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enzymes in the parenchyma and stroma of the pancreas with permanent destruction,
tissue, occurrence of pseudocysts, calcification of pancreas and disorders in its exo- and
The inflammatory component in the development of CP is not the only and even leading, it
The incidence of chronic pancreatitis has a constant upward trend and a range from 2 to
10 cases per 100 thousand populations annually, and its overall frequency is from 50 to 75
patients per 100 thousand populations. According to autopsy data, CP occurs from 0.18 to
9%, on average, about 1%. The disease is most often diagnosed at the age of 40-60
years.
Etiology
associated with at least 100 reasons, the main ones of which are:
1) chronic alcoholism
2) gallstone disease
8) hyperparathyroidism (hypercalcemia)
Gallstone disease and alcohol intake are the most common causes of the development of CP,
amounting to 60-80%. In different countries (geographical regions) and sociodemographic groups of
the population one of these two main causes of CP is leading. The third place in terms of frequency
of occurrence is the so-called idiopathic CP, the etiological factors of which cannot be ascertained.
Idiopathic CP is 10-15% of all patients. All other causes of CP are relatively rare, they account for up
to 10% in total. There are several theories of the pathogenesis of CP, of which enzyme is considered
the most recognized. According to this theory, each of the etiological factors leads to the activation
of enzymes produced by the pancreas, autolysis of the gland, necrobiosis and necrosis of acinar
tissue and stroma of the gland, followed by its replacement with connective tissue and the
development of fibrosis.
- violation of the secretory function of the pancreas: changes in the characteristics of pancreatic
juice, leading to precipitation of the protein in the ductal system and it obstruction;
- enhanced secretion with bile products of free radical oxidation of fatty acids and peroxide
compounds penetrating into the pancreatic duct and supporting the inflammatory process in the
pancreas.
The main mechanism of CP in cholelithiasis, according to the theory of “common channel” is biliary-
pancreatic reflux resulting blocked stone in large papilla of the duodenum, trauma and prolonged
spasm of sphincter hepato-pancreatic ampoule, papillostenosis due to frequent injury papilla by
small stones. ( Normally, pressure in the gallbladder and common bile duct when they are empty is
250 mm of water. And in the main pancreatic duct - 300-500 mm of water. It prevents the
occurrence of bile reflux in the pancreatic duct. The gallstone disease, in particular
choledocholithiasis, complicated by stenotic papillitis may be the cause of CP due to the disruption
of the normal passage of bile and its throwing into the pancreatic ducts). It is also possible the direct
transition of inflammation from the gallbladder, bile ducts to the pancreas through the venous and
lymphatic vessels in the absence of biliary-pancreatic reflux.
CP classification
Since CP is in fact a very heterogeneous disease, having a different etiology, morphological, clinical
variants, the creation of a comprehensive and generally accepted classification is a big problem. A
number of CP classifications have been proposed, which can be grouped as follows:
2. morphological, which take into account both the preferential localization of the pathological
process in different parts of the pancreas, and the nature of the morphological changes in the tissue
of the organ,
4. complex classification schemes based on mixed principles, with this can be taken into account
several parameters: clinic, morphology, the nature of the functional impairment and lesions of
adjacent organs, the degree of activity of the inflammatory process in the pancreas, etc.
One of the most accepted and used classifications of CP is the clinical classification of CP,
proposed by A.A. Shelagurov. According to this classification, there are:
patient’s condition remains relatively good in the period of remission (the most frequent
form of CP),
3. Chronic latent pancreatitis, in which disorders of the external and internal secretion of the
pancreas are determined
pancreatic head mainly with signs of compression of the common bile duct, duodenum
Clinical manifestations of CP
The symptoms of CP are determined by the nature of the lesion of this organ, the stage of the
disease (period of exacerbation or remission), the extent of lesions of the gland and its adjacent
organs, and in some cases other organs and systems, finally, the presence, nature and severity of
complications and consequences of pancreatic lesions.
2) dyspeptic symptoms;
3) weight loss;
5) fever;
6) jaundice;
7) sometimes glycosuria;
8) ascites;
9) multiple thrombosis;
1) pain syndrome;
diabetes of varying severity, less often - hypoglycemic syndrome, in some cases - signs of impaired
secretion of other pancreatic hormones;
4) syndrome of biliary hypertension (cholestasis) with its clinical manifestations (hepaticcolic,
pruritus, jaundice, acholia, Courvoisier’s symptom), as well as a characteristic laboratory picture;
In addition clinical manifestations of inflammatory and purulent-septic lesions of the pancreas and
adjacent organs and tissues are often encountered in chronic pancreatitis. 2. Laboratory and
instrumental diagnosis, differential diagnosis of chronic pancreatitis;
Diagnostics
The diagnosis of CP is based on the clinical presentation, laboratory data and instrumental methods
of diagnostics. Diagnosis of CP has the following objectives:
2. To establish the severity of the disease (morphological changes in the parenchyma and ductal
system of the pancreas, adjacent organs, the severity of loss of gland functions),
3. Identify the presence of complications, their nature, 4. Outline a reasonable treatment plan.
Laboratory diagnosis of CP
Uncomplicated CP does not lead to marked changes in laboratory parameters. An increase in the
activity of pancreatic enzymes in the blood and urine indicates an exacerbation of the inflammatory
process in the gland, and leukocytosis can also be detected with a characteristic shift in leukocyte
formula. Laboratory diagnosis of CP is used primarily to study the function of the pancreas and
determine the degree of its exocrine and endocrine insufficiency. For this purpose, the following
methods can be applied:
2) study of the exocrine function of the pancreas as a state of the digestive capacity of its secret
(indirect methods). First of all, these include coprological studies, etc.;
1) detection of insufficient B-cell endocrine function, i.e. essentially the diagnosis of secondary
(pancreatogenic) diabetes mellitus;
severity of morphological changes in the parenchyma and the ductal system of the
pancreas:
2) ultrasound,
5) endoscopic ultrasonography,
6) angiography
7) radioisotope scanning,
Differential Diagnoses
• Ampullary Carcinoma
• Cholangitis
• Cholecystitis
• Chronic Gastritis
• Crohn Disease
• Intestinal Perforation
• Myocardial Infarction
• Pancreatic Cancer
3. Treatment of chronic pancreatitis. Conservative therapy. Indications for surgical treatment, types
of operations;
Treatment
recurrences, relief of pain and stabilization of the anatomical and functional changes of the
pancreas.
In the treatment of patients with CP two main methods of treatment can be applied conservative
and surgical, each of which has its own goals, indications, possibilities and limitations.
Conservative treatment of CP
organ failure,
prevention of exacerbations of CP
Surgical treatment of CP
2) relief of pain,
All options for the surgical treatment of CP can be grouped as follows (Danilov MV):
2. Gastrointestinal surgery.
e) total duodenopancreatectomy.
The choice of the optimal method of treatment of CP and the most adequate method of surgical
treatment may at least stop the further progression of the disease.
Chronic pancreatitis has the potential to cause numerous complications. You’re at greater risk of
developing complications if you continue to drink alcohol after you’ve been diagnosed.
• Nutrient malabsorption is one of the most common complications. Since your pancreas isn’t
producing enough digestive enzymes, your body isn’t absorbing nutrients properly. This can lead to
malnutrition.
• The development of diabetes is another possible complication. Pancreatitis damages the cells that
produce insulin and glucagon, which are the hormones that control the amount of sugar in your
blood. This can lead to an increase in blood sugar levels. About 45
• Some people will also develop pseudocysts, which are fluid-filled growths that can form inside or
outside of your pancreas. Pseudocysts are dangerous because they can block important ducts and
blood vessels. They may become infected in some cases.
Pancreatic cysts
Pancreatic cysts are fluid-filled and capsule-limited cavities that can be located both in the
parenchyma of the pancreas (intrapancreatic) and in the adjacent sections of the retroperitoneal
tissue, omental bag (extrapancreatic).
Most often (almost 50%), cyst formation is the outcome of severe forms of acute destructive
pancreatitis. Chronic pancreatitis is combined with cyst formation in 25%, pancreatic injury leads to
the formation of a cyst in 20%, approximately 5% of all cases of cystic lesions of the pancreas are
tumor cyst - cystadenoma and cystadenocarcinoma.
a) congenital
b) acquired
parasitic,
- tumor.
- false (pseudocyst)
posttraumatic,
- idiopathic.
2. by localization:
- organ (intrapancreatic), located in the parenchyma of the pancreas, in any of its parts,
often have a relatively small size and are often associated with the ductal system of the
pancreas,
- extraorganic (extrapancreatic), located outside the parenchyma of the pancreas (in the
tissue of the retroperitoneal space, in the cavity of the omentum, in the mesentery of the
small intestine or transverse colon), are almost always the outcome of pancreatic
- perforation into the abdominal cavity (less often in the pleural or in the pericardial cavity),
The classification of pancreatic cysts based on the fundamental classification criteria and
proposed by G.D. Vilyavin and al. (1977). According to this classification cysts of the
a) in operated patients;
b) in non-operated patients.
2. Posttraumatic cysts.
3. Parasitic.
5. Congenital.
a) simple;
III. Primary and recurrent cysts. The clinical presentation of pancreatic cysts is determined by its
nature, size, location, presence or absence of complications. To verify the diagnosis, all methods of
laboratory and instrumental studies can be applied, the main of which should be recognized as
methods that allow identifying the anatomical and morphological characteristics of cysts, their
localization, wall structure, complications.
The main method of treatment of cysts of the pancreas is surgical. Single cases of selfhealing of
formed pancreatic cysts cannot justify all the dangers of the passive tactics of their treatment, due
to the high probability (at least in 15-20% of patients) of the occurrence of different and severe
complications. Most of these complications are accompanied by high mortality, even under the
condition of performing emergency operations, and the technical implementation of surgical
interventions against the background of a developed complication is much more difficult, while the
radicalness of the intervention is much less. It is important to remember that cystic formation of the
pancreas, interpreted clinically as a complication of pancreatitis, may actually be a cystic tumor or a
malignant cyst.
Thus, the identification using clinical and instrumental methods in patients with pancreatitis formed
pancreatic cyst should be considered an absolute indication for surgery. More difficult is the choice
of the optimal duration of surgery, as well as the method of treatment, especially in case of
incompletely formed cysts.
5. closure of the fistulous passage and ductal system of the pancreas. Surgery used for
It should be understood that the surgical treatment of pancreatic cysts should be pathogenetically
substantiated, i.e. first aimed at eliminating the causes of cyst formation
injuries;
The closed abdominal trauma is the kind of injury of the abdomen when the skin remains intact.
2) Neck
3) Chest
4) Abdomen
The most frequent ruptures occur in the spleen, kidney, small intestine and its mesentery, liver.
• POLYTRAUMA it is a trauma of internal organs in two or more areas when it is exposed to one
factor.
Causes: traffic injury, household, falling down from high amplitudes (katatravma), industrial and
sports injuries.
CLASSIFICATION
b) Retroperitoneal hematoma.
a) hollow organs;
b) parenchymal organs;
d) Retroperitoneal organs.
a) the aorta;
c) Contusion, tear, break, crush injury of retroperitoneal organs (pancreas and kidneys), followed by
development of cellulitis or retroperitoneal hematoma. A two-stage lesion of parenchymatous organ
- an injury of organ with the subcapsular hematoma formation at the first and second stage after a
certain time period (hours, days, weeks) hematoma breakthrough into the
6. The clinical picture of abdominal injuries. Laboratory and instrumental diagnosis, differential
diagnosis;
CLINIC
• Closed abdominal injury without damaging internal organs - hematoma, painful abrasions, bruises
in the anterior abdominal wall.
• The main manifestation of abdominal trauma with internal injuries: shock, bleeding and peritonitis.
The
• Tachycardia and decrease blood pressure, caused by damage and blood loss;
• The frequency, rhythm and depth of breathing are violated parallel to the severity of the injury;
• Dry tongue, white or brown bloom; - pain during abdominal palpation;
• Anterior abdominal wall is not involved in the act of breathing or its movements are limited;
Symptoms:
• Bloomberg - the appearance of pain after the sudden withdrawal of the hands during palpation of
the abdomen;
• Rosanov - an attempt to change the body position of the patient, he returns to the initial forced
position, usually on the back and on the side with legs bent or tries to sit down;
• Kulenkampf - sharp pain on palpation of soft or slightly tense of anterior abdominal wall;
• Joyce - percussion change when the patient is rotated to one side indicates hemoperitoneum,
preservation blunting indicate retroperitoneal hematoma, or bleeding in the root of the mesentery;
• Disappearance of hepatic dullness indicates the presence of gas in rupture of the hollow organ;
Factors affecting the clinical presentation and timely diagnosis: shock, significant blood loss, a
combination of internal injuries, alcohol and drug intoxication of the patient.
DIAGNOSIS
Anamnesis, nature and mechanism of injury, it may be asked to medical professionals, relatives
and spectators.
Laboratory methods:
CBC: reduction of red blood cells, hemoglobin, hematocrit, the proportion with bleeding;
leukocytosis to 35х109/l at admission and bleeding of the hollow organs contents into the peritoneal
cavity. It is necessary to study the dynamics of these indicators in 30-60 minutes.
Urine analysis: hematuria due to damaged organs of urinary system; raising the level of alpha-
amylase in trauma of pancreas; appearance of bile pigments from biliary tract.
Radiological methods:
General radiography and fluoroscopy of abdominal organs depending on the severity of injury in
an upright position, sitting, lateroposition: the presence of gas, liquid in the abdominal cavity and
retroperitoneal fat; pneumatization of the stomach and intestines; deformation and displacement of
organs; impaired function, the position and shape of the diaphragm.
Indirect signs of damage to internal organs: fractures of the lower right and left edges (suspected
damage to the liver and spleen), lower thoracic or upper lumbar vertebrae (suspected damage to
the pancreas and kidney), pelvis (suspected bladder rupture).
Computed tomography is used in general stable condition of patient when it is necessary to clarify
the status of parenchymal organs, aorta, foci of hemorrhage in the abdominal cavity and
retroperitoneal space.
Instrumental methods:
Bladder catheterization. In the case of obtaining more than 1 liter of bloody urine, i.e. volume
exceeding the capacity of the bladder due to the flow of fluid from the abdominal cavity, we can
assume its rupture (Zeldovich sign). Lack of urine, like its small amount, with urinary retention is
likely to indicate its accumulation outside the bladder (the patient “urinates inside himself”).
Ultrasound to determine the presence of free fluid and gas in the peritoneal cavity,
Invasive methods:
hematoma.
Laparotomy is indicated when all other methods have been exhausted, and doubts about the
diagnosis remains.
7. Treatment of injuries of the abdomen. Indications for surgery, options for interventions;
Surgical tactics
INDICATIONS
1) The presence of a clinical presentation of the internal bleeding and peritonitis in patients with
abdominal trauma is an indication for urgent surgery.
2) Presence of growing hematoma of the anterior abdominal wall serves as an indication for surgery.
3) Conservative treatment is efficient for patients with bruises, abrasions, stable hematomas of the
abdominal wall, stable intraorgan hematomas of parenchymatous organs and small stable
subcapsular hematomas, as well as the majority of patients with closed kidney injury without
damage of the vascular pedicle.
Surgery
The growing hematoma of the abdominal wall should be opened, the cavity should be emptied of
blood and clots, the bleeding vessel should be ligated, suturing of the wound, leaving drainage.
Surgery on damaged organs: suturing of lesion, suturing with fixation of a large omentum, an
organ suture, hepatopexy, a large omentum tamponade, resection and removal of an organ,
removal of the damaged intestine to the anterior abdominal wall, nephrostoma.
Breast injury refers to a violation of the anatomical integrity, physiological functions of the
chest and (or) the organs of the chest cavity due to exposure to a mechanical agent.
- without complications;
- with complications.
- with the phenomena of acute respiratory failure (I, II, III degree);
- With the phenomena of acute cardiovascular failure (I, II and III degree).
The clinical picture of closed chest injuries is determined by the presence of various
injuries of the skeleton, chest organs and other anatomical areas, which leads to
case.
1. General manifestations:
tachycardia, oliguria);
- bleeding symptoms (weakness, dizziness, dry tongue, pallor of the skin, sticky sweat,
2. Local signs:
- abrasions, bruises in the form of continuous blue-purple spots or stripes, swelling of the
- restriction of excursions of the chest when breathing on the side of the injury;
- chest rotation, i.e. the retraction of its fragment during inhalation when the rest of the
chest expands and prolapse on the exhale when the rest of the chest decreases.
- upon palpation in the area of damage, pain intensifying with deep inspiration and
- during percussion, dullness of sound (hemothorax, contusion of the lung), box sound or
(pneumothorax), etc .;
rales (lung contusion, pneumonia), etc. It should be emphasized that the most common
3. Bronchiolospasm.
The combination of several of the above factors leads to the development of severe
respiratory distress syndrome and may be called “shock lung”. In severe types of breast
Fractures of the ribs are the most common damage to a chest injury, which is manifested
fragments of broken ribs are secondary damaging agents, and with an increase in their
number, the probability of typical pleural (pneumo-, hemothorax) and pulmonary (bruising,
rupture) complications increases proportionally. More often 3-9 ribs break, in the case of
1-3 neurological and vascular injuries are common, and with fractures of 9-12, concomitant
abdominal injury.
Multiple, especially bilateral, terminal rib fractures are accompanied by respiratory failure.
The paradoxical mobility (otation) of the chest wall occurs with multiple fractures of the ribs
along two or more lines (terminal or oating fractures), as well as their combination with a
fracture of the sternum. Finite is called fracture of the ribs along several anatomical lines,
with the formation of a sash (valve) of the chest wall. The otation otates when breathing:
during inspiration, it sinks, during exhalation it prolapses. This leads to a violation of the
The main complaint is severe pain at the site of a rib fracture, shortness of breath.
Closed heart damage. Allocate concussion, bruise, rupture. With a concussion, a spasm of
violation of conduction, rhythm, and a decrease in blood pressure. In the case of a heart
injury, in addition to spasm of the coronary vessels, hemorrhages occur in the epi-, myo-,
endocardium and are manifested by more signicant disturbances in the function of the
heart. On the ECG, nonspecic changes in the ST segment , blockade of the legs of the
fracture of the sternum; at the same time, it can proceed without signicant changes in
To diagnose heart damage, it is necessary to study and determine the values of the most
informative symptoms: the nature of chest damage, pulse properties, central venous
Ultrasound can provide valuable information. The differential diagnosis is carried out with
which is made taking into account the ECG data in dynamics, laboratory tests (biochemical
markers).
injuries;
Anamnesis: patient complaints and clarication of the nature and circumstances of the
injury. Important information can be provided by medical personnel, relatives of the victim,
Laboratory methods:
- UAC: a decrease in the level of red blood cells, hemoglobin, hematocrit, specic gravity
with hemothorax; leukocytosis with bleeding and the entry of the contents of a hollow
organ into the pleural cavity. The denition of these indicators in dynamics is important.
X-ray methods:
a) fluoroscopy and chest radiography are leading diagnostic studies. They allow you to
identify damage to the bone skeleton of the chest; accumulation of air under the skin
b) tomography and CT specify the nature and localization of damage to internal organs.
c) angiography reveals damage to the vessels of the chest and mediastinum, pulmonary
embolism.
Instrumental methods:
- ECG, ultrasound of the heart establish the localization and nature of its damage.
- Ultrasound of the pleural cavity reveals hemothorax, inammatory effusion in the pleural
cavity, and also determines the areas of compaction of the lung tissue.
- Pleural puncture establishes the nature and amount of pathological contents in the
pathological conditions when. The method allows you to adequately assess the
Special methods:
- Ruvilua-Gregoire test - coagulation in a test tube of blood poured out of the pleural cavity
troponin).
post-operative period;
1. Elimination of pain.
Adequate analgesia provides a protective function against traumatic shock, allows the
victim to breathe adequately, which is the basis for the prevention of pneumonia. Of the
An important place in the complex of treatment for patients with closed chest injuries
places” blockade (medial to the fracture zone, lateral to the fracture zone and in the
pleural cavity, performed according to emergency indications in the 1st minutes of the
victim’s admission, allows confirming or eliminating the accumulation of air or blood in the
pleural cavity even before obtaining the results of the X-ray examination, conducting their
aspiration, which will improve the patient’s condition and will help determine further tactics
of patient management. Drainage is the method of choice for breast injury, accompanied
by an accumulation of air and blood in the pleural cavity. allows not only to completely
remove the pathological contents, but also to promptly display indications for thoracotomy.
This principle is largely ensured by adequate analgesia. Patients are shown massage,
moderate trauma, the half-sitting position of the patient provides lowering of the diaphragm
and additional adequate breathing due to intercostal muscles. Inhalation of oxygen, even
Indications for thoracotomy (in some cases video thoracoscopy is possible) with closed
- damage to the vessels of the upper aperture of the chest and vessels of the
mediastinum;
- progressive hemothorax;
- curled hemothorax;
acute respiratory distress is eliminated. For this, drainage of the vocal cavity is performed
immediately upon admission. Further, the patient is given anesthesia with one-lung intubation - an
intact (less) lung is ventilated.
Lung damage. In victims, to achieve hemo- and aerostasis, suturing of lung ruptures is used, atypical
resection using staplers is possible. Performing anatomical resections of the lung is usually not used.
Damage to the trachea, bronchi. In case of incomplete tears, suturing is performed. With a complete
gap (more often, the right main bronchus is torn off at the place of departure from the trachea),
integrity can be restored by forming an anastomosis.
Damage to the heart and large vessels. Such patients are immediately sent to the operating room,
where they perform a thoracotomy, the purpose of which is to stop bleeding, restore the integrity of
damaged organs, eliminate tamponade of the heart, acute respiratory disorders.
Paradoxical mobility (rotation) of the chest. The stabilization of the skeleton of the chest is
performed. Elimination of pathological mobility of the damaged section of the chest wall is achieved
by skeletal traction over the ribs or sternum, osteosynthesis is performed. In recent years,
stabilization with a metal plate according to the type of operation “ Nuss ” is often used for funnel
chest deformities. Sometimes they resort to internal stabilization of the costal “valve” with the help
of prolonged (up to 10-15 days) mechanical ventilation, which is often accompanied by the
development of infectious complications and higher mortality.
Relatively immediate and long-term indications for surgery include the following:
• Massive hemothorax or continued high rate of blood loss via the chest tube (ie,
1500 mL of blood upon chest-tube insertion or continued loss of 250 mL/hr for 3
consecutive hours)
esophageal injury
Relatively immediate and long-term indications for surgery include the following:
• Empyema
• Traumatic lung abscess
• Tracheoesophageal fistula
• Cardiac tamponade
Relatively immediate and long-term indications for surgery include the late recognition of a great-
vessel injury (eg, development of traumatic
pseudoaneurysm).
No distinct, absolute contraindications exist for surgery in blunt thoracic trauma. Rather, guidelines
have been instituted to define which patients have clear indications for surgery (eg, massive
hemothorax, continued high rates of blood loss via chest tube).
A controversial area has been the use of emergency department (ED) thoracotomy in patients with
blunt trauma who present without vital signs. The results of this approach in this particular patient
population have been dismal and have led many authors to condemn it.
Postoperative Care
Patients are extubated as soon as feasible in the postoperative period. Monitoring devices are kept
in place while needed but are removed as soon as possible. Intravenous fluids are provided until the
patient has had a return of GI function, at which time the patient can be fed. Patients with severe
associated injuries, especially those in a coma, may require prolonged enteral tube feedings.
Pain control is important in these patients because it facilitates breathing and helps to prevent
pulmonary complications such as atelectasis and pneumonia. Chest physiotherapy and nebulizer
treatments are used as necessary, and the use of an incentive spirometer is encouraged.
Chest tubes are placed for suction until fluid drainage has fallen sufficiently and the lung is
completely expanded without evidence of air leak. Tubes may then be placed to water seal and may
be removed if a chest radiograph demonstrates continued lung expansion.
treatment; Patients with blunt thoracic trauma are subject to myriad complications during the
course of their care.
• Wound infection
• Myocardial infarction
• Arrhythmias
• Pericarditis
• Septal defects
• Valvular insufficiency
• Atelectasis
• Pneumonia
• Pulmonary abscess
• Empyema
• Clotted hemothorax
• Fibrothorax
• Bronchopleural fistula
• Graft infection
• Pseudoaneurysm
• Graft thrombosis
• Pulmonary embolism
• Paraplegia (the spinal cord is at risk during repair of a ruptured thoracic aorta)
• Stroke
• Leakage of repair
• Mediastinitis
• Esophageal fistula
• Esophageal stricture, late (click here to complete a Medscape CME activity on treating esophageal
strictures)
• Skeletal deformity
• Chronic pain
Pneumothorax. They distinguish between open (free communication of the pleural cavity with the
external environment, in connection with which air enters and leaves through the wound of the
chest wall), closed (air intake occurs at the time of damage and stops due to displacement of soft
tissues) and valve, or tense (occurs
whenviolationoftheintegrityofthebronchiortheformationofavalveintheareaofthewoundofthechest,th
e air entering during the inhalation into the pleural cavity does not exit or partially leaves it upon
exhalation) pneumothorax.
Apical (collapse of the apex of the lung, partial or paracostal (band of air up to the diaphragm),
incomplete (lung collapsed by 1/3 - 1⁄4), total (collapse of the entire pulmonary parenchyma) are
distinguished by the volume of collapse of the lung tissue.
In the case of total pneumothorax, patients are restless, the presence of severe acrocyanosis,
shortness of breath is noteworthy. Breathing shallow, rapid. With a deep breath, the pain intensies
sharply. Compensatory tachycardia is noted, blood pressure is normal or low. When examining the
chest, there is a noticeable restriction of the mobility of the affected half of the chest, gentle
breathing on the affected side, the presence of a wound and emphysema around it, and air suction
through the wound heard from a distance when breathing in and out of the wound when exhaling.
Percussion is determined by tympanitis, and in the presence of hemothorax - dullness over its
surface. Auscultation -a sharp weakening of breathing in the projection of the upper lobe of the lung
and its almost complete absence in the projection of the lower lobes.
The most severe is the total valve pneumothorax in which the mediastinum mixes, the deformation
of large vessels and bronchi occurs, which is accompanied by severe cardiorespiratory failure.
Cyanosis of the skin, and visible mucous membranes, swelling of the cervical veins, tachycardia,
arterial hypotension in combination with a decrease in pulse pressure are noted. Respiratory
movements on the affected side are absent or weakened, tympanitis and a mixture of cardiac
dullness in a healthy direction are determined percussion.
Hemothorax - accumulation of blood in the pleural cavity due to damage to the vessels of the lung,
chest wall, wounded heart and large vessels of the chest. According to P.A.Kupriyanov, on the basis
of direct radiography in a vertical direction along the rear landmarks of the chest wall, the following
are distinguished: small (100–200 ml in the pleural sinuses), medium (up to the level of the scapular
angle - 500–700 ml), large (up to the middle of the scapula - 1000-1500 ml) and total hemothorax
(2000 ml or more).
The condition of victims with moderate to severe hemothorax. Pallor of the skin, frequent shallow
breathing, tachycardia, arterial hypotension are characteristic. With percussion, dullness of sound is
detected, the displacement of the borders of the heart in the opposite direction, with auscultation,
weakening of respiratory sounds.
Hemopneumothorax. Combines the signs of the above conditions.
It should be remembered that a chest injury can be combined with damage to the abdomen, with
tears (a sharp increase in pressure; broken ribs) of the spleen and liver most often occur. In this case,
the clinical picture will present symptoms of acute blood loss, irritation of the peritoneum.
16. Indications for surgical treatment of congenital heart defects, methods and
difficulties due to the huge number of types of defects and principles that can be put in its
foundation.
· Cross-discharge;
· Valvular defects;
· Cardiomyopathy;
characteristic of blood flow in the small circulation and the presence of cyanosis.
Features of
hemodynamics
Presence of cyanosis
Present Absent
Enrichment of the
pulmonary circulation
ventricular septal defect, atrial
veins, incomplete
atrioventricular communication
transposition of great
left heart,
circulation
isolated stenosis
pulmonary artery
Ebstein's disease,
coarctation
defects.
The majority of congenital defects are heart defects with enrichment of the pulmonary
arteriovenous shunt. The discharge of blood through a defect is determined by its size and
vascular resistance of the blood circulation circles. Secondary sclerotic changes in the
pulmonary vessels that develop under the inuence of increased pulmonary blood ow and
between pulmonary artery pressure and the aorta, changing the direction of the blood ow
(“changing shunt”).
Pulmonary hypertension causes hypertrophy and systolic overload of the right heart and
impairs the effectiveness of the surgical correction. With a high degree of pulmonary
hypertension, venoarterial shunt of blood through a defect in the aorta appears and
gradually increases, despite the appearance of cyanosis, this reduces the load on the right
heart and partially relieves the pulmonary circulation. In this situation, the surgical closure
of the defect quickly eliminates this shunt, and the right ventricle has to throw out the entire
stroke volume against high resistance into the pulmonary artery. Therefore, in the acute
situation of a new hemodynamic situation, the right parts of the heart are unable to cope
with the increased load and postoperative acute right ventricular failure develops, which is
In children suffering from congenital heart disease with the enrichment of the pulmonary
circulation, the formation of pulmonary hypertension goes through three main phases:
No significant
hemodynamic
disturbances
dextrocardia, vascular
disease
blood ow 2-3 times may not be accompanied by a signicant increase in pressure in the
pulmonary artery. For the mixed phase, a protective increase in pressure in the pulmonary
mainly due to hypervolemia and increased vascular wall tone due to vasoconstriction and
hypertrophy of the middle lay of the small muscular arteries. After a successful surgical
correction of the defect, the pressure in the pulmonary artery in most patients is almost
completely normalized. For the sclerotic phase, destructive changes in the vascular wall
are characteristic, when, against the background of hypertrophy of the middle sheath of
the small muscular arteries, sclerosis of the inner lining occurs, followed by thinning of the
arterial wall and their generalized dilation with the development of necrotizing arteritis. In
the sclerotic phase, there is a high irreversible pulmonary hypertension, expansion of the
pulmonary artery, persistent cyanosis, and severe hypertrophy with systolic overload of the
right heart, often with manifestations of chronic right ventricular failure. Surgical
intervention, predict the results of surgical correction, the nature of rehabilitation, the
• Dyspnea;
• Heart hump;
• Heart murmur;
• An increase in the size of the liver (edema, ascites are observed only in the terminal
stage).
In the formation of arterial hypoxemia in CHD, three main mechanisms may play a role:
intracardiac discharge of blood from right to left and its entry into the aorta; reduced
pulmonary blood ow and reduced pulmonary return of arterial blood to the heart;
separation of large and small circles of blood circulation. With the majority of CHD of the
cyanotic type, arterial hypoxemia is associated with the rst two mechanisms.
Heart failure is a pathological condition in which the heart is unable to provide the blood
circulation necessary to meet the needs of the body. It most often develops either due to
myocardial contractility during hypoxia or an inammatory process in the heart muscle. The
main symptoms of heart failure are tachycardia, shortness of breath, signs of stagnation in
a small or large circle of blood circulation. In young children, heart failure is almost always
biventricular in nature.
Complications of CHD:
· Dystrophy
· Anemia
· Recurrent pneumonia
· Infective endocarditis
· Thromboembolic syndrome
· ECG during which you can identify overload of various parts of the heart,
myocardial changes
The open arterial duct (OAD, PDA) - the presence of a connection between the aorta
and the pulmonary artery, which is considered an anomaly in the postnatal period (Fig. 1).
