SKRIPTA IZ HIRURGIJE Eng PDF
SKRIPTA IZ HIRURGIJE Eng PDF
SKRIPTA IZ HIRURGIJE Eng PDF
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In few months enthusiastic followers of ether narcosis appeared in all civilized countries.
At the beginning of February 1847 this type of narcosis was performed by professor F.I.
Inozemtsev in Moscow clinic, two weeks later it was performed in St. Petersburg by our
compatriot, surgeon Mykola Ivanovych Pirogov. This outstanding surgeon and the first
anaesthesiologist played prominent role in the history of ether narcosis. He was the first to
argument theoretical basis for the action mechanism of ether on the central nervous system; he
proposed alternative ways of administration of ether (into the trachea, in the blood, into the
gastrointestinal tract). Invaluable experience of ether narcosis M. I. Pirogov described in his
monograph On the application of sulphuric ether vapours in operational medicine published in
1847.
In the Crimean-Turkish war (1853 1856) our compatriot performed hundreds of
successful ether anaesthesias during surgeries on gunshot injuries.
In 1937 Guedel determined the clinical stages of ether narcosis, which are still considered
to be classic.
In 1847 a prominent scientist Simpson introduced into clinical practice another
preparation for narcosis - chloroform.
Since that time anaesthesiology has begun its scientific development.
For 150 years of anaesthesiology history scientists proposed and implemented in clinical
practice dozens of anaesthetic preparations, both inhalation and non-inhalation, as long as various
types and methods of pain relief. This stimulated development of operative surgery and allowed
various range of surgical interventions in all organs and systems of the body.
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Anaesthesiology is a science that studies how to protect the organism from operating
injuries. It improves the well-known and develops new methods of preparing patients for
surgeries, providing anaesthesia, controlling the body functions during the operation and in
postoperative period.
In the preoperative period it is essential to clarify the nature of operation: planned, urgent
or emergency:
a) in case of planned surgeries with decompensated comorbidities there should be an
adequate therapy performed at first; If necessary ask other specialists to take part in the treatment;
b) if an operation is urgent the main vital parameters should be stabilized in short term,
further correction should be made during the operation;
c) in case of emergency the patient is transferred to the operating room as soon as
possible, as anaesthesia and surgery are critical factors in saving his/her life. Stabilization of vital
functions is achieved on the operating table.
During the examination of the patient special attention should be paid to the condition of
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the central and peripheral nervous system (mental and emotional lability, sleep disorders, the
presence of anxiety and fear, paresis and paralysis). Constitution of the body, anthropometric data
(weight and height) should be determined. The attention is paid to the subcutaneous fat and its
distribution, peripheral veins.
While examination should be assessed: the skin and its colour, temperature, humidity and
turgor of tissues (particular attention is paid to the capillary refill - press the nail of the patient for
5 seconds and if the white spot after pressing will not disappear in 2 seconds microcirculation is
violated); anatomical features of the upper respiratory tract: the width of mouth opening, the size
of oral cavity, presence of dentures, caries teeth, type of bite, the size of the tongue, size of
tonsils, size of the nasal passages; shape of the neck and its size, the size of the thyroid gland.
Reserves of respiratory system are determined by spirometry tests (breath-holding after
maximal inspiration and expiration tests of Stange and Hench). Normally they are 50 - 60 sec.
and 35 - 45 sec., respectively. If necessary, more detailed study called spirography is made.
The breathing rate should be determined and the chest should be examined (palpation,
percussion and auscultation).
While assessing the state of the cardiovascular system, it is necessary to auscultate the
heart, measure blood pressure and evaluate the pulse. In case of cardiac rhythm disorders, it is
necessary to measure pulse deficit (the difference between the heart rate and the pulse rate on the
radial artery per minute). An electrocardiogram should be made in order to make a detailed study
of the disorder.
Examination of the digestive system should start from the tongue, which gives
information about the degree of organism dehydration (dry tongue, marked buds, available
longitudinal grooves), the severity of stomach inflammation (the tongue is coated), convulsions in
anamnesis (scars on the tongue from biting), manifestations of avitaminosis and fungal diseases
("geographic", raspberry tongue). Also the inspection, palpation, percussion and auscultation of
the abdomen should be made. Always check the symptoms of peritoneal irritation and muscular
defence of the anterior abdominal wall. Ask the patient about the distension of the abdomen,
nature, and frequency of defecations.
The urinary system should be assessed by palpation of the kidneys and lower abdomen
(projection areas of the bladder), check of Pasternacki symptom. The frequency, volume and
nature of urination, colour and odour of the urine should be determined. In urgent and emergency
surgery with suspicion of renal insufficiency the bladder should be always catheterized in order to
control the urination during surgery.
Don't forget to assess the probability of thrombosis: identify peripheral veins of lower
extremities, swelling and pain of the ankles. Laboratory tests and instrumental examinations are
also very important. The required minimum of these examinations depends on the urgency of an
operation.
In emergency surgery as soon as possible (often right during the operation) the following
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contents into the airways (one of the most common and severe complications of anaesthesia).
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- pain relieve;
- neuro-vegetative protection;
- muscle relaxation;
- adequate ventilation;
-optimal level of blood circulation;
- normalization of metabolic processes in tissues.
Narcosis (from narkosis - get torpid) is the process of temporary reversible depression of
the central nervous system caused by pharmacological agents.
Analgesia (from Greek analgesio - no pain) absence of pain sensitivity.
Anaesthesia (from Greek anaestesio loss of sensation) - a set of methods used to
remove all kinds of sensitivity.
Anaesthetics - pharmacological agents, which eliminate sensitivity.
Anaesthetics can have general (agents for narcosis) or local action (medicines for regional
anaesthesia).
Depending on the way of admission anaesthetics are divided into inhalational and
non-inhalational (mostly intravenous).
During inhalation anaesthesia gases or vapour of anaesthetics enter the patients through
the airways and lungs (anaesthesia machines are connected with the mask, endotracheal tube,
tracheostomy tube, etc.) This type of anaesthesia is characterized by the simplicity of the method
and high degree of control. The most common anaesthetics are: nitrous oxide, sevoflurane,
isoflurane, xenon. Ether and phtorotan have now historical meaning.
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Unlike general anaesthesia (narcosis), during regional anaesthesia patients are conscious.
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1. Nitrous oxide ( N2O) is a gas stored in liquefied state under the pressure of 50
atmospheres in the cylinders of grey colour (in French-speaking countries, these tanks are painted
blue!). From 1 kg of liquid N2O about 500 litres of colourless inflammable stable gas are formed.
To prevent gas freezing at the outlet of the container it is necessary to use a special type of
reductors (ribbed). Gas supply of the anaesthetic machine is performed through a high-pressure
hose. Dosage control is made with special flow measurement devices (rotameters).
Nitrous oxide should be always combined with oxygen in the anaesthetic mix, otherwise
patient can die; usually a ratio of 1:1, 2:1, 3:1 are used.
Note that false connection of nitrous oxide supply hose to the oxygen supply inlet is
dangerous for the patient!
This gas does not cause unconsciousness, has a weak anaesthetic and mild analgesic
(pain-relieving) properties. It is not toxic for the patient and it can be combined with other
inhalation and intravenous anaesthetics.
Harmful effects of nitrous oxide are noticeable when its concentrations in the respiratory
mixture is over 75 - 80% (in these cases, the oxygen content in the mixture is lower than 20%,
which is life-threatening).
Nitrous oxide is used in combination with other anaesthetics to enhance their effects
during various anaesthesias, in the form of oxide-oxygen mixture - for pain relief during attacks of
angina pectoris, myocardial infarction, complicated and uncomplicated childbirth.
2. Anaesthetic ether was widely used in anaesthesiology for about 150 years.
Although currently ether is not used it is a classic of anaesthesiology.
Ether is a colourless volatile liquid with a specific odour. It is produced in orange bottles
of 100 and 150 ml. Boiling point of ether is 37. It is explosive!
Ether is a potent anaesthetic, which causes unconsciousness, analgesia and muscle
relaxation. It has sympathomimetic effects (causes tachycardia, increases blood pressure,
stimulates the activity of the salivary and bronchial glands, increases level of sugar in the blood,
stimulates the respiratory centre).
In toxic doses, ether depresses the activity of the heart, liver and kidneys. It irritates the
respiratory tract. Therefore, rapid increase of its concentration in the breathing mix can cause
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Pre-agonal signs of ether overdose: clammy cold sweat, grey skin colour, the sphincter
relaxation and spontaneous urination and defecation.
During the recovering of the patient the same stages are observed, however in reverse
order.
3. Fluothane (halothane) was widely used at the end of the 20th century, hoqever now its
not popular. It was discovered by Raventos in 1956. It is a clear liquid with a sweet odour, not
explosive. It is produced in bottles dark glass (capacity 50, 150, 250 ml).
Fluothane is characterized by severe anaesthetic and weak analgesic effect. It depresses
the secretion of the salivary and the bronchial glands, extends the bronchi. The drug depresses the
larynx and throat reflexes, the respiratory centre and relaxes the cross - striated muscles. It also
causes myocardial depression.
Fluothane has a short therapeutic range, its overdose is characterised by hypotension and
bradycardia.
During fluothane narcosis it is contraindicated to use sympathomimetics! Fluothane
increases catecholamine sensitivity of the myocardium. Adrenaline, noradrenaline and other drugs
of this group during fluothane anaesthesia can cause myocardial fibrillation, followed by cardiac
arrest.
For the narcosis fluothane should be filled in special evaporators of anaesthetic machines,
which are situated beyond the circulation circuits. This is the way of overdose prevention.
Mask fluothane-oxide-oxygen narcosis was widely used in paediatric anaesthesiology,
during short-term and small traumatic surgery. As medical narcosis - (manipulation of despair) - it
is used for the immediate spasm relief when there is no venous access (epileptic state, seizures in
case of eclampsia, meningitis, tetanus) for the treatment of bronchial spasm in patients with
asthmatic conditions.
Fluothane anaesthesia is contraindicated for the patients with low blood pressure,
deficiency of circulating blood volume (massive haemorrhage), heart failure, insufficiencies of
parenchymal organs (liver-kidney failure).
4. Sevoflurane (Sevoran) was first synthesized in 1969 in the USA, now it is leading
among the inhalational anaesthetics. It is a clear, colourless, mobile liquid with floral odour. It is
produced in bottles of 100 and 200 ml.
Sevoran can be applied for initial anaesthesia, and for its maintaining. Sevoran is easily
controlled: rapid induction of patients and quick recovery after termination of anaesthetic supply
are its known benefits.
Initial narcosis is characterized by minimal excitement and absence of upper respiratory
tract irritation. Sevoran causes dose-dependent inhibition of respiratory function and decrease of
blood pressure. Therefore, its dose should be selected individually to achieve the desired effect,
taking into account age and state of the patient.
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7. Xenon.
Xenon has been allowed for medical use as a preparation for inhalation general
anaesthesia since 1999. This drug belongs to inert gases, that is why it does not enter into any
chemical reaction in the body and it is not subjected to biological transformation. However, it has
significant analgesic and anaesthetic effects (1.5-2 times more potent than nitrous oxide).
Clinical course of Xenon narcosis: after 5-6 inhalations of narcotic concentration of
xenon the first stage occurs peripheral paraesthesia and hypalgesia. Numbness and heaviness in
the legs gradually rises upwards, spreading onto the skin of the abdomen, chest, neck and the
head. In 2-3 minutes appears the second stage of euphoria and psychomotor activity, that is
rapidly changing into the third stage of complete analgesia and partial amnesia. With the loss of
consciousness, there is the fourth stage of complete analgesia and anaesthesia (corresponding to
the first surgical stage of ether narcosis). At this stage, in conditions of mono-narcosis and
spontaneous respiration, it is possible to perform surgery without the narcotic analgesics.
Cardiovascular and respiratory systems (gas exchange) are stable.
Analgesia occurs in case of inhalation of 30-40% mixture with oxygen, the loss of
consciousness occurs during inhalation of 65-70% of mixture. Muscle relaxation is quite
significant. Recovery fast: in 2-3 minutes after gas supply is turned off, the patient is entirely
conscious with pleasant subjective sensations.
Xenon can be used as an anaesthetic for various surgical operations, childbirth, painful
manipulations; for relieving of pain attacks and treatment of pain syndromes and depression states
in all fields of medicine, especially in patients of high risk groups. It is not toxic, that is why
xenon should become an anaesthetic of choice, "gold reserve" during operations of patients with
high anaesthesiology risk.
Xenon is used as a single component of anaesthesia (mask and endotracheal option) or in
combination with various intravenous preparations: sedatives, narcotic and non-narcotic
analgesics, neuroplegics, tranquilizers, gangliolytics etc.
Xenon can also be used for treatment at pre-hospital stage (emergency and urgent medical
care to relieve pain in case of myocardial infarction, angina pectoris, burn or skeletal injuries,
asthma attacks with the usage a special devices (mixture of Xe: O2 - 50:50). It can be used as an
antidepressant in neurotic and stress-anxiety disorders and other neurological conditions, to
relieve abstinent syndrome, in treatment of motor aphasia, dysarthria.
Non-inhalational anaesthesia occurs in case of the parenteral injection of
anaesthetics. The most common way of administration is intravenous route.
1. Derivatives of barbituric acid.
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Sodium thiopental (hexenal) was first described by Lundy in 1934. It is a powder of green
(sodium thiopental) or white (hexenal) colour. It is produced in bottles of 0.5 and 1 gram.
Immediately prior to anesthesia, this powder is dissolved with distilled water (isotonic solution of
sodium chloride) up to 1% concentration.
Barbiturates have narcotic effect (cause unconsciousness) with minor pain relief effect.
Therefore, they are used for initial narcosis, during the painless manipulations. For anaesthesia
during barbituric narcosis it is necessary to introduce additional narcotic analgesics (morphine
hydrochloride, phentanyl).
Easy, pleasant for the patient falling asleep and lack of excitement at the same time led to
widespread use of sodium thiopental and hexenal in the practice of an anaesthesiologist.
In addition, due to strong anticonvulsant effect barbiturates are used for removal of
cramps in patients with epilepsy, tetanus, meningitis, eclampsia etc.
Derivatives of barbituric acid have parasympathomimetic properties. Therefore, at the use
of them the following complications are possible: cough, bronchial spasm, laryngeal spasm. They
inhibit the activity of the respiratory centre, with fast intravenous administration of large doses of
sodium thiopental or hexenal respiratory arrest is possible.
Barbiturates may be used only when the apparatus for artificial ventilation of the lungs is
available!
A nurse anaesthetist should prepare anaesthetic for anaesthesia and give it to the patient
by the anaesthesiologists instruction. She should dissolve in aseptic conditions 1 gram of sodium
thiopental in 100 ml of 0.9% solution of sodium chloride (up to 1% concentration). After venous
puncture and managing system for infusion therapy (only by the anaesthesiologists instruction)
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she should introduce 1-2 ml of anaesthetic intravenously. Waiting for 1 - 2 minutes, she should
determine if the patient has sensitivity to thiopental sodium, if the solution is not under the skin.
Then she should introduce the rest of the drug. The dose of anaesthetic is especially individual
(from 4 to 8 mg / kg of body weight). Barbituric narcosis lasts 15 - 30 minutes. To continue
narcotic sleeping the patient should be administered 10 - 20 ml of 1% solution or use other
anaesthetics.
2. Sodium oxybutyrate (GOBA).
Sodium salt of gamma-oxybutyric acid (GOBA) was first described by H. Laborit in 1960.
It is produced in ampoules of 10 ml of 20% solution. It has sedative and narcotic effect.
Anaesthetic effect is not significant.
Sodium oxybutyrate - derivative of gamma-aminobutyric acid - a natural metabolite of the
organism. Therefore, its use does not cause toxic effects in patients. Involving in metabolic
processes, GOBA normalizes cellular respiration, transmembrane potential, moving potassium
from blood plasma into the cells, due to that excitation processes of cells of the heart, brain, etc.
decrease.
Sodium oxybutyrate also belongs to the group of anti-hypoxants, so it is widely used in
intensive care of patients with disabilities of the cardiovascular system (in shock), with severe
hypoxic conditions (after having survived clinical death, brain damage, in obstetrics).
Anti-hypoxic dose (20-40mg/kg body weight) effectively affects tissue respiration, optimizing it.
GOBA at this dose does not influence on consciousness of the patient.
As a means of anaesthesia, it is a method of choice in accompanying diseases of the
cardiovascular system, the liver, the kidneys, diseases of the endocrine organs, in neurosurgical
operations and in the pathology of pregnancy. In the intravenous method, it can be used
intramuscularly, orally, rectally.
For anaesthesia GOBA is used at a dose of 70 - 120 mg / kg of body weight. A nurse -
anaesthetist introduces it, following doctors instructions, intravenously slowly by 10 ml. In order
to prevent spasms, GOBA should be introduced together with barbiturates. For this 20-milliliter
syringe should be filled with sodium oxybutyrate (10 ml) and sodium thiopental (10 ml). This
mixture can be administered quickly. After repeated (3-5 times) injection of the mixture in 5 - 10
minutes the patient falls asleep, which resembles the physiological sleep. A rare, deep breathing,
muscle relaxation, inhibition of reflexes are observed. Haemodynamics is not disturbed. Narcotic
sleep lasts for 1 1,5 hours, its after-effect - up to 5 hours. At this time the patient needs to be
looked after because retraction of the tongue, disorder of the lung ventilation may occur.
3. Ketamine.
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Ketamine (ketanest, kalipsol, ketalar, velonarkon, petar) was described by Karsen and
Domino in 1965. This group of drugs, has the ability to depress the function of some parts of the
central nervous system and increase the activity of others, causing a so-called dissociative
narcosis. Ketamine is a clear liquid, unstable to light, produced as 1 or 5% solution in bottles of
darkened glass (10 ml), or in ampoules (2 ml). Ketamine is a strong anaesthetic, causing a deep
sleep with moderate anesthesia. Due to selective stimulation of certain parts of the brain (limbic
structures), during ketamine mono-narcosis patients may have visual hallucinations. In addition,
ketamine causes a slight neuro-vegetative inhibition, relaxation of the cross - striated muscles with
preserved tendon reflexes. It increases blood pressure, heart rate, slightly depresses respiration
and stimulates the production of cerebrospinal fluid (liquor).
According to its characteristics ketamine is a tool of choice in patients with deficiency of
circulating blood volume (hypohydration, hypotension, and various types of shock, collapse), in
the need of anaesthesia with preserved spontaneous breathing. Due to its universal administration
(intravenous, intramuscular and rectal) this anaesthetic is widely used in paediatric
anaesthesiology.
Ketamine can be administered intravenously at doses of 2 - 3 mg / kg or intramuscularly at
doses of 7-15 mg / kg. To avoid unwanted hallucinatory effect it is used with tranquilizer solution
(1 - 2 ml of 0.5% sibazon solution).
Ketamine can be combined with various inhalation and non-inhalation preparations in the
combined narcosis.
Ketamine anaesthesia is contraindicated for patients with hypertension, liquor
hypertension (traumatic brain injury, epilepsy), with mental disorders.
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After diprivan narcosis (even long-term) the patients wake up fast during 10 minutes. This
feature, as well as normalization of haemodynamics during laparoscopic surgery, the minimum
number of complications and contraindications make propofol a drug of choice in modern
anaesthesiology.
Combined general anaesthesia with muscle relaxants.
To achieve general anaesthesia most effectively use a combination of several anaesthetics
should be. In these cases, the dose of each anaesthetic is reduced (and, respectively, their toxicity),
therapeutic effect is increased. The use of muscle relaxants and muscle relaxation by themselves
still reduce the need for anaesthetic, facilitating optimal performance of surgeons in the depth of
the wound.
Muscle relaxants are divided into depolarizing and anti-depolarizing. The first are
short-term, causing febrile twitching of the facial muscles, muscles of the trunk, the limbs, the
diaphragm, followed by relaxation of the muscles and vocal cords up to 4-6 minutes. Ditylin
(succinylcholine) is produced in ampoules of 5 ml of 2% solution, usually used for tracheal
intubation at a dose of 2 mg / kg (7 - 10 ml) intravenously.
Anti-depolarizing muscle relaxants cause long-term (from 25 min. to 1,5 hours) muscle
relaxation in patients without prior fibrillation, so they are used during prolonged operation on
the organs of the abdominal cavity, the chest, etc. They include tubocurarine chloride, pavulon,
arduan, tracrium. Arduan is produced in bottles, 4 mg of dry substance. Before the administration
muscle relaxant should be dissolved in 2 ml of isotonic solution of sodium chloride, applied at a
dose of 0.04 mg / kg (1.5-2 ml) intravenously, every 40 - 45 minutes the drug is re-administered in
the half dose.
As a multi component intravenous narcosis with muscle relaxation and artificial
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ventilation of the lungs neuroleptanalgesia, ataralgesia, central analgesia are often used.
Neuroleptanalgesia (NLA). For NLA neuroleptic droperidolum and narcotic analgesics
phentanyl are used either alone or in combination with other inhalation or non-inhalation
anaesthetics.
Droperidolum is produced in bottles: of 10 ml transparent colourless liquid, which
contains 25 mg of preparation (0.25% solution). The drug has a marked antishock effect: it blocks
extra excitement of the sympathic-adrenal system, normalizes the activity of the reticular
formation, relieves spasm of arterioles (alpha adrenolytic influence on the system of
microcirculation), does not cause unconsciousness. Duration of the drug action is up to 3-4 hours.
Phentanyl is produced in ampoules of 2 ml of 0.005% solution. It has short-term
analgesic effect (up to 30 minutes), which allows to manage anaesthesia by minimizing the risk of
drug inhibition of the respiratory centre in patients in the postoperative period.
When using the classic technique of NLA is administered intravenously 0,25-0,5 mg/kg of
droperidolum and 0.005 mg/kg of phentanyl (6-8 ml of droperidolum solution and 6-8 ml of
phentanyl solution for 1 hour anaesthesia). To cause unconsciousness the respiratory mixture of
dinitrogen oxide and oxygen in the ratio 70%: 30% is used. After the introduction of muscle
relaxants the patient is intubated, artificial ventilation of the lungs is performed. To maintain
narcosis 1-2 ml of droperidolum and phentanyl should be administered every 20-30 minutes.
Tachycardia is indication for re-administration of phentanyl, hypertension for re-administration of
droperidolum.
Neuroleptanalgesia is used for very weak patients with high operational risk, in disorder
of haemodynamics and the need of artificial ventilation of the lungs in the postoperative period.
Ataralgesia is the way of general anaesthesia with sedation preparations (ataractics) and
narcotic analgesics.
Ataractic seduxen (diazepam, relanium, sibazon) is produced in ampoules of 2 ml of 0.5%
solution. It cannot be dissolved or mixed with other drugs (white precipitate is formed!).
For narcosis seduxen is administered at a dose of 0.3-0.5 mg/kg and intravenously
mixture of dinitrogen oxide with oxygen (2:1) is used. Anaesthetic effect is obtained by
introducing phentanyl fractionally or other narcotic analgesic (morphine hydrochloride, dipidolor,
pentazocine) at doses as for NLA. To achieve muscle relaxation muscle relaxants are used, and to
ensure adequate breathing - artificial ventilation of the lungs is used. During the surgery by
indications (tachycardia, increased blood pressure) seduxen is re-administered (usually in 1,5
hour) and phentanyl (in 20-30 min.)
The advantage of this narcosis is its minimal adverse effects on various organs and
systems so that ATA is used in patients with accompanying pathology of the heart, the liver, the
kidneys etc.
Central analgesia is the way of narcosis in which anaesthesia, hyporeflexia and neuro-
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purpose, he closes by his finger adapter of breathing circuit of working apparatus, following the
manometer. In its indications of 300 mm.of water column dehermetisation valve must operate;
-efficiency work of electric suction machine (having closed a rubber hose by finger,
follows the vacuum manometer deflection);
-working condition of laryngoscopes. After its turning on the lamp must light;
-state of cardiomonitor, pulse oximeter.
Preparing an anaesthetists working place
While preparing the anaesthetists table to work one should follow the order of setting
instruments and medical preparation for narcosis and intensive care.
First, a table is covered with a sterile cloth. Then successively disposable syringes are put:
in the lower left corner - two of 20-milliliter for 1% thiopental sodium solution (hexenal,
propofol) in the lower right corner - syringes for muscle relaxants: 10 ml of capacity for 2%
Dithylin solution (listenon , myorelaxant) and 2 ml for 0.2% for arduan solution. Behind them
5-milliliter syringe is located for narcotic analgesics (0.005%. phentanyl solution). In the upper
right corner there should be 5 ml syringe for solutions of sibazon, droperidolum, ketamine. In the
upper left corner - syringes of 5 and 10 ml capacity for other drugs (ganglioblockers, clopheline,
dalargin, etc.). Among them there are placed two glass vessels (of 100 ml of capacity) filled with
0.9%, sodium chloride solution. In the left bowl the powder of sodium thiopental is dissolved up
to 1% concentration; 0.9% sodium chloride solution in the right bowl is used for dissolving other
drugs just before their intravenous introduction.
In a separate tray must be sterile gauze wipes and forceps, next to a bottle with antiseptic
solution (70% of ethyl alcohol).
The desk drawer is designed to store pharmacological preparations needed during surgery,
intravenous catheters, disposable system for transfusions, adhesive plaster, etc.
On the shelf under the box an anaesthetist places the bottles of infusion-transfusion
preparations.
In a separate tray a set for tracheal intubation is form: laryngoscopes with a set of blades
(large, medium, small), intubation tubes of various sizes and throat mask, air-way, mouth dilator, a
connector of the intubation tube, syringe for cuff blow of the intubation tube, Kocher clamp,
napkins.
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consciousness, they can remember some episodes of the operation. It is very unpleasant
complications of anaesthesia, however, it is quite a rare event, since the modern system of
monitoring can prevent the development of such complication.
Rare and very rare side effects and complications of anaesthesia.
Nerve injury, as a complication of anaesthesia. This type of complication is characterized
by a sense of numbness, tingling or pain. There may be a disorder of heat or cold sensitivity.
Additionally, there may be a feeling of weakness or paralysis. Typically, all complaints disappear
in a few days or months. Complete recovery can sometimes be delayed up to a year. The most
common is ulnar nerve injury in the ulna nerve area and fibular nerve in the knee.
Nerves may be injured during epidural and spinal anaesthesia. This complication is rare
and usually disappears within a few weeks or months. Cases of temporary immobilization
(paralysis) of one or two extremities are very rare (1:50 000).
Reasons that may cause nerve injury:
- Nerve may be injured by a surgeon during some operations (it is sometimes difficult and
unavoidable);
- The position in which the patient lies on the operating table can lead to nerve
compression or tension, damaging it;
- The use of turnstiles by a surgeon to reduce the amount of blood loss during surgery
puts pressure on the nerve, also contributing to its injury;
- The cause of nerve compression may be post-operative swelling of the tissues.
Allergic reaction (anaphylaxis). During anaesthesia, as well as, during the patients stay in
hospital medications may cause severe allergic reaction - anaphylaxis. The frequency of
development is 1:15000 of anaesthesia. Usually, an anaesthesiologist successfully diagnoses and
treats this terrible complication, however, statistically one of twenty of such severe reactions can
lead to death.
Injury of the eyes during general anaesthesia. This is a rare complication of narcosis. The
most frequent type of eye injury during and after general anaesthesia is damage of the cornea
(1:2000 anaesthesias). This condition does not affect visual acuity, but may cause a dark point in
the damaged eye. Most corneal injury is due to the fact, that during anaesthesia the patient's
eyelids are not always completely closed. Consequently, the cornea becomes dry and the eyelid
"sticks" to it from inside. Then, when the patient opens the eyes and corneal injury occurs.
Death or brain injury.
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Tracheal intubation
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cords.
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Epidural anaesthesia.
Indications: anaesthesia in surgery on the abdomen, the pelvis and the lower
extremities; intensive therapy of pathological conditions in which a temporary medication
denervation of appropriate segments of the body is necessary (asthmatic status, myocardial
infarction, pulmonary oedema, acute pancreatitis, paralytic intestinal obstruction, frostbite of
the lower limbs etc.).
Picture 1.4 Choice of the place for puncture in epidural anaesthesia, depending on the
required level of anaesthesia
Necessary equipment: a needle with a stylet for puncture of epidural space (Tyoxi),
Dyufo needle, a needle for intramuscular injections, syringes of 2 ml of capacity with a light
piston moving and of 10 ml with the adapter to the catheter, epidural catheter, Kocher clamp,
sterile gauze tampons, a solution of ethanol, adhesive plaster, the solution of local anaesthetic.
Methods of administration
The equipment is placed on the sterile surface (a nappy) of the manipulation table.
The patient is placed on the operating table lying on his side or sitting, bending his
body maximum (moving the head to the knees).
A place for puncture is chosen, according to the indications (the required level of
anaesthesia).
The operating field and the anaesthesiologists hands are washed according to the
rules of asepsis and antisepsis.
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Infiltration anaesthesia of soft tissues from the puncture along the needle (introducing
it in the sagittal direction, in the middle between the osseous processes of the spine) is
administered.
Piercing the skin and subcutaneous fat tissue with Dyufo needle, creating a channel of
2 - 2.5 cm in depth.
Along the channel in the sagittal direction Tyoxi needle with a stylet is introduced in a
depth of 3 - 4 cm, piercing upper osseous and intra-osseous ligaments.
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In case of a long-term anaesthesia the epidural space is catherized, moving the catheter
through the Tyoxi needle to a depth of 7 - 8 cm. The needle is carefully removed, an aseptic
bandage is put on the place of the puncture, and the catheter is fixed to the skin by adhesive
plaster. A syringe with adapter is attached to the outer end of the catheter. First a test dose is
administered and then, in the absence of symptoms of spinal anaesthesia - the rest of the
required dose of anaesthetic.
Conductive anaesthesia.
In large traumatic operations (femur amputation, under-knee leg amputation) the most
reasonable is the use of methods of conductive anaesthesia by blocking the sciatic and femoral
nerve in the proximal regions.
The rear (proximal) blockade of the sciatic nerve (according to Rai).
Indications: In case of large operations (usually amputation of the lower third of the
thigh), especially when the patient in some reason cannot be placed on the side or on the
abdomen.
Necessary equipment: a 10-centimeter needle type UP 20G cut on 15-30 degrees; an
anaesthetic - 20-30 ml of 1% xylonest solution (or mepivacaine, or lidocaine).
Anatomical orientation: a large trochanter of the femur, a sciatic tuber.
Methods of administration. The patients position: on the back, the assistant lifts up
the patients leg, bending it at 90 degrees in the hip and knee joints. An anaesthesiologist
marks the line between the large trochanter and the sciatic tuber, strictly in the middle of
which, perpendicular to the skin introduces the needle, pushing it into the cranial direction.
At a depth of 5-10 cm during electrical stimulation (0.3 mA / 0.1 ms) foot bending
appears (fibular nerve stimulation) or its extension (tibial nerve stimulation);
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Blockade of the femoral nerve in the inguinal region (by Vinnie Rosenblatt).
Indications: In case of large operations (amputation of the lower limb).
Necessary equipment: a 5-centimeter needle type UP 18G; an anaesthetic - 20-30 ml of
1% xylonest solution (or mepivacaine, or lidocaine).
Anatomical orientation: the inguinal fold, the femoral artery.
Methods of administration. The patients position on his/her back, the lower limb is
slightly drawn aside and rotated outward. The place of injection: 2 cmbelow the inguinal fold
and 1.5 cm outside of the artery. A needle with electric stimulator is injected at an angle of 30
degrees into the skin in cranial direction to the sense of a double downfall on the passage of
two fascias. Motor response is proved by contraction of the quadratus femoris muscle and the
patella tingling during electrical stimulation 0.3 mA / 0.1 ms
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this purpose the needle 19,5 G and catheter 20G should be used, which is injected to a depth of
4-5 cm cranially from needle cut. The anaesthetic is administered at a speed of 6 ml/hour, with
optimum use of continuous administration of anesthetic by infusion pump.
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cyanotic, the neck veins became swollen, the pupils became dilated.
Specify the complication, its probable causes and sequence of nurse (anaesthetist)
actions.
Task 3
What preoperative preparation does a 73-year-old patient S. need? He has been admitted
to the surgical department with clinical signs of adhesive intestinal obstruction. On examination
of the patient hypotension (BP -90 and 60 mm Hg.), tachycardia (heart rate - 112 per minute) have
been revealed
Task 4
During intravenous anaesthesia the patients breathing became discontinuous, noisy,
"gurgling": from the mouth gastric content appeared. What has happened? Determine the sequence
of emergency aid.
Task 5
While performing tracheal intubation, an anaesthesiologist observed stomach contents in
the mouth of the patient, which slowly moved between the vocal chords into the trachea.
Determine the type of complication, its cause and probable course of the disease, and
emergency aid that is necessary for the patient.
Task 6
An anaesthesiologist performed intubation to the patient and connected the intubation
tube to the breathing apparatus. With air supply there appeared typical "gurgling" sound.
Simultaneously, in the patient began to project epigastric area of the abdomen, breathing in the
chest was not available.
Determine the type of complication and urgent aid.
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Dehydration signs: weight loss, decrease of skin turgor and eyeballs tone, dry skin and
mucous membranes; low central venous pressure, cardiac output and blood pressure (collapse is
possible); decreased urine output and peripheral veins tone; capillary refill over 2 seconds
(microcirculation disorders) and low skin temperature; intracellular dehydration is characterized
with thirst and consciousness disorders. Laboratory tests show blood concentration: hematocrit,
hemoglobin concentration, protein level and red blood cells concentration increase.
Overhydration appears in case of:
- excessive water consumption, inadequate infusion therapy;
- acute and chronic renal failure, hepatic and cardiac insufficiency;
- disorders of fluid balance regulation;
- low protein edema.
Clinical findings in case of overhydration are: weight gain, peripheral oedema,
transudation of the plasma into the body cavities (pleural, abdominal), high blood pressure and
central venous pressure. In case of intracellular overhydration appear additional symptoms:
nausea, vomiting, signs of cerebral edema (spoor, coma). Laboratory tests prove hemodilution.
According to the osmotic concentration of plasma dehydration and overhydration are
divided into hypotonic, isotonic and hypertonic.
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Isotonic dehydration is caused by equal loss of electrolytes and fluid from the
extracellular space (without cellular disorders).Blood tests show hemoconcentration; sodium level
and osmotic concentration are normal.
To treat this type of water imbalance use normal saline solution, Ringer solution, glucose-
saline solutions, etc.. The volumes of infusions can be calculated according to the formula:
VH2O= 0,2*BW* (Htp-0,4)/0,4 ,
Hypertonic dehydration is caused by mostly water loss: first it appears in the vascular bed,
than in the cells. Laboratory tests show hemoconcentration: elevated levels of proteins, red blood
cells, hematocrit. Plasma sodium is over 155 mmol/l and osmotic concentration increases over 310
mOsm/l.
Intensive treatment: if there is no vomiting allow patients to drink. Intravenously give
0,45% saline solution and 2,5 % glucose solution, mixed with insulin. The volume of infusions is
calculated according to the formula:
VH2O=0,6*BW (Nap -140)/140,
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Sodium is the main extracellular cation. Its normal plasma concentration is 135-155
mmol/l. Daily required amount of potassium is 2 mmol/kg of body weight.
Sodium concentration which is lower than 135 mmol/l is known as hyponatraemia.
This condition is caused by sodium deficiency or water excess. Sodium deficiency is
calculated according to the formula:
Nad= (140-Nap)*0,2 BW,
Na- sodium deficiency, mmol;
Nap sodium concentration of the patient mmol/l;
0,2*BW extracellular fluid volume, l.
To treat it use normal saline (1000 ml contains 154 Na mmol) or 5,8% solution of
sodium chloride your choice will depend on osmotic concentration.
Sodium concentration over 155 mmol/l is a state called hypernatremia. This condition
usually appears in case of hypertonic dehydration or hypertonic overhydration. Treatment was
described in the text above.
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Chlorine is the main extracellular anion. Its normal plasma concentration is 98-107
mmol/l. Daily requirement of chlorine is 215 mmol.
Hypochloremia is a condition of decreased plasma chlorine concentration (less than 98
mmol/l).
Chlorine deficiency is calculated according to the formula:
Cld = (100-Clp)*0,2 BW,
Cld- chlorine deficiency, mmol
Clp plasma chlorine concentration of the patient, mmol/l
0,2*BW extracellular fluid volume, l.
To treat hypochloremia use normal saline (1000 ml contains 154 mmol of chlorine) or
5,8% sodium chlorine solution (1 ml contains 1 mmol of chlorine). The choice of solution
depends on the osmotic concentration of the plasma.
Hyperchloremia is a condition of increased chlorine concentration (over 107 mmol/l).
Intensive therapy of this state includes treatment of the disease, which caused it (decompensated
heart failure, hyperchloremic diabetes insipidus, glomerulonephritis). You can also use glucose,
albumin solutions and dialysis.
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BW body weight, kg
Control tasks.
Task 1.
Calculate the total body water volume and its extracellular and intracellular volumes of
the Patience, the patient of 48 years and body weight 88 kg.
Task 2.
Patience, the patient of 23 with body weight 70 kg has sodium level 152 mmol/l and
hematocrit 0,49 l/l. Name the type of water balance disorder.
Task 3.
Patience, the patient of 54 with body weight 76 kg has sodium level 128 mmol/l.
Calculate the volume of saline and 7,5% sodium chloride solution necessary for the treatment of
this condition.
Task 4.
Patience, the patient of 60 with body weight 60 kg has sodium level 140 mmol/l and
hematocrit 0,55 l/l. Name the type of disorder and prescribe infusion therapy.
Task 5.
Patience, the patient of 42 with body weight 80 kg has potassium level 2,6 mmol/l.
Calculate the volume of 4% potassium chloride solution necessary for treatment of this
condition.
Task 6.
Patience, the patient of 33 with body weight 67 kg and diagnosis gastric ulcer,
complicated with pylorostenosis has potassium concentration 3 mmol/l, chlorine concentration
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Physiologically insignificant amounts of water are distributed beyond the tissues in the
body cavities: gastrointestinal tract, cerebral ventricles, joint capsules (nearly 1% of the body
weight). However during different pathologic conditions this third space can cumulate large
amounts of fluid: for example in case of ascites caused by chronic cardiac insufficiency or
cirrhosis abdominal cavity contains up to 10 liters of fluid. Peritonitis and intestinal obstructions
remove the fluid part of blood from the vessels into the intestinal cavity.
Severe dehydration is extremely dangerous for the patient. Water gets to the body with
food and drinks, being absorbed by the mucous membranes of gastro-intestinal tract in total
amount of 2-3 liters per day. Additionally in different metabolic transformations of lipids,
carbohydrates and proteins nearly 300 of endogenous water are created. Water is evacuated from
the body with urine (1,5-2 liters), stool (300 ml), perspiration and breathing (those two reasons
are combined as perspiration loss and make from 300 to 1000 ml per day).
Water balance is regulated through complicated, but reliable mechanisms. Control over
water and electrolytes excretion is realized by osmotic receptors of posterior hypothalamus,
volume receptors of the atrial walls, baroreceptors of carotid sinus, juxtaglomerular apparatus of
the kidneys and adrenal cortical cells.
When there is a water deficiency or electrolytes excess (sodium, chlorine) thirst appears
and this makes us drink water. At the same time posterior pituitary produces antidiuretic hormone,
which decreases urine output. Adrenals reveal into the blood flow aldosterone, which stimulates
reabsorption of sodium ions in the tubules and thus also decreases diuresis (due to osmosis laws
water will move to the more concentrated solution). This way organism can keep precious water.
On the contrary, in case of water excess endocrine activity of glands is inhibited and water
is actively removed from the body through the kidneys.
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another. For example, when there is a tissue damage concentration of active osmotic parts
increases and water diffuses to this compartment, causing oedema. On the contrary plasma
osmolarity decreases, when there is a loss of electrolytes and osmotic concentration of the cellular
fluid stays on the previous level. This brings cellular oedema, because water moves through the
intracellular space to the cells due to their higher osmotic concentration.
Cerebral oedema appears when the plasma osmolarity is lower than 270 mOsm/l. Activity
of central nervous system is violated and hypoosmolar coma occurs. Hyperosmolar coma appears
when the plasma osmolarity is over 320 mOsm/l: water leaves the cells and fills the vascular bed
and this leads to cellular dehydration. The sensitive to cellular dehydration are the cells of the
brain.
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Dehydration signs: weight loss, decrease of skin turgor and eyeballs tone, dry skin and
mucous membranes; low central venous pressure, cardiac output and blood pressure (collapse is
possible); decreased urine output and peripheral veins tone; capillary refill over 2 seconds
(microcirculation disorders) and low skin temperature; intracellular dehydration is characterized
with thirst and consciousness disorders. Laboratory tests show blood concentration: hematocrit,
hemoglobin concentration, protein level and red blood cells concentration increase.
Overhydration appears in case of:
- excessive water consumption, inadequate infusion therapy;
- acute and chronic renal failure, hepatic and cardiac insufficiency;
- disorders of fluid balance regulation;
- low protein edema.
Clinical findings in case of overhydration are: weight gain, peripheral oedema,
transudation of the plasma into the body cavities (pleural, abdominal), high blood pressure and
central venous pressure. In case of intracellular overhydration appear additional symptoms:
nausea, vomiting, signs of cerebral edema (spoor, coma). Laboratory tests prove hemodilution.
According to the osmotic concentration of plasma dehydration and overhydration are
divided into hypotonic, isotonic and hypertonic.
Isotonic dehydration is caused by equal loss of electrolytes and fluid from the
extracellular space (without cellular disorders).Blood tests show hemoconcentration; sodium level
and osmotic concentration are normal.
To treat this type of water imbalance use normal saline solution, Ringer solution, glucose-
saline solutions, etc.. The volumes of infusions can be calculated according to the formula:
VH2O= 0,2*BW* (Htp-0,4)/0,4 ,
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Hypertonic dehydration is caused by mostly water loss: first it appears in the vascular bed,
than in the cells. Laboratory tests show hemoconcentration: elevated levels of proteins, red blood
cells, hematocrit. Plasma sodium is over 155 mmol/l and osmotic concentration increases over 310
mOsm/l.
Intensive treatment: if there is no vomiting allow patients to drink. Intravenously give
0,45% saline solution and 2,5 % glucose solution, mixed with insulin. The volume of infusions is
calculated according to the formula:
VH2O=0,6*BW (Nap -140)/140,
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Treat the reason of imbalance: cardiac failure, liver insufficiency, etc. Prescribe cardiac
glycosides, limit salt and water consumption. Give osmotic diuretics (mannitol solution 1,5 g/kg),
saluretics (furosemide solution 2 mg/kg), aldosterone antagonists (triamterene 200 mg), steroids
(prednisolone solution 1-2 mg/kg) albumin solution if necessary (0,2-0,3 g/kg).
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insulin 12 units
Give it intravenously slowly, during one hour. Forced bolus infusion of potassium
solutions (10-15 ml) can bring cardiac arrest.
Potassium level over 5,2 mmol/l is a state called hyperkalemia. To treat this condition
use calcium gluconate or calcium chloride solutions (10 ml of 10% solution intravenously),
glucose and insulin solution, saluretics, steroids, sodium bicarbonate solution. Hyperkalemia
over 7 mmol/l is an absolute indication for dialysis.
Sodium is the main extracellular cation. Its normal plasma concentration is 135-155
mmol/l. Daily required amount of potassium is 2 mmol/kg of body weight.
Sodium concentration which is lower than 135 mmol/l is known as hyponatraemia.
This condition is caused by sodium deficiency or water excess. Sodium deficiency is
calculated according to the formula:
Nad= (140-Nap)*0,2 BW,
Na- sodium deficiency, mmol;
Nap sodium concentration of the patient mmol/l;
0,2*BW extracellular fluid volume, l.
To treat it use normal saline (1000 ml contains 154 Na mmol) or 5,8% solution of
sodium chloride your choice will depend on osmotic concentration.
Sodium concentration over 155 mmol/l is a state called hypernatremia. This condition
usually appears in case of hypertonic dehydration or hypertonic overhydration. Treatment was
described in the text above.
Chlorine is the main extracellular anion. Its normal plasma concentration is 98-107
mmol/l. Daily requirement of chlorine is 215 mmol.
Hypochloremia is a condition of decreased plasma chlorine concentration (less than 98
mmol/l).
Chlorine deficiency is calculated according to the formula:
Cld = (100-Clp)*0,2 BW,
Cld- chlorine deficiency, mmol
Clp plasma chlorine concentration of the patient, mmol/l
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To treat hypochloremia use normal saline (1000 ml contains 154 mmol of chlorine) or
5,8% sodium chlorine solution (1 ml contains 1 mmol of chlorine). The choice of solution
depends on the osmotic concentration of the plasma.
Hyperchloremia is a condition of increased chlorine concentration (over 107 mmol/l).
Intensive therapy of this state includes treatment of the disease, which caused it (decompensated
heart failure, hyperchloremic diabetes insipidus, glomerulonephritis). You can also use glucose,
albumin solutions and dialysis.
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ventilation (through the mask or tube; when the necessity of ventilation lasts longer than 3 days
perform tracheostomy).
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To treat this condition use acid solutions, which contain chlorides (saline, potassium
chloride). In case of kaliopenia give potassium solutions.
Respiratory and metabolic imbalances can mix in case of severe decompensated diseases
due to failure of compensatory mechanisms. Correct interpretation of these violations is possible
only in case of regular and iterative gasometry blood tests.
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Terminal pause ends within a minute and final stage agony begins. According
to the complete exhaustion of superior control centers of the CNS
lower centers (bulbar respiratory and vasomotor centers, reticular
formation) are getting more active. Muscular tone, reflexes and
external respiration (chaotic, with auxiliary respiratory muscles
participation) are restored.
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Fig. Defibrilation
You can also use simple airway adjuncts such as oropharyngeal
and nasopharyngeal airways.
II. Breathing (B). Respiratory support in conditions of BLS is
usually mouth_to_mouth ventilation. If only there is a chance use
devices for pre_hospital ventilation: pocket resuscitation masks of
different types or at least handkerchief. Place closely your mouth
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over that of the patient and make a normal exhale (volume 600_800
ml). Remember to keep the airways conductive using the methods
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Fig. Defibrilation
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Fig. Conicotomia
During the CPR think about reversible cardiac arrest reasons
and try to treat them: there are easy mnemonic schemes of 4 H and 4
T for this purpose. So, the reversible causes of the clinical death are:
hypoxia tension pneumothorax hypovolemia tamponade (cardiac)
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On the first stage of this care check again the patients condition:
monitor constantly condition of cardiovascular and respiratory
systems, measure blood pressure and central venous pressure,
evaluate CNS state (reflexes, neurological deficiency), perform
laboratory tests (take blood and urine samples, liquor if necessary),
etc. Well_planned, comprehensive examination allows us to identify
homoeostasis disorder and choose optimal treatment. After main
parameters are stabilized central nervous system becomes your main
concern: protect the brain from hypoxia by all available means,
because hypoxic damage of neurons is usually irreversible. To achieve
this purpose you should:
provide adequate oxygenation (however excess of oxygen is
no longer recommended, so keep blood saturation at the level 94_
98%); hyperventilation might be used in case of brain oedema (first
12_24 hours of artificial ventilation);
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Fig. Trainings
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gloves if available.
Procedure: First of all free upper airways open the mouth of
the patient and clear oral cavity as mentioned above: turn the head
aside, open the mouth and remove vomit, blood cloths, foreign bodies
with a finger. Then title head backwards and thrust the jaw forward.
To make mouth_to_mouth ventilation less unpleasant you can put a
napkin or a piece of bandage on the mouth of the victim. Close
patients nostrils with your fingers, press your mouth against the
mouth of the patient and make a forced expiration. Inhaling the air
observe the chest: if it moves according to your respiratory efforts
breathing is effective. However if chest is not rising check again
airways patency: thrust the jaw placing your fingers over its angle
and moving them forward (lower teeth should overlap upper teeth).
Your aim is to exhale nearly 600_800 ml of air with the frequency of
10 times per minute (2 breathes to 30 compressions) during CPR. If
it is respiratory arrest alone you can make 15_20 breathes per minute.
Chest compressions (External heart massage).
Indications: cardiac arrest (clinical death).
Necessary equipment: doesnt need any; gloves if they are
available.
Procedure: place the patient on the firm flat surface in supine
position; if you have an assistant one of you should provide airways
patency and breathing, another chest compressions. Staying on
your knees aside the patient place one hand in the middle of the chest
and cover it with another. Your fingers should not touch the chest,
otherwise while compressions you will break the ribs. Frequency of
compressions should be 100 per minute*, depth 5_6 cm. Keep your
elbows straight and use mainly mussels of your back (weight of the
body): thus you will exhaust slower. In case of effectively provided
CPR you might observe constriction of pupils, normalization of skin
color, pulse on peripheral vessels, sometimes its even possible to
measure blood pressure.
Heart punction.
There are two types of heart punction: punction of heart cavity
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D. 5_7 minutes
E. 10 minutes
5. Name the exact hand placement during heart massage:
A. on the chest, fingers to chin
B. lower third of the sternum, fingers along ribs
C. middle of the chest
D. 4_th intercostal space, left part of the chest
E. on the chest in the heart area
6. What are the signs of effective artificial ventilation?
A. narrowing of the pupils
B. noises during ventilation
C. silent chest movements
D. bulged out epigastrium
E dizziness of the rescuer
7. Choose an absolute sign of cardiac arrest:
A. flat line on ECG
B. unconsciousness
C. cyanotic color of skin
D. lack of pulse over carotid arteries
E. lack of blood pressure
8. Choose the place of heart puncture:
A. 5_th intercostal space, in the place of apex projection
B. 3_d intercostal space, on the left from sternum
C. lower edge of the 4_th rib
D. 4_th intercostal space, 1,5 cm on the left from the sternum
E. in the place where heart action is noticeable
9. What medicines are usually used during CPR?
A. adrenaline, atropine, cordaron
B. adrenalin, dopamine
C. atropine, dopamine
D. atropine, steroids, dopamine, magnesium
E. adrenaline, magnesium
10. What is the reason of Sodium bicarbonate usage during CPR?
A. correction of metabolic acidosis
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that they putted her on her back, attached with a pin her tongue to the
chin (in order to provide airways potency). Next they started CPR: forced
maximal breathes (14 per minute) together with chest compressions (4 cm
deep, 60 per minute). Name 5 mistakes of The layman.
Task 5.
The Dream team, group of professional rescuers, started CPR of a
patient in a state of clinical death. Then they cleared the upper airways
with an electric suction machine, connected respiratory machine. Next
they gave adrenaline (0,5 ml of 0,1% solution) sodium bicarbonate (4%
solution, 10 ml), calcium chloride (10%, 5 ml) and atropine (0,5 ml of 0,1%
solution) at the same time and connected patient to a monitor (flat line on
the ECG). After that rescuers did a defibrillation of 300 J, which resulted
in a flat line on the ECG. They repeated everything again, this time with
defibrillation of 400J. Unfortunately there was no effect. Patient died.
Name 5 mistakes of The Dream team
The importance of the water to the organism.
Life on earth was born in the water environment. Water is a universal solvent for all the
biochemical processes of the organism. Only in case of stable quantitative and qualitative
composition of both intracellular and extra cellular fluids homoeostasis is remained.
The body of an adult human contains 60% of water. Intracellular water makes 40% of
the body weight, the water of intercellular space makes 15% of body weight and 5% of body
weight are made by the water in the vessels. It is considered that due to unlimited diffusion of
water between vessels and extra vascular space the volume of extracellular fluid is 20% of body
weight (15%+5%).
Physiologically insignificant amounts of water are distributed beyond the tissues in the
body cavities: gastrointestinal tract, cerebral ventricles, joint capsules (nearly 1% of the body
weight). However during different pathologic conditions this third space can cumulate large
amounts of fluid: for example in case of ascitescaused by chronic cardiac insufficiency or
cirrhosis abdominal cavity contains up to 10 liters of fluid. Peritonitis and intestinal
obstructions remove the fluid part of blood from the vessels into the intestinal cavity.
Severe dehydration is extremely dangerous for the patient. Water gets to the body with
food and drinks, being absorbed by the mucous membranes of gastro-intestinal tract in total
amount of 2-3 liters per day. Additionally in different metabolic transformations of lipids,
carbohydrates and proteins nearly 300 of endogenous water are created. Water is evacuated
from the body with urine (1,5-2 liters), stool (300 ml), perspiration and breathing (those two
reasons are combined as perspiration loss and make from 300 to 1000 ml per day).
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Water balance is regulated through complicated, but reliable mechanisms. Control over
water and electrolytes excretion is realized by osmotic receptors of posterior hypothalamus,
volume receptors of the atrial walls, baroreceptors of carotid sinus, juxtaglomerular apparatus
of the kidneys and adrenal cortical cells.
When there is a water deficiency or electrolytes excess (sodium, chlorine) thirst
appears and this makes us drink water. At the same time posterior pituitary
produces antidiuretic hormone, which decreases urine output. Adrenals reveal into the blood
flow aldosterone, which stimulates reabsorption of sodium ions in the tubules and thus also
decreases diuresis (due to osmosis laws water will move to the more concentrated solution).
This way organism can keep precious water.
On the contrary, in case of water excess endocrine activity of glands is inhibited and
water is actively removed from the body through the kidneys.
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Dehydration signs: weight loss, decrease of skin turgor and eyeballs tone, dry skin and
mucous membranes; low central venous pressure, cardiac output and blood pressure (collapse
is possible); decreased urine output and peripheral veins tone; capillary refill over 2 seconds
(microcirculation disorders) and low skin temperature; intracellular dehydration is
characterized with thirst and consciousness disorders. Laboratory tests show blood
concentration: hematocrit, hemoglobinconcentration, protein level and red blood cells
concentration increase.
Overhydration appears in case of:
- excessive water consumption, inadequate infusion therapy;
- acute and chronic renal failure, hepatic and cardiac insufficiency;
- disorders of fluid balance regulation;
- low protein edema.
Clinical findings in case of overhydration are: weight gain, peripheral oedema,
transudation of the plasma into the body cavities (pleural, abdominal), high blood pressure and
central venous pressure. In case of intracellular overhydration appear additional symptoms:
nausea, vomiting, signs of cerebral edema (spoor, coma). Laboratory tests prove hemodilution.
According to the osmotic concentration of plasma dehydration and overhydration are
divided into hypotonic, isotonic and hypertonic.
Isotonic dehydration is caused by equal loss of electrolytes and fluid from the
extracellular space (without cellular disorders).Blood tests showhemoconcentration; sodium
level and osmotic concentration are normal.
To treat this type of water imbalance use normal saline solution, Ringer solution,
glucose-saline solutions, etc.. The volumes of infusions can be calculated according to the
formula:
VH2O= 0,2*BW* (Htp-0,4)/0,4 ,
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Hypertonic dehydration is caused by mostly water loss: first it appears in the vascular
bed, than in the cells. Laboratory tests show hemoconcentration: elevated levels of proteins, red
blood cells, hematocrit. Plasma sodium is over 155 mmol/l and osmotic concentration increases
over 310 mOsm/l.
Intensive treatment: if there is no vomiting allow patients to drink. Intravenously give
0,45% saline solution and 2,5 % glucose solution, mixed with insulin. The volume of infusions
is calculated according to the formula:
VH2O=0,6*BW (Nap -140)/140,
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Give it intravenously slowly, during one hour. Forced bolus infusion of potassium
solutions (10-15 ml) can bring cardiac arrest.
Potassium level over 5,2 mmol/l is a state called hyperkalemia. To treat this
condition use calcium gluconate or calcium chloride solutions (10 ml of 10% solution
intravenously), glucose and insulin solution, saluretics, steroids, sodium bicarbonate
solution. Hyperkalemia over 7 mmol/l is an absolute indication for dialysis.
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To treat hypochloremia use normal saline (1000 ml contains 154 mmol of chlorine) or
5,8% sodium chlorine solution (1 ml contains 1 mmol of chlorine). The choice of solution
depends on the osmotic concentration of the plasma.
Hyperchloremia is a condition of increased chlorine concentration (over 107 mmol/l).
Intensive therapy of this state includes treatment of the disease, which caused it
(decompensated heart failure, hyperchloremic diabetes insipidus, glomerulonephritis). You can
also use glucose, albumin solutions and dialysis.
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acute and chronic respiratory violations. When pCO2 is over 60 mm Hg begin artificial lung
ventilation (through the mask or tube; when the necessity of ventilation lasts longer than 3 days
perform tracheostomy).
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BE 3,0 mmol/l.
To treat this condition use acid solutions, which contain chlorides (saline, potassium
chloride). In case of kaliopenia give potassium solutions.
Respiratory and metabolic imbalances can mix in case of
severe decompensated diseases due to failure of compensatory mechanisms. Correct
interpretation of these violations is possible only in case of regular and
iterative gasometry blood tests.
Control tasks.
Task 1.
Calculate the total body water volume and its extracellular and intracellular volumes of
the Patience, the patient of 48 years and body weight 88 kg.
Task 2.
Patience, the patient of 23 with body weight 70 kg has sodium level 152 mmol/l
and hematocrit 0,49 l/l. Name the type of water balance disorder.
Task 3.
Patience, the patient of 54 with body weight 76 kg has sodium level 128 mmol/l.
Calculate the volume of saline and 7,5% sodium chloride solution necessary for the treatment
of this condition.
Task 4.
Patience, the patient of 60 with body weight 60 kg has sodium level 140 mmol/l
and hematocrit 0,55 l/l. Name the type of disorder and prescribe infusion therapy.
Task 5.
Patience, the patient of 42 with body weight 80 kg has potassium level 2,6 mmol/l.
Calculate the volume of 4% potassium chloride solution necessary for treatment of this
condition.
Task 6.
Patience, the patient of 33 with body weight 67 kg and diagnosis gastric ulcer,
complicated with pylorostenosis has potassium concentration 3 mmol/l, chlorine
concentration 88 mmol/l. pH 7,49, pCO2a 42 mm Hg, BE + 10 mmol/l. Name the type of
disorder.
Task 7.
Patience, the patient of 50 with body weight 75 kg, was transported to the admission
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unit of the hospital with: unconsciousness, cyanotic skin, low blood pressure, shallow
breathing. Blood tests show: pH 7,18, pCO2a 78 mm Hg, pO2A 57 mm Hg, BE -4,2 mmol/l.
Name the type of acid-base disorder and prescribe treatment.
Task 8.
Patience, the patient with body weight 62 kg and renal insufficiency has: potassium
concentration 5,2 mmol/l, sodium concentration 130 mmol/l, calcium concentration
1,5 mmol/l, pH 7,22, pCO2a 34 mm Hg, BE -9,2 mmol/l. Name the type of disorder.
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Introduction
Acute circulatory insufficiency
Anatomy and physiology
Life is provided through a variety of mechanisms, however all of
them depend on proper circulation. Circulation itself consists of 2
parts: work of heart (pump of the body) and vessels, through which
blood is pumped to the most remote organs and tissues. During every
systolic contraction heart pumps 70_80 ml of blood (so called stroke
volume). So if the heart rate is 70 beats per minute, heart pumps
nearly 5 liters of blood, what makes more than 7 tones per day.
From the left ventricle blood gets to the arterial system of the
systemic circuit. Arteries contain 15% of the whole circulating blood
volume; they carry blood from the heart to their distal departments
arterioles (vessels of resistance). Arterioles themselves are defining
blood distribution: in condition of constriction (spasm) they make
blood supply of the capillaries impossible (ischemia appears). On the
contrary, in condition of dilatation they provide maximal
oxygenation. When arterioles are blocked due to the spasm blood is
flowing through the arterio_venous anastomoses directly to the
venous system.
Distribution of blood in the vascular bed (% of CBV).
a. heart cavity 3%
b. arteries 15%
c. capillaries 12%
d. venous system 70%
Among the natural vasoconstrictors (agents, which cause
constriction of the blood vessel) are epinephrine, norepinephrine,
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During alveolar edema not only the plasma, but also blood
components (red and white blood cells, platelets) get out from the
vessels. During the respiratory act blood mixes with the air creating
large amount of foam, which violates gas exchange. This way, in
addition to circulatory hypoxia, hypoxic hypoxia appears.
Condition of the patient gets worth quickly. Sitting position is
optimal, but not as helping as previously. Respiratory rate is nearly
30_35 breathes per minute, but attacks of breathlessness are constant.
Skin is pale with acrocyanosis. Hypoxia of central nervous system
usually causes psychomotor agitation. Respiratory acts are noisy;
during cough pink blood_tinged phlegm is released. Auscultation
allows you to hear different wet rales, sometimes its even possible to
hear them standing aside the patient without phonendoscope.
Pulmonary edema can be also divided according to the blood
pressure level: the one with elevated pressure is caused by a
hypertonic disease, aorta valve insufficiency or disorders of cerebral
perfusion; another one is caused by total myocardial infarction, acute
inflammation of myocardial muscle, terminal valve defects, severe
pneumonia and is characterized with normal or low blood pressure.
Immediate aid
make sure patient is sitting with his legs down (orthopnea)
provide oxygenation through nasal catheter (before placing
oil it with glycerin, insert it to the depth of 10_12 cm distance from
the wing of the nose to auricle) or face mask. Do not use Vaseline,
because it can burn in atmosphere with high concentration of oxygen.
However if catheter is not deep enough patient will suffer from
an unpleasant burning feeling, because oxygen flow will dry mucosa
layer of the nasal cavity; also in this situation concentration of oxygen
will be lower than expected.
put venous tourniquets on the limbs in order to reduce amount
of blood returning to heart: venous bed of limbs can reserve up to 1,7
liters of blood;
constantly control heart and kidney activity (ECG, SaO2 , and
blood pressure are checked automatically trough the monitor; to
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ECG = electrocardiogram.
The initial working diagnosis is based on the clinical presentation and the initial
electrocardiogram (ECG) findings and, in particular, the presence or absence of ST-segment
elevation. As the vast majority of patients who present with initial ST-segment elevation
develop biochemical evidence of myonecrosis, the term ST-segment-elevation myocardial
infarction (STEMI) is often used from the outset in these patients.
ACS without ST-segment elevation on the presenting ECG represent a broad spectrum of risk,
but are collectively referred to as NSTEACS. This grouping is useful because emergency
reperfusion therapy is not indicated (unless ST-segment elevation develops later), and further
investigation is required to classify the patients risk and determine the most suitable treatment
(see sections on Investigations and Management of patients with STEMI for further details).
Final diagnosis
The final diagnostic attribution (ie, clinical label) has important and persisting implications for
the patient, both prognostically and socially. Current international criteria for the diagnosis of
myocardial infarction have a strong emphasis on biomarkers, specifically troponin, given its
high sensitivity and, in particular, specificity for myonecrosis.5 The diagnostic criteria for
acute, evolving or recent myocardial infarction are defined as:
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Typical rise in the serum level of troponin or a more rapid rise in the serum level of the
MB isoenzyme of creatine kinase (CK-MB) with at least one of the following:
Ischaemic symptoms;
Development of pathological Q waves on the ECG;
ECG changes indicative of ischaemia (ST-segment elevation or depression); and
Coronary artery intervention (eg, coronary angioplasty or coronary bypass surgery);
or
Pathological findings of an acute myocardial infarction.
This definition requires a temporal appreciation of the cardiac markers, and therefore
differentiation between non-ST-segment-elevation myocardial infarction and unstable angina
(without evidence of myonecrosis) must be delayed.
Acute management of chest pain
Getting to hospital
Chest discomfort at rest or for a prolonged period (more than 10 minutes, not relieved by
sublingual nitrates), recurrent chest discomfort, or discomfort associated with syncope or acute
heart failure are considered medical emergencies. Other presentations of ACS may include
back, neck, arm or epigastric pain, chest tightness, dyspnoea, diaphoresis, nausea and vomiting.
Very atypical pain, including sharp and pleuritic pain, is more common in women, people with
diabetes and older people.3,7,8
People experiencing such symptoms should seek help promptly and activate emergency medical
services to enable transport to the nearest appropriate health care facility for urgent assessment
(grade D recommendation). Ideally, transport should be by ambulance. However, where
ambulance response times are long, alternatives may need to be considered. Patients should be
strongly discouraged from driving themselves because of the risk to other road users.
The most important initial requirement is access to a defibrillator to avoid early cardiac death
from reversible arrhythmias. All Australian ambulances now carry defibrillators, and there is
promise in further exploring public access defibrillation opportunities. In the case of cardiac
arrest occurring in a setting where a defibrillator is not immediately available, cardiopulmonary
resuscitation should be commenced immediately.
Actions in transit
Aspirin (300 mg) should be given unless already taken or contraindicated (grade A
recommendation), and should preferably be given early (eg, by emergency or ambulance
personnel) (grade D recommendation). Oxygen should also be given (grade D
recommendation).
Glyceryl trinitrate and intravenous morphine should be given as required (grade D
recommendation).
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Where appropriate, a 12-lead ECG should be taken en route and transmitted to a medical
facility (grade B recommendation).
Receiving medical facilities should be given warning of incoming patients in whom there is a
high suspicion of ACS, particularly STEMI, or those whose condition is unstable (grade B
recommendation).
Where formal protocols are in place, prehospital treatment should be given, including
fibrinolysis in appropriate cases (grade A recommendation). See section on management of
patients with STEMI for further discussion of prehospital fibrinolysis.
On arrival
All patients presenting with suspected ACS should be subject to ongoing surveillance and have
an ECG completed within 5 minutes of arrival at the medical facility (grade A
recommendation). The ECG should be assessed promptly by an appropriately qualified person
(grade D recommendation).
Oxygen and pain control should be given as required (grade D recommendation).
People experiencing symptoms of ACS should seek help promptly and activate emergency
medical services.
The most important initial requirement is access to a defibrillator to avoid early cardiac death
from reversible arrhythmias.
Aspirin should be given early (eg, by emergency or ambulance personnel) unless already taken
or contraindicated.
Oxygen should be given, as well as glyceryl trinitrate and intravenous morphine as required.
As a minimum, receiving medical facilities should be given warning of incoming patients in
whom there is a high suspicion of ACS, particularly STEMI, or whose condition is unstable.
Where appropriate, a 12-lead ECG should be taken en route and transmitted to a medical
facility.
Where formal protocols are in place, prehospital treatment (including fibrinolysis in
appropriate cases) should be facilitated.
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Electrocardiography
Electrocardiography is necessary to detect ischaemic changes or arrhythmias. It should be
noted that the initial ECG has a low sensitivity for ACS, and a normal ECG does not rule out
ACS. However, the ECG is the sole test required to select patients for emergency reperfusion
(fibrinolytic therapy or direct PCI). Patients with STEMI who present within 12 hours of the
onset of ischaemic symptoms should have a reperfusion strategy implemented promptly (grade
A recommendation) see the section on management of patients with STEMI for
recommendations.
Accurate ECG interpretation in a patient with chest pain is critical. Basically, there can be
three types of problems - ischemia is a relative lack of blood supply (not yet an
infarct), injury is acute damage occurring right now, and finally, infarct is an area of dead
myocardium. It is important to realize that certain leads represent certain areas of the left
ventricle; by noting which leads are involved, you can localize the process. The prognosis often
varies depending on which area of the left ventricle is involved (i.e. anterior wall myocardial
infarct generally has a worse prognosis than an inferior wall infarct).
anteroseptal wall
V1-V2
V3-V4 anterior wall
V5-V6 anterolateral wall
II, III,
inferior wall
aVF
I, aVL lateral wall
posterior wall
V1-V2
(reciprocal)
Infarct
Represented by symmetrical T wave
1.
inversion(upside down). The definitive leads for
Ischemia
ischemia are: I, II, V2 - V6.
Acute damage - look for elevated ST segments.
(Pericarditis and cardiac aneurysm can also cause
2. Injury
ST elevation; remember to correlate it with the
patient.
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Figure 36: Infarct: Note Q waves in leads II, III, and aVF (inferior wall).
For the posterior wall, remember that vectors representing depolarization of the anterior and
posterior portion of the left ventricle are in opposite directions. So, a posterior process shows
up as opposite of an anterior process in V1. Instead of a Q wave and ST elevation, you get an R
wave and ST depression in V1.
Figure: Posterior wall infarct. Notice tall R wave in V1. Posterior wall infarcts are often
associated with inferior wall infarcts (Q waves in II, III and aVF).
Two other caveats: One is that normally the R wave gets larger as you go to V1 to V6. If there
is no R wave "progression" from V1 to V6 this can also mean infarct. The second caveat is that,
with a left bundle branch block, you cannot evaluate "infarct" on that ECG. In a patient with
chest pain and left bundle branch block, you must rely on cardiac enzymes (blood tests) and
the history.
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Blood tests
Further investigations
Patients without ST-segment elevation on the initial ECG should be further observed and
investigated to promptly identify patients suitable for an emergency reperfusion strategy (based
on ECG changes) and/or determine the best management protocol for NSTEACS based on risk
stratification (see section on Management of patients with NSTEACS).
The ECG is the sole test required to select patients for emergency reperfusion (fibrinolytic
therapy or direct PCI).
Patients with STEMI who present within 12 hours of the onset of ischaemic symptoms should
have a reperfusion strategy implemented promptly.
Patients with a suspected ACS without ST-segment elevation on the ECG should undergo
further observation and investigation to rule out other diagnoses, enable risk stratification and
determine the most appropriate treatment strategy.
Patients with a normal ECG and cardiac biomarker levels after an appropriate period of
observation should, where practicable, undergo provocative testing (eg, stress test) before
discharge.
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biomarker
Troponin On arrival Troponin rise
level(Cardiac indicates
troponin I or myonecrosis,
T) and is a
high-risk
feature in
NSTEACS.
Troponin is
the preferred
marker
because
about a third
of patients
with elevated
troponin, but
normal CK
and CK-MB
levels, will
develop an
adverse
outcome.9
Not repeated if Troponin
positive remains
elevated for
514 days,
and therefore
may not be
useful for
identifying
early
re-infarction.
Repeated Troponin
> 8 hours after elevation is
last episode of often delayed
pain or other by
symptoms of 46 hours.
coronary Therefore,
insufficiency if repeat
initially troponin
negative testing is
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necessary to
identify
patients at
high risk
who may
benefit from
aggressive
therapy and
an early
invasive
strategy.
Serial troponin Appearance
measurements of typical
in patients with rise of
NSTEACS troponin
suspected to be indicates
at high risk high risk
NSTEACS
and may be
an indication
for more
aggressive
therapy.
Total CK Serial Can be
level measurements remeasured
performed for to confirm a
48 hours in second event
patients with if
myocardial re-infarction
infarction is suspected
later.
CK-MB Should be While
level measured in all troponin is
patients with an the preferred
ACS if troponin marker of
assay myocardial
unavailable damage, if it
is
unavailable
CK-MB is
more specific
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than CK for
myocardial
injury.
CK-MB may
also be used
to confirm a
re-infarction.
STEMI is defined as presentation with clinical symptoms consistent with an acute coronary
syndrome with ECG features including any of:
Patients with STEMI usually have a completely occluded coronary artery with thrombus at the
site of a ruptured plaque. Restoring coronary patency as promptly as possible is a key
determinant of short-term and long-term outcomes (level I evidence).14-18
Patients with STEMI who present within 12 hours of the onset of ischaemic symptoms should
have a reperfusion strategy implemented promptly (grade A recommendation).
Reperfusion therapy
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Antiplatelet therapy
Aspirin (300 mg) should be given to all patients with STEMI unless contraindicated and, in the
absence of significant side effects, low-dose therapy should be continued in the long term
(grade A recommendation).16,20
There is evidence that clopidogrel (300600 mg loading dose) should be prescribed in addition
to aspirin for patients undergoing PCI with a stent.21-23 In patients selected for fibrinolytic
therapy, clopidogrel (300 mg) should be given in addition to aspirin, unless contraindicated
(grade B recommendation).24 Note, however, that if it is thought that the patient is likely to
require CABG acutely, clopidogrel should be withheld.
Clopidogrel (75 mg daily) should be continued for at least a month after fibrinolytic therapy,
and for up to 12 months after stent implantation, depending on the type of stent and
circumstances of implantation (level II evidence; grade B recommendation).25
Antithrombin therapy
With PCI: Antithrombin therapy should be used in conjunction with PCI (grade A
recommendation). The dose of unfractionated heparin therapy will depend on concomitant use
of glycoprotein (GP) IIb/IIIa inhibitors. The aim should be to obtain an activated clotting time
(ACT) between 200 and 300 seconds if using GP IIb/IIIa inhibitors, or between 300 and
350 seconds if these drugs are not used (grade B recommendation). It may be advisable to give
a bolus of heparin while the patient is in transit to the catheterisation laboratory (grade D
recommendation).
The role of enoxaparin in acute STEMI in conjunction with PCI remains to be determined, but
it appears to be safe and effective at a dose of 0.75 mg/kg (grade D recommendation).
With fibrinolysis: Antithrombin therapy should be used with fibrin-specific fibrinolytic agents
(grade A recommendation).26,27
Unfractionated heparin should be given as an initial bolus dose of 60 units per kilogram of
body weight (with a maximum dose of 4000 units) followed by an initial infusion of 12 units
per kilogram per hour (maximum units 1000 per hour), adjusted to attain the activated partial
thromboplastin time (APTT) at 1.5 to 2 times control (about 5070 seconds; grade B
recommendation).12
Enoxaparin may be used in conjunction with fibrin-specific fibrinolytic agents in patients
under the age of 75 years, provided they do not have significant renal dysfunction. An
intravenous bolus dose of 30 mg followed by a 1 mg/kg subcutaneous injection every 12 hours
in combination with tenecteplase is the most comprehensively studied therapy.12 Care should
be taken in patients who are aged over 75 years, or who have renal dysfunction, as dose
adjustment is required.12
The use of antithrombin therapy in conjunction with streptokinase therapy is optional.28
Glycoprotein IIb/IIIa inhibitors
It is reasonable to use abciximab with primary PCI, although there are conflicting data (grade B
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recommendation). It appears the earlier it is used, the greater the advantage.29 When used in
patients with STEMI undergoing primary PCI, the timing of administration of abciximab is a
matter of clinical judgement.30,31
Full-dose GP IIb/IIIa inhibitors should be avoided with fibrinolytic therapy (grade B
recommendation) as there is evidence of excessive bleeding (including intracranial
haemorrhage) with this combination.32 It is unclear how early full-dose GP IIb/IIIa inhibitors
can be safely given after fibrinolysis, but it is probably at least 4 hours after administration of
fibrin-specific fibrinolytic agents and 24 hours after administration of streptokinase.32
The combination of GP IIb/IIIa inhibitors with reduced doses of fibrinolytic therapy is not
recommended. There is no significant advantage over full-dose fibrinolytic therapy alone, and
the risk of bleeding is increased, particularly in the elderly.32 This combination has been used
for facilitated PCI.32
All patients undergoing reperfusion therapy (PCI or fibrinolysis) for STEMI should be
given aspirin and clopidogrel unless contraindicated.
Antithrombin therapy should be given in combination with PCI or fibrinolytic therapy
with fibrin-specific fibrinolytic agents, but its use in conjunction with streptokinase is
optional.
It is reasonable to use abciximab with primary PCI, but GP IIb/IIIa inhibitors should
generally be avoided with full or reduced doses of fibrinolytic therapy.
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Choice of reperfusion strategy depends on a number of factors, with time delay (both
to presentation and potential PCI or fibrinolytic therapy) playing a major role in determining
best management.
In general, PCI is the treatment of choice, provided it can be performed promptly by a
qualified interventional cardiologist in an appropriate facility.
In general, the maximum acceptable delay from presentation to balloon inflation is:
60 minutes if a patient presents within 1 hour of symptom onset; and
90 minutes if a patient presents later.
Note: for patients who present late (312 hours after symptom onset) to a facility without PCI
capability, it is appropriate to consider transfer for primary PCI if balloon inflation can be
achieved within 2 hours (including transport time).
All PCI facilities should be able to perform angioplasty within 90 minutes of patient
presentation.
Fibrinolysis should be considered early if PCI is not readily available, particularly in
rural and remote areas.
When there are major delays to hospitalisation (more than 30 minutes), prehospital
fibrinolysis should be considered.
Reperfusion is not routinely recommended in patients who present more than 12 hours
after symptom onset and who are asymptomatic and haemodynamically stable.
Assuming no contraindications to fibrinolytic therapy see Box 5. Time delay refers to time
from first medical contact to balloon. Patients with ongoing symptoms or instability should
be transferred for PCI.
Note: Reperfusion after 12 hours is indicated for cardiogenic shock, ongoing pain or
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Absolute contraindications
Risk of bleeding
Active bleeding or bleeding diathesis (excluding menses)
Significant closed head or facial trauma within 3 months
Suspected aortic dissection (including new neurological symptoms)50
Risk of intracranial haemorrhage
Any prior intracranial haemorrhage
Ischaemic stroke within 3 months
Known structural cerebral vascular lesion (eg, arteriovenous malformation)
Known malignant intracranial neoplasm (primary or metastatic)
Relative contraindications
Risk of bleeding
Current use of anticoagulants: the higher the international normalised ratio (INR), the
higher the risk of bleeding
Non-compressible vascular punctures
Recent major surgery (< 3 weeks)
Traumatic or prolonged (> 10 minutes) cardiopulmonary resuscitation
Recent (within 4 weeks) internal bleeding (eg, gastrointestinal or urinary tract
haemorrhage)
Active peptic ulcer
Risk of intracranial haemorrhage
History of chronic, severe, poorly controlled hypertension
Severe uncontrolled hypertension on presentation (> 180 mmHg systolic or
> 110 mmHg diastolic)
Ischaemic stroke more than 3 months ago, dementia, or known intracranial abnormality
not covered in contraindications
Other
Pregnancy
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There are four fibrinolytic agents currently available in Australia; streptokinase and the tissue
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fibrin-specific fibrinolytic agents alteplase, reteplase and tenecteplase. The properties of these
agents are summarised in Box 7.
Fibrin-specific fibrinolytic agents have been shown to reduce mortality compared with
streptokinase in patients with STEMI who present within 6 hours of symptom onset (level I
evidence).55 Fibrin-specific fibrinolytic agents also lack the significant acute side effects of
hypotension and allergy caused by streptokinase (level I evidence). Streptokinase may be
associated with a lower incidence of intracranial haemorrhage, particularly in older people
(level I evidence), but the overall mortality is still lower with the use of fibrin-specific
fibrinolytic agents (level II evidence).56 Tenecteplase is associated with a lower rate of
bleeding than alteplase (level II evidence).57
Second-generation fibrin-specific fibrinolytic agents can be given as either single or double
bolus injections, which makes them significantly easier to use than streptokinase.
In combination therapy, PCI combined with fibrin-specific fibrinolytic agents appears to have
greater efficacy and results in fewer complications than PCI combined with streptokinase (level
III evidence, grade B recommendation).58
Streptokinase should not be given to patients with previous exposure (more than 5 days ago) to
the drug (grade B recommendation). There is also evidence that streptokinase may be less
effective in Aboriginal and Torres Strait Islander peoples because of the high levels of skin
infection (and thus streptococcal antibodies), particularly in remote populations.45,59 It is
therefore an inappropriate choice of agent in these populations (level III evidence, grade B
recommendation). Making second-generation fibrin-specific fibrinolytic agents the standard
choice is likely to decrease inequalities of care between Indigenous and non-Indigenous
populations, in addition to providing superior reperfusion.
Therefore, second-generation fibrin-specific fibrinolytic agents which are available as a bolus
(ie, reteplase, tenecteplase) are the fibrinolytics of choice (grade A recommendation). These
agents should be available at all centres where fibrinolysis may be required (grade D
recommendation).
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information) units (50 mg) on basis of apart (give 15 mg bolus; units over
body weight: < 60 kg each bolus then 50 mg 3060 minutes
6000 units 6070 kg slowly over no over 30
7000 units 7080 kg more than minutes and
8000 units 8090 kg 2 minutes) 35 mg over
9000 units > 90 kg the next
10 000 units 60 minutes
For patients
65 kg: 15 mg
bolus; then
0.75 mg/kg
over
30 minutes
and 0.5 mg/kg
over the next
60 minutes.
Bolus Yes Yes No No
administration
Antigenic12 No No No Yes
Systemic Minimal Moderate Mild Marked
fibrinogen
depletion12
Lives saved per 3553 3554 3555 2514
1000 patients
treated
(approximate
number at
30 days)
Patients who have had STEMI should be considered for early transfer to a tertiary
cardiac centre with PCI facilities and links to cardiac surgical facilities.
If early transfer is not possible, all patients should be transferred or referred as soon as
is practicable for assessment of the need for revascularisation through PCI or CABG.
The initial objective of evaluation is to define the likelihood of an ACS as the cause of a
patients presentation. Most patients will present with prolonged or recurrent central chest
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discomfort but others, particularly the elderly, people with diabetes and women, may present
with atypical symptoms. These include neck, jaw, back or epigastric discomfort or dyspnoea,
diaphoresis, nausea and vomiting. Age is an important risk factor, and the presence (or
absence) of coronary risk factors adds little to the accuracy of the diagnosis in middle-aged or
elderly patients, but is more useful in making a diagnosis in younger patients. A history of
physical or emotional stress before symptom onset increases the likelihood of an ACS. Most
patients with NSTEACS are normal on physical examination. An abnormal ECG, particularly
dynamic ST-segment deviation ( 0.5 mm) or new T-wave inversion ( 2 mm) will confirm the
diagnosis, but the ECG may be normal or show minor changes in up to 50% of cases.
The second objective of evaluation is to determine the risk of short-term adverse outcomes,
which will direct the management strategy. Box 8 provides a paradigm for the risk stratification
of patients presenting with suspected NSTEACS, and a simplified risk assessment algorithm is
shown in Box 9. Most patients admitted to hospital with possible NSTEACS will have
intermediate-risk or high-risk features (Box 8), and these patients are best managed with a
structured clinical pathway (see Investigationssection). Patients with clinical features
consistent with NSTEACS and high-risk features are best managed with aggressive medical
and invasive therapy (detailed later). Patients with diabetes or chronic kidney disease with
typical symptoms of ACS would be considered to be at high risk, but those with atypical
symptoms and normal ECGs and cardiac biomarker levels may initially be considered at
intermediate risk until a diagnosis is made. Patients with low-risk unstable angina may be
managed with upgraded medical therapy and outpatient cardiac referral.
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Treatment of NSTEACS
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Fig. ECG with MI
Additional risk stratification on the basis of a TIMI risk score of greater than three for deciding
which patients might be transferred for early invasive management may be considered where
funding is constrained, but it must be remembered that 14-day cardiac event rates are still
considerable, even for those with low scores (see Box 12). Appropriate patients should be
transferred for angiography within 48 hours, and aggressive medical therapy with initial
stabilisation of symptoms does not mitigate the need for early angiography.
0/1 4.7%
2 8.3%
3 13.2%
4 19.9%
5 26.2%
6/7 40.9%
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All patients with NSTEACS should have their risk stratified to direct management
decisions.
All patients with NSTEACS should be given aspirin unless contraindicated.
Patients with high-risk NSTEACS should be treated with aggressive medical
management (including aspirin and clopidogrel, unfractionated heparin or subcutaneous
enoxaparin, intravenous tirofiban or eptifibatide, and a -blocker), and arrangements should be
made for coronary angiography and revascularisation, except in those with severe
comorbidities.
Patients with intermediate-risk NSTEACS should undergo an accelerated diagnostic
evaluation and further assessment to allow reclassification into low-risk or high-risk categories.
Patients with low-risk NSTEACS, after an appropriate period of observation and
assessment, may be discharged on upgraded medical therapy for urgent outpatient cardiac
follow-up.
Before discharge of patients who have had an ACS, therapy with an appropriate
medication regimen should be initiated, including antiplatelet agent(s), -blocker, angiotensin-
converting enzyme inhibitor, statin and other therapies as appropriate.
Implantable cardiac defibrillators should be considered in some patients who, despite
optimal medical therapy, have persistently depressed left ventricular function more than
6 weeks after STEMI.
Patients should be given advice on lifestyle changes that will reduce the risk of further
coronary heart disease events, including smoking cessation, good nutrition, moderate alcohol
intake, regular physical activity and weight management, as appropriate.
All patients should have access, and be actively referred, to comprehensive ongoing
prevention and cardiac rehabilitation services.
All patients should be provided with a written action plan for chest pain.
Depression and coronary heart disease frequently coexist, and in patients with heart
disease, depression, social isolation and lack of social support are more likely to lead to poorer
outcomes. All patients with coronary heart disease should be assessed for depression and level
of social support.
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This algorithm is for suggested management in an area which is still evolving.There may be
considerable resource issues that will need to be explored, and cost-effectiveness data are
currently lacking. Other factors such as comorbidities and conditions that significantly shorten
life expectancy and reduce quality of life should be considered before ICD implantation. The
evidence for benefit is strongest in patients with a left-ventricular ejection fraction 30% and
New York Heart Association Class II or III heart failure.
Overview of keypoints
Acute coronary syndrome (ACS) refers to a group of clinical conditions caused by myocardial
ischemia including unstable angina pectoris (UA), non-ST-segment elevation myocardial
infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI) (Fig. 1).
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Patients presenting with acute chest pain and persistent (>20 min.) ST-elevation on
electrocardiogram (ECG) will have the working diagnosis of ST-elevation ACS. Most of these
patients will ultimately develop STEMI and progress to Q wave myocardial infarction (MI).
Patients with acute chest pain, but without persistent ST-segment elevation (presenting with
persistent or transient ST depression or T-wave inversion, flat T waves, pseudo-normalization
of T waves or normal ECG) will have the working diagnosis of non-ST-elevation ACS. On the
basis of troponin measurements patients with non-ST-elevation ACS will be further qualified
as having NSTEMI or UA.
The distinction between nonST segment elevation ACS and ST-segment elevation ACS is
clinically important because rapid recanalization therapy is critical for improving the outcome
in ST elevation ACS/STEMI, but is less urgent in nonST-segment elevation ACS.
MI is defined pathologically as myocardial cell death due to prolonged ischemia. In the clinical
setting, these conditions are met when the following criteria are present: detection of a rise
and/or fall of cardiac biomarkers with at least one value above the 99th percentile of the upper
reference limit (URL) together with evidence of myocardial ischemia as recognized by at least
one of the following:
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- symptoms of ischemia;
- ECG changes of new ischemia (ST-elevation or depression) or development of pathologic Q
waves; or
- imaging evidence of new loss of viable myocardium or new regional wall motion abnormality.
Pathophysiology
Acute coronary syndrome represents a life-threatening manifestation of atherosclerosis. ACS
most frequently develops as a result of plaque rupture or erosion with overlying thrombosis. A
thin fibrous cap is more likely to rupture than a thick one. Factors such as the lipid and tissue
factor content of the plaque, the severity of the plaque rupture, the degree of inflammation at
the site, the blood flow in the area, and the patient's antithrombotic and prothrombotic balance
are important in determining whether a given plaque rupture will result in ACS.
Less frequent pathophysiological causes of ACS include dynamic obstruction due to coronary
vasospasm as in Prinzmetal angina or in cocaine use, coronary dissection, secondary UA in
patients with fever, thyrotoxicosis, severe anemia, hypoxemia or hypotension.
Clinical presentation
The typical clinical presentation of ACS is prolonged (>20 min.) retrosternal pressure or
heaviness radiating to the left arm, neck or jaw. These complaints may be accompanied by other
symptoms such as diaphoresis, nausea, abdominal pain and syncope(Table 1).
Feature Likelihood
High Intermediate Low
Absence of high-likelihood Absence of high- or
features and presence of intermediate- likelihood
any of the following: features and presence of
Any of the following: any of the following:
History - Chest or left arm pain - Chest or left arm pain or - Probable ischemic
reproducing previously discomfort; symptoms in absence of any
documented angina; - age>70 years; of the intermediate-likelihood
- known history of CAD, - male gender; characteristics;
including MI - diabetes mellitus - recent cocaine use
Examination Transient MR murmur, Extracardiac vascular Chest discomfort reproduced
hypotension, diaphoresis, disease by palpation
pulmonary edema, rles
ECG New, or presumably new - Fixed Q-waves; - T wave flattening or
ST-segment elevation (0,1 - ST-segment depression inversion <0,1 mV in leads
mV) or T wave inversion 0,05-0,1 mV or T wave with dominant R waves;
(0,2 mV) in multiple inversion >0,1 mV - normal ECG
precordial leads
Cardiac Elevated cardiac TnI, TnT, or Normal Normal
CK-MB
markers
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CAD = coronary artery disease; ECG = electrocardiogram; MI = myocardial infarction; MR = mitral regurgitation;
Tn = troponin; CK-MB = creatine kinase MB isoenzyme
From Sabatine M.S., Cannon C.P. Approach to patient with chest pain. In: Bonow R.O., Mann D.L., Zipes D.P.,
Libby P., eds. Braunwald's Heart Disease: a textbook of cardiovascular medicine. 9th ed. Philadelphia, Pa:
Saunders Elsevier; 2011:chap. 53.
Atypical presentations include epigastric pain, neck, jaw, ear, arm discomfort. Some patients,
especially those who are elderly or who have diabetes, present with no pain, complaining only
of episodic shortness of breath, severe weakness, light-headedness, diaphoresis, or nausea and
vomiting. Elderly persons may also present only with altered mental status (Table 2).
The physical examination is frequently normal. Worrisome findings include hypotension, new
jugular venous distension, pulmonary edema, or a new systolic murmur. An important goal of
the physical examination is to exclude non-cardiac causes of chest pain (e.g., pulmonary
embolism, aortic dissection, pericarditis, valvular heart disease, pneumothorax, pneumonia, or
pleural effusion). The Killip classification system (Table 2) and TIMI risk score (Table 3) are
helpful in using physical exam findings to assess a patient's 30-day mortality.
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Diagnosis
The diagnosis is based on a combination of history, ECG, and biochemical markers of cardiac
injury.
ECG. ST segment elevation of 2 mm in two adjacent chest leads and of 1 mm in adjacent
limb leads suggests of STEMI. Other associated findings may include tall peaked T waves and
reciprocal ST-segment depression. Pathological Q waves indicating significant transmural
myocardial damage should be 25% of the R wave, 0.04 sec in duration. The infarction site
can be localized from ECG changes (Table 4).
Patients with UA/NSTEMI may have a normal ECG or may have changes ranging from new T
wave inversions, ST segment depression, or normalization of previously inverted T waves
(pseudonormalization).
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Treatment
Stabilizing measures are similar in all patients with ACS. Patients should be placed in an
environment with continuous ECG monitoring and defibrillation capacity. Patients should
receive aspirin 300 mg orally, analgesia, secure i.v. access and oxygen. Intramuscular injections
and not be given as they cause rise in total CK and risk of bleeding with
thrombolysis/anticoagulation.
STEMI
Patients presenting with ST-segment elevation or left bundle branch block on ECG benefit
significantly from immediate reperfusion and are treated as one group under the term STEMI.
1. Relief of pain, breathlessness and anxiety.
Titrated i.v. opioids (e.g. morphine) are the analgesics most commonly used in this context.
Repeated doses may be necessary. Side-effects include nausea and vomiting,
hypotension with bradycardia, and respiratory depression. Anti-emetics (e.g., metoclopramide
10 mg i.v.) may be administered concurrently with opioids to minimize nausea.
Nitrates (sublingual or intravenous) may lessen pain and can be given, providing the patient is
not hypotensive.
Oxygen (at 2-5 L/min for at least 2-3 hours by mask or nasal prongs) should be administered
to those who are breathless, hypoxic (SaO2<95%), or who have heart failure. Non-invasive
monitoring of blood oxygen saturation greatly helps when deciding on the need to administer
oxygen or ventilatory support.
Anxiety is a natural response to the pain and the circumstances surrounding a heart attack.
Reassurance of patients and those closely associated with them is of great importance. If the
patient becomes excessively disturbed, it may be appropriate to administer a tranquillizer, but
opioids are frequently all that is required.
2. Correction of electrolytes. Potassium and magnesium should be supplemented as both low
potassium and magnesium may be arrhythmogenic.
3. Strategies to limit infarct size (beta-blockade, ACE-inhibitors, reperfusion).
Beta-blockade. Metoprolol i.v. 1-2 mg at a time repeated at 1-2 min. intervals to a maximum
dose of 15-20 mg under continuous ECG and BP monitoring. Aim at a pulse rate of 60 bpm
and systolic BP 100-110 mmHg.
ACE-inhibitors. After receiving aspirin, beta-blockade (if appropriate), and reperfusion,
patients with STEMI should receive an ACE-inhibitor within the first 24 hours of presentation.
Reperfusion.
Primary percutaneous coronary intervention (PCI) is the current gold standard reperfusion
strategy for the treatment of STEMI and demonstrates superior outcome in comparison with
thrombolysis. In settings where primary PCI cannot be performed within 120 min of first
medical contact by an experienced team, thrombolysis should be considered, particularly if it
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can be given pre-hospital (e.g. in the ambulance) and within the first 120 min of symptom
onset. As an adjuct to thrombolysis, rescue PCI should be reserved for patients who remain
symptomatic post thrombolysis or develop cardiogenic shock.
Thrombolysis (fibrinolysis). Fibrinolytic therapy (Table 5) is recommended within 12 h of
symptom onset if primary PCI cannot be performed within 90 min of being able to administer
fibrinolysis and within 120 min from first medical contact and there are no contraindications
(Table 6). The later the patient presents (particularly after 6 h), the more consideration should
be given to transfer for primary PCI (in preference to fibrinolytic therapy) as the efficacy and
clinical benefit of fibrinolysis decrease over time, which, in later presentations, has the effect
of increasing the acceptable time delay before transfer for primary PCI.
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- recent trauma (within 2-4 weeks), prolonged CPR (>10 min.), or major surgery (within 3 weeks);
- noncompressible vascular punctures;
- recent internal bleeding (within 2-4 weeks);
- pregnancy;
- active peptic ulcer disease;
- for streptokinase or anistreplase: prior exposure to either agent or prior allergic reaction
4. Additional therapies
Heparin. Unfractionated heparin (UFH) should be used routinely with rt-PA and its derivatives
for 24-48 hours for a target aPTT (activated partial thromboplasin time) 50-70 sec or 1.5-2.0
times control (to be monitored at 3, 6, 12 and 24 h). Low molecular weight heparin (LMWH)
can be used as an alternative to UFH.
Clopidogrel (loading dose of 600 mg orally followed by a maintenance dose of 75 mg/day)
should be administerd to all patients undergoing primary PCI. If coronary stents are used,
patients should remain on clopidogrel for at least 1 month in bare-metal stents and 12 months
in coated stents.
Glycoprotein IIb/IIIa inhibitors (abciximab, eptifibatide, tirofiban) are recommended
routinely in the context of STEMI treated with primary PCI.
NSTEMI/UA
Timing of angiography and revascularization should be based on patient risk profile. The
GRACE risk score provides the most accurate stratification of risk both on admission and at
discharge due to its good discriminative power. However, the complexity of the estimation
requires the use of computer or personal digital assistant software for risk calculations, which
can also be performed online:
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- recurrent angina despite intense antianginal treatment, associated with ST depression (2 mm)
or deep negative T waves;
- clinical symptoms of heart failure or haemodynamic instability (shock);
- life-threatening arrhythmias (ventricular fibrillation or ventricular tachycardia).
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In other low risk patients without recurrent symptoms a non-invasive assessment of inducible
ischaemia should be performed before hospital discharge. Coronary angiography should be
performed if the results are positive for reversible ischaemia.
Medical management
All patients should be treated with adequate analgesia, i.v. nitrates, beta-blockers and statins (if
not contraindicated). Other agents can also be added depending on the clinical picture.
1. Anti-ischaemic agents
Anti-ischaemic drugs either decrease myocardial oxygen demand (by decreasing heart rate,
lowering blood pressure, reducing preload, or reducing myocardial contractility) or increase
myocardial oxygen supply (by inducing coronary vasodilatation).
Beta-blockers competitively inhibit the myocardial effects of circulating catecholamines and
reduce myocardial oxygen consumption by lowering heart rate, blood pressure, and
contractility. Beta-blockers should be started on presentation, initially using a short-acting
agent (e.g., metoprolol 12.5-50 mg t.i.d) which, if tolerated, may be converted to a longer-
acting agent. Aim for HR of 50-60 bpm.
Nitrates
E.g., glyceryl trinitrate (GTN) infusion (50 mg in 50 mL 1 M saline at 1-10 mL/h). Tolerance to
continuous infusion develops within 24 hours, therefore the lowest eficaceous dose should be
used.
The use of nitrates in unstable angina is largely based on pathophysiological considerations
and clinical experience. The therapeutic benefits of nitrates and similar drug classes such as
syndonimines are related to their effects on the peripheral and coronary circulation. The major
therapeutic benefit is probably related to the venodilator effects that lead to a decrease in
myocardial preload and LV end-diastolic volume, resulting in a decrease in myocardial oxygen
consumption. In addition, nitrates dilate normal as well as atherosclerotic coronary arteries and
increase coronary collateral flow.
Nitrates should not be given to patients on phosphodiesterase-5 inhibitors (sildenafil,
vardenafil, or tadalafil) because of the risk of profound vasodilatation and critical blood
pressure drop.
Calcium channel blockers
Calcium channel blockers are vasodilating drugs. In addition, some have direct effects on
atrioventricular conduction and heart rate. There are three subclasses of calcium blockers,
which are chemically distinct and have different pharmacological effects: dihydropyridines
(such as nifedipine), benzothiazepines (such as diltiazem), and phenylethylamines (such as
verapamil). The agents in each subclass vary in the degree to which they cause vasodilatation,
decrease myocardial contractility, and delay atrioventricular conduction. Atrioventricular block
may be induced by non-dihydropyridines. Nifedipine and amlodipine produce the most marked
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peripheral arterial vasodilatation, whereas diltiazem has the least vasodilatory effect. All
subclasses cause similar coronary vasodilatation. Therefore, calcium channel blockers are the
preferred drugs in vasospastic angina. Diltiazem and verapamil show similar efficacy in
relieving symptoms and appear equivalent to beta-blockers.
E.g., diltiazem 60-360 mg orallt, verapamil 40-120 mg orally t.i.d. Amlodipine/felodipine 5-10
mg PO can also be used.
Other antianginal drugs
Nicorandil, a potassium channel opener, reduced the rate of the primary composite endpoint in
patients with stable angina, but was never tested in ACS patients. Ivabradine selectively
inhibits the primary pacemaker current in the sinus node and may be used in selected patients
with -blocker contraindications.
Ranolazine exerts antianginal effects by inhibiting the late sodium current. It was not effective
in reducing major cardiovascular events in a clinical trial, but reduced the rate of recurrent
ischaemia.
Statins (e.g., atorcvastatin 80 mg qd) have been shown to reduce mortality and recurrent MI in
the acute setting.
2. Antiplatelet agents
Platelet activation and subsequent aggregation play a dominant role in the propagation of
arterial thrombosis and consequently are the key therapeutic targets in the management of
ACS. Antiplatelet therapy should be instituted as early as possible when the diagnosis of
NSTE-ACS is made in order to reduce the risk of both acute ischaemic complications and
recurrent atherothrombotic events. Platelets can be inhibited by three classes of drugs, each of
which has a distinct mechanism of action.
Aspirin (acetylsalicylic acid) targets cyclo-oxygenase (COX-1), inhibiting thromboxane
A2 formation and inducing a functional permanent inhibition in platelets. However, additional
complementary platelet aggregation pathways must be inhibited to ensure effective treatment
and prevention of coronary thrombosis. ADP binding to the platelet P2Y12 receptor plays an
important role in platelet activation and aggregation, amplifying the initial platelet response to
vascular damage. The antagonists of the P2Y12receptor are major therapeutic tools in ACS.
The prodrug thienopyridines such as clopidogrel and prasugrel are actively biotransformed into
molecules that bind irreversibly to the P2Y12 receptor. A new class of drug is the pyrimidine
derivative ticagrelor, which without biotransformation binds reversibly to the P2Y12 receptor,
antagonizing ADP signalling and platelet activation. I.v. GP IIb/IIIa receptor antagonists
(abciximab, eptifibatide, and tirofiban) target the final common pathway of platelet
aggregation.
Aspirin
A daily maintenance dose of 75100 mg should be continued indefinitely. It has the same
efficacy as higher doses and carries a lower risk of gastrointestinal intolerance.
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3. Anticoagulants
Several anticoagulants, which act at different levels of the coagulation cascade, have been
investigated or are under investigation in NSTE-ACS:
Indirect inhibitors of coagulation (need antithrombin for their full action)
Indirect thrombin inhibitors: UFH
LMWHs
Indirect factor Xa inhibitors: LMWHs
fondaparinux
Direct inhibitors of coagulation
Direct factor Xa inhibitors: apixaban, rivaroxaban, otamixaban
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6. Statin: titrate to achieve target LDL-C levels <1.8 mmol/L (<70 mg/dL)
7. Lifestyle: risk-factor counselling, referral to cardiac rehabilitation / secondary prevention
programme.
References.
A - Basic:
1. Davidsons Principles and practice of medicine (21st revised ed.) / by Colledge N.R., Walker
B.R., and Ralston S.H., eds. Churchill Livingstone, 2010. 1376 p.
2. Harrisons principles of internal medicine (18th edition) / by Longo D.L., Kasper D.L.,
Jameson J.L. et al. (eds.). McGraw-Hill Professional, 2012. 4012 p.
3. The Merck Manual of Diagnosis and Therapy (nineteenth Edition)/ Robert Berkow, Andrew
J. Fletcher and others. published by Merck Research Laboratories, 2011.
4. Web -sites:
a) http://emedicine.medscape.com/
b) http://meded.ucsd.edu/clinicalmed/introduction.htm
B - Additional:
1. Braunwalds Heart Disease: a textbook of cardiovascular medicine (9th ed.) /
by Bonow R.O., Mann D.L., and Zipes D.P., and Libby P. eds. Saunders, 2012. 2048 p.
2. Braunwalds Heart Disease: review and assessment (9th ed.) / Lilly L.S., editor. Saunders,
2012. 320 p.
3. Cardiology Intensive Board Review. Question Book (2nd ed.) / by Cho
L., Griffin B.P., Topol E.J., eds. Lippincott Williams & Wilkins, 2009. 385 p.
4. Cleveland Clinic Cardiology Board Review / Griffin B.P., Kapadia S.R., Rimmerman C.M.,
eds. Lippincott Williams & Wilkins, 2012. 952 p.
5. Hursts the Heart (13th ed.) / by Fuster V., Walsh R.A., Harrington R., eds. McGraw-Hill,
2010. 2500 p.
5. Oxford Handbook of Cardiology (2nd ed.) / by Ramrakha P., Hill J., eds.
Oxford University Press, 2012. 851 p.
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Comatous states
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(interview relatives and witnesses) and clinical observations are very important.
First of all ask about the duration of unconsciousness and was it lost suddenly or
there were other levels of altered consciousness. Ask about the events prior to incident: did
the patient fell and was there a chance of head injury? Did he have fever, flu or jaundice?
Are there any sings of chronic diseases like diabetes, epilepsy, hypertonic disease? Have the
patient ever suffered from similar unconsciousness episodes? Were there any suicide
attempts? If the comatose condition was not sudden, have the patient complained of
vomiting, convulsions? Pay attention to the personal things of the patient: you can find
medical documents, medicine packages, diabetic bracelets or necklaces, etc.
If the anamnesis failed to reveal the coma etiology, concentrate on objective
symptoms.
Skin colour: extreme paleness can be a sign of great blood loss, circulatory
collapse, blood diseases. Cyanosis is a symptom of hypercapnic coma caused by respiratory
failure or asphyxia (hanging, drowning, convulsions). Hyperaemic face allows you to think
about atropine and carbon monoxide poisonings, hyperglycaemic coma or infectious
disease.
Head position: tilted back head is a sign of meningitis, tetanus, hysteria; head
turned aside can be the symptom of stroke.
Pathological types of breathing are also helpful in coma diagnostics: Cheyne-
Stokes breathing (periods of apnoea, which are followed with chaotic frequent breathing)
and Biots breathing (periods of apnoea which are followed with breathing of equal
amplitude) show deep affection of central nervous system. Kussmaul breathing (deep and
laboured) proves accumulation of acid metabolites (metabolic acidosis) of exogenous (in
case of poisonings) or endogenous (diabetic ketoacidosis) nature. Fever and rapid deep
breathing are probable signs of infectious coma. Remember that per each excess body
temperature degree there are 5-7 excess breathes and 10 excess heart beats.
Generally when you are coming to the patient with consciousness disorders try to
do this from the side of patients head (nape): this way you can easily improve airways
patency if necessary (thrust the jaw forward for example) and avoid accidental injuries from
the patient if his moves are uncontrolled.
You can always identify simulation or hysteric coma by opening the eyes of the
patient: in case of simulating conscious patients or hysteric patients you will feel the
resistance of the eyelids. Unconscious patients never resist when you try to open their eyes.
Pressing the eyeballs toy can evaluate their tone: soft eyeballs with decreased
tone are the symptom of hypovolemia (bleeding, dehydration) or shock condition. However
they can also be part of hyperglycaemic coma clinic.
The depth of coma is assessed with the reflexes reduction. If patient reacts to the
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external stimuli - its a moderate coma. If corneal reflexes are preserved with depressed
other reflexes its a deep coma. Lack of photoreaction is a symptom of terminal coma.
Pupils diameter varies: pupils are narrowed in case of sleeping pills overdose or
organophosphate poisonings; terminally narrow pupils you can see in patients after drugs
admission; pupils are dilated in case of hypoxia, neuroleptic poisonings, antihistamine
medicines intoxications; the widest pupils you can observe in atropine poisoning.
Anisocoria (pupils of different size) is a symptom of local CNS injuries. In most
cases you notice this sign when a trauma causes intracranial haematoma. Examine those
patients carefully: look for bruises and scratches on the head (including parts covered with
hear). Sometimes you can even notice eyeballs deviation to the side of injury. Lack of
patellar and heelstring reflexes proves deep CNS affection. Pathological Babinskis reflex
shows organic CNS injury. Muscular tone asymmetry is a sign of stroke, tumour,
haematoma, etc.
Dont forget to assess other systems and organs, because brain reaction can be only
the response to a serious visceral pathology. For example unconsciousness can be a
consequence of cardiac arrhythmia (Morgagni-Adams-Stokes syndrome). And on the
contrary: CNS violations can cause rhythm disorders.
Pericardial murmur and pleural rub can indicate uraemic coma. Changes of liver
size are features of hepatic coma. Enlarged spleen is a symptom of bone marrow or liver
diseases.
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In case of comatose patients use all your laboratory and instrumental possibilities:
perform head X-ray, CT, liquor tests, encephalography, angiography, usual blood tests, etc.
For assessment of central nervous system condition Glasgow Coma Scale was
proposed in 1974.
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b. turn patient aside by pulling the flexed knee and shoulder on the same side; then
press the hand of the upper arm to the chick; make sure breathing is not difficult.
Some comatose patients can be hyperreflexive, hyperkinetic and disposed to
cramps.
In case of cramps you should:
- lay patient in a supine position on a flat surface (to avoid injuries);
- prevent tongue biting inserting the gag or any available items (like
stick or spoon wrapped with cloth);
- keep the airways open (usual methods described above) and hold the
head in order to prevent trauma and asphyxia;
- provide oxygenation with the mask;
- between the attacks get an i/v access and give the patient 10-20 ml of
25% magnesium sulphate solution, 2 ml of 0,5% Diazepam solution;
- clean the oral cavity from blood, saliva, gastric contents;
- if patients breathing is inadequate provide artificial ventilation.
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Hyperlactacidemic coma
Hyperlactacidemic coma is a diabetic coma, which appears in decompensated
diabetic patients who suffer from hypoxia (disorders of respiration or oxygen
transportation). In case of oxygen deficiency intracellular respiration is blocked and acid
metabolites (including lactic acid) are accumulated. This brings acidosis and diabetic
decompensation.
The most common reasons of hypoxia are pneumonia, shocks and anaemia.
Intensive treatment includes usual steps of hyperglycaemia therapy, but main accent
is made over the liquidation hypoxia:
- check the efficiency of respiration and improve it if necessary (mask
oxygenation or even artificial ventilation);
- provide shock treatment if the it is the reason of patients comatose
condition;
- transfuse blood components if the cause was anaemia;
- inhibit excessive metabolic reactions (normalize body temperature, use
sedative medicines or neuroleptics if patient has psychomotor excitement and
agitation);
- use antihypoxants (cytochrome c for example).
Hypoglycaemic coma
As you can see from the name hypoglycaemic coma is a condition of low glucose
concentration in the blood. Unlike most of the previous types of diabetic coma it develops
really quickly: within 30-60 minutes. The most common reason for this coma is improper
insulin admission or diet violations (insulin overdose or lack of meal after insulin
injection). Among the other reasons are: overdose of oral hypoglycaemic drugs
(sulfonylurea), physical exercises without insulin dose correction, chronic alcoholism
(violated glycogenolysis), hepatic diseases, postoperative gastric diseases (influence speed
of glucose absorption).
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Your clinical findings will be mostly connected with brain energetic deficiency:
weakness, dizziness, coordination violations, dysphoria and inadequate behaviour,
unconsciousness and cramps appear as a result of neuroglycopenia (as you remember
glucose is the only energetic substrate for neurons, unlike other organs brain is 100%
dependable on this monosaccharide).
Hypoglycaemia is classified according to the severity of the symptoms as mild
(consciousness preserved, patient is able to take care of himself and hypoglycaemia is
liquidated by oral admission of simple carbohydrates), moderate (patient needs help, but his
condition is improving after oral admission of simple carbohydrates) and severe (patient is
unconscious, needs help and his hypoglycaemia is liquidated only with parenteral glucose
infusion).
When glucose concentration is 3,33-2,77 mmol/l you observe only mild
hypoglycaemic symptoms. When it diminishes to the level 2,77-1,66 mmol/l the clinical
picture is complete (except the unconsciousness). Glucose concentration less than 1, 66
mmol/l induces coma. Hypoglycaemia lasting 4-6 hours can end up with irreversible
cellular damages and even brain death.
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Clinical picture is characterized with: pale skin wet from sweat; hemodynamics
(central venous pressure, blood pressure) and other systems might be not involved in the
initial stages; eyeballs tone and skin turgor are normal, mucous membranes are moist.
Breathing is normal, not pathological Kussmaul breathing of ketoacidosis. There is no
acetone-like breath odour. Urinary output is normal.
Those clinical features are quite typical, but to prove hypoglycaemia you should
wait laboratory results (blood tests will show low glucose concentration).
Immediate aid.
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Intensive therapy.
In case of severe hypoglycaemia use usual algorithms:
- provide oxygenation and adequate ventilation;
- get an i/v access as soon as possible;
- give 20-40-60-80-100 ml of 40% glucose solution (actually lately it is
recommended to use 20% solutions because they cause less irritation of the
peripheral veins); the precise dose you will choose according to clinical improvement
of CNS condition (but not more than 120 ml);
- in glucose solutions are not effective prescribe 1 mg of glukagon s/c; 1
ml of 0,1% adrenaline solution s/c, 3060 mg of prednisolone solution i/v;
- additionally you can use: 100 mg of cocarboxylase i/v, 5 ml of 5%
ascorbic acid solution,- or any required symptomatic medicines;
- in case of brain oedema use 15% mannitol solution (0,5-1,0 g/kg) i/v;
- even after clinical improvement patients should stay in the ITU for a
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while, because his condition is still unstable and encephalopathy is still probable.
In children: when you are out of hospital use glukagon subcutaneously (0,5 mg with
children under 5 years and 1 mg with elder kids). When you are in the ITU use i/v infusions
of 20% glucose (1 ml/kg) during first 3 minutes, then 10% solution of glucose (2-4 ml/kg),
check the glycemia and if you will not see the CNS improvement continue with 10-20%
solutions of glucose and keep glucose concentration at the level of 7-11 mmol/l. Check
glycemia level every half an hour or hour.
Control tests.
1. According to the GCS deep coma is characterized with:
A. 4-5 points
B.13-14 points
C.11-12 points
D. 3 points
E. complete lack of reaction to external stimuli
2. What is the condition of normal CNS functioning?
A. getting of 20-25 % of circulation blood volume every minute;
B. glycemia level not less than 3 mmol/l;
C. normal concentration of blood proteins and lipids;
D. brain should get at least 10% of total blood oxygen;
E. plasma osmolality should be 185-210 mOsm/l
3. Hyperglycaemic ketoacidotic coma is not characterized with:
A. metabolic acidosis;
B. overhydration;
C. low central venous pressure;
D. respiratory alkalosis;
E. severe paleness.
4. Hypoglycaemic coma is characterized with:
A. critically low blood pressure;
B. decreased tone of eyeballs;
C. wet skin;
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Task 1.
Andrew, the doctor, is examining Patience, the patient of 52. Patience is
unconscious. His breathing is noisy and frequent; he has acetone-like breath odor; his
skin and mucous membranes are dry; his blood pressure is low.
1. What symptoms will help Andrew to make a proper diagnosis?
2. Write the algorithm of Andrews actions: clinical examination and laboratory
diagnostics.
Task 2.
Choose the symptoms typical for:
a. hyperglycaemic coma;
b. hypoglycaemic coma.
1. Acetone-like breath odour. 2. Paleness.3. Dry skin and mucous membranes. 4.
Wet skin.5. Hyperaemic face. 6. Tachycardia.7. Normal heart rate. 8. Decreased tone of
eyeballs.9.Normal eyeballs tone. 10. Usual breathing rate.11. Deep breathing. 12.
Normal blood pressure. 13. Hypotension. 14. Normal urine output. 15. Oliguria. 16.
Hyperkalemia. 17. Normal potassium concentration. Hypokalemia.19. Increased
hematocrit. 20. Unchanged hematocrit. 21. Hyperglycaemia. 22. Hypoglycemia. 23.
Central venous pressure over 4 cm H2O. 24. Central venous pressure 6-10 cm H2O.
Task 3. What medicines are not allowed for patients with hyperosmolar
nonketotic coma and why?
a. Insulin; b. saline solution; c. 2,5 % glucose solution; d. 4% sodium
bicarbonate solution; e. 10% calcium chloride solution; e. 0,45% sodium chloride
solution; f. mannitol solution; g. heparin; h. spironolalactone; i. prednisolone.
Task 4.
Andrew, the student of medicine, is a witness of such situation: in the street man
suddenly felt and in few seconds cramps began.
What should Andrew do? What is the probable reason of this situation?
Task 5.
Patience, the patient of 50, was found unconscious by the ambulance workers at
4 oclock in the morning. During the admission to the hospital: patient is not reacting to
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pain stimuli. Respiration is normal, however in supine position airways loose patency.
Alcohol odour is quite evident. Pupils are asymmetric, right is wider than the
left, photoreaction is inhibited. Haemodynamics is stable. Abdomen is soft, peristalsis is
active. Urination is not controlled.
What is the probable diagnosis? What treatment should be prescribed?
Acute poisonings.
Acute poisoning is a chemical injury, which occurs when chemical substance gets to
the organism and violates its vital functions. If the substance is aggressive enough and
proper treatment is not provided on time poisoning will bring death.
Although there are over 500 toxic substances which may cause acute poisoning,
clinical picture is made up of quite similar syndromes. Proper diagnostics of these
syndromes allows avoiding life-threatening complications and gets the chance to make
correct preliminary conclusions about the nature of poisoning.
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and toxic coma. One of the comas deepness criteria is reaction of the patient to the painful
stimuli (you can also check reaction to smell of ammonium chloride). Lack of reaction is a
sign of coma. Dont live such patient without observation, because his condition is severe
and at any moment life-threatening complications may appear: those patients have tendency
to bradypnoea up to complete respiratory arrest. Also you should not forget that decreased
tone of soft palate and tongue in a supine position will violate patency of the airways and
patient can die of asphyxia. In addition comatose condition influences reflexes and lack of
swallowing can lead to entrance of saline and gastric contents into the airways (and thus to
development of aspiration pneumonia).
Usually CNS depression is caused by excessive alcohol consumption or admission
of its surrogates, overdose of neuroleptics, sleeping pills, drugs, sedative medicines,
antidepressants and carbon monoxide poisoning. You can remind intensive treatment of
comatose patients in the chapter 5.
Some poisoning are followed with acute intoxication psychosis (mental disorders,
hallucinations, time and space disorientation, inadequate behavior). This clinical picture
you can observe in case of atropine poisoning (and also atropine-like agents: tincture of
dope, henbane, amanita) or cocaine, tubazid, antihistaminic drugs and organophosphates
poisoning.
In case of psychosis you will have to immobilize patient in the bed for his own
good and safety (to avoid injuries both patients and those of the stuff). You will also have
to do this in order to maintain i/v lines for antidotes and sedative infusions (aggressive
patient will try to remove everything he or she considers irritating). Constantly observe the
patients vital functions.
Toxic affection of the respiratory system can progress as the violation of:
a. external respiration - neurogenic form, aspirations and obstructions of the
airways which bring hypoxic hypoxia;
b. hemoglobins function aniline and nitrobenzene create methmoglobin, carbon
monoxide connected with hemoglobin creates carboxyhemoglobin and neither the first nor
the second is capable of normal oxygen transportation; heavy metal, organic acids and
arsenic poisonings lead to destruction of the red blood cells and emission of the free
hemoglobin into the plasma;
c. oxygen transportation due to the decrease of circulating blood volume exotoxic
shock;
d. cellular respiration tissue hypoxia occurs when cytochromes are blocked with
toxins like cyanides.
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Practically all severe poisonings earlier or later lead to hypoxia, because they
violate oxygen supply, transportation and consumption.
Your immediate therapy actions in this situation will be:
- to assess of respiratory system (described above);
- to provide of airways patency (cleaning of the oral cavity, aspiration of
the saline and gastric contents, conicotomy if necessary, etc.);
- to begin oxygen supply (face mask, nasal catheter);
- to start artificial ventilation if necessary;
- to prescribe antidotes if they are available (methylene-blue in case of
nitro compounds poisonings, unithiolum in case of heavy metals and arsenic
poisonings, cytochrome c in case of tissue hypoxia);
- to start hyperbaric oxygenation in case of carbon monoxide poisoning;
- to begin infusion therapy in order to stabilize the hemodynamics;
- to start general detoxification;
- to prescribe symptomatic treatment and provide prevention of the
complications (for example prescription of antibiotics).
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shade of skin is a symptom of cardiac disorders. Wet skin might be the symptom of
hypoglycaemic coma, hypercapnia or organophosphate poisoning, which are covered with
the obvious clinic of alcohol poisoning. In case of moderate coma vital functions are usually
not involved. Pupils are narrowed or dilated, photoreaction is preserved. Objective criterion
of alcohol poisoning is alcohol concentration of the blood:
- less than 1,5 light inebriation
- 1,5-3,5 moderate inebriation
- 3,5 and more severe inebriation
Lethal concentration of alcohol is 5-6.
The most common complications of alcohol poisoning are next:
- obstruction of the airways with the tongue, soft palate or biological
fluids (vomit, saline, sputum, blood) in supine position;
- regurgitation of the gastric contents and development of aspiration
pneumonia; lethality is nearly 70%;
- head traumas with brain injuries: patients usually fell and hurt
themselves; the problem with such injuries is that the clinic of hematoma (subdural,
epidural, intracerebtal) is quite often covered with alcohol intoxication and this is
why you should always remember about the differential diagnostics. To make a
correct diagnosis in case of coma you should check the specific symptoms such as
anisocoria (there is no poisoning which causes pupils asymmetry!), signs of head
injury (scratches, bruises, skull deformations, oto-liquorrhea and nasal liquorrhea,
nasal and ear bleeding), asymmetric tendon reflexes and muscle tone, disparity
between the amount of alcohol and deepness of coma, prolonged unconsciousness
(alcohol coma even without proper treatment lasts only 3-4 hours);
- other traumatic injuries (rib fractures which violate external breathing,
spleen or liver ruptures with haemorrhagic shock, ruptures of hollow organs with
peritonitis; limb fractures);
- compartment syndrome appears when certain enclosed space within
the body for several hours suffers from the decreased blood flow (for example when
patients spends few hours in one inconvenient position); even when blood supply
will be restored necrotic products will continue pathological process through toxic
affection of the life-important organs (for example free myoglobin can cause renal
failure).
There is always possibility of chronic diseases exacerbations on the background
of alcohol poisoning (stroke, myocardial infarction). Remember about the necessity of
complete examination (inspection, palpation, percussion and auscultation of undressed
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patient) of such alcohol victims it is the only way to find all the diagnostic mysteries
patients hide!
Intensive treatment:
- evaluate CNS condition (deepness of the coma);
- provide airways patency and adequate respiration (described above; if
necessary intubate the patient and begin artificial ventilation);
- check the cardiovascular system: heart rate, pulse, blood pressure;
- in case of severe hemodynamic disorders provide infusion therapy;
- insert the stomach probe and remove its contents using lavage with
water;
- take blood samples and check blood alcohol level (obligatory!);
- prescribe intravenously: 60-80 ml of 40% glucose solution, 60-80 ml
of 4% sodium bicarbonate solution, 5-10 ml of 5% ascorbic acid, 1-2 ml of vitamin
B1 solution;
- if there are no comorbidities add analeptic solutions i/m (2-3 ml of
caffeine or 2 ml of cordiamin);
- in case of severe intoxication begin forced diuresis.
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the burn. Systemic disorders are characterized with exotoxic shock which develops as
burn shock (unbearable pain, dehydration, toxic affection of the heart, decrease of
cardiac output, spasm of arterioles and microcirculation block). Organic acids also
provoke hemolysis of red blood cells: free haemoglobin transforms into hydrochloric
haematin and obturates renal tubules, causing acute renal failure.
Intensive treatment principles:
- evaluate patients condition: external respiration, consciousness,
cardiovascular system;
- adequate pain relief with narcotic painkillers and non-steroidal
anti-inflammatory drugs (1-2 ml of 1% morphine solution; 2 ml of 50% analgin
solution);
- liquidate the spasm of gastric cardia and oesophagus (1 ml of 0,1%
atropine solution i/m, 5 ml of baralgin solution);
- clean the stomach during first 10 hours after poisoning; insert the
stomach probe (cover it thickly with Vaseline and dont push too hard); use water for
lavage and dont try to perform chemical inactivation of the poison, because during
the reaction carbon dioxide can exude and acute expansion of the stomach leads to it
rupture;
- provide treatment of shock (sometimes up to 10-12 liters/day of
infusions);
- in case of organic acids poisonings (acetic acid, oxalic acid get into the
blood) give 1500-2000 of 4% sodium bicarbonate solution intravenously slowly with
diuretics; these actions will help to remove hemoglobin (released due to red blood
cells hemolysis) and thus to prevent acute renal failure;
- in case of obstructive breathing disorders (mucous membrane edema)
use steroids (90-120 mg of prednisolone), antihistamine drugs (2 ml of 1% dimedrol
solution intravenously), sedative medicines (2 ml of 0,5% diazepam solution);
perform tracheostomy or conicotomy if necessary;
- prescribe antibiotics for infectious diseases prevention (for example in
case of prolonged artificial ventilation);
- symptomatic treatment.
During the recovering period patient may need surgeries for restoration of
gastrointestinal tract: the most common practice is the bouginage of the oesophagus or,
if necessary, oesophagus plastic.
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Among the toxic gases are carbon monoxide, car exhausts, propane and butane,
ammoniac gases. The last one is the most toxic: few inhales are enough to cause
unconsciousness.
The foundation of the pathology lies within the atypical haemoglobin
carboxyhemoglobin combination of normal haemoglobin and toxic gas. Oxygen
transportation if violated (in case of severe poisonings there are nearly 70-80% of
changed haemoglobin) and thus haemic hypoxia appears. In addition within the tissues
cytochromes are connected with toxic substances and this leads to tissue hypoxia.
Clinical findings in case of carbon monoxide poisoning depend on the severity
of the poisoning. In case of mild intoxication they are: headache, nausea, vomiting.
Moderate intoxication shows unconsciousness for 12-16 hours and severe intoxication
is characterized with coma, central disorders of breathing, toxic affection of heart and
other organs, etc.
If intoxication advances changes of central nervous system become irreversible
(brain death is possible).
Intensive treatment.
In case of mild and moderate poisonings you should you should carry the patient
out of the toxic atmosphere as soon as possible. In hospital conditions you should
provide oxygen supply, get an intravenous line for crystalloids infusion and prescribe
vitamins.
In case of severe intoxication begin artificial ventilation with high oxygen flow.
Luckily there is an antidote for carbon monoxide poisoning: hyperbaric oxygenation.
Connection with oxygen is more natural for haemoglobin and when the pressure of
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oxygen is higher than its usual partial pressure carbon monoxide is replaced from the
haemoglobin. Usually in case of comatose patients 40-50 minutes sessions every 6-12
hours are enough.
To normalize tissue metabolism prescribe antihypoxants: 20% solution of
sodium oxybutirate (20-40 mg/kg i/v) and cytochrome c (2-3 ml i/v) every 4-6 hours. To
improve microcirculation dilute the blood with crystalloid infusions (check the level of
hemodilution with hematocrit stop when it will reach 0,3-0,35 l/l).
Prevent the infectious complications and brain oedema with standard methods.
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Forced diuresis.
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Control tests.
1. What medicine should be used as an antidote in case of severe soporific drugs
poisoning?
A. bemegride
B. cordiamin
C. there is no such meidicine
D. unithiol
E. cytiton
2. What is the most common death reason in case of alcohol poisoning?
A. acute liver failure
B. acute respiratory failure
C. acute renal failure
D. acute heart insufficiency
E. collapse
3. What is necessary for the patient, who took 60 ml of acetic essence?
A. to give 4% sodium bicarbonate solution i/v
B. to clean the stomach with alkaline solution in order to neutralize the acid
C. to use unithiol as an antidote
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Task 1.
Patience, the patient of 19 is transported to the ITU by witnesses from the street.
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Clinical findings: unconscious, cyanotic wet skin, 6 breathes per minute, respiration
shallow, blood pressure 70/40 mm Hg, heart rate 112/minute. Name the reason of vital
disorder and write the principles of intensive care (algorithm).
Task 2.
Patience, the patient of 19, was found unconscious in his own apartment by the
ambulance workers. Clinical findings: total cyanosis, shallow breathing, respiration rate
5/min, pupils extremely narrowed, photoreaction is absent, blood pressure 80/40 mm Hg.
In the elbow area there are noticeable signs of injections. Name the reason of vital
disorder and write the principles of intensive care (algorithm).
Task 3.
Patience, the patient of 23 was hospitalized into ITU with the diagnosis:
mushroom poisoning. It turned out, that yesterday she was eating cooked champignons.
8 hours later she noticed vomiting and diarrhoea. Clinical findings: scleral icterus, dry
coated white tongue; painful abdomen (epigastrium and right hypogastric area), painful
and enlarged liver (2 cm); hemodynamics and respiration are not violated.
Write the diagnosis and the phase of the disease.
Task 4.
Patience, the patient of 18, is transported to the toxicology unit with delirium.
Clinical findings: hyperaemic face, dry skin, dilated pupils. Blood pressure 140/70 mm
Hg, heart rate 127/minute. It is know, that 2 hours ago she took 10 unknown tablets
during the suicidal attempt. What is the diagnosis and what are your actions?
Task 5.
Patience, the patient of middle age, was found by the ambulance workers in his
own kitchen unconscious. Clinical findings: specific smell of organophosphates in the
room, signs of vomit on the clothes, miosis, cold clammy skin with cyanotic shade,
foamy white sputum in the mouth, blood pressure 90/50 mm Hg, heart rate 54/minute.
What is the diagnosis? What immediate aid should be provided during pre-hospital
stage?
Task 6.
Adams family were celebrating the New Year Eve near the fireplace. In the
morning came the carol singers and found hosts in a condition of deep sleep. Dream
team, the ambulance workers, who came to the place of the accident, stated: 2 adults
and their children in comatose condition, vomit signs on the clothes, rapid
breathing, pupils dilated with weak photoreaction; heart rate is 110-120 per minute,
rhythmic; blood pressure is high.
Name the reason of the accident and describe the actions of the Dream team.
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Task 7.
Name the poisoning agent for each antidote: a. atropine, b. unithiol, c. naloxone,
d.tetacinum, e. ethylic alcohol, f. dipiroximum, g. lipoic acid?
Among the natural vasoconstrictors (agents, which cause constriction of the blood
vessel) are epinephrine, norepinephrine, serotonin, angiotensin II. Stress enhances the secretion
of cathecholamines, their blood concentration increases and arterioles constrict. Spasm of the
arterioles is the basis of blood flow centralization: peripheral flow is disregarded in order to
provide brain with the oxygenated blood as long as possible. To the group of vasodilatators
(agents, which provide dilatation of the vessels) belong acid metabolites (lactate, pyruvate,
adenylic acid, inosinic acid), bradykinin, acetylcholine, different medicines (neuroleptics,
-adrenergic antagonists, peripheral vasodilatators, ganglionic blocking agents, etc.), some
exogenous poisons. All of them cause blood flow decentralization: opening of arterioles and
distribution of the blood from central vessels to the capillary bed.
Capillaries are the interweaving network of the smallest body vessels with the general
length of 90-100 thousands of kilometers. However simultaneously work only 20-25% of them.
They provide metabolic exchange bringing oxygen and nutrients to the tissues and take back
wastes of metabolism. Periodically, every 30-40 seconds one of them get closed and others
open (vasomotion effect). Capillaries contain 12% of the whole circulating blood volume, but
different pathological conditions can increase this amount even 3 and more times.
Used blood from the capillaries flows to the venous system. Veins are the blood
reservoir, which contains 70% of the total circulating blood volume. Unlike arteries they are
capable of volume control and thus they influence the amount of blood, which returns to the
heart.
The most important haemodynamic index of venous system is central venous pressure.
CVP represents the pressure which blood causes to the walls of cava veins and right atrium.
This parameter is an integral index of circulating blood volume, systemic vascular resistance
and pump function of the heart. It can be measure with a special device called
phlebotonometer (pic. 4.9) or with a usual infusion set and a ruler. Normally CVP measured
from the sternum point is 0-14 cm H2O and from midaxillary line is 8-15 cm H2O.
Central venous pressure decreases (sometimes even to negative) in case of:
- blood loss
- excessive water loss (dehydration)
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MAP defines the level of pressure necessary for the metabolic exchange in the tissues.
Its measurement allows the evaluation of tissue perfusion level.
Blood pressure depends on different factors, but the most important are cardiac output
and vascular resistance (mostly arterioles). This dependence is direct, thus you can increase
blood pressure using:
- infusion of vasoconstrictors - solutions of epinephrine, phenylephrine
(mesaton), etc. (they will increase the vascular resistance);
- infusion of hydroxyethyl starch solutions or saline (they will increase
circulating blood volume)
- infusion of cardiac glycosides or other medicine which stimulate
myocardium
General volume of blood in the body of a healthy adult is nearly 7% from the body
weight: 70 ml per kilogram for male and 65 mil per kilogram of body weight for female. Of
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course circulating blood volume is lower, because part of blood is out of metabolic processes
as a reserve. CBV can be measured with the infusion of coloring substance to the blood flow
(Evans blue, polyglucin) and later evaluation of its dissolution degree.
Therefore measurement of CVP, BP, cardiac output and circulating blood volume allow
to evaluate condition of circulation system of the patients and to provide adequate correction.
The reasons of the failure vary greatly: mechanic injuries, blood loss, burns,
dehydration, exogenous and endogenous intoxications, immediate hypersensitivity reaction,
ischemic heart disease, neural and humoral regulation disorders of vascular tone.
Acute cardiac failure is a disorder of heart pumping action. It develops due to primary
heart problems or secondary, under the influence of extracardiac factors such as infection or
intoxication. There are two types of heart failure: left-sided and right-sided.
Left-sided heart failure is an inability of left ventricle to pump blood from the
pulmonary circuit to the systemic circuit. The most common reasons of it are myocardial
infarction, mitral insufficiency, left AV valve stenosis, aortic valve stenosis, aortal
insufficiency, hypertonic disease, coronary sclerosis, acute pneumonia.
Coronary circulation is possible only during the diastole and in those conditions every
violation of coronary passability decreases cardiac output. This way during the systole part of
the blood is not injected into aorta, but stays in the left ventricle. Diastolic pressure in the left
ventricle increases and blood is literally forced to stagnate in the left atrium. At the same time
right ventricle functions normally and continues to pump usual amounts of blood to the
pulmonary circuit. Thus hydrostatic pressure in the vessels of pulmonary circulation increases,
fluid part of the blood moves first to the lung tissue and then, through alveolar-capillary
membrane, to the alveolar lumen.
Clinically pulmonary edema begins with dyspnea (during physical activity or rest).
Later attacks of dyspnea are connected with persistent cough with white or pink blood-tinged
phlegm. During the attack patient tries to sit as in this position breathing is easier. This
condition is called heart asthma. When hydrostatic pressure is over 150-200 mm Hg, fluid
part of blood moves to the alveolar lumen causing development of pulmonary edema.
Pulmonary edema is divided into interstitial and alveolar edema.
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Interstitial edema is a condition during which serous part of stagnated in the pulmonary
circuit blood infiltrates the lung tissue, including peribronchial and perivascular spaces.
During alveolar edema not only the plasma, but also blood components (red and white
blood cells, platelets) get out from the vessels. During the respiratory act blood mixes with the
air creating large amount of foam, which violates gas exchange. This way, in addition to
circulatory hypoxia, hypoxic hypoxia appears.
Condition of the patient gets worth quickly. Sitting position is optimal, but not as
helping as previously. Respiratory rate is nearly 30-35 breathes per minute, but attacks of
breathlessness are constant. Skin is pale with acrocyanosis. Hypoxia of central nervous system
usually causes psychomotor agitation. Respiratory acts are noisy; during cough pink blood-
tinged phlegm is released. Auscultation allows you to hear different wet rales, sometimes its
even possible to hear them standing aside the patient without phonendoscope.
Pulmonary edema can be also divided according to the blood pressure level: the one
with elevated pressure is caused by a hypertonic disease, aorta valve insufficiency or disorders
of cerebral perfusion; another one is caused by total myocardial infarction, acute inflammation
of myocardial muscle, terminal valve defects,severe pneumonia and is characterized with
normal or low blood pressure.
Immediate aid
- make sure patient is sitting with his legs down (orthopnea)
- provide oxygenation through nasal catheter (before placing oil it with
glycerin, insert it to the depth of 10-12 cm distance from the wing of the nose to
auricle) or face mask. Do not use Vaseline, because it can burn in atmosphere with high
concentration of oxygen.
However if catheter is not deep enough patient will suffer from an unpleasant
burning feeling, because oxygen flow will dry mucosa layer of the nasal cavity; also in
this situation concentration of oxygen will be lower than expected.
- put venous tourniquets on the limbs in order to reduce amount of blood
returning to heart: venous bed of limbs can reserve up to 1,7 liters of blood;
- constantly control heart and kidney activity (ECG, SaO2 , and blood
pressure are checked automatically trough the monitor; to control diuresis you should
insert Foley catheter;
- catheterize central vein, because amount of infusions should be based on
central venous pressure;
- use medical defoamers if they are available (ethyl alcohol or
antiphomsylan solution) combined with oxygen inhalation
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Collapse is a vascular failure. It occurs when body is not able to provide blood flow
according to the new level of its needs (either because reaction is not fast enough or
because sympathetic activation fails).Vascular bed volume and circulating blood volume are
disproportional: too much blood gets to the microcirculation vascular reserve and the
amount, which returns to the heart is not enough for the systemic needs (so called
decentralization of the blood flow). Cardiac output and blood pressure decrease, that
causes hypoperfusion of the central nervous system and thus unconsciousness and
life-threatening complications.
Collapse definition is a bit nominal, because if such reaction extends in time the
state of shock develops. Shock itself can equally run as a vascular failure or as a sudden
clinical death.
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Water deficiency brings lowering of cardiac output, blood pressure and central venous
pressure (through decrease of blood volume returning to the heart, which leads to
compensatory adrenergic vasoconstriction).
Dehydration causes body weight loss, skin and mucosa dryness, decrease of
subcutaneous turgor and eyeballs tone, hypothermia, tachycardia, oliguria, thirst. While
dehydration progresses compensatory mechanisms weaken and central nervous system suffers:
patients become sluggish, confused; hallucinations, cramps and unconsciousness are also
possible. Laboratory tests show blood concentration.
One of the most important things in treatment of dehydrated patients is daily balance
of fluid: check it carefully trough measuring of daily received and lost fluids (food, infusions,
stool and urine output). In case of fever or tachypnea make necessary corrections. Balance
should be calculated every 12-24 hours (special paper forms make this easier).
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Daily fluid balance is calculated by adding all the received fluids (both enteral and
parenteral ways) and deducting urine output, stool, perspiration and breathing water loss.
You should remember, that perspiration depends on body temperature: in case of
normal temperature (36,6C) patient looses 0,5 ml/kg of water during every hour; 1 degree of
temperature elevation adds 0,25 ml/kg to normal value of 0,5 ml/kg.
According to the fluid balance infusion therapy is divided into positive (for dehydrated
patients), negative (for overhydrated patients) and zero (for patients without balance
disorders).
Water deficiency is calculated according to the formula:
W def = (Htp-Htn)* 0,2 BW/ Htn,
W def water deficiency, l;
Htp hematocrit of the patient, l/l;
Htn - normal hematocrit, l/l;
BW body weight, kg.
Use crystalloids to treat water deficiency: saline solution, Ringers solution, Ringer-
lactate solution, electrolytic solutions, 5%, 10, 20% glucose solution. To control potassium
concentration (during dehydration this cation is widely lost) prescribe polarizing GIK mixture
(pic.9.4), but dont you ever infuse concentrated potassium solutions quickly it can cause
cardiac arrest (not more than 400 of GIK solution ml per hour).
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Kidneys are exclusively hard-working organ. Their total weigh is hardly 0,4% of
the total body weight, however they receive 25 % of cardiac output. 10% of total inhaled
oxygen are used for their metabolic needs. During the day nearly 150 liters of primary urine
are ultrafiltrated out of the blood. Ultrafiltration is possible only when effective filtration
pressure is not less than 12 mm Hg. It is defined as a difference between hydrostatic (47
mm Hg), oncotic (25 mm Hg) andintracapsular pressure (10 mm Hg).
EFP=Hp(47)-Op(25)-ICp(10)= 12 mm Hg
So when hydrostatic pressure (mean arterial pressure) is decreasing or
when intracapsular pressure is reaching critical values filtration stops and renal failure
appears.
In tubules water, electrolytes and glucose are reabsorbed and metabolic wastes are
secreted to the urine. Eventually during one day only 1 % of primary urine is evacuated
from the organism in the form of secondary urine with high concentration of toxic
substances.
Kidneys participate in haematopoiesis, regulation of fluid balance, electrolytes
metabolism and acid-base balance.
Kidneys are also organs of secretion: their parenchyma produces rennin substance
very important for vascular tone regulation.
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Intensive treatment depends on the primary disease. So you have next possibilities:
1. Hypovolemic shock: profuse bleeding, plasma loss, dehydration.
a. restore the circulating blood volume (blood components transfusions, colloids
and crystalloids infusions, glucose solutions) on time provided correction of circulating
blood volume (and you will notice it through normalization of blood pressure,
pulse, haemoconcentration indexes and especially central venous pressure) in most cases
means restore of the diuresis.
b. if there is no effect of infusion therapy: to liquidate renal arteries spasm and
restore microcirculation give -adrenoceptor antagonists
(droperydol,aminazin, ganglionic blockers, epidural anesthesia); stimulate diuresis with
30% mannitol solution 1 g/kg 1/v with the speed 80-100 drops per minute (with 40%
glucose solution), 1% furosemid solution (beginning with 2-4 ml every 7-10 minutes and up
to 40-50 ml); use additionally spasmolytics (10 ml of 2% euphillinsolution i/v with saline).
This triple shot combined with infusions can liquidate the functional renal failure.
2. Acute vascular insufficiency: anaphylaxis, toxic collapse, orthostatic collapse
caused by overdose of ganglionic agents or -adrenoceptor antagonists; warm phase of
bacterial shock; reflectory cardiogenic shock.
a. stabilize vascular tone and perfusion pressure
with adrenomimetics (epinephrine, dopamine, mezaton i/v, best of all with infusion pump).
b. use steroids, colloids and crystalloids, steroids and then stimulate
the diuresis (described above).
3. Hemolysis (reactions after blood transfusions, hemolytic poisonings, true
drowning in sweet water, some snakebites and insect bites, myolisis during crash-
syndrome):
a. increase the circulating blood volume providing hemodilution through
infusion therapy;
b. increase blood pH infusing 4% solution of sodium bicarbonate (however dont
forget to control its level);
c. liquidate spasm of renal arteries;
d. stimulate diuresis.
In case of intense hemolysis, injuries with massive muscle disintegration it would
be wise to begin preventive hemodyalisis.
4. Renal diseases: normalize hemodynamic indexes, give spasmolytics,
stimulate diuresis and use antihypoxic treatment.
5. Postrenal reasons of acute kidneys injury demands immediate consultation of
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urologist and decision about operative liquidation of urine flow obstruction (insertion of
catheters into the bladder, ureters; epicystostomy, prostatectomy, lithotomy, etc.). Do not
stimulate urine output with diuretics until the reason of obturation is not removed!!!
Lack of diuretic effects after stimulation states severe organic injury
of nephrons and you should make a diagnosis acute renal failure, stage of oligoanuria.
II. Second stage- oligoanuria- lasts from several days to 3 weeks (duration depends
on the degree of the damage and regeneration ability of the nephrons). It can manifest
as oliguria (urine output less than 500 ml/day) or anuria (urine output less than 50 ml/day).
The severity of this stage is determined with its symptoms:
1. Overhydration: quite often it is caused by iatrogenic reasons doctors try to
overfill patient with the water to stimulate diuresis (outdated and dangerous conception!)
or simply calculate the daily fluid balance in a wrong way (too positive balance).In
addition this phase is characterized with intensive catabolism (tissues destruction) and thus
excessive endogenous water production (up to 1500 ml/day). Clinical findings: increase of
the body weight, circulating blood volume, blood pressure, central venous pressure,
peripheral oedema, possibly pulmonary oedema.
2. Electrolytic disorders: hyperkalemia, hypermagnesemia, hypocalcemia.
Clinical findings: depression, somnolence, hyporeflexia, respiratory and cardiac disorders.
3. Metabolic acidosis is caused by accumulation of hydrogen ions due to
disorders of their renal secretion. Clinical findings: noisy rapid deep breathing
(compensatory Kussmaul breathing), vomiting, evident haemodynamic disorders.
4. Uraemic intoxication. Clinical findings: consciousness disorders (up to coma),
ammonia breath odour, uraemic polyserositis (pleuritis, pericarditis), ulceration of
oesophageal mucous membrane and gastric mucous membrane, diarrhoea.
5. Disorders of synthetic renal function. Clinical findings: anaemia due to
erythropoietin deficiency and hypertension (connected with renin-angiotensindisorders).
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Intensive treatment.
Your therapeutic tactic will differ a lot in comparing with the previous phase.
1. Fight with overhydration. First of all medical stuff should control carefully
body weight gain: ideally correct treatment excludes increase of the weight. Everyday
patient loses 400-500 ml of water with respiration. Dont forget to count water loss with
vomiting and diarrhea. Infusion therapy should not exceed this total fluid loss and the only
solutions you should use are normal saline and 20-40% glucose solutions (with insulin).
2. Control and treat electrolyte disorders: prescribe calcium chloride or
calcium gluconate solutions (40-50 ml of 10% solution intravenously). Calcium acts as
potassium and magnesium antagonist and thus lowers their plasma concentrations.
3. Treat metabolic acidosis with 4% sodium bicarbonate solution (up to 400-500
ml per day with acid-base control tests). Normalization of blood pH also normalizes
potassium level.
4. Catabolism inhibition: to prevent tissues destruction use anabolic hormones
(Nerobol, Retabolil) which prevent muscle disintegration and breakdown of the proteins.
This helps to reduce endogenous water production and toxins production. For this purpose
we are also using concentrated glucose solutions.
5. To eliminate the wastes from the body there are different
methods: enterosorbtion (enterodez, polisorb, activated charcoal, etc.),
intestinal lavage(cleansing enemas 4-6 times a day), extracorporeal detoxification methods
(hemodyalisis, plasmapheresis, hemosorbtion), peritoneal dialysis.
6. Symptomatic treatment: prescribe hypotensive medicines if necessary,
preparations for cardiac support, transfuse washed red blood cells. Prevent infectious
complications.
Dont forget, that in case of acute kidneys injury withdrawal of many drugs is
delayed or interrupted and thus accumulation effects are possible!
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Hemodialysis is the process of extracorporeal waste products removal with the help
of artificial kidney. The principle of its work is quite simple: special pump pushes the
blood through the tubes to the dialyzer. Dialyzer itself is a system of capillaries, made
of semipermeable membrane (kuprofan, cellophane), which are immersed into
the dializing solution (something chemically very close to plasma). When blood passes
through the capillaries dialysis, osmosis andultrafiltration take place. During this process
toxic wastes (creatinine, urea, uric acid, phosphates, potassium and hydrogen ions) and
excessive water move to thedializing solution. Simultaneously ions of sodium and calcium
move from the dializing solution into the blood.
According to the method of blood taking and blood return dialysis is conducted
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III. Third stage is a stage of diuretic function restoring. It begins when the daily
urine output becomes more than 500 ml and lasts for 3-5 days. Due to regeneration of
the glomeruli blood filtration is gradually restored. Tubules epithelium regenerates a bit
slower and thus water reabsorption is still inadequate. Diuresisgrowth every day and at the
end of this phase reaches 1500-2000 ml per day. However urine has low specific gravity and
contains large amount of red blood cells and
protein. Hyperkalaemia and uraemic intoxication are still dangerous, because wastes
elimination is not adequate.
So the intensive treatment is quite similar to the previous stage. You can change the
volume of infusions (but again control the fluid daily balance). When daily urine output
will reach physiologic point of 2-3 liters next stage starts.
IV. Forth stage is a diuretic stage (polyuria). It lasts up to 2 weeks.
Daily diuresis increase is 800-1000 ml and daily urine output reaches 7-9 liters.
Biochemical blood tests get to the norm (urea, creatinine). Due to
excessive diuresis dehydration and electrolyte imbalance develop: potassium and
magnesium ions are lost in large amounts and this can bring life-threatening complications.
Intensive treatment is changed: now your task is to restore the circulating blood
volume and lost electrolytes reserves. Correction is made according to the laboratory tests
and special formulas.
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Control tests.
1. What is the normal renal blood flow?
A. 5-10% of circulating blood volume
B. 500 ml/ minute
C. of cardiac output
D. depends on renal activity
E. 40-50% of cardiac output.
2. During the first stage of acute renal failure you should:
A. begin hemodialysis;
B. provide intensive therapy of shock, normalize microcirculation and
stimulate diuresis;
C. stop infusions due to overhydration risk;
D. perform paranephral block;
E. prescribe high doses of furosemide
3. What is a contraindication to hemodialysis?
A. potassium level more than 7,0 mmol/l
B. CVP>13 cm H2O
C. pH<7,2;
D. acute renal failure of III or IV stages;
E. prolonged compression of the kidneys
4. Name the symptom atypical for uraemic intoxication:
A. metabolic alkalosis
B. overhydration
C. azotemia;
D. anemia;
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E. hypocalcaemia
5. In case of III stage of acute renal failure you should:
A. obligatory prescribe furosemide
B. give infusions in the rate 5-10 ml/kg
C. treat respiratory alkalosis
D. first of all begin with the dialysis
E. avoid diuretics
6. The forth stage of acute renal failure:
A. is terminal
B. shows overhydration and hyperkalemia;
C. is characterized with potassium ions loss;
D. needs hemodialysis;
E. shows metabolic acidosis and compensated dyspnea.
Task 1.
What medicines should not be used for treatment of patient with the II stage of
acute renal failure?
a. mannitol; b. concentrated glucose solutions; c. heparin; d. plasma; e. panangin; f.
normal saline; g. calcium chloride; h. enterodez; i. rheopolyglucin j. magnesium
chloride; k.nerobol.
Task 2.
Here are the clinical and laboratory findings of the patient, who is suffering from
the lack of urine for 5 days:
Creatinine 0,64 mmol/l; potassium 7,1 mmol/l; urea 41 mmol/l; CVP 14,5 cm H2O;
blood pressure 170/110 mm Hg; heart rate 96/minute.
What treatment should be prescribed?
Task 3.
One week after restore of the diuresis patient with acute renal failure shows such
laboratory results: hematocrit 0,5 l/l, plasma sodium 148 mmol/l, plasma potassium
3 mmol/l, chlorine 98 mmol/l. What is the reason for these changes? What changes should
be done in the prescriptions?
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On the contrary, in case of water excess endocrine activity of glands is inhibited and
water is actively removed from the body through the kidneys.
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Dehydration signs: weight loss, decrease of skin turgor and eyeballs tone, dry skin
and mucous membranes; low central venous pressure, cardiac output and blood pressure
(collapse is possible); decreased urine output and peripheral veins tone; capillary refill over
2 seconds (microcirculation disorders) and low skin temperature; intracellular dehydration
is characterized with thirst and consciousness disorders. Laboratory tests show blood
concentration: hematocrit, hemoglobinconcentration, protein level and red blood cells
concentration increase.
Overhydration appears in case of:
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Isotonic dehydration is caused by equal loss of electrolytes and fluid from the
extracellular space (without cellular disorders).Blood tests showhemoconcentration; sodium
level and osmotic concentration are normal.
To treat this type of water imbalance use normal saline solution, Ringer solution,
glucose-saline solutions, etc.. The volumes of infusions can be calculated according to the
formula:
VH2O= 0,2*BW* (Htp-0,4)/0,4 ,
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To treat hypochloremia use normal saline (1000 ml contains 154 mmol of chlorine)
or 5,8% sodium chlorine solution (1 ml contains 1 mmol of chlorine). The choice of
solution depends on the osmotic concentration of the plasma.
Hyperchloremia is a condition of increased chlorine concentration (over
107 mmol/l). Intensive therapy of this state includes treatment of the disease, which caused
it (decompensated heart failure, hyperchloremic diabetes insipidus, glomerulonephritis).
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pH>7,45,
pCO2a <33 mm Hg
BE < +1,5 mmol/l.
However prolong alkalosis brings decrease of BE due to compensatory retain of H+
ions. To improve this imbalance treat its reason: normalize ventilation parameters; if
patients breathing has rate over 40 per minute sedate the patient, perform the intubation
and begin artificial ventilation with normal parameters.
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Control tasks.
Task 1.
Calculate the total body water volume and its extracellular and intracellular
volumes of the Patience, the patient of 48 years and body weight 88 kg.
Task 2.
Patience, the patient of 23 with body weight 70 kg has sodium level 152 mmol/l
and hematocrit 0,49 l/l. Name the type of water balance disorder.
Task 3.
Patience, the patient of 54 with body weight 76 kg has sodium level 128 mmol/l.
Calculate the volume of saline and 7,5% sodium chloride solution necessary for the
treatment of this condition.
Task 4.
Patience, the patient of 60 with body weight 60 kg has sodium level 140 mmol/l
and hematocrit 0,55 l/l. Name the type of disorder and prescribe infusion therapy.
Task 5.
Patience, the patient of 42 with body weight 80 kg has potassium level 2,6 mmol/l.
Calculate the volume of 4% potassium chloride solution necessary for treatment of this
condition.
Task 6.
Patience, the patient of 33 with body weight 67 kg and diagnosis gastric ulcer,
complicated with pylorostenosis has potassium concentration 3 mmol/l, chlorine
concentration 88 mmol/l. pH 7,49, pCO2a 42 mm Hg, BE + 10 mmol/l. Name the type of
disorder.
Task 7.
Patience, the patient of 50 with body weight 75 kg, was transported to the
admission unit of the hospital with: unconsciousness, cyanotic skin, low blood pressure,
shallow breathing. Blood tests show: pH 7,18, pCO2a 78 mm Hg, pO2A 57 mm Hg, BE
-4,2 mmol/l. Name the type of acid-base disorder and prescribe treatment.
Task 8.
Patience, the patient with body weight 62 kg and renal insufficiency has: potassium
concentration 5,2 mmol/l, sodium concentration 130 mmol/l, calcium concentration
1,5 mmol/l, pH 7,22, pCO2a 34 mm Hg, BE -9,2 mmol/l. Name the type of disorder.
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will bring oxygenation disorders first of all to the tissues of the liver. This evolutionary
resulted in unique regeneration abilities of the liver: death of 70% of cells will end up with
a failure; however after a certain adaptation period hepatic tissues will restore their quantity
and quality.
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encephalopathy appears because of violations of uric acid synthesis (it is made from
ammonia and without this process ammonia concentration increases several times). Food
reach with proteins stimulates ammonia encephalopathy onset, as well as gastrointestinal
bleedings, hypnotic medicines and opiates, alcohol, surgeries, infections and metabolic
alkalosis. In the CNS tissues false mediators like octopamine, amino acids and their toxic
metabolites are accumulated. On the background
of hypoproteinemia interstitial edema appears and this brings respiratory hypoxia of tissues.
At the same time violated synthesis of enzymes, disordered metabolism of carbohydrates
and lipids, metabolic alkalosis withhypokalaemia just advance the encephalopathy.
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Clinical findings:
- skin: jaundice, vascular spiders, hepatic palm, extension of small
superficial face vessels;
- fever;
- hepatic breath odour, hepatic smell of sweat and urine (this smell
occurs due to transformation of methionine into methyl mercaptan);
- digestion disorders (nausea, hiccups, inappetence, smooth red tongue,
abdominal pain, meteorism, defecation disorders);
- obstructive and diffuse respiration disorders hypoxic hypoxia;
- cardiovascular disorders (arterial hypotension,
tachycardia, extrasystoles);
- haemorrhagic syndrome, anemia (due to interruption of coagulation
factors synthesis and bleeding of gastric or oesophageal erosions and ulcers);
- frequent additional complications: renal failure, hepatorenal syndrome
is prognostically dangerous.
If liver failure progresses CNS damage deepens and you can clinically observe:
weakness, headache, sluggishness, apathy, inversion of sleep and awakening. Disorientation
develops gradually, there is possibility of excitement periods and cramps. You can also find
overactive tendon reflexes, foot clonus,Babinskis sign. One of the most significant
symptoms is flapping: trepidation of limbs and face, especially of hands in prone position
(arms extended). In case of deepest coma you will see dilated pupils, eyeballs are
fixed, tendon reflexes are absent.
Progressive and quick decrease of liver size is a prognostically bad sign. However
when the disease is chronic and fibrous changes took place this symptom is not noticed
(liver stays enlarged).
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Intensive treatment.
The basic principle of liver failure treatment is etiologically aimed therapy: you
should treat the reason of the failure. Two other important components are prevention and
treatment of liver failure complications during 10-14 days necessary for the regeneration of
the hepatocytes.
Necessary treatment measures:
1. Patient should follow strictly bed regiment in isolated ward. Medical stuff should
follow aseptic and antiseptic rules.
2. Eliminate animal fats and proteins from the patients diet to prevent
encephalopathy.
3. Liquidate hepatotoxic factors (hypoxia, hypovolemia, haemorrhagic syndrome,
intoxication):
- provide oxygen supply (nasal catheter, face mask with the flow 3-4 l/min);
sometimes hyperbaric oxygenation and even intestinal oxygenation (0,2-0,3 ml/kg/min) are
possible;
- to increase hepatic blood flow restore the circulating blood volume, improve
rheological properties of the blood, restore the peristalsis. To achieve this you should:
infuse crystalloids and glucose solutions, spasmolytics, 2 % euphyllin solution (20-30
ml/day). 10% albumin solution (200-300 ml) and mannitol solution (1 g/kg)
increase oncotic blood pressure and thus help to prevent interstitial oedema of the liver;
- prevent ulceration of stomach and gastrointestinal bleeding by prescription
of famotidine or omeprazole (40 mg twice a day); oesophageal bleedings are stopped with
Blackmore probe;
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- if you suspect stagnated blood in the intestines remove it, because otherwise
intoxication will get more intense;
- use only fresh blood stabilized with heparin for transfusions.
Prevent and treat intoxication with:
- intestinal lavage and enemas;
- antibiotics which are not toxic to the liver (for example ampicillin 1,0 every 4
hours);
- extracorporeal blood detoxification
(plasmapheresis, hemosorbtion or hemodialysis; usage of artificial liver or artificial spleen);
- prescribe antagonists of ammonium (40-50 ml of 1% glutamic acid solution with
glucose 3 times a day; 2,0 of alfa-arginine solution i/v every 8 hours).
4. To stimulate energetic metabolism in hepatocytes prescribe concentrated glucose
solutions (10-20% solutions, up to 5g/kg/day). This will also prevent proteins breakdown
and thus wastes accumulation.
5. To stabilize the membranes of the hepatocytes prescribe steroids (10-15 mg/kg of
hydrocortisone).
6. To stabilize the energetic exchange and stimulate transportation of the lipids
prescribe choline chloride (10 ml of 10% solution with 200 ml of glucose solution after
previous atropine admission, twice a day).
7. Additionally prescribe vitamins (ascorbic acid, B1, B2, B6, K, E, B12, folic and
nicotinic acids in doses 2-3 times higher than daily needs), cardiac glycosides, panangin,
antioxidants (cytochrome c, sodium gamma-hydroxybutyrate).
8. Symptomatic treatment helps to stabilize homoeostasis if not to treat failure
itself: if necessary use anticonvulsive medicines, antipyretics, etc.
Control tests.
1. The reason of exogenous liver failure is:
A. acute exogenous poisoning
B. exogenous shock
C. hepatitis B
D. hepatic cirrhosis
E. hyperbilirubinemia
2. The reason of endogenous liver failure is:
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A. oesophageal bleeding
B. acute carbon monoxide poisoning
C. infectious shock
D. damage of hepatocytes
E. endocrinological diseases
Task 1.
What is typical for exogenous (a.) and endogenous (b.) liver failure?
a. unconsciousness; b. rapid noisy breathing; c. bleeding varicose veins of
oesophagus; d. ascites; e. anaemia f. elevated transaminases; g. acute exogenous poisonings;
h. viral hepatitis i. alcohol abuse.
Task 2.
Patience, the patient with liver failure, receives:
a. enteral nutrition reached with proteins; b. oxygenation; c. albumin
infusion; d. blood transfusion; e. sodium thiopental for cramps treatment f. steroids
g. vitamins h. gentamicin i. diuretics.
Acute poisonings.
Acute poisoning is a chemical injury, which occurs when chemical substance gets to
the organism and violates its vital functions. If the substance is aggressive enough and
proper treatment is not provided on time poisoning will bring death.
Although there are over 500 toxic substances which may cause acute poisoning,
clinical picture is made up of quite similar syndromes. Proper diagnostics of these
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syndromes allows avoiding life-threatening complications and gets the chance to make
correct preliminary conclusions about the nature of poisoning.
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Toxic affection of the respiratory system can progress as the violation of:
a. external respiration - neurogenic form, aspirations and obstructions of the
airways which bring hypoxic hypoxia;
b. hemoglobins function aniline and nitrobenzene create methmoglobin, carbon
monoxide connected with hemoglobin creates carboxyhemoglobin and neither the first nor
the second is capable of normal oxygen transportation; heavy metal, organic acids and
arsenic poisonings lead to destruction of the red blood cells and emission of the
free hemoglobin into the plasma;
c. oxygen transportation due to the decrease of circulating blood volume
exotoxic shock;
d. cellular respiration tissue hypoxia occurs when cytochromes are blocked with
toxins like cyanides.
Practically all severe poisonings earlier or later lead to hypoxia, because they
violate oxygen supply, transportation and consumption.
Your immediate therapy actions in this situation will be:
- to assess of respiratory system (described above);
- to provide of airways patency (cleaning of the oral cavity, aspiration of
the saline and gastric contents, conicotomy if necessary, etc.);
- to begin oxygen supply (face mask, nasal catheter);
- to start artificial ventilation if necessary;
- to prescribe antidotes if they are available (methylene-blue in case of
nitro compounds poisonings, unithiolum in case of heavy metals and arsenic
poisonings, cytochrome c in case of tissue hypoxia);
- to start hyperbaric oxygenation in case of carbon monoxide poisoning;
- to begin infusion therapy in order to stabilize the hemodynamics;
- to start general detoxification;
- to prescribe symptomatic treatment and provide prevention of the
complications (for example prescription of antibiotics).
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vascular bed to provide adequate blood supply of the organs, which leads to metabolic
disorders and in the worst case to death. Severe toxic damage of cardiovascular system
brings acute cardiovascular failure: primary toxic collapse,exotoxic shock,
secondary somatogenic collapse.
Primary toxic collapse appears in case of massive poison admission, when
compensatory mechanisms are not quick enough to resist the chemical aggression.
Immediately or minutes after poisoning patients begin to suffer from reduced cardiac output
and thus from decreased blood flow in the tissues. Peripheral pulse is weak or absent, blood
pressure critically lowers and cardiac arrest can appear. In most cases of primary toxic
collapse ambulance is not able to save the life of the patient due to
the fulminant development of life-threatening complication. However you should remember
that such collapse occurs only in 5 % of the cases.
Exotoxic shock is the reason of death for 70 % of poisoning victims. Violations
of hemodynamics on one hand are caused by direct heart and vessels damage and on the
other hand by compensatory sympathetic and adrenal reactions. On the background of CNS
and gastrointestinal system violations you will observe disorders of
systemic hemodynamics and microcirculation: arrhythmias, decrease of blood pressure,
central venous pressure, cardiac output and diuresis. The peripheral vascular tone changes:
toxins induce spasm or dilation of arterioles with the ischemia of one and hyperemia of
other tissues. Depending on the body reaction on intensive treatment shock can be
compensated, decompensated reversible and decompensated irreversible.
In case of toxic shock you should:
- get an i/v line (preferably several, including central venous access);
- start infusions of colloids
(albumin, rheopolyglucin, hydroxyethylstarch solutions) and crystalloids (saline,
glucose solutions, polarizing solution) in order to normalize blood pressure, heart
rate and diuresis; sometimes infusion dose is up to 100-150 ml/kg, (7-10 l/day);
- constantly control patients condition: monitor the heart action, blood
pressure and central venous pressure;
- provide antidote treatment and detoxification; remember that
extracorporeal detoxification is possible only after the stabilization of
thehemodynamics (systolic blood pressure >90 mm Hg ).
Secondary somatogenic collapse is the reason of death in 25% of the cases. It
can occur few days after poisoning, when the toxin is already eliminated from the body,
however the tissue changes (in the lungs, liver, kidneys, heart) are irreversible. Necessary
treatment: hemodynamics stabilization, improvement of microcirculation, intensive
therapy of functional disorders and organic changes (artificial lung
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sensitive to hypoxia.
Light forms of toxic and hypoxic affections can develop without clinical
manifestation. However they will be noticeable in laboratory tests (elevation
oftransaminases, bilirubin, phosphates). Severe poisoning will bring to toxic hepatitis and
even hepatic coma.
Among the hepatotoxic substances are: heavy metals salts, dichloroethane, ethylene
glycol, deadly amanita toxins.
To protect the liver you should:
- eliminate the toxic substance from the gastrointestinal tract;
- give antidotes if they exist (unithiol for heavy metals salts, lipoic acid
for deadly amanita);
- prescribe cleansing enemas 2-4 times a day (to prevent intoxication
with the wastes accumulated in the intestine);
- use extracorporeal detoxification (hemosorbtion, plasmapheresis,
artificial liver);
- provide adequate oxygenation and blood supply of the liver;
- prescribe symptomatic treatment.
Kidneys are very important for the elimination of the poisons circulating in the
blood. So in many cases they are also the target of the toxin. They can be damaged
primary (poison affect their tissues directly) and secondary though the violations of vital
functions (for example hemodynamics in case of exotoxicshock). Their condition you
can control with the help of urine output per hour, which normally is not less than
0,5 ml/kg.
To prevent the renal failure you should:
- eliminate the poison as soon as possible (gastric lavage and enemas for
gastrointestinal tract; hemodialysis, hemosorbtion, plasmapheresis for blood);
- give antidotes if they exist (unithiol for heavy metals salts, sodium
bicarbonate for hemolytic poisons, ethylic alcohol for ethylene glycol and methanol);
- treat disorders of hemodynamics (therapy against exotoxic shock);
- stimulate the urine output with the diuretics on the background of
previous rehydration: this will allow you to eliminate diluted in the plasma toxins
faster and to prevent renal failure; kidney is an organ which functions normally only
if works intense;
Clinical observations tell us, that incredibly massive infusions (10-20-30 l/day)
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with diuresis stimulation really help patient to dilute and eliminate the toxin without
kidneys damage.
In case of acute renal failure you should treat the patient according to the
principles described in chapter 6.
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etc.
Clinical picture is usually connected with CNS affection. There are phases of
somnolence, sleep and coma. Depending on involvement of other systems coma can be
complicated or uncomplicated. Usually respiratory complications appear: inspiration centre
depression, violations of airways patency due to soft tissues (tongue, soft palate) or biologic
fluids (blood, sputum, saline), pneumonia. In 15-20% of cases the poisoning development is
complicated with the exotoxicshock. The peculiarities of this shock are next: circulatory
disorders with blood stagnation in the pulmonary circuit, toxic affection of the myocardium
and decrease of energy metabolism of the organism.
To indicate the poison you should ask relatives and witnesses and check things of
the patient (for example you can find medicine packages). Evaluate the size of the pupils:
extremely narrowed pupils (poppy seeds) are the effect of narcotics admission; narrowed
pupils might be the sign of sleeping or sedative medicines overdose; dilated pupils are the
symptom of clofelin, antidepressants or neuroleptics administration; wide pupils covering
the whole iris are usually the sign of atropine poisoning (or a poisoning with atropine-like
substances: dope, henbane, amanita).
Principles of the intensive treatment in the toxicology unit:
- clean the gastrointestinal tract as soon as possible (gastric and
intestinal lavage, enterosorbtion, cleansing enemas) and as often as necessary;
- provide adequate respiration (check airways patency);
- in case of comatose patients intubate the trachea and begin artificial
ventilation (sometimes it is necessary for weeks);
- control hemodynamics and treat its violations (infusion therapy and
adrenergic agonists or antagonists if necessary);
- stimulate diuresis: patients with barbiturate poisoning should be
treated with alkaline forced diuresis in order to eliminate the toxin (add to the
infusion 400-600 ml of 4% sodium bicarbonate solution and prescribe diuretics);
- use antidotes: naloxone for opiates, pharmacological antagonists
for anticholinergic and cholinomimetic agents; dont you ever prescribe central
analeptics for comatose patients with drugs poisoning cordiamin,
caffeine, bemegride , cytiton, lobelinum can cause cerebral blood flow steeling
effect and thus they deepen the hypoxia of brain cells!
- provide extracorporeal detoxification to eliminate toxins
(hemodialysis, hemosorbtion, plasmapheresis);
- prescribe antibiotics for infectious diseases prevention (for example in
case of prolonged artificial ventilation);
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- symptomatic treatment.
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- in case of organic acids poisonings (acetic acid, oxalic acid get into the
blood) give 1500-2000 of 4% sodium bicarbonate solution intravenously slowly with
diuretics; these actions will help to remove hemoglobin (released due to red blood
cells hemolysis) and thus to prevent acute renal failure;
- in case of obstructive breathing disorders (mucous membrane edema)
use steroids (90-120 mg of prednisolone), antihistamine drugs (2 ml of
1% dimedrol solution intravenously), sedative medicines (2 ml of 0,5% diazepam
solution); perform tracheostomy or conicotomy if necessary;
- prescribe antibiotics for infectious diseases prevention (for example in
case of prolonged artificial ventilation);
- symptomatic treatment.
During the recovering period patient may need surgeries for restoration of
gastrointestinal tract: the most common practice is the bouginage of the oesophagus or,
if necessary, oesophagus plastic.
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vitamins.
In case of severe intoxication begin artificial ventilation with high oxygen flow.
Luckily there is an antidote for carbon monoxide poisoning: hyperbaric oxygenation.
Connection with oxygen is more natural for haemoglobin and when the pressure of
oxygen is higher than its usual partial pressure carbon monoxide is replaced from the
haemoglobin. Usually in case of comatose patients 40-50 minutes sessions every 6-12
hours are enough.
To normalize tissue metabolism prescribe antihypoxants: 20% solution of
sodium oxybutirate (20-40 mg/kg i/v) and cytochrome c (2-3 ml i/v) every 4-6 hours. To
improve microcirculation dilute the blood with crystalloid infusions (check the level
of hemodilution with hematocrit stop when it will reach 0,3-0,35 l/l).
Prevent the infectious complications and brain oedema with standard methods.
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- clean the stomach with large amounts of cold water; repeat it several
times, because these substances are excreted through the mucous membranes of
gastrointestinal tract;
- give saline laxative;
- if the poison affected skin wash it with alkaline solution.
Antidotes:
a. use peripheral m-anticholinergic drug atropine: during the first few
hours 2-3 ml of 0,1% atropine solution (up to 30-35 ml during the whole period of
intensive atropinization); pay attention to the signs of atropine administration as they
are the measure of your antidote treatment effectiveness: termination of excessive
bronchial secretion, dilation of the pupils, tachycardia (90-110/min). During next 3-5
days continue atropine prescription (from 10-15 mg to 100-150 mg/day period of
supportive atropinization). Control clinically the level of atropinization.
b. use cholinesterase reactivators: 1-2 ml of 15% dipiroxim solution i/m,
up to 600 mg; 3 ml of 40% izonotrozin solution i/m up to 3-4 grams. However
remember, that cholinesterase reactivators can be used only 24 hours after poisoning.
Later administered reactivators will ne not only ineffective, but also toxic for the
patient.
You should also provide usual treatment as soon as possible: infusion therapy,
forced diuresis, hemosorbtion, plasmapheresis, hemodialysis and antibiotics for
infection preventions.
In case of ineffective external respiration and comatose patients
condition intubate the patient and start artificial respiration. Convulsions in case of
organophosphate poisoning are treated with sodium oxybate (75-100 mg/kg i/v every 4
hours). Cardiac glycosides, calcium chloride, euphillinum are forbidden in case of
organophosphate poisonings, because they induce toxic heart affection.
Be aware of the possibility of second poisoning wave: even 4-8 days after the
stabilization of the patients condition clinical picture of the poisoning might return and
this time hemodynamics will decompensate quickly.
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- extracorporeal detoxification
(hemodialysis, hemosorbtion, plasmapheresis, artificial spleen or liver) as soon as
possible;
- antibiotics if necessary (penicillin); vitamins (B,C,E);
- external drainage of thoracic duct (decreases intoxication through
elimination of toxic lymph).
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One-time water doe is nearly 200 ml: it will flow out when you will lower the
probe or you will have to evacuate the water with the syringe. Repeat these actions until
the water wash out the stomach will be clean (usually it takes nearly 10 liters of water).
Forced diuresis.
Indications: intoxications of different origin (poisonings, infectious diseases,
endogenous intoxications).
Medicines required: normal saline (3-5 liters); detoxification solutions;
polarizing solution (400 ml of 10% glucose solution, 10 ml of 7,5% potassium chloride
solution, 12 units of insulin), osmotic diuretics ( mannitol in the dose 1
g/kg), furosemid solution (40-80 mg)
Procedure: get and i/v line (central or peripheral) and insert urinary catheter.
During the first phase of forced diuresis water the patient with crystalloids and
detoxification solutions (30-40 ml/kg). During the second phase infuse osmotic diuretics
and furosemide solution. Excessive urine output brings potassium loss, which you
should treat with polarizing solution. Balance the speed of infusion with the speed
of diuresis: generally per 5-7 liters of infused solutions you should receive at
least 5 liters of urine.
Constantly control hemodynamics and blood electrolytes.
Control tests.
1. What medicine should be used as an antidote in case of severe soporific drugs
poisoning?
A. bemegride
B. cordiamin
C. there is no such meidicine
D. unithiol
E. cytiton
2. What is the most common death reason in case of alcohol poisoning?
A. acute liver failure
B. acute respiratory failure
C. acute renal failure
D. acute heart insufficiency
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E. collapse
3. What is necessary for the patient, who took 60 ml of acetic essence?
A. to give 4% sodium bicarbonate solution i/v
B. to clean the stomach with alkaline solution in order to neutralize the acid
C. to use unithiol as an antidote
D. to stimulate intestinal cleansing with saline laxatives
E. central analeptics
4. What is the symptom of organophosphate poisoning?
A. pale and dry skin
B. maximal pupils dilation
C. tachycardia
D. muscle fasciculation
E. acute liver failure
5. What is used as an antidote in case of severe carbon monoxide poisoning?
A. cytochrome c
B. cordiamin solution
C. unithiol
D. prednisolone
E. antidotes are not used
6. What is typical for deadly amanita poisonings?
A. first symptoms appear in2-3 hours after mushroom meal;
B. low-grade fever
C. latent period of 6-12 hours
D. first symptoms are haemostatic disorders (bleeding)
E. early unconsciousness
7. What is the necessary aid in case of narcotic painkillers overdose?
A. artificial ventilation
B. cordiamin
C. oxygen supply
D. immobilization of the patient in order to avoid self-injuries during the
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excitement-phase;
E. cardiac medicines
Task 1.
Patience, the patient of 19 is transported to the ITU by witnesses from the street.
Clinical findings: unconscious, cyanotic wet skin, 6 breathes per minute, respiration
shallow, blood pressure 70/40 mm Hg, heart rate 112/minute. Name the reason of vital
disorder and write the principles of intensive care (algorithm).
Task 2.
Patience, the patient of 19, was found unconscious in his own apartment by the
ambulance workers. Clinical findings: total cyanosis, shallow breathing, respiration rate
5/min, pupils extremely narrowed, photoreaction is absent, blood pressure 80/40 mm Hg.
In the elbow area there are noticeable signs of injections. Name the reason of vital
disorder and write the principles of intensive care (algorithm).
Task 3.
Patience, the patient of 23 was hospitalized into ITU with the diagnosis:
mushroom poisoning. It turned out, that yesterday she was eating cooked champignons.
8 hours later she noticed vomiting and diarrhoea. Clinical findings: scleral icterus, dry
coated white tongue; painful abdomen (epigastrium and righthypogastric area), painful
and enlarged liver (2 cm); hemodynamics and respiration are not violated.
Write the diagnosis and the phase of the disease.
Task 4.
Patience, the patient of 18, is transported to the toxicology unit with delirium.
Clinical findings: hyperaemic face, dry skin, dilated pupils. Blood pressure 140/70 mm
Hg, heart rate 127/minute. It is know, that 2 hours ago she took 10 unknown tablets
during the suicidal attempt. What is the diagnosis and what are your actions?
Task 5.
Patience, the patient of middle age, was found by the ambulance workers in his
own kitchen unconscious. Clinical findings: specific smell of organophosphates in the
room, signs of vomit on the clothes, miosis, cold clammy skin with cyanotic shade,
foamy white sputum in the mouth, blood pressure 90/50 mm Hg, heart rate 54/minute.
What is the diagnosis? What immediate aid should be provided during pre-hospital
stage?
Task 6.
Adams family were celebrating the New Year Eve near the fireplace. In the
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morning came the carol singers and found hosts in a condition of deep sleep. Dream
team, the ambulance workers, who came to the place of the accident, stated: 2 adults
and their children in comatose condition, vomit signs on the clothes, rapid
breathing, pupils dilated with weak photoreaction; heart rate is 110-120 per minute,
rhythmic; blood pressure is high.
Name the reason of the accident and describe the actions of the Dream team.
Task 7.
Name the poisoning agent for each antidote: a. atropine, b. unithiol,
c. naloxone, d.tetacinum, e. ethylic alcohol, f. dipiroximum, g. lipoic acid?
The essential components of the human cardiovascular system are the heart, blood,
and blood vessels. It includes: the pulmonary circulation, a "loop" through the lungs where
blood is oxygenated; and the systemic circulation, a "loop" through the rest of the body to
provide oxygenated blood. An average adult contains five to six quarts (roughly 4.7 to 5.7
liters) of blood, accounting for approximately 7% of their total body weight.
While it is convenient to describe the flow of the blood through the right side of the
heart and then through the left side, it is important to realize that both atria contract at the same
time and that both ventricles contract at the same time. The heart works as two pumps, one on
the right and one on the left that works simultaneously. The right pump pumps the blood to the
lungs or the pulmonary circulation at the same time that the left pump pumps blood to the rest
of the body or the systemic circulation. Venous blood from systemic circulation (deoxygenated)
enters the right atrium through the superior and inferior vena cava. The right atrium contracts
and forces the blood through the tricuspid valve (right atrioventricular valve) and into the right
ventricles. The right ventricles contract and force the blood through the
pulmonary semilunar valve into the pulmonary trunk and out the pulmonary artery. This takes
the blood to the lungs where the blood releases carbon dioxide and receives a new supply of
oxygen. The new blood is carried in the pulmonary veins that take it to the left atrium. The left
atrium then contracts and forces blood through the left atrioventricular, bicuspid, or mitral,
valve into the left ventricle. The left ventricle contracts forcing blood through the
aortic semilunar valve into the ascending aorta. It then branches to arteries carrying oxygen rich
blood to all parts of the body.
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capillaries, exchange of oxygen and carbon dioxide takes place. Red blood cells inside the
capillary releases their oxygen which passes through the wall and into the surrounding tissue.
The tissue then releases waste, such as carbon dioxide, which then passes through the wall and
into the red blood cells.
The Circulatory System
The circulatory system is extremely important in sustaining life. Its proper functioning
is responsible for the delivery of oxygen and nutrients to all cells, as well as the removal of
carbon dioxide, waste products, maintenance of optimum pH, and the mobility of the elements,
proteins and cells, of the immune system. In developed countries, the two leading causes of
death, myocardial infarction and stroke are each direct results of an arterial system that has
been slowly and progressively compromised by years of deterioration.
Arteries
Arteries are muscular blood vessels that carry blood away from the heart, oxygenated
and deoxygenated blood . The pulmonary arteries will carry deoxygenated blood to the lungs
and the sytemic arteries will carry oxygenated blood to the rest of the body. Arteries have a
thick wall that consists of three layers. The inside layer is called the endothelium, the middle
layer is mostly smooth muscle and the outside layer is connective tissue. The artery walls are
thick so that when blood enters under pressure the walls can expand.
Arterioles
An arteriole is a small artery that extends and leads to capillaries. Arterioles have thick
smooth muscular walls. These smooth muscles are able to contract (causing vessel constriction)
and relax (causing vessel dilation). This contracting and relaxing affects blood pressure; the
higher number of vessels dilated, the lower blood pressure will be. Arterioles are just visible to
the naked eye.
Capillaries
Capillaries are the smallest of a bodys vessels; they connect arteries and veins, and
most closely interact with tissues. They are very prevalent in the body; total surface area is
about 6,300 square meters. Because of this, no cell is very far from a capillary, no more than 50
micrometers away. The walls of capillaries are composed of a single layer of cells, the
endothelium, which is the inner lining of all the vessels. This layer is so thin that molecules
such as oxygen, water and lipids can pass through them by diffusion and enter the tissues.
Waste products such as carbon dioxide and urea can diffuse back into the blood to be carried
away for removal from the body.
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The "capillary bed" is the network of capillaries present throughout the body. These
beds are able to be opened and closed at any given time, according to need. This process is
called autoregulation and capillary beds usually carry no more than 25% of the amount of
blood it could hold at any time. The more metabolically active the cells, the more capillaries it
will require to supply nutrients.
Veins
Veins carry blood to the heart. The pulmonary veins will carry oxygenated blood to the
heart awhile the systemic veins will carry deoxygenated to the heart. Most of the blood volume
is found in the venous system; about 70% at any given time. The veins outer walls have the
same three layers as the arteries, differing only because there is a lack of smooth muscle in the
inner layer and less connective tissue on the outer layer. Veins have low blood pressure
compared to arteries and need the help of skeletal muscles to bring blood back to the heart.
Most veins have one-way valves called venous valves to prevent backflow caused by gravity.
They also have a thick collagen outer layer, which helps maintain blood pressure and stop
blood pooling. If a person is standing still for long periods or is bedridden, blood can
accumulates in veins and can cause varicose veins. The hollow internal cavity in which the
blood flows is called the lumen. A muscular layer allows veins to contract, which puts more
blood into circulation. Veins are used medically as points of access to the blood stream,
permitting the withdrawal of blood specimens (venipuncture) for testing purposes, and
enabling the infusion of fluid, electrolytes, nutrition, and medications (intravenous delivery).
Venules
A venule is a small vein that allows deoxygenated blood to return from the capillary
beds to the larger blood veins, except in the pulmonary circuit were the blood is
oxygenated. Venules have three layers; they have the same makeup as arteries with less smooth
muscle, making them thinner.
The double circulatory system of blood flow refers to the separate systems of
pulmonary circulation and the systemic circulation in amphibians, birds and mammals
(including humans.) In contrast, fishes have a single circulation system. For instance, the adult
human heart consists of two separated pumps, the right side with the right atrium and ventricle
(which pumps deoxygenated blood into the pulmonary circulation), and the left side with the
left atrium and ventricle (which pumps oxygenated blood into the systemic circulation). Blood
in one circuit has to go through the heart to enter the other circuit. Blood circulates through the
body two to three times every minute. In one day, the blood travels a total of 19,000
km (12,000 miles), or four times the distance across the U.S. from coast to coast.
The Pulmonary Circuit
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In the pulmonary circuit, blood is pumped to the lungs from the right ventricle of the
heart. It is carried to the lungs via pulmonary arteries. At lungs, oxygen in the alveolae diffuses
to the capillaries surrounding the alveolae and carbon dioxide inside the blood diffuses to
the alveolae. As a result, blood is oxygenated which is then carried to the heart's left half -to
the left atrium via pulmonary veins. Oxygen rich blood is prepared for the whole organs and
tissues of the body. This is important because mitochondria inside the cells should use oxygen
to produce energy from the organic compounds.
The Systemic Circuit
The systemic circuit supplies oxygenated blood to the organ system. Oxygenated blood
from the lungs is returned to the left atrium, then the ventricle contracts and pumps blood into
the aorta. Systemic arteries split from the aorta and direct blood into the capillaries. Cells
consume the oxygen and nutrients and add carbon dioxide, wastes, enzymes and hormones.
The veins drain the deoxygenated blood from the capillaries and return the blood to the right
atrium.
Pic. 4.1 Distribution of blood in the body:
a. hear cavity itself 0 3% (% of blood volume)
b.arteries -15%
c. capillares -12%
d. venous system 70%
Cardiac cycle is the term used to describe the relaxation and contraction that occur, as
a heart works to pump blood through the body. Heart rate is a term used to describe the
frequency of the cardiac cycle. It is considered one of the four vital signs. Usually it is
calculated as the number of contractions (heart beats) of the heart in one minute and expressed
as "beats per minute" (bpm). When resting, the adult human heart beats at about
70 bpm (males) and 75 bpm (females), but this rate varies between people. However, the
reference range is nominally between 60 bpm (if less termed bradycardia) and 100 bpm (if
greater, termed tachycardia). Resting heart rates can be significantly lower in athletes, and
significantly higher in the obese. The body can increase the heart rate in response to a wide
variety of conditions in order to increase the cardiac output (the amount of blood ejected by the
heart per unit time). Exercise, environmental stressors or psychological stress can cause the
heart rate to increase above the resting rate. The pulse is the most straightforward way of
measuring the heart rate, but it can be deceptive when some strokes do not lead to much cardiac
output. In these cases (as happens in some arrhythmias), the heart rate may be considerably
higher than the pulse. Every single 'beat' of the heart involves three major stages: atrial systole,
ventricular systole and complete cardiac diastole. Throughout the cardiac cycle, the blood
pressure increases and decreases. As ventricles contract the pressure rise, causing the AV valves
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to slam shut.
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by spirometer or volumeter. But not the whole air of one respiratory effort gets to the alveoli:
part of it stays in oral cavity, nasal cavity, pharynx, trachea, bronchi and thus does not
participate in the act of respiration itself. It is so called dead space- volume of airways which
are ventilated, but are not involved in gas exchange. Dead space makes nearly 30% of the tidal
volume (2,22 ml/kg of body weight).
Normal respiration rate (RR) is 14-20 per minute. Thus minute ventilation is calculated
according to the formula:
Minute ventilation =Tidal volume* Respiratory rate (ml)
However the parameter, which helps to characterize the efficiency of breathing, is
alveolar ventilation (AV): it shows the exact amount of the air which gets to the alveoli during
the minute. The difference between minute ventilation and alveolar ventilation is the volume of
dead space:
According to this formula breathing with lower frequency and higher tidal volume is
more effective. In addition efficiency of breathing is increased through reduction of dead space
volume. Thus endotracheal tube or tracheostomy make it two times less.
Oxygen gets to the arterial blood due to the difference of gas partial pressures. If the
atmospheric pressure is 740-740 mm of Mercury and the amount of oxygen in the air is
20-21% partial pressure of Oxygen (pO2) will be 160-150 mm of Mercury. In the airways air is
being mixed with used gases and water steam, so the partial pressure of oxygen inside the
alveoli is 95-85 mm of Mercury. With such values pO2a , 3 ml of oxygen will be dissolved in
one liter of blood (plasma).
The main amount of oxygen in blood is being bound to the haemoglobin. One gram of
haemoglobin bounds 1,34-1,39 ml of oxygen. In normal conditions haemoglobin of arterial
blood (HbO2a)is saturated to the extent of 96%. So, with the concentration of haemoglobin
120-140 grams per liter, one liter of arterial blood contains 170-190 ml of oxygen (VO2a).
From every litre of blood only one third of oxygen amount (nearly 50 ml) is being used
for the needs of the tissues. Thus venous blood contains nearly 120-140 ml of oxygen
(VO2v) and its HbO2v is 70-75% and pO2v 45-55 mm of Mercury.
Partial pressure of carbon dioxide in the arterial blood (pCO2a) is an important index
of ventilation adequacy. Normally it is 36-46 mm of Mercury. Worsening of lung ventilation
causes increasing of pCO2a over 44 mm of Mercury hypercapnia appears. Excessive
ventilation, on the contrary, helps in elimination of carbon dioxide and appearance of
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illustrative.
In case of external respiration disorders the amount of oxygenated haemoglobin is
decreased and thus quantity of reduced haemoglobin. Arterial blood becomes venous
(dark): skin and mucosa become cyanotic (blue, purple). First of all their colour change
lips, nail plates, earlobes, afterwards face and other body parts. In case of anaemic patients
with haemoglobin level 60 grams per litre and lower skin stays pale even in terminal stages
of respiratory insufficiency. In case of cyanic and carbon monoxide intoxication skin, nail
plates and mucosa turn bright pink, although patients are greatly suffering from hypoxia.
Hydrosis is quite significant feature of hypercapnia. Terminal respiratory insufficiency is
characterized with dark-grey color cold skin covered with clammy sweat.
Disorders of external respiration are the most obvious symptoms of respiratory
insufficiency. Clinically in case of those patients next symptoms might be observed:
complete breathing arrest (apnea);
low respiratory rate less than 12 per minute (bradypnea);
high respiratory rate more than 20 per minute (tachypnea);
shallow breathing (respiratory volume less than 5 ml per kilogram of body weight);
respiratory anarchy (irregular breathing with pauses and uneven amplitude of
respiratory movements);
pathological types of respiration:
a. Cheyne-Stokes breathing (periods of apnea, which are followed with
chaotic frequent breathing);
b. Biots breathing (periods of apnea which are followed with breathing
of equal amplitude);
c. Difficult breathing (noticeable at a distance, correlation between
inspiration and expiration is violated, with active participation of additional
muscles):
1. inspiratory dyspnea (difficult inspiration) inspiration is
prolonged, intercostals spaces, jugular fossa and subclavian fossa are
retracted; sometimes stridorous noise can be heard
2. expiratory dyspnea (difficult expiration) patients should
make a great physical effort in order to exhale; exhalation is prolonged,
noisy, heard at a distance; chest is enlarged, becomes barrel shaped
Cardiovascular system at the beginning reacts trough compensative hyperdynamic
reaction. Cardiac output, heart rate, systolic and diastolic pressure increase. Tissue perfusion
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improves, what makes cellular oxygen supply and carbon dioxide elimination more effective.
But due to hypoxia development vessel tone decreases and heart action is depressed. Blood
pressure critically lowers and in case of inadequate treatment cardiac arrest appears.
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It is quite often observed that in case of unconscious patients oral cavity and pharynx
are overfilled with saline and trachea, bronchi filled with mucus, which normally should be
swallowed or spitted out. Mucus gets infected quickly and thus inflammatory reactions begin,
causing complications such as purulent bronchitis and tracheitis, pneumonia, which may lead
coma patient to death.
Respiratory disorders of unconscious patients can be explained with passive outflow of
gastric contents from stomach to the oral cavity and its father aspiration into airways (trachea
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and bronchi). According to A. Zilber (1989) aspiration of 10-15 ml of acid gastric contents in
most cases end with the death of the patient.
Prevention and treatment of this disease belong to the most urgent.
Urgent help:
1. Evaluate central nervous system condition deepness of coma (chapter 5)
2. To prevent aspiration turn patient into save position (side position with
head turned aside and if possible lower upper part of the body thus gastric contents
will probably flow out rather than into trachea).
3. Open the mouth of the patient and clean the oral cavity, if necessary, using
your finger or forceps with surgical drape).
4. Titled the head backwards (use roll or small cushion if possible). Thus
airways should stay clear.
5. Thrust the jaw forward: place your thumbs over the chin and the rest of
your fingers put on the jaw (little fingers on the angles of the jaw), push the jaw forward
and up, in a position of malocclusion (lower teeth in front of upper). After this action is
done further providing of airways patency is quite simple and can be achieved with one
finger.
6. You can also use simple airway adjuncts such as oropharyngeal and
nasopharyngeal airways. Guedel tube is inserted between teeth with its curved distal end
turned up, than moved toward soft palate and turned 180 and placed over the tongue.
In case of inadequate breathing or complete lack of it artificial ventilation should
be provided (mouth to mouth or with apparatus for ventilation).
Constantly check patients condition: control the heart and respiratory rate, blood
pressure, body temperature, ECG. When there will be a possibility take biological material
for the laboratory tests.
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4. Get the intravenous access, peripheral or central and start the infusion.
5. In case of further inadequacy of breathing give 0,5 ml of 0,1% of atropine
intravenous and intubate the patient, because probably artificial ventilation will be
prolonged.
6. Insert gastric sound and aspirate its contents.
7. Write down all the current data about patients condition and performed
treatment actions.
8. Continue observation using laboratory and instrumental techniques.
9. Continue etiological and symptomatic treatment.
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later cardiovascular system fails. Those patients should be ventilated with the help of
respiratory apparatus immediately, as in their case oxygenation itself will not help (hypoxia
will be corrected, but never the less elimination of carbon dioxide will not be improved and
hypercapnia will cause cardiac arrest).
Residual relaxants effect is eliminated with anticholinergic drugs ( 1-2 ml of 0,05%
proserin solution intravenous with previous administration of 0,1% atropine sulphate solution).
For hypokalemia correction special mix glucose, potassium and insulin is used (so
called polarizing solution).
Low cholinesterase activity of plasma is compensated with fresh frozen plasma.
Organophosphate poisonings are treated with special antidotes (8.2); for elimination of
convulsions specific medicines are used (5.3).
Brief lung ventilation (up to 30 minutes) can be provided with the mask. Ventilation up
to 3 days needs intubation. If self-breathing is still inadequate after this time tracheostomy is
recommended.
History of medicine knows cases, when patients were artificially ventilated for 18-20
years.
Team of medical professionals, responsible for treatment of patient with
hypoventilation should follow all the asepsis and antiseptic rules and should be very careful
and attentive to the patients condition and apparatus work.
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monitored), record in the papers parameters of ventilation, heart rate, blood pressure and
central venous pressure, consciousness, physiologic and pathological liquid loss and
medicines administered.
2. All the time control work of the respiratory apparatus (respiratory rate,
volumes of respiration, minute ventilation, pressure in the airways during inspiration and
expiration). If self-breathing is present, but inadequate its important to achieve
synchronized patient-apparatus breathing (choose the correct mode or sometimes use
pharmacological sleep to turn off the respiratory centre of the patient if respiratory
efforts are exhausting for the organism).
3. Every 30 minutes change parameters of respiration, making tidal volume
40-50% more than the necessary every 5-10 minutes. This way you prevent the
development of atelectasis.
4. Every hour carry our oral, tracheal and bronchial suction using plastic
catheters with side foramina and blunt end. Catheters generally should not be reused, but
if its necessary you can use them for one patient several times keeping them in
antiseptic solution between suctions. Procedure: doctor or nurse puts on gloves and face
mask, disconnects tube from the apparatus, carefully and at the same time quickly inserts
the plastic catheter, previously connected to the vacuum suction, into the tube and turns
it clockwise and counterclockwise. For cleaning of principal bronchi try to turn head of
the patient and to push catheter deeper, but try not to make single suction try longer than
10-12 seconds. In necessary continue suction after a ventilation break (during this
pause you can carefully clap over the chest of the patient to remove mucus from lower
airways to their upper parts). After suction is done clean the catheter and place it into the
antiseptic solution.
Cleaning of the trachea through tracheostomy tube has 2 main points:
- inserting the catheter keep the side foramen of its upper end open
- during the suction shut it with your finger to create negative pressure and
aspirate mucus; taking it our dont forget to scroll it.
The same technique should be used for oral and nasal cavities (right and left
nostril), but not the same catheter. Every catheter container with antiseptic should be signed.
5. Every hour change the position of the patient: make it lateral, supine or
prone, Fowlers or Trendelenberg. Changing body position you change perfusion and
ventilation correlations in the lungs and thus arterial blood becomes more oxygenated.
This way appearance of bedsores is also prevented.
6. Every12-24 hours change the endotracheal or tracheostomy tube.
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Status asthmaticus
Status asthmaticus is an acute exacerbation of asthma that is caused by bronchial
spasm and does not respond to standard treatments of bronchodilators and steroids. It occurs
when parasympathetic-sympathetic balance is greatly violated. Pathological stimulation of
vagus causes spasms of smooth bronchi muscles, what brings increasing of resistance
worsening of their patency. In addition excessive secretion and oedema of bronchial walls make
airways almost not conductive.
Such exacerbation can be caused by allergens, stress or endocrinological factors.
Main clinical asthma symptom is dyspnea attack, which begins with dry cough. Those
attacks are sudden; patients feel more comfortably sitting in bed with their arms based on bed.
This position is called orthopnea, it help to use additional muscles (abdominal, muscles of the
shoulder girdle) in respiratory act. Extreme wheezing is heard at distance. Inspiration is
extremely short and expiration much prolonged and forced. Lack of mucus is rather warning
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symptom. In case of complete obturation silent lung appears: breathing is asymmetric, there
are silent parts of the lungs which do not contain any auscultative phenomena. Patients suffer
from hypoxia and hypercapnia which earlier or later result in unconsciousness.
Treatment.
Most asthma attacks are successfully treated with inhalation of short
acting 2-adrenoreceptor agonists (SABA), such as salbutamol. Anticholinergic medications,
such as ipratropium bromide, might be used in addition for severe cases. Steroids are generally
considered the most effective treatment available for long term control. When neither steroids,
nor adrenomimetics work for treatment of a long and severe attack (or series of attacks)
In case of status asthmaticus spasm of bronchioles, inflammation and edema of
bronchial wall and violation of mucus excretion and evacuation (due to abnormal cilia work)
create pathogenetic base. Hyperventilation leads to greater water loss, what makes surface of
bronchi dry and mucus more thick. This sick mucus can not be evacuated from airways during
cough and thus it obstructs small bronchi and bronchioles, making ventilation impossible.
There are two types of status asthmaticus: anaphylactic and metabolic. Anaphylactic
type is connected with allergic and immune reactions. It might appear after administration of
some medicines (antibiotics, enzymes, aspirin, etc.) and develops very fast. Metabolic type of
status asthmaticus is caused by metabolism disorders, which block -adrenoreceptors.
Long-term administration of sympatomimetics (asthmopent, ephedrine) can also cause
metabolic type of status asthmaticus.
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140 per minute, blood pressure lowers to critical values. Biochemical blood test results show
mixed decompensated acidosis (pH <7,2) and serious homoeostatic disorders. Acute
cardiopulmonary insufficiency may lead to death.
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There are many important points in general asthma treatment. Among them: rational
antibiotic treatment, elimination of allergens, treatment of comorbidities and adequate asthma
attacks treatment, in order to avoid development of status asthmaticus.
Chest injuries
Multiple rib fractures, especially that causing flail chest, violate greatly biomechanics
of breathing. Clinically one can see reduction of chest excursion, retraction of certain chest
wall parts and asymmetric breathing movements. Patients show decreasing of tidal volume,
cyanosis, violations of haemodynamics, microcirculation disorders and depression of central
nervous system.
Rib fractures can also cause hemothorax and pneumothorax.One of the most dangerous
complications of chest injury is a tension pneumothorax, which end with a severe hypoxia,
mediastinum organs dislocation and thus death.
Chest trauma patients should be treated very carefully: use all your diagnostic
possibilities, including inspection, palpation, percussion, auscultation and additional
laboratory and instrumental tests. Especially important is such approach with unconscious
victims.
The choice of treatment depends on specific type of injury and its complications:
hemothorax and pneumothorax need to be drained; tension pneumothorax should be
punctuated (transformed into open pneumothorax); ineffective spontaneous ventilation should
be replaced with artificial; antibiotics and painkillers are generally recommended.
Coronary Caf-syndrome
This name is used for a sudden asphyxia, which appears when foreign body gets
between the vocal cords and obturates the airways.
It is caused by a violation of swallowing and breathing. Imagine a situation in which
the victim speaks loudly during the meal and then suddenly stops talking and jumps to his feet.
His efforts to inhale are ineffective, hands try to free the neck rending the clothes, face gets
cyanotic and swollen, eyes get filled with fear. In 3-4 minutes patient losses the consciousness,
convulsions begin and finally clinical death appears (respiratory efforts cease, pulse gets
weaker, defecation and urination are possible).
Thus, during acute foreign body obturation of glottis we can see 3 subsequent stages:
1- patient conscious, on his feet
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This manoeuvre allows to create a high pressure in the windpipe of the patient and
thus exhaled air forces the foreign body to get out from the glottis. If the try will be
unsuccessful only urgent conicotomy will save the life of the patient.
Procedure of conicotomy: put a roll (improvised one if necessary) under the neck of the
patient, extending his neck as much as possible. In case of convulsions just ask someone to
hold the patient. Then cover tightly with the first and third fingers of your left hand the thyroid
cartilage and slide down with your index finger to the fossa, which divides thyroid and
cricoid cartilages. At this place the thickness of the membrane is only few millimetres, so it can
be easily pricked with a sharp object (for example kitchen knife). Limit the blade of the knife
to 1cm long with the fingers of your right hand and sliding over the nail of your left hand index
finger prick or cut the membrane. If it is possible insert a tube into the opening you made to
prevent its closing (you can even use your ball pen for this purpose). The faster this
manipulation will be done, the higher are chances of the patient to get fully recovered.
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If the victim is in a state of clinical death (the third stage) perform the conicotomy
immediately and start CPR. You can ventilate the patient through the conicotomy tube.
Advanced medical help includes direct laryngoscopy and extraction of a foreign body
with a forceps. If necessary those patients can be treated with a bronchoscopy or tracheostomy.
Laryngospasm
Laryngospasm is a pathological muscular contraction of the laryngeal cords, which
manifests itself with a difficult or impossible inspiration. It appears as a consequent of
pathological reflex or excessive stimulation of vagal nerve.
Usual reasons for laryngospasm are traumatic operations on reflex zones (vocal cords,
trachea bifurcation, epiglottis, eye bulbs, periosteums). Irritation of vocal cords by food, saline,
gastric contents, chemical or thermal stimuli as long as allergic reaction are the most common
reasons for laryngospasm.
There are two types of laryngospasm: total and partial. Both cases are sudden and
characterized by an inspiration dyspnea. Patient tries to inhale, his respiratory muscles
contract, retracting intercostals spaces, jugular and supraclavicular fossae. During partial
laryngospasm a small amount of air gets through the vocal cords and the sound of this air
movement reminds cry of a rooster. Total laryngospasm is silent (aphonic). Within few seconds
patient becomes cyanotic, his blood pressure and heart rate rise, later victim becomes
unconscious, reflexes are inhibited. In some cases after this muscles of larynx relaxes
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spontaneously and thus laryngospasm stops. But if deep hypoxia lasted for a while cardiac
arrest still might appear.
Immediate aid
- begin oxygenation though the face mask as without proper oxygen supply partial
laryngospasm becomes total
- whatever the reason of laryngospasm was eliminate it (remove the stimulator from the
reflex zone if necessary, stop the operation for example)
- give intravenously atropine solution ( 0,01 mg per kilogram of body weight),
euphillinum (5-10 ml of 2,4% solution, diluted in 10 ml of saline). If the initial damage was
caused by thermal, chemical or allergic stimuli use antihistamine medicine (2 ml of 2,5%
promethazine solution, 2 ml of 2% dimedrol solution) and steroids (60-90 mg of prednisolone).
Intensive treatment
- inhalation of bronchial spasmolytics (salbutamol);
- repeat the medicines mentioned above;
- in case of partial laryngospasm start artificial respiration through the mask with high
oxygen speed and large ventilation volume;
- if your previous actions are not successful use depolarising muscle relaxants (give
10 ml of 2% suxamethonium solution intravenously) and after total muscle relaxation perform
direct laryngoscopy and trachea intubation. Of course if you have time and possibilities
previously use hypnotics (for example 5-10 ml of propofol solution);
- if there are no conditions for intubation or your tries were unsuccessful, but situation
is worsening into life-threatening (extreme bradycardia, unconsciousness, blood pressure less
then 70 mm of Hg, general convulsions) perform conicotomy with the equipment you have and
insert tube for oxygenation;
- in case of cardiac arrest start CPR according to general standards.
Bronchial spasm
Bronchial spasm is an acute disorder of external respiration caused by spasm of small
bronchi smooth muscles. It can be total or partial. The reasons are the same as those for
laryngospasm. Treatment for bronchial and laryngeal spasm are much alike, however muscle
relaxants and conicotomy are not effective and thus death is almost unavoidable. What could
be really useful is prophylactic premedication: before operations on reflex zones use atropine
solution (0,01 mg per kg of body weight) in order to avoid pathological reflexes.
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Tracheostomy
There are 3 types of tracheostomy according to anatomic placement of the incision:
upper medial and low.
Indications: violations of airways patency in case of tumors, laryngeal stenosis;
prolonged artificial ventilation of ITU patients.
Required equipment: tracheostomy tubes of different sizes, scalpel, clamps, tissue
retraction blades, stitch material and dressing, antiseptics, electric suction, respiratory
apparatus, anaesthetics.
Procedure: perfect conditions for tracheostomy are those in operating room,
however it can be done in ITU with specific antiseptic and aseptic measures.
After antiseptic preparation of the operative field immobilize the trachea with
fingers of your left hand and cut the skin strictly along the midline of the neck right under
the thyroid cartilage (the length of the incision should be 4-5 cm). After skin, hypodermic
tissue and aponeurosis are cut start blunt separating of the cricoid cartilage and pull it
upwards with a surgical hook. Cut the fascia, which covers the thyroid isthmus, along the
lower edge of the cartilage and with a blunt hook pull the isthmus down. Make horizontal
incision between the second and third or third and fourth tracheal rings, then cut one or two
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distal tracheal rings and insert the tube (use dilatator if necessary). Dont make opening too
large, not more than 1/3 of trachea diameter. After tube is fixated put an aseptic bandage
around the wound.
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Pic.3.3 Pic.3.4
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Task1.
Patience, the patient of 56 years, was transported by ambulance to the hospital
reception with breathlessness and difficult breathing. He is restless, excited: his skin is
cyanotic and dry. Respiration rate is 26, respiratory movements are deep, additional muscles
participate respiration. Blood pressure is 180/110 mm of Mercury, heart rate 106 per minute.
Gasometry results are: pO2A 67 mm of Mercury, pCO2a 49 mm of Mercury. Name the
disorder and principles of its treatment.
Task 2.
Calculate normal spirography indexes of Andrew, medical student of 22 years
(height 170 cm, weight 70 kg): respiratory rate, tidal volume, minute ventilation, dead space
volume, alveolar ventilation.
Task 3.
Patience, the patient, during cleaning of his nasal cavity suddenly felt, that inspiration
became difficult. His skin gets cyanotic, blood pressure increases. Name the type of
complication and describe the urgent help, which is necessary in this situation.
Task 4.
Andrew, the medical student, during a casual meeting in a caf was laughing and at the
same time chewing his sandwich. Suddenly he became quiet, grabbed his neck and stopped
breathing. His face turns blue.
what should be done immediately
What should be done if Bonnie, student of medicine, has convulsions. He is
unconscious, his pulse is weak. Describe CPR.
What will be your decision if You find Clyde, student of medicine, 3 minutes after
cardiac arrest?
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Task 5.
Patience, the patient, was transported to the hospital in a severe condition:
unconscious, skin cyanotic, respiratory rate 64 per minute, heart rate 124 per minute, blood
pressure 90/60 mm of Mercury, body temperature normal. Choose the type of help and
algorithm of your actions.
Task 6.
Patience, the patient, suffers from bronchial asthma. After regular ambulance visit he
doesn't feel better, although medicines were given intravenously. His condition is critical:
central nervous system depressed, skin is wet and cyanotic, expiration is prolonged greatly,
sibilant rales are combined with silent lung parts. Blood pressure is 110/70 mm of Mercury.
Heart rate is 116 per minute. Describe your immediate actions and algorithm of intensive care.
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from the body with urine (1,5-2 liters), stool (300 ml), perspiration and breathing (those two
reasons are combined as perspiration loss and make from 300 to 1000 ml per day).
Water balance is regulated through complicated, but reliable mechanisms. Control over
water and electrolytes excretion is realized by osmotic receptors of posterior hypothalamus,
volume receptors of the aerial walls, bar receptors of carotid sinus, juxtaglomerular apparatus
of the kidneys and adrenal cortical cells.
When there is a water deficiency or electrolytes excess (sodium, chlorine) thirst
appears and this makes us drink water. At the same time posterior pituitary produces
antidiuretic hormone, which decreases urine output. Adrenals reveal into the blood flow
aldosterone, which stimulates reabsorption of sodium ions in the tubules and thus also
decreases diuresis (due to osmosis laws water will move to the more concentrated solution).
This way organism can keep precious water.
On the contrary, in case of water excess endocrine activity of glands is inhibited and
water is actively removed from the body through the kidneys.
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Dehydration signs: weight loss, decrease of skin turgor and eyeballs tone, dry skin and
mucous membranes; low central venous pressure, cardiac output and blood pressure (collapse
is possible); decreased urine output and peripheral veins tone; capillary refill over 2 seconds
(microcirculation disorders) and low skin temperature; intracellular dehydration is
characterized with thirst and consciousness disorders. Laboratory tests show blood
concentration: hematocrit, hemoglobin concentration, protein level and red blood cells
concentration increase.
Overhydration appears in case of:
- excessive water consumption, inadequate infusion therapy;
- acute and chronic renal failure, hepatic and cardiac insufficiency;
- disorders of fluid balance regulation;
- low protein edema.
Clinical findings in case of overhydration are: weight gain, peripheral oedema,
transudation of the plasma into the body cavities (pleural, abdominal), high blood pressure and
central venous pressure. In case of intracellular overhydration appear additional symptoms:
nausea, vomiting, signs of cerebral edema (spoor, coma). Laboratory tests prove hemodilution.
According to the osmotic concentration of plasma dehydration and overhydration are
divided into hypotonic, isotonic and hypertonic.
Isotonic dehydration is caused by equal loss of electrolytes and fluid from the
extracellular space (without cellular disorders).Blood tests show hemoconcentration; sodium
level and osmotic concentration are normal.
To treat this type of water imbalance use normal saline solution, Ringer solution,
glucose-saline solutions, etc.. The volumes of infusions can be calculated according to the
formula:
VH2O= 0,2*BW* (Htp-0,4)/0,4 ,
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Hypertonic dehydration is caused by mostly water loss: first it appears in the vascular
bed, than in the cells. Laboratory tests show hemoconcentration: elevated levels of proteins, red
blood cells, hematocrit. Plasma sodium is over 155 mmol/l and osmotic concentration increases
over 310 mOsm/l.
Intensive treatment: if there is no vomiting allow patients to drink. Intravenously give
0,45% saline solution and 2,5 % glucose solution, mixed with insulin. The volume of infusions
is calculated according to the formula:
VH2O=0,6*BW (Nap -140)/140,
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Give it intravenously slowly, during one hour. Forced bolus infusion of potassium
solutions (10-15 ml) can bring cardiac arrest.
Potassium level over 5,2 mmol/l is a state called hyperkalemia. To treat this
condition use calcium gluconate or calcium chloride solutions (10 ml of 10% solution
intravenously), glucose and insulin solution, saluretics, steroids, sodium bicarbonate
solution. Hyperkalemia over 7 mmol/l is an absolute indication for dialysis.
Sodium is the main extracellular cation. Its normal plasma concentration is 135-155
mmol/l. Daily required amount of potassium is 2 mmol/kg of body weight.
Sodium concentration which is lower than 135 mmol/l is known as hyponatraemia.
This condition is caused by sodium deficiency or water excess. Sodium deficiency is
calculated according to the formula:
Nad= (140-Nap)*0,2 BW,
Na- sodium deficiency, mmol;
Nap sodium concentration of the patient mmol/l;
0,2*BW extracellular fluid volume, l.
To treat it use normal saline (1000 ml contains 154 Na mmol) or 5,8% solution of
sodium chloride your choice will depend on osmotic concentration.
Chlorine is the main extracellular anion. Its normal plasma concentration is 98-107
mmol/l. Daily requirement of chlorine is 215 mmol.
Hypochloremia is a condition of decreased plasma chlorine concentration (less than 98
mmol/l).
Chlorine deficiency is calculated according to the formula:
Cld = (100-Clp)*0,2 BW,
Cld- chlorine deficiency, mmol
Clp plasma chlorine concentration of the patient, mmol/l
0,2*BW extracellular fluid volume, l.
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To treat hypochloremia use normal saline (1000 ml contains 154 mmol of chlorine) or
5,8% sodium chlorine solution (1 ml contains 1 mmol of chlorine). The choice of solution
depends on the osmotic concentration of the plasma.
Hyperchloremia is a condition of increased chlorine concentration (over 107 mmol/l).
Intensive therapy of this state includes treatment of the disease, which caused it
(decompensated heart failure, hyperchloremic diabetes insipidus, glomerulonephritis). You can
also use glucose, albumin solutions and dialysis.
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acute and chronic respiratory violations. When pCO2 is over 60 mm Hg begin artificial lung
ventilation (through the mask or tube; when the necessity of ventilation lasts longer than 3 days
perform tracheostomy).
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BE 3,0 mmol/l.
To treat this condition use acid solutions, which contain chlorides (saline, potassium
chloride). In case of kaliopenia give potassium solutions.
Respiratory and metabolic imbalances can mix in case of severe decompensated
diseases due to failure of compensatory mechanisms. Correct interpretation of these violations
is possible only in case of regular and iterative gasometry blood tests.
Control tasks.
Task 1.
Calculate the total body water volume and its extracellular and intracellular volumes of
the Patience, the patient of 48 years and body weight 88 kg.
Task 2.
Patience, the patient of 23 with body weight 70 kg has sodium level 152 mmol/l and
hematocrit 0,49 l/l. Name the type of water balance disorder.
Task 3.
Patience, the patient of 54 with body weight 76 kg has sodium level 128 mmol/l.
Calculate the volume of saline and 7,5% sodium chloride solution necessary for the treatment
of this condition.
Task 4.
Patience, the patient of 60 with body weight 60 kg has sodium level 140 mmol/l and
hematocrit 0,55 l/l. Name the type of disorder and prescribe infusion therapy.
Task 5.
Patience, the patient of 42 with body weight 80 kg has potassium level 2,6 mmol/l.
Calculate the volume of 4% potassium chloride solution necessary for treatment of this
condition.
Task 6.
Patience, the patient of 33 with body weight 67 kg and diagnosis gastric ulcer,
complicated with pylorostenosis has potassium concentration 3 mmol/l, chlorine
concentration 88 mmol/l. pH 7,49, pCO2a 42 mm Hg, BE + 10 mmol/l. Name the type of
disorder.
Task 7.
Patience, the patient of 50 with body weight 75 kg, was transported to the admission
unit of the hospital with: unconsciousness, cyanotic skin, low blood pressure, shallow
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breathing. Blood tests show: pH 7,18, pCO2a 78 mm Hg, pO2A 57 mm Hg, BE -4,2 mmol/l.
Name the type of acid-base disorder and prescribe treatment.
Task 8.
Patience, the patient with body weight 62 kg and renal insufficiency has: potassium
concentration 5,2 mmol/l, sodium concentration 130 mmol/l, calcium concentration 1,5
mmol/l, pH 7,22, pCO2a 34 mm Hg, BE -9,2 mmol/l. Name the type of disorder.
Among the natural vasoconstrictors (agents, which cause constriction of the blood
vessel) are epinephrine, norepinephrine, serotonin, angiotensin II. Stress enhances the secretion
of cathecholamines, their blood concentration increases and arterioles constrict. Spasm of the
arterioles is the basis of blood flow centralization: peripheral flow is disregarded in order to
provide brain with the oxygenated blood as long as possible. To the group of vasodilatators
(agents, which provide dilatation of the vessels) belong acid metabolites (lactate, pyruvate,
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MAP defines the level of pressure necessary for the metabolic exchange in the tissues.
Its measurement allows the evaluation of tissue perfusion level.
Blood pressure depends on different factors, but the most important are cardiac output
and vascular resistance (mostly arterioles). This dependence is direct, thus you can increase
blood pressure using:
- infusion of vasoconstrictors - solutions of epinephrine, phenylephrine
(mesaton), etc. (they will increase the vascular resistance);
- infusion of hydroxyethyl starch solutions or saline (they will increase
circulating blood volume)
- infusion of cardiac glycosides or other medicine which stimulate
myocardium
General volume of blood in the body of a healthy adult is nearly 7% from the body
weight: 70 ml per kilogram for male and 65 mil per kilogram of body weight for female. Of
course circulating blood volume is lower, because part of blood is out of metabolic processes
as a reserve. CBV can be measured with the infusion of coloring substance to the blood flow
(Evans blue, polyglucin) and later evaluation of its dissolution degree.
Therefore measurement of CVP, BP, cardiac output and circulating blood volume allow
to evaluate condition of circulation system of the patients and to provide adequate correction.
The reasons of the failure vary greatly: mechanic injuries, blood loss, burns,
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Left-sided heart failure is an inability of left ventricle to pump blood from the
pulmonary circuit to the systemic circuit. The most common reasons of it are myocardial
infarction, mitral insufficiency, left AV valve stenosis, aortic valve stenosis, aortal
insufficiency, hypertonic disease, coronary sclerosis, acute pneumonia.
Coronary circulation is possible only during the diastole and in those conditions every
violation of coronary passability decreases cardiac output. This way during the systole part of
the blood is not injected into aorta, but stays in the left ventricle. Diastolic pressure in the left
ventricle increases and blood is literally forced to stagnate in the left atrium. At the same time
right ventricle functions normally and continues to pump usual amounts of blood to the
pulmonary circuit. Thus hydrostatic pressure in the vessels of pulmonary circulation increases,
fluid part of the blood moves first to the lung tissue and then, through alveolar-capillary
membrane, to the alveolar lumen.
Clinically pulmonary edema begins with dyspnea (during physical activity or rest).
Later attacks of dyspnea are connected with persistent cough with white or pink blood-tinged
phlegm. During the attack patient tries to sit as in this position breathing is easier. This
condition is called heart asthma. When hydrostatic pressure is over 150-200 mm Hg, fluid
part of blood moves to the alveolar lumen causing development of pulmonary edema.
Pulmonary edema is divided into interstitial and alveolar edema.
Interstitial edema is a condition during which serous part of stagnated in the pulmonary
circuit blood infiltrates the lung tissue, including peribronchial and perivascular spaces.
During alveolar edema not only the plasma, but also blood components (red and white
blood cells, platelets) get out from the vessels. During the respiratory act blood mixes with the
air creating large amount of foam, which violates gas exchange. This way, in addition to
circulatory hypoxia, hypoxic hypoxia appears.
Condition of the patient gets worth quickly. Sitting position is optimal, but not as
helping as previously. Respiratory rate is nearly 30-35 breathes per minute, but attacks of
breathlessness are constant. Skin is pale with acrocyanosis. Hypoxia of central nervous system
usually causes psychomotor agitation. Respiratory acts are noisy; during cough pink blood-
tinged phlegm is released. Auscultation allows you to hear different wet rales, sometimes its
even possible to hear them standing aside the patient without phonendoscope.
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Pulmonary edema can be also divided according to the blood pressure level: the one
with elevated pressure is caused by a hypertonic disease, aorta valve insufficiency or disorders
of cerebral perfusion; another one is caused by total myocardial infarction, acute inflammation
of myocardial muscle, terminal valve defects, severe pneumonia and is characterized with
normal or low blood pressure.
Immediate aid
- make sure patient is sitting with his legs down (orthopnea)
- provide oxygenation through nasal catheter (before placing oil it with
glycerin, insert it to the depth of 10-12 cm distance from the wing of the nose to
auricle) or face mask. Do not use Vaseline, because it can burn in atmosphere with high
concentration of oxygen.
However if catheter is not deep enough patient will suffer from an unpleasant
burning feeling, because oxygen flow will dry mucosa layer of the nasal cavity; also in
this situation concentration of oxygen will be lower than expected.
- put venous tourniquets on the limbs in order to reduce amount of blood
returning to heart: venous bed of limbs can reserve up to 1,7 liters of blood;
- constantly control heart and kidney activity (ECG, SaO2 , and blood
pressure are checked automatically trough the monitor; to control diuresis you should
insert Foley catheter;
- catheterize central vein, because amount of infusions should be based on
central venous pressure;
- use medical defoamers if they are available (ethyl alcohol or
antiphomsylan solution) combined with oxygen inhalation
Scheme of oxygenation set connected to defoamer container
a. oxygen source (cylinder with oxygen)
b. tube with numerous holes sunk into container with defoamer
c. tube for humidified oxygen (its opening should be over the level of fluid);
d. patient
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them in case of low blood pressure; diuretic effect will last up to 3 hours after i/v
infusion, the expected diuresis is 2-3 liters
- if blood pressure allows you can try to use nitroglycerin to reduce
intravascular pressure of pulmonary circuit (1 or 2 tablets with 10 minutes interval)
- cardiac glycosides for improvement of heart action (0,025% digoxin
solution, 0,05% strophanthin solution, 0,06% corglicon solution);
- in case of high pressure (over 150 mm Hg) use ganglionic blocking agents
(1 ml of 5% pentamin solution diluted in 150 ml of saline, give i/v slowly; diluted with
saline 250 mg of trimethaphan solution), because they reduce pressure in pulmonary
circuit and lower the amount of blood getting to right half of the heart, however be
careful with the dosage and monitor blood pressure level carefully;
- never use osmotic diuretics in case of pulmonary edema they will
increase blood volume and thus heart load!!!
- when everything listed above failed and patient is worsening with every
second you should intubate him and start artificial ventilation with positive end
expiratory pressure (begin with 4-6 cm H2O)
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Collapse is a vascular failure. It occurs when body is not able to provide blood flow
according to the new level of its needs (either because reaction is not fast enough or
because sympathetic activation fails).Vascular bed volume and circulating blood volume are
disproportional: too much blood gets to the microcirculation vascular reserve and the
amount, which returns to the heart is not enough for the systemic needs (so called
decentralization of the blood flow). Cardiac output and blood pressure decrease, that
causes hypoperfusion of the central nervous system and thus unconsciousness and
life-threatening complications.
Collapse definition is a bit nominal, because if such reaction extends in time the
state of shock develops. Shock itself can equally run as a vascular failure or as a sudden
clinical death.
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(crush-syndrome).
In cases described above electrolytes are also lost (cations of sodium, potassium,
calcium, magnesium; anions of chlorine, hydrocarbonate). It causes complex osmolar, acid-base
and electrolytic disorders.
Stage of dehydration shock is evaluated according to the actual fluid loss:
less than 5% of body weight mild dehydration
5-10% of body weight moderate dehydration
over 10% of body weight severe dehydration
Water deficiency brings lowering of cardiac output, blood pressure and central venous
pressure (through decrease of blood volume returning to the heart, which leads to
compensatory adrenergic vasoconstriction).
Dehydration causes body weight loss, skin and mucosa dryness, decrease of
subcutaneous turgor and eyeballs tone, hypothermia, tachycardia, oliguria, thirst. While
dehydration progresses compensatory mechanisms weaken and central nervous system suffers:
patients become sluggish, confused; hallucinations, cramps and unconsciousness are also
possible. Laboratory tests show blood concentration.
One of the most important things in treatment of dehydrated patients is daily balance
of fluid: check it carefully trough measuring of daily received and lost fluids (food, infusions,
stool and urine output). In case of fever or tachypnea make necessary corrections. Balance
should be calculated every 12-24 hours (special paper forms make this easier).
Daily fluid balance is calculated by adding all the received fluids (both enteral and
parenteral ways) and deducting urine output, stool, perspiration and breathing water loss.
You should remember, that perspiration depends on body temperature: in case of
normal temperature (36,6C) patient looses 0,5 ml/kg of water during every hour; 1 degree of
temperature elevation adds 0,25 ml/kg to normal value of 0,5 ml/kg.
According to the fluid balance infusion therapy is divided into positive (for dehydrated
patients), negative (for overhydrated patients) and zero (for patients without balance
disorders).
Water deficiency is calculated according to the formula:
W def = (Htp-Htn)* 0,2 BW/ Htn,
W def water deficiency, l;
Htp hematocrit of the patient, l/l;
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The essential components of the human cardiovascular system are the heart, blood,
and blood vessels. It includes: the pulmonary circulation, a "loop" through the lungs where
blood is oxygenated; and the systemic circulation, a "loop" through the rest of the body to
provide oxygenated blood. An average adult contains five to six quarts (roughly 4.7 to 5.7
liters) of blood, accounting for approximately 7% of their total body weight.
While it is convenient to describe the flow of the blood through the right side of the
heart and then through the left side, it is important to realize that both atria contract at the same
time and that both ventricles contract at the same time. The heart works as two pumps, one on
the right and one on the left that works simultaneously. The right pump pumps the blood to the
lungs or the pulmonary circulation at the same time that the left pump pumps blood to the rest
of the body or the systemic circulation. Venous blood from systemic circulation (deoxygenated)
enters the right atrium through the superior and inferior vena cava. The right atrium contracts
and forces the blood through the tricuspid valve (right atrioventricular valve) and into the right
ventricles. The right ventricles contract and force the blood through the pulmonary semilunar
valve into the pulmonary trunk and out the pulmonary artery. This takes the blood to the lungs
where the blood releases carbon dioxide and receives a new supply of oxygen. The new blood
is carried in the pulmonary veins that take it to the left atrium. The left atrium then contracts
and forces blood through the left atrioventricular, bicuspid, or mitral, valve into the left
ventricle. The left ventricle contracts forcing blood through the aortic semilunar valve into the
ascending aorta. It then branches to arteries carrying oxygen rich blood to all parts of the body.
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Capillaries
Capillaries are the smallest of a bodys vessels; they connect arteries and veins, and
most closely interact with tissues. They are very prevalent in the body; total surface area is
about 6,300 square meters. Because of this, no cell is very far from a capillary, no more than 50
micrometers away. The walls of capillaries are composed of a single layer of cells, the
endothelium, which is the inner lining of all the vessels. This layer is so thin that molecules
such as oxygen, water and lipids can pass through them by diffusion and enter the tissues.
Waste products such as carbon dioxide and urea can diffuse back into the blood to be carried
away for removal from the body.
The "capillary bed" is the network of capillaries present throughout the body. These
beds are able to be opened and closed at any given time, according to need. This process is
called autoregulation and capillary beds usually carry no more than 25% of the amount of
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blood it could hold at any time. The more metabolically active the cells, the more capillaries it
will require to supply nutrients.
Veins
Veins carry blood to the heart. The pulmonary veins will carry oxygenated blood to the
heart awhile the systemic veins will carry deoxygenated to the heart. Most of the blood volume
is found in the venous system; about 70% at any given time. The veins outer walls have the
same three layers as the arteries, differing only because there is a lack of smooth muscle in the
inner layer and less connective tissue on the outer layer. Veins have low blood pressure
compared to arteries and need the help of skeletal muscles to bring blood back to the heart.
Most veins have one-way valves called venous valves to prevent backflow caused by gravity.
They also have a thick collagen outer layer, which helps maintain blood pressure and stop
blood pooling. If a person is standing still for long periods or is bedridden, blood can
accumulates in veins and can cause varicose veins. The hollow internal cavity in which the
blood flows is called the lumen. A muscular layer allows veins to contract, which puts more
blood into circulation. Veins are used medically as points of access to the blood stream,
permitting the withdrawal of blood specimens (venipuncture) for testing purposes, and
enabling the infusion of fluid, electrolytes, nutrition, and medications (intravenous delivery).
Venules
A venule is a small vein that allows deoxygenated blood to return from the capillary
beds to the larger blood veins, except in the pulmonary circuit were the blood is oxygenated.
Venules have three layers; they have the same makeup as arteries with less smooth muscle,
making them thinner.
The double circulatory system of blood flow refers to the separate systems of
pulmonary circulation and the systemic circulation in amphibians, birds and mammals
(including humans.) In contrast, fishes have a single circulation system. For instance, the adult
human heart consists of two separated pumps, the right side with the right atrium and ventricle
(which pumps deoxygenated blood into the pulmonary circulation), and the left side with the
left atrium and ventricle (which pumps oxygenated blood into the systemic circulation). Blood
in one circuit has to go through the heart to enter the other circuit. Blood circulates through the
body two to three times every minute. In one day, the blood travels a total of 19,000
km (12,000 miles), or four times the distance across the U.S. from coast to coast.
The Pulmonary Circuit
In the pulmonary circuit, blood is pumped to the lungs from the right ventricle of the
heart. It is carried to the lungs via pulmonary arteries. At lungs, oxygen in the alveolae diffuses
to the capillaries surrounding the alveolae and carbon dioxide inside the blood diffuses to the
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alveolae. As a result, blood is oxygenated which is then carried to the heart's left half -to the
left atrium via pulmonary veins. Oxygen rich blood is prepared for the whole organs and tissues
of the body. This is important because mitochondria inside the cells should use oxygen to
produce energy from the organic compounds.
The Systemic Circuit
The systemic circuit supplies oxygenated blood to the organ system. Oxygenated blood
from the lungs is returned to the left atrium, then the ventricle contracts and pumps blood into
the aorta. Systemic arteries split from the aorta and direct blood into the capillaries. Cells
consume the oxygen and nutrients and add carbon dioxide, wastes, enzymes and hormones.
The veins drain the deoxygenated blood from the capillaries and return the blood to the right
atrium.
Pic. 4.1 Distribution of blood in the body:
a. hear cavity itself 0 3% (% of blood volume)
b.arteries -15%
c. capillares -12%
d. venous system 70%
Cardiac cycle is the term used to describe the relaxation and contraction that occur, as
a heart works to pump blood through the body. Heart rate is a term used to describe the
frequency of the cardiac cycle. It is considered one of the four vital signs. Usually it is
calculated as the number of contractions (heart beats) of the heart in one minute and expressed
as "beats per minute" (bpm). When resting, the adult human heart beats at about 70 bpm
(males) and 75 bpm (females), but this rate varies between people. However, the reference range
is nominally between 60 bpm (if less termed bradycardia) and 100 bpm (if greater, termed
tachycardia). Resting heart rates can be significantly lower in athletes, and significantly higher
in the obese. The body can increase the heart rate in response to a wide variety of conditions in
order to increase the cardiac output (the amount of blood ejected by the heart per unit time).
Exercise, environmental stressors or psychological stress can cause the heart rate to increase
above the resting rate. The pulse is the most straightforward way of measuring the heart rate,
but it can be deceptive when some strokes do not lead to much cardiac output. In these cases
(as happens in some arrhythmias), the heart rate may be considerably higher than the pulse.
Every single 'beat' of the heart involves three major stages: atrial systole, ventricular systole and
complete cardiac diastole. Throughout the cardiac cycle, the blood pressure increases and
decreases. As ventricles contract the pressure rise, causing the AV valves to slam shut.
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Water balance is regulated through complicated, but reliable mechanisms. Control over
water and electrolytes excretion is realized by osmotic receptors of posterior hypothalamus,
volume receptors of the atrial walls, baroreceptors of carotid sinus, juxtaglomerular apparatus
of the kidneys and adrenal cortical cells.
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through the intracellular space to the cells due to their higher osmotic concentration.
Cerebral oedema appears when the plasma osmolarity is lower than 270 mOsm/l.
Activity of central nervous system is violated and hypoosmolar coma occurs. Hyperosmolar
coma appears when the plasma osmolarity is over 320 mOsm/l: water leaves the cells and fills
the vascular bed and this leads to cellular dehydration. The sensitive to cellular dehydration are
the cells of the brain.
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Dehydration signs: weight loss, decrease of skin turgor and eyeballs tone, dry skin and
mucous membranes; low central venous pressure, cardiac output and blood pressure (collapse
is possible); decreased urine output and peripheral veins tone; capillary refill over 2 seconds
(microcirculation disorders) and low skin temperature; intracellular dehydration is
characterized with thirst and consciousness disorders. Laboratory tests show blood
concentration: hematocrit, hemoglobin concentration, protein level and red blood cells
concentration increase.
Overhydration appears in case of:
- excessive water consumption, inadequate infusion therapy;
- acute and chronic renal failure, hepatic and cardiac insufficiency;
- disorders of fluid balance regulation;
- low protein edema.
Clinical findings in case of overhydration are: weight gain, peripheral oedema,
transudation of the plasma into the body cavities (pleural, abdominal), high blood pressure and
central venous pressure. In case of intracellular overhydration appear additional symptoms:
nausea, vomiting, signs of cerebral edema (spoor, coma). Laboratory tests prove hemodilution.
According to the osmotic concentration of plasma dehydration and overhydration are
divided into hypotonic, isotonic and hypertonic.
Isotonic dehydration is caused by equal loss of electrolytes and fluid from the
extracellular space (without cellular disorders).Blood tests show hemoconcentration; sodium
level and osmotic concentration are normal.
To treat this type of water imbalance use normal saline solution, Ringer solution,
glucose-saline solutions, etc.. The volumes of infusions can be calculated according to the
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formula:
VH2O= 0,2*BW* (Htp-0,4)/0,4 ,
Hypertonic dehydration is caused by mostly water loss: first it appears in the vascular
bed, than in the cells. Laboratory tests show hemoconcentration: elevated levels of proteins, red
blood cells, hematocrit. Plasma sodium is over 155 mmol/l and osmotic concentration increases
over 310 mOsm/l.
Intensive treatment: if there is no vomiting allow patients to drink. Intravenously give
0,45% saline solution and 2,5 % glucose solution, mixed with insulin. The volume of infusions
is calculated according to the formula:
VH2O=0,6*BW (Nap -140)/140,
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Sodium is the main extracellular cation. Its normal plasma concentration is 135-155
mmol/l. Daily required amount of potassium is 2 mmol/kg of body weight.
Sodium concentration which is lower than 135 mmol/l is known as hyponatraemia.
This condition is caused by sodium deficiency or water excess. Sodium deficiency is
calculated according to the formula:
Nad= (140-Nap)*0,2 BW,
Na- sodium deficiency, mmol;
Nap sodium concentration of the patient mmol/l;
0,2*BW extracellular fluid volume, l.
To treat it use normal saline (1000 ml contains 154 Na mmol) or 5,8% solution of
sodium chloride your choice will depend on osmotic concentration.
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Chlorine is the main extracellular anion. Its normal plasma concentration is 98-107
mmol/l. Daily requirement of chlorine is 215 mmol.
Hypochloremia is a condition of decreased plasma chlorine concentration (less than 98
mmol/l).
Chlorine deficiency is calculated according to the formula:
Cld = (100-Clp)*0,2 BW,
Cld- chlorine deficiency, mmol
Clp plasma chlorine concentration of the patient, mmol/l
0,2*BW extracellular fluid volume, l.
To treat hypochloremia use normal saline (1000 ml contains 154 mmol of chlorine) or
5,8% sodium chlorine solution (1 ml contains 1 mmol of chlorine). The choice of solution
depends on the osmotic concentration of the plasma.
Hyperchloremia is a condition of increased chlorine concentration (over 107 mmol/l).
Intensive therapy of this state includes treatment of the disease, which caused it
(decompensated heart failure, hyperchloremic diabetes insipidus, glomerulonephritis). You can
also use glucose, albumin solutions and dialysis.
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Control tasks.
Task 1.
Calculate the total body water volume and its extracellular and intracellular volumes of
the Patience, the patient of 48 years and body weight 88 kg.
Task 2.
Patience, the patient of 23 with body weight 70 kg has sodium level 152 mmol/l and
hematocrit 0,49 l/l. Name the type of water balance disorder.
Task 3.
Patience, the patient of 54 with body weight 76 kg has sodium level 128 mmol/l.
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Calculate the volume of saline and 7,5% sodium chloride solution necessary for the treatment
of this condition.
Task 4.
Patience, the patient of 60 with body weight 60 kg has sodium level 140 mmol/l and
hematocrit 0,55 l/l. Name the type of disorder and prescribe infusion therapy.
Task 5.
Patience, the patient of 42 with body weight 80 kg has potassium level 2,6 mmol/l.
Calculate the volume of 4% potassium chloride solution necessary for treatment of this
condition.
Task 6.
Patience, the patient of 33 with body weight 67 kg and diagnosis gastric ulcer,
complicated with pylorostenosis has potassium concentration 3 mmol/l, chlorine
concentration 88 mmol/l. pH 7,49, pCO2a 42 mm Hg, BE + 10 mmol/l. Name the type of
disorder.
Task 7.
Patience, the patient of 50 with body weight 75 kg, was transported to the admission
unit of the hospital with: unconsciousness, cyanotic skin, low blood pressure, shallow
breathing. Blood tests show: pH 7,18, pCO2a 78 mm Hg, pO2A 57 mm Hg, BE -4,2 mmol/l.
Name the type of acid-base disorder and prescribe treatment.
Task 8.
Patience, the patient with body weight 62 kg and renal insufficiency has: potassium
concentration 5,2 mmol/l, sodium concentration 130 mmol/l, calcium concentration 1,5
mmol/l, pH 7,22, pCO2a 34 mm Hg, BE -9,2 mmol/l. Name the type of disorder.
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weight (15%+5%).
Physiologically insignificant amounts of water are distributed beyond the tissues in the
body cavities: gastrointestinal tract, cerebral ventricles, joint capsules (nearly 1% of the body
weight). However during different pathologic conditions this third space can cumulate large
amounts of fluid: for example in case of ascites caused by chronic cardiac insufficiency or
cirrhosis abdominal cavity contains up to 10 liters of fluid. Peritonitis and intestinal
obstructions remove the fluid part of blood from the vessels into the intestinal cavity.
Severe dehydration is extremely dangerous for the patient. Water gets to the body with
food and drinks, being absorbed by the mucous membranes of gastro-intestinal tract in total
amount of 2-3 liters per day. Additionally in different metabolic transformations of lipids,
carbohydrates and proteins nearly 300 of endogenous water are created. Water is evacuated
from the body with urine (1,5-2 liters), stool (300 ml), perspiration and breathing (those two
reasons are combined as perspiration loss and make from 300 to 1000 ml per day).
Water balance is regulated through complicated, but reliable mechanisms. Control over
water and electrolytes excretion is realized by osmotic receptors of posterior hypothalamus,
volume receptors of the atrial walls, baroreceptors of carotid sinus, juxtaglomerular apparatus
of the kidneys and adrenal cortical cells.
When there is a water deficiency or electrolytes excess (sodium, chlorine) thirst
appears and this makes us drink water. At the same time posterior pituitary produces
antidiuretic hormone, which decreases urine output. Adrenals reveal into the blood flow
aldosterone, which stimulates reabsorption of sodium ions in the tubules and thus also
decreases diuresis (due to osmosis laws water will move to the more concentrated solution).
This way organism can keep precious water.
On the contrary, in case of water excess endocrine activity of glands is inhibited and
water is actively removed from the body through the kidneys.
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changes in one sector the whole fluid of the body will be redistributed (water will move to the
environment with higher concentration). Over hydration of one sector will bring dehydration of
another. For example, when there is a tissue damage concentration of active osmotic parts
increases and water diffuses to this compartment, causing oedema. On the contrary plasma
osmolarity decreases, when there is a loss of electrolytes and osmotic concentration of the
cellular fluid stays on the previous level. This brings cellular oedema, because water moves
through the intracellular space to the cells due to their higher osmotic concentration.
Cerebral oedema appears when the plasma osmolarity is lower than 270 mOsm/l.
Activity of central nervous system is violated and hypoosmolar coma occurs. Hyperosmolar
coma appears when the plasma osmolarity is over 320 mOsm/l: water leaves the cells and fills
the vascular bed and this leads to cellular dehydration. The sensitive to cellular dehydration are
the cells of the brain.
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Dehydration signs: weight loss, decrease of skin turgor and eyeballs tone, dry skin and
mucous membranes; low central venous pressure, cardiac output and blood pressure (collapse
is possible); decreased urine output and peripheral veins tone; capillary refill over 2 seconds
(microcirculation disorders) and low skin temperature; intracellular dehydration is
characterized with thirst and consciousness disorders. Laboratory tests show blood
concentration: hematocrit, hemoglobin concentration, protein level and red blood cells
concentration increase.
Overhydration appears in case of:
- excessive water consumption, inadequate infusion therapy;
- acute and chronic renal failure, hepatic and cardiac insufficiency;
- disorders of fluid balance regulation;
- low protein edema.
Clinical findings in case of overhydration are: weight gain, peripheral oedema,
transudation of the plasma into the body cavities (pleural, abdominal), high blood pressure and
central venous pressure. In case of intracellular overhydration appear additional symptoms:
nausea, vomiting, signs of cerebral edema (spoor, coma). Laboratory tests prove hemodilution.
According to the osmotic concentration of plasma dehydration and overhydration are
divided into hypotonic, isotonic and hypertonic.
Isotonic dehydration is caused by equal loss of electrolytes and fluid from the
extracellular space (without cellular disorders).Blood tests show hemoconcentration; sodium
level and osmotic concentration are normal.
To treat this type of water imbalance use normal saline solution, Ringer solution,
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glucose-saline solutions, etc.. The volumes of infusions can be calculated according to the
formula:
VH2O= 0,2*BW* (Htp-0,4)/0,4 ,
Hypertonic dehydration is caused by mostly water loss: first it appears in the vascular
bed, than in the cells. Laboratory tests show hemoconcentration: elevated levels of proteins, red
blood cells, hematocrit. Plasma sodium is over 155 mmol/l and osmotic concentration increases
over 310 mOsm/l.
Intensive treatment: if there is no vomiting allow patients to drink. Intravenously give
0,45% saline solution and 2,5 % glucose solution, mixed with insulin. The volume of infusions
is calculated according to the formula:
VH2O=0,6*BW (Nap -140)/140,
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Sodium is the main extracellular cation. Its normal plasma concentration is 135-155
mmol/l. Daily required amount of potassium is 2 mmol/kg of body weight.
Sodium concentration which is lower than 135 mmol/l is known as hyponatraemia.
This condition is caused by sodium deficiency or water excess. Sodium deficiency is
calculated according to the formula:
Nad= (140-Nap)*0,2 BW,
Na- sodium deficiency, mmol;
Nap sodium concentration of the patient mmol/l;
0,2*BW extracellular fluid volume, l.
To treat it use normal saline (1000 ml contains 154 Na mmol) or 5,8% solution of
sodium chloride your choice will depend on osmotic concentration.
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Chlorine is the main extracellular anion. Its normal plasma concentration is 98-107
mmol/l. Daily requirement of chlorine is 215 mmol.
Hypochloremia is a condition of decreased plasma chlorine concentration (less than 98
mmol/l).
Chlorine deficiency is calculated according to the formula:
Cld = (100-Clp)*0,2 BW,
Cld- chlorine deficiency, mmol
Clp plasma chlorine concentration of the patient, mmol/l
0,2*BW extracellular fluid volume, l.
To treat hypochloremia use normal saline (1000 ml contains 154 mmol of chlorine) or
5,8% sodium chlorine solution (1 ml contains 1 mmol of chlorine). The choice of solution
depends on the osmotic concentration of the plasma.
Hyperchloremia is a condition of increased chlorine concentration (over 107 mmol/l).
Intensive therapy of this state includes treatment of the disease, which caused it
(decompensated heart failure, hyperchloremic diabetes insipidus, glomerulonephritis). You can
also use glucose, albumin solutions and dialysis.
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breathing has rate over 40 per minute sedate the patient, perform the intubation and begin
artificial ventilation with normal parameters.
Control tasks.
Task 1.
Calculate the total body water volume and its extracellular and intracellular volumes of
the Patience, the patient of 48 years and body weight 88 kg.
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Task 2.
Patience, the patient of 23 with body weight 70 kg has sodium level 152 mmol/l and
hematocrit 0,49 l/l. Name the type of water balance disorder.
Task 3.
Patience, the patient of 54 with body weight 76 kg has sodium level 128 mmol/l.
Calculate the volume of saline and 7,5% sodium chloride solution necessary for the treatment
of this condition.
Task 4.
Patience, the patient of 60 with body weight 60 kg has sodium level 140 mmol/l and
hematocrit 0,55 l/l. Name the type of disorder and prescribe infusion therapy.
Task 5.
Patience, the patient of 42 with body weight 80 kg has potassium level 2,6 mmol/l.
Calculate the volume of 4% potassium chloride solution necessary for treatment of this
condition.
Task 6.
Patience, the patient of 33 with body weight 67 kg and diagnosis gastric ulcer,
complicated with pylorostenosis has potassium concentration 3 mmol/l, chlorine
concentration 88 mmol/l. pH 7,49, pCO2a 42 mm Hg, BE + 10 mmol/l. Name the type of
disorder.
Task 7.
Patience, the patient of 50 with body weight 75 kg, was transported to the admission
unit of the hospital with: unconsciousness, cyanotic skin, low blood pressure, shallow
breathing. Blood tests show: pH 7,18, pCO2a 78 mm Hg, pO2A 57 mm Hg, BE -4,2 mmol/l.
Name the type of acid-base disorder and prescribe treatment.
Task 8.
Patience, the patient with body weight 62 kg and renal insufficiency has: potassium
concentration 5,2 mmol/l, sodium concentration 130 mmol/l, calcium concentration 1,5
mmol/l, pH 7,22, pCO2a 34 mm Hg, BE -9,2 mmol/l. Name the type of disorder.
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biochemical processes of the organism. Only in case of stable quantitative and qualitative
composition of both intracellular and extra cellular fluids homoeostasis is remained.
The body of an adult human contains 60% of water. Intracellular water makes 40% of
the body weight, the water of intercellular space makes 15% of body weight and 5% of body
weight are made by the water in the vessels. It is considered that due to unlimited diffusion of
water between vessels and extra vascular space the volume of extracellular fluid is 20% of body
weight (15%+5%).
Physiologically insignificant amounts of water are distributed beyond the tissues in the
body cavities: gastrointestinal tract, cerebral ventricles, joint capsules (nearly 1% of the body
weight). However during different pathologic conditions this third space can cumulate large
amounts of fluid: for example in case of ascites caused by chronic cardiac insufficiency or
cirrhosis abdominal cavity contains up to 10 liters of fluid. Peritonitis and intestinal
obstructions remove the fluid part of blood from the vessels into the intestinal cavity.
Severe dehydration is extremely dangerous for the patient. Water gets to the body with
food and drinks, being absorbed by the mucous membranes of gastro-intestinal tract in total
amount of 2-3 litters per day. Additionally in different metabolic transformations of lipids,
carbohydrates and proteins nearly 300 of endogenous water are created. Water is evacuated
from the body with urine (1,5-2 liters), stool (300 ml), perspiration and breathing (those two
reasons are combined as perspiration loss and make from 300 to 1000 ml per day).
Water balance is regulated through complicated, but reliable mechanisms. Control over
water and electrolytes excretion is realized by osmotic receptors of posterior hypothalamus,
volume receptors of the aerial walls, bar receptors of carotid sinus, juxtaglomerular apparatus
of the kidneys and adrenal cortical cells.
When there is a water deficiency or electrolytes excess (sodium, chlorine) thirst
appears and this makes us drink water. At the same time posterior pituitary produces
antidiuretic hormone, which decreases urine output. Adrenals reveal into the blood flow
aldosterone, which stimulates reabsorption of sodium ions in the tubules and thus also
decreases diuresis (due to osmosis laws water will move to the more concentrated solution).
This way organism can keep precious water.
On the contrary, in case of water excess endocrine activity of glands is inhibited and
water is actively removed from the body through the kidneys.
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of osmosis. Osmosis is a movement of water through a partially permeable membrane from the
solution with lower concentration to a solution with higher concentration.
Osmotic concentration (osmolarity) is the concentration of active parts in one liter of
solution (water). It is defined as a number of miliosmoles per liter (mOsm/l). Normally osmotic
concentration of plasma, intracellular and extracellular fluids is equal and varies between
285mOsm/l. This value is one of the most important constants of the organism, because if it
changes in one sector the whole fluid of the body will be redistributed (water will move to the
environment with higher concentration). Over hydration of one sector will bring dehydration of
another. For example, when there is a tissue damage concentration of active osmotic parts
increases and water diffuses to this compartment, causing oedema. On the contrary plasma
osmolarity decreases, when there is a loss of electrolytes and osmotic concentration of the
cellular fluid stays on the previous level. This brings cellular oedema, because water moves
through the intracellular space to the cells due to their higher osmotic concentration.
Cerebral oedema appears when the plasma osmolarity is lower than 270 mOsm/l.
Activity of central nervous system is violated and hypoosmolar coma occurs. Hyperosmolar
coma appears when the plasma osmolarity is over 320 mOsm/l: water leaves the cells and fills
the vascular bed and this leads to cellular dehydration. The sensitive to cellular dehydration are
the cells of the brain.
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Dehydration signs: weight loss, decrease of skin turgor and eyeballs tone, dry skin and
mucous membranes; low central venous pressure, cardiac output and blood pressure (collapse
is possible); decreased urine output and peripheral veins tone; capillary refill over 2 seconds
(microcirculation disorders) and low skin temperature; intracellular dehydration is
characterized with thirst and consciousness disorders. Laboratory tests show blood
concentration: hematocrit, hemoglobin concentration, protein level and red blood cells
concentration increase.
Overhydration appears in case of:
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Isotonic dehydration is caused by equal loss of electrolytes and fluid from the
extracellular space (without cellular disorders).Blood tests show hemoconcentration; sodium
level and osmotic concentration are normal.
To treat this type of water imbalance use normal saline solution, Ringer solution,
glucose-saline solutions, etc.. The volumes of infusions can be calculated according to the
formula:
VH2O= 0,2*BW* (Htp-0,4)/0,4 ,
Hypertonic dehydration is caused by mostly water loss: first it appears in the vascular
bed, than in the cells. Laboratory tests show hemoconcentration: elevated levels of proteins, red
blood cells, hematocrit. Plasma sodium is over 155 mmol/l and osmotic concentration increases
over 310 mOsm/l.
Intensive treatment: if there is no vomiting allow patients to drink. Intravenously give
0,45% saline solution and 2,5 % glucose solution, mixed with insulin. The volume of infusions
is calculated according to the formula:
VH2O=0,6*BW (Nap -140)/140,
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Sodium is the main extracellular cation. Its normal plasma concentration is 135-155
mmol/l. Daily required amount of potassium is 2 mmol/kg of body weight.
Sodium concentration which is lower than 135 mmol/l is known as hyponatraemia.
This condition is caused by sodium deficiency or water excess. Sodium deficiency is
calculated according to the formula:
Nad= (140-Nap)*0,2 BW,
Na- sodium deficiency, mmol;
Nap sodium concentration of the patient mmol/l;
0,2*BW extracellular fluid volume, l.
To treat it use normal saline (1000 ml contains 154 Na mmol) or 5,8% solution of
sodium chloride your choice will depend on osmotic concentration.
Chlorine is the main extracellular anion. Its normal plasma concentration is 98-107
mmol/l. Daily requirement of chlorine is 215 mmol.
Hypochloremia is a condition of decreased plasma chlorine concentration (less than 98
mmol/l).
Chlorine deficiency is calculated according to the formula:
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To treat hypochloremia use normal saline (1000 ml contains 154 mmol of chlorine) or
5,8% sodium chlorine solution (1 ml contains 1 mmol of chlorine). The choice of solution
depends on the osmotic concentration of the plasma.
Hyperchloremia is a condition of increased chlorine concentration (over 107 mmol/l).
Intensive therapy of this state includes treatment of the disease, which caused it
(decompensated heart failure, hyperchloremic diabetes insipidus, glomerulonephritis). You can
also use glucose, albumin solutions and dialysis.
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pH<7,35,
pCO2a > 46 mm Hg
BE - normal values
However when the respiratory acidosis progresses renal compensation fails to maintain
normal values and BE gradually increases. In order to improve this condition you should treat
acute and chronic respiratory violations. When pCO2 is over 60 mm Hg begin artificial lung
ventilation (through the mask or tube; when the necessity of ventilation lasts longer than 3 days
perform tracheostomy).
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Control tasks.
Task 1.
Calculate the total body water volume and its extracellular and intracellular volumes of
the Patience, the patient of 48 years and body weight 88 kg.
Task 2.
Patience, the patient of 23 with body weight 70 kg has sodium level 152 mmol/l and
hematocrit 0,49 l/l. Name the type of water balance disorder.
Task 3.
Patience, the patient of 54 with body weight 76 kg has sodium level 128 mmol/l.
Calculate the volume of saline and 7,5% sodium chloride solution necessary for the treatment
of this condition.
Task 4.
Patience, the patient of 60 with body weight 60 kg has sodium level 140 mmol/l and
hematocrit 0,55 l/l. Name the type of disorder and prescribe infusion therapy.
Task 5.
Patience, the patient of 42 with body weight 80 kg has potassium level 2,6 mmol/l.
Calculate the volume of 4% potassium chloride solution necessary for treatment of this
condition.
Task 6.
Patience, the patient of 33 with body weight 67 kg and diagnosis gastric ulcer,
complicated with pylorostenosis has potassium concentration 3 mmol/l, chlorine
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Among the natural vasoconstrictors (agents, which cause constriction of the blood
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vessel) are epinephrine, norepinephrine, serotonin, angiotensin II. Stress enhances the secretion
of cathecholamines, their blood concentration increases and arterioles constrict. Spasm of the
arterioles is the basis of blood flow centralization: peripheral flow is disregarded in order to
provide brain with the oxygenated blood as long as possible. To the group of vasodilatators
(agents, which provide dilatation of the vessels) belong acid metabolites (lactate, pyruvate,
adenylic acid, inosinic acid), bradykinin, acetylcholine, different medicines (neuroleptics,
-adrenergic antagonists, peripheral vasodilatators, ganglionic blocking agents, etc.), some
exogenous poisons. All of them cause blood flow decentralization: opening of arterioles and
distribution of the blood from central vessels to the capillary bed.
Capillaries are the interweaving network of the smallest body vessels with the general
length of 90-100 thousands of kilometers. However simultaneously work only 20-25% of them.
They provide metabolic exchange bringing oxygen and nutrients to the tissues and take back
wastes of metabolism. Periodically, every 30-40 seconds one of them get closed and others
open (vasomotion effect). Capillaries contain 12% of the whole circulating blood volume, but
different pathological conditions can increase this amount even 3 and more times.
Used blood from the capillaries flows to the venous system. Veins are the blood
reservoir, which contains 70% of the total circulating blood volume. Unlike arteries they are
capable of volume control and thus they influence the amount of blood, which returns to the
heart.
The most important haemodynamic index of venous system is central venous pressure.
CVP represents the pressure which blood causes to the walls of cava veins and right atrium.
This parameter is an integral index of circulating blood volume, systemic vascular resistance
and pump function of the heart. It can be measure with a special device called
phlebotonometer (pic. 4.9) or with a usual infusion set and a ruler. Normally CVP measured
from the sternum point is 0-14 cm H2O and from midaxillary line is 8-15 cm H2O.
Central venous pressure decreases (sometimes even to negative) in case of:
- blood loss
- excessive water loss (dehydration)
- distributive shock (decrease of peripheral resistance due to venous and arterial
dilatation)
In those conditions decreases volume of blood returning to the heart and thus suffers
cardiac output. In case of negative CVP cardiac arrest is highly probable.
Central venous pressure increases in case of:
- heart failure (insufficiency of left or right ventricle)
- hypervolemia (excessive blood infusion, improper infusion therapy)
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MAP defines the level of pressure necessary for the metabolic exchange in the tissues.
Its measurement allows the evaluation of tissue perfusion level.
Blood pressure depends on different factors, but the most important are cardiac output
and vascular resistance (mostly arterioles). This dependence is direct, thus you can increase
blood pressure using:
- infusion of vasoconstrictors - solutions of epinephrine, phenylephrine
(mesaton), etc. (they will increase the vascular resistance);
- infusion of hydroxyethyl starch solutions or saline (they will increase
circulating blood volume)
- infusion of cardiac glycosides or other medicine which stimulate
myocardium
General volume of blood in the body of a healthy adult is nearly 7% from the body
weight: 70 ml per kilogram for male and 65 mil per kilogram of body weight for female. Of
course circulating blood volume is lower, because part of blood is out of metabolic processes
as a reserve. CBV can be measured with the infusion of coloring substance to the blood flow
(Evans blue, polyglucin) and later evaluation of its dissolution degree.
Therefore measurement of CVP, BP, cardiac output and circulating blood volume allow
to evaluate condition of circulation system of the patients and to provide adequate correction.
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adequate supply of tissue metabolic needs with oxygenated blood and nutrients. This, earlier or
later, causes cellular death.
The reasons of the failure vary greatly: mechanic injuries, blood loss, burns,
dehydration, exogenous and endogenous intoxications, immediate hypersensitivity reaction,
ischemic heart disease, neural and humoral regulation disorders of vascular tone.
Acute cardiac failure is a disorder of heart pumping action. It develops due to primary
heart problems or secondary, under the influence of extracardiac factors such as infection or
intoxication. There are two types of heart failure: left-sided and right-sided.
Left-sided heart failure is an inability of left ventricle to pump blood from the
pulmonary circuit to the systemic circuit. The most common reasons of it are myocardial
infarction, mitral insufficiency, left AV valve stenosis, aortic valve stenosis, aortal
insufficiency, hypertonic disease, coronary sclerosis, acute pneumonia.
Coronary circulation is possible only during the diastole and in those conditions every
violation of coronary passability decreases cardiac output. This way during the systole part of
the blood is not injected into aorta, but stays in the left ventricle. Diastolic pressure in the left
ventricle increases and blood is literally forced to stagnate in the left atrium. At the same time
right ventricle functions normally and continues to pump usual amounts of blood to the
pulmonary circuit. Thus hydrostatic pressure in the vessels of pulmonary circulation increases,
fluid part of the blood moves first to the lung tissue and then, through alveolar-capillary
membrane, to the alveolar lumen.
Clinically pulmonary edema begins with dyspnea (during physical activity or rest).
Later attacks of dyspnea are connected with persistent cough with white or pink blood-tinged
phlegm. During the attack patient tries to sit as in this position breathing is easier. This
condition is called heart asthma. When hydrostatic pressure is over 150-200 mm Hg, fluid
part of blood moves to the alveolar lumen causing development of pulmonary edema.
Pulmonary edema is divided into interstitial and alveolar edema.
Interstitial edema is a condition during which serous part of stagnated in the pulmonary
circuit blood infiltrates the lung tissue, including peribronchial and perivascular spaces.
During alveolar edema not only the plasma, but also blood components (red and white
blood cells, platelets) get out from the vessels. During the respiratory act blood mixes with the
air creating large amount of foam, which violates gas exchange. This way, in addition to
circulatory hypoxia, hypoxic hypoxia appears.
Condition of the patient gets worth quickly. Sitting position is optimal, but not as
helping as previously. Respiratory rate is nearly 30-35 breathes per minute, but attacks of
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breathlessness are constant. Skin is pale with acrocyanosis. Hypoxia of central nervous system
usually causes psychomotor agitation. Respiratory acts are noisy; during cough pink blood-
tinged phlegm is released. Auscultation allows you to hear different wet rales, sometimes its
even possible to hear them standing aside the patient without phonendoscope.
Pulmonary edema can be also divided according to the blood pressure level: the one
with elevated pressure is caused by a hypertonic disease, aorta valve insufficiency or disorders
of cerebral perfusion; another one is caused by total myocardial infarction, acute inflammation
of myocardial muscle, terminal valve defects, severe pneumonia and is characterized with
normal or low blood pressure.
Immediate aid
- make sure patient is sitting with his legs down (orthopnea)
- provide oxygenation through nasal catheter (before placing oil it with
glycerin, insert it to the depth of 10-12 cm distance from the wing of the nose to
auricle) or face mask. Do not use Vaseline, because it can burn in atmosphere with high
concentration of oxygen.
However if catheter is not deep enough patient will suffer from an unpleasant
burning feeling, because oxygen flow will dry mucosa layer of the nasal cavity; also in
this situation concentration of oxygen will be lower than expected.
- put venous tourniquets on the limbs in order to reduce amount of blood
returning to heart: venous bed of limbs can reserve up to 1,7 liters of blood;
- constantly control heart and kidney activity (ECG, SaO2 , and blood
pressure are checked automatically trough the monitor; to control diuresis you should
insert Foley catheter;
- catheterize central vein, because amount of infusions should be based on
central venous pressure;
- use medical defoamers if they are available (ethyl alcohol or
antiphomsylan solution) combined with oxygen inhalation
Scheme of oxygenation set connected to defoamer container
a. oxygen source (cylinder with oxygen)
b. tube with numerous holes sunk into container with defoamer
c. tube for humidified oxygen (its opening should be over the level of fluid);
d. patient
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Collapse is a vascular failure. It occurs when body is not able to provide blood flow
according to the new level of its needs (either because reaction is not fast enough or
because sympathetic activation fails).Vascular bed volume and circulating blood volume are
disproportional: too much blood gets to the microcirculation vascular reserve and the
amount, which returns to the heart is not enough for the systemic needs (so called
decentralization of the blood flow). Cardiac output and blood pressure decrease, that
causes hypoperfusion of the central nervous system and thus unconsciousness and
life-threatening complications.
Collapse definition is a bit nominal, because if such reaction extends in time the
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state of shock develops. Shock itself can equally run as a vascular failure or as a sudden
clinical death.
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However not only the complete fluid loss can be the reason of shock, but also its
pathological distribution into the extracellular space (intestinal cavity in case of intestinal
paralysis, abdominal cavity in case of ascites, pleural cavity in case of pleurisy). This way
will can also act prolonged heavy tissue inflammations (peritonitis) or massive injuries
(crush-syndrome).
In cases described above electrolytes are also lost (cations of sodium, potassium,
calcium, magnesium; anions of chlorine, hydrocarbonate). It causes complex osmolar, acid-base
and electrolytic disorders.
Stage of dehydration shock is evaluated according to the actual fluid loss:
less than 5% of body weight mild dehydration
5-10% of body weight moderate dehydration
over 10% of body weight severe dehydration
Water deficiency brings lowering of cardiac output, blood pressure and central venous
pressure (through decrease of blood volume returning to the heart, which leads to
compensatory adrenergic vasoconstriction).
Dehydration causes body weight loss, skin and mucosa dryness, decrease of
subcutaneous turgor and eyeballs tone, hypothermia, tachycardia, oliguria, thirst. While
dehydration progresses compensatory mechanisms weaken and central nervous system suffers:
patients become sluggish, confused; hallucinations, cramps and unconsciousness are also
possible. Laboratory tests show blood concentration.
One of the most important things in treatment of dehydrated patients is daily balance
of fluid: check it carefully trough measuring of daily received and lost fluids (food, infusions,
stool and urine output). In case of fever or tachypnea make necessary corrections. Balance
should be calculated every 12-24 hours (special paper forms make this easier).
Daily fluid balance is calculated by adding all the received fluids (both enteral and
parenteral ways) and deducting urine output, stool, perspiration and breathing water loss.
You should remember, that perspiration depends on body temperature: in case of
normal temperature (36,6C) patient looses 0,5 ml/kg of water during every hour; 1 degree of
temperature elevation adds 0,25 ml/kg to normal value of 0,5 ml/kg.
According to the fluid balance infusion therapy is divided into positive (for dehydrated
patients), negative (for overhydrated patients) and zero (for patients without balance
disorders).
