Gs Preparation

Suggested Answers for General Surgery Final Examination 2008 1
1. History of surgery
Ancient period
Ancient Greek, Rome, Chinese and Indian civilizations made significant contributions to the development of surgery. Babylonian physicians were able to
open purulent cavities with bronze knives. Wound irrigation was accomplished using honey, milk and plain water. They were able to close wounds using
animal hair or tendons. The Chinese used the wine and bread for the care of a wound. Cosmetic surgery and anesthesia using inhaled opium were firstly
attempted in China. Ancient Indian physicians described more than 100 surgical instruments, including scalpels, lancets, scarifies, saws, trocars and
needles. They were widely renowned for skills in plastic surgery, introduction of skin pedicle flaps, etc. However, the Greek civilization was considered
as the most ancient and influencing one. It gifted the world with the word "surgery" Hyros (hand) - and urge (action).
At around 400 B C. the first systematic description of wounds, dislocations, fractures, and their treatment was done by Hippocrates. He introduced the
term "desmurgy" desmos - connecting, urge - action. His Corpus Hippocraticum was the collection of knowledge precisely describing different types of
wounds, ulcers, injuries, fractions, and their treatments.
Galen, a famous physician whose views dominated European medicine for almost 15 centuries, until the time of Renaissance, considered that diseases
were caused by the humors - yellow bile, black bile, blood and phlegm.
Medieval Period
In 1125 AD, The French University was opened. Doctors used the same approach at treatment as 1000 years ago. Surgery during the middle Ages was
performed predominantly by barber surgeons. Lack of knowledge and ban of surgery by church were most important obstacles. Anatomy was still
shaded; autopsy for education purposes was permitted only twice a year.
In 1338 AD, the invention of gunpowder led to a widespread of gunshot wounds. In 1400 AD, the French army used wine to irrigate wounds and spider's
web to stop bleeding.
Renaissance Period
During the Renaissance, surgery did slowly begin to regain a higher social position. Most prominent physicians and anatomists were Vesalius, Fabricius,
William Harvey, and Paracelsus.
Paracelsus considered a pus in the wound as a negative event, comparing it with the rotted apple justifying necrectomy as a part of treatment. He blamed
it on the bloodletting procedure.
Vesalius presented an anatomy which broke former views of Galen's human structure. He created a practical anatomy atlas for students at those times
which were most accurate and complete. Anatomy of muscular and venous systems was shown. But still achievements were not used fully.
Ambroise Pare introduced dressing soaked by rose oil and egg yolk instead of former wound treatment with boiling oil. He described debridement of
gunshot wound, ligation of vessels, etc. In 1597, The method of Italian plasty using migrating flap was introduced. The military time were considered to
be the real opportunity for practice and innovations in surgery. New influx of knowledge was gained during Napoleon wars. In 1794-1814 Jean Larrey as
a doctor performed more than 200 amputations daily, stressed an importance of extremities’ immobilization. Formerly, immobilization was usually done
using wooden boards.
In 1851-1855, a Flemish surgeon, Matise invented plaster cast. It does not differ a lot from the modern type we are using now.
Modern Period
In the nineteenth century, the surgeon emerged as a specialist and a respected medical practitioner. But at the first half of century the scope of surgery
remained limited. Surgeons treated only simple fractures, dislocations and abscesses and performed amputations technically perfect but with high
mortality rate. They managed to ligate major arteries for common and accessible aneurysms and made attempts to excise external tumors, but the
abdominal surgery was virtually unknown.
There were numerous obstacles to the advance of surgery. Pain, infection, hemorrhage and shock were four of the most difficult to overcome. Narcotic
and analgesics agents such as opium, alcoholic beverages, mandrake root, or even reduction of blood flow to the brain to diminish sensibility had been
used for thousands of years to alleviate human pain. In 1831, 3 main anesthetics were introduced: ether, nitrous oxide, and chloroform, but without
practical application.
The effective use of general anesthesia can be precisely dated to the 1840s. William Morton successfully used ether. It became obvious that these
substances could be applicable to surgical operations. First successful surgery of vascular tumor under ether anesthesia was done 1846 by Jon Warren.
Besides, for thousands of years, different materials were used as dressing eg lint and canvases. Purulent complications were common after even perfectly
performed surgery.
During 1847-1848, the second crucial step was an introduction of antisepsis as part of wound treatment. Phillip Shimmelvaise (Hungarian surgeon)
introduced disinfection of hands before taking the birth care;
Louis Pasteur discovered microorganisms responsible for fermentation and developed a ‘germ theory’ of disease. He showed that the pus formation and
inflammation were caused by living, multiplying matter. Joseph Lister continued his research from the practical point of view.In 1867, he introduced the
method of soaking gauze in carbolic acid. 1870 Listers’ concept was that everything that was in contact with wound must be sterile (hand washing,
wound and instrument irrigation, air spraying). He introduced a new suture material known as catgut, which is absorbed by tissues in several weeks.In
1870-80 An antiseptic concept had already developed. Special operating rooms, dressing rooms, their separation, clean and dirty areas, shaving, cleaning,
and other rules were invented
1874 German surgeon, Kirsh, had introduced a split-thickness skin graft, special stainless wires (treatment of fractures), etc. Theodor Billroth, Esmarch
1879 introduced tourniquet to stop bleeding and special device for wound irrigation. Mikulicz, Volkmann, Bergmann were the famous surgeons who
made great contributions in the history of German abdominal surgery.
1878-80 Robert Koch at first described specific microorganisms (different species like mycobacterium tuberculosis, staph, etc.) responsible for different
forms of infection.
1883-84 Kocher’s (German) surgical treatment of goiter, earned Kocher a Nobel Prize in 1909 – the first time it was awarded to a surgeon.
The new view on the origin of diseases was that a disease was localized and hence remediable by surgical intervention. Rudolf Virchow was the first, who
localized disease process within the cell especially cellular changes developing during inflammation (leukocytosis), and vessels’ change (thrombosis,
etc.).
First steps in neurosurgery were done by Harvey Cushing. He introduced the practice of sphygmomanometry into the operating room (beginning of the
monitoring during surgical operation). 1895 instruments used to cutting end exploration of tissues were invented.
In 1895 pressurized irrigation set was invented for the evacuation of necrotic materials and pressurized pulsatile irrigation of the wound in 1971-73.
The discovery of X-rays by Roentgen in 1995. Primarily used to bones and tissues, within a few years the use of rays was expanded and include
physiologic studies such as those of swallowing and intestinal motion.
1905 William Halsted, an American surgeon, made numerous important contributions to surgical technique and teaching. He introduced the use of rubber
gloves into the surgery, developed improved methods for operating on hernias and cancer of the breast. He took part in the establishing the "surgical
residency system", new program of education provided systematic way of young surgeons training.
Organ transplantation. Alexis Carrel overcame the problem of blood supply of transplanted organ by reconnecting the blood vessels by means of end-to-
end suture. In honour of that, he was awarded the Nobel Prize in 1912.
Non Operative Surgical Techniques
2. Central venous access and venous cut-down: indications and contraindications, procedure, complications
Central venous access can be performed by using the subclavian vein and the internal jugular vein.
Indications:
a) central venous pressure (CVP) monitoring;
b) poor peripheral access;
c) long term infusion of drugs;
d) total parenteral nutrition (TPN).
Contraindications:
a) venous thrombosis;
b) coagulopathy (PC below 50,000);
c) sepsis.
Seldinger needle and guide wire for introducing an arterial catheter
Procedure:
1. Trendelenburg’s position of a patient is used for puncture of the central neck veins.
2. The area is prepped (with antiseptic) and draped (sterile environment).
3. Anesthesia is done as usual (with 1% Lidocaine 2-3ml).
4. The needle is passed under the clavicle horizontally, while aspirating, towards the sternal notch. It is advanced to 5 cm. The venous blood in the
syringe appears once the needle has entered the vein.
5. The Seldinger’s technique is further used. The J wire is introduced through the needle, after that the needle is removed and the dilator and scalpel may
be used to increase the size of the skin puncture. Introduce the CV catheter over the wire and aspirate the blood. Flush the line with sterile solution, suture
the catheter to the skin and apply steriledressing. (Subclavian vein puncture using Hickman’s catheter or supraclavicular approach may also be
accomplished)
6. Auscultation, percussion, or plain chest X-ray are used to rule out pneumothorax.
Complications:
a) arterial puncture;
b) air embolism;
c) pneumothorax;
d) disrhythmias;
e) hemothorax;
f) injury to brachial plexus, trachea, or esophagus;
g) chylothorax.
Venous cut-down
Indications: when the peripheral access cannot be gained;
Site: at the middle of the ankle is preferred. Position is supine.
Procedure: With transverse incision after local anesthesia the vein is exposed, dissected, the distal ends ligated. Insert the catheter through a venotomy
and tie the proximal suture. The wound is closed with skin suture.
Complications: bleeding, infection, phlebitis.
3. Arterial access: indications and contraindications, procedure, complications

Indications:
a) continuous hemodynamic monitoring (PR, BP, systemic arterial pressure, etc);
b) those who receive inotropic agents;
c) thermodynamically unstable patient;
d) frequent assessment of arterial blood gases – Pa CO2, Pa O2, lactate level,.
Preference of the arteries: Radial → Ulnar → Femoral → Dorsalis pedis → Axillary;

Prep solution - alcohol 70% (povidon-iodine or chlorhexidine), mask, gown, gloves, towels, dressings are necessary to secure an aseptic technique.
needles, syringes, local anesthetic (usually 1% lidocaine 2-3ml), and arterial catheter.
Procedure (E.g. Radial artery cannulation)

The needle is oriented at 45 degrees towards radial artery till aspiration of the blood. May be used quick catheter (needle is already covered by the
catheter, so the J wire as well as Seldinger’s technique are not necessary. Direction must be from the periphery to center. Then the system is flushed and
sensors are attached to monitor to assess arterial waveforms.
Contraindications: positive Allen's test (it evaluates the ulnar blood flow through a palmar arch).
“Allen’s test: 1) occlude both ulnar and radial artery till exsanguination; 2) release the ulnar artery while keeping the radial artery compressed; 3) if
hand color doesn't return to normal in less then 5 sec, Allen's test is positive and cannulation is aborted.”
Complications: ischemic digits (remove the catheter), thrombosis, septic complications.
4. Placement of Swan-Ganz catheter and intraaortic balloon pump: indications and contraindications, procedure, complications.
Swan Ganz Cathether (pulmonary artery catheter)
Indications:
a) severe cardiopulmonary disarrangement (myocardial failure, infarction), assessment of the efficacy of certain drugs (inotropes), diagnosis of pericardial
tamponade, mitral regurgitation;
b) hypovolemic shock not responding to resuscitation;
c) severe pulmonary disorders (pulmonary edema and ARDS due to shock);
Contraindications: vein thrombosis, severe pulmonary hypertension, coagulopathy, ongoing sepsis.

Sites of insertion:
Priority is the following: right jugular → left subclavian → left jugular → right subclavian vein
Procedure (posture, equipment, anesthesia are the same).
1. Test all ports for all lines by inflating and deflating the balloon and flushing all the ports.
2. Connect the catheter to pressure monitoring line.
3. The sheath is placed over the catheter and it is inserted according to Seldinger technique.
Placement of the Swan - Ganz catheter according to pressure changes which vary depending on localization of the catheter. PAWP is evident by
appearance of dampened wave forms at the screen.
Localization of the catheter should be confirmed by X-ray at least once daily.

Complications: infectious, those associated with CV puncture, ventricular arrhythmias or complete heart block, lodging of the catheter at the trabeculae,
puncture of the right ventricle (followed by cardiac tamponade)
damage of valves (if inflated and long in place), intracardiac knotting, distal migration with pulmonary infarction (also may be caused by over inflation of
the balloon),perforation of the pulmonary artery, disruption of the balloon (due to overinflation).
NB! The catheter should never be left in wedge position.
CVP (v. cava and right atrium = 5-15 mmHg or 50-150 mm of water column);
Normally the PAWP is approximately 15 mmHg, it reflects left ventricular end-diastolic pressure(LVEDP) but does not reflect end-diastolic volume and
stroke volume;
Increase of PAWP higher than 25 mmHg leads to pulmonary edema.
Intraaortic balloon pump counterpulsation (IABPC).
Indications:
a) cardiogenic shock;
b) refractory left ventricular failure;
c) unstable angina refractory to medical treatment;
d) support during PT coronary angioplasty;
Contraindications: end stage heart disease, aortic aneurysm, aortic insufficiency, peripheral vascular disease of femoral or iliac artery.
Procedure: IABPC insertion.

1. The approach is the same as for right femoral artery access (1-2cm distally to inguinal ligament over the pulsation of femoral artery).
2. Using Seldinger’s technique, the balloon is passed over guidewire.
3. If placed properly, the tip of the balloon is approximately 2 cm distal to the take off of the left subclavian artery in the descending thoracic aorta.
Secure the catheter with suture and attach to IABP system. X-ray is used to confirm right position after insertion (final position)
4. After removal a manual pressure is applied during 30 min. Monitoring of the distal pulse and possible expanding hematoma is required.
Complications: limb ischemia, aortic dissection, renal injury, thromboembolism, bleeding, infection.
5. Bladder puncture and laparocentesis: indications and contraindications, procedure, complication

Percutaneous suprapubic cystostomy.(Bladder puncture)
Indications: acute urine retention due to urethral stricture, inability to catheterize, acute prostatitis, traumatic urethral disruption, periuretral abscess.
Several types of suprapubic catheters are present. Bonanno and Stamey (below, with self-retaining mechanism) catheters.
Contraindications: prior midline infraumbilical incision, non distended bladder, coagulopathy, pregnancy.
Procedure:
1. Shave, prep, and drape the area above symphysis pubis.
2. Puncture of the bladder is done with spinal needle (anesthesia and guide).
3. After penetration through the second point of resistance remove the obturator, attach the syringe, and aspirate the urine.
4. Assembled suprapubic catheter is inserted parallel to spinal needle.
5. The catheter is secured with skin suture and connected to urinary drainage system.
Complications: bowel perforation, hematuria.
Laparocentesis (paracentesis).
Indications:
a) diagnostic (to evaluate an effusion);
b) treatment (evacuation of ascitis);
Contraindications: skin infection, previous abdominal surgery (adhesions), pregnancy, coagulopathy.
Procedure:
Sites of puncture: Lower quadrant (anterior superior iliac spine), Lateral to the rectus muscle at the level of or below the umbilicus, infraumbilically in the
midline.
1. A patient should empty the bladder before the procedure.
2. The catheter is advanced using Seldinger or alternatively the procedure may be accomplished with trocar technique (can’t ensure complete evacuation
of the fluid).
3. Catheter for continuous laparocentesis are used (with fixating subcutaneous cuffs). The patient is at supine position. Sitting position is employed with
trocar technique.
4. Final position of the catheter is in the Douglas pouch.
Complications:
Hypotension, bowel perforation, hemorrhage, persistent ascetic leak, bladders’ perforation, infections.
6. Joint’s puncture: indications and contraindications, procedure, complications
Indications to procedure of joint puncture (arthrocentesis):
1) Diagnostic aim: to evaluate an effluent (blood, pus, etc.);
2) Treatment aim: to treat the diseased joint (evacuation of pus, drug’s injection, etc.);
Contraindications: Local infections (underlying cellulitis), systemic infections with possible bacteremia, coagulopathy, hemophilia.
Procedures: (Diagrams are available in lecture notes “Non Operative Surgical Techniques”)
Sites of puncture:
a) Shoulder joint:
1. Make a triangle with the coracoid process as the medial point, tubercle of the head of humerus as the lateral point and tip of the acromion as the
superior point.
2. Insert the needle at the center of the triangle to a depth of 1 – 2cm with the needle pointing posteriorly. (Arm may need to be rotated internally and
externally to find entrance point.)
b) Elbow joint – Insert a needle at posterior aspect just lateral to the olecranon.
c) Wrist joint – Insert a needle at the base of snuffbox just adjacent to the radial aspect of extensor pollicis longus. (The Snuffbox can be palpated with
the thumb in extension)
d) Knee joint – Insert a needle laterally at the level of superior pole of patella, then advance into the joint.
e) Ankle joint – Insert a needle 2.5cm proximal and 1.3 cm medial to the tip of lateral malleolus.
Techniques:
1. Patient is placed in a comfortable position, preferably supine.
2. Identify site of puncture.
3. Clean skin with povidone iodine and prep the entire joint.
4. Inject 1% Lidocaine subcutaneously at the point of needle entry and raise a wheal with a needle.
5. With a longer needle, inject lidocaine into the periarticular tissues.
6. Attach the longer needle to a large syringe and insert into the joint.
7. Aspirate and later stabilize the needle with a clamp to enable the exchange of syringe.
Complications:
Infections, intraarticular and periarticular bleeding, allergic reaction, Tendon rupture, weakness of extremity due to injection of nerves, etc.
7. Pericardiocentesis: indications and contraindications, procedure, complications

Indications:
a) diagnostic (to evaluate an effusion);
b) treatment (evacuation of the blood to relief the cardiac tamponade);
Contraindications:
a) Coagulopathy (Platelets< 50 000, PT or PTT >1.3)
b) Post coronary bypass surgery because of risk of injury to grafts.

c) Acute traumatic hemopericardium
d) Small pericardial effusion (<200 ml)
e) Absence of anterior effusion or if effusion is loculated.
Procedure
1. Sterile prep and drape the chest and subxiphoid area.
2. Identify site of entry : 0.5 cm laterally from the left xiphoid tip.
3. Administer 1% Lidocaine solution.
4. Insert a long needle through the anesthetized skin at the same point.
5. Attach a precordial limb lead of the ECG to the needle for monitoring.
6. Advance the needle through the skin at a 45o angle to the thorax and directed posteriorly, aiming towards the left shoulder.
7. When contact is made with the epicardium of the pericardial sac, negative deflection of the QRS complex will be seen. Advance the needle further into
the pericardial space where blood or effusion may be encountered. If ST elevation is present, it indicates contact with myocardium. In this case, withdraw
the needle back to the pericardial space and aspirate all the fluid present.
8. For continuous drainage, place a catheter using the Seldinger technique.
Complications: cardiac puncture, laceration of the coronary artery, air embolus, cardiac arrhythmias, hemo- or pneumothorax.
8. Thoracentesis and thoracostomy: indications and contraindications, procedure, complications
Thoracentesis is used to evacuate an effusion from the pleural cavity :

Indications:
1) Diagnostic purpose (to obtain the specimen of effusion);
2) Treatment purpose (evacuation of the effusion from the pleural cavity to relieve dyspnea).
Contraindications: coagulopathy (platelets less than 50,000), small-volume effusion, mechanical ventilation, uncooperative patient.
Procedure:
Patient is seated straight, erect with the body leaning anteriorly against the back of a chair.
1) Prep and drape the area of 7th- 8th ICS. (Lines that can be used: Midaxillary, posterior axillary, scapular line)
2) Administer 1% Lidocaine solution.
3) Place a needle on a syringe and insert it into the pleural space.
4) Place a catheter using the Seldinger’s technique. A three-way stopcock prevents backflow of fluid once closed. If one-way valve is not available, the
clamp may help prevent the air to reenter the pleural cavity.
5) The catheter is connected to extension tubing and vacuum apparatus. Having completed an evacuation of the fluid, remove the catheter and place
sterile dressing. X-ray, auscultation, and percussion are used to assess effect.
Complications: intercostal vessel damage (hemothorax), pneumothorax, lung injury.
Antisepsis and Asepsis

9. Antisepsis definition and types –complete characteristics of all types (chemical, physical, etc.)
Antisepsis is a complex of measures oriented on removing, inhibition of growth or killing of microorganisms which are already present in the wound.
It can be divided into the following types:
 Mechanical antisepsis (e.g. surgical debridement, amputation)
 Physical antisepsis (e.g. use of UV, laser)
 Chemical antisepsis (e.g. chemical antiseptic agents)
 Biological antisepsis (e.g. antibiotics, serums, enzymes)
 Combined (mixed) antisepsis
Mechanical antisepsis
Surgical debridement is the procedure of removal of all necrotized, nonviable tissues (affected parts of the skin, subcutaneous fat, muscles or even
bone). The purpose of the procedure is to remove all nonviable tissues and create the best environment for the healing process and prompt closure of the
wound.
Amputation is the removal of the distal part of an extremity. It is absolutely indicated if the extremity is obviously nonviable. Relative indications are
when the condition of the limb presents a direct threat to patient’s life. They are the severe infections, incurable conditions, etc.
Physical antisepsis
Pressurized pulsatile irrigation of the wound is a necessary adjunctive therapy of the wound cleaning. It helps to fulfil finer debridement, remove all
pus, tiny particles, and foreign bodies. The procedure requires 1-7 L of fluid. Commonly used agents are saline solution, furacilline, chlorhexidine,
aqueous antibiotics, etc.
Low frequency ultrasound action onto the wound cavity. The mechanism of action of the ulrasound is provided by the mechanical cleaning of the
wound due to disintegrative action on the necrotized areas and improvement of blood circulation. The period of action varies from 2 to 8 minutes. This
procedure is effective during the first period of wound healing.
High intensity laser action onto the wound. It produces local heat leading to prompt evaporation of necrotized tissues with destruction of bacteria by
high temperature. Simultaneous cauterisation of vessels minimizes blood loss.
Managed abacterial environment (MAE). It is a special device which is able to isolate the part of the body into a sterile environment. Special plastic
chamber is placed over the affected part. Air humidity, PaO2, etc can be controlled. This method is especially useful at treatment of suppurative wounds
and burns. The wound does not require any covering with dressing.
Drains are different appliances used to evacuate any fluid stagnating in the cavities, wounds, etc. All draining systems are divided into open and closed:
1) Closed drains are tubes connecting a body cavity to a sealed reservoir.
2) Open drains are not sealed at either end (high risk of infection).
Types of closed drains