Anatomic closure or obliteration occurs during the rst 2 weeks of postnatal life. Such
congenital pneumonia, birth asphyxia prevent the closure of the PDA. The volume of blood
discharged from the aorta into the pulmonary artery leads to the development of diastolic
overload and dilatation of the left heart, especially the left atrium, hypervolemia in the
lungs with the formation of pulmonary hypertension. The clinical picture of PDA is typical of
the CHD, occurring with the enrichment of the small circle of blood circulation, and will
depend on the size of the duct. With the natural course the life of patients lasts for 20-25
years. After 12 months of age, spontaneous closure of the ductus arteriosus rarely occurs.
The main complications of PDA are heart failure, pulmonary hypertension, infective
Surgical treatment involves dressing or intersection with the closure of the aortic and
pulmonary duct ends, but lately catheter endovascular occlusion of the duct has also been
used
Atrial septal defect (ASD) is a group of heart defects that are characterized by abnormal
Hemodynamic changes in ASD develop gradually due to the difference in pressurein the
large and small circles of blood circulation, due to which a left-right discharge of blood
through a defect is formed. Due to the receipt of an excess amount of blood in the right
atrium and right ventricle, their dilatation and hypertrophy develop over time. A
hemodynamic (relative) stenosis of the pulmonary artery is formed, the noise of which is
heard during auscultation. Changes in the vessels of the pulmonary circulation occur
according to general laws, but much more slowly than with VSD. It is difficult to suspect
ASD in the neonatal period. Signs of circulatory failure develop, as a rule, much later - at
1-3 years of age, when there is an increase in the motor activity of the child. Indicators of
physical development in children with ASD, as a rule, correspond to the age norm.
16–25.
Treatment of heart failure is carried out according to general principles. Surgical treatment
Ventricular septal defect (VSD) - occurs most often, both in an isolated form, and as part
There are 3 sections in the interventricular septum: the upper part is membranous,
adjacent to the central brous body, the middle part is muscular, and the lower part is
trabecular. According to these sections, ventricular septal defects are also named, but
most of them have perimembranous localization. In order to properly assess the size of the
defect, its size must be compared with the diameter of the aorta. Minor defects of 1-2 mm
in size, located in the muscular part of the interventricular sept, are called Tolochinov –
after birth, as a rule, after 3-5 days of life. In the early neonatal period, heart murmur may
be absent due to the same pressure in the right and left ventricles due to so-called
system and in the right ventricle creates a difference (gradient) of pressures between the
ventricles, as a result of which there is a discharge of blood from left to right (from the high
pressure area to the low pressure area). The additional volume of blood entering the right
ventricle and the pulmonary artery leads to an overow of vessels in the pulmonary
If the surgical correction of CHD is not performed, the processes of pulmonary vascular
pathological process does not reverse development and leads to a signicant increase in
pressure in the pulmonary artery (sometimes up to 100-120 mm Hg). In the clinical picture
of the disease there are many pathological signs: heart “hump”, the expansion of the
borders of relative cardiac dullness, more to the right. The most characteristic feature of
Eisenmenger syndrome is a gradual increase in cyanosis, rst peripheral, and later diffuse.
This is due to cross-ow of blood in the area of the ventricular septal defect, which, if the
pressure in the right ventricle is exceeded, becomes right-left, i.e. changes its direction.
The clinical picture of VSD is in the symptom complex of heart failure, which develops at
1-3 months of life (depending on the size of the defect). In addition to signs of heart failure,
Surgical interventions are divided into palliative operations (narrowing of the pulmonary
artery) and a radical correction of the defect - plastic surgery of an interventricular septal
defect.
Abnormal drainage of the pulmonary veins (ADPV) is a congenital heart disease, which
is characterized by the conuence of the pulmonary veins into the right atrium or into the
caval veins of the greater circulation. Normally, all four pulmonary veins are drained into
the left atrium. With partial abnormal drainage of pulmonary veins, one or two pulmonary
veins ow into the right atrium (or, alternatively, into the superior vena cava, lower hepatic
or portal vein). With total abnormal drainage, all pulmonary veins are not properly drained
(Figure 6). At the same time there is a different degree of severity of stagnation in the
pulmonary circulation and overload of the right atrium, which increases signicantly. To
discharge the latter, the presence of an atrial septal defect, through which blood from the
right atrium will ow into the left atrium, carrying mixedblood there, is a prerequisite. In the
The clinical picture depends on the type of defect and, rst of all, on the number of
abnormally draining veins. With total ADPV, the clinical picture is specic and develops
shortly after birth: dyspnea progresses and becomes pronounced, mild cyanosis takes
place, symptoms of biventricular heart failure develop rapidly and increase, there is a
With partial ADPV, the clinical picture develops more slowly and the defect can be
detected by chance, most often in the second year of life. Children tend to develop
With total abnormal drainage of pulmonary veins, patients die from refractory heart failure
Average life expectancy is 2-6 months. Partial abnormal drainage of pulmonary veins is
Surgical correction is carried out in different age periods and depends on the type of CHD.
The operative lethality at this defect makes up to 25% in the period of a neonatality and
progressively decreases with age of the child. Newborns sometimes undergo palliative
surgery is to create a wide anastomosis of the pulmonary veins with the left atrium, closing
the ASD.
Fallot’s tetrad (FT) belongs to the most common heart disease of the blue type (Fig. 7). In
the classic Fallot’s tetrad, there are 4 signs: narrowing of the right ventricular ejection at
various levels, ventricular septal defect, which is always large, high, perimembranous, right
ventricular myocardial hypertrophy and aortic dextraction. Defect refers to the CHD of the
cyanotic type with the impoverishment of the small circle of blood circulation.
Fallot’s triad is distinguished when there is no ventricular septal defect. Fallot’s tetrad can
be combined with other CHDs: with the simultaneous presence of ASD, the variant is
called Fallot’s pentad. Most often, FT is combined with PDA, due to which a compensatory
blood supply to the lungs occurs. With the “extreme” form of FT, the defect is “ductus” -
dependent.
pulmonary artery. Obstruction may be at the level of the output section of the right
ventricle, at the level of the valve of the pulmonary artery, along the trunk and branches of
the pulmonary artery, and at several levels simultaneously. During systole, blood flows
from both ventricles to the aorta and, in smaller quantities, into the pulmonary artery. Due
to the fact that the aorta is wide and shifted to the right, the blood passes through it without
hindrance, therefore, with the classical form of the Fallot’s tetrad, there is never a
circulatory insufficiency. Due to the large ventricular septal defect, the pressure in both
ventricles is the same. The degree of hypoxia and the severity of the patients correlate
with the degree of stenosis of the pulmonary artery. In patients with the extreme form of
Fallot’s tetrad, the blood enters the lungs through the open arterial duct or through the
utero, but more often - postnatally. Compensation of blood circulation occurs due to: 1)
right ventricular hypertrophy; 2) the operation of the PDA and / or collaterals; 3) the
is the main symptom of Fallot’s tetrad. The degree of cyanosis and the time of its
appearance depend on the severity of stenosis of the pulmonary artery. In children of the
first days of life, only severe forms of the defect — the “extreme” form of Fallot’s tetrad —
are diagnosed on the basis of cyanosis. Basically, the gradual development of cyanosis
(by 3 months - 1 year), which has various shades (from pale bluish to “blue-crimson” or
“iron-blue”), is characteristic: 1st, cyanosis of the lips, then mucous membranes, fingertips,
skin of the face, limbs and trunk. Cyanosis increases with the activity of the child. Early
develop “drum sticks” and “watch glasses”. Permanent symptom is shortness of breath,
which is noted at rest and sharply increasing with the slightest exertion. Gradually
develops a delay in physical development. Almost from birth, a rough systolic murmur is
heard along the left edge of the sternum. A formidable clinical symptom in Fallot’s tetrad,
which is responsible for the severity of the condition of the patients, is undesired cyanotic
attacks. They arise, as a rule, between the ages of 6 and 24 months on the background of
anemia. The pathogenesis of the onset of an attack is associated with a sharp spasm of
the infundibular section of the right ventricle, with the result that all venous blood enters
the aorta, causing the most acute hypoxia of the central nervous system. Blood oxygen
saturation during an attack drops to 35%. The intensity of the noise in this case decreases
sharply until complete disappearance. The child becomes restless, the expression on his
face is frightened, the pupils are dilated, shortness of breath and cyanosis are increasing,
the extremities are cold; followed by loss of consciousness, convulsions, and possible
development of hypoxic coma and death. Attacks vary in severity and duration (from 10–
15 seconds to 2–3 minutes). In the post-attack period, the patients remain sluggish and
adynamic for a long time. Sometimes the development of hemiparesis and severe forms of
cerebrovascular accident is occurred. By the age of 4-6 years, the frequency and severity
collaterals, through which more or less adequate blood supply to the lungs occurs.
Depending on the characteristics of the clinic, there are three phases of defect:
Phase I - relative well-being (from 0 to 6 months), when the patient’s condition is relatively
Phase III - transitional, when the clinical picture of vice begins to take on adult features;
With a pale form of FT, the course and clinical signs resemble those with septal defects.
With the natural course of CHD, the average life expectancy is 12-15 years. Causes of
allows the patient to survive and grow stronger before carrying out a radical correction,
which is carried out in 2-3 years. Radical surgery involves the simultaneous elimination of
The optimal age for the surgical treatment of certain congenital heart defects
CHD - critical
2. Sharp coarctation of the aorta and Complete obliteration of the aortic arch - Urgent
Currently, the vast majority of heart defects are operated on. Operations are usually
operations are resorted to in cases of a serious condition of the patient and / or torpid in
the treatment of congestive heart failure. For example, in CHD, proceeding with the
the pulmonary artery by applying a squeezing cuff to the vessel. Subsequently, a radical
correction of the CHD is carried out. When “ductus”-dependent heart defects perform an
Radical heart operations are performed under conditions of arterial blood circulation,
surgery is impossible due to the anatomical features of the heart defect, for example, in
hypoplasia of the left calving, double separation of the vessels from the right ventricle, etc.
puncture of the main artery according to Seldinger (usually the femoral or radial) with the
catheter being guided along the guide proximal to the aortic root and the catheter
positioned alternately at the mouth of the right and left coronary arteries.
Indications:
• Patients with post-infarction aneurysm and progressive (left ventricular) heart failure
• Patients with stable angina FC III-IV with inefficiency anti- anginal therapy
• Patients with stable angina pectoris with blockade of the legs of the bundle of His in
• Patients with coronary heart disease combined with aortic valvular disease requiring
surgical correction
• Patients with ischemic heart disease with severe cardiac arrhythmias requiring
Contraindications:
· fever
arterial occlusion, stenosis of more than 75%, stenosis of 50% or more (the main trunk of
Intra-coronary ultrasound is an image of the lumen of the coronary arteries with a high
resolution of the transverse section using a piezoelectric crystal rotating through 360 ° or
sequential activation of many crystals of the sensor introduced into the artery lumen.
Initially, the technique was developed as an alternative to angiography, which does not
require radiation exposure and contrast, but at the moment it does not allow replacing the
The main objectives of invasive visualization techniques for examining coronary blood ow
you to determine the tactics and preferred method of re-vascularization. The choice of re-
vascularization method is based on risk stratification. There are two main approaches to
and coronary artery bypass grafting. Each of the methods has soy advantages and
disadvantages.
ECG during which you can identify overload of various parts of the heart, myocardial
hypertrophy;
General radiography of the chest organs, on which a change in the conguration of the
investigate the condition of the valvular apparatus, to identify the aneurysm in the cavity of
ECHO-CG - the main method - allows you to see the morphology of the defect and
Cardiopulmonary bypass - temporary shutdown of the heart from the blood circulation
and the implementation of blood circulation in the body using an artificial blood circulation
apparatus. Used in operations on the heart and aorta. In most cases, cardioplegia is used
during cardiac surgery, including cardiac arrest and myocardial protection. Cardiac arrest
in the diastole phase reduces myocardial oxygen consumption. Most modern strategies for
cardioplegia are based on the introduction into the coronary bed of cold solutions
Auxiliary blood circulation is a method of partial replacement of cardiac function with the
A device with a balloon is inserted through the femoral artery, which is installed below the
left subclavian artery. By periodically inflating and deflating the balloon in accordance with
the phases of the cardiac cycle, temporary support of the pumping function of the heart is
provided. The artificial ventricle of the heart is a mechanical device that partially or
completely replaces the function of the heart in heart failure (Fig. 11). The principle of their
work consists in mechanical unloading of the left or right or two ventricles of the heart. In
the case of a bypass of the left ventricle, the cannula is implanted in the apex of the
ventricle or atrium, then blood passes through the pump of the auxiliary device into the
cannula implanted into the aorta. In the case of using the right artificial ventricle, blood
from the right ventricle through the pump enters the pulmonary artery.
The artificial ventricle of the heart can be used temporarily - while the patient is
expecting a donor heart, and the heart’s own pumping function is insufficient, or recovery
of the heart’s function is expected, for example, after an acute myocardial infarction
complicated by cariogenic shock. Long-term therapy is also possible for patients with
(blood sampling from a vein, oxygenation, return to the artery) ECMO can be considered
The mechanical support of the heart is associated with the risk of ischemic and
Indications for surgical treatment and types of surgical interventions for acquired heart
defects.
Surgical treatment of patients with aortic insufficiency is indicated for all symptomatic
patients who are in NYHA functional class II or above, as well as with an ejection fraction
of> 20-30%. Patients with damage to the contractile function of the left ventricle have a
higher risk of surgery and postoperative mortality. Aortic valve replacement is indicated for
all patients with aortic stenosis with symptoms of the disease, as well as for patients
without symptoms with a high trans-valvular pressure gradient (greater than 60 mmHg),
opening area ≤ 0.6 cm 2, coronary or other valve pathology, up to of how left ventricular
decompensation develops.
Surgical correction of aortic defect is carried out with the help of its prosthetic mechanical,
Indications for surgery for mitral stenosis are determined by the area of the left
critical. The indication for surgery is a reduction in the area of MV <1.5 cm2 and II and
The indication for an operation for mitral insufficiency is the area of the effective opening of
NYHA class.
Surgical correction of mitral disease is carried out with the help of prosthetics with artificial
reconstructive operations on the mitral valve. For this, various methods of reconstruction
are used: annuloplasty on hard and soft rings, resection of the valves, implantation of
artificial chords.
The indication for surgery for tricuspid valve stenosis is the effective orifice area <1.5 cm2,
and in case of insufficiency, blood regurgitation to the right atrium of II - III degree.
annuloplasty. Ways to reduce the diameter of the tricuspid valve ring consist in holding a
purse-string plastics and using rigid or flexible corrective rings. In some cases, when it is
TAVI (Transcatheter Aortic Heart Valve ) The prosthesis for TAVI is a tricuspid bovine
pericardial valve, fixed in a metal frame (stent). The folded bioprosthesis inserted into the
femoral artery using a catheter is delivered to the orifice of the affected native aortic valve
and opens up on its own or inflates with a balloon. The operation is performed under x-ray
control. The delivery system is removed, the valve begins to function. TAVI is the treatment
of choice for patients older than 75 years with severe aortic stenosis, who have
performed to correct severe mitral insufficiency in patients with a high risk of surgical
intervention (Fig. 15). This device is a clip designed to connect the valves at the center of
the mitral valve (an analogue of the open operation Alfieri is the elimination of prolapse of
the anterior valve of the mitral valve with a suture attaching the anterior prolapse to the
unchanged posterior cusp with the formation of a double lumen atrioventricular orifice
ensuring valve tightness). The clip of the mitral valve with the help of the delivery device is
carried out through the femoral vein, then by transseptal access (puncture of the interatrial
septum) is delivered from the right atrium to the left, and then to the mitral valve area.
Fixing the clips to the valve leaflets is carried out under the control of transesophageal
echocardiography.
19. Indications for surgical treatment and surgical interventions with acquired
defects. Prosthetic heart valves. Pre- and post- operative period and outcomes;
Severe lesions of the valve apparatus need replaced valves. Most often carry out the
replacement of the mitral and aortic valves. Mechanical prostheses - made of plastic,
carbon or metal. They are durable and can last long enough. Since blood when in contact
with mechanical valves is prone to the formation of blood clots, patients with such
prostheses should take anticoagulants (warfarin) for life. Biological - made from animal
tissues (xenografts) or from the heart of a human donor (allografts). Patients with
Long experience of using artificial mechanical valves of the heart has shown that despite
their reliability and durability, the use of prostheses is not an ideal solution. The
strengths and weaknesses of allo and xeno materials. Along with the advantages, they
have the disadvantage - the fragility caused by the destruction of biological tissue in the
long-term period. On the one hand, this leads to the rejection of the use of bio-prostheses
in patients of middle (up to 65 years) age, on the other, to the search for methods capable
of realizing the use of allografts not as prostheses, but as viable valves or vessels.
The preoperative preparation of the patient for surgery on the heart valves is aimed at
conducting the necessary examinations, planning the course of the surgery. Diagnosis of
concomitant pathology is carried out and the degree of its severity is assessed, which is
very important in terms of reducing the risk of developing intraoperative complications and
If you find any additional somatic problems, you should achieve an optimal general
condition of the patient, in which unwanted negative points will be minimized. Patients
which is to teach the patient to help himself in stress situations emotional states, such as
fear or depression, to develop the ability to psychological adaptation to the effects of the
Currently, no single implanted biological or mechanical prosthetic heart valve provides the
Prostheses of different designs have individual behavior in the long-term period, which is
high probability of pannus and thrombosis. All prostheses are vulnerable to complications
associated with infectious endocarditis.
surgical treatment;
Infectious endocarditis is an infectious lesion of the tissue of the valve apparatus of the
The criteria for establishing the diagnosis of endocarditis are positive blood cultures and
vascular phenomena (large arterial embolism, septic lung infarction, mycotic aneurysms,
From the point of view of surgery in the pathogenesis of infective endocarditis, the most
important is the fact of the rapid destruction of the valvular apparatus of the heart. This
leads to a catastrophic increase in heart failure, since the myocardium does not have time
The decision about the need for surgical treatment arises, as a rule, with the development
these cases, surgical treatment is more successful than the therapeutic approach.
Indications for surgical treatment - CHF, ineffective antibiotic therapy or sepsis, large,
In case of severe damage or destruction of the valve, prosthetics are usually performed. In
21. Indications for surgical treatment of coronary heart diseases. The choice of
angioplasty (PTBA) and stenting or coronary artery bypass surgery and mammary
coronary artery bypass graft has become the main method of surgical treatment of
A key factor in studying the topic of surgical treatment is a clear understanding of the
nature of coronary heart disease (CHD). CHD is a myocardial damage caused by a
disorder of the coronary circulation, resulting from an imbalance between the coronary
blood flow and the delivery of oxygen to the heart muscle. CHD is based on organic lesion
atherosclerosis, to which thrombosis can join. As a result, the main directions of the
treatment of coronary artery disease are medical therapy aimed at restoring the balance
between myocardial need and oxygen delivery. Indications for surgical treatment occur in
cases where the balance can not be achieved with medication. Such situations may be
urgent (acute coronary syndrome) or develop over a long period of time (stable exertional
separation of the valve chord with the development of acute failure, etc.).
Questions of classification, drug therapy and prevention of coronary artery disease are
discussed in detail in the course of internal diseases. More details on the issues related to
surgical care.
The range of surgical interventions for ischemic heart disease is reduced not only to
revascularization issues, but also to the aspect of invasive diagnostics - coronary
puncture of the main artery according to Seldinger (usually femoral or radial) with a
catheter guided along the guide wire to the aortic root and positioning the catheter
Indications:
• Patients with stable angina pectoris NYHA I-II, who have had myocardial infarction
• Patients with postinfarction aneurysm and progressive (left ventricular) heart failure
• Patients with stable angina pectoris NYHA III-IV with the ineffectiveness of antianginal
therapy
• Patients with stable exertional angina with blockade of the His’ bundle in combination
• Patients with coronary artery disease in combination with aortic heart disease, requiring
surgical correction
• Patients with coronary artery disease with severe cardiac arrhythmias requiring
Contraindications:
· fever
Ventriculography - contrasting of the left ventricle, performed during CAG, which makes it
• Diagnose a LV aneurysm
Functionally significant is the detection of the following signs during angiography: artery
occlusion, stenosis of more than 75%, stenosis of 50% or more (main trunk of the left
coronary artery).
Intracoronary ultrasound is an image of the lumen of the coronary arteries with a high
resolution cross section using a 360 ° rotating piezoelectric crystal or the sequential
activation of a multitude of sensor crystals inserted into the artery lumen. Initially, the
radiation exposure and contrast, but at present it is not possible to replace the standard
angiographic study.
The main objectives of invasive imaging techniques for examining coronary blood flow is to
determine the morphological substrate of coronary blood flow disorders, which allows you
to decide on the tactics and preferred method of re-vascularization. The choice of revascularization
method is based on risk stratification. There are two main approaches to
the artery is restored by performing balloon angioplasty (crushing a plaque with a high
pressure balloon) followed by the installation of a stent (metal mesh tube with or without
drug coating). The introduction and positioning of the balloon and the stent is carried out
using the same technique as angiography - with Seldinger’s puncture of the femoral artery
using different conductors to pass through the narrowing site. The operation is performed
Indications
• Progressive angina .
• Stable angina with low quality of life on the background of adequate drug therapy.
examination methods.
Advantages of stenting
• Short-term hospitalization.
Disadvantages of stenting
• The risk of thrombosis, heart attack, restenosis (up to 15-60% within 6 months).
• At high risk of restenosis, it is necessary to set expensive stents with a drug coating.
• Despite visible minor injuries, the stent implantation procedure is laborious, especially in
the arteries, stenosis of the left coronary artery, not applicable for the lesion of small
The direct effect of PTBA in patients with stable angina with proper selection of patients
reaches 95%. In patients with a single vascular lesion, the mortality associated with the
procedure itself is less than 0.2%; with multiple lesions of the arteries - 0.5%, the
frequency of Q-infarction is less than 1%.
surgery. This intervention involves the formation of bypass routes of blood flow past the
and skills of the surgeon, various options for this intervention are possible, from standard
minimally invasive thoracotomic and endoscopic approaches on the working heart. For the
formation of bypass anastomoses can be used as native arteries (left and right internal
thoracic arteries, gastro-epiploic arteries - which are skeletized, cut off in the distal part,
after which they anastomose with the affected coronary artery distal to the stenosis /
occlusion site), the displaced arteries (usually radial artery) or autovenes (vv. saphena
magna or parva) that anastomose with the aortic root and the affected artery. Arterial
shunts are preferable to venous because of the lower frequency and later periods of
restenosis (10 years after surgery, 90% of the internal mammary artery transplants
continue to function).
• Stenosis of the three coronary arteries (especially with left ventricular dysfunction),
• Stenosis of the proximal left descending coronary artery over 75% with concurrent
Benefits of CABG
Can be performed with the defeat of any arteries (including the left coronary trunk)
Does not lead to a limitation when performing MRI (compared with stenting with
holometalic stents)
Disadvantages of CABG
invasive monitoring.
• Long duration (up to 6 hours), depending on the method and number of superimposed
shunts.
• Traumatic surgery is difficult to tolerate.
Mortality in CABG in patients with lesions of several arteries and severe dysfunction of the
left ventricle reaches 4-5%, about the same incidence of Q-infarction. Currently, there is a
tendency to increase the frequency of operations performed on the working heart and from
In conclusion, it should be noted that CABG and stenting in most cases are not
surgical approaches for the treatment of coronary artery disease in various clinical
situations.
operations;
Cicatricle myocardial changes as a result of a heart attack can lead to the formation of
rare cases due to trauma or a congenital defect. In most cases, aneurysms are localized in
the apex or on the anterior wall of the left ventricle. The existence of an aneurysm changes
the nature of blood flow in the ventricles, significantly reducing the ejection fraction and the
shortness of breath, interruptions in the work of the heart - i.e. the clinic of angina, due to a
heart attack.
Physical examination can reveal a paradoxical pulsation in the fourth intercostal space on
heart shadow due to the sacculate protrusion), ECG (characteristic features of the heart
aneurysm: QS or QR complex, persistent elevation of the interval S-T and negative T wave
in the chest leads), Echo-CG (the location of the aneurysm is clearly defined its size, the
presence of thrombotic masses in the cavity of the aneurysm). Additionally Echo-CG
assess changes in hemodynamic parameters and the state of the valves and papillary
muscles.
Coronarography (with a view to clear diagnosis of lesions in the vascular bed) and
ventriculography (to determine the size of the aneurysm, localization, myocardial changes
due to the pathological process, to evaluate the overall contractile ability of the remaining
With the natural course of the disease, patients with post-infarction aneurysms die within
arrhythmias.
Surgical treatment of a ventricular aneurysm consists in excision of the aneurysm wall with
removal of parietal thrombi and closure of the resulting defect. If necessary, the
walls and containing in its cavity the heart and roots of the main vessels (aorta, pulmonary
trunk, caval veins). In the pericardium, there are two layers - serous, covering the heart
(epicardium), and fibrous parietal layer. The functions of the pericardium are the fixation of
the heart in the region of the mediastinum, protective function and reduction of friction
during heart contractions. Pericardial diseases can be both isolated and part of systemic
diseases. The following main pericardial lesions are distinguished: pericarditis, pericardial
Classification of pericarditis:
· viral pericarditis;
· bacterial pericarditis;
· tuberculosis pericarditis;
· traumatic pericarditis;
· radiation pericarditis;
· idiopathic pericarditis
diseases. In this regard, often there is no specific clinic. However, patients most often
present the following complaints: general malaise, weakness, shortness of breath, chest
pain, heart palpitations and dry cough. As the heart is expelled with an effusion, signs of
impaired cardiac activity increase: cyanosis of the lips and extremities appears, swelling of
the neck veins, severe shortness of breath, and a drop in blood pressure. Given the nature
The main diagnostic tools for the detection of pericarditis are imaging techniques -
information on the nature of pericardial inflammation and do not give direct indications and
the need for one or another treatment option. Reliable differential diagnosis can be
used to perform invasive studies, which is convenient for obtaining diagnostic material.
Invasive diagnostic studies are completed with pericardial drainage to prevent tamponade.
risk of severe complications - puncture of the pleural cavity, heart cavity, liver, development
of pneumothorax, hemothorax, hemopericardium. Such invasive diagnostic procedures
The treatment of acute pericarditis in most patients takes place in parallel with the
treatment of the underlying disease and according to the same principles: antimicrobial
therapy, heart remedies, painkillers, anti-inflammatory therapy. There are no drugs with
carried out on the basis of the etiology of the underlying disease, and for primary bacterial
pericarditis - depending on the sensitivity of the pathogen. Surgical care in the treatment of
Drainage of the pericardial cavity with exudative serous pericarditis is possible through
Drainage of the pericardial cavity is necessary after open cardiac surgery, suturing the
formed - communication between the pericardial cavity and the pleural cavity in order to
thoracoscopy. This type of drainage is less effective and radical than pericardectomy, but
Pericardiectomy - open excision of the altered pericardium, usually required for the
treatment of chronic constrictive pericarditis (i.e., in situations where the contractions of the
heart are not limited by effusion in the cavity, but by changes in the pericardial sheets
themselves). Decortication is the most complete, but with preservation of the phrenic
nerves. It is necessary to exempt from the parietal and visceral sheets of the pericardium,
the right atrium, the vena cava, the lower part of the right ventricle. A full pericardectomy
can be performed only from sternotomy access. This operation requires cardiopulmonary
bypass. Although artificial blood circulation is not required to perform pericardectomy, the
Heart rhythm disorders have a high prevalence in the population. Even normally with a
daily ECG recording, the supraventricular extrasystoles (mostly atrial) are found in
43-63% of cases, ventricular extrasystoles can be caught in 2/3 of people with a healthy
heart. For heart diseases, the number of extrasystoles is usually higher, their nature and
their negative effect on hemodynamics and the ability to provoke more severe rhythm
fibrillation occurs in approximately 0.4% of the adult population, in individuals older than 60
Disorders of the conduction of the cardiac impulse are a frequent pathology in persons
with diseases of the cardiovascular system. Often, these disorders limit the possibilities of
drug therapy, putting the doctor in front of the need to determine indications and
Basic concepts
Arrhythmias are changes in the normal frequency, regularity, and source of excitation of
the heart, as well as impulse conduction disorders, communication disorders, and (or) the
Extrasystoles - premature in relation to the basic rhythm of arousal of the whole heart or
atrial muscle fibers with a loss of mechanical atrial systole and irregular excitations and
ventricular contractions.
with a frequency of usually between 250 and 350 beats per minute.
reflex influences);
impairment of ABB;
3. Physical and chemical effects: caffeine, nicotine, alcohol, drugs, hypoxia, hypo-and
The clinical manifestations of arrhythmias and blockades and related complaints are
due to two main factors: irregular heartbeats and a decrease in the efficiency of cardiac
output. Patients complain about the feeling of interruptions, pauses, “fading” of the heart,
heart palpitations, sometimes seizures, fast fatigue, weakness, swelling, and sometimes
loss of consciousness.
The diagnosis is made on the basis of clinical data. However, to determine the nature and
form of rhythm disturbances, as well as the complications that prevent some invasive
heart.
excitability of the heart, controlling heart rate (cardiac glycosides, β-blockers, calcium
flutter / atrial fibrillation, WPW syndrome), non-drug treatment is indicated in the following
cases:
tachi-arrhythmias are:
A pacemaker is a small device (pulse generator), like a pocket watch, which is implanted
under local anesthesia under the skin, near the heart, to control heart rhythm. A modern
device is a complex device made of inert medical titanium alloy, in the case of which a
battery and a microprocessor unit are placed, oriented towards the heart’s own electrical
activity. When the heart rhythm is disturbed, the stimulator begins to generate an electrical
single chamber - the active electrode is located only in the ventricle and only its stimulation
occurs (deficiency - the atria contract in their own rhythm, if the atrial and ventricular
contractions coincide, blood flows from the ventricle to the atrium, which can cause serious
consequences);
two-chamber - two electrodes: to the atrium and ventricle, provides consistent reductions
three-chamber (last generation) - three electrodes: to the atrium, to the right and left
ventricles, creates a physiological movement of blood through the chambers of the heart.
Pacemaker implantation: A flexible insulated wire is inserted into the left subclavian vein,
a transvenous endocardial electrode is passed to the heart under x-ray control: the distal
end is attached to the right ventricle, the proximal to a pulse generator (single-chamber
pacemaker); 2 wires are often inserted, the second is attached to the right atrium (twochamber).
The operation lasts 1-2 hours. In the hospital the patient spends 1-2 days.
Modern artificial pacemakers are reliable in operation, their service life reaches 5-10 years,
after which, if necessary, the stimulator bolt can be replaced. A portable pacemaker, the
subclavian region.
All modern pacemakers have at least two functions: 1) carry out electrical stimulation of
the corresponding heart section and 2) have the ability to perceive their own electrical
activity of the atria and ventricles, being included in the stimulation mode only in the period
when the critical heart rate decreases or asystole develops (“on demand”).
Some modern artificial pacemakers also have additional functions, for example, the ability
to change the frequency of heart stimulation depending on the size of the load performed
the pacemaker using special devices or the ability to automatically recognize and stop
tachycardia paroxysm.
The pacemaker is programmed based on the individual parameters of the activity of the
atrial fibrillation.
widespread, since it is well eliminated foci of arrhythmias, and healthy areas of the
2. Laser destruction.
The operation is performed under local anesthesia. Through the femoral artery or the left
subclavian vein, electrodes are administered under fluoroscopic control into the heart
tests that provoke arrhythmia are performed. Having found an arrhythmogenic point, it is
affected by radio frequency energy supplied through one of the electrodes. After 20
minutes, repeat the electrophysiological study to assess the effectiveness of the performed
manipulation. If the therapeutic effect is achieved, the catheters are removed, hemostatic
pressure bandages are applied to the place of punctures. The patient is prescribed strict
than normal.
impulse movement from the atria to the ventricles. In the clinic, AV blockades are
classified:
I. By stability:
• Acute transient;
• Intermittent;
• AV node (node)
• Both legs of the His’ bundle (blockade of the legs of the His’ bundle)
From surgical positions, the following types of bradyarrhythmias are important: sick sinus
disturbances caused by a decrease in cardiac output and hypoxia of organs, primarily the
brain. Especially dangerous are periods of ventricular asystole, i.e. periods of absence of
complete AV block, when the new ectopic ventricular rhythm driver located below the level
of the blockade had not yet begun to function. In such situations, the period of asystole
may last for a few seconds and be accompanied by a short-term sudden loss of
fibrillation.