Water deficiency is calculated according to the formula:
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A Multidisciplinary Approach
The multidisciplinary team in the SICU consists of intensivists, physicians, mid-level
practitioners and critical care nurses trained in critical care, surgery and trauma care of adult
patients. Many of the nurses are certified through The American Association of Critical Care
Nurses and are CCRN recipients. Other multidisciplinary services include:
Respiratory therapy
Physical and occupational therapy
Dietary services
Pharmacy services
Social work
Case management
Ancillary support
Patient Population
The SICU's patient population includes:
General surgery
Trauma services
ENT
Orthopaedic surgery
Vascular surgery
Urology
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Plastic surgery
Bariatric surgery
OB/GYN
Thoracic surgery
Immediately after your surgery, you will be taken to the intensive care unit (ICU) to recover,
where a team of specially trained cardiothoracic nurses will take care of you. Their goal is to
help you recover as quickly and safely as possible. Along with your surgeon, members of the
cardiothoracic anesthesia and surgical teams who took care of you in the operating room will
continue to follow your progress in the ICU.
Because the ICU is a busy place, you can expect bright lights and a great deal of activity during
the day. Many of the sounds you will hear are made by monitors and different types of
equipment. Your medications, including those for pain control, will be given through
intravenous (IV) tubes at very controlled rates using pumps.
To help you breathe, an endotracheal tube (breathing tube) was inserted while you were asleep.
This tube is connected to a respirator that assists your breathing. Because you will not be able
to talk or swallow while this tube is in place, your nurse will anticipate your needs and ask you
questions that require only a yes or no answer. Nod your head to say yes, and shake your head
to say no. When you are fully awake and breathing on your own, the breathing tube will be
removed, and you will be able to talk.
It's normal to feel cold and to shiver for a short while after you arrive in the ICU. Your nurse
will give you blankets to keep you warm. It's also normal to wake up feeling thirsty, because of
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the medications you received before or during the surgery, or because you had nothing to eat or
drink before your operation. Despite your thirst, you will be limited in what and how much you
may drink while in the ICU.
Controlling Pain
Although all patients are concerned about the pain they will experience, pain after surgery is
not as severe as most patients anticipate. To control your pain, you will be given medication
that is injected, given orally or by suppository. While you are in the ICU, pain medications will
be given to you as scheduled. While doses are calculated to keep you as comfortable as
possible, if the medications affect your breathing and/or blood pressure, your physician may
decrease the amount of pain medication given to you.
As you recover in the ICU, the nurses will monitor your blood pressure, pulse rate and
breathing. The endotracheal tube (breathing tube) will continue to help you breathe. To prevent
postoperative pneumonia, the nurses and respiratory therapists will periodically remove any
secretions that may have settled in your lungs during surgery. As soon as your breathing tube is
removed, you should begin using your incentive spirometer, followed by coughing exercises.
You should continue these exercises every hour while you are awake when you are transferred
to your hospital room.
While lying in bed, moving and changing position will help improve blood flow in your legs
and remove secretions in your lungs. You can move your feet, wiggle your toes and point your
toes up toward your head and then down toward the foot of the bed. Your nurse will help you
change positions by turning you from one side to another.
Your surgeon, anesthesiologist and pulmonologist will determine the best time for you to be
transferred from the ICU to the Cardiothoracic Unit Floor (CT Unit). Most patients are
transferred the day after surgery. If you remain in the ICU for more than a day, your surgeon or
a member of your surgery team will explain the specific reasons for the delay. The extra time
spent in ICU is often for precautionary reasons and does not indicate any problem.
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Incentive Spirometer
While recover from surgery, it might be uncomfortable or painful to breathe in as deeply as you
normally would. But in order for your lungs to function properly, you need to use your
incentive spirometer. You will be given one to take home to practice. You do not need to bring
it back to the hospital.
The incentive spirometer is a small, handheld device that is used after surgery to help you
expand your lungs and cough up any secretions from your lungs. It also helps maintain normal
breathing pattern and measures your inspiratory volume, or how well your lungs are being
filled with air when breathe in. In addition, the incentive spirometer will help exercise lungs,
just as if you were going through your normal daily routine.
PEP Therapy
Positive Expiratory Pressure (PEP) therapy uses a breathing device that helps expand lungs and
remove pulmonary secretions, or mucus. Therapist will assist you with this treatment.
Breathing through the PEP valve, you will inhale normally, then exhale through the PEP valve,
which has some resistance. This resistance will work out your lungs. After two series of ten
breaths, follow with 2-3 huff coughs.
Huff Coughing
Coughing is a natural way to force mucus out of lungs. During huff coughing, gently say the
word "huff". Therapist will help you with this breathing exercise.
Introduction
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Initial reports by Frerichs (1861) and Flint (1863), who had noted an association between
advanced liver disease with ascites and acute oliguric renal failure in the absence of significant
histological changes in the kidneys, led Heyd , and later Helwig and Schutz , to introduce the
concept of the hepatorenal syndrome (HRS) to explain the increased frequency of acute renal
failure after biliary surgery. However, because HRS could not be reproduced in animal models,
pathophysiological concepts remained speculative and its clinical entity was not generally
accepted. During the 1950s, HRS was more specifically characterised as a functional renal
failure in patients with advanced liver disease, electrolyte disturbances and low urinary sodium
concentrations. Hecker and Sherlock showed its temporal reversibility by norepinephrine
administration. Over the next few decades, haemodynamic and perfusion studies by Epstein
and other investigators identified splanchnic and systemic vasodilatation and active renal
vasoconstriction as the pathophysiological hallmarks of HRS. Improved models of ascites and
circulatory dysfunction contributed to therapeutic advances, including the introduction of
large-volume paracentesis, vasopressin analogues, and transjugular intrahepatic stent-shunt
(TIPS), which in turn have led to an improved pathophysiological understanding of HRS.
Definition HRS is defined as the development of renal failure in patients with severe liver
disease (acute or chronic) in the absence of any other identifiable cause of renal pathology. It is
diagnosed following the exclusion of other causes of renal failure in patients with liver disease,
such as hypovolaemia, drug nephrotoxicity, sepsis or glomerulonephritis. A similar syndrome
can also occur in the setting of acute liver failure. In the kidney there is marked renal
vasoconstriction, resulting in a low glomerular filtration rate (GFR). In the extrarenal
circulation arterial vasodilatation predominates, resulting in reduction of the total systemic
vascular resistance and arterial hypotension.
Diagnostic Criteria
The International Ascites Club (1996) group has defined the diagnostic criteria for HRS, and
these are listed in Table 1.
Major criteria
Chronic or acute liver disease with advanced hepatic failure and portal hypertension
Low GFR, as indicated by serum creatinine > 1.5 mg/dl or 24-h creatinine clearance <> 500
g/d for several days in patients with ascites without peripheral oedema or > 1000 ml in patients
with peripheral oedema)
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No sustained improvement in renal function (decrease of serum creatinine to 1.5 mg/dl or less
or increase in 24 h creatinine clearance to 40 ml/min or more) after withdrawal of diuretics and
expansion of plasma volume with 1.5 l of isotonic saline
Proteinuria
Additional criteria
Urine sodium <> plasma osmolality
Urine red blood cells <>
Epidemiology
HRS occurs in about 4% of patients admitted to hospital with decompensated cirrhosis, the
cumulative probability being 18% at 1 year, increasing to 39% at 5 years. Retrospective
studies indicate that HRS is present in approximately 17% of patients admitted to hospital
with ascites and in more than 50% of cirrhotic patients dying of liver failure. The most frequent
cause of renal failure in cirrhosis is spontaneous bacterial peritonitis (SBP). Approximately
30% of patients with SBP develop renal failure. Type 1 HRS is characterised by rapid and
progressive renal impairment and is precipitated most commonly by SBP. Type 1 HRS occurs
in approximately 25% of patients with SBP, even when rapid resolution of the infection is
obtained with antibiotics. Without treatment, the median survival of patients with HRS type 1
is less than 2 weeks, and virtually all patients die within 10 weeks after the onset of renal
failure. Type 2 HRS is characterised by a moderate and stable reduction in GFR and commonly
occurs in patients with relatively well-preserved hepatic function. The median survival is 36
months. Although this is markedly longer than that in type 1 HRS, it is still shorter than that of
patients with cirrhosis and ascites who do not have renal failure. People of all races who have
chronic liver disease are at risk of HRS, and its frequency is equal in both sexes; most patients
with chronic liver disease are in the 4th8th decade of life.
Prognosis
In a prospective study published by Gines et al., once HRS had developed the median survival
was only 1.7 weeks, and it was poorer particularly in patients with apparent precipitating
factors. Overall survival at 4 and 10 weeks was 20% and 10%, respectively. Patients with low
urinary sodium excretion
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Pathophysiology
The hallmark of HRS is renal vasoconstriction, although the pathogenesis is not fully
understood.Multiple mechanisms are probably involved and include interplay between
disturbances in systemic haemodynamics, activation of vasoconstrictor systems and a reduction
in activity of the vasodilator systems. The haemodynamic pattern of patients with HRS is
characterised by increased cardiac output, low arterial pressure and reduced systemic vascular
resistance. Renal vasoconstriction occurs in the absence of reduced cardiac output and blood
volume, which is a point of contrast to most clinical conditions associated with renal
hypoperfusion. Although the pattern of increased renal vascular resistance and decreased
peripheral resistance is characteristic of HRS, it also occurs in other conditions, such as
anaphylaxis and sepsis. Doppler studies of the brachial, middle cerebral and femoral arteries
suggest that extrarenal resistance is increased in patients with HRS, while the splanchnic
circulation is responsible for arterial vasodilatation and reduced total systemic vascular
resistance. The renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous
system (SNS) are the predominant systems responsible for renal vasoconstriction. The activity
of both systems is increased in patients with cirrhosis and ascites, and this effect is magnified
in HRS. In contrast, an inverse relationship exists between the activity of these two systems
and renal plasma flow (RPF) and the glomerular filtration rate (GFR). Endothelin is another
renal vasoconstrictor that is present in increased concentration in HRS, although its role in the
pathogenesis of this syndrome has yet to be identified. Adenosine is well known for its
vasodilator properties, although it acts as a vasoconstrictor in the lungs and kidneys. Elevated
levels of adenosine are more common in patients with heightened activity of the RAAS and
may work synergistically with angiotensin II to produce renal vasoconstriction in HRS. This
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effect has also been described with the powerful renal vasoconstrictor, leukotriene E4. The
vasoconstricting effect of these various systems is antagonised by local renal vasodilatory
factors, the most important of which are the prostaglandins. Perhaps the strongest evidence
supporting their role in renal perfusion is the marked decrease in RPF and the GFR when
nonsteroidal medications known to bring about a sharp reduction in PG levels are
administered. Nitrous oxide (NO) is another vasodilator that is believed to play an important
part in renal perfusion. Preliminary studies, predominantly based on animal experiments, have
demonstrated that NO production is increased in the presence of cirrhosis, although NO
inhibition does not result in renal vasoconstriction owing to a compensatory increase in PG
synthesis.However, when both NO and PG production are inhibited, marked renal
vasoconstriction develops. These findings demonstrate that renal vasodilators have a critical
role in maintaining renal perfusion, particularly in the presence of overactivity of renal
vasoconstrictors. However, we do not yet know for certain whether vasoconstrictor activity
becomes the predominant system in HRS and whether a reduction in the activity of the
vasodilator system contributes to this.Various theories have been proposed to explain the
development of HRS in cirrhosis. The two main ones are the arterial vasodilatation theory and
the hepatorenal reflex theory. The first not only describes sodium and water retention in
cirrhosis, but may also be the most rational hypothesis for the development of HRS.
Splanchnic arteriolar vasodilatation in patients with compensated cirrhosis and portal
hypertension may be mediated by several factors, the most important of which is probably NO.
In the early phases of portal hypertension and compensated cirrhosis, this underfilling of the
arterial bed causes a decrease in the effective arterial blood volume and results in homeostatic
reflex activation of the endogenous vasoconstrictor systems. Activation of the RAAS and SNS
occurs early with antidiuretic hormone secretion, a later event when a more marked
derangement in circulatory function is present. This results in vasoconstriction not only of the
renal vessels, but also in the vascular beds of the brain,muscle, spleen and extremities. The
splanchnic circulation is resistant to these effects because of the continuous production of
local vasodilators, such as NO. In the early phases of portal hypertension, renal perfusion is
maintained within normal or near-normal limits as the vasodilatory systems antagonise the
renal effects of the vasoconstrictor systems. However, as liver disease progress in severity, a
critical level of vascular underfilling is achieved; renal vasodilatory systems are unable to
counteract the maximal activation of the endogenous vasoconstrictors and/or intrarenal
vasoconstrictors, which leads to uncontrolled renal vasoconstriction. Support for this
hypothesis is provided by studies in which the administration of splanchnic vasoconstrictors in
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combination with volume expanders results in improvement in arterial pressure, RPF and GFR.
The alternative theory proposes that renal vasoconstriction in HRS is not related to systemic
haemodynamics but is due either to a deficiency in the synthesis of a vasodilator factor or to a
hepatorenal reflex that leads to renal vasoconstriction. Evidence points to the vasodilatation
theory as a more tangible explanation for the development of HRS.
Histopathology of HRS
In previous definitions of HRS, changes in renal histology were reported to be absent or
minimal, which reflected a rapid progression to death after development of HRS. Considering
that many patients with HRS currently receive aggressive supportive treatment including renal
replacement therapy to prolong survival until liver transplantation, it seems obvious that
prolonged renal hypoperfusion, renal medullary hypoxia and the high frequency of infectious
complications ultimately contribute to histologically detectable renal damage. However, it is
increasingly recognised that structural renal damage may already be found even before renal
dysfunction becomes manifest. In a series of cirrhotic patients undergoing liver
transplantation, 100% of renal biopsies showed glomerular abnormalities. Tubular function is
usually well preserved at the time when HRS develops, but tubular abnormalities, including
increased B2 microglobulin excretion, have been reported in deeply jaundiced patients with
HRS. With progressive circulatory dysfunction, prolonged renal hypoperfusion may eventually
result in acute tubular necrosis by increasing the susceptibility to additional insults by
radiographic contrast agents, aminoglycosides, haemorrhage, endotoxinaemia or any other
cause of medullary hypoxia. The presence of acute tubular necrosis could partially explain the
slow or absent renal recovery in HRS type 1 even after the initiation of vasopressor support.
For instance, a recent case study reports full recovery of renal function in dialysis-dependent
HRS after 7 weeks of treatment with ornipressin, dopamine and intravenous albumin.
Prevention
The following measures may decrease the incidence of renal failure or HRS in patients with
liver disease.
Prophylaxis Against
Bacterial Infections Bacterial infections occur in approximately 50% of patients with variceal
haemorrhage, and antibiotic prophylaxis improves survival by approximately 10%. Patients
who have had a previous episode of SBP have a 68% chance of recurrent infection at 1 year,
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and this carries a 33% chance of developing renal failure. As bacterial infections are an
important cause of renal dysfunction in cirrhotic patients, prophylaxis with antibiotics is
recommended in two clinical settings, namely variceal bleeding and a history of previous SBP.
Volume Expansion
To prevent the development of renal failure in patients who develop SBP, it is now
recommended that plasma volume expansion should be implemented in these patients by giving
20% albumin (11.5 g/kg over 13 days) at diagnosis to prevent circulatory dysfunction, renal
impairment and mortality. Use of low-salt albumin as fluid replacement in patients undergoing
large-volume paracentesis (8 g for each litre of ascitic fluid removed) is known to prevent
paracentesis-induced circulatory dysfunction.
Treatment
The ideal treatment for HRS is liver transplantation; however, because of the long waiting lists
in the majority of transplant centres, most patient die before being offered a transplant. There is
an urgent need for effective alternative therapies to increase survival chances for patients with
HRS until transplantation can be performed. Treatment can be divided into initial management,
pharmacological treatment and surgical manoeuvres.
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Pharmacological Treatment
All the drugs that have been investigated in HRS have one overriding aim: to increase renal
blood flow. This has been achieved either indirectly, by splanchnic vasoconstriction, or
directly, using renal vasodilators. One of the principal difficulties has been the lack of agents
that act purely on the splanchnic circulation. Drugs that spill over into the systemic
circulation may actually exacerbate the intense renal vasoconstriction already present.
Currently, there is significant enthusiasm for the use of vasoconstrictor agents in HRS.
However, the numbers of patients studied have been small, mortality remains high and there
have been no randomised placebo-controlled trials. This deficit clearly needs to be addressed
but the possibilities are limited by the relative rarity of patients with pure HRS without such
confounding variables as sepsis and gastrointestinal bleeding. Important aspect of the situation
mentioned in these reports are the need for a pressor response to the agents used and the
recurrence of abnormal renal function after the cessation of vasoconstrictor therapy. HRS is
effectively a marker of poor hepatic function, and these agents are probably best utilised as a
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bridge to further improvement in liver function following either cessation of alcohol abuse or
liver transplantation. Thus, the decision to use vasoconstrictor agents for HRS should be based
on whether the patient is a realistic transplant candidate and, if not, whether liver function
might improve. Patients who do not satisfy these criteria will be tested unnecessarily, merely
prolonging the process of dying when palliative care would be more appropriate. Dopamine.
Nonpressor renal doses of dopamine [25 g kg1 min1) are frequently prescribed to patients
with acute deterioration of renal function. As shown by a recent, large scale, randomised trial,
early renal dose dopamine has no role in the prevention of acute renal failure in critically ill
patients and does not significantly improve renal function in patients with HRS.At higher
doses, dopamine worsens the hyperdynamic circulation by exaggerating splanchnic hyperaemia
and increasing portal pressure and may cause tachyarrhythmia. Thus, the use of dopamine
monotherapy seems to offer no benefit in HRS. Combination therapy with dopamine and
vasopressors has produced inconsistent results in HRS. Because beneficial renal effects have
been reported only with vasopressor, and not with dopamine, monotherapy, it seems unlikely
that dopamine contributed to renal improvement in these studies. Misoprostol. Misoprostol, a
synthetic prostaglandin E-1 analogue, has been used to reverse renal vasoconstriction in HRS.
Low doses of misoprostol are vasodilatory, natriuretic and diuretic, whereas high-dose
misoprostol increases renal vascular tone and inhibits sodium and water excretion. None of the
five studies investigating misoprostol in HRS seems to indicate substantial benefit.
Improvement of renal function occurred in 1 of these studies, but could also be explained by
volume expansion. N-Acetylcysteine. In 1999, the group at the Royal Free Hospital reported
their experience with N-acetylcysteine (NAC) for the treatment of HRS. This was based on
experimental models of acute cholestasis, in which the administration of NAC resulted in an
improvement in renal function. Twelve patients with HRS were treated with intravenous NAC,
without any adverse effects, and the survival rates were 67% and 58% at 1 month and 3
months, respectively (this included 2 patients who received liver transplantation after
improvement in renal function). The mechanism of action remains unknown, but this
interesting study encourages further optimism for medical treatment of a condition that once
carried a hopeless diagnosis without liver transplantation. Controlled studies with longer
follow-up may help answer these pressing questions. Renal vasoconstrictor antagonists.
Saralasin, an antagonist of angiotensin II receptors, was first used in 1979 in an attempt to
reverse renal vasoconstriction. Because this drug inhibited the homeostatic response to
hypotension commonly observed in patients with cirrhosis, it led to worsening hypotension and
deterioration in renal function. Poor results were also observed with phentolamine, an alpha-
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according to this study, terlipressin with albumin is a safe and effective treatment for HRS.
Alpha adrenergic agonists.Angeli et al. showed that long-term administration of midodrine (an
alpha-adrenergic agonist) and octreotide improved renal function in patients with HRS type 1.
All patients also received albumin, and the results obtained with this approach were compared
against those observed with dopamine at nonpressor doses. None of the patients treated with
dopamine showed any improvement in renal function, but in all the patients treated with
midodrine, octreotide and volume expansion renal function did improve. No adverse effects
were reported in these patients. Gulberg et al. treated seven patients who had cirrhosis and
HRS type 1 with a combination of ornipressin and dopamine for infusion periods as long as 27
days, but only three of the seven patients survived. This treatment can be used as a bridge to
liver transplantation. Aquaretic agents. K-Opioid antagonists inhibit antidiuretic hormone
secretion by the neurohypophysis and induce water excretion.Administration of niravoline at
doses ranging from 0.5 to 2 mg induced a strong aquaretic response and was well tolerated in
18 cirrhotic patients with preserved renal function, but no data are available on the use of
niravoline in patients with HRS.
Surgical Manoeuvres
Transjugular intrahepatic portosystemic shunting. It is well documented that portal
hypertension plays a central role in the development of refractory ascites and HRS. Earlier
studies showed improved renal function after sideto- side portocaval shunting, but at the cost
of a high surgical mortality in advanced cirrhosis. The transjugular intrahepatic portosystemic
shunt (TIPS) was introduced as a less invasive method of reducing increased portal pressure.
Guevarra et al. have investigated hepatic and renal haemodynamic changes after placement of
TIPS in patients with HRS. One month after placement of TIPS a marked improvement in renal
function was observed, as indicated by a significant reduction in serum creatinine and blood
urea nitrogen and increased urine volume, RPF and GFR. These improvements were associated
with a reduction in plasma rennin, aldosterone and norepinephrine activity. These changes were
statistically significant, albeit less pronounced than observed in a similar group of patients
receiving ornipressin and albumin infusions. Renal improvements were more pronounced at 30
days than at 7 days, possibly because of the deleterious effects of contrast media or the
resolution of concomitant problems. After TIPS, GFR improved significantly but did not reach
normal values, suggesting that TIPS does not correct all mechanisms contributing to HRS.
Brensing et al. found a sustained improvement of renal function after TIPS in 31 patients with
type 1 or 2 HRS, allowing the discontinuation of haemodialysis in four of seven patients.After
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TIPS 3-, 6-, 12- and 18-month survival rates were 81%, 71%, 48% and 35%, respectively, in
the total patient cohort, with survival in HRS type 1 patients being significantly worse than in
the others. The use of TIPS to prolong survival until liver transplantation seems promising.
Other surgical shunts. Despite the theoretical benefit of improving portal hypertension and thus
HRS by means of a portosystemic shunt, only a few scattered case reports have shown any
benefit. Currently, particularly with the recent introduction of TIPS, portocaval shunts are not
indicated in this setting. Renal replacement therapy. Many clinicians are reluctant to institute
renal replacement therapy in advanced cirrhosis, because the outcome is poor unless liver
transplantation is a realistic option. Intermittent haemodialysis can be a problem because
patients with HRS are prone to develop circulatory and coagulation problems, and
biocompatibility is also a problematic issue. In an early study in the United Kingdom 100%
mortality was observed in cirrhotic patients with HRS despite early institution of renal support.
However, modern renal replacement therapies such as continuous endogenous haemofiltration
(CVVH) are certainly capable of prolonging life in patients with type 1 HRS who have not
responded to medical therapies or TIPS. Because the underlying hepatic problem persists, the
long-term prognosis is grim and treatment should be confined to patients who are candidates
for liver transplantation or have a realistic chance of hepatic recovery. The molecular adsorbent
recirculating system (MARS) is a modified dialysis method that uses albumin-containing
dialysate in a closed-loop secondary circuit for adsorptive removal of albumin-bound toxins. In
a randomised study, short-term survival of eight HRS patients treated with MARS was superior
to that of five other HRS patients treated with CVVH. In contrast to previous reports on
haemodialysis, treatment was well tolerated. Unfortunately, the study was terminated after
enrolment of only 13 patients, which makes evaluation of any influence on mortality
difficult.Moreover, the control group seems to have received a smaller dialytic dose: creatinine
levels were decreased in the MARS group only.Nonetheless, the favourable effects of this
system deserve evaluation in a prospective study of adequate power. Liver transplantation.
Liver transplantation is the ideal treatment for HRS, but is completely dependent on the
availability of Donors. Patients with HRS have a higher risk of postoperative morbidity, early
mortality and longer hospitalisation than other transplant recipients.Gonwa et al. reported that
at least one third of such patients require haemodialysis postoperatively, with a smaller
proportion (5%) requiring long-term dialysis. Because renal dysfunction is common in the first
few days after transplantation, avoidance nephrotoxic immunosuppressants is generally
recommended until renal function is recovered. However, the GFR gradually improves to an
average of 4050 ml/min by the 6th postoperative week. The systemic and neurohumoral
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abnormalities associated with HRS also resolve in the 1st postoperative month. Long-term
survival rates are excellent, with the survival rate at 3 years approaching approximately 60%.
This is only slightly lower than the 7080% survival rate of transplant recipients without HRS
and is markedly better than the survival rate of patients with HRS who do not receive
transplants, which is virtually nil at 3 years.
HANDWASHING
Handwashing is mandatory (and often overlooked) before the insertion of vascular devices.
Scrubbing with antimicrobial cleansing solutions does not reduce the incidence of catheter-
related sepsis, so a simple soap-and-water scrub is sufficient.
UNIVERSAL PRECAUTIONS
In 1985, the Centers for Disease Control introduced a strategy for blood and body fluid
precautions known as universal precautions. This strategy is based on the assumption that all
patients are potential sources of human immunodeficiency virus (HIV) and other blood-borne
pathogens (e.g., hepatitis viruses) until proven otherwise. The following recommendations
apply to the insertion of vascular catheters.
Use sterile gloves for all cannulations except those involving the introduction of a short
catheter into a peripheral vein.
Caps, gowns, masks, and protective eyewear are not necessary unless splashes of blood are
anticipated (e.g., in a trauma victim). These measures do not reduce the incidence of catheter-
related sepsis.
Avoid needlestick injuries. Do not recap needles or manually remove needles from syringes.
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If a needlestick injury is sustained during the procedure, follow the recommendations in Table
4.1.
Needlestick injuries are reported in up to 80% of medical students and interns. Therefore, in
patients who are known risks for transmitting HIV or viral hepatitis, vascular cannulation
should be performed only by an experienced senior-level resident or fellow.
LATEX ALLERGY
The increased use of rubber gloves (made of latex or vinyl) as protection against HIV infections
has resulted in an increased recognition of allergic reactions to latex. These reactions can be
manifest as a contact dermatitis (urticarial lesions of the hands and face), or as a conjunctivitis,
rhinitis, or asthma. The latter three manifestations are reactions to airborne latex particles, and
they do not require direct physical contact with gloves. They often appear when the affected
individual enters an area where latex gloves are being used. Therefore, a latex allergy should be
suspected in any ICU team member who develops atopic symptoms when in the ICU. When
this occurs, a switch to vinyl gloves will eliminate the problem. Latex allergy can be manifest
as anaphylaxis , so the transition to vinyl gloves for suspected latex allergy should not be
delayed.
Agents that reduce skin microflora are called antiseptics, whereas agents that reduce the
microflora on inanimate objects are called disinfectants. Common antiseptic agents are listed in
Table 4.2 (11,12). The most widely used antiseptic agents are alcohol and iodine, both of which
have a broad spectrum of antimicrobial activity. Alcohol (commonly used as a 70% solution)
may not work well on dirty skin (that is, it does not have a detergent action), so it is often used
in combination with another antiseptic agent. The most popular antiseptic solution currently in
use is a povidone-iodine preparation (e.g., Betadine), also known as an iodophor, a water-
soluble complex of iodine and a carrier molecule. The iodine is released slowly from the carrier
molecule, and this reduces the irritating effects of iodine on the skin. This preparation should
be left in contact with the skin for at least 2 minutes to allow sufficient time for iodine to be
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HAIR REMOVAL
Shaving is not recommended for hair removal because it abrades the skin and promotes
bacterial colonization. If hair removal is necessary, the hair can be clipped or a depilatory can
be applied.
Vascular cannulation can be performed by advancing the catheter over a needle or guidewire
that is in contact with the lumen of a blood vessel.
CATHETER-OVER-NEEDLE
A catheter-over-needle device is shown in Figure 4.1. The catheter fits snugly over the insertion
needle, and has a tapered end to minimize damage to the catheter tip and soft tissues during
insertion. This device can be held like a pencil (i.e., between the thumb and forefinger) as it is
inserted through the skin and directed to the target vessel. When the tip of the needle enters the
lumen of a patent blood vessel, blood moves up the needle by capillary action and enters the
flashback chamber. When this occurs, the catheter is threaded over the needle and into the
lumen of the blood vessel as the needle is withdrawn.
CATHETER-OVER-GUIDEWIRE
Guidewire-assisted vascular cannulation was introduced in the early 1950s and is often called
the Seldinger technique, after its inventor. This technique is illustrated in Figure 4.2. A
small-bore needle (usually 20 gauge) is used to probe for the target vessel. When the tip of the
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needle enters the vessel, a thin wire with a flexible tip (called a J-tip because of its shape) is
passed through the needle and into the vessel lumen. The needle is then removed, leaving the
wire in place to serve as a guide for cannulation of the vessel. When cannulating deep vessels, a
rigid dilator catheter is first threaded over the guidewire and removed; this creates a tract that
facilitates insertion of the vascular catheter.
The guidewire technique has the presumed advantage of minimizing damage to soft tissues and
blood vessels by using a small-bore probe needle. However, the use of a rigid dilator catheter
(as explained above) seems to nullify this advantage. Nevertheless, the guidewire technique is
currently the preferred method for central venous and arterial cannulation.
THE CATHETERS
Vascular catheters are composed of plastic polymers impregnated with barium or tungsten salts
to enhance radiopacity. Catheters intended for short-term cannulation (days) are usually made
of polyurethane; catheters used for long-term venous access (weeks to months) are composed
of a more flexible and less thrombogenic derivative of silicone. The silicone catheters (e.g.,
Hickman and Broviac catheters) are too flexible for routine percutaneous insertion, and are not
appropriate for use in the ICU.
HEPARIN BONDING
Some vascular catheters are impregnated or coated with heparin to reduce thrombogenicity.
However, this measure has not proven effective in reducing the incidence of catheter-associated
thrombosis. Because heparin-coated catheters can be a source of heparin-induced
thrombocytopenia, catheters used in the ICU should not be impregnated or coated with heparin.
CATHETER SIZE
The size of vascular catheters is commonly expressed in terms of the outside diameter, and the
units of measurement are shown in Table 4.3. The French size is a metric derivative equivalent
to the outside diameter in millimeters multiplied by 3; that is, French size = outside diameter
(in mm) 3. The gauge system was developed for wires and needles, and has been adopted for
catheters. There is no simple mathematical relationship between gauge size and other units of
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measurement, and a table of reference values such as Table 4.3 is needed to make the
appropriate conversions. Gauge sizes usually range from 14 (largest diameter) to 27 (smallest
diameter).
The steady or laminar flow through a rigid tube is influenced most by the radius of the tube
(see the Hagen-Poisseuille equation in the section on peripheral blood flow in Chapter 1). The
influence of tube diameter on flow rate is demonstrated in Table 4.3 for gravity flow of one unit
of packed red blood cells diluted with 250 mL normal saline flowing through catheters of equal
length. Note that a little more than a doubling of tube diameter (from 0.7 mm to 1.65 mm) is
associated with almost a quadrupling of flow rate (from 24.7 to 96.3 mL/minute). Thus,
catheter size (diameter) is an important consideration if rapid flow rates are desired.
MULTILUMEN CATHETERS
Multilumen catheters were introduced for clinical use in the early 1980s, and are now used
routinely for central venous cannulation. The design of a triple-lumen catheter is shown in
Figure 4.3. These catheters have an outside diameter of 2.3 mm (6.9 French) and may have
three channels of equal diameter (usually 18 gauge) or may have one larger channel (16 gauge)
and two smaller channels of equal diameter (18 gauge). The distal opening of each channel is
separated from the other by at least 1 cm to help minimize mixing of infusate solutions.
Multilumen catheters have proven to be valuable aids because they minimize the number of
venipunctures needed for monitoring and infusion therapy, yet they do not increase the risk of
thrombosis or infection when compared with single-lumen catheters.
INTRODUCER CATHETERS
Another valuable addition to the family of vascular catheters is the introducer catheter, shown
in Figure 4.3. These large-bore catheters (8 to 9 French) can be used as conduits for insertion
and removal of smaller vascular catheters (including multilumen catheters and pulmonary artery
catheters) through a single venipuncture. The side-arm infusion port on the catheter provides an
additional infusion line, and allows a continuous flush to prevent thrombus formation around
smaller catheters that sit in the lumen of the introducer catheter. This side-arm infusion port
also allows the introducer catheter to be used as a stand-alone infusion device (a rubber
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membrane on the hub of the catheter provides an effective seal when fluids are infusing through
the side-arm port of the catheter). The large diameter of introducer catheters makes them
particularly valuable as infusion devices when rapid infusion rates are necessary (e.g., in the
resuscitation of massive hemorrhage).
ACCESS ROUTES
The following is a brief description of common vascular access routes in the arm (antecubital
veins and radial artery), the thoracic inlet (subclavian and jugular veins), and the groin (femoral
artery and vein).
ANTECUBITAL VEINS
The veins in the antecubital fossa provide rapid and safe vascular access for acute resuscitative
therapy. Although long catheters can be inserted into the antecubital veins and advanced into
the superior vena cava, such peripherally inserted central venous catheters (PICC devices) are
more appropriate for home infusion therapy than for treating critically ill patients. Short
catheters (5 to 7 cm) are preferred for acute resuscitation via the antecubital veins because they
are more easily inserted and allow more rapid infusion rates than the longer PICC catheters.
Anatomy
The surface anatomy of the antecubital veins is shown in Figure 4.4. The basilic vein runs
along the medial aspect of the antecubital fossa, and the cephalic vein is situated on the
opposite side. The basilic vein is preferred for cannulation because it runs a straighter and less
variable course up the arm than the cephalic vein.
Insertion Technique
The patient need not be supine, but the arm should be straight and abducted. The antecubital
veins can be distended by tourniquet or by inflating a blood pressure cuff to just above the
diastolic pressure (this allows arterial inflow while impeding venous outflow). Once the veins
are visible or palpable, a catheter-over-needle device is used to insert a short 16- or 18-gauge
catheter into the basilic or cephalic vein.
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Blind Insertion
If the antecubital veins are neither visible nor palpable, palpate the brachial artery pulse at a
point 1 inch above the antecubital crease. The basilic vein (or brachial vein) should lie just
medial to the palpated pulse at this point, and can be entered by inserting the catheter-
over-needle device through the skin at a 35 to 45 angle and advancing the needle until blood
return is noted. This approach has a reported success rate of 80%. Injury to the median nerve
(which is also medial to the artery, but deep to the veins) can occur with excessive movement of
the probe needle.
Comment
Remember that the shorter the catheter, the more rapid the flow rate through the catheter (see
Chapter 1). Thus, insertion of short catheters into the antecubital veins permits more rapid
volume resuscitation than insertion of the longer central venous catheters.
RADIAL ARTERY
The radial artery is a favored site for arterial cannulation because the vessel is superficial and
accessible and the insertion site is easy to keep clean. The major disadvantage of the radial
artery is its small size, which limits the success rate of cannulation and promotes vascular
occlusion.
Anatomy
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The surface anatomy of the radial and ulnar arteries is shown in Figure 4.4. The radial artery is
usually palpable at a point just medial to the styloid process of the radius. The ulnar artery is
on the opposite (medial) side of the wrist, just lateral to the pisiform bone. Although the radial
artery is preferred, the ulnar artery is the larger of the two arteries and should be easier to
cannulate.
The Allen test evaluates the capacity of the ulnar artery to supply blood to the digits when the
radial artery is occluded. The test is performed by first occluding the radial and ulnar arteries
with the thumb and index finger. The patient is then instructed to raise the wrist above the head
and to make a fist repeatedly until the fingers turn white. The ulnar artery is then released, and
the time required for return of the normal color to the fingers is recorded. A normal response
time is 7 seconds or less, and a delay of 14 seconds or greater is evidence of insufficient flow
in the ulnar artery.
Although a positive Allen test (i.e., 14 seconds or longer for return of color to the digits) is
often stated as a contraindication to radial artery cannulation, in numerous instances the Allen
test has indicated inadequate flow in the ulnar artery, yet subsequent radial artery cannulation
has been uneventful (2,21). Thus, a positive Allen test is not a contraindication to radial artery
cannulation. Another limitation is the need for patient cooperation to perform the test.
Therefore, this test is not worth the time it takes.
Insertion Technique
The wrist should be hyperextended to bring the artery closer to the surface. A short 20-gauge
catheter is appropriate, and can be inserted by a catheter-over-needle device or by the guidewire
technique. When using a catheter-over-needle device, the following through-and-through
technique is recommended: When the needle tip first punctures the artery (and blood appears
in the flashback chamber), the tip of the catheter is just outside the vessel. To position the
catheter tip in the lumen of the vessel, the needle is passed completely through the artery and
then withdrawn until blood returns again through the needle. At this point, the catheter tip
should be in the lumen of the artery, and the catheter can be advanced while the needle is
retracted. If two attempts at cannulation are unsuccessful, switch to an alternative site (to
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Comment
Arterial occlusion occurs in as many as 25% of radial artery cannulations, but digital ischemia
is rare (2,22). Despite being well tolerated in most patients, cannulation of the radial artery (or
any artery) should be reserved for monitoring blood pressure, and is not to be used as a
convenience measure for monitoring blood gases or other blood components.
More than 3 million central venous cannulations are performed yearly in the United States ,
and a majority of these procedures are performed via the subclavian vein. The subclavian vein is
well suited for cannulation because it is a large vessel (about 20 mm in diameter) and is
prevented from collapsing by its surrounding structures. The immediate risks of subclavian vein
cannulation include pneumothorax (1% to 2%) and hemothorax ( less than 1%). The incidence
of bleeding is no different in the presence or absence of a coagulopathy ; that is, the presence
of a coagulation disorder is not a contraindication to subclavian vein cannulation.
Anatomy
The subclavian vein is a continuation of the axillary vein as it passes over the first rib, and the
apical pleura lies about 5 mm deep to the vein at its point of origin. As shown in Figure 4.5,
the subclavian vein runs most of its course along the underside of the clavicle. The vein runs
along the outer surface of the anterior scalene muscle, which separates the vein from its
companion artery on the underbelly of the muscle. At the thoracic inlet, the subclavian vein
meets the internal jugular vein to form the brachiocephalic vein. The convergence of the right
and left brachiocephalic veins forms the superior vena cava.
Anatomic Distances
The lengths of the vascular segments involved in subclavian (and internal jugular) vein
cannulation are shown in Table 4.4. The average distance from venipuncture site to the right
atrium is 14.5 cm and 18.5 cm for right-sided and left-sided cannulations, respectively. These
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distances are far shorter than catheter lengths recommended for right-sided (20 cm) and
left-sided (30 cm) central venous cannulations, and are more consistent with a recent report
showing that the average distance to the right atrium is 16.5 cm in central venous cannulation
from either side in adults. Therefore, to avoid placing catheter tips in the right atrium (which
can lead to cardiac perforation and fatal cardiac tamponade), all central venous catheters should
be no longer than 15 or 16 cm in length.
INSERTION TECHNIQUE
The patient is placed supine, with arms at the sides and head faced away from the insertion site.
A towel roll can be placed between the shoulder blades, but this is uncomfortable and
unnecessary. Identify the clavicular insertion of the sternocleidomastoid muscle. The
subclavian vein lies just underneath the clavicle where the muscle inserts onto the clavicle. The
vein can be entered from either side of the clavicle.
Infraclavicular Approach (Insertion Site 1 in Figure 4.5). Identify the lateral margin of the
sternocleidomastoid muscle as it inserts on the clavicle. The catheter is inserted in line with
this margin, but below the clavicle. Insert the probing needle (18 or 20 gauge) with the bevel
pointing upward (toward the ceiling) and advance the needle along the underside of the clavicle
and toward the suprasternal notch. The path of the needle should be parallel to the patient's
back. When the vein is entered, turn the bevel of the needle to 3 o'clock so the guidewire
threads in the direction of the superior vena cava.
Supraclavicular Approach (Insertion Site 2 in Figure 4.5). Identify the angle formed by the
lateral margin of the sternocleidomastoid muscle and the clavicle. The probe needle is inserted
so that it bisects this angle. Keep the bevel of the needle facing upward and direct the needle
under the clavicle in the direction of the opposite nipple. The vein should be entered at a
distance of 1 to 2 cm from the skin surface (the subclavian vein is more superficial in the
supraclavicular approach). When the vein is entered, turn the bevel of the needle to 9 o'clock so
the guidewire threads in the direction of the superior vena cava.
Comment
Patient comfort and ease of insertion are the most compelling reasons to select the subclavian
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vein for central venous access. Selection of the infraclavicular versus supraclavicular approach
is largely a matter of personal preference. Some recommend avoiding the subclavian vein in
ventilator-dependent patients because of the risk of pneumothorax. However, the risk of
pneumothorax is too small to justify abandoning the subclavian vein in patients with
respiratory failure.
Cannulation of the internal jugular vein reduces (but does not eliminate) the risk of
pneumothorax, but introduces new risks (e.g., carotid artery puncture and thoracic duct injury).
Anatomy
The internal jugular vein is located under the sternocleidomastoid muscle in the neck and, as
shown in Figure 4.5, the vein follows an oblique course as it runs down the neck. When the
head is turned to the opposite side, the vein forms a straight line from the pinna of the ear to
the sternoclavicular joint. Near the base of the neck, the internal jugular vein becomes the most
lateral structure in the carotid sheath (which contains the carotid artery sandwiched between
the vein laterally and the vagus nerve medially).
Insertion Technique
The right side is preferred because the vessels run a straighter course to the right atrium. The
patient is placed in a supine or Trendelenburg position, with the head turned to the opposite
side. The internal jugular vein can be entered from an anterior or posterior approach.
The Anterior Approach (Insertion Site 4 in Figure 4.5). The anterior approach is through a
triangular region created by two heads of the sternocleidomastoid muscle. The carotid artery is
palpated in the triangle and retracted medially. The probe needle is inserted at the apex of the
triangle with the bevel facing up, and the needle is advanced toward the ipsilateral nipple, at a
45 angle with the skin surface. If the vein is not encountered by a depth of 5 cm, the needle is
withdrawn 4 cm and advanced again in a more lateral direction. When a vessel is entered, look
for pulsations. If the blood is red and pulsating, you have entered the carotid artery. In this
situation, remove the needle and tamponade the area for 5 to 10 minutes. When the carotid
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artery has been punctured, no further attempts should be made on either side because puncture
of both arteries can have serious consequences.
The Posterior Approach (Insertion Site 3 in Figure 4.5). The insertion site for this approach is
1 centimeter superior to the point where the external jugular vein crosses over the lateral edge
of the sternocleidomastoid muscle. The probe needle is inserted with the bevel positioned at 3
o'clock. The needle is advanced along the underbelly of the muscle in a direction pointing to
the suprasternal notch. The internal jugular vein should be encountered 5 to 6 cm from the skin
surface with this approach.
Carotid Artery Puncture. If the carotid artery has been punctured with a probing needle, the
needle should be removed and pressure should be applied to the site for at least 5 minutes (10
minutes is recommended for patients with a coagulopathy). No further attempts should be made
to cannulate the internal jugular vein on either side, to avoid puncture of both carotid arteries.
If the carotid artery has been inadvertently cannulated, the catheter should not be removed, as
this could provoke serious hemorrhage. In this situation, a vascular surgeon should be
consulted immediately.
Comment
As with the subclavian vein, cannulation of the internal jugular vein is safe and effective when
performed by skilled operators. However, several disadvantages of internal jugular cannulation
deserve mention. (a) Accidental puncture of the carotid artery is reported in 2 to 10% of
attempted cannulations. (b) Awake patients often complain of the limited neck mobility when
the internal jugular vein is cannulated. (c) In agitated patients, inappropriate neck flexion can
result in thrombotic occlusion of the catheter and vein. (d) In patients with tracheostomies, the
insertion site can be exposed to infected secretions that drain from the tracheal stoma.
Cannulation of the external jugular vein has two advantages: (a) There is no risk of
pneumothorax, and (b) hemorrhage is easily controlled. The major drawback is difficulty
advancing the catheter.
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Anatomy
The external jugular vein runs along a line extending from the angle of the jaw to a point
midway along the clavicle. The vein runs obliquely across the surface of the
sternocleidomastoid muscle and joins the subclavian vein at an acute angle. This acute angle is
the major impediment to advancing catheters that have been inserted into the external jugular
vein.
Insertion Technique
The patient is placed in the supine or Trendelenburg position, with the head turned away from
the insertion site. If necessary, the vein can be occluded just above the clavicle (with the
forefinger of the nondominant hand) to engorge the entry site. As many as 15% of patients so
not have an identifiable external jugular vein, even under optimal conditions of vein
engorgement.
The external jugular vein has little support from surrounding structures, so the vein should be
anchored between the thumb and forefinger when the needle is inserted. The bevel of the
needle should be pointing upward when it enters the vein. The recommended insertion point is
midway between the angle of the jaw and the clavicle (see Fig. 4.5). Use a 16-gauge
single-lumen catheter that is 10 to 15 cm in length. If the catheter does not advance easily, do
not force it, as this may result in vascular perforation at the junction between the external
jugular and subclavian veins.
Comment
This approach is best reserved for temporary access in patients with a severe coagulopathy,
particularly when the operator is inexperienced and does not feel comfortable cannulating the
subclavian or internal jugular veins. Contrary to popular belief, cannulation of the external
jugular is not always easier to accomplish than central venous cannulation because of the
difficulty in advancing catheters past the acute angle at the junction of the subclavian vein.
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The femoral vein is the easiest of the large veins to cannulate and also does not carry a risk of
pneumothorax. The disadvantages associated with this route are venous thrombosis (10%),
femoral artery puncture (5%), and limited ability to flex the hip (which can be bothersome for
awake patients). Contrary to popular belief, the infection rate with femoral vein catheters is no
different from that of subclavian or internal jugular vein catheters.
Anatomy
The anatomy of the femoral sheath is shown in Figure 4.6. The femoral vein is the most medial
structure in the femoral sheath and is situated just medial to the femoral artery. At the inguinal
ligament, the femoral vessels are just a few centimeters below the skin surface.
Insertion Technique
Palpate the femoral artery just below the inguinal crease and insert the needle (bevel up) 1 to 2
cm medial to the palpated pulse. Advance the needle at a 45 angle to the skin surface, entering
the vein at a depth of 2 to 4 cm. Once in the vessel, if the catheter or guidewire will not pass
beyond the tip of the needle, tilt the needle so that it is more parallel to the skin surface (this
may move the needle tip away from the far side of the vessel wall and into more direct contact
with the lumen of the vessel). Femoral vein catheters should be at least 15 cm long.
Blind Insertion
If the femoral artery pulse is not palpable, draw an imaginary line from the anterior superior
iliac crest to the pubic tubercle, and divide the line into three equal segments. The femoral
artery lies at the junction between the middle and most medial segment, and the femoral vein is
1 to 2 cm medial to this point. This method of locating the femoral vein has a reported success
rate of over 90%.
Comment
Femoral vein cannulation is usually reserved for patients who are paralyzed or comatose and
immobile. This approach is not recommended for cardiopulmonary resuscitation (because of
the delayed transit times for bolus drug injections) or in patients with bleeding disorders.
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Cannulation of the femoral artery is usually reserved for situations where radial artery
cannulation is unsuccessful or contraindicated. Despite its reserve status, the femoral artery is
larger than the radial artery, and is easier to cannulate. The complications of femoral artery
cannulation are the same as for radial artery cannulation (thrombosis, bleeding, and infection).
The incidence of infection is the same with radial and femoral artery catheters, and the
incidence of thrombosis is lower with femoral artery cannulation. Thrombosis of the femoral
artery, like that in the radial artery, only rarely results in troublesome ischemia in the distal
extremity.
Localization and cannulation of the femoral artery proceeds as described in the section on
femoral vein cannulation. The Seldinger technique is preferred for catheter insertion, and
catheters should be 18 gauge in diameter and 15 to 20 cm long.
Comment
Femoral artery cannulation is a viable alternative and may be preferable to radial artery
cannulation in patients who are paralyzed or otherwise immobile, unless they have a significant
coagulopathy (in which case the radial artery is preferred). The incidence of thrombotic
complications is lower in femoral artery cannulations, and the pressure in the femoral artery
more closely approximates the pressure in the aorta than does the pressure in the radial artery
(see Chapter 8).
IMMEDIATE CONCERNS
Inadvertent air entry is one of the most feared complications of central venous cannulation. The
importance of maintaining a closed system during insertion is highlighted by the following
statement:
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Preventive Measures
Prevention is the hallmark of reducing the morbidity and mortality of venous air embolism. The
most effective method of preventing air entry is to keep the venous pressure more positive than
atmospheric pressure. This is facilitated by placing the patient in the Trendelenburg position
with the head 15 below the horizontal plane. Remember that the Trendelenburg position does
not prevent venous air entry because patients still generate negative intrathoracic pressures
while in the Trendelenburg position. When changing connections in a central venous line, a
temporary positive pressure can be created by having the patient hum audibly. This not only
produces a positive intrathoracic pressure, but allows clinicians to hear when the intrathoracic
pressure is positive. In ventilator-dependent patients, the nurse or respiratory therapist should
initiate a mechanical lung inflation when changing connections.
Clinical Presentation
The usual presentation is acute onset of dyspnea that occurs during the procedure. Hypotension
and cardiac arrest can develop rapidly. Air can pass across a patent foramen ovale and obstruct
the cerebral circulation, producing an acute ischemic stroke. A characteristic "mill wheel"
murmur can be heard over the right heart, but this murmur may be fleeting.
Therapeutic Maneuvers
If a venous air embolism is suspected, immediately place the patient with the left side down,
and attempt to aspirate air directly from the venous line. In dire circumstances, a needle should
be inserted through the chest wall and into the right ventricle to aspirate the air. Unfortunately,
the mortality in severe cases of venous air embolism remains high despite these maneuvers.
PNEUMOTHORAX
Pneumothorax is a concern primarily with subclavian vein cannulation but can also complicate
jugular vein cannulation (2,30). This is one reason that postinsertion chest films are
recommended after all central venous cannulations (or attempts). If possible, postinsertion
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films should be obtained in the upright position and during expiration. Expiratory films
facilitate the detection of small pneumothoraxes because expiration decreases the volume of air
in the lungs, but not the volume of air in the pleural space. Thus, during expiration, the volume
of air in the pleural space is a larger fraction of the total volume of the hemithorax, thereby
magnifying the radiographic appearance of the pneumothorax.
Upright films are not always possible in ICU patients. When supine films are necessary,
remember that pleural air does not often collect at the apex of the lung when the patient is in
the supine position (32,33). In this situation, pleural air tends to collect in the subpulmonic
recess and along the anteromedial border of the mediastinum (see Chapter 28).
Delayed Pneumothorax
Pneumothoraxes may not be radiographically evident until 24 to 48 hours after central venous
cannulation (31,33). Therefore, the absence of a pneumothorax on an immediate postinsertion
chest film does not absolutely exclude the possibility of a catheter-induced pneumothorax.
This is an important consideration in patients who develop dyspnea or other signs of
pneumothorax in the first few days after central venous cannulation. In the absence of signs
and symptoms, there is little justification for serial chest films following central venous
catheter placement.
The properly placed central venous catheter should run parallel to the superior vena cava, and
the tip of the catheter should be positioned above the junction of the superior vena cava and
right atrium. The following conditions warrant corrective measures.
Catheters inserted from the left side must make an acute turn downward when they reach the
superior vena cava. If they fail to make this turn, the catheters can end up in a position like the
one shown in Figure 4.7. The tip of the catheter is up against the lateral wall of the vena cava,
and in this position, the catheter tip can stab the vessel wall and perforate the vena cava.
Therefore, catheters that abut the wall of the vena cava should be repositioned as soon as
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possible. (The problem of vascular perforation is discussed in more detail in Chapter 5.)
The Food and Drug Administration has issued a strong warning about the risk of cardiac
perforation from catheter tips that are advanced into the heart. However, cardiac perforation is a
rare complication of central venous cannulation , even though over half of central venous
catheters may be misplaced in the right atrium. Nevertheless, tamponade is often fatal, so
cardiac placement of catheters should be avoided. A few measures help to minimize the risk of
cardiac perforation. The most effective measure is to use shorter catheters, as recommended
earlier. The tip of indwelling catheters should be above the third right costal cartilage (this is
the level where the vena cava meets the right atrium). If the anterior portion of the third rib
cannot be visualized, keep the catheter tip at or above the tracheal carina.
Cardiopulmonary resuscitation
Many countries have official guidelines on how CPR should be provided, and these naturally
override the general description of CPR in this article.
In 2005, new CPR guidelines were published with input from International Resuscitation
Councils, and was agreed at the 2005 International Consensus Conference on
Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science. The primary goal
was to simplify CPR for lay rescuers and healthcare providers alike to maximise the potential
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for early resuscitation. The important changes for 2005 are as follow.
A universal compression-ventilation ratio (30:2) is recommended for all single rescuers of
infant (less than one year old), child (1 year old to puberty), and adult (puberty and above)
victims (excluding newborns). The only difference between the age groups is that with adults
the rescuer uses two hands for the chest compressions, while with children it is only one, and
with infants only two fingers (pointer and middle fingers). It is worth noting that paediatric
guidelines for healthcare professionals differ from the 30:2 compression-ventilation ratio stated
here.
Lay rescuers do not need to assess for pulse or signs of circulation for an unresponsive adult
victim.
Lay rescuers do not need to provide rescue breathing without chest compressions for an adult
victim.
As research has shown that lay personnel cannot accurately detect a pulse in about 40% of
cases and cannot accurately discern the absence of pulse in about 10%, the pulse check step
has been removed from the CPR procedure completely for lay persons and de-emphasized for
healthcare professionals.
Cardiac arrest and the place of CPR
The medical term for the condition in which a person's heart has stopped is cardiac arrest (also
referred to as cardiorespiratory arrest). CPR appropriate for cardiac arrest. If the patient still
has a pulse, but is not breathing, this is called respiratory arrest and rescue breathing is more
appropriate.
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However, since people often can't tell the difference (can't accurately feel a pulse to determine
whether the heart is still beating), CPR is often recommended for both.
The most common cause of cardiac arrest outside of a hospital is ventricular fibrillation (VF), a
potentially fatal arrhythmia that is usually (but not always) caused by a heart attack. Other
causes of cardiac arrest include drowning, drug overdose, poisoning, electrocution.
Sudden cardiac arrest is a leading cause of death, approximately 250,000 per annum outside a
hospital setting in the USA. CPR can double or triple the victim's chances of survival when
commenced immediately. According to American Heart Association, only two thirds of victims
of a witnessed cardiac arrest are administered CPR. Rapid access to defibrillation is also vital.
Blood circulation and lung ventilation are absolute requirements in transporting oxygen to the
tissues. The brain may sustain damage after four minutes and irreversible damage after about
seven minutes The heart also rapidly loses the ability to maintain a normal rhythm. Low body
temperatures as seen in drownings prolong the time the brain survives. Following cardiac
arrest, effective CPR enables enough oxygen to reach the brain to delay brain death, and allows
the heart to remain responsive to defibrillation attempts.
CPR is taught to the general public because they are the only ones present in the crucial few
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minutes before emergency personnel are available. Simple training is the goal of the 2005
guidelines to maximise the prospect that CPR will be performed successfully.
Effectiveness
CPR is almost never effective if started more than 15 minutes after collapse because permanent
brain damage has probably already occurred, especially if the person has stopped breathing,
since the brain can only survive for 4-6 minutes without oxygen.[citation needed] A notable
exception is cardiac arrest occurring in conjunction with exposure to very cold temperatures.
Hypothermia seems to protect the victim by slowing down metabolic and physiologic
processes, greatly decreasing the tissues' need for oxygen.[citation needed] There are cases
where CPR, defibrillation, and advanced warming techniques have revived victims after
substantial periods of hypothermia.
Used alone, few patients will make a complete recovery, and those that do survive often
develop serious complications. Estimates vary, but many organizations[citation needed] stress
that CPR does not "bring anyone back," it simply preserves the body for defibrillation and
advanced life support. However, in the case of "non-shockable" rhythms such as Pulseless
Electrical Activity (PEA), defibrillation is not indicated, and the importance of CPR rises. On
average, only 5%-10% of people who receive CPR survive. The purpose of CPR is not to
"start" the heart, but rather to circulate oxygenated blood, and keep the brain alive until
advanced care (especially defibrillation) can be initiated. As many of these patients may have a
pulse that is unpalpable by the layperson rescuer, the current consensus is to perform CPR on a
patient that is not breathing. A pulse check is not required in basic CPR since it is so often
missed when present, or even felt when absent, even by health care professionals
Studies have shown the importance of immediate CPR followed by defibrillation within 35
minutes of sudden VF cardiac arrest improve survival. In cities such as Seattle where CPR
training is widespread and defibrillation by EMS personnel follows quickly, the survival rate is
about 30 percent. In cities such as New York City, without those advantages, the survival rate is
only 1-2 percent.
CPR is often severely misportrayed in movies and television as being highly effective in
resuscitating a person who is not breathing and has no circulation. A 1996 study published in
the New England Journal of Medicine showed that CPR success rates in television shows was
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75%.
It is considered by a number of international bodies that in order for CPR to be effective, the
guidelines must be simple and easy to remember.[citation needed]
CPR training
CPR is a practical skill and needs professional instruction followed up by regular practice on a
resuscitation mannequin to gain and maintain full competency. Training is available through
many commercial, volunteer and government organizations worldwide.
CPR training is not confined to the medical professionals. To be effective, CPR must be
applied almost immediately after a patient's heart has stopped. Early CPR on the scene of an
incident is essential to the prevention of brain damage during a cardiac arrest. Blood flow and
air supply to the brain and other major organs is maintained until a defibrillator and
professional medical help arrives. Almost anyone is able to perform CPR with training, and
health organizations advocate the development of CPR skills throughout the general public.
It is best to obtain training in CPR before a medical emergency occurs. One needs hands-on
training by experts to perform CPR safely, and guidelines change, so that training should be
repeated every one or two years. Training in first aid is often available through community
organizations such as the Red Cross and St. John Ambulance. In many countries in
the Commonwealth of Nations, St. John Ambulance and the Medic First Aid Organization
provide CPR training. In Scotland, St. Andrew's Ambulance Association provides first aid
training. In the United States, the American Red Cross, American Heart Association and
American CPR Training also offer CPR training. In addition, many employees at public areas
or community centres are trained in CPR. Lifeguards are also trained in CPR and other first aid
protocols.
In most CPR Classes a simple shortform is used for people to remember everything they need
to do. The most common one used worldwide is DRABCD which stands for Danger, Response,
Airway, Breathing, Compressions and Defibrillation.
History
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CPR has been known in theory, if not practice, for many hundreds or even thousands of years;
some claim it is described in the Bible, discerning a superficial similarity to CPR in a passage
from the Books of Kings (II 4:34), wherein the Hebrew prophet Elisha warms a dead boy's
body and "places his mouth over his". In the 19th century, doctor H. R. Silvester described a
method (The Silvester Method) of artificial respiration in which the patient is laid on their
back, and their arms are raised above their head to aid inhalation and then pressed against their
chest to aid exhalation. The procedure is repeated sixteen times per minute. This type of
artificial respiration is occasionally seen in movies made in the early part of the 20th century.
A second technique, described in the first edition of the Boy Scout Handbook in the United
States in 1911, described a form of artificial respiration where the person was laid on their
front, with their head to the side, and a process of lifting their arms and pressing on their back
was utilized, essentially the Silvester Method with the patient flipped over. This form is seen
well into the 1950s (it is used in an episode of Lassie during the Jeff Miller era), and was often
used, sometimes for comedic effect, in theatrical cartoons of the time. This method would
continue to be shown, for historical purposes, side-by-side with modern CPR in the Boy Scout
Handbook until its ninth edition in 1979.
However it wasn't until the middle of the 20th century that the wider medical community
started to recognise and promote it as a key part of resuscitation following cardiac arrest. Peter
Safar wrote the book ABC of resuscitation in 1957. In the U.S., it was first promoted as a
technique for the public to learn in the 1970s. Early marketing efforts oversold the
effectiveness of CPR in rescuing heart attack and other victims, and this misperception
continues even today, as the success rate for CPR is only 1/20.
Self-CPR
A form of "self-CPR" termed "Cough CPR" may help a person maintain blood flow to the brain
during a heart attack while waiting for medical help to arrive and has been used in a hospital
emergency room in cases where "standard CPR" was contraindicated. While this technique is
not in widespread use, one researcher has recommended that it be taught broadly to the public
However, the American Heart Association (AHA), does not endorse "Cough CPR", which it
terms a misnomer as it is not a recognized form of resuscitation. The AHA does recognize a
limited legitimate use of the coughing technique:
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This coughing technique to maintain blood flow during brief arrhythmias has been useful in the
hospital, particularly during cardiac catheterization. In such cases the patient's ECG is
monitored continuously, and a physician is present.
"Cough CPR" was the subject of a hoax chain e-mail entitled "How to Survive a Heart Attack
When Alone" which wrongly cited "ViaHealth Rochester General Hospital" as the source of the
technique.Rochester General Hospital has denied any connection with the technique.
References
1. http://circ.ahajournals.org/cgi/content/full/112/24_suppl/IV-19
2. http://circ.ahajournals.org/cgi/content/full/112/24_suppl/IV-156
3. http://circ.ahajournals.org/cgi/content/full/112/22_suppl/III-5
1. To check an unconscious victim, place two fingers under his chin and a hand on his
forehead. Tilt his head back to open his airway. Remove any obstructions from his mouth.
2. Listen and feel for victim's breathing. If he is breathing, place him in the recovery position. If
he is not breathing, begin rescue breathing.
3. Check the victim's circulation by feeling for a pulse at the side of his windpipe (carotid
artery). If there is no pulse, begin CPR immediately.
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1. If a victim is unconscious but breathing, bend his near arm up at a right angle to his body.
Hold the back of his far hand to his near cheek. With the near leg straight, pull the far knee
toward you.
2. With the victim on his side, place his uppermost leg at a right angles to his body. His head
will be supported by the hand of the uppermost arm. Tilt his head back so that he will not
choke if he vomits.
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Rescue Breathing
1. To ensure an open airway, first clear the victim's mouth of obstructions, then place one hand
under his chin and one on his forehead, and tilt his head back.
2. Pinching the victim's nose shut, clamp your mouth over his mouth, and blow steadily for
about two seconds until his chest rises. Remove your mouth and let his chest fall, then repeat.
3. Listen for the victim's breathing and check his pulse. If he still has a pulse, give 10 breaths
per minute until help arrives or the victim is breathing by himself. If the pulse has stopped,
combine rescue breathing with chest compressions.
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If a person's heart has stopped, give cardiopulmonary resuscitation (CPR). This consists of
chest compressions to maintain the blood flow to the brain, combined with rescue breathing to
oxygenate the blood. Give chest compressions at a rate of 80 per minute, counting "one-and-
two-and..."
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1. Place the heel of your hand two finger-widths up from the end of the sternum and your other
hand on top of the first. Press down firmly, then release.
2. Check for a pulse. After 15 chest compressions, give the victim two breaths of rescue
breathing. Repeat until the pulse restarts, professional help arrives, or you are too exhausted to
continue.
Control of the airway is the single most important task for emergency resuscitation. If the
patient has inadequate oxygenation or ventilation, inability to protect the airway due to altered
sensorium from illness or drugs, or external forces compromising the airway (i.e., trauma), he
or she may need advanced airway techniques as described in this chapter.
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It is done in supine position. But in very rare cases, where supine position is not possible it can
be done in prone position also.
The rescuer stand (or bend on knee if the victim is on floor) on side (usually right side), lock
one hand over other and provide compression over the lower third of sternum (2 fingers above
xiphoid process).
The force generated during massage should be able to depress sternum by 114-2 inches (approx
73 of chest wall diameter). During massage compression relaxation (chest to recoil) should be
equal.
Patient should lie flat on hard surface.
Physiological Considerations of Cardiac Massage
Heart compressed between sternum and spine results in ejection of blood from heart (cardiac
pump theory) but another convincing theory is thoracic pump theory which states that cardiac
compression raises intrathoracic pressure forcing blood out of chest and dynamic venous
compression preventing backward flow, heart acting only as a passive conduit.
Chest compression can generate a systolic BP of 80-100 mmHg but diastolic only 10-40 mmHg
(which may compromise coronary flow). Effective cardiac output generated by successful
massage is only 30% of normal. So all efforts to restore spontaneous cardiac activity should be
started immediately.
Monitoring of CPR
1. Capnography: It is considered as most reliable and best Indicator to see the
effectiveness of CPR. Successful cardiac massage should be able to produce ETCO2 of at least
20 mmHg and ETCO2 becoming normal (40 mmHg), is the earliest indicator of return of
normal circulation.
2. Palpation of pulses (carotid): It is the most effective clinical monitor to see the
effectiveness of cardiac massage. A successful cardiac massage should be able to generate a
major peripheral pulse especially carotid.
3. Coronary perfusion pressure: Good guide but very difficult to measure.
COMPRESSION (C) TO VENTILATION (V) RATIO
Before advanced airway ( e. by mouth to mouth, bag and mask ventilation), the ratio should be
30:2 (30 compressions followed by 2 breaths)'irrespective of duration of resuscitation
(previously this ratio was 15:2). The reason for change in ratio is to minimize interruption in
chest compression (this is the most important goal of latest recommendations).
After advanced airway ( e. endotracheal tube, LM A or combitube): Compression will be
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Paddle size
For adults: 13 cm.
For children: 8 cm.
For infants :4.5cm.
Latest Recommendations for Energy selection and shock protocol.
1. Contrary to previous recommendation of 3 successive shocks (200,300 & 360 J) now a
days Only Single Shock of 360J by monophasic defibrillators, and 150-200J withbiphasic
[biphasic 150-200J is equivalent to 360 J of monophasic) is given.
2. Immediately after giving shock, give 5 cycles of 30:2 (without advance airway) or 2
minutes of CPR (with advance airway) before checking rhythm [Earlier rhythm was checked
just after giving shock]. The rationale for this recommendation is that it actually takes around 2
minutes for heart to recover completely after ventricular fibrillation so CPR during this 2
minutes is required to maintain coronary and cerebral perfusion.
So the protocol for advance life support maybe in continuation of basic life support (where
BLS is provided by lay rescuers/paramedicals) or fresh management in hospital arrest.
Consider termination of efforts if there is no response after 20 minutes.
MANAGEMENT OF PULSELESS ELECTRIAL ACTIVITY AND ASYSTOLE
PULSELESS ELECTRICAL ACTIVITY (PEA)
Also called as electromechanical dissociation (EMD). It is the condition in which peripheral
pulses are not palpable but heart shows some electrical activity on ECG other than ventricular
tachycardia and ventricular fibrillation.
Causes are
1. Hypovolemia (most common cause).
2. Cardiac tamponade.
3. Tension pneumothorax.
4. Pulmonary embolism.
5. Hypoxia.
6. Hyperkalemia.
7. Hypothermia.
8. Acidosis.
9. Overdosage of digitalis, (5 blockers, calcium channel blockers.
(Conditions 6 to 9 show idioventricular rhythm).
Treatment
Treatment of PEA lies in treating the cause, adrenaline
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Start
CPR with compression rate of 100/min and ventilation with 8-10 breath/min
with advance airway and 30:2 without advance airway
a. whenever possible defibrillation should precede intubation and IV access (should not delay
defibrillation if ventilation is achieved without intubation, like bag & mask)
Assess Rhythm
Shockable (VF, pulseless V tachy)
1. Give one shock (360 J with monophasic & 200 J with biphasic)
Continue CPR for 2 min (or 5 cycles of 30:2 if airway is still not maintained by advance
methods)
Check Rythm
Still shockable rhythm
(Asystole)
Non shockable (Asystole, PEA)
Continue CPR
Adrenaline 1 mg IV and repeat every 3-5 minutes (if IV access not possible than use
intraoss-eous or endotracheal route) Consider vasopressin 40U after 1st or 2nd dose of
adrenaline Atropine 1 mg, repeat every 3-5 minutes (to a max. of 3 doses) Keep on checking
rhythm every 2 min, if non shockable, continue same treatment and if becomes shockable treat
like shockable.
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Still shockable
Recovered
Non shockable
3. Continue CPR
Repeat adrenaline 1 mg or vasopressin 40 U (as an alternative to adrenaline)
1 Shock (360 J - Monophasic, 200 J - Biphasic)
Continue CPR for 2 minutes 1
Continue CPR
Give amiodarone / gnocaine / magnesium sulphate
Shock (with 360 J - monophasic with 200 J biphasic)
Proceed like non shockable
Recovered Shockable
Go back to stage 2 and continue same protocol
Non shockable
Treat like non shockable and pacing as immediate measures to tide over the crisis.
MANAGEMENT OF ASYSTOLE
Asystole is the terminal event of all arrhythmias.
Management
Intubate immediately and start pulmonary ventilation and cardiac massage
Consider possible causes like hyperkalemia, hypokalemia, hypothermia, hypoxia, acidosis,
I Adrenaline 1 mg IV and repeat every 3 minutes Vasopressin 40 Units after 1s' or 2nd dose of
adrenaline Atropine 1 mg IV and repeat every 3 minutes to a total of 0.04 mg/kg
Transcutaneous pacing
No response Consider termination of efforts
PAEDIATRIC CPR (excluding NEWBORN)
Age classification: From CPR point of view.
Neonate: First 4 weeks after birth.
Infants: 4 weeks to I year.
Child: 1-14 years (previously children were considered 1 -8 years) for medical staff but
for lay rescuers children still mean 1-8 years.
Adults: > 14 years for medical staff. > 8 years for lay rescuers.
Differences from Adults
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Ratio of compression to breathing without advance airway: 30:2 for one rescuer and
15:2 for 2 rescuers. (While for adults it is 30:2 irrespective of rescuers).
With Advance airway: 100 compressions per minute (even for infants which was earlier
120/min) with 8-10 breaths/min. and unsynchronized e. no pause for ventilation (similar to
adults) [contrary to previous 5:1 ratio and synchronized].
If pulses are palpable then give breath at a rate of 12-20/min (Adults 10-12/min).
Pulse check:
- Infants: Brachial/Femoral.
- Children: Carotid.
- Adult: Carotid/Femoral.
In emergency cuffed tubes can be used in paediatric age group if inflation pressure is
less than 20 cmH20.
If heart rate is <60/min with signs of poor prfusion (pallor/cyanosis) start compressions.
Cardiac arrest in children is not usually because of ventricular fibrillation and cause is
usually asphyxial (respiratory) so the difference from adults in protocol of basic life support is
that after assessing responsiveness immediately start CPR and give five cycle of30:2 and then
call for Emergency medical system (EMS) while in adults (see algorithm for BLS) first step
after assessing responsiveness is activation of EMS and than start CPR, further protocol for
BLS remains same.
Advance life support protocol for paediatric patient remains same with some differences
like:
1. Energy selection for shock (manual) is 2 J/kg for first shock and 4 J/kg subsequently. If
AED is used it automatically select energy and do attenuation accordingly. Paediatric AED
are only recommended for children < 8yrs (or <25 kg). Children > 8 years (> 25 kg) should be
defibrillated with adult defibrillators.
2. Another important difference from adults in management of asytole is that atropine and
vasopressin are not recommended for paediatric age group.
3. Endotracheal concentration of adrenaline for adults is 1:10,000 but for paediatric 1 :
1000.
NEWBORN CPR
The detailed discussion of newborn CPR is beyond the scope of this book but some of the
notable differences are:
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1. Rate of ventilation (breathing) is 40-60 breaths/ min (if only ventilation is given).
2. The primary measure for successful ventilation is increase in heart rate.
3. Indication of chest compression is HR (Heart rate) < 60/min. inspite of adequate
ventilation with 100% oxygen for 30 seconds.
4. 2 thumbs with encircled chest is preferred method for compression over only 2 thumb
technique.
5. Compression ventilation ratio is 3:1 (90 compression with 30 breaths) and
synchronized.
6. Reassessment to be made every 30 sec. and continue compression till HR > 60/min.
7. Adrenaline indicated if HR < 60 /min.
8. Stop resuscitation if no signs of life after 10 minutes.
Lay Rescuers
1. Pulse check not expected from them therefore they can start compression even if not
able to palpate pulse of an unresponsive victim.
2. Paediatric means 1-8 years (for health care professionals pead. means 1-14 years).
CPR IN PREGNANCY
1. External cardiac massage should be combined with lateral tilt.
2. Sodium bicarbonate administration is advocated early.
3. Early insertion of endotracheal tube (as pregnant patients are very vulnerable for
aspiration) therefore during mask ventilation continously apply cricoid pressure till patient is
intubated.
4. More prone for hypoxia so use high FIO2.
5. Chest compression should be performed harder.
6. Emergency LSCS (cesarean section) should be considered only if:
- Fetus > 25 week.
- Uterine decompression is mandatory for patients life (fetus can be saved only if LSCS is
performed within 5 min. of arrest).
OPEN CHEST MASSAGE
Indications are:
1. Cardiac tamponade.
2. Penetrating blunt trauma.
3. Air embolism.
4. Arrest during intrathoracic procedures.
5. Chest deformities.
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COMPLICATIONS OF CPR
1. Rib fracture.
2. Pneumothorax.
3. Pneumopericardium.
4. Pneumomediastinum.
5. Injury to diaphragm.
6. Gastric injury.
7. Lung injury.
8. Injury to major vessels particularly by fractured rib.
9. Injury to abdominal organs: Liver, spleen and stomach.
OUTCOME OF CPR
Depends on the:
1. Cause.
2. ThetimeofinitiationofCPRand
3. Duration for which CPR is performed.
Survival is better, if basic life support (BLS) is
initiated within 4 minutes of arrest and ALS within 8 minutes.
Fortunately most common cause of cardiac arrest is ventricular fibrillation which if detected in
time can have 50 to 60% success rate. Average survival rate of in hospital arrest is 8 to 21 %.
Survival is better if arrest time (onset of arrest to start of CPR) is less than 6 minutes and CPR
time (time required for successful CPR) is less than 30 minutes.
NEWER TECHNIQUES OF CPR
1. Simultaneous abdominal compression: Limits
caudal movement of diaphragm and limits dissipation of intrathoracic pressure.
2. Vest CPR: Increasing intrathoracic pressure by physically inflating the bladder around
chest.
3. Simultaneous ventilation with every compression.
4. Cardiopulmonary bypass.
5. Cough CPR (applicable to conscious patient having VF): If a patient cough during VF,
increase in intrathoracic pressure can maintain cerebral (perfusion ( e. consciousness) for 90
sec. So ask him to cough every 1-3 sec. till he/she is defibrillated.
6. High frequency (120/min) CPR: Not better than standard CPR.
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INITIAL APPROACH
The initial approach to airway management is simultaneous assessment and management of the
adequacy of airway patency (the A of ABCs) and oxygenation and ventilation (the B of ABCs).
1.The patient's color and respiratory rate must be assessed; marked hypoventilation with or
without cyanosis may be an indication for immediate intubation.
2.The airway should be opened with head tiltchin lift maneuver (jaw thrust should be used if
C-spine injury is suspected). If needed, the patient should be bagged with the bag-valve-mask
device, including an O2 reservoir. For a good seal, the proper size mask should be ensured.
This technique may require an oral or nasal airway or two rescuers to both seal the mask (two
hands) and bag the patient.
3.The patient should be placed on a cardiac monitor, pulse oximetry, and possibly
capnography (end-tidal CO2), while the remaining vitals, pulse, and blood pressure
(temperature is important but can be delayed to assure the ABCs) can be collected.
4.The need for invasive airway management techniques must be determined as described later.
It is essential to not wait for arterial blood gas analyses (ABG) if the initial assessment declares
the need for invasive airway management. If the patient does not require immediate airway or
ventilation control, he or she should be administered oxygen by face mask, as necessary, to
assure an O2 saturation of 95%. Laboratory studies should be collected as needed. Do not
remove a patient from oxygen to draw an ABG unless deemed safe from the initial assessment.
OROTRACHEAL INTUBATION
The most reliable means to ensure a patent airway, prevent aspiration, and provide oxygenation
and ventilation is endotracheal (ET) intubation. Many conscious patients require intubation
(see the section, Rapid Sequence Induction later). Selection of the blade should be
considered in advance, if possible. The curved blade rests in the vallecula above the epiglottis
and indirectly lifts it off the larynx because of traction on the frenulum. The straight blade is
used to lift the epiglottis directly. The curved blade does a better job of clearing the tongue
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from view and may be less traumatic and reflex-stimulating. The straight blade is mechanically
easier to insert in many patients.
1.Adequate ventilation must be ensured while the equipment is prepared. The patient should be
preoxygenated, with or without a bag-valve-mask device, depending on the clinical need. Vital
signs must be monitored and pulse oximetry used throughout the procedure.
2.The blade type and size (usually #3 or #4 curved blade, or #2 or #3 straight blade) should be
selected; the blade light should be tested. The tube size (usually 7.5 to 8.0 in women, 8.0 to 8.5
in men) must be selected and the balloon cuff tested. The end of the tube should be lubricated
with lidocaine jelly or similar lubricant. The use of a flexible stylet should be considered; the
distal end should be bent upward if the patient's anatomy requires it. The tube and tonsillar tip
suction should be placed within easy reach. If there is an assistant, he or she should be asked to
pass the items when needed.
3.The patient should be positioned with the head extended and neck flexed, possibly with a
rolled towel under the occiput. If C-spine injury is suspected, the head or neck should not be
moved. Rapid sequence induction with in-line traction, nasotracheal intubation, or
cricothyrotomy should be considered.
4.The blade should be inserted on the right and slowly advanced in search of the epiglottis. The
patient should be suctioned as necessary. If the curved blade is used, the tip should be slid into
the vallecula and lifted (indirectly lifting the epiglottis); if a straight blade is used, the
epiglottis should be lifted directly in the direction the handle points, that is, 90 to the blade. It
is important to not rock back on the teeth.
5.Once the vocal cords are visualized, it is important to not lose sight of them. The assistant
should be asked to place the tube in the physician's hand. Pass the tube between the cords,
avoiding force. The stylet should be removed, the balloon cuff inflated. Ventilate the patient
with a bag-valve device and check for bilateral breath sounds. Placement should be confirmed
with an end-tidal CO2 detector (not reliable if the patient is in cardiac arrest) or capnography.
Tube length should be checked; the usual distance (marked on the tube) from the corner of the
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6.The tube should be taped in place and a bite block inserted. Correct intubation and tube
placement can be verified with a portable chest x-ray.
NASOTRACHEAL INTUBATION
1.Both nares should be sprayed with a topical vasoconstrictor and anesthetic. Between 4 to
10% cocaine solution is an appropriate single agent, but may cause unwanted systemic
cardiovascular effects. Topical neosynephrine is an effective vasoconstrictor, and tetracaine is a
safe effective topical anesthetic.
2.The tube size must be chosen, usually between 7.0 to 7.5 in women and 7.5 to 8.0 in men.
The balloon cuff of the tube should be checked for leaks. The tube should be lubricated with
lidocaine jelly or similar lubricant.
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3.The largest nares should be used or the right side if the nares are equal. Some operators
recommend dilating the nares with a lubricated nasal airway. The patient may be sitting up or
supine.
4.An assistant can immobilize the patient's neck. The physician should stand to the patient's
side, with one hand on the tube and with the thumb and index finger of the other hand
straddling the larynx. The tube should be advanced slowly, with steady gentle pressure. The
tube should be twisted to help move past obstructions in the nose and nasopharynx. The tube
should be advanced until maximal airflow is heard through the tube; this means the larynx is
now close by.
5.The physician should listen carefully to the rhythm of inspiration and expiration. The tube
should then be gently but swiftly advanced during the beginning of inspiration. Entrance into
the larynx may initiate a cough, and most expired air should exit the tube even though the cuff
is uninflated. If the tube is foggy the cuff should be inflated.
6.If intubation is unsuccessful, the physician should carefully look for a bulge lateral to the
larynx (usually the tip of the tube is in the pyriform fossa on the same side as the nares used).
If found, the tube must be retracted until maximal breath sounds are heard and then intubation
should be reattempted by manually displacing the larynx toward the bulge. If no bulge is seen,
it is possible that the tube has gone posteriorly into the esophagus. In this case, the tube should
be withdrawn until maximal breath sounds are heard. Intubation should again be reattempted
after the patient's head is extended and a Sellick's maneuver performed. Another option is to
use a directional control tip (Endotrol) or fiberoptic laryngoscope. The head should not be
moved if C-spine injury is suspected.
Complications other than local bleeding are rare. Occasionally, marked bleeding will prompt
the need for orotracheal intubation or cricothyrotomy.
CRICOTHYROTOMY
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laryngeal disease due to trauma or infection or recent prolonged intubation and should not be
used in children below the age of 12.
1.Sterile technique should be used. The cricothyroid membrane should be palpated with digital
stabilizion of the larynx (see With a #11 scalpel, a vertical 3 to 4 cm incision should be started
at the superior border of the thyroid cartilage and incised caudally toward the suprasternal
notch.
2.The membrane should be repalpated and a horizontal stab should be made through its inferior
aspect. The blade should be kept temporarily in place.
3.The larynx should be stabilized by inserting the tracheal hook into the cricothyroid space and
retracting upon the inferior edge of the thyroid cartilage (an assistant should hold after the
hook is placed). Leaving the blade tip in the space, a slightly open hemostat should be inserted
straddling the blade and spread open horizontally.
4.The scalpel should be removed and a dilator inserted (LaBorde or Trousseau). The tracheal
hook can then be removed.
5.A Shiley tracheostomy tube should be introduced (or the largest tube that will fit).
Alternatively, a small cuffed endotrachial tube may be used (#6 or the largest tube that will fit).
The balloon should be inflated and the tube secured in place.
6.The physician should check for bilateral breath sounds. Make sure subcutaneous air is not
introduced. Placement can be checked with an end-tidal CO2 detector and chest x-ray.
Complex airway emergencies in select nonfasted patients may require rapid sequence
induction. This technique couples sedation to induce unconsciousness (induction) with
muscular paralysis. Intubation follows laryngoscopy while maintaining cricoid pressure to
prevent aspiration. The principle contraindication is any condition preventing mask ventilation
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or intubation.
1.The cardiac monitor, oximetry, and capnography should be set up, if available. Equipment
should be checked.
3.Lidocaine (1.5 mg/kg intravenously) should be considered in a head trauma patient to prevent
increased intracranial pressure. Atropine (0.4 mg/kg intravenously) should be considered to
prevent reflex bradycardia, but is not essential.
4.Medication for sedation or analgesia should be considered, if such agents are not being used
for induction.
5.A defasciculating dose of a nondepolarizing agent (i.e., vecuronium at 0.02 mg/kg) is used if
succinylcholine is given for paralysis.
7.In a patient needing analgesia in addition to sedation, opiates should be considered for
induction. These agents are reversible with naloxone. Fentanyl, 2 to 10 g/kg, is commonly
used.
8.Cricoid pressure should be applied before paralysis and maintained until intubation is
accomplished.
9.Succinylcholine (1.0 mg/kg) is chosen for paralysis in many cases because of its rapid onset
and short duration of action; it should not be used in a patient with preexisting paralysis or > 2
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h after severe burns, as hyperkalemia may occur. A nondepolarizing agent such as vecuronium
(0.2 mg/kg) may be chosen for a patient with increased intracranial pressure, one in status
asthmaticus, or at operator discretion.
11.The physician should be prepared to bag the patient if intubation proves unsuccessful.
Invasive airway techniques should be considered as indicated.
Alternative drugs for rapid sequence induction are listed in Chap. 15 of Emergency Medicine,
A Comprehensive Study Guide, 5th ed. Airway management alternatives to the methods
described earlier include retrograde tracheal intubation, translaryngeal ventilation, digital
intubation, transillumination, fiberoptic assistance, and formal tracheostomy. Translaryngeal
ventilation may be used to temporarily provide ventilation until a more definitive procedure is
possible. When oral intubation is indicated but has been unsuccessful, and the patient can be
temporarily ventilated with a bag-valve-mask unit, the following assist methods are warranted.
Retrograde tracheal intubation, digital intubation, transillumination, or fiberoptic assistance
may be helpful. Formal tracheostomy is reserved for those experienced in the technique when
less-invasive or more-rapid methods (cricothyrotomy) are unsuccessful.
2 Dysrhythmia Management
If sustained junctional escape rhythms are producing symptoms, the underlying cause should
be treated. Atropine can be used to accelerate temporarily the sinus node discharge rate and
enhance AV nodal conduction.
VENTRICULAR DYSRHYTHMIAS
Differentiation between ectopic beats of ventricular origin and those of supraventricular origin
that are conducted aberrantly, can be difficult, especially in sustained tachycardias with wide
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QRS complexes (WCT). In general, the majority of patients with WCT have ventricular
tachycardia, which should be approached as ventricular tachycardia, until proved otherwise.
Several guidelines follow:
1.A preceding ectopic P wave is good evidence favoring aberrancy, although coincidental atrial
and ventricular ectopic beats or retrograde conduction can occur. During a sustained run of
tachycardia, AV dissociation favors a ventricular origin of the dysrhythmia.
2.Postectopic pause: A fully compensatory pause is more likely after a ventricular beat, but
exceptions occur.
3.Fusion beats are good evidence for ventricular origin but, again, exceptions occur.
5.Coupling intervals are usually constant with ventricular ectopic beats, unless parasystole is
present. Varying coupling intervals suggest aberrancy.
6.Response to carotid sinus massage or other vagal maneuvers will slow conduction through
the AV node and may abolish reentrant SVT and slow the ventricular response in other
supraventricular tachydysrhythmias. These maneuvers have essentially no effect on ventricular
dysrhythmias.
7.A QRS duration of longer than 0.14 s is usually found in ventricular ectopy or tachycardia.
8.Historical criteria also have been found to be useful: a patient over 35 years old or a history
of MI, CHF, or coronary artery bypass graft strongly suggest ventricular tachycardia in patients
with WCT.
1.As with ventricular tachycardia lidocaine 1 to 1.5 mg/kg intravenously should be started and
may be repeated up to 3 mg/kg.
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Clinical Features
Premature ventricular contractions (PVCs) are due to impulses originating from single or
multiple areas in the ventricles. The ECG characteristics of PVCs are (a) a premature and wide
QRS complex; (b) no preceding P wave; (c) the ST-segment and T wave of the PVC are
directed opposite the major QRS deflection; (d) most PVCs do not affect the sinus node, so
there is usually a fully compensatory postectopic pause, or the PVC may be interpolated
between 2 sinus beats; (e) many PVCs have a fixed coupling interval (within 0.04 s) from the
preceding sinus beat; and (f) many PVCs are conducted into the atria, producing a retrograde P
wave.
PVCs are common, occur in most patients with ischemic heart disease, and are universally
found in patients with acute MI. Other common causes of PVCs include digoxin toxicity, CHF,
hypokalemia, alkalosis, hypoxia, and sympathomimetic drugs.
1.Most acute patients with PVCs will respond to intravenous lidocaine (1 mg/kg
intravenously), although some patients may require procainamide. Although single studies have
suggested benefit, pooled data and meta-analysis find no reduction in mortality from either
suppressive or prophylactic treatment of PVCs.
Clinical Features
The ECG characteristics of accelerated idioventricular rhythm (AIVR) are (a) wide and regular
QRS complexes; (b) rate between 40 and 100, often close to the preceding sinus rate; (c) most
runs of short duration (3 to 30 beats); and (d) an AIVR often beginning with a fusion beat.
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1.Treatment is not necessary. On occasion, AIVR may be the only functioning pacemaker, and
suppression with lidocaine can lead to cardiac asystole.
Ventricular Tachycardia
Clinical Features
Ventricular tachycardia is rare in patients without underlying heart disease. The most common
causes of ventricular tachycardia are ischemic heart disease and acute MI. Ventricular
tachycardia cannot be differentiated from SVT with aberrancy on the basis of clinical
symptoms, blood pressure, or heart rate. Patients who are unstable should be cardioverted,
which is effective for both dysrhythmias. In general, it is best to treat all wide complex
tachycardias as ventricular tachycardia with lidocaine or procainamide. Adenosine appears to
cause little harm in patients with ventricular tachycardia and has potential merit for the
treatment of wide QRS complex tachycardias.
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b.Procainamide can be administered intravenously at less than 30 mg/min until the dysrhythmia
converts, the total dose reaches 15 to 17 mg/kg in normals (12 mg/kg in patients with CHF), or
early signs of toxicity develop, with hypotension or QRS prolongation. The loading dose
should be followed by a maintenance infusion of 2.8 mg/kg/h in normal subjects.
Torsades de Pointes
Atypical ventricular tachycardia (torsade de pointes, or twisting of the points) is where the
QRS axis swings from a positive to negative direction in a single lead (Fig. 2-14).
FIG. 2-14 Two examples of short runs of atypical ventricular tachycardia showing sinusoidal
variation in amplitude and direction of the QRS complexes: Le torsade de pointes (twisting
of the points). Note that the top example is initiated by a late-occurring PVC (lead II).
2.To date, treatment for torsades de pointes consisted of accelerating the heart rate (thereby
shortening ventricular repolarization) with isoproterenol (2 to 8 g/min), while making
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arrangements for a ventricular pacemaker to overdrive the heart at rates of 90 to 120. Temporary
pacing is the most effective and safest method to treat torsades de pointes and prevent its
recurrence.
Ventricular Fibrillation
Clinical Features
Ventricular fibrillation is the totally disorganized depolarization and contraction of small areas
of ventricular myocardiumthere is no effective ventricular pumping activity. The ECG of
ventricular fibrillation shows a fine-to-coarse zigzag pattern without discernible P waves or
QRS complexes (Fig. 2-15). Ventricular fibrillation is never accompanied by a pulse or a
measurable blood pressure.
Ventricular fibrillation is most commonly seen in patients with severe ischemic heart disease,
with or without an acute MI. Primary ventricular fibrillation occurs suddenly, without
preceding hemodynamic deterioration, whereas secondary ventricular fibrillation occurs after a
prolonged period of left ventricular failure or circulatory shock.
2.If the initial 3 attempts at defibrillation are unsuccessful, cardiopulmonary resuscitation and
intubation should be initiated.
4.Defibrillation should be attempted after each drug administration, at 360 J, unless lower
energy levels have been previously successful.
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6.Amiodarone, 150 mg over 10 min followed by 1 mg/min for 6 h, may become a preferred
treatment for
References
http://circ.ahajournals.org/cgi/content/full/112/24_suppl/IV-19
http://circ.ahajournals.org/cgi/content/full/112/24_suppl/IV-156
http://circ.ahajournals.org/cgi/content/full/112/22_suppl/III-5
http://www.cts.usc.edu/lpg-breathingcoughingexercisesafterlungsurgery.html
http://intesivecareunit.blogspot.com/2009/04/hepatorenal-syndrome.html
..
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The word shock is used differently by the medical community and the general public. The
connotation by the public is an intense emotional reaction to a stressful situation or bad news.
The medical definition of shock is much different.
Medically, shock is defined as a condition where the tissues in the body don't receive enough
oxygen and nutrients to allow the cells to function. This ultimately leads to cellular death,
progressing to organ failure, and finally, if untreated, whole body failure and death.
Cells need two things to function: oxygen and glucose. This allows the cells to generate energy
and do their specific jobs.
Oxygen in the air enters the body through the lungs; where oxygen molecules cross into the
smallest blood vessels, the capillaries, and are picked up by red blood cells and attached to
hemoglobin molecules. The red blood cells are pushed through the body by the actions of the
pumping heart and deliver the oxygen to cells in all the tissues of the body. The hemoglobin
then picks up carbon dioxide, the waste product of metabolism, where it is then taken back to
the lungs and breathed out into the air, whereby the whole cycle begins again.
Glucose is generated in the body from the foods we eat. Glucose travels in the blood stream
and uses an insulin molecule to "open the door," where it then enters the cell to provide energy
for cellular metabolism.
Shock Causes
If cells are deprived of oxygen, instead of using aerobic (with oxygen) metabolism to function,
the cells use the anaerobic (without oxygen) pathway to produce energy. Unfortunately, lactic
acid is formed as a by product of anaerobic metabolism. This acid changes the acid-base
balance in the blood, making it more acidic, and this leads to situation in which cells begin to
leak toxic chemicals into the bloodstream, causing blood vessel walls to become damaged. The
anaerobic process ultimately leads to the death of the cell. If enough cells die, organs start to
fail, and the body starts to fail and death occurs.
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Think of the cardiovascular system of the body as similar to the oil pump in your car. For
efficient functioning, the electrical pump needs to work to pump the oil, there needs to be
enough oil, and the oil lines need to be intact. If any of these components fail, oil pressure falls
and the engine may be damaged. In the body, if the heart, blood vessels, or bloodstream
(circulation) fail, then the body fails.
The oxygen delivery system to the body's cells can fail in a variety of ways.
The lung may be injured and not be able to transfer oxygen to the blood stream. Examples of
causes include:
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The heart may not be able to adequately pump the blood to the tissues of the body. Examples
of causes examples include:
Heart attack in which muscle tissue is lost and the heart cannot beat as strong and pump
blood throughout the body.
A rhythm disturbance of the heart occurs when the heart can't beat in a coordinated way.
Inflammation of the sac around the heart (pericarditis) or inflammation of the heart
muscle due to infections or other causes, in which the effective beating capabilities of the
heart are lost.
There may not be enough red blood cells in the blood. If there aren't enough red blood cells
(anemia), then not enough oxygen can be delivered to the tissues with each heart beat.
Examples of causes may include:
There may not be enough other fluids in the blood vessels. The blood stream contains the
blood cells (red, white, and platelets), plasma (which is more than 90% water), and many
important proteins and chemicals. Loss of body water or dehydration can cause shock.
The blood vessels may not be able to maintain enough pressure within their walls to allow
blood to be pumped to the rest of the body. Normally, blood vessel walls have tension on them
to allow blood to be pumped against gravity to areas above the level of the heart. This tension
is under the control of the unconscious central nervous system, balanced between the action of
two chemicals, adrenaline (epinephrine) and acetylcholine. If the adrenaline system fails, then
the blood vessel walls dilate and blood pools in the parts of the body closest to the ground
(lower extremities), and may have a difficult time returning to heart to be pumped around the
body.
Since one of the steps in the cascade of events causing shock is damage to blood vessel walls,
this loss of integrity can cause blood vessels to leak fluid, leading to dehydration which
initiates a vicious circle of worsening shock.
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Stages of shock
There are four stages of shock. As it is a complex and continuous condition there is no sudden
transition from one stage to the next.
Initial
During this stage, the hypoperfusional state causes hypoxia, leading to the mitochondria being
unable to produce adenosine triphosphate (ATP). Due to this lack of oxygen, the cell
membranes become damaged, they become leaky to extra-cellular fluid, and the cells perform
anaerobic respiration. This causes a build-up of lactic and pyruvic acid which results in
systemic metabolic acidosis. The process of removing these compounds from the cells by the
liver requires oxygen, which is absent.
Compensatory (Compensating)
This stage is characterised by the body employing physiological mechanisms, including neural,
hormonal and bio-chemical mechanisms in an attempt to reverse the condition. As a result of
the acidosis, the person will begin to hyperventilate in order to rid the body of carbon dioxide
(CO2). CO2 indirectly acts to acidify the blood and by removing it the body is attempting to
raise the pH of the blood. The baroreceptors in the arteries detect the resulting hypotension,
and cause the release of adrenaline and noradrenaline.
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vascular tone; the combined effect results in an increase in blood pressure. Renin-angiotensin
axis is activated and arginine vasopressin is released to conserve fluid via the kidneys.
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Should the cause of the crisis not be successfully treated, the shock will proceed to the
progressive stage and the compensatory mechanisms begin to fail. Due to the decreased
perfusion of the cells, sodium ions build up within while potassium ions leak out. As anaerobic
metabolism continues, increasing the body's metabolic acidosis, the arteriolar smooth muscle
and precapillary sphincters relax such that blood remains in the capillaries. Due to this, the
hydrostatic pressure will increase and, combined with histamine release, this will lead to
leakage of fluid and protein into the surrounding tissues. As this fluid is lost, the blood
concentration and viscosity increase, causing sludging of the micro-circulation. The prolonged
vasoconstriction will also cause the vital organs to be compromised due to reduced perfusion.
If the bowel becomes sufficiently ischemic, bacteria may enter the blood stream, resulting in
the increased complication of endotoxic shock.
Refractory (Irreversible)
At this stage, the vital organs have failed and the shock can no longer be reversed. Brain
damage and cell death have occurred. Death will occur imminently.
A medical emergency is an injury or illness that is acute and poses an immediate risk to a
person's life or long term health. These emergencies may require assistance from another
person, who should ideally be suitably qualified to do so, although some of these emergencies
can be dealt with by the victim themselves. Dependent on the severity of the emergency, and the
quality of any treatment given, it may require the involvement of multiple levels of care, from a
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Classification of shock
Shock is identified in most patients by hypotension and inadequate organ perfusion, which
may be caused by either low cardiac output or low systemic vascular resistance. Circulatory
shock can be subdivided into 4 distinct classes on the basis of underlying mechanism and
characteristic hemodynamics, as follows:
Hypovolemic shock
Obstructive shock
Distributive shock
Cardiogenic shock
These classes of shock should be considered and systemically differentiated before establishing
a definitive diagnosis of septic shock.
Hypovolemic shock results from the loss of blood volume caused by such conditions as
gastrointestinal (GI) bleeding, extravasation of plasma, major surgery, trauma, and severe burns.
The patient demonstrates tachycardia, cool clammy extremities, hypotension, dry skin and
mucus membranes, and poor turgor.
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Hypovolemic Shock
There needs to be enough red blood cells and water in the blood for the heart to push the fluids
around within the blood vessels. When the body becomes dehydrated, there may be enough red
blood cells, but the total volume of fluid is decreased, and pressure within the system
decreases. Cardiac output is the amount of blood that the heart can pump out in one minute. It
is calculated as the stroke volume (how much blood each heart beat can push out) multiplied by
the heart rate (how fast the heart beats each minute). If there is less blood in the system to be
pumped, the heart speeds up to try to keep its output steady.
Water makes up 90% of blood. If the body becomes dehydrated because water is lost or fluid
intake is inadequate, the body tries to maintain cardiac output by making the heart beat faster.
But as the fluid losses mount, the body's compensation mechanisms fail, and shock may ensue.
Hypovolemic (hypo=low + volemic=volume) shock due to water loss can be the endpoint of
many illnesses, but the common element is the lack of fluid within the body.
Gastroenteritis can cause significant water loss from vomiting and diarrhea, and is a common
cause of death in third world countries. Heat exhaustion and heat stroke is caused by excessive
water loss through sweating as the body tries to cool itself. Patients with infections can lose
significant amounts of water from sweating. People with diabetes who have diabetic
ketoacidosis lose significant water because of because of elevated blood sugar that cause
excess water to be excreted in the urine.
Ultimately in hypovolemic shock, the patient cannot replace the amount of fluid that was lost
by drinking enough water, and the body is unable to maintain blood pressure and cardiac
output. In all shock states, when cells start to malfunction waste products build up, a
downward spiral of cell death begins, increased acidosis occurs, and a worsening body
environment leads to further cell death - and ultimately organ failure.
Hemorrhagic Shock
A subset of hypovolemic shock occurs when there is significant bleeding that occurs relatively
quickly. Trauma is the most common example of bleeding or hemorrhage, but bleeding can
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Hemorrhage classes
Class Blood loss Response Treatment
I <15 %(0.75 l) min. fast heart rate, normal blood pressure minimal
II 15-30 %(0.75-1.5 l) fast heart rate, min. low blood pressure intravenous fluids
III 30-40 %(1.5-2 l) very fast heart rate, low blood pressure, confusion fluids and packed RBCs
IV >40 %(>2 l) critical blood pressure and heart rate aggressive interventions
Blood loss has two effects on the body. First, there is a loss of volume within blood vessels to
be pumped (see hypovolemic shock) and second, a reduced oxygen carrying capacity occurs
because of the loss of red blood cells. Otherwise healthy people can lose up to 10% of their
blood volume (about the amount that a person donates at a blood drive) without becoming
symptomatic with weakness, lightheadedness, or shortness of breath.
The treatment of hemorrhagic shock depends on the cause. Finding and controlling the source
of bleeding is of paramount importance. Intravenous fluids are used to help with resuscitation
to increase the fluid volume within the blood vessel space, but blood transfusion is not always
mandatory. If the bleeding is controlled and the patient becomes more stable, the bone marrow
may be allowed to replenish the red blood cells that were lost.
If the red blood cell count in the blood decreases gradually over time, either because of
bleeding or the inability of the body to make enough new red cells, the body can adjust to the
lower levels to maintain adequate cell perfusion, but the individual's exercise tolerance may
decrease. This means that they may do well in normal daily activities but find that routine
exercise or household activities bring on weakness or shortness of breath. The treatment
depends on the underlying diagnosis, since it isn't a total fluid problem as in hypovolemic
shock.
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Cardiogenic Shock
When the heart loses its ability to pump blood to the rest of the body, blood pressure
decreases. Although there may be enough red blood cells and oxygen, they can't get to the cells
that need them.
The heart is a muscle itself and needs blood supply to work. When a heart attack occurs, the
blood supply to part of the heart is lost, and that can stun and irritate the heart muscle so that it
isn't able to beat with an appropriate squeeze to push blood out to the rest of the body. This
decreases stroke volume, and cardiac output falls.
Treatment includes trying to restore blood supply and the use of medications to support blood
pressure. In more dire circumstances, machines can be used to assist the heart to support blood
pressure.
Neurogenic Shock
There are involuntary muscles within blood vessel walls that maintain the squeeze so that the
volume within the vessels stays constant even if the body changes position against gravity. As
an analogy, is when you get up out of bed in the morning. If your blood vessels didn't squeeze a
little tighter, gravity would make the blood flow to your feet, the lowest part of your body,
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away from your brain, and you might pass out. The squeeze is maintained by signals from
nerves in the sympathetic trunk, a long bundle of fibers running from the skull to the tailbone
alongside the vertebral column.
In brain or spinal injury, the sympathetic trunk stops working and blood vessels dilate and
result in blood pooling away from the heart. Since there isn't enough blood returning to the
heart, the heart has a hard time pumping blood through the body.
Treatment includes fluids and medications to increase the tone in the blood vessel walls.
High or low blood sugars are almost always associated with diabetes. In people with diabetes,
the body does not make enough insulin to permit glucose to enter the cells for aerobic
metabolism. As treatment, insulin needs to be injected, or medication needs to be taken to
boost the body's lower insulin production. There must be a balance between how much
medication is taken and how much food is eaten.
If not enough food is ingested, then the blood sugar drops (hypoglycemia) and no glucose is
available to enter the cells, even if there is enough insulin to permit glucose to enter the cells.
The brain is very susceptible to low blood sugars, and coma has a very quick onset. Treatment
is providing sugar. If the person is awake enough to swallow, a sugar solution by mouth is
used, otherwise, intravenous fluids containing glucose are provided. If the lack of sugar was of
short duration, the person will awaken almost immediately after treatment. If blood sugars
remain low for prolonged periods of time, the brain's ability to recover is potentially lost.
When blood sugar levels spiral high out of control, there is risk of significant dehydration and
shock. If there is not enough insulin in the blood stream, cells cannot use the glucose that is
present, and instead turn to an alternative anaerobic metabolism to generate energy. Since
glucose can't enter cells to be used, hyperglycemia (hyper= high + gly=sugar = emia) occurs
as the glucose level builds up in the blood stream. The kidneys try to excrete excess sugar, but
because of chemical concentration gradients between blood and urine, significant amounts of
water also are lost. The body quickly becomes dehydrated and blood pressure drops, decreasing
blood flow to cells. Cells which are now lacking glucose inside them are now starved of
oxygen and turn to anaerobic metabolism, causing acid waste product build up. Excess acid in
the body changes the metabolism for all organs, making it more difficult for oxygen to be used.
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Conditions will continue worsen until insulin and significant fluids are given to the patient.
Anaphylactic Shock
When the body develops an allergic reaction to some outside chemical or substance, it can
activate its immune system to combat that substance. On occasion, there can be an excess
response and multiple organ systems in the body can be affected and fail. This is known as
anaphylaxis. Mast cells and basophils (a type of white blood cell) that contain histamine
become unstable and leak their contents to affect the muscles of the lung, heart and blood
vessels. These are smooth muscles that are part of the regulatory system of the body and are not
under conscious control.
The muscles that surround bronchial tubes go into spasm and cause wheezing and
shortness of breath.
The muscles that surround blood vessels dilate, causing blood pressure to drop.
The histamine also causes flushing of the skin, urticaria (hives), vomiting and diarrhea.
A variety of mechanisms cause the heart muscle to pump weakly and blood vessels to leak
fluid.
The combination of these effects decrease blood flow and oxygen supply to cells in the body
and can result in shock.
The most common causes of anaphylactic shock include allergic reactions to foods (especially
peanuts), antibiotics, and bee and wasp stings. Children are often allergic to eggs, soy, and
milk.
These allergens can cause the immune system to turn on the potential cascade to shock. Many
patients have allergic reactions that are less severe and can just involve hives, but others can
develop shortness of breath, wheezing, swelling of the tongue and mouth, and difficulty
swallowing.
Patients with major allergic reactions must try to avoid the chemical trigger. They also often
carry an Epipen (epinephrine injection kit) to inject themselves with epinephrine should an
allergic reaction occur.
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Shock Symptoms
Shock is defined as abnormal metabolism at the cellular level. Since it is not easy to directly
measure cellular problems, the symptoms of shock are indirect measurements of cellular
function. Shock is the end stage of all diseases, and symptoms will often be dependant on the
underlying cause.
Vital signs
As the patient goes through the various stages of shock, vital signs change. In the early stages,
the body tries to compensate by moving fluids around from within cells to the blood stream
with an attempt to maintain blood pressure in a normal range. However, there may be a slight
rise in the heart rate (tachycardia = tachy or fast + cardia or heart). For example, donating
blood. A unit of blood (or about 10% of the bloods volume) is removed, yet the body
compensates well, except for a little lightheadedness, which is often resolved by drinking
fluids. Another example is exercising and forgetting to drink enough fluids and feeling a little
tired at the end of the day.
As the body loses the ability to compensate, the breathing rate gets faster and the tachycardia
increases as the body tries to pack as much oxygen onto the remaining red blood cells as
possible and deliver them to the cells. Unfortunately, blood pressure starts to drop
(hypotension=hypo or low + tension= pressure) as compensation mechanisms fail.
Body function
Cells don't receive enough oxygen and the organs that they comprise begin to fail. All organs
may be affected.
As the brain is affected, the patient may become confused or lose consciousness (coma).
There may be chest pain as the heart itself doesn't get an adequate oxygen supply.
Diarrhea may occur as the large intestine becomes irritated due to hypotension.
Kidneys may fail and the body may stop producing urine.
The skin becomes clammy and pale.
Shock Diagnosis
The approach to the patient in shock requires that treatment occur at the same time as the
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diagnosis occurs. The source of the underlying disease needs to be found. Sometimes it is
obvious, for example, a trauma victim bleeding from a wound. Other times, the diagnosis is
elusive. The type of tests will depend upon the underlying condition.
The diagnosis is most often found through the medical history. A thorough physical
examination will be undertaken and the patients vital signs monitored.
Patient vital signs monitored might include continual blood pressure and heart rate
monitoring, and oxygen measurement. Special catheters may be inserted into the large
veins in the neck, chest, arm, or groin and threaded near the heart or into the pulmonary
artery, to measure pressures close to the heart, which may be a better indicator of the
body's fluid status. Other catheters may be inserted into arteries (arterial lines) to measure
blood pressures more directly. Tubes may be placed in the bladder (Foley catheter) to
measure urine output.
Blood laboratory tests will be performed (the type dependent on the underlying disease
or condition).
Radiologic tests may be performed dependent on the underlying illness.
Differential diagnosis
Shock is a common end point of many medical conditions. It has been divided into four
main types based on the underlying cause: hypovolemic, distributive, cardiogenic and
obstructive. A few additional classifications are occasionally used including:
endocrinologic shock.
Hypovolemic
This is the most common type of shock and is caused by insufficient circulating volume. Its
primary cause is hemorrhage (internal and/or external), or loss of fluid from the circulation.
Vomiting and diarrhea are the most common cause in children. With other causes including
burns, environmental exposure and excess urine loss due to diabetic ketoacidosis and
diabetes insipidus.
Cardiogenic
This type of shock is caused by the failure of the heart to pump effectively. This can be due
to damage to the heart muscle, most often from a large myocardial infarction. Other causes
of cardiogenic shock include dysrhythmias, cardiomyopathy/myocarditis, congestive heart
failure (CHF), contusio cordis, or cardiac valve problems.
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Obstructive
Obstructive shock is due to obstruction of blood flow outside of the heart. Several
conditions can result in this form of shock.
Cardiac tamponade in which fluid in the pericardium prevents inflow of blood into the
heart (venous return). Constrictive pericarditis, in which the pericardium shrinks and
hardens, is similar in presentation.
Tension pneumothorax Through increased intrathoracic pressure, bloodflow to the heart
is prevented (venous return).
Pulmonary embolism is the result of a thromboembolic incident in the blood vessels of
the lungs and hinders the return of blood to the heart.
Aortic stenosis hinders circulation by obstructing the ventricular outflow tract
Distributive
Distributive shock is due to impaired utilization of oxygen and thus production of energy
by the cell. Examples of this form of shock are:
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peripheral blood vessels. (This term can be confused with spinal shock which is a
recoverable loss of function of the spinal cord after injury and does not refer to the
haemodynamic instability per se.)
Endocrine
Based on endocrine disturbances such as:
Shock Treatment
If you come upon a person in shock, the initial response should be to call 101 in Ukraine
(911 in Usa) and activate the emergency response system. Self-care at home is not
appropriate.
Lay the person down in a safe place and try to keep them warm and comfortable.
If the patient is not awake, is not breathing, and has no heartbeat, it is appropriate to start chest
compressions following the American Heart Association guidelines. It is important to send
someone to get an AED if one is available.
EMS personnel are well trained in the initial assessment of the patient in shock. The first
course of action is to make certain that the ABCs have been assessed. The so-called
ABCs are:
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Airway: assessment of whether the patient is awake enough to try to take their own
breaths and/or if there is there anything blocking the mouth or nose.
Breathing: assessment of the adequacy of breathing and whether it may need to be
assisted with mouth-to-mouth resuscitation or more aggressive interventions like a bag
and mask or intubation with an endotracheal tube and a ventilator.
Circulation: assessment of the adequacy of the blood pressure adequate and
determination of whether intravenous lines are needed for delivery of fluid or medications
to support the blood pressure.
If there is bleeding that is obvious, attempts to control it with direct pressure will be
attempted.
A fingerstick blood sugar will be checked to make certain that hypoglycemia (low blood
sugar) does not exist.
In the emergency department, diagnosis and treatment will occur at the same time.
Patients will be treated with oxygen supplementation through nasal cannulae, a face
mask, or endotracheal intubation. The method and amount of oxygen will be titrated to
make certain enough oxygen is available for the body to use. Again, the goal will be to
pack each hemoglobin molecule with oxygen.
Blood may be transfused if bleeding (hemorrhage) is the cause of the shock state. If
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bleeding is not the case, intravenous fluids will be given to bolster the volume of fluids
within the blood vessels.
Intravenous drugs can be used to try to maintain blood pressure (vasopressors). They
work by stimulating the heart to beat stronger and by squeezing blood vessels to increase
the flow within them.
Shock Prognosis
Shock is a culmination of multiple organ systems in the body that have failed or are in the
process of failing. Even with the best of care, there is a significant risk of death. The mortality
rate for shock depends upon the type and reason for the shock, and the age and underling
health condition of the patient.
Background
Shock is a state of inadequate perfusion, which does not sustain the physiologic needs of organ
tissues. Many conditions, including blood loss but also including nonhemorrhagic states such
as dehydration, sepsis, impaired autoregulation, obstruction, decreased myocardial function,
and loss of autonomic tone, may produce shock or shocklike states.
Pathophysiology
In hemorrhagic shock, blood loss exceeds the body's ability to compensate and provide
adequate tissue perfusion and oxygenation. This frequently is due to trauma, but it may be
caused by spontaneous hemorrhage (eg, GI bleeding, childbirth), surgery, and other causes.
Most frequently, clinical hemorrhagic shock is caused by an acute bleeding episode with a
discrete precipitating event. Less commonly, hemorrhagic shock may be seen in chronic
conditions with subacute blood loss.
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Epidemiology
Frequency
United States
Accidental injuries remain the leading cause of death in individuals aged 1-44
years.Hemorrhagic shock is a leading cause of death among trauma patients.
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History
Specific details of the mechanism of trauma or other cause of hemorrhage are essential.
Inquire about a history of bleeding disorders and surgery.
Prehospital interventions, especially the administration of fluids, and changes in vital
signs should be determined. Emergency medical technicians or paramedics should share
this information.
Physical
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when blood is present. However, the patient with altered mental status or multiple
concomitant injuries may not have the classic signs and symptoms at physical
examination.
Progressive abdominal distention in hemorrhagic shock is highly suggestive of intra-
abdominal hemorrhage.
Pelvis
Fractures can produce massive bleeding. Retroperitoneal bleeding must be
suspected.
Flank ecchymosis may indicate retroperitoneal hemorrhage.
Extremities
Hemorrhage from extremity injuries may be apparent, or tissues may obscure
significant bleeding.
Femoral fractures may produce significant blood loss.
Nervous system
Agitation and combativeness may be seen in the initial stages of hemorrhagic shock.
These signs are followed by a progressive decline in level of consciousness due to
cerebral hypoperfusion or concomitant head injury.
Differential Diagnoses
Abdominal Trauma, Blunt
Abdominal Trauma, Penetrating
Abortion, Complications
Anemia, Acute
Anemia, Chronic
Blast Injuries
Disseminated Intravascular Coagulation
Pneumothorax, Tension and Traumatic
Pregnancy, Ectopic
Pregnancy, Postpartum Hemorrhage
Pregnancy, Trauma
Shock, Cardiogenic
Shock, Hypovolemic
Shock, Septic
Spinal Cord Injuries
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Laboratory Studies
Imaging Studies
Cervical spine, chest, and pelvis radiographs are the standard screening images for severe
trauma. Other radiographs may be indicated for orthopedic injuries.
Computed tomography can be used to image the appropriate region of suspected injury. CT
scanning frequently is the method of choice for evaluating possible intra-abdominal and/or
retroperitoneal sources of hemorrhage in stable patients (see the image below). Oral contrast
material may not increase the diagnostic yield of abdominal CT scanning in blunt trauma.
Scanning should not be delayed to administer oral contrast material.
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Fig. CT scan of a 26-year-old man after a motor vehicle crash shows a significant amount of
intra-abdominal bleeding.
Bedside ultrasonography abdominal ultrasonography can be very useful for the rapid detection
of AAA and free intra-abdominal fluid. Thoracic ultrasonographic findings can immediately
confirm hemothorax or pericardial tamponade.
Directed angiography may be diagnostic and therapeutic. Interventional radiologists have had
good success achieving hemostasis in hemorrhage caused by a variety of vessels and organs.
Other Tests
An ECG can be useful for detecting dysrhythmias and cardiac sequelae of shock.
Tissue oximetry using Near Infrared Spectroscopy (NIRS) shows promise for continuous
noninvasive measurement of perfusion in hemorrhagic shock and other conditions.
Procedures
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of hemorrhage.
Prehospital Care
The standard care consists of rapid assessment and expeditious transport to an appropriate
center for evaluation and definitive care.
Intravenous access and fluid resuscitation are standard. However, this practice has become
controversial.
For many years, aggressive fluid administration has been advocated to normalize
hypotension associated with severe hemorrhagic shock. Recent studies of urban patients
with penetrating trauma have shown that mortality increases with these interventions;
these findings call these practices into question.
Reversal of hypotension prior to the achievement of hemostasis may increase hemorrhage,
dislodge partially formed clots, and dilute existing clotting factors. Findings from animal
studies of uncontrolled hemorrhage support these postulates. These provocative results
raise the possibility that moderate hypotension may be physiologically protective and
should be permitted, if present, until hemorrhage is controlled.
These findings should not yet be clinically extrapolated to other settings or etiologies of
hemorrhage. The ramifications of permissive hypotension in humans remain speculative,
and safety limits have not been established yet.
Diagnosis and treatment of the underlying hemorrhage must be performed rapidly and
concurrently with management of shock.
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Determination of the site and etiology of hemorrhage is critical to guide further interventions
and definitive care.
Control of hemorrhage may be achieved in the ED, or control may require consultations and
special interventions.
Consultations
Medication Summary
Achievement of hemostasis, fluid resuscitation, and use of blood products are the mainstays of
treatment. Pressor agents may be useful in some settings (eg, spinal shock), but these agents
should not be substitutes for adequate volume resuscitation and blood product replacement.
Tranexamic acid (TXA) is an inexpensive antifibrinolytic drug that promotes blood clotting by
preventing blood clots from breaking down. It has been shown to reduce mortality in trauma
patients with uncontrolled hemorrhage. Further studies are planned to determine specific
recommendations for TXA administration.
Vasopressors
Class Summary
These agents augment both coronary and cerebral blood flow during the low-flow state
associated with shock.
Dopamine (Intropin)
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Norepinephrine (Levophed)
Vasopressin (Pitressin)
Has vasopressor and ADH activity. Increases water resorption at distal renal tubular epithelium
(ADH effect) and promotes smooth muscle contraction throughout the vascular bed of the renal
tubular epithelium (vasopressor effects); however, vasoconstriction also is increased in
splanchnic, portal, coronary, cerebral, peripheral, pulmonary, and intrahepatic vessels.
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Transfer
Complications
Hypovolemic shock refers to a medical or surgical condition in which rapid fluid loss results in
multiple organ failure due to inadequate circulating volume and subsequent inadequate
perfusion. Most often, hypovolemic shock is secondary to rapid blood loss (hemorrhagic
shock).
Acute external blood loss secondary to penetrating trauma and severe GI bleeding disorders are
2 common causes of hemorrhagic shock. Hemorrhagic shock can also result from significant
acute internal blood loss into the thoracic and abdominal cavities.
Two common causes of rapid internal blood loss are solid organ injury and rupture of an
abdominal aortic aneurysm. Hypovolemic shock can result from significant fluid (other than
blood) loss. Two examples of hypovolemic shock secondary to fluid loss include refractory
gastroenteritis and extensive burns. The remainder of this article concentrates mainly on
hypovolemic shock secondary to blood loss and the controversies surrounding the treatment of
this condition. The reader is referred to other articles for discussions of the pathophysiology
and treatment for hypovolemic shock resulting from losses of fluid other than blood.
The many life-threatening injuries experienced during the wars of the 1900s have significantly
affected the development of the principles of hemorrhagic shock resuscitation. During World
War I, W.B. Cannon recommended delaying fluid resuscitation until the cause of the
hemorrhagic shock was repaired surgically. Crystalloids and blood were used extensively
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during World War II for the treatment of patients in unstable conditions. Experience from the
Korean and Vietnam wars revealed that volume resuscitation and early surgical intervention
were paramount for surviving traumatic injuries resulting in hemorrhagic shock. These and
other principles helped in the development of present guidelines for the treatment of traumatic
hemorrhagic shock. However, recent investigators have questioned these guidelines, and today,
controversies exist concerning the optimal treatment of hemorrhagic shock.
Pathophysiology
The human body responds to acute hemorrhage by activating the following major physiologic
systems: the hematologic, cardiovascular, renal, and neuroendocrine systems.
The hematologic system responds to an acute severe blood loss by activating the coagulation
cascade and contracting the bleeding vessels (by means of local thromboxane A2 release). In
addition, platelets are activated (also by means of local thromboxane A2 release) and form an
immature clot on the bleeding source. The damaged vessel exposes collagen, which
subsequently causes fibrin deposition and stabilization of the clot. Approximately 24 hours are
needed for complete clot fibrination and mature formation.
The cardiovascular system initially responds to hypovolemic shock by increasing the heart rate,
increasing myocardial contractility, and constricting peripheral blood vessels. This response
occurs secondary to an increased release of norepinephrine and decreased baseline vagal tone
(regulated by the baroreceptors in the carotid arch, aortic arch, left atrium, and pulmonary
vessels). The cardiovascular system also responds by redistributing blood to the brain, heart,
and kidneys and away from skin, muscle, and GI tract.
The renal system responds to hemorrhagic shock by stimulating an increase in renin secretion
from the juxtaglomerular apparatus. Renin converts angiotensinogen to angiotensin I, which
subsequently is converted to angiotensin II by the lungs and liver. Angiotensin II has 2 main
effects, both of which help to reverse hemorrhagic shock, vasoconstriction of arteriolar smooth
muscle, and stimulation of aldosterone secretion by the adrenal cortex. Aldosterone is
responsible for active sodium reabsorption and subsequent water conservation.
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The pathophysiology of hypovolemic shock is much more involved than what was just listed.
To explore the pathophysiology in more detail, references for further reading are provided in
the bibliography. These intricate mechanisms list above are effective in maintaining vital organ
perfusion in severe blood loss. Without fluid and blood resuscitation and/or correction of the
underlying pathology causing the hemorrhage, cardiac perfusion eventually diminishes, and
multiple organ failure soon follows.
History
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whereas a patient with a history of hematemesis from the start is more likely to have
peptic ulcer disease or esophageal varices.
If a gynecologic cause is being considered, gather information about the following: last
menstrual period, risk factors for ectopic pregnancy, vaginal bleeding (including amount
and duration), vaginal passage of products of conception, and pain. All women of
childbearing age should undergo a pregnancy test, regardless of whether they believe that
they are pregnant. A negative pregnancy test typically excludes ectopic pregnancy as a
diagnosis.
Physical
The physical examination should always begin with an assessment of the airway, breathing, and
circulation. Once these have been evaluated and stabilized, the circulatory system should be
evaluated for signs and symptoms of shock.
Do not rely on systolic BP as the main indicator of shock; this practice results in delayed
diagnosis. Compensatory mechanisms prevent a significant decrease in systolic BP until the
patient has lost 30% of the blood volume. More attention should be paid to the pulse,
respiratory rate, and skin perfusion. Also, patients taking beta-blockers may not present with
tachycardia, regardless of the degree of shock.
Classes of hemorrhage have been defined, based on the percentage of blood volume loss.
However, the distinction between these classes in the hypovolemic patient often is less
apparent. Treatment should be aggressive and directed more by response to therapy than by
initial classification.
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In the pregnant patient, perform a sterile speculum examination. However, with third-
trimester bleeding, the examination should be performed as a "double set-up" in the
operating room. Check for abdominal, uterine, or adnexal tenderness.
Causes
The causes of hemorrhagic shock are traumatic, vascular, GI, or pregnancy related.
Traumatic causes can result from penetrating and blunt trauma. Common traumatic
injuries that can result in hemorrhagic shock include the following: myocardial laceration
and rupture, major vessel laceration, solid abdominal organ injury, pelvic and femoral
fractures, and scalp lacerations.
Vascular disorders that can result in significant blood loss include aneurysms,
dissections, and arteriovenous malformations.
GI disorders that can result in hemorrhagic shock include the following: bleeding
esophageal varices, bleeding peptic ulcers, Mallory-Weiss tears, and aortointestinal
fistulas.
Pregnancy-related disorders include ruptured ectopic pregnancy, placenta previa, and
abruption of the placenta. Hypovolemic shock secondary to an ectopic pregnancy is
common. Hypovolemic shock secondary to an ectopic pregnancy in a patient with a
negative urine pregnancy test is rare but has been reported.
Differential Diagnoses
Abruptio Placentae
Aneurysm, Abdominal
Aneurysm, Thoracic
Fractures, Femur
Fractures, Pelvic
Gastritis and Peptic Ulcer Disease
Placenta Previa
Pregnancy, Ectopic
Pregnancy, Postpartum Hemorrhage
Pregnancy, Trauma
Shock, Hemorrhagic
Shock, Hypovolemic
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Toxicity, Iron
Laboratory Studies
After the history is taken and the physical examination is performed, further workup
depends on the probable cause of the hypovolemia, as well as on the stability of the
patient's condition.
Initial laboratory studies should include analysis of the CBC, electrolyte levels (eg, Na,
K, Cl, HCO3, BUN, creatinine, glucose levels), prothrombin time, activated partial
thromboplastin time, ABGs, urinalysis (in patients with trauma), and a urine pregnancy
test. Blood should be typed and cross-matched.
Imaging Studies
Patients with marked hypotension and/or unstable conditions must first be resuscitated
adequately. This treatment takes precedence over imaging studies and may include
immediate interventions and immediately taking the patient to the operating room.
The workup for the patient with trauma and signs and symptoms of hypovolemia is
directed toward finding the source of blood loss.
The atraumatic patient with hypovolemic shock requires ultrasonographic examination in
the ED if an abdominal aortic aneurysm is suspected. If GI bleeding is suspected, a
nasogastric tube should be placed, and gastric lavage should be performed. An upright
chest radiograph should be obtained if a perforated ulcer or Boerhaave syndrome is a
possibility. Endoscopy can be performed (usually after the patient has been admitted) to
further delineate the source of bleeding.
A pregnancy test should be performed in all female patients of childbearing age. If the
patient is pregnant and in shock, surgical consultation and the consideration of bedside
pelvic ultrasonography should be immediately performed in the ED. Hypovolemic shock
secondary to an ectopic pregnancy is common. Hypovolemic shock secondary to an
ectopic pregnancy in a patient with a negative pregnancy test, although rare, has been
reported.
If thoracic dissection is suspected because of the mechanism and initial chest
radiographic findings, the workup may include transesophageal echocardiography,
aortography, or CT scanning of the chest.
If a traumatic abdominal injury is suspected, a focused abdominal sonography for trauma
(FAST) ultrasonography examination may be performed in the stable or unstable patient.
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Prehospital Care
The treatment of patients with hypovolemic shock often begins at an accident scene or at home.
The prehospital care team should work to prevent further injury, transport the patient to the
hospital as rapidly as possible, and initiate appropriate treatment in the field. Direct pressure
should be applied to external bleeding vessels to prevent further blood loss.
Prevention of further injury applies mostly to the patient with trauma. The cervical spine
must be immobilized, and the patient must be extricated, if applicable, and moved to a
stretcher. Splinting of fractures can minimize further neurovascular injury and blood loss.
Although in selected cases stabilization may be beneficial, rapid transport of sick patients
to the hospital remains the most important aspect of prehospital care. Definitive care of
the hypovolemic patient usually requires hospital, and sometimes surgical, intervention.
Any delay in definitive care, eg, such as delayed transport, is potentially harmful.
Most prehospital interventions involve immobilizing the patient (if trauma is involved),
securing an adequate airway, ensuring ventilation, and maximizing circulation.
In the setting of hypovolemic shock, positive-pressure ventilation may diminish
venous return, diminish cardiac outcome, and worsen the shock state. While
oxygenation and ventilation are necessary, excessive positive-pressure ventilation
can be detrimental for a patient suffering hypovolemic shock.
Appropriate treatment usually can be initiated without delaying transport. Some
procedures, such as starting intravenous (IV) lines or splinting of extremities, can be
performed while a patient is being extricated. However, procedures in the field that
prolong transportation should be delayed. Benefits to giving IV fluids prior to
departure from the scene are not clear; however, IV lines and fluid resuscitation
should be started and continued once the patient is en route to definitive care.
In recent years, there has been considerable debate regarding the use of military antishock
trousers (MAST). MAST were introduced in the 1960s and, based mostly on anecdotal
reports of success, their use became standard therapy in the prehospital treatment of
hypovolemic shock in the late 1970s. By the 1980s, the American College of Surgeons
Committee on Trauma included their use in the standard of care for all patients with
trauma and signs or symptoms of shock. Since that time, studies have failed to show
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improved outcome with the use of MAST. The American College of Surgeons Committee
on Trauma no longer recommends the use of MAST.
Three goals exist in the emergency department treatment of the patient with hypovolemic shock
as follows: (1) maximize oxygen delivery - completed by ensuring adequacy of ventilation,
increasing oxygen saturation of the blood, and restoring blood flow, (2) control further blood
loss, and (3) fluid resuscitation. Also, the patient's disposition should be rapidly and
appropriately determined.
The patient's airway should be assessed immediately upon arrival and stabilized if necessary.
The depth and rate of respirations, as well as breath sounds, should be assessed. If pathology
(eg, pneumothorax, hemothorax, flail chest) that interferes with breathing is found, it should be
addressed immediately. High-flow supplemental oxygen should be administered to all patients,
and ventilatory support should be given, if needed. Excessive positive-pressure ventilation can
be detrimental for a patient suffering hypovolemic shock and should be avoided.
Two large-bore IV lines should be started. The Poiseuille law states that flow is inversely
related to the length of the IV catheter and directly related to its radius to the fourth power.
Thus, a short large-caliber IV catheter is ideal; the caliber is much more significant than the
length. IV access may be obtained by means of percutaneous access in the antecubital veins,
cutdown of saphenous or arm veins, or access in the central veins by using the Seldinger
technique. If central lines are obtained, a large-bore single-lumen catheter should be used.
Intraosseous access has and continues to be used for hypotensive children younger than 6
years. Intraosseous access has also been used in hypotensive adults. The most important factor
in determining the route of access is the practitioner's skill and experience.
Placement of an arterial line should be considered for patients with severe hemorrhage. For
these patients, the arterial line will provide continuous blood pressure monitoring and also ease
arterial blood gas testing.
Once IV access is obtained, initial fluid resuscitation is performed with an isotonic crystalloid,
such as lactated Ringer solution or normal saline. An initial bolus of 1-2 L is given in an adult
(20 mL/kg in a pediatric patient), and the patient's response is assessed.
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If vital signs return to normal, the patient may be monitored to ensure stability, and blood
should be sent for typed and cross-matched. If vital signs transiently improve, crystalloid
infusion should continue and type-specific blood obtained. If little or no improvement is seen,
crystalloid infusion should continue, and type O blood should be given (type O Rh-negative
blood should be given to female patients of childbearing age to prevent sensitization and future
complications).
If a patient is moribund and markedly hypotensive (class IV shock), both crystalloid and type O
blood should be started initially. These guidelines for crystalloid and blood infusion are not
rules; therapy should be based on the condition of the patient.
The position of the patient can be used to improve circulation; one example is raising the
hypotensive patient's legs while fluid is being given. Another example of useful positioning is
rolling a hypotensive gravid patient with trauma onto her left side, which displaces the fetus
from the inferior vena cava and increases circulation. The Trendelenburg position is no longer
recommended for hypotensive patients, as the patient is predisposed to aspiration. In addition,
the Trendelenburg position does not improve cardiopulmonary performance and may worsen
gas exchange.
Autotransfusion may be a possibility in some patients with trauma. Several devices that allow
for the sterile collection, anticoagulation, filtration, and retransfusion of blood are available. In
the trauma setting, this blood almost always is from a hemothorax collected by means of tube
thoracostomy.
Control of further hemorrhage depends on the source of bleeding and often requires surgical
intervention. In the patient with trauma, external bleeding should be controlled with direct
pressure; internal bleeding requires surgical intervention. Long-bone fractures should be
treated with traction to decrease blood loss.
In the patient whose pulse is lost in the ED or just prior to arrival, an emergency thoracotomy
with cross-clamping of the aorta may be indicated to preserve blood flow to the brain. This
procedure is palliative at best and requires immediate transfer to the operating room.
In the patient with GI bleeding, intravenous vasopressin and H2 blockers have been used.
Vasopressin commonly is associated with adverse reactions, such as hypertension, arrhythmias,
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Somatostatin and octreotide infusions have been shown to reduce gastrointestinal bleeding
from varices and peptic ulcer disease. These agents possess the advantages of vasopressin
without the significant side effects.
Virtually all causes of acute gynecological bleeding that cause hypovolemia (eg, ectopic
pregnancy, placenta previa, abruptio placenta, ruptured cyst, miscarriage) require surgical
intervention.
Early consultation and definitive care are the keys. The goal in the ED is to stabilize the
hypovolemic patient, determine the cause of bleeding, and provide definitive care as quickly as
possible. If transfer to another hospital is necessary, resources should be mobilized early.
In patients with trauma, if the emergency medical services personnel indicate potential serious
injury, the surgeon (or trauma team) should be notified prior to the patient's arrival. In a
55-year-old patient with abdominal pain, for example, emergency ultrasonography of the
abdomen may be necessary to identify an abdominal aortic aneurysm before the vascular
surgeon is notified. Every patient should be individually evaluated, because delaying definitive
care can increase morbidity and mortality.
Resuscitation
Whether crystalloids or colloids are best for resuscitation continues to be a matter for
discussion and research. Many fluids have been studied for use in resuscitation; these include
isotonic sodium chloride solution, lactated Ringer solution, hypertonic saline, albumin,
purified protein fraction, fresh frozen plasma, hetastarch, pentastarch, and dextran 70.
Proponents of colloid resuscitation argue that the increased oncotic pressure produced with
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these substances decreases pulmonary edema. However, the pulmonary vasculature allows
considerable flow of material, including proteins, between the intravascular space and
interstitium. Maintenance of the pulmonary hydrostatic pressure at less than 15 mm Hg appears
to be a more important factor in preventing pulmonary edema.
Another argument is that less colloid is needed to increase the intravascular volume. Studies
have shown this to be true. However, they still have not demonstrated any difference in
outcome with colloids compared with crystalloids.
Synthetic colloid solutions, such as hetastarch, pentastarch, and dextran 70, have some
advantages compared with natural colloids such as purified protein fraction, fresh frozen
plasma, and albumin. They have the same volume-expanding properties, but because of their
structures and high molecular weights, they remain mostly in the intravascular space, reducing
the occurrence of interstitial edema. Although theoretic advantages exist, studies have failed to
show a difference in ventilatory parameters, pulmonary function test results, days using a
ventilator, total hospital days, or survival.
The European Society of Intensive Care Medicine (ESICM) advises against the use of colloids-
hydroxyethyl starches (HES) in patients with severe sepsis or risk of acute kidney injury.
Physicians should also avoid using colloids in patients with head injury and refrain from
administering gelatins and HES in organ donors
The combination of hypertonic saline and dextran also has been studied because of previous
evidence that it may improve cardiac contractility and circulation. Studies in the US and Japan
have failed to show any difference when this combination was compared with isotonic sodium
chloride solution or lactated Ringer solution. Thus, despite the many available resuscitation
fluids, current recommendations still advocate the use of normal saline or lactated Ringer
solution. In the US, one reason for the predominant use of crystalloids over the other
resuscitative fluids is cost.
Recent literature suggests that the early administration of FFP and platelets improves survival
and decreases overall PRBC need in patients undergoing a massive transfusion
Although some data indicate that a systolic BP of 80-90 mm Hg may be adequate in penetrating
truncal trauma without head injury, further studies are needed.
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Current recommendations are for aggressive fluid resuscitation with lactated Ringer solution or
normal saline in all patients with signs and symptoms of shock, regardless of underlying cause.
Medication Summary
Antisecretory agents
Class Summary
These agents have vasoconstrictive properties and can reduce blood flow to portal systems.
Somatostatin (Zecnil)
Naturally occurring tetradecapeptide isolated from the hypothalamus and pancreatic and enteric
epithelial cells. Diminishes blood flow to portal system because of vasoconstriction. Has
similar effects as vasopressin but does not cause coronary vasoconstriction. Rapidly cleared
from the circulation, with an initial half-life of 1-3 min.
Octreotide (Sandostatin)
Complications
Neurologic sequelae
Death
Prognosis
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Cardiogenic Shock
Background
Cardiogenic shock is a physiologic state in which inadequate tissue perfusion results from
cardiac dysfunction, most often systolic. It is a major, and frequently fatal, complication of a
variety of acute and chronic disorders, occurring most commonly following acute myocardial
infarction (MI). (See Pathophysiology, Etiology, and Prognosis.)
Patient with an acute anterolateral myocardial infarction who developed cardiogenic shock.
Coronary angiography images showed severe stenosis of the left anterior descending
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Echocardiogram image from a patient with cardiogenic shock shows enlarged cardiac
chambers; the motion study showed poor left ventricular function. Courtesy of R. Hoeschen,
MD.
The clinical definition of cardiogenic shock is decreased cardiac output and evidence of tissue
hypoxia in the presence of adequate intravascular volume. Hemodynamic criteria for
cardiogenic shock are sustained hypotension (systolic blood pressure < 90 mm Hg for at least
30 min) and a reduced cardiac index (< 2.2 L/min/m2) in the presence of elevated pulmonary
capillary wedge pressure (>15 mm Hg). (See DDx, Workup.)
The diagnosis of cardiogenic shock can sometimes be made at the bedside by observing
hypotension, absence of hypovomeia, and clinical signs of poor tissue perfusion, which include
oliguria, cyanosis, cool extremities, and altered mentation. These signs usually persist after
attempts have been made to correct hypovolemia, arrhythmia, hypoxia, and acidosis. (See
Presentation, DDx.)
Pathophysiology
Cardiogenic shock is recognized as a low cardiac output state secondary to extensive left
ventricular infarction, development of a mechanical defect (eg, ventricular septal defect or
papillary muscle rupture), or right ventricular infarction.
Disorders that can result in the acute deterioration of cardiac function and lead to cardiogenic
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shock include myocardial infarction (MI) or myocardial ischemia, acute myocarditis, sustained
arrhythmia, severe valvular dysfunction, and decompensation of end-stage cardiomyopathy
from multiple etiologies. Autopsy studies show that cardiogenic shock is generally associated
with the loss of more than 40% of the left ventricular myocardial muscle.
Myocardial pathology
Cardiogenic shock is characterized by systolic and diastolic dysfunction. Patients who develop
cardiogenic shock from acute MI consistently have evidence of progressive myocardial necrosis
with infarct extension. Decreased coronary perfusion pressure and increased myocardial
oxygen demand play a role in the vicious cycle that leads to cardiogenic shock.
Patients suffering from cardiogenic shock often have multivessel coronary artery disease with
limited coronary blood flow reserve. Ischemia remote from the infarcted zone is an important
contributor to shock. Myocardial diastolic function is also impaired, because ischemia causes
decreased myocardial compliance, thereby increasing left ventricular filling pressure, which
may lead to pulmonary edema and hypoxemia.
Cellular pathology
Tissue hypoperfusion, with consequent cellular hypoxia, causes anaerobic glycolysis, the
accumulation of lactic acid, and intracellular acidosis. Also, myocyte membrane transport
pumps fail, which decreases transmembrane potential and causes intracellular accumulation of
sodium and calcium, resulting in myocyte swelling.
If ischemia is severe and prolonged, myocardial cellular injury becomes irreversible and leads
to myonecrosis, which includes mitochondrial swelling, the accumulation of denatured proteins
and chromatin, and lysosomal breakdown. These events induce fracture of the mitochondria,
nuclear envelopes, and plasma membranes.
Additionally, apoptosis (programmed cell death) may occur in peri-infarcted areas and may
contribute to myocyte loss. Activation of inflammatory cascades, oxidative stress, and
stretching of the myocytes produces mediators that overpower inhibitors of apoptosis, thus
activating the apoptosis.
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Large areas of myocardium that are dysfunctional but still viable can contribute to the
development of cardiogenic shock in patients with MI. This potentially reversible dysfunction
is often described as myocardial stunning or as hibernating myocardium. Although hibernation
is considered a different physiologic process than myocardial stunning, the conditions are
difficult to distinguish in the clinical setting and they often coexist.
The main mechanical defect in cardiogenic shock is a shift to the right for the left ventricular
end-systolic pressure-volume curve, because of a marked reduction in contractility. As a result,
at a similar or even lower systolic pressure, the ventricle is able to eject less blood volume per
beat. Therefore, the end-systolic volume is usually greatly increased in persons with
cardiogenic shock.
The stroke volume is decreased, and to compensate for this, the curvilinear diastolic pressure-
volume curve also shifts to the right, with a decrease in diastolic compliance. This leads to
increased diastolic filling, which is associated with an increase in end-diastolic pressure. The
attempt to enhance cardiac output by this mechanism comes at the cost of having a higher left
ventricular diastolic filling pressure, which ultimately increases myocardial oxygen demand
and causes pulmonary edema.
As a result of decreased contractility, the patient develops elevated left and right ventricular
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filling pressures and low cardiac output. Mixed venous oxygen saturation falls because of the
increased tissue oxygen extraction, which is due to the low cardiac output. This, combined
with the intrapulmonary shunting that is often present, contributes to substantial arterial
oxygen desaturation.
Systemic effects
When a critical mass of left ventricular myocardium becomes ischemic and fails to pump
effectively, stroke volume and cardiac output are curtailed. Myocardial ischemia is further
exacerbated by compromised myocardial perfusion due to hypotension and tachycardia.
The pump failure increases ventricular diastolic pressures concomitantly, causing additional
wall stress and thereby elevating myocardial oxygen requirements. Systemic perfusion is
compromised by decreased cardiac output, with tissue hypoperfusion intensifying anaerobic
metabolism and instigating the formation of lactic acid, which further deteriorates the systolic
performance of the myocardium.
Depressed myocardial function also leads to the activation of several physiologic compensatory
mechanisms. These include sympathetic stimulation, which increases the heart rate and cardiac
contractility and causes renal fluid retention, hence augmenting the left ventricular preload.
The raised heart rate and contractility increases myocardial oxygen demand, further worsening
myocardial ischemia.
Fluid retention and impaired left ventricular diastolic filling triggered by tachycardia and
ischemia contribute to pulmonary venous congestion and hypoxemia. Sympathetically mediated
vasoconstriction to maintain systemic blood pressure amplifies myocardial afterload, which
additionally impairs cardiac performance. Finally, excessive myocardial oxygen demand with
simultaneous inadequate myocardial perfusion worsens myocardial ischemia, initiating a
vicious cycle that ultimately ends in death, if uninterrupted.
Shock state
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Shock state, irrespective of the etiology, is described as a syndrome initiated by acute systemic
hypoperfusion that leads to tissue hypoxia and vital organ dysfunction. All forms of shock are
characterized by inadequate perfusion to meet the metabolic demands of the tissues. A
maldistribution of blood flow to end organs begets cellular hypoxia and end organ damage, the
well-described multisystem organ dysfunction syndrome. The organs of vital importance are the
brain, heart, and kidneys.
A decline in higher cortical function may indicate diminished perfusion of the brain, which
leads to an altered mental status ranging from confusion and agitation to flaccid coma. The
heart plays a central role in propagating shock. Depressed coronary perfusion leads to
worsening cardiac dysfunction and a cycle of self-perpetuating progression of global
hypoperfusion. Renal compensation for reduced perfusion results in diminished glomerular
filtration, causing oliguria and subsequent renal failure.
Etiology
Cardiogenic shock can result from the following types of cardiac dysfunction:
Systolic dysfunction
Diastolic dysfunction
Valvular dysfunction
Cardiac arrhythmias
Coronary artery disease
Mechanical complications
The vast majority of cases of cardiogenic shock in adults are due to acute myocardial ischemia.
Indeed, cardiogenic shock is generally associated with the loss of more than 40% of the left
ventricular myocardium, although in patients with previously compromised left ventricular
function, even a small infarction may precipitate shock. Cardiogenic shock is more likely to
develop in people who are elderly or diabetic or in persons who have had a previous inferior
myocardial infarction (MI).
Complications of acute MI, such as acute mitral regurgitation, large right ventricular infarction,
and rupture of the interventricular septum or left ventricular free wall, can result in cardiogenic
shock. Conduction abnormalities (eg, atrioventricular blocks, sinus bradycardia) are also risk
factors.
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Many cases of cardiogenic shock occurring after acute coronary syndromes may be due to
medication administration. The use of beta blockers and angiotensin-converting enzyme (ACE)
inhibitors in acute coronary syndromes must be carefully timed and monitored.
In children, preceding viral infection may cause myocarditis. In addition, children and infants
may have unrecognized congenital structural heart defects that are well compensated until there
is a stressor. These etiologies plus toxic ingestions make up the 3 primary causes of
cardiogenic shock in children.
A systemic inflammatory response syndrometype mechanism has also been implicated in the
etiology of cardiogenic shock. Elevated levels of white blood cells, body temperature,
complement, interleukins, and C-reactive protein are often seen in large myocardial infarctions.
Similarly, inflammatory nitric oxide synthetase (iNOS) is also released in high levels during
myocardial stress. Nitric oxide production induced by iNOS may uncouple calcium metabolism
in the myocardium resulting in a stunned myocardium. Additionally, iNOS leads to the
expression of interleukins, which may themselves cause hypotension.
Systolic dysfunction
Ischemia/MI
Global hypoxemia
Valvular disease
Myocardial depressant drugs - Eg, beta blockers, calcium channel blockers, and
antiarrhythmics
Myocardial contusion
Respiratory acidosis
Metabolic derangements - Eg, acidosis, hypophosphatemia, and hypocalcemia
Severe myocarditis
End-stage cardiomyopathy - Including valvular causes
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Diastolic dysfunction
Increased left ventricular diastolic chamber stiffness contributes to cardiogenic shock during
cardiac ischemia, as well as in the late stages of hypovolemic shock and septic shock. Increased
diastolic dysfunction is particularly detrimental when systolic contractility is also depressed.
The causes of cardiogenic shock due primarily to diastolic dysfunction can be summarized as
follows:
Ischemia
Ventricular hypertrophy
Restrictive cardiomyopathy
Prolonged hypovolemic or septic shock
Ventricular interdependence
External compression by pericardial tamponade
Increased afterload, which can impair cardiac function, can be caused by the following:
Aortic stenosis
Hypertrophic cardiomyopathy
Dynamic aortic outflow tract obstruction
Coarctation of the aorta
Malignant hypertension
Valvular dysfunction may immediately lead to cardiogenic shock or may aggravate other
etiologies of shock. Acute mitral regurgitation secondary to papillary muscle rupture or
dysfunction is caused by ischemic injury. Rarely, acute obstruction of the mitral valve by a left
atrial thrombus may result in cardiogenic shock by means of severely decreased cardiac output.
Aortic and mitral regurgitation reduce forward flow, raise end-diastolic pressure, and aggravate
shock associated with other etiologies.
Valvular and structural abnormalities associated with cardiogenic shock include the following:
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Mitral stenosis
Endocarditis
Mitral aortic regurgitation
Obstruction due to atrial myxoma or thrombus
Papillary muscle dysfunction or rupture
Ruptured septum or free wall arrhythmias
Tamponade
Decreased contractility
Afterload increase associated with right ventricular failure can result from the following:
Pulmonary embolism
Pulmonary vascular disease - Eg, pulmonary arterial hypertension and veno-occlusive
disease
Hypoxic pulmonary vasoconstriction
Peak end-expiratory pressure
High alveolar pressure
Acute respiratory distress syndrome
Pulmonary fibrosis
Sleep disordered breathing
Chronic obstructive pulmonary disease
Arrhythmias
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Epidemiology
International occurrence
Race-stratified mortality rates from cardiogenic shock are as follows (race-based mortality
differences disappear with revascularization):
Hispanics - 74%
African Americans - 65%
Whites - 56%
Asians/others - 41%
The overall incidence of cardiogenic shock is higher in men than in women, with females
accounting for 42% of patients with cardiogenic shock. This difference results from the
increased prevalence of coronary artery disease in males. However, a higher percentage of
female patients with MI develop cardiogenic shock than do males with MI.
Median age for cardiogenic shock mirrors the bimodal distribution of disease. For adults, the
median age ranges from 65-66 years. For children, cardiogenic shock presents as a
consequence of fulminant myocarditis or congenital heart disease.
Prognosis
Cardiogenic shock is the leading cause of death in acute myocardial infarction (MI). In the
absence of aggressive, highly experienced technical care, mortality rates among patients with
cardiogenic shock are exceedingly high (up to 70-90%). The key to achieving a good outcome
is rapid diagnosis, prompt supportive therapy, and expeditious coronary artery
revascularization in patients with myocardial ischemia and infarction.
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Cardiopulmonary arrest
Dysrhythmia
Renal failure
Multisystem organ failure
Ventricular aneurysm
Thromboembolic sequelae
Stroke
Death
The following predictors of mortality were identified from the Global Utilization of
Streptokinase and Tissue-Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I)
trial :
Increasing age
Prior MI
Altered sensorium
Cold, clammy skin
Oliguria
Echocardiographic findings such as left ventricular ejection fraction and mitral regurgitation
are independent predictors of mortality. An ejection fraction of less than 28% is associated
with a survival rate of 24% at 1 year, compared with a survival rate of 56% with a higher
ejection fraction. Moderate or severe mitral regurgitation was found to be associated with a
1-year survival rate of 31%, compared with a survival rate of 58% in patients with no
regurgitation.
Outcomes in cardiogenic shock significantly improve only when rapid revascularization can be
achieved. The SHOCK (Should We Emergently Revascularize Occluded Coronaries for
Cardiogenic Shock?) trial demonstrated that overall mortality when revascularization occurs is
38%.When rapid revascularization is not attempted, mortality rates approach 70%. Rates vary
depending on the procedure (eg, percutaneous transluminal coronary angioplasty, stent
placement, thrombolytic therapy).
Physical Examination
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Patients in shock usually appear ashen or cyanotic and have cool skin and mottled
extremities
Peripheral pulses are rapid and faint and may be irregular if arrhythmias are present
Jugular venous distention and crackles in the lungs are usually (but not always) present;
peripheral edema also may be present.
Heart sounds are usually distant, and third and fourth heart sounds may be present
The pulse pressure may be low, and patients are usually tachycardic
Patients show signs of hypoperfusion, such as altered mental status and decreased urine
output
A systolic murmur is generally heard in patients with acute mitral regurgitation or ventricular
septal rupture. The associated parasternal thrill indicates the presence of a ventricular septal
defect, whereas the murmur of mitral regurgitation may be limited to early systole.
The systolic murmur, which becomes louder upon Valsalva and prompt standing, suggests
hypertrophic obstructive cardiomyopathy (idiopathic hypertropic subaortic stenosis).
Diagnostic Considerations
Conditions to consider in the differential diagnosis of cardiogenic shock include the following:
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Right ventricular infarction occurs in up to 30% of patients with inferior myocardial infarction
(MI) and becomes hemodynamically unstable in 10% of these patients. The diagnosis is made
by identifying an ST-segment elevation in the right precordial leads (V3 or V4 R) and/or typical
hemodynamic findings after right heart catheterization. These are elevated right atrial and right
ventricular end-diastolic pressures with normal to low pulmonary artery wedge pressure and
low cardiac output.
Echocardiography findings can also be very helpful in the diagnosis of right ventricular
infarction. Patients with cardiogenic shock due to this condition have a better prognosis than
do patients when compared to those with cardiogenic shock due to left ventricular systolic
failure.
Regarding the management of cardiogenic shock due to right ventricular infarction, supportive
therapy begins with the restoration and maintenance of right ventricular preload with fluid
administration. However, excessive fluid resuscitation may compromise left ventricular filling
by introducing an interventricular septal shift.
Inotropic therapy with dobutamine may be effective in increasing cardiac output in patients
with right ventricular infarction. Maintenance of systemic arterial pressure in order to maintain
adequate coronary artery perfusion may require vasoconstricting agents, such as
norepinephrine. In unstable patients, an intra-aortic balloon pump (IABP) may be useful for
ensuring adequate blood supply to the already compromised right ventricle.
Acute mitral regurgitation is usually associated with inferior MI due to ischemia or infarction
of the papillary muscle. It occurs in approximately 1% of MIs, and posteromedial papillary
muscle is involved more frequently than anterolateral muscle. Acute mitral regurgitation
usually happens 2-7 days following acute MI and manifests with an abrupt onset of pulmonary
edema, hypotension, and cardiogenic shock.
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Doppler study can be used to document the severity of mitral regurgitation. Right heart
catheterization is often required for stabilizing the patient. Tall V waves identified on
pulmonary arterial and wedge pressure waveforms indicate acute mitral regurgitation. However,
the diagnosis must be confirmed based on echocardiography or left ventriculography findings
before definitive therapy or surgery is initiated.
Cardiac rupture
Rupture of the free wall of the left ventricle occurs within 2 weeks of the MI and may occur
within the first 24 hours. The rupture may involve the anterior, posterior, or lateral wall of the
ventricle.
Cardiac rupture often presents as sudden cardiac death. Premortem symptoms include chest
pain, agitation, tachycardia, and hypotension. This diagnosis should be considered in patients
with electromechanical dissociation who have a history of anginal pain. Patients rarely, if ever,
survive cardiac rupture.
Approximately 1-3% of acute MIs are associated with ventricular septal rupture. Most septal
ruptures occur within the week following MI. Patients with acute ventricular septal rupture
develop acute heart failure and/or cardiogenic shock, with physical findings of a harsh
holosystolic murmur and left parasternal thrill.
Rapid stabilization using an IABP and pharmacologic measures, followed by emergent surgical
repair, is lifesaving. The timing of surgical intervention is controversial, but most experts
suggest operative repair within 48 hours of the rupture.
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Myocardial dysfunction may vary from mild to severe and may lead to cardiogenic shock. For
patients in cardiogenic shock, cardiovascular support with inotropic agents may be required
until recovery, which generally occurs after the underlying disease process resolves.
Differential Diagnoses
Myocardial Infarction
Myocardial Ischemia
Myocardial Rupture
Myocarditis
Pulmonary Edema, Cardiogenic
Pulmonary Embolism
Sepsis, Bacterial
Septic Shock
Shock, Distributive
Shock, Hemorrhagic
Initial management includes fluid resuscitation to correct hypovolemia and hypotension, unless
pulmonary edema is present. Central venous and arterial lines are often required. Swan-Ganz
catheterization and continuous percutaneous oximetry are routine.
Oxygenation and airway protection are critical; intubation and mechanical ventilation are
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commonly required. However, although positive pressure ventilation may improve oxygenation,
it may also compromise venous return, preload, to the heart. In any event, the patient should be
treated with high-flow oxygen. Studies in patients with acute cardiogenic pulmonary edema
have shown noninvasive ventilation to improve hemodynamics and reduce the intubation rate.
Mortality is, however, unaffected.
Pharmacologic therapy
Patients with myocardial infarction (MI) or acute coronary syndrome are given aspirin and
heparin. Both of these medications have been shown to be effective in reducing mortality in
separate studies. Before initiating therapy, however, care should be taken to ensure that the
patient does not have a myocardial wall rupture that is amenable to surgery.
The glycoprotein IIb/IIIa inhibitors improve the outcome of patients with nonST-segment
elevation acute coronary syndrome (NSTACS). They have been found to reduce recurrent MI
following percutaneous coronary intervention (PCI) and in cardiogenic shock.
Hemodynamic Support
Dopamine, norepinephrine, and epinephrine are vasoconstricting drugs that help to maintain
adequate blood pressure during life-threatening hypotension and help to preserve perfusion
pressure for optimizing flow in various organs. The mean blood pressure required for adequate
splanchnic and renal perfusion (mean arterial pressure [MAP] of 60 or 65 mm Hg) is based on
clinical indices of organ function.
In patients with inadequate tissue perfusion and adequate intravascular volume, initiation of
inotropic and/or vasopressor drug therapy may be necessary. Dopamine increases myocardial
contractility and supports the blood pressure; however, it may increase myocardial oxygen
demand. Dobutamine may be preferable if the systolic blood pressure is higher than 80 mm Hg;
it has the advantage of not affecting myocardial oxygen demand as much as dopamine does.
However, the resulting tachycardia may preclude the use of this inotropic agent in some
patients.
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Dopamine is usually initiated at a rate of 5-10 mcg/kg/min intravenously, and the infusion rate
is adjusted according to the blood pressure and other hemodynamic parameters. Often, patients
may require high doses of dopamine (as much as 20 mcg/kg/min).
If the patient remains hypotensive despite moderate doses of dopamine, a direct vasoconstrictor
(eg, norepinephrine) should be started at a dose of 0.5 mcg/kg/min and titrated to maintain an
MAP of 60 mm Hg. The potent vasoconstrictors (eg, norepinephrine) have traditionally been
avoided because of their adverse effects on cardiac output and renal perfusion.
Dopamine
Norepinephrine
The dose of norepinephrine may vary from 0.2-1.5 mcg/kg/min, and large doses, as high as 3.3
mcg/kg/min, have been used because of the alpha-receptor down-regulation in persons with
sepsis.
Epinephrine
Administration of this agent is associated with an increase in systemic and regional lactate
concentrations. The use of epinephrine is recommended only in patients who are unresponsive
to traditional agents. The undesirable effects are an increase in lactate concentration, a
potential to produce myocardial ischemia, the development of arrhythmias, and a reduction in
splanchnic flow.
Dobutamine
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In the setting of acute myocardial infarction (MI), dobutamine use could increase the size of
the infarct because of the increase in myocardial oxygen consumption that may ensue. In
general, avoid dobutamine in patients with moderate or severe hypotension (eg, systolic blood
pressure < 80 mm Hg) because of the peripheral vasodilation.
Phosphodiesterase inhibitors
PDIs are beneficial in persons with cardiac pump failure, but they may require concomitant
vasopressor administration. Unlike catecholamine inotropes, these drugs are not dependent on
adrenoreceptor activity; therefore, patients are less likely to develop tolerance to these
medications.
Thrombolytic Therapy
Although thrombolytic therapy (TT) reduces mortality rates in patients with acute myocardial
infarction (MI), its benefits for patients with cardiogenic shock secondary to MI are
disappointing. When used early in the course of MI, TT reduces the likelihood of subsequent
development of cardiogenic shock after the initial event.
In the Gruppo Italiano Per lo Studio Della Streptokinase Nell'Infarto Miocardio trial, 30-day
mortality rates were 69.9% in patients with cardiogenic shock who received streptokinase,
compared to 70.1% in patients who received a placebo.
Similarly, other studies employing a tissue plasminogen activator did not show reductions in
mortality rates from cardiogenic shock. Lower rates of reperfusion of the infarct-related artery
in patients with cardiogenic shock may help to explain the disappointing results from TT.
Other reasons for the decreased efficacy of TT are the existence of hemodynamic, mechanical,
and metabolic causes of cardiogenic shock that are unaffected by TT.
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The use of the IABP reduces systolic left ventricular afterload and augments diastolic coronary
perfusion pressure, thereby increasing cardiac output and improving coronary artery blood
flow. The IABP is effective for the initial stabilization of patients with cardiogenic shock.
However, an IABP is not definitive therapy; the IABP stabilizes patients so that definitive
diagnostic and therapeutic interventions can be performed.[18, 19]
The IABP also may be a useful adjunct to thrombolysis for initial stabilization and transfer of
patients to a tertiary care facility. Some studies have shown lower mortality rates in patients
with myocardial infarction (MI) and cardiogenic shock treated with an IABP and subsequent
revascularization, as previously mentioned.
Complications may be documented in up to 30% of patients who undergo IABP therapy; these
relate primarily to local vascular problems, embolism, infection, and hemolysis.
The impact of treatment with an IABP on long-term survival is controversial and depends on
the patients hemodynamic status and the etiology of the cardiogenic shock. Patient selection is
the key issue; inserting the IABP early, rather than waiting until full-blown cardiogenic shock
has developed, may result in clinical benefit.
Ramanathan et al found that rapid and complete reversal of systemic hypoperfusion with IABP
counterpulsation in the SHOCK trial and SHOCK registry was independently associated with
improved inhospital, 30-day, and 1-year survival, regardless of early revascularization. This
suggests that complete reversal of systemic hypoperfusion with IABP counterpulsation is an
important early prognostic feature.
In the IABP-SHOCK II study, 600 patients with cardiogenic shock complicating acute
myocardial infarction were randomized to intraaortic balloon counterpulsation or no intraaortic
balloon counterpulsation. All patients were expected to undergo early revascularization. Use of
intraaortic balloon counterpulsation did not significantly reduce 30-day mortality in these
patients.
In recent years, left ventricular assist devices (LVADs) capable of providing complete
short-term hemodynamic support have been developed. The application of LVAD during
reperfusion, after acute coronary occlusion, causes reduction of the left ventricular preload,
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increases regional myocardial blood flow and lactate extraction, and improves general cardiac
function. The LVAD makes it possible to maintain the collateral blood flow as a result of
maintaining the cardiac output and aortic pressure, keeping wall tension low and reducing the
extent of microvascular reperfusion injury.
A pooled analysis from 17 studies showed that the mean age of this group of patients with
LVADs was 59.5 4.5 years and that mean support duration was 146.2 60.2 hours. In 78.5%
of patients (range, 53.8-100%), adjunctive reperfusion therapy, mainly percutaneous
transluminal coronary angioplasty (PTCA), was used. Mean weaning and survival rates were
58.5% (range, 46-75%) and 40% (range, 29-58%), respectively.
In any case, comparing studies is difficult because important data are usually missing, mean age
of patients were different, and time to treatment is not standardized. Hemodynamic
presentation seems to be worse compared with data reported in the SHOCK trial, with lower
cardiac index, lower systolic aortic pressure, and higher serum lactates. Taking these
considerations into account, LVAD support seems to give no survival improvement in patients
with cardiogenic shock complicating acute myocardial infarction (MI), compared with early
reperfusion alone or in combination with IABP.
However, LVADs as a bridging option for patients with cardiogenic shock must be considered
cautiously and must be avoided in patients who are unlikely to survive or are not likely to be
transplant candidates. Further investigations are required to better define indications, support
modalities, and outcomes.
The indications for insertion of a ventricular assist device are controversial. Such an aggressive
approach to support the circulatory system in cardiogenic shock is appropriate (1) after the
failure of medical treatment and an IABP, (2) when the cause of cardiogenic shock is
potentially reversible, or (3) if the device can be used as a bridging option.
The retrospective and prospective data favor aggressive mechanical revascularization in patients
with cardiogenic shock secondary to myocardial infarction (MI).
Reestablishing blood flow in the infarct-related artery may improve left ventricular function
and survival following MI. In acute MI, studies show that percutaneous transluminal coronary
angioplasty (PTCA) can achieve adequate flow in 80-90% of patients, compared with 50-60%
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Several retrospective clinical trials have shown that patients with cardiogenic shock due to
myocardial ischemia benefitted (reduction in 30d mortality rates) when treated with
angioplasty. A study of direct (primary) PTCA in patients with cardiogenic shock reported
lower mortality rates in patients treated with angioplasty combined with the use of stents than
in patients treat with medical therapy.
Critical left main artery disease and 3-vessel coronary artery disease are common findings in
patients who develop cardiogenic shock. The potential contribution of ischemia in the
noninfarcted zone contributes to the deterioration of already compromised myocardial
function.
Coronary artery bypass grafting (CABG) in the setting of cardiogenic shock is generally
associated with high surgical morbidity and mortality rates. Because the results of
percutaneous interventions can be favorable, routine bypass surgery is often discouraged for
these patients.
REFERENCES
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4. Zink KA, Sambasivan CN, Holcomb JB, Chisholm G, Schreiber MA. A high ratio
of plasma and platelets to packed red blood cells in the first 6 hours of massive
transfusion improves outcomes in a large multicenter study. Am J Surg. May
2009;197(5):565-70; discussion 570.
5. http://emedicine.medscape.com/article/760145-followup#showall
6. http://emedicine.medscape.com/article/827930-overview#showall
7. National Center for Injury Control and Prevention. Ten Leading Causes of Death
by age group. 2004. Center for Disease Control and Prevention;
8. Tsang BD, Panacek EA, Brant WE, Wisner DH. Effect of oral contrast
administration for abdominal computed tomography in the evaluation of acute
blunt trauma. Ann Emerg Med. Jul 1997;30(1):7-13.
9. Ward KR, Ivatury RR, Barbee RW, Terner J, Pittman R, Filho IP. Near infrared
spectroscopy for evaluation of the trauma patient: a technology review.
Resuscitation. Jan 2006;68(1):27-44.
10. Gonzalez EA, Moore FA, Holcomb JB, Miller CC, Kozar RA, Todd SR.
Fresh frozen plasma should be given earlier to patients requiring massive
transfusion. J Trauma. Jan 2007;62(1):112-9.
11. Armstrong, D.J. (2004) "Shock". In: Alexander, M.F., Fawcett, J.N.,
Runciman, P.J. Nursing Practice. Hospital and Home. The Adult.(2nd
edition). Edinburgh: Churchill Livingstone.
12. Collins, T. (2000) "Understanding Shock". Nursing Standard. Vol. 14(49),
pp. 3541.
13. Cuthbertson, B.H. and Webster, N.R. (1995) "Nitric oxide in critical care
medicine". British Journal of Hospital Medicine. Vol. 54(11), pp. 579582.
14. Emerson, William R.: Shock: A Universal Malady (Prenatal and Perinatal
Origins of Suffering), excerpted from Origins of Adversity: the Treatment of
Prenatal and Perinatal Shock, Petaluma: Emerson Training Seminars
15. Hand, H. (2001) "Shock". Nursing Standard. Vol. 15(48), pp. 4555.
16. Hobler, K, Napadono,R, "Tolerance of Swine to Acute Blood Volume
Deficits", Journal of Trauma, 1974, August 14 (8):7168.
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17. Irwin, R.S. and Rippe, J.M. (2003) Irwin and Rippe's Intensive Care
Medicine (5th edition). Boston: Lippincott, Williams and Wilkins
18. Irwin, R.S., Rippe, J.M., Curley, F.J., Heard, S.O. (1997) Procedures and
Techniques in Intensive Care Medicine (3rd edition). Boston: Lippincott,
Williams and Wilkins.
19. Ledingham, I.M. and Ramsey, G. (1986) "Shock". British Journal of
Anaesthesia Vol. 58, pp. 169189.
20. Marino, P. (1997) The ICU Book. (2nd edition). Philadelphia: Lippincott,
Williams and Wilkins.
21. Porth, C.M. (2005) Pathophysiology: Concepts of Altered Health States.
(7th edition). Philadelphia: Lippincott, Williams and Wilkins
22. Sheppard, M. (2005) Principles and practice of high dependency
nursing. Edinburgh: Bailliere Tindall.
23. Society of Critical Care Medicine. Fundamental Critical Care Support, A
standardized curriculum of critical care. SSCM Illinois, 2001.
24. Tortora, G.J. (2005) Principles of anatomy and physiology New Jersey:
John Wiley, Inc
..
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a. heart cavity 3%
b. arteries 15%
c. capillaries 12%
d. venous system 70%
Among the natural vasoconstrictors (agents, which cause constriction of the blood
vessel) are epinephrine, norepinephrine, serotonin, angiotensin II. Stress enhances the secretion
of cathecholamines, their blood concentration increases and arterioles constrict. Spasm of the
arterioles is the basis of blood flow centralization: peripheral flow is disregarded in order to
provide brain with the oxygenated blood as long as possible. To the group
of vasodilatators (agents, which provide dilatation of the vessels) belong acid metabolites
(lactate, pyruvate, adenylic acid, inosinic acid), bradykinin, acetylcholine, different medicines
(neuroleptics, -adrenergic antagonists, peripheral vasodilatators, ganglionic blocking agents,
etc.), some exogenous poisons. All of them cause blood flow decentralization: opening of
arterioles and distribution of the blood from central vessels to the capillary bed.
Capillaries are the interweaving network of the smallest body vessels with the general
length of 90-100 thousands of kilometers. However simultaneously work only 20-25% of them.
They provide metabolic exchange bringing oxygen and nutrients to the tissues and take back
wastes of metabolism. Periodically, every 30-40 seconds one of them get closed and others
open (vasomotion effect). Capillaries contain 12% of the whole circulating blood volume, but
different pathological conditions can increase this amount even 3 and more times.
Used blood from the capillaries flows to the venous system. Veins are the blood
reservoir, which contains 70% of the total circulating blood volume. Unlike arteries they are
capable of volume control and thus they influence the amount of blood, which returns to the
heart.
The most important haemodynamic index of venous system is central venous pressure.
CVP represents the pressure which blood causes to the walls of cava veins and right atrium.
This parameter is an integral index of circulating blood volume, systemic vascular resistance
and pump function of the heart. It can be measure with a special device called
phlebotonometer (pic. 4.9) or with a usual infusion set and a ruler. Normally CVP measured
from the sternum point is 0-14 cm H2O and from midaxillary line is 8-15 cm H2O.
Central venous pressure decreases (sometimes even to negative) in case of:
- blood loss
- excessive water loss (dehydration)
- distributive shock (decrease of peripheral resistance due to venous and arterial
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dilatation)
In those conditions decreases volume of blood returning to the heart and thus suffers
cardiac output. In case of negative CVP cardiac arrest is highly probable.
MAP defines the level of pressure necessary for the metabolic exchange in the tissues.
Its measurement allows the evaluation of tissue perfusion level.
Blood pressure depends on different factors, but the most important are cardiac output
and vascular resistance (mostly arterioles). This dependence is direct, thus you can increase
blood pressure using:
- infusion of vasoconstrictors - solutions of
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epinephrine, phenylephrine (mesaton), etc. (they will increase the vascular resistance);
- infusion of hydroxyethyl starch solutions or saline (they will increase
circulating blood volume)
- infusion of cardiac glycosides or other medicine which stimulate
myocardium
General volume of blood in the body of a healthy adult is nearly 7% from the body
weight: 70 ml per kilogram for male and 65 mil per kilogram of body weight for female. Of
course circulating blood volume is lower, because part of blood is out of metabolic processes
as a reserve. CBV can be measured with the infusion of coloring substance to the blood flow
(Evans blue, polyglucin) and later evaluation of its dissolution degree.
Therefore measurement of CVP, BP, cardiac output and circulating blood volume allow
to evaluate condition of circulation system of the patients and to provide adequate correction.
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The reasons of the failure vary greatly: mechanic injuries, blood loss, burns,
dehydration, exogenous and endogenous intoxications, immediate hypersensitivity reaction,
ischemic heart disease, neural and humoral regulation disorders of vascular tone.
Acute cardiac failure is a disorder of heart pumping action. It develops due to primary
heart problems or secondary, under the influence of extracardiac factors such as infection or
intoxication. There are two types of heart failure: left-sided and right-sided.
Left-sided heart failure is an inability of left ventricle to pump blood from the
pulmonary circuit to the systemic circuit. The most common reasons of it are myocardial
infarction, mitral insufficiency, left AV valve stenosis, aortic valve stenosis, aortal
insufficiency, hypertonic disease, coronary sclerosis, acute pneumonia.
Coronary circulation is possible only during the diastole and in those conditions every
violation of coronary passability decreases cardiac output. This way during the systole part of
the blood is not injected into aorta, but stays in the left ventricle. Diastolic pressure in the left
ventricle increases and blood is literally forced to stagnate in the left atrium. At the same time
right ventricle functions normally and continues to pump usual amounts of blood to the
pulmonary circuit. Thus hydrostatic pressure in the vessels of pulmonary circulation increases,
fluid part of the blood moves first to the lung tissue and then, through alveolar-capillary
membrane, to the alveolar lumen.
Clinically pulmonary edema begins with dyspnea (during physical activity or rest).
Later attacks of dyspnea are connected with persistent cough with white or pink blood-tinged
phlegm. During the attack patient tries to sit as in this position breathing is easier. This
condition is called heart asthma. When hydrostatic pressure is over 150-200 mm Hg, fluid
part of blood moves to the alveolar lumen causing development of pulmonary edema.
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Pulmonary edema can be also divided according to the blood pressure level: the one with
elevated pressure is caused by a hypertonic disease, aorta valve insufficiency or disorders of
cerebral perfusion; another one is caused by total myocardial infarction, acute inflammation of
myocardial muscle, terminal valve defects,severe pneumonia and is characterized with normal
or low blood pressure.
Immediate aid
- make sure patient is sitting with his legs down (orthopnea)
- provide oxygenation through nasal catheter (before placing oil it with
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glycerin, insert it to the depth of 10-12 cm distance from the wing of the nose to
auricle) or face mask. Do not use Vaseline, because it can burn in atmosphere with high
concentration of oxygen.
However if catheter is not deep enough patient will suffer from an unpleasant
burning feeling, because oxygen flow will dry mucosa layer of the nasal cavity; also in
this situation concentration of oxygen will be lower than expected.
- put venous tourniquets on the limbs in order to reduce amount of blood
returning to heart: venous bed of limbs can reserve up to 1,7 liters of blood;
- constantly control heart and kidney activity (ECG, SaO2 , and blood
pressure are checked automatically trough the monitor; to control diuresisyou should
insert Foley catheter;
- catheterize central vein, because amount of infusions should be based on
central venous pressure;
- use medical defoamers if they are available (ethyl alcohol
or antiphomsylan solution) combined with oxygen inhalation
Scheme of oxygenation set connected to defoamer container
a. oxygen source (cylinder with oxygen)
b. tube with numerous holes sunk into container with defoamer
c. tube for humidified oxygen (its opening should be over the level of fluid);
d. patient
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mechanisms mobilization).
Stimulation of sympathetic nervous system - production of catecholamines and
other vasoactive substances by hypothalamus and adrenal glands are the universal response
of the body to the stress. Those mediators interact with the receptors of peripheral vessels
causing their constriction and at the same time theydilatate the vascular bed of
life-important organs. This is so called centralization of the flow: rational decrease of
blood flow in less important tissues (skin, organs of abdominal cavity, kidneys) in case of
aggressive external influence for protecting life itself (brain, heart, lungs).
However influence of shock agents (pain, hypovolemia, destroyed cells, toxic
metabolites), extended microcirculation violations (vascular spasm,microthrombosis and
sludge) and caused by them tissue ischemia lead to hypoxic affection and cellular death of
the internal organs. Further it can bring multiple organ dysfunction syndrome.
Collapse is a vascular failure. It occurs when body is not able to provide blood flow
according to the new level of its needs (either because reaction is not fast enough or
because sympathetic activation fails).Vascular bed volume and circulating blood volume are
disproportional: too much blood gets to the microcirculation vascular reserve and the
amount, which returns to the heart is not enough for the systemic needs (so called
decentralization of the blood flow). Cardiac output and blood pressure decrease, that
causes hypoperfusion of the central nervous system and thus unconsciousness and
life-threatening complications.
Collapse definition is a bit nominal, because if such reaction extends in time the
state of shock develops. Shock itself can equally run as a vascular failure or as a sudden
clinical death.
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- dehydration shock;
- burn shock;
- septic shock;
- anaphylactic shock;
- cardiogenic shock;
- exotoxic shock.
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Blood loss and tissue fluid loss decrease the subcutaneous turgor, eyeballs tone, blood
filling of the subcutaneous veins. Peripheral pulse is weak, rapid andthready; blood pressure
and central venous pressure are low. Hypotension and compensatory spasm of renal arteries
decreases urine output through reduction of the renal blood flow. This brings state of oliguria-
condition in which urine output is less than 0,5 ml per kilogram of body weight per hour.
In case of traumatic shock erectile and torpid phases are described. Erectile phase is
not obligatory: it begins during pre-hospital stage and doesnt last long (minutes). This phase
is characterized with agitation, restlessness and stimulation of all vital systems. Torpid phase is
much more dangerous, because patients suffer from CNS disorders and their lifesaving systems
are as close to breakdown as possible.
To calculate the actual blood loss and thus to know class of shock you can
use Allgower index (shock index).
It is a correlation between heart rate and systolic blood pressure:
AI = HR/ Psyst.
Normally its value is 0,5-0,7 (for example in case of HR 60 and Psyst 120 mm Hg it
will be 0,5). Shock conditions causes lowering of blood pressure which is compensated
through tachycardia and thus increase of shock index.
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This method of blood loss evaluation is simple and allows quick evaluation of blood
loss and its immediate adequate concentration of circulating blood volume. Perhaps you will
better understand those calculations using this example:
patient weights 80 kilograms, his blood pressure is 80/50 mm Hg, HR 120 per minute.
His perfect circulating blood volume is 70 ml per kilogram: 70*80=5600 ml.
SI= 120/80=1,5.
According to the table above he has 2 stage of shock and he lost nearly 30% (2 stage
means from 20% to 40%, lets take 30%) from his CBV. So you will have to compensate 30%
from 5 600 ml or: 5600*0,3=1680 ml of blood.
Until shock is not liquidated, even if the bleeding is stopped, lowering of CBL
continues (so called relative blood loss, caused by stagnation, aggregation and sequestration of
red blood cells in the microcirculation vessels).
During shock compensatory mechanisms of the organism try to fill the vascular bed
with whatever fluid they can; this includes water from intercellular space, which causes so
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called blood dilution. The last one is detected in laboratory tests, which show decrease of
blood concentration: subnormal indexes ofhematocrit, hemoglobin, red blood cells and
protein. This mechanism begins within first few minutes after the injury. However final
evaluation of blood concentration indexes is possible only 12-24 hours after the initial
trauma.
Profuse acute bleeding (over 30% of CBV during 1 hour) is life threatening. In case
of chronic anemia organism is used to hemoglobin deficiency and hemorrhagic lack of even
70% of red blood cells and 30% of plasma might be acceptable (of course it does not mean,
that you should not treat the bleeding or blood loss).
Immediate aid.
First hour of shock is called golden because of its prognostic value and great
therapeutic possibilities so dont waste even minute of it!
- first of all stop arterial bleeding (press artery to the bone, use special
devices like tourniquets or tamponade the wound); be careful with the time of
compression, because prolonged total block of blood flow will cause necrosis;
- constantly evaluate patients condition (pulse over peripheral and central
arteries, consciousness, airways patency, effectiveness of external breathing );
- if patient is unconscious and you cant control his airways all the time use
the recovery position (three-quarters prone position); be careful with the neck of the
patient if you suspect backbone injuries those patients should be placed in supine
position on the firm surface with immobilized neck; patients with pelvic fractures should
lay on back with flexed knees;
- immobilize injured limbs with standard splints or improvised material;
- put on the wounds aseptic dressings; bandage is all you need to stop
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capillary and venous bleeding; in case of pneumothorax use specialAsherman seal or just
a three-sided airtight dressing;
- use pain killers: either narcotic analgesics (1% promedol solution) or
non-steroidal anti-inflammatory drugs like 50% analgin solution (depends on the pain
intensity); patients with shock are unstable, so after giving of analgesics be very attentive
to the changes in patients condition, because pain was sympathetic system stimulator
and without it blood pressure will probably lower and respiratory center might be
inhibited; if you cant control the state of the patient (too many victims, dangerous
environment, transportation) try to use ketamine (2-3 ml of 5% solution, i/m) instead of
narcotic drugs: it has analgesic properties, however it will not influence blood pressure
or breathing (but to avoid hallucinations use it with 1-2 ml of 5% diazepam solution);
local anesthetic infiltration of tissues around the fracture also can be used to reduce
pain (10-20 ml of 0,5% Novocain solution);
Transfusion scheme for patients with blood loss (according to P. Brusov, 1997).
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Patient in critical condition with an urgent need of surgical treatment should be taken
to the operating room immediately: in their case intensive therapy of shock will be conducted
directly on the operating table during surgery (of course general anesthesia is necessary).
In case of every open wound take care about tetanus prevention
(antitetanic immunization according to the scheme).
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Water deficiency brings lowering of cardiac output, blood pressure and central venous
pressure (through decrease of blood volume returning to the heart, which leads to
compensatory adrenergic vasoconstriction).
Dehydration causes body weight loss, skin and mucosa dryness, decrease of
subcutaneous turgor and eyeballs tone, hypothermia, tachycardia, oliguria, thirst. While
dehydration progresses compensatory mechanisms weaken and central nervous system suffers:
patients become sluggish, confused; hallucinations, cramps and unconsciousness are also
possible. Laboratory tests show blood concentration.
One of the most important things in treatment of dehydrated patients is daily balance
of fluid: check it carefully trough measuring of daily received and lost fluids (food, infusions,
stool and urine output). In case of fever or tachypnea make necessary corrections. Balance
should be calculated every 12-24 hours (special paper forms make this easier).
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Burn shock.
Burn shock is a type of hypovolemic shock, caused by thermal or chemical agents.
It appears in adults in case if burns cover over10-15% of the body surface. Huge
plasma loss and pain stimulation of sympathetic nervous system bringhypovolemia, blood flow
centralization and low cardiac output syndrome.
At the beginning patients complain of pain, nausea, vomiting, and thirst. Erectile phase
of shock changes into torpid, central nervous system after stimulation becomes inhibited (stage
depends on burn surface). Breathing and heart rate are increased, blood pressure is decreased.
Undamaged skin is cold and mottled. If burning area covers airways asphyxia is highly
possible.
Laboratory tests show concentration of the blood.
Immediate aid.
As soon as possible eliminate thermal or chemical agent (cover the fire with wet tissue,
wash off chemicals with cold water). Generally use cold water (snow if you dont have an
alternative) as cooling agent (not oils, not other organic substances). Take of smoldering
clothes, cut them if necessary (dont try to take off something what is soldered with the skin
by fire). Put a sterile bandage on burn areas. You should use general principles of shock
treatment, including rule of 4catheters: central venous catheter, urinary catheter, stomach
probe and endotrachel tube or nasal catheter for oxygenation depending on condition of the
patient. Take care about the proper pain reliving: prescribe narcotic analgesics (2 ml of
2% promedol solution), neuroleptics (2-3 ml of 0,25% droperidol solution). Infusion therapy is
provided with crystalloids, colloids and glucose solutions (in the ratio 1:1:1 in case of mild
shock, 2:1:1 in case of severe shock). Constantly monitor condition of the patient: monitor
heart rate, blood pressure, central venous pressure and diuresis (make sure its not lower than
0,5 ml/kg per hour). When you suspect a thermal airways injury always intubate the patient:
you will not have much time in case if edema will bring asphyxia.
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Anaphylactic shock
Anaphylactic shock is a type of distributive shock, caused by allergen inducted
immediate hypersensitivity reaction.
Various factors can cause anaphylactic reaction: serums, antibiotics, blood
preparations, local anesthetics (Novocain), hypnotics (Sodium thiopental,
Diazepam), radiocontrast agents, etc. Among non-medical allergens most common are:
alimentary substances, chemical cleaning agents, cosmetics, insect poisons, fur, etc.
The main condition of anaphylactic reaction is presence of antibodies in
previously sensibilized organism. Antigen-antibody reaction reveals bioactive substances, such
as histamine, bradykinin, slow-reacting substance of anaphylaxis. Those mediators cause
vasodilatation and leakage of fluid from vessels into the tissues. The amount of blood returning
to the heart decreases greatly, cardiac output reduces and thus blood pressure is lowering until
the cardiac arrest appears (usually PEA).
Form of the shock depends on the time of reaction:
- fulminant form develops within 10 minutes;
- immediate form pre-shock phase continues 30-40 minutes;
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Septic shock
Septic shock is a type of distributive shock, caused by generalized reaction of the
organism to microorganisms and their toxins. Its etiology can be connected with
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gram-positive and gram-negative bacteria, rickettsia or fungi and any mucosa can be their
entrance (intestine, abdominal cavity, urinary tracts, woundsurface). Sepsis has its
terminology:
SIRS systemic inflammatory response syndrome is a systemic answer of
organism to the intensive stimuli (infection, injury, operation, etc.)
When the toxins get to the blood flow tissue macrophages answer their appearance
with production of cytokines. Cytokines are mediators of systemic inflammatory response;
they trigger a whole number of immune reactions (both humoral and cellular immune
response). This bring to circulation and microcirculation disorders and thus to
tissue hypoperfusion and tissue anoxemia. Lethality in this type of shock is 60-80%.
Disorders of circulation can be
both hyperdynamic and hypodynamic. Hyperdynamic syndrome is characterized with high
cardiac output and uninterrupted microcirculation. Hypodynamic reaction appears in case of
low cardiac output connected with high vascular resistance; during terminal phase of shock
vascular resistance drops drastically and hypotension becomes incurable.
Sepsis has its own terminology. We diagnose SIRS if two of the symptoms listed below
are present:
- fever over 38C or temperature less than 36C;
- heart rate over 90 pre minute;
- respiration rate over 20 per minute or PaCO2 < 32 mm HG;
- leucocytosis over 12*109 or less than 4*109 or more than 10% of young
forms
Sepsis itself we state if SIRS is combined with source of infection. Severe sepsis is a
sepsis connected with multiple organ dysfunction of two and more systems (for
example oliguria and encephalopathy).
Components of multiple organ failure are: septic encephalopathy, polyneuropathy of
terminal stages, acute respiratory distress-syndrome, septic shock, ileusand bacterial
translocation, renal failure, acute tubular necrosis, DIC syndrome.
Signs of tissue dysfunction:
- arterial hypoxemia (PaO2 / FiO2 <300);
- acute oliguria (diuresis less than 0,5 ml/kg per hour);
- creatinine concentration over 0,5 mg/dl;
- activated partial thromboplastin time over 60 seconds;
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- enteroparesis;
- thrombocytopenia (less than 100 *109 );
- hyperbilirubinemia (general bilirubin over 4 mg/dl or 70 mkmol/l).
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Cardiogenic shock.
Cardiogenic shock is a state of acute heart failure, caused by primary heart affection.
Usually it happens due to myocardial infarction: necrosis or heart rhythm violations influence
negatively pump function of the heart and low cardiac output syndrome appears. This situation
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is characterized with high central venous pressure, low blood pressure and compensatory
peripheral vascular spasm.
Myocardial infarction according to modern classification is a part of wider category of
acute coronary syndrome (together with unstable angina). It is divided into ST elevation MI and
non-ST elevation MI (with or without elevation of ST segment on ECG). Those clinical
syndromes are different forms of one pathological process: rapture of vulnerable atherosclerotic
plaque in coronary artery. Ruptured plaque is filled with blood and this way it blocks blood
flow in the artery (additionally affected vessel constricts and blood clot is formed in the place
of rupture).
Clinical picture.
Angina pectoris is a burning chest pain or a discomfort feeling, caused by myocardial
ischemia. There is also a possibility of referred pain in the jaw, one or both shoulders (usually
left), back, neck area or epigastrium. Some of the patients actually never complain of chest
pain, but give other pain and discomfort localizations. Unstable angina is suspected when pain
pattern changes into more severe, it occurs in rest or minimal exertion and lasts over 10
minutes.
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hours; normal values 22-66 mkg/l), MB fraction of creatine phosphokinase (rises during first
3-4 hours, maximal level within first 24-36 hours; normal value0-24 IU/l), lactate
dehydrogenase-1 (rises during first 8-10 hours, stays 8-10 days; normal value 240-480 IU/l,
LDH-1 is 15-25% of general LDH). There are different express-tests for infarction markers, in
many countries they are available even for ambulance service. Additional information can
give coagulogram, echocardioscopy (decrease of ejection
fraction, hypokinetic and akinetic areas). Chronography is very important for further treatment
tactic; it performed within first hours in case of ST-MI and 24 hours after non-ST-MI onset.
Intensive treatment.
In all cases of acute coronary syndrome are required:
morphine (1 ml , i/v, but dont forget to dilute it with saline and give it very slowly),
oxygen (can be provided through the mask, 6-8 l/min),
nitroglycerin (tablets or 1% solution i/v with blood pressure control),
aspirin (300 mg per os as soon as possible).
The main point of therapy during the first stage of infarction (the most acute) is
re-perfusion. After first 12 hours from the moment of pain onset risk of re-perfusion is
overwhelming its benefits. Thrombolytics do not provide reperfusion in all patients, however
they are dangerous because of haemorrhagic complications. So the choice we actually have
during first hours is percutaneous coronary intervention (in case if it is not slowing
re-perfusion).
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Schemes of thrombolysis
- streptokinase 250 000 U, diluted in 20 ml of saline, given during 30
minutes; then 100 000 U are given i/v during 24-48 hours;
- actilyse 15 mg in bolus, then 0,75 mg/kg during 30 minutes, later 0,5
mg/kg during 60 minutes;
- urokinase 4400 U/kg during 10 minutes, then 4400 U/kg/hour during
12-24 hours.
Relative contraindications to thrombolytic therapy are: early postoperative period,
recent injury or gastrointestinal bleeding, vascular cerebral pathology, hypertension with
systolic blood pressure over 180 mm Hg or diastolic pressure over 110 mm Hg, high probability
of left atrium clot (mitral stenosis with atrialfibrillation),
acute pericarditis, subacute bacterial endocarditis, functional disorder of coagulation system,
hepatic failure, pregnancy, diabetic hemorrhagic retinopathy, septic thrombophlebitis, patients,
who take warfarin constantly.
Absolute contraindications: previous usage of streptokinase (within 4 years);
streptococcus infection, active internal bleeding, state after cerebrovascularaccident, recent
cerebral or spinal operation, intracerebral aneurism.
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advancethe cannula. When You are sure, that catheter is in the vein, release the tourniquet and
flush the line with saline (connect the giving set with the cannula). Cover the insertion area
with special dressing or simply with the plaster. Make sure everything is working properly
(no extravasation signs, no blood in the giving set, quick infusion is possible) and access cant
be easily removed. In you notice, that growing oedema near the insertion place probably you
will have to make another i/v access, because this catheter should be removed and its place
should be bandaged in order to prevent further extravasation, i/v insertion of cardiac electrodes.
Central vein catheterization (subclavian vein)
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Ask the nurse or assistant to disinfect the punction area (swab with antiseptic solution
3 times). Wash your hands and put on sterile gloves according to general standards of aseptic.
Take the necessary equipment from the kit and position it on a sterile surface in a way you find
handy. Find the place of punction: palpate with the fingers of your right hand point between
the middle and medial third of the clavicle, 1-1,5 cm below it. Fill the 5 ml syringe with local
anesthetic and infiltrate the tissues around this point. Then take the needle from the set and
connect it to the syringe filled with saline. Fix the collar bone over the point of puncture with
the fingers of your left hand and perforate the skin, holding the hub firmly. Move forward
between collar bone and first rib, until you will feel the increase of resistance (fascia is lying
few centimeters deep). After this moment move forward the needle in the direction
of sternocostal articulation with continuous aspiration. When you will see the blood in the
barrel disconnect the syringe from the needle (close the lumen with the fingertip of your left
thumb to prevent air embolism) and insert carefully wire guide until the last of its marks.
Holding the wire withdraw the needle. Try not to make unnecessary movements, because needle
disconnection and wire insertion are the most uncertain steps of central
vein cannulation (accidentally you can loose the vein). If it is needed use dilators: thread
them over the wire and enlarge the entry site (use twisting movements pushing the dilator
forward). When you will find the entry wide enough to let the catheter through without much
resistance thread the catheter over the wire until the wire will exit the distal lumen of catheter
(grasp it there with your left hand). Continue moving the catheter forward (simultaneously pool
the wire out) until it will be at the mark your desire. Take out the wire completely and check
the placement of catheter by aspiration with the syringe. If you receive venous blood you can
flash the catheter with saline and connect giving set (or take blood samples, measure CVP or
infuse medicines). Dont forget to fix the external part of the catheter with the special dressing
or suture. After all this is done check the catheter placement with an X-ray (it should not end in
the right atrium).
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Control tests.
1. Choose the wrong statement:
A. venous vessels contain 5 times blood more than arterial
B. central venous pressure is normally 60-120 mm of water column
C. arterioles tone influences blood pressure
D. serotonin constricts vessels
E. in case of pulmonary edema, due to blood accumulation, central venous pressure
lowers.
2. If blood pressure is 80/40 mm of Mercury and the heart rate is 120 per minute,
what will be the shock index?
A. could not be calculated, as we dont know the blood loss
B. (80+40)/120=1
C. 120/80=1,5
D.80/120=0,67
E.120/40=3
3. Which statement is wrong in case of traumatic shock?
A. shock index is very low
B. low cardiac output occurs
C. centralization of the circulation develops
D. central venous pressure lowers
E. erythrocytes begin to stick together
4. Choose the best treatment of fulminant anaphylactic shock:
A. dimedrol, prednisolone, cordiamin - intravenously
B. atropine, pipolfen, prednisolone - ointravenously
C. poliglukin, calcium chloride, hydrocortisone - intravenously
D. adrenalin, polyglucin, prednisolone - intravenously
E. local usage of adrenalin in the place of injection, antihistamine medications
intravenously
5. In case of cardiogenic shock you will not observe:
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Task 1.
Patience, the patience of 44 years, has the central venous pressure 100 mm of water
column What are probable reasons of such value? Describe the therapy.
Task 2.
During the class students of group N were checking blood volume. Results were
lost. Calculate blood volume according to the parameters below:
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Water balance is regulated through complicated, but reliable mechanisms. Control over
water and electrolytes excretion is realized by osmotic receptors of posterior hypothalamus,
volume receptors of the atrial walls, baroreceptors of carotid sinus, juxtaglomerular apparatus
of the kidneys and adrenal cortical cells.
When there is a water deficiency or electrolytes excess (sodium, chlorine) thirst
appears and this makes us drink water. At the same time posterior pituitary
produces antidiuretic hormone, which decreases urine output. Adrenals reveal into the blood
flow aldosterone, which stimulates reabsorption of sodium ions in the tubules and thus also
decreases diuresis (due to osmosis laws water will move to the more concentrated solution).
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Dehydration signs: weight loss, decrease of skin turgor and eyeballs tone, dry skin and
mucous membranes; low central venous pressure, cardiac output and blood pressure (collapse
is possible); decreased urine output and peripheral veins tone; capillary refill over 2 seconds
(microcirculation disorders) and low skin temperature; intracellular dehydration is
characterized with thirst and consciousness disorders. Laboratory tests show blood
concentration: hematocrit, hemoglobinconcentration, protein level and red blood cells
concentration increase.
Overhydration appears in case of:
- excessive water consumption, inadequate infusion therapy;
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Isotonic dehydration is caused by equal loss of electrolytes and fluid from the
extracellular space (without cellular disorders).Blood tests showhemoconcentration; sodium
level and osmotic concentration are normal.
To treat this type of water imbalance use normal saline solution, Ringer solution,
glucose-saline solutions, etc.. The volumes of infusions can be calculated according to the
formula:
VH2O= 0,2*BW* (Htp-0,4)/0,4 ,
Hypertonic dehydration is caused by mostly water loss: first it appears in the vascular
bed, than in the cells. Laboratory tests show hemoconcentration: elevated levels of proteins, red
blood cells, hematocrit. Plasma sodium is over 155 mmol/l and osmotic concentration increases
over 310 mOsm/l.
Intensive treatment: if there is no vomiting allow patients to drink. Intravenously give
0,45% saline solution and 2,5 % glucose solution, mixed with insulin. The volume of infusions
is calculated according to the formula:
VH2O=0,6*BW (Nap -140)/140,
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To treat hypochloremia use normal saline (1000 ml contains 154 mmol of chlorine) or
5,8% sodium chlorine solution (1 ml contains 1 mmol of chlorine). The choice of solution
depends on the osmotic concentration of the plasma.
Hyperchloremia is a condition of increased chlorine concentration (over 107 mmol/l).
Intensive therapy of this state includes treatment of the disease, which caused it
(decompensated heart failure, hyperchloremic diabetes insipidus, glomerulonephritis). You can
also use glucose, albumin solutions and dialysis.
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Control tasks.
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Task 1.
Calculate the total body water volume and its extracellular and intracellular volumes of
the Patience, the patient of 48 years and body weight 88 kg.
Task 2.
Patience, the patient of 23 with body weight 70 kg has sodium level 152 mmol/l
and hematocrit 0,49 l/l. Name the type of water balance disorder.
Task 3.
Patience, the patient of 54 with body weight 76 kg has sodium level 128 mmol/l.
Calculate the volume of saline and 7,5% sodium chloride solution necessary for the treatment
of this condition.
Task 4.
Patience, the patient of 60 with body weight 60 kg has sodium level 140 mmol/l
and hematocrit 0,55 l/l. Name the type of disorder and prescribe infusion therapy.
Task 5.
Patience, the patient of 42 with body weight 80 kg has potassium level 2,6 mmol/l.
Calculate the volume of 4% potassium chloride solution necessary for treatment of this
condition.
Task 6.
Patience, the patient of 33 with body weight 67 kg and diagnosis gastric ulcer,
complicated with pylorostenosis has potassium concentration 3 mmol/l, chlorine
concentration 88 mmol/l. pH 7,49, pCO2a 42 mm Hg, BE + 10 mmol/l. Name the type of
disorder.
Task 7.
Patience, the patient of 50 with body weight 75 kg, was transported to the admission
unit of the hospital with: unconsciousness, cyanotic skin, low blood pressure, shallow
breathing. Blood tests show: pH 7,18, pCO2a 78 mm Hg, pO2A 57 mm Hg, BE -4,2 mmol/l.
Name the type of acid-base disorder and prescribe treatment.
Task 8.
Patience, the patient with body weight 62 kg and renal insufficiency has: potassium
concentration 5,2 mmol/l, sodium concentration 130 mmol/l, calcium concentration
1,5 mmol/l, pH 7,22, pCO2a 34 mm Hg, BE -9,2 mmol/l. Name the type of disorder.
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In medicine, systemic inflammatory response syndrome (SIRS) is an inflammatory state affecting the whole
body, frequently in response of the immune system to infection, but not necessarily so. It is related to sepsis, a
condition in which individuals both meet criteria for SIRS and have a known or highly suspected infection.
The latest finding shows that SIRS in trauma patients may be caused by immune reaction to mitochondria
massively released into bloodstream from dying cells at the site of injury. [1]Contents [hide]
1 Classification
2 Definition
3 Complications
4 Causes
5 Treatment
6 See also
7 References
[edit]
Classification
SIRS is a serious condition related to systemic inflammation, organ dysfunction, and organ failure. It is a
subset of cytokine storm, in which there is abnormal regulation of various cytokines.[citation needed] SIRS is
also closely related to sepsis, in which patients satisfy criteria for SIRS and have a suspected or proven
infection.[2][3][4]
[edit]
Definition
SIRS was first described by Dr. Nelson, of the University of Toronto, at the Nordic Micro Circulation meeting
in Geilo, Norway in February of 1983. The intent of creating an encompassing definition was to bring together
the multiple etiologies of post episode organ dysfunction (fibrin deposition, platelet aggregation,
coagulopathies, leukocyte lysosomal release) into a family of negatively synergistic responses to injury and/or
infection which can collectively lead to micro circulatory dysfunction. The implication of such a definition
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suggested that recognition of the activation of one of the above noted humoral pathways suggests that
additional processes are also active. The aggregate of such pathophysiology would lead to clinical conditions
such as renal failure and/or pulmonary edema.
Criteria for SIRS were established in 1992 as part of the American College of Chest Physicians/Society of
Critical Care Medicine Consensus Conference.[2] The conference concluded that the manifestations of SIRS
include, but are not limited to:
Body temperature less than 36C or greater than 38C
Heart rate greater than 90 beats per minute
Tachypnea (high respiratory rate), with greater than 20 breaths per minute; or, an arterial partial pressure of
carbon dioxide less than 4.3 kPa (32 mmHg)
White blood cell count less than 4000 cells/mm (4 x 109 cells/L) or greater than 12,000 cells/mm (12 x 109
cells/L); or the presence of greater than 10% immature neutrophils (band forms)
SIRS can be diagnosed when two or more of these criteria are present.[3][4][5][6]
The International Pediatric Sepsis Consensus has proposed some changes to adapt these criteria to the
pediatric population.
Fever and leukocytosis are features of the acute-phase reaction, while tachycardia is often the initial sign of
hemodynamic compromise. Tachypnea may be related to the increased metabolic stress due to infection and
inflammation, but may also be an ominous sign of inadequate perfusion resulting in the onset of anaerobic
cellular metabolism.
Note that SIRS criteria are very non-specific, and must be interpreted carefully within the clinical context.
These criteria exist primarily for the purpose of more objectively classifying critically-ill patients so that
future clinical studies may be more rigorous and more easily reproducible.
As an alternative, when two or more of the systemic inflammatory response syndrome criteria are met
without evidence of infection, patients may be diagnosed simply with "SIRS." Patients with SIRS and acute
organ dysfunction may be termed "severe SIRS."
[edit]
Complications
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SIRS is frequently complicated by failure of one or more organs or organ systems.[2][3][4] The complications
of SIRS include:
Acute lung injury
Acute kidney injury
Shock
Multiple organ dysfunction syndrome
[edit]
Causes
The causes of SIRS are broadly classified as infectious or noninfectious. As above, when SIRS is due to an
infection, it is considered sepsis. Noninfectious causes of SIRS include trauma, burns, pancreatitis, ischemia,
and hemorrhage.[2][3][4]
Generally, the treatment for SIRS is directed towards the underlying problem or inciting cause (i.e. adequate
fluid replacement for hypovolemia, IVF/NPO for pancreatitis, epinephrine/steroids/benadryl for
anaphylaxis).[1] Selenium, glutamine, and eicosapentaenoic acid have shown effectiveness in improving
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symptoms in clinical trials.[10] Other antioxidants such as vitamin E may be helpful as well.[11]
[edit]
See also
Sepsis
Septicemia
Septic shock
Acute respiratory distress syndrome
Inflammatory response
immune system
[edit]
Health science Medicine Medical specialities Intensive care medicine / Critical care medicine and Critical
care nursing
General terms Intensive-care unit (ICU) Neonatal intensive care unit (NICU) Pediatric intensive care unit
(PICU) Coronary care unit (CCU) Critical illness insurance
Organ failure: Acute renal failure Acute respiratory distress syndrome Acute liver failure Respiratory
failure Multiple organ dysfunction syndrome
Polytrauma Coma
Diagnosis Arterial blood gas catheter (Arterial catheter, Central venous catheter, Pulmonary artery
catheter) Blood cultures Screening cultures
Life supporting treatments Airway management Chest tube Dialysis Enteral feeding Goal-directed
therapy Induced coma Mechanical ventilation Therapeutic hypothermia Total parenteral nutrition
Tracheal intubation
ICU scoring systems APACHE II Glasgow Coma Scale PIM2 SAPS II SAPS III SOFA
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ARDS is a severe lung disease caused by a variety of direct and indirect issues. It is
characterized by inflammation of the lung parenchyma leading to impaired gas exchange with
concomitant systemic release of inflammatory mediators causing inflammation, hypoxemia and
frequently resulting in multiple organ failure. This condition is often fatal, usually requiring
mechanical ventilation and admission to an intensive care unit. A less severe form is called
acute lung injury (ALI).
The first description of acute respiratory distress syndrome appeared in 1967, when Ashbaugh
and colleagues described 12 patients with acute respiratory distress, cyanosis refractory to
oxygen therapy, decreased lung compliance, and diffuse infiltrates evident on the chest
radiograph. Initially called the adult respiratory distress syndrome, this entity is now termed the
acute respiratory distress syndrome, since it does occur in children. Because the initial
definition lacks specific criteria that could be used to identify patients systematically, there was
controversy over the incidence and natural history of the syndrome and the mortality associated
with it. In 1988, an expanded definition was proposed that quantified the physiologic
respiratory impairment through the use of a four-point lung-injury scoring system that was
based on the level of positive end-expiratory pressure, the ratio of the partial pressure of
arterial oxygen to the fraction of inspired oxygen, the static lung compliance, and the degree of
infiltration evident on chest radiographs. Other factors included in the assessment were the
inciting clinical disorder and the presence or absence of nonpulmonary organ dysfunction
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Although the lung-injury scoring system has been widely used to quantify the severity of lung
injury in both clinical research and clinical trials, it cannot be used to predict the outcome
during the first 24 to 72 hours after the onset of the acute respiratory distress syndrome and
thus has limited clinical usefulness. When the scoring system is used four to seven days after
the onset of the syndrome, scores of 2.5 or higher may be predictive of a complicated course
with the need for prolonged mechanical ventilation.
Epidemiology
Incidence
An accurate estimation of the incidence of acute lung injury and the acute respiratory distress
syndrome has been hindered by the lack of a uniform definition and the heterogeneity of the
causes and clinical manifestations. An early estimate by the National Institutes of Health (NIH)
suggested that the annual incidence in the United States was 75 per 100,000 population. More
recent studies reported lower incidences of 1.5 to 8.3 per 100,000. However, the first
epidemiologic study to use the 1994 consensus definition reported considerably higher annual
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incidences in Scandinavia: 17.9 per 100,000 for acute lung injury and 13.5 per 100,000 for the
acute respiratory distress syndrome. On the basis of the results of screening of large numbers of
patients by the NIH Acute Respiratory Distress Syndrome Network over the past three years,
some investigators believe that the original estimate of 75 per 100,000 per year may be
accurate. To settle this issue, a prospective epidemiologic study that is using the 1994
consensus definition is under way in Seattle.
ARDS Causes
c) fat emboli
d) near drowning
e) inhalation injury
a) sepsis
d) cardiopulmonary bypass
e) acute pancreatitis
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ARDS was defined as the ratio of arterial partial oxygen tension (PaO2) as fraction of inspired
oxygen (FiO2) below 200 mmHg in the presence of bilateral alveolar infiltrates on the chest
x-ray. These infiltrates may appear similar to those of left ventricular failure, but the cardiac
silhouette appears normal in ARDS. Also, the pulmonary capillary wedge pressure is normal
(less than 18 mmHg) in ARDS, but raised in left ventricular failure.
A PaO2/FiO2 ratio less than 300 mmHg with bilateral infiltrates indicates acute lung injury
(ALI). Although formally considered different from ARDS, ALI is usually just a precursor to
ARDS. (Consensus after 1967 and 1994)
ARDS is characterized by
Acute onset
Bilateral infiltrates on chest radiograph sparing costophrenic angles
Pulmonary artery wedge pressure < 18 mmHg (obtained by pulmonary artery catheterization), if
this information is available; if unavailable, then lack of clinical evidence of left ventricular
failure suffices:
if PaO2:FiO2 < 300 mmHg (40 kPa) acute lung injury (ALI) is considered to be present
if PaO2:FiO2 < 200 mmHg (26.7 kPa) acute respiratory distress syndrome (ARDS) is
considered to be present
To summarize and simplify, ARDS is an acute (rapid onset) syndrome (collection of symptoms)
that affects the lungs widely and results in a severe oxygenation defect, but is not heart failure.
ARDS Symptoms
Anxiety
Agitation
Fever
The definitions discussed above identify patients early in the course of acute lung injury and
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the acute respiratory distress syndrome. However, the syndrome is often progressive,
characterized by distinct stages with different clinical, histopathological, and radiographic
manifestations. The acute, or exudative, phase is manifested by the rapid onset of respiratory
failure in a patient with a risk factor for the condition. Arterial hypoxemia that is refractory to
treatment with supplemental oxygen is a characteristic feature.
An arterial blood gas analysis and chest X-ray allow formal diagnosis by the aforementioned
criteria. Although severe hypoxemia is generally included, the appropriate threshold defining
abnormal PaO2 has never been systematically studied. Note though, that a severe oxygenation
defect is not synonymous with ventilatory support. Any PaO2 below 100 (generally saturation
less than 100%) on a supplemental oxygen fraction of 50% meets criteria for ARDS. This can
easily be achieved by high flow oxygen supplementation without ventilatory support.
Any cardiogenic cause of pulmonary edema should be excluded. This can be done by placing a
pulmonary artery catheter for measuring the pulmonary artery wedge pressure. However, this is
not necessary and is now rarely done as abundant evidence has emerged demonstrating that the
use of pulmonary artery catheters does not lead to improved patient outcomes in critical illness
including ARDS.
Plain Chest X-rays are sufficient to document bilateral alveolar infiltrates in the majority of
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cases. While CT scanning leads to more accurate images of the pulmonary parenchyma in
ARDS, it has little utility in the clinical management of patients with ARDS, and remains
largely a research tool.
Although acute lung injury and the acute respiratory distress syndrome may resolve completely
in some patients after the acute phase, in others it progresses to fibrosing alveolitis with
persistent hypoxemia, increased alveolar dead space, and a further decrease in pulmonary
compliance. Pulmonary hypertension, owing to obliteration of the pulmonary-capillary bed,
may be severe and may lead to right ventricular failure. Chest radiographs show linear
opacities, consistent with the presence of evolving fibrosis. Pneumothorax may occur, but the
incidence is only 10 to 13 percent and is not clearly related to airway pressures or the level of
positive end-expiratory pressure. Computed tomography of the chest shows diffuse interstitial
opacities and bullae. Histologically, there is fibrosis along with acute and chronic inflammatory
cells and partial resolution of the pulmonary edema
The recovery phase is characterized by the gradual resolution of hypoxemia and improved lung
compliance. Typically, the radiographic abnormalities resolve completely. The degree of
histologic resolution of fibrosis has not been well characterized, although in many patients
pulmonary function returns to normal.
The ability to identify patients at risk for acute lung injury and the acute respiratory distress
syndrome is important if therapies are to be developed to prevent the disorder. The commonly
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associated clinical disorders can be divided into those associated with direct injury to the lung
and those that cause indirect lung injury in the setting of a systemic process.
Overall, sepsis is associated with the highest risk of progression to acute lung injury or the
acute respiratory distress syndrome, approximately 40 percent. The presence of multiple
predisposing disorders substantially increases the risk, as does the presence of secondary
factors including chronic alcohol abuse, chronic lung disease, and a low serum pH.
Outcomes
Until recently, most studies of acute lung injury and the acute respiratory distress syndrome
have reported a mortality rate of 40 to 60 percent. The majority of deaths are attributable to
sepsis or multiorgan dysfunction rather than primary respiratory causes, although the recent
therapeutic success of ventilation with low tidal volumes indicates that in some cases death is
directly related to lung injury. Two reports suggest that mortality from this disease may be
decreasing. The first, from a large county hospital in Seattle, found that the mortality rate was
36 percent in 1993 as compared with rates of 53 to 68 percent in the period from 1983 to 1987.
The second, from a hospital in the United Kingdom, reported a decline in the mortality rate
from 66 percent to 34 percent between 1990 to 1993 and 1994 to 1997. Possible explanations
for the decrease include more effective treatments for sepsis, changes in the method of
mechanical ventilation, and improvement in the supportive care of critically ill patients. The
possibility that mortality is decreasing emphasizes the importance of the use of randomized
control subjects rather than historical controls in clinical studies of the disorder.
Factors whose presence can be used to predict the risk of death at the time of diagnosis of
acute lung injury and the acute respiratory distress syndrome include chronic liver disease,
nonpulmonary organ dysfunction, sepsis, and advanced age. Surprisingly, initial indexes of
oxygenation and ventilation, including the ratio of the partial pressure of arterial oxygen to the
fraction of inspired oxygen and the lung-injury score, do not predict outcome. In three large
studies, the mortality rate among patients with an initial ratio of partial pressure of arterial
oxygen to fraction of inspired oxygen of 300 or less was similar to that among patients with a
ratio of 200 or less. However, the failure of pulmonary function to improve during the first
week of treatment is a negative prognostic factor.
In most patients who survive, pulmonary function returns nearly to normal within 6 to 12
months, despite the severe injury to the lung. Residual impairment of pulmonary mechanics
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may include mild restriction, obstruction, impairment of the diffusing capacity for carbon
monoxide, or gas-exchange abnormalities with exercise, but these abnormalities are usually
asymptomatic. Severe disease and prolonged mechanical ventilation identify patients at highest
risk for persistent abnormalities of pulmonary function. Those who survive the illness have a
reduced health-related quality of life as well as pulmonary-diseasespecific health-related
quality of life.
Pathogenesis
Stages of ARDS
4. Recovery
Two separate barriers form the alveolarcapillary barrier, the microvascular endothelium and
the alveolar epithelium. The acute phase of acute lung injury and the acute respiratory distress
syndrome is characterized by the influx of protein-rich edema fluid into the air spaces as a
consequence of increased permeability of the alveolarcapillary barrier. The importance of
endothelial injury and increased vascular permeability to the formation of pulmonary edema in
this disorder has been well established.
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The critical importance of epithelial injury to both the development of and recovery from the
disorder has become better recognized. The degree of alveolar epithelial injury is an important
predictor of the outcome. The normal alveolar epithelium is composed of two types of cells.
Flat type I cells make up 90 percent of the alveolar surface area and are easily injured.
Cuboidal type II cells make up the remaining 10 percent of the alveolar surface area and are
more resistant to injury; their functions include surfactant production, ion transport, and
proliferation and differentiation to type I cells after injury.
The loss of epithelial integrity in acute lung injury and the acute respiratory distress syndrome
has a number of consequences. First, under normal conditions, the epithelial barrier is much
less permeable than the endothelial barrier. Thus, epithelial injury can contribute to alveolar
flooding. Second, the loss of epithelial integrity and injury to type II cells disrupt normal
epithelial fluid transport, impairing the removal of edema fluid from the alveolar space. Third,
injury to type II cells reduces the production and turnover of surfactant, contributing to the
characteristic surfactant abnormalities. Fourth, loss of the epithelial barrier can lead to septic
shock in patients with bacterial pneumonia. Finally, if injury to the alveolar epithelium is
severe, disorganized or insufficient epithelial repair may lead to fibrosis.
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Clinical and experimental studies have provided circumstantial evidence of the occurrence of
neutrophil-mediated injury in acute lung injury and the acute respiratory distress syndrome.
Histologic studies of lung specimens obtained early in the course of the disorder show a
marked accumulation of neutrophils. Neutrophils predominate in the pulmonary edema fluid
and bronchoalveolar-lavage fluid obtained from affected patients, and many animal models of
acute lung injury are neutrophil-dependent. Some of the mechanisms of the sequestration and
activation of neutrophils and of neutrophil-mediated lung injury are summarized in.
New evidence raises the question of whether neutrophilic inflammation is the cause or the
result of lung injury. Acute lung injury and the acute respiratory distress syndrome may
develop in patients with profound neutropenia, and some animal models of acute lung injury
are neutrophil-independent. In clinical trials in which patients with severe pneumonia received
granulocyte colony-stimulating factor in order to increase the number of circulating
neutrophils, the incidence or severity of lung injury did not increase. The neutrophil has a
critical role in host defense in this disorder, a factor that may explain, in part, why
antiinflammatory strategies have largely been unsuccessful.
Inflammation
Inflammation alone, as in sepsis, causes endothelial dysfunction, fluid extravasation from the
capillaries and impaired drainage of fluid from the lungs. Dysfunction of type II pulmonary
epithelial cells may also be present, with a concomitant reduction in surfactant production.
Elevated inspired oxygen concentration often becomes necessary at this stage, and they may
facilitate a 'respiratory burst' in immune cells.
In a secondary phase, endothelial dysfunction causes cells and inflammatory exudate to enter
the alveoli. This pulmonary edema increases the thickness of the alveolo-capillary space,
increasing the distance the oxygen must diffuse to reach blood. This impairs gas exchange
leading to hypoxia, increases the work of breathing, eventually induces fibrosis of the airspace.
Moreover, edema and decreased surfactant production by type II pneumocytes may cause whole
alveoli to collapse, or to completely flood. This loss of aeration contributes further to the right-
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to-left shunt in ARDS. As the alveoli contain progressively less gas, more blood flows through
them without being oxygenated resulting in massive intrapulmonary shunting.
Collapsed alveoli (and small bronchi) do not allow gas exchange. It is not uncommon to see
patients with a PaO2 of 60 mmHg (8.0 kPa) despite mechanical ventilation with 100% inspired
oxygen.
The loss of aeration may follow different patterns according to the nature of the underlying
disease, and other factors. In pneumonia-induced ARDS, for example, large, more commonly
causes relatively compact areas of alveolar infiltrates. These are usually distributed to the lower
lobes, in their posterior segments, and they roughly correspond to the initial infected area.
In sepsis or trauma-induced ARDS, infiltrates are usually more patchy and diffuse. The
posterior and basal segments are always more affected, but the distribution is even less
homogeneous.
Loss of aeration also causes important changes in lung mechanical properties. These alterations
are fundamental in the process of inflammation amplification and progression to ARDS in
mechanically ventilated patients.
Cytokines
A complex network of cytokines and other proinflammatory compounds initiate and amplify
the inflammatory response in acute lung injury and the acute respiratory distress syndrome.
Proinflammatory cytokines may be produced locally in the lung by inflammatory cells, lung
epithelial cells, or fibroblasts. The regulation of cytokine production by extrapulmonary factors
has also been described. Macrophage inhibitory factor is a regulatory cytokine produced by the
anterior pituitary that is found in high concentrations in the bronchoalveolar-lavage fluid of
patients with the syndrome. This cytokine increases production of the proinflammatory
cytokines interleukin-8 and tumor necrosis factor and can override glucocorticoid-mediated
inhibition of cytokine secretion.
New evidence indicates that it is not only the production of proinflammatory cytokines that is
important, but also the balance between proinflammatory and antiinflammatory mediators.
Several endogenous inhibitors of proinflammatory cytokines have been described, including
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Mechanical ventilation is an essential part of the treatment of ARDS. As loss of aeration (and
the underlying disease) progress, the work of breathing (WOB) eventually grows to a level
incompatible with life. Thus, mechanical ventilation is initiated to relieve respiratory muscles
of their work, and to protect the usually obtunded patient's airways.
Older studies focused on the potential toxic effects of high fractions of inspired oxygen, but
experimental evidence indicates that mechanical ventilation at high volumes and pressures can
injure the lung, causing increased permeability pulmonary edema in the uninjured lung and
enhanced edema in the injured lung. Initial theories formulated to explain these deleterious
effects focused on capillary stress failure due to alveolar overdistention. More recently, cyclic
opening and closing of atelectatic alveoli during mechanical ventilation have been shown to
cause lung injury independently of alveolar overdistention. Alveolar overdistention coupled
with the repeated collapse and reopening of alveoli can initiate a cascade of proinflammatory
cytokines.
However, mechanical ventilation may constitute a risk factor for the development, or the
worsening, of ARDS.
Aside from the infectious complications arising from invasive ventilation with tracheal
intubation, positive-pressure ventilation directly alters lung mechanics during ARDS. The
result is higher mortality, i.e. through baro-trauma, when these techniques are used.
In 1998, Amato et al. published a paper showing substantial improvement in the outcome of
patients ventilated with lower tidal volumes (Vt) (6 mLkg-1).This result was confirmed in a
2000 study sponsored by the NIH.Although both these studies were widely criticized for
several reasons, and although the authors were not the first to experiment lower-volume
ventilation, they shed new light on the relationship between mechanical ventilation and ARDS.
One opinion is that the forces applied to the lung by the ventilator may work as a lever to
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induce further damage to lung parenchyma. It appears that shear stress at the interface between
collapsed and aerated units may result in the breakdown of aerated units, which inflate
asymmetrically due to the 'stickiness' of surrounding flooded alveoli. The fewer such interfaces
around an alveolus, the lesser the stress.
Indeed, even relatively low stress forces may induce signal transduction systems at the cellular
level, thus inducing the release of inflammatory mediators.
This form of stress is thought to be applied by the transpulmonary pressure (gradient) (Pl)
generated by the ventilator or, better, its cyclical variations. The better outcome obtained in
patients ventilated with lower Vt may be interpreted as a beneficial effect of the lower Pl.
Transpulmonary pressure, is an indirect function of the Vt setting on the ventilator, and only
trial patients with plateau pressures (a surrogate for the actual Pl) were less than 32 cmH2O
(3.1 kPa) had improved survival.
The way Pl is applied on alveolar surface determines the shear stress to which lung units are
exposed. ARDS is characterized by a usually inhomogeneous reduction of the airspace, and
thus by a tendency towards higher Pl at the same Vt, and towards higher stress on less diseased
units.
The different mechanical properties of alveoli in ARDS may be interpreted as having varying
time constants (the product of alveolar compliance resistance). A long time constant indicates
an alveolus which opens slowly during tidal inflation, as a consequence of contrasting pressure
around it, or altered water-air interface inside it (loss of surfactant, flooding).
Slow alveoli are said to be 'kept open' using positive end-expiratory pressure, a feature of
modern ventilators which maintains a positive airway pressure throughout the whole respiratory
cycle. A higher mean pressure cycle-wide slows the collapse of diseased units, but it has to be
weighed against the corresponding elevation in Pl/plateau pressure. Newer ventilatory
approaches attempt to maximize mean airway pressure for its ability to 'recruit' collapsed lung
units while minimizing the shear stress caused by frequent openings and closings of aerated
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units.
The prone position also reduces the inhomogeneity in alveolar time constants induced by
gravity and edema. If clinically appropriate, mobilization of the ventilated patient can assist in
achieving the same goal.
In patients with acute lung injury and the acute respiratory distress syndrome, ventilation at
traditional tidal volumes (10 to 15 ml per kilogram of predicted body weight) may overdistend
uninjured alveoli, perhaps promoting further lung injury, inhibiting resolution of the disorder,
and contributing to multiorgan failure. The failure of traditional ventilatory strategies to
prevent end-expiratory closure of atelectatic alveoli may also contribute to lung injury. These
issues have led to a number of clinical trials of protective ventilatory strategies to reduce
alveolar overdistention and increase the recruitment of atelectatic alveoli. Interestingly, a recent
study found that a strategy of protective ventilation could reduce both the pulmonary and the
systemic cytokine response.
Like any form of inflammation, acute lung injury and the acute respiratory distress syndrome
represent a complex process in which multiple pathways can propagate or inhibit lung injury.
For example, abnormalities of the coagulation system often develop, leading to plateletfibrin
thrombi in small vessels and impaired fibrinolysis within the distal air spaces of the injured
lung. Also, abnormalities in the production, composition, and function of surfactant probably
contribute to alveolar collapse and gas-exchange abnormalities.
Fibrosing Alveolitis
After the acute phase of acute lung injury and the acute respiratory distress syndrome, some
patients have an uncomplicated course and rapid resolution of the disorder. Others have
progression to fibrotic lung injury, and such injury can be observed histologically as early as
five to seven days after the onset of the disorder. The alveolar space becomes filled with
mesenchymal cells and their products, along with new blood vessels. The finding of fibrosing
alveolitis on histologic analysis correlates with an increased risk of death, and patients who die
of the condition have a marked accumulation of collagen and fibronectin in the lung at autopsy.
The process of fibrosing alveolitis apparently begins early in the course of the disorder and
may be promoted by early proinflammatory mediators such as interleukin-1. Levels of
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procollagen III peptide, a precursor of collagen synthesis, are elevated in the alveolar
compartment very early in the course of the illness, even at the time of intubation and the
initiation of mechanical ventilation. Furthermore, the early appearance of procollagen III in the
alveolar space is associated with an increased risk of death.
Resolution
Strategies that hasten the resolution of the illness may ultimately be as important as those that
attenuate early inflammatory lung injury. Alveolar edema is resolved by the active transport of
sodium and perhaps chloride from the distal air spaces into the lung interstitium. Water follows
passively, probably through transcellular water channels, the aquaporins, located primarily on
type I cells. In clinical studies, clearance of alveolar fluid can occur surprisingly early and is
often apparent within the first few hours after intubation and the initiation of mechanical
ventilation. Maintenance of the ability to remove alveolar fluid is associated with improved
oxygenation, a shorter duration of mechanical ventilation, and an increased likelihood of
survival.
A considerable quantity of both soluble and insoluble protein must also be removed from the
air spaces. The removal of insoluble protein is particularly important, since hyaline membranes
provide a framework for the growth of fibrous tissue. Soluble protein appears to be removed
primarily by diffusion between alveolar epithelial cells. Insoluble protein may be removed by
endocytosis and transcytosis by alveolar epithelial cells and by phagocytosis by macrophages
The alveolar epithelial type II cell is the progenitor for reepithelialization of a denuded alveolar
epithelium. Type II cells proliferate to cover the denuded basement membrane and then
differentiate into type I cells, restoring the normal alveolar architecture and increasing the
fluid-transport capacity of the alveolar epithelium. This proliferation is controlled by epithelial
growth factors, including keratinocyte and hepatocyte growth factors.
The mechanisms underlying the resolution of the inflammatory-cell infiltrate and fibrosis are
unclear. Apoptosis (programmed cell death) is thought to be a major mechanism for the
clearance of neutrophils from sites of inflammation and may be important in the clearance of
neutrophils from the injured lung. However, in one study of bronchoalveolar-lavage fluid from
patients with acute lung injury and the acute respiratory distress syndrome, the numbers of
apoptotic neutrophils were low, perhaps because of the presence of antiapoptotic factors such
as granulocyte colony-stimulating factor and granulocytemacrophage colony-stimulating
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factor. Nevertheless, high concentrations of the markers of apoptosis are present in the
pulmonary edema fluid of patients, and exposure in vitro to bronchoalveolar-lavage fluids from
these patients can promote epithelial-cell apoptosis. These are potentially important
observations, since the mechanisms that alter epithelial integrity need to be identified. The role
of proapoptotic and antiapoptotic mechanisms in both the injury and repair of the alveolar
epithelium and the lung endothelium is an important area for future research.
Arterial blood gas analysis reveals hypoxemia (reduced levels of oxygen in the blood).
A complete blood count may be taken. The number of white blood cells is increased in
sepsis.
CT scan of the chest may be required only in some situations (routine chest x-ray is
sufficient in most cases).
Echocardiogram (an ultrasound of the heart) may help exclude any heart problems that
can cause fluid build-up in the lung.
Monitoring with a pulmonary artery catheter may be done to exclude a cardiac cause for
the difficulty in breathing.
Bronchoscopy (a procedure used to look inside the windpipe and large airways of the
lung) may be considered to evaluate the possibility of lung infection.
Treatment
Approach to Treatment
Improvement in the supportive care of patients with acute lung injury and the acute respiratory
distress syndrome may have contributed to the recent decline in the mortality rate. There should
be a careful search for the underlying cause, with particular attention paid to the possibility of
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An improved understanding of the pathogenesis of acute lung injury and the acute respiratory
distress syndrome has led to the assessment of several novel treatment strategies. Although
many specific therapies have not proved beneficial, it is encouraging that the quality of clinical
trials is improving. An important advance has been the establishment of a network supported
by the NIH that includes 10 centers, 24 hospitals, and 75 intensive care units and that provides
the infrastructure for well-designed, multicenter, randomized trials of potential new therapies.
General
Acute respiratory distress syndrome is usually treated with mechanical ventilation in the
Intensive Care Unit. Ventilation is usually delivered through oro-tracheal intubation, or
tracheostomy whenever prolonged ventilation (2 weeks) is deemed inevitable.
The possibilities of non-invasive ventilation are limited to the very early period of the disease
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or, better, to prevention in individuals at risk for the development of the disease (atypical
pneumonias, pulmonary contusion, major surgery patients).
Treatment of the underlying cause is imperative, as it tends to maintain the ARDS picture.
The origin of infection, when surgically treatable, must be operated on. When sepsis is
diagnosed, appropriate local protocols should be enacted.
Mechanical Ventilation
The most appropriate method of mechanical ventilation in the acute respiratory distress
syndrome has been controversial since the syndrome was first described. Although the tidal
volume in normal persons at rest is 6 to 7 ml per kilogram, historically a volume of 12 to 15 ml
per kilogram was recommended in patients with acute lung injury and the acute respiratory
distress syndrome. This comparatively high tidal volume may cause further lung injury.
Interestingly, the possibility of ventilator-associated lung injury was first considered in the
1970s, leading to a study of extracorporeal membrane oxygenation in which the tidal volume
was reduced to 8 to 9 ml per kilogram. However, this strategy, like extracorporeal removal of
carbon dioxide in a subsequent study, failed to decrease mortality.
As described in this issue of the Journal, the NIH Acute Respiratory Distress Syndrome
Network compared a traditional tidal volume (12 ml per kilogram of predicted body weight)
with a lower tidal volume (6 ml per kilogram of predicted body weight) in 861 patients. In the
group receiving lower tidal volumes, plateau pressure (airway pressure measured after a
0.5-second pause at the end of inspiration) could not exceed 30 cm of water and a detailed
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protocol was used to adjust the fraction of inspired oxygen and positive end-expiratory
pressure. The in-hospital mortality rate was 39.8 percent in the group treated with traditional
tidal volumes and 31.0 percent in the group treated with lower tidal volumes (P=0.007). Thus,
mortality was reduced by 22 percent in the group treated with lower tidal volumes, a finding of
major importance. This large multicenter trial provides convincing evidence that a specific
therapy for the acute respiratory distress syndrome can reduce mortality. It also provides
evidence of the clinical significance of ventilator-associated lung injury and provides a
well-defined protocol for ventilation against which future strategies can be compared.
The positive results of this trial differed from those of two previous studies of low tidal
volumes, a Canadian study of 120 patients and a European study of 116 patients. There are
several possible explanations for the discrepant results. First, the NIH study had the lowest
tidal volume when the tidal volumes were compared with the use of the same calculation of
ideal body weight. Thus, the NIH study may have been better able to show a difference between
the treatment groups. Second, the study treated respiratory acidosis associated with alveolar
hypoventilation and hypercapnia by allowing the respiratory rate to increase to 35 breaths per
minute and by the administration of sodium bicarbonate. Conceivably, respiratory acidosis
could have had deleterious effects in the groups treated with low tidal volumes in the other two
studies. Finally, the other studies had many fewer patients, thus reducing the statistical power
to find a treatment effect.
APRV (Airway Pressure Release Ventilation) and ARDS / ALI
Some practitioners favor airway pressure release ventilation (APRV). Advantages to APRV
ventilation include: decreased airway pressures, decreased minute ventilation, decreased
dead-space ventilation, promotion of spontaneous breathing, almost 24 hour a day alveolar
recruitment, decreased use of sedation, near elimination of neuromuscular blockade, optimized
arterial blood gas results, mechanical restoration of FRC (functional residual capacity), a
positive effect on cardiac output (due to the negative inflection from the elevated baseline with
each spontaneous breath), increased organ and tissue perfusion, potential for increased urine
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A patient with ARDS on average spends 8 to 11 days on a mechanical ventilator; APRV may
reduce this time significantly and conserve valuable resources.
A study is needed to evaluate whether APRV will reduce patient mortality when compared to
the ARDSNet protocol. However, there seems to be little political will, within the medical
community, to address the need for this study, in spite of the clinical successes seen with
APRV.
There has also been considerable interest in the optimal level of positive end-expiratory
pressure in patients with acute lung injury and the acute respiratory distress syndrome. It was
noted early on that the use of positive end-expiratory pressure could improve oxygenation in
these patients, allowing the fraction of inspired oxygen to be reduced. The best-documented
effect of positive end-expiratory pressure on lung function is an increase in functional residual
capacity, probably as a result of the recruitment of collapsed alveoli. Although lung injury was
prevented in rats by the prophylactic use of positive end-expiratory pressure, the prophylactic
use of a positive end-expiratory pressure of 8 cm of water in patients at risk for the acute
respiratory distress syndrome was not successful.
Recently, Amato et al. used an open-lung approach to mechanical ventilation in patients with
acute lung injury and the acute respiratory distress syndrome. In addition to a low tidal volume
and pressure-controlled inverse-ratio ventilation, the protocol included raising the level of
positive end-expiratory pressure above the lower inflection point on a pressurevolume curve
for each patient in an attempt to ensure adequate recruitment of atelectatic lung. With this
approach, mortality was reduced. However, the adoption of this approach cannot yet be
recommended for several reasons. First, this study was small, involving only 53 patients and
only a single center. Second, mortality in the group treated with conventional ventilation was
unusually high (71 percent), suggesting that the high tidal volume used may have been
especially injurious. Furthermore, the difference in mortality between the two groups was only
apparent at 28 days; the rates of survival until hospital discharge were not significantly
different between the two groups. Third, a reliable measurement of the lower inflection point of
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the pressurevolume curve is technically difficult and usually requires sedation and paralysis of
the patient.
The 'best PEEP' used to be defined as 'some' cmH2O above the lower inflection point (LIP) in
the sigmoidal pressure-volume relationship curve of the lung. Recent research has shown that
the LIP-point pressure is no better than any pressure above it, as recruitment of collapsed
alveoli, and more importantly the overdistension of aerated units, occur throughout the whole
inflation. Despite the awkwardness of most procedures used to trace the pressure-volume curve,
it is still used by some to define the minimum PEEP to be applied to their patients. Some of
the newest ventilators have the ability to automatically plot a pressure-volume curve. The
possibility of having an 'instantaneous' tracing trigger might produce renewed interest in this
analysis.
PEEP may also be set empirically. Some authors suggest performing a 'recruiting maneuver'
(i.e., a short time at a very high continuous positive airway pressure, such as 50 cmH2O (4.9
kPa), to recruit, or open, collapsed units with a high distending pressure) before restoring
previous ventilation. The final PEEP level should be the one just before the drop in PaO2 (or
peripheral blood oxygen saturation) during a step-down trial.
Intrinsic PEEP (iPEEP), or auto-PEEP, first described by John Marini of St. Paul Regions
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Prone position
The rationale for restricting fluids in patients with acute lung injury and the acute respiratory
distress syndrome is to decrease pulmonary edema. Studies in animals with acute lung injury
indicated that the degree of edema was reduced if left atrial pressure was lowered. Some
clinical studies have supported this hypothesis. Soon, a randomized trial of fluid management
designed to compare restricted with liberal fluid management based on monitoring
hemodynamics with either a pulmonary-artery catheter or a central venous catheter will be
carried out by the NIH Acute Respiratory Distress Syndrome Network. While we await these
results, a reasonable objective is to maintain the intravascular volume at the lowest level that is
consistent with adequate systemic perfusion, as assessed by metabolic acidbase balance and
renal function. If systemic perfusion cannot be maintained after the restoration of intravascular
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volume, as is the case in patients with septic shock, treatment with vasopressors is indicated to
restore end-organ perfusion and normalize oxygen delivery. However, on the basis of the
negative results of clinical trials, the use of supranormal levels of oxygen delivery cannot be
recommended.
Surfactant Therapy
Nitric oxide is a potent vasodilator that can be delivered to the pulmonary vasculature by
inhalation without causing systemic vasodilation. Although observational studies suggested
that inhaled nitric oxide might be beneficial in patients with acute lung injury and the acute
respiratory distress syndrome, the results of randomized, double-blind studies have been
discouraging. In a phase 2 study, inhaled nitric oxide did not reduce mortality or reduce the
duration of mechanical ventilation. The improvements in oxygenation with this treatment were
small and were not sustained, and pulmonary-artery pressure decreased very little, and only on
the first day of treatment. Also, a recent phase 3 study of inhaled nitric oxide showed that it
had no effect on either mortality or the duration of mechanical ventilation. Thus, inhaled nitric
oxide cannot be recommended for the routine treatment of acute lung injury and the acute
respiratory distress syndrome, but it may be useful as a rescue therapy in patients with
refractory hypoxemia. Treatment with several less selective vasodilators, including sodium
nitroprusside, hydralazine, alprostadil (prostaglandin E1), and epoprostenol (prostacyclin), has
also not been shown to be beneficial.
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Recognition of the inflammatory nature of the lung injury in acute lung injury and the acute
respiratory distress syndrome prompted interest in antiinflammatory treatments, particularly
glucocorticoids. However, glucocorticoids had no benefit when they were given before the
onset of the disease or early in its course. More recently, glucocorticoids have been used to
treat the later, fibrosing-alveolitis phase of the disease. Encouraging results were reported in
preliminary studies and in a small randomized trial of 24 patients. A larger randomized,
multicenter U.S. trial of treatment with high-dose methylprednisolone for at least seven days is
under way. Because treatment with high-dose methylprednisolone may increase the incidence
of infection, the routine use of this drug in patients with established acute lung injury and the
acute respiratory distress syndrome cannot be recommended until results of a large multicenter
trial become available.
Acceleration of Resolution
Recognition of the importance of the resolution phase of acute lung injury and the acute
respiratory distress syndrome has stimulated interest in strategies to hasten patients' recovery
from lung injury. Experimentally, removal of pulmonary edema fluid from the alveolar space
can be enhanced by both catecholamine-dependent and catecholamine-independent
mechanisms, including those increased by inhaled and systemic beta-agonists. Beta-agonists
are appealing candidates because they are already in wide clinical use and have no serious side
effects, even in critically ill patients. Treatment with beta-agonists may also increase the
secretion of surfactant and perhaps exert an antiinflammatory effect, thus helping to restore
vascular permeability of the lung.
Since acute injury to epithelial type I cells causes denudation of the alveolar epithelium, an
additional approach to hastening the resolution of acute lung injury and the acute respiratory
distress syndrome is to accelerate reepithelialization of the alveolar barrier. The proliferation of
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alveolar epithelial type II cells is controlled by a number of epithelial growth factors, including
keratinocyte growth factor. Experimentally, administration of keratinocyte growth factor
protects against lung injury, probably in part by increasing the proliferation of alveolar type II
cells and the clearance rate of alveolar fluid and by inducing antioxidant effects, and perhaps
by reducing lung endothelial injury. These findings raise the possibility that an epithelium-
specific growth factor could be used to accelerate the resolution of the syndrome. Overall,
strategies directed at restoring the function of alveolar epithelium deserve careful evaluation.
Conclusions
In conclusion, substantial progress has been made in the understanding of acute lung injury
and the acute respiratory distress syndrome. More information regarding epidemiology and
pathogenesis has become available, and the importance of the resolution phase of the illness
has been recognized, opening up new avenues for therapeutic intervention. Although progress
in specific treatments has lagged behind basic research, the formation of the NIH Acute
Respiratory Distress Syndrome Network led to a clinical trial of a ventilation strategy involving
low tidal volumes, which reduced mortality by 22 percent. Large, prospective, randomized
trials of new ventilatory and pharmacologic strategies may further reduce mortality from this
common clinical syndrome.
Physical Examination :
The first priority: ABCs Airway, breathing, and circulation Watch chest for rhythmic breathing;
listen near mouth and nose for air movement Palpate the carotid and peripheral pulses Once
respiration and circulation established, assess for uncontrolled bleeding and shock If none,
assess systematic head-to-toe
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defibrillation Exposure Secondary survey (head-to-toe): Head, face, neck, neurologic status
Chest Abdomen/genitourinary system Limbs Log roll
Cardiopulmonary Arrest :
Cardiopulmonary Arrest Absence of a heartbeat and respirations Causes Myocardial infarction,
heart failure, electrocution, drowning, drug overdose, anaphylaxis, and asphyxiation Signs and
symptoms Collapse and quickly lose consciousness No pulse or respiration
Cardiopulmonary Arrest :
Cardiopulmonary Arrest Interventions Determine responsiveness Open airway Check for
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breathing (look, listen, feel) If nonresponsive and not breathing, palpate for a pulse If no pulse
in 10 seconds, begin compression:ventilation cycles of 30:2 If a pulse, deliver 10-12 rescue
breaths per minute In no advanced airway, continue the 30:2 ratio With advanced airway,
compressions of 100 per minute without pausing for ventilations which are done at a rate of
8-10 per minute
Figure: Airway :
Cardiopulmonary Arrest :
Cardiopulmonary Arrest Two-rescuer CPR One rescuer compresses the chest at a rate of 100
per minute without pausing for ventilations Second rescuer ventilates with 8-10 breaths/minute
Swap roles about every 2 minutes to avoid tiring Recovery position Unresponsive victim who is
breathing should be log-rolled to one side if no cervical trauma is suspected
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Choking or Airway Obstruction Assessment Universal sign of choking is grabbing the throat
with one or both hands First determine if airway completely blocked If victim is able to speak,
breathe, or cough with good air exchange, do nothing If unable to speak, breathe, or cough with
good air exchange, act quickly to prevent suffocation
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Straddle the victims thighs, place one hand on top of the other, and deliver up to five
abdominal thrusts Repeat these three steps until the airway is clear
Shock :
Shock Results from acute circulatory failure caused by inadequate blood volume, heart failure,
overwhelming infection, severe allergic reactions, or extreme pain or fright
Hemorrhage :
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Hemorrhage The loss of a large amount of blood Loss of more than 1 liter (L) of blood in an
adult may lead to hypovolemic shock Death from continued uncontrolled bleeding Bleeding
may be external or internal Internal bleeding is suspected if signs of shock but no external
bleeding is evident
Exsanguination :
Exsanguination To Bleed Out all the Blood from the body
Hemorrhage :
Hemorrhage Apply direct, continuous pressure Elevate and immobilize the injured part (unless
fracture is suspected) After bleeding stops, secure a large dressing, if available, over the wound
Reinforce the dressing but do not change it If direct wound pressure and elevation fail to
control bleeding, apply indirect pressure to the main artery that supplies the area
Hemorrhage Epistaxis Blood from anterior or posterior portion of the nose Most anterior
nosebleeds respond to pressure Instruct the patient to sit down and lean the head forward Pinch
the nostrils shut for at least 10 minutes Advise patient not to blow or pick at nose for several
hours Continued bleeding or bleeding from the posterior area of the nose requires medical
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treatment
Fracture :
Fracture A break in a bone Simple (closed) fracture Does not break the skin Compound (open)
fracture Broken bone protrudes through the skin Complete fracture Broken ends are separated
Incomplete fracture Bone ends are not separated
Fracture :
Fracture Assessment Primary symptom is pain Numbness/tingling from nerve injury and blood
vessels Signs: deformity, swelling, discoloration, decreased function, and bone fragments
protruding through the skin
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Head Injury :
Head Injury Suspected with any type of blow to the head or any unexplained loss of
consciousness Assessment Inspection and palpation of the head Evaluate for signs and
symptoms of increased intracranial pressure Be alert for the leakage of cerebrospinal fluid that
occurs with basilar skull fractures
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Head Injury :
Head Injury Must be assessed by a physician as soon as possible Immobilize neck and keep
victim flat with proper alignment of the neck and head Backboard used for transporting victim
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Neck and Spinal Injuries Immediately summon expert emergency team In remote or
life-threatening settings, the victim may have to be moved A rolled towel or article of clothing
can be used as a collar to support the neck The victim can then be moved by log-rolling to one
side and then rolling back onto a board, keeping the spine as straight as possible Throughout
the movement, one rescuer supports the head while two others support the shoulders, hips, and
legs
Eye Injury :
Eye Injury Assessment Inspect eyelid for trauma and the eye for redness, foreign bodies, or
penetrating objects To inspect for foreign bodies, evert the eyelids
Ear Trauma :
Ear Trauma Assessment Assess extent of injury; note if any tissue is fully separated and
severity of bleeding Apply direct pressure to injury to control bleeding
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Ear Trauma :
Ear Trauma If injured part is actually separated, reattachment may be possible Retrieve the
tissue, wrap it in plastic, keep it cool, and transport it with the victim
Chest Injury :
Chest Injury Critical injuries: open pneumothorax, flail chest, massive hemothorax, and cardiac
tamponade
Pneumothorax
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Cardiac Tamponade
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Assessment of Pt with Chest Injuries rate and character of respirations, skin color, pulse rate
and rhythm symmetry of the chest wall movement presence of any apparent injuries to the chest
Signs and symptoms of chest injuries Dyspnea Tachycardia Restlessness Cyanosis asymmetric
or other abnormal chest wall movement, abnormal sounds of breathing Note mental state and
level of consciousness
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Abdominal
Injury: Assessment :
Abdominal Injury: Assessment Assess abdomen for evidence of injury Nausea/ Vomiting
Inspect Suspect internal abdominal injuries if victim complains of abdominal pain or abdomen
shows evidence of trauma or distention Protrusion of internal organs through a wound is called
evisceration
Abdominal Injury :
Abdominal Injury Cullens Sign- Bluish tinge around umbilicus may indicates abdominal
hemorrhage
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Traumatic Amputation :
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Amputated Hand :
Amputated Hand
:
Shark Bite Amputation
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Burns: Assessment :
Burns: Assessment Determine the type of burn If patient has a flame burn or was in a closed,
smoke-filled area, assess respirations first Determine the extent and depth of the burns Inspect
skin for color, blisters, tissue destruction Superficial burns: typically pink or red and painful
Deeper burns: red, white, or black; may destroy not only the skin but also the underlying
tissues Electrical: difficult to assess; full extent of tissue damage may not be apparent for
several days Chemical: immediately remove any remaining chemical
Burns: Interventions :
Burns: Interventions Ensure a patent airway and respirations for burn victims Rescue breathing,
if needed
Hyperthermia :
Hyperthermia Body temperature >37.2 C (99 F) Heat edema and heat cramps are mild degrees
of hyperthermia Can be treated by moving individual into cool place and providing fluids with
electrolytes Heat exhaustion and heat stroke more serious See Table 16-5, p. 236
Hypothermia :
Hypothermia Decrease in body core temperature to <36 C (95 F) Caused by prolonged
exposure to cold, extremely cold temperatures, or immersion in cold water Causes depression
of vital functions, and if not corrected, death results from cardiac dysrhythmias
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Hypothermia :
Hypothermia Mild stage Patient shivers in an effort to generate body heat Blood vessels in the
extremities are constricted, and performing complex motor tasks is impaired Moderate
hypothermia Appears dazed, poor motor coordination, slurred speech, and violent shivering
May behave irrationally Severe hypothermia Waves of shivering, rigid muscles, and pale skin
Pulse rate is slow and the pupils are dilated
Hypothermia
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Interventions :
Interventions Immediately move the victim to fresh air If person not breathing, start rescue
breathing Seek emergency medical assistance immediately Give oxygen as soon as it is
available At the hospital the patient may be placed in a hyperbaric oxygen chamber
Prevention :
Prevention Keep gas furnaces and stoves in proper repair Burners that use gas must be vented
to the outside Dont use charcoal or wood-burning devices in closed area Never let automobile
engine run in closed garage Install carbon monoxide detector alarm
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Food Poisoning :
Food Poisoning Assessment Symptoms: nausea, vomiting, abdominal cramps, and diarrhea
Botulism caused by Clostridium botulinum has neurotoxic effects: difficulty breathing, seeing,
and swallowing Clue that food poisoning is causing victims symptoms is that all who
consumed a certain food become ill To assist in identifying poisons, collect samples of stool or
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Food Poisoning :
Food Poisoning Ptomaine poisoning Bacterial or chemical Cleanliness, good personal hygiene,
and proper preparation and handling of foods Symptoms and treatment (Also refer to Health
Promotion Points 44-2.)
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Healthy People 2010 Food Safety Focus area # 10: Food Safety. To reduce food-borne
illnesses.
Animal Bites :
Animal Bites Animal bites and Animal Control Agency: Wash area with warm soapy water for
5-10 minutes Rabies immunization or 5 IM injections given over a period of 3 weeks
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Copperhead Snake :
Snakebite: :
Snakebite: Poisonous snakes and venomous snakebite Treatment Wash area Immobilize Apply
suction Go to hospital Give antivenin
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Health Promotion Points : Anaphylaxis Kit Individuals who have known allergies to insect
bites or other common environmental allergens should carry an anaphylaxis kit. Family and
friends should know how to use the contents in case the individual is unable to treat herself.
Coral Snake
Snakebite: :
Snakebite: Poisonous snakes and venomous snakebite Treatment Wash area Immobilize Apply
suction Go to hospital Give antivenin
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Remove Stinger
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Acts of Bioterrorism Deliberate release of pathogens to kill people Anthrax, botulism, plague,
smallpox, tularemia: most common biologic agents in terrorist attack Easily spread; potential to
cause many deaths Health care providers must know how to protect themselves and others Staff
should know where to obtain personal protective equipment and what types of precautions (i.e.,
patient isolation) should be taken
Disaster Planning :
Disaster Planning A challenge for the health care system is to be ready for natural disasters that
often occur with short warning American Red Cross and the Salvation Army are experienced in
handling these situations and quickly move in to help A call for nurse volunteers usually
follows Regardless of the area of clinical expertise, there is certain to be a way each nurse can
contribute
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Psychological Emergencies :
Psychological Emergencies Combative patient Domestic violence/abuse Child abuse Elder
abuse Psychological trauma
Legal Aspects of Emergency Care Emergency doctrine In emergencies, person may be unable to
consent to care Treatment can be provided under the assumption that the patient would have
consented if able Good Samaritan laws Limit liability and provide protection against
malpractice claims when health care providers render first aid at the scene of an emergency
These laws do not protect the nurse in the event of gross negligence or willful misconduct
Source Information
From the Cardiovascular Research Institute (L.B.W., M.A.M.) and the Departments of
Medicine (L.B.W., M.A.M.) and Anesthesia (M.A.M.), University of California, San
Francisco, San Francisco.
Address reprint requests to Dr. Matthay at CVRI, Box 0130, 505 Parnassus Ave., University of
California, San Francisco, San Francisco, CA 94143-0130, or at [email protected].
..
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of myocardial metabolic activity and myocardial oxygen demand. Increases in the heart rate and
myocardial contractile state result in increased myocardial oxygen demand. Increases in both
afterload (ie, aortic pressure) and preload (ie, ventricular end-diastolic volume) result in a
proportional elevation of myocardial wall tension and, therefore, increased myocardial oxygen
demand. Oxygen supply to any organ system is determined by blood flow and oxygen
extraction. Because the resting coronary venous oxygen saturation is already at a relatively low
level (approximately 30%), the myocardium has a limited ability to increase its oxygen
extraction during episodes of increased demand. Thus, an increase in myocardial oxygen
demand (eg, during exercise) must be met by a proportional increase in coronary blood flow.
The ability of the coronary arteries to increase blood flow in response to increased cardiac
metabolic demand is referred to as coronary flow reserve (CFR). In healthy people, the
maximal coronary blood flow after full dilation of the coronary arteries is roughly 4-6 times the
resting coronary blood flow. CFR depends on at least 3 factors: large and small coronary artery
resistance, extravascular (ie, myocardial and interstitial) resistance, and blood composition.
Myocardial ischemia can result from (1) a reduction of coronary blood flow caused by fixed
and/or dynamic epicardial coronary artery (ie, conductive vessel) stenosis, (2) abnormal
constriction or deficient relaxation of coronary microcirculation (ie, resistance vessels), or (3)
reduced oxygen-carrying capacity of the blood.
Atherosclerosis is the most common cause of epicardial coronary artery stenosis and, hence,
angina pectoris. Patients with a fixed coronary atherosclerotic lesion of at least 50% show
myocardial ischemia during increased myocardial metabolic demand as the result of a
significant reduction in CFR. These patients are not able to increase their coronary blood flow
during stress to match the increased myocardial metabolic demand, thus they experience
angina. Fixed atherosclerotic lesions of at least 90% almost completely abolish the flow
reserve; patients with these lesions may experience angina at rest.
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Coronary spasm can also reduce CFR significantly by causing dynamic stenosis of coronary
arteries. Prinzmetal angina is defined as resting angina associated with ST-segment elevation
caused by focal coronary artery spasm. Although most patients with Prinzmetal angina have
underlying fixed coronary lesions, some have angiographically normal coronary arteries.
Several mechanisms have been proposed for Prinzmetal angina: focal deficiency of nitric oxide
production, hyperinsulinemia, low intracellular magnesium levels, smoking cigarettes, and
using cocaine.
Approximately 30% of patients with chest pain referred for cardiac catheterization have normal
or minimal atherosclerosis of coronary arteries. A subset of these patients demonstrates
reduced CFR that is believed to be caused by functional and structural alterations of small
coronary arteries and arterioles (ie, resistance vessels). Under normal conditions, resistance
vessels are responsible for as much as 95% of coronary artery resistance, with the remaining
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5% being from epicardial coronary arteries (ie, conductive vessels). The former is not
visualized during regular coronary catheterization. Angina due to dysfunction of small coronary
arteries and arterioles is called microvascular angina. Several diseases, such as diabetes
mellitus, hypertension, and systemic collagen vascular diseases (eg, systemic lupus
erythematosus, polyarteritis nodosa), are believed to cause microvascular abnormalities with
subsequent reduction in CFR.
The syndrome that includes angina pectoris, ischemialike ST-segment changes and/or
myocardial perfusion defects during stress testing, and angiographically normal coronary
arteries is referred to as syndrome X. Most patients with this syndrome are postmenopausal
women, and they usually have an excellent prognosis. Syndrome X is believed to be caused by
microvascular angina. Multiple mechanisms may be responsible for this syndrome, including
(1) impaired endothelial dysfunction, (2) increased release of local vasoconstrictors, (3)
fibrosis and medial hypertrophy of the microcirculation, (4) abnormal cardiac adrenergic nerve
function, and/or (5) estrogen deficiency.
A number of extravascular forces produced by contraction of adjacent myocardium and
intraventricular pressures can influence coronary microcirculation resistance and thus reduce
CFR. Extravascular compressive forces are highest in the subendocardium and decrease toward
the subepicardium. Left ventricular (LV) hypertrophy together with a higher myocardial oxygen
demand (eg, during tachycardia) cause greater susceptibility to ischemia in subendocardial
layers.
Myocardial ischemia can also be the result of factors affecting blood composition, such as
reduced oxygen-carrying capacity of blood, as is observed with severe anemia (hemoglobin, <8
g/dL), or elevated levels of carboxyhemoglobin. The latter may be the result of inhalation of
carbon monoxide in a closed area or of long-term smoking.
Recently, ambulatory ECG monitoring has shown that silent ischemia is a common
phenomenon among patients with established coronary artery disease. In one study, as many as
75% of episodes of ischemia (defined as transient ST depression of >1 mm persisting for at
least 1 min) occurring in patients with stable angina were clinically silent. Silent ischemia
occurs most frequently in early morning hours and may result in transient myocardial
contractile dysfunction (ie, stunning). The exact mechanism(s) for silent ischemia is not
known. However, autonomic dysfunction (especially in patients with diabetes), a higher pain
threshold in some individuals, and the production of excessive quantities of endorphins are
among the more popular hypotheses.
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a frequent lack of classic anginal symptoms. The estimated age-adjusted prevalence of angina is
greater in women than in men.
Age: The prevalence of angina pectoris increases with age. Age is a strong independent risk
factor for mortality.
CLINICAL
History: Most patients with angina pectoris report of retrosternal chest discomfort rather than
frank pain. The former is usually described as a pressure, heaviness, squeezing, burning, or
choking sensation. Anginal pain may be localized primarily in the epigastrium, back, neck, jaw,
or shoulders. Typical locations for radiation of pain are arms, shoulders, and neck. Typically,
angina is precipitated by exertion, eating, exposure to cold, or emotional stress. It lasts for
approximately 1-5 minutes and is relieved by rest or nitroglycerin. Chest pain lasting only a
few seconds is not usually angina pectoris. The intensity of angina does not change with
respiration, cough, or change in position. Pain above the mandible and below the epigastrium
is rarely anginal in nature.
Fig.3 Coronarographia
Ask patients about the frequency of angina, severity of pain, and number of nitroglycerin pills
used during angina episodes.
Angina decubitus is a variant of angina pectoris that occurs at night while the patient is
recumbent. Some have suggested that it is induced by an increase in myocardial oxygen
demand caused by expansion of the blood volume with increased venous return during
recumbency.
The Canadian Cardiovascular Society grading scale is used for classification of angina severity,
as follows:
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Fig. Angiography
Physical:
For most patients with stable angina, physical examination findings are normal. Diagnosing
secondary causes of angina, such as aortic stenosis, is important.
A positive Levine sign (characterized by the patient's fist clenched over the sternum when
describing the discomfort) is suggestive of angina pectoris.
Look for physical signs of abnormal lipid metabolism (eg, xanthelasma, xanthoma) or of
diffuse atherosclerosis (eg, absence or diminished peripheral pulses, increased light reflexes or
arteriovenous nicking upon ophthalmic examination, carotid bruit).
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Examination of patients during the angina attack may be more helpful. Useful physical findings
include third and/or fourth heart sounds due to LV systolic and/or diastolic dysfunction and
mitral regurgitation secondary to papillary muscle dysfunction.
Pain produced by chest wall pressure is usually of chest wall origin.
Causes:
Decrease in myocardial blood supply due to increased coronary resistance in large and small
coronary arteries
Significant coronary atherosclerotic lesion in the large epicardial coronary arteries (ie,
conductive vessels) with at least a 50% reduction in arterial diameter
Coronary spasm (ie, Prinzmetal angina)
Abnormal constriction or deficient endothelial-dependent relaxation of resistant vessels
associated with diffuse vascular disease (ie, microvascular angina)
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Congenital anomalies of the origin and/or course of the major epicardial coronary arteries
Structural abnormalities of the coronary arteries
Congenital coronary artery aneurysm or fistula
Coronary artery ectasia
Coronary artery fibrosis after chest radiation
Coronary intimal fibrosis following cardiac transplantation
Risk factors
Major risk factors for atherosclerosis: These include a family history of premature coronary
artery disease, cigarette smoking, diabetes mellitus, hypercholesterolemia, or systemic
hypertension.
Other risk factors: These include LV hypertrophy, obesity, and elevated serum levels of
homocysteine, lipoprotein (a), plasminogen activator inhibitor, fibrinogen, serum triglycerides,
or low high-density lipoprotein (HDL).
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demand.
Preventive factors: Factors associated with reduced risk of atherosclerosis are a high serum
HDL cholesterol level, physical activity, estrogen, and moderate alcohol intake (1-2 drinks/d).
DIFFERENTIALS
Anemia, Anxiety Disorders , Aortic Dissection ,Aortic Stenosis ,Biliary Colic
,Cardiomyopathy, Hypertrophic ,Cholecystitis ,Coronary Artery Atherosclerosis ,Coronary
Artery Vasospasm ,Diabetes Mellitus, Type 1 ,Diabetes ,ellitus, Type 2 ,Gastric Ulcers
,Gastritis, Acute ,Gastroesophageal Reflux Disease ,Hiatal Hernia ,Hypercholesterolemia,
Familial ,Hypercholesterolemia, Polygenic ,Hypertension ,Hyperthyroidism ,Isolated Coronary
Artery ,nomalies ,Kawasaki Disease ,Mitral Regurgitation ,Mitral Valve Prolapse ,Panic
Disorder ,Pericarditis, Acute ,Pleurodynia ,Pneumothorax ,Polyarteritis Nodosa ,Pott Disease
(Tuberculous Spondylitis) ,Pulmonary Embolism ,Pulmonary Hypertension, Primary
,Pulmonary Hypertension, Secondary ,Scleroderma ,Systemic Lupus Erythematosus ,Takayasu
Arteritis ,Toxicity, Cocaine ,Varicella-Zoster Virus
Imaging Studies:
Chest radiograph findings are usually normal in patients with angina pectoris. However, they
may show cardiomegaly in patients with previous MI, ischemic cardiomyopathy, pericardial
effusion, or acute pulmonary edema. Calcification of coronary arteries frequently correlates
with major coronary artery disease.
Graded exercise stress testing is the most widely used test for the evaluation of patients
presenting with chest pain. In patients with established stable angina pectoris, it also can
provide prognostic information about the extent of disease.
Exercise stress testing can be performed alone and in conjunction with echocardiography or
myocardial perfusion scintigraphy tests. Stress echocardiography has an overall sensitivity of
78% and specificity of 86%; myocardial perfusion scintigraphy has an overall sensitivity of
83% and specificity of 77%. Exercise stress testing alone generally has somewhat lower
sensitivity and specificity, but it is cheaper and therefore is a reasonable choice in those with a
low probability of disease.
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These test results must be interpreted in the context of the likelihood of the presence of
coronary artery disease determined from the patient's history and physical examination
findings. In a population with low prevalence, the predictive abilities of these tests are low;
however, in patients with a high likelihood of coronary artery disease, the predictive value is
much higher.
Stress echocardiography can be used to evaluate segmental wall motion during exercise. It
detects changes in regional wall motion that occur during myocardial ischemia. Normal
myocardium becomes hyperdynamic during exercise; ischemic segments become hypokinetic or
akinetic.
Stress echocardiography has the advantage of simultaneous evaluation of LV function, cardiac
dimensions, and valvular disease. It is especially useful in patients with baseline ECG
abnormalities and those with systolic murmurs suggestive of aortic stenosis or hypertrophic
cardiomyopathy.
It is also helpful for localizing ischemia and evaluating its severity.
Signs of severe coronary artery disease during exercise stress echocardiography include LV
dilation, a decrease in global systolic function, and new or worsening mitral regurgitation.
However, with dobutamine stress echocardiography, even in patients with severe coronary
artery disease, the LV cavity may not dilate and global systolic function may improve.
A major problem with stress echocardiography is the technical difficulty with obtaining
adequate images in some patients.
Thallium Tl 201 and technetium Tc 99m sestamibi are the most frequently used myocardial
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perfusion scintigraphy tests. These tests are especially useful in patients with baseline ECG
abnormalities, to localize the region of ischemia, and as prognostic indicators. The presence of
increased lung uptake upon thallium imaging is associated with a poor prognosis. Increased
lung uptake, together with poststress dilation of the LV and multiple perfusion defects, is
suggestive of either left main coronary artery disease or severe 3-vessel disease. The number of
affected myocardial segments is predictive of long-term survival. Smaller perfusion defects are
usually associated with peripheral coronary artery lesions, which are associated with a better
prognosis. The absence of perfusion defects even in the presence of symptoms indicates an
excellent prognosis.
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Other Tests:
ECG is useful for evaluating persons with angina pectoris; however, findings are variable
among patients.
Approximately 50% of patients with angina pectoris have normal findings after a resting ECG.
However, abnormalities such as evidence for prior MI, intraventricular conduction delay,
various degrees of atrioventricular block, arrhythmias, or ST-Twave changes may be seen.
During an attack of angina pectoris, 50% of patients with normal findings after resting ECG
show abnormalities. A 1-mm or greater depression of the ST segment below the baseline,
measured 80 milliseconds from the J point, is the most characteristic change. Reversible
ST-segment elevation occurs with Prinzmetal angina. Some patients with coronary artery
disease may show pseudonormalization of the resting ECG ST-Twave abnormalities during
episodes of chest pain.
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Exercise with ECG monitoring alone is the initial procedure of choice in patients without
baseline ST-segment abnormalities or in whom anatomic localization of ischemia is not a
consideration.
Horizontal or down-sloping ST-segment depression of at least 1 mm, measured 80 milliseconds
from the J point, is considered the characteristic ischemic response.