 Gravity drainage (passive draining) uses forces of gravity - posture of a patient, placement of the drain below the affected region (pleural empyema,
etc.)
 Underwater-sealed drainage (passive draining) system prevents air and fluid from reentering the body. This system is used for tubes in the pleural
space.
 Continuous irrigation drainage (active draining)
 Suction drainage (active draining) applies a low level of suction to the drainage tube (very effective to evacuate fluid and close the “dead space”
allowing a better approximation of tissue surfaces.
 Sump drains (active draining) are double-lumen catheters that allow air or irrigation fluid to enter through one lumen while suction is applied to the
other lumen.
Sump drain is commonly used to decrease intestinal dilation, nausea, and vomiting (paralytic ileus after GIT surgery).
 Sometime a rubber strip (passive draining) is inserted into the wound to prevent sealing of edges and wound cavity. It improves the outflow of
collecting fluid. An insertion of the gauze strip (pledget) may limit the contact of contaminated tissues with sterile ones. Also it helps to control bleeding.
Improvement of outflow of drainage from the wound may be promoted by soaking the dressing with NaCl 10%.
Chemical antisepsis
Antiseptics are chemicals which can be applied to living tissue to kill or to inhibit the growth of microorganisms.
Disinfection involves the killing or removal of microorganisms on inanimate objects. After application of both, the bacterial spores are not killed, but the
growing “vegetative” bacteria are.
1. Acids and alkalis: boric acid 2-3% solution (Eusol) - broad spectrum and locally toxic
2. Halogens: Chlorine and Iodine.
Iodine (Lugol's solution) - broad spectrum, cheap, hypersensitivity is common;
Povidone-iodine - broad spectrum, some hypersensitivity and local wound toxicity, rapidly inactivated by blood;
Dilute sodium hypochloride - broad spectrum and locally toxic.
3. Salts of heavy metals: silver nitrate, aqueous solution of silver, mefenide acetate, mercuric chloride, Zn etc.
4. Antiseptics of phenol group: First representative was carbolic acid, or phenol. Due to it’s significant tissue toxicity only derivatives are currently used:
- chlorhexidine (is referred to detergents) - non-toxic, persistent action, good activity against Gram + and moderate against Gram – (Savlon is a
compound of chlorhexidine and cetrimede) is widely used in burns, wound care, etc.)
- hexachlorophane is used in soap and powder form (on skin as prophylaxis against Staph infection.
- cresols. Solution of cresols in soaps (lysol) – possesses tissue toxicity;
5. Oxidising agents: H2O2 (Hydrogen peroxide) - weakly and slowly bactericidal, cheap. Ozone, potassium permanganate.
6. Dyes: brilliant green, methylene blue, acriflavin, acridine orange.
7. Surface acting agents: quaternary ammonium compounds, soaps.
8. Alcohols: most active in 70% concentration, broad spectrum and rapid action.
9. Derivatives of nitrofuran: aqueous furacillin, Furagin and furasolidon are available in tablets and for i.v. injections.
10. 5-nitro-imidazole derivatives: metronidazole (flagil) is available in tablets, solution, and for i.v. injections. Most effective against anaerobes;
dioxidin.
Some chemical agents are used only locally (topical chemotherapy), another are administered systemically (systemic chemotherapy).
Utility of the topical chemotherapy
 Application on operative and traumatic wounds and indwelling devices (intravenous cannulas);
 Treatment of established infection of wound and body cavities;
 Clearance of colonization with pathogenic or antibiotic-resistant organisms.
Recommended antiseptics for local care
 Traumatic wounds: aqueous chlorhexidine; saline.
 Surgical incisions: chlorhexidine; saline.
 Peritoneal, pleural and wound irrigation: chlorhexidine; saline; noxythiolin
 Removal of slough: chlorinated lime and boric acid (Eusol)
Biological antisepsis
Biological antisepsis uses administration of antibacterial therapy Examples of antibiotics are:
Penicillin, Cephalosporin, Quinolones, Vancomycin, etc.
10. Biological antisepsis definition –complete characteristics of all groups of antibiotics, rules of therapy, etc.
Biological antisepsis uses administration of antibacterial medicines. Among the groups of antibiotics are:
Penicillin.
 Natural penicillin
 penicillin, benzyl- penicillin, penicillin G (bicillin), extencillin
 Penicillinase-resistant penicillin (or semisynthetic)
 methicillin, oxacillin, nafcillin, cloxacillin, dicloxacillin
 Aminopenicillin
 ampicillin, amoxicillin (more effective)
 Carboxipenicillin
 carbenicillin, ticarcillin (more effective): Against G- infection especially.
 Ureidopenicillin
 azlocillin, piperacillin, mezlocillin: very broad spectrum of activity, but are susceptable to B-lactamase (should be used with B-lactamase inhibitors)
General characteristic:
Common rate of administration is 4 times a day, mostly are effective against G+ infection.
Adverse effects: allergic reactions (anaphylaxis, rashes) diarrhea, occasionally anemia, rarely seizures.
Cephalosporin
First generation:
- cefazolin, cephalothin.
Mostly against G+ bacteria, little effect on the G- bacteria.
Treatment of skin infections, osteomyelitis. They were used with aminoglycosides to provide broad-spectrum coverage. But bacterial resistance to first
generation is very high.
Second generation:
- cefotetan, cefoxitine, cefuroxime, cefamandole. Broader activity against G- bacteria
Third generation:
- cefotaxime, ceftriaxone, cefoperazone. They have broader action against G- than against G+ bacteria. That group can be used instead of
aminoglycosides. But now they are not so popular because of incomplete spectrum of activity that may be present at polimicrobial infections, unexpected
toxicity, high propensity for inducing resistancy.
Still the gold standard for treatment of abdominal infections includes aminoglycoside to cover enteric G- organisms and clindamycin or metronidazole to
cover anaerobes. If the third-generation cephalosporin is used for emperical therapy of serious intraabdominal infection it should be combined with
clindamycin or metronidazole to cover anaerobes
New cephalosporins (fourth generation) : cefepime, cefpirome.
Generally they are administered 2 times a day, 3 times in severe cases

Adverse effects: they are relatively nontoxic. Hypersensitivity, local pain, GIT disturbances. Reactions are usually mild and reversible.
Aminoglycosides
-Streptomycin, kanamycine, neomycine, tobramycine, gentamycine, amikacin
Characteristic: poor intestinal absorption (parenteral route is preferred),
Bactericidal effect due to inhibition of protein synthesis. In anaerobic conditions it cannot penetrate the cell. So in that circumstances better penetration is
achieved with inhibitor of cell wall synthesis, such as B-lactam AB or vancomycin. Gentamycine is commonly used for severe intraabdominal infections.
Adverse effects: ototoxicity, nephrotoxicity.
Tetracycline
- Tetracycline, doxicicline, minocicline.
They are metabolized by the liver, here is the highest concentration, penetrate body tissues well crossing blood-brain barrier and placenta. Very effective
for sexually transmitted diseases (STD).
Adverse effects: GIT irritation, hepatotoxicity, fetus toxicity, nephrotoxicity, vestibular toxicity (dizziness,vomiting)
Macrolides
- erythromycin and oleandomycin- metabolized by the liver, here is the highest concentration, commonly used at ambulance patients and those allergic to
penicillins. Rate of administration is 4 times a day.
New macrolides - azithromycin, clarithromycin: well absorbed and widely distributed. Broad spectrum. Standard oral therapy respiratory and soft tissue
infections. Can be given once a day.
Adverse effects: GIT irritation
Clindamycin
Active against anaerobes and is useful at therapy of serious intraabdominal pelvic and pulmonary infections. Only few side effects.
Chloramphenicol
Has the same point of action but one very negative side effect limiting its utility. Bone marrow supression starts usually 5-7 days after initiation of
therapy - pancytopenia (reticulo, leyco-, neutro-, thrombocytopenia).
Vancomycin
Main feature is the effectiveness against resistant penicillinase-producing staph inhibiting synthesis of cell wall peptidoglicane. Mainly administered i.v.
and effective against G+. Agent of choice in trreatment of methicillin-resistant staph. Aureus, useful for multiple resistant infections of CSF shunt,
prosthetic valve infections.
Side effects: anaphylactoid reactions (pruritis, hypotension, cardiac arrest)
Carbapenems:
Extraordinary effective against anaerobes as well as G+ and G- bacteria.
- Thienamycin, Imipenem- cilastatin.
Cilastatin is added to prolongate action. Highly effective against most species likely to be encountered in severe intraabdominal infections. Can be used to
replace combination therapy in mixed infections or exclude toxicity of other AB.
Side effects: potentiation of seizures, diarrhea.
Monobactams
Aztreonam only inhibits aerobic G-, two-three times daily, may be useful to replace side effects of aminoglycosides.
B-lactamase inhibitors.
- Clavulonate, sulbactam, tazobactam.
 Amoxicillin-clavulonat is used for treatment of upper respiratory tract infections caused by B-lactamaze producing flora.
 Ticarcillin-clavulonat is used for treatment of intraabdominal, gynecologic infections where the flora commonly has B-lactamaze activity.
 Piperacillin is commonly combined with any of clavulonate, sulbactam, tazobactam and effective against G- B-lactamaze producing flora.
Quinolones
Characteristic: wide spectrum, used orally or parenterally, less toxic.
- Ciprofloxacin, ofloxacin, norfloxacin, enoxacin, pefloxacin.
Exellent activity against most Enterobac. including organisms resistant to aminoglycosides and cephalosporines, very effective against Staph,
including methicillin-resistant isolates.
Treatment of urinary infections, prostatitis, bacterial diarrhea, skin infections, pneumonia.
Side effects: CNS -headache, dizziness; GIT- diarrhea, vomiting; rushes, pruritis.
Initial systemic antibacterial therapy
Culture may be done with most rapid test not less than 24 h. And antibiotic sensitivity is obtained in not less than 48-72 h. But some patients require
antibiotic to be started as soon as diagnosis is established. Therapy is initiated with an agent or combination of agents whose action is broad enough to
cover all the suspected microbial pathogens. Initiation of such broad spectrum antibiotic therapy in the absence of microbial confirmation is termed
emperical therapy. In deciding the emperical therapy, one should know the common pathogens of the site, host defense status, severity of infection, and
response of the host. If the chosen therapy is appropriate, the patient will get well (normalization of body temperature, clinical improvement, and
normalization of lab picture).
Risk patients: Advanced age, malnutrition, preexisting diseases.

Route of administration: I.V., I.A., I.M., instillations into the body cavity or the wound.
In administering an antibiotic, we need to consider these factors:

I. Distribution of an agent
II. Toxicity
III. Cost
IV. Dosage
V. Route of administration
VI. Duration (treatment - 5-14 days (longer therapy may require change of AB), till resolution of symptoms; prophylaxis - intraoperatively and 1-2 days
after surgery)
VII. Single-agent or multi-agent therapy.
VIII. Careful evaluation of drug history, previous administration and allergy. Caution in pregnant women (possible toxicity to mother or fetus)
Complications of AB therapy: -
Widespread resistance to AB, development of suprainfections which are more difficult to eradicate.
Attention:
 AB are not used in treatment of viral infections.
 During AB therapy the close observation of a patient is necessary for possible complications (anemia, leycopenia, allergy, etc.).
 If the purulent focus (abscess, etc.) is not drained or soiling is continued (uncontrolled peritonitis, empyema, etc.) an AB will not be effective.
 After AB treatment an intestinal disbiosis is common. Bificol, lactobacteriin, colibacteriin, etc. may restore normal intestinal flora.
 After AB treatment the fungi associations are common. Nistatin or levorin are used parallel to AB treatment to suppress growth of fungi.
Development of drug resistance.

 After exposure to AB most germs are killed. Sometimes, however, there is a microbe with a mutation that makes it resistant to a drug. Then a colony
grows back, all germs are drug resistant.
 Drug resistance that develops in harmless bacteria may be transferred to harmful one. One microorganism attaches itself to another and a tube is
opened between them in a process of conjugation.
 A virus may infect a bacterial cell and incorporate bacterial genes into its own genes. Later the virus may infect another bacteria so it may transfer the
deadly gene to the bacterium making the bacteria more dangerous.
 Arising of new viruses from wild environment (from animals)
 Often bacteria links up with another microorganism of the same species and expose genetic material.
11. Asepsis definition and types –complete characteristics of all types (chemical, physical, etc.)
Asepsis is the prevention of microbial contamination of tissues and sterile materials by excluding, removing, or killing microorganisms.
Measures oriented on reduction of possibility of preoperative cross-infection

Preoperative shaving of the operative site. Shaving may damage the epidermis. The depilatory creams may cause irritation. It is done on the evening
before operation or immediately before the incision. If Prophylactic AB are required, they should begin with the induction of anesthesia and continue in
high dosage for a maximum of 24h.
Measures oriented on reduction of possibility of cross-infection in theatre

For staffs: Reduction of medical staffs ; removal of ordinary outer clothes and putting on operating theater wear; carriers or staff with septic lesions of
the skin must be excluded from the theater.
Masks - do not reduce the infectiveness of a surgeon with sore throat ( provide only some protection against coughs and sneezes). Types of masks - paper
disposable mask; - cotton reusable after sterilization.
Gowns are put on before surgery.Head – hair should be completely covered with a well-fitting cap.
Shoe covers are useful to protect shoes from spills.
For theatre:
1) ventilation:
- with "plenum" system (changing room air 20-25 times each hour, uses special filters and positive pressure);
- laminar flow ultraclean air system or occlusive gowns are used for high-risk operation such as insertion of a prosthetic joint, etc.
-Air decontamination using UV, etc.
2) Design and construction of the surgical block (separation of clean traffic and dirty traffic):
 Sterile zone (operating theater, scrub-up room, room for sterilization)
 Clean zone (rooms for personal hygiene and changing clothes of the stuff)
 Technical zone (for surgical equipment)
 Dirty zone (rooms for dirty clothes, rooms of nurses, etc.).
The floor should be seamless, hard, and easily cleaned. Operating room temperature varies from 180 to 260 C (22 is preferred). Humidity is maintained at
between 50 and 60%. The operating light and the general lights should be flexible, adjustable, and controllable.
3) regular cleaning with detergents (disinfectants for spilled body fluids) e.g. using 70%-96% alcohol requires at least 15 min contact, flammable;
Quaterny Ammonium (Roccal, Cetylcide) – rapidly inactivated.
Measures oriented on reduction of possibility of infection during direct contact with the wound:
They include:
I. Sterilization of reusable surgical instruments, dressing materials, etc.
II. Surgeon’s hands preparation (scrubbing)

Surgeon’s hands preparation (scrubbing):
Options:
a) Using C-4 solution (compound of 85% formic acid with 33% H2O2 ). First part is washing of hands under running water during 1 min followed by 1
min exposure to antiseptic.
b) Using Chlorhexidine 0,5% alcoholic solution. Washing of hands under running water during 1 min followed by 3 min exposure in antiseptic.
c) AHD, Eurosept. Washing of hands under running water during 1 min followed by two 5 ml applications rubbed to dryness over the hands and
forearms.
d) The use of two 5 ml applications of alcoholic chlorhexidine gluconate, with emollients rubbed to dryness over the hands and forearms after standard
wash with soap.
III. Operation site.

Prepping is a preparation or cleaning of the operative area before surgery using antiseptic solution during at least 1 minute. Options are, Povidon-iodine
or chlorhexidine are commonly used, exposure to 70% alcohol solution and
C-4 solution is also practiced.
Drepping. Sterile drapes are used to cover the areas that surround the operation field.
Additional barriers to separate sterile and nonsterile areas include adhesive incise plastic barrier sheets and plastic ring drapes (the last one is inserted into
the wound and covers the wound edges during the procedure).
12. Sterilization (complete characteristics of all stages and types.)

Sterilization is a complete elimination or destruction of all forms of microbial life.
Stages of sterilization:
I. Preparation of materials (cleaning).

II. Preparing for sterilization
III. Sterilization
IV. Self-keeping of sterilized materials
Preparation of materials.
All instruments to be sterilized must first be thoroughly cleaned to remove all organic matter.
a) Instruments were used but not infected: 5 min washing with the brush under running water.
b) Instruments were used and blood-stained: Washed immediately and then soaked in one of special washing solutions during 15-20 min at temperature
500 C:
Solution A: perhydrol – 20g; washing detergent – 5; water 975 ml;

Solution B: H2O2 2,5% – 200 ml; ; washing detergent – 5; water 795 ml;
After that 5 min washing with the brush in the same solution
After that 5 min rinsing in warm water;
c) Instruments were used and contaminated with pus or intestinal contents: Firstly are soaked for 30 min in lysol 5%. After that 5 min washing with the
brush in the same solution. After that rinsing in running water and then soaked in one of special washing solutions repeating steps for “b” instruments;
d) Instruments were used to operate a patient with anaerobic infection:

Firstly are soaked for 1 hour in special solution containing H2O2 6% and washing agent 0,5%;
After that 5 min washing with the brush in the same solution
After that 90 min. boiling.
Arrangement and package for sterilization

For sterilization using dry heat (in the dry heat oven) instruments are placed onto the metal tray , the lid is left open to dry out instruments for 30 min.
For sterilization using moist heat under pressure (in the autoclave) the instruments should be wrapped in cotton. Instruments are placed into special
cumber (sterilizer) which is then placed into the autoclave. The sterilization indicator is placed at the same time.
Sterilization (is a complete elimination or destruction of all forms of microbial life, whereas a disinfection is a process that eliminates many or all
pathogenic microorganisms on inanimate objects with the exception of bacterial spores) After sterilization if the material is sealed it should be used
within 25-30 days; At the sterilizer chamber the material can stay sterile no longer then 3 days.
Self-keeping of sterilized materials.

After sterilization if the material is sealed it should be used within 25-30 days; At the sterilizer chamber the material can stay sterile no longer then 3
days.
Types of sterilization:
I. In the dry heat oven: only instruments able to withstand high temperature, may take up to 24 hours to be completed.
a) The lid is left open for 30 min to dry out instruments.
b) 60 min sterilization at 1800 C, after that cooling of instruments
II. In the autoclave: for instruments unable to withstand high temperature (above 1300 C)
a) 20 min sterilization at 132,90 C, 2 atm. (for instruments, towels, etc.)
b) or 45 min sterilization at 1200 C, 1.1 atm. (for plastic tubes, gloves, etc.)
III. Gas sterilization: for instruments intolerant to heat (fiberoptic endoscopes.)
a) Ethylene oxide during 16 hours at temperature 180 C followed by prolonged airing (high toxicity, irritation, carcinogenic action).
IV. Ionizing radiation ( -rays) requires special equipment, commonly used by manufacturers to sterilize disposable items (gowns, needle, scalpels, etc.).
V. Chemical sterilization: aldehydes (formaldehyde 6%, gluteraldehyde - many hours are required for sterilization – 6-10hours, corrosive), H2O2 6%,
etc.
13. Preparation of a surgeon's hands, gowning and gloving, prepping and draping
Preparation of surgeon’s hand (Fuerbringer’s and Alfred’s method)
 Soap is applied to the brush, which is kept on the right hand. After soaping the brush, the soap is placed on top of the brush and held at the hand that
holds the brush.
 The brush should always be moved from outside the fingers to the elbow, with the fingers kept higher than the elbow and the stream of running water
from the fingers to the elbows.
 Scrubbing starts from the palmar aspect of each finger, then dorsal aspects, nail lodges, between the fingers of the left followed by the right, palms an
dorsum of the left and right and lastly the hands up to the upper third
of the forearm towards the elbow joint.
 The soapy foam is constantly washed off under running water.
 Throughout the process, it is forbidden to touch the tap.
 At the end of the scrubbing, the brush and soap are put on the table, hands rinsed and with fingers at the level of the chest, dry with sterile gauze or
napkin, without touching parts which is not scrubbed.
 Finally, the hands are wiped with gauze soaked with alcohol solution and other antiseptics.
Gowning and Gloving

Gowning by own self Gowning by scrub nurse
Prepping and drepping

Prepping is a preparation or cleaning of the operative area before surgery using antiseptic solution during at least 1 minute.
Povidon-iodine or chlorhexidine are commonly used. Exposure to 70% alcohol solution, C-4 solution is also practiced.
Drepping. Sterile drapes are used to cover the areas that surround the operation field.
14. Common disinfectant and antiseptic agents: general characteristic.

Iodine
 Cleaning the skin around the wound, superficial wounds, bruises, operative field
Povidone – Iodine
 Scrubbing the hands, cleaning operative site.
Chloramine B
 Disinfecting the hands, items used for patient care, non metallic instruments, rooms.
Formaldehyde
 Disinfecting gloves, catheters, drainage systems
Chlorhexidine
 Cleaning operative site and disinfecting instruments.
Formic acid
 Cleaning hands before surgery, washing surgical instruments and gloves.
Bleeding and Hemostasis
15. Hemorrhage: Pathophysiologic changes, classifications, clinical picture

Hemorrhage is the escape of blood from vessels due to injury or increased permeability. It represents an intravascular depletion through loss of plasma
and RBC mass.
Pathophysiologic changes that occur are:

 Increase in sympathetic activity (vasoconstriction)
 Release of stress hormones (vasoconstriction)
 Resorption of interstitial fluid
 Conservation of fluids and electrolyte by kidneys.
Classification of hemorrhage:
i. According to source of bleeding – Venous, Arterial, Mixed
ii. According to area of bleeding – Internal, External

iii. According to degree of blood loss – Mild(Class I), Moderate (Class II), Severe (Class III)
Clinical picture
General signs are: Pale and clammy skin, fainting and dizziness, tachycardia, hypotension
Specific Signs:
 Class I – Blood pressure is maintained by peripheral vasoconstriction (PVC), pallor, delayed capillary refill, increased pulse rate, mild oliguria.
 Class II – Classic findings of hemorrhagic shock, obvious signs of mental status alteration.
 Class III- Obtundation, loss of consciousness, undetectable pulse and BP if blood loss exceeds 50%.
16. Hemorrhage: Estimation of blood lost volume (degrees of hemorrhage) and management.
We can estimate the degree of blood loss by looking at the clinical signs. Check the Pulse rate (PR), Respiratory rate( RR), Urine output(UO), Mental
status, CVP.
In Class I hemorrhage, In Class II hemorrhage In Class III hemorrhage

PR: 100-120/min PR: 120-140/min PR >140/min
RR: 20-30/min RR: 30 – 40/min RR>35 /min
UO: 20-30 ml/hr UO: 5-15ml/hr UO: Negligible
Mental status: Mildly anxious Mental status: anxious, confused Mental status: Confused, lethargic .
CVP: Decreased CVP: Decreased CVP: Decreased.
.
Besides, lab values may also be useful in determining the degree of hemorrhage. Levels of hemoglobin (Hb), Red blood cells (RBC) and hematocrit (Ht)
are checked.
Class I Class II Class III

Hb: 120g/l Hb: 80 – 120g/l Hb: >80g/l
RBC: RBC: RBC:
Ht: > 35 ml/dl Ht: 25 – 35 ml/dl Ht: < 25 ml/dl
Volume of blood loss: Volume of blood loss: 1500 – 2 000 ml (30- Volume of blood loss: > 2000ml (>40%)
<1500 ml (15-30%) 40%)
Management:
Treatment is oriented on achieving 2 primary goals

 To control ongoing blood loss.
 To reexpand the circulating volume.
17. Hemorrhage: Replenishment of circulating volume

 200 – 500ml of blood loss do not require replenishment as our body is able to restore blood by:
i. Extravascular reserves.
ii. Regeneration of proteins and RBC
 Class I – Reinfusion therapy by crystalloid solutions. E.g. Normal Saline (NS), Lactated Ringer Solution (LR), etc. They are administered according to
the ratio of 3:1 ( of crystalloid to of blood loss)
 Class II – Reinfusion therapy by a combination of crystalloid and colloid solutions. E.g. Albumin, Starch, dextrans etc. (Administered at ratio of 1:1)
 Class III – Blood transfusion is required. Besides, these patients also require platelets and clotting factors (Fresh Frozen Plasma) replacement.
18. External and internal hemorrhage: Clinical picture

External hemorrhage – Diagnosis is prompt and obvious. Differentiation of arterial (bright red, pulsating) or venous blood (dark red) is required.
Internal hemorrhage – Diagnosis is more difficult. General signs are: pale and clammy skin, fainting, dizziness, tachycardia, drop of arterial blood
pressure. More specific signs are when blood escapes through original body openings and manifested as:
 Hemoptysis (bright red and foamy) – Pulmonary bleeding.
 Hematuria – Renal bleeding.
 Epistaxis – Nasal bleeding.
19. Hemoperitoneum: Etiology, Clinical picture, Diagnosis