Blockade treatment
the form of dizziness and fainting, it is possible to restrict yourself to dynamic observation
of the patient or an attempt to administer drugs that improve performance in C-A or A-B
• AV-blockade of the II degree of the Mobitz I type (in rare cases with the development of
• Class II AV-blockade of the Mobitz II type (since the risk of the development of the full
AV-blockade is high)
Since conduction disturbances with bradyarrhythmias can be the result of not only organic,
but also functional, electrolyte, and drug changes, implantation of a pacemaker is rarely
considered the first treatment method. The first step is to eliminate the influence of
corrected factors, including with temporary cardiac pacing, and only in the absence of
penetration into the heart chambers and implantation of a foreign body, which is
• The displacement of the electrode and the inability to stop the stimulation;
• Thrombophlebitis;
• Sepsis;
• Embolism (air);
• Pneumothorax;
In view of the severity of possible complications, the implantation of the pacemaker should
Currently, implantation of permanent pacemaker is the only effective way to treat severe
surgical treatment;
treatment;
The aneurysms of the thoracic aorta include cases of irreversible local sacciform or diffuse
Classification.
According to the localization of the aneurysm of the thoracic aorta is divided as follows;
1.Valsalva’s sinus aneurysms, which include the initial segment of the aorta from the
fibrous ring of the aortic valve to the synotubular sulcus, the line on which the upper points
of the commissures of the semilunar valves of the ascending aorta are projected. These
aneurysms are usually innate in nature. The aneurysms of the ascending aorta - from the
level of the sinotubular sulcus to the mouth of the brachiocephalic trunkAt the suggestion
the aortic valve, Valsalva’s sinuses and loss of the synotubular sulcus were divided into a
2. Aortic arch aneurysm, including a segment of the thoracic aorta from the mouth of the
nameless artery to the level of discharge of the left subclavian artery;
3. Aneurysms of the descending aorta, located in the segment of the thoracic aorta
between the left subclavian artery and the aortic orifice of the diaphragm;
extending to its abdominal region. To characterize the latter, use the Crawford
classification
Type 1 - the lesion begins in the proximal half of the descending aorta and above the level
Type 2 - aneurysm also spreads from proximal half of the descending thoracic aorta to a
Type 3 - begins in the distal half of the descending aorta and continues for a different
Type 4 - the aneurysm begins at the level of the aortic orifice of the diaphragm and
According to etiology
1. Congenital diseases.
- Cardiovascular system (double or single aortic valve, aortic stenosis, coarctation of the
2. Acquired diseases.
- Non-inflammatory, degenerative:
patches).
- Inflammatory:
b) Mycotic;
- Post -traumatic.
1. Hypertension,
2. Age,
3. Smoking
4. Cocaine addiction.
The clinical picture of aneurysms of the thoracic aorta depends on the location and size
symptoms in aneurysms of the ascending aorta are chest pain due to aortic wall lesions,
of the superior vena cava is accompanied by edema of the upper limbs, head and neck.
Symptoms of heart failure are typical for ascending aortic aneurysm due to frequent
With aneurysms of the arch and the descending part of the thoracic aorta, pain syndrome
can occur both behind the sternum and in the interscapular region. With this arrangement,
dysphonia occurs during compression of the recurrent nerve, and during compression of
the vagus nerve, bradycardia and salivation occur. Compression of the trachea and the left
congestion in the lungs. The defeat of aneurysmal process branches of the aortic arch
especially in the epigastric region; they are characterized by symptoms associated with the
involvement in the process of branches of the abdominal aorta and the development of
ischemia of the relevant organs. These are signs of chronic abdominal ischemia with
lesions of the celiac trunk and superior mesenteric artery, renovascular hypertension, and
ischemia of the lower extremities. Rarely, with occlusion of the intercostal arteries,
a pronounced collapse often against the background of persisting pain syndrome. The
remaining symptoms are associated with the localization of the gap, for ascending aortic
aneurysms, this is the hemopericardium. For localization of a gap in the descending part or
pulmonary hemorrhage.
or retroperitoneal space, less commonly into the stomach or duodenum, when vomiting
with red blood and / or melena is noted. The rarest localization of rupture of aneurysms of
the ascending aorta and the thoracoabdominal department is a breakthrough into the
superior vena cava and the inferior vena cava, respectively. The clinical picture in these
dominant manner and is associated with a defect in the gene responsible for the synthesis
of fibrillin, the main protein component of microfibrils that make up elastin fibers.
(shoulder, hip, patella, Steyberg positive sign (maximum reduced thumb protrudes beyond
the rest of the fingers that cover it), joint flexion of the joints, increased length of the lower
extremities relative to the length of the body (dolichostenomelia), tall, scoliosis (in 72% of
women and 50% of men in), protrusion of the acetabulum, extension of the knee joints,
flat-footedness, spina bifida occulata (hidden spina bifida or dural ectasia), kyphoscoliosis,
thoracic lordosis, expansion of the large cistern, lumbosacral meningocele, high arch of
the sky;
30-50% of patients have mitral regurgitation. Nearly 80% of patients have aortic root
of the syndrome include annuloaortic ectasia, dissection and aortic aneurysm. The severity
of aortic injury increases with age. Usually, aortic dissection begins with the Valsalva’s
sinuses, then dilated, the sinotubular sulcus and further the aortic arch and arc.
The average life expectancy for patients with Marfan’s syndrome is 32 years. The main
The intensity of the expansion of the aorta in Marfan syndrome is inhibited by the use of
rupture. In planned situations, when the normal aortic diameter is twice exceeded or
extremely high risk of a rupture or separation. Indications for surgery are also heart failure
Aortic dissection is the discrepancy (division) of the aortic media into two layers due to
penetration of the intraluminal blood through the intimal gap and the occurrence of a
pathological connection between the true lumen of the aorta and the channel formed in the
Type 3a - dissection begins below the orifice of the left subclavian artery and extends only
3b type - dissection is the same as with type 3a, but extends through the aortic orifice of
Stanford Classification:
Type A - exfoliation of the ascending aorta (regardless of the location of the intima strain
For aortic dissection in the thoracoabdominal region, the Crawford classification is used for
Etiology. The main causes of dissection are degenerative aortic media lesion and
stratification itself in the absence of degenerative aortic disease, due to the occurrence of
mechanical and metabolic stresses in the aortic wall in response to a pulse wave.
instantaneous onset of high blood pressure with the development of intense pain
syndrome, expressed so that outwardly, despite hypertension, the patient looks like being
in a collaptoid state (lethargy, gaze fixation, cold sticky sweat, weak peripheral ripple). The
causes of often persistent and severe hypertension are damage to the baro-receptors of
the aorta, the release of catecholamines, and in some cases, as a rule, with involvement in
the bundle of the left renal artery - activation of the renin-angiotensin system. A decrease
in blood pressure leads to the suspension of aortic dissection and a decrease in the
severity of pain syndrome with stabilization of the general condition, but then a wave-like
growth of this process is possible again and again. The causes of hypotension in aortic
redistribution of the BCC), can be heart tamponade, aortic regurgitation, aortic rupture,
coronary artery occlusion. Localization of pain depends on the place of the beginning of
the stratification. With the spread of the bundle, the source of the pain shifts and can reach
the lumbar region, in some cases the stratification is almost asymptomatic, and signs of
ischemia of other organs and systems may be the first symptoms of the
transient disorders of cerebral circulation, clinic mesenteric thrombosis, acute renal failure,
acute arterial impassability of the lower extremities. Aortic valve insufficiency is observed
Symptoms of chronic dissection and its complications (rupture) are determined by theType
1 - stratification begins in the ascending section, goes through the arc in the descending s
extensiveness of the dissection, the degree of involvement in the process of various parts
The natural course of aortic dissection. In acute proximal stratification, mortality during the
first 24 and 48 hours is at least 33 and 50%, respectively, i.e. at least 1% of non-operated
patients die every hour. During the week, 80% die, and during the first month - 95% of
patients with acute proximal aortic dissection. Among patients with chronic proximal
bundles, after 5 years, 10–5% survive. In distal separations, 75% of patients remain alive
within a month.
Surgery.
The choice of the type of operation depends on the prevalence of the aneurysm, the
degree of involvement of the aortic root and aortic valve, comorbidity, the life expectancy
of the patient, the desired status of anticoagulant therapy. For correction of the pathology
of the ascending aorta, operations are performed to replace the aortic segment involved in
the aneurysm with a vascular prosthesis, and for aortic valve pathology, aortic valve
In the reconstruction of the aortic arch, hypothermic (280C) antegrade cerebral perfusion
through the right subclavian artery and/or additional branches from the aortic artery is used
to protect the brain. Surgical correction of aortic arch aneurysms is most often performed
Dissecting aneurysm of the thoracic aorta is characterized by an intimal rupture and partial
redirection of blood flow from its natural lumen to a false one, located within the media
between intima and adventitia. A type A dissecting aneurysm is an absolute indication for
surgery. The state of aortic dissection is not a factor influencing the decision about surgical
treatment - in cases of thrombosis of the false lumen there remains the risk of fatal
complications and surgery is necessary. Currently, hybrid interventions are possible: the
ascending aorta and the arch are replaced with a vascular prosthesis if necessary the reimplantation
of the aortic valve is performed, and to reduce the morbidity of the operation
and close the false lumen of the descending thoracic aorta, stentgraft is used.
Aneurysms of the abdominal aorta (AAA) are in many ways similar to the aneurysmal
changes of the thoracic aorta (especially thoracoabdominal aneurysms, which are a direct
continuation of the enlarged part of the descending aorta), but also have certain
differences. According to the literature data, the frequency of abdominal aneurysms varies
within fairly wide limits, which is caused by the difference in approaches (population
screening, autopsy assessment). In general, abdominal aortic aneurysm is not the most
common disease of the arteries - according to various sources, it ranges from 0.6 to 7%,
and the incidence of the disease increases with age, but AAA occurs in individuals of any
age. However, despite the relatively low frequency, this pathology has a high proportion in
the structure of mortality, since it is characterized by high mortality with the development of
uncomplicated course.
processes, infection, connective tissue pathology. Unlike thoracic aortic aneurysms, the
now, there is no single concept for the development of aneurysms, which allows to explain
pathogenetic changes in the aortic wall, leading to its dilatation, are inflammatory or
degenerative. However, these data were obtained at certain stages of change, while the
true dynamics of changes have not yet been completely studied. In the pathogenesis of
aneurysm development, genetic factors, high blood pressure, sex, and many other causes
allows to systematically reflect the essence of the processes taking place. Therefore,
morphological, clinical, etc. The main classification approaches are listed below.
• congenital
• acquired
- Posttraumatic / anastomotic.
• Bag-shaped.
• Spindly.
According to size:
• true
• false
• Asymptomatic.
• Painless course.
• Stage of complications:
- threatening gap;
- gap, breakthrough;
- stratification;
By anatomical localization:
• Type II - infrarenal with adequate proximal isthmus, extending to the aortic bifurcation
(IIa), with the involvement of the common (IIb) and the mouths of the internal iliac (IIc)
arteries
Clinical picture
In case of uncomplicated abdominal aortic aneurysm, they may not manifest themselves
for a long time, therefore they are often found by chance when screening ultrasound of the
abdominal organs or when searching for a different pathology of the abdominal cavity and
retroperitoneal space. In some cases, patients (especially those with asthenic physique)
independently note the presence of a volume pulsating formation in the abdomen (usually
abdominal mass formation (dislocation of the shadow of the intestinal loops during
radiography, constipation, etc.). During the physical examination, in addition to the most
compression of the duodenum, stomach, bile ducts, disturbances in the kidney intestinal
abdominal aortic aneurysms, as a rule, is not typical. The appearance of pain in patients
complication of AAA is its rupture. The clinic for rupture of the abdominal aortic aneurysm
largely depends on the location of the rupture and the conditions that provoked it
(increased blood pressure, physical exertion). The main clinical manifestations of the
rupture are associated with hematoma formation and tissue stratification, which causes
pain, and loss of BCC. Depending on the location of the gap and hematoma, the pain
syndrome may have a different character. Gaps in the back wall are sometimes
accompanied by moderately severe aching pain in the lumbar region, sometimes even
without falling of the BCC, since the dense tissues of the ligaments of the spine do not
allow the hematoma to spread widely. In such cases, it happens that the patient is
examined for pain for a long time and is operated on in a planned manner, when a rupture
hematoma is formed with severe pain in the lumbar region, radicular pain, impaired
innervation of the lower extremities and blood supply, since the hematoma squeezes the
terminal part of the aorta. It often happens that such ruptures occur after lifting weights or
other physical activities, and since they are manifested by severe weakness, especially of
attack of radiculitis. If the patient has a history of AAA, the complaints described should be
necessary to evaluate the pulsation of the femoral arteries and the appearance of the
lower extremities (when aneurysm ruptures, as a rule, pale cyanotic, marble color,
pulsation is reduced). A rupture of the aneurysm on the front / side surface is usually
accompanied by sharp pain in the abdomen or lower back and the clinic of acute blood
loss. The most severe are tears in the free abdominal cavity or the lumen of a hollow
organ. In both cases, acute blood loss syndrome will prevail, due to the lack of conditions
for restricting hematoma. In case of rupture, there will be a pronounced acute pain
syndrome in the abdominal cavity, in the second case there will be practically no pain
syndrome, but there will be a clinic of acute gastrointestinal bleeding. Severely diagnosed
aneurysms are diagnosed and flow into the lumen of the inferior vena cava, accompanied
by a clinic of acute heart failure and volume overload of the right heart, as well as acute
venous insufficiency.
of delamination, i.e. double contour in the vessel lumen occurs with great frequency.
However, this phenomenon is not caused by intimal detachment, but by the presence of a
thrombotic bowl that performs the cavity of the aneurysm, leaving the central lumen, which
can be shifted from the axis of the vessel, which creates the impression of separation.
True AAA dissection occurs rarely and is characterized by pain in the lumbar region and
The presence in the aneurysm of the thrombotic bowl can cause non-cardiogenic
thromboembolism of the arteries of the lower extremities with the development of the clinic
thrombotic bowl or its complete displacement can lead to aortic thrombosis, i.e. complete
blockage of the lumen. With acutely developed aortic thrombosis, the clinic of acute
ischemia of both lower limbs, pelvic organs in combination with acute heart failure prevails.
Diagnostics
abdominal aortic aneurysms requires the use of imaging techniques. Ultrasound allows
you to extract AAA, evaluate its lumen and permeability, measure the diameter of the
aneurysm, determine the location relative to the renal arteries, in some cases to identify
the hematoma around the aneurysm (extensive). Being an excellent screening technology,
ultrasound is not able to provide answers to all the questions necessary for planning an
intervention. More reliable information is provided by CT with contrast and MRI (Fig. 6): the
communication with the lumen, contrast flow, structure, shape and size of the aneurysm,
lumen, intima condition. Ideally, the survey should be performed under MSCT conditions.
Angiography of the aorta and arteries of the lower extremities is somewhat inferior in terms
of the effectiveness of MSCT, but it provides a spatial representation of the lesions of the
angiography should not include a clear estimate of the size of aneurysms, since only their
lumen contrasts, and the outer diameter can be estimated with a calcified aortic wall or in
Treatment
course, the main criteria for determining indications for surgical treatment are the size and
shape of the aneurysms and the growth rate. The presence of a bag-shaped aneurysm
serves as an independent indication for surgical treatment, since the risk of rupture of baglike
aneurysms is quite large. With a spindle-shaped aneurysm, indications for planned
surgical treatment will be “medium” and “large” aneurysms (d> 5 cm), since upon reaching
such a diameter, the risk of aneurysm rupture during the year is 5-10%, which exceeds the
risk of surgery (2-3 %). A separate indication for the planned treatment of asymptomatic
Drug therapy for aneurysms is aimed at reducing the risk of rupture and slowing the
growth of the aneurysm. Depending on the etiology, therapy may include antibacterial
blood pressure in patients with hypertension, preferably with the use of β-blockers as a
component of therapy (reduce the risk of rupture). But it should be remembered that
therapeutic agents are only ancillary. Patients require regular screening for timely
necessary for health reasons. Without surgical treatment, mortality for complications of
aortic aneurysms reaches 100%. In the surgical treatment of patients with aneurysm
rupture, mortality reaches 25-75%. Such high rates of mortality and severity of the
surgical treatment.
The principal task of surgical intervention for abdominal aortic aneurysms is to turn off the
enlarged portion of the aorta with a thinned wall of blood flow with the formation of a safe
The main methods of surgical treatment of AAA at the moment are resection of the
aneurysm with prosthetics and staging of the stentgraft. In exceptional cases, aortic
ligation is possible against the background of a rupture, however, the mortality rate for
such operations exceeds 90% and at the moment they are practically not performed.
Each of the methods of surgical treatment has its own advantages and disadvantages.
accompanied by severe blood loss, a relatively high incidence of complications, but leaves
ample opportunities for surgical maneuver in case of irregular anatomy, involvement of the
renal arteries, occlusion of the distal channel segments, the need to preserve the lower
mesenteric artery, etc. The operation can be performed in the form of a linear prosthesis
resection of the aortic area, bifurcation prosthetics with the launch of blood flow to the iliac
arteries or femoral, as well as extranatomical shunting of the aortic area off (from the
subclavian artery) with a compromised neck of the aneurysm. Although the immediate
risk of complications, but the distant complications almost does not have. Endovascular
shutdown of the aneurysm with a stent graft implies the performance of the lumen of the
aorta with a stent covered with an impermeable tissue material. This intervention is less
graft selection, as well as lifelong observation and control using CT and angiography to
lesions of the arteries of the lower extremities and, as a rule, is considered as one of the
approaches in this case do not apply. However, there are fundamentally important points
that require separate instructions. First, it is the prognostically more severe character of
the lesion than in the case of even both common iliac arteries, since collaterals along the
lumbar arteries are turned off, which is especially important in acute thrombosis. Mortality
in acute aortic thrombosis is very high. Secondly, chronic occlusion of the terminal part of a
large vessel such as the aorta leads to a significant increase in total peripheral resistance
and the development of heart failure. Therefore, occlusion of the terminal aorta is an
independent indication for surgical treatment, even with a low degree of chronic arterial
insufficiency. And thirdly, endovascular reconstruction with occlusive lesion of the terminal
aortic region is not indicated. Fourthly, when planning surgery, the question clearly arises
as to the need for aortic clamping, which requires an assessment of the function and
reserve of the myocardium, invasive blood pressure monitoring during the operation, as
The remaining therapeutic and diagnostic approaches are similar to those used in patients
treatment, principles;
Coarctation of the aorta (CA) is a congenital segmental narrowing of the aorta in the area
of the arc, isthmus, lower thoracic or abdominal regions.In most cases in infants,
coarctation is located on the site from the left subclavian artery to the open arterial duct or
immediately after it, called the aortic isthmus.In the fetus and newborn, the aorta isthmus
region is normally narrowed, since during the prenatal period only one third of the blood
volume flows through the descending aorta, the other two thirds pass through the
PDA. Soon after the closure of the PDA, all the blood begins to pass through the isthmus,
it gradually expands and almost reaches the diameter of the descending aorta. In the
presence of pathology, the isthmus region remains narrowed in one or another area. The
constriction may take the form of a constriction (then a membrane with a small opening is
found inside the vessel, but there may be a complete break in the aortic arch) or a tubular
constriction for some distance. In relation to the PDA, aortic coarctation is subdivided as
follows:
1. Narrowing proximal to the site of PDA discharge - preductal coarctation of the aorta;
2. Narrowing at the level of the PDA discharge - juxtaductal coarctation of the aorta;
3. Narrowing distal to the PDA discharge - post-ductal aortic coarctation.
Hemodynamics significantly depends on the type and location of coarctation, the degree of
narrowing, as well as the presence of concomitant CHD. With an isolated spacecraft in the
large circle of blood circulation, two modes of blood circulation are established: proximal
(arterial hypertension) and distal (arterial hypotension and lack of blood flow) of the
narrowing site.
circulation, the flow of the defect is less severe. Collateral blood flow occurs through the
subclavian, intercostal, internal thoracic, scapular, epigastric, and vertebral arteries, which
over time expand due to increased pressure in them. With inadequate development of
collaterals, blood pressure rises significantly to the site of constriction and blood under
pressure is discharged from the aorta through the PDA into the pulmonary artery. The
amount of discharge depends on the gradient between the aorta and the pulmonary artery
and, as a rule, is significant. In response to the arrival of a large additional blood volume in
the vessels of the pulmonary circulation, pulmonary hypervolemia and hypertension are
developed.
In case of pre-ductal coarctation of the aorta, the direction of blood shunting will depend on
the pressure ratio in the descending aorta and the pulmonary artery. When the degree of
narrowing is pronounced, venous arterial blood shunt is noted, which leads to the
appearance of differentiated cyanosis (there is on the legs, but not on the arms).
When CA is combined with other CHDs, in particular, with VSD, the value of arterio-venous
discharge is very large, and pulmonary hypertension develops faster.The result of longterm
hemodynamic stress is the development of left ventricular fibroelastosis of the
signs of left ventricular hypertrophy and left atrium refractory to treatment of heart
failure.With postductal CA localization, the clinical picture develops quite quickly - in the
first weeks of life. For children, marked anxiety, shortness of breath, difficulty in feeding,
the development of malnutrition are characteristic. Pale skin, with an ashy tint (especially
during anxiety attacks). The legs in children are always cold to the touch due to a lack of
peripheral blood flow. Chest deformity of the “heart-hump” type may develop. In the lungs,
congestive crepitus are heard, and pneumonia is possible. Cardiac impulse strengthened,
spilled. Borders of the heart are extended left and right, with fibroelastosis -
rhythm. The noise picture is nonspecific - most often systolic or systolic-diastolic PDA
noise is heard. Medium or low intensity systolic murmur in the interscapular region can be
heard. The most specific clinical symptom, by the presence of which coarctation can be
suspected, is a decrease in pulsation in the femoral artery. When measuring systolic blood
pressure there is a significant increase in the upper half of the body. Other clinical signs
In case of pre-octal coarctation, along with the above-mentioned symptoms, the presence
In older children, the clinical picture is significantly different from that in nursing
patients. As a rule, children develop normally. Defect is detected by chance (more often at
school age) when high blood pressure is detected. Characteristic is the appearance of
such children with a developed upper half of the body and an asthenic physique of the
At the stage of primary adaptation, a high mortality rate of children due to severe heart
failure and the accession of pneumonia is noted. In the future, the condition of the patients
the closure of the PDA) and they live, on average, to 30-35 years. The main complications
in adults are exfoliating aneurysm and aortic rupture, severe strokes and infective
endocarditis.
Surgical correction consists of excision of the site of aortic narrowing and joining of
the cut ends “end to end”, “side to side”, “end to side”, or subsequent ismoplasty. In
children with coarctation according to the type of internal membrane, balloon angioplasty
Blood vessels
Occlusive peripheral arterial disease is blockage or narrowing of an artery in the legs (or
rarely the arms), usually due to atherosclerosis and resulting in decreased blood flow.
Symptoms depend on which artery is blocked and how severe the blockage is.
Occlusive peripheral arterial disease is common among older people because it often
results from
• atherosclerosis (plaque or disease buildup in the wall of the blood vessel), which
When people suddenly develop a painful, cool, and pale arm or leg, they should seek
Bypass surgery may be done to treat arteries that are narrowed or blocked. In this
procedure, blood is rerouted around the affected artery—for example, around part of the
femoral artery in the thigh or part of the popliteal artery in the knee. A graft consisting of a
tube made of a synthetic material or part of a vein from another part of the body is joined
diagnosis;
30. Chronic limb ischemia treatment. Indications for surgical treatment, types of
operations;
Chronic limb ischaemia is peripheral arterial disease that results in a symptomatic reduced
blood supply to the limbs.It is typically caused by atherosclerosis (rarely vasculitis) and will
commonly affect the lower limbs (however the upper limbs and gluteals can also be
The Framingham study demonstrated an increase in the prevalence of the disease from
0.4 per 1000 males aged 35-45yrs to 6 per 1000 males aged >65yrs.
Risk Factors
• Smoking
• Diabetes mellitus
• Hypertension
• Hyperlipidaemia
• Increasing age
• Family history
The clinical features of chronic limb ischaemia depend on its severity, as shown in Table 1.
One of the earlier symptoms is intermittent claudication, a cramping-type pain in the calf,
thigh, or buttock after walking a fixed distance (the ‘claudication distance’), relieved by rest
within minutes.
Buerger’s test involves lying the patient supine and raising their legs until they go pale and
then lowering them until the colour returns (or even becoming hyperaemic). The angle at
which limb goes pale is termed Buerger’s angle; an angle of less than 20
• Ischaemic rest pain for greater than 2 weeks duration, requiring opiate analgesia
occlusive disease
Stage I Asymptomatic
On examination, the limbs may be pale and cold, with weak or absent pulses.Other signs
include limb hair loss, skin changes (atrophic skin, ulceration, or gangrene), and thickened
nails.
Differential Diagnoses
There are two major differential diagnoses* for a patient presenting with limb ischaemia
symptoms:
• Typically have pain from the back radiating down the lateral aspect of the leg
• Clinical features that are less than 14 days duration, often presenting within
hours.
embolic event in a patient with previous peripheral arterial disease. These patients are
sub-classified as they typically have a longer duration in which the limb is salvageable.
Investigations
index (ABPI, Fig. 2) is used to confirm the diagnosis and quantify severity of chronic limb
ischaemia:
Any ABPI value >1.2 should be interpreted with caution, as calcification and hardening of
Any critical limb ischaemia should be investigated initially with a Doppler ultrasound, used
to assess the severity and anatomical location of any occlusion. Further imaging can be
Due to concurrent cardiovascular risk factors seen in patients with chronic limb ischaemia,
patients should also have a cardiovascular risk assessment. This includes blood pressure,
In addition, any patient presenting with chronic limb ischaemia <50yrs without significant
risk factors should also have a thrombophilia screen and homocysteine levels* checked.
Severity ABPI
Normal >0.9
Mild 0.8-0.9
Moderate 0.5-0.8
Severe <0.5
*A lower homocysteine level has been associated with reduced risk of cardiovascular
events
The ankle-brachial pressure index (ABPI); a value of less than 0.9 indicates a reduce
Management
1. Medical Management
Most patients with chronic limb ischaemia require cardiovascular risk factor modification:
Enrollment into a local supervised exercise programme has been shown to improve
walking distance and claudication distance, and should be used as first line therapy in any
The course of chronic limb ischaemia is variable and many patients’ symptoms do improve
2. Surgical Management
NICE guidance states that surgical intervention can be offered in suitable patients if (i) risk
factor modification has been discussed; and (ii) supervised exercise has failed to improve
symptoms.
Any patients with critical limb ischaemia should be urgently referred for surgical
intervention.
Amputations are considered for any patients who are unsuitable for revascularisation with
Complications
Chronic limb ischaemia can result in sepsis (secondary to infected gangrene), acute-onchronic
ischaemia, amputation*, and reduced mobility and quality of life.
further above knee amputation, 30% have died, and only 40% have full mobility.
The 5 year mortality rate in those diagnosed with chronic limb ischaemia is around 50%
31. Chronic and acute disorders of visceral blood flow. Classification, clinical
operations;
For the first time at autopsy, he revealed and described the asymptomatic occlusion of the
superior mesenteric artery Tiedeman in 1843. Until recently, the incidence of this disease
has not been studied. According to the literature, the frequency of damage to the superior
mesenteric artery is 30–40%, and the celiac trunk is 20–40%. The following forms of
mortality, disability of patients. The main cause of acute abdominal ischemia is mesenteric
thrombectomy from the main vessels of the mesentery is usually not advisable due to the
low tolerance of the intestine to ischemia. In most cases, patients with mesothrombosis
enter the operating table when irreversible changes in the intestinal wall have already
occurred.
Differential diagnosis of acute violation of mesenteric circulation must be carried out with
disorders of the abdominal cavity caused by impaired visceral artery patency due to extra -
or intravasal causes (A. V. Pokrovsky, 1979). Since the disease manifests itself in
abdominal pain during the maximum activity of the digestive organs in the literature, this
condition is also known as "abdominal toad." The mechanism of pain is identical to angina
organ due to impaired blood ow through the arteries. Extravascular and intravascular
causes lead to circulatory disorders in the abdominal organs. Extravascular causes include
compression of the mesenteric arteries with the crescent ligament of the diaphragm, nerve
ganglia of the solar plexus, medial leg of the diaphragm, tumors. In this case, the celiac
At the beginning of the development of the disease, ischemic changes are compensated
by the developed system of collateral organs of the abdominal cavity. Ischemic disorders
in the digestive tract are manifested in incomplete digestion of foods, especially fats. For a
long time, existing ischemia of the intestinal muscle layer is manifested in impaired motor
that occurs some time after a meal 2) impaired intestinal functions, which are expressed in
subcompensated, decompensated.
gastrointestinal tract, which is manifested by pain. Pain, as a rule, is caused by occlusalstenotic lesion
of the branches of the celiac trunk. It occurs after eating a large volume of
food regardless of its quality (“small portions” syndrome). Also, a pain attack can provoke
prolonged walking or mental stress. The pain is usually localized in the epigastrium. The
attack lasts from several minutes to 1.5 to 3 hours. As a diagnostic criterion, a test with
nitroglycerin can be used. The meaning of which is that when taking nitroglycerin, the pain
syndrome stops.
inferior mesenteric artery, patients are concerned about constipation, which is due to
in the region of the superior mesenteric artery, patients are disturbed by episodic attacks of
diarrhea, unstable stool, which leads to a progressive decrease in body weight. The longterm
symptoms described above lead to the development of astheno-hypochondria
With the development of the decompensated stage of chronic abdominal ischemia, the
progressive depletion.
In the diagnosis of chronic ischemia of the abdominal organs, an important role is given to
the inefficiency of conservative therapy. The use of laboratory diagnostic methods allows
If the patient has the entire previously listed symptom complex, the absence of the clinical
effect of conservative treatment, the patient is shown to perform an X-ray contrast study
An ultrasound scan of the abdominal organs with duplex angioscanning can also be used
Surgical treatment in the rst stage of the disease is not advisable. The most justified is
conservative therapy. Indications for surgical treatment in the stage of sub compensation
and decompensation are set individually, taking into account the severity of the disease
Surgical treatment of disorders in the pathways of blood ow to the organs of the abdominal
occlusion-stenotic lesions of the vascular bed are corrected by performing various types of
the celiac trunk and superior mesenteric artery is carried out from the left
trunk and reconstruction of the inferior mesenteric artery, it is most advisable to use
laparotomy. In cases of extravascular compression of the celiac trunk, the medial leg of the
diaphragm is intersected, the median fibrous ligament of the diaphragm is dissected, and
and stenting of visceral arteries are increasingly being used. The use of these methods of
treatment is more promising in terms of reducing surgical trauma, but they require further
arteries. Renal artery stenosis (SPA) not only leads to the development of vaso-renal
hypertension, but can also cause renal failure, heart failure with pulmonary edema, and
The causes of stenotic lesions of the renal arteries can be both congenital and acquired,
• Arteriovenous fistula
• Extravascular renal vascular compression of various genesis (tumor, scar tissue, etc.).