ST-segment depression of more than 2 mm at a low workload or that persists for more than 5
minutes after termination of exercise and a failure of blood pressure to rise or an actual drop in
blood pressure are signs of severe ischemic heart disease and a poor prognosis.
Withhold beta-blockers for approximately 48 hours before the stress test, whenever possible.
Patients on digoxin and those with LV hypertrophy with repolarization abnormalities more
often show positive results. Exercise stress tests have lower sensitivity and specificity in
women and in patients with left bundle-branch block.
Pharmacologic agents (eg, dobutamine, dipyridamole, adenosine) can be used in patients who
are unable to exercise.
Ambulatory ECG monitoring can be used for diagnostic purposes in patients with chest pain
suggestive of Prinzmetal angina but is primarily used to evaluate the frequency of silent
ischemia. Silent ischemia has been shown to be an independent predictor of mortality in
patients with angina pectoris.
Several studies have shown that calcium in the coronary arteries as detected by electron-beam
computed tomography is an important indicator of coronary artery stenosis. In these studies,
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the sensitivity of a positive electron-beam computed tomography scan ranged from 85-100%
and the specificity varied from 41-76%, while the positive predictive value varied from 55-84%
and the negative predictive value varied from 84-100%. However, several studies have shown
inconsistent reproducibility in repeated measures of coronary calcium with electron-beam
computed tomography. Thus, its proper role at this time remains controversial.
Procedures:
Selective coronary angiography is the definitive diagnostic test for evaluating the anatomic
extent and severity of coronary artery disease.
Consider coronary angiography in symptomatic patients with inconclusive noninvasive study
results, in survivors of sudden cardiac death, in those who are considered to have a poor
prognosis based on the results of noninvasive studies, in those with occupational requirements
for a definite diagnosis (eg, pilots), or in patients with coronary artery disease who are severely
symptomatic despite maximal medical therapy.
In patients in whom Prinzmetal angina is suggested, provocative testing with ergonovine
maleate during coronary angiography may be useful.
Intra-aortic balloon counterpulsation can be used in patients who continue to have unstable
angina pectoris despite maximal medical treatment. This procedure should be followed
promptly by coronary angiography with possible coronary revascularization.
In patients whose angina is refractory to medical therapy who are not suitable candidates for
either percutaneous or surgical revascularization, enhanced external counterpulsation is a safe
and noninvasive alternative therapy. It increases coronary perfusion and reduces myocardial
oxygen demand by diastolic augmentation of the central aortic pressure. Several studies have
shown that patients treated with enhanced external counterpulsation have a significantly
reduced number of anginal episodes, improved exercise tolerance, and decreased daily use of
nitroglycerin tablets. Its therapeutic effects on quality of life are noted to remain at 1-year
follow-up.
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TREATMENT
Medical Care: The main goals of treatment in angina pectoris are to relieve the symptoms,
slow the progression of disease, and reduce the possibility of future events, especially MI and
premature death.
General measures
Smoking cessation results in a significant reduction of acute adverse effects on the heart and
may reverse, or at least slow, atherosclerosis. Strongly encourage patients to quit smoking, and
take an active role in helping them to achieve this goal.
Treat risk factors, including hypertension, diabetes mellitus, obesity, and hyperlipidemia.
Several clinical trials have shown that in patients with established coronary artery disease,
reduction of low-density lipoprotein (LDL) level with a beta-hydroxy-beta-methylglutaryl
coenzyme A reductase inhibitor (ie, statin) is associated with significant reductions in both
mortality rate and major cardiac events.
These benefits are present even in patients with mild-to-moderate elevations of LDL
cholesterol level.
Recent trials with cholesterol-lowering agents have confirmed the benefits of the therapeutic
LDL lowering in older persons.
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Angiographic studies demonstrate that a reduction of the LDL level in patients with coronary
artery disease could cause slowing of progression, stabilization, or even regression of coronary
artery lesions.
A recent study demonstrates a significant reduction of symptomatic myocardial ischemia in
patients with unstable angina or nonQ-wave infarction with the administration of a statin
during the early acute phase.
In a more recent study of 10,001 patients with stable coronary artery disease, an aggressive
cholesterol-lowering approach with atorvastatin 80 mg daily (mean cholesterol level of 77
mg/dL) compared to a less-aggressive approach with atorvastatin 10 mg daily (mean cholesterol
level of 101 mg/dL) resulted in a 2.2% absolute reduction and a 22% relative reduction in the
occurrence of a first major cardiovascular event (defined as death from coronary heart disease;
nonfatal, nonprocedure-related myocardial infarction; resuscitation from cardiac arrest; or
fatal or nonfatal stroke).This occurred with a greater incidence of elevated aminotransferase
levels with the aggressive cholesterol-lowering approach (1.2% vs 0.2%, p<0.001).
On the basis of several recent studies that have demonstrated the benefits of more aggressive
LDL-lowering therapies in high-risk patients with coronary artery disease, the Committee of
the National Cholesterol Education Program recently made the following modifications to the
Adult Treatment Panel III (ATP III) guidelines.
In high-risk patients, a serum LDL cholesterol level of less than 100 mg/dL is the goal.
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In very high-risk patients, an LDL cholesterol level goal of less than 70 mg/dL is a therapeutic
option. Patients in the category of very high risk are those with established coronary artery
disease with one of the following: multiple major risk factors (especially diabetes), severe and
poorly controlled risk factors (especially continued cigarette smoking), multiple risk factors of
the metabolic syndrome (especially high triglyceride levels [>200 mg/dL] plus non-HDL
cholesterol level [>130 mg/dL] with low HDL cholesterol level [<40 mg/dL]), and patients with
acute coronary syndromes.
For moderately high-risk persons (2+ risk factors), the recommended LDL cholesterol level is
less than130 mg/dL, but an LDL cholesterol level of 100 mg/dL is a therapeutic option.
Some triglyceride-rich lipoproteins, including partially degraded very LDL levels, are believed
to be independent risk factors for coronary artery disease. In daily practice, non-HDL
cholesterol level (ie, LDL + very LDL cholesterol [total cholesterol - HDL cholesterol]) is the
most readily available measure of the total pool of these atherogenic lipoproteins. Thus, the
ATP III has identified non-HDL cholesterol level as a secondary target of therapy in persons
with high triglyceride levels (>200 mg/dL). The goal for non-HDL cholesterol level (for
persons with serum triglyceride levels >200 mg/dL) is 30 mg/dL higher than the identified LDL
cholesterol level goal.
Patients with established coronary disease and low HDL cholesterol levels are at high risk for
recurrent events and should be targeted for aggressive nonpharmacological (ie, dietary
modification, weight loss, physical exercise) and pharmacological treatment.
A recent study demonstrated that in patients with established coronary artery disease who have
low HDL and low-risk LDL levels, drug therapy with medications that raise HDL cholesterol
levels and lower triglyceride levels but have no effect on LDL cholesterol levels (eg,
gemfibrozil) could significantly reduce the risk of major cardiac events.
Currently, the accepted approach to the management of patients with coronary artery disease
and low HDL levels is as follows:
In all persons with low HDL cholesterol levels, the primary target of therapy is to achieve the
ATP III guideline LDL cholesterol level goals with diet, exercise, and drug therapy as needed.
After reaching the targeted LDL level goal, emphasis shifts to other issues. That is, in patients
with low HDL cholesterol levels who have associated high triglyceride levels (>200 mg/dL),
the secondary priority is to achieve the non-HDL cholesterol level goal of 30 mg/dL higher
than the identified LDL cholesterol level goal. In patients with isolated low HDL cholesterol
levels (triglycerides <200 mg/dL), drugs to raise the HDL cholesterol level (eg, gemfibrozil,
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In fact, these studies even demonstrated an increased risk of coronary artery disease and stroke
in patients on hormone replacement therapy.
The Women's Health Initiative study demonstrated that the use of hormone replacement therapy
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for 1 year in 10,000 healthy postmenopausal women is associated with 7 more instances of
coronary artery disease, 8 more strokes, 8 more pulmonary emboli, 8 more invasive breast
cancers, 5 fewer hip fractures, and 6 fewer colorectal cancers.
Based on these data, the risks and benefits of hormone replacement therapy must be assessed
on an individual basis for each patient.
Sublingual nitroglycerin has been the mainstay of treatment for angina pectoris. Sublingual
nitroglycerin can be used for acute relief of angina and prophylactically before activities that
may precipitate angina. No evidence indicates that long-acting nitrates improve survival in
patients with coronary artery disease.
Beta-blockers are also used for symptomatic relief of angina and prevention of ischemic events.
They work by reducing myocardial oxygen demand and by decreasing the heart rate and
myocardial contractility. Beta-blockers have been shown to reduce the rates of mortality and
morbidity following acute MI.
Long-acting heart rateslowing calcium channel blockers can be used to control anginal
symptoms in patients with a contraindication to beta-blockers and in those in whom
symptomatic relief of angina cannot be achieved with the use of beta-blockers, nitrates, or both.
Avoid short-acting dihydropyridine calcium channel blockers because they have been shown to
increase the risk of adverse cardiac events.
Anginal symptoms in patients with Prinzmetal angina can be treated with calcium channel
blockers with or without nitrates. In one study, supplemental vitamin E added to a calcium
channel blocker significantly reduced anginal symptoms among such patients.
In patients with syndrome X and hypertension, ACE inhibitors may normalize thallium
perfusion defects and increase exercise capacity.
Surgical Care:
Revascularization therapy (ie, coronary revascularization) can be considered in patients with
left main artery stenosis greater than 50%, 2- or 3-vessel disease and LV dysfunction (ejection
fraction, <45%), poor prognostic signs during noninvasive studies, or severe symptoms despite
maximum medical therapy. The 2 main coronary revascularization procedures are percutaneous
transluminal coronary angioplasty, with or without coronary stenting, and coronary artery
bypass grafting.
Patients with 1- or 2-vessel disease and normal LV function who have anatomically suitable
lesions are candidates for percutaneous transluminal coronary angioplasty and coronary
stenting. Restenosis is the major complication, with symptomatic restenosis occurring in
20-25% of patients. Restenosis mostly occurs during the first 6 months after the procedure and
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can be managed by repeat angioplasty. Several recent trials have demonstrated that the use of
drug-eluting stents (eg, sirolimus-eluting stents, paclitaxel-coated stents) can remarkably
reduce the rate of in-stent restenosis. Recently, with the introduction of these drug-coated
stents, patients with multivessel coronary artery disease are more frequently treated with
percutaneous revascularization as opposed to the surgical revascularization.
Patients with single-vessel disease and normal ventricular function treated with percutaneous
transluminal coronary angioplasty show improved exercise tolerance and fewer episodes of
angina compared with those who receive medical treatment. However, no difference in the
frequency of MI or death has been shown between these two groups.
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study demonstrated that off-pump coronary surgery was as safe as on-pump surgery and caused
less myocardial damage. However, the graft-patency rate was lower at 3 months in the off-pump
group than in the on-pump group.
Recently, laser transmyocardial revascularization has been used as an experimental therapy for
the treatment of severe, chronic, stable angina refractory to medical or other therapies. This
technique has been performed with either an epicardial surgical technique or by a percutaneous
approach. In both approaches, a series of transmural endomyocardial channels are created to
improve myocardial perfusion. The surgical transmyocardial revascularization technique has
been associated with symptomatic relief for end-stage chronic angina in the short term.
However, no published data address the long-term efficacy of surgical transmyocardial
revascularization. Nonetheless, this technique appears to provide at least symptomatic relief for
end-stage chronic angina in the short term.
Diet: A diet low in saturated fat and dietary cholesterol is the mainstay of the Step I and Step II
diet from the American Heart Association.
Activity: The level of activity that aggravates anginal symptoms is different for each patient.
However, most patients with stable angina can avoid symptoms during daily activities simply
by reducing the speed of activity.
MEDICATION
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
Drug Category: Antiplatelet agents -- Prevent thrombus formation by inhibiting platelet
aggregation. Aspirin is proven beneficial in primary and secondary prevention of coronary
artery disease. In patients with aspirin intolerance, use clopidogrel. Clopidogrel is also used in
combination with aspirin after coronary stent placement. Recently, clopidogrel use in addition
to aspirin has been shown to be significantly superior to aspirin alone in patients with acute
coronary syndrome without ST-segment elevation MI.
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Drug Category: Calcium channel blockers -- Reduce transmembrane flux of calcium via
calcium channels. Cause smooth muscle relaxation, resulting in peripheral arterial vasodilation
and afterload reduction. Indicated when symptoms persist despite treatment with beta-blockers
or when beta-blockers are contraindicated. Also indicated in patients with Prinzmetal angina
with or without nitrates.
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Drug Category: Short-acting nitroglycerins -- Suitable for immediate relief of exertional or rest
angina. Can also be used for prophylaxis several minutes before planned exercise to avoid
angina. Reduce myocardial oxygen demand by reduction of LV and arterial pressure, primarily
by reducing preload.
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Drug Category: Long-acting nitroglycerins -- Reduce LV preload and afterload by venous and
arterial dilation, which subsequently reduces myocardial oxygen consumption and relieves
angina. Also cause dilation of epicardial coronary arteries, which is beneficial in patients with
coronary spasm. In addition, nitroglycerin has antithrombotic and antiplatelet effects in
patients with angina pectoris. No evidence suggests that nitrates improve survival or slow
progression of coronary artery disease.
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FOLLOW-UP
Deterrence/Prevention:
Coronary atherosclerosis is the main preventable cause of mortality in the United States. A
rigorous effort to address correctable risk factors is the mainstay of preventive cardiovascular
medicine.
Smoking cessation is the single most effective preventive intervention to reduce coronary
atherosclerosis prevalence. It has been associated with a coronary artery disease reduction of
7-47% in primary prevention settings.
Aggressive treatment of diabetes mellitus, hypertension, LV hypertrophy, hyperlipidemia, and
obesity has an important role in the prevention of coronary artery disease.
The most important recent development in coronary atherosclerosis risk modification is the
introduction of inhibitors of beta-hydroxy-beta-methylglutaryl coenzyme A reductase.
Reductions of total and LDL cholesterol levels by 25% and 35%, respectively, can achieve a
similar reduction in rates of total and coronary mortality, MI, and need for coronary
revascularization.
Complications:
Complications of angina pectoris include unstable angina, MI, and death.
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Prognosis:
Important prognostic indicators in patients with angina pectoris include LV function, severity
and location of atherosclerotic lesions, and response of symptoms to medical treatment.
LV function is the strongest predictor of long-term survival. Elevated LV end-diastolic pressure
and volume along with reduced LV ejection fraction (<40%) are poor prognostic signs.
Critical lesions of left main and proximal left anterior descending coronary arteries are
associated with a greater risk. Mortality rates are also directly associated with the number of
epicardial arteries involved.
Unstable angina, recent MI, or both is a sign of atherosclerotic plaque instability, which is a
strong predictor of increased risk of short-term coronary events.
A number of signs during noninvasive testing are predictive of a higher risk of coronary events,
including ST-segment depression of more than 2 mm at a low workload, ST-segment depression
that persists for more than 5 minutes after termination of exercise, and failure of blood pressure
to rise or an actual drop in blood pressure.
Patients who continue to smoke after an MI have a 22-47% increased risk of reinfarction and
death.
In general, Prinzmetal angina and syndrome X are associated with excellent long-term
prognoses.
Patient Education:
Educating patients about the benefits of smoking cessation, a low-cholesterol diet, physical
activity, and periodic screening for diabetes mellitus and hypertension is the prime component
of a long-term management plan.
For excellent patient education resources, visit eMedicine's Circulatory Problems Center,
Cholesterol Center, Heart Center, and Statins Center. Also, see eMedicine's patient education
articles Angina Pectoris, High Cholesterol, Understanding Your Cholesterol Level, Lifestyle
Cholesterol Management, Understanding Cholesterol-Lowering Medications, Chest Pain,
Coronary Heart Disease, and Heart Attack.
MISCELLANEOUS
Medical/Legal Pitfalls:
In patients with stable angina pectoris, even the most carefully performed history and physical
examination have limitations. Classification of these patients solely on the basis of history and
physical examination findings may lead to serious mistakes. Some type of stress testing is
usually indicated to confirm the diagnosis and quantitate the severity of ischemia.
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In women, elderly persons, and diabetic patients, coronary artery disease may manifest with
atypical presentations other than angina pectoris, such as silent ischemia or infarction.
Physicians should use a careful approach when evaluating these patients.
Background: Myocardial infarction (MI) is the irreversible necrosis of heart muscle secondary
to prolonged ischemia. This usually results from an imbalance of oxygen supply and demand.
The appearance of cardiac enzymes in the circulation generally indicates myocardial necrosis.
MI is considered, more appropriately, part of a spectrum referred to as acute coronary
syndromes (ACSs), which also includes unstable angina and nonST-elevation MI (NSTEMI).
Patients with ischemic discomfort may or may not have ST-segment elevation. Most of those
with ST-segment elevation will develop Q waves. Those without ST elevations will ultimately
be diagnosed with unstable angina or NSTEMI based on the presence of cardiac enzymes.
Fig. Pathogenesis of MI
MI may lead to impairment of systolic function or diastolic function and to increased
predisposition to arrhythmias and other long-term complications.
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Pathophysiology: Atherosclerosis is the disease primarily responsible for most ACS cases.
Approximately 90% of MIs result from an acute thrombus that obstructs an atherosclerotic
coronary artery. Plaque rupture is considered to be the major trigger of coronary thrombosis.
Following plaque rupture, platelet activation and aggregation, coagulation pathway activation,
and endothelial vasoconstriction occur and lead to coronary thrombosis and occlusion.
Atherogenesis
Fig. Atherogenesis
Frequency: In the US: Approximately 1.5 million cases of MI occur each year.
Internationally: Cardiovascular diseases cause 12 million deaths throughout the world each
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year, according to the third monitoring report of the World Health Organization, 1991-93. They
cause half of all deaths in several developed countries and are one of the main causes of death
in many developing countries; they are the major cause of death in adults everywhere.
Mortality/Morbidity: Cardiovascular disease is the leading cause of death in the United
States; approximately 500,000-700,000 deaths related to the coronary artery occur each year.
Ischemic heart disease is the leading cause of death worldwide. Approximately 6.3 million
deaths due to heart disease occurred in 1990 worldwide, which represents 29% of all deaths.
The prevalence of coronary artery disease (CAD) is increasing rapidly in nonindustrialized
countries.
Race: Cardiovascular disease is the leading cause of morbidity and mortality among African
American, Hispanic, and white populations in the United States.
Sex: A male predominance in incidence exists up to approximately age 70 years, when the
sexes converge to equal incidence.
Premenopausal women appear to be somewhat protected from atherosclerosis, possibly owing
to the effects of estrogen.
Age:Incidence increases with age. Most patients who develop an acute MI are older than 60
years. Elderly people also tend to have higher rates of morbidity and mortality from their
infarcts.
CLINICAL
History:
Chest pain
This is usually described as a substernal pressure sensation that also may be described as
squeezing, aching, burning, or even sharp pain.
Prolonged chest discomfort lasting longer than 30 minutes is most compatible with infarction.
Radiation to the left arm or neck is common.
The sensation is precipitated by exertion and relieved by rest and nitroglycerin.
Chest pain may be associated with nausea, vomiting, diaphoresis, dyspnea, fatigue, or
palpitations.
Atypical chest pain is common, especially in patients with diabetes and in elderly patients.
However, any patient may present with atypical symptoms. These symptoms are considered the
anginal equivalent for that patient.
Shortness of breath
Shortness of breath may be the patient's anginal equivalent or a symptom of heart failure.
It is due to elevated end-diastolic pressures secondary to ischemia, which may then lead to
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Physical: Physical examination findings can vary; one patient may be comfortable in bed, with
normal examination results, while another may be in severe pain with significant respiratory
distress requiring ventilatory support.
Low-grade fever may be present.
Hypotension or hypertension can be observed depending on the extent of the MI.
Fourth heart sound (S4) may be heard in patients with ischemia. With ischemia, diastolic
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dysfunction is the first physiologically measurable effect and this can then cause a stiff
ventricle and an audible S4.
Dyskinetic cardiac bulge (in anterior wall MI) can occasionally be palpated.
Systolic murmur can be heard if mitral regurgitation (MR) or ventricular septal defect (VSD)
develops.
Other findings include cool, clammy skin and diaphoresis.
Signs of congestive heart failure (CHF) may be found, including the following:
Third heart sound (S3) gallop
Pulmonary rales
Lower extremity edema
Elevated jugular venous pressure
Fig Stages of MI
Causes: Atherosclerosis with occlusive or partially occlusive thrombus formation,
Nonmodifiable risk factors for atherosclerosis, Age, Sex, Family history of premature coronary
heart disease, Modifiable risk factors for atherosclerosis, Smoking or other tobacco use,
Diabetes mellitus, Hypertension, Dyslipidemia, Obesity, New and other risk factors for
atherosclerosis, Elevated homocysteine levels, Male pattern baldness. Sedentary lifestyle
and/or lack of exercise, Psychosocial stress, Presence of peripheral vascular disease, Poor oral
hygiene, Nonatherosclerotic causes, Vasculitis , Coronary emboli , Congenital coronary
anomalies, Coronary trauma, Coronary spasm, Drug use (cocaine), Factors that increase oxygen
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requirement, such as heavy exertion, fever, or hyperthyroidism , Factors that decrease oxygen
delivery, such as hypoxemia of severe anemia
Other Problems to be Considered:
Pneumonia
Pancreatitis
Lab Studies:
Cardiac enzymes: In patients with suspected MI, obtain cardiac enzymes at regular intervals,
starting upon admission and serially for as long as 24 hours.
Creatine kinase level
Creatine kinase comprises 3 isoenzymes, including creatine kinase with muscle subunits
(CK-MM), which is found mainly in skeletal muscle; creatine kinase with brain subunits
(CK-BB), predominantly found in the brain; and myocardial muscle creatine kinase (CK-MB),
which is found mainly in the heart.
Serial measurements of CK-MB isoenzyme levels were previously the standard criterion for
diagnosis of MI. CK-MB levels increase within 3-12 hours of onset of chest pain, reach peak
values within 24 hours, and return to baseline after 48-72 hours. Levels peak earlier (wash out)
if reperfusion occurs. Sensitivity is approximately 95%, with high specificity. However,
sensitivity and specificity are not as high as for troponin levels, and the trend has favored using
troponins for the diagnosis of MI.
Troponin levels
Troponin levels are now considered the criterion standard in defining and diagnosing MI,
according to the American College of Cardiology (ACC)/American Heart Association (AHA)
consensus statement on MI (Braunwald, 2000).
Cardiac troponin levels (troponin-T and troponin-I) have a greater sensitivity and specificity
than CK-MB levels in detecting MI. They have important diagnostic and prognostic roles.
Positive troponin levels are considered virtually diagnostic of MI in the most recent ACC/AHA
revisions, as they are without equal in combined specificity and sensitivity in this diagnosis.
Serum levels increase within 3-12 hours from the onset of chest pain, peak at 24-48 hours, and
return to baseline over 5-14 days.
Myoglobin levels
Urine myoglobin levels rise within 1-4 hours from the onset of chest pain.
Myoglobin levels are highly sensitive but not specific, and they may be useful within the
context of other studies and in early detection of MI in the ED.
Complete blood cell count
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Obtain a CBC count if MI is suspected to rule out anemia as a cause of decreased oxygen
supply and prior to giving thrombolytics.
Leukocytosis is also common, but not universal, in the setting of acute MI.
A platelet count is necessary if a IIb/IIIa agent is considered; furthermore, the patient's WBC
count may be elevated modestly in the setting of MI, signifying an acute inflammatory state.
Chemistry profile
In the setting of MI, closely monitor potassium and magnesium levels.
Creatinine level is also needed prior to initiating treatment with an angiotensin-converting
enzyme (ACE) inhibitor.
Lipid level profile: This may be helpful if obtained upon presentation because levels can
change after 12-24 hours of an acute illness.
C-reactive protein (CRP) levels: Consider measuring CRP levels and other markers of
inflammation upon presentation if an ACS is suspected.
Imaging Studies:
Chest radiography
Upon presentation, obtain a chest radiograph to assess the patient's heart size and the presence
or absence of decompensated CHF with or without pulmonary edema.
A chest radiograph may also assist in diagnosing concomitant disease, such as pneumonia in an
elderly patient, as a precipitating cause for MI.
Echocardiography
An echocardiogram may play an important role in the setting of MI.
Regional wall motion abnormalities can be identified, which are especially helpful if the
diagnosis is questionable.
An echocardiogram can also define the extent of the infarction and assess overall left ventricle
(LV) and right ventricle (RV) function. In addition, an echocardiogram can identify
complications, such as acute MR, LV rupture, or pericardial effusion.
Myocardial perfusion imaging
Prior to discharge, obtain myocardial perfusion imaging to assess the extent of residual
ischemia if the patient has not undergone cardiac catheterization. The extent of ischemia can
guide further therapy as to whether to proceed with catheterization or to continue conservative
therapy.
Myocardial perfusion has been shown to be a valuable method for triage of patients with chest
pain in the ED. Significant variability exists among centers, and the results of the trials can be
applied only to those centers with proven reliability and experience.
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Cardiac angiography
Cardiac catheterization defines the patient's coronary anatomy and the extent of the disease.
Most investigators recommend that all patients with MI should undergo cardiac catheterization,
if it is available.
Patients with cardiogenic shock, intractable angina despite medications, or severe pulmonary
congestion should undergo cardiac catheterization immediately.
Other Tests:
The electrocardiogram (ECG) is the most important tool in the initial evaluation and triage of
patients in whom an ACS is suspected (see Images 1-3). It is confirmatory of the diagnosis in
approximately 80% of cases.
Obtain an ECG immediately if MI is considered or suspected.
In patients with inferior MI, record a right-sided ECG to rule out RV infarct.
Qualified personnel should review the ECG as soon as possible.
Perform ECGs serially upon presentation to evaluate progression and assess changes with and
without pain.
Obtain daily serial ECGs for the first 2-3 days and additionally as needed.
Convex ST-segment elevation with upright or inverted T waves is generally indicative of MI in
the appropriate clinical setting.
ST depression and T-wave changes may also indicate evolution of NSTEMI.
TREATMENT
Medical Care: Initial therapy for acute MI is directed toward restoration of perfusion in order
to salvage as much of the jeopardized myocardium as possible. This may be accomplished
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through medical or mechanical means, such as angioplasty or coronary artery bypass grafting.
Further treatment is based on (1) restoration of the balance between the oxygen supply and
demand to prevent further ischemia, (2) pain relief, and (3) prevention and treatment of any
complications that may arise.
Thrombolytic therapy has been shown to improve survival rates in patients with acute MI if
administered in a timely fashion in the appropriate group of patients. If PCI capability is not
available or will cause a delay greater than 90 minutes, then the optimal approach is to
administer thrombolytics within 12 hours of onset of symptoms in patients with ST-segment
elevation greater than 0.1 mV in 2 or more contiguous ECG leads, new left bundle-branch
block (LBBB), or anterior ST depression consistent with posterior infarction. Tissue
plasminogen activator (t-PA) is superior to streptokinase in achieving a higher rate of coronary
artery patency; however, the key to efficacy lies in the speed of the delivery of therapy. Recent
trials show a high patency rate if a IIb/IIIa receptor antagonist is combined with a half dose of a
thrombolytic agent as the initial reperfusion strategy. The reduced dose of a thrombolytic agent
combined with a potent platelet inhibitor may prove to be the preferred method for medical
reperfusion. Larger clinical trials are pending.
Aspirin and/or antiplatelet therapy Aspirin has been shown to decrease mortality and
re-infarction rates after MI. Administer aspirin immediately, which the patient should chew if
possible upon presentation. Continue aspirin indefinitely unless an obvious contraindication,
such as a bleeding tendency or an allergy, is present. Clopidogrel may be used as an alternative
in cases of a resistance or allergy to aspirin. Recent data from the CLARITY trial (CLopidogrel
as Adjunctive ReperfusIon Therapy Thrombolysis in Myocardial Infarction [TIMI] 28) suggest
that adding clopidogrel to this regimen is safe and effective. The clopidogrel dose used was
300 mg.
Administer a platelet glycoprotein (GP) IIb/IIIa-receptor antagonist, in addition to
acetylsalicylic acid and unfractionated heparin (UFH), to patients with continuing ischemia or
with other high-risk features and to patients in whom a percutaneous coronary intervention
(PCI) is planned. Eptifibatide and tirofiban are approved for this use. Abciximab also can be
used for 12-24 hours in patients with unstable angina or NSTEMI in whom a PCI is planned
within the next 24 hours.
Beta-blockers reduce the rates of reinfarction and recurrent ischemia and possibly reduce the
mortality rate if administered within 12 hours after MI. Administer routinely to all patients
with MI unless a contraindication is present.
Heparin (and other anticoagulant agents) has an established role as an adjunctive agent in
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patients receiving t-PA but not with streptokinase. Heparin is also indicated in patients
undergoing primary angioplasty. Little data exist with regard to efficacy in patients not
receiving thrombolytic therapy in the setting of acute MI. Lowmolecular-weight heparins
(LMWHs) have been shown to be superior to UFHs in patients with unstable angina or
NSTEMI.
Nitrates have no apparent impact on mortality rate in patients with ischemic syndromes. Their
utility is in symptomatic relief and preload reduction. Administer to all patients with acute MI
within the first 48 hours of presentation, unless contraindicated (ie, in RV infarction).
ACE inhibitors reduce mortality rates after MI. Administer ACE inhibitors as soon as
possible as long as the patient has no contraindications and remains in stable condition. ACE
inhibitors have the greatest benefit in patients with ventricular dysfunction. Continue ACE
inhibitors indefinitely after MI. Angiotensin-receptor blockers may be used as an alternative in
patients who develop adverse effects, such as a persistent cough, although initial trials need to
be confirmed.
Surgical Care:
Percutaneous coronary intervention
PCI is the treatment of choice in most patients with STEMI, assuming a door to needle time of
less than 90 minutes. PCI provides greater coronary patency (>96% thrombolysis in myocardial
infarction [TIMI] 3 flow), lower risk of bleeding, and instant knowledge about the extent of the
underlying disease. Studies have shown that primary PCI has a mortality benefit over
thrombolytic therapy.
The choice of primary PCI should be individualized to each institution and to the patient's
presentation and timing.
The widespread use of stenting and adjunctive IIb/IIIa therapy are improving the results of
primary PCI. A recently published trial showed that, in patients with acute MI, coronary
stenting and abciximab lead to a greater degree of myocardial salvage and a better clinical
outcome than fibrinolysis with thrombolytic therapy. Improvement of long- and short-term
outcomes, however, depends highly on the speed with which reperfusion is achieved.
Primary PCI is also the treatment of choice in patients with cardiogenic shock, patients in
whom thrombolysis failed, and those with high risk of bleeding or contraindications to
thrombolytic therapy.
Only an experienced operator should perform primary PTCA, and PTCA should be performed
only where the appropriate facilities are available. Operators should have at least 75 cases per
year, while the center should perform at least 200 cases per year as per the recommendations of
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the ACC.
Emergent or urgent coronary artery graft bypass surgery is indicated in patients in whom
angioplasty fails and in patients who develop mechanical complications such as a VSD, LV, or
papillary muscle rupture.
Consultations:
ED personnel should initiate evaluation and treatment, including administering a thrombolytic
agent.
Obtain cardiology consultation immediately if primary PCI is considered. Otherwise,
cardiology consultation may be obtained as needed and upon admission. Consultation may be
obtained sooner if the patient presents with significant heart failure, mechanical complications,
arrhythmias, or other complicating factors.
Diet: Initially, keep the patient on nothing by mouth (NPO) until his or her condition has been
stabilized and treated. Following initial therapy and admission, a dietitian should instruct the
patient regarding appropriate diet, as recommended by the AHA.
A low-salt, low-fat, and low-cholesterol diet is generally recommended.
Activity: Confine patients to bed rest to minimize oxygen consumption until reperfusion and
initial therapy are complete. This usually lasts about 24-48 hours; after that, the patient's
activity may be accelerated slowly as tolerated and as the clinical situation allows.
Initiate cardiac rehabilitation prior to discharge.
MEDICATION
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
Drug Category: Salicylates -- The antiplatelet effects of these agents may improve
mortality rate.
Aspirin (Anacin, Ascriptin, Bayer Aspirin) --
Early administration of aspirin in patients
Drug Name
with acute MI has been shown to reduce
cardiac mortality rate by 23% in first mo.
Adult Dose 160-325 mg PO or chewed
Pediatric Dose 10-15 mg/kg/dose PO q4-6h
Documented hypersensitivity, liver
damage; hypoprothrombinemia; vitamin K
Contraindications deficiency; bleeding disorders; asthma
Because of association with Reye
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FOLLOW-UP
Further Inpatient Care: Admit patients with MI to a coronary care unit. Monitor patients
carefully for arrhythmia, recurrent ischemia, and other possible complications. The patient may
be transferred to a telemetry unit 24-48 hours after admission if no complications occur.
Hospitalize the patient for approximately 4-5 days after MI. Patients who undergo primary PCI
or have an immediate cardiac catheterization may be discharged sooner if their hospital course
is without incident.
Perform a coronary angiography on high-risk patients prior to discharge to evaluate their need
for revascularization.
In the case of patients who have not had a cardiac catheterization and have no complications,
perform a submaximal stress test prior to discharge to assess their subsequent risk.
Further Outpatient Care:
Arrange for follow-up within 2 weeks of discharge.
Arrange for cardiac rehabilitation.
In/Out Patient Meds:
The long-term use of aspirin in patients who have had an MI results in significant reduction in
subsequent mortality rate.
Beta-blocker therapy has confirmed therapeutic benefit in survivors of acute MI. This therapy
is most beneficial in patients with the highest risk.
ACE inhibitor use in patients with known CAD has been shown to reduce mortality rate.
Many trials have shown a clear benefit of lipid-lowering therapy in the secondary and primary
prevention of CAD. The National Cholesterol Education Panel has set guidelines for target
cholesterol levels. In general, patients who have experienced MI should achieve low-density
lipoprotein (LDL) level less than 100 mg/dL, high-density lipoprotein (HDL) level greater than
40 mg/dL, and triglyceride level less than 200 mg/dL. High-risk patients should be treated to a
target LDL level of less than 70 mg/dL.
Schwartz et al recently showed in the MIRACL trial that initiating atorvastatin during
hospitalization for an ACS, irrespective of lipid levels, reduces the frequency of recurrent
ischemic events. This treatment significantly reduced the frequency of the combined end point
of death, recurrent death, MI, or worsening unstable angina requiring hospitalization.
Clopidogrel should be prescribed for a year following discharge if the patient has no
contraindications and cost is not prohibitive. To reduce the risk of bleeding, the aspirin dose
can be reduced to 81 mg.
Transfer: A patient in whom thrombolytic therapy fails should be transferred to a facility
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causes. Atrial fibrillation and other atrial tachycardias may also occur. Treat any tachycardia by
correcting the cause first or by pharmacotherapy, because persistent tachycardias may lead to
further ischemia.
Conduction abnormalities may result from ischemia, necrosis, or chronotropic drugs, or as a
vagal response. Recognition and treatment of these abnormalities are important in short- and
long-term outcomes. Possible therapies include medications, such as atropine, or even
placement of a transvenous pacemaker if indicated. Conduction disturbances are seen more
commonly in the setting of inferior MI but are more ominous when seen with an anterior
infarct.
Recurrent ischemia may be due to incomplete reperfusion. Postinfarct angina occurs in 20-30%
of patients. This is an indication to proceed to cardiac catheterization followed by mechanical
revascularization as needed.
CHF can be due to systolic dysfunction or diastolic dysfunction in the setting of MI. The
severity of the heart failure and systolic dysfunction depends on the extent of the infarct and
the presence of any other complications, such as acute mitral regurgitation. Aggressive
treatment is indicated to avoid worsening of the situation. Treatment may include any or all of
the following: nitrates, morphine, diuretics, ACE inhibitors, and other vasodilators if needed.
Digoxin has no role in the setting of acute CHF due to ischemia.
Cardiogenic shock is defined as a systolic BP less than 90 mm Hg in the presence of organ
hypoperfusion. The mortality rate due to cardiogenic shock is as high as 70% in some series.
Patients usually require inotropic agents, such as dopamine or dobutamine, and occasionally an
intraaortic balloon pump is required. Patients presenting with cardiogenic shock should
proceed directly to the catheterization lab, if available, for mechanical revascularization.
Acute MR is most common in the setting of an inferoposterior MI. This is secondary to
ischemia, necrosis, or rupture of the LV papillary muscle (especially the posteromedial
papillary muscle). This can lead to mild-to-severe MR with CHF. Diagnosis can be made on
physical examination, but an echocardiogram is necessary to confirm the diagnosis and assess
the severity, which helps in the choice of therapy. Treatment consists of aggressive afterload
reduction, intraaortic balloon pump insertion, and immediate surgical repair.
Ventricular rupture occurs in the interventricular septum or the LV free wall. Both are
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catastrophic events with mortality rates greater than 90%. Prompt recognition, stabilization,
and surgical repair are crucial to any hope of survival. Ventricular rupture is more common in
women, patients with hypertension, and those receiving NSAIDs or steroids. An
echocardiogram can usually define the abnormality, and a right heart catheterization can show
an oxygen saturation step-up in the case of a septal rupture.
Other complications include pericarditis, ventricular aneurysms, mural thrombi, and
hypertension. Recognition and treatment can be life saving.
Prognosis:
Acute MI is associated with a 30% mortality rate; half of the deaths occur prior to arrival at the
hospital.
An additional 5-10% of survivors die within the first year after their MI.
Approximately half of all patients with an MI are rehospitalized within 1 year of their index
event.
Overall, prognosis is highly variable and depends largely on the extent of the infarct, the
residual LV function, and whether the patient underwent revascularization.
Patient Education:
Diet
Diet plays an important role in the development of CAD. Educate post-MI patients about the
role of a low-cholesterol and low-salt diet.
Educate patients about the AHA dietary guidelines regarding a low-fat, low-cholesterol diet.
A dietitian should see and evaluate all post-MI patients prior to their discharge.
Smoking cessation
Educate all post-MI patients regarding the critical role of smoking in the development of CAD.
Smoking cessation classes should be offered to help patients avoid smoking after their MI.
For excellent patient education resources, visit eMedicine's Cholesterol Center. Also, see
eMedicine's patient education articles High Cholesterol, Understanding Your Cholesterol
Level, Lifestyle Cholesterol Management, Understanding Cholesterol-Lowering Medications,
Chest Pain, Coronary Heart Disease, and Heart Attack.
MISCELLANEOUS
Medical/Legal Pitfalls:
Failure to make the diagnosis of an MI is the leading cause of litigation against ED physicians
and cardiologists.
Consider atypical presentations in elderly patients, patients with diabetes, and women. Assess
all patients carefully, especially if they have significant cardiac risk factors.
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Review all ECGs that are obtained in a prompt fashion because time is crucial.
Obtain cardiology consultation whenever the diagnosis is questionable.
Consider an echocardiogram to assess wall motion abnormalities in difficult cases with
nondiagnostic ECGs, such as with an LBBB.
Special Concerns:
Right ventricular infarction
Approximately one third of patients with inferior MI develop RV infarction. RV infarction
presents a special challenge because the adjunctive therapy, other than reperfusion, is
somewhat different.
A right-sided ECG with greater than 1 mm ST elevation in V3R or V4R leads describes an RV
infarct. An echocardiogram may be helpful in confirming the diagnosis. On physical
examination, signs of right heart failure, such as elevated jugular venous pulsation, right-sided
S3, Kussmaul sign, or hypotension, may be present, and the patient may have clear lung fields.
The patient becomes volume dependent to maintain adequate LV and RV filling. Occasionally,
dobutamine may be needed, or even an intraaortic balloon pump for hemodynamic support.
Avoid nitrates or any medications that lower preload in this setting. A pulmonary artery
catheter can be helpful in guiding therapy.
Elderly patients
Elderly patients with acute MI are at increased risk of developing complications. Treat these
patients aggressively.
Elderly patients have an increased risk of bleeding with thrombolytic therapy, but they also
have the most to gain from this therapy.
Very elderly patients should undergo primary angioplasty if available, but they should receive
thrombolytics if excessive delay is anticipated before angioplasty can be performed.
LITERATURE
Antman EM, McCabe CH, Gurfinkel EP, et al: Enoxaparin prevents death and cardiac ischemic
events in unstable angina/non-Q-wave myocardial infarction. Results of the thrombolysis in
myocardial infarction (TIMI) 11B trial. Circulation 1999 Oct 12; 100(15): 1593-601.
Braunwald E, Antman EM, Beasley JW, et al: ACC/AHA guidelines for the management of
patients with unstable angina and non-ST-segment elevation myocardial infarction. A report of
the American College of Cardiology/American Heart Association Task Force on Practice
Guidelines (Committee on the Manag. J Am Coll Cardiol 2000 Sep; 36(3): 970-1062.
Califf RM: Acute myocardial infarction and other acute ischemic syndromes. In: Braunwald E,
ed. Atlas of Heart Disease. 8th ed. St. Louis, Mo: Mosby; 1996: 1.1-15.13.
Ornato JP: Chest pain emergency centers: improving acute myocardial infarction care. Clin
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344(8934): 1383-9.
Shepherd J, Blauw GJ, Murphy MB, et al: Pravastatin in elderly individuals at
risk of vascular disease (PROSPER): a randomised controlled trial. Lancet
2002 Nov 23; 360(9346): 1623-30.
Yusuf S, Zhao F, Mehta SR, et al: Effects of clopidogrel in addition to aspirin in
patients with acute coronary syndromes without ST-segment elevation. N Engl J
Med 2001 Aug 16; 345(7): 494-502.
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Primary valvular heart disease ranks well below coronary heart disease, stroke, hypertension,
obesity, and diabetes as major threats to the public health. Nevertheless, it is the source of
significant morbidity and mortality. Rheumatic fever is the dominant cause of valvular heart
disease in developing countries. Its prevalence has been estimated to range from as low as 1.0
per 100,000 school-age children in Costa Rica to as high as 150 per 100,000 in China.
Rheumatic heart disease accounts for 1265% of hospital admissions related to cardiovascular
disease and 210% of hospital discharges in some developing countries. Prevalence and
mortality rates vary among communities even within the same country as a function of
crowding and the availability of medical resources and population-wide programs for detection
and treatment of Group A streptococcal pharyngitis. In economically deprived areas, tropical
and subtropical climates (particularly on the Indian subcontinent), Central America, and the
Middle East, rheumatic valvular disease progresses more rapidly than in more-developed
nations and frequently causes serious symptoms in patients <20 years of age. This accelerated
natural history may be due to repeated infections with more virulent strains of rheumatogenic
streptococci.
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TS, a relatively uncommon valvular lesion in North America and Western Europe, is more
common in tropical and subtropical climates, especially in southern Asia and in Latin America.
As of the year 2000, worldwide death rates for rheumatic heart disease approximated 5.5 per
100,000 population (n = 332,000), with the highest rates reported from Southeast Asia.
Although there have been reports of recent isolated outbreaks of streptococcal infection in
North America, valve disease in developed countries is now dominated by degenerative or
inflammatory processes that lead to valve thickening, calcification, and dysfunction. The
prevalence of valvular heart disease increases with age. Important left-sided valve disease may
affect as many as 1213% of adults over the age of 75.
The incidence of infective endocarditis has increased with the aging of the population, the
more widespread prevalence of vascular grafts and intracardiac devices, the emergence of more
virulent multidrug-resistant microorganisms, and the growing epidemic of diabetes. Infective
endocarditis has become a more frequent cause of acute valvular regurgitation.
Bicuspid aortic valve disease affects as many as 12% of the population, and an increasing
number of childhood survivors of congenital heart disease present later in life with valvular
dysfunction. The past several years have witnessed significant improvements in surgical
outcomes with progressive refinement of relatively less-invasive techniques. Percutaneous heart
valve replacement or repair is under active clinical investigation.
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Ankylosing spondylitis
Root disease
Aortic dissection
Cystic medial degeneration
Marfan syndrome
Bicuspid aortic valve
Nonsyndromic familial aneurysm
Aortitis
Hypertension
Tricuspid stenosis Rheumatic
Congenital
Tricuspid regurgitation Primary
Rheumatic
Endocarditis
Myxomatous (TVP)
Carcinoid
Congenital (Ebstein's)
Trauma
Papillary muscle injury (post-MI)
Secondary
RV and tricuspid annular dilatation
Multiple causes of RV enlargement (e.g., long-standing pulmonary
HTN)
Chronic RV apical pacing
Pulmonic stenosis Congenital
Carcinoid
Pulmonic regurgitation Valve disease
Congenital
Postvalvotomy
Endocarditis
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Annular enlargement
Pulmonary hypertension
Idiopathic dilatation
Marfan syndrome
Mitral regurgitation
Mitral regurgitation affects more than 2 million people in the USA. The main causes are
classified as degenerative (with valve prolapse) and ischaemic (ie, due to consequences of
coronary disease) in developed countries, or rheumatic (in developing countries). This disorder
generally progresses insidiously, because the heart compensates for increasing regurgitant
volume by left-atrial enlargement, causes left-ventricular overload and dysfunction, and yields
poor outcome when it becomes severe. Doppler-echocardiographic methods can be used to
quantify the severity of mitral regurgitation. Yearly mortality rates with medical treatment in
patients aged 50 years or older are about 3% for moderate organic regurgitation and about 6%
for severe organic regurgitation. Surgery is the only treatment proven to improve symptoms and
prevent heart failure. Valve repair improves outcome compared with valve replacement and
reduces mortality of patient with severe organic mitral regurgitation by about 70%. The best
short-term and long-term results are obtained in asymptomatic patients operated on in advanced
repair centres with low operative mortality (<1%) and high repair rates (8090%). These
results emphasise the importance of early detection and assessment of mitral regurgitation.
Mitral regurgitation is defined as systolic retrograde flow from the left ventricle into the left
atrium. Although a trivial form of this valve disease is often seen in healthy people,
epidemiological data show that moderate or severe regurgitation is the most frequent valve
disease in the USA and is the second most common form of valvular heart disease needing
surgery in Europe. Despite substantial reduction in the incidence of rheumatic heart disease,
mitral regurgitation is a growing public health problem. Moderate or severe regurgitation is
frequent, its prevalence increases with age, and it was estimated to affect 2025 million
people in the USA in 2000a number expected to almost double by 2030 because of
population ageing and growth. Although no large epidemiological studies are available, mitral
regurgitation is prevalent in young adults in countries with endemic rheumatic fever.
Substantial progress has been achieved to improve its diagnosis, quantification, and surgical
treatment. Improved knowledge of clinical outcome of patients with mitral regurgitation
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Major causes of surgical mitral regurgitation in western countries are degenerative (primary
myxomatous disease, primary flail leaflets, annular calcification), representing 6070% of
cases, followed by ischaemic mitral regurgitation (20%), endocarditis (25%), rheumatic
(25%), and miscellaneous causes (cardiomyopathies, inflammatory diseases, drug-induced,
traumatic, congenital). Ischaemic disease probably represents a large proportion of the
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non-surgical disease burden. Nomenclature and mechanisms of major causes are summarised
below.
Degenerative mitral regurgitation is usually related to mitral-valve prolapse and rarely to
isolated mitral annular calcification. Mitral-valve prolapse is an abnormal systolic valve
movement into the left atrium (2 mm beyond saddle-shaped annular level). This excessive
movement can be seen with other causes such as endocarditis. Prolapse might be of moderate
magnitude (leaflet tips remain in the left ventricleie, billowing mitral valve) or can be severe
(eversion of leaflet tip into left atriumie, flail leafletusually caused by ruptured chordae).
The main phenotypes of mitral prolapse are diffuse myxomatous degeneration (mitral-valve
prolapse syndrome or Barlow's disease, sometimes with posterior annular translocation into left
atrium) or primary flail leaflets with ruptured chordae affecting the posterior leaflet in 70% of
cases, and accompanied by myxomatous degeneration localised to the flail segment and
generally normal valve morphology elsewhere. Myxomatous degeneration remodels valve tissue
by increasing the spongiosa layer and valve water content and thickness, with
mucopolysaccharide and matrix changes, as a functional manifestation of metalloproteinase
alterations. These mitral tissue changes and prolapse might be genetically transmitted and
X-chromosome linked. Degenerative mitral regurgitation is the most reparable form, warranting
early and careful assessment.
Echocardiographic appearance of the two main anatomical types of mitral regurgitation from apical views
centred on the mitral valve
(A) An example of a flail posterior leaflet with the tip of the leaflet floating in the left atrium. Note the
otherwise grossly normal anterior leaflet. (B) An example of functional mitral regurgitation. Strut chordae
(long arrows) to the anterior and posterior leaflets exert an abnormal traction on the body of the leaflets,
which displaces (arrowheads) the leaflets towards the ventricular apex, creating an area of tenting above the
mitral annulus and an incomplete coaptation. LA=left atrium. LV=left ventricle.
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The ischaemic form of this disease rarely results from an organic mechanism (papillary-muscle
rupture) and is rarely acute. Frequently, it is functional (structurally normal leaflets) and
chronic, epitomising left-ventricular disease that causes valvular dysfunction. Papillary-muscle
dysfunction plays little part in the generation of functional mitral regurgitation, which is
mostly caused by apical and inferior-papillary-muscle displacement due to ischaemic
left-ventricular remodelling. Because chordae are non-extensible, papillary-muscle
displacement exerts traction on leaflets through strut chordae implanted on the body of leaflets,
resulting in tethered and apically displaced leaflets (tenting). Coupled with annular flattening,
enlargement, and decreased contraction, mitral valve tenting results in coaptation loss that
yields functional mitral regurgitation. Asymmetric tenting due to regional scarring (inferior
infarction) might explain commissural jets of ischaemic disease. Rheumatic mitral
regurgitationpast the acute phasecauses chordal and leaflet retraction, which, amplified by
annular dilatation, results in coaptation loss. Postinflammatory and postradiation mitral
regurgitations have similar mechanisms. Retraction of tissue is a major limitation to successful
valve repair.
Endocarditic mitral regurgitation might be caused by ruptured chordae or perforations. In all
causes, annular enlargement is common, is located mostly or exclusively on the posterior part
of the annular circumference, and surgical repair almost always requires annuloplasty.
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functional mitral regurgitation, ERO area is dynamic during systole, with large area during
short isovolumic contraction and relaxation phases caused by lesser ventricular pressure
apposing leaflets. This type of regurgitation is also dynamic with decreased loading or inotrope
administration, and might disappear with these interventions, whereas exercise most often
results in augmentation of ERO area. Long-term progression of organic disease is about 57
mL per year for RVol and is determined by ERO area progression caused by new lesions or
annular enlargement. Thus, mitral regurgitation is self-sustained, causing atrial and annular
enlargement, which in turn leads to increased ERO area.
The ventricular and atrial consequences of organic mitral regurgitation are initiated by volume
overload with increased preload and left-ventricular and left-atrial enlargement. Impedance to
ejection is reduced despite normal or increased vascular resistances, whereas myocardial
afterload (end-systolic wall stress) is normal with an end-systolic volume that is normal to
slightly increased. Thus, in organic disease, altered left-ventricular function might coexist with
normal or high ejection fraction. Borderline normal ejection fraction, between 5060%,
already implies overt left-ventricular dysfunction. Ventricular dysfunction should be suspected
when end-systolic dimensions are large but is often masked by a large ejection volume and is
revealed after surgical elimination of mitral regurgitation, with a postoperative average
immediate ejection fraction drop of about 10%. Diastolic ventricular dysfunction is difficult to
characterise, but seems to reduce exercise capacity.
Physiology of functional mitral regurgitation is even more complex than that of organic mitral
regurgitation since ventricular dysfunction predates the regurgitation. Nevertheless, functional
mitral regurgitation further increases atrial pressure, which leads to pulmonary hypertension
and heart failure. With increased atrial pressure and low driving force, functional regurgitation
often has low RVol and can be silent.
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and atrial fibrillation. These signs are important but not specific enough to rely solely on them
to suggest surgery.
Doppler echocardiography is the main method for assessment of patients with mitral
regurgitation. Transthoracic or transoesophageal echocardiography provides functional
anatomical information that is crucial for assessment of reparability by defining cause,
mechanism, presence of calcification, and localisation of lesions. Transoesophageal
echocardiography provides better imaging quality than transthoracic echocardiography but its
ability to detect details such as ruptured chordae rarely changes management. Transoesophageal
echocardiography essentially provides incremental clinically meaningful information (such as
reparability) when transthoracic echocardiography is of poor quality or when complex,
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flow is of uniform colour. It fills only part of the left atrium and might underestimate the regurgitation. The
observation of a large flow convergence should lead to suspicion of severe regurgitation. (B) Measurement of
the flow convergence with colour-flow imaging. The baseline of the colour scale has been brought down to
decrease the aliasing velocity to 53 cm/s (velocity at the blue-yellow border), which allows the flow
convergence (yellow) to be seen. The radius (r) of the flow convergence is used in the formula for calculation
of the instantaneous regurgitant flow (258 mL/s). Flow=628Valiasingr2=628530882=258 mL/s. Division
of this value by the jet velocity allows calculation of the effective regurgitant orifice of mitral regurgitation.
LA=left atrium. LV=left ventricle.
Doppler echocardiography also measures left-ventricular and left-atrial consequences of mitral
regurgitation. End-diastolic left-ventricular diameter and volume indicate volume overload
whereas end-systolic dimension shows volume overload and ventricular function. Patients with
left-ventricular ejection fraction less than 60% or end-systolic diameter of at least 4045 mm
are regarded as having overt left-ventricular dysfunction. Left-atrial diameter indicates volume
overload but also conveys important prognostic information. Left-atrial volume was
recommended as the preferred measure of atrial overload, (at least 40 mL/m2 for severe
dilatation) and predicts the occurrence of atrial fibrillation.
Exercise tests are used to define functional capacity. One in five asymptomatic patients shows
severe functional limitations during cardiopulmonary exercise. Peak oxygen consumption
compared with that expected for age, sex, and weight objectively measures functional
limitations versus normal reference values. Other exercise modalities, such as supine-bike
exercise, examine changes in severity of mitral regurgitation with activity, especially seen in
ischaemic and functional disease and might reveal poor prognosis when ERO area increases.
Standard postexercise echocardiography was used to detect exertional ventricular volume
increase as a predictor of postoperative left-ventricular dysfunction, but difficulties in
measurement of monoplane ventricular volumes hinder this approach. Other stress tests are
rarely used. Dobutamine echocardiography reduces mitral regurgitation universally, but in
selected patients with ischaemic disease it might reveal viability and ischaemia.
MRI shows mitral regurgitation jets, with limitations similar to those of colour-flow imaging;
quantitative measurements are possible but validation studies are few. This imaging method is
unique in revealing ventricular scars and in assessment of viability in ischaemic disease and is
useful in measurement of ventricular volumes but its incremental diagnostic role remains
unknown.
Detection of hormonal activation is important in many cardiac diseases. Atrial natriuretic
peptide has little specificity for mitral regurgitation and is strongly activated by arrhythmias,
irrespective of mitral regurgitation severity. B-type natriuretic peptide is of greater value than
atrial natriuretic peptide in patients with regurgitation. Its activation in organic disease is
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those with severe mitral regurgitation had, under medical management, yearly cardiac event
rates of 1012%including about 9% for heart failure and 5% for atrial fibrillation. Within
10 years of diagnosis, cardiac events arise in most patients with severe mitral regurgitation, and
death occurs or cardiac surgery is needed in at least 90%, making surgery an almost
unavoidable consideration in such patients. The risk of stroke is low, but in excess of that
expected in old patients and is strongly linked to occurrence of atrial fibrillation, and thus to
left-atrial size. Predictors of reduced survival under medical management are symptoms (class
III or IV), even if transient, reduced ejection fraction, severe mitral regurgitation with ERO area
of 40 mm2 or more, and hormonal activation, although not as well substantiated. Predictors of
cardiac events are atrial fibrillation, left-atrial enlargement of at least 4050 mm diameter, ,
flail leaflet or large ERO areaall markers of severe mitral regurgitationand, during
exercise, reduced peak oxygen consumption and possibly reduced right ventricular function.
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6575 years, and 45% for older than 75 years. Increased surgical risk is also linked to
preoperative severe symptoms or heart failure whereas ejection fraction has less effect. Surgery-
related determinants of operative risk are governed by mitral reparability, which ensures
reduced risk, whereas risk is increased with concomitant coronary artery bypass grafting. Other
associated procedures, such as tricuspid repair or replacement, or those aimed at treatment or
prevention of atrial fibrillation need a longer bypass time, which can increase risk. Long-term,
patient-related factors continue to affect outcome, particularly coronary disease or reduced
renal function. Age determines mortality but restoration of life expectancy is similar in young
and old patients. After surgery, patients with severe symptoms before surgery continue to have
increased mortality despite symptom relief, whereas in those with no or few symptoms,
restoration of life expectancy can be achieved. Similarly, patients with overt preoperative
ventricular dysfunction have increased postoperative mortality, especially with ejection fraction
less than 50%. Generally, a 10% early postoperative reduction in ejection fraction happens
after elimination of volume overload, whereas end-systolic characteristics (volume, wall stress)
are unchanged. This reduction is lowest after valve repairand is minimised by preservation of
subvalvular apparatus during valve replacement. Nevertheless, 2530% of patients with mitral
regurgitation present with postoperative left-ventricular dysfunction, especially those with
preoperative ejection fraction of less than 60% or end-systolic diameter at least of 4045 mm.
Occasional unexpected ventricular dysfunctions arise in patients with ejection fraction greater
than 60% and no perfect predictor has been identified. Hence, in some centres, prevention of
postoperative left-ventricular dysfunction relies on performance of early surgery when no sign
of left-ventricular alteration is present.
Coronary disease (even in the absence of angina) increases the risk of left-ventricular
dysfunction despite the performance of coronary artery bypass grafting. Although no clinical
trial has compared outcomes of patients randomised to repair versus replacement, observational
evidence suggests that the major surgical determinant of improved long-term outcome is valve
repair, which allows restoration of life expectancy and reduces the risk of heart failure after
surgery. Although mitral regurgitation can recur after repair, reoperation rates do not differ after
repair compared with replacement. Thus, mitral valve repair is widely regarded as the preferred
mode of correction of organic mitral regurgitation, especially degenerative.
For ischaemic mitral regurgitation, the natural history of the functional form is incompletely
definedwhereas that of papillary-muscle rupture is known to be rapidly fatal. Whether
functional regurgitation intrinsically causes poor outcome, or whether it indicates
left-ventricular alterations, is still disputed. However, association of severe ischaemic mitral
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regurgitation with severe outcomes, independent of ejection fraction, age, and presentation,
suggests that the regurgitation is indeed causal of the poor outcome. This prognostic role of
mitral regurgitation is now substantiated by results from studies of patients with acute or
chronic myocardial infarction, by clinical trials and by population studies. Another important
concept is that even modest regurgitation is associated with substantially increased mortality, a
fact proved by quantitative data. ERO area of ischaemic mitral regurgitation independently
predicts excess mortality. Patients with an area larger than 20 mm2 incur about a two-fold
increase in mortality risk and about a four-fold increase in the risk of heart failure compared
with those with a similar ischaemic left-ventricular dysfunction but no mitral regurgitation. The
better predictive value of ERO area than that of RVol is explained by the strong link between
ERO area and filling pressure. Increase in ERO area with exercise might additionally affect
clinical outcome, survival, and heart failure. Nevertheless, a clinical trial is needed to determine
whether surgical correction of the valvular consequence (ischaemic mitral regurgitation)
improves mortality and heart failure in this mainly ventricular disease. Clinical outcome of
functional disease caused by cardiomyopathy is not well defined but few data suggest that
mitral regurgitation yields poor outcomes.
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Outcomes after surgery for functional disease remain suboptimum. Operative mortality is still
high despite definite surgical improvements. Long-term mortality and heart failure rates are
high, although not unexpected in patients with coronary disease, previous myocardial
infarction, reduced ventricular function, and vascular comorbidity. These suboptimum
outcomes explain uncertainties in surgical indications. However, with low operative mortality,
postoperative heart failure and symptomatic improvements are possible.
Treatment
The natural history of untreated organic and functional mitral regurgitation emphasises the
importance of treatment of patients with severe regurgitation. Because the effects of various
treatments on survival have not been tested in randomised clinical trials, the value of any
approach is estimated on the basis of outcome studies.
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Fig Management strategy for patients with chronic severe mitral regurgitation. *Mitral valve (MV)
repair may be performed in asymptomatic patients with normal left ventricular (LV) function if performed by
an experienced surgical team and if the likelihood of successful MV repair is >90%. AF, atrial fibrillation;
Echo, echocardiography; EF, ejection fraction; ESD, end-systolic dimension; eval, evaluation; HT,
hypertension; MVR, mitral valve replacement. (From Bonow et al.)
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restricted to localised prolapse of the central segment of the anterior and posterior leaflets.
Second, annular dilatation is not addressed by the procedure and might cause residual
regurgitation.
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mechanical valve replacement is associated with high risk of embolism and haemorrhagic
complications (due to intensive warfarin treatment) but has potential for long-lasting durability.
Results of randomised trials showed that within 10 years of surgery these risks are balanced.
Older age determines the probability that bioprosthetic durability will be longer than life
expectancy, and is the main bioprosthesis insertion indication (usually >65 years of age).
Ability to achieve high-quality anticoagulation and patient's desire also affect the choice of
prosthesis. Irrespective of the prosthesis selected, conservation of subvalvular apparatus is
essential for preservation of ventricular function. The risk of prosthetic complications makes
surgical indications more restrictive when valve replacement is likely.
In view of the experimental nature of medical and interventional treatments for mitral
regurgitation, surgery is the only treatment recommended by management guidelines. Because
surgery is associated with small but definite risks, those patients with a higher risk of
spontaneous complications than of surgery-related complications are selected. Guidelines
should, in our opinion, be interpreted as a minimum to be applied by all physicians but should
not deter centres with better results than those of other centres from providing advanced care to
patients with mitral regurgitation. Furthermore, the absence of clinical trials and few
prospective studies create ample controversy, which should be addressed in future studies.
Although approaches to surgical indications are detailed in clinical guidelines, they are
summarised here. Rescue surgical indicationsclass I by guidelinesare compulsory. Patients
with organic mitral regurgitation who have developed severe symptoms (class III or IV), heart
failure, or signs of overt left-ventricular dysfunction (ejection fraction <60% or end-systolic
dimension 4045 mm) have an immediate high risk and therefore prompt surgeryrepair
(preferable) or replacementis indicated. Even with advanced heart failure or ventricular
dysfunction, contraindications to surgery are rare as long as mitral regurgitation remains severe,
emphasising the importance of quantitative assessment of disease. Such rescue surgery is
indispensable, but is not the preferred timing for surgery in organic disease. Indeed, patients
who need to be operated on at such a late stage of their disease have increased mortality after
surgery. This outcome emphasises the importance of early detection and assessment of mitral
regurgitation. In functional regurgitation, rescue surgery is the most frequent surgical
indication, but consideration should be given to surgery in symptomatic patients before heart
failure becomes intractable.
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Rheumatic fever is the leading cause of mitral stenosis (MS) (Table). Other less common
etiologies of obstruction to left atrial outflow include congenital mitral valve stenosis, cor
triatriatum, mitral annular calcification with extension onto the leaflets, systemic lupus
erythematosus, rheumatoid arthritis, left atrial myxoma, and infective endocarditis with large
vegetations.
Pure or predominant MS occurs in approximately 40% of all patients with rheumatic heart
disease and a history of rheumatic fever. In other patients with rheumatic heart disease, lesser
degrees of MS may accompany mitral regurgitation (MR) and aortic valve disease. With
reductions in the incidence of acute rheumatic fever, particularly in temperate climates and
developed countries, the incidence of MS has declined considerably over the past few decades.
However, it remains a major problem in developing nations, especially in tropical and
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semitropical climates.
In rheumatic MS, the valve leaflets are diffusely thickened by fibrous tissue and/or calcific
deposits. The mitral commissures fuse, the chordae tendineae fuse and shorten, the valvular
cusps become rigid, and these changes, in turn, lead to narrowing at the apex of the funnel-
shaped ("fish-mouth") valve. Although the initial insult to the mitral valve is rheumatic, the
later changes may be a nonspecific process resulting from trauma to the valve caused by altered
flow patterns due to the initial deformity. Calcification of the stenotic mitral valve immobilizes
the leaflets and narrows the orifice further. Thrombus formation and arterial embolization may
arise from the calcific valve itself, but in patients with atrial fibrillation (AF), thrombi arise
more frequently from the dilated left atrium (LA), particularly the left atrial appendage.
Pathophysiology
In normal adults, the area of the mitral valve orifice is 46 cm2. In the presence of significant
obstruction, i.e., when the orifice area is reduced to < ~2 cm2, blood can flow from the LA to
the left ventricle (LV) only if propelled by an abnormally elevated left atrioventricular pressure
gradient, the hemodynamic hallmark of MS.
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When the mitral valve opening is reduced to <1 cm2, often referred to as "severe" MS, a LA
pressure of ~25 mmHg is required to maintain a normal cardiac output (CO). The elevated
pulmonary venous and pulmonary arterial (PA) wedge pressures reduce pulmonary compliance,
contributing to exertional dyspnea. The first bouts of dyspnea are usually precipitated by
clinical events that increase the rate of blood flow across the mitral orifice, resulting in further
elevation of the LA pressure (see below).
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Fig. Pathophysiology of MS
To assess the severity of obstruction hemodynamically, both the transvalvular pressure gradient
and the flow rate must be measured. The latter depends not only on the CO but on the heart
rate as well. An increase in heart rate shortens diastole proportionately more than systole and
diminishes the time available for flow across the mitral valve. Therefore, at any given level of
CO, tachycardia including that associated with AF augments the transvalvular pressure gradient
and elevates further the LA pressure. Similar considerations apply to the pathophysiology of
tricuspid stenosis.
Cardiac Output
In patients with moderate MS (mitral valve orifice 1.0 cm21.5 cm2), the CO is normal or
almost so at rest but rises subnormally during exertion. In patients with severe MS (valve area
<1.0 cm2), particularly those in whom pulmonary vascular resistance is markedly elevated, the
CO is subnormal at rest and may fail to rise or may even decline during activity.
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Pulmonary Hypertension
The clinical and hemodynamic features of MS are influenced importantly by the level of the
PAP. Pulmonary hypertension results from: (1) passive backward transmission of the elevated
LA pressure; (2) pulmonary arteriolar constriction, which presumably is triggered by LA and
pulmonary venous hypertension (reactive pulmonary hypertension); (3) interstitial edema in the
walls of the small pulmonary vessels; and (4) organic obliterative changes in the pulmonary
vascular bed. Severe pulmonary hypertension results in RV enlargement, secondary tricuspid
regurgitation (TR) and pulmonic regurgitation (PR), as well as right-sided heart failure.
Symptoms
In temperate climates, the latent period between the initial attack of rheumatic carditis (in the
increasingly rare circumstances in which a history of one can be elicited) and the development
of symptoms due to MS is generally about two decades; most patients begin to experience
disability in the fourth decade of life. Studies carried out before the development of mitral
valvotomy revealed that once a patient with MS became seriously symptomatic, the disease
progressed continuously to death within 25 years.
In patients whose mitral orifices are large enough to accommodate a normal blood flow with
only mild elevations of LA pressure, marked elevations of this pressure leading to dyspnea and
cough may be precipitated by sudden changes in the heart rate, volume status, or CO, as for
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example with severe exertion, excitement, fever, severe anemia, paroxysmal AF and other
tachycardias, sexual intercourse, pregnancy, and thyrotoxicosis. As MS progresses, lesser
stresses precipitate dyspnea, and the patient becomes limited in daily activities, and orthopnea
and paroxysmal nocturnal dyspnea develop. The development of permanent AF often marks a
turning point in the patient's course and is generally associated with acceleration of the rate at
which symptoms progress.
Pulmonary Changes
In addition to the aforementioned changes in the pulmonary vascular bed, fibrous thickening of
the walls of the alveoli and pulmonary capillaries occurs commonly in MS. The vital capacity,
total lung capacity, maximal breathing capacity, and oxygen uptake per unit of ventilation are
reduced. Pulmonary compliance falls further as pulmonary capillary pressure rises during
exercise.
In patients with severe MS, there may be a malar flush with pinched and blue facies. In patients
with sinus rhythm and severe pulmonary hypertension or associated tricuspid stenosis (TS), the
jugular venous pulse reveals prominent a waves due to vigorous right atrial systole. The
systemic arterial pressure is usually normal or slightly low. An RV tap along the left sternal
border signifies an enlarged RV. A diastolic thrill may be present at the cardiac apex, with the
patient in the left lateral recumbent position.
Auscultation
The first heart sound (S1) is usually accentuated and slightly delayed. The pulmonic
component of the second heart sound (P2) also is often accentuated, and the two components
of the second heart sound (S2) are closely split. The opening snap (OS) of the mitral valve is
most readily audible in expiration at, or just medial to the cardiac apex. This sound generally
follows the sound of aortic valve closure (A2) by 0.050.12 s. The time interval between A2
and OS varies inversely with the severity of the MS. The OS is followed by a low-pitched,
rumbling, diastolic murmur, heard best at the apex with the patient in the left lateral recumbent
position. It is accentuated by mild exercise (e.g., a few rapid sit-ups) carried out just before
auscultation. In general, the duration of this murmur correlates with the severity of the stenosis
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in patients with preserved CO. In patients with sinus rhythm, the murmur often reappears or
becomes louder during atrial systole (presystolic accentuation). Soft grade I or II/VI systolic
murmurs are commonly heard at the apex or along the left sternal border in patients with pure
MS and do not necessarily signify the presence of MR. Hepatomegaly, ankle edema, ascites,
and pleural effusion, particularly in the right pleural cavity, may occur in patients with MS and
RV failure.
Associated Lesions
Laboratory Examination
ECG
In MS and sinus rhythm, the P wave usually suggests LA enlargement . It may become tall and
peaked in lead II and upright in lead V1 when severe pulmonary hypertension or TS
complicates MS and right atrial (RA) enlargement occurs. The QRS complex is usually normal.
However, with severe pulmonary hypertension, right axis deviation and RV hypertrophy are
often present.
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Echocardiogram
Chest X-Ray
The earliest changes are straightening of the upper left border of the cardiac silhouette,
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prominence of the main pulmonary arteries, dilatation of the upper lobe pulmonary veins, and
posterior displacement of the esophagus by an enlarged LA. Kerley B lines are fine, dense,
opaque, horizontal lines that are most prominent in the lower and mid-lung fields and that
result from distention of interlobular septae and lymphatics with edema when the resting mean
LA pressure exceeds approximately 20 mmHg.
Differential Diagnosis
Like MS, significant MR may also be associated with a prominent diastolic murmur at the apex
due to increased flow, but in MR this diastolic murmur commences slightly later than in
patients with MS, and there is often clear-cut evidence of LV enlargement. An apical
pansystolic murmur of at least grade III/VI intensity as well as an S3 suggests significant
associated MR. Similarly, the apical mid-diastolic murmur associated with severe AR (Austin
Flint murmur) may be mistaken for MS but can be differentiated from it because it is not
intensified in presystole. TS, which occurs rarely in the absence of MS, may mask many of the
clinical features of MS or be clinically silent.
Treatment
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Management strategy for patients with mitral stenosis (MS) and mild symptoms. There is controversy as
to whether patients with severe MS (MVA <1.0 cm2) and severe pulmonary hypertension(PH) (PASP >60
mmHg) should undergo percutaneous mitral balloon valvotomy (PMBV) or mitral valve replacement (MVR)
to prevent right ventricular failure. CXR, chest x-ray; ECG, electrocardiogram; echo, echocardiography; LA,
left atrial; MR, mitral regurgitation; MVA, mitral valve area; MVG, mean mitral valve pressure gradient;
NYHA, New York Heart Association; PASP, pulmonary artery systolic pressure; PAWP, pulmonary artery
wedge pressure; 2D, 2-dimensional. (From Bonow et al.)
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Note: Antibiotic prophylaxis is recommended according to current American Heart Association guidelines.
For patients with these forms of valvular heart disease, prophylaxis is indicated for a prior history of
endocarditis. HF is an indication for surgical or percutaneous treatment, and the recommendations here
pertain to short-term therapy prior to definitive correction of the valve lesion. For patients whose
comorbidities prohibit surgery, the medical therapies listed can be continued according to available guidelines
for the management of HF. See text.
Abbreviations: AF, atrial fibrillation; HF, heart failure; HTN, systemic hypertension; PCN, penicillin; RF,
rheumatic fever.
Source: Adapted from NA Boon, P Bloomfield: The medical management of valvular heart disease. Heart
87:395, 2002
Mitral Valvotomy
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as high as 8090% over 37 years. Therefore, PMBV has become the procedure of choice for
such patients when it can be performed by a skilled operator in a high-volume center.
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Inoue balloon technique for mitral balloon valvotomy. A. After transseptal puncture, the deflated balloon
catheter is advanced across the inter-atrial septum, then across the mitral valve and into the left ventricle.
B-D. The balloon is then inflated stepwise within the mitral orifice.
Successful valvotomy is defined by a 50% reduction in the mean mitral valve gradient and a
doubling of the mitral valve area. Successful valvotomy, whether balloon or surgical, usually
results in striking symptomatic and hemodynamic improvement and prolongs survival.
However, there is no evidence that the procedure improves the prognosis of patients with slight
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Mitral valve replacement (MVR) is necessary in patients with MS and significant associated
MR, those in whom the valve has been severely distorted by previous transcatheter or operative
manipulation, or those in whom the surgeon does not find it possible to improve valve function
significantly. MVR is now routinely performed with preservation of the chordal attachments to
optimize LV functional recovery. Perioperative mortality rates with MVR vary with age, LV
function, the presence of CAD, and associated comorbidities. They average 5% overall but are
lower in young patients and may be twice as high in older patients with comorbidities. Since
there are also long-term complications of valve replacement, patients in whom preoperative
evaluation suggests the possibility that MVR may be required should be operated on only if
they have severe MSi.e., an orifice area 1 cm2and are in NYHA Class III, i.e.,
symptomatic with ordinary activity despite optimal medical therapy. The overall 10-year
survival of surgical survivors is ~70%. Long-term prognosis is worse in older patients and
those with marked disability and marked depression of the CO preoperatively. Pulmonary
hypertension and RV dysfunction are additional risk factors for poor outcome.
Aortic stenosis
Aortic stenosis (AS) most often is due to calcification of a congenitally bicuspid or normal
trileaflet valve. Calcific changes are due to an active disease process characterized by lipid
accumulation, inflammation, and calcification. Once initiated, progressive leaflet calcification
and fibrosis eventually result in reduced leaflet motion with obstruction to left ventricular (LV)
outflow . Aortic stenosis often is first diagnosed by the finding of a murmur on auscultation.
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However, while a soft murmur with a physiologic split S2 reliably excludes severe stenosis and
a grade 4 murmur with diminished carotid upstrokes confirms severe obstruction, between
these extremes physical examination is not accurate for evaluation of disease severity.
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AS occurs in about one-fourth of all patients with chronic valvular heart disease;
approximately 80% of adult patients with symptomatic valvular AS are male.
AS in adults may be due to degenerative calcification of the aortic cusps. It may be congenital
in origin or it may be secondary to rheumatic inflammation. Age-related degenerative calcific
AS (also known as senile or sclerocalcific AS) is now the most common cause of AS in adults
in North America and Western Europe. About 30% of persons >65 years exhibit aortic valve
sclerosis; many of these have a systolic murmur of AS but without obstruction, while 2%
exhibit frank stenosis. Aortic sclerosis is defined echocardiographically as focal thickening or
calcification of the valve cusps with a peak Doppler transaortic velocity of 2.5 m/s. Aortic
sclerosis appears to be a marker for an increased risk of coronary heart disease events. On
histologic examination these valves frequently exhibit changes similar to those seen with
atherosclerosis and vascular inflammation. Interestingly, risk factors for atherosclerosis, such
as age, male sex, smoking, diabetes mellitus, hypertension, chronic kidney disease, increased
LDL, reduced HDL cholesterol, and elevated C-reactive protein are all risk factors for aortic
valve calcification.
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The congenitally affected valve may be stenotic at birth and may become progressively more
fibrotic, calcified, and stenotic. In other cases the valve may be congenitally deformed, usually
bicuspid [bicuspid aortic valve (BAV)], without serious narrowing of the aortic orifice during
childhood; its abnormal architecture makes its leaflets susceptible to otherwise ordinary
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Rheumatic disease of the aortic leaflets produces commissural fusion, sometimes resulting in a
bicuspid-appearing valve. This condition in turn makes the leaflets more susceptible to trauma
and ultimately leads to fibrosis, calcification, and further narrowing. By the time the
obstruction to LV outflow causes serious clinical disability, the valve is usually a rigid calcified
mass, and careful examination may make it difficult or even impossible to determine the
etiology of the underlying process. Rheumatic AS is almost always associated with
involvement of the mitral valve and with AR.
Pathophysiology
The obstruction to LV outflow produces a systolic pressure gradient between the LV and aorta.
When severe obstruction is suddenly produced experimentally, the LV responds by dilatation
and reduction of stroke volume. However, in some patients the obstruction may be present at
birth and/or increase gradually over the course of many years, and LV output is maintained by
the presence of concentric LV hypertrophy. Initially, this serves as an adaptive mechanism
because it reduces toward normal the systolic stress developed by the myocardium, as predicted
by the Laplace relation (S = Pr/h, where S = systolic wall stress, P = pressure, r = radius, and h
= wall thickness). A large transaortic valvular pressure gradient may exist for many years
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A mean systolic pressure gradient >40 mmHg with a normal CO or an effective aortic orifice
area < ~1.0 cm2 (or ~<0.6 cm2/m2 body surface area in a normal-sized adult)i.e., less than
approximately one-third of the normal orificeis generally considered to represent severe
obstruction to LV outflow. The elevated LV end-diastolic pressure observed in many patients
with severe AS signifies the presence of LV dilatation and/or diminished compliance of the
hypertrophied LV wall. Although the CO at rest is within normal limits in most patients with
severe AS, it usually fails to rise normally during exercise. Loss of an appropriately timed,
vigorous atrial contraction, as occurs in AF or atrioventricular dissociation, may cause rapid
progression of symptoms. Late in the course, the CO and LVaortic pressure gradient decline,
and the mean LA, PA, and RV pressures rise.
Symptoms
AS is rarely of clinical importance until the valve orifice has narrowed to approximately 1.0
cm2. Even severe AS may exist for many years without producing any symptoms because of the
ability of the hypertrophied LV to generate the elevated intraventricular pressures required for a
normal stroke volume.
Most patients with pure or predominant AS have gradually increasing obstruction for years but
do not become symptomatic until the sixth to eighth decades. Exertional dyspnea, angina
pectoris, and syncope are the three cardinal symptoms. Often there is a history of insidious
progression of fatigue and dyspnea associated with gradual curtailment of activities. Dyspnea
results primarily from elevation of the pulmonary capillary pressure caused by elevations of LV
diastolic pressures secondary to reduced left ventricular compliance. Angina pectoris usually
develops somewhat later and reflects an imbalance between the augmented myocardial oxygen
requirements and reduced oxygen availability; the former results from the increased myocardial
mass and intraventricular pressure, while the latter may result from accompanying CAD, which
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is not uncommon in patients with AS, as well as from compression of the coronary vessels by
the hypertrophied myocardium. Therefore, angina may occur in severe AS even without
obstructive epicardial CAD. Exertional syncope may result from a decline in arterial pressure
caused by vasodilatation in the exercising muscles and inadequate vasoconstriction in
nonexercising muscles in the face of a fixed CO, or from a sudden fall in CO produced by an
arrhythmia.
Since the CO at rest is usually well maintained until late in the course, marked fatigability,
weakness, peripheral cyanosis, cachexia, and other clinical manifestations of a low CO are
usually not prominent until this stage is reached. Orthopnea, paroxysmal nocturnal dyspnea,
and pulmonary edema, i.e., symptoms of LV failure, also occur only in the advanced stages of
the disease. Severe pulmonary hypertension leading to RV failure and systemic venous
hypertension, hepatomegaly, AF, and TR are usually late findings in patients with isolated
severe AS.
When AS and MS coexist, the reduction in CO induced by MS lowers the pressure gradient
across the aortic valve and thereby masks many of the clinical findings produced by AS.
Physical Findings
The rhythm is generally regular until late in the course; at other times, AF should suggest the
possibility of associated mitral valve disease. The systemic arterial pressure is usually within
normal limits. In the late stages, however, when stroke volume declines, the systolic pressure
may fall and the pulse pressure narrow. The peripheral arterial pulse rises slowly to a delayed
sustained peak (pulsus parvus et tardus. In the elderly, the stiffening of the arterial wall may
mask this important physical sign. In many patients the a wave in the jugular venous pulse is
accentuated. This results from the diminished distensibility of the RV cavity caused by the
bulging, hypertrophied interventricular septum.
Auscultation
An early systolic ejection sound is frequently audible in children and adolescents with
congenital noncalcific valvular AS. This sound usually disappears when the valve becomes
calcified and rigid. As AS increases in severity, LV systole may become prolonged so that the
aortic valve closure sound no longer precedes the pulmonic valve closure sound, and the two
components may become synchronous, or aortic valve closure may even follow pulmonic valve
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closure, causing paradoxic splitting of S2. The sound of aortic valve closure can be heard most
frequently in patients with AS who have pliable valves, and calcification diminishes the
intensity of this sound. Frequently, an S4 is audible at the apex and reflects the presence of LV
hypertrophy and an elevated LV end-diastolic pressure; an S3 generally occurs late in the
course, when the LV dilates.
A. Schematic representation of ECG, aortic pressure (AOP), left ventricular pressure (LVP),
and left atrial pressure (LAP). The shaded areas indicate a transvalvular pressure difference
during systole. HSM, holosystolic murmur; MSM, midsystolic murmur. B. Graphic
representation of ECG, aortic pressure (AOP), left ventricular pressure (LVP), and left atrial
pressure (LAP) with shaded areas indicating transvalvular diastolic pressure difference. EDM,
early diastolic murmur; PSM, presystolic murmur; MDM, middiastolic murmur.
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severe stenosis with heart failure in whom the stroke volume and therefore the transvalvular
flow rate are reduced, the murmur may be relatively soft and brief.
Laboratory Examination
ECG
Left ventricular hypertrophy (LVH) increases the amplitude of electrical forces directed
to the left and posteriorly.
In advanced cases, ST-segment depression and T-wave inversion (LV "strain") in standard leads
I and aVL and in the left precordial leads are evident. However, there is no close correlation
between the ECG and the hemodynamic severity of obstruction, and the absence of ECG signs
of LV hypertrophy does not exclude severe obstruction.
Echocardiogram
The key findings are LV hypertrophy and, in patients with valvular calcification (i.e., most
adult patients with symptomatic AS), multiple, bright, thick, echoes from the valve.
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Still frame two-dimensional echocardiographic image from the parasternal long axis view of a patient with
aortic stenosis. The aortic valve is calcified with restricted opening during systole. Ao, aorta; RV, right
ventricle; LA, left atrium; LV, left ventricle.
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Standard evaluation of aortic stenosis (AS) severity is based on measurement of left ventricular outflow tract
(LVOT) diameter (D) in a parasternal long-axis view for calculation of a circular cross-sectional area (CSA),
outflow tract velocity (V) from an apical approach using pulsed Doppler, and the maximum aortic jet (AS-Jet,
Vmax) from the continuous-wave Doppler recording. Either velocity-time integrals (VTIs) or maximum
velocities can be used in the continuity equation for aortic valve area (AVA).
. The valve gradient and aortic valve area can be estimated by Doppler measurement of the
transaortic velocity. Severe AS is defined by a valve area <1.0 cm2, whereas moderate AS is
defined by a valve area of 1.01.5 cm2 and mild AS by a valve area of 1.52.0 cm2. LV
dilatation and reduced systolic shortening reflect impairment of LV function.
Chest X-Ray
The chest x-ray may show no or little overall cardiac enlargement for many years. Hypertrophy
without dilatation may produce some rounding of the cardiac apex in the frontal projection and
slight backward displacement in the lateral view; severe AS is often associated with
poststenotic dilatation of the ascending aorta. As noted above, however, aortic enlargement may
be an independent process and mediated by the same type of structural changes that occur in
patients with Marfan syndrome. Aortic calcification is usually readily apparent on fluoroscopic
examination or by echocardiography; the absence of valvular calcification in an adult suggests
that severe valvular AS is not present. In later stages of the disease, as the LV dilates there is
increasing roentgenographic evidence of LV enlargement, pulmonary congestion, and
enlargement of the LA, PA, and right side of the heart.
Medical Treatment
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Management strategy for patients with severe aortic stenosis. Preoperative coronary angiography should
be performed routinely as determined by age, symptoms, and coronary risk factors. Cardiac catheterization
and angiography may also be helpful when there is discordance between clinical findings and
echocardiography. AVA, aortic valve area; BP, blood pressure; CABG, coronary artery bypass graft surgery;
echo, echocardiography; LV, left ventricle; Vmax, maximal velocity across aortic valve by Doppler
echocardiography. (From Bonow et al. Modified from CM Otto: J Am Coll Cardiol 47:2141, 2006.)
In patients with severe AS (<1.0 cm2), strenuous physical activity should be avoided, even in
the asymptomatic stage. Care must be taken to avoid dehydration and hypovolemia to protect
against a significant reduction in CO. Medications used for the treatment of hypertension or
CAD, including beta blockers and ACE inhibitors, are generally safe for asymptomatic patients
with preserved left ventricular systolic function. Nitroglycerin is helpful in relieving angina
pectoris. Retrospective studies have shown that patients with degenerative calcific AS who
receive HMG-CoA reductase inhibitors ("statins") exhibit slower progression of leaflet
calcification and aortic valve area reduction than those who do not. One prospective
randomized clinical trial using high-dose atorvastatin failed to show a measurable benefit,
although a more recent trial using rosuvastatin did show a beneficial effect. The role of statin
medications may be more clearly defined with further study.
Surgical Treatment
Asymptomatic patients with calcific AS and severe obstruction should be followed carefully
for the development of symptoms and by serial echocardiograms for evidence of deteriorating
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LV function. Operation is indicated in patients with severe AS (valve area <1.0 cm2 or 0.6
cm2/m2 body surface area) who are symptomatic, those who exhibit LV dysfunction (EF
<50%), as well as those with an aneurysmal or expanding aortic root (maximal dimension >4.5
cm or annual increase in size >0.5 cm/year), even if they are asymptomatic. In patients without
heart failure, the operative risk of AVR is approximately 3% . It is prudent to postpone
operation in patients with severe calcific AS who are truly asymptomatic and who exhibit
normal LV function, i.e., EF >50%, since they may continue to do well for years. However,
some advocate AVR in patients with severe valve calcification and rapid progression of
obstruction. The risk of surgical mortality exceeds that of sudden death in asymptomatic
patients. Exercise testing is employed in many centers to assess objectively the functional
capacity of asymptomatic patients for whom the history is ambiguous. As many as one-third of
patients will show signs of functional impairment during exercise for which AVR should be
considered. AVR is carried out in asymptomatic patients with severe or moderately severe
stenosis who undergo coronary artery bypass grafting. AVR is also routinely performed in
patients with moderate AS who are undergoing coronary bypass grafting or aortic root
reconstruction.
Operation should, if possible, be carried out before frank LV failure develops; at this late stage,
the aortic valve pressure gradient declines as the CO, stroke volume, and EF decline (low
gradient, low output AS). In such patients the perioperative risk is high (1520%), and
evidence of myocardial disease may persist even when the operation is technically successful.
Furthermore, long-term postoperative survival also correlates inversely with preoperative LV
dysfunction. Nonetheless, in view of the even worse prognosis of such patients when they are
treated medically, there is usually little choice but to advise surgical treatment, especially in
patients in whom contractile reserve can be demonstrated by dobutamine echocardiography
(defined by a 20% in stroke volume after dobutamine challenge). In patients in whom severe
AS and CAD coexist, relief of the AS and revascularization of the myocardium by means of
aortocoronary bypass grafting may result in striking clinical and hemodynamic improvement.
Because many patients with calcific AS are elderly, particular attention must be directed to the
adequacy of hepatic, renal, and pulmonary function before AVR is recommended. Age alone is
not a contraindication to AVR for AS. The mortality rate depends to a substantial extent on the
patient's preoperative clinical and hemodynamic state. The 10-year survival rate of patients with
AVR is approximately 60%. Approximately 30% of bioprosthetic valves evidence primary valve
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This procedure is preferable to operation in children and young adults with congenital,
noncalcific AS. It is not commonly used in adults with severe calcific AS because of a very
high restenosis rate and the risk of procedural complications, but on occasion it has been used
successfully as a "bridge to operation" in patients with severe LV dysfunction and shock who
are too ill to tolerate surgery.
In approximately two-thirds of patients with valvular AR, the disease is rheumatic in origin,
resulting in thickening, deformity, and shortening of the individual aortic valve cusps, changes
that prevent their proper opening during systole and closure during diastole. A rheumatic origin
is much less common in patients with isolated AR who do not have associated mitral valve
disease. Patients with congenital BAV disease may develop predominant AR. Congenital
fenestrations of the aortic valve occasionally produce mild AR. Membranous subaortic stenosis
often leads to thickening and scarring of the aortic valve leaflets with secondary AR. Prolapse
of an aortic cusp, resulting in progressive chronic AR, occurs in approximately 15% of patients
with ventricular septal defect but may also occur as an isolated phenomenon or as a
consequence of myxomatous degeneration sometimes associated with mitral and/or tricuspid
valve involvement.
AR may result from infective endocarditis, which can develop on a valve previously affected by
rheumatic disease, a congenitally deformed valve, or, rarely, on a normal aortic valve, and may
lead to perforation or erosion of one or more leaflets. The aortic valve leaflets may become
scarred and retracted during the course of syphilis or ankylosing spondylitis and contribute
further to the AR that derives primarily from the associated root disease. Although traumatic
rupture or avulsion of the aortic valve is an uncommon cause of acute AR, it does represent the
most frequent serious lesion in patients surviving nonpenetrating cardiac injuries. The
coexistence of hemodynamically significant AS with AR usually excludes all the rarer forms of
AR because it occurs almost exclusively in patients with rheumatic or congenital AR. In
patients with AR due to primary valvular disease, dilatation of the aortic annulus may occur
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Pathophysiology
The total stroke volume ejected by the LV (i.e., the sum of the effective forward stroke volume
and the volume of blood that regurgitates back into the LV) is increased in patients with AR. In
patients with wide-open (free) AR, the volume of regurgitant flow may equal the effective
forward stroke volume. In contrast to MR, in which a fraction of the LV stroke volume is
delivered into the low-pressure LA, in AR the entire LV stroke volume is ejected into a
high-pressure zone, the aorta. An increase in the LV end-diastolic volume (increased preload)
constitutes the major hemodynamic compensation for AR. The dilatation and eccentric
hypertrophy of the LV allow this chamber to eject a larger stroke volume without requiring any
increase in the relative shortening of each myofibril. Therefore, severe AR may occur with a
normal effective forward stroke volume and a normal left ventricular EF [total (forward plus
regurgitant) stroke volume/end-diastolic volume], together with an elevated LV end-diastolic
pressure and volume. However, through the operation of Laplace's law, LV dilatation increases
the LV systolic tension required to develop any given level of systolic pressure. Chronic AR is
thus a state in which LV preload and afterload are both increased. Ultimately, these adaptive
measures fail. As LV function deteriorates, the end-diastolic volume rises further and the
forward stroke volume and EF decline. Deterioration of LV function often precedes the
development of symptoms. Considerable thickening of the LV wall also occurs with chronic
AR, and at autopsy the hearts of these patients may be among the largest encountered,
sometimes weighing >1000 g.
The reverse pressure gradient from aorta to LV, which drives the AR flow, falls progressively
during diastole, accounting for the decrescendo nature of the diastolic murmur. Equilibration
between aortic and LV pressures may occur toward the end of diastole in patients with chronic
severe AR, particularly when the heart rate is slow. In patients with acute severe AR, the LV is
unprepared for the regurgitant volume load. LV compliance is normal or reduced, and LV
diastolic pressures rise rapidly, occasionally to levels >40 mmHg. The LV pressure may exceed
the LA pressure toward the end of diastole, and this reversed pressure gradient closes the mitral
valve prematurely.
In patients with chronic severe AR, the effective forward CO usually is normal or only slightly
reduced at rest, but often it fails to rise normally during exertion. Early signs of LV
dysfunction include reduction in the EF. In advanced stages there may be considerable
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elevation of the LA, PA wedge, PA, and RV pressures and lowering of the forward CO at rest.
Physical Findings
In chronic severe AR, the jarring of the entire body and the bobbing motion of the head with
each systole can be appreciated, and the abrupt distention and collapse of the larger arteries are
easily visible. The examination should be directed toward the detection of conditions
predisposing to AR, such as Marfan syndrome, ankylosing spondylitis, and ventricular septal
defect.
Arterial Pulse
A rapidly rising "water-hammer" pulse, which collapses suddenly as arterial pressure falls
rapidly during late systole and diastole (Corrigan's pulse), and capillary pulsations, an alternate
flushing and paling of the skin at the root of the nail while pressure is applied to the tip of the
nail (Quincke's pulse), are characteristic of free AR. A booming "pistol-shot" sound can be
heard over the femoral arteries (Traube's sign), and a to-and-fro murmur (Duroziez's sign) is
audible if the femoral artery is lightly compressed with a stethoscope.
The arterial pulse pressure is widened, and there is an elevation of the systolic pressure,
sometimes to as high as 300 mmHg, and a depression of the diastolic pressure. The
measurement of arterial diastolic pressure with a sphygmomanometer may be complicated by
the fact that systolic sounds are frequently heard with the cuff completely deflated. However,
the level of cuff pressure at the time of muffling of the Korotkoff sounds (Phase IV) generally
corresponds fairly closely to the true intraarterial diastolic pressure. As the disease progresses
and the LV end-diastolic pressure rises, the arterial diastolic pressure may actually rise as well,
since the aortic diastolic pressure cannot fall below the LV end-diastolic pressure. For the same
reason, acute severe AR may also be accompanied by only a slight widening of the pulse
pressure. Such patients are invariably tachycardic as the heart rate increases in an attempt to
preserve the CO.
Auscultation
In patients with severe AR, the aortic valve closure sound (A2) is usually absent. An S3 and
systolic ejection sound are frequently audible, and occasionally an S4 also may be heard. The
murmur of chronic AR is typically a high-pitched, blowing, decrescendo diastolic murmur,
heard best in the third intercostal space along the left sternal border.
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A. Schematic representation of ECG, aortic pressure (AOP), left ventricular pressure (LVP), and left atrial
pressure (LAP). The shaded areas indicate a transvalvular pressure difference during systole. HSM,
holosystolic murmur; MSM, midsystolic murmur. B. Graphic representation of ECG, aortic pressure (AOP),
left ventricular pressure (LVP), and left atrial pressure (LAP) with shaded areas indicating transvalvular
diastolic pressure difference. EDM, early diastolic murmur; PSM, presystolic murmur; MDM, middiastolic
murmur.
In patients with mild AR, this murmur is brief but, as the severity increases, generally becomes
louder and longer, indeed holodiastolic. When the murmur is soft, it can be heard best with the
diaphragm of the stethoscope and with the patient sitting up, leaning forward, and with the
breath held in forced expiration. In patients in whom the AR is caused by primary valvular
disease, the diastolic murmur is usually louder along the left than the right sternal border.
However, when the murmur is heard best along the right sternal border, it suggests that the AR
is caused by aneurysmal dilatation of the aortic root. "Cooing" or musical diastolic murmurs
suggest eversion of an aortic cusp vibrating in the regurgitant stream.
A mid-systolic ejection murmur is frequently audible in isolated AR. It is generally heard best
at the base of the heart and is transmitted along the carotid vessels. This murmur may be quite
loud without signifying aortic obstruction. A third murmur frequently heard in patients with
severe AR is the Austin Flint murmur, a soft, low-pitched, rumbling mid-diastolic murmur. It is
probably produced by the diastolic displacement of the anterior leaflet of the mitral valve by
the AR stream but does not appear to be associated with hemodynamically significant mitral
obstruction. The auscultatory features of AR are intensified by strenuous handgrip, which
augments systemic resistance.
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In acute severe AR, the elevation of LV end-diastolic pressure may lead to early closure of the
mitral valve, an associated mid-diastolic sound, a soft or absent S1, a pulse pressure that is not
particularly wide, and a soft, short diastolic murmur of AR.
Laboratory Examination
ECG
In patients with chronic severe AR, the ECG signs of LV hypertrophy become manifest . In
addition, these patients frequently exhibit ST-segment depression and T-wave inversion in
leads I, aVL, V5, and V6 ("LV strain"). Left axis deviation and/or QRS prolongation denote
diffuse myocardial disease, generally associated with patchy fibrosis, and usually signify a
poor prognosis.
Echocardiogram
The extent and velocity of wall motion are normal or even supernormal, until myocardial
contractility declines. A rapid, high-frequency fluttering of the anterior mitral leaflet produced
by the impact of the regurgitant jet is a characteristic finding. The echocardiogram is also
useful in determining the cause of AR, by detecting dilatation of the aortic annulus and root or
aortic dissection. Thickening and failure of coaptation of the leaflets also may be noted. Color
flow Doppler echocardiographic imaging is very sensitive in the detection of AR, and Doppler
echocardiography is helpful in assessing its severity. With severe AR, the central jet width
exceeds 65% of the left ventricular outflow tract, the regurgitant volume is 60 ml/beat, the
regurgitant fraction is 50%, and there is diastolic flow reversal in the proximal descending
thoracic aorta. The continuous wave Doppler profile shows a rapid deceleration time in
patients with acute severe AR, due to the rapid increase in LV diastolic pressure. Serial
two-dimensional echocardiography is valuable in assessing LV performance and in detecting
progressive myocardial dysfunction.
Chest X-Ray
In chronic severe AR, the apex is displaced downward and to the left in the frontal projection.
In the left anterior oblique and lateral projections, the LV is displaced posteriorly and
encroaches on the spine. When AR is caused by primary disease of the aortic root, aneurysmal
dilatation of the aorta may be noted, and the aorta may fill the retrosternal space in the lateral
view. Echocardiography and CT angiography are more sensitive than the chest x-ray for the
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Clinically, bounding arterial pulses, a widened pulse pressure, a loud diastolic murmur, and a
third heart sound are signs of severe regurgitation but are not always specific. Doppler
echocardiography has become the mainstay of the assessment of the severity of aortic
regurgitation. Suggestive of severe regurgitation are signs of a broad jet width on color-flow
imaging, steep jet velocity deceleration (reflecting equalization of aortic and ventricular
pressure), and prolonged diastolic flow reversal in the aorta. The use of Doppler
echocardiography makes it possible to quantify the effective regurgitant orifice (severe if 0.30
cm2) and regurgitant volume (severe if 60 ml per beat)
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A simple, reliable measurement is the "vena contracta" that is, the width of the regurgitant
flow at the orifice, a surrogate measurement for the size of the orifice. Measurements that are
0.5 cm or more have a high sensitivity for the diagnosis of severe regurgitation, and
measurements that are 0.7 cm or more have a high specificity for the diagnosis. On rare
occasions, this approach is inconclusive, and either transesophageal echocardiography or
angiography of the aortic root is necessary to determine the severity of aortic regurgitation. Left
ventricular size and function (particularly, the end-systolic diameter and ejection fraction)
should be routinely assessed, as should dilatation of the ascending aorta. If transthoracic
imaging is suboptimal for the latter, transesophageal echocardiography, computed tomography,
or magnetic resonance imaging can be used. Exercise testing may be warranted in asymptomatic
patients with limited physical activity to evaluate functional limitations and may also provide
information about changes of left ventricular function with stress.
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Treatment
Patients with acute severe AR may respond to intravenous diuretics and vasodilators (such as
sodium nitroprusside), but stabilization is usually short-lived and operation is indicated
urgently. Intraaortic balloon counterpulsation is contraindicated. Beta-blockers are also best
avoided so as not to reduce the CO further or slow the heart rate, which might allow
proportionately more time in diastole for regurgitation to occur. Surgery is the treatment of
choice.
Early symptoms of dyspnea and effort intolerance respond to treatment with diuretics and
vasodilators (ACE inhibitors, dihydropyridine calcium channel blockers, or hydralazine) may
be useful as well. Surgery can then be performed in more controlled circumstances. The use of
vasodilators to extend the compensated phase of chronic severe AR before the onset of
symptoms or the development of LV dysfunction is more controversial. Expert consensus is
strong regarding the need to control systolic blood pressure (goal <140 mmHg) in patients with
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chronic AR, and vasodilators are an excellent first choice as antihypertensive agents. It is often
difficult to achieve adequate control in such patients because of the increased stroke volume.
Cardiac arrhythmias and systemic infections are poorly tolerated in patients with severe AR
and must be treated promptly and vigorously. Although nitroglycerin and long-acting nitrates
are not as helpful in relieving anginal pain as they are in patients with ischemic heart disease,
they are worth a trial. Patients with syphilitic aortitis should receive a full course of penicillin
therapy. Beta blockers may be useful to retard the rate of aortic root enlargement in young
patients with Marfan syndrome and aortic root dilatation with no or only mild AR. Patients
with severe AR should avoid isometric exercises.
Surgical Treatment
In deciding on the advisability and proper timing of surgical treatment, two points should be
kept in mind: (1) patients with chronic severe AR usually do not become symptomatic until
after the development of myocardial dysfunction; and (2) when delayed too long (defined as >1
year from onset of symptoms or LV dysfunction), surgical treatment often does not restore
normal LV function. Therefore, in patients with chronic severe AR, careful clinical follow-up
and noninvasive testing with echocardiography at approximately 6-month intervals are
necessary if operation is to be undertaken at the optimal time, i.e., after the onset of LV
dysfunction but prior to the development of severe symptoms. Operation can be deferred as
long as the patient both remains asymptomatic and retains normal LV function.
Surgical options for management of aortic valve and root disease have expanded considerably
over the past decade. AVR with a suitable mechanical or tissue prosthesis is generally
necessary in patients with rheumatic AR and in many patients with other forms of
regurgitation. Rarely, when a leaflet has been perforated during infective endocarditis or torn
from its attachments to the aortic annulus by thoracic trauma, primary surgical repair may be
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possible. When AR is due to aneurysmal dilatation of the annulus and ascending aorta rather
than to primary valvular involvement, it may be possible to reduce the regurgitation by
narrowing the annulus or by excising a portion of the aortic root without replacing the valve.
Resuspension of the native aortic valve leaflets is possible in approximately 50% of patients
with acute AR in the setting of Type A aortic dissection. In other conditions, however,
regurgitation can be eliminated only by replacing the aortic valve, excising the dilated or
aneurysmal ascending aorta responsible for the regurgitation, and replacing it with a graft. This
formidable procedure entails a higher risk than isolated AVR.
As in patients with other valvular abnormalities, both the operative risk and the late mortality
are largely dependent on the stage of the disease and on myocardial function at the time of
operation. The overall operative mortality for isolated AVR is about 3%. However, patients
with marked cardiac enlargement and prolonged LV dysfunction experience an operative
mortality rate of approximately 10% and a late mortality rate of approximately 5% per year due
to LV failure despite a technically satisfactory operation. Nonetheless, because of the very poor
prognosis with medical management, even patients with LV failure should be considered for
operation.
Patients with acute severe AR require prompt surgical treatment, which may be lifesaving.
TS, much less prevalent than MS in North America and Western Europe, is generally rheumatic
in origin and is more common in females than in males. It does not occur as an isolated lesion
and is usually associated with MS. Hemodynamically significant TS occurs in 510% of
patients with severe MS; rheumatic TS is commonly associated with some degree of TR.
Nonrheumatic causes of TS are rare.
Pathophysiology
A diastolic pressure gradient between the RA and RV defines TS. It is augmented when the
transvalvular blood flow increases during inspiration and declines during expiration. A mean
diastolic pressure gradient of 4 mmHg is usually sufficient to elevate the mean RA pressure to
levels that result in systemic venous congestion. Unless sodium intake has been restricted and
diuretics administered, this venous congestion is associated with hepatomegaly, ascites, and
edema, sometimes severe. In patients with sinus rhythm, the RA a wave may be extremely tall
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and may even approach the level of the RV systolic pressure. The y descent is prolonged. The
CO at rest is usually depressed, and it fails to rise during exercise. The low CO is responsible
for the normal or only slightly elevated LA, PA, and RV systolic pressures despite the presence
of MS. Thus, the presence of TS can mask the hemodynamic and clinical features of the MS,
which usually accompanies it.
Symptoms
Since the development of MS generally precedes that of TS, many patients initially have
symptoms of pulmonary congestion. Spontaneous improvement of these symptoms should raise
the possibility that TS may be developing. Characteristically, patients complain of relatively
little dyspnea for the degree of hepatomegaly, ascites, and edema that they have. However,
fatigue secondary to a low CO and discomfort due to refractory edema, ascites, and marked
hepatomegaly are common in patients with TS and/or TR. In some patients, TS may be
suspected for the first time when symptoms of right-sided failure persist after an adequate
mitral valvotomy.
Physical Findings
Severe TS is associated with marked hepatic congestion, often resulting in cirrhosis, jaundice,
serious malnutrition, anasarca, and ascites. Congestive hepatomegaly and, in cases of severe
tricuspid valve disease, splenomegaly are present.
Laboratory Examination
The ECG features of RA enlargement include tall, peaked P waves in lead II, as well as
prominent, upright P waves in lead V1. The absence of ECG evidence of right ventricular
hypertrophy (RVH) in a patient with right-sided heart failure who is believed to have MS
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should suggest associated tricuspid valve disease. The chest x-ray in patients with combined
TS and MS shows particular prominence of the RA and superior vena cava without much
enlargement of the PA and with less evidence of pulmonary vascular congestion than occurs in
patients with isolated MS. On echocardiographic examination, the tricuspid valve is usually
thickened and domes in diastole; the transvalvular gradient can be estimated by Doppler
echocardiography. TTE provides additional information regarding mitral valve structure and
function, LV and RV size and function, and PA pressure.
Patients with TS generally exhibit marked systemic venous congestion; intensive salt
restriction, bed rest, and diuretic therapy are required during the preoperative period. Such a
preparatory period may diminish hepatic congestion and thereby improve hepatic function
sufficiently so that the risks of operation, particularly bleeding, are diminished. Surgical relief
of the TS should be carried out, preferably at the time of surgical mitral valvotomy or MVR, in
patients with moderate or severe TS who have mean diastolic pressure gradients exceeding ~4
mmHg and tricuspid orifice areas <1.52.0 cm2. TS is almost always accompanied by
significant TR. Operative repair may permit substantial improvement of tricuspid valve
function. If repair cannot be accomplished, the tricuspid valve may have to be replaced with a
prosthesis, preferably a large bioprosthetic valve. Mechanical valves in the tricuspid position
are more prone to thromboembolic complications than in other positions.
Most commonly, TR is functional and secondary to marked dilatation of the tricuspid annulus.
Functional TR may complicate RV enlargement of any cause, including inferior wall infarcts
that involve the RV. It is commonly seen in the late stages of heart failure due to rheumatic or
congenital heart disease with severe pulmonary hypertension (pulmonary artery systolic
pressure >55 mmHg), as well as in ischemic heart disease and dilated cardiomyopathy. It is
reversible in part if pulmonary hypertension is relieved. Rheumatic fever may produce organic
(primary) TR, often associated with TS. Infarction of RV papillary muscles, tricuspid valve
prolapse, carcinoid heart disease, endomyocardial fibrosis, infective endocarditis, and trauma
all may produce TR. Less commonly, TR results from congenitally deformed tricuspid valves,
and it occurs with defects of the atrioventricular canal, as well as with Ebstein's malformation
of the tricuspid valve. TR also develops eventually in patients with chronic RV apical pacing.
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As is the case for TS, the clinical features of TR result primarily from systemic venous
congestion and reduction of CO. With the onset of TR in patients with pulmonary
hypertension, symptoms of pulmonary congestion diminish, but the clinical manifestations of
right-sided heart failure become intensified. The neck veins are distended with prominent v
waves and rapid y descents, marked hepatomegaly, ascites, pleural effusions, edema, systolic
pulsations of the liver, and a positive hepatojugular reflux. A prominent RV pulsation along
the left parasternal region and a blowing holosystolic murmur along the lower left sternal
margin, which may be intensified during inspiration and reduced during expiration or the strain
of the Valsalva maneuver (Carvallo's sign), are characteristic findings; AF is usually present.
The ECG usually shows changes characteristic of the lesion responsible for the enlargement of
the RV that leads to TR, e.g., inferior wall myocardial infarction or severe RVH.
Echocardiography may be helpful by demonstrating RV dilatation and prolapsing, flail,
scarred, or displaced tricuspid leaflets; the diagnosis of TR can be made by color flow Doppler
echocardiography, and its severity can be estimated by Doppler examination.
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Severe TR is accompanied by hepatic vein systolic flow reversal. Continuous wave Doppler is
also useful in estimating PA pressure. Roentgenographic examination usually reveals
enlargement of both the RA and RV.
In patients with severe TR, the CO is usually markedly reduced, and the RA pressure pulse may
exhibit no x descent during early systole but a prominent c-v wave with a rapid y descent. The
mean RA and the RV end-diastolic pressures are often elevated.
Ebstein's Anomaly
Ebstein's anomaly is an abnormality of the tricuspid valve in which the septal leaflets and often
the posterior leaflets are displaced into the right ventricle and the anterior leaflet is usually
malformed, excessively large, and abnormally attached or adherent to the right ventricular free
wall. Thus, a portion of the right ventricle is "atrialized" in that it is located on the atrial side of
the tricuspid valve, and the remaining functional right ventricle is small (Figure 6). The
tricuspid valve is usually regurgitant but may be stenotic. Eighty percent of patients with
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Ebstein's anomaly have an interatrial communication (atrial septal defect or patent foramen
ovale) through which right-to-left shunting of blood may occur.
The severity of the hemodynamic derangements in patients with Ebstein's anomaly depends on
the degree of displacement and the functional status of the tricuspid-valve leaflets. Patients
with mild apical displacement of the tricuspid leaflets have normal valvular function, whereas
those with severe tricuspid-leaflet displacement or abnormal anterior leaflet attachment, with
valvular dysfunction, have elevated right atrial pressure and right-to-left interatrial shunting.
Similarly, the clinical presentation of Ebstein's anomaly varies from severe heart failure in a
fetus or neonate to the absence of symptoms in an adult in whom it is discovered incidentally.
When Ebstein's anomaly is discovered during fetal life, the rate of intrauterine mortality is
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high. Neonates with severe disease have cyanosis, with heart failure and a murmur noted in the
first days of life. Transient improvement may occur as pulmonary vascular resistance falls, but
the condition worsens after the ductus arteriosus closes, thereby decreasing pulmonary blood
flow. Older children with Ebstein's anomaly often come to medical attention because of an
incidental murmur, whereas adolescents and adults present with a supraventricular arrhythmia.
In adults with Ebstein's anomaly, the most important predictors of outcome are the New York
Heart Association (NYHA) functional class, the heart size, the presence or absence of cyanosis,
and the presence or absence of paroxysmal atrial tachycardias. Such tachycardias may lead to
cardiac failure, worsening cyanosis, and even syncope. Patients with Ebstein's anomaly and an
interatrial communication are at risk for paradoxical embolization, brain abscess, and sudden
death.
Tall and broad P waves are common on the electrocardiogram, as is right bundle-branch block.
First-degree atrioventricular block occurs frequently. Since about 20 percent of patients with
Ebstein's anomaly have ventricular preexcitation by way of an accessory electrical pathway
between the atrium and ventricle (WolffParkinsonWhite syndrome), a delta wave may be
present. The radiographic findings depend on the severity of the anatomical abnormality. In
mild cases, the heart size and pulmonary vasculature are normal. In more severe cases, marked
cardiomegaly, which is largely due to right atrial enlargement, is present. In severe cases (with
little functional right ventricle and marked right-to-left shunting), pulmonary vascular markings
are decreased. Echocardiography is used to assess right atrial dilatation, anatomical
displacement and distortion of the tricuspid-valve leaflets, and the severity of tricuspid
regurgitation or stenosis; in addition, the presence and magnitude of interatrial shunting can be
determined (by color Doppler imaging or bubble study), as can the presence of associated
cardiac abnormalities. Electrophysiologic evaluation is warranted in patients with atrial
tachyarrhythmias.
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Repair or replacement of the tricuspid valve in conjunction with closure of the interatrial
communication is recommended for older patients who have severe symptoms despite medical
therapy. When possible, valve repair is preferable to valve replacement, because it is associated
with lower mortality and has fewer long-term complications. The complications of surgery to
correct Ebstein's anomaly include complete heart block, persistence of supraventricular
arrhythmias, residual tricuspid regurgitation after valve repair, and prosthetic-valve dysfunction.
Ebstein's Anomaly
Ebstein's anomaly is an abnormality of the tricuspid valve in which the septal leaflets and often
the posterior leaflets are displaced into the right ventricle and the anterior leaflet is usually
malformed, excessively large, and abnormally attached or adherent to the right ventricular free
wall. Thus, a portion of the right ventricle is "atrialized" in that it is located on the atrial side of
the tricuspid valve, and the remaining functional right ventricle is small (Figure 6). The
tricuspid valve is usually regurgitant but may be stenotic. Eighty percent of patients with
Ebstein's anomaly have an interatrial communication (atrial septal defect or patent foramen
ovale) through which right-to-left shunting of blood may occur.
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The severity of the hemodynamic derangements in patients with Ebstein's anomaly depends on
the degree of displacement and the functional status of the tricuspid-valve leaflets. Patients
with mild apical displacement of the tricuspid leaflets have normal valvular function, whereas
those with severe tricuspid-leaflet displacement or abnormal anterior leaflet attachment, with
valvular dysfunction, have elevated right atrial pressure and right-to-left interatrial shunting.
Similarly, the clinical presentation of Ebstein's anomaly varies from severe heart failure in a
fetus or neonate to the absence of symptoms in an adult in whom it is discovered incidentally.
When Ebstein's anomaly is discovered during fetal life, the rate of intrauterine mortality is
high. Neonates with severe disease have cyanosis, with heart failure and a murmur noted in the
first days of life. Transient improvement may occur as pulmonary vascular resistance falls, but
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the condition worsens after the ductus arteriosus closes, thereby decreasing pulmonary blood
flow. Older children with Ebstein's anomaly often come to medical attention because of an
incidental murmur, whereas adolescents and adults present with a supraventricular arrhythmia.
In adults with Ebstein's anomaly, the most important predictors of outcome are the New York
Heart Association (NYHA) functional class, the heart size, the presence or absence of cyanosis,
and the presence or absence of paroxysmal atrial tachycardias. Such tachycardias may lead to
cardiac failure, worsening cyanosis, and even syncope. Patients with Ebstein's anomaly and an
interatrial communication are at risk for paradoxical embolization, brain abscess, and sudden
death.
Tall and broad P waves are common on the electrocardiogram, as is right bundle-branch block.
First-degree atrioventricular block occurs frequently. Since about 20 percent of patients with
Ebstein's anomaly have ventricular preexcitation by way of an accessory electrical pathway
between the atrium and ventricle (WolffParkinsonWhite syndrome), a delta wave may be
present. The radiographic findings depend on the severity of the anatomical abnormality. In
mild cases, the heart size and pulmonary vasculature are normal. In more severe cases, marked
cardiomegaly, which is largely due to right atrial enlargement, is present. In severe cases (with
little functional right ventricle and marked right-to-left shunting), pulmonary vascular markings
are decreased. Echocardiography is used to assess right atrial dilatation, anatomical
displacement and distortion of the tricuspid-valve leaflets, and the severity of tricuspid
regurgitation or stenosis; in addition, the presence and magnitude of interatrial shunting can be
determined (by color Doppler imaging or bubble study), as can the presence of associated
cardiac abnormalities. Electrophysiologic evaluation is warranted in patients with atrial
tachyarrhythmias.
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Repair or replacement of the tricuspid valve in conjunction with closure of the interatrial
communication is recommended for older patients who have severe symptoms despite medical
therapy. In addition, repair or replacement should be considered for patients with less severe
symptoms who have cardiac enlargement, since this condition has a poor prognosis. When
possible, valve repair is preferable to valve replacement, because it is associated with lower
mortality and has fewer long-term complications. However, when valve replacement is required,
a bioprosthesis is preferable to a mechanical prosthesis. The complications of surgery to correct
Ebstein's anomaly include complete heart block, persistence of supraventricular arrhythmias,
residual tricuspid regurgitation after valve repair, and prosthetic-valve dysfunction.
With d-transposition of the great arteries (also known as complete transposition), the aorta
arises in an anterior position from the right ventricle and the pulmonary artery arises from the
left ventricle (Figure 7A). Therefore, there is complete separation of the pulmonary and
systemic circulations: systemic venous blood traverses the right atrium, right ventricle, aorta,
and systemic circulation, whereas pulmonary venous blood traverses the left atrium, left
ventricle, pulmonary artery, and pulmonary circulation. In order for an infant with this
condition to survive, there must be a communication between the two circuits. In about two
thirds of patients, no other associated cardiac defect is present, so that the ductus arteriosus
and foramen ovale allow communication between the two circuits. Infants with this condition
have severe cyanosis. The one third of patients with other associated defects that permit
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intracardiac mixing (e.g., atrial septal defect, ventricular septal defect, or patent ductus
arteriosus) are less critically ill, since they have less severe cyanosis. However, they are at risk
for left ventricular failure due to volume overload caused by left-to-right shunting.
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In d-transposition of the great arteries (complete transposition) (Panel A), systemic venous
blood returns to the right atrium, from which it goes to the right ventricle and then to the aorta.
Pulmonary venous blood returns to the left atrium, from which it goes to the left ventricle and
then to the pulmonary artery. Survival is possible only if there is a communication between the
two circuits, such as a patent ductus arteriosus. With the "atrial switch" operation (Panel B), a
pericardial baffle is created in the atria, so that blood returning from the systemic venous
circulation is directed into the left ventricle and then the pulmonary artery (blue arrows),
whereas blood returning from the pulmonary venous circulation is directed into the right
ventricle and then the aorta (red arrow). With the "arterial switch" operation (Panel C), the
pulmonary artery and ascending aorta are transected above the semilunar valves and coronary
arteries, then switched (neoaortic and neopulmonary valves).
Patients with complete transposition have cyanosis from birth and often have heart failure in
the newborn period. The findings on physical examination are nonspecific. Infants have
cyanosis and tachypnea. The second heart sound is single and loud (due to the anterior position
of the aorta). In patients with mild cyanosis, a holosystolic murmur caused by a ventricular
septal defect may be heard. Likewise, a soft systolic ejection murmur (due to pulmonary
stenosis, ejection into the anteriorly located aorta, or both) may be audible. The
electrocardiogram shows right-axis deviation and right ventricular hypertrophy (since the right
ventricle is the systemic ventricle). Patients with a large ventricular septal defect or patent
ductus arteriosus, as well as those with pulmonary stenosis, have left ventricular hypertrophy.
The chest radiograph shows cardiomegaly with increased pulmonary vascularity. Classically,
the cardiac silhouette is described as being egg-shaped, with a narrow "stalk."
Without intervention, patients with complete transposition have a poor prognosis. Unless
intracardiac mixing is improved, progressive hypoxemia and acidosis develop; the mortality
rate is 90 percent by six months of age. Infants who have less severe cyanosis (because of a
sizable ventricular septal defect or patent ductus arteriosus) fare better in the neonatal period,
but pulmonary vascular obstructive disease (due to increased pulmonary blood flow) is more
likely to develop than in infants with more severe cyanosis; infants with less severe cyanosis
are also more likely to have higher operative mortality and are less likely to have complete
repair of their defect.
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Two surgical procedures have been used in patients with complete transposition of the great
arteries. With the initial approach, known as the "atrial switch" operation (the Mustard or
Senning operation), the atrial septum was excised, then a "baffle" within the atria was
constructed to direct systemic venous blood across the mitral valve into the left ventricle and
pulmonary venous blood across the tricuspid valve into the right ventricle (Figure 7B). Thus,
physiologic circulation was restored; however, after this procedure was performed, the right
ventricle continued to function as the "systemic ventricle." This operation corrected cyanosis
and improved survival. The complications associated with it were leakage of the atrial baffle
(often clinically inconsequential); obstruction of the baffle (often insidious and frequently
asymptomatic); sinus-node dysfunction and atrial arrhythmias, particularly atrial flutter; right
(systemic) ventricular dysfunction; and an increased risk of sudden death.
The atrial-switch operation has been replaced by the arterial-switch operation, in which the
pulmonary artery and ascending aorta are transected above the semilunar valves and coronary
arteries and then switched, so that the aorta is connected to the neoaortic valve (formerly the
pulmonary valve) arising from the left ventricle, and the pulmonary artery is connected to the
neopulmonary valve (formerly the aortic valve) arising from the right ventricle (Figure 7C). The
coronary arteries are relocated to the neoaorta to restore normal coronary circulation. This
operation can be performed in neonates and is associated with a low operative mortality and an
excellent long-term outcome.
Eisenmenger's Syndrome
A patient with Eisenmenger's syndrome has a large left-to-right shunt that causes severe
pulmonary vascular disease and pulmonary hypertension, with resultant reversal of the
direction of shunting (Figure 8). With substantial left-to-right shunting, the exposure of the
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pulmonary vasculature to increased blood flow as well as increased pressure often results in
pulmonary vascular obstructive disease. The initial morphologic alterations (medial
hypertrophy of the pulmonary arterioles, intimal proliferation and fibrosis, and occlusion of
capillaries and small arterioles) are potentially reversible. However, as the disease progresses,
the more advanced morphologic changes (plexiform lesions and necrotizing arteritis) are
irreversible. The result is obliteration of much of the pulmonary vascular bed, leading to
increased pulmonary vascular resistance. As the pulmonary vascular resistance approaches or
exceeds systemic resistance, the shunt is reversed.
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shown), but it also may occur in association with an atrial septal defect or patent ductus
arteriosus.
The morphologic changes in the pulmonary vasculature that occur with Eisenmenger's
syndrome usually begin in childhood, but symptoms may not appear until late childhood or
early adulthood. In many patients, pulmonary congestion in early infancy (a result of the large
left-to-right shunt) resolves in later infancy or early childhood as pulmonary vascular resistance
increases and the magnitude of shunting decreases. Likewise, the patient may have a murmur in
early childhood that disappears (as the pulmonary disease progresses and the magnitude of
shunting decreases), leading to the mistaken assumption that the intracardiac communication
has closed. Occasionally, patients have no history of pulmonary congestion or a murmur in
childhood.
As right-to-left shunting develops, cyanosis appears. Most patients will have impaired exercise
tolerance and exertional dyspnea, but these symptoms may be well compensated for years.
Palpitations are common and are most often due to atrial fibrillation or flutter. As
erythrocytosis due to arterial desaturation develops in patients with Eisenmenger's syndrome,
symptoms of hyperviscosity (visual disturbances, fatigue, headache, dizziness, and
paresthesias) may appear. Hemoptysis may occur, as a result of pulmonary infarction or rupture
of dilated pulmonary arteries, arterioles, or aorticopulmonary collateral vessels. Since patients
with arterial desaturation have abnormal hemostasis, they are at risk for both bleeding and
thrombosis. Cerebrovascular accidents may occur as a result of paradoxical embolization,
venous thrombosis of cerebral vessels, or intracranial hemorrhage. In addition, patients with
this condition are at risk for brain abscess. Patients with Eisenmenger's syndrome may have
syncope owing to inadequate cardiac output or, less commonly, an arrhythmia. Symptoms of
heart failure, which are uncommon until the disease is far advanced, portend a poor prognosis.
Finally, these patients are at risk for sudden death.
On physical examination, patients have digital clubbing and cyanosis, the severity of which
depends on the magnitude of right-to-left shunting. The jugular venous pressure may be normal
or elevated, and prominent V waves are seen if tricuspid regurgitation is present. Arterial pulses
are small in volume. A right parasternal heave (due to right ventricular hypertrophy) is present,
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and the pulmonary component of the second heart sound is loud (and often palpable). The
murmur caused by a ventricular septal defect, patent ductus arteriosus, or atrial septal defect
disappears when Eisenmenger's syndrome develops. Many patients have a decrescendo diastolic
murmur caused by pulmonary regurgitation or a holosystolic murmur caused by tricuspid
regurgitation. A right-sided fourth heart sound is usually present. The lungs are clear.
Peripheral edema and hepatic congestion are absent unless there is substantial right ventricular
dysfunction.
The electrocardiogram shows right ventricular hypertrophy. Atrial arrhythmias may be present,
particularly in patients with atrial septal defect. The chest film reveals prominent central
pulmonary arteries and decreased vascular markings ("pruning") of the peripheral vessels. The
size of the heart is normal in patients with a ventricular septal defect or patent ductus
arteriosus, but cardiomegaly (due to right ventricular enlargement) is usually seen in those with
atrial septal defect. On transthoracic echocardiography, there is evidence of right ventricular
pressure overload and pulmonary hypertension. The underlying cardiac defect can usually be
visualized, although shunting across the defect may be difficult to demonstrate by color
Doppler imaging because of the low velocity of the jet. Contrast echocardiography permits the
location of the shunt to be determined. Catheterization should be performed in any patient with
suspected Eisenmenger's syndrome in order to assess the severity of pulmonary vascular disease
and to quantify the magnitude of intracardiac shunting. Pulmonary vasodilators such as
oxygen, inhaled nitrous oxide, or intravenous adenosine or epoprostenol should be
administered to permit assessment of the reversibility of pulmonary hypertension.
The rate of survival among patients with Eisenmenger's syndrome is 80 percent 10 years after
diagnosis, 77 percent at 15 years, and 42 percent at 25 years. Death is usually sudden,
presumably caused by arrhythmias, but some patients die of heart failure, hemoptysis, brain
abscess, or stroke. A history of syncope, clinically evident right ventricular systolic
dysfunction, low cardiac output, and severe hypoxemia portend a poor outcome.
Patients with Eisenmenger's syndrome should avoid intravascular volume depletion, heavy
exertion, high altitude, and the use of vasodilators. Because of high maternal and fetal
morbidity and mortality, pregnancy should be avoided. Although no therapy has been proved to
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Patients with Eisenmenger's syndrome who are undergoing noncardiac surgery require
meticulous management of anesthesia, with attention to the maintenance of systemic vascular
resistance, the minimization of blood loss and intravascular volume depletion, and the
prevention of iatrogenic paradoxical embolization. In preparation for noncardiac surgery,
prophylactic phlebotomy (usually of 1 to 2 units of blood, with isovolumic replacement) is
recommended for patients with a hematocrit above 65 percent in order to reduce the likelihood
of perioperative hemorrhagic and thrombotic complications. In general, anticoagulants and
antiplatelet agents should be avoided, since they exacerbate the hemorrhagic diathesis.
Lung transplantation with repair of the cardiac defect or combined heartlung transplantation is
an option for patients with Eisenmenger's syndrome who have markers of a poor prognosis
(syncope, refractory right-sided heart failure, a high NYHA functional class, or severe
hypoxemia). Because of the somewhat limited success of transplantation and the reasonably
good survival among patients treated medically, careful selection of patients for transplantation
is imperative.
For Guidelines on the Management of Adults With Congenital Heart Disease, please visit here.
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presence of a secundum atrial septal defect with moderate right ventricular dilation.
Atrial septal defects are some of the most common congenital cardiac malformations in adults,
representing up to 40% of acyanotic shunt lesions in patients older than 40 years. They arise
from either excessive resorption of the septum primum or from deficient growth of the septum
secundum, and are occasionally associated with anomalous pulmonary venous connection
(about 10%). The degree of left-to-right atrial shunting depends on the size of the defect and
the diastolic filling properties of the two ventricles. A substantial shunt (Qp/Qs >15/10) will
probably cause symptoms over time, and the movement of such patients will become
progressively more restricted with age. Effort dyspnoea is seen in about 30% of patients by
their third decade whereas supraventricular arrhythmias (atrial fibrillation or flutter) and right
heart failure develop in about 10% of patients by age 40 years.
Treatment
Haemodynamically unimportant atrial septal defects (Qp/Qs <15) do not need closure, except
for the prevention of paradoxical emboli in patients who have had cryptogenic stroke. In the
absence of clinically significant pulmonary hypertension, closure is recommended for severe
defects (Qp/Qs >15, or those associated with right ventricular volume overload). In patients
without symptoms, indications for closure are somewhat controversial. In those younger than
40 years, severe defects should probably be closed. The appropriate treatment for patients who
are older than 40 years is in some dispute, although results of one randomised clinical trial
which showed an overall survival benefit among surgical patients would suggest that closure is
advisable.
Surgical closure of these defects can be done by primary suture closure or by an autologous
pericardial or synthetic patch. Surgical mortality in adults with no pulmonary hypertension
should be less than 1%, with a low morbidity related mainly to the development of
perioperative arrhythmias (atrial flutter or fibrillation, or junctional rhythm). The use of devices
to close defects percutaneously under fluoroscopy and transoesophageal echocardiographic
guidance is gaining popularity.
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LA=left atrium. RA=right atrium. Arrows point at both sides of the Amplatzer device after
insertion.
Indications for closure by devices are the same as for surgical closure but selection criteria are
stricter than for surgery. Devices are available only for patients with one secundum atrial septal
defect and with an adequate septal margin for proper device support. Anomalous pulmonary
venous connection precludes the use of this technique. This procedure is safe and effective
when done by a skilled cardiologist, and major complications (eg, device embolisation, atrial
perforation) arise in less than 1% of patients. Complete closure is achieved in 80% or more of
patients. Long-term follow-up data, however, are not available. Notwithstanding, closure by
device can be appealing to a patient wishing to avoid the consequences of surgery (general
anaesthesia, cardiopulmonary bypass, pain, scar, and time for convalescence), or to a patient
believed to be at high surgical risk.
The incidence of isolated persistent patency of the ductus arteriosus is estimated at one in 2000
to one in 5000 births. The ductus arteriosus derives from the left sixth primitive aortic arch and
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connects the proximal left pulmonary artery to the descending aorta, distal to the left
subclavian artery. Occasionally, the ductus fails to close at birth and presents as a potential
clinical problem.
Physiological consequences of a patent ductus arteriosus depend on the degree of left-to-right
shunting, which is determined by both the size of the duct and the difference between systemic
and pulmonary vascular resistances. A small ductus accompanied by a small shunt does not
cause significant haemodynamic disruption but might predispose to endarteritis, especially if
accompanied by an audible murmur. A moderate sized duct and shunt put a volume load on the
left atrium and ventricle that results in dilation and often dysfunction of the left ventricle, and
development of a trial fibrillation, or both. A large duct results initially in left-ventricular
volume overload (which disappears after pulmonary hypertension develops), with a progressive
rise in pulmonary artery pressure. This rise in pressure leads to high pulmonary vascular
resistance and eventually, irreversible pulmonary vascular changes and systemic pulmonary
pressures.
Treatment
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is unknown,24 and appropriate clinical management of such patients is unclear. Some would
recommend closure by device in this patient to eliminate the risk of endarteritis. In our view
however, there is no evidence for that approach. Others might choose a non-interventional
approach with the use of prophylactic treatment for subacute bacterial endocarditis when
needed.
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Bicuspid aortic valve has a male preponderance of 4 to 1. This lesion accounts for about half
the cases of surgically important isolated aortic stenosis in adults. A bicuspid aortic valve
consists of two cusps, often of unequal size, the larger usually containing a false raphe. This
lesion generally arises in isolation but is associated with other abnormalities in 20% of
patients, the most common of which is coarctation of the aorta and patent ductus arteriosus.
At least half the patients with a bicuspid aortic valve have no complications, although there is
always the risk of endocarditis. Mild aortic stenosis or regurgitation from bicuspid aortic valve
generally progresses as the patient ages, but the rate is variable. Enlargement of the aortic root
resulting from cystic medial changes in patients with bicuspid aortic valve has a high
prevalence, and occurs irrespective of altered haemodynamics or age. Aortic dissection is rare.
Treatment
Bicuspid aortic valves need intervention for stenosis when symptoms (exertional dyspnoea,
angina, pre-syncope, or syncope) are present and should be considered before pregnancy when
the stenosis is severe. Intervention for asymptomatic severe aortic stenosis to allow safe
pregnancy is controversial, but severe aortic stenosis has proved to be a risk factor for cardiac
decompensation during pregnancy.30 Bicuspid aortic stenosis can be treated with balloon
valvuloplasty if the patient is younger than 30 years and if the valve is not calcified. Other
treatment options include open aortic valvotomy, or valve replacement with a mechanical valve,
a biological valve, or a pulmonary autograft (Ross procedure).
Prophylactic surgery for proximal aortic dilation (>55 mm), in the context of bicuspid
aortopathy, seems better than waiting for the aorta to dissect or rupture, although there is no
agreement about the diameter at which referral for surgery is appropriate. With the added
haemodynamic load of pregnancy (50% increase in cardiac output) and the high oestrogen
concentrations that tend to lessen the strength of the aortic wall, any patient with a dilated
ascending aorta should be closely monitored during their pregnancy.
This patient would be best treated with close medical follow-up and echocardiography every 3
months or so, to look for signs of progressive aortic root dilation. Treatment with blockers (if
blood pressure is normal) and bedrest, with or without early delivery, should be considered
when rapid progression of the ascending aortopathy is seen or the ascending aorta reaches more
than 55 mm. Vaginal delivery at term with a rapid (forceps-assisted) second stage labour would
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Coarctation of the aorta is seen most frequently in men with a ratio of almost 3 to 1. It usually
resides in the region of the ligamentum arteriosum. It might be discrete or associated with
hypoplasia of the aortic arch and isthmus. Related abnormalities include bicuspid aortic valve
in 50-85% of cases. Despite initial successful correction of coarctation, the risk of late
systemic hypertension (due to residual or recurrent coarctation, or merely to abnormal aortic
wall compliance) in these patients is fairly high. If inadequately controlled, hypertension leads
to an increased risk of premature death from late heart failure. Other causes of premature death
might be coronary artery disease with or without aortic rupture or dissection. Careful long-term
follow-up and aggressive management of patients with hypertension is therefore recommended.
Local complications such as re-coarctation and aneurysm formation at the site of previous
transcatheter or surgical correction should be identified through periodic chest radiography,
echocardiogram, MRI, or spiral CT examinations.
Treatment
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available. If the anatomy is not suitable (ie, long tunnel-like stenosis) surgery might be needed.
After surgical repair of isolated aortic coarctation, the obstruction is usually relieved with
minimum mortality (<2%). However, mortality is increased for reoperation (5-15%).
Angiograms of mild re-coarctation of the aorta (A); balloon dilatation and stenting of the
re-coarctation segment of the descending aorta (B); and stented descending aorta (C)
Arrow in (A) indicates re-coarctation segment.
This patient has mild re-coarctation of the aorta (peak gradient >20 mm Hg) at the site of
previous surgical repair with superimposed mild systolic hypertension. Balloon dilatation and
stenting of the re-coarctation segment (if the anatomy is suitable) should be done to reduce
proximal systolic blood pressure. The procedure should only be done, however, by experienced
cardiologists. Surgical revision or antihypertensive medication, or both, might also be
appropriate.
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The patient has a history of repaired tetralogy of Fallot in childhood. She was lost to
follow-up. Physical examination showed a right ventricular impulse and a low-pitched diastolic
murmur grade 3/6 best heard along the left sternal border. Transthoracic echo showed a dilated
right ventricle and severe pulmonary regurgitation. Cardiac MRI confirmed a severely dilated
right ventricle (right ventricular end-diastolic volume 350 mLnormal range up to 108
mL/m2), severe pulmonary regurgitation, and fairly normal right ventricular systolic function.
MRI showing right right ventricular dilation in a patient after repair of tetralogy of Fallot
LA=left atrium. LV=left ventricle. RA=right atrium. RV=right ventricle.
Tetralogy of Fallot is the most common form of cyanotic congenital heart disease after 1 year of
age, with a frequency of almost 10% of all congenital heart disease. The defect is caused by
anterocephalad deviation of the outlet septum resulting in four features: (1) a non-restrictive
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ventricular septal defect; (2) an overriding aorta (<50% override); (3) obstruction of the right
ventricular outflow tract which may be infundibular, valvar, or (usually) both, with or without
supravalvar or branch pulmonary artery stenosis; and (4) consequent right ventricular
hypertrophy.
Reparative surgery is usually done early in infancy, by closure of the ventricular septal defect
with a Dacron patch and relief of the right ventricular outflow tract obstruction. Obstruction
relief might include resection of infundibular muscle and insertion of a right ventricular
outflow tract or transannular patcha patch across the pulmonary valve annulus that disrupts
the integrity of the pulmonary valve and causes important pulmonary regurgitation. Significant
pulmonary regurgitation is almost always encountered when the transannular patch repair
technique is used. Pulmonary regurgitation is usually well-tolerated indefinitely, if mild to
moderate. Severe chronic pulmonary regurgitation might be well tolerated for 20 years or more,
but could then lead to symptomatic right ventricular dysfunction, and increase the
susceptibility to ventricular tachycardia and sudden cardiac death.
Residual obstruction of the right ventricular outflow tract can arise in the infundibulum, the
pulmonary valve, and the main pulmonary trunk or branches of the left and right pulmonary
arteries, or both branches. Right ventricular dilation in this setting is usually due to
longstanding free pulmonary regurgitation, but might result from operative injury. Substantial
tricuspid regurgitation might occur because of right ventricular dilation, which then leads to
further dilation of the right ventricle.
Atrial tachyarrhythmia arises in about a third of adults and contributes to late morbidity and
even mortality. It usually takes the form of atrial flutter or intra-atrial re-entrant tachycardia.
Often indicative of haemodynamic trouble (significant right ventricular dilation and
dysfunction, increased tricuspid regurgitation), the substrate is most likely a surgical scar in the
atria and the trigger, atrial dilation.
Sustained monomorphic ventricular tachycardia is rare, compared with other types, and is
highly associated with pronounced right ventricular dilation. The QRS duration from the
standard surface ECG has been shown to correlate well with right ventricle size in these
patients. A maximum QRS duration of 180 ms or more is a highly sensitive marker for
sustained ventricular tachycardia and sudden cardiac death in adults with previous tetralogy
repair, although its positive predictive value is low. Dilation of the right ventricle is thought to
trigger ventricular tachycardia, whereas surgical scars (near the right ventricular outflow tract or
ventricular septal defect patch) form the arrhythmia substrate. The reported frequency of
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sudden death, presumably due to arrhythmia, in late follow-up series is 056% over 30 years,
accounting for about a third to a half of late deaths. Older age at repair, severe left ventricular
dysfunction, postoperative right ventricular hypertension, transannular patching (causing free
pulmonary regurgitation), and an accelerated rate of QRS prolongation are all predictors of
sudden death in these patients.
Treatment of complications
Replacement of the pulmonary valve (with either a homograft or porcine bioprosthesis) might
be necessary for severe pulmonary regurgitation leading to right ventricular dilation, sustained
arrhythmias or symptoms, or both. Such replacement might also be needed for a grossly
calcified pulmonary valve. It has a low operative risk and leads to symptomatic improvement.
Timely pulmonary valve replacement, before irreversible severe right ventricular dilation and
systolic right ventricular dysfunction begins, is a major clinical goal. Concomitant tricuspid
valve annuloplasty might also be necessary when at least moderate tricuspid regurgitation is
present.
Patients presenting with sustained atrial flutter, atrial fibrillation, or ventricular tachycardia,
should undergo a thorough assessment of their haemodynamics and should have residual
haemodynamic lesions repairedeg, significant right ventricular dilation from pulmonary
regurgitation with resulting tricuspid regurgitation that needs pulmonary valve replacement and
tricuspid valve annuloplasty50, 51. Radiofrequency ablation, after mapping for atrial re-entry
tachycardia, now yields better results than before for classic atrial flutter or incisional atrial
reentrant tachycardia, or both, and should be done either percutaneously (if there is no need for
concomitant surgery) or intraoperatively at the time of surgical repair of underlying
haemodynamic lesions. For atrial fibrillation, a biatrial maze procedure should also be
considered, and ideally done at reoperation. Likewise, transcatheter (when surgery is
unnecessary) or concomitant intraoperative ablative procedures of the ventricular tachycardial
pathway should be done when appropriate. Antiarrhythmic medications and the new generation
of atrial antitachycardia pacemakers (for supraventricular tachycardia) can be used as adjunct
treatments. Patients who were resuscitated after sudden cardiac death and are in need of
surgery without a haemodynamic substrate should probably receive an automated implantable
cardioverter defibrillator (AICD).
This patient should probably have pulmonary valve replacement since the right ventricle is
severely dilated, with repair of the ventricular septal defect patch as well as cryoablation of the
ventricular tachycardia focus at the time of surgery. Pulmonary valve replacement will lead to a
smaller right ventricle and cryoablation of the ventricular tachycardia focus would eliminate the
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arrhythmia substrate and probably prevent a further episode of sudden cardiac death.
In patients with complete transposition of the great arteries, the connections between the atria
and ventricles are concordant (normal), and the connections between ventricles and great
arteries are discordant. Thus, the pulmonary and systemic circulations are connected in parallel
rather than the normal in-series connection. In one circuit, systemic venous blood passes to the
right atrium, the right ventricle, and then to the aorta. In the other, pulmonary venous blood
passes through the left atrium and ventricle to the pulmonary artery. This situation is fatal
unless the two circuits mix. About half of patients with transposition of the great arteries have
additional abnormalities, most often a ventricular septal defect.
The most common previously done surgical procedure seen in adults is the atrial switch
operation. Patients will have had either a Mustard or a Senning procedure. Blood is redirected
at atrial level with a baffle made of Dacron or pericardium (Mustard operation) or with atrial
flaps (Senning operation), to achieve physiological correction. Systemic venous return is
diverted through the mitral valve into the subpulmonary morphological left ventricle and the
pulmonary venous return is rerouted via the tricuspid valve into the subaortic morphological
right ventricle. This repair, however, leaves the morphological right ventricle to support the
systemic circulation.
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Diagram showing atrial baffle in a patient with D-transposition of the great arteries
RA=right atrium. RV=right ventricle. LA=left atrium. LV=left ventricle. PA=pulmonary artery,
AO=aorta. Arrows indicate systemic venous baffle, and black dots pulmonary venous baffle.
After atrial baffle surgery, most patients reaching adulthood will be in New York Heart
Association class III. During 25 years of follow-up, about half these patients will have
moderate systemic dysfunction of the right ventricle with only a few presenting with symptoms
of congestive heart failure. Severe systemic tricuspid regurgitation is present in about a third,
which exacerbates right ventricular dysfunction. Atrial flutter arises in 20% of patients by age
20 and progressive sinus node dysfunction is seen in half the patients by that time. These
rhythm disturbances are thought to be a result of atrial and sinus node damage at the time of
atrial baffle surgery. Baffle leak or obstruction can also occur.
The atrial switch operation was gradually replaced by the arterial switch operation (Jatene) in
the 1980s, but few of these patients have yet become adults. Blood is redirected at the great
artery level by switching the aorta and pulmonary arteries such that the morphological left
ventricle becomes the subaortic ventricle and the morphological right ventricle becomes the
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subpulmonary ventricle. Reliable data for the clinical outcome in adults after the arterial switch
procedure should be available over the next decade. Clinical arrhythmia promises to be less of
a problem in this group of patients, but concerns about the development of supra neopulmonary
artery stenosis, ostial coronary artery disease, and progressive neoaortic valve regurgitation
warrant serial follow-up
Treatment
The Fontan procedure is the palliative, non-curative, surgical treatment for patients with
univentricular hearts. The principle is diversion of the systemic venous return directly to the
pulmonary arteries without the need for a subpulmonary ventricle. Many modifications of this
procedure have been described, egdirect atrio-pulmonary connection, total cavopulmonary
connection, and extracardiac conduit. Progressive deterioration of functional status with time is
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the rule, with survival at 10 years after the procedure reported to be 6071%. The most
common complications after a Fontan procedure include atrial flutter or fibrillation, right atrial
thrombus formation, obstruction of the Fontan circuit, and ventricular dysfunction.
Atrial flutter or fibrillation are common (1520% at 5-year follow-up), and increases with
duration of follow-up. They are associated with serious morbidity (especially the development
of atrial thrombi within hours), and can lead to profound haemodynamic deterioration. Such
patients need prompt and expert medical attention. The combination of atrial incisions and
multiple suture lines at the time of Fontan surgery with increased right atrial pressure and size
probably accounts for the high frequency of atrial arrhythmias in these patients. Obstruction of
the Fontan connection should be ruled out in all patients presenting with new onset atrial
arrhythmias.
The reported frequency of thromboembolic complications in the Fontan circuit varies from 6%
to 33%, dependent on the diagnostic method used and the length of follow-up. Right atrial
thrombus formation relates to the presence of atrial flutter or fibrillation, right atrial dilation,
right atrial smoke (spontaneous echo contrast), and the presence of artificial material used to
construct the Fontan circuit.
Part obstruction of the Fontan connection leads to exercise intolerance, atrial
tachyarrhythmias, and right-sided heart failure. Sudden total obstruction presents as sudden
death. Protein-losing enteropathy is seen in about 23% of patients after the Fontan
procedure. Patients present with generalised oedema, ascites, pleural effusion, or chronic
diarrhoea. The diagnosis is confirmed by low serum albumin and protein and high
1-antitrypsin stool clearance. The prognosis is poor, with a 5-year survival of 4659%.
Treatment of complications
In patients with atrial fibrillation or flutter, prompt anticoagulation and transoesophageal echo
assessment to rule out atrial thrombi before cardioversion is recommended. Long-term
management with antiarrhythmic therapy is successful in less than 50%. Transcatheter atrial
ablation can be done in specialised centres, with a 50% success rate. For recalcitrant cases,
surgical revision with antiarrhythmic surgery is recommended.
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For established thrombus, thrombolytic therapy or surgical removal of the clot and conversion
of the Fontan circuit have been described. Long-term anticoagulation is recommended for
patients with known thrombi. Some centres anticoagulate all Fontan circuits for the rest of the
patient's life. For patients with Fontan obstruction, surgical revision of the Fontan connection
is usually needed. Alternatively, balloon angioplasty with or without stenting can be used when
appropriate. Patients with protein-losing enteropathy might be candidates for creation of a
fenestration in the atrial septum or revision of the Fontan. Alternatively, subcutaneous heparin,
octreotide treatment, and prednisone treatment have also been tried with variable success, No
particular treatment seems more successful than any other.
In this patient, who is haemodynamically stable, ventricular rate should be controlled with
digoxin or other agents, and prompt anticoagulation with heparin should be started. The patient
should be transferred to a highly specialised hospital for transoesophageal echo to rule out
right atrial clot before cardioversion. Fontan obstruction as the cause of atrial fibrillation
(conduit obstruction with secondary right atrial stretch) should be ruled out either at the time
of transoesophageal echo or by cardiac catheterisation. Long-term coumadin is recommended
for all patients with Fontan obstruction who have a history of atrial fibrillation. Maintenance
of sinus rhythm after cardioversion is probably best achieved with amiodarone, although the
success rate is low at 50%. Antitachycardia pacing, catheter ablation or surgical revision, or
both, with concomitant biatrial maze procedure are used as second-line treatment in patients
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with Fontan obstruction and chronic or paroxysmal atrial fibrillation that is unresponsive to
medical management. Other causes of atrial fibrillation such as ethanol binge or
hyperthyroidism should also be ruled out.
..
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ESOPHAGEAL DIVERTICULA
The esophageal diverticula are the sacciform outpouchings of the esophageal wall, which
filled with mucus and undigested food.
Pathology
The restricted blind herniation of the wall of esophagus could be single or multiple,
ring-shaped, cylindrical, oval or sacciform-shaped. The muscle coat atrophies, that makes
difficult differentiation between true and false diverticula. The latter caused by inflammatory
processes. In such cases the paraesophageal scarring resulting from extrapharyngeal abscesses,
mediastinitis, specific and nonspecific inflammatory processes of bifurcational lymph nodes
(traction diverticula) are revealed.
The small size of the opening of pouch, for example, in globular diverticula, leads to
congestion of contents with the further development of inflammation (diverticulitis erosive,
catarrhal, gangrenous, purulent).
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Classification
1. According to the origin:
a) congenital;
b) acquired.
2. According to number:
a) single;
b) multiple.
3. According to histological structure:
a) true (have all layers of esophageal wall);
b) false (absent muscular layer of esophageal wall).
4. According to localization:
a) pharyngoesophageal (Zenker's);
b) bifurcational;
c) epiphrenic.
5. According to the clinical course:
a) complicated;
b) uncomplicated.
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Types of diverticula:
1 pharyngoesophageal (Zenker's)
2 bifurcational
3 epiphrenic
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Bifurcational diverticula are usually less 2 cm in size and therefrom rarely complicated
and clinically manifested. At its greater size the complications can arise rather frequently and
determine the course and manifestations of the disease.
Diverticula that occur in the distal esophagus, in the lower 6-10 cm, are termed
epiphrenic diverticula (see the image below).
The epiphrenal diverticula can achieve considerably size, and more frequently
complicated by diverticulitis. Being filled with food, such diverticulum can compress cervical
organs, and sometimes is complicated with achalasia.
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Diverticula of the mid and distal esophagus may have various etiologies. For instance,
some diverticula in the mid esophagus are congenital in origin; others are of the traction
variety. With the latter, diverticula develop by traction from contiguous mediastinal
inflammation and adenopathy, eg, pulmonary tuberculosis and histoplasmosis. The diverticula
that develop by traction and adenopathy usually are asymptomatic.
Retention of undigested food in large diverticula occasionally results in regurgitation,
nocturnal cough, and aspiration pneumonia.
Occasional epiphrenic diverticula occur in the setting of long-standing peptic
esophagitis and strictures, and they rarely are symptomatic. Other rare causes of diverticula of
the mid and distal esophagus include iatrogenic surgical injury to the esophagus and Ehlers-
Danlos syndrome (weakness of collagen). Perhaps the most common causes of mid esophageal
and epiphrenic diverticula are motility disorders of the esophageal body, including achalasia,
diffuse esophageal spasm, and hypertensive lower esophageal sphincter.
Dysphagia is the most common symptom associated with mid esophageal and epiphrenic
diverticula, although it usually is related more to the underlying motility disturbance than to
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the diverticulum per se. However, on occasion, the diverticulum may be responsible for the
dysphagia, particularly if it is very large and filled with food or a bezoar. Regurgitation and
aspiration may be related to large mid esophageal and epiphrenic diverticula; however, in
patients with achalasia, regurgitation and aspiration are more likely to be related to poor
esophageal emptying from the underlying motility disturbance (eg, hypertensive lower
esophageal sphincter that fails to relax, absence of esophageal body peristalsis).
The diagnosis is confirmed by the findings of barium swallow, and also esophagoscopy.
Diverticulitis. The anginal pain, or the pain in epigastric region, which can resemble
stenocardia or gastric disorders, belching, are the chief manifestations. Sometimes observed
nausea and vomiting.
The perforation of diverticulum can be directed into pleural space, trachea, bronchus or
pericardium. The clinical picture depends on the place of perforation. In part the perforation in
trachea or bronchus results in occurrence of esophago-bronchial fistula. Clinically such
complication is commonly shown by cough during meal. An everlasting esophago-bronchial
fistula can cause the aspiration pneumonia with the further abscessing.
Bleeding from diverticula frequently results from erosion of esophageal mucosa on the
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background of diverticulitis. Nevertheless such bleedings, as a rule, are not profuse and rather
easily stopped by conservative treatment.
Malignancy rarely occurs and most often as the outcome of recurrent diverticulites.
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Differential diagnostics
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In many patients with mid esophageal and epiphrenic diverticula, dysphagia is related to
underlying dysmotility; thus, treatment should be directed to the motility disorder when
feasible. For instance, achalasia can be treated with pneumatic dilation, botulinum toxin
injection into the lower esophageal sphincter, or surgical Heller esophagomyotomy.
Treatment of esophageal intramural pseudodiverticulosis is directed toward underlying
strictures or dysmotility.
The bifurcational diverticula require operative treatment only in one patient in ten. The
indications for such operation are frequently recurrent diverticulites, bleeding, perforation,
esophago-bronchial fistula or suspicion on malignancy.
Treatment of Zenker diverticulum traditionally has been surgical, although the specific
operation used still is controversial. Surgical options include diverticulectomy with
cricopharyngeal myotomy, diverticular suspension (diverticulopexy) with cricopharyngeal
myotomy, and cricopharyngeal myotomy alone.
Consider diverticulectomy when esophageal body diverticula are believed to be the cause
of aspiration. An abdominal laparoscopic approach may be feasible for some patients with
epiphrenic diverticula. Case reports of endoscopic treatment of giant midesophageal diverticula
have been reported. However, patients who are being considered for diverticulectomy should
first undergo careful study with barium swallow, flexible endoscopy, and esophageal
manometry. Treatment directed at an underlying esophageal motility disorder, such as
achalasia, cannot be ignored.
Diverticulectomy usually is not performed by itself because it does not correct the defect
in cricopharyngeal function that usually contributes to the formation of a Zenker diverticulum.
While the transcervical approach has been used traditionally, the transoral route using a
rigid esophagoscope also may be used.
Good results have been obtained by performing a diverticulotomy using a flexible
endoscope and needle-knife papillotome to cut the common wall between the diverticulum and
the oropharynx as well as the cricopharyngeus while the patient is consciously sedated. Data
suggest that this technique offers good results with a relatively high success rate, but it should
be performed in large centers with surgeons who are experienced with this technique. In some
variations of this technique, the diverticulum is stapled.
Other novel techniques are being developed. Flexible endoscopic diverticulotomy
approaches have been explored using various techniques, including argon plasma coagulation,
monopolar coagulation forceps, and needle-knife incision. These techniques typically use a cap
or hood attached to the endoscope. The goal of these techniques is the division of the septum
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between the diverticulum and the esophagus, thus performing a cricopharyngeal myotomy.
Increased efforts to a laparoscopic approach to repair both epiphrenic diverticula and
Zenker diverticula have been explored. The literature supports open surgery and a laparoscopic
approach as appropriate methods of repair. The laparoscopic technique uses stapler closure,
and multiple case reports cite wound leakage from stapler failure as a complication. With
complication rates as high as 20%, a skilled surgeon with experience in this procedure is
beneficial. Benefits of the laparoscopic approach include decreased morbidity because of no
thoracotomy wounds and chest tubes and a less invasive approach.
A study of 229 endoscopic diverticulotomies (in 189 patients), conducted by Kos et al,
indicated that better results can be achieved using a combination of CO2 laser and Acuspot in
the endoscopic procedure than by employing endoscopic diverticulotomy with electrocautery or
with a carbon dioxide (CO2) laser alone. The investigators reported the following postsurgical
results:
Endoscopy with CO2 laser
Dysphagia - Absent following 78.4% of procedures
Repeat surgery - Required following 19.6% of procedures
Endoscopy with electrocautery
Dysphagia - Absent following 72% of procedures
Repeat surgery - Required following 24.3% of procedures
Endoscopy with CO2 laser and Acuspot
Dysphagia - Absent following 84.6% of procedures
Repeat surgery - Required following 13% of procedures
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Cervical
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Etiology
The cause of this disease is still unknown. Among the underlying mechanisms are the
psycho-emotional trauma, disturbance of parasympathetic and sympathetic innervation and
influence of vegetotrophic substances on muscular fibers.
Pathology
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Frequency
United States. The incidence of achalasia is approximately 1 per 100,000 people per
year.
Sex
The male-to-female ratio of achalasia is 1:1.
Age
Achalasia typically occurs in adults aged 25-60 years. Less than 5% of cases occur in
children.
Classification
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Dysphagia in the onset of the disease wears a temporary intermittent character with
further permanent interchange. The passing of food after several swallows delayed on the level
of a lower part of breastbone. In some cases during meal the dysphagia arises suddenly without
any cause. The majority of the patients with dysphagia swallow better warm or hot food.
Esophageal vomiting (regurgitation) is the outcome of accumulation in esophagus of two
and more l. of fluid. In initial stages of the disease the regurgitation can arise during or at once
after meal and is accompanied by discomfort pain sensations. In advanced stages observed
regurgitation with a rotten smell. The regurgitation can occur during sleeping the sign "of a
wet pillow".
Splashing sounds and gurgling behind breastbone are rarely observed.
The sign of nocturnal cough arises owing to aspiration of fluid from esophagus into
trachea. Thereby, the patients try to sleep in a sedentary position.
Pain and sense of tightness in the chest is the result of spasm and esophageal distention.
With the developing of esophagitis, the pain wears a burning character.
Loss of weight is the outcome of prolonged disturbed food intake.
It is necessary to consider roentgenological contrast examination with barium swallow as the
chief method, which enables to confirm the diagnosis. In the beginning of the disease revealed
an inappreciable esophageal dilation and temporary delay of barium above the level of the
inferior esophageal sphincter. In advanced stages of the disease observed a considerable
esophageal dilation and elongation with a long delay of barium. Contours of a distal
constricted part of esophagus described as the "rat tail" or "bird-beak" sign, without filling
defects .
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Esophageal achalasia
The endoscopic procedure reveals erosive changes of esophageal mucosa and enables to
take a biopsy to rule out malignancy. Frequently in advanced stages it is failed to pass by
endoscope a constricted part of esophagus and cardia.
The disease is characterized by remittent course with the change of the periods of
dysphagia from inappreciable to intensive. Even in advanced stages in minority of patients
observed a latent course with complete disappearance of dysphagia in considerable esophageal
dilation and cicatrical stenosis of cardia. Nevertheless later (from several months to several
years) there comes an exacerbation of the disease with more severe course.
The bleeding arises owing to complications of erosive esophagitis at long duration of the
disease.
The malignancy occurs in the patients with phenomena of a chronic esophagitis and
chronic character of the disease.
Pneumonia, abscesses, bronchiectases, atelectases and pneumosclerosis are frequently
the outcomes of decreasing pulmonary excursion which results from compression by dilated
esophagus.
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Esophageal achalasia
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Esophageal achalasia
Differential diagnostics
Cancer of the lower part of esophagus and cardial part of stomach. The predominant
place in differential diagnostics possesses X-ray examination. As opposed to achalasia, the
cancer is characterized by irregular contours of constricted part of esophagus with filling
defect. Endoscopic examination and biopsy allows to confirm the diagnosis.
Diaphragmatic hypotonia with inflection of esophagus also can be accompanied with
dysphagia. However chest X-radiography enables to find out high standing of the left dome of
diaphragm.
Pneumothorax. On the plain chest X-radiography the edge of dilated esophagus can
resemble the edge of collapsed lung. Nevertheless in the patient with pneumothorax on the
roentgenogram the lung pattern is absent.
The goal of therapy for achalasia is to relieve symptoms by eliminating the outflow
resistance caused by the hypertensive and nonrelaxing LES. Once the obstruction is
relieved, the food bolus can travel through the aperistaltic body of the esophagus by
gravity.
Calcium channel blockers and nitrates are used to decrease LES pressure.
Approximately 10% of patients benefit from this treatment. This treatment is used
primarily in elderly patients who have contraindications to either pneumatic dilatation or
surgery.
Endoscopic treatment includes an intrasphincteric injection of botulinum toxin to block
the release of acetylcholine at the level of the LES, thereby restoring the balance
between excitatory and inhibitory neurotransmitters. This treatment has limited value.
Only 30% of patients treated endoscopically still have relief of dysphagia 1 year after
treatment. Most patients need repeated botulinum toxin injections, with short-lasting
clinical benefits. This treatment can cause an inflammatory reaction at the level of the
gastroesophageal junction, making a subsequent myotomy very difficult. Compared with
pneumatic dilation, botulinum toxin injection is associated with significantly higher
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follow-up periods.
Based on the limited evidence available, POEM seems to be a promising new procedure.
However, there are some concerns about this new technique. Endoscopic myotomy is a
very demanding procedure, requiring major skills, with a very long learning curve. Even
though several studies have reported significant reduction of LES pressure as
demonstrated by manometry, the LES pressure was often between 15 and 20 mm Hg. It is
known that a predictor of long-term success is an LES pressure around 10 mm Hg.
Gastroesophageal reflux is reported in up to 50% of patients after POEM, replicating the
results obtained when a myotomy alone was performed without an antireflux operation.
Surgical revision in patients with recurrent dysphagia after POEM might be challenging.
The presence of adhesions between the submucosal and longitudinal muscular layers
after POEM might make the dissection at this level very difficult.
Diet. The food should be semisoft, without pungent relishes, chemically inactive and
enriched with proteins, fat, carbohydrates and vitamins.
The medicament treatment should include local anesthetics, spasmolytics, and sedative
drugs. Atropin and other anticholinergic agents only increase the spasm of a cardial sphincter,
therefrom their usage is undesirable. The medicament treatment results only in temporary relief.
Cardiodilatation is indicated in - stage of achalasia. It is one of the chief methods of
the treatment of this pathology. The treatment is performed as follows: under local anesthesia
by aerosol or solution of anesthetic agent (lidocain, trimecain) through constricted part of the
cardia under roentgenological check cardiodilatator (metal, pneumatic) is passed. The air is
pumped up in balloon making pressure 200-350 mm H2O. Repeated procedure is performed in
2-3 days. The course of dilatation includes 3-10 procedures, depending on obtained effect.
Surgical treatment is managed in -V stage of achalasia or in recurrence of the disease
after dilatation.
Because of excellent results, a short hospital stay, and a fast recovery time, the primary
treatment is considered by many to be a laparoscopic Heller myotomy and partial
fundoplication. In the author's experience and in the experience of many authors, this
treatment provides a fine balance in relieving symptoms of dysphagia by performing the
myotomy and in preventing gastroesophageal reflux by adding a partial wrap. A
prospective, randomized study from Vanderbilt University indicated that there is
significantly less risk of postoperative reflux following a Heller myotomy plus a partial
fundoplication than there is after a Heller myotomy alone. The authors of this study also
showed that in patients with achalasia, adding a partial fundoplication not only is more
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Heller's operation:
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Nissen fundoplication
The defect of a muscular layer of esophageal wall is covered with a gastric fundus or by
means of interrupted suture or diaphragmatic flap.
Patients remain hospitalized for 24-48 hours and return to regular activities in about 2
weeks.
The operation relieves symptoms in 85-95% of patients, and the incidence of
postoperative reflux is about 20%.
For patients in whom surgery fails, they may be treated with an endoscopic dilatation
first. If this fails, a second operation (extending the previous myotomy onto the anterior
gastric wall) can be attempted once the cause of failure has been identified with imaging
studies. The last resort is to surgically remove the esophagus (ie, esophagectomy).
Treatment options vary for patients with different degrees of illness severity. A study by
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have been reported in several series of patients previously treated with endoscopic
treatments. These findings may be related to scar tissue at the level of the
gastroesophageal junction, which makes surgical dissection of the anatomic planes much
more difficult.
In 2011, Boeckxstaens et al[22] reported the results of a multicenter, randomized trial
comparing pneumatic dilatation (95 patients) to laparoscopic Heller myotomy with Dor
fundoplication (106 patients) for untreated esophageal achalasia. The perforation rate
during pneumatic dilatation and laparoscopic Heller myotomy was 4% and 12%,
respectively. Therapeutic success was defined as a drop in Eckardt score below 3. The
study showed similar success rates after laparoscopic Heller myotomy (90%) and
pneumatic dilatation (86%) over a 2-year follow-up period.
In conclusion, while pneumatic dilatation was considered the main treatment modality
for patients with achalasia in the 1980s, with surgery having a secondary role in case of
dilatation failure, in current practice pneumatic dilatation should be reserved for when
surgical expertise is not available and for the treatment of recurrent dysphagia after
myotomy.
One study only has compared in a retrospective fashion POEM and laparoscopic Heller
myotomy.[28] Eighteen patients undergoing POEM were compared in a nonrandomized
fashion to 55 patients treated by laparoscopic Heller myotomy. No differences were
observed in terms of length of the myotomy, complication rate, and length of hospital
stay. Veress needle decompression of the pneumoperitoneum was required
intraoperatively in 7 (39%) patients undergoing POEM. Treatment success (Eckardt
score 3) after POEM was achieved in 16 (89%) patients at median 6-month follow-up.
Six weeks after POEM, routine follow-up manometry and timed-esophagram showed
normalization of esophagogastric junction pressures and contrast column heights.
Only long-term follow-up and prospective trials comparing POEM with laparoscopic
Heller myotomy and fundoplication will determine the role of this new technique in the
treatment of esophageal achalasia.
Helerovsky's method. The operation is indicated for the patients with -V stage of the
disease in case of considerable esophageal dilation, when performance of Heller's operation is
impossible owing to cicatrical changes. However the indication for this operation should be
restricted, because of frequent development of expressed esophagitis in postoperative period.
The same accesses, as in Heller's operation are applied. Constricted part of esophagus to its
dilation exposed and cardial part of stomach is mobilized. Dilated part of the esophagus is
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ESOPHAGEAL STICTURE
The cicatrical esophageal stenosis can arise owing to chemical, thermal and radial burns,
and as a result of esophagitis or peptic ulcers. The most frequent cause of cicatrical strictures is
considered to be chemical burns of esophagus, which are usually the result of accidentally or
purposely (suicide) drink of acids or alkalis.
Disease processes that can produce esophageal strictures can be grouped into 3 general
categories: (1) intrinsic diseases that narrow the esophageal lumen through inflammation,
fibrosis, or neoplasia; (2) extrinsic diseases that compromise the esophageal lumen by direct
invasion or lymph node enlargement; and (3) diseases that disrupt esophageal peristalsis and/or
lower esophageal sphincter (LES) function by their effects on esophageal smooth muscle and
its innervation.
Many diseases can cause esophageal stricture formation. These include acid peptic,
autoimmune, infectious, caustic, congenital, iatrogenic, medication-induced, radiation-induced,
malignant, and idiopathic disease processes.
The etiology of esophageal stricture can usually be identified using radiologic and
endoscopic modalities and can be confirmed by endoscopic visualization and tissue biopsy.
Use of manometry can be diagnostic when dysmotility is suspected as the primary process.
Computed tomography (CT) scanning and endoscopic ultrasonography are valuable aids in the
staging of malignant stricture. Fortunately, most benign esophageal strictures are amenable to
pharmacologic, endoscopic, and/or surgical interventions.
Because peptic strictures account for 70-80% of all cases of esophageal stricture, peptic
stricture is the focus of this article. A detailed discussion of possible benign and malignant
processes associated with esophageal stricture and its management is beyond the scope of this
article.
Frequency
United States Gastroesophageal reflux affects approximately 40% of adults. Esophageal
strictures are estimated to occur in 7-23% of untreated patients with reflux disease.
Gastroesophageal reflux disease accounts for approximately 70-80% of all cases of
esophageal stricture. Postoperative strictures account for about 10%, and corrosive strictures
account for less than 5%.
The overall frequency of initial and subsequent dilations for peptic stricture appears to
have decreased gradually since the introduction of proton pump inhibitors (PPIs) in the market
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in 1989. This has been borne out by data at the author's institution and in 2 large community
hospitals in Wisconsin. It is also in keeping with the general experience of gastroenterologists
in the United States.
Mortality/Morbidity
The mortality rate of peptic strictures is not increased unless a procedure-related
perforation occurs or the stricture is malignant. However, the morbidity for peptic strictures is
significant.
Most patients undergo a chronic relapsing course with an increased risk of food
impaction and pulmonary aspiration.
Frequently, coexistent Barrett esophagus and its attendant complications occur.
The need for repeated dilatation potentially increases the risk of perforation.
Race
Peptic strictures are 10-fold more common in whites than blacks or Asians. However,
this is controversial as a recent retrospective study reported comparable frequencies between
blacks and non-Hispanic whites. The authors reported that distribution of reflux esophagitis
and grade and frequency of reflux-related esophageal ulcer and hiatal hernia were also similar
in non-Hispanic whites and blacks. However, heartburn was more frequent and nausea/vomiting
less frequent in non-Hispanic whites compared with blacks with erosive esophagitis or its
complications.[2]
Sex
Peptic strictures are 2- to 3-fold more common in men than in women.
Age
Patients with peptic stricture tend to be older, with a longer duration of reflux
symptoms.
Pathology
Peptic esophageal strictures are sequelae of gastroesophageal reflux -induced
esophagitis, and they usually originate from the squamocolumnar junction and average 1-4 cm
in length.
Two major factors involved in the development of a peptic esophageal stricture are as
follows:
Dysfunctional lower esophageal sphincter: Mean LES pressures are lower in patients
with peptic strictures compared with healthy controls or patients with milder degrees of reflux
disease. A study by Ahtaridis et al showed that patients with peptic esophageal strictures had a
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Classification
According to the clinical course:
I. The period of acute manifestation has three degrees of severity:
1 - mild;
2 - moderate;
3 - severe.
. The latent period (false improvement).
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The clinical signs of esophageal burn directly depend on the period of lesion and degree
of gravity.
Acute period
The mild degree of clinical course manifests by satisfactory general state of the patient.
At swallowing the patient feels a moderate pain, sometimes salivation, hoarseness.
Roentgenologically the lumen of esophagus without changes, with free passage of barium,
the mucous folds with regular contours, but in some places it is possible to observe its
graduation. The esophageal peristalsis is maintained. As a rule, in 5-7 days the clinical
manifestations of the burn disappear.
The moderate degree of gravity of acute period is characterized by acute substernal and
pharyngeal pain at swallowing, repeated vomiting, feeling of fear and excitement. Tachycardia
120-130 beats/min. The body temperature rises to 39C. Oliguria develops frequently.
Roentgenologically the esophagus dilated, but in some places can be constricted as a result
of edema or spasm. The lumen is filled with considerable amount of slime. The contours of
mucosal folds are irregular, the peristalsis is weakened or absent at all. If there will be no
complication, in 10-15 days the clinical manifestation of the disease disappear and general
state of the patient is improved.
Severe degree is characterized by the clinic of shock. Pulse of weak filling and tension,
expressed tachycardia, acute substernal pain. The excitement of the patient is accompanied by
feeling of fear, further transmits into adynamia, frequently the patients are unconsciousness.
The skin is pale, covered with cold sweat. One patient in four except esophageal burns, suffers
from burn of the stomach. The clinical course of the disease is worsened by oliguria, which can
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transfer into anuria, and also occurrence of other complications. It determines the unfavorable
forecast.
The barium swallow in the majority of patients is problematic. Nevertheless if the
general state of the patient allows to carry out it, on the first day after a burn already have been
observed expressed manifestations of esophagitis: the esophagus dilated, mucosal folds are
failed to reveal. The deposits of destructive changed tissues in the lumen of esophagus
resemble the picture of filling defects; the peristalsis is absent, complete atony.
Latent period
This period is connected with replacement of necrotic tissues by granulations. The
general state of the patient is improved. The acute signs disappear. The patient swallows freely,
without feeling of discomfort at passage of food.
Period of cicatrize
It frequently lasts from 1 to 12 months. It is connected with replacement of granulations
by cicatrical tissue that results in progressing of esophageal stricture and disturbance of
swallowing at first of solid, and further of liquid food. Such strictures develop at the orifice of
esophagus, in projection of tracheal bifurcation and in the place of gastroesophageal juncture.
The passage of food through the constricted regions of esophagus is possible at first only due
to careful grinding and watering, but further it is inefficient. Thereafter food delay in
esophagus, choking, salivation, belching and vomiting develop. If the stricture is located in the
lower part of esophagus, the vomitis can be of putrefactive character. Progressing loss of
weight observed, which without correction can transfer into cachexia. The level and degree of
the stricture, its extension circumstantiated after X-ray examination.
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History
Patients with peptic strictures may present with heartburn, dysphagia, odynophagia, food
impaction, weight loss, and chest pain.
Progressive dysphagia for solids is the most common presenting symptom. This may
progress to include liquids.
Atypical presentations include chronic cough and asthma secondary to aspiration of food
or acid.
The clinician cannot rely on the presence or absence of heartburn to definitely determine
whether dysphagia is secondary to a peptic esophageal stricture.
Of patients with peptic esophageal strictures, 25% have no previous history of
heartburn.
Heartburn may resolve with worsening of a peptic stricture.
Approximately two thirds of patients with adenocarcinoma in Barrett esophagus
have a history of long-standing heartburn.
The abnormal esophageal motor activity in achalasia can produce a heartburn
sensation.
Important points regarding dysphagia
The obstruction is usually perceived at a point that is either above or at the level
of the lesion.
Dysphagia for solids and liquids simultaneously should alert the clinician to the
possibility of a motility disorder such as achalasia or collagen vascular disorders.
Dysphagia secondary to a Schatzki ring is usually intermittent and
nonprogressive.
Dysphagia for solids and liquids early in the course of disease should alert the
clinician to the possibility of achalasia as an etiology of a peptic esophageal
stricture.
Benign esophageal strictures usually produce dysphagia with slow and insidious
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progression (ie, months to years) of frequency and severity with minimal weight
loss.
Malignant esophageal strictures result in a rapid progression (ie, weeks to
months) of severity and frequency of dysphagia and are associated frequently with
significant weight loss.
Determining whether the patient takes any medications known to cause pill esophagitis
is important.
Determining whether a history of collagen vascular disease or immunosuppression exists
may provide clues to the underlying etiology.
Physical
Physical examination frequently does not provide clues to the cause of dysphagia.
Assessing the patient's nutritional status is important.
Patients with collagen vascular diseases may exhibit joint abnormalities, calcinosis,
telangiectasias, sclerodactyly, or rashes.
The presence of atypical gastroesophageal reflux disease may be suggested by hoarse
voice, posterior oropharyngeal erythema, diffuse dental erosions, wheezing, or epigastric
tenderness.
Patients with adenocarcinoma of the gastroesophageal junction may have left
supraclavicular lymphadenopathy (Virchow node).
Causes
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the anatomic site of narrowing, with the middle one-third behind the left atrium
predominating in 75.6%.[6]
Diseases of the skin - Pemphigus vulgaris, benign mucous membrane (cicatricial)
pemphigoid, epidermolysis bullosa dystrophica
Graft versus host disease
Idiopathic eosinophilic esophagitis
Extrinsic compression
Squamous cell carcinoma
Sequela of endoscopic submucosal dissection for superficial squamous cell
neoplasms.[7]
Miscellaneous - Trauma to the esophagus from external forces, foreign body,
surgical anastomosis/postoperative stricture, congenital esophageal stenosis
Distal esophageal strictures
Peptic stricture - Gastroesophageal reflux disease, Zollinger-Ellison syndrome
Adenocarcinoma
Collagen vascular disease - Scleroderma, systemic lupus erythematosus (SLE),
rheumatoid arthritis
Extrinsic compression
Alkaline reflux following gastric resection
Sclerotherapy and prolonged nasogastric intubation
Crohn disease
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narrowings of the esophagus such as those caused by rings and peptic strictures
that are greater than 10 mm in diameter.
This study has 100% sensitivity with luminal diameter less than 9 mm, and 90%
sensitivity with luminal diameter greater than 10 mm.
3. Chest X-radiography.
Chest radiograph, posteroanterior (PA) and lateral: Chest radiography should be
used as an adjunct if extrinsic compression is considered a possible etiology of
esophageal stricture.
CT scanning
CT scans can be used to stage malignancies that produce esophageal strictures.
Accuracy in estimating the depth of tumor invasion is 60-69%.
Accuracy in determining spread to other organs is 82%.
4. Endoscopic examination of esophagus, stomach and duodenum.
This procedure can be used to establish or confirm the diagnosis of esophageal
stricture, to seek evidence of esophagitis, to exclude malignancy, to obtain
biopsy and brush cytology specimens, and to implement therapy.
EGD is more sensitive than barium esophagram in the identification of subtle
mucosal lesions.
Subtle strictures may be missed when smaller and thinner endoscopes are
employed, especially in the setting of minimal sedation.
5. General blood analysis.
6. Coagulogram.
7. Biochemical investigation of plasma.
Complete blood cell (CBC) count: Usually, the results of a CBC are within the
reference range; however, anemia may develop due to chronic bleeding from
severe esophagitis or carcinoma.
Liver profile: Usually, the findings are within the reference range; however, the
liver profile may be abnormal if metastatic disease in underlying malignancy is
present.
Complete metabolic panel: This study may allow assessment of the patient's
nutritional status, especially in conjunction with weight loss.
8. Histologic Findings
Initial histologic changes in the peptic stricture process include edema, cellular
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infiltration, basal cell hyperplasia, and vascular changes with a slight increase in
type III collagen deposition on healing.
If untreated, the process can lead to progressive inflammation and ulceration
involving the submucosa and muscularis mucosa. This can lead to damage of the
muscular layer and the intrinsic nervous system of the esophagus, resulting in
deposition of type I collagen with subsequent formation of scar tissue and
stricture formation.
Differential diagnostics
The treatment of esophageal burns first of all should be guided to save the life of the
patient, and also to prevent the development of esophageal strictures. The first aid must be
given as soon as possible after taking of the chemical substance, which have caused the burn.
In such cases by means of gastric tube and great amount of water (to 10-15 l.) immediately
wash out the esophagus and stomach. It is better to use for this purpose the neutralizing
solutions. If the burn is caused by acid applied 2 % solution of sodium hydrocarbonatis, and in
the burns by alkalis vinegar in the ratio 1:20 with water. For prophylaxis of shock and
decreasing of psychoemotional excitement of the patient instituted anesthetizing agents. If
asphyxia arise owing to edema of pharynx and epiglottis, a tracheostomy is performed.
The further aid the treatment of shock and hypovolemia by massive intravenous
infusions (up to 4-5 l. per day) of saline solutions, solutions of glucose, dextrans and blood
plasma. With the purpose of detoxycation also applied forced diuresis.
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Traditionally, more emphasis has been placed on mechanical dilatation, and coexistent
esophagitis has been relatively ignored. However, several studies have demonstrated that
aggressive acid suppression using PPIs is extremely beneficial in the initial treatment of
esophageal stricture, as well as long-term management.
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Surgical Care
In advanced cases if failed to reach the restore of esophageal patency by a bougienage,
the esophagoplasty by stomach, small and large intestine is applied.
The following discussion concerns the endoscopic and surgical modalities employed for the
management of peptic esophageal stricture. The choice of dilator and technique is dependent
on many factors, the most important being stricture characteristics. It is also based on other
factors, including patient tolerance, operator preference, and experience. No clear consensus on
the optimal end point exists. In summary, dilation therapy should be tailored individually.
Endoscopic dilation dates to the 16th century, when physicians used wax wands for esophageal
dilation.[13, 14] The word bougie is derived from Boujiyah, an Algerian city that was the
center of the medieval candle trade. The following 3 types of dilators are used:
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o Many authors have questioned the need for mandatory fluoroscopy, and no
published data exist to advocate safety of fluoroscopy. However, one may consider
using fluoroscopy in complicated strictures, especially in guiding the blind
passage of a guidewire.
o Rule of 3s: The first bougie passed should be approximately equal to the
estimated diameter of the stricture. Pass no more than 3 consecutive bougies of
progressively increasing size after the first one that meets moderate resistance
during any one dilation session. The rule of 3s has been questioned because of a
lack of data verifying the increased efficacy or safety if one adheres to this rule.
This rule was formulated for dilation using mercury-filled bougies resulting in
dilation no greater than 1.3 mm in one session. However, polyvinyl dilators may
not provide adequate tactile perception to follow this rule.
o A study by Kozarek et al showed only one perforation in 400 patients dilated
with polyvinyl dilators to greater than 2 mm in one session.
o Balloon dilators frequently dilate greater than that prescribed by the rule of 3s
without any increased risk of complications.
No consensus exists regarding the end point of esophageal dilation for peptic strictures.
o Most patients experience complete relief when dilated to 40-54F. Therefore,
using this end point as a benchmark is recommended.
o In summary, the extent of the dilatation should be individualized based on
symptomatic response and technical difficulty encountered during therapy.
Intralesional steroid injection
o Limited anecdotal data exist showing that intralesional steroid injection of peptic
strictures may be beneficial. The mechanism is unclear; it may inhibit collagen
formation and enhance collagen degradation, thus increasing stricture compliance.
o Triamcinolone 10 mg/mL in 0.5 mL aliquots was injected in 4 quadrants in 2
patients with a successful outcome as reported by Kirsch et al.
o Lee at al showed a higher rate of achieving greater luminal diameters and
duration between dilations in a nonrandomized cohort of patients with strictures
of varying etiologies.[20] Similar results were obtained by Kochhar et al in 71
patients, although 8 injections of 20 mg of triamcinolone in 0.5-mL aliquots were
given at the proximal margin and into the stricture itself.
o A randomized prospective trial of Savary dilation with or without intralesional
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Esophageal plastic
By stomach
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By large intestine
By small intestine
ESOPHAGEAL CANCER
Esophageal cancer is cancer that occurs in the esophagus a long, hollow tube that
runs from your throat to your stomach. Your esophagus carries food you swallow to your
stomach to be digested.
Esophageal cancer usually begins in the cells that line the inside of the esophagus.
Esophageal cancer can occur anywhere along the esophagus, but in people in the United States,
it occurs most often in the lower portion of the esophagus. More men than women get
esophageal cancer.
Esophageal cancer isn't common in the United States. In other areas of the world, such
as Asia and parts of Africa, esophageal cancer is much more common.
Etiology
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It's not clear what causes esophageal cancer. Esophageal cancer occurs when cells in
your esophagus develop errors (mutations) in their DNA. The errors make cells grow and
divide out of control. The accumulating abnormal cells form a tumor in the esophagus that can
grow to invade nearby structures and spread to other parts of the body.
Esophageal cancer is classified according to the type of cells that are involved. The type
of esophageal cancer you have helps determine your treatment options. Types of esophageal
cancer include:
Adenocarcinoma. Adenocarcinoma begins in the cells of mucus-secreting glands in the
esophagus. Adenocarcinoma occurs most often in the lower portion of the esophagus.
Adenocarcinoma is the most common form of esophageal cancer in the United States,
and it affects primarily white men.
Squamous cell carcinoma. The squamous cells are flat, thin cells that line the surface of
the esophagus. Squamous cell carcinoma occurs most often in the middle of the
esophagus. Squamous cell carcinoma is the most prevalent esophageal cancer worldwide.
Other rare types. Rare forms of esophageal cancer include choriocarcinoma, lymphoma,
melanoma, sarcoma and small cell
Risk factors
It's thought that chronic irritation of your esophagus may contribute to the DNA changes
that cause esophageal cancer. Factors that cause irritation in the cells of your esophagus and
increase your risk of esophageal cancer include:
Drinking alcohol
Having bile reflux
Chewing tobacco
Having difficulty swallowing because of an esophageal sphincter that won't relax
(achalasia)
Drinking very hot liquids
Eating few fruits and vegetables
Eating foods preserved in lye, such as lutefisk, a Nordic recipe made from
whitefish, and some olive recipes
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Diagnostic
Using a scope to examine your esophagus (endoscopy). During endoscopy, your doctor
passes a hollow tube equipped with a lens (endoscope) down your throat and into your
esophagus. Using the endoscope, your doctor examines your esophagus looking for cancer or
areas of irritation.
X-rays of your esophagus. Sometimes called a barium swallow, an upper gastrointestinal
series or an esophagram, this series of X-rays is used to examine your esophagus. During the
test, you drink a thick liquid (barium) that temporarily coats the lining of your esophagus, so
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When you're diagnosed with esophageal cancer, your doctor works to determine the
extent (stage) of the cancer. Your cancer's stage helps determine your treatment options. Tests
used in staging esophageal cancer include computerized tomography (CT) and positron
emission tomography (PET).
The stages of esophageal cancer are:
Stage I. This cancer occurs only in the top layer of cells lining your esophagus.
Stage II. The cancer has invaded deeper layers of your esophagus lining and may have
spread to nearby lymph nodes.
Stage III. The cancer has spread to the deepest layers of the wall of your esophagus and
to nearby tissues or lymph nodes.
Stage IV. The cancer has spread to other parts of your body.
Surgery
Surgery to remove the cancer can be used alone or in combination with other treatments.
Operations used to treat esophageal cancer include:
Surgery to remove very small tumors. If your cancer is very small, confined to the
superficial layers of your esophagus and hasn't spread, your surgeon may recommend removing
the cancer and margin of healthy tissue that surrounds it. Surgery for very early-stage cancers
can be done using an endoscope passed down your throat and into your esophagus.
Surgery to remove a portion of the esophagus (esophagectomy). Your surgeon removes
the portion of your esophagus that contains the tumor and nearby lymph nodes. The remaining
esophagus is reconnected to your stomach. Usually this is done by pulling the stomach up to
meet the remaining esophagus. In some situations, a portion of the colon is used to replace the
missing section of esophagus.
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Surgery to remove part of your esophagus and the upper portion of your stomach
(esophagogastrectomy). Your surgeon removes part of your esophagus, nearby lymph nodes and
the upper part of your stomach. The remainder of your stomach is then pulled up and
reattached to your esophagus. If necessary, part of your colon is used to help join the two.
Esophageal cancer surgery carries a risk of serious complications, such as infection,
bleeding and leakage from the area where the remaining esophagus is reattached. Surgery to
remove your esophagus can be performed as an open procedure using large incisions or with
special surgical tools inserted through several small incisions in your skin (laparoscopically).
How your surgery is performed depends on your situation and your surgeon's experience and
preferences.
Besides treating the disease, surgery can help relieve symptoms or allow you to eat.
Relieving esophageal obstruction. A number of treatments are available to relieve
esophageal obstruction. One option includes using an endoscope and special tools to widen the
esophagus and place a metal tube (stent) to hold the esophagus open. Other options include
surgery, radiation therapy, chemotherapy, laser therapy and photodynamic therapy.
Providing nutrition. A surgeon inserts a feeding tube (percutaneous gastronomy) so you
can receive nutrition directly into your stomach or intestine. This is usually temporary until the
surgical site heals or until you're finished with chemotherapy and radiation therapy.
Chemotherapy
Chemotherapy is drug treatment that uses chemicals to kill cancer cells. Chemotherapy
drugs are typically used before (neoadjuvant) or after (adjuvant) surgery in people with
esophageal cancer. Chemotherapy can also be combined with radiation therapy. In people with
advanced cancer that has spread beyond the esophagus, chemotherapy may be used alone to
help relieve signs and symptoms caused by the cancer.
The chemotherapy side effects you experience depend on which chemotherapy drugs
you receive.
Radiation therapy
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Radiation therapy uses high-powered energy beams to kill cancer cells. Radiation can
come from a machine outside your body that aims the beams at your cancer (external beam
radiation). Or radiation can be placed inside your body near the cancer (brachytherapy).
Radiation therapy is most often combined with chemotherapy in people with esophageal
cancer. It can be used before or after surgery. Radiation therapy is also used to relieve
complications of advanced esophageal cancer, such as when a tumor grows large enough to
stop food from passing to your stomach.
Side effects of radiation to the esophagus include sunburn-like skin reactions, painful
or difficult swallowing, and accidental damage to nearby organs, such as the lungs and heart.
Combining chemotherapy and radiation therapy may enhance the effectiveness of each
treatment. Combined chemotherapy and radiation may be the only treatment you receive, or
combined therapy can be used before surgery. But combining chemotherapy and radiation
treatments increases the likelihood and severity of side effects.
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Lung abscess is defined as necrosis of the pulmonary tissue and formation of cavities
containing necrotic debris or fluid caused by microbial infection. The formation of multiple
small (< 2 cm) abscesses is occasionally referred to as necrotizing pneumonia or lung gangrene.
Both lung abscess and necrotizing pneumonia are manifestations of a similar pathologic
process. Failure to recognize and treat lung abscess is associated with poor clinical outcome.
Lung abscess was a devastating disease in the preantibiotic era, when one third of the
patients died, another one third recovered, and the remainder developed debilitating illnesses
such as recurrent abscesses, chronic empyema, bronchiectasis, or other consequences of
chronic pyogenic infections. In the early postantibiotic period, sulfonamides did not improve
the outcome of patients with lung abscess until the penicillins and tetracyclines were available.
Although resectional surgery was often considered a treatment option in the past, the role of
surgery has greatly diminished over time because most patients with uncomplicated lung
abscess eventually respond to prolonged antibiotic therapy.
Lung abscesses can be classified based on the duration and the likely etiology. Acute
abscesses are less than 4-6 weeks old, whereas chronic abscesses are of longer duration.
Primary abscess is infectious in origin, caused by aspiration or pneumonia in the healthy host;
secondary abscess is caused by a preexisting condition (eg, obstruction), spread from an
extrapulmonary site, bronchiectasis, and/or an immunocompromised state.
Most patients with primary lung abscess improve with antibiotics, with cure rates
documented at 90-95%
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Abscessing pneumonia is characterized by the multiple destructive foci 0,3-0,5 cm in size within 1-2
segments of lungs, which are not disposed to progression. The destruction is accompanied by expressed
perifocal infiltration of a pulmonary tissue.
Abscess of lungs - purulent or ichorous destruction of necrotic sites of pulmonary tissue of one segment with
formation of one or several cavities, filled by pus, and detached from adjacent parenchyma by a pyogenic
capsule and expressed perifocal infiltration of surrounding pulmonary tissue. It arises at the persons with a
maintained reactivity of the organism.
Gangrenous abscess is a purulent, ichorous necrosis of a pulmonary tissue within 2-3 segments, detached from
adjacent pulmonary parenchyma, with the liability to formation of sequesters. Depending on reactivity of the
organism it can transform into purulent abscess (after the lysis of sequesters) or gangrene.
Gangrene of lungs a diffuse purulent, ichorous necrosis of the tissue without the tendency to defined
demarcation with prompt dynamics of spreading of necrotic zone and destruction of the parenchyma. It is
characterized by a grave intoxication, liability to a pleural complications and pulmonary bleeding. If only the
one lobe is affected the gangrene is considered to be limited, if affected extensive areas of lungs the gangrene
is wide-spread.
Lung abscesses have numerous infectious causes. Anaerobic bacteria continue to be accountable for most
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cases. These bacteria predominate in the upper respiratory tract and are heavily concentrated in areas of
oral-gingival disease. Other bacteria involved in lung abscesses are gram-positive and gram-negative
organisms. However, lung cavities may not always be due to an underlying infection. Some evidence suggests
that individuals with cyanotic heart disorders may also be more prone to lung abscess formation. The
continuous hypoperfusion of the pulmonary tissues may predispose the individuals to chronic pulmonary
infections.
The embodiment of these factors occurs in condition of the changed reactivity of the organism.
The states which result in the aspiration of contents of the upper parts of alimentary tract (traumas of head,
craniovascular disturbances, alcoholism, narcomania, narcoses, epilepsy etc.) contribute to the pulmonary
abscessing. And also factors, which are capable to provoke secondary immunodeficiency and suppression of
reactive processes: diabetes mellitus, irradiation, long application of corticosteroids, antineoplastic therapy,
some hematological disease, AIDS favor the purulent processes.
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Esophageal disease
Achalasia
Reflux disease
Depressed cough and gag reflex
Esophageal obstruction
Bronchial obstruction
Tumor
Foreign body
Stricture
Generalized sepsis
Pathology
The abscesses mainly develop in and V segments of lungs. They may be single and multiple. The abscess is
confined from adjacent pulmonary tissue by a capsule, which represents a granulating tissue and dense
leukocytic rampart. Usually it is possible to find out a draining bronchus. Later on in the wall of the abscess
the amount of connective tissue fibers is enlarged.
In gangrene the pulmonary tissue is of black color, swollen, with cavities, and in some places transfers into
the sites with dark green coloring. The macropreparatus is characteristically fetid.
Classification
According to pathogenesis:
- postpneumonic;
- aspirative;
- obturative;
- posttraumatic;
- hematogenous or septic;
- lymphogenous;
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- thromboembolic.
- limited gangrene;
- wide-spread gangrene.
According to stages:
- acute;
- chronic.
Complications:
- pulmonary bleeding;
- pyopneumothorax;
- pleural empyema;
- sepsis;
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- bronchogenic dissemination.
The clinical manifestations of acute purulent destruction of lungs depend on the size of the focus and
character of destruction, reactivity of the organism and stage of the disease, peculiarities of the drainage of
purulent cavities and complications.
At the first stage of acute abscess the patients complain of general weakness, headache, malaise, suppressed
appetite, moderate chest pain, dyspnea, subfebrile temperature.
At the second stage the state of the patients is worsened. The fever rises to as high as 39-40 and has a
hectic character. At the same time the chest pain increases, which associates with a troubling cough and
dyspnea. The condition of the patients is worsened and the intoxication increases. One can feel a
foul-smelling from the mouth at cough. The amount of sputum is small, with a rusty tone. With the beginning
of the draining of destructive cavities through bronchus the daily quantity of the sputum reaches 500 ml and
more. At this time is possible hemoptysis. The sputum is foul-smelling. At sedimentation it divides into three
layers:
- inferior resembling a grey mass with detrites and flaps of a pulmonary tissue;
Further in favourable cases there is a considerable improvement of state of the patients. The body
temperature falls, the signs of intoxication reduce and the appetite increases.
The disease grades into the third stage, which is characterized by the regress of clinical manifestations, up to
their complete disappearance.
The physical signs good are well revealed at peripheral localization of the process. By palpation weakened
vocal fremitus. At percussion a blunted sound over the site of the purulent focus and perifocal infiltration
(at subpleural location of the abscess). By auscultation tubular sound with a moist rales in the zone of
purulent focus. Well-generated subpleural cavities of major sizes can be revealed by percussion by bandbox
sound, on auscultation by moist rales on the background of amphoric respiration.
At X-ray of the chest at the stage of necrotic pneumonia is found out a rounded lesion with irregular contour.
For the second stage is characteristic the enlightenment of the shadow with a further developing of the
rounded cavity with air-fluid level (Kordins symptom), gentle pyogenic sheath and the perifocal infiltration.
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At the third stage on the place of suppuration observed expressed fibrosis, sometimes as a thin-walled annular
formation.
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Gangrenous abscess is characterized by a grave state of the patient, expressed purulent intoxication, cough
with expectoration of a great amount (500 ml and more) of grey-green sputum with a foul-smelling, hectic
body temperature. Roentgenologically the inline of the cavity is poorly defined, it contains a visible
sequesters that look as a polymorphous shadow. The adjacent pulmonary tissue is infiltrated.
Gangrenous abscess
The clinic of a pulmonary gangrene differs by a terminal expression of signs. The state of the patients is
critical. The patient is adynamic, exhausted, with edemas on legs. Dyspnea in rest, hemodynamic disturbances
are evident. Dirty-grey or brown sputum with detrites, pieces of necrotic parenchyma and threads of blood
excretes out with the cough up to 1 l. Early pleural complications are usual and represent with pulmonary
bleeding, which may be profuse. Often it is associated with vital organ dysfunction and loss of consciousness.
The intensive shadow which borrows a considerable area of lungs with a visible cavities, that contain
sequesters, fluid levels, is roentgenologically revealed. The shadow outline is irregular, but could be well
defined if the process is within interlobar sulcus.
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Pulmonary gangrene
Roentgenologically chronic abscess is shown by one or several cavities of a spherical shape with a thick,
dense pyogenic sheath. Exacerbation of the process manifests by a cavity with horizontal air-fluid level. The
size of surrounding perifocal infiltration depends on the phase of process.
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The blood analysis in pulmonary destruction is characterized by leukocytosis with deviation of the differential
count to the left, lymphocytopenia, elevation of the erythrocyte sedimentation rate. Gangrenous change of the
process is accompanied by a progressing anemia, sometimes by leukopenia. The hypoproteinemia arises from
major losses of protein with purulent sputum. Intoxication and toxic lesion of liver leads to disproteinemia. It
is associated with the enlarged concentration of mucoprotein, sialine acids, seromucoid, and fibrinogen.
The immunogram reveals the suppression of cellular and humoral immunity with a liability to hyperergy and
autoaggression, depression of the mechanisms of nonspecific protection.
According to the clinical course, there are such variants of the development of purulent diseases of lungs:
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1. Favorable course. The adequate treatment results in prompt positive clinical, roentgenological and
laboratory dynamics, and terminates by recovery.
2. Non-progressive course. A poor drainage of the suppurative focus and permanent purulent intoxication
result in transferring of the process in chronic form.
3. Progressing course. Is predetermined by combination of a series of the unfavorable factors (low resistance
of the organism, autoimmune aggression, high virulence of the infecting agent etc.). Characterized by
diffusion of the zone of necrosis and destruction with transferring in gangrene.
4. Incapsulated process. Caused by the absence or complete obstruction of the draining bronchus under
condition of satisfactory resistance of the organism.
5. Complicated course. Mostly is the result of progressive development of the pathological process.
Pulmonary bleeding arise suddenly, are associated with coughing out of a foamy, red blood and clots by
portions or continuous stream. The most often source of a pulmonary bleeding are the bronchial arteries and
vessels of a pulmonary tissue. The clinical manifestations of a pulmonary suppuration are accompanied by
dizziness, weakness, dyspnea, chest pain. The hemodynamic disturbances depend on intensity of the bleeding.
The auscultation of lungs from both sides reveals the moist rales (aspiration). If the pulmonary destruction is
present the plain film of the chest shows the localization of the source of bleeding. After hospitalization of the
patient with this complication the exclusive information is obtained with a fibrobronchoscopy.
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1. Single hemoptysis.
2. Multiple hemoptysis.
1. Single bleeding:
2. Multiple bleeding:
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1. Massive bleeding.
The degree of a pulmonary bleeding manifests by coughing out the sputum tinged with blood, the
hemodynamic disturbance usually absent. At bleeding of degree are observed decreasing of arterial
pressure on 20-30 mm Hg, tachycardia to 100 beats/min, contents of hemoglobin within 60-80 g/l. The
bleeding of degree are accompanied with sharp decreasing of arterial pressure, rapid (more than 100-120
beats/min), small, sometimes thread pulse, and even its disappearance on peripheral arteries, tachypnea to 40
per 1 min, hemoglobin to 50-60 g/l. Probable the fulminant course up to the terminal state with prompt failure
of cardiac activity and asphyxia by blood.
Sepsis manifests by multisystem lesions with progression of the syndrome of polyorganous failure,
hematosepsis, purulent metastasizing (frequently in brain).
Characteristic complications for suppurative diseases of lungs such as pleural empyema and
pyopneumothorax are described in separate parts.
Generally, most of the patients admitted to the hospital with a diagnosis of lung abscess
have had symptoms for at least 2 weeks. These patients typically have an intermittent febrile
course, productive cough, weight loss, general malaise, and night sweats. Initially, foul sputum
is not observed in the course of the infection; however, after cavitation occurs, putrid
expectorations are quite prevalent. The odor of the breath and sputum of a patient with an
anaerobic lung abscess is often quite pronounced and noxious and may provide a clue to the
diagnosis. Hemoptysis may occasionally follow the expectoration of putrid sputum.
Symptoms depend on whether the abscess is caused by anaerobic or other bacterial
infection.
Anaerobic infection in lung abscess
o Patients often present with indolent symptoms that evolve over a period of
weeks to months.
o The usual symptoms are fever, cough with sputum production, night
sweats, anorexia, and weight loss.
o The expectorated sputum characteristically is foul smelling and bad
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tasting.
o Patients may develop hemoptysis or pleurisy
Other pathogens in lung abscess
o These patients generally present with conditions that are more emergent in
nature and are usually treated while they have bacterial pneumonia.
o Cavitation occurs subsequently as parenchymal necrosis ensues.
o Abscesses from fungi, Nocardia species, and Mycobacteria species tend to
have an indolent course and gradually progressive symptoms.
2. Physical findings.
The findings on physical examination of a patient with lung abscess are variable.
Physical findings may be secondary to associated conditions such as underlying pneumonia or
pleural effusion. The physical examination findings may also vary depending on the organisms
involved, the severity and extent of the disease, and the patient's health status and
comorbidities.
Patients with lung abscesses may have low-grade fever in anaerobic
infections and temperatures higher than 38.5C in other infections.
Generally, patients with in lung abscess have evidence of gingival disease.
Clinical findings of concomitant consolidation may be present (eg,
decreased breath sounds, dullness to percussion, bronchial breath sounds, course
inspiratory crackles).
The amphoric or cavernous breath sounds are only rarely elicited in
modern practice.
Evidence of pleural friction rub and signs of associated pleural effusion,
empyema, and pyopneumothorax may be present. Signs include dullness to percussion,
contralateral shift of the mediastinum, and absent breath sounds over the effusion.
Digital clubbing may develop rapidly.
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The wall thickness of a lung abscess progresses from thick to thin and
from ill-defined to well-circumscribed as the surrounding lung infection resolves. The
cavity wall can be smooth or ragged but is less commonly nodular, which raises the
possibility of cavitating carcinoma.
The extent of the air-fluid level within a lung abscess is often the same in
posteroanterior or lateral views. The abscess may extend to the pleural surface, in which
case it forms acute angles with the pleural surface.
Anaerobic infection may be suggested by cavitation within a dense
segmental consolidation in the dependent lung zones.
Lung infection with a virulent organism results in more widespread tissue
necrosis, which facilitates progression of underlying infection to pulmonary gangrene.
5. Tomogram of lungs.
6. Computed tomography
CT scanning of the lungs may help visualize the anatomy better than chest
radiography. CT scanning is very useful in the identification of concomitant empyema or
lung infarction.
On CT scans, an abscess often is a rounded radiolucent lesion with a thick
wall and ill-defined irregular margins.
The vessels and bronchi are not displaced by the lesion, as they are by an
empyema.
The lung abscess is located within the parenchyma compared with
loculated empyema, which may be difficult to distinguish on chest radiographs.
The lesion forms acute angles with the pleural surface chest wall.
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culture is requested.
Blood culture may be helpful in establishing the etiology.
Obtain sputum for ova and parasite whenever a parasitic cause for lung
abscess is suspected.
10. Immunogram.
11. Fibrobronchoscopy.
Differential diagnostics
Pneumonia
Primary bacterial pneumonias caused by single bacterial species other than the pneumococcus may account
for up to 25% of community-acquired and 80% of hospital-acquired pneumonias. All of these pneumonias
may have somewhat similar physical find- ings and x-ray evidence of pulmonary infiltration or consolidation.
For proper treatment, it is crucial to identify the causative agent by blood culture and by sputum examination
with stained smear and culture. Transtracheal aspiration, fiberoptic bronchoscopy, or even lung biopsy may be
needed for specific diagnosis and treatment.
Streptococcal Pneumonia
Pneumonia due to hemolytic streptococci occurs usually as a sequela to viral infection of the respiratory tract,
especially influenza or measles, or in persons with underlying pulmonary disease. The patients are usually in a
severely toxic condition and cyanotic. Pleural effusion develops frequently and early and progresses to
empyema in one-third of untreated pa- tients. The diagnosis rests on finding large numbers of streptococci in
smears of sputum and culturing hemolytic streptococci from blood and sputum.
The treatment of choice is with penicillin G in a dosage similar to that for pneumococcal pneumonia (see
above). If treatment is started early, the prognosis is good.
Pneumonia caused by Staphylococcus aureus occurs as a sequela to viral infections of the respiratory tract
(eg, influenza) and in debilitated (eg, postsurgical) patients or hospitalized infants, especially after
antimicrobial drug administration. There is often a history of a mild illness with headache, cough, and
generalized aches that abruptly changes to a very se- vere illness with high fever, chills, and exaggerated
cough with purulent or blood-streaked sputum and deep cyanosis. There may be early signs of pleural
effusion, empyema, or tension pneumothorax. X-ray examination reveals lung consolidation, pneumatoceles,
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abscesses, empyema, and pneumothorax. The demonstration of pyopneumothorax and of cavities with
air-fluid levels by x-ray is highly suggestive of Staphylococcal pneumonia. The diagnosis must be confirmed
by stained smear of sputum (masses of white cells and gram-positive cocci, many intra- cellular) and culture
(predominantly S aureus), and
also by means of cultures of pleural fluid and blood. The white count is usually more than 20,000//zL.
Initial therapy (based on sputum smear) consists of nafcillin, 6-12 g/d, or vancomycin, 2 g/d, given
intravenously in divided doses as a bolus. If the staphylococcus proves to be penicillin-sensitive by laboratory
test, penicillin G, 20-60 million units/d intravenously, is the antibiotic of choice. Drugs should be continued
for several weeks. If empyema develops, drainage must be established. The prognosis varies with the
underlying condition of the patient and the drug susceptibility of the organism.
Legionella Pneumonia
The eponym legionnaires' disease has been given to a serious pneumonia that afflicted people attending the
American Legion Convention in Philadelphia in 1976. Other outbreaks have been diagnosed ret- rospectively
at least since 1965, and sporadic infec- tions have occurred at least since 1947 in many places.
Legionella pneumophila is a poorly staining gram-negative bacterium that grows slowly on special media (eg,
charcoal-yeast extract) at 35 C. There are at least 8 species of Legionella, some with multiple serotypes.
These organisms can be recovered in human disease from sputum, bronchial washings, pleural fluid, lung
biopsies, or blood. Legionella species occur in the environment and are acquired by humans from aerosols,
dust from air-conditioning systems, water, or soil. The infection is not usually communi- cable from patient to
contacts. Asymptomatic infec- tion is common at all ages, whereas symptomatic infection is most often an
opportunistic pneumonia in immunocompromised individuals.
Asymptomatic infection is evident only by a rise in specific antibodies. Symptomatic infection is ob- served
mainly in elderly persons, smokers, and pa- tients undergoing hemodialysis or renal transplant.
The incubation period is estimated to be 2-10 days. Initial symptoms are malaise, diffuse myalgias, and
headache, followed in 12-48 hours by high, non- remittent fever and chills. Nausea, vomiting, and diarrhea
are frequent early in the illness. On the third day a dry cough begins that is nonproductive or produces scanty
mucoid, sometimes blood-streaked sputum. Dyspnea and hypoxia become marked as signs of consolidation
develop. Pleuritic chest pain occurs in one-third of patients. Severe confusion or delirium may occur.
There is leukocytosis with a shift to the left, hyponatremia, abnormal liver function tests, and, occasionally,
microscopic hematuria. Chest x-rays reveal patchy, often multilobar pulmonary con- solidation, and,
occasionally, small pleural effusions. The illness usually worsens for 4-7 days before im- provement begins in
those who recover. During severe outbreaks, the mortality rate has been 10% in those with manifest disease.
Death is attributed to respi- ratory or renal failure or shock, with disseminated intravascular coagulation.
The diagnosis is based on a clinical picture com- patible with the specific features of the disease and on
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negative results of bacteriologic laboratory tests for other pneumonias. The organism can be identified by
immunofluorescence in cultures, lung biopsy, and, rarely, sputum specimens. A retrospective diagnosis is
based on a significant rise in specific serum antibodies detected by immunofluorescence.
The treatment of choice is erythromycin, 0.5-1 g every 6 hours intravenously or orally for 2-3 weeks. This
usually results in improvement in 2-3 days. Rifampin, 10-20 mg/kg/d, has been suggested for patients who fail
to respond to erythromycin. Assisted ventilation and management of shock are essential.
This parasitic infection occurs in debilitated children or immunodeficient adults. It has been a prominent
opportunistic infection in AIDS patients. The diagnosis is made by lung biopsy and the demonstration of
typical cysts of P carinii in impression smears of lung tissue stained with methena- mine-silver. Early
treatment with sulfamethoxazole- trimethoprim can cure the pneumonia. The same drug has been effective in
prophylaxis during immunosuppression. An alternative, more toxic drug is pentamidine isethionate .
Essentials of Diagnosis
General Considerations
Mixed bacterial pneumonias include those in which culture and smear reveal several organisms, not one of
which can clearly be identified as the causative agent. These pneumonias usually appear as complica- tions of
anesthesia, surgery, aspiration, trauma, or various chronic illnesses (cardiac failure, advanced carcinoma,
uremia). They are common complications of chronic pulmonary diseases such as bronchiectasis and
emphysema. Old people are most commonly affected ("terminal" pneumonia). Patients treated with
intermittent positive pressure breathing apparatus or immunosuppressive drugs may develop pneumonia
caused by gram-negative rods.
The following findings in a debilitated, chroni- cally ill, or aged person suggest a complicating pneumonia: (1)
worsening of cough, dyspnea, cyanosis; (2) low-grade, irregular fever; (3) purulent sputum; and (4) patchy
basal densities on a chest film (in addition to previously noted densities caused by a primary underlying
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Clinical Findings
A. Symptoms and Signs: The onset is usually insidious, with low-grade fever, cough, expectoration, and
dyspnea that may become marked and lead to cyanosis. Physical findings are extremely variable and may not
be impressive against a background of cardiac or pulmonary disease. The signs listed under Other Bacterial
Pneumonias may also be present.
B. Laboratory Findings: The appearance of a greenish or yellowish (purulent) sputum should suggest a
complicating pneumonia. Smears and cul- tures reveal a mixed flora, often including anaerobes. Predominant
types should be noted. Leukocytosis is often absent in the aged and debilitated patient present- ing with a
mixed infection.
C. X-Ray Findings: X-ray (Picture 3) shows patchy, irregular infiltrations, most commonly posterior and basal
(in bedridden patients). Abscess formation may be observed. Careful interpretation will avoid confusion with
shadows due to preexisting heart or lung disease.
Differential Diagnosis
Mixed bacterial pneumonias must be differ- entiated from tuberculosis, carcinoma, and other spe- cific
mycotic, bacterial, and viral pulmonary infec- tions (to which they may be secondary).
Treatment
Clear the airway and correct hypoxia. Unless a probably significant etiologic agent can be identified, give one
of the new cephalosporins (eg, cefotaxime, 12 g/d intravenously) as initial therapy. This will be modified
according to clinical and laboratory results.
Prognosis
The prognosis depends upon the nature and sever- ity of the underlying pulmonary disease and varies with the
predominating organism.
ASPIRATION PNEUMONIA
Aspiration pneumonia is an especially severe type of pneumonia, often with a high mortality rate. It results
from the aspiration of gastric contents in addition to aspiration of upper respiratory flora in secretions.
Important predisposing factors include impairment of the swallowing mechanism (eg, esopha- geal disease),
inadequate cough reflex (eg, anesthesia, postoperative state, central nervous system disease, drug abuse), and
impaired gastric emptying (eg, pyloric obstruction). Pulmonary injury is due in large part to the low pH (< 2.5)
of gastric secretions.
Scattered areas of pulmonary edema and bron- chospasm occur, and the x-ray appearance (pictures 4-5) may
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be confused with that of pulmonary emboli, atelectasis, bronchopneumonia, and congestive heart failure.
Removal of aspirated material by catheter suction or bronchoscopy may be attempted, but this
usually fails to remove all aspirate completely. Corticosteroids (eg, prednisone, 100 mg orally
on the first or second day) may reduce the intensity of the inflammatory reaction to acidic
gastric secretion, but the value of corticosteroids in the treatment of aspiration pneumo- nia is
not proved, and they increase the risk of superinfection. Some aspiration pneumonias have no
bacterial component, but in many others a mixed bacterial flora is involved. Antimicrobial
drugs directed against the latter (eg, penicillin G plus an aminoglycoside or the best available
cephalosporin) are sometimes adminis- tered without waiting for evidence of progressive pul-
monary infection. In doing so, however, there is a risk of favoring the development of resistant
mi- croorganisms. Therefore, administration of antimi- crobials should not continue without
laboratory and clinical evidence of microbial infection. Assisted ventilation and supplementary
oxygen are beneficial.
The cancer of the central location due to the obturation of bronchus results in atelectasis of a segment or lobe
of lungs, with probable further abscessing. For the differentiation used tomography (reveals the obturation of
bronchus by tumour, lesion of central lymph nodes), cytological examination of sputum and bronchial
outwashes. The determinant role belongs to fibrobronchoscopy with a biopsy and verification of the
diagnosis.
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The peripheral cancer of lungs with destruction on tomograms is characterized by cavity with irregular inner
surface, which external outline connects with root of the lung because of lymphatic metastatic spreading. The
central lymph nodes frequently enlarged. The diagnosis is improved by results of transthoracic puncture or
catheterizing biopsy with cytological investigation, fibrobronchoscopy. If it is impossible to confirm the
diagnosis the thoracotomy is indicated.
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The tubercular cavern is mainly located in the upper lobes of lungs, roentgenologically revealed on the
background of characteristic changes in adjacent pulmonary tissue (calcification, dissemination), sometimes
detected a draining bronchus. In the sputum mycobacteria of tuberculosis are frequently found.
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The suppurative cyst of lungs differs by a gradual onset, slow course of the suppuration, less expressed
intoxication. Roentgenologically its cavity has the oval or rounded shape with a thin sheath and regular
contour. Perifocal infiltration is not characteristic.
With the purpose of maximal concentration of drugs in the pathological focus applied:
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- Introduction of medicinal agents into respiratory tracts (in the second stage) through the
endotracheal microirrigator, nasogastric tube, during bronchoscopies, endoscopic catheterization
of the abscess cavity through the draining bronchus, in aerosolic inhalations. The composition of
medical admixtures includes: antibiotics, antiseptics (10 % dimexid, dioxydin, microcid etc.),
enzymes;
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Skin wound
- Transcutaneous in the focus of destruction by means of puncture or draining with the usage of
physical antiseptics (US, UVR, laser).
- Intrapleural;
- By means of electrophoresis.
- Non-specific (pirimidine and purine derivates, drugs of a thymus gland, splenin, levamisol,).
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7. Correction of dysfunction of the vital organs and systems, prevention of complications, symptomatic
therapy.
Contraindications: decompensation of the vital functions and systems in the terminal stage, bilateral purulent
destruction of lungs, concomitant incurable malignant tumours.
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gram-negative and opportunistic organisms. These factors have increased the incidence of lung
abscess and the associated morbidity.
A great deal of caution is needed during anesthesia when patients with lung abscess
undergo surgery because spillage of the abscess material into the uninvolved lung can occur.
Therefore, a double-lumen endotracheal tube is used in all cases.
A study by Nagasawa et al has shown that thoracoscopic surgery can lead to effective
drainage of pediatric lung abscess without major complications. In addition, other benefits of
thoracoscopy include rapid recovery, less pain, and minimal morbidity.
Operational incisions anterolateral, lateral and posterolateral thoracotomy. The operation suggests
segmental, polysegmental resection, lobectomy, bilobectomy combined intervention (with the decortication,
pleurectomy).
Lateral access
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Anterior access
Posterior access
The patients with chronic abscesses should be undergone the operative treatment after complete liquidation of
exacerbation.
In a pulmonary gangrene the stabilization of the process on the background of active conservative treatment
allows in future to apply conservative tactics up to recovery or making optimal conditions for operation
(liquidation of intoxication, aggressive panbronchitis, diffuse infiltration of the parenchyma, pleural
complications). The headlong progression of the gangrene during first days, despite the active correction,
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occurrence of pulmonary bleeding requires urgent performance of operative management. Volume of the
operation pneumonectomy, bilobectomy, lobectomy.
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The pleural empyema is a purulent inflammation of its visceral and parietal membranes, which is associated
with accumulation of pus in a pleural space.
The causes of occurrence of acute pleural empyema are inflammatory, or purulent and destructive processes
of lungs, abscesses of abdominal cavity (secondary pleural empyema), open and closed damages of chest, and
also, in some cases, operative approaches on thoracic organs (primary pleural empyema).
A secondary pleural empyema occurs in 88 % of the patients. Thus develops fibrinous, exsudative, and then
purulent pleurisy.
In case of pulmonary gangrene, purulent mediastinitis, subphrenic abscess the stage of exsudative pleurisy
extremely short. The progression of the process results in transferring of focal pleural empyema into
wide-spread.
Pathology
Classification
1. Specific.
2. Nonspecific.
1. Primary.
2. Secondary.
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1. Acute.
2. Chronic.
1. Focal.
2. Wide-spread.
3. Pyopneumothorax.
bronchopleural fistula;
thoracopleural fistula;
thoracopleurobronchial fistula;
cribrate lung.
The clinic of an acute pleural empyema depends on extension of the process, reactivity of organism and
presence of complications.
The pain is the sign, which denote the involvement of pleural membranes in the process. Its intensity
increases depending on depth of respiration and body position.
The dyspnea arises from accumulation of a purulent content in a pleural space and exception of particular
volume of a pulmonary tissue from respiration. It's in direct ratio to amount of exudation in a pleural space.
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The cough is manifestation of inflammation or purulent and destructive process in a pulmonary tissue.
Fever to 39-40C, headache, sleeplessness, general malaise, and anorexia all these are manifestations of
intoxication.
The forced patient's position and restriction of breathing should be considered as outcomes of a pain
syndrome. The extension of pleural empyema causes the swelling of thoracic wall, smoothing of intercostal
spaces.
The data of percussion and auscultation depend on extension of the process and amount of pus in a pleural
space. At percussion over the exudate it is possible to reveal short sound with oblique upper contour. Above
the exudate tympanic sound resulting from consolidation of pulmonary tissue. By auscultation diminished
or absent sound in a great amount of exudate.
The predominant roentgenological sign of a focal or wide-spread empyema the presence of exudate. In
localized acute pleural empyema observed a local intensive homogeneous shadow. Roentgenologically
according to localization distinguished such types of a focal empyema:
1) apical;
2) paramediastinal;
3) parietal;
4) interlobar;
5) epiphrenic.
The wide-spread pleural empyema manifests by intensive homogeneous shadow in a basal parts with oblique
upper contour (Damuaso' line). The diaphragmatic dome is failed to observe. The more pus contents in a
pleural space, the higher the upper measure of exudate.
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Pleural empyema
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Pleural empyema
Pleural empyema
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Pleural empyema
The clinic of a focal pleural empyema depends on the site of the process. The apical empyema, due to
involvement in the process of a vascular-nervous fascicle, manifests by intensive pain. The soft tissues of
supraclavicular region are swelled. The percussion and auscultation has no information.
The pain syndrome in parietal (paracostal) empyema is more expressed. Thoracic excursion is restricted. The
diminishing of respiratory sound can be obtained over the exudate.
The chief complaint in paramediastinal empyema is the heart pain. The location of the process in the upper
mediastinum can cause the superior vena cava syndrome. The physical findings are vague.
In case of the basal (epiphrenic) empyema the patients complain of pain in subcostal area, which increases at
respiration and irradiates in supraclavicular region. In some cases the pain irradiates in epigastric region. The
palpation of intercostal spaces and hypochondrium is painful.
The clinical course of postoperative empyema depends on the character of operative approach (marginal
resection of lung, lobectomy, pneumonectomy, operation on esophagus) and infection of the pleural space.
The clinical manifestations of posttraumatic empyema depend on the size of damage of the chest, lungs,
mediastinal organs and complications (suppuration, hemothorax).
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The involvement in the purulent process of a pulmonary tissue in acute empyema results in its fusion of
membranes with formation of a bronchial or thoracopleural fistula (discharge of abscess through thoracic
wall).
The inappropriate elimination of empyema results in chronic course, cribrate lung and pleurogenic cirrhosis of
lungs.
2. Physical findings.
4. Pleural puncture.
Pleural puncture:
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Local anesthesia
Thoracentesis
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Differential diagnostics
Pleuropneumonia complicated with exsudative pleurisy, in some cases resembles acute pleural empyema: a
chest pain, fever, dyspnea, cough, and general weakness. The chest roentgenogram reveals hydrothorax
(exsudative pleurisy, pleural empyema, hemothorax). The chief diagnostic method for differentiation is the
thoracentesis. The presence of a serous (lucent, faint-yellow) exudate testifies about the pleuropneumonia,
complicated with pleural effusion, and cloudy, foul-smelling exudate of white or greenish color about acute
empyema.
The major difficulties in differential diagnostics cause the limited forms of empyema.
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The Pancoast cancer clinically and roentgenologically in most cases has almost the similar course to apical
form of empyema. The transthoracic biopsy permits to confirm the diagnosis.
The acute cholecystitis is necessary to differentiate with the epiphrenic empyema. The pain in the right
hypochondrium, fever, phrenic symptom are common for both diseases. However the objective findings,
X-radiography of chest and the thoracentesis allow to differentiate these pathological processes.
The tumour of anterior mediastinum complicated by superior vena cava syndrome is necessary to
differentiate with paramediastinal empyema. Nevertheless the body temperature in such patients, as a rule,
normal. The upper cavography is possible to find out the shift of cava vein and its irregular contours (filling
defect) due to growth of the mediastinal tumour.
There are some difficulties in differential diagnostics of empyema with a posttraumatic diaphragmatic hernia.
Such X-ray findings as deformation of diaphragm, additional shadows with a liquid level, intestinal loop
suggest a diaphragmatic hernia. A laterography and contrast study of gastrointestinal tract is basic in
differential diagnostics of this disease.
The atelectasis of a segment, and lobe of lung in some cases can cause misdiagnostics. Except X-ray chest
examination (in two planes and tomography), these situations require necessity of diagnostic bronchoscopy,
which reveals the cause of bronchial obturation (foreign body, endobronchial cancer etc.).
The presence of pus in a pleural space is the indication for its elimination. In the place of performed
diagnostic thoracentesis carried out the draining of empyema's cavity, its sanation by means of antiseptic
solutions. In a focal empyema the aspiration of pus is performed by thoracentesis and only in its inefficiency
carried out a draining of pleural space.
Pleural drainage:
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Trocar insertion
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Active aspiration
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Intensive antibacterial and antiinflammatory therapy should be immediately instituted. For general improving
used detoxication therapy (infusion of saline solutions, hemotransfusion, transfusion of proteins, solutions of
dextran, haemodes, forced diuresis, hemosorption if necessary), therapy for rising up of immunological
resistance of the organism.
During the empyema's sanation decreases the amount of pus which discharges out through the drainage. The
optimal variant of such course is the liquidation of empyema's cavity, then the drainage must be removed.
Transferring of the process into the chronic form (10-12 weeks) results in formation of a residual empyema's
cavity, which is possible is to reveal by means of pleurography introduction through the drainage of water-
soluble contrast with the further X-radiography in 2 planes.
Operative approach is applied when the process has transferred into the chronic form, that is in case of
residual empyema's cavity. Volume of the operation pleurectomy, decortication of lung.
In some cases, when a bronchial fistula and great empyema's cavity has been formed, there is the necessity of
performance of resection of lung and corrective thoracoplasty.
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The cysts of lungs are the thin-walled cavitary formations, filled with air or liquid contents.
Inherent cysts arise from the abnormalities of the development of lungs under influence of the multiple
chemical, physical, biological factors. Whether they can develop from a bronchial tree (bronchial) of from
alveolar tissue (alveolar). Their occurrence resulting from the delay of the development of peripheral parts of
bronchus with their expansion or agenesia of alveoli with dilatation of terminal bronchioles. Congenital cysts
at first develop and grow as secretory formations. After communication with bronchus they finally form as air
or hydroair cavities.
The acquired cysts represent fibrous cavities, which remain after abscesses, tubercular caverns, echinococci,
posttraumatic intrapulmonary hematomas. The degenerative changes in the wall of bronchus with obliteration
of its lumen by a cloggy secret owing to repeated inflammatory processes result in occurrence of acquired
retentional cysts.
Pathology
Congenital cyst can be located in any part of lungs. The walls of bronchogenic cavities contain chaotically
disposed elements of bronchus (cartilagous plates, muscle fibers, mucous glands), they are lined from inside
by cylindrical or cubic epithelium. Squeezed alveolar cells line the walls of alveolar formations.
The acquired cyst are revealed in places of localization of previous diseases,. Their walls mainly consist of
connective tissue. Epithelization is possible due to transferring of the epithelium from a draining bronchus at
long existence.
The cysts could be uni- or multichamber, closed and open (depending on the presence of communication with
bronchus).
Classification
According to parentage:
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- congenital;
- acquired.
According to displacement:
- single, multiple;
- unilateral, bilateral.
Complications:
- Suppuration;
- Bleeding;
- Malignancy.
Clinical manifestations of uncomplicated pulmonary cysts are vague. Sometimes patients complain of a chest
pain, periodic cough, and inflammatory diseases of respiratory tract in history. In children the signs are much
expressed, the dyspnea associates with the compression of airways.
In great, superficially disposed cysts revealed delayed respiratory movements on affected side during
breathing.
At routine chest films the closed congenital cyst forms a homogeneous shadow of the spherical or oval shape
of average intensity with rather regular edge on the background of an intact pulmonary tissue. During
roentgenoscopy sometimes observed the change of its shape depending on the phase of breathing elongation
in inspiration (Escudero's syndrome). The character of the shadow is better to study on tomograms.
Acquired retentional cyst is roentgenologically shown by a shadow of irregular shape (piriform, spindle-
shaped etc.), that displays the shape of the distended bronchus. The adjacent tissue, as a rule, changed due to
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Open cysts are observed as thin-walled, good defined cavities of annular or oval shape.
On bronchograms congenital cysts are observed hypoplasia of segmental or lobar bronchus, lack of bronchial
bifurcations, which tends to bone. Sometimes observed bronchiectases in the neighboring parts of lungs. A
cystic cavity is infrequently defined.
The angiopulmonography reveals deformation of vascular branches, which circumflex the cyst.
The suppuration of the closed cysts resembles the development of a lung abscess with lesser expression of
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Infection of the open cysts is characterized by a gradual long course, moderate manifestation of suppuration
and late intoxication.
The tension (valvular) cysts arise more often in children. They are characterized by severe respiratory and
hemodynamic disturbances, up to terminal, owing to inflexion of venous trunks, shift of mediastinum and
compression of lungs. The predominant signs are increased dyspnea, cyanosis, chest pain, respiratory lag on
affected side, auscultatory absence or weakening of respiration, bandbox percussion sound over the cavity
at mediastinal shift to the opposite side of the chest.
Pleural complications of pulmonary cysts, and also bleeding described in the relevant parts.
4. Lung tomography.
5. Bronchography.
6. Angiopulmonography.
Differential diagnostics
The abscess of lungs, in contrast with a suppurative cyst, is characterized by prompt course, expressed
purulent intoxication, roentgenologically its wall is irregular, with proper considerable perifocal infiltration.
The cancer with destruction differs by a thick wall with a tuberous inner surface, phenomena of lymphangitis
in adjacent tissue. The determinant value has endoscopic examination or puncture with a biopsy and
following morphological investigation.
The tubercular cavern displaced in the upper lobes, in adjacent tissue revealed fibrosis, petrifactions,
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Opposite to cyst, in termed diseases, the circumflex deformation of vascular branches never observed at
angiopulmonography.
The considerable difficulties can arise at differentiation of the closed congenital cysts.
The tuberculoma differs from them by characteristic localization. At X-ray examination the heterogeneity of
the shadow with calcifications, early excentric destruction, "tubercular" background is observed.
The benign tumours sometimes possible to differentiate only after the results of cytological investigation of
punctate or after operation.
The echinococci cysts on tomogram can have a double contour of chitinous and fibrous sheaths. In blood
analyses observed eosinophilia. The final decision is taken out after carrying out immunological (indirect
microagglutination test) allergic (Cacconi's reaction) tests.
Huge cysts, in contrast with open air cysts, are characterized by a subpleural location.
The diagnostic doubts at suspicion on a diaphragmatic hernia are solved by radiopaque examination of a
gastrointestinal tract.
The acquired cysts differ from congenital by roentgenological signs of the lesion of surrounding tissues
(pneumofibrosis, deforming bronchitis, secondary bronchiectases, and calcifications). Postpneumonic cavities
are of irregular shape, with grooves and pockets, their walls different thick. During bronchography they filled
through some small bronchi. Sometimes the verification is possible only after postoperative morphological
investigation.
The pulmonary cysts require the surgical treatment. In case of complications the indication for operation
becomes absolute. Contraindications: the severe respiratory disturbance, concomitant malignant
nonresectable tumors, vital organs dysfunction in the stage of permanent decompensation, elderly age of the
patients.
The volume of the operation: if the adjacent pulmonary tissue is intact cystectomy, otherwise segmental or
wedged resection, lobectomy.
The conservative therapy is applied in suppuration of cysts with the purpose of preoperative preparation. It is
the similar, which applied for abscesses of lungs.
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SPONTANEOUS PNEUMOTHORAX
Spontaneous pneumothorax is the entry of air in a pleural space with the further lung collapse, which not
associated with traumatic damage of chest or pulmonary tissue.
As a result of spontaneous disrupture of lung blebs and subpleural air cysts occurs the damage of pleural
visceral membrane. It causes entry of air in pleural space. Owing to its leakage the elastic pulmonary tissue
collapses. The degree of the collapse of lung depends on amount of air, that has penetrated a pleural space.
Pathology
Morphologically in spontaneous pneumothorax found out a focal bullous emphysema with disrupture of blebs,
subpleural air cyst, and also disorders, which have caused disturbances of ventilating ability of bronchi. It can
be bronchitis, pneumosclerosis, tuberculosis and fibrous alveolitis.
Classification
1. Unilateral or bilateral.
5. Tension or valvular (complete collapse of lungs and shift of mediastinum in the opposite side).
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The onset of the disease is sudden. A state of the patient and expression of clinical manifestations depends on
amount of air, which has entered the pleural space. Usually in normal conditions, and sometimes after
physical activity, the patients suddenly feel acute pain on the side of lesion, dyspnea, pain in the heart region
and heartbeating. An available also Acrocyanosis or total cyanosis of skin is observed. The circulatory
disturbance depends on degree of hypoxia. Intensity of pain and dyspnea gradually decrease, but a dry
troublesome cough appears.
Examination of the chest allows to observe expansion of intercostal spaces and restriction of respiratory
excursion. By palpation - diminishing of vocal fremitus on the affected side. At percussion a chief sign of
pneumothorax is the tympanic sound. Auscultation reveals weakened or sharply weakened breathing sounds.
The cardiac tones are muffled, tachycardia.
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Thoracoscopy in pneumothorax possible to find out subpleural blebs of different sizes (0,5-3 cm), which are
mainly disposed on the apex of lung.
The atypical (asymptomatic) spontaneous pneumothorax occurs in 20 % of the patients, and mainly revealed
at X-ray examination. In most cases it is the partial pneumothorax.
The expressed pain syndrome and dyspnea, which resulting from collapse of lung, characterize subtotal and
total pneumothorax.
The tension spontaneous pneumothorax is the most severe form of pneumothorax. It manifests by sudden
onset, progressive increase of dyspnea, expressed cyanosis. The breathing is superficial, rapid, with active
participation of auxiliary muscles. Mediastinal shift and flexion of vessels result in disturbance of cardiac
activity up to the cardiac arrest, and requires urgent management.
Rigid pneumothorax (rigid lung). The neglected pneumothorax causes fibrinous exsudative pleurisy. On the
surface of lung (visceral pleura) commissures are formed, that give no opportunity for lung expansion. The
presence of residual pleural cavity and progressive development of a purulent infection result in occurrence
of acute pleural empyema. In such cases the patients complain of the fever up to 38-38,5C, general
weakness and increasing of dyspnea. The phenomena of intoxication increase. Thus such patients require the
treatment of pleural empyema.
2. Physical findings.
4. Thoracentesis
5. Thoracoscopy.
6. Tomography of lungs.
Differential diagnostics
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Pleural effusion. This pathology manifests by more gradual onset. As opposite to pneumothorax, the
complaints of chest pain predominate above the complaints of dyspnea. Frequently such patients specify on
transferred undercooling.
As well as the spontaneous pneumothorax, the pleural effusion is characterized by diminishing of vocal
fremitus, dullness of percussion sound, weakened of absent breathing sounds over the exudate. Nevertheless
in the routine roentgenogram in such cases observed a homogeneous intensive shadow of a pleural space with
oblique upper contour. The puncture of pleural space enables finally to confirm the diagnosis of pleural
effusion.
Intercostal neuralgia. A predominant sign in clinical pattern is acute pain, which intensifies at physical
activity, changes of body position and body movements, at deep breathing. The localization of pain coincides
with zone of innervation of intercostal nerves.
Conservative treatment is applied in the patients with a partial pneumothorax. Thus thoracentesis in
intercostal space in the midclavicular line with aspiration of air is performed. The cases of its inefficiency, and
also subtotal, total and tension pneumothorax require drainage of a pleural space with active aspiration of air.
The operative management is necessary, if there is no efficiency from active aspiration (in incomplete
expansion of lung), recurrent of course of the process, presence of great subpleural blebs and rigid
pneumothorax. Volume of operation depends on extension of the process: liquidation of alveolar fistula,
wedged resection of lung or lobectomy.
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PYOPNEUMOTHORAX
Pyopneumothorax is the discharge of lung abscess of into pleural space, which is accompanied by purulent
inflammation of pleural membranes with a collapse of lung.
Peripheral placement of the purulent focus in a pulmonary tissue results in destruction (fusion) of visceral
membrane. As a result of, the pus and air penetrate into a pleural space that leads to a purulent inflammation
of parietal and visceral membranes of pleura. The disorder of hermeticity of a pleural space results in a lung
collapse.
Among other causes of pyopneumothorax are the chest trauma, which results in collapse of lung, infection
and purulent inflammation of pleural membranes.
- gangrene of lung;
- abscessing pneumonia;
- bronchiectatic disease;
- damage of esophagus;
- mediastinitis;
- chest trauma;
Pathology
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Morphologically in pyopneumothorax pus and air are present in pleural space. In the lungs subpleural
disposed purulent or necrotic foci, which connected with a pleural space through a pleuro-pulmonary fistula.
From the outside the zone of disrupture is confined by perifocal inflammation. In the draining bronchus it is
possible to see manifestations of deforming, frequently polypous bronchitis.
Classification
1. Specific.
2. Nonspecific.
1. Primary.
2. Secondary.
1. Asymptomatic form.
2. Mild form.
3. Acute form.
1. Localized pyopneumothorax:
a) parietal;
b) apical;
c) epiphrenic;
d) paramediastinal;
e) polychamber.
2. Subtotal pyopneumothorax.
3. Total pyopneumothorax.
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4. Tension pyopneumothorax.
The clinic of pyopneumothorax depends on the size of the focus of destruction, which influences on degree of
lung collapse, and on amount of purulent content in a pleural space.
The pain owing to discharge of the focus of destruction into pleural space often arises suddenly.
The dyspnea occurs as a result of collapse of lung owing to leakage of pus and air into pleural space. Its
expression is in direct ratio to lung collapse. Therefore a dyspnea in rest observed in a subtotal and total
pyopneumothorax. It sharply amplifies even at minor physical activity. Auxiliary muscles take part in order to
force respiration.
The expectoration of sputum with ichorous smell is the outcome of destructive process in a pulmonary tissue.
Its amount decreases after discharge of pus into pleural space.
Hectic fever with caused by enlargement of the area of resorption. The patients are adynamic, flaccid. Some
of them are unconsciousness.
By objective examination the position of patients is forced, they sit in bed leaning upon the bed (subtotal,
total pyopneumothorax). The affected hemithorax takes no part in respiration.
Percussion reveals a sharp shortening of sound over the zone of exudate and bandbox sound above the region
of collapsed lung.
By auscultation there are no breathing sounds on the affected side. In case of localized pyopneumothorax
weakened or sharply weakened sound with a bronchial or amphoric tone.
The X-ray picture of pyopneumothorax depends on its form, but the obligatory sign is the air-fluid level in a
pleural space with well-defined edge of collapsed lung on its background.
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Pyopneumothorax
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Pyopneumothorax
The clinical course of pyopneumothorax depends on adhesions between pleural membranes. It sometimes
changes typical clinical course of a total lung collapse. The clinic of disease depends also on amount of a
purulent exudate. Therefore according to extension of the process and size of destruction of lung
distinguished acute, mild and asymptomatic forms of pyopneumothorax. Especially difficult for diagnostics is
the asymptomatic form of localized pyopneumothorax. Dyspnea for such pathology not characteristic, as the
adhesion of membranes prevents complete collapse of lung. Dyspnea is vague or absent at all in partial
collapse. A diminished vocal fremitus on side of pathological process, shortening of percussion sound and
weakened or sharply weakened breathing sounds over the collapsed lung and exudate are revealed.
Roentgenological manifestations in localized pyopneumothorax not expressed and include horizontal fluid
level, margin of partially collapsed lung and minor air in the pleural space.
In most cases after discharge of the destructive focus in a pleural space and collapse of lung observed the
closure of bronchopleural fistula. Nevertheless the inflammatory process in a pulmonary tissue and pleural
space is going on.
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2. Physical findings.
4. Thoracentesis.
5. Pleurography.
Differential diagnostics
They're no special necessity for differential diagnostics of pyopneumothorax in the majority of patients.
History (presence of the purulent focus in a pulmonary tissue), clinical course (acute pain and dyspnea at
abscess discharge into pleural space), and also chest X-ray findings and thoracentesis frequently reliably
permit to make the diagnosis.
In some cases a localized pyopneumothorax according to clinical course resembles a huge acute abscess of
lungs. But the differences of roentgenological symptomatology permit to verify these pathological processes.
In acute lung abscess the cavity of destruction localized in a pulmonary parenchyma, it is of rounded form
with horizontal fluid level and expressed perifocal infiltration.
The purpose of treatment should include sanation of the destructive focus in pulmonary tissue and liquidation
of complications; that means elimination of pus and air from a pleural space and prompt expanding of lung.
2. Draining of pleural space, active aspiration of its content (air, pus) to expand the lungs.
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5. The therapy for rising up of immunological resistance of the organism (staphylococcal anatoxin according
to scheme, antistaphylococcal gamma-globulin, antistaphylococcal plasma).
The indications for operative management are the same, as in pleural empyema.
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Lung abscess is defined as necrosis of the pulmonary tissue and formation of cavities
containing necrotic debris or fluid caused by microbial infection. The formation of multiple
small (< 2 cm) abscesses is occasionally referred to as necrotizing pneumonia or lung gangrene.
Both lung abscess and necrotizing pneumonia are manifestations of a similar pathologic
process. Failure to recognize and treat lung abscess is associated with poor clinical outcome.
Lung abscess was a devastating disease in the preantibiotic era, when one third of the
patients died, another one third recovered, and the remainder developed debilitating illnesses
such as recurrent abscesses, chronic empyema, bronchiectasis, or other consequences of
chronic pyogenic infections. In the early postantibiotic period, sulfonamides did not improve
the outcome of patients with lung abscess until the penicillins and tetracyclines were available.
Although resectional surgery was often considered a treatment option in the past, the role of
surgery has greatly diminished over time because most patients with uncomplicated lung
abscess eventually respond to prolonged antibiotic therapy.
Lung abscesses can be classified based on the duration and the likely etiology. Acute
abscesses are less than 4-6 weeks old, whereas chronic abscesses are of longer duration.
Primary abscess is infectious in origin, caused by aspiration or pneumonia in the healthy host;
secondary abscess is caused by a preexisting condition (eg, obstruction), spread from an
extrapulmonary site, bronchiectasis, and/or an immunocompromised state.
Most patients with primary lung abscess improve with antibiotics, with cure rates
documented at 90-95%
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Abscessing pneumonia is characterized by the multiple destructive foci 0,3-0,5 cm in size within 1-2
segments of lungs, which are not disposed to progression. The destruction is accompanied by expressed
perifocal infiltration of a pulmonary tissue.
Abscess of lungs - purulent or ichorous destruction of necrotic sites of pulmonary tissue of one segment with
formation of one or several cavities, filled by pus, and detached from adjacent parenchyma by a pyogenic
capsule and expressed perifocal infiltration of surrounding pulmonary tissue. It arises at the persons with a
maintained reactivity of the organism.
Gangrenous abscess is a purulent, ichorous necrosis of a pulmonary tissue within 2-3 segments, detached from
adjacent pulmonary parenchyma, with the liability to formation of sequesters. Depending on reactivity of the
organism it can transform into purulent abscess (after the lysis of sequesters) or gangrene.
Gangrene of lungs a diffuse purulent, ichorous necrosis of the tissue without the tendency to defined
demarcation with prompt dynamics of spreading of necrotic zone and destruction of the parenchyma. It is
characterized by a grave intoxication, liability to a pleural complications and pulmonary bleeding. If only the
one lobe is affected the gangrene is considered to be limited, if affected extensive areas of lungs the gangrene
is wide-spread.
Lung abscesses have numerous infectious causes. Anaerobic bacteria continue to be accountable for most
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cases. These bacteria predominate in the upper respiratory tract and are heavily concentrated in areas of
oral-gingival disease. Other bacteria involved in lung abscesses are gram-positive and gram-negative
organisms. However, lung cavities may not always be due to an underlying infection. Some evidence suggests
that individuals with cyanotic heart disorders may also be more prone to lung abscess formation. The
continuous hypoperfusion of the pulmonary tissues may predispose the individuals to chronic pulmonary
infections.
The embodiment of these factors occurs in condition of the changed reactivity of the organism.
The states which result in the aspiration of contents of the upper parts of alimentary tract (traumas of head,
craniovascular disturbances, alcoholism, narcomania, narcoses, epilepsy etc.) contribute to the pulmonary
abscessing. And also factors, which are capable to provoke secondary immunodeficiency and suppression of
reactive processes: diabetes mellitus, irradiation, long application of corticosteroids, antineoplastic therapy,
some hematological disease, AIDS favor the purulent processes.
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Esophageal disease
Achalasia
Reflux disease
Depressed cough and gag reflex
Esophageal obstruction
Bronchial obstruction
Tumor
Foreign body
Stricture
Generalized sepsis
Pathology
The abscesses mainly develop in and V segments of lungs. They may be single and multiple. The abscess is
confined from adjacent pulmonary tissue by a capsule, which represents a granulating tissue and dense
leukocytic rampart. Usually it is possible to find out a draining bronchus. Later on in the wall of the abscess
the amount of connective tissue fibers is enlarged.
In gangrene the pulmonary tissue is of black color, swollen, with cavities, and in some places transfers into
the sites with dark green coloring. The macropreparatus is characteristically fetid.
Classification
According to pathogenesis:
- postpneumonic;
- aspirative;
- obturative;
- posttraumatic;
- hematogenous or septic;
- lymphogenous;
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- thromboembolic.
- limited gangrene;
- wide-spread gangrene.
According to stages:
- acute;
- chronic.
Complications:
- pulmonary bleeding;
- pyopneumothorax;
- pleural empyema;
- sepsis;
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- bronchogenic dissemination.
The clinical manifestations of acute purulent destruction of lungs depend on the size of the focus and
character of destruction, reactivity of the organism and stage of the disease, peculiarities of the drainage of
purulent cavities and complications.
At the first stage of acute abscess the patients complain of general weakness, headache, malaise, suppressed
appetite, moderate chest pain, dyspnea, subfebrile temperature.
At the second stage the state of the patients is worsened. The fever rises to as high as 39-40 and has a
hectic character. At the same time the chest pain increases, which associates with a troubling cough and
dyspnea. The condition of the patients is worsened and the intoxication increases. One can feel a
foul-smelling from the mouth at cough. The amount of sputum is small, with a rusty tone. With the beginning
of the draining of destructive cavities through bronchus the daily quantity of the sputum reaches 500 ml and
more. At this time is possible hemoptysis. The sputum is foul-smelling. At sedimentation it divides into three
layers:
- inferior resembling a grey mass with detrites and flaps of a pulmonary tissue;
Further in favourable cases there is a considerable improvement of state of the patients. The body
temperature falls, the signs of intoxication reduce and the appetite increases.
The disease grades into the third stage, which is characterized by the regress of clinical manifestations, up to
their complete disappearance.
The physical signs good are well revealed at peripheral localization of the process. By palpation weakened
vocal fremitus. At percussion a blunted sound over the site of the purulent focus and perifocal infiltration
(at subpleural location of the abscess). By auscultation tubular sound with a moist rales in the zone of
purulent focus. Well-generated subpleural cavities of major sizes can be revealed by percussion by bandbox
sound, on auscultation by moist rales on the background of amphoric respiration.
At X-ray of the chest at the stage of necrotic pneumonia is found out a rounded lesion with irregular contour.
For the second stage is characteristic the enlightenment of the shadow with a further developing of the
rounded cavity with air-fluid level (Kordins symptom), gentle pyogenic sheath and the perifocal infiltration.
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At the third stage on the place of suppuration observed expressed fibrosis, sometimes as a thin-walled annular
formation.
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Gangrenous abscess is characterized by a grave state of the patient, expressed purulent intoxication, cough
with expectoration of a great amount (500 ml and more) of grey-green sputum with a foul-smelling, hectic
body temperature. Roentgenologically the inline of the cavity is poorly defined, it contains a visible
sequesters that look as a polymorphous shadow. The adjacent pulmonary tissue is infiltrated.
Gangrenous abscess
The clinic of a pulmonary gangrene differs by a terminal expression of signs. The state of the patients is
critical. The patient is adynamic, exhausted, with edemas on legs. Dyspnea in rest, hemodynamic disturbances
are evident. Dirty-grey or brown sputum with detrites, pieces of necrotic parenchyma and threads of blood
excretes out with the cough up to 1 l. Early pleural complications are usual and represent with pulmonary
bleeding, which may be profuse. Often it is associated with vital organ dysfunction and loss of consciousness.
The intensive shadow which borrows a considerable area of lungs with a visible cavities, that contain
sequesters, fluid levels, is roentgenologically revealed. The shadow outline is irregular, but could be well
defined if the process is within interlobar sulcus.
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Pulmonary gangrene
Roentgenologically chronic abscess is shown by one or several cavities of a spherical shape with a thick,
dense pyogenic sheath. Exacerbation of the process manifests by a cavity with horizontal air-fluid level. The
size of surrounding perifocal infiltration depends on the phase of process.
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The blood analysis in pulmonary destruction is characterized by leukocytosis with deviation of the differential
count to the left, lymphocytopenia, elevation of the erythrocyte sedimentation rate. Gangrenous change of the
process is accompanied by a progressing anemia, sometimes by leukopenia. The hypoproteinemia arises from
major losses of protein with purulent sputum. Intoxication and toxic lesion of liver leads to disproteinemia. It
is associated with the enlarged concentration of mucoprotein, sialine acids, seromucoid, and fibrinogen.
The immunogram reveals the suppression of cellular and humoral immunity with a liability to hyperergy and
autoaggression, depression of the mechanisms of nonspecific protection.
According to the clinical course, there are such variants of the development of purulent diseases of lungs:
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1. Favorable course. The adequate treatment results in prompt positive clinical, roentgenological and
laboratory dynamics, and terminates by recovery.
2. Non-progressive course. A poor drainage of the suppurative focus and permanent purulent intoxication
result in transferring of the process in chronic form.
3. Progressing course. Is predetermined by combination of a series of the unfavorable factors (low resistance
of the organism, autoimmune aggression, high virulence of the infecting agent etc.). Characterized by
diffusion of the zone of necrosis and destruction with transferring in gangrene.
4. Incapsulated process. Caused by the absence or complete obstruction of the draining bronchus under
condition of satisfactory resistance of the organism.
5. Complicated course. Mostly is the result of progressive development of the pathological process.
Pulmonary bleeding arise suddenly, are associated with coughing out of a foamy, red blood and clots by
portions or continuous stream. The most often source of a pulmonary bleeding are the bronchial arteries and
vessels of a pulmonary tissue. The clinical manifestations of a pulmonary suppuration are accompanied by
dizziness, weakness, dyspnea, chest pain. The hemodynamic disturbances depend on intensity of the bleeding.
The auscultation of lungs from both sides reveals the moist rales (aspiration). If the pulmonary destruction is
present the plain film of the chest shows the localization of the source of bleeding. After hospitalization of the
patient with this complication the exclusive information is obtained with a fibrobronchoscopy.
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1. Single hemoptysis.
2. Multiple hemoptysis.
1. Single bleeding:
2. Multiple bleeding:
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1. Massive bleeding.
The degree of a pulmonary bleeding manifests by coughing out the sputum tinged with blood, the
hemodynamic disturbance usually absent. At bleeding of degree are observed decreasing of arterial
pressure on 20-30 mm Hg, tachycardia to 100 beats/min, contents of hemoglobin within 60-80 g/l. The
bleeding of degree are accompanied with sharp decreasing of arterial pressure, rapid (more than 100-120
beats/min), small, sometimes thread pulse, and even its disappearance on peripheral arteries, tachypnea to 40
per 1 min, hemoglobin to 50-60 g/l. Probable the fulminant course up to the terminal state with prompt failure
of cardiac activity and asphyxia by blood.
Sepsis manifests by multisystem lesions with progression of the syndrome of polyorganous failure,
hematosepsis, purulent metastasizing (frequently in brain).
Characteristic complications for suppurative diseases of lungs such as pleural empyema and
pyopneumothorax are described in separate parts.
Generally, most of the patients admitted to the hospital with a diagnosis of lung abscess
have had symptoms for at least 2 weeks. These patients typically have an intermittent febrile
course, productive cough, weight loss, general malaise, and night sweats. Initially, foul sputum
is not observed in the course of the infection; however, after cavitation occurs, putrid
expectorations are quite prevalent. The odor of the breath and sputum of a patient with an
anaerobic lung abscess is often quite pronounced and noxious and may provide a clue to the
diagnosis. Hemoptysis may occasionally follow the expectoration of putrid sputum.
Symptoms depend on whether the abscess is caused by anaerobic or other bacterial
infection.
Anaerobic infection in lung abscess
o Patients often present with indolent symptoms that evolve over a period of
weeks to months.
o The usual symptoms are fever, cough with sputum production, night
sweats, anorexia, and weight loss.
o The expectorated sputum characteristically is foul smelling and bad
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tasting.
o Patients may develop hemoptysis or pleurisy
Other pathogens in lung abscess
o These patients generally present with conditions that are more emergent in
nature and are usually treated while they have bacterial pneumonia.
o Cavitation occurs subsequently as parenchymal necrosis ensues.
o Abscesses from fungi, Nocardia species, and Mycobacteria species tend to
have an indolent course and gradually progressive symptoms.
2. Physical findings.
The findings on physical examination of a patient with lung abscess are variable.
Physical findings may be secondary to associated conditions such as underlying pneumonia or
pleural effusion. The physical examination findings may also vary depending on the organisms
involved, the severity and extent of the disease, and the patient's health status and
comorbidities.
Patients with lung abscesses may have low-grade fever in anaerobic
infections and temperatures higher than 38.5C in other infections.
Generally, patients with in lung abscess have evidence of gingival disease.
Clinical findings of concomitant consolidation may be present (eg,
decreased breath sounds, dullness to percussion, bronchial breath sounds, course
inspiratory crackles).
The amphoric or cavernous breath sounds are only rarely elicited in
modern practice.
Evidence of pleural friction rub and signs of associated pleural effusion,
empyema, and pyopneumothorax may be present. Signs include dullness to percussion,
contralateral shift of the mediastinum, and absent breath sounds over the effusion.
Digital clubbing may develop rapidly.
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The wall thickness of a lung abscess progresses from thick to thin and
from ill-defined to well-circumscribed as the surrounding lung infection resolves. The
cavity wall can be smooth or ragged but is less commonly nodular, which raises the
possibility of cavitating carcinoma.
The extent of the air-fluid level within a lung abscess is often the same in
posteroanterior or lateral views. The abscess may extend to the pleural surface, in which
case it forms acute angles with the pleural surface.
Anaerobic infection may be suggested by cavitation within a dense
segmental consolidation in the dependent lung zones.
Lung infection with a virulent organism results in more widespread tissue
necrosis, which facilitates progression of underlying infection to pulmonary gangrene.
5. Tomogram of lungs.
6. Computed tomography
CT scanning of the lungs may help visualize the anatomy better than chest
radiography. CT scanning is very useful in the identification of concomitant empyema or
lung infarction.
On CT scans, an abscess often is a rounded radiolucent lesion with a thick
wall and ill-defined irregular margins.
The vessels and bronchi are not displaced by the lesion, as they are by an
empyema.
The lung abscess is located within the parenchyma compared with
loculated empyema, which may be difficult to distinguish on chest radiographs.
The lesion forms acute angles with the pleural surface chest wall.
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culture is requested.
Blood culture may be helpful in establishing the etiology.
Obtain sputum for ova and parasite whenever a parasitic cause for lung
abscess is suspected.
10. Immunogram.
11. Fibrobronchoscopy.
Differential diagnostics
Pneumonia
Primary bacterial pneumonias caused by single bacterial species other than the pneumococcus may account
for up to 25% of community-acquired and 80% of hospital-acquired pneumonias. All of these pneumonias
may have somewhat similar physical find- ings and x-ray evidence of pulmonary infiltration or consolidation.
For proper treatment, it is crucial to identify the causative agent by blood culture and by sputum examination
with stained smear and culture. Transtracheal aspiration, fiberoptic bronchoscopy, or even lung biopsy may be
needed for specific diagnosis and treatment.
Streptococcal Pneumonia
Pneumonia due to hemolytic streptococci occurs usually as a sequela to viral infection of the respiratory tract,
especially influenza or measles, or in persons with underlying pulmonary disease. The patients are usually in a
severely toxic condition and cyanotic. Pleural effusion develops frequently and early and progresses to
empyema in one-third of untreated pa- tients. The diagnosis rests on finding large numbers of streptococci in
smears of sputum and culturing hemolytic streptococci from blood and sputum.
The treatment of choice is with penicillin G in a dosage similar to that for pneumococcal pneumonia (see
above). If treatment is started early, the prognosis is good.
Pneumonia caused by Staphylococcus aureus occurs as a sequela to viral infections of the respiratory tract
(eg, influenza) and in debilitated (eg, postsurgical) patients or hospitalized infants, especially after
antimicrobial drug administration. There is often a history of a mild illness with headache, cough, and
generalized aches that abruptly changes to a very se- vere illness with high fever, chills, and exaggerated
cough with purulent or blood-streaked sputum and deep cyanosis. There may be early signs of pleural
effusion, empyema, or tension pneumothorax. X-ray examination reveals lung consolidation, pneumatoceles,
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abscesses, empyema, and pneumothorax. The demonstration of pyopneumothorax and of cavities with
air-fluid levels by x-ray is highly suggestive of Staphylococcal pneumonia. The diagnosis must be confirmed
by stained smear of sputum (masses of white cells and gram-positive cocci, many intra- cellular) and culture
(predominantly S aureus), and
also by means of cultures of pleural fluid and blood. The white count is usually more than 20,000//zL.
Initial therapy (based on sputum smear) consists of nafcillin, 6-12 g/d, or vancomycin, 2 g/d, given
intravenously in divided doses as a bolus. If the staphylococcus proves to be penicillin-sensitive by laboratory
test, penicillin G, 20-60 million units/d intravenously, is the antibiotic of choice. Drugs should be continued
for several weeks. If empyema develops, drainage must be established. The prognosis varies with the
underlying condition of the patient and the drug susceptibility of the organism.
Legionella Pneumonia
The eponym legionnaires' disease has been given to a serious pneumonia that afflicted people attending the
American Legion Convention in Philadelphia in 1976. Other outbreaks have been diagnosed ret- rospectively
at least since 1965, and sporadic infec- tions have occurred at least since 1947 in many places.
Legionella pneumophila is a poorly staining gram-negative bacterium that grows slowly on special media (eg,
charcoal-yeast extract) at 35 C. There are at least 8 species of Legionella, some with multiple serotypes.
These organisms can be recovered in human disease from sputum, bronchial washings, pleural fluid, lung
biopsies, or blood. Legionella species occur in the environment and are acquired by humans from aerosols,
dust from air-conditioning systems, water, or soil. The infection is not usually communi- cable from patient to
contacts. Asymptomatic infec- tion is common at all ages, whereas symptomatic infection is most often an
opportunistic pneumonia in immunocompromised individuals.
Asymptomatic infection is evident only by a rise in specific antibodies. Symptomatic infection is ob- served
mainly in elderly persons, smokers, and pa- tients undergoing hemodialysis or renal transplant.
The incubation period is estimated to be 2-10 days. Initial symptoms are malaise, diffuse myalgias, and
headache, followed in 12-48 hours by high, non- remittent fever and chills. Nausea, vomiting, and diarrhea
are frequent early in the illness. On the third day a dry cough begins that is nonproductive or produces scanty
mucoid, sometimes blood-streaked sputum. Dyspnea and hypoxia become marked as signs of consolidation
develop. Pleuritic chest pain occurs in one-third of patients. Severe confusion or delirium may occur.
There is leukocytosis with a shift to the left, hyponatremia, abnormal liver function tests, and, occasionally,
microscopic hematuria. Chest x-rays reveal patchy, often multilobar pulmonary con- solidation, and,
occasionally, small pleural effusions. The illness usually worsens for 4-7 days before im- provement begins in
those who recover. During severe outbreaks, the mortality rate has been 10% in those with manifest disease.
Death is attributed to respi- ratory or renal failure or shock, with disseminated intravascular coagulation.
The diagnosis is based on a clinical picture com- patible with the specific features of the disease and on
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negative results of bacteriologic laboratory tests for other pneumonias. The organism can be identified by
immunofluorescence in cultures, lung biopsy, and, rarely, sputum specimens. A retrospective diagnosis is
based on a significant rise in specific serum antibodies detected by immunofluorescence.
The treatment of choice is erythromycin, 0.5-1 g every 6 hours intravenously or orally for 2-3 weeks. This
usually results in improvement in 2-3 days. Rifampin, 10-20 mg/kg/d, has been suggested for patients who fail
to respond to erythromycin. Assisted ventilation and management of shock are essential.
This parasitic infection occurs in debilitated children or immunodeficient adults. It has been a prominent
opportunistic infection in AIDS patients. The diagnosis is made by lung biopsy and the demonstration of
typical cysts of P carinii in impression smears of lung tissue stained with methena- mine-silver. Early
treatment with sulfamethoxazole- trimethoprim can cure the pneumonia. The same drug has been effective in
prophylaxis during immunosuppression. An alternative, more toxic drug is pentamidine isethionate .
Essentials of Diagnosis
General Considerations
Mixed bacterial pneumonias include those in which culture and smear reveal several organisms, not one of
which can clearly be identified as the causative agent. These pneumonias usually appear as complica- tions of
anesthesia, surgery, aspiration, trauma, or various chronic illnesses (cardiac failure, advanced carcinoma,
uremia). They are common complications of chronic pulmonary diseases such as bronchiectasis and
emphysema. Old people are most commonly affected ("terminal" pneumonia). Patients treated with
intermittent positive pressure breathing apparatus or immunosuppressive drugs may develop pneumonia
caused by gram-negative rods.
The following findings in a debilitated, chroni- cally ill, or aged person suggest a complicating pneumonia: (1)
worsening of cough, dyspnea, cyanosis; (2) low-grade, irregular fever; (3) purulent sputum; and (4) patchy
basal densities on a chest film (in addition to previously noted densities caused by a primary underlying
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Clinical Findings
A. Symptoms and Signs: The onset is usually insidious, with low-grade fever, cough, expectoration, and
dyspnea that may become marked and lead to cyanosis. Physical findings are extremely variable and may not
be impressive against a background of cardiac or pulmonary disease. The signs listed under Other Bacterial
Pneumonias may also be present.
B. Laboratory Findings: The appearance of a greenish or yellowish (purulent) sputum should suggest a
complicating pneumonia. Smears and cul- tures reveal a mixed flora, often including anaerobes. Predominant
types should be noted. Leukocytosis is often absent in the aged and debilitated patient present- ing with a
mixed infection.
C. X-Ray Findings: X-ray (Picture 3) shows patchy, irregular infiltrations, most commonly posterior and basal
(in bedridden patients). Abscess formation may be observed. Careful interpretation will avoid confusion with
shadows due to preexisting heart or lung disease.
Differential Diagnosis
Mixed bacterial pneumonias must be differ- entiated from tuberculosis, carcinoma, and other spe- cific
mycotic, bacterial, and viral pulmonary infec- tions (to which they may be secondary).
Treatment
Clear the airway and correct hypoxia. Unless a probably significant etiologic agent can be identified, give one
of the new cephalosporins (eg, cefotaxime, 12 g/d intravenously) as initial therapy. This will be modified
according to clinical and laboratory results.
Prognosis
The prognosis depends upon the nature and sever- ity of the underlying pulmonary disease and varies with the
predominating organism.
ASPIRATION PNEUMONIA
Aspiration pneumonia is an especially severe type of pneumonia, often with a high mortality rate. It results
from the aspiration of gastric contents in addition to aspiration of upper respiratory flora in secretions.
Important predisposing factors include impairment of the swallowing mechanism (eg, esopha- geal disease),
inadequate cough reflex (eg, anesthesia, postoperative state, central nervous system disease, drug abuse), and
impaired gastric emptying (eg, pyloric obstruction). Pulmonary injury is due in large part to the low pH (< 2.5)
of gastric secretions.
Scattered areas of pulmonary edema and bron- chospasm occur, and the x-ray appearance (pictures 4-5) may
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be confused with that of pulmonary emboli, atelectasis, bronchopneumonia, and congestive heart failure.