Hemoperitoneum is a collection of blood in the peritoneum.
Etiology:
 Injury to parenchymal organ. (spleen , liver)
 Injury to arteries and veins. (aorta, mesenteric vessels, cava veins, etc)
 Ectopic pregnancy.
 Postoperative complication or failure of intraoperative hemostasis.
Clinical picture:
Abdominal pain which increases at the change of position, alteration of vital signs according to severity of blood loss.
Diagnosis:
Inspection: Thoracic pattern of breathing, Sign of changing posture.
Auscultation: Decreased bowel sounds (Paralytic ileus)

Palpation: Tenderness and muscle guarding, rebound tenderness (moderate), Phrenic sign and Ker’s sign are possible.
Percussion: Mendel’s sign and sign of shifting dullness.
Instrumental diagnosis can be performed using invasive and non invasive tools.
 Non invasive – Ultrasound, Computed Tomography (CT), Magnetic Resonance Imaging (MRI)
 Invasive – Culdocentesis, paracentesis(laparocentesis), diagnostic peritoneal lavage, video assisted laparoscopy.
If diagnosis still cannot be established even after above-mentioned manipulations, exploration and control of bleeding (surgery) is indicated.
20. Hemothorax: Etiology, Clinical picture, Diagnosis

Hemothorax is an accumulation of blood in the pleural cavity.
Etiology:
 Injury to lung tissues or pulmonary vessels
 Injury to thoracic wall (Intercostal arteries, internal thoracic artery) or adjacent thoracic organs.
Clinical picture:
Pain, dyspnea, universally changed vital signs.
Diagnosis:
Inspection: Unequal chest expansion, bulging intercostals spaces
Palpation: Vocal fremitus is normal.
Percussion: Dull sound over area of fluid accumulation, displacement of heart and arch of aorta towards healthy side.(in severe hemothorax)
Auscultation: Reduced/absent breathing sounds over fluid.
Instrumental diagnosis:
Plain Anteroposterior Chest X ray, Ultrasound, CT, MRI, Thoracocentesis
21. Hemopericardium: Etiology, Clinical picture, Diagnosis Diagnosis can be established by

Hemopericardium is a collection of blood in the pericardial the so called Beck’s Triad which cavity which may lead to cardiac tamponade
includes:
(constrictive heart failure) Low ABP
Jugular Vein Dilation
Etiology: Muffled heart sounds
 Penetrative heart injury.
 Ruptured aortic aneurysm or cardiac aneurysm
Clinical picture:
Chest pain and dyspnea, low arterial BP
Diagnosis:
Inspection: Jugular vein dilation (CVP is raised)
Palpation: Weak and rapid pulse
Percussion: Increased heart dullness
Auscultation: Muffled heart sounds.
Plain AP chest X ray (increased, round heart shape), Ultrasound, CT, MRI, pericardiocentesis.
22. Hemarthrosis and hematoma: Clinical picture, Diagnosis

Hemarthrosis
Etiology: Coagulation disturbances (hemophilia), joints injury
Clinical picture: Limited movements, change of shape of the joints.
Diagnosis:
 Bulge sign:
1. Milk the medial aspect of the knee firmly upwards with your hand 2-3 times to displace any fluid.
2. Then press or tap the knee just behind the lateral margin of the patella.
3. Watch out for a bulge or returning of the fluid at medial aspect of the knee.
4. A bulge of returning fluid (+ve sign) indicates a small effusion within the knee joint.
 Ballotte sign (Floating patella)
1. Grab the thigh immediately above the patella firmly with one hand.
2. With fingers of another hand, compress the suprapatellar pouch by pushing the patella sharply against the femur.
3. Feel for a palpable tap (+ve sign)
4. If fluid is absent, no tap is heard as the patella is already fixed to the femur by the ballottement.
5. If the patella is separated by fluid, a sharp push makes the patella collide with the femur this creating a tapping sound.
Instrumental diagnosis is performed using X ray, Ultrasound and arthrocentesis.
Hematoma
Hematoma is a localized collection of blood within soft tissues. It is caused by different trauma, eg Blunt, penetrating, iatrogenic trauma.
Clinical picture:
Intracranial hematoma – Lateralized weakness (paralysis), pupil dilation, alteration of consciousness
Pulsating hematoma – The mass at projection of vascular bundle, its rhythm coincides with the pulse, auscultation reveals bruit.
Diagnosis
Clinical signs, Ultrasound, duplex scan, CT, MRI, angiography.
23. Temporary and permanent methods of hemostasis.

Temporary hemostasis
 Tourniquet (on padded extremity, released each 20 min)
 Air-filled cuff
 Digital compression against the bone.
 Digital compression of the vessel in the wound.
 Flexion of the extremity at the joint.
 Tamponade (wound packing) followed by tight application of compressive bandage
 Applying a clamp of forceps on vessel.
 Pressing of vessel proximally (artery) or distally (vein) to the bleeding point.
 Elevation of extremity
Permanent hemostasis
Methods can be divided into 5 groups:
 Mechanical methods
 Physical methods
 Chemical methods
 Biological methods
 Combined methods
Mechanical methods  Vascular anastomoses.

 Ligation of distal and proximal ends of bleeding vessel.
 Tying the vessels with surrounding tissues. Physical methods
 Ligation along the course of the bleeding vessel.  Ice (over the wound or swallowed to stop stomach bleeding)
 Twisting of the bleeding vessel.  Tamponade (package of bleeding wound ) with gauze soaked in hot
 Tamponade (wound packaging) saline.
 Metal stitches.  Electrocoagulation of the bleeding point with cautery/diathermy
 Embolization (cauterization)
 Vascular suture  Laser or cryomethods.
Chemical and biological methods  Cryoprecipitate, fibrinogen

a) With systemic action.  Platelet mass
 Fresh frozen plasma
 Concentrated definitive factors are used at states of deficiency of  Trasilol (biologic)

exact factor.  Contrical (biologic)
Angioprotectors
 Vit C
 Rutin b) With Topical action
 Dicinone  Hemostatic sponge
 Etamsylate  Hemostatic pads
 Vit K
 Calcium (CaCL 10% IV)  Fibrin application
 Thrombin application.
Anti fibrinolytic agents

24. Physical, Chemical and Biological methods methods of hemostasis.
(Refer to above)
Coagulation disturbances of surgical patients

25. Normal coagulation process: vessel and platelet response, coagulation and fibrinolysis
Hemostasis is a natural physiologic process by which bleeding is controlled. It consists of the following components:
a) Vessel response.
b) Platelet activation and aggregation.
c) Coagulation mechanism.
d) Fibrinolytic system.
Vessel response
I. Constriction (Spasm)
II. Retraction
a. Caused by the release of Thromboxane.
b. Potentiated by sympathetic activity – The release of cathecholamines, cholinesterase and heat.
c. Supressed by adrenergic blockage, acetylcholine and cold.
Platelet activation and aggregation
Circulating platelets adhere to the von Willebrand factor , collagen and other subendothelial elements at the site of endothelial injury. Activated platelets
begin clumping together and more platelets are recruited to the thrombus. Simultaneously, activated platelets trigger the arachidonic acid cascade,
inducing more platelets to adhere to each other.
Coagulation mechanism
It consists of 2 mechanisms: The intrinsic pathway and the extrinsic pathway.
Fibrinolytic system
It functions in the lysis of excessive thrombus to restore normal blood flow to distal organs.
26. Clinical and laboratory assessment for bleeding risk.
Clinical assessment
Subjective examination
 History of previous abnormal bleeding (from wounds, easy bruisability, etc)
 Family history – E.g Hemophillia.
 Drug history – E.g. Prolonged therapy of NSAIDs.
Objective examination
 Skin observation : presence of petechia, ecchymoses
 Liver and hepatic diseases: Jaundice, hepatomegaly, ascites, or small liver.
 Spleen: Splenomegaly
If the above assessment is negative, an operation can usually proceed without lab test.
If the patient has a positive history for bleeding, further screening is needed using lab test.
Lab assessment
 Bleeding time – Reflects function and number of platelets, vascular response to injury. (Norm: 3-8min)
 Coagulation time (Norm: 5-15 min)
 Prothrombin time (PT) – Reflects extrinsic pathway (Norm: 12-14 s)
 Activated partial Thromboplastin Time (aPTT) – Reflects all factors except for Factor VII. (Norm: 16-25 s)
 Assay of clotting factors
 Fibrin split products (<10mg/L)
 Fibrinogen (2.0-4.0 g/L)
 International Normalized Ratio (INR) – Norm 2.0 – 3.0
If there is an evidence of coagulation abnormality, the suspected drug should be discontinued prior to an elective surgery.
If it is an emergency surgery, the specific defect must first be corrected.
27. Disorders of hemostasis: Vessel wall abnormalities and platelet disorders: Reasons, Types, Diagnosis, Treatment.
Vessel wall abnormalities
 Reason :Hypovitaminosis ,Endocrine disturbances.,Hereditary predisposition (autoimmune)
 Types
o Scurvy
o Henoch-Schonlein purpura – inflammation of the capillaries with increased permeability. It presents as an eruption of purpuric lesions due to dermal
leukocytoclastic vasculitis with Ig A in vessel wall. It is associated with joint pain and swelling, colic and bloody stools. A characteristic children
infection.
o Ehlers-Danlos syndrome – A group of inherited generalized connective tissue diseases characterized by overelasticity and friability of the skin,
hypermobility of the joints, fragility of blood vessels due to lack of collagen’s quality or quantity.
Platelet disorders
 It may be thrombocytopenia and thrombocytopathy.
Thrombocytopenia is the decrease platelet number to less than 100 000. The reasons are following:
a) Reduced number of platelets (commonly due to bone marrow failure) as a result of:
a. Congenital (Faconi’s syndrome)
b. Acquired – Drugs, radiation, Bone marrow neoplasm.
b) Abnormal platelet maturation
Deficiency of Vit , Vit
c) Abnormal platelet distribution

a. Liver pathology
b. Splenomegaly
d) Increased platelet destruction
a. Autoimmune disorders – Idiopathic Thrombocytopenic Purpura (ITP) – Presence of extensive ecchymoses and hemorrhage from mucous membrane
and very low platelet count resulting from platelet destruction by macrophages in the spleen due to anti platelet factor. Treated by steroids, platelet
transfusion, splenectomy.
b. Hypersensitivity reactions to drugs
c. DIC
d. Hemorrhage
e. Dilutional thrombocytopenia due to transfusion of stored blood.
Thrombocytopathy is the disorder of abnormal platelet function.(platelet number is normal)\

a. Von Willebrand’s disease
b. Uremia
c. Drug effects (ASA, NSAID, some AB)
d. Glanzmann’s thrombosathenia – Rare hereditary disease
e. Idiopathic causes.
28. Disorders of blood coagulation: etiology, types, diagnosis, treatment

It can be divided into 2 types: Inherent and acquired. Bleeding usually occurs 2 hours after trauma.
Inherent
a. Hemophilia A (deficit of Factor VIII)

 Sex-linked recessive disorder.
 Treated by administration of Factor VIII till sufficient level.
 Besides, Desmopressin can be used to increase Factor VIII production.
b. Hemophillia B (Christmas Disease – Deficit of Factor IX)

c. Inherent deficiency of any clotting factors.
Acquired
a. Vit K deficiency – Vit K is required for the synthesis of Factors II, VII, IX, X. The vitamin is produced by intestinal (gut) flora.
Etiology: Antibiotics intake, poor nutrition, obstructive jaundice, Total Parenteral Nutrition with low Vit K, short gut syndrome.
b. Liver diseases
c. Administration of exogenous anticoagulants, eg Heparin, Warfarin, etc
29. DIC-syndrome: causes, classification and pathophysiology, clinical and laboratory diagnosis. treatment.
Disseminated Intravascular coagulation syndrome occurs as a consequence of severe underlying disorder resulting in the simultaneous activation of the
coagulation and fibrinolytic system.
Etiology:
a) Obstetric: amniotic fluid embolism, ecclampsia, placental separation, septic abortion, etc
b) Medical: Anaphylactic shock, drowning, heatstroke, Gram –ve sepsis, hemolytic anemia, advanced malignancy, snake bite, viral or fungal septicemia.
c) Surgical: Head injury, ischemic tissue, pancreatitis, severe shock, severe soft tissue injury, transfusion reaction, transplant rejection.
Classification:
I. Mild: Hypercoagulable state. Clinically manifested by tendence to clot at areas of stasis. (risk of embolism)
II. Moderate: Clinically, it is manifested by systemic vascular permeability alteration (need large volume of infusion, ARDS)
III. Severe: DIC per se, manifested by bleeding syndrome.
Pathophysiology:
Extreme stimulus
Massive coagulation
Activation of factor XII accompanied by activation of pro inflammatory mediators.
(Complement, Kinin, Prostaglandin, Histamine, Serotonin, etc)
Increase vascular permeability with third space sequestration of fluid
Consumption coagulopathy
Platelets and clotting factors are consumed
Deprivation of clotting factors
Fibrinolysis activation
Hypocoagulable state with simultaneous fibrinolysis activation.Lysis of clot (release D-dimer).Widespread hemorrhage.
Diagnosis
Mostly clinical picture – Aortic aneurysm, shock,etc
Laboratory data – Levels of D-dimers, No of platelets, increase bleeding time, Increased PT and aPTT, decreased fibrinogen level.
Treatment
 Removal of the source and treatment of shock (stop blood transfusion, restore perfusion, debridement, control of infection – AB, fetus removal, etc
 Maintenance of circulating volume (Blood transfusion components or fresh whole blood)
If bleeding still can’t be controlled, use heparin 10000 IU followed by infusion of FFP and platelet mass. (To prevent further consumption)
Also, we can administer antifibrinolytic agents simultaneously with heparin (Inhibit fibrinolysis)
30. Etiology and management of intraoperative bleeding

Etiology
I. Platelet deficiency after massive blood transfusion due to dilution and use of blood components without platelets.
II. Hemolytic reaction due to transfusion of incompatible blood.
III. Hypothermia-induced coagulopathy where patient’s body temperature is (patient should be warmed)
IV. Consumption coagulopathy in DIC
V. Elevated levels of circulating anticoagulants (Mistakenly administered)
Management
Autologous blood transfusion

I. Reinfusion therapy – Blood is cleansed and reinjected into the body. (Contraindicated if blood is contaminated)
II. Intraoperative hemodilution – Blood is taken out prior to surgery, replaced with colloid. This blood can be used later on if needed.
III. Predeposited autologous blood
IV. Blood substitute – Perfluorocarbon
V. Recombinant erythropoietin
31. Characteristic of blood components used for transfusion.

Whole blood
 Rarely used nowadays due to potential loss of function of RBC, platelet and clotting factors and change in pH (pH 6.7).
 Stored in plastic bags or glass ampoules.
 Use acid-citrate dextrose as anticoagulant.
 Labeling is necessary.
 Stored at
Packed RBC
 High Ht level (70%)
 Free of biological impurities – Vasoactive substances and antigens.
 Primarily used to increase oxygen carrying capacity.
Fresh frozen plasma (FFP)

 Has all coagulation factors.
 Primarily used to replace clotting factors during massive transfusion of packed RBC or to correct coagulation factor abnormalities as in DIC.
Cryoprecipitate ( Plasma derivative)

 High level of Factor VIII and fibrinogen.
 Low level of other factors.
 Primarily used to replace deficit of Factor VIII and treatment of DIC.
Specific clotting factor concentrates

 Provide replacement therapy for inherent deficiency states and liver diseases.
Albumin
 5% concentration is commonly used.
 It is a volume expander – used in shock treatment, to increase BP.
 Also used in states of hypoproteinemia.

 Free of risk transmission of infections.
Platelets concentrates
 Commonly require donation from several patients, used soon after preparation.
 Used in bleeding due to thrombocytopenia and after massive blood replacement or 7hemorrhage.
(Hemostatic process)
32. Classification of transfused solutions

Solutions for transfusion can be classified into the following:
1. With hemodynamic action (Antishock).
2. For detoxification therapy.
3. For parenteral nutrition.
4. Blood substitutes.
5. Solutions used to maintain acid – base balance.
With hemodynamic action

i. Low molecular dextrans – Rheopolyglucin or Dextran 40 (MW=40 000) is used a plasma volume extender and blood flow adjuvant.
ii. Moderate molecular dextrans – Polyglucin or Dextran 70 (MW= 70 000) is used as a plasma volume expander.
iii. Starch products or synthetic colloids – Hetastarch or pentastarch are used as plasma volume expander.
a. Hetastarch – High MW (450 KD), has a significant volume expanding effect that last 24 hours, resulting volume expansion is approximately equal to
the volume administered.
b. Pentastarch – Lower MW (260 KD), has significant volume expanding effect that last for 12 hours, resulting volume expansion is about 1.5 times the
volume administered.
For detoxification therapy – Povidone (MW = 20 000) is used as a plasma extender. It is not metabolized and
excreted unchanged by the kidneys.
For parenteral nutrition

i. Protein solutions (amino acids)
ii. Dextrose solutions (D40W)
iii. Fat emulsions (10 – 20%)
Blood Substitutes – Fluorocarbon, Perftoran, and RBC substitutes (Polymerized stroma-free Hb)
Solutions used to maintain acid – base balance

i. 0.9% NaCl (NS) – ECF replacement, correction of hypovolemia.

ii. 0.45% NaCl – Na maintenance, gastric fluid replacement.
iii. 0.27 % NaCl – as for D5W.

iv. LR – ECF replacement, correction of isotonic deficit.
v. D5W – Correction of insensible water loss, hyperosmolar dehydration, cause dilutional hyponatriemia in overuse.
33. Immunologic aspects of blood transfusion
 Risk of immunologic response – absent only in identical twins.

 Antigen difference – provided by ABO, Rh and HLA (Kell and other minor blood group antibodies system).
 Antigens on cells – manifested by agglutination reaction induced by different antisera.
 Transfusion reactions are caused by different of antigen structure.
34. Blood typing for ABO system

There are 3 methods if blood typing according to the ABO system. They are:
 With standard isohemagglutination serum.
 With anti – A and anti – B monoclonal antibodies.
 With standard washed red blood cells of the known group.
With standard isohemagglutination serum.

Requirements:
2 sets of standard sera I(O), II(A), III(B) of different serial groups, an ampoule of serum IV(AB), a vial of normal saline, pipette, clean dry plate, ground
slide, sterile spear-like needles for finger prick, sterile swabs, alcohol.
Procedures:
1. Divide the plate into 4 parts with a colour pencil and label the parts clockwise – I(O), II(A), III(B).
2. Place the serum of the 2 series of groups I(O), II(A), III(B) in the corresponding areas using pipettes.
3. Then, clean the finger with alcohol and prick it using the sterile needle.
4. Clear away the first blood drop with a swab, while further blood drops are placed on the slide, thoroughly mixed with a drop of serum.
5. Shake the plate to facilitate mixing of the serum and blood.
6. Check the initial results in 3 minutes, add a few drops of normal saline and shake the plates again.
7. Finally, examine the mixture of agglutination.
Results:
In a positive reaction, flakes and granulations of RBC that have clung together do not separate upon dilution with normal saline or shaking.
In a negative reaction, drops of serum on the plate appears transparent or even pink with no visible flakes or granules.
4 patterns of agglutination reaction are possible:

1. The agglutination reaction is negative with the three sera in both series – Group I(O) blood.
2. The agglutination reaction is negative with serum II(A) but positive with serum I(O) and III(B) – Group II(A).
3. The agglutination reaction is negative with serum III(B) but positive with serum I(O) and serum II(A) – Group III(B) blood.
4. The agglutination reaction is positive with the three sera in both series – Group IV(AB) blood.
*Diagrams are available in lecture slides of ‘Principles of blood transfusion’ or Gostichev Textbook Fig. 33
With anti – A and anti – B monoclonal antibodies.
Principles: The detection of antigens A and B in the red blood cells by antibodies contained in celiclones.
(Celiclone is a diluted ascetic fluid of mice carriers of hybridomas producing IgM against antigen A or B).
Procedures:
1. Place big drops of anti –A and anti – B celiclones on a labeled plate.
2. Put the drops of blood in question.
3. Shake the plate slightly and observe for about 2.5 min.
(Reaction normally occurs in 3-4 seconds)
Results:
1. Negative agglutination with both anti A and anti B celiclones – Group I(O) blood.
2. Positive agglutination with anti A but negative with anti B – Group II(A) blood.
3. Positive agglutination with anti B but negative with anti A – Group III(B) blood.
4. Positive agglutination with both anti A and anti B – Group IV (AB) blood.
With standard washed RBC of the known group.
Procedures:
1. Place 3 – 4 ml of patient’s blood into a glass tube and centrifuge it.
2. Put a few drops of the serum on a labeled plate accordingly and add a few drops of standard RBC.
3. Mix them using the edge of a slide and shake the plate for 3 minutes.
4. Then mix one drop of normal saline with each portion and keep shaking the plate.
5. Observe the reaction after 5 minutes.
Results:
1. A negative reaction with Group I(O) RBC but a positive one with Group II(A) RBC – Group I(O) blood.
2. A negative reaction with Group II(A) RBC but a positive one with Group 1(O) RBC – Group II(A) blood.
3. A negative reaction with Group I(O) and Group III(B) RBC – Group III(B) blood.
4. A negative reaction with Group I(O), II(A) and III(B) RBC – Group IV(AB) blood.
35. Blood typing for Rh systems.

Requirements:
2 different series of standard anti-RH serum , petri dish, water bath, pipette, glass rod.
Procedure:
1. Put 3 big drops of the anti –RH serum of one serial type into the petri dish.
2. Add 3 drops of that of another series to arrange the drops in 2 parallel lines.
3. Place a few small drops of blood on the anti-RH drops on the first row.
4. Put the same small amount of standard RH positive RBC in the second vertical row (To check for it’s strength).
5. Add drops of RH negative standard RBC to serum drops in third row.(To check for its specificity).
6. Mix the serum and RBC in each row separately, with different glass rods, cover the petri dish and place it in the water bath at .
7. Observe the results in 10 min.
Results:
1. The drop with the standard Rh-positive RBC should give a positive reaction of agglutination.
2. The drop with the standard Rh-negative RBC should be negative.
3. The agglutination seen with drops in both series of the serum with the RBC of the blood in question – Rh positive.
4. Otherwise, it is Rh negative
36. Methods and procedure of blood transfusion

There are the following methods of blood transfusion:
a. Intravenous (IV) – preferred method.
b. Intraarterial (IA)
c. Intraaortic
d. Intraosseous
Procedures of blood transfusion.

I. Consider indications.
II. Consider contraindications.
III. Consider transfuse agents.

IV. Assess suitability of agent for transfusion.
V. Retype the blood of donor and recipient.
VI. Cross matching ( Individual compatibility test)
VII. Biological compatibility test.
If everything is fine, blood transfusion can be performed.
After blood transfusion, monitor body temperature, BP, pulse rate and lab values of RBC and urinalysis.
37. Indications and contraindications to blood transfusion.