• Traumatic injuries
There are several clinical signs indicating a high risk of SPA; if they are present, this
• Malignant hypertension;
In the natural course of SPA, a gradual occlusion of the renal artery occurs over time, loss
of kidney mass and weakening of its function. The rate of progression of SPA, according to
angiographic studies, varies from 39% to 49%. With the most severe stenosis, complete
In a prospective study on the medical treatment of SPA, progression was noted in 42% of
patients (11% developed occlusion). It should be noted that the progression of SPA and
the loss of renal function do not correlate with the possibility of drug control of
hypertension.
Atherosclerotic stenosis of the renal artery, the most common cause of secondary
hypertension, is found in less than 5% of the total hypertensive population, but at the same
people older than 50 years, in 5-15% of cases, this leads to renal failure and the need for
dialysis. As a Swedish study showed, in patients with renal artery stenosis more than 50%,
the overall risk of death is 3.3 times higher than in the general population (with equal age
groups), and the risk of death from cardiovascular disease is 5.7 times above.
Stenotic lesions of the renal arteries represent a significant public health problem not only
in the Republic of Belarus but also in foreign countries. So, according to rough estimates,
in the Russian Federation the number of patients with vasorenal hypertension is about 1.5
million people, in the USA, according to 1977, about 1 million people suffered from this
pathology. A number of studies have shown that atherosclerotic lesions of the renal
· Refractory hypertension
Currently, balloon dilatation and stenting of the renal arteries is the operation of choice in
the presence of veried hemodynamically signicant renal artery stenosis with a decrease in
the nitrogen-excreting function of the kidneys. Open surgical procedures are practically not
Differential diagnosis;
Atherosclerosis obliterans- a systemic, chronic, slowly progressing, incurable disease,
which is accompanied by deep changes in the arterial wall and impaired patency due to
the growth of atherosclerotic plaque. The main reason for the development of occlusalstenotic
lesions of the arterial bed is atherosclerosis. The development of atherosclerotic
plaques, as a rule, occurs in the arteries of large and medium caliber elastic and muscle
type. It should be remembered that atherosclerosis is a systemic disease that affects the
entire arterial bed of a person, but manifests the disease in one of the most affected
vascular pools. The degree of atherosclerotic lesion of the vascular bed increases with
age. According to scientific studies, atherosclerotic plaques in the vessels begin to form
even in childhood, however, the clinical manifestations of the disease appear mainly in
adulthood. This phenomenon is due to the high adaptive potential of the human vascular
of the artery of at least 75% of its diameter. The growth rate of atherosclerotic plaque
depends on many factors, the main of which are smoking, low level of physical activity and
improper eating behavior. In the majority of modern international recommendations for the
treatment of occlusal- stenotic lesions of the vascular bed, the modification of the above
risk factors plays a huge role with a high level of evidence. So hemodynamically significant
stenosis is considered to be a narrowing of the lumen of the artery of at least 75% of its
diameter. The growth rate of atherosclerotic plaque depends on many factors, the main of
which are smoking, low level of physical activity and improper eating behavior. In the
lesions of the vascular bed, the modification of the above risk factors plays a huge role
considered to be a narrowing of the lumen of the artery of at least 75% of its diameter. The
growth rate of atherosclerotic plaque depends on many factors, the main of which are
smoking, low level of physical activity and improper eating behavior. In the majority of
the vascular bed, the modification of the above risk factors plays a huge role with a high
level of evidence.
(accumulation of lipids and smooth muscle cells) occurs in combination with lipid infiltration
and the accumulation of blood elements in an atherosclerotic plaque. Gradually, the wall of
the artery loses its elasticity and becomes like a “bamboo stick”. The disease proceeds for
a long time and imperceptibly, leading to a gradual narrowing of the lumen of the vessel
and impaired blood ow in the organ. Gradually, the development of atherosclerotic plaque
atherosclerotic plaque protruding into the lumen of the artery), damage to the endothelium
(due to destruction of the fibrous capsule of the plaque), a change in the rheological
treatment;
narrowing of the lumen of the medium and large arteries with a primary lesion of the aorta
and its branches. This pathology is more characteristic of young and middle-aged women
in Asian countries. Frequency of occurrence from 1.2 to 2.6 people per one million of the
vessels of the retina, and Dr. Onisi and Kagoshima at the same meeting reported similar
The etiology of the disease is still unknown. It is believed that there is a certain genetic
52, HLA - DR 2. In the pathogenesis of the disease, the leading role is played by the
immunological theory.
( vasavasorum ) and the outer layers of copper on the walls of large and medium arteries.
formation of granulomas. In the future, fibrosis of granulomas occurs, sclerosis and tears
of a blood clot.
· I type - an isolated lesion of the aortic arch and arteries extending from it, usually
a combination of pathology of the left subclavian and left common carotid artery is noted;
· Type II - an isolated lesion of the thoracic or abdominal aorta and its branches;
· III type - a combined lesion of the aortic arch and its branches with changes in the
· IV type - the pulmonary artery, its branches are involved, while a combination with
Most often with non-specific aortoarteritis, subclavian arteries are affected (90%), common
carotid arteries (60%), abdominal aorta (60%), aortic arch (40%). For diagnosis,
gold standard for diagnosing Takayasu disease. During angiography, it is determined that
the lesion is localized mainly in the places where the aortic branches discharge, the lumen
of the artery is not uniform and the stenosis sections alternate with the areas of the
cytostatics. Surgical treatment of nonspecific aortoarteritis is indicated only during the first
ve years from the onset of the disease, in an inactive stage and with the development of
stenosis of the main arteries more than 70%. However, it should be remembered that
angiosurgical reconstructions in this case have a limited service life due to intraoperative
trauma to the artery, which leads to the activation of processes of intimal hyperproliferation
with the subsequent development of stenosis or occlusion of anastomoses. For the same
methods of treatment.
lesion of small and medium caliber arteries of the distal lower extremities. Obliterating
endarteritis takes the second place after obliterating atherosclerosis in the frequency of
of the trigger mechanism in this disease is played by factors that cause a prolonged
(chills) of the lower extremities (men who are fond of winter fishing, drivers, builders),
sciatic nerve, injuries of limbs), some chronic intoxications (e.g. lead). An important role in
the development of obliterating endarteritis has a chronic overstrain of the nervous system
and, first of all, its central departments, because activation of the sympathetic nervous
system leads to prolonged vascular spasms. The autonomic nervous system dysfunction
that develops at the same time is also important, which leads to disorganization of
endocrine activity and a violation of the hormonal function of the sex glands and adrenal
glands. An increase in the incidence was observed during the period of world warriors,
of this pathology.
represented as follows: first, a long spasm of small and medium caliber vessels develops
the development of metabolic acidosis due to tissue hypoperfusion and the accumulation
of free radicals. The destruction of cell membranes and the release of inflammatory
mediators: serotonin, gestamine, kinin, which leads to increased pain impulse and a
number of humoral changes that contribute to thrombosis. On the other hand, as a result
of compression of vasa vasorum by spasmodic muscles of the vessel, blood supply to the
vascular wall suffers, which leads to a violation of its trophism and the development of
degenerative changes in it. Endotheliocytes die, and blood clots also form in parts of the
vessel devoid of endothelium. The pathological process extends not only to the great
vessels, but also to the collateral ones. The defeat of the collateral bed can occur
simultaneously or somewhat later compared to the main. At the beginning of the disease,
collateral circulation is not enough only during exercise of the limb. With the progression of
leads to the appearance of severe pains not only when walking, but also at rest,
intensifying in the horizontal position of the limb. At the beginning of the disease, collateral
circulation is not enough only during exercise of the limb. With the progression of the
to the appearance of severe pains not only when walking, but also at rest, intensifying in
the horizontal position of the limb. At the beginning of the disease, collateral circulation is
not enough only during exercise of the limb. With the progression of the pathological
appearance of severe pains not only when walking, but also at rest, intensifying in the
During obliterating endarteritis, the following stages are distinguished: ischemic, trophic
At the initial stages of the disease, the treatment is conservative with the obligatory
glucocorticosteroid hormones and cytostatics is considered not entirely justified due to the
of the elastic tissue of blood vessels with the simultaneous growth of fibrous and smooth
muscle tissue, not caused by inflammation or atherosclerosis. Most often, the renal
arteries are involved in the pathological process, less often the branches of the aortic arch,
cerebral vessels.
In view of the rather rare frequency of this disease, the etiology and pathogenesis are still
anomalies in the structure of the elastic frame of the vascular wall. Congenital deficiency of
elastic fibers in the walls of the artery leads to the growth of muscle and fibrous tissue.
multiple sections of narrowing of the artery are visible, alternating with aneurysmal
dilatations or sections of the unaffected vessel, and the x-ray image resembles a “chain of
beads”.
The treatment of bro-muscular dysplasia is mostly conservative and comes down to the
(renal arteries, upper parts of the internal carotid artery at the base of the skull) and
suture arteriotomy holes. The use of endovascular methods of treatment in this situation is
The following factors exist that have a teratogenic effect and cause vascular tube
ionizing radiation.
All vascular abnormalities are divided into vascular tumors and malformations, which differ
in their specific structure, pathophysiology, clinical features and treatment tactics. Of the
hyperplasia and is a benign tumor. Most of the vascular malformations are venous, arterial,
defect that occurs during embryo and vasculogenesis. Currently, the Classification of the
International Society for the Study of Vascular Anomalies ( ISSVA) is used to classify
Classification of the International Society for the Study of Vascular Anomalies ( ISSVA ,
2014)
I. Vascular tumors
Benign
infantile hemangioma
retiform hemangioendothelioma
capochiform hemangioendothelioma
composite hemangioendothelioma
Kaposi's sarcoma
Malignant
Angiosarcoma
Epitheloid hemangioendothelioma
Simple capillary
• normal sporadic
• Bean syndrome
• Glomangioma
• Mafucci syndrome
lymphatic
• arteriovenous malformations
• arteriovenous stula
combined
1. directions
2. quantities
3. lengths
enchondroma
Microcephaly - CM (MICCAP) G
The most common vascular tumor is infantile hemangioma, which occurs in 10% of the
population. Recent studies have shown that they are more common in low-weight girls
hemangiomas are of 2 types: rapidly involving and generally not involutional. Infantile
hemangioma appears in the first days after birth. It is a clearly defined at red spot on the
skin surface. At this stage, hemangioma can be confused with other vascular diseases,
however, rapid vertical growth allows you to make the correct diagnosis. With intradermal
localization, the hemangioma has a bright red color. In cases where the hemangioma is
located subcutaneously, it loses the clarity of its relief and borders and has a bluish color.
The development of hemangioma has the following stages: growth phase (first weeks and
up to the 3–6th month of life), stabilization phase (from the 6–8th month and up to the 12–
20th month), the regression phase (up to 6–7 years ) With spontaneous involution,
sclerosis of the hemangioma occurs. On the head and neck, the hemangioma is usually
localized in the projection of the trigeminal nerve, and the location in the region of its lower
Therapeutic tactics for simple hemangiomas are expectant, with the goal of the onset of
located on the face, around natural openings, the presence of episodes of bleeding,
ulceration or inflammation, active therapeutic tactics are used. Propranolol is the rst-line
systemic drug in the treatment of hemangiomas. In 2008, it was found that the use of
a slowdown in the growth of the latter. This observation was confirmed by many studies
that showed a pronounced decrease in tumor size within 1-2 weeks after the start of
impossible to perform surgery or use wait and see tactics. The most successful use of the
mechanism of action has not yet been fully studied. There is an assumption that
Despite the relatively high efficiency of propranolol in half the cases, it is nevertheless
often used.
terminal arteries and arterioles. The disease affects mainly the upper limbs. It occurs in
3-5% of the population, mainly female, aged 20-40 years. Women get sick 5 times more
often than men. First described in 1862 by the French physician Maurice Reynaud.
At the heart of the disease is a genetic predisposition. Factors that trigger the onset of the
disease include:
Diseases are more common among pianists and typists. In pathogenesis, an important
role is played by increased muscle tone in the distal upper limbs, due to hyperactivation of
the sympathetic nervous system. Often the disease is combined with migraine.
1. angiospastic
2. angioparalytic
3. trophoparalytic
In the first stage of the disease, spasms of the vessels of the terminal phalanges of the
In the second stage of the disease, the hands and fingers acquire a pale, cyanotic color,
necrosis. With the rejection of necrotic tissue, long-lasting non-healing ulcers are formed.
Patients suffering from Raynaud's disease are characterized by a specific reaction to cold,
which manifests itself in the form of chilliness of fingers and pain. Even washing your
The treatment methods for this disease are divided into two groups: conservative and
disease and preventing the causes that cause the onset of the disease. At the first stage of
the disease, the relief of a pain attack is possible by warming the limbs in warm water.
Drug therapy consists in the use of vasodilator drugs. It is recommended that patients
avoid hypothermia of the extremities, chronic trauma and stay in a state of psychoemotional
comfort. With the progression of the disease and the development of trophic
ulcers, various dressings are used depending on the phase of the wound process. In
the main blood ow in the extremities is preserved. The pulsation on the arteries of the
wrists and legs is distinct, and the pathological process is localized at the level of the
on the side of the lesion. As a rule, after surgery, in most patients, a stable remission of the
disease can be achieved with the exception of provoking factors and regular courses of
progression of the disease and leveling the achieved positive results from conservative
and surgical treatment. Only after complete cessation of smoking is it possible to perform
on the side of the lesion. As a rule, after surgery, in most patients, a stable remission of the
disease can be achieved with the exception of provoking factors and regular courses of
progression of the disease and leveling the achieved positive results from conservative
and surgical treatment. Only after complete cessation of smoking is it possible to perform
on the side of the lesion. As a rule, after surgery, in most patients, a stable remission of the
disease can be achieved with the exception of provoking factors and regular courses of
progression of the disease and leveling the achieved positive results from conservative
and surgical treatment. Only after complete cessation of smoking is it possible to perform
of the disease with the exception of provocative factors and regular courses of
progression of the disease and leveling the achieved positive results from conservative
and surgical treatment. Only after complete cessation of smoking is it possible to perform
of the disease with the exception of provocative factors and regular courses of
progression of the disease and leveling the achieved positive results from conservative
and surgical treatment. Only after complete cessation of smoking is it possible to perform
sympathectomy.
36. Stenotic lesions of the terminal aorta, iliac arteries and lower limb arteries:
Atherosclerosis is the main cause of occlusal-stenotic diseases of the terminal aorta, iliac
arteries and lower limb arteries. Also, non-specific aortoarteritis, thromboangiitis obliterans,
endarteritis obliterans and Raynaud's disease lead to the development of damage to the
arterial bed of the lower extremities and pelvic organs. However, the share of these
diseases in the development of stenotic lesions of the arterial bed is significantly less than
Stage I - asymptomatic lesion of the arteries, which is detected only when using
Fundamentally important is the division of this stage. You can start thinking about the
It should be noted that the selection of such a term as “critical ischemia” is fundamental. It
includes III and IV stages of classification A.V. Pokrovsky. If the patient has pain at rest or
Occlusion of aortic bifurcation was described and analyzed in detail by R. Lerish in 1923.
The symptom complex described by R. Lerish included five signs: 1) unstable and
incomplete erection; 2) severe fatigue of the lower extremities; 3) diffuse muscle atrophy of
the lower extremities; 4) the absence of trophic disorders; 5) the pallor of the legs and feet,
even in the upright position of the patient. To date, occlusion of aortic bifurcation is called
Lerish syndrome.
The main symptom of chronic arterial insufficiency is the pain that occurs when walking.
First, the pain syndrome occurs with a significant level of physical activity and is
manifested by painful sensations in the muscles of the leg. With a decrease or cessation of
the load, the symptoms disappear. As the atherosclerotic process progresses, the distance
of painless walking decreases, the time required for rest increases. Upon transition to the
stage of critical ischemia, pain at rest is disturbing. Patients sleep with their limbs down or
in a sitting position to relieve pain. However, a prolonged forced position with a limb
lowered down leads to the development of edema, which in turn compresses the
As the progression of atherosclerotic lesions in the arterial bed, patients lose leg hair.
Atrophy of muscles, skin and subcutaneous tissue occurs. Toenails become brittle,
characterized by fungal infection.
The basic principles for diagnosing chronic arterial insufficiency of the lower extremities
are reduced to determining the distance of painless walking, the severity of pain and the
Differential diagnosis of chronic arterial insufficiency must be carried out with chronic
venous insufficiency, neuralgia, arthrosis and arthritis. The main symptom of chronic
venous insufficiency is edema, which progressively grows throughout the day. Ripple on
the main vessels preserved. In case of neurological lesions, patients complain of burning,
shooting pains that spread from the buttocks along the lateral surface of the thigh and
lower leg. There is no intermittent claudication and pulsation is preserved on the main
arteries. Pain occurs during palpation of paravertebral points in the lumbar spine, as well
as exit points of the sciatic nerve in the buttocks. With the development of arthritis or
determine the possibility and extent of angiosurgical treatment, the “gold standard” of
Treatment of occlusal-stenotic lesions of the arterial bed is divided into: conservative and
surgical. All patients with a clinic of chronic arterial insufficiency should be recommended
to walk at least one hour a day under the supervision of relatives. Walking is indicated at
all stages of the disease. It is necessary to explain to patients that at least once every 6
of the condition of the leg. Only systematic treatment can slow the progression of
atherosclerosis. The main principles of conservative therapy include: leveling risk factors
(actovegin, solcoseryl),
An indication for surgical treatment is dissatisfaction with the distance of painless walking
can be used: reversible endarterectomy, endarterectomy with plastic artery patch, various
Endovascular treatment methods include balloon angioplasty and stenting. With limited,
great advantages. It should be noted that the use of hybrid revascularization technologies
include the combined implementation of open angiosurgical treatment of one vascular pool
obstruction;
39. Treatment of acute limb ischemia: conservative therapy, indications for surgery,
types of operations;
Acute arterial obstruction - a sudden cessation of arterial blood ow. The main causes are
represented by a part of a blood clot that has torn off from the main source and migrates
The famous Berlin pathologist Rudolf Virchow in the second half of the 19th century
formulated three main reasons for the formation of a blood clot: a violation of the integrity
of the vascular wall, changes in the rheological properties of blood and a slowdown in
blood ow.
Sources:
1) The left half of the heart - atrial fibrillation, post-infarction aneurysm of the left ventricle,
infectious endocarditis with vegetation on the alignment of the valve, stenosis of the mitral
valve, tumor. The greatest embologous danger is represented by episodes of the transition
of the sinus rhythm into fibrillation and vice versa. The most common cause of arterial
thromboembolism is atrial fibrillation.
2) Aorta and large major vessels - separation of fragments of the thrombotic cup of the
3) The right heart and veins of a large circle of blood circulation - with extensive defects of
the interventricular and atrial septa. In arterial thromboembolism of the extremities, emboli
Complete or even partial occlusion of the arterial supply to a limb can lead to rapid
Etiology
Acute limb ischaemia has an incidence of around 1.5 per 10,000 person years. Its causes
• The original thrombus source may be as a result of AF, post-MI muralthrombus, abdominal aortic
aneurysm, or prosthetic heart valves
Clinical Features
Classically, the signs and symptoms of acute limb ischaemia can be described using the
6 Ps (the first three here being the most common initial features):
• Pain
• Pallor
• Pulselessness
• Paresthesia
• Perishingly cold
• Paralysis
In the history, the causes of potential embolisation should be explored. These include
The later the patient presents to a hospital, the more likely that irreversible damage to the
neuromuscular structures will have occurred (more common >6hrs post-symptom onset),
Loss
Motor
Deficit
Arterial
Doppler
Venous
Doppler
I – Viable No Immediate
IIA –
Marginally
Threatened
Salvageable,
if promptly
treated
Minimal
(toes) or
none
Differential Diagnosis
The differential diagnoses for acute limb ischaemia include critical chronic limb ischaemia,
acute DVT (can present as Phlegmasia cerulea dolens and Phlegmasia alba dolens), or
Routine bloods, including a serum lactate (to assess the level of ischaemia), a
thrombophilia screen (if <50yrs without known risk factors), and a group and save, should
regarding the anatomical location of the occlusion and can help decide the operative
Management
1. Initial Management
Acute limb ischaemia is a surgical emergency. Complete arterial occlusion will lead
to irreversible tissue damage within 6 hours. Early senior surgical support is vital.
Start the patient on high-flow oxygen and ensure adequate IV access. A therapeutic
dose heparin or preferably a bolus dose then heparin infusion should be initiated as
soon as is practical.
2. Conservative Management
Any patient started on conservative management via heparin will need regular
assessment to determine its effectiveness through monitoring APPT and clinical review.
IIB –
Immediately
Threatened
Salvageable if
immediately
revascularised
More
than
toes, rest
pain
Mild/
III –
Irreversible
Major tissue
loss,
permanent
nerve damage
inevitable
Profound
Profound
paralysis
Inaudible Inaudible
3. Surgical Intervention
• Angioplasty (Fig. 2)
• Bypass surgery
Most post-operative cases require a high level of care, typically at a high dependency unit,
for Rutherford 2a
conditions to the acute limb ischaemia should be treated, e.g. uncontrolled AF.
Cases resulting in amputation will require occupational therapy and physiotherapy, with
centre.
Complications
Acute limb ischaemia has a mortality rate of around 20%, with the 30-day mortality rate
• Compartment syndrome
It is imperative that patients at risk of compartment syndrome are closely monitored and
rapidly treated. Electrolyte imbalance due to reperfusion injury requires close monitoring
I stage of ischemia - stage of functional disorders (sensitivity and movement of the limb
preserved, acute pain in the limb, pallor and cooling of the skin, lack of pulse in the
peripheral arteries).
II stage of ischemia - stage of organic changes. Its duration is 12-24 hours. Pain and
tactile sensitivity are absent, active and passive movements in the joints are limited,
III of stage ischemia - necrotic. The duration of the stage is 24-48 hours. Lost all kinds of
Differential Diagnostics:
2. Diabetic angiopathy.
3. Transverse myelitis.
4. Sciatica
further treatment are determined by the duration of the disease, the prevalence and
localization of the lesion of the vascular bed, the degree of ischemic tissue damage, and
performed - embolectomy using a Fogarty catheter. The success of this type of surgical
treatment depends on the duration of the disease. The most successful embolectomy in
the first 6 hours after the onset of limb ischemia. Angiosurgical reconstructions are not
performed if the patient has severe concomitant pathology and muscle contracture in large
joints. In the presence of subfascial edema, fasciotomy is additionally performed with the
80. Anatomical and physiological information about the diaphragm, classification of diseases of the
diaphragm.
The diaphragm is the fibromuscular structure separating the thorax from the abdomen.
The attachments of diaphragm can be divided into peripheral and central attachments.
The parts of the diaphragm that arise from the vertebrae are tendinous in structure, and are
known as the right and
left crura:
Right crus – Arises from L1-L3 and their intervertebral discs. Some fibres from the right crus
surround the
oesophageal opening, acting as a physiological sphincter to prevent reflux of gastric contents into
the
oesophagus.
Muscular part consists of skeletal muscle. The muscular part is located on the periphery. It is
divided into the
The muscle fibres of the diaphragm combine to form a central tendon. This tendon ascends to fuse
with the
Either side of the pericardium, the diaphragm ascends to form left and right domes. At rest, the
right dome lies
slightly higher than the left – this is thought to be due to the presence of the liver.
There are three openings that act as conduit for these structures:
VASCULATURE:
The majority is provided inferior phrenic arteries, which arise directly from the abdominal aorta.
The remaining supply is from the superior phrenic, pericardiacophrenic, and musculophrenic
arteries which
branches off from the internal thoracic, as well as six lower intercostal arteries..
The draining veins follow the aforementioned arteries, azygous & hemiazygous veins and
oesophageal veins.
INNERVATION
The halves of the diaphragm receives motor innervation from a phrenic nerve.
The left half of the diaphragm (known as a hemidiaphragm) is innervated by the left phrenic nerve,
and vice
versa.
Each phrenic nerve is formed in the neck within the cervical plexus, and contains fibres from spinal
roots C3-C5.
leading to breathlessness.
trauma.
Unless there is severe bleeding or strangulation of the viscera it is best managed after an interval.
In a severely injured patient being ventilated it can wait until other injuries are dealt with and
weaning from the
When the diaphragm is breached, as in anatomical disorders, repair with either primary closure or
with a mesh is
81. Damage and injuries of the diaphragm, causes, clinic, diagnosis, treatment.
Iatrogenic causes (medical intervention, for example during surgery to the abdomen or chest)
MECHANISM
It is proposed that a blow to the abdomen may raise the pressure within the abdomen so high that
the diaphragm
bursts.
Blunt trauma creates a large pressure gradient between the abdominal and thoracic cavities; this
gradient, in
addition to causing the rupture, can also cause abdominal contents to herniate into the thoracic
cavity.
Abdominal contents in the pleural space interfere with breathing and cardiac activity.
They can interfere with the return of blood to the heart and prevent the heart from filling
effectively,
If ventilation of the lung on the side of the tear is severely inhibited, hypoxemia (low blood oxygen)
results.
Usually the rupture is on the same side as an impact. A blow to the side is three times more likely
to cause
CLINIC
2. Bowel sounds may be heard in the chest, and shoulder or epigastric pain may be present.
3. When the injury is not noticed right away, the main symptoms are those that indicate bowel
obstruction. These people present months later, with vague symptoms that do not necessarily relate
to an
injury.
With penetrating trauma, the contents of the abdomen may not herniate into the chest cavity
right away, but they
DIAGNOSIS
A nasogastric tube from the stomach may appear on the film in the chest cavity; this sign
is pathognomonic for diaphragmatic rupture, but it is rare. A contrast medium that shows up on X-
ray can be
The X-ray is better able to detect the injury when taken from the back with the patient upright, but
this is not
usually possible because the patient is usually not stable enough; thus it is usually taken from the
front with the
Positive pressure ventilation helps keep the abdominal organs from herniating into the chest
cavity, but this also can
2. Computed tomography
3. Thoracoscopy
4. Laparotomy
LOCATION
It is possible that the liver, which is situated in the right upper quadrant of the abdomen, cushions
the
diaphragm.
However, injuries occurring on the left side are also easier to detect in X-ray films.
Half of diaphragmatic ruptures that occur on the right side are associated with liver injury. Injuries
occurring
on the right are associated with a higher rate of death and more numerous and serious
accompanying
injuries.
Bilateral diaphragmatic rupture, which occurs in 1–2% of ruptures, is associated with a much
higher death
TREATMENT
82. Hiatal hernias, etiology and pathogenesis, classification, clinic, diagnosis, treatment.
A hiatal hernia is a type of hernia in which portion of the stomach prolapses through the
diaphragmatic
Most hiatal hernias are asymptomatic and are discovered incidentally, but rarely, a life-threatening
complication
This may result in gastroesophageal reflux disease (GERD) or laryngopharyngeal reflux (LPR).
ETIOLOGY
Hard sneezing
Violent vomiting
Pregnancy
The most common risk factors are obesity and older age. Other risk factors include major trauma,
scoliosis, and
Type I: A type I hernia, also known as a sliding hiatal hernia, occurs when part of the
disease.
Sliding hernias are the most common type and account for 95% of all hiatal
hernias. (C)
Type II: A type II hernia, also known as a paraesophageal or rolling hernia, occurs when
the fundus and greater curvature of the stomach roll up through the diaphragm, forming a pocket
alongside the
esophagus.
It results from a localized defect in the phrenoesophageal ligament while the gastroesophageal
junction
remains fixed to the pre aortic fascia and the median arcuate ligament.
Although type II hernias are associated with reflux disease, their primary clinical significance lies in
the
Type III: Type III hernias have elements of both types I and II hernias.
With progressive enlargement of the hernia through the hiatus, the phrenoesophageal ligament
stretches,
displacing the gastroesophageal junction above the diaphragm, thereby adding a sliding element to
the type II
hernia.
Type IV: Type IV hiatus hernia is associated with a large defect in the phrenoesophageal ligament,
allowing other
organs, such as colon, spleen, pancreas and small intestine to enter the hernia sac.
The end stage of type I and type II hernias occurs when the whole stomach migrates up into the
chest by rotating
180° around its longitudinal axis, with the cardia and pylorus as fixed points.
CLINIC
Called the "great mimic" because its symptoms can resemble many disorders.
1. Dull pains in the chest, shortness of breath (caused by the hernia's effect on the diaphragm)
3. Swallowed food "balling up" and causing discomfort in the lower esophagus until it passes on to
the stomach.
4. In addition, hiatal hernias often result in heartburn but may also cause chest pain or pain with
eating.
The pain and discomfort that a patient experiences is due to the reflux of gastric acid, air, or bile.
While there are several causes of acid reflux, it occurs more frequently in the presence of hiatal
hernia.
5. GORD symptoms Regurgitation of food/ liquids into the esophagus; Heart burn.
6. Vomiting of blood; Black stool (melaena) from associated esophagitis, erosions (Cameron ulcers),
or a discrete
7. In newborns, the presence of Bochdalek hernia can be recognized from symptoms such as
difficulty
DIAGNOSIS
1. Upper GI series An upper gastrointestinal series, also called a barium meal, is a series of
radiographs used
to examine the gastrointestinal tract for abnormalities. A contrast medium, usually a radiocontrast
agent such
as barium sulfate mixed with water, is ingested or instilled into the gastrointestinal tract, and X-rays
are used to
2. Endoscopy
TREATMENT
If there is pain or discomfort 3 or 4 sips of room temperature water will usually relieve the pain.
Symptomatic patients
CONSERVATIVE
2. Elevate the head of their beds and avoid lying down directly after meals.
5. Medications that reduce the lower esophageal sphincter (LES) pressure should be avoided.
SURGERY
Indications
It is necessary only in the very few patients who have complications of GERD despite aggressive PPI
treatment.
Esophageal stricture or severe discomfort due to unusually large hiatal hernia or paraesophageal
type. About 5%
If symptoms from such a hernia are severe for example if chronic acid reflux threatens to severely
injure
Complications from surgical procedures to correct a hiatal hernia may include gas bloat
syndrome, dysphagia (trouble swallowing), dumping syndrome, excessive scarring, and rarely,
achalasia
Surgical procedures sometimes fail over time, requiring a second surgery to make repairs.
Procedures:
Thoracotomy).
procedure)
2. Belsey fundoplication
3. Hill repair
herniation of the stomach through the hiatus in the diaphragm and the
Diaphragmatic paralysis is due to an interruption in its nervous supply. This can occur in the phrenic
nerve, cervical
spinal cord, or the brainstem. It is most often due to a lesion of the phrenic nerve.
ETIOLOGY
Bilateral-Motor neuron disease (most common): Amyotrophic lateral sclerosis; Post-polio syndrome
Unilateral -Compression: due to a tumour within the chest cavity(e.g., metastatic lung cancer)
Unilateral -Supraclavicular brachial plexus block Neuropathies: such diabetic neuropathy, multiple
sclerosis
DIAGNOSIS
Physical examination
Unilateral Dullness to percussion and absent breath sounds over the lower chest on the involved
side.
Excursion on the involved hemithorax is decreased when compared with the healthy side.
Bilateral Chest examination reveals limitation of diaphragmatic excursions and bilateral lower
chest dullness
The diagnostic finding is a paradoxical inward movement of the abdomen with inspiration.
ventilation-perfusion mismatching.
The hallmark of patients with diaphragmatic paralysis is hypercapnia and a respiratory acidosis.
2. Pulmonary function test Vital capacity in the upright and supine positions is the most important
part of
4. Electromyography & phrenic nerve stimulation May reveal a neuropathic versus myopathic
pattern
Measured by placing a thin-walled balloon transnasally at the lower end of the esophagus,
allowing
Then, a second balloon manometer is placed in the stomach to measure changes in intra-
abdominal pressure.
Gastric pressure should become more positive during inspiration. Esophageal pressure should
become more
Imaging Studies
(Unilateral paralysis can usually be diagnosed with only radiographic studies, unlike bilateral.)