Removal of aspirated material by catheter suction or bronchoscopy may be attempted, but this
usually fails to remove all aspirate completely. Corticosteroids (eg, prednisone, 100 mg orally
on the first or second day) may reduce the intensity of the inflammatory reaction to acidic
gastric secretion, but the value of corticosteroids in the treatment of aspiration pneumo- nia is
not proved, and they increase the risk of superinfection. Some aspiration pneumonias have no
bacterial component, but in many others a mixed bacterial flora is involved. Antimicrobial
drugs directed against the latter (eg, penicillin G plus an aminoglycoside or the best available
cephalosporin) are sometimes adminis- tered without waiting for evidence of progressive pul-
monary infection. In doing so, however, there is a risk of favoring the development of resistant
mi- croorganisms. Therefore, administration of antimi- crobials should not continue without
laboratory and clinical evidence of microbial infection. Assisted ventilation and supplementary
oxygen are beneficial.
The cancer of the central location due to the obturation of bronchus results in atelectasis of a segment or lobe
of lungs, with probable further abscessing. For the differentiation used tomography (reveals the obturation of
bronchus by tumour, lesion of central lymph nodes), cytological examination of sputum and bronchial
outwashes. The determinant role belongs to fibrobronchoscopy with a biopsy and verification of the
diagnosis.
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The peripheral cancer of lungs with destruction on tomograms is characterized by cavity with irregular inner
surface, which external outline connects with root of the lung because of lymphatic metastatic spreading. The
central lymph nodes frequently enlarged. The diagnosis is improved by results of transthoracic puncture or
catheterizing biopsy with cytological investigation, fibrobronchoscopy. If it is impossible to confirm the
diagnosis the thoracotomy is indicated.
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The tubercular cavern is mainly located in the upper lobes of lungs, roentgenologically revealed on the
background of characteristic changes in adjacent pulmonary tissue (calcification, dissemination), sometimes
detected a draining bronchus. In the sputum mycobacteria of tuberculosis are frequently found.
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The suppurative cyst of lungs differs by a gradual onset, slow course of the suppuration, less expressed
intoxication. Roentgenologically its cavity has the oval or rounded shape with a thin sheath and regular
contour. Perifocal infiltration is not characteristic.
With the purpose of maximal concentration of drugs in the pathological focus applied:
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- Introduction of medicinal agents into respiratory tracts (in the second stage) through the
endotracheal microirrigator, nasogastric tube, during bronchoscopies, endoscopic catheterization
of the abscess cavity through the draining bronchus, in aerosolic inhalations. The composition of
medical admixtures includes: antibiotics, antiseptics (10 % dimexid, dioxydin, microcid etc.),
enzymes;
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Skin wound
- Transcutaneous in the focus of destruction by means of puncture or draining with the usage of
physical antiseptics (US, UVR, laser).
- Intrapleural;
- By means of electrophoresis.
- Non-specific (pirimidine and purine derivates, drugs of a thymus gland, splenin, levamisol,).
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7. Correction of dysfunction of the vital organs and systems, prevention of complications, symptomatic
therapy.
Contraindications: decompensation of the vital functions and systems in the terminal stage, bilateral purulent
destruction of lungs, concomitant incurable malignant tumours.
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gram-negative and opportunistic organisms. These factors have increased the incidence of lung
abscess and the associated morbidity.
A great deal of caution is needed during anesthesia when patients with lung abscess
undergo surgery because spillage of the abscess material into the uninvolved lung can occur.
Therefore, a double-lumen endotracheal tube is used in all cases.
A study by Nagasawa et al has shown that thoracoscopic surgery can lead to effective
drainage of pediatric lung abscess without major complications. In addition, other benefits of
thoracoscopy include rapid recovery, less pain, and minimal morbidity.
Operational incisions anterolateral, lateral and posterolateral thoracotomy. The operation suggests
segmental, polysegmental resection, lobectomy, bilobectomy combined intervention (with the decortication,
pleurectomy).
Lateral access
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Anterior access
Posterior access
The patients with chronic abscesses should be undergone the operative treatment after complete liquidation of
exacerbation.
In a pulmonary gangrene the stabilization of the process on the background of active conservative treatment
allows in future to apply conservative tactics up to recovery or making optimal conditions for operation
(liquidation of intoxication, aggressive panbronchitis, diffuse infiltration of the parenchyma, pleural
complications). The headlong progression of the gangrene during first days, despite the active correction,
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occurrence of pulmonary bleeding requires urgent performance of operative management. Volume of the
operation pneumonectomy, bilobectomy, lobectomy.
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The pleural empyema is a purulent inflammation of its visceral and parietal membranes, which is associated
with accumulation of pus in a pleural space.
The causes of occurrence of acute pleural empyema are inflammatory, or purulent and destructive processes
of lungs, abscesses of abdominal cavity (secondary pleural empyema), open and closed damages of chest, and
also, in some cases, operative approaches on thoracic organs (primary pleural empyema).
A secondary pleural empyema occurs in 88 % of the patients. Thus develops fibrinous, exsudative, and then
purulent pleurisy.
In case of pulmonary gangrene, purulent mediastinitis, subphrenic abscess the stage of exsudative pleurisy
extremely short. The progression of the process results in transferring of focal pleural empyema into
wide-spread.
Pathology
Classification
1. Specific.
2. Nonspecific.
1. Primary.
2. Secondary.
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1. Acute.
2. Chronic.
1. Focal.
2. Wide-spread.
3. Pyopneumothorax.
bronchopleural fistula;
thoracopleural fistula;
thoracopleurobronchial fistula;
cribrate lung.
The clinic of an acute pleural empyema depends on extension of the process, reactivity of organism and
presence of complications.
The pain is the sign, which denote the involvement of pleural membranes in the process. Its intensity
increases depending on depth of respiration and body position.
The dyspnea arises from accumulation of a purulent content in a pleural space and exception of particular
volume of a pulmonary tissue from respiration. It's in direct ratio to amount of exudation in a pleural space.
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The cough is manifestation of inflammation or purulent and destructive process in a pulmonary tissue.
Fever to 39-40C, headache, sleeplessness, general malaise, and anorexia all these are manifestations of
intoxication.
The forced patient's position and restriction of breathing should be considered as outcomes of a pain
syndrome. The extension of pleural empyema causes the swelling of thoracic wall, smoothing of intercostal
spaces.
The data of percussion and auscultation depend on extension of the process and amount of pus in a pleural
space. At percussion over the exudate it is possible to reveal short sound with oblique upper contour. Above
the exudate tympanic sound resulting from consolidation of pulmonary tissue. By auscultation diminished
or absent sound in a great amount of exudate.
The predominant roentgenological sign of a focal or wide-spread empyema the presence of exudate. In
localized acute pleural empyema observed a local intensive homogeneous shadow. Roentgenologically
according to localization distinguished such types of a focal empyema:
1) apical;
2) paramediastinal;
3) parietal;
4) interlobar;
5) epiphrenic.
The wide-spread pleural empyema manifests by intensive homogeneous shadow in a basal parts with oblique
upper contour (Damuaso' line). The diaphragmatic dome is failed to observe. The more pus contents in a
pleural space, the higher the upper measure of exudate.
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Pleural empyema
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Pleural empyema
Pleural empyema
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Pleural empyema
The clinic of a focal pleural empyema depends on the site of the process. The apical empyema, due to
involvement in the process of a vascular-nervous fascicle, manifests by intensive pain. The soft tissues of
supraclavicular region are swelled. The percussion and auscultation has no information.
The pain syndrome in parietal (paracostal) empyema is more expressed. Thoracic excursion is restricted. The
diminishing of respiratory sound can be obtained over the exudate.
The chief complaint in paramediastinal empyema is the heart pain. The location of the process in the upper
mediastinum can cause the superior vena cava syndrome. The physical findings are vague.
In case of the basal (epiphrenic) empyema the patients complain of pain in subcostal area, which increases at
respiration and irradiates in supraclavicular region. In some cases the pain irradiates in epigastric region. The
palpation of intercostal spaces and hypochondrium is painful.
The clinical course of postoperative empyema depends on the character of operative approach (marginal
resection of lung, lobectomy, pneumonectomy, operation on esophagus) and infection of the pleural space.
The clinical manifestations of posttraumatic empyema depend on the size of damage of the chest, lungs,
mediastinal organs and complications (suppuration, hemothorax).
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The involvement in the purulent process of a pulmonary tissue in acute empyema results in its fusion of
membranes with formation of a bronchial or thoracopleural fistula (discharge of abscess through thoracic
wall).
The inappropriate elimination of empyema results in chronic course, cribrate lung and pleurogenic cirrhosis of
lungs.
2. Physical findings.
4. Pleural puncture.
Pleural puncture:
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Local anesthesia
Thoracentesis
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Differential diagnostics
Pleuropneumonia complicated with exsudative pleurisy, in some cases resembles acute pleural empyema: a
chest pain, fever, dyspnea, cough, and general weakness. The chest roentgenogram reveals hydrothorax
(exsudative pleurisy, pleural empyema, hemothorax). The chief diagnostic method for differentiation is the
thoracentesis. The presence of a serous (lucent, faint-yellow) exudate testifies about the pleuropneumonia,
complicated with pleural effusion, and cloudy, foul-smelling exudate of white or greenish color about acute
empyema.
The major difficulties in differential diagnostics cause the limited forms of empyema.
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The Pancoast cancer clinically and roentgenologically in most cases has almost the similar course to apical
form of empyema. The transthoracic biopsy permits to confirm the diagnosis.
The acute cholecystitis is necessary to differentiate with the epiphrenic empyema. The pain in the right
hypochondrium, fever, phrenic symptom are common for both diseases. However the objective findings,
X-radiography of chest and the thoracentesis allow to differentiate these pathological processes.
The tumour of anterior mediastinum complicated by superior vena cava syndrome is necessary to
differentiate with paramediastinal empyema. Nevertheless the body temperature in such patients, as a rule,
normal. The upper cavography is possible to find out the shift of cava vein and its irregular contours (filling
defect) due to growth of the mediastinal tumour.
There are some difficulties in differential diagnostics of empyema with a posttraumatic diaphragmatic hernia.
Such X-ray findings as deformation of diaphragm, additional shadows with a liquid level, intestinal loop
suggest a diaphragmatic hernia. A laterography and contrast study of gastrointestinal tract is basic in
differential diagnostics of this disease.
The atelectasis of a segment, and lobe of lung in some cases can cause misdiagnostics. Except X-ray chest
examination (in two planes and tomography), these situations require necessity of diagnostic bronchoscopy,
which reveals the cause of bronchial obturation (foreign body, endobronchial cancer etc.).
The presence of pus in a pleural space is the indication for its elimination. In the place of performed
diagnostic thoracentesis carried out the draining of empyema's cavity, its sanation by means of antiseptic
solutions. In a focal empyema the aspiration of pus is performed by thoracentesis and only in its inefficiency
carried out a draining of pleural space.
Pleural drainage:
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Trocar insertion
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Active aspiration
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Intensive antibacterial and antiinflammatory therapy should be immediately instituted. For general improving
used detoxication therapy (infusion of saline solutions, hemotransfusion, transfusion of proteins, solutions of
dextran, haemodes, forced diuresis, hemosorption if necessary), therapy for rising up of immunological
resistance of the organism.
During the empyema's sanation decreases the amount of pus which discharges out through the drainage. The
optimal variant of such course is the liquidation of empyema's cavity, then the drainage must be removed.
Transferring of the process into the chronic form (10-12 weeks) results in formation of a residual empyema's
cavity, which is possible is to reveal by means of pleurography introduction through the drainage of water-
soluble contrast with the further X-radiography in 2 planes.
Operative approach is applied when the process has transferred into the chronic form, that is in case of
residual empyema's cavity. Volume of the operation pleurectomy, decortication of lung.
In some cases, when a bronchial fistula and great empyema's cavity has been formed, there is the necessity of
performance of resection of lung and corrective thoracoplasty.
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The cysts of lungs are the thin-walled cavitary formations, filled with air or liquid contents.
Inherent cysts arise from the abnormalities of the development of lungs under influence of the multiple
chemical, physical, biological factors. Whether they can develop from a bronchial tree (bronchial) of from
alveolar tissue (alveolar). Their occurrence resulting from the delay of the development of peripheral parts of
bronchus with their expansion or agenesia of alveoli with dilatation of terminal bronchioles. Congenital cysts
at first develop and grow as secretory formations. After communication with bronchus they finally form as air
or hydroair cavities.
The acquired cysts represent fibrous cavities, which remain after abscesses, tubercular caverns, echinococci,
posttraumatic intrapulmonary hematomas. The degenerative changes in the wall of bronchus with obliteration
of its lumen by a cloggy secret owing to repeated inflammatory processes result in occurrence of acquired
retentional cysts.
Pathology
Congenital cyst can be located in any part of lungs. The walls of bronchogenic cavities contain chaotically
disposed elements of bronchus (cartilagous plates, muscle fibers, mucous glands), they are lined from inside
by cylindrical or cubic epithelium. Squeezed alveolar cells line the walls of alveolar formations.
The acquired cyst are revealed in places of localization of previous diseases,. Their walls mainly consist of
connective tissue. Epithelization is possible due to transferring of the epithelium from a draining bronchus at
long existence.
The cysts could be uni- or multichamber, closed and open (depending on the presence of communication with
bronchus).
Classification
According to parentage:
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- congenital;
- acquired.
According to displacement:
- single, multiple;
- unilateral, bilateral.
Complications:
- Suppuration;
- Bleeding;
- Malignancy.
Clinical manifestations of uncomplicated pulmonary cysts are vague. Sometimes patients complain of a chest
pain, periodic cough, and inflammatory diseases of respiratory tract in history. In children the signs are much
expressed, the dyspnea associates with the compression of airways.
In great, superficially disposed cysts revealed delayed respiratory movements on affected side during
breathing.
At routine chest films the closed congenital cyst forms a homogeneous shadow of the spherical or oval shape
of average intensity with rather regular edge on the background of an intact pulmonary tissue. During
roentgenoscopy sometimes observed the change of its shape depending on the phase of breathing elongation
in inspiration (Escudero's syndrome). The character of the shadow is better to study on tomograms.
Acquired retentional cyst is roentgenologically shown by a shadow of irregular shape (piriform, spindle-
shaped etc.), that displays the shape of the distended bronchus. The adjacent tissue, as a rule, changed due to
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Open cysts are observed as thin-walled, good defined cavities of annular or oval shape.
On bronchograms congenital cysts are observed hypoplasia of segmental or lobar bronchus, lack of bronchial
bifurcations, which tends to bone. Sometimes observed bronchiectases in the neighboring parts of lungs. A
cystic cavity is infrequently defined.
The angiopulmonography reveals deformation of vascular branches, which circumflex the cyst.
The suppuration of the closed cysts resembles the development of a lung abscess with lesser expression of
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Infection of the open cysts is characterized by a gradual long course, moderate manifestation of suppuration
and late intoxication.
The tension (valvular) cysts arise more often in children. They are characterized by severe respiratory and
hemodynamic disturbances, up to terminal, owing to inflexion of venous trunks, shift of mediastinum and
compression of lungs. The predominant signs are increased dyspnea, cyanosis, chest pain, respiratory lag on
affected side, auscultatory absence or weakening of respiration, bandbox percussion sound over the cavity
at mediastinal shift to the opposite side of the chest.
Pleural complications of pulmonary cysts, and also bleeding described in the relevant parts.
4. Lung tomography.
5. Bronchography.
6. Angiopulmonography.
Differential diagnostics
The abscess of lungs, in contrast with a suppurative cyst, is characterized by prompt course, expressed
purulent intoxication, roentgenologically its wall is irregular, with proper considerable perifocal infiltration.
The cancer with destruction differs by a thick wall with a tuberous inner surface, phenomena of lymphangitis
in adjacent tissue. The determinant value has endoscopic examination or puncture with a biopsy and
following morphological investigation.
The tubercular cavern displaced in the upper lobes, in adjacent tissue revealed fibrosis, petrifactions,
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Opposite to cyst, in termed diseases, the circumflex deformation of vascular branches never observed at
angiopulmonography.
The considerable difficulties can arise at differentiation of the closed congenital cysts.
The tuberculoma differs from them by characteristic localization. At X-ray examination the heterogeneity of
the shadow with calcifications, early excentric destruction, "tubercular" background is observed.
The benign tumours sometimes possible to differentiate only after the results of cytological investigation of
punctate or after operation.
The echinococci cysts on tomogram can have a double contour of chitinous and fibrous sheaths. In blood
analyses observed eosinophilia. The final decision is taken out after carrying out immunological (indirect
microagglutination test) allergic (Cacconi's reaction) tests.
Huge cysts, in contrast with open air cysts, are characterized by a subpleural location.
The diagnostic doubts at suspicion on a diaphragmatic hernia are solved by radiopaque examination of a
gastrointestinal tract.
The acquired cysts differ from congenital by roentgenological signs of the lesion of surrounding tissues
(pneumofibrosis, deforming bronchitis, secondary bronchiectases, and calcifications). Postpneumonic cavities
are of irregular shape, with grooves and pockets, their walls different thick. During bronchography they filled
through some small bronchi. Sometimes the verification is possible only after postoperative morphological
investigation.
The pulmonary cysts require the surgical treatment. In case of complications the indication for operation
becomes absolute. Contraindications: the severe respiratory disturbance, concomitant malignant
nonresectable tumors, vital organs dysfunction in the stage of permanent decompensation, elderly age of the
patients.
The volume of the operation: if the adjacent pulmonary tissue is intact cystectomy, otherwise segmental or
wedged resection, lobectomy.
The conservative therapy is applied in suppuration of cysts with the purpose of preoperative preparation. It is
the similar, which applied for abscesses of lungs.
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SPONTANEOUS PNEUMOTHORAX
Spontaneous pneumothorax is the entry of air in a pleural space with the further lung collapse, which not
associated with traumatic damage of chest or pulmonary tissue.
As a result of spontaneous disrupture of lung blebs and subpleural air cysts occurs the damage of pleural
visceral membrane. It causes entry of air in pleural space. Owing to its leakage the elastic pulmonary tissue
collapses. The degree of the collapse of lung depends on amount of air, that has penetrated a pleural space.
Pathology
Morphologically in spontaneous pneumothorax found out a focal bullous emphysema with disrupture of blebs,
subpleural air cyst, and also disorders, which have caused disturbances of ventilating ability of bronchi. It can
be bronchitis, pneumosclerosis, tuberculosis and fibrous alveolitis.
Classification
1. Unilateral or bilateral.
5. Tension or valvular (complete collapse of lungs and shift of mediastinum in the opposite side).
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The onset of the disease is sudden. A state of the patient and expression of clinical manifestations depends on
amount of air, which has entered the pleural space. Usually in normal conditions, and sometimes after
physical activity, the patients suddenly feel acute pain on the side of lesion, dyspnea, pain in the heart region
and heartbeating. An available also Acrocyanosis or total cyanosis of skin is observed. The circulatory
disturbance depends on degree of hypoxia. Intensity of pain and dyspnea gradually decrease, but a dry
troublesome cough appears.
Examination of the chest allows to observe expansion of intercostal spaces and restriction of respiratory
excursion. By palpation - diminishing of vocal fremitus on the affected side. At percussion a chief sign of
pneumothorax is the tympanic sound. Auscultation reveals weakened or sharply weakened breathing sounds.
The cardiac tones are muffled, tachycardia.
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Thoracoscopy in pneumothorax possible to find out subpleural blebs of different sizes (0,5-3 cm), which are
mainly disposed on the apex of lung.
The atypical (asymptomatic) spontaneous pneumothorax occurs in 20 % of the patients, and mainly revealed
at X-ray examination. In most cases it is the partial pneumothorax.
The expressed pain syndrome and dyspnea, which resulting from collapse of lung, characterize subtotal and
total pneumothorax.
The tension spontaneous pneumothorax is the most severe form of pneumothorax. It manifests by sudden
onset, progressive increase of dyspnea, expressed cyanosis. The breathing is superficial, rapid, with active
participation of auxiliary muscles. Mediastinal shift and flexion of vessels result in disturbance of cardiac
activity up to the cardiac arrest, and requires urgent management.
Rigid pneumothorax (rigid lung). The neglected pneumothorax causes fibrinous exsudative pleurisy. On the
surface of lung (visceral pleura) commissures are formed, that give no opportunity for lung expansion. The
presence of residual pleural cavity and progressive development of a purulent infection result in occurrence
of acute pleural empyema. In such cases the patients complain of the fever up to 38-38,5C, general
weakness and increasing of dyspnea. The phenomena of intoxication increase. Thus such patients require the
treatment of pleural empyema.
2. Physical findings.
4. Thoracentesis
5. Thoracoscopy.
6. Tomography of lungs.
Differential diagnostics
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Pleural effusion. This pathology manifests by more gradual onset. As opposite to pneumothorax, the
complaints of chest pain predominate above the complaints of dyspnea. Frequently such patients specify on
transferred undercooling.
As well as the spontaneous pneumothorax, the pleural effusion is characterized by diminishing of vocal
fremitus, dullness of percussion sound, weakened of absent breathing sounds over the exudate. Nevertheless
in the routine roentgenogram in such cases observed a homogeneous intensive shadow of a pleural space with
oblique upper contour. The puncture of pleural space enables finally to confirm the diagnosis of pleural
effusion.
Intercostal neuralgia. A predominant sign in clinical pattern is acute pain, which intensifies at physical
activity, changes of body position and body movements, at deep breathing. The localization of pain coincides
with zone of innervation of intercostal nerves.
Conservative treatment is applied in the patients with a partial pneumothorax. Thus thoracentesis in
intercostal space in the midclavicular line with aspiration of air is performed. The cases of its inefficiency, and
also subtotal, total and tension pneumothorax require drainage of a pleural space with active aspiration of air.
The operative management is necessary, if there is no efficiency from active aspiration (in incomplete
expansion of lung), recurrent of course of the process, presence of great subpleural blebs and rigid
pneumothorax. Volume of operation depends on extension of the process: liquidation of alveolar fistula,
wedged resection of lung or lobectomy.
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PYOPNEUMOTHORAX
Pyopneumothorax is the discharge of lung abscess of into pleural space, which is accompanied by purulent
inflammation of pleural membranes with a collapse of lung.
Peripheral placement of the purulent focus in a pulmonary tissue results in destruction (fusion) of visceral
membrane. As a result of, the pus and air penetrate into a pleural space that leads to a purulent inflammation
of parietal and visceral membranes of pleura. The disorder of hermeticity of a pleural space results in a lung
collapse.
Among other causes of pyopneumothorax are the chest trauma, which results in collapse of lung, infection
and purulent inflammation of pleural membranes.
- gangrene of lung;
- abscessing pneumonia;
- bronchiectatic disease;
- damage of esophagus;
- mediastinitis;
- chest trauma;
Pathology
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Morphologically in pyopneumothorax pus and air are present in pleural space. In the lungs subpleural
disposed purulent or necrotic foci, which connected with a pleural space through a pleuro-pulmonary fistula.
From the outside the zone of disrupture is confined by perifocal inflammation. In the draining bronchus it is
possible to see manifestations of deforming, frequently polypous bronchitis.
Classification
1. Specific.
2. Nonspecific.
1. Primary.
2. Secondary.
1. Asymptomatic form.
2. Mild form.
3. Acute form.
1. Localized pyopneumothorax:
a) parietal;
b) apical;
c) epiphrenic;
d) paramediastinal;
e) polychamber.
2. Subtotal pyopneumothorax.
3. Total pyopneumothorax.
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4. Tension pyopneumothorax.
The clinic of pyopneumothorax depends on the size of the focus of destruction, which influences on degree of
lung collapse, and on amount of purulent content in a pleural space.
The pain owing to discharge of the focus of destruction into pleural space often arises suddenly.
The dyspnea occurs as a result of collapse of lung owing to leakage of pus and air into pleural space. Its
expression is in direct ratio to lung collapse. Therefore a dyspnea in rest observed in a subtotal and total
pyopneumothorax. It sharply amplifies even at minor physical activity. Auxiliary muscles take part in order to
force respiration.
The expectoration of sputum with ichorous smell is the outcome of destructive process in a pulmonary tissue.
Its amount decreases after discharge of pus into pleural space.
Hectic fever with caused by enlargement of the area of resorption. The patients are adynamic, flaccid. Some
of them are unconsciousness.
By objective examination the position of patients is forced, they sit in bed leaning upon the bed (subtotal,
total pyopneumothorax). The affected hemithorax takes no part in respiration.
Percussion reveals a sharp shortening of sound over the zone of exudate and bandbox sound above the region
of collapsed lung.
By auscultation there are no breathing sounds on the affected side. In case of localized pyopneumothorax
weakened or sharply weakened sound with a bronchial or amphoric tone.
The X-ray picture of pyopneumothorax depends on its form, but the obligatory sign is the air-fluid level in a
pleural space with well-defined edge of collapsed lung on its background.
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Pyopneumothorax
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Pyopneumothorax
The clinical course of pyopneumothorax depends on adhesions between pleural membranes. It sometimes
changes typical clinical course of a total lung collapse. The clinic of disease depends also on amount of a
purulent exudate. Therefore according to extension of the process and size of destruction of lung
distinguished acute, mild and asymptomatic forms of pyopneumothorax. Especially difficult for diagnostics is
the asymptomatic form of localized pyopneumothorax. Dyspnea for such pathology not characteristic, as the
adhesion of membranes prevents complete collapse of lung. Dyspnea is vague or absent at all in partial
collapse. A diminished vocal fremitus on side of pathological process, shortening of percussion sound and
weakened or sharply weakened breathing sounds over the collapsed lung and exudate are revealed.
Roentgenological manifestations in localized pyopneumothorax not expressed and include horizontal fluid
level, margin of partially collapsed lung and minor air in the pleural space.
In most cases after discharge of the destructive focus in a pleural space and collapse of lung observed the
closure of bronchopleural fistula. Nevertheless the inflammatory process in a pulmonary tissue and pleural
space is going on.
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2. Physical findings.
4. Thoracentesis.
5. Pleurography.
Differential diagnostics
They're no special necessity for differential diagnostics of pyopneumothorax in the majority of patients.
History (presence of the purulent focus in a pulmonary tissue), clinical course (acute pain and dyspnea at
abscess discharge into pleural space), and also chest X-ray findings and thoracentesis frequently reliably
permit to make the diagnosis.
In some cases a localized pyopneumothorax according to clinical course resembles a huge acute abscess of
lungs. But the differences of roentgenological symptomatology permit to verify these pathological processes.
In acute lung abscess the cavity of destruction localized in a pulmonary parenchyma, it is of rounded form
with horizontal fluid level and expressed perifocal infiltration.
The purpose of treatment should include sanation of the destructive focus in pulmonary tissue and liquidation
of complications; that means elimination of pus and air from a pleural space and prompt expanding of lung.
2. Draining of pleural space, active aspiration of its content (air, pus) to expand the lungs.
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5. The therapy for rising up of immunological resistance of the organism (staphylococcal anatoxin according
to scheme, antistaphylococcal gamma-globulin, antistaphylococcal plasma).
The indications for operative management are the same, as in pleural empyema.
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CHEST TRAUMA .
Chest trauma is a significant source of morbidity and mortality in the United States. This
article focuses on chest trauma caused by blunt mechanisms. Penetrating thoracic injuries are
addressed in Penetrating Chest Trauma.
Blunt injury to the chest can affect any one or all components of the chest wall and
thoracic cavity. These components include the bony skeleton (ribs, clavicles, scapulae,
sternum), lungs and pleurae, tracheobronchial tree, esophagus, heart, great vessels of the chest,
and the diaphragm. In the subsequent sections, each particular injury and injury pattern
resulting from blunt mechanisms is discussed. The pathophysiology of these injuries is
elucidated, and diagnostic and treatment measures are outlined.
Frequency
Trauma is responsible for more than 100,000 deaths annually in the United States.
Estimates of thoracic trauma frequency indicate that injuries occur in 12 persons per million
population per day. Approximately 33% of these injuries require hospital admission. Overall,
blunt thoracic injuries are directly responsible for 20-25% of all deaths, and chest trauma is a
major contributor in another 50% of deaths.
Pathophysiology
The major pathophysiologies encountered in blunt chest trauma involve derangements in
the flow of air, blood, or both in combination. Blunt trauma commonly results in chest wall
injuries (eg, rib fractures). The pain associated with these injuries can make breathing difficult,
and this may compromise ventilation.
Direct lung injuries, such as pulmonary contusions, are frequently associated with major
chest trauma and may impair ventilation by a similar mechanism.
Space-occupying lesions, such as pneumothoraces, hemothoraces, and
hemopneumothoraces, interfere with oxygenation and ventilation by compressing otherwise
healthy lung parenchyma. A situation of special concern is tension pneumothorax in which
pressure continues to build in the affected hemithorax as air leaks from the pulmonary
parenchyma into the pleural space. This can push mediastinal contents toward the opposite
hemithorax. Distortion of the superior vena cava by this mediastinal shift can result in
decreased blood return to the heart, circulatory compromise, and shock.
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Relevant Anatomy
The thorax is bordered superiorly by the thoracic inlet, just cephalad to the clavicles.
The major arterial blood supply to and venous drainage from the head and neck pass through
the thoracic inlet.
The thoracic outlets form the superolateral borders of the thorax and transmit branches
of the thoracic great vessels that supply blood to the upper extremities. The nerves that
comprise the brachial plexus also access the upper extremities via the thoracic outlet. The veins
that drain the arm, most importantly the axillary vein, empty into the subclavian vein, which
returns to the chest via the thoracic outlet.
Inferiorly, the pleural cavities are separated from the peritoneal cavity by the
hemidiaphragms. Communication routes between the thorax and abdomen are supplied by the
diaphragmatic hiatuses, which allow egress of the aorta, esophagus, and vagal nerves into the
abdomen and ingress of the vena cava and thoracic duct into the chest.
The chest wall is composed of layers of muscle, bony ribs, costal cartilages, sternum,
clavicles, and scapulae. In addition, important neurovascular bundles course along each rib,
containing an intercostal nerve, artery, and vein. The inner lining of the chest wall is the
parietal pleura. The visceral pleura invests the lungs. Between the visceral and parietal pleurae
is a potential space, which, under normal conditions, contains a small amount of fluid that
serves mainly as a lubricant.
The lungs occupy most of the volume of each hemithorax. Each is divided into lobes.
The right lung has 3 lobes, and the left lung has 2 lobes. Each lobe is further divided into
segments.
The trachea enters through the thoracic inlet and descends to the carina at thoracic
vertebral level 4, where it divides into the right and left mainstem bronchi. Each mainstem
bronchus divides into lobar bronchi. The bronchi continue to arborize to supply the pulmonary
segments and subsegments.
The heart is a mediastinal structure contained within the pericardium. The right atrium
receives blood from the superior vena cava and inferior vena cava. Right atrial blood passes
through the tricuspid valve into the right ventricle. Right ventricular contraction forces blood
through the pulmonary valve and into the pulmonary arteries. Blood circulates through the
lungs, where it acquires oxygen and releases carbon dioxide. Oxygenated blood courses
through the pulmonary veins to the left atrium. The left heart receives small amounts of
nonoxygenated blood via the thebesian veins, which drain the heart, and the bronchial veins.
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Left atrial blood proceeds through the mitral valve into the left ventricle.
Left ventricular contraction propels blood through the aortic valve into the coronary
circulation and the thoracic aorta, which exits the chest through the diaphragmatic hiatus into
the abdomen. A ligamentous attachment (remnant of ductus arteriosus) exists between the
descending thoracic aorta and pulmonary artery just beyond the take-off of the left subclavian
artery.
The esophagus exits the neck to enter the posterior mediastinum. Through much of its
course, it lies posterior to the trachea. In the upper thorax, it lies slightly to the right with the
aortic arch and descending thoracic aorta to its left. Inferiorly, the esophagus turns leftward and
enters the abdomen through the esophageal diaphragmatic hiatus. The thoracic duct arises
primarily from the cisterna chyli in the abdomen. It traverses the diaphragm and runs cephalad
through the posterior mediastinum in proximity to the spinal column. It enters the neck and
veers to the left to empty into the left subclavian vein.
Clinical
The clinical presentation of patients with blunt chest trauma varies widely and ranges
from minor reports of pain to florid shock. The presentation depends on the mechanism of
injury and the organ systems injured.
Obtaining as detailed a clinical history as possible is extremely important in the
assessment of a patient with a blunt thoracic trauma. The time of injury, mechanism of injury,
estimates of MVA velocity and deceleration, and evidence of associated injury to other systems
(eg, loss of consciousness) are all salient features of an adequate clinical history. Information
should be obtained directly from the patient whenever possible and from other witnesses to the
accident if available.
Classification
1. Isolated trauma.
2. Combined trauma (craniocerebral, with damage of abdominal organs, with damage of bones).
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1. Contusion.
2. Compression.
3. Commotion.
4. Fracture.
2. With damage of viscerae (lungs, trachea, bronchi, esophagus, heart, vessels, diaphragm etc.).
1. Uncomplicated.
2. Complicated:
1. Mild.
2. Moderate.
3. Severe.
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RIB FRACTURE
Simple rib fractures are the most common injury sustained following blunt chest trauma, accounting for more
than half of thoracic injuries from nonpenetrating trauma. Approximately 10% of all patients admitted after
blunt chest trauma have one or more rib fractures. These fractures are rarely life-threatening in themselves
but can be an external marker of more severe visceral injury inside the abdomen and the chest.
The most common mechanism of injury for rib fractures in elderly persons is a fall from height or from
standing. In adults, motor vehicle accident (MVA) is the most common mechanism. Youths sustain rib
fractures most often secondary to recreational and athletic activities.
Rib fractures may compromise ventilation by a variety of mechanisms. Pain from rib fractures can cause
respiratory splinting, resulting in atelectasis and pneumonia. Multiple contiguous rib fractures (ie, flail chest)
interfere with normal costovertebral and diaphragmatic muscle excursion, potentially causing ventilatory
insufficiency. Fragments of fractured ribs can also act as penetrating objects leading to the formation of a
hemothorax or a pneumothorax. Ribs commonly fracture at the point of impact or at the posterior angle
(structurally their weakest area). Ribs four through nine (4-9) are the most commonly injured.
Physical
Rib fractures are the most common blunt thoracic injuries. Ribs 4-10 are most frequently involved. Patients
usually report inspiratory chest pain and discomfort over the fractured rib or ribs. Physical findings include
local tenderness and crepitus over the site of the fracture. If a pneumothorax is present, breath sounds may be
decreased and resonance to percussion may be increased. Rib fractures may also be a marker for other
associated significant injury, both intrathoracic and extrathoracic. In one report, 50% of patients with blunt
cardiac injury have rib fractures. Fractures of ribs 8-12 should raise the suggestion of associated abdominal
injuries. Lee and colleagues reported a 1.4- and 1.7-fold increase in the incidence of splenic and hepatic
injury, respectively, in those with rib fractures.
Paradoxical chest wall excursion with inspiration is seen with flail chest. A flail chest occurs when a large
segment of ribs is not attached to the spine. These ribs are broken in at least 2 places on each rib. The
paradoxical movement occurs because the middle section of the rib between the 2 fracture sites moves in
response to intrathoracic pressure changes not intercostal muscle contractions.
Specific signs of ventilatory insufficiency include cyanosis, tachypnea, retractions, and use of accessory
muscles for ventilation.
If fracture of the lower ribs is suspected, assess the patient for abdominal tenderness and costal margin
tenderness, which could raise suspicion for injury to intra-abdominal organs.[14]
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Chest radiographs
Anteroposterior (AP) and lateral chest films are used routinely to assist in the diagnosis of rib fractures, yet
sensitivity as low as 50% has been reported. Delayed or follow-up radiographs can be very helpful.
Chest radiographs are much more useful in the diagnosis of underlying injuries, including hemothorax,
pneumothorax, lung contusion, atelectasis, pneumonia, and vascular injuries.
Findings of sternal fracture[3] or scapular fracture[15] should increase suspicion for rib fractures.
Chest CT scan
A chest CT scan is more sensitive than plain radiographs for detecting rib fractures. The modality can also
provide information regarding the number of ribs involved.
If complications from rib fractures are suspected clinically or diagnosed by plain radiographs, a chest CT scan
may be helpful to document specific injuries, to characterize extent of injury, and to plan for definitive
management.
An associated CT scan of the abdomen with intravenous contrast should be considered in cases involving
lower rib fractures with suspected or known injury to the liver and/or the spleen.
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First and second rib fractures are considered a separate entity from other rib fractures because of the
excessive energy transfer required to injure these sturdy and well-protected structures. First and second rib
fractures are harbingers of associated cranial, major vascular, thoracic, and abdominal injuries. The clinician
should aggressively seek to exclude the presence of these other injuries.
Pain control and pulmonary toilet are the specific treatment measures for rib fractures. First and second rib
fractures do not require surgical therapy. An exception to this would be the need to excise a greatly displaced
bone fragment.
Treatment
Elderly patients with 3 or more rib fractures have been shown to have a 5-fold increased mortality rate and a
4-fold increased incidence of pneumonia. Effective pain control is the cornerstone of medical therapy for
patients with rib fractures. For most patients, this consists of oral or parenteral analgesic agents. Intercostal
nerve blocks may be feasible for those with severe pain who do not have numerous rib fractures. A local
anesthetic with a relatively long duration of action (eg, bupivacaine) can be used. Patients with multiple rib
fractures whose pain is difficult to control can be treated with epidural analgesia.
Adjunctive measures in the care of these patients include early mobilization and aggressive pulmonary toilet.
Rib fractures do not require surgery. Pain relief and the establishment of adequate ventilation are the
therapeutic goals for this injury. Rarely, a fractured rib lacerates an intercostal artery or other vessel, which
requires surgical control to achieve hemostasis acutely. In the chronic phase, nonunion and persistent pain
may also require an operation.
The direct force of traumatizing factor on the chest wall results in rib fracture.
The pain localized in the zone of damage, is the chief clinical manifestation. The pain intensifies at
respiration, cough and change of a body position of the patient. The overwhelming majority of the patients
complain of crepitation of ribs in the fracture site.
Crepitating of osseous fragment revealed by palpation, and depending on number of injured ribs diminished
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This is one of the most severe complication of the closed trauma of the chest. The floation arises from
fracture of three and more ribs along two anatomic lines. The multiple rib fractures produce an unstable
segment of chest wall that moves paradoxically inward upon inspiration and balloons outward during
expiration (flail chest). Thereby the respiration disturbed not only in the area of a floating segment, but also in
all lungs. The permanent movement of flail chest result in rocking shift of mediastinum, which causes
deviation of its organs. As a result the respiratory failure is associated with cardiovascular.
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In an attempt to stabilize the chest wall and to avoid endotracheal intubation and mechanical ventilation,
various operations have been devised for correcting flail chest. These include pericostal sutures, the
application of external fixation devices, or the placement of plates or pins for internal fixation. With improved
understanding of pulmonary mechanics and better mechanical ventilatory support, surgical therapy has not
been proven superior to the supportive and medical measures discussed. However, most authors would agree
that stabilization is warranted if a thoracotomy is indicated for another reason.
Flail chest
Classification
1. Central floative segment a multiple rib fracture along parasternal or midclavicular lines.
2. Anterolateral floative segment a multiple rib fracture along parasternal and anteaxillary lines.
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3. Lateral floative segment a multiple rib fracture along anterior and posterior axillary lines.
4. Posterior floative segment a multiple rib fracture along postaxillary and paravertebral lines.
The patients state is grave or extremely grave. The expressed pain syndrome frequently results in traumatic
shock. The patient is restless. Observed the cyanosis of skin, tachypnea, and tachycardia to 120-160 beat/min
of weak filling and tension. Arterial pressure at first elevated, then its decrease observed. At examination
characteristic paradoxical respiratory movements of chest, inward upon inspiration and outward during
expiration, crepitus of bone fragments by palpation are revealed. Breathing sounds diminished on the side of
damage by auscultation.
In case of floative rib fracture the chest X-ray examination reveals multiple, double rib fracture with
deformity of the chest.
Flail chest
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In 75 % of cases the multiple rib fracture is the cause of injury of lungs, pneumothorax or
pneumohemothorax.
Treatment
Pain relief in closed trauma of the chest is achieved by means of different blocks:
1. Vagosympathetic block;
3. Paravertebral block.
Except blocks, in some cases analgesics and opiates are instituted. On 2-3 day desirable the administration of
electrophoresis with novocaine. For prophylaxis of congested phenomena in a pulmonary tissue used
respiratory gymnastics, forced ventilation of lungs, inhalations.
The methods of reduction of the skeleton of the flail chest are divided onto three groups:
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1. External fixation of a movable segment by means of suturing for intercostal muscles and traction
during 2-3 weeks;
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BREASTBONE FRACTURE
Most sternal fractures are caused by MVAs. The upper and middle thirds of the bone are most commonly
affected in a transverse fashion. Patients report pain around the injured area. Inspiratory pain or a sense of
dyspnea may be present. Physical examination reveals local tenderness and swelling. Ecchymosis is noted in
the area around the fracture. A palpable defect or fracture-related crepitus may be present.
Associated injuries occur in 55-70% of patients with sternal fractures. The most common associated injuries
are rib fractures, long bone fractures, and closed head injuries. The association of blunt cardiac injuries with
sternal fractures has been a source of great debate. Blunt cardiac injuries are diagnosed in fewer than 20% of
patients with sternal fractures. Caution should be used before completely excluding myocardial injury. The
workup should begin with an ECG.
Most sternal fractures require no therapy specifically directed at correcting the injury. Patients are treated
with analgesics and are advised to minimize activities that involve the use of pectoral and shoulder girdle
muscles. The most important aspect of the care for these patients is to exclude blunt myocardial and other
associated injuries. Patients who are experiencing severe pain related to the fracture and those with a badly
displaced fracture are candidates for open reduction and internal fixation. Various techniques have been
described, including wire suturing and the placement of plates and screws. The latter technique is associated
with better outcomes.
The fracture of breastbone is commonly caused by direct forces at the site of the sternum. Usually it is the
outcome of compression or result of trauma to vehicle helm.
The fracture in most cases located in the upper and medial thirds of breastbone.
The patients complain of severe pain in the site of fracture, which intensifies at respiration and movements.
The pain behind the sternum and in the heart area follows the contusion of lungs and heart. Sometimes
hemoptysis is observed.
Examination reveals the deformity of breastbone in the site of fracture. Displaced fragments are palpated
here, that accompanied by severe pain syndrome.
By auscultation, if there are no intrapleural complications, the respiration in the first 2-3 days is vesicular
from both sides. Then the fine bubbling rales are auscultated which is the first objective manifestation of a
posttraumatic pneumonia.
The complete fracture of breastbone is characterized by a break in continuity of both cortical plates with a
local dislocation of fragments.
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Fracture of breastbone
2. Physical findings.
Treatment
The sternal fracture without displacement of fragments requires conservative treatment. The fracture of the
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corpus of breastbone with dislocation of fragments quite often requires operative treatment with performance
of osteosynthesis.
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POSTTRAUMATIC PNEUMOTHORAX
Pneumothorax is defined as the presence of air or gas in the pleural cavity, that is, in the
potential space between the visceral and parietal pleura of the lung. The result is collapse of the
lung on the affected side. Air can enter the intrapleural space through a communication from
the chest wall (ie, trauma) or through the lung parenchyma across the visceral pleura.
Spontaneous pneumothorax is a commonly encountered problem with approaches to
treatment that can vary from observation to aggressive intervention. Spontaneous pneumothorax
occurs in people without underlying lung disease and in the absence of an inciting event. In
other words, air is present in the intrapleural space without preceding trauma and without
underlying clinical or radiologic evidence of lung disease. However, many patients whose
condition is labeled as spontaneous pneumothorax have subclinical lung disease. Patients are
typically between age 18 and 40 years.
Spontaneous pneumothoraces in most patients occur from the rupture of blebs and
bullae. Although primary spontaneous pneumothorax (PSP) is defined as a lack of underlying
pulmonary disease, these patients have asymptomatic blebs and bullae detected on computed
tomography scans or upon thoracotomy. PSP is typically observed in tall, young people
without parenchymal lung disease and is thought to be related to increased shear forces in the
apex.
Traumatic pneumothorax results from injury, typically blunt trauma or penetrating
trauma that disrupts the parietal or visceral pleura (see the images below). The mechanisms of
injury are secondary to medical or surgical procedures. Pneumothoraces due to trauma are
relatively straightforward and usually require tube thoracostomy.
Pathophysiology
The pleural space has a negative pressure, with the chest wall tending to spring outward
and the lung's elastic recoil tending to collapse. If the pleural space is invaded by gas from a
ruptured bleb, the lung collapses until equilibrium is achieved or the rupture is sealed. As the
pneumothorax enlarges, the lung becomes smaller. The main physiologic consequence of this
process is a decrease in vital capacity and partial pressure of oxygen.
Tension pneumothorax occurs anytime a disruption involves the visceral pleura, parietal
pleura, or the tracheobronchial tree. This condition develops when injured tissue forms a 1-way
valve, allowing air inflow into the pleural space and prohibiting air outflow. The volume of this
nonabsorbable intrapleural air increases with each inspiration because of the 1-way valve
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effect. In addition to this mechanism, the positive pressure used with mechanical ventilation
therapy can cause air trapping. As a result, pressure rises within the affected hemithorax.
As the pressure increases, the ipsilateral lung collapses and causes hypoxia. Further
pressure build-up causes the mediastinum to shift toward the contralateral side and impinge on
and compress both the contralateral lung and the vasculature entering the right atrium of the
heart. Hypoxia results as the collapsed lung on the affected side and the compressed lung on
the contralateral side compromise effective gas exchange. This hypoxia and decreased venous
return caused by compression of the relatively thin walls of the atria impair cardiac function.
The inferior vena cava is thought to be the first to kink and restrict blood flow back to the
heart. It is most evident in trauma patients who may be hypovolemic with reduced venous blood
return to the heart.
Arising from numerous causes, this condition rapidly progresses to respiratory
insufficiency, cardiovascular collapse, and, ultimately, death if unrecognized and untreated.
Classification
1. Unilateral.
2. Bilateral.
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1. Closed.
2. Open.
3. Valvular.
The closed pneumothorax is the complication, which arises from the damage of visceral pleural membrane,
which results in entry of air in a pleural space and atelectasis of lung. In chest trauma the cause of occurrence
of the closed pneumothorax is the perforation of a visceral pleura and pulmonary tissue by the fragment of
fractured rib.
The open pneumothorax results from formation of hole in a chest wall at massive trauma and free entry of air
during inspiration inward a pleural space, and during expiration outward.
The valvular pneumothorax occurs at damage of a pulmonary tissue or chest wall with formation of the valve,
when the air during inspiration enters a pleural space, and during expiration, due to valve closure, does not
exits outside. It is the most dangerous form of pneumothorax, which results in a complete pulmonary collapse,
shift of mediastinum, inflection of major vessels and cardiac arrest.
The chief clinical manifestation of posttraumatic pneumothorax, which results from a pulmonary collapse, is
the rest dyspnea, which amplifies at a minor exertion. This sign arises due to atelectasis of lung and its
exclusion from breathing. On the background of collapsed lung only the main and lobar bronchi and pleural
space are ventilated. The oxygenation of blood in collapsed lungs does not occur, therefore the shunting of a
venous blood arise.
The chest pain is more characteristic manifestation for trauma with the damage of ribs, however pulmonary
collapse also can associate with a pain syndrome. Nevertheless the patients promptly adapt for it and the
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On the background of severe trauma of the chest the signs of damage dominate in clinical manifestation on
inappreciable entry of air in a pleural space. Pneumothorax mostly revealed during X-ray examination.
Progressing of air entry in a pleural space and pulmonary collapse cause the respiratory lag on affected side.
By palpation the vocal fremitus is absent. It indicates the origin of the complication rib fracture.
Percussion obtains bandbox sound, or pulmonary sound with tympanitis. By auscultation - weak or absent
breathing sounds, sometimes amphoric respiration. The expressiveness of clinical pattern depends on degree
of a pulmonary collapse.
Pulmonary atelectasis and presence of air in a pleural space are the X-ray findings that enable to establish the
final diagnosis.
Right-side pneumothorax
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pneumothorax.
Spontaneous and iatrogenic pneumothorax
Despite descriptions of Valsalva maneuvers and increased intrathoracic pressures as
inciting factors, spontaneous pneumothorax usually develops at rest. By definition,
spontaneous pneumothorax is not associated with trauma or stress. Symptoms of iatrogenic
pneumothorax are similar to those of a spontaneous pneumothorax and, depend on the age of
the patient, the presence of underlying lung disease, and the extent of the pneumothorax.
Until a bleb ruptures and causes pneumothorax, no clinical signs or symptoms are
present in primary spontaneous pneumothorax (PSP). Young and otherwise healthy patients
can tolerate the main physiologic consequences of a decrease in vital capacity and partial
pressure of oxygen fairly well, with minimal changes in vital signs and symptoms, but those
with underlying lung disease may have respiratory distress. The most common underlying
abnormality in secondary spontaneous pneumothorax is chronic obstructive pulmonary disease
(COPD), and cystic fibrosis carries one of the highest associations, with more than 20%
reporting spontaneous pneumothorax.
In one series, acute onset of chest pain and shortness of breath were present in all
patients in one series; typically, both symptoms are present in 64-85% of patients. The chest
pain is described as severe and/or stabbing, radiates to the ipsilateral shoulder and increases
with inspiration (pleuritic). In PSP, chest often improves over the first 24 hours, even without
resolution of the underlying air accumulation. Well-tolerated primary pneumothorax can take
12 weeks to resolve. In secondary pneumothorax (SSP), the chest pain is more likely to persist
with more significant clinical symptoms.
Shortness of breath/dyspnea in PSP is generally of sudden onset and tends to be more
severe with secondary spontaneous pneumothoraces (SSPs) because of decreased lung reserve.
Anxiety, cough, and vague presenting symptoms (eg, general malaise, fatigue) are less
commonly observed.
A history of previous pneumothorax is important, as recurrence is common, with rates
reported between 15% and 40%. Up to 15% of recurrences can be on the contralateral side.
Secondary pneumothoraces are often more likely to recur, with cystic fibrosis carrying the
highest recurrence rates at 68-90%. No study has shown that the number or size of blebs and
bullae found in the lung can be used to predict recurrence.
Signs and symptoms of tension pneumothorax are usually more impressive than those
seen with a simple pneumothorax, and clinical interpretation of these is crucial for diagnosing
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and treating the condition. Unlike the obvious patient presentations oftentimes used in medical
training courses to describe a tension pneumothorax, actual case reports include descriptions of
the diagnosis of the condition being missed or delayed because of subtle presentations that do
not always present with the classically described clinical findings of this condition.
Symptoms of tension pneumothorax may include chest pain (90%), dyspnea (80%),
anxiety, fatigue, or acute epigastric pain (a rare finding).
2. Physical examination.
The general appearance of the patient with pneumothorax may vary from asymptomatic
to respiratory distress. It may include diaphoresis, splinting chest wall to relieve pleuritic pain,
and cyanosis (in the case of tension pneumothorax). Findings on lung auscultation also vary
depending on the extent of the pneumothorax. Affected patients may also reveal altered mental
status changes, including decreased alertness and/or consciousness (a rare finding).
Respiratory findings may include the following:
Respiratory distress (considered a universal finding) or respiratory arrest
Tachypnea (or bradypnea as a preterminal event)
Asymmetric lung expansion: A mediastinal and tracheal shift to the contralateral
side can occur with a large tension pneumothorax.
Distant or absent breath sounds: Unilaterally decreased or absent lung sounds is a
common finding, but decreased air entry may be absent even in an advanced state
of the disease.
Lung sounds transmitted from the unaffected hemithorax are minimal with
auscultation at the midaxillary line
Hyperresonance on percussion: This is a rare finding and may be absent even in
an advanced state of the disease.
Decreased tactile fremitus
Adventitious lung sounds (crackles, wheeze; an ipsilateral finding)
Cardiovascular findings may include the following:
Tachycardia: This is the most common finding. If the heart rate is faster than 135
beats per minute (bpm), tension pneumothorax is likely.
Pulsus paradoxus
Hypotension: This should be considered as an inconsistently present finding;
although hypotension is typically considered a key sign of a tension
pneumothorax, studies suggest that hypotension can be delayed until its
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Although expiratory images are thought to better depict subtle pneumothoraces (the
volume of the pneumothorax is constant and hence proportionally higher on expiratory
images), a randomized controlled trial revealed no difference in the ability of radiologists to
detect pneumothoraces on inspiratory and expiratory images after procedures with the potential
to cause pneumothoraces.
4. Thoracentesis.
5. ECG.
6. Chest CT Scanning
Computed tomography (CT) scanning is the most reliable imaging study for the
diagnosis of pneumothorax, but it is not recommended for routine use in pneumothorax. This
imaging modality can help to accomplish the following:
Distinguish between a large bulla and a pneumothorax
Indicate underlying emphysema or emphysemalike changes (ELCs)
Determine the exact size of the pneumothorax, especially if it is small
Confirm the diagnosis of pneumothorax in patients with head trauma who are
mechanically ventilated
Detect occult/small pneumothoraces and pneumomediastinum (although the
clinical significance of these occult pneumothoraces is unclear, particularly in the
stable nonintubated patient)
CT scanning is widely used in actual clinical practice to assess the possibility of
associated concurrent pulmonary disease because of the inherent superiority of CT scans to
visualize the details of lung parenchyma and pleura, as can be seen in the images below.
When performed on primary spontaneous pneumothorax patients, CT detects multiple
blebs and bullae in the setting of negative chest radiographic findings. This may not impact
management, as there has been no correlation between number of blebs and recurrence.
However, CT scanning may have a role in secondary spontaneous pneumothorax, especially to
differentiate from giant bullous emphysema.
CT scanning can detect occult pneumothorax in patients who will require mechanical
ventilation in trauma and emergency surgery settings. This modality has also been shown to be
more sensitive than radiography for hemothorax and pulmonary contusion.
Collapse of the lung, air in the pleural cavity, and deviation of mediastinal structures are
present in tension pneumothorax.
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Treatment
A chest trauma, which complicated by pneumothorax with a partial pulmonary collapse (to 1/3 of volume) is
indication to aspiration of air by means of thoracentesis. The cases, if the negative pressure in a pleural space
is not obtained, and also subtotal, and total pneumothorax require closed drainage of a pleural space.
Under the local anesthesia by solution of novocaine in intercostal space in the midclavicular line by means
of a trocar in a pleural space inserted a plastic tube, which fixed to skin. The drainage connects to aspirative
system or according to method of Bulau. In the majority of patients the pneumothorax liquidates in some
hours, or during 1-2 days.
The absence of effect (incomplete expansion of lung) of active aspiration, and also valvular closed
pneumothorax is the indications to operative management suturing of the pulmonary wound. In some cases
a segmental resection of lung, or lobectomy is carried out.
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treatment of tube thoracostomy. The catheter is left in place until the chest tube is placed.
Needle Aspiration
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intercostal space.
Insert a large-bore Angiocath (14-gauge in an adult, 18- or 20-gauge in an infant)
or ready-to-use aspiration kit into the chosen intercostal space over the top of the
rib and perpendicular to the chest wall.
For simple needle aspiration, withdraw air once the pleural cavity is entered, and
when resistance is felt, withdraw the needle.
For catheter aspiration, once the pleural cavity is entered, a soft pigtail catheter is
advanced over the needle into the pleural space. A scalpel may be necessary to
enlarge the entry site at the skin. Remove the needle once the pleural cavity is
entered, and attach the catheter to a 3-way stopcock and large syringe (eg, 60-mL
syringe) to evacuate air.
When no more air can be aspirated (discontinue if resistance is felt, if the patient
coughs excessively, or if more than 2.5 L is aspirated) or the patient suddenly
coughs, the lung most likely has reexpanded.
Close the stopcock, and secure the catheter to the chest wall.
Obtain a chest radiograph to assess the degree of success, and obtain another
radiograph 4 hours later to confirm the absence of recurring accumulation.
If no recurrence is present, remove the catheter and massage the insertion site with
sterile gauze to seal the channel into the pleural space.
Discharge the patient with appropriate return instructions. (Some authors suggest
observation for an additional 2 h after catheter removal.)
If the pneumothorax persists, attach a Heimlich valve or a water seal and admit the
patient.
Potential complications associated with needle aspiration includes pneumothorax (with
potential to later tension pneumothorax), cardiac tamponade, hemorrhage (which can be life
threatening), loculated intrapleural hematoma, atelectasis, pneumonia, arterial air embolism
(when needle thoracostomy is performed and no tension pneumothorax is present), and pain to
the patient.
Tube Thoracostomy
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of anchoring and closure techniques exist, all of which are probably equivalent
Obtain a follow-up chest x-ray to assess tube positioning and lung reexpansion.
Complications of tube thoracostomy include death, injury to lung or mediastinum,
hemorrhage (usually from intercostal artery injury), neurovascular bundle injury, infection,
bronchopleural fistula, and subcutaneous or intraperitoneal tube placement.
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HEMOTHORAX
Accumulation of blood within the chest, or hemothorax, is a relatively common problem,
most often resulting from injury to intrathoracic structures or the chest wall. Hemothorax
unrelated to trauma is considerably less common and can result from various causes. Prompt
identification and treatment of traumatic hemothorax is an essential part of the care of the
injured patient. In cases of hemothorax unrelated to trauma, a careful investigation for the
underlying source must be performed while treatment is occurring.
Pathophysiology
Bleeding into the pleural space can occur with virtually any disruption of the tissues of
the chest wall and pleura or the intrathoracic structures.
The physiologic response to the development of a hemothorax is manifested in 2 major
areas: hemodynamic and respiratory. The degree of hemodynamic response is determined by the
amount and rapidity of blood loss.
Normal respiratory movement may be hampered by the space-occupying effect of a large
accumulation of blood within the pleural space. In trauma cases, abnormalities of ventilation
and oxygenation may result, especially if associated with injuries to the chest wall. In some
cases of nontraumatic origin, especially those associated with pneumothorax and a limited
amount of bleeding, respiratory symptoms may predominate.
Hemodynamic changes vary depending on the amount of bleeding and the rapidity of
blood loss. Blood loss of up to 750 mL in a 70-kg man should cause no significant
hemodynamic change. Loss of 750-1500 mL in the same individual will cause the early
symptoms of shock, ie, tachycardia, tachypnea, and a decrease in pulse pressure.
Significant signs of shock with signs of poor perfusion occur with loss of blood volume
of 30% or more (1500-2000 mL). Because the pleural cavity of a 70-kg man can hold 4 or more
liters of blood, exsanguinating hemorrhage can occur without external evidence of blood loss.
Blood occupying the pleural cavity takes up space that the lung would fill in normal
respiratory excursion. A large enough collection causes the patient to complain of dyspnea and
may produce the clinical finding of tachypnea. The volume of blood required to produce these
symptoms in a given individual varies depending on a number of factors, including organs
injured, severity of injury, and underlying pulmonary and cardiac reserve.
Dyspnea is a common symptom in cases in which hemothorax develops in an insidious
manner, such as those secondary to metastatic disease. Blood loss in such cases is not acute as
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to produce a visible hemodynamic response, and dyspnea is often the predominant complaint.
Two pathologic states are associated with the later stages of hemothorax. These include
empyema and fibrothorax.
Empyema results from bacterial contamination of the retained hemothorax. If undetected
or improperly treated, this can lead to bacteremia and septic shock.
Fibrothorax results when fibrin deposition develops in an organized hemothorax and
coats both the parietal and visceral pleural surfaces, trapping the lung. The lung is fixed in
position by this adhesive process and is unable to fully expand. Persistent atelectasis of
portions of the lung and reduced pulmonary function result from this process.
Classification
. According to extent:
1. Unilateral.
2. Bilateral.
1. Coagulated.
2. No- coagulated.
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1. Not infected.
2. Infected (suppurative).
If hemothorax is the complication of blunt chest trauma, the clinical manifestations depend on the gravity of
trauma and degree of hemorrhage. Also hemothorax by itself results in pulmonary compression and shift of
mediastinum.
In case of small hemothorax clinical manifestations of hemorrhage are slightly expressed or absent at all.
Dyspnea, cough, general malaise and dizziness are obvious in moderate hemothorax. The skin is pale. The
hemodynamic disturbances tachycardia and decreased arterial pressure are observed.
The great and total hemothorax are associated with extremely grave condition. The patients are troubled with
expressed general malaise, dizziness, dyspnea and difficult breathing. In some cases they enter medical
hospitals in a terminal state. The skin is sharply pale. The peripheral pulse impaired or absent. Tachycardia,
weak cardiac tones, low arterial pressure are obvious.
By percussion the dullness is revealed. On auscultation - the breathing over the site of hemothorax is sharply
diminished or is not heard.
The X-ray picture of hemothorax is rather specific. The intensive homogeneous shadow on the side of the
lesion with oblique upper contour (Damuaso' line) is observed. The costal sinus does not visualized. In small
hemothorax, depending on the degree of intrapleural bleeding, the shadow observed only in the region of
sinus. In moderate hemothorax it achieves a scapular angle (on the back surface) or V rib on anterior surface
of the chest wall. In great hemothorax this shadow achieves rib, and total hemothorax characterized by
complete shadow of a pleural space, and in some cases mediastinal shift to the healthy side.
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2. Physical examination.
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Symptoms and physical findings associated with hemothorax in trauma vary widely
depending on the amount and rapidity of bleeding, the existence and severity of underlying
pulmonary disease, the nature and degree of associated injuries, and the mechanism of injury.
Hemothorax is rarely a solitary finding in blunt trauma. Associated chest wall or
pulmonary injuries are nearly always present.
Simple bony injuries consisting of one or multiple rib fractures are the most common
blunt chest injuries. A small hemothorax may be associated with even single rib fractures but
often remains unnoticed during the physical examination and even after chest radiography.
Such small collections rarely need treatment.
Complex chest wall injuries are those in which either 4 or more sequential single rib
fractures are present or a flail chest exists. These types of injuries are associated with a
significant degree of chest wall damage and often produce large collections of blood within the
pleural cavity and substantial respiratory impairment. Pulmonary contusion and pneumothorax
are commonly associated injuries. Injuries resulting in laceration of intercostal or internal
mammary arteries may produce a hemothorax of significant size and significant hemodynamic
compromise. These vessels are the most common source of persistent bleeding from the chest
after trauma.
Delayed hemothorax can occur at some interval after blunt chest trauma. In such cases,
the initial evaluation, including chest radiography, reveals findings of rib fractures without any
accompanying intrathoracic pathology. However, hours to days later, a hemothorax is seen. The
mechanism is believed to be either rupture of a trauma-associated chest wall hematoma into the
pleural space or displacement of rib fracture edges with eventual disruption of intercostal
vessels during respiratory movement or coughing.
Large hemothoraces are usually related to injury of vascular structures. Disruption or
laceration of major arterial or venous structures within the chest may result in massive or
exsanguinating hemorrhage.
Hemodynamic manifestations associated with massive hemothorax are those of
hemorrhagic shock. Symptoms can range from mild to profound, depending on the amount and
rate of bleeding into the chest cavity and the nature and severity of associated injuries.
Because a large collection of blood will compress the ipsilateral lung, related respiratory
manifestations include tachypnea and, in some cases, hypoxemia.
A variety of physical findings such as bruising, pain, instability or crepitus upon
palpation over fractured ribs, chest wall deformity, or paradoxical chest wall movement may
lead to the possibility of coexisting hemothorax in cases of blunt chest wall injury. Dullness to
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percussion over a portion of the affected hemithorax is often noted and is more commonly
found over the more dependent areas of the thorax if the patient is upright. Decreased or absent
breath sounds upon auscultation are noted over the area of hemothorax.
The upright chest radiograph is the ideal primary diagnostic study in the evaluation of
hemothorax.
In the normal unscarred pleural space, a hemothorax is noted as a meniscus of fluid
blunting the costophrenic angle or diaphragmatic surface and tracking up the pleural margins of
the chest wall when viewed on the upright chest x-ray film. This is essentially the same chest
radiographic appearance found with any pleural effusion.
In cases in which pleural scarring or symphysis is present, the collection may not be free
to occupy the most dependent position within the thorax, but will fill whatever free pleural
space is available. This situation may not create the classic appearance of a fluid layer on a
chest x-ray film.
As much as 400-500 mL of blood is required to obliterate the costophrenic angle as seen
on an upright chest radiograph.
In the acute trauma setting, the portable supine chest radiograph may be the first and
only view available from which to make definitive decisions regarding therapy. The presence
and size of a hemothorax is much more difficult to evaluate on supine films. As much as 1000
mL of blood may be missed when viewing a portable supine chest x-ray film. Only a general
haziness of the affected hemithorax may be noted.
In blunt trauma cases, hemothorax is frequently associated with other chest injuries
visible on the chest radiograph, such as rib fractures (see below), pneumothorax, or a widening
of the superior mediastinum.
Additional studies such as ultrasonography or CT scan may sometimes be required for identification
and quantification of a hemothorax noted on a plain chest radiograph
4. Thoracentesis.
6. Test by Revilour-Greguar.
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The coagulated hemothorax. The patient's late apply for medical aid or major bleeding results in formation of
clots in a pleural space, and in some cases all blood, which has accumulated in a pleural space, forms by itself
a major entire clot.
Depending on degree of bleeding and, consequently, size of clot, the patients complain of chest pain, which
intensifies at respiration, dyspnea, general malaise, and dizziness. As a rule, on 3-5 day the fever to 37,5-38
is observed.
The physical findings (diminishing and absence of vocal fremitus by palpation, dullness by percussion and
sharply diminished or absent breathing by auscultation) suggest the presence of pathological process in a
pleural space.
Chest roentgenogram reveals the intensive shadow, sometimes heterogeneous (with enlightenments and
multiple levels).
The needle aspiration obtains small amount of a liquid hemolyzed blood and small bloody thrombi (according
to inner diameter of the needle).
Suppurative hemothorax. The coagulated hemothorax in overwhelming majority is infected, that results in
occurrence of a pleural empyema (clinical manifestations, diagnostics and treatment look in chapter " pleural
empyema").
Treatment
A treatment of small hemothorax requires needle aspiration or drainage of pleural space and elimination of
blood. The manipulation is carried out in V-V intercostal spaces in the postaxillary or scapular lines.
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Total, great or moderate hemothorax with persistent bleeding (positive test by Revilour-Greguar) requires
thoracotomy for liquidation of a bleeding source.
The bleeding wounds of lungs are sewed up by twist suture. If the pleural space contains liquid blood, the
surgeon carries out its reinfusion. The clots are removed from pleural space.
Tube thoracostomy drainage is the primary mode of treatment for hemothorax. In adult
patients, large-bore chest tubes, usually 36-42F, should be used to achieve adequate drainage in
adults. Smaller-caliber tubes are more likely to occlude. In pediatric patients, chest tube size
varies with the size of the child. In patients older than 12 years, the chest tube size used is
usually the same as that for adults. In smaller children, a 24-34F chest tube should be used,
depending on the size of the child.
Thoracostomy tube placement for hemothorax should ideally be in the sixth or seventh
intercostal space at the posterior axillary line. In the supine trauma victim, a common error in
chest tube insertion is placement too anteriorly and superiorly, making complete drainage very
unlikely.
After tube thoracostomy is performed, a repeat chest radiograph should always be
obtained. This helps identify chest tube position, helps determine completeness of the
hemothorax evacuation, and may reveal other intrathoracic pathology previously obscured by
the hemothorax. If drainage is incomplete as visualized on the postthoracostomy chest
radiograph, placement of a second drainage tube should be considered. Preferably, a video-
assisted thoracic surgery (VATS) operative procedure should be undertaken to evacuate the
pleural space.
In cases of hemopneumothorax, 2 chest tubes may be preferred, with the tube draining
the pneumothorax placed in a more superior and anterior position.
Surgical exploration in cases of traumatic hemothorax should be performed in the
following circumstances:
Greater than 1000 mL of blood is evacuated immediately after tube thoracostomy. This is
considered a massive hemothorax.
Bleeding from the chest continues, defined as 150-200 mL/h for 2-4 hours.
Persistent blood transfusion is required to maintain hemodynamic stability.
In the majority of trauma cases requiring chest exploration, the bleeding source is from
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the chest wall, most commonly intercostal or internal mammary arteries. Once identified, these
can be easily controlled with suture ligatures in most cases. After control of obvious bleeding
and evacuation of clot and blood, a rapid but thorough exploration of the entire chest cavity
should be performed.
Unstable rib fractures found at the time of surgery may require some debridement of
sharp rib edges to prevent further injury to the lung or adjacent chest wall structures. At some
centers, flail segments or extensive rib fractures are stabilized with wires or other types of
support in an attempt to improve postoperative chest wall mechanics.
A thoracic surgeon should be present or immediately available at the time of emergency
thoracic exploration because control of bleeding from difficult areas such as the hilum of the
lung, the heart, or the great vessels may require a surgeon with expertise in that field.
Adequate drainage of the chest after control of bleeding is very important. Because chest
drainage tubes are placed under direct vision, the complication of retained hemothorax should
occur with extreme infrequency. A minimum of 2 large-bore chest tubes should be used, with
one positioned posteriorly and the other positioned anteriorly. Some surgeons prefer the
addition of a right-angled chest tube positioned over the diaphragm.
The late sequelae of hemothorax, including residual clot, infected collections, and
trapped lung, require additional treatment and, most often, surgical intervention.
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SUBCUTANEOUS EMPHYSEMA
The cause of this complication of blunt chest trauma is the damage by edge of the broken rib of parietal and
visceral pleural membranes with the following entering of air from a pulmonary tissue into a pleural space and
through damaged chest wall (ruptured intercostal muscles) into subcutaneous fat.
In overwhelming majority the subcutaneous emphysema is the outcome of a valvular pneumothorax and
pneumothorax in obliterated pleural space.
Classification
1. Localized.
2. Widespread.
3. Total.
As the subcutaneous emphysema is the outcome of trauma complicated by a rib fracture and posttraumatic
pneumothorax, the chief complaints are of chest pain and dyspnea, which intensify at respiration, movements
and minor physical activity.
In localized subcutaneous emphysema the patients the complaints of the chest trauma are predominant in
symptomatology. On examination observed a swelling of a chest wall in the place of damage. By palpation a
subcutaneous crepitation is felt over this region. Percussion reveals a bandbox sound or tympanitis.
Auscultation of lungs over subcutaneous emphysema is usually impossible.
The widespread and total subcutaneous emphysema represents a serious moral problem for the patient. Owing
to extent of air all over the chest, abdominal wall, neck (wide-spread emphysema), and also face, arms and
legs (total emphysema), the patients has a specific appearance: swelling face, thick neck, enlargement of the
chest, arms, and legs. Subcutaneous emphysema by itself usually causes no respiratory and cardiovascular
disturbances. However the patients note the change of the quality of voice. By palpation the subcutaneous
emphysema is felt in whole body ("crisping snow").
It is necessary to note, that in widespread and total emphysema the auscultation is impossible. However the
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presence of subcutaneous emphysema at the closed trauma of the chest enables to suspect the presence of
posttraumatic pneumothorax.
On the chest roentgenogram the enlightenment of a subcutaneous fat (presence of air) is observed.
Subcutaneous emphysema
2. Physical findings.
3. Chest X-radiography.
Treatment
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Widespread and total subcutaneous emphysema requires the draining of subcutaneous space by plastic tubes
in infra- and supraclavicular region, and also in the zone of the most expressed emphysema. Also performed
the drainage of a pleural space.
The subcutaneous emphysema resolves depending on its extent from several days to 2-3,5 weeks.
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The isolated injuries of trachea and bronchi as the result of blunt trauma of the chest occur rarely and located
mainly in a cervical part.
1) shearing forces, which arises at the moment of trauma owing to a sudden rise of intraluminal
pressure against a closed glottis when the airway is compressed against the spine.;
3) shift of lungs in sudden and rapid deceleration or acceleration of a body occurs with greater
amplitude, than fixed bifurcation of trachea.
Such disruptions most often occurs as a result of vehicular impacts, falls from great heights, direct blows to
the chest. In most cases disruption of trachea and bronchi are accompanied with the other visceral damages:
lungs, skull and brain, heart, liver and flail chest.
Classification
1. Partial:
3. Complete transverse disruption of all walls without disjunction of the of trachea, (bronchus)
(V degree).
1. Longitudinal.
2. Oblique.
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3. Transversal.
4. Mixed.
1. Tracheo-laryngeal.
2. Cervico-tracheal.
3. Mediastino-bronchial.
4. Bifurcational.
5. Bronchial.
3. Damage of a trachea (bronchi). adjacent organs and other segments of the body.
The clinical manifestations of the injury of trachea depend on the type of disruption, its degree and presence
of concomitant damages.
Incomplete isolated disruption of trachea commonly manifests by cough and hemoptysis. Respiration is not
disturbed as a rule.
The small disruptions are characterized by various clinics. If the hole is occluded by clot and mediastinal
tissues, the signs, which had appeared earlier (cough, hemoptysis, mediastinal emphysema), can disappear.
Nevertheless the repeated occurrence of cough, as a rule, leads to severe aggravation of the patient state.
Major and circular disruptions of trachea cause a grave state of the patients. They manifest except difficult
breathing by such signs:
2) compression syndrome compression and inflection of major vessels due to tension pneumothorax
or mediastinal emphysema with transmission into acute cardiopulmonary failure;
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3) hemorrhage syndrome;
4) aspiration syndrome, which is the outcome of bleeding into airways or aspirations of the gastric
content;
5) traumatic shock.
The injuries of bronchi occur in the way of abruption of main bronchi or their disruption in the zone of
bifurcation. In the zone of a tracheal bifurcation observed multiple (2-4) disruptions, which can be
longitudinal, transversal or oblique.
Depending on the character of trauma, it is necessary to distinguish direct and secondary disruptions of
bronchi. The direct injuries arise from the gunshot and knife wounds, penetration of rib fragments or other
subjects in mediastinum or endoscopic manipulations.
The overwhelming majority of bronchial disruption is the part of blunt trauma of the chest. By the way, the
damage of vessels of a lung root occurs in 41,3 %.
The predominant clinical signs of a bronchial disruption are the respiratory disturbance, gas syndrome,
hemoptysis and hemothorax. However these signs may be observed only in isolated injuries of lungs.
The patients state is grave. Rest dyspnea and acute pain behind a breastbone are the most troubling
manifestations. The difficult swallowing, hoarseness, swelling face and subcutaneous crepitation are
observed. Auscultatory on the side of trauma the breathing sounds are weak or absent at all.
The sequence of examination of the patients with injuries of trachea and bronchi depends on the character
and gravity of trauma, clinical signs and concomitant damages, which threatening life.
If the state of the patient allows, a chest X-radiography is performed. Commonly it is possible to find out
mediastinal emphysema, sometimes the sign of discontinuing of trachea.
The injuries of bronchi manifest by the distension of mediastinum and presence of air strips along its borders,
and in some cases total or tension pneumothorax observed.
Final and most informative diagnostic method is the tracheobronchoscopy, which can be also the therapeutic
method. However it is necessary to carry out decompression of a mediastinal emphysema and pneumothorax
before such investigation.
Before examination the clots and liquid blood are aspirated from airways, then adjusted the localization and
character of disruption. The incomplete disruptions are usually longitudinal and oblique and located on the
line of membranous and cartilaginous part, circular mainly in a cervical part of trachea. Except disruption of
the wall, observed the absence of cartilaginous rings in this region and filled by blood parabronchial fat.
The open damages of trachea take place mainly in a cervical part and rarely - in thoracic. In all cases of neck
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trauma it is necessary always suspect the opportunity of damage of trachea and esophagus.
1. The initial stage (lasts during 2 days after the trauma with typical signs of disruption; the urgent
resuscitation measures are required).
2. The stage of temporary compensation (lasts during 2 weeks; at this time it is possible to carry out
diagnostic examination).
3. The stage of persistent compensation (lasts during 30 days; during this time a stenosis and other
persistent complications of disruption of trachea and bronchi develops).
2. Physical findings.
3. Chest X-radiography.
4. Diagnostic thoracentesis.
7. Tracheobronchoscopy.
8. Tomography.
Treatment
There are primary operations in acute stage (first two days after the trauma) and late repairing operations (in
1 month after the trauma). The operation is based in resection of injured tissues, edges of bronchus with the
further suturing of disruption, or wedge-like or circular resection with following anastomosis. In series of
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MEDIASTINAL EMPHYSEMA
Mediastinal emphysema is the complication of the blunt trauma of the chest, which is characterized by
entering and accumulation of air in mediastinum.
The causes of mediastinal emphysema is partial (damage of a membranous part) or complete disruptions of
trachea, bronchi, esophagus and in some cases tension pneumothorax.
The entry of air in mediastinum leads to compressing of superior cava vein and right atrium, which results in
the expressed discirculation.
The patients complain of difficult breathing and swallowing, pain behind breastbone, hoarseness, cough
attacks. As a rule, the patient's position is forced semi-sitting. The neck and face are thickened, cervical
veins distended, the skin is cyanotic. By palpation the crepitation of neck, face, and shoulder area. By
auscultation heart tones are diminished with tachycardia.
On X-ray film on the background of enlightenment observed well-defined contour of a mediastinal pleura. If
there is the damage of mediastinal pleural membrane a pneumothorax (mainly total or intense) is revealed.
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2. Physical findings.
6. ECG.
Progressing mediastinal emphysema requires the urgent drainage of a forward mediastinum in order to
prevent external cardiac tamponade.
Tension mediastinal emphysema resulting from disruption of trachea or bronchus operative management,
pneumothorax, etc., requires the treatment, which is described in previous chapters.
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SHOCK
Circulatory shock, commonly known as just shock, is a serious, life-threatening medical
condition where insufficient blood flow reaches the body tissues. As the blood carries oxygen
and nutrients around the body, reduced flow hinders the delivery of these components to the
tissues, and can stop the tissues from functioning properly. The process of blood entering the
tissues is called perfusion, so when perfusion is not occurring properly this is called a
hypoperfusional (hypo = below) state.
Circulatory shock should not be confused with the emotional state of shock, as the two
are not related. Medical shock is a life-threatening medical emergency and one of the most
common causes of death for critically-ill people. Shock can have a variety of effects, all with
similar outcomes, but all relate to a problem with the body's circulatory system. For example,
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shock may lead to hypoxemia (a lack of oxygen in arterial blood) or cardiac arrest (the heart
stopping
Fig. Classes of hemorragical shock
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perfusion[1]. If the bowel becomes sufficiently ischemic, bacteria may enter the blood stream,
resulting in the increased complication of endotoxic shock[1].
Refractory (Irreversible)
At this stage, the vital organs have failed and the shock can no longer be reversed. Brain
damage and cell death have occurred. Death will occur imminently.
A medical emergency is an injury or illness that is acute and poses an immediate risk to a
person's life or long term health. These emergencies may require assistance from another
person, who should ideally be suitably qualified to do so, although some of these emergencies
can be dealt with by the victim themselves. Dependent on the severity of the emergency, and the
quality of any treatment given, it may require the involvement of multiple levels of care, from a
first aider to an emergency physician through to specialist surgeons.
Any response to an emergency medical situation will depend strongly on the situation,
the patient involved and availability of resources to help them. It will also vary depending on
whether the emergency occurs whilst in hospital under medical care, or outside of medical care
(for instance, in the street or alone at home).
For emergencies starting outside of medical care, a key component of providing proper
care is to summon the emergency medical services (usually an ambulance), by calling for help
using the appropriate local emergency telephone number, such as 999, 911, 112 or 000 or 111.
After determining that the incident is a medical emergency (as opposed to, for example, a
police call), the emergency dispatchers will generally run through a questioning system such as
AMPDS in order to assess the priority level of the call, along with the caller's name and
location.
Those trained to perform first aid can act within the bounds of the knowledge they have,
whilst awaiting the next level of definitive care. Those who are not able to perform first aid can
also assist by remaining calm and staying with the injured or ill person. A common complaint
of emergency service personnel is the propensity of people to crowd around the scene of victim,
as it is generally unhelpful, making the patient more stressed, and obstructing the smooth
working of the emergency services. If possible, first responders should designate a specific
person to ensure that the emergency services are called. Another bystander should be sent to
wait for their arrival and direct them to the proper location. Additional bystanders can be
helpful in ensuring that crowds are moved away from the ill or injured patient, allowing the
responder adequate space to work.
Many states of the USA have "Good Samaritan Laws" which protect civilian responders
who choose to assist in an emergency. Responders acting within the scope of their knowledge
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and training as a "reasonable person" in the same situation would act are often immune to
liability in emergency situations. Usually, once care has begun, a first responder or first aid
provider may not leave the patient or terminate care until a responder of equal or higher
training (e.g., fire department or emergency medical technicians) assumes care. This can
constitute abandonment of the patient, and may subject the responder to legal liability. Care
must be continued until the patient is transferred to a higher level of care, the situation
becomes too unsafe to continue, or the responder is physically unable to continue due to
exhaustion or hazards.
The principles of the chain of survival apply to medical emergencies where the patient
has an absence of breathing and heartbeat. This involves the four stages of Early access, Early
CPR, Early defibrillation and Early advanced life support
Unless the situation is particularly hazardous, and is likely to further endanger the
patient, evacuating an injured victim requires special skills, and should be left to the
professionals of the emergency medical and fire service.
Within hospital settings, an adequate staff is generally present to deal with the average
emergency situation. Emergency medicine physicians have training to deal with most medical
emergencies, and maintain CPR and ACLS certifications. In disasters or complex emergencies,
most hospitals have protocols to summon on-site and off-site staff rapidly.
Both emergency room and inpatient medical emergencies follow the basic protocol of
Advanced Cardiac Life Support. Irrespective of the nature of the emergency, adequate blood
pressure and oxygenation are required before the cause of the emergency can be eliminated.
Possible exceptions include the clamping of arteries in severe hemorrhage.
While the golden hour (medicine) is a trauma treatment concept, two emergency medical
conditions have well-documented time-critical treatment considerations: stroke and myocardial
infarction (heart attack). In the case of stroke, there is a window of three hours within which
the benefit of clot-busting drugs outweighs the risk of major bleeding. In the case of a heart
attack, rapid stabilization of fatal arrhythmias can prevent sudden cardiac death. In addition,
there is a direct relationship between time-to-treatment and the success of reperfusion
(restoration of blood flow to the heart), including a time dependent reduction in the mortality
and morbidity.In 1972 Hinshaw and Cox suggested the following classification which is still
used today.[2] It uses four types of shock: hypovolemic, cardiogenic, distributive and
obstructive shock:[3][4][5][8][10]
Hypovolemic shock This is the most common type of shock and based on insufficient
circulating volume. Its primary cause is loss of fluid from the circulation from either an internal
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or external source. An internal source may be haemorrhage. External causes may include
extensive bleeding, high output fistulae or severe burns.
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DIAPHRAGMATIC HERNIAS
Diaphragmatic hernia represents herniation of abdominal organs through natural openings of diaphragm, its weak places or ruptures.
A hiatal hernia occurs when a portion of the stomach prolapses through the diaphragmatic esophageal hiatus. Although the
existence of hiatal hernia has been described in earlier medical literature, it has come under scrutiny only in the last century or so
because of its association with gastroesophageal reflux disease (GERD) and its complications. There is also an association between
obesity and the presence of hiatal hernia. By far, most hiatal hernias are asymptomatic and are discovered incidentally. On rare
occasion, a life-threatening complication, such as gastric volvulus or strangulation, may present acutely.
The cause of occurrence of congenital hernia is the disturbance of embryogenesis with transformation in anomaly of diaphragm. The acquired
diaphragmatic hernia more often arise owing to age-dependent involution of diaphragm, its ptosis in the people with a mainly sedentary mode of life,
increase of intraperitoneal pressure, obesity, cough, overfeeding, constipation, meteorism and pregnancy. The cause of sliding hernias can be draw of
esophagus upward in reflux esophagitis owing to intensive contraction of its longitudinal musculature.
Diaphragmatic hernias may be congenital or acquired. Acquired hiatal hernias are divided further into nontraumatic and
traumatic hernias. The most common types of hernias are those acquired in a nontraumatic fashion. Hernias acquired in a
nontraumatic fashion are divided into 2 types, (1) sliding hiatal hernia and (2) paraesophageal hiatal hernia. A mixed variety with
coexisting sliding and paraesophageal components is possible.
Sliding hiatal hernia by far is the most common type of hiatal hernia. It occurs when the gastroesophageal
junction, along with a portion of the stomach, migrates into the mediastinum through the esophageal hiatus (see the image
below). The majority of patients with demonstrated hiatal hernias are asymptomatic. This type of hernia interferes with the
reflux barrier mechanism in several ways. As the LES moves into the chest, it no longer is exposed to positive intra-
abdominal pressure and, therefore, is less effective as a sphincter. In fact, the sphincter moves into an area of low pressure,
which interferes with the sphincter activity. In addition, the widening hiatus affects the competence of the diaphragmatic
crura. The angle of His is lost, making regurgitation of gastric contents more likely. These changes not only predispose to
reflux of gastric contents into the esophagus, but also prolong the acid contact time with the epithelium of the esophagus.
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In paraesophageal hernia, also called rolling-type hiatal hernia, the widened hiatus permits the fundus of the
stomach to protrude into the chest, anterior and lateral to the body of the esophagus; however, the gastroesophageal junction
remains below the diaphragm (see Figure 3 of the image above). This causes the stomach to rotate in a counter-clockwise
direction. As the hiatus widens, increasing amounts of the greater curvature of the stomach and, sometimes, the gastric-colic
omentum, follow. The fundus eventually comes to lie above the gastroesophageal junction, with the pylorus being pulled
towards the diaphragmatic hiatus. In this type of hernia, the anatomic relation of the stomach to the lower end of the
esophagus (angle of His) tends to remain unchanged, so gross acid reflux does not occur.
Pathology
The esophagus passes through the diaphragmatic hiatus in the crural part of the diaphragm to reach the stomach. The
diaphragmatic hiatus itself is approximately 2 cm in length and chiefly consists of musculotendinous slips of the right and left
diaphragmatic crura arising from either side of the spine and passing around the esophagus before inserting into the central tendon
of the diaphragm. The size of the hiatus is not fixed, but narrows whenever intra-abdominal pressure rises, such as when lifting
weights or coughing.
The lower esophageal sphincter (LES) is an area of smooth muscle approximately 2.5-4.5 cm in length. The upper part of the
sphincter normally lies within the diaphragmatic hiatus, while the lower section normally is intra-abdominal. At this level, the
visceral peritoneum and the phrenoesophageal ligament cover the esophagus. The phrenoesophageal ligament is a fibrous layer of
connective tissue arising from the crura, and it maintains the LES within the abdominal cavity. The A-ring is an indentation
sometimes seen on barium studies, and it marks the upper part of the LES. Just below this is a slightly dilated part of the esophagus,
forming the vestibule. A second ring, the B-ring, may be seen just distal to the vestibule, and it approximates the Z-line or
squamocolumnar junction. The presence of a B-ring confirms the diagnosis of a hiatal hernia. Occasionally, the B-ring also is called
the Schatzki ring.
Any sudden increase in intra-abdominal pressure also acts on the portion of the LES below the diaphragm to increase the
sphincter pressure. An acute angle, the angle of His, is formed between the cardia of the stomach and the distal esophagus and
functions as a flap at the gastroesophageal junction and helps prevent reflux of gastric contents into the esophagus (see the image
below).
The gastroesophageal junction acts as a barrier to prevent reflux of contents from the stomach into the esophagus by a
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combination of mechanisms forming the antireflux barrier. The components of this barrier include the diaphragmatic crura, the LES
baseline pressure and intra-abdominal segment, and the angle of His. The presence of a hiatal hernia compromises this reflux barrier
not only in terms of reduced LES pressure but also reduced esophageal acid clearance. Patients with hiatal hernias also have longer
transient LES relaxation episodes particularly at night time. These factors increase the esophageal mucosa acid contact time
predisposing to esophagitis and related complications.
Frequency
Hiatal hernias are more common in Western countries. The frequency of hiatus hernia increases with age, from 10% in patients
younger than 40 years to 70% in patients older than 70 years.
Paraesophageal hernias generally tend to enlarge with time, and sometimes the entire stomach is found within the chest. The risk of
these hernias becoming incarcerated, leading to strangulation or perforation, is approximately 5%. This complication is potentially
lethal, and surgical intervention is necessary. Because of the high mortality associated with this condition, elective repair often is
advised wherever a paraesophageal hernia is found.
Classification
1) congenital;
2) acquired;
3) posttraumatic;
4) true;
5) false.
. Diaphragmatic hernia.
1) esophageal;
2) cardial;
3) cardiofundal.
1) fundal;
2) antral;
5) epiploic.
1) subtotal gastric;
2) total gastric.
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V. A short esophagus:
B. Parasternal hernias:
1) retrosternal;
2) retrocostosternal.
Esophageal hernias:
Esophageal
Cardiofundal
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Mixed paraesophageal
Paraesophageal fundal
The predominant manifestations resulting from sliding diaphragmatic hernia (about 90 % of diaphragmatic hernias) are the signs of gastroesophageal
reflux. It is characterized by the pain behind breastbone or epigastric region. It more often appears in supine position after meal or after intensive
physical exertion.
Heartburn is the second according to the frequency sign and caused by the injury of esophageal mucosa by gastric juice as a result in turn of
gastroesophageal reflux.
Belching by air, as a rule, observed, which commonly results in pain relief and decrease of arching feeling in epigastric region.
Regurgitation arises owing to gastroesophageal reflux, which reaches pharynx and oral cavity. More often observed regurgitation by gastric acid or bitter
liquid or food.
The sign of "lacing shoes" is expressed when the patient bends down after liquid food, and the latter is partially poured out into the mouth. It is caused
by incompetence of the lower esophageal sphincter (gastroesophageal junction).
Nausea and vomiting are rare. The latter some patients cause by themselves to achieve some relief.
Dysphagia is rarely observed. More often it is the outcome of complications of diaphragmatic hernia (esophageal stricture, malignancy).
Roentgenological signs: 1) the sign of "bell"; 2) blunt His angle; 3) lack of air bubble of the stomach.
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The clinical manifestations of paraesophageal, retrosternal or lumbocostal hernias basically depend on the character of organs, which the hernial sac
contents, and their compressing by hernial ring. Sometimes the clinical course even of major hernias is asymptomatic, and they are occasionally found
out during X-ray examinations. For the first time the disease can manifest under the influence of physical exertion, trauma, pregnancy, labors etc.
Paraesophageal hernia
The sliding hiatal hernia commonly has typical clinical course and rather rich symptomatology, which enable to establish the diagnosis with a great
degree of probability. Nevertheless occasionally gastroesophageal reflux as the sequel of a sliding hiatal hernia can result in misdiagnostics (stenocardia,
acute cholelithiasis etc.).
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The most often complications of sliding diaphragmatic hernia are gastric bleeding, peptic stricture of esophagus and malignancy.
The causes of the bleeding can be erosion and ulcers of stomach, which result from compression of the organ in esophageal hiatus. More often observed
small bleeding, but at long-stand recurrent course they result in chronic anemia. The profuse bleeding arise rarely. The strangulation of a sliding
diaphragmatic hernia never occurs.
Nevertheless for diaphragmatic hernias of other locations the most dangerous complication is naturally strangulation. Such pathology manifests by the
signs of s strangulation intestinal obstruction. However the correct diagnosis frequently possible to establish only during operation.
Hiatal hernias are relatively common and, in themselves, do not cause symptoms. For this reason, most people with hiatal
hernias are asymptomatic. Hiatal hernias may predispose to reflux or worsen existing reflux in a minority of individuals. Physicians
should resist the temptation to label hiatal hernia as a disease.
Patients can have reflux without a demonstrable hiatal hernia. When a hernia is present in a patient with symptomatic GERD,
the hernia may worsen symptoms for several reasons, including the hiatal hernia acting as a fluid trap for gastric reflux and
increasing the acid contact time in the esophagus. In addition, with a hiatal hernia, episodes of transient relaxation of the LES are
more frequent and the length of the high-pressure zone is reduced. The main symptoms of a sliding hiatal hernia are those
associated with reflux and its complications.
No clear correlation exists between the size of a hiatal hernia and the severity of the symptoms. A very large hiatal hernia may
be present with no symptoms at all. Some complications are specific for a hiatal hernia.
Esophageal complications
o By far, the majority of hiatal hernias are asymptomatic.
o Often, patients are left with the impression that they have a disease when a hiatal hernia is diagnosed.
o In rare cases, however, a hiatal hernia may be responsible for intermittent bleeding from associated
esophagitis, erosions (Cameron ulcers), or a discrete esophageal ulcer, leading to iron-deficiency anemia. The
prevalence of large hiatal hernias in patients with iron deficiency anemia is 6-7%. This particular complication is more
likely in patients who are bed-bound or those who take nonsteroidal anti-inflammatory drugs. Massive bleeding is rare.
Nonesophageal complications
o Incarceration of a hiatal hernia is rare and is observed only with paraesophageal hernia.
o When this occurs, it can present abruptly, with a sudden onset of vomiting and pain, sometimes
requiring immediate operative intervention.
Although a chest radiograph may reveal a large hiatal hernia (see the first image below), and many incidentally diagnosed
hiatal hernias are discovered in this manner, a barium study of the esophagus helps establish the diagnosis with greater accuracy
(see the second image below).
Typical findings include an outpouching of barium at the lower end of the esophagus, a wide hiatus through which gastric
folds are seen in continuum with those in the stomach, and, occasionally, free reflux of barium.
A barium study helps distinguish a sliding from a paraesophageal hernia (see the images below).
In rare cases, the entire stomach may herniate into the chest
The stomach may then undergo volvulus (see the image below) and subsequent incarceration and strangulation.
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Esophageal manometry has a low sensitivity for diagnosing hiatal hernia, as compared to endoscopy, and is therefore not appropriate in helping to
establish a diagnosis.
4. Contrast X-radiography of esophagus and stomach in three positions: upward, supine and upside-down position.
6. Coagulogram.
Sliding hernia
Paraesophageal hernia
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Mixed hernia
Differential diagnostics
Stenocardia. Diaphragmatic hernias frequently cause the pain, which character not only the patient, but also doctor can identify as anginal. However in
diaphragmatic hernia the pain more often is vague, spread to the stomach region and depends on body position. The pain, as a rule, arises in supine
position and disappears, if the patient upward. More often it spreads to the right and anginal vice versa to the left. In diaphragmatic hernia the ECG can
manifest the coronary failure, nevertheless standing up, owing to the stop of strangulation leads to disappearance of these pathological sings. The pain
caused by diaphragmatic hernia does not relieve after nitroglycerin. In this case more effective and prompt is atropine.
Peptic ulcer. The pain in gastric and duodenal ulcer frequently localized in epigastric region with irradiation in the left or right hypochondrium.
Nevertheless, it is characterized by periodicity, which caused by meal and disappears after the usage of soda.
Lung atelectasis, pleurisy, pneumonia are also should be differentiated with diaphragmatic hernia. Thus it is always necessary to remember, that the
extrapulmonary shadow of supradiaphragmatic disposed hernia on a plain roentgenogram can resemble intrapulmonary. For correct diagnosis it is
possible to recommend polypositional X-radiography, contrast roentgenography of esophagus and stomach.
Hypochromic anemia frequently associated due to repeated or permanent small bleedings. They are caused by a regional destruction a gastric mucosa.
In the females of senior age if it is fail to explain genesis of the revealed anemia, it is necessary to think about the opportunity of diaphragmatic hernia
and carry out appropriate X-ray examination.
The medical tactics toward diaphragmatic hernias of different localization essentially differs.
In case of sliding hiatal hernia the method of a choice is the conservative therapy:
An appropriate diet maintains an ideal body mass index. Obesity predisposes to reflux disease. Burkitt et al suggest that the
Western, fiber-depleted diet leads to a state of chronic constipation and straining during bowel movement, which would explain the
higher incidence of this condition in Western countries.
2) position of the patient during sleeping with elevated upside, during exacerbation sedentary;
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6) avoidance of constipation;
The indication for surgical treatment of sliding diaphragmatic hernia is the considerable expression of clinical signs, diminish of patient's working
capacity, fail of conservative treatment, bleeding, peptic stricture, malignancy.
When hiatal hernias are symptomatic, acid reflux usually produces the symptoms. If the hernia itself is causing chest
discomfort or other symptoms, surgery may be necessary.
When symptoms are due to GERD, the goals of treatment include prevention of reflux of gastric contents,
improved esophageal clearance, and reduction in acid production. This is achieved in the majority of patients by a
combination of the following:
o Modifying lifestyle factors
o Neutralizing acid or inhibiting acid production
o Enhancing esophageal and gastric motility
The treatment of GERD is beyond the scope of this article and is discussed in Gastroesophageal Reflux
Disease.
Large hiatal hernias may cause iron deficiency anemia regardless of whether Cameron ulcers are present. This
anemia responds well to PPI therapy with surgery offering no clear advantage over medical therapy.
Surgical treatment. Upper median laparotomy is mainly used. Nevertheless some surgeons prefer transthoracic accesses.
A patient with a large hiatal hernia may experience vague intermittent chest discomfort or pain. The paraesophageal hernia
may strangulate and frequently is operated on prophylactically to prevent this complication. Paraesophageal hernias may present in
infants or adults as a potentially life-threatening complication of strangulation, and prompt surgical repair is key. When found in
asymptomatic individuals, laparoscopic repair is often undertaken, with large defects in the diaphragm being closed with mesh.
Surgery is necessary only in the minority of patients with complications of GERD despite aggressive treatment with proton
pump inhibitors (PPIs). Because only a minority of patients with hiatal hernia have any problems, this represents a very small
proportion of patients with sliding hiatal hernia; most patients with problems are managed medically.
By far, the majority of patients who would have undergone surgery in the past are managed successfully today with PPIs.
However, young patients with severe or recurrent complications of GERD, such as strictures, ulcers, and bleeding, who cannot
afford lifelong PPI treatment or would prefer to avoid taking medications long term, may be surgical candidates.
Another group of patients who are surgical candidates are those with pulmonary complications, in particular, asthma,
recurrent aspiration pneumonia, chronic cough, or hoarseness linked to reflux disease.
Three major types of surgical procedures correct gastroesophageal reflux and repair the hernia in the process. They can be
performed by open laparotomy or with laparoscopic approaches, which currently are being employed more frequently.
Nissen fundoplication
o The Nissen fundoplication performed laparoscopically has gained popularity because of its lower
morbidity and shorter hospital stay compared to the open procedure performed previously. Although a relatively high
incidence of postoperative complications, such as dysphagia and gas bloating, are reported, DeMeester and Peters[7]
have shown that placing a larger bougie in the esophagus during this procedure, along with a shorter wrap and more
complete mobilization of the stomach, have markedly reduced postoperative complications.[8, 9]
o This procedure involves a 360 fundic wrap around the gastroesophageal junction. The diaphragmatic
hiatus also is repaired.
o A transthoracic approach may be used in patients who have had a previous Nissen wrap or those who
have an irreducible hernia.
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o The Toupet procedure is a variant of the Nissen wrap and involves a 180 wrap in an attempt to lessen
the likelihood of postoperative dysphagia.
Belsey (Mark IV) fundoplication: This operation involves a 270 wrap in an attempt to reduce the incidence of
gas bloating and postoperative dysphagia. It also is preferred when minimal esophageal dysmotility is suspected. To complete
this operation, the left and right crura of the diaphragm are approximated.
Hill repair: In this procedure, the cardia of the stomach is anchored to the posterior abdominal areas, such as
the medial arcuate ligament. This also has the effect of augmenting the angle of His and thus strengthening the antireflux
mechanism.
The antireflux procedures discussed above offer relief of symptoms in 80-90% of patients. In most cases, the
procedure of choice is the one with which the surgeon is most familiar. These procedures carry low mortality and morbidity
rates, lower than 15-20%. DeMeester et al found the Nissen procedure superior to the Belsey and Hill repairs with regard to
symptom relief and prevention of reflux postoperatively (as judged by pH monitoring). Good long-term results have been
reported for antireflux surgery, with adequate control of reflux in the range of 80% at 10 years.
Most patients with a paraesophageal hernia remain asymptomatic. In this type of hernia, symptoms from acid
reflux usually do not occur. Instead, the most common symptom is epigastric or substernal pain. Some patients complain of
substernal fullness, nausea, and dysphagia.
o A significant proportion of patients with this type of hernia develop incarceration of the hernia and
possible gastric volvulus, which can lead to perforation.
o If perforation occurs, the mortality rate is high. Because of this, many surgeons advise elective repair
when the diagnosis is made.
o The goal of surgery is to remove the hernia sac and close the abnormally wide esophageal hiatus.
o Some surgeons then tack the stomach down in the abdomen to prevent it from migrating upwards again,
or, they perform a temporary gastrostomy to help decompress the stomach and anchor it in place in the abdominal
cavity.
1. Drawing of the stomach into abdominal vacuity by disjunction of adhesions in the region of its cardial part, esophagus, excision of hernial
sac.
2. The plastics of esophageal hiatus of diaphragm (cruroplasty). The most widespread cruroplasty by Hill and narrowing of esophageal ring
according to Garrington.
3. Elimination of valvular failure of esophagocardial junction. The purpose of operation is to prevent gastroesophageal reflux by means of
formation of His angle and esophagocardial valve. Also Nissen fundoplication is applied.
Another tactics is applied in the patients with paraesophageal, parasternal and lumbocostal hernias. The method of choice is the surgery. Such tactics is
explained by the hazard of strangulation. The essence of the operation consists of drawing down of hernial content (stomach, intestine, omentum) into
abdominal cavity, removing of hernial sac and liquidation (suturing) of hernial ring.
Steps of cruroplastic
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The cause of the disease is the congenital or acquired decrease of diaphragmatic resistance, which during elevation of intraperitoneal pressure results in
its outpouching. The great importance in the development of acquired relaxation belongs to the damage of diaphragmatic nerve. The cause of the latter
could be inflammatory processes in chest and abdominal cavity, intoxication, poisoning, operations on chest organs and birth injury.
Pathology
In congenital form of a diaphragmatic relaxation revealed muscular aplasia, in acquired atrophy of muscular fibers.
Classification
Minor manifestation or asymptomatic course characterizes diaphragmatic relaxation. Therefrom, it is always necessary to thoroughly analyze the
occurrence of multiple signs from the organs of digestive, respiratory and cardiovascular system. The clinical symptomatology basically depends on
dysfunction of the diaphragm by itself and organs, which adjoin to it both in chest, and in abdominal cavity. In left-side diaphragmatic relaxation the
asymptomatic course rarely occurs.
General symptomatology. The patients with diaphragmatic relaxation can feel a pain of different character, localization and intensity. The pain syndrome
frequently results from gastric inflection or compression of vessels and nerves by filled stomach. Inflection of vascular bundles of pancreas, lien,
kidneys, mesentery of small and large intestines as a result of shift of abdominal organs also contribute to the development of pain syndrome. Frequently
patients complain of general weakness and loss of weight.
Gastrointestinal symptomatology. Dysphagia almost always arises as a result of inflection of abdominal part of esophagus. The heaviness after meal
should be caused by atony of stomach and its evacuation dysfunction. Ulceration and erosive gastritis, which occurs in some patients, are the outcome
of a regional ischemia from gastric inflection or torsion. Chronic constipation is basically caused by disturbance of massage influence of the diaphragm
on intestine. Meanwhile heartburn, belching, nausea, vomiting and meteorism also observed.
A phrenocardiac Uden-Ramcheld's syndrome represents cardiopulmonary signs. It is characterized by dyspnea, discomfort in the region of heart, anginal
pain, extrasystole and ECG changes (elongation of wave, Q interval and complex QRS).
Respiratory disturbances result from dynamic dysfunction of the diaphragm. The high standing of the diaphragm leads to compression of lung on the
side of lesion and disturbed ventilation of the lower part. It causes the diminishing of vital capacity of the lungs and development of dyspnea.
Roentgenologically revealed the high standing of diaphragmatic dome (to - intercostal space), restriction of its excursion and reduce of the inferior
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pulmonary field. Frequently observed the mediastinal shift to the opposite side. The contrast X-radiography of esophagogastric junction can find out the
inflection of abdominal part of esophagus. The X-ray examination enables to establish the diagnosis with a high degree of reliability.
Diaphragmatic relaxation
Asymptomatic course of diaphragmatic relaxation in the majority of patients has caused interpretation of this pathology as "innocent disease".
Nevertheless the shift and rotation of heart can cause the heart failures, and the restriction of pulmonary excursion sometimes leads to chronic
pneumonia. The gastric inflection frequently may result in disturbance of the valvular mechanism of esophagogastric junction and occurrence of reflux
esophagitis.
3. Esophagogastroduodenoscopy.
Differential diagnostics
Diaphragmatic elevation is the secondary high standing, which can arise as a result of ascites, pregnancy, expressed meteorism, peritonitis, tumours of
abdomen, splenomegaly or megacolon.
Pneumothorax, pyopneumothorax, pleurisy. Such misdiagnostics in the patients with diaphragmatic relaxation frequently caused by chest pain, cough,
dullness and tympanic sound revealed at percussion, and weak breathing at auscultation. Chest X-radiography rather contributes to exact diagnostics.
Diaphragmatic hernia. The differential diagnosis of diaphragmatic relaxation with this pathology is the most difficult. Nevertheless it has the important
practical value, because the threat of strangulation of diaphragmatic hernia requires an active surgical tactics. During the establishment of the diagnosis
it is always necessary to remember, that clinical manifestation of diaphragmatic hernia more expressed. However, the sharp inflection of abdominal
organs in the patients with diaphragmatic relaxation also can associate with severe pain, which resembles strangulation. Thereafter, a reliably
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Cancer of esophagus and cardial part of stomach. A sharp gastric shift upward with inflection of abdominal part of esophagus can lead to dysphagia,
substernal pain, disturbance of digestion, considerable loss of weight etc. For differential diagnostics applied a contrast X-ray examination of esophagus
and stomach.
In difficult for differential diagnostics cases a pneumoperitoneum with further X-ray examination is performed. This method allows with a major degree
of reliability to establish the diagnosis of diaphragmatic relaxation.
In most cases the asymptomatic course of diaphragmatic relaxation requires no special treatment.
2) diet eating by small portions and exception of food, which form waste and gases;
3) therapeutic gymnastics for improving of intestinal function and decrease of the patient's weight;
The indication for operation: gastric torsion or severe cardiorespiratory dysfunction. If clinical manifestations are absent, the surgical treatment can be
recommended only for women with further pregnancy and labors, because these conditions cause a sharp increase of intraperitoneal pressure with
further shift of the diaphragm and abdominal organs.
Surgical treatment. By means of a lateral access in V intercostal space a phrenoplasty is performed, which consist of incision of diaphragm from costal
edge to esophageal ring with following diaphragmatic duplication.
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ACUTE MEDIASTINITIS
The penetration of pathogenic agents into mediastinum can result from perforation and chemical burns of esophagus; injuries of trachea, bronchi,
operations on mediastinal organs and lungs. Also is possible the contamination from neck fat tissue and tracheobronchial lymph nodes.
Classification of mediastinitis
According to localization:
1) anterior;
2) posterior;
3) superior;
4) medial;
5) inferior.
According to pathogenesis:
1) primary;
2) secondary.
2) chronic.
1) nonspecific;
2) specific.
The clinical manifestation of acute mediastinitis is characterized by prompt progressing course, dependence on extent of the process, gravity of infection
and peculiarities of underlying disease.
Body temperature raises up to 39-40 and of hectic character, the patients complain of dyspnea, cyanosis, fever and profuse sweating.
The local symptomatology of the disease depends on location of the process and involvement of esophagus, trachea, heart, n. vagus, n. hrnus, n.
recurrens, tr. smtus.
Also is possible dysphagia, dyspnea, constant cough, hoarseness, change of cardiac rhythm.
X-ray examination. The method of X-ray examination should be chosen according to the cause of occurrence of acute mediastinitis. If the disease is
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caused by cervical phlegmon the X-radiography examination should be restricted only by chest X-ray film in three plains. In such situations observed
widening of mediastinum, shadowing of its anterior part and shift of trachea. Compression of esophagus revealed by barium swallow.
The contrast X-ray examination of esophagus after its iatrogenic perforation it is possible to see penetration of barium into mediastinum, shadowing and
widening of its consequent parts. Fiberesophagoscopy as the method of diagnostics of esophageal perforation is not recommended due to pneumatic
pressure during this manipulation.
According to the features of clinical symptomatology, acute mediastinitis is divided into anterior and posterior mediastinites.
The most often complications of acute mediastinitis are: pyopneumothorax, which has arisen after the abscess discharge into pleural space, pleural
empyema, purulent pericarditis, erosive bleeding and lung abscesses.
2. Physical findings.
4. Contrast esophagography.
5. ECG.
6. Fibrobronchoscopy.
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Acute mediastinitis
Differential diagnostics
Acute pneumonia, as a rule, is the outcome of catarrhal factor, which evidence is showed by the patients. Besides, more long duration, high temperature,
and cough with expectoration of mucopurulent sputum characterize the pneumonia; on auscultation fine bubbling wet rales on the side of lesion and
infiltration of pulmonary tissue at chest X-ray examination. All these findings enable to confirm or to rule out pneumonia.
Exsudative pleurisy mostly arises as the result of complication of pleuropneumonia. The process lasts, as a rule, 5-7 days. The most typical
manifestations are cough and chest pain on the side of lesion, which intensifies at deep breathing. Percussion reveals a shortening of percussion sound.
On auscultation weak breathing sounds and pleural friction rub. The presence of intensive homogeneous shadow with oblique upper contour on chest
X-radiography and also thoracentesis confirm the diagnosis of pleurisy.
Exsudative pericarditis. It most often results from rheumatic lesion of heart, acute myocardial infarction or polyserositis. Dyspnea, pain, heavy feeling
behind breastbone, general malaise, forced sedentary patient's position are the chief signs of pericarditis. On X-ray films observed a trapezoid shape of
heart, and on ECG diminished waves. Puncture of the pericardium with obtaining of exudate finally confirms the diagnosis.
The treatment of mediastinitis is only surgical. Its character and volume significantly depend on the cause, location and extent of purulent process.
Established perforation of esophagus, trachea or bronchus requires an urgent operation. The foreign bodies thus removed, and operation ends by
drainage. If the process located in anterosuperior mediastinum used a cervical mediastinotomy.
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Cervical mediastinotomy
Nevertheless cervical mediastinotomy is insufficient at low localization of the process. In such cases performed anterior mediastinotomy. Meanwhile,
isolated posterior mediastinitis is the indication for drainage by means of posterior extrapleural mediastinotomy.
In postoperative period is necessary application of intensive antibacterial, antiinflammatory and detoxycation therapy, and also treatment direct on the
increase of immunological resistance of the organism. The mortality after such operative approaches has been 26-36 %, and after conservative treatment
about 70 %.
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MEDIASTINAL TUMORS
Classification of tumours
1. Neurogenic tumours:
a) ganglioneuroma;
b) neurinoma;
c) neurogenic sarcoma;
d) neuroblastoma;
e) sympathoblastoma.
2. Mesenchymal tumours:
a) fibroma;
b) lipoma;
c) hemangioma;
d) fibrosarcoma;
e) liposarcoma;
f) angiosarcoma.
a) lymphosarcoma;
b) reticulosarcoma;
c) lymphogranulomatosis.
4. Tumour originated from thymus (thymoma), and thyroid gland (substernal, intrathoracic goiter).
a) dermoid cyst;
b) teratoma;
c) mediastinal seminoma;
d) choriocarcinoma.
a) mesothelial cyst;
b) pericardial diverticula;
c) bronchogenic cyst;
d) enteric cyst.
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On early stages of the development the tumours are almost asymptomatic, and 40 % of mediastinal neoplasms are revealed at preventive chest X-ray
examination. The patients most often complain of chest pain. The intensity of pain depends on degree of tumour compression or growth into nervous
structures. In malignant growth the pain has more intensive character, than in benign. Frequently the pain precedes by feeling of heaviness, discomfort
and foreign body in chest. Sometimes observed dyspnea caused by compression of airways, and major vessels both of anterior, and posterior
mediastinum.
Owing to compression of the lumen of superior vena cava the syndrome of superior vena cava develops, which manifest by cyanosis of face, neck and
upper half of chest, distend cervical veins, edema and dyspnea. Resulting from the rise of blood pressure and disrupture of venous walls, the nasal,
esophageal and pulmonary bleedings develop. As the characteristic features considered headache, loss of consciousness and hallucinations. In
overwhelming cases superior vena cava syndrome results from malignant tumours of lungs and mediastinum. Only in 5-7 % of patients they are benign.
The basic method of diagnostics is a complex X-ray examination: roentgenoscopy, polypositional X-radiography, tomography, computer tomography.
The examination should be start from roentgenoscopy in different plains (multiaxial roentgenoscopy). It gives the possibility to find out a pathological
shadow, its location, shape, size, mobility, intensity, contours and to reveal the presence or lack of pulsation of walls. Computer tomography is also a
high-grade method of diagnostics. It helps to receive the image of transversal plain of chest at any level, to confirm the location of mediastinal tumour
and its communication with adjacent organs. In suspicion on a vascular nature of the process, angiography is used. It enables to rule out aneurysm of
heart, aorta and its branches, reveal compression of superior vena cava and growth of the tumour into major arterial trunks.
If it is necessary to differentiate the tumour from cyst and reveal its different deposits, it is expedient to apply ultrasonic examination (sonography).
With the purpose of improvement of localization, size of mass, its communication with mediastinal organs performed pneumomediastinography
(X-radiography of mediastinum with introducing of oxygen or air). For pneumomediastinography, depending on tumour locating the gas is introduced
through a puncture above jugular incissure of breastbone, under xyphoid process or parasternally. Thus gas at first is spread in anterior mediastinum, and
in 45-60 min. penetrates in posterior. The introduced gas achieves a good visualization of tumour contours and its growth into adjacent organs.
Sometimes an artificial pneumothorax is performed on the affected side. In such patients collapse of lung gives the opportunity to differentiate
pulmonary tumour from mediastinal tumours and cysts.
- thoracoscopy, which allows to examine a pleural space, to take biopsy from mediastinal lymph nodes or tumour;
- mediastinoscopy (through a small incision above the breastbone exposed trachea, and along its position performed the canal in anterior
mediastinum with following insertion of a special endoscope) enables to examine anterior mediastinum, and take a biopsy from lymph nodes
and tumour;
During diagnostics of mediastinal neoplasms applied according to indications bronchography, esophagography and pneumoperitoneum.
Neurogenic tumours are the most common neoplasms of mediastinum, which occur in 20 % among the tumours of this location. There arise in any age
and more often benign. Their predominant localization is the posterior mediastinum. The origin of such tumours could be nervous trunks, ganglions and
other nervous structures of mediastinum. From the cells of sympathetic nervous trunk arise ganglioneuromas, neuroblastomas and sympathoblastomas.
Slide
The tumours, which arise from peripheral nerves are represent by neuromas and neurofibromas. The paragangliomas and mediastinal
pheochromocytoma develop from chemoceptor cells of and according to the structure resemble the tumours of sinocarotid zone. They frequently
produce hormones, and manifests by hypertension with often crises. In half of patients these tumours are malignant.
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Neurogenic sarcoma is a malignant tumour of nervous sheath. It is usually solitary, or in association with von Recklinhausen's disease.
The neurogenic tumours commonly manifest by backache, hyperalgesia, pareses and paralyses at tumour growth trough the spinal canal. The pain
reaction varies from slight to severe expressed neuralgias. Frequently ganglioneuroma is asymptomatic for many years. In the clinical pattern of
malignant neurogenic tumours prevail general intoxication, loss of weight and pain syndrome.
Roentgenologically in neurogenic tumour of a vertebrocostal angle observed characteristic intensive rounded shadow, with vertebral and costal
usuration, rib. Frequently revealed hemorrhagic pleural effusion on the side of lesion by malignant tumour.
Ganglioneuroma
Mesenchymal tumours. According to the histological origin mesenchymal benign tumours are represented by:
Lipomas are the most frequent mesenchymal benign tumours with predominant location in cardiodiaphragmatic angle.
The clinical symptomatology of these tumours is atypical. At the small sizes they are usually asymptomatic. The malignant neoplasms manifest much
earlier as the result of prompt infiltrative growth of the tumour and intoxication of the organism. Nevertheless, despite the malignant character,
liposarcoma can grow rather slowly with late metastatic spread.
On roentgenogram such masses represented by homogeneous formations, that applies to heart shadow.
The lymphomas occur in 3-5 % of patients with mediastinal tumors and in 20-25 % with all malignant neoplasms of mediastinum. The lymphomas arise
from mediastinal lymph nodes. Their common localization anterior mediastinum, nevertheless lymph nodes of any part can be affected. There are
three types of lymphomas: lymphosarcoma, reticulosarcoma and lymphogranulomatosis. All of them are characterized by malignant course. The initial
signs of this pathology mainly caused by intoxication: malaise, subfebrile or febrile temperature with further remittent character, sweating and loss of
weight. One of most typical manifestation of the disease should be considered itching of skin. Abnormally enlarged lymph nodes can compress
mediastinal organs, which lead to dry cough, chest pain, and dyspnea. In lymphogranulomatosis, in contrast with other mediastinal tumours, the signs of
compression are weakly expressed. It is characterized by bilateral lesion and blood changes (leukocytosis or leukopenia and elevation of erythrocyte
sedimentation rate). Lymphosarcoma differs by more prompt course and considerable progression of mediastinal compression syndrome. X-ray
examination, mediastinoscopy and biopsy of lymph nodes are the most valuable for diagnostics.
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The dermoid cysts and teratomas arise owing to disturbance of embryogenesis and occur in 5-8 % of the patients with mediastinal tumors. The origin of
dermoid cysts is the ectoderm, which transforms to a fibrous connecting tissue. The cystic cavity frequently contains similar to fat viscous mass of
brown color with deposits of skin and hair. The teratomas arise from several germinal laminas and contain different structural tissues. They are divided
on mature and immature. All mature teratomas, as a rule, are characterized by well-defined capsule, irregular rounded or oval shape, different size, and
look like a cyst on slit. Immature ones look like solitary nodes, sometimes with small cavities. The structure of teratomas can include parts of glands,
teeth, bones and sometimes even underdeveloped fetus. According to degree of cellular differentiation teratoma divided on benign (80-90 %) and
malignant (10-20 %). Although this disease is always congenital, it diagnosed, mainly, in elderly age at occurrence of pain and "compression syndrome".
95 % of such cysts are located in anterior mediastinum and frequently are accompanied with cardiovascular disturbances (tachycardia, pressing pain in
the region of heart). The compression of major bronchi and trachea results in occurrence of dyspnea, paroxysmal cough and hemoptysis. The infection
of the tumour frequently leads to fever and increase of intoxication. The presence in sputum of hair and other tissues is considered to be the sign of
bronchial fistula.
In diagnostics of teratomas the major value has a complex X-ray examination. It is possible to find out teeth, calcification of cystic capsule and its
contents. Prompt growth of the tumour, disappearance of its regular contours suspects the malignancy.
Cysts of pericardium are the cavity thin-walled formations, which according to the structure resemble pericardium. They occur in 7-8 % of cases of all
mediastinal tumors. Their most often location is the right cardiodiaphragmatic angle, much less often left one. A true cyst may be single-, double- or
multichamber, connected or non-connected with pericardium. The cases, when the cystic cavity communicates with the cavity of pericardium, it should
be considered as diverticulum. The disease, as a rule, asymptomatic and it is casually revealed only during prophylactic photoroentgenography. In cases
of great size of cyst the patients complain of pain in the region of heart and cardiac arrhythmia. During X-ray examination mesothelial cyst or
pericardial diverticulum observed as oval or semicircular homogeneous shadow with regular outline, which intimately applies to the shadow of heart.
Bronchogenic and enteric cysts of mediastinum arise in the period of intrauterine development and originated from dystopic germs of bronchial or
intestinal epithelium.
Bronchogenic cysts, as a rule, are single chamber, with location either in mediastinum, or in pulmonary tissue. The neighborhood of cyst with bifurcation
of trachea can cause paroxysmal cough, dyspnea and respiratory disturbances. Paraesophageal location of the cyst manifests by dysphagia. The clinical
manifestations of such pathology can be caused by inflammatory process in cyst or its sudden discharge into airways. If the cyst is communicated with
airways, the roentgenogram reveals a fluid level, and during bronchography a contrast agent fills in the lumen of cyst. The diagnosis is possible to
confirm by means of pneumomediastinography.
The enteric cyst (enterocystoma) arises from the dorsal parts of a primary intestinal tube, located more often in lower parts of posterior mediastinum and
applies to esophagus. Depending on histology they are divided on esophageal, gastric and intestinal cyst. In cases, when a cystic wall is covered by
gastric epithelium, which produces hydrochloric acid, an ulceration of wall, bleeding and its perforation can develop.
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Frequently enteric cyst suppurates with the hazard of discharge into pleural space or pericardium, esophagus and bronchi. The most often signs of the
disease is dyspnea and chest pain. Due to characteristic localization of the pathological focus in posterior mediastinum, to the right from median line, the
roentgenological diagnostics is usually not difficult. In order to determine mutual relation of neoplasm to trachea, bronchi, and esophagus it is possible to
apply pneumomediastinography. As there is always a danger of the development of complications, it is necessary to consider such pathology as absolute
indication for operative removal.
Echinococcosis of mediastinum occurs rarely (1-2 % of all mediastinal tumors). If the parasite is of small size, the disease most often asymptomatic. The
enlargement of echinococcal cyst causes pain, dyspnea, dysphagia and superior vena cava syndrome. Sometimes in such patients the cyst can discharge
into bronchus or trachea. The suppuration of parasitogenic cysts is transformed into abscess and purulent mediastinitis. Roentgenological method should
be considered to be predominant in the diagnostics of echinococcosis of mediastinum. The presence of homogeneous, round or oval shadow with regular
outline (with further calcification) suggests echinococcosis. For confirming of the diagnosis reaction of latex-agglutination is performed. Echinococcosis
of mediastinum frequently associated with anatomical lesion of lungs.
The presence of mediastinal tumors requires surgical treatment. Expectant tactics and dynamic observation in such cases are unjustified.
In connection with a constant and substantial threat of infection, perforation and development of purulent intrapleural complications, the pericardial,
bronchogenic and enteric cysts of mediastinum are the subjects to operative remove.
The operative treatment of malignant mediastinal tumors should be applied on early stages of the disease. In advanced cases it is expedient to apply
antineoplastic and radiotherapy.
The benign neurogenic tumours are removed in surgical way through thoracotomy incision. If the tumour grow like a " sandglasses" a fragment of the
tumour removed with following resection of vertebral arches. The malignant tumours are removed "n mass", with maximal excision of the tumour,
affected ribs, paraaortic, esophageal and paratracheal lymph nodes.
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Pathophysiology
Extrinsic compression of the superior vena cava is possible because it has a thin wall coupled with a low intravascular
pressure. Because the superior vena cava is surrounded by rigid structures, it is relatively easy to compress. The low intravascular
pressure also allows for the possibility of thrombus formation, such as catheter-induced thrombus.
The subsequent obstruction to flow causes an increased venous pressure, which results in interstitial edema and retrograde
collateral flow.
Epidemiology
Superior vena cava syndrome is chiefly associated with malignancy. Currently, more than 90% of patients with superior vena
cava syndrome have an associated malignancy as the cause. This contrasts with studies in the early 1950s in which a large
proportion of cases were nonmalignant. Infectious causes (eg, syphilis, tuberculosis) have decreased because of improvements in
antibiotic therapy. Of the nonmalignant causes of superior vena cava syndrome, thrombosis from central venous instrumentation
(catheter, pacemaker, guidewire) is an increasingly common event, especially as these procedures become more common.
Causes
Today, the most common etiology of superior vena cava syndrome is related to malignancy.
Prior to modern antibiotics, infectious causes including syphilis, tuberculosis, and fungi occurred with almost
equal frequency.
The most common cause of malignancy-related superior vena cava syndrome is bronchogenic carcinoma, which
accounts for nearly 80% of cases.
Lymphoma accounts for approximately 15% of cases.
Other cases have various causes, including infectious and catheter-related etiologies. Increasingly, dialysis
catheters and pacemaker leads are becoming associated with superior vena cava syndrome due to thrombosis.
Symptoms
The symptoms of SVCS are more severe if the vein becomes blocked quickly. This is because the other veins in the area do
not have time to widen and take over the blood flow that cannot pass through the superior vena cava.
The most common symptoms are:
Trouble breathing.
Coughing.
Swelling in the face, neck, upper body, or arms.
Less common symptoms include the following:
Hoarse voice.
Trouble swallowing or talking.
Coughing up blood.
Swollen veins in the chest or neck.
Chest pain.
Reddish skin color.
Laboratory Studies
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The diagnosis of superior vena cava syndrome (SVCS) is often made on clinical grounds alone, combining clinical
presentation with an often-obtained history of thoracic malignancy.
Imaging Studies
Plain radiography is often helpful and reveals a mediastinal mass in most patients (as is seen in the image below).
When in doubt, venography can aid in the diagnosis, but this is usually not necessary.
Thoracic CT scanning is helpful, but the histologic diagnosis is important in initiating therapy.
Treatment
Treatment for SCVS caused by cancer depends on the following:
The type of cancer.
The cause of the blockage.
How severe the symptoms are.
The prognosis (chance of recovery).
Whether treatment is to cure, control, or relieve the symptoms of cancer.
The patient's wishes.
Treatment may include the following:
Watchful waiting
Watchful waiting is closely monitoring a patients condition without giving any treatment unless symptoms appear or change.
A patient who has good blood flow through smaller veins in the area and mild symptoms may not need treatment.
The following may be used to relieve symptoms and keep the patient comfortable:
Keeping the upper body raised higher than the lower body.
Corticosteroids (drugs that reduce swelling).
Diuretics (drugs that make excess fluid pass from the body in urine). Patients taking diuretics are closely
watched because these drugs can cause dehydration (loss of too much fluid from the body).
Chemotherapy
Chemotherapy is the usual treatment for tumors that respond to anticancer drugs, including small cell lung cancer and
lymphoma. Chemotherapy uses drugs to stop the growth of cancer cells, either by killing the cells or by stopping them from
dividing. When chemotherapy is taken by mouth or injected into a vein or muscle, the drugs enter the bloodstream and can reach
cancer cells throughout the body (systemic chemotherapy). When chemotherapy is placed directly into the cerebrospinal fluid, an
organ, or a body cavity such as the abdomen, the drugs mainly affect cancer cells in those areas (regional chemotherapy). The way
the chemotherapy is given depends on the type and stage of the cancer being treated.
Radiation therapy
If the blockage of the superior vena cava is caused by a tumor that does not usually respond to chemotherapy, radiation
therapy may be given. Radiation therapy is a cancer treatment that uses high-energy x-rays or other types of radiation to kill cancer
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cells. External radiation therapy uses a machine outside the body to send radiation toward the cancer. The way the radiation therapy
is given depends on the type and stage of the cancer being treated.
Thrombolysis
SVCS may occur when a thrombus (blood clot) forms in a partly blocked vein. Thrombolysis is a way to break up and remove
blood clots. This may done by a thrombectomy. Thrombectomy is surgery to remove the blood clot or the use of a device inserted
into the vein to remove the blood clot. This may be done with or without the use of drugs to break up the clot.
Stent placement
If the superior vena cava is partly blocked by the tumor, an expandable stent (tube) may be placed inside the superior vena
cava to help keep it open and allow blood to pass through. This helps most patients. Drugs to keep more blood clots from forming
may also be used.
Surgery
Surgery to bypass (go around) the blocked part of the vein is sometimes used for cancer patients, but is used more often for
patients without cancer.
Palliative care may be given to relieve symptoms in patients with SVCS.
Superior vena cava syndrome is serious and the symptoms can be upsetting for the patient and family. It is important that
patients and family members ask questions about superior vena cava syndrome and how to treat it. This can help relieve anxiety
about symptoms such as swelling, trouble swallowing, coughing, and hoarseness.
Patients with advanced cancer sometimes decide not to have any serious treatment. Palliative treatment can help keep patients
comfortable by relieving symptoms to improve their quality of life.
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Causes
When you eat, food passes from the throat to the stomach through the esophagus (also called the food pipe or swallowing
tube). Once food is in the stomach, a ring of muscle fibers prevents food from moving backward into the esophagus. These muscle
fibers are called the lower esophageal sphincter, or LES.
If this sphincter muscle doesn't close well, food, liquid, and stomach acid can leak back into the esophagus. This is called
reflux or gastroesophageal reflux. Reflux may cause symptoms, or it can even damage the esophagus.
The risk factors for reflux include:
Alcohol (possibly)
Hiatal hernia (a condition in which part of the stomach moves above the diaphragm, which is the muscle that separates
the chest and abdominal cavities)
Obesity
Pregnancy
Scleroderma
Smoking
Heartburn and gastroesophageal reflux can be brought on or made worse by pregnancy and many different medications. Such
drugs include:
Anticholinergics (e.g., for seasickness)
Beta-blockers for high blood pressure or heart disease
Bronchodilators for asthma
Calcium channel blockers for high blood pressure
Dopamine-active drugs for Parkinson's disease
Progestin for abnormal menstrual bleeding or birth control
Sedatives for insomnia or anxiety
Tricyclic antidepressants
If you suspect that one of your medications may be causing heartburn, talk to your doctor. Never change or stop a medication
you take regularly without talking to your doctor.
Symptoms
More common symptoms are:
Feeling that food is stuck behind the breastbone
Heartburn or a burning pain in the chest (under the breastbone)
Increased by bending, stooping, lying down, or eating
More likely or worse at night
Relieved by antacids
Nausea after eating
Less common symptoms are:
Bringing food back up (regurgitation)
Cough or wheezing
Difficulty swallowing
Hiccups
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A positive stool occult blood test may diagnose bleeding that is coming from the irritation in the esophagus, stomach, or
intestines.
Treatment
You can make many lifestyle changes to help treat your symptoms. Avoid foods that cause problems for you. Making changes
to your routine before you go to sleep may also help.
Avoid drugs such as aspirin, ibuprofen (Advil, Motrin), or naproxen (Aleve, Naprosyn). Take acetaminophen (Tylenol) to
relieve pain. Take your medicines with plenty of water. When your doctor gives you a new medicine, remember to ask whether it will
make your heartburn worse.
You may use over-the-counter antacids after meals and at bedtime, although they do not last very long. Common side effects
of antacids include diarrhea or constipation.
Other over-the-counter and prescription drugs can treat GERD. They work more slowly than antacids but give you longer
relief. Your pharmacist, doctor, or nurse can tell you how to take these drugs.
Proton pump inhibitors (PPIs) decrease the amount of acid produced in your stomach
H2 blockers (antagonists) lower the amount of acid released in the stomach
Anti-reflux operations (fundoplication and others) may be an option for patients whose symptoms do not go away with
lifestyle changes and drugs. Heartburn and other symptoms should improve after surgery, but you may still need to take drugs for
your heartburn.
There are also new therapies for reflux that can be performed through an endoscope (a flexible tube passed through the mouth
into the stomach).
Outlook (Prognosis)
Most people respond to lifestyle changes and medications. However, many patients need to continue taking drugs to control
their symptoms.
Possible Complications
Asthma
Barrett's esophagus (a change in the lining of the esophagus that can increase the risk of cancer)
Bronchospasm (irritation and spasm of the airways due to acid)
Chronic cough or hoarseness
Dental problems
Esophageal ulcer
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Peritonitis
Peritonitis is the acute or chronic peritoneal inflammation with characteristic local and general changes
in the organism and severe dysfunction of organs and vital systems of the organism. Peritonitis is
an inflammation of the peritoneum, the thin tissue that lines the inner wall of the abdomen and covers most
of the abdominal organs. Peritonitis may be localized or generalised, and may result from infection (often
due to rupture of a hollow organ as may occur in abdominal trauma or appendicitis) or from a non-infectious
process.
Anatomy
The peritoneum is the largest and most complex serous membrane in the body. It forms a closed sac (ie,
coelom) by lining the interior surfaces of the abdominal wall (anterior and lateral), by forming the boundary
to the retroperitoneum (posterior), by covering the extraperitoneal structures in the pelvis (inferior), and by
covering the undersurface of the diaphragm (superior). This parietal layer of the peritoneum reflects onto the
abdominal visceral organs to form the visceral peritoneum. It thereby creates a potential space between the 2
layers (ie, the peritoneal cavity).
The peritoneum consists of a single layer of flattened mesothelial cells over loose areolar tissue. The
loose connective tissue layer contains a rich network of vascular and lymphatic capillaries, nerve endings, and
immune-competent cells, particularly lymphocytes and macrophages. The peritoneal surface cells are joined
by junctional complexes, thus forming a dialyzing membrane that allows passage of fluid and certain small
solutes. Pinocytotic activity of the mesothelial cells and phagocytosis by macrophages allow for clearance of
macromolecules.
Normally, the amount of peritoneal fluid present is less than 50 mL, and only small volumes are
transferred across the considerable surface area in a steady state each day. The peritoneal fluid represents a
plasma ultrafiltrate, with electrolyte and solute concentrations similar to that of neighboring interstitial spaces
and a protein content of less than 30 g/L, mainly albumin. In addition, peritoneal fluid contains small
numbers of desquamated mesothelial cells and various numbers and morphologies of migrating immune cells
(reference range is < 300 cells/ L, predominantly of mononuclear morphology).
The peritoneal cavity is divided incompletely into compartments by the mesenteric attachments and
secondary retroperitonealization of certain visceral organs. A large peritoneal fold, the greater omentum,
extends from the greater curvature of the stomach and the inferior aspect of the proximal duodenum
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downward over a variable distance to fold upon itself (with fusion of the adjacent layers) and ascends back to
the taenia omentalis of the transverse colon. This peritoneal fold demonstrates a slightly different microscopic
anatomy, with fenestrated surface epithelium and a large number of adipocytes, lymphocytes, and
macrophages, and it functions as a fat storage location and a mobile immune organ.
The compartmentalization of the peritoneal cavity, in conjunction with the greater omentum, influences
the localization and spread of peritoneal inflammation and infections.
The main causes of peritonitis are the acute inflammation of abdominal viscera, discontinuity and
disturbed permeability of their walls, open and closed traumas of the abdomen with the damage of viscera
with following microbial contamination of peritoneal space.
Despite the cause of peritonitis, the disease is characterized by a typical bacterial inflammation. The
infectious agents are represented by Escherichia colli, Staphylococcus and Enterococcus, Proteus,
Streptococcus and also nonclostridial anaerobes. At least in 30 % of cases association of two or more agents
occur.
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Primary peritonites occur very rarely and result from pneumococcal, streptococcal and staphylococcal
infection.
Besides microbial peritonites, caused by peritoneal contamination, distinguished also aseptic peritoneal
inflammation, which result from entering of different chemical noninfectious agents into peritoneal cavity
(blood, urine, bile, pancreatic juice, etc.). Its so called toxico-chemical peritonitis. But with the development
of aseptic inflammation bacteria penetrate into peritoneal space with transformation of peritonitis into
bacterial.
Chronic peritonitis is mainly caused by tuberculosis, which agents are usually located extraperitoneally
(lungs, mediastinal lymph nodes) or in mesenteric lymph nodes and by hematogenous way enter the
peritoneum.
Risk Factors:
The following factors may increase the risk for primary peritonitis:
Infected peritonitis
Perforation of part of the gastrointestinal tract is the most common cause of peritonitis. Examples
include perforation of the distal oesophagus (Boerhaave syndrome), of thestomach (peptic ulcer, gastric
carcinoma), of the duodenum (peptic ulcer), of the
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Aerobic
Enterobacter/Klebsiella 26%
Proteus 22%
Pseudomonas 8%
Enterococci 17%
Staphylococci 7%
Eubacteria 24%
Clostridia 17%
Peptostreptococci 14%
Peptococci 11%
Fungi Candida 2%
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Disruption of the peritoneum, even in the absence of perforation of a hollow viscus, may also cause
infection simply by letting micro-organisms into the peritoneal cavity. Examples include trauma, surgical
wound, continuous ambulatory peritoneal dialysis, and intra-peritoneal chemotherapy. Again, in most cases,
mixed bacteria are isolated; the most common agents include cutaneous species such as Staphylococcus
aureus, and coagulase-negative staphylococci, but many others are possible, including fungi such as Candida.
Spontaneous bacterial peritonitis (SBP) is a peculiar form of peritonitis occurring in the absence of an
obvious source of contamination. It occurs in patients with ascites, in particular, in children. See the article
on spontaneous bacterial peritonitis for more information.
Intra-peritoneal dialysis predisposes to peritoneal infection (sometimes named "primary peritonitis" in
this context).
Systemic infections (such as tuberculosis) may rarely have a peritoneal localisation.
Non-infected peritonitis
Leakage of sterile body fluids into the peritoneum, such as blood (e.g., endometriosis, blunt
abdominal trauma), gastric juice (e.g., peptic
ulcer, gastriccarcinoma), bile(e.g., liverbiopsy), urine (pelvic trauma), menstruum (e.g., salpingitis), pancreatic
juice (pancreatitis), or even the contents of a ruptured dermoid cyst. It is important to note that, while
these body fluids are sterile at first, they frequently become infected once they leak out of their organ, leading
to infectious peritonitis within 24 to 48 hours.
Sterile abdominal surgery, under normal circumstances, causes localised or minimal generalised
peritonitis, which may leave behind a foreign body reaction and/or fibroticadhesions. However, peritonitis
may also be caused by the rare case of a sterile foreign body inadvertently left in
the abdomen after surgery (e.g., gauze, sponge).
Much rarer non-infectious causes may include familial Mediterranean fever, TNF receptor associated
periodic syndrome, porphyria, and systemic lupus erythematosus.
Classification
Peritonites are classified:
According to the character of microbial contamination:
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A: primary
B: secondary.
According to clinical course:
A: acute
B: chronic.
According to the etiological agents:
A: peritonites, which caused by bacteria of digestive tract (E. colli, staphylococci, streptococci, proteus,
anaerobes, etc.)
B: which caused by bacteria, which exist out of gastrointestinal tube (gonococci, pneumococci,
streptococcus haemolyticus, etc.).
C: distinguished aseptic (nonbacterial peritonites), resulting from irritation by blood, bile, pancreatic
juice or urine.
According to the character of exudate:
A: serous;
B: fibrinous;
C: fibrinopurulent;
D: purulent;
E: hemorrhagic;
F: "peritonitus sicca".
According to the extension of inflammatory process:
A: local;
B: diffuse;
C: generalized.
Dependent on duration of the disease and degree of pathological alterations in the clinical course of
peritonitis distinguished three stages:
reactive (first 24 hours) maximal manifestation of local signs of the disease;
toxic (24-72 hours) gradual reducing of local signs and increasing of general intoxication.
terminal (after 72 hours) severe, often unreversable intoxication on the background of sharply
expressed local manifestations of peritoneal inflammation.
Primary peritonitis.
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Spontaneous bacterial peritonitis (SBP) is an acute bacterial infection of ascitic fluid. Contamination of
the peritoneal cavity is thought to result from translocation of bacteria across the gut wall or mesenteric
lymphatics and, less frequently, via hematogenous seeding in the presence of bacteremia.
SBP can occur as a complication of any disease state that produces the clinical syndrome of ascites,
such as heart failure and Budd-Chiari syndrome. Children with nephrosis or systemic lupus erythematosus
who have ascites have a high risk of developing SBP. The highest risk of SBP, however is in patients with
cirrhosis who are in a decompensated state. In particular, decreased hepatic synthetic function with
associated low total protein level, low complement levels, or prolonged prothrombin time (PT) is associated
with maximum risk. Patients with low protein levels in ascitic fluid (< 1 g/dL) have a 10-fold higher risk of
developing SBP than those with a protein level greater than 1 g/dL. Approximately 10-30% of patients with
cirrhosis and ascites develop SBP. The incidence rises to more than 40% with ascitic fluid protein contents of
less than 1 g/dL (which occurs 15% of patients), presumably because of decreased ascitic fluid opsonic
activity.
More than 90% of cases of SBP are caused by a monomicrobial infection.
Secondary peritonitis
Common etiologic entities of secondary peritonitis (SP) include perforated appendicitis; perforated
gastric or duodenal ulcer; perforated (sigmoid) colon caused by diverticulitis, volvulus, or cancer; and
strangulation of the small bowel. Necrotizing pancreatitis can also be associated with peritonitis in the case of
infection of the necrotic tissue.
The pathogens involved in SP differ in the proximal and distal GI tract. Gram-positive organisms
predominate in the upper GI tract, with a shift toward gram-negative organisms in the upper GI tract in
patients on long-term gastric acid suppressive therapy. Contamination from a distal small bowel or colon
source initially may result in the release of several hundred bacterial species (and fungi); host defenses
quickly eliminate most of these organisms. The resulting peritonitis is almost always polymicrobial, containing
a mixture of aerobic and anaerobic bacteria with a predominance of gram-negative organisms.
As many as 15% of patients who have cirrhosis with ascites who were initially presumed to have SBP
have SP. In many of these patients, clinical signs and symptoms alone are not sensitive or specific enough to
reliably differentiate between the 2 entities. A thorough history, evaluation of the peritoneal fluid, and
additional diagnostic tests are needed to do so; a high index of suspicion is required.
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Iatrogenic
The most common cause of postoperative peritonitis is anastomotic leak, with symptoms generally
appearing around postoperative days 5-7. After elective abdominal operations for noninfectious etiologies,
the incidence of SP (caused by anastomotic disruption, breakdown of enterotomy closures, or inadvertent
bowel injury) should be less than 2%. Operations for inflammatory disease (ie, appendicitis, diverticulitis,
cholecystitis) without perforation carry a risk of less than 10% for the development of SP and peritoneal
abscess. This risk may rise to greater than 50% in gangrenous bowel disease and visceral perforation.
After operations for penetrating abdominal trauma, SP and abscess formation are observed in a small
number of patients. Duodenal and pancreatic involvement, as well as colon perforation, gross peritoneal
contamination, perioperative shock, and massive transfusion, are factors that increase the risk of infection in
these cases.
Peritonitis is also a frequent complication and significant limitation of peritoneal dialysis. Peritonitis
leads to increased hospitalization and mortality rates.
Tertiary peritonitis.
Tertiary peritonitis (see Table 3, below) develops more frequently in immunocompromised patients and
in persons with significant preexisting comorbid conditions. Although rarely observed in uncomplicated
peritoneal infections, the incidence of tertiary peritonitis in patients requiring ICU admission for severe
abdominal infections may be as high as 50-74%.
Tuberculous peritonitis (TP) is rare in the United States (< 2% of all causes of peritonitis), but it
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continues to be a significant problem in developing countries and among patients with human
immunodeficiency virus (HIV) infection. The presenting symptoms are often nonspecific and insidious in
onset (eg, low-grade fever, anorexia, weight loss). Many patients with TP have underlying cirrhosis. More
than 95% of patients with TP have evidence of ascites on imaging studies, and more than half of these
patients have clinically apparent ascites.
In most cases, chest radiographic findings in patients with TP peritonitis are abnormal; active pulmonary
disease is uncommon (< 30%). Results on Gram stain of ascitic fluid are rarely positive, and culture results
may be falsely negative in up to 80% of patients. A peritoneal fluid protein level greater than 2.5 g/dL, a
lactate dehydrogenase (LDH) level greater than 90 U/mL, or a predominantly mononuclear cell count of
greater than 500 cells/ L should raise suspicion of TP but have limited specificity for the diagnosis.
Laparoscopy and visualization of granulomas on peritoneal biopsy specimens, as well as cultures (requires
4-6 wk), may be needed for the definitive diagnosis; however, empiric therapy should begin immediately.
Chemical peritonitis. Chemical (sterile) peritonitis may be caused by irritants such as bile, blood, barium,
or other substances or by transmural inflammation of visceral organs (eg, Crohn disease) without bacterial
inoculation of the peritoneal cavity. Clinical signs and symptoms are indistinguishable from those of SP or
peritoneal abscess, and the diagnostic and therapeutic approach should be the same.
Peritoneal abscess. Peritoneal abscess describes the formation of an infected fluid collection
encapsulated by fibrinous exudate, omentum, and/or adjacent visceral organs. The overwhelming majority of
abscesses occurs subsequent to SP. Abscess formation may be a complication of surgery. The incidence of
abscess formation after abdominal surgery is less than 1-2%, even when the operation is performed for an
acute inflammatory process. The risk of abscess increases to 10-30% in cases of preoperative perforation of
the hollow viscus, significant fecal contamination of the peritoneal cavity, bowel ischemia, delayed diagnosis
and therapy of the initial peritonitis, and the need for reoperation, as well as in the setting of
immunosuppression. Abscess formation is the leading cause of persistent infection and development of
tertiary peritonitis.
The clinical picture of acute peritonitis is determined by the character of primary causative lesion,
duration of inflammatory process, its extension and also the stage of the disease. Predominant clinical sign is
the abdominal pain, which gradually increases. Firstly it is localized in the region of the source of peritonitis
and then extends all over the abdomen. Elderly patients may experience lacking pain and even pay no
attention on it, but general malaise, loss of appetite, and weakness are evident. This course is also
characteristic for postoperative peritonitis, which results from parting of sutures (of anastomosis or site of
perforation) or leaking colon carcinoma. Simultaneously with the increase of pain also change the general
appearance. The patient looks anxious, with drawn features, hollowed-eyed. Further this is accompanied by
nausea and vomiting: on initial stages vomit is of gastric contents, later duodenal and thereafter is of
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intestinal contents. With progression of the disease vomiting becomes constant, effortless and overcomes into
frequent regurgitation by brown fluid with foul-smelling. Patient's lips and tongue are dry, with brown fur.
Respiration is of thoracic type and is shallow and rapid. In order to prevent pain the patient speaks very quite.
Every change of position results in increase of pain, thus the patient lies with the knee drawn up to relax the
abdominal wall.
Often the vomiting is accompanied by hiccup, which results from irritation of diaphragmatic
peritoneum. This is considered to be an unfavorable prognostic sign. The patient tries to retain distended
abdomen by his hands during hiccup and thus provokes increase of pain.
During examination observed restricted movements of abdominal wall, which is mainly expressed over
the inflammatory focus. Abdominal percussion reveals the region of maximal painfulness, which response
the site of lesion, high tympanic sound as a result of intestinal gaseous dilatation, but sometimes dullness,
caused by cumulation of great amount of exudate. On palpation revealed muscular tension of abdominal
wall. Especially expressed the muscular rigidity in case of perforation of hollow organs ("board-like
abdomen"). Pelvic location of peritonitis usually causes less clinical manifestations. In such cases a diagnostic
value has digital examination of the rectum and bimanual palpation of the pelvis and lower abdomen, which
reveals overhanging and painfulness of anterior rectal wall or posterior vaginal vault owing to accumulation
of the exudate.
The clinical manifestation of peritonitis is various and individual. It depends on the character of primary
lesion, extension of inflammatory process, and defensive properties of the organism. The main manifestations
of peritonitis are acute abdominal pain, abdominal tenderness, and abdominal guarding, which are
exacerbated by moving the peritoneum, e.g., coughing (forced cough may be used as a test), flexing one's
hips, or eliciting the Blumberg sign (a.k.a. rebound tenderness, meaning that pressing a hand on the abdomen
elicits less pain than releasing the hand abruptly, which will aggravate the pain, as the peritoneum snaps back
into place). The presence of these signs in a patient is sometimes referred to as peritonism. The localization
of these manifestations depends on whether peritonitis is localized (e.g., appendicitis or diverticulitis before
perforation), or generalized to the whole abdomen. In either case, pain typically starts as a generalized
abdominal pain (with involvement of poorly localizing innervation of the visceral peritoneal layer), and may
become localized later (with the involvement of the somatically innervated parietal peritoneal layer).
Peritonitis is an example of an acute abdomen.
Collateral manifestations: diffuse abdominal rigidity ("washboard abdomen") is often present, especially
in generalized peritonitis, Fever, Sinus tachycardia, Development of ileus paralyticus (i.e., intestinal
paralysis), which also causes nausea, vomiting and bloating.
In reactive stage of the disease the most common are the pain, muscular rigidity and positive Shchotkin-
Blumberg's symptom. The general state changed a little the patient is active, sometimes excite. A moderate
tachycardia and hypertension commonly observed.(Fig.1)
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In toxic stage of the disease the pain and muscular defense tend to diminish, but on palpation the
muscular tenderness and Shchotkin-Blumberg's symptom retain on the same level. More evident the signs of
intestinal paresis (abdominal distension, absence of peristalsis). The general state is worsened. The patient is
apathetic, the skin is blanched or cyanotic. Observed progressing of tachycardia, decreasing of blood
pressure and rising of temperature. In blood analysis revealed leukocytosis and deviation of the differential
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The specific complications of acute peritonitis include inflammatory infiltrates and abscesses of
abdominal cavity (Fig.2) (subphrenic, subhepatic, interintestinal and pelvic), dynamic ileus, intestinal fistula,
suppuration of postoperative wound, eventration, peritoneal adhesions, etc.
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chest, which irradiates into the shoulder and increases during cough and deep breathing. Sometimes revealed
painfulness during digital pressing and swelling of soft tissues in the region of 7-10th Intercostals space. The
patients are suffering from nausea, hiccup, and high temperature. Sometimes they must stay in forced
position: supine or semisedentary. The tongue is dry, the abdomen is slightly bloated, and rebound tenderness
symptoms are usually absent. In blood revealed leukocytosis, deviation of the differential count to the left.
The abscess requires a surgical treatment. If the abscess is located near anterior abdominal wall, it is drained
by means of oblique access under the costal arch. The abscesses, which located in posterior subphrenic
space, are drained after the previous puncture through the access after resection of X rib. (Fig.4)
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Subhepatic abscess is characterized by the pain and presence of infiltrate below right costal arch,
positive Shchotkin-Blumberg symptom. The abscess is drained through the incision along right costal arch.
The clinical pattern of interintestinal abscess is vague. It is formed mostly on the 12-14th day after
appearance of peritonitis. The patients complain of the high temperature and dull pain in the site of its
location. The abdomen is soft, but during palpation revealed dense, painful infiltrate. In case of localization
near to abdominal wall one can observe muscular tension and positive Shchotkin-Blumberg symptom. The
roentgenological or ultrasound investigation often reveals focal shadow with air-fluid level. The abscess is
drained over the site of its localization, dividing the bowel loops.
Abscesses of small pelvis mostly occur as a result of appendicitis(Fig.5) or accumulation of the exudates
in Douglas space in diffuse peritonitis.
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Such patients complain of constant pain in the lower abdomen, high temperature, painful urinary
excretion and tenesmus. The palpation of the abdomen usually reveals no pathology. But the digital rectal
examination finds out a painful infiltrate that drawn into the rectum. (Fig.6) The mucosa over the infiltrate is
edematous and immovable. The vaginal examination of the female patients reveals overhanging of posterior
vaginal vault and painfulness of cervical shift. Often on the background of solid consistency of the infiltrate
the softened regions are palpated, which respond to accumulation of pus. The purulent sites of small pelvis in
males are drained through the anterior wall of the rectum and in females through the posterior vaginal
vault. For this purpose the infiltrate is punctured by thick needle and under its check the abscess is drained by
means of scalpel incision. Then the incision is expanded by clamp, the pus is aspirated and the abscess cavity
is drained by rubber strap, which is fixed to perineum.
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Laparocentesis.
To diagnose peritonitis, your doctor will talk with you about your medical history and perform a physical
exam. When peritonitis is associated with peritoneal dialysis, your signs and symptoms, particularly cloudy
dialysis fluid, may be enough for your doctor to diagnose the condition.
In cases of peritonitis in which the infection may be a result of other medical conditions (secondary
peritonitis) or in which the infection arises from fluid buildup in your abdominal cavity (spontaneous
peritonitis), your doctor may recommend the following tests to confirm a diagnosis:
Peritoneal fluid analysis. Using a thin needle, your doctor may take a sample of the fluid in your
peritoneum (paracentesis). If you have peritonitis, examination of this fluid may show an increased white
blood cell count, which typically indicates an infection or inflammation. A culture of the fluid may also reveal
the presence of bacteria.
Diagnostic paracentesis should be performed in all patients who do not have an indwelling peritoneal
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catheter and are suspected of having SBP. In peritoneal dialysis patients with a peritoneal catheter, fluid
should be withdrawn using sterile technique. Ultrasonography may aid paracentesis if ascites is minimally
detectable or questionable.
The results of aerobic and anaerobic bacterial cultures, used in conjunction with the cell count, prove
the most useful in guiding therapy for those with SBP. With regard to ascitic fluid culture, direct inoculation
of routine blood culture bottles at the bedside with 10 mL of ascitic fluid has been reported to significantly
increase the sensitivity of microbiologic studies.
The single best predictor of SBP is an ascitic fluid neutrophil count of greater than 500 cells/L, which
carries a sensitivity of 86% and a specificity of 98%. By lowering the ascitic fluid neutrophil count threshold
to 250 cells/ L, the sensitivity increases to 93% with only a minimal decrease in specificity to 94%.
The fluid should be evaluated for glucose, protein, lactate dehydrogenase (LDH), cell count, Gram
stain, and aerobic and anaerobic cultures. If pancreatitis or a pancreatic leak is suspected, amylase analysis
should be added to the panel. Bilirubin and creatinine levels can be analyzed as well, if a biliary or urinary
leak is suspected as a possible etiology. The peritoneal/ascitic fluid characteristics or levels are then compared
with their respective serum values.
The fluid in bacterial peritonitis generally demonstrates a low pH and low glucose levels with elevated
protein and LDH levels. Traditionally, ascitic fluid pH of less that 7.34 was consistent with a diagnosis of
SBP; however, ascitic pH is less commonly measured because it is unreliable and lacks specificity for the
condition.
SBP is established when the polymorphonuclear neutrophil (PMN) count is 250 cells/L or greater in
conjunction with a positive bacterial culture result. In most of these cases, as mentioned previously, cultures
are positive for a single organism. Obviously, these patients should receive antibiotic therapy. Although up to
30% of cultures remain negative, most of these patients are presumed to have bacterial peritonitis; they
should be treated. A significantly decreased peritoneal fluid glucose level (< 50 mg/dL), a peritoneal fluid
LDH level much greater than the serum LDH, a peritoneal fluid WBC count greater than 10,000 cells/L, a
pH lower than 7.0, high amylase levels, multiple organisms on Gram stain, or recovery of anaerobes from the
culture raises the suspicion of SP in these patients. Some authors recommend repeating the paracentesis in
48-72 hours to monitor treatment success (decrease in neutrophil count to < 50% of the original value).
Culture-negative neutrocytic ascites (probable SBP) is established when the ascitic fluid culture results
are negative but the PMN count is 250 cells/L or greater. This may happen in as many as 50% of patients
with SBP and may not actually represent a distinctly different disease entity. Rather, it may be the result of
poor culturing techniques or late-stage resolving infection. Nonetheless, these patients should be treated just
as aggressively as those with positive culture results.
Monomicrobial nonneutrocytic bacterascites exists when a positive culture result coexists with a PMN
count 250 cells/L or greater. Although this may often be the result of contamination of bacterial cultures,
38% of these patients develop SBP. Therefore, monomicrobial nonneutrocytic bacterascites may represent an
early form of SBP. All study patients described who eventually developed SBP were symptomatic. For this
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reason, any patient suspected clinically of having SBP in this setting must be treated.
Tuberculous peritonitis is identified by ascites with high protein content, a low glucose and low SAAG,
elevated ascitic fluid WBC count, and lymphocyte predominance. In TP, the fluid Gram stain and acid-fast
stain results are rarely positive, and routine culture results are falsely negative in as many as 80% of cases. A
peritoneal fluid protein level greater than 2.5 g/dL, LDH level greater than 90 U/mL, and predominantly
mononuclear cell count of more than 500 cells/L should raise the suspicion of TP, but specificity for the
diagnosis is limited. Laparoscopy with visualization of granulomas on peritoneal biopsy and specific culture
(which requires 4-6 wk) may be needed for definitive diagnosis.
Peritonitis in patients receiving continuous ambulatory peritoneal dialysis (CAPD) is indicated by
contamination of the dialysis catheter; cloudy effluent, total fluid WBC count of greater than 100
neutrophils/L, or presence of organisms on Gram stain.
Routine intraoperative peritoneal fluid cultures in defined acute disease entities (ie, gastric or duodenal
ulcer perforation, appendicitis, diverticulitis or perforation of the colon caused by obstruction or ischemia)
are controversial. Several studies found no significant difference in patients with appendicitis, diverticulitis,
and other common etiologies for bacterial peritonitis with regard to postoperative complication rates or
overall outcomes. The antibiotic regimen was altered only 8-10% of the time based on operative culture data.
In patients who had previous abdominal operations or instrumentation (eg, peritoneal dialysis catheter,
percutaneous stents) and patients with prolonged antibiotic therapy, critical illness, and/or hospitalization,
these cultures may reveal resistant or unusual organisms that should prompt alteration of the antibiotic
strategy.
For a summary of ascitic fluid analysis, see table, below.
Table. Ascitic Fluid Analysis Summary
protein (LDH)
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Glycosaminoglycans
Blood tests. A sample of your blood may be drawn and sent to a lab to check for a high white blood cell
count. A blood culture also may be performed to determine if there are bacteria in your blood.
Most patients will have leukocytosis (>11,000 cells/ L), with a shift to the immature forms on the
differential cell count. Patients who have severe sepsis, are immunocompromised, or have certain types of
infections (eg, fungal, cytomegaloviral) may not have leukocytosis or leukopenia. In cases of suspected SBP,
hypersplenism may reduce the polymorphonuclear leukocyte count.
Blood chemistry findings may reveal dehydration and acidosis. PT, PTT, and INR are indicated. Liver
function tests may be indicated. Amylase and lipase levels should be obtained if pancreatitis is suspected.
Blood culture results are positive for the offending agent in as many as 33% of patients with SBP and may
help guide antibiotic therapy. Measurement of serum albumin allows calculation of the serum-to-ascites
albumin gradient (SAAG). A SAAG of more than 1.1 is noted in SBP.
Imaging tests. Your doctor may want to use an X-ray to check for holes or other perforations in your
gastrointestinal tract. Ultrasound may also be used. In some cases, your doctor may use a computerized
tomography (CT) scan instead of an X-ray.
Radiography.Plain films of the abdomen (eg, supine, upright, and lateral decubitus positions) are often
the first imaging studies obtained in patients presenting with peritonitis. Their value in reaching a specific
diagnosis is limited.
Ultrasonography. Abdominal ultrasonography may be helpful in the evaluation of pathology in the right
upper quadrant (eg, perihepatic abscess, cholecystitis, biloma, pancreatitis, pancreatic pseudocyst), right
lower quadrant, and pelvis (eg, appendicitis, tubo-ovarian abscess, Douglas pouch abscess). However, the
examination is sometimes limited because of patient discomfort, abdominal distention, and bowel gas
interference. Ultrasonography may detect increased amounts of peritoneal fluid (ascites), but its ability to
detect quantities of less than 100 mL is limited. The central (perimesenteric) peritoneal cavity is not
visualized well with transabdominal ultrasonography. Examination from the flank or back may improve the
diagnostic yield, and providing the ultrasonographer with specific information about the patient's condition
and the suspected diagnosis before the examination is important. With an experienced ultrasonographer, a
diagnostic accuracy of greater than 85% has been reported in several series. Ultrasonographically guided
aspiration and placement of drains has evolved into a valuable tool in the diagnosis and treatment of
abdominal fluid collections. Advantages of ultrasound include low cost, portability, and availability.
Disadvantages are that the test is operator dependent, and there is reduced visualization in the presence of
overlying bowel gas and abdominal dressings.
CT scanning. If the diagnosis of peritonitis is made clinically, a CT scan is not necessary and generally
delays surgical intervention without offering clinical advantage. However, CT scanning is indicated in all
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cases in which the diagnosis cannot be established on clinical grounds and findings on abdominal plain films.
CT scans of the abdomen and pelvis remain the diagnostic study of choice for peritoneal abscess and related
visceral pathology.
Whenever possible, the CT scan should be performed with enteral and intravenous contrast. CT scans
can detect small quantities of fluid, areas of inflammation, and other GI tract pathology, with sensitivities that
approach 100%. (See the image below.) CT scanning can be used to evaluate for ischemia, as well as to
determine bowel obstruction. An abscess is suggested by the presence of fluid density that is not bound by
the bowel or other known structures. Gas within an abdominal mass or the presence of an enhancing wall
and adjacent inflammatory changes are also highly suggestive of an abscess. Ischemia can be demonstrated
by a clot in a large vessel or by the absence of blood flow. Gas within the intestinal wall or in the portal vein
may also suggest ischemia.
Free air is present in most cases of anterior gastric and duodenal perforation but is much less frequent
with perforations of the small bowel and colon and is unusual with appendiceal perforation. Upright films are
useful for identifying free air under the diaphragm (most often on the right) as an indication of a perforated
viscus. Remember that the presence of free air is not mandatory with visceral perforation and that small
amounts of free air are missed easily on plain films.
In abscess formation subsequent to secondary peritonitis (SP), approximately half of patients have a
simple abscess without loculation, and the other half have complex abscesses secondary to fibrinous septation
and organization of the abscess material. Abscess formation occurs most frequently in the subhepatic area,
the pelvis, and the paracolic gutters, but it may also occur in the perisplenic area, the lesser sac, and between
small bowel loops and their mesentery.
Peritoneal abscesses and other fluid collections may be aspirated for diagnosis and drained under CT
guidance; this technique has become a mainstay of therapy.
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MRI. MRI is an emerging imaging modality for the diagnosis of suspected intra-abdominal abscesses.
Abdominal abscesses demonstrate decreased signal intensity on T1-weighted images and homogeneous or
heterogeneous increased signal intensity on T2-weighted images; abscesses are observed best on gadolinium-
enhanced, T1-weighted, fat-suppressed images as well-defined fluid collections with rim enhancement.
Limited availability and high cost, as well as the need for MRI-compatible patient support equipment
and the length of the examination, currently limit its usefulness as a diagnostic tool in acute peritoneal
infections, particularly for patients who are critically ill.
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The above tests may also be necessary if you're receiving peritoneal dialysis and a diagnosis of peritonitis
is uncertain after a physical exam and an examination of the dialysis fluid.\
Differential diagnostics
Thoracic processes with diaphragmatic irritation (eg, empyema), extraperitoneal processes (eg,
pyelonephritis, cystitis, acute urinary retention), and abdominal wall processes (eg, infection, rectus
hematoma) may mimic certain signs and symptoms of peritonitis. Always examine the patient for the
presence of external hernias to rule out intestinal incarceration.
According to Adler and Gasbarra, the following should be considered in the differential diagnosis:
Aneurysm, Abdominal
Angioedema
Appendicitis, Acute
Mesenteric Ischemia
Urinary Tract Infection in Females
Whipple Disease
Chemical irritants (eg, bile, blood, gastric juice, barium, enema or douche contents)
Chronic peritoneal dialysis
Chylous peritonitis
Eosinophilic peritonitis
Familial Mediterranean fever
Fungal infections (eg, histoplasmosis, cryptococcosis, coccidioidomycosis)
Granulomatous peritonitis (eg, parasitic infestations, sarcoidosis, tumors, Crohn disease, starch granules)
Gynecologic disorders (Chlamydia peritonitis, salpingitis, endometriosis, teratoma, leiomyomatosis,
dermoid cyst)
HIV-associated peritonitis (from opportunistic organisms)
Mesothelial hyperplasia and metaplasia
Neoplasms (eg, primary mesothelioma, secondary carcinomatosis, Pseudomyxoma peritonei)
Parasitic infections (eg, schistosomiasis, ascariasis, enterobiasis, amebiasis, strongyloidiasis)
Perforated viscus
Peritoneal encapsulation
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The differential diagnostics in toxic and terminal stage of peritonitis when the typical signs of the disease
are present commonly makes no difficulties. But in initial (reactive) stage the sings are similar to
manifestation of causative disease appendicitis, cholecystitis, pancreatitis, etc.). But there are variety of
disorders, which according to their manifestation resemble peritonitis, renal colic for instance. A sharp pain,
nausea, vomiting, intestinal paralysis, and false Shchotkin-Blumberg symptom (peritonism) frequently lead to
misdiagnostics. A periodical pain attack with typical irradiation in thigh, perineum, dysuria, positive
Pasternatsky's symptom, lack of inflammatory changes in blood analysis, presence of erythrocytes in urine
help to make correct diagnosis. For its improvement applied x-ray film of the abdomen, urography and
chromocystoscopy.
A diffuse abdominal pain, muscular tension of abdominal wall and peritonism often accompany
hemorrhagic diatheses (Schonlein-Henoch's disease). This disorder mostly occurs in young people and
manifests by multiple small hemorrhages on skin (forearm, chest, and thigh), mucous membranes of cheeks,
tongue and peritoneum as well. The rectal examination reveals tarry stool or melena. In blood
thrombocytopenia is observed.
Myocardial infarction especially in its location on posterior wall (abdominal form) usually accompanied
by epigastric pain, nausea and vomiting. Also revealed abdominal wall tension with phenomena of
peritonism. But ischemic heart disease in history and characteristic ECG changes can favor correct
diagnostics.
Basal pleurisy and acute lower lobe pneumonia, causing the pain and muscular guard in epigastrium,
also resemble peritonitis. Only thorough clinical examination leads to correct diagnostics.
Approach considerations. The current approach to peritonitis and peritoneal abscesses targets correction
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of the underlying process, administration of systemic antibiotics, and supportive therapy to prevent or limit
secondary complications due to organ system failure. treatment success is defined as adequate source control
with resolution of sepsis and clearance of all residual intra-abdominal infection.
Early control of the septic source is mandatory and can be achieved by operative and nonoperative
means.
Peritonitis is a medical emergency and should be treated by a medical doctor. Do not try to treat
peritonitis with herbs or supplements. However, a comprehensive treatment plan for recovering from
peritonitis may include a range of complementary and alternative therapies. Ask your team of health care
providers about the best ways to incorporate these therapies into your overall treatment plan. Always tell your
health care provider about the herbs and supplements you are using or considering using.
These good nutrition habits may help you recover from any serious illness:
Eat antioxidant foods, including fruits (such as blueberries, cherries, and tomatoes) and
vegetables (such as squash and bell peppers).
Eat foods high in B-vitamins and calcium, such as almonds, beans, whole grains (if no
allergy), dark leafy greens (such as spinach and kale), and sea vegetables.
Avoid refined foods, such as white breads, pastas, and especially sugar.
Eat fewer red meats and more lean meats, cold-water fish, tofu, or beans for protein.
Use healthy oils in foods, such as olive oil or vegetable oil.
Avoid caffeine, alcohol, and tobacco.
Drink 6 - 8 glasses of filtered water daily.
Ask your doctor about taking a multivitamin daily, containing the antioxidant vitamins A,
C, E, the B-complex vitamins, and trace minerals such as magnesium, calcium, zinc, and selenium.
Probiotic supplement (containing Lactobacillus acidophilus among other species), 5 - 10
billion CFUs (colony forming units) a day, for gastrointestinal and immune health. Probiotics can be
especially helpful when taking antibiotics, because probiotics can help restore the balance of "good"
bacteria in the intestines.
Operative management addresses the need to control the infectious source and to purge bacteria and
toxins.
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The type and extent of surgery depends on the underlying disease process and the severity of intra-
abdominal infection. Definitive interventions to restore functional anatomy involve removing the source of
the antimicrobial contamination and repairing the anatomic or functional disorder causing the infection. This
is accomplished by surgical intervention. Occasionally, this can be achieved during a single operation;
however, in certain situations, a second or a third procedure may be required. In some patients, definitive
intervention is delayed until the condition of the patient improves and tissue healing is adequate to allow for a
(sometimes) lengthy procedure.
To see complete information on the Surgical Approach to Peritonitis and Abdominal Sepsis, please go to
the main article by clicking here.
Nonoperative interventions include percutaneous abscess drainage, as well as percutaneous and
endoscopic stent placements. If an abscess is accessible for percutaneous drainage and if the underlying
visceral organ pathology does not clearly require operative intervention, percutaneous drainage is a safe and
effective initial treatment approach. With percutaneous treatment, the definition of success includes the
avoidance of further operative intervention and, in some cases, the delay of surgery until after resolution of
the initial sepsis.
The general principles guiding the treatment of infections are 4-fold, as follows:
Control the infectious source
Eliminate bacteria and toxins
Maintain organ system function
Control the inflammatory process
The treatment of peritonitis is multidisciplinary, with complementary application of medical, operative,
and nonoperative interventions. Medical support includes the following:
Systemic antibiotic therapy
Intensive care with hemodynamic, pulmonary, and renal support
Nutrition and metabolic support
Inflammatory response modulation therapy
Early control of the septic source is mandatory and can be achieved by operative and nonoperative
means. Nonoperative interventional therapies include percutaneous drainage of abscesses and percutaneous
and endoscopic stent placements.
Treatment of peritonitis and intra-abdominal sepsis always begins with volume resuscitation, correction
of potential electrolyte and coagulation abnormalities, and empiric broad-spectrum parenteral antibiotic
coverage.
The treatment of acute peritonitis should be always carried out with appreciation of clinical form and
stage of the disease, causative factor, extension of inflammatory process, degree of metabolic disturbances
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2. Beginning of intubation
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The preoperative preparation in patients with peritonitis should be individual and lasted at least 2-3
hours. In extremely advanced cases, which associated with toxic shock and low arterial pressure it can last to
4-6 hours and must include nasogastric decompression of the stomach with active aspiration, catheterization
of two veins, one of which is central, catheterization of bladder for diuresis control, infusion therapy.
The infusion therapy includes 5 % solution of glucose, solution of albumins, plasma, rheopolyglucin,
vitamins of B and C group, solution of sodium hydrocarbonatis. The volume of fluid infusion should be at
least 1.5-2 l. If there are no improvement of patient's condition before the operation, the infusion therapy
must go on during operative approach.
The most common access in diffuse peritonitis is a median laparotomy, which is the most suitable for
abdominal revision. In case of localized peritonitis (acute appendicitis) oblique incision may be used. The
main goal of surgery must be elimination of infectious focus (appendectomy, cholecystectomy) or closure of
stomach opening (perforating ulcer) or disrupture of hollow viscera. The exudate must be maximum
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removed and peritoneal cavity washed up by antiseptic solutions and thereafter the intestinal decompression
and draining of peritoneal space is performed.
In diffuse peritonitis the peritoneal cavity is drained in right and left hypochondrium and both left and
right inguinal regions. It is better to use double or multiple polyethylene tubes, which are the most suitable for
peritoneal dialysis. ( Fig.9);( Fig.10);( Fig.11)
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Thus the infectious exudate and toxic substances are eliminated and antibiotics and antiseptic solutions
are flown into the abdomen through these tubes. In 1.5-2 hours after the operation before the dialysis the
patient takes a semisedentary position. Then the solutions flow in through the upper tubes and flow out
through the lower. This procedure is performed as far as the solution from the lower tubes becomes clear,
using for this purpose 10-25 l. of fluid.
In recent years instead of dialysis applied peritoneal lavage. Controllable peritoneostomy(Fig.12) in
association with lavage, epidural anesthesia and intestinal intubation allow to rather promptly carry out
sanation of peritoneal cavity and liquidation of inflammatory process. These procedures are repeated in 1-2
days up to complete elimination of pus, fibrin and necrotic tissues. After the last sanation the abdominal wall
is closed.
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detoxycation therapy. For restitution of peristalsis used proserin, 10 % solution of sodium chloride,
hypertonic enema. One of the most important factors in the treatment of peritonitis is the complete restore of
the volume of circulating blood, correction of acid-base balance, blood electrolytes, protein metabolism. The
total amount of fluid is calculated with account of its loss during vomiting, urinary excretion, drainage
discharges and also respiration. For energetic compensation infused concentrated solution of glucose, sorbitol
and lipid emulsion. Also plasma, erythrocyte and blood transfusions are used. In order to prevent hypoxia
oxygenotherapy or hyperbaric oxygenation are applied.
References:
1. Runyon BA. Treatment and prophylaxis of spontaneous bacterial peritonitis.
2. "Biology Online's definition of peritonism". Retrieved 2008-08-14.
3. Prasad AG, et al. Peritonitis, secondary. In: Ferri FF. Ferri's Clinical Advisor 2011: Instant Diagnosis
and Treatment. Philadelphia, Pa.: Mosby Elsevier; 2011.
4. "Peritonitis: Emergencies: Merck Manual Home Edition". Retrieved 2007-11-25.
5. Acute abdominal pain. The Merck Manuals: The Merck Manual for Healthcare Professionals.
6. Fort GG, et al. Peritonitis, spontaneous bacterial. In: Ferri FF. Ferri's Clinical Advisor 2011: Instant
Diagnosis and Treatment. Philadelphia, Pa.: Mosby Elsevier; 2011.
7. Picco MF (expert opinion). Mayo Clinic, Rochester, Minn. June 13, 2011.
8. Badgwell B, Turnage RH. Abdominal Wall, umbilicus, peritoneum,mesenteries, omentum, and
retroperitoneum. In: Townsend CM Jr, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of
Surgery.19th ed. Philadelphia, Pa: Saunders Elsevier; 2012:chap 45.
9. Prather C. Inflammatory and anatomic diseases of the intestine, peritoneum, mesentery, and
omentum. In: Goldman L, Schafer AI, eds. Cecil Medicine. 24th ed. Philadelphia, Pa: Saunders Elsevier;
2011:chap 144.
10.Pavlidis TE. Cellular changes in association with defense mechanisms in intra-abdominal
sepsis. Minerva Chir. Dec 2003;58(6):777-81.
11.Appenrodt B, Grnhage F, Gentemann MG, Thyssen L, Sauerbruch T, Lammert F. Nucleotide-
binding oligomerization domain containing 2 (NOD2) variants are genetic risk factors for death and
spontaneous bacterial peritonitis in liver cirrhosis. Hepatology. Apr 2010;51(4):1327-33.
12.Barretti P, Montelli AC, Batalha JE, Caramori JC, Cunha Mde L. The role of virulence factors in the
outcome of staphylococcal peritonitis in CAPD patients. BMC Infect Dis. Dec 22 2009;9:212.
13.Runyon BA. Management of adult patients with ascites due to cirrhosis. Hepatology. Mar
2004;39(3):841-56.
14.Lata J, Stiburek O, Kopacova M. Spontaneous bacterial peritonitis: a severe complication of liver
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Historical Background
While the term minimally-invasive surgery is relatively recent, the history of its component
parts is nearly 100 years old. What is considered the newest and most popular variety of MIS,
laparoscopy, is in fact the oldest. Primitive laparoscopy, placing a cystoscope within an inflated
abdomen, was first performed by Kelling in 1901. 1 Illumination of the abdomen required hot
elements at the tip of the scope and was dangerous. In the late 1950s Hopkins described the rod
lens, a method of transmitting light through a solid quartz rod with no heat and little light loss.
1 Around the same time, thin quartz fibers were discovered to be capable of trapping light
internally and conducting it around corners, opening the field of fiberoptics and allowing the
rapid development of flexible endoscopes. 2,3 In the 1970s the application of flexible
endoscopy grew faster than that of rigid endoscopy except in a few fields such as gynecology
and orthopedics. 4 By the mid-1970s rigid and flexible endoscopes made a rapid transition
from diagnostic instruments to therapeutic ones. The explosion of video-assisted surgery in the
past 10 years was a result of the development of compact, high-resolution charge-coupled
devices which could be mounted on the internal end of flexible endoscopes or on the external
end of a Hopkins telescope. Coupled with bright light sources, fiberoptic cables, and
high-resolution video monitors, the videoendoscope has changed our understanding of surgical
anatomy and reshaped surgical practice.
While optical imaging produced the majority of MIS procedures, other (traditionally
radiologic) imaging technologies allowed the development of innovative procedures in the
1970s. Fluoroscopic imaging allowed the adoption of percutaneous vascular procedures, the
most revolutionary of which was balloon angioplasty. Balloon-based procedures spread into all
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MIS procedures using ultrasound imaging have been limited to fairly crude exercises, such
as fragmenting kidney stones and freezing liver tumors, because of the relatively low resolution
of ultrasound devices. Newer, high-resolution ultrasound methods with high-frequency crystals
may act as a guide while performing minimally-invasive resections of individual layers of the
intestinal wall.
FIG. 1.
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With the transvenous intrahepatic portosystemic shunt (TIPS), percutaneous access to the
superior vena cava is followed by the retrograde cannulation of the hepatic veins. Next a needle
is advanced through the hepatic parenchyma until the portal venous radicle is located. A
guidewire is passed across this connection, and after dilation a metallic stent is expanded with
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a balloon. While not often performed by surgeons, TIPS represents a particularly creative
example of minimally-invasive surgery. (Reproduced with permission from Hunter JG, Sackier
JM (eds): Minimally-Invasive Surgery. New York: McGraw-Hill, 1993, p 271.)
Axial imaging, such as computed tomography (CT), has allowed the development of an area of
MIS that is not often recognized because it requires only a CT scanner and a long needle.
CT-guided drainage of abdominal fluid collections and percutaneous biopsy of abnormal
tissues are minimally-invasive means of performing procedures that previously required a
celiotomy. Recently, CT-guided percutaneous radiofrequency ablation has emerged as a useful
treatment for primary and metastatic liver tumors. This procedure has also been performed
laparoscopically under ultrasound guidance. 5
A powerful, noninvasive method of imaging that will allow the development of the least
invasiveand potentially noninvasivesurgery is magnetic resonance imaging (MRI).
MRI is an extremely valuable diagnostic tool, but it is only slowly coming to be of therapeutic
value. One obstacle to the use of MRI for MIS is that image production and refreshment of the
image as a procedure progresses are slow. Another is that all instrumentation must be
nonmetallic when working with the powerful magnets of an MRI scanner. Moreover, MRI
magnets are bulky and limit the surgeon's access to the patient. Open magnets have been
developed that allow the surgeon to stand between two large MRI coils, obtaining access to the
portion of the patient being scanned. The advantage of MRI, in addition to the superb images
produced, is that there is no radiation exposure to patient or surgeon. Some neurosurgeons are
accumulating experience using MRI to perform frameless stereotactic surgery.
From the beginning, the tremendous success of minimally-invasive surgery has been founded
on the understanding that a team approach is necessary. The numerous laparoscopic procedures
range from basic to advanced complexity, and require that the surgical team have an intimate
understanding of the operative conduct (Table 13-1). Minimally-invasive procedures require
complicated and fragile equipment that demands constant maintenance. In addition, multiple
intraoperative adjustments to the equipment, camera, insufflator, monitors, and patient/surgeon
position are made during these procedures. As such, a coordinated team approach is mandated
in order to ensure patient safety and excellent outcomes.
A typical MIS team may consist of a laparoscopic surgeon and an operating room nurse with an
interest in laparoscopic surgery. Adding dedicated laparoscopic assistants and circulating staff
with an intimate knowledge of the equipment will add to and enhance the team nucleus.
Studies have demonstrated that having a designated laparoscopic team reduces the conversion
rate and overall operative time, which is translated into a cost savings for patient and hospital.
6
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Physiology
Even with the least invasive of the MIS procedures, physiologic changes occur. Many
minimally-invasive procedures require minimal or no sedation, and there are few alterations to
the cardiovascular, endocrinologic, or immunologic systems. The least invasive of such
procedures include stereotactic biopsy of breast lesions and flexible gastrointestinal
endoscopy. Minimally-invasive procedures that require general anesthesia have a greater
physiologic impact because of the anesthetic agent, the incision (even if small), and the
induced pneumoperitoneum.
Laparoscopy
The unique feature of endoscopic surgery in the peritoneal cavity is the need to lift the
abdominal wall from the abdominal organs. Two methods have been devised for achieving this.
7 The first, used by most surgeons, is the induction of a pneumoperitoneum. Throughout the
early twentieth century intraperitoneal visualization was achieved by inflating the abdominal
cavity with air, using a sphygmomanometer bulb. 8 The problem with using air insufflation is
that nitrogen is poorly soluble in blood and is slowly absorbed across the peritoneal surfaces.
Air pneumoperitoneum was believed to be more painful than nitrous oxide pneumoperitoneum
but less painful than carbon dioxide pneumoperitoneum. Subsequently, carbon dioxide and
nitrous oxide were used for inflating the abdomen. N2O had the advantage of being
physiologically inert and rapidly absorbed. It also provided better analgesia for laparoscopy
performed under local anesthesia when compared with CO2 or air. 9 Despite initial concerns
that N2O would not suppress combustion, controlled clinical trials have established its safety
within the peritoneal cavity. 10 In addition, nitrous oxide has recently been shown to reduce
the intraoperative end-tidal CO2 and minute ventilation required to maintain homeostasis when
compared to CO2 pneumoperitoneum. 10 The effect of N2O on tumor biology and the
development of port site metastasis are unknown. As such, caution should be exercised when
performing laparoscopic cancer surgery with this agent. Finally, the safety of N2O
pneumoperitoneum in pregnancy has yet to be elucidated.
The physiologic effects of CO2 pneumoperitoneum can be divided into two areas: (1)
gas-specific effects and (2) pressure-specific effects (FIG. 2). CO2 is rapidly absorbed across
the peritoneal membrane into the circulation. In the circulation, CO2 creates a respiratory
acidosis by the generation of carbonic acid. 11 Body buffers, the largest reserve of which lies in
bone, absorb CO2 (up to 120 L) and minimize the development of hypercarbia or respiratory
acidosis during brief endoscopic procedures. 11 Once the body buffers are saturated,
respiratory acidosis develops rapidly, and the respiratory system assumes the burden of keeping
up with the absorption of CO2 and its release from these buffers.
FIG. 2.
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Carbon dioxide gas insufflated into the peritoneal cavity has both local and systemic effects
that cause a complex set of hemodynamic and metabolic alterations. [Reproduced with
permission from Hunter JG (ed): Baillire's Clinical Gastroenterology Laparoscopic Surgery.
London/Philadelphia: Baillire Tindall, 1993, p 758.]
In patients with normal respiratory function this is not difficult; the anesthesiologist increases
the ventilatory rate or vital capacity on the ventilator. If the respiratory rate required exceeds 20
breaths per minute, there may be less efficient gas exchange and increasing hypercarbia. 12
Conversely, if vital capacity is increased substantially, there is a greater opportunity for
barotrauma and greater respiratory motioninduced disruption of the upper abdominal
operative field. In some situations it is advisable to evacuate the pneumoperitoneum or reduce
the intra-abdominal pressure to allow time for the anesthesiologist to adjust for hypercarbia. 13
While mild respiratory acidosis probably is an insignificant problem, more severe respiratory
acidosis leading to cardiac arrhythmias has been reported. 14 Hypercarbia also causes
tachycardia and increased systemic vascular resistance, which elevates blood pressure and
increases myocardial oxygen demand. 11,14
The pressure effects of the pneumoperitoneum on cardiovascular physiology also have been
studied. In the hypovolemic individual, excessive pressure on the inferior vena cava and a
reverse Trendelenburg position with loss of lower extremity muscle tone may cause decreased
venous return and cardiac output. 11,15 This is not seen in the normovolemic patient. The most
common arrhythmia created by laparoscopy is bradycardia. A rapid stretch of the peritoneal
membrane often causes a vagovagal response with bradycardia and occasionally hypotension.
16 The appropriate management of this event is desufflation of the abdomen, administration of
vagolytic agents (e.g., atropine), and adequate volume replacement. 17
With the increased intra-abdominal pressure compressing the inferior vena cava, there is
diminished venous return from the lower extremities. This has been well documented in the
patient placed in the reverse Trendelenburg position for upper abdominal operations. Venous
engorgement and decreased venous return promote venous thrombosis. 18,19 Many series of
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advanced laparoscopic procedures in which deep venous thrombosis (DVT) prophylaxis was
not used demonstrate the frequency of pulmonary embolus. This usually is an avoidable
complication with the use of sequential compression stockings, subcutaneous heparin, or
low-molecular-weight heparin. 20 In short-duration laparoscopic procedures, such as
appendectomy, hernia repair, or cholecystectomy, the risk of DVT may not be sufficient to
warrant extensive DVT prophylaxis.
The increased pressure of the pneumoperitoneum is transmitted directly across the paralyzed
diaphragm to the thoracic cavity, creating increased central venous pressure and increased
filling pressures of the right and left sides of the heart. If the intra-abdominal pressures are kept
under 20 mm Hg, the cardiac output usually is well maintained. 19,20,21 The direct effect of
the pneumoperitoneum on increasing intrathoracic pressure increases peak inspiratory pressure,
pressure across the chest wall, and also the likelihood of barotrauma. Despite these concerns,
disruption of blebs and consequent pneumothoraces are rare after uncomplicated laparoscopic
surgery. 21
Increased intra-abdominal pressure decreases renal blood flow, glomerular filtration rate, and
urine output. These effects may be mediated by direct pressure on the kidney and the renal
vein. 22,23 The secondary effect of decreased renal blood flow is to increase plasma renin
release, thereby increasing sodium retention. Increased circulating antidiuretic hormone (ADH)
levels also are found during the pneumoperitoneum, increasing free water reabsorption in the
distal tubules. 24 Although the effects of the pneumoperitoneum on renal blood flow are
immediately reversible, the hormonally mediated changes, such as elevated ADH levels,
decrease urine output for up to 1 hour after the procedure has ended. Intraoperative oliguria is
common during laparoscopy, but the urine output is not a reflection of intravascular volume
status; intravenous fluid administration during an uncomplicated laparoscopic procedure
should not be linked to urine output. Because fluid losses through the open abdomen are
eliminated with laparoscopy, the need for supplemental fluid during a laparoscopic surgical
procedure is rare.
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Thoracoscopy
The physiology of thoracic MIS (thoracoscopy) is different from that of laparoscopy. Because
of the bony confines of the thorax it is unnecessary to use positive pressure when working in
the thorax. 29 The disadvantages of positive pressure in the chest include decreased venous
return, mediastinal shift, and the need to keep a firm seal at all trocar sites. Without positive
pressure, it is necessary to place a double-lumen endotracheal tube so that the ipsilateral lung
can be deflated when the operation starts. By collapsing the ipsilateral lung, working space
within the thorax is obtained. Because insufflation is unnecessary in thoracoscopic surgery, it
can be beneficial to utilize standard instruments via extended port sites in conjunction with
thoracoscopic instruments. This approach is particularly useful when performing advanced
procedures such as thoracoscopic anatomic pulmonary resection.
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FIG. 3.
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Balloons are used to create extra-anatomic working spaces. In this example a balloon is
introduced into the space between the posterior rectus sheath and the rectus abdominis muscle.
The balloon is inflated in the preperitoneal space to create working room for extraperitoneal
endoscopic hernia repair.
Anesthesia
The most important factors in appropriate anesthesia management are related to CO2
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The most natural ports of access for MIS are the anatomic portals of entry and exit. The nares,
mouth, urethra, and anus are used to access the respiratory, gastrointestinal, and urinary
systems. The advantage of using these points of access is that no incision is required. The
disadvantages lie in the long distances between the orifice and the region of interest.
Access to the vascular system may be accomplished under local anesthesia by cutting down and
exposing the desired vessel, usually in the groin. Increasingly, vascular access is obtained with
percutaneous techniques using a small incision, a needle, and a guidewire, over which are
passed a variety of different sized access devices. This approach, known as the Seldinger
technique, is most frequently used by general surgeons for placement of Hickman catheters, but
also is used to gain access to the arterial and venous system for performance of minimally-
invasive procedures. Guidewire-assisted, Seldinger-type techniques also are helpful for gaining
access to the gut for procedures such as percutaneous endoscopic gastrostomy, for gaining
access to the biliary system through the liver, and for gaining access to the upper urinary tract.
In thoracoscopic surgery, the access technique is similar to that used for placement of a chest
tube. In these procedures general anesthesia and split-lung ventilation are essential. A small
incision is made over the top of a rib and, under direct vision, carried down through the pleura.
The lung is collapsed, and a trocar is inserted across the chest wall to allow access with a
telescope. Once the lung is completely collapsed, subsequent access may be obtained with
direct puncture, viewing all entry sites through the videoendoscope. Because insufflation of the
chest is unnecessary, simple ports that keep the small incisions open are all that is required to
allow repeated access to the thorax.
Laparoscopic Access
The requirements for laparoscopy are more involved, because the creation of a
pneumoperitoneum requires that instruments of access (trocars) contain valves to maintain
abdominal inflation.
Two methods are used for establishing abdominal access during laparoscopic procedures.
34,35 The first, direct puncture laparoscopy, begins with the elevation of the relaxed abdominal
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wall with two towel clips or a well-placed hand. A small incision is made in the umbilicus, and
a specialized spring-loaded (Veress) needle is placed in the abdominal cavity (FIG. 4A and B).
With the Veress needle, two distinct pops are felt as the surgeon passes the needle through the
abdominal wall fascia and the peritoneum. The umbilicus usually is selected as the preferred
point of access because in this location the abdominal wall is quite thin, even in obese patients.
The abdomen is inflated with a pressure-limited insufflator. CO2 gas is usually used, with
maximal pressures in the range of 14 to 15 mm Hg. During the process of insufflation it is
essential that the surgeon observe the pressure and flow readings on the monitor to confirm an
intraperitoneal location of the Veress needle tip (FIG. 5). Laparoscopic surgery can be
performed under local anesthesia, but general anesthesia is preferable. Under local anesthesia,
N2O is used as the insufflating agent, and insufflation is stopped after 2 L of gas is insufflated
or when a pressure of 10 mm Hg is reached.
FIG. 4.
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A. Insufflation of the abdomen is accomplished with a Veress needle held at its serrated
collar with a thumb and forefinger. B. Because linea alba is fused to the umbilicus, the
abdominal wall is grasped with fingers or penetrating towel clip in order to elevate the
abdominal wall away from the underlying structures.
It is essential to be able to interpret the insufflator pressure readings and flow rates. These
readings indicate proper intraperitoneal placement of the Veress needle.
After peritoneal insufflation, direct access to the abdomen is obtained with a 5- or 10-mm
trocar. The critical issues for safe direct-puncture laparoscopy include the use of a vented stylet
for the trocar, or a trocar with a safety shield or dilating tip. The trocar must be pointed away
from the sacral promontory and the great vessels. 36 Patient position should be surveyed prior
to trocar placement to ensure a proper trajectory. For performance of laparoscopic
cholecystectomy, the trocar is angled toward the right upper quadrant.
Occasionally the direct peritoneal access (Hasson) technique is advisable. 37 With this
technique, the surgeon makes a small incision just below the umbilicus and under direct vision
locates the abdominal fascia. Two Kocher clamps are placed on the fascia, and with a curved
Mayo scissors a small incision is made through the fascia and underlying peritoneum. A finger
is placed into the abdomen to make sure that there is no adherent bowel. A sturdy suture is
placed on each side of the fascia and secured to the wings of a specialized trocar, which is then
passed directly into the abdominal cavity (FIG. 6). Rapid insufflation can make up for some of
the time lost with the initial dissection. This technique is preferable for the abdomen of
patients who have undergone previous operations in which small bowel may be adherent to the
undersurface of the abdominal wound. The close adherence of bowel to the peritoneum in the
previously operated abdomen does not eliminate the possibility of intestinal injury, but should
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make great vessel injury extremely unlikely. Because of the difficulties in visualizing the
abdominal region immediately adjacent to the primary trocar, it is recommended that the
telescope be passed through a secondary trocar in order to inspect the site of initial abdominal
access. 35 Secondary punctures are made with 5- and 10-mm trocars. For safe access to the
abdominal cavity, it is critical to visualize all sites of trocar entry. 35,36 At the completion of
the operation, all trocars are removed under direct vision and the insertion sites are inspected
for bleeding. If bleeding occurs, direct pressure with an instrument from another trocar site or
balloon tamponade with a Foley catheter placed through the trocar site generally stops the
bleeding within 3 to 5 minutes. When this is not successful, a full-thickness abdominal wall
suture has been used successfully to tamponade trocar site bleeding.
FIG. 6.
The open
laparoscopy technique involves identification and incision of the peritoneum, followed by the
placement of a specialized trocar with a conical sleeve to maintain a gas seal. Specialized wings
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on the trocar are attached to sutures placed through the fascia to prevent loss of the gas seal.
It is generally agreed that 5-mm trocars need no site suturing. Ten-millimeter trocars placed off
the midline and above the transverse mesocolon do not require repair. Conversely, if the fascia
has been dilated to allow the passage of the gallbladder, all midline 10-mm trocar sites should
be repaired at the fascial level with interrupted sutures. Specialized suture delivery systems
similar to crochet needles have been developed for mass closure of the abdominal wall in obese
patients, in whom it is difficult to visualize the fascia through a small skin incision. Failure to
close lower abdominal trocar sites that are 10 mm in diameter or larger can lead to an
incarcerated hernia.
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FIG. 8.
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This is an example of hand-assisted laparoscopic surgery during left colectomy. The surgeon
uses a hand to provide retraction and counter tension during mobilization of the colon from its
retroperitoneal attachments, as well as during division of the mesocolon. This technique is
particularly useful in the region of the transverse colon.
Port Placement
Trocars for the surgeon's left and right hand should be placed at least 10 cm apart. For most
operations it is possible to orient the telescope between these two trocars and slightly retract
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from them. The ideal trocar orientation creates an equilateral triangle between the surgeon's
right hand, left hand, and the telescope, with 10 to 15 cm on each leg. If one imagines the target
of the operation (e.g., the gallbladder or gastroesophageal junction) oriented at the apex of a
second equilateral triangle built on the first, these four points of reference create a diamond
(FIG. 9). The surgeon stands behind the telescope, which provides optimal ergonomic
orientation but frequently requires that a camera operator (or robotic arm) reach between the
surgeon's hands to guide the telescope.
FIG. 9.
The diamond configuration created by placing the telescope between the left and the right
hand, recessed from the target by about 15 cm. The distance between the left and the right hand
is also ideally 10 to 15 cm. In this "baseball diamond" configuration, the surgical target
occupies the second base position.
The position of the operating table should permit the surgeon to work with both elbows in
at the sides, with arms bent 90 at the elbow. 43 It usually is necessary to alter the operating
table position with left or right tilt with the patient in the Trendelenburg or reverse
Trendelenburg position, depending on the operative field. 44,45
Imaging Systems
Two methods of videoendoscopic imaging are widely used. Both methods use a camera with
a charge-coupled device (CCD), which is an array of photosensitive sensor elements (pixels)
that convert the incoming light intensity to an electric charge. The electric charge is
subsequently converted into a black-and-white image. 46 The first of these is flexible
videoendoscopy, where the CCD camera is placed on the internal end of a long, flexible
endoscope. In the second method, thin quartz fibers are packed together in a bundle, and the
CCD camera is mounted on the external end of the endoscope. Most standard gastrointestinal
endoscopes have the CCD chip at the distal end, but small, delicate choledochoscopes and
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nephroscopes are equipped with fiberoptic bundles. 47 Distally-mounted CCD chips were
developed for laparoscopy, but are unpopular.
Video cameras come in two basic designs. The one-chip camera has a black-and-white video
chip that has an internal processor capable of converting gray scales to approximate colors.
Perfect color representation is not possible with a one-chip camera, but perfect color
representation is rarely necessary for endosurgery. The most accurate color representation is
obtained using a three-chip video camera. A three-chip camera has red, green, and blue (RGB)
input, and is identical to the color cameras used for television production. 46 RGB imaging
provides the highest fidelity, but is probably not necessary for everyday use. An additional
feature of newer video cameras is digital enhancement. Digital enhancement detects edges,
areas where there are drastic color or light changes between two adjacent pixels. 48 By
enhancing this difference, the image appears sharper and surgical resolution is improved.
Digital enhancement is available on one- and three-chip cameras. Priorities in a video system
for MIS are illumination first, resolution second, and color third. Without the first two
attributes, video surgery is unsafe. Imaging for laparoscopy, thoracoscopy, and subcutaneous
surgery uses a rigid metal telescope, usually 30 cm in length. This telescope contains a series of
quartz optical rods with differing optical characteristics that provide a specific character to
each telescope. 49 These metal telescopes vary in size from 2 to 10 mm in diameter. Since light
transmission is dependent on the cross-sectional area of the quartz rod, when the diameter of a
rod/lens system is doubled, the illumination is quadrupled. Little illumination is needed in
highly-reflective, small spaces such as the knee, and a very small telescope will suffice. When
working in the abdominal cavity, especially if blood is present, the full illumination of a
10-mm telescope usually is necessary.
Rigid telescopes may have a flat or angled end. The flat end provides a straight view (0),
and the angled end provides an oblique view (30 or 45). 46 Angled scopes allow greater
flexibility in viewing a wider operative field through a single trocar site (FIG. 10); rotating an
angled telescope changes the field of view. The use of an angled telescope has distinct
advantages for most videoendoscopic procedures, particularly in visualizing the common bile
duct during laparoscopic cholecystectomy or visualizing the posterior esophagus or the tip of
the spleen during laparoscopic fundoplication.
FIG. 10.
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The laparoscope tips come in a variety of angled configurations. All laparoscopes have a 70
field of view. A 30 angled scope enables the surgeon to view this field at a 30 angle to the
long axis of the scope.
Light is delivered to the endoscope through a fiberoptic light cable. These light cables are
highly inefficient, losing more than 90% of the light delivered from the light source. Extremely
bright light sources (300 watts) are necessary to provide adequate illumination for video
endosurgery.
The quality of the videoendoscopic image is only as good as the weakest component in the
imaging chain (FIG. 11). Therefore it is important to use a video monitor that has a resolution
equal to or greater than the camera being used. 49 Resolution is the ability of the optical
system to distinguish between line pairs. The larger the number of line pairs per millimeter, the
sharper and more detailed the image. Most high-resolution monitors have up to 700 horizontal
lines. High definition television (HDTV) can deliver up to eight times more resolution than the
standard NTSC/PAL monitors; when combined with digital enhancement, a very sharp and
well-defined image can be achieved. 46,49 A heads-up display (HUD) is a high-resolution
liquid crystal monitor that is built into eyewear worn by the surgeon. 50 This technology
allows the surgeon to view the endoscopic image and operative field simultaneously. The
proposed advantages of HUD include a high-resolution monocular image, which affords the
surgeon mobility and reduces vertigo and eyestrain. However, this technology has not yet been
widely adopted.
FIG. 11.
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The Hopkins rod lens telescope includes a series of optical rods that effectively transmit light
to the eyepiece. The video camera is placed on the eyepiece to provide the working image. The
image is only as clear as the weakest link in the image chain. (Reproduced with permission
from Prescher et al. 46 )
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back receives the flow of electrons that originate at a point source, the surgical electrode. A
fine-tipped electrode causes a high current density at the site of application and rapid tissue
heating. Monopolar electrosurgery is inexpensive and easy to modulate to achieve different
tissue effects. 53 A short-duration, high-voltage discharge of current (coagulation current)
provides extremely rapid tissue heating. Lower-voltage, higher-wattage current (cutting current)
is better for tissue desiccation and vaporization. When the surgeon desires tissue division with
the least amount of thermal injury and least coagulation necrosis, a cutting current is used.
With bipolar electrosurgery the electrons flow between two adjacent electrodes. The tissue
between the two electrodes is heated and desiccated. There is little opportunity for tissue
cutting when bipolar current is used, but the ability to coapt the electrodes across a vessel
provides the best method of small-vessel coagulation without thermal injury to adjacent tissues
54 (FIG. 12).
FIG. 12.
An example of bipolar coagulation devices. The flow of electrons passes from one electrode
to the other and the intervening tissue is heated and desiccated.
In order to avoid thermal injury to adjacent structures, the laparoscopic field of view must
include all uninsulated portions of the electrosurgical electrode. In addition, the integrity of the
insulation must be maintained and assured. Capacitive coupling occurs when a plastic trocar
insulates the abdominal wall from the current; in turn the current is bled off of a metal sleeve or
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laparoscope into the viscera 52 (Fig. 1313A). This may result in thermal necrosis and a
delayed fecal fistula. Another potential mechanism for unrecognized visceral injury may occur
with the direct coupling of current to the laparoscope and adjacent bowel 52 (FIG. 13B).
FIG. 13.
A. Capacitive coupling occurs as a result of high current density bleeding from a port sleeve or
laparoscope into adjacent bowel. B. Direct coupling occurs when current is transmitted directly
from the electrode to a metal instrument or laparoscope, and then into adjacent tissue.
(Reproduced with permission from Odell. 52 )
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Gas, liquid, and solid-state lasers have been available for medical application since the
mid-1960s. 57 The CO2 laser (wavelength 10.6 m) is most appropriately used for cutting
and superficial ablation of tissues. It is most helpful in locations unreachable with a scalpel
such as excision of vocal cord granulomas. The CO2 laser beam must be delivered with a series
of mirrors and is therefore somewhat cumbersome to use. The next most popular laser is the
neodymium yttrium-aluminum-garnet (Nd:YAG) laser. Nd:YAG laser light is 1.064 m
(1064 nm) in wavelength. It is in the near-infrared portion of the spectrum, and, like CO2 laser
light, is invisible to the naked eye. A unique feature of the Nd:YAG laser is that 1064-nm light
is poorly absorbed by most tissue pigments and therefore travels deep into tissue. 58 Deep
tissue penetration provides deep tissue heating (FIG. 14). For this reason the Nd:YAG laser is
capable of the greatest amount of tissue destruction with a single application. 57 Such
capabilities make it the ideal laser for destruction of large fungating tumors of the
rectosigmoid, tracheobronchial tree, or esophagus. A disadvantage is that the deep tissue
heating may cause perforation of a hollow viscus.
When it is desirable to coagulate flat lesions in the cecum, a different laser should be chosen.
The frequency-doubled Nd:YAG laser, also known as the KTP laser (potassium thionyl
phosphate crystal is used to double the Nd:YAG frequency), provides 532-nm light. This is in
the green portion of the spectrum, and at this wavelength, selective absorption by red pigments
in tissue (such as hemangiomas and arteriovenous malformations) is optimal. The depth of
tissue heating is intermediate, between those of the CO2 and the Nd:YAG lasers. Coagulation
(without vaporization) of superficial vascular lesions can be obtained without intestinal
perforation. 58
In flexible gastrointestinal endoscopy, the CO2 and Nd:YAG lasers have largely been replaced
by heater probes and endoluminal stents. The heater probe is a metal ball that is heated to a
temperature (60 to 100C) that allows coagulation of bleeding lesions without perforation.
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to become established.
A unique application of laser technology provides extremely rapid discharge (<106 s) of large
amounts of energy (>103 volts). These high-energy lasers, of which the pulsed dye laser has
seen the most clinical use, allow the conversion of light energy to mechanical disruptive energy
in the form of a shock wave. Such energy can be delivered through a quartz fiber, and with
rapid repetitive discharges, can provide sufficient shock-wave energy to fragment kidney stones
and gallstones. 60 Shock waves also may be created with miniature electric spark-plug
discharge systems known as electrohydraulic lithotriptors. These devices also are inserted
through thin probes for endoscopic application. Lasers have the advantage of pigment
selectivity, but electrohydraulic lithotriptors are more popular because they are substantially
less expensive and are more compact.
Methods of producing shock waves or heat with ultrasonic energy are also of interest.
Extracorporeal shockwave lithotripsy creates focused shock waves that intensify as the focal
point of the discharge is approached. When the focal point is within the body, large amounts of
energy are capable of fragmenting stones. Slightly different configurations of this energy can be
used to provide focused internal heating of tissues. Potential applications of this technology
include the ability to noninvasively produce sufficient internal heating to destroy tissue
without an incision.
A third means of using ultrasonic energy is to create rapidly-oscillating instruments that are
capable of heating tissue with friction; this technology represents a major step forward in
energy technology. 61 An example of its application is the laparoscopic coagulation shears
(LCS) device (Harmonic Scalpel), which is capable of coagulating and dividing blood vessels
by first occluding them and then providing sufficient heat to weld the blood vessel walls
together and to divide the vessel (FIG. 15). This nonelectric method of coagulating and
dividing tissue with a minimal amount of collateral damage has facilitated the performance of
numerous endosurgical procedures. 62 It is especially useful in the control of bleeding from
medium-sized vessels that are too big to manage with monopolar electrocautery and require
bipolar desiccation followed by cutting.
FIG. 15.
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Instrumentation
Hand instruments for MIS usually are duplications of conventional surgical instruments
made longer, thinner, and smaller at the tip. It is important to remember that when grasping
tissue with laparoscopic instruments, a greater force is applied over a smaller surface area,
which increases the risk for perforation or injury. 63
Certain conventional instruments such as scissors are easy to reproduce with a diameter of 3
to 5 mm and a length of 20 to 45 cm, but other instruments, such as forceps and clamps, cannot
provide remote access. Different configurations of graspers were developed to replace the
various configurations of surgical forceps and clamps. Standard hand instruments are 5 mm in
diameter and 30 cm in length, but smaller and shorter hand instruments are now available for
pediatric surgery, for microlaparoscopic surgery, and for arthroscopic procedures. 63 A unique
laparoscopic hand instrument is the monopolar electrical hook. This device is usually
configured with a suction and irrigation apparatus to eliminate smoke and blood from the
operative field. The monopolar hook allows tenting of tissue over a bare metal wire with
subsequent coagulation and division of the tissue.
Robotic Assistance
The term "robot" defines a device that has been programmed to perform specific tasks in
place of those usually performed by people. The equipment that has been introduced under the
heading of robotic assistance would perhaps be more aptly termed computer-assisted surgery,
as it is controlled entirely by the surgeon for the purpose of improving team performance. An
example of computer-assisted surgery includes laparoscopic camera holders, which enable the
surgeon to maneuver the laparoscope either with head movements or voice activation (FIG. 16).
Randomized studies with such camera holders have demonstrated a reduction in operative time,
steadier image, and a reduction in the number of required laparoscope cleanings. 64 This
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device has the advantage of eliminating the need for a human camera holder, which serves to
free valuable operating room personnel for other duties.
FIG. 16.
The surgeon controlled computer-assisted camera holder obviates the need for an additional
assistant. This device may reduce operative times and provide a steadier image.
Another form of computer assistance involves the use of voice-activated system controls for the
camera, light source, insufflators, and telephone. Studies have demonstrated a reduction in the
time required to perform these tasks when compared to human intervention. 65
Nearly all MIS, whether using fluoroscopic, ultrasound, or optical imaging, incorporates a
video monitor as a guide. Occasionally two images are necessary to adequately guide the
operation, as in procedures such as endoscopic retrograde cholangiopancreatography (ERCP),
laparoscopic common bile duct exploration, and laparoscopic ultrasonography. When two
images are necessary, the images should be displayed on two adjacent video monitors or
projected on a single screen with a picture-in-picture effect. The video monitor(s) should be set
across the operating table from the surgeon. The patient should be interposed between the
surgeon and the video monitor; ideally, the operative field also lies between the surgeon and
the monitor. In pelviscopic surgery it is best to place the video monitor at the patient's feet, and
in laparoscopic cholecystectomy, the monitor is placed at the 10 o'clock position (relative to
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the patient) while the surgeon stands on the patient's left at the 4 o'clock position. The
insufflating and patient-monitoring equipment ideally also is placed across the table from the
surgeon, so that the insufflating pressure and the patient's vital signs and end-tidal CO2 tension
can be monitored.
Patient Positioning
Patients usually are placed in the supine position for laparoscopic surgery. When the
operative field is the gastroesophageal junction or the left lobe of the liver, it is easiest to
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operate from between the legs. The legs may be elevated in Allen stirrups or abducted on leg
boards to achieve this position. When pelvic procedures are performed, it usually is necessary
to place the legs in Allen stirrups to gain access to the perineum. A lateral decubitus position
with the table flexed provides the best access to the retroperitoneum when performing
nephrectomy or adrenalectomy. For laparoscopic splenectomy, a 45-tilt of the patient provides
excellent access to the lesser sac and the lateral peritoneal attachments to the spleen. For
thoracoscopic surgery, the patient is placed in the lateral position with table flexion in order to
open the intercostal spaces and the distance between the iliac crest and costal margin (FIG. 18).
When the patient's knees are to be bent for extended periods or the patient is going to be
placed in a reverse Trendelenburg position for more than a few minutes, deep venous
thrombosis prophylaxis should be used. Sequential compression of the lower extremities
during prolonged (more than 90 min) laparoscopic procedures increases venous return and
provides inhibition of thromboplastin activation.
Special Considerations
Pediatric Considerations
The advantages of MIS in children may be more significant than in the adult population. 67
MIS in the adolescent is little different from that in the adult, and standard instrumentation and
trocar positions can usually be used. However, laparoscopy in the infant and young child
requires specialized instrumentation. The instruments are shorter (15 to 20 cm), and many are 3
mm in diameter rather than 5 mm. 68 Because the abdomen of the child is much smaller than
that of the adult, a 5-mm telescope provides sufficient illumination for most operations. The
development of 5-mm clippers and bipolar devices has obviated the need for 10-mm trocars in
pediatric laparoscopy. 68 Because the abdominal wall is much thinner in infants, a
pneumoperitoneum pressure of 8 mm Hg can provide adequate exposure. Deep venous
thrombosis is rare in children, and prophylaxis against thrombosis is probably unnecessary.
Pregnancy
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should be used in favor of direct puncture laparoscopy. The patient should be positioned
slightly on the left side in order to avoid compression of the vena cava by the uterus. Because
pregnancy poses a risk for thromboembolism, sequential compression devices are essential for
all procedures.
Cancer
MIS techniques have been used for many decades to provide palliation for the patient with an
obstructive cancer. Laser treatment, intracavitary radiation, stenting, and dilation are outpatient
techniques that can be used to reestablish the continuity of an obstructed esophagus, bile duct,
ureter, or airway. MIS techniques also have been used in the staging of cancer.
Mediastinoscopy is still used occasionally before thoracotomy to assess the status of the
mediastinal lymph nodes. Laparoscopy also is used to assess the liver in patients being
evaluated for pancreatic, gastric, or hepatic resection. New technology and greater surgical
skills allow for accurate minimally-invasive staging of cancer. 71 Occasionally it is appropriate
to perform palliative measures (e.g., laparoscopic gastrojejunostomy to bypass a pancreatic
cancer) at the time of diagnostic laparoscopy if diagnostic findings preclude attempts at
curative resection. 72
The most controversial role of MIS techniques is that of providing potentially curative surgery
to the patient with cancer. It is possible to perform laparoscopy-assisted colectomy,
gastrectomy, pancreatectomy, and hepatectomy in patients with intra-abdominal malignant
disease, as well as thoracoscopic esophagectomy and pneumonectomy in patients with
intrathoracic malignant disease. There are not yet enough data to indicate whether minimally-
invasive surgical techniques provide survival rates or disease-free intervals comparable to those
of conventional surgical techniques. It has been proven that in laparoscopy-assisted colectomy
and gastrectomy a number of lymph nodes equal to that of an open procedure can be removed
without any compromise of resection margins. A second concern centers on excessive tumor
manipulation and the possibility that cancer cells would be shed during the dissection.
Alarming reports of trocar site implantation with viable cancer cells have appeared in the
literature.
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decreased mobility. By allowing rapid and early mobilization, laparoscopic surgery has made
possible the safe performance of procedures in the elderly and infirm.
Patients with hepatic insufficiency pose a significant challenge for any type of surgical
intervention. 74 The ultimate surgical outcome in this population relates directly to the degree
of underlying hepatic dysfunction. 75 Often, this group of patients has minimal reserve, and the
stress of an operation will trigger complete hepatic failure or hepatorenal syndrome. These
patients are at risk for major hemorrhage at all levels, including trocar insertion, operative
dissection in a field of dilated veins, and secondary to an underlying coagulopathy. 75
Additionally, ascitic leak from a port site may occur, leading to bacterial peritonitis. Therefore
a watertight port site closure should be carried out in all patients.
It is essential that the surgeon be aware of the Child class of severity of cirrhosis of the patient
prior to intervening so that appropriate preoperative optimization can be completed. For
example, if a patient has an eroding umbilical hernia and ascites, a preoperative paracentesis or
transjugular intrahepatic portosystemic shunt (TIPS) procedure in conjunction with aggressive
diuresis may be considered. Because these patients commonly are intravascularly depleted,
insufflation pressures should be reduced in order to prevent a decrease in cardiac output and
minimal amounts of low-salt intravenous fluids should be given.
Minimally-invasive surgical procedures reduce the costs of surgery most when length of
hospital stay can be shortened. For example, shorter hospital stays can be demonstrated in
laparoscopic cholecystectomy, fundoplication, splenectomy, and adrenalectomy. Procedures
such as inguinal herniorrhaphy that are already performed as outpatient procedures are less
likely to provide cost advantage. Procedures that still require a 4- to 7-day hospitalization, such
as laparoscopy-assisted colectomy, are even less likely to deliver a lower bottom line than their
open-surgery counterparts. Nonetheless, with responsible use of disposable instrumentation
and a commitment to the most effective use of the inpatient setting, most laparoscopic
procedures can be made less expensive than their conventional equivalents.
Robotic Surgery
With the development of advanced laparoscopic procedures, the limitations of minimally-
invasive surgical techniques and instrumentation have become accentuated. For example, the
mobility and positioning of a laparoscopic instrument is limited by the placement of the port
site on the abdominal wall. This may prevent the surgeon from obtaining the desired instrument
angle and position to perform a complex maneuver. In addition, the fine motor movements
required to perform complex minimally-invasive surgical procedures may be difficult to
perform with standard laparoscopic instruments and imaging. Computer-enhanced ("robotic")
surgery was developed with the intent of circumventing the limitations of laparoscopy and
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Robotic instruments and hand controls. The surgeon is in a sitting position and the arms
and wrists are in an ergonomic and relaxed position.
FIG. 20.
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Room set-up and position of surgeon and assistant for robotic surgery.
Because this equipment is very costly, a primary limitation to its uniform acceptance has
been attempting to achieve increased value in the form of improved clinical outcomes. There
have been two randomized controlled trials that compared robotic and conventional
laparoscopic approaches to Nissen fundoplication. 78,79 While there was a reduction in
operative time, there was no difference in ultimate outcome. Similar results have been achieved
for laparoscopic cholecystectomy. 80 Finally, it may be too early in its development (due to
bulky equipment, difficulty in accessing patients, and limited instrumentation) for widespread
adoption of this technology.
Endoluminal Surgery
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fluoroscopically guided. Balloon dilators all have low compliancethat is, the balloons do not
stretch as the pressure within the balloon is increased. The high pressures achievable in the
balloon create radial expansion of the narrowed vessel or orifice, usually disrupting the
atherosclerotic plaque, the fibrotic stricture, or the muscular band (e.g., esophageal achalasia).
82
Once the dilation has been attained, it is frequently beneficial to hold the lumen open with a
stent. 83 Stenting is particularly valuable in treating malignant lesions and in endovascular
procedures (FIG. 21). Stenting usually is not applicable for long-term management of benign
gastrointestinal strictures except in patients with limited life expectancy 8385 (FIG. 22A and
B).
FIG. 21.
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The deployment of a metal stent across an isolated vessel stenosis is illustrated. [Reproduced
with permission from Hunter JG, Sackier JM (eds): Minimally-Invasive Surgery. New York:
McGraw-Hill, 1993, p 325.]
FIG. 22.
A variety of stents are available that are divided into two basic categories, plastic stents and
expandable metal stents 84 (FIG. 23). Plastic stents came first and are used widely as
endoprostheses for temporary bypass of obstructions in the biliary or urinary systems. Metal
stents generally are delivered over a balloon and expanded with the balloon to the desired size.
These metal stents usually are made of titanium or nitinol. Although great progress has been
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made with expandable metal stents, two problems remain: propensity for tissue ingrowth
through the interstices of the stent and stent migration. Ingrowth may be an advantage in
preventing stent migration, but such tissue ingrowth may occlude the lumen and cause
obstruction anew. This is a particular problem when stents are used for palliation of
gastrointestinal malignant growth, and may be a problem for the long-term use of stents in
vascular disease. Filling the interstices with Silastic or other materials may prevent tumor
ingrowth, but also makes stent migration more likely. In an effort to minimize stent migration,
stents have been incorporated with hooks and barbs.
FIG. 23.
Most recently, anticoagulant-eluding coronary artery stents have been placed in specialized
centers. 86 This exciting technological advance may dramatically increase the long-term
patency rates of stents placed in patients with coronary artery disease and peripheral
atherosclerosis.
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Intraluminal Surgery
FIG. 24.
An illustration of a radially expanding trocar used for intraluminal surgery. The stomach is
insufflated using a nasogastric tube, and the anterior gastric wall is pierced with the trocar
under laparoscopic guidance. A balloon is inflated and used to draw the stomach up to the
anterior abdominal wall. [Reproduced with permission from Eubanks WS, Swanstrom LL,
Soper NJ (eds): Mastery of Endoscopic and Laparoscopic Surgery. Philadelphia: Lippincott
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The location of the lesion within the gastrointestinal tract is of utmost importance when
considering an intraluminal approach. For example, a leiomyoma that is located on the anterior
gastric wall may not be amenable to intraluminal resection because the working ports must also
penetrate the anterior surface of the stomach. Preoperative endoscopy and endoscopic
ultrasound should be routinely employed in order to determine resectability. 87
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Teleconsultation and telementoring are carried out between two providers who are
geographically separated. The console has a video camera, microphone, and flat screen display
which can be positioned at the operating room table or in the clinic.
The revolution in minimally-invasive general surgery, which occurred in 1990, created ethical
challenges for the profession. The problem was this: If competence is gained from experience,
how was the surgeon to climb the competence curve (otherwise known as the learning curve)
without injuring patients? If it was indeed impossible to achieve competence without making
mistakes along the way, how should one effectively communicate this to patients such that they
understand the weight of their decisions? Even more fundamentally important is determining
the path that should be followed before one recruits the first patient for a new procedure.
Although procedure development is fundamentally different than drug development (i.e., there
is great individual variation in the performance of procedures, but no difference between one
tablet and the next), adherence to a process similar to that used to develop a new drug is a
reasonable path for a surgical innovator. At the outset the surgeon must identify the problem
that is not solved with current surgical procedures. For example, while the removal of a
gallbladder through a Kocher incision is certainly effective, it creates a great deal of disability,
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pain, and scarification. As a result of those issues, many patients with very symptomatic biliary
colic delayed operation until life-threatening complications occurred. Clearly there was a need
for developing a less invasive approach (FIG. 26).
Once the opportunity has been established, the next step involves a search through other
disciplines for technologies and techniques that might be applied. Again, this is analogous to
the drug industry, where secondary drug indications have often turned out to be more
therapeutically important than the primary indication for drug development. The third step is in
vivo studies in the most appropriate animal model. Certainly these types of studies are
controversial because of the resistance to animal experimentation, and yet without such studies
many humans would be injured or killed during the developmental phase of medical drugs,
devices, and techniques. These steps are often called the preclinical phase of procedure
development.
The decision as to when such procedures are ready to come out of the lab is a difficult one. Put
simply, the procedure should be reproducible, provide the desired effect, and not have serious
side effects. Once these three criteria are reached, the time for human application has arrived.
Before the surgeon discusses the new procedure with his patient, it is important to achieve full
institutional support. Clearly, involvement of the medical board, the chief of the medical staff,
and the institutional review board are essential before commencing on a new procedure. These
bodies are responsible for the use of safe, high quality medical practices within their
institution, and they will demand that great caution and all possible safeguards are in place
before proceeding.
The dialogue with the patient who is to be first must be thorough, brutally honest, and well
documented. The psychology that allows a patient to decide to be first is quite interesting, and
may under certain circumstances require psychiatric evaluation. Certainly if a dying cancer
patient has a chance with a new drug, this makes sense. Similarly, if the standard surgical
procedure has a high attendant morbidity and the new procedure offers a substantially better
outcome, the decision to be first is understandable. On the other hand, when the benefits of the
new approach are small and the risks are largely unknown, a more complete psychological
profile may be necessary before proceeding.
For new surgical procedures, it is generally wise to assemble the best possible operative team,
including a surgeon experienced with the old technique, and assistants who have participated
in the earlier animal work. This initial team of experienced physicians and nurses should
remain together until full competence with the procedure is attained. This may take 10
procedures, or it may take 50 procedures. The team will know that it has achieved competence
when the majority of procedures take the same length of time, and the team is relaxed and sure
of the flow of the operation. This will complete phase I of the procedure development.
In phase II, the efficacy of the procedure is tested in a nonrandomized fashion. Ideally, the
outcome of new techniques must be as good or better than the procedure that is being replaced.
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This phase should occur at several medical centers to prove that good outcomes are achievable
outside of the pioneering institution. These same requirements may be applied to the
introduction of new technology into the operating room. The value equation requires that the
additional measurable procedure quality exceeds the additional measurable cost to the patient
or health care system. In phase III, a randomized trial pits the new procedure against the old.
Once the competence curve has been climbed, it is appropriate for the team to engage in the
education of others. During the ascension of the competence curve, other learners in the
institution (i.e., surgical residents) may not have the opportunity to participate in the first case
series. While this may be difficult for them to swallow, the best interest of the patient must be
put before the education of the resident.
The second stage of learning occurs when the new procedure has proven its value and a handful
of experts exist, but the majority of surgeons have not been trained to perform the new
procedure. In this setting, it is relatively unethical for surgeons to forge ahead with a new
procedure in humans as if they had spent the same amount of time in intensive study that the
first team did. The fact that one or several surgical teams were able to perform an operation
does not ensure that all others with the same medical degrees can perform the operation with
equal skill. It behooves the learners to contact the experts and request their assistance to ensure
an optimal outcome at the new center. While it is important that the learners contact the
experts, it is equally important that the experts be willing to share their experience with their
fellow professionals. As well, the experts should provide feedback to the learners as to whether
they feel the learners are equipped to forge ahead on their own. If not, further observation and
assistance from the experts are required. While this approach may sound obvious, it is fraught
with difficulties. In many situations ego, competitiveness, and monetary concerns have short-
circuited this process and led to poor patient outcomes. To a large extent, MIS has recovered
from the black eye that it received early in development, when inadequately trained surgeons
caused an excessive number of significant complications.
If innovative procedures and technologies are to be developed and applied without the mistakes
of the past, surgeons must be honest when they answer these questions: Is this procedure safe?
Would I consider undergoing this procedure if I developed a surgical indication? Is the
procedure as good or better than the procedure it is replacing? Do I have the skills to apply this
procedure safely and with equivalent results to the more experienced surgeon? If the answer to
any of these questions is "no," or "I don't know," there is a professional obligation to seek
another procedure or outside assistance before subjecting a patient to the new procedure.
The management of biliary stones diseases has dramatically changed with the advent of the
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In the past few years, our surgical team has designed and revised numerous management protocols
for various clinical settings effectively achieving impressive improvements in our surgical
performance for the treatment of biliary stone diseases. This chapter will describe these
management protocols and our latest technical updates.
In order to achieve the level of Maximum Surgical Performance with this procedure,
patients at high risk of presenting with Common Bile Duct Stones need to be identified
pre-operatively. The simplest methods to initially identify these patients are:
1) History and Physical Examination,
2) Liver Function Studies,
3) Sonographic Findings.
Patients with a recent history of gallstone pancreatitis, jaundice, or presenting with such
symptoms are at a high risk of having common bile duct pathology; the same is valid for
patients with altered liver function studies. The most accurate studies are the Serum
Transaminases (SGOT, SGPT). Elevations of these enzymes over 20% of their normal values
are significant. But patients with severe, acute cholecystitis can occasionally generate such
elevations. Also, extreme elevations of these two enzymes could represent hepatocytes
necrosis as seen in hepatitis. The bilirubin level may also be elevated in certain patients with
acute cholecystitis, but elevations above 2.5 or 3.0 mg/dl could identify a patient with
choledocholithiasis. Finally, we find the enzymes LDH and GGTP to have no real specific
value in this clinical setting.
It is interesting that in spite of our intensive efforts to identify Common Bile Duct
pathology preoperatively, missed Common Bile Duct Stones are found in 1.92% of all patients.
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This technology is being used with increasing frequency in our surgical service to identify
patients with choledocholithiasis. A GE Magnetic Resonance machine was used for all studies.
To date the specificity and accuracy of these studies in our services is 98.2% for common bile
duct stones over 1 mm in size.
Significant problems have impaired the growth of Laparoscopic Common Bile Duct
exploration. This technique is simply not easy to perform and good results are only achieved by
experienced operators. In addition, this procedure is hardware intensive and the
choledochoscopes are not as reliable as they are touted to be. For these reasons it quickly
become obvious to us, the indications for this procedure were becoming more and more
limited.
Our surgical team promotes the use of Endoscopic Retrograde Cholangiography and
Papillotomy. When not feasible, a laparoscopic transcystic or via anterior choledochotomy
CBDE is performed. It should be mentioned that some critics claim there are no studies
available on the long term effects of endoscopic papillotomies and that it represents a
significant additional cost. Although, this statement is correct, there are also no reports of long
term adverse effects of such procedures.
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Asymptomatic
Incidental Finding on Sonogram
Cholelithiasis
Cholelithiasis on Sonogram, clinical Cholecystitis diagnosis or Positive
Acute Cholecystitis
Pipida Scan
Symptomatic
Positive Sonogram, normal Liver Function Tests
Cholelithiasis
Cholelithiasis with
Abnormal Liver Function Tests (Serum Transaminases elevation or
Suspected
Bilirubin >3.0, gallstone pancreatitis)
Choledocholithiasis
Cholelithiasis with
CBD Stone on Sonogram, MR Cholangiography or Jaundice
Choledocholithiasis
Cholelithiasis with
Pancreatitis on Sonogram, CT or MER Cholangiography or clinically,
Resolving
Documented High Serum Amylase and Lipase - WITH - Decreasing
Gallstone
Serum Pancreatic Enzymes after initial attack
Pancreatitis
MANAGEMENT
PROTOCOLS FOR
UNCOMPLICATED PROPOSED MANAGEMENT
BILIARY STONE
DISEASES
Asymptomatic Cholelithiasis No Surgical Intervention
Asymptomatic Cholelithiasis
No Surgical Intervention
in Diabetic Patients
Symptomatic Cholelithiasis
LapChole
or Acute Cholecystitis
Symptomatic Cholelithiasis
LapChole with Insertion of Cystic Duct Cannula with
with Suspected
Cholangiography, if Choledocholithiasis, postop ERCP
Choledocholithiasis
Symptomatic Cholelithiasis LapChole with Insertion of Cystic Duct Cannula with
with Choledocholithiasis Cholangiography, if Choledocholithiasis, postop ERCP
Cholelithiasis with LapChole with Insertion of Cystic Duct Cannula with
Resolving Pancreatitis Cholangiography, if Choledocholithiasis, postop ERCP
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THE TECHNIQUES
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TROCARS PLACEMENT
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The pneumoperitoneum is obtained in the usual fashion. The trocars are inserted as
indicated.
The stationary grasper [1: lateral position] is utilized to grasp the tip of the gallbladder and
push it over the anterior edge of the liver by progressive traction. Hartmann's pouch is pulled
upward. This exposes the cystic duct and artery as well as the common bile duct. It is important
to constantly maintain this traction. In most cases, the scrub nurse or assistant hold this
retractor. In difficult, longer cases, the handle of the grasper is clamped onto the skin of the
abdomen or onto the protective field. The patient is now positioned head down.
CAUTION: It is not always possible to push the tip of the gallbladder (Re: cirrhotic
patients) over the anterior hepatic edge. In these cases, gently push its tip against the liver,
being very meticulous not to penetrate the parenchyma of the liver.
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Once the field is exposed, Hartmann's pouch is grasped with the lateral working grasper and
pulled laterally, further exposing Calot's triangle. The operator will then pass a dissecting
grasper through the subxyphoid trocar and begin to identify the cystic duct. In acute
cholecystitis, edematous layers of tissue will have to be stripped downward to expose the cystic
duct.
The subxyphoid Dolphin Nose Grasper instrument is passed behind the cystic duct or
actually between the cystic duct and the cystic artery. In most cases, the duct is anterior to the
artery.
CAUTION : Hartmann's pouch should always be identified and visualized. The dissection
of Calot's triangle can be done safely starting from the pouch and moving toward the cystic
duct. This is particularly important in acute cases, when anatomical landmarks are difficult to
find. It is essential to visualize Calot's triangle, which includes the cystic artery, cystic duct and
the common bile duct. If visualization of this area becomes difficult, always check the tension
on the stationary grasper and the intra-abdominal pressure.
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At this juncture, the cystic window is created (i.e., free space behind the cystic duct and the
cystic artery). The clip applier is inserted via the subxyphoid trocar. The cystic duct and artery
are clipped (three clips) as close as possible to the gallbladder. The ENDO CLIP* Applier is
then withdrawn and the EndoShears instrument is inserted to cut them.
CAUTION: Be very careful to clearly identify the junction of the gallbladder and cystic
duct and plan your transection from this anatomical landmark. In doubt, always check with an
IOC.
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Hartmann's pouch is now retracted upward. Using the EndoShears* instrument, the most
lower lateral aspect of Hartmann's pouch should be dissected meticulously.
A 10 mm, large grasper is introduced via the sub-xyphoid trocar. The two lateral graspers
holding the gallbladder present the gallbladder to the newly introduced large grasper. The
gallbladder is pulled from the the intra-abdominal cavity through the same trocar site. This
trocar site can enlarged bluntly with a peon clamp of a few millimeters. An Endocatch
Instrument can be used to remove the specimen.
The intra-abdominal cavity is then thoroughly irrigated with normal saline. All stones that
have dropped into the intra-abdominal cavity are retrieved with a morcilator or stone retrieving
forceps.
The abdomen is deflated; the trocars removed, and the trocar insertion sites are closed in the
usual fashion.
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Additional Instruments:
1. Storz Cholangiograsper 5 mm
2. 1 Ureteral Catheter 4 or 5 F with Adapter
3. Dye Used: Renographin 60
The cystic duct is dissected meticulously as close as possible to the gallbladder. The ENDO
CLIP* Applier is inserted via the sub-xyphoid trocar and the cystic duct is clipped at its
junction with the gallbladder. While maintaining the same exposure, the ENDO CLIP* applier
is withdrawn, an ENDO SHEARS* instrument is inserted via the subxyphoid trocar.
An anterior incision is made on the cystic duct.
The ENDO SHEARS* instrument is then withdrawn and a cholangiocatheter grasper with a
French #4 catheter is inserted. All the side ports of the catheter have been eliminated by cutting
the last 3 cm of the tip. The catheter is inserted into the duct.
In most cases, the intraluminal valves on the cystic duct will make this insertion difficult.
However, with the cholangiocatheter only the very tip of the catheter needs to be inserted to
ensure the flow of bile enters the common bile duct. The grasper is closed around the duct; the
jaws should enclose the entire width of the duct for better performance. The catheter is
irrigated, and no leak should be seen around the entry site.
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If the injection of dye is difficult and slow, and in most cases it is, use a 10cc syringe to
inject the dye.
After completing the operative cholangiogram, the cholangiocatheter and grasper are
removed.
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Pre-exploration Work-up: A correct diagnosis should be made prior to the actual initiation
of the procedure. An intraoperative cholangiogram or another imaging study should
demonstrate common bile duct pathology unequivocally.
1 - 5 mm trocar (available)
Additional Instruments
1 Phantom 5 Plus Balloon Catheter (Microvasive /75cm, 5 Fr./6 mm, 18 Fr.) with Catheter
Introducer
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The Phantom 5 Plus Catheter is connected to the LeVeen Inflator with Pressure Gauge. The
catheter is inserted via the lateral 5 mm trocar into the intraabdominal cavity. A long 4.5 mm
sealed, steel shaft is used to minimize air leaks and to facilitate insertion of the catheter into
the cystic duct.
A glide wire is inserted into the central channel of the Phantom 5 Plus Catheter. This glide
wire is inserted into the Cystic duct and into the common bile duct using direct vision. The
dilating catheter is then passed over the glide wire into the common bile duct. The balloon of
the catheter entering the cystic duct is positioned at the entrance of the cystic duct. The balloon
is inflated for five minutes at 12 atmospheres of pressure. The entrance of the cystic duct has
now been dilated to accommodate a standard 3.0 mm ureteroscope.
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The Phantom 5 Plus Catheter is then removed and replaced by the ureteroscope. This scope
is either connected to an additional camera and monitor, or to an additional camera with a
image splitter. The ureteroscope is inserted into the cystic duct with a high pressure saline flow.
It is pushed into the common bile duct which is visualized and fully explored.
Once a stone is seen, the tip of the ureteroscope is placed proximal to the stone. A Segura
Basket is inserted into the working channel of the ureteroscope, advanced into the common
bile duct and passed beyond the stone. It is then opened and slowly withdrawn under direct
vision. When the stone is in the basket, the basket is closed and the stone grasped. The entire
apparatus, including the ureteroscope and the wire basket, is pulled out of the common bile
duct and the cystic duct. The stone is then released into the intraabdominal cavity and retrieved
in the usual manner.
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Laparoscopic Sutures
T Tube ( Sizes 12 - 18 should be available)
The Technique
This can be performed at the time of a laparoscopic cholecystectomy or in the
post-cholecystectomy patient. In the latter group, the trocars used are the same as for a standard
laparoscopic cholecystectomy.
The common bile duct should be equivocally identified. We rarely proceed with a common
bile duct exploration if the duct is 1cm or less in diameter. A confirmation of the diagnosis is
imperative either via an intra-operative cholangiography or with an intra-operative sonographic
study. A meticulous dissection of the common bile duct is performed using the ENDO
SHEARS* Instrument and a non traumatic grasper from the hepatic bifurcation to the superior
aspect of the pancreas. A section of the common bile duct of about 2 cm should be exposed. In
some cases, the gallbladder is used to give additional retraction as demonstrated in the
following picture. An endoscopic suture can be placed on the lower portion of the gallbladder
and the lateral aspect of the common bile duct. In most cases however, we perform a
choledochotomy without retraction sutures.
Once the choledochotomy is done, the common bile duct is flushed using our high pressure
irrigation device. A Biliary Fogarty Catheter is then used. It is inserted via the subxyphoid
trocar and into the common bile duct, run proximally and distally. This step usually retrieves
most of the common bile stones.
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Once the common bile duct is shown to be free of stones, a T Tube is inserted. The T Tube
is usually inserted via the subxyphoid trocar after its limbs have been cut (each should be 1.0
cm in length). It is then inserted entirely into the intra-abdominal cavity. An additional 5 mm
trocar is inserted in the RUQ. A grasper is inserted via this new trocar to grasp the long limb of
the T Tube. The T Tube is then pulled through the anterior abdominal wall along with the
trocar. The T Tube is then inserted into the common bile duct, using two graspers or ENDO
DISSECT*. The common bile duct is sutured closed with endoscopic sutures. A completion
Cholangiogram is then obtained.
Indications: Acute, severe, gangrenous Cholecystitis and the inability to complete a safe
standard laparoscopic Cholecystectomy.
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The Technique
A standard laparoscopic cholecystectomy has been initiated by the surgeon, at which time
he assesses an anterior laparoscopic cholecystectomy should be performed.
Using the stationary or lateral 5 mm grasper, the tip of the fundus of the gallbladder is
grasped and retracted cephalad. An ENDO SHEARS* Instrument is inserted via the
sub-xyphoid trocar (with electrocautery connection). Using the other lateral grasper, the
anterior aspect of the gallbladder is dissected meticulously. The dissection should be extended
as low as possible toward the cystic duct without compromising the safety of the procedure.
Using the ENDO SHEARS* Instrument, the gallbladder is entered and the anterior wall of
the gallbladder should be resected. Hemostasis should be controlled with the ENDO
SHEARS* Instrument connected to an electrocautery source. Spilled gallstones should be
retrieved and removed with a morcilator-type grasper (10 mm). The specimen should be
removed via the sub-xyphoid trocar. The gallbladder fossa should be flushed thoroughly with
normal saline.
Two Blake drains are inserted into the intra-abdominal cavity. The best method for the
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insertion of these drains is to insert a 5 mm grasper via one of the lateral trocars into the intra-
abdominal cavity and out through the sub-xyphoid trocar. The sub-xyphoid trocar is removed.
The end of the Blake drain is grasped by the grasper outside the abdominal cavity and pulled
back into the intra-abdominal cavity. The lateral grasper pulls it via the 5 mm trocar site. One
drain is inserted into the open gallbladder fossa and the other into the sub-hepatic fossa.
The procedure is completed as usual.
Technical Notes
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cholecystectomies (LC) per year. LC's have largely superceded open cholecystectomies (OC) as
the preferred method of gallbladder removal, accounting for 80% of such procedures in this
country. One limitation of LC as compared to OC is the difficulty in dealing with common bile
duct (CBD) stones. CBD stones are present in approximately 15% of patients, and are
responsible for considerable morbidity and mortality (specifically pancreatitis and ascending
cholangitis) which mandates the removal of such stones.
In OC, surgeons can routinely remove CBD stones via common bile duct exploration
(CBDE), a natural extension of the operative procedure. In LC however, techniques for
detection of CBD stones (intraoperative cholangiography or IOC) and subsequent removal are
beset with pitfalls. IOC, performed by injection of dye via a cystic duct catheter placed
surgically, adds significant time to the operative procedure. It also requires commitment of
additional equipment and personnel to the operating room, and has a false positive rate of stone
detection of up to 12%, sometimes resulting in unnecessary CBDE. Furthermore, the finding of
stones on operative cholangiogram obligates the surgeon to perform CBDE, either laparoscopic
or open . A laparoscopic CBDE is a time consuming, hardware intensive procedure, has a steep
learning curve, is associated with up to a 50% failure rate, and risks injury to the CBD.
Conversion to open CBDE negates the value of a laparoscopic procedure. Another alternative
in patients with stones seen on IOC is to refer the patient postoperatively for ERCP,
papillotomy, and stone removal. However, a technical failure rate of up to 15% in some series
could lead to a second operative procedure, open CBDE.
A number of researchers have attempted to define parameters which could be useful in
preoperative prediction of CBD stones. This includes the presence of any of several
parameters: 1) Increased liver enzymes, 2) Preoperative pancreatitis, jaundice, or cholangitis, 3)
A dilated CBD or intraductal stone on ultrasound, is predictive of CBD stones 25-48% of the
time. Furthermore, stones can be present up to 8% of the time in the absence of such
parameters or risk factors. Strategies to deal with possible CBD stones in patients with risk
factors are complex. One strategy is to do preoperative ERCP with removal of stones (if
present). The problem is that 50-75% of ERCP's performed because of the presence of a risk
factor will show no stones. Thus, a large number of unnecessary ERCP's will be performed,
with a complication rate of 5-10%, and a technical failure rate of up to 15% (i.e. failure to
cannulate CBD). A second strategy is to do IOC on patients with risk factors, and to do
intraoperative stone removal if stones are detected. The problem with this, as mentioned is that
IOC, is time-consuming and associated with up to 12% false positive rate. Subsequent
intraoperative stone removal is both time consuming and risky, and often subjects the patient to
an open procedure. A third strategy is to do postoperative ERCP if the IOC shows stones.
Again, the problem here is that up to a 15% failure risk associated with ERCP would subject
the patient to another surgical procedure to remove the stones.
We have developed a new and simple technique for cholangiography that we believe will
largely supplant existing complicated algorithms for dealing with CBD stones. In this
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Technique
The procedure is initiated as described in the Standard LAPCHOLE Chapter.
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We routinely advance the cannula for about 5-6 cm, and then withdraw the cannula to leave
approximately 1.5 to 2 cm inside the cystic duct.
3. Securing the Cannula in the Cystic Duct
The ENDO DISSECT*or grasper is removed from the intraabdominal cavity and replaced
with the ENDO CLIP* Applier. It is essential to use a USSC ENDO CLIP* or a SURGICON
applier. They are the only instruments that will allow the performance of the next maneuver.
Two clips are placed on the cystic duct. It is essential NOT to close the entire clip around
the cystic duct so as not to entirely obliterate the duct and cannula. The partial closing of the
clip can only be performed with the USSC ENDO CLIP* applier. ( The Ethicon clip Applier
does not have this capability.) Another clip is tightly placed behind the cannula. If using the
SURGICON clip applier, only one clip is used on the cannula and behid it.
The ENDO CLIP* applier is now replaced with the ENDO DISSECT* Grasper. The
Cannula is grasped outside the cystic duct and pulled .5 cm to check that the cannula is not
crushed or locked onto the cystic duct. Then additional cannula is inserted into the
intraabdominal cavity to provide slack, so it can be placed laterally to allow for the completion
of the laparoscopic cholecystectomy. A Blake Drain is inserted at the end of the procedure.
An intraoperative cholangiogram can be performed. If negative, the cannula is removed. We
routinely do not perform an intraoperative cholangiogram. We order it a few hours after the
procedure.
POST-OP ERCP
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ERCP Technique
The cystic duct catheter provides a portal through which a guidewire can be directed into
the duodenum at the time of ERCP. The ability to place a guidewire greatly facilitates
cannulation of the CBD during ERCP, especially in technically difficult cases.
Equipment
Technique
STEP 1. A cholangiogram is first performed via transcystic catheter. This helps identify
CBD and facilitates cannulation of papilla.
STEP 2. ERCP is then performed in the standard fashion.
STEP 3. If cannulation takes longer than 15 minutes, then a 400 cm Zebra wire is advanced
through the transcystic catheter and directed by fluoroscopy into the CBD and through the
papilla.
STEP 4. The endoscopist passes a snare through the biopsy channel of the ERCP scope,
snares the end of the Zebra wire, and pulls it out of the scope.
STEP 5. The papillotomy is flushed with saline and advanced over the wire, through the
scope, and into position in the papilla and CBD.
STEP 6. Endoscopist performs papillotomy over the guidewire and removes
guidewire/papillotomy assembly.
STEP 7. The duct is then swept with an 8.5 mm or 11 mm balloon or a stone retrieval basket
to remove stone(s).
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The transcystic cannula is removed by firmly pulling on it at the bedside or in the ERCP
suite. The Blake drain is left in place and the patient is discharged. The Blake drain is then
removed a few days later as an outpatient.
NOTE: There has been no reported leak following this protocol. However, the Blake drains
are left in place should a bile leak occur.
The Cannula is removed by exerting firm traction. The Blake Drain is left in place and
removed 48 hours later as an outpatient.
Advantages
This technique offers many advantages over existing strategies for dealing with CBD stones.
First, ERCP's will be limited only to those patients who have a stone visualized on transcystic
cholangiogram. For those surgeons or gastroenterologists who currently stratify patients' need
for ERCP according to preoperative risk factors for CBD stones, the TCC approach will
eliminate the need to perform ERCP on up to 80% of patients with positive risk factors but
who have no stones (False Positives). The ERCP associated complications will thereby be
eliminated. Second, the 15% risk of postoperative ERCP failure to cannulate or clear stones
(even up to 10% in biliary referral centers) will be largely eliminated by the ability to place a
transcystic, transpapillary guidewire. This safety valve will greatly facilitate endoscopic access
to the bile duct, eliminate the need for a risky precut papillotomy to gain access to the CBD,
and reduce the potential need for a second operation in patients in whom ERCP was a
technical failure. Third, the TCC should eliminate the need for IOC and CBDE. Since the
TCC/ERCP technique reduces the risks associated with ERCP and optimizes the chance of a
successful outcome, the need for IOC and /or CBDE (laparoscopic or open) is greatly reduced
(including those CBDE's done for false positive IOC's). Fourth, if this technique is applied to
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all laparoscopic cholecystectomies, then all CBD stones will be detected including up to 8% of
patients who have no preoperative risk factors for stones.
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HERNIA
Hernia of the abdominal wall or external hernia (herniae abdominalis externae) is such surgical disease, which is characterized by outlet of the visceral organs from the place of their physiological
placement through the natural channels or defects of the abdominal and pelvic wall. In such case all visceral organs covered by parietal peritoneum and skin cover are not damaged.
Internal hernia (herniae abdominalis internae) is such disease, visceral organs hit the peritoneum pouch. It formed in the place of natural peritoneum fold or recess and generally kept in the abdominal
cavity.
Localizations of the abdominal wall hernias :1 Linea alba; 2Umbilical; 3 Spigelian li-nea; 4Incisional hernia; 5Direct inquinalis hernia;6Femoral hernia;7Indirect
inquinalis hernia
Hernias are divided into two main groups: congenital (herniae conqenitae) and acquired (herniae acguisitae). The main reason of congenital hernias is malformation. Thus, inguinal hernia arose in case of
noclosure of the process of peritoneum, which passes by inguinal channel during descending the testis. On such hernias testis is located in the hernia pouch. Acquired inguinal hernia has hernia pouch and testis
located outside it. Many factors are of great importance in the beginning and developing of the acquired hernia. One of them contributes, other - causes disease. The first are hereditary, anatomical inferiority of the
abdominal wall, sex (inguinal area weakness in males and largeness internal femoral ring in females), age (atrophic processes in older age, anatomical inferiority of the abdominal wall in babies), weight loss,
injury, postoperative scar, physical activity, pregnancy, during which abdominal wall stretched (for example, midline increased in 12 times).
Such reasons, as increased abdominal pressure and weakness of the abdominal wall, cause hernia. That arise after hard physical activity, continued cough, constipation, nerves palsy, which innervated
abdominal wall, injury of muscles or aponeurosis of the abdomen.
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Inguinal hernia
Postoperative hernia
Pathomorphology
Each abdominal hernia consists of hernia gate, hernia sac and hernia contents. Hernia sac forms by outpouching of parietal peritoneum and can contain any organ from abdominal cavity, but mostly small
intestine and omentum. Sometimes it containes other organs: large intestine, urinary bladder, ovary, and appendix.
The main parts of the hernia pouch are neck, body and fundus. Through the hernias gate, peritoneum is outpouching. In the case of sliding hernia organ in the hernia pouch has mesoperitoneal disposition
and not enclosed by peritoneum.
Classification
Clinical management
The typical symptom of hernia is swelling, which arises on vertical position of the patient or during rise of intraperitoneal pressure. These can disappear in a state of dormancy, on vertical position of the
patient or after applying small pressure. Such factors make it possible to confirm hernia.
In the case of hernia primary formation skin over the swelling almost not changed. Hernia is determined by finger examination of the inguinal channel. We can feel positive symptom of the "cough push",
which is caused by cough or by the rise of intraperitoneal pressure. In the case of late stage of hernia developing evagination appear on changing body position from horizontal to verticalor after rising of the
intraperitoneal pressure. If hernia sac contained small intestine than every next tension of the abdominal muscle inflated hernia sac by intestinal loop.
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Diagnostics of the noncomplicated external abdominal hernias is easy. Anamnesis of patients and clinical data are enough. However, we should remember about nonreducible hernias. Such hernia's shape
and dimension often does not change. Patients complicated for continuous pain in the hernia region, which irradiated to other abdominal organs. The main danger of the nonreducible hernias is jamming.
Inguinal hernias is developed in two ways: through the internal (middle) inguinal cavity and external (lateral). In the first case formed direct in other - indirect inguinal hernia.
Indirect hernias could be congenital and acquired. Direct hernias are only acquired and occur in older patients.
There are two main signs, which differentiate direct and indirect hernias. Direct hernia is always located medially from a. epigastrica inf. Indirect hernia is always located laterally from a. epigastrica inf.
The other sign is: direct hernia located medially from deferent duct, indirect hernia located inside it
Femoral hernias are such pathological formation, which is encountered 10-20 times more often in males then females. This is explained by anatomical peculiarity of the females pelvis, wider interval
between femoral vein and lacunar [Gimbernat's] ligament and inguinal [Poupart's] ligament weakness.
There are distinguished femoral hernias, vasculo-lacunar, rural pectineal [Cloquet's] hernia, Hesselbach's hernia.
In addition, there are some kinds of femoral hernias, which can be identified only during the operation:
1) Medial vascular-lacunar femoral hernia, most common;
2) Hernia, which passed through the middle part of vascular lacuna or through the vascular sheath;
3) Lateral vascular-lacunar hernia, which pass outside of the femoral vessels.
Besides, there is middle or prevascular hernia.
Medial vascular -lacunar femoral hernia has three stages of developing:
1) Beginning femoral hernia - swelling does not pass outside internal femoral ring;
2) Incomplete (interstitial) hernia - swelling does not pass outside of superficial fascia;
3) Complete femoral hernia - swelling passed through all anatomical part of the femoral channel and outgoing to the subcutaneous cellular tissue on the anterior femoral surface below inguinal [Poupart's]
ligament.
In spite of small size of the hernia sac, femoral hernia could contain omentum, small intestine and urinary bladder. It is more difficult to diagnose femoral hernia in overweight patients because of
inexpressive clinical signs.
We should differentiate femoral hernias with inguinal hernias, increased or varicose changed lymphatic nodes. In those cases, we should determine external inguinal ring and inguinal ligament.
Midline [epigastric] hernia usually has males in giving age.
There are distinguished supraumbilical, umbilical and paraumbilical hernias.
Very often, such kind of the hernia has no clinical signs and can be determined on the medical examinations. The usual clinical signs are: swelling on linea alba and intermittent pain.
Umbilical hernias occur in 2 % from all kinds of hernia. The most frequent hernias in females (the ratio is 5:1), which is explained by anatomical peculiarity of the females umbilicus after pregnancy. Such
hernia often has two- and three-chambers hernia sacs, which could contain omentum, small intestine, and sometime stomach. Clinical signs depend on those contents. However, it always characterized by pain and
swelling. In some patients swelling is very large.
Diagnosis of the umbilical hernia in typical case is not very difficult. Sometimes it is arduous to differentiate incarcerated umbilical hernia and umbilical metastasis of tumor. We should remember about
umbilical evagination (without organs) in the patients with liver cirrhosis because of presence ascitic fluid in the abdominal cavity.
Lumbar hernias are abdominal wall or retroperitoneal outpouchings. It does not occur very often. The area of the hernia orifice includes the superior costolumbar triangle and the inferior iliolumbar triangle.
Besides that, it could be in aponeurosis slit.
Lumbar hernias could be congenital and acquired. Congenital lumbar hernias are frequently the result of aponeurosis slit or enlargement of the Pti triangle or Hrunfeld interval. Acquired lumbar hernias are
usually result of injury those anatomical structure or after pyoinflammatory diseases.
The most frequent clinical sign is pain. The other signs depend on hernia content. The hernia contents may include any intra- and retroperitoneal structures, e.g., the kidney, small bowel, and omentum.
Diagnosis is made by clinical examination: in the horizontal patient position on healthy side, swelling disappeared, and on the vertical patient position appeared again.
Obturator hernia is the result of wide obturator channel. In those cases hernia sac formes inside pelvic cavity, and than passes through the obturator channel, and arises on internal femoral surface.
Diagnosis of the obturator hernias is not easy, especially in the patients without swelling on the hip. In such cases, patients have complaints for pain along obturator nerve with irradiation to knee joint or
hip joint. Pain increases during leg rotation or abduction. Sometime pain irradiates to the foot.
Sciatic hernias is divided into two main types: hernia of the major sciatic foramen, which passes above and under piriform muscle and hernias of the small sciatic foramen, which passes under sciatic
muscle. Patients complained for pain in the sciatic region, which increased during walking. Sometime pain irradiated along sciatic nerve.
Ischiorectal [perineal] hernia is formed in the urogenital diaphragm or in the perineum muscle. Anterior and posterior hernias are distinguished depending on whether the hernia is anterior or posterior to
the transverse perineal muscle and sacrospinal ligament. Hernia ring formed by rectouterine [Douglas'] pouch in the female and by retrovesical pouch [Proust's space] in the male. Anterior hernias usually contained
internal genital organs or urinary bladder. Posterior hernias usually contained omentum or small intestine loops.
Diagnosis of the anterior ischiorectal hernias, which passed to perineum, usually is not difficult. Diagnostic pitfall should be on the patients with posterior hernias, which is located under large sciatic
muscle and looks like sciatic hernia. In such cases, we performed vaginal and rectal examination or X-Ray examination of the urinary bladder and intestine as required.
There are three types of the lateral abdominal hernias:
1) Acquired hernia of the rectus sheath;
2) Acquired hernias of the Spigelian line;
3) Congenital hernias because of congenital hypoplasia of the abdominal wall.
Clinical signs of lateral abdominal hernias are the same as for other types of hernias, so diagnosis is not very difficult.
The most common complications for all those hernias are incarceration.
Diagnosis program
Inguinal hernia usually should be surgically repaired. On oblique inguinal hernias, we should strengthen anterior wall of the inguinal channel. On direct inguinal hernias, we should strengthen posterior wall
of the inguinal channel. On recurrence hernias - we should strengthen anterior and posterior wall of the inguinal channel.
Bassini repair. After extraction of the hernia sac, we are taking spermatic duct on holders. Between the borders of transverse muscle, internal oblique muscle, transverse fascia and inguinal ligament
interrupted sutures placed. Except that, couples sutures placed between border of abdominal rectus muscle sheath and pubic bone periosteum.
In such way, inguinal space closured and posterior wall strengthened. Spermatic duct placed on the new-formed posterior wall of the inguinal channel. Over the spermatic duct aponeurosis restored by
interrupted sutures.
Girard in such kind of the operations propose to attach the edges of the internal oblique muscle and transversal muscle to the inguinal ligament over the spermatic duct. The aponeurosis of the external
oblique muscle sutured by second layer of the suture. Excess of the aponeurosis is fixed to the muscle in the form of duplication.
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Spasokukotskyy proposed to catch the edges of the internal oblique muscle and transversal muscle with aponeurosis of the external oblique muscles by single-layer interrupted suture.
Martynov proposed the fixation to the Poupart's ligament only internal edge of the external oblique muscle aponeurosis without muscles. External edge of the aponeurosis sutured over internal in the form
of duplication.
Kimbarovskyy, based on the principles of joining similar tissues, proposed special suture: Sutures placed on 1 cm from the edge of the external oblique abdominal muscle aponeurosis, grasped the part of
the internal oblique and transversal muscle. After that, aponeurosis is sutured one more time from behind to the front and attached to the Pouparts ligament.
Kukudganov proposed to restore back wall of inguinal interval. Sutures are placed between the Coupers ligamentum, vagina of direct abdominal muscle and aponeurosis of the transversal muscle.
Postempskyy proposed the deaf closing of inguinal interval with the moving of spermatic duct.
The plastic narrowing of internal inguinal ring of to 0,8 cm is the important moment of this modification. On occasion, when internal and external inguinal rings are in one plane, a spermatic duct is
displaced inlateral direction by transversal incision of the oblique and transversal muscles. Then edge of the vagina of direct muscle and aponeurosis of the internal and transversal muscles is fixed to the Coupers
ligament.
LAPAROSCOPIC HERNIOPLASTY
Laparoscopic hernioplasty:
a view from inside; b cutting of the peritoneum; c remuving the hernia; d fixation by mesh material; e suturing
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video
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HERNIOPLASY BY LICHTENSTEIN
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FEMORAL HERNIA
The are some methods of surgical treatment of the femoral hernia, when the plastic are performed intraperitoneal from the side of thigh through the inguinal channel.
The Bassini method is attributed to femoral. It is performed from a cut, that passes under inguinal fold. After removal of hernia sack a hernia gate is liquidated by suturing of inguinal to the pectineal
ligament.
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The Rudgi-Parlavecho Method. A cut passes parallel to the inguinal fold and higher it (the same as at inguinal hernia). A hernia sack is removed. After that the edges of the transversal and internal oblique
muscles and inguinal ligament sutured to the periosteum of pubic bone.
UMBILICAL HERNIA
For operative treatment of umbilical hernia a few methods are used. The Lexer operation is most widespread. It performed by imposition of sutures on an umbilical ring.
After the Meyo method defect of anterior abdominal wall in the umbilical ring is sutured by U-shaped stitches in transversal direction.
Meyo method
Sapezhko proposed to form duplication of the abdominal white line by stitches in longitudinal direction.
Sapezhko method
At surgical treatment of hernia of abdominal white line, abdominal lateral hernia, lumbar and obturator hernia, sciatic and ischiorectal hernias after deleting of hernia sack it is needed to try to close a hernia
orifice by suturing of fissures in aponeurosis and muscles.
INCARCERATED HERNIA
Incarcerated hernia is sudden pressing of hernia contents in a hernia orifice. Incarceration is the most frequent and most dangerous complication of hernia diseases.
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Depending on mechanism, the elastic and fecal incarceration is distinguished. At the elastic incarceration, after increasing intraabdominal pressure, one or a few organs relocated from an abdominal cavity
to the hernia sack, where it is compressed with following ischemia and necrosis in the area of hernia gate. At the fecal incarceration in the intestinal loop which is in a hernia sack, plenty of excrement passed
quickly. Proximal part of loop is overfilled, and distal is compressed in a hernia gate. So, arose its strangulation, as well as at the elastic incarceration.
Most often the loop of bowel is incarcerated. Thus three parts are distinguished in it: proximal, distal loop, central part. The heaviest pathological changes during incarceration takes place in a strangulated
furrow in the central part of the incarcerated bowel.
Pathomorphology
At incarcerated hernia an important role has all internal rings: inguinal, umbilical, weak places in a diaphragm, orifice of the omental bursa, numeral and variant folds of peritoneum.
In the place of compressing of the bowels and mesentery, as a rule, it is possible to find a strangulation furrow. If circulation of blood changes, the wall of bowel cyanotic, with hemorrhages and necrosis of a
different size. The loop of bowel which is located proximally the places of strangulation are extended, and distal loop mainly without changes.
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The incarcerated hernia is divided into the complete and incomplete. The other types of incarceration is partial (the Richters hernia) and retrograde. The incarcerated hernia can be without the destructive
changes of hernia contents and with the phlegmon of hernia sack.
Clinical management
The clinic of the incarcerated hernia depends on pulling in organ, character and duration of jamming. The clinical signs of the incarcerated hernia can be divided into three groups: 1) local changes; 2)
common signs; 3) complication. From the most characteristic signs of local changes the most common is sharp pain, irreducible hernia, tension of hernia sack that and negative symptom of the "cough push".
Pain sometimes is so intensive that causes pain shock. In the case of intestinal obstruction a pain is attack-like. In case of occurring of peritonitis pain changes the character and becomes permanent.
It is necessary to mean that tensions of hernia sack and incarceration of the hernia, as signs of jamming, lose it value, if hernia was irreducible.
From other side, the isolation of hernia sack from an abdominal region during jamming is the reason of the negative symptom of the "cough push".
The common signs at the incarcerated hernia has phase character. Nausea and vomits during first hours of disease has reflex reason, and on 2nd and 3rd days has toxic reason, that is consequence of
antiperistaltic and reflux of intestinal contents to the stomach.
The temperature of body at first time is normal, and than rises, but usually low grade fever.
The clinic of acute intestinal obstruction and peritonitis develops at the protracted jamming of intestine. The phlegmon of hernia sack can develop in the area of the hernia swelling.
There are different forms of incarceration of internal organs, and accordingly different clinical variants.
Retrograde incarceration. In such cases a hernia sack contains no less than two loops of intestine. But these loops are damaged less, than loop which is in an abdominal cavity. At this variant of jamming
peritonitis arose quicker. So, surgeon during operation must always remember about the necessity of careful revision of the incarcerated loops of bowel.
Parietal incarceration (the Richters hernia). Unlike retrograde, which has wide hernia gate, a similar pathology arises in case of narrow hernia gate. In a hernia sack in such patients located part of bowel
wall, opposite it mesentery edge.
Thus, as a rule, patency of bowel is not broken. Such variant of jamming is dangerous, because there are no evident clinical signs or some of them are quite absent and intestinal patency almost is always
present. Necrosis of bowel wall comes quickly and in 2-3 days the perforation with subsequent development of peritonitis begins after jamming.
The Littres hernia. Jamming of Meckel's diverticulum can come at oblique inguinal hernia. Clinical signs of this pathology reminds the parietal incarceration. Sometimes is possible to palpate dense, short,
thick tension bar in a hernia sack.
Incarceration at sliding hernia. It is observed at patients with inguinal hernia. At sliding hernia of colon, as a rule, there is the fecal incarceration. A bowel is the external wall of hernia sack in such cases.
About it is necessary to remember during opening of hernia sack. Jammings of urinary bladder meet enough rarely, mainly at older-men at oblique sliding hernia of inguinal channel. It is necessary to ask before the
operation, whether a patient had disorders of urination before jamming. Frequent urges, or, opposite, the reflex delay of urination is arose at the beginning of jamming already, and in urine expose macro- or
microhematuria. If during operation at opening of hernia sack it medial wall has dense, doughy consistency, it is an urinary bladder.
At the incarcerated hernia the contents of hernia sack can be also omentum, appendages of colon, internal female genital organs. Sometimes combination of the incarcerated inguinal hernia with different
pathological changes of testicle and deferent duct can take place.
Rough manual reduction of the incarcerated hernia can bring to pseudoreduction. Then the local signs of the incarcerated hernia disappear, and jamming of organs and its consequences is kept. There are five
variants of the pseudoreduction: 1) at multicompartment hernia sacks there is the possible moving of strangulated organs from one chamber in other, that located more deep or in a preperitoneal adipose tissue; 2)
separation and reduction of hernia sack together with it content in an abdominal cavity or in a preperitoneal adipose tissue; 3) abruption of the neck from other part of hernia sack and reduction it together with
content in an abdominal cavity or in a preperitoneal adipose tissue; 4) abruption of the neck from a hernia sack and from a parietal peritoneum with reduction of the incarcerated organs in an abdominal cavity; 5)
break of the incarcerated bowel at the rough reduction of hernia.
Untimely operative at the incarcerated hernia, usually, is complicated by the gangrene of bowel, peritonitis or phlegmon of hernia sack. Such complications considerably worsen clinical status of patient and
require other surgical tactic.