Indications
I. Acute blood loss (>100ml/min)
II. Hypovolemic (hemorrhagic) shock after restoration of circulatory volume.
III. Major surgery with expected significant blood loss.
IV. Severe anemia: Drop of Hb level below 70-80g/l
Contraindications
Congestive heart failure
Septic endocarditis
HPT
Thromboembolism
Hepatic failure
Renal failure
Asthma (Hypersensitivity)
38. Option of transfused product, assessment of viability
Probable agents for transfusion are:
 Packed RBC
 Platelet concentrate
 Cryoprecipitate
 Whole blood
 Fresh frozen plasma
 6% albumin
 6% dextran 70
 10% dextran 40
 6% Hetastarch
Assessment for viability
 Check for the wholeness of the package, expiry date and possible violations of the storage.
 Best blood – not stored for more than 5-7 days.

 Macroscopically, blood should have 3 layers – Red layer of RBC (Base), layer of leukocytes, transparent yellowish layer of plasma (Top).
 Signs showing blood is unfit for transfusion:
o Blood being suspended.
o No labeling.
o Vial is not closed airtight.
o Presence of blood clot.
o Hemolysis.
o Contaminated blood.
39. Assessment of individual and biological compatibility.

Individual compatibility
 Patient’s serum is added to donor’s blood in a 2:1 ratio and they are mixed in a low ionic strength saline or NS.
 Incubate at for 10-15 min.
 Look out for presence of agglutination or hemolysis.
Biological compatibility
 Three 20ml infusions of the blood is done.
 Between each portion, the patient is examined for signs of adverse reactions.
 Tachycardia, dyspnea, facial hyperemia and hypotension suggest incompatibility.
40. Complications of blood transfusion: Allergic reactions and febrile reaction, other complications.
i. Febrile reactions.
ii. Bacterial contamination.
iii. Metabolic complications: Hyperkalemia, Hypocalcemia, citrate toxicity.
iv. Hemorrhagic reactions: DIC
v. Transmission of disease: HIV, Hepatitis, Syphillis, etc.
41. Hemolytic reactions: Etiology, clinical picture, diagnosis and treatment.
Etiology: Transfusion of incompatible blood.
Clinical picture:
Fever, chills, itching, chest and back pain, dyspnea.
Vital signs: Rise of pulse rate, drop of arterial blood pressure (Shock)
Diagnosis:
Clinical signs, oliguria or anurea, shock.
Treatment:
1. Stop transfusion.
2. Foley catheter inserted for hourly urine output monitoring.
3. Mannitol 25-50g – to maintain urine output.
4. Infusion therapy with crystalloid.
5. Antihistamine or steroids.
6. Oxygen supply
7. Dialysis
42. Methods of autologous blood transfusion: Characteristic

i. Reinfusion therapy – Blood is cleansed and reinjected into the body. (Contraindicated if blood is contaminated)
ii. Preoperative hemodilution – Blood is taken out immediately prior to surgery, replaced with colloid. This blood can be used later on if needed.
iii. Predeposited autologous blood – Blood is taken out 4-6 days before surgery. Blood is collected in bottles with preservatives and stored for a maximum
of 4-5 days.
iv. Blood substitute – Perfluorocarbon
v. Recombinant erythropoietin
43. Distribution of fluid, colloids, and crystalloids.

 Crystalloid solutions are distributed in extracellular fluid (ECF).
 Most colloid solutions are distributed in intravascular fluid (IVF)
 Sodium concentration in the IVF is higher (135-145 ) compared to intracellular fluid (ICF).
 The predominant intracellular cation is potassium (serum concentration is approx 3,5-5,3)
 Albumin represents the most important osmotically active constituent of the extracellular fluid (ECF) - Serum concentration is 4,0 g/dL .
 Total Body Water (TBW) is the distribution volume of sodium-free water.
44. Causes of dehydration.

1) Hemorrhage: Intravascular volume depletion
2) Surgical patients: NPO regimen, anesthesia, trauma, sepsis
3) Loss of plasma volume through:
a) GIT: prolonged vomiting, severe diarrhea,
b) Insensible losses: caused by fever (perspiration), hyperventilation, and burns.
c) Urinary: diabetes insipidus, loop diuretics.
d) Extravascular volume sequestration or "third space" fluid losses. A result of local inflammation process (pancreatitis) leading to change in
permeability, resulting in fluid extravasation from the intravascular space to the interstitium. In a another instance, small bowel obstruction causes
hypovolemia that results from fluid loss into the interstitium, bowel lumen and exudation of the fluid into the peritoneal cavity.
45. Diagnosis of dehydration (clinical and laboratory).

I. History of fluid losses:
External losses such as bleeding, melena, vomiting, diarrhea are obvious;
Internal losses such as lost into obstructed bowel, pancreatitis, or internal bleeding may be subtle;
II. Physical examination:
Vital signs (heart rate, blood pressure), weight change, skin turgor, moistness of mucous membranes, venous filling, urine output (UO);
III. Laboratory tests: Hematocrit (Ht), serum Na, K, HCO3, Cl, and glucose; blood urea nitrogen (BUN) and creatinine.
Other tests if needed – serum osmolality 285-295 mOsm/L
Posm = 2x serum [Na] + glucose/18 + BUN/2.8;
Urine osmolality;
IV. Indirect measurement of circulating volume: CVP, PAWP may be useful for diagnosis or to guide rehydration.
46. Degrees of dehydration.

I. Mild dehydration (1st degree 3% of TBW): Thirst
II. Moderate dehydration (2nd degree 6% of TBW): Marked thirst and dry mucous membranes (groin, armpit), loss of skin turgor
III. Severe dehydration (3rd degree 10% of TBW): plus orthostatic hypotension, confusion, or delirious, sunken eyes.
Progressive changes of the following values: heart rate increases, CVP decreases, urine output low (oliguria)
47. Management of dehydration depending on the type.

Existing volume deficits
Deficit is caused by any reason of hypovolemia. Estimation of existing deficit and its correction has top priority. It is evaluated using:
 clinical picture
 estimate using vital signs
Replace half of the calculated deficit quickly (over 12-24 hours), then re-examine the patient and reassess the need for further deficit correction.
Composition of used for therapy solutions has to take into account an etiology of deficit.
On Going Losses
It is the continuous losses from or within the body through nasogastric tubes, drains, fistula, stomas, third space losses.
Replacement of ongoing loses (so-called replacement therapy) has second priority in F/E treatment. It is done with fluids possessing approximately
similar composition to lost one.
 Gastric losses are replaced using 0,45% NaCl plus 20-30 mEq KCl/L
 Intestinal juice is replaced with lactated Ringer’s solution plus 10 mEq KCl/L;
 Third space losses are most difficult to evaluate, they vary with magnitude of the injury. Lactated Ringer’s solution or normal saline plus albumin is
used for replacement.
Maintenance requirements of fluid

Maintenance requirements are defined as the fluid and electrolytes necessary to maintain daily fluid and electrolyte balance in an individual.
This includes usual daily fluid losses: insensible, urinary, and stool.
Common average daily requirements for fluid are 35-40 ml/kg.
Maintenance solution D5W + 1/2 NS or 2/3 D5W +1/2 NS.

Potassium is often added to this solutions at concentration approximating 20 mEq/L.
Maintenance electrolyte requirements
Na 1-2mEq/Kg/d
K 0.5 - 1 mEq/Kg/d
 Usually no K given until after urine output is adequate
 Always give K with care, in an infusion slowly - never bolus
 Ca, PO4, Mg are not required for short term treatment.
48. Causes, clinical presentation and management of hyponatremia and hypernatremia.

Hyponatremnia Hypernatremia
Hyperglycemia - It results shifts of water from the Causes Excessive insensible loses caused by fever, hyperventilation, and
cells leading to dilutional hyponatremia, burns, or hypotonic fluid loses due to perspiration, or severe diarrhea.
inappropriate ADH secretion.
Acute drop of BP below 120 mmHg Clinical Confusion, coma, and intracranial hemorrhage.
Weakness presentations
Fatigue
Confusion
Cramps
Nausea/vomiting
Headache/delirium/seizures/coma
Permanent CNS damage
A reduction in extracellular volume (plasma, gastric Management Rapid correction may cause irreversible neurological deficit.
loses, administration of Na-free solutions) is due to Sufficient free water should by administered to reduce plasma Na.
Na+ loss. The treatment involves replenishment the
extravascular volume with isotonic solutions in

concert with restriction of free water.
Hyponatremia in the presence of increased EVV

(dilutional hyponatremia). This represents
edematous states.Both water restriction and sodium
restriction are necessary. Loop diuretic may be
required to increase both water and sodium loss.
This induce of excess of urinary water loss over Na+
loss and should correct hyponatremia.
Patients with a normal ECV may have the syndrome

of inappropriate ADH secretion. It causes
overconservation of free water. The treatment is
water restriction.
49. Causes, clinical presentation and management of hypokalemia and hyperkalemia.

Hypokalemia Hyperkalemia
Losses from GIT, kidneys, or skin. Diarrhea, Causes Severe methabolic acidosis, insulin deficiency (diabetes mellitus),
vomiting and massive burns. rabdomyolisis, oliguric renal disfunction
Cardiac arrhythmia. Clinical Weakness and myocardial irritability. If untreated it can ultimately
presentations cause ventricular fibrillation.
K supplementation should by administered orally. Management -Mild hyperkalemia (less than 6mmol) can usually be treated
Potassium can by administered IV with conservatively by reducing daily intake.
administration rate no greater than 20-40 mEq/L - IV infusion of Calcium gluconate (antagonizing effect);
per hour, with continuous monitoring. Depending on the cause: glucose, insulin, sodium bicarbonate can
be administered. (translocation of potassium into cells),
-kidney dialysis.
50. Causes, clinical presentation and management of calcium disorders.

Hypocalcemia Hypercalcemia
Acute pancreatitis, massive soft tissue infections, Causes Primary hyperparathyroidism (malignancy).
small-bowel fistulae and hypoparathyroidism.
Numbness in the region of the tips of the fingers. Clinical Confusion, lethargy, coma, muscle weakness, anorexia, nausea,
Tetany or seizures may arise at more profound presentations vomiting, pancreatitis or constipation.
hypocalcemia.
10ml ampoule of either 10% Ca gluconate or Management Most patients will respond to vigorous hydration. After rehydration,
CaCl in 50-100ml D5W, or oral supplementation furosemide may be administered to further increase calcium excretion.
may by sufficient. Treatment should by oriented on the underlying cause.
51. Metabolic acidosis: causes and diagnosis.

Causes: Retention (or administration) of fixed acids, the loss of bicarbonate ions.
Types of metabolic acidosis:
 Lactic acidosis.
o Inadequate tissue perfusion (hypovolemia) aerobic metabolism is inadequate triggering anaerobic metabolism production and cumulation
of lactic acid.
 Diabetic ketoacidosis
o Diabetus mellitus insulin deficiency impaired glucose utilization energy deficit liver produces ketones from free fatty acids to supply
alternative source of Energy acetoacetic acid B-hydroxybutyrate aceton. Ketones are organic acids.
 Alcoholic ketoacidosis
o After sudden abstinence, one or three days after heavy drinking. Commonly associated with starvation or vomiting (volume depletion).
 Rhabdomylysis.
o Excessive muscle breakdown caused by myonecrosis. Accumulation of organic acids and possible development of renal failure (block of renal
tubules).
 Acute and chronic renal failure
o Decreased excretion of acids, leading to their accumulation.
 Excessive bicarbonate loss
o Hypoaldesteronism and Addison's disease
Aldosteron deficit reduction of acid secretion in the distal nephron (defect of acidification)
 Excessive acid administration
o Administration of large volume of blood preserved with citrate.
Diagnosis: Arterial lactate concentration, serum and urine ketone level, blood glucose level, serum [K], BUN, creatinine, blood alcohol level. For
rhabdomyolysis - urine myoglobin concentration, methanol and ethylene glycol levels and serum osmolality. They are necessary to determine the cause
of acidosis.
But if a patient is obviously underperfused and metabolic acidosis improves with therapy, further workup is not necessary.
52. Metabolic acidosis: Treatment depending on the reason.

 Lactic acidosis –
o Restoration of tissue oxygenation helps to metabolize lactic acid by the liver and kidneys resolving acidosis.
o All efforts should be oriented to restoration of perfusion. Oxygen delivery is improved by increase of cardiac output (volume resuscitation or sometime
inotropic agents), increase of Hb concentration (RBC transfusion) if indicated. Dichloracetate improves cardiac output and oxidation processes - can be
used.
o Restoration of perfusion and correction of underlying disorder. Correction of IVV can be guided by simple UO measurement. In cardiac patients or
patients with renal insufficiency - CVP or PAWP is used to guide resuscitation. In rare cases is necessary to administer sodium bicarbonate parallel to
fluid resuscitation and underlying disorder only if pH is below 7,2. (only in life-threatening situations and judiciously).
 Diabetic ketoacidosis
o Aim – Correction of hypovolemia, hyperglycemia, ketoacidosis, and K depletion.
o Insulin administration: I.V., bolus, subsequently by continuous IV infusion.
o Fluid resuscitation - Control of hypovolemia (CVP to titrate volume repletion)
o Repletion of K under continuous ECG monitoring.
 Alcoholic Ketoacidosis
o Infusion therapy – D5W decreases keto acid formation in the liver, saline solution promotes renal excretion of keto acid.
 Rhabdomyolysis
o Aggressive fluid resuscitation to prevent renal failure.
53. Respiratory acidosis: causes, diagnosis, and treatment.

Causes:
 Common cause in postoperative patients is central respiratory depression due to excessive postoperative sedation or narcotics (and CNS lesions).
 Airway obstruction: Laringospasm
 External compression of airways by tumors, thyroid gland - usually surgical treatment is indicated.
 Pneumonia, pulmonary edema, ARDS, aspiration pneumonia.- treatment of the cause.
 Respiratory muscle weakness: due to neuromuscular blocking agents; neurologic diseases (multiple sclerosis, etc.)
 Depressed respiratory drive (depressing drugs, narcotics)
Diagnosis:
Dyspnea, cyanosis, increased in the blood, increased urine bicarbonate level.
Treatment:
Improvement of ventilation, correction of the cause.
54. Metabolic alkalosis: causes, diagnosis, and treatment.

Causes:
 Loss of acids from the GIT or urine;

 Administration of HCO3, such as citrate (after massive blood transfusion)
 Loss of fluid with a high chloride/bicarbonate ratio.
Diagnosis:
 Reduction of minute ventilation.
 Rare manifestations: Neuromuscular excitability including paresthesias, carpopedal spasms or lightheadedness.
Treatment:
 Vomiting results in both hypovolemia and loss of and ions. Administration of NaCl replenishes the depleted levels and restore ECV.
 At life-threatening situations the acetazolamide should be considered (inhibitor of carbonic anhydrase). If it is not effective an exogenous acid can be
given (100 mEq/L of hydrochloric acid) via IV line under the monitoring of arterial blood gases.
 Primary aldosteronism: Treatment is removal of source of mineralocorticoid excess. The action of mineralocorticoid can be blocked by means of
spironolactone or amiloride.
55. Respiratory alkalosis: causes, diagnosis, and treatment.

Causes:
Generally, due to increased loss of carbon dioxide due to hyperventilation.
Pulmonary causes: Diseases that affect the alveolar-capillary membrane leading to ventilation-perfusion mismatch and finally to hypoxia. The body
responds by hyperventilation resulting in respiratory alkalosis (asthma, pneumonia, congestive heart failure, pulmonary embolism, atelectasis,
pneumothorax).
Diagnosis:
Arterial blood gases show decreased PaCO2 and increased pH.
Treatment:
Directed towards the underlying cause. Decrease ventilation (e.g., sedatives) or rebreathing in the same air to decrease carbon dioxide loss. In life-
threatening cases, mechanical ventilation is required.
Critical conditions at surgical patients

56. Acute hepatic failure: etiology and classification
Etiology:
 Vascular abnormalities obstruction of venous flow.
 Billiary obstruction due to gallstones, sclerosing cholangitis or compression of common bile by carcinoma can also lead to hepatic failure.
 Other reasons include prolonged hypotension, MODS, ingestion of some hepatropic poisonous agents.
Classification:
 Posthepatic block: thrombosis of hepatic vein (Budd Chiari syndrome)
 Intrahepatic block: cirrhosis due to chronic hepatis (viral or billiary)
 Prehapatic block/ extrahepatic: obstruction of portal/ splenic vein (congenital, maglignancy)
57. Acute hepatic failure: clinical and laboratory presentation

Clinical presentation:
 Jaundice
 Obtundation/ encephalopathy
 Ascitis
 Peripheral oedema
 Nasal bleeding
 Asterixis
Laboratory presentation:
 Increase prothrombin time (PT) and active partial thromboplastin time (aPTT)
 Thrombocytopenia
 AST and alkaline phosphate elevated
 Increase serum bilirubin more than 4.0
58. Acute hepatic failure: etiology and management of bleeding

Etiology:
 GIT bleeding commonly occurs from Curling’s ulcer (acute ulcers of the stomach) at patients with billirary obstruction or after shock
 Bleeding from esophageal varices (at patients with portal hypertension)
Management of bleeding:
 GIT bleeding commonly occurs from Curling’s ulcer (acute ulcers of the stomach) at patients with billirary obstruction or after shock, can manage by:
(a) Fresh frozen plasma (FFP), cryoprecipitate, platelet concentrate

(b)Antacids
(c) Vitamin K parenterally
(d)Folic acid
 Bleeding from esophageal varices (at patients with portal hypertansion), can manage by:
(a) Iced saline lavage of the stomach
(b)Blood components (e.g FFP) or fresh whole blood
(c) Vasopressine or somatostatine i.v
(d)Placement of Blackemore balloon or sclerotherapy
(e) Surgery
59. Acute hepatic failure: etiology and management CNS dysfunction

Etiology:
 Constipation, hypokalemic, hyponatremia and products of GIT flora metabolism
Management:
 Diet rich of branched chain aminoacids
 Catharsis with lactulose, magnesium citrate
 Intestinal sterilization with oral aminoglycosides
 Zinc and thiamine to decrease encephalopathy
60. Acute hepatic failure: management of ascitis and electrolyte disturbances

Management of ascites:
 Diuretics
 A peritoneal venous shunt for recirculating ascitis fluid. Changes in pressure during ventilation open and close the intraperitoneal valve, which moves
fluid from the peritoneum into venous circulation. Repeated paracentesis also can be used.
Management of electrolyte disturbances:

 Increase excretion of fluid by using loop diuretic (furosemide). It is combined with K-sparing diuretic, a spironolactone
61. Acute renal failure: etiology and classification

Etiology:
 Prerenal: hypovolemia, cardiac pathology (BP less than 80-70mmHg)
 Renal: ionic radiopaque contrast material, myoglobin (crash syndrome), Hb (intravascular hemolysis), cyclosporine, NSAID, aminoglycosides, DIC
 Postrenal: prostatic enlargement, stones, plugged Foley catheter, compression due to malignancy, iatrogenic reasons.
Classification: classification according to etiology

 Prerenal form
 Renal form
 Postrenal form
62. Acute renal failure: clinical and laboratory presentation

 Decrease in urine output
 Rise in serum creatinine
 Acute onset of oliguria (0.5ml/kg/h) or anuria (less than 100ml/day)
 Increased in serum cratinine (less than 0.6-1.2mg/dL)
63. Acute renal failure: prerenal form: etiology, diagnosis and treament
Etiology:
 Prerenal: hypovolemia, cardiac pathology (BP less than 80-70mmHg)
Diagnose:
Due to hypovolemia
 Flat veins
 Rise in pulse rate
 Dry mucous membrane
 Hypotension
 Poor capillary refilling
 Low carotid venous pressure
Due to poor heart contractility

 Specific complaint (e.g: chest pain, palpitation etc)
 History of heart disease
 Physical data (sounds, rhythm etc)
 Instrument: changes of ECG, EchoCG, specific lab changes, etc
Treatment:
Due to hypovolemia
 Volume expander
 Crystalloid
 FFP, platelets, etc, if accompanied by bleeding
Due to poor heart contractility (cardiac pathology)

 Inotropes
 Dimetic
 Nitrofusin
64. Acute renal failure: renal form: etiology, diagnosis and treatment
Etiology:
 Renal: ionic radiopaque contrast material, myoglobin (crash syndrome), Hb (intravascular hemolysis), cyclosporine, NSAID, aminoglycosides, DIC
Diagnosis:
 Specific complaints
 History of blood transfusion, severe soft tissue trauma, exposure to nephrotoxic agents, etc
 Physical data
 Specific lab changes are possible: myoglobine or free Hb
 Presence of protein, RBC, WBC in the urinalysis is less specific
65. Acute renal failure: postrenal form: etiology, diagnose and treatment
Etiology:
 Postrenal: prostatic enlargement, stones, plugged Foley catheter, compression due to malignancy, iatrogenic reasons.
Diagnose:
 Specific complaints are possible

 History of renal disease (stones)
 Characteristic physical data
 Instrumental diagnosis: US, i.v.pielography
 Plane abdominal X-ray
Treatment:
 Decompression of obstruction area using Foley catheter or suprapubic catheter.
 Uretral obstruction may be corrected with percutaneous nephrostomy tubes
66. Acute respiratory failure: etiology and classification

Etiology:
Primary acute respiratory failure
 Affected patency of the airway (e.g: aspiration, mechanical obstruction, tumors, bronchospasm, etc)
 Affected respiratory surface area of the lung (e.g: pneumonia, hemothorax, pleuritis etc)
 Impairment of the central respiratory drive (e.g: head trauma)
 Impairment of synase transmission of impulses (e.g: tetanus)
Secondary acute respiratory
 Pulmonary thromboembolism
 ARDS (e.g: low pressure pulmonary edema)
 High pressure pulmonary edema (e.g: left heart failure)
 Hypovolemia
Classification:
 Primary acute respiratory failure
 Secondary acute respiratory failure
67. Acute respiratory failure: clinical and laboratory presentation

 Dyspnea and tachypnea
 Chest pain
 Hypoxia
 Hypercapnea
 Cyanosis
 Po2 lesser that 70- hypoxia
 Pco2 greater than 55- hypercapnea
68. Acute respiratory failure: indication to endotracheal intubation

 Impaired airway patency(edema, burn, trauma)
 Inadequate airway protection (at patients risky to aspiration due to trauma, neurologic, etc)
 Inadequate pulmonary toilet (to prevent obstruction by mucosa and atelectasis) when coughing is inadequate
 Need for positive ventilation (when spontaneous ventilation is inadequate)
69. Acute respiratory failure: diagnosis of respiratory failure

 Specific complaints (dyspnea, chest pain, etc)
 Characteristic physical data (auscultation, percussion, palpation)
 Objective data(jugular distention, dysrrhythmias, murmurs, sign of congestive heart)
 Instrumental (plain chest X-ray, ECG, EchoCG)
70. Acute respiratory failure: management of respiratory failure

 Treatment of underlying cause (AB for infection, debridement of crashed tissues, stabilization of fracture, etc)
 Careful infusion therapy (pulmonary catheter may be required )
 Supplementary O2 or even supportive ventilation using positive end-expiratory pressure (PEEP)
 Inotropes may be used (norepinephrine, epinephrine, dopamine, dobutamine, etc )
 Vitamin C, E and glutamine
71. Acute left heart failure: etiology

 Ischemic heart disease
 Systemic hypertension
 Mitral and aortic valve disease
 Cardiomyopathies
72. Acute left heart failure: pathology changes