However, can be misleading as accessory muscle contraction may create the appearance of
diaphragmatic movement.
5. Ultrasonography
TREATMENT
a) Patients who do not have intrinsic lung pathology Non-invasive ventilation, such as a CPAP
(continuous
b) In patients with central respiratory paralysis and upper cervical spinal cord injury (lesions above
C3) to wean
Electrodes can be implanted intrathoracically via thoracotomy and, more recently, with VATS.
In this approach, intramuscular electrodes are placed near the entrance points of the phrenic
nerves using
Negative-pressure systems
c) Patients with mild-to-moderate diaphragmatic weakness usually maintain daytime gas exchange
but worsen
e) Patients who are not candidates for less invasive methods or in whom less invasive methods fail
f) Nerve reconstruction techniques Neurolysis, nerve grafting, and neurotization for returning
function to
unilateral phrenic nerve injury that occurred as a result of anesthetic procedures and operative and
nonoperative
muscle recruitment and help those with mild symptoms from diaphragmatic paralysis.
Diaphragmatic hernia is a defect or hole in the diaphragm that allows the abdominal contents to
move into the chest cavity.
Types
1. Congenital diaphragmatic
hernia
Morgagni's hernia
Bochdalek hernia
2. Hiatal hernia
Pathophysiology
3. Pulmonary hypoplasia
CLASSIFICATION
1. True hernia Have a hernial sac with hernial contents. A hernial sac is composed of parietal
peritoneum,
covered by pleura.
2. False hernia Without a hernia sac, i.e.the abdominal viscera lying free within the thoracic cavity.
Traumatic
Non-traumatic false congenital hernias of the diaphragms, true CDH of weak zones, true hernias of
atypical localization, hiatal hernias (esophageal opening, physiological foramen).
a) False congenital hernias of the diaphragm are formed due to failure of the diaphragm to
completely close during embryonic development.
b) True hernias of the weak areas of the diaphragm occur when the intraperitoneal pressure
increases resulting in exit
hernia/retrosternal/parasternal hernia). It is
Common hernial sac contents omentum, transverse colon, preperitoneal fatty tissue
(parasternal lipoma).
development.
treatment principles.
vena cava)
CLINIC
Antenatal
The diagnosis of congenital diaphragmatic hernia (CDH) is frequently made antenatally prior to
25 weeks' gestation.
CDH is usually detected in the antenatal period (46-97%), depending on the use of level II
ultrasonography (US)
techniques
Postnatal
History and clinical findings vary with the presence of associated anomalies and the degree of
pulmonary
hypoplasia and visceral herniation, the degree of lung collapse and displacement of the
mediastinum and the size
Factors leading to increase intra-abdominal pressure, increase the severity of the symptoms of
the disease.
In the infant presenting in the neonatal period without antenatal diagnosis, variable
respiratory distress and
Auscultation breath sounds are diminished, bowel sounds may be heard in the chest, and
heart sounds are
distant or displaced.
Bochdalek hernias are more likely to be asymptomatic if it is on the right side of the chest.
Complaints:
After heavy intake food Feeling of heaviness and pain in the epigastric region, chest &
hypochondria;
Regurgitation of recently eaten food brings relief. Increased shortness of breath in a horizontal
position.
Reduction in chest movement and smoothing of intercostal spaces on the affected side,
Presence of dullness or tympanic sound over the affected half of the chest.
Depending on the degree of herniation of the stomach and intestines, auscultation of intestinal
peristalsis or
splash sound in this area while decreased or completely absent respiratory noises.
Late presentation
Patients may present outside of the neonatal period with respiratory symptoms, intestinal
obstruction, bowel
Laboratory Studies
(CDH)
3. Assess arterial blood gas values Hypoxemia, hypercarbia, and respiratory or metabolic
acidosis depend
Imaging
4. Chest Radiography
5. CT
(more commonly, ventricular hypoplasia, atrial septal defects, and ventricular septal defects).
TREATMENT
hypertension.
Prior to surgery:
If the infant cannot be stabilized using medical treatments and mechanical ventilation, the
alternate pathway
involves putting the infants on a temporary heart/lung bypass machine, called ECMO, which
stands for extracorporeal membrane oxygenation.
ECMO allows oxygen to be regulated into the blood and then pumps the blood throughout the
entire body.
During ECMO the pulmonary artery has a chance to rest, as it were, thus hopefully reducing the
presence of
pulmonary hypertension, one of the biggest complication of CDH cases. Normally, this machine
is used to
Window of opportunity is 24-48 hours after birth to achieve normal pulmonary arterial
pressures and
However, surgical repair can often be safely delayed in stable patients, and the operation can
be scheduled on a
semielective basis. Urgent surgical repair is almost never necessary and may worsen the
pulmonary
hypertension.
The association of CDH with lethal congenital abnormalities is a relative contraindication for
repair of the
diaphragmatic defect.
Procedure:
After the baby is stable and his or her state has improved, the diaphragm can be fixed and the
misplaced organs
That is either done via primary repair where the remaining diaphragm is stretched to cover the
hole, or an
abdominal muscle is split so it can be used to stretch over the hole, and the last option is with a
Gor-Tex patch,
Any organ displacement is corrected during surgery; the heart and lungs will usually move back
into position on
their own, once displaced organs such as bowel, liver, or stomach, are out of the way.
The incision is then closed. Sometimes, the incision site will be left open to allow the body to
adjust to newly
moved organs and the pressure associated with that, and then closed later once swelling and
drainage has
decreased.
Prognosis Congenital diaphragmatic hernia has a mortality rate of 40–62%, with outcomes
being more favourable in the absence of other congenital abnormalities.
12. Specific methods of examination of focal liver lesions. Differential diagnosis of liver lesions;
1. Hepatic hemangioma
• Benign vascular lesions of the liver and commonest liver tumor (F>M) (30-50 years)
• Usually asymptomatic
• Hemangioma are compose of many endothelium lined vascular spaces separated by fibrous
septa
•2
3. Hepatic adenoma
• Rare hepatic tumor. In women aged 20-40 years (associated with oral contraceptive use)
• Dx CT and MRI
4. Liver cysts
• Maybe single or multiple
1. HCC
2. Regenerating nodules
3. Dysplastic nodules
• No arterial enhancement
5. Metastatic disease
• Common primaries are colon, breast, lung, stomach, pancreas, and melanoma
1. Simple cysts
4. Cystic tumors
5. Abscesses
These conditions can usually be distinguished using patient's symptoms, clinical history, and
the
Ductal cysts, choledochal cysts, and Caroli disease are differentiated from hepatic cysts by
involvement of the
In patients with simple liver cysts, it is generally agreed that laparoscopic unroofing offers the
best balance
How patients with PCLD should be treated remains less clear because the failure rates for
laparoscopic
unroofing and fenestration are high. Liver resection, though more effective, carries higher risks.
indications for PAIR (puncture, aspiration, injection, reaspiration) versus surgery are delineated.
Simple cysts
• The cause of simple liver cysts is not known, but they are believed to be congenital in origin.
• The cysts are lined by biliary-type epithelium, and perhaps result from progressive dilatation of
biliary
microhamartomas.
• Because these cysts seldom contain bile, the current hypothesis is that the microhamartomas
fail to develop
• Typically, the fluid within the cyst has an electrolyte composition that mimics plasma. Bile,
amylase, and white
• Adult PCLD (AD-PCLD) is congenital and is usually associated with autosomal dominant
polycystic kidney
disease (AD-PKD).
• Mutations in these patients have been identified in PKD1 and PKD2 genes.
• Occasionally, PCLD has been reported in the absence of polycystic kidney disease (PKD). In
these patients, a
third gene, protein kinase C substrate 80K-H (PRKCSH), has been identified.
• Despite these differences in genotype, patients with PCLD are similar phenotypically.
• In patients with PKD, the kidney cysts usually precede the liver cysts. PKD often results in renal
failure,
whereas liver cysts only rarely are associated with hepatic fibrosis and liver failure.
Neoplastic cysts
• Liver tumors with central necrosis visualized on imaging studies are often misdiagnosed as liver
cysts. True
• The cause of cystadenomas and cystadenocarcinomas is unknown, but they may represent
proliferation of
• These cystic tumors are lined with biliary-type cuboidal or columnar cells and are surrounded
by ovarian like
stroma.
In a retrospective study, Kim et al investigated the value of quantitative color mapping of the
liver’s arterial
• The investigators determined that when the color maps were analyzed in combination with
multiphasic
computed tomography (CT) scans, the mean sensitivity for HCC detection reached 88.8%, in
comparison with
71.7% sensitivity for HCC detection using the multiphasic CT scans alone.
Hydatid cysts
• Hydatid cysts are caused by infestation with the parasite Echinococcus granulosus.
• The adult tapeworm lives in the digestive tract of carnivores, such as dogs or wolves.
• Eggs are released into the stool and are ingested by the intermediate hosts, such as sheep,
cattle, or humans.
The egg larvae invade the bowel wall and mesenteric vessels of the intermediate host, allowing
circulation to
the liver.
• In the liver, the larvae grow and become encysted. The hydatid cyst develops an outer layer of
inflammatory
• When carnivores ingest the liver of the intermediate host, the scolices of the daughter cysts
are released in the
small intestines and grow into adult worms, thus completing the life cycle of the worm.
Hepatic abscesses
water contaminated by the cyst stage of the parasite. Amebiasis generally only involves the
intestine but
can invade the mesenteric venules resulting in liver abscesses. Its only host is the human.
• Pyogenic abscesses can be a result of instrumentation but are most often caused by ascending
cholangitis in
the setting of biliary obstruction. Microorganisms isolated are most often bowel flora. Other
routes of
• Patients with intra-abdominal infections may present with liver abscesses with extension of
bacteria through
the portal venous system. Hematogenous spread via the hepatic artery in patients with
septicemia is rare.
Laboratory Studies
bilirubin, prothrombin time (PT), and activated partial thromboplastin time (aPTT) are usually
within the
reference range.
In the setting of polycystic liver disease (PCLD), greater abnormalities in LFT results are found,
but liver failure
is uncommon.
2. Renal function test results, including blood urea nitrogen (BUN) and creatinine levels, are
often abnormal and
3. GBA - In the presence of hydatid cysts, eosinophilia is noted in approximately 40% of patients,
and echinococcal
With cystic tumors, as with simple cysts, LFT results are normal. There may be mild
abnormalities in some patients.
4. Carbohydrate antigen (CA) 19-9 levels are elevated in some patients. Cyst fluid can be sent for
CA 19-9 testing at
Patients with hepatic abscesses can usually be easily identified on the basis of the clinical
presentation.
Imaging Studies
The clinician has a number of options for imaging the liver in patients with hepatic cysts.
2. CT (see the image below) is also highly sensitive and is easier for most clinicians to interpret,
particularly
3. Magnetic resonance imaging (MRI), nuclear medicine scanning, and hepatic angiography have
a limited
Simple cysts have a typical radiographic appearance. They are thin-walled with a homogenous
lowdensity interior.
PCLD is confirmed by means of ultrasonography or CT, with multiple liver cysts identified at the
time
initial of evaluation.
Central necrosis of large solid neoplasms can mimic cystic hepatic tumors, in that this area of
necrosis appears
cystic.
density, and irregularities in the cyst wall. Unlike many tumors, cystadenoma and
cystadenocarcinoma are rarely
A practical problem in the evaluation of a patient with a cystic hepatic lesion is differentiating
cystic neoplasms
1. Cystic neoplasms tend to have thicker, irregular, hypervascular walls, whereas simple cysts
tend to be
2. Simple cysts tend to have homogenous low-density interiors, whereas neoplastic cysts usually
have
MEDICAL THERAPY
Simple cysts
No medical therapy has proved effective in reducing the size of simple hepatic cysts.
has been abandoned because the recurrence rates are nearly 100%.
Aspiration combined with sclerosis with alcohol or other agents has been successful in some
patients but has
high failure and recurrence rates. Successful sclerosis depends on complete decompression of
the cyst and
apposition of the cyst walls. This is not possible if the cyst wall is thickened or if the cyst is large.
Percutaneous catheters should not be placed to drain simple cysts, because the cavity
becomes contaminated,
No options are available for the medical treatment of PCLD or cystadenocarcinoma because of
the malignant
Hydatid cysts
disease.
In this minimally invasive method, a needle is introduced into the cyst under ultrasonographic
guidance.
Cyst fluid is aspirated and analyzed. Hypertonic saline or ethanol is then injected and
reaspirated.
PAIRD (puncture, aspiration, injection, reaspiration, drainage) is similar to PAIR except that a
catheter is
left in place after completion of the procedure. PAIRD is most often used for large cysts.
Patients should be followed clinically after PAIR treatment. Recurrence is increased in more
complicated
PAIR should only be performed in highly specialized centers with appropriately trained and
experienced staff.
In addition, an anesthesiologist should be present for monitoring and treatment in the event of
anaphylactic
In surgical patients, antihydatid agents are generally given perioperatively; and continued only
in those
who have spillage of cyst fluid at the time of operation or to those with cyst rupture.
Antihydatid agents are used with percutaneous treatment. Medical therapy should be started
4 days before
percutaneous treatment and continued either for 1 month (albendazole) or for 3 months
(mebendazole).
Hepatic abscesses
More likely, these patients will require the addition of percutaneous drainage for eradication.
SURGICAL THERAPY
Simple cysts
Most patients with simple cysts are asymptomatic and require no treatment. When the cysts
become large and
"Unroofing" the cyst by excising the portion of the wall that extends to the surface of the liver.
Excision of this portion of the cyst wall at the liver surface produces a saucer-type appearance
in the
remaining cyst so that any fluid secreted from the remaining epithelium leaks into the peritoneal
cavity
Although ablating the remaining epithelium with electrocautery or an argon beam coagulator
is possible, this
generally is not required because the volume of fluid secreted each day can be absorbed by the
peritoneum
without any consequence. Furthermore, ablation of the cyst wall can lead to bleeding or bile
leak secondary
The cyst wall should be sent to pathology to confirm the diagnosis and exclude cystadenoma
or
Can be done via laparotomy, but today, cyst unroofing can be successfully performed
laparoscopically.
In adult PCLD (AD-PCLD), enlargement of the liver occurs slowly and only rarely compromises
liver function.
Only those patients with clearly disabling pain should be considered for surgery.
In patients with PCLD, the surgical goal is to decompress as much of the cystic liver as possible.
This can be
accomplished by a combination of unroofing and fenestration or, in selected patients, by
resection of the
Recurrence of symptoms with either procedure is high as new cysts replace those that have
been resected. Small
Neoplastic cysts
Several surgical methods for treatment of cystadenoma and cystadenocarcinoma have been
described.
Regardless of surgical technique, all surgical options should result in complete ablation of the
tumor.
Fenestration and complete fulguration have also been implemented, although, in this method,
complete
Hydatid cysts
All patients with hydatid disease should be considered for percutaneous or surgical treatment
because of the risk of
1. Risk of anaphylaxis from spillage of cyst fluid containing eggs and larvae into the peritoneal
cavity and
To prevent these problems, most surgeons use a technique in which the cyst contents are
aspirated and replaced
with a hypertonic saline solution to kill residual daughter cysts in the germinal membrane before
unroofing and
pericystectomy.
The goal of the latter procedure is to excise the germinal membrane, leaving the inflammatory
and fibrous
components of the cyst wall in situ. Attempts to excise the entire cyst wall or to perform formal
hepatectomy
for hydatid cysts have largely been abandoned because of increased surgical morbidity.
Hepatic abscesses
Other surgical indications include large cysts at risk of rupture and abscesses not anatomically
amenable to
percutaneous treatment.
POSTOPERATIVE CARE
In patients undergoing laparoscopic unroofing of simple hepatic cysts, the orogastric and
bladder catheters
A light diet is offered the evening of surgery, and most patients can be discharged home the
following day.
Generally, recovery is rapid, and most patients resume full activity within 1 week.
Patients can shower with the waterproof dressings in place the day after surgery. The
dressings can be
Complications
Unexpected leakage of bile from the cut edges of the cyst can lead to a subhepatic or
subphrenic fluid
In patients with PCLD, unroofing and fenestration procedures should be performed with care
to avoid injury
to biliary or vascular structures in the compressed hepatic parenchyma between the cysts.
In patients with hydatid cysts, spillage of cyst contents into the peritoneal cavity, which may
cause
Long-Term Monitoring
After successful laparoscopic unroofing of a simple liver cyst, the patient is seen at a follow-up
visit within 2
weeks and again 6 weeks after surgery to assess symptomatic relief and to identify
complications, such as
14. Liver abscesses: etiology, pathogenesis, clinical features, diagnosis, and treatment.
TYPES
2. Amoebic liver abscess due to Entamoeba histolytica accounts for 10% of cases. The incidence
is much
3. Fungal abscess, most often due to Candida species, accounts for less than 10% of cases.
The most common organisms are Streptococcus milleri and Escherichia coli, but other enteric
organisms such
as Streptococcus faecalis, Klebsiella and Proteus vulgaris also occur, and mixed growths are
common.
Common causes
infection is of biliary origin. Abscesses involving K pneumoniae have been associated with
multiple
cases of endophthalmitis
2. Instrumentation
3. Other routes of contamination include the portal vein and hepatic artery (sepsis).
a) Haematogenous spread through the portal vein: Other causes of intra-abdominal sepsis
intraabdominal infections, including appendicitis or diverticulitis
b) Hematogenous spread via the hepatic artery in patients with septicemia is rare.
CLINIC
Chills
Anorexia
Malaise
Cough or hiccoughs due to diaphragmatic irritation may be reported. Referred pain to the right
shoulder may
be present.
DIAGNOSIS
TREATMENT
More likely, these patients will require the addition of ultrasound-guided percutaneous
drainage for
Other surgical indications include large cysts at risk of rupture and abscesses not anatomically
amenable to
percutaneous treatment.
CLINIC
The most common presentation is with dysentery, but it may also present with an amoebic
abscess, the common
DIAGNOSIS
Isolation of the parasite from the liver lesion or the stool and confirming its nature by
microscopy.
TREATMENT
Often patients with clinical signs of an amoebic abscess Empirical tx with metronidazole
(400–
800 mg t.d.s. for 7–10 days) and investigated further only if they do not respond.
For abscess that is expected to rupture Aspiration; also helps the penetration of
metronidazole.
Mediastinum - part of the chest cavity, bounded by the rear surface of the sternum - in
front; thoracic spine - back; right and left mediastinal pleura - on the sides; the upper
The mediastinum is divided along the horizontal plane through the upper edge of the III rib,
into the upper and lower. By a conventional plane passing frontally through the trachea
and the main bronchi, the mediastinum is divided into anterior and posterior.
The anterior mediastinum contains: the thymus gland, superior vena cava and its
tributaries - brachiocephalic and unpaired, ascending part and aortic arch, pulmonary
trunk, pulmonary veins, phrenic nerves, lymph nodes, trachea and main bronchi; in its
lower section is the heart and pericardium.
In the posterior mediastinum are located: esophagus, lymphatic duct, thoracic aorta,
unpaired and semi-unpaired veins, vagus nerves, sympathetic trunks, pectoral aortic
plexus.
The mediastinum is innervated by the thoracic aortic plexus and its derivatives - the
Blood supply to the mediastinum is carried out by numerous arterial branches originating
directly from the aorta - mediastinal, bronchial, esophageal, pericardial, and from its
branches of the posterior intercostal arteries, from the internal mammary arteries.
The outflow of venous blood occurs in unpaired, semi-unpaired, and internal chest veins.
Lymphatic vessels from the mediastinal organs go to the following lymph nodes:
mediastinitis;
MEDIASTINITIS CLASSIFICATION
I of . Primary or traumatic;
II . Secondary
B. By prevalence:
3. Spilled (phlegmon).
1. Serous.
2. Purulent.
3. Putrid.
4. Anaerobic.
5. Gangrenous.
D. Localization:
1.The front.
2. The rear.
3. Total.
I Acute mediastinitis:
- fulminant form;
- acute form;
- simple form.
- primarily chronic;
- secondarily chronic.
CAUSES
1. Traumatic mediastinitis due to open and closed injuries; intraoperative injuries, damage
4. The appearance of putrefactive and anaerobic forms of crepitus in the jugular cavity.
inhalation).
4. The appearance of putrefactive and anaerobic forms of crepitus in the jugular cavity.
inhalation).
6. The appearance of putrefactive and anaerobic forms of crepitus over the clavicle.
7. Paravertebral symptom of Rawicz-Shcherbo and Steinberg (the appearance of rigidity of
of the intercostal veins, effusion in the pleural cavity and in the pericardium.
9. Extension of the boundaries of dullness on both sides of the lower thoracic vertebrae.
11. X-ray - shadows in the posterior part of the mediastinum, with perforation of the
Pathogens.
Mixed aerobic and anaerobic microflora - 74%; 26% - only aerobic flora.
Diagnostics:
- MRI;
-CT.
Razumovsky.
2. In case of anterior mediastinitis - rib-sternal drainage from the jugular notch to the
xiphoid process.
The most universal and reliable way is mediastinotomy via right-sided thoracotomy.
treatment;
treatment;
Mediastinal tumors are relatively uncommon and there are many different types.
CLASSIFICATION- PATHOLOGICAL
• NEUROGENIC TUMOURS
• LYMPHOMA – HODGKINSDISEASE ,
Mediastinal Tumors
– Many years are needed to develop adequate clinical experience Includes a wide variety
of lesions
– The approach used by authors is the opposite of what the clinician needs
• Age, gender
• Radiographic characteristics
❖ Often available:
• Duration of symptoms
❖ Sometimes available:
SLE)
and associated
❖ Non-invasive (Imaging)
• CT • CT/PET • MRI
• TTNA
❖ Surgical techniques
• Mediastinoscopy • Mediastinotomy
• A few are teratoma in age 40-49 ü ~15% comprised of miscellaneous rare tumors
Thymoma
• Age onset: 30-40 yrs (with MG); 60-70 yrs (without MG)
Myasthenia Gravis
Lymphoma
• Symptoms: fever, wt loss, night sweats, compressive symtoms like pain, dyspnoea,
• Malignant, Neurofibrosarcoma
• Benign, ganglioneuroma
❖ Paraganglionic tissue
• MRI
• Observation
Conclusion
to assign the tumor to one of the mediastinal anatomic compartments. MRI and PET-CT
• Histological confirmation is most often needed for suspected lymphomas and in locally
• More than half of the tumors are in the anterior region, the remaining are equally
• In the anterior region the most common tumors are thymomas in adults and lymphomas
• In the visceral region more than half of the tumors are cysts. The remaining are
• In the paravertebral region almost all tumors are from nervous structures. Malignant
esophageal diseases;
The length of the esophagus depends on age, head position, body length and gender,
fluctuating in women within 23-24 cm, and in men within 25-30 cm. Currently, it is believed
The beginning of the esophagus is normal in a 2-year-old child located at the level of 4
cervical vertebra, by the age of 12 - C5, in an adult - C6, and in the elderly - C7. The lower
border is at the level of Th10-11. The cardia is projected onto the anterior surface of the
chest at the level of the VII left rib. The width of the lumen of the esophagus at the level of
the upper border is usually 18 mm, at the level of the lower - 22 mm, and at the level of the
thoracic region 21-25 mm. The thickness of the esophagus wall is on average 3-4 mm.
The entrance to the esophagus is formed from the inside by a lip-shaped fold due to the
abdominal. However, it seems fair to single out the fourth, functionally important
The cervical esophagus begins at C6 and ends at Th2. This rather short section of the
esophagus (5-6 cm), is completely covered with a layer of loose connective tissue that
passes into the tissue of the upper mediastinum, which makes it quite mobile and supple
when swallowed. In this section, 2 / 3-3 / 4 foreign bodies get stuck. The anterior surface
of this section of the esophagus is adjacent to the trachea and the left lobe of the thyroid
gland, the posterior to the spinal column (C6-Th2.), The lateral to the thyroid gland, carotid
The thoracic esophagus begins at the upper border of the posterior mediastinum (Th2)
and is pumped at the entrance to the esophageal opening of the diaphragm at the level of
Th9-10. This longest section of the esophagus (16 - 18 cm) is closely adjacent to the
mediastinal pleura and is separated from the prevertebral fascia with a thin layer of loose
fiber. From Th2-6, the esophagus lies to the left of the trachea, at the level of Th3 in front it
crosses with the aortic arch, at the level of Th6 - with an unpaired vein. At a height of Th5,
the esophagus is quite closely adjacent to the left main bronchus and tracheal bifurcation
The embryological community of the trachea and esophagus results in dense connective
the left of the esophagus at this level are the thoracic lymphatic duct, recurrent nerve,
aortic arch, or subclavian artery. At the level of bifurcation, the left and right behind the
esophagus are the vagus nerves. Below the esophagus is adjacent the posterior wall of
the left atrium, separated by the pericardium. 2-3 cm above the diaphragm near the
surface of the left ventricle, the esophagus deviates to the left at an angle. Mediastinal,
esophagus and very rarely at the level of the general aortic-esophagus, normally at a level
of Th9-10 2-3 cm in front of the spinal column and 1 cm to the left of the midline of the
body. The bro-muscular ring involved in the opening of the cardia ensures its tightness,
and the rather loose fiber inside the diaphragm provides the esophagus with mobility in the
longitudinal direction. This functionally important part of the esophagus, which does not
The subphrenic (or abdominal) section of the esophagus , referred to in the literature as
the vestibule of the cardia, has an average length of 3-4 cm (1-7 cm). Its length depends
on the standing of the domes of the diaphragm, the breathing phase, the mobility of the
This section between the dome of the diaphragm and the anatomical cardia is adjacent to
the posterior surface of the left lobe of the liver and is covered in the front and sides of the
peritoneum. In the surrounding loose fiber are the lymph nodes of the cardia and branches
of the vagus and sympathetic nerves. The diaphragmatic and abdominal esophagus are
The outer lower border of the cardia is considered to be the acute angle of the esophagus
entering the stomach, usually formed by the end of the first year of life, - the
angle of His. It represents the angle of transition of one side wall of the esophagus into a
large curvature of the stomach, while the other side wall smoothly passes into a small
curvature. It is believed that functionally this place prevents regurgitation and its
effectiveness directly depends on the severity of the angle of His. The internal lower border
of the cardia is usually recognized as a fold of the mucous membrane (plica cardiaca). The
air bladder of the stomach and intragastric pressure contribute to a snug t of the valve of
the mucous membrane to the right wall, thereby preventing the contents of the stomach
from being thrown into the esophagus. Together with plica cardiaca the antireflux function
is performed by the muscular structures of the cardia at the Z-line level and the cardia
outlet.
more than 1/3). In places of narrowing, foreign bodies are more often delayed, injuries,
esophagitis, scars and neoplasms occur. The first narrowing is formed at the entrance to
the esophagus by the pharyngeal-esophageal sphincter at level C6. The second
narrowing, aortic, is less noticeable, its origin is explained by the pressure of the aortic
arch on the esophagus at the Th3 level: this narrowing becomes more pronounced at the
time of passage of food or with aortic sclerosis. At the level of Th5, there is a third
narrowing, due to the depression of the left main bronchus into the wall of the esophagus.
The fourth narrowing is caused by a squeezed esophagus with the legs of the diaphragm
at the level of - Th10. This zone (epicardia) can in pathological cases increase to 7-8 cm.
Esophageal vascularizationin comparison with other parts of the digestive tract, it is less
pronounced due to the lack of a single esophageal artery. The cervical esophagus is
supplied with branches of the lower thyroid and partly the left subclavian arteries. The
thoracic section is vascularized by the branches of the bronchial and intercostal arteries
and the thoracic aorta. The abdominal section covered with the peritoneum is better
supplied with blood than others, receiving food from the lower diaphragmatic and left
gastric arteries (Figure 2). The intramural vasculature is most developed in the
submucosa, from which the arterial plexus nourishes the mucous membrane and muscle.
Blood flows through the venules into a rather complex structure of the venous plexus, the
main collector of which is the central submucosal plexus, lying next to the arterial. The
main venous arteries in the cervical spine are the thyroid and bronchial, in the chest -
paired and unpaired (system of the superior vena cava), in the abdominal - veins of the
stomach and liver (portal vein system). Thus, the veins of the thoracic and abdominal
Esophagus lymph nodes are conditionally divided into 5 groups: lymph nodes of the
common carotid artery, jugular and subclavian veins, bifurcation, paraaortic and cardiac
nodes. Lymphatic drainage is carried out through well-developed lymphatic plexuses in the
mucosa and submucous membranes. For the lymphatic system of the esophagus, a
pharynx or down towards the stomach. In this regard, metastases in cancer of the
esophagus initially spread intramurally and only later are found in regional lymph nodes.
Sometimes the lymphatic vessels open directly into the thoracic duct, which should
be taken into account in the diagnosis and surgical treatment of cancer. Usually, the lymph
of the cervical esophagus is sent to regional nodes near the trachea (paratracheal nodes)
or along the jugular vein. Lymph of the middle third of the esophagus flows into the
mediastinal, bifurcation and tracheobronchial lymph nodes. From the lower esophagus,
lymph is directed along the organ, so with cancer of this part of the esophagus, cardia or
upper stomach, metastasis to the supraclavicular lymph nodes is possible. The common
development of the esophagus and stomach is also confirmed by the outflow of lymph
from the lower segments of the esophagus to the lymph nodes of the upper stomach and
carried out through the vagus and recurrent nerves, sympathetic through the nodes of the
border and aortic plexuses, branches of the pulmonary and cardiac plexuses, the fibers of
the solar plexus and ganglia of the subcardia. Numerous nerve branches form the
superficial anterior and posterior plexuses of the esophagus. The anterior one is formed
mainly by the fibers of the right vagus nerve, the posterior by the left. It is considered
proven the existence of many anastomoses between the nerve structures in the plexuses.
adventitious, intermuscular and submucosal. They have peculiar ganglion cells (Dogel
cells) that determine autonomous internal innervation and local regulation of the motor
function of the esophagus. The vagus nerves, with their meat fibers, are connected with
the intramural plexuses, and the non-vagus nerves with other intraparietal plexuses. Some
of the soft fibers are pumped into muscle cells. Thus, the esophagus, like the heart, has its
own autonomous nervous system. Reflex self-regulation is carried out mainly by intramural
plexuses.
The cervical part of the esophagus is innervated by the recurrent nerve, the pectoral part
by the branches of the vagus and sympathetic nerves, and the lower celiac nerve. The
fibers of the recurrent nerve innervate the striated muscles, the sympathetic - the smooth
muscles of the esophagus. Efferent nerve fibers, in addition to muscles, innervate the
glands of the esophagus, and afferent fibers (Th5-7) carry out sensory innervation. The
mucous membrane of the esophagus is sensitive to thermal, pain and tactile irritations,
with the most susceptible distal segments and cardia. The area of the mouth of the
esophagus and the place of physiological constrictions are most sensitive to mechanical
irritation. Sensory innervation is carried out by the vagus nerve, the main regulator of
esophageal motility. The sympathetic nervous system controls the tone of the esophagus.
In this way, the esophagus and cardia contain their own intramural neuromuscular
apparatus, regulated by the central and autonomic nervous system. The innervation of the
legs of the diaphragm, especially the right one, is provided by the branches of the phrenic
nerves.
Histology. The wall of the esophagus consists of 4 layers - the mucosa, submucosa,
muscle and adventitia. Adventitia of the abdominal esophagus passes into the serous
cover.
The mucous membrane of the esophagus consists of 20-25 layers of stratified squamous
epithelium. Its thickness is 0.5-0.8 mm. Closer to the lumen are layers of rejected cells,
scaly cells are located deeper, and behind them are layers of prickly cells on a thin
basement membrane. The esophagus epithelium lies on a thin elastic connective tissue
plate, which in turn is separated from the submucosa by the smooth muscle layer with a
longitudinal arrangement of muscle fibers. Due to the elasticity of the mucous membrane
and its larger surface, in comparison with a powerful annular muscle layer, 3-4 longitudinal
folds are formed in it, most pronounced in the middle and lower parts of the organ.