Diagnosis program
1. Anamnesis examination.
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2. Physical examination.
3. Blood analysis and urine analysis.
4. Digital investigation of the rectum.
5. Survey X-Ray of abdominal cavity organs.
Differential diagnostics
As experience shows, the incarcerated hernia we should differentiate with irreducible, which as a rule, is not tense, positive symptom of the "cough push", painful on palpation. A patient complained for long
duration of the disease. The incarcerated hernia needs to be differentiated with coprostasis. In such patients disorder of bowel loop patency, that is in a hernia sack, creates accumulation of excrement. Coprostasis
mostly found at fecal hernia in older people, that suffer from intractable constipation. Clinically it develops gradually and slowly. The hernia swelling almost not painfully, some tense, a positive symptom of the
"cough push". Beginning of coprostasis is unconnected with physical tension. Application of cleansing siphon enema washed of excrement and liquidated coprostasis.
Unreal jamming of hernia. In clinical practice there are often such situation, when during the acute surgical diseases of organs of abdominal cavity free external abdominal hernia becomes irreducible,
painfully and tense, and looks like incarcerated. This is the unreal jamming of hernia, which can be observed at the acute surgical diseases of organs of abdominal cavity, ascites. During examination of such
patients it is necessary to remember, that at the unreal jamming abdominal pain, vomiting, worsening of the general condition and signs of the intestine obstruction come earlier, than changes in a hernia sack.
In addition, during the operation in patients with incarcerated hernia, it is needed to make sure, whether there is a strangulation furrow, or organ, that is in a hernia sack, fixed in a hernia gate. When these
signs are absent, it is possible to consider that jamming is unreal.
The incarcerated femoral hernia must be differentiated with inguinal lymphadenitis, by varicose expansion of large hypodermic vein, varicose knot and their thrombophlebitis, tumor and abscess.
From such pathology without surgical procedure it is possible to differentiate only varicose expansion of veins (varicose knot), for which the positive Valsalv test at horizontal position of patient with the
leg heaved up a knot is empty.
The incarcerated inguinal hernia needs to be differentiated also with hydrocele and orchiepididymitis, cyst of deferent duct, cyst of round ligamentum of uterus, bartholinitis. Patients, who have with such
diseases, a process usually does not spread higher external ring of inguinal channel. Also, absence of testicle in scrotum can be cryptorchiism sign.
The common clinical signs of the internal incarcerated hernia is abdominal pain and symptoms of the intestinal obstruction. A final diagnosis is set during the operation.
Differential diagnostics and clinical variants
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beneath the abcupula, there are dysuric disorders, diarrhea and tenesmus. The temperature of body rises to 38,039,0o, and rectal to considerably higher numbers. In the blood test leukocytosis, change of
formula of blood is fixed to the left.
During the rectal examination the weakened sphincter of anus is found. The front wall of rectum at first is only painful, and then its overhanging is observed as dense painful infiltrate.
A subdiaphragmatic abscess develops at the high placing of appendix. The pain in the lower parts of thorax and in a upper quarter of abcupula ofn to the right, that increases at deep inhalationis except for
the signs of intoxication, is characteristic of it. A patient, generally, occupies semisitting position. Swelling in an epigastric area is observed in heavy cases, smoothing and painful intercostal intervals. The
abcupula ofn during palpation is soft, although tension in the area of right hypochondrium is possible. Painfulness at pressure on bottom (911) ribs is the early and permanent symptom of subdiaphragmatic
abscess (the Krukovs symptom).
Roentgenologically the right half of diaphragm can fall behind from left one while breathing, and there is a present reactive exudate in the right pleura cavity. A gas bubble is considered the roentgenologic
sign of subdiaphragmatic abscess with the horizontal level of liquid, which is placed under the diaphragm.
Interloop abscesses are not frequent complications of acute appendicitis. As well as all abscesses of abdominal cavity, they pass the period of infiltrate and abscess formation with the recreation of the proper
clinic.
The poured festering peritonitis develops as a result of the timely unoperated appendicitis. Diagnostics of this pathology does not cause difficulties.
Pylephlebitis is a complication of both appendicitis and after-operative period of appendectomy.
The reason of this pathology is acute retrocecal appendicitis. At it development the thrombophlebitis process from the veins of appendix, passes to the veins of bowels mesentery, and then on to the portal
vein. Patients complain at the expressed general weakness, pain in right hypochondrium, high hectic temperature of body, fever and strong sweating. Patients are adynamic, with expressed subicteritiousness of the
scleras. During palpation painfulness is observed in the right half of abcupula ofn and the symptoms of irritation of peritoneum are not acutely expressed.
In case with rapid passing of disease the icterus appears, the liver is increased, kidney-hepatic insufficiency makes progress, and patients die in 7-10 days from the beginning of disease. At gradual subacute
development of pathology the liver and spleen is increased in size, and after the septic state of organism ascites arises.
Acute appendicitis is differentiated with the diseases which are accompanied by pain in the abcupula ofn.
Food toxicoinfection. Complaints for pain in the epigastric area of the intermittent character, nausea, vomitings and liquid emptying are the first signs of disease. The state of patients progressively gets
worse from the beginning. Next to that, it is succeeded to expose that a patient used meal of poor quality. However, here patients do not have phase passing, which is characteristic of acute appendicitis, and clear
localization of pain. Defining the symptoms of irritation of peritoneum is not succeeded, the peristalsis of intestine is, as a rule, increased.
Acute pancreatitis. In anamnesis in patients with this pathology there is a gallstone disease, violation of diet and use of alcohol. Their condition from the beginning of a disease is heavy. Pain is considerably
more intensive, than during appendicitis, and is concentrated in the upper half of abcupula ofn. Vomiting is frequent and does not bring to the recovery of patients.
Perforative peptic and duodenum ulcer. Diagnostic difficulties during this pathology arise up only on occasion. They can be in patients with the covered perforation, when portion of gastric juice flows out
in an abdominal cavity and stays too long in the right iliac area, or in case of atipical perforations. Taking it into account, it is needed to remember, that the pain in the perforative ulcer is considerably more
intensive in epigastric, instead of in the right iliac area. On the survey roentgenogram of organs of abdominal cavity under the right cupula of diaphragms free gases can be found.
The apoplexy of ovary more frequent is with young women and, as a rule, on 10-14 day after menstruation. Pain appears suddenly and irradiate in the thigh and perineum. At the beginning of disease there
can be a collapse. However, the general condition of patients suffers insignificantly. When not enough blood was passed in the abdominal cavity, all signs of pathology of abdominal cavity organs calm down after
some time. Signs, which are characteristic of acute anaemia, appear at considerable hemorrhage. Abdomen more frequent is soft and painful down, (positive Kulenkampff's symptom: acute pain during palpation of
stomach and absent tension of muscles of the front abdominal wall).
During paracentesis of back fornix the blood which does not convolve is got.
Extra-uterine pregnancy. A necessity to differentiate acute appendicitis with the interrupted extra-uterine pregnancy arises, when during the examination the patient complains at the pain only down in the
stomack, more to the right. Taking it into account, it is needed to remember, that at extra-uterine pregnancy a few days before there can be intermittent pain in the lower part of the abdomen, sometimes excretions
of coffee colour appear from vagina. In anamnesis often there are the present gynaecological diseases, abortions and pathological passing of pregnancy. For the clinical picture of such patient inherent sudden
appearance of intensive pain in lower part of the abdomen. Often there is a brief loss of consciousness. During palpation considerable painfulness is localized lower, than at appendicitis, the abdomen is soft, the
positive Kulenkampff's symptom is determined. Violations of menstrual cycle testify for pregnancy, characteristic changes are in milk glands, vagina and uterus. During the vaginal examination it is sometimes
possible to palpate increased tube of uterus. The temperature of body more frequently is normal. If hemorrhage is small, the changes in the blood test are not present. The convincing proof of the broken extra-
uterine pregnancy is the dark colour of blood, taken at punction of back fornix of vagina.
Acute cholecystitis. The high placing of vermiform appendix in the right half of abdomen during its inflammation can cause the clinic somewhat similar to acute cholecystitis. But unlike appendicitis, in
patients with cholecystitis the pain is more intensive, has cramp-like character, is localized in right hypochondrium and irradiate in the right shoulder and shoulder-blade. Also the epigastric phase is absent. The
attack of pain can arise after the reception of spicy food and, is accompanied by nausea and frequent vomiting by bile. In anamnesis patients often have information about a gallstone disease. During examination
intensive painfulness is observed in right hypochondrium, increased gall-bladder and positive symptoms Murphy's and Ortner's.
Right-side kidney colic. For this disease tormina at the level of kidney and in lumbus is inherent, hematuria and dysuric signs which can take place at the irritation of ureter by the inflamed appendix.
Intensity of pain in kidney colic is one of the basic differences from acute appendicitis. Pain at first appears in lumbus and irradiate downward after passing of ureter in genital organs and front surface of the thigh.
In diagnostics urogram survey is important, and if necessary chromocystoscopy. Absence of function of right kidney to some extent allows to eliminate the diagnosis of acute appendicitis.
As experience of surgeons of the whole world testifies, in acute appendicitis timely operation is the unique effective method of treatment.
Access for appendectomy must provide implementation of operation. McBurney's incision is typical.
When during operation the appendix without the special difficulties can be shown out in a wound, antegrade appendectomy is executed. On clamps its mesentery is cut off and ligated. Near the basis the
appendix is ligated and cut. Stump is processed by solution of antiseptic and peritonized by a purse-string suture (Pic. 3.3.2).
If only the basis of appendix is taken in a wound, and an apex is fixed in an abdominal cavity, more rationally retrograde appendectomy is conducted (Pic. 3.3.3). Thus the appendix near basis is cut between
two ligatures. Stump is processed by antiseptic and peritonized. According to it the appendix is removed in the direction from basis to the apex. According to indication operation is concluded by draining of
abdominal cavity (destructive appendicitis, exudate in an abdominal cavity, capillary hemorrhage from the bed). In recent years the laparoscopy methods of appendectomy are successfully performed.
In patients with appendiceal infiltrate it is necessary to perform conservative-temporizing tactic. Taking it into account, bed rest is appointed, protective diet, cold on the area of infiltrate, antibiotic therapy.
According to resorption of infiltrate, in two months, planned appendectomy is executed.
Treatment of appendiceal abscess must be only operative. Opening and drainage of abscess, from retroperitoneal access, is performed. To delete here the appendix is not necessary, and because of denger of
bleeding, peritonitis and intestinal fistula even dangerously.
Intestinal obstruction is a complete or partial violation of passing of maintenance by the intestinal truct.
The principal reasons of intestinal obstruction can be:
1) commissures of abdominal cavity after traumas, wounds, previous operations and inflammatory diseases of organs of abdominal cavity and pelvis;
2) long mesentery of small intestine or colon, that predetermines considerable mobility of their loops;
3) tumours of abdominal cavity and retroperitoneal space.
Such principal reasons can cause violation of passing of intestinal maintenance, disorder of suction from the intestine and loss of plenty of electrolytes both from vomiting and in the intestine cavity as a
result of disorders of bloodflow in its wall.
The morphological signs of dynamic intestinal obstruction are: small thickening of wall (at considerable paresis is thinning), friability of tissue (the bowel breaks easily) and presence of liquid maintenance
and gases in cavity of bowel. At mechanical obstruction it is always possible to expose the obstacle: strang, commissures, tumours, jammings of hernia, cicatricial strictures, wrong entered drainages, tampons and
others like that. In place of compression strangulation is exposed. The bowel loop higher strangulation is extended, and distally collapsed. In case of released invagination on small distance two strangulation
furrows are observed, and distally from the second ring cylinder expansion of bowel lumen is observed.
Beginning of clinical signs of intestinal obstruction is sudden in 12 hours after taking the meal. The pain in the abdomen has the intermittent character and is met in all forms of mechanical intestinal
obstruction. However, some types of strangulated intestinal obstruction (node formation, volvulus of thin and colons) can be accompanied by permanent pain. It is needed to mark that at spike intestinal
obstruction, invagination and obturation cramp-like pain can be considered as pathognomic sign of disease. For paralytic intestinal obstruction more frequent is inherent permanent pain which is accompanied by
the progressive swelling of abdomen. At spastic obstruction of intestine the pain is mainly acute, the abdomen is not blown away, sometimes pulled in.
Nausea and vomiting are met in 7580 % patients with the heaviest forms of high level of intestinal obstruction (node formation, volvulus of small intestine, spike obstruction). At obturation obstruction and
invagination they are observed not so often.
There is a characteristic thirst which can be considered as an early symptom. Besides, the higher intestinal obstruction, the greater the thirst.
Swelling of abdomen, the delay of emptying and gases are observed in 8590% patients, mainly, with the high forms of obstruction (volvulus of small intestine, spike intestinal obstruction).
Together with that, for invagination emptying by liquid excrement with the admixtures of mucus and blood are more characteristic.
In patients during palpation the soft abdomen is observed, sometimes with easy resistance of front abdominal wall, and at percussion high tympanitis. At auscultation at the beginning of disease
increased peristaltic noises are present, then gradual fading of peristalsis is positive (the Mondors symptom, noise of beginning, quietness of end).
There are other symptoms pathognomic for intestinal obstruction.
The Valas symptom is the limited elastic sausage-shaped formation.
The Sklarovs symptom is the noise of intestinal splash.
The Kywul's symptom is the clang above the exaggerated bowel.
The Schlange's symptom is the peristalsis of bowel, that arises after palpation of abdomen.
The Spasokukotsky's symptom is noise of falling drop.
The Hochenegg's symptom incompletely closed anus in combination with balloon expansion of ampoule of rectum.
At survey roentgenoscopy or -graphy of the abdominal cavity in the loops of bowels liquids and gas are observed the Klojbers bowl (Pic. 3.3.4).
Strangulated obstruction. The ischemic component is the characteristic feature of this form of intestinal obstruction, that is investigation of squeezing of mesentery vessels, which determines the dynamics of
pathomorphologic changes and clinical signs of disease, and the basic place among them belongs to the pain syndrome. Consequently, sudden appearance of disease, acuteness of pain syndrome and ischemic
disorders in the wall of bowel cause necrosis changes of area of bowel pulling in a process. It is accompanied by the making progress worsening of the patient condition and origin of endotoxicosis.
Obturation intestinal obstruction, unlike strangulated, pass not so quickly. In its clinical picture on the first place there are the symptoms of violation of passage on the intestine (protracted intermittent pain,
flatulence), instead of symptoms of bowel destruction and peritonitis.
For high, especially strangulated, intestinal obstruction progressive growth of clinical signs of disease and violation of secretory function of intestine is inherent. Thus the volume of circulatory blood
diminishes, the level of haematocritis rises and leukocytosis grows. There are also deep violations of homeostasis (hypoproteinemia, hypokalemia, hyponatremia, hypoxia and others like that). In patients with low
intestinal obstruction above-named signs are less expressed, and their growth is related to more protracted passing of disease. Invagination of bowel which can be characterized by the triad of characteristic signs is
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the special type of intestinal obstruction with the signs of both obturation and strangulation: 1) periodicity of appearance of the intermittent attacks of pain in the abdomen; 2) presence of elastic, insignificantly
painful, mobile formation in an abdominal cavity; 3) appearance of blood in the excrement or its tracks (at rectal examination).
The special forms of obturation intestinal obstruction is the obstruction caused by gall-stones. The last are got in the small intestine as a result of bedsore in the walls of gall-bladder and bowel, that adjoins
to it. It is needed to mention that intestinal obstruction can be caused by concrement with considerably more small diameter than bowel lumen. The mechanism of such phenomenon is related to irritating action of
bilious acids on the bowel wall. The last answers this action by a spasm with the dense wedging of stone in the bowel lumen.
Development of intestinal obstruction caused by gall-stones the attack of colic and clinic of acute cholecystitis precede always. Characteristically, that in the process of development of disease the pain
caused by acute cholecystitis calms down, whereupon the new pain characteristic of other pathology intestinal obstruction appears.
Dynamic intestinal obstruction is divided into paralytic and spastic. Paralytic obstruction often arises after different abdominal operations, inflammatory diseases of organs of abdominal cavity, traumas and
poisonings. The reason of spastic intestinal obstruction can be the lead poisonings, low-quality meal, neuroses, hysterias, helminthiasis and others like that. Clinic of dynamic intestinal obstruction is always
variable in signs and depends on a reason, that caused it. Disease is characterized by pain in the abdomen, delay of gases and emptying. During palpation the abdomen is blown away, painful, however soft. To
diagnose this form of intestinal obstruction is not difficult, especially, if its etiology is known.
Hemostatic intestinal obstruction develops after embolism or thromboses of mesenteric arteries and thromboses of veins, there can be mixed forms. Embolism of mesenteric arteries arises in patients with
heart diseases (mitral and aortic failings, heart attack of myocardium, warty endocarditis) and declared by damaging, mainly, upper mesentery arteries. Beginning of disease, certainly, is acute, with nausea,
sometimes vomiting. At first there is a picture of acute abdominal ischemic syndrome, that is often accompanied by shock (frequent pulse, decline of arterial and pulse pressure, death-damp, cyanosys of mucus
membranes and acrocyanosis). Patients become excitative, uneasy, occupy the forced knee-elbow position or lie on the side with bound legs.
During the examination the abdomen keeps symmetry, abdominal wall is soft, the increased peristalsis is heard from the first minutes during 12 hours (hypoxic stimulation of peristalsis), which later goes
out gradually (grave quiet). According to the phenomena of intoxication peritonitis grow quickly. At the beginning of disease the delay of gases and emptying is observed, later there is diarrhea with the
admixtures of blood in an excrement. When the last is heavy to set macroscopically, it is needed to explore scourage of intestine.
Intestinal obstruction must be differentiated with the acute diseases of organs of abdominal cavity.
The perforation of gastroduodenal ulcer, as well as intestinal obstruction, passes acutely with inherent to it by sudden intensive pain and tension of muscles of abdomen. However, in patients with this
pathology, unlike intestinal obstruction, the abdomen is not exaggerated, and pulled in with wooden belly tension of muscles of front abdominal wall. There is also characteristic ulcerous anamnesis.
Roentgenologic and by percussion pneumoperitoneum is observed. Certain difficulties in conducting of differential diagnostics of intestinal obstruction can arise at atipical passing and in case of the covered
perforations.
Acute pancreatitis almost always passes with the phenomena of dynamic intestinal obstruction and symptoms of intoxication and repeated vomiting, with rapid growth. During the examination in such
patients, unlike intestinal obstruction, rigidity of abdominal wall and painfulness is observed in the projections of pancreas and positive Korte's symptom and Mayo-Robson's. The examination of diastase of urine
and amylase of blood have important value in establishment of diagnosis.
Acute cholecystitis. Unlike intestinal obstruction, patients with this pathology complain for pain in right hypochondrium, that irradiate in the right shoulder-blade, shoulder and right subclavian area.
Difficulties can arise, when the symptoms of dynamic intestinal obstruction appear on the basis of peritonitis.
The clinic of kidney colic in the signs and character of passing are similar to intestinal obstruction, however, attacks of pain in the lumbar area with characteristic irradiation in genital parts, the thigh and
dysuric disorders help to set the correct diagnosis. Certain difficulties in conducting of differential diagnostics also can arise in difficult patients, at frequent vomiting which sometimes can be observed in patients
with kidney colic.
During the first 1,52 hours after hospitalization of patient complex conservative therapy which has the differential-diagnostic value and can be preoperative preparation is conducted.
It is directed on warning of the complications related to pain shock, correction of homeostasis and, simultaneously, is the attempt of liquidation of intestinal obstruction by unoperative methods.
1. The measures directed for the fight against abdominal pain shock include conducting of neuroleptanalgesia, procaine paranephric block and introduction of spasmolytics. Patients with the expressed pain
syndrome and spastic intestinal obstruction positive effect can be attained by epidural anaesthesia also.
2. Liquidation of hypovolemia with correction of electrolyte, carbohydrate and albuminous exchanges is achieved by introduction of salt blood substitutes, 510 % solution of glucose, gelatinol, albumen
and plasma of blood. There are a few methods suitable for use in the urgent surgery of calculation of amount of liquid necessary for liquidation of hypovolemia. Most simple and accessible is a calculation by the
values of hematocrit. If to consider 40 % for the high bound of hematocrit norm, on each 5 % above this size it is needed to pour 1000 ml of liquids.
3. Correction of hemodynamic indexes, microcirculation and disintoxication therapy is achieved by intravenous infusion of Reopolyhlukine and Neohemodes.
4. Decompression of intestine truct is achieved by conducting of nasogastric drainage and washing of stomach, and also conducting of siphon enema. It is needed to underline that technically the correct
conducting of siphon enema has the important value for the attempt of liquidation of intestinal obstruction by conservative facilities, therefore this manipulation must be conducted in presence of a doctor. For
such enema the special device is used with the rectal tip, by a PVC pipe by a diameter of 1,52,0 cm and watering-can of very thin material. A liquid into the colon is brought to appearance of the pain feeling, then
drop the watering-can below the level of patient who lies. The passage of gases and excrement is looked after. As a rule, this manipulation is to repeat repeatedly with the use of plenty of warm water (to 1520 and
more litres).
Liquidating of the intestinal obstruction by such conservative facilities is succeeded in 5060 % patients with mechanical intestinal
obstruction.
Patients with dynamic paralytic intestinal obstruction are expedient to stimulation of peristalsis of intestine to be conducted, besides, necessarily after infusion therapy and correction of hypovolemia. A lot
of kinds of stimulation of intestine peristalsis are offered. Most common of them are:
1) hypodermic introduction of 1,0 ml of 0,05 % solution of proserin; 2) through 10 min 60 ml intravenously stream of 10 % solution of chlorous sodium; 3) hypertensive enema.
Surgical treatment of intestinal obstruction must include such important moments:
1. According to middle laparotomy executed the novocaine blockade of mesentery of small and large intestine and operative exploration of abdominal cavity organs during which the reason of intestinal
obstruction and expose viability of intestine is set.
The revision at small intestine obstruction begins from the Treitz' ligament to iliocecal corner. At large intestine obstruction the hepatic, splenic and rectosigmoid parts are observed intently. Absence of
pathological processes after revision needs the examination of places of cavity and jamming of internal hernia: internal inguinal and femoral rings, obturator openings, pockets of the Treitz' ligament, Winslow's
opening, diaphragm and periesophageal opening.
2. Liquidation of reasons of obstruction (scission of connection, that squeezes a bowel, violence of volvulus and node formation of loops, desinvagination, deleting of obturative tumours and others like
that).
It is needed to mark that the unique method of liquidation of acute intestinal obstruction does not exist. At the lack of viability of bowel the resection of nonviable area is executed with 3040 cm of afferent
and 1520 cm of efferent part with imposition of side-to-side anastomosis (Pic. 3.3.5) or end-to-end (Pic. 3.3.6).
3. Intubation. Decompression of intestine foresees conducting in the small intestine of elastic probe by thickness of 89 mm and length of 33,5 with the plural openings by a diameter 22,5 mm along all
probe, except for part, that will be in the oesophagus, pharynx and outwardly. A few methods of conducting of probe are offered in a bowel (nasogastric, through gastrostomy, ceco- or appendicostoma). Taking it
into account, such procedure needs to be executed individually and according to indications.
Each of them has the advantages and failings. In connection with the threat of origin of pneumonia, entering an intubation probe to the patients of old ages is better by means of gastrostomy. Most surgeons
avoid the method of introduction of probe through ceco- or appendicostoma because of technical difficulties of passing in a small intestine through a Bauhin's valve. Today the most wide clinical application has
intubation of intestine extracted by the nasogastric method with the use of other thick probe as explorer of the first (by L.J. Kovalchuk, 1981). Such method not only simplifies procedure of intubation but also
facilitates penetration through the piloric sphincter and duodenojejunal bend, and also warns passing of intestinal maintenance in a mouth cavity and trachea. Thus probe is tried to be conducted in the small
intestine as possible farther and deleted the next day after appearance of peristalsis and passage of gases, however not later than on 7th days, because more protracted sign of probe carries the real threat of
formation of bedsores in the wall of bowel.
4. Sanation and draining of abdominal cavity is executed by the generally accepted methods of washing of antiseptic. Draining of the abdominal cavity it is needed from four places: in both iliac areas and
both hypochondrium, better by the coupled synthetic drainpipes.
Crohns disease is an unspecific inflammatory process of submucosal membrane of gastrointestinal truct with propensity to the segmental lesions and recurrent passing. The local signs of disease exist in
different areas of digestive truct organs, however, most frequent and most intensive they are in the distal segment of small intestine, therefore it was named terminal ileitis.
The reason of origin of the Crohns disease for today is not finally found out. An infection and allergy are infringement factors. Together with that, granuloma, which is exposed at histological examination
with present in its lymphocytic and protoplasmatic infiltrations, grounds to consider that the defined value in the origin of the Crohns disease have immune factors. Thus inflammation begins in the submucosal
membrane, and afterwards engulfs all bowel walls. The mucus membrane acquires the crimson colouring, there are deep cracks and ulcers. Combination of the damaged areas of mucus membrane with healthy
creates a picture similar to the roadway. In future granuloma appears, an inflammatory process goes out outside the wall of bowel and gets to the contiguous organs (large and small intestines, urinary bladder,
abdominal wall). In the eventual result there are infiltrate, abscesses and fistula. Finally, it is needed to mark that the people of young ages mainly are ill by terminal ileitis.
The morphological changes are concentrated, mainly, in the terminal part of iliac bowel, anal segment of rectum and appendix. Internal surface is hilly, thickened, swelling, deep ulcers are intermittent with
the unchanged areas of mucus. The serous tunic is covered by plural, similar on tuberculosis, knots. Mesentery is sclerosed, regional lymphatic knots are hyperplastic, of whiter-rose color. By the most
characteristic microscopic sign of Crohns disease is presence of unspecific sarcoid granuloma. Hyperplasia of lymphoid elements of submucosal membrane and formation of fissured ulcers is observed also.
The Crohns disease begins from the insignificant signs as a general weakness, increase of temperature of body, intermittent pain, that arises after the reception of meal, diarrhea without some visible features
or with the admixture of blood. As this process strikes the terminal segment of small intestine, pain is concentrated in the right iliac area. Together with that, at localization of pathological focus in a colon with an
anal segment pain is concentrated by its passing to the anal opening. A granuloma process takes place in the area of oesophagus, abdomen or duodenum, pain can arise up in the area of lesions. With progress of
disease on endoscopy examination (proctosigmoidoscopy, fiberoptic colonoscopy, fiberoptic gastroscopy) hyperemia and deep cracks of mucus membrane, ulcers, symptom of roadway and stenosis are observed.
At roentgenoscopy survey of organs of abdominal cavity in patients with the perforation it is possible to expose pneumoperitoneum, and at contrasting sciagraphy stenosis of initial part of stomach, presence of
ulcers or granuloma in the oesophagus. The examination of the passage on the small intestine enables to eliminate or confirm stenosis (Pic. 3.3.7). Irrigoscopy determines the defect of filling.
At acute passing of terminal ileitis, the pain appears acute in the right iliac area, sometimes intermittent, accompanied by nausea, vomitings, emptying by a liquid excrement with the admixture of blood or
delay of emptying. During the examination of patient the abdomen can be exaggerated, tension of muscles and positive symptoms of irritation of peritoneum, high temperature is observed. In the general analysis of
blood leukocytosis is present with the change of leukocyte formula to the left. In such difficult situation often only laparotomy helps to specify the diagnosis. The swollen segment of iliac bowel is thus observed
with increased mesentery lymphatic knots. The changed area of bowel can perforate in the free abdominal cavity or penetrate in the contiguous loops of large or small intestine. It causes forming of inflammatory
infiltrate, and in future abscess formation. The unoperated abscesses are always inclined to the independent opening in surrounding organs with subsequent formation of fistula ducts.
The disease with the lesions of other parts of small and large intestine passes acutely (granulomatous enteritis, colitis). By palpation in these patients painful infiltrate is exposed, which by the character
remind the clinic of invagination. Only the meticulous examination and present data analysis enable to set correct diagnosis. At granulomatous proctitis the plural cracks of mucus membrane without the signs of
spasm of sphincter appear often, on the basis of which afterwards there are ulcers, that badly granulate. The same changes can develop on skin round the anal opening.
The chronic forms of disease often pass with insignificant symptoms. From the beginning of disease to establishment of diagnosis sometimes 12 years and more pass. Such patients periodically complain
for pain, diarrhea, weight loss, increase of body temperature, nausea, vomitings and bleeding from a rectum.
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Objectively in the abdominal cavity painful infiltrate is determined, and at laboratory examination anaemia and hypoproteinemia.
Complications of the Crohns disease can be divided into local and general. Among local, formations of fistula which arise on the front abdominal wall between the damaged bowel and surrounding organs
are most characteristic (ileoileal fistula, entero-entero, enterovesical fistula). Sometimes fistulas are opened in the area of scars after the operations on the lateral wall of abdomen or in the area of anus. Next to
that, stenosis inflammatory infiltrate of bowel can be transformed in acute or chronic intestinal obstruction. Some patients have the obvious threat of perforation of the changed wall of bowel or intestinal bleeding.
The protracted passing of disease can be also complicated by malignization. The aphthous ulcers of tongue, node erythema, arthritises and chronic lesionss of liver are general complications.
The Crohns disease must be differentiated with the unspecific ulcerous colitis and cancer of colon.
An unspecific ulcerous colitis mainly initially strikes the mucus membrane of all colon. The disease is accompanied by the excreta with the excrement of plenty of blood and mucus. For Crohns disease
languid passing of disease is characteristic. Acute passing of disease is met considerably rarer, than chronic. The modern methods of endoscopic examination with the biopsy of mucus membrane, which helps to
specify diagnosis, are helpful in differential diagnostics.
The cancer of colon is mostly accompanied by formation of deep ulcers and infiltrate. However, for the cancer process slowly progressive passing without the periods of remission is more inherent, thus the
disease more frequently ends with the phenomena of intestinal obstruction. At roentgenologic examination on the background the relatively unchanged colon the lonely defect of filling is observed, and during
colonoscopy thrusting out in the lumen of bowel with an erosive surface or signs of disintegration. Histological examination of biopsy material enables to expose cancer cells.
Conservative treatment. The diet of patient, generally, must be ordinary, except for products with bad intestinal uptake. The medicine of the first row is 5-S (aminosalicylic acid, sulfasalazone and
glucocorticoid). The medicines of the second row are: 6- mercaptopurine, azatiopurine and metronidazole. At diarrhea diphenoxilate is used 5 ml peroral three times per days, loperamide 2 mg peroral 34
times per days, smecta 1 pack 3 times per days. At the expressed anaemia, to the considerable loss of weight, system complications, relapse of disease after operation prednisolone is applied for 4060 mg
peroral every day during 12 weeks. After that its day's dose is diminished to 1020 mg during 46 weeks and, in the end, stopped. For patients which are irresponsive to steroid, asatioprine is appointed (2 /)
peroral. Metronidazole in a dose of 400 mg twice a days is used in the case of granulomatous disease of perineum.
The presence of external and internal fistula, stenosis of bowel, perforation and recurrent bleeding is an indication to operative treatment. The method of choice of operation is the segmental resection of the
pathologically changed bowel in the distance of 3035 cm of proximal and distal from the damaged area. The regional limph nodes is also deleted. In case of the perforation of bowel with poured peritonitis, it is
recommend not to perform primary anastomosis because of possible insolvency of stitches after the resection. In this connection, afferent and efferent loops exteriorizes on the wall of abdomen as two-channel
stoma (Pic. 3.3.8). The passage by an intestine (liquidation of stoma) is restored in 24 months after liquidation of the peritonitis signs.
An unspecific ulcerous colitis is a diffuse inflammatory process that is accompanied by the ulcerous-necrosis changes in the mucus membrane of colon and rectums.
Etiology of unspecific ulcerous colitis to this time is not finally found out. This disease is suffered by people in the age from 20 to 40 years. An infectious factor in development of disease for today is not
confirmed. However, as the exception of meal of food allergens (milk, eggs) results in the improvement of passing of disease, it is possible to consider that allergy assists to development of inflammatory process.
Important significance in genesis of this pathology is also attached to immunological violations. In the blood of patient sensibilizing on the antigen of mucus membrane of colon specifically lymphocytes and
immune complexes are found. The antigen-antibody reaction can cause colitis. In most patients with the chronic recurrent unspecific ulcerous colitis a stress situation causes the process of acutening. In future,
obviously, there are violations of microcirculation and cellular structures, and also the transport system of cells membranes suffers, that carries potassium and sodium ions. Taking it into account, the timely
exposure of disease in which the process is localized and has a reverse tendency, can result in the positive therapeutic effect.
In patients with an unspecific ulcerous colitis the relatively isolated damages of rectum and sigmoid colon, sigmoid colon and transverse colon, so total colitis are met. The necrosis component prevails as
the acute form. The wall of bowel in such cases is swollen, hyperemic, with plural erosions and ulcers of irregular form. Its infiltration by lymphocytes, plasmocytes and eosinophils with characteristic formation of
granulation, crypt and abscesses are microscopically observed. In patients with a chronic process prevail, mainly, reparative-sclerotic processes. A bowel is deformed, dense, segmentally narrowed. As a result of
the disfigured regeneration plural granulomatous and adenomatous pseudopolypuses appear.
Pain in the abdomen and diarrhea is one of basic signs of unspecific ulcerous colitis with emptying from 3 to 20 and more times per days. Thus during defecation the mixture of liquid excrement, mucus and
blood are observed. As far as progress of disease the pain has the intermittent character and is localized by the passing of colon. By palpation it is spastic and painful. Frequent diarrhea is brought to dehydration,
loss of electrolytes, albumen and anaemia. Patients are weak, there are the strongly expressed signs of intoxication, the temperature of body rises to 40 o and the psyche is repressed. Characteristic also are
tachycardia, decline of arterial pressure, avitaminosises and edemata. Hypochromic anaemia is exposed in the general analysis of blood, leukocytosis, change of leukocyte formula to the left and increased ESR. In
plasma of blood the decline of maintenance of potassium and sodium ions and level of general protein, especially albumen are marked. In future there are the progressive degenerative changes of parenchymatous
organs.
At endoscopic examination (proctoscopy, fiberoptic colonoscopy) hyperemia of mucus membrane, swollen, contact bleeding, plural erosions, ulcers, festering and necrosis stratifications, are observed. At
heavy passing of disease fiberoptic colonoscopy or irrigoscopy always has the danger of perforation or acute bowel dilatation, therefore more rationally it is to conduct it in the period of calming down of
inflammatory process. During roentgenoscopy survey of organs of abdominal cavity in case of disease, complicated of acute toxic dilatation, the extended (from 10 to 20 cm and more) pneumatizated bowel is
exposed. During the perforation of bowel signs of pneumoperitoneum are present (air under the right cupula of diaphragm). Contrasting irrigoscopy examination in such patients enables to establish the presence
of water-pipe symptom. Thrusting out of tailings of well-kept mucus membrane on the background of plural ulcers and cicatricial changes of bowel walls at pseudopolyposis creates roentgenologic reality of
shot target throughsymptom (Pic. 3.3.9). Often in case of transformation of ulcerous colitis in the cancer on roentgenograms, stenosis cavity of bowel or defect of filling is observed (Pic. 3.3.10).
Acute, especially fulminant form of the unspecific ulcerous colitis passes the heaviest, so the prognosis is always doubtful. Taking it into account, death can come in the first days of disease. Thus an
inflammatory process will strike all colon. During 12 days the heavy clinical picture is observed with frequent diarrhea with mucus, blood and pus, vomiting, dehydration and loss of weight of body. Next to that,
deep intoxication, darkened consciousness, and the temperature of body rises to 3940 is present. The expressed anaemia, tachycardia and hypovolemia are observed. The loss of albumens causes the decline of
oncotic pressure and causes dehydration. The disbalance of electrolytes grows with progress of disease, microcirculation gets worse and day's diuresis goes down. In most cases this form of disease requires
urgentoperative treatment (absolute indications).
A chronic recurrent unspecific ulcerous colitis is characterized by the periods of acuteening and remission. Thus in patients with the total lesions of colon in the period of acuteening the heavy degree of
disease is observed, and in the period of remission middle or even easy degree of disease, thus, such calming down can last 6 months and more.
A chronic continuous unspecific ulcerous colitis at the total lesions of intestine in most patients passes as middle heavy degree, and in the period of worsening the disease takes heavy shape. The easy form
is met, mainly, at presence of inflammatory process in the rectum and sigmoid colon, considerably rarer it is at the lesions of left half of colon and quite rarely at the total lesions in the period of calming down
of the process. Conventionally, the unspecific ulcerous colitis begins from the rectum and engulfs all parts of colon. Thus emptying are 23 times per days with the admixtures of mucus, sometimes blood. Thus,
diarrhea can be intermittent with constipation. The temperature of body remains within the limits of norm. From the side of global and biochemical analysis of blood noticeable changes do not arise. Weight of
body does not diminish. At endoscopic examination hyperemia of mucus membrane, contact bleeding, expressed vascular picture, erosions, point hemorrhages and superficial ulcers are observed. It is needed also
to mark that in this situation the presence of erosions must be equated with an ulcerous process.
The middle heavy form of disease of the unspecific ulcerous colitis can be met in patients with the ulcerous colitis and proctosigmoiditis in the period of process acutening. Thus there are the subjective
feelings with considerable expression of tenesmus and heartburns.
The chronic forms of unspecific ulcerous colitis both at total and at the left-side lesions of colon, pass at the level of middle heavy degree. Frequency of emptying reaches to 510 times with mucus, blood
and pain. Low grade fever, general weakness, nausea and loss of appetite appear, and weight of body diminishes on 58 kg. Moderate anaemia is exposed in the general analysis of blood, leukocytosis, increased
ESR. Among the biochemical indexes of blood hypoproteinemia and hypokalemia are marked. At endoscopic examination of colon there is a considerable hyperemia and edema of mucus membrane, plural
erosions, contact bleeding and superficial ulcers.
The heavy form of unspecific ulcerous colitis is at the total lesions, especially with acute, and also chronic recurrent passing of disease. The temperature of body in such patient rises to 3940 , there is
diarrhea (more than 10 times per days) with mucus, blood and pus, vomitings, heavy intoxication grows, weight loss on 2530 kg, acutely expressed anaemia, leukocytosis with the change of leukocyte formula to
the left, considerable changes of albuminous and electrolyte exchanges. At endoscopic examination of colon the blood is exposed in its cavity, slid, pus, fibrin incrustation, often pseudopolypuses and almost
complete absence of mucus membrane. Roentgenologically some signs of complications of unspecific ulcerous colitis are confirmed.
The complications are divided into local and general. Local complications are: profuse intestinal bleeding, perforation, acute toxic dilatation, stenosis and malignization. To general the following are
included: damage of liver (hepatitis, cirrhosis), stomatitis, ulcer of lower extremities, lesions of joints, eyes and skin.
Acute dysentery passes with bloody diarrheas, increased temperature of body, pain in the abdomen. Bacteriological examination of excrement enables to expose dysenteric bacillus and specify diagnosis.
Crohns disease (granulomatous colitis) is this local process, that begins from the submucosal layer of bowel and distributes outside of walls with subsequent formation of infiltrate, abscesses and fistula.
Exposure of granulomas, and during microscopic examination accumulation of lymphocytes, neutrophils, protoplasmatic cells and the Pyrohov-Lunghans' cells are confirmed diagnosis.
The cancer of colon, in particular its enterocolitis and toxicoanemic forms, also often can simulate an unspecific ulcerous colitis. Irrigoscopy, fiberoptic colonoscopy with biopsy and subsequent histological
examination almost always help to diagnose cancer process.
Treatment of unspecific ulcerous colitis, certainly, begins with application of conservative facilities. Thus patients with easy and middle heavy forms must be under protracted conservative treatment.
The leading role is taken to the parenteral feed of patients with heavy common exhaustion (hydrolyzate of casein, aminopeptid, amynosol, vamin, alvesin, moriamin, intralipid, lipofundin, glucose and
others like that). Electrolytes (chloride of sodium, sulfate of magnesium, chloride of potassium, panangin) and vitamins are entered (6, 12, , , and others). Intensity and methods of conservative therapy
always must depend on the phase of disease:
) moderately expressed passing of disease or proctitis corticosteroid enema and sulfasalazone peroral;
) at heavy passing is parenteral introduction of liquids, nutritives, blood transfusion, system use of corticosteroids, surgical treatment;
) at chronic passing is corticosteroids peroral, asatioprine, surgical treatment;
) at remission is preparations of 5-aminosalicylic acid peroral, examination for the exception of cancer of colon.
The heavy form of passing of disease is absent of effect from the conducted conservative treatment during two weeks and progress of process testifies to the necessity of surgical treatment.
The conservative treatment must include antibacterial agent, antidiarrheal preparations, steroid hormone.
A diet is considered an important factor in treatment of such patient (diet 4). Thus it is recommended to take a meal to 6 times per days by small portions, withdrawing milk, fruit, vegetables, wheat and
rye bread from it. It is possible to appoint unfat meat and fish. Parenteral introduction of vitamins B, , A, folic acid are helpful.
The basic antiinflammatory facilities are: sulfasalazopreparations (sulfasalazone, salazopirine), salicylazosulfanilamide (salazosulfapyridine, salazodimetoxine) and corticosteroids. Practice showed that
sulfasalazone was one of the best antirecurrent facilities.
In patients with easy and middle heavy forms (distal or left-side lesions of colon) sulfasalazone is applied in a dose about 5 g per days, and salazopiridazine and salazodimetoxine about 2 g during that
time. The course of treatment must proceed 12 months. For local steroid therapy prednisolone is used as powder in a dose 6080 mg or hydrocortisone to 125 mg. It is dissolved in 100 ml physiologic saline
and entered rectal dropwise one time per days during 34 weeks.
At erosive proctitis and proctosigmoiditis 5 % (100,0 ml) solution of kolargole or extract of camomile in microclyster is applied.
At the heavy forms of ulcerous colitis with fulminant passing and frequent vomiting the treatment is needed to begin with intravenous introduction of 350380 mg hydrocortisone per day. Thus procedures
must proceed to appearance of positive clinical effect and realization of possibility of transition on enteral treatment. Such period lasts on the average of 67 days. In future it is recommended to adopt
prednisolone peroral.
Sulfasalazopreparations is used in the same dose, as at the middle heavy form of flow of disease. As in patients at this form of disease water-electrolyte and albuminous exchanges are considerably violated,
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there are the expressed intoxication and anaemia, it is expedient to conduct adequate therapy (intravenously - NaCl solution, glucose, chlorous potassium, albumen, hemodes, protein, whole blood), and also
hemodialysis and oxygenotherapy is used.
An absolute indication for surgical treatment is the presence of such complications of unspecific ulcerous colitis as: perforation of wall of bowel, acute toxic dilatation, stenosis, profuse bleeding and
malignization. By the choice of method of operation at such pathology it is needed to count colproctectomy with exteriorization of ileostomy.
However, during the perforation of colon or toxic dilatation the operative treatment can be limited to colectomy because proctectomy will be conducted as the next stage.
For patients with total ulcerous colitis with chronic heavy passing and without the tendency to the visible improvement expedient radical operative treatment colproctectomy with exteriorization of
ileostomy. At such tactic postoperative lethality is diminished in 5-6 times, comparative with palliative operations which were conducted earlier.
In Western Europe and North America colorectal cancer (CRC) is one of most widespread malignant neoplasm. Morbidity in these regions exceeds 20,0 on a 100000 of population. In Japan, South America,
Africa and countries of Asia this tumour is met rarer (6,0:100000). There is an annual increase of frequency of cancer of colon approximately by 3 % in the developed countries. Morbidity of population of
Ukraine by malignant neoplasm in 1995 was 16,3:100000.
Approximately 85 % of patients for CRC are of over 50 years old, with age frequency of cancer is increased.
The nutrition by fat and albuminous food promotes the elimination to the intestine of bile. Under the act of bacterial flora there is transformation of primary bilious acids to the secondary, which has the
carcinogenic and mutagenic activity. A meal with vitamins A, C and that which contains plenty of vegetable cellulose has a braking carcinogenic influence.
The factors of risk which predetermine the origin of cancer of bowel are:
1) diffuse (family) poliposis, which is considered obligate precancer;
2) plural and single adenomatous polypuses;
3) chronic unspecific ulcerous colitis (anamnesis more than 10 years);
4) Crohns disease (granulomatous colitis).
Localization. A tumour is mostly lacalized in sigmoid (3540 % cases) and blind (2025 % cases) bowels.
Macroscopic forms. Exophytic tumours grow in the lumen of bowel as a polypus or knot and at disintegration have the appearance of ulcer with a dense bottom that is swelling by edges which come forward
above the surface of the damaged mucus (saucer-shaped cancer). The endophytic (infiltrate) cancer grows in walls of bowel. The tumour spreads on the perimeter of bowel and engulfs it circular, causing narrowing
of its lumen. In the right half of colon exophytic tumours grow, as a rule, in left endophytic tumours.
Histological structure. Cancer of colon in 95 % cases has the structure of adenocarcinoma. Metastasis takes place by lymphatic and hematogenic ways in regional retroperitoneal lymphatic knots, liver,
lungs.
The symptoms of cancer of colon are so numerous and various, that many authors group them in such clinical forms: toxico-anemic, dyspeptic, enterocolitic, obturation, pseudoinflammatory and tumular.
A toxico-anemic form shows up by indisposition, weakness, rapid fatigability, increase of temperature, progressive anaemia. Characteristic for the cancer of right half of colon.
The enterocolitic form is characterized by symptom of complex intestinal disorders: diarrhea, constipation, swelling, grumbling, pain.
The dyspeptic form is characterized by functional disorders of gastrointestinal truct.
An obturation form shows up by intestinal obstruction.
A pseudoinflammatory form is characterized by the symptoms of inflammatory process in the abdominal cavity.
A tumour form passes asymptomatic. A tumour is exposed by chance by a patient or doctor.
Obturation and enterocolitic forms more characteristic for the cancer of left half, other ones of the right. For the cancer of right half of colon tendency to gradual progress is characteristic, and the
tumours of left half often show up suddenly by intestinal obstruction.
Intestinal obstruction, germination in neighbouring organs and tissue, perforation, bleeding are considered as the most frequent complications of colon cancer.
Depending on the clinical signs of colon cancer, a differential diagnosis is to be conducted with appendiceal infiltrate, by different chronic specific and unspecific diseases of colon, and also other organs of
abdominal cavity and retroperitoneal space (gall-bladder, pancreas, kidneys, genital organs and others like that), with the tumours of other organs of abdominal cavity and retroperitoneal space.
Radical treatment. Operative treatment is the unique method of radical treatment of colon cancer. The choice of method of operation depends on localization of tumour (Pic. 3.3.11). At cancer of right half of
colon right hemicolectomy, (deleting of all right half of colon, including right third of transversal colon and distal segment of iliac bowel by length 2025 cm) is conducted. In patients with tumours of left half of
colon left hemicolectomy (segment from middle or from left third of transversal colon to overhead part of sigmoid is resected) is executed. At cancer of transversal colon, middle and distal parts of sigmoid bowels
the resection of the damaged area is conducted, stepping back 5-6 cm from the edge of tumour. In patients who are hospitalized in an urgent order with the signs of intestinal obstruction, perforations and
peritonitis, after intensive preoprative preparation the Hartmann operation is executed (at tumours of left half of colon). It is the resection of the damaged area of intestine and exteriorization of proximal segment
on a front abdominal wall as colostomy. A distal end is sutured and is remained in the abdominal cavity. Through half-year there is a possibility of reconstructive operation. To the patients with the damage of right
half of colon operation in a radical volume can be executed (right hemicolectomy).
During treatment with palliative purpose (at presence of solitary metastases) operations in a radical volume with removing of metastatic knot (in a liver) or subsequent chemotherapy (by 5- fluorouracil) can
be used.
In recent years for the improvement of remote results treatment is applied by the adjuvant chemotherapy and intensive preoperative gamut-therapy.
The remote results of treatment of patients on the initial stages of CRC are fully satisfactory. At I stages the five-year survival is 85-100 %, at II 6570 %, at III 2530 %. On the whole at the IIII
stages the five-year survival is 45 %.
Persons who refused from operative treatment perish in a short time. The combined treatment improves remote results approximately on 1520%.
The gastric ulcer is the chronic disease with polycyclic passing. The main typical of peptic ulcer is the presence of ulcerous defect in a mucous tunic. One of basic places belongs among the gastroenterology
diseases to this pathology. Such phenomenon explained by not only considerable distribution of disease but also those dangerous complications which always accompany gastric ulcers.
Frequency of morbidity on the peptic ulcer among the adult population is about 4 %. More frequent age in patients with gastric ulcers is 5060 years.
To development mechanism of disease is still not enough studied. From a plenty of different theories in relation to genesis of peptic ulcer no one able to explain the disease. So, each of such factors as
neurogenic, mechanical, inflammatory, vascular is present in the mechanism of development of peptic ulcer. Consider for today, that disturbance between the factors of aggression and defense of mucous tunic
arose peptic ulcer. To the first factors belong: hydrochloric acid, pepsin, reverse diffusion of ions of hydrogen, products of lipid hyperoxidizing. To the second: mucus and alkaline components of gastric juice,
property of epithelium of mucous tunic to permanent renewal, local blood flow of mucous tunic and submucous membrane.
In the terminal stage of mechanism of origin of gastric ulcers important role has the peptic factor and disturbance of trophism of gastric wall as a result of local ischemia. It confirmed by decreasing of blood
flow in the wall of stomach at patients with ulcers on 3035 % compared to the norm. It is proved, that a local and functional ischemia more frequent arises up on small curvature of stomach in the areas of ectopy
of the antral mucous tunic in acid-forming. Exactly there ulcers appear.
Important part in ulcerogenesis is acted by duodenogastric reflux and gastritis. Also, gastrostasis can provoke hypergastrinaemia and hypersecretion and formed gastric ulcers.
Numeral scientific developments of the last years testify to the important infectious factor in the mechanism of origin of peptic ulcer conditioned, mainly, by helicobacter pylori.
Such stages of disease are distinguished: erosion, acute and chronic ulcers.
Erosions, mainly, are plural. Their bottom as a result of formation of muriatic haematine is black, edges infiltrated by leucocytes. A defect usually does not penetrate outside muscular tissue of the
mucous tunic. If necrosis gets to more deep layers of wall of stomach, a acute ulcer develops. It has a funnel-shaped form. Bottom is also black, edges is swelled. Chronic ulcers are mainly single, sometimes arrive
to the serous layer. A bottom is smooth, sometimes hilly, edges is like elevation, dense.
For today the most known classification of gastric ulcers by Johnson (1965). There are three types of gastric ulcers are distinguished: I ulcers of small curvature (for 3 cm higher from a goalkeeper); II
double localization of ulcers simultaneously in a stomach and duodenum; III ulcers of goalkeeper part of stomach (not farther as 3 cm from a goalkeeper). In the area of small curvature of body of stomach is
localized 70,9 % ulcers, on a back wall, nearer to small curvature 4,8 %, in the area of cardial part 12,9 %, in a goalkeeper part 11,4 %. The ulcers of large curvature of stomach are casuistry and meet
infrequently.
The complaints of patients with the gastric ulcer always give valuable information about the disease. The detailed analysis of their anamnesis allows to pay attention to the possible reasons of origin of ulcer,
time of the first complaints, to the changes of symptoms.
Pain. A pain symptom in the peptic ulcer disease is very important. There are typical passing for this disease: hunger pain food intake facilitation again hunger pain food intake facilitation (so
during all days). Night pain for the gastric ulcer is not typical. The such patients rarely wake up in order to take a food. For diagnostics of ulcer localization it is important to know the time of appearance of pain.
Between acceptance of food and appearance of pain it is the shorter, than the higher placed gastric ulcer. Thus, at patients with a cardial ulcer pain arises at once after the food intake, with the ulcers of small
curvature in 5060 minutes, at pyloric localization approximately in two hours. However this feature it is enough relative and some patients in general do not mark dependence between food intake and pain.
In other patients the pain attack is accompanied by the salivation.
A epigastric region near the xiphoid process is typical localization of pain. The irradiation of pain is not usual for gastric ulcers. Irradiation occur in patients with penetration and depended from organ, in
which an ulcer penetrates.
At the examination of ulcerous patient it is expedient to determine the special pain points: Boas (pain at pressure on the left of the II pectoral vertebrae), Mendel (pain at percussion on the left to
epigastric region).
Vomiting, the sign of disturbance of motility function of stomach, is the second typical symptom of gastric ulcer. More frequent gastrostasis arises as a result of failure of stomach muscular, it atony which
can be effect of organ ischemia. Vomiting could arises both on empty stomach and after food intake.
Heartburn is one of early symptoms of gastric ulcer, however at the prolonged passing of disease it can be hidden or quite disappear. Often it precedes of pain arising (initial heartburn) or accompanies a pain
symptom. Mostly heartburn arises after the food intake, but can appear independently. it is observed not only at hypersecretion of the hydrochloric acid, but at normal secretion, even reduced acidity of gastric
juice.
The belching at gastric ulcers is examined rarely, more frequent in patients with cardial and subcardial ulcers. It is necessary to bind to disturbance of function of cardial valve.
The general condition of patients with the uncomplicated gastric ulcer usually satisfactory, and in a period between the attacks even good. However for most patients lost of the body weight and pallor are
typical. In a epigastric region hyperpigmental spots are examined after the prolonged application of hot-water bottle. At palpation of stomach in this area sometimes appears local painful. It is needed also to check
up noise of splash, the presence of which can be the sign of possible gastrostasis.
At the examination of mouth cavity a tongue has whiter-yellow incrustation. In patients with penetration ulcers and disturbances evacuations from a stomach examined dryness of tongue.
Stomach, as a rule, regular rounded shape, however during the pain attack is pulled in. There is antiperistalsis arises during the pylorostenosis.
The increased secretion of hydrochloric acid in patients with gastric ulcers observed rarely and, mainly, at prepyloric ulcer localizations. Mostly secretion is normal, and in some patients is even reduced.
X-Ray examination. The direct signs of ulcer at X-Ray examinations are: symptom of Haudek's niche (Pic. 3.2.1), ulcerous billow and convergence of folds of mucous tunic. Indirect signs: symptom of
forefinger (circular spasm of muscles), segmental hyperperistalsis, pylorospasm, delay of evacuation from a stomach, duodenogastric reflux, disturbance of function of cardial part (gastroesophageal reflux).
Gastroscopy can give important information about localization, sizes, kind of ulcer, dynamics of its cicatrization, and also allow to perform biopsy with subsequent histological examination.
The gastric ulcer passing can be acute and chronic. Acute ulcers arise as answer for the stress situations, related to the nervous overstrain, trauma, loss of blood, some infectious and somatic diseases. By a
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diameter ulcers has from a few millimeters to centimeter, a round or oval form with even edges. Thus in most cases clinically observed clear ulcerous clinical signs. If complications is absent (bleeding, perforation)
such ulcers treated and mostly heal over.
G.J. Burchynskyy (1965) such variants of clinical flow distinguished:
1. Chronic ulcer which does not heal over long time.
2. Chronic ulcer which after the conservative therapy heals over relatively easily, however inclined to the relapses after the periods of remission of a different duration.
3. Ulcers, which localization are had migrant character. Observed in people with acute ulcerous process of stomach.
4. Special form of gastric ulcer passing after the already carried disease. Passed with the expressed pain syndrome. Characterized by the presence in place of ulcerous defect of scars or deformations and
absence of symptom of niche.
There are such complications can develop in patients with gastric ulcer: penetration, stenosis, perforation, bleeding and malignization.
Chronic gastritis, as well as at an gastric ulcer, characterized by the pain syndrome, that arises after the food intake. In such patients it is possible to observe nausea and vomiting by gastric content,
heartburn and belch. However, unlike an gastric ulcer, for gastritis typical symptom of quick satiation by a food. Unsteady emptying, diarrhea also more inherent to gastritises. At gastric ulcer more frequent the
delays are observed, constipation for 45 days.
The cancer of stomach, it is comparative with an gastric ulcer, has considerably more short anamnesis. The most typical clinical signs of this pathology are: absence of appetite, weight loss, rapid fatigability,
depression, unsociability, apathy. In such patients X-Ray examination expose the defect of filling, related to exophytic tumor and deformation of walls of organ. A final diagnosis is set after the results of
multiposition biopsy of shady areas of mucous tunic of stomach.
Differential diagnostics also needs to be conducted with the so called precancerous states: gastritis with the achlorhydria; chronic, continuously recurrence ulcers, poliposis and Addison-Biermer anemia.
Conservative treatment of gastric ulcer always must be complex, individually differentiated, according to the etiology, pathogeny, localization of ulcer and character of clinical signs (disturbance of functions
of gastroduodenal organs, complication, accompanying diseases).
Conservative therapy must include: a) anticholinergic drugs (atropine, methacin, platyphyllin) and myolitics (papaverine, halidor, nospanum); antiacid drugs in accordance with the results of pH-metry; b)
2- blocker histamine receptor (ranitidine) 150 mg in the evening, famotidine 40 mg at night, roxatidine 150 mg in the evening, c) reparative drugs (dalargin, solcoseryl, actovegin) for 2 ml 12 times
per days; ) antimicrobial drugs (de-nol, metronidazole, semisynthetic antibiotic); ) vitamins of group B and symptomatic medicine.
Treatment of patient with a gastric ulcer must continues not less than 68 weeks.
Surgical treatment must performed in cases:
a) at the relapse of ulcer after the course of conservative therapy;
b) in the cases when the relapses arise during supporting antiulcer therapy;
c) when an ulcer does not heal over during 1,52 months of intensive treatment, especially in families with ulcerous anamnesis.
d) at the relapse of ulcer in patients with complications (perforation or bleeding);
e) at suspicion on malignization ulcers, in case of negative cytological analysis.
The choice of method of surgical treatment of gastric ulcer depended from localization and sizes of ulcer, presence of gastro- and duodenostasis, accompanying gastritis, complications of peptic ulcer
(penetration, stenosis, perforation, bleeding, malignization), age of patient, general condition and accompanying diseases. In patients with cardial localization of ulcer the operation of choice is the proximal
resection of stomach, which, from one side, allows to remove an ulcer, and from other to save considerable part of organ, providing it functional ability (Pic. 3.2.2). In case with large cardial ulcers, when the
vagus nerves pulled in the inflammatory infiltrate and it is impossible to save integrity even one of them, operation needs to be complemented by pyloroplasty. It will give possibility to warn pylorospasm and
gastrostasis, which in an early postoperative period can be the reason of anastomosis insufficiency and other complications.
At the choice of method of surgical treatment of gastric ulcers with subcardial localization on small curvature without duodenostasis it is better to apply the methods of stomach resection with saving of
passage through a duodenum.
For this purpose we are developed the method of segmental resection of stomach with addition selective proximal vagotomy. The redistribution of gastric blood flow between the functional parts of stomach
as reply to medicinal vagotomy (intravenous introduction 1,0 ml 0,1 % solution of atropine of sulfate) is studied. Hyperemia of acid-forming part of stomach comes after introduction of preparation. The functional
scopes of stomach parts are determined. The border between acid-forming and antral parts are the most frequent localization of gastric ulcers.
During this operation middle laparotomy is performed, intravenously entered 1,0 ml 0,1 % solution of atropine, then the scopes of functional stomach parts are identified and by stitches-holders is marked a
intermedial segment. Selective proximal vagotomy is performed. After mobilization of large curvature of stomach within the limits of intermedial segment it resection is performed. After that gastro-gastro
anastomosis end-to-end is formed (Pic. 3.2.3).
The analysis of supervisions of the patients operated by such method in postoperative period has good results. It allows to recommend this operation for clinical practice, in case of gastric ulcers of
subcardial localizations, without duodenostasis, penetration, malignization or nerves Latarjet damaging.
The operation of choice in patients with subcardial ulcers and duodenostasis is gastric resection by Billroth II.
At the choice of method of surgical treatment of ulcers which are localized in upper and middle third of stomach, it is necessary to consider such factors, as absence of penetration in a small omentum and
absence of the duodenostasis. In such patients is performed segmental resection of stomach with ulcer removing with selective proximal vagotomy. In case of penetration ulcer in a small omentum with involvement
in infiltrate Latarjet nerves, such operation is impossible because of future spasm of pylorus and gastrostasis. If duodenostasis is absence than better to apply pylorus-saving resection by Maki-Shalimov. In
patients with duodenostasis better to apply gastric resection by Billroth II.
At the border of gastric resection near pyloric sphincter can be spasm and gastrostasis in a postoperative period . Avoiding such complication is possible, if this border of gastric resection passes no more
than 1,5 cm from a pyloric sphincter (M.M. Risaev, 1986). So, at a resection, that passes higher than 2,0 cm from a pylorus, integrity of both loops is kept.
Patients with antral ulcers without the duodenostasis performed the gastric resection by Billroth I (Pic. 3.2.6), and on presence of duodenostasis Billroth II.
Prepiloric ulcers is similar to the ulcers of duodenum. Such localization of gastric ulcers without malignization allow to perform selective proximal vagotomy. However, at large prepyloric ulcers with
penetration without duodenostasis is better to perform the gastric resection by Billroth I and on presence of duodenostasis by Billroth II.
By contra-indication to operations with saving of food passing through the duodenum are also decompensated pylorostenosis , functional gastrostasis and duodenostasis. In such patients it is better to
perform gastric resection by Billroth II.
The duodenal ulcer is the chronic recurrent disease which characterized by ulcerous defect on a mucous tunic of duodenum. Pathology often makes progress with complications development.
There are some etiologic factors of the duodenal ulcer: Helicobacter pylori, emotion tension and neuropsychic stress overstrain, heredity and genetic inclination, presence of chronic gastroduodenitis,
disturbance of diet and harmful habits (alcohol, smoking). In pathogenesis of peptic ulcer a leading role is played disturbance of equilibrium between aggressive and projective properties of secret of stomach and
it mucous tunic. The aggressive factors are vagus hyperfunctioning and hypergastrinemia; hyperproduction of hydrochloric acid and pepsin, and also reverse diffusion of the ions +, action of bilious acids and
isoleucine, toxins and enzymes of helicobacter pylori (HP). There are factors which are contribute to ulcerogenic action: disturbance of motility of stomach and duodenum, ischemia of duodenum, and metaplasia
of the epithelium.
Morphogenesis of duodenal ulcer fundamentally does not differ from ulcer in a stomach. Chronic ulcers are mainly single, is localized on the front or back wall of bulb (bulbar ulcer) and only in 78 %
cases below it (postbulbar ulcer). The plural ulcers of duodenum are met in 25 % cases.
Pain in the epigastric region is the most expressed symptom of duodenal ulcer, often with displacement to the right in the projection area of bulb of duodenum and gall-bladder. Also for this pathology is
typical the pain, that arises in 1,52 hours after food intake, hungry and nightly pain. As a rule, it is acute, sometimes unendurable, and is halted only after the use of food or water. Such patients complains for
the seasonal exacerbation, more frequent in spring and in autumn. However exacerbation can be also in winter or in summer. In the acute period of disease heartburn often increases. However heartburn is the
frequent symptom of cardial insufficiency and gastroesophageal reflux. For an duodenal ulcer the acute burning feeling of acid in a esophagus, pharynx and even in the cavity of mouth is especially typical. Often
are belch by air or sour content, excessive salivation. Vomiting is not a typical symptom for duodenal ulcer. More typical sign is nausea. Sometimes for facilitation patients wilfully cause vomiting. These
symptoms, arises in the late periods of passing of duodenal ulcer.
Intensity of pain and dyspepsia syndromes depends both on the depth of penetration and from distribution of ulcerous and periulcerous processes. Superficial ulceration within the mucous tunic, as a rule,
does not cause the pain because it does not have sensible receptors. However, more deep layers of wall (muscular and especially serous) have plural sensible vegetative receptors. Therefore, on deepening and
distribution of process arises visceral pain. At evident periulcerous processes and penetration of ulcers to neighboring organs and tissues, usually, a parietal peritoneum, that has spinal innervation, is pulled in.
Pain becomes viscero-somatic, more intensive. A such pain syndrome (with an irradiation in the back) is typical for low postbulbar ulcers and bulbous ulcers of back wall, which penetrates in a pancreas and
hepato-duodenal ligament. Usually such patients has good appetite. Some of them limit themselves in acceptance of ordinary food, go into to the dietary feed by small portions, and some even hold back from a
food, being afraid to provoke pain, and as a result of it weight is lost. Some of patients feeds more intensive and often.
The psychical status of patients often are changed as a asthenoneurotic syndrome: irritates, decline of working capacity, indisposition, hypochondria, abusiveness.
An inspection, as a rule, gives insignificant information. In many cases on the abdominal skin it is possible to notice hyperpigmentation after application of hot-water bottle. During the pain attack patients
often occupy the forced position. At superficial palpation on the abdominal wall determined hyperesthesia in ulcer projection. In the epigastric region, during deep palpation, it is possible to define pain and
muscular tension, mostly moderate intensity. There is important symptom of local percussion painful (Mendels symptom): percussion by fingers in the symmetric epigastric areas provoke pain in the ulcer, which
is increased after the deep breath. The roentgenologic and endoscopic are main diagnostic methods. The symptom of ulcerous niche is a classic roentgenologic sign. It is depot of contrast agent, which is
corresponded to ulcerous defect, with clear contours and light bank to which converged fold mucus. Cicatricial deformation of bulb of duodenum as a shamrock, butterfly, narrowing, tube, diverticulum and other
forms is the important sign of chronic ulcerous process. A roentgenologic method is especially important for determination of configuration and sizes of stomach and duodenum, and also for estimation of motility
functions. X-Ray examination is the main method at the peptic ulcer complicated by stenosis, with disturbance of evacuation, duodenostasis, duodenal-gastric reflux, gastroesophageal reflux, diverticulum. But by
X-Ray examination is difficult to diagnose small superficial ulcers, acute ulcers, erosions, gastritises and duodenitises. The most informing method in such cases it endoscopy.
During endoscopy examination it is possible to define localization, form, sizes and depth of ulcer. During bleeding grumes, trickle or pulsating of blood are observed. By irrigation by styptic solutions, by
cryocoagulation, by laser coagulation endoscopy allows to secure hemostasis. Endoscopy allows to perform the biopsy of ulcer tissues for determination of possible malignization.
In patients with low postbulbar ulcers the clinical signs are more expressed. It characterized by late (in 23 hours after food intake) and intensive hungry and nightly pain, that often irradiate to the back
and to the right hypochondrium. The postbulbar ulcers are inclined to more frequent exacerbation, and also to more frequent complications, such, as penetration, stenosis and bleeding.
The are more frequent ulcerous bleeding (the bulbous happen in 2025 % cases, postbulbar in 5075 %), perforations (1015 % cases). Penetration, stenosis and malignization in patients with duodenal
ulcers are observed rarely.
Penetration is frequent complication of low and postbulbar ulcers of duodenum, which are placed on posterior, posterior superior and posterior inferior walls. Penetrates, usually, deep chronic ulcers, by
passing through all layers of duodenum in neighboring organs and tissues (head of pancreas, hepato-duodenal ligament, small and large omentum, gall-bladder, liver). Such penetration is accompanied by
development of inflammatory process in the neighboring organs and surrounding tissues and forming of cicatrical adhesions. A pain syndrome becomes more intensive, permanent and often pain irradiated in the
back. Sometimes in the area of penetration it is possible to palpate painfully infiltrate.
The duodenal ulcer must be differentiated from acute and chroniccholecystitis, pancreatitis, gastroduodenitis. Endoscopy is help to diagnose duodenal ulcer.
Conservative treatment. In most patients after conservative treatment an ulcer heals over in 46 weeks. Warning of relapses can be carried out by only supporting therapy during many years.
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The best therapy of duodenal ulcer is associated with a helicobacter infection, there is the use of antagonists of 2- receptors of histamine (renitidine 300 mg in the evening or 150 mg twice for days;
famotidine 40 mg in the evening or 20 mg twice for days; nisatidine 300 mg in the evening or 150 mg twice for days; roxatidine 150 mg in the evening) in combination with sucralfate (venter) for 1
three times for days and antacid (almagel, maalox or gaviscon 1 dessert-spoon in a 1 hour after food intake). To this complex it is needed to add antibacterial preparations (De-nol 1 tabl. 4 times per a day
during 46 weeks + oxacylline for 0,5 g 4 times per a day 10 days + Tryhopol (metronidazole) for 0,5 g 4 times per a day 15 days).
In treatment of duodenal ulcer used chinolitics and miolitics (atropine, methacin, platyphyllin), and also mesoprostol (200 mg 4 times per days) and omeprasole (20 or 40 mg on days).
Such treatment of patients with the duodenal ulcer must be 46 weeks. If complications absents there is no necessity in the special diet.
Because of appearance of new pharmaceutical preparations and modern therapeutic treatment, indication to the operative methods narrowed. But the number of acute complications of duodenal ulcer does
not go down, especially bleeding and perforations which require the urgent surgery.
Indications to the elective operation:
1. Passing of duodenal ulcer with the frequent relapses which could not treated conservatively.
2. Repeated ulcerous bleeding.
3. Stenosis of outcome part of stomach.
4. Chronic penetration ulcers with the pain syndrome.
5. Suspicion for malignization ulcers.
Methods of surgical treatment.
At patients with the duodenal ulcer three types of operations are distinguished:
organ-saving operations;
organ-sparing operations;
resection.
From them the better are: organ-saving operations with vagotomy, excision of ulcer and drainage operation.
Types of vagotomy: trunk (TrV) (Pic.. 3.2.7), selective (SV) (Pic. 3.2.8), selective proximal (SPV) (Pic. 3.2.9). Selective proximal vagotomy is optimal in the elective surgery of duodenal ulcer. However in
urgent surgery a trunk, selective or selective proximal is often used in combination with drainage operations.
Drainage of the stomach operations are: Heineke-Mikulicz pyloroplasty, Finney pyloroplasty, submucous pyloroplasty by Diver-Barden-Shalimov, gastroduodenostomy by Jaboulay,
gastroenteroanastomosis.
It is necessary to mark that clean isolated SPV, performed in patients with duodenal ulcer, often (in 1520 % cases) results in the relapses. The considerably less number of relapses (810 %) is observed
after SPV in combinations with drainage operations. Especially dangerous is the relapses of the ulcers placed in the projection of large duodenal papilla, after gastroduodenostomy by Jaboulay.
The least number of relapses of duodenal ulcer is observed after organ-saving operations, that combine SPV and ulcer excision.
If ulcer localized on the anterior surface of duodenal bulb it can be performed by the method Jade (Pic. 3.2.13) with subsequent to the pyloroplasty by Heineke-Mikulich.
At patients with decompensate stenosis and expressed dilatation and by the atony of stomach it is needed to apply the classic resection of stomach depending on possible damping-syndrome by Billroth -I or
Billroth -II.
The choice of subtotal resection of stomach needs to be done at suspicion for malignization or at histological confirmed malignization ulcers. In a duodenum this process happens very rarely.
Ulcerous stenosis is complication of Peptic ulcer or duodenum, which characterized by narrowing.
Stenosis of outgoing part of stomach and duodenum of ulcerous origin arises as a result of scarring and common morphological changes around an ulcer. Narrowing, disturbance of the coordinated motility
of goalkeeper come as a result of it and creates the obstacle to the even moving of stomach content to the duodenum.
Such pathology in the compensation stage arises hypertrophy of the stomach walls. The pyloric ring has a 0,50,7 cm in diameter. The mucous tunic of pyloric part of stomach is thickened, with rough folds.
Muscular fibers are hypertrophied and solid. Histological hyperplasia of pyloric glands is observed.
During decompensation the muscular layer of stomach higher stenosis becomes thinner, tone of him goes down, and a pyloric ring narrows to a few millimetres. Microscopically present atrophy of mucous
tunic and muscular fibers, vessels sclerosis. A stomach collects the form of the stretched sack which goes down to the level of small pelvis.
The first signs of stenosis can be exposed already in eight-ten years from the beginning of the peptic ulcer disease., Mainly, this is narrowing and rigidity and disturbance of retractive activity of goalkeeper,
which create a barrier for transition of stomach content to the duodenum.
In the stage of the compensated stenosis hypertrophy of wall of stomach develops and tone of muscular shell rises. Hereupon gastric content, slowly, but passes through the narrowed area of stomach output.
In this stage patients, usually, complained about feeling of plenitude in a epigastric area after food intake, periodic vomitings by sour gastric content. On empty a stomach by a stomach pump 200300 ml gastric
content is removed.
In the subcompensated stage muscular layer of stomach becomes thinner. Tone of him goes down, a peristalsis relaxes, and it looks like the stretched sack. Evacuation disorders is increased. Fermentation
and rotting developed in stagnant gastric content. On this stage of disease development patients, usually, complain for the permanent feeling of weight in epigastric region and regurgitation with an unpleasant
rotten smell of sulphuretted hydrogen.
Vomiting becomes systematic (once or twice on a day) up to half of liter per day. On empty a stomach it possible to aspirate from it more 500 ml of content with the food used the day before.
In the decompensation stage of the clinical sighn make progress quickly. There are heavy disturbances of the general condition of patient, considerable loss of weight (to 3040 %), acutely expressed
dehydration of organism, hypoproteinemia, hypokalemia, azotemia and alkalosis. In case of the protracted neglected disease, as a result of progress of disturbances of metabolism, there can be a convulsive
syndrome (gastric tetany). Vomiting in this stage not always can be considered by a typical sign, in fact patients often renounce to adopt a food, and a stomach acquires considerable sizes, overdistension form, it
tone is violated and atrophy of wall comes. In such patients in a epigastric area it is possible to define the contours of the stretched stomach, with a slow peristalsis,. In the distance it is possible to hearken the
splash. By a probe from a stomach to 1.5-2 litres of food with a putrid smell are removed. There can be gastric tetany at considerable disturbances of electrolyte metabolism.
A diagnosis is set according to a typical syndrome, results of sounding of stomach, rontgenoscopy, at which by contrasting of a barium expose stenosis of initial part of stomach or duodenum, determines it
origin and estimate a degree.
Roentgenologically in the compensation stage stomach in normal sizes, it peristalsis deep, increased, evacuation of content proceeds no more than 6 hours. In the stage of subcompensation a stomach is
megascopic, a peristalsis is loosened, evacuation stays too long to 24 hours. During decompensation a stomach is considerably extended as a sack, deformed, the waves of antiperistalsis can take place, a contrast
stays too long more than 2448 hours. The method of the double contrasting by a barium and air considerably facilitates diagnostics.
Determination of stomach motility has not only diagnostic but also prognostic value for the choice of method of operation.
In the stage of compensation motility of stomach is well-kept, often even increased. With the increasing the degree of stenosis the motility disturbance increased, up to gastroplegia.
In the biochemical blood test is marked the decline of content of albumen to 5448 g/l; potassium to 2,92,5 mmol/l; chlorides to 8587 mmol/l. The changes of such indexes are most expressed at
patients with gastrogenous tetany.
The study of secretory function of stomach allows to define the degree of compensation of stenosis and importent at the choice of adequate method of operation.
Gastroscopy with a biopsy is the enough informing method of examination of such patients. By this method is possible to determine a reason and degree of stenosis, and also state of mucous tunic of
stomach.
Stenosis of the output part of stomach and duodenum of ulcerous origin it is needed to differentiate with functional gastrostasis and narrowing of tumour and chemical genesis.
Functional gastrostasis more frequent meets at women. Basic, that distinguishes it from other pathologies, there is absence of some organic changes in the area of pyloric part of stomach or in a duodenum,
that can be exposed during fibergastroscopy.
Differential diagnostics of stenosis of tumour genesis, as a rule, also does not cause the special difficulties. A diagnosis is finally confirmed by histological examinations of the biopsy material taken during
endoscopy.
Postburn stenosis of piloroantral area of stomach observed, from data of statistics, more than in 25 % cases of patients with the burn of esophagus. In anamnesis in each of such patients takes place by
mistake or the intentionally taken an a swig at acid, alkali or other chemical matter. Some diagnostic difficulties can arise up at the isolated postburn stenosis of pyloric part of stomach. The however attentively
collected anamnesis and professionally conducted endoscopic examination enable to set a correct diagnosis.
Treatment of ulcerous stenosis of piloroantral part of stomach and duodenum must be exceptionally operative. A method depend on many factors: degree of stenosis, these secretory and motility functions of
stomach, age of patient, presence of accompanying diseases and others like that. In the compensated and subcompensated stages of stenosis and at enough well-kept functions of stomach it is possible to perform
of organ-saving operations (vagotomy with drainage stomach operations, economy resection of stomach). At growth of the signs of stenosis and disturbance of basic functions of stomach, the volume of operation
must be increased up resection by the Bilroths second method.
At the patients and older age persons with heavy accompanying pathology is performed minimum surgery gastroenteroanastomosis.
Preoperative preparation must be strictly individual.
At patients with insignificant disturbances of gastric motor activity (stage of compensation, subcompensations) and with good level of metabolism indexes it is better to shorten preoperative preparation in
time. Such patients, usually, operated on 34 day. Preparation before operation at patients with decompensated pilorostenosis must be directed for the correction of metabolism disturbances. Such patients must
receive transfusion of liquid up to 2,53 l per day with content of the ions +, Na+, ++, amino acid and glucose; plasma, albumen. Twice on days performed decompression and washing of stomach and
anti-ulcerous therapy. Effective preoperative preparation in such patients requires 57 days, sometimes more.
The typical perforation of gastric or duodenum ulcer is strengthening of necrosis process in the area of ulcerous crater with subsequent disturbance of integrity of wall, that result to the permanent effluence
of gastroduodenal content and air in a free abdominal cavity.
In 50,7 % cases perforates the ulcers of duodenum, in 42,8 % are ulcers of pyloric part of stomach, in 4,8 % are ulcers of small curvature of body of stomach and in 0,7 % are cardial ulcers.
Ulcers, which lie on the front wall of stomach and duodenum more frequent give the perforation with general peritonitis, while ulcers on a back wall perforation with adhesive inflammation.
The reasons of ulcers perforation are: exacerbation of peptic ulcer, harmful habits, stresses, professional, athletic overexertion, faults in the feed and abuses by strong waters.
In pathogeny of acute perforation important: progressive necrosis processes in the area of ulcerous crater with activating of virulent infection; hyperergic type of local vaculo-stromal reaction with the
thrombosis of veins of stomach and duodenum; local manifestation of autoimmune conflict with accumulation of sour mucopolysaccharides on periphery of ulcer and high coefficient of plasmatization of mucous
tunic (.I. Mishkin, .. Frankfurt, 1971).
The clinical picture of perforation is very typical and depends on distribution of inflammatory process and infection of abdominal cavity. In clinical passing of the perforations distinguish three phases:
shock, imaginary prosperity and peritonitis (Mondor, 1939).
For the phase of shock (to 6 hours last) typical very acute pain in epigastric region (Delafua compares it to pain from the stab with a dagger) with an irradiation in a right shoulder and collar-bone, a face is
pale, with expression of strong fear, lines become (facies abdominalis) acute, a death-damp irrigates skin covers. A pulse is at first slow (vagus pulse), later becomes frequent and less filling. Sometime observed
the reflex vomiting and delay of gases. Arterial pressure is reduced. On examination stomach is pulls in, does not take part in the act of breathing. At palpation is wooden belly stomach, especially in an upper
part, where, usually, there is most pain. Positive Blumberg's sign. At percussion is disappearance of hepatic dullness (the Spizharnyy symptom). At rectal examination expose painful in the area of rectouterine or
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almost always there are considerable disturbances of blood circulation with disturbance of functions of liver and kidneys.
The III degree of hemorrhage characterizes heavy clinical passing. There is a pulse in such patients 130140 per min., and arterial pressure from 60 to 0 mm Hg. Consciousness is almost always
darkened, acutely expressed adynamy. Central vein pressure is low. Oliguria is observed, that can change by anuria. Without active and directed correction of hemorrhage a patient can die.
But, not always weight of bleeding which is conditioned by the degree of hemorrhage correspond the general condition of patient. On occasion the considerable loss of blood during the set time is
accompanied by the relatively satisfactory condition of patient. And vice versa, moderate hemorrhage can bring to the considerable worsening of general condition. It can depend both on compensate possibilities
of organism and from the presence of accompanying pathology.
It is needed to remember, that the ulcerous bleeding can accompanying with the perforation of ulcer. During perforation ulcers are often accompanied by bleeding. Correct diagnostics of these two
complications has the important value in tactical approach and in the choice of method of surgical treatment. In fact simple suturing of perforated and bleeding ulcer can complicated in postoperative period by the
profuse bleeding and cause the necessity of the repeated operation.
At wide introduction of gastroduodenoscopy of question of differential diagnostics of bleeding lost the actuality. However much a problem arises up at impossibility to execute this examination through the
heavy general condition of patient or taking into account other reasons. Differential diagnostics is conducted with bleeding of unulcerous origin, which arise up in different parts of digestive tract.
For bleeding from the varicose extended veins of esophagus during portal hypertension at patients with the cirrhosis of liver the acute beginning without pain is characteristic, like during exacerbation of
ulcerous disease. These bleeding differ by the special massiveness and considerable hemorrhage. Vomiting by fresh blood, expressed tachycardia, falling of arterial pressure are observed. In such patients it is
possible to find the signs of cirrhosis of liver and portal hypertension (head of jelly-fish, hypersplenism, ascites, often is icterus).
Sliding hernia of the esophagus opening of diaphragm can be accompanied by formation of ulcers in the place of clench of the stomach by the legs of diaphragm and bleeding from them. However for this
pathology are more typical microbleeding, that is hidden. In such patients often the present protracted anaemia which can achieve the critical values. Sometimes in them observe more expressed bleeding with
classic vomiting coffee-grounds and melena. During the roentgenologic examination with barium is possible to expose the signs of sliding hernia of the esophagus opening: the obtuse cardial angle, absence or
diminishment of gas bubble of stomach or ringing symptom.
The cancer tumour of stomach in the destruction stage can be also complicated by bleeding. However, such bleeding are massive, and chronic character is carried mostly with gradual growth of anaemia. For
this pathology there are the inherent worsenings of the general condition of patient, loss of weight of body, decline of appetite and waiver of meat food. At the roentgenologic examination the defect of filling is
exposed in a stomach.
The gastric bleeding can be related to the diseases of the cardio-vascular system (atherosclerosis, hypertensive disease), however such happens mainly in the older years people. Clearly, that in such patients
during the endoscopic examination the source of bleeding exposing is not succeeded.
Among other diseases, with which it is necessary to differentiate the ulcerous bleeding, it is needed to remember the Mallory-Weiss syndrome, benign tumours of stomach and duodenum (more frequent
leiomyoma), hemorrhagic gastritis, acute (stress) erosive defeats of stomach, arteriovenous fistula of mucous tunic.
Often differential diagnostics performed according to the level of localization of source of bleeding in different parts of gastrointestinal tract. For the upper parts of digestive tract (esophagus and stomach)
typical there is vomiting by grume or coffee-grounds content and emptying by melena. The farther aboral placed source of bleeding, the bloody emptying changes the more so. During the bleeding from a thin
bowel excrement looks as melena. In case of such pathology of colon (polypuses, tumours, unspecific ulcerous colitis) emptying have the appearance of fresh red blood, mostly as packages.
The conservative therapy indicated to patients with the stopped bleeding of I degree and bleeding of the IIIII degrees at patients which have heavy accompanying pathology, because of operative risk.
Conservative therapy must include:
prescription of hemostatic preparations (intravenously the aminocapronic acid 5 % 200400 ml, chlorous calcium 10 % 10,0 ml, vicasol 1 % 3,0 ml);
addition to the volume of circulatory blood (gelatin, poliglukine, salt blood substitutes);
preparations of blood (fibrinogen 23 , cryoprecipitate);
blood substitutes therapy (red corpuscles mass, washed red corpuscles, plasma of blood);
antiulcerous preparations blocker of 2- receptor (ranitidine, roxatidine, nasatidine for 150 mg 12 times per days);
antacid and adsorbents (almagel, phosphalugel, maalox for 12 dessert-spoons through 1 hour after food intake).
It is expedient to apply washing of stomach by water with ice and the use 5 % solution of aminocapronic acid inward for to a 1 soupspoon in every 2030 minutes.
The endoscopic methods of stop of bleeding are used also. Among them most effective is a laser and electro-coagulation.
Absolute indications to surgical treatment are: 1) lasting bleeding I degree; 2) recurrent bleeding after hemorrhage I degree; 3) bleeding of the IIIII degrees; 4) stopped bleeding with hemorrhage of the IIIII
degrees at the endoscopically exposed ulcerous defect with a presence on the ulcer bottom thrombosed vessels or erosive vessels covered by the package of blood.
The choice of method of surgical treatment always needs to be decided individually. On today the best tactic which gives advantage to organ-saving and organsparing methods of operations. The removing
ulcer as sources of bleeding must be an obligatory condition. The methods of sewing of bleeding vessels or edging of ulcer and bandaging of vessels which feed a stomach and duodenum did not justify itself
through the real threat of relapse of bleeding already in an early postoperative period (912 days).
Palliative operations (cutting of ulcer, forming of roundabout anastomosis) can be justified only taking into account the general condition of patient and on a necessity as possible quick and least
traumatically to make off operation.
At the bleeding ulcers of duodenum it is better to apply excision of ulcer or it exteritirization after methods, developed by V.Zajtsev and Velihotskyy. Operation complemented by one of types of vagotomy,
it is better by a selective proximal with piliroplastic. The resection of stomach on the second or first method of Bilroth can be realized only in the stable general condition of patient. During the resection of
stomach in case of low bleeding duodenal ulcers it is better to execute mobilization of duodenum and suturing of its stump on transcholedochus drainage which formed as transcholedochus duodenotomy (Laqey,
1942). This method warns the possible intraoperative damages of choledoch, that are the possible at low duodenal ulcers. Transcholedochus duodenotomy by performing the decompression of stump of duodenum,
warns insufficiency of its stitches, that can arise up in an early postoperative period.
In case of bleeding gastric ulcers, the resection methods of operations are also usable. Only on occasion, when patients has the grave general condition, it is possible to assume the wedge cutting of ulcer.
The origin of acute linear breaks of mucous tunic of esophagus and cardial part of stomach, which are accompanied by bleeding of a different degree of weight to the gastrointestinal tract lumen, is named
the Mallory-Weiss Syndrome. First described by . Mallory and . Weiss in 1929. As the reason of the gastroduodenal bleeding observed in 10 % cases. Men are ill mainly in age 3050 years.
The predetermining factors of origin of syndrome are: protracted whooping, attacks of cough, physical overstrain after the surplus food intake, alcohol with vomiting, chronic diseases of stomach, with the
acute increase of intaragastric pressure as a result of discoordinated function of cardial and pyloric sphincter, especially at older patients with atrophy gastritis. The increase of intaragastric pressure causes change
of blood flow in the wall of the stretched stomach. Spontaneous break of mucous tunic of cardial part of stomach, is accompanied by bleeding in the gastrointestinal tract lumen. The break takes not only mucous
tunic but also muscular layer, that weight of bleeding is predetermined. Most often the breaks are localized on small curvature, on the back wall of stomach and esophagus.
The main symptom of syndrome is bloody vomiting which the dyspeptic signs preceded: nausea and unbloody vomiting. Sometimes patients complain for pain in a epigastric area, in the lower part of
thorax, which is related to sudden cardial and lower part of esophagus distension.
Weight of bleeding depends on length and depth of breaks and caliber of the damaged vessels. In one case at first the some dark blood is excreted and only at the repeated vomiting is a lot of bright red
blood. In other case at once there is vomiting by a bright red blood. Sometimes bleeding looked as the tar-like emptying. The degree of hemorrhage and its weight is determined after the generally accepted chart.
Taking into account that a syndrome arises up after acceptance of a plenty of alcohol and food, the clinical forms of passing are distinguished: simple, delirious, with the signs of acute hepatic insufficiency,
without the signs of acute hepatic insufficiency, that matters very much for the choice of medical tactic.
Urgent esophagogastroscopy is the basic method of diagnostics of syndrome. During it in the cardial part of stomach or esophagus single or plural fissures are diagnosed by length 0,54,0 cm, by width
0,50,8 cm which pass longitudinally, bleeding. The edges of mucus round a fissures swelled, elevated, covered by a fibrin. Often the muscular layer of stomach or esophagus is the bottom of fissure.
Conservative treatment of the Mallory-Weiss syndrome is indicated at the small rupture of mucus stomach, to the stop of bleeding, absence of bleeding. Treatment of patients is begun with active
conservative therapy, which includes blood transfusion, infusion of hemostatic, application of antacid, Meulengracht's diet. At the rupture of the III degrees indicated endoscopy by a monopolar
electrocoagulation of the fissure and covering of aerosol film-forming preparation Lifusol. The conservative method of stop of bleeding in such patients is especially perspective, because most of them has the
delirious state or acute hepatic insufficiency.
Operative treatment is indicated at the deep large ruptures of mucus and muscular layers, cardial part of stomach, which are complicated by bleeding. In such cases conduct gastrotomy and suturing of
raptures by interrupted suture or 8-shaped stitch, applying nonabsorbable filaments. Sewings of ruptures of mucus stomach often supplement with vagotomy with pyloroplasty. At deep, especially plural ruptures
which are accompanied by the edema of tissues, sewing of ruptures is supplement with bandaging of left gastric artery.
Hemorrhagic erosive gastritis is diffuse bleeding from mucous tunic stomach as a result of single or plural superficial defects (erosions) of mucous tunic. The gastrointestinal bleeding during erosive gastritis
meet in a clinic in 1317 % cases of acute hemorrhage in a gastrointestinal tract and take first place among bleeding of unulcerous etiology. The disease is met both at men and at women, but more frequent observe
in declining years.
The spasm of large vessels in the deep layers of gastric wall, which results in disturbance of local microcirculation, hypoxia and increases of permeability of vascular wall, matters in etiology and
pathogenesis of hemorrhage erosive gastritis. The local reaction causes strengthening of reverse diffusion of hydrogen ions, liberation of pepsin, histamine. Such process often is consequence of local damaging
factor action of medicinal or toxic factors for the vessels of mucus. Damaging factor could be the matters which violate a blood flow in mucus stomach (aspirin, reserpine, hormones of adrenal glands cortex).
The large value in formation of erosions is had by the anatomic features of blood flow of stomach in a cardial part on small curvature. In connection with absence of submucosal vascular plexus, eventual vessels on
small curvature are disposed in relation to mucus tangentially. It results in shelling of epithelium, origin of erosions. Veins damaged at first, that predetermines a hemorrhage and then bleeding. In the origin of
acute hemorrhage gastritis matter also acute damage of mucus stomach by mechanical, chemical (burns) and other factors, accompanying diseases (uremia and others like that).
For hemorrhage erosive gastritis there are typical two clinical syndromes: ulcerous and hemorrhagic. The ulcerous syndrome is the most frequent sign of hemorrhage gastritis. Typical ulcerous pain is
observed in such patients. A hemorrhagic syndrome shows up by the repeated gastric bleeding and moderately increasing anaemia. Bleeding are capillary and are not such catastrophic, as at gastric ulcers.
The clinical picture of hemorrhage gastritis is characterized by dull pain in a epigastric area, which appears at faults in a food, reception of alcohol. Patients disturbs vomiting like coffee-grounds,
melena, which arise up among a complete health, symptoms of hemorrhage (dizziness, general weakness, acceleration of pulse, decline of arterial pressure). The decline of amount of red corpuscles is observed
in the blood test, haemoglobin, haemathokritis, leukocytosis. During the roentgenologic examination observed the thickened winding folds of mucus stomach with the small depots of barium. At endoscopic
diagnostics of bleeding the presence of single or plural erosions on mucus up to 57 mm in diameter are noticed, symptom of morning dew (weeps all mucus stomach).
Treatment of hemorrhage erosive gastritis, mainly, is conservative. Washing of stomach an effective by cold water or by 5 % solution of aminocapronic acid with subsequent irrigation of mucous tunic by
film-forming preparations through endoscope and introduction of hemostatic. It is important the neutralization of hydrochloric acid in a stomach (antacid, additional introduction of atropine of sulfate, aspiration
of gastric content), setting of preparations which stimulate reparative processes in a mucous tunic (methyluracyl, sayotek, sea-buckthorn oil), antihelicobacter preparation (de-nol). If under the endoscopy control
effect from conservative treatment is absent and it is the obvious threat of life of the patients, operative treatment is indicated.
Surgical treatment must be minimum. Sewing and edging of bleeding areas, selective vagotomy with pyloroplasty in most cases is effective. Only at bleeding from arising acute erosions after submucosal
telangiectasia, indicated resection of stomach. It is needed to remember, that the additional focus of bleeding can be in fundal and cardial part of stomach. Without their edging and local hemostasis operation can
not be radical. At the considerable damage of stomach by an erosive process, for a patient indicated resection of stomach or gastrectomy.
The hereditary hemorrhagic teleangiectasia, Rendu-Osler-Weber Disease hemorrhage angiopathy, which is characterized by focus microvascular expansion by the type of teleangiectasia and angiomas
with the break of which possible bleeding. Meets rarely, inherited after a autosomal-dominant type, sometimes arises up sporadically.
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Teleangiectasia and angiomas develops as a result of thinning and expansion of shallow vessels. At the same time local hemostasis is violated as a result of hypoplasia of subendothelium and collagen
deficiency. Bleeding is related to small resistance and easy vulnerability of vascular wall, by weak stimulation in these areas of aggregation of thrombocyte and blood coagulation. Teleangiectasia is disposed on
the mucous tunics of mouth cavity, rarer is mucus of the trachea, bronchial tubes, gastrointestinal tract, urinary bladder and liver.
The disease is characterized by the frequent nose-bleeds which appear in early child's age, teleangiectasias and angiomas with certain localization. The gastrointestinal bleeding can be profuse and result in
lethal termination, chronic, with the expressed anaemia. At differential diagnostics of bleeding it is necessary to observe the skin and mucous tunics. Teleangiectasias and angiomas is characterized by expansion of
granulomatous vessels and is disposed, mainly, on a head, skin, mucus of the mouth, nose, on hands, finger-tips, genital organs.
Treatment of the Rendu-Osler-Weber disease is conservative, symptomatic, including hemostatic therapy. There is the indicated blood transfusion at considerable hemorrhage. Often during recrudescent and
profuse gastrointestinal bleeding the resection of stomach is indicated. It is represents a problem for a surgeon, because teleangiectasias after the decline of arterial pressure, become pale and unnoticeable. A
prognosis is often unfavorable, because not always it is possible to expose teleangiectasias in other organs.
Menetrie syndrome is pseudotumor gastritis. The disease rarely. Etiology and pathogenesis is unknown. During disease observed the increasing of folds of mucus stomach by the height up to 3 cm and
thickness up to 2 cm. Deep cracks, which the massive bleeding are from, appear between folds. Diagnostics of bleeding is confirmed by endoscopy. Treatment is conservative, including the hemostatic therapy. If
conservative treatment are uneffective, indicated resection of stomach. During operation round a stomach the megascopic lymphatic knots with soft consistency are observed.
Hemobilia is bleeding from bilious ways and liver to the intestine. Meets in 0,01 % all gastric bleeding of unulcerous genesis.
The most frequent reason of hemobilia is the traumas of liver. Among other reasons are inflammatory processes of liver, external bilious ways (abscesses, cholangitis), vascular anomalies as aneurism of
hepatic artery and vein gate.
The typical signs of hemobilia: attack-like pain in right hypochondrium, moderate icterus, anaemia, presence of grume in vomiting masses and in the excrement which looks like a pencil or worm (imprints
of bilious ducts). Bleeding have cyclic passing (repeat oneself in 68 days). A diagnosis is based on the clinical signs, information of endoscopy, at which founded the blood flow to the duodenum from a general
bilious duct or bloody clot in the papilla Fateri. The most diagnostic value has selective angiography of the hepatic artery and cholangiography, which allow to expose the flowline of contrasting matter in tissues
of liver.
Bleeding from biliary tracts during the damage of large vessels can be severe. So, operation is the unique treatment method in such cases. In patients with hemobilia performed opening, draining and
tamponade of the haematomas with obligatory draining of general bilious channel for decompression of biliary tracts. The most radical method some surgeons count opening of haematoma with bandaging of
bleeding vessel and bilious channel or resection of liver. Bandaging of hepatic artery after angiographic study of the intraorgan arterial vessels is sometimes recommended only. Better to bandage that branch of
hepatic artery from which observed bleeding.
The particle of the rare extragastric diseases complicated by the acute gastrointestinal bleeding is 2 %. Among them the diseases of blood are met, blood vessels, system diseases (leukosis, haemophilia,
autoimmune thrombocytopenia, hemorrhagic vasculitis, the Werlhof's disease and others like that).
Leukosis are tumours which developed from hemopoietic cells. Etiology and pathogenesis to this time is not exposed. Patients with a leucosis with the gastrointestinal bleeding is 1 % of all patients with
the unulcerous bleeding.
During leucosis in the process of extramedullar hematosis the cells of vascular wall and vessel are pulled in and from the circulatory changed into hemopoietic, that results in disturbance of permeability of
vessel wall. In development of hemorrhage diathesis large part is acted the changes of thrombocytopesis, declines of growth of tissues basophiles, which produce heparin, that shows up by wide hemorrhages in a
gastrointestinal tract. Bleeding can be both insignificant and threatening to life of patient. In establishment of diagnosis sometimes there is enough simple examination of blood (hyperleukocytosis), to suspect
leucosis bleeding. During endoscopy in such patients observe the presence of flat, superficial defects of mucus stomach. A final diagnosis is based on the results of biopsy and haematological examination of bone
marrow.
Treatment includes complex application of hemostatic, preparations of blood and cytostatic agents, that results in the stop of bleeding and even to bring a patient into remission.
Haemophilia is the innate form of bleedingwhich coused by the deficit of one of three antihemophilic factors (VIII, IX, XI). The gastrointestinal bleeding is observed in 624 % patients with haemophilia.
Absence or insufficient content in the blood of antihemophilic globulin lies in basis of disease. At diminishment of it level below 30 % there is bleeding. Haemophilia is inherited, men are ill more frequent.
Pointing in anamnesis on bleeding from babyhood allow to suspect haemophilia. Roentgenologic information and results of fibergastroscopy does not expose the substantial changes in a gastrointestinal
tract. Main in diagnostics of haemophilia examination of the system of blood coagulation. Time of blood coagulation continued to 1030 minutes, sometimes a blood does not coagulate by hours.
Treatment is directed on compensation of insufficient components of the of blood coagulation system. In patients with haemophilia A, for which typical deficit of antihemophilic globulin, fresh blood
transfusion is indicated, because in a banked blood a antihemophilic globulin collapses during a few hours. At haemophilia B and are used dry and native plasma, cryoprecipitate, banked blood, because factors
IX, XI, which predetermine the form of haemophilia, is kept in them long. ordinary hemostyptic preparation (vicasol, the vitamin, chloride of calcium and others like that) does not give the effect. So, if form of
haemophilia does not established, the treatment is necessary to begin from fresh blood transfusion, antihemophilic plasma and antihemophilic globulin transfusion.
Autoimmune thrombocytopenia, or idiopathic thrombocytopenic purpura, is accompanied by the gastrointestinal bleeding and is arisen up in 0,52 % patients. Often bloody vomiting and black excrement
conditioned by swallowing of blood from a nose and gums.
The disease shows up by plural hypodermic hemorrhages and hemorrhages into submucous membrane. At girls and women the uterine bleeding is often observed. Thrombocytopenia on very low numbers
and it is the most pathognomonic sign of disease. Typical acute increase of duration of bleeding, especially in the period of acute hemorrhage.
Fresh blood and thrombocyte mass transfusion is the most effective treatment in the case of the gastrointestinal bleeding during autoimmune thrombocytopenia. Other hemostatic preparations are indicated
also. During operative treatment performed splenectomy. The absolute indications to it are frequent and protracted bleeding, threat of hemorrhage in a brain.
The Schonlein-Henoch disease is hemorrhagic vasculitis, which caused by plural microfocus microthrombovasculitis. The gastrointestinal bleeding at the Schonlein-Henoch disease is observed in 0,51 %
cases and accompanied with great pain in a epigastric area like abdominal colic. For this disease typical presence of purpura which has the symmetric location on the external surface of feet, legs, shoulders,
buttocks, also joint syndrome with pain and edema in large joints, kidney syndrome by the type of acute or chronic glomerulonephritis. Women have the possible uterine bleeding. The intestinal bleeding can be
accompanied by the edema of wall of intestine, that results in invagination or perforation of wall of bowel.
The basic and pathogenetic treatment method of patients is early application of heparin with blood transfusion, introduction of heparinized blood under the control of blood coagulation, which after
adequate therapy must be increased in two times, comparative with a norm. For a patient in the initial form of disease indicated introduction of antibiotics of wide spectrum of action, hormones of adrenal glands
cortex.
The diseases of the operated stomach (postgastrectomy and postvagotomy syndromes) are the diseases which arise up after surgical treatment of peptic or duodenum ulcer or other pathology of these organs.
Dumping syndrome is frequent complication of operations which are related to deleting or disturbance of function of goalkeeper (resection of stomach, vagotomy with antrectomy, vagotomy with drainage
operations). It takes place in 1030 % patients.
The rapid receipt (dumping) is considered the starting mechanism of dumping syndrome. During this concentrated, mainly carbohydrate, food passed from a stomach in an empty bowel.
In the phase changes of motility of thin bowel during dumping syndrome important part is acted by the hormones of thin bowel. In endocrine cells of APUD- on during dumping-syndrome observed
degranulation and presence of hormones of mothiline, neurotensin and enteroglucagon.
The inadequate mechanical, chemical and osmotic irritation of mucous tunic of thin bowel by chymus results for the acute increase of blood flow in a bowel. The last is accompanied by the considerable
redistribution of blood, especially in heavy case of dumping syndrome : blood supply of head, lower extremities is diminishes, a blood flow in a liver is multiplied.
The numeral examinations resulted in creation of osmotic theory the principal reason of dumping syndrome is the decline of volume of circulatory plasma as a result of coming a plenty of liquid into the
lumen of thin bowel from an of circulatory system and intercellular space.
For the clinical finding of dumping syndrome typical there is the origin of attacks of general weakness during acceptance of food or during the first 1520 minutes after it. The attack begins from feeling of
plenitude in a epigastric area and is accompanied by the unpleasant feeling of heat, that spills in the overhead half of trunk or on all body. Thus is acutely multiplied sweating. Then there is a fatigue, appear
somnolence, dizziness, noise in ears, shaking of extremities and worsening of sight. These signs sometimes achieve such intensity, that patients forced to lie down. Loss of consciousness could be in the first
months after operation. The attacks are accompanied by tachycardia, sometimes by the shortness of breath, headache, paresthesia of upper and lower extremities, polyuria and vasomotor rhinitis. At the end of
attack or after it patients often notice grumbling in a stomach and diarrhea.
A milk or carbohydrate food is the most frequent provoking factor of dumping syndrome. In a period between the attacks patients complain about rapid fatigueability, weakening of memory, decline of
working capacity, change of mood, irritates, apathy. During roentgenologic examination after 515 minutes observed the increased evacuation of barium mixture through anastomosis by a wide continuous stream,
expansion of efferent loop and rapid advancement of contrasting matter in the distal parts of thin bowel (Pic. 3.2.16).
By the expression of symptoms dumping syndrome is divided into three degrees of weight:
I degree is easy. Patients have the periodic attacks of weakness with dizziness, nausea, that appear after the use of carbohydrates and milk food and last no more than 1520 min. During the attack a pulse
becomes more frequent on 1015 per min., arterial pressure rises or sometimes goes down on 1.3-2 KPa (1015 mm Hg), the volume of circulatory blood diminishes on 200300 ml. The deficit of mass of body of
patient does not exceed 5 kg. A working capacity is well-kept. Medicinal and dietary treatment gives a good effect.
II degree middle weight. Attacks of weakness with dizziness, pain in the region of heart, hyperhidrosis, diarrhea. Such signs last, usually, 2040 min., arise up after the use of ordinary portions of some
food. During such state a pulse becomes more frequent on 2030 per min., arterial pressure is rises (sometimes goes down) on 22,7 KPa (1520 mm Hg), the volume of circulatory blood diminishes on 300500
ml. The deficit of mass of body of patient achieves 510 kg. A working capacity is reduced. Conservative treatment sometimes has a positive effect, but brief.
The III degree is hard. Patients are disturbed by the permanent, acutely expressed attacks with the collaptoid state, by a fainting fit, by diarrhea, which do not depend on character and amount of the accepted
food and last about 1 hour. During the attack is multiplied frequency of pulse on 2030 per 1 min; arterial pressure goes down on 2,74 KPa (2030 mm Hg), the volume of circulatory blood diminishes more than
on 500 ml. The deficit of mass of body exceeds 10 kg. Patients, as a rule, are disabled. Conservative treatment is uneffective.
The problem of treatment of patients with dumping syndrome is not easy. Before the surgical treatment, as a rule, must precede conservative. Patients with the disease of easy and middle degrees respond to
conservative treatment, mainly with an enough quite good effect. At the heavy degree of disease such treatment more frequent serves as only preparation to operative treatment. If a patient does not give a consent
for operation or at presence of contra-indications to operative treatment (disease of heart, livers, kidneys), conservative therapy is also applied. Such treatment must include dietotherapy, blood and plasma
transfusion, correction of metabolism, hormonal preparations, symptomatic therapy, electro-stimulation of motility function of digestive tract.
The dietotherapy: using of high-calorie, various food rich in squirrel, by vitamins, by mineral salts, with normal content of fats and exception from the ration of carbohydrates which are easily assimilation
(limitation of sugar, sweet drinks, honey, jam, pastry wares, kissel and fruit compotes). All it is needed to use by small portions (56 times per days). If the signs of dumping syndrome appear after a food, such
patients it is needed to lie down and be in horizontal position not less than 1 hour. At the heavy degree of dumping syndrome patients need to eat slowly, desirably lying on left. Such position creates the best
terms for evacuation of food from a stomach. Thus recommend also to repudiate from too hot and cold foods.
Medicinal treatment must include sedative, replaceable, antiserotonin, hormonal and vitamin therapy. The indications to operative treatment of patients with dumping syndrome are: heavy passing of disease,
combination of dumping syndrome of middle degree with other postgastrectomy syndromes (with the syndrome of efferent loop, hypoglycemic syndrome and progressive exhaustion) and uneffective of
conservative treatment of the dumping syndrome of middle degree. Most methods of operative treatment of dumping syndrome are directed on renewal of natural way of passing of food on a stomach and intestine,
improvement of reservoir function of stomach and providing of proportioning receipt of food in a thin bowel.
Depending on reasons and mechanisms of development of dumping syndrome there are different methods of the repeated reconstructive operations. All of them can be divided into four basic groups: I.
Operations which slow evacuation from stump of stomach. II. Redoudenization. III. Redoudenization with deceleration of evacuation from stump of stomach. IV. Operations on a thin bowel and its nerves.
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Basic stages of reconstructive operations: 1) disconnection of adhesions in an abdominal cavity, releasing of gastrointestinal and interintestinal anastomosis and stump of duodenum; 2) cutting or resection
of efferent and afferent loops; 3) renewal of continuity of upper part of digestive tract.
For correction of the accompany postgastrectomy pathology it is better to apply combined anti- (iso-) peristaltic gastrojejunoplasty. Thus transplant by length 2022 cm, located between a stomach and
duodenum, must consist of two parts: antiperistaltic (78 cm), connected with a stomach, and isoperistaltic, connected with a duodenum. An antiperistaltic segment brakes dumping of stomach stump, and
isoperistaltic hinders the reflux of duodenum content.
The attacks of weakness at a hypoglycemic syndrome arise up as a result of decline of content of sugar in a blood. It is accompanied by a acute muscular weakness, by headache, by falling of arterial
pressure, by feeling of hunger and even by the loss of consciousness. It is needed to remember, that at this pathology, unlike dumping-syndrome, acceptance of food especially sweet facilitates the state of patient.
However in some patients both syndromes unite and the attacks of weakness can arise up as directly after food intake, so in a few hours after it. In patients with such pathology the best results are got after
antiperistaltic gastrojejunoplasty (Fink, 1976).
The postgastrectomy (agastric) asthenia arises up as a result of disturbance of digestive function of stomach, pancreas, liver and thin bowel.
In patients with such pathology stump of stomach almost fully loses ability to digest a food. It is related to the small capacity of stump and rapid evacuation of food from it, and also with the acute decline of
production of hydrochloric acid and pepsin. In the mucous tunics of stump of stomach, duodenum and thin bowels as a result of fall of trophic role of gastrin and other hormones of digestive tract there are the
progressive atrophy changes. Absence in gastric juice of free hydrochloric acid is the reason of acute diminishment of digestive ability of gastric juice and decline of it bactericidal. Such situation is assist in
advancement to ascending direction of virulent flora, to development duodenitis, hepatitis, cholecystitis, dysbacteriosis, hypovitaminosis and decline of antitoxic function of liver. All it results in acute disturbance
of evacuation from a stomach.
The clinical signs of postgastrectomy asthenia arise up after a some latent period which can last from a few months to some years. During this period patients often complain for a general weakness and bad
appetite. The basic symptoms of postgastrectomy asthenia are: general weakness, edemata, acute weight loss, diarrhea, skin and endocrine abnormalities. The postgastrectomy asthenia more frequent meets at men
at 4050 years. In most cases diarrhea is the first symptom of disease, that can arise up in 2 months after operation. Diarrhea, usually, has permanent character and sometimes becomes profuse.
Weight loss appears too early, the deficit of mass of body achieves 2030 kg. A patient quickly loses forces.
Conservative treatment is the blood, plasma and albumen transfusions. These preparations are prescribed 23 times per a week. Correction of disturbances of electrolyte exchange is conducted at the same
time (transfusion of solutions to potassium, calcium and others like that). For the improvement of processes of albumen synthesis anabolic hormones are prescribed.
Operative treatment foresees the inclusion in the digestion process of duodenum, increase of capacity of stump of stomach and deceleration of evacuation of its content.
The afferent loop consists of part of duodenum, that stopped behind after a resection, area of empty bowel between a duodenojejunal fold and stump of stomach. The syndrome of afferent loop can arise up
after the resection of stomach after the Bilrhoth-II method. Violation of evacuation from a afferent loop and vomiting by a bile are its basic signs.
Acute and chronic obstruction of afferent loop are distinguished. The reason of acute obstruction is mechanical factors: postoperative commissure, volvulus, internal hernia, invagination, jamming behind
mesentery of loop of bowel and stenosis of anastomosis.
Frequency of origin of sharp obstruction of afferent loop hesitates within the limits of 0,52 %. The disease can arise up in any time after operation: in a few days or a few years.
Chronic obstruction of afferent loop (actually syndrome of afferent loop), as well as acute, can arise up in any time after operation, however more often it develop after the resection of stomach with
gastroenteroanastomosis on a long loop, especially when operation is performed without entero-enteroanastomosis by Brown.
The etiologic factors of syndrome of afferent loop are divided into two groups: 1) mechanical (postoperative commissure, invagination, disturbance of evacuation on a afferent loop, wrong location of
afferent loop, very long afferent loop, fall of mucous tunic of afferent loop into a stomach); 2) functional (hypertensive dyskinesia of bilious ways and duodenum, damage and irritation of trunks of vagus nerves,
hypotensive and spastic states of upper part of digestive tract, heightened secretion of bile and juice of pancreas under act of secretin and cholecystokinin).
For the clinical picture of acute obstruction typical is permanent, with a tendency to strengthening, pain in a epigastric area or in right hypochondrium, nausea and vomiting. At complete obstruction a bile in
vomiting masses is absent. The general condition of patient progressively gets worse, the temperature of body rises, leukocytosis grows, tachycardia grows. At the objective examination painful and tension of
muscles of abdominal wall is observed. In a epigastric area it is often possible to palpate tumular lump. Possible cases, when the increase of pressure in a bowel is passed on bilious ways and channels of pancreas.
There can be pain and icterus in such patients. There are necrosis and perforation of duodenum with development of peritonitis during further progress of process. Acute obstruction of afferent loop in an early
postoperative period can be the reason of insufficiency of stump of duodenum also.
During the roentgenologic examination of organs of abdominal cavity it is visible round form area of darkening and extended, filled by gas, bowels loop.
Patients, usually, complain for feeling of weight in a epigastric area and arching in right hypochondrium, that arises in 1015 min. after acceptance of food and gradually grows. Together with that, appear
nausea, bitter taste in a mouth, heartburn. Then there is increasing pain in a right to epigastric area. During this pain arises intensive, sometimes repeated vomiting by a bile, after which the all symptoms disappear.
It could be after certain kind of food (milk, fats) or its big amount. Very rarely vomiting by bile unconnected with the feed. In heavy case patients lose up to 1 liter of bile with vomiting masses. During the
objective examination observed subicteritiousness of the sclera, sign of dehydration of organism (decline of turgor of skin, dry tongue, oliguria, concentrated urine). Emptying is irregular, grey color, with
considerable content of undigested fat and muscular fibres. Anaemia can develop at heavy passing of disease.
Distinguished easy, middle and heavy degrees of afferent loop syndrome. In patients with the easy degree of disease vomiting is 12 times per a month, and insignificant regurgitation arise up through 20 min
2 hour after a food, more frequent after the use of milk or sweet food. At middle degree of afferent loop syndrome such attacks repeat 23 times per week, patients are disturbed by the considerably expressed
pain syndrome, and with vomiting up to 200300 ml of bile is lost. For a heavy degree the daily attacks of pain are typical, that is accompanied by vomiting by a bile (up to 500 ml and more).
A roentgenologic examination of the patients with the afferent loop syndrome is unspecific. Neither the passing of contrasting matter nor absence of filling of afferent loop can be considered as pathognomic
signs of syndrome of afferent loop.
Treatment of acute obstruction of afferent loop is mainly operative. Essence of it is the removal of barriers of evacuation of content from an afferent loop. Adhesions are dissected, volvulus is straightened,
invagination or internal hernia is liquidated. For the improvement of evacuation between afferent and efferent loops performes the entero-enteroanastomosis type end-to-end or after the Roux method.
Conservative treatment of syndrome of afferent loop is ineffective and, mainly, is mean the removal of hypoproteinemia and anaemia, spasmolytic preparations and vitamin are appointed. With this purpose a
blood, plasma and glucose is poured with insulin, a novocaine lumbar blockade and blockade of neck-pectoral knot, washing of stomach is also done.
All operative methods of treatment of afferent loop syndrome can be divided into three groups:
I. Operations, that will liquidate the bends of afferent loop or shorten it.
II. Drainage operations.
III. Reconstructive operations.
The operations of the first group, directed on the removal of bends and invagination of afferent loop, can not be considered as radical. They need to be performed only at the grave general condition of
patient.
The widest application in clinical practice at the syndrome of afferent loop has the operation offered by Roux (Pic. 3.2.17).
For the prophylaxis of afferent loop syndrome it is necessary to watch after correct imposition of anastomosis during the resection of stomach: to use for the gastroenteroanastomosis short loop of thin
bowel (68 cm from the Treits ligament) for imposition, to sew afferent loop to small curvature for creation of spur, to fix reliably stump of stomach in peritoneum of transverse colon.
The origin of reflux after the distal resection of stomach is conditioned by some factors:
I. Traumatic factors: 1) traction of stomach during operation as reason of sprain of ligament of proximal part of stomach and mobilization of large curvature of stomach; 2) cutting of vessels of stomach and
oblique muscles of it wall, in particular on small curvature; 3) vagotomy, that is accompanied by cutting of phrenico-esophageal and gastrophrenic ligaments; 4) imposition of gastrointestinal anastomosis,
especially direct gastroduodenoanastomosis by Billroth-I, that results in smoothing of the Hisa corner; 5) frequent aspiration of gastric content in a postoperative period, that causes superficial esophagitis.
II. Trophic factors: 1) damage of vessels which are the reason of ischemia in the area of esophago-gastric connection, and thrombophlebitis of cardial part of stomach; 2) disturbance of influencing of
neurohumoral factors which take part in innervations of esophagus; 3) disturbance of trophism of diaphragm as a result of hypoproteinemia and weight loss; 4) ulcerous diathesis and megascopic volume of gastric
secretion (especially nightly); 5) regurgitation of alkaline content of duodenum in stump of stomach which reduces tone of it muscular shell.
III. Mechanical factors: 1) gastric stasis; 2) diminishment of volume of gastric reservoir, that is accompanied by the increase of intragastric pressure.
The clinical picture of gastroesophageal reflux is conditioned by the mechanical and chemical irritations of esophagus by content of stomach or thin bowel. As a result, there is esophagitis, which can be
catarrhal, erosive or ulcerous-necrotic. The symptoms of reflux are very various and can simulate different diseases of both pectoral and abdominal cavity organs.
The basic complaint of patients with this pathology is a smart behind a breastbone, especially in the area of the its lower part. It, usually, spreads upwards and can be accompanied by considerable salivation.
Strengthening of pain at inclinations of trunk gave to the French authors an occasion to name this sign the symptom of laces. Unendurable heartburn is the second complaint, that arises up approximately in 12
hours after the food intake. Patients forced often to drink, somehow to decrease the unpleasant feelings, however this, certainly, does not bring them facilitation. Some of them, in addition, complain for bitter taste
in a mouth.
Pain behind a breastbone often can remind the attack of stenocardia with typical irradiation. Sometimes such reflux is able to provoke real stenocardia.
Hypochromic anaemia is the frequent symptom of gastroesophageal reflux too.
The diagnosis of gastroesophageal reflux, mainly, is based on clinical information, results of roentgenologic examination, esophagoscopy.
The edema, hyperemia of mucous tunic of esophagus, easy bleeding and vulnerability it during examination, surplus of mucus and erosions covered by fibrin tape is considered the endoscopic signs of
esophagitis. In doubtful case at the insignificantly expressed macroscopic changes the biopsy of mucous tunic helps to set a diagnosis.
Treatment of patients with gastroesophageal reflux is mainly conservative. Very important is diet, which avoid spicy, rough and hot food. Eating is needed often, by small portions. It is impossible also to lie
down after the food intake, because the gastric content can flow in a esophagus. A supper must be not later than for 34 hours before sleep. Between the reception of food does not recommend to use a liquid.
Next to that, it is necessary to remove factors which promote intraperitoneal pressure (carrying to the bracer, belt, constipation, flatulence). Sleeping is needed in position with a lift head and trunk. From
medicinal preparations it is useful to recommend enveloping preparation.
Operative treatment of gastroesophageal reflux, that arose up after the distal resection of stomach, it is needed to recommend to the patients with the protracted passing and uneffective of conservative
treatment. During operation, mainly, performed renewal of the broken Hisa angle. In addition, performed esophagoplasty, fundoplication by Nessen's and esophagofrenofundoplication.
The prophylaxis of this complication consists in the study of the state of cardial part of stomach before and during every resection and fixing of bottom of stomach to the diaphragm and abdominal part of
esophagus during leveling the Hisa angle.
Alkaline reflux-gastritis meets in 535 % operated patients after the resection of stomach, antrectomy, gastroenterostomy, vagotomy with pyloroplasty, and also cholecystectomy and papillosphincteroplasty.
The reason of this complication is influence of duodenum content for the mucous tunic of stomach (bilious acids, enzymes of pancreas and isolecithin). Last, forming from bile lecithin under act of
phospholipase A, able to destroy the cells of superficial epithelium of mucous tunic of stomach by removing of lipid from their membranes. As a result the erosions and ulcers are formed in the patient organism.
Bilious acids also has the expressed detergents properties. As isolecithin and bilious acids, the very important bacterial flora which directly and through toxins can cause the damage of mucous tunic of stomach
stump. Also, alkaline environment and disturbance of evacuation from the operated stomach influence favourably on microflora growth.
For the clinical picture of alkaline reflux-gastritis the permanent poured out pain in a epigastric area, belch and vomiting by a bile are typical. At some patients heartburn and pain is observed behind a
breastbone also. In majority patients so proof loss of weight takes place, that even the protracted complex therapy and valuable feed does not provide addition to the deficit of mass of body. There are typical signs
also anaemia, hypo- or achlorhydria.
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Reliable diagnostics of alkaline reflux-gastritis became possible after wide introduction in clinical practice of endoscopic examination. In such patients during gastroscopy hyperemia of mucous tunic of
stomach is observed. It is often possible to observe reflux in the stomach of duodenum content. During histological examination of biopsy material a chronic inflammatory process, intestinal metaplasia,
diminishment of mass of coating cells and area of hemorrhages are found. All it testifies the deep degenerative changes in the mucous tunic of stomach. The some authors underlines that the inflammatory changes,
at least in the area of anastomosis, are observed in most persons which carried the resection of stomach. So, endoscopic examination can not be considered deciding in diagnostics. Even the diffuse inflammatory
changes can take place in absent of clinical symptoms and, opposite, in case with expressed clinical symptoms the minimum changes of mucous tunic of stomach are sometimes observed.
Conservative treatment of reflux-gastritis (sparing diet, antacides, enveloping preparations), usually, is ineffective. Existent methods of surgical treatment, mainly, directed on the removal of reflux of
duodenum content to the stomach. Most popular is operation by the Roux method. The some surgeons considers that distance from gastroenteroanastomosis to interintestinal anastomosis must be 4550 cm.
Main reason of origin of peptic ulcer of anastomosis is leaving of the hyperacid state of stomach mucous, even after the performed operation. Such phenomenon can be consequence of many reasons:
primary economy resection, wrong executed resection (when the mucous tunic of pyloric part is abandoned in stump of duodenum or stomach), heightened tone of vagus nerves and the Zollinger-Ellison syndrome.
Peptic ulcers, usually, arise up after operation during the first year. Typical signs are pain, vomiting, weight loss, bleeding, penetration and perforation.
Pain is the basic symptom of peptic ulcer. Often it has the same character and localization, as well as at peptic ulcer. However often observe it moving to the left or in the umbilical area. At first patients bind
such feelings to the use of food, but then specify nightly and hungry pain. It at first is halted after a food, but in course of time is become permanent, unendurable, independent from food intake. It can increase
during the flounces, the walk, can irradiate in the back, thorax or shoulder.
During the objective examination of patients is often possible to expose on a stomach hyperpigmentation from a hot-water bottle. During palpation to the left from epigastric area near a umbilicus the
painful and moderate muscles tension of abdominal wall is observed. Sometimes is possible to palpate inflammatory infiltrate of different sizes. During the examination of patients with a peptic ulcer the important
role has determination of gastric secretion against a background of histamine and insulin stimulation. There is a necessity also examination of basal secretion. These preoperative examinations in most patients
enable to set the reason of hypersecretion which can be: 1) heightened tone of vagus nerves (positive Hollander test); 2) economy resection of stomach, often in combination with the heightened tone of vagus
nerve (considerable increase of gastric secretion after histamine or pentagastrin stimulation in combination with the positive Hollander test); 3) abandoned part of mucous tunic of antral part of stomach (high basal
secretion and small increase of secretion in reply to histamine and insulin stimulator); 4) the Zollinger-Ellison syndrome.
Roentgenologic diagnostics of peptic ulcer, usually, is difficult, especially at shallow, flat ulcers, bad mobility and insufficient function of anastomosis. A niche is the direct sign of a similar pathology,
indirect are the expressed inflammatory changes of mucous tunic of stump of stomach and bowel, painful point in the projection of stump of stomach and anastomosis and bad function of anastomosis. The
deciding value in diagnostics has endoscopic examination.
Conservative treatment of peptic ulcers, as a rule, is ineffective. So, operation must be the basic type of treatment. The choice of method of operative treatment depends on character of previous operation
and from abdominal cavity pathology found during the revision. For today the most important parts of the repeated operations is vagotomy. There is obligatory also during the resection of stomach on the exception
the revision of duodenum stump for liquidation of possibly abandoned mucous tunic of antral area.
Operative treatment at a peptic ulcer must consist of certain stages. Laparotomy and disconnection of adhesions through a considerable spike process (increasing of stomach, loops of intestine and liver to
the postoperative scar) almost always causes large difficulties.
After the selection of anastomosis with afferent and efferent loops the last cut by the UKL-60 appliance, within the limits of healthy tissues with renewal of intestine continuity by end-to-end type
anastomosis.
At patients with a peptic ulcer, that developed after gastroenterostomy, cut a duodenum and sutured its stump by one of the described methods. During it there can be the difficulties related to the presence in
it active ulcer. When peptic ulcers do not cause rough deformation of stomach, apply degastroenterostomy, vagotomy and drainage operations.
In the case of the considerably expressed spike process it is possible to execute trunk subdiaphragmatic vagotomy, and in case of the insignificantly changed topography of this area selective gastric
vagotomy.
It is important to note, that stomach resected together with anastomosis, peptic ulcer and eliminated area of empty bowel by one block.
This pathology arises up as a result of perforated of peptic ulcer in a transverse colon with formation of connection between a stomach, small or large intestine.
Diagnostics of gastro-colon fistula at patients with expressed clinical signs of disease does not difficult. However, symptoms are often formed and is indicated up slowly, so such patients with different
diagnoses long time treat oneself in the therapeutic or infectious parts.
The typical signs of this pathology is considered diminishment or disappearance of pain, that was before, and proof, profuse, that does not respond to treatment, diarrhea. Patients has emptying up to 1015
times per days and even more frequent. An excrement contains a plenty of undigested muscular fibres and fat acids (steatorrhea). In case of wide fistula an undigested food can be with an excrement.
Excrement smell from a mouth, usually, notice surrounding. The patients does not feel it. However appearance of excrement belch is indicate the hit into the stomach of excrement masses and gases, and
could confirm this pathology.
The such patients very quickly lose weight (mass of body goes down on 5060 %), their skin becomes pale with a grey tint. The protein-free edemata, ascites, hydrothorax, anasarca, signs of avitaminosis
appear in non-treated case.
Through the severe losses of liquid and nonassimilable food there can be the increased appetite and unendurable thirst in such patients. However, they adopt a plenty of liquid and food but the state of them
continues to get worse.
Headache, apathy and depression is observed, and at the objective examination is exhaustion (ochre colour of skin, dryness and decline of it turgor, edemata or slurred of swelling extremities, atrophy of
muscles). A stomach often moderately pigmented from hot-water bottles, subinflated, with the visible peristalsis of intestine. During the changes of patient position it is possible to hear grumbling, splash and
transfusion of liquid. The examination of blood can expose hypochromic anaemia.
Roentgenologic examination is a basic diagnostic method. There are three varieties of such examinations of gastro-colon fistula. During the examination with introduction of barium mixture through a
mouth the hit of contrasting matter directly from a stomach into a colon is the typical roentgenologic symptom of such pathology. Irrigoscopy is more perfect and effective method. With suspicion on gastro-colon
fistula it is better to perform irrigoscopy. Passing of contrasting matter to the stomach at this manipulation testifies the presence of fistula. The third method is insufflation of air in a rectum. With it help on the
screen it is possible to observe the location and passing of fistula, and also, as a result, hit of air in a stomach, increase of it gas bubble. Thus there can be the belch with an excrement smell.
The important role played the tests with dyes: at peroral introduction of methylene-blue after the some time it found in excrement masses or, opposite, after an enema with methylene-blue dye appears in a
stomach.
Treatment of gastro-colon fistula is exceptionally operative. It needs to be conducted after intensive preoperative preparation with correction of metabolism. All operations which can be applied at treatment
of patients with gastro-colon fistula divide into palliative and radical (single-stage operation and multi-stage operation).
During the palliative operations the place of fistula of stomach, transverse colon and jejunum is disconnected and then sutured the created defects. Other variant is disconnection of stomach and transverse
colon and leaving the gastroenteroanastomosis. It is necessary to remember, that during such operations the only fistula always removed and does not performed the resection of stomach. Clearly, that such
situation also does not eliminate possibility of relapse of peptic ulcer and development of its complications. Taking into account it, palliative operations can be recommended in those case only, when the general
condition of patient does not allow to perform radical operation.
Single-stage operation radical operations. The most widespread is degastroenterostomy with the resection of stomach. However, it is needed to remember that operation of disconnection of fistula, suturing
of opening in the jejunum and transverse colon on the lines of fistula and resection of stomach applies only in case of absent of infiltrate and deformation and in the conditions of possibility to close a defect in
bowels without narrowing of their lumen. This operation is the simplest, is enough easily carried by patients and it is enough radical.
Such complications appear through considerable time after operation (from 1 month to one year). Disturbances of function of gastrointestinal anastomosis can be caused by the reasons, related both to the
technical mistakes during operation and with pathological processes which arose up in the area of anastomosis.
The clinical picture of disturbance of anastomosis function, mainly, depends from the degree of its closing. At complete it obstruction in patients arise up intensive vomiting, pain in a epigastric area, the
symptoms of dehydration and other similar signs appear. In other words, the clinic of stenosis of the stomach output develops. Clearly, that during incomplete narrowing the clinical signs will be expressed less,
and growth of them more slow. Sometimes disturbance of evacuation can unite with the syndrome of afferent loop with a inherent clinical picture. At the roentgenologic examination of such patients expansion
of stomach stump is exposed with the horizontal level of liquid and small gas bubble. Evacuation from it is absent or acutely slow.
Treatment of scar deformations and narrowing of anastomosis must be operative and directed for the disconnection of accretions and straightening of the deformed areas. In case of presence in patients large
inflammatory infiltrate it does not need to perform disconnection. In such cases it is the best to apply roundabout anastomosis. If a resection by Finsterer was done in such patient, better to perform anterior
gastroenteroanastomosis, and after a resection by Billroth-I posterior. As a result of conducting of such operations the state of patient, as a rule, gets better, and often recovered the function of primary
anastomosis.
Removing of all stomach and exception of duodenum from the process of digestion of food cause plural functional disturbances in an organism. Some of them meet already after the resection of stomach
(dumping-syndrome, hypoglycemic syndrome), other more inherent for gastrectomy (anaemia, reflux- esophagitis and others like that).
Most patients, that carried gastrectomy, complain for a considerable physical weakness, heightened fatigueability, sometimes is complete weakness, loss of activity and acute decline of work capacity.
Almost all of them notice bad sleep, worsening of memory and heightened irritates. The appearance of patients is typical. Their skin insignificantly hyperpigmentated, dry, its turgor reduced, noticeable atrophy of
muscles. Can be the signs of chronic coronal insufficiency in such patients, and in older-year persons is typical picture of stenocardia. Except for it, can be hypotension, bradycardia and decline of voltage on
EKG; during auscultation deafness of tones is observed. From the side of the hormonal system the decline of function of sexual glands is typical: in men declines of potency, in women disturbances of
menstrual cycle, early climax. Can be the signs of hypovitaminosis A, B, and decline of resistibility of organism to chill, infectious diseases and tuberculosis.
The decline of mass of body is observed in 75 % patients, that carried gastrectomy. It is conditioned by the decline of power value of food as a result of disturbance of digestion, bad appetite and wrong diet.
As a result of progressive hypoproteinemia there can be the protein-free edemata.
Patients with such pathology must be under the permanent clinical supervision and 12 times per year during a month to have the course of stationary prophylactic treatment which includes psycho-, diet-,
vitaminotherapy, correcting and replaceable therapy, and also prophylaxis of anaemia.
Psychotherapy is especially indicated in the psychodepressive and asthenic states. It is performed in combination with medicinal treatment. Hypnotic preparation, bromide, tranquilizers are applied.
A food must be correctly prepared, without the protracted cooking. Patients need to feed on 610 times per days by small portions.
Next to dietotherapy, it is constantly necessary to apply replaceable therapy (Pancreatine, Pansinorm, Festal, Intestopan). In case of absent of esophagitis hydrochloric acid is appointed. For the improvement
of albuminous exchange anabolic hormones are applied.
In case of reflux-esophagitis there are indicated feeds by small portions with predominance of liquid, ground, jelly-like foods, astringent, coating, anticholinergic preparations. Between the receptions of
food does not recommend to use a liquid. In case of dysphagy appoints a sparing diet.
For the prophylaxis of iron-deficiency anaemia, that arises up in the first 23 years after gastrectomy, important the indication of iron preparations.
For warnings and treatments of pernicious anaemia applied cyanocobalamin for 200 mcg through a day and folic acid. Packed red blood cells is indicated in heavy case.
The relapse of ulcer is enough frequent complication of vagotomy. It meets in 812 % patients. The reasons of such relapses of ulcer can be: 1) inadequate decline of products of hydrochloric acid
(incomplete vagotomy, reinnervation); 2) disturbance of emptying of stomach (ulcerous pylorostenosis after selective proximal vagotomy or after pyloroplasty); 3) local factors (duodenogastric reflux with
development of chronic atrophy gastritis, disturbance of circulation of blood and decline of resistibility of mucous tunic); 4) exogenous factors (alcohol, smoking, medicinal preparations); 5) endocrine factors
(hypergastrinaemia: hyperplasia of antral G-cells, the Zollinger-Ellison syndrome; hyperparathyroidism).
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Three variants of clinical passing of relapse of ulcer are distinguished after vagotomy: 1) symptomless, when an ulcer is found during endoscopic examination; 2) recurrent with protracted lucid space; 3)
persisting ulcer with typical periodicity and seasonality of exacerbation.
It is needed to underline that the clinical signs of this pathology during the relapse are less expressed, than before operation, and absence of pain does not eliminate the presence of ulcer. Sometimes
bleeding can be first its sign. Complex examination, that includes roentgenologic, endoscopic examination, study of gastric secretion and determination of content of gastrin in the blood, allows not only to expose
an ulcer but also, in most cases, to set its reason. The interpretation the results of gastric secretion examination in such patients are heavy. Taking into account it, it is needed to study both a basal secretion and
secretion in reply to introduction of insulin and pentagastrin, and also level of pepsin.
Approximately in 35 % patients, mainly with the first two variants of clinical passing of disease, the relapses of ulcers, are treated by ordinary methods of conservative therapy. Yet in 3040 % cicatrization
of ulcers comes after application of preparations which stop a gastric secretion (cimetidine, ranitidine150 mg for night). At other 1020 % patients, mainly with the third variant of clinical passing, is necessary
operative treatment.
The question of choice of the repeated operation in patients with the relapse of ulcer after vagotomy still does not decided. Some surgeons execute revagotomy, trunk vagotomy with drainage operation,
revagotomy with antrectomy or resection of stomach. However much majority from them in case of relapse ulcer after vagotomy performed antrectomy in combination with trunk vagotomy.
Frequency of postvagotomy diarrhea hesitates from 2 to 30 %. The basic sign of complication in patient is present the liquid watery emptying about three times per days. The reasons of diarrhea are: gastric
stasis and achlorhydria, denervation of pancreas, small intestine and liver, and also disturbance of motility of digestive tract. Discoordination of evacuations from a stomach, stagnation and hypochlorhydria assist
to development in it different microorganisms, and it also can be the reason of diarrhea.
The clinical signs of postvagotomy diarrhea are specific. Acute beginning are typical patient often does not have time to reach to the rest room. Such suddenness repressing operates on patients. As a result
they are forced whole days to be at home, expecting the duty attack. An excrement changes colorings as a result of breeding of pigment and becomes more light.
Treatment of diarrhea must be complex. Above all things it is needed to recommend a diet with the exception of milk and other provoking products. For the removal of bacterial factor antibiotics are applied.
Favourable action in case of the signs of stagnation in a stomach are had weak solutions of organic acids (lemon, apple and others like that).
Among other most distribution was got by the .. Kuragin and S.D. Hroismann (1971) suggestion to treat postvagotomy diarrhea by benzohexamethonium (for 1 ml 2,5 % solution 23 times per a day).
Reported also about successful application of cholesteramine (for 4 g 3 times per a day with the subsequent decline of dose to 4 g per days).
At heavy passing of postvagotomy diarrhea, that does not respond to conservative treatment, it is needed to recommend operative treatment degastroenterostomy with pyloroplasty. However, the type of
drainage operation, as practice shows, does not influence on frequency of diarrhea origin. In this connection, some surgeons with success applied the inversion of the segment of thin bowel, located distal from the
area of maximal absorption.
The cancer of stomach is a malignant formation, that develops from epithelium tissue of mucus stomach. Among the tumours of organs of digestion this pathology takes first place and is the most frequent,
by the reason of death from malignant formations in many countries of world. Frequency of it at the last 30 years considerably diminished in the countries of Western Europe and North America, but yet remains
high in Japan, China, countries of East Europe and South America.
Etiology of cancer of stomach is unknown. It is known that, as other diseases of gastrointestinal tract, a cancer damages a stomach. According to statistical information, it meets approximately in 40 % of all
localizations of cancer.
The factors of external environment has the substantial influencing on frequency of this pathology. Above all things, feed, smoke food, salting, freezing of products and their contamination of aflatoxin.
Consider that a food factor can be: a) by a carcinogen; b) by the solvent of carcinogens; c) to grow into a carcinogen in the process of digestion; d) to be instrumental in action of carcinogens; e) not enough to
neutralize carcinogens.
In the USA and countries of Western Europe frequency of cancer of stomach in 2 times more large in the lower socio-economic groups of population. Some professional groups also can it (miners, farmers,
works of rubber, woodworking and asbestine industry). High correlation communication is set between frequency of cancer of stomach and use of alcohol and smoking. The value of genetic factors (heredity, blood
type) is not led to.
The cancer of stomach arises up mainly in age 60 years and above, more frequent men are ill.
Precancer. The precancer diseases of stomach are: a) chronic metaplastic disregenerator gastritis conditioned by helicobacter pylori; b) villous polypuses of stomach and chronic ulcers; c) nutritional anemia
due to vitamin B12 deficiency (pernicious); d) resected stomach concerning an ulcer.
The presence of precancer changes of mucous tunic of stomach has substantial influence for frequency of stomach cancer. In those countries, where morbidity on the cancer of stomach is higher,
considerably more frequent chronic gastritises are diagnosed. Lately in etiology of chronic gastritises take the important value helicbacter pylori. In Japan, where the cancer of stomach is in 40 % cases is the
reason of death, chronic gastritis appears in 80 % cases of resected stomach, concerning a cancer.
Connection between polypuses, chronic gastric ulcers and possible it malignization comes into question in literature during many decades. Most authors consider that polypuses could be malignant
differently. There are three histological types of polypuses: hyperplastic, villous and hamartoma. There are hyperplastic polypuses, but it not malignant.
Hamartoma is accumulation of cells of normal mucous tunic of stomach. They never becomes malignant.
Villous polypuses are potentially malignant in 40 % cases, but it happen in 10 times less, than hyperplastic. The possibility of malignization of chronic gastric ulcers is not proved. The American scientists
support a hypothesis, that the cancer of stomach can be ulcerous often, but malignization of ulcers takes place rarely (no more than 3 %). From data of the Japanese scientists, on 5070th there was higher
correlation connection between chronic gastric ulcers and cancer of stomach. The frequent decline of this correlation is lately noticed (70 % on 5070th and 10 % on 80th).
Frequency of cancer of stomach at patients with pernicious anaemia hesitates within the 510 %, that in 20 times higher, compare with control population. In patients with a resected stomach after peptic
ulcers is multiplied the risk of origin of stomach cancer in 23 times (duration of latent period hesitates from 15 to 40 years). The reason of such dependence is not found out, but there is a version, that this is
linked with a gastric epithelium metaplasia by an intestinal type.
From all malignant formations of the stomach in 95 % adenocarcinoma is observed. Epidermoid cancer, adeno-acanthoma and carcinoid tumours do not exceed 1 %. Frequency of leiomyosarcoma hesitates
within the limits of 13 %. Lymphoma of gastrointestinal tract is localized in a stomach.
The prognosis of localization depends on the degree of invasion, histological variants of tumour.
The macroscopic forms of cancer of stomach in different times were described variously. More than 60 years ago the German pathologist Bermann described 5 macroscopic forms of cancer of stomach: 1)
polypoid or mushroom-like; 2) saucer-shaped or with ulcerous and expressly salient edges; 3) with ulcerous and infiltration of walls of stomach; 4) diffuse -infiltrate; 5) unclassified.
American pathopsychologs is selected 4 forms. The tumours of stomach with ulcerous are the most frequent macroscopic form of cancer of stomach and arise up on soil of chronic ulcer. The signs suspicious
on malignization are: the sizes of ulcer more than 2 cm in a diameter, appearance of the heightened edges.
The polypoid tumours of stomach observed only in 10 %. These tumours can achieve considerable sizes without an invasion and metastasis. Scirrhous carcinoma is the third macroscopic type. This category
of tumours also does not exceed 10 %. The scirrhous carcinoma is the signs of infiltration by anaplastic cancer cells, diffusely developed connecting tissue which results in the bulge and rigidity of wall of
stomach. So called small cancers belong to the fourth macroscopic type. It meet comparative rarely (no more than 5 %) and is characterized by superficial accumulation of cancer cells which substitute for normal
mucus in such kind: a) superficial flat layer which does not rise above the level of mucus; b) salient (bursting) formation; c) erosions.
Mainly (more than 50 %) tumours arise up in a antral part or in distal (lower) third of stomach, rarer (to 15 %) in a body and in cardia (to 25 %).
However, lately more often observed cardioesophageal cancers and diminishment of frequency of tumours of distal parts of stomach. In 2 % cases meet the multicentric focuses of growth, but from data of
some authors, this percent could be multiplied in 10 times after carefully histological inspection of the resected stomaches. This assertion is based on the theory of the tumour field (D.I. Holovin, 1992).
Especially this typically for patients which has pernicious anaemia or chronic metaplastic disregenerative gastritis.
Metastasis is carried out by lymphogenic, hematogenic and implantation ways mostly. Three (from data of some authors, four) pools of lymphogenic metastasis are selected: left gastric (knots on passing of
small curvature of stomach in a gastro-subgastric ligament and pericardial); splenic (mainly, suprainfrapancreatic knots); hepatic (knots in a hepato-duodenal ligament, right gastric omentum that lower pyloric
groups, right gastric and suprapyloric groups, pancreatoduodenal group).
However, the such way of lymphogenic metastasis is conditional and incomplete, as at presence of block lymph flow passes retrograde metastasis, so called jumping metastases which predetermine the
origin of remote lymphogenic metastases in left supraclavicular lymph nodes (Virhov metastasis) appear, in Lymph nodes of left axillar and inguinal areas, metastases in a umbilicus.
Direct distribution: small and large omentum, esophagus and duodenum; liver and diaphragm; pancreas, spleen, bile ducts.
Front wall of stomach: colon bowel and mesocolon; organs and tissues of retroperitoneal space.
Lymphogenic metastasis: regional lymph nodes, remote lymph nodes, left supraclavicular lymph node (Virhov), lymph node of axillar area (Irish); in a umbilicus (sisters Joseph).
Hematogenic metastasis: liver, lungs, bones, cerebrum.
Peritoneal metastasis: peritoneum, ovarium (the Krukenberg metastasis), Duglas space (the Shnicler metastasis).
All authors which are engaged in the study of problem of cancer of stomach underline absence or vagueness, no specificity of symptoms, especially on the early stages of disease. The displays of cancer of
stomach are very various and depend on localization of tumour, character of its growth, morphological structure, distribution on contiguous organs and tissues. At localization of tumour in a cardial part patient
complains firstly, as a rule, for appearance of dysphagy.
At careful, purposeful collection of anamnesis it is not succeeded to expose some other, most early symptoms, which precedes to dysphagy and forces a patient to appeal to the doctor. The unpleasant feeling
behind a breastbone and feeling of unpassing of hard food on a esophagus appear at the beginning of disease. After some time (as a rule, it is enough quickly, during a few weeks, sometimes even days) a hard food
does not pass (it is to wash down by water or other liquid). This period can be during 13 months. Patients address a doctor exactly in this period. Other symptoms appear to this time: regurgitation, pain behind a
breastbone, loss of mass of body, sometimes even exhaustion, the grey colouring of person, a skin is dry, quickly grows general weakness. Sometimes patients address a doctor, when already with large effort a
spoon-meat passes only or complete stenosis came.
At localization of tumour in the antral part of stomach the first complaints, as a rule, are up to appearance of feeling of weight in epigastric region after the reception of food (even in a two-bit), feeling of
saturation (after the reception of glass of water), belch (at first it is simple by air, and then with a smell). Feeling of weight grows for a day, patients forced to cause vomiting. In the morning there can be vomiting
by mucus with the admixtures of coffee-grounds (so called cancer water). Patients loses weight (mass of body is lost), a weakness, anaemia grows.
Tumours localized in the body of stomach show up either a pain syndrome or syndrome of so called small signs (.I. Savitskyy, 1947), which is characterized by appearance of amotivational general
weakness, decline of capacity, rapid fatigueability, depression (by the loss of interest to the environment), proof decline of appetite, gastric discomfort, making progress weight lost.
The carried chronic diseases of stomach, for which typical seasonality, can influence on the clinical sign of cancer of stomach. At appearance of gastric complaints out of season or in absent of effect from
the got therapy concerning the exacerbation of gastritis, ulcers must guard a patient and doctor (symptom of precipice of gastric anamnesis).
In case of occurring of gastric symptoms first in persons in age 50 years and older it is foremost necessary to eliminate the cancer of stomach.
In parts of patients cancer of stomach shows up only the metastatic damage of other organs or complications. More than twenty so called atypical forms, which are characterized by causeless anaemia,
ascites, icterus, fever, edemata, hormonal disturbances, changes of carbohydrate exchange, intestinal symptoms, are distinguished.
During the examination of patients with the cancer of stomach the pallor of skin covers (at anaemia) is observed, in neglected case is frog stomach (sign of ascites).
During palpation determined painful in a epigastric area, sometimes possible to palpate the tumour.
During auscultation of patients with pylorostenosis it is possible to define noise of splash.
Laboratory information: hypochromic anaemia, neutrophilic leukocytosis, megascopic ESR; during examination of gastric secretion: hypo- and anacidity and achlorhydria.
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Gastroduodenoscopy enables to diagnose a tumour even smaller 5 mm and conduct an aiming biopsy with histological examination of the taken material.
Roentgenoscopy and roentgenography examination of stomach. Basic signs: defect of filling, local absence of peristalsis, malignant relief of mucous tunic (Pic. 3.2.18).
Ultrasonic examination: presence of metastases in a liver, pancreas.
Computer tomography allows to estimate the basic parameters of tumour, germination in neighbouring organs and presence of metastases.
It is expedient to apply laparoscopy, mainly, for the decision of question about operable of tumour (diagnostics of metastatic defeat of organs of abdominal cavity).
At an early cancer complaints depend on the previous gastric diseases. Therefore, on the basis of clinical information, suspecting a tumour is possible only on occasion, when in patients next to clear pain
symptoms an appetite goes down, appear anaemia, general weakness. In practice an early cancer is recognized at purposeful screening, and also in the process of endoscopic or roentgenologic examination of
gastric patients.
A differential diagnosis is conducted with an peptic ulcer, gastritis, polyposis, other gastric and ungastric diseases. For a cancer there is typical firmness of symptoms, instead of their seasonality (typical
syndrome of precipice of gastric anamnesis) or tendency to their gradual progress.
The row of diseases, with which the cancer of stomach is to differentiate to the doctor, depends from character of complaints of patients.
Five basic clinical syndromes are selected:
1) pain;
2) gastric discomfort;
3) anaemic;
4) dysphagic;
5) disturbance of evacuation from a stomach.
At patients, at what cancer of stomach shows up a pain syndrome and syndrome of gastric discomfort, a differential diagnosis is conducted with the peptic ulcer, gastritis, cancer of body of pancreas.
It is oriented on features dynamics of development of pain syndrome, ingravescent of the general condition, change of character of complaints.
A question about character of anaemia, source and nature of bleeding decides at an anaemic syndrome. In the process of examination attention is paid to the state of bottom of stomach, where bleeding
malignant formations can be.
At a dysphagic syndrome a differential diagnosis is conducted with the cicatrical narrowing, achalasia of esophagus. For malignant formations testify short anamnesis, gradual progress of symptoms, signs of
gastric discomfort, general weakness, weight lost.
At disturbance of evacuation from a stomach during stenosis of pyloric part, absence of ulcerous anamnesis, declining years of patients, relatively quick (weeks, months) growth of stenosis testify for tumor.
The presence of cancer of stomach is a indications for surgical treatment. However, counting on success is possible only at presence of the limited tumours (within the limits of the 0II stages). At the III
stage of disease implementation of the widespread combined operations in a radical volume is possible, however most patients die during 12 years. A distal or proximal subtotal resection (Pic. 3.2.19) and total
gastrectomy (Pic. 3.2.20) is performed with removing of large and small omentumes and regional areas of metastasis with obligatory histological examination of stomach on the lines of resections.
During the combined operations organs which are pulled in to the pathological process are removed.
In case of IV stage of disease and satisfactory state of patient palliative operations which improve quality of life of patient are performed.
In case of presence of complications (mainly stenosis) and grave common condition of patient perform symptomatic operative treatments.
Symptomatic is operations which will liquidate one of symptoms of cancer of stomach. In this group of operations include: 1) roundabout gastrojejunoanastomosis (Pic. 3.2.21) and jejunostoma (in case of
the stenosis tumours of stomach output); 2) gastrostoma (Pic. 3.2.22) in case of the cancer of cardial part of stomach with disturbance of patency; 3) edging of bleeding vessels in case of complication of cancer
by bleeding; 4) tamponade by omentum during the perforation of tumour.
The value of radial therapy and chemotherapy, as independent methods of treatment of cancer of stomach, is limited. Radial therapy is indicated for patients with cardial cancer as preoperative course or as
palliative treatment. Adjuvant mono- or polychemotherapy (mainly by 5-phtoruracil) is conducted in a postoperative period as combined therapy and in case of dissemination of the tumours.
Prognosis. The indexes of five-year survival of patients with the cancer of stomach hesitate within the limits of 530 %, but, from data of most authors, they do not exceed 10 %.
The incarcerated hernia, regardless of time of its origin, localization and age of patient, must be operated on. However, if a patient is hospitalized already with the expressed symptoms of intestinal
obstruction, than should be preoperative treatment. Such conservative therapy must be brief (11,5 hours), but always actively directed for correction of violations of metabolism and prophylaxis of possible
pulmonary and cardiovascular complications. It is necessary also to conduct evacuation of the gastric contents and other preparatory procedures.
Patient with reduced hernia must be hospitalized and observed during 12 days. If a abdominal pain is contained or is growing, the signs of peritonitis and intoxication appear, than performed urgent
laparotomy and necessary operation. If the symptoms of acute abdomen are not present, a patient examined and prepared for elective operation.
Operation at the incarcerated hernia is executed under the general anesthesia. A hernia sack is selected from surrounding tissue, cut it in the area of bottom and remove hernia water, defining its character and
sending to bacterial inoculation. Retaining the damaged organs, a strangulated ring is cut. It is necessary to remember, that at the incarcerated femoral hernia ring cut up and some medially, because a femoral vein
passes from a lateral side.
If a bowel is contents of hernia sack, we must estimate its viability. Remembering about possibility of the retrograde jamming, special attention must be paid to the state of strangulation furrow. About
viability of the bowels testify: 1) renewal of its normal color; 2) presence or renewal of peristalsis; 3) renewal of pulsation of vessels of mesentery and bowel. If there are the certain doubting, a bowel is dipped on
a holder in an abdominal cavity and in 1520 minutes it is examined repeatedly. If one of the resulted signs of viability is absent even, it is necessary to conduct the resection of bowel. The resection is executed,
receded from the strangulation furrow on a proximal loop 3040 cm and distal 1520 cm. Anastomosis between proximal and distal loops it is better to impose end-to-end. The plastic of hernia gate are
conducted depending on indications after one of the surgical methods.
When the necrosis elements of omentum or fatty pendants of colon are contents of hernia sack, they must be removed within the limits of healthy tissue.
There can be necrosis of wall of colon or urinary bladder at sliding hernia. In such cases it is needed to be limited to the minimum surgical procedure: to dip a necrosis area by sutures inside the bowel or use
it for forming of colostomy or epicystostomy. These are the best to conclude operation.
In similar situations at the incarcerated parietal hernia in most patients it is possible to be limited to peritonization of displaced area of wall of bowel. If after the peritonization there is the threat of
narrowing of bowel or necrosis goes outside of the strangulation furrow, it is needed to conduct the resection of bowel.
Because of insufficient blood floow of Meckel's diverticulum and, permanent threat of it necrosis, at patients with Littres hernia it resection must be performed.
At the phlegmon of hernia sack operation is begun with herniotomy. If the incarcerated organ is damaged by necrosis, and in a hernia sack present pus, than there is a necessity for surgeon to perform
laparotomy. After that incarcerated organ resected within the limits of healthy tissue (in the generally accepted limits 40 cm of proximal loop and 20 cm distal) and impose anastomosis. An abdominal cavity is
sewn up. Incarcerated loops of bowel, together with it blind ends which lacated in an abdominal cavity, removed through a hernia sack, a peritoneum is sutured, the hernia sack is drained, the plastic of hernia gate
are not performed. Skin is sewn up by widely spaced sutures.
video1
video
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1. The Safety of Mesh Repair for Primary Inguinal Hernias: Results of 3019 Operations from Five Diverse Surgical Sources; Shulman, AG, Amid, PK, Lichtenstein, IL; The American Surgeon; 1992; 58:255-7.
2. The Tension-Free Hernioplasty; Lichtenstein, IL, Shulman, AG, Amid, PK, Montllor, MM; Am J Surg; 1989; 157:188-193.
3. Inguinal Hernia Repair: Biomaterials and Sutures Repair; Gilbert, AI; Perspectives in General Surgery; 1991; 2:113-129.
4. The Mesh-Plug Hernioplasty; Robbins, AW, Rutkow, IM, Surgical Clinics of North America; 1993; 73:501-12.
5. Abdominal Wall Hernias; Wantz, GE, in Principles of Surgery; Schwartz et al.; 6th Edition; 1994; McGraw-Hill, Inc.; New York.
6. The Shouldice Repair for Inguinal Hernia; Glassow, F; in Hernia; Nyhus, LM & Condon, RE; Second Edition; 1978; J. B. Lippincott Co.; Philadelphia.
7. The Cause, Prevention, and Treatment of Recurrent Groin Hernia; Lichtenstein, IL, Shulman, AG, Amid, PK; Surgical Clinics of North America; 1993;73:529-44.
8. "Tension-free" inguinal herniorrhaphy: A preliminary report on the "mesh plug" technique; Rutkow, IM, Robbins, AW; Surgery; 1993; 114: 3-8.
9. Sutures Repair of Inguinal Hernia; Gilbert, AI; Am J Surg; 1992; 163: 331-5.
10. The "Plug" Repair of 1402 Recurrent Inguinal Hernias; 20 Year Experience; Shulman, AG, Amid, PK, Lichtenstein, IL; Arch Surg; 1990; 125:265-7.
11. Inguinal and femoral hernioplasty utilizing polypropylene patch and plug; Amid, PK, Shulman, AG, Lichtenstein, IL; Ann Ital Chir; 1993; 44: 119-25.
12. Improved Sutureless Technique--Advice to Experts; Gilbert, AI, Graham, MF; Problems in General Surgery; 1995; 12:117-9.
13. Technical and Scientific Objections to Laparoscopic Herniorrhaphy; Gilbert, AI, Graham, MF; Presented at 15th Anniversary Meeting of the Shouldice Hospital; June 16, 1995.
14. Laparoscopic mesh repair vs. open repair with and without mesh graft for inguinal hernia. Preliminary study; Johansson, B, et al.; Surgical Endoscopy; 1997; 11: 170 (Abstract).
15. Laparoscopic TEP versus open Lichtenstein hernia Repair, Randomized Trial; Merello, J; Surgical Endoscopy; 1997; 11: 545 (Abstract).
16. Moran Repair for Inguinal Hernias; Moran, RM, Brauns, J, Petrie, CR, Novak, BP, Johnsrud, JM,; Am Surg; 1997: 63: 430-3.
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various injuries and illnesses, i.e. acute pancreatitis. Paralytic ileus causes constipation
and bloating. On listening to the abdomen with a stethoscope, no bowel sounds are
heard because the bowel is inactive.
A temporary paralysis of a portion of the intestines occurs typically after an
abdominal surgery. Since the intestinal content of this portion is unable to move
forward, food or drink should be avoided until peristaltic sound is heard from
auscultation of the area where this portion lies.
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Myocardial infarction
Pneumonia
Trauma (eg, fractured ribs, fractured spine)
Biliary colic and renal colic
Head injury and neurosurgical procedures
Intra-abdominal inflammation and peritonitis
Retroperitoneal hematomas
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Perforation may occur in an ischemic segment (typically small bowel) or when marked
dilation occurs. The risk is high if the cecum is dilated to a diameter 13 cm.
Perforation of a tumor or a diverticulum may also occur at the obstruction site.
Pathomorphology
The morphological signs of dynamic intestinal obstruction are: small thickening
of wall (at considerable paresis is thinning), friability of tissue (the bowel breaks easily)
and presence of liquid maintenance and gases in cavity of bowel. At mechanical
obstruction it is always possible to expose the obstacle: strang, commissures, tumours,
jammings of hernia, cicatricial strictures, wrong entered drainages, tampons and others
like that. In place of compression strangulation is exposed. The bowel loop higher
strangulation is extended, and distally collapsed. In case of released invagination on
small distance two strangulation furrows are observed, and distally from the second
ring cylinder expansion of bowel lumen is observed.
Classification
(by D.P.Chuhrienko, 1958)
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Clinical management
Main symptoms:
moderate, diffuse abdominal discomfort
constipation
abdominal distension
nausea/vomiting, especially after meals
lack of bowel movement and/or flatulence
excessive belching
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In its clinical picture on the first place there are the symptoms of violation of
passage on the intestine (protracted intermittent pain, flatulence), instead of symptoms
of bowel destruction and peritonitis.
For high, especially strangulated, intestinal obstruction progressive growth of
clinical signs of disease and violation of secretory function of intestine is inherent.
Thus the volume of circulatory blood diminishes, the level of haematocritis rises and
leukocytosis grows. There are also deep violations of homeostasis (hypoproteinemia,
hypokalemia, hyponatremia, hypoxia and others like that). In patients with low
intestinal obstruction above-named signs are less expressed, and their growth is related
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During the examination the abdomen keeps symmetry, abdominal wall is soft,
the increased peristalsis is heard from the first minutes during 12 hours (hypoxic
stimulation of peristalsis), which later goes out gradually (grave quiet). According to
the phenomena of intoxication peritonitis grow quickly. At the beginning of disease the
delay of gases and emptying is observed, later there is diarrhea with the admixtures of
blood in an excrement. When the last is heavy to set macroscopically, it is needed to
explore scourage of intestine.
Small-bowel obstruction (SBO). The most common cause of small-bowel
obstruction (SBO) is postsurgical adhesions. Postoperative adhesions can be the cause
of acute obstruction within 4 weeks of surgery or of chronic obstruction decades later.
The incidence of SBO parallels the increasing number of laparotomies performed in
developing countries. Another commonly identified cause of SBO is an incarcerated
groin hernia. Other etiologies include malignant tumor (20%), hernia (10%),
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inflammatory bowel disease (5%), volvulus (3%), and miscellaneous causes (2%). The
causes of SBO in pediatric patients include congenital atresia, pyloric stenosis, and
intussusception.
History. Obstruction can be characterized as either partial or complete versus
simple or strangulated. No accurate clinical picture exists to detect early strangulation
of obstruction.
Abdominal pain, often described as crampy and intermittent, is more prevalent
in simple obstruction. Often, the presentation may provide clues to the approximate
location and nature of the obstruction. Usually, pain that occurs for a shorter duration
of time and is colicky and accompanied by bilious vomiting may be more proximal.
Pain that lasts as long as several days, is progressive in nature, and is accompanied by
abdominal distention may be typical of a more distal obstruction.
Changes in the character of the pain may indicate the development of a more
serious complication (ie, constant pain of a strangulated or ischemic bowel).
Patients also report the following:
Nausea
Physical Examination
Abdominal distention is present. The duodenal or proximal small bowel has less
distention when obstructed than the distal bowel has when obstructed. Hyperactive
bowel sounds occur early as GI contents attempt to overcome the obstruction;
hypoactive bowel sounds occur late.
Exclude incarcerated hernias of the groin, femoral triangle, and obturator
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foramina. Proper genitourinary and pelvic examinations are essential. Look for the
following during rectal examination:
Gross or occult blood, which suggests late strangulation or malignancy
Masses, which suggest obturator hernia
Check for symptoms commonly believed to be more diagnostic of intestinal
ischemia, including the following:
Fever (temperature >100F)
Tachycardia (>100 beats/min)
Peritoneal signs
No reliable way exists to differentiate simple from early strangulated obstruction
on physical examination. Serial abdominal examinations are important and may detect
changes early.
Complications of SBO include the following:
Sepsis
Intra-abdominal abscess
Wound dehiscence
Aspiration
Short-bowel syndrome (as a result of multiple surgeries)
Death (secondary to delayed treatment)
Large-bowel obstruction (LBO) is an emergency condition that requires early
identification and intervention. Approximately 60% of mechanical large-bowel
obstructions (LBOs) are caused by malignancies, 20% are caused by diverticular
disease, and 5% are the result of colonic volvulus. The most common causes of adult
large-bowel obstruction are as follows:
Neoplasm (benign or malignant)
Stricture (diverticular or ischemic)
Volvulus (eg, colonic, sigmoid, cecal)
Incarcerated hernia
Intussusception, usually with an identifiable anatomic abnormality in adults
but not in children
Impaction or obstipation
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Gallstone ileus
Volvuli
A colonic volvulus results when the colon twists on its mesentery, which impairs
the venous drainage and arterial inflow. Symptoms of this condition are usually abrupt.
A sigmoid volvulus typically occurs in older, debilitated individuals with a history
of chronic constipation, or those living in an institutionalized setting.
A cecal volvulus is caused by a congenital defect in the peritoneum, which
results in inadequate fixation of the cecum, and increased cecal mobility. Patients
usually present with this disorder in the sixth decade of life.
Intussusception
Intussusception is primarily a pediatric disease; however, it is estimated that
between 5% and 16% of all intussusceptions in the Western world occur in adults, of
which approximately two thirds of adult intussusception cases are caused by tumors.
Two main types of intussusception affect the large bowel: enterocolic and colocolic.
Enterocolic intussusceptions involve both the small bowel and the large bowel.
These are composed of either ileocolic intussusceptions or ileocecal intussusceptions,
depending on where the lead point is located.
Colocolic intussusceptions involve only the colon. They are classified as either
colocolic or sigmoidorectal intussusceptions.
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severe illness. In a retrospective review of more than 1400 cases of acute colonic
pseudo-obstruction, the most common predisposing conditions were operative and
nonoperative trauma (11%), infections (10%), and cardiac disease (10-18%).
History. Obtain the patient's history of bowel movements, flatus, obstipation (ie,
no gas or bowel movement), and symptoms. Attempt to distinguish complete bowel
obstruction from partial obstruction, which is associated with passage of some gas or
stool, and from ileus. Also inquire about the patient's current and past history in an
attempt to determine the most likely cause.
Major complaints in patients with large-bowel obstruction (LBO) include
abdominal distention, nausea, vomiting, and crampy abdominal pain. An abrupt onset
of symptoms makes an acute obstructive event (eg, cecal or sigmoid volvulus) a more
likely diagnosis. A history of chronic constipation, long-term cathartic use, and
straining at stools implies diverticulitis or carcinoma.
Changes in the patient's caliber of stools (eg, passage of melanotic bloody stools)
strongly suggest carcinoma. When associated with weight loss, the likelihood of
neoplastic obstruction increases.
A history of recurrent left lower quadrant abdominal pain over several years is
more consistent with diverticulitis, a diverticular stricture, or similar problems.
A history of aortic surgery suggests the possibility of an ischemic stricture.
Diagnostic program
1. Anamnesis and physical methods of examination (auscultation of abdomen,
percussion and others like that).
2. General analysis of blood, urines and biochemical blood test.
3. Survey sciagraphy of organs of abdominal cavity.
4. Coagulogramm.
5. Electrocardiography.
6. Irrigography.
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early obstructions. Essential laboratory tests are needed; these include the following:
Serum chemistries - Results are usually normal or mildly elevated
Blood urea nitrogen (BUN) level - If the BUN level is increased, this may
indicate decreased volume state (eg, dehydration)
Creatinine level - Creatinine level elevations may indicate dehydration
Complete blood count (CBC) - The white blood cell (WBC) count may be
elevated with a left shift in simple or strangulated obstructions; increased hematocrit is
an indicator of volume state (ie, dehydration)
Lactate dehydrogenase tests
Urinalysis
Type and crossmatch - The patient may require surgical intervention
Laboratory tests to exclude biliary or hepatic disease are also needed; they
include the following:
Phosphate level
Creatine kinase level
Liver panels
Studies have been performed to evaluate the use of water-soluble oral contrast as
a tool in the management of SBO and as a predictive tool for nonoperative resolution
of adhesive SBO. It does not cause resolution of the SBO, but it may reduce the
hospital stay in patients not requiring surgery.
Plain Radiography
Obtain plain radiographs first for patients in whom small-bowel obstruction
(SBO) is suspected. At least 2 views, supine or flat and upright, are required. Plain
radiographs are diagnostically more accurate in cases of simple obstruction. However,
diagnostic failure rates of as much as 30% have been reported.
In one small study, the sensitivity of plain radiography was reported to be 75%,
and specificity was reported to be 53%; similar findings were reported in a second
study. In another study, plain films were more accurate in the detection of acute SBO
and the accuracy was higher if interpreted by more-experienced radiologists.
Plain radiography is of little assistance in differentiating strangulation from
simple obstruction. Some have used abdominal radiography to distinguish between
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CT scanning
Computed tomography (CT) scanning is the study of choice if the patient has
fever, tachycardia, localized abdominal pain, and/or leukocytosis.
CT scanning is useful in making an early diagnosis of strangulated obstruction
and in delineating the myriad other causes of acute abdominal pain, particularly when
clinical and radiographic findings are inconclusive. It also has proved useful in
distinguishing the etiologies of small-bowel obstruction (SBO), that is, in distinguishing
extrinsic causes (such as adhesions and hernia) from intrinsic causes (such as
neoplasms and Crohn disease). In addition, CT scanning differentiates the above from
intraluminal causes, such as bezoars. The modality may be less useful in the evaluation
of small bowel ischemia associated with obstruction.
CT scanning is capable of revealing abscess, inflammatory process, extraluminal
pathology resulting in obstruction, and mesenteric ischemia and enables the clinician to
distinguish between ileus and mechanical small bowel obstruction in postoperative
patients.
The modality does not require oral contrast for the diagnosis of SBO, because
the retained intraluminal fluid serves as a natural contrast agent.
Obstruction is present if the small-bowel loop is greater than 2.5 cm in diameter
dilated proximal to a distinct transition zone of collapsed bowel less than 1 cm in
diameter. A smooth beak indicates simple obstruction without vascular compromise; a
serrated beak may indicate strangulation. Bowel wall thickening, portal venous gas, or
pneumatosis indicates early strangulation.
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Plain Radiography
Obtain an upright chest radiograph to determine whether free air is present,
which would suggest perforation of a hollow viscus and ileus rather than organic
obstruction, as well as flat and upright abdominal radiographs, which may demonstrate
dilatation of the small and/or large bowel and air-fluid levels.
Chest radiographs will demonstrate free air if perforation has occurred (see the
first image below); abdominal radiographs may be diagnostic of sigmoid or cecal
volvulus (ie, kidney bean appearance on the radiograph) (see the second and third
images below, respectively). Intramural air is an ominous sign that suggests colonic
ischemia. The absence of free air does not exclude perforation (this finding may be
absent in half of all perforations).
Tracing colonic air around the colon, into the left gutter, and down into the
rectum or demonstrating an abrupt cut-off in colonic air suggests the anatomic location
of the obstruction.
A dilated colon without air in the rectum is more consistent with obstruction.
The presence of air in the rectum is consistent with obstipation, ileus, or partial
obstruction. However, this finding can be misleading, particularly if the patient has
undergone rectal examinations or enemas.
Radiocontrast Radiography
Contrast studies include an enema with water-soluble contrast (ie, Gastrografin)
(see the following images) or computed tomography (CT) scanning with intravenous
(IV) and oral (PO) or rectal (PR) contrast. Contrast studies that reveal a column of
contrast ending in a "bird's beak" are suggestive of colonic volvulus.
Indications for imaging with contrast
Radiopaque contrast material may be administered and imaging of the colon
may be performed under the following circumstances:
Perform it if the diagnosis of large bowel obstruction is suspected but not
proven
If differentiation between obstipation and obstruction is required
If localization is required for surgical intervention
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Flexible Endoscopy
Flexible endoscopy preceded by rectal enema may be useful in evaluating
left-sided colonic obstruction, including the anatomic location and pathology of the
lesion. Because the cecum is not reached in such cases, the endoscopist must be alert
to the possibility of incorrectly identifying anatomic landmarks and the location of the
obstruction.
An abdominal radiograph with the tip of the endoscope at the site of the
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Differential diagnostics
Abortion, Threatened
Alcoholic Ketoacidosis
Cholangitis
Cholecystitis and Biliary Colic in Emergency Medicine
Cholelithiasis
Constipation
Diverticular Disease
Dysmenorrhea
Endometriosis
Inflammatory Bowel Disease
Mesenteric Ischemia
Intestinal obstruction must be differentiated with the acute diseases of organs of
abdominal cavity.
The perforation of gastroduodenal ulcer, as well as intestinal obstruction, passes
acutely with inherent to it by sudden intensive pain and tension of muscles of
abdomen. However, in patients with this pathology, unlike intestinal obstruction, the
abdomen is not exaggerated, and pulled in with wooden belly tension of muscles of
front abdominal wall. There is also characteristic ulcerous anamnesis. Roentgenologic
and by percussion pneumoperitoneum is observed. Certain difficulties in conducting of
differential diagnostics of intestinal obstruction can arise at atipical passing and in case
of the covered perforations.
Acute pancreatitis almost always passes with the phenomena of dynamic
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intestinal obstruction and symptoms of intoxication and repeated vomiting, with rapid
growth. During the examination in such patients, unlike intestinal obstruction, rigidity
of abdominal wall and painfulness is observed in the projections of pancreas and
positive Korte's symptom and Mayo-Robson's. The examination of diastase of urine
and amylase of blood have important value in establishment of diagnosis.
Acute cholecystitis. Unlike intestinal obstruction, patients with this pathology
complain for pain in right hypochondrium, that irradiate in the right shoulder-blade,
shoulder and right subclavian area. Difficulties can arise, when the symptoms of
dynamic intestinal obstruction appear on the basis of peritonitis.
The clinic of kidney colic in the signs and character of passing are similar to
intestinal obstruction, however, attacks of pain in the lumbar area with characteristic
irradiation in genital parts, the thigh and dysuric disorders help to set the correct
diagnosis. Certain difficulties in conducting of differential diagnostics also can arise in
difficult patients, at frequent vomiting which sometimes can be observed in patients
with kidney colic.
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Cleansing enemas
Perform cleansing enemas if obstipation is suspected rather than true large-bowel
obstruction. These can also be performed to prepare the distal colon for endoscopic
evaluation.
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absent, which would imply dead bowel or perforation. This procedure is also indicated
when evidence of mucosal ischemia is not present upon endoscopy. An experienced
person should perform the procedure.
Endoscopic reduction is not indicated for the less common cecal or transverse colon
volvulus.
A rigid sigmoidoscope may be used if a flexible instrument is not available. The
endoscopist must have sufficient experience with this technique.
Reduction of a volvulus does not imply cure. The sigmoid usually revolvulizes if
definitive treatment is not carried out.
These patients are generally admitted to the hospital, subjected to mechanical bowel
preparation, and managed surgically by sigmoid resection, unless contraindications are
present.
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Dietary considerations
Patients with complete large-bowel obstruction should receive nothing by mouth
(NPO). Patients with a partial obstruction may tolerate minimal clear liquids, oral
medications, and a gradual bowel preparation.
It is directed on warning of the complications related to pain shock, correction of
homeostasis and, simultaneously, is the attempt of liquidation of intestinal obstruction by
unoperative methods.
1. The measures directed for the fight against abdominal pain shock include
conducting of neuroleptanalgesia, procaine paranephric block and introduction of
spasmolytics. Patients with the expressed pain syndrome and spastic intestinal obstruction
positive effect can be attained by epidural anaesthesia also.
2. Liquidation of hypovolemia with correction of electrolyte, carbohydrate and
albuminous exchanges is achieved by introduction of salt blood substitutes, 510 %
solution of glucose, gelatinol, albumen and plasma of blood. There are a few methods
suitable for use in the urgent surgery of calculation of amount of liquid necessary for
liquidation of hypovolemia. Most simple and accessible is a calculation by the values of
hematocrit. If to consider 40 % for the high bound of hematocrit norm, on each 5 %
above this size it is needed to pour 1000 ml of liquids.
3. Correction of hemodynamic indexes, microcirculation and disintoxication therapy
is achieved by intravenous infusion of Reopolyhlukine and Neohemodes.
4. Decompression of intestine truct is achieved by conducting of nasogastric
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drainage and washing of stomach, and also conducting of siphon enema. It is needed to
underline that technically the correct conducting of siphon enema has the important value
for the attempt of liquidation of intestinal obstruction by conservative facilities, therefore
this manipulation must be conducted in presence of a doctor. For such enema the special
device is used with the rectal tip, by a PVC pipe by a diameter of 1,52,0 cm and
watering-can of very thin material. A liquid into the colon is brought to appearance of the
pain feeling, then drop the watering-can below the level of patient who lies. The passage
of gases and excrement is looked after. As a rule, this manipulation is to repeat repeatedly
with the use of plenty of warm water (to 1520 and more litres).
Liquidating of the intestinal obstruction by such conservative facilities is succeeded
in 5060 % patients with mechanical intestinal
obstruction.
Surgical Intervention
Surgical intervention is directed at relieving the obstruction.
A diverting transverse loop colostomy may be the least invasive procedure for a very
ill patient with a left colonic obstruction. It permits relief of the obstruction and further
resuscitation without compromising chances for a subsequent resection. A case report
described the use of hand-assisted laparoscopy via the loop colostomy site for subsequent
resection of the obstructing lesion.
A sigmoid colostomy without resection may be used in patients with a rectal
obstruction that cannot be managed without a combined abdominoperineal approach.
Cecostomy should not be performed, because the diversion is inadequate.
In younger patients without substantial comorbidity, some surgeons would consider
primary anastomosis, rather than ileostomy, in the right colon, assuming no intraoperative
hypotension, blood loss, or other complications are present.
If resection and proximal colostomy or ileostomy are performed, a mucous fistula is
generally extracted from the distal end, unless the obstruction is rectosigmoid, in which
case the distal end may be oversewn or stapled and left to drain transanally.
If the cause of the obstruction can be relieved nonsurgically, through procedures
such as decompressing a volvulus, or if the obstruction is only partial, deferring surgery
temporarily and supporting the patient while the large bowel is cleansed so that primary
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Carcinoma
In most patients, the obstructing lesion is resected. Because the colon has not been
cleansed, anastomosis is often risky. After resection, most surgeons perform a proximal
colostomy if the obstruction is on the left side or ileostomy if it is on the right side.
In patients with substantial comorbidity and surgical risk or in the presence of an
unresectable tumor, a diverting proximal colostomy or ileostomy may be performed
without resection.
Left vs right colon carcinoma. Surgical treatment of left colon carcinoma includes
resection without primary anastomosis or resection with primary anastomosis and
intraoperative lavage. Endoscopically placed expandable metal stents can be used to
relieve the large-bowel obstruction, thus allowing for a primary colorectal anastomosis.
Right colonic obstructions are treated with a right colectomy and a primary
anastomosis between the ileum and the transverse colon. Patients with high-risk features
for surgery (advanced age, complete obstruction, or severe comorbidities) may benefit
from stent placement until patient can be optimized for a surgical procedure. Palliative
colorectal stents are an option in patients who are poor surgical candidates or have
advanced cancer.
Diverticulitis
Patients with persistent obstruction secondary to diverticular disease despite
appropriate medical management are treated surgically. Surgical resection follows the
same principles as the treatment of carcinomas. Elective colonic resection is offered to
patients with recurrent disease.
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Fig.9.Intestinal obstruction.
Overblowning of small intestine
The revision at small intestine obstruction begins from the Treitz' ligament to
iliocecal corner. At large intestine obstruction the hepatic, splenic and rectosigmoid parts
are observed intently. Absence of pathological processes after revision needs the
examination of places of cavity and jamming of internal hernia: internal inguinal and
femoral rings, obturator openings, pockets of the Treitz' ligament, Winslow's opening,
diaphragm and periesophageal opening.
2. Liquidation of reasons of obstruction (scission of connection, that squeezes a
bowel, violence of volvulus and node formation of loops, desinvagination, deleting of
obturative tumours and others like that).
It is needed to mark that the unique method of liquidation of acute intestinal
obstruction does not exist. At the lack of viability of bowel the resection of nonviable
area is executed with 3040 cm of afferent and 1520 cm of efferent part with
imposition of side-to-side(Fig. 10; Fig. 11) anastomosis or end-to-end(Fig.12).
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ABC
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Today the most wide clinical application has intubation of intestine extracted by the
nasogastric method with the use of other thick probe as explorer of the first (by L.J.
Kovalchuk, 1981)(Fig.15). Such method not only simplifies procedure of intubation but
also facilitates penetration through the piloric sphincter and duodenojejunal bend, and
also warns passing of intestinal maintenance in a mouth cavity and trachea. Thus probe is
tried to be conducted in the small intestine as possible farther and deleted the next day
after appearance of peristalsis and passage of gases, however not later than on 7th days,
because more protracted sign of probe carries the real threat of formation of bedsores in
the wall of bowel.
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References
1. Livingston EH, Passaro EP Jr. Postoperative ileus. Dig Dis Sci. Jan
1990;35(1):121-32.
2. Shibata Y, Toyoda S, Nimura Y, Miyati M. Patterns of intestinal motility
recovery during the early stage following abdominal surgery: clinical and manometric
study. World J Surg. Oct 1997;21(8):806-9; discussion 809-10.
3. Holte K, Kehlet H. Postoperative ileus: a preventable event. Br J Surg. Nov
2000;87(11):1480-93.
4. Vasquez W, Hernandez AV, Garcia-Sabrido JL. Is gum chewing useful for
ileus after elective colorectal surgery? A systematic review and meta-analysis of
randomized clinical trials. J Gastrointest Surg. Apr 2009;13(4):649-56.
5. Resnick J, Greenwald DA, Brandt LJ. Delayed gastric emptying and
postoperative ileus after nongastric abdominal surgery: part I. Am J Gastroenterol. May
1997;92(5):751-62.
6. Resnick J, Greenwald DA, Brandt LJ. Delayed gastric emptying and
postoperative ileus after nongastric abdominal surgery: part II. Am J Gastroenterol. Jun
1997;92(6):934-40.
7. Kalff JC, Schraut WH, Simmons RL, Bauer AJ. Surgical manipulation of the
gut elicits an intestinal muscularis inflammatory response resulting in postsurgical ileus.
Ann Surg. Nov 1998;228(5):652-63.
8. Boeckxstaens GE, de Jonge WJ. Neuroimmune mechanisms in post-operative
ileus. Gut. Sept 2009;58(9):1300-11.
9. Espat NJ, Cheng G, Kelley MC, Vogel SB, Sninsky CA, Hocking MP.
Vasoactive intestinal peptide and substance P receptor antagonists improve postoperative
ileus. J Surg Res. Jun 1995;58(6):719-23.
10. Kalff JC, Schraut WH, Billiar TR, Simmons RL, Bauer AJ. Role of inducible
nitric oxide synthase in postoperative intestinal smooth muscle dysfunction in rodents.
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2007;30(3):167-72.
34. Traut U, Brgger L, Kunz R, Pauli-Magnus C, Haug K, Bucher HC, et al.
Systemic prokinetic pharmacologic treatment for postoperative adynamic ileus following
abdominal surgery in adults. Cochrane Database Syst Rev. Jan 23 2008;CD004930.
35. Wattchow DA, De Fontgalland D, Bampton PA, et al. Clinical trial: the impact
of cyclooxygenase inhibitors on gastrointestinal recovery after major surgery - a
randomized double blind controlled trial of celecoxib or diclofenac vs. placebo. Aliment
Pharmacol Ther. Nov 15 2009;30(10):987-98.
36. Yeh YC, Klinger EV, Reddy P. Pharmacologic options to prevent postoperative
ileus. Ann Pharmacother. Sep 2009;43(9):1474-85.
37. Abd-El-Maeboud KH, Ibrahim MI, Shalaby DA, Fikry MF. Gum chewing
stimulates early return of bowel motility after caesarean section. BJOG. Sep
2009;116(10):1334-9.
38. Iyer S, Saunders WB, Stemkowski S. Economic burden of postoperative ileus
associated with colectomy in the United States. J Manag Care Pharm. Jul-Aug
2009;15(6):485-94.
39. Bauer AJ, Boeckxstaens GE. Mechanisms of postoperative ileus.
Neurogastroenterol Motil. Oct 2004;16 Suppl 2:54-60.
40. Behm B, Stollman N. Postoperative ileus: etiologies and interventions. Clin
Gastroenterol Hepatol. Mar 2003;1(2):71-80.
41. Carter S. The surgical team and outcomes management: focus on postoperative
ileus. J Perianesth Nurs. Apr 2006;21(2A Suppl):S2-6.
42. Correia MI, da Silva RG. The impact of early nutrition on metabolic response
and postoperative ileus. Curr Opin Clin Nutr Metab Care. Sep 2004;7(5):577-83.
43. Delaney CP. Clinical perspective on postoperative ileus and the effect of
opiates. Neurogastroenterol Motil. Oct 2004;16 Suppl 2:61-6.
44. Delaney CP, Senagore AJ, Viscusi ER, Wolff BG, Fort J, Du W, et al.
Postoperative upper and lower gastrointestinal recovery and gastrointestinal morbidity in
patients undergoing bowel resection: pooled analysis of placebo data from 3 randomized
controlled trials. Am J Surg. Mar 2006;191(3):315-9.
45. Houwen RH, van der Doef HP, Sermet I, et al. Defining DIOS and
constipation in cystic fibrosis with a multicentre study on the incidence, characteristics,
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Pic. The anatomic relationships in the upper abdomen. The stomach is bounded on its
left by the spleen, posteriorly (dorsally) by the pancreas, inferiorly (caudally) by the
colon, and to its right by the duodenum along the liver's edge.
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Pic. Anatomically, the stomach is divided into several segments. Functionally, the
cardia and the antrum differ from the body in that they contain no acid secretory
properties. The incisura is an area on the lesser curvature, which marks the antrum-body
junction and is often easily seen on barium upper intestinal series.
video
GASTRIC ULCER
Video
The gastric ulcer is the chronic disease with polycyclic passing. The main typical
of peptic ulcer is the presence of ulcerous defect in a mucous tunic. One of basic places
belongs among the gastroenterology diseases to this pathology. Such phenomenon
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explained by not only considerable distribution of disease but also those dangerous
complications which always accompany gastric ulcers.
Frequency of morbidity on the peptic ulcer among the adult population is about 4
%. More frequent age in patients with gastric ulcers is 5060 years.
To development mechanism of disease is still not enough studied. From a plenty of
different theories in relation to genesis of peptic ulcer no one able to explain the disease.
So, each of such factors as neurogenic, mechanical, inflammatory, vascular is present in
the mechanism of development of peptic ulcer. Consider for today, that disturbance
between the factors of aggression and defense of mucous tunic arose peptic ulcer. To the
first factors belong: hydrochloric acid, pepsin, reverse diffusion of ions of hydrogen,
products of lipid hyperoxidizing. To the second: mucus and alkaline components of
gastric juice, property of epithelium of mucous tunic to permanent renewal, local blood
flow of mucous tunic and submucous membrane.
In the terminal stage of mechanism of origin of gastric ulcers important role has
the peptic factor and disturbance of trophism of gastric wall as a result of local ischemia.
It confirmed by decreasing of blood flow in the wall of stomach at patients with ulcers on
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3035 % compared to the norm. It is proved, that a local and functional ischemia more
frequent arises up on small curvature of stomach in the areas of ectopy of the antral
mucous tunic in acid-forming. Exactly there ulcers appear.
Important part in ulcerogenesis is acted by duodenogastric reflux and gastritis.
Also, gastrostasis can provoke hypergastrinaemia and hypersecretion and formed gastric
ulcers.
Numeral scientific developments of the last years testify to the important
infectious factor in the mechanism of origin of peptic ulcer conditioned, mainly, by
helicobacter pylori.
Pathomorphology
Such stages of disease are distinguished: erosion, acute and chronic ulcers.
Erosions, mainly, are plural. Their bottom as a result of formation of muriatic
haematine is black, edges infiltrated by leucocytes. A defect usually does not
penetrate outside muscular tissue of the mucous tunic. If necrosis gets to more deep
layers of wall of stomach, a acute ulcer develops. It has a funnel-shaped form. Bottom is
also black, edges is swelled. Chronic ulcers are mainly single, sometimes arrive to the
serous layer. A bottom is smooth, sometimes hilly, edges is like elevation, dense.
Classification
For today the most known classification of gastric ulcers by Johnson (1965). There
are three types of gastric ulcers are distinguished: I ulcers of small curvature (for 3 cm
higher from a goalkeeper); II double localization of ulcers simultaneously in a stomach
and duodenum; III ulcers of goalkeeper part of stomach (not farther as 3 cm from a
goalkeeper). In the area of small curvature of body of stomach is localized 70,9 % ulcers,
on a back wall, nearer to small curvature 4,8 %, in the area of cardial part 12,9 %, in
a goalkeeper part 11,4 %. The ulcers of large curvature of stomach are casuistry and
meet infrequently.
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Clinical management
The complaints of patients with the gastric ulcer always give valuable information
about the disease. The detailed analysis of their anamnesis allows to pay attention to the
possible reasons of origin of ulcer, time of the first complaints, to the changes of
symptoms.
Pain. A pain symptom in the peptic ulcer disease is very important. There are
typical passing for this disease: hunger pain food intake facilitation again hunger
pain food intake facilitation (so during all days). Night pain for the gastric ulcer is
not typical. The such patients rarely wake up in order to take a food. For diagnostics of
ulcer localization it is important to know the time of appearance of pain. Between
acceptance of food and appearance of pain it is the shorter, than the higher placed gastric
ulcer. Thus, at patients with a cardial ulcer pain arises at once after the food intake, with
the ulcers of small curvature in 5060 minutes, at pyloric localization
approximately in two hours. However this feature it is enough relative and some patients
in general do not mark dependence between food intake and pain. In other patients the
pain attack is accompanied by the salivation.
A epigastric region near the xiphoid process is typical localization of pain. The
irradiation of pain is not usual for gastric ulcers. Irradiation occur in patients with
penetration and depended from organ, in which an ulcer penetrates.
At the examination of ulcerous patient it is expedient to determine the special pain
points: Boas (pain at pressure on the left of the II pectoral vertebrae), Mendel (pain
at percussion on the left to epigastric region).
Vomiting, the sign of disturbance of motility function of stomach, is the second
typical symptom of gastric ulcer. More frequent gastrostasis arises as a result of failure of
stomach muscular, it atony which can be effect of organ ischemia. Vomiting could arises
both on empty stomach and after food intake.
Heartburn is one of early symptoms of gastric ulcer, however at the prolonged
passing of disease it can be hidden or quite disappear. Often it precedes of pain arising
(initial heartburn) or accompanies a pain symptom. Mostly heartburn arises after the food
intake, but can appear independently. it is observed not only at hypersecretion of the
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hydrochloric acid, but at normal secretion, even reduced acidity of gastric juice.
The belching at gastric ulcers is examined rarely, more frequent in patients with
cardial and subcardial ulcers. It is necessary to bind to disturbance of function of cardial
valve.
The general condition of patients with the uncomplicated gastric ulcer usually
satisfactory, and in a period between the attacks even good. However for most patients
lost of the body weight and pallor are typical. In a epigastric region hyperpigmental spots
are examined after the prolonged application of hot-water bottle. At palpation of stomach
in this area sometimes appears local painful. It is needed also to check up noise of
splash, the presence of which can be the sign of possible gastrostasis.
At the examination of mouth cavity a tongue has whiter-yellow incrustation. In
patients with penetration ulcers and disturbances evacuations from a stomach examined
dryness of tongue.
Stomach, as a rule, regular rounded shape, however during the pain attack is pulled
in. There is antiperistalsis arises during the pylorostenosis.
The increased secretion of hydrochloric acid in patients with gastric ulcers
observed rarely and, mainly, at prepyloric ulcer localizations. Mostly secretion is normal,
and in some patients is even reduced.
X-Ray examination. The direct signs of ulcer at X-Ray examinations are: symptom
of Haudek's niche (Pic. 3.2.1), ulcerous billow and convergence of folds of mucous
tunic. Indirect signs: symptom of forefinger (circular spasm of muscles), segmental
hyperperistalsis, pylorospasm, delay of evacuation from a stomach, duodenogastric
reflux, disturbance of function of cardial part (gastroesophageal reflux).
Gastroscopy can give important information about localization, sizes, kind of
ulcer, dynamics of its cicatrization, and also allow to perform biopsy with subsequent
histological examination.
The gastric ulcer passing can be acute and chronic. Acute ulcers arise as answer for
the stress situations, related to the nervous overstrain, trauma, loss of blood, some
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infectious and somatic diseases. By a diameter ulcers has from a few millimeters to
centimeter, a round or oval form with even edges. Thus in most cases clinically observed
clear ulcerous clinical signs. If complications is absent (bleeding, perforation) such
ulcers treated and mostly heal over.
G.J. Burchynskyy (1965) such variants of clinical flow distinguished:
1. Chronic ulcer which does not heal over long time.
2. Chronic ulcer which after the conservative therapy heals over relatively easily,
however inclined to the relapses after the periods of remission of a different duration.
3. Ulcers, which localization are had migrant character. Observed in people with
acute ulcerous process of stomach.
4. Special form of gastric ulcer passing after the already carried disease. Passed
with the expressed pain syndrome. Characterized by the presence in place of ulcerous
defect of scars or deformations and absence of symptom of niche.
There are such complications can develop in patients with gastric ulcer:
penetration, stenosis, perforation, bleeding and malignization.
Diagnosis program
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Differential diagnostics
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syndrome, that arises after the food intake. In such patients it is possible to observe
nausea and vomiting by gastric content, heartburn and belch. However, unlike an gastric
ulcer, for gastritis typical symptom of quick satiation by a food. Unsteady emptying,
diarrhea also more inherent to gastritises. At gastric ulcer more frequent the delays are
observed, constipation for 45 days.
The cancer of stomach, it is comparative with an gastric ulcer, has considerably
more short anamnesis. The most typical clinical signs of this pathology are: absence of
appetite, weight loss, rapid fatigability, depression, unsociability, apathy. In such patients
X-Ray examination expose the defect of filling, related to exophytic tumor and
deformation of walls of organ. A final diagnosis is set after the results of multiposition
biopsy of shady areas of mucous tunic of stomach.
Differential diagnostics also needs to be conducted with the so called
precancerous states: gastritis with the achlorhydria; chronic, continuously recurrence
ulcers, poliposis and Addison-Biermer anemia.
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Treatment of patient with a gastric ulcer must continues not less than 68 weeks.
Surgical treatment must performed in cases:
) at the relapse of ulcer after the course of conservative therapy;
) in the cases when the relapses arise during supporting antiulcer therapy;
) when an ulcer does not heal over during 1,52 months of intensive treatment,
especially in families with ulcerous anamnesis.
) at the relapse of ulcer in patients with complications (perforation or bleeding);
) at suspicion on malignization ulcers, in case of negative cytological analysis.
The choice of method of surgical treatment of gastric ulcer depended from
localization and sizes of ulcer, presence of gastro- and duodenostasis, accompanying
gastritis, complications of peptic ulcer (penetration, stenosis, perforation, bleeding,
malignization), age of patient, general condition and accompanying diseases. In patients
with cardial localization of ulcer the operation of choice is the proximal resection of
stomach, which, from one side, allows to remove an ulcer, and from other to save
considerable part of organ, providing it functional ability (Pic. 3.2.2). In case with large
cardial ulcers, when the vagus nerves pulled in the inflammatory infiltrate and it is
impossible to save integrity even one of them, operation needs to be complemented by
pyloroplasty. It will give possibility to warn pylorospasm and gastrostasis, which in an
early postoperative period can be the reason of anastomosis insufficiency and other
complications.
At the choice of method of surgical treatment of gastric ulcers with subcardial
localization on small curvature without duodenostasis it is better to apply the methods of
stomach resection with saving of passage through a duodenum.
For this purpose we are developed the method of segmental resection of stomach
with addition selective proximal vagotomy. The redistribution of gastric blood flow
between the functional parts of stomach as reply to medicinal vagotomy (intravenous
introduction 1,0 ml 0,1 % solution of atropine of sulfate) is studied. Hyperemia of
acid-forming part of stomach comes after introduction of preparation. The functional
scopes of stomach parts are determined. The border between acid-forming and antral
parts are the most frequent localization of gastric ulcers.
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At the border of gastric resection near pyloric sphincter can be spasm and
gastrostasis in a postoperative period . Avoiding such complication is possible, if this
border of gastric resection passes no more than 1,5 cm from a pyloric sphincter (M.M.
Risaev, 1986). So, at a resection, that passes higher than 2,0 cm from a pylorus, integrity
of both loops is kept.
Patients with antral ulcers without the duodenostasis performed the gastric
resection by Billroth I (Pic. 3.2.6), and on presence of duodenostasis Billroth II.
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large prepyloric ulcers with penetration without duodenostasis is better to perform the
gastric resection by Billroth I and on presence of duodenostasis by Billroth II.
By contra-indication to operations with saving of food passing through the
duodenum are also decompensated pylorostenosis , functional gastrostasis and
duodenostasis. In such patients it is better to perform gastric resection by Billroth II.
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DUODENAL ULCER
There are some etiologic factors of the duodenal ulcer: Helicobacter pylori,
emotion tension and neuropsychic stress overstrain, heredity and genetic inclination,
presence of chronic gastroduodenitis, disturbance of diet and harmful habits (alcohol,
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Pathomorphology
Classification
(by A.L.Hrebenev, A.O.Sheptulin, 1989)
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Clinical management
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Pain in the epigastric region is the most expressed symptom of duodenal ulcer,
often with displacement to the right in the projection area of bulb of duodenum and
gall-bladder. Also for this pathology is typical the pain, that arises in 1,52 hours after
food intake, hungry and nightly pain. As a rule, it is acute, sometimes unendurable, and
is halted only after the use of food or water. Such patients complains for the seasonal
exacerbation, more frequent in spring and in autumn. However exacerbation can be also
in winter or in summer. In the acute period of disease heartburn often increases. However
heartburn is the frequent symptom of cardial insufficiency and gastroesophageal reflux.
For an duodenal ulcer the acute burning feeling of acid in a esophagus, pharynx and even
in the cavity of mouth is especially typical. Often are belch by air or sour content,
excessive salivation. Vomiting is not a typical symptom for duodenal ulcer. More typical
sign is nausea. Sometimes for facilitation patients wilfully cause vomiting. These
symptoms, arises in the late periods of passing of duodenal ulcer.
Intensity of pain and dyspepsia syndromes depends both on the depth of
penetration and from distribution of ulcerous and periulcerous processes. Superficial
ulceration within the mucous tunic, as a rule, does not cause the pain because it does not
have sensible receptors. However, more deep layers of wall (muscular and especially
serous) have plural sensible vegetative receptors. Therefore, on deepening and
distribution of process arises visceral pain. At evident periulcerous processes and
penetration of ulcers to neighboring organs and tissues, usually, a parietal peritoneum,
that has spinal innervation, is pulled in. Pain becomes viscero-somatic, more intensive. A
such pain syndrome (with an irradiation in the back) is typical for low postbulbar ulcers
and bulbous ulcers of back wall, which penetrates in a pancreas and hepato-duodenal
ligament. Usually such patients has good appetite. Some of them limit themselves in
acceptance of ordinary food, go into to the dietary feed by small portions, and some
even hold back from a food, being afraid to provoke pain, and as a result of it weight is
lost. Some of patients feeds more intensive and often.
The psychical status of patients often are changed as a asthenoneurotic syndrome:
irritates, decline of working capacity, indisposition, hypochondria, abusiveness.
An inspection, as a rule, gives insignificant information. In many cases on the
abdominal skin it is possible to notice hyperpigmentation after application of hot-water
bottle. During the pain attack patients often occupy the forced position. At superficial
palpation on the abdominal wall determined hyperesthesia in ulcer projection. In the
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epigastric region, during deep palpation, it is possible to define pain and muscular
tension, mostly moderate intensity. There is important symptom of local percussion
painful (Mendels symptom): percussion by fingers in the symmetric epigastric areas
provoke pain in the ulcer, which is increased after the deep breath. The roentgenologic
and endoscopic are main diagnostic methods. The symptom of ulcerous niche is a
classic roentgenologic sign. It is depot of contrast agent, which is corresponded to
ulcerous defect, with clear contours and light bank to which converged fold mucus.
Cicatricial deformation of bulb of duodenum as a shamrock, butterfly, narrowing, tube,
diverticulum and other forms is the important sign of chronic ulcerous process. A
roentgenologic method is especially important for determination of configuration and
sizes of stomach and duodenum, and also for estimation of motility functions. X-Ray
examination is the main method at the peptic ulcer complicated by stenosis, with
disturbance of evacuation, duodenostasis, duodenal-gastric reflux, gastroesophageal
reflux, diverticulum. But by X-Ray examination is difficult to diagnose small superficial
ulcers, acute ulcers, erosions, gastritises and duodenitises. The most informing method in
such cases it endoscopy.
During endoscopy examination it is possible to define localization, form, sizes and
depth of ulcer. During bleeding grumes, trickle or pulsating of blood are observed. By
irrigation by styptic solutions, by cryocoagulation, by laser coagulation endoscopy
allows to secure hemostasis. Endoscopy allows to perform the biopsy of ulcer tissues for
determination of possible malignization.
In patients with low postbulbar ulcers the clinical signs are more expressed. It
characterized by late (in 23 hours after food intake) and intensive hungry and nightly
pain, that often irradiate to the back and to the right hypochondrium. The postbulbar
ulcers are inclined to more frequent exacerbation, and also to more frequent
complications, such, as penetration, stenosis and bleeding.
The are more frequent ulcerous bleeding (the bulbous happen in 2025 % cases,
postbulbar in 5075 %), perforations (1015 % cases). Penetration, stenosis and
malignization in patients with duodenal ulcers are observed rarely.
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Diagnostic program
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Pic. Duodenoscopy
Differential diagnostics
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the method Jade (Pic. 3.2.13) with subsequent to the pyloroplasty by Heineke-Mikulich.
At patients with decompensate stenosis and expressed dilatation and by the atony
of stomach it is needed to apply the classic resection of stomach depending on possible
damping-syndrome by Billroth -I or Billroth -II.
The choice of subtotal resection of stomach needs to be done at suspicion for
malignization or at histological confirmed malignization ulcers. In a duodenum this
process happens very rarely.
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ULCEROUS STENOSIS
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Pathomorphology
Such pathology in the compensation stage arises hypertrophy of the stomach walls.
The pyloric ring has a 0,50,7 cm in diameter. The mucous tunic of pyloric part of
stomach is thickened, with rough folds. Muscular fibers are hypertrophied and solid.
Histological hyperplasia of pyloric glands is observed.
During decompensation the muscular layer of stomach higher stenosis becomes
thinner, tone of him goes down, and a pyloric ring narrows to a few millimetres.
Microscopically present atrophy of mucous tunic and muscular fibers, vessels sclerosis.
A stomach collects the form of the stretched sack which goes down to the level of small
pelvis.
Classification
(by .. Shalimov and V.F.Saenko, 1987)
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stenosis:
I stenosis of goalkeeper;
II stenosis of bulb of duodenum;
III postbulbar duodenal stenosis.
First two types of stenosis are similar by functional and the organic changes. It
united them by one name pyloroduodenal, or high duodenal stenosis. The second
group is postbulbar duodenal stenosis. Feature of them is that a goalkeeper does not take
participation in the cicatricial- ulcerous process and it function is not broken.
Clinical management
The first signs of stenosis can be exposed already in eight-ten years from the
beginning of the peptic ulcer disease., Mainly, this is narrowing and rigidity and
disturbance of retractive activity of goalkeeper, which create a barrier for transition of
stomach content to the duodenum.
In the stage of the compensated stenosis hypertrophy of wall of stomach develops
and tone of muscular shell rises. Hereupon gastric content, slowly, but passes through the
narrowed area of stomach output. In this stage patients, usually, complained about feeling
of plenitude in a epigastric area after food intake, periodic vomitings by sour gastric
content. On empty a stomach by a stomach pump 200300 ml gastric content is removed.
In the subcompensated stage muscular layer of stomach becomes thinner. Tone of
him goes down, a peristalsis relaxes, and it looks like the stretched sack. Evacuation
disorders is increased. Fermentation and rotting developed in stagnant gastric content.
On this stage of disease development patients, usually, complain for the permanent
feeling of weight in epigastric region and regurgitation with an unpleasant rotten smell
of sulphuretted hydrogen.
Vomiting becomes systematic (once or twice on a day) up to half of liter per day.
On empty a stomach it possible to aspirate from it more 500 ml of content with the food
used the day before.
In the decompensation stage of the clinical sighn make progress quickly. There are
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heavy disturbances of the general condition of patient, considerable loss of weight (to
3040 %), acutely expressed dehydration of organism, hypoproteinemia, hypokalemia,
azotemia and alkalosis. In case of the protracted neglected disease, as a result of progress
of disturbances of metabolism, there can be a convulsive syndrome (gastric tetany).
Vomiting in this stage not always can be considered by a typical sign, in fact patients
often renounce to adopt a food, and a stomach acquires considerable sizes,
overdistension form, it tone is violated and atrophy of wall comes. In such patients in a
epigastric area it is possible to define the contours of the stretched stomach, with a slow
peristalsis,. In the distance it is possible to hearken the splash. By a probe from a
stomach to 1.5-2 litres of food with a putrid smell are removed. There can be gastric
tetany at considerable disturbances of electrolyte metabolism.
A diagnosis is set according to a typical syndrome, results of sounding of stomach,
rontgenoscopy, at which by contrasting of a barium expose stenosis of initial part of
stomach or duodenum, determines it origin and estimate a degree.
Roentgenologically in the compensation stage stomach in normal sizes, it
peristalsis deep, increased, evacuation of content proceeds no more than 6 hours. In the
stage of subcompensation a stomach is megascopic, a peristalsis is loosened, evacuation
stays too long to 24 hours. During decompensation a stomach is considerably extended
as a sack, deformed, the waves of antiperistalsis can take place, a contrast stays too long
more than 2448 hours. The method of the double contrasting by a barium and air
considerably facilitates diagnostics.
Determination of stomach motility has not only diagnostic but also prognostic
value for the choice of method of operation.
In the stage of compensation motility of stomach is well-kept, often even
increased. With the increasing the degree of stenosis the motility disturbance increased,
up to gastroplegia.
In the biochemical blood test is marked the decline of content of albumen to
5448 g/l; potassium to 2,92,5 mmol/l; chlorides to 8587 mmol/l. The changes
of such indexes are most expressed at patients with gastrogenous tetany.
The study of secretory function of stomach allows to define the degree of
compensation of stenosis and importent at the choice of adequate method of operation.
Gastroscopy with a biopsy is the enough informing method of examination of such
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patients. By this method is possible to determine a reason and degree of stenosis, and
also state of mucous tunic of stomach.
Diagnosis program
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Differential diagnostics
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In 50,7 % cases perforates the ulcers of duodenum, in 42,8 % are ulcers of pyloric
part of stomach, in 4,8 % are ulcers of small curvature of body of stomach and in 0,7 %
are cardial ulcers.
Ulcers, which lie on the front wall of stomach and duodenum more frequent give
the perforation with general peritonitis, while ulcers on a back wall perforation with
adhesive inflammation.
The reasons of ulcers perforation are: exacerbation of peptic ulcer, harmful habits,
stresses, professional, athletic overexertion, faults in the feed and abuses by strong
waters.
Pathomorphology
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Classification
(by V.S. Savelev, 1986)
Clinical management
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Covered perforation (.. Shnicler, 1912). At this pathology the perforative hole
after a perforation is closed by a fibrin, by a omentum, by the fate of liver, sometimes
piece of food. After that some amount of stomach content and air gets in an abdominal
cavity. After the protection a stomach-ache diminishes, but proof tension of muscles of
front abdominal wall, especially overhead quadrant of stomach is kept. At percussion
hepatic dullness is doubtful. During x-Ray examination it is not always possible to mark
gas in right hypochondrium (Pic. 3.2.14).
Consequences of passing of the covered perforation: the repeated perforation with
development of classic clinical signs can come; at separation of process from a free
abdominal cavity a subdiaphragmatic or subhepatic abscess is formed; complete closing
of defect by surrounding tissue with gradual convalescence of patient.
The atypical perforation is the perforation, at which gastric or intestinal content
gets not to the abdominal cavity, but in retroperitoneal space (ulcers of back wall of
duodenum), large or small omentum (ulcers of small curvature of stomach), hepato-
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duodenal ligament.
In such patients during a perforation pain is not acutely expressed. During
palpation observed insignificant rigidity of muscles of front abdominal wall. On
occasion, especially on the late stages of disease, there can be hypodermic emphysema
and crepitation.
Diagnosis program
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operation. Preoperative preparation must include: in I phase are antishock action; in the
II and III phases reanimation preparations, introductions of antibiotics for 23 hours
before operation, liquidation of hypovolemia by salt blood substitutes (solution of
chlorous sodium), solutions of dextran (polyhlukine, reopolihlukine, hemodes). Amount
of liquid necessary for correction of hypovolemia, calculate after hematokrit by central
vein pressure. Taking for the norm of hematokrit 40 %, on each 5 % higher norms need to
be poured 1000,0 ml liquids.
Conservative treatment (method of Tejlor, 1946) can be justified at the refusal of
patient from operation or in default of conditions for its implementation.
It must include:
permanent nasogastral aspiration of gastric content;
introduction of preparations which brake a gastric secretion (atropine, 2-
blockers and others like that);
introduction of antibiotics;
correction of metabolism;
laparocentesis with drainage and closed lavage of the abdominal cavity.
In the decision of question about the choice of method of operative treatment of
perforated gastroduodenal ulcers the important value has the following factors:
localization of ulcer, clinico-morphological description of ulcer (perforation of acute or
chronic ulcer), connected with the perforation such complications of ulcer, as bleeding,
cicatricial-ulcerous stenosis, penetration, degree of risk of operation and feature of
clinical situation.
Operative treatments at a perforated ulcer divide into palliative and radical.
Palliative operations
Palliative operations are: closure of the perforative hole of ulcer, tamponade of the
perforative hole by a omentum on a leg by .. Oppel - P.N.Polikarpov -
..Pidhorbunskyy (1896, 1927, 1948) (Pic. 3.2.15). Indications and terms for their
implementation are:
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perforation of acute duodenal ulcer in youth and young age without anamnesis;
perforation of acute ulcer in the IIIII phases of passing;
perforation of callous gastric ulcer in the IIIII phases of passing;
expressed and high degrees of risk of operation.
Radical operations
The radical operations at perforated ulcers are: resection of stomach and excision
of the perforative hole of ulcer in combination with pyloroplasty and StV, SV or SPV.
Indications and terms for implementation of resection of stomach are:
perforation of callous gastric ulcer in I phase of clinical passing;
repeated perforation of ulcer;
perforation of ulcer in I phase of clinical passing in combination with stenosis
and bleeding of ulcer;
perforation of duodenal ulcer in I phase of passing in combination with a
gastric ulcer;
unexpressed and moderate degree of risk of operation;
sufficient qualification of surgeon and material resources of operating-
anaesthetic brigade.
Indications for implementation of operation of excision of the perforative hole of
ulcer with pyloroplasty, StV, SV and SPV are: perforation of ulcer of front wall of
duodenum or pyloric part of stomach in the III phases of passing;
perforation of ulcer of front wall of duodenum in the III phases of passing in
combination with the bleeding ulcer of back wall;
perforation of duodenal ulcer in the III phases of passing in combination with
the compensated stenosis of outgoing part of stomach;
increased gastric secretion;
insignificant and moderate degree of risk of operation;
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Pathomorphology
Strengthening of necrosis process are leading factors in the origin of the ulcerous
bleeding in the area of ulcerous crater with distribution of this process to a vessel and
subsequent melting of vascular wall; activation of fibrinolysis in tissues of stomach and
duodenum; ischemia of tissues of wall of stomach.
Classification
Bleeding gastroduodenal ulcers after the degree of weight of loss of blood (by
.. Shalimov and V.F.Saenko, 1987) are divided:
I degree is easy observed at the loss to 20 % volume of circulatory blood (at a
patient with weight of body 70 kg it is up to 1000 ml);
II degree middle weight is loss from 20 to 30 % volume of circulatory blood
(10001500 ml);
The III degree is heavy is observed at loss of blood more than 30 % volume of
circulatory blood (15002500 ml).
Clinical management
At patients with an peptic ulcer disease, bleeding pops up, mainly at night.
Vomiting can be the first sign of it, mostly, at gastric localization of ulcers. Vomiting
masses, as a rule, looks like coffee-grounds. Sometimes they are as a fresh red blood or
its grume.
The black tar-like emptying are the permanent symptom of the ulcerous bleeding,
with an unpleasant smell (melena), that can take place to a few times per days.
Bloody vomiting and emptying as melena is accompanied by worsening of the
general condition of patient. A acute weakness, dizziness, noise in a head and darkening
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Diagnosis program
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Differential diagnostics
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tachycardia, falling of arterial pressure are observed. In such patients it is possible to find
the signs of cirrhosis of liver and portal hypertension (head of jelly-fish,
hypersplenism, ascites, often is icterus).
Sliding hernia of the esophagus opening of diaphragm can be accompanied by
formation of ulcers in the place of clench of the stomach by the legs of diaphragm and
bleeding from them. However for this pathology are more typical microbleeding, that is
hidden. In such patients often the present protracted anaemia which can achieve the
critical values. Sometimes in them observe more expressed bleeding with classic
vomiting coffee-grounds and melena. During the roentgenologic examination with
barium is possible to expose the signs of sliding hernia of the esophagus opening: the
obtuse cardial angle, absence or diminishment of gas bubble of stomach or ringing
symptom.
The cancer tumour of stomach in the destruction stage can be also complicated by
bleeding. However, such bleeding are massive, and chronic character is carried mostly
with gradual growth of anaemia. For this pathology there are the inherent worsenings of
the general condition of patient, loss of weight of body, decline of appetite and waiver of
meat food. At the roentgenologic examination the defect of filling is exposed in a
stomach.
The gastric bleeding can be related to the diseases of the cardio-vascular system
(atherosclerosis, hypertensive disease), however such happens mainly in the older years
people. Clearly, that in such patients during the endoscopic examination the source of
bleeding exposing is not succeeded.
Among other diseases, with which it is necessary to differentiate the ulcerous
bleeding, it is needed to remember the Mallory-Weiss syndrome, benign tumours of
stomach and duodenum (more frequent leiomyoma), hemorrhagic gastritis, acute (stress)
erosive defeats of stomach, arteriovenous fistula of mucous tunic.
Often differential diagnostics performed according to the level of localization of
source of bleeding in different parts of gastrointestinal tract. For the upper parts of
digestive tract (esophagus and stomach) typical there is vomiting by grume or coffee-
grounds content and emptying by melena. The farther aboral placed source of
bleeding, the bloody emptying changes the more so. During the bleeding from a thin
bowel excrement looks as melena. In case of such pathology of colon (polypuses,
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tumours, unspecific ulcerous colitis) emptying have the appearance of fresh red blood,
mostly as packages.
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individually. On today the best tactic which gives advantage to organ-saving and
organsparing methods of operations. The removing ulcer as sources of bleeding must be
an obligatory condition. The methods of sewing of bleeding vessels or edging of ulcer
and bandaging of vessels which feed a stomach and duodenum did not justify itself
through the real threat of relapse of bleeding already in an early postoperative period
(912 days).
Palliative operations (cutting of ulcer, forming of roundabout anastomosis) can be
justified only taking into account the general condition of patient and on a necessity as
possible quick and least traumatically to make off operation.
At the bleeding ulcers of duodenum it is better to apply excision of ulcer or it
exteritirization after methods, developed by V.Zajtsev and Velihotskyy. Operation
complemented by one of types of vagotomy, it is better by a selective proximal with
piliroplastic. The resection of stomach on the second or first method of Bilroth can be
realized only in the stable general condition of patient. During the resection of stomach
in case of low bleeding duodenal ulcers it is better to execute mobilization of duodenum
and suturing of its stump on transcholedochus drainage which formed as
transcholedochus duodenotomy (Laqey, 1942). This method warns the possible
intraoperative damages of choledoch, that are the possible at low duodenal ulcers.
Transcholedochus duodenotomy by performing the decompression of stump of
duodenum, warns insufficiency of its stitches, that can arise up in an early postoperative
period.
In case of bleeding gastric ulcers, the resection methods of operations are also
usable. Only on occasion, when patients has the grave general condition, it is possible to
assume the wedge cutting of ulcer.
video
MALIGNIZATION
CANCER OF STOMACH
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first place and is the most frequent, by the reason of death from malignant formations in
many countries of world. Frequency of it at the last 30 years considerably diminished in
the countries of Western Europe and North America, but yet remains high in Japan,
China, countries of East Europe and South America.
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Pathomorphology
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primary tumour.
0 is a primary tumour is not determined.
not enough data for estimation of primary tumour.
is is invasive carcinoma: intraepithelial tumour without the invasion of own shell
mucus (Carcinoma in situ).
1 is a tumour infiltrate the wall of stomach to the submucous layer.
2 is a tumour damages mucus, submucous and muscular layers.
3 is a tumour germinates in a serous shell.
4 is a tumour passes to the neighbouring structures.
N are regional lymphatic nodes.
N not enough information for the damage assessment of lymphatic nodes.
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Groupment by stages
Stage 0 No Mo.
Stage I 1-2 No Mo.
Stage II T2-3 No Mo.
Stage III T1-4 N1-2 Mo.
Stage IV any T, any N M1.
Except for clinical classification (NM or TNM), for the most detailed study
pathological classification (postsurgical, posthistological) which is signed N.
G histopathological differentiation:
G1 is the well differentiated tumour;
G2 is the moderately differentiated tumour;
G3-4 it is badly or undifferentiated tumour.
Clinical management
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All authors which are engaged in the study of problem of cancer of stomach
underline absence or vagueness, no specificity of symptoms, especially on the early
stages of disease. The displays of cancer of stomach are very various and depend on
localization of tumour, character of its growth, morphological structure, distribution on
contiguous organs and tissues. At localization of tumour in a cardial part patient
complains firstly, as a rule, for appearance of dysphagy.
At careful, purposeful collection of anamnesis it is not succeeded to expose some
other, most early symptoms, which precedes to dysphagy and forces a patient to appeal to
the doctor. The unpleasant feeling behind a breastbone and feeling of unpassing of hard
food on a esophagus appear at the beginning of disease. After some time (as a rule, it is
enough quickly, during a few weeks, sometimes even days) a hard food does not pass (it
is to wash down by water or other liquid). This period can be during 13 months.
Patients address a doctor exactly in this period. Other symptoms appear to this time:
regurgitation, pain behind a breastbone, loss of mass of body, sometimes even
exhaustion, the grey colouring of person, a skin is dry, quickly grows general weakness.
Sometimes patients address a doctor, when already with large effort a spoon-meat passes
only or complete stenosis came.
At localization of tumour in the antral part of stomach the first complaints, as a
rule, are up to appearance of feeling of weight in epigastric region after the reception of
food (even in a two-bit), feeling of saturation (after the reception of glass of water),
belch (at first it is simple by air, and then with a smell). Feeling of weight grows for a
day, patients forced to cause vomiting. In the morning there can be vomiting by mucus
with the admixtures of coffee-grounds (so called cancer water). Patients loses weight
(mass of body is lost), a weakness, anaemia grows.
Tumours localized in the body of stomach show up either a pain syndrome or
syndrome of so called small signs (.I. Savitskyy, 1947), which is characterized by
appearance of amotivational general weakness, decline of capacity, rapid fatigueability,
depression (by the loss of interest to the environment), proof decline of appetite, gastric
discomfort, making progress weight lost.
The carried chronic diseases of stomach, for which typical seasonality, can
influence on the clinical sign of cancer of stomach. At appearance of gastric complaints
out of season or in absent of effect from the got therapy concerning the exacerbation of
gastritis, ulcers must guard a patient and doctor (symptom of precipice of gastric
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anamnesis).
In case of occurring of gastric symptoms first in persons in age 50 years and
older it is foremost necessary to eliminate the cancer of stomach.
In parts of patients cancer of stomach shows up only the metastatic damage of
other organs or complications. More than twenty so called atypical forms, which are
characterized by causeless anaemia, ascites, icterus, fever, edemata, hormonal
disturbances, changes of carbohydrate exchange, intestinal symptoms, are distinguished.
During the examination of patients with the cancer of stomach the pallor of skin
covers (at anaemia) is observed, in neglected case is frog stomach (sign of ascites).
During palpation determined painful in a epigastric area, sometimes possible to
palpate the tumour.
During auscultation of patients with pylorostenosis it is possible to define noise
of splash.
Laboratory information: hypochromic anaemia, neutrophilic leukocytosis,
megascopic ESR; during examination of gastric secretion: hypo- and anacidity and
achlorhydria.
Gastroduodenoscopy enables to diagnose a tumour even smaller 5 mm and conduct
an aiming biopsy with histological examination of the taken material.
Roentgenoscopy and roentgenography examination of stomach. Basic signs: defect
of filling, local absence of peristalsis, malignant relief of mucous tunic (Pic. 3.2.18).
Ultrasonic examination: presence of metastases in a liver, pancreas.
Computer tomography allows to estimate the basic parameters of tumour,
germination in neighbouring organs and presence of metastases.
It is expedient to apply laparoscopy, mainly, for the decision of question about
operable of tumour (diagnostics of metastatic defeat of organs of abdominal cavity).
Diagnosis program
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(Pic. 3.2.21) and jejunostoma (in case of the stenosis tumours of stomach output); 2)
gastrostoma (Pic. 3.2.22) in case of the cancer of cardial part of stomach with disturbance
of patency; 3) edging of bleeding vessels in case of complication of cancer by bleeding;
4) tamponade by omentum during the perforation of tumour.
The value of radial therapy and chemotherapy, as independent methods of
treatment of cancer of stomach, is limited. Radial therapy is indicated for patients with
cardial cancer as preoperative course or as palliative treatment. Adjuvant mono- or
polychemotherapy (mainly by 5-phtoruracil) is conducted in a postoperative period as
combined therapy and in case of dissemination of the tumours.
Prognosis. The indexes of five-year survival of patients with the cancer of stomach
hesitate within the limits of 530 %, but, from data of most authors, they do not exceed
10 %.
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20. Gisbert JP, Pajares R, Pajares JM. Evolution of Helicobacter pylori therapy from a
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21. Svanes C, Lie RT, Svanes K, Lie SA, Sreide O. Adverse effects of delayed
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mortality in patients with bleeding peptic ulcers after therapeutic endoscopy. Clin
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31. Kikkawa A, Iwakiri R, Ootani H, Ootani A, Fujise T, Sakata Y, et al. Prevention of
the rehaemorrhage of bleeding peptic ulcers: effects of Helicobacter pylori
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32. Lisbert JP, Calvet X, Feu F, Bory F, Cosme A, Almela P, et al. Eradication of
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34. Barkun A, Bardou M, Marshall JK. Consensus recommendations for managing
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Gastroenterol Rep. Jun 2008;10(3):208-14.
36. Laine L, Shah A, Bemanian S. Intragastric pH with oral vs intravenous bolus plus
infusion proton-pump inhibitor therapy in patients with bleeding ulcers.
Gastroenterology. Jun 2008;134(7):1836-41.
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37. Chan WH, Khin LW, Chung YF, Goh YC, Ong HS, Wong WK. Randomized
controlled trial of standard versus high-dose intravenous omeprazole after
endoscopic therapy in high-risk patients with acute peptic ulcer bleeding. Br J
Surg. May 2011;98(5):640-4.
38. [Best Evidence] Andriulli A, Loperfido S, Focareta R, Leo P, Fornari F, Garripoli
A, et al. High- versus low-dose proton pump inhibitors after endoscopic
hemostasis in patients with peptic ulcer bleeding: a multicentre, randomized study.
Am J Gastroenterol. Dec 2008;103(12):3011-8.
39. Sari YS, Can D, Tunali V, Sahin O, Koc O, Bender O. H pylori: Treatment for the
patient only or the whole family?. World J Gastroenterol. Feb 28
2008;14(8):1244-7.
40. Konno M, Yokota S, Suga T, Takahashi M, Sato K, Fujii N. Predominance of
mother-to-child transmission of Helicobacter pylori infection detected by random
amplified polymorphic DNA fingerprinting analysis in Japanese families. Pediatr
Infect Dis J. Nov 2008;27(11):999-1003.
41. Singh V, Mishra S, Maurya P, Rao G, Jain AK, Dixit VK, et al. Drug resistance
pattern and clonality in H. pylori strains. J Infect Dev Ctries. Mar 1
2009;3(2):130-6.
42. [Guideline] Lanza FL, Chan FK, Quigley EM. Guidelines for prevention of
NSAID-related ulcer complications. Am J Gastroenterol. Mar
2009;104(3):728-38.
43. Chan FK, Hung LC, Suen BY, Wu JC, Lee KC, Leung VK, et al. Celecoxib versus
diclofenac and omeprazole in reducing the risk of recurrent ulcer bleeding in
patients with arthritis. N Engl J Med. Dec 26 2002;347(26):2104-10.
44. Chan KL, Ching YL, Hung CY. Clopidogrel versus aspirin and esomeprazole to
prevent ulcer bleeding. N Eng J Med. 2005;352:238-44.
45. Lai KC, Chu KM, Hui WM, Wong BC, Hung WK, Loo CK, et al. Esomeprazole
with aspirin versus clopidogrel for prevention of recurrent gastrointestinal ulcer
complications. Clin Gastroenterol Hepatol. Jul 2006;4(7):860-5.
46. Hsu PI, Lai KH, Liu CP. Esomeprazole with clopidogrel reduces peptic ulcer
recurrence, compared with clopidogrel alone, in patients with atherosclerosis.
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ULCERATIVE DISEASE OF THE STOMACH (UDS) AND THE DUO... http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
The aim. To master clinics, diagnostics, differential diagnostics of various clinical forms of UDS and UDD. To learn the treatment tactics, indications and contraindications for operative intervention, operative intervention type
at various clinical forms of UDS and UDD, principles of postoperative period course, expertise of the working ability after operations for UDS and UDD.
Professional orientation of students. UDS and UDD is one of the most frequent surgical illnesses of organs of gastric-intestinal tract. Morbidity reaches the level of 10-15%. Major complications of UDS and UDD are
perforation, bleeding, ulcerative stenosis, malignization. They are vitally dangerous and require urgent or pressing surgical interventions. Postoperative lethality after urgent operations because of UDS and UDD
complications sometimes reaches 15-20%.
Theme 1. Modern principles of diagnostics of surgical treatment of the ulcerative disease of stomach and duodenum.
1.Anatomic and physiologic features of the stomach and the duodenum.
2.Factors of the ulcerative disease development.
3.Pathogenesis of the ulcerative disease of the stomach and the duodenum.
4.Classification of ulcerative disease of the stomach and the duodenum.
5.Diagnosis methods of the ulcerative disease of the stomach and the duodenum.
6. Curing tactics at the ulcerative disease.
7.Modern principles of conservative and surgical treatment of UDS and UDD.
8.Choice of the operative treatment method at UDS and UDD.
9. Types of radical (organ-sparing and organ-preserving) and palliative operations for the reason of UDS and UDD.
10.Peculiarities of the postoperative period course after the operations for UDS and UDD reason.
11.Evaluation of treatment results of patients with UDS and UDD.
11.Disablement expertise after the operations for UDS and UDD reason.
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BREAK 12.00-12.30
4. In patients with bleeding duodenal ulcers, the endoscopic finding associated with the highest incidence of rebleeding is:
A. Visible vessel.
B. Cherry-red spot.
C. Clean ulcer bed.
D. Duodenitis.
E. Shallow, 3-mm. ulcer.
5. All of the following are contraindications for highly selective vagotomy except:
A. Intractable duodenal ulcer disease.
B. Peptic ulcer disease causing gastric outlet obstruction.
C. Fundic peptic ulceration.
D. Cigarette chain smoking.
E. Perforated peptic ulcer disease with more than 24 hours' soilage.
6. Appropriate management of severe vomiting associated with gastric outlet obstruction from peptic ulcer disease includes all of the following except:
A. Nasogastric suction.
B. Intravenous hydration.
C. Nutritional assessment; upper endoscopy to rule out malignancy.
D. Intravenous H 2 antagonist.
E. Oral antacid therapy.+
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8. All of the following are contraindications for highly selective vagotomy except:
A. Intractable duodenal ulcer disease.+
B. Peptic ulcer disease causing gastric outlet obstruction.
C. Fundic peptic ulceration.
D. Cigarette chain smoking.
E. Perforated peptic ulcer disease with more than 24 hours' soilage.
9. Numerous epidemiologic associations have been made between (1) environmental and dietary factors and (2) the incidence of gastric cancer, including all except:
A. Dietary nitrites.
B. Dietary salt.
C. Helicobacter pylori infection.
D. Dietary ascorbic acid.+
10. All of the following benign conditions are associated with increased rates of gastric cancer except:
A. Pernicious anemia.
B. Multiple endocrine neoplasia type I (MEN 1).+
C. Adenomatous polyps.
D. Chronic atrophic gastritis.
1 C.
2 E.
3 C.
4 B.
5 A.
6 E.
7 D.
8 A.
9 D.
10 B.
Information sourses:
Main
1. Townsend CM, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery. 19th ed. Philadelphia, Pa: Saunders Elsevier; 2012.
2. L.Ya.Kovalchuck, Yu.P.Spizhenko, V.F.Sayenko and others Hospital surgery. Ternopil: Ukrmendknyga, 1999.
3. Practical classes materials http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/classes_stud/en/med/lik/ptn/Surgery
/4/Topic%2004%20Ulcerative%20disease%20of%20the%20stomach%20and%20the%20duodenum.%20Diseases%20of%20operated%20stomach.%20Postresection%20and%20postvagotomy%20syndromes..htm
Additional
1. Manual Facultative Surgery under the edition of V.O.Shidlovsky Ternopil: Ukrmedknyga, 2002, section Diseases of the rectum and the colon,
2. Compact disc Facultative surgery.
3. Schwartz's Principles of Surgery, Ninth Edition. F. Brunicardi. Philadelphia, Pa: Saunders Elsevier; 2009
4. Zollinger's Atlas of Surgical Operations, 9th Edition. Robert Zollinger Jr., Elsevier; 2010
5. Chen, Herbert. Illustrative Handbook of General Surgery. Berlin: Springer, 2010.
"11" 2013 . 9
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Clinical management
For the clinical finding of dumping syndrome typical there is the origin of attacks of
general weakness during acceptance of food or during the first 1520 minutes after it. The
attack begins from feeling of plenitude in a epigastric area and is accompanied by the
unpleasant feeling of heat, that spills in the overhead half of trunk or on all body. Thus is
acutely multiplied sweating. Then there is a fatigue, appear somnolence, dizziness, noise in
ears, shaking of extremities and worsening of sight. These signs sometimes achieve such
intensity, that patients forced to lie down. Loss of consciousness could be in the first months
after operation. The attacks are accompanied by tachycardia, sometimes by the shortness of
breath, headache, paresthesia of upper and lower extremities, polyuria and vasomotor rhinitis.
At the end of attack or after it patients often notice grumbling in a stomach and diarrhea.
A milk or carbohydrate food is the most frequent provoking factor of dumping
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syndrome. In a period between the attacks patients complain about rapid fatigueability,
weakening of memory, decline of working capacity, change of mood, irritates, apathy. During
roentgenologic examination after 515 minutes observed the increased evacuation of barium
mixture through anastomosis by a wide continuous stream, expansion of efferent loop and
rapid advancement of contrasting matter in the distal parts of thin bowel (Pic. 3.2.16).
By the expression of symptoms dumping syndrome is divided into three degrees of
weight:
I degree is easy. Patients have the periodic attacks of weakness with dizziness, nausea,
that appear after the use of carbohydrates and milk food and last no more than 1520 min.
During the attack a pulse becomes more frequent on 1015 per min., arterial pressure rises or
sometimes goes down on 1.3-2 KPa (1015 mm Hg), the volume of circulatory blood
diminishes on 200300 ml. The deficit of mass of body of patient does not exceed 5 kg. A
working capacity is well-kept. Medicinal and dietary treatment gives a good effect.
II degree middle weight. Attacks of weakness with dizziness, pain in the region of
heart, hyperhidrosis, diarrhea. Such signs last, usually, 2040 min., arise up after the use of
ordinary portions of some food. During such state a pulse becomes more frequent on 2030 per
min., arterial pressure is rises (sometimes goes down) on 22,7 KPa (1520 mm Hg), the
volume of circulatory blood diminishes on 300500 ml. The deficit of mass of body of patient
achieves 510 kg. A working capacity is reduced. Conservative treatment sometimes has a
positive effect, but brief.
The III degree is hard. Patients are disturbed by the permanent, acutely expressed attacks
with the collaptoid state, by a fainting fit, by diarrhea, which do not depend on character and
amount of the accepted food and last about 1 hour. During the attack is multiplied frequency of
pulse on 2030 per 1 min; arterial pressure goes down on 2,74 KPa (2030 mm Hg), the
volume of circulatory blood diminishes more than on 500 ml. The deficit of mass of body
exceeds 10 kg. Patients, as a rule, are disabled. Conservative treatment is uneffective.
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The problem of treatment of patients with dumping syndrome is not easy. Before the
surgical treatment, as a rule, must precede conservative. Patients with the disease of easy and
middle degrees respond to conservative treatment, mainly with an enough quite good effect. At
the heavy degree of disease such treatment more frequent serves as only preparation to
operative treatment. If a patient does not give a consent for operation or at presence of contra-
indications to operative treatment (disease of heart, livers, kidneys), conservative therapy is
also applied. Such treatment must include dietotherapy, blood and plasma transfusion,
correction of metabolism, hormonal preparations, symptomatic therapy, electro-stimulation of
motility function of digestive tract.
The dietotherapy: using of high-calorie, various food rich in squirrel, by vitamins, by
mineral salts, with normal content of fats and exception from the ration of carbohydrates which
are easily assimilation (limitation of sugar, sweet drinks, honey, jam, pastry wares, kissel and
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fruit compotes). All it is needed to use by small portions (56 times per days). If the signs of
dumping syndrome appear after a food, such patients it is needed to lie down and be in
horizontal position not less than 1 hour. At the heavy degree of dumping syndrome patients
need to eat slowly, desirably lying on left. Such position creates the best terms for evacuation
of food from a stomach. Thus recommend also to repudiate from too hot and cold foods.
Medicinal treatment must include sedative, replaceable, antiserotonin, hormonal and
vitamin therapy. The indications to operative treatment of patients with dumping syndrome are:
heavy passing of disease, combination of dumping syndrome of middle degree with other
postgastrectomy syndromes (with the syndrome of efferent loop, hypoglycemic syndrome and
progressive exhaustion) and uneffective of conservative treatment of the dumping syndrome of
middle degree. Most methods of operative treatment of dumping syndrome are directed on
renewal of natural way of passing of food on a stomach and intestine, improvement of reservoir
function of stomach and providing of proportioning receipt of food in a thin bowel.
Depending on reasons and mechanisms of development of dumping syndrome there are
different methods of the repeated reconstructive operations. All of them can be divided into
four basic groups: I. Operations which slow evacuation from stump of stomach. II.
Redoudenization. III. Redoudenization with deceleration of evacuation from stump of stomach.
IV. Operations on a thin bowel and its nerves.
Basic stages of reconstructive operations: 1) disconnection of adhesions in an abdominal
cavity, releasing of gastrointestinal and interintestinal anastomosis and stump of duodenum; 2)
cutting or resection of efferent and afferent loops; 3) renewal of continuity of upper part of
digestive tract.
For correction of the accompany postgastrectomy pathology it is better to apply
combined anti- (iso-) peristaltic gastrojejunoplasty. Thus transplant by length 2022 cm,
located between a stomach and duodenum, must consist of two parts: antiperistaltic (78 cm),
connected with a stomach, and isoperistaltic, connected with a duodenum. An antiperistaltic
segment brakes dumping of stomach stump, and isoperistaltic hinders the reflux of
duodenum content.
Signs beghins after 2-2,5 h after food intake, 2-3 times per
stage
week. Patients does not feel it.
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Clinical management
The clinical signs of postgastrectomy asthenia arise up after a some latent period which
can last from a few months to some years. During this period patients often complain for a
general weakness and bad appetite. The basic symptoms of postgastrectomy asthenia are:
general weakness, edemata, acute weight loss, diarrhea, skin and endocrine abnormalities. The
postgastrectomy asthenia more frequent meets at men at 4050 years. In most cases diarrhea is
the first symptom of disease, that can arise up in 2 months after operation. Diarrhea, usually,
has permanent character and sometimes becomes profuse.
Weight loss appears too early, the deficit of mass of body achieves 2030 kg. A patient
quickly loses forces.
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The afferent loop consists of part of duodenum, that stopped behind after a resection,
area of empty bowel between a duodenojejunal fold and stump of stomach. The syndrome of
afferent loop can arise up after the resection of stomach after the Bilrhoth-II method. Violation
of evacuation from a afferent loop and vomiting by a bile are its basic signs.
Acute and chronic obstruction of afferent loop are distinguished. The reason of acute
obstruction is mechanical factors: postoperative commissure, volvulus, internal hernia,
invagination, jamming behind mesentery of loop of bowel and stenosis of anastomosis.
Frequency of origin of sharp obstruction of afferent loop hesitates within the limits of
0,52 %. The disease can arise up in any time after operation: in a few days or a few years.
Chronic obstruction of afferent loop (actually syndrome of afferent loop), as well as
acute, can arise up in any time after operation, however more often it develop after the resection
of stomach with gastroenteroanastomosis on a long loop, especially when operation is
performed without entero-enteroanastomosis by Brown.
The etiologic factors of syndrome of afferent loop are divided into two groups: 1)
mechanical (postoperative commissure, invagination, disturbance of evacuation on a afferent
loop, wrong location of afferent loop, very long afferent loop, fall of mucous tunic of afferent
loop into a stomach); 2) functional (hypertensive dyskinesia of bilious ways and duodenum,
damage and irritation of trunks of vagus nerves, hypotensive and spastic states of upper part of
digestive tract, heightened secretion of bile and juice of pancreas under act of secretin and
cholecystokinin).
Clinical management
For the clinical picture of acute obstruction typical is permanent, with a tendency to
strengthening, pain in a epigastric area or in right hypochondrium, nausea and vomiting. At
complete obstruction a bile in vomiting masses is absent. The general condition of patient
progressively gets worse, the temperature of body rises, leukocytosis grows, tachycardia grows.
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At the objective examination painful and tension of muscles of abdominal wall is observed. In
a epigastric area it is often possible to palpate tumular lump. Possible cases, when the increase
of pressure in a bowel is passed on bilious ways and channels of pancreas. There can be pain
and icterus in such patients. There are necrosis and perforation of duodenum with development
of peritonitis during further progress of process. Acute obstruction of afferent loop in an early
postoperative period can be the reason of insufficiency of stump of duodenum also.
During the roentgenologic examination of organs of abdominal cavity it is visible round
form area of darkening and extended, filled by gas, bowels loop.
Patients, usually, complain for feeling of weight in a epigastric area and arching in right
hypochondrium, that arises in 1015 min. after acceptance of food and gradually grows.
Together with that, appear nausea, bitter taste in a mouth, heartburn. Then there is increasing
pain in a right to epigastric area. During this pain arises intensive, sometimes repeated vomiting
by a bile, after which the all symptoms disappear. It could be after certain kind of food (milk,
fats) or its big amount. Very rarely vomiting by bile unconnected with the feed. In heavy case
patients lose up to 1 liter of bile with vomiting masses. During the objective examination
observed subicteritiousness of the sclera, sign of dehydration of organism (decline of turgor of
skin, dry tongue, oliguria, concentrated urine). Emptying is irregular, grey color, with
considerable content of undigested fat and muscular fibres. Anaemia can develop at heavy
passing of disease.
Distinguished easy, middle and heavy degrees of afferent loop syndrome. In patients with
the easy degree of disease vomiting is 12 times per a month, and insignificant regurgitation
arise up through 20 min 2 hour after a food, more frequent after the use of milk or sweet
food. At middle degree of afferent loop syndrome such attacks repeat 23 times per week,
patients are disturbed by the considerably expressed pain syndrome, and with vomiting up to
200300 ml of bile is lost. For a heavy degree the daily attacks of pain are typical, that is
accompanied by vomiting by a bile (up to 500 ml and more).
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. 2. Resection by Roux
All operative methods of treatment of afferent loop syndrome can be divided into three
groups:
I. Operations, that will liquidate the bends of afferent loop or shorten it.
II. Drainage operations.
III. Reconstructive operations.
The operations of the first group, directed on the removal of bends and invagination of
afferent loop, can not be considered as radical. They need to be performed only at the grave
general condition of patient.
The widest application in clinical practice at the syndrome of afferent loop has the
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The origin of reflux after the distal resection of stomach is conditioned by some factors:
I. Traumatic factors: 1) traction of stomach during operation as reason of sprain of
ligament of proximal part of stomach and mobilization of large curvature of stomach; 2) cutting
of vessels of stomach and oblique muscles of it wall, in particular on small curvature; 3)
vagotomy, that is accompanied by cutting of phrenico-esophageal and gastrophrenic ligaments;
4) imposition of gastrointestinal anastomosis, especially direct gastroduodenoanastomosis by
Billroth-I, that results in smoothing of the Hisa corner; 5) frequent aspiration of gastric content
in a postoperative period, that causes superficial esophagitis.
II. Trophic factors: 1) damage of vessels which are the reason of ischemia in the area of
esophago-gastric connection, and thrombophlebitis of cardial part of stomach; 2) disturbance
of influencing of neurohumoral factors which take part in innervations of esophagus; 3)
disturbance of trophism of diaphragm as a result of hypoproteinemia and weight loss; 4)
ulcerous diathesis and megascopic volume of gastric secretion (especially nightly); 5)
regurgitation of alkaline content of duodenum in stump of stomach which reduces tone of it
muscular shell.
III. Mechanical factors: 1) gastric stasis; 2) diminishment of volume of gastric reservoir,
that is accompanied by the increase of intragastric pressure.
Clinical management
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mouth.
Pain behind a breastbone often can remind the attack of stenocardia with typical
irradiation. Sometimes such reflux is able to provoke real stenocardia.
Hypochromic anaemia is the frequent symptom of gastroesophageal reflux too.
The diagnosis of gastroesophageal reflux, mainly, is based on clinical information,
results of roentgenologic examination, esophagoscopy.
The edema, hyperemia of mucous tunic of esophagus, easy bleeding and vulnerability it
during examination, surplus of mucus and erosions covered by fibrin tape is considered the
endoscopic signs of esophagitis. In doubtful case at the insignificantly expressed macroscopic
changes the biopsy of mucous tunic helps to set a diagnosis.
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and through toxins can cause the damage of mucous tunic of stomach stump. Also, alkaline
environment and disturbance of evacuation from the operated stomach influence favourably on
microflora growth.
Clinical management
For the clinical picture of alkaline reflux-gastritis the permanent poured out pain in a
epigastric area, belch and vomiting by a bile are typical. At some patients heartburn and pain is
observed behind a breastbone also. In majority patients so proof loss of weight takes place, that
even the protracted complex therapy and valuable feed does not provide addition to the deficit
of mass of body. There are typical signs also anaemia, hypo- or achlorhydria.
Reliable diagnostics of alkaline reflux-gastritis became possible after wide introduction
in clinical practice of endoscopic examination. In such patients during gastroscopy hyperemia
of mucous tunic of stomach is observed. It is often possible to observe reflux in the stomach of
duodenum content. During histological examination of biopsy material a chronic inflammatory
process, intestinal metaplasia, diminishment of mass of coating cells and area of hemorrhages
are found. All it testifies the deep degenerative changes in the mucous tunic of stomach. The
some authors underlines that the inflammatory changes, at least in the area of anastomosis, are
observed in most persons which carried the resection of stomach. So, endoscopic examination
can not be considered deciding in diagnostics. Even the diffuse inflammatory changes can take
place in absent of clinical symptoms and, opposite, in case with expressed clinical symptoms
the minimum changes of mucous tunic of stomach are sometimes observed.
Tactic and choice of treatment method
Conservative treatment of reflux-gastritis (sparing diet, antacides, enveloping
preparations), usually, is ineffective. Existent methods of surgical treatment, mainly, directed
on the removal of reflux of duodenum content to the stomach. Most popular is operation by the
Roux method. The some surgeons considers that distance from gastroenteroanastomosis to
interintestinal anastomosis must be 4550 cm.
Main reason of origin of peptic ulcer of anastomosis is leaving of the hyperacid state of
stomach mucous, even after the performed operation. Such phenomenon can be consequence of
many reasons: primary economy resection, wrong executed resection (when the mucous tunic
of pyloric part is abandoned in stump of duodenum or stomach), heightened tone of vagus
nerves and the Zollinger-Ellison syndrome.
Clinical management
Peptic ulcers, usually, arise up after operation during the first year. Typical signs are
pain, vomiting, weight loss, bleeding, penetration and perforation.
Pain is the basic symptom of peptic ulcer. Often it has the same character and
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localization, as well as at peptic ulcer. However often observe it moving to the left or in the
umbilical area. At first patients bind such feelings to the use of food, but then specify nightly
and hungry pain. It at first is halted after a food, but in course of time is become permanent,
unendurable, independent from food intake. It can increase during the flounces, the walk, can
irradiate in the back, thorax or shoulder.
During the objective examination of patients is often possible to expose on a stomach
hyperpigmentation from a hot-water bottle. During palpation to the left from epigastric area
near a umbilicus the painful and moderate muscles tension of abdominal wall is observed.
Sometimes is possible to palpate inflammatory infiltrate of different sizes. During the
examination of patients with a peptic ulcer the important role has determination of gastric
secretion against a background of histamine and insulin stimulation. There is a necessity also
examination of basal secretion. These preoperative examinations in most patients enable to set
the reason of hypersecretion which can be: 1) heightened tone of vagus nerves (positive
Hollander test); 2) economy resection of stomach, often in combination with the heightened
tone of vagus nerve (considerable increase of gastric secretion after histamine or pentagastrin
stimulation in combination with the positive Hollander test); 3) abandoned part of mucous
tunic of antral part of stomach (high basal secretion and small increase of secretion in reply to
histamine and insulin stimulator); 4) the Zollinger-Ellison syndrome.
Roentgenologic diagnostics of peptic ulcer, usually, is difficult, especially at shallow,
flat ulcers, bad mobility and insufficient function of anastomosis. A niche is the direct sign of a
similar pathology, indirect are the expressed inflammatory changes of mucous tunic of stump of
stomach and bowel, painful point in the projection of stump of stomach and anastomosis and
bad function of anastomosis. The deciding value in diagnostics has endoscopic examination.
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In the case of the considerably expressed spike process it is possible to execute trunk
subdiaphragmatic vagotomy, and in case of the insignificantly changed topography of this area
selective gastric vagotomy.
It is important to note, that stomach resected together with anastomosis, peptic ulcer and
eliminated area of empty bowel by one block.
Clinical management
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method is insufflation of air in a rectum. With it help on the screen it is possible to observe the
location and passing of fistula, and also, as a result, hit of air in a stomach, increase of it gas
bubble. Thus there can be the belch with an excrement smell.
The important role played the tests with dyes: at peroral introduction of methylene-blue
after the some time it found in excrement masses or, opposite, after an enema with
methylene-blue dye appears in a stomach.
Such complications appear through considerable time after operation (from 1 month to
one year). Disturbances of function of gastrointestinal anastomosis can be caused by the
reasons, related both to the technical mistakes during operation and with pathological
processes which arose up in the area of anastomosis.
Clinical management
The clinical picture of disturbance of anastomosis function, mainly, depends from the
degree of its closing. At complete it obstruction in patients arise up intensive vomiting, pain in
a epigastric area, the symptoms of dehydration and other similar signs appear. In other words,
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the clinic of stenosis of the stomach output develops. Clearly, that during incomplete
narrowing the clinical signs will be expressed less, and growth of them more slow.
Sometimes disturbance of evacuation can unite with the syndrome of afferent loop with a
inherent clinical picture. At the roentgenologic examination of such patients expansion of
stomach stump is exposed with the horizontal level of liquid and small gas bubble. Evacuation
from it is absent or acutely slow.
Removing of all stomach and exception of duodenum from the process of digestion of
food cause plural functional disturbances in an organism. Some of them meet already after the
resection of stomach (dumping-syndrome, hypoglycemic syndrome), other more inherent for
gastrectomy (anaemia, reflux- esophagitis and others like that).
Most patients, that carried gastrectomy, complain for a considerable physical weakness,
heightened fatigueability, sometimes is complete weakness, loss of activity and acute decline of
work capacity. Almost all of them notice bad sleep, worsening of memory and heightened
irritates. The appearance of patients is typical. Their skin insignificantly hyperpigmentated,
dry, its turgor reduced, noticeable atrophy of muscles. Can be the signs of chronic coronal
insufficiency in such patients, and in older-year persons is typical picture of stenocardia.
Except for it, can be hypotension, bradycardia and decline of voltage on EKG; during
auscultation deafness of tones is observed. From the side of the hormonal system the decline of
function of sexual glands is typical: in men declines of potency, in women disturbances
of menstrual cycle, early climax. Can be the signs of hypovitaminosis A, B, and decline of
resistibility of organism to chill, infectious diseases and tuberculosis.
The decline of mass of body is observed in 75 % patients, that carried gastrectomy. It is
conditioned by the decline of power value of food as a result of disturbance of digestion, bad
appetite and wrong diet. As a result of progressive hypoproteinemia there can be the
protein-free edemata.
Patients with such pathology must be under the permanent clinical supervision and 12
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times per year during a month to have the course of stationary prophylactic treatment which
includes psycho-, diet-, vitaminotherapy, correcting and replaceable therapy, and also
prophylaxis of anaemia.
Psychotherapy is especially indicated in the psychodepressive and asthenic states. It is
performed in combination with medicinal treatment. Hypnotic preparation, bromide,
tranquilizers are applied.
A food must be correctly prepared, without the protracted cooking. Patients need to feed
on 610 times per days by small portions.
Next to dietotherapy, it is constantly necessary to apply replaceable therapy
(Pancreatine, Pansinorm, Festal, Intestopan). In case of absent of esophagitis hydrochloric acid
is appointed. For the improvement of albuminous exchange anabolic hormones are applied.
In case of reflux-esophagitis there are indicated feeds by small portions with
predominance of liquid, ground, jelly-like foods, astringent, coating, anticholinergic
preparations. Between the receptions of food does not recommend to use a liquid. In case of
dysphagy appoints a sparing diet.
For the prophylaxis of iron-deficiency anaemia, that arises up in the first 23 years after
gastrectomy, important the indication of iron preparations.
For warnings and treatments of pernicious anaemia applied cyanocobalamin for 200 mcg
through a day and folic acid. Packed red blood cells is indicated in heavy case.
Differential diagnostics and clinical variants
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succeeded.
Four phases are distinguished in clinical passing of acute appendicitis: 1) epigastric; 2)
local symptoms; 3) calming down; 4) complications.
The disease begins with a sudden pain in the abdomen. It is localized in a right iliac
area, has moderate intensity, permanent character and not irradiate. With 70 % of patients the
pain arises in a epigastric area - it is an epigastric phase of acute appendicitis. In 24 hours it
moves to the place of appendix existance (the Kocher's symptom). At coughing patients mark
strengthening of pain in a right iliac area it is a positive cough symptom.
Together with it, nausea and vomiting that have reflex character can disturb a patient.
Often there is a delay of gases. The temperature of body of most patients rises, but high
temperature can occur rarely and, mainly, it is a low grade fever. The general condition of
patients gets worse only in case of growth of destructive changes in appendix.
During the examinationIt is possible to mark, that the right half of stomach falls behind
in the act of breathing, and a patient wants to lie down on a right side with bound leg.
Painfulness is the basic and decisive signs of acute appendicitis during the examination
by palpation in a right iliac area, tension of muscle of abdominal wall, positive symptoms of
peritoneum irritation. About 100 pain symptoms characteristic of acute appendicitis are known,
however only some of them have the real practical value.
The Blumberg's symptom. After gradual pressing by fingers on a front abdominal wall
from the place of pain quickly, but not acutely, the hand is taken away. Strengthening of pain is
considered as a positive symptom in that place. Obligatory here is tension of muscles of front
abdominal wall.
The Voskresenkyy Symptom. By a left hand the shirt of patient is drawn downward and
fixed on pubis. By the taps of 2-4 fingers of right hand epigastric area is pressed and during
exhalation of patient quickly and evenly the ha nd slides in the direction of right iliac area,
without taking the hand away. Thus there is an acute strengthening of pain.
The Bartomier's symptom is the increase of pain intensity during the palpation in right
iliac area of patient in position on the left side. At such pose an omentum and loops of thin
intestine is displaced to the left, and an appendix becomes accessible for palpation.
The Sitkovsky's symptom. A patient, that lies on left, feels the pain which arises or
increases in a right iliac area. The mechanism of intensification of pain is explained by
displacement of blind gut to the left, by drawing of mesentery of the inflamed appendix.
The Rovsing's symptom. By a left hand a sigmoid bowel is pressed to the back wall of
stomach. By a right hand by ballotting palpation a descending bowel is pressed. Appearance of
pain in a right iliac area is considered as a sign characteristic of appendicitis.
The Obrazcovs symptom. With the position of patient on the back by index and middle
fingers the right iliac area of most painful place is pressed and the patient is asked to heave up
the straightened right leg. At appendicitis pain increases acutely.
The Rozdolskyys symptom. At percussion there is painfulness in a right iliac area.
The general analysis of blood does not carry specific information, which would specify
the presence of acute appendicitis. However, much leukocytosis and change of formula to the
left in most cases can point to the present inflammatory process.
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Acute appendicitis in children. With children of infancy acute appendicitis can be seen
infrequently, but, quite often carries atipical character. All this is conditioned, mainly, by the
features of anatomy of appendix, insufficient of plastic properties of the peritoneum, short
omentum and high reactivity of child's organism. The inflammatory process in the appendix of
children quickly makes progress and during the first half of days from the beginning of disease
there can appear its destruction, even perforation. The child, more frequent than an adult,
suffers vomiting. Its general condition gets worse quickly, and already the positive symptoms of
irritation of peritoneum can show up during the first hours of a disease. The temperature
reaction is also expressed considerably acuter. In the blood test there is high leukocytosis. It is
necessary to remember, that during the examination of calmless children it is expedient to use a
chloral hydrate enema.
Acute appendicitis of the people of declining and old ages can be met not so often, as of
the persons of middle ages and youth. This contingent of patients is hospitalized to hospital
rather late: in 23 days from the beginning of a disease. Because of the promoted threshold of
pain sensitiveness, the intensity of pain in such patients is small, therefore they almost do not
fix attention on the epigastric phase of appendicitis. More frequent are nausea and vomiting,
and the temperature reaction is expressed poorly. Tension of muscles of abdominal wall is
absent or insignificant through old-age relaxation of muscles. But the symptoms of irritation of
peritoneum keep the diagnostic value with this group of patients. Thus, the sclerosis of vessels
of appendix results in its rapid numbness, initially-gangrenous appendicitis develops. Because
of such reasons the destructive forms of appendicitis prevail, often there is appendiceal
infiltrate.
With pregnant women both the bend of appendix and violation of its blood flow are
causes of the origin of appendicitis. Increased in sizes uterus causes such changes. It,
especially in the second half of pregnancy, displaces a blind gut together with an appendix
upwards, and an overdistension abdominal wall does not create adequate tension. It is needed
also to remember, that pregnant women periodically can have a moderate pain in the abdomen
and changes in the blood test. Together with that, psoas-symptom and the Bartomier's symptom
have a diagnostic value at pregnant women.
Clinical passing of acute appendicitis at the atipical placing (not in a right iliac area)
will differ from a classic vermiform appendix (Pic. 3.3.1).
Appendicitis at retrocecal and retroperitoneal location of appendiceal appendix can be
with 820 % patients. Thus an appendix can be placed both in a free abdominal cavity and
retroperitoneal. An atipical clinic arises, as a rule, at the retroperitoneal location. The patients
complain at pain in lumbus or above the wing of right ilium. There they mark painfulness
during palpation. Sometimes the pain irradiates to the pelvis and in the right thigh. The positive
symptom of Rozanov painfulness during palpation in the right Pti triangle is characteristic.
In transition of inflammatory process on an ureter and kidney in the urines analysis red
corpuscles can be found.
Appendicitis at the pelvic location of appendix can be met in 1130 % cases. In such
patients the pain is localized above the right Poupart's ligament and above pubis. At the very
low placing of appendix at the beginning of disease the reaction of muscles of front abdominal
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A subdiaphragmatic abscess develops at the high placing of appendix. The pain in the
lower parts of thorax and in a upper quarter of abcupula ofn to the right, that increases at deep
inhalationis except for the signs of intoxication, is characteristic of it. A patient, generally,
occupies semisitting position. Swelling in an epigastric area is observed in heavy cases,
smoothing and painful intercostal intervals. The abcupula ofn during palpation is soft, although
tension in the area of right hypochondrium is possible. Painfulness at pressure on bottom
(911) ribs is the early and permanent symptom of subdiaphragmatic abscess (the Krukovs
symptom).
Roentgenologically the right half of diaphragm can fall behind from left one while
breathing, and there is a present reactive exudate in the right pleura cavity. A gas bubble is
considered the roentgenologic sign of subdiaphragmatic abscess with the horizontal level of
liquid, which is placed under the diaphragm.
Interloop abscesses are not frequent complications of acute appendicitis. As well as all
abscesses of abdominal cavity, they pass the period of infiltrate and abscess formation with the
recreation of the proper clinic.
The poured festering peritonitis develops as a result of the timely unoperated
appendicitis. Diagnostics of this pathology does not cause difficulties.
Pylephlebitis is a complication of both appendicitis and after-operative period of
appendectomy.
The reason of this pathology is acute retrocecal appendicitis. At it development the
thrombophlebitis process from the veins of appendix, passes to the veins of bowels mesentery,
and then on to the portal vein. Patients complain at the expressed general weakness, pain in
right hypochondrium, high hectic temperature of body, fever and strong sweating. Patients are
adynamic, with expressed subicteritiousness of the scleras. During palpation painfulness is
observed in the right half of abcupula ofn and the symptoms of irritation of peritoneum are not
acutely expressed.
In case with rapid passing of disease the icterus appears, the liver is increased, kidney-
hepatic insufficiency makes progress, and patients die in 7-10 days from the beginning of
disease. At gradual subacute development of pathology the liver and spleen is increased in size,
and after the septic state of organism ascites arises.
Acute appendicitis is differentiated with the diseases which are accompanied by pain in
the abcupula ofn.
Food toxicoinfection. Complaints for pain in the epigastric area of the intermittent
character, nausea, vomitings and liquid emptying are the first signs of disease. The state of
patients progressively gets worse from the beginning. Next to that, it is succeeded to expose
that a patient used meal of poor quality. However, here patients do not have phase passing,
which is characteristic of acute appendicitis, and clear localization of pain. Defining the
symptoms of irritation of peritoneum is not succeeded, the peristalsis of intestine is, as a rule,
increased.
Acute pancreatitis. In anamnesis in patients with this pathology there is a gallstone
disease, violation of diet and use of alcohol. Their condition from the beginning of a disease is
heavy. Pain is considerably more intensive, than during appendicitis, and is concentrated in the
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upper half of abcupula ofn. Vomiting is frequent and does not bring to the recovery of patients.
Perforative peptic and duodenum ulcer. Diagnostic difficulties during this pathology
arise up only on occasion. They can be in patients with the covered perforation, when portion
of gastric juice flows out in an abdominal cavity and stays too long in the right iliac area, or in
case of atipical perforations. Taking it into account, it is needed to remember, that the pain in
the perforative ulcer is considerably more intensive in epigastric, instead of in the right iliac
area. On the survey roentgenogram of organs of abdominal cavity under the right cupula of
diaphragms free gases can be found.
The apoplexy of ovary more frequent is with young women and, as a rule, on 10-14 day
after menstruation. Pain appears suddenly and irradiate in the thigh and perineum. At the
beginning of disease there can be a collapse. However, the general condition of patients suffers
insignificantly. When not enough blood was passed in the abdominal cavity, all signs of
pathology of abdominal cavity organs calm down after some time. Signs, which are
characteristic of acute anaemia, appear at considerable hemorrhage. Abdomen more frequent is
soft and painful down, (positive Kulenkampff's symptom: acute pain during palpation of
stomach and absent tension of muscles of the front abdominal wall).
During paracentesis of back fornix the blood which does not convolve is got.
Extra-uterine pregnancy. A necessity to differentiate acute appendicitis with the
interrupted extra-uterine pregnancy arises, when during the examination the patient complains
at the pain only down in the stomack, more to the right. Taking it into account, it is needed to
remember, that at extra-uterine pregnancy a few days before there can be intermittent pain in
the lower part of the abdomen, sometimes excretions of coffee colour appear from vagina. In
anamnesis often there are the present gynaecological diseases, abortions and pathological
passing of pregnancy. For the clinical picture of such patient inherent sudden appearance of
intensive pain in lower part of the abdomen. Often there is a brief loss of consciousness.
During palpation considerable painfulness is localized lower, than at appendicitis, the
abdomen is soft, the positive Kulenkampff's symptom is determined. Violations of menstrual
cycle testify for pregnancy, characteristic changes are in milk glands, vagina and uterus. During
the vaginal examination it is sometimes possible to palpate increased tube of uterus. The
temperature of body more frequently is normal. If hemorrhage is small, the changes in the
blood test are not present. The convincing proof of the broken extra-uterine pregnancy is the
dark colour of blood, taken at punction of back fornix of vagina.
Acute cholecystitis. The high placing of vermiform appendix in the right half of
abdomen during its inflammation can cause the clinic somewhat similar to acute cholecystitis.
But unlike appendicitis, in patients with cholecystitis the pain is more intensive, has
cramp-like character, is localized in right hypochondrium and irradiate in the right shoulder
and shoulder-blade. Also the epigastric phase is absent. The attack of pain can arise after the
reception of spicy food and, is accompanied by nausea and frequent vomiting by bile. In
anamnesis patients often have information about a gallstone disease. During examination
intensive painfulness is observed in right hypochondrium, increased gall-bladder and positive
symptoms Murphy's and Ortner's.
Right-side kidney colic. For this disease tormina at the level of kidney and in lumbus is
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inherent, hematuria and dysuric signs which can take place at the irritation of ureter by the
inflamed appendix. Intensity of pain in kidney colic is one of the basic differences from acute
appendicitis. Pain at first appears in lumbus and irradiate downward after passing of ureter in
genital organs and front surface of the thigh. In diagnostics urogram survey is important, and if
necessary chromocystoscopy. Absence of function of right kidney to some extent allows to
eliminate the diagnosis of acute appendicitis.
As experience of surgeons of the whole world testifies, in acute appendicitis timely
operation is the unique effective method of treatment.
Access for appendectomy must provide implementation of operation. McBurney's
incision is typical.
When during operation the appendix without the special difficulties can be shown out in
a wound, antegrade appendectomy is executed. On clamps its mesentery is cut off and ligated.
Near the basis the appendix is ligated and cut. Stump is processed by solution of antiseptic and
peritonized by a purse-string suture (Pic. 3.3.2).
If only the basis of appendix is taken in a wound, and an apex is fixed in an abdominal
cavity, more rationally retrograde appendectomy is conducted (Pic. 3.3.3). Thus the appendix
near basis is cut between two ligatures. Stump is processed by antiseptic and peritonized.
According to it the appendix is removed in the direction from basis to the apex. According to
indication operation is concluded by draining of abdominal cavity (destructive appendicitis,
exudate in an abdominal cavity, capillary hemorrhage from the bed). In recent years the
laparoscopy methods of appendectomy are successfully performed.
In patients with appendiceal infiltrate it is necessary to perform conservative-temporizing
tactic. Taking it into account, bed rest is appointed, protective diet, cold on the area of
infiltrate, antibiotic therapy. According to resorption of infiltrate, in two months, planned
appendectomy is executed.
Treatment of appendiceal abscess must be only operative. Opening and drainage of
abscess, from retroperitoneal access, is performed. To delete here the appendix is not necessary,
and because of denger of bleeding, peritonitis and intestinal fistula even dangerously.
Intestinal obstruction is a complete or partial violation of passing of maintenance by the
intestinal truct.