 Reduction ineffective left ventricular output for a given pulmonary venous or left atrial pressure
 Acute increase in left atrial pressure lead to pulmonary congestion or pulmonary edema
73. Acute left heart failure: clinical presentation

 Pulmonary edema
 Dyspnoe, paroxysmal nocturnal dyspnoe
 Orthopnoe
 Fatigue, weakness
 Nocturia
74. Acute left heart failure: diagnosis (laboratory, instrumental)

 ECG: right or left ventricular hypertrophy, signs of myocardial ischemia or infraction
 X- ray chest: prominent upper lobe veins, Karley B lones
 Fluid in fissures or interlobar effusion
 Increase in broncho- ventricular marking- features of pulmonary edema
 Cardiomegaly
75. Acute left heart failure: treatment

 Diet: salt free diet
 Oxygen therapy
 Diuretics
 Vasodilation
 Arteriolar dilator- Hydralazim
 venodilator- Isosorbid 5- mononatritrate
 ACE inhibitors- Prestarium
 Digoxin
76. Multiorgan dysfunction syndrome: etiology

 Infections (peritonitis, pneumonia, necrotizing soft tissue infections)
 Inflammation (pancreatitis)
 Injury (multiple trauma, burn injury)
 Ischemia (ruptured aneurysm, hypovolemia shock, mesenteric vascular occlusion)
 Immune reactions
 Iatrogenic (incompatible blood transfusion)
77. Multiorgan dysfunction syndrome: pathologic changes

 Respiratory dysfunction in the form of ARDS
 Renal dysfunction in the form of prerenal failure
 Hepatic dysfunction in the form of acute ischemia hepatic
 Cardiovascular dysfunction develops due to reduction of peripheral vascular resistance and increased vascular permeability.
 Neurologic dysfunction is manifested by thrombocytopenia, anemia, etc
 Gastrointestinal dysfunction is manifested by Curling ulcers, paralytic ileus, intolerance of GIT feeding
 Endocrine dysfunction is manifested by hyperglycemia, impaired healing
78. Multiorgan dysfunction syndrome: clinical presentation

 ARDS- tachypnea, dyspnea, cyanosis, hypoxia, hypercapnea
 Prerenal failure- flat veins, rise in pulse rate, dry mucous membrane, hypotension, poor capillary refilling, polyurea
 Acute ischemia hepatic- increased in AST, ALT, alkaline phosphotase, PT, aPPT, direct and indirect billirubin
 Cardiovascular dysfunction- hypotension
 Neurologic dysfunction- thrombocytopenia, anemia, leucocytosis
 Gastrointestinal dysfunction-melena, hematemesis
 Endocrine dysfunction- hyperglycemia, impaired healing
79. Multiorgan dysfunction syndrome: lab and instrumental diagnosis

 Red blood count show blood congestion and anemia
 White blood count show inflammatory changes and leucopenia
 Blood chemistry show AST and ALT increase, dysproteinemia, reduced amount of protein, changes in electrolytes , elevation of creatinine, plasma
urea and bilirubin
 Leukocyte intoxication index
 Lymphocyte intoxication index
 Low and moderate molecular weight molecules (is the depicition value for all plasma urea, creatinine, glucose, lactic acid, fatty acids, etc.which are
accumulated in the body more than their normal concentration)
 Immunological test
 Resistance of leukocytes and erythrocytes
80. Multiorgan dysfunction: common principle of treatment

 Worsening of dysfunction should prompt a search for potentially correctable cause
 Indentification and treatment of the cause
 Occult infection
 Special attention for postoperative patients, such as site of incision, use of clinical and instrumental diagnose tools
 Example:
1. Respiratory support (to achieve adequate saturation)
- Oxygen supplementation (nasal cannula)
- Use positive end respiratory pressure, PERP to limit formation of intestinal fluid
2. Cardiovascular support
- Carefully administration of fluid for cardiac patient, ARDS and head trauma patients
- Maybe guided by pulmonary catheter
3. Renal support
- Dopamine at low doses to improve renal blood flow
- Renal replacement therapy, but used only on stable cardiovascular function patient.
4. Liver support
- Platelet and clotting factors
- AB are used to treat infection but not for prophylactic aim
- Steroid are not used, it is not effective
81. Evaluation of patient’s condition

 Evaluation of patient’s condition is generally based on:
- Consciousness level
- Change of vital signs: CVS (ABR, PR) and RS (breathing rate, pattern)
 Alteration of consciousness varies from clear to coma. The special score sys is used in the assessment of consciousness level – GCS. These score sys
takes into account three most important aspects of consciousness:
- eye opening
- verbal response
- motor response
82. criteria and degrees of patient’s condition

 satisfactory: GCS = 15; no changes of vital functions (SI = 0.5)
 moderate severity: GCS = 13-15; mild changes of vital functions (SI = 1.0)
 severe: GCS = 9-12; moderate changes of the respiratory or CVS (SI = 1.5)
 extremely severe: GCS = 5-8; significant changes of the respiratory and/or CVS (SI = 2.0)
83. assessment of condition according to Glosgow coma scale, GCS

GCS takes into account three most important aspects of consciousness:
1. eye opening
2. verbal response
3. motor response
Glasgow Coma Scale (GCS)
84. clinical and biological death: criteria

Clinical death:
 heartbeat and breathing have stopped
 it may be averted or reversible
Biological death:
 permanent brain death due to lack of oxygen
 This death is final
85. cardiopulmonary resuscitation: common sequence of measures

 Establishment of Airway (head tilt, chin lift, jaw-thrust maneuver, etc.)
 Maintenance of Breathing (artificial ventilations, etc.)
 Maintenance of Circulation (cardiac massage)
86. Causes and signs of sudden cardiac arrest

Causes of sudden cardiac arrest: Signs of sudden cardiac arrest:
 MI  Absence of carotid and peripheral pulse.
 Upper airway obstruction  Absence of arterial pressure
 Heart injury  Absence of heart sounds
 Electric trauma  Dilated unrespond pupils
 Anaphylactic shock  Apnea
 Drowning  Unconsciousness
 Hyperkalemia and metabolic acidosis  Pallor
87. Cardiopulmonary resuscitation: definition, sequence of measures

Definition:
 Method of resuscitation which stimulate both the heart and the lung consisting of external chest compression and mouth to mouth ventilation.
Sequence of measures:
 Establishment of airway (head tilt, chin lift, jaw-thrust maneuver, etc.)
 Maintenance of breathing (artificial ventilations, etc.)
 Maintenance of circulation (cardiac massage)
88. Methods of airways securing: types
 Heimlich maneuver
Used to expel an obstructing bolus of food from the throat by placing a first on the abdomen between the navel and costal margin, grasping the first with
another hand and forcefully thrusting it inward and upward so as to force the diaphragm upward, forcing air up the trachea to dislodge the obstruction.
 Jaw-thrust maneuver – used to open the airway
Hands are placed on the mandibular rami and pushed anteriorly, so opening the airway.
 Chin-lift maneuver – used to open the airway
Tip of the fingers are placed beneath the patient’s chin and the jaw is lifted anteriorly while the mouth is opened by drawing down on the lower lip with
the thumb of the same hand.
 Head-tilt maneuver
 Advanced airway maintenance require special equipment. Endotracheal intubation using orotracheal or nasotracheal tube.
 Needle cricothyroidotomy with jet insufflation
 Cricothyroidotomy
 Tracheostomy
89. Maintainance of ventilation, types, rate, efficacy

Types:
 Mouth to mouth
 Mouth to nose
 Mouth to mouth to nose
Rate: 12 per min
Efficacy: until the present of chest expansion and breathing sound
90. Maintenance of circulation (cardiac massage), types, rate, efficacy

Types:
 Closed chest/ indirect cardiac message- usually done before the patient arrive to the hospital
 Open/ direct cardiac message- applied in chest surgery, chest injuries or in chest rigidity that precludes adequate external message.
Rate: 60 pressing per min
Efficacy: until the pupil back to its original size and the present of carotid pulse
91. Shock: definition, pathologic changes in the body

Definition: It’s a clinical syndrome arising as a result of inadequate tissue perfusion, i.e. inadequate O2 delivery. This impaired perfusion causes of some
organ dysfunction (end-organ) with corresponding clinical manifestation.
Pathologic changes in the body:

Poor perfusion → cellular injury → elaboration of proinflammatory mediators →
impairment of microvasculature (2º injury) → further impairment of perfusion → vicious circle.
Activation of potent inflammatory cells may lead to systemic inflammatory response syndrome (SIRS), that may be causative in the development of
multiple organ dysfunction syndrome (MODS).
92. Classification and common clinical presentation of shock
Classification:  Pale, clammy skin

According to the pathophysiologic mechanism:  Delayed capillary refill
 Hypovolemic  Alteration of consciousness (mental changes)
 Traumatic
 Tachypnea
 Cardiogenic (intrinsic and compressive)
 Septic  Tachycardia
 Neurogenic  Low BP
 Anaphylactic  Oligo- or even anuria
Common clinical presentation: Septic shock:

Hypovolemia shock  Tachypnea, tachycardia, oliguria, changes in mental status, fever
 Pale, clammy skin  Specific clinical findings characteristic to some infections.
 Delayed capillary refill  Lab changes: leukocytosis, rise of ESR, etc.
 Alteration of consciousness (mental changes)
Anaphylactic shock:
 Tachypnea  Generalized pruritis
 Tachycardia  Bronchospasm
 Low BP  hypotension.
 Oligo- or even anuria
Neurogenic shock:
Cardiogenic shock
 Peripheral edema  skin is warm
 perfused
93. Anaphylactic shock: Etiology, pathogenesis

Etiology:
 exposure to allergen (contrast agent, blood products, antibiotics, anesthetics, etc.)
Pathogenesis:
Exposure to allergens → release of proinflammatory cytokines → vasodilation and increases in vascular permeability → hypotension → pooling in large
capacitance vessels → reduction of circulating blood vol. → hypoperfusion → shock.
94. Anaphylactic shock: clinical presentation, diagnose

 Generalized pruritis
 Bronchospasm
 Hypotension
 Warm skin
 Utricaria, agioedema, bronchospasms, wheeze and facial edema
Diagnosis:
 Specific complaints
 Lab changes: leucocytosis, rise in ESR
 Cardiogenic: low CVP
95. Anaphylactic shock: treatment

 Epinephrine 5mg/kg subcutaneously followed by additional epinephrine 10-50ng/kg/min I.V.
 Prednisolone 50mg I.V.
 Fluids in 20ml/kg I.V. bolus over 5mins followed by additional continuous I.V. infusion
96. Hypovolemia shock: etiology and division depending on the different reason
Etiology:
 hemorrhage (intravascular volume depletion through loss of RBC mass)
 Loss of plasma volume due to GI, urinary, and insensible losses or through extravascular volume sequestration
Division:
 Hemorrhagic form of hypovolemic shock
 Non hemorrhagic form of hypovolemic shock
97. Hypovolemic shock: compensatory body response, pathology

 Low intravascular volume → reduction in preload → diminished cardiac output →drop of BP → activation of sympathetic sys (stimulation of
baroreceptors) →increase in heart rate, myocardial contractility, and arterial and venous vasoconstriction.
 Drop of BP → poor renal perfusion → activation of renin-angiotensin sys → additional vasoconstriction and salt and water retention, release ADH
further increases water retention.
 → centralization of hemodynamic due to peripheral vasoconstriction → microvascular hypoperfusion → accumulation of lactate → lactic acidosis →
cellular injury → elaboration of proinflammatory mediators → increase of permeability → further impairment of microvasculature → further impairment
of perfusion → vicious cycle, SIRS, MODS.
98. Hypovolemic shock: clinical presentation, diagnosis (clinical and laboratory), treatment
 Pale, clammy skin
 Delayed capillary refill
 Tachypnea
 Tachycardia
 Low BP
Diagnosis:
Clinical diagnosis:
 Hemorrhage is obvious
 Hypovolemia due to burns, sequestration of fluid (small bowel obstruction, pancreatitis), etc. → occult loss → more difficult to diagnose
Lab changes:
 Nonhemorrhagic forms → hemoconcentration
 Hemorrhagic form → the oncotic induced shifts may take several hours to achieve.
Treatment:
 Rapid infusion of normal saline or lactated ringer 2 to 3 L over 10-30 min should restore adequate intravascular vol. in most cases as a result of its
large vol. of distribution.
 Hemorrhagic form: of shock crystalloid with 1:3 ratio or predicted vol. of lost blood.
 If blood pressure does not improve after admin of 2L, this suggests that blood loss is in excess of 1500 ml, there is ongoing active bleeding or another
cause of shock. Further vol. resuscitation should include simultaneous blood transfusion, lactated Ringer.
 Other crystalloids – HS
 Colloids – human albumin, plasma, dextrans, synthetic colloids.
99. Cardiogenic shock: left heart failure: etiology, pathology, clinical presentation
Etiology:
 intrinsic causes: MI, arrhythmia, valvular heart disease, contusion from direct chest trauma, cardiomyopathy
 compressive cardiogenic shock occurs as a result of extrinsic compression of the heart. The cause is accumulation of blood or fluid within pericardial
sac that causes pericardial tamponade.
Pathology:
 Heart pathology → impairment of heart contractility → diminished cardiac output → drop of blood pressure → activation of sympathetic system
(stimulation of baroreceptor) → increase in heart rate, myocardial contractility and arterial and venous vasoconstriction.
 Drop of BP → poor renal perfusion → activation of renin-angiotensin sys → additional vasoconstriction and salt and water retention, release of ADH
further increases water retention.
 → peripheral vasoconstriction → microvascular hypoperfusion → accumulation of lactate → impairment of perfusion.
 The reduction in BP and elevated left-ventricular end-diastolic BP (LVEDBP) → reduced coronary perfusion pressure and thus coronary O2 delivery.
 Meanwhile, the increase in heart rate, systemic vascular resistance (afterload) and contractility, vol. overload (preload), all increase myocardial O2
consumption and demand. The discrepancy between myocardial O2 demand and once delivery further impairs left-ventricular function and will lead to
circulation collapse unless appropriate and timely intervention interrupt the vicious cycle.
 Low cardiac output
 tissue hypoxia
 presence of inadequate circulating volume
 signs of myocardial failure- raised in JVP, gallop rhythm, basal crepitation, pulmonary edema
Right-sided failure: clinical picture of blood accumulation in systemic veins and capacitance vessels. Peripheral edema, hepatomegaly and hepatojugular
reflux may develop.
Left-sided failure: an increase of extravascular lung water. The large capacitance pulmonary vasculature initially accommodates the increase in blood
volume. Pulmonary interstitial fluid flow overwhelms the capacity of pulmonary lymphatics, and edema develops at capillary pressure higher than
20mmHg (PAWP which reflects LVEDBP).
100. Cardiogenic shock: diagnosis (laborartory, instrument), treatment

Diagnosis:
 Change in heart sound
 Cardiac enzymes
 ECG
 EchoCG
 Chest radiograph
 Arterial blood gases

 Elevated urinary osmolality
 In some situations pulmonary artery catheter may provide additional diagnostic info.
Treatment:
Medical treatment
In patients with inadequate tissue perfusion and adequate circulating volume, infusion of inotropic or vasopressor drugs should begin immediately.
 Dobutamin because it’s beneficial effects on afterload reduction is preferable.
 In the presence of moderate hypotension, dopamine is the preferred agent.
 Norepinephrine is reserved for cases of profound hypotension.
 Afterload reduction (vasodilators) may be beneficial (risk of hypotension). Either I.V. nitroglycerin or sodium nitroprusside may be used.
 Preload reduction through the use of diuretics.
Surgical treatment
Intra-aortic balloon pump:
This pump is a catheter-based device that is inserted via the common femoral artery. The balloon is positioned in the descending thoracic aorta.
Balloon inflation during cardiac diastole increases coronary arterial perfusion. Balloon deflation during cardiac systole provides afterload reduction
thereby facilitating cardiac ejection.
Temporary left heart bypass using the centrifugal pump:
Inflow to the pump is provided via a cannula in the left superior pulmonary vein and outflow via a cannula in the descending aorta.
Longer-duration left heart assist device (Novacor left ventricular assist device):
Inflow to the device is via a Dacron graft sewn to the left ventricular apex and outflow via a Dacron graft sewn to the ascending aorta.
Abiomed BVS 5000 ventricular assist device:
For left ventricular assistance, blood is withdrawn from the left atrium and returned to the ascending aorta. For right ventricular assistance, blood is
withdrawn frm the right atrium and returned to the main pulmonary artery. Two blood pumps can be employed for biventricular support. The cannulas
leave the patient in the subcostal region and the air driven blood pumps are located at the patient’s bedside. The device is designed to give temporary
support to the function of either the right or left heart.when the patient’s ventricular function returns, usually within 7-10 days, the blood pump is removed
Implantable AB-180 centrifugal pump:
Used to maintain systemic blood flow in patients who have cardiogenic shock
101. Compressive cardiogenic shock: etiology, pathology, clinical presentation, diagnosis, treatment
Etiology:
 Occurs as a result of extrinsic compression of the heart due to pericardial tamponade.

 Tension pneumothorax, diaphragmatic hernia, intraabdominal compartment pressure
Pathology:
 The extrinsic compression limits diastolic filling, effectively reducing preload which adversely affects stroke vol. and cardiac output.
 Jugular venous distention
 muffled heart sounds
 hypotension (Beck’s triad)
Diagnosis: EchoCG
Treatment:
 surgical( sternotomy,etc)
102. Traumatic shock: Etiology, pathology, clinical presentation, diagnosis, treatment

Etiology: hemorrhage
Pathology:
significant trauma (massive crush injury, multiple fractures) → cellular injury, devitalized tissues, bacterial contamination → systemic circulation is
flooded with BAS and necrotic products from damaged tissues → SIRS – loss of the plasma into interstitium of injured tissues, activation of coagulation
cascade and systemic fibrinolysis (DIC), ARDS, etc.
 Pale, clammy skin
 Delayed capillary refill
 Tachypnea
 Tachycardia
 Low BP
Diagnosis:
 Hemorrhagic is obvious
Treatment:
 early reestablishment of circulation to ischemic tissues, prompt debridement of devitalized or necrotic tissues, and early fracture fixation
 analgesics
103. Septic shock: Etiology, pathology, clinical presentation, diagnosis, treatment

Etiology: Any germs, virus, fungi, or protozoa may be causative agent
Pathology:
 bacteria and their products (endo- and exotoxin, proteases, enterotoxins, peptidoglycan) → release of endothelial and macrophage derived
proinflammatory cytokines (TNF-α and IL 1) → stimulate the release of other mediators: thromboxanes, leucotriens, platlet-activating factor,
prostaglandins, complement and nitric oxide (NO).
Effect of mediators:
 → cardiac dysfunction
 → activation of coagulation cascade microthrombosis → capillary plugging → opening of arteriovenous shunts → deprivation of tissues of adequate
perfusion.
 → increases endothelial and vascular permeability → loss of intravascular vol. into the interstitium → hypotension and edema.
End results : hypotension mostly due to decrease in vascular tone → pooling in large capacitance vessels → reduction of circulating blood vol. →
hypoperfusion → shock.
 Tachypnea, tachycardia, oliguria, changes in mental status, fever
 Specific clinical findings characteristic to some infections.
 Lab changes: leukocytosis, rise of ESR, etc.
Treatment:
 Fluid resuscitation – empiric broad-spectrum antibiotic
 Treatment of ongoing soiling: drainage or control of contamination, necrotic infected tissues debridement, etc.
104. Definition of anesthesia, local and general anesthesia, classification and types of anesthesia
Anesthesia is a partial or complete loss of sensation of pain with or without the loss of consciousness
General anesthesia is a period of reversible inconsciousness, the absence of pain, reflexes and relaxation of skeletal muscles as a result of the effect of
narcotic substanceson the central nervous system. (Gostichev)
Local anesthesia is a reversible loss of sensation in some part of the body induced by a local anesthetic agent. (Gostichev)
Local anesthesia - epidural
 Topical (aerosol, creams crioanasthesia, etc.)

 Local infiltration General anesthesia
 Local intravenous anesthesia Acc to route of admin:
 Electrostimulation  intramusculary
 Regional anesthesia:  intravenous
- plexus (celiac, brachial, etc.)  inhalation (via mask, endotracheal tbe, etc.)
- nerve trunk (digitalis nerve block, etc.)  combined
- spinal (intrathecal, subdural)
105. Stages of narcosis with characteristic

Stages of narcoses (depth)
Four stages are as follows:
1. Analgesia
the patient is conscious but confused and answers ques reluctantly. Not sensitive to superficial pain. Touch n heat sensitivity intact. Minor opt (e.g.
incision and drainage of abscess and ds procedure) can b performed. Short: 3 – 4 mins.
2. Excitement/agitation
inhibit cortical centers. Subcortical excited: unconscious, increased motor and speech rxn. Shout, attempt to get off opt table. Hyperemic skin, pulse
accelerated, BP increase. Pupil dilated but react to light, tears appear in the eyes. Cough, bronchial secretion is increased and vomit may occur. Opt is
prohibited. 7 – 15 mins.
3. Surgical stage (of 4 lvls)

calms down, breate smoothly, pulse n BP near basal values. Surgical intervention may b performed. Divided to 4 lvls:
 Lvl 1: calm, breathes smoothly, BP and pulse approach initial values. Pupils begin to constrict, still rx to light. Eyeballs placed eccentrically and move
rolling. Corneal and swallow reflexes are maintained. Muscle tone is maintained, difficult to perform opt on visceral organs.
 Lvl 2: eyeballs stop moving and located centrally. Pupils start to grad dilate; rxn to light abates. Corneal and swallow reflexes weaken and at the end
absent. Breathing is quiet n smooth. BP and PR are normal. Muscle tone starts to decrease, which allows opt on visceral organs
 Lvl 3: deep narcosis. Pupils are dilated, do not rx to light, swallow reflex is absent. Skeletal muscle incl intercostal ones are fully relaxed. Breathing is
shallow and diaphragmatic. Relaxation of muscle of the mandibnle which can hang and tongue can fall back to block the entrance of the larynx and cause
resp arrest. To prevent this complication the mandible should be helf fwd and kept there. Keep anes this cond may b fatal
 Lvl 4: max dilation of the pupils with no rxn to light, cornea is dry. Breathing is shallow thru movement of diaphragm, intercostal muscles are
paralysed. Pulse is fast and faint. BP is low and can hardly b assessed. May b fatal since resp n circulatory arrest can easily set in
4. Awakening
supply of narcotic is stopped, its blood concentration falls, patient in a reverse way goes thru all the stages passed and wakes up.
106. Preparation before general anesthesia, monitoring

The patient is examined before the operation. History is taken not only for the principal disease but also details of the concurrent conditions as well. If the
surgery is scheduled, the patient should be treated for any underlying ailments. Besides, examination has to be done to exclude possible allergies,
previous operations (if any) and the anesthesia used.
Features of the face, the chest, type of neck, nutritive status are evaluated.
Examples of underlying ailments:

CV disease
 Uncontrolled hypertension and angina, dysrhythmia and cardiac failure are common reasons for postponement of elective procedures
 Correction of HPT and IHD (medical therapy, pacemaker insertion before anesthesia,etc.)
 recent myocardial infarction is strong contraindication to elective anesthesia (delayed until at least 6 mths have elapsed)
 Any electrolyte abnormality (especially hypokalemia) or anemia should be corrected and the circulatory volume should be maintained at normal lvl
(an adequate urine output, etc.)
Respiratory disease
 Specific preoperative tests of respiratory function: spirometry and blood gas analysis
 Resp infection and asthma are the common prob needing trtment bfore anesthesia
 Regional anesthesia is advantageous in resp disease
Metabolic disorders
 insulin-dependent diabetes always needs preoperative conversion to control with rapidly acting insulin
Coagulation disorders
 coagulation disorders need careful assessment before surgery with a coagulation screen and platelet measurements
 patients receiving therapeutic warfarin need to cease trtment several days preopt and have prothrombin time measurement till international normalized
ratio falls to about 1.5 fr the therapeutic range of 2.0 - 4.2
 the heparin can be stopped or reversed with protamine for the period of surgery
Lab test
 Routine hematological and biochem screen
 Serum sample for transfusion cross-match a check for hepatitis antigen
Instrumental
 ECG and chest radiography in elderly ppl receiving gen anesthesia for all but minor surgery
One important measure to do prior to administration of anesthesia is the evacuation of gastrointestinal contents. It can be done through gastric lavage or
cleansing enema.
Fasting before surgery

 Standard practice is 6 hrs abstinence from food and 4 hrs abstinence fr fluids (recently a clear, nonfizzy fluids up to 2 hours preopt are allowed)
 Emptying of the bowel is attained by cleansing enema
Consent for surgery and anesthesia

 Informed Consent should be obtained before any sedation is given
 The anesthetist should explain anesthetic procedures, especially regional and spinal techniques, and discuss potential sequelae
Preoperative medications
Preoperative drugs
 At day case procedures preoperative sedation is avoided
 Reduction of anxiety: oral short-acting benzodiazepines 1 -2 hours preopt
30 mins before surgery

 The anticholinergic agents, atropine (0.1% 1ml) is used to reduce respiratory and oral secretions
 Powerful opioid analgesic (promedol 2% 1ml)
 Antihistamine agent (dimerol1% 1ml)
 Antiemetic may be given
107. Characteristic of anesthetic device. types of inhalation anesthetic administration

The anesthetic device consist of the following parts:
a) Cylinder for the gaseous substances – Gases are kept under the pressure of 150 atm.
b) Vaporiser – Steam forming narcotic substances.
c) Dosimeter – For measurement of accurate dosage of gaseous anesthetic drug and oxygen.
d) Breathing contour – Consist of a mechanical ventilator, a bag, hose, valves and absorbers. 4 types of breathing contour: Open, partly open, closed,
partly closed ( often used).
Types of inhalational anesthetic administration
a) Mask
b) Endotracheal
c) Endobronchial
108. Characteristic and examples of used inhalation and intravenous anesthetics

Inhalation anesthesia (isoflurane, sevoflurane, NO, ftorotane, etc) is given by an anesthetic machine
1. gas bags
2. dosimeters and evaporators
3. ventilators
Intravenous anesthesia: ketamine, propofol, thiopental, hexenal, sodium oxibutirate, etc.