In the area of transition of the squamous epithelium of the esophagus into the cylindrical
epithelium of the stomach, a dentate border is often located above the anatomical cardia.
The folds of the mucous membrane are collected in the form of a socket and close the
cardia. In the mucous membrane of the thoracic esophagus are small shallow branched
tubular glands that secrete mucus. In their excretory ducts, islets of ciliated epithelium can
most often in the abdominal part, there are cardiac glands containing pepsin-producing
parietal cells (similar to the cardiac glands of the stomach). Parts of the mucous
the gastric epithelium are of great importance in the development of peptic ulcers and
strictures.
The submucous membrane is a layer of loose connective tissue with less mobility, but with
a more powerful network of blood vessels, nerves and glands than the mucous membrane.
In the upper segments of the esophagus, the submucosa contains about 200 deep, or
true, glands. Their long excretory ducts open caudally at an angle into the lumen of the
esophagus. These glands secrete thick mucus that has protective properties. The
submucous membrane has sufficient extensibility, therefore, suturing during surgery does
The muscular membrane, the most massive (up to 0.2 cm thick), consists of 2 layers - a
powerful circular and twice as thin longitudinal. Blood vessels and the intramuscular nerve
plexus are located in a small layer of connective tissue. The longitudinal muscle layer of
the esophagus is a continuation of a similar layer of the pharynx and, in turn, passes into
the external muscle layer of the stomach, forming a single functional system. The fibers of
this layer communicate with the vessels supplying them with the muscles of the left main
bronchus and mediastinal pleura. The muscular membrane of the upper third of the
esophagus consists of striated fibers, the lower of smooth muscle, and the middle of mixed
esophagus is represented only by striated fibers or only smooth muscles. This structure
predisposes to the development of intramural muscle tumors. Such muscle tumors can
probably arise from islands of “dormant” muscle germ cells, which begin to grow rapidly at
a certain stage.
The thickenings of the circular and spiral-like muscle fibers that are quite visible in the
sections, performing the function of the pulp, are located at the entrance to the esophagus
retrograde throwing of food into the throat, and the pharyngeal muscle prevents air from
entering the stomach during breathing - the “air-tight sphincter”. The existence of an
independent sphincter in the area of the anatomical cardia has not been conclusively
established.
The outer connective tissue membrane consists of interwoven bundles of collagen and
elastic fibers through which the blood, lymph vessels and nerves supplying all layers pass.
Advent occurs in the periophageal tissue and connective tissue of adjacent organs of the
stomach. The swallowing process is divided into 3 consecutive phases. The first phase is
to push liquid or chewed solid food from the mouth into the throat. It is proved that as soon
as an arbitrarily swallowed lump of food passes the base of the tongue and palatine
arches, swallowing becomes uncontrollable and the second purely reflex phase of
swallowing begins. The center of the swallowing reflex lies in the medulla oblongata and
the brain bridge. With lesions of these parts of the brain, a violation of the second, reflex,
phase of swallowing is manifested by regurgitation of food in the nasal cavity, mouth and
its aspiration. The third phase is the passage of food through the esophagus through the
cardia into the stomach. The function of the esophagus at this stage seems very simple
and understandable, but in fact it remains to this day the subject of heated debate.
The main importance is given to the advancement of food along the esophagus by the
energy supply created by the spraying effect of the pharynx, others consider gravity and
the hydrostatic pressure of food as the main ones, while others recognize only the role of
active wall contraction. At present, the action of all these factors is recognized with a
predominance of each depending on the quantity and quality of food, body position,
condition of the neuromuscular apparatus of the esophagus and the whole organism. So, a
sip of water quickly, in 2-3 seconds, slips into the stomach, significantly ahead of the active
motility of the esophagus. If you drink a lot of fluid in one gulp, then the esophagus and
cardia gape for a long time without movement and only after the last sip does a peristaltic
wave appear, covering the lumen of the esophagus and cardia. Believed that the third
phase of the act of swallowing liquid food is provided mainly by gravity, hydrostatic
pressure and the injecting effect of the pharynx. The experiment with nerve transection
causing the swallowing reflex and the injecting effect, and observations of the astronauts
in zero gravity showed that the act of swallowing under such conditions does not suffer
important role of esophageal motility in promoting any food. The leading role of the
peristaltic wave is clearly manifested when a dense or viscous food lump passes through
the esophagus - swallowing slows down 3-5 times and lasts from 6 to 15 seconds. From
the open mouth of the esophagus, it spreads to the walls of the esophagus, causing a
propulsive peristaltic wave directed towards the stomach. The walls of the esophagus in
front of the food lump open and close behind it. The segmented segmental contraction is
5-6 cm long; ahead of him, an expansion of the lumen of the esophagus is noticeable. The
contraction of the longitudinal muscles causes the food lump to move towards the
stomach, and the ring of circular muscles, contracting behind the lump, does not allow it to
go back. Thus, the advancement of the food lump is ensured by a uniform and consistent
reduction of the muscle layers of the esophagus. The average velocity of the peristaltic
wave is 3-5 cm / s, the duration of the reduction of the upper section is about 2 seconds,
and the lower one is about 3 seconds. The segmented segmental contraction is 5-6 cm
long; ahead of him, an expansion of the lumen of the esophagus is noticeable. The
contraction of the longitudinal muscles causes the food lump to move towards the
stomach, and the ring of circular muscles, contracting behind the lump, does not allow it to
go back. Thus, the advancement of the food lump is ensured by a uniform and consistent
reduction of the muscle layers of the esophagus. The average velocity of the peristaltic
wave is 3-5 cm / s, the duration of the reduction of the upper section is about 2 seconds,
and the lower one is about 3 seconds. The segmented segmental contraction is 5-6 cm
long; ahead of him, an expansion of the lumen of the esophagus is noticeable. The
contraction of the longitudinal muscles causes the food lump to move towards the
stomach, and the ring of circular muscles, contracting behind the lump, does not allow it to
go back. Thus, the advancement of the food lump is ensured by a uniform and consistent
reduction of the muscle layers of the esophagus. The average velocity of the peristaltic
wave is 3-5 cm / s, the duration of the reduction of the upper section is about 2 seconds,
and the lower one is about 3 seconds. the advancement of the food lump is ensured by a
uniform and consistent reduction of the muscle layers of the esophagus. The average
velocity of the peristaltic wave is 3-5 cm / s, the duration of the reduction of the upper
section is about 2 seconds, and the lower one is about 3 seconds. the advancement of the
food lump is ensured by a uniform and consistent reduction of the muscle layers of the
esophagus. The average velocity of the peristaltic wave is 3-5 cm / s, the duration of the
reduction of the upper section is about 2 seconds, and the lower one is about 3 seconds.
esophagus. Art. Upper and lower physiological sphincters separate this zone of
weakly negative pressure from positive pressure in the pharynx and stomach. The tonic
tension of the circular fibers of these sphincters normally creates the upper and
accompanied first by a sharp increase in pressure in the area of the upper sphincter for
tenths of a second, and then within 1 second, a drop in pressure not lower than
atmospheric. The resulting primary peristaltic wave creates an average pressure of 70-90
cm
of water. Art., ranging from 30 to 140 cm of water. Art. As food moves through the
esophagus, the pressure and speed of the peristaltic wave weaken to a minimum. The
lower zone of high pressure creates the abdominal segment of the esophagus. The
pressure in this zone is usually 10 cm water. Art. higher pressure in the cavity of the
stomach. The lower elevated pressure zone is a powerful anti-regurgitation barrier due to
its one-way cross-country ability. If the pressure of 5 cm of water is enough to pass food
from the esophagus into the stomach. Art., then for the artificial reproduction of reflux, it is
necessary to raise the pressure to 100 cm of water. Art. This explains the
positions and space frights. If the pressure of 5 cm of water is enough to pass food from
the esophagus into the stomach. Art., then for the artificial reproduction of reflux, it is
necessary to raise the pressure to 100 cm of water. Art. This explains the absence of
gastroesophageal reflux with sharp abdominal compression, upside down positions and
space frights. If the pressure of 5 cm of water is enough to pass food from the esophagus
into the stomach. Art., then for the artificial reproduction of reflux, it is necessary to raise
the pressure to 100 cm of water. Art. This explains the absence of gastroesophageal reflux
with sharp abdominal compression, upside down positions and space frights.
Usually, the lower esophageal sphincter opens reflexively 3-5 seconds earlier than the
primary wave of esophageal motility. Recently, much attention has been paid to the
hormonal regulation of the digestive system. Some authors associate the pathology of the
cardiac sphincter with the hormones of the APUD system - gastrin and secretin. Gastrin
increases the tone of the sphincter and further increases the level of high blood pressure.
Intravenous infusions of secretin, on the contrary, reduce the pressure and tone of the
cardiac sphincter. Thus, the functioning of the esophagus is regulated not only by the
central and autonomic nervous system, but also by the endocrine system of the digestive
tract. This ensures a normal act of swallowing, coordination of the activity of sphincters
and muscle, layers of the esophagus, creating propulsive peristalsis. Outside of the act of
swallowing, a secondary peristaltic wave can occur in the esophagus, inferior in amplitude
and force to the primary. This non-swallowing peristalsis is called “purifying” or “sentinel”. It
factors and somatic suffering of the organs of the abdominal and thoracic cavities
(viscerovisceral and vago-vagal reflexes). The type of food or thoughts about it, fear, fright, joy
change the tone of the esophagus and sometimes lead to its motor dysfunction. Irritation
of the trachea and bronchi of the stomach, duodenum, gall bladder, diaphragm and other
1. Atresia.
2. Strictures.
3. Idiopathic expansion.
a) achalasia or cardiospasm;
2. Esophageal diverticula:
a) closed and open injuries of the esophagus; b) foreign bodies of the esophagus;
· Concentrated alkalis.
1. X-ray method. This is a simple, safe and quite physiological method. It allows one to
study with great confidence the topography, anatomical structure and, in particular, the
It can be performed even in patients in an extremely serious condition, when the use of
other instrumental methods is completely excluded. In all cases, the radiologist must
adhere to the principle of “from simple to complex” and strive with a minimum of methods
An X-ray examination begins with an overview uoroscopy of the organs of the chest and, if
necessary, the abdominal cavity (first stage). The purpose of a chest x-ray in patients with
pathological changes in the lungs and heart, as well as the detection of foreign bodies and
signs of organ wall perforation. This tactic of pre-contrast research often reveals important
radiological symptoms.
The next stage is a contrast polypositional study of the esophagus, combining uoroscopy
and radiography. Contrasting of the esophagus should begin with the use of a regular
liquid barium suspension of sour cream-like consistency (100 g of barium sulfate in 100 g
of water). Good pneumorelief and contrast of the esophagus can be obtained by asking
the patient to drink liquid barium suspension in one gulp, in large sips or in small portions,
like hot tea. Sometimes for a more detailed study of the relief it is necessary to examine
patients in the positions of Trendelenburg or Quincke (the pelvis or legs are located above
the head). For better visibility of the folds of the esophagus, substances that increase its
esophagus. When using the “tight lling” method with liquid barium suspension, such
nodes of varicose veins, paraesophageal and sliding hernias of the esophageal opening of
the diaphragm, ulcerative defects of the mucous membrane are well detected. More
precisely, the localization and size of foreign bodies can be determined. To detect
recommended.
Since the use of X-ray examination is especially useful in assessing the contractility of the
gastroesophageal reux disease, cardiac achalasia and cardiospasm. In this case, the aim
of the study is to identify the ability of the cardia to open in response to swallowing, to
insufficiency, and to evaluate the speed and effectiveness of expelling the reflux contrast
When using the double contrasting technique by using a suspension of finely dispersed
barium, which has more pronounced adhesive properties, and simultaneously spraying the
organ with gas, it is possible to more accurately assess the relief of the mucous
membrane, to reveal small erosions and ulcers, to diagnose not only pronounced, but also
interpret the physiology and pathophysiology of the esophagus in the clinic. Diagnostic
esophagus. In practical work, the following pharmacological tests are more often
subcutaneously with an examination of the esophagus after 7-10 minutes), atropine (1-1, 5
ml of a 0.1% solution subcutaneously with a study after 10-15 minutes), metacin (2-4 ml of
prostigmine (1 ml)
possible to most objectively assess the condition of the esophageal mucosa: to determine
the severity of inflammatory changes, mechanical and chemical damage, to identify ulcers
and erosion, fistulas, and metaplasia zones of the epithelium. The method is highly
informative in identifying benign and malignant neoplasms, including in the early stages of
their development. Significant help in this can be provided by chromoscopy - the use of
various dyes (Lugol's solution, indigo carmine, toluidine blue) in order to contrast the
surface of the mucous membrane. Thanks to this technique, areas with altered epithelial
lining become more visible. The indisputable advantage of endoscopy is the ability to
perform targeted biopsies from clearly pathologically altered or suspicious sections of the
mucosa and obtain material for histological and cytological studies. In addition, during the
study, the elasticity and extensibility of the wall of the esophagus can be determined,
which is especially important in the diagnosis and determination of treatment tactics for
bougon guide, and then the esophagus is dilated and dilated. For the treatment of postburn
strictures, lidase can be injected directly into the scar tissue through an endoscope.
of the dilated veins of the esophagus is widely used by chipping the bed of a vessel or
indications.
the esophagus with exciting forceps, loops, baskets, scissors and other special devices.
3. The manometry of the esophagus. It is rarely used in practice, however, with its help it
is possible to quantify the speed and amplitude of peristaltic waves, the duration of the
opening of the lower esophageal sphincter, obtain information about the length and tone of
the lower esophageal sphincter, its localization with respect to the diaphragm, and in some
cases reveal a sliding hernia of the esophagus aperture. Thus, the method is very useful in
the differential diagnosis between diseases such as insufficiency of the lower esophageal
4. Sample with a solution of methylene blue. This is a less sensitive than pH meter
consists in aspirating the esophageal contents through a probe after introducing a glass of
liquid through it into the cavity of the stomach, tinted with 3 drops of a methylene blue
5. CT. With the help of CT, which allows to obtain a series of images of transverse
sections of the neck, chest, upper floor of the abdominal cavity, the depth of structural
damage to the esophagus wall can be most reliably estimated, which is especially
important when determining the local spread of the tumor process. In this case, computed
tomography with great accuracy reveals metastases in distant organs. This allows you to
more accurately determine both the stage of the malignant neoplasm, as well as
indications for surgical and combined treatment methods, to evaluate the effectiveness of
the therapy in repeated studies. In addition, with the help of CT, benign formations of the
nodes. The accuracy in determining the T and N stages of esophageal carcinoma with
endoscopic sonography reaches 85% and 75%, respectively, and with CT - 60% and 74%.
The method owes its accuracy to the analysis of the details of the image of the five- layer
structure of the wall of the upper gastrointestinal tract. The disadvantages of the method
include the impossibility of holding the instrument further than the proximal edge of the
lesion site in case of severe stenosis of the esophagus, as well as low specificity in
7. pH Metrics of the esophagus. The method can be used both for a monitor study of the
intraesophageal medium, and for various functional tests characterizing the motor activity
of the esophagus and the effectiveness of the cardiac closure mechanism. 24-hour
intraesophageal pH monitoring is the most sensitive and specific test for the diagnosis of
gastroesophageal reflux disease and is considered the “gold standard”. At present, 6- and
disorders of the motor function of the esophagus and its transport ability. The researcher is
given a drink of a colloid labeled with technetium (99mTc) diluted in water. Using a gamma
esophagus and stomach are performed. Only as a result of this study is it possible to
quantify gastroesophageal reflux and the rate of emptying of the esophagus. The
sensitivity of the method reaches 90%. Thus, radionuclide scintigraphy is the most
9. Acid perfusion test . It was proposed in 1958 by Bernstein and Baker, which serves to
elucidate the causes of the appearance of typical symptoms of esophagitis and the
differential diagnosis of cardiac and esophageal genesis of pain. A 0.9% solution of sodium
chloride is injected into the esophagus of the subject at a rate of 6-7.5 ml / min for 15-30
minutes. Then the solution is replaced with 0.1N hydrochloric acid. The test is considered
positive if the administration of 0.1 N hydrochloric acid causes pain, heartburn and other
typical symptoms of esophagitis, and with the repeated administration of a 0.9% sodium
As follows from the foregoing, a fairly wide range of diagnostic methods are currently used
for instrumental examination of the esophagus, from which it is necessary to choose the
Upper esophageal dysphagia is caused by diseases of the thyroid gland, lymph nodes,
muscles, spine and other organs, as well as numerous central and peripheral disorders of
the nervous regulation of the functions of the mouth, pharynx and mouth of the esophagus.
Muscular discoordination, paresis or paralysis of one or more muscles involved in the act
of swallowing leads to its disorder. Nutrition, especially the intake of liquid food, in such
patients is difficult due to its easier throwing into the nose or respiratory tract. Swallowing
its derivatives. This often painful dysphagia should be called dry. After the abolition of
moments, eating dry food or in a hurry and other factors can cause even a healthy person
posterior mediastinal organs (vessels, nerves, lymph nodes, heart, pleura, connective
tissue, etc.). Expansion of the heart chambers (to a “bovine heart”), atriomegaly with mitral
defect, abnormalities of the heart, aorta, subclavian artery, tumors and pericardial cysts,
mediastinum are usually accompanied by mild dysphagia, and malignant tumors and
Tumors and cysts of the diaphragm, Bohdalek hernia, hepatomegaly, splenomegaly cause
diverticula, foreign bodies, acute and chronic inflammations of the oral mucosa, pharynx
and larynx, xerosis, Plummer-Winson syndrome, and others are mildly severe mild
disorders and organic lesions (esophagitis, ulcers, strictures, tumors, diverticula, etc.).
Dysphagia after ingestion of any food is more characteristic for esophagitis, after liquid -
for functional pathology, after solid - for organic narrowing of the lumen by a tumor,
stricture, stenosis.
Lower intraesophageal dysphagia often reflects chalasia and achalasia, hiatal hernia,
reflux esophagitis, ulcers, strictures, including circular stricture of the esophagus, tumors,
transcardial displacement of the mucous membrane, epiphrenic diverticuli, and others from
rare , hernias and tumors) there is a special type of dysphagia with variable intolerance to
The paradoxical dysphagia, in which solid food passes better than liquid, and large pieces
of food is better than small ones, is described in the literature as a symptom of
dysphagia with a horizontal position of the body, although this symptom is also
that dysphagia does not always indicate cancer stenosis, however, it should always cause
the thought of cancer. When dysphagia appears, patients tend to panic, identifying it with
Typically, patients refuse first solid and rough food (second courses), then from porridge
and soups (first courses) and, finally, from liquids (third courses). Sometimes in the
dynamics of dysphagia can weaken or even disappear, allowing you to completely eat
lunch, which is explained by ulceration and decay inside the tumor. This “bright” period of
false remission is usually short-lived, and dysphagia again becomes a cardinal clinical
Pain is a frequent manifestation of both functional disorders and organic lesions of the
esophagus and cardia. Painful sensations are usually localized at the level of the lesion -
usually behind the sternum, occasionally with radiation to the neck, jaw, shoulder, back,
epigastric region (pain abdominal syndrome). Pain along the esophagus can be
Functional disorders are accompanied by pain behind the sternum during meals or in
infarction in such cases. Dysphagia and pain with dysfunction are not associated with
physical activity, the ECG is normal, taking nitroglycerin does not help. Esophageal hernia
or large epiphrenic diverticulum when filled with food leads to afternoon pain. Reflux
esophagitis and esophagitis are accompanied by pain after taking acidic or spicy foods,
after belching with eaten food, in a prone position. With achalasia, pain can occur either on
an empty stomach in the morning or at night in the form of prolonged pain crises and
combined with dysphagia. The decompensated stages of achalasia weaken the pain
syndrome until it completely disappears (an important difference from cancer), apparently
due to a decrease in the sensitivity of the mucous membrane. Pain in cancer of the
esophagus can occur during or immediately after a meal, localizing above the tumor (prestenotic
esophagitis and cramping) or be constant, localizing below the tumor
the mediastinal tissue causes irradiation of pain and the interscapular region, and
along the esophagus is sometimes explained not by a tumor of the organ itself, but by
metastases to the spine. Constant pain or its constant irradiation with cancer of the
the mediastinal tissue causes irradiation of pain and the interscapular region, and
along the esophagus is sometimes explained not by a tumor of the organ itself, but by
metastases to the spine. Constant pain or its constant irradiation with cancer of the
the mediastinal tissue causes irradiation of pain and the interscapular region, and
along the esophagus is sometimes explained not by a tumor of the organ itself, but by
metastases to the spine. Constant pain or its constant irradiation with cancer of the
Heartburn is a burning sensation behind the sternum in the xiphoid process. Heartburn
happens on an empty stomach or after a hearty meal, a lot of sweets, spices or spicy
dishes. Often it appears in a horizontal position, with physical work and a bent state,
during pregnancy. The mechanism of the occurrence of heartburn has not been fully
clarified, but it is considered the response of an already irritated wall of the esophagus (for
discoordination syndrome, and other conditions. Alkalis, alkaline mineral waters and
adsorbents relieve heartburn, but often it soon arises with renewed vigor. Heartburn
associated with alkaline reflux (with achilic gastritis, after gastrectomy) is relieved by weak
solutions of organic acids or diluted hydrochloric acid. Using pH-metry and
esophagotonokimograi it was shown that in patients suffering from heartburn, the pH in the
sternum in coronary insufficiency. Functional tests with nitroglycerin or soda can help
Belching and regurgitation - involuntary sharp ejection of air or a mixture of air with gastric
contents into the mouth from the esophagus or stomach cavity. Often this unpleasant
process for the patient is accompanied by a loud sound. Belching is close to belching, i.e.,
Belching with air after a plentiful meal, carbonated drinks is physiological. In neuropaths,
and sometimes in healthy individuals, with salivation, forced feeding of lying, diseases of
the abdominal cavity (peptic ulcer, tumors, cholecystitis), aerophagy causes a sonorous
burping of air.
Belching usually occurs spontaneously 10-20 minutes after eating. It can be acidic in
belching with rancid oil reflects fermentative dyspepsia of the stomach. The putrid smell of
belching is due to the decomposition of tissue and food debris with stenotic cancer of the
Bad breath - can be a sign of not only a tumor, but also esophagitis, peptic ulcer and
odors, one should reckon with the patient's subjective perception of the smell from his
mouth.
Subjective cacosmia means a constant or periodic sensation by the patient himself of bad
breath (rot, rotten eggs, etc.), but objectively the source of bad breath is not detected. With
consists in re-chewing and swallowing food thrown from the stomach into the mouth in
humans or into the cavity of the room (the initial part of the stomach) in ruminants.
Sometimes the term is called regurgitation of food only in infants, recognizing this
the esophagus (expulsion), i.e., emptying of the filled esophagus. True esophageal
esophagus with organic cardia stenosis (tumor, ulcer, achalasia). The upper esophageal
sphincter does not withstand the pressure created by a sharp spasm with a distorted
longitudinal orientation. In fact, this is chalazia of the mouth of the esophagus with
achalasia of the cardia. Fountain vomiting more often occurs after a hearty meal with the
last piece of food or when going to bed, tilting the body, straining. Esophageal vomiting
indicates a neglected pathology of the cardia. Sometimes cardia failure, pyloric stenosis
cause vomiting similar to esophageal, but in these cases it is accompanied by nausea and
Esophagus bleeding- This is a spontaneous discharge from the mouth of red blood. The
vomiting. With esophageal bloody vomiting, a real source (varicose veins, cancer, ulcer) of
bleeding is located in the esophagus itself, profuse bleeding from the mouth with relatively
little pronounced chalk occurs, bleeding begins at night or after a hearty meal (increased
blood ow). A similar picture can be given by cardia cancer, ruptures of the mucous
aortic aneurysms, tracheoesophageal fistulas. Esophageal varicose nodes are the most
common cause, but profuse bleeding can cause damage to the lungs, blood vessels, and
even capillaries.
Hiccups in patients with damage to the esophagus indicate involvement of the phrenic
nerve. Most often this happens with cancer of the esophagus, but can be observed with
local and general clinical manifestations that are closely related to the underlying disease:
recurrent laryngeal nerve tumor, heaviness in the chest, shortness of breath, weakness,
loss of appetite, exhaustion in cancer, attacks of nocturnal cough with achalasia, nervous
93. Chemical burns to the esophagus. Clinic of the acute period. First aid and
Damage to the esophagus caused by ingestion of acids or alkalis is called toxic toxic
esophagitis. These substances are taken for the purpose of suicide or by mistake. Acids
cause coagulation necrosis of tissues with the formation of a dense, dry scab of curled
proteins, which protects the deeper layers of the organ from damage. Caustic alkalis
cause coalification necrosis with the destruction of neutral fats and complex lipids by the
type of saponification, therefore such burns are deeper with a more unpleasant prognosis.
The severity of the burn depends on the concentration, amount, chemical nature of the
substance taken, the duration of its contact with the esophagus wall, the degree of filling of
When the esophagus chemical burns can occur simultaneously burns of the mouth, larynx,
from e to the lung, acute respiratory failure. This is observed in at e IU acetic acid and
ammonia because of their volatility and vapor when exposed to concentrated acids.
As a result of a chemical burn, the mucous membrane of the oral cavity, pharynx,
esophagus, and stomach is damaged. Followed by hyperemia and e com mucosa tissue
necrosis occurs rapidly. By the end of the 1st week, the rejection of necrotic areas from the
underlying tissues begins and the formation of superficial or deep ulcerations. Superficial
ulcerations epiteliziruyutsya (1 - 2 months yatsa ) deep - to heal with the formation of
esophagus is formed more often in several places; the surrounding tissue is often involved
in the process. The cicatricial-ulcerative process in the esophagus after chemical burns
can last for years. As a result, in individual patientscicatricial narrowing of the esophagus
Stage IV - scarring.
Clinic and diagnosis . The clinical picture of a chemical burn of the esophagus consists of
symptoms caused by the local action of chemically active substances, and manifestations
of intoxication.
Stage III - the stage of stricture formation (organic narrowing of the esophagus);
According to the severity of acute phase in three degrees isolated esophageal burn: light
The first degree burn is the result at e ma inwardly a small amount of caustic agent in a
low concentration. In this case, the surface layers of the epithelium are damaged in a
The second degree of burn is characterized by more extensive necrosis of the epithelium
The third degree of burn - necrosis captures the mucous membrane, submucosal and
The defeat of esophageal acid may be accompanied by lesions of the stomach, and initial
jejunum with the emergence of areas of necrosis and perforation of that Veda e t to the
development of peritonitis in acute as well as scar deformity of the stomach afterwards.
The I acute phase (5 - 10 hours) in patients after at e ma acid or caustic appear severe
pain in the mouth, pharynx, chest, epigastric, profuse salivation, frequent vomiting,
dysphagia due to esophageal spasm in the burn area and by mucosa. Swallowing is
difficult or impossible. Patients excited, scared. The skin is pale, moist. Breath is frequent,
tachycardia, decreased blood pressure, dull heart sounds, decreased urine up to anuria. A
few hours after the burn along with symptoms of burn shock symptoms of toxemia:
delirium, muscle under. Respiration is frequent, shallow, pulse rate up to 120 - 130 per
minute, blood pressure is reduced due to hypovolemia. In patients painful thirst appears as
a result of dehydration, with electrolytemia. During a blood test, leukocytosis, a shift of the
leukocyte formula to the left, an increase in ESR, an increase in hematocrit, hypo- and
dysproteinemia are noted. The cord e mated cases there is hyperkalemia, hyponatremia
With concomitant burn larynx and the vocal cords may be hoarseness, difficult g Goes
breath asphyxia. The cord e mated cases develops toxic damage of parenchymal organs
(acute printed e night and renal failure). Poisoning with vinegar essence can cause the
aspiration, patients may develop tracheobronchitis, pneumonia. With direct damage to the
Stage II - the stage of "imaginary well-being" (lasts from 7 to 30 days). By the end of the
1st week, the rejection of necrotic tissues of the esophagus begins. Ingestion of liquid food
becomes somewhat freer, bleeding is possible. With deep necrosis, perforation of the
empyema of the pleura, esophageal-bronchial fistula. Amplified chest pain and back pain,
shortness of breath and tachycardia increases body temperature becomes hectic nature,
chills replaced by heavy sweats, formation of subcutaneous emphysema, cough
appearance at at e IU of liquid food. Aspiration that occurs in the acute period can be
gIn rare cases, in the presence of extensive wound surfaces on the walls of the
esophagus, sepsis may develop. The latent period is characterized by dysfunction of the
By the end of the month (stricture formation step) under the influence of treatment of
burned esophageal areas heal. In 10 - 15% of patients with the X-ray examination show no
esophagus Length. In 20% of cases, by the end of the month, the phenomena of
where healing occurs slowly. The wound surfaces are covered with a dense scab, bleed
easily.
In the long term (up to 2 - 3 years) after a burn (stage of late complications), dysphagia
comes first in the clinical course. From starvation, the patient's condition progresses with
Emergency care for chemical burns of the esophagus and treatment in the acute period
papaverine, ganglion blockers are administered. It is advisable to rinse the mouth, the
gastric lavage with a rubber probe. Depending on the nature of the received substances
for gastric lavage using weak solutions or acid. When the drink is expedient burn acids 2%
at Poisoning alkalis - 1 - 1.5% acetic acid solution. In the first 6 to 7 hours, antidotes are
administered.
electrolyte solutions).
In order to prevent esophageal cicatricial narrowing of patients with 1st day given every 30
novocaine solution, an antibiotic, a 3rd of the day they are fed Cooling food. When taking
medicine and food early, it’s as if carrying out a “soft” bougienage of the esophagus. The
scars. It is now recognized expedient to hold early (9 - 11 days) bougienage esophagus for
weeks. Too early, before this term started probing yes e t the opposite effect, causing an
exacerbation of inflammation in the esophagus and increased scarring. Before starting the
Gulping of the esophagus is unsafe and may be complicated by its perforation with the
development of purulent mediastinitis and pleurisy, therefore it should be carried out with
great care.
oxygenation, which reduces the depth of necrosis zone delimits leukocyte infiltration
contributes to the clearance of the wound surface and causes epithelialization e g the end
of 1 month. Hyperbaric oxygenation inhibits the formation of connective tissue, which leads
to the development of a more loose, thin and elastic scar of the esophagus.
hemolysis, alkalizing therapy (5% sodium bicarbonate solution) and forced diuresis are
necessary.
94. Cicatricial narrowing of the esophagus: location and shape of the constriction,
Cicatricial narrowing of the esophagus. Post-burn strictures have significant Length and
depth of damage esophageal wall are formed of different stricture Length. Allocate Space
strictures that are thin membrane thickness of a few millimeters, annular - thickness of 2 -
3 cm, tubular - length of 5 - 10 cm and more, subtotal and total. The strictures can be
single or multiple, complete or incomplete. The course of the stricture is often tortuous,
occurs.