The principal reasons of intestinal obstruction can be:
1) commissures of abdominal cavity after traumas, wounds, previous operations and
inflammatory diseases of organs of abdominal cavity and pelvis;
2) long mesentery of small intestine or colon, that predetermines considerable mobility
of their loops;
3) tumours of abdominal cavity and retroperitoneal space.
Such principal reasons can cause violation of passing of intestinal maintenance, disorder
of suction from the intestine and loss of plenty of electrolytes both from vomiting and in the
intestine cavity as a result of disorders of bloodflow in its wall.
The morphological signs of dynamic intestinal obstruction are: small thickening of wall
(at considerable paresis is thinning), friability of tissue (the bowel breaks easily) and presence
of liquid maintenance and gases in cavity of bowel. At mechanical obstruction it is always
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possible to expose the obstacle: strang, commissures, tumours, jammings of hernia, cicatricial
strictures, wrong entered drainages, tampons and others like that. In place of compression
strangulation is exposed. The bowel loop higher strangulation is extended, and distally
collapsed. In case of released invagination on small distance two strangulation furrows are
observed, and distally from the second ring cylinder expansion of bowel lumen is observed.
Beginning of clinical signs of intestinal obstruction is sudden in 12 hours after
taking the meal. The pain in the abdomen has the intermittent character and is met in all forms
of mechanical intestinal obstruction. However, some types of strangulated intestinal
obstruction (node formation, volvulus of thin and colons) can be accompanied by permanent
pain. It is needed to mark that at spike intestinal obstruction, invagination and obturation
cramp-like pain can be considered as pathognomic sign of disease. For paralytic intestinal
obstruction more frequent is inherent permanent pain which is accompanied by the progressive
swelling of abdomen. At spastic obstruction of intestine the pain is mainly acute, the abdomen
is not blown away, sometimes pulled in.
Nausea and vomiting are met in 7580 % patients with the heaviest forms of high level
of intestinal obstruction (node formation, volvulus of small intestine, spike obstruction). At
obturation obstruction and invagination they are observed not so often.
There is a characteristic thirst which can be considered as an early symptom. Besides,
the higher intestinal obstruction, the greater the thirst.
Swelling of abdomen, the delay of emptying and gases are observed in 8590% patients,
mainly, with the high forms of obstruction (volvulus of small intestine, spike intestinal
obstruction).
Together with that, for invagination emptying by liquid excrement with the admixtures of
mucus and blood are more characteristic.
In patients during palpation the soft abdomen is observed, sometimes with easy
resistance of front abdominal wall, and at percussion high tympanitis. At auscultation at the
beginning of disease increased peristaltic noises are present, then gradual fading of peristalsis
is positive (the Mondors symptom, noise of beginning, quietness of end).
There are other symptoms pathognomic for intestinal obstruction.
The Valas symptom is the limited elastic sausage-shaped formation.
The Sklarovs symptom is the noise of intestinal splash.
The Kywul's symptom is the clang above the exaggerated bowel.
The Schlange's symptom is the peristalsis of bowel, that arises after palpation of
abdomen.
The Spasokukotsky's symptom is noise of falling drop.
The Hochenegg's symptom incompletely closed anus in combination with balloon
expansion of ampoule of rectum.
At survey roentgenoscopy or -graphy of the abdominal cavity in the loops of bowels
liquids and gas are observed the Klojbers bowl (Pic. 3.3.4).
Strangulated obstruction. The ischemic component is the characteristic feature of this
form of intestinal obstruction, that is investigation of squeezing of mesentery vessels, which
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determines the dynamics of pathomorphologic changes and clinical signs of disease, and the
basic place among them belongs to the pain syndrome. Consequently, sudden appearance of
disease, acuteness of pain syndrome and ischemic disorders in the wall of bowel cause necrosis
changes of area of bowel pulling in a process. It is accompanied by the making progress
worsening of the patient condition and origin of endotoxicosis.
Obturation intestinal obstruction, unlike strangulated, pass not so quickly. In its clinical
picture on the first place there are the symptoms of violation of passage on the intestine
(protracted intermittent pain, flatulence), instead of symptoms of bowel destruction and
peritonitis.
For high, especially strangulated, intestinal obstruction progressive growth of clinical
signs of disease and violation of secretory function of intestine is inherent. Thus the volume of
circulatory blood diminishes, the level of haematocritis rises and leukocytosis grows. There are
also deep violations of homeostasis (hypoproteinemia, hypokalemia, hyponatremia, hypoxia
and others like that). In patients with low intestinal obstruction above-named signs are less
expressed, and their growth is related to more protracted passing of disease. Invagination of
bowel which can be characterized by the triad of characteristic signs is the special type of
intestinal obstruction with the signs of both obturation and strangulation: 1) periodicity of
appearance of the intermittent attacks of pain in the abdomen; 2) presence of elastic,
insignificantly painful, mobile formation in an abdominal cavity; 3) appearance of blood in the
excrement or its tracks (at rectal examination).
The special forms of obturation intestinal obstruction is the obstruction caused by
gall-stones. The last are got in the small intestine as a result of bedsore in the walls of
gall-bladder and bowel, that adjoins to it. It is needed to mention that intestinal obstruction can
be caused by concrement with considerably more small diameter than bowel lumen. The
mechanism of such phenomenon is related to irritating action of bilious acids on the bowel
wall. The last answers this action by a spasm with the dense wedging of stone in the bowel
lumen.
Development of intestinal obstruction caused by gall-stones the attack of colic and clinic
of acute cholecystitis precede always. Characteristically, that in the process of development of
disease the pain caused by acute cholecystitis calms down, whereupon the new pain
characteristic of other pathology intestinal obstruction appears.
Dynamic intestinal obstruction is divided into paralytic and spastic. Paralytic
obstruction often arises after different abdominal operations, inflammatory diseases of organs
of abdominal cavity, traumas and poisonings. The reason of spastic intestinal obstruction can
be the lead poisonings, low-quality meal, neuroses, hysterias, helminthiasis and others like
that. Clinic of dynamic intestinal obstruction is always variable in signs and depends on a
reason, that caused it. Disease is characterized by pain in the abdomen, delay of gases and
emptying. During palpation the abdomen is blown away, painful, however soft. To diagnose
this form of intestinal obstruction is not difficult, especially, if its etiology is known.
Hemostatic intestinal obstruction develops after embolism or thromboses of mesenteric
arteries and thromboses of veins, there can be mixed forms. Embolism of mesenteric arteries
arises in patients with heart diseases (mitral and aortic failings, heart attack of myocardium,
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warty endocarditis) and declared by damaging, mainly, upper mesentery arteries. Beginning of
disease, certainly, is acute, with nausea, sometimes vomiting. At first there is a picture of
acute abdominal ischemic syndrome, that is often accompanied by shock (frequent pulse,
decline of arterial and pulse pressure, death-damp, cyanosys of mucus membranes and
acrocyanosis). Patients become excitative, uneasy, occupy the forced knee-elbow position or lie
on the side with bound legs.
During the examination the abdomen keeps symmetry, abdominal wall is soft, the
increased peristalsis is heard from the first minutes during 12 hours (hypoxic stimulation of
peristalsis), which later goes out gradually (grave quiet). According to the phenomena of
intoxication peritonitis grow quickly. At the beginning of disease the delay of gases and
emptying is observed, later there is diarrhea with the admixtures of blood in an excrement.
When the last is heavy to set macroscopically, it is needed to explore scourage of intestine.
Intestinal obstruction must be differentiated with the acute diseases of organs of
abdominal cavity.
The perforation of gastroduodenal ulcer, as well as intestinal obstruction, passes acutely
with inherent to it by sudden intensive pain and tension of muscles of abdomen. However, in
patients with this pathology, unlike intestinal obstruction, the abdomen is not exaggerated, and
pulled in with wooden belly tension of muscles of front abdominal wall. There is also
characteristic ulcerous anamnesis. Roentgenologic and by percussion pneumoperitoneum is
observed. Certain difficulties in conducting of differential diagnostics of intestinal obstruction
can arise at atipical passing and in case of the covered perforations.
Acute pancreatitis almost always passes with the phenomena of dynamic intestinal
obstruction and symptoms of intoxication and repeated vomiting, with rapid growth. During
the examination in such patients, unlike intestinal obstruction, rigidity of abdominal wall and
painfulness is observed in the projections of pancreas and positive Korte's symptom and
Mayo-Robson's. The examination of diastase of urine and amylase of blood have important
value in establishment of diagnosis.
Acute cholecystitis. Unlike intestinal obstruction, patients with this pathology complain
for pain in right hypochondrium, that irradiate in the right shoulder-blade, shoulder and right
subclavian area. Difficulties can arise, when the symptoms of dynamic intestinal obstruction
appear on the basis of peritonitis.
The clinic of kidney colic in the signs and character of passing are similar to intestinal
obstruction, however, attacks of pain in the lumbar area with characteristic irradiation in
genital parts, the thigh and dysuric disorders help to set the correct diagnosis. Certain
difficulties in conducting of differential diagnostics also can arise in difficult patients, at
frequent vomiting which sometimes can be observed in patients with kidney colic.
During the first 1,52 hours after hospitalization of patient complex conservative
therapy which has the differential-diagnostic value and can be preoperative preparation is
conducted.
It is directed on warning of the complications related to pain shock, correction of
homeostasis and, simultaneously, is the attempt of liquidation of intestinal obstruction by
unoperative methods.
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1. The measures directed for the fight against abdominal pain shock include conducting
of neuroleptanalgesia, procaine paranephric block and introduction of spasmolytics. Patients
with the expressed pain syndrome and spastic intestinal obstruction positive effect can be
attained by epidural anaesthesia also.
2. Liquidation of hypovolemia with correction of electrolyte, carbohydrate and
albuminous exchanges is achieved by introduction of salt blood substitutes, 510 % solution
of glucose, gelatinol, albumen and plasma of blood. There are a few methods suitable for use in
the urgent surgery of calculation of amount of liquid necessary for liquidation of hypovolemia.
Most simple and accessible is a calculation by the values of hematocrit. If to consider 40 % for
the high bound of hematocrit norm, on each 5 % above this size it is needed to pour 1000 ml of
liquids.
3. Correction of hemodynamic indexes, microcirculation and disintoxication therapy is
achieved by intravenous infusion of Reopolyhlukine and Neohemodes.
4. Decompression of intestine truct is achieved by conducting of nasogastric drainage
and washing of stomach, and also conducting of siphon enema. It is needed to underline that
technically the correct conducting of siphon enema has the important value for the attempt of
liquidation of intestinal obstruction by conservative facilities, therefore this manipulation must
be conducted in presence of a doctor. For such enema the special device is used with the rectal
tip, by a PVC pipe by a diameter of 1,52,0 cm and watering-can of very thin material. A liquid
into the colon is brought to appearance of the pain feeling, then drop the watering-can below
the level of patient who lies. The passage of gases and excrement is looked after. As a rule, this
manipulation is to repeat repeatedly with the use of plenty of warm water (to 1520 and more
litres).
Liquidating of the intestinal obstruction by such conservative facilities is succeeded in
5060 % patients with mechanical intestinal
obstruction.
Patients with dynamic paralytic intestinal obstruction are expedient to stimulation of
peristalsis of intestine to be conducted, besides, necessarily after infusion therapy and
correction of hypovolemia. A lot of kinds of stimulation of intestine peristalsis are offered.
Most common of them are:
1) hypodermic introduction of 1,0 ml of 0,05 % solution of proserin; 2) through 10 min
60 ml intravenously stream of 10 % solution of chlorous sodium; 3) hypertensive enema.
Surgical treatment of intestinal obstruction must include such important moments:
1. According to middle laparotomy executed the novocaine blockade of mesentery of
small and large intestine and operative exploration of abdominal cavity organs during which the
reason of intestinal obstruction and expose viability of intestine is set.
The revision at small intestine obstruction begins from the Treitz' ligament to iliocecal
corner. At large intestine obstruction the hepatic, splenic and rectosigmoid parts are observed
intently. Absence of pathological processes after revision needs the examination of places of
cavity and jamming of internal hernia: internal inguinal and femoral rings, obturator openings,
pockets of the Treitz' ligament, Winslow's opening, diaphragm and periesophageal opening.
2. Liquidation of reasons of obstruction (scission of connection, that squeezes a bowel,
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needed to mark that the people of young ages mainly are ill by terminal ileitis.
The morphological changes are concentrated, mainly, in the terminal part of iliac bowel,
anal segment of rectum and appendix. Internal surface is hilly, thickened, swelling, deep ulcers
are intermittent with the unchanged areas of mucus. The serous tunic is covered by plural,
similar on tuberculosis, knots. Mesentery is sclerosed, regional lymphatic knots are
hyperplastic, of whiter-rose color. By the most characteristic microscopic sign of Crohns
disease is presence of unspecific sarcoid granuloma. Hyperplasia of lymphoid elements of
submucosal membrane and formation of fissured ulcers is observed also.
The Crohns disease begins from the insignificant signs as a general weakness, increase
of temperature of body, intermittent pain, that arises after the reception of meal, diarrhea
without some visible features or with the admixture of blood. As this process strikes the
terminal segment of small intestine, pain is concentrated in the right iliac area. Together with
that, at localization of pathological focus in a colon with an anal segment pain is concentrated
by its passing to the anal opening. A granuloma process takes place in the area of oesophagus,
abdomen or duodenum, pain can arise up in the area of lesions. With progress of disease on
endoscopy examination (proctosigmoidoscopy, fiberoptic colonoscopy, fiberoptic gastroscopy)
hyperemia and deep cracks of mucus membrane, ulcers, symptom of roadway and stenosis are
observed. At roentgenoscopy survey of organs of abdominal cavity in patients with the
perforation it is possible to expose pneumoperitoneum, and at contrasting sciagraphy
stenosis of initial part of stomach, presence of ulcers or granuloma in the oesophagus. The
examination of the passage on the small intestine enables to eliminate or confirm stenosis (Pic.
3.3.7). Irrigoscopy determines the defect of filling.
At acute passing of terminal ileitis, the pain appears acute in the right iliac area,
sometimes intermittent, accompanied by nausea, vomitings, emptying by a liquid excrement
with the admixture of blood or delay of emptying. During the examination of patient the
abdomen can be exaggerated, tension of muscles and positive symptoms of irritation of
peritoneum, high temperature is observed. In the general analysis of blood leukocytosis is
present with the change of leukocyte formula to the left. In such difficult situation often only
laparotomy helps to specify the diagnosis. The swollen segment of iliac bowel is thus observed
with increased mesentery lymphatic knots. The changed area of bowel can perforate in the free
abdominal cavity or penetrate in the contiguous loops of large or small intestine. It causes
forming of inflammatory infiltrate, and in future abscess formation. The unoperated
abscesses are always inclined to the independent opening in surrounding organs with
subsequent formation of fistula ducts.
The disease with the lesions of other parts of small and large intestine passes acutely
(granulomatous enteritis, colitis). By palpation in these patients painful infiltrate is exposed,
which by the character remind the clinic of invagination. Only the meticulous examination and
present data analysis enable to set correct diagnosis. At granulomatous proctitis the plural
cracks of mucus membrane without the signs of spasm of sphincter appear often, on the basis
of which afterwards there are ulcers, that badly granulate. The same changes can develop on
skin round the anal opening.
The chronic forms of disease often pass with insignificant symptoms. From the
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beginning of disease to establishment of diagnosis sometimes 12 years and more pass. Such
patients periodically complain for pain, diarrhea, weight loss, increase of body temperature,
nausea, vomitings and bleeding from a rectum.
Objectively in the abdominal cavity painful infiltrate is determined, and at laboratory
examination anaemia and hypoproteinemia.
Complications of the Crohns disease can be divided into local and general. Among
local, formations of fistula which arise on the front abdominal wall between the damaged
bowel and surrounding organs are most characteristic (ileoileal fistula, entero-entero,
enterovesical fistula). Sometimes fistulas are opened in the area of scars after the operations on
the lateral wall of abdomen or in the area of anus. Next to that, stenosis inflammatory infiltrate
of bowel can be transformed in acute or chronic intestinal obstruction. Some patients have the
obvious threat of perforation of the changed wall of bowel or intestinal bleeding. The
protracted passing of disease can be also complicated by malignization. The aphthous ulcers of
tongue, node erythema, arthritises and chronic lesionss of liver are general complications.
The Crohns disease must be differentiated with the unspecific ulcerous colitis and
cancer of colon.
An unspecific ulcerous colitis mainly initially strikes the mucus membrane of all colon.
The disease is accompanied by the excreta with the excrement of plenty of blood and mucus.
For Crohns disease languid passing of disease is characteristic. Acute passing of disease is
met considerably rarer, than chronic. The modern methods of endoscopic examination with the
biopsy of mucus membrane, which helps to specify diagnosis, are helpful in differential
diagnostics.
The cancer of colon is mostly accompanied by formation of deep ulcers and infiltrate.
However, for the cancer process slowly progressive passing without the periods of remission is
more inherent, thus the disease more frequently ends with the phenomena of intestinal
obstruction. At roentgenologic examination on the background the relatively unchanged colon
the lonely defect of filling is observed, and during colonoscopy thrusting out in the lumen
of bowel with an erosive surface or signs of disintegration. Histological examination of biopsy
material enables to expose cancer cells.
Conservative treatment. The diet of patient, generally, must be ordinary, except for
products with bad intestinal uptake. The medicine of the first row is 5-S (aminosalicylic
acid, sulfasalazone and glucocorticoid). The medicines of the second row are: 6-
mercaptopurine, azatiopurine and metronidazole. At diarrhea diphenoxilate is used 5 ml
peroral three times per days, loperamide 2 mg peroral 34 times per days, smecta 1 pack 3
times per days. At the expressed anaemia, to the considerable loss of weight, system
complications, relapse of disease after operation prednisolone is applied for 4060 mg
peroral every day during 12 weeks. After that its day's dose is diminished to 1020 mg during
46 weeks and, in the end, stopped. For patients which are irresponsive to steroid, asatioprine
is appointed (2 /) peroral. Metronidazole in a dose of 400 mg twice a days is used in the
case of granulomatous disease of perineum.
The presence of external and internal fistula, stenosis of bowel, perforation and recurrent
bleeding is an indication to operative treatment. The method of choice of operation is the
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patients with the ulcerous colitis and proctosigmoiditis in the period of process acutening.
Thus there are the subjective feelings with considerable expression of tenesmus and heartburns.
The chronic forms of unspecific ulcerous colitis both at total and at the left-side lesions
of colon, pass at the level of middle heavy degree. Frequency of emptying reaches to 510
times with mucus, blood and pain. Low grade fever, general weakness, nausea and loss of
appetite appear, and weight of body diminishes on 58 kg. Moderate anaemia is exposed in the
general analysis of blood, leukocytosis, increased ESR. Among the biochemical indexes of
blood hypoproteinemia and hypokalemia are marked. At endoscopic examination of colon
there is a considerable hyperemia and edema of mucus membrane, plural erosions, contact
bleeding and superficial ulcers.
The heavy form of unspecific ulcerous colitis is at the total lesions, especially with
acute, and also chronic recurrent passing of disease. The temperature of body in such patient
rises to 3940 , there is diarrhea (more than 10 times per days) with mucus, blood and pus,
vomitings, heavy intoxication grows, weight loss on 2530 kg, acutely expressed anaemia,
leukocytosis with the change of leukocyte formula to the left, considerable changes of
albuminous and electrolyte exchanges. At endoscopic examination of colon the blood is
exposed in its cavity, slid, pus, fibrin incrustation, often pseudopolypuses and almost complete
absence of mucus membrane. Roentgenologically some signs of complications of unspecific
ulcerous colitis are confirmed.
The complications are divided into local and general. Local complications are: profuse
intestinal bleeding, perforation, acute toxic dilatation, stenosis and malignization. To general
the following are included: damage of liver (hepatitis, cirrhosis), stomatitis, ulcer of lower
extremities, lesions of joints, eyes and skin.
Acute dysentery passes with bloody diarrheas, increased temperature of body, pain in the
abdomen. Bacteriological examination of excrement enables to expose dysenteric bacillus and
specify diagnosis.
Crohns disease (granulomatous colitis) is this local process, that begins from the
submucosal layer of bowel and distributes outside of walls with subsequent formation of
infiltrate, abscesses and fistula. Exposure of granulomas, and during microscopic examination
accumulation of lymphocytes, neutrophils, protoplasmatic cells and the Pyrohov-Lunghans'
cells are confirmed diagnosis.
The cancer of colon, in particular its enterocolitis and toxicoanemic forms, also often
can simulate an unspecific ulcerous colitis. Irrigoscopy, fiberoptic colonoscopy with biopsy
and subsequent histological examination almost always help to diagnose cancer process.
Treatment of unspecific ulcerous colitis, certainly, begins with application of
conservative facilities. Thus patients with easy and middle heavy forms must be under
protracted conservative treatment.
The leading role is taken to the parenteral feed of patients with heavy common
exhaustion (hydrolyzate of casein, aminopeptid, amynosol, vamin, alvesin, moriamin,
intralipid, lipofundin, glucose and others like that). Electrolytes (chloride of sodium, sulfate of
magnesium, chloride of potassium, panangin) and vitamins are entered (6, 12, , , and
others). Intensity and methods of conservative therapy always must depend on the phase of
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disease:
) moderately expressed passing of disease or proctitis corticosteroid enema and
sulfasalazone peroral;
) at heavy passing is parenteral introduction of liquids, nutritives, blood transfusion,
system use of corticosteroids, surgical treatment;
) at chronic passing is corticosteroids peroral, asatioprine, surgical treatment;
) at remission is preparations of 5-aminosalicylic acid peroral, examination for the
exception of cancer of colon.
The heavy form of passing of disease is absent of effect from the conducted conservative
treatment during two weeks and progress of process testifies to the necessity of surgical
treatment.
The conservative treatment must include antibacterial agent, antidiarrheal preparations,
steroid hormone.
A diet is considered an important factor in treatment of such patient (diet 4). Thus it
is recommended to take a meal to 6 times per days by small portions, withdrawing milk, fruit,
vegetables, wheat and rye bread from it. It is possible to appoint unfat meat and fish. Parenteral
introduction of vitamins B, , A, folic acid are helpful.
The basic antiinflammatory facilities are: sulfasalazopreparations (sulfasalazone,
salazopirine), salicylazosulfanilamide (salazosulfapyridine, salazodimetoxine) and
corticosteroids. Practice showed that sulfasalazone was one of the best antirecurrent facilities.
In patients with easy and middle heavy forms (distal or left-side lesions of colon)
sulfasalazone is applied in a dose about 5 g per days, and salazopiridazine and
salazodimetoxine about 2 g during that time. The course of treatment must proceed 12
months. For local steroid therapy prednisolone is used as powder in a dose 6080 mg or
hydrocortisone to 125 mg. It is dissolved in 100 ml physiologic saline and entered rectal
dropwise one time per days during 34 weeks.
At erosive proctitis and proctosigmoiditis 5 % (100,0 ml) solution of kolargole or extract
of camomile in microclyster is applied.
At the heavy forms of ulcerous colitis with fulminant passing and frequent vomiting the
treatment is needed to begin with intravenous introduction of 350380 mg hydrocortisone per
day. Thus procedures must proceed to appearance of positive clinical effect and realization of
possibility of transition on enteral treatment. Such period lasts on the average of 67 days. In
future it is recommended to adopt prednisolone peroral.
Sulfasalazopreparations is used in the same dose, as at the middle heavy form of flow of
disease. As in patients at this form of disease water-electrolyte and albuminous exchanges are
considerably violated, there are the expressed intoxication and anaemia, it is expedient to
conduct adequate therapy (intravenously - NaCl solution, glucose, chlorous potassium,
albumen, hemodes, protein, whole blood), and also hemodialysis and oxygenotherapy is used.
An absolute indication for surgical treatment is the presence of such complications of
unspecific ulcerous colitis as: perforation of wall of bowel, acute toxic dilatation, stenosis,
profuse bleeding and malignization. By the choice of method of operation at such pathology it
is needed to count colproctectomy with exteriorization of ileostomy.
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However, during the perforation of colon or toxic dilatation the operative treatment can
be limited to colectomy because proctectomy will be conducted as the next stage.
For patients with total ulcerous colitis with chronic heavy passing and without the
tendency to the visible improvement expedient radical operative treatment colproctectomy
with exteriorization of ileostomy. At such tactic postoperative lethality is diminished in 5-6
times, comparative with palliative operations which were conducted earlier.
In Western Europe and North America colorectal cancer (CRC) is one of most
widespread malignant neoplasm. Morbidity in these regions exceeds 20,0 on a 100000 of
population. In Japan, South America, Africa and countries of Asia this tumour is met rarer
(6,0:100000). There is an annual increase of frequency of cancer of colon approximately by 3
% in the developed countries. Morbidity of population of Ukraine by malignant neoplasm in
1995 was 16,3:100000.
Approximately 85 % of patients for CRC are of over 50 years old, with age frequency of
cancer is increased.
The nutrition by fat and albuminous food promotes the elimination to the intestine of
bile. Under the act of bacterial flora there is transformation of primary bilious acids to the
secondary, which has the carcinogenic and mutagenic activity. A meal with vitamins A, C and
that which contains plenty of vegetable cellulose has a braking carcinogenic influence.
The factors of risk which predetermine the origin of cancer of bowel are:
1) diffuse (family) poliposis, which is considered obligate precancer;
2) plural and single adenomatous polypuses;
3) chronic unspecific ulcerous colitis (anamnesis more than 10 years);
4) Crohns disease (granulomatous colitis).
Localization. A tumour is mostly lacalized in sigmoid (3540 % cases) and blind (2025
% cases) bowels.
Macroscopic forms. Exophytic tumours grow in the lumen of bowel as a polypus or knot
and at disintegration have the appearance of ulcer with a dense bottom that is swelling by edges
which come forward above the surface of the damaged mucus (saucer-shaped cancer). The
endophytic (infiltrate) cancer grows in walls of bowel. The tumour spreads on the perimeter of
bowel and engulfs it circular, causing narrowing of its lumen. In the right half of colon
exophytic tumours grow, as a rule, in left endophytic tumours.
Histological structure. Cancer of colon in 95 % cases has the structure of
adenocarcinoma. Metastasis takes place by lymphatic and hematogenic ways in regional
retroperitoneal lymphatic knots, liver, lungs.
The symptoms of cancer of colon are so numerous and various, that many authors group
them in such clinical forms: toxico-anemic, dyspeptic, enterocolitic, obturation,
pseudoinflammatory and tumular.
A toxico-anemic form shows up by indisposition, weakness, rapid fatigability, increase
of temperature, progressive anaemia. Characteristic for the cancer of right half of colon.
The enterocolitic form is characterized by symptom of complex intestinal disorders:
diarrhea, constipation, swelling, grumbling, pain.
The dyspeptic form is characterized by functional disorders of gastrointestinal truct.
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structure of acute pathology of organs of abdominal cavity this disease takes the third place
after acute appendicitis and cholecystitis. Women suffer from acute pancreatitis 33,5 times
more frequently than men.
Acute pancreatitis is a polyetiology disease. Its secondary forms, which arise on the
background of pathologies of bile-excreting system and duodenum are closely associated with
anatomic and functionally with pancreas, and are met in clinical practice.
Among the starting factors of origin of cholelithiasis disease (biliary pancreatitis)
abuse by an alcohol and food overloads (fat and irritating products), traumas of pancreas,
operating-room in particular, and also separate infectious diseases (parotitis, mononucleosis)
are most frequent, especially infection of bilious ways. However, in 1020 % of patients the
reason of acute pancreatitis remains unknown (cryptogenic form).
In the basis of such damages of pancreas and enzymic toxemia lies mainly activating of
pancreatic, and then the tissue enzymes (tripsin, lipase, amylase). Often the combination of the
broken outflow of pancreatic secret and promoted secretion takes place, which provokes
intraductal hypertension.
Among explanations of primary mechanisms of activating of pancreatic enzymes the
most value belongs to: a) theory of general duct with reflux of bile in the ducts of pancreas;
b) blockade of outflow of pancreatic juice with development of intraductal hypertension and
penetration of secret in interstitial tissue; in) violation of blood flow of pancreas (vasculitis,
thrombophlebitis and embolisms, cardiac insufficiency and others like that); g) toxic and
allergic damages of gland. The role of alcohol in such situations can be dual: stimulation of
secretion of pancreas and direct damaging action on its tissue.
The process of acute inflammation of pancreas consistently passes the stages of edema,
pancreatonecrosis and festering pancreatitis. In the stage of edema there is pancreas of
hyperemic, increased in volume, with the shallow hearths of necrosis or, as it is in swingeing
majority of cases, without them.
Pancreatonecrosis can pass with fatty or hemorrhagic character. In the first case, as a
rule, pancreas is increased, dense, cut whity-yellow hearths are selected to necrosis. Increase of
crimson-black pancreas with darkly-brown infiltrate on a cut is characteristic for hemorrhagic
pancreatonecrosis.
Dystrophy of parenchyma is exposed microscopically, up to necrosis, hemorrhages,
thromboses of vessels and signs of inflammatory infiltration.
The disease begins suddenly, after the surplus reception of rich spicy food and use of
alcohol. Pain, vomiting and phenomena of dynamic intestinal obstruction are considered the
most characteristic signs of acute pancreatitis.
A stomach-ache is permanent and so strong, that can result in shock, localized in an
epigastric area and left hypochondrium. Some patients feel pain in right hypochondrium with
irradiation in the back, loin or breastbone.
In a short period of time after appearance of pain there is a repeated strong vomiting, that
does not facilitate the state of patient.
In general vomiting is considered a frequent and characteristic symptom. It is repeated or
continuous and never brings facilitation. Vomit masses contain bile, as admixture, and at the
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Laparoscopy and laparocentesis are often used for a doubtful diagnosis or necessity of
taking away the exudation of abdominal cavity for biochemical or bacteriological examination.
Retrograde endoscopic cholangiopancreatography is used in case of mechanical icterus
and suspicion of choledocholithiasis. The last methods are invasive and can if it is necessary
transform from diagnostic to manipulation treatments: laparoscopic draining of abdominal
cavity at pancreatogenic peritonitis and endoscopic papillotomy at choledocholithiasis and
biliary pancreatitis.
Clinical passing of disease can be abortive, slowly or quickly progressive. At abortive
passing the process is limited to acute edema of pancreas with convalescence in 710 days.
Rapid progress is characteristic for pancreatonecrosis. In patients expressed toxemia,
impregnation by exudation of retroperitoneal cellulose and development of fermentative
hemorrhagic peritonitis can be seen. Strengthening of stomachache, continuous vomiting, proof
paresis of intestine, positive symptoms of irritation of peritoneum and growth of hemodynamic
violations are the clinical signs of necrosis of pancreas.
There is a formation of parapancreatic infiltrate at slow progress.
Among early complications of acute pancreatitis shock, peritonitis and acute cardiac,
pulmonary, hepatic and kidney insufficiency can be distinguished.
Before later complications it is needed to deliver the abscesses of pancreas,
subdiaphragmatic, interintestinal abscesses, pyogenic abscess omentum bag, phlegmons of
retroperitoneal space and erosive bleeding.
In future formations of pseudocysts, fistula of pancreas, intestinal fistula and
development of saccharine diabetes are possible.
Acute pancreatitis needs to be differentiated with the row of acute diseases of organs of
abdominal cavity.
Acute mechanical intestinal obstruction. In patients with this pathology pain is of the
alternated character and is accompanied by nausea, vomiting, delay of gases and emptying. It is
possible to see the Klojber bowls on the sciagram survey of organs of abdominal cavity.
Acute cholecystitis runs with characteristic localization of pain and muscular defense,
with presence of increased, painful gall-bladder or infiltrate in right hypochondrium. Often
acute (especially lately) pancreatitis develops on the background of gallstone disease (biliary
pancreatitis).
Thrombosis or embolism of mesenteric vessels. Both for pancreatitis and for the
thrombosis of mesenteric vessels great pain at soft abdomen (absence of defense muscles of
front abdominal wall), that precedes to development of peritonitis, is inherent. Yet from the
beginning the disease gains heavy character of passing. In anamnesis in such patients a heart
disease or heart attack of myocardium rheumatic is met. As a result of gangrene of intestine, the
symptoms of peritonitis appear very quickly and intoxication grows. The fragments of mucus
shell are found in flushing waters of intestine at the detailed examination, which have the
appearance of meat flushing.
A perforated gastric and duodenum ulcer is distinguished by the presence of dagger pain,
defense of abdominal wall, ulcerous anamnesis.
The conservative method is considered the basic one for treatment of acute pancreatitis,
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but in connection with that unsuccessful conservative treatment of patients with acute
pancreatitis can often put a question about the necessity of operation, therefore patients must
be in permanent surgical establishment. Thus acute pancreatitis with heavy passing is necessary
to be treated under the conditions of separation of intensive therapy.
Before conservative treatment hunger, bed rest, fight against pain and enzymic toxemia,
conducting of acid-base state, prophylaxis of festering infection and acute ulcers of digestive
duct are to be entered .
Patients stomach is washed by cold soda solution and a cold on an epigastric area and
left hypochondrium is used. Medicinal therapy is prescribed also: spasmolytics (papaverine,
platyphyllin, no-shparum, baralgine, atropine); inhibitor of protease (contrical, trasilol, gordox,
antagosan); cytostatic agent (5-fluorouracil, ftorafur). Positive action of inhibitor of protease is
marked only in the first days of disease which are subject to conditioned application of large
doses. Antibiotics of wide spectrum of action: a) tienam, which most effective in the
prophylaxis of festering pancreatitis, as is selected by pancreatic juice; b) cephalosporins
(kefzol, cefazoline); c) cefamizine (mefoxine).
Disintoxication therapy is conducted also (5 % but 10 % solutions of glucose, hemodes,
reopolyhlukine, polyhlukine, plasma of blood, only from 3 to 5 liters on days, in accordance
with a necessity).
For the improvement of rheological properties of blood heparine is prescribed (5 000
ODES every 4 hours).
If patients have the expressed pain syndrome and phenomena of general intoxication
during all pain period plus 48 hours (by Bakulev), hunger is used. Such mode lasts on the
average of 24 days. The parenteral feed of albuminous hydrolyzate is thus conducted, by the
mixtures of amino acid and fatty emulsion. Alkaline water of to 12 l. and albuminous-
carbohydrate diet are also appointed. Infusion therapy is complemented by plasma, by albumen,
hemodes, reopolyhlukine. The improvements of microcirculation in pancreas are achieved due
to introduction of reopolyhlukine, komplamine, trental and heparin 5000 ODES 6 times per
days under the control the indexes of the coagulation system of blood. Anticholinergic drug
(sulfate of atropine, methacin, platyphyllin), 2-histamin blocker (cimetidine, ranisan,
ranitidine, famotidine, omeprazol) are also applied. For the removal of pain: 1) sulfate of the
atropine 0,1 % 1 ml + promedol 2 % 1 ml + papaverine 2 % 2 ml + analgin 50 % 2
ml; 2) isotonic solution of chloride of sodium 500 ml + baralgine 5 ml +
diphenhydramine hydrochloride 1 % 1 ml + papaverine 2 % 2 ml + magnesium the
sulfate 25 % 5 ml + ascorbic acid 5 ml + lipoic acid 0,5 % 2 ml + novocaine 0,5 %
10 ml. are used. From the first days by a nasogastral probe the permanent aspiration of gastric
maintenance is conducted also. The Motility function of gastro-intestinal highway gets better at
application of cerucal or primperane. With the same purpose forced diuresis (maninil,
furosemide, aminophylline) is used on the background of intravenous introduction of plenty of
liquid.
At uneffective conservative treatment of patients with acute pancreatitis of middle weight
and heavy form it is expedient to apply surgical treatment.
Surgical treatment is carried out for patients with biliary pancreatitis (for a day long
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from the beginning of disease) in combination with the destructive forms of cholecystitis, at
complications of acute pancreatitis by peritonitis, abscess of omentum bag or phlegmon of
retroperitoneal cellulose.
Overhead-middle laparotomy, which allows to estimate the state of pancreas, bilious
ways and other organs of abdominal cavity, is the best access in this situation. In case of
destructive pancreatitis the possible use of lumbar laparotomy from left to right hypochondrium
through a mesogastric area is useful.
Cholecystectomy is executed at calculous cholecystitis, phlegmonous inflammation of
walls of gall-bladder and biliary pancreatitis. If there are more than 0,9 cm at expansion of
choledochus, presence of concrement, ointment-like bile in it, increase of concentration of
bilirubin in the whey of blood over 21 mmol/L, choledochuslithotomy is complemented by
external draining of choledochus. Information of lithiasis of general bilious duct is absent,
cholecystectomy in patients with acute pancreatitis is complemented by external draining of
choledochus, better by Pikovskyy method (through stump of cystic duct).
Transduodenal sphincteroplasty is shown at fixed concrement of large duodenal papilla
(Pic. 3.5.2), if they are diagnosed intraoperative, and also in the cases of papillotomy with
extraction of concrement when there is no possibility to execute endoscopic operation .
Omentopancreatopexy. After laparotomy and cutting of gastro-colon and gastro-
pancreatic ligament mobile part of large omentum through opening in gastro-colon ligament is
conducted and fixed by separate stitches to the peritoneum along the overhead and lower edges
of pancreas. Such operation needs to be considered rational at the expressed edema of pancreas
and presence of necrosis in it.
Abdominisation of pancreas. A cellulose round pancreas (along the lower and overhead
edges of body and tail) is infiltrated by solution of novocaine, after it parietal peritoneum is
cut. Under the body and tail glands free end of omentum is conducted and is bundled by a
gland. This operation is able to warn the hit of enzymes and products of disintegration in
retroperitoneal space.
Sequestrectomy is deleting of necrosis part of gland within the limits of nonviable
tissue. Operation is executed in a dull way.
Necrectomy (deleting of necrosis part of gland within the limits of healthy tissue) is
executed by an acute way: tissue of gland is cut on verge of necrosis and bleeding vessels are
carefully bandaged.
The resection of pancreas is deleting the part of organ with its transversal cutting within
the limits of the unchanged (ad ulus) tissue of gland. The resections of tail and body of
pancreas are distinguished (Pic. 3.5.3).
Pancreatectomy is a complete deleting of pancreas. Operative treatment is applied
infrequently. After the resection of pancreas adequate draining of its bed is very responsible.
The prognosis of disease depends on character of morphological changes of
parapancreatic to the cellulose in pancreas. The more difficult destructive changes, the worst
the prognosis.
Chronic pancreatitis is a progressive inflammation of pancreas with the periodic
acutening and remission, related to the process of autolysis, that shows up by pain, by violation
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of exocrine and endocrine functions of gland with the eventual result of fibrosis of organ and
high risk of malignization.
A gallstone disease is considered the most frequent reason of chronic pancreatitis.
Pathogenesis of cholangiogenic pancreatitis acted in pancreatic ducts (theory of general duct)
is in part of difficulty of outflow of pancreatic secret and reflux of infected bile or maintenance
of duodenum. Dyskinesia, spasms and stenosis of the Fater's papilla of duodenum are
instrumental in reflux. Bile or duodenal maintenance, that gets Wirsung's duct, activates the
enzymes of pancreas and is instrumental in the origin of its inflammation. Development of
pancreatitis potentiates infection. The last can penetrate pancreas not only due to reflux but
also in a hematogenic or lymphogenic way.
Thus, chronic pancreatitis develops as a result of functional violations of pancreas,
which with the flow of time pass to organic. The reasons of such violations are the attack of
acute pancreatitis suffered the in past, alcoholism, traumas of gland, pathology of its vessels,
gastroduodenal ulcers, gastritis or duodenostasis.
The morphological changes in pancreas at chronic pancreatitis are mainly taken to
development of passionately-degenerative processes and atrophy of parenchyma. Connecting
tissue in such cases develops both in the particles of gland and between them. In one case the
process has diffuse character, in the other it is limited. Thus pancreas becomes dense as a result
of excrescence of connecting tissue. It can be multiplied, taking shape of chronic hypertrophy
pancreatitis. Atrophy of gland comes in other cases, besides, not evenly in different parts.
The inflammatory edema of parenchyma is exposed in case of acutening of process.
Hemorrhages, fatty necrosis and pseudocysts are exposed on the surface of cut.
As passing of disease has cyclic character with the periodic changes of remission and
acuteening, the clinic of chronic pancreatitis depends on the phase of development of
inflammatory process. Violation of excretory and incretory functions of pancreas influences
polymorphic of symptoms which remission is especially determining in the phase.
Pain, dyspepsia phenomena and progressive loss of weight of body are the basic signs of
chronic pancreatitis. Besides, pain, is permanent, changes only its intensity, mainly in
epigastric region, sometimes on the left, burning, squeezing or prickly, comes forward the
unique symptom of disease, complaints about it precede other symptoms. In some patients the
pain feelings increase in lying position. Therefore patients occupy forced sitting position.
Intensity of pain can change throughout a day. Patients explain it by acceptance of rich, fried
food, boiled eggs, coffee. The last is the principal reason of acutening of process with acute
pain syndrome.
It is needed to mark, that occasionally passing of chronic pancreatitis can take hidden,
smooth shapes, with the moderately expressed pain syndrome or pain, that has atipical
character, for example, stenocardia. In such patients the symptoms related to violations of
exogenous function of pancreas come forward. They complain about absence of appetite,
nausea, belch, sometimes vomiting and diarrhea with putrid smell. Thirst, general weakness and
progressive loss of weight is observed also.
At palpation of abdomen pain does not arise, or it is quite insignificant. It is sometimes
succeeded to palpate horizontally placed pancreas as dense, moderately painful tension bar.
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The transmission of pulsation of aorta at palpation in a epigastric area count characteristic for
pathology.
During intervals between the attacks the feeling of patients remains satisfactory.
Development of saccharine diabetes is the basic sign of endocrine insufficiency,
hypoglycemia is rarer. The feature of this form of saccharine diabetes consists in the fact that it
shows up in a few years after the beginning of disease, runs easier and often carries latent
character. There can be hypoglycemia at the insufficient products of glucagon.
The syndrome of biliary hypertension with development of mechanical icterus and
cholangitis determining it can develop in some patients. The reasons for such cholestasis more
frequently are tubular stenosis of choledochus, choledocholithiasis or stenotic papillitis. There
is duodenal obstruction in some cases.
Important information about it can be given by the laboratory and instrumental methods
of examination.
Examination of excretory function of pancreas is based on establishment of level of
amylase in the whey of blood and urine. In acutening period of chronic pancreatitis this level of
amylase rises, the numbers of tripsin and lipase grow.
Coprologic examination. Macroscopic picture of excrement gets greyish color, in large
masses with unpleasant smell. Steatorrhea (increase of amount of neutral fat) and
creatorrhea are characteristic for it (a plenty of muscular fibres).
Examination of incretory function of pancreas includes: 1) determination of sugar in
blood and urine (characteristic is hyperglycemia and glycosuria); 2) radioimmunoassay of
hormones (insulin, -peptide and glucagon).
Sciagraphy survey of organs of abdominal cavity in two projections enables to expose
existent concrement in ducts and calcificat in parenchyma of pancreas.
Relaxation duodenography. Thus the development of horseshoe of duodenum and
change of relief of its mucus can be seen (Pic. 3.5.4).
Cholecystocholangiography with the purpose of diagnostics of gallstone disease and
second damaging of bilious ways is conducted.
Ultrasonic examination (sonography) is one of the basic methods of diagnostics. With
the help of symptoms of chronic pancreatitis it is possible to expose inequality of contours of
gland, increase of closeness of its parenchyma, increase or diminishment of sizes of organ,
expansion of pancreatic duct and wirsungolithiasis or presence of concrement of parenchyma.
Thus it is necessary to inspect gall-bladder, liver and bile-excreting ways for diagnostics of
gallstone disease and choledocholithiasis (Pic. 3.5.5).
Scintigraphy of pancreas. On early stages strengthening of scintigraphic picture is
observed, on later ones defects of accumulation to radionuclide (symptom of sieve or bee
honeycomb).
Computer tomography allows to expose the increase or diminishment of sizes of gland,
presence of calcificats, concrement, inequality of contours of organ, focuses or diffuse changes
of its structure (Pic. 3.5.6, Pic. 3.5.7).
Endoscopic retrograde cholangiopancreatography (ERCPG). Expansion of pancreatic
duct its deformation, wirsungolithiasis is marked, (Pic. 3.5.8).
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arises at once after the reception of meal, somewhat diminishes after application of
spasmolytics. For the disease considerable weight loss and waiver of meal in connection with
dread of pain attack can be characteristic. The basic method of examination, with a necessity
for differential diagnostics, celiacography is useful, which enables to expose oclusion of
abdominal trunk or its compression. During conducting of differential diagnostics with two last
nosologies it is necessary to state a possibility of origin of secondary pancreatitis.
Cancer of pancreas. Mechanical icterus and presence of Courvoisier's symptom are
considered the clearest and most important displays of cancer of head of pancreas, and
carcinoma of body and tail is a proof pain syndrome. For the cancer the damage of pancreas,
rapid progress of symptomatology are characteristic, and for chronic pancreatitis the protracted
passing with proper clinical symptomatology and changes which can be exposed by the
laboratory, roentgenologic and instrumental methods of examination are characteristic. The
most informative among methods of diagnostics of cancer of pancreas are sonography (echo-
producing formations in parenchyma of pancreas), computer tomography (tumor knots) and
puncture biopsy of gland with the histological examination (reliable diagnostics of cancer).
Heart attack of myocardium. In anamnesis of patients with the heart attack of
myocardium it is possible to expose pain behind breastbone, that arises at the physical activity
and emotional stress, it is irradiated in left shoulder-blade and left shoulder, unrelated with the
reception of meal and disappears as a result of action of coronarolytics. The typical changes of
ECG confirm the diagnosis of heart attack of myocardium. In addition, no violations of
external and incretions of pancreas are characteristic. The roentgenologic and instrumental
methods of examination can help in differential diagnostics.
Treatment is conducted in the phase of acutening of chronic pancreatitis, as well as at its
acute form. In the first days the bed rest and medical starvation is prescribed without limitation
of alkaline drink (mineral water). The fight against pain syndrome includes application of
anaesthetic preparations and spasmolytics (promedol, analgin, baralgine, papaverine,
no-shparum, platyphyllin). Preparation action is directed on the decline of pancreatic secretion
(atropine, methacin, sandostatine, dalargine, stilamine, somatostatine) or on oppression of
gastric secretion: 2-blockers (hystodil, cimetidine, hastrocepin, ranisan, tagamet and others
like that), antiacides (almagel, gastropan). Appoint, next to it, and antihistaminic preparations
(diphenhydramine hydrochloride, suprastine, fenkarol, tavegil). Antienzymic therapy is also
important: a) inhibitor of protease (contrical, trasilol, hordox, antagosan), the dose of which
must depend on the level of hyperenzymeemia; b) cytostatic agent (ftorafur, 5-fluorouracil); c)
chemical inhibitor of tripsin (aminocapronic acid, pentoxil). For the improvement of
microcirculation at this pathology heparin, reopolyhlucine and reohluman are applied. The
ponderable value is achieved by disintoxication therapy (hemodes, hluconeodes, enterodes).
With the purpose of parenteral feed 51040 % glucose with insulin, plasma, albumen,
alvesyn, polyamin and lipofundine are used. Normalization of agile function of organs of
digestion is achieved by settings of cerucal and reglan. In complex treatment it is necessary to
include vitamins (, 1, 6, 12) and anabolic hormones (retabolil, nerobol).
At calming down of the inflammatory phenomena a diet 5 is prescribed in pancreas
and conduct correction of excretory insufficiency of pancreas (festal, pansinorm,
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panccreosymin, digestal and others like that). With the purpose of stimulation of function of
pancreas it is possible to apply secretin.
Correction of endocrine insufficiency of pancreas. At development of the secondary
saccharine diabetes of easy degree a diet is recommended with limitation of carbohydrates,
bukarban, maninil and other peroral preparations, at middle and heavy degrees
insulinotherapy.
Physical therapy procedures. Except medical treatment it is possible to apply
inductothermy, microwave therapy (high frequency) and electro-stimulation of duodenum. For
spa treatment visiting of Morshyn, Husjatyn, Shidnytsja is recommend.
Indication to operation and its volume depend on the form of pancreatitis. Acutening of
chronic cholangiogenic pancreatitis at presence of gallstone disease must be examined as
indication to operation in first 24 hours since diseases beginning. Operative treatment is done
in case of:
1) calcinosis pancreas with the expressed pain syndrome;
2) violation of patency of duct of pancreas;
3) presence of cyst or fistula of resistance to conservative therapy during 24 months;
4) mechanical icterus on soil of tubular stenosis of distal part of general bilious duct;
5) compression and thrombosis of portal vein;
6) gallstone disease complicated by chronic pancreatitis;
7) ulcerous disease of stomach and duodenum complicated by secondary pancreatitis;
8) duodenostasis, complicated by chronic pancreatitis;
9) impossibility of exception to operation tumors or violations of arterial circulation of
blood of pancreas.
Cholecystectomy at presence of calculous cholecystitis and secondary pancreatitis, acute
destructive cholecystitis or hydropsy of gall-bladder.
Choledochuslithotomy is executed for patients with cholangiolithiasis: a) with the deaf
stitch of general bilious duct (use rarely); b) with its external draining for taking of infected
bile (cholangitis), decline of biliary hypertension (at the edema of head of pancreas); c) with
internal draining (at tubular stenosis of distal part of general bilious duct, acute expansion of
choledochus with the complete loss of elasticity of its wall (execute one of variants of
choledochoduodenostomy).
Papillosphincterotomy: a) execute transduodenal with papillosphincteroplasty; b)
endoscopic is recommended at the isolated or connected with choledocholithiasis stenosis of
large duodenal papilla, fixed concrement of large papilla of duodenum.
Wirsungoplasty is scission of plastic arts of narrow part or distal part of main pancreatic
duct (apply at patients with stricture of proximal part of duct by a slowness no more than 2
cm). Lately at the isolated stenosis of bee-entrance of main pancreatic duct endoscopic
wirsungotomy is executed.
Pancreatojejunostomy: a) longitudinal (it is executed at considerable expansion of
pancreatic duct); ) caudal (by Duval) with the resection of distal part of pancreas (Pic. 3.5.9).
Resection of pancreas: a) distal or caudal; b) distal subtotal; c) pancreatoduodenal
(PDR); e) total duodenopancreatectomy heads or bodies of gland (execute in case of fibrous-
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degenerative pancreatitis).
Oklusion of ducts of pancreas by polymeric connections (cianocrylat, prolamine,
neopren and others like that) results in atrophy of exocrine parenchyma, but keeps to the islet
of tissue.
Operations on the nervous system are used in case of the pain forms of chronic
indurative pancreatitis, resistant to conservative therapy, in default of rough morphological
changes of parenchyma, stroma of gland and deformation of main pancreatic duct: a) left-side
splanchnicectomy; b) bilateral pectoral splanchnicectomy and sympathectomy; c)
postganglionic neurotomy of pancreas.
Cyst of pancreas is a cavity, filled by liquid (pancreatic juice, exudation, pus), intimately
soldered with head, body or tail of organ, is limited by capsule, which has epithelium on
internal surface.
Pseudocyst (unreal cyst) is a cavity in pancreas which appears as a result of its
destruction, limited by capsule, that does not have epithelium on internal surface.
The reasons of pseudocysts are destructive pancreatitis, traumas of pancreas, oklusion of
Wirsung's duct by parasite, concrement, tumors, innate anomalies of development.
To the real cysts belong: innate (dysontogenetic) cysts which are anomalic in
development; acquired retention cysts which develop as a result of difficult outflow of
pancreatic juice, cystadenoma and cystadenocarcinoma (by mechanism the origins belong more
frequently to proliferative, sometimes degenerative cysts).
The mechanism of development of pseudocysts consists in the focus necrosis of gland,
difficult normal outflow of its secret, there is a destruction of walls of pancreatic ducts with
overrun of pancreatic juice gland that causes reactive inflammation of peritoneum of
surrounding organs which form the walls of pseudocyst.
Morphologically the cysts of pancreas are divided into: pseudocysts retention to the duct
are innate, single and multiple.
Pseudocysts are fresh and old. The internal surface of fresh pseudocyst is rough,
granulating, grey-red. The table of contents is alkaline, grey or with a brown tint. In an old
pseudocyst the wall is smooth and shiny, pale-grey. The table of contents is lighter. Epithelium
pseudocysts is absent. More frequently they are met in body and tail of gland and are not
connected with ducts.
Retention cysts connected with an obturated duct. The cavity has smooth, grey-white
surface, maintenance is transparent, watery or mucous-like. Innate cysts are mainly multiple
and shallow. A simple retention cyst differ from those that are always connected with the
anomalies of development of ducts and are unite with polycystosis buds and liver.
Rarely there are echinococcus cysts, which have a clear chitinous shell, liquid in cavity
and daughter's blisters. They are localized in the area of head of pancreas.
According to clinical passing pseudocysts are divided into acute, subacute and chronic.
According to weight of passing into simple (uncomplicated) and complicated.
In patients with the cystic damaging of pancreas there can be pain of different character
and intensity (dull, permanent, cramp-like and belting). It is localized more frequently in right
hypochondrium, epigastric area (cyst of head and body of gland), left hypochondrium (cyst of
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tail of pancreas). Pain is irradiated in the back, left shoulder-blade, shoulder and spine.
Dyspepsia violations are characteristic. Nausea, vomiting and belch are observed.
The syndrome of functional insufficiency of pancreas shows up by disorders of exocrine
and endocrine insufficiency and depends on the degree of damage of organ. The unsteady
emptying, replacement of diarrhea of constipation, steatorrhea and creatorrhea, development of
the second diabetes are marked.
Compression syndrome. Arises as a result of compression of neighbouring organs.
Clinically the compression of organs of gastro-intestinal highway shows up by complete or
partial obstruction of general bilious duct (mechanical icterus), vein (portal hypertension) gate,
splenic vein (splenomegaly).
During the examination patients with large cysts are marked by asymmetry of abdomen
in epigastric and mesogastric areas. At palpation of abdomen tumular formation of elastic
consistency with an even, immobile surface is found.
Sonography examination shows echo-free formation with a clear capsule, determines
localization and sizes of cyst (Pic. 3.5.10).
Contrasting roentgenologic examination of stomach and duodenum with the sulfate of
barium at the cyst of head of pancreas exposes moving of pyloric part of stomach upwards and
breeding of ,,horseshoe duodenum (at relaxation duodenography in the conditions of low
artificial blood pressure). If a cyst is localized in the area of body of gland, displacement of
stomach is marked forward and upwards or downward, rapprochement of its walls, moving of
duodenal transition and loops of thin bowel downward and to the right; at lateral projection the
distance between stomach and spine is increased. The cyst localized in the area of tail of gland,
displaces the stomach forward and upwards, to the left or to the right (Pic. 3.5.11).
Cholecystocholangiography exposes calculous cholecystitis and cholelithiasis.
Retrograde pancreatocholangiography exposes the changed and deformed, infrequently
extended pancreatic duct, occasionally there can be filling of cavity of cyst by the contrasting
matter.
Computer tomography shows accumulation of liquid limited by the capsule of different
closeness and thickness (Pic. 3.5.12).
Laboratory examinations exposes hyperamylasemia, steatorrhea and creatorrhea,
sometimes hyperglycemia and glycosuria.
Clinical passing of cysts of pancreas depends on their kind, localization, size, stage of
forming and complications.
Four stages of forming of pseudocyst are distinguished (.G. Karaguljan, 1972).
I stage (11,5 months last) in the center of inflammatory process the cavity of
disintegration, which takes surrounding tissue, appears in an omentum bag.
The II stage (23 months) is characterized by the beginning of forming of capsule of
pseudocyst. Cyst is magnificent, unformed, acute inflammatory phenomena calms down.
The III stage (312 months) is completion of forming of capsule of pseudocyst. Last
accretes with surrounding organs.
The IV stage (begins an in year from the origin of cyst) is a separated cyst. The cyst is
mobile, easily selected from connections with surrounding organs.
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Retention cysts arise at closing of lumen of pancreatic duct (concrement, sclerosis). The
internal surface of cyst is covered with epithelium. Pain syndrome, violation of exocrine
function of gland are characteristic.
Traumatic cysts belong to the pseudocysts with similar passing and clinic, as well as
inflammatory pseudocysts.
Parasite cysts (to echinococcus, cysticercotic) are met as casuistry. In such patients
Kaconi test and serological Weinberg's reaction are positive.
The variants of clinical passing of the real and unreal cysts depend on their
complications.
Perforation in free abdominal cavity. Clinic of the poured peritonitis is characteristic.
Tormina, positive symptoms of irritation of peritoneum, possible shock state as a result of
irritation of peritoneum by pancreatic juice arise.
Perforation in stomach, duodenum, small, rarer in large intestine is accompanied by
diminishment of cyst in sizes or complete disappearance, sometimes diarrhea appears.
Suppuration of maintenance of cyst is accompanied by pain which becomes more
intensive, temperature rises, leucocytosis grows.
The erosive bleeding appears suddenly and is accompanied by the symptoms of internal
bleeding (expressed general weakness, dizziness). The pallor of skin and mucus shells, sticky
death-damp, tachycardia and anemia are observed.
Mechanical icterus arises as a result of compression of cyst on the terminal part of
choledochus. The icterus of skin and mucus shells, acholic excrement, dark urine,
hyperbilirubinemia, increase of the AlT and AsT level are exposed.
Portal hypertension develops as a result of compression of portal vein. Ascites, varicose
expansion of veins of esophagus and stomach, moderate icterus are diagnosed.
Reactive exudation pleurisy more frequently arises in left pleura cavity, where
roentgenologic exudation is diagnosed with high maintenance of amylase.
At malignization the walls of cyst specific symptoms are absent, a diagnosis is set during
operation (surgical biopsy of cyst wall).
The cysts of pancreas are differentiated with the tumors of abdominal cavity and of
retroperitoneal space.
Cancer of pancreas. For the cancer tumor of pancreas syndrome of small signs
(discomfort in epigastric area, loss of appetite, general weakness), permanent dull pain,
unrelated with the reception and composition of meal, icterus (cancer of head of gland),
Courvoisier's symptom (increased, unpainfully gall-bladder) are characteristic. Inconstant pain
at cysts of pancreas is more frequently related to faults in a diet; in anamnesis destructive
pancreatitis, traumas of gland are carried. Sonography examination, retrograde
pancreatocholangiography and computer tomography help in establishment of diagnosis.
Tumors of retroperitoneal space are passed asymptomatic, clinic shows up by a
considerable compression on neighbouring organs. Nausea, vomit, chronic intestinal
obstruction, dysuric disorders arise. Clinic of cysts of pancreas, on the opposite, are expressed
on early stages. Pain, dyspepsia syndromes, syndrome of exocrine and endocrine insufficiency
of pancreas are characteristic. Pain is related to the reception of meal and alcohol.
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Aneurism of abdominal aorta. Dull, indefinite pain in abdomen which is unrelated with
the reception of meal, pulsation and pulsating formation in abdomen are characteristic,
auscultatory is systolic murmur. Aortography allows to confirm a diagnosis.
The cyst of mesentery of thin bowel has painless passing, at palpation it is mobile, easily
changes position in abdomen. The cysts of pancreas are practically immobile, pain, anamnesis
and laboratory information are characteristic.
The cyst of liver has protracted asymptomatic passing. Pain appears at infection of cyst.
For this pathology symptoms which take place at the cysts of pancreas are not typical (pain
related to the reception of rich food, alcohol, hyperamylasemia). Topic diagnostics is carried
out at ultrasonic examination, scintigraphy, computer tomography.
Conservative treatment. Treatment of acute or chronic pancreatitis is conducted in
accordance with principles. At the unfavorable dynamics of passing the diseases hunger with
the permanent sucking of gastric maintenance, parenteral feed and intravenous introduction of
liquids are appointed. Puncture of cysts is used through abdominal wall under sonography
control with aspiration of maintenance.
Surgical treatment is the method of choice of treatment of cysts of pancreas. The choice
of treatment method depends on the stage of forming of pancreas cysts.
On the I stage operation is not used, conservative treatment of pancreatitis is conducted.
On the II stage it is used at suppuration of pseudocyst (external draining of cyst). On the III
internal draining of cyst is used. More frequently cystojejunostomy on the eliminated loop of
thin bowel by Roux (Pic. 3.5.13), cystojejunostomy with entero-entero anastomosis by Brawn
and closing of afferent loop by Shalimov. Cystogastrostomy (Pic. 3.5.14) are executed and
cystoduodenostomy is now not applied because of possible complications (infection of cyst,
erosive bleeding). Marsupialization (opening and sewing down of cyst to the parietal
peritoneum and skin) is used infrequently (at suppuration of cyst is seriously patientsing with
the septic state). On the IV stage external and internal draining of cyst and radical operations
are applied: a) enucleation of cysts (executed very rarely); b) distal resection of pancreas with a
cyst.
The cancer of pancreas is a malignant tumor of epithelium tissue. Its specific gravity
among all malignant tumors makes 10 %. Greater part of patients with cancer of pancreas (to
80 %) is made by the persons of capable working age.
The origin of cancer of pancreas is related to character of nutrition: with the promoted
maintenance of albumens and fats in meal.
Shortage of vitamins, especially B and , harmful habits (abuse of alcohol, smoking),
presence of carcinogenic matters in food (nitrite, nitrates and others like that), tonsillectomy
suffered in the past also belong to etiologic factors. The cancer tumor of pancreas can arise on
the background of protracted period of chronic pancreatitis.
A cancer tumor is localized in the head. Rarer in the area of body or tail, rarer there is
a diffuse damage of pancreas.
A tumor has the appearance of a dense knot or conglomerate of knots of different sizes.
It resembles epithelium of pancreatic ducts or epithelium of acinous tissue, sometimes the
Langerhans' islet.
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Clinical management
Three variants of clinical passing of relapse of ulcer are distinguished after vagotomy: 1)
symptomless, when an ulcer is found during endoscopic examination; 2) recurrent with
protracted lucid space; 3) persisting ulcer with typical periodicity and seasonality of
exacerbation.
It is needed to underline that the clinical signs of this pathology during the relapse are
less expressed, than before operation, and absence of pain does not eliminate the presence of
ulcer. Sometimes bleeding can be first its sign. Complex examination, that includes
roentgenologic, endoscopic examination, study of gastric secretion and determination of
content of gastrin in the blood, allows not only to expose an ulcer but also, in most cases, to
set its reason. The interpretation the results of gastric secretion examination in such patients
are heavy. Taking into account it, it is needed to study both a basal secretion and secretion in
reply to introduction of insulin and pentagastrin, and also level of pepsin.
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Approximately in 35 % patients, mainly with the first two variants of clinical passing of
disease, the relapses of ulcers, are treated by ordinary methods of conservative therapy. Yet in
3040 % cicatrization of ulcers comes after application of preparations which stop a gastric
secretion (cimetidine, ranitidine150 mg for night). At other 1020 % patients, mainly with
the third variant of clinical passing, is necessary operative treatment.
The question of choice of the repeated operation in patients with the relapse of ulcer
after vagotomy still does not decided. Some surgeons execute revagotomy, trunk vagotomy with
drainage operation, revagotomy with antrectomy or resection of stomach. However much
majority from them in case of relapse ulcer after vagotomy performed antrectomy in
combination with trunk vagotomy.
Postvagotomy diarrhea
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Clinical management
The clinical signs of postvagotomy diarrhea are specific. Acute beginning are typical
patient often does not have time to reach to the rest room. Such suddenness repressing
operates on patients. As a result they are forced whole days to be at home, expecting the duty
attack. An excrement changes colorings as a result of breeding of pigment and becomes more
light.
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coagulation system. In patients with haemophilia A, for which typical deficit of antihemophilic
globulin, fresh blood transfusion is indicated, because in a banked blood a antihemophilic
globulin collapses during a few hours. At haemophilia B and are used dry and native plasma,
cryoprecipitate, banked blood, because factors IX, XI, which predetermine the form of
haemophilia, is kept in them long. ordinary hemostyptic preparation (vicasol, the vitamin,
chloride of calcium and others like that) does not give the effect. So, if form of haemophilia
does not established, the treatment is necessary to begin from fresh blood transfusion,
antihemophilic plasma and antihemophilic globulin transfusion.
Autoimmune thrombocytopenia, or idiopathic thrombocytopenic purpura, is
accompanied by the gastrointestinal bleeding and is arisen up in 0,52 % patients. Often
bloody vomiting and black excrement conditioned by swallowing of blood from a nose and
gums.
The disease shows up by plural hypodermic hemorrhages and hemorrhages into
submucous membrane. At girls and women the uterine bleeding is often observed.
Thrombocytopenia on very low numbers and it is the most pathognomonic sign of disease.
Typical acute increase of duration of bleeding, especially in the period of acute hemorrhage.
Fresh blood and thrombocyte mass transfusion is the most effective treatment in the case
of the gastrointestinal bleeding during autoimmune thrombocytopenia. Other hemostatic
preparations are indicated also. During operative treatment performed splenectomy. The
absolute indications to it are frequent and protracted bleeding, threat of hemorrhage in a brain.
The Schonlein-Henoch disease is hemorrhagic vasculitis, which caused by plural
microfocus microthrombovasculitis. The gastrointestinal bleeding at the Schonlein-Henoch
disease is observed in 0,51 % cases and accompanied with great pain in a epigastric area like
abdominal colic. For this disease typical presence of purpura which has the symmetric
location on the external surface of feet, legs, shoulders, buttocks, also joint syndrome with
pain and edema in large joints, kidney syndrome by the type of acute or chronic
glomerulonephritis. Women have the possible uterine bleeding. The intestinal bleeding can be
accompanied by the edema of wall of intestine, that results in invagination or perforation of
wall of bowel.
The basic and pathogenetic treatment method of patients is early application of heparin
with blood transfusion, introduction of heparinized blood under the control of blood
coagulation, which after adequate therapy must be increased in two times, comparative with a
norm. For a patient in the initial form of disease indicated introduction of antibiotics of wide
spectrum of action, hormones of adrenal glands cortex.
The diseases of the operated stomach (postgastrectomy and postvagotomy syndromes)
are the diseases which arise up after surgical treatment of peptic or duodenum ulcer or other
pathology of these organs.
Dumping syndrome is frequent complication of operations which are related to deleting
or disturbance of function of goalkeeper (resection of stomach, vagotomy with antrectomy,
vagotomy with drainage operations). It takes place in 1030 % patients.
The rapid receipt (dumping) is considered the starting mechanism of dumping syndrome.
During this concentrated, mainly carbohydrate, food passed from a stomach in an empty bowel.
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In the phase changes of motility of thin bowel during dumping syndrome important part
is acted by the hormones of thin bowel. In endocrine cells of APUD- on during
dumping-syndrome observed degranulation and presence of hormones of mothiline,
neurotensin and enteroglucagon.
The inadequate mechanical, chemical and osmotic irritation of mucous tunic of thin
bowel by chymus results for the acute increase of blood flow in a bowel. The last is
accompanied by the considerable redistribution of blood, especially in heavy case of dumping
syndrome : blood supply of head, lower extremities is diminishes, a blood flow in a liver is
multiplied.
The numeral examinations resulted in creation of osmotic theory the principal reason
of dumping syndrome is the decline of volume of circulatory plasma as a result of coming a
plenty of liquid into the lumen of thin bowel from an of circulatory system and intercellular
space.
For the clinical finding of dumping syndrome typical there is the origin of attacks of
general weakness during acceptance of food or during the first 1520 minutes after it. The
attack begins from feeling of plenitude in a epigastric area and is accompanied by the
unpleasant feeling of heat, that spills in the overhead half of trunk or on all body. Thus is
acutely multiplied sweating. Then there is a fatigue, appear somnolence, dizziness, noise in
ears, shaking of extremities and worsening of sight. These signs sometimes achieve such
intensity, that patients forced to lie down. Loss of consciousness could be in the first months
after operation. The attacks are accompanied by tachycardia, sometimes by the shortness of
breath, headache, paresthesia of upper and lower extremities, polyuria and vasomotor rhinitis.
At the end of attack or after it patients often notice grumbling in a stomach and diarrhea.
A milk or carbohydrate food is the most frequent provoking factor of dumping
syndrome. In a period between the attacks patients complain about rapid fatigueability,
weakening of memory, decline of working capacity, change of mood, irritates, apathy. During
roentgenologic examination after 515 minutes observed the increased evacuation of barium
mixture through anastomosis by a wide continuous stream, expansion of efferent loop and
rapid advancement of contrasting matter in the distal parts of thin bowel (Pic. 3.2.16).
By the expression of symptoms dumping syndrome is divided into three degrees of
weight:
I degree is easy. Patients have the periodic attacks of weakness with dizziness, nausea,
that appear after the use of carbohydrates and milk food and last no more than 1520 min.
During the attack a pulse becomes more frequent on 1015 per min., arterial pressure rises or
sometimes goes down on 1.3-2 KPa (1015 mm Hg), the volume of circulatory blood
diminishes on 200300 ml. The deficit of mass of body of patient does not exceed 5 kg. A
working capacity is well-kept. Medicinal and dietary treatment gives a good effect.
II degree middle weight. Attacks of weakness with dizziness, pain in the region of
heart, hyperhidrosis, diarrhea. Such signs last, usually, 2040 min., arise up after the use of
ordinary portions of some food. During such state a pulse becomes more frequent on 2030 per
min., arterial pressure is rises (sometimes goes down) on 22,7 KPa (1520 mm Hg), the
volume of circulatory blood diminishes on 300500 ml. The deficit of mass of body of patient
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achieves 510 kg. A working capacity is reduced. Conservative treatment sometimes has a
positive effect, but brief.
The III degree is hard. Patients are disturbed by the permanent, acutely expressed attacks
with the collaptoid state, by a fainting fit, by diarrhea, which do not depend on character and
amount of the accepted food and last about 1 hour. During the attack is multiplied frequency of
pulse on 2030 per 1 min; arterial pressure goes down on 2,74 KPa (2030 mm Hg), the
volume of circulatory blood diminishes more than on 500 ml. The deficit of mass of body
exceeds 10 kg. Patients, as a rule, are disabled. Conservative treatment is uneffective.
The problem of treatment of patients with dumping syndrome is not easy. Before the
surgical treatment, as a rule, must precede conservative. Patients with the disease of easy and
middle degrees respond to conservative treatment, mainly with an enough quite good effect. At
the heavy degree of disease such treatment more frequent serves as only preparation to
operative treatment. If a patient does not give a consent for operation or at presence of contra-
indications to operative treatment (disease of heart, livers, kidneys), conservative therapy is
also applied. Such treatment must include dietotherapy, blood and plasma transfusion,
correction of metabolism, hormonal preparations, symptomatic therapy, electro-stimulation of
motility function of digestive tract.
The dietotherapy: using of high-calorie, various food rich in squirrel, by vitamins, by
mineral salts, with normal content of fats and exception from the ration of carbohydrates which
are easily assimilation (limitation of sugar, sweet drinks, honey, jam, pastry wares, kissel and
fruit compotes). All it is needed to use by small portions (56 times per days). If the signs of
dumping syndrome appear after a food, such patients it is needed to lie down and be in
horizontal position not less than 1 hour. At the heavy degree of dumping syndrome patients
need to eat slowly, desirably lying on left. Such position creates the best terms for evacuation
of food from a stomach. Thus recommend also to repudiate from too hot and cold foods.
Medicinal treatment must include sedative, replaceable, antiserotonin, hormonal and
vitamin therapy. The indications to operative treatment of patients with dumping syndrome are:
heavy passing of disease, combination of dumping syndrome of middle degree with other
postgastrectomy syndromes (with the syndrome of efferent loop, hypoglycemic syndrome and
progressive exhaustion) and uneffective of conservative treatment of the dumping syndrome of
middle degree. Most methods of operative treatment of dumping syndrome are directed on
renewal of natural way of passing of food on a stomach and intestine, improvement of reservoir
function of stomach and providing of proportioning receipt of food in a thin bowel.
Depending on reasons and mechanisms of development of dumping syndrome there are
different methods of the repeated reconstructive operations. All of them can be divided into
four basic groups: I. Operations which slow evacuation from stump of stomach. II.
Redoudenization. III. Redoudenization with deceleration of evacuation from stump of stomach.
IV. Operations on a thin bowel and its nerves.
Basic stages of reconstructive operations: 1) disconnection of adhesions in an abdominal
cavity, releasing of gastrointestinal and interintestinal anastomosis and stump of duodenum; 2)
cutting or resection of efferent and afferent loops; 3) renewal of continuity of upper part of
digestive tract.
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The afferent loop consists of part of duodenum, that stopped behind after a resection,
area of empty bowel between a duodenojejunal fold and stump of stomach. The syndrome of
afferent loop can arise up after the resection of stomach after the Bilrhoth-II method. Violation
of evacuation from a afferent loop and vomiting by a bile are its basic signs.
Acute and chronic obstruction of afferent loop are distinguished. The reason of acute
obstruction is mechanical factors: postoperative commissure, volvulus, internal hernia,
invagination, jamming behind mesentery of loop of bowel and stenosis of anastomosis.
Frequency of origin of sharp obstruction of afferent loop hesitates within the limits of
0,52 %. The disease can arise up in any time after operation: in a few days or a few years.
Chronic obstruction of afferent loop (actually syndrome of afferent loop), as well as
acute, can arise up in any time after operation, however more often it develop after the resection
of stomach with gastroenteroanastomosis on a long loop, especially when operation is
performed without entero-enteroanastomosis by Brown.
The etiologic factors of syndrome of afferent loop are divided into two groups: 1)
mechanical (postoperative commissure, invagination, disturbance of evacuation on a afferent
loop, wrong location of afferent loop, very long afferent loop, fall of mucous tunic of afferent
loop into a stomach); 2) functional (hypertensive dyskinesia of bilious ways and duodenum,
damage and irritation of trunks of vagus nerves, hypotensive and spastic states of upper part of
digestive tract, heightened secretion of bile and juice of pancreas under act of secretin and
cholecystokinin).
For the clinical picture of acute obstruction typical is permanent, with a tendency to
strengthening, pain in a epigastric area or in right hypochondrium, nausea and vomiting. At
complete obstruction a bile in vomiting masses is absent. The general condition of patient
progressively gets worse, the temperature of body rises, leukocytosis grows, tachycardia grows.
At the objective examination painful and tension of muscles of abdominal wall is observed. In
a epigastric area it is often possible to palpate tumular lump. Possible cases, when the increase
of pressure in a bowel is passed on bilious ways and channels of pancreas. There can be pain
and icterus in such patients. There are necrosis and perforation of duodenum with development
of peritonitis during further progress of process. Acute obstruction of afferent loop in an early
postoperative period can be the reason of insufficiency of stump of duodenum also.
During the roentgenologic examination of organs of abdominal cavity it is visible round
form area of darkening and extended, filled by gas, bowels loop.
Patients, usually, complain for feeling of weight in a epigastric area and arching in right
hypochondrium, that arises in 1015 min. after acceptance of food and gradually grows.
Together with that, appear nausea, bitter taste in a mouth, heartburn. Then there is increasing
pain in a right to epigastric area. During this pain arises intensive, sometimes repeated vomiting
by a bile, after which the all symptoms disappear. It could be after certain kind of food (milk,
fats) or its big amount. Very rarely vomiting by bile unconnected with the feed. In heavy case
patients lose up to 1 liter of bile with vomiting masses. During the objective examination
observed subicteritiousness of the sclera, sign of dehydration of organism (decline of turgor of
skin, dry tongue, oliguria, concentrated urine). Emptying is irregular, grey color, with
considerable content of undigested fat and muscular fibres. Anaemia can develop at heavy
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passing of disease.
Distinguished easy, middle and heavy degrees of afferent loop syndrome. In patients with
the easy degree of disease vomiting is 12 times per a month, and insignificant regurgitation
arise up through 20 min 2 hour after a food, more frequent after the use of milk or sweet
food. At middle degree of afferent loop syndrome such attacks repeat 23 times per week,
patients are disturbed by the considerably expressed pain syndrome, and with vomiting up to
200300 ml of bile is lost. For a heavy degree the daily attacks of pain are typical, that is
accompanied by vomiting by a bile (up to 500 ml and more).
A roentgenologic examination of the patients with the afferent loop syndrome is
unspecific. Neither the passing of contrasting matter nor absence of filling of afferent loop can
be considered as pathognomic signs of syndrome of afferent loop.
Treatment of acute obstruction of afferent loop is mainly operative. Essence of it is the
removal of barriers of evacuation of content from an afferent loop. Adhesions are dissected,
volvulus is straightened, invagination or internal hernia is liquidated. For the improvement of
evacuation between afferent and efferent loops performes the entero-enteroanastomosis type
end-to-end or after the Roux method.
Conservative treatment of syndrome of afferent loop is ineffective and, mainly, is mean
the removal of hypoproteinemia and anaemia, spasmolytic preparations and vitamin are
appointed. With this purpose a blood, plasma and glucose is poured with insulin, a novocaine
lumbar blockade and blockade of neck-pectoral knot, washing of stomach is also done.
All operative methods of treatment of afferent loop syndrome can be divided into three
groups:
I. Operations, that will liquidate the bends of afferent loop or shorten it.
II. Drainage operations.
III. Reconstructive operations.
The operations of the first group, directed on the removal of bends and invagination of
afferent loop, can not be considered as radical. They need to be performed only at the grave
general condition of patient.
The widest application in clinical practice at the syndrome of afferent loop has the
operation offered by Roux (Pic. 3.2.17).
For the prophylaxis of afferent loop syndrome it is necessary to watch after correct
imposition of anastomosis during the resection of stomach: to use for the
gastroenteroanastomosis short loop of thin bowel (68 cm from the Treits ligament) for
imposition, to sew afferent loop to small curvature for creation of spur, to fix reliably stump of
stomach in peritoneum of transverse colon.
The origin of reflux after the distal resection of stomach is conditioned by some factors:
I. Traumatic factors: 1) traction of stomach during operation as reason of sprain of
ligament of proximal part of stomach and mobilization of large curvature of stomach; 2) cutting
of vessels of stomach and oblique muscles of it wall, in particular on small curvature; 3)
vagotomy, that is accompanied by cutting of phrenico-esophageal and gastrophrenic ligaments;
4) imposition of gastrointestinal anastomosis, especially direct gastroduodenoanastomosis by
Billroth-I, that results in smoothing of the Hisa corner; 5) frequent aspiration of gastric content
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23 times per a day). Reported also about successful application of cholesteramine (for 4 g 3
times per a day with the subsequent decline of dose to 4 g per days).
At heavy passing of postvagotomy diarrhea, that does not respond to conservative
treatment, it is needed to recommend operative treatment degastroenterostomy with
pyloroplasty. However, the type of drainage operation, as practice shows, does not influence on
frequency of diarrhea origin. In this connection, some surgeons with success applied the
inversion of the segment of thin bowel, located distal from the area of maximal absorption.
The cancer of stomach is a malignant formation, that develops from epithelium tissue of
mucus stomach. Among the tumours of organs of digestion this pathology takes first place and
is the most frequent, by the reason of death from malignant formations in many countries of
world. Frequency of it at the last 30 years considerably diminished in the countries of Western
Europe and North America, but yet remains high in Japan, China, countries of East Europe and
South America.
Etiology of cancer of stomach is unknown. It is known that, as other diseases of
gastrointestinal tract, a cancer damages a stomach. According to statistical information, it meets
approximately in 40 % of all localizations of cancer.
The factors of external environment has the substantial influencing on frequency of this
pathology. Above all things, feed, smoke food, salting, freezing of products and their
contamination of aflatoxin. Consider that a food factor can be: a) by a carcinogen; b) by the
solvent of carcinogens; c) to grow into a carcinogen in the process of digestion; d) to be
instrumental in action of carcinogens; e) not enough to neutralize carcinogens.
In the USA and countries of Western Europe frequency of cancer of stomach in 2 times
more large in the lower socio-economic groups of population. Some professional groups also
can it (miners, farmers, works of rubber, woodworking and asbestine industry). High
correlation communication is set between frequency of cancer of stomach and use of alcohol
and smoking. The value of genetic factors (heredity, blood type) is not led to.
The cancer of stomach arises up mainly in age 60 years and above, more frequent men
are ill.
Precancer. The precancer diseases of stomach are: a) chronic metaplastic disregenerator
gastritis conditioned by helicobacter pylori; b) villous polypuses of stomach and chronic
ulcers; c) nutritional anemia due to vitamin B12 deficiency (pernicious); d) resected stomach
concerning an ulcer.
The presence of precancer changes of mucous tunic of stomach has substantial influence
for frequency of stomach cancer. In those countries, where morbidity on the cancer of stomach
is higher, considerably more frequent chronic gastritises are diagnosed. Lately in etiology of
chronic gastritises take the important value helicbacter pylori. In Japan, where the cancer of
stomach is in 40 % cases is the reason of death, chronic gastritis appears in 80 % cases of
resected stomach, concerning a cancer.
Connection between polypuses, chronic gastric ulcers and possible it malignization
comes into question in literature during many decades. Most authors consider that polypuses
could be malignant differently. There are three histological types of polypuses: hyperplastic,
villous and hamartoma. There are hyperplastic polypuses, but it not malignant.
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frequency of tumours of distal parts of stomach. In 2 % cases meet the multicentric focuses of
growth, but from data of some authors, this percent could be multiplied in 10 times after
carefully histological inspection of the resected stomaches. This assertion is based on the
theory of the tumour field (D.I. Holovin, 1992). Especially this typically for patients which
has pernicious anaemia or chronic metaplastic disregenerative gastritis.
Metastasis is carried out by lymphogenic, hematogenic and implantation ways mostly.
Three (from data of some authors, four) pools of lymphogenic metastasis are selected: left
gastric (knots on passing of small curvature of stomach in a gastro-subgastric ligament and
pericardial); splenic (mainly, suprainfrapancreatic knots); hepatic (knots in a hepato-duodenal
ligament, right gastric omentum that lower pyloric groups, right gastric and suprapyloric
groups, pancreatoduodenal group).
However, the such way of lymphogenic metastasis is conditional and incomplete, as at
presence of block lymph flow passes retrograde metastasis, so called jumping metastases
which predetermine the origin of remote lymphogenic metastases in left supraclavicular lymph
nodes (Virhov metastasis) appear, in Lymph nodes of left axillar and inguinal areas, metastases
in a umbilicus.
Direct distribution: small and large omentum, esophagus and duodenum; liver and
diaphragm; pancreas, spleen, bile ducts.
Front wall of stomach: colon bowel and mesocolon; organs and tissues of retroperitoneal
space.
Lymphogenic metastasis: regional lymph nodes, remote lymph nodes, left supraclavicular
lymph node (Virhov), lymph node of axillar area (Irish); in a umbilicus (sisters Joseph).
Hematogenic metastasis: liver, lungs, bones, cerebrum.
Peritoneal metastasis: peritoneum, ovarium (the Krukenberg metastasis), Duglas space
(the Shnicler metastasis).
All authors which are engaged in the study of problem of cancer of stomach underline
absence or vagueness, no specificity of symptoms, especially on the early stages of disease. The
displays of cancer of stomach are very various and depend on localization of tumour, character
of its growth, morphological structure, distribution on contiguous organs and tissues. At
localization of tumour in a cardial part patient complains firstly, as a rule, for appearance of
dysphagy.
At careful, purposeful collection of anamnesis it is not succeeded to expose some other,
most early symptoms, which precedes to dysphagy and forces a patient to appeal to the doctor.
The unpleasant feeling behind a breastbone and feeling of unpassing of hard food on a
esophagus appear at the beginning of disease. After some time (as a rule, it is enough quickly,
during a few weeks, sometimes even days) a hard food does not pass (it is to wash down by
water or other liquid). This period can be during 13 months. Patients address a doctor exactly
in this period. Other symptoms appear to this time: regurgitation, pain behind a breastbone,
loss of mass of body, sometimes even exhaustion, the grey colouring of person, a skin is dry,
quickly grows general weakness. Sometimes patients address a doctor, when already with large
effort a spoon-meat passes only or complete stenosis came.
At localization of tumour in the antral part of stomach the first complaints, as a rule, are
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up to appearance of feeling of weight in epigastric region after the reception of food (even in a
two-bit), feeling of saturation (after the reception of glass of water), belch (at first it is simple
by air, and then with a smell). Feeling of weight grows for a day, patients forced to cause
vomiting. In the morning there can be vomiting by mucus with the admixtures of coffee-
grounds (so called cancer water). Patients loses weight (mass of body is lost), a weakness,
anaemia grows.
Tumours localized in the body of stomach show up either a pain syndrome or syndrome
of so called small signs (.I. Savitskyy, 1947), which is characterized by appearance of
amotivational general weakness, decline of capacity, rapid fatigueability, depression (by the
loss of interest to the environment), proof decline of appetite, gastric discomfort, making
progress weight lost.
The carried chronic diseases of stomach, for which typical seasonality, can influence on
the clinical sign of cancer of stomach. At appearance of gastric complaints out of season or
in absent of effect from the got therapy concerning the exacerbation of gastritis, ulcers
must guard a patient and doctor (symptom of precipice of gastric anamnesis).
In case of occurring of gastric symptoms first in persons in age 50 years and older it is
foremost necessary to eliminate the cancer of stomach.
In parts of patients cancer of stomach shows up only the metastatic damage of other
organs or complications. More than twenty so called atypical forms, which are characterized
by causeless anaemia, ascites, icterus, fever, edemata, hormonal disturbances, changes of
carbohydrate exchange, intestinal symptoms, are distinguished.
During the examination of patients with the cancer of stomach the pallor of skin covers
(at anaemia) is observed, in neglected case is frog stomach (sign of ascites).
During palpation determined painful in a epigastric area, sometimes possible to palpate
the tumour.
During auscultation of patients with pylorostenosis it is possible to define noise of
splash.
Laboratory information: hypochromic anaemia, neutrophilic leukocytosis, megascopic
ESR; during examination of gastric secretion: hypo- and anacidity and achlorhydria.
Gastroduodenoscopy enables to diagnose a tumour even smaller 5 mm and conduct an
aiming biopsy with histological examination of the taken material.
Roentgenoscopy and roentgenography examination of stomach. Basic signs: defect of
filling, local absence of peristalsis, malignant relief of mucous tunic (Pic. 3.2.18).
Ultrasonic examination: presence of metastases in a liver, pancreas.
Computer tomography allows to estimate the basic parameters of tumour, germination in
neighbouring organs and presence of metastases.
It is expedient to apply laparoscopy, mainly, for the decision of question about operable
of tumour (diagnostics of metastatic defeat of organs of abdominal cavity).
At an early cancer complaints depend on the previous gastric diseases. Therefore, on the
basis of clinical information, suspecting a tumour is possible only on occasion, when in
patients next to clear pain symptoms an appetite goes down, appear anaemia, general weakness.
In practice an early cancer is recognized at purposeful screening, and also in the process of
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jejunostoma (in case of the stenosis tumours of stomach output); 2) gastrostoma (Pic. 3.2.22)
in case of the cancer of cardial part of stomach with disturbance of patency; 3) edging of
bleeding vessels in case of complication of cancer by bleeding; 4) tamponade by omentum
during the perforation of tumour.
The value of radial therapy and chemotherapy, as independent methods of treatment of
cancer of stomach, is limited. Radial therapy is indicated for patients with cardial cancer as
preoperative course or as palliative treatment. Adjuvant mono- or polychemotherapy (mainly by
5-phtoruracil) is conducted in a postoperative period as combined therapy and in case of
dissemination of the tumours.
Prognosis. The indexes of five-year survival of patients with the cancer of stomach
hesitate within the limits of 530 %, but, from data of most authors, they do not exceed 10 %.
1. The Safety of Mesh Repair for Primary Inguinal Hernias: Results of 3019 Operations from Five
Diverse Surgical Sources; Shulman, AG, Amid, PK, Lichtenstein, IL; The American Surgeon; 1992;
58:255-7.
2. The Tension-Free Hernioplasty; Lichtenstein, IL, Shulman, AG, Amid, PK, Montllor, MM; Am J
Surg; 1989; 157:188-193.
3. Inguinal Hernia Repair: Biomaterials and Sutures Repair; Gilbert, AI; Perspectives in General
Surgery; 1991; 2:113-129.
4. The Mesh-Plug Hernioplasty; Robbins, AW, Rutkow, IM, Surgical Clinics of North America; 1993;
73:501-12.
5. Abdominal Wall Hernias; Wantz, GE, in Principles of Surgery; Schwartz et al.; 6th Edition; 1994;
McGraw-Hill, Inc.; New York.
6. The Shouldice Repair for Inguinal Hernia; Glassow, F; in Hernia; Nyhus, LM & Condon, RE;
Second Edition; 1978; J. B. Lippincott Co.; Philadelphia.
7. The Cause, Prevention, and Treatment of Recurrent Groin Hernia; Lichtenstein, IL, Shulman, AG,
Amid, PK; Surgical Clinics of North America; 1993;73:529-44.
8. "Tension-free" inguinal herniorrhaphy: A preliminary report on the "mesh plug" technique;
Rutkow, IM, Robbins, AW; Surgery; 1993; 114: 3-8.
9. Sutures Repair of Inguinal Hernia; Gilbert, AI; Am J Surg; 1992; 163: 331-5.
10. The "Plug" Repair of 1402 Recurrent Inguinal Hernias; 20 Year Experience; Shulman, AG, Amid,
PK, Lichtenstein, IL; Arch Surg; 1990; 125:265-7.
11. Inguinal and femoral hernioplasty utilizing polypropylene patch and plug; Amid, PK, Shulman, AG,
Lichtenstein, IL; Ann Ital Chir; 1993; 44: 119-25.
12. Improved Sutureless Technique--Advice to Experts; Gilbert, AI, Graham, MF; Problems in General
Surgery; 1995; 12:117-9.
13. Technical and Scientific Objections to Laparoscopic Herniorrhaphy; Gilbert, AI, Graham, MF;
Presented at 15th Anniversary Meeting of the Shouldice Hospital; June 16, 1995.
14. Laparoscopic mesh repair vs. open repair with and without mesh graft for inguinal hernia.
Preliminary study; Johansson, B, et al.; Surgical Endoscopy; 1997; 11: 170 (Abstract).
15. Laparoscopic TEP versus open Lichtenstein hernia Repair, Randomized Trial; Merello, J; Surgical
Endoscopy; 1997; 11: 545 (Abstract).
16. Moran Repair for Inguinal Hernias; Moran, RM, Brauns, J, Petrie, CR, Novak, BP, Johnsrud, JM,;
Am Surg; 1997: 63: 430-3.
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Abdominal pain (or stomach ache) is a common symptom associated with transient disorders or serious disease.
Diagnosing the cause of abdominal pain can be difficult, because many diseases can cause this symptom. Most
frequently the cause is benign and/or self-limiting, but more serious causes may require urgent intervention.
DIFFERENTIAL DIAGNOSIS
Gastrointestinal
GI tract
Inflammatory: gastroenteritis, appendicitis, gastritis, esophagitis, diverticulitis,Crohn's
disease, ulcerative colitis, microscopic colitis
Obstruction: hernia, intussusception, volvulus, post-surgical adhesions,tumours, superior
mesenteric artery syndrome, severe constipation,hemorrhoids
Vascular: embolism, thrombosis, hemorrhage, sickle cell disease, abdominal angina, blood vessel
compression (such as celiac artery compression syndrome), Postural orthostatic tachycardia syndrome
digestive: peptic ulcer, lactose intolerance, coeliac disease, food allergies
Glands
Bile system
Inflammatory: cholecystitis, cholangitis
Obstruction: cholelithiasis, tumours
Liver
Inflammatory: hepatitis, liver abscess
Pancreatic
Inflammatory: pancreatitis
Renal and urological
Inflammation: pyelonephritis, bladder infection
Obstruction: kidney stones, urolithiasis, Urinary retention, tumours
Vascular: left renal vein entrapment
Gynaecological or obstetric
Inflammatory: pelvic inflammatory disease
Mechanical: ovarian torsion
Endocrinological: menstruation, Mittelschmerz
Tumors: endometriosis, fibroids, ovarian cyst, ovarian cancer
Pregnancy: ruptured ectopic pregnancy, threatened abortion
Abdominal wall
muscle strain or trauma
muscular infection
neurogenic pain: herpes zoster, radiculitis in Lyme disease, abdominal cutaneous nerve entrapment
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shoulder)
Duodenal ulcer, diverticulitis
Appendicitis (starts here, after several times moves to lower right abdomen)
Upper right abdominal pain
Liver (caused by hepatomegaly due to fatty liver, hepatitis, or caused by liver cancer, abscess)
Gallbladder and biliary tract (gallstones, inflammation, roundworms)
Colon pain (below the area of liver - bowel obstruction, functional disorders, gas accumulation, spasm,
inflammation, colon cancer)
Upper left abdominal pain
Spleen pain (splenomegaly)
Pancreas
Colon pain (below the area of spleen - bowel obstruction, functional disorders, gas accumulation, spasm,
inflammation, colon cancer)
Middle abdominal pain (pain in the area around belly button)
Appendicitis (starts here)
Small intestine pain (inflammation, intestinal spasm, functional disorders)
Lower abdominal pain
Lower right abdominal pain
Cecum (intussusception, bowel obstruction)
Appendix point (Appendicitis location)
Lower left abdominal pain
Sigmoid colon (polyp), sigmoid volvulus, obstruction or gas accumulation)
Pelvic pain
bladder (cystitis, may secondary to diverticulum and bladder stone, bladder cancer)
pain in women (uterus, ovaries, fallopian tubes)
Right lumbago and back pain
liver pain (hepatomegaly)
right kidney pain (its location below the area of liver pain)
Left lumbago and back pain
less in spleen pain
left kidney pain
Low back pain
kidney pain (kidney stone, kidney cancer, hydronephrosis)
Ureteral stone pain
DIAGNOSTIC APPROACH
When a physician assesses a patient to determine the etiology and subsequent treatment for abdominal pain the patient's
history of the presenting complaint and physical examination should derive a diagnosis in over 90% of cases.
It is important also for a physician to remember that abdominal pain can be caused by problems outside the abdomen,
especially heart attacks and pneumonias which can occasionally present as abdominal pain.
Investigations that would aid diagnosis include
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Blood tests including full blood count, electrolytes, urea, creatinine, liver function tests, pregnancy
test, amylase and lipase.
Urinalysis
Imaging including erect chest X-ray and plain films of the abdomen
An electrocardiograph to rule out a heart attack which can occasionally present as abdominal pain
If diagnosis remains unclear after history, examination and basic investigations as above then more advanced
investigations may reveal a diagnosis. These as such would include
Computed Tomography of the abdomen/pelvis
Abdominal or pelvic ultrasound
Endoscopy and colonoscopy (not used for diagnosing acute pain)
ACUTE APPENDICITIS
Most frequent causes of acute appendicitis are festering microbes: intestinal stick, streptococcus, staphylococcus.
Moreover, microflora can be in cavity of appendix or get there by hematogenic way, and for women by lymphogenic
one.
Factors which promote the origin of appendicitis, are the following: a) change of reactivity of organism; b)
constipation and atony of intestine; c) twisting or bends of appendix; d) excrement stone in its cavity; e) thrombosis of
vessels of appendix and gangrene of wall as a substance of inflammatory process (special cases).
Pathomorphology
Simple (superficial) and destructive (phlegmonous, gangrenous primary and gangrenous secondary) appendicitises
which are morphological expressions of phases of acute inflammation that is completed by necrosis can be
distinguished.
In simple appendicitis the changes are observed, mainly, in the distant part of appendix. There are stasis in
capillaries and venule, edema and hemorrhages. Focus of festering inflammation of mucus membrane with the defect of
the epithelium covering is formed in 12 hours (primary affect of Ashoff). This characterizes acute superficial
appendicitis. The phlegmon of appendix develops to the end of the day. The organ increases, it serous tunic becomes
dimmed, sanguineous, stratifications of fibrin appear on its surface, and there is pus in cavity.
In gangrenous appendicitis the appendix is thickened, the its serous tunic is covered by dimmed fibrinogenous tape,
differentiating of the layer structure through destruction is not succeeded.
Classification
(by V.I. Kolesnikov)
1. Appendiceal colic.
2. Simple superficial appendicitis.
3. Destructive appendicitis:
) phlegmonous;
) gangrenous;
) perforated.
4. Complicated appendicitis:
) appendicular infiltrate;
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) appendicular abscess;
) diffuse purulent peritonitis.
5. Other complications of acute appendicitis (pylephlebitis, sepsis, retroperitoneal phlegmon, local abscesses of
abdominal cavity).
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almost do not fix attention on the epigastric phase of appendicitis. More frequent are nausea and vomiting, and the
temperature reaction is expressed poorly. Tension of muscles of abdominal wall is absent or insignificant through
old-age relaxation of muscles. But the symptoms of irritation of peritoneum keep the diagnostic value with this group of
patients. Thus, the sclerosis of vessels of appendix results in its rapid numbness, initially-gangrenous appendicitis
develops. Because of such reasons the destructive forms of appendicitis prevail, often there is appendiceal infiltrate.
With pregnant women both the bend of appendix and violation of its blood flow are causes of the origin of
appendicitis. Increased in sizes uterus causes such changes. It, especially in the second half of pregnancy, displaces a
blind gut together with an appendix upwards, and an overdistension abdominal wall does not create adequate tension. It
is needed also to remember, that pregnant women periodically can have a moderate pain in the abdomen and changes in
the blood test. Together with that, psoas-symptom and the Bartomier's symptom have a diagnostic value at pregnant
women.
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Clinical course of acute appendicitis at the atipical location (not in a right iliac area) will differ from a classic
vermiform appendix .
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Appendicitis at retrocecal and retroperitoneal location of appendiceal appendix can be with 820 % patients. Thus
an appendix can be placed both in a free abdominal cavity and retroperitoneal. An atypical clinic arises, as a rule, at the
retroperitoneal location. The patients complain at pain in lumbus or above the wing of right ileum. There they mark
painfulness during palpation. Sometimes the pain irradiates to the pelvis and in the right thigh. The positive symptom of
Rozanov painfulness during palpation in the right Pti triangle is characteristic. In transition of inflammatory process
on an ureter and kidney in the urines analysis red corpuscles can be found.
Appendicitis at the pelvic location of appendix can be met in 1130 % cases. In such patients the pain is localized
above the right Poupart's ligament and above pubis. At the very low placing of appendix at the beginning of disease the
reaction of muscles of front abdominal wall on an inflammatory process can be absent. With transition of inflammation
on an urinary bladder or rectum either the dysuric signs or diarrhea developes, mucus appears in an excrement.
Distribution of process on internal genital organs provokes signs characteristic of their inflammation.
Appendicitis at the medial placing of appendix. The appendix in patients with such pathology is located between
the loops of intestine, that is the large field of suction and irritation of peritoneum. At these anatomic features mesentery
is pulled in the inflammatory process, acute dynamic of the intestinal obstruction develops in such patients. The pain in
the abdomen is intensive, widespread, the expressed tension of muscles of abdominal wall develops, that together with
symptoms of the irritation of peritoneum specify the substantial threat of peritonitis development.
For the subhepatic location of appendix the pain is characteristic in right hypochondrium. During palpation
painfulness and tension of musclescan be marked.
Left-side appendicitis appears infrequently and, as a rule, in case of the reverse placing of all organs, however it can
occur at a mobile blind gut. In this situation all signs which characterize acute appendicitis will be exposed not on the
right, as usually, but on the left.
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Among complications of acute appendicitis most value have appendiceal infiltrates and abscesses.
Appendiceal infiltrate is the conglomerate of organs and tissue not densely accrete round the inflamed vermiform
appendix. It develops, certainly, on 35th day from the beginning of disease. Acute pain in the stomach calms down thus,
the general condition of a patient gets better. Dense, not mobile, painful, with unclear contours, formation is palpated in
the right iliac area. There are different sizes of infiltrate, sometimes it occupies all right iliac area. The stomach round
infiltrate during palpation is soft and unpainful.
At reverse development of infiltrate (when resorption comes) the general condition of a patient gets better, sleep and
appetite recommence, activity grows, the temperature of body and indexes of blood is normalized. Pain in the right iliac
area calms down, infiltrate diminishes in size. In this phase of infiltrate physiotherapeutic procedure is appointed,
warmth on the iliac area.
In two months after resorption of infiltrate appendectomy is conducted.
At abscessing of infiltrate the condition of a patient gets worse, the symptoms of acute appendicitis become more
expressed, the temperature of body, which in most cases gains hectic character, rises, the fever appears. Next to that, pain
in the right iliac area increases. Painful formation is felt there. In the blood test high leukocytosis is present with the
acutely expressed change of leukocyte formula to the left.
Local abscesses of abdominal cavity, mainly, develops as a result of the atypical placing of appendix or suppuration.
More frequent from other there are pelvic abscesses. Thus a patient is disturbed by pain beneath the abcupula, there are
dysuric disorders, diarrhea and tenesmus. The temperature of body rises to 38,039,0o, and rectal to considerably
higher numbers. In the blood test leukocytosis, change of formula of blood is fixed to the left.
During the rectal examination the weakened sphincter of anus is found. The front wall of rectum at first is only
painful, and then its overhanging is observed as dense painful infiltrate. Slide.
A subdiaphragmatic abscess develops at the high placing of appendix. The pain in the lower parts of thorax and in
a upper quarter of abcupula ofn to the right, that increases at deep inhalationis except for the signs of intoxication, is
characteristic of it. A patient, generally, occupies semisitting position. Swelling in an epigastric area is observed in heavy
cases, smoothing and painful intercostal intervals. The abcupula ofn during palpation is soft, although tension in the
area of right hypochondrium is possible. Painfulness at pressure on bottom (911) ribs is the early and permanent
symptom of subdiaphragmatic abscess (the Krukovs symptom).
Roentgenologically the right half of diaphragm can fall behind from left one while breathing, and there is a present
reactive exudate in the right pleura cavity. A gas bubble is considered the roentgenologic sign of subdiaphragmatic
abscess with the horizontal level of liquid, which is placed under the diaphragm.
Interloop abscesses are not frequent complications of acute appendicitis. As well as all abscesses of abdominal
cavity, they pass the period of infiltrate and abscess formation with the recreation of the proper clinic.
The poured festering peritonitis develops as a result of the timely unoperated appendicitis. Diagnostics of this
pathology does not cause difficulties.
Pylephlebitis is a complication of both appendicitis and after-operative period of appendectomy.
The reason of this pathology is acute retrocecal appendicitis. At it development the thrombophlebitis process from
the veins of appendix, passes to the veins of bowels mesentery, and then on to the portal vein. Patients complain at the
expressed general weakness, pain in right hypochondrium, high hectic temperature of body, fever and strong sweating.
Patients are adynamic, with expressed subicteritiousness of the scleras. During palpation painfulness is observed in the
right half of abcupula ofn and the symptoms of irritation of peritoneum are not acutely expressed.
In case with rapid passing of disease the icterus appears, the liver is increased, kidney-hepatic insufficiency makes
progress, and patients die in 7-10 days from the beginning of disease. At gradual subacute development of pathology the
liver and spleen is increased in size, and after the septic state of organism ascites arises.
Diagnostic program
1. Anamnesis information.
2. Information of objective examination.
3. General analysis of blood and urine.
4. Vaginal examination for women.
5. Rectal examination for men.
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Differential diagnostics
Acute appendicitis is differentiated with the diseases which are accompanied by pain in the abcupula ofn.
Food toxicoinfection. Complaints for pain in the epigastric area of the intermittent character, nausea, vomiting and
liquid emptying are the first signs of disease. The state of patients progressively gets worse from the beginning. Next to
that, it is succeeded to expose that a patient used meal of poor quality. However, here patients do not have phase passing,
which is characteristic of acute appendicitis, and clear localization of pain. Defining the symptoms of irritation of
peritoneum is not succeeded, the peristalsis of intestine is, as a rule, increased.
Acute pancreatitis. In anamnesis in patients with this pathology there is a gallstone disease, violation of diet and
use of alcohol. Their condition from the beginning of a disease is heavy. Pain is considerably more intensive, than during
appendicitis, and is concentrated in the upper half of abcupula ofn. Vomiting is frequent and does not bring to the
recovery of patients.
Perforative peptic and duodenum ulcer. Diagnostic difficulties during this pathology arise up only on occasion.
They can be in patients with the covered perforation, when portion of gastric juice flows out in an abdominal cavity and
stays too long in the right iliac area, or in case of atypical perforations. Taking it into account, it is needed to remember,
that the pain in the perforative ulcer is considerably more intensive in epigastric, instead of in the right iliac area. On the
survey roentgenogram of organs of abdominal cavity under the right cupula of diaphragms free gases can be found.
The apoplexy of ovary more frequent is with young women and, as a rule, on 10-14 day after menstruation. Pain
appears suddenly and irradiate in the thigh and perineum. At the beginning of disease there can be a collapse. However,
the general condition of patients suffers insignificantly. When not enough blood was passed in the abdominal cavity, all
signs of pathology of abdominal cavity organs calm down after some time. Signs, which are characteristic of acute
anemia, appear at considerable hemorrhage. Abdomen more frequent is soft and painful down, (positive Kulenkampff's
symptom: acute pain during palpation of stomach and absent tension of muscles of the front abdominal wall).
During paracentesis of back fornix the blood which does not convolve is got.
Extra-uterine pregnancy. A necessity to differentiate acute appendicitis with the interrupted extra-uterine
pregnancy arises, when during the examination the patient complains at the pain only down in the stomack, more to the
right. Taking it into account, it is needed to remember, that at extra-uterine pregnancy a few days before there can be
intermittent pain in the lower part of the abdomen, sometimes excretions of coffee colour appear from vagina. In
anamnesis often there are the present gynaecological diseases, abortions and pathological passing of pregnancy. For the
clinical picture of such patient inherent sudden appearance of intensive pain in lower part of the abdomen. Often there is
a brief loss of consciousness. During palpation considerable painfulness is localized lower, than at appendicitis, the
abdomen is soft, the positive Kulenkampff's symptom is determined. Violations of menstrual cycle testify for pregnancy,
characteristic changes are in milk glands, vagina and uterus. During the vaginal examination it is sometimes possible to
palpate increased tube of uterus. The temperature of body more frequently is normal. If hemorrhage is small, the changes
in the blood test are not present. The convincing proof of the broken extra-uterine pregnancy is the dark colour of blood,
taken at punction of back fornix of vagina.
Acute cholecystitis. The high placing of vermiform appendix in the right half of abdomen during its inflammation
can cause the clinic somewhat similar to acute cholecystitis. But unlike appendicitis, in patients with cholecystitis the
pain is more intensive, has cramp-like character, is localized in right hypochondrium and irradiate in the right shoulder
and shoulder-blade. Also the epigastric phase is absent. The attack of pain can arise after the reception of spicy food
and, is accompanied by nausea and frequent vomiting by bile. In anamnesis patients often have information about a
gallstone disease. During examination intensive painfulness is observed in right hypochondrium, increased gall-bladder
and positive symptoms Murphy's and Ortner's.
Right-side kidney colic. For this disease tormina at the level of kidney and in lumbus is inherent, hematuria and
dysuric signs which can take place at the irritation of ureter by the inflamed appendix. Intensity of pain in kidney colic is
one of the basic differences from acute appendicitis. Pain at first appears in lumbus and irradiate downward after passing
of ureter in genital organs and front surface of the thigh. In diagnostics urogram survey is important, and if necessary
chromocystoscopy. Absence of function of right kidney to some extent allows to eliminate the diagnosis of acute
appendicitis.
As experience of surgeons of the whole world testifies, in acute appendicitis timely operation is the unique effective
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method of treatment.
Access for appendectomy must provide implementation of operation. McBurney's incision is typical.
When during operation the appendix without the special difficulties can be shown out in a wound, antegrade
appendectomy is executed. On clamps its mesentery is cut off and ligated. Near the basis the appendix is ligated and cut.
Stump is processed by solution of antiseptic and peritonized by a purse-string suture .
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If only the basis of appendix is taken in a wound, and an apex is fixed in an abdominal cavity, more rationally
retrograde appendectomy is performed. Thus the appendix near basis is cut between two ligatures. Stump is processed by
antiseptic and peritonized. According to it the appendix is removed in the direction from basis to the apex.
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According to indication operation is concluded by draining of abdominal cavity (destructive appendicitis, exudate
in an abdominal cavity, capillary hemorrhage from the bed). In recent years the laparoscopy methods of appendectomy
are successfully performed.
In patients with appendiceal infiltrate it is necessary to perform conservative-temporizing tactic. Taking it into
account, bed rest is appointed, protective diet, cold on the area of infiltrate, antibiotic therapy. According to resorption
of infiltrate, in two months, planned appendectomy is executed.
Treatment of appendiceal abscess must be only operative. Opening and drainage of abscess, from retroperitoneal
access, is performed. To delete here the appendix is not necessary, and because of denger of bleeding, peritonitis and
intestinal fistula even dangerously.
Acute pancreatitis
The basis of disease of pancreas is degenerative-inflammatory processes which are considered to be acute pancreatiti
tissue by its own enzymes. In the structure of acute pathology of organs of abdominal cavity this disease takes the
appendicitis and cholecystitis. Women suffer from acute pancreatitis 33,5 times more frequently than men.
Anatomy(Fig.1;Fig.2; Fig.3.)
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Acute pancreatitis is a polyetiology disease. Its secondary forms, which arise on the background of pathologies of
bile-excreting system and duodenum are closely associated with anatomic and functionally with pancreas, and are met in
clinical practice.
Among the starting factors of origin of cholelithiasis disease (biliary pancreatitis) abuse by an alcohol and food
overloads (fat and irritating products), traumas of pancreas, operating-room in particular, and also separate infectious
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diseases (parotitis, mononucleosis) are most frequent, especially infection of bilious ways. However, in 1020 % of
patients the reason of acute pancreatitis remains unknown (cryptogenic form).
In the basis of such damages of pancreas and enzymic toxemia lies mainly activating of pancreatic, and then the
tissue enzymes (tripsin, lipase, amylase). Often the combination of the broken outflow of pancreatic secret and promoted
secretion takes place, which provokes intraductal hypertension.
Among explanations of primary mechanisms of activating of pancreatic enzymes the most value belongs to: a)
theory of general duct with reflux of bile in the ducts of pancreas; b) blockade of outflow of pancreatic juice with
development of intraductal hypertension and penetration of secret in interstitial tissue; in) violation of blood flow of
pancreas (vasculitis, thrombophlebitis and embolisms, cardiac insufficiency and others like that); g) toxic and allergic
damages of gland. The role of alcohol in such situations can be dual: stimulation of secretion of pancreas and direct
damaging action on its tissue.
Pathomorphology
The process of acute inflammation of pancreas consistently passes the stages of edema, pancreatonecrosis and
festering pancreatitis. In the stage of edema there is pancreas of hyperemic, increased in volume, with the shallow
hearths of necrosis or, as it is in swingeing majority of cases, without them.
Pancreatonecrosis can pass with fatty or hemorrhagic character. In the first case, as a rule, pancreas is increased,
dense, cut whity-yellow hearths are selected to necrosis. Increase of crimson-black pancreas with darkly-brown infiltrate
on a cut is characteristic for hemorrhagic pancreatonecrosis.
Dystrophy of parenchyma is exposed microscopically, up to necrosis, hemorrhages, thromboses of vessels and signs
of inflammatory infiltration.
Classification
(V All-russian convention of surgeons, 1978)
I. Clinico-anatomy forms:
1. Arching form.
2. Fatty pancreatonecrosis.
3. Hemorrhagic pancreatonecrosis.
II. Prevalence of necrosis:
1. Local (focus) damage of gland.
2. Subtotal damage of gland.
3. Total damage of gland.
III. Ran across: abortive, progressive.
IV. Periods of disease:
1. Period of hemodynamic violations and pancreatogenic shock.
2. Period of functional insufficiency of parenchymatous organs.
3. Period of degenerative and festering complications.
The disease begins suddenly, after the surplus reception of rich spicy food and use of alcohol. Pain, vomiting and
phenomena of dynamic intestinal obstruction are considered the most characteristic signs of acute pancreatitis.
A stomach-ache is permanent and so strong, that can result in shock, localized in an epigastric area and left
hypochondrium. Some patients feel pain in right hypochondrium with irradiation in the back, loin or breastbone. (Fig.4)
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In a short period of time after appearance of pain there is a repeated strong vomiting, that does not facilitate the state
of patient.
In general vomiting is considered a frequent and characteristic symptom. It is repeated or continuous and never
brings facilitation. Vomit masses contain bile, as admixture, and at the difficult form of acute pancreatitis remind
coffee-grounds.
Nausea, hiccup, belch and dryness in a mouth are attributed as less characteristic symptoms of this pathology.
During the examination the skin is pale, often subicterus. Some patients have cyanosys with a marble picture as a
result of violation of microcirculation. Later the component of respiratory insufficiency can join it. At progressive
general condition the patient quickly gets worse to passing of acute pancreatitis, intoxication grows. The skin takes
shelter with sticky sweat.
The temperature of body of patients at the beginning of disease can be normal. It rises at resorption of products of
autolysis tissue and development of inflammatory process in bilious ways.
The pulse in most cases is at first slow, then becomes frequent, notedly passing ahead the increase of temperature of
body.
Arterial pressure goes down.
The tongue in the first hour of disease is moist, assessed by white and grey raid. At vomiting by bile the raid has
yellow or greenish tint.
The abdominal is blown away, peristaltic noises are loosened. The signs of paresis of stomach and intestine
demonstrate early. They need to be included in the pathological process of mesentery root of bowel. At palpation
painfulness in an epigastric area and in right, and sometimes and in left, hypochondrium is marked. However, in spite of
great pain in stomach, it remains soft for a long time. A little later there is moderate tension or resistance of muscles of
front abdominal wall.
Poor local symptoms during heavy intoxication are characteristic for the early period of acute pancreatitis. Later
there are symptoms of irritation of peritoneum, and at percussion dulling is marked in lateral parts of abdominal as a
result of accumulation of liquid, and also the sign of aseptic phlegmon of retroperitoneal cellulose as slurred or edema of
lumbar area is seen. For diagnostics of acute pancreatitis there is the row of characteristic symptoms which have
different clinical value.
The Mondors symptom is violet spots on face and trunk.
The Lagermph's symptom is acute cyanosys of person.
The Halsted's Symptom is cyanosys of abdominal skin.
The Gray's symptom is cyanosys of lateral walls of abdomen.
The Kullen's symptom is the yellow colouring of skin near a belly-button.
The Korte's symptom is painful resistance as a lumbar bar in a epigastric area on 67 cm higher belly-button.
The Voskresynskyy's symptom is absence of pulsation of abdominal aorta in an epigastric area.
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The Mayo-Robson's symptom is feeling of pain at pressure by fingers in the left costal-vertebral corner.
The Rozdolskyy's symptom painfulness at percussion above pancreas.
The Blumberg's symptom in patients with acute pancreatitis more frequently is low-grade. Such feature of this
sign of irritation of peritoneum needs to be explained by character of localization of pathological process, mainly in
retroperitoneal spacious.
In clinical passing of pancreatonecrosis it is possible to select three periods (V.S. Saveljev, 1978).
The I period (hemodynamic violations and pancreatogenic shock) lasts during 23 days. Violation of central
hemodynamics, diminishment of volume of circulatory blood and disorders of microcirculation, which at first arise as a
result of angiospasm, are considered the most characteristic signs, and later as a result of joining of the intravascular
rolling up and laying of elements of blood.
The II period (insufficiency of parenchymatous organs) lasts from 3rd to the 7th day of disease. Violation of
functions of basic organs and systems, sign of cardio-vascular, hepatic and kidney insufficiency and growth of violations
of breathing are thus observed. In this period there is possible damaging of the central nervous system, which is erected
mainly to disorders of psyche, appearances of delirium and commas which in the eventual result are the main reasons of
patients death.
The III period (postnecrosis dystrophic and festering complications) comes in 12 weeks after the beginning of
disease. During it, on the background of progress of necrosis processes in pancreas, the regenerative changes develop,
there are parapancreatic infiltrate and cysts, cystic fibrosis of pancreas. Aseptic retroperitoneal phlegmon which
strengthens intoxication can also develop. There is festering pancreatitis at joining of infection. During this period such
complications, as erosive bleeding, internal or external fistula, retroperitoneal phlegmon, can develop in patients. (Fig.5)
From laboratory information leucocytosis which at the necrosis and hemorrhagic forms of pancreatitis sometimes
arrives at 25-30 10G/l, lymphopenia, change of leukocytic formula to the left and the increased ESR are characteristic.
Growth of activity of amylase of blood and urine is very often marked, and is the important sign of pancreatitis. For
estimation of the state of other organs maintenance of general albumen and its factions, glucose of blood, bilirubin, urea,
electrolytes, acid-base equilibrium (ABE), and also the state of blood coagulation are determined. It is necessary to mark
that the exposure of hypocalcemia is considered a bad predictive sign of heavy passing of acute pancreatitis.
Ultrasonic examination of gall-bladder and pancreas often specifies the increase of their sizes, bulge of walls and
presence or absence of concrement of gall-bladder and general bilious duct.
Computer tomography enables to describe in details the changes in pancreas and surrounding organs.
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At sciagraphy survey of organs of abdominal cavity gives a possibility to expose the unfolded horseshoe of
duodenum, pneumatization, expansion of transverse colon (the Gobia's symptom). On the 1st stage of diagnostics in the
plan of differential diagnosis of acute destructive pancreatitis with other diseases of abdominal cavity, diagnostics of
distribution of destructive damaging of different parts of pancreas and estimation of distribution of parapancreatitis is
possible only by the method of computer tomography which depending on clinico-laboratory signs and weight of
passing is needed to apply in a different period, and sometimes a few times in dynamics with interval of 45 days.
Laparoscopy and laparocentesis are often used for a doubtful diagnosis or necessity of taking away the exudation
of abdominal cavity for biochemical or bacteriological examination.
Retrograde endoscopic cholangiopancreatography is used in case of mechanical icterus and suspicion of
choledocholithiasis. The last methods are invasive and can if it is necessary transform from diagnostic to manipulation
treatments: laparoscopic draining of abdominal cavity at pancreatogenic peritonitis and endoscopic papillotomy at
choledocholithiasis and biliary pancreatitis.
Clinical passing of disease can be abortive, slowly or quickly progressive. At abortive passing the process is limited
to acute edema of pancreas with convalescence in 710 days.
Rapid progress is characteristic for pancreatonecrosis. In patients expressed toxemia, impregnation by exudation of
retroperitoneal cellulose and development of fermentative hemorrhagic peritonitis can be seen. Strengthening of
stomachache, continuous vomiting, proof paresis of intestine, positive symptoms of irritation of peritoneum and growth
of hemodynamic violations are the clinical signs of necrosis of pancreas.
There is a formation of parapancreatic infiltrate at slow progress.
Among early complications of acute pancreatitis shock, peritonitis and acute cardiac, pulmonary, hepatic and kidney
insufficiency can be distinguished.
Before later complications it is needed to deliver the abscesses of pancreas, subdiaphragmatic, interintestinal
abscesses, pyogenic abscess omentum bag, phlegmons of retroperitoneal space and erosive bleeding.
In future formations of pseudocysts, fistula of pancreas, intestinal fistula and development of saccharine diabetes
are possible.
Diagnosis program
Differential diagnostics
Acute pancreatitis needs to be differentiated with the row of acute diseases of organs of abdominal cavity.
Acute mechanical intestinal obstruction. In patients with this pathology pain is of the alternated character and is
accompanied by nausea, vomiting, delay of gases and emptying. It is possible to see the Klojber bowls on the sciagram
survey of organs of abdominal cavity.
Acute cholecystitis runs with characteristic localization of pain and muscular defense, with presence of increased,
painful gall-bladder or infiltrate in right hypochondrium. Often acute (especially lately) pancreatitis develops on the
background of gallstone disease (biliary pancreatitis).
Thrombosis or embolism of mesenteric vessels. Both for pancreatitis and for the thrombosis of mesenteric vessels
great pain at soft abdomen (absence of defense muscles of front abdominal wall), that precedes to development of
peritonitis, is inherent. Yet from the beginning the disease gains heavy character of passing. In anamnesis in such
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patients a heart disease or heart attack of myocardium rheumatic is met. As a result of gangrene of intestine, the
symptoms of peritonitis appear very quickly and intoxication grows. The fragments of mucus shell are found in flushing
waters of intestine at the detailed examination, which have the appearance of meat flushing.
A perforated gastric and duodenum ulcer is distinguished by the presence of dagger pain, defense of abdominal
wall, ulcerous anamnesis.
The conservative method is considered the basic one for treatment of acute pancreatitis, but in connection with that
unsuccessful conservative treatment of patients with acute pancreatitis can often put a question about the necessity of
operation, therefore patients must be in permanent surgical establishment. Thus acute pancreatitis with heavy passing is
necessary to be treated under the conditions of separation of intensive therapy.
Before conservative treatment hunger, bed rest, fight against pain and enzymic toxemia, conducting of acid-base
state, prophylaxis of festering infection and acute ulcers of digestive duct are to be entered .
Patients stomach is washed by cold soda solution and a cold on an epigastric area and left hypochondrium is used.
Medicinal therapy is prescribed also: spasmolytics (papaverine, platyphyllin, no-shparum, baralgine, atropine); inhibitor
of protease (contrical, trasilol, gordox, antagosan); cytostatic agent (5-fluorouracil, ftorafur). Positive action of inhibitor
of protease is marked only in the first days of disease which are subject to conditioned application of large doses.
Antibiotics of wide spectrum of action: a) tienam, which most effective in the prophylaxis of festering pancreatitis, as is
selected by pancreatic juice; b) cephalosporins (kefzol, cefazoline); c) cefamizine (mefoxine).
Disintoxication therapy is conducted also (5 % but 10 % solutions of glucose, hemodes, reopolyhlukine,
polyhlukine, plasma of blood, only from 3 to 5 liters on days, in accordance with a necessity).
For the improvement of rheological properties of blood heparine is prescribed (5 000 ODES every 4 hours).
If patients have the expressed pain syndrome and phenomena of general intoxication during all pain period plus 48
hours (by Bakulev), hunger is used. Such mode lasts on the average of 24 days. The parenteral feed of albuminous
hydrolyzate is thus conducted, by the mixtures of amino acid and fatty emulsion. Alkaline water of to 12 l. and
albuminous-carbohydrate diet are also appointed. Infusion therapy is complemented by plasma, by albumen, hemodes,
reopolyhlukine. The improvements of microcirculation in pancreas are achieved due to introduction of reopolyhlukine,
komplamine, trental and heparin 5000 ODES 6 times per days under the control the indexes of the coagulation system of
blood. Anticholinergic drug (sulfate of atropine, methacin, platyphyllin), 2-histamin blocker (cimetidine, ranisan,
ranitidine, famotidine, omeprazol) are also applied. For the removal of pain: 1) sulfate of the atropine 0,1 % 1 ml +
promedol 2 % 1 ml + papaverine 2 % 2 ml + analgin 50 % 2 ml; 2) isotonic solution of chloride of sodium
500 ml + baralgine 5 ml + diphenhydramine hydrochloride 1 % 1 ml + papaverine 2 % 2 ml + magnesium the
sulfate 25 % 5 ml + ascorbic acid 5 ml + lipoic acid 0,5 % 2 ml + novocaine 0,5 % 10 ml. are used. From
the first days by a nasogastral probe the permanent aspiration of gastric maintenance is conducted also. The Motility
function of gastro-intestinal highway gets better at application of cerucal or primperane. With the same purpose forced
diuresis (maninil, furosemide, aminophylline) is used on the background of intravenous introduction of plenty of liquid.
At uneffective conservative treatment of patients with acute pancreatitis of middle weight and heavy form it is
expedient to apply surgical treatment.
Surgical treatment is carried out for patients with biliary pancreatitis (for a day long from the beginning of disease)
in combination with the destructive forms of cholecystitis, at complications of acute pancreatitis by peritonitis, abscess
of omentum bag or phlegmon of retroperitoneal cellulose.
Overhead-middle laparotomy, which allows to estimate the state of pancreas, bilious ways and other organs of
abdominal cavity, is the best access in this situation. In case of destructive pancreatitis the possible use of lumbar
laparotomy from left to right hypochondrium through a mesogastric area is useful.
Cholecystectomy is executed at calculous cholecystitis, phlegmonous inflammation of walls of gall-bladder and
biliary pancreatitis. If there are more than 0,9 cm at expansion of choledochus, presence of concrement, ointment-like
bile in it, increase of concentration of bilirubin in the whey of blood over 21 mmol/L, choledochuslithotomy is
complemented by external draining of choledochus. Information of lithiasis of general bilious duct is absent,
cholecystectomy in patients with acute pancreatitis is complemented by external draining of choledochus, better by
Pikovskyy method (through stump of cystic duct).
Transduodenal sphincteroplasty(Fig.6) is shown at fixed concrement of large duodenal papilla, if they are diagnosed
intraoperative, and also in the cases of papillotomy with extraction of concrement when there is no possibility to execute
endoscopic operation.
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Omentopancreatopexy. After laparotomy and cutting of gastro-colon and gastro-pancreatic ligament mobile part of
large omentum through opening in gastro-colon ligament is conducted and fixed by separate stitches to the peritoneum
along the overhead and lower edges of pancreas. Such operation needs to be considered rational at the expressed edema
of pancreas and presence of necrosis in it.
Abdominisation of pancreas. A cellulose round pancreas (along the lower and overhead edges of body and tail) is
infiltrated by solution of novocaine, after it parietal peritoneum is cut. Under the body and tail glands free end of
omentum is conducted and is bundled by a gland. This operation is able to warn the hit of enzymes and products of
disintegration in retroperitoneal space.
Sequestrectomy is deleting of necrosis part of gland within the limits of nonviable tissue. Operation is executed in a
dull way.
Necrectomy (deleting of necrosis part of gland within the limits of healthy tissue) is executed by an acute way:
tissue of gland is cut on verge of necrosis and bleeding vessels are carefully bandaged.
The resection of pancreas is deleting the part of organ with its transversal cutting within the limits of the unchanged
(ad ulus) tissue of gland. The resections of tail and body of pancreas are distinguished.
Pancreatectomy is a complete deleting of pancreas. Operative treatment is applied infrequently. After the resection
of pancreas adequate draining of its bed is very responsible.
The prognosis of disease depends on character of morphological changes of parapancreatic to the cellulose in
pancreas. The more difficult destructive changes, the worst the prognosis.
INCARCERATED HERNIA
Incarcerated hernia is sudden pressing of hernia contents in a hernia orifice. Incarceration is the most
frequent and most dangerous complication of hernia diseases.
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Depending on mechanism, the elastic and fecal incarceration is distinguished. At the elastic incarceration,
after increasing intraabdominal pressure, one or a few organs relocated from an abdominal cavity to the hernia sack,
where it is compressed with following ischemia and necrosis in the area of hernia gate. At the fecal incarceration in
the intestinal loop which is in a hernia sack, plenty of excrement passed quickly. Proximal part of loop is
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overfilled, and distal is compressed in a hernia gate. So, arose its strangulation, as well as at the elastic
incarceration.
Most often the loop of bowel is incarcerated. Thus three parts are distinguished in it: proximal, distal loop,
central part. The heaviest pathological changes during incarceration takes place in a strangulated furrow in the
central part of the incarcerated bowel.
Pathomorphology
At incarcerated hernia an important role has all internal rings: inguinal, umbilical, weak places in a
diaphragm, orifice of the omental bursa, numeral and variant folds of peritoneum.
In the place of compressing of the bowels and mesentery, as a rule, it is possible to find a strangulation furrow.
If circulation of blood changes, the wall of bowel cyanotic, with hemorrhages and necrosis of a different size. The
loop of bowel which is located proximally the places of strangulation are extended, and distal loop mainly without
changes.
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The incarcerated hernia is divided into the complete and incomplete. The other types of incarceration is partial
(the Richters hernia) and retrograde. The incarcerated hernia can be without the destructive changes of hernia
contents and with the phlegmon of hernia sack.
Clinical management
The clinic of the incarcerated hernia depends on pulling in organ, character and duration of jamming. The
clinical signs of the incarcerated hernia can be divided into three groups: 1) local changes; 2) common signs; 3)
complication. From the most characteristic signs of local changes the most common is sharp pain, irreducible
hernia, tension of hernia sack that and negative symptom of the "cough push".
Pain sometimes is so intensive that causes pain shock. In the case of intestinal obstruction a pain is
attack-like. In case of occurring of peritonitis pain changes the character and becomes permanent.
It is necessary to mean that tensions of hernia sack and incarceration of the hernia, as signs of jamming, lose it
value, if hernia was irreducible.
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From other side, the isolation of hernia sack from an abdominal region during jamming is the reason of the
negative symptom of the "cough push".
The common signs at the incarcerated hernia has phase character. Nausea and vomits during first hours of
disease has reflex reason, and on 2nd and 3rd days has toxic reason, that is consequence of antiperistaltic and
reflux of intestinal contents to the stomach.
The temperature of body at first time is normal, and than rises, but usually low grade fever.
The clinic of acute intestinal obstruction and peritonitis develops at the protracted jamming of intestine. The
phlegmon of hernia sack can develop in the area of the hernia swelling.
There are different forms of incarceration of internal organs, and accordingly different clinical variants.
Retrograde incarceration. In such cases a hernia sack contains no less than two loops of intestine. But these
loops are damaged less, than loop which is in an abdominal cavity. At this variant of jamming peritonitis arose
quicker. So, surgeon during operation must always remember about the necessity of careful revision of the
incarcerated loops of bowel.
Parietal incarceration (the Richters hernia). Unlike retrograde, which has wide hernia gate, a similar
pathology arises in case of narrow hernia gate. In a hernia sack in such patients located part of bowel wall, opposite
it mesentery edge.
Thus, as a rule, patency of bowel is not broken. Such variant of jamming is dangerous, because there are no
evident clinical signs or some of them are quite absent and intestinal patency almost is always present. Necrosis of
bowel wall comes quickly and in 2-3 days the perforation with subsequent development of peritonitis begins after
jamming.
The Littres hernia. Jamming of Meckel's diverticulum can come at oblique inguinal hernia. Clinical signs of
this pathology reminds the parietal incarceration. Sometimes is possible to palpate dense, short, thick tension bar
in a hernia sack.
Incarceration at sliding hernia. It is observed at patients with inguinal hernia. At sliding hernia of colon, as a
rule, there is the fecal incarceration. A bowel is the external wall of hernia sack in such cases. About it is necessary
to remember during opening of hernia sack. Jammings of urinary bladder meet enough rarely, mainly at older-men
at oblique sliding hernia of inguinal channel. It is necessary to ask before the operation, whether a patient had
disorders of urination before jamming. Frequent urges, or, opposite, the reflex delay of urination is arose at the
beginning of jamming already, and in urine expose macro- or microhematuria. If during operation at opening of
hernia sack it medial wall has dense, doughy consistency, it is an urinary bladder.
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At the incarcerated hernia the contents of hernia sack can be also omentum, appendages of colon, internal
female genital organs. Sometimes combination of the incarcerated inguinal hernia with different pathological
changes of testicle and deferent duct can take place.
Rough manual reduction of the incarcerated hernia can bring to pseudoreduction. Then the local signs of the
incarcerated hernia disappear, and jamming of organs and its consequences is kept. There are five variants of the
pseudoreduction: 1) at multicompartment hernia sacks there is the possible moving of strangulated organs from one
chamber in other, that located more deep or in a preperitoneal adipose tissue; 2) separation and reduction of hernia
sack together with it content in an abdominal cavity or in a preperitoneal adipose tissue; 3) abruption of the neck
from other part of hernia sack and reduction it together with content in an abdominal cavity or in a preperitoneal
adipose tissue; 4) abruption of the neck from a hernia sack and from a parietal peritoneum with reduction of the
incarcerated organs in an abdominal cavity; 5) break of the incarcerated bowel at the rough reduction of hernia.
Untimely operative at the incarcerated hernia, usually, is complicated by the gangrene of bowel, peritonitis or
phlegmon of hernia sack. Such complications considerably worsen clinical status of patient and require other
surgical tactic.
Diagnosis program
1. Anamnesis examination.
2. Physical examination.
3. Blood analysis and urine analysis.
4. Digital investigation of the rectum.
5. Survey X-Ray of abdominal cavity organs.
Differential diagnostics
As experience shows, the incarcerated hernia we should differentiate with irreducible, which as a rule, is not
tense, positive symptom of the "cough push", painful on palpation. A patient complained for long duration of the
disease. The incarcerated hernia needs to be differentiated with coprostasis. In such patients disorder of bowel loop
patency, that is in a hernia sack, creates accumulation of excrement. Coprostasis mostly found at fecal hernia in
older people, that suffer from intractable constipation. Clinically it develops gradually and slowly. The hernia
swelling almost not painfully, some tense, a positive symptom of the "cough push". Beginning of coprostasis is
unconnected with physical tension. Application of cleansing siphon enema washed of excrement and liquidated
coprostasis.
Unreal jamming of hernia. In clinical practice there are often such situation, when during the acute surgical
diseases of organs of abdominal cavity free external abdominal hernia becomes irreducible, painfully and tense, and
looks like incarcerated. This is the unreal jamming of hernia, which can be observed at the acute surgical diseases
of organs of abdominal cavity, ascites. During examination of such patients it is necessary to remember, that at the
unreal jamming abdominal pain, vomiting, worsening of the general condition and signs of the intestine obstruction
come earlier, than changes in a hernia sack.
In addition, during the operation in patients with incarcerated hernia, it is needed to make sure, whether there
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is a strangulation furrow, or organ, that is in a hernia sack, fixed in a hernia gate. When these signs are absent, it is
possible to consider that jamming is unreal.
The incarcerated femoral hernia must be differentiated with inguinal lymphadenitis, by varicose expansion of
large hypodermic vein, varicose knot and their thrombophlebitis, tumor and abscess.
From such pathology without surgical procedure it is possible to differentiate only varicose expansion of veins
(varicose knot), for which the positive Valsalv test at horizontal position of patient with the leg heaved up a knot
is empty.
The incarcerated inguinal hernia needs to be differentiated also with hydrocele and orchiepididymitis, cyst of
deferent duct, cyst of round ligamentum of uterus, bartholinitis. Patients, who have with such diseases, a process
usually does not spread higher external ring of inguinal channel. Also, absence of testicle in scrotum can be
cryptorchiism sign.
The common clinical signs of the internal incarcerated hernia is abdominal pain and symptoms of the
intestinal obstruction. A final diagnosis is set during the operation.
The incarcerated hernia, regardless of time of its origin, localization and age of patient, must be operated on.
However, if a patient is hospitalized already with the expressed symptoms of intestinal obstruction, than should be
preoperative treatment. Such conservative therapy must be brief (11,5 hours), but always actively directed for
correction of violations of metabolism and prophylaxis of possible pulmonary and cardiovascular complications. It
is necessary also to conduct evacuation of the gastric contents and other preparatory procedures.
Patient with reduced hernia must be hospitalized and observed during 12 days. If a abdominal pain is
contained or is growing, the signs of peritonitis and intoxication appear, than performed urgent laparotomy and
necessary operation. If the symptoms of acute abdomen are not present, a patient examined and prepared for
elective operation. On oblique inguinal hernias, we should strengthen anterior wall of the inguinal channel. On
direct inguinal hernias, we should strengthen posterior wall of the inguinal channel. On recurrence hernias - we
should strengthen anterior and posterior wall of the inguinal channel.
Bassini repair. After extraction of the hernia sac, we are taking spermatic duct on holders. Between the
borders of transverse muscle, internal oblique muscle, transverse fascia and inguinal ligament interrupted sutures
placed. Except that, couples sutures placed between border of abdominal rectus muscle sheath and pubic bone
periosteum.
In such way, inguinal space closured and posterior wall strengthened. Spermatic duct placed on the
new-formed posterior wall of the inguinal channel. Over the spermatic duct aponeurosis restored by interrupted
sutures.
Girard in such kind of the operations propose to attach the edges of the internal oblique muscle and
transversal muscle to the inguinal ligament over the spermatic duct. The aponeurosis of the external oblique muscle
sutured by second layer of the suture. Excess of the aponeurosis is fixed to the muscle in the form of duplication.
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Spasokukotskyy proposed to catch the edges of the internal oblique muscle and transversal muscle with
aponeurosis of the external oblique muscles by single-layer interrupted suture.
Martynov proposed the fixation to the Poupart's ligament only internal edge of the external oblique muscle
aponeurosis without muscles. External edge of the aponeurosis sutured over internal in the form of duplication.
Kimbarovskyy, based on the principles of joining similar tissues, proposed special suture: Sutures placed on 1
cm from the edge of the external oblique abdominal muscle aponeurosis, grasped the part of the internal oblique
and transversal muscle. After that, aponeurosis is sutured one more time from behind to the front and attached to
the Pouparts ligament.
Kukudganov proposed to restore back wall of inguinal interval. Sutures are placed between the Coupers
ligamentum, vagina of direct abdominal muscle and aponeurosis of the transversal muscle.
Postempskyy proposed the deaf closing of inguinal interval with the lateral moving of spermatic duct.
The plastic narrowing of internal inguinal ring of to 0,8 cm is the important moment of this modification. On
occasion, when internal and external inguinal rings are in one plane, a spermatic duct is displaced inlateral
direction by transversal incision of the oblique and transversal muscles. Then edge of the vagina of direct muscle
and aponeurosis of the internal and transversal muscles is fixed to the Coupers ligament.
Operation at the incarcerated hernia is executed under the general anesthesia. A hernia sack is selected from
surrounding tissue, cut it in the area of bottom and remove hernia water, defining its character and sending to
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bacterial inoculation. Retaining the damaged organs, a strangulated ring is cut. It is necessary to remember, that at
the incarcerated femoral hernia ring cut up and some medially, because a femoral vein passes from a lateral side.
If a bowel is contents of hernia sack, we must estimate its viability. Remembering about possibility of the
retrograde jamming, special attention must be paid to the state of strangulation furrow. About viability of the
bowels testify: 1) renewal of its normal color; 2) presence or renewal of peristalsis; 3) renewal of pulsation of
vessels of mesentery and bowel. If there are the certain doubting, a bowel is dipped on a holder in an abdominal
cavity and in 1520 minutes it is examined repeatedly. If one of the resulted signs of viability is absent even, it is
necessary to conduct the resection of bowel. The resection is executed, receded from the strangulation furrow on a
proximal loop 3040 cm and distal 1520 cm. Anastomosis between proximal and distal loops it is better to
impose end-to-end. The plastic of hernia gate are conducted depending on indications after one of the surgical
methods.
When the necrosis elements of omentum or fatty pendants of colon are contents of hernia sack, they must be
removed within the limits of healthy tissue.
There can be necrosis of wall of colon or urinary bladder at sliding hernia. In such cases it is needed to be
limited to the minimum surgical procedure: to dip a necrosis area by sutures inside the bowel or use it for forming
of colostomy or epicystostomy. These are the best to conclude operation.
In similar situations at the incarcerated parietal hernia in most patients it is possible to be limited to
peritonization of displaced area of wall of bowel. If after the peritonization there is the threat of narrowing of
bowel or necrosis goes outside of the strangulation furrow, it is needed to conduct the resection of bowel.
Because of insufficient blood floow of Meckel's diverticulum and, permanent threat of it necrosis, at patients
with Littres hernia it resection must be performed.
At the phlegmon of hernia sack operation is begun with herniotomy. If the incarcerated organ is damaged by
necrosis, and in a hernia sack present pus, than there is a necessity for surgeon to perform laparotomy. After that
incarcerated organ resected within the limits of healthy tissue (in the generally accepted limits 40 cm of
proximal loop and 20 cm distal) and impose anastomosis. An abdominal cavity is sewn up. Incarcerated loops of
bowel, together with it blind ends which lacated in an abdominal cavity, removed through a hernia sack, a
peritoneum is sutured, the hernia sack is drained, the plastic of hernia gate are not performed. Skin is sewn up by
widely spaced sutures.
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1. The Safety of Mesh Repair for Primary Inguinal Hernias: Results of 3019 Operations from Five Diverse Surgical Sources;
Shulman, AG, Amid, PK, Lichtenstein, IL; The American Surgeon; 1992; 58:255-7.
2. The Tension-Free Hernioplasty; Lichtenstein, IL, Shulman, AG, Amid, PK, Montllor, MM; Am J Surg; 1989; 157:188-193.
3. Inguinal Hernia Repair: Biomaterials and Sutures Repair; Gilbert, AI; Perspectives in General Surgery; 1991; 2:113-129.
4. The Mesh-Plug Hernioplasty; Robbins, AW, Rutkow, IM, Surgical Clinics of North America; 1993; 73:501-12.
5. Abdominal Wall Hernias; Wantz, GE, in Principles of Surgery; Schwartz et al.; 6th Edition; 1994; McGraw-Hill, Inc.; New York.
6. The Shouldice Repair for Inguinal Hernia; Glassow, F; in Hernia; Nyhus, LM & Condon, RE; Second Edition; 1978; J. B.
Lippincott Co.; Philadelphia.
7. The Cause, Prevention, and Treatment of Recurrent Groin Hernia; Lichtenstein, IL, Shulman, AG, Amid, PK; Surgical Clinics of
North America; 1993;73:529-44.
8. "Tension-free" inguinal herniorrhaphy: A preliminary report on the "mesh plug" technique; Rutkow, IM, Robbins, AW; Surgery;
1993; 114: 3-8.
9. Sutures Repair of Inguinal Hernia; Gilbert, AI; Am J Surg; 1992; 163: 331-5.
10. The "Plug" Repair of 1402 Recurrent Inguinal Hernias; 20 Year Experience; Shulman, AG, Amid, PK, Lichtenstein, IL; Arch Surg;
1990; 125:265-7.
11. Inguinal and femoral hernioplasty utilizing polypropylene patch and plug; Amid, PK, Shulman, AG, Lichtenstein, IL; Ann Ital
Chir; 1993; 44: 119-25.
12. Improved Sutureless Technique--Advice to Experts; Gilbert, AI, Graham, MF; Problems in General Surgery; 1995; 12:117-9.
13. Technical and Scientific Objections to Laparoscopic Herniorrhaphy; Gilbert, AI, Graham, MF; Presented at 15th Anniversary
Meeting of the Shouldice Hospital; June 16, 1995.
14. Laparoscopic mesh repair vs. open repair with and without mesh graft for inguinal hernia. Preliminary study; Johansson, B, et
al.; Surgical Endoscopy; 1997; 11: 170 (Abstract).
15. Laparoscopic TEP versus open Lichtenstein hernia Repair, Randomized Trial; Merello, J; Surgical Endoscopy; 1997; 11: 545
(Abstract).
16. Moran Repair for Inguinal Hernias; Moran, RM, Brauns, J, Petrie, CR, Novak, BP, Johnsrud, JM,; Am Surg; 1997: 63: 430-3.
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Embryology
The embryonic gastrointestinal tract begins developing during the fourth week of gestation.
The primitive gut is derived from the endoderm and divided into three segments: foregut,
midgut, and hindgut. Both midgut and hindgut contribute to the colon, rectum, and anus.
The midgut develops into the small intestine, ascending colon, and proximal transverse colon,
and receives blood supply from the superior mesenteric artery. During the sixth week of
gestation, the midgut herniates out of the abdominal cavity, and then rotates 270 degrees
counterclockwise around the superior mesenteric artery to return to its final position inside the
abdominal cavity during the tenth week of gestation.
The hindgut develops into the distal transverse colon, descending colon, rectum, and proximal
anus, all of which receive their blood supply from the inferior mesenteric artery. During the
sixth week of gestation, the distal-most end of the hindgut, the cloaca, is divided by the
urorectal septum into the urogenital sinus and the rectum.
The distal anal canal is derived from ectoderm and receives its blood supply from the internal
pudendal artery. The dentate line divides the endodermal hindgut from the ectodermal distal
anal canal.
Anatomy
The large intestine extends from the ileocecal valve to the anus. It is divided anatomically and
functionally into the colon, rectum, and anal canal. The wall of the colon and rectum comprise
five distinct layers: mucosa, submucosa, inner circular muscle, outer longitudinal muscle, and
serosa. In the colon, the outer longitudinal muscle is separated into three teniae coli, which
converge proximally at the appendix and distally at the rectum, where the outer longitudinal
muscle layer is circumferential. In the distal rectum, the inner smooth-muscle layer coalesces to
form the internal anal sphincter. The intraperitoneal colon and proximal one third of the rectum
are covered by serosa; the mid and lower rectum lack serosa.
Colon Landmarks
The colon begins at the junction of the terminal ileum and cecum and extends 3 to 5 feet to the
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rectum. The rectosigmoid junction is found at approximately the level of the sacral promontory
and is arbitrarily described as the point at which the three teniae coli coalesce to form the outer
longitudinal smooth muscle layer of the rectum. The cecum is the widest diameter portion of
the colon (normally 7.5 to 8.5 cm) and has the thinnest muscular wall. As a result, the cecum is
most vulnerable to perforation and least vulnerable to obstruction. The ascending colon is
usually fixed to the retroperitoneum. The hepatic flexure marks the transition to the transverse
colon. The intraperitoneal transverse colon is relatively mobile, but is tethered by the
gastrocolic ligament and colonic mesentery. The greater omentum is attached to the
anterior/superior edge of the transverse colon. These attachments explain the characteristic
triangular appearance of the transverse colon observed during colonoscopy. The splenic flexure
marks the transition from the transverse colon to the descending colon. The attachments
between the splenic flexure and the spleen (the lienocolic ligament) can be short and dense,
making mobilization of this flexure during colectomy challenging. The descending colon is
relatively fixed to the retroperitoneum. The sigmoid colon is the narrowest part of the large
intestine and is extremely mobile. Although the sigmoid colon is usually located in the left
lower quadrant, redundancy and mobility can result in a portion of the sigmoid colon residing
in the right lower quadrant. This mobility explains why volvulus is most common in the
sigmoid colon and why diseases affecting the sigmoid colon, such as diverticulitis, may
occasionally present as right-sided abdominal pain. The narrow caliber of the sigmoid colon
makes this segment of the large intestine the most vulnerable to obstruction.
The arterial supply to the colon is highly variable (Fig. 28-1). In general, the superior
mesenteric artery branches into the ileocolic artery (absent in up to 20% of people), which
supplies blood flow to the terminal ileum and proximal ascending colon, the right colic artery,
which supplies the ascending colon, and the middle colic artery, which supplies the transverse
colon. The inferior mesenteric artery branches into the left colic artery, which supplies the
descending colon, several sigmoidal branches, which supply the sigmoid colon, and the
superior rectal artery, which supplies the proximal rectum. The terminal branches of each
artery form anastomoses with the terminal branches of the adjacent artery and communicate via
the marginal artery of Drummond. This arcade is complete in only 15 to 20% of people.
The lymphatic drainage of the colon originates in a network of lymphatics in the muscularis
mucosa. Lymphatic vessels and lymph nodes follow the regional arteries. Lymph nodes are
found on the bowel wall (epicolic), along the inner margin of the bowel adjacent to the arterial
arcades (paracolic), around the named mesenteric vessels (intermediate), and at the origin of the
superior and inferior mesenteric arteries (main). The sentinel lymph nodes are the first one to
four lymph nodes to drain a specific segment of the colon, and are thought to be the first site of
metastasis in colon cancer. The utility of sentinel lymph node dissection and analysis in colon
cancer remains controversial.
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Anorectal Landmarks
The rectum is approximately 12 to 15 cm in length. Three distinct submucosal folds, the valves
of Houston, extend into the rectal lumen. Posteriorly, the presecral fascia separates the rectum
from the presacral venous plexus and the pelvic nerves. At S4, the rectosacral fascia
(Waldeyer's fascia) extends forward and downward and attaches to the fascia propria at the
anorectal junction. Anteriorly, Denonvilliers' fascia separates the rectum from the prostate and
seminal vesicles in men and from the vagina in women. The lateral ligaments support the lower
rectum. The surgical anal canal measures 2 to 4 cm in length and is generally longer in men
than in women. It begins at the anorectal junction and terminates at the anal verge. The dentate
or pectinate line marks the transition point between columnar rectal mucosa and squamous
anoderm. The 1 to 2 cm of mucosa just proximal to the dentate line shares histologic
characteristics of columnar, cuboidal, and squamous epithelium and is referred to as the anal
transition zone. The dentate line is surrounded by longitudinal mucosal folds, known as the
columns of Morgagni, into which the anal crypts empty. These crypts are the source of
cryptoglandular abscesses
In the distal rectum, the inner smooth muscle is thickened and comprises the internal anal
sphincter that is surrounded by the subcutaneous, superficial, and deep external sphincter.
The deep external anal sphincter is an extension of the puborectalis muscle. The puborectalis,
iliococcygeus, and pubococcygeus muscles form the levator ani muscle of the pelvic floor.
The superior rectal artery arises from the terminal branch of the inferior mesenteric artery and
supplies the upper rectum. The middle rectal artery arises from the internal iliac; the presence
and size of these arteries are highly variable. The inferior rectal artery arises from the internal
pudendal artery, which is a branch of the internal iliac artery. A rich network of collaterals
connects the terminal arterioles of each of these arteries, thus making the rectum relatively
resistant to ischemia
The venous drainage of the rectum parallels the arterial supply. The superior rectal vein drains
into the portal system via the inferior mesenteric vein. The middle rectal vein drains into the
internal iliac vein. The inferior rectal vein drains into the internal pudendal vein, and
subsequently into the internal iliac vein. A submucosal plexus deep to the columns of
Morgagni forms the hemorrhoidal plexus and drains into all three veins.
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Lymphatic drainage of the rectum parallels the vascular supply. Lymphatic channels in the
upper and middle rectum drain superiorly into the inferior mesenteric lymph nodes. Lymphatic
channels in the lower rectum drain both superiorly into the inferior mesenteric lymph nodes
and laterally into the internal iliac lymph nodes. The anal canal has a more complex pattern of
lymphatic drainage. Proximal to the dentate line, lymph drains into both the inferior mesenteric
lymph nodes and the internal iliac lymph nodes. Distal to the dentate line, lymph primarily
drains into the inguinal lymph nodes, but can also drain into the inferior mesenteric lymph
nodes and internal iliac lymph nodes.
Both sympathetic and parasympathetic nerves innervate the anorectum. Sympathetic nerve
fibers are derived from L1-L3 and join the preaortic plexus. The preaortic nerve fibers then
extend below the aorta to form the hypogastric plexus, which subsequently joins the
parasympathetic fibers to form the pelvic plexus. Parasympathetic nerve fibers are known as the
nervi erigentes and originate from S2-S4. These fibers join the sympathetic fibers to form the
pelvic plexus. Sympathetic and parasympathetic fibers then supply the anorectum and adjacent
urogenital organs.
The internal anal sphincter is innervated by sympathetic and parasympathetic nerve fibers; both
types of fibers inhibit sphincter contraction. The external anal sphincter and puborectalis
muscles are innervated by the inferior rectal branch of the internal pudendal nerve. The
levator ani receives innervation from both the internal pudendal nerve and direct branches of
S3 to S5. Sensory innervation to the anal canal is provided by the inferior rectal branch of the
pudendal nerve. While the rectum is relatively insensate, the anal canal below the dentate line
is sensate.
Congenital Anomalies
Perturbation of the embryologic development of the midgut and hindgut may result in anatomic
abnormalities of the colon, rectum, and anus. Failure of the midgut to rotate and return to the
abdominal cavity during the tenth week of gestation results in varying degrees of intestinal
malrotation and colonic nonfixation. Failure of canalization of the primitive gut can result in
colonic duplication. Incomplete descent of the urogenital septum may result in imperforate
anus and associated fistulas to the genitourinary tract. Many infants with congenital anomalies
of the hindgut have associated abnormalities in the genitourinary tract.
Normal Physiology
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The colon is a major site for water absorption and electrolyte exchange. Approximately 90% of
the water contained in ileal fluid is absorbed in the colon (1000 to 2000 mL/d), and up to 5000
mL of fluid can be absorbed daily. Sodium is absorbed actively via a Na-K ATPase. The colon
can absorb up to 400 mEq of sodium per day. Water accompanies the transported sodium and is
absorbed passively along an osmotic gradient. Potassium is actively secreted into the colonic
lumen and absorbed by passive diffusion. Chloride is absorbed actively via a chloride
bicarbonate exchange.
Short-chain fatty acids (acetate, butyrate, and propionate) are produced by bacterial
fermentation of dietary carbohydrates. Short-chain fatty acids are an important source of energy
for the colonic mucosa, and metabolism by colonocytes provides energy for processes such as
active transport of sodium. Lack of a dietary source for production of short-chain fatty acids, or
diversion of the fecal stream by an ileostomy or colostomy, may result in mucosal atrophy and
"diversion colitis."
Approximately 30% of fecal dry weight is composed of bacteria (1011 to 1012 bacteria/g of
feces). Anaerobes are the predominant class of microorganism, and Bacteroides species are the
most common (1011 to 1012 organisms/mL). Escherichia coli are the most numerous aerobes
(108 to 1010 organisms/mL). Endogenous microflora are crucial for the breakdown of
carbohydrates and proteins in the colon and participate in the metabolism of bilirubin, bile
acids, estrogen, and cholesterol. Colonic bacteria also are necessary for production of vitamin
K. Endogenous bacteria also are thought to suppress the emergence of pathogenic
microorganisms, such as Clostridium difficile. However, the high bacterial load of the large
intestine may contribute to sepsis in critically ill patients and may contribute to intra-
abdominal sepsis, abscess, and wound infection following colectomy.
Intestinal gas arises from swallowed air, diffusion from the blood, and intraluminal production.
Nitrogen, oxygen, carbon dioxide, hydrogen, and methane are the major components of
intestinal gas. Nitrogen and oxygen are largely derived from swallowed air. Carbon dioxide is
produced by the reaction of bicarbonate and hydrogen ions, and by the digestion of
triglycerides to fatty acids. Hydrogen and methane are produced by colonic bacteria. The
production of methane is highly variable. The gastrointestinal tract usually contains between
100 and 200 mL of gas and 400 to 1200 mL per day are released as flatus, depending upon the
type of food ingested.
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Motility
Unlike the small intestine, the large intestine does not demonstrate cyclic motor activity
characteristic of the migratory motor complex. Instead, the colon displays intermittent
contractions of either low or high amplitude. Low-amplitude, short-duration contractions occur
in bursts and appear to move the colonic contents both antegrade and retrograde. It is thought
that these bursts of motor activity delay colonic transit and thus increase the time available for
absorption of water and exchange of electrolytes. High-amplitude contractions occur in a more
coordinated fashion and create "mass movements." Bursts of "rectal motor complexes" also
have been described. In general, cholinergic activation increases colonic motility.
Defecation
Continence
Clinical Evaluation
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Clinical Assessment
A complete history and physical examination is the starting point for evaluating any patient
with suspected disease of the colon and rectum. Special attention should be paid to the
patient's past medical and surgical history to detect underlying conditions that might contribute
to a gastrointestinal problem. If patients have had prior intestinal surgery, it is essential that
one understand the resultant gastrointestinal anatomy. In addition, family history of colorectal
disease, especially inflammatory bowel disease, polyps, and colorectal cancer, is crucial.
Medication use must be detailed as many drugs cause gastrointestinal symptoms. Before
recommending operative intervention, the adequacy of medical treatment must be ascertained.
In addition to examining the abdomen, visual inspection of the anus and perineum and careful
digital rectal exam are essential.
Endoscopy
Anoscopy
The anoscope is a useful instrument for examination of the anal canal. Anoscopes are made in a
variety of sizes and measure approximately 8 cm in length. A larger anoscope provides better
exposure for anal procedures such as rubber band ligation or sclerotherapy of hemorrhoids.
The anoscope, with obturator in place, should be adequately lubricated and gently inserted into
the anal canal. The obturator is withdrawn, inspection of the visualized anal canal is done, and
the anoscope should then be withdrawn. It is rotated 90 degrees and reinserted to allow
visualization of all four quadrants of the canal. If the patient complains of severe perianal pain
and cannot tolerate a digital rectal examination, anoscopy should not be attempted without
anesthesia.
Proctoscopy
The rigid proctoscope is useful for examination of the rectum and distal sigmoid colon and is
occasionally used therapeutically. The standard proctoscope is 25 cm in length and available in
various diameters. Most often, a 15- or 19-mm diameter proctoscope is used for diagnostic
examinations. The large (25-mm diameter) proctoscope is useful for procedures such as
polypectomy, electrocoagulation, or detorsion of a sigmoid volvulus. A smaller "pediatric"
proctoscope (11-mm diameter) is better tolerated by patients with anal stricture. Suction is
necessary for an adequate proctoscopic examination.
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sedation. Colonoscopes measure 100 to 160 cm in length and are capable of examining the
entire colon and terminal ileum. A complete oral bowel preparation is usually necessary for
colonoscopy and the duration and discomfort of the procedure usually require conscious
sedation. Both sigmoidoscopy and colonoscopy can be used diagnostically and therapeutically.
Electrocautery should generally not be used in the absence of a complete bowel preparation
because of the risk of explosion of intestinal methane or hydrogen gases. Diagnostic
colonoscopes possess a single channel through which instruments such as snares, biopsy
forceps, or electrocautery can be passed; this channel also provides suction and irrigation
capability. Therapeutic colonoscopes possess two channels to allow simultaneous
suction/irrigation and the use of snares, biopsy forceps, or electrocautery.
Imaging
Despite advanced radiologic techniques, plain x-rays and contrast studies continue to play an
important role in the evaluation of patients with suspected colon and rectal diseases. Plain
x-rays of the abdomen (supine, upright, and diaphragmatic views) are useful for detecting free
intra-abdominal air, bowel gas patterns suggestive of small or large bowel obstruction, and
volvulus. Contrast studies are useful for evaluating obstructive symptoms, delineating fistulous
tracts, and diagnosing small perforations or anastomotic leaks. While Gastrografin cannot
provide the mucosal detail provided by barium, this water-soluble contrast agent is
recommended if perforation or leak is suspected. Double-contrast barium enema has been
reported to be 70 to 90% sensitive for the detection of mass lesions greater than 1 cm in
diameter. 1 Detection of small lesions can be extremely difficult, especially in a patient with
extensive diverticulosis. For this reason, a colonoscopy is preferred for evaluating
nonobstructing mass lesions in the colon. Double-contrast barium enema has been used as a
back-up examination if colonoscopy is incomplete.
Computed Tomography
Virtual Colonoscopy
Virtual colonoscopy is a new radiologic technique that is designed to overcome some of the
limitations of traditional CT scanning. This technology uses helical CT and three-dimensional
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reconstruction to detect intraluminal colonic lesions. Oral bowel preparation, oral and rectal
contrast, and colon insufflation are used to maximize sensitivity. Early evaluation of virtual
colonoscopy suggests that accuracy may approach that of colonoscopy for detection of lesions
1 cm in diameter or greater.
The main use of magnetic resonance imaging (MRI) in colorectal disorders is in evaluation of
pelvic lesions. MRI is more sensitive than CT for detecting bony involvement or pelvic
sidewall extension of rectal tumors. MRI also can be helpful in the detection and delineation of
complex fistulas in ano. The use of an endorectal coil may increase sensitivity.
Positron emission tomography (PET) is used for imaging tissues with high levels of anaerobic
glycolysis, such as malignant tumors. 18 F-fluorodeoxyglucose (FDG) is injected as a tracer;
metabolism of this molecule then results in positron emission. PET has been used as an adjunct
to CT in the staging of colorectal cancer and may prove useful in discriminating recurrent
cancer from fibrosis. At present, the efficacy and utility of PET in the detection of recurrent
and/or metastatic colorectal cancer remains unproven.
Angiography
Angiography is occasionally used for the detection of bleeding within the colon or small
bowel. To visualize hemorrhage angiographically, bleeding must be relatively brisk
(approximately 0.5 to 1.0 mL per minute). If extravasation of contrast is identified, infusion of
vasopressin or angiographic embolization can be therapeutic.
Endorectal ultrasound is primarily used to evaluate the depth of invasion of neoplastic lesions
in the rectum. The normal rectal wall appears as a five-layer structure (Fig. 28-6). Ultrasound
can reliably differentiate most benign polyps from invasive tumors based upon the integrity of
the submucosal layer. Ultrasound can also differentiate superficial T1-T2 from deeper T3-T4
tumors. Overall, the accuracy of ultrasound in detecting depth of mural invasion ranges
between 81 and 94%. 3 This modality also can detect enlarged perirectal lymph nodes, which
may suggest nodal metastases; accuracy of detection of pathologically positive lymph nodes is
58 to 83%. Ultrasound may also prove useful for early detection of local recurrence after
surgery.
Endoanal ultrasound is used to evaluate the layers of the anal canal. Internal anal sphincter,
external anal sphincter, and puborectalis muscle can be differentiated. Endoanal ultrasound is
particularly useful for detecting sphincter defects and for outlining complex anal fistulas.
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Anorectal physiologic testing uses a variety of techniques to investigate the function of the
pelvic floor. These techniques are useful in the evaluation of patients with incontinence,
constipation, rectal prolapse, obstructed defecation, and other disorders of the pelvic floor.
Manometry
Neurophysiology
Rectal evacuation studies include the balloon expulsion test and video defecography. Balloon
expulsion assesses a patient's ability to expel an intrarectal balloon. Video defecography
provides a more detailed assessment of defecation. In this test, barium paste is placed in the
rectum and defecation is then recorded fluoroscopically. Defecography is used to differentiate
nonrelaxation of the puborectalis, obstructed defecation, increased perineal descent, rectal
prolapse and intussusception, rectocele, and enterocele. The addition of vaginal contrast and
intraperitoneal contrast is useful in delineating complex disorders of the pelvic floor.
Laboratory Studies
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Fecal occult blood testing (FOBT) is used as a screening test for colonic neoplasms in
asymptomatic, average-risk individuals. The efficacy of this test is based upon serial testing
because the majority of colorectal malignancies will bleed intermittently. FOBT has been a
nonspecific test for peroxidase contained in hemoglobin; consequently, occult bleeding from
any gastrointestinal source will produce a positive result. Similarly, many foods (red meat,
some fruits and vegetables, and vitamin C) will produce a false-positive result. Patients were
counseled to eat a restricted diet for 2 to 3 days prior to the test. Increased specificity is now
possible by using immunochemical FOBT. These tests rely on monoclonal or polyclonal
antibodies to react with the intact globin portion of human hemoglobin. Because globin does
not survive in the upper gastrointestinal tract, the immunochemical tests are more specific for
identifying occult bleeding from the colon or rectum. Dietary restrictions are not necessary.
Any positive FOBT mandates further investigation, usually by colonoscopy.
Stool Studies
Stool studies are often helpful in evaluating the etiology of diarrhea. Wet-mount examination
reveals the presence of fecal leukocytes, which may suggest colonic inflammation or the
presence of an invasive organism such as invasive E. coli or Shigella. Stool cultures can detect
pathogenic bacteria, ova, and parasites. C. difficile colitis is diagnosed by detecting bacterial
toxin in the stool. 4 Steatorrhea may be diagnosed by adding Sudan red stain to a stool sample.
Serum Tests
Specific laboratory tests that should be performed will be dictated by the clinical scenario.
Preoperative studies generally include a complete blood count and electrolyte panel. The
addition of coagulation studies, liver function tests, and blood typing/cross-matching depends
upon the patient's medical condition and the proposed surgical procedure.
Tumor Markers
Genetic Testing
Although familial colorectal cancer syndromes, such as familial adenomatous polyposis (FAP)
and hereditary nonpolyposis colon cancer (HNPCC) are rare, information about the specific
genetic abnormalities underlying these disorders has led to significant interest in the role of
genetic testing for colorectal cancer. 6 Tests for mutations in the adenomatous polyposis coli
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(APC) gene responsible for FAP, and in mismatch repair genes responsible for HNPCC, are
commercially available and extremely accurate in families with known mutations. Although
many of these mutations are also present in sporadic colorectal cancer, the accuracy of genetic
testing in average-risk individuals is considerably lower and these tests are not recommended
for screening. Because of the potential psychosocial implications of genetic testing, it is
strongly recommended that professional genetic counselors be involved in the care of any
patient considering these tests.
Pain
Abdominal Pain
Abdominal pain is a nonspecific symptom with a myriad of causes. Abdominal pain related to
the colon and rectum can result from obstruction (either inflammatory or neoplastic),
inflammation, perforation, or ischemia. Plain x-rays and judicious use of contrast studies
and/or a CT scan can often confirm the diagnosis. Gentle retrograde contrast studies (barium or
Gastrografin enema) may be useful in delineating the degree of colonic obstruction.
Sigmoidoscopy and/or colonoscopy performed by an experienced endoscopist can assist in the
diagnosis of ischemic colitis, infectious colitis, and inflammatory bowel disease. However, if
perforation is suspected, colonoscopy and/or sigmoidoscopy are generally contraindicated.
Evaluation and treatment of abdominal pain from a colorectal source should follow the usual
surgical principles of a thorough history and physical examination, appropriate diagnostic
tests, resuscitation, and appropriately timed surgical intervention.
Pelvic Pain
Pelvic pain can originate from the distal colon and rectum or from adjacent urogenital
structures. Tenesmus may result from proctitis or from a rectal or retrorectal mass. Cyclical
pain associated with menses, especially when accompanied by rectal bleeding, suggests a
diagnosis of endometriosis. Pelvic inflammatory disease also can produce significant
abdominal and pelvic pain. The extension of a peridiverticular abscess or periappendiceal
abscess into the pelvis may also cause pain. CT scan and/or MRI may be useful in
differentiating these diseases. Proctoscopy (if tolerated) also can be helpful. Occasionally,
laparoscopy will yield a diagnosis.
Anorectal Pain
Anorectal pain is most often secondary to an anal fissure or perirectal abscess and/or fistula.
Physical examination can usually differentiate these conditions. Other, less common causes of
anorectal pain include anal canal neoplasms, perianal skin infection, and dermatologic
conditions. Proctalgia fugax results from levator spasm and may present without any other
anorectal findings. Physical exam is critical in evaluating patients with anorectal pain. If a
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patient is too tender to examine in the office, an examination under anesthesia is necessary.
MRI may be helpful in select cases where the etiology of pain is elusive.
The first goal in evaluating and treating a patient with gastrointestinal hemorrhage is adequate
resuscitation. The principles of ensuring a patent airway, supporting ventilation, and
optimizing hemodynamic parameters apply and coagulopathy and/or thrombocytopenia should
be corrected. The second goal is to identify the source of hemorrhage. Because the most
common source of gastrointestinal hemorrhage is esophageal, gastric, or duodenal, nasogastric
aspiration should always be performed; return of bile suggests that the source of bleeding is
distal to the ligament of Treitz. If aspiration reveals blood or nonbile secretions, or if symptoms
suggest an upper intestinal source, esophagogastroduodenoscopy is performed. Anoscopy
and/or limited proctoscopy can identify hemorrhoidal bleeding. A technetium-99
(99mTc)-tagged red blood cell (RBC) scan is extremely sensitive and is able to detect as little
as 0.1 mL/h of bleeding; however, localization is imprecise. If the 99mTc-tagged RBC scan is
positive, angiography can then be employed to localize bleeding. Infusion of vasopressin or
angioembolization may be therapeutic. Alternatively, a catheter can be left in the bleeding
vessel to allow localization at the time of laparotomy. If the patient is hemodynamically stable,
a rapid bowel preparation (over 4 to 6 hours) can be performed to allow colonoscopy.
Colonoscopy may identify the cause of the bleeding, and cautery or injection of epinephrine
into the bleeding site may be used to control hemorrhage. Colectomy may be required if
bleeding persists despite these interventions. Intraoperative colonoscopy and/or enteroscopy
may assist in localizing bleeding. If colectomy is required, a segmental resection is preferred if
the bleeding source can be localized. "Blind" subtotal colectomy may very rarely be required in
a patient who is hemodynamically unstable with ongoing colonic hemorrhage of an unknown
source. In this setting, it is crucial to irrigate the rectum and examine the mucosa by
proctoscopy to ensure that the source of bleeding is not distal to the resection margin
Occult blood loss from the gastrointestinal tract may manifest as iron-deficiency anemia or may
be detected with fecal occult blood testing. Because colon neoplasms bleed intermittently and
rarely present with rapid hemorrhage, the presence of occult fecal blood should always prompt
a colonoscopy. Unexplained iron-deficiency anemia is also an indication for colonoscopy.
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Constipation is an extremely common complaint, affecting more than 4 million people in the
United States. Despite the prevalence of this problem, there is lack of agreement about an
appropriate definition of constipation. Patients may describe infrequent bowel movements,
hard stools, or excessive straining. A careful history of these symptoms often clarifies the
nature of the problem.
Medical management is the mainstay of therapy for constipation and includes fiber, increased
fluid intake, and laxatives. Outlet obstruction from nonrelaxation of the puborectalis often
responds to biofeedback. 7 Surgery to correct rectocele and rectal prolapse has a variable effect
on symptoms of constipation, but can be successful in selected patients. Subtotal colectomy is
considered only for patients with severe slow-transit constipation (colonic inertia) refractory to
maximal medical interventions. While this operation almost always increases bowel movement
frequency, complaints of diarrhea, incontinence, and abdominal pain are not infrequent, and
patients should be carefully selected. 8
Chronic diarrhea may present a more difficult diagnostic dilemma. Chronic ulcerative colitis,
Crohn's colitis, infection, malabsorption, and short gut syndrome can cause chronic diarrhea.
Rarely, carcinoid syndrome and islet cell tumors (vasoactive intestinal peptide-secreting tumor
[VIPoma], somatostatinoma, gastrinoma) present with this symptom. Large villous lesions may
cause secretory diarrhea. Collagenous colitis can cause diarrhea without any obvious mucosal
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abnormality. Along with stool cultures, tests for malabsorption, and metabolic investigations,
colonoscopy can be invaluable in differentiating these causes. Biopsies should be taken even if
the colonic mucosa appears grossly normal.
Incontinence
The incidence of fecal incontinence has been estimated to occur in 10 to 13 individuals per
1000 people older than age 65 years. Incontinence ranges in severity from occasional leakage
of gas and liquid stool to daily loss of solid stool. The underlying cause of incontinence is
often multifactorial and diarrhea is often contributory. In general, causes of incontinence can
be classified as neurogenic or anatomic. Neurogenic causes include diseases of the central
nervous system and spinal cord along with pudendal nerve injury. Anatomic causes include
congenital abnormalities, procidentia, overflow incontinence secondary to impaction or
neoplasm, and trauma. The most common traumatic cause of incontinence is injury to the anal
sphincter during vaginal delivery. Other causes include anorectal surgery, impalement, and
pelvic fracture.
After a thorough medical evaluation to detect underlying conditions that might contribute to
incontinence, evaluation focuses on assessment of the anal sphincter and pudendal nerves.
Pudendal nerve terminal motor latency testing may detect neuropathy. Anal manometry can
detect low resting and squeeze pressures. Defecography can detect rectal prolapse. Endoanal
ultrasound is invaluable in diagnosing sphincter defects.
Hemorrhoids from Greek mean bleeding. Nowadays hemorrhoids are volume increase
or dilation of cavernous bodies in rectum.
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Pathomorphology
External hemorrhoids have their origin from veins of lower hemorrhoidal plexus,
internal from upper. External hemorrhoids are soft, of bluish color, they have not
smooth surface and are filled with blood. Sometimes they are dense and filled with
thrombs. Sometimes external hemorrhoids are prolapsed internal nodes. They have long
leg deeply in anal canal.
Histologically they observe wall atrophy, anomalies of development, often signs of
thrombophlebitis.
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Classification
Early signs of hemorroids are rush feeling in asnal region that appears due to skin
maceration by mucous excretions from rectum. This sign is increased in diet violations
that may be a consequence of constipation or diarrhea.
There define three degrees of hemorrhoids. At I degree nodes prolabe from anus
during defecation, but they replace independently and are painful during palpation. At II
degree there is a need to replace nodes. There is edema in perianal region and pain. At III
degree nodes prolabe at very low physical loading, edema and pain are severe. The
speciality of chronic hemorrhoids is that there are conditions for appearance of mucosal
fissures, polipes and paraproctitis.
Diagnostic program
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Differential diagnostics
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For treatment of such patients they use massage through Diet therapy means
excluding from ration spicy and salty food. rectum, recommend carrying of bandages.
They also prescribe enemas (micro enemas with warm water, oils, antiseptics), warm as
sitting bath, perineal shower, warming compresses.
In acute period they use bandages with cold water, cooling bandages with plumbum
water or furacilinum.
Medicamentous therapy includes prescription of anti bleeding remedies and
analgetics, antiseptics, anti-inflammatory remedies (orally, intravenously and locally as
rectal suppositoria).
They also use physiotherapeutic methods (UHF, darsonvalization), treating physical
training for strengthening of abdominal muscles and diaphragm, pelvis, spa treatment
(H2S baths, mud and radon sanatoria).
Indications for surgical treatment are frequent bleedings from hemorrhoidal nodes
that are accompanied with anemia, big nodes that worsen defecationm inflammation,
prolapse and strangulation of nodes.
There are known more than 30 methods of hemorrhoids extraction. The main
moments of operation are divulsion of sphincter, extraction and ligation of hemorrhoidal
nodes situated in zones on 3, 7, and 11 hours at position of patient on back.
Hemorrhoidal nodes are cut from external area to internal, leg is ligated by silk ligature
and extracted. The most wide spread method is by Milligan-Morgan extraction of nodes
with renewal of mucosa in anus (Pic. 4.1.1).
In patients with complication of secondary hemorrhoids by bleeding that may not be
treated by conservative therapy as a rule there is provided only ligation of bleeding areas.
Medical Therapy
Bleeding from first- and second-degree hemorrhoids often improves with the
addition of dietary fiber, stool softeners, increased fluid intake, and avoidance of
straining. Associated pruritus may often improve with improved hygiene. Many over-the-
counter topical medications are desiccants and are relatively ineffective for treating
hemorrhoidal symptoms.
Persistent bleeding from first-, second-, and selected third-degree hemorrhoids may
be treated by rubber band ligation.
Mucosa located 1 to 2 cm proximal to the dentate line is grasped and pulled into a
rubber band applier. After firing the ligator, the rubber band strangulates the underlying
tissue, causing scarring and preventing further bleeding or prolapse (Fig. 28-30). In
general, only one or two quadrants are banded per visit. Severe pain will occur if the
rubber band is placed at or distal to the dentate line where sensory nerves are located.
Other complications of rubber band ligation include urinary retention, infection, and
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Infrared photocoagulation is an effective office treatment for small first- and second-
degree hemorrhoids. The instrument is applied to the apex of each hemorrhoid to
coagulate the underlying plexus. All three quadrants may be treated during the same visit.
Larger hemorrhoids and hemorrhoids with a significant amount of prolapse are not
effectively treated with this technique.
Sclerotherapy
Operative Hemorrhoidectomy
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This technique, often called the Milligan and Morgan hemorrhoidectomy, follows the
same principles of excision described above, but the wounds are left open and allowed to
heal by secondary intention.
Whitehead's Hemorrhoidectomy
Stapled Hemorrhoidectomy
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Milligan-Morgan operation
After operation hemorrhoidectomy may appear early (bleeding from the wound) and
later (stricture of anal canal) complications. With the aim of prevention of bleeding at
hemorrhoidectomy leg is ligated with silk ligation, and the wound by node ligations to
bottom. For prevention of stricture of anal canal there makes sense to extract nodes not
more than in 4 places. During this between extracted nodes there must stay not injured
mucosa. When indicated, if after operation surgeon revealed the stricture of entrance into
anal canal, hemorrhoidectomy is finished by dosed sphincterectomia.
During appearance of stricture of anal canal by posterior comissure scar in extracted,
there is provided dosed sphincterectomia, and then mucosa is connected with perianal
skin with further fixation by separate ligations.
Complications of Hemorrhoidectomy
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Rectal fissures are linear or triangle shaped defects of anal mucosa. This disease
takes 3rd place after hemorrhoids and paraproctitis by frequency.
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The most wide spread theories of appearance of fissures are mechanic and infectious.
Due to the first, appearance of fissures is conditioned by injury of anal mucosa by dense
feces in combination with constipation and diarrhea. Diseases that promote formation of
fissures are proctosigmoiditis, enterocolitis and hemorrhoids. Often fissures accompany
gastritis, gastric and duodenal ulcers.
By infectious theory fissures appear at inflammation of anal glands (criptitis) that
lead to tissue fibrosis and decrease of their elasticity. Appearance of disease also may be
promoted by syphilis, tuberculosis, homosexualism.
Classification
Rectal fissures by clinical course are divided onto acute and chronic. They may be
complicated (paraproctitis, malignization, bleeding, pectenosis) and combined with other
diseases of anal canal (hemorrhoids, criptitis, polypus).
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Rectal fissures
Such disease is seen mostly in women of middle age. Fissures are mostly situated in
area of posterior comissure on 6 hours by clock dial in patients position laying on back.
More rarely fissures are situated on anterior and lateral walls. On posterior wall of anal
canal conditions of bleeding are worse, thats why there is more danger of mucosal injury
during defecation, it is connected with pressure of feces during their motion onto
posterior and anterior commissures. Fissure mostly has longitudinal direction and hides
between skin folds in anal area. In chronic course near external edge of fissure there
appear skin fold with undermined edges, so called terminal tuberculum. On internal edge
of fissure there is tuberculum of smaller size. In rare cases there are seen two fissures at
the same time.
Clinical picture of anal fissure includes triad of symptoms: pain during or after
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Diagnostic program
Differential diagnostics
Chronic fissures of rectum should be often differentiated with other diseases that
may have the same local signs.
Proctalgia. Pain is localized in the area of rectum. Consider, that the reason of
proctalgia is pathology of the higher nervous system (neuroses, hysteria). At objective
examination the visible organic changes are not exposed.
The anal form of non specific ulcerous colitis is characterized by the superficial
damage of rectum hyperemia and edema of mucus, formation of shallow ulcers and
erosions. As a rule, non specific ulcerous colitis with all its signs begins from the distal
part of rectum.
Krons disease of rectum begins from submucosal layer, ulcers do not spread much,
they mostly are like fissures that penetrate onto all depth of intestinal wall, have
longitudinal and transversal directions, and may cause formation of fistules and
abscesses. At histological investigation during Krons disease there is revealed granuloma.
Cancer of rectum. Presence in anal canal of formation with not smooth edges and
additions of blood in feces gives a possibility to suspect malignization of fissure.
Morphological investigation of bioptates with presence of atypical cells proves malignant
process.
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Rectally they use micro enemas (oily, antiseptic), rectal suppositoria (with
belladonna, anaesthesinum and their standard forms proctosedylum, G preparation).
Under the fissure by injection they introduce hydrocortizonum with novocainum.
Transverse cut of the mucosa above the upper merge of the Rectal fissures
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Polyps are non malignant tumors on legs that grow from mucosa.
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Pathomorphology
Polypus of inflammatory origin differ from adenomatous ones by their incorrect form
and size variety. They are soft, filled with blood, often with ulceration and hematomas.
Such polypus usually combine with other signs of inflammation in intestine.
Adenomatous polypus are often part of syndromes. Thus, combination with non
malignant tumors of bones, skin and soft tissues is characteric for Gardners syndrome,
combination with focal melanosis of mucosa for Peitz-Eggers syndrome, combination
with brain tumors for Turcos syndrome.
Classification
By etiology:
Innate (hereditary, family)
Acquired (at inflammatory processes)
Separately they define also children (juvenile, innate and acquired).
By process spreading:
Single
Multiple
Total (injury of all intestines).
By external appearance and microscopic structure:
True (glandular, fleesy, from multi layer epithelium)
False (hypertrophic at ulceric colitis, fibrose).
Men get this disease in 2-3 times more than women. Single polypus of colon and
rectum have usually latent course and are often revealed accidentally.
Multiple polypus may lead to diarrhea, bleeding, changes in morphological and
biochemical blood composition. At this children do not devlop properly. At distal
localization in some patients polypus prolapse and strangulate in anal ring causing pain.
Low situated polypus irritate rectum and cause tenesmas, sometimes they cause prolapse
of intestinal wall.
Among diseases symptoms first palce belongs to disorders of defecation and blood
in feces with further anemia, hypoproteinemia, decrease of workability. Fleesy polypus
leads to disorders of water-salt and protein metabolism, because mucus excretion at
defecation may achieve 1.5 liters,
At multiple polyposis they define triad of symptoms:
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1. Pigment spots (on the face, lips, mucosal membranes of cheeks, fingers,
and other areas of covering epithelium).
2. Polyposis of digestive tract.
3. Hereditary character of disease.
Finger examination of rectum and observation with rectal mirror give a possibility
to investigate its lower part. During this procedures you can reveal polypus of different
size situated on jucosa of rectum and also polypus prolapsed with invaginate of sygmoid
colon.
Irigography reveals single and multiple defects of filling (Pic. 4.1.13), so called
symptom of shooted aim that may be seen in different parts of colon. At presence of
invaginate as complication of polypus there is charactering defect of filling.
With the help of rectoromanoscope you can examine rectum and sigmoid colon on
average height 30 cm, and fibrocolonoscope is to examine all parts of colon. This
investigation method gives a possibility to reveal exact place of polypus localization, its
appearance including leg width, to provide excisional byopsia and also
electrocoagulation.
Polypus of small size at the onset have latent course. With their growth during
moving of feces may occur disorder of their completeness with further possible
complications. More often is bleeding that in most cases occur defecation. Depending on
the height of polypus localization in intestine blood may be dark red to bright red color.
Blood loss may be from small, light to severe, with signs of small and incredible anemia.
In most patients polypus have a tendense to malignization. Provided biopsia in pre
operation period with morphological investigation reveals malignant transformation of
tissues and proves this diagnosis not in all cases. It depends on that in what part polypus
becomes malignant. Final diagnosis may be put after the operation during histological
investigation of all polypus.
Polypus of big size situated in rectum usually strangulate. During this strangulation
takes place on the level of anal ring and is accompanied with severe pain. Not reducible
polypus may necrotize.
Polypus are situated in caecum, colon and sigmoid colon. In the most motile areas
they may lead to intestinal invagination. In this case there appear spastic pain, blood
excretion with feces. During abdominal palpation they reveal painful infiltrate.
Invagination may prolapse into rectal lumen.
Diagnostic program
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4. Rectoromanoscopy.
5. Irigography.
6. Fibrocolonoscopy.
7. General analysis of blood and urine.
8. Coagulogram
Differential diagnosis
Polypus of colon and rectum should be differentiated with malignant and non
epithelial tumors, non specific ulcer colitis and rectal fissures.
Cancer of right part of colon ahs a course with incredible anemia (toxicoanemic
form) due to absorption of tumors toxic products, their action on hemopoetic organs.
Cancer of left part of colon is usually accompanied with signs of obturative intestinal
impassability. Additional examination (finger rectal examination, irigography, endoscopic
methods) give a possibility to prove the diagnosis.
At chronic course of non specific ulcer colitis there is injured mucosa of intestine,
and little islands of not injured mucosa between multiple big ulcers look like polypus, so
called pseudopolyposis. Detailed anamnesis, specialities of clinical course of the disease,
irigography and colonoscopy exclude presence of true polypus.
Not epithelial tumors (leyomyoma, lipoma) are situated under intestinal mucosa and
at their small size do not cause any symptoms. With their growth mucosa is injured, there
occurs bleeding with its signs. X-ray and endoscopic methods of investigation, and also
histological investigation prove the final diagnosis.
Chronic fissure of rectum with not smooth edges and terminal tuberculum often
simulates true polypus. Removal of this formation both with fissure and provided
histological investigation help in proving of diagnosis.
Conservative method of treatment is rarely used. For this is used solution of green
greater celandine for its introduction in enemas (3-4 grams of green mass for 1 kg of
patient weight, on the average 50 g for adults). A celandine is ground down on a meat
grinder, conduct in hot water in the ratio 1:10. A medical cycle includes 1530 enemas.
Per treatments course is conducted three cycles at intervals in one month. The low located
polypuses from a stratified epithelium, pseudopolypuses and malignant polypuses are not
treated by celandine.
Because of polypuses of small intestine and rectums are inclined to malignization,
the basic method of its treatment is surgical .
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Acute paraproctitis is acute inflammation of pararectal cellular tissue. They take near
30% of all diseases of rectum.
Pathomorphology
Classification
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Paraproctitis has as local as general symptoms. The most often are pain in anal
region of rectum, swelling, hyperemia, fluctuation, constipation, sometimes - disuria,
increase of body temperature, loss of appetite and workability.
During general blood analysis there are leukocytosis with left disposition of
leukocyte formula, SES increase. If in-time operative treatment shouldn't be provided,
period of disease may increase to 10 days and more. After that there comes independent
opening of abscess into rectum (chronic paraproctitis), formation of recurrent
paraproctitis or reconvalescense.
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Diagnostic program
Differential diagnosis
Method of choice for treatment of acute paraproctitis is surgical. But on early stages
of pelviorectal paraproctitis with deep infiltration of tissues surrounding rectum, without
signs of softening there is indicated conservative treatment (warming compress on area of
perineum with 20% spiritus aethylicus, antibioitics of wide spectrum of stion, lumbal
novocainum blocade, strict bed regime, exclusion of cellulose from food, usage of
cleaning enemas). Surgical treatment means early operation by opening of abscess by
semilunar incision with dreanging and liquidation of its inner opening (removal of crypt)
through which abscess cavity is connected with rectum.
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Rectal fistulas are tubular purulent canals in cellular tissue surrounding rectum and
anus.
Rectal fistulas occur mostly on the basis of acute paraproctitis. Reasons of chronic
fistulas are:
- opening of purulent paraproctitis without cutting of crypt;
- shortening of external anal sphincter at which fistula's canal is pressed and
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Classification
Self feeling and general status of patient with chronic course of paraproctitis in most
cases is satisfacting. At long time existing inflammatory focus workability decreases,
increased irritability appears, sleep becomes worse. Depending on activity of
inflammatory process, character of excretions fro fistula changes. After abscess opening
pain decreases and may be back when process becomes acute. In most patients with rectal
fistulas there are observed signs of proctosigmoiditis and chronic recurrent paraproctitis.
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When process becomes acute pain appears and temperature increases. There is formed
purulent focus with formation of new fistula's canals.
In most patients fistula situated near anal ring goes inside the sphincter. Fistula
situated 4-5 cm from anus and deeper is situated mostly outside the sphincter and may be
of IV degree.
Patients with fistulas feel rush and heaviness in areas of rectum and anus. Long
existing fistulas are accompanied with scar changes of anal ring (pectenosis) that
difficults defecation. After fistulas closing (between acute periods) patients have no
troubles and feel healthy. In some patients there stay painful infiltrates where
inflammatory process may renew. The most dangerous and rare complication of chronic
paraproctitis is malignant transformation of rectal fistulas.
Diagnostic program
Differential disagnosis
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At conservative treatment of chronic paraproctitis (fistulas) they use sitting baths and
warming compresses with 20% spiritus aethylicus. They also prescribe physiotherapeutic
procedures (ultraviolet radiation, local darsonvalization, electrophoresis with 1% solution
of potassium iodide, 1% novocainum solution), lavage of fistula with diluted solutions of
antiseptics.
Operative treatment is indicated if fistula is present for a long time or closes for some
time and then opens again after acute inflammatory period. In patients with intrasphincter
fistulas there is used operation by Gabriel. Its basis is that fistula is cut from inner to
external opening. Skin that covers the fistula is cut as triangle. Its peak includes internal
opening, and basis is situated outside (Pic. 4.1.8).
In case of fistula going through inner parts of sphincter (transsphincter fistula)
during canal removal there are injured fibers of sphincter. For renewal of cut sphincter
there are used node of -like ligations. At extrasphincter fistulas there are used such
operations:
Ryzhykh-I they remove fistula's canal in perineal wound to rectal wall and cut in
basis. Stump of fistula's canal is emptied with Folkmanns spoon, cleaned with iodine
solution and ligated with two or three layers of catgut ligations. During this ligated stump
of fistula's canal is covered by surrounding tissues. Operaiton is finished with dosed
sphincterotomia of inner fibers. This method is used when inner fistula's opening is
localized in posterior crypt.
Ryzhykh-II (second variant) is used when inner fistula's opening is localized in
anterior crypt or on lateral wall. Removal offistula in perineal wound is provided the same
as in the first variant. Further, upon the inner fistula's opening there is separated piece of
mucosa (width 1-1.5 cm and length to 4 cm). Inner fistula's opening is ligated with node
catgut ligations. With this aim threads are knotted after removal of rectal mirror. Then
there should be put several ligations between separated and partially cut pieces of mucosa
and distal part of the wound. At the end of operation there is provided posterior dosed
sphincterotomia.
By Blinnitchev, opening in rectal mucosa is closed by catgut ligations in two stairs.
There is separated mucosa upon the ligated opening, it should be fixed including
submucosal layer to muscular membrane and ligated by silk ligations to perianal skin.
Sometimes mobilized piece is moved downwards. Mobilized mucosal-muscular piece is
ligated in such a way that needle should go near the edge of terminal fold to the basis of
mobilized piece. After that by separate silk ligations they fix pieces edge to perianal skin.
Ligation method (by Hippocrates). On the wall of anal canal there should be cut
inner fistula's opening and perianal skin together with narrow stripe of mucosa. Into this
layer there are put ligations No.6 and sphincter fibers are tightened. Thus, thread stretches
with 1-1.5 cm width intestinal wall and sphincter fibers. Ligation is tightened again till
complete cutting of tissues and sphincter with cellular tissue (Pic. 4.1.9).
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Classification
There define such stages of course of epithelial paracoccygeal canals (by Yu.V.
Dooltsev and L.V. Ryvkin, 1988):
I. Epithelial paracoccygeal canals without any clinical findings.
II. Acute inflammation of epithelial paracoccygeal canals:
(a) infiltrative stage;
(b) abscess formation.
III. Chronic inflammation of epithelial paracoccygeal canals:
(a) infiltrative stage;
(b) recurrent abscess;
(c) purulent fistula.
IV. Remission of inflammation of epithelial paracoccygeal canals.
Epithelial paracoccygeal canals may have no clinical findings, thats why they are
often revealed accidentally during medical examination. In such cases I distal part of
intergluteal fold near occygeal apex upon the edge of anal region there are seen one or
several point openings where sometimes hair grows. Diameter of those openings is
from 1 to 3 mm, they are situated by middle line one by one. During pressing on the
skin upper from epithelial opening you can see excretion of drops of non transparent
or purulent fluid. Self feeling and general status of patients are usually not changed.
But when there appears also inflammation in coccygeal region there occurs abscess
formation. Then patients feel pain, body temperature increases. Investigation of
general blood analysis reveals leukocytosis with formula moving to the left, increase of
SES.
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At non complicated epithelial paracoccygeal canals patients suffer from dull pain,
feeling of pressing in coccygeal region, especially during long time walking. Increased
sweating in intergluteal region is accompanied with rush, sometimes there appears
painful infiltrate that disappears independently.
Acute stage of the disease is characterized by changes of general and local
character. Body temperature, as a rule, increases to 39-40 degrees centigrade and is
accompanied with chilling. Local symptoms are severe pain in coccygeal region,
sometimes with irradiation into rectum. At the same time there appear swelling,
infiltration of intergluteal region, skin upon the place of inflammation becomes bluish-
violet. Further, abscess is formed. During independent opening of abscess there goes
purulent content of dark color with bad smell. Sometimes abscess from coccygeal
region spreads to pararectal and even pelviorectal spaces, but as a rule it does not open
into rectal lumen.
Diagnostic program
Differential diagnosis
Presacral cyst teratoma both with epithelial paracoccygeal canal at the initial stage
and period of complications absence are differentiated easily, because when teratoma is
present, finger examination of rectum gives a possibility to reveal tumor-like formation in
presacral region. Complication of cyst teratoma with fistulas is differentiated with
suppurated paracoccygeal canal with incredible difficulties. Provided contrast
fistulography of fistula's canals at cyst teratoma gives a possibility to define its
localization in presacral region, and epithelial canal may often be branched and ends
blindly in soft tissues behind the coccygeum.
At paraproctitis epithelial opening in intergluteal fold is usually absent, and fistula's
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canal in most cases is connected with rectal lumen and is revealed during finger
examination or investigation by rectal mirror. At pressing on pararectal region from
fistula's canals there appears purulent content. Preliminarly introduced tampon is stained
by methylene blue at the moment of its getting into external opening of fistula.
Osteomyellitis of pterygoideal bone and coccygeum is often connected with injury of
this region. On observing X-ray grams there is revealed characteristic picture of injured
bone (foci of osteoporosis and sequesters). Fistulography helps in proving of diagnosis.
Two independent diseases epithelial paracoccygela canals and osteomyelitis of sacral
bone and coccygeum at the same time may be combined in one patient extremely rarely.
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In rare cases when after opening and removal of abscesses there stays big wound
surface, wound should be treated by opened method. For sanation of such wounds, except
usual remedies, they use laser and ultrasound.
At abscesses and secondary fistulas in most cases there should be provided radical
operation: wound edges are to be ligated to its bottom. During removal of lateral fistula's
canals because of absence of fossa in this region there are applied rare situational
ligations onto wound edges not including the bottom.
In surgical practice in treatment epithelial paracoccygeal canals there should be taken
into account anatomical variants of structure of sacral-coccygeal-gluteal region. In most
patients there may be high position of buttocks, deep intergluteal fold, acute angle
between buttocks and middle line of sacrococcygeal region, close position of primary
epithelial opening from anus.
References
1. Smith RA, von Eschenbach AC, Wender R, et al: American Cancer Society guidelines for the early
detection of cancer: Update of early detection guidelines for prostate, colorectal and endometrial cancers. CA
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POLYPOSIS
Polyps are non malignant tumors on legs that grow from mucosa.
Reasons of polyps appearance are disorders in embryonal development , inflammatory processes of mucosa and also
viral infection.
Pathomorphology
Polypus of inflammatory origin differ from adenomatous ones by their incorrect form and size variety. They are soft,
filled with blood, often with ulceration and hematomas. Such polypus usually combine with other signs of inflammation in
intestine.
Adenomatous polypus are often part of syndromes. Thus, combination with non malignant tumors of bones, skin and
soft tissues is characteric for Gardners syndrome, combination with focal melanosis of mucosa for Peitz-Eggers syndrome,
combination with brain tumors for Turcos syndrome.
Classification
By etiology:
Innate (hereditary, family)
Acquired (at inflammatory processes)
Separately they define also children (juvenile, innate and acquired).
By process spreading:
Single
Multiple
Total (injury of all intestines).
By external appearance and microscopic structure:
True (glandular, fleesy, from multi layer epithelium)
False (hypertrophic at ulceric colitis, fibrose).
Men get this disease in 2-3 times more than women. Single polypus of colon and rectum have usually latent course and
are often revealed accidentally.
Multiple polypus may lead to diarrhea, bleeding, changes in morphological and biochemical blood composition. At this
children do not devlop properly. At distal localization in some patients polypus prolapse and strangulate in anal ring causing
pain. Low situated polypus irritate rectum and cause tenesmas, sometimes they cause prolapse of intestinal wall.
Among diseases symptoms first palce belongs to disorders of defecation and blood in feces with further anemia,
hypoproteinemia, decrease of workability. Fleesy polypus leads to disorders of water-salt and protein metabolism, because
mucus excretion at defecation may achieve 1.5 liters,
At multiple polyposis they define triad of symptoms:
1. Pigment spots (on the face, lips, mucosal membranes of cheeks, fingers, and other areas of covering
epithelium).
2. Polyposis of digestive tract.
3. Hereditary character of disease.
Finger examination of rectum and observation with rectal mirror give a possibility to investigate its lower part. During
this procedures you can reveal polypus of different size situated on jucosa of rectum and also polypus prolapsed with
invaginate of sygmoid colon.
Irigography reveals single and multiple defects of filling, so called symptom of shooted aim that may be seen in
different parts of colon. At presence of invaginate as complication of polypus there is charactering defect of filling.
With the help of rectoromanoscope you can examine rectum and sigmoid colon on average height 30 cm, and
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fibrocolonoscope is to examine all parts of colon. This investigation method gives a possibility to reveal exact place of
polypus localization, its appearance including leg width, to provide excisional byopsia and also electrocoagulation.
Polypus of small size at the onset have latent course. With their growth during moving of feces may occur disorder of
their completeness with further possible complications. More often is bleeding that in most cases occur defecation.
Depending on the height of polypus localization in intestine blood may be dark red to bright red color. Blood loss may be
from small, light to severe, with signs of small and incredible anemia.
In most patients polypus have a tendense to malignization. Provided biopsia in pre operation period with morphological
investigation reveals malignant transformation of tissues and proves this diagnosis not in all cases. It depends on that in what
part polypus becomes malignant. Final diagnosis may be put after the operation during histological investigation of all
polypus.
Polypus of big size situated in rectum usually strangulate. During this strangulation takes place on the level of anal ring
and is accompanied with severe pain. Not reducible polypus may necrotize.
Polypus are situated in caecum, colon and sigmoid colon. In the most motile areas they may lead to intestinal
invagination. In this case there appear spastic pain, blood excretion with feces. During abdominal palpation they reveal
painful infiltrate. Invagination may prolapse into rectal lumen.
Diagnostic program
Differential diagnosis
Polypus of colon and rectum should be differentiated with malignant and non epithelial tumors, non specific ulcer colitis
and rectal fissures.
Cancer of right part of colon ahs a course with incredible anemia (toxicoanemic form) due to absorption of tumors toxic
products, their action on hemopoetic organs.
Cancer of left part of colon is usually accompanied with signs of obturative intestinal impassability. Additional
examination (finger rectal examination, irigography, endoscopic methods) give a possibility to prove the diagnosis.
At chronic course of non specific ulcer colitis there is injured mucosa of intestine, and little islands of not injured
mucosa between multiple big ulcers look like polypus, so called pseudopolyposis. Detailed anamnesis, specialities of clinical
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course of the disease, irigography and colonoscopy exclude presence of true polypus.
Not epithelial tumors (leyomyoma, lipoma) are situated under intestinal mucosa and at their small size do not cause any
symptoms. With their growth mucosa is injured, there occurs bleeding with its signs. X-ray and endoscopic methods of
investigation, and also histological investigation prove the final diagnosis.
Chronic fissure of rectum with not smooth edges and terminal tuberculum often simulates true polypus. Removal of this
formation both with fissure and provided histological investigation help in proving of diagnosis.
Conservative method of treatment is rarely used. For this is used solution of green greater celandine for its introduction
in enemas (3-4 grams of green mass for 1 kg of patient weight, on the average 50 g for adults). A celandine is ground down on
a meat grinder, conduct in hot water in the ratio 1:10. A medical cycle includes 1530 enemas. Per treatments course is
conducted three cycles at intervals in one month. The low located polypuses from a stratified epithelium, pseudopolypuses
and malignant polypuses are not treated by celandine.
Because of polypuses of small intestine and rectums are inclined to malignization, the basic method of its treatment is
surgical .
Methods of operative treatment at polypus are divided into two groups:
1. Local operations (endoscopic electrocoagulation, polypuss removal). Indication for electrocoaguclation
is presence of single polypus on narrow leg, rarely multiple polypus. Depending on the localization polypus on wide
leg are removed through rectum of by laparotomy with further colotomy.
2. Radical operations as resection of separate segments of colon, right-side, left-side, subtotal colectomy or
coleproctectomy are provided at multiple polypus. video video2 video3
Embryology
The embryonic gastrointestinal tract begins developing during the fourth week of gestation. The primitive gut is derived from the
endoderm and divided into three segments: foregut, midgut, and hindgut. Both midgut and hindgut contribute to the colon,
rectum, and anus.
The midgut develops into the small intestine, ascending colon, and proximal transverse colon, and receives blood supply from the
superior mesenteric artery. During the sixth week of gestation, the midgut herniates out of the abdominal cavity, and then rotates
270 degrees counterclockwise around the superior mesenteric artery to return to its final position inside the abdominal cavity
during the tenth week of gestation.
The hindgut develops into the distal transverse colon, descending colon, rectum, and proximal anus, all of which receive their
blood supply from the inferior mesenteric artery. During the sixth week of gestation, the distal-most end of the hindgut, the cloaca,
is divided by the urorectal septum into the urogenital sinus and the rectum.
The distal anal canal is derived from ectoderm and receives its blood supply from the internal pudendal artery. The dentate line
divides the endodermal hindgut from the ectodermal distal anal canal.
Anatomy
The large intestine extends from the ileocecal valve to the anus. It is divided anatomically and functionally into the colon, rectum,
and anal canal. The wall of the colon and rectum comprise five distinct layers: mucosa, submucosa, inner circular muscle, outer
longitudinal muscle, and serosa. In the colon, the outer longitudinal muscle is separated into three teniae coli, which converge
proximally at the appendix and distally at the rectum, where the outer longitudinal muscle layer is circumferential. In the distal
rectum, the inner smooth-muscle layer coalesces to form the internal anal sphincter. The intraperitoneal colon and proximal one
third of the rectum are covered by serosa; the mid and lower rectum lack serosa.
Colon Landmarks
The colon begins at the junction of the terminal ileum and cecum and extends 3 to 5 feet to the rectum. The rectosigmoid junction
is found at approximately the level of the sacral promontory and is arbitrarily described as the point at which the three teniae coli
coalesce to form the outer longitudinal smooth muscle layer of the rectum. The cecum is the widest diameter portion of the colon
(normally 7.5 to 8.5 cm) and has the thinnest muscular wall. As a result, the cecum is most vulnerable to perforation and least
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vulnerable to obstruction. The ascending colon is usually fixed to the retroperitoneum. The hepatic flexure marks the transition to
the transverse colon. The intraperitoneal transverse colon is relatively mobile, but is tethered by the gastrocolic ligament and
colonic mesentery. The greater omentum is attached to the anterior/superior edge of the transverse colon. These attachments
explain the characteristic triangular appearance of the transverse colon observed during colonoscopy. The splenic flexure marks the
transition from the transverse colon to the descending colon. The attachments between the splenic flexure and the spleen (the
lienocolic ligament) can be short and dense, making mobilization of this flexure during colectomy challenging. The descending
colon is relatively fixed to the retroperitoneum. The sigmoid colon is the narrowest part of the large intestine and is extremely
mobile. Although the sigmoid colon is usually located in the left lower quadrant, redundancy and mobility can result in a portion
of the sigmoid colon residing in the right lower quadrant. This mobility explains why volvulus is most common in the sigmoid
colon and why diseases affecting the sigmoid colon, such as diverticulitis, may occasionally present as right-sided abdominal pain.
The narrow caliber of the sigmoid colon makes this segment of the large intestine the most vulnerable to obstruction.
The arterial supply to the colon is highly variable (Fig. 28-1). In general, the superior mesenteric artery branches into the ileocolic
artery (absent in up to 20% of people), which supplies blood flow to the terminal ileum and proximal ascending colon, the right
colic artery, which supplies the ascending colon, and the middle colic artery, which supplies the transverse colon. The inferior
mesenteric artery branches into the left colic artery, which supplies the descending colon, several sigmoidal branches, which
supply the sigmoid colon, and the superior rectal artery, which supplies the proximal rectum. The terminal branches of each artery
form anastomoses with the terminal branches of the adjacent artery and communicate via the marginal artery of Drummond. This
arcade is complete in only 15 to 20% of people.
The lymphatic drainage of the colon originates in a network of lymphatics in the muscularis mucosa. Lymphatic vessels and lymph
nodes follow the regional arteries. Lymph nodes are found on the bowel wall (epicolic), along the inner margin of the bowel
adjacent to the arterial arcades (paracolic), around the named mesenteric vessels (intermediate), and at the origin of the superior
and inferior mesenteric arteries (main). The sentinel lymph nodes are the first one to four lymph nodes to drain a specific segment
of the colon, and are thought to be the first site of metastasis in colon cancer. The utility of sentinel lymph node dissection and
analysis in colon cancer remains controversial.
The colon is innervated by both sympathetic (inhibitory) and parasympathetic (stimulatory) nerves, which parallel the course of
the arteries. Sympathetic nerves arise from T6-T12 and L1-L3. The parasympathetic innervation to the right and transverse colon is
from the vagus nerve; the parasympathetic nerves to the left colon arise from sacral nerves S2-S4 to form the nervi erigentes.
Anorectal Landmarks
The rectum is approximately 12 to 15 cm in length. Three distinct submucosal folds, the valves of Houston, extend into the rectal
lumen. Posteriorly, the presecral fascia separates the rectum from the presacral venous plexus and the pelvic nerves. At S4, the
rectosacral fascia (Waldeyer's fascia) extends forward and downward and attaches to the fascia propria at the anorectal junction.
Anteriorly, Denonvilliers' fascia separates the rectum from the prostate and seminal vesicles in men and from the vagina in women.
The lateral ligaments support the lower rectum. The surgical anal canal measures 2 to 4 cm in length and is generally longer in
men than in women. It begins at the anorectal junction and terminates at the anal verge. The dentate or pectinate line marks the
transition point between columnar rectal mucosa and squamous anoderm. The 1 to 2 cm of mucosa just proximal to the dentate line
shares histologic characteristics of columnar, cuboidal, and squamous epithelium and is referred to as the anal transition zone. The
dentate line is surrounded by longitudinal mucosal folds, known as the columns of Morgagni, into which the anal crypts empty.
These crypts are the source of cryptoglandular abscesses
In the distal rectum, the inner smooth muscle is thickened and comprises the internal anal sphincter that is surrounded by the
subcutaneous, superficial, and deep external sphincter. The deep external anal sphincter is an extension of the puborectalis
muscle. The puborectalis, iliococcygeus, and pubococcygeus muscles form the levator ani muscle of the pelvic floor.
The superior rectal artery arises from the terminal branch of the inferior mesenteric artery and supplies the upper rectum. The
middle rectal artery arises from the internal iliac; the presence and size of these arteries are highly variable. The inferior rectal
artery arises from the internal pudendal artery, which is a branch of the internal iliac artery. A rich network of collaterals connects
the terminal arterioles of each of these arteries, thus making the rectum relatively resistant to ischemia
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The venous drainage of the rectum parallels the arterial supply. The superior rectal vein drains into the portal system via the
inferior mesenteric vein. The middle rectal vein drains into the internal iliac vein. The inferior rectal vein drains into the internal
pudendal vein, and subsequently into the internal iliac vein. A submucosal plexus deep to the columns of Morgagni forms the
hemorrhoidal plexus and drains into all three veins.
Lymphatic drainage of the rectum parallels the vascular supply. Lymphatic channels in the upper and middle rectum drain
superiorly into the inferior mesenteric lymph nodes. Lymphatic channels in the lower rectum drain both superiorly into the inferior
mesenteric lymph nodes and laterally into the internal iliac lymph nodes. The anal canal has a more complex pattern of lymphatic
drainage. Proximal to the dentate line, lymph drains into both the inferior mesenteric lymph nodes and the internal iliac lymph
nodes. Distal to the dentate line, lymph primarily drains into the inguinal lymph nodes, but can also drain into the inferior
mesenteric lymph nodes and internal iliac lymph nodes.
Both sympathetic and parasympathetic nerves innervate the anorectum. Sympathetic nerve fibers are derived from L1-L3 and join
the preaortic plexus. The preaortic nerve fibers then extend below the aorta to form the hypogastric plexus, which subsequently
joins the parasympathetic fibers to form the pelvic plexus. Parasympathetic nerve fibers are known as the nervi erigentes and
originate from S2-S4. These fibers join the sympathetic fibers to form the pelvic plexus. Sympathetic and parasympathetic fibers
then supply the anorectum and adjacent urogenital organs.
The internal anal sphincter is innervated by sympathetic and parasympathetic nerve fibers; both types of fibers inhibit sphincter
contraction. The external anal sphincter and puborectalis muscles are innervated by the inferior rectal branch of the internal
pudendal nerve. The levator ani receives innervation from both the internal pudendal nerve and direct branches of S3 to S5.
Sensory innervation to the anal canal is provided by the inferior rectal branch of the pudendal nerve. While the rectum is
relatively insensate, the anal canal below the dentate line is sensate.
Congenital Anomalies
Perturbation of the embryologic development of the midgut and hindgut may result in anatomic abnormalities of the colon, rectum,
and anus. Failure of the midgut to rotate and return to the abdominal cavity during the tenth week of gestation results in varying
degrees of intestinal malrotation and colonic nonfixation. Failure of canalization of the primitive gut can result in colonic
duplication. Incomplete descent of the urogenital septum may result in imperforate anus and associated fistulas to the genitourinary
tract. Many infants with congenital anomalies of the hindgut have associated abnormalities in the genitourinary tract.
Normal Physiology
The colon is a major site for water absorption and electrolyte exchange. Approximately 90% of the water contained in ileal fluid is
absorbed in the colon (1000 to 2000 mL/d), and up to 5000 mL of fluid can be absorbed daily. Sodium is absorbed actively via a
Na-K ATPase. The colon can absorb up to 400 mEq of sodium per day. Water accompanies the transported sodium and is absorbed
passively along an osmotic gradient. Potassium is actively secreted into the colonic lumen and absorbed by passive diffusion.
Chloride is absorbed actively via a chloridebicarbonate exchange.
Bacterial degradation of protein and urea produces ammonia. Ammonia is subsequently absorbed and transported to the liver.
Absorption of ammonia depends in part upon intraluminal pH. A decrease in colonic bacteria (e.g., broad spectrum antibiotic
usage) and/or a decrease in intraluminal pH (e.g., lactulose administration) will decrease ammonia absorption.
Short-chain fatty acids (acetate, butyrate, and propionate) are produced by bacterial fermentation of dietary carbohydrates.
Short-chain fatty acids are an important source of energy for the colonic mucosa, and metabolism by colonocytes provides energy
for processes such as active transport of sodium. Lack of a dietary source for production of short-chain fatty acids, or diversion of
the fecal stream by an ileostomy or colostomy, may result in mucosal atrophy and "diversion colitis."
Approximately 30% of fecal dry weight is composed of bacteria (1011 to 1012 bacteria/g of feces). Anaerobes are the predominant
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class of microorganism, and Bacteroides species are the most common (1011 to 1012 organisms/mL). Escherichia coli are the most
numerous aerobes (108 to 1010 organisms/mL). Endogenous microflora are crucial for the breakdown of carbohydrates and
proteins in the colon and participate in the metabolism of bilirubin, bile acids, estrogen, and cholesterol. Colonic bacteria also are
necessary for production of vitamin K. Endogenous bacteria also are thought to suppress the emergence of pathogenic
microorganisms, such as Clostridium difficile. However, the high bacterial load of the large intestine may contribute to sepsis in
critically ill patients and may contribute to intra-abdominal sepsis, abscess, and wound infection following colectomy.
Intestinal gas arises from swallowed air, diffusion from the blood, and intraluminal production. Nitrogen, oxygen, carbon dioxide,
hydrogen, and methane are the major components of intestinal gas. Nitrogen and oxygen are largely derived from swallowed air.
Carbon dioxide is produced by the reaction of bicarbonate and hydrogen ions, and by the digestion of triglycerides to fatty acids.
Hydrogen and methane are produced by colonic bacteria. The production of methane is highly variable. The gastrointestinal tract
usually contains between 100 and 200 mL of gas and 400 to 1200 mL per day are released as flatus, depending upon the type of
food ingested.
Motility
Unlike the small intestine, the large intestine does not demonstrate cyclic motor activity characteristic of the migratory motor
complex. Instead, the colon displays intermittent contractions of either low or high amplitude. Low-amplitude, short-duration
contractions occur in bursts and appear to move the colonic contents both antegrade and retrograde. It is thought that these bursts
of motor activity delay colonic transit and thus increase the time available for absorption of water and exchange of electrolytes.
High-amplitude contractions occur in a more coordinated fashion and create "mass movements." Bursts of "rectal motor complexes"
also have been described. In general, cholinergic activation increases colonic motility.
Defecation
Defecation is a complex, coordinated mechanism involving colonic mass movement, increased intra-abdominal and rectal pressure,
and relaxation of the pelvic floor. Distention of the rectum causes a reflex relaxation of the internal anal sphincter (the rectoanal
inhibitory reflex) that allows the contents to make contact with the anal canal. This "sampling reflex" allows the sensory
epithelium to distinguish solid stool from liquid stool and gas. If defecation does not occur, the rectum relaxes and the urge to
defecate passes (the accommodation response). Defecation proceeds by coordination of increasing intra-abdominal pressure via
the Valsalva maneuver, increased rectal contraction, relaxation of the puborectalis muscle, and opening of the anal canal.
Continence
The maintenance of fecal continence is at least as complex as the mechanism of defecation. Continence requires adequate rectal
wall compliance to accommodate the fecal bolus, appropriate neurogenic control of the pelvic floor and sphincter mechanism, and
functional internal and external sphincter muscles. At rest, the puborectalis muscle creates a "sling" around the distal rectum,
forming a relatively acute angle that distributes intraabdominal forces onto the pelvic floor. With defecation, this angle straightens,
allowing downward force to be applied along the axis of the rectum and anal canal. The internal and external sphincters are
tonically active at rest. The internal sphincter is responsible for most of the resting, involuntary sphincter tone (resting pressure).
The external sphincter is responsible for most of the voluntary sphincter tone (squeeze pressure). Branches of the pudendal nerve
innervate both the internal and external sphincter. Finally, the hemorrhoidal cushions may contribute to continence by
mechanically blocking the anal canal. Thus, impaired continence may result from poor rectal compliance, injury to the internal
and/or external sphincter or puborectalis, or nerve damage or neuropathy.
Clinical Evaluation
Clinical Assessment
A complete history and physical examination is the starting point for evaluating any patient with suspected disease of the colon
and rectum. Special attention should be paid to the patient's past medical and surgical history to detect underlying conditions that
might contribute to a gastrointestinal problem. If patients have had prior intestinal surgery, it is essential that one understand the
resultant gastrointestinal anatomy. In addition, family history of colorectal disease, especially inflammatory bowel disease, polyps,
and colorectal cancer, is crucial. Medication use must be detailed as many drugs cause gastrointestinal symptoms. Before
recommending operative intervention, the adequacy of medical treatment must be ascertained. In addition to examining the
abdomen, visual inspection of the anus and perineum and careful digital rectal exam are essential.
Endoscopy
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Anoscopy
The anoscope is a useful instrument for examination of the anal canal. Anoscopes are made in a variety of sizes and measure
approximately 8 cm in length. A larger anoscope provides better exposure for anal procedures such as rubber band ligation or
sclerotherapy of hemorrhoids. The anoscope, with obturator in place, should be adequately lubricated and gently inserted into the
anal canal. The obturator is withdrawn, inspection of the visualized anal canal is done, and the anoscope should then be
withdrawn. It is rotated 90 degrees and reinserted to allow visualization of all four quadrants of the canal. If the patient complains
of severe perianal pain and cannot tolerate a digital rectal examination, anoscopy should not be attempted without anesthesia.
Proctoscopy
The rigid proctoscope is useful for examination of the rectum and distal sigmoid colon and is occasionally used therapeutically.
The standard proctoscope is 25 cm in length and available in various diameters. Most often, a 15- or 19-mm diameter proctoscope
is used for diagnostic examinations. The large (25-mm diameter) proctoscope is useful for procedures such as polypectomy,
electrocoagulation, or detorsion of a sigmoid volvulus. A smaller "pediatric" proctoscope (11-mm diameter) is better tolerated by
patients with anal stricture. Suction is necessary for an adequate proctoscopic examination.
Video or fiberoptic flexible sigmoidoscopy and colonoscopy provide excellent visualization of the colon and rectum.
Sigmoidoscopes measure 60 cm in length. Full depth of insertion may allow visualization as high as the splenic flexure, although
the mobility and redundancy of the sigmoid colon often limit the extent of the examination. Partial preparation with enemas is
usually adequate for sigmoidoscopy and most patients can tolerate this procedure without sedation. Colonoscopes measure 100 to
160 cm in length and are capable of examining the entire colon and terminal ileum. A complete oral bowel preparation is usually
necessary for colonoscopy and the duration and discomfort of the procedure usually require conscious sedation. Both
sigmoidoscopy and colonoscopy can be used diagnostically and therapeutically. Electrocautery should generally not be used in the
absence of a complete bowel preparation because of the risk of explosion of intestinal methane or hydrogen gases. Diagnostic
colonoscopes possess a single channel through which instruments such as snares, biopsy forceps, or electrocautery can be passed;
this channel also provides suction and irrigation capability. Therapeutic colonoscopes possess two channels to allow simultaneous
suction/irrigation and the use of snares, biopsy forceps, or electrocautery.
Imaging
Despite advanced radiologic techniques, plain x-rays and contrast studies continue to play an important role in the evaluation of
patients with suspected colon and rectal diseases. Plain x-rays of the abdomen (supine, upright, and diaphragmatic views) are
useful for detecting free intra-abdominal air, bowel gas patterns suggestive of small or large bowel obstruction, and volvulus.
Contrast studies are useful for evaluating obstructive symptoms, delineating fistulous tracts, and diagnosing small perforations or
anastomotic leaks. While Gastrografin cannot provide the mucosal detail provided by barium, this water-soluble contrast agent is
recommended if perforation or leak is suspected. Double-contrast barium enema has been reported to be 70 to 90% sensitive for
the detection of mass lesions greater than 1 cm in diameter. 1 Detection of small lesions can be extremely difficult, especially in a
patient with extensive diverticulosis. For this reason, a colonoscopy is preferred for evaluating nonobstructing mass lesions in the
colon. Double-contrast barium enema has been used as a back-up examination if colonoscopy is incomplete.
Computed Tomography
Computed tomography (CT) is commonly employed in the evaluation of patients with abdominal complaints. Its utility is primarily
in the detection of extraluminal disease, such as intra-abdominal abscesses and pericolic inflammation, and in staging colorectal
carcinoma, because of its sensitivity in detection of hepatic metastases. 2 Extravasation of oral or rectal contrast may also confirm
the diagnosis of perforation or anastomotic leak. Nonspecific findings such as bowel wall thickening or mesenteric stranding may
suggest inflammatory bowel disease, enteritis/colitis, or ischemia. A standard CT scan is relatively insensitive for the detection of
intraluminal lesions.
Virtual Colonoscopy
Virtual colonoscopy is a new radiologic technique that is designed to overcome some of the limitations of traditional CT scanning.
This technology uses helical CT and three-dimensional reconstruction to detect intraluminal colonic lesions. Oral bowel
preparation, oral and rectal contrast, and colon insufflation are used to maximize sensitivity. Early evaluation of virtual
colonoscopy suggests that accuracy may approach that of colonoscopy for detection of lesions 1 cm in diameter or greater.
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The main use of magnetic resonance imaging (MRI) in colorectal disorders is in evaluation of pelvic lesions. MRI is more sensitive
than CT for detecting bony involvement or pelvic sidewall extension of rectal tumors. MRI also can be helpful in the detection and
delineation of complex fistulas in ano. The use of an endorectal coil may increase sensitivity.
Positron emission tomography (PET) is used for imaging tissues with high levels of anaerobic glycolysis, such as malignant
tumors. 18 F-fluorodeoxyglucose (FDG) is injected as a tracer; metabolism of this molecule then results in positron emission. PET
has been used as an adjunct to CT in the staging of colorectal cancer and may prove useful in discriminating recurrent cancer from
fibrosis. At present, the efficacy and utility of PET in the detection of recurrent and/or metastatic colorectal cancer remains
unproven.
Angiography
Angiography is occasionally used for the detection of bleeding within the colon or small bowel. To visualize hemorrhage
angiographically, bleeding must be relatively brisk (approximately 0.5 to 1.0 mL per minute). If extravasation of contrast is
identified, infusion of vasopressin or angiographic embolization can be therapeutic.
Endorectal ultrasound is primarily used to evaluate the depth of invasion of neoplastic lesions in the rectum. The normal rectal
wall appears as a five-layer structure (Fig. 28-6). Ultrasound can reliably differentiate most benign polyps from invasive tumors
based upon the integrity of the submucosal layer. Ultrasound can also differentiate superficial T1-T2 from deeper T3-T4 tumors.
Overall, the accuracy of ultrasound in detecting depth of mural invasion ranges between 81 and 94%. 3 This modality also can
detect enlarged perirectal lymph nodes, which may suggest nodal metastases; accuracy of detection of pathologically positive
lymph nodes is 58 to 83%. Ultrasound may also prove useful for early detection of local recurrence after surgery.
Endoanal ultrasound is used to evaluate the layers of the anal canal. Internal anal sphincter, external anal sphincter, and
puborectalis muscle can be differentiated. Endoanal ultrasound is particularly useful for detecting sphincter defects and for
outlining complex anal fistulas.
Anorectal physiologic testing uses a variety of techniques to investigate the function of the pelvic floor. These techniques are
useful in the evaluation of patients with incontinence, constipation, rectal prolapse, obstructed defecation, and other disorders of
the pelvic floor.
Manometry
Anorectal manometry is performed by placing a pressure-sensitive catheter in the lower rectum. The catheter is then withdrawn
through the anal canal and pressures recorded. A balloon attached to the tip of the catheter also can be used to test anorectal
sensation. The resting pressure in the anal canal reflects the function of the internal anal sphincter (normal: 40 to 80 mm Hg),
while the squeeze pressure, defined as the maximum voluntary contraction pressure minus the resting pressure, reflects function of
the external anal sphincter (normal: 40 to 80 mm Hg above resting pressure). The high-pressurezone estimates the length of the
anal canal (normal: 2.0 to 4.0 cm). The rectoanal inhibitory reflex can be detected by inflating a balloon in the distal rectum;
absence of this reflex is characteristic of Hirschsprung's disease.
Neurophysiology
Neurophysiologic testing assesses function of the pudendal nerves and recruitment of puborectalis muscle fibers. Pudendal nerve
terminal motor latency measures the speed of transmission of a nerve impulse through the distal pudendal nerve fibers (normal: 1.8
to 2.2 msec); prolonged latency suggests the presence of neuropathy. EMG recruitment assesses the contraction and relaxation of
the puborectalis muscle during attempted defecation. Normally, recruitment increases when a patient is instructed to "squeeze," and
decreases when a patient is instructed to "push." Inappropriate recruitment is an indication of paradoxical contraction
(nonrelaxation of the puborectalis). Needle EMG has been used to map both the pudendal nerves and the anatomy of the internal
and external sphincters. However, this examination is painful and poorly tolerated by most patients. Needle EMG has largely been
replaced by pudendal nerve motor-latency testing to assess pudendal nerve function and endoanal ultrasound to map the sphincters.
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Rectal evacuation studies include the balloon expulsion test and video defecography. Balloon expulsion assesses a patient's ability
to expel an intrarectal balloon. Video defecography provides a more detailed assessment of defecation. In this test, barium paste is
placed in the rectum and defecation is then recorded fluoroscopically. Defecography is used to differentiate nonrelaxation of the
puborectalis, obstructed defecation, increased perineal descent, rectal prolapse and intussusception, rectocele, and enterocele. The
addition of vaginal contrast and intraperitoneal contrast is useful in delineating complex disorders of the pelvic floor.
Laboratory Studies
Fecal occult blood testing (FOBT) is used as a screening test for colonic neoplasms in asymptomatic, average-risk individuals. The
efficacy of this test is based upon serial testing because the majority of colorectal malignancies will bleed intermittently. FOBT has
been a nonspecific test for peroxidase contained in hemoglobin; consequently, occult bleeding from any gastrointestinal source
will produce a positive result. Similarly, many foods (red meat, some fruits and vegetables, and vitamin C) will produce a false-
positive result. Patients were counseled to eat a restricted diet for 2 to 3 days prior to the test. Increased specificity is now possible
by using immunochemical FOBT. These tests rely on monoclonal or polyclonal antibodies to react with the intact globin portion of
human hemoglobin. Because globin does not survive in the upper gastrointestinal tract, the immunochemical tests are more specific
for identifying occult bleeding from the colon or rectum. Dietary restrictions are not necessary. Any positive FOBT mandates
further investigation, usually by colonoscopy.
Stool Studies
Stool studies are often helpful in evaluating the etiology of diarrhea. Wet-mount examination reveals the presence of fecal
leukocytes, which may suggest colonic inflammation or the presence of an invasive organism such as invasive E. coli or Shigella.
Stool cultures can detect pathogenic bacteria, ova, and parasites. C. difficile colitis is diagnosed by detecting bacterial toxin in the
stool. 4 Steatorrhea may be diagnosed by adding Sudan red stain to a stool sample.
Serum Tests
Specific laboratory tests that should be performed will be dictated by the clinical scenario. Preoperative studies generally include a
complete blood count and electrolyte panel. The addition of coagulation studies, liver function tests, and blood typing/cross-
matching depends upon the patient's medical condition and the proposed surgical procedure.
Tumor Markers
Carcinoembryonic antigen (CEA) may be elevated in 60 to 90% of patients with colorectal cancer. Despite this, CEA is not an
effective screening tool for this malignancy. Many practitioners follow serial CEA levels after curative-intent surgery in order to
detect early recurrence of colorectal cancer. However, this tumor marker is nonspecific, and no survival benefit has yet been proven.
Other biochemical markers (ornithine decarboxylase, urokinase) have been proposed, but none has yet proven sensitive or specific
for detection, staging, or predicting prognosis of colorectal carcinoma. 5
Genetic Testing
Although familial colorectal cancer syndromes, such as familial adenomatous polyposis (FAP) and hereditary nonpolyposis colon
cancer (HNPCC) are rare, information about the specific genetic abnormalities underlying these disorders has led to significant
interest in the role of genetic testing for colorectal cancer. 6 Tests for mutations in the adenomatous polyposis coli (APC) gene
responsible for FAP, and in mismatch repair genes responsible for HNPCC, are commercially available and extremely accurate in
families with known mutations. Although many of these mutations are also present in sporadic colorectal cancer, the accuracy of
genetic testing in average-risk individuals is considerably lower and these tests are not recommended for screening. Because of the
potential psychosocial implications of genetic testing, it is strongly recommended that professional genetic counselors be involved
in the care of any patient considering these tests.
Pain
Abdominal Pain
Abdominal pain is a nonspecific symptom with a myriad of causes. Abdominal pain related to the colon and rectum can result from
obstruction (either inflammatory or neoplastic), inflammation, perforation, or ischemia. Plain x-rays and judicious use of contrast
studies and/or a CT scan can often confirm the diagnosis. Gentle retrograde contrast studies (barium or Gastrografin enema) may
be useful in delineating the degree of colonic obstruction. Sigmoidoscopy and/or colonoscopy performed by an experienced
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endoscopist can assist in the diagnosis of ischemic colitis, infectious colitis, and inflammatory bowel disease. However, if
perforation is suspected, colonoscopy and/or sigmoidoscopy are generally contraindicated. Evaluation and treatment of abdominal
pain from a colorectal source should follow the usual surgical principles of a thorough history and physical examination,
appropriate diagnostic tests, resuscitation, and appropriately timed surgical intervention.
Pelvic Pain
Pelvic pain can originate from the distal colon and rectum or from adjacent urogenital structures. Tenesmus may result from
proctitis or from a rectal or retrorectal mass. Cyclical pain associated with menses, especially when accompanied by rectal
bleeding, suggests a diagnosis of endometriosis. Pelvic inflammatory disease also can produce significant abdominal and pelvic
pain. The extension of a peridiverticular abscess or periappendiceal abscess into the pelvis may also cause pain. CT scan and/or
MRI may be useful in differentiating these diseases. Proctoscopy (if tolerated) also can be helpful. Occasionally, laparoscopy will
yield a diagnosis.
Anorectal Pain
Anorectal pain is most often secondary to an anal fissure or perirectal abscess and/or fistula. Physical examination can usually
differentiate these conditions. Other, less common causes of anorectal pain include anal canal neoplasms, perianal skin infection,
and dermatologic conditions. Proctalgia fugax results from levator spasm and may present without any other anorectal findings.
Physical exam is critical in evaluating patients with anorectal pain. If a patient is too tender to examine in the office, an
examination under anesthesia is necessary. MRI may be helpful in select cases where the etiology of pain is elusive.
The first goal in evaluating and treating a patient with gastrointestinal hemorrhage is adequate resuscitation. The principles of
ensuring a patent airway, supporting ventilation, and optimizing hemodynamic parameters apply and coagulopathy and/or
thrombocytopenia should be corrected. The second goal is to identify the source of hemorrhage. Because the most common source
of gastrointestinal hemorrhage is esophageal, gastric, or duodenal, nasogastric aspiration should always be performed; return of
bile suggests that the source of bleeding is distal to the ligament of Treitz. If aspiration reveals blood or nonbile secretions, or if
symptoms suggest an upper intestinal source, esophagogastroduodenoscopy is performed. Anoscopy and/or limited proctoscopy
can identify hemorrhoidal bleeding. A technetium-99 (99mTc)-tagged red blood cell (RBC) scan is extremely sensitive and is able
to detect as little as 0.1 mL/h of bleeding; however, localization is imprecise. If the 99mTc-tagged RBC scan is positive,
angiography can then be employed to localize bleeding. Infusion of vasopressin or angioembolization may be therapeutic.
Alternatively, a catheter can be left in the bleeding vessel to allow localization at the time of laparotomy. If the patient is
hemodynamically stable, a rapid bowel preparation (over 4 to 6 hours) can be performed to allow colonoscopy. Colonoscopy may
identify the cause of the bleeding, and cautery or injection of epinephrine into the bleeding site may be used to control
hemorrhage. Colectomy may be required if bleeding persists despite these interventions. Intraoperative colonoscopy and/or
enteroscopy may assist in localizing bleeding. If colectomy is required, a segmental resection is preferred if the bleeding source can
be localized. "Blind" subtotal colectomy may very rarely be required in a patient who is hemodynamically unstable with ongoing
colonic hemorrhage of an unknown source. In this setting, it is crucial to irrigate the rectum and examine the mucosa by
proctoscopy to ensure that the source of bleeding is not distal to the resection margin
Occult blood loss from the gastrointestinal tract may manifest as iron-deficiency anemia or may be detected with fecal occult blood
testing. Because colon neoplasms bleed intermittently and rarely present with rapid hemorrhage, the presence of occult fecal blood
should always prompt a colonoscopy. Unexplained iron-deficiency anemia is also an indication for colonoscopy.
Hematochezia is commonly caused by hemorrhoids or fissure. Sharp, knife-like pain and bright-red rectal bleeding with bowel
movements suggest the diagnosis of fissure. Painless, bright-red rectal bleeding with bowel movements is often secondary to a
friable internal hemorrhoid that is easily detected by anoscopy. In the absence of a painful, obvious fissure, any patient with rectal
bleeding should undergo a careful digital rectal examination, anoscopy, and proctosigmoidoscopy. Failure to diagnose a source in
the distal anorectum should prompt colonoscopy.
Constipation is an extremely common complaint, affecting more than 4 million people in the United States. Despite the prevalence
of this problem, there is lack of agreement about an appropriate definition of constipation. Patients may describe infrequent bowel
movements, hard stools, or excessive straining. A careful history of these symptoms often clarifies the nature of the problem.
Constipation has a myriad of causes. Underlying metabolic, pharmacologic, endocrine, psychologic, and neurologic causes often
contribute to the problem. A stricture or mass lesion should be excluded by colonoscopy or barium enema. After these causes have
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been excluded, evaluation focuses upon differentiating slow-transit constipation from outlet obstruction. Transit studies, in which
radiopaque markers are swallowed and then followed radiographically, are useful for diagnosing slow-transit constipation.
Anorectal manometry and electromyography can detect nonrelaxation of the puborectalis, which contributes to outlet obstruction.
The absence of an anorectal inhibitory reflex suggests Hirschsprung's disease and may prompt a rectal mucosal biopsy.
Defecography can identify rectal prolapse, intussusception, rectocele, or enterocele.
Medical management is the mainstay of therapy for constipation and includes fiber, increased fluid intake, and laxatives. Outlet
obstruction from nonrelaxation of the puborectalis often responds to biofeedback. 7 Surgery to correct rectocele and rectal
prolapse has a variable effect on symptoms of constipation, but can be successful in selected patients. Subtotal colectomy is
considered only for patients with severe slow-transit constipation (colonic inertia) refractory to maximal medical interventions.
While this operation almost always increases bowel movement frequency, complaints of diarrhea, incontinence, and abdominal
pain are not infrequent, and patients should be carefully selected. 8
Diarrhea is also a common complaint and is usually a self-limited symptom of infectious gastroenteritis. If diarrhea is chronic or is
accompanied by bleeding or abdominal pain, further investigation is warranted. Bloody diarrhea and pain are characteristic of
colitis; etiology can be an infection (invasive E. coli, Shigella, Salmonella, Campylobacter, Entamoeba histolytica, or C. difficile),
inflammatory bowel disease (ulcerative colitis or Crohn's colitis), or ischemia. Stool wet-mount and culture can often diagnose
infection. Sigmoidoscopy or colonoscopy can be helpful in diagnosing inflammatory bowel disease or ischemia. However, if the
patient has abdominal tenderness, particularly with peritoneal signs, or any other evidence of perforation, endoscopy is
contraindicated.
Chronic diarrhea may present a more difficult diagnostic dilemma. Chronic ulcerative colitis, Crohn's colitis, infection,
malabsorption, and short gut syndrome can cause chronic diarrhea. Rarely, carcinoid syndrome and islet cell tumors (vasoactive
intestinal peptide-secreting tumor [VIPoma], somatostatinoma, gastrinoma) present with this symptom. Large villous lesions may
cause secretory diarrhea. Collagenous colitis can cause diarrhea without any obvious mucosal abnormality. Along with stool
cultures, tests for malabsorption, and metabolic investigations, colonoscopy can be invaluable in differentiating these causes.
Biopsies should be taken even if the colonic mucosa appears grossly normal.
Irritable bowel syndrome is a particularly troubling constellation of symptoms consisting of crampy abdominal pain, bloating,
constipation, and urgent diarrhea. Work-up reveals no underlying anatomic or physiologic abnormality. Once other disorders have
been excluded, dietary restrictions and avoidance of caffeine, alcohol, and tobacco may help to alleviate symptoms.
Antispasmodics and bulking agents may be helpful.
Incontinence
The incidence of fecal incontinence has been estimated to occur in 10 to 13 individuals per 1000 people older than age 65 years.
Incontinence ranges in severity from occasional leakage of gas and liquid stool to daily loss of solid stool. The underlying cause of
incontinence is often multifactorial and diarrhea is often contributory. In general, causes of incontinence can be classified as
neurogenic or anatomic. Neurogenic causes include diseases of the central nervous system and spinal cord along with pudendal
nerve injury. Anatomic causes include congenital abnormalities, procidentia, overflow incontinence secondary to impaction or
neoplasm, and trauma. The most common traumatic cause of incontinence is injury to the anal sphincter during vaginal delivery.
Other causes include anorectal surgery, impalement, and pelvic fracture.
After a thorough medical evaluation to detect underlying conditions that might contribute to incontinence, evaluation focuses on
assessment of the anal sphincter and pudendal nerves. Pudendal nerve terminal motor latency testing may detect neuropathy. Anal
manometry can detect low resting and squeeze pressures. Defecography can detect rectal prolapse. Endoanal ultrasound is
invaluable in diagnosing sphincter defects.
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The prevalence of diverticular disease in the general population ranges between 35% and 50%, as estimated by several large
autopsy and radiographic series.13 Prevalence directly correlates with age, estimated to be less than 5% at age 40, increasing to
30% by age 60, and as high as 65% by age 85.25 Males and females appear to be affected equally. Geographically, diverticular
disease is much more common in the United States and Western Europe than in other less industrialized regions such as
Africa, South America, and Asia. Although diet is thought by many to contribute significantly to the development of
diverticular disease, the complete etiology is likely to involve other, as yet unrecognized, factors. For example, diverticular
disease in Asian populations is localized predominantly to the right colon, in distinct contrast to the left-sided predilection
observed in Western civilizations. Such variations in the anatomic distribution of diverticula among civilizations might suggest
that factors other than diet alone exert a substantial influence on the character of this disease worldwide.
Mechanical Factors. Clinical studies within the past 30 years have implicated low fiber diets as a prominent etiologic
factor in the development of diverticular disease.24, 25 Diets lacking vegetable fiber are presumed to predispose to the
development of diverticula by altering colonic motility. Colonic motility is a complex process serving to transport feces
distally while also permitting storage, thereby facilitating fluid and electrolyte absorption. Colonic motility is modulated by
myogenic, hormonal, and neural influences. There is evidence that patients with diverticular disease manifest exaggerated
contractile responses to feeding and hormonal stimuli. Resting pressures are usually normal, however. These abnormal
muscular contractions are believed to cause colonic smooth muscle hypertrophy, a characteristic of diverticular disease.
The possible role of dietary fiber in the development of diverticula is best explained by effects on colonic diameter and
stool consistency. It has been postulated that colonic segments with bulky fecal contents and large luminal diameters are less
likely to exhibit exaggerated segmentation. Low-fiber diets are associated with a narrowed colon filled with small, hardened
feces; segmentation is enhanced, and high luminal pressures tend to develop. Although this concept has been widely
disseminated, definitive evidence for a causal relationship between low dietary fiber and the development of diverticular
disease does not exist.31, 39 Nonetheless, high-residue diets are in widespread use in the management of diverticular disease.
Whether such therapy has a significant influence on the natural history of diverticular disease is unclear.
Anatomic Features. Diverticula tend to develop at specific points in the circumference of the colon. This localization is
determined, in part, by the anatomic relationship between the colonic musculature and its nutrient blood supply. Diverticula
form at so-called weak points where the nutrient blood vessels (vasa recta) penetrate the circular muscle layer en route to the
mucosa. These perforating vessels tend to penetrate the colonic wall along the mesenteric border of the two antimesenteric
taeniae. The gaps in the circular muscle layer where the vasa recta penetrate constitute points of potential weakness through
which the mucosa and submucosa can herniate, forming diverticula. Diverticula, therefore, are usually located between the
single mesenteric taenia and either of the two antimesenteric taeniae. Less commonly, diverticula form in the area between the
antimesenteric taeniae. Although also consisting of mucosal herniation through the muscular layers of the colonic wall, these
diverticula tend to be less prominent. In many instances the mucosal herniation does not quite extend to the serosa, causing
these to be referred to as intramural diverticula.
The distribution of diverticula throughout the colon also tends to follow a pattern, but with considerable individual
variation. The overwhelming majority of diverticula occur in the descending and sigmoid colon. It is estimated that 90% to
95% of patients with diverticulosis will have involvement of the sigmoid colon. Approximately 65% of patients will have
disease limited to the sigmoid colon alone. Conversely, only a small number of patients (2% to 10%) will have disease
confined to the right colon. Solitary diverticula occur most commonly in the cecum.
NATURAL HISTORY
After the first episode of diverticulitis, approximately one third of patients will sustain a second attack, usually within 3 to
5 years. Another 30% to 40% will suffer from intermittent symptoms of discomfort and crampy abdominal pain, without
requiring hospitalization. The remainder can be expected to remain symptom free. The prognosis is worse after a second attack,
with only 10% of patients remaining symptom free. The morbidity and the mortality from recurrent attacks are also higher than
that associated with an initial episode. Complications such as abscess formation or fistulization develop in approximately 20%
of patients after a single attack of diverticulitis, while the complication rate approaches 60% in patients who have had previous
episodes.
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Because diverticulosis is an acquired disease, the incidence of which clearly increases with age, it would seem logical that
the number and size of diverticula would also increase with time. However, only 30% of patients demonstrate radiologic
evidence of progression of their disease, either in the form of an increased number of diverticula or involvement of other
segments of the colon. Progression of disease after resection of involved colon is also unusual, occurring in less than 10% to
15% of patients. video video2 video3 video4
CROHNS DISEASE
Crohns disease is a chronic, nonspecific inflammatory disease of the gastrointestinal tract of unknown etiology. It
involves mainly the ileum and large intestine, most often producing symptoms of obstruction or localized perforation with
fistula. Both medical and surgical treatments are palliative. Nonetheless, operative excision provides effective symptomatic
relief and produces reasonable long-term benefit.
Epidemiology
Crohn's disease is a chronic, idiopathic inflammatory disease with a propensity to affect the distal ileum, although any
part of the alimentary tract can be involved. Recent estimates of the incidence of Crohn's disease in the United States have
ranged from 3.6 to 8.8 per 100,000. 34 A dramatic increase in incidence in the United States was observed to occur from the
mid-1950s through the early 1970s. Incidence rates have been stable since the 1980s. Substantial regional variations in
incidence have been observed, with the highest incidences reported to exist in northern latitudes. The incidence of Crohn's
disease varies among ethnic groups within the same geographic region. For example, members of the East European
Ashkenazi Jewish population are at two- to fourfold higher risk of developing Crohn's disease than are members of other
populations living in the same location.
Most studies suggest that Crohn's disease is slightly more prevalent in females than in males. The median age at which
patients are diagnosed with Crohn's disease is approximately 30 years; however, age of diagnosis can range from early
childhood through the entire life span.
Both genetic and environmental factors appear to influence the risk for developing Crohn's disease. The relative risk
among first-degree relatives of patients with Crohn's disease is 14 to 15 times higher than that of the general population.
Approximately 1 of 5 patients with Crohn's disease will report having at least one affected relative. The concordance rate
among monozygotic twins is as high as 67%; however, Crohn's disease is not associated with simple mendelian inheritance
patterns. Although there is a tendency within families for either ulcerative colitis or Crohn's disease to be present exclusively,
mixed kindreds also occur, suggesting the presence of some shared genetic traits as a basis for both diseases.
Higher socioeconomic status is associated with an increased risk of Crohn's disease. Most studies have found breast-
feeding to be protective against the development of Crohn's disease. Crohn's disease is more prevalent among smokers.
Furthermore, smoking is associated with the increased risk for both the need for surgery and the risk of relapse after surgery
for Crohn's disease.
Crohn's disease is characterized by sustained inflammation. Whether this inflammation represents an appropriate
response to a yet unrecognized pathogen or an inappropriate response to a normally innocuous stimulus is unknown. Various
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hypotheses on the roles of environmental and genetic factors in the pathogenesis of Crohn's disease have been proposed.
Many infectious agents have been suggested to be the causative organism of Crohn's disease. Candidate organisms have
included Chlamydia, Listeria monocytogenes, Pseudomonas species, reovirus, Mycobacterium paratuberculosis, and many
others. There is no conclusive evidence that any of these organisms is the causative agent.
Studies using animal models suggest that in a genetically susceptible host, nonpathogenic, commensal enteric flora are
sufficient to induce a chronic inflammatory response resembling that associated with Crohn's disease. In these models, the
sustained intestinal inflammation is the result of either abnormal epithelial barrier function or immune dysregulation. Poor
barrier function is hypothesized to permit inappropriate exposure of lamina propria lymphocytes to antigenic stimuli derived
from the intestinal lumen. In addition, a variety of defects in immune regulatory mechanisms, e.g., overresponsiveness of
mucosal T cells to enteric flora-derived antigens, can lead to defective immune tolerance and sustained inflammation.
Specific genetic defects associated with Crohn's disease in human patients are beginning to be defined. For example,
the presence of a locus on chromosome 16 (the so-called IBD1 locus) has been linked to Crohn's disease. The IBD1 locus has
been identified as the NOD2 gene. 35,36 Persons with allelic variants on both chromosomes have a 40-fold relative risk of
Crohn's disease when compared to those without variant NOD2 genes. The relevance of this gene to the pathogenesis of
Crohn's disease is biologically plausible, because the protein product of the NOD2 gene mediates the innate immune
response to microbial pathogens.
Although the pathologic hallmark of Crohn's disease is focal, transmural inflammation of the intestine, a spectrum of
pathologic lesions can be present. The earliest lesion characteristic of Crohn's disease is the aphthous ulcer. These superficial
ulcers are up to 3 mm in diameter and are surrounded by a halo of erythema. In the small intestine, aphthous ulcers typically
arise over lymphoid aggregates. Granulomas are highly characteristic of Crohn's disease and are reported to be present in up
to 70% of intestinal specimens obtained during surgical resection. These granulomas are noncaseating and can be found in
both areas of active disease and apparently normal intestine, in any layer of the bowel wall, and in mesenteric lymph nodes.
As disease progresses, aphthae coalesce into larger, stellate-shaped ulcers. Linear or serpiginous ulcers may form when
multiple ulcers fuse in a direction parallel to the longitudinal axis of the intestine. With transverse coalescence of ulcers, a
cobblestone appearance of the mucosa may arise.
With advanced disease, inflammation can be transmural. Serosal involvement results in adhesion of the inflamed bowel
to other loops of bowel or other adjacent organs. Transmural inflammation also can result in fibrosis, with stricture formation,
intra-abdominal abscesses, fistulas, and, rarely, free perforation. Inflammation in Crohn's disease can affect discontinuous
portions of intestine: so-called "skip lesions" that are separated by intervening normal-appearing intestine.
A feature of Crohn's disease that is grossly evident and helpful in identifying affected segments of intestine during
surgery is the presence of fat wrapping (Fig. 27-17). This finding is virtually pathognomonic of Crohn's disease. It is the
encroachment of mesenteric fat onto the serosal surface of the bowel. The presence of fat wrapping correlates well with the
presence of underlying acute and chronic inflammation.
ETIOLOGY
No specific etiology of the disease has been identified. There are two main schools of investigation: the microbiologic
and the immunologic. Microbiologists have long sought a specific micro-organism that might be the cause of the disease;
however, none has yet been identified. Recent reports of the isolation of Mycobacterium paratuberculosis from segments of
bowel affected with Crohns disease excited interest, but this organism as a specific etiology for the disease has yet to be
proved. Also, no virus has been identified as an etiologic agent.
An immunologic origin of the disease has also been sought. No doubt an immunologic response to the condition does
exist. Some have postulated that a childhood sensitization to milk impairs mucosal integrity and allows bacteria or
bacteriologic products to enter the body. A cellular and humoral immune response to these products then ensues. The
ileocolic epithelium, in particular, may be the target of a necrotizing immune response, with ensuing ulceration, tissue
destruction, and the clinical appearance of the disease. Although an immunologic response certainly plays a role in the
pathogenesis of the condition, its role as an etiologic agent is still unclear.
Other data suggest that environmental factors have an etiologic role in the disease. The disease is more common among
persons living in temperate climates than among those living in tropical climates. Smoking may exert a stimulating effect on
the disease; many patients with Crohns disease are heavy smokers. Spouses of persons with Crohns disease have a higher
incidence of the disease than persons in the general population. Although these data suggest that environmental factors have a
role, no specific environmental factor has been identified.
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SYMPTOMS
The most common symptoms of Crohns disease are those from the intestinal lesions, with abdominal pain, especially of a
cramping nature, topping the list. Diarrhea is frequent. The stools may contain blood, although they often do not. Patients
experience abdominal distention or flatulence and sometimes nausea and vomiting. Eating becomes difficult, because it induces
symptoms. Patients therefore decrease their food intake and lose weight. Should fistulas develop, the pain and discharge of
intestinal content at the site of the fistulas to the skin or in the perianal area produce localized symptoms in these areas. Systemic
responses include fever and malaise; localized pain and discomfort are related to the sites of extraintestinal involvement in the
skin, eyes, and joints.
The course of the disease is one of exacerbations and remissions, but as the lesions mature and complications develop, the
symptoms continue unabated and the disease becomes relentlessly progressive. About 70% of patients eventually come to
operation, in spite of spontaneous remissions and medical or dietary therapy.
DIAGNOSIS
Diagnosis is based on the history, physical findings, and appropriate laboratory tests. The physical findings include the
palpation of the thickened bowel wall or adjacent inflammatory response or abscesses in the abdomen. Hyperactive bowel tones are
heard using auscultation, and peristaltic rushes in the small intestine may even be seen through a thin abdominal wall. Abdominal
distention occurs. Fistulas are apparent, and probes and catheters can be passed through the cutaneous openings and into the
lumen of the bowel through the tracts. On inspection, the perianal skin appears bluish, and perianal fissures, abscesses, and
fistulas can be identified.
Proctoscopy often reveals the characteristic rectal aphthous ulcer with surrounding normal-appearing mucosa. With
progressive and extensive involvement, the ulcerations involve more and more of the lumen of the bowel, with diminishing isolated
segments of normal mucosa remaining. Anoscopy can show perianal abscesses, perianal fistulas, and even rectovaginal fistulas.
Colonoscopy delineates the extent of the lesions in the large intestine. Sometimes the colonoscope can be passed through the
colon and into the ileum to identify the ileal lesions of the disease. The hallmarks of Crohns disease are the discontinuous and
asymmetrical nature of the endoscopic findings. Biopsies taken during endoscopy show chronic inflammation and sometimes
granulomas.
Roentgenographic examination of the gastrointestinal tract using BaSO4. Proximal dilatation of the bowel accompanies
obstructing lesions. Long lengths of narrowed terminal ileum may reduce the caliber of the lumen to the size of a string. Areas of
dilatation may alternate with areas of constriction. The cobblestone appearance of the mucosa may be apparent, as may the rake
ulcers. Fissures, fistulas, and perienteric abscesses may be found. Computed axial tomography may help delineate thickened
bowel, perienteric abscesses, and perforations. In toxic megacolon, the transverse colon is greatly dilated and the bowel wall is
thickened. A mass accompanying a narrowed or ulcerated area suggests cancer. Free air in the abdomen is present with free
perforation.
The differential diagnosis includes both specific and nonspecific causes of intestinal inflammation. Specific microbiologic
diseases that may be confused with Crohns disease include bacterial inflammations such as those caused by salmonella and
shigella, typhoid fever, intestinal tuberculosis, and protozoan infections such as amebiasis. Appropriate cultures and biopsies
reveal the causative organisms in these conditions and rule them out. In regard to nonspecific intestinal inflammation, chronic
ulcerative colitis can usually be differentiated from Crohns disease. Although ulcerative colitis involves the mucosa of the large
intestine, it does not extend deep into the wall of the bowel, as does Crohns disease. Ulcerative colitis nearly always involves the
rectum most severely, with lessening inflammation from the rectum to the ileocolic area. In contrast, Crohns disease may be worse
on the right side of the colon than on the left side, sometimes sparing the rectum. Ulcerative colitis also shows continuous
involvement from rectum to proximal segments, whereas Crohns disease shows segmental lesions. Although nonspecific, so-called
backwash ileitis may be present in ulcerative colitis, ileal and small intestinal involvement suggests Crohns disease. Bleeding is a
more common symptom in ulcerative colitis and is less common in Crohns disease. Perianal involvement and rectovaginal fistulas
are unusual in ulcerative colitis but are more common in Crohns disease. In most instances, the two diseases can be clearly
separated, but a subgroup of 5% to 10% of all patients with chronic nonspecific inflammatory bowel disease cannot be clearly
classified as having ulcerative colitis or Crohns disease. These patients are usually given a diagnosis of indeterminate colitis.
The true diagnosis often becomes apparent as the patients are followed through the years.
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Endoscopic view
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Crohns disease. Hyperemia and deep cracks of mucus membrane of colon, ulcers, symptom of roadway
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Acute distal ileitis may be a manifestation of early Crohns disease, but it also may be unrelated, such as when it is caused
by a bacteriologic agent such as Campylobacter or Yersinia. Patients usually present in a manner similar to patients with acute
appendicitis. They have a sudden onset of right lower quadrant pain, nausea, vomiting, and fever, with tenderness over the area of
involvement. The diagnosis is made at operation by identifying an acutely inflamed segment of terminal ileum. No biopsy or
resection should be done. The condition almost always subsides spontaneously, and the segment should not be excised. If the
cecum is not involved, the appendix should be removed to prevent subsequent bouts of right lower quadrant inflammation from
being confused with appendicitis.
THERAPY
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Orally administered glucocorticoids are used to treat patients with mildly to moderately severe disease that does not respond
to aminosalicylates. Patients with severe active disease usually require intravenous administration of glucocorticoids. Although
glucocorticoids are effective in inducing remission, they are ineffective in preventing relapse and their adverse side-effect profile
makes long-term use hazardous. Therefore, they should be tapered once remission is achieved. Some patients are unable to undergo
glucocorticoid tapering without suffering recurrence of symptoms. Such patients are said to have glucocorticoid dependence and
are candidates for therapy with glucocorticoid-sparing immune modulators.
The thiopurine antimetabolites azathioprine and 6-mercaptopurine have demonstrated efficacy in inducing remission, in
maintaining remission, and in allowing for glucocorticoid tapering in glucocorticoid-dependent patients. There is also some
evidence that they decrease the risk of relapse after intestinal resection for Crohn's disease. These agents are relatively safe, but can
induce bone marrow suppression and promote infectious complications. For patients who do not respond to the thiopurines,
methotrexate is an alternative. There is little role for cyclosporine in Crohn's disease; its efficacy/toxicity profile in this disease is
poor.
Infliximab is a chimeric monoclonal antitumor-necrosis-factor antibody that has efficacy in inducing remission and in
promoting closure of enterocutaneous fistulas. 37 Infliximab is generally well tolerated but should not be used in patients with
ongoing septic processes, such as undrained intra-abdominal abscesses.
Surgical Therapy
Indications for Operation. Patients with Crohns disease are usually operated on because an intestinal complication of
Crohns disease mandates the operation. All in all, about 70% of patients with Crohns disease will come to operation. The most
common complications leading to operation are recurrent intestinal obstruction, intestinal perforation with fistula formation and
abscess, or a gastrointestinal bleeding.2 Obstruction is usually partial and is seldom complete. With nasogastric suction and
intravenous nutrition, the distended bowel usually decompresses, and bowel movements resume. Failure to achieve complete
resolution or recurrence of obstructive symptoms with the resumption of oral feedings usually leads to operation. Perforation with
fistula formation and resultant abdominal mass usually causes continuing pain, fever, malaise, and weight loss until operation can
be accomplished. Perianal complications, such as abscess and fistula, commonly lead to operation. Bleeding, a less frequent cause
of operation, is usually not massive, but it may be persistent and contribute to chronic anemia until the offending lesion or lesions
can be resected. Patients with small intestinal Crohns disease usually require operation for obstruction or perforation, whereas
those with large intestinal Crohns are usually operated on for chronic debility and failure to respond to medical therapy.
Severe systemic symptoms, intractable medical therapy, and weight loss, especially with growth failure in children, can also
lead to operation. Prepubertal and early pubertal patients experiencing growth failure from Crohns can be expected to sustain
catch-up and accelerated growth after resection.16 Toxic megacolon and cancer of the small or large intestine are less common
intestinal complications requiring operation. Extraintestinal complications in and of themselves seldom require intestinal
operation, but they often contribute to the decision to operate. Most of the extraintestinal complications, with the exception of
ankylosing spondylitis and the hepatic complications, subside with the excision of intestine grossly involved with Crohns disease.
Preoperative Preparation. The nutritional status of the patient is optimized before operation. This sometimes, but not
often, requires parenteral caloric supplementation. Anemia is treated by blood transfusion. For patients currently on or recently
receiving corticoid therapy, additional steroids usually 100 mg. of hydrocortisone intravenously every 8 hoursare given to
ensure an adequate supply during the operative stress. The bowels are cleansed with laxatives and enemas the day prior to
operation. Alternatively, 4 liters of an electrolyte solution (GoLYTELY) can be given by mouth the night before operation.36 Diet
is restricted to clear liquids the day before operation.
The growth of enteric bacteria in patients having the laxative-enema preparation is suppressed by giving oral neomycin 0.5
gm. every 4 hours, and tetracycline, erythromycin, or metronidazole 250 mg. every 4 hours, for 18 hours prior to operation. When
the GoLYTELY preparation is used, 2 gm. neomycin and 2 gm. metronidazole are given by mouth 12 hours and 8 hours before
operation. With both preparations, cefazolin 0.5 gm. is given intravenously just prior to operation and is continued every 8 hours
for two more doses.
General Principles of Operation. Because Crohns disease involves nearly the entire gastrointestinal tract in most patients,
total excision of the disease is not possible. Thus, surgical treatment is directed at the most severe areas of involvement, including
those that account for the complications of obstruction, bleeding, or perforation.
The two main operative approaches are to excise the lesions or to bypass them. Currently, most surgeons advise excision
rather than bypass. Bypass allows the diseased intestine to remain in place, where it can cause continuing symptoms, require
treatment, and perhaps even develop malignancy. The risk of cancer in bypassed small and large intestine with Crohns disease is
greater than the risk in healthy bowel. Excision is done with 3-cm. disease-free margins on both sides of the area of involvement.
The disease-free margins are established by gross inspection. Most surgeons do not use microscopic confirmation of healthy
borders. Although the authors have found that when borders are free of microscopic involvement there are fewer recurrences over
the long term than when the border is involved,37 others have not found a higher recurrence rate when histologic findings of
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Crohns are present in the margins. Certainly, demanding microscopic borders that are free of disease may lead to excessively large
resections and result in the short bowel syndrome. Patients with this syndrome do not have enough intestine remaining to digest
and absorb their food properly.
After resection and anastomosis of the index segment (or segments) of intestine that has led to the operation, fistulas from
the index segment to adjacent organs, such as the stomach, colon, duodenum, bladder, or vagina, can usually be closed by suture of
the entrance of the fistula into the adjacent segment. Resection of the adjacent segment is seldom required, unless it is primarily
involved with gross Crohns disease.
Ulcerative colitis, a diffuse inflammatory disease of the mucosal lining of the colon and rectum, is characterized by bloody
diarrhea that exacerbates and abates without apparent cause. It is difficult to realize that a disease so devastating remains
without an identified etiology or specific medical therapy. Total removal of the affected organsthe colon and rectum
provides a complete cure, but at a sacrifice, since patients so treated must learn to live with an external abdominal stoma (an
ileostomy) for the remainder of their lives. Since the disease has its peak onset in early and middle adulthood, this represents a
long time span for most patients. Fortunately, new surgical alternatives have eliminated the need for a permanent ileostomy
without sacrificing definitive treatment of the disease.
ETIOLOGY
The etiology of ulcerative colitis remains unknown despite intensive work by many investigators. The examination of
bacterial and viral agents continues to be an area of great activity. Whether the infectious agents are more likely to be triggers
of disease or perpetuators of disease is of great controversy. To be a trigger, an infectious agent would have to act by initiation
or reactivation. Agents could initiate an autoimmune response by altering antigens, affecting molecular immunity, or increasing
immune responsiveness. The microbial agent might also trigger the pathologic response by increasing mucosal permeability or
stimulating epithelial injury or localized ischemia. The microbial agent could reactivate the inflammatory process directly, by
secondary infection, or by the release of toxins. Evidence for microbial agents as triggers in inflammatory bowel disease is
only indirect.
Psychologic factors have long been thought to have a critical role in exacerbations of the disease. It is now clear that
patients with ulcerative colitis have no unusual predisposing factors when compared with matched controls. Moreover,
colectomy is usually followed by a marked improvement in pre-existing morbid psychologic states such as depression or social
estrangement. Psychosomatic factors most likely only facilitate the colonic mucosal reaction to another as yet unidentified
causative agent.
Another area of great interest has been that of cytokines and immunoregulatory molecules involved in the control of the
immune response.61 The production of interferon during inflammation could have a significant role in the differentiation of
mature memory and effector cells within the intestine. Specific activities of interleukins that are potentially relevant to
inflammatory bowel disease have been identified. Most important of these may be interleukin-1 (IL-1), which activates T and B
lymphocytes as well as macrophages and neutrophils. IL-1 stimulates production of eicosanoids, cytokines, growth factors, and
destructive enzymes; increases adhesion of neutrophils and monocytes to endothelial cells; induces acute-phase response as
well as fever, anorexia, and sleep; and stimulates collagen production and thus fibrosis. IL-1 has been shown to be elevated in
ulcerative colitis as well as in experimental models of colitis. The increase in IL-1 levels seems to correlate with severity of
disease. Alterations in IL-2, IL-6, IL-8, and interferon-gamma have been identified in tissues from patients with ulcerative
colitis. The production of interferon during inflammation could play a significant role in the differentiation of mature memory
and effector cells within the intestine. Tumor necrosis factor may also be particularly important in the activation of
mesenchymal cells but has not been fully evaluated in ulcerative colitis. Thus, it appears that cytokines are integrally involved
in the pathogenesis of inflammatory bowel disease with both immunoregulatory and proinflammatory properties.
PATHOLOGY
Ulcerative colitis is, for the most part, a disease confined to the mucosal and submucosal layers of the colonic wall,
progressing from mucosal edema and lipemia to vascular congestion, superficial ulcers, increased cellular infiltration of the
lamina propria, and cyst abscesses beginning in the rectum and advancing proximally to involve the entire colon. In 10% of
patients, the terminal ileum may show mild inflammation and dilation, a process that has been called backwash ileitis. On
gross inspection, the colonic mucosa demonstrates healed granular superficial ulcers superimposed on a friable and thickened
mucosa with increased vascularity. Patients may also demonstrate superficial fissures and small and regular pseudopolyps. This
is in contradistinction to the transmural inflammatory changes found in Crohns disease of the colon, in which all layers may
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be involved in a granulomatous inflammatory process. The pathologic changes observed in ulcerative colitis, however, are
nonspecific and can be seen in shigellosis, amebiasis, and gonorrheal colitis.
CLINICAL MANIFESTATIONS
The initial presentation of ulcerative colitis can take many forms. Bloody diarrhea is the most common early symptom.