Rapid action, easy to perform, short period of action.
109. Combined anesthesia: general characteristic, stages, examples of used medicines

General combined anesthesia
It usually requires endotracheal intubation (best control of an airway) with parallel admin of inhalation and i.v. anesthetics, myorelaxants, etc.
I. induction of anesthesia
 intravenous injection is most common. For intravenous induction, ketamine (propofol, thiopental, hexenal, sodium oxibutirate) with its rapid recovery
is currently practiced
 sevofluorane may also be used for inhalational induction
 analgesic agents are frequently also injected at the time of anesthetic induction
II. Maintenance of anesthesia

 following the induction of anesthesia, inhalational volatile or i.v. anesthetic agents are continuously admin to maintain an adequate depth of anesthesia
 adding nitrous oxide contributes analgesic and weak anesthetic effects
 ether has generally been replaced by halothane, enflurane and isoflurane. Desflurane and sevoflurane are the most recently introduced agents
conferring the advantages of fewer side effects and more rapid recovery
 total i.v. anesthesia avoids the use of inhalational anesthetic agents (enhanced quality and rapidity of recovery)
 it is also used when inhalayional anesthesia may be mpractical such as during airway laser surgery or endoscopy, and is popilar for cardiopulmonary
bypass
 i.v. anesthesia avoids atmospheric pollution and is usually conducted by neurolepanalgesia: propofol and a short acting opioid analgesic agent
(fentanyl) with droperidol (sedative) in combination with neuromuscular block and pulmonary ventilation with a mixture of air and oxygen
Neuromuscular blockade during surgery

 pharmacological bloackade of neuromuscular transmission provides relaxation of muscles ti facilitate surgery and mechanical positive pressure
ventilation
 muscle tone may also be reduced by very deep anesthesisa but may compromise the circulation
 neuromuscular blockade demands complete control of the airway and ventilation by the anesthetist
used agents
 depolarizing muscle relaxants: suxamethonium (rapidly provides excellent intubation conditions of brief duration)
 curare agents: atracurium, cisatracurium, vecuronium and rocuronium
 a peripheral nerve stimulator is also used to check for adequate depth of bloackade during surgery, and to confirm satisfactory recovery of
neuromuscular fx prior to extubation of the trachea
management of the airway during anesthesia

 general anesthesia reduces the tone of the muscles required to preserve airway patency (e.g. jaw thrust), or devices such as the Guedel or laryngeal
mask airways of endotracheal tubes)
instruments for control of the airway describing from the mouth to the bronchus: face mask and oro or nasopharyngeal tube (cuff inflated); cuffed
traheostomy tube; double lumen right endotracheal tube (tracheal and bronchial cuffs)
Airway contol with endotracheal tube (lung ventilation). It is usually placed by direct laryngoscopy, using a laryngoscope
A ciffed endotracheal tube is used to facilitate artificial ventilation or surgery around the face or airway, and to protect the lungs if there is a risk of
pulmonary aspiration. If fluid may collect in the mouth from above (as in nasal surgery) a throat pack is placed in the oropharynx.
Endotracheal tube
In pulmonary and open oesophageal surgery, selective intubation of either bronchus is usual to facilitate deflation of the lung on the operated side. Its use
is essential to protect the normal lung in the presence of a bronchopleural fistula.
Endotracheal intubation complications

 accidental and unrecognized oerophageal intubation
 accidental intubationof a main bronchus
 trauma to larynx, trachea or teeth
 aspiration of vomitus during neuromuscular blockade for intubation
 failure to intubate and loss of airway control
 disconnection or bloackage of the tube

 delayed tracheal stenosis, in children or after prolonged intubation
 careful observation of physical signs and constant vigilance, aided by pulse oximetry, capnography of the expiratory gases, inspiratory oxygen
concentration measurement and ventilator disconnection alarms are mandatory to minimize these risks
Haemostasis and blood pressure control

 20 – 30% reduction of mean arterial bp fr the awake preopt lvl in fit patients is acceptable, and can greatly improve the quality of the operative field
and reduce total blood loss. Reduction of venous pressure at the wound by correct patient positioning and avoidance of any causes of venous obstruction
and maintenance of satisfactorily deep anesthesia and slightly reduced arterial carbon dioxide tension, further contribute to providing a dry surgical field.
 Hypotensive drugs may be used to produce deliberate controlled hypotension if there is a clear surgical benefit to be obtained
Monitoring during anesthesia

 Accurate monitoring of vital funcions during anesthesia is obligatory
The basic parameters monitored are:

 Inspiratory oxygen concentration
 Oxygen saturation by pulse oximetry
 Expiratory carbon dioxide tension measurement
 Blood pressure
 Electrocardiogram
 For major surgery, invasive, direct monitoring of the circulation is used but the potential value of information gained must be weighed against the
possible dangers of placing intra arterial or central venous or pulmonary artery catherter. Hourly observation of urine output via a urinary catheter is most
helpful in assessing renal profusion. Ventilators should all have airway pressure monitors and disconnection alarms.
Anesthetic monitoring devices.

Cardiac monitoring: ecg, heart rate, arterial and central venous pressure, pulse oxymetry and body temperature
Respiratory parameters: including spirograph and volatile agent concentration
III. Conclusion or recovery from general anesthesia

 Recovery from general anesthesia should be closely supervised by trained nursing staff in an area equipped with the means of resuscitation and with
adequate monitoring devices. An anesthetist should be readily available.
 For the seriously ill patient, an intensive care unit may be necessary until the patient’s condition is satisfactory and stable
 The transition from tracheal intubation with ventilatory support to spontaneous be=reathing with an unprotected airway is a time of increased risk,
when respiratory arrest or obstruction may occur
Complication of gen anesthesia

 Airway obstruction (dentures, tongue, aspiration, malposition of an endotracheal tube, etc.)
 Intubation complications (mentioned above)
 Neurologic complications (brain edema, etc)
110. characteristic of neuroleptanalgesia, complications of narcosis

Neuroleptoanalgesia – used in maintanence of anaesthesia
- nitrous oxide with oxygen, fentanyl, droperidol and muscle relaxants
- anaesthesia is maintained with nitrous oxide + oxygen in the ratio of 2:1, fractional injection of fentanyl and droperidol 1-2ml each 15-20 minutes is
provided.
- tachycardia requires injection of fentanyl, whereas hypertension necessitates administration of droperidol
- this type of anaesthesia is the safest for patient
111. spinal and epidural anesthesia: indications, advantages and disadvantages

Indications
Genitourinary (caesaren section, prostatectomy, etc) and lower limb surgery
Indicated for operation on the organs below the diaphragm (stomach, intestine, liver, bile ducts, spleen, pelvic organs)
Advantages: Rapid action, usually within 5 min (e.g hyperbaric solutions of bupivicane)
Disadvantages: May lead to severe hypotension and respiratory failure.
112. spinal and epidural anesthesia: contraindications, procedure, specific complications.

Spinal anesthesia
Contraindications:
 Traumatic shock
 Severe Intoxication
 Concurrent hypotension
 Myocarditis
 Cutaneous infection of the spine
 Vertebral column deformity.
Procedure
1. Special spinal needles are used.
2. The patient is set on a table, the feet put on a step, the knees raised a little and the spine maximally flexed.
3. The nurse stands in front of the patient to keep him in the required posture.
4. The lumbar pucture is usually performed at the level between L2 and L3 or L3 and L4 vertebra process.
5. The skin of the injection site is infiltrated with novocaine.
6. The needle is placed in the midline between the bone precesses and tilted a little downwards.
7. As the needle passes through the intervertebral yellow ligaments, some resistance can be felt. Advance further till resistance is not felt.
8. Further resistance can be felt at the point of entry of through t he spinal dura mater.
9. The syringe is remove while the needle is pushed forward, piercing the internal layer of the dura mater.
10. The appearance of colourless fluid suggest a successful puncture.
11. Upon successful puncture, 2-3ml of CSF is withdrawn into the syringe, mixed with solution of bupivacaine and injected as a single shot into the
CSF.
12. The patient is immediately placed on the operating table with the head end of the table raised. This is to prevent the spread of the anesthetic to the
midbrain.
Complications: Hypotension, Respiratory arrest (due to spread of anesthesia upwards along the subarachnoid space), headache, lower limb paresis and
purulent menigitis
Epidural anesthesia
Indications
 Trauma and orthopedic surgeries on the lower limbs.
 Abdominal operations
 Pelvic operations.
 Elderly patients
 Patients with cardiovascular and respiratory diseases.
 Patients with metabolic disorders.(obesity, diabetes mellitus)
Procedure:
1. Puncture can be done at any level of the vertebral column.
2. Puncture is done with a needle connected to a syringe with NS solution.
3. Resistance will be felt as the needle passes through the intervertebral ligament and enters the epidural space, where no resistance is felt and the liquid
is easily injected.
4. Needle is in the correct space when the CSF do not gush out when the syringe is removed.
5. Anethetic can be given with a needle or through a catheter (for longer duration)
Complications epidural anesthesia

 Rare
 bradycardia and hypotension
 urinary retention is common necessitating catheterization of the bladder
 headache
 back pain
113. Characteristic and examples of drugs used in local anesthesia

Upper dose limits suitable for a 70kg adult
Lignocaine
 200 mg (10ml of 2%)
 50 ml lignocaine 1% with adrenaline (1:200 000)
Bupivacaine (for about 6 hours)

 150 mg (30 ml of 0.5%)
 Addition of adrenaline would enhance the safety of this high dose. Bupivacaine is more cardiotoxic than lignocaine. Bupivacaine 0.25% is effective
for sensory block against moderate stimulus. Bupivacaine must never be injected into a vein, and is absolutely contraindicated from use for intravenous
regional anesthesia
Prilocaine
 400mg (40ml of 1%)
Ropivacaine 225mg (30ml of 0.75%)
114. Indications and contraindications to local infiltration anesthesia

 Infiltration Anaesthesia / Vishnevsky anaesthesia
- anaesthetic admin to subcutaneus tissue, affecting nerve ending
- large volume needed = 100mL / 80 mL (conc. 0.5%)
- can lead to toxicity (10mL of 2%) – overdosage

- in small vol. (1%) – 1 – 2mL
- safest : 0.5%
- into dermis, them a further 20mL given, can change position of needle  deep fascia (20-40mL)  muscle
- eg: Herniatomy
o operation of abd, eg: appendicitis, gastrotomy
o inflammatory disease
Contraindications
 Local infection (infection spread, ineffective in acid environment)
 Clotting disorder (haemorrhage)
115. advantages and disadvantages of local infiltration anesthesia

Local infiltration (into or around a wound)
Advantages
 Fasting is no necessary.
Disadvantages
 Administration in the presence of clotting disorder , may result in hemorrhage or hematoma.
 In the presence of a local infection, it may be responsible for the spreading of the infection
116. procedure of local infiltration anesthesia

Infiltration anesthesia for thyroid surgery
1. Skin and subcutaneous anesthesia along the course of incision.
2. Anesthesia of cervical muscles
3. Thyroid gland anesthesia
117. Local anesthesia: specific complications and management
Complications
 Local (infection, hematoma)
 Systemic: overdosage or accidental intravascular injection
Systemic toxicity
 Depressed consciousness and light headedness
 Convulsions
 Circum oral parastesia

 Cardiac arrest (bupivacaine)
Management:
 Use recently introduced anesthetics e.g, ropivacaine and levo-bupivacaine with lesser side effects.
 Do not use adrenaline in hypertensive patients .
 Ensure the availability of skilled personnel and resuscitation equipment including oxygen.
118. Digital nerve block anesthesia: used drugs, indications, procedure, complications
- Digital nerve block anaesthesia
o for outpatients
o to area of med and lat.
o from dorsal aspect of finger towards bone ( 2 -3 mL enough for all fingers)
o treat finger pathology eg: abscess
o to ↓ bleeding – torniquet placed at end / base of finger
119. Intercostal nerve block anesthesia: indications, procedure

- Costal nerve / rib anaesthesia
o at patients with rib fractures
o at area of muscular bundle, lower border
o should aspirate continuously
120. anesthesia of the brachial plexus: indications, procedure

- Brachial plexus anaesthesia
o for whole arm
o neddle towards plexus
o using sensitive needles for guide, attached to device
o current: if touch nerve, muscle movements seen – right position, inject anaesthetics
o done in ischiatic nerve for lower extremities too, celiac plexus
121. Blocking of the upper arm, forearm, thigh: Indications, procedure.

122. Intraveneous and intraosseous anesthesia: indications, procedure.
Wound and Healing Process

123. Primary and Secondary Healing. Definition and characteristic

Wound healing is a complex of biological processes intiated by tissue injury that terminates with restoration of tissue integrity. The end result is fibrosis
and scar.
The biological processes involved are:

 Inflammation
 Proliferation
 Remodelling
Primary healing – Occurs when wound edges are approximated, healing proceeds rapidly to closure.
Secondary healing – If wound edges are separated as in tissue loss, the biological processes occur but rapid closure is impossible
124. Open wound healing: stages and characteristic
125. Closed wound healing: stages and characteristic
Inflammation
- within 24 hrs, neutrophil efflux into the wound. The neutrophils scavenge debris, bacteria and secrete cytokines for monocyte and lymphocyte
attraction and activation. Keratinocytes begin migration when provisional matrix is present.
- At 2 - 3 days after injury, macrophage becomes the predominant inflammatory cell type in clean noninfected wounds. These cells then regulate the
repair process by secretion of a myriad of growth factors including types that induce fibroblast and endothelial cell migration and proliferation.
Proliferation
a) Fibroplasia - synthesis and secretion of extracellualar matrix products. It is composed of fibrin, glycosaminoglycan and hyaluronic acid. As fibroblasts
enter and populate the wound they digest the provisional matrix and concomitantly deposit collagens. Fibroblast are activated and present at the wound by
3 -5 days after injury. These cells secrete matrix components and growth factors that contribute to stimulate healing. Keratinocytes migration (epiboly)
begins over the new matrix. Migration starts from the wound edges as well as from epidermal cell nests at sweat glands and hair follicles in the center of
the wound.
b) Granulation – granulation tis is present in tissue healing by secondary intention. This tis is clinically characterized by its beefy-red appearance (rich
bed of new capillary network due to neoangiogenesis)
c) Contraction – contraction is a feature of the open wound (such as after trauma, burns, dehiscence due to local infection). Contraction is the process in
which surrounding skin is pulled circumferentially towards the wound, decreasing its size without new tissue formation.
d) Epithilization - new epithelial cells for wound closure are provided by fixed basal cells in a zone near the edge of the wound. Their daughter cells
flatten and migrate over the wound matrix as a sheet.
Remodeling
The extracellular matrix is the scaffold that supports cells. The ECM is dynamic and during repair is constantly undergoing remodeling. Simplistically it
is a balance between synthesis, deposition and degradation.
Scar formation is the outcome of healing in postoatal skin. Scar is composed of densely packed disorganized collagen fiber bundles, remodeling occurs up
to 1 – 2 years after injury and consists of further collagen cross-linking and regression of capillary which account for the softening of scar and its color
change from red to white.
Scar is char by lack of tissue organization compared to normal tissue architecture. The scar is less elastic n does not contain any skin appendages such as
hair follicles and sweat glands.
126. Wound pathology: types and characteristic of chronic wounds
WOUND PATHOLOGY
Nonhealing wounds
1) pressure sores. The trtment option is to close these wounds surgically with flap of normal skin and muscles over the bony prominence
2) lower extremity ulcers. They are caused by venous(80 – 90%) or arterial insufficiency
3) radiation injury. Trtment modalities are hyperbaric oxygen therapy or coverage with vascularized tissue flaps.
127. Clinical factors, affecting repair

Clinical factors affecting repair
1) infection (>105 organisms/g tis)
2) nutrition: malnutrition , ascorbic acid deficiency, vit A (retinoic acid), vit B6(pyridoxine), vit B1 (thiamine), vit B2 (riboflavin), Zn, copper are also
impt for normal process of healing
3) oxygen n perfusion. Wound ischemia occurs secondary to:
- occlusive vascular disease
- hypovolemia
- vasoconstriction due to pain, tight sutures
4) diabetes mellitus and obesity
5) corticosteroids
6) radiation therapy
7) chemotherapy
128. Hypertrophic scar: etiology, pathology, clinical picture, treatment

Excessive healing
Hypertrophic scars. Trtments options include application of pressure garment(for 14 months) or topical silicone sheets, laser therapy, physical therapy
with range of motion exercise or reexcision with primary closure (for scars caused by infection r dehiscence)
The treatment of hypertrophic scars with pressure garments. A typical eg of active hypertrophic scaring following a full thickness scald. Pressure
garments were worn continuously for 14months and the scar matured with reduced contracture formation.
129. Keloid: etiology, pathology, clinical picture, treatment

the keloid scar continues to enlarge and behave like a benign skin tumor with continued slow growth.
a)steroid injection directly into keloid
b)short course of low dose radiation therapy
c)topical silicone sheeting placement
130. Classifications of wounds

CLASSIFICATON OF TRAUMATIC WOUNDS Contamination:
According to character: - tidy
- stab - untidy
- incised Tidy wounds (trtment is usually by primary closure)
- contused - clean incision
- crushed - uncontaminated
- lacerated - less thn 6 hours old
- gunshot - low energy trauma
- bite
Untidy wounds (commonly left open)
Relation to body cavity: - ragged edge
- penetrating (with and without organ injury) - contaminated
- non penetrating - more than 12 hrs
- high energy trauma
Presence of complications: - crushed tissue
- complicated (vascular injury, gas gangrene etc) - burns
- noncomplicated
131. Diagnosis of wounds, local wound examination

Examination of a patient
 Complaints: pain, bleeding, tissue defect
 History of trauma
 Objective exmn; can be found characteristic features of blood los or signs of internal bleeding, etc
*Any type of wound should be considered for tetanus and rabies prophylaxis
Examination of a wound(local status)

 presence of foreign bodies
 viability
 coexisting injury to adjacent nerves (sensation), muscles (active movements) and vessels (distal pulsation)
132. characteristic of different sorts of wounds

Gunshot wounds
-3 areas
1)wound canal
2)area of primary traumatic necrosis
3)area of molecular concussion
e.g. High velocity wound.

Extensive exploration of the entrance wound in the groin was required in order to adequately complete wound debridement and gain proximal control of
the femoral artery should this have been damaged. The extend of the skin incision is clearly demonstrated; this was partially restored at initial opt aft
exploration of the large vessels.
The exit wound in the buttocks undergoes wound debridement before delayed primary closure some days later.
133. Pathology, diagnosis and first aid of penetrating injuries into the pleural cavity
Diagnosis and management of penetrating chest wound
Manifested by:
 subcutaneous emphysema (crepitation) around the wound
 whistling sound produced by passage of air thru the wound during inspiration and expiration
 bubbling of air in the depth of wound
 exmn of the chest may detect objective signs of pneumo- or hemothorax (dyspnea, change in breathing sound, expansion and percussion note)
First aid for open and tension pneumothorax

Treatment of sucking chest wound. on inspiration, the dressing seals the wound preventing entry of air. on expiration, trapped air is able to escape thru the
untapped section of the dressing
134. Pathology, diagnosis and first aid of penetrating injuries into the abdominal cavity
Diagnosis and management of penetrating abdominal wound
 Typical localization of the wound
 passage of urine, bile, intestinal content, loop of intestine thru the wound. Cover the wound with clean dressing and transport a patient for definitive
trtment in the hospital.
 Sign of peritonitis (damage to hollow intraabdominal organ)
 Signs of hemoperitoneum (damage to solid intraabdominal organ)
 Exploration of wound for penetration during surgical debridement
135. Management of wounds: first aid
136. Primary surgical debridement: types, procedure and characteristic

SURGICAL DEBRIMENT represent the procedure of removal of all necrotized ,nonviable tissue (affected parts of the skin, s/c fat, muscles, or even
bone). The purpose of the procedure is to remove all nonviable tis and create the best environment for healing process and prompt closure of wound
PRIMARY SURGICAL DEBRIMENT is performed according primary indications. It means the procedure is done after trauma approx w/in 6-12 hrs
after injury.
Wound draining
In some circumstances a surgical debridement is finished by insertion of the plastic drain
PRIMARY CLOSURE WITH HEALING by PRIMARY INTENTION

PI healing occurs in closed wounds which are wounds with the edges approximated. Direct approximation of wound edge can be accomplished by the
following (closure):
-suturing
-adhesive strip
-metal clips
-biological glues and sealants (fibrin and oth)
TOPICAL WOUND T’MENT

local care for open wound left for healing by secondary intention
 excision of the skin lacerations by sharp dissection (secondary surgical debriment) together with copius wound irrigaton with normal saline till
undamaged cells shud be performed in order to convert the wound into a tidy one. Normal wound bleeding is a hallmark of viability. necrotic material
shud be removed fm open wound on initial presentation n subsequently as it accumulates. The only exception to immediate debridement is dry, chronic,
arterial insufficiency eschar without evidence of infection.
 open wounds heals optimally in moist, sterile environment. by keeping wound covered n moist without infection, desiccation necrosis and healing
delay are prevented
SECONDARY SURGICAL DEBRIMENT is always performed acc to secondary indication. It means the procedure is done to treat complications such as
suppurative complications, pus loculation at the primary wound, etc.
Wound dressing
The optimal open wound dressing maintains a moist, clean environment, reduces edema, stimulate repair, require less frequent dressing, prevent skin
irritation and is inexpensive
137. Wound closure: general rules, types, indications and contraindications

DEFINITIVE CARE OF THE WOUND
Whether to close the defect:
a) primary closure is common for tidy wounds (at the time of presentation)
is not done for:
1) uncontrollable bleeding
2) presence of necrotic or foreign materials that cant be removed fr the wound
3) excessive contamination
b) left open. It is acceptable for contaminated wounds (untidy wounds)

- quantitative bacteriology (more thn 10 0000 organisms).
- age of wound (6 hrs, maybe slightly prolonged by use of irrigation, antibiotics and debridement)
- mechanism of injury (bite and agricultural wounds)
- location (well vascularized area is more safely to close)
- malnutrition
- steroids and cytostatics
How aggressively the wound can be treated before closure?