Clinic and diagnosis . The main symptom of post-burn stricture is dysphagia, which
appears from 3 to 4 weeks after the onset of the disease. At first, dysphagia is not
sternum. Over time, narrowing of the esophagus progresses, as the surface of the
process. The severity of dysphagia increases, complete obstruction of the esophagus may
develop. Food retention causes chest pain and regurgitation. With high stenosis of the
esophagus, food during ingestion can enter the respiratory tract, causing laryngospasm,
time after eating. Among other symptoms of post-burn narrowing of the esophagus often
have chest pain when under g food IU, increased salivation, belching, heartburn. As a
obstruction of the esophagus with food, which requires emergency medical attention
(esophagoscopy to remove the food lump). Chronic inflammatory diseases of the bronchi
and often develop l e soft due to regurgitation and aspiration of food e g in the respiratory
the area of stricture. In patients with stenosis, more often than in healthy people,
with a liquid and a thick contrast medium (Figure 3) . The narrowing of the esophagus has
a tubular shape, the relief of the mucous membrane in the area of narrowing is absent,
peristalsis is not determined. As a result of scarring and inflammation, the lumen of the
esophagus in the narrowing area has an irregular shape. Above the stricture, there is often
Both methods allow the investigation to clarify the extent, location, Length narrowing its
Treatment . The main method of treating esophageal stricture after a chemical burn is
Unlike the early one, later bougienage is carried out in order to expand the already
shown all patients with post-burn esophageal strictures when conduct through the
bougienage must be carried out for many weeks and even months . Apply:
conductor;
5) retrograde bougieurage.
Probing blindly through the mouth it is indicated in small-Length annular strictures of upper
and middle chest esophagus. Treatment is carried out using a special set of bougie. If the
bougie is easy, bouge is carried out next to the thickness of the number.
The method of bougieument was improved with the use of metal conductors and
radiopaque hollow bougie. They provide the opportunity for x-ray control to determine the
course of stricture and advance the bougie along the esophagus, which increases the
effectiveness of the procedure and reduces the risk of perforation of the esophagus.
"Probing without end" is used in the presence of gastrostomy in patients with tubular,
convoluted or multiple strictures, enter constant derived through the mouth and through
the gastrostomy tube is attached rubber tubes of different diameters. Stretching, they are
carried out through the narrowed area and left for several hours. Retrograde bougienage
In some cases, mechanical expansion of the cicatricial strictures of the esophagus can
At present, balloon plastic surgery of cicatricial narrowing of the esophagus under the
Indications for surgery for cicatricial strictures of the esophagus: 1) complete obliteration of
In COG g scrap depletion for feeding patients applied gastrostomy as the rst stage of
treatment.
When choosing a method of operation take into account the age and general condition of
the patient , location and Length narrowing of the esophagus. In most cases , one-stage
.
With segmental strictures, various types of partial plastics of the esophagus are produced.
When defeat lower esophagus or gastric cardia used: overlay bypass gastroesophageal
anastomosis resection hitting g nnogo portion and its replacement by a tube formed from a
large curvature of the stomach, the graft from the small or large intestine. With damage to
Use transplants from the small or large intestine. One end of the graft is anastomosed with
the esophagus above and the other below the narrowing. With extensive strictures, the
total plasticity of the esophagus with pre- sternal or intrathoracic (retrosternal, intrapleural,
The creation of an artificial esophagus should not be started earlier than 2 years after the
burn. Only after this period, the degree of scarring of the esophagus can be revealed and it
becomes clear that the formed scar tissue will not allow to expand the lumen of the
manifested by a violation of the passage of food masses into the stomach due to
persistent disturbance of the reflex opening of the cardia during swallowing, changes in
The incidence rate is 0.5-0.8 cases per 100,000 population. The first symptoms of the
disease are more likely to occur at the age of 20-40 years. More often women are ill.
uerbahova) plexus);
Infectious toxic lesions of the nerve plexuses n the esophagus and cardia.
physiological cardia. In healthy people, he is at rest in a state of tonic contraction, and after
swallowing, he relaxes.
With cardiospasm, increased cardia pressure is observed, the gradient of esophagealgastric
pressure can reach 20 mm Hg. Art. and more at a rate of 10 + 3 mm RT. Art. The
preganglionic neurons of the dorsal nuclei of the vagus nerves and, to a lesser extent, in
the postganglionic neurons of the Auerbach plexus of the esophagus. It is believed that
due to a violation of central innervation during cardiospasm, the smooth muscles of the
lower esophageal sphincter become more than usual sensitive to its physiological
regulator - endogenous gastrin. Thus, with this variant of the course of the disease, a true
With achalasia of the cardia, on the contrary, mainly postganglionic neurons are affected,
as a result, the reflex of opening the cardia to the throat falls out. Manometrically and a
weakening of the motility of the esophagus. With achalasia, there are no conditions for the
Therefore, the main differences between cardiospasm and achalasia of the cardia are
different levels of parasympathetic nervous system damage and the related changes in the
sensitivity of the smooth muscles of the lower esophageal sphincter to its main
Dysphagia is the main and in most cases the first symptom of the disease. It can occur
in the majority of patients is observed after neural stimulation, during a hasty meal, while at
g IU dense, dry and bad living or e bathroom food. Sometimes paradoxical dysphagia is
observed: dense food passes into the stomach better than liquid and semi-liquid.
A number of patients dysphagia depends on the temperature of the food: bad passes or
does not pass t e Playa food, and cold runs, or vice versa. Patients gradually adapted to
facilitate the passage of food into the stomach via the series for g mov (walking, gymnastic
exercises, saliva and swallowing of air when g m large amount Ploy water, etc.). Severe
with a significantly expanded esophagus it is more rare, but plentiful and is due to strong
spastic contractions of the esophagus that occur when it is full. Regurgitation at position l g
Ms and under strong torso content due to mechanical pressure on the esophageal
The pain behind the sternum is diverse. It may be associated with spasm of the
patients, pain occurs when the esophagus is full and disappears after burping or passing
food into the stomach. In some cases , there were sporadic attacks of pain in the chest on
the type of pain crises Such pain is more often observed in the initial period of the disease,
sometimes the development of dysphagia and regurgitation, which are not always
dystrophic process in the intramural nerve plexus of the esophagus. Pain on an empty
Belching by air, nausea, increased salivation, burning along the esophagus, bad breath
The most common complication of the disease is congestive esophagitis, which occurs
with prolonged retention of food masses in the esophagus. The L g mild cases, it is
manifested by hyperemia and e com mucosa, more COG g mated - presence of rough and
uneven folds, erosions, ulcers, which usually are located slightly above the necked portion.
caused by compression of the enlarged esophagus of the recurrent nerve, right main
Stage I - functional intermittent spasm of the cardia, expansion of the esophagus is not
observed;
Stage II - stable spasm of the cardia with an unsharp expansion of the esophagus;
Stage III - cicatricial changes in the muscle layers of the cardia with a pronounced
Stage IV - pronounced stenosis of the cardia with dilatation of the esophagus, often Sshaped,
and esophagitis.
With a non-contrast radiological examination of the chest, an additional bulging of the right
mediastinal contour, the presence of a fluid level in the projection of the posterior
mediastinum, and the absence of a gas bubble of the stomach are revealed. Basic
radiographic signs - narrowing of esophagus with terminal h e IMT, smooth and flexible
circuits ( "ame pens g rnutoy candle", "Mouse tail"). The folds of the mucous membrane in
the narrowing area are preserved. The first sips of barium can freely enter the stomach,
then the contrast mass is retained for a long time in the esophagus. A layer of liquid and
food debris are determined above the barium suspension. The expansion of the
esophagus over the site of its narrowing is expressed to varying degrees. In a number of
The peristalsis of the esophagus in all patients is sharply impaired: contractions are
weakened, have a spastic character and insufficient amplitude. With the development of
esophagitis, changes in the relief of the mucous membrane of the esophagus are visible:
Esophagoscopy allows you to conrm the diagnosis, identify complications and conduct a
picture depends on the duration of the disease. At the beginning of the disease esophagus
widened slightly, as the disease progresses the lumen Sun g more expanded and in some
patients it becomes crimped. The mucous membrane has signs of inflammation: the folds
are thickened, the arteries and veins are enlarged, and areas of hyperemia, erosion,
leukoplakia, and ulceration are often visible. Typically, the end esophagoscope navigate
through the narrowed portion, which supports advantageously the functional nature of the
changes in the esophagus. The mucous membrane at the site of narrowing is most often
not changed.
clinical symptoms of the disease. The study is carried out using a special multichannel
probe with rubber cartridges or "open" catheters that record reductions in the esophagus
and changes in the esophageal pressure. Normally, after swallowing, a peristaltic wave
and the pressure decreases. After the passage of the peristaltic wave, the cardia closes
again. With cardiospasm (cardiac achalasia), there is no reflex relaxation of the cardiac
sphincter during swallowing, and intraluminal pressure remains at the previous figures.
In doubtful cases, pharmacological tests are used to confirm the diagnosis. Nitroglycerin
reduces the tone of the esophagus and physiological cardiac sphincter, which facilitates
the passage of the contents of the esophagus into the stomach. The introduction of
the muscular layer of the esophagus wall and on the cardiac sphincter. With
cardioesophageal cancer and organic stenosis of the esophagus, both samples are
negative.
Treatment . Conservative treatment is used only in the initial stages of the disease, and is
also used as an addition to cardiodilation and in preparing patients for surgical treatment.
Food should be mechanically and thermally gentle, rich in proteins, vitamins. The food is
fractional, the last meal 3 to 4 hours before bedtime. Reducing dysphagia in I - II stages of
disease can achieve put g m nitro application of preparations - nitroglycerin, amyl nitrite
electrophoresis (iontophoresis) with novocaine, deep diathermy in the region of the cardia,
The main method of treatment is cardiodilation, which consists in violent stretching and
partial tearing of the muscles of the distal esophagus and cardia. Cardiodilation can be
Contraindication to the use are, portal hypertension with esophageal varices, expressed
are:
1) the inability to carry out cardiodilation;
4) pronounced peptic strictures that developed after overstretching of the cardia and are
dissection of the muscular membrane of the terminal esophagus along the front and back
during normal cardia function. More often men are ill, mostly middle and old.
The cause of primary esophagospasm is a violation of the function of the nervous system
Clinic and diagnosis. The clinical picture is dominated by pain behind the breastbone that
appears during the passage of food through the esophagus, has a different intensity, may
radiate to the back, jaw, neck, arms and others. The pain can occur is when yo food ma,
dysphagia and often e e paradoxical character, which allows to differentiate this disease
from cancer, esophageal stricture and achalasia, in which less dense food passes and
zapivanie e e relieves water. During severe spastic contractions of the esophagus, there
may be regurgitation of a small amount of just taken food in the mouth.
"pseudodiverticulum", "spin" (Figure 5) . The diameter of the esophagus above and below
the narrowed areas is not changed, the walls of the esophagus are elastic, the folds of the
mucous membrane are longitudinal, the peristalsis is uneven and irregular. Repeated x-ray
esophagus.
form of waves of various shapes and amplitudes, while peristaltic contractions are also
performed to the level of the aortic arch. Treatment of secondary esophagospasm should
be aimed primarily at eliminating the root cause, then it is necessary to influence the
Classication. According to the pathogenetic origin, diverticula are divided into pulsion,
Pulsed diverticulums are formed due to protrusion of the esophageal wall under the action
Traction diverticulums are formed due to the involvement of the esophagus wall in
inflammatory and adhesion processes that develop in the mediastinal tissue , most often
The traction mechanism is observed at the very beginning of the development of the
diverticulum, then the pulsion factors join, as a result of which the diverticulum becomes
pulsion-traction.
Distinguish congenital and acquiring diverticula esophagus true (retaining body structure)
and false (lacking the tunica muscularis). False diverticula at substantially are hernia
(protrusion mucosa through weaknesses muscular wall), which indicates that their
acquired character.
times more often than women, they come from the posterior pharyngeal wall at the level of
the cricoid cartilage of the trachea, where between the constrictors there is an area that is
not covered by muscles (the Lanier-Hackerman triangle), and are by the mechanism of
occurrence of pulsion. Purely esophageal diverticula are less commonly observed in this
area. They come from the Lymer triangle, which is bounded above by the cricoidpharyngeal
muscle, and from below and on the sides by bundles of longitudinal muscles of
the esophagus.
An increase in pressure in the pharyngeal cavity and in the area of the “mouth” of the
esophagus can lead to the formation of a diverticulum along with the discoordination of
muscle contractions. With small sizes, the diverticulum bag is located behind the pharynx
and esophagus, large diverticuli, reaching significant sizes, are localized to the left of the
midline. Traction diverticulums of this area, developing after operations on the neck
The Zenker diverticulum in the initial stage may not show anything, sometimes patients are
disturbed by a feeling of awkwardness, “scratching” in the throat while eating - then such
patients are mistakenly treated for diseases of the pharynx or larynx. As the diverticulum
symptoms appear - dysphagia, regurgitation (often during sleep, which can lead to
aspiration), halitosis. With large diverticula in the region of the left half of the neck, elastic
Bifurcation diverticulums (Figure 8) are located mainly on the anterior or anterior-right wall
Inflammatory processes in the lymph nodes and other formations of the mediastinum lead
to the development of adhesions, scarring and stretching of the wall of the esophagus.
This is confirmed by operational ndings, in which dense adhesions of the diverticulum with
lymph nodes, trachea, and bronchi are always revealed. Bifurcation diverticuli are smaller
in an X-ray contrast study. With more or less large diverticulums with a long and narrow
neck that prevents their emptying, characteristic chest pain (sometimes simulating angina
esophageal spasm) appear. Pain can be associated with both diverticulitis and
peridiverticulitis, and with the development of segmental esophagitis in the neck of the
palpitations, shortness of breath. Bifurcation diverticula are often combined with a cardiac
hernia of the esophageal aperture of the diaphragm and reflux esophagitis, with symptoms
characteristic for this suffering (heartburn, belching, regurgitation, epigastric pain). With the
Epiphrenic diverticula, first described by Deguis in 1804, are pulsional and are often of
considerable size, usually located on the anterior or anterior-right wall of the lowest third of
the esophagus. It is believed that the main role in their occurrence is played by congenital
weakness of the esophagus wall in this area. Here he deviates to the right of the midline,
and then to the left, so the food lump, constantly acting on the right wall of the esophagus
more than the left, can lead to the formation of a diverticulum. The pulsed mechanism of
the occurrence of epiphrenic diverticula is confirmed by the fact that they are often
Epiphrenal diverticula with small sizes and a wide neck may not manifest clinically. With
large diverticulums, especially complicated by diverticulitis, the clinical picture becomes
bright: chest pain is characteristic (sometimes as with angina pectoris), less often -
when foreign bodies get into the diverticulum. In approximately 20% of patients with such
which must be taken into account when developing a treatment plan. Against the
In the diagnosis of all types of esophageal diverticulums, the main role is played by a
suspension is retained in the cavity of the diverticulum for more than 2 minutes, then
wall allows you to exclude the diagnosis of a tumor (polyp, cancer), as well as various
complications (fistula). The exact localization of the diverticulum, as well as the condition
of the cardia, is necessary for the selection of rational surgical access (it is known that a
diaphragm is possible).
the mucous membrane of the esophagus and the diverticulum itself, localization, size of
the neck, and the presence of various complications - bleeding, fistula, polyp, and cancer.
without diverticulitis, a poor clinical picture, and also if there are contraindications for
sparing diet - optimal temperature food, well-machined, not causing irritation of the
mucous membrane of the esophagus (spicy foods and alcohol are excluded). For
meals, and after a meal to drink several sips of water. With a combination of a diverticulum
cervical access. The diverticulum is isolated, excised, the wound is sutured in the
transverse direction in layers on a thick probe inserted into the esophagus to prevent
stenosis. Sometimes, staplers are used to remove the diverticulum, with which the neck is
stitched in the transverse direction, and then the clips are covered with a second row of
interrupted sutures. For the prevention of relapse, it is also advisable to cross in the
longitudinal direction the lower constrictor of the pharynx along the posterior wall below the
invagination are used. The operation is performed by transpleural access. Perform rightsided
thoracotomy in the fifth or sixth intercostal space. Having highlighted the diverticulum
from all sides, its base is stitched either with the help of staplers, or a U- shaped catgut
seam is applied. When applying U-shaped catgut sutures after removing the diverticulum,
the mucosa is stitched again with the same thread. Then impose nodal sutures on the
muscular membrane of the esophagus. The seam lines can be strengthened with a pleural
flap, diaphragm, and alloplastic tissues. Diverticulum invagination is used for small
diverticula, which when immersed in the lumen can not cause narrowing of the lumen of
suture,
diverticulectomy. Use left or right access on the seventh-eighth intercostal space. Dissect
the mediastinal pleura, distinguish a diverticulum; the diverticulum neck is stitched with a
needle. The second row of sutures is applied to the muscular membrane of the
pleura, lung, alloplastic tissues. Since epiphrenic diverticula are sometimes combined with
Heller's esophagocardioplasty.
Foreign bodies are a rather frequent and dangerous pathology of the esophagus. Most
often, sh, meat and bird bones, dentures, coins, buttons, pins, nails get stuck in the
esophagus. The main reasons for foreign bodies to enter the esophagus are hasty food
with swallowing poorly chewed pieces of food, bones, careless cooking with leaving bones
keep nails, needles, pins in their mouths when working. , oral pathology in elderly patients
(poorly fitted false jaws, decreased sensitivity of the oral mucosa), children's habit of taking
A swallowed foreign body can pass from the esophagus to the stomach and exit naturally
strictures, tumors, diverticula, cramps, achalasia). However, in more than 90% of cases,
foreign bodies are found in a healthy esophagus. The predominant localization of foreign
bodies in the esophagus is the place of physiological constriction. Most often, foreign
bodies linger at the level of the jugular notch of the sternum. Less commonly, delay occurs
at the level of the aortic arch and bifurcation of the trachea and cricopharyngeal narrowing.
Clinic.The clinical picture largely depends on the size, shape, localization, duration of a
foreign body in the esophagus. After ingestion of a foreign body, the patient notes pain, a
feeling of compression in the throat or behind the sternum, which intensifies when
swallowing. Pain can be absent with foreign bodies with a at, smooth surface. The pain
radiates to the back, between the shoulder blades. In addition to pain, dysphagia,
regurgitation, and salivation are characteristic. If the esophagus wall is injured, bleeding
may occur. In rare cases, with large foreign bodies, complete obstruction of the esophagus
occurs. This is largely facilitated by concomitant muscle spasm and inflammatory edema
of the mucous membrane. Sometimes the clinical picture is dominated by signs of sudden
suffocation. With damage to the wall of the esophagus and the attachment of inflammatory
phenomena, there is constant pain in the neck, back, behind the sternum. Dysphagia is
rapidly increasing. The general condition of the patient worsens, the temperature rises,
chills appear. On the neck, more often on the left, there is a painful swelling, crepitus. The
body, tends to occupy a forced position. With foreign bodies in the upper third of the
esophagus, he extends his neck, tilts his head down. When a foreign body is retained in
the thoracic region, the body is tilted down, the patient prefers to lie in a bent position.
When swallowing, a painful expression appears on the face. painful swelling, crepitus is
noted. The patient’s appearance is characteristic, which, depending on the location of the
foreign body, tends to occupy a forced position. With foreign bodies in the upper third of
the esophagus, he extends his neck, tilts his head down. When a foreign body is retained
in the thoracic region, the body is tilted down, the patient prefers to lie in a bent position.
When swallowing, a painful expression appears on the face. painful swelling, crepitus is
noted. The patient’s appearance is characteristic, which, depending on the location of the
foreign body, tends to occupy a forced position. With foreign bodies in the upper third of
the esophagus, he extends his neck, tilts his head down. When a foreign body is retained
in the thoracic region, the body is tilted down, the patient prefers to lie in a bent position.
Diagnostics. The examination begins with an instrumental examination of the pharynx and
pharynx with the help of a laryngeal mirror. Sometimes in this way it is possible to detect a
foreign body in the pear-shaped sinuses. After examination, the pharynx proceeds to an Xray
examination of the esophagus. X-ray contrast metallic foreign bodies (coins, needles,
For negative X-ray data, a contrast agent test is used. With negative data from an X-ray
examination and persistent persistent complaints of the patient for pain, dysphagia, with
Treatment. The presence of a foreign body in the esophagus serves as an indication for its
immediate removal. For this purpose, esophagoscopy using special forceps is used. In
adults, it is performed under local anesthesia, in children and excited patients under
methods are used. When localizing a foreign body in the cervical region, at a distance of
25 - 26 cm from the edge of the upper incisors, esophagotomy is used by cervical access
on the left. Foreign bodies of the thoracic esophagus are removed using thoracotomy or
dorsal mediastinotomy.
99. Benign tumors of the esophagus: clinical features, diagnosis, indications for
surgical treatment;
Benign tumors of the esophagus are histologically divided into tumors of epithelial and
non-epithelial origin. The first group includes polyps, adenomas, papillomas and cysts of
a benign tumor can range from the size of the cherry to the tumors, which occupy a
In frequency, the first place among benign tumors of the esophagus is occupied by
leiomyoma (50-70% of all benign tumors of the esophagus). Other tumors are very rare.
Leiomyomas in most cases are localized in the lower third of the esophagus, less often in
the middle third. Most often, leiomyomas occur between the ages of 20-60, although cases
of this tumor have been described in children and senile individuals. More often,
The second most common benign tumor of the esophagus is esophageal cysts.
Depending on the origin of the esophagus cysts are divided into the following groups:
1) retention cysts;
3) publication cysts;
7) dermoid cysts;
8) parasitic cysts.
The esophagus cyst is a thin-walled formation of a round shape, the cavity of which is
By the nature of the growth of the tumor (inside the lumen of the esophagus or inside its
wall), their division into intraparietal and intraluminal is based. The rst group includes
papillomas.
Clinic.Due to their small size, intra-esophageal tumors of the esophagus often do not give
any symptoms and are an accidental finding during an X-ray examination. In clinically
pronounced cases, the main symptoms of intradenal tumors of the esophagus are
dysphagia, pain behind the sternum or in the epigastric region, dyspepsia, and
respiratory disorders. The first two symptoms are most common, although their severity
varies widely. Dysphagia in most cases is negligible, but slowly grows as the tumor grows.
The pain is usually localized behind the sternum or in the epigastrium. Some patients
belching, nausea, vomiting, sensations of fullness in the epigastric region. Some patients
diseases of the bronchi and lungs. Pulmonary symptoms are usually the result of
regurgitation of food masses into the bronchial tree or the result of compression of the
Most intraluminal tumors are localized in the upper half of the esophagus. Single tumors
are more common. In many cases, these tumors are asymptomatic. With large sizes, they
usually manifest with certain symptoms. Patients may have dysphagia, regurgitation, loss
characteristic. Sharp pain may appear when the legs of the tumor are twisted. The most
unpleasant and life-threatening patient is the ejection of a tumor on a long leg during
vomiting in the mouth. A tumor can block the entrance to the larynx, cause an asthma
attack or even death. Complications of benign tumors include bleeding due to ulceration of
Diagnostics.The main diagnostic methods for benign tumors of the esophagus are x-ray
esophagus. In this case, part of the defect extends into the lumen of the esophagus, and
the other part is located outside it, against the background of the posterior mediastinum.
The severity of each of these symptoms depends on the location of the tumor in relation to
the axis of the esophagus. The relief of the mucous membrane over the filling defect is
usually little changed or smoothed due to the stretching of the mucous membrane by the
tumor. The elasticity and peristalsis of the walls of the esophagus are preserved. It is
characteristic that suprastenotic expansion is usually absent and appears in rare cases
only with stenosis of the lumen of the esophagus. With an uneven tuberous surface of the
tumor, the filling defect has uneven contours. The lateral projection is characterized by a
sharply defined angle between the edge of the tumor and the unchanged wall of the
esophagus. When swallowing, a synchronous shift in the shadow of the tumor is observed.
Intra-luminal tumors are characterized by the presence of a filling defect with clear, even
contours, located in the lumen of the esophagus and changing its location. The folds of the
mucous membrane near the tumor are usually not changed and bend around its base. In
and CT can be used, in which the shadow of the tumor and its relation to surrounding
organs are clearly visible. When swallowing, a synchronous shift in the shadow of the
defect with clear, even contours, located in the lumen of the esophagus and changing its
location. The folds of the mucous membrane near the tumor are usually not changed and
bend around its base. In difficult cases, in addition to conventional research methods,
pneumomediastinography and CT can be used, in which the shadow of the tumor and its
relation to surrounding organs are clearly visible. When swallowing, a synchronous shift in
the shadow of the tumor is observed. Intra-luminal tumors are characterized by the
presence of a filling defect with clear, even contours, located in the lumen of the
esophagus and changing its location. The folds of the mucous membrane near the tumor
are usually not changed and bend around its base. In difficult cases, in addition to
the shadow of the tumor and its relation to surrounding organs are clearly visible.
Esophagoscopy is indicated for all patients with a tumor of the esophagus. A typical
membrane of the esophagus above the tumor protruding into the lumen. The lumen of the
esophagus can be narrowed on the one hand and compensatory widened on the other, so
that the esophagoscope can usually be held below the tumor. Sometimes pathology with
esophagoscopy is not determined. This may be due to the fact that the esophagoscope
Treatment . Surgical treatment of benign tumors. In this case, five types of operations are
used:
4) excision of the tumor with a section of the wall of the esophagus; 5) resection of the
esophagus.
Removal of a tumor through the mouth is used for polyps in the initial esophagus.
Endoscopic removal of the tumor is resorted to with small polyps on a narrow leg. The
operation consists in crossing the tumor leg with a loop and removing it with forceps. In
case of intraparietal tumors and large polyps, especially on a broad base, cervical,
transpleural, or abdominal access is used depending on the location of the tumor. In the
case of a cervical tumor, the esophagus is exposed with a cut along the front edge of the
left sternocleidomastoid muscle. With tumors of the upper 2/3 of the thoracic esophagus,
right-sided thoracotomy in the fifth intercostal space is convenient, with tumors in the lower
third of the esophagus, left-side access in the seventh intercostal space is usually used.
Damage to the esophagus is divided into closed (internal) from the mucous membrane
and open (external) with penetrating wounds of the neck and chest.
Closed injuries of the esophagus are possible during the implementation of diagnostic and
to the esophagus can occur from the inside when foreign bodies enter it. Pressure ulcers
of the esophagus wall occur when the probes are in it for a long time, from the pressure of
the cuff of the endotracheal or tracheostomy tube. Perforation of the wall of the esophagus
can occur with its various diseases: tumors, peptic ulcer, chemical burns. Closed injuries of
the neck, chest and abdomen can lead to malnutrition and necrosis of the esophagus wall
as a result of squeezing it between the sternum and vertebral bodies. In this case, damage
to neighboring organs is often noted. Direct trauma to the esophagus can occur during
Open (external) esophageal injuries in peacetime are rare. Usually they are combined with
multiple injuries of neighboring organs (thyroid gland, trachea, heart, lungs, large vessels,
etc.).
Clinic. When the cervical esophagus is injured, patients complain of pain when
swallowing, subcutaneous emphysema occurs on the neck. Esophagitis, periesophagitis
In case of damage to the thoracic esophagus, patients note a sharp pain behind the
body sensation in the esophagus. Characteristically forced position - the body is tilted
forward. There is vomiting with an admixture of blood, a subtle emphysema of the neck,
described in 1724 - there is a rupture of the lower thoracic esophagus during an attack of
pressure (the pressure in the stomach during vomiting can increase to 200 mm Hg. ). A
rupture of the esophagus can also occur when trying to artificially suppress an attack of
vomiting (the syndrome is described in the literature under the name “banquet injury”). The
rupture often takes the form of a linear wound, can spread to the stomach. azvivaetsya
of the esophagus pain occurs suddenly (usually during vomiting) in the xiphoid, may
radiate to the epigastric region, back, left shoulder noted hematemesis,.. mediastinal and
subcutaneous emphysema, shock develops, body temperature rises. With damage to the
esophagus. It starts with a review uroscopy and radiography, in which you can detect
emphysema. In the absence of air in the mediastinum, the esophagus with a contrast
agent is examined in the patient's position, lying on his back, on the right and left side, on
his stomach. If there is a suspicion of a defect in its wall due to rupture or perforation,
water-soluble contrast agents should be used, since a suspension of barium, leaving the
defect in the esophagus wall into the mediastinal tissue, imbibes it and makes subsequent
easily penetrate through small defects in the wall of the esophagus, do not cause an
inflammatory reaction of the surrounding fiber, are quickly absorbed. Often this study is
enough to determine the location and size of the perforation hole. In doubtful cases,
esophagoscopy is used.
anti-inflammatory drugs) is carried out: 1) until a final diagnosis is established and when
Surgical treatment (radical and palliative) is indicated for extensive damage to the
Radical surgical treatment consists in suturing the defect with prescription of damage to
the esophagus up to 1 day. Suturing of the defect in the wall of the esophagus produce
two rows of sutures in the longitudinal direction. The tightness of the sutures and their
isolation from the infected mediastinum and pleural cavity is provided by hemming around
them depending on the location of the defect in the muscles of the neck, parietal pleura,
pericardium, diaphragm, and the bottom wall of the stomach. The mediastinum and pleural
cavity are drained for aspiration of exudate, the introduction of antibiotics, antiseptics,
proteolytic enzymes.
Recently, with perforation of the esophagus, the method of active and tight drainage of the
mediastinum has become widespread. In this case, a mediastinotomy is performed taking into
account the place of damage to the esophagus, often from an incision in the neck, and a double-
lumen drainage tube is brought to the perforation site, which is removed away from the surgical
wound. The surgical wound is sutured in layers. The method is based on the principle of
simultaneous infusion of a mediastinum of an antiseptic solution into the area of the destroyed
and inflamed periophageal fiber and aspiration of this solution together with the contents that
accumulate in the area of post-traumatic purulent inflammation.
40. The etiology and pathogenesis of suppurative pulmonary diseases and pleura.
Classification;
Classification of purulent lung diseases:
b) lung gangrene.
a) uncomplicated;
mechanisms.;
42. The clinical course and diagnosis of acute suppurative diseases of the lungs;
diagnosis;
Two phases: before the breakthrough of the abscess in the bronchus and after its
breakthrough.
The clinical and radiological symptoms of the first phase are typical for croupous or focal
pneumonia. Kryukov’s symptom is pain when pressing and tapping on the part of the chest
In the second phase, more typical symptoms appear: separation of purulent sputum,
sometimes with an admixture of blood. Sputum, settling, is divided into three layers: pusserous
fluid-foam.
Diagnostic methods for suppurative lung diseases: laboratory blood and sputum tests,
external respiration tests, X-ray methods, computed tomography, bronchobroscopy,
Lung Gangrene
Clinic: fetid exhaled air, severe shortness of breath, fetid sputum of the form: meat slops ”,
- bronchiectasis;
Treatment:
exercise therapy.
6. Immunocorrective therapy.
Conservative treatment is futile with abscesses with a diameter of more than 6 cm, a very
Complications in the acute period: a breakthrough of the abscess into the pleural cavity
with the development of intense pneumothorax; bleeding into the bronchial tree with
possible asphyxia; aspiration of pus into the unaffected areas of the bronchial tree and the
development of new abscesses; the formation of ulcers in distant organs, more often in the
brain.
45. Chronic lung abscess: the development, clinical course and differential
diagnosis;
Etiology:
1. Features of the pathological process: large, with a diameter of more than 6 cm cavities
in the lung; the presence of sequestration in the cavity; poor drainage conditions; sluggish
2. Errors in the treatment of the patient: inadequate antibiotic therapy; poor drainage;
First type - Against the background of remission of the lung abscess, frequent relapse of
the disease occurs in 1-2 weeks. They lead to the phenomena of purulent bronchitis,
An acute period
without%remissiongoesintothechronicstage.Severeintoxicationanddystrophyofparenchyma
disease.
Symptoms
- cough;
- hemoptysis;
- chest pain;
- shortness of breath;
- sweating;
- osteoarthropathy.
47. Acute empyema and pleural empyema. The clinical course. Diagnosis and
differential diagnosis;
48. The principles of treatment of acute pleural empyema. Indications for surgical
Empyema is a condition that affects the space between the outermost layer of the lungs
and the layer touching the chest wall, known as the pleural space. This space exists to
help the lungs expand and contract.The pleural space naturally contains a small amount of
fluid. Empyema happens when extra fluid begins to collect in the pleural space.Different
strains of bacteria cause fluid and pus to build up in the pleural space. Very
• a fever
• chest pain
• a cough
• pus in mucus
• difficulty breathing
Empyema can progress through three stages if a person does not receive treatment.