Occasionally, extraintestinal manifestations, including arthritis, iritis, hepatic dysfunction, and skin lesions, may be
paramount. The disease presents as a chronic, relatively low-grade illness in most patients. In a small number of patients
(15%), it has an acute and catastrophic fulminating course. Such patients present with frequent bloody bowel movements (up
to 30 per day), high fever, and abdominal pain. The disease therefore has a wide spectrum of clinical manifestations, ranging
from a mild diarrheal illness to an overwhelming life-threatening event of short duration that demands immediate medical
attention.
Onset of the disease occurs in patients less than 15 years of age in approximately 15% of cases, and presentation in patients
over 40 years of age is not uncommon. The incidence of ulcerative colitis is 3.5 to 6.5 per 100,000 population, and the
prevalence is 60 per 100,000. A slight female predominance has been reported.
Physical findings are directly related to the duration and presentation of the disease. Weight loss and pallor are usually
present. In the active phase, the abdomen, in the region of the colon, is usually tender to palpation. There may be signs of an
acute abdomen accompanied by fever and decreased bowel sounds. This is especially true during acute attacks or in the
fulminating form of the disease. Abdominal distention is unusual, except in patients who have toxic megacolon, in which case
the patient is usually febrile and has signs of an acute abdomen. The perianal area may be excoriated from the numerous
wipings associated with bowel movements. There may be evidence of perianal inflammation in the form of a fissure, abscess, or
fistula in ano, although the last is more common in Crohns disease. Rectal examination is almost always painful and, in the
presence of perianal inflammation, should be done with gentle care. Examination of the integument, tongue, joints, and eyes is
important, since the presence of disease in these areas suggests ulcerative colitis as a likely cause of the diarrheal illness.
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Proctosigmoidoscopy is a helpful and specific diagnostic aid, since ulcerative colitis involves the distal colon and rectum in
90% to 95% of cases. In fact, the mucosa of both the rectum and the sigmoid colon is usually erythematous and granular and
bleeds easily when touched by the endoscope or rubbed with a cotton swab. Normal colonic vascular markings may be absent,
or the mucosa may be hyperemic; in the disease-bearing mucosa, superficial (less than 2 mm.) mucosal alterations are seen.
The intercolonic haustra are thick and blunted. Cobblestoning and deep linear ulceration, which are common endoscopic
findings in Crohns disease, are unusual in ulcerative colitis. In advanced disease, ulcers may be present, surrounded by
hyperplastic areas of granulation tissue and edematous mucosa, which may assume a polypoid appearance (pseudopolyps).
Mucosal bridging is also commonly found. In chronic advanced disease, the lumen of the rectosigmoid may be remarkably
contracted. The use of flexible sigmoidoscopy has improved diagnostic accuracy and patient acceptance. Colonoscopic
examination is of value in determining the extent and activity of the disease. Unless a distinct granuloma is identified,
endoscopic biopsies are of little value in differentiating ulcerative colitis from Crohns colitis.
Although recent studies suggest that previous reports may have overestimated the risk of cancer in the adult population with
ulcerative colitis, patients with this disease still appear to be confronted with at least a 10% to 20% likelihood of developing
carcinoma within 20 years of the diagnosis of ulcerative colitis.100 Adenocarcinoma in association with ulcerative colitis is
multicentric in 15% of patients. In addition, the cancers tend to be flatter and perhaps more infiltrating. These tumors are more
evenly distributed throughout the colon, with approximately 50% being found proximal to the splenic flexure. Carcinoma in
association with ulcerative colitis is more difficult to diagnose by history and physical examination, stool guaiac testing, and
radiographic studies. The likelihood of carcinoma in patients with ulcerative colitis appears to relate to both the extent of
colonic involvement and the duration of disease. Although it is generally accepted that patients with extensive total ulcerative
colitis are at increased risk of developing carcinoma, the question of what constitutes extensive colitis is still not fully
resolved. In addition, the assessment is variable if judged radiographically or colonoscopically. The evidence that patients with
left-sided ulcerative colitis, by any criteria, are at increased risk when compared with the general populationwhich carries a
4% to 6% likelihood of developing colorectal carcinoma, with three fourths of these cancers occurring on the left sideis far
from overwhelming. The likelihood of cancer may be related to duration of activity and age of onset, although this has not been
clearly established. Although it was held for some time that the carcinoma associated with ulcerative colitis was more
aggressive than that in the general population, recent studies have demonstrated that the natural evolution of the cancer is
likely the same in both groups.
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Rectal biopsies have also been advocated to assess the presence or absence of dysplasia. Morson and Pang71 advocate a
surveillance program of rectal biopsy to assess the point at which a patient becomes at high risk for colonic cancer. When
dysplasia of the rectal mucosa is identified, colectomy has been advocated. Other investigators in this field have found the test
less useful, with false-negative results of 20% to 40% and false-positive results of 30% to 40%.90 Colonoscopy may improve
the accuracy of surveillance; however, random biopsies have a very low yield because of the immense sampling problem.
Between 20 and 25 equally spaced biopsies are required on a 10-cm. length of colon to reasonably detect a patch of dysplasia
2 cm. in diameter. Moreover, the endoscopic appearances of both dysplasia and carcinoma in ulcerative colitis remain nearly
undocumented. The biopsy of target lesions, that is, any lesion that cannot be reasonably accepted as part of the chronic
disease state, is recommended. In addition, the end-point of surveillance remains controversial. Many gastroenterologists
recommend colectomy only in the presence of high-grade dysplasia, a dysplasia-associated mass lesion, or a frank carcinoma.
Unfortunately, the presence of dysplasia, whether low-grade or high-grade, can give rise directly to an invasive carcinoma, and
all large centers have had patients under surveillance who developed and died of colorectal carcinoma. Some evidence suggests
that even low-grade dysplasia unassociated with severe inflammation, if it is unequivocal, should prompt colectomy. To date,
no prospective study has clearly demonstrated that surveillance lowers the mortality from colorectal cancer in association with
ulcerative colitis, although a large review from St. Marks suggested an overall 5-year survival of 87% in those patients who
underwent surveillance and 55% in those who did not.
A plain abdominal film may reveal a variant of the disease called toxic megacolon, in which there may be free air within the
peritoneal cavity from perforation of the colon. A more common sign is a remarkable dilation of the transverse colon.
Barium enema examination, usually with air contrast, can be performed safely in most patients and is extremely helpful in
identifying the extent and severity of the disease. Barium roentgenographic signs include loss of haustral markings and
irregularities of the colon wall, which represent small ulcerations. These are well demonstrated in picture, which contrasts the
appearance of the left side of the splenic flexure and that of the right. As the disease progresses, pseudopolyps become a
prominent roentgenographic sign. In advanced disease, the colon assumes the appearance of a rigid contracted tube. The
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barium roentgenogram, although useful, should be avoided in the presence of toxic megacolon, since it may exacerbate the
colitis. When diarrhea is not present, a liquid diet for 3 days prior to examination is recommended. Barium roentgenogram
should be omitted when the clinical signs of toxic megacolon are present. Upper gastrointestinal contrast studies are also
indicated in most patients to exclude Crohns disease.
The aforementioned clinical manifestations and simple diagnostic tests usually help identify the presence of ulcerative
colitis. It is necessary, however, to obtain stool smears and cultures to exclude colitis due to viruses, Chlamydia, bacterial
pathogens, and parasites. Particularly important and difficult to exclude are pseudomembranous colitis, the proctocolitis seen
increasingly in homosexual males, and travelers diarrhea. Cello and Meyer12 provided a useful schema for distinguishing
ulcerative colitis from granulomatous colitis. Note, however, the low frequency of discriminating clinical characteristics,
except for associated small bowel disease or skip areas within the colon, when the etiology is Crohns disease.
The strong association of cancer of the colon with ulcerative colitis bears further emphasis.115 For example, 40% of
patients with total colonic involvement may die of cancer if they survive their disease and the colon is left in place.62 Three
percent of children with ulcerative colitis have cancer of the colon at 10 years; 20% develop cancer during each ensuing
decade.20 With the availability of far more acceptable surgical alternatives to proctocolectomy and ileostomy, it is hoped that
patients will obtain definitive treatment for the disease well before they enter the phase of accelerating cancer risk. These data
support close medical management for such patients and surgical intervention, on this basis alone, when chronicity is well
established.
The extracolonic manifestations of ulcerative colitis can be categorized as the colitis group, the pathophysiologic group,
and the miscellaneous group of disorders. The colitis group of extracolonic manifestations generally parallels the activity of
the underlying bowel disease, being present and most active when the colitis is active and usually subsiding when the colitis
goes into remission induced by medical therapy, by surgical intervention, or spontaneously. It appears most likely that these
extracolonic disorders represent antigen-antibody immune complex disorders. Ocular manifestations are common in ulcerative
colitis and include conjunctivitis, iritis, and choroiditis. These are closely related to disease activity and respond to steroid
therapy. More severe and rare eye diseases, including ulcerative panophthalmitis, are more difficult to treat, even with
high-dose steroid suppression. Articular disorders, including peripheral joint disease, arthralgias, swelling, pain, and redness
with migratory involvement, usually parallel the intensity of the colitis and respond to medical or surgical treatment. The joints
of the lower extremities are most frequently involved. Fortunately, permanent deformity of these joints is very uncommon. A
certain percentage of patients go on to develop clear evidence of rheumatoid arthritis even after colectomy. Ankylosing
spondylitis and sacroiliitis, in contrast, can cause permanent fixation of the spine and need to be treated aggressively. Bone
involvement specific to the axial skeleton is less closely related to the severity of the inflammatory state of the colon and, in
fact, may precede frank evidence of ulcerative colitis. Patients with ulcerative colitis frequently experience dermatologic
disorders, including erythema nodosum and pyoderma gangrenosum. Although these difficult problems resolve after colectomy
in most patients, in others, they may precede the colonic disease or may not become manifest until after proctocolectomy has
been performed.
Pathophysiologic disorders are more often seen in Crohns disease than in ulcerative colitis, since in ulcerative colitis, the
normal physiology of the terminal ileum is not disturbed. Liver disease is common in patients with both ulcerative colitis and
Crohns disease. Nonspecific inflammation and fatty metamorphosis manifested by mild increases in the serum transaminase
values are common in ulcerative colitis. Pruritus and elevation of the alkaline phosphatase are commonly associated with the
pericholangitis that occasionally accompanies ulcerative colitis. The most dreaded complication, sclerosing cholangitis,
presents with pruritus, alkaline phosphatase elevation, right upper quadrant pain and tenderness, and jaundice. The diagnosis
is most often made by endoscopic retrograde cholangiopancreatography or transhepatic cholangiography. It has been estimated
that 50% of patients who present with sclerosing cholangitis already have or will develop frank ulcerative colitis. Controversy
surrounds the treatment of this disorder. Whereas some patients respond to colectomy, many others show progression of their
disease even after colon resection. Surgical drainage, internal stent placement, antibiotics, and ultimately liver transplantation
have all been reported to be of value in the treatment of symptomatic sclerosing cholangitis. Cholangiocarcinomas have also
been reported in patients with ulcerative colitis, usually after many years of sclerosing cholangitis.
MEDICAL MANAGEMENT
The outcome of an acute episode of ulcerative colitis relates to the severity of the disease as manifested by systemic
symptoms. Duration of the disease and extent of involvement of the colon do not appear to be determinants of survival if
ulcerative proctitis is excluded from consideration. Those who present with advanced signs of acute illness require
hospitalization and supportive, as well as specific, therapy for associated metabolic and hematologic derangements. Because of
the massive fluid and electrolyte loss per rectum, such patients often present with metabolic acidosis, contracted extravascular
volume, and prerenal azotemia. The serum potassium level is usually low because of excessive loss in stool and urine.
Intravenous administration of balanced salt solutions in amounts sufficient to replace these losses is an initial step in
management. Patients with long-standing disease may have lost considerable protein and probably are in a depleted nutritional
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state. The precise role of specialized nutritional support in ulcerative colitis and, in particular, of total parenteral nutrition is
unclear. Despite early enthusiasm, total parenteral nutrition does not appear to have a specialized therapeutic role in this
disease. Total parenteral nutrition improves the overall nutritional state of patients with ulcerative colitis and may reverse
growth retardation in children, but it certainly does not replace conventional medical treatment or prevent or delay colectomy.
In fact, in patients with severe acute colitis, it may be impossible to attain a positive nitrogen balance while the colon is still in
place.
Corticosteroids and immunosuppressive agents have both been demonstrated to be effective in the management of ulcerative
colitis. Both agents, however, are capable of producing significant side effects. In general, corticosteroids have been more
readily accepted by the medical community as therapeutic agents and remain the mainstay of therapy in acute attacks. Between
40 and 60 mg. of prednisone in a single daily dose is effective in inducing remission.110 Rectal steroids have been shown to
be effective in left colon disease or proctitis and may have therapeutic efficacy in universal colitis as well, perhaps because
approximately 30% of the steroid given rectally is absorbed into the systemic circulation. In an attempt to avoid systemic
effects of steroid enemas, tixocortol pivalate was synthesized by adding a thiol ester group at position 21 on the
hydrocortisone molecule. In trials, this agent has been useful for treating patients with left-sided colitis and has resulted in a
reduction in systemic steroid side effects. The controversy over intravenous steroids versus intravenous adrenocorticotropic
hormone (ACTH) has now been resolved by a randomized trial that revealed a similar response to equipotent doses of either
hormone.49 A recent study suggests that ACTH may be more effective in patients not previously treated with corticosteroids,
whereas corticosteroids appear to be preferable for patients already receiving steroid therapy.68 A steroid-induced remission is
not more likely to exacerbate than a spontaneous remission, and an ACTH-induced remission is not more likely to exacerbate
than a corticosteroid-induced remission. The usual recommended doses are 300 mg. of hydrocortisone or 40 units of ACTH
per day. Occasionally, massive doses of steroids (over 1 gm. per day) are required. The usual response is rapid, and acute signs
of inflammation subside within a few days. The optimal duration of intravenous steroid therapy is 5 to 7 days, although this
may be extended in patients supported nutritionally with total parenteral nutrition. Proctoscopic examination is useful in
following response to therapy. There is still controversy as to whether maintenance steroid thereby reduces recurrence of the
disease. Although maintenance steroids may be useful in controlling symptoms of patients with continuing activity,
maintenance therapy with low-dose corticosteroids for patients with inactive disease has not been demonstrated to prevent
relapse.59 Patients must be monitored carefully for the long-term adverse sequelae of corticosteroid use, including
hypertension, hyperglycemia, cataracts, osteoporosis, and osteomalacia.
Sulfasalazine has enjoyed widespread use in the chronic phases of ulcerative colitis. Its mode of action is unknown.
Sulfasalazine may exert this prophylactic effect by inhibiting mucosal prostaglandin synthesis,49 although not all studies have
supported this mechanism.81 Whatever the mechanism of action, sulfasalazine appears to be associated with fewer
exacerbations as assessed by controlled randomized trials.21, 108 The drug appears to be of lesser value in severe ulcerative
colitis. Sulfasalazine is metabolized by bacteria to 5-aminosalicylic acid (5-ASA) and sulfapyridine. Dose-related side effects
of sulfasalazine include nausea, vomiting, headache, and abdominal discomfort. Reversible hypospermia and infertility are
observed in males. Hypersensitivity effects include fever, skin rash, agranulocytosis, and hemolytic anemia. Studies have
indicated that the sulfapyridine produced by bacterial degradation of sulfasalazine is responsible for the majority of the side
effects, whereas the 5-ASA component appears to be the effective moiety of the drug. Five-aminosalicylic acid is now available
in this country for clinical use. In all studies to date, these compounds have been shown to be as efficacious as sulfasalazine in
treating acute ulcerative colitis as well as in preventing relapse.
A third approach has been the use of immunosuppressive agents. Rosenberg and colleagues88 concluded, based on a
well-controlled study, that azathioprine allows reduction of the use of steroids in chronic cases but does not, in itself, control
exacerbation of the disease. In a more recent controlled trial, however, Kirk and Lennard-Jones54 demonstrated that clinical
improvement may occur in about 25% of patients treated with a dose of azathioprine at 2 to 2.5 mg. per kg. Uncontrolled trials
have demonstrated a favorable response to 6-mercaptopurine (6-MP) in 64% to 70% of patients with refractory ulcerative
colitis.81 Because these drugs do not produce a clinical response for several months, they have no role in the treatment of
acute flares of ulcerative colitis. Cyclosporine (CS), which has a more rapid onset of action, has been advocated for the
treatment of severe, refractory acute ulcerative colitis. Both uncontrolled trials and one controlled study suggest that high-dose
CS is efficacious for severe ulcerative colitis. There is, however, significant theoretical risk of irreversible CS-associated
nephropathy following treatment with high-dose CS. Severe infectious complications may also occur.92 A trial of 6-MP or CS
may be warranted when steroids and sulfasalazine have failed, when the disease is confined to the left side of the colon or
rectum, when the patient is compliant, and when there is no absolute indication for immediate surgical therapy.80 However,
before prescribing these immunosuppressive agents, one must be fully familiar with the dosing, monitoring, toxicity, and
possible induction of lymphoma or other malignancies associated with these drugs.
Although widely prescribed for both ulcerative colitis and Crohns disease, metronidazole and other antibiotics have no
proven value in the treatment of inflammatory bowel disease.
The major therapeutic problem between acute episodes is control of diarrhea and maintenance of nutrition. Diet therapy is
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no longer recommended, and patients are encouraged to eat a substantial diet of their choice. Milk products are to be avoided
only if they cause problems such as increasing diarrhea or cramps (as they may in about half of patients with ulcerative colitis).
The reason for this is not clear but relates to something specific in cows milk rather than to the lactase deficiency that exists
in many patients with ulcerative colitis. Opiates such as codeine or paregoric should be avoided. Nocturnal diarrhea can be
controlled by anticholinergics or diphenoxylate with atropine. The synthetic peripheral-acting opioid loperamide may be more
effective than diphenoxylate in this situation and avoids the atropine side effect associated with this drug.74 Stool bulk
formers, such as psyllium, are also helpful. Finally, the importance of rest and peace of mind cannot be overemphasized.
Patients are advised to remain at rest during episodes of exacerbation.
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provided the patient is stable, initial medical trial is warranted in order to make the operation elective rather than urgent. If no
clear response is obtained within 24 to 48 hours, surgical therapy is warranted. Larger doses of steroids after initial medical
failure probably will not benefit the patient and, as noted, may be deleterious. During medical therapy, serial blood counts,
serum electrolyte levels, and abdominal roentgenograms should be closely monitored.
In the presence of acute toxic megacolon caused by ulcerative colitis, surgical therapy can be associated with a high
operative morbidity and mortality. Block and colleagues6 noted an overall mortality following emergency operation of 8.7%;
6.1% after total abdominal colectomy, and 14.7% after proctocolectomy. This suggests that more conservative surgical
intervention is appropriate in the acute setting. Also, with the recent popularity of anal sphinctersparing procedures, when
operating for acute ulcerative colitis, one should weigh the possibility of subsequent surgical correction for continence.
Specifically, leaving the rectum intact allows its use for subsequent surgical mucosal proctectomy and ileoanal anastomosis.
When urgent colectomy is required, total abdominal colectomy, Brooke ileostomy, and Hartmanns pouch are appropriate.39,
97 Although ileostomy alone for acute complications has been abandoned, it has been used in the recent past with good
success by Turnbull and co-workers,111 in combination with skin-level transverse and sigmoid colostomies, for toxic
megacolon. This is a relatively simple procedure that spares such desperately ill patients a major operative intervention until
their acute illness has subsided. Because the procedure involves only decompression of the colon and does not remove the
acutely inflamed tissue, most surgeons prefer colon resection.
SURGICAL MANAGEMENT
Total proctocolectomy with permanent Brooke ileostomy offers definitive treatment for ulcerative colitis by eliminating
diseased mucosa and the risk of malignant transformation. Nevertheless, it remains controversial and is poorly accepted by
patients and their physicians. Patients with a permanent ileostomy are incontinent of gas and stool and must wear a collecting
bag day and night. As many as 40% to 50% of patients with Brooke ileostomies have appliance-related problems, and the
psychologic and social implications, particularly for young patients, are tremendous.78, 89 Therefore, the search has continued
for adequate alternatives to proctocolectomy and ileostomy.
Until recently, single-stage total proctocolectomy was the procedure of choice when complications of the disease were treated
electively. This procedure is performed through a midline incision. The rectum is excised from the abdomen after mobilization and
circumferential incision from the perineum. When cancer is not suspected, excision is performed rapidly, with division of the
mesentery close to the bowel wall. This principle is especially important in the pelvic colon and rectum, where injury to the sacral
parasympathetic nerves may lead to bladder and sexual dysfunction. Endorectal mucosal resection, as described later, appears to
offer the best way to avoid such serious complications.34 After standard proctocolectomy, management of the perineal wound is a
problem, since chronic infection and poor healing may cause a lingering sinus tract between the buttocks. The authors preference
is to apply active closed drainage to this area for 3 to 5 days following operation. Gauze packing of the perineum should be
reserved for pelvic hemorrhage that cannot otherwise be controlled. Perineal wound problems may be reduced by performing an
intersphincteric proctectomy, which entails dissecting between the internal and external anal sphincter when removing the rectum,
thus preserving the levator ani and external anal sphincter muscles. These muscles can then be included in the closure of the
perineum. Using this technique, complete healing of the perineum approaches 95% at 6 months.
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The most important modification of the operation was the creation of an ileal pouch or reservoir proximal to the ileoanal
anastomosis.
The most frequent late complication in patients undergoing ileoanal anastomosis is ileal pouch dysfunction or pouchitis, which
has been reported to occur in 10% to 50% of patients undergoing this procedure for ulcerative colitis. Pouchitis is an incompletely
defined and poorly understood clinical syndrome consisting of increased stool frequency, watery stools, cramping, urgency,
nocturnal leakage of stool, arthralgias, malaise, and fever. The syndrome is similar to that found in patients with Kock continent
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ileostomy pouches. The etiology of this condition is unknown; speculations have included early Crohns disease, bacterial
overgrowth or bacterial dysbiosis, either primary or secondary malabsorption, stasis, ischemia, and nutritional or immune
deficiencies.
Mortality for elective surgical therapy is in the range of 0% to 2%; for emergency operation, it is about 4% to 5%; and for toxic
megacolon, it rises to 17%.5 These are remarkable statistics when one considers the debilitating nature of the disease and the fact
that many patients have had long-term steroid therapy. The major complication in all reported series is sepsis, either in the wound
or in the intra-abdominal cavity. There is little evidence that the development of more potent and specific antibiotics has
significantly reduced the incidence of this complication; attention to the details of operative management continues to be the best
way to ensure a smooth postoperative course. The most common late complication of resectional therapy with ileostomy or ileoanal
anastomosis is intestinal obstruction, which occurs in about 10% of patients. Other bothersome but nonlethal complications
following proctocolectomy include delay in perineal closure (25%), sexual dysfunction (5% to 10%), and renal stones (10%).
Ileostomy dysfunction as a consequence of stenosis has been reduced to 2% by the Brooke-Turnbull ileostomy. Additional
uncommon complications include prolapse, herniation, and ulceration of the stoma, which is usually a sign of the development of
Crohns disease within the ileal stoma. Whether the outcome following surgical therapy for Crohns disease of the colon is as
favorable as for ulcerative colitis continues to be a source of controversy.
The formation of social groups (ileostomy clubs) has provided an important mechanism for the education of patients by
those who have already mastered the technique of ileostomy management. Some hospitals have enterostomal therapists. These
professionals are highly skilled in dealing with the physical and emotional problems of stomal management. In institutions that
perform a large number of ileal pouch operations, specialized patient-oriented support groups are essential.
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50. Pignone M, Rich M, Teutsch SM, et al: Screening for colorectal cancer in adults at average risk: A summary of the evidence for the U.S. Preventive
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[PMID: 11711741]
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Rev 2, 2002.
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Oncol 8:94, 2001.
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75. Moore HG, Guillem JG: Adenocarcinoma of the anal canal. Clin Colon Rectal Surg 15:255, 2002.
76. Mutch MG, Roberts PL: Anal and peri-anal melanoma. Clin Colon Rectal Surg 15:271, 2002.
77. Bullard K, Tuttle T, Rothenberger D, et al: Surgical therapy for anorectal melanoma. J Am Coll Surg 196:206, 2003. [PMID: 12595048]
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81. Ganio E, Altomare DF, Gabrielli F, et al: Prospective randomized multicentre trial comparing stapled with open haemorrhoidectomy. Br J Surg
88:669, 2001. [PMID: 11350437]
82. Ho YH, Seow-Choen F, Tsang C, et al: Randomized trial assessing anal sphincter injuries after stapled hemorrhoidectomy. Br J Surg 88:1449, 2001.
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83. Ho Y-H, Cheong W-K, Tsang C, et al: Stapled hemorrhoidectomyCost and effectiveness. Randomized, controlled trial including incontinence
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84. Madoff R, Fleshman J: AGA technical review on the diagnosis and care of patients with anal fissure. Gastroenterology 124:235, 2003. [PMID:
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86. Bailey H, Beck D, Billingham R, et al: A study to determine the nitroglycerin ointment dose and dosing interval that best promote the healing of
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Biliary Anatomy
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video
OBTURATIVE ICTERUS
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Obstruction of external bilious ducts can arise for many reasons: as a result of
inflammatory processes of surrounding organs (pancreas, paracholedochus lymphatic
knots), damage of walls of ducts during operations. However, in most cases it is a
gallstone disease, choledocholithiasis and related to them scar changes of large papilla of
duodenum. The second place among the reasons of obturation icterus is taken by
tumours of which the cancer of head of pancreas and large papilla of duodenum is most
widespread.
Disregarding the fact that each of the adopted diseases has special clinical passing,
obturation of bilious ducts causes the changes which have general character. At complete
blockade of external bilious ducts and growth of pressure higher than 300 mm of waters.
an item or 2,94 kPa (after a norm not higher 150 mm or 1,47 kPa) in them,
excretions of bile in bilious capillaries are halted. It is conditioned by the fact that the
secretory mechanism of hepatic cells (hepatocyte) can not overcome such resistance.
Thus bile through the blasted particles and lymphatic and vein vessels of liver gets into
blood, causing the syndrome of mechanical icterus.
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Classification
(by .. Shalimov, 1993)
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The clinical picture of obturative icterus is founded, first of all, on the symptoms
caused by violation of outflow of bile.
A pain syndrome is a characteristic accomponiment of gallstone disease and
choledocholithiasis, that run with the attacks of hepatic colic. However, pain syndrome at
these pathologies can often be not acutely expressed or quite absent. Pain is often
observed at stricture of bilious ducts, but it is not quite typical of patients with the cancer
of bile ducts.
An icterus is an important sign of obstruction of bilious ways, speed of origin and
intensity of which depend on whether well-kept or broken passage of bile in intestine is.
For choledocholithiasis with valve character of concrement transitional passing of
icterus is inherent, and for cancer it is more proof and progressive.
The itch of body is a frequent accomponiment of icterus, that arises up as a result
of action of bilious acids. It is thus needed to remember, that under the conditions of
damage by tumour the itch which proceeds for a long time appears at first, only later
there appears icterus. During examination the yellowness of sclera, mucus shells and skin
are observed. At the same time patients specify urines and discolorations of excrement
darkening (argil). The increase of temperature of body testifies the development of
cholangitis, metastasis of tumors in liver is rarer.
In emaciated patients in right hypochondrium it is sometimes possible to see
formation, that moves during breathing, probably it is a gall-bladder. If it is elastic,
unpainful and it is accompanied by icterus (the Courvoisier's symptom), a patient then
suffers from cancer of head of pancreas or distal parts of general bilious ducts.
However, it is necessary to warn, that determination of character of icterus only
on the basis of clinical signs to a great extent carries only conditional character. It must be
connected to the fact that at parenchymatous hepatitis expressed cholestasis often is
observed, and at obturation icterus damage of hepatic cells is characteristic. Therefore for
establishment of diagnosis of obturative icterus, except for clinical information, special
methods of examination are necessary.
Laboratory information. For obturative icterus a cholestatic syndrome with high
bilirubinmia mainly due to direct faction of bilirubin and bilirubinuria is characteristic,
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Sonography examination
Duodenography in the conditions of artificial low blood pressure apply for the
exposure of pathology of organs of pancreatoduodenal area.
Retrograde cholangiopancreatography enables to examine stomach, duodenum
by endoscope, to conduct biopsy, to extract bile and pancreatic juice for examination, to
get the roentgenologic image of ducts: external and internal hepatic ducts and duct of
pancreas, and in a number of cases at presence of concrement to conduct endoscopic
papillotomy and extraction of them through papillotomic access.
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Retrograde cholangiopancreatography
Intraoperative cholangiography
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Cholangiomanometry
Debitomanometry
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Choledochoscopy
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Diagnosis program
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7. Endoscopy.
8. Retrograde cholangiopancreatography.
9. Laparoscopy with biopsy.
10. Percutaneous transhepatic cholangioduodenography.
11. Computer tomography.
Asymptomatic
Incidental Finding on Sonogram
Cholelithiasis
Acute Cholelithiasis on Sonogram, clinical Cholecystitis diagnosis
Cholecystitis or Positive Pipida Scan
Symptomatic
Positive Sonogram, normal Liver Function Tests
Cholelithiasis
Cholelithiasis
Abnormal Liver Function Tests (Serum Transaminases
with Suspected
elevation or Bilirubin >3.0, gallstone pancreatitis)
Choledocholithiasis
Cholelithiasis
CBD Stone on Sonogram, MR Cholangiography or
with
Jaundice
Choledocholithiasis
Cholelithiasis
Pancreatitis on Sonogram, CT or MER Cholangiography
with Resolving
or clinically, Documented High Serum Amylase and Lipase -
Gallstone
WITH - Decreasing Serum Pancreatic Enzymes after initial attack
Pancreatitis
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MANAGEMENT
PROTOCOLS FOR
UNCOMPLICATED PROPOSED MANAGEMENT
BILIARY STONE
DISEASES
Asymptomatic
No Surgical Intervention
Cholelithiasis
Asymptomatic
Cholelithiasis in Diabetic No Surgical Intervention
Patients
Symptomatic
Cholelithiasis or Acute LapChole
Cholecystitis
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Asymptomatic
No Surgical Intervention
Gallbladder Polyps
Symptomatic
LapChole
Gallbladder Polyps
Severe, Gangrenous
LapChole, if not safely feasible, Anterior-
Cholecystitis with
subtotal LapChole
Subhepatic Phlegmon
Post Cholecystectomy
(Lap or open) Suspected MR Cholangiogram or ERC
Choledocholithiasis
Post Cholecystectomy
ERCP, if failure Laparoscopic Common Bile
(Lap or open)
Duct Exploration.
Choledocholithiasis
Differential diagnostics
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Normal /
Total bilirubin Increased
Increased
Conjugated
Normal Increased Increased
bilirubin
Unconjugated Normal /
Increased Normal
bilirubin Increased
Normal / Decreased /
Urobilinogen Increased
Increased Negative
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Dark Dark
Urine Color Normal (urobilinogen + (conjugated
conjugated bilirubin) bilirubin)
Alkaline
Increased
phosphatase levels
Alanine Normal
transferase and
Increased
Aspartate transferase
levels
Conjugated
Not Present Present
Bilirubin in Urine
Final diagnosis, that maximally represents the character of obturative icterus and
volume of the most operative treatment, as a rule, is set only during the intraoperative
revision. At determination of medical tactics and choice of method of surgical treatment
of such icterus it is needed also to objectively estimate weight of general condition of
patients. For this purpose it is necessary to take into account the character of icterus,
stage of hepatic insufficiency keeping in mind the duration and intensity of cholestasis,
presence and character of cholangitis, weight and expression of accompanying pathology,
eyelids of patients.
Medical measures in preoperative period must be directed on correction of
violations of homeostasis, hemocoagulation (aminocapronic acid, vicasol, 10 % solution
of chlorous calcium, one-group fresh-frozen plasma, inhibitor of protease), improvement
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The management of biliary stones diseases has dramatically changed with the
advent of the Laparoscopic Cholecystectomy. It has now become a true outpatient
laparoscopic procedure with negligible morbidity.
In the past few years, our surgical team has designed and revised numerous
management protocols for various clinical settings effectively achieving impressive
improvements in our surgical performance for the treatment of biliary stone diseases.
This chapter will describe these management protocols and our latest technical updates.
The original Laparoscopic Cholecystectomy technique has undergone a vast
maturation process over the past decade. Various technical steps has been modified and
adapted to improve surgical performance and clinical outcome. As a result, nowadays,
most surgeons in the Western World can safely perform a Laparoscopic Cholecystectomy
with a minimal conversion rate.
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This technology is being used with increasing frequency in our surgical service to
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Portal hypertension refers to abnormally high pressure in the hepatic portal vein.
It is defined as a portal pressure of 12 mm Hg or more (compared with the normal 5-10
mm Hg).
See related articles dealing with ascites, cirrhosis, hepatic encephalopathy,
hepatorenal syndrome, liver failure and oesophageal varices, listed below under
'Complications'.
Etiology
Causes can be divided into: prehepatic, hepatic and posthepatic. Cirrhosis is a
common cause.
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Circulatory disturbances:
Portal hypertension and cirrhosis produce a hyperdynamic circulation, with
splanchnic vasodilatation, increased cardiac output, arterial hypotension, and
hypervolaemia.
There is salt and water retention, ascites and hyponatraemia.
Presentation
History
For causes of liver disease:
History of jaundice.
Alcohol consumption.
Blood transfusion, especially abroad; lifestyles that predispose to hepatitis B or
hepatitis C.
Family history, eg Wilson's disease or hereditary haemochromatosis.
For complications of portal hypertension:
Haematemesis or melaena - suggest bleeding varices.
Lethargy, irritability and changes in sleep pattern - suggest encephalopathy.
Increased abdominal girth, weight gain - suggest ascites.
Abdominal pain and fever - suggest spontaneous bacterial peritonitis.
Examination
Signs of portal hypertension:
Dilated veins in the anterior abdominal wall and caput medusae (tortuous
collaterals around the umbilicus). A venous hum, loudest during inspiration, is sometimes
heard over large upper abdominal collaterals.
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Splenomegaly.
Ascites.
Signs of liver disease:
Jaundice, spider naevi, palmar erythema.
Confusion, liver flap and fetor hepaticus are signs of encephalopathy.
Signs of hyperdynamic circulation: bounding pulse, low blood pressure, warm
peripheries.
Enlarged or small liver.
Gynaecomastia and testicular atrophy.
Investigations
Blood tests:
LFTs, U&Es, glucose, FBC, clotting screen.
Investigations for liver disease if the cause not known, e.g ferritin (for
haemochromatosis), hepatitis serology, autoantibodies, alpha-1-antitrypsin (for alpha-
1-antitrypsin deficiency), ceruloplasmin (for Wilson's disease).
Scans:
Abdominal ultrasound - for liver and spleen size, ascites, portal blood flow and
thrombosis of the portal or splenic veins.
Doppler ultrasound - can show direction of flow in blood vessels.
CT scan, especially spiral CT, may show portal vasculature - can be useful if
ultrasound was inconclusive.
MRI scan - gives similar information to CT.
Elasticity measurement (FibroScan) - a new technique based on the velocity of
an elastic wave via an intercostally placed transmitter. Results correlate with liver stiffness
and so with fibrosis.
Endoscopy - for oesophageal varices - essential for those with suspected portal
hypertension. Varices indicate portal hypertension, but their absence does not exclude it.
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Hepatopulmonary syndrome.
Budd-Chiari syndrome.
Surgical procedures
Surgical portosystemic shunts:
These require major surgery and an experienced surgeon. They are less likely to
stenose than TIPS and can be used where TIPS is not feasible.
Shunts may be total, partial or selective.
Devascularisation procedures:
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develop varices, but only 30% of varices bleed. The first episode of variceal
haemorrhage is estimated to carry a mortality rate of 30-50%.
Acute liver failure (ALF) is a rare condition in which rapid deterioration of liver
function results in altered mentation and coagulopathy in previously normal individuals.
U.S. estimates are placed at approximately 2,000 cases per year.4 The most
prominent causes include druginduced liver injury, viral hepatitis, autoimmune liver
disease and shock or hypoperfusion; many cases (20%) have no discernible cause. Acute
liver failure often affects young persons and carries a high morbidity and mortality.
Prior to transplantation, most series suggested less than 15% survival. Currently,
overall short-term survival with transplantation is greater than 65%. Because of its rarity,
ALF has been difficult to study in depth and very few controlled therapy trials have been
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performed. As a result, standards of intensive care for this condition have not been
established.
The most widely accepted definition of ALF includes evidence of coagulation
abnormality, usually an INR 1.5, and any degree of mental alteration (encephalopathy) in
a patient without preexisting cirrhosis and with an illness of 26 weeks duration. Patients
with Wilson disease, vertically-acquired HBV, or autoimmune hepatitis may be included
in spite of the possibility of cirrhosis if their disease has only been recognized for 26
weeks. A number of other terms have been used including fulminant hepatic failure and
fulminant hepatitis or necrosis. Acute liver failure is a better overall term that should
encompass all durations up to 26 weeks. Terms used signifying length of illness such as
hyperacute (7 days), acute (7-21 days) and subacute (21 days and 26 weeks) are not
particularly helpful since they do not have prognostic significance distinct from the cause
of the illness. For example, hyperacute cases may have a better prognosis but this is
because most are due to acetaminophen toxicity.
All patients with clinical or laboratory evidence of moderate to severe acute
hepatitis should have immediate measurement of prothrombin time and careful
evaluation for subtle alterations in mentation. If the prothrombin time is prolonged by 4-6
seconds or more (INR 1.5) and there is any evidence of altered sensorium, the diagnosis
of ALF is established and hospital admission is mandatory. Since the condition may
progress rapidly, with changes in consciousness occurring hour-by-hour, early transfer to
the intensive care unit (ICU) is preferred once the diagnosis of ALF is made. History
taking should include careful review of possible exposures to viral infection and drugs or
other toxins. If severe encephalopathy is present, the history may be provided entirely by
the family or may be unavailable. In this setting, limited information is available,
particularly regarding possible toxin/drug ingestions. Physical examination must include
careful assessment and documentation of mental status and a search for stigmata of
chronic liver disease. Jaundice is often but not always seen at presentation.
Right upper quadrant tenderness is variably present. Inability to palpate the liver
or even to percuss a significant area of dullness over the liver can be indicative of
decreased liver volume due to massive hepatocyte loss.
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An enlarged liver may be seen early in viral hepatitis or with malignant infiltration,
congestive heart failure, or acute Budd-Chiari syndrome. History or signs of cirrhosis
should be absent as such features suggest underlying chronic liver disease, which may
have different management implications. Furthermore, the prognostic criteria mentioned
below are not applicable to patients with acute-on-chronic liver disease.
Initial laboratory examination must be extensive in order to evaluate both the
etiology and severity of ALF. In addition to coagulation parameters, early testing should
include routine chemistries (especially glucose as hypoglycemia may be present and
require correction), arterial blood gas measurements, complete blood counts, blood
typing, acetaminophen level and screens for other drugs and toxins, viral hepatitis
serologies (most prominently A and B), tests for Wilson disease, autoantibodies (anti-
nuclear and anti-smooth muscle antibodies) and a pregnancy test in females. Plasma
ammonia, preferably arterial,7,8 may also be helpful. A liver biopsy, most often done via
the transjugular route because of coagulopathy, may be indicated when certain conditions
such as autoimmune hepatitis, metastatic liver disease, lymphoma, or herpes simplex
hepatitis are suspected. As the evaluation continues, several important decisions must be
made: whether to admit the patient to an ICU, whether to transfer the patient to a
transplant facility, and (if already at a transplant center) whether and when to place the
patient on the list for transplantation. For patients in a non-transplant center, the
possibility of rapid progression of ALF makes early consultation with a transplant facility
critical. Specific prognostic indicators may point toward the need for transplantation. For
patients with acetaminophenrelated ALF in particular, an arterial pH of 7.3 should
prompt immediate consideration for transfer to a transplant center and placement on a
transplant list.
Patients with altered mentation should generally be admitted to an ICU. Planning
for transfer to a transplant center should begin in patients with grade I or II
encephalopathy because they may worsen rapidly.
Early transfer is important as the risks involved with patient transport may
increase or even preclude transfer once stage III or IV encephalopathy develops.
Evaluation for transplantation should begin as early as possible. In these critically ill
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patients with potential for rapid deterioration it is necessary to make treatment plans
promptly. Social and financial considerations are unavoidably tied to the overall clinical
assessment where transplantation is contemplated. It is important to inform the patients
family or other next of kin of the potentially poor prognosis and to include them in the
decision-making process.
Table. Initial Laboratory Analysis
Prothrombin time/INR
Chemistries
sodium, potassium, chloride, bicarbonate, calcium, magnesium,
phosphate
glucose
AST, ALT, alkaline phosphatase, GGT, total bilirubin, albumin
creatinine, blood urea nitrogen
Arterial blood gas
Arterial lactate
Complete blood count
Blood type and screen
Acetaminophen level
Toxicology screen
Viral hepatitis serologies
anti-HAV IgM, HBSAg, anti-HBc IgM, anti-HEV, anti-HCV*
Ceruloplasmin Level#
Pregnancy test (females)
Ammonia (arterial if possible)
Autoimmune markers
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Etiology of ALF provides one of the best indicators of prognosis, and also
dictates specific management options.
LIVER BIOPSY
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greater than 2 in homozygotes and less than 2 in patients with alcoholic siderosis. Finally,
tissue obtained from the heart, pancreas, or skin of patients with hemochromatosis shows
heavy infiltration of stainable iron.
ACETAMINOPHEN HEPATOTOXICITY
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WILSON DISEASE
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is a risk of hypersensitivity to this agent; acute lowering of the copper is more effectively
accomplished using direct plasma copper reduction techniques, especially when renal
function is impaired.40 Although such copper lowering measures should be considered,
recovery is infrequent without transplantation. Wilson disease is one of the special
circumstances in which patients may already have evidence of cirrhosis and still be
considered to have a diagnosis of ALF when rapid deterioration occurs. Please refer to
the AASLD Practice Guideline on Wilson Disease for more detailed information
regarding the diagnosis and management of patients with this condition.
BUDD-CHIARI SYNDROME
The Budd-Chiari syndrome (acute hepatic vein thrombosis) can also present as
ALF. Abdominal pain, ascites and striking hepatomegaly are often present. The diagnosis
should be confirmed with hepatic imaging studies (computed tomography, doppler
ultrasonography, venography, magnetic resonance venography). In the presence of
significant liver failure, transplantation may be required as opposed to venous
decompression. As malignancy-associated hypercoagulability is one of the causes of
Budd-Chiari syndrome, it is important to rule out underlying cancer prior to
transplantation of these patients.
While patients with ALF represent a heterogeneous group, they have consistent
clinical features, and share the common disease process of acute hepatocyte loss and its
sequelae. Despite decades of research, however, no agent or therapy that is beneficial to
all patients with ALF has been found. Systemic corticosteroids are ineffective in this
condition.
Because most patients with ALF tend to develop some degree of circulatory
dysfunction, agents that may improve hemodynamics have been of particular interest.
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While prostacyclin and other prostaglandins have appeared promising in some reports,
others have not supported their efficacy in ALF. NAC may improve systemic circulation
parameters in patients with ALF, but this was not observed in all studies. NAC has been
shown to improve liver blood flow and function in patients with septic shock. Use
ofNACin all forms of ALF cannot be justified based on current evidence. A large, multi-
center, randomized, double-blind controlled trial of intravenous NAC versus placebo for
non-acetaminophen ALF is currently under way. Because there is no proven therapy for
ALF in general, management consists of intensive care support once treatments for
specific etiologies have been initiated. While some patients with evidence of acute liver
injury but without significant coagulopathy or encephalopathy may be monitored on a
medicine ward, any patient with altered mental status warrants admission to an ICU as
the condition may deteriorate quickly. Careful attention must be paid to fluid
management, hemodynamics and metabolic parameters as well as surveillance for and
treatment of infection.
Maintenance of nutrition and prompt recognition and resuscitation of
gastrointestinal bleeding are crucial as well. Coagulation parameters, complete blood
counts, metabolic panels (including glucose) and arterial blood gas should be checked
frequently. Serum aminotransferases and bilirubin are generally measured daily to follow
the course of the condition, however changes in aminotransferase levels correlate poorly
with prognosis.
Specific Issues. See Table.
Table. Intensive Care of Acute Liver Failure
Cerebral Edema/Intracranial Hypertension
Grade I/II Encephalopathy
Consider transfer to liver transplant facility and listing for transplantation
Brain CT: rule out other causes of decreased mental status; little utility to
identify cerebral edema
Avoid stimulation, avoid sedation if possible
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Cerebral edema and intracranial hypertension (ICH) have long been recognized as
the most serious complications of ALF. Uncal herniation may result and is uniformly
fatal. Cerebral edema may also contribute to ischemic and hypoxic brain injury, which
may result in long-term neurological deficits in survivors. The pathogenic mechanisms
leading to the development of cerebral edema and ICH in ALF are not entirely
understood. It is likely that multiple factors are involved, including osmotic disturbances
in the brain and heightened cerebral blood flow due to loss of cerebrovascular
autoregulation. Inflammation and/or infection, as well as factors yet unidentified may also
contribute to the phenomenon. Several measures have been proposed and used with
varying success to tackle the problem of cerebral edema and the associated ICH in
patients with ALF. Some interventions are supported by more evidence than others; no
uniform protocol has been established.
Prevention/Management of Elevated Intracranial Pressure (ICP). The occurrence
of cerebral edema and ICH in ALF is related to severity of encephalopathy (Table).
Cerebral edema is seldom observed in patients with
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grade I-II encephalopathy. The risk of edema increases to 25% to 35% with
progression to grade III, and 65% to 75% or more in patients reaching grade IV coma. A
stepwise approach to management is therefore advised.
Grades I-II. Depending on the overall clinical picture, patients with only grade I
encephalopathy may sometimes be safely managed on a medicine ward withskilled
nursing in a quiet environment to minimize agitation, although management in an ICU is
preferable. Frequent mental status checks should be performed with transfer to an ICU if
level of consciousness declines. With progression to grade II encephalopathy, an ICU
setting is indicated. Head imaging with computerized tomography (CT) is used to
exclude other causes of decline in mental status such as intracranial hemorrhage.
Sedation is to be avoided if possible; unmanageable agitation may be treated with short-
acting benzodiazepines in small doses.
GRADES III-IV.
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CLASSIFICATION according to
Seizures.
Seizures, which may be seen as a manifestation of the process that leads to
hepatic coma and ICH, should be controlled with phenytoin. Use of any sedative is
discouraged in light of its effects on the evaluation of mental status. Only minimal doses
of benzodiazepines should be used given their delayed clearance by the failing liver.
Seizure activity may acutely elevate ICP81 and may also cause cerebral hypoxia and thus
contribute to cerebraledema. Some experts have advocated prophylactic use of
phenytoin, especially as seizure activity may be inapparent.
A small randomized controlled trial of prophylactic phenytoin in ALF showed no
difference in overall survival, but a striking diminution in cerebral edema at autopsy in
the treated group. A recent clinical trial did not show beneficial effects on the prevention
of seizures, brain edema or survival Further studies may clarify the value of this
treatment, but it cannot be recommended as a prophylactic measure at this time.
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COMPLICATION
Infection.
All patients with ALF are at risk for acquisition of bacterial or fungal infection or
sepsis, which may preclude transplantation or complicate the post-operative course.
Prophylactic antimicrobial therapy reduces the incidence of infection in certain groups of
patients with ALF, but no actual survival benefit has been shown, making it difficult to
recommend antibiotic prophylaxis uniformly. Although often given, poorly absorbable
antibiotics for selective bowel decontamination have not been shown to impact survival
either. Deterioration of mental status in hospital, particularly in patients with
acetaminophen toxicity, may represent the onset of infection. If antibiotics are not given
prophylactically, surveillance for infection (including chest radiography and periodic
cultures of sputum, urine and blood for fungal and bacterial organisms) should be
undertaken, while maintaining a low threshold for starting appropriate anti-bacterial or
anti-fungal therapy. There are no controlled trials available to confirm whether the use of
prophylactic antimicrobials decreases the likelihood of progression of encephalopathy
and/or development of cerebral edema in ALF. Recent studies have suggested an
association between infection and/or the systemic inflammatory response syndrome
(SIRS) and progression to deeper stages of encephalopathy. Given that prophylactic
antibiotics have been shown to reduce the risk of infection, that later stages of
encephalopathy are associated with increased incidence of cerebral edema, and that fever
may worsen ICH, it is possible that antibiotic and antifungal prophylaxis may decrease
the risk of cerebral edema and ICH. This hypothesis is yet to be proven, however.
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DIAGNOSIS
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most common agents. Pneumococcus and Streptococcus organisms are responsible for as
many as 20% of cases. In nearly half of cases, blood cultures are positive for the same
organism found in the ascitic fluid.
TREATMENT
COAGULOPATHY.
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GASTROINTESTINAL BLEEDING.
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hours and coagulopathy were the only significant risk factors for bleeding in critically ill
patients of all types. Additional risk factors for bleeding reported in smaller studies have
included hepatic and renal failure, sepsis, shock and others. Patients with acute liver
failure are thus at high risk for gastrointestinal hemorrhage. Histamine 2 receptor (H2)
blocking agents such as ranitidine have long been used in the prophylaxis of GI bleeding
in critically ill patients; their efficacy has been supported in several trials. Sucralfate has
also been found to be effective in many studies, and there have been smaller randomized
trials and a meta-analysis which suggested that sucralfate may be as effective in
preventing gastrointestinal bleeding and might be associated with lower risk of
nosocomial pneumonia than H2 blockers which lower gastric pH. More recently,
however, a much larger (1,200 patients), well-designed trial comparing ranitidine to
sucralfate in mechanically-ventilated patients found that ranitidine but not sucralfate
decreased the risk of clinically significant bleeding; the incidence of pneumonia was
similar for the two groups. Limited studies of proton pump inhibitors (PPIs) as bleeding
prophylaxis have demonstrated their effectiveness in maintaining elevated intragastric pH.
Two trials found no significant bleeding in PPI-treated patients on mechanical ventilation,
but study size may have precluded detection of significant bleeding. H2 blockers have
been proven to be effective and PPIs are almost certainly effective as well. PPIs may
provide superior protection but this remains to be proven. Sucralfate may be acceptable
as second-line treatment.
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preferred shunt procedure is the one with which the surgeon is most experienced. A
distal splenorenal shunt with concomitant gastroesophageal devasc ularization selectively
decompresses esophageal varices while maintaining mesenteric blood flow to the liver. In
most but not all studies, use of the distal splenorenal shunt reduced the incidence of
severe encephalopathy as a late complication after surgery, compared with conventional
shunts. The procedure is technically difficult; time will reveal if it possesses any
long-term advantages.
Because the first episode of variceal bleeding can result in significant morbidity
and mortality, there has been considerable interest in the prophylactic treatment of
esophageal varices in persons who have never bled. Prophylactic portosystemic shunts
decrease rebleeding but do not enhance survival. Prophylactic sclerotherapy has been
studied in several centers with mixed results. In the largest study, which was restricted to
alcoholic patients, this approach proved harmful. The experience with the
beta-adrenergic antagonists propranolol and nadolol has been somewhat more
encouraging because the drugs appear both to prevent the first episode of bleeding and to
reduce mortality associated with bleeding in patients who have moderate or large
esophageal varices.51 If a patient known to have large varices is well motivated and
tolerates the medication, beta-adrenergic antagonists may be considered.
Isosorbide-5- mononitrate, a long-acting nitrate, may also help prevent the first variceal
hemorrhage.
HEMODYNAMICS/RENAL FAILURE
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SCITES
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PARACENTESIS
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blood flow. Serious complications of the shunt include bacterial infection of the
peritoneum, disseminated intravascular coagulation, and rupture of esophageal varices.
Because of these complications, the peritoneovenous shunt is seldom used.
TRANSPLANTATION
Orthotopic liver transplantation remains the only definitive therapy for patients
who are unable to achieve regeneration of sufficient hepatocyte mass to sustain life. As
mentioned previously, the advent of transplantation has coincided with improvement in
overall survival rates from as low as 15% in the pre-transplant era to 60% presently.
Advances in critical care and changing trends toward more benign etiologies such as
acetaminophen (having a better overall outcome) have likely helped. Spontaneous
survival rates are now around 40%,5 compared to 15% in the pre-transplant era.
Post-transplant survival rates for ALF have been reported to be as high as 80% to
90%,5,93 but accurate long-term outcome data are not yet available. In the largest U.S.
study, only 29% of patients received a liver graft, while 10% of the overall group (1/4 of
patients listed for transplantation) died on the waiting list.5 Other series have reported
death rates of those listed for transplant as high as 40%,150,151 despite the fact that
ALF remains the one condition for which the most urgent (UNOS status 1) listing is
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AUXILIARY TRANSPLANTATION
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A support device to replace the acutely failing liver seems a reasonable but elusive
goal. The ideal replacement for the failing liver would detoxify, metabolize and
synthesize; in short, perform all the livers many functions. A variety of systems have
been tested to date, with no certain evidence of efficacy. Sorbent systems embody only
detoxification and no hepatocyte replacement. Such systems, employing charcoal or
other adherent particles in a capsule or column device placed in an extracorporeal circuit,
may show loss of platelets and worsening of coagulation parameters across the device.
Transient improvement of hepatic encephalopathy may be observed but no improvement
in hepatic function or long-term benefit has been shown. Hepatocytes, whether of human
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or other mammalian origin, have been used in cartridges in extracorporeal circuits, either
with or without sorbent columns.
Few controlled trials have been published, and some preliminary reports suggest
no benefit to outcome, with or without transplantation. One recent multicenter trial did
report improved short-term survival for a subgroup of patients with ALF who were
treated with a porcine hepatocyte-based bioartificial liver, but corroboration of these
results by further studies will likely be required before the true utility of this device can
be established. All such trials are difficult to perform and to control properly due to the
rarity of well-characterized patients, the heterogeneity of etiologies, varying levels of
disease severity and varying access to transplantation. A recent meta-analysis, considering
all forms of devices together, demonstrated no efficacy for bio-artificial liver devices for
the treatment of ALF. A variety of other strategies have been employed including
exchange transfusion, charcoal hemoperfusion, extracorporeal liver perfusions, and intra-
portal hepatocyte infusions. To date, none can be recommended, and their use remains
experimental. Efforts to improve hepatocyte regeneration have likewise been futile thus
far.160 When heterotopic or partial replacement transplantations have been performed it
appears that the native liver can recover in some but not all situations, but this may
require weeks or months to occur, underscoring the real challenge to liver replacement
devices, that is, that liver assist devices might well be required for long periods of time.
PROGNOSIS
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Mushroom poisoning
Wilson disease
Budd-Chiari syndrome
Indeterminate cause
Coma grade on admission
III
IV
Kings College Criteria:
Acetaminophen-induced ALF:
Arterial pH _7.3 (following adequate volume resuscitation) irrespective of
coma grade OR
PT _100 seconds (INR _ 6.5) _ serum creatinine _300 _mol/L (3.4 mg/
dL) in patients in grade III/IV coma
Non-acetaminophen-induced ALF:
PT _100 seconds irrespective of coma grade OR
Any three of the following, irrespective of coma grade:
Drug toxicity, indeterminate cause of ALF
Age _10 years or _40 years
Jaundice to coma interval _7 days
PT _50 seconds (INR _3.5)
Serum bilirubin _300 _mol/L (17.5 mg/dL)
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large numbers of patients, still fail to achieve success, given the wide variety of etiologies
that lead to this end stage syndrome. The traditional Kings College Hospital criteria have
been the most commonly utilized and most frequently tested of the numerous proposed
prognostic criteria for ALF Several studies evaluating these criteria have shown positive
predictive values ranging from just below 70% to nearly 100% and negative predictive
values ranging from 25% to 94%. Overall, such prognostic scores have proven to have
acceptable specificity but low sensitivity to determine outcome. Criteria based on
decreased levels of factor V in patients with encephalopathy predicted death in acute viral
hepatitis cases with a positive predictive value of 82% and a negative predictive value of
98%, butsubsequent studies in both acetaminophen and nonacetaminophen ALF have
shown these criteria to be less accurate than Kings College Hospital criteria in predicting
outcome.
In a recent meta-analysis, Bailey et al. compared various prognostic criteria in
patients with ALF due to acetaminophen, including Kings College Hospital criteria,
various combinations of elevated serum creatinine, encephalopathy, and prothrombin
time elevations (both single and serial measurements), decreased factor V levels, the
Acute Physiology and Chronic Health Evaluation (APACHE) II scores and Gc globulin
(vitaminDbinding protein, a liver-derived component of the actin-scavenging system170).
The analysis found that Kings College Hospital criteria and pH 7.30 alone were both
fairly specific in predicting a poor outcome. While the Kings College Hospital criteria
were more sensitive than pH alone (69% versus 57% sensitivity), use of both criteria was
still likely to miss many patients who would ultimately require transplantation. The
authors also found that an APACHE II score of 15 on admission had a specificity of 92%
(comparable to Kings College Hospital criteria) with a much better sensitivity of 81%,
but this measure was only examined in one limited studyOther factors such as age and
the length of time between onset of illness and onset of encephalopathy have previously
been proposed as important prognostic indicators in ALF, these parameters did not affect
outcome in the largest U.S. multi-center study of ALF to date. Patients presenting in
grade III or IV encephalopathy were less likely than those patients presenting in grade I
or II encephalopathy to survive without receiving a liver graft. The most significant
predictor of outcome in this study was etiology of ALF, as patients with ALF due to
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REFERENCES
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20:180, 1975.
21. Gurusamy, K. S.; Samraj, K. (2006). Early versus delayed laparoscopic
cholecystectomy for acute cholecystitis. In Gurusamy, Kurinchi Selvan. "Cochrane
Database of Systematic Reviews". Cochrane database of systematic reviews (Online)
22. Howard, R. J.: Acute acalculous cholecystitis. Am. J. Surg., 141:194, 1981.
23. Isch, J. H., Finneran, J. C., and Nahrwold, D. L.: Perforation of the
gallbladder. Am. J. Gastroenterol., 55:451, 1971.
24. Jarvinen, H. J., and Hastabacka, J.: Early cholecystectomy for acute
cholecystitis, a prospective randomized study. Ann. Surg., 191:501, 1980.
25. Keighley, M. R. B.: Microorganisms in the bile. Ann. R. Coll. Surg. Engl.,
59:329, 1977.
26. Levene, A.: Acute torsion of the gallbladder: Postmortem finding in two
cases. Br. J. Surg., 45:338, 1958.
27. Long, T. N., Heimbach, D. M., and Carrico, C. J.: Acalculous cholecystitis
in critically ill patients. Am. J. Surg., 136:31, 1978.
28. Lou, M. A., Mandal, A. K., Alexander, J. L., and Thadepalli, H.:
Bacteriology of the human biliary tract and the duodenum. Arch. Surg., 112:965, 1977.
29. Mentzer, R. M., Jr., Golden, G. T., Chandler, J. G., and Horsley, J. S., III:
A comparative appraisal of emphysematous cholecystitis. Am. J. Surg., 129:10, 1975.
30. Norrby, S., Herlin, P., Holmin, T., Sjodahl, R., and Tagesson, C.: Early or
delayed cholecystectomy in acute cholecystitis? A clinical trial. Br. J. Surg., 70:163,
1983.
31. Ostrow, J. D.: Absorption of bile pigments by the gallbladder. J. Clin.
Invest., 46:2035, 1967.
32. Ottinger, L. W.: Acute cholecystitis as a postoperative complication. Ann.
Surg., 184:162, 1976.
33. Petersen, S. R., and Sheldon, G. F.: Acute acalculous cholecystitis: A
complication of hyperalimentation. Am. J. Surg., 138:814, 1979.
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34. Richards, C.; Edwards, J.; Culver, D.; Emori, T. G.; Tolson, J.; Gaynes, R.;
National Nosocomial Infections Surveillance (Nnis) System, C. F. D. C. P. (2003).
35. Rodriguez-Noriega, E., Andrade-Villanueva, J., and Amaya-Tapia, G.:
Quinolones in the treatment of Salmonella carriers. Rev. Infect. Dis., 11:S1179, 1989.
36. Serpe, S. J., Todd, D., and Baruch, H.: Cholecystitis due to granular cell
myoblastoma of the cystic duct. Am. J. Dig. Dis., 5:824, 1960.
37. Silbernagl S, Despopoulos A (2009). Color atlas of physiology (6 ed.).
Thieme. p. 252.
38. Stephenson, S. E., Jr., and Nagel, C. B.: Acute cholecystitis: An
experimental study. Ann. Surg., 157:687, 1963.
39. Stone, H. H., Hooper, C. A., Kolb, L. D., Geheber, C. E., and Dawkins, E.
J.: Antibiotic prophylaxis in gastric, biliary and colonic surgery. Ann. Surg., 184:443,
1976.
40. Strasberg, S. M., Hertl, M., and Soper, N. J.: An analysis of the problem of
biliary injury during laparoscopic surgery. J. Am. Coll. Surg., 180:101, 1995.
41. Strasberg, S. M. (2008). "Acute Calculous Cholecystitis". New England
Journal of Medicine 358 (26): 28042811.
42. Strohl, E. L., Diffenbaugh, W. G., Baker, J. H., and Cheema, M. H.:
Gangrene and perforation of the gallbladder (Int. Abstr. Surg.). Surg. Gynecol. Obstet.,
114:1, 1962.
Weissmann, H. S., Badia, J., Sugarman, L. A., Kluger, L., Rosenblatt, R., and
Freeman, L. M.: Spectrum of
38. Werbel, G. B., Nahrwold, D. L., Joehl, R. J., Vogelzang, R. L., and Rege,
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in the high-risk patient. Arch. Surg., 124:782, 1989.
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Classification
(by O.O.Shalimov, 1988)
PCES is distinguished:
1. PCES, related to the diseases of gall-bladder and changes in bilious ducts which were
uncorrected at cholecystectomy (51 %):
a) stenotic papillitis;
b) stenosises of bilious ducts;
c) tubular stenosis of choledochus on soil of chronic pancreatitis;
d) residual choledocholithiasis;
e) mechanical violations of patency of duodenum (chronic duodenojejunal obstruction and
arteriomesenteric obstruction);
f) cysts of bilious ducts;
g) parasite diseases of bilious ducts.
2. PCES, conditioned by the changes which arose as a result of operative treatment
concerning cholecystitis (19 %):
a) iatrogenic damage of bilious ducts;
b) scar stricture and deformation of bilious ducts with violation of outflow of bile;
c) deformation of duodenum with violation of evacuation of its maintenance;
d) remaining gall-bladder;
e) strange bodies of bilious ways (filaments, needles, prosthetic appliances, fragments of
drainages);
f) reflux after transduodenal sphincteroplasty or choledochoduodenostomia;
g) neurinoma of the cut nerves.
3. Disease of hepatopancreatoduodenal area, connected with protracted cholecystitis (17
%):
a) chronic cholangiohepatitis;
b) chronic pancreatitis;
c) pericholedocheal lymphadenitis;
d) intrahepatic and parahepatic abscesses;
e) cholangiogenic sepsis;
f) tumour of liver, bilious ducts and pancreas.
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4. Organic and functional diseases of other organs and systems, not connected with the
disease of gall-bladder and its deleting (7 %):
a) hernia of the esophagus opening of diaphragm;
b) ulcerous disease of stomach and duodenum;
c) chronic gastroduodenitis, colitis;
d) tumours of stomach and intestine;
e) nephroptosis;
f) kidney-stone disease and chronic pyelonephritis;
g) solar plexitis;
h) diencephalic syndrome;
i) asthenovegetative syndrome, psychopathy, hysteria;
j) Abdominal ischemic syndrome;
k) deforming spondylarthrosis.
5. Nervously-kinetic violations of bilious ducts and duodenum (6 %):
a) dyskinesia of bilious ducts and large papilla of duodenum (LDP);
b) blood pressure LDP low;
c) LDP hypertension;
d) hypokinesia of duodenum;
e) reflux-gastritis.
During intravenous cholegraphy on sciagrams dilatation ducts can be seen and their
emptying from the contrasting matter is slow. Retrograde pancreatocholangiography (Pic.
3.4.32) can set a level and character of obstruction of ducts (stone, tumour, indurative
pancreatitis and others like that). In the PCES diagnostics ultrasonic examination occupies
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important place by which it is possible to verify the sizes of bilious ways and expose
concrement (Pic. 3.4.33).
The presence of external bilious fistula or drainpipe in biliary passings enables to contrast
both intrahepatic and external bilious ducts (Pic. 3.4.34). External fistula are localized in the
area of postoperative scar. Thus bile and pancreatic juice cause maceration of skin, races and
infiltrate are formed. External fistula periodically can be closed and opened, accompanied by
icterus and cholangitis, presence of gases in bilious ways and contrasting mass during the
roentgenologic inspection of patient.
PCES engulfs different types of pathology, which differ by both the reasons of origin and
clinical signs. At the PCES development conditioned by the uncorrected changes at
cholecystectomy, a leading role belongs to concrement forgotten in a general bilious duct
during cholecystectomy (3540 %).
The real relapse of cholelithiasis is met seldom, only in 57 % and, as a rule, in people
with the protracted anamnesis of gallstone disease, after choledocholithotomy and previous
choledocholithiasis. Both the first and the second variants of pathology (forgotten stone or
recurrent cholelithiasis), can cause pain of a different character in the area of liver, icterus and
cholangitis. Distinguishing the real relapse of choledocholithiasis from unreal is difficult,
therefore acquired concrement cholegraphy, sonography, retrograde pancreatocholangiography
have the decisive value in diagnostics.
Scar stricture of large duodenal papilla (LDP) is met in 30 % cases. They are divided into
primary and secondary. Under the concept of scar of LDP stricture the damage of distal part
of general bilious duct by length from 5 to 10 mm is understood, the most widespread reason of
which can be a gallstone disease. This complication usually shows up the attacks of hepatic
colic or permanent aching pain in right hypochondrium. At intravenous cholegraphy
contrasting of all parts of bilious ways is marked in such patients, expressed ectasia and delay
of selection of contrast. Retrograde pancreatocholangiography has the decisive value in
diagnostics of this complication.
It is needed to mark that except for the organic stenosises LDP, occasionally there are
undiagnosed before operation functional, transitional forms of defeats of bilious ways which
can be accompanied by high blood pressure or low blood pressure of sphincter. Operating
trauma of nervous branches, formation of connections and scars always negatively influence the
LDP function. Violation of function of sphincter is accompanied by pain and dyspepsia
disorders.
Scar strictures of distal part of choledochus on soil of chronic pancreatitis (tubular
stenosis) are considered to be a difficult type of pathology of bilious ways (1516 %). The first
signs of this disease, as a rule, arise during 23 months after operation and show up by
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permanent dull pain in right hypochondrium, dyspepsia disorders, cholangitis and mechanical
icterus. Valuable information in diagnostics of tubular stenosis can be got from retrograde
pancreatocholangiography and percutaneous transhepatic cholangioduodenography.
The frequent reason of origin of pain after cholecystectomy is an inflammatory process in
regional lymphatic knots. The so called pericholedocheal lymphadenitis can squeeze a general
bilious duct, cause violation of function of the Oddi sphincter and predetermine development
of pancreatitis.
Pancreatitis, which is connected with cholecystectomy, can be met in 3040 % patients
with PCES. Similar pancreatitis arises up as a result of the undiagnosed stenosis of the Oddi
sphincter and distal part of Wirsung's duct during operation on bilious ways. It results in
violation of outflow of bile and pancreatic maintenance and provokes acutening of existing or
origin of acute pancreatitis.
In 2025 % cases the reason of PCES is duodenostasis undiagnosed before operation.
Nausea, bitter taste in the mouth, periodic vomitting and loss of weight are the basic signs of
this disease. Facilitation, as a rule, comes, when patients occupy knee-elbow position or lie
down on the right side. Duodenomanometry is the basic method of diagnostics of
duodenostasis (CDS) (normal pressure in a duodenum is 100120 mm of col. or 1,17 kPa).
During roentgenologic examination (tube relaxation duodenogram) violation of duodenal
patency is exposed. The last can be conditioned by high duodenojejunal corner,
arteriomesenteric compression, cicatricial periduodenitis, lacks of development of duodenum
and others. Uncorrected during cholecystectomy such changes of duodenum can be the reason
of unsatisfactory results of operative treatment of patients with cholecystitis.
The organic and functional diseases of other organs and systems (hernia of diaphragm,
ulcerous disease of stomach, duodenum and others like that), which are not connected with the
disease of gall-bladder and its deleting, always require their preoperative diagnostics and
previous treatment.
Diagnosis program
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Choledohoscopia. Choledochoitiasis.
Supraduodenal choledohotomy
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Choledocholithiasis, ERCP
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Choledocholithiasis, fistulocholangiography.
Differential diagnostics
Chronic pancreatitis. Everyday medical practice testifies that in patients with the diseases
of bilious ways the symptoms of damage of pancreas appear very often. Actually biliary
pancreatitis is the most widespread form of chronic pancreatitis. For this disease belting pain
and positive Mayo-Robson's symptom are characteristic. Thus, pain can be of hepatic colics
character, accompanied by icterus or cholangitis. By palpation patients feel painfulness in the
overhead half of abdomen.
At acutening of chronic pancreatitis there is growth of diastase activity in urines and
amylase in blood. Ultrasonic examination, computer tomography have the important value in
diagnostics of chronic pancreatitis.
Ulcerous disease of stomach and duodenum. Considerable difficulties can arise during
conducting of the differential diagnostics of PCES with ulcerous disease, especially at its
complications by penetration.
For diagnostics of this pathology character of pain, it intensity, time of origin and
periodicity of appearance have the important value. In all doubtful cases it is necessary to
conduct the x-Ray examination of both bilious ways and gastro-intestinal tract. Final
confirmation of diagnosis can be got by endoscopy.
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Choledohojejunostomy by Roux.
If the process spreads on liver or pancreas, correction is brought in medicinal therapy. The
uneffective of the conducted conservative therapy is an indication to the repeated operative
treatment on bile-excreting ways.
1. Tumours of duodenal papilla, scar stricture of bilious duct, large stump of cystic duct
and tubular stenosis of choledochus.
2. Mechanical icterus, internal and external fistula, expressed with the frequent relapses
cholangitis.
In argumentation of method of operative treatment of postcholecystectomy syndrome the
intraoperative revision of bilious ways is of important value. In this plan of expansion of
general bilious duct more than 10 mm is considered as a sign of bilious hypertension.
Considerable methods of the PCES diagnostics are also intraoperative cholangiography,
choledochoscopy, cholangiomanometry and debitometry.
The choice of method of surgical treatment of postcholecystectomy syndrome, first of all,
depends on character of pathology. Basic of them at postcholecystectomy syndrome are: 1)
choledochoduodenostomy (by Finsterer, Flerken, Jurash, Kirschner); 2)
choledochojejunostomy (on the eliminated loop for Roux and after the Brawn method with
choke by O.O. Shalimov); 3) transduodenal papillosphincteroplasty and wirsungoplasty.
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Classification
According to the causal factors the syndromes of portal hypertension are divided into three
kinds:
1. Intrahepatic, that arises at different forms of cirrhosis of liver.
2. The suprahepatic arises at the thrombosis of hepatic veins (the Badda-Kiari syndrome).
3. Pre-hepatic is thrombosis of basic trunk of portal vein.
Stages of development of portal hypertension.
1. Preclinical.
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Cirrhosis of liver.
Intrahepatic
portal hypertension
The cirrhosis of liver is a chronic progressive disease, the characteristic signs of which are
the defeats of parenchymatous and interstitial tissue of organ, necrosis and dystrophy of
hepatic cells, with the subsequent node regeneration as diffuse excrescence of connecting
tissue. All this finally results in a different degree of insufficiency of functions of liver and
origin of syndrome of portal hypertension.
video
Pathomorphology
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The histological signs of cirrhosis are: dystrophy and necrosis of hepatocytes, disfigured
regeneration, diffuse sclerosis, structural alteration and deformation of organ.
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Classification
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passing.
Together with that, quick progressive passing is a transitional form from subacute atrophy
of liver to the cirrhosis. Death of patients at such passing of pathology, as a rule, comes as a
result of hepatic insufficiency during a few months from the beginning of disease.
Most characteristic for the alcoholic cirrhosis of liver after the absolute exception of
reception alcohol and adjusting of valuable nutrition is regressive passing.
Protracted periods of remission which come on the early stages of cirrhosis after adequate
conservative treatment are inherent to stable character of passing.
Complications: bleeding from the varicose extended veins of esophagus and stomach,
haemorrhoidal veins, choleic bleeding, thrombosis of portal vein, hepatogenic gastric ulcers,
hepatic insufficiency, hepatic comma, transition of cirrhosis in cancer and encephalopathy.
Complication of portal hypertension by bleeding from the varicose extended veins of
esophagus carries the instant danger for life of patient, if portal pressure grows over 250300
mm of waters (2,452,94 kPa). Lethality of patients after the first bleeding makes 25 %, after
the second about 50 % and after the third over 75 %. Such complications can arise both
during complete rest and after the physical loading. Bleeding, as a rule, is profuse, and is
accompanied by vomitting by coffee-grounds and grume of fresh blood. Thus patients often
have collapse with the acute falling of arterial pressure and eclipse of consciousness. The
frequent liquid emptying of black can also take place (melena).
Diagnosis program
Differential diagnostics
Insufficiency of circulation of blood after the right ventricle type can be accompanied by
an increased painfulness of liver. It can be the reason of such symptomatic complex as
rheumatism, atherosclerotic cardiosclerosis, innate lacks of heart and chronic pulmonary heart.
However, for this pathology edemata on lower extremities which arises long before
development of ascites is characteristic. It is needed to remember, that ascites well responds to
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treatment by cardiac glycoside and diuretic. And yet, except for anasarca, for insufficiency of
circulation of blood the shortness of breath is characteristic, acrocyanosis and the stagnant
phenomena in lungs, changes of ECG. The icterus in such patients is very rarely, and the
functional tests of liver change insignificantly.
Pericarditic pseudocirrhosis. This pathology develops at squeezing pericarditis. Except
for development of ascites, that can be observed, for this pathology symptoms of constructional
pericarditis are characteristic also: increase of vein pressure over 200 mm of waters. item (1,96
kPa), paradoxical pulse (disappearance during inhalation) and decline of amplitude of
pulsation of heart on roentgenokymography. Roentgenologicly , laying of salts of calcium in a
pericardium, little and quiet heart are found in patients. For this disease characteristic are
the typical changes at ECG and phonocardiography.
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Palliative operations
Among them the widespread are used:
1. Operations directed on stimulation of regeneration of liver: a) partial (regional)
resection of liver; b) electro-coagulation of surface of liver; c) cryogenic and laser destructions
of surface of liver; d) periarterial neurectomy of general hepatic artery; e) bandaging of splenic
artery and splenectomy; f) endovascular embolization of splenic artery.
2. Organanastomosis:
a) omentopexy;
b)omentodiaphragmopexy;
c) omentohepatopexy.
3. Operations at ascites:
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a) laparocentesis; VIDEO
b) taking of ascites liquid in preperitoneal, retroperitoneal and hypodermic cellulose, in
urethra;
c) lymph-venous anastomosis (between a pectoral lymphatic duct and internal or external
jugular vein);
d) peritoneovenous shunting by the synthetic tube with a valvular device, taken in an
abdominal wall;
e) extraperitonization of the livers (formation of vascular communications between a liver
and diaphragm).
Treatment of patients at bleeding from the varicose veins of esophagus needs to be begun
with the tamponade internal surface of esophagus and cardial part of stomach by the special
double-balloon Sengstaken-Blakemore tube. Some other conservative measures directed on the
stop of bleeding without the use of this probe are considered ineffective and tactically wrong.
The Sengstaken-Blakemore tube has three ducts, two of which are connected with rubber
bulbs, one with the cavity of stomach. (Fig.4)
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probe through the block, the load is suspended weighing about 1 kg It warns reverse
advancement of probe in stomach and by this provides stability of compression of the varicose
extended veins. The control after hemostasis is carried out through the third, connected with
stomach, duct of probe. By such method it can be succeeded to attain to hemostasis in 8090
% cases. The probe in such position is held 23 days. After this decompression of repeated
bleeding can come almost in half of patients. Therefore deleting the probe is not needed.
Taking this into account, it is expedient to carry out decompression of bulbs in the light
intervals of days and inflate bulbs at night, when the control after the possible bleeding is
complicated.
Conservative treatment is reasonable: 1) at the easy degree of loss of blood and I degree of
hepatic insufficiency (basic biochemical indexes either are not changed or with insignificant
deviations from a norm; ascites and encephalopathy are absent);
2) at the III degree of hepatic insufficiency, progressive ascites and encephalopathy,
regardless of degree of loss of blood.
Conservative therapy of bleeding from the varicose veins of esophagus must engulf the
whole volume of medical measures, as at similar pathology of ulcerous genesis (hemostatic
therapy, antacid, 2- blocker histamine receptors).
For the decline of portal pressure pituitrin is entered. The endoscopic methods of stop of
bleeding are applied also (imposition of clips on veins, sclerosis therapy 76 % ethyl
alcohol, Varicocide, 66 % solution of glucose, endovascular occlusion of veins, laser
coagulation of veins). It is needed to count setting of preparations for stimulation of
regeneration of liver (esenciale, lif-52 and others like that), application of disintoxication
therapy.
Surgical treatment is considered applicable at bleeding of middle and heavy degrees with
the I and the II degrees of hepatic insufficiency (general bilirubin not more large 50 mcmol/L,
general albumen not more small 60 g/, prothrombin index not more low 60 %, present
transient ascites) in the cases when the valuable conservative treatment directed on the stop of
bleeding is not effective during 2448 hours.
Types of operations
I. Operations directed to disconnection of gastroesophageal vein way.
1. The Taners operation:
a) transversal cutting and sewing together of stomach in subcardial part;
b) cutting with the next sewing together of esophagus in supradiaphragmatic segment.
2. Operation by .. Shalimov is cutting and sewing together of esophagus by the device
for circular anastomosis.
3. Sewing of cardioesophageal transition circular by U-shaped stitches after V.M.
Korotkyy.
4. Operation developed by M.D. Paciora, is sewing and bandaging by separate ligatures of
bleeding veins of cardial part of stomach and esophagus from the side of mucus shell.
5. Resection of distal part of esophagus and proximal part of stomach.
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II. Operations which reduce portal pressure: portocaval anastomosis (direct and selective),
splenectomy.
In children the basic etiologic factor which predetermines the thrombosis of portal vein, is
infectious aggression. Inflammatory processes of abdominal cavity (acute appendicitis,
cholecystitis traumas), the getting wet belly-button of new-born are those principal reasons
which predetermine the origin of pylephlebitis and thrombopylephlebitis. In adults the most
frequent reasons of thrombosis of portal vein are the cirrhosis of liver and hepatoma. Similar
pathology can develop after splenectomy or operations on bilious ways. The reason of
thrombosis can be the cardiovascular anomalies of development, in particular, innate defect of
portal vein. However, it is needed to mark that in the half of patients reason of origin of
thrombosis of portal vein is not succeeded to set.
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In patients with portal hypertension, that arose on soil of thrombosis of portal vein, acute
symptoms, as a rule, are absent. However, it is possible to observe the dyspeptic phenomena in
them: nausea, bad appetite, flatulence. Moderate pain is felt in right hypochondrium, that is
multiplied after acceptance of meal.
At this pathology appearance of early ascites which mainly carries temporal, transitional
character is characteristic, sometimes it takes out chronic shape. On more late stages
hypersplenism can develop and bleeding arise from the varicose extended veins of esophagus
and cardia.
The general condition of patients here can remain satisfactory, the relapses of bleeding
from the varicose extended veins of esophagus and cardia are seldom. If they arise, they are
carried by patients relatively well. It can account for favourable passing of portal hypertension
by development of collateral circulation of blood. Together with that, productively
unfavourable passing of disease is observed on the background development of chronic ascites
and portocaval encephalopathy.
The diagnosis is usually confirmed by sonography and splenoportography. Valuable
information about such patients can be given by computer tomography on the background rapid
introduction of contrasting matter to the portal system (computerized axial tomography).
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For the clinic of disease, as a rule, stormy passing is peculiar. Thus patients feel great pain
in stomach, liver is increased, painful. Increasing ascites is often observed. As experience
shows, development and expression of symptoms of disease depend on the depth of damage by
the thrombosis process of hepatic veins and joining of thrombosis of lower hollow vein.
The disease is also accompanied by development of polycythemia, which is the second and
conditioned, from one side, by concentration of blood, and from other investigation of
increased products of erythropoietin, that is selected by a regenerating liver.
At endoscopy the varicose extended veins of esophagus and cardial part of stomach are
exposed.
In some patients it is possible to observe acute passing of the Budd-Chiari syndrome, that
usually has bad prognosis and is often closed lethally. Portal hypertension in these patients, as
a rule, develops early and has the expressed character, sometimes arriving at maximal numbers
(390400 mm of waters). Bleeding which arise on this background carries difficult profuse
character.
Conservative therapy in such cases is ineffective. At acute passing of disease lethal end
can be warned only by forming of direct or selective portocaval anastomosis. The protracted
(chronic) passing of disease is also accompanied by early and expressed portal hypertension,
that can be complicated by bleeding from the varicose extended veins of esophagus. In such
cases, as well as at acute forms, although not so quickly, the operative treatment directed on
decompression of the portal system is possibly conducted.
LIVER TRANSPLANTATION
History
Canine liver grafts were shown to function after transplantation to the pelvis by Welch in 1955.
Orthotopic liver transplantation in dogs was attempted by Cannon in 1956 and performed
successfully by Moore in 1959. The first attempt at liver allotransplantation in man was made
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by Starzl at the University of Colorado on March 1, 1963. The 3-year-old recipient with
extrahepatic biliary atresia died of hemorrhage on the day of transplantation. Ensuing attempts
in Denver, Boston, and Paris were unsuccessful until 1967, when the first extended survival of
a human liver allograft recipient was achieved by Starzl. The addition of cyclosporine
immunosuppression by Calne in 1978 and then combination therapy with cyclosporine and
prednisone by Starzl in 1980, as well as better liver preservation and surgical techniques,
improved the prospects for clinical liver transplantation
The specific indications for liver transplantation have become more standardized owing to
the better knowledge of the natural history of a number of liver diseases and concomitant
improvement in short- and long-term results of orthotopic liver transplantation (OLT).As with
most aspects of this topic, however, significant controversy remains about several disease states
leading to end-stage liver failure.
Cholestatic Liver Diseases. Cholestatic diseases, including primary biliary cirrhosis (PBC),
secondary biliary cirrhosis, and primary sclerosing cholangitis (PSC), are the diseases most
successfully treated by liver transplantation.Operative survival is greater than 90%, and 5-year
survival is approximately 80%. This rate is due mostly to the slow onset of illness, which
allows for preoperative preparation of the recipient and appropriate timing of the procedure, as
well as absence of recurrence of the disease in the graft. As a result of this success, cholestatic
disease is one of the most frequent indications for transplantation, accounting for 22% of all
transplants performed in the United States. Clearly, the timing of operation is critical, and a
substantial literature has addressed the rate of disease progression.
The indications for transplantation in patients with PSC are based on refractory symptoms
resulting from recurrent cholangitis or impaired synthetic function. The risk of
cholangiocarcinoma, approximately 15% in these patients, is an additional relative indication
for OLT. A current trend toward earlier intervention with liver transplantation in PSC is
underway, with retrospective comparisons of transplant versus nontransplant therapy weighing
heavily in favor of the transplant approach. Clearly, however, some patients, particularly those
with predominantly extrahepatic biliary strictures do well with conventional bypass or
endoscopic procedures. Thus, timing remains a matter of clinical judgment, with most patients
benefiting from allotransplantation.
Several models of survival have been established to predict outcome in patients with
PBC. All prognostic scores are based in part on the rise in serum bilirubin. In general,
transplantation is recommended when the bilirubin level exceeds 15 mg./100 ml., although
earlier transplantation for severe associated symptoms such as pruritus or fatigue, refractory
ascites, or variceal bleeding is appropriate. Although close monitoring of asymptomatic
patients is reasonable, it is important not to delay intervention until the clinical status of the
patient deteriorates, because OLT is the only definitive treatment.
Alcoholic Liver Disease. Nineteen percent of all liver transplants performed in the United
States have been for alcoholic cirrhosis. Although the procedure was originally avoided
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progressing to coma in less than 2 weeks having a 36% survival and those progressing in 2 to 8
weeks having a 7% survival. Despite the dramatic rate of progression of disease, these patients
have very acceptable results from OLT (about 60% 5-year survival).Predictably, survival after
OLT improves with improved health of the patient at the time of transplant. Survival for all
etiologies of FHF has doubled in the past decade, primarily due to great strides in supportive
intensive care. Unlike chronic viral diseases, recurrence of disease for viral causes of FHF is
unusual.
Care of patients with FHF is complex, and OLT should be considered early. Thus, prompt
transfer to a liver transplantation center is critical. In patients with rapid deterioration,
supportive care (e.g., hyperventilation, diuresis) should be supplemented with monitoring of
intracranial pressure (ICP) for best results. Subdural ICP monitors have obviated the need for
intraventricular devices and have thus reduced the bleeding risks of this approach. Perfusion
pressures (mean arterial pressure minus ICP) of less than 40 mm. Hg, especially when
combined with pupillary fixation, suggest that irreversible brain injury has occurred, and OLT
should be avoided. Patient decompensation can be rapid and unpredictable. In the absence of a
suitable donor, several aggressive maneuvers can successfully delay the onset of brain death
from intracranial pressure. These include hepatectomy with end-to-side portacaval shunt,
xenogeneic ex vivo perfusion, and bioartificial hepatic support (see later). Donor criteria may
be liberalized to achieve timely hepatic replacement, and ABO incompatibility is acceptable.
Chronic Hepatitis B. Transplantation for chronic hepatitis B virus (HBV) cirrhosis
remains a controversial topic.The discouraging reinfection rate of over 80% of recipients
associated with a high rate of clinical hepatitis recurrence (60% at 1 year) and high related
mortality (30% at 1 year and 52% at 5 years) raises questions about the procedure.Although
generally contraindicated, transplantation may be appropriate in certain settings. Recent
intense investigation in this area has identified several factors affecting reinfection. In general,
the state of viral replication at the time of transplantation is critical in establishing reinfection.
Identification of active viral replication (serum HBV DNA and HBeAg detection) at the time of
transplantation clearly worsens the prognosis. Immunoprophylaxis with anti-HBV antibodies
improves outcome for replication-negative patients, but long-term results for patients so treated
remain to be seen. In general, OLT in the presence of HBV infection should be reserved for
patients enrolled in specific viral prophylaxis protocols.
Intrahepatic Malignancy. Predictably, transplantation for primary and metastatic cancer
has been associated with a high recurrence of tumor and a poor 5-year survival. Thus, there is
little indication for OLT in a patient with known malignancy. Liver transplantation is no longer
an accepted therapy for hepatic metastasis except perhaps in some patients with rare
neuroendocrine tumors. Today, liver transplantation is usually limited to patients with
nonresectable hepatoma fulfilling the following criteria: asymptomatic hepatoma (i.e., not
associated with recent weight loss, ascites, or constitutional symptoms); tumor less than 5 cm.
in diameter; and fewer than or equal to three intrahepatic tumors. If feasible, liver resection
should always be considered first. Extensive evaluation is required to exclude the presence of
extrahepatic spread. Transplantation for cholangiocarcinoma is even more controversial and
should probably be performed only under the guidance of specific protocols. The role of
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status and overall medical condition. Finally, education of the patient must be initiated early to
ensure that complications of medical noncompliance are avoided postoperatively.
For all liver recipients, thorough preoperative evaluation to determine the antibody titer
directed against hepatitis A, B, and C as well as cytomegalovirus, human immunodeficiency
virus, Epstein-Barr virus, and herpes simplex is mandatory. In addition, viral antigen detection
is required to identify active infection. The role of transplantation for primary viral hepatitis
was discussed previously. Active infection with cytomegalovirus or herpesvirus requires
clinical resolution before transplantation, but viral carriers can receive transplants given
appropriate antiviral prophylaxis. Human immunodeficiency virus infection contraindicates
OLT. In addition to the recipient's status, the donor's status for these viruses should be
ascertained before implantation, again to allow for antiviral prophylaxis when indicated.
Several alternative therapies should be considered in the candidate for transplantation, not
necessarily to obviate the need for transplantation but to improve the medical condition before
transplantation. Patients with good synthetic function (normal bilirubin, normal coagulation,
normal albumin), such as an individual with Child's A cirrhosis and recurrent variceal bleeding,
may benefit from nontransplant surgical palliation such as a Warren shunt. The TIPS procedure
is also a useful palliative step for refractory complications of portal hypertension. Stabilization
of disease with these interventions gives more time to evaluate patients and optimize
preoperative conditions. It allows for a more thorough evaluation of a patient's ability to
comply with the posttransplant medical regimen, particularly alcoholic patients who present
abstinent because they are too sick to drink. This compliance alone may stabilize the disease in
an alcoholic patient with Child's A cirrhosis and avoid the need for transplantation. Reduction
in the degree of portal hypertension may also minimize intraoperative bleeding during the
recipient hepatectomy. Problems with these palliative procedures are frequent and require
surveillance with particular attention to portal vein patency. Identified candidates should be
treated at a center with transplant expertise to facilitate palliation that does not jeopardize
future transplantation. Alternative treatment should not delay transplantation.
SELECTION OF DONORS
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preservation injury or prolonged cold ischemia, prolonged rewarming time, and reperfusion
injury after implantation.
Several factors have been investigated to aid in the prediction of PNF. The most widely
noted is the estimated parenchymal fat content. Donor liver biopsy specimens that show a 40%
or greater parenchymal replacement by fat have a higher chance of PNF, and in some settings
this is a reasonable indicator of the adequacy of a donor organ. This must, however, be
balanced against the severity of the recipient's disease and the urgency of the planned
operation. Other factors used to evaluate the donor's status include the age of the donor, the
level of inotropic support, the mechanism of the donor's death, the level of hepatic or intra-
abdominal trauma, the presence of hypernatremia, and the biochemical studies of liver
function. No single parameter has been established absolutely governing the acceptance of a
donor for organ harvest. Rather, combinations of risk factors are generally responsible for
discarding a potential donor liver. In case of doubt about the quality of an organ, the personal
inspection of the liver by an experienced transplant surgeon is often critical for decision about
the use of an organ.
Donor use has been improved with the introduction of UW preservation solution as
mentioned earlier. Until 1987 the outer limit for cold storage of the liver using EuroCollins
solution was about 8 hours. Use of UW solution has extended the time to about 24 hours,
allowing for better allocation of the organ and preparation of the recipient. The specifics of this
and other preservation solutions are detailed in Part VII of this chapter.
The considerations of ABO typing and other immunologic concerns are discussed later. An
additional issue is size compatibility. Smaller organs are easily adapted to a large recipient, but
the converse is not true. One advance has been the use of reduced-size allografts, particularly in
children. Usually the left lateral lobe (segments 2 and 3) or left lobe (segments 2, 3, and 4) is
used, allowing up to 1/10 weight mismatch. This has been the most important factor in the
success of transplantation in small children. This technique is sometimes used in adults when
an emergency transplantation is required. Finally, male recipients of female organs have 10%
worse survival than other sex-match combinations, according to the 1994 UNOS registry.
Harvest of the donor organ should be performed by an experienced surgeon, with particular
care taken to optimize the preharvest resuscitation of the heart-beating cadaver. Because
immediate hepatic function after transplantation is required, there is no room for error. Errors
in resuscitation include injudicious use of vasopressors, prolonged acidosis, and hypoperfusion
from hypovolemia. Visual inspection and palpation of the liver with knowledge of the potential
recipient's status and size aid in the assessment of the appropriateness of a donor liver.
The liver is generally procured through a midline incision from jugular notch to pubis,
including median sternotomy. Harvest is coordinated with the harvest teams for other organs.
Complete mobilization of the liver is required, including division of both triangular ligaments
and the falciform ligament. The hepatogastric ligament is divided. Particular attention is paid to
the vascular supply, including preservation of aberrant hepatic arteries (20% aberrant right from
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the superior mesenteric artery, 15% aberrant left from the left gastric artery). Unlike the relative
impunity associated with arterial ligation in nontransplanted livers, failure to complete the
arterial revascularization due to an unrecognized arterial supply is poorly tolerated after cold
storage. PNF, late biliary stricture, or intrahepatic abscess may result. Additional care must be
taken when simultaneous pancreas harvest is performed to avoid hepatic artery injury or portal
vein transection. The suprahepatic vena cava should be preserved for the hepatic graft, and care
should be taken to avoid caval injury during cardiac retrieval. The gallbladder is removed either
in situ or after explantation.
Once mobilization is completed, perfusion with UW solution is initiated through the distal
aorta or common iliac arteries with ligation of the supraceliac aorta. The inferior mesenteric
vein or splenic vein is used for portal perfusion. When pancreatic harvest is performed, some
surgeons prefer to use the portal vein for cold perfusion. UW solution is also flushed into the
biliary tree. Topical slush is rapidly applied. Hepatic extirpation is performed after
cardiopulmonary retrieval and before harvest of the pancreas and kidney. The iliac artery and
vein should be harvested in the event that vascular reconstruction is required.
Patients awaiting liver transplantation are prioritized on a national waiting list based on
severity of disease as defined by the UNOS. Status 4 patients are at home and functioning
normally, status 3 patients can be at home but require continuous medical care. Status 2
patients are continuously hospitalized in an acute care unit for at least 5 days or are in the
intensive care unit. Status 1 patients are in the intensive care unit because of acute or chronic
liver failure with a life expectancy without a liver transplant of less than 7 days. Status 7 is
reserved for patients taken from the active list for a temporary medical contraindication such as
sepsis. These patients can accrue points for time on the list despite not being able to accept an
organ. Strict adherence to guidelines for proper categorization is required to allow for ethical
allocation of organs. As soon as a donor is identified, the organ is paired with a potential
recipient, who is called to the hospital for preoperative evaluation before organ harvest.
Appropriate perioperative management of a transplant recipient begins with a thorough
preoperative physical examination (including rectal and dental examinations) to rule out the
possibility of ongoing infection or malignancy. Routine screening includes a complete blood
cell count, electrolyte and metabolic profile, urinalysis, and chest film. Blood is crossmatched.
Intravenous lines, including arterial lines and pulmonary artery catheters, should be placed with
strict attention to aseptic technique because cutaneous contamination with bacteria or fungi can
cause serious postoperative complications in the transplant patient. Selective decontamination
of the gut and mechanical preparation of the bowel are advocated at many centers, as is a
shower with an antimicrobial soap.
For patients in the intensive care unit, supportive measures are continued as needed. Of
specific concern is the potential for neurologic recovery in patients with advanced
encephalopathy and cerebral edema. A recent advance has been the use of intracranial pressure
monitoring in the perioperative period. This was once shunned as a prohibitive risk for cerebral
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bleeding in the coagulopathic fulminant hepatic failure patient, but routine assessment is now
possible through minimally invasive techniques. Small-gauge catheter pressure monitors can be
placed into the subdural space without the need for parenchymal puncture, thus decreasing the
risk of the intervention substantially. Greatly elevated intracerebral pressures, especially in
association with signs of transtentorial herniation in a Grade 5 coma patient, suggest an
irreversible lesion that is unlikely to resolve after transplantation.
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the additional manipulation required by bypass. It has thus become policy at many centers to
employ this technique selectively after an intraoperative trial of portal vein and vena caval
occlusion.
The implantation procedure begins with the suprahepatic vena caval anastomosis followed
by the infrahepatic caval anastomosis. Alternatively, the donor vena cava can be anastomosed
side to side with the recipient vena cava if it is left in situ during the recipient hepatectomy
(piggyback technique). The operation then proceeds to the portal anastomosis. After all venous
connections, the liver is reperfused with the suprahepatic vena cava temporarily occluded and
the infrahepatic vena cava vented to allow washout of the hyperkalemic and adenosine-rich UW
solution. The hepatic artery anastomosis is the final vascular step in the procedure. Some
groups perform simultaneous arterial and venous reperfusion.
The biliary reconstruction remains an additional area of debate. Options include
choledochocholedochostomy with or without externalized T-tube stents. This has the advantage
of easy access for subsequent biliary manipulations or evaluation of bile, as well as
preservation of the sphincter mechanism. Unfortunately, the anastomosis is particularly
sensitive to ischemic injury of the common duct, and complications of leak when the T tube is
removed remain vexing. The incidence of technical complications related to this method ranges
from 12% to 50% in published series, with the cumulative average being 25%. These problems
are obviated for the most part by use of a Roux-en-Y choledochojejunostomy at the expense of
convenient biliary access. Leak or stricture is still observed in 4% to 30% of cases (mean
14%). This method is frequently used in pediatric transplants. One report of 300 transplants
performed with a side-to-side choledochocholedochostomy technique has reported a
remarkable 2.2% technical complication rate. This technique awaits confirmation in other
centers.
POSTOPERATIVE MANAGEMENT
Management in the postoperative intensive care unit is similar to that after any major
procedure. Ventilatory support and volume replacement are standard. Isolation is not required
beyond standard universal precautions. No sedation is given until extubation. For unclear
reasons, postoperative pain is usually mild, and any major discomfort should alert one for
possible complications. Close monitoring of serologic liver enzymes is critical because
increasing enzymes or a failure of enzyme values to correct rapidly suggests PNF or technical
complications such as hepatic artery thrombosis. Liberal use of the Doppler ultrasonography
and rapid return to the operating room are mandatory in these situations because early
detection is the only factor separating a return to normal liver function from complete graft
necrosis and patient death.
Use of drains and antibiotics is no different in this operation from that in any other major
abdominal procedure. Closed-suction drains should be used and removed early after the threat
of postoperative hemorrhage is over. Brief antibiotic prophylaxis is appropriate with an agent
with adequate skin and biliary organism coverage. Prolonged use of prophylactic antibiotics is
contraindicated. A protocol for decontaminating the small bowel can be used but is usually
discontinued within a few weeks of transplantation. At Duke University Medical Center,
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decontamination (colistin, 100 mg./10 ml.; gentamicin, 80 mg./10 ml.; nystatin, 2 106/10
ml.) is discontinued at the time of normal enteral feeding, often within the first postoperative
week).
If a T tube is used in the biliary reconstruction, a T-tube cholangiogram is obtained within a
week with internalization contingent on a normal result. Patients are discharged when they are
familiar with their medications. Patients living more than 2 hours from the transplant center
generally stay in the vicinity for an additional 2 to 4 weeks. Close monitoring of hepatic
function and medical compliance is continued twice a week for 4 weeks and weekly for an
additional 4 weeks. After this outpatient evaluation, patients are returned to their referring
community for chronic follow-up. It is important to establish open lines of communication
between the community physician and the transplant center to ensure prompt recognition and
referral of postoperative complications.
IMMUNOLOGIC MANAGEMENT
The liver must be considered separately from other solid organs with regard to immunologic
management. Many well-established concepts of donor-host interaction after kidney or heart
transplantation do not apply after hepatic transplantation, and failure to recognize the unique
properties of this situation can lead to detrimental perioperative treatment.
HLA Typing. HLA matching is not feasible before liver transplantation. However, because
new techniques have been developed that allow donor HLA data to be provided in a timely
manner, the future use of these data is pertinent. Although matching donors and recipients with
regard to HLA type clearly improves outcome after kidney, heart, and pancreas transplantation,
no such correlation exists with liver transplantation. Indeed, matching may, in fact, reduce
overall survival.The reasons for this lie in the dualistic nature of HLA in the pathophysiology
of liver disease. T-cellmediated rejection of the organ is mechanistically the same as with
other organs, so rejection is reduced with improved HLA compatibility. However, the
physiologic role of HLA is to present viral peptides to T cells to initiate destruction of virally
infected cells. Thus, HLA compatibility potentiates the inflammation during viral reinfection
after transplantation for viral hepatitis and increases the chance for clinical recurrence of the
original disease. Similarly, T-cellmediated autoimmune diseases (e.g., PBC) are etiologically
based on T-cell recognition of HLA presented peptides. Therefore, recurrence of autoimmune
diseases may be potentiated as well. Further knowledge regarding specific disease states
worsened by certain HLA matches may be useful in selective typing in the future.
Crossmatch and ABO Matching. The lymphocytotoxic crossmatch is not used
prospectively before liver transplantation. Again, temporal concerns are most pressing; but in
this case, the value of a positive crossmatch in predicting subsequent poor outcome from
hyperacute rejection is minimal. Indeed, hyperacute rejection is rarely seen even in the face of
documented preformed antibodies and ABO incompatibility.The reasons for this remain
controversial because hyperacute rejection can be readily produced experimentally. Although
preformed antibodies reduce long-term graft survival somewhat, early results appear to be
minimally affected. Grafts unmatched for ABO antigens can cause antibody-mediated graft-
versus-host disease with mild hemolytic anemia and fever occurring between postoperative days
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5 and 12. This is the result of intrahepatic B cells that secrete antibody directed against the
recipient ABO antigens. Although it is usually self-limited, increased immunosuppression may
be required. Alternatively, some groups suggest a decrease in immunosuppression to allow for a
limited rejection of the offending B cells. It is preferred that rules for ABO compatibility be
followed for elective transplantation. In the emergent setting, however, ABO-incompatible
grafts can be used with acceptable results. The 5-year survival for grafts that are ABO
incompatible is approximately 15% lower than that for grafts without ABO discrepancy. This
not only reflects some immune preference but also the patient population that receives ABO
mismatched grafts, that is, emergent transplants for FHF and PNF.
Acute Rejection. As with other allografts, T-cellmediated destruction of the liver is
inevitable without immunosuppressive therapy. The primary targets for T-cell recognition are
HLA antigens on the biliary epithelium and vascular endothelium. The characteristics of this
rejection, termed acute rejection, are similar to those of kidney or heart in that it develops in
most of the cases during the first 6 months after transplantation, usually within the first 4
postoperative weeks. More than half of patients develop at least one episode of rejection.
Symptoms are nonspecific, often including mild intermittent fever and general malaise with
alteration in liver tests. The diagnosis should be confirmed by liver biopsy. Most episodes are
readily reversible (90%), given prompt recognition and initiation of antirejection therapy. This
contrasts sharply to chronic rejection, discussed later.
Monitoring for acute rejection is a continuous process. Needle-core biopsy of the allograft
is the best diagnostic test. Histologically it appears as a predominantly T-cell and monocyte
infiltrate in the portal tracts, with subendothelial (endotheliitis) and biliary epithelial
aggregates. Eosinophils and polymorphonuclear leukocytes are present to a lesser degree but
are more prevalent in hepatic rejection than in infiltrate seen in other organs. Although
protocol biopsies are performed in some centers, most groups rely on monitoring of the liver
function studies and/or the serum beta2-microglobulin value, with biopsy used to clarify
detected abnormalities. Because a primary target in acute rejection is biliary epithelium, it
often presents initially as a cholestatic process with rapid increases in the alkaline phosphatase
and bilirubin values. However, changes in hepatic biochemical parameters are nonspecific and
can also indicate technical or infectious complications where alterations in the
immunosuppressive regimen would be ineffective or even detrimental. Thus, liberal use of
biopsy and Doppler ultrasound evaluation of hepatic blood flow and bile duct integrity is
critical. Once acute rejection is diagnosed, rescue immunosuppression is initiated as described
later.
Chronic Rejection. The development of liver allograft dysfunction over a period of months
to years is termed chronic rejection and, like other allografts, is controversial and multifactorial
in its etiology, and is usually not reversible. Histologically it appears as a paucity of bile duct
epithelium without conspicuous lymphocytic infiltration and has thus been described as the
vanishing bile duct syndrome. Additionally, an obliterative vasculopathy can occur with
parenchymal fibrosis. The time course, histology, and refractory nature of chronic rejection
suggest that direct cell-mediated destruction is not a primary mechanism. It is likely that the
cumulative effects of mild subclinical immune recognition by several limbs of the immune
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system, and the resulting exposure to soluble factors including fibrogenic cytokines, eventually
take their toll on the fragile epithelium. Chronic rejection often requires retransplantation.
Immunosuppressive Pharmacology. Manipulation of the immune system is required to
avoid graft loss from rejection. Identifying a safe, effective, and minimally immunosuppressive
regimen requires a careful balance aimed at reducing infectious and neoplastic complications
without a resultant increase in allograft rejection and/or dysfunction. Thus, rational, selective
use of several immunosuppressive agents is required to manage successfully the broad array of
patients who are transplanted. Three general classifications of immunosuppression are used:
(1) induction therapy, a relatively intense initial conditioning of the newly transplanted
recipient; (2) maintenance therapy, drugs given at minimal doses required to maintain graft
function; and (3) rescue therapy, heightened immunosuppression given to reverse an episode of
acute rejection. Most transplant centers have specific protocols for each situation.
Several issues specific to liver transplantation should be mentioned. Of major importance is
that the liver appears to have less immunostimulatory antigenicity than other organs. The
specifics of this perceived resistance remain somewhat controversial but may relate to several
peculiarities of hepatic physiology. First, the portal circulation is exposed regularly to enteric
pathogens and, more importantly, to absorbed peptides, which have potential antigenicity. A
generalized perihepatic anergy has been postulated as protective in this setting to prevent
vascular thrombosis and inappropriate hepatic inflammation. Clearly the reticuloendothelial
system of the liverthe Kupffer cellsis important in establishing appropriate versus
inappropriate presentation of portal antigen. Most of the Kupffer cells of the liver are replaced
with those of recipient HLA type within a few weeks after transplantation. In addition, the
Kupffer cells of the donor have been described as migrating to other recipient tissues and
establishing a state of chimerism. Whether this chimerism creates specific tolerance or is the
result of it remains to be seen. From a practical standpoint, maintenance immunosuppression
after liver transplantation can be comparatively low, and many patients have been weaned to
little or no immunosuppression for years. Also of importance in this regard, the liver can
tolerate brief periods on immunosuppression withdrawal if it becomes necessary to combat a
potentially lethal infection.
A recent issue of particular importance in liver transplant immunosuppressive pharmacology
has been the development of the drug tacrolimus (FK 506). This agent has been suggested as
having particular efficacy in the setting of liver transplantation, with truly remarkable results in
early, uncontrolled trials performed at the University of Pittsburgh.48 Tacrolimus has a
mechanism of action similar to that of cyclosporin A and it has been used as a replacement for
this drug. A possible benefit is the potential steroid-sparing effect of tacrolimus, exceeding that
of cyclosporine. Single-drug maintenance therapy is being actively investigated. Multicenter,
randomized, prospective trials comparing cyclosporine to tacrolimus are underway, with the
initial 1-year follow-up demonstrating a significant reduction in rejection episodes and a lower
need for rescue therapy with OKT3 in the tacrolimus group.No graft or patient survival
advantage has been demonstrated. The side effect profile for tacrolimus differs from that of
cyclosporine in that the cosmetic complications of hirsutism, acne, and gingival hyperplasia are
not present but the potential for neurologic abnormalities, diabetes mellitus, and renal
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a fundamental priority in our society. Outcomes can be defined either from a physician's,
patient's, payer's, or society's perspective. The medical perspective is in the traditional purview
of the clinician and clinician investigator, who use objective and quantifiable medical
parameters, whereas the patient's perspective involves a more subjective assessment of quality
of life. Today, survival has become the norm after OLT, and thus the next decade should clearly
define outcome with regard to each of these perspectives.
Medical Perspective. Despite the recent advances in all aspects of liver transplantation, the
procedure remains one with considerable morbidity. Most patients have some complications
that deviate from an ideal recovery, and all patients accept the trade of their liver disease for the
disease of immunosuppression. These negative outcomes are generally remedied by prompt
recognition of problems and aggressive corrective intervention. It is, therefore, critical that the
potential obstacles arising postoperatively are thoroughly understood. The authors have
recently categorized negative outcomes under three headings: negative sequel, complications,
and failure to cure.
A negative sequel is an adverse effect inherent to the transplant procedure. Transplantation
in general carries with it the risk of lifelong immunosuppression. Patients must adapt their
lifestyle to ensure that medications are taken as prescribed and that the immune system and
organ function are monitored when necessary. The risk of opportunistic infection and
malignancy that accompanies chronic immunosuppression persists for life. These factors,
however, are less intrusive for liver transplant patients than for recipients of other solid organs
because of their reduced need for immunosuppression, especially after the first transplant year.
Failure to cure refers to pre-existing conditions that remain unchanged or recur after the
transplant procedure. The likelihood of cure reflects the primary disease. Metabolic and
cholestatic diseases are generally resolved, as are the physiologic disorders of alcoholic
cirrhosis. Unfortunately, viral infections remain generally uncured by liver replacement. As
mentioned earlier, clinically significant recurrence of hepatitis B and hepatitis C may limit
long-term cure. The cure for these illnesses remains in more potent antiviral therapeutics.
Practically, however, viral reinfection that creates a clinically insignificant carrier state is
viewed as a cure by the patient. Obviously, no extrahepatic malignancy can be cured by OLT,
and the potential for cure in patients with intrahepatic malignancy is solely related to the
presence or absence of metastatic disease at the time of recipient hepatectomy.
A complication is any other negative outcome that does not fit clearly into the definition of
negative sequel or failure to cure. Complications of some kind occur in almost all patients, but
the significance of these setbacks varies greatly. For example, acute rejection must be
considered a complication of sorts, but most episodes are treated without significant alteration
of a patient's comfort or residual disability. Conversely, PNF at best leads to retransplantation
and at worst to death. The lack of uniform reporting of complications makes interpretation of
the results of OLT difficult. The authors have presented a classification of complications
stratified by severity. With the heightened requirement for outcomes-based research in the
current economic environment, standardized evaluation of transplant programs with regard to
complication rates will likely increase.
Several common complications, such as acute and chronic rejection, have been discussed.
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Some complications deserve particular attention because of their seriousness and requirement
for prompt intervention. PNF presents as a complete lack of synthetic function from the time of
reperfusion. The patient develops encephalopathy, increased intracranial pressure,
coagulopathy, hyperbilirubinemia, and hypertransaminasemia. Aggressive supportive therapy
and prompt retransplantation are required within 72 hours. Total transplant hepatectomy with
portacaval shunt can improve the hemodynamic and metabolic status of the patient for 24 to 36
hours if a suitable liver is not found immediately.
Hepatic artery thrombosis remains a complication, especially in the pediatric population.
This presents as a rapid rise in serum transaminase levels. The transplanted liver does not
tolerate loss of arterial flow, and failure to restore flow produces graft loss. Hepatic artery
stricture or stenosis generally presents as a lesser degree of metabolic change later in the
postoperative course. An alternative presentation of dearterialization is bile leak resulting from
hepatic duct necrosis. An additional vascular complication that is less frequent but equally
devastating is early portal vein thrombosis. Given the rapid and serious but reversible nature of
these vascular complications, any suspect change in hepatic function requires immediate
evaluation of the hepatic vasculature by Doppler ultrasonography, followed by either
re-exploration or a confirmatory arteriogram.
Biliary complications, which occur in 15% to 30% of patients, suggest vascular
compromise. Both leaks and strictures can occur regardless of the method of reconstruction.
Percutaneous or endoscopic management is generally considered an acceptable first alternative,
but reoperation should not be avoided for appropriate lesions at the expense of hepatic
function or cholangitis.
Patient Perspective. Today, increasing emphasis is given to patient-oriented subjective
outcomes such as quality of life and well-being. Subjective outcomes have inherent limitations,
but they are arguably more relevant to individual patients. Well-being represents a composite of
several different aspects, including mental, physical, and social criteria.
Due to the initial formidable technical issues of OLT, analyses of quality of life have been
almost absent from the literature. With improved results these past few years, researchers in
numerous centers are evaluating the effects of OLT on quality of life. Successful
transplantation allows a return to an active lifestyle free from the metabolic and hematologic
complications of hepatic failure or portal hypertension. Preliminary studies have already shown
that self-image, functioning ability, and perception of health status are significantly improved
after OLT. Currently, about 60% of patients undergoing OLT return to work within the first
year,4 a figure that continues to increase long term.
Payer's Perspective. Once therapy has been shown to be effective, it is necessary to
determine whether the treatment is cost-effective in order to compare it with other competing
technologies. Analysis of cost-effectiveness is difficult to apply to liver transplantation because
there is no alternative therapy with which the results of the procedure can be compared. Thus,
the cost issue becomes one of establishing a monetary value for one's life. There is no doubt
that OLT is expensive. The total first-year expenses for a new liver average $200,000, with an
additional $10,000 to $20,000 per year required thereafter. Cost for patients in the intensive
care unit at the time of transplant are 3 to 5 times higher than those called in from home for the
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procedure. With current health care reform underway, these amounts are falling somewhat. In
addition, consolidation of transplant centers in the United States is likely to improve efficiency
and reduce costs. As new immunosuppressive agents are introduced, competition is also likely
to drive the cost down. Nonetheless, the extent to which physicians should go to return
patients to health and to work is a matter of great societal debate. As with all other aspects of
liver transplantation, rational selection of patients is the most important factor affecting cost.
EMERGING TECHNIQUES
Split and Reduced-Size Transplantation. The remarkable ability of the liver to regenerate
and support the metabolic needs of an individual despite major resection has allowed for
correction of most conditions with partial hepatic transplantation.10 This is useful for major
size mismatches, especially in children, and can also help address the growing donor organ
shortage. Anatomic division of the lobes of the liver with preservation of hepatic venous and
arterial, portal, and biliary branches has become increasingly successful but remains technically
formidable. The anatomic boundaries are based on the segmental anatomic system of Couinaud
and Bismuth.17 Left lateral segments 2 and 3 or left lobe grafts (segments 2, 3, and 4) can be
placed in recipients who are substantially smaller than the donor. Because of the anterior to
posterior dimensions of the right lobe (segments 5 through 8), placement of this graft requires a
recipient similar in size to the donor.
Several major centers have initiated protocols for split and reduced-size transplantation with
excellent results. Predictably, biliary complications are increased in this procedure, but in
children the problem of hepatic artery thrombosis is improved, owing to the comparatively
large vasculature present in the graft when an adult liver is reduced for use in a child. Patient
survival is as good as or better than full-size grafts in children. Use of reduced-size grafts has
decreased the mortality of pediatric recipients on the waiting list to approximately 3%.
Living-Related Transplantation. Arising from the success of reduced-size grafting, living-
related transplantation has been initiated at selected centers.This involves a reduced-size graft
usually derived from a donor left lobe (segments 2 and 3 or 2, 3, and 4). Technically, this has
been quite successful and has the benefits of reduced ischemic time, better HLA match, and
better timing of transplantation, producing excellent graft survival. Because most of the
transplants are performed for congenital anomalies, the negative aspects of HLA typing have
not been problematic. The most pressing concern with this procedure is ethics. Although
hepatic resection is generally safe, the mortality is not zero. One donor perioperative death has
been reported, and many argue that with the success of reduced-size cadaveric allografts, a
procedure that places a healthy parent at risk is not necessary. The concept of informed consent
is difficult to establish because most parents disregard personal safety when the life of their
child is at risk. One consensus hearing on the matter has approved this procedure, with the
caveat that only centers with established success in reduced cadaveric grafts, pediatric
transplantation, and adult hepatic surgery be involved.
Heterotopic Liver Transplantation. Placement of an allograft in an anatomically altered
site has the advantages of avoiding the recipient hepatectomy (often the most morbid portion of
the procedure) and preserving the orthotopic position for future use in the event of graft
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ALTERNATIVE THERAPIES
The development of artificial support devices has revolutionized perioperative management
in all areas of transplantation except hepatic. Renal dialysis, ventricular assist and intra-aortic
counterpulsation devices, total parenteral nutrition, and insulin have all helped optimize the
condition of solid organ recipients to some degree, making emergent transplantation unusual
for any organ other than the liver. The importance of preoperative condition is clear from the
survival statistics presented in this chapter. Thus, great effort has been directed toward finding
adequate hepatic replacement.
Xenogeneic Support. Xenotransplantation, the use of organs from other species, has many
theoretical advantages. A renewable supply of organs subject to genetic manipulation available
on an elective basis would greatly alter the course of patients with liver failure. In addition, the
hepatotrophic viruses responsible for most hepatitis are generally specific for human
hepatocytes, so the specter of reinfection would be abolished. Unfortunately, the immune
barriers to transspecies transplantation remain formidable. Organs from discordant species,
those phylogenetically distant animals to which preformed natural antibodies exist, are
hyperacutely rejected. Organs from these animals also produce plasma proteins that are similar
but not identical to their human homologues, thus raising the possibility of antigenic proteins
subject to immune clearance. Concordant species, namely primates, are rejected in a more
conventionally acute manner, but antibody-mediated rejection occurs. Although the immune
barrier is less daunting, primates are slow-breeding animals that could quickly become extinct
if widespread use were initiated. Of additional concern is the potential for introducing new
viruses from primates to man.
Several efforts in xenogeneic organ use have been made in the past 5 years. Baboon livers
were used to treat two patients with hepatitis B at the University of Pittsburgh. Both livers
functioned well enough to carry out the major physiologic functions of the liver. Interpretation
of the immune implications of these procedures, however, is difficult because one patient was
infected with the human immunodeficiency virus with an inverted T4:T8 ratio pretransplant and
the other received a concurrent baboon bone marrow transplant. An orthotopic pig liver
transplant performed at Cedars Sinai Hospital in Los Angeles was hyperacutely rejected (L.
Makowka, personal communication, 1994).
Ex vivo perfusion with porcine livers has been successfully employed as a bridge to
orthotopic allotransplantation by the authors' group. Biochemical improvement in all measured
parameters, including reversal of cerebral edema and reduction of coma, has been demonstrated
by the authors' group and others. This approach has the advantage of being reversible without
requiring a surgical procedure. It is, however, logistically difficult and temporary.
Bioartificial Liver. The ability of porcine hepatocytes to perform many of the functions of
human hepatocytes has been exploited by several investigators by development of an ex vivo
apparatus for hepatic support consisting of porcine hepatocytes attached to a hollow-fiber
dialysis cassette. Early clinical trials have shown promise in reducing cerebral edema as well as
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SUMMARY
Liver transplantation has evolved in the past decade from an experimental procedure to an
accepted, effective therapy for end-stage diseases of the liver. Extended survival of over 75% in
appropriately selected patients is now commonplace with return to an excellent quality of life.
Continued improvements in perioperative management and operative technique are being
realized. The most important predictors of success are the state of the patient at the time of
transplantation and the disease being transplanted. Early intervention once end-stage disease is
diagnosed is preferable. A critical shortage of suitable donor organs remains the single most
important barrier to transplantation
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Pathomorphology
Classification
(by O.O. Shalimov)
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As passing of disease has cyclic character with the periodic changes of remission and
acuteening, the clinic of chronic pancreatitis depends on the phase of development of
inflammatory process. Violation of excretory and incretory functions of pancreas influences
polymorphic of symptoms which remission is especially determining in the phase.
Pain, dyspepsia phenomena and progressive loss of weight of body are the basic signs of
chronic pancreatitis. Besides, pain, is permanent, changes only its intensity, mainly in
epigastric region, sometimes on the left, burning, squeezing or prickly, comes forward the
unique symptom of disease, complaints about it precede other symptoms. In some patients the
pain feelings increase in lying position. Therefore patients occupy forced sitting position.
Intensity of pain can change throughout a day. Patients explain it by acceptance of rich, fried
food, boiled eggs, coffee. The last is the principal reason of acutening of process with acute
pain syndrome.
It is needed to mark, that occasionally passing of chronic pancreatitis can take hidden,
smooth shapes, with the moderately expressed pain syndrome or pain, that has atipical
character, for example, stenocardia. In such patients the symptoms related to violations of
exogenous function of pancreas come forward. They complain about absence of appetite,
nausea, belch, sometimes vomiting and diarrhea with putrid smell. Thirst, general weakness and
progressive loss of weight is observed also.
At palpation of abdomen pain does not arise, or it is quite insignificant. It is sometimes
succeeded to palpate horizontally placed pancreas as dense, moderately painful tension bar.
The transmission of pulsation of aorta at palpation in a epigastric area count characteristic for
pathology.
During intervals between the attacks the feeling of patients remains satisfactory.
Development of saccharine diabetes is the basic sign of endocrine insufficiency,
hypoglycemia is rarer. The feature of this form of saccharine diabetes consists in the fact that it
shows up in a few years after the beginning of disease, runs easier and often carries latent
character. There can be hypoglycemia at the insufficient products of glucagon.
The syndrome of biliary hypertension with development of mechanical icterus and
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cholangitis determining it can develop in some patients. The reasons for such cholestasis more
frequently are tubular stenosis of choledochus, choledocholithiasis or stenotic papillitis. There
is duodenal obstruction in some cases.
Important information about it can be given by the laboratory and instrumental methods of
examination.
Examination of excretory function of pancreas is based on establishment of level of
amylase in the whey of blood and urine. In acutening period of chronic pancreatitis this level of
amylase rises, the numbers of tripsin and lipase grow.
Coprologic examination. Macroscopic picture of excrement gets greyish color, in large
masses with unpleasant smell. Steatorrhea (increase of amount of neutral fat) and
creatorrhea are characteristic for it (a plenty of muscular fibres).
Examination of incretory function of pancreas includes: 1) determination of sugar in blood
and urine (characteristic is hyperglycemia and glycosuria);
2) radioimmunoassay of hormones (insulin, -peptide and glucagon).
Sciagraphy survey of organs of abdominal cavity in two projections enables to expose
existent concrement in ducts and calcificat in parenchyma of pancreas.
Relaxation duodenography. Thus the development of horseshoe of duodenum and
change of relief of its mucus can be seen.
Cholecystocholangiography with the purpose of diagnostics of gallstone disease and
second damaging of bilious ways is conducted.
Ultrasonic examination (sonography) is one of the basic methods of diagnostics. With the
help of symptoms of chronic pancreatitis it is possible to expose inequality of contours of
gland, increase of closeness of its parenchyma, increase or diminishment of sizes of organ,
expansion of pancreatic duct and wirsungolithiasis or presence of concrement of parenchyma.
Thus it is necessary to inspect gall-bladder, liver and bile-excreting ways for diagnostics of
gallstone disease and choledocholithiasis.
Scintigraphy of pancreas. On early stages strengthening of scintigraphic picture is
observed, on later ones defects of accumulation to radionuclide (symptom of sieve or bee
honeycomb).
Computer tomography allows to expose the increase or diminishment of sizes of gland,
presence of calcificats, concrement, inequality of contours of organ, focuses or diffuse changes
of its structure .
Endoscopic retrograde cholangiopancreatography (ERCPG). Expansion of pancreatic duct
its deformation, wirsungolithiasis is marked.
It is expedient to apply laparoscopy in the phase of acutening of chronic pancreatitis at
development of fatty and hemorrhagic pancreatonecrosis (stearin name-plates, exudation).
The puncture biopsy of pancreas under sonography control can have an important value for
differential diagnostics of pancreatitis and cancer.
Percutaneous transhepatic cholangioduodenography and -stomy. This method is used both
for differential diagnostics of pseudo tumor-like form of chronic pancreatitis and cancer of
pancreas and with the purpose of preoperative preparation at presence of icterus. During it
there is a possibility to expose expansion of intra- and out-of-hepatic ducts, localization and
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Chronic recurrent pancreatitis. The changes of periods of acuteening and remission are
characteristic for it. The first period shows up by the attacks of pain of different frequency and
duration, and during remission patients feel satisfactory.
Chronic pain pancreatitis. Intensive pain in the overhead half of abdomen with an
irradiation in loin and region of heart is inherent for this form. Also belting pain often appears.
Chronic painless (latent) pancreatitis. In patients with this form of pathology for a long
time the pain is either absent in general or arises after the reception of spicy food rich and can
be insignificantly expressed. Violation of excretory or incretory function of pancreas come
forward on the first plan.
Chronic pseudo tumor-like pancreatitis. Dull pain in the projection of head of pancreas,
dyspepsia disorders and syndrome of biliary hypertension are clinical its signs.
Chronic cholangiogenic pancreatitis. Both clinic of chronic cholecystitis and
cholelithiasis and clinic of pancreatitis are characteristic for this form.
Chronic indurative pancreatitis. In patients with this diseases symptoms of excretory and
incretory insufficiency of pancreas are present. The low indexes of amylase in blood and urine
are characteristic. At the expressed sclerosis of head of pancreas the with including process of
general bilious duct, development of mechanical icterus is possible.
Among complications of chronic pancreatitis, fatty dystrophy and cirrhosis of liver,
stricture of terminal part of general bilious duct, ulcers of duodenum, thrombosis of splenic
vein, saccharine diabetes, pseudocysts of pancreas, exudation pleurisy and pericarditis and
heart attack of myocardium are observed.
Diagnosis program
Differential diagnostics
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Disease of gall-bladder and bilious ways (gallstone disease, dyskinesia of bilious ways).
For these diseases pain in right hypochondrium is inherent, that irradiates in right
shoulder-blade and shoulder. At chronic pancreatitis pain is localized in epigastric area, left
hypochondrium, often is of belting character. One of the basic additional methods of
inspection for confirmation of diseases of gall-bladder and ducts is sonography.
Ulcerous disease of stomach and duodenum. Pain at ulcerous disease is seasonal
(relapses more frequent in spring and autumn), unites with heartburn and has tendency to
diminishment after vomiting. In patients with chronic pancreatitis pain arises after faults in a
diet, often is of belting character. Frequent vomiting is determining, that does not bring
facilitation to the patient. Also violations of excretory and incretory functions of pancreas can
take place.
Abdominal ischemic syndrome. Patients with this pathology complain about pain, that
arises at once after the reception of meal, somewhat diminishes after application of
spasmolytics. For the disease considerable weight loss and waiver of meal in connection with
dread of pain attack can be characteristic. The basic method of examination, with a necessity
for differential diagnostics, celiacography is useful, which enables to expose oclusion of
abdominal trunk or its compression. During conducting of differential diagnostics with two last
nosologies it is necessary to state a possibility of origin of secondary pancreatitis.
Cancer of pancreas. Mechanical icterus and presence of Courvoisier's symptom are
considered the clearest and most important displays of cancer of head of pancreas, and
carcinoma of body and tail is a proof pain syndrome. For the cancer the damage of pancreas,
rapid progress of symptomatology are characteristic, and for chronic pancreatitis the protracted
passing with proper clinical symptomatology and changes which can be exposed by the
laboratory, roentgenologic and instrumental methods of examination are characteristic. The
most informative among methods of diagnostics of cancer of pancreas are sonography (echo-
producing formations in parenchyma of pancreas), computer tomography (tumor knots) and
puncture biopsy of gland with the histological examination (reliable diagnostics of cancer).
Heart attack of myocardium. In anamnesis of patients with the heart attack of myocardium
it is possible to expose pain behind breastbone, that arises at the physical activity and
emotional stress, it is irradiated in left shoulder-blade and left shoulder, unrelated with the
reception of meal and disappears as a result of action of coronarolytics. The typical changes of
ECG confirm the diagnosis of heart attack of myocardium. In addition, no violations of
external and incretions of pancreas are characteristic. The roentgenologic and instrumental
methods of examination can help in differential diagnostics.
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Indication to operation and its volume depend on the form of pancreatitis. Acutening of
chronic cholangiogenic pancreatitis at presence of gallstone disease must be examined as
indication to operation in first 24 hours since diseases beginning. Operative treatment is done
in case of:
1) calcinosis pancreas with the expressed pain syndrome;
2) violation of patency of duct of pancreas;
3) presence of cyst or fistula of resistance to conservative therapy during 24 months;
4) mechanical icterus on soil of tubular stenosis of distal part of general bilious duct;
5) compression and thrombosis of portal vein;
6) gallstone disease complicated by chronic pancreatitis;
7) ulcerous disease of stomach and duodenum complicated by secondary pancreatitis;
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Cysts of pancreas
Cyst of pancreas is a cavity, filled by liquid (pancreatic juice, exudation, pus), intimately
soldered with head, body or tail of organ, is limited by capsule, which has epithelium on
internal surface.
Pseudocyst (unreal cyst) is a cavity in pancreas which appears as a result of its destruction,
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Pathomorphology
Morphologically the cysts of pancreas are divided into: pseudocysts retention to the duct
are innate, single and multiple.
Pseudocysts are fresh and old. The internal surface of fresh pseudocyst is rough,
granulating, grey-red. The table of contents is alkaline, grey or with a brown tint. In an old
pseudocyst the wall is smooth and shiny, pale-grey. The table of contents is lighter. Epithelium
pseudocysts is absent. More frequently they are met in body and tail of gland and are not
connected with ducts.
Retention cysts connected with an obturated duct. The cavity has smooth, grey-white
surface, maintenance is transparent, watery or mucous-like. Innate cysts are mainly multiple
and shallow. A simple retention cyst differ from those that are always connected with the
anomalies of development of ducts and are unite with polycystosis buds and liver.
Rarely there are echinococcus cysts, which have a clear chitinous shell, liquid in cavity
and daughter's blisters. They are localized in the area of head of pancreas.
Classification
(by A.N. Bakulev and V.V. Vinogradov, 1952)
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3. Innate adenomas.
4. Fibrocystic degeneration.
5. Polycystic degeneration.
II. Inflammatory cysts:
1. Pseudocysts.
2. Retention cysts.
III. Traumatic cysts:
1. As a result of direct damage of gland.
2. As a result of indirect damage of gland.
IV. Parasite cysts:
1. Echinococcosis glands.
2. Cysticercosis glands.
V. Neoplasty cysts:
1. Cyst-adenoma.
2. Cyst-adenocarcinoma.
3. Cavernous hemangioma.
4. Cystic epithelioma.
Pathomorphology cysts are divided on:
1. The true cyst.
2. Pseudocysts.
According to clinical passing pseudocysts are divided into acute, subacute and chronic.
According to weight of passing into simple (uncomplicated) and complicated.
In patients with the cystic damaging of pancreas there can be pain of different character
and intensity (dull, permanent, cramp-like and belting). It is localized more frequently in right
hypochondrium, epigastric area (cyst of head and body of gland), left hypochondrium (cyst of
tail of pancreas). Pain is irradiated in the back, left shoulder-blade, shoulder and spine.
Dyspepsia violations are characteristic. Nausea, vomiting and belch are observed.
The syndrome of functional insufficiency of pancreas shows up by disorders of exocrine
and endocrine insufficiency and depends on the degree of damage of organ. The unsteady
emptying, replacement of diarrhea of constipation, steatorrhea and creatorrhea, development of
the second diabetes are marked.
Compression syndrome. Arises as a result of compression of neighbouring organs.
Clinically the compression of organs of gastro-intestinal highway shows up by complete or
partial obstruction of general bilious duct (mechanical icterus), vein (portal hypertension) gate,
splenic vein (splenomegaly).
During the examination patients with large cysts are marked by asymmetry of abdomen in
epigastric and mesogastric areas. At palpation of abdomen tumular formation of elastic
consistency with an even, immobile surface is found.
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Diagnosis program
1. Anamnesis.
2. Biochemical blood test (amylase, sugar, bilirubin).
3. Analysis of urine on diastase.
4. Coprograma.
5. Sonography.
6. Contrasting sciagraphy of stomach and duodenum (relaxation duodenography).
7. Retrograde pancreatocholangiography.
8. Computer tomography.
Differential diagnostics
The cysts of pancreas are differentiated with the tumors of abdominal cavity and of
retroperitoneal space.
Cancer of pancreas. For the cancer tumor of pancreas syndrome of small signs
(discomfort in epigastric area, loss of appetite, general weakness), permanent dull pain,
unrelated with the reception and composition of meal, icterus (cancer of head of gland),
Courvoisier's symptom (increased, unpainfully gall-bladder) are characteristic. Inconstant pain
at cysts of pancreas is more frequently related to faults in a diet; in anamnesis destructive
pancreatitis, traumas of gland are carried. Sonography examination, retrograde
pancreatocholangiography and computer tomography help in establishment of diagnosis.
Tumors of retroperitoneal space are passed asymptomatic, clinic shows up by a
considerable compression on neighbouring organs. Nausea, vomit, chronic intestinal
obstruction, dysuric disorders arise. Clinic of cysts of pancreas, on the opposite, are expressed
on early stages. Pain, dyspepsia syndromes, syndrome of exocrine and endocrine insufficiency
of pancreas are characteristic. Pain is related to the reception of meal and alcohol.
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Aneurism of abdominal aorta. Dull, indefinite pain in abdomen which is unrelated with
the reception of meal, pulsation and pulsating formation in abdomen are characteristic,
auscultatory is systolic murmur. Aortography allows to confirm a diagnosis.
The cyst of mesentery of thin bowel has painless passing, at palpation it is mobile, easily
changes position in abdomen. The cysts of pancreas are practically immobile, pain, anamnesis
and laboratory information are characteristic.
The cyst of liver has protracted asymptomatic passing. Pain appears at infection of cyst.
For this pathology symptoms which take place at the cysts of pancreas are not typical (pain
related to the reception of rich food, alcohol, hyperamylasemia). Topic diagnostics is carried
out at ultrasonic examination, scintigraphy, computer tomography.
Differential diagnostics and clinical variants
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unique symptom of disease, complaints about it precede other symptoms. In some patients the
pain feelings increase in lying position. Therefore patients occupy forced sitting position.
Intensity of pain can change throughout a day. Patients explain it by acceptance of rich, fried
food, boiled eggs, coffee. The last is the principal reason of acutening of process with acute
pain syndrome.
It is needed to mark, that occasionally passing of chronic pancreatitis can take hidden,
smooth shapes, with the moderately expressed pain syndrome or pain, that has atipical
character, for example, stenocardia. In such patients the symptoms related to violations of
exogenous function of pancreas come forward. They complain about absence of appetite,
nausea, belch, sometimes vomiting and diarrhea with putrid smell. Thirst, general weakness and
progressive loss of weight is observed also.
At palpation of abdomen pain does not arise, or it is quite insignificant. It is sometimes
succeeded to palpate horizontally placed pancreas as dense, moderately painful tension bar.
The transmission of pulsation of aorta at palpation in a epigastric area count characteristic for
pathology.
During intervals between the attacks the feeling of patients remains satisfactory.
Development of saccharine diabetes is the basic sign of endocrine insufficiency,
hypoglycemia is rarer. The feature of this form of saccharine diabetes consists in the fact that it
shows up in a few years after the beginning of disease, runs easier and often carries latent
character. There can be hypoglycemia at the insufficient products of glucagon.
The syndrome of biliary hypertension with development of mechanical icterus and
cholangitis determining it can develop in some patients. The reasons for such cholestasis more
frequently are tubular stenosis of choledochus, choledocholithiasis or stenotic papillitis. There
is duodenal obstruction in some cases.
Important information about it can be given by the laboratory and instrumental methods of
examination.
Examination of excretory function of pancreas is based on establishment of level of
amylase in the whey of blood and urine. In acutening period of chronic pancreatitis this level of
amylase rises, the numbers of tripsin and lipase grow.
Coprologic examination. Macroscopic picture of excrement gets greyish color, in large
masses with unpleasant smell. Steatorrhea (increase of amount of neutral fat) and
creatorrhea are characteristic for it (a plenty of muscular fibres).
Examination of incretory function of pancreas includes: 1) determination of sugar in blood
and urine (characteristic is hyperglycemia and glycosuria); 2) radioimmunoassay of hormones
(insulin, -peptide and glucagon).
Sciagraphy survey of organs of abdominal cavity in two projections enables to expose
existent concrement in ducts and calcificat in parenchyma of pancreas.
Relaxation duodenography. Thus the development of horseshoe of duodenum and
change of relief of its mucus can be seen (Pic. 3.5.4).
Cholecystocholangiography with the purpose of diagnostics of gallstone disease and
second damaging of bilious ways is conducted.
Ultrasonic examination (sonography) is one of the basic methods of diagnostics. With the
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choledochoduodenostomy).
Papillosphincterotomy: a) execute transduodenal with papillosphincteroplasty; b)
endoscopic is recommended at the isolated or connected with choledocholithiasis stenosis of
large duodenal papilla, fixed concrement of large papilla of duodenum.
Wirsungoplasty is scission of plastic arts of narrow part or distal part of main pancreatic
duct (apply at patients with stricture of proximal part of duct by a slowness no more than 2
cm). Lately at the isolated stenosis of bee-entrance of main pancreatic duct endoscopic
wirsungotomy is executed.
Pancreatojejunostomy: a) longitudinal (it is executed at considerable expansion of
pancreatic duct); ) caudal (by Duval) with the resection of distal part of pancreas (Pic. 3.5.9).
Resection of pancreas: a) distal or caudal; b) distal subtotal; c) pancreatoduodenal (PDR);
e) total duodenopancreatectomy heads or bodies of gland (execute in case of fibrous-
degenerative pancreatitis).
Oklusion of ducts of pancreas by polymeric connections (cianocrylat, prolamine, neopren
and others like that) results in atrophy of exocrine parenchyma, but keeps to the islet of tissue.
Operations on the nervous system are used in case of the pain forms of chronic indurative
pancreatitis, resistant to conservative therapy, in default of rough morphological changes of
parenchyma, stroma of gland and deformation of main pancreatic duct: a) left-side
splanchnicectomy; b) bilateral pectoral splanchnicectomy and sympathectomy; c)
postganglionic neurotomy of pancreas.
Cyst of pancreas is a cavity, filled by liquid (pancreatic juice, exudation, pus), intimately
soldered with head, body or tail of organ, is limited by capsule, which has epithelium on
internal surface.
Pseudocyst (unreal cyst) is a cavity in pancreas which appears as a result of its destruction,
limited by capsule, that does not have epithelium on internal surface.
The reasons of pseudocysts are destructive pancreatitis, traumas of pancreas, oklusion of
Wirsung's duct by parasite, concrement, tumors, innate anomalies of development.
To the real cysts belong: innate (dysontogenetic) cysts which are anomalic in development;
acquired retention cysts which develop as a result of difficult outflow of pancreatic juice,
cystadenoma and cystadenocarcinoma (by mechanism the origins belong more frequently to
proliferative, sometimes degenerative cysts).
The mechanism of development of pseudocysts consists in the focus necrosis of gland,
difficult normal outflow of its secret, there is a destruction of walls of pancreatic ducts with
overrun of pancreatic juice gland that causes reactive inflammation of peritoneum of
surrounding organs which form the walls of pseudocyst.
Morphologically the cysts of pancreas are divided into: pseudocysts retention to the duct
are innate, single and multiple.
Pseudocysts are fresh and old. The internal surface of fresh pseudocyst is rough,
granulating, grey-red. The table of contents is alkaline, grey or with a brown tint. In an old
pseudocyst the wall is smooth and shiny, pale-grey. The table of contents is lighter. Epithelium
pseudocysts is absent. More frequently they are met in body and tail of gland and are not
connected with ducts.
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Retention cysts connected with an obturated duct. The cavity has smooth, grey-white
surface, maintenance is transparent, watery or mucous-like. Innate cysts are mainly multiple
and shallow. A simple retention cyst differ from those that are always connected with the
anomalies of development of ducts and are unite with polycystosis buds and liver.
Rarely there are echinococcus cysts, which have a clear chitinous shell, liquid in cavity
and daughter's blisters. They are localized in the area of head of pancreas.
According to clinical passing pseudocysts are divided into acute, subacute and chronic.
According to weight of passing into simple (uncomplicated) and complicated.
In patients with the cystic damaging of pancreas there can be pain of different character
and intensity (dull, permanent, cramp-like and belting). It is localized more frequently in right
hypochondrium, epigastric area (cyst of head and body of gland), left hypochondrium (cyst of
tail of pancreas). Pain is irradiated in the back, left shoulder-blade, shoulder and spine.
Dyspepsia violations are characteristic. Nausea, vomiting and belch are observed.
The syndrome of functional insufficiency of pancreas shows up by disorders of exocrine
and endocrine insufficiency and depends on the degree of damage of organ. The unsteady
emptying, replacement of diarrhea of constipation, steatorrhea and creatorrhea, development of
the second diabetes are marked.
Compression syndrome. Arises as a result of compression of neighbouring organs.
Clinically the compression of organs of gastro-intestinal highway shows up by complete or
partial obstruction of general bilious duct (mechanical icterus), vein (portal hypertension) gate,
splenic vein (splenomegaly).
During the examination patients with large cysts are marked by asymmetry of abdomen in
epigastric and mesogastric areas. At palpation of abdomen tumular formation of elastic
consistency with an even, immobile surface is found.
Sonography examination shows echo-free formation with a clear capsule, determines
localization and sizes of cyst (Pic. 3.5.10).
Contrasting roentgenologic examination of stomach and duodenum with the sulfate of
barium at the cyst of head of pancreas exposes moving of pyloric part of stomach upwards and
breeding of ,,horseshoe duodenum (at relaxation duodenography in the conditions of low
artificial blood pressure). If a cyst is localized in the area of body of gland, displacement of
stomach is marked forward and upwards or downward, rapprochement of its walls, moving of
duodenal transition and loops of thin bowel downward and to the right; at lateral projection the
distance between stomach and spine is increased. The cyst localized in the area of tail of gland,
displaces the stomach forward and upwards, to the left or to the right (Pic. 3.5.11).
Cholecystocholangiography exposes calculous cholecystitis and cholelithiasis.
Retrograde pancreatocholangiography exposes the changed and deformed, infrequently
extended pancreatic duct, occasionally there can be filling of cavity of cyst by the contrasting
matter.
Computer tomography shows accumulation of liquid limited by the capsule of different
closeness and thickness (Pic. 3.5.12).
Laboratory examinations exposes hyperamylasemia, steatorrhea and creatorrhea,
sometimes hyperglycemia and glycosuria.
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Clinical passing of cysts of pancreas depends on their kind, localization, size, stage of
forming and complications.
Four stages of forming of pseudocyst are distinguished (.G. Karaguljan, 1972).
I stage (11,5 months last) in the center of inflammatory process the cavity of
disintegration, which takes surrounding tissue, appears in an omentum bag.
The II stage (23 months) is characterized by the beginning of forming of capsule of
pseudocyst. Cyst is magnificent, unformed, acute inflammatory phenomena calms down.
The III stage (312 months) is completion of forming of capsule of pseudocyst. Last
accretes with surrounding organs.
The IV stage (begins an in year from the origin of cyst) is a separated cyst. The cyst is
mobile, easily selected from connections with surrounding organs.
Retention cysts arise at closing of lumen of pancreatic duct (concrement, sclerosis). The
internal surface of cyst is covered with epithelium. Pain syndrome, violation of exocrine
function of gland are characteristic.
Traumatic cysts belong to the pseudocysts with similar passing and clinic, as well as
inflammatory pseudocysts.
Parasite cysts (to echinococcus, cysticercotic) are met as casuistry. In such patients Kaconi
test and serological Weinberg's reaction are positive.
The variants of clinical passing of the real and unreal cysts depend on their complications.
Perforation in free abdominal cavity. Clinic of the poured peritonitis is characteristic.
Tormina, positive symptoms of irritation of peritoneum, possible shock state as a result of
irritation of peritoneum by pancreatic juice arise.
Perforation in stomach, duodenum, small, rarer in large intestine is accompanied by
diminishment of cyst in sizes or complete disappearance, sometimes diarrhea appears.
Suppuration of maintenance of cyst is accompanied by pain which becomes more
intensive, temperature rises, leucocytosis grows.
The erosive bleeding appears suddenly and is accompanied by the symptoms of internal
bleeding (expressed general weakness, dizziness). The pallor of skin and mucus shells, sticky
death-damp, tachycardia and anemia are observed.
Mechanical icterus arises as a result of compression of cyst on the terminal part of
choledochus. The icterus of skin and mucus shells, acholic excrement, dark urine,
hyperbilirubinemia, increase of the AlT and AsT level are exposed.
Portal hypertension develops as a result of compression of portal vein. Ascites, varicose
expansion of veins of esophagus and stomach, moderate icterus are diagnosed.
Reactive exudation pleurisy more frequently arises in left pleura cavity, where
roentgenologic exudation is diagnosed with high maintenance of amylase.
At malignization the walls of cyst specific symptoms are absent, a diagnosis is set during
operation (surgical biopsy of cyst wall).
The cysts of pancreas are differentiated with the tumors of abdominal cavity and of
retroperitoneal space.
Cancer of pancreas. For the cancer tumor of pancreas syndrome of small signs
(discomfort in epigastric area, loss of appetite, general weakness), permanent dull pain,
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unrelated with the reception and composition of meal, icterus (cancer of head of gland),
Courvoisier's symptom (increased, unpainfully gall-bladder) are characteristic. Inconstant pain
at cysts of pancreas is more frequently related to faults in a diet; in anamnesis destructive
pancreatitis, traumas of gland are carried. Sonography examination, retrograde
pancreatocholangiography and computer tomography help in establishment of diagnosis.
Tumors of retroperitoneal space are passed asymptomatic, clinic shows up by a
considerable compression on neighbouring organs. Nausea, vomit, chronic intestinal
obstruction, dysuric disorders arise. Clinic of cysts of pancreas, on the opposite, are expressed
on early stages. Pain, dyspepsia syndromes, syndrome of exocrine and endocrine insufficiency
of pancreas are characteristic. Pain is related to the reception of meal and alcohol.
Aneurism of abdominal aorta. Dull, indefinite pain in abdomen which is unrelated with the
reception of meal, pulsation and pulsating formation in abdomen are characteristic,
auscultatory is systolic murmur. Aortography allows to confirm a diagnosis.
The cyst of mesentery of thin bowel has painless passing, at palpation it is mobile, easily
changes position in abdomen. The cysts of pancreas are practically immobile, pain, anamnesis
and laboratory information are characteristic.
The cyst of liver has protracted asymptomatic passing. Pain appears at infection of cyst.
For this pathology symptoms which take place at the cysts of pancreas are not typical (pain
related to the reception of rich food, alcohol, hyperamylasemia). Topic diagnostics is carried
out at ultrasonic examination, scintigraphy, computer tomography.
Conservative treatment. Treatment of acute or chronic pancreatitis is conducted in
accordance with principles. At the unfavorable dynamics of passing the diseases hunger with
the permanent sucking of gastric maintenance, parenteral feed and intravenous introduction of
liquids are appointed. Puncture of cysts is used through abdominal wall under sonography
control with aspiration of maintenance.
Surgical treatment is the method of choice of treatment of cysts of pancreas. The choice of
treatment method depends on the stage of forming of pancreas cysts.
On the I stage operation is not used, conservative treatment of pancreatitis is conducted.
On the II stage it is used at suppuration of pseudocyst (external draining of cyst). On the III
internal draining of cyst is used. More frequently cystojejunostomy on the eliminated loop of
thin bowel by Roux (Pic. 3.5.13), cystojejunostomy with entero-entero anastomosis by Brawn
and closing of afferent loop by Shalimov. Cystogastrostomy (Pic. 3.5.14) are executed and
cystoduodenostomy is now not applied because of possible complications (infection of cyst,
erosive bleeding). Marsupialization (opening and sewing down of cyst to the parietal
peritoneum and skin) is used infrequently (at suppuration of cyst is seriously patientsing with
the septic state). On the IV stage external and internal draining of cyst and radical operations
are applied: a) enucleation of cysts (executed very rarely); b) distal resection of pancreas with a
cyst.
The cancer of pancreas is a malignant tumor of epithelium tissue. Its specific gravity
among all malignant tumors makes 10 %. Greater part of patients with cancer of pancreas (to
80 %) is made by the persons of capable working age.
The origin of cancer of pancreas is related to character of nutrition: with the promoted
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unfolded horseshoe of duodenum, and in case of localization of tumor in the body of gland
displacement of back wall of stomach forward. At duodenoscopy rigidity of mucus shell of
descending part of duodenum, narrowing of its lumen are determined, and sometimes there is
germination of bowel by tumor.
Scanning is an informing method of examination with the use of 75 Se-methionine. Such
examinations can expose the hearths of reduced accumulation of isotope or its absence in
tissue of gland at the damage by tumor.
During laparoscopy the cancer of pancreas is visualized infrequently, however,
dissemination of peritoneum and its metastatic hearths in liver are diagnosed without
difficulties.
By ultrasonic (sonography) examination it is succeeded to expose the places of promoted
closeness of tissue of gland, sign of mechanical icterus at localization of tumor in the head.
Most informing among all is computer tomography (Pic. 3.5.15). It is possible to define
both the tumor of gland and its size and metastatic knots. The changes of main duct of pancreas
as segmental stenosis or breaking are fixed on retrograde endoscopic pancreatography.
Clinical passing of cancer of pancreas in 70 % patients is marked by the background
diseases and complications. This circumstance allows to select a few clinical forms of the
cancer of pancreas before appearance of icterus: pancreatitic, diabetogenic, cholangitic and
gastritis-like. The names specify the feature of clinical signs of different forms of disease.
Mechanical icterus is the heaviest complication of cancer of pancreas. With the increase of
duration and growth of its intensity development of such dangerous complications, as hepatic
or hepatic-kidney insufficiency, cholemic bleeding is possible.
Anamnesis has an important value for differential diagnostics. The presence of attacks of
pain or intermittent icterus testifies its calculous origin. A pain syndrome at the cancer of
pancreas does not have such acuteness and intensity, as at gallstone disease. Icterus in cancer
patients, unlike cholelithiasis, develops gradually, incessantly grows and is of proof character.
Often substantial difficulties arise during conducting the differential diagnostics of
obturative and infectious icterus. It is necessary to remember, that at viral hepatitis the level of
transaminase and aldolase in the whey of blood rises by 23 times. At obturation icterus their
level does not change substantially, and the increase of activity of alkaline phosphatase and
instead of that the level of cholesterol is marked.
However, most operation difficulties are met during conducting the differential diagnosis
of the cancer of pancreas and chronic indurative pancreatitis. In fact both processes during
examination and palpation produce similar pictures. In such cases puncture of the densest area
of pancreas is executed and cytologic examination is quickly conducted.
Treatment of cancer of pancreas is mainly surgical. The choice of method and volume of
operation depends on localization of tumor, stage of process, age of patient and his general
condition.
Taking it into account, as practice shows, radical operations in the moment of
establishment of final diagnosis are successfully executed only in 1520 % of patients.
Pancreatoduodenal resection is the method of choice of operation in patients with the damage
of head of pancreas. Operation foresees deleting one block of head of pancreas, distal part of
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stomach, duodenum and distal part of general bilious duct. Four anastomosis are thus imposed:
gastroenteroanastomosis, cholecystoenteroanastomosis or choledochoenteroanastomosis,
pancreatoenteroanastomosis and enteroenteroanastomosis. Sometimes this operation is
executed in two stages. On the first one biliary-enteric anastomosis is formed for taking bile
and improvement of function of liver, and the second stage is carried out in 34 weeks.
However, more frequently symptomatic operations are to be executed:
cholecystoenteroanastomosis or choledochoduodenoanastomosis. They are able to liquidate
icterus and prolong the life of patients for 59 months. In case of damage of body and tail of
pancreas the distal subtotal resection of gland with spleen is radical.
Chemotherapy can give partial remission. With this purpose 5-fluorouracil, adriablastine,
methotrexate are mainly used.
Some palliative effect also comes after gamma-ray telethepary.
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Fig.5
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ACUTE PANCREATITIS
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toward the center of the abdomen; the middle section is called the neck and the body of
the pancreas; the thin end is called the tail and extends to the left side. Several major
blood vessels surround the pancreas, the superior mesenteric artery, the superior
mesenteric vein, the portal vein and the celiac axis, supplying blood to the pancreas and
other abdominal organs.
Exocrine Function: The pancreas contains exocrine glands that
produceenzymes important to digestion. When food enters the stomach, these pancreatic
juices are released into a system of ducts that culminate in the mainpancreatic duct. The
pancreatic duct joins the common bile duct to form theampulla of Vater which is
located at the first portion of the small intestine, called the duodenum. The common bile
duct originates in the liver and thegallbladder and produces another important digestive
juice called bile. The pancreatic juices and bile that are released into the duodenum, help
the body to digest fats, carbohydrates, and proteins.
Endocrine Function: The endocrine component of the pancreas consists of islet
cells that create and release important hormones directly into the bloodstream. Two of
the main pancreatic hormones are insulin, which acts to lower blood sugar,
and glucagon, which acts to raise blood sugar. Maintaining proper blood sugar levels is
crucial to the functioning of key organs including the brain, liver, and kidneys.
Acute pancreatitis
The basis of disease of pancreas is degenerative-inflammatory processes which are
considered to be acute pancreatitis, the so called autolysis tissue by its own enzymes. In
the structure of acute pathology of organs of abdominal cavity this disease takes the third
place after acute appendicitis and cholecystitis. Women suffer from acute pancreatitis
33,5 times more frequently than men.
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In the basis of such damages of pancreas and enzymic toxemia lies mainly activating
of pancreatic, and then the tissue enzymes (tripsin, lipase, amylase). Often the
combination of the broken outflow of pancreatic secret and promoted secretion takes
place, which provokes intraductal hypertension.
Among explanations of primary mechanisms of activating of pancreatic enzymes the
most value belongs to: a) theory of general duct with reflux of bile in the ducts of
pancreas; b) blockade of outflow of pancreatic juice with development of intraductal
hypertension and penetration of secret in interstitial tissue; in) violation of blood flow of
pancreas (vasculitis, thrombophlebitis and embolisms, cardiac insufficiency and others
like that); g) toxic and allergic damages of gland. The role of alcohol in such situations
can be dual: stimulation of secretion of pancreas and direct damaging action on its
tissue.
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Pathomorphology
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Classification
(V All-russian convention of surgeons, 1978)
I. Clinico-anatomy forms:
1. Arching form.
2. Fatty pancreatonecrosis.
3. Hemorrhagic pancreatonecrosis.
II. Prevalence of necrosis:
1. Local (focus) damage of gland.
2. Subtotal damage of gland.
3. Total damage of gland.
III. Ran across: abortive, progressive.
IV. Periods of disease:
1. Period of hemodynamic violations and pancreatogenic shock.
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The disease begins suddenly, after the surplus reception of rich spicy food and use
of alcohol. Pain, vomiting and phenomena of dynamic intestinal obstruction are
considered the most characteristic signs of acute pancreatitis.
A stomach-ache is permanent and so strong, that can result in shock, localized in an
epigastric area and left hypochondrium. Some patients feel pain in right hypochondrium
with irradiation in the back, loin or breastbone.
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repeated or continuous and never brings facilitation. Vomit masses contain bile, as
admixture, and at the difficult form of acute pancreatitis remind coffee-grounds.
Nausea, hiccup, belch and dryness in a mouth are attributed as less characteristic
symptoms of this pathology.
During the examination the skin is pale, often subicterus. Some patients have
cyanosys with a marble picture as a result of violation of microcirculation. Later the
component of respiratory insufficiency can join it. At progressive general condition the
patient quickly gets worse to passing of acute pancreatitis, intoxication grows. The skin
takes shelter with sticky sweat.
The temperature of body of patients at the beginning of disease can be normal. It
rises at resorption of products of autolysis tissue and development of inflammatory
process in bilious ways.
The pulse in most cases is at first slow, then becomes frequent, notedly passing
ahead the increase of temperature of body.
Arterial pressure goes down.
The tongue in the first hour of disease is moist, assessed by white and grey raid. At
vomiting by bile the raid has yellow or greenish tint.
The abdominal is blown away, peristaltic noises are loosened. The signs of paresis of
stomach and intestine demonstrate early. They need to be included in the pathological
process of mesentery root of bowel. At palpation painfulness in an epigastric area and in
right, and sometimes and in left, hypochondrium is marked. However, in spite of great
pain in stomach, it remains soft for a long time. A little later there is moderate tension or
resistance of muscles of front abdominal wall.
Poor local symptoms during heavy intoxication are characteristic for the early period
of acute pancreatitis. Later there are symptoms of irritation of peritoneum, and at
percussion dulling is marked in lateral parts of abdominal as a result of accumulation of
liquid, and also the sign of aseptic phlegmon of retroperitoneal cellulose as slurred or
edema of lumbar area is seen. For diagnostics of acute pancreatitis there is the row of
characteristic symptoms which have different clinical value.
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Saveljev, 1978).
The I period (hemodynamic violations and pancreatogenic shock) lasts during 23
days. Violation of central hemodynamics, diminishment of volume of circulatory blood
and disorders of microcirculation, which at first arise as a result of angiospasm, are
considered the most characteristic signs, and later as a result of joining of the
intravascular rolling up and laying of elements of blood.
The II period (insufficiency of parenchymatous organs) lasts from 3rd to the 7th day
of disease. Violation of functions of basic organs and systems, sign of cardio-vascular,
hepatic and kidney insufficiency and growth of violations of breathing are thus observed.
In this period there is possible damaging of the central nervous system, which is erected
mainly to disorders of psyche, appearances of delirium and commas which in the
eventual result are the main reasons of patients death.
The III period (postnecrosis dystrophic and festering complications) comes in 12
weeks after the beginning of disease. During it, on the background of progress of
necrosis processes in pancreas, the regenerative changes develop, there are
parapancreatic infiltrate and cysts, cystic fibrosis of pancreas. Aseptic retroperitoneal
phlegmon which strengthens intoxication can also develop. There is festering pancreatitis
at joining of infection. During this period such complications, as erosive bleeding,
internal or external fistula, retroperitoneal phlegmon, can develop in patients.
From laboratory information leucocytosis which at the necrosis and hemorrhagic
forms of pancreatitis sometimes arrives at 25-30 109, lymphopenia, change of
leukocytic formula to the left and the increased ESR are characteristic. Growth of activity
of amylase of blood and urine is very often marked, and is the important sign of
pancreatitis. For estimation of the state of other organs maintenance of general albumen
and its factions, glucose of blood, bilirubin, urea, electrolytes, acid-base equilibrium
(ABE), and also the state of blood coagulation are determined. It is necessary to mark
that the exposure of hypocalcemia is considered a bad predictive sign of heavy passing of
acute pancreatitis.
Ultrasonic examination of gall-bladder and pancreas often specifies the increase of
their sizes, bulge of walls and presence or absence of concrement of gall-bladder and
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Pic. Sonography.
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Among early complications of acute pancreatitis shock, peritonitis and acute cardiac,
pulmonary, hepatic and kidney insufficiency can be distinguished.
Before later complications it is needed to deliver the abscesses of pancreas,
subdiaphragmatic, interintestinal abscesses, pyogenic abscess omentum bag, phlegmons
of retroperitoneal space and erosive bleeding.
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Diagnosis program
1. Anamnesis and physical methods of inspection.
2. General analysis of blood and urine.
3. Biochemical blood test (amylase, bilirubin, sugar).
4. Analysis of urine on diastase.
5. Sonography.
6. Computer tomography.
7. Cholecystocholangiography.
8. Endoscopic retrograde cholangiopancreatography.
9. Laparoscopy.
10. Laparocentesis.
Physical Examination:
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The following physical examination findings may be noted, varying with the severity
of the disease:
Fever (76%) and tachycardia (65%) are common abnormal vital signs; hypotension
may be noted
Abdominal tenderness, muscular guarding (68%), and distention (65%) are
observed in most patients; bowel sounds are often diminished or absent because of
gastric and transverse colonic ileus; guarding tends to be more pronounced in the upper
abdomen
A minority of patients exhibit jaundice (28%)
Some patients experience dyspnea (10%), which may be caused by irritation of the
melena sometimes develops (5%); in addition, patients with severe acute pancreatitis are
often pale, diaphoretic, and listless
Occasionally, in the extremities, muscular spasm may be noted secondary to
hypocalcemia
A few uncommon physical findings are associated with severe necrotizing
pancreatitis:
The Cullen sign is a bluish discoloration around the umbilicus resulting from
hemoperitoneum
The Grey-Turner sign is a reddish-brown discoloration along the flanks resulting
from retroperitoneal blood dissecting along tissue planes; more commonly, patients may
have a ruddy erythema in the flanks secondary to extravasated pancreatic exudate
Erythematous skin nodules may result from focal subcutaneous fat necrosis; these
are usually not more than 1 cm in size and are typically located on extensor skin surfaces;
in addition, polyarthritis is occasionally seen
Rarely, abnormalities on funduscopic examination may be seen in severe
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pancreatitis. Termed Purtscher retinopathy, this ischemic injury to the retina appears to
be caused by activation of complement and agglutination of blood cells within retinal
vessels. It may cause temporary or permanent blindness.
Differential diagnostics
Acute Mesenteric Ischemia
Acute Respiratory Distress Syndrome
Bacterial Pneumonia
Cholangitis
Cholecystitis
Choledocholithiasis
Cholelithiasis
Chronic Pancreatitis
Colon Adenocarcinoma
Colonic Obstruction
Community-Acquired Pneumonia
Duodenal Ulcers
Gastric Cancer
Gastroenteritis in Emergency Medicine
Irritable Bowel Syndrome
Myocardial Infarction
Pancreatic Cancer
Pancreatic Pseudocysts
Viral Hepatitis in Emergency Medicine
Acute pancreatitis needs to be differentiated with the row of acute diseases of organs
of abdominal cavity.
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Before conservative treatment hunger, bed rest, fight against pain and enzymic
toxemia, conducting of acid-base state, prophylaxis of festering infection and acute ulcers
of digestive duct are to be entered .
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Patients stomach is washed by cold soda solution and a cold on an epigastric area
and left hypochondrium is used. Medicinal therapy is prescribed also: spasmolytics
(papaverine, platyphyllin, no-shparum, baralgine, atropine); inhibitor of protease
(contrical, trasilol, gordox, antagosan); cytostatic agent (5-fluorouracil, ftorafur). Positive
action of inhibitor of protease is marked only in the first days of disease which are
subject to conditioned application of large doses. Antibiotics of wide spectrum of action:
a) tienam, which most effective in the prophylaxis of festering pancreatitis, as is selected
by pancreatic juice; b) cephalosporins (kefzol, cefazoline); c) cefamizine (mefoxine).
Disintoxication therapy is conducted also (5 % but 10 % solutions of glucose,
hemodes, reopolyhlukine, polyhlukine, plasma of blood, only from 3 to 5 liters on days,
in accordance with a necessity).
For the improvement of rheological properties of blood heparine is prescribed (5
000 ODES every 4 hours).
If patients have the expressed pain syndrome and phenomena of general intoxication
during all pain period plus 48 hours (by Bakulev), hunger is used. Such mode lasts on
the average of 24 days. The parenteral feed of albuminous hydrolyzate is thus
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conducted, by the mixtures of amino acid and fatty emulsion. Alkaline water of to 12 l.
and albuminous-carbohydrate diet are also appointed. Infusion therapy is complemented
by plasma, by albumen, hemodes, reopolyhlukine. The improvements of microcirculation
in pancreas are achieved due to introduction of reopolyhlukine, komplamine, trental and
heparin 5000 ODES 6 times per days under the control the indexes of the coagulation
system of blood. Anticholinergic drug (sulfate of atropine, methacin, platyphyllin),
2-histamin blocker (cimetidine, ranisan, ranitidine, famotidine, omeprazol) are also
applied. For the removal of pain: 1) sulfate of the atropine 0,1 % 1 ml + promedol 2
% 1 ml + papaverine 2 % 2 ml + analgin 50 % 2 ml; 2) isotonic solution of
chloride of sodium 500 ml + baralgine 5 ml + diphenhydramine hydrochloride 1 %
1 ml + papaverine 2 % 2 ml + magnesium the sulfate 25 % 5 ml + ascorbic
acid 5 ml + lipoic acid 0,5 % 2 ml + novocaine 0,5 % 10 ml. are used. From
the first days by a nasogastral probe the permanent aspiration of gastric maintenance is
conducted also. The Motility function of gastro-intestinal highway gets better at
application of cerucal or primperane. With the same purpose forced diuresis (maninil,
furosemide, aminophylline) is used on the background of intravenous introduction of
plenty of liquid.
At uneffective conservative treatment of patients with acute pancreatitis of middle
weight and heavy form it is expedient to apply surgical treatment.
Surgical treatment is carried out for patients with biliary pancreatitis (for a day long
from the beginning of disease) in combination with the destructive forms of cholecystitis,
at complications of acute pancreatitis by peritonitis, abscess of omentum bag or
phlegmon of retroperitoneal cellulose.
Overhead-middle laparotomy, which allows to estimate the state of pancreas, bilious
ways and other organs of abdominal cavity, is the best access in this situation. In case of
destructive pancreatitis the possible use of lumbar laparotomy from left to right
hypochondrium through a mesogastric area is useful.
Cholecystectomy is executed at calculous cholecystitis, phlegmonous inflammation
of walls of gall-bladder and biliary pancreatitis. If there are more than 0,9 cm at
expansion of choledochus, presence of concrement, ointment-like bile in it, increase of
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CYSTS OF PANCREAS
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Pseudocysts are fresh and old. The internal surface of fresh pseudocyst is rough,
granulating, grey-red. The table of contents is alkaline, grey or with a brown tint. In an
old pseudocyst the wall is smooth and shiny, pale-grey. The table of contents is lighter.
Epithelium pseudocysts is absent. More frequently they are met in body and tail of gland
and are not connected with ducts.
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Retention cysts connected with an obturated duct. The cavity has smooth,
grey-white surface, maintenance is transparent, watery or mucous-like. Innate cysts are
mainly multiple and shallow. A simple retention cyst differ from those that are always
connected with the anomalies of development of ducts and are unite with polycystosis
buds and liver.
Rarely there are echinococcus cysts, which have a clear chitinous shell, liquid in
cavity and daughter's blisters. They are localized in the area of head of pancreas.
Classification
(by A.N. Bakulev and V.V. Vinogradov, 1952)
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V. Neoplasty cysts:
1. Cyst-adenoma.
2. Cyst-adenocarcinoma.
3. Cavernous hemangioma.
4. Cystic epithelioma.
Pathomorphology cysts are divided on:
1. The true cyst.
2. Pseudocysts.
According to clinical passing pseudocysts are divided into acute, subacute and
chronic.
According to weight of passing into simple (uncomplicated) and complicated.
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Diagnosis program
1. Anamnesis.
2. Biochemical blood test (amylase, sugar, bilirubin).
3. Analysis of urine on diastase.
4. Coprograma.
5. Sonography.
6. Contrasting sciagraphy of stomach and duodenum (relaxation duodenography).
7. Retrograde pancreatocholangiography.
8. Computer tomography.
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Sonography
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The CT scan provides a very good appreciation of the wall thickness of the
pseudocyst, which is useful in planning therapy.
pseudocysts and acute pancreatitis and reported that a change in management occurred
35% of the time after the ERCP findings in pseudocysts were evaluated. Therefore,
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MRI:
MRI is not necessary to establish a diagnosis of pseudocysts; however, it is useful
acute necrotizing pancreatitis with resultant pseudocyst, an MRI may be very important
before a planned catheter drainage procedure.
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Endoscopic ultrasound:
Endoscopic ultrasound (EUS) is not necessary to establish a diagnosis but is very
undetected portal hypertension that may increase bleeding risks with transmural drainage.
Transmural drainage may be performed only when the symptomatic pseudocyst is
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to exclude tumors in any patient who does not have a clear history of pancreatitis.
oCarcinoembryonic antigen (CEA) and carcinoembryonic antigen-125
(CEA-125) tumor marker levels are low in pseudocysts and elevated in tumors.
o Fluid viscosity is low in pseudocysts and elevated in tumors.
o Amylase levels are usually high in pseudocysts and low in tumors.
o Cytology is occasionally helpful in diagnosing tumors, but a negative result does
not exclude tumors.
o A CEA level of greater than 400 ng/mL within the cyst fluid strongly suggests
malignancy.
Clinical passing of cysts of pancreas depends on their kind, localization, size, stage
of forming and complications.
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Differential diagnostics
Pancreatic Cancer
Pancreatic Necrosis and Pancreatic Abscess
Pancreatic Pseudoaneurysm
Pancreatitis, Acute
Pancreatitis, Chronic
von Hippel-Lindau Disease
The cysts of pancreas are differentiated with the tumors of abdominal cavity and of
retroperitoneal space.
Cancer of pancreas. For the cancer tumor of pancreas syndrome of small signs
(discomfort in epigastric area, loss of appetite, general weakness), permanent dull pain,
unrelated with the reception and composition of meal, icterus (cancer of head of gland),
Courvoisier's symptom (increased, unpainfully gall-bladder) are characteristic. Inconstant
pain at cysts of pancreas is more frequently related to faults in a diet; in anamnesis
destructive pancreatitis, traumas of gland are carried. Sonography examination,
retrograde pancreatocholangiography and computer tomography help in establishment of
diagnosis.
Tumors of retroperitoneal space are passed asymptomatic, clinic shows up by a
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Conservative
treatment. Treatment of acute or chronic pancreatitis is conducted in accordance with
principles. At the unfavorable dynamics of passing the diseases hunger with the
permanent sucking of gastric maintenance, parenteral feed and intravenous introduction
of liquids are appointed. Puncture of cysts is used through abdominal wall under
sonography control with aspiration of maintenance.
Peripancreatic fluid collections persisting for more than 4 weeks are referred to as
acute pseudocysts. Pseudocysts lack an epithelial layer and thus are not considered true
cysts. They also differ from true cysts in that they are usually filled with necrotic debris
rather than fluid. Accordingly, pseudocysts may be better described by the term
organized necrosis.
Surgical treatment is the method of choice of treatment of cysts of pancreas. The
choice of treatment method depends on the stage of forming of pancreas cysts.
In selected patients with very large fluid collections, percutaneous aspiration of
pancreatic pseudocysts is a reasonable approach. Even though treatment failures are
common when the pseudocyst communicates with the pancreatic ductal system,
percutaneous drainage serves as a temporizing measure that may later lead to successful
endoscopic or surgical intervention. Often, an infected pseudocyst (which by definition is
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Cystoejunostomy
Complications:
Bleeding is the most feared complication and is caused by the erosion of the
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fever or an elevated WBC count. Treat infection with antibiotics and urgent drainage.
GI obstruction, manifesting as nausea and vomiting, is an indication for drainage.
The pseudocyst can also rupture.
o A controlled rupture into an enteric organ occasionally causes GI bleeding.
o On rare occasions, a profound rupture into the peritoneal cavity causes
peritonitis and death.
REFERENCES
1. Li H, Qian Z, Liu Z, Liu X, Han X, Kang H. Risk factors and outcome of acute
renal failure in patients with severe acute pancreatitis. J Crit Care. Jun
2010;25(2):225-9.
2. Whitcomb DC, Yadav D, Adam S, et al. Multicenter approach to recurrent
acute and chronic pancreatitis in the United States: the North American Pancreatitis
Study 2 (NAPS2). Pancreatology. 2008;8(4-5):520-31.
3. Granger J, Remick D. Acute pancreatitis: models, markers, and mediators.
Shock. Dec 2005;24 Suppl 1:45-51.
4. Singla A, Csikesz NG, Simons JP, Li YF, Ng SC, Tseng JF, et al. National
hospital volume in acute pancreatitis: analysis of the Nationwide Inpatient Sample
1998-2006. HPB (Oxford). Aug 2009;11(5):391-7.
5. Banks PA. Epidemiology, natural history, and predictors of disease outcome in
acute and chronic pancreatitis. Gastrointest Endosc. Dec 2002;56(6 Suppl):S226-30.
6. Morinville VD, Barmada MM, Lowe ME. Increasing incidence of acute
pancreatitis at an American pediatric tertiary care center: is greater awareness among
physicians responsible?. Pancreas. Jan 2010;39(1):5-8.
7. Akhtar AJ, Shaheen M. Extrapancreatic manifestations of acute pancreatitis in
African-American and Hispanic patients. Pancreas. Nov 2004;29(4):291-7.
8. Whitcomb DC. Clinical practice. Acute pancreatitis. N Engl J Med. May 18
2006;354(20):2142-50.
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2001;48(1):62-9.
19. [Best Evidence] Aboulian A, Chan T, Yaghoubian A, Kaji AH, Putnam B,
Neville A, et al. Early cholecystectomy safely decreases hospital stay in patients with mild
gallstone pancreatitis: a randomized prospective study. Ann Surg. Apr
2010;251(4):615-9.
20. Ai X, Qian X, Pan W, Xu J, Hu W, Terai T, et al. Ultrasound-guided
percutaneous drainage may decrease the mortality of severe acute pancreatitis. J
Gastroenterol. 2010;45(1):77-85.
21. [Best Evidence] van Santvoort HC, Besselink MG, Bakker OJ, Hofker HS,
Boermeester MA, Dejong CH, et al. A step-up approach or open necrosectomy for
necrotizing pancreatitis. N Engl J Med. Apr 22 2010;362(16):1491-502.
22. Acosta, J. M., Pelligrini, C. A., and Skinner, D. B.: Etiology and pathogenesis
of acute biliary pancreatitis. Surgery, 88:118, 1980.
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th
METHODICAL INSTRUCTIONS FOR 5 YEAR STUDENTS
METHODOLOGICAL INSTRUCTION TO LESSON 9
. AIM. To be able to diagnose, to know symptoms of cirrhosis and portal hypertension, their complications
depending on clinical type of the disease. Principles of conservative and surgical treatment. To be able to diagnose, to
know symptoms of chronic pancreatitis, cysts and cancer of the panceras, depending on clinical type of the disease.
Principles of conservative and surgical treatment. To be able to diagnose, to know symptoms of euthyreoid and toxic goiter,
depending on clinical type of the disease, principles of conservative and surgical treatment.
Hepatic cirrhosis progressing causes dangerous complications. Conservative treatment of these complecations is
not always effective. The knowledge of surgical treatment principles gives a possibility to correct patients management,
saving his life.
The consequences of chronic pancreatitis, pancreatic cancer are rather resistant to treatment. In-time diagnosing of of
these diseases and adequate surgical intervention leads to healing or significant improving of patients state.
Diseases of thyroid gland set the sirst place in surgical endicrinology. Untimely and not proper choice of the
method of treatment frequently causes irreversible consequences appearing, that cause patients disablement or even are
threatening to his life.
1. Anatomical, morphological and functional peculiarities of liver (anatomy, topographical anatomy, anatomical
pathology, histology, propaedeutical therapy).
2. Etiology, pathogenesis of hepatic cirrhosis and types of portal hypertension (pathological physiology,
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propaedeutical therapy).
3. Estimation of laboratory and x-ray (transumbilical portography, splenoportography, celiacography) data, and also
of radionuclide scanning, reography, echography, percutaneous transhepatic cholangioduodenography,
laparoscopy, puncture biopsy.
4. Mechanism of hepatoprotectors, blood specimens, protamine sulfate solution action.
1. Anatomical, morphological and functional peculiarities of pancreas (anatomy, anatomical pathology, histology).
2. Etiology, pathogenesis and classification of chronic pancreatitis, cysts and cancer of pancreas (pathological
physiology, propaedeutical therapy).
3. Estimation of functional, x-ray, endoscopic findings (rhoetgenology).
4. Mechanism of pancreatic proteases inhibitors action.
Break 12.00-12.30
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Technical means and material provision of lectures (names and numbers of tables, compact discs, instruments
quantity, subjectpatients, etc.)
Multimedia projection of demonstration material (pictures, tables, videofilms) from compact disc Clinical Surgery,
videofilms with operations.
1. 51-year old patient, has alcohol abuse for a long time, suffers on hepatic cirrhosis. Duting recent months periodically
noticed black stool. Once there vas a bloody vomiting. The patient passed treatment courses in gastroenterological
department, took syrepar, essentiale, albumin, aminocapronic acid infusions, vicasol, multivitamins. After course of
treatment bleeding stopped. After repeated alcohol abuse bleeding has appeared again. Blood analysis data reveal
insignificant anemia. Serum bilirubin is on normal level. Liver is insignificantly atrophied in size. Ascites is absent.
Management tactics?
2. 38-year old patient, had severe form of viral hepatitis in young age. During course of treatment hormonal therapy
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was used. The patient keeps diet, has no alcohol abuse. During last year periodically notices dull pain in right
hypochondrium. Liver is 2-3 sm under costal arch. Serum bilirubin periodically rises up to 28-32 mkmol/l.
Presumptive diagnosis?
Following tactics?
3. 54-years old patient, suffers on frequent attacks of chronic pancreatitis. On intravenous cholangiocholecystography
3 concrements in the distant part of choledochus were found. Whole blood bilirubin is 260 mkmol/l, the level of urine
diastase is not increased. During an operation pancreas is dense. By means of supraduodenal choledochotomy only 1
stone was removed; the probe doesnt pass into duodenum.
Surgeons tactics?
4. During an operation upon stomach cancer, no malignant process was found. The cyst of pancreas body, 15x15 cm
in size, that is intimately adhered with back wall of the stomach, mesocolon and mesentery was found.
Surgeons tactics?
5. 40-years old female patient, is ill with diffuse toxic goiter for 3 years. During all this time she has been undergoing the
conservative treatment, in spite of what gradual increasing of thyroid gland up to the IV degree is observed. She mentions
body weight loss and progressing of nerve-psychic disorders.
Tactics of treatment?
6. 50-years old patient with diagnosis Diffuse toxic goiter of IV degree; thyreotoxicosis of severe degree. At the same
time, he has chronic pneumonia with signs of lung insufficiency of II degree.
Surgeons tactics?
Information sourses:
Main
1. Townsend CM, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery. 19th ed.
Philadelphia, Pa: Saunders Elsevier; 2012.
2. L.Ya.Kovalchuck, Yu.P.Spizhenko, V.F.Sayenko and others Hospital surgery. Ternopil: Ukrmendknyga, 1999.
3. Practical classes materials http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/classes_stud/en/med
/lik/ptn/Surgery/4/Topic%2009%20Postcholecystectomy%20syndrome.%20Obsructive%20jaundice.htm
Additional
1. Manual Facultative Surgery under the edition of V.O.Shidlovsky Ternopil: Ukrmedknyga, 2002, section
Diseases of the rectum and the colon,
2. Compact disc Facultative surgery.
3. Schwartz's Principles of Surgery, Ninth Edition. F. Brunicardi. Philadelphia, Pa: Saunders Elsevier; 2009
4. Zollinger's Atlas of Surgical Operations, 9th Edition. Robert Zollinger Jr., Elsevier; 2010
5. Chen, Herbert. Illustrative Handbook of General Surgery. Berlin: Springer, 2010.
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"11" 2013 . 9
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Endemic goiter is the pathology of thyroid gland, which occurs in biogeochemical regions with iodine
deficiency in environment (regional pathology).
Sporadic goiter is the disease of thyroid gland, which occurs in unendemic for goiter regions.
(Fig.1;Fig.2;Fig.3.)
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Except iodine deficiency, the goitrous endemia is contributed by excessive contents of calcium in
environment, deficiency of bromine, poor sanitary and hygienic conditions. Decreased contents of cobalt,
manganese, and zinc in environment also influence on expression of goitrous endemia. The lack of iodine in
the organism blocks the synthesis of thyroid hormones. It results in hypersecretion of thyroidstimulating
hormone of hypophysis, which in turn leads to hypertrophy and hyperplasia of thyroid epithelium that on
initial stages can be compensated, but further transformed into the goiter.
1) relationship between men and women with goiter (if it approaches to 1, the endemia is more
severe);
3) presence of cretinism;
4) goiter in animals;
Sporadic goiter arises from relative iodine deficiency, which results from disturbance of iodine ingestion, liver
dysfunction.
Macroscopically the goiter is divided onto diffuse, nodular and mixed. According to histological structure
distinguished parenchymatous and colloid ones. Sometimes occur cystic transformation of the gland and
calcification. The enlarged nodes may result in atrophy of adjacent tissues and organs. So, the advanced forms
of goiter can cause compression of trachea and its softening (tracheomalacia). The sings of hyperthyroid
transformation of euthyroid goiter include: the transformation of thyroid epithelium from squamous cell into
cubic and cylindrical, presence of papillomatous overgrowth, agglomeration of lymphocytes, liquid
vacuolated colloid.
1) diffuse goiter;
2) nodular goiter;
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3) mixed goiter.
I - the isthmus of the gland is noticeable during swallowing and could be palpated;
III - the enlargement of gland results in evident thickening of neck ("a thick neck");
Diffuse enlargement of thyroid of I-II degrees without disturbances of function and nodular transformation
referred to compensatory hyperplasia of the gland.
2) retrosternal goiter;
5) presternal goiter.
In the patients with endemic euthyroid goiter the clinical sings are basically caused by mechanical and
reflex influence of enlarged thyroid gland on adjacent organs. Patients mainly complain of the presence of
"tumour" and neck deformity. Sense of tightness in the neck, difficult breathing, swallowing, and also sudden
attacks of cough (owing to compression of laryngeal nerves by goiter) trouble them. In case of great goiter
(particularly retrosternal,) periodical dyspnea may develop (especially in the night), up to asphyxia, which is
result of compression and inflection of trachea. Retrosternal goiter frequently accompanied with hoarseness,
distended veins of face and neck.
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The goiter with low thyroid function, as a rule, clinically manifests by general weakness, malaise,
sleepiness, hypomnesia, chilliness, dry skin and edemas, particularly around eyes. Sometimes in such patients
observed constipation.
The patients with hyperthyroid goiter complain of irritability, heartbeat, excessive sweating, and tremor of
arms, sleeplessness, feeling of fever. Sometimes observed loss of weight, diarrhea. The thyroid hyperfunction
in endemic goiter mainly slightly expressed, and not associated with exophthalmus.
Enlargement of thyroid gland in patients with endemic goiter mostly often has nodular or mixed character,
and only in small number of the patients (mainly of younger age) observed diffuse enlargement of thyroid
gland.
Nodular goiter is palpated as painless tumour with regular contours, smooth surface, not connected with
adjacent tissues and displaced during swallowing. Such goiter is characterized by elastic or dense consistence.
Long-term goiter leads to formation of fibrosis and calcification, it becomes solid, and tuberous.
The shape of diffuse goiter resembles the butterfly. It retains the contours, its surface is smooth, consistence
mostly elastic, sometimes soft or dense. Mixed goiters combine manifestations of the nodular and diffuse
one, however tactically, the mixed goiters refer to nodular group.
The separate nodes or entire goiter can partially or completely be displaced behind breastbone. Palpation of
such goiter requires the special devices. The examination is performed when the patient is supine with the
bolster under scapulas. During the procedure the patient must force by himself or cough, that causes the
emergence of the upper pole or entire goiter above breastbone.
Features of the clinical course of endemic and sporadic goiter caused by its form (nodular, diffuse, mixed),
degree of thyroid enlargement, character of functional state (euthyroid, hypothyroid, hyperthyroid), location
(typical, retrosternal, ectopic, aberrant goiter), constitutional features of the patient, duration of the disease
and character of previous treatment.
Complication: inflammation of the goitrous thyroid gland (strumitis), hemorrhage in the tissue of goiter,
asphyxia, malignancy.
3. Determining of thyroid function (serum hormones, serum iodine, and thyroid-iodine uptake)
(Fig.5;Fig.6;Fig.7;Fig.8.).
4. According to indications: X-radiography of the neck (calcification, ossified foci) with barium
swallow (compression of esophagus, trachea, their shift, and deformity).
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6. Puncture biopsy(Fig.9.)
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Endemic and sporadic goiter requires the differential diagnostics with chronic autoimmune thyroiditis
(Hashimoto's thyroiditis), Riedel's fibrous thyroiditis, neck cysts, lipomas and other tumours of the neck and
mediastinum, malignant neoplasms of thyroid gland, metastases of tumours in cervical lymph nodes.
In case of Riedel's goiter the gland is tuberous, of woody consistency, quite often knitted with adjacent
tissues (except skin).
The cysts, tumours of the neck, metastases in lymph nodes are well defined on sonograms, do not displace
at swallowing and accumulate radioactive iodine.
The suspicion on thyroid cancer makes the necessity to carry out morphological verification by puncture
biopsy with further cytological examination.
Endemic goiter is the subject for treatment in all its forms and all stages of the development. The choice of
treatment depends on type of the goiter (diffuse, nodular, mixed), degree of enlargement of the thyroid (I-V)
and character of complications of the goiter (inflammation, hemorrhage, asphyxia, and malignancy).
Conservative treatment includes the drugs of inorganic iodine, thyroidine and pure hormonal drugs
(thyroxine, triiodothyronine). Thyroxine is the most effective one. The iodine drugs less effective and
frequently are the cause of secondary hyperthyroidism. The medicament treatment is administered in diffuse
thyroid enlargement without sings of compression of neck organs. Polynodular goiter (particularly in elder
women) sometimes complicated by malignancy and consequently, even if the sings of compression of neck
organs and hyperthyroidism are absent, also treated by conservative agents. The important argument of
medicament treatment is their often recurrences after operation.
The surgical approach in endemic and sporadic goiter are determined by their spread and character of the
lesion. There used the principle that all transformed into the goiter parenchyma should be removed, and
healthy preserved as much as possible.
The nodular and mixed form of the goiter, despite its function and size, is the subject for surgery. The
hypothyroidism is not contraindication for operation, as the removal of the goiter results in functional
normalization of unaltered, paranodular tissue. The operation, first of all, is indicated if present the sings of
compression of neck organs, goiter of the major sizes, secondary hyperthyroidism and suspicion on
malignancy. The goiter of additional thyroid glands (aberrant goiter) is the subject for obligatory surgical
removal. The operation consists of removal of the aberrant gland with revision of the basic thyroid gland.
The intrathoracic goiter, which develops in retrosternal ectopy of thyroid gland, also requires obligatory
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surgical removal(Fig.10.). The best access is the longitudinal sternotomy. The cervical goiter is possible to
remove by means of cervical access without the special technical efforts.
In tongue ectopy if there are no severe disturbances of speech, swallow and breathe also possible observation
and conservative treatment. Progressive growth of the goiter, presence of sings of compression, dysphagia,
traumatic bleeding and suspicion on malignancy require the surgical treatment removal of the goiter mostly
through a lateral pharyngeal incision.
The optimal method of anesthesia is the endotracheal narcosis. This method prevents mechanical asphyxia
during operation resulting from compression or inflection of trachea at the moment of mobilization and
drawing out of the goiter. The method permits to perform careful revision of entire gland and neck spaces,
first of all retrosternal, retrotracheal, retroesophageal, where there can be separate thyroid nodes. It is
necessary to consider a local anesthesia, and also other methods of general anesthesia as reserve.
For removal of goiter used transversal incision by Kocher in the inferior part of the neck above the
sternoclavicular junctions. Operation on thyroid gland must begin from careful revision and intraoperative
diagnostics that permits to choose the adequate operative tactics. Trachea must be mobilized by means of
isthmus dissection. It permits better orientation in topographic situation caused by the goiter, and to perform
tracheostomy at occurrence of asphyxia. Further isthmus and pyramidal lobe must be removed as the most
dangerous as for relapse of the goiter.
The volume of thyroid resection in endemic and sporadic goiter is determined individually. The resection is
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performed subfascially that prevent the removal of parathyroid glands and trauma of laryngeal nerves. The
node is necessary to eliminate together with paranodular tissue, as it is functionally failed. It is justified also
by oncologic reasons. The operation of nodular enucleation is considered to be inadequate, thus never used.
Meanwhile, in multinodular bilateral goiter, when practically entire thyroid gland is affected, it is necessary to
eliminate separate nodes from healthy parenchyma, preserving its maximal amount, as the parenchyma is
mainly disposed as lamina on their surface. This layer of parenchyma is necessary to dissect and draw aside
by scissors out of node, having preserved its vascularization.(Fig.11-15.)
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In endemic and sporadic goiter applied saving, extent and subtotal resection of the thyroid with obligatory
indication of amount and site of leaving parenchyma.
For oncologic standpoint it is necessary in all cases to carry out intraoperative express cytology of the
removed tissue.
For prophylaxis of goiter relapse after the operation necessary long-termed institution of thyroid hormones
with the purpose to block thyroid stimulation by pituitary gland.
Diffuse goiter with hyperthyroidism (Grave's or Basedow's disease, thyrotoxicosis, hyperthyroidism) is severe
autoimmune and neuroendocrine disease resulting from excessive secretion of thyroid hormones by diffuse-
enlarged thyroid gland with lesion of all organs and systems of the body.
The diffuse goiter with hyperthyroidism (thyrotoxicosis) mostly occurs at women. In 5 % of persons with
hyperthyroidism develop ophthalmopathy and pretibial myxedema.
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The scientific investigation and clinical examination testify that the diffuse goiter with hyperthyroidism is
autoimmune disease. This disease is commonly results from infections, intoxication, craniocerebral injury,
dysfunction of other endocrine glands, first of all genital, acute and chronic mental disorder, sunstroke. The
disease develops under the influence of these factors directly on generically predisposed to thyrotoxicosis
organism.
The thyroid gland is 2-5 times enlarged, moderately dense, on incision pulpy, sanguineous, of grey-pink color.
Histologically revealed a polymorphism of follicles. Follicular epithelium is cylindrical with papillomatous
growths. The colloid is eosinophilic, contains plenty of resorptive vacuoles. In interstitial space lot of
lymphocytes, which form follicles. The severe form of thyrotoxicosis results in thyrotoxic heart, thyrotoxic
liver cirrhosis, thyrotoxic ophthalmopathy, osteoporosis, and cachexia.
According to the clinical course distinguished mild, moderate and severe forms of the disease.
II stage neurohormone, marked sings of thyrotoxicosis, the thyroid is noticeably enlarged in size.
A diffuse toxic goiter affects practically all organs and systems and disturbs all types of metabolism. Except
described in 1842 by Basedow classical triad (goiter, tachycardia and eye bulging), today is known about 70
signs, proper for thyrotoxicosis, which can be combined in three basic syndromes: hyperthyroidism, eye signs
(ophthalmopathy) and lesion of skin (pretibial myxedema). By the may, the hyperthyroidism is the permanent
phenomenon, and ophthalmopathy and pretibial myxedema occurs rather seldom (in 1-5 % of patients).
To initial sings of thyrotoxicosis can be regarded: general weakness, prompt fatigability, decreased work
ability and muscular force, nervousness, irritability, sleeplessness, sweating and hyperemia of skin.
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The basic signs of thyrotoxicosis are enlargement of thyroid gland (goiter), palpitation, exophthalmos, tremor
and progressing loss of weight. (Fig. 16)
Fig.16. Thyrotoxicosis
The thyroid gland in the patients with thyrotoxicosis is diffuse enlarged and of moderate density. In some of
them due to excessive blood supply it can pulsate. After long treatment by iodine the gland becomes dense
and painless. Such long-term conservative treatment causes the development of sclerotic degenerative
processes, sometimes with nodular transformation of the tissue, and the degree of thyroid enlargement
frequently does not relate to the gravity of thyrotoxicosis.
Secretory activity of thyroid hyperplasia in the form of excessive releasing of its hormones (triiodothyronine
and thyroxine) underlies the hyperthyroidism. The majority of effects of thyroid hyperfunction manifest
through sympathetic nervous system: palpitation, tremor of fingers, tongue, and whole body (sign of
"telegraphpole"), sweating. In the patients with thyrotoxicosis the protein, carbohydrate and lipid metabolism
is elevated, which manifests by simultaneous excessive appetite and loss of weight.
The changes, which develop in organs of cardiovascular system and manifests by tachycardia, high systolic
and low diastolic pressure, increase of pulse pressure and complete arrhythmia with the development of heart
failure form a syndrome of thyrotoxic heart.
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The excessive formation of heat owing to intensive metabolism, which results from the influence of thyroid
hormones, leads to hyperthermal syndrome (feeling of fever, high body temperature). The sings of nervous
dysfunction include irritability, anxiety, fear sensation, nervousness, sleeplessness, hyperactive tendon
reflexes. The dysfunction of genitals manifests by oligo- or amenorrhea, and in the men by gynecomastia,
which is the outcome of disturbed relation between estrogens and androgens. Thereafter libido and potency
are reduced.
The thyrotoxicosis without treatment results in loss of weight, in advanced cases not only the subcutaneous
fat disappears, but also a muscular tissue reduced, down to cachexia. Degenerative changes in muscles, and
lesion of peripheral nervous system result in thyrotoxic myopathy.
In majority of patients develop characteristic eye signs. The predominant one is the exophthalmos. By the
way, eye bulging, which occurs in 50 % of cases, frequently can be the initial manifestation of the disease,
assigned by patient. Three types exophthalmos are distinguished: slight (14-17 mm), moderate (17-20 mm)
and considerable (more than 20 mm). The exophthalmos in thyrotoxicosis is symmetric, the eye trophic and
movements of does not disturbed. Except exophthalmos, there are lot of other eye signs observed in the
patients with thyrotoxicosis.
Graefe's sign the upper lid lag when the patient looks downward;
The eye signs of diffuse toxic goiter are necessary to differentiate from ophthalmopathy (malignant
exophthalmos), which observed approximately in 5 % of the patients with thyrotoxicosis. Such exophthalmos
simultaneously associated with pain in the eyeballs, gritty sensation and eyewatering. Also detected lid
edema, ocular injection. In considerable ophthalmopathy the eyeballs bulge from orbits, eyelids and
conjunctiva are swollen, with sings of inflammation. It can result in keratitis with corneal ulceration, which
finally can lead to blindness. The high orbital pressure caused by lymphoid infiltration, accumulation of fluid
and edema of retroorbital tissues result in not only eye bulging exophthalmoses, but also compression of
optic nerve and loss of sight. It is necessary also to specify that the ophthalmopathy in thyrotoxicosis, as a
rule, develops on the background of encephalopathy and has an autoimmune genesis. (Fig.17.)
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Fig.17. Exophthalmoses
Pretibial myxedema arises on the anterior surface of lower legs. The skin becomes dense, thickened, of
purple-red color, and hair follicles jut out of its surface.
Thyroid hypersecretion also negatively influences on the liver parenchyma. In severe cases it can result in
toxic hepatitis, jaundice and further hepatargy. It is necessary to consider the toxic hepatitis in such patients
unfavorable as for prognosis.
Under the direct cytotoxic influence of thyroid hormones on intestinal mucosa suppressed its enzymatic
function that leads to intestinal hyperkinesis and osmotic diarrhea thyrotoxic enteric syndrome. It is
accompanied by gluco- and mineralocorticoid dysfunction of suprarenal gland, and leukopenia, granulocytosis
and lymphocytosis in blood.
In clinical course of thyrotoxicosis distinguished the mild, moderate and severe forms.
The mild form of thyrotoxicosis is characterized by following signs: pulse 100 beat/min, loss of weight
approximately 3-5 kg, slight sweating, eye signs absent or slightly expressed, normal arterial pressure, basal
metabolism to +30 %, elevated thyroid-iodine uptake, and the maximum of iodine accumulation, which
exceeds 30 % is detected after 24 hours.
The moderate gravity of the disease manifests by expressed symptomatology: loss of weight to 8-10 kg,
tachycardia 101-120 beat/min, systolic pressure is elevated, and diastolic decreased or normal. Frequently
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observed exophthalmos, basal metabolism +31-50 %, thyroid-iodine uptake has been excessive since first
hours.
The severe form of thyrotoxicosis is characterized by the sharply expressed symptomatology, which is caused
by considerable visceral dysfunction. The pulse rate in such patients exceeds 120 per minute, and complete
arrhythmia develops. Tremor and profuse sweating sharply expressed, pulse pressure considerably elevated
circulatory failure and ophthalmopathy frequently observed. The loss of weight can overtop 10 kg, basal
metabolism more than +50 %, the maximum of radioactive iodine accumulation detected in 4-6 hours after
taking of isotope, and decreasing of accumulation curve exceed 24 hours.
According to the clinical course two forms of thyrotoxicosis distinguished: ) thyrotoxicosis with slow
development; ) acute form of diffuse toxic goiter, which is characterized by an acute onset and prompt,
sometimes within several hours, development. The acute thyrotoxicosis seldom occurs and in most cases ends
lethally from thyrotoxic coma.
The clinics of acute thyrotoxicosis develop within some hours or days. Thus the thyroid gland is not enlarged,
high temperature, vomiting, diarrhea, sharp loss of weight are observed.
The special forms of thyrotoxicosis include the thyrotoxicosis in childhood, in pregnant, in climacteric
women, and people of the elderly age.
Among complications during the course of disease the most dangerous for the life is thyroid storm. It is
observed in 0,02-0,05 % of the patients and develops, mainly, as the outcome of the lesion of provoking
factor. Among them considered trauma (surgical intervention on thyroid gland or other organs), harsh
palpation of the gland, mental trauma, emotional stress, infections, pregnancy, labors and radioiodine therapy.
The manifestation of initial, vague and slightly expressed forms of thyrotoxicosis can resemble neuroses,
rheumatic disease, tuberculosis, chroniosepsis, postcastrate syndrome, diencephalic lesions, and also
malignant tumours. It particularly concerns those cases, when the enlargement of thyroid gland is slight or it is
failed to detect.
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All the mentioned diseases are characterized by palpitation, heart pain excessive sweating, subfebrile fever
and loss of weight.
The acute development of thyrotoxicosis sometimes makes the necessity to rule out such acute infectious
diseases, as dysentery, influenza or camp-fever.
Laboratory tests are important for differential diagnostics of thyrotoxicosis: detecting of thyroid hormones,
serum protein-bounded iodine, thyroid-iodine uptake, biochemical, immunological investigations, sonography
and scanning with the radioiodine or technetium.
The thyrotoxicosis revealed for the first time, and also its severe and moderate forms require institutional
treatment. Three methods of treatment of thyrotoxicosis are commonly employed: ) antithyroid drugs; b)
treatment by radioactive iodine; c) surgery.
The antithyroid drug therapy of the patients with thyrotoxicosis, first of all, should be directed to
ameliorate hyperthyroidism. This is gained by the usage of iodine and thyrostatic agents, particularly
mercasolil synthetic antithyroid drug. In severe cases the treatment begins from 45-60 mg (9-12 tablets) per
day, in the moderate form from 30 mg (6 tablets), in mild from 15 mg (3 tablets) per day. The maximal
initial dose ordered within 2-4 weeks to gain expressed clinical relief of the disease (decrease of irritability,
normalization of pulse rate, increase of weight). After that, if the state of the patient gradually improves, the
dosage is reduced every 3-4 weeks by 1-2 tablets per day to supportive dose (1 or 1/2 tablets per day during
2-3 months). Commonly, the course of the treatment by mercasolil should be lasted for 1-1,5 years. Among
complications, which can arise during the treatment, it is necessary to mention leukopenia, agranulocytosis
and allergy.
In case of allergic response to mercasolil or development of complications used a reserve drug lithium
carbonate.
Such long conservative treatment of thyrotoxicosis is desirable in those patients, who gained euthyoidism in
1-3 months, that is the gradual reduce of goiter and eye signs. If during the treatment periodically
exacerbation occurs, which manifests by thyroid enlargement, development of encephalopathy, activation of
ophthalmopathy the surgery is indicated.
More recent studies showed that the treatment by radioactive iodine is a radical method of therapy of
thyrotoxicosis. The radioactive iodine, which deposits in thyroid gland, irradiating its parenchyma, results in
destruction of the active thyrocytes with their further replacement by connective tissue (bloodless
thyroidectomy). The standard dosage is 0,1 mCi per gram of thyroid tissue, and it can be introduced at one
time or partly.
Nevertheless such therapy has series of essential drawbacks. The lack of precise methods of determining the
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weight of the gland results in miscalculations at selection of total dose of the isotope. It is also impossible to
exclude the harmful influence of the isotope on the genetic kettle of the patient. Almost in 70 % of the
patients the hypothyroidism develops after the treatment by radioactive iodine and there is a potential threat
of the development of radioactive thyroid cancer. That's why the indication for application of this method
rather restricted.
The treatment by radioactive iodine is commonly indicated for the patients with thyrotoxicosis after 40, with
recurrent thyrotoxicosis, and after operations particularly, in combination with severe concomitant diseases
and in case of refuse of surgery. It is not justified at young age, pregnancy and during lactation, thyrotoxic
multinodular adenoma, expressed leukopenia, and kidney dysfunction or at severe acute thyrotoxicosis.
Sometimes introduction of radioactive iodine can cause the exacerbation of thyrotoxicosis, up to the
development of thyroid storm. Thus, before administration of the radioactive iodine, particularly in patient
with severe form of thyrotoxicosis in order to relieve thyrotoxicosis it is necessary to institute antithyroid
drugs.
The surgical method of treatment is considered to be radical and the most effective. The operation almost
always allows to liquidate the manifestations of hyperthyroidism together with its morphological base. The
efficiency of this method in the specialized clinics reaches 95-97 %.
The indications for surgery include thyrotoxicosis of moderate gravity when the conservative treatment is
inefficient during 2-3 months, severe forms of thyrotoxicosis, goiter of IV-V degree despite the gravity of
thyrotoxicosis, and also nodular transformation of toxic goiter.
The surgical method is not recommended for the patients with thyrotoxicosis with severe concomitant
diseases and dysfunction of vital systems.
The obligatory requirement of successful surgery of the patients with thyrotoxicosis is the careful
preoperative preparation, which goal is the liquidation or decreasing of hyperthyroidism, that achievement
of euthyroid state. Preoperative preparation should be complex, pathogenically proved and individual.
The appropriate place in preoperative period should possess psychological preparation. The patients stay in
chambers together with patients recovering after operation. In severe form of thyrotoxicosis a strict bed
regime is ordered. The diet should be high-caloric, rich with proteins, vitamins. The patient must take
antithyroid drugs under the control of general blood analysis. To prevent leukopenia and agranulocytosis
instituted leukopoetic agents. Besides antithyroid therapy, are advisable reserpin that characterized by
hypotensive, sedative and antithyroid activity, beta-blockers and tranquilizers for decreasing stimulation of
CNS.
The preoperative preparation is considered to be sufficient, if the state of the patient is regarded to euthyroid
or approximate to it. It is testified by normalization of pulse (90-80 per minute), increase of weight on 3-5 kg,
liquidation of nervousness and irritability, disappearance of tremor, regulation of function of cardiovascular
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Operation. The most effective and rational surgery approach for thyrotoxicosis is the subtotal subfascial
resection of the thyroid (O.V.Nickolayev, 1951) or thyroidectomy. The main difference of this procedure is
the refuse of ligation of thyroid vessels before they enter the gland and subfascial resection of the gland. The
goal of this technique is to gain bloodless and atraumatic procedure of operation, to prevent damage
(removal) of parathyroid glands and laryngeal nerves. This procedure also favors the formation of a gland
stumps in the site of parathyroid glands and passage of recurrent nerves. The volume of resection and,
consequently, the size of the gland stamp must be based on the account of gravity of thyrotoxicosis, age of the
patient, duration of the disease, previous treatment, morphology of the organ and immune state of the patient.
(Fig.18)
It is generally accepted, that the more severe the form of thyrotoxicosis, more young the patient, more short
duration of the disease, more intensive vascularization, more dark color of the gland, the smaller tissue
remnant is necessary to leave (mainly less 6 g, on 1-3 g from each side). Morphologically in such patients
revealed hyperfunctional type of histogram and autoimmune processes on initial stage of the development.
The elderly age of the patients with long conservative treatment, reduced blood supply of the gland,
expressed plasmolymphatic infiltration of the tissue requires to leave greater thyroid remnant (6-10 g).
Morphologically in such patients detected regenerate type of histogram.
Sometimes a long anamnesis and conservative treatment, in association with expressed sclerosis of the gland
or its nodular or cystic transformation requires performing of thyroidectomy.
Postoperative period. The clinical course of early postoperative period in the patients undergone the
operation mainly depends both on quality of preoperative preparation, and on technique of the surgical
intervention. In some patients, particularly with severe form of thyrotoxicosis, during first days after the
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There are three degrees of postoperative thyrotoxic response: mild, moderate gravity and severe.
Characteristic sings of mild degree is the tachycardia up to 120 per minute, fever as high as 38, satisfactory
state of the patient, tachypnea.
The moderate gravity of thyrotoxic response manifests by mild psychomotor excitement. They complain of
general weakness, headache, fever sensation, rapid pulse to 120-140 per minute (rhythmic, tense), sometimes
extrasystole. Temperature raises as high as 38,5-39. Characteristic the considerable sweating, tachypnea,
superficial sleep.
Severe degree of thyrotoxic response is characterized by expressed psychomotor excitement. The patients are
restless, frequently change positions in the bed, they complain of considerable sweating, permanent fever
sensation and expressed tremor. Hyperemia of the face, pulsate vessels of the neck and cyanosis of leaps are
evident. The pulse rate usually exceeds 140 per minute, irregular and soft. The breathing is superficial. Body
temperature is 39-40. The sleeplessness in such patients is almost impossible to liquidate by hypnotic and
narcotics agents.
1. Thyroid storm is the severe complication of postoperative period in the patients with thyrotoxicosis
(thyrotoxic crisis, acute postoperative thyrotoxicosis). The crisis develops mainly on the second or third day
after the operation. If is failed to liquidate it in a day after the onset, the patient can die.
The clinical development of such crisis is acute or fulminant. It manifests by excitement, up to psychosis and
coma, motor disorders, tachycardia (pulse rate 150-200 per minute), complete arrhythmia, fever as high as
40 and more, hyperemia of the face, neck, limbs, cyanosis, extremely sweating, diarrhea.
Pathogenically thyroid storm is caused by excessive releasing of thyroid hormones. It can arise as the result of
rough palpation of the thyroid, treatment by antithyroid drugs, radioactive iodine, infections and traumas.
The crisis requires an urgent and complex treatment. Infusion therapy includes transfusion of haemodes,
solutions of glucose with vitamins, plasma, and albumin. Major doses of glycocorticoids, narcotics,
neuroleptanalgesia are instituted. Also desirable administration of sedative antihistamine drugs, adrenergic
blockers, cardiac glycosides, oxygenotherapy, hypothermia, particularly on regions of major vessels, medical
narcosis, extracorporal method of detoxycation.
The prophylaxis of thyroid storm suggests an adequate preoperative preparation in order to gain euthyroid
state of the patient, and also atraumatic performance of surgical intervention.
2. The damage of laryngeal nerves is the severe complication of operations on thyroid gland. Thus the
paralysis of laryngeal nerves can be unilateral or bilateral, temporary or permanent. The basic causes of the
paralysis: cutting off the nerve, its crushing or ligating, distention or compression. It is also necessary to
specify that the bilateral injury of inferior laryngeal nerves is particularly dangerous.
The prophylaxis of the damages of laryngeal nerves basically consists of careful technique of subfascial
resection of thyroid gland. It is always necessary gently manipulate in the region of inferior poles and
"dangerous zone". The hemostasis in order to obtain "dry" operative wound should be carried out only under
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3. Asphyxia. It is caused, except bilateral injury of inferior laryngeal nerves, by the damage of trachea,
tracheomalacia, laryngeal edema or inflection of trachea.
The tracheal wall injuries must be sutured by atraumatic needle with further muscular plastics.
Tracheomalacia requires supporting sutures on trachea or application of prosthetics from synthetic material.
Sometimes it is necessary to perform temporary tracheostomy.
4. Air embolism. The cause of this infrequent complication is the entering of air in the neck veins owing to
suctional activity of chest and negative venous pressure. The prophylaxis of such complications consists of
clamping of veins before cutting.
5. Parathyroid tetany is a difficult postoperative complication, which is hardly to undergo rehabilitation. The
basic cause parathyroid tetany is the removal of parathyroid glands together with thyroid tissue. Besides it can
result from impaired blood supply of the glands after the operation. The tetany develops on the base of
mineral metabolism disorders, first of all, extremely reduced serum calcium (less 2,5 mEq/l)
It manifests by acute attack of wide-spread or localized cramps of separate groups of muscles of the upper or
lower limbs. The most dangerous in this plan is the development of laryngospasm or tonic contraction of
diaphragm.
Early clinical manifestation of parathyroid tetany is the Chvostek's signs (percussion near mandible angle
causes muscular contractions of the face), Ttrousseau (occurrence of paresthesias and the sign of
"obstetrician's" hand" after applying of tourniquet on brachium.
The treatment of parathyroid tetany consists of prompt administration of calcium agents. The usage of
parathormone in complex with vitamin D is usually beneficial. Simultaneously with conservative treatment
also performed transplantation of bony tissue.
The careful technique of subfascial resection of thyroid gland prevents the damage of parathyroid glands
(except cases of their thyroid ectopy).
6. Bleeding. The cause of intra- and postoperative bleedings is insufficient mechanical hemostasis.
The postoperative bleedings are observed within first hours after operation as the result of unreliable
hemostasis or slipping of ligature from vessels. Bleedings are clinically characterized by the prompt
enlargement of swelling in the region of neck, considerable sopping of bandage by blood. Meanwhile, the
patients complain of feeling of tightness in the neck, fear, tachycardia, cyanosis and dyspnea. The treatment
of this complication is only surgical. The goal consists of complete disclosure and revision of the wound,
carrying out of careful hemostasis.
The prophylaxis of postoperative bleeding includes a complex of measures, the most important of which is a
subfascial technique of thyroid resection, careful reliable hemostasis and anatomic operating. The special
attention is necessary to pay on lateral thyroid veins (Kocher's veins), which are short and empty directly into
interior jugular vein. If the vessels are sclerosed, fragile and easily broken, they should be tied at once after
cutting, instead of leaving on clamps up to the end of gland removal.
The damage of larynx, esophagus, major vessels of neck, lymph duct and pleura very seldom occurs. The
laryngeal defects are sewed up with further covering by muscles. The esophageal wound is sewed up tightly,
and feeding of the patient during 7 days is carried out through the tube.
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PURULENT THYROIDITIS
The purulent thyroiditis is a suppurative septic lesion of thyroid parenchyma. There are also cases of purulent
inflammation goitrous thyroid gland acute purulent strumitis.
The purulent thyroiditis arises owing to invasion of the thyroid by bacterial infection which spreads by
hematogenous or lymphogenous way. The infecting agent most often represented by pyogenic streptococcus
or staphylococcus aureus.
Morphologically according to the character of inflammation distinguished the plain and specific thyroiditis,
according to the course acute, subacute and chronic.
The acute thyroiditis mainly develops in one lobe. Histologically revealed formation of the necrotic foci,
hemorrhages, leukocytic infiltration of stroma with admixture of lymphocytes and macrophages.
The subacute thyroiditis (de Kerven) is histologically represented by the developments granulomatous
inflammation. The stroma is commonly infiltrated by lymphocytes, leukocytes and large cells, which remind
the cells of foreign bodies.
The chronic thyroiditis can manifest in the form of Hashimoto's and Riedel's goiter or specific thyroiditis
caused by tuberculosis, lues or actinomycosis.
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Distinguished acute purulent thyroiditis as diseases, which arise in unaltered thyroid gland, and acute purulent
strumitis the lesion of the goitrous transformed thyroid gland.
The onset of the disease is usually acute. It manifests by spontaneous sharp pain in the region of the neck,
which amplifies at movements, speech and swallowing, fever, chills, weakness, sweating and tachycardia. On
examination it is possible to note local reddening and swelling. Palpation reveals tissue tension, thyroid
enlargement, density, with fluctuation in the site of lesion. In blood observed neutrophil leukocytosis and
increased erythrocyte sedimentation rate.
The clinical course of the disease is characterized by the sings of purulent septic pathology of the neck. The
process spreads outside the thyroid. Late diagnostics and inappropriate treatment result in discharge of the
abscess outside, development of neck phlegmon, mediastinitis and sepsis. Nevertheless, in general, the
outcome is favorable, on the site of abscess replaced by fibrous tissue, and the function of gland tends to
norm.
The purulent thyroidites must be differentiated from simple thyroiditis and strumitis. The stormy course and
transformation of plane inflammation into purulent that detected clinically, and by means of diagnostic
puncture (purulent exudate) distinguish acute thyroiditis from the other inflammatory processes in thyroid
gland.
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Diagnostic puncture is necessary in order to confirm the diagnosis. If present fluctuation and purulent exudate
it is necessary to carry out surgical management (drainage of suppurative focus). Such patients require
antibiotics, analgesics, antiinflammatory and sedative agents.
AUTOIMMUNE THYROIDITIS
Autoimmune (lymphomatous) thyroiditis is the disease described by Hashimoto in 1912. In most cases it
occurs in women of age 40-50.
The basic etiologic factor in the development of autoimmune thyroiditis is the release and entering of thyroid
antigens into the blood as the result of inflammatory processes and traumas combined with surgical operations
on thyroid gland. It has been found the presence of antibodies to thyroglobulins, colloidal component of
thyroid gland and microsomal fraction. However the presence of antithyroid antibodies not always results in
the damage of the thyroid. The cytotoxic properties of these antibodies manifest only after their interaction
with -lymphocytes and HLA antigens.
The histological sign of autoimmune thyroiditis is the diffuse or focal thyroid infiltration by lymphocytes and
plasma cells, which results in destruction of follicles and their basal membranes. Further thyroid tissue is
replaced by connecting that leads to the focal fibrosis, which resemble nodes.
Distinguished diffuse and focal, and also hypertrophic and atrophic form of autoimmune thyroiditis.
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Hashimoto's thyroiditis is characterized by the slow growth of goiter, the thyroid density, and gradual
hypothyroidism. Besides develops the symptomatology, resulting from compression of organs and tissues of
the neck by goiter. The patients complain of enlargement of thyroid gland, sense of tightness in the neck,
difficult swallowing and breathing, pain in the region of gland and general weakness.
Enlargement of the thyroid is symmetric, it, as a rule, of dense consistence, and on palpation detected its
nodular character. During pressing on one of the lobe of thyroid gland the elevation of contrlateral lobe is
observed (the sign of "swing").
Autoimmune thyroiditis is characterized by the development of hypothyroidism. Nevertheless there are also
atypical clinical forms of the disease: autoimmune thyroiditis with thyrotoxicosis (Hashitoxicosis) with
gradual transferring into hypothyroidism, lesion of one lobe with clinical course according to the nodular type
of euthyroid or hypothyroid goiter. The autoimmune thyroiditis can arise in thyroid stump after surgery for
different forms of goiter. The combination of autoimmune thyroiditis with thyroid adenoma or cancer and its
transferring into chronic rarely occur.
Autoimmune thyroiditis can complicated with hypothyroidism, compression of neck organs, in some cases -
malignancy.
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It should be carried out with endemic and sporadic goiter, Riedel's fibrous goiter and thyroid cancer.
Symmetric enlargement of thyroid gland, its dense consistence, nodular character, presence of autoimmune
diseases in family history, high antibody capacity to thyroglobulins and microsomal fraction, development of
hypothyroidism, positive response as reducing of goiter at prednisolone assay (20 mg of prednisolone during
7-10 days) all these distinguish autoimmune thyroiditis from endemic and sporadic goiter, Riedel's
thyroiditis. It is usually impossible to differentiate autoimmune thyroiditis from thyroid cancer on the base of
clinical, instrumental and laboratory findings. In this case exclusive value has the morphological investigation
biopsy of thyroid gland or express histological investigation during operation. Macroscopically the gland is
of pale-pink- greyish color with yellowish tone (instead of red-brown in norm), with atrophic sheath and
thin-walled veins.
There is no specific therapy of autoimmune thyroiditis for today. The phenomena of hypothyroidism require
nominating of replaceable therapy by thyroid hormones (thyroidine, thyroxine). Glycocorticoids and
antihistamine agents are used in subacute form of autoimmune thyroiditis.
Surgery is applied in case of compression of the neck organs and suspicion on malignant tumour of the
thyroid. The volume of operation has been still controversial. Preserving operation (isthmusectomy in
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combination with wedge-like resection of lateral lobes, resection of thyroid gland) expedient only on initial
stages of the disease with maintained thyroid activity. Taking into account a reality of malignancy, often
relapses of goiter after small resections, the role of thyroid remnants as the foci of autoimmune aggression,
the thyroidectomy is performed. After such operation the patients till the end of life should take substitution
therapy by thyroid hormones. Is has been noticed, that after thyroidectomy, in comparison with thyroid
resection, the patients considerably better response to substitution therapy by thyroid hormones.
RIEDEL'S THYROIDITIS
Invasive fibrous Riedel's thyroiditis (synonyms Riedel's goiter, "woody" goiter) is the extremely rare
pathology, which consist of 0,005 % of persons undergone the surgery for different thyroid lesions. The
disease described by Riedel in 1894 and 1897, occurs mainly in males.
The etiology of the disease is still unknown. There is the hypothesis that the Riedel's thyroiditis is the similar
to such diseases, as idiopathic fibrous mediastinitis, sclerosing cholangitis and retrobulbar fibrosis. It gives the
suggestion that the fibrous lesions of different organs can be the manifestation of one disease. Some authors
suggest its infectious origin, though there are no reliable findings.
This disease is represented by the development of connective tissue in thyroid gland with further
transformation into a thick-fibber fibrous tissue. Between its layers there are small foci of adenomatous
parenchyma, mainly of a microfollicular structure. The fibrous connective tissue spreads outside the thyroid,
penetrates into muscles of the neck, untimely adherents to esophagus and trachea, causing their constriction
and deformity.
The patients complain of goiter, dysphagia, difficult respiration and changes of a vote quality (chestvoice)
down to aphonia. The gland becomes of woody or iron consistence, with change of configuration. Frequently
observed the signs of tracheal and esophageal compression.
The disease is characterized by severe "malignant" course with aggressive growth of a fibrous tissue, which
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can go on even after thyroid resection and after repeated operations for goiter relapse.
The function of the gland commonly preserved, though occasionally the course of disease complicated with
hypothyroidism.
The most common complication of the disease is compression of organs and tissues of the neck, which results
in dysphagia, dyspnea, and vocal changes.
Riedel's thyroiditis is necessary to differentiate with thyroid cancer. Such sings as nodular character,
metastases in lymph nodes of neck and paralysis of recurrent nerves, are characteristic for cancer. Owing to
high density of Riedel's thyroiditis a puncture biopsy of the thyroid is usually hardly performed. Thus, it is
necessary to carry out intraoperative histological investigation.
Macroscopically the adhesion of neck muscles with thyroid capsule is observed. The tissue of the gland is
grey, with pink foci, according to consistence resemble cartilage and homogeneous on incision.
The treatment of invasive fibrous Riedel's thyroiditis only surgical and consists of complete removal of
affected thyroid tissue. The advantage should be given to thyroidectomy.
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ANATOMY
Knowledge of the anatomy and embryology of the breast and the chest structures under it is
required not only for the performance of surgical procedures but also in planning therapeutic
radiation, predicting sites of locally recurrent disease, and assessing the adequacy of surgical
procedures used in an increasing number of therapeutic trials. Embryologically, the human
breast develops in the thickened portion of ectodermal tissue known as the milk streak coursing
from the pubis to the axilla in early fetal life. Late in the first trimester, the milk streak
atrophies, leaving only its pectoral portion, which continues to thicken and to form the nipple
bud. The entire gland then forms as a dermally derived organ lying within the subcutaneous
tissue in a manner similar to that of sweat gland development. The ductal system develops from
the nipple bud by invasion and downgrowth of primitive ectodermal cells from the nipple
surface. The mature breast parenchyma lies cushioned in fat between the layers of superficial
pectoral fascia. Between the deep layer of the superficial fascia and the fascial investment of
the pectoralis major muscle, the breast rests on a thin layer of loose areolar tissue, the
retromammary space, containing lymphatics and small vessels. When a total mastectomy is
performed, the correct plane is found under the pectoral fascia and includes the retromammary
space as emphasized by earlier surgeons and anatomists.
Deep to the pectoralis major muscle, the pectoralis minor muscle is enclosed in the
clavipectoral fascia that envelopes it and extends laterally to fuse with the axillary fascia. In a
standard modified radical mastectomy, dissection along the lateral border of the pectoralis
minor muscle divides the axillary fascia and exposes the contents of the axilla. The number of
lymph nodes found in the axillary space of patients undergoing mastectomy varies depending
on the extent of dissection and the diligence of methods used to identify these nodes. An upper
limit is established by the work of Durkin and Haagensen using ethanol clearing. These
investigators found an average of 50 nodes in 100 specimens obtained in the course of a
Halsted-type radical mastectomy. The current approach to less radical procedures has reduced
the number of nodes retrieved.
To standardize the extent of axillary dissection, the axillary space is arbitrarily divided into
three levels. Level I nodes are those in the external mammary, scapular, axillary vein, and
central axillary groups, which lie lateral to the lateral border of the pectoralis minor muscle.
Level II nodes are those in the central axillary group, which lie under the pectoralis minor
muscle. The level III nodes are difficult to visualize and remove unless the pectoralis minor
muscle is sacrificed or divided and include those subclavicular nodes medial to the minor
muscle. The apex of the axilla is defined by the costoclavicular ligament (Halsted's ligament),
at which point the axillary vein passes into the thorax and becomes the subclavian vein. Lymph
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nodes in the space between the pectoralis major and minor muscles are known as the
interpectoral group, or Rotter's nodes, described by Grossman and Rotter. Unless this group is
specifically exposed, they are not encompassed in surgical procedures that preserve the
pectoral muscles.
The lymphatic drainage of the breast is rich, and appreciation of the major pathways allows
one to predict the sites most commonly containing lymph-borne metastases. Lymphatic
channels within the breast follow centrifugal pathways from the subareolar plexus along major
lactiferous ducts and then along efferent veins to draining nodal beds. The major site of
drainage is to central axillary nodes. The internal mammary and interpectoral nodes, although
primary routes of lymph flow, are rarely the sites of nodal metastasis from breast cancer in the
absence of simultaneous axillary disease. Secondarily, the lymphatic spread of cancer is into
the high axillary nodes in the subclavicular chain and henceforth into the supraclavicular fossa.
As the surgeon endeavors to remove the lymph nodes of the axilla, a keen knowledge of the
nerve structures in the axilla is required to avoid their sacrifice. Coursing close to the chest
wall on the medial side of the axilla is the long thoracic nerve, or the external respiratory nerve
of Bell, which innervates the serratus anterior muscle. This muscle is important in fixation of
the scapula to the chest wall during adduction of the shoulder and extension of the arm, and its
denervation results in the winged scapula deformity. For this reason, the long thoracic nerve is
carefully preserved during standard axillary dissection. The second major nerve trunk
encountered during axillary dissection is the thoracodorsal nerve to the latissimus dorsi muscle
at the lateral border of the axilla. This nerve arises from the posterior cord of the brachial
plexus and enters the axillary space under the axillary vein, close to the entrance of the long
thoracic nerve, and then crosses the axilla to the medial surface of the latissimus dorsi muscle.
The thoracodorsal nerve is usually preserved during dissection of axillary nodes, unless its
sacrifice is required for complete removal of tumor-containing nodes.
Innervation of the pectoralis major muscle has gained the attention of some who emphasize
the advantage of protecting these nerves during modified radical mastectomy. Loss of
innervation results in a flaccid and atrophic muscle and a diminished tissue covering over the
chest wall after amputation of the breast. These investigators have named the pectoral nerves
according to their actual position as encountered during axillary dissection. The lateral pectoral
nerve has a variable course. In the majority of patients, the lateral pectoral nerve travels around
the lateral margin of the pectoralis minor muscle and is in a vulnerable position during the
division of the clavipectoral fascia and exposure of the axillary space. If possible, this branch
can be saved without compromising the dissection.
The final nerves of interest to the surgeon are the large sensory intercostal brachial or
brachial cutaneous nerves that span the axillary space and supply sensation to the undersurface
of the upper arm and skin of the chest wall along the posterior margin of the axilla. Cutting
these nerves, which is routinely done in removing the lymph node-containing tissues, causes
cutaneous anesthesia in these areas. It is helpful to emphasize this to the patients before
operation. Denervation of the areas supplied by these sensory nerves can cause chronic and
uncomfortable pain syndromes in a small percentage of patients. Contemporary surgeons have
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advocated preservation of the most superior brachial cutaneous nerve, which crosses the central
axilla to supply cutaneous sensation to the posterior upper arm. This nerve can be preserved
without compromising the axillary dissection in many patients.
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With pregnancy, there is diminution of the fibrous stroma to accommodate the hyperplasia
of the lobular units. This formation of many new acini or lobules is termed the adenosis of
pregnancy and is influenced by high circulating levels of estrogen and progesterone and by
levels of prolactin that steadily rise during gestation. After birth, there is sudden loss of the
placental hormones and the continued high level of prolactin. This may be the principal trigger
for lactation. The actual expulsion of milk is under hormonal control and is caused by the
contraction of the myoepithelial cells that surround breast ducts and terminal ductules. There is
no evidence for innervation of the myoepithelial cells; their contraction appears to be in
response to the pituitary-derived peptide oxytocin. Stimulation of the nipple appears to be the
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physiologic signal for continued pituitary secretion of prolactin and for the acute release of
oxytocin.
When breast feeding ceases there is a fall in prolactin and no stimulus for release of
oxytocin. The breast then returns to a resting state and to the cyclic changes induced when
menstruation begins again. With the approach of menopause, phases of the menstrual cycle
may not be as symmetrical and regular. This irregularity can induce functional nodularity and
breast pain where there had been none in earlier years. Menopause is defined by a cessation in
menstrual flow for a significant period of time (i.e., 6 months or more) and the variable
appearance of constitutional systems such as diaphoresis, minor psychological disturbances, or
even clinical depression. For the breast, menopause results in involution and a general decrease
in the epithelial elements of the resting breast. These changes include increased fat deposition,
diminished connective tissue, and the virtual disappearance of the lobular units. The
persistence of lobules, hyperplasia of the ductal epithelium, and even cyst formation can all
occur under the influence of exogenous ovarian hormones. Most commonly, hormones are
administered to relieve the symptoms of menopause, to prevent demineralization of bone, or to
slow the appearance of atherosclerosis. The surgeon evaluating patients at any age for breast
disease should inquire about the menstrual history, establish the cessation of menses in
postmenopausal women, and record the use of any exogenous hormones. It is important that the
pathologist who is examining biopsy material also have this information.
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nipples) are both common. Supernumerary nipples are usually rudimentary and occur along the
milk line from the axilla to the pubis in both males and females. They may be mistaken by the
patient for a small mole. However, accessory nipples are removed only for cosmetic reason.
True polythelia refers to more than one nipple serving a single breast and is very rare.
Accessory breast tissue is commonly located above the breast in the axilla. Rudimentary
nipple development may be present, and lactation is possible with more complete development.
Accessory breast tissue, which may present as an enlarging mass in the axilla during pregnancy,
is treated by surgical removal if it is large, cosmetically deforming, or to prevent enlargement
during future pregnancy.
Breast Imaging
The goal of any technique that seeks to image the breast is to extend the capability of
physical examination to either detect smaller abnormalities or to provide more information
about palpable abnormalities. Mammography is clearly the most sensitive and specific test that
can be used to complement the physical examination of the breast. It is used either as a
diagnostic modality that seeks to answer specific questions about the health of the breast or as
a screening test that seeks to find any abnormality within the breast. A variety of other methods
have been used to generate useful images of the breast. Of these, ultrasonography is the only
one in common use today. Thermography, which images heat generated by the breast, was
added to the Breast Cancer Detection Demonstration Project (BCDDP) to evaluate its
usefulness as a screening tool. However, because of a low overall yield, thermography was
dropped from the project. Computed tomography (CT) has been used by some investigators
with success but can require contrast medium enhancement, has limited ability to resolve small
abnormalities, and requires a larger exposure of radiation. CT appears to be the best way to
image internal mammary nodes and to evaluate the chest and axilla after mastectomy. Magnetic
resonance imaging (MRI) is a technique that requires expensive equipment. The long times
required to construct a suitable image are acceptable for diagnostic applications but prohibit
MRI as a screening tool. MRI may have a role in evaluating breasts that are difficult to image
or after prosthetic implantation. Digital imaging is an evolving hybrid technology that has
found application in chest radiography and may be used to store radiographic information in a
digital format or to directly produce images. This technology is improving and may have
application in mammography.
Diagnostic Mammography. Film-screen mammography has replaced xeromammography as
the standard breast imaging technology. Xeromammography was developed by the Xerox
corporation and produced a blue image viewed in ambient reflected light. Modern film-screen
mammography uses a combination of an enhancing screen and a molybdenum anode tube that
produces low kilovolt electron photons. The enhancing screen converts and amplifies a
low-energy radiation beam into high-energy photons that, in turn, expose a standard x-ray film.
This technique uses compression of the breast between plexiglass plates to lessen the thickness
of the tissue through which the radiation must pass and to separate adjacent structures and
improve resolution. The image, like standard x-rays, is viewed using transmitted light and is a
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negative image. Film-screen mammography delivers an average glandular dose of radiation that
is less than 100 mrad. (0.1 cGy. or 0.1 rad.). In comparison, the average dose to the center of
the breast in patients undergoing barium swallow is more than 10-fold the dose of two-view
mammography.
The mammographic features of malignancy can be broadly divided into density
abnormalities (including masses, asymmetries, and architectural distortions) and
microcalcifications. Each mammogram should also be assessed for the presence of
abnormalities in the axillary nodes and for the presence of skin or nipple changes, such as
thickening or retraction. These mammographic features can coexist in any one particular
abnormality and may exist in the presence or absence of physical findings. In fact, integration
of each of the radiographic features and the physical findings leads to a prediction of
malignancy.
Nonpalpable Mammographic Abnormalities. Mammographic abnormalities that cannot
be detected by physical examination are classified in three broad categories: (1) lesions
consisting of microcalcifications only, (2) density lesions (masses, architectural distortions,
and asymmetries), and (3) those with both calcifications and density abnormalities. The
incidence of malignancy after biopsy depends on the characteristics of the radiographic
finding. Lesions with both microcalcifications and a mass effect, spiculated masses, and linear
branching calcifications carry the highest probability of being malignant. However, even
well-defined densities can be malignant. To be certain, not every abnormality should undergo
biopsy, and recommendations must be made by the surgeon in consultation with an experienced
radiologist. For those patients not undergoing biopsy, interval mammograms must be done to
ensure stability of the abnormality.
If a biopsy is performed, it is usually done after mammographic placement of a needle or
hook wire. A newer alternative is automated stereotactic core-needle biopsy. This procedure
requires a large and dedicated unit, which is expensive. The patient generally lies prone with
the breast hanging through the table. A robotic arm and biopsy gun is positioned by
computerized analysis of triangulated mammographic images. A small amount of local
anesthesia is used at the point of core-needle entry into the breast. Firing the machine obtains a
core biopsy through the abnormality. Many series containing hundreds of patients have shown
good correlation between stereotactic biopsy and subsequent needle-placement open biopsy.
For lesions with calcification, a specimen radiograph must be done to confirm the presence of
the abnormality in the specimen. This is true for both stereotactic and open biopsy procedures.
Cooperation is required between the radiologist, surgeon, and pathologist for the correct
interpretation of biopsy material obtained by either technique. If stereotactic biopsy is available
to the surgeon, judgment must be used to determine the optimal biopsy strategy. Because
stereotactic biopsy does not remove the abnormality, a subsequent localization and open
procedure will be required if a cancer is found and the patient wishes to attempt breast
conservation. If the abnormality proves benign after stereotactic biopsy, follow-up
mammography needs to be done if the lesion is indeterminate. The false-negative rate of
stereotactic biopsy is low but finite.
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blue dome cysts, and they reflect the dark cyst fluid contained within. Grossly, they are usually
unilocular and lined by a smooth and glistening surface, although larger cystic structures may
be trabeculated and multiloculated. Histologically, cysts are frequently lined by a flattened
epithelium. However, the epithelial layer may display apocrine metaplasia or may have
papillary features. Intracystic carcinoma is exceedingly rare. Rosemond was able to report only
three examples in over 3000 cyst aspirations (0.1%), and other investigators confirm this
exceedingly low incidence. Regarding the risk of developing cancer for women with cystic
disease, no studies demonstrate an increased risk in women with small or microscopic cysts.
For patients with large cysts, called gross cystic disease by Haagensen, there remains some
controversy. Patey and Nurick found no increase in cancers subsequent to cyst aspiration. Of
810 cancers treated by Patey, only 10 had a previous history of gross cysts. Other recent
reviews have emphasized that women with gross cysts have a risk of twofold to fourfold that of
age-matched women without cysts. The studies of Page and associates and of Dupont and Page
do not show a significant increase in cancers after long-term follow-up of over 2000 women
who underwent biopsy of palpable cysts when compared with the slight increase borne by
women who have had breast biopsy alone.
Fibroadenoma and Related Tumors. Fibroadenoma (adenofibroma) is a benign tumor
composed of both stromal and epithelial elements in the breast.After carcinoma, fibroadenoma
is the second most common solid tumor in the breast and is the most common tumor in women
younger than age 30 years. The benign nature of this lesion was recognized in 1840 by Cooper,
who referred to the lesions as chronic mammary tumors. Clinically, they present as firm,
solitary tumors that may increase in size over several months of observation. They may be
lobulated but will slip easily under the examining fingers. At operation, fibroadenomas appear
to be well-encapsulated masses that may easily detach from the surrounding breast tissue. By
history, fibroadenoma is favored over cyst in the adolescent or young adult; and on
examination, these tumors are distinguished from cysts by the needle aspiration that yields no
fluid. Mammography is of little help in distinguishing between cysts and fibroadenomas;
however, ultrasound usually clearly shows the cavity of a cyst. The gross appearance and
histopathology are distinctive of fibroadenoma. Grossly, the tumor appears well encapsulated,
with smooth borders that may be lobulated. Histologically, a variable proportion of epithelial
and stromal proliferation is present, and the stroma may be quite cellular or replaced by
acellular swirls of collagen. In older patients, the lesions may contain deposits of calcium
within dense fibrosis. The epithelium can display the entire spectrum of proliferative changes
seen elsewhere in the breast. Although fibroadenomas are not considered to have a malignant
potential, the epithelial elements appear to be at risk for neoplasia just as epithelium elsewhere
in the breast. More than 100 invasive and noninvasive carcinomas have been reported in
preexisting fibroadenomas since 1985. Most of these (50%) have been lobular carcinoma in
situ, 35% were infiltrating carcinomas, and 15% were intraductal carcinoma. The risk of cancer
in a newly discovered fibroadenoma found in the breast of a young woman is obviously
exceedingly rare and is not an issue that influences treatment. A modest risk of subsequent
carcinoma in women who have previously been treated for fibroadenoma has been reported, but
the magnitude is about two times the general population. This is only slightly higher than the
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reported excess risk for all women who have had a breast biopsy.
The treatment of fibroadenoma follows that for any unexplained solid mass within the
breast. The great majority of patients in the United States are treated by excisional biopsy to
remove the tumor and establish the diagnosis. It is worth recognizing that a different approach
is taken by physicians in other countries. A typical fibroadenoma is frequently left untreated by
European physicians when the tumor is encountered in the breast of a young women. If
excision is recommended, the approach to a young women with a typical fibroadenoma on
examination should be very different than the approach in older women with indeterminate
masses. Cosmetic incisions around the areola with a modest amount of tunneling to remove the
lesion are commonly used techniques and are proper for the treatment of fibroadenoma.
Emphasis should be placed on removing a minimum amount of breast tissue adjacent to a
typical fibroadenoma. If the gross appearance is that of a fibroadenoma, frozen section is
superfluous, the patient can be immediately reassured, and final diagnosis can be established
by inspecting permanent sections.
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Breast Abscess and Infections. Breast abscess commonly occurs in the subareolar breast
tissue and may be recurrent and difficult to treat. Although the exact cause is not known,
subareolar duct ectasia and obstruction of major ducts may lead to proliferation of bacteria and
subsequent abscess. Further destruction of the normal ductal openings leads to fistula
formation and chronic recurrent abscess. Mammary duct ectasia, first named by Haagensen, is
an inflammatory condition that causes distortion and dilation of the lactiferous sinuses under
the nipple. It is a common entity and is frequently responsible for nipple inversion in older
women. In understanding subareolar abscess and probably mastitis in general, it is useful to
remember that the nipple and areolar complex contains secretory ducts that are exposed to the
environment. Chronic inflammation, duct dilation, and obstruction may combine at the nipple
to produce circumstances that favor bacterial invasion.
The treatment of acute abscess of periareolar tissue should be conservative if possible.
Antibiotics with broad-spectrum coverage should be used initially. More severe infections may
require hospitalization and intravenous antibiotics. A small incision with drainage is preferred
if the process cannot be controlled by antibiotics alone. Needle aspiration may be attempted,
but the abscess cavity is usually multiloculated. Recurrent infection is best treated by excision
of the diseased subareolar ducts as described by Haagensen and others. However, recurrence is
common and leads to chronic and recurring infection.
Mastitis describes a more generalized cellulitis of breast tissue that may involve a large area
of the breast but may not form a true abscess. The etiology appears to be an ascending infection
beginning in subareolar ducts and extending outward from the nipple. Occasionally, mastitis
involves areas of cystic disease and may be sterile. Mastitis presents with erythema of the
overlying skin, pain, and tenderness to palpation. There is induration of the skin and
underlying breast parenchyma. Especially in young women, an apparent mastitis may develop
that is dramatic in its presentation and responds poorly to antibiotics but resolves
spontaneously. The etiology is unknown but may be related to menstrual cycle irregularity.
More commonly, mastitis complicates lactation, possibly due to inspissation of milk,
obstruction, and secondary infection. Local measures such as application of heat, ice packs, or
use of a mechanical breast pump on the affected side have all been recommended. If
conservative measures are not effective, administration of broad-spectrum antibiotics is usually
indicated. In many situations, the differential diagnosis of acute mastitis includes inflammatory
carcinoma. It is important to follow patients with mastitis and confirm that there has been a
complete resolution of symptoms and signs. The erythema produced by an inflammatory
carcinoma will not resolve with conservative measures and generally will worsen in a short
period of follow-up.
Papilloma and Related Ductal Tumors. Solitary intraductal papillomas are true polyps
of epithelial-lined breast ducts. Solitary papillomas are located under the areola in the majority
of cases. In contrast, certain patients have multiple intraductal papillomas that Haagensen
believes are more likely to be peripherally located and associated with an increased risk of
cancer. Solitary papillomas may be located in peripheral ducts and can grow to large size,
presenting as a breast mass. When papillomas attain a large size, they may appear to arise
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within a cystic structure, probably representing a greatly expanded duct. In general, these
lesions are less than 1 cm. but can grow to as large as 4 or 5 cm.
Tumors under the nipple and areolar complex often present with a bloody nipple discharge.
Less frequently, they are discovered as a palpable mass under the areola or as a density lesion
on the mammogram. Treatment is total excision through a circumareolar incision. The surgeon
must keep in mind that one of the most difficult areas in differential diagnosis is between a
papilloma and invasive papillary carcinoma. Because these lesions can infarct, scar, and even
develop squamous metaplasia, they can appear bizarre and disordered. Most pathologists urge
evaluation on permanent sections for the majority of papillary lesions before more extensive
surgery is undertaken.
It is also important not to confuse the commonly used term papillomatosis with either
solitary or multiple papillomas. Papillomatosis refers to epithelial hyperplasia that commonly
occurs in younger women or is associated with fibrocystic change. This lesion is not composed
of true papillomas. Hyperplastic epithelium in papillomatosis may fill individual ducts like a
true polyp but has no stalk of fibrovascular tissue nor the frondlike growth. Solitary papillomas
are entirely benign and do not predispose to development of cancer in the patients who have
them. Page and Anderson state that the degree of subsequent risk for breast cancer in patients
with either papillomatosis or with true papillomas, either solitary or multiple, relates to the
degree of atypical epithelial proliferation associated with them.
Epidemiology
The likelihood of developing breast cancer is highly dependent on both age and the interval
over which an individual is at risk. Although the lifetime risk of developing breast cancer is
estimated at 10%, more than one half of patients with breast cancer are older than 65.
Furthermore, the 10% figure is based on a hypothetical interval that extends from birth to age
110. A more realistic view considers risk starting at a particular age and extends over a finite
period of time. For instance, the chance that a woman age 35 will develop breast cancer during
the next two decades of her life, until age 55, is only 2.5%. A woman who is 50 has close to a
5% chance of developing cancer before she turns 75 and a 65-year-old woman has a 5.5%
chance of getting breast cancer before she turns 85 years of age. These figures apply to white
women in the United States; the same idealized African-American woman has a lifetime risk of
breast cancer that is 7% or 8%.
The odds of dying of breast cancer over the ideal lifetime of birth to 110 are about 3.6%.
Although carcinoma of the lung has overtaken breast cancer as the leading cause of cancer-
related death in American women, breast cancer remains far more common. Of 595,000 new
cases of cancer among women in 1996, 186,000 occurred in the breast while 78,000 arose in
the lung.
Several studies based on cancer registries in the SEER program of the NCI have reported an
increasing attack rate for breast cancer in the United States. In Washington State there has been
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an annual estimated increase of 2.5%. A greater increase was apparent among black and
low-income women. In the Connecticut Tumor Registry the overall annual incidence rose from
53 cases per 100,000 women during the years 1935 to 1939 to an average annual rate of 86.4
per 100,000 for the years 1975 to 1979. The annual rate of increase during 1980 to 1985
averaged 3%; during the past 5 years, this rate of increase has declined to about 1% per year.
Data from other studies and from other western countries confirm the increase in the incidence
of breast cancer. Despite this increased incidence, the age-adjusted death rate from carcinoma
of the breast was stable until 1979 and may have decreased in the 5-year period between 1979
and 1984. Although it is tempting to speculate that this is a real improvement attributable to
early diagnosis or improved therapy, no direct proof can be cited.
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central detritus can undergo dystrophic calcification that is fine, focally clustered, and even
linear and branching when seen on high-quality mammography. This process can locally
produce a palpable mass if multiple ducts are involved.
Subtypes of DCIS are now well recognized and frequently reported pathologically. The
solid or comedo type is most common and probably more virulent. Papillary or cribriform
DCIS are characterized by papillary projections of tumor cells into the ductal lumen or by the
presence of a branching, cribriform pattern filling ducts. These types are less likely to form
palpable masses and uncommonly calcify to produce a mammographic abnormality. However, it
is important to emphasize that these subtypes can coexist and that DCIS is best described by
the pathologist in terms of its extent, multicentricity, and involvement of the surgical margin.
Confusion arises in a number of ways. First, the uninitiated may confuse the term infiltrating
ductal carcinoma with the term intraductal carcinoma; the former is invasive disease and the
latter is noninvasive disease. Second, these two stages of tumorigenesis usually coexist,
particularly when they are carefully searched for in pathologic specimens. Finally, as discussed
later, the treatment and outcome for patients with intraductal disease may depend on variables
such as multifocality, multicentricity, and extent of disease in a way more demanding for the
pathologists and surgeons than in the past.
Lobular Carcinoma in Situ (LCIS) or Lobular Neoplasia. This disease of the breast
lobules or acini was first clearly delineated by Foote and Stewart in 1941, who gave it the name
lobular carcinoma in situ. Haagensen first used the term lobular neoplasia to emphasize its
more benign course. Pathologically, it is a proliferation of small round epithelial cells within
lumens of multiple breast acini. The resulting picture is multiple clusters of epithelial cells
forming islands of neoplastic cells but maintaining a lobular architecture. Although the ducts
expand with proliferating cells, they usually do not reach the large size seen with DCIS.
Unlike DCIS, LCIS never forms a palpable mass by itself and is therefore not recognized on
physical examination. In addition, there are no mammographic findings in LCIS. It does not
form a density and rarely calcifies, both of which are typical for DCIS. Therefore, this is a
disease that is recognized incidentally after biopsy for another abnormality that is producing a
clinical or mammographic finding. The treatment of this incidental pathologic entity remains
controversial and is reviewed later.
Infiltrating Ductal Carcinoma. This is the most common malignant tumor in the breast
recognized after biopsy. The term ductal carcinoma refers to its origin from ductal epithelium;
infiltrating describes its growth pattern and distinguishes this lesion from noninvasive
carcinoma. Some add the terms not otherwise specified (NOS) and no special type (NST) to
emphasize that this disease is diagnosed after the other, more distinctive histologies have been
eliminated. The tumor infiltrates into a variable amount of stroma as cords or islands of
malignant epithelium. It may form primitive glandular forms, but not to the extent of a pure
tubular carcinoma. As discussed, and as reflected in the WHO classification, many infiltrating
carcinomas display an in situ component. This fact reflects its ductal origin and may be used to
prove a mammary origin of the tumor. The stromal reaction may be intense and has led to the
older term scirrhous carcinoma of the breast.
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cell layer, and with an open central space. The tumor is characteristically small, is scirrhous,
and has an excellent prognosis after treatment. The descriptions of these histologic variants
refer to their predominant features. However, each may coexist with more undifferentiated
infiltrating carcinoma of the usual type. In general, if the tumor is composed of definite
infiltrating ductal carcinoma of poor differentiation, the final diagnosis reflects the poorest
histologic pattern. Because tubular and mucinous variants are less likely to metastasize, some
modern breast surgeons tailor their primary approach to these lesions by, for instance, omitting
axillary node dissections for small and well-differentiated lesions.
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the application of this procedure alone. Other studies document both the strengths and
weaknesses of maximal local therapy represented by this procedure. The personal series of
Haagensen reports results from treatment of 1036 patients; 727 patients with clinically negative
nodes (Stage A, Columbia clinical staging) had a survival of 72.4% at 10 years. In contrast,
only 42.3% of clinically node-positive patients (Stage B) survived at 10 years. These figures
were confirmed by the National Surgical Adjuvant Breast and Bowel Project (NSABP) early
trial of adjuvant thiotepa. By 10 years, 76% of patients with histologically positive nodes
suffered recurrence of breast cancer and one fourth of patients with negative nodes failed
surgical treatment. In contrast, local failure rates have been extremely low since introduction of
the Halsted radical mastectomy. Published figures are generally between 5% and 7% and
provide the standard against which newer procedures are judged.
The extended radical mastectomy is a standard radical mastectomy to which en bloc removal
of internal mammary nodes is added. This procedure was popularized in the United States by
Urban, who reported a 35.5% 10-year survival in patients undergoing extended radical
mastectomy. Other studies have resulted in abandonment of the extended procedure. A large
prospective trial and several uncontrolled series have failed to provide evidence of improved
clinical outcome after extended radical mastectomy.
Modified Radical Mastectomy.Modified radical mastectomy refers to a procedure
combining total mastectomy with removal of axillary lymph nodes in continuity with the
mastectomy specimen. This is the most widely used procedure to treat operable breast cancer
and is the alternative to breast-sparing procedures described later. Modified radical mastectomy
leaves the pectoralis major muscle intact, providing a soft tissue covering over the chest wall
and a normal-appearing junction of the shoulder with the anterior chest wall and avoiding the
hollow defect inferior to the clavicle that accompanies the removal of the pectoralis muscle.
The patient is left with intact musculature around the shoulder and a situation that is well
suited to prosthetic reconstruction. Two forms of the procedure are in use by surgeons: the
Patey procedure and modifications described by Scanlon and the procedure described by
Auchincloss.
Patey, at the Middlesex Hospital in London, developed a procedure that preserves the
pectoralis major muscle and sacrifices the underlying pectoralis minor muscle to remove levels
I, II, and III lymph nodes in the axilla. A large number of Patey procedures performed by
Handley, who wrote extensively about this procedure, were reviewed independently and
reported by Donegan and associates. The survival of patients with negative axillary nodes was
82% at 10 years with a local recurrence rate of 5%. For patients with positive nodes, the
survival was 48%, very similar to results with radical mastectomy. Thus, preservation of the
pectoralis major muscle did not appear to produce inferior results. Scanlon modified the Patey
procedure by dividing but not removing the pectoralis minor muscle, allowing removal of apical
(level III) nodes and preservation of the lateral pectoral nerves to the major muscle.
The procedure described by Auchincloss differs from the Patey procedure by not removing
or dividing the pectoralis minor muscle. This modification limits the complete removal of high
axillary nodes but is justified by Auchincloss, who calculated that only 2% of patients will
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potentially benefit by removal of the highest level nodes. It is probable that the Auchincloss
mastectomy was the most popular procedure for breast cancer in the United States during the
past decade.
Wide Local Excision and Primary Radiation Therapy. Excision of the primary tumor
with preservation of the breast has been referred to by many names, including partial
mastectomy, segmentectomy, tylectomy, or lumpectomy. Wide local excision seems to be the
most descriptive term for the procedure, which removes the malignancy with a surrounding rim
of grossly normal breast parenchyma. An even more aggressive local procedure designed to
remove 1 to 2 cm. of adjacent breast and overlying skin is called quadrantectomy. In modern
practice, these more limited surgical procedures are applied as part of a multidisciplinary
approach to breast cancer and always include postoperative radiation therapy, giving at least
4500 cGy. to the whole breast and usually including a boost of radiation to the tumor bed.
Axillary dissection is done through a separate incision in the majority of patients. Therefore,
conservative breast surgery or breast preservation usually refers to wide local excision of the
primary tumor, whole breast radiation, and a separate axillary dissection.
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were present in only 5 of these; in one case a second primary invasive cancer in the ipsilateral
breast was present. Although not all patients underwent axillary dissection, there were no
nodal recurrences during the follow-up of these patients. Significantly, all patients with
positive nodes had large tumors, palpable tumors, or microscopic invasion
Many authors who have written about intraductal carcinoma are influenced by the high
incidence of multicentric, multifocal, and even bilateral disease. Multifocal is a term referring
to disease within the vicinity or same quadrant as the dominant lesion. Multicentric refers to
disease in distant sites or quadrants within the same breast. Bilateral implies the concurrent
finding of disease in both breasts. The existence of multicentric disease has led many to favor
mastectomy for the treatment of DCIS, and concerns about bilaterality have prompted the use
of prophylactic procedures on the contralateral breast. The most widely reported figure for the
incidence of multicentric disease within the ipsilateral breast is 33%, or one third of cases in
which a biopsy discloses intraductal cancer as the predominant lesion. However, estimates vary
depending on how extensively other quadrants of the breast are examined. For example,
although a large review of NSABP material failed to find multicentric disease, only a single
random section from remote quadrants was examined. In contrast, Schwartz reported an
incidence of approximately 37% after examining four random sections from each remote
quadrant and from under the areola. Other estimates range between the results of these two
studies. The risk of multicentric disease appears to depend both on the histologic type of the
intraductal tumor and on the size or extent of the primary cancer. In the study of Lagios and
associates, 2 of 24 small tumors less than 2 cm. (8%) were associated with disease in other
quadrants of the breast. In moderate size tumors, between 2 and 5 cm., 2 breasts of 16
examined (12.5%) had multicentric disease. In large tumors whose extent was greater than 5
cm., all 13 cases examined had disease in remote quadrants of the ipsilateral breast. The study
of Patchefsky and colleagues examined multicentricity as a function of the histology of the
primary tumor. In agreement with other authors, this series found that micropapillary pathology
was associated with a high (80%) incidence of multicentric disease. An intermediate percentage
(40%) of papillary and comedocarcinomas were associated with remote disease, and solid and
cribriform types were lowest. Size was not noted in this study. Pathologic review of DCIS
should include an estimate of size, a comment about pathologic margins, and assessment of
multifocal disease within the surgical specimen. Histologic type should be noted and a
statement made about the presence or absence of microscopic invasion.
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LCIS (lobular neoplasia) treated by biopsy and careful observation, Haagensen determined the
actuarial probability of developing carcinoma at the end of 35 years was 21.4%. Compared
with the Connecticut Tumor Registry data, a risk ratio (observed to expected cases) of 7:1 was
calculated. Significantly, 40% of the carcinomas that subsequently developed were purely in
situ lesions and one half of all subsequent carcinomas occurred in the contralateral breast.
Haagensen preferred a practice of close observation after a biopsy diagnosis of LCIS. Similar
data have led others to express doubts about the need for mastectomy. These authors have
recommended a conservative policy of close observation after a biopsy diagnosis of LCIS or
lobular neoplasia.
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17. Orgiazzi J, Madec AM, Ducottet X: The role of stimulating, function-blocking and growth-blocking
anti-TSH receptor antibodies (TRAbs) in GD, Hashimoto's disease and in atrophic thyroiditis. Ann Endocrinol
(Paris) 64:31, 2003. [PMID: 12707631]
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18. Pasieka JL: Hashimoto's disease and thyroid lymphoma: Role of the surgeon. World J Surg 24:966, 2000.
[PMID: 10865042]
19. Owen PJ, Lazarus JH: Subclinical hypothyroidism: The case for treatment. Trends Endocrinol Metab
14:257, 2003. [PMID: 12890589]
20. De M, Jaap A, Dempster J: Tamoxifen therapy in steroid-resistant Riedel's disease. Scott Med J 47:12,
2002. [PMID: 11980291]
21. Knudsen N, Laurberg P, Perrild H, et al: Risk factors for goiter and thyroid nodules. Thyroid 12:879,
2002. [PMID: 12487770]
22. Williams D: Cancer after nuclear fallout: Lessons from the Chernobyl accident. Nat Rev Cancer 2:543,
2002. [PMID: 12094241]
23. Hemminki K, Li X: Familial risk of cancer by site and histopathology. Int J Cancer 103:105, 2003.
[PMID: 12455061]
24. Morgan JL, Serpell JW, Cheng MS: Fine-needle aspiration cytology of thyroid nodules: How useful is it?
Aust N Z J Surg 73:480, 2003. [PMID: 12864820]
25. Segev DL, Umbricht C, Zeiger MA: Molecular pathogenesis of thyroid cancer. Surg Oncol 12:69, 2003.
[PMID: 12946479]
26. Nikiforov YE: RET/PTC rearrangement in thyroid tumors. Endocr Pathol 13:3, 2002. [PMID: 12114746]
27. Cheung L, Messina M, Gill A, et al: Detection of the PAX8-PPAR gamma fusion oncogene in both
follicular thyroid carcinomas and adenomas. J Clin Endocrinol Metab 88:354, 2003. [PMID: 12519876]
28. Hay ID, Grant CS, Taylor WF, et al: Ipsilateral lobectomy versus bilateral lobar resection in papillary
thyroid carcinoma: A retrospective analysis of surgical outcome using a novel prognostic scoring system.
Surgery 102:1088, 1987. [PMID: 3686348]
29. Cady B, Rossi R: An expanded view of risk-group definition in differentiated thyroid carcinoma. Surgery
104:947, 1988. [PMID: 3194846]
30. AJCC Cancer Staging Manual, 6th ed. New York: Springer-Verlag, 2002.
31. DeGroot LJ, Kaplan EL, McCormick M, et al: Natural history, treatment, and course of papillary thyroid
carcinoma. J Clin Endocrinol Metab 71:414, 1990. [PMID: 2380337]
32. Kebebew E, Clark OH: Differentiated thyroid cancer: "Complete" rational approach. World J Surg
24:942, 2000. [PMID: 10865038]
33. Cady B, Sedgwick CE, Meissner WA, et al: Risk factor analysis in differentiated thyroid cancer. Cancer
43:810, 1979. [PMID: 427722]
34. Mazzaferri EL, Jhiang SM: Long-term impact of initial surgical and medical therapy on papillary and
follicular thyroid cancer. Am J Med 97:418, 1994. [PMID: 7977430]
35. Hay ID, Grant CS, Bergstralh EJ, et al: Unilateral total lobectomy: Is it sufficient surgical treatment for
patients with AMES low-risk papillary thyroid carcinoma? Surgery 124:958, 1998. [PMID: 9854569]
36. Mazzaferri EL, Massoll N: Management of papillary and follicular (differentiated) thyroid cancer: New
paradigms using recombinant human thyrotropin. Endocr Relat Cancer 9:227, 2002. [PMID: 12542401]
37. Sivanandan R, Soo KC: Pattern of cervical lymph node metastases from papillary carcinoma of the
thyroid. Br J Surg 88:1241, 2001. [PMID: 11531874]
38. Haigh PI: Follicular thyroid carcinoma. Curr Treat Options Oncol 3:349, 2002. [PMID: 12074771]
39. Thompson LD, Wieneke JA, Paal E, et al: A clinicopathologic study of minimally invasive follicular
carcinoma of the thyroid gland with a review of the English literature. Cancer 91:505, 2001. [PMID:
11169933]
40. Lopez-Penabad L, Chiu AC, Hoff AO, et al: Prognostic factors in patients with Hrthle cell neoplasms of
the thyroid. Cancer 97:1186, 2003. [PMID: 12599224]
41. Mazzaferri EL, Robbins RJ, Spencer CA, et al: A consensus report of the role of serum thyroglobulin as a
monitoring method for low-risk patients with papillary thyroid carcinoma. J Clin Endocrinol Metab 88:1433,
2003. [PMID: 12679418]
42. Kim TH, Yang DS, Jung KY, et al: Value of external irradiation for locally advanced papillary thyroid
cancer. Int J Radiat Oncol Biol Phys 55:1006, 2003. [PMID: 12605980]
43. Clayman GL, el-Baradie TS: Medullary thyroid cancer. Otolaryngol Clin North Am 36:91, 2003. [PMID:
53 of 56 1.5.2014 18:16
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12803011]
44. Brandi ML, Gagel RF, Angeli A, et al: Guidelines for diagnosis and therapy of MEN type 1 and type 2. J
Clin Endocrinol Metab 86:5658, 2001. [PMID: 11739416]
45. Pasieka JL: Anaplastic thyroid cancer. Curr Opin Oncol 15:78, 2003. [PMID: 12490766]
46. Giuffrida D, Ferrau F, Pappalardo A, et al: Metastasis to the thyroid gland: A case report and review of
the literature. J Endocrinol Invest 26:560, 2003. [PMID: 12952372]
47.Hedayati N, McHenry CR: The clinical presentation and operative management of nodular and diffuse
substernal thyroid disease. Am Surg 68:245, 2002. [PMID: 11893102]
48. Fewins J, Simpson CB, Miller FR: Complications of thyroid and parathyroid surgery. Otolaryngol Clin
North Am 36:189, 2003. [PMID: 12803016]
49. Akerstrom G, Malmaeus J, Bergstrom R: Surgical anatomy of human parathyroid glands. Surgery 95:14,
1984. [PMID: 6691181]
50. Gilmour JR: The gross anatomy of the parathyroid glands. J Pathol 46:133, 1938.
51.Carling T: Molecular pathology of parathyroid tumors. Trends Endocrinol Metab 12:53, 2001. [PMID:
11167122]
52. Awad SS, Miskulin J, Thompson N: Parathyroid adenomas versus four-gland hyperplasia as the cause of
primary hyperparathyroidism in patients with prolonged lithium therapy. World J Surg 27:486, 2003. [PMID:
12658498]
53. Skogseid B: Multiple endocrine neoplasia type 1. Br J Surg 90:383, 2003. [PMID: 12673737]
54. Arnold A, Shattuck TM, Mallya SM, et al: Molecular pathogenesis of primary hyperparathyroidism. J
Bone Miner Res 17:N30, 2002.
55. Talpos GB, Bone HG 3rd, Kleerekoper M, et al: Randomized trial of parathyroidectomy in mild
asymptomatic primary hyperparathyroidism: Patient description and effects on the SF-36 health survey.
Surgery 128:1013, 2000. [PMID: 11114637]
56. Sheldon DG, Lee FT, Neil NJ, et al: Surgical treatment of hyperparathyroidism improves health-related
quality of life. Arch Surg 137:1022, 2002. [PMID: 12215152]
57. Pasieka JL, Parsons LL, Demeure MJ, et al: Patient-based surgical outcome tool demonstrating alleviation
of symptoms following parathyroidectomy in patients with primary hyperparathyroidism. World J Surg
26:942, 2002. [PMID: 12016473]
58. Nappi S, Saha H, Virtanen V, et al: Left ventricular structure and function in primary hyperparathyroidism
before and after parathyroidectomy. Cardiology 93:229, 2000. [PMID: 11025348]
59. Vestergaard P, Mollerup CL, Frokjaer VG, et al: Cardiovascular events before and after surgery for
primary hyperparathyroidism. World J Surg 27:216, 2003. [PMID: 12616440]
60. Wermers RA, Khosla S, Atkinson EJ, et al: Survival after the diagnosis of hyperparathyroidism: A
population-based study. Am J Med 104:115, 1998. [PMID: 9528728]
61. Deftos LJ: Hypercalcemia in malignant and inflammatory diseases. Endocrinol Metab Clin North Am
31:141, 2002. [PMID: 12055985]
62. Scholz DA, Purnell DC: Asymptomatic primary hyperparathyroidism: 10-Year prospective study. Mayo
Clin Proc 56:473, 1981. [PMID: 7266058]
63. Silverberg SJ, Shane E, Jacobs TP, et al: A 10-year prospective study of primary hyperparathyroidism with
or without parathyroid surgery. N Engl J Med 341:1249, 1999. [PMID: 10528034]
64. Anonymous: Proceedings of the NIH Consensus Development Conference on diagnosis and management
of asymptomatic primary hyperparathyroidism. Bethesda, Maryland, October 2931, 1990. J Bone Miner Res
6:S1, 1991.
65. Bilezikian JP, Potts JT Jr., El-Hajj Fuleihan G, et al: Summary statement from a workshop on
asymptomatic primary hyperparathyroidism: A perspective for the 21st century. J Clin Endocrinol Metab
87:5353, 2002. [PMID: 12466320]
66. Hedback G, Oden A: Increased risk of death from primary hyperpar-athyroidismAn update. Eur J Clin
Invest 28:271, 1998. [PMID: 9615902]
67. Sosa JA, Udelsman R: Minimally invasive parathyroidectomy. Surg Oncol 12:125, 2003. [PMID:
12946483]
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68.Fujii H, Kubo A: Sestamibi scintigraphy for the application of minimally invasive surgery of
hyperfunctioning parathyroid lesions. Biomed Pharmacother 56:7s, 2002.