If the wound can be completely excised to fresh tis primary closure can be carried out even in unfavourable wounds (may be limited by lack of tis,
adjacent nerves, vessels or bones)
Primary closure is not feasible

 Wound with uncontrollable bleeding – tamponage with tight bandaging
 necrotc and contaminated wound - dressing change with wet environment using collagenolytic ointments, antiseptics
 since the problem has been controlled the wound can be closed
To heal secondary (contraction and granulation, etc.)

The secondary healing is preferred for infected wounds, superficial wounds, small and puncture wounds. The forming scar is aesthetic and acceptable.
Delayed primary closure

when doubts exist about status of a wound, it can be maintained in optimal condition with wet dressings and antiseptics for up to 72 hrs. dead tis will
“declare” itself and can be excised allowing subsequent delayed primary closure.
Wound closure
-direct wound approximation (most lacerations n wounds with limited tissue loss)
-skin graft (for more intensive wounds)
-local flaps and focal flaps
Direct wound approximation

Generally it involves 5 steps:
1) anesthesia
2) wound irrigation
3) shaving n prepping of the wounded area
4) wound debridement
5) wound closure
138. Care for closed and open wounds

Clinical management of open wounds healing by secondary intention
Open wound edges are not approximated but are instead separated, therefore each sequence lasts most longer, especially proliferative phase
A bed of granulation tissue forms during proliferation phase
if no infection is present (less thn 10 000 organisms/g) the wound can be closed using the following methods:
-Secondary suturing
-placement of skin graft if the area is of sufficient size that healing is not be completed for at least 2-3 weeks
-skin flap is used at the areas of poor bld supply and absence of “padding”
after 2 weeks a closure of the wound with secondary suturing requires excision of already formed scar tissue to closer approximation of the wound edges
Local care for closed wound

-closed wound shud be kept sterile for 24-48 hrs. tensile strength is only 20% of normal skin at 3 weeks thn collagen cross linking bcoming significant. at
6 weeks wounds are at 70% of the tensile strength of normal skin (heavy activity shud be limited for at min of 6 weeks while healing of deep fascial
structures like an abdominal aponeurosis)
-skin structure are remved depending on the localization (bld supply) of the wound
PHARMACOLOGICAL T’MENT
-open wounds are colonized by bacteria and systemic antibiotics are indicated if invasive infection is present. topical antibiotics shud not be used becoz of
risk of developing an invasive infection by resistant bacteria is very high
-antibiotic ointments are commonly used in burn wound care
-collagenases are useful to treat wounds that require fine debridement
-growth factors
TETANUS PROPHYLAXIS
-Evalute patients immunization status
-patients with tetanus prone wounds who have undergone previous active immunization within 5 years of the time of injury require no further prophylaxis
-patients with tetanus prone wounds who received their most recent booster injection more thn 5 years.
Surgical infections: Suppurative diseases of the skin, glands and subcutaneous cellular tissue.
139. Purulent infection: definition, etiology

Purulent infections is the group of diseases caused by pyogenic bacteria that may localize at different body areas and have different features
Classification of surgical infections Acc to clinical course and char local changes
 Acute surgical infection: Acc to localization

o Purulent  Skin and subcutaneous tis
o Anaerobic  Skull, brain, meninges
o Specific (tuberculosis, syphilis, anthrax, etc)  Neck
 Chest wall, pleura, lungs
 Chronic surgical infection:  Mediastinum
o Nonspecific (pyogenic)  Peritoneum and peritoneal organs
o Specific (tuberculosis, syphilis, actinomycosis, etc.)  Pelvic organs
 Bones and joints
Acc to etio
 Staphylococcal, streptococcal, clostridial, etc. Etiology
 Different spp of MO (G+ ; G- ; anaerobic, etc,)
 Invasion may occur by exo- or endogenous route
140. Purulent infection: pathogenesis, stages of the inflammatory process

Pathogenesis
Invasion (due to trauma, predisposition) → inflammatory response → outcome (stops or progress)
141. Purulent infection: factors, determining outcomes of infection

Factors determining course and outcome of purulent disease
 Immunity status
 Immune response (hyperergic, hypoergic and normoergic response varies with an age)
 Immunodeficiency states (taking corticosteroids, immunosuppressive and cytostatic agents, radiation)
 Metabolic abnormalities
 Nutrition state
 Tissue perfusion
 Amount of bacteria and their virulence
 Anatomophysiologic conditions of the area
Two stages
Early serous inflammation (infiltrative stage)
Localization of the process (suppurative stage) is characterized by pus formation and loculation
Body response (local and general changes)

 Local reaction (response) includes rise of local T, pain, loss of fx, edema, hyperemia. Its manifestation is influenced by a type of imm resp and oth
factors. The process may loculate or extend deeper
 General rxn (changes). Its manifestation is influenced by a no. of factors (virulence and extend of infection, etc.)
 Intoxication (due to toxemia – bact toxins, devitalized tis, etc.) → depletion of circulating volume (nonhemorrhagic dehydration), electrolyte and acid-
base changes (are most prominent at severe infections – peritonitis, mediastinitis, etc.) If the pathology is severe and progresses it may lead to SIRS and
MODS.
142. Examination of a patient with purulent infection

Clinical features and patient’s examination
 Local manifestation depends on the stage (infiltration or loculation), localization (deep or superficial), and character (peritonitis, empyema, etc.) of
process
 Progression of local inflammation increases general manifestation and intoxication)
General manifestation
 Fever (hectic type is common), chills, gen debilitation, (change of consciousness, hypothermia are at severe cases), malaise, vomit, headache, loss of
appetite
 Rise of RR
 Rise of HR
 Oth signs of hypovolemia
 At severe cases complicated by organ dysfunction a clinical evidence of their alteration may be present
Laboratory changes may be different depending on severity of infection

 Complete blood count:
o WBC changes are characteristic – leukocytosis, increase band form
o RBC
o ESR – increased in infection
 Blood chemistry
o Dysproteinema
o At severe cases complicated by organ dysfunction may be characteristic lab evidence of their alteration
o Rise of AST, ALT
o Rise of alkaline phosphatase
o C-reactive protein, etc.
 Urinanalysis may show dysfunction of the kidney

 Blood culture (signs despite control of local infection)
 Glucose level
 Aspiration of exudate (puncture)
 Immune tests (immunogram)
After correction of the reason (pus draining) all signs of infection rapidly decrease
Instrumental investigation methods are extremely useful in identification of occult infection focus (deep localization) and atypical clinical presentation
The list of used tools may vary with an exact type of pathology
 US
 CT and MRI
 Endoscopy
 Plane and contrast X-ray studies
 Etc.
143. Purulent infection: general principles of treatment

Surgical treatment:
Indications: loculation of the pus has completed or conservative treatment has failed,
Stages of surgery
 Surgical access to purulent locus (best draining)
 Debridement and irrigation
 Draining of the wound (passive or active)
 Management of the wound acc to common rules of care for open wounds
Note: closure with primary sutures (or tissue flap) can only be done if complete excision of the purulent focus has been accomplished. It is always
finished by active draining of the wound.
Medical therapy (conservative treatment):

 Antibiotics, antiseptics, physiotherapy may abrupt the process at the stage of serous inflammation (before localization of the pus)
 Immobilization and elevation of the affected part
 Infusion and detoxification therapy (severe cases)
 Correction of acid-base and fluid-electrolyte disorders
 Immunotherapy
 Nutrition of a patient
Detoxification therapy
 Intracorporal detoxification (infusion therapy, forced diuresis, etc.)
 Extracorporal detoxification (plasmapheresis, hemosorption, hemodialysis, etc.)
Pyogenic diseases of the skin, glands and subcutaneous tissue

 Abscess  Hydradenitis
 Phlegmon  Erysipelas
 Folliculitis  Lymphangitis and lymphadenitis
 Furuncle  Acute mastitis
 Carbuncle  Coccygealsinus
144. Abscess: definition, etiology, clinical picture, treatment
abscess is a localized collection of the pus due to purulent infection which has already passed a phase of serous inflammation. Commonly it is caused by
complication of purulent processes (furuncle, carbuncle, etc.)
Pathophysio, loculation of an abscess is caused by the formation of pyogenic capsule which demarcated viable tis fr the collected pus. Clinical pic is
determined by localization of the abscess.
Clinical pic and ds

An abscess may form anywhere in the body. Clinic pic is determined by localization of the abscess. Ds is based on signs of infection (local and general),
presence of fluctuation. A diagnostic puncture may be useful.
Deeply situated abscess may require instrumental investigation

In 85% of cases the responsible for the abscess bact are staph or streptococcus
Treatment
Treatment of the abscess is surgical. It consist of inclusion, evacuation of the pus, excision of the capsule, active draining of the wound and closure of the
wound with primary suture. Only if a surgeon is sure of the completeness of excision of necrotic materials.
Active draining with continuous irrigation of the wound using antiseptics is accomplished at the early postopt period
Small abscess do not require closure with primary sutures. After evacuation of the pus and secondary debridement they are managed as an open wound
which may heal by secondary intention. Closure of the wound may be done using secondary sutures.
Nowadays a puncture, draining, and further management of an abscess may be done using sophisticated endoscopic techniques and imaging studies (US,
CT and MRI). This mtd are extremely useful in trtment of deeply situated abscesses (intrahepatic, subphrenic, pulmonary, pleural empyema, etc.)
145. Phlegmon: definition, etiology, clinical picture, diagnosis and treatment

phlegmon is a diffuse suppurative inflammation of fatty tissue without clear loculation of the process
Etio: postinjection complication, complication of an abscess, osteomyelitis, infection of the hematoma, etc.
Classification acc to localization

 Superficial (mostly G+) – subcutaneous, paraproctitis
 Deeply (mostly G-, anaerobes) – retroperioneal, intramuscular, mediastinitis, paranephritis.
Superficial phlegmon
 Overt signs of inflammation
 Absence of clear boundaries
 Gradually developing fluctuation followed by skin necrosis
Deep phlegmon are dangerous due to possibility of their spread along the fascial planes
Ds
Ds is based on analysis of clinical data
Deep phlegmons more significantly affect a general condition of a patient
Clinical ds of a deep phlegmon is more difficult. An instrumental techniques are very useful
Treatment
Medical therapy is done acc to common rules of incision, evacuation of the pus, excision of debris and loculation of the pus, active draining of the wound
and closure of the wound with primary sutures. They can be applied only if a surgeon is sure of completeness of excision of necrotic materials.
Active draining in that case is mandatory. Active irrigation is done with several liters of antiseptic. Drains are removed 6 -7 days after surgery.
If the wound is left open its further treatment is done acc to care for open wounds. Secondary wound closure is preferred and done if any uncertainty are
present about completeness of removal of necrotic tis.
Different localization of pyogenic infection diseases in the skin and subcutaneous tis
1. carbuncle
2. hydradenitis
3. furuncle
4. erysipelas
5. phlegmon of subcutaneous tis
146. Lymphangitis and lymphadenitis: definition, etiology, clinical picture, treatment
lymphangitis is an inflammation of lymphatics commonly developing as a complication of different purulent infection processes
pathology
absorption of toxins and extension of infection from a primary focus at the beginning leads to lymphangitis. If the process is not stopped it may extend
onto the regional lymph nodes resulting in lymphadenitis
clinically the lymphangitis is char by several red strips running fr infected area towards a regional lymph node. Both the lymphangitis and lymphadenitis
are accompanied by prominent local and general signs of infection
treatment
both the lymphangitis and lymphadenitis well respond to trtment of primary focus of infection (surgical debridement, etc). surgery is indicated at the
purulent stage of luphadenitis.
147. Furuncle: definition, etiology, clinical picture, treatment

localization: the back, thighs, buttocks
etio: staph
predisposition: poor hygiene, continuous microtrauma of the skin, hypovitaminosis, metabolic disoders
Clinical pic
Superficial reddish lesion which later becomes yellow (pustule) 2-3 mm size with indurated basis
Treatment of the furuncle is commonly conservative. Surgical treatment is indicated if the furuncle is complicated by abscess formation. In unfavourable
circumstances the inflammation may progress leading to carbuncle.
148. Hydradenitis: definition, etiology, clinical picture, treatment

hydradenitis is an acute inflammation of the sweat glands (armpit, rarely at the groin). Bact commonly pass via the orifices of sweat glands.
Clinical pic and treatment

It commonly has protracted course with recurrence of symptoms. It may require surgical resection of affected tis w/in borders of nonaffected skin.
149. Acute mastitis: definition and etiology, classification

mastitis is an acute purulent inflammation of the mammary gland
predisposing factors: lactostasis (poor development of milk ducts), microtrauma and poor hygiene
classification
1. galactophoritis
2. subareolar abscess
3. intramammary abscess
4. retromammary abscess
150. Acute mastitis: clinical picture, diagnosis and treatment, prophylaxis

clinical pic
severe pain and infiltration in the gland, fever
ds
clinical pic, puncture, imaging studies
treatment
early period: conservative measures – prevention of milk stagnation, AB, Novocain blocks.
Surgery is indicated if there is a purulent stage of mastitis. A type of incision varies depending on localization of the process
The abscess requires excision of a necrotic tissues, draining of the wound with gauze pads.
Also the mtd of active wound care using complete excision of necrotic materials, active draining and primary or secondary wound closure can be
accomplished.
151. Carbuncle: definition, etiology, clinical picture, treatment

carbuncle is an inflammation of several hair follicles and sebaceous glands. It has a tendency to extension onto surrounding tis. Local changes are always
more prominent when those caused by furuncle.
Clinical pic
Dark area of skin necrosis may be of large size. Signs of local inflammation are always accompanied by general body response. Inflammation involves
surrounding noninvolved structures leading to multiple subcutaneous abscesses.
Surgical treatment requires excision of an infiltrate till the borders of noninvolved tis which is followed by common care for the open wound
Closure of the wound defect may be done by secondary sutures, skin graft or flap
152. Erysipelas: definition, etiology, clinical picture, clinical forms, treatment

erysipelas is an acute infection disease char by inflammation of the skin leading to hyperemia and swelling of a clear demarcated area.
Etio: B-hemolytic streptococcus
 Erythematous-bullous form
 Erythematous-hemorrhagic form
 Bullous-hemorrhagic (phlegmonous) form
 Necrotic form
Treatment
AB therapy is done using penicillinase-resistant penicillins and acc to results of sensitivity
UVI of the skin
Complicated forms of the erysipelas are treated acc to general rules of surgery
The wound may be treated with MAE. Closure of the extensive skin defect is later done with skin graft or flap.
Recurrence of the erysipelas may lead to chronic lymphatic insufficiency. Prevention may be achieved using long-acting penicillin.
153. Folliculitis: definition, etiology, clinical picture, treatment

Folliculitis is an inflammation of hair follicle. Small superficial yellow lesion.
154. General aspects: predisposing conditions, stages of inflammation.
Purulent Infections of the Hand and Foot
155. Etiology and classification of the hand suppurative infections.

 Suppurative hand infection etiology :
- skin n subcutaneous tissue –corn , interphalengeal phlegmon ,supraaponeurotic phlegmon of palm
- facial n intersisitial space – mid palmar space thenar n hypothenar phlegmon
- dorsal aspect – subcutaneous phlegmon
 Classification :
- superficial forms: cutaneous, subcutaneous , paronychial , hyponychial .
- Deeper forms : tendinous ,osteal, articular and pandactilitis .
156. Cutaneous panatrium (felon): pathology, clinical picture, treatment

 Pathology:
o formation of blisters- the content may be serous, purulent, hemorrhagic
 Clinical picture
- High temperature at the infected region
 Treatment:
- Surgical treatment
1. Types of insisions: depending on the localization of infection (an incision never crosses the skin creases and area of median nerve distribution)
2. adequate draining by using plastic tube drain.
- antibiotics
157. Subcuatneous panatrium (felon): pathology, clinical picture, treatment

 Pathology
- Pain- tissue bands cause in the subcutaneous layer, connect skin to periosteum , prevent pus from spreading from the periphery.tension in this tissue
bands cause intensive pain in finger ,puss in subcutaneous panaritum tends to spread to deep lying tissue .
- Infection is commonly localized under the skin with apparent local sign. Movement are not painful
 Clinical picture
- Pain increase with throbbing and pulsating character
- Presence of tenderness at the focus of inflammation
- During examination- show tension in the tissue of the finger fold at the interphalangeal
 Treatment:
Types of insisions: depending on the localization of infection (an incision never crosses the skin creases and area of median nerve distribution)
adequate draining by using plastic tube drain.
- antibiotics
158. Paranychia and Hyponyhia: pathology, clinical pictures, treatment

 Pathology :
Paranychia
- Inflammation in the area of the nail fold.
- tender swelling and hyperemia of the skin around it .
- palpation of the edematous area around the nail phalanxis tender.
- sometimes is can spread beneath the nail plate dividing it from dividing it from lateral and purulent
Hyponyhia
- Pus beneath the nail plate.
- signs are loosing of the nail bed n it only fix to the proximal ends .
- Oedema of the skin is minimal in hyponychial panaaritium.
- The main sympthom are pulsating throbbing pain at the nail phalanx.there is tenderness on palpation.
 Clinical pictures
Paranychia
- tender swelling and hyperemia of the skin around it .
- palpation of the edematous area around the nail phalanxis tender.
- sometimes is can spread beneath the nail plate dividing it from dividing it from lateral and purulent
Hyponyhia
- Pus beneath the nail plate.
- signs are loosing of the nail bed n it only fix to the proximal ends .
- Oedema of the skin is minimal in hyponychial panaaritium.

- The main sympthom are pulsating throbbing pain at the nail phalanx.
- tenderness on palpation.
 Treatment:
- Surgical:
The nail root should be exposed. Incision proximal to the corner of the involved nail. If the abscess extends around the nail base or lateral margin, the
base or margin should be excised for adequate drainage and removal of nonviable nail. The fingernail will regenerate from the nail bed.
- Antibiotics
159. Tendon panaritium (felon) or bacteria flexor tenosynovits: pathology, clinical pictures, treatment
 Pathology
- infection to the tendon of flexor digitorum muscles
- pain is like shooting and throobing pain towards the finger .
- the finger appears to be like sausage like and slightly bent due to the tension
- lymphangitis
- lymphadenitis
 treatment
- surgical
a) the incision is placed at the neutral midaxial line
b) End-on view of incision, the web extension of incision is not always necessary for exposure
c) Surgical maneuvers
d) Implantation of irrigating catheters and multiple postoperative instillations effectively control many infections
e) Closed irrigation of flexor sheath infection using two incisions and a small catheter
- postoperative immobilization at the position of function, antibiotics, and elevation of the hand are to be done
160. Articular panaritium (felon) or acute suppurative arthritis: pathology, clinical pictures, treatment
 Pathology:
- Injuries to the dorsum, interphalangeal or carpophalangeal aspects where the joints are covered by the layer of soft tissue
- local signs of infection, (with advanced infection pathologic mobility, and crepitation develop due to destruction of ligaments)
- painful movements .
- Pain when bend finger .

- increase in tempreture , oedema and hyperemia .
- puncture of the reveals turbid fluid
 Treatment
- surgical wide arthrotomy and draining are used if joint surface is not damaged. Damaged surfaces need to be resected
161. Osteal panaritium (felon) or osteomyelitis: pathology, clinical pictures, diagnose, treatment
 Pathology
- usually results from further progress of infection caused by subcutaneous panaritium
- radiological picture of bone destruction is evident only at 10-14 days after beginning of clinical picture
- Dull and nagging pain
- minimal purulent discharge .
- finger- clubbed and puffy and tender on palpation.
- In x-ray sign of bone distruction in the 2nd -3rd week .
 Diagnose
- In x-ray sign of bone distruction in the 2nd -3rd week
 Treatment .
- surgical wide incision and draining are used .
- Damaged surfaces need to be resected
162. Web infection: pathology, clinical pictures, treatment

Pathology:
163. U- phlegmon or horseshoe abcess: etiology, pathology, clinical pictures, treatment

Etiology:
 Purulent tendovaginits of the 1st or the 5th finger with a spread of the purulent exudates to radial and ulnar synovial sacs
Pathology:
 Hand is edematous, bluish- violet in colour
 Absence of active movement of the finger
Clinical pictures:
 Pronounced intoxication, high temperature, headache, body weekness

 Hand is edematous, bluish- violet in colour and palpation is extremely tender
 Finger bend forward and active movement of the finger is absence, movement of the finger may cause pain too
Treatment:
 Incision for draining the abcess
 Antibiotics
164. Thenar and midpalmar space suppurative infectious: pathology, clinical pictures, treatment
Pathology:
 Swelling in the central palmar area
 Skin is tense, skin folds are smooth
 Dorsum of the hand is very edematous
 2nd – 5th finger are slightly bent in the interphalangeal joint
Clinical pictures:
 Swelling in the central palmar area
 Skin is tense, skin folds are smooth and fluctuation is impossible to elicit
 Palpation over the region may cause pain
 Dorsum of the hand is very edematous
 2nd-5th fingers are slightly bent in the interphalangeal joint, movement of the fingers may cause pain
Treatment:
 Incision for draining of the abcess
 Antibiotics
165. Surgical treatment of hand infection (indications to surgery, incisions etc.)