The first stage of empyema is called simple empyema. It occurs when extra fluid begins to
build up in the pleural cavity. This fluid can become infected and may contain pus.
In complicated empyema, the fluid in the pleural cavity begins to thicken and form
“pockets.”
Finally, the infected fluid causes scarring to the inner layers that line the pleural cavity in
the lungs. This causes difficulty breathing as it stops the lungs from inflating properly.
Causes
Pneumonia is the most common cause of empyema. People who have undergone
Risk factors
The biggest risk factor for empyema is having had pneumonia recently.
In low-risk populations, empyema was generally less severe, and people were more likely
Statistically, people with the following conditions are also more likely to develop empyema.
• diabetes
• heart disease
• previous cancer
• lung disease
Diagnosis
The first step to diagnosing empyema is a chest X-ray. An X-ray can only identify
empyema when there is a specific amount of fluid in the pleural cavity, however.
If the doctor suspects there is liquid in the pleural cavity after a chest X-ray, they will carry
out an ultrasound. Ultrasounds are more sensitive and better at detecting fluid in the
pleural cavity.
CT scans are also a useful method of detecting empyema. This allows doctors to see the
Treatment
Antibiotics
Doctors usually prescribe antibiotics as the first treatment for simple cases of empyema.
Because different strains of bacteria cause empyema, finding the right antibiotic is crucial.
Drainage
To drain the fluid, a doctor performs a tube thoracostomy, which involves inserting an
ultrasound or computer-guided tube into the chest cavity and removing the liquid from the
pleural space.
Surgery
For advanced cases of empyema, surgery may be the best treatment option. One study
found that a surgery called decortication yielded better results than tube drainage in
Decortication involves removing the pus “pockets” and fibrous tissue from the pleural
There are two types of surgeries available. In most cases, a surgeon will perform a videoassisted
thoracotomy (VATS). This procedure is less invasive, less painful, and has a
shorter recovery time than an open-thoracotomy, which requires a surgeon to open the
specific criteria to decide when surgery is necessary for empyema. One study found that
those with symptoms lasting less than 4 weeks had better surgery results than people who
Fibrinolytic therapy
A doctor may also recommend fibrinolytic therapy, which uses drugs known as fibrinolytic
agents. The therapy helps to drain pleural fluid, and doctors may use it in combination with
comparison to fibrinolytic therapy after tube thoracostomy found that both methods are
highly effective.
Rare complications
• Fibrosis, which is when damaged lung tissue causes difficulty breathing that affects
• Empyema necessitatis, which is an extension of the infection into the chest wall
and soft tissue. This is very rare and requires immediate medical attention.
Outlook
Getting early medical attention can stop empyema from becoming a more severe
condition.
Treatment for empyema can vary depending on the severity of a person’s symptoms.
Antibiotics and drainage are the first steps, followed by surgery in more advanced cases.
Clinic: long course; cough, sputum, pulmonary hemorrhage, chest pain, shortness of
stages:
- initial stage)
g) the same, as well as severe disorders of cardiac, respiratory, liver, renal failure.
Differential diagnosis:
- lung abscess;
- pulmonary tuberculosis.
Treatment:
Stage I - conservative;
II - III and stage - operational (removal of the affected part of the lung); Stage III -
conservative.
51. Cyst of the lung. Etiology, clinical features, diagnosis, indications for surgery,
types of operations;
lung cysts -- sacs of tissue filled with air or fluid. Treatments can help, but your options
The symptoms are similar, so your doctor may suggest you get an imaging test called
high-definition computed tomography (CT) to figure out which cystic lung disease you
have. If that doesn't work, you may need to get a lung biopsy. Your doctor will remove a
small piece of tissue from your lung and send it to a lab for testing.
Other conditions can look like cystic lung disease, such as emphysema and honeycomb
lung. To confirm that you have it, your doctor will check things like how much air your lungs
can hold. He'll also look at the size, wall thickness, shape, and location of your cysts.
Cystic lung disease is rare. Most adults who get it have one of these four types:
Lymphangioleiomyomatosis (LAM)
LAM happens when muscle cells in the lung tissue grow out of control and form cysts,
which eventually damage your lung tissue. It mostly affects women between ages 20 and
40.
TSC-LAM is when you have LAM and a rare disease called tuberous sclerosis
complex (TSC). Sporadic LAM means you have LAM but not TSC.
Both kinds are thought to be due to changes in the tuberous sclerosis gene.
Doctors believe that estrogen plays a part in both types of LAM. The disease may get
worse during menstruation and pregnancy, and after using birth control pills with estrogen.
• Chest pain
• Tiredness
• Shortness of breath
• Wheezing
You may also have fluid collect in the space between your lungs and chest wall, a problem
called pleural effusion. It can make it hard to catch your breath. Fluid can also build up in
your belly, legs, and feet.You might get a collapsed lung if a cyst tears through the lining of
your lung. A collapsed lung happens when air leaks into the space between your lung and
chest wall and flattens part of your lung. This is an emergency and needs treatment right
away.
LAM doesn't have a cure, but you can treat it with sirolimus (Rapamune), a medicine that
can slow the disease and may even improve how well your lungs work.You could also
take bronchodilators, medicines that can help open up your airways and
make breathing easier.LAM can get worse over time. If it does, you may need oxygen
PLCH mostly shows up in young adults who are smokers or former smokers. In the early
stages, you may not have any symptoms, but if you do, they might include mild shortness
• Chest pain
• Fever
• Night sweats
• Tiredness
• Weight loss
PLCH begins when chemicals in cigarette smoke cause cells to grow abnormally in your
lungs. As the disease gets worse, scars form and the tissue becomes stiff and thick. You
may find it harder to breathe in enough air, and you'll get short of breath, even during
normal activities.
PLCH can cause a lung to collapse, sometimes more than once. Your doctor may suggest
you get a procedure called a pleurodesis. It closes up the space between your lungs and
chest wall and stops air or fluid from filling the space.It's not clear if PLCH is a cancer or an
immune disorder.
Either way, the first and most important treatment is to quit smoking. PLCH may stop
getting worse and even get better when you quit.You may also take a steroid medicine to
reduce inflammation. Some people with PLCH take a chemotherapy drug if steroids don't
help. If you're very short of breath, you may need to get extra oxygen from a machine or
tank.
BHD is caused by an abnormal gene that you inherit from a parent who has the disease.
You might also get BHD if there are changes to one of your genes, called a gene mutation.
Symptoms usually happen when you're in your 20s or 30s. Small skin bumps on your face
are the most common signs of BHD. These bumps are benign tumors (not cancer) in
the hair follicles. You may also have them on your neck, ears, or upper body.About 80% of
people with BHD have lung cysts. The cysts usually don't cause symptoms, and your lungs
work normally.Up to a third of people with BHD can have repeated lung collapses, and
15% to 30% can get kidney tumors. The tumors are usually slow growing and are
diagnosed at around age 48 to 50. You should get regular CT scans of your belly to find
The treatment for BHD depends on the symptoms you have. For example, your doctor
may remove skin bumps with a laser. If you have frequent lung collapses, he may
LIP is extremely rare. Doctors believe it's both a disease and a reaction to something in
LIP may happen if you also have an autoimmune disease, especially Sjögren’s syndrome.
In that condition, your immune system -- the body's defense against germs -- attacks the
glands that make your tears and saliva.About twice as many women as men get LIP. It's
typically diagnosed when you're between ages 52 and 56. The usual symptoms are
Your doctor may suggest you treat it with steroids to lessen inflammation. If steroids aren't
helpful, you may need to take medicine that tamps down the actions of your immune
system.
77. Anatomical and physiological information about the spleen. Classification of surgical diseases
of the
spleen.
ANATOMY
Size: The weight of the normal adult spleen is 75–250 g and it measures up to 10 × 7 × 3 cm.
Localization: It lies in the left hypochondrium between the gastric fundus and the left
hemidiaphragm, with its long
Topography:
The hilum sits in the angle between the stomach and the kidney and is in contact with the tail
of the pancreas.
The concave visceral surface lies in contact with these structures, and the lower pole extends no
further than the
mid-axillary line.
There is a notch on the inferolateral border, and this may be palpated when the spleen is
enlarged.
Arterial BS:
The tortuous splenic artery arises from the coeliac axis, usually from a common stem with a
hepatic artery, and
runs along the upper border of the body and tail of the pancreas, to which it gives small
branches.
The short gastric and left gastroepiploic branches pass between the layers of the gastrosplenic
ligament.
The main splenic artery generally divides into superior and inferior branches, which, in turn,
subdivide into
Venous drainage:
The splenic vein is formed from several tributaries that drain the hilum.
The vein runs behind the pancreas, receiving several small tributaries from the pancreas
before joining the
superior mesenteric vein at the neck of the pancreas to form the portal vein.
The splenic pulp is invested by an external serous and internal fibroelastic coat which is
reflected inwards at the
Lymphatics:The lymphatic drainage comprises efferent vessels in the white pulp that run with
the arterioles and
emerge from nodes at the hilum. These nodes and lymphatics drain via retropancreatic nodes to
the coeliac nodes.
Innervation: Sympathetic nerve fibres run from the coeliac plexus and innervate splenic arterial
branches.
PHYSIOLOGY
muscle fibres.
with germinal centres and periarterial lymphatic sheaths that provide a framework filled with
lymphocytes and
macrophages.
Arteries from the central artery and the peripheral‘penicillar’ arteries pass into the marginal
zone that lies at
Plasma-rich blood that has passed through the central lymphatic nodules is filtered as it passes
through the
Immunoglobulins produced in the lymphatic nodules enter the circulation through the sinuses
in the marginal
zone, beyond which lies the red pulp, which consists of cords and sinuses.
Cell-concentrated blood passes in the trabecular artery through the centre of the white pulp to
the red pulp cords.
Red cells must elongate and become thinner to pass from the cords to the sinuses, a process
that removes
As 90% of the blood passing through the spleen moves through an open circulation in which
blood flows from
arteries to cords, and thence sinuses, splenic pulp pressure reflects the pressure throughout the
portal system.
The remaining 10% of the blood flow through the spleen bypasses the cords and sinuses by
direct arteriovenous
1. Immune function.
The spleen contains 66.5% and 10–15% of the body’s total T and B lymphocyte population,
respectively.
It processes foreign antigens and is the major site of specific immunoglobulin M (IgM)
production.
These antibodies are of B- and T-cell origin and bind to the specific receptors on the surface of
macrophages
2. Filter function.
Macrophages in the reticulum capture cellular and non-cellular material from the blood and
plasma.
This will include the removal of effete platelets and red blood cells.
This process takes place in the sinuses and the splenic cords by the action of the endothelial
macrophages.
Iron is removed from the degraded haemoglobin during red cell breakdown and is returned to
plasma.
3. Pitting.
Particulate inclusions from red cells are removed, and the repaired red cells are returned to
the circulation.
These include Howell–Jolly and Heinz bodies, which represent nuclear remnants and
precipitated
4. Reservoir function.
This function in humans is less marked than in other species, but the spleen does contain
approximately 8%
An enlarged spleen may contain a much larger proportion of the blood volume.
5. Cytopoiesis.
From the fourth month of intrauterine life,some degree of haemopoiesis occurs in the fetal
spleen.
Stimulation of the white pulp may occur following antigenic challenge, resulting in the
proliferation of T and
This may also occur in myeloproliferative disorders, thalassaemias and chronic haemolytic
anaemias.
8. Plays a role in the endocrine system (connection with the thymus, thyroid, and sex glands - for
example, in
women, splenomegaly leads to the cessation of menstruation, and splenectomy returns this
function)
2. Traumatic injuries:
a) Open - closed
b) Isolated - combined
3. Acute diseases of the spleen (inversion of the spleen, spontaneous rupture, heart attack due
to embolism or
According to etiology:
hemaoma)
2. Parasitic
1. Nonparasitic cysts:
True (internally coated with endothelium). True cysts congenital and occur due to a violation
of
embryogenesis.
False (not having endothelial lining). False cysts acquired and arise most often after injuries,
infectious
According to number:
Single
Multiple.
Serous
Hemorrhagic character.
NON-PARASITIC CYSTS.
CLINIC
1) Persistent dull pain in the left hypochondrium with radiation to the left shoulder and shoulder
girdle.
2) With large sizes of cysts, pain can increase significantly, symptoms of compression and
displacement of
3) During physical examination, bulging in the left hypochondrium, some asymmetry of the
abdomen,
DIAGNOSIS
In the diagnosis of spleen cysts, the same methods are used as for abscesses of the spleen
1) Ultrasound scanning
avascular zone is determined on an x-ray in the projection of the spleen, displacing its intraorgan
vessels.
TREATMENT
Surgical Splenectomy
PARASITIC CYSTS
Ways of penetration of the parasite into the spleen is hematogenous, less commonly
lymphogenous.
spleen abscess.
DIAGNOSIS
TREATMENT
ETIOLOGY:
3) Embolic disorders – Atrial fibrillation, Mitral stenosis, Cholesterol embolus, Patent foramen
ovale, Bacterial
septic endocarditis
Gaucher disease, Sickle cell crisis in patients with sickle cell anemia, Vasculitis & DIVC
CLINIC
1) The infarct may be asymptomatic. or give rise to left upper quadrant and pain.
2) If symptomatic begins suddenly with intense sharp pains in the left hypochondrium,
sometimes radiating
The severity of the clinical picture depends on the size of the infected area of the organ.
4) Minor heart attacks can occur with minimal clinical manifestations or may be asymptomatic.
In most patients, self-healing occurs with the organization and scarring of the infarcted zone.
Less often, an infected
and purulent fusion of the infarcted zone is observed with the formation of an abscess of the
spleen, sometimes a false spleen cyst develops in the infarction zone.
DIAGNOSIS
Contrast-enhanced CT will show the characteristic perfusion defect in the enlarged spleen
TREATMENT
60. Definition of basic concepts: the transplantation, the recipient, donor, transplant
classification;
61. The immunological basis of Transplantation. Legal and ethical issues of organ
transplantation;
In accordance with the law of the Republic of Belarus dated July 13, 2012, a living donor is
a person who voluntarily gave consent in accordance with the established procedure for
the collection of organs and (or) human tissues for transplantation of organs and (or)
disorders (diseases), persons with a disease that is dangerous to the life and health of the
Organ harvesting for transplantation from a living donor is permitted subject to the
conditions:
• written warning of the donor by the attending physician to the state healthcare
organization about the possible deterioration of his health, organs for transplantation;
• the availability of the voluntary consent of the donor for the collection of organs,
expressed in writing, notarized;
• conducting a comprehensive medical examination of this living donor and the presence
The bone marrow is taken from a minor who has not acquired full legal capacity, with the
written consent of his legal representative, notarized, and the guardianship authority. In
Only one of the paired organs, a fragment of an unpaired organ, tissue, the absence of
which does not cause irreversible processes in the body, can be taken from a living donor
for transplantation.
Before organ harvesting, a living donor has the right to receive complete and objective
information about his state of health and the consequences that may arise in connection
Consent to organ harvesting can be revoked at any time, unless the doctors have already
started organ harvesting and its termination or return to its original state is impossible or is
Brain death is denied as the permanent loss of all brain functions in a beating heart
subject. Brain death is the result of a complete stop in cerebral circulation. At the same
time, the function of the remaining organs is preserved if the correct intensive therapy
continues, adapted to new conditions. Brain destruction stops the central commands of
A detailed history and clinical neurological examination are without a doubt the basis for a
The US Presidential Ethical Medicine Research Company in the United States formulates
the concept of “brain death” as follows: “Irreversible termination of the entire function of the
whole brain, including the cortex and brain stem, denied in accordance with accepted
medical standards.”
The list of data on the history of mandatory methods for examining a potential living kidney
donor (RLD) includes: ultrasound of the abdominal cavity, kidney, bladder, prostate, pelvic
organs. For a kidney recipient, the same examinations and dopplerography of the iliac
hypertension and decreased kidney function (GFR less than 80 liters per minute)
Criteria for selecting potential cadaveric kidney donors for transplantation: severe
Contraindications are: over 65 years of age and younger and 50 years old, bacterial
sepsis, active viral or bacterial infection (HIV, syphilis), chronic kidney disease, primary
kidney disease, oliguric acute renal failure, systemic disease with kidney damage,
malignant neoplasms.
A relative contraindication is: age over 60 years, arterial hypertension, treated infections,
including hepatitis, neoliguric acute renal failure, diabetes mellitus, covered intestinal
perforation, prolonged cold ischemia, poor hypodynamics (hypotension less than 50-60
The list of necessary studies for a living kidney donor: tissue typing, determination of
kidneys, if treatment has not been carried out or less than two years have passed since
the radical removal, the presence of infection in the body, decompensation of chronic
diseases of any organ (heart failure, UBJ, sugar diabetes), failure to follow the doctor’s
personality changes.
Assessment of renal transplant (TP): topometry of TP, assessment of the state of the
perinephric space, color and spectral Doppler ultrasound. When assessing the state of TP,
the contour of the kidney, the uniformity and echogenicity of the parenchyma, the state of
the renal sinus, ChLS and the ureter are evaluated. The cortical layer is calculated by
three measurements at the poles and in the middle segment, the height of the pyramids,
the size of the central echocomplex are estimated, the sizes of the cups, pelvis and ureter
are measured. Assessment of the condition of the perinephric space includes the search
for free fluid around TP, which can be observed with the formation of hematomas, urine,
and lymphocele. CDK allows you to assess the patency of the main vessels of TP, arteries
and veins, as well as the uniformity and degree of perfusion of the vascular bed up to the
blood ow velocity and the resistance index of the main, lobar, segmental, arc and
Ultrasound examination of TP is carried out at 1, 3, 5, 7, 10, 14, 21, 30, 60. 90 days.
Clinical observation is carried out 1 time in 30 days during the rst year according to clinical
With spectral Dopplerography, RI is less than 0.7 clinically - adequate diuresis and a
indicator. When RI is greater than 0.8, the clinically functional state of TP is denied as
An increase in RI of more than 0.8 is a reliable criterion that makes it possible to ascertain
a violation in the operation of TP. At the same time, a decrease in RI is a good prognostic
sign. The causes of the acute reaction of rejection of TP are: acute tubular necrosis, acute
TP rejection reaction:
- super acute several hours after transplantation, not amenable to treatment; - acute
Complications after transplantation are: bleeding, failure of the anastomosis of the ureter
with the bladder and the formation of urinary fistulas, infection of the wound and bed of the
management;
Classification of heart failure Strazhenko-Vasilenko:
Stage I. Initial latent circulatory failure, which manifests itself only during physical exertion,
Stage II. Severe prolonged circulatory failure, hemodynamic disturbances in the small and
Period B.'s period the end of a long stage, the expressed hemodynamic disturbances in
which all cardiovascular system is involved (and big and small circles of blood circulation).
Stage III. The final dystrophic with severe hemodynamic disorders, persistent metabolic
changes and irreversible changes in the structure of organs and tissues. Functional
Class II: slight limitation of physical activity: at rest, there are no symptoms, habitual
Class III: a marked limitation of physical activity, at rest there are no symptoms, physical
appearance of symptoms.
Class IV: the inability to perform any physical activity without the appearance of discomfort;
symptoms of heart failure are noted at rest and intensify with minimal physical exertion.
Indications for inclusion in the waiting list on the vehicle are divided into:
unstable uid balance, which is not associated with the patient's observation of body weight
In 50% of the recipients included in the waiting list, the average life expectancy according
to generally accepted indications for DCMP was 5.6 ± 2.7 months, and for coronary artery
Epidemiology
The disease is common in the Indian subcontinent, Africa and parts of Central and South
America, where almost
The mode of infection is via the faeco-oral route, thus insanitary conditions and poor personal
hygiene encourage
Therefore, the population from the poorer socioeconomic strata are more vulnerable.
Patients who are immunocompromised and alcoholics are more susceptible to infection.
Amoebic liver abscess, the commonest extraintestinal manifestation, occurs in less than 10%
of the infected
population and, in endemic areas, is much more common than pyogenic abscess.
Pathogenesis
In the small intestine, the parasite hatches into trophozoites, which invade the submucosa to
produce flask-shaped
ulcers.
In the portal circulation, the parasite causes liquefactive necrosis in the liver, producing an
abscess, the commonest
extraintestinal manifestation.
The majority of abscesses occur high in the diaphragmatic surface of the right lobe of the liver.
One possible explanation for the more common involvement of the right lobe of the liver is
that blood from
the superior mesenteric vein runs on a straighter course through the portal vein into the larger
lobe.
The abscess cavity contains chocolate-coloured, odourless, ‘anchovy sauce’-like fluid that is a
mixture of
There may be secondary infection of the abscess which causes the pus to smell.
While pus in the abscess is sterile unless secondarily infected, trophozoites may be found in
the abscess
Chronic infection of the large bowel may result in a granulomatous lesion along the large
bowel, most commonly
CLINICAL FEATURES
1. Gradual in onset, with symptoms presenting over 1-2 weeks cramping abdominal pain,
watery or bloody
2. Bloody mucoid diarrhea (raspberry jelly) in a patient from an endemic area or following a
recent visit to
such a country
The typical patient with amoebic liver abscess is a young adult male
1. Insidious onset of non-specific symptoms abdominal pain, anorexia, fever, night sweats,
malaise,
2. Gradually progress to more specific symptoms pain in the right upper abdomen and right
shoulder
tip, hiccoughs and a non-productive cough.
Examination
2. The patient will have upper abdominal rigidity, tender hepatomegaly, tender and bulging
intercostal
spaces, overlying skin oedema, a pleural effusion and basal pneumonitis – the last feature is
usually a late
manifestation.
4. Rarely, the patient may present as an emergency due to the effects of rupture of an abscess
into the
DIAGNOSIS
Laboratory tests
3. Rigid sigmoidoscopy using a disposable instrument rectosigmoid show shallow skip lesions
and ‘flaskshaped’ or ‘collar-stud’ ulcers, punctuate hemorrhages.
4. These can be biopsied or scrapings can be taken along with mucus for immediate microscopic
examination. The presence of trophozoites distinguishes the condition from ulcerative colitis.
Imaging techniques
1. US
2. CT
3. MRI
Diagnostic aspiration is of limited value except for establishing the typical colour of the
aspirate, which is sterile
and odourless unless it is secondarily infected.
TREATMENT
Medical treatment is very effective and should be the first choice in the elective situation, with
surgery being
CONSERVATIVE TREATMENT
Follwed by diloxanide furoate, which is not effective against hepatic infestation, for 10 days
to destroy any
intestinal amoebae.
EXTRA:
Amoeboma
This is a chronic granuloma arising in the large bowel, most commonly seen in the caecum.
It is prone to occur in chronic amoebic infection that has been treated intermittently with
drugs without
An amoeboma should be suspected when a patient from an endemic area with generalised ill
health and
pyrexia has a mass in the right iliac fossa with a history of blood-stained mucoid diarrhoea.
Such a patient is highly unlikely to have a carcinoma because altered bowel habit is not a
feature of rightsided colonic carcinoma.
While iron deficiency anaemia is a classical elective presentation of a caecal carcinoma, the
same is present in
For abscess that is expected to rupture Aspiration; also helps the penetration of
metronidazole.
The threshold for aspirating an abscess in the left lobe should be lower because of its proximity
to the pericardium.
SURGICAL TREATMENT
Only for complications rupture into the pleural (usually the right side), peritoneal or pericardial
cavities; severe
1. Rupture into the pleural (usually the right side), peritoneal or pericardial cavities
Resuscitation,
drainage and appropriate lavage with vigorous medical treatment are the key principles.
2. Toxic megacolon surgical emergency, the principles of management being the same as for
any toxic
megacolon.
All such cases are managed in the intensive care unit, as would any patient with toxic
megacolon whatever
the cause.
3. An amoeboma that has not regressed after full medical treatment colonic resection,
particularly if cancer
cannot be excluded.
86. Echinococcosis (Hyatid disease). Clinic, diagnosis, treatment, indications for surgical
treatment, types
of operations.
Hydatid disease is caused by Ecchinococcus granulosus, commonly called the dog tapeworm.
Close contact with an infected dog, sheep or cattle causes contamination by the oral route,
with the ovum thus
The parasite can affect any organ or several organs in the same patient. The liver is the organ
most often affected.
The lung is the next most common. Can also affect the spleen, brain, heart and kidneys,
CLINICAL FEATURES
1. LIVER enlarging painful mass in the right upper quadrant with the physical findings of a liver
swelling.
Dull pain from stretching of the liver capsule.
2. Daughter cysts may communicate with the BILIARY TREE obstructive jaundice and its usual
clinical
features.
3. LUNGS, if cyst is large enough dyspnea, cough, expectoration, fever, chest pain and
sometimes
haemoptysis. Silent cysts may present as an emergency due to rupture or an allergic reaction.
The patient may present as an emergency with severe abdominal pain following minor trauma,
when the CT scan
may be diagnostic.
Rarely, emergency presentation anaphylactic shock due to rupture of cyst. Such a patient
may subsequently
cough up white material that contains scolices that have travelled into the tracheobronchial tree
from rupture of a
DIAGNOSIS
TREATMENT
LIVER
Surgical treatment PAIR (puncture, aspiration, injection of scolicidal agents and reaspiration).
echinococcus accidental spillage of fluid during PAIR or to minimize cyst size before surgery.
10% solution). This may cause sclerosing cholangitis if biliary radicles are in communication with
the cyst wall.
Cysts in other organs need to be treated in accordance with the actual anatomical site, along
with the general
principles described.
LUNGS
pneumonectomy.
87. Alveococcosis. Clinic, diagnosis, treatment, indications for surgical treatment, types of
operations.
The lung is the second commonest organ affected after the liver.
The size of the cyst can vary from very small to a considerable size.
The right lung and lower lobes are slightly more often involved.
The cyst is usually single, although multiple cysts do occur and concomitant hydatid cysts in
other organs, such
CLINICAL FEATURES
2. Symptomatic patients’ dyspnea, cough, expectoration, fever, chest pain and sometimes
haemoptysis.
EXTRA;
Laparoscopic management
In the initial steps, the cyst is aspirated, taking care not to spill any contents, using povidone
iodine or hypertonic
Any communication with the biliary tree is oversewn and pedicled omentum is sutured to the
margins of the cyst.
If the cyst is small, superficial and in the left lobe, cystopericystectomy is performed at centres
experienced enough
DIAGNOSIS
Erosion of the bronchioles results in air being introduced between the pericyst and the
laminated membrane
3. CT scan when the cyst ruptures, the crumpled collapsed endocyst floats in the residual fluid,
giving rise to
TREATMENT
pneumonectomy.
Medical treatment is less successful and considered when surgery is not possible because of
poor general
88. Opisthorchiasis. Clinic, diagnosis, treatment, indications for surgical treatment, types of
operations.
Liver flukes: Opisthorchis (specifically, Opisthorchis viverrini and Opisthorchis felineus).
Chronic infection may lead to cholangiocarcinoma, a malignant cancer of the bile ducts.
Pathology
In humans, the parasite matures into the adult worm in the intrahepatic biliary ducts where
they may reside for
many years causing chronic inflammation of the bile ducts dilation of intrahepatic bile ducts,
with
These changes may lead to dysplasia, causing cholangiocarcinoma – the most serious and
dreaded
The eggs or dead worms stone formation in the gallbladder or common bile duct, which
becomes
Intrahepatic bile duct stones are also caused by the parasite producing mucin-rich bile.
The dilated intrahepatic bile ducts may lead to cholangitis, liver abscess and hepatitis.
CLINIC
The disease may remain dormant for many years. Most infected persons are asymptomatic and
exhibit no physical
signs.
Symptomatic:
1. Non-specific symptoms mild fever, malaise, anorexia and upper abdominal discomfort.
2. Heavier infection The complete clinical picture can consist of fever with rigors due to
ascending
cholangitis, lack of appetite (anorexia), fatigue, obstructive jaundice, biliary colic and pruritus
from stones
Acute pancreatitis may occur because of obstruction of the pancreatic duct by an adult worm.
1. Accumulation of fluid in the legs (edema) and in the peritoneal cavity (ascites);
DIAGNOSIS
Lab Tests
1. GBA Oesinophilia
4. PCR
Instrumental Tests
1. Ultrasound scan of the hepatobiliary system dilatation of intrahepatic bile ducts with only
minimal
dilatation of the common hepatic and common bile ducts, (but latter are much more dilated
when the
The thickened duct foci in the bile ducts representing the worms or eggs.
TREATMENT
CONSERVATIVE TX
Alternative Albendazole
SURGERY
89. Ascariasis. Clinic, diagnosis, treatment, indications for surgical treatment, types of
operations.
Epidemiology
Typically found in a humid atmosphere and poor sanitary conditions, hence is seen in the
tropics and
resource-poor countries
Pathogenesis
Larvae cause pulmonary symptoms; adult worms cause gastrointestinal, biliary and pancreatic
symptoms
Distal ileal obstruction is due to a bolus of worms; ascending cholangitis and obstructive
jaundice from
CLINICAL FEATURES
1. The larval stage in the lungs causes pulmonary symptoms Loeffler’s syndrome: dry cough,
chest pain,
3. Small intestine malnutrition, failure to thrive, particularly in children, and abdominal pain.
Small intestinal obstruction can occur, particularly in children, due to a bolus of adult worms
incarcerated
Rarely, perforation of the small bowel may occur from ischaemic pressure necrosis from the
bolus of
worms.
6. Allergies Ascariasis may result in allergies to shrimp and dustmites due to the shared
antigen, tropomyosin;
7. Others Ascaris have an aversion to some general anesthetics and may exit the body,
sometimes through the
If a person from a tropical country, or one who has recently returned after spending some time
in an endemic area,
peritonitis; biliary colic; acute cholecystitis; acute pancreatitis; acute cholangitis; hepatic abscess.
DIAGNOSIS
Laboratory Tests
1. GBA Eosinophilia
Instrumental Tests
PULMONARY TESTS
GIT TRACTS
3. A barium meal and follow-through may show a bolus of worms in the ileum or lying freely
within the small
bowel.
4. Ultrasound may show a worm in the common bile duct or pancreatic duct.
Intestinal obstruction:
6. Plain abdominal radiograph may show tubular structures within dilated small bowel,
denoting the
presence of worms.
TREATMENT
CONSERVATIVE TX
2. Intestinal disease patients should ideally be under the care of a physician for treatment with
anthelmintic
drugs.
Certain drugs may cause rapid death of the adult worms and, if there are many worms in the
terminal ileum,
the treatment may actually precipitate acute intestinal obstruction from a bolus of dead worms.
3. Children who present with features of intermittent or subacute obstruction should be given a
trial of conservative
management in the form of intravenous fluids, nasogastric suction and hypertonic saline
enemas.
The last of these helps to disentangle the bolus of worms and also increases intestinal motility.
SURGERY
Indications: Surgery is reserved for complications, such as intestinal obstruction that has not
resolved on a
1. At laparotomy, the bolus of worms in the terminal ileum is milked through the ileocaecal valve
into the colon
for natural passage in the stool. Postoperatively, hypertonic saline enemas may help force out
the worms.
3. If the bowel wall is healthy enterotomy and removal of the worms may be performed.
4. Rarely, when perforation occurs the parasites may be found lying free in the peritoneal
cavity. It is safer to
bring out the site of perforation as an ileostomy because, in the presence of a large number of
worms, the
closure of an anastomosis may be at risk of breakdown from the activity of the worms.
laparoscopic or open exploration of the common bile duct is necessary. Cholecystectomy is also
carried out.
actual diagnosis at operation may turn out to be acute appendicitis, typhoid perforation or a
tuberculous stricture,
and the presence of roundworms is an incidental finding. Such a patient requires the appropriate
surgery depending
INTERVENTION