69. Banzo I, Pena FJ, Allende RH, et al: MIBI SPECT and radioguided surgery in the accurate location of a
posterior mediastinal parathyroid adenoma. Clin Nucl Med 28:584, 2003. [PMID: 12819415]
70. Proctor MD, Sofferman RA: Intraoperative parathyroid hormone testing: What have we learned?
Laryngoscope 113:706, 2003. [PMID: 12671433]
71. Udelsman R, Donovan PI, Sokoll LJ: One hundred consecutive minimally invasive parathyroid
explorations. Ann Surg 232:331, 2000. [PMID: 10973383]
72. Perrier ND, Ituarte PH, Morita E, et al: Parathyroid surgery: Separating promise from reality. J Clin
Endocrinol Metab 87:1024, 2002. [PMID: 11889156]
73. Perrier ND, Ituarte P, Kikuchi S, et al: Intraoperative parathyroid aspiration and parathyroid hormone
assay as an alternative to frozen section for tissue identification. World J Surg 24:1319, 2000. [PMID:
11038200]
74. Lentsch EJ, Withrow KP, Ackermann D, et al: Parathyromatosis and recurrent hyperparathyroidism. Arch
Otolaryngol Head Neck Surg 129:894, 2003. [PMID: 12925351]
75. Wells SA Jr., Debenedetti MK, Doherty GM: Recurrent or persistent hyperparathyroidism. J Bone Miner
Res 17:N158, 2002.
76. Ziegler R: Hypercalcemic crisis. J Am Soc Nephrol 12:S3, 2001.
77. Llach F, Velasquez Forero F: Secondary hyperparathyroidism in chronic renal failure: Pathogenic and
clinical aspects. Am J Kidney Dis 38:S20, 2001.
78. Chou FF, Lee CH, Shu K, et al: Improvement of sexual function in male patients after parathyroidectomy
for secondary hyperparathyroidism. J Am Coll Surg 193:486, 2001. [PMID: 11708504]
79. Nichol PF, Starling JR, Mack E, et al: Long-term follow-up of patients with tertiary hyperparathyroidism
treated by resection of a single or double adenoma. Ann Surg 235:673, 2002. [PMID: 11981213]
80. Marx SJ: Hyperparathyroid and hypoparathyroid disorders. N Engl J Med 343:1863, 2000. [PMID:
11117980]
81. Auchus RJ: Aldo is back: Recent advances and unresolved controversies in hyperaldosteronism. Curr
Opin Nephrol Hypertens 12:153, 2003. [PMID: 12589175]
82. Jackson RV, Lafferty A, Torpy DJ, et al: New genetic insights in familial hyperaldosteronism. Ann N Y
Acad Sci 970:77, 2002. [PMID: 12381543]
83. Stewart PM: Mineralocorticoid hypertension. Lancet 353:1341, 1999. [PMID: 10218547]
84. Espiner EA, Ross DG, Yandle TG, et al: Predicting surgically remedial primary aldosteronism: Role of
adrenal scanning, posture testing, and adrenal vein sampling. J Clin Endocrinol Metab 88:3637, 2003.
[PMID: 12915648]
85. Raff H, Findling JW: A physiologic approach to diagnosis of the Cushing syndrome. Ann Intern Med
138:980, 2003. [PMID: 12809455]
86. Putignano P, Toja P, Dubini A, et al: Midnight salivary cortisol versus urinary free and midnight serum
cortisol as screening tests for Cushing's syndrome. J Clin Endocrinol Metab 88:4153, 2003. [PMID:
12970280]
87. Ng L, Libertino JM: Adrenocortical carcinoma: Diagnosis, evaluation and treatment. J Urol 169:5, 2003.
[PMID: 12478091]
88. Copeland PM: The incidentally discovered adrenal mass. Ann Intern Med 98:940, 1983. [PMID:
6344711]
89. Baudin E, Pellegriti G, Bonnay M, et al: Impact of monitoring plasma 1,1-dichlorodiphenildichloroethane
(op'-DDD) levels on the treatment of patients with adrenocortical carcinoma. Cancer 92:1385, 2001. [PMID:
11745214]
90. Gmyrek GA, New MI, Sosa RE, et al: Bilateral laparoscopic adrenalectomy as a treatment for classic
congenital adrenal hyperplasia attributable to 21-hydroxylase deficiency. Pediatrics 109:E28, 2002.
91. Pederson LC, Lee JE: Pheochromocytoma. Curr Treat Options Oncol 4:329, 2003. [PMID: 12943613]
92. Lenders JW, Pacak K, Walther MM, et al: Biochemical diagnosis of pheochromocytoma: Which test is
best? JAMA 287:1427, 2002. [PMID: 11903030]
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93. Sackett WR, Bambach CP: Bilateral subtotal laparoscopic adrenalectomy for phaeochromocytoma. Aust
N Z J Surg 73:664, 2003. [PMID: 12887546]
94. Kanauchi H, Wada N, Clark OH, et al: Apoptosis regulating genes, bcl-2 and bax, and human telomerase
reverse transcriptase messenger RNA expression in adrenal tumors: Possible diagnostic and prognostic
importance. Surgery 132:1021, 2002. [PMID: 12490850]
95. Brunt LM, Moley JF: Adrenal incidentaloma. World J Surg 25:905, 2001. [PMID: 11572032]
96. Reincke M: Subclinical Cushing's syndrome. Endocrinol Metab Clin North Am 29:43, 2000. [PMID:
10732263]
97. Libe R, Dall'Asta C, Barbetta L, et al: Long-term follow-up study of patients with adrenal incidentalomas.
Eur J Endocrinol 147:489, 2002. [PMID: 12370111]
98. Arlt W, Allolio B: Adrenal insufficiency. Lancet 361:1881, 2003. [PMID: 12788587]
99. Kebebew E, Siperstein AE, Clark OH, et al: Results of laparoscopic adrenalectomy for suspected and
unsuspected malignant adrenal neoplasms. Arch Surg 137:948, 2002. [PMID: 12146996]
100. Kelly PA, Samandouras G, Grossman AB, et al: Neurosurgical treatment of Nelson's syndrome. J Clin
Endocrinol Metab 87:5465, 2002. [PMID: 12466338]
56 of 56 1.5.2014 18:16
ABDOMINAL HERNIAS http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
The aim. To master clinics, diagnostics, differential diagnostics of reducible and complicated abdominal hernias. To
choose the treatment tactics, indications and contraindications for operative intervention, analgesia, type of plastics,
principles of postoperative period course, expertise of the ability to work and the rehabilitation after operations for
hernias.
Professional orientation of students. Abdominal hernias are common for 3-5% of population. Hernia limits the
working ability of the hernia carrier and is a vitally dangerous illness due to eventual complications (incarceration,
inflammation). The lethality at incarcerated hernias depend on many factors and therefore it ranges from 2 to 17%
according to various authors.
Theme 2. Femoral, umbilical hernias, hernia of the linea alba, hernia of semilunar line (Spigelius').
1. Anatomo-topographic features of the femoral channel, linea alba, Spigelius' line and other weak sites of the
abdominal wall.
2. Femoral hernias. Classification. Clinical features, differential diagnostics.
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BREAK 12.00-12.30
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coprostasis.
8. Indications and contraindications for conservative and operative treatment of complicated hernias.
9. Main peculiarities of operative treatment of complicated hernias.
Technical means and material provision of lectures (names and numbers of tables, compact discs, instruments
quantity, subjectpatients, etc.)
Multimedia projection of demonstration material (pictures, tables, videofilms) from compact disc Facultative Surgery,
file Hernias.
2. Staples may safely be placed during laparoscopic hernia repair in each of the following structures except:
A. Cooper's ligament.
B. Tissues superior to the lateral iliopubic tract.
C. The transversus abdominis aponeurotic arch.
D. Tissues inferior to the lateral iliopubic tract.
E. The iliopubic tract at its insertion onto Cooper's ligament.
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4. Which of the following statements about the causes of inguinal hernia is correct?
A. Excessive hydroxyproline has been demonstrated in the aponeuroses of hernia patients.
B. Obliteration of the processus vaginalis is a contributing factor for the development of an indirect inguinal hernia.
C. Physical activity and athletics have been shown to have a protective effect toward the development of inguinal
hernias.
D. Elevated levels of circulating serum elastalytic activity have been demonstrated in patients with direct herniation
who smoke.
E. The majority of inguinal hernias are acquired.
5. The following statements about the repair of inguinal hernias are true except:
A. The conjoined tendon is sutured to Cooper's ligament in the Bassini hernia repair.
B. The McVay repair is a suitable option for the repair of femoral hernias.
C. The Shouldice repair involves a multilayer, imbricated repair of the floor of the inguinal canal.
D. The Lichtenstein repair is accomplished by prosthetic mesh repair of the inguinal canal floor in a tension-free
manner.
E. The laparoscopic transabdominal preperitoneal (TAPP) and totally extraperitoneal approach (TEPA) repairs are
based on the preperitoneal repairs of Cheattle, Henry, Nyhus, and Stoppa.
1 C.
2 D.
3 E.
4 D.
5 A.
6E
Information sourses:
Main
1. Townsend CM, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery. 19th ed.
Philadelphia, Pa: Saunders Elsevier; 2012.
2. L.Ya.Kovalchuck, Yu.P.Spizhenko, V.F.Sayenko and others Hospital surgery. Ternopil: Ukrmendknyga, 1999.
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ABDOMINAL HERNIAS http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
Additional
1. Manual Facultative Surgery under the edition of V.O.Shidlovsky Ternopil: Ukrmedknyga, 2002, section
Diseases of the rectum and the colon,
2. Compact disc Facultative surgery.
3. Schwartz's Principles of Surgery, Ninth Edition. F. Brunicardi. Philadelphia, Pa: Saunders Elsevier; 2009
4. Zollinger's Atlas of Surgical Operations, 9th Edition. Robert Zollinger Jr., Elsevier; 2010
5. Chen, Herbert. Illustrative Handbook of General Surgery. Berlin: Springer, 2010.
"11" 2013 . 9
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ACUTE APPENDICITIS http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
The aim. To master clinics, diagnostics, differential diagnostics of the acute simple, complicated and chronic
appendicitis, peculiarities of acute appendicitis course in children, elderly people, pregnant women. To learn the
treatment tactics, indications and contraindications for operative intervention, operative intervention, principles of
postoperative period course, expertise of the working ability to and the reablement.
Professional orientation of students. Acute appendicitis is the most frequent urgent surgical illness. Its share makes
up 60-70% of all urgent surgical illnesses. The lethality after appendectomy varies in the ranges of 0,1-0,15% and is
determined also by diagnostic mistakes at untypical forms of the acute appendicitis, by diseases in children, elderly
people and pregnant women
Theme 2. Acute complicated appendicitis (infiltrate, abscess, peritonitis, pylephlebitis). Untypical forms of
the acute appendicitis. Peculiarities of the acute appendicitis course in children, elderly people and pregnant
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ACUTE APPENDICITIS http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
women.
1.Classification of the acute appendicitis complications.
2.Clinics, diagnostics and treatment of the appendicular infiltrate.
3.Clinics, diagnostics and treatment of the appendicular abscess.
4.Clinics, diagnostics and treatment of the appendicular peritonitis.
5.Clinical features of the retrocecal appendicitis.
6.Clinical features of the acute appendicitis at the pelvic appendix.
7.Clinical features of the acute appendicitis at the subhepatic appendix.
8.Clinical features of the acute appendicitis at the medial appendix.
9.Peculiarities of clinical course of the diagnosis of the acute appendicitis in children.
10.Peculiarities of clinical course of the diagnosis of the acute appendicitis in elderly people.
11. Peculiarities of clinical course of the diagnosis of the acute appendicitis in pregnant women.
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ACUTE APPENDICITIS http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
2. To reveal main clinical signs and symptoms of different forms of the acute and the chronic appendicitis.
3. To argue and formulate the preliminary diagnosis.
4. To make a plan of the examination of the patient and explain the examination results
(general blood test, general urine test, ultrasound diagnostics).
5. To define indications and contraindications for operative intervention, to choose properly the type anesthesia,
operative access and tuype of intervention according to the clinical form of the appendicitis.
Technical means and material provision of lectures (names and numbers of tables, compact discs, instruments
quantity, subjectpatients, etc.)
Multimedia projection of demonstration material (pictures, tables, videofilms) from compact disc Facultative Surgery,
file Hernias.
1. Which of the following most often initiates the development of acute appendicitis?
A. A viral infection.
B. Acute gastroenteritis.
C. Obstruction of the appendiceal lumen.
D. A primary clostridial infection.
3. Once a diagnosis of acute appendicitis has been made and appendectomy decided upon, which of the following
is/are true?
A. Prophylactic antibiotics should be administered.
B. Prophylactic antibitics are not necessary unless there is evidence of perforation.
C. If the appendix is not ruptured and not gangrenous, antibiotics may be discontinued after 24 hours.
D. Multiple antibiotics are in all cases preferable to a single agent.
4. Which of the following statements about pyogenic abscess of the liver are true?
A. The right lobe is more commonly involved than the left lobe.
B. Appendicitis with perforation and abscess is the most common underlying cause of hepatic abscess.
C. Mortality is largely determined by the underlying disease.
D. Mortality from hepatic abscess is currently greater than 40%.
5. Acute appendicitis is most commonly associated with which of the following signs?
A. Temperature above 104 F.
B. Frequent loose stools.
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1 C.
2 C.
3 A.
4 D.
5 C.
6C
7 B.
Information sourses:
Main
1. Townsend CM, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery. 19th ed.
Philadelphia, Pa: Saunders Elsevier; 2012.
2. L.Ya.Kovalchuck, Yu.P.Spizhenko, V.F.Sayenko and others Hospital surgery. Ternopil: Ukrmendknyga, 1999.
3. Practical classes materials http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/classes_stud/en/med
/lik/ptn/Surgery/4/Topic%2001%20Acute%20appendicitis.htm
Additional
1. Manual Facultative Surgery under the edition of V.O.Shidlovsky Ternopil: Ukrmedknyga, 2002, section
4 of 5 1.5.2014 18:55
ACUTE APPENDICITIS http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
"11" 2013 . 9
5 of 5 1.5.2014 18:55
ACUTE INTESTINAL OBSTRUCTION http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
The aim. To master clinics, diagnostics, differential diagnostics of various clinical forms of AIO. To learn the treatment
tactics, indications and contraindications for operative intervention, operative intervention type at various clinical forms
of AIO principles of postoperative period course, expertise of the working ability after operations for AIO.
Professional orientation of students. The acute intestinal obstruction makes up to 3,5% among the patients of
surgical stationaries and up to 10% of patients with acute diseases of abdominal organs. The lethality at AIO according
to different data, varies from 6 to 18-20%.
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ACUTE INTESTINAL OBSTRUCTION http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
4.Clinics, diagnostics, differential diagnostics of various types of the strangulation intestinal obstruction.
5.Differential diagnosis of the strangulation intestinal obstruction.
6.Modern verification methods of diagnosis (ultrasonic examination, laparoscopy, roengenologic methods).
7.Curing tactics at the strangulation intestinal obstruction.
8.Choice of scope and method of operative interventions at various clinical types of the strangulation intestinal
obstruction.
9.Peculiarities of the preoperative preparation and postoperative period course at the strangulation intestinal
obstruction.
10.Principles of operative treatment of the strangulation intestinal obstruction.
11.Peculiarities of the postoperative period course.
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1.To take the history of the patient with the suspect for AIO.
2.To reveal main clinical features and symptoms at various clinical forms of the obturative ileus.
3.To reveal main clinical features and symptoms at various clinical forms of the strangulation AIO.
4.To reveal main clinical features and symptoms at various clinical forms of the dynamic AIO.
5.To define free and limited liquid in the abdominal cavity, splash noise, characteristics of peristaltic violations.
6.To argue and explain the preliminary diagnosis.
7.To make a plan of patient examination and explain the examination results
(general blood test, general urine test, roentgenologic examination of the alimentary tract, general view
roentgenogram, barium passage, irriography, ultrasonic examination, biochemical blood test).
8.To define indications and contraindications for operative intervention, to choose properly the preoperative
preparation, anesthesia type, operative access and type of intervention according to the clinical form of mechanical
AIO.
9.To define principles of conservative treatment of the dynamic AIO.
1. History and physical examination permit the diagnosis of intestinal obstruction in most cases. Which of the following
are important for the clinical diagnosis of small bowel obstruction?
A. Crampy abdominal pain.
B. Fever.
C. Vomiting.
D. Abdominal distention.
E. Leukocyte count above 12,000.
F. Abdominal tenderness.
2. Patients with established, complete, simple, distal small bowel obstruction usually have the following findings on
plain and upright abdominal radiographs:
A. Distended small bowel identifiable by the valvulae conniventes.
B. Multiple air-fluid levels.
C. Modest amount of gas in the pelvis.
D. Peripheral, rather than central, distribution of gas.
E. Prominent haustral markings.
F. Free air.
3. Which of the following statement(s) about gallstone ileus is/are not true?
A. The condition is seen most frequently in women older than 70.
B. Concomitant with the bowel obstruction, air is seen in the biliary tree.
C. The usual fistula underlying the problem is between the gallbladder and the ileum.
D. When possible, relief of small bowel obstruction should be accompanied by definitive repair of the fistula since
there is a significant incidence of recurrence if the fistula is left in place.
E. Ultrasound studies may be of help in identifying a gallstone as the obstructing agent.
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1 A,B,C,D,F.
2 A,B.
3 C.
4 A,B,C,D,E.
Information sourses:
Main
1. Townsend CM, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery. 19th ed.
Philadelphia, Pa: Saunders Elsevier; 2012.
2. L.Ya.Kovalchuck, Yu.P.Spizhenko, V.F.Sayenko and others Hospital surgery. Ternopil: Ukrmendknyga, 1999.
3. Practical classes materials http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/classes_stud/en/med
/lik/ptn/Surgery/4/Topic%2005%20Acute%20intestinal%20obstruction.htm
4.
Additional
1. Manual Facultative Surgery under the edition of V.O.Shidlovsky Ternopil: Ukrmedknyga, 2002, section
Diseases of the rectum and the colon,
2. Compact disc Facultative surgery.
3. Schwartz's Principles of Surgery, Ninth Edition. F. Brunicardi. Philadelphia, Pa: Saunders Elsevier; 2009
4. Zollinger's Atlas of Surgical Operations, 9th Edition. Robert Zollinger Jr., Elsevier; 2010
5. Chen, Herbert. Illustrative Handbook of General Surgery. Berlin: Springer, 2010.
"11" 2013 . 9
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CHOLELITHIASIS, ACUTE PANCREATITIS http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
The aim. To master clinics, diagnostics, differential diagnostics of various clinical forms of the cholelithiasis and
pancreatitis. To learn to choose the treatment tactics, indications and contraindications for operative intervention,
analgesia type, operative intervention type, principles of postoperative period course, expertise of the working ability
after operations for biliary ducts and pancreas.
Professional orientation of students. Cholelithiasis and pancreatitis is the most frequent surgical illness of outer
biliary ducts. The disease is constantly growing and is covering now up to 10-15% of the population; it is especially
common for women after 40-50. Cholecystectomy still remains the main surgical treatment method. During the recent
years endoscopic (laparoscopic) operative interventions on biliary ducts have become widely used in surgical practice.
1 of 6 1.5.2014 18:55
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BREAK 12.00-12.30
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CHOLELITHIASIS, ACUTE PANCREATITIS http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
1.Anatomic and physiologic data about the liver and the outer biliary ducts.
2.Modern theories and stages of biliary lithogenesis.
3.Definition and classification of various clinical forms of the cholelithiasis.
4.Modern pre-, intra- and postoperative examination methods of biliary ducts.
5.Clinical and biochemical characteristics of violations of hepatic functions at cholelithiasis.
6.Clinics, diagnostics, differential diagnostics of various clinical forms of the cholelithiasis (acute and chronic calculous
cholecystitis, choledocholithiasis, biliodigestive fistula).
7.Indications and contraindications for conservative or operative treatment of various clinical versions of the
cholelithiasis.
8.Peculiarities of the preoperative preparation.
9.Types of operative interventions at various clinical forms of the cholelithiasis.
10.Peculiarities of the postoperative period course.
11.Anatomic and physiologic features of the pancreas.
12.Modern theories of apperance of acute and chronic pancreatitis.
13.Acute pancreatitis classification.
14.Chronic pancreatitis classification.
15.Clinical and biochemical characteristics of secretory nad incretory functions of the pancreas.
16.Clinics, diagnostics, differential diagnostics and curing tactics choice at various clinical forms of acute pancreatitis.
17.Clinics, diagnostics, differential diagnostics and curing tactics choice at various clinical forms of chronic pancreatitis.
18.Curing tactics at the acute pancreatitis.
19.Indications and contraindications for conservative and operative treatment of various clinical forms of acute
pancreatitis.
20.Complex of conservative treatment of acute pancreatitis.
21.Types of operative interventions at various clinical forms of acute pancreatitis.
22.Complex of conservative treatment of chronic pancreatitis.
23.Types of operative interventions at various clinical forms of chronic pancreatitis. 24.Peculiarities of postoperative
period course after operations at acute and chronic pancreatitis.
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1. Which of the following statements about the diagnosis of acute calculous cholecystitis are true?
A. Pain is so frequent that its absence almost precludes the diagnosis.
B. Jaundice is present in a majority of patients.
C. Ultrasonography is the definitive diagnostic test.
D. Cholescintigraphy is the definitive diagnostic test.
3. True statements about the surgical management of patients with acute calculous cholecystitis include:
A. Operation should be performed in all patients as soon as the diagnosis is made.
B. Antibiotic therapy should be initiated as soon as the diagnosis is made.
C. Dissection of the gallbladder is facilitated by decompression of the organ with the use of a trocar.
D. An operative cholangiogram should be done in every patient.
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8. Which of the following parameters is/are not included in the Ranson's prognostic signs useful in the early evaluation
of a patient with acute pancreatitis?
A. Elevated blood glucose.
B. Leukocytosis.
C. Amylase value greater than 1000 U per dl.
D. Serum lactic dehydrogenase (LDH) greater than 350 IU per dl.
E. Alanine aminotransferase greater than 250 U per dl.
9. Standard supportive measures for patients with mild pancreatitis include the following:
A. Intravenous fluid and electrolyte therapy.
B. Withholding of analgesics to allow serial abdominal examinations.
C. Subcutaneous octreotide therapy.
D. Nasogastric decompression.
E. Prophylactic antibiotics.
10. Which of the following statements about chronic pancreatitis is/are correct?
A. Chronic pancreatitis is the inevitable result after repeated episodes of acute pancreatitis.
B. Patients with chronic pancreatitis commonly present with jaundice, pruritus, and fever.
C. Mesenteric angiography is useful in the evaluation of many patients with chronic pancreatitis.
D. Total pancreatectomy usually offers the best outcome in patients with chronic pancreatitis.
E. For patients with disabling chronic pancreatitis and a dilated pancreatic duct with associated stricture formation, a
longitudinal pancreaticojejunostomy (Peustow procedure) is an appropriate surgical option.
11. Which of the following statements about pancreatic ascites is/are correct?
A. Patients typically present with painful ascites, reflecting the release of toxic pancreatic enzymes into the peritoneal
cavity.
B. The standard evaluation of a patient with new-onset ascites includes abdominal paracentesis. In cases of
pancreatic ascites, the peritoneal fluid contains high concentrations of both amylase and protein.
C. Pancreatic ascites can follow an episode of acute pancreatitis.
D. Patients with pancreatic ascites may fail to improve with nonoperative therapy and require surgical procedures. At
abdominal exploration an acceptable approach to the pancreatic duct disruption involves suture ligation with omental
patching.
12. Which of the following statements about adenocarcinoma of the pancreas is/are correct?
A. It is the fifth most common cause of cancer death in the U.S.
B. Most cases occur in the body and tail of the pancreas, making distal pancreatectomy the most commonly performed
resectional therapy.
C. For cancers of the head of the pancreas resected by pancreaticoduodenectomy, prognosis appears to be
independent of nodal status, margin status, or tumor diameter.
D. The most accurate screening test involves surveillance of stool for carbohydrate antigen (CA 199).
1 A,D.
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CHOLELITHIASIS, ACUTE PANCREATITIS http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
2 A,B,C,D.
3 B,C.
4 A.
5 A,B.
6 B,C,D.
7 A.
8 C,E.
9 A.
10 E.
11 B.
12 A.
Information sourses:
Main
1. Townsend CM, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery. 19th ed.
Philadelphia, Pa: Saunders Elsevier; 2012.
2. L.Ya.Kovalchuck, Yu.P.Spizhenko, V.F.Sayenko and others Hospital surgery. Ternopil: Ukrmendknyga, 1999.
3. Practical classes materials http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/classes_stud/en/med
/lik/ptn/Surgery/4/Topic%2002%20Acute%20cholecystitis.htm
Additional
1. Manual Facultative Surgery under the edition of V.O.Shidlovsky Ternopil: Ukrmedknyga, 2002, section
Diseases of the rectum and the colon,
2. Compact disc Facultative surgery.
3. Schwartz's Principles of Surgery, Ninth Edition. F. Brunicardi. Philadelphia, Pa: Saunders Elsevier; 2009
4. Zollinger's Atlas of Surgical Operations, 9th Edition. Robert Zollinger Jr., Elsevier; 2010
5. Chen, Herbert. Illustrative Handbook of General Surgery. Berlin: Springer, 2010.
"11" 2013 . 9
6 of 6 1.5.2014 18:55
DISEASES OF THE RECTUM AND THE COLON http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
The aim. To master clinics, diagnostics, differential diagnostics of diseases of rectum and colon: hemorrhoids, anal
fissures, acute and chronic paraproctitis, Crohns disease, nonspecific ulcerative colitis, rectal prolapse. To learn the
treatment tactics, indications and contraindications for conservative and operative treatment, analgesia type, operative
intervention type, principles of the pre- and postoperative periods, expertise of the working ability after operations on
rectum and colon.
Professional orientation of students. Diseases of the rectum and the colon are very common for people regardless
their sex, especially in mature and elderly age. Say, 10-20% of the population suffer with hemorrhoids, 0,5-6,1% of
people of able to work age have rectal fistulas. Therefore, a doctor of any profile, especially a family one, must be
accustomed with the peculiarities of curing-diagnostic tactics at those illnesses.
1 of 5 1.5.2014 18:59
DISEASES OF THE RECTUM AND THE COLON http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
BREAK 12.00-12.30
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DISEASES OF THE RECTUM AND THE COLON http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
inflammatory process.
14.Chronic paraproctitis. Concept definition and classification.
15.Clinical characteristics, diagnostics and differential diagnostics and diagnosis verification methods of chronic
paraproctitis.
16.Curing tactics and treatment method of chronic paraproctitis depending on the clinical form.
17.Crohns disease. Classification.
18.Clinical characteristics of Crohns disease depending on the clinical form and course stage, complications.
19.Curing tactics and methods of conservative and operative treatment of Crohns disease depending on the clinical
form, course stage and complications.
20.Nonspecific ulcerative colitis (NUC). Concept definition and classification.
21. NUC clinics depending on the allocation, clinical course, complications.
22.Verification methods of NUC diagnosis.
23.Curing tactics and principles of conservative and operative treatment of NUC depending on the clinical form, course
and complications.
24.Rectal prolapse. Concept definition and classification.
25.Clinics of the rectal prolapse depending on the course stage.
26.Curing tactics and treatment methods of the rectal prolapse depending on the course stage.
2. Which answers are true? In contrast to ulcerative colitis, Crohn's disease of the colon:
A. Is not associated with increased risk of colon cancer.
B. Seldom presents with daily hematochezia.
C. Is usually segmental rather than continuous.
D. Has a lower incidence of perianal fistulas.
E. Never develops toxic megacolon.
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DISEASES OF THE RECTUM AND THE COLON http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
3. Which of the following statements about the etiology of chronic ulcerative colitis are true?
A. Ulcerative colitis is 50% less frequent in nonwhite than in white populations.
B. Psychosomatic factors play a major causative role in the development of ulcerative colitis.
C. Cytokines are integrally involved in the pathogenesis of ulcerative colitis.
D. Ulcerative colitis has been identified with a greater frequency in family members of patients with confirmed
inflammatory bowel disease.
E. Ulcerative colitis is two to four times more common in Jewish than in non-Jewish populations.
4. Surgical alternatives for the treatment of ulcerative colitis include all of the following except:
A. Colectomy with ileal pouchanal anastomosis.
B. Left colectomy with colorectal anastomosis.
C. Proctocolectomy with Brooke ileostomy or continent ileostomy.
D. Subtotal colectomy with ileostomy and Hartmann closure of the rectum.
6. Which finding(s) suggest(s) the diagnosis of chronic ulcerative colitis as opposed to Crohn's colitis?
A. Endoscopic evidence of backwash ileitis.
B. Granulomas on biopsy.
C. Anal fistula.
D. Rectal sparing.
E. Cobblestone appearance on barium enema.
7. Axial twisting of the right colon or cecal volvulus has been shown to be associated with each of the following except:
A. A history of abdominal operation.
B. A mobile cecum.
C. An obstructing lesion in the transverse or left colon.
D. Inflammatory bowel disease.
1 C.
2 B,C.
3 A,C,D,E.
4 B.
5 A,C.
6 A.
4 of 5 1.5.2014 18:59
DISEASES OF THE RECTUM AND THE COLON http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
7 D.
Information sourses:
Main
1. Townsend CM, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery. 19th ed.
Philadelphia, Pa: Saunders Elsevier; 2012.
2. L.Ya.Kovalchuck, Yu.P.Spizhenko, V.F.Sayenko and others Hospital surgery. Ternopil: Ukrmendknyga, 1999.
3. Practical classes materials http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/classes_stud/en/med
/lik/ptn/Surgery/4/Topic%2011%20HEMORRHOIDS.%20ANAL%20FISSURES.%20PARAPROCTITIS.htm
Additional
1. Manual Facultative Surgery under the edition of V.O.Shidlovsky Ternopil: Ukrmedknyga, 2002, section
Diseases of the rectum and the colon,
2. Compact disc Facultative surgery.
3. Schwartz's Principles of Surgery, Ninth Edition. F. Brunicardi. Philadelphia, Pa: Saunders Elsevier; 2009
4. Zollinger's Atlas of Surgical Operations, 9th Edition. Robert Zollinger Jr., Elsevier; 2010
5. Chen, Herbert. Illustrative Handbook of General Surgery. Berlin: Springer, 2010.
"11" 2013 . 9
5 of 5 1.5.2014 18:59
DISEASES OF THE RECTUM AND THE COLON http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
The aim. To master clinics, diagnostics, differential diagnostics of diseases of rectum and colon: hemorrhoids, anal
fissures, acute and chronic paraproctitis, Crohns disease, nonspecific ulcerative colitis, rectal prolapse. To learn the
treatment tactics, indications and contraindications for conservative and operative treatment, analgesia type, operative
intervention type, principles of the pre- and postoperative periods, expertise of the working ability after operations on
rectum and colon.
Professional orientation of students. Diseases of the rectum and the colon are very common for people regardless
their sex, especially in mature and elderly age. Say, 10-20% of the population suffer with hemorrhoids, 0,5-6,1% of
people of able to work age have rectal fistulas. Therefore, a doctor of any profile, especially a family one, must be
accustomed with the peculiarities of curing-diagnostic tactics at those illnesses.
1 of 5 1.5.2014 18:59
DISEASES OF THE RECTUM AND THE COLON http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
BREAK 12.00-12.30
2 of 5 1.5.2014 18:59
DISEASES OF THE RECTUM AND THE COLON http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
inflammatory process.
14.Chronic paraproctitis. Concept definition and classification.
15.Clinical characteristics, diagnostics and differential diagnostics and diagnosis verification methods of chronic
paraproctitis.
16.Curing tactics and treatment method of chronic paraproctitis depending on the clinical form.
17.Crohns disease. Classification.
18.Clinical characteristics of Crohns disease depending on the clinical form and course stage, complications.
19.Curing tactics and methods of conservative and operative treatment of Crohns disease depending on the clinical
form, course stage and complications.
20.Nonspecific ulcerative colitis (NUC). Concept definition and classification.
21. NUC clinics depending on the allocation, clinical course, complications.
22.Verification methods of NUC diagnosis.
23.Curing tactics and principles of conservative and operative treatment of NUC depending on the clinical form, course
and complications.
24.Rectal prolapse. Concept definition and classification.
25.Clinics of the rectal prolapse depending on the course stage.
26.Curing tactics and treatment methods of the rectal prolapse depending on the course stage.
2. Which answers are true? In contrast to ulcerative colitis, Crohn's disease of the colon:
A. Is not associated with increased risk of colon cancer.
B. Seldom presents with daily hematochezia.
C. Is usually segmental rather than continuous.
D. Has a lower incidence of perianal fistulas.
E. Never develops toxic megacolon.
3 of 5 1.5.2014 18:59
DISEASES OF THE RECTUM AND THE COLON http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
3. Which of the following statements about the etiology of chronic ulcerative colitis are true?
A. Ulcerative colitis is 50% less frequent in nonwhite than in white populations.
B. Psychosomatic factors play a major causative role in the development of ulcerative colitis.
C. Cytokines are integrally involved in the pathogenesis of ulcerative colitis.
D. Ulcerative colitis has been identified with a greater frequency in family members of patients with confirmed
inflammatory bowel disease.
E. Ulcerative colitis is two to four times more common in Jewish than in non-Jewish populations.
4. Surgical alternatives for the treatment of ulcerative colitis include all of the following except:
A. Colectomy with ileal pouchanal anastomosis.
B. Left colectomy with colorectal anastomosis.
C. Proctocolectomy with Brooke ileostomy or continent ileostomy.
D. Subtotal colectomy with ileostomy and Hartmann closure of the rectum.
6. Which finding(s) suggest(s) the diagnosis of chronic ulcerative colitis as opposed to Crohn's colitis?
A. Endoscopic evidence of backwash ileitis.
B. Granulomas on biopsy.
C. Anal fistula.
D. Rectal sparing.
E. Cobblestone appearance on barium enema.
7. Axial twisting of the right colon or cecal volvulus has been shown to be associated with each of the following except:
A. A history of abdominal operation.
B. A mobile cecum.
C. An obstructing lesion in the transverse or left colon.
D. Inflammatory bowel disease.
1 C.
2 B,C.
3 A,C,D,E.
4 B.
5 A,C.
6 A.
4 of 5 1.5.2014 18:59
DISEASES OF THE RECTUM AND THE COLON http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
7 D.
Information sourses:
Main
1. Townsend CM, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery. 19th ed.
Philadelphia, Pa: Saunders Elsevier; 2012.
2. L.Ya.Kovalchuck, Yu.P.Spizhenko, V.F.Sayenko and others Hospital surgery. Ternopil: Ukrmendknyga, 1999.
3. Practical classes materials http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/classes_stud/en/med
/lik/ptn/Surgery/4/Topic%2011%20HEMORRHOIDS.%20ANAL%20FISSURES.%20PARAPROCTITIS.htm
Additional
1. Manual Facultative Surgery under the edition of V.O.Shidlovsky Ternopil: Ukrmedknyga, 2002, section
Diseases of the rectum and the colon,
2. Compact disc Facultative surgery.
3. Schwartz's Principles of Surgery, Ninth Edition. F. Brunicardi. Philadelphia, Pa: Saunders Elsevier; 2009
4. Zollinger's Atlas of Surgical Operations, 9th Edition. Robert Zollinger Jr., Elsevier; 2010
5. Chen, Herbert. Illustrative Handbook of General Surgery. Berlin: Springer, 2010.
"11" 2013 . 9
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DISEASES OF THE THYROID AND MAMMARY GLAND http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
The aim. To master clinics, diagnostics, differential diagnostics of various clinical forms of goiter, thyroiditis. To learn the treatment tactics, indications and contraindications for operative
intervention, operative intervention type at various clinical forms of goiter, principles of postoperative period course, expertise of the working ability after operations for endemic, sporadic,
diffuse toxic goiters, thyroidites.
Professional orientation of students. Thyroid gland diseases (endemic, sporadic, diffuse, toxic goiters, thyroidites) occupy the leading place among surgical illnesses of endocrine
glands. The actuality of the problem is connected with the endemic character of many geographical regions of Ukraine and also with the accident at Chernobyl Power Atomic Station.
BREAK 12.00-12.30
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1. When progressive enlargement of a multinodular goiter causes symptomatic tracheal compression, the preferred management in otherwise good-risk patients is:
A. Iodine treatment.
B. Thyroid hormone treatment.
C. Surgical resection of the abnormal thyroid.
D. Radioactive iodine treatment.
2. The most precise diagnostic screening procedure for differentiating benign thyroid nodules from malignant ones is:
A. Thyroid ultrasonography.
B. Thyroid scintiscan.
C. Fine-needle-aspiration biopsy (FNAB).
D. Thyroid hormone suppression.
4. Which of the following statements is true about the synthesis of thyroid hormone and its physiology?
A. The iodine utilized in hormone synthesis is derived principally from dietary sources.
B. The role of thyroid-stimulating hormone (TSH) in thyroid physiology is limited to regulation of the release of thyroid hormone in plasma.
C. Enough thyroxine (T 4) is stored in the normal thyroid to provide a euthyroid state for 3 weeks despite absence of iodine intake.
D. The regulation of thyroid function involves pituitary, but not hypothalamic, input.
5. Correct statements about thyroid function tests include which of the following?
A. Contraceptive pills and pregnancy increase the amount of thyroxin-binding globulin (TBG), and, consequently, the total T 4 level.
B. Anticonvulsive medications and chronic debilitating illnesses decrease the amount of TBG and, consequently, the total T 4 level.
C. Intravenous pyleography can lower the rate of active iodine uptake by the thyroid.
D. A triiodothyronine (T 3) suppression test that demonstrates nonsuppressibility of thyroid function is compatible with the diagnosis of Graves' disease, toxic adenoma, or functioning
carcinoma.
E. An increased serum cholesterol level in a hypothyroid patient indicates a thyroid cause.
7. Arrange the following complications of thyroid surgery (bilateral subtotal thyroidectomy) in decreasing order of incidence in patients with Graves' disease.
A. Laryngeal nerve paralysis.
B. Hypoparathyroidism.
A. Hypothyroidism.
B. Recurrent hyperthyroidism.
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1 C.
2 C.
3 D.
4 A,C.
5 A,B,C,D.
6 E.
7 A,B,C,D.
Information sourses:
Main
1. Townsend CM, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery. 19th ed. Philadelphia, Pa: Saunders Elsevier; 2012.
2. L.Ya.Kovalchuck, Yu.P.Spizhenko, V.F.Sayenko and others Hospital surgery. Ternopil: Ukrmendknyga, 1999.
3. Practical classes materials http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/classes_stud/en/med/lik/ptn/Surgery
/4/Topic%2012%20Endemic,%20sporadic%20goiters.%20Diffuse%20toxic%20goiter.%20Thyrotoxicosis.%20Dishormonous%20diseases%20of%20the%20mammary%20gland.htm
Additional
1. Manual Facultative Surgery under the edition of V.O.Shidlovsky Ternopil: Ukrmedknyga, 2002, section Diseases of the rectum and the colon,
2. Compact disc Facultative surgery.
3. Schwartz's Principles of Surgery, Ninth Edition. F. Brunicardi. Philadelphia, Pa: Saunders Elsevier; 2009
4. Zollinger's Atlas of Surgical Operations, 9th Edition. Robert Zollinger Jr., Elsevier; 2010
5. Chen, Herbert. Illustrative Handbook of General Surgery. Berlin: Springer, 2010.
"11" 2013 . 9
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EMPLOYMENT 19 (Practical - 7 hours http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
Purpose: to learn the modern approaches to operative medical treatment with the use of endoscopic
technologies. To know prospects, possibilities and to be able to ground testimonies to implementation of
endoscopic operative interferences. Learn modern approaches to operative medical treatment with the use of
sonography and X-Ray control. To know prospects, possibilities and to be able to ground a testimony to
implementation of operative interferences under the control sonography and X-Ray control. To know diagnostic
potential of modern medical telecommunication equipment. To familiarize with the basic systems vehicles,
which is used in remote diagnostics of surgical pathology. Learn the principles of action, testimonies and contra-
indications to application and diagnostic value of modern telemedical equipment.
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2. Friendly behavour.
3. To explain to the patient a purpose of the visit, duration of conversation and to get his agreement.
4. Correct and quiet conversation with a patient.
5. To get the agreement of patient for the performance of the examination.To take complaints. Correct and
quiet conversation with a patient. A patient is in vertical position persons to the doctor, neck and
shoulders of patient is maximally weakened.
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Break 12.00-12.30
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EMPLOYMENT 19 (Practical - 7 hours http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
The basic level of knowledges and abilities is checked up by the undoing of situation tasks to every theme, by
answers for tests and structural questions.
(presence of complete sets of tests and situation tasks at a teacher)
1. Patient To., 46 years, first days after laparoscopic operation concerning chronic calculous cholecystitis
grumbles about a general weakness, nausea, multiple vomiting by a bile, pain and swelling of stomach. To the
peristalsis is hearkened, gases do not depart. On a X-Ray film is free gas in an abdominal region.
Clinical diagnosis?
Medical tactic?
2. At a patient, 40 years, about of 5 month after carried laparoscopic cholecystectomy there recover the
cramping hepatic colic, which was accompanied icteric of the skin covers, excrement of color of argil. What
method of diagnostics will be most informing?
Answers:
. Peroral cholangiography
. Retrograde pankreatocholangiography
. Ultrasonografy hepatobiliary area
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. Radionuclide scanning
. Laparoscopy
3. A patient 78 years is hospitalized in the planned order with complaints about jaundice making
progress, which appeared over 3 weeks to that ago, without a pain syndrome, general weakness, bad appetite.
Objectively: temperature of body 36, 80, pulse of 78/, a stomach is soft painless, symptoms of irritation of
the peritoneum not exposed. From data of sonography tumular education in the area of gate of liver by sizes 4*6
sm, intrahepatic bilious duct is extended. On the X-Ray sciagram of organs of pectoral cavity extended plural
metastases in both 0,5 - 1 sm easy by sizes. What operative medical treatment will be most optimum?
Answers:
. Cholecystoenterostomy
. Hepatoenteroanastomosis on a excluded loop for Ru
C. cholecystectomy, external drenagine of choledoch
. Choledochoduodenostomy
. Throughskin throughhepatic drenagine of intrahepatic bilious ducts under the control sonography
4. Patient of 53 years, entered a clinic concerning the gastro-intestinal bleeding of unclear etiology.
During laparotomy there is a revel big vascular tumour, which coverage on a duodenum, the Treyts copula and
head of the pancreas. Deleting a tumour is not possible. During postoperative period it is conducted to the
angiography gastroduodenal artery. On angiography was determined characteristic picture of vascular tumour.
What next medical tactic in relation to this patient?
. Embolization systems of gastroduodenal artery.
. Conservative hemostatic therapy.
C. Chemotherapy.
. Radial therapy.
. Embolization of abdominal trunk branches of aorta.
5. During telemedical vydeoteleconsultations you advise a domestic doctor, who is appealed to the patient
in 62, during 10 years is ill gallstone illness. Three days to that ago he fell dull pain in right hypochondriac
region, almost at once at a patient the turn of sclera and skin covers appeared yellow, at the same time of patient
marked the complete lighting up of color of excrement the masses almost. Your recommendations?
And. Urgent hospitalization in surgical permanent establishment
B. Setting of diet 5 for Pevznerom
C. Supervision after a patient in the conditions of policlinic
D. Conservative therapy in ambulatory terms
E. Conducting of diagnostic measures for clarification of diagnosis
6. To your electronic address came a latter from a patient 50 years, in which she grumbles about pain in
right hypochondriac region, nausea, arose up after the reception of rich food. After 6 hours of spasmolytics
using she fell better. Similar to pain colic it was to 3 mounts that before. A patient did sonography - in a
gall-bladder find out the concretion in diameter of 30 mm. What can be advised this patient?
A. To apply medicinal dissolution of stone
B. To offer conservative medical treatment
C. Ambulatory supervision following to new pain colic
D. To apply extracorporal lithotripsy
E. To offer cholecystectomy
Information sourses:
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Main
1. Townsend CM, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery. 19th ed. Philadelphia, Pa: Saunders
Elsevier; 2012.
2. L.Ya.Kovalchuck, Yu.P.Spizhenko, V.F.Sayenko and others Hospital surgery. Ternopil: Ukrmendknyga, 1999.
3. Practical classes materials http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/classes_stud/en/med/lik/ptn/Surgery
/4/Topic%2013.%20New%20technologies%20in%20surgery.%20Modern%20methods%20of%20diagnostic%20and%20treatment.htm
Additional
1. Manual Facultative Surgery under the edition of V.O.Shidlovsky Ternopil: Ukrmedknyga, 2002, section Diseases of the rectum
and the colon,
2. Compact disc Facultative surgery.
3. Schwartz's Principles of Surgery, Ninth Edition. F. Brunicardi. Philadelphia, Pa: Saunders Elsevier; 2009
4. Zollinger's Atlas of Surgical Operations, 9th Edition. Robert Zollinger Jr., Elsevier; 2010
5. Chen, Herbert. Illustrative Handbook of General Surgery. Berlin: Springer, 2010.
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The aim: To be able to diagnose the acute and chronic abscess of lung depending on their localization and
complications, to give urgent help to the patients with the acute abscess of lung complicated by the
pulmonary bleeding, to diagnose and liquidate complications, indications for conservative and operative
treatment, to know the methods of their operative treatment.
Work 2. Students independently inspect sick purulent diseases of lung, meet with a medical document,
confirm diagnosis and methods of treatment. After it the survey sciagrams of organs of thorax are analysed,
differential diagnostics is performed with urgent thoracic pathology.
Work 3. Students independently inspect patients with different types of purulent diseases of lung, meet with
the methods of diagnostics, by a medical document, confirm diagnosis and methods of treatment, the survey
sciagrams of organs of thorax are analysed, CT, information of clinical methods of examination, differential
diagnostics is performed with urgent thoracic pathology.
Individual Students Program.
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Work 4. Students independently examine patients with the purulent diseases of pleura, meet with the methods
of diagnostics, by a medical document, confirm diagnosis and methods of treatment, information of the survey
sciagrams is analysed, clinical methods of examination, differential diagnostics is performed with urgent
thoracic pathology.
Individual Students Program.
1. Acute empyema of pleura: Etiology, pathogeny, clinic.
2. Clinical signs of the limited empyema pleura: roentgenologic picture.
3. Clinic of limited piopneumothorax: roentgenologic signs.
4. Reasons of origin and clinic of total piopneumothorax.
5. Additional methods of examination at the chronic purulent processes of pleura.
6. Differential diagnostics of empyema pleura and piopneumothorax.
7. Clinic of chronic empyema.
8. Additional methods of examination at piopneumothorax.
9. Tactic of treatment of patients with piopneumothorax.
10. Indication to puncture of pleura cavity.
11. Technique of execution of pleura puncture.
12. Indication to drainage of pleura cavity.
13. Technique of execution of drainage of pleura cavity.
14. Features of conservative treatment of piopneumothorax.
Break 12.00-12.30
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A. Chest pain
B. Vomiting
C. Regurgitation
D. Dysphagia
E. Dilated cervical veins
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A. Emphysema
B. Pulmonary bleeding
C. Rib fracture
D. Malignancy
E. Esophageal bleeding
A. Rib fracture
B. Emphysema
C. Pyopneumothorax
D. Malignancy
E. Esophageal bleeding
A. Esophageal bleeding
B. Rib fracture
C. Emphysema
D. Sepsis
E. Malignancy
A. Esophageal bleeding
B. Rib fracture
C. Bronchogenic dissemination
D. Emphysema
E. Malignancy
8. In the patient of 35 years old during physical exertion have appeared a sharp pain in the left half of
the chest. On examination: the patient is covered with cold sweat, difficult breathing on the left side.
A tachycardia. By percussion: the bandbox sound from the left side. By auscultation: respiration on
the right side is vesicular, on the left side is absent. The probable diagnosis?
A. Spontaneous pheumothorax
B. Angina on exertion
C. Acute myocardial infarction
D. Left pleurisy
E. Pneumonia
9. The patient ., 37 years old, has entered with the complaints of cough with daily excretion of a
purulent sputum to 150 ml, pain in the right half of the chest, increase of temperature to 38C. Has
been ill for 2 weeks. Before the day of entrance in clinic appeared expectoration of 300 ml of purulent
sputum during cough. On examination: a shortening of percussion pulmonary sound and harsh
breathing with coarse rales over the right scapula. What is the previous diagnosis?
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A. Acute bronchitis
B. Acute abscess of lung
C. Exacerbation of a chronic abscess
D. Exacerbation of bronchiectatic disease
E. Pleural empyema
10. The patient ., 42 years old entered the clinic. During two months was treated for acute abscess of
the upper lobe of the right lung. The treatment included intramuscular injections of antibiotics.
Improvement inappreciable as there stayed a cough with expectoration of a purulent fetid-odor
sputum to 80-100 ml per day, high temperature. The diagnosis?
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2. To expose the basic variants of clinical display of acute and chronic abscess of lung, ground and
formulate a diagnosis, to perform a differential diagnosis, to ground conservative and operative
treatment.
3. To expose the basic clinical signs of acute empyema of pleura and pyopneumothorax, to formulate a
clinical diagnosis, to perform a differential diagnosis, to ground the shows and methods of operative
treatment.
4. To expose the basic clinical aspects of purulent processes of lung.
5. To ground and formulate a clinical diagnosis.
6. To perform a differential diagnosis.
7. To formulate the shows to surgical and conservative treatment.
References:
Main
1. Manual Facultative Surgery under the edition of V.O.Shidlovsky Ternopil: Ukrmedknyga, 2002,
section Diseases of the lung,compact disc Facultative surgery, file Diseases of the lung.
2. Wang JL, Chen KY, Fang CT, Hsueh PR, Yang PC, Chang SC. Changing bacteriology of adult
community-acquired lung abscess in Taiwan: Klebsiella pneumoniae versus anaerobes. Clin Infect Dis.
Apr 1 2005;40(7):915-22.
3. Takayanagi N, Kagiyama N, Ishiguro T, Tokunaga D, Sugita Y. Etiology and outcome of community-
acquired lung abscess. Respiration. 2010;80(2):98-105.
4. Mwandumba HC, Beeching NJ. Pyogenic lung infections: factors for predicting clinical outcome of
lung abscess and thoracic empyema. Curr Opin Pulm Med. May 2000;6(3):234-9.
5. Celli BR. Diseases of the diaphragm, chest wall, pleura, and mediastinum. In: Goldman L, Ausiello D,
eds. Cecil Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 100.
6. Broaddus VC, Light RW. Pleural effusion. In: Mason RJ, Broaddus VC, Martin TR, et al, eds. Murray
and Nadel's Textbook of Respiratory Medicine. 5th ed. Philadelphia, Pa: Saunders Elsevier; 2010:chap
68.
7. Website of the Ternopil University
Additional
1. L.Ya.Kovalchuck, Yu.P.Spizhenko, V.F.Sayenko and others. Hospital surgery. Ternopil:
Ukrmendknyga, 1999- 590C.
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5. To get the agreement of patient for the performance of the examination.To take
complaints
6. To take anamnesis (to pay attention on the character, period of the onset of
complaints, presence of the intermittent claudication)
7. To examine the patient (examination of the skin, presence of destructive changes,
presence of pulsation on different levels of the arterial system of the lower
extremities)
8. To detect the degree of arterial insufficiency of the lower extremities
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"Determination of the valvular function of subcutaneous and deep veins of the lower
extremities"
Medical cure of the patient with the purulent destructive diseases of lungs
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2. Friendly behavour.
3. To explain to the patient a purpose of the visit, duration of conversation and to get his
agreement.
4. Correct and quiet conversation with a patient.
5. To get the agreement of patient for the performance of the examination.To take
complaints
6. To take anamnesis (to pay attention to the onset of the disease, development of purulent
destructive processes in pulmonary tissue, clinical course of the pathological process
before to and after discharge into bronchial tube)
7. To examine the patient (physical examination, palpation, percution, auscultation)
8. Interpretation of laboratory and instrumental methods of investigation, establishment of
diagnosis
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The aim. To master clinics, diagnostics, differential diagnostics of various clinical forms of peritonitis. To learn the
treatment tactics, indications and contraindications for operative intervention, operative intervention type at various
clinical forms of peritonitis, principles of postoperative period course.
Professional orientation of students. The course of acute surgical illnesses of peritoneal organs is complicated
with peritonitis development in 20-30% of the cases. The lethality at the extensive forms of peritonitis depends on the
skilled early diagnosis and in-time complex treatment.
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Theme 3. Correction principles of water-electrolytic and acid-alkaline balance. Pre- and postoperative
periods course in patients with acute extensive peritonitis.
1.Classification of dehydration and electrolytic violations.
2.Clinical characteristics of water-electrolytic violations at various course phases of the acute extensive peritonitis.
3.Classification of blood substitutes, hydroionic solutions which are used to correct the hydroionic violations.
4.Major principles of intravascular dehydration correction.
5.Principles of intravascular and mixed dehydration correction.
6.Concrete example of calculation of hyponatremia correction.
7. Concrete example of calculation of hypopotassiumemia correction.
8.General rules of infusion therapy.
BREAK 12.00-12.30
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8.Peculiarities of clinical course and differential diagnosis of the false peritonitis (at diabetes mellitus, uremia,
Schonlein-Henoch disease).
9.Peculiarities of the preoperative preparation in patients with the extensive peritonitis.
10.Principles of operative treatment of patients with various clinical versions of the peritonitis.
11.Peculiarities of the postoperative course in patients with the peritonitis.
2. The most common indication for surgery secondary to acute diverticulitis is:
A. Abscess.
B. Colonic obstruction.
C. Colovesical fistula.
D. Free perforation.
E. Hemorrhage.
3. Which of the following statements most accurately describes the current therapy for pyogenic hepatic abscess?
A. Antibiotics alone are adequate for the treatment of most cases.
B. All patients require open surgical drainage for optimal management.
C. Optimal treatment involves treatment of not only the abscess but the underlying source as well.
D. Percutaneous drainage is more successful for multiple lesions than for solitary ones.
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1 C.
2 A.
3 C.
4 B,C.
Information sourses:
Main
1. Townsend CM, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery. 19th ed.
Philadelphia, Pa: Saunders Elsevier; 2012.
2. L.Ya.Kovalchuck, Yu.P.Spizhenko, V.F.Sayenko and others Hospital surgery. Ternopil: Ukrmendknyga, 1999.
3. Practical classes materials http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/classes_stud/en/med
/lik/ptn/Surgery/4/Topic%2006%20Acute%20peritonitis.htm
Additional
1. Manual Facultative Surgery under the edition of V.O.Shidlovsky Ternopil: Ukrmedknyga, 2002, section
Diseases of the rectum and the colon,
2. Compact disc Facultative surgery.
3. Schwartz's Principles of Surgery, Ninth Edition. F. Brunicardi. Philadelphia, Pa: Saunders Elsevier; 2009
4. Zollinger's Atlas of Surgical Operations, 9th Edition. Robert Zollinger Jr., Elsevier; 2010
5. Chen, Herbert. Illustrative Handbook of General Surgery. Berlin: Springer, 2010.
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th
METHODICAL INSTRUCTIONS FOR 5 YEAR STUDENTS
METHODOLOGICAL INSTRUCTION TO LESSON 8
. AIM. To be able to diagnose, to know symptoms of diseases of operated stomach, depending on clinical type of the disease.
Principles of conservative and surgical treatment. To be able to diagnose, to know symptoms and principles of conservative and surgical
treatment of of postcholecystectomic syndrome.
Knowledge of symptoms, appearing after performed stomach resections and vagotomies, causes proper approach to choosing of
operative intervention and the techniques of its performing.
Cholecystectomy is one of frequently performed operations in surgical clinics. Knowledge of symptoms, clinical signs and
diagnosing of the diseases, that are grouped into the term PCES, gives us a possibility to prevent its appearing in one cases, and to
determine the expediency of conservative or surgical treatment in another ones.
1. Anatomical, morphological and functional peculiarities of stomach (anatomy, topographical anatomy, anatomical pathology,
histology).
2. Etiology, pathogenesis and classification of diseases of operated stomach (pathological physiology, propaedeutical therapy, faculty
surgery).
3. Estimation of x-ray, endoscopic, laboratory findings (rhoetgenology, functional diagnostics).
4. Mechanism of antiulcerogenic agents action, correction of electrolytes metabolism violation, use of digestive enzymes, hormones,
vitamins, methods of operative intervention (pharmacology, faculty surgery).
5. Rontgenoscopy, estimation of x-ray reports, gastric juices test.
1. Anatomical, morphological and functional peculiarities of biliary tracts (anatomy, topographical anatomy, anatomical pathology).
2. Classification of postcholecystectomic syndrome (propaedeutical therapy)
3. Estimation of clinical and laboratory, x-ray, ultrasonographical, endoscopic, findings (rhoetgenology, infectious diseases,
biochemistry).
4. Mechanism of antiinflammatory, spasmolytic, detoxicative, replacement agents action, methods of operative intervention on biliary
tracts (pharmacology, topographical anatomy and operative surgery).
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Break 12.00-12.30
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Technical means and material provision of lectures (names and numbers of tables, compact discs, instruments quantity,
subjectpatients, etc.)
Multimedia projection of demonstration material (pictures, tables, videofilms) from compact disc Clinical Surgery, videofilms with
operations.
1. 40-years old patient, 3 years ago had an operation of stomach resection by Hoffmeister-Finsterer because of duodenum ulcer with
petetration into the head of pancreas. Duting the last year notices everyday pain in right subcostal region, that are attended by bile vomiting
up to 1 l in volume. After vomiting pain disappeares. The patient several times have passed treatment courses in surgical department, but
there was no improving of his state. The patient has lost 16 kg of weight. During x-ray examination the contrast gets into the afferent loop.
Your diagnosis?
Surgeons tactics?
2. 45-year old patient, 3 years ago had an operation of 2/3 stomach resection by Hoffmeister-Finsterer because of stenosing ulcer of the
antrum. Now the expressed dumping syndrome of severe degree with ptogressive weight loss is observed, despite repeated courses of
in-patient and health resort treatment. Psychoneurological dusorders are expressed slightly. There is no bile vomiting. At x-ray examination
of gastric stump the accelerated evacuation is observed.
Your diagnosis?
Surgeons tactics?
3. 48-years old patient, that has undergone an operation of cholecystectomy 3 years ago, has complaints on cramping pains, that were
followed by raised temperature up to 380C, scleral and mucous membranes icteritiousness. Whole bilirubin 128,0 mkmol/l, leukocites
15,0x109/l, stab neutrophils 16 %.
What methods of examination should be used?
Your diagnosis?
Treatment tactics?
4. 35-year old female patient, a month ago had an operation of cholecystectomy. Now she complains on circumferential pain in
abdomen, nausea, vomiting, icteritiousness of scleras and visible mucous membranes. Whole bilirubin is 60,0 mkmol/l. While palpation the
patient feels pain in left mesogastral region. Symptoms of rebound stomach tenderness are absent.
Your diagnosis?
Surgeons tactics?
Information sourses:
Main
1. Townsend CM, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery. 19th ed. Philadelphia, Pa: Saunders
Elsevier; 2012.
2. L.Ya.Kovalchuck, Yu.P.Spizhenko, V.F.Sayenko and others Hospital surgery. Ternopil: Ukrmendknyga, 1999.
3. Practical classes materials http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/classes_stud/en/med/lik/ptn/Surgery
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SURGICAL GASTROENTEROLOGY AND ENDOCRINOLOGY http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/metod_rozrobky...
/4/Topic%2008%20POSTRESECTION%20AND%20POSTVAGOTOMY%20SYNDROMES.%20CLASSIFICATION.%20CLINICS.htm
Additional
1. Manual Facultative Surgery under the edition of V.O.Shidlovsky Ternopil: Ukrmedknyga, 2002, section Diseases of the
rectum and the colon,
2. Compact disc Facultative surgery.
3. Schwartz's Principles of Surgery, Ninth Edition. F. Brunicardi. Philadelphia, Pa: Saunders Elsevier; 2009
4. Zollinger's Atlas of Surgical Operations, 9th Edition. Robert Zollinger Jr., Elsevier; 2010
5. Chen, Herbert. Illustrative Handbook of General Surgery. Berlin: Springer, 2010.
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2. Friendly behavour.
3. To explain to the patient a purpose of the visit, duration of conversation and to get
his agreement.
4. Correct and quiet conversation with a patient.
5. To get the agreement of patient for the performance of the examination. To take
complaints
6. To take anamnesis (to pay attention to the onset of the disease, defecation, swelling
of the abdomen, development of the pain irradiation)
7. To examine the patient (palpation of the large and small intestine, auscultation of
peristalsis, determination of particular symptoms)
8. Interpretation of laboratory and instrumental methods of investigation,
establishment of the diagnosis (X-Ray films)
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anamnesis)
7. To examine the patient (examination, palpation and percution of suprapubic area,
determination of Pasternacky's sign, digital rectal examination)
8. To detect the cause of acute urine delay
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General Approach to the Vascular Patient http://intranet.tdmu.edu.ua/data/kafedra/internal/surgery2/classes_stud/en...
Because the vascular system involves every organ system in our body, the symptoms of
vascular disease are as varied as those encountered in any medical specialty. Lack of adequate
blood supply to target organs typically presents with pain; for example, calf pain with lower
extremity (LE) claudication, postprandial abdominal pain from mesenteric ischemia, and arm
pain with axillosubclavian arterial occlusion. In contrast, stroke and transient ischemic attack
(TIA) are the presenting symptoms from middle cerebral embolization as a consequence of a
stenosed internal carotid artery (ICA). The pain syndrome of arterial disease usually is divided
clinically into acute and chronic types, with all shades of severity between the two extremes.
Sudden onset of pain can indicate complete occlusion of a critical vessel, leading to more
severe pain and critical ischemia in the target organ, resulting in lower limb gangrene or
intestinal infarction. Chronic pain results from a slower, more progressive atherosclerotic
occlusion, which can be totally or partially compensated by developing collateral vessels.
Acute on chronic is another pain pattern in which a patient most likely has an underlying
arterial stenosis that suddenly occludes; for example, the patient with a history of calf
claudication who now presents with sudden, severe acute limb-threatening ischemia. The
clinician should always try to understand and relate the clinical manifestations to the
underlying pathologic process.
Vascular History
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The patient with carotid disease in most cases is completely asymptomatic, having been
referred based on the finding of a cervical bruit or duplex finding of stenosis. Symptoms of
carotid territory TIAs include transient monocular blindness (amaurosis), contralateral
weakness or numbness, and dysphasia. Symptoms persisting longer than 24 hours constitute a
stroke. In contrast, the patient with chronic mesenteric ischemia is likely to present with
postprandial abdominal pain and weight loss. The patient fears eating because of the pain,
avoids food, and loses weight. It is very unlikely that a patient with abdominal pain who has
not lost weight has chronic mesenteric ischemia.
The patient with LE pain on ambulation has intermittent claudication that occurs in
certain muscle groups; for example, calf pain upon exercise usually reflects superficial femoral
artery (SFA) disease, while pain in the buttocks reflects iliac disease. In most cases, the pain
manifests in one muscle group below the level of the affected artery, occurs only with exercise,
and is relieved with rest only to recur at the same location, hence the term window gazers
disease. Rest pain (a manifestation of severe underlying occlusive disease) is constant and
occurs in the foot (not the muscle groups), typically at the metatarsophalangeal junction, and is
relieved by dependency. Often, the patient is prompted to sleep with their foot hanging off one
side of the bed to increase the hydrostatic pressure.
Specific vascular examination should include abdominal aortic palpation, carotid artery
examination, and pulse examination of the LE (femoral, popliteal, posterior tibial, and dorsalis
pedis arteries). The abdomen should be palpated for an abdominal aortic aneurysm (AAA),
detected as an expansile pulse above the level of the umbilicus. It also should be examined for
the presence of bruits. Because the aorta typically divides at the level of the umbilicus, an
aortic aneurysm is most frequently palpable in the epigastrium. In thin individuals, a normal
aortic pulsation is palpable, while in obese patients even large aortic aneurysms may not be
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The carotids should be auscultated for the presence of bruits, although there is a higher
correlation with coronary artery disease (CAD) than underlying carotid stenosis. A bruit at the
angle of the mandible is a significant finding, leading to follow-up duplex scanning. The
differential diagnosis is a transmitted murmur from a sclerotic or stenotic aortic valve. The
carotid is palpable deep to the sternocleidomastoid muscle in the neck. Palpation, however,
should be gentle and rarely yields clinically useful information.
For LE vascular examination, the femoral pulse usually is palpable midway between the
anterior superior iliac spine and the pubic tubercle. The popliteal artery is palpated in the
popliteal fossa with the knee flexed to 45 and the foot supported on the examination table to
relax the calf muscles. Palpation of the popliteal artery is a bimanual technique. Both thumbs
are placed on the tibial tuberosity anteriorly and the fingers are placed into the popliteal fossa
between the two heads of the gastrocnemius muscle. The popliteal artery is palpated by
compressing it against the posterior aspect of the tibia just below the knee. The posterior tibial
pulse is detected by palpation 2 cm posterior to the medial malleolus. The dorsalis pedis is
detected 1 cm lateral to the hallucis longus extensor tendon, which dorsiflexes the great toe
and is clearly visible on the dorsum of the foot. Pulses can be graded using either the
traditional four-point scale or the basic two-point scale system (Table 2). The foot also should
be carefully examined for pallor on elevation and rubor on dependency, as these findings are
indicative of chronic ischemia. Note should also be made of nail changes and loss of hair.
Ulceration and other findings specific to disease states are described in relevant sections below.
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After reconstructive vascular surgery, the graft may be available for examination,
depending on its type and course. The in situ LE graft runs in the subcutaneous fat and can be
palpated along most of its length. A change in pulse quality, aneurysmal enlargement, or a new
bruit should be carefully noted. Axillofemoral grafts, femoral-to-femoral grafts, and
arteriovenous access grafts usually can be easily palpated as well.
Ankle-Brachial Index
There is increasing interest in the use of the ankle-brachial index (ABI) to evaluate
patients at risk for cardiovascular events. An ABI <0.9 correlates with increased risk of
myocardial infarction and indicates significant, although perhaps asymptomatic, underlying
peripheral vascular disease. The ABI is determined in the following ways. Blood pressure (BP)
is measured in both upper extremities using the highest systolic BP as the denominator for the
ABI. The ankle pressure is determined by placing a BP cuff above the ankle and measuring the
return to flow of the posterior tibial and dorsalis pedis arteries using a pencil Doppler probe
over each artery. The ratio of the systolic pressure in each vessel divided by the highest arm
systolic pressure can be used to express the ABI in both the posterior tibial and dorsalis pedis
arteries (Fig. 1). Normal is more than 1. Patients with claudication typically have an ABI in the
0.5 to 0.7 range, and those with rest pain are in the 0.3 to 0.5 range. Those with gangrene have
an ABI of <0.3. These ranges can vary depending on the degree of compressibility of the
vessel. The test is less reliable in patients with heavily calcified vessels. Due to
noncompressibility, some patients such as diabetics and those with end-stage renal disease may
have an ABI of 1.40 or greater and require additional noninvasive diagnostic testing to evaluate
for peripheral arterial disease (PAD). Alternative tests include toe-brachial pressures, pulse
volume recordings, transcutaneous oxygen measurements, or vascular imaging (duplex
ultrasound).
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By placing serial BP cuffs down the LE and then measuring the pressure with a Doppler
probe as flow returns to the artery below the cuff, it is possible to determine segmental
pressures down the leg. These data can then be used to infer the level of the occlusion. The
systolic pressure at each level is expressed as a ratio, with the highest systolic pressure in the
upper extremities as the denominator. Normal segmental pressures commonly show high thigh
pressures 20 mmHg or greater in comparison to the brachial artery pressures. The low thigh
pressure should be equivalent to brachial pressures. Subsequent pressures should fall by no
more than 10 mmHg at each level. A pressure gradient of 20 mmHg between two subsequent
levels is usually indicative of occlusive disease at that level. The most frequently used index is
the ratio of the ankle pressure to the brachial pressure, the ABI. Normally the ABI is >1.0, and
a value <0.9 indicates some degree of arterial obstruction and has been shown to be correlated
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with an increased risk of coronary heart disease.1 Limitations of relying on segmental limb
pressures include: (a) missing isolated moderate stenoses (usually iliac) that produce little or
no pressure gradient at rest; (b) falsely elevated pressures in patients with diabetes and
end-stage renal disease; and (c) the inability to differentiate between stenosis and occlusion.2
Patients with diabetes and end-stage renal disease have calcified vessels that are difficult to
compress, thus rendering this method inaccurate, due to recording of falsely elevated pressure
readings. Noncompressible arteries yield ankle systolic pressures of 250 mmHg or greater and
an ABI of >1.40. In this situation, absolute toe and ankle pressures can be measured to gauge
critical limb ischemia. Ankle pressures <50 mmHg or toe pressures <30 mmHg are indicative of
critical limb ischemia. The toe pressure is normally 30 mmHg less than the ankle pressure, and
a toe-brachial index of <0.70 is abnormal. False-positive results with the toe-brachial index are
unusual. The main limitation of this technique is that it may be impossible to measure
pressures in the first and second toes due to pre-existing ulceration.
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Fig. 2 A Pulse volume recording is done by connecting blood pressure cuffs and plethysmograph to
various levels of the leg
Fig. 2 B Typical report of peripheral vascular study with arterial segmental pressure measurement
plus Doppler evaluation of the lower extremity.
Although isolated segmental limb pressures and PVR measurements are 85% accurate
when compared with angiography in detecting and localizing significant atherosclerotic
lesions, when used in combination, accuracy approaches 95%.3 For this reason, it is suggested
that these two diagnostic modalities be used in combination when evaluating PAD.
Ultrasound
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speed of image acquisition and resolution will continue to increase. The major limitations of
multidetector CTA are use of contrast and presence of artifacts caused by calcification and
stents. CTA can overestimate the degree of instent stenosis, while heavy calcification can limit
the diagnostic accuracy of the method by causing a ''blooming artifact."5 The artifacts can be
overcome with alteration in image acquisition technique. There are no randomized trials to
document the superiority of multidetector CTA over traditional angiography, but there is
emerging evidence to support the claim that multidetector CTA has sensitivity, specificity, and
accuracy that rival invasive angiography.
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Magnetic resonance angiography (MRA) has the advantage of not requiring iodinated
contrast agents to provide vessel opacification (Fig. 5). Gadolinium is used as a contrast agent
for MRA studies, and as it is generally not nephrotoxic, it can be used in patients with elevated
creatinine. MRA is contraindicated in patients with pacemakers, defibrillators, spinal cord
stimulators, intracerebral shunts, cochlear implants, and cranial clips. Patients with
claustrophobia may require sedation to be able to complete the test. The presence of metallic
stents causes artifacts and signal dropout; however, these can be dealt with using alternations
in image acquisition and processing. Nitinol stents produce minimal artifact.6 Compared to
other modalities, MRA is relatively slow and expensive. However, due to its noninvasive nature
and decreased nephrotoxicity, MRA is being used more frequently for imaging vasculature in
various anatomic distributions.
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Fig. 5. Magnetic resonance angiogram of aortic arch and carotid arteries. This study can
provide a three-dimensional analysis of vascular structures such as aortic arch branches, as well
as carotid and vertebral arteries
Diagnostic Angiography
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patient to the risks of both ionizing radiation and intravascular contrast. Nevertheless, contrast
angiography remains the most common invasive method of vascular investigation for both
diagnostic and therapeutic intervention. The angiogram usually provides the final information
needed to decide whether or not to proceed with operation or endovascular interventions.
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angiography study, multilevel lesions are demonstrated that include a focal left iliac artery
stenosis (large arrow), right superficial femoral occlusion (curved arrows), left superficial
femoral stenosis (small arrow), and multiple tibial artery stenoses (arrowheads).
The most important and controversial aspect of preoperative evaluation in patients with
atherosclerotic disease requiring surgical intervention is the detection and subsequent
management of associated CAD. Several studies have documented the existence of significant
CAD in 40 to 50% or more of patients requiring peripheral vascular reconstructive procedures,
10 to 20% of whom may be relatively asymptomatic largely because of their inability to
exercise. Myocardial infarction is responsible for the majority of both early and late
postoperative deaths. Most available screening methods lack sensitivity and specificity to
predict postoperative cardiac complications. There have been conflicting reports regarding the
utility of preoperative dipyridamole-thallium nuclear imaging or dobutamine-echocardiography
to stratify vascular patients in terms of perioperative cardiac morbidity and mortality. In nearly
one half of patients, thallium imaging proves to be unnecessary because cardiac risk can be
predicted by clinical information alone. Even with coronary angiography, it is difficult to relate
anatomic findings to functional significance, and hence, surgical risk. There are no data
confirming that percutaneous coronary interventions or surgical revascularization before
vascular surgical procedures impacts mortality or incidence of myocardial infarctions. In fact,
coronary angiography is associated with its own inherent risks, and patients undergoing
coronary artery bypass grafting or coronary percutaneous transluminal angioplasty (PTA)
before needed aortoiliac reconstructions are subjected to the risks and complications of both
procedures.
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The distal abdominal aorta and the iliac arteries are common sites affected by
atherosclerosis. The symptoms and natural history of the atherosclerotic process affecting the
aortoiliac arterial segment are influenced by the disease distribution and extent. Atherosclerotic
plaques may cause clinical symptoms by restricting blood flow due to luminal obstruction or
by embolizing atherosclerotic debris to the LE circulation. If the aortoiliac plaques reach
sufficient mass that impinge on the arterial lumen, obstruction of blood flow to lower
extremities occurs. Various risk factors exist that can lead to the development of aortoiliac
occlusive disease. Recognition of these factors and understanding this disease entity will
enable physicians to prescribe the appropriate treatment strategy that may alleviate symptoms
and improve quality of life.
Diagnostic Evaluation
On clinical examination, patients often have weakened femoral pulses and a reduced
ABI. Verification of iliac occlusive disease is usually made by color duplex scanning that
reveals either a peak systolic velocity ratio of 2.5 or greater at the site of stenosis and/or a
monophasic waveform. Noninvasive tests such as pulse volume recording (PVR) of the LE with
estimation of the thigh-brachial pressure index may be suggestive of aortoiliac disease. MRA
and multidetector CTA are increasingly being used to determine the extent and type of
obstruction. DSA offers the interventionalist the benefit of making a diagnosis and the option
of performing an endovascular treatment in a single session. Angiography provides important
information regarding distal arterial runoff vessels as well as the patency of the profunda
femoris artery (PFA). Presence of pelvic and groin collaterals is important in providing crucial
collateral flow in maintaining lower limb viability. It must be emphasized, however, that
patients should be subjected to angiography only if their symptoms warrant surgical
intervention.
Differential Diagnosis
Degenerative hip or spine disease, lumbar disc herniation, spinal stenosis, diabetic
neuropathy, and other neuromuscular problems can produce symptoms that may be mistaken
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for vascular claudication. Such cases can be distinguished from true claudication by the fact
that the discomfort from neuromuscular problems often is relieved by sitting or lying down, as
opposed to cessation of ambulation. In addition, complaints that are experienced upon standing
suggest nonvascular causes. When confusion persists, the use of noninvasive vascular
laboratory testing modalities, including treadmill exercise, can help establish the diagnosis.
The principal collateral pathways in severe aortoiliac artery occlusive disease or chronic
aortic occlusion that may provide blood flow distal to the aortoiliac lesion include: (a) the
SMA to the distal IMA via its superior hemorrhoidal branch to the middle and inferior
hemorrhoidals to the internal iliac artery (39%); (b) the lumbar arteries to the superior gluteal
artery to the internal iliac system (37%); (c) the lumbar arteries to the lateral and deep
circumflex arteries to the common femoral artery (CFA) (12%); and (d) Winslow's pathway
from the subclavian to the superior epigastric artery to the inferior epigastric artery to the
external iliac arteries at the groin (Fig. 7). In general, treatment indications for aortoiliac artery
occlusive disease include disabling claudication, ischemic rest pain, nonhealing LE tissue
wound, and LE microembolization that arise from aortoiliac lesions.
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Fig. 7. Pertinent collateral pathways are developed in the event of chronic severe aortoiliac
occlusive disease. As illustrated in this multidetector computed tomography angiography, these
collaterals include epigastric arteries (large white arrows), an enlarged inferior mesenteric
artery (white arrowhead), and enlarged lumbar arteries (black arrows).
Disease Classification
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Fig. 8. Aortoiliac disease can be classified into three types. Type I represents focal disease
affecting the distal aorta and proximal common iliac artery. Type II represents diffuse aortoiliac
disease above the inguinal ligament. Type III represents multisegment occlusive disease
involving aortoiliac and infrainguinal arterial vessels.
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Fig. 9. Type I aortoiliac disease is confined to the distal abdominal aorta (long arrow) or
proximal common iliac arteries. Due to the localized nature of this type of aortic obstruction
and formation of collateral blood flow around the occluded segment (short arrows),
limb-threatening symptoms are rare in the absence of more distal disease.
Fig. 10. Multidetector computed tomography angiography of the aortoiliac artery circulation in
a 63-year-old man with buttock claudication. Three-dimensional image reconstruction showing
intra-arterial calcification of the aorta (large arrows) and right common iliac artery (small
arrows). This is consistent with a type I aortoiliac occlusive disease.
Fig. 11. Atherosclerotic disease involving the aortoiliac segment can result in
microembolization of the lower leg circulation, resulting in trash foot or digital gangrene of
toes.
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Fig. 12. Type III aortoiliac occlusive disease is a multilevel disease pattern that affects the
aortoiliac segment as well as infrainguinal femoropopliteal vessels. Most patients with this
disease pattern tend to present with symptoms of advanced ischemia and require
revascularization for limb salvage rather than for claudication.
The most commonly used classification system of iliac lesions has been set forth by the
TASC II group with recommended treatment options. This lesion classification categorizes the
extent of atherosclerosis and has suggested a therapeutic approach based on this classification
(Table 3 and Fig. 13). According to this consensus document, endovascular therapy is the
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treatment of choice for type A lesions, and surgery is the treatment of choice for type D lesions.
Endovascular treatment is the preferred treatment for type B lesions, and surgery is the
preferred treatment for good-risk patients with type C lesions. In comparison to the 2000 TASC
II document, the commission has not only made allowances for treatment of more extensive
lesions, but also took into account the continuing evolution of endovascular technology and
the skills of individual interventionalists when stating that the patient's comorbidities, fully
informed patient preference, and the local operator's long-term success rates must be
considered when making treatment decisions for type B and type C lesions
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There is no effective medical therapy for the management of aortoiliac disease, but
control of risk factors may help slow progression of atherosclerosis. Patients should have
hypertension, hyperlipidemia, and diabetes mellitus controlled. They should be advised to stop
smoking. Most patients are empirically placed on antiplatelet therapy. A graduated exercise
program may improve walking efficiency, endothelial function, and metabolic adaptations in
skeletal muscle, but, there is usually minimal improvement in patients with aortoiliac disease
who are treated with these measures. Failure to respond to exercise and/or drug therapy should
prompt consideration for limb revascularization. Patients with buttock claudication and
reduced or absent femoral pulses who fail to respond to exercise and drug therapy should be
considered for revascularization because they are less likely than patients with more distal
lesions to improve without concomitant surgical or endovascular intervention.
Aortobifemoral Bypass
Both femoral arteries are initially exposed to ensure that they are adequate for the distal
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anastomoses. The abdomen is then opened in the midline, the small intestine is retracted to the
right, and the posterior peritoneum overlying the aorta is incised. A retroperitoneal approach
may be selected as an alternative in certain situations. This approach involves making a left
flank incision and displacing the peritoneum and its contents to the right. Such an approach is
contraindicated if the right renal artery is acutely occluded, because visualization from the left
flank is very poor. Tunneling of a graft to the right femoral artery also is more difficult from a
retroperitoneal approach, but can be achieved. The retroperitoneal approach has been reputed
to be better tolerated than midline laparotomy for patients with multiple previous abdominal
operations and with severe pulmonary disease. Further proposed advantages of the
retroperitoneal approach include less GI disturbance, decreased third-space fluid losses, and
ease with which the pararenal aorta can be accessed. There are randomized reports, however,
that support and refute the superiority of this approach. A collagen-impregnated, knitted
Dacron graft is used to perform the proximal aortic anastomosis, which can then be made in
either an end-to-end or end-to-side fashion using 3-0 polypropylene suture. The proximal
anastomosis should be made as close as possible to the renal arteries to decrease the incidence
of restenosis from progression of the atherosclerotic occlusive process in the future.
An end-to-end proximal aortic anastomosis is necessary in those patients with an aortic
aneurysm or complete aortic occlusion extending up to the renal arteries (Fig. 14). Although in
theory, the end-to-end configuration allows for less turbulence and less chance of competitive
flow with still patent host iliac vessels, there have not been consistent results to substantiate
differences in patency between end-to-end and end-to-side grafts. Relative indications for an
end-to-side proximal aortic anastomosis include the presence of large aberrant renal arteries, an
unusually large IMA with poor back-bleeding, suggesting inadequate collateralization, and/or
occlusive disease involving bilateral external iliac arteries. Under such circumstances,
end-to-end bypass from the proximal aorta to the femoral level devascularizes the pelvic region
because there is no antegrade or retrograde flow in the occluded external iliac arteries to supply
the hypogastric arteries. As a result of the pelvic devascularization, there is an increased
incidence of impotence, postoperative colon ischemia, buttock ischemia, and paraplegia
secondary to spinal cord ischemia, despite the presence of excellent femoral and distal pulses.
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Fig. 14. In an end-to-end proximal aortic anastomosis, the aorta is divided in half. The
proximal end of the aorta is anastomosed to the end of a prosthetic graft while the distal
divided aortic stump is oversewn.
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Fig. 15. In an end-to-side aortic anastomosis, the end of a prosthetic graft is connected to the
side of an aortic incision
Aortic Endarterectomy
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diameter, increased length, and exposure issues. The ability to establish an appropriate
endarterectomy plane is compromised due to the muscular and inherently adherent nature of the
media in this location. There is a higher incidence of early thrombosis and late failure with
extended aortoiliofemoral endarterectomy when compared to bypass grafting as a result of
recurrent stenosis.
Axillofemoral Bypass
Iliofemoral Bypass
One option for patients with unilateral occlusion of the distal common iliac or external
iliac arteries is iliofemoral grafting (Fig. 16). Long-term patency is comparable to
aortounifemoral bypass and because the procedure can be performed using a retroperitoneal
approach without clamping the aorta, the perioperative mortality is less.
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Fig. 16 B. A prosthetic bypass graft is used for an iliofemoral artery bypass in which the
proximal anastomosis is connected to the common iliac artery (long arrow) while the distal
anastomosis is connected to the common femoral artery (short arrow).
Femorofemoral Bypass
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patients with multiple comorbidities, because it is not necessary to cross-clamp the aorta. There
are no studies supporting the superiority of unsupported or externally supported PTFE over
Dacron for choice of conduit. The fear of the recipient extremity stealing blood from the
extremity ipsilateral to the donor limb is not realized unless the donor iliac artery and donor
outflow arteries are diseased. Depending on the skills of the interventionalist/surgeon, many
iliac lesions classified as TASC II B, C, or D can now be addressed using an endovascular
approach, thus obviating the need to perform a femorofemoral bypass. Additionally,
femorofemoral bypass can be used as an adjuvant procedure after iliac inflow has been
optimized with endovascular methods.
Obturator Bypass
An obturator bypass is used to reconstruct arterial anatomy in patients with groin sepsis
resulting from prior prosthetic grafting, intra-arterial drug abuse, groin neoplasm, or damage
from prior groin irradiation. This bypass can originate from the CIA, EIA, or uninvolved limb
of an ABF. A conduit of Dacron, PTFE, or autologous vein is tunneled through the
anteromedial portion of the obturator membrane to the distal superficial femoral or popliteal
artery. The obturator membrane must be divided sharply so as to avoid injury to adjacent
structures, and care must be taken to identify the obturator artery and nerve that pass
posterolaterally. After the bypass is completed and the wounds isolated, the infected area is
entered, the involved arteries are dbrided to healthy tissue, and vascularized muscle flaps are
mobilized to cover the ligated ends. There have been varied results in terms of patency and limb
salvage for obturator bypass. Some authors have reported 57% 5-year patency and 77% 5-year
limb salvage rates, whereas others have shown a high rate of reinfection and low patency
requiring reintervention.
Thoracofemoral Bypass
The indications for thoracofemoral bypass are (a) multiple prior surgeries with a failed
infrarenal aortic reconstruction and (b) infected aortic prosthesis. This procedure is more
physiologically demanding than other extra-anatomic reconstructions because the patient must
not only tolerate clamping the descending thoracic aorta but also performance of a left
thoracotomy. The graft is tunneled to the left CFA from the left thorax posterior to the left
kidney in the anterior axillary line using a small incision in the periphery of the diaphragm and
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an incision in the left inguinal ligament to gain access to the extraperitoneal space from below.
The right limb is tunneled in the space of Retzius in an attempt to decrease kinking that is more
likely to occur with subcutaneous, suprapubic tunneling. Thoracofemoral bypass has long-term
patency comparable to aortofemoral bypass.
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The symptoms of LE occlusive disease are classified into two large categories: ALI and
chronic limb ischemia (CLI). Ninety percent (90%) of acute ischemias are either thrombotic or
embolic. Frequently, sudden onset of limb-threatening ischemia may be the result of acute
exacerbation of the pre-existing atherosclerotic disease. Chronic ischemia is largely due to
atherosclerotic changes of the LE that manifest from asymptomatic to limb-threatening
gangrene. As the population ages, the prevalence of chronic occlusive disease of the LE is
increasing and it significantly influences lifestyle, morbidity, and mortality. In addition,
multiple comorbid conditions increase risks of surgical procedures. Endovascular interventions
become an important alternative in treating LE occlusive disease. However, despite rapid
evolving endovascular technology, LE endovascular intervention continues to be one of the
most controversial areas of endovascular therapy.
Epidemiology
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Diagnostic Evaluation
The diagnosis of LE occlusive disease often is made based upon a focused history and
physical examination, and confirmed by the imaging studies. A well-performed physical
examination often reveals the site of lesions by detecting changes in pulses, temperature, and
appearances. The bedside ABIs using BP cuff also aid in diagnosis. Various clinical signs and
symptoms are useful to differentiate conditions of viable, threatened, and irreversible limb
ischemia caused by arterial insufficiency.
Noninvasive studies are important in documenting the severity of occlusive disease
objectively. Ultrasound Dopplers measuring ABIs and segmental pressures are widely used in
North America and Europe. Normal ABI is >1.0. In patients with claudication, ABIs decrease
to 0.5 to 0.9 and to even lower levels in patients with rest pain or tissue loss. Segmental
pressures are helpful in identifying the level of involvement. Decrease in segmental pressure
between two segments indicates significant disease. Ultrasound duplex scans are used to
identify the site of lesion by revealing flow disturbance and velocity changes. A meta-analysis
of 71 studies by Koelemay and associates confirmed that duplex scanning is accurate for
assessing arterial occlusive disease in patients suffering from claudication or critical ischemia,
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with an accumulative sensitivity of 80% and specificity of over 95%. Adding an ultrasound
contrast agent further increases sensitivity and specificity to ultrasound technology. Other
noninvasive imaging technologies such as MRA and CTA are rapidly evolving and gaining
popularity in the diagnosis of LE occlusive disease (Figs. 17 and 18).
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Fig 18 B. Pedal arterial circulation. The high spatial resolution and image quality of
these images show three patent infrapopliteal runoff vessels and patent pedal vessels at the foot
level
Contrast angiography remains the gold standard in imaging study. Using contrast
angiography, interventionists can locate and size the anatomic significant lesions and measure
the pressure gradient across the lesion, as well as plan for potential intervention. Angiography
is, however, semi-invasive and should be confined to patients for whom surgical or
percutaneous intervention is contemplated. Patients with borderline renal function may need to
have alternate contrast agents such as gadolinium or carbon dioxide to avoid contrast-induced
nephrotoxicity.
Differential Diagnosis
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not always the result of arterial insufficiency. Ischemic ulcers occur on the toes or lateral side
of the foot and are painful. By comparison, venous ulcers, which also are common, occur above
the medial malleolus. These venous stasis ulcers are typically surrounded by a peripheral area
of darkened skin discoloration that is also known as lipodermatosclerosis. Neuropathic ulcers
usually are found on weight-bearing surfaces, have thick calluses, and are pain free. Ulcers may
be the result of more than one etiology. Rest pain must be distinguished from peripheral
neuropathy, which is prevalent in diabetic patients. Patients with diabetic neuropathy tend to
have decreased vibration and position sense and decreased reflexes. Spinal stenosis causes pain
that is exacerbated with standing and back extension.
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Table 7 Classification of Peripheral Arterial Disease Based on the Fontaine and Rutherford
Classifications
The Rutherford classification has four grades (0III) and seven categories (06).
Asymptomatic patients are classified into category 0; claudicants are stratified into grade I and
divided into three categories based on the severity of the symptoms; patients with rest pain
belong to grade II and category 4; patients with tissue loss are classified into grade III and
categories 5 and 6, based on the significance of the tissue loss. These clinical classifications
help to establish uniform standards in evaluating and reporting the results of diagnostic
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In a similar fashion, infrapopliteal arterial diseases are classified into four types based
on TASC II guideline (Fig. 19). Type A lesions are single lesions <1 cm in length not involving
the trifurcation; Type B lesions are multiple lesions <1 cm in length or single lesions shorter
than 1 cm involving the trifurcation; Type C lesions are those lesions extensively involving
trifurcation or those that are 1- to 4-cm stenotic or 1- to 2-cm occlusive lesions; Type D lesions
are occlusions longer than 2 cm or diffuse diseases.
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The term chronic limb ischemia is reserved for patients with objectively proven arterial
occlusive disease and symptoms lasting for more than 2 weeks. Symptoms include rest pain and
tissue loss such as ulceration or gangrene (Table 9). The diagnosis should be corroborated with
noninvasive diagnostic tests such as the ABI, toe pressures, and transcutaneous oxygen
measurements. Ischemic rest pain most commonly occurs below an ankle pressure of 50 mmHg
or a toe pressure <30 mmHg.2 Ulcers are not always of an ischemic etiology (Table 10). In
many instances, there are other etiologic factors (traumatic, venous, or neuropathic) that are
contributory, but it is underlying peripheral arterial disease (PAD) that may be responsible for
delayed or absent healing (Fig. 20). Healing of ulcers requires an inflammatory response and
greater perfusion than is required to support intact skin and underlying tissues. As a result, the
ankle and toe pressure levels needed for healing are higher than the pressures seen with
ischemic rest pain. For patients with ulcers or gangrene, the presence of CLI is suggested by an
ankle pressure <70 mmHg or a toe systolic pressure <50 mmHg.2 It is important to understand
that there is no definite consensus regarding the vascular hemodynamic parameters required to
make the diagnosis of CLI.
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Table 10. Symptoms and Signs of Neuropathic Ulcer versus Ischemic Ulcer
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Fig. 20 B An ischemic ulcer is characterized by a gangrenous skin change in the foot or toes.
The foot is usually cold to touch with absent pedal pulses. The foot is painful to touch with
decreased distal capillary refills.
One of the most common sites for occlusive disease is in the distal SFA as it passes deep
through the adductor canal. It may be that the entrapment by the adductor hiatus prevents the
compensatory dilation that occurs in atherosclerotic vessels. Stenoses, which develop here,
progress to occlusion of the distal third of the SFA (Fig. 21). When distal SFA occlusion
develops slowly, it may be totally asymptomatic because of development of collaterals from the
proximal SFA or the profunda femoris artery (PFA) can bypass the occlusion and reconstitute
the popliteal artery. Symptom development is a function of the extent of occlusion, adequacy of
collaterals, and also the activity level of the patients.
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Fig. 21. Computed tomography angiogram of a patient with an occluded left superficial femoral
artery (single long arrow) with reconstituted superficial femoral artery at the level of midthigh.
Diffuse arterial calcifications (double small arrows) are noted in the mid and distal left
superficial femoral arteries.
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foot off the side of the bed. The pain is severe and relentless, even with narcotics. Ischemic
ulceration most commonly involves the toes. Any toe can be affected. Occasionally, ulcers
develop on the dorsum of the foot. Ulceration can occur in atypical positions in an ischemic
foot from trauma such as friction from poorly fitting shoes. Injury to a foot with borderline
ischemia can convert an otherwise stable situation into one that is limb-threatening. The initial
development of gangrene commonly involves the digits. As with all vascular patients, it is
important to evaluate their risk factors, intercurrent cardiac diseases, and any prior vascular
interventions.
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and patency rates of endovascular intervention are closely related to the anatomic and
morphologic characters of the treated lesions. The TASC II work group made recommendations
on the intervention strategies of LE arterial diseases based on the morphologic characters.
Based on the TASC II guidelines, endovascular treatment is recommended for type A lesions,
open surgery is recommended for Type D lesions, and no recommendations were made for
Types B and C lesions. However, with rapid advancement in endovascular technologies, there
are increased numbers of lesions amendable to endovascular interventions.
There is less literature support on infrapopliteal endovascular intervention due to higher
complication and lower success rates. The treatment is restricted to patients with
limb-threatening ischemia who lack surgical alternatives. However, with further advancement of
endovascular technology and the development of new devices, endovascular intervention will
become an integral part of treatment (Table 11). By itself or combined with open technique,
percutaneous intervention plays an important role in therapeutic options for LE occlusive
disease. As described by the TASC II guidelines, four criteria should be measured to evaluate
the clinical success of the treatment: improvement in walking distance, symptomatic
improvement, quality of life, and overall graft patency. These criteria should all be carefully
weighed and evaluated for each individual before endovascular therapy.
Endovascular Treatment
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Technical Considerations
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seconds on the catheter insertion and subsequently 1000 units for each additional hour of the
procedure. Newer agents such as low molecular weight heparin, platelet IIb/IIIa inhibitor, direct
thrombin inhibitor, or recombinant hirudin have been available and can be used either alone or
in conjunction with heparin, particularly in patients sensitive to unfractionated heparin. After
procedures, all patients are placed on antiplatelet therapy such as aspirin. Additional
antiplatelet agents such as clopidogrel (Plavix) are given to selected patients with stent
placement for at least 6 weeks after LE interventions, unless otherwise contraindicated.
After the lesion is crossed with a wire, an appropriate balloon angioplasty catheter is
selected and tracked along the wire to traverse the lesion. The length of the selected catheter
should be slightly longer than the lesion and the diameter should be equal to the adjacent
normal vessel. The balloon tends to be approximately 10 to 20% oversized. The radiopaque
markers of the balloon catheter are placed so that they will straddle the lesion. Then, the
balloon is inflated with saline and contrast mixture to allow visualization of the insufflation
process under the fluoroscopy (Fig. 22). The patient may experience mild pain, which is not
uncommon. However, severe pain can be indicative of vessel rupture, dissection, or other
complications. An angiography is crucial in confirming the intraluminal location of the catheter
and absence of contrast extravasation. The inflation is continued until the waist of the
atherosclerotic lesion disappears and the balloon is at full profile. Frequently, several inflations
are required to achieve full profile of the balloon (Fig. 23). Occasionally, a lower profile
balloon is needed to predilate the tight stenosis so that the selected balloon catheter can cross
the lesion.
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Fig. 22 B. This lesion was treated with a balloon angioplasty catheter that inflated a
dilating balloon and expanded the flow lumen
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Fig. 23 B. This lesion was treated with cryoplasty, which lowered the balloon catheter
temperature to a temporary freezing state during the balloon angioplasty procedure (double
arrows)
Besides length and diameter, the operators need to be familiar with several balloon
characters. Noncompliant and low-compliant balloons tend to be inflated to their preset
diameter and offer greater dilating force at the site of stenosis. Low-compliant balloons are the
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mainstay for peripheral intervention. A balloon with a low profile is used to minimize
complication at the entry site and for crossing the tight lesions. Upon inflation, most balloons
do not rewrap to their preinflation diameter and assume a larger profile. Furthermore,
trackability, pushability, and crossability of the balloon should be considered when choosing a
particular type. Lastly, shoulder length is an important characteristic when performing PTA to
avoid injury to the adjacent arterial segments. After PTA, a completion angiogram is performed
while the wire is still in place. Leaving the wire in place provides access for repeating the
procedure if the result is unsatisfactory.
PTA is an established and effective therapy for select patients with LE occlusive
diseases. Studies have shown that PTA of the femoropopliteal segment achieved over a 90%
technical success rate and a 38 to 58% 5-year primary patency rate. However, efficacy of PTA
is highly dependent upon anatomic selection and patient condition. PTA of lesions longer than
7 to 10 cm offer limited patency, while PTA of shorter lesions, such as those that are <3 cm,
have fairly good results. Lofberg and associates performed 127 femoropopliteal PTA
procedures and reported a primary 5-year success rate of 12% in limbs with an occlusion
longer than 5 cm vs. 32% in limbs with an occlusion <5 cm in length.151 Occlusive lesions
have much worse initial technical success rates than stenotic lesions. Concentric lesions
respond better to PTA than eccentric lesions, and heavy calcifications have a negative impact
on success rates. A meta-analysis by Hunink and associates showed that adjusted 5-year
primary patencies after angioplasty of femoropopliteal lesions varied from 12 to 68%, the best
results being for patients with claudication and stenotic lesions. Distal runoff is another
powerful predictor of long-term success. Johnston analyzed 254 consecutive patients who
underwent femoral and popliteal PTA and reported that 5-year patency rates of 53% for
stenotic lesions and 36% for occlusive lesions in patients with good runoffs vs. a 5-year
patency of 31% for stenotic lesions and 16% for occlusive lesions in patients with poor runoff.
Literature reviews showed that 5-year patency rates varied from 27 to 67% based on the runoff
statuses.
Due to limited success with infrapopliteal PTA, the indication for infrapopliteal artery
PTA is stringent, reserved for limb salvage. Current patency rates from infrapopliteal PTA can
be improved further by proper patient selection, ensuring straight-line flow to the foot in at
least one tibial vessel, and close patient surveillance for early reintervention. Possible future
advances including the use of drug-eluting stents (DES), cutting balloons, and atherectomy
devices are being investigated to improve clinical outcomes following endovascular
interventions on the tibial arteries. Varty and associates reported a 1-year limb salvage rate of
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77% in patients with critical ischemia who underwent infrapopliteal PTA. In patients with
favorable anatomies, a 2-year limb salvage rate after infrapopliteal artery PTA is expected to
exceed 80 %.
Subintimal Angioplasty
The technique of SA was first described in 1987 when successful establishment of flow
was made by accidental creation of a subintimal channel during treatment of a long popliteal
artery occlusion. SA is recommended for chronic occlusion, long segments of lesion, and
heavily calcified lesions. In addition, this technique is applicable for vessels with diffuse
diseases and for vessels that had previously failed an intraluminal approach because it is
difficult to negotiate the wire across the entire diseased segment without dissection.
The principle of this technique is to bypass the occlusion by deliberately creating a
subintimal dissection plan commencing proximal to the lesion and continuing in the subintimal
space before breaking back into the true lumen distal to the lesion. The occluded lumen is
recanalized through the subintimal plan. SA can be performed through either ipsilateral
antegrade or contralateral retrograde using the CFA approach. If selecting contralateral CFA
puncture, a long guiding sheath is placed across the aortic bifurcation to provide access for the
femoropopliteal and infrapopliteal vessels. The subintimal dissection is initiated at the origin
of an occlusion by directing the tip of an angled guidewire, usually an angled hydrophilic wire
such as Glidewire. A supporting catheter is used to guide the tip of the guidewire away from
the important collaterals. When the wire is advanced, a loop is naturally formed at the tip of the
guidewire. Once the subintimal plan is entered, the wire tends to move freely in the dissection
space. Subintimal location of the wire and the catheter can be confirmed by injecting a small
amount of diluted contrast. At this point, the wire and the catheter are then advanced along the
subintimal plan until the occlusion segment is passed. A loss of resistance is often encountered
as the guidewire re-enters the true lumen distal to the occlusion. Recanalization is confirmed
by advancing the catheter over the guidewire beyond the point of re-entry and obtaining an
angiogram. This is followed by a balloon angioplasty. To confirm the patency following
balloon dilatation, a completion angiogram is performed before withdrawing the catheter and
wire. If flow is impaired, repeat balloon dilatation may be necessary. Frequently, a stent is
required to maintain a patent lumen and treat residual stenosis if more than a 30% luminal
reduction is confirmed on completion angiogram.
Multiple studies have demonstrated the efficacy of SA. Bolia and his colleagues and
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London and his colleagues reported their extensive experiences on SA for treating long
segment occlusions of infrainguinal vessels. They achieved a technical success rate of over
80% for both femoropopliteal and tibial arteries. One-year patency rates varied from 53% for
infrapopliteal vessels to 71% for femoropopliteal segments. Limb salvage rates reached over
80% at 12 months. They also reported that the factors influencing patency are smoking, number
of runoff vessels, and occlusion length. Studies by other groups showed similar results.
Treiman and colleagues treated 25 patients with 6- to 18-cm femoropopliteal occlusion and
achieved a technical success rate of 92% and a 12-month primary patency rate of 92%, while
Lipsitz and associates reported a technical success rate of 87% in treating 39 patients and
achieved a 12-month cumulative patency rate of 74%. Additionally, Ingle and associates
reported a technical success rate of 87% on 67 patients with femoropopliteal lesions and a
36-month limb salvage rate of 94%. As demonstrated herein, although technical success rates
are similar in most series, the patency rates vary widely in different studies. Patient selection,
anatomic character, and lesion locations may account for the wide range of outcomes.
Stent Placement
Although suggested by Dotter during the late 1960s, the use of an endoluminal stent was
not pursued until the limitations of PTA were widely recognized. There are several situations
where stent placement is appealing. The primary indication is the potential salvage of an
unacceptable angioplasty result. Stent placement is typically used when residual stenosis after
PTA is 30% or greater. An endoluminal stent is also used for dissection, perforation, and other
PTA complications. Primary stent placement has become a viable alternative for treating
ulcerative lesions that may potentially be the source for embolization. Primary stent is also
used to treat occlusive lesions that have a tendency of reocclusion and distal embolization after
PTA. In addition, an endoluminal stent is potentially beneficial for early restenosis post-PTA.
DESs are currently under investigation in the United States and may be promising in
decreasing restenotic rates.
Even though technical success rates are high, a published series on femoropopliteal
artery stents show that patency rates are comparable to PTA alone with primary patency rates
varying from 18 to 72% at 3 years. Gray and associates stented 58 limbs after suboptimal PTA
for long SFA lesions and demonstrated a 1-year primary patency rate of 22%. However,
Mewissen treated 137 limbs using self-expanding SMART nitinol stents in patients with TASC
II A, B, and C femoropopliteal lesions and reported a 1-year primary patency rate of 76% and a
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24-month primary patency rate of 60%. Appropriate patient selection and the anatomic
characteristics of the lesions are crucial in the success of treatment outcomes. Additionally,
stent characteristics may contribute to the patency rate.
Several clinical studies have demonstrated the significant improvements of the new
generation of nitinol stents for the SFA lesions: the German Multicenter Experience, the
Mewissen trial, the BLASTER Trial, and the SIROCCO trials.161 The German Multicenter
Experience was a retrospective review of 111 SFA stenting procedures and found the 6-month
patency rates for Smart stents and Wall stents were 82% and 37%, respectively. The BLASTER
(Bilateral Lower Arterial Stenting Employing Reopro) Trial evaluated the feasibility of using
nitinol stents with and without IV abciximab for the treatment of femoral artery disease.
Preliminary results showed a 1-year clinical patency rate of 83%.
Furthermore, DESs, which proved effective at decreasing restenosis in coronary
intervention, may offer another promising alternative in LE diseases. The drug, released over a
period of time, interferes with smooth muscle cell proliferation, the main cellular element and
source of extracellular-matrixproducing restenosis. The first DES clinical trial used Cordis
Cypher SMART stents coated with sirolimus (SIROCCO trial). The SIROCCO results showed
binary inlesion restenosis rates of 0% in the sirolimus-eluting group vs. 23.5% in the
noneluting group at 6-month follow-up angiography.
Stent Graft
The concept of endobypass using stent graft in treating atherosclerotic SFA disease has
been entertained. A stent graft is placed percutaneously across a long segment or multiple
segments of lesions and is used to create a femoropopliteal bypass. Theoretically, endobypass
has the potential of being as successful as surgical bypass graft by relining the vessel wall in its
anatomical position without the negative impact of anastomosis. Stent grafts can be divided
into two categories: unsupported and fully supported. The unsupported grafts consist of
segments of bypass graft, such as PTFE, with an expandable stent at one or both ends. The
unsupported grafts are flexible with a low profile, but prone to external compression. The
supported stent grafts consist of a metallic skeleton covered with graft fabric. The presence of a
dense metal skeleton promotes an extensive inflammatory response and increases the risk of
thrombosis. There is no FDA-approved stent graft for peripheral intervention. However,
Viabahn (WL Gore, Calif) is the most commonly used device in the United States, composed of
an ultrathin PTFE graft externally supported by a self-expanding nitinol meshwork. The
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Viabahn device has a specific delivery mechanismpulling back the attached stringwhich
results in a proximal-to-distal delivery of the endoprosthesis.
Although it is an intriguing concept, data on endobypass results are limited and the graft
thrombosis rate is high. Additionally, covering major collateral vessels can potentially
jeopardize the viability of the limb if stent graft occlusion occurs. Bauermeister treated 35
patients with Hemobahn and reported a 28.6% occlusion rate on an average 7-month follow-up.
Kedora and colleagues recently conducted a prospective, randomized study comparing covered
PTFE/nitinol self-expanding stent grafts with prosthetic above-the-knee femoropopliteal
bypass. Fifty limbs were randomized into each group. Primary patency at 1-year was
approximately 74% for both cohorts, with a mean follow-up of 18 months. The covered nitinol
PTFE stent graft in the SFA had a 1-year patency rate comparable to surgical bypass, with a
significantly shorter hospital stay (0.9 vs. 3.1 days).
Atherectomy
The basic principle of atherectomy is to remove the atheroma from obstructed arterial
vessels. There are currently five atherectomy devices approved by the FDA: Simpson
AtheroCath (DVI, Redwood City, Calif), Transluminal Extraction Catheter (Interventional
Technologies, San Diego, Calif), Theratec recanalization arterial catheter (Trac-Wright), Auth
Rotablator (Heart Technologies, Redmond, Wash), and SilverHawk system (FoxHollow
Technologies, Redwood City, Calif). These devices either cut and remove or pulverize the
atheroma plaques.
The Simpson AtheroCath has a directional cutting element that is exposed to one third
of the circumference of the arterial wall. The atheroma protruding into the window is excised
and pushed into the collection chamber. The Transluminal Extraction Catheter has an
over-the-wire, nondirectional cutter mounted on the distal end of a torque tube. The excised
atheroma is simultaneously removed by aspiration through the torque tube. The Theratec
recanalization arterial catheter is a nondirectional, noncoaxial, atheroablative device. The
rotating cam tip pulverizes the atheromatous lesion into minute particles. The Auth Rotablator
is a nondirectional, coaxial, atheroablative device with a metal burr embedded with fine
diamond chips. Lastly, the SilverHawk device, approved by the FDA for peripheral use in
2003, is a monorail catheter designed to overcome the drawback of direction atherectomy
catheter, such as the Simpson AtheroCath. The working end consists of a hinged housing unit
containing a carbide cutting blade. The blade is activated from the motor drive unit and the
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catheter is then advanced through the length of the lesion. Once each pass is completed, the
cutter then packs the tissue into the distal end of the nosecone to maximize collection capacity.
The SilverHawk can then either be removed or torqued to treat a different quadrant in the same
lesion or other lesions.
Despite the promising early technical and clinical success, the mid- and long-term results
have been disappointing due to a high incidence of restenosis. However, a multicenter clinical
registry of plaque atherectomy in patients with femoropopliteal occlusive disease showed
potential clinical efficacy of this technology as the 6- and 12-month rates of survival free of
target lesion revascularization were 90 and 80%, respectively. Importantly, nearly three fourths
(73%) of patients treated with plaque excision modality did not require adjunctive
endovascular therapy as infrainguinal stenting was necessary in only 6.3% of lesions. Results
from the TALON registry support the role of plaque excision in selective patients with LE
arterial disease.
Laser Atherectomy
Since laser atherectomy was reported in the 1960s, a variety of innovative approaches
have been developed in an effort to overcome the limitation of laser angioplasty. Recent
developments in excimer laser technology have led to increased optimism regarding the ability
to safely deliver laser energy. Excimer laser atherectomy approved by the FDA for peripheral
artery intervention uses precision laser energy control (shallow tissue penetration) and safer
wavelengths (ultraviolet as opposed to the infrared spectra in older laser technology), which
decreases perforation and thermal injury to the treated vessels.
A laser atherectomy catheter, with diameters varying from 0.9 mm to 2.5 mm, is tracked
over the guidewire to the desired target. Once activated, the excimer laser uses ultraviolet
energy to ablate the lesion and create a nonthrombogenic arterial lumen. This lumen is further
dilated by an angioplasty balloon. Because the excimer laser can potentially reduce the rate of
distal embolization by evaporating the lesion, it may be used as an adjunct tool for ostial
lesions and lesions that can be traversed by a wire but not an angioplasty balloon catheter.
Several studies regarding the use of excimer laser atherectomy combined with balloon
angioplasty on LE occlusive disease have shown promising clinical outcomes. Peripheral
excimer laser angioplasty trials involved 318 patients with chronic SFA occlusion. They
achieved a technical success rate of 83.2%, a 1-year primary patency rate of 33.6%, and an
assisted primary patency rate of 65%.168 Steinkamp and his colleagues treated 127 patients
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with long-segment of popliteal artery occlusion using laser atherectomy followed by balloon
angioplasty and reported a 3-year primary patency rate of 22%. The multicenter clinical trial
evaluating the use of laser angioplasty for critical limb ischemia supports the efficacy of this
treatment modality in selective patients as the 6-month primary patency rate and clinical
improvement were 33 and 89%, respectively.
Angioplasty-Related Complications
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Fig. 24. Due to various geometric forces, including torsion, compression, extension, and
flexion, which exert on the superficial femoral artery, stent fracture (arrows) is a known
complication following superficial femoral artery stent placement.
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Overall complication rates associated with atherectomy range from 15.4 to 42.8% and
include spasm, thrombosis, dissection, perforation, distal emboli, no reflow, and hematoma.
Jahnke and associates conducted a prospective study evaluating high-speed, rotational
atherectomy in 15 patients with infrapopliteal occlusive disease. They yielded a 94% technical
success rate, which was complicated by vessel rupture (5%), distal embolization (5%), and
arterial spasm (5%). Although the excimer laser atherectomy reduces embolic events by
evaporating the lesion, embolization still remains a problematic complication. Studies show
that distal embolic events occur in 3 to 4% of procedures, and perforation in 2.2 to 4.3% of
cases. Other complications compromising laser atherectomy therapy include acute reocclusion,
vasospasm, direct vessel injury, and dissection.
Endarterectomy
Bypass grafting
Bypass grafting remains the primary intervention for LE occlusive disease. The type of
bypass and conduit are important variables to consider. Patients with occlusive disease limited
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to the SFA, who have at least 4 cm (ideally 10 cm) of normal popliteal artery reconstituted
above the knee joint and at least one continuous vessel to the foot, can be treated with an
above-knee (AK) femoropopliteal bypass graft. Despite the fact that in this above-knee
location, the differential patencies between prosthetic (PTFE) and vein graft are comparable;
undoubtedly, it remains ideal to use a saphenous vein as the bypass conduit, if possible. Saving
the vein for future coronary artery bypass or distal leg bypass grafting has been shown to be a
flawed argument. One must also take into consideration that the consequences to the vascular
outflow after a thrombosed prosthetic are worse than after a thrombosed vein graft.
When the disease extends to involve the popliteal artery or the tibial vessels, the surgeon
must select an appropriate outflow vessel to perform a bypass. Suitable outflow vessels are
defined as uninterrupted flow channels beyond the anastomosis into the foot. In order of
descending preference, they are: AK popliteal artery, below-knee (BK) popliteal artery,
posterior tibial artery, anterior tibial artery, and peroneal artery. In patients with diabetes, it is
frequently the peroneal artery that is spared. Although the peroneal artery has no direct flow
into the foot, collateralization to the posterior tibial and anterior tibial arteries makes it an
appropriate outflow vessel. There is no objective evidence to preferentially select tibial over
peroneal arteries if they are vessels of equal caliber and quality. The dorsalis pedis, which is
the continuation of the anterior tibial in the foot, is frequently spared from atherosclerotic
disease and can be used as a target for distal bypasses. Patency is affected by the length of the
bypass (longer bypasses have reduced patency), quality of the recipient artery, extent of runoff
to the foot, and quality of the conduit (saphenous vein/graft). Five-year assisted patency rates
for infrapopliteal venous bypasses are 60%. Venous conduits also have been shown to be
suitable for bypasses to plantar arteries. In this location, venous conduits have a 3-year limb
salvage of 84% and a 3-year secondary patency of 74%. A meta-analysis suggests
unsatisfactory results when PTFE-coated grafts are used to bypass to infrapopliteal arteries. In
this location, prosthetic grafts have a 5-year primary patency rate of 30.5%. Additionally, due
to distal embolization and compromise of outflow vessels, prosthetic graft occlusion may have
more severe consequences than vein graft occlusion.
Two techniques are used for distal bypass grafting: reversed saphenous vein grafting and
in situ saphenous vein grafting. There is no difference in outcomes (patency or limb salvage)
between these techniques. In the former, the vein is excised in its entirety from the leg using
open or endoscopic vein harvest, reversed to render the valves nonfunctional, and tunneled
from the CFA inflow to the distal target vessels. End-to-side anastomoses are then created.
Several adjunctive techniques have been tried to improve the patency of bypass grafts to
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tibial arteries. Creation of an arteriovenous fistula at the distal anastomosis is one option, but it
has not been shown to improve patency. Another method involves creating various
configurations of vein cuffs or patches at the distal anastomosis in an attempt to streamline the
flow and to reduce the likelihood of neointimal hyperplasia. Results with this approach are
more promising, especially when done to improve patency of a below-the-knee prosthetic;
however, there are no definitive comparative trials that support the superiority of one
configuration over another.
Amputation
Fifteen percent of vein grafts will develop intrinsic stenoses within the first 18 months
following implantation. Consequently, patients with a vein graft were entered into duplex
surveillance protocols (scans every 3 months) to detect elevated (>300 cm/s) or abnormally low
(<45 cm/s) graft velocities early. Stenoses greater than 50%, especially if associated with
changes in ABI, should be repaired to prevent graft thrombosis. Repair usually entails patch
angioplasty or short-segment venous interposition, but PTA/stenting is an option for short,
focal lesions. Grafts with stenoses that are identified and repaired before thrombosis have
assisted primary patency identical to primary patency, whereas a thrombosed autogenous
bypass has limited longevity, resulting from ischemic injury to the vein wall. Secondary
patency is markedly inferior to primary assisted patency. The recommendation for routine
duplex ultrasound surveillance of autogenous infrainguinal bypasses was recently brought into
question by a randomized, controlled trial that demonstrated no cost benefit or quality-of-life
improvement after 18 months in patients with femoropopliteal venous bypasses. Many
surgeons continue with programs of vein graft surveillance, as has been suggested in older
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trials, awaiting further confirmation of the findings from the more recent study. When
intervening on a failing infrainguinal bypass, the original indication for surgery is an important
consideration. Limb salvage rates for occluded grafts are better if the indication for the original
bypass was claudication rather than rest pain or tissue loss. An acutely occluded infrainguinal
graft (30 postoperative days) has a 25% limb salvage rate.
Limb Swelling
Wound Infection
Because the most common inflow vessel for distal bypass is the CFA, groin infection is
common and occurs in 7% of cases. When an autogenous conduit such as a saphenous vein is
used, most infection can be managed with local wound care because it involves the
subcutaneous tissue or skin rather than infection of the actual vein. When a prosthetic graft has
been used, management of graft infection is a major undertaking. Infection of a LE prosthetic
bypass graft is associated with a significant amputation rate because of the tendency for graft
thrombosis and anastomotic disruption. Prosthetic graft infections cannot be eradicated with
antibiotics, and they mandate graft excision and complex revascularization using a vein, if
available.
Autogenous Vein
Autogenous vein is superior to prosthetic conduits for all infrainguinal bypasses, even in
the AK position. This preference is applicable not only for the initial bypass but also for
reoperative cases. For long bypasses, ipsilateral great saphenous vein (GSV), contralateral
GSV, small saphenous vein, arm vein, and spliced vein are used, in decreasing order of
preference. If only a short segment of vein is missing, the SFA can be endarterectomized and
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the proximal anastomosis performed distally to decrease the length of the conduit and to avoid
harvesting and splicing additional vein. When GSV is not available and a relatively short
bypass is necessary, arm vein or small saphenous vein is effective. Small saphenous vein is of
particular use when a posterior approach is used. If a longer bypass with vein is necessary, arm
vein is preferable because it is less awkward to harvest. Another conduit alternative is to
harvest the upper arm basilic, median cubital, and cephalic veins in continuity, while incising
valves in the basilic segment and using the cephalic segment in reversed configuration to
provide a relatively long, unspliced autogenous conduit.
Cryopreserved Grafts
Cryopreserved grafts are usually cadaveric arteries or veins that have been subjected to
rate-controlled freezing with dimethyl sulfoxide and other cryopreservants. Cryopreserved vein
grafts are more expensive than prosthetic grafts and are more prone to failure. The endothelial
lining is lost as part of the freezing process, making these grafts prone to early thrombosis.
Cryopreserved grafts also are prone to aneurysmal degeneration. Despite the fact that these
grafts have not performed as well as prosthetic bypasses and autogenous vein in clinical
practice, they can still play a role when revascularization is required following removal of
infected prosthetic bypass grafts, especially when autogenous vein is unavailable to create a
new bypass through clean tissue planes.
Human umbilical vein (HUV) is less commonly used than PTFE, because it is thicker
and more cumbersome to handle and because of concerns about aneurysmal degeneration. HUV
allografts are stabilized with glutaraldehyde and do not have viable cells or antigenic reactivity.
These grafts have poor handling characteristics and require extra care when suturing because of
an outer Dacron mesh wrapping, which is used to decrease aneurysmal degeneration. Dardik
and colleagues have reported favorable results after using HUV and an adjunctive distal
arteriovenous fistula. One trial comparing HUV with PTFE and saphenous vein showed that
HUV was better than PTFE but worse than saphenous vein in terms of 5-year patency in the
AK location. In a systematic review, HUV appears to perform better than cryopreserved veins.
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If vein is truly unavailable, PTFE or Dacron is the best option for AK bypass. The
addition of rings to PTFE did not confer benefit in a single prospective, randomized clinical
trial. For infrageniculate prosthetic bypasses, use of a vein patch, cuff, or other venous
anastomotic modification can improve patency (52% patency at 2 years for PTFE with vein cuff
vs. 29% for PTFE with no cuff) and also improve limb salvage (84% vs. 62%).
Although prosthetic grafts are readily available, easy to handle, and do not require
extensive dissection to harvest, their propensity to undergo thrombosis and develop neointimal
hyperplasia makes them a less favorable alternative when compared to vein. In a recent review
of vein and prosthetic AK femoropopliteal bypasses, the 5-year primary patency rates were
reported to be 74 and 39%, respectively. Outcomes were even worse for BK prosthetic
bypasses. Unfortunately, the use of autologous venous conduits is not possible in as many as
30% of patients. The GSV may be unsuitable because of small size and poor quality or
unavailable due to prior harvest.
Methods to improve prosthetic graft performance have consisted of altering the geometry
at the distal anastomosis to get the benefit obtained with vein cuffs (Distaflo, Bard Peripheral
Vascular, Tempe, Ariz) and covalently bonding agents onto the luminal surface with
anticoagulant, anti-inflammatory and antiproliferative characteristics (Propaten, Gore,
Flagstaff, Ariz). One randomized trial that compared precuffed PTFE and PTFE with a vein
cuff enrolled 104 patients at 10 centers. Eighty-nine patients were randomized to 47 precuffed
PTFE bypasses and 44 bypasses with a vein cuff. At 1 and 2 years, primary patency rates were
52 and 49% for the precuffed group and 62 and 44% for the vein cuffed group, respectively. At
1 year and 2 years, the limb salvage rate was 72 and 65% for the precuffed group and 75 and
62% in the vein cuffed group, respectively. Although numbers are small and follow-up short,
the midterm analysis revealed that Distaflo precuffed grafts and PTFE grafts with vein cuff had
similar results. The authors concluded that a precuffed graft was a reasonable alternative for
infragenicular reconstruction in the absence of saphenous vein. Other authors have been less
optimistic and question if there is any benefit derived from geometrically altering prosthetic
conduits.
Another approach for improving outcomes when using prosthetic for bypass grafts
involves bonding anticoagulants to the conduit. The Gore Propaten graft has heparin bonded
onto the luminal surface of the PTFE graft using Carmeda BioActive Surface technology,
which immobilizes the heparin molecule with a single covalent bond that does not alter its
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anticoagulant properties. The heparin binding does not alter the microstructure and handling
characteristics of the PTFE. A prospective, randomized trial by Devine and associates
suggested that heparin-bonded Dacron or PTFE was superior to plain PTFE for AK popliteal
bypasses. The 3-year primary patency for the heparin-bonded grafts was 55% compared with
42% for PTFE (P <.044). Both of these patency rates are inferior to GSV; however, if the
improved results with heparin bonding continue to be substantiated, then heparin-bonded
prosthetic grafts will become the preferred conduit for AK bypass in the absence of suitable
vein. A recent review of available studies with this graft showed an 80% 1-year patency for BK
bypasses.195 Randomized, controlled clinical trials with more patients and longer follow-up
are necessary to validate whether the PROPATEN vascular graft is superior to other prosthetics,
and if, indeed, it is comparable to autogenous vein for BK interventions.
Balloon angioplasty of the femoropopliteal vessels has not enjoyed the degree of success
seen with iliac angioplasty. Patency in this region is dependent upon whether the patient
presents with claudication vs. limb-threatening ischemia, the status of the distal runoff vessels,
and lesion morphology. Initial technical success for femoropopliteal angioplasty is seen in 80
to 90% of cases, with failures to cross a lesion occurring in 7% of stenoses and 18% of
occlusive lesions. Studies have shown that PTA of the femoropopliteal segment achieved
greater than a 90% technical success rate and had a 59% primary patency rate at 5-years. PTA
of lesions longer than 7 to 10 cm results in compromised patency, while PTA of shorter lesions
(<3 cm) gives fairly good results. Lofberg and associates performed 127 femoropopliteal PTA
procedures and reported a primary patency rate at 5-year follow-up of 12% in limbs with
occlusion longer than 5 cm vs. 32% in limbs with occlusion <5 cm in length. Occlusive lesions
have much worse initial technical success rates than stenotic lesions. Concentric lesions
respond better to PTA than eccentric lesions, and heavy calcifications have a negative impact
on success rates. Distal runoff is another powerful predictor of long-term success.
Johnston and associates analyzed 254 consecutive patients who underwent
femoropopliteal PTA and reported a 5-year patency rate of 53% for stenotic lesions and 36%
for occlusive lesions in patients with good runoff vs. 5-year patency of 31% for stenotic lesions
and 16% for occlusive lesions in patients with poor runoff. A meta-analysis by Hunink and
colleagues showed that adjusted 5-year primary patencies after angioplasty of femoropopliteal
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lesions varied from 12 to 68%, the best results occurring in patients with claudication and
stenotic lesions. Although the initial technical success is better for stenoses than occlusions,
long-term patency rates for stenoses and short occlusions have been variable and there have
been conflicting results regarding the efficacy of stent use. Early published series that
examined efficacy of femoropopliteal artery stents showed patency rates that were comparable
to stand-alone PTA with primary patency rates varying from 18 to 72% at 3 years. Patient
selection and the anatomic character of the lesions may play important roles in the outcomes.
Additionally, stent characteristics may contribute to the patency rate. Several clinical studies
have demonstrated significant improvements in patency when the newer generations of nitinol
stents are used to treat SFA lesions.
Mewissen treated 137 lower limbs in 122 patients with CLI, secondary to TASC II A (n
= 12) or TASC II B or C (n = 125) lesions in the SFA. Patients were treated with Cordis
SMART self-expanding nitinol stents. Binary restenosis (>50%) was measured by standard
duplex velocity criteria at various postintervention intervals. Primary stent patency, defined as
absence of binary restenosis in this study, was calculated by life table methods from the time of
intervention. The mean lesion length was 12.2 cm (range, 4 to 28 cm). The technical success
was 98%. Mean follow-up was 302 days. The primary stent patency rates were 92%, 76%,
66%, and 60% at 6, 12, 18, and 24-months, respectively. Fereira and associates treated 59
patients who had 74 femoropopliteal lesions (60% TASC II D) with Zilver nitinol
self-expanding stents (COOK, Bloomington, Ind). Mean recanalization length was 19 cm
(range 3 to 53 cm). Mean follow-up time was 2.4 years (range 3 days to 4.8 years).
Kaplan-Meier estimates for primary patency rates were 90%, 78%, 74%, 69%, and 69% at 1, 2,
3, 4, and 4.8 years, respectively.
There is general agreement that for suboptimal PTA of an SFA lesion, stent placement is
indicated, but a recent randomized trial by Schillinger and associates suggests that primary
stenting results in lower restenosis rates than PTA and selective stenting. Restenosis rates at 2
years were 45.7% vs. 69.2% in favor of primary stenting compared with PTA and optional
secondary stenting using an intention-to-treat analysis (P = .031). Consistently, stenting, both
primary and selective, was superior to stand-alone PTA with respect to the occurrence of
restenosis (49.2% vs. 74.3%; P = .028) by a treatment-received analysis.
Nitinol bare metal stents that are designed specifically for BK interventions are showing
very encouraging results. Bosiers and colleagues reported their 12-month results using the
commercially available nondrug-eluting Xpert (Abbott Vascular, Santa Clara, Calif) nitinol
stent system in BK arterial interventions. They had a 12-month primary patency rate of 76.3%,
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and a limb salvage rate of 95.9%. They followed patients to 12 months and performed
angiography with quantitative vessel analysis on the 73% of patients available. Angiography
revealed a binary restenosis rate (>50%) of only 20.5%, which is comparable to well-accepted
coronary DES study outcomes. The authors attributed this optimal performance to the
maintenance of flow dynamics because the stent was specifically designed for use in small
vessels. Kickuth and colleagues also have obtained good results using the Xpert stent. After
stent placement, the primary cumulative patency rate at 6 months for the study group of 35
patients was 82%. The sustained clinical improvement rate as evidenced by improved ABI was
80%, and freedom from major amputation was 100% at the 6-month follow-up. The rate of
major complications was 17%.
Wolf and associates published a multicenter, prospective randomized trial comparing
PTA with bypass in 263 men who had iliac, femoral, or popliteal artery obstruction. In 56
patients, cumulative 1-year primary patency after PTA was 43% and, after bypass surgery, was
82%, demonstrating that for long SFA stenoses or occlusions, surgery is better than PTA.
Another recent randomized study (BASIL trial) of 452 patients with CLI demonstrated no
difference in amputation-free survival at 6 months between surgery and PTA/stenting. The
authors commented that surgery was somewhat more expensive and recommended that
endovascular intervention should be used as first-line therapy, especially in medically unfit
patients. They did conclude that at 2-year follow-up, healthy patients without medical
comorbidities derived greater benefit from surgery because it was associated with decreased
need for reintervention and had a decreased hazard ratio in terms of all-cause mortality. Using
the 2000 TASC II definitions and a Markov state transition model decision analysis, Nolan and
colleagues showed that PTA/stenting surpasses bypass efficacy for TASC II C lesions if
PTA/stenting primary patency is greater than 32% at 5 years, patient age is >80 years, and/or
GSV bypass operative mortality is greater than 6%.
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of cases. Other etiologies exist and include FMD, panarteritis nodosa, arteritis, and celiac
artery (CA) compression from a median arcuate ligament, but they are unusual and have an
incidence of one in nine compared to that of atherosclerosis.
Chronic mesenteric ischemia is related to a lack of blood supply in the splanchnic region
and is caused by disease in one or more visceral arteries: the celiac trunk, the SMA, and the
IMA. Mesenteric ischemia is thought to occur when two of the three visceral vessels are
affected with severe stenosis or occlusion; however, in as many as 9% of cases, only a single
vessel is involved [superior mesenteric artery (SMA) in 5% and celiac trunk in 4% of cases].73
This disease process may evolve in a chronic fashion, as in the case of progressive luminal
obliteration due to atherosclerosis. On the other hand, mesenteric ischemia can occur suddenly,
as in the case of thromboembolism. Despite recent progress in perioperative management and
better understanding in pathophysiology, mesenteric ischemia is considered one of the most
catastrophic vascular disorders, with mortality rates ranging from 50 to 75%. Delay in
diagnosis and treatment are the main contributing factors in its high mortality. It is estimated
that mesenteric ischemia accounts for one in every 1000 hospital admissions in this country.
The prevalence is rising due in part to the increased awareness of this disease, the advanced age
of the population, and the significant comorbidity of these elderly patients. Early recognition
and prompt treatment before the onset of irreversible intestinal ischemia are essential to
improve the outcome.
Mesenteric arterial circulation is remarkable for its rich collateral network. Three main
mesenteric arteries provide the arterial perfusion to the GI system: the CA, SMA, and IMA. In
general, the CA provides arterial circulation to the foregut (distal esophagus to duodenum),
hepatobiliary system, and spleen; the SMA supplies the midgut (jejunum to midcolon); and the
IMA supplies the hindgut (midcolon to rectum). The CA and SMA arise from the ventral
surface of the infradiaphragmatic suprarenal abdominal aorta, while the IMA originates from
the left lateral portion of the infrarenal aorta. These anatomic origins in relation to the aorta are
important when a mesenteric angiogram is performed to determine the luminal patency. To fully
visualize the origins of the CA and SMA, it is necessary to perform both an anteroposterior and
a lateral projection of the aorta because most arterial occlusive lesions occur in the proximal
segments of these mesenteric trunks.
Because of the abundant collateral flow between these mesenteric arteries, progressive
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diminution of flow in one or even two of the main mesenteric trunks is usually tolerated,
provided that uninvolved mesenteric branches can enlarge over time to provide sufficient
compensatory collateral flow. In contrast, acute occlusion of a main mesenteric trunk may
result in profound ischemia due to lack of sufficient collateral flow. Collateral network
between the CA and the SMA exist primarily through the superior and inferior
pancreaticoduodenal arteries. The IMA may provide collateral arterial flow to the SMA through
the marginal artery of Drummond, the arc of Riolan, and other unnamed retroperitoneal
collateral vessels termed meandering mesenteric arteries (Fig. 25). Lastly, collateral visceral
vessels may provide important arterial flow to the IMA and the hindgut through the hypogastric
arteries and the hemorrhoidal arterial network.
Fig. 25. An aortogram showing a prominent collateral vessel that is the arc of Riolan
(arrow) in a patient with an inferior mesenteric artery occlusion. This vessel network provides
collateral flow between the superior mesenteric artery and inferior mesenteric artery
Regulation of mesenteric blood flow is largely modulated by both hormonal and neural
stimuli, which characteristically regulate systemic blood flow. In addition, the mesenteric
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There are three major mechanisms of visceral ischemia involving the mesenteric arteries,
which include: (a) acute mesenteric ischemia, which can be either embolic or thrombotic in
origin; (b) chronic mesenteric ischemia; and (c) nonocclusive mesenteric ischemia. Despite the
variability of these syndromes, a common anatomic pathology is involved in these processes.
The SMA is the most commonly involved vessel in acute mesenteric ischemia. Acute
thrombosis occurs in patients with underlying mesenteric atherosclerosis, which typically
involves the origin of the mesenteric arteries while sparing the collateral branches. In acute
embolic mesenteric ischemia, the emboli typically originate from a cardiac source and
frequently occur in patients with atrial fibrillation or following myocardial infarction (Figs. 26
and 27). Nonocclusive mesenteric ischemia is characterized by a low flow state in otherwise
normal mesenteric arteries, and most frequently occurs in critically ill patients on vasopressors.
Finally, chronic mesenteric ischemia is a functional consequence of a long-standing
atherosclerotic process that typically involves at least two of the three main mesenteric vessels.
The gradual development of the occlusive process allows the development of collateral vessels
that prevent the manifestations of acute ischemia, but are not sufficient to meet the high
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Fig. 27. A lateral mesenteric angiogram showing an abrupt cutoff of the proximal
superior mesenteric artery, which is consistent with superior mesenteric artery embolism
(arrow).
Mesenteric arteriography also can play a therapeutic role. Once the diagnosis of
nonocclusive mesenteric ischemia is made on the arteriogram, an infusion catheter can be
placed at the SMA orifice and vasodilating agents such as papaverine can be administered
intra-arterially. The papaverine infusion may be continued postoperatively to treat persistent
vasospasm, a common occurrence following mesenteric reperfusion. Transcatheter thrombolytic
therapy has little role in the management of thrombotic mesenteric occlusion. Although
thrombolytic agents may transiently recannulate the occluded vessels, the underlying occlusive
lesions require definitive treatment. Furthermore, thrombolytic therapy typically requires a
prolonged period of time to restore perfusion, during which the intestinal viability will be
difficult to assess.
A word of caution would be appropriate here regarding patients with typical history of
chronic intestinal angina who present with an acute abdomen and classical findings of
peritoneal irritation. Arteriography is the gold standard for the diagnosis of mesenteric
occlusive disease; however, it can be a time-consuming diagnostic modality. In this group of
patients, immediate exploration for assessment of intestinal viability and vascular
reconstruction is the best choice.
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Surgical Repair
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In general, bypass grafting may be performed either antegrade from the supraceliac aorta or
retrograde from either the infrarenal aorta or iliac artery. Both autogenous saphenous vein
grafts and prosthetic grafts have been used with satisfactory and equivalent success. An
antegrade bypass also can be performed using a small-caliber bifurcated graft from the
supraceliac aorta to both the CA and SMA, which yields an excellent long-term result.
Endovascular Treatment
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mortality rate that ranges from 15 to 70%. This is particularly true when the SMA is involved.
Mesenteric angioplasty and stenting is particularly suitable for this patient subgroup given its
low morbidity and mortality. Because of the limited experience with stent use in mesenteric
vessels, appropriate indications for primary stent placement have not been clearly defined.
Guidelines generally include calcified ostial stenoses, high-grade eccentric stenoses, chronic
occlusions, and significant residual stenosis greater than 30% or the presence of dissection
after angioplasty. Restenosis after PTA is also an indication for stent placement.
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mesenteric segment, a balloon angioplasty is advanced over the guidewire through the guiding
sheath and positioned across the stenosis. The balloon diameter should be chosen based on the
vessel size of the adjacent normal mesenteric vessel. Once balloon angioplasty is completed, a
postangioplasty angiogram is necessary to document the procedural result. Radiographic
evidence of either residual stenosis or mesenteric artery dissection constitutes suboptimal
angioplasty results that warrant mesenteric stent placement. Moreover, atherosclerotic
involvement of the proximal mesenteric artery or vessel orifice should be treated with a
balloon-expandable stent placement. These stents can be placed over a low profile 0.014- or
0.018-in guidewire system. It is preferable to deliver the balloon-mounted stent through a
guiding sheath, which is positioned just proximal to the mesenteric orifice while the balloon-
mounted stent is advanced across the stenosis. The stent is next deployed by expanding the
angioplasty balloon to its designated inflation pressure. The balloon is then deflated and
carefully withdrawn through the guiding sheath.
Completion angiogram is performed by hand injecting a small volume of contrast though
the guiding sheath. It is critical to maintain the guidewire access until a satisfactory completion
angiogram is obtained. If the completion angiogram reveals suboptimal radiographic results,
such as residual stenosis or dissection, additional catheter-based intervention can be performed
through the same guidewire. These interventions may include repeat balloon angioplasty for
residual stenosis or additional stent placement for mesenteric artery dissection. During the
procedure, intra-arterial infusion of papaverine or nitroglycerine can be used to decrease
vasospasm. Administration of antiplatelet agents is also recommended, for at least 6 months or
even indefinitely if other risk factors of cardiovascular disease are present.
Complications are not common and rarely become life threatening. These include access
site thrombosis, hematomas, and infection. Dissection can occur during PTA and is managed
with placement of a stent. Balloon-mounted stents are preferred over the self-expanding ones
because of the higher radial force and the more precise placement. Distal embolization has also
been reported but it never resulted in acute intestinal ischemia, likely due to the rich network
of collaterals already developed.
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Acute ischemia in the upper extremity constitutes 1015% of all acute extremity
ischemia. The etiology is emboli in 90% of the patients. The reason for this higher rate
compared with the leg is that atherosclerosis is less common in arm arteries. Emboli have the
same origins as in the lower extremity and usually end up obstructing the brachial artery.
Sometimes plaques or an aneurysm in the subclavian or axillary arteries is the primary source
of emboli. Embolization to the right arm is more common than to the left due to the vascular
anatomy. For the 10% of patients with atherosclerosis and acute thrombosis as the main cause
for their arm ischemia, the primary lesions are located in the brachiocephalic trunk or in the
subclavian artery. Such pathologies are usually asymptomatic due to well-developed collaterals
around the shoulder joint until thrombosis occurs, and they cause either micro- or
macroembolization. Other less frequent causes of acute upper extremity ischemia are listed in
Table 1
Subclavian artery thrombosis is a condition in which the blood flow through the vessel
is obstructed. The condition usually occurs secondary to some form of antecedent injury to the
vessel, hypercoagulable state, or atherosclerotic changes. The condition is common in young
athletic individuals who exert a significant amount of upper body activity. Sudden occlusion
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from emboli followed by thrombosis of the artery is common in the population with signs of
significant atherosclerotic disease.
The patient presenting with acute subclavian artery occlusion usually has a history of
repetitive use and/or stress injury to the upper extremity on the affected side. A history of
upper extremity claudication is common.
THROMBOSIS
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Reports suggest that 5% of cases in population studies and 9% to 35% in surgical series
are due to thrombosi. Jivegard et al. estimated that in patients who had embolectomy, the
chance of thrombosis being the true cause was 5.5% in the arm. Most of the proximal arterial
lesions that can cause emboli can also result in thrombosis, including atherosclerotic plaques,
aneurysm, acute aortic dissection, and arteritis (Takayasu's disease).
Atherosclerosis in the upper extremity appears especially prominent in older men. The
disease may be at the origin of the great vessels or distally in the axillary or brachial arteries.
Aneurysms of the subclavian or axillary arteries may also result in upper extremity ischemia
through two mechanisms. They may directly cause ischemic symptoms by thrombosis or by
producing emboli that occlude the distal circulation (Raynaud's phenomenon).
Less common causes include arteritis from connective tissue disorders (scleroderma),
radiation arteritis, hyperthrombotic conditions and thrombosis associated with malignancy or
steroid use.
Clinical Presentation
Acute arm ischemia is usually apparent on the basis of the physical examination. The
symptoms are often relatively discreet, especially early after onset. The explanation for this is
the well developed collateral system circumventing the brachial artery around the elbow, which
is the most common site for embolic obstruction. The six Ps pain, pallor, paresthesia,
paralysis, pulselessness, poikilothermia are applicable also for acute arm ischemia, but
coldness and color changes are more prominent than for the legs. Accordingly, the most
common findings in the physical examination are a cold arm with diminished strength and
disturbed hand and finger motor functions. Tingling and numbness are also frequent. The radial
pulse is usually absent but is pounding in the upper arm proximal to the obstruction. Gangrene
and rest pain appear only when the obstruction is distal to the elbow and affects both of the
paired arteries in a finger or in the lower arm. Ischemic signs or symptoms suggesting acute
digital artery occlusion in only one or two fingers, imply microembolization.
Diagnostics
Only the few patients with uncertain diagnosis, and those with a history and physical
findings that indicates thrombosis, need additional work-up. Examples include patients with a
history of chronic arm ischemia (arm fatigue, muscle atrophy, and microembolization) and
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bruits over proximal arteries. Angiography should then be performed to reveal the site of the
causing lesion. Duplex ultrasound is rarely needed to diagnose acute arm ischemia but may
occasionally be helpful.
Even though symptoms and examination findings may be so subtle that conservative
treatment is tempting, surgical removal of the obstruction is almost always preferable. It has
been suggested that in patients with a lower-arm blood pressure >60 mmHg embolectomy can
be omitted, but such a strategy has not to our knowledge been evaluated systematically. In a
patient series of nearly symptomless acute arm ischemia, which was left to resolve
spontaneously or with anticoagulation as the only treatment, late symptoms developed in up to
45% of the cases. Surgical treatment is also fairly straightforward. It can be performed using
local anesthesia and is associated with few complications. Very often an embolus is a
manifestation of severe cardiac disease, so the patients cardiopulmonary function should be
assessed and optimized as soon as possible. Preoperative preparations include an
electrocardiogram (ECG) and laboratory tests to guide anticoagulation treatment. Heparin
treatment is started perioperatively and continued postoperatively in most patients.
Operation
Embolectomy
As mentioned previously, the most common site for embolic obstruction is the brachial
artery.
The arm is placed on an arm table. We prefer to perform embolectomy using local
anesthesia. Often a transverse incision placed over the palpable brachial pulse can be used. If
proximal extension of the incision is required, this should be done in parallel with and dorsal
to the dorsal aspect of the biceps muscle. It has to be kept in mind that 1020% of patients may
have a different brachial artery anatomy. The most common variation is a high bifurcation of
the radial and ulnar arteries, and next in frequency is a doubled brachial artery.
An alternative location for embolectomy in the arm is to expose the brachial artery in the
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bicipital groove. A longitudinal incision starting 10 cm above the elbow that is extended
proximally is then used.
If it is hard to achieve a good inflow, a proximal lesion may cause the embolization or
thrombosis. More complicated vascular procedures are then required to reestablish flow. The
embolectomy attempt is then discontinued and the patient taken to the angiography suite for a
complete examination. If practically feasible, an alternative is to obtain the angiogram in the
operating room. Frequently, however, the preferred treatment is endovascular, and this is better
done in the angiography suite. Occasionally the films will reveal a proximal obstruction that
needs open repair. Examples of such are carotid-subclavian, subclavian-axillary, and axillary-
brachial bypasses.
The incision is made along the posterior border of the biceps muscle; a length of 68 cm
is usually enough.
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Fig. Transverse incision in the elbow for exposing the brachial artery and with possible
elongations (dottedlines) when access to the ulnar and radial branches as well as to more
proximal parts of the brachial artery is needed
The muscles are retracted medially and laterally, and the artery lies in the neurovascular
bundle immediately below the muscles. The sheath is incised and the artery freed from the
median nerve and the medial cutaneous nerve that surrounds it.
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The incision is placed 2 cm below the elbow crease and should continue up on the
medial side along the artery. If possible, veins transversing the wound should be preserved, but
they can be divided if necessary for exposure. The medial insertion of the biceps tendon is
divided entirely, and the artery lies immediately beneath it. By following the wound proximally,
more of the artery can be exposed . If the origins of the radial and ulnar artery need to be
assessed, the wound can be elongated distally on the ulnar side of the volar aspect of the arm.
The median nerve lies close to the brachial artery, and it is important to avoid injuring it.
A transverse arteriotomy in the brachial artery is made as close as possible to the
bifurcation of the ulnar and radial arteries. The embolectomy is performed in proximal and
distal directions with #2 and #3 Fogarty catheters. Separate embolectomy in each branch
should be done if technically simple. The Fogarty catheter otherwise slips down into the larger
and straighter ulnar artery. The route of the catheter can be checked by palpation at the wrist
level when the inflated balloon passes. On the other hand, restored flow in one of the arteries is
usually enough for a result that is sufficient for adequate hand perfusion. The arteriotomy is
closed with interrupted 6-0 sutures, and distal pulses and the perfusion in the hand are
evaluated. If the result is inadequate poor backflow after embolectomy, absence of pulse, a
weak continuous-wave Doppler signal, and questionable hand perfusion the arteriotomy
should be reopened and intraoperative angiography performed.
Endovascular Treatment
Thrombolysis is as feasible for acute upper extremity ischemia as it is in the leg. The
limited ischemia that often occurs after most embolic events because of the collateral network
around the elbow also allows the time needed for planning and moving the patient to the
angiosuite. The technique involves cannulation in the groin with a 7-French sheath. Long guide
wires and catheters are required to reach the occluded site and makes identification of proximal
lesions possible. A new arterial puncture in the brachial artery may be necessary for
thrombolysis of distal occlusions.It can be argued that thrombolysis in spite of acceptable
results, rarely is needed for treating this disease because open embolectomy can be performed
under local anesthesia with good results and little surgical morbidity. The advantages with
endovascular treatment are indeed limited. For patients in whom suspicion of thrombosis is
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strong or when proximal lesions are likely, it should be attempted first. However, case series
indicates that results of thrombolysis are inferior for forearm occlusions. In summary,
thrombolysis is an alternative but has little to offer in reducing risk or improving outcome
compared with embolectomy for most patients.
Patients usually regain full function of their hand immediately after the procedure, and
postoperative regimens consist of anticoagulation and a search for the embolic source. The
search for cardiac sources may advocate repeated ECGs, echocardiography, and duplex
ultrasound of proximal arteries.
The number of salvaged arms after surgical intervention is very high, 9095 %, and arm
function is usually fully recovered. The remaining 510% represents patients with extensive
thrombosis involving many vascular segments and most branches of the distal arteries. The
postoperative mortality is around 1040% in most patient series, reflecting that embolization
often is a consequence of severe cardiac disease. Postoperative mortality is similar for
thrombolysis to treat acute arm ischemia, while early technical success is slightly lower or
similar. Less favorable results with thrombolysis are achieved when the distal arteries also are
obstructed.
Acute leg ischemia is associated with a great risk for amputation and death. The age of
the patients is high, and to some extent acute leg ischemia can be considered an end-of-life
disease. Patients symptoms and the clinical signs of the afflicted leg vary. Sometimes grave
ischemia immediately threatens limb viability, such as after a large embolization to a healthy
vascular bed. Other times the symptoms are less dramatic, appearing as onset of rest pain in a
patient with claudication. This is usually due to thrombosis of a previously stenosed artery.
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It is the severity of ischemia that determines management and treatment. To minimize the
risk for amputation or persistent dysfunction it is important to rapidly restore perfusion if an
extremity is immediately threatened. When the leg shows signs of severe ischemia but is clearly
viable, it is equally important to thoroughly evaluate and optimize the patient before any
intervention is initiated. These basic management principles are generally applicable.
Accordingly, we recommend management by severity rather than management by etiology
(thrombosis versus embolus) but recognize that the latter can also be an effective strategy.
Embolism
Embolism is by far the most common cause of acute arm ischaemia, accounting for
74100% of cases.
In the lower extremities, controversy exists regarding the ratio between arterial embolism
and thrombosis, with diferent studies giving numbers ranging from 4:1 to 1:9.
The heart is invariably the most common origin of peripheral arterial emboli, and is
responsible for 5893% of cases. However, the pattern of the underlying heart disease has
changed recently as the incidence of rheumatic valvular disease has decreased significantly
Nowadays, the most common sources of arterial emboli of cardiac origin are:
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atrial ibrillation due to atherosclerotic heart disease, accounting for 3275% of cases,
followed by
myocardial infarction with mural thrombi formation, which is responsible for 2132% of
peripheral emboli.
Noncardiac Sources
Noncardiac sources of emboli are being identiied with increasing frequency, at the
expense of undetermined causes, the frequency of which has steadily decreased due to
improvements in diagnostic methods. Noncardiac sources of emboli are nowadays found in
512% of patients, while in 912% the source of the emboli remains unknown.
Aneurysms are the most common noncardiac source of peripheral embolism, accounting
for about 5% of distal emboli.
Ulcerated atherosclerotic plaques follow in order of frequency, carrying the risk of distal
embolism from white thrombi adherent on their surface. Such emboli are usually sizeable,
capable of obstructing major peripheral arteries.
A distinct variant of peripheral embolization due to an atherosclerotic plaque is
atheroembolism, in which a portion of the plaque breaks of and undergoes embolization to
peripheral arteries. Such emboli may evolve in three clinical forms:
1. The asymptomatic form, not diagnosed during the subjects lifetime and only
recognized in autopsy studies.
2. A benign form such as blue toe syndrome or cutaneous livedo, with a spontaneous
mild prognosis.
3. A difuse multisystemic form with a very poor prognosis.
Cryptogenic Emboli
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Thrombosis
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It is difficult to find accurate incidence figures on acute leg ischemia. Data from some
reports are given in Table 2. The numbers listed do not include conservatively treated patients
or those whose legs were amputated as a primary procedure. The incidence increases with age
and is seen with equal frequency in men and women. Regardless, the frequency indicates that it
is a very common problem.
Pathogenesis
Acute leg ischemia is caused by a sudden deterioration of perfusion to the distal parts of
the leg. While the abrupt inhibition of blood flow causes the ischemia, its consequences are
variable because acute leg ischemia is multifactorial in origin. Hypercoagulable states, cardiac
failure, and dehydration predispose the blood for thrombosis and make the tissue more
vulnerable to decreased perfusion. Besides the fact that a healthy leg is more vulnerable than
one accustomed to low perfusion, it is unknown what determines the viability of the tissue. The
most important factor is probably the duration of ischemia. The type of tissue affected also
influences viability. In the leg, the skin is more ischemia-tolerant than skeletal muscle.
The etiology of the occlusion is not what determines the management process. It is,
however, of importance when choosing therapy. Embolus is usually best treated by
embolectomy, whereas arterial thrombosis is preferably resolved by thrombolysis, percutaneous
transluminal angioplasty (PTA), or a vascular reconstruction. The reason for this difference is
that emboli often obstruct a relatively healthy vascular bed, whereas thrombosis occurs in an
already diseased atherosclerotic artery. Consequently, emboli more often cause immediate
threatening ischemia and require urgent restoration of blood flow. Thrombosis, on the other
hand, occurs in a leg with previous arterial insufficiency with well-developed collaterals. In the
latter case it is important not only to solve the acute thrombosis but also to get rid of the cause.
It must be kept in mind that emboli can be lodged in atherosclerotic arteries as well, which then
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Table 3 summarizes typical findings in the medical history and physical examination that
suggest thrombosis or embolism. Many risk factors, such as cardiac disease, are common for
both embolization and thrombosis. Atrial fibrillation and a recent (less than 4 weeks)
myocardial infarction with intramural thrombus are the two dominating sources for emboli
(8090%). Other possible origins are aneurysms and atherosclerotic plaques located proximal
to the occluded vessel. The latter are often associated with microembolization (discussed later)
but may also cause larger emboli.
Table 3. History and clinical indings diferentiating the etiology of acute ischemia
Plaque rupture, immobilization, and hypercoagulability are the main causes of acute
thrombosis. Severe cardiac failure, dehydration, and bleeding are less common causes.
Hypoperfusion due to such conditions can easily turn an extremity with longstanding slightly
compromised perfusion into acute ischemia.
Location of embolic obstruction
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Clinical Presentation
Medical History
The typical patient with acute leg ischemia is old and has had a recent myocardial
infarction. He or she describes a sudden onset of symptoms a few hours of pain, coldness,
loss of sensation, and poor mobility in the foot and calf. Accordingly, all signs of threatened
leg viability are displayed. The event is most likely an embolization, and the patient needs
urgent surgery. Unfortunately, such patients are unusual among those who are admitted for
acute leg ischemia. The history is often variable, and sometimes it is difficult to decide even the
time of onset of symptoms. It is important to obtain a detailed medical history to reveal any
underlying conditions or lesions that may have caused the ischemia. Moreover, identifying and
treating comorbidities may improve the outcome after surgery or thrombolysis.
The symptoms and signs of acute ischemia are often summarized as the five Ps: pain,
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pallor, pulselessness, paresthesia, and paralysis. Besides being helpful for establishing
diagnosis, careful evaluation of the five Ps is useful for assessing the severity of ischemia.
Sometimes a sixth Ps is used poikolothermia, meaning a low skin temperature that does not
vary with the environment.
Pain: For the typical patient, as the one described above, the pain is severe, continuous,
and localized in the foot and toes. Its intensity is unrelated to the severity of ischemia. For
instance, it is less pronounced when the ischemia is so severe that the nerve fibers transmitting
the sensation of pain are damaged. Patients with diabetes often have neuropathy and a
decreased sensation of pain.
Pallor: The ischemic leg is pale or white initially, but when ischemia aggravates the color
turns to cyanotic blue. This cyanosis is caused by vessel dilatation and desaturation of
hemoglobin in the skin and is induced by acidic metabolites in combination with stagnant
blood flow. Consequently, cyanosis is a graver sign of ischemia than pallor.
Pulselessness: A palpable pulse in a peripheral artery means that the flow in the vessel is
sufficient to give a pulse that is synchronous with vessel dilatation, which can be palpated with
the fingers. In general, palpable pulses in the foot therefore exclude severe leg ischemia. When
there is a fresh thrombus, pulses can be felt in spite of an occlusion, so this general principle
must be applied with caution. Palpation of pulses can be used to identify the level of
obstruction and is facilitated by comparing the presence of pulses at the same level in the
contralateral leg.
When the examiner is not convinced that palpable pulses are present, distal blood
pressuresmust be measured. It is prudent to always measure the ankle blood pressure. This is a
simple way to verify ischemia and the measurement can be used to grade the severity and serve
as a baseline for comparison with repeated examinations during the course of treatment. (This
will be discussed further later.) The continuous-wave (CW) Doppler instrument does not give
information about the magnitude of flow because it registers only flow velocities in the vessel.
Therefore, an audible signal with a CW Doppler is not equivalent to a palpable pulse, and a
severely ischemic leg can have audible Doppler signals.
Paresthesia: The thin nerve fibers conducting impulses from light touch are very
sensitive to ischemia and are damaged soon after perfusion is interrupted. Pain fibers are less
ischemia-sensitive. Accordingly, the most precise test of sensibility is to lightly touch the skin
with the fingertips, alternating between the affected and the healthy leg. It is a common mistake
to believe that the skin has been touched too gently when the patient actually has impaired
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sensitivity. The examiner then may proceed to pinching and poking the skin with a needle.
Such tests of pain fibers evaluate a much later stage of ischemic damage. The
anatomiclocalization of impaired sensation is sometimes related to which nerves are involved.
Frequently, however, it does not follow nerve distribution areas and is circumferential and most
severe distally. Numbness and tingling are other symptoms of ischemic disturbance of nerve
function.
Paralysis: Loss of motor function in the leg is initially caused by ischemic destruction of
motor nerve fibers and at later stages the ischemia directly affects muscle tissue. When
palpated, ischemic muscles are tender and have a spongy feeling. Accordingly, the entire leg
can become paretic after proximal severe ischemia and misinterpreted as a consequence of
stroke. Usually paralysis is more obscure, however, presenting as a decreased strength and
mobility in the most distal parts of the leg where the ischemia is most severe. The most
sensitive test of motor function is to ask the patient to try to move and spread the toes. This
gives information about muscular function in the foot and calf. Bending the knee joint or
lifting the whole leg is accomplished by large muscle groups in the thigh that remain intact for
a long time after ischemic damage in the calf muscle and foot has become irreversible.
Classiication
When a patient has been diagnosed to have acute leg ischemia, it is extremely important
to evaluate its grade. Ischemic severity is the most important factor for selecting a management
strategy, and it also affects treatment outcome. Classification according to severity must be
done before the patient is moved to the floor or sent to the radiology department. We have
found that the simple classification suggested by the Society for Vascular Surgery ad hoc
committee (1997) is helpful for grading. It is displayed in Table 4.
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Viable Leg
As indicated in Figure 2, a viable ischemic leg is not cyanotic, the toes can be moved
voluntarily, and the ankle pressure is measurable. The rationale for choosing these parameters
is that cyanosis and impaired motor function are of high prognostic value for outcome. The
limit of 30mmHg for the ankle pressure is not important per se but is a practical limit useful to
make sure that it is the arterial, and not a venous, pressure that has been measured. The dorsalis
pedis, posterior tibial arteries, or branches from the peroneal artery can be insonated. The latter
can be found just ventral to the lateral malleolus. If no audible signal is identified in any of
these arteries or if there only is a weak signal that disappears immediately when the tourniquet
is inflated, the ankle blood pressure should be recorded as zero. It is important to rely on the
obtained results and not assume that there is a signal somewhere that is missed due to
inexperience. Qualitative analysis of the Doppler signal is seldom useful when evaluating acute
leg ischemia.
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Threatened Leg
As shown in Table 4, the threatened leg differs from the viable one in that the sensibility
is impaired and there is no measurable ankle blood pressure. The threatened limb is further
separated into marginally threatened and immediately threatened by the presence or absence of
normal motor function. The threatened leg differs from the irreversibly damaged leg by the
quality of the venous Doppler signal. In the irreversibly damaged leg, venous blood flow is
stagnant and inaudible.
Management Strategy
A viable leg does not require immediate action and can be observed in the ward. A
threatened leg needs urgent operation or thrombolysis. The latter is more time-consuming and
recommended for the marginally threatened leg. The immediately threatened leg must be treated
as soon as possible, usually with embolectomy or a vascular reconstruction. Irreversible
ischemia is quite unusual but implies that the patients leg cannot be saved. Figure 2 is
intended to show a simplified algorithm to further support the management of acute leg
ischemia.
Diagnostics
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The arteriogram provides an anatomical map of the vascular bed and is very helpful in
discriminating embolus and thrombosis. The former is essential for planning the surgical
procedure, and the latter may be of importance for selecting the treatment strategy.
Angiographic signs of embolism are an abrupt, convex start of the occlusion and lack of
collaterals. Thrombosis is likely when the arteriogram shows well-developed collaterals and
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Viable Leg
If the leg is viable the patient is admitted for observation. A checklist of what needs to
be done in the emergency department follows below:
2. Start infusion of fluids. Because dehydration is often a part of the pathogenic process,
Ringers acetate is usually preferred. Dextran is another option that also is beneficial for blood
rheology.
3. Draw blood for hemoglobin and hematocrit, prothrombin time, partial thromboplastin
time, complete blood count, creatinine, blood urea nitrogen, fibrinogen, and antithrombin.
Consider the need to type and cross-match blood.
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Repeated assessments of the patients clinical status are mandatory in the intensive care
unit and when the patient has been moved to the ward. The time interval depends on the
severity of ischemia and the medical history. This examination includes evaluating skin color,
sensibility, and motor function as well as asking the patient about pain intensity.
Dextran is administered throughout the observation period. The risk for deterioration of
heart failure due to dextran treatment is substantial and for patients at risk the volume load
must be related to the treatments expected possible benefits. For such patients it is wise to
reduce the normal dose of 500ml in 12h to 250ml. Another option is to prolong the infusion
time to 24h.
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needed. If no improvement occurs, angiography can be performed during the daytime, followed
by thrombolysis, PTA, or vascular reconstruction.
Threatened Leg
If the leg is immediately threatened, the patient is prepared for operation right away. This
includes the steps listed above for the viable leg, including contact with an anesthesiologist.
When there is no cyanosis and motor function is normal that is, the extremity is only
marginally threatened there is time for immediate angiography followed by thrombolysis or
operation. An option is cautious monitoring and angiography as soon as possible.
Before starting the operation, the surgeon needs to consider the risk for having to
perform a complete vascular reconstruction. It is probable that a bypass to the popliteal artery
or a calf artery will be needed to restore circulation. If thrombosis is the likely cause and the
obstruction is distal (a palpable pulse is felt in the groin but not distally), a bypass may also be
required even when embolization is suspected.
Operation
a A longitudinal skin incision starting 12 cm cranial to the inguinal skin fold and
continued lateral to the artery is used to avoid the inguinal lymph nodes. A common mistake is
to place the incision too far caudally, which usually means the dissection is taking place distal
to the deep femoral.
b The dissection is continued sharply with the knife straight down to the fascia lateral
to the lymph nodes and is then angulated 90 medially to reach the area over the artery. It
should then be palpable. Lymph nodes should be avoided to minimize the risk for infection and
development of seroma. The fascia is incised, and the anterior and lateral surfaces of the artery
are approached.
c At this stage the anatomy is often unclear regarding the relation of branches to the
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common femoralartery. Encircle the exposed artery with a vessel-loop, and gently lift the artery.
Continue dissection until the bifurcation into superficial and deep femoral artery is identified.
Its location varies from high up under the inguinal ligament up to 10 cm further down. At this
stage, the surgeon must decide whether exposure and clamping of the common femoral are
enough. This is usually the case for proximal control in trauma distally in the leg. In acute
ischemia it is more common that the entire bifurcation needs to be exposed.
During the continued dissection, attention must be given to important branches that
should be controlled and protected from iatrogenic injuries. These are, in particular, the
circumflex iliac artery on the dorsal aspect of the common femoral artery and the deep femoral
vein crossing over the anterior aspect of the deep femoral artery just after its bifurcation. To
provide a safe and good exposure of the deep femoral to a level below its first bifurcation, this
vein must be divided and suture-ligated. Partial division of the inguinal ligament is
occasionally needed for satisfactory exposure.
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A skin incision is made along the dorsal aspect of the sartorius muscle at a midthigh
level. It is important to avoid injuries to the greater saphenous vein, which usually is located in
the posterior flap of the incision. The incision can be elongated as needed. After the deep
fascia is opened and the sartorius muscle is retracted anteriorly, the femoral artery is found and
can be mobilized. Division of the adductor tendon is sometimes required for exposure.
a The knee is supported on a sterile, draped pillow. The skin incision is started at the
medial aspect of the femoral condyle and follows the anterior border of the sartorius muscle
1015 cm in a proximal direction. Protect the greater saphenous vein and the saphenous nerve
during dissection down to the fascia. After dividing the fascia longitudinally, continue the
dissection in the groove between the sartorius and gracilis muscles, which leads to the fat in the
popliteal fossa.
b The popliteal artery and adjacent veins and nerve are then, without further division of
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muscles, easily found and separated in the anterior aspect of the fossa.
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a A sterile pillow or pad is placed under the distal femur. The incision is placed 1 or 2
cm posterior to the medial border of the tibia, starting at the tibial tuberosity and extending
1012 cm distally. Subcutaneous fat and fascia are sharply divided, with caution to the greater
saphenous vein.
b The popliteal fossa is reached by retracting the gastrocnemius muscle dorsally. The
deep fascia is divided and the artery usually easier to identifiy. Occasionally, pes anserinus
must be divided for adequate exposure. The popliteal artery is often located just anterior to the
nerve and in close contact with the popliteal vein and crossing branches from concomitant
veins. If it is necessary to expose the more distal parts of the popliteal artery, the soleus muscle
has to be divided and partly separated from the posterior border of the tibia.
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Embolectomy
It is beyond the scope of this book to cover the technique for vascular reconstructions.
But because embolectomy from the groin with balloon catheters (known as Fogarty catheters)
is one of the most common emergency vascular operations in a general surgical clinic and may
be performed by surgeons not so familiar with vascular surgery.
TECHNICAL TIPS
Embolectomy
Use an operating table that allows x-ray penetration. Local anesthesia is used if embolus
is likely and the obstruction seems to be in the upper thigh or in pelvic vessels (no pulse in the
groin). Make a longitudinal incision in the skin, and identify and expose the common,
superficial, and deep femoral arteries . If the common femoral artery is soft-walled and free
from arteriosclerosis especially if a pounding pulse is felt proximal to the origin of the deep
femoral artery an embolus located in its bifurcation is likely. Make a short transverse
arteriotomy including almost half the circumference. Place the arteriotomy only a few mm
proximal to the origin of the profunda artery so it can be inspected and cannulated with ease. In
most other cases, a longitudinal arteriotomy is preferable because it allows elongation and can
be used as the site for the inflow anastomosis of a bypass. For proximal embolectomy, a #5
catheter is used.
Before the catheter is used the balloon should be checked by insufflation of a suitable
volume of saline. Check the position of the lever of the syringe when the balloon is starting to
fill, which gives a good idea of what is happening inside the artery. Wet the connection piece
for the syringe to get a tight connection. It is smart to get external markers of the relationship
between the catheter length and important anatomical structures; for example, the aortic
bifurcation (located at the umbilicus level), the trifurcation level (located approximately 10 cm
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below the knee joint), as well as the ankle level. The catheters have centimeter grading, which
simplifies the orientation.
It is common for the embolus to already be protruding when the arteriotomy is done and
a single pull with the catheter starting with the tip in the iliac artery is enough to ensure
adequate inflow. This means that a strong pulse can be found above the arteriotomy, and a
pulsatile heavy blood flow comes through the nole. For distal clot extraction, a #3 or #4
catheter is recommended. A slight bending of the catheter tip between the thumb and index
finger might, in combination with rotation of the catheter, make it easier to pass down the
different arterial branches (Fig. 8).
Fig. 8. Use of Fogarty catheter for embolectomy. Note that withdrawal is parallel to the
artery
When the catheter is inserted into the artery and while the surgeon is working with it,
hemostasis of the arteriotomy is achieved by a vessel-loop or by a thumbindex finger grip over
the artery and the catheter. In a typical case, an embolus, including a possible secondary
thrombus, can be passed relatively easily or with only slight resistance. If a major part of the
catheter can be inserted the tip will be located in one of the calf arteries, most probably the
posterior tibial artery or the peroneal artery. The balloon is insufflated simultaneously as the
catheter is slowly withdrawn, which makes it easier to get a feeling for the dynamics and to not
apply too much pressure against the vascular wall.
A feeling of touch is preferable, but a feeling of pull against the vascular wall
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should be avoided.
To get the right feeling the same person needs to hold the catheter, pull it, and insufflate
the balloon at the same time. To avoid damage in the arteriotomy, the direction of withdrawal
should be parallel with the artery .
When the catheter is withdrawn it moves into larger segments of the artery and has to be
successively insufflated until it reaches the arteriotomy. The reverse is, of course, valid when
the embolectomy is done in a proximal direction. The thromboembolic masses can be suctioned
or pulled out with forceps, and the arteriotomy should be inspected to be clean from remaining
materials before the catheter is reinserted. The maneuver should be repeated until the catheter
has been passed at least once without any exchange of thromboembolic materials and until
there is an acceptable backflow from the distal vascular bed.
Depending on the degree of ischemia and collaterals, the backflow is, however, not
always brisk.
If a catheter runs into early and hard resistance, this might be due to previously occluded
segment that forced the catheter into a branch. It should then be withdrawn and reinserted,
using great caution to avoid perforation. If the resistance cannot be passed and if acute
ischemia is present, angiography should always be considered to examine the possibility of a
vascular reconstruction.
Besides performing embolectomy in the superficial femoral, popliteal, and calf arteries,
the deep femoral artery must be checked for an obstructing embolus or clot that needs to be
extracted. Separate declamping of the superficial femoral and deep femoral arteries to check the
backflow is the best way to do this. Remember the possibility that backflow from the distal
vascular bed after embolectomy might emanate from collaterals located proximal to distally
located clots. Back flow does not always assure that the peripheral vascular bed is free from
further embolic masses. A basic rule is that every operation should be completed with
intraoperative angiography to ensure good outflow and to rule out remaining emboli and
secondary thrombus. To dissolve small amounts of remaining thrombus local infusion of 24 cc
recombinant tissue plasminogen activator (rtPA) can be administered before the angiography
catheter is pulled out.
Finally, the arteriotomy is closed. If necessary a patch of vein or synthetic material is
used to avoid narrowing of the lumen. As mentioned before, the embolectomy procedure
includes intraoperative angiography. If this examination indicates significant amounts of
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emboli remaining in the embolectomized arteries or if the foot still appears as being
inadequately perfused after the arteriotomy is closed, other measures need to be taken. If there
are remaining emboli in the superficial femoral or popliteal arteries, another embolectomy
attempt from the arteriotomy in the groin can be made. Clots, if seen in all the calf arteries,
need to be removed through a second arteriotomy in the popliteal artery. This is done by a
medial incision below the knee; note that localanesthesia is not sufficient for this. It is usually
necessary to restore flow in two, or occasionally in only one, of the calf arteries.
Embolectomy at the popliteal level is the first treatment step when ischemia is limited to
the distal calf and foot and when there is a palpable pulse in the groin or in the popliteal fossa.
Thrombosis
The preliminary diagnosis of embolus must be reconsidered if the exposed femoral artery
in the groin is hard and calcified. In most situations, clot removal with Fogarty catheters will
then fail. It is usually difficult or even impossible to pass the catheter distally, indicating the
presence of stenoses or occlusions. Even if the embolectomy appears successful, early
reocclusion is common. Such secondary thrombosis is usually more extensive and will
aggravate the ischemia. Accordingly, angiography should be considered as the first step if the
femoral artery is grossly arteriosclerotic and if it is hard to pass the catheter down to the calf
level. It will confirm the etiology and reveal whether a bypass is required and feasible. Vascular
reconstruction in acute leg ischemia is often rather difficult andexperience in vascular surgery
is required.
Intraoperative angiography
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The use of contrast in the Fogarty catheter balloon during fluoroscopy allows the calf
vessel into which the catheter slides to be identified. The technique for intraoperative
angiography is also a prerequisite for interoperative use of endovascular treatment options such
asangioplasty (Fig. 9).
Thrombolysis
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is continued slowly over 612h with 1mg/h. If the initial thrombolysis fails, a variety of
mechanical catheters can be used to try to further dissolve and aspirate the thrombus. Examples
include the AngioJet and the Amplatz.
Because of the risk of bleeding and systemic complications, and also because the
ischemic leg may deteriorate, careful monitoring during con-tinued thrombolysis is necessary.
This is best done in an intensive care or step-down unit. The patient should be kept supine in
bed throughout the procedure. During this time the other measures suggested for optimizing
coagulation and central circulation are continued. It is also necessary to check fibrinogen
concentration to make sure the value does not decline to <1.0 mg/ml. Below this level surgical
hemostasis is insufficient and the infusion should be stopped. Angiographic control of the
result is performed afterwards, usually the following morning, and occasionally during the slow
infusion to check the effect and allow repositioning of the catheter. The part of the thrombus
surrounding the catheter is lysed first, which is why it often is beneficial to advance the
catheter further into the thrombus after a few hours.
Finally, the lesion that caused the thrombosis is treated with angioplasty. To avoid
unnecessary bleeding from the puncture site, the fibrinogen concentration is checked again
before the sheath is withdrawn to ensure that the level exceeds 1.0 mg/ml.
Anticoagulation
Patients with embolic disease caused by cardiac arrhythmia or from other cardiac sources
proven by ECG, medical history, or clinical signs should be anticoagulated postoperatively.
Treatment regimens described previously are employed, followed by treatment with coumadin.
Anticoagulation has no proven positive effect for the prognosis of the ischemic leg but is
administered to reduce the risk of new emboli. The patients abilities to comply with treatment
and the risk for bleeding complications have to be weighed against the benefits. If the source of
the emboli is not clear, it should be investigated. Findings of atrial fibrillation and heart
thrombus can then be treated. If the ECG is normal, echocardiography is ordered to search for
thrombus and valve deficiencies. If the left atrium is a likely embolic source, transesophageal
echocardiography may be indicated.
When the etiology of leg ischemia is uncertain it is difficult to give general advice. There
is no scientific evidence that long-term postoperative anticoagulation reduces the risk of
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reocclusion or influences patient survival. Continued treatment with dextran or low molecular
weight heparin is recommended at least during hospitalization.
If hypercoagulable states are suspected the patient needs to be worked up during the
postoperative period to reduce the risk of reocclusion. Examples are patients with
hyperhomocysteinemia, who may be treated with folates, and patients with antiphospholipid
antibodies, who need coumadin and salicylic acid.
Reperfusion Syndrome
Patients treated for severe acute leg ischemia are at risk of developing reperfusion
syndrome. This occurs when ischemic muscles are reperfused and metabolites from damaged
and disintegrated muscle cells are spread systemically. A part of this process consists of
leakage of myoglobin; it may be nephrotoxic and colors the urine red. The metabolites also
affect central circulation and may cause arrhythmia and heart failure. The risk for reperfusion
syndrome is higher when occlusions are proximal and the affected muscle mass is large. One
example is saddle emboli located in the iliac bifurcation. The risk is also higher when the
ischemia time is longer than 46 h.
The elevated mortality associated with severe acute leg ischemia may be due to
reperfusion syndrome. Survival may therefore be improved by avoiding reperfusion and a lower
mortality has been reported from hospitals where primary amputation is favored. It has also
been suggested that thrombolysis saves lives by restoring perfusion gradually. For a threatened
leg this is seldom an option because rapid restoration of perfusion is necessary to save it.
The best treatment for reperfusion syndrome is prevention by expeditious restoration of
flow.
There are no clinically proven effective drugs but many have been successful in animal
models, including heparin, mannitol, and prostaglandins.
Because heparin and mannitol also have other potential benefits and few side effects
they are recommended during the postoperative period. Obviously, acidosis and hyperkalemia
must be corrected, and the patient needs to be well hydrated and have good urine output. For
patients with suspected reperfusion syn-
drome urine acidosis and high serum myoglobin levels alkalinization of the urine is
often recommended in order to avoid renal failure despite weak support in the literature. If the
urine is red, the urine pH <7.0, and serum myoglobin >10,000 mg/ml, 100 ml sodium
bicarbonate is given IV. The dose is repeated until the pH is normalized.
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Compartment Syndrome
The acute inflammation in the muscle after reestablishing perfusion leads to swelling
and a risk for compartment syndrome. The available space for the muscles is limited in the leg
and when the increased pressure in the compartments reduces capillary perfusion below the
level necessary for tissue viability, nerve injury and muscle necrosis occur.
The essential clinical feature of compartment syndrome is pain often very strong and
out of proportion, which is accentuated by passive extension. The muscle is hard and tender
when palpated. Unfortunately, nerves within the compartments are also affected, causing
disturbance of sensibility and motor function. This makes diagnosis more difficult. Moreover,
the patient is often not fully awake or disoriented, but early diagnosis is still important to save
the muscle tissue. For that reason measurement of intracompartmental pressure is performed for
diagnosis in some hospitals.
There are no precise limits that advocate fasciotomy, but 30mmHg has been proposed.
The specificity for a correct diagnosis using this limit is high, but the sensitivity is much lower.
To notice signs of compartment syndrome after operation or thrombolysis for acute
ischemia, frequent physical examinations are vital. Fasciotomy should be performed
immediately following the procedure if any suspicion of compartment syndrome exists.
Common advice is to always perform fasciotomy right after the vascular procedure when the
ischemia is severe and has lasted over 46 h. To open all four compartments, we recommend
using two long incisions, one placed laterally and one medially in the calf.
The outlook for patients with acute leg ischemia has generally been poor. The 30-day
mortality when an embolus is the etiology varies between 10% and 40%. Survival is better
when arterial thrombosis is the cause, around 90%. When considering the amputation rate after
surgical treatment the figures are reversed lower for embolic disease, at 1030%, than for
thrombosis, which of ten has an early amputation rate of around 40%.
A substantial number of the patients die or require amputation after 30 days. This is due
to a combined effect of the patients advanced age and comorbidities. In studies not
differentiating between etiologies, only 3040% of the patients were alive 5 years after surgery,
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A substantial number of patients have chronic leg ischemia and have undergone vascular
reconstructions, so there is a high likelihood that emergency department physicians will have to
take care of problems with postoperative acute leg ischemia in the operated leg. The clinical
presentation of graft failure or occlusion is variable. An abrupt change in leg function and skin
temperature accompanied by the onset of pain can occur any time after surgery, but especially
within the first 6 months. Several years after the reconstruction it is slightly more common for
progressive deterioration to occur and an eventual graft occlusion to pass unnoticed.
As discussed previously in this chapter the management principles are roughly the same
as for primary acute leg ischemia. It is the status of the leg and the severity of ischemia that
lead workup and management. Most patients will undergo angiography to establish diagnosis
and to provide information about possibilities to restore blood flow. Thrombolysis is often the
best treatment option because it exposes the underlying lesions that may have caused the
occlusion. As for patients with acute ischemia, those with an immediately threatened leg after a
reconstruction should be taken to the operating room and treated as fast as possible.
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A toe that suddenly becomes cool, painful, and cyanotic, while pulses can be palpated in
the foot, characterizes the classic presentation of blue toe syndrome. This has occasionally led
to the assumption that the discoloration of the toe is not of vascular origin, and patients have
been sent home without proper vascular assessment. Although coagulation disorders or
vasculitis may contribute, such an assumption is dangerous. Atheroembolism is the main cause
for blue toe syndrome and atheromatous plaques in the iliac or femoral arteries or thrombi in
abdominal or popliteal aneurysms are the main sources. Blue toe syndrome can also present
without palpable foot pulses. The presentation may then be less dramatic.
It is common that the patient does not notice the initial insult and wait to seek medical
care until after several weeks. Ischemic ulceration at the tip of the toe may then be found in the
examination. During the foot examination more signs of microembolization are usually found,
including blue spots or patchy discoloration of the sole and heel. When both feet are affected it
suggests an embolic source above the aortic bifurcation. The clinical examination should
include assessing the aorta and all peripheral arteries, including pulses and auscultation for
bruits. When pulses in the foot are not palpable, ankle blood pressure needs to be measured. In
the search for aneurysms and stenoses patients need to be investigated with duplex ultrasound
to verify examination findings. To prevent future embolization episodes lesions or aneurysms
found should be treated as soon as possible.
Occasionally the pain is transient and the blue color will disappear within a few weeks.
More common, however, is an extremely intense pain in the toe that is continuous and difficult
to treat. Unfortunately, the pain often lasts several months until the toe is either amputated or
healed.
The pain is best treated with oral opiates, and quite high doses are often required to ease
the pain. A tricyclic antidepressant drug may be added to the regimen if analgesics are not
enough.
While waiting for diagnostic studies and final treatment of the lesions, the patient is put
on aspirin therapy. There is no scientific evidence for using other medications such as
coumadin, steroids, or dipyramidole. Still, if suspicion for a popliteal aneurysm is high we
recommend anticoagulation with low molecular weight heparin until the aneurysm is corrected.
Popliteal Aneurysms
A common reason for acute leg ischemia is thrombosis of a popliteal aneurysm. Such
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aneurysms are also one of the main sources for embolization to the digits in the foot and blue
toe syndrome. Besides the clinical signs of acute ischemia discussed previously, a prominent
wide popliteal pulse or a mass in the popliteal fossa is often palpated when popliteal aneurysm
is the reason for the obstrution.
Popliteal aneurysms are frequent in men but rare in women. They are often bilateral
more than 50% and associated with the presence of other aneurysms. For instance, 40% of
patients with popliteal aneurysms also have an aneurysm in the abdominal aorta. Most
popliteal aneurysms are identified during angiography performed as part of the management
process for acute leg ischemia. When an aneurysm is suspected during angiography or
examination, duplex ultrasound is performed to verify the finding and estimate the aneurysms
diameter.
If the severity of ischemia corresponds to the immediately threatened stage described
earlier, the patient needs urgent surgery. The revascularization procedure is then often quite
difficult. Exposure of the popliteal artery below the knee, including the origins of the calf
arteries, should be followed by intraoperative angiography and an attempt to remove the
thrombus. It is hoped that angiography can identify a spared calf artery distally. The calf
arteries are sometimes slightly dilated in this patient group and can serve as a good distal
landing site for a bypass excluding the aneurysm. Often, however, it is impossible to open up
the distal vascular bed due to old embolic occlusions and the prognosis for the leg is poor. In
such situations every possible alternative solution should be considered, including local
thrombolysis, systemic prostaglandin infusion, and profundaplasty.
If the ischemia is less severe, thrombolysis may be considered following the angiography
before surgical exclusion of the aneurysm. While thrombolysis previously has been considered
questionable because of the risk for further fragmentation of thrombus within the popliteal
aneurysm, this strategy may prove very favorable. Over the last few years several studies
reporting restored calf vessels by thrombolysis have been published. This may lead to more
successful bypasses and improved limb salvage. Once the bypass is accomplished good
long-term results are probable. Interestingly, vein grafts used for bypasses in patients with
popliteal aneurysms appear to be wider and stay patent longer than for other patient groups.
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Mesenteric artery thrombosis has the highest mortality rate of all causes of mesenteric
ischemia. First described in the late 15th century, little progress was made in its treatment
before the 20th century.
In 1901, a patient with a long history of postprandial pain was found to have an
atherosclerotic plaque with overlying thrombus of the superior mesenteric artery (SMA). The
physician concluded that if a patient could develop pain of the lower extremities secondary to
atherosclerosis, it would stand to reason that a patient could present with postprandial pain due
to narrowing of the mesenteric vessels. An example of complete occlusion is illustrated in the
image below. The pathophysiologic mechanism by which ischemia produces pain remains
poorly understood.
The arterial circulation to the gut has extensive collaterals and arcades providing
multiple sources of blood inflow. This explains why vascular occlusion is well tolerated as
evidenced by the relative lack of clinical intestinal ischemia despite the high prevalence of
atherosclerotic disease of the aorta and visceral arteries. Certain collateral patterns are
recognized, depending on which artery is blocked. When either the celiac or superior
mesenteric artery (SMA) is compromised, the main collateral circulation is by the
gastroduodenal and pancreaticoduodenal arteries. The main collateral channels between the
SMA and inferior mesenteric artery (IMA) occur in the region of the splenic flexure between
the middle and left colic arteries. In the presence of either SMA or IMA occlusion, the
marginal artery of Drummond and the arch of Riolan (an ascending branch of the left colic
artery anastomosing with branches of the SMA) enlarge significantly. In the presence of an
IMA occlusion, another important collateral circulation is between the internal iliac artery and
the left colic artery via the superior hemorrhoidal arteries.
The SMA is the critically important vessel in maintaining visceral perfusion, as
demonstrated by increased blood flow after eating. This is not seen in the celiac artery. In
chronic ischemia, all patients have SMA stenosis or occlusion, in addition to celiac artery
and/or IMA involvement.
Etiology
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OCCLUSIVE DISEASE
Emboli. The SMA is the most common site of embolic occlusion although the celiac
artery can be affected. There is classically an underlying cardiac problem giving rise to the
organized thrombus that embolizes. This is usually atrial fibrillation or less commonly a mural
thrombus from an acute myocardial infarction. A history of previous embolic events is not
uncommon. Other causes of emboli include iatrogenic intra-aortic manipulations, paradoxical
emboli through a septal defect, atrial myxoma or primary aortic tumors.
The history is of constant severe epigastric or periumbilical pain of sudden onset. It is
frequently followed by copious vomiting and explosive diarrhea.
Typically the patient has been previously well and asymptomatic. The abdominal signs
are often lacking or nonspecific, with distension in association with absent or normal bowel
sounds without any signs of peritonism. This combination of severe abdominal pain out of
proportion to the clinical findings is typical. Peritonism or blood in the stool or vomitus
indicates severe advanced intestinal ischemia with likely infarction and is generally a late
clinical feature.
The presence of proximal SMA pulsation and the distribution of intestinal ischemia are
intra-operative clues for an embolus. The occlusion in embolism is usually distal to the origin
of the pancreaticoduodenal and middle colic branches, which allows some blood flow to the
small intestine to be maintained. The stomach, duodenum, and proximal jejunum are normal
with ischemia extending to the mid transverse colon.
Thrombosis.
Thrombosis of the superior mesenteric or celiac arteries is most often associated with a
preexisting atherosclerotic lesion that already compromises flow. The most common
preexisting pathology found in patients with acute mesenteric thrombosis is atherosclerosis.
Many patients present with histories consistent with chronic mesenteric ischemia.
Wasting, postprandial pain, and phagophobia (fear of eating) are all common.
Typically, the atherosclerotic lesion gradually compromises flow to the gut, causing a
progressive worsening of symptoms. During a period of low flow, the artery thromboses, and
flow to the gut is compromised.
Unlike embolic events that occur in arterial branches and result in limited bowel
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ischemia, thrombosis occurs at the vessel origin, resulting in extensive bowel involvement.
Superior mesenteric arterial thrombosis may occur as the result of progression of SMA
stenosis that had not previously been diagnosed or treated. There is often a history of intestinal
or food fear with severe weight loss, the hallmark of chronic intestinal ischemia in about 65%
of patients. The typical patient is female and a heavy smoker, often with evidence of
widespread arterial disease including previous myocardial infarction or daudication. As with
embolic occlusion, the combination of severe abdominal pain out of proportion to the clinical
findings is typical. The thrombosis of the SMA occurs at the origin of the artery.
In contrast to embolic disease, the proximal SMA pulse is absent and the distribution of
intestinal ischemia is more extensive. Only the stomach, duodenum and distal colon are spared.
In the young patients, fibromuscular dysplasia can cause mesenteric arterial thrombosis
with equally devastating results. Intravenous cocaine abuse is another increasing problem
accounting for intestinal ischemia in the young patients. The extent of intestinal ischemia and
infarction tends to be foca and less than that seen with atherosclerotic thrombosis. The
mechanism of ischemia appears to be occlusive rather than due to vasospasm. Mesenteric
ischemia should be considered in the differential diagnosis when evaluating a young patient
with a history of cocaine abuse presenting with an acute abdomen.
Some prothrombotic states such as hyperhomocysteinemia or the 20210 A prothrombin
gene mutation have resulted in primary arterial thrombosis.
Mesenteric venous thrombosis (MVT) is rare and accounts for 5% to 15% of all acute
mesenteric ischemia. It is classified as primary (where no cause is recognized) or secondary.
Secondary MVT may follow hypercoagulable states, portal venous stasis and hypertension,
intra-abdominal infection and inflammation or malignancy, use of oral contraceptives and
splenectomy. Long-term anticoagulation is required for MVT, because of the high recurrence
rates. The clinical presentation is usually less acute than that of arterial occlusion.
Severe but vague abdominal pain that tends to be colicky and slowly progressive is
usually present. Few abdominal signs are present except tenderness, distension and decreased
bowel sounds. The pain is out of proportion to the physical findings. Fecal occult blood is
present in the majority of patients.
There is a pyrexia of greater than 38 C in 25% to 50% of patients, and 20% have a
tachycardia. Leucocytosis ranges from 12000 to 29000.
Frank peritonitis is seen only when transmural infarction or perforation has occurred.
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Surgical findings include blood-stained free peritoneal fluid at laparotomy. The affected
bowel is cyanotic and edematous with a rubbery texture.
Mesenteric arterial pulsations are present but the veins contain fresh thrombus that
extrude when the veins are cut. Infarction is most common in the mid small bowel.
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Diagnosis
The majority of cases are diagnosed more than 12 hours after the onset of symptoms.
Delayed diagnosis accounts for the majority of malpractice claims involving acute mesenteric
ischemia in the United States. Diagnosis depends on a high index of suspicion. The main
presenting feature is the combination of severe abdominal pain out of proportion to the clinical
findings, as discussed above.
Serum levels of lactate and leucocytes are elevated in the majority (65% to 90%) of
patients to greater than 50 U/L and 15000/mL, respectively.
Hyperamylasemia is seen in just under half the patients with acute mesenteric ischemia.
Elevation of serum inorganic phosphate levels have been proposed as a marker of mesenteric
ischemia, as it is extensively found in gut, but this only occurs in 15% to 33% of such patients.
However, in those patients who did have elevated phosphate levels, it predicted extensive
injury and poor prognosis. The fibrinolytic marker D-dimer is elevated in thrombo-embolic
occlusion of the SMA, although levels are also raised in other conditions of acute bowel
ischemia such as strangulation or ruptured aortic aneurysm.
Animal studies have suggested intestinal fatty acid binding protein (I-FABP) as a serum
marker reflecting bowel ischemia. Early human studies show promise, as patients with ischemic
bowel disease demonstrate significantly higher I-FABP levels than either healthy subjects or
patients with acute abdominal pain. Patients with mesenteric infarction had the highest serum
I-FABP levels.
Plain radiographs of the abdomen may reveal nonspecific bowel dilatation or, in MVT,
wall edema (thumbprinting); or gas in the bowel wall or portal vein. Unfortunately they are not
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Mesenteric angiography will confirm the diagnosis of arterial occlusion but at the cost of
delay in treatment. If there are clear abdominal signs of peritonitism, urgent laparotomy without
angiography is the best course of action. In the remainder of patients suspected of acute
intestinal ischemia with-out abdominal signs, angiography is indicated with lateral views of the
visceral aorta and its branches.
In acute SMA thrombosis, there is usually no visualization of the entire artery because of
the ostial nature of the disease, although delayed views may show slow filling of the distal
SMA. SMA embolization usually allows visualization of the proximal artery to just beyond the
level of the middle colic artery.
Treatment
Nonsurgical
In all cases, the patient should be initially resuscitated, given broadpectrum intravenous
antibiotics and fully heparinized. As yet, the twin goals of mesenteric revascularization and
resection of nonviable bowel can only be achieved by surgical means.
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SURGICAL
Laparotomy is indicated in patients with peritonitis after rapid resuscitation. The first
step is to assess the degree and extent of bowel viability. Free, foul smelling peritoneal fluid is
a sign of advanced necrosis even if perforation has not occurred. Ischemic bowel has a
characteristic appearance with loss of its normal sheen. It is dull, gray in color and flabby in
tone without any peristalsis. Infarcted bowel is purplish black in color, often friable and
perforated. In many cases the bowel ischemia will be so extensive and advanced that no further
surgical treatment is undertaken and palliative care given. Where there is hope of sufficient
bowel viability, revascularization should be performed before any bowel resection is
considered. After successful revascularization, previously precarious segments of intestine may
recover and resection of clearly ischemic bowel can then take place.
SMA embolectomy. The proximal portion of the SMA is dissected free from the
surrounding fat and lymphatic tissue just as it emerges from the pancreatic neck into the base
of the mesentery. Approximately 3 to 4 centimeters of artery is cleared, with care taken not to
damage the branches. Heparin (5000 units) is given intravenously. A transverse arteriotomy is
made and a 3F or 4F embolectomy catheter is passed proximally and distally to clear the
embolus and reestablish vigorous pulsatile flow. If proximal flow cannot be established, SMA
thrombosis is likely and reconstructive surgery will be required.
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Atherosclerotic occlusive plaque is by far the most common pathology seen in the
carotid artery bifurcation. Thirty to 60% of all ischemic strokes are related to atherosclerotic
carotid bifurcation occlusive disease. In the following section, discussion will be focused on
clinical presentation, diagnosis, and management, including medical therapy, surgical carotid
endarterectomy, and stenting of atherosclerotic carotid occlusive disease. In the second part of
the section, a brief review will be focused on other less common non-atherosclerotic diseases
involving the extracranial carotid artery, including kink and coil, fibromuscular dysplasia
(FMD), arterial dissection, aneurysm, radiation arteritis, Takayasu's arteritis, and carotid body
tumor.
Approximately 700,000 Americans suffer a new or recurrent stroke each year. Eighty-five
percent of all strokes are ischemic and 15% are hemorrhagic. Hemorrhagic strokes are caused
by head trauma or spontaneous disruption of intracerebral blood vessels. Ischemic strokes are
due to hypoperfusion from arterial occlusion, or less commonly due to decreased flow resulting
from proximal arterial stenosis and poor collateral network. Common causes of ischemic
strokes are cardiogenic emboli (35%), carotid artery disease (30%), lacunar (10%),
miscellaneous (10%), and idiopathic (15%). The term cerebrovascular accident (CVA) often is
used interchangeably to refer to an ischemic stroke. A transient ischemic attack (TIA) is
defined as a temporary focal cerebral or retinal hypoperfusion state that resolves spontaneously
within 24 hours after its onset. However, the majority of TIAs resolve within minutes, and
longer lasting neurologic deficits more likely represent a stroke. Recently, the term brain attack
has been coined to refer to an acute stroke or TIA, denoting the condition as a medical
emergency requiring immediate attention, similar to a heart attack.
Stroke due to carotid bifurcation occlusive disease usually is caused by atheroemboli
(Fig. 1). The carotid bifurcation is an area of low-flow velocity and low-shear stress. As the
blood circulates through the carotid bifurcation, there is separation of flow into the
low-resistance ICA, and the high-resistance external carotid artery. Characteristically,
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atherosclerotic plaque forms in the outer wall opposite to the flow divider (Fig. 2).
Atherosclerotic plaque formation is complex, beginning with intimal injury, platelet
deposition, smooth muscle cell proliferation, and fibroplasia, and leading to subsequent
luminal narrowing. With increasing degree of stenosis in the ICA, flow becomes more
turbulent, and the risk of atheroembolization escalates. The severity of stenosis is commonly
divided into three categories according to the luminal diameter reduction: mild (less than 50%),
moderate (50 to 69%), and severe (70 to 99%). Severe carotid stenosis is a strong predictor for
stroke. In turn, a prior history of neurologic symptoms (TIA or stroke) is an important
determinant for recurrent ipsilateral stroke. The risk factors for the development of carotid
artery bifurcation disease are similar to those causing atherosclerotic occlusive disease in other
vascular beds. Increasing age, male gender, hypertension, tobacco smoking, diabetes mellitus,
homocysteinemia, and hyperlipidemia are well-known predisposing factors for the development
of atherosclerotic occlusive disease.
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Fig.2 A. The carotid bifurcation is an area of low-flow velocity and low-shear stress. As
the blood circulates through the carotid bifurcation, there is separation of flow into the
low-resistance internal carotid artery and the high-resistance external carotid artery
Fig. 2 B. The carotid atherosclerotic plaque typically forms in the outer wall opposite to
the flow divider due in part to the effect of the low-shear stress region, which also creates a
transient reversal of flow during cardiac cycle.
TIA is a focal loss of neurologic function, lasting for <24 hours. Crescendo TIAs refer to
a syndrome comprising repeated TIAs within a short period of time that is characterized by
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complete neurologic recovery in between. At a minimum the term should probably be reserved
either for those with daily events or multiple resolving attacks within 24 hours. Hemodynamic
TIAs represent focal cerebral events that are aggravated by exercise or hemodynamic stress and
typically occur after short bursts of physical activity, postprandially or after getting out of a hot
bath. It is implied that these are due to severe extracranial disease and poor intracranial
collateral recruitment. Reversible ischemic neurologic deficits refer to ischemic focal
neurologic symptoms lasting longer than 24 hours but resolving within 3 weeks. When a
neurologic deficit lasts longer than 3 weeks, it is considered a completed stroke. Stroke in
evolution refers to progressive worsening of the neurologic deficit, either linearly over a
24-hour period, or interspersed with transient periods of stabilization and/or partial clinical
improvement.
The patients who suffer CVAs typically present with three categories of symptoms,
including ocular symptoms, sensory/motor deficit, and/or higher cortical dysfunction. The
common ocular symptoms associated with extracranial carotid artery occlusive disease include
amaurosis fugax and presence of Hollenhorst plaques. Amaurosis fugax, commonly referred to
as transient monocular blindness, is a temporary loss of vision in one eye that patients
typically describe as a window shutter coming down or gray shedding of the vision. This partial
blindness usually lasts for a few minutes and then resolves. Most of these phenomena (>90%)
are due to embolic occlusion of the main artery or the upper or lower divisions. Monocular
blindness progressing over a 20-minute period suggests a migrainous etiology. Occasionally,
the patient will recall no visual symptoms while the optician notes a yellowish plaque within
the retinal vessels, which is also known as the Hollenhorst plaque. These are frequently
derived from cholesterol embolization from the carotid bifurcation and warrant further
investigation. Additionally, several ocular symptoms may be caused by microembolization from
the extracranial carotid diseases, including monocular vision loss due to retinal artery or optic
nerve ischemia, the ocular ischemia syndrome, and visual field deficits secondary to cortical
infarction and ischemia of the optic tracts. Typical motor and/or sensory symptoms associated
with CVAs are located in either an ipsilateral or contralateral neurologic deficit. Ischemic
events tend to have an abrupt onset, with the severity of the insult being apparent from the
onset and not usually associated with seizures or paraesthesia. In contrast, they represent loss
or diminution of neurologic function. Furthermore, motor or sensory deficits can be unilateral
or bilateral, with the upper and lower limbs being variably affected depending on the site of the
cerebral lesion.
The combination of a motor and sensory deficit in the same body territory is suggestive
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Diagnostic Evaluation
Duplex ultrasonography is the most widely used screening tool to evaluate for
atherosclerotic plaque and stenosis of the extracranial carotid artery. It is also commonly used
to monitor patients serially for progression of disease, or after intervention (carotid
endarterectomy or angioplasty). Duplex ultrasound of the carotid artery combines B-mode
gray-scale imaging and Doppler waveform analysis. Characterization of the carotid plaque on
gray-scale imaging provides useful information about its composition. However, there are
currently no universal recommendations that can be made based solely on the sonographic
appearance of the plaque. On the other hand, criteria have been developed and well refined for
grading the degree of carotid stenosis based primarily on Doppler-derived velocity waveforms.
The external carotid artery has a high-resistance flow pattern with a sharp systolic peak
and a small amount of flow in diastole. In contrast, a normal ICA will have a low-resistance
flow pattern with a broad systolic peak and a large amount of flow during diastole. The flow
pattern in the common carotid artery (CCA) resembles that in the ICA, as 80% of the flow is
directed to the ICA, with waveforms that have broad systolic peaks and a moderate amount of
flow during diastole. Conventionally, velocity measurements are recorded in the common,
external carotid bulb, and the proximal, mid-, and distal portions of the ICA. Characteristically,
the peak systolic velocity is increased at the site of the vessel stenosis. The end-diastolic
velocity is increased with a greater degree of stenosis. In addition, stenosis of the ICA can lead
to color shifts with color mosaics indicating a poststenotic turbulence. Dampening of the
Doppler velocity waveforms are typically seen in areas distal to severe carotid stenosis where
blood flow is reduced. It is well known that occlusion of the ipsilateral ICA can lead to a
"falsely" elevated velocity on the contralateral side due to an increase in compensatory blood
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flow. In the presence of a high-grade stenosis or occlusion of the ICA, the ipsilateral CCA
displays high flow resistance waveforms, similar to that seen in the external carotid artery. If
there is a significant stenosis in the proximal CCA, its waveforms may be dampened with low
velocities.
The Doppler grading systems of carotid stenosis were initially established by
comparison to angiographic findings of disease. Studies have shown variability in the
measurements of the duplex properties by different laboratories, as well as heterogeneity in the
patient population, study design, and techniques. One of the most commonly used
classifications was established at the University of Washington School of Medicine in Seattle.
Diameter reduction of 50 to 79% is defined by peak systolic velocity >125 cm/sec with
extensive spectral broadening. For stenosis in the range of 80 to 99%, the peak systolic
velocity is >125 cm/sec and peak diastolic velocity is >140 cm/sec. The ratio of internal carotid
to common carotid artery (ICA/CCA) peak systolic velocity has also been part of various
ultrasound diagnostic classifications. A ratio >4 is a great predictor of angiographic stenosis of
70 to 99%. A multispecialty consensus panel has developed a set of criteria for grading carotid
stenosis by duplex examination (Table 1).
Table 1. Carotid Duplex Ultrasound Criteria for Grading Internal Carotid Artery
Stenosis
MRA is increasingly being used to evaluate for atherosclerotic carotid occlusive disease
and intracranial circulation. MRA is noninvasive and does not require iodinated contrast
agents. MRA uses phase contrast or time-of-flight, with either two-dimensional or three-
dimensional data sets for greater accuracy. Three-dimensional, contrast-enhanced MRA allows
data to be obtained in coronal and sagittal planes with improved image qualities due to shorter
study time. In addition, the new MRA techniques allow for better reformation of images in
various planes to allow better grading of stenosis. There have been numerous studies
comparing the sensitivity and specificity of MRA imaging for carotid disease to duplex and
selective contrast angiography. Magnetic resonance imaging (MRI) of the brain is essential in
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the assessment of acute stroke patients. MRI with diffusion-weighted imaging can differentiate
areas of acute ischemia, areas still at risk for ischemia (penumbra), and chronic cerebral
ischemic changes. However, computed tomographic (CT) imaging remains the most expeditious
test in the evaluation of acute stroke patients to rule out intracerebral hemorrhage. Recently,
multidetector CTA has gained increasing popularity in the evaluation of carotid disease. This
imaging modality can provide volume rendering, which allows rotation of the object with
accurate anatomic structures from all angles (Fig. 3). The advantages of CTA over MRA
include faster data acquisition time and better spatial resolution. However, grading of carotid
stenosis by CTA requires further validation at the time of this writing before it can be widely
applied.
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Fig.3
B. The entire segment of extracranial carotid artery is visualized from the thoracic
compartment to the base of skull.
Historically, DSA has been the gold standard test to evaluate the extra- and intracranial
circulation (Fig. 4). This is an invasive procedure, typically performed via a transfemoral
puncture, and involves selective imaging of the carotid and vertebral arteries using iodinated
contrast. The risk of stroke during cerebral angiography is generally reported at approximately
1%, and is typically due to atheroembolization related to wire and catheter manipulation in the
arch aorta or proximal branch vessels. Over the past decades, however, the incidence of
neurologic complications following angiography has been reduced, due to the use of improved
guidewires and catheters, better resolution digital imaging, and increased experience. Local
access complications of angiography are infrequent and include development of hematoma,
pseudoaneurysm, distal embolization, or acute vessel thrombosis. Currently, selective
angiography is particularly used for patients with suspected intracranial disease and for
patients in whom percutaneous revascularization is considered. The techniques of carotid
angioplasty and stenting for carotid bifurcation occlusive disease are described in the
"Techniques of Carotid Angioplasty and Stenting" section. Preoperative CTA or MRA is
routinely utilized to get information about the aortic arch anatomy and presence of concomitant
intracranial disease and collateral pathway in planning our strategy for carotid stenting or
endarterectomy.
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Fig. 4. A carotid angiogram reveals an ulcerated carotid plaque (arrow) in the proximal
internal carotid artery, which also resulted in a high-grade, internal, carotid artery stenosis
Conventionally, patients with carotid bifurcation occlusive disease are divided into two
broad categories: patients without prior history of ipsilateral stroke or TIA (asymptomatic) and
those with prior or current ipsilateral neurologic symptoms (symptomatic). It is estimated that
15% of all strokes are preceded by a TIA. The 90-day risk of a stroke in a patient presenting
with a TIA is 3 to 17%. According to the Cardiovascular Health Study, a longitudinal,
population-based study of CAD and stroke in men and women, the prevalence of TIA in men
was 2.7% between the ages of 65 to 69 and 3.6% for ages 75 to 79; the prevalence in women
was 1.4% and 4.1%, respectively. There have been several studies reporting on the effectiveness
of stroke prevention with medical treatment and carotid endarterectomy for symptomatic
patients with moderate to severe carotid stenosis. Early and chronic aspirin therapy has been
shown to reduce stroke recurrence rate in several large clinical trials.
Currently, most stroke neurologists prescribe both aspirin and clopidogrel for secondary
stroke prevention in patients who had experienced a TIA or stroke. In patients with
symptomatic carotid stenosis, the degree of stenosis appears to be the most important predictor
in determining risk for an ipsilateral stroke. The risk of a recurrent ipsilateral stroke in patients
with severe carotid stenosis approaches 40%. Two large multicenter randomized clinical trials,
the European Carotid Surgery Trial and the North American Symptomatic Carotid
Endarterectomy Trial, have both shown a significant risk reduction in stroke for patients with
symptomatic high-grade stenosis (70 to 99%) undergoing carotid endarterectomy when
compared to medical therapy alone. There has been much discussion regarding the different
methodology used in the measurement of carotid stenosis and calculation of the life-table data
between the two studies, which still led to similar results. Findings of these two landmark trials
have also been reanalyzed in many subsequent publications. The main conclusions of the trials
remain validated and widely acknowledged. Briefly, the North American Symptomatic Carotid
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Endarterectomy Trial study showed that, for high-grade carotid stenosis, the cumulative risk of
ipsilateral stroke was 26% in the medically treated group and 9% in the surgically treated
group at 2 years. For patients with moderate carotid artery stenosis (50 to 69%), the benefit of
carotid endarterectomy is less but still favorable when compared to medical treatment alone;
the 5-year fatal or nonfatal ipsilateral stroke rate was 16% in the surgically treated group vs.
22% in the medically treated group. The risk of stroke was similar for the remaining group of
symptomatic patients with less than 50% carotid stenosis, whether they had endarterectomy or
medical treatment alone. The European Carotid Surgery Trial reported similar stroke risk
reduction for patients with severe symptomatic carotid stenosis and no benefit in patients with
mild stenosis, when carotid endarterectomy was performed vs. medical therapy.
The optimal timing of carotid intervention after acute stroke, however, remains
debatable. Earlier studies showed an increased rate of postoperative stroke exacerbation and
conversion of a bland to hemorrhagic infarction when carotid endarterectomy was carried out
within 5 to 6 weeks after acute stroke. The dismal outcome reported in the early experience was
likely related to poor patient selection. The rate of stroke recurrence is not insignificant during
the interval period and may be reduced with early intervention for symptomatic carotid
stenosis. Contemporary series have demonstrated acceptable low rates of perioperative
complications in patients undergoing carotid endarterectomy within 4 weeks after acute stroke.
In a recent retrospective series, carotid artery stenting, when performed early (<2 weeks) after
the acute stroke, was associated with higher mortality than when delayed (>2 weeks).
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total occlusion of the ICA or new symptoms. The major risk factors associated with disease
progression were cigarette smoking, diabetes mellitus, and age. This study supported the
contention that it is prudent to follow a conservative course in the management of
asymptomatic patients presenting with a cervical bruit.
One of the first randomized clinical trials on the treatment of asymptomatic carotid
artery stenosis was the Asymptomatic Carotid Atherosclerosis Study, which evaluated the
benefits of medical management with antiplatelet therapy vs. carotid endarterectomy. Over a
5-year period, the risk of ipsilateral stroke in individuals with a carotid artery stenosis greater
than 60% was 5.1% in the surgical arm. On the other hand, the risk of ipsilateral stroke in
patients treated with medical management was 11%. Carotid endarterectomy produced a
relative risk reduction of 53% over medical management alone. The results of a larger
randomized trial from Europe, The Asymptomatic Carotid Surgery Trial, confirmed similar
beneficial stroke risk reduction for patients with asymptomatic greater than 70% carotid
stenosis undergoing endarterectomy compared to medical therapy. An important point derived
from this latter trial was that even with improved medical therapy, including the addition of
statin drugs and clopidogrel, medical therapy was still inferior to endarterectomy in the primary
stroke prevention for patients with high-grade carotid artery stenosis. It is generally agreed that
asymptomatic patients with severe carotid stenosis (80 to 99%) are at significantly increased
risk for stroke and stand to benefit from either surgical or endovascular revascularization.
However, revascularization for asymptomatic patients with a less severe degree of stenosis (60
to 79%) remains controversial.
Currently, the argument is no longer that medical therapy alone is inferior to surgical
endarterectomy in stroke prevention for severe carotid stenosis. Rather, the debate now revolves
around whether carotid angioplasty and stenting produces the same benefit that has been
demonstrated by carotid endarterectomy. Since carotid artery stenting was approved by the
FDA in 2004 for clinical application, this percutaneous procedure has become a treatment
alternative in patients who are deemed "high-risk" for endarterectomy (Table 2). In contrast to
many endovascular peripheral arterial interventions, percutaneous carotid stenting represents a
much greater challenging procedure, because it requires complex, catheter-based skills using
the 0.014-in guidewire system and distal protection device. Moreover, current carotid stent
devices predominantly use the monorail guidewire system that requires more technical agility,
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Table 2. Conditions Qualifying Patients as "High Surgical Risk" for Carotid Endarterectomy
Although carotid endarterectomy is one of the earliest vascular operations ever described
and its techniques have been perfected in the last two decades, surgeons continue to debate
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many aspects of this procedure. For instance, there is no universal agreement with regard to the
best anesthetic of choice, the best intraoperative cerebral monitoring, whether to "routinely"
shunt, open vs. eversion endarterectomy, and patch vs. primary closure. Various anesthetic
options are available for a patient undergoing carotid endarterectomy including general, local,
and regional anesthesia. Typically, the anesthesia of choice depends on the preference of the
surgeon, anesthesiologist, and patient. However, depending on the anesthetic given, the surgeon
must decide whether intraoperative cerebral monitoring is necessary or intra-arterial carotid
shunting will be used. In general, if the patient is awake, then his or her abilities to respond to
commands during carotid clamp period determine the adequacy of collateral flow to the
ipsilateral hemisphere. On the other hand, intraoperative electroencephalogram or transcranial
power Doppler (TCD) has been used to monitor for adequacy of cerebral perfusion during the
clamp period for patients undergoing surgery under general anesthesia. Focal ipsilateral
decreases in amplitudes and slowing of electroencephalogram waves are indicative of cerebral
ischemia. Similarly, a decrease to less than 50% of baseline velocity in the ipsilateral middle
cerebral artery is a sign of cerebral ischemia. For patients with poor collateral flow exhibiting
signs of cerebral ischemia, intra-arterial carotid shunting with removal of the clamp will restore
cerebral flow for the remaining part of the surgery. Stump pressures have been used to
determine the need for intra-arterial carotid shunting. Some surgeons prefer to shunt all
patients on a routine basis and do not use intraoperative cerebral monitoring.
The patient's neck is slightly hyperextended and turned to the contralateral side, with a
roll placed between the shoulder blades. An oblique incision is made along the anterior border
of the sternocleidomastoid muscle centered on top of the carotid bifurcation (Fig. 5). The
platysma is divided completely. Typically, tributaries of the anterior jugular vein are ligated and
divided. The dissection is carried medial to the sternocleidomastoid. The superior belly of the
omohyoid muscle is usually encountered just anterior to the CCA. This muscle can be divided.
The carotid fascia is incised and the CCA is exposed. The CCA is mobilized cephalad toward
the bifurcation. The dissection of the carotid bifurcation can cause reactive bradycardia related
to stimulation of the carotid body. This reflex can be blunted with injection of lidocaine 1%
into the carotid body or reversed with administration of IV atropine. A useful landmark in the
dissection of the carotid bifurcation is the common facial vein. This vein can be ligated and
divided. Frequently, the twelfth cranial nerve (hypoglossal nerve) traverses the carotid
bifurcation just behind the common facial vein. The external carotid artery is mobilized just
enough to get a clamp across. Often, a branch of the external carotid artery crossing to the
sternocleidomastoid can be divided to allow further cephalad mobilization of the ICA. For high
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bifurcation, division of the posterior belly of the digastric muscle is helpful in establishing
distal exposure of the ICA.
IV heparin sulfate (1 mg/kg) is routinely administered just before carotid clamping. The
ICA is clamped first using a soft, noncrushing vascular clamp to prevent distal embolization.
The external and common carotid arteries are clamped subsequently. A longitudinal
arteriotomy is made in the distal CCA and extended into the bulb and past the occlusive plaque
into the normal part of the ICA. Endarterectomy is carried out to remove the occlusive plaque
(Fig. 6). If necessary, a temporary shunt can be inserted from the CCA to the ICA to maintain
continuous antegrade cerebral blood flow (Fig. 7). Typically, a plane is teased out from the
vessel wall, and the entire plaque is elevated and removed. The distal transition line in the ICA
where the plaque had been removed must be examined carefully and should be smooth. Tacking
sutures are placed when an intimal flap remains in this transition to ensure no obstruction to
flow (Fig. 8). The occlusive plaque is usually removed from the origin of the external carotid
artery using the eversion technique. The endarterectomized surface is then irrigated and any
debris removed. A patch (autogenous saphenous vein, synthetic such as polyester, PTFE, or
biologic material) is sewn to close the arteriotomy (Fig. 9). Whether patch closure is necessary
in all patients and which patch is the best remain controversial. However, most surgeons agree
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that patch closure is indicated particularly for the small vessel (<7 mm). The eversion technique
also has been advocated for removing the plaque from the ICA. In the eversion technique, the
ICA is transected at the bulb, the edges of the divided vessel are everted, and the occluding
plaque is "peeled" off the vessel wall. The purported advantages of the eversion technique are
no need for patch closure and a clear visualization of the distal transition area. Reported series
have not shown a clear superiority of one technique over the others. Surgeons will likely
continue to use the technique of their choice. Just before completion of the anastomosis to
close the arteriotomy, it is prudent to flush the vessels of any potential debris. When the
arteriotomy is closed, flow is restored to the external carotid artery first and to the ICA second.
IV protamine sulfate can be given to reverse the effect of heparin anticoagulation following
carotid endarterectomy. The wound is closed in layers. After surgery, the patient's neurologic
condition is assessed in the operating room (OR) before transfer to the recovery area.
Fig. 6 A. During carotid endarterectomy, vascular clamps are applied in common carotid,
external carotid, and internal carotid arteries. Carotid plaque is elevated from the carotid lumen
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Fig. 6 B. Carotid plaque is removed and the arteriotomy is closed either primarily or
with a patch angioplasty
Fig. 7. A temporary carotid shunt is inserted from the common carotid artery (long
arrow) to the internal carotid artery (short arrow) during carotid endarterectomy to provide
continuous antegrade cerebral blood flow.
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Fig. 8. The distal transition line (left side of the picture) in the internal carotid artery
where the plaque had been removed must be examined carefully and should be smooth. Tacking
sutures (arrows) are placed when an intimal flap remains in this transition to ensure no
obstruction to flow.
Fig. 9 A. An autologous or synthetic patch can be used to close the carotid arteriotomy
incision, which maintains the luminal patency
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Most patients tolerate carotid endarterectomy very well and typically are discharged
home within 24 hours after surgery. Complications after endarterectomy are infrequent but can
be potentially life threatening or disabling. Acute ipsilateral stroke is a dreaded complication
following carotid endarterectomy. Cerebral ischemia can be due to either intraoperative or
postoperative events. Embolizations from the occlusive plaque or prolonged cerebral ischemia
are potential causes of intraoperative stroke. The most common cause of postoperative stroke is
due to embolization. Less frequently, acute carotid artery occlusion can cause acute
postoperative stroke. This is usually due to carotid artery thrombosis related to closure of the
arteriotomy, an occluding intimal flap, or distal carotid dissection. When patients experience
acute symptoms of neurologic ischemia after endarterectomy, immediate intervention may be
indicated. Carotid duplex scan can be done expeditiously to assess patency of the extracranial
ICA. Re-exploration is mandated for acute carotid artery occlusion. Cerebral angiography can
be useful if intracranial revascularization is considered.
Local complications related to surgery include excessive bleeding and cranial nerve
palsies. Postoperative hematoma in the neck after carotid endarterectomy can lead to
devastating airway compromise. Any expanding hematoma should be evacuated and active
bleeding stopped. Securing an airway is critical and can be extremely difficult in patients with
large postoperative neck hematomas. The reported incidence of postoperative cranial nerve
palsies after carotid endarterectomy varies from 1 to 30%. Well-recognized injuries involve the
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marginal mandibular, vagus, hypoglossal, superior laryngeal, and recurrent laryngeal nerves.
Often these are traction injuries but can also be due to severance of the respective nerves.
Percutaneous carotid artery stenting has become an accepted alternative treatment in the
management of patients with carotid bifurcation disease (Fig. 10). The perceived advantages of
percutaneous carotid revascularization are related to the minimal invasiveness of the procedure
compared to surgery. There are anatomical conditions based on angiographic evaluation in
which carotid artery stenting should be avoided due to increased procedural-related risks
(Table 3). In preparation for carotid stenting, the patient should be given oral clopidogrel 3
days before the intervention if the patient was not already taking the drug. The procedure is
done in either the OR with angiographic capabilities or in a dedicated angiography room. The
patient is placed in the supine position. The patient's BP and cardiac rhythm are closely
monitored.
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in the ipsilateral external carotid artery. Anticoagulation with IV bivalirudin bolus (0.75mg/kg)
followed by an infusion rate of 2.5 mg/kg per hour for the remainder of the procedure is
routinely administered. Next, the diagnostic catheter is withdrawn and a 90-cm 6F guiding
sheath is advanced into the CCA over the stiff glide wire. It is critical not to advance the sheath
beyond the occlusive plaque in the carotid bulb. The stiff wire is then removed and preparation
is made to deploy the distal embolic protection device (EPD). Several distal EPDs are available
(Table 4). The EPD device is carefully deployed beyond the target lesion. With regard to the
carotid stents, there are several stents that have received approval from the FDA and are
commercially available for carotid revascularization (Table 5). All current carotid stents use the
rapid-exchange monorail 0.014-in platform. The size selection is typically based on the size of
CCA. Predilatation using a 4-mm balloon may be necessary to allow passage of the stent
delivery catheter. Once the stent is deployed across the occlusive plaque, postdilatation is
usually performed using a 5.5-mm or less balloon. It's noteworthy that balloon dilation of the
carotid bulb may lead to immediate bradycardia due to stimulation of the glossopharyngeal
nerve. The EPD is then retrieved and the procedure is completed with removal of the sheath
from the femoral artery. The puncture site is closed using an available closure device or with
manual compression. Throughout the procedure, the patient's neurologic function is closely
monitored. The bivalirudin infusion is stopped, and the patient is kept on clopidogrel (75 mg
daily) for at least 1 month and aspirin indefinitely.
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Although there have been no randomized trials comparing carotid stenting with and
without EPD, the availability of EPDs appears to have reduced the risk of distal embolization
and stroke. The results of the various clinical trials and registries of carotid stenting have been
reported and compared. It is well known that distal embolization as detected by TCD is much
more frequent with carotid stenting, even with EPD, when compared to carotid endarterectomy.
However, the clinical significance of the distal embolization detected by TCD is not clear, as
most are asymptomatic. Acute carotid stent thrombosis is rare. The incidence of instent carotid
restenosis is not well known but is estimated at 10 to 30%. Duplex surveillance shows elevated
peak systolic velocities within the stent after carotid stenting can occur frequently. However,
velocity criteria are being formulated to determine the severity of instent restenosis after carotid
stenting by ultrasound duplex. It appears that systolic velocities exceeding 300 to 400 cm/s
would represent greater than 70 to 80% restenosis. Bradycardia and hypotension occurs in up
to 20% of patients undergoing carotid stenting. Systemic administration of atropine is usually
effective in reversing the bradycardia. Other technical complications of carotid stenting are
infrequent and include carotid artery dissection, and access site complications such as groin
hematoma, femoral artery pseudoaneurysm, distal embolization, and acute femoral artery
thrombosis.
A carotid coil consists of an excessive elongation of the ICA producing tortuosity of the
vessel (Fig. 11). Embryologically, the carotid artery is derived from the third aortic arch and
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dorsal aortic root, and is uncoiled as the heart and great vessels descend into the mediastinum.
In children, carotid coils appear to be congenital in origin. In contrast, elongation and kinking
of the carotid artery in adults is associated with the loss of elasticity and an abrupt angulation
of the vessel. Kinking is more common in women than men. Cerebral ischemic symptoms
caused by kinks of the carotid artery are similar to those from atherosclerotic carotid lesions,
but are more likely due to cerebral hypoperfusion than embolic episodes. Classically, sudden
head rotation, flexion, or extension can accentuate the kink and provoke ischemic symptoms.
Most carotid kinks and coils are found incidentally on carotid duplex scan. However,
interpretation of the Doppler frequency shifts and spectral analysis in tortuous carotid arteries
can be difficult because of the uncertain angle of insonation. Cerebral angiography, with
multiple views taken in neck flexion, extension, and rotation, is useful in the determination of
the clinical significance of kinks and coils.
Fig. 11. Excessive elongation of the carotid artery can result in carotid kinking (arrow), which
can compromise cerebral blood flow and lead to cerebral ischemia.
Fibromuscular Dysplasia
FMD usually involves medium-sized arteries that are long and have few branches (Fig.
12). Women in the fourth or fifth decade of life are more commonly affected than men.
Hormonal effects on the vessel wall are thought to play a role in the pathogenesis of FMD.
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FMD of the carotid artery is commonly bilateral, and in about 20% of patients, the vertebral
artery also is involved. An intracranial saccular aneurysm of the carotid siphon or middle
cerebral artery can be identified in up to 50% of the patients with FMD. Four histological
types of FMD have been described in the literature. The most common type is medial
fibroplasia, which may present as a focal stenosis or multiple lesions with intervening
aneurysmal outpouchings. The disease involves the media with the smooth muscle being
replaced by fibrous connective tissue. Commonly, mural dilations and microaneurysms can be
seen with this type of FMD. Medial hyperplasia is a rare type of FMD, with the media
demonstrating excessive amounts of smooth muscle. Intimal fibroplasia accounts for 5% of all
cases and occurs equally in both sexes. The media and adventitia remain normal, and there is
accumulation of subendothelial mesenchymal cells with a loose matrix of connective tissue
causing a focal stenosis in adults. Finally, premedial dysplasia represents a type of FMD with
elastic tissue accumulating between the media and adventitia. FMD also can involve the renal
and the external iliac arteries. It is estimated that approximately 40% of patients with FMD
present with a TIA due to embolization of platelet aggregates. DSA demonstrates the
characteristic "string of beads" pattern, which represents alternating segments of stenosis and
dilatation. The string of beads can also be shown noninvasively by CTA or MRA. FMD should
be suspected when an increased velocity is detected across a stenotic segment without
associated atherosclerotic changes on carotid duplex ultrasound. Antiplatelet medication is the
generally accepted therapy for asymptomatic lesions. Endovascular treatment is recommended
for patients with documented lateralizing symptoms. Surgical correction is rarely indicated.
Fig. 12. A carotid fibromuscular dysplasia with typical characteristics of multiple stenosis with
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intervening aneurysmal outpouching dilatations. The disease involves the media, with the
smooth muscle being replaced by fibrous connective tissue
Dissection of the carotid artery accounts for approximately 20% of strokes in patients
younger than 45 years of age. The etiology and pathogenesis of spontaneous carotid artery
dissection remains incompletely understood. Arterial dissection involves hemorrhage within
the media, which can extend into the subadventitial and subintimal layers. When the dissection
extends into the subadventitial space, there is an increased risk of aneurysm formation.
Subintimal dissections can lead to intramural clot or thrombosis. Traumatic dissection is
typically a result of hyperextension of the neck during blunt trauma, neck manipulation,
strangulation, or penetrating injuries to the neck. Even in supposedly spontaneous cases, a
history of preceding unrecognized minor neck trauma is not uncommon. Connective disorders
such as Ehlers-Danlos syndrome, Marfan syndrome, alpha1-antitrypsin deficiency, or FMD
may predispose to carotid artery dissection. Iatrogenic dissections also can occur due to
catheter manipulation or balloon angioplasty.
Typical clinical features of carotid artery dissection include unilateral neck pain,
headache, and ipsilateral Horner's syndrome in up to 50% of patients, followed by
manifestations of the cerebral or ocular ischemia and cranial nerve palsies. Neurologic deficits
can result either because of hemodynamic failure (caused by luminal stenosis) or by an artery
to artery thromboembolism. The ischemia may cause TIAs or infarctions, or both. Catheter
angiography has been the method of choice to diagnose arterial dissections, but with the advent
of duplex ultrasonography, MRI/MRA, and CTA, most dissections can now be diagnosed using
noninvasive imaging modalities (Fig. 13). The dissection typically starts in the ICA distal to
the bulb. Uncommonly, the dissection can start in the CCA, or is an extension of a more
proximal aortic dissection. Medical therapy has been the accepted primary treatment of
symptomatic carotid artery dissection. Anticoagulation (heparin and warfarin) and antiplatelet
therapy have been commonly used, although there have not been any randomized studies to
evaluate their effectiveness. The prognosis depends on the severity of neurologic deficit but is
generally good in extracranial dissections. The recurrence rate is low. Therapeutic interventions
have been reserved for recurrent TIAs or strokes, or failure of medical treatment. Endovascular
options include intra-arterial stenting, coiling of associated pseudoaneurysms, or more recently,
deployment of covered stents.
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Fig. 13. Carotid ultrasound reveals a patient with a carotid artery dissection in which
carotid flow is separated in the true flow lumen (long arrow) from the false lumen (short
arrow).
Carotid artery aneurysms are rare, encountered in less than 1% of all carotid operations
(Fig. 14). The true carotid artery aneurysm generally is due to atherosclerosis or medial
degeneration. The carotid bulb is involved in most carotid aneurysms, and bilaterality is present
in 12% of the patients. Patients typically present with a pulsatile neck mass. The available data
suggest that, untreated, these aneurysms lead to neurologic symptoms from embolization.
Thrombosis and rupture of the carotid aneurysm is rare. Pseudoaneurysms of the carotid artery
can result from injury or infection. Mycotic aneurysms often involve syphilis in the past, but
are now more commonly associated with peritonsillar abscesses caused by Staphylococcus
aureus infection. FMD and spontaneous dissection of the carotid artery can lead to the
formation of true aneurysms or pseudoaneurysms. Whereas conventional surgery has been the
primary mode of treatment in the past, carotid aneurysms are currently being treated more
commonly using endovascular approaches.
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The carotid body originates from the third branchial arch and from neuroectodermal-
derived neural crest lineage. The normal carotid body is located in the adventitia or
periadventitial tissue at the bifurcation of the CCA (Fig. 15). The gland is innervated by the
glossopharyngeal nerve. Its blood supply is derived predominantly from the external carotid
artery, but also can come from the vertebral artery. Carotid body tumor is a rare lesion of the
neuroendocrine system. Other glands of neural crest origin are seen in the neck, parapharyngeal
spaces, mediastinum, retroperitoneum, and adrenal medulla. Tumors involving these structures
have been referred to as paraganglioma, glomus tumor, or chemodectoma. Approximately 5 to
7% of carotid body tumors are malignant. Although chronic hypoxemia has been invoked as a
stimulus for hyperplasia of carotid body, approximately 35% of carotid body tumors are
hereditary. The risk of malignancy is greatest in young patients with familial tumors.
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Fig. 15 A. A carotid body tumor (arrow) located adjacent to the carotid bulb
Symptoms related to the endocrine products of the carotid body tumor are rare. Patients
usually present between the fifth and seventh decade of life with an asymptomatic lateral neck
mass. The diagnosis of carotid body tumor requires confirmation on imaging studies. Carotid
duplex scan can localize the tumor to the carotid bifurcation, but CT or MR imaging usually is
required to further delineate the relationship of the tumor to the adjacent structures.
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Classically, a carotid body tumor will widen the carotid bifurcation. The Shamblin
classification describes the tumor extent: I. tumor is <5 cm and relatively free of vessel
involvement; II. tumor is intimately involved but does not encase the vessel wall; and III. tumor
is intramural and encases the carotid vessels and adjacent nerves. With good resolution CT and
MR imaging, arteriography usually is not required. However, arteriography can provide an
assessment of the vessel invasion and intracranial circulation, and allows for preoperative
embolization of the feeder vessels, which has been reported to reduce intraoperative blood loss.
Surgical resection is the recommended treatment for suspected carotid body tumor.
Introduction
A blood vessel has 3 layers: the intima (inner layer made of endothelial cells), media
(contains muscular elastic fibers), and adventitia (outer connective tissue). Aneurysms are
either true or false. The wall of a true aneurysm involves all 3 layers, and the aneurysm is
contained inside the endothelium. The wall of a false or pseudoaneurysm only involves the
outer layer and is contained by the adventitia. An aortic dissection is formed by an intimal tear
and is contained by the media; hence, it has a true lumen and a false lumen.
Most aortic aneurysms (AA) occur in the abdominal aorta; these are termed abdominal
aortic aneurysms (AAA). Although most abdominal aortic aneurysms are asymptomatic at the
time of diagnosis, the most common complication remains life-threatening rupture with
hemorrhage.
Aneurysmal degeneration that occurs in the thoracic aorta is termed a thoracic aneurysm
(TA). Aneurysms that coexist in both segments of the aorta (thoracic and abdominal) are termed
thoracoabdominal aneurysms (TAA). Thoracic aneurysms and thoracoabdominal aneurysms are
also at risk for rupture. A recent population-based study suggests an increasing prevalence of
thoracic aortic aneurysms. Thoracic aortic aneurysms are subdivided into 3 groups depending
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Dissection is another condition that may affect the thoracic aorta. An intimal tear causes
separation of the walls of the aorta. A false passage for blood develops between the layers of
the aorta. This false lumen may extend into branches of the aorta in the chest or abdomen,
causing malperfusion, ischemia, or occlusion with resultant complications. The dissection can
also progress proximally, to involve the aortic sinus, aortic valve, and coronary arteries.
Dissection can lead to aneurysmal change and early or late rupture. A chronic dissection is one
that is diagnosed more than 2 weeks after the onset of symptoms. Dissection should not be
termed dissecting aneurysm because it can occur with or without aneurysmal enlargement of
the aorta.
The shape of an aortic aneurysm is either saccular or fusiform. A fusiform (or true)
aneurysm has a uniform shape with a symmetrical dilatation that involves the entire
circumference of the aortic wall. A saccular aneurysm is a localized outpouching of the aortic
wall, and it is the shape of a pseudoaneurysm.
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Most of these initial successful repairs involved the use of preserved aortic allografts,
thus triggering the establishment of numerous aortic allograft banks. Simultaneously, Gross
and colleagues successfully used allografts to treat complex thoracic aortic coarctations,
including those with aneurysmal involvement.
In 1951, Lam and Aram reported the resection of a descending thoracic aneurysm with
allograft replacement.3 Ascending aortic replacement required the development of
cardiopulmonary bypass and was first performed in 1956 by Cooley and DeBakey. They
successfully replaced the ascending aorta with an aortic allograft. Successful replacement of
the aortic arch, with its inherent risk of cerebral ischemia, was understandably more
challenging and was not reported until 1957 by DeBakey et al.
Although the use of aortic allografts as aortic replacement was widely accepted in the
early 1950s, the search for synthetic substitutes was well underway. Dacron was introduced by
DeBakey. By 1955, Deterling and Bhonslay believed that Dacron was the best material for
aortic substitution.6 Numerous types of intricately woven hemostatic grafts have since been
developed and are now used much more extensively than their allograft counterparts. Such
Dacron grafts are used to replace ascending, arch, thoracic, and thoracoabdominal aortic
segments.
However, some patients required replacement of the aortic root, as well. Subsequently,
combined operations that replaced the ascending aneurysm in conjunction with replacement of
the aortic valve and reimplantation of the coronary arteries were performed by Bentall and De
Bono in 1968, using a mechanical valve with a Dacron conduit. Ross, in 1962, and Barratt-
Boyes, in 1964, successfully implanted the aortic homograft in the orthotopic position. In
1985, Sievers reported the use of stentless porcine aortic roots.
More recently, less invasive therapy for descending thoracic aortic aneurysm have been
developed. Dake et al reported the first endovascular thoracic aortic repair in 1994.11 In March
2005, the US Food and Drug Administration (FDA) approved the first thoracic aortic stent
graft, the GORE TAG graft (W.L. Gore and Associates; Newark, Del).
Problem
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Aneurysms are usually defined as a localized dilation of an arterial segment greater that
50% its normal diameter. Most aortic aneurysms occur in the infrarenal segment (95%). The
average size for an infrarenal aorta is 2 cm; therefore, abdominal aortic aneurysms are usually
defined by diameters greater than 3 cm.
The normal size for the thoracic and thoracoabdominal aorta is larger than that of the
infrarenal aorta, and aneurysmal degeneration in these areas is defined accordingly. The average
diameter of the mid-descending thoracic aorta is 26-28 mm, compared with 20-23 mm at the
level of the celiac axis.
Frequency
Although findings from autopsy series vary widely, the prevalence of aortic aneurysms
probably exceeds 3-4% in individuals older than 65 years.
Death from aneurysmal rupture is one of the 15 leading causes of death in most series.
The estimated incidence of thoracic aortic aneurysms is 6 cases per 100,000 person-years. In
addition, the overall prevalence of aortic aneurysms has increased significantly in the last 30
years. This is partly due to an increase in diagnosis based on the widespread use of imaging
techniques. However, the prevalence of fatal and nonfatal rupture has also increased,
suggesting a true increase in prevalence. Population-based studies suggest an incidence of
acute aortic dissection of 3.5 per 100,000 persons; an incidence of thoracic aortic rupture of
3.5 per 100,000 persons; and an incidence of abdominal aortic rupture of 9 per 100,000
persons. An aging population probably plays a significant role.
Etiology
Aneurysmal degeneration occurs more commonly in the aging population. Aging results
in changes in collagen and elastin, which lead to weakening of the aortic wall and aneurysmal
dilation. According to the Laplace law, luminal dilation results in increased wall tension and
the vicious cycle of progressive dilation and greater wall stress. Pathologic sequelae of the
aging aorta include elastic fiber fragmentation and cystic medial necrosis. Arteriosclerotic
(degenerative) disease is the most common cause of thoracic aneurysms.
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A previous aortic dissection with a persistent false channel may produce aneurysmal
dilation; such aneurysms are the second most common type. False aneurysms are more common
in the descending aorta and arise from the extravasation of blood into a tenuous pocket
contained by the aortic adventitia. Because of increasing wall stress, false aneurysms tend to
enlarge over time.
Aneurysmal degeneration occurs more commonly in the aging population. Aging results
in changes in collagen and elastin, which lead to weakening of the aortic wall and aneurysmal
dilation. According to the law of Laplace, luminal dilation results in increased wall tension and
the vicious cycle of progressive dilation and greater wall stress. Pathologic sequelae of the
aging aorta include elastic fiber fragmentation and cystic medial necrosis. Arteriosclerotic
(degenerative) disease is the most common cause of thoracic aneurysms.
A previous aortic dissection with a persistent false channel may produce aneurysmal
dilation; such aneurysms are the second most common type. False aneurysms are more common
in the descending aorta and arise from the extravasation of blood into a tenuous pocket
contained by the aortic adventitia. Because of increasing wall stress, false aneurysms tend to
enlarge over time.
Authorities strongly agree that genetics play a role in the formation of aortic aneurysms.
Of first-degree relatives of patients with aortic aneurysms, 15% have an aneurysm. This appears
especially true in first-degree relatives of female patients with aortic aneurysms. Thus, inherited
disorders of connective tissue appear to contribute to the formation of aortic aneurysms.
Pathophysiology
The occurrence and expansion of an aneurysm in a given segment of the arterial tree
probably involves local hemodynamic factors and factors intrinsic to the arterial segment itself.
The medial layer of the aorta is responsible for much of its tensile strength and elasticity.
Multiple structural proteins comprise the normal medial layer of the human aorta. Of these,
collagen and elastin are probably the most important. The elastin content of the ascending aorta
is high and diminishes progressively in the descending thoracic and abdominal aorta. The
infrarenal aorta has a relative paucity of elastin fibers in relation to collagen and compared with
the thoracic aorta, possibly accounting for the increased frequency of aneurysms in this area. In
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addition, the activity and amount of specific enzymes is increased, which leads to the
degradation of these structural proteins. Elastic fiber fragmentation and loss with degeneration
of the media result in weakening of the aortic wall, loss of elasticity, and consequent dilation.
Hemodynamic factors probably play a role in the formation of aortic aneurysms. The
human aorta is a relatively low-resistance circuit for circulating blood. The lower extremities
have higher arterial resistance, and the repeated trauma of a reflected arterial wave on the distal
aorta may injure a weakened aortic wall and contribute to aneurysmal degeneration. Systemic
hypertension compounds the injury, accelerates the expansion of known aneurysms, and may
contribute to their formation.
Aneurysm formation is probably the result of multiple factors affecting that arterial
segment and its local environment.
Presentation
Most patients with aortic aneurysms are asymptomatic at the time of discovery. Thoracic
aneurysms are usually found incidentally after chest radiographs or other imaging studies.
Abdominal aortic aneurysms may be discovered incidentally during imaging studies or a
routine physical examination as a pulsatile abdominal mass.
Patients with a variant of abdominal aortic aneurysm may present with fever and a
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painful aneurysm with or without an obstructive uropathy. These patients may have an
inflammatory aneurysm that can be treated with surgical repair.
Patients with thoracic aneurysms are often asymptomatic. Most patients are hypertensive
but remain relatively asymptomatic until the aneurysm expands. Their most common presenting
symptom is pain. Pain may be acute, implying impending rupture or dissection, or chronic,
from compression or distension. The location of pain may indicate the area of aortic
involvement, but this is not always the case. Ascending aortic aneurysms tend to cause anterior
chest pain, while arch aneurysms more likely cause pain radiating to the neck. Descending
thoracic aneurysms more likely cause back pain localized between the scapulae. When located
at the level of the diaphragmatic hiatus, the pain occurs in the mid back and epigastric region.
Large ascending aortic aneurysms may cause superior vena cava obstruction manifesting
as distended neck veins. Ascending aortic aneurysms also may develop aortic insufficiency,
with widened pulse pressure or a diastolic murmur, and heart failure. Arch aneurysms may
cause hoarseness, which results from stretching of the recurrent laryngeal nerves. Descending
thoracic aneurysms and thoracoabdominal aneurysms may compress the trachea or bronchus
and cause dyspnea, stridor, wheezing, or cough. Compression of the esophagus results in
dysphagia. Erosion into surrounding structures may result in hemoptysis, hematemesis, or
gastrointestinal bleeding. Erosion into the spine may cause back pain or instability. Spinal cord
compression or thrombosis of spinal arteries may result in neurologic symptoms of paraparesis
or paraplegia. Descending thoracic aneurysms may thrombose or embolize clot and
atheromatous debris distally to visceral, renal, or lower extremities.
Patients who present with ecchymoses and petechiae may be particularly challenging
because these signs probably indicate disseminated intravascular coagulation (DIC). The risk
of significant perioperative bleeding is extremely high, and large amounts of blood and blood
products must be available for resuscitative transfusion.
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The most common complications of thoracic aortic aneurysms are acute rupture or
dissection. Some patients present with tender or painful nonruptured aneurysms. Although
debate continues, these patients are thought to be at increased risk for rupture and should
undergo surgical repair on an emergent basis.
Marfan syndrome is a potentially lethal connective-tissue disease characterized by
skeletal, heart valve, and ocular abnormalities. Individuals with this disease are at risk for
aneurysmal degeneration, especially in the thoracic aorta. Marfan syndrome is an autosomal
dominant genetic condition that results in abnormal fibrillin, a structural protein found in the
human aorta. Patients with Marfan syndrome may develop annuloaortic ectasia of the sinuses
of Valsalva, commonly associated with aortic valvular insufficiency and aneurysmal dilation of
the ascending aorta.
Traumatic dissection is a result of shearing from deceleration injury due to high speed
motor vehicle accidents (MVA) or a fall from heights. The dissection occurs at a point of
fixation, usually at the aortic isthmus (ie, at the ligamentum arteriosum, distal to the origin of
the left subclavian artery), the ascending aorta, the aortic root, and the diaphragmatic hiatus.
The true etiology of aortic aneurysms is probably multifactorial, and the condition
occurs in individuals with multiple risk factors. Risk factors include smoking, chronic
obstructive pulmonary disease (COPD), hypertension, atherosclerosis, male gender, older age,
high BMI, bicuspid or unicuspid aortic valves, genetic disorders, and family history. Aortic
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aneurysms are more common in men than in women and are more common in persons with
COPD than in those without lung disease.
Indications
Indications for surgery of thoracic aortic aneurysms are based on size or growth rate and
symptoms. Because the risk of rupture is proportional to the diameter of the aneurysm,
aneurysmal size is the criterion for elective surgical repair. Elefteriades published the natural
history of thoracic aortic aneurysms and recommends elective repair of ascending aneurysms at
5.5 cm and descending aneurysms at 6.5 cm for patients without any familial disorders such as
Marfan syndrome. These recommendations are based on the finding that the incidence of
complications (rupture and dissection) exponentially increased when the size of the ascending
aorta reached 6.0 cm (31% risk of complications) or when the size of the descending aorta
reached 7.0 cm (43% risk).15,14 Patients with Marfan syndrome or familial aneurysms should
undergo earlier repair, when the ascending aorta grows to 5.0 cm or the descending aorta grows
to 6.0 cm.
In addition, relative aortic aneurysm size in relation to body surface area may be more
important than absolute aortic size in predicting complications.16 Using the aortic size index
(ASI) of aortic diameter (in cm) divided by body surface area (m2), patients are stratified into 3
groups: ASI <2.75 cm/m2 are at low risk for rupture (4%/y), ASI 2.75-4.25 cm/m2 are at
moderate risk (8%/y), and ASI >4.25cm/m2 are at high risk (20-25%/y).
Rapid expansion is also a surgical indication. Growth rates average 0.07 cm/y in the
ascending aorta and 0.19 cm/y in the descending aorta.14 A growth rate of 1 cm/y or faster is
an indication for elective surgical repair.
Patients with acute aortic dissection of the ascending aorta require emergent operation.
They may present with rupture, tamponade, acute aortic insufficiency, myocardial infarction, or
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end-organ ischemia. Acute dissection of the descending aorta does not require surgical
intervention, unless complicated by rupture, malperfusion (eg, visceral, renal, neurologic, leg
ischemia), progressive dissection, persistent recurrent pain, or failure of medical management.
Patients who undergo surgery for symptomatic aortic insufficiency or stenosis with an
associated enlarged aneurysmal aorta should have concomitant aortic replacement if the aorta
reaches 5 cm in diameter. Concomitant aortic replacement should be consider for patients with
bicuspid aortic valves with an aorta >4.5 cm in diameter.
Summary of indications
Aortic size
Ascending aortic diameter 5.5 cm or twice the diameter of the normal contiguous aorta
Descending aortic diameter 6.5 cm
Subtract 0.5 cm from the cutoff measurement in the presence of Marfan syndrome,
family history of aneurysm or connective tissue disorder, bicuspid aortic valve, aortic stenosis,
dissection, patient undergoing another cardiac operation
Growth rate 1 cm/y
Symptomatic aneurysm
Traumatic aortic rupture
Acute type B aortic dissection with associated rupture, leak, distal ischemia
Pseudoaneurysm
Large saccular aneurysm
Mycotic aneurysm
Aortic coarctation
Bronchial compression by aneurysm
Aortobronchial or aortoesophageal fistula
Relevant Anatomy
Ascending aortic aneurysms occur as proximally as the aortic annulus and as distally as
the innominate artery. They may compress or erode into the sternum and ribs, causing pain or
fistula. They also may compress the superior vena cava or airway. When symptomatic by
rupture or dissection, they may involve the pericardium, aortic valve, or coronary arteries. They
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may rupture into the pericardium, causing tamponade. They may dissect into the aortic valve,
causing aortic insufficiency, or into the coronary arteries, causing myocardial infarction.
Aortic arch aneurysms involve the aorta where the innominate artery, left carotid, and left
subclavian originate. They may compress the innominate vein or airway. They may stretch the
left recurrent laryngeal nerve, causing hoarseness.
Descending thoracic aneurysms originate beyond the left subclavian artery and may
extend into the abdomen. Thoracoabdominal aneurysms are stratified based on the Crawford
classification. Type I involves the descending thoracic aorta from the left subclavian artery
down to the abdominal aorta above the renal arteries. Type II extends from the left subclavian
artery to the renal arteries and may continue distally to the aortic bifurcation. Type III begins at
the mid-to-distal descending thoracic aorta and involves most of the abdominal aorta as far
distal as the aortic bifurcation. Type IV extends from the upper abdominal aorta and all or none
of the infrarenal aorta. Descending thoracic aneurysms and thoracoabdominal aneurysms may
compress or erode into surrounding structures, including the trachea, bronchus, esophagus,
vertebral body, and spinal column.
Contraindications
Laboratory Studies
CBC count
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Imaging Studies
Chest radiograph
In the case of ascending aortic aneurysms, chest x-rays may reveal a widened
mediastinum, a shadow to the right of the cardiac silhouette, and convexity of the right superior
mediastinum. Lateral films demonstrate loss of the retrosternal air space. However, the
aneurysms may also be completely obscured by the heart, and the chest x-ray appear normal.
Plain chest radiographs may show a shadow anteriorly and slightly to the left for arch
aneurysms and posteriorly and to the left for descending thoracic aneurysms. Aortic
calcification may outline the borders of the aneurysm in the anterior, posterior, and lateral
views in both the chest and abdomen.
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Transthoracic echocardiography demonstrates the aortic valve and proximal aortic root. It
may help detect aortic insufficiency and aneurysms of the sinus of Valsalva, but it is less
sensitive and specific than transesophageal echocardiography.
Transesophageal echocardiography images show the aortic valve, ascending aorta, and
descending thoracic aorta, but they are limited in the area of the distal ascending aorta,
transverse aortic arch, and upper abdominal aorta. Transesophageal echocardiography can help
accurately differentiate aneurysm and dissection, but the images must be obtained and
interpreted by skilled personnel.
Ischemia may be evaluated using dipyridamole-thallium or dobutamine echocardiography
scans.
Ultrasonography
Aortography
Aortography images can delineate the aortic lumen, and they can help define the extent
of the aneurysm, any branch vessel involvement, and the stenosis of branch vessels. It describes
the takeoff of the coronary ostia.
For patients older than 40 years or those with a history suggestive of coronary artery
disease, aortography helps evaluate coronary anatomy, ventricular function by ventriculography,
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and aortic insufficiency. It does not help in defining the size of the aneurysm because the outer
diameter is not measured, which may miss dissections.
Disadvantages include the use of nephrotoxic contrast and radiation. The risk of
aortography includes embolization from laminated thrombus and carries a 1% stroke risk.
CT scans with contrast have become the most widely used diagnostic tool. They rapidly
and precisely evaluate the thoracic and abdominal aorta to determine the location and extent of
the aneurysm and the relationship of the aneurysm to major branch vessels and surrounding
structures. They can help accurately determine the size of the aneurysm and assesses
dissection, mural thrombus, intramural hematoma, free rupture, and contained rupture with
hematoma.
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Sagittal, coronary, and axial images may be obtained with 3-dimensional reconstruction.
Stent graft planning for endovascular descending thoracic aneurysm repairs requires fine-cut
images from the neck through the pelvis to the level of the femoral heads. The takeoff of the
arch vessels is critical to determine the adequacy of the proximal landing zone, as is assessing
the patency of the vertebral arteries, if the left subclavian artery should be covered by the stent
graft. Assessment of the common femoral artery access is essential to determine the feasibility
of large-bore sheath access. A spiral CT scan with 1-mm cuts and 3-dimensional reconstruction
with the ability to make centerline measurements is crucial to stent graft planning.
CT angiography may create multiplanar reconstructions and cines. This requires
nephrotoxic contrast and radiation, but the procedure is noninvasive.
Fig.18. Descending thoracic aortic aneurysm with mural thrombus at the level of the left
atrium
MRI and magnetic resonance angiography have the advantage of avoiding nephrotoxic
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Other Tests
Electrocardiogram: Baseline ECG should be performed. Transthoracic echocardiograms
noninvasively screen for valvular abnormalities and cardiac function.
Pulmonary function tests: Patients with a smoking history and COPD should be
evaluated using pulmonary function tests with spirometry and room-air arterial blood gas
determinations.
Diagnostic Procedures
Cardiac catheterization: Patients with a history of coronary artery disease or those older
than 40 years should undergo cardiac catheterization.
Histologic Findings
Histologic findings may include elastic fiber fragmentation, loss of elastic fibers, loss of
smooth muscle cells, cystic medial necrosis, intraluminal thrombus, and atherosclerotic plaque
and ulceration.
Treatment
Medical Therapy
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For acute aortic dissections, the first-line treatment of hypertension is with a short-
acting beta-blocker (eg, esmolol). Beta blockade decreases the force of contraction, thus
decreasing the dP/dt and shear force exerted on the dissection by minimizing the rate of rise of
the aortic pressure. It also decreases the heart rate and the inotropic state of the myocardium,
and reduces the likelihood of propagation of the dissection. A second-agent added is a
vasodilator (eg, nitroprusside), which reduces the systolic blood pressure to, in turn, decrease
the aortic wall stress and the possibility of rupture.
Surgical Therapy
Most aneurysm repairs involve aortic replacement with a Dacron tube graft. Dacron
grafts allow ingrowth in the interstices to form a pseudoendothelial layer to minimize the risk
of embolization. They may be knitted or woven. Knitted grafts are more porous and incorporate
tissue well; however, they are prone to more bleeding. Woven grafts are more impervious and
therefore are the most commonly used for aortic replacement. Grafts are typically impregnated
with collagen to avoid preclotting the graft and to promote optimal healing.
Surgical treatment of ascending aortic aneurysms depends on the extent of the aneurysm
both proximally (eg, involvement of the aortic valve, annulus, sinuses of Valsalva, sinotubular
junction, coronary orifices) and distally (eg, involvement to the level of the innominate artery).
The choice of operation also depends on the underlying pathology of the disease, the patient's
life expectancy, the desired anticoagulation status, and the surgeon's experience and preference.
Ascending aortic aneurysms with normal aortic valve leaflets, annulus, and sinuses of
Valsalva are typically replaced with a simple supracoronary Dacron tube graft from the
sinotubular junction to the origin of the innominate artery, with the patient under
cardiopulmonary bypass.
If the aortic valve is diseased but the aortic sinuses and annulus are normal, the aortic
valve is replaced separately and the ascending aortic aneurysm is replaced with a supracoronary
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synthetic graft, leaving the coronary arteries intact (ie, Wheat procedure).
Sinus of Valsalva aneurysms with normal aortic valve leaflets and aortic insufficiency
due to dilated sinuses may be repaired with a valve-sparing aortic root replacement. Two valve-
sparing procedures have been developed: the remodeling method and the reimplantation
method. The remodeling method involves resecting the aneurysmal sinus tissue while
maintaining the tissue along the valve leaflets and scalloping the Dacron graft to form new
sinuses to remodel the root. The reimplantation method involves reimplanting the scalloped
native valve into the Dacron graft. Both require reimplantation of the coronary ostia into the
Dacron graft.
Patients with an abnormal aortic valve and aortic root require aortic root replacement
(ARR). In nonelderly patients who can undergo anticoagulation with reasonable safety, the
aortic root may be replaced with a composite valve-graft consisting of a mechanical valve
inserted into a Dacron graft coronary artery reimplantation (eg, classic or modified Bentall
procedure, Cabrol procedure).
For elderly patients, young active patients who do not desire anticoagulation, women of
childbearing age, and patients with contraindications to warfarin, the options include stentless
porcine roots, aortic homografts, and pulmonary autografts (ie, Ross procedure). For elderly
patients who cannot undergo a complex operation, another option is reduction aortoplasty (ie,
wrapping of the ascending aorta with a prosthetic graft).
Patients with Marfan syndrome have abnormal aortas and cannot undergo tube graft
replacement alone. They must have either a valve-sparing aortic root replacement or a complete
aortic root replacement.
Aortic root replacement with a homograft is ideal in the setting of aortic root abscess
from endocarditis.
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facilitate reanastomosis of the arch vessels. Aortic arch reconstruction techniques vary
depending on the arch pathology.
In patients with proximal arch involvement extending from the ascending aorta, a
hemiarch replacement may be performed. The ascending aorta is replaced with a Dacron graft
beveled as a tongue along the undersurface of the arch. In patients whose conditions mandate
replacement of the entire arch, the distal anastomosis is the Dacron graft to the descending
thoracic aorta. The head vessels are reimplanted individually or as an island. Grafts have been
developed with a trifurcated head-vessel attachment and with a fourth attachment for the
cannula. In this case, the head vessels are attached individually to the trifurcated branches.
For patients in whom the arch replacement is part of a staged procedure, preceding the
delayed repair of a concomitant descending thoracic aneurysm, an "elephant trunk" is used.
That is, the Dacron graft used to reconstruct the transverse arch ends distally in an extended
sleeve that is telescoped into the descending thoracic aorta, facilitating later replacement of the
descending thoracic/abdominal aneurysm (2-stage procedure).
Descending thoracic aneurysms may be repaired with open surgery or, if appropriate,
with endovascular stent grafting techniques. Stent graft repair of descending thoracic aortic
aneurysms should be performed if the predicted operative risk is lower than that of an open
repair. Patient age, comorbidities, symptoms, life expectancy, aortic diameter, characteristics
and extent of the aneurysm, and landing zones, should also be taken into consideration.
Surgically, descending thoracic aneurysms may be repaired with or without the use of a
bypass circuit from the left atrium to the femoral artery or femoral veinfemoral artery
cardiopulmonary bypass, depending on the length of the anticipated ischemic cross-clamping
and the experience of the surgeon. Discrete aneurysms with an anticipated clamp time of less
than 30 minutes may be repaired without left heart or cardiopulmonary bypass (ie, "clamp and
go" technique). More complex or larger aneurysms are probably safer to repair with the aid of
either left heart, partial, or full cardiopulmonary bypass with hypothermic circulatory arrest.
The use of left heart or cardiopulmonary bypass is favored to reduce hemodynamic instability
and the risk of spinal cord paraplegia.
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Descending thoracic aneurysms with the appropriate anatomy may now be repaired by
endovascular stent grafts. The GORE TAG is an FDA-approved nitinol-based stent graft
designed for descending thoracic aneurysm repair. An appropriate proximal neck of 2 cm prior
to the aneurysm is required. Ideally, the proximal landing zone is beyond the left subclavian
artery, though, in some circumstances, the stent may be placed proximal to the left subclavian
artery. Distally, a sufficient landing zone of 2 cm prior to the celiac artery is required. The
aortic inner neck diameters in the proximal and distal landing zones must fall within 23-37
mm. In addition, appropriately sized femoral and iliac arteries (typically >8 mm in diameter)
that lack tortuosity and calcium are required for implantation.
The GORE TAG graft has been FDA-approved since March 2005. More recently, the
Zenith TX2 endovascular graft (Cook Medical Inc.; Bloomington, Ind) was approved in March
2008, followed by the Talent Thoracic Stent Graft (Medtronic Inc.; Minneapolis, Minn) in
June 2008.29,30 The Valiant Thoracic Stent Graft (Medtronic Inc.; Minneapolis, Minn) is
approved for use outside the United States.
Under investigational trials, Dr. Timothy Chuter at the University of California at San
Francisco Medical Center and Dr. Roy Greenberg at the Cleveland Clinic have treated
thoracoabdominal aneurysms using custom-built fenestrated and branched stent grafts. Such
devices require precise anatomic tailoring of the grafts to the specific patient's anatomy for
placement of the scallops (for visceral flow) or branches (for direct stenting into the visceral
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vessels).
Preoperative Details
Preoperative assessment of coronary artery disease is essential to determine the need for
concomitant coronary artery bypass grafting. Transesophageal echocardiography is crucial
preoperatively to examine the need for aortic valve replacement. Patients with aortic stenosis or
aortic insufficiency in whom the valve leaflets are anatomically abnormal require replacement,
whereas patients with aortic insufficiency and normal aortic valve leaflets may be candidates
for valve-sparing procedures. Transesophageal echocardiography is valuable for accurate
delineation of the aortic root at the sinuses of Valsalva and sinotubular junction.
The major morbidities from aortic arch aneurysm repair are neurologic, cardiac, and
pulmonary in nature. All patients require preoperative assessment of cardiac function and
evaluation for coronary artery disease. In the operating room, transesophageal
echocardiography is used to monitor ventricular function and to assess for atherosclerosis of
the aorta.
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aneurysm repair is spinal cord injury with paraparesis or paraplegia. Preoperatively, some
groups perform spinal arteriograms to attempt to localize the artery of Adamkiewicz for
reimplantation during surgery. Neurologic monitoring with somatosensory evoked potentials or
motor evoked potentials is used by some to assess spinal cord ischemia and identify critical
segmental arteries for spinal cord perfusion. Lastly, preoperative placement of catheters for
cerebrospinal fluid drainage is performed to increase spinal cord perfusion pressure during
aortic cross-clamping.
Spinal cord injury is less prevalent with endovascular stent grafting than with open
repair but exists with both types of surgical treatment.24,25,27,28 For endovascular stent
grafting, cerebrospinal fluid (CSF) drainage and avoidance of hypotension are the primary
mechanisms used to prevent paraplegia. The use of CSF drainage is selective among most
centers. For some discrete aneurysms, stent graft coverage may allow for preservation of spinal
arteries. Others require coverage of the entire descending thoracic aorta. Indications for use of
CSF drains include anticipated endograft coverage of T9-T12, coverage of the long segment of
the thoracic aorta, compromised collateral pathways from prior infrarenal AAA repair, and
symptomatic spinal ischemia.
Brain protection
Methods used for brain protection during deep hypothermic circulatory arrest (DHCA)
include intraoperative EEG monitoring, evoked somatosensory potential monitoring,
hypothermia (to temperatures <20o C), packing the patient's head in ice, Trendelenburg
positioning (ie, head down), mannitol, CO2 flooding, thiopental, steroids, and antegrade and
retrograde cerebral perfusion.
Intraoperative Details
Venous access is obtained with 2 large-bore peripheral IVs and a central line. Filling
pressures and cardiac output monitoring are performed with a pulmonary artery catheter.
Continuous blood pressure monitoring is performed with a radial arterial line. Nasopharyngeal
and bladder probes monitor systemic temperature. Intraoperative transesophageal
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Cardiopulmonary bypass is established and the aorta is cross-clamped just below the
innominate artery. The heart is arrested with cardioplegia. The aorta is transected at the
sinotubular junction and sized for the appropriate Dacron tube graft. The tube graft is sutured
to the proximal aorta with running 4-0 Prolene with a strip of felt. The tube graft is measured
to length distally and sutured to the distal aorta using running 4-0 Prolene with a strip of felt.
Once the aorta is transected at the sinotubular junction, the valve is inspected for normal
anatomy. If sparing is feasible, the appropriate size tube graft is chosen to allow coaptation of
the aortic valve leaflets without aortic insufficiency. In the remodeling technique, the tube graft
is tailored to form aortic sinuses. The sinuses of Valsalva of the native aorta are removed, and
the coronary ostia are mobilized. The neosinuses of the tube graft are sutured to the scalloped
aortic valve with running 4-0 Prolene and a strip of felt.
In the reimplantation technique, Tycron sutures are placed along the subannular
horizontal plane and passed through the tube graft. The scalloped aortic valve is placed within
the tube graft, and the proximal suture line is secured. The scalloped aortic valve is positioned
in the graft to achieve valve competence, and the subcoronary suture line along the scalloped
valve is performed with running 4-0 Prolene. The valve is examined for competence within the
graft. The coronary ostia are reimplanted in the graft. The graft is measured to length distally
and sutured to the distal aorta.
In the reimplantation technique, Tycron sutures are placed along the subannular
horizontal plane and passed through the tube graft. The scalloped aortic valve is placed within
the tube graft, and the proximal suture line is secured. The scalloped aortic valve is positioned
in the graft to achieve valve competence, and the subcoronary suture line along the scalloped
valve is performed with running 4-0 Prolene. The valve is examined for competence within the
graft. The coronary ostia are reimplanted in the graft. The graft is measured to length distally
and sutured to the distal aorta.
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The aorta is transected, and the aortic valve is removed. The annulus is sized, and the
appropriate valved conduit, stentless root, mechanical composite, or homograft is brought to
the field. The coronary ostia are mobilized. Annular sutures are placed and are passed through
the valve conduit. The proximal suture is thus secured. The coronary ostia are reimplanted. The
distal suture line is performed for the mechanical valve composite, but an additional Dacron
graft extension may be required for the stentless roots or homografts, depending on their
length.
Modified Bentall procedure ("buttons"): The right and left coronary arteries are
dissected as a button, which is then reimplanted into the Dacron composite graft as an aortic
button.
Cabrol procedure: Rarely performed, this technique may be used when the aortic tear or
dissection extends into the coronary ostia. It may also be used when adequate mobilization of
the coronary ostia is not possible (i.e., from scarring in a reoperation), or when the coronary
ostia are too low. The coronary buttons are dissected and anastomosed to a separate 6- or 8-mm
Dacron interposition graft; this graft is then anastomosed into the Dacron composite graft. This
technique results in a tension-free anastomosis of the coronary buttons and also allows for
easier access for hemostasis. However, it is subject to twisting and kinking with resultant
myocardial ischemia and, thus, is not as reproducible as the modified Bentall.
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Air (ie, nitrogen) is poorly soluble in blood. The risk of air embolism is reduced by
flooding the surgical field with carbon dioxide. Carbon dioxide is denser than air and displaces
air. It is rapidly soluble in blood and causes less risk of embolization. Any carbon dioxide
absorbed in the blood is removed by increasing the sweep speed of cardiopulmonary bypass.
Cannulation for arch repairs varies among groups. They include the femoral artery, right
axillary artery, and ascending aorta. Hypothermic circulatory arrest is required for arch repairs,
but the safe period of arrest to avoid neurologic injury is 30-45 minutes at 18C (64.4F), but
some advocate a shorter period of 25 minutes. Antegrade cerebral perfusion to minimize
neurologic injury is thus advocated. Others advocate cooling to 11-14C (51.8-57.2F).
Once the patient is cooled to the desired temperature, the circuit is turned off. For
retrograde cerebral perfusion, flow is established through the superior vena cava as the arch
reconstruction is performed. For antegrade cerebral perfusion, flow is continued through the
axillary artery with the innominat