Cutaneous panatrium (felon):
Treatment:
Subcuatneous panatrium (felon):

Treatment:
Paranychia and Hyponyhia

Treatment:
- Surgical:
The nail root should be exposed. Incision proximal to the corner of the involved nail. If the abscess extends around the nail base or lateral margin, the
base or margin should be excised for adequate drainage and removal of nonviable nail. The fingernail will regenerate from the nail bed.
Tendon panaritium (felon) or bacteria flexor tenosynovits

Treatment
- surgical
f) the incision is placed at the neutral midaxial line
g) End-on view of incision, the web extension of incision is not always necessary for exposure
h) Surgical maneuvers
i) Implantation of irrigating catheters and multiple postoperative instillations effectively control many infections
j) Closed irrigation of flexor sheath infection using two incisions and a small catheter
Articular panaritium (felon) or acute suppurative arthritis:

Treatment
- surgical wide arthrotomy and draining are used if joint surface is not damaged. Damaged surfaces need to be resected
Osteal panaritium (felon) or osteomyelitis:

Treatment .
- surgical wide incision and draining are used .
- Damaged surfaces need to be resected
U- phlegmon or horseshoe abcess:

Treatment:
 Incision for draining the abcess
Thenar and midpalmar space suppurative infectious

Treatment:
 Incision for draining of the abcess
166. Ingrown nail: etiology, pathology, clinical pictures, principles of treatment

Etiology:
 tight shoes
 flat-foot
 excessive weight distribution onto the thumb (neurologic disorders, etc.)
Pathology:
 introduction of the nail plate into the skin fold, which may lead to constant trauma and associated infection (fungi)
Principles of treatment:
 Medical therapy includes eradication of cause, proper nail care, and local antiseptics (they are not always effective).
 Surgery treatment
- surgery of ingrown nail using phenol application
- surgery is indicated if the conservative therapy fails. Types of surgical treatment
a) removal of the nail with necrotic tissues
b) removal of the nail with wage shape resection of skin folds at both sides
c) removal of the nail with wage shape resection of skin fold and resection of growth zone
167. Bite wounds of the hand: etiology, pathology, clinical pictures, principles of treatment
Etiology and pathology:
 Bites from carnivores – e.g. dogs, cats (small, sharp, incised wounds)
 Bites from herbivores – e.g. horses (severe tissue crushing),
 Accidentl bite wound of humans resulting from an attacker striking the victim’s incisor teeth with the knuckles.
Clinical picture:
 Radiological examination reveals parts of tooth within metacarparphalangeal joints.
Treatment:
 Open surgical exploration, excision of skin margins, irrigation of joints and antibiotic therapy.

168. Diabetic foot: Etiology, pathology
Etiology:
 Alteration of peripheral nerves, vessels, skin and soft tissue
Pathology:
 Changes of the bones, joints and purulent- necrotic processes at patients suffered by diabetes mellitus
169. Diabetic foot: types with characteristics

 Diabetic sensory neuropathy is characterized by
- weakness, burning sensation, muscle cramps, paraesthesias, etc. Loss of sensation predisposes a patient to overlooked skin trauma and development of
ulcers and even advanced infection.
- development of Charcot cubic foot. It is characterized by destruction of plantar metatarsal joints followed by excessive loading of several areas of the
foot by body weight
 Motor neuropathy
- leads to changes in the foot muscles leading to change of gait and appearance of areas of excessive pressure at the foot during walking. These changes
also predispose a patient to formation of calluses and ulcers at the foot.
 Autonomic neuropathy is caused by
- sympathetic denervation of vessels and dilation of arterio-venous shunts, depriving the cells of oxygen.
- The second event is a loss of sweating followed by dryness, calluses and cracks of the skin and development of ulcers and even advanced infection.
170. Diabetic foot: diagnosis and classification

Diagnosis:
 Clinical presentation
- In neuropathic foot: disproportion between lesions and absence of pain; plantar ulcer; deformities if foot and toes; loss of sense of touch, pain and
vibration; venous congestion; edema; warm dry feet etc
- In ischemic foot: painful lesion; black gangrene; slow venous filling; reduced reflexes and sensation, etc
 Laboratory and instrument investigation
- Common laboratory and instrumental investigation:CBC, urine analysis, blood chemistry, glucose level, glycemic profile, coagulogramm,
immunogramm, ECG, Echo–CG, Chest X-ray
- Assessment of extend of necrotic process:foot X-ray (two planes), CT of the foot and calf, culture and AB sensitivity
- Assessment of arterial involvement: Doppler US, duplex scanning, arteriography, transcutaneous partial oxygen pressure
- Assessment of peripheral neuropathy: investigation of pain, vibration, and temperature sensitivity, tendon reflexes
Classification:
 neuropathic infected form is associated with development of purulent and necrotic processes on the ground of diabetic neuropathy
 neuro-ischemic form is associated with development of purulent and necrotic processes on the ground of alteration of both nerves (diabetic
neuropathy), and major arteries (diabetic arteriopathy). Coexistence of two pathologic factors and surgical infection is associated with poor prognosis the
extremity to survive.
171. Diabetic foot: general principles of medical and surgical treatment

Medical treatment:
 Symptomatic: NSAID, Vitamins of B group, cease smoking
 Antibacterial: empirical (to cover G+, G-, and anaerobes) is followed by accurate administration according to results of antibacterial sensitivity test.
Parenteral route is preferred, duration is 2 to 3 weeks (at patients with deep necroses even if well drained)
 Andiaggregative (antiplatelet drags): “vessel due F” i.v., i.m., (glicosaminoglican containing agent reduces platelet aggregation); orally – ticlopidin,
dipyridamole, aspirin.
 Prostagandin based agents are used at critical ischemia – alprostadil, vasoprostane – vasodilating, angioprotective, rrheolytic, antiaggregative, and
fibrinlytic action
Surgical treatment: is based on Wagner’s classification, but the general principle of surgical treatment are-
 wide incision, adequate draining and excision of necrotic tissues to prevention of further spread of infection.
Purulent inflammation of Serous Cavities
172. Pleural effusion and empyema: definition and etiology, pathology, clinical picture
Definition:
Pleural effusion is the accumulation of non bacterial fluid in pleural cavity.
Pleural empyema is the suppurative inflammation of the parietal and visceral pleural that is associated with local changes and intoxication.
Etiology:
Pneumonia (56%), lung abscess, after surgery (thoracotomy, thoracentasis, etc), infected hemathorax, esophageal perforation, subdiaphragmal infection,
septicemia, trauma.
Pathology:
Clinical picture:
 Complaints: pains in the side of the chest, cough, a feeling of fullness or heaviness in the side, difficulty in breathing, being unable to inhale deeply,
dyspnea, a rise in body temperature (39-40˚C ) and weakness.
 Physical examination of the patient reveals pallor, dyspnea and uncomfortable position in bed – half-sitting or on the side which reduces the pain on
inhalation. Breathing rate increases to 20-25 and in extreme cases to 30-40 per min.
 Inspection of the chest reveals limitations in the braeathing excursion of the chest with the sick side impaired or even not taking part in the process.
When large amounts of fluid are accumulated in the pleural cavity, a swelling in the posterior lower parts of the chest is found and the intercostal spaces
are filled up.
 Palpation of the intercostal spaces causes some tenderness. Tactile fremitus on the affected side is reduced or is not determined at all.
 Percussion of the chest reveals dullness in the percussion note over the areas of accumulation.
 Auscultation reveals a marked decrease in breath sounds or their total absence over the areas of accumulation.
173. Pleural effusion and empyema: laboratory and instrumental diagnosis, medical and surgical treatment
Laboratory diagnosis: blood test shows leukocytosis, a shift of the leucocyte formula to the left and a high ESR.
Instrumental diagnosis: Plane chest radiograph, Ultrasound and CT examination is done to determine the presence of fluid in the pleural cavity.
Medical therapy: Antibiotics: B-lactam are used for 2-4 weeks, Emperical AB (fluorquinolone), infusion therapy, detoxication therapy, mucolytics,
improvement of ventilation.
Surgical treatment: Chest drainage using thoracentesis, video assisted thoracoscopy (lysis of adhesion), thoracostomy and decortications, persistent
bronchopleural fistulas may be closed by muscle flap followed by obliteration of a cavity.
174. Bacterial pericarditis: definition and etiology, pathology, clinical picture

Definition: Pericarditis is an acute or chronic inflammation of the membranous sac (pericardium) surrounding the heart.
Etiology: idiopathic causes, viral infection, malignancy, uremia, collagen vascular diseases (SLE, RA, etc)
Pathology: inflammation →secretion of fluid (effusion) and cells → resolution or progress to fibrous thickening without or with constriction (obliteration
of the pericardial space and calcification is followed by constrictive pericarditis)
Clinical picture: Commonly develops during the course of severe systemic infection, Signs of acute illness with general signs (fever, malaise, etc) maybe
attribute to the underlying disease. Chest pain (retrosternal with irradiation to the shoulder). Vital signs change (dyspnea, tachycardia, etc). Respiratory
examination: pericardial friction rub is possible, maybe signs of underlying disorder.
175. Bacterial pericarditis: laboratory and instrumental diagnosis, medical and surgical treatment
Laboratory diagnosis: inflammatory changes (leukocytosis shift to the left, ESR increse)
Instrumental diagnosis: ESG, EchoCG, CT show abnormal amount of fluid in the pericardial sac.
Treatment: Surgical drainage of the pericardium, pericadioectomy is reserved for those who failed to improve or deteriorate, appropriate antibacterial
therapy and treatment of the main disorder.
176. Peritonitis: definition and etiology

Definition: This is the inflammation of the parietal and visceral peritoneal layers accompanied by local changes and intoxication.
Etiology:
a) Penetrating or blunt abdominal trauma with injury to intraabdominal organs (hollow)
b) Inflammatory disease s of intraabdominal organs such as acute appendicitis, cholecystitis, pancreatitis, tumor necrosis, incarcerated hernia, etc which
may be complicated by secondary peritonitis.
c) Perforation of hollow intraabdominal organs (perforated duodenal or stomach ulcer, perforated diverticulitis):
- Volvulus and bowel obstruction, diseases of female genital organs (inflammatory process in uterus, adnexitis or salpingo oophoritis)
- Intestinal ischemia due to thrombosis of mesenterial vessels and some other disorders.
177. Peritonitis: pathology and classification

Pathology:
 Invasion of bacteria → inflammation (exudation of fluid) → hypovolemia (third space dequestration, vomiting, paralytic ileus) and electrolyte
disbalance → peripheral vasoconstriction → poor perfusion → lactic acidosis → microcirculatory disorders → SIRS and MODS
 Intoxication is caused by absorption of necrotic materials and bacterial toxins.
Classification:
I. According to etiology
II. According to stage (initial or reactive, intermediate or toxic and terminal or MOD)
III. According to extend (local, diffuse, total)
178. Peritonitis: clinical picture, laboratory and instrumental diagnosis

Obtained clinical data may vary depending on the stage (initial, intermediate, and terminal) and extend (local, diffuse, total) of the peritonitis.
 Complaints: abdominal pain of different localization, high body temperature, vomiting.
 History (of trauma, progression of signs, etc)
 Physical examination: signs of hypovolemia
 Inspection: dryness of mouth, presence of any scar, hernia, wound, etc, thoracic breathing.
 Auscultation: absence of sounds (paralytic ileus)
 Palpation: tenderness and muscle guarding, rebound tenderness.
 Percussion: Mendel’s sign is possible.

 Rectal / vaginal examination (tenderness)
Laboratory diagnosis:
 Blood analysis: eosinophilic leukocytosis, ESR increase
 Stool examination: present of parasites.
 Laboratory changes characteristics to severe inflammation
 Plane abdominal (chest) X-ray
 US, MRI, CT may detect free abdominal fluid.
 Invasive tools: culdocentesis, paracentesis, diagnostic peritoneal lavage (DPL) and video assisted laparoscopy may be done at difficult diagnostic
cases.
179. Peritonitis: medical and surgical treatment

 Medical: antibiotics against G- and anaerobe microbs, correction of hypovolemia by infusion therapy, detoxication therapy, GIT decompression (NG),
oxygen supplementation, analgesia.
 Surgery:
 Correction of hypovolemia (shock) is required before surgery.
 Wide midline laparotomy

 Exploration of intraabdominal organs
 Cleaning of purulent materials
 Treatment of injured organ
 Draining of the peritoneal cavity
 Closure of the surgical wound
 Peritoneal lavage is done at the postoperative period.
Suppurative diseases of the Bones and Joints
180. Osteomyelitis: definition, etiology, classification, forms of acute osteomyelitis

Definition: Osteomyelitis represents nonspecific purulent-necrotic process with alteration of bone (osteitis), bone marrow (myelitis), periosteum
(periostitis), and surrounding tissues. The term was introduced by Reynauld at a1831
Etiology: Mycobacterium tuberculosis (acid-fast slow growing bacillus is spread by air-born infection)
Classification:
According to their etiology factors:
a) Nonspecific osteomyelitis
b) Specific osteomyelitis
According to the mode of infection (transmission)

a) Haematogenic
b) Non-hemaetogenic
i. Trauma
ii. Gunshot
iii. Contact
According to the clinical manifestation:

a) Haematogenic
i. Acute (toxic form, septicopyemia, localized form)
ii. Primary chronic
iii. Secondary chronic
b) Non-haematogenic
i. Acute
ii. Chronic
Forms of acute osteomyelitis:

i. Acute haematogenic osteomyelitis: toxic form, septicophyaemic form and localized form.
ii. Acute non-haemorrhagic form.
181. Primary-chronic osteomyelitis: pathology, clinical picture, diagnosis

Forms of primary chronic osteomyelitis:
 Brodie’s abscess
 Garre’s disease
 Ollier’s albuminous osteomyelitis
Pathology:
Clinical picture:
 Intermittent local pain, absence of sequesters and fistulas are the commonest signs for all the primary-chronic forms.
 Usually they result from pyogenic septicemia from which the patient has recovered, leaving the bone abscess which may remain dormant for years
(due to low virulent bacteria, good host defense, and exposure to antibiotics)
Diagnosis:
 Blood analysis: neutrophilic leukocytosis, ESR increase, disproteinemia
 Urinalysis: traces of protein, leukocytes and cylinders present in urine.
 Serology investigation: present of staphylococcal and gram negative strains microbs.
 Immunological investigation: slightly lowered titres of staphylococcal antitoxin and indices of immunobiological reactions such as complement titres,
phagocyte activity, leucocytes and T-lymphocytes.
 X-ray examination, CT scan, radiography: found bone sequester
 Fistulography: it gives evidence of the direction of the fistula tract, its connection with the bone cavity which is necessary in planning surgery.
182. Acute hematogenous osteomyelitis: etiology, pathogenesis, clinical presentation

Etiology: Endogenic suppurative infection gains access to bone via the bloodstream.
Pathogenesis: Infection spreads from the primary endogenous focus via the blood leading to embolism of the feeding the bone vessel. That form
commonly affects young teenage boys.
 First days of infection: general signs of infection are marked. Change of general condition, signs of intoxication.
 Local status: scarce data (localized pain over metaphysis, special maneuvers)
183. Acute hematogenous osteomyelitis: laboratory and instrumental diagnosis, medical and surgical treatment
 Laboratory changes are not specific.
 Blood culture has to be obtained (before antibacterial treatment if possible)
 At early stage an intraosseal pressure may be measured
Characteristic radiologic picture becomes obvious only 12-14 days after beginning of the disease (thickening of the periosteum, vague contour of the bone
morrow channel)
Medical and surgical treatment:

 Within first 48 hours the pus has not yet been loculated and an infection may be aborted by appropriate AB, splintage, and parallel infusion and
detoxication therapy.
 After that period the pus must be evacuated through a wide incision. Continuous irrigation of a former osteomyelitic area is done after surgery.
 Vacuum or long-term drainage with solutions of antiseptics conducted for at least 7-10 days and discontinued only when the suppuration has been
eliminated nd the patient’s condition has improved.
 Extensive trepanation of the bone in acute haematogenic osteomyelitis is not recommended since it creates the hazerd of generalized infection.
184. Acute posttraumatic osteomyelitis etiology, pathogenesis, clinical presentation, treatment

Etiology: Posttraumatic osteomyelitis results from traumatic bone fracture with subsequent local infections.
Pathogenesis:
Microorganisms introduced into bone as a direct result of trauma or by contiguous spread from injury to overlying soft tissue proliferate in the presence of
devitalized or traumatized soft tissues containing clotted blood, necrotic bone, and dead space. In addition, biofilm formation and slime production help
bacteria resist host defense mechanisms and establish infection. The likelihood of developing infection following an open fracture is increased if the
inoculum of microorganisms is high, if the fracture remains unstable, or if host defenses are impaired because of diabetes, peripheral vascular disease, or
immune suppression.
 First days of infection: general signs of infection are marked. Change of general condition, signs of intoxication.
 Local status: scarce data (localized pain over metaphysis, special maneuvers)
185. Chronic osteomyelitis etiology, pathogenesis, clinical presentation

Etiology:
 Natural outcome of non-treated acute osteomyelitis
 Inadequate surgical treatment of acute osteomyelitis
 Inadequate antibacterial treatment of acute osteomyelitis
Pathogenesis:
Chronic osteomyelitis may result from any form of acute osteomyelitis. It is accompanied by necrosis of segment of the bone (sequester), suppuration,
and purulent fistula formation. Sometime it is complicated by pathologic fracture.
It is comprises of two phases: relapse and remission.
 Relapse of disease occurs when active pathogenic strains attack again and the body is weakened by disease, exposure to radiation, injury and other
factors, reactivation of the chronic process of osteomyelitis occurs. Patient’s general condition is deteriorated. Patient complains of general malaise,
weakness, headache, rise in body temperature, sweating, chills, pain in the limbs, and purulent fistula opens up. Skin over the focus of osteomyelitis
becomes hyperemic, intensive pain and indurations of the soft tissue occur followed by the fluctuation sign.
 Under the effect of antimicrobial therapy or as a result of spontaneous healing of the active process, the whole condition may resolve and the phase of
remission sets in. Patient’s condition may improved in this phase.
186. Chronic osteomyelitis laboratory and instrumental diagnosis, medical and surgical treatment
 Blood analysis: neutrophilic leukocytosis, ESR increase, disproteinemia
 Urinalysis: traces of protein, leukocytes and cylinders present in urine.
 Serology investigation: present of staphylococcal and gram negative strains microbs.
 Immunological investigation: slightly lowered titres of staphylococcal antitoxin and indices of immunobiological reactions such as complement titres,
phagocyte activity, leucocytes and T-lymphocytes.
 X-ray examination, CT scan, radiography: found bone sequester
 Fistulography: it gives evidence of the direction of the fistula tract, its connection with the bone cavity which is necessary in planning surgery.
Surgical treatment:
 Necrectomy is done to eliminate the chronic focus of infection in the bone and its surrounding tissues. The sequestrum is removed, all osteomyelitic
cavities are incised and liquidated together with their internal wall granulations and detritus and all purulent fistulas are excised.
 Then sanitation (long-term methods of washing and drainage as well as vacuum drainage using different antiseptic solutions such as antibiotics,
dioxidin, soluble furagin and sodium hypochloride) and plasty of the bone cavity is done (achieved by using muscle pedicle flaps, bone plates,
chondroplasty and cutaneous flaps).
Medical treatment:
1. Antibiotic therapy
2. Immunotherapy
3. Local physiotherapeutic measures: ultrasound therapy, electrophoresis with drug preparation.
Fluid management is initiated during the post operative period: blood transfusion, protein blood substitutes, electrolyte solutions, correction of metabolic
disorders, and immobilization of the limb followed by exercise therapy to improve the functions of locomotive system.
187. Acute suppurative arthritis: etiology, pathogenesis, clinical presentation, treatment

Etiology: staphylococcus infection
Pathogenesis:
1. Serous arthritis represents inflammation in the synovial bursa and accompanied by collection of effusion in the joint.
2. Contamination of effusion results in joint empyema.

3. Further progress of infection onto the joint surfaces, joint’s capsula, and ligaments leads to panarthritis
4. If an inflammation extends onto the bone epypheses and methaphyses the condition is named osteoarthritis.
 Sudden onset, severe pain and limitations in joint movement, tension, induration and hyperemia of the integument as well as a change in the joint size
and shape.
 In complicated cases local signs of phlegmon are encounter. General clinical symptoms include the presence of suppurative intoxication: high body
temperature, weakness, malaise, chills, sweating, depression, progressive anemia etc.
Treatment:
Treatment of acute suppurative arthritis combines both local and general therapeutic measures.
 Local measures include:
a. Puncture of the joint with aspiration of its content, irrigation or washing of the joint cavity with antiseptic followed by infusion of antibiotics. It is done
daily till the accumulation of inflammatory exudates into the joint has stopped.
b. Immobilization of the joint using POP slab or therapeutic splint.
c. Physiotherapy: high-frequency therapy, quartz irradiation, electrophoresis with trypsin and antibiotics.
d. After the inflammation has subsided the patient is prescribed exercise therapy, massage and other manipulations to restore the joint functions.
 General therapeutics measure include antibiotic therapy tailored to the results of microbiological investigations, immunotherapy, blood transfusion,
plasma, protein blood substitutes, detoxication therapy, rational nutrition rich in protein and vitamins.
 Surgical treatment involves arthrotomy, which is indicated only where the puncture and aspiration, local and general antibiotics therapy prove
unsuccessful. During arthrotomy the joint cavity is cleared of all the purulent effusion and fibrinous deposit whereupon a drainage tube is places for long-
term washing sanitation. Paraarticular phlegmon has to be incised and drained followed by subsequent treatment along the standard lines.
Tetanus, Gas Gangrene, Necrotizing Fasciitis
188. Tetanus: epidemiology, etiology, pathogenesis, clinical picture

Epidemiology n etiology: Cl. Tetani is widespread in manure n soil.
Pathogenesis:
 m/o enter the body thru wounds-traumatic, umbilical stump(sometimes cryptogenic). Bacteria multiplies n produces powerful toxins(tetanospasmin n
tetano lysin)
 The exotoxin (tetanospasmin) produced in the inoculation site inhibits the cholinesterases at the motor endplates, resulting in an excess acetylcholine
locally n therefore a sustained state of tonic muscle spasm. The exotoxin also travel along the nerves thru CNS n causes extreme hyperexcitability of
motor neurons in anterior horm cells, thereby evoking explosive n widespread reflex spasms of muscle in response to sensory stimuli.
 Once fixed in the nerve tissue, the toxin no longer can be neutralized by antitoxin.
Clinical picture:
 Dysphagia, jaw stiffness, severe pain in neck, back and abdomen precede the tonic muscle spasm.
 Sardonic smile of tetanus (risus sardonicus) and trismus.
 Respiration n swallowing become progressively more difficult, reflex convulsions occur affecting all muscles n causing great pain.
 Opisthotonus – spasm of the extensors of the neck, back and legs to form backward curvature which may lead to muscle rupture.
 Temp is elevated, pulse is rapid, respiratory failure, and death during a cyanotic attack will usually follow if no treatment done.
189. Tetanus: diagnosis, treatment, prophylaxis

Diagnosis: Mostly based on characteristic clinical picture. see ques 188
Treatment:
 Isolation
 Airway control –endotracheal tube or tracheostomy
 Nasogastric tube passed to feed patient
 Spasm control –Diazepam, Benzdiazepam
 Immunizations of a patient- Human antitetanus globulin(eg:Humotet) I.M. 250-500U plus tetanus toxoid(tetanus vaccine) I.M.
 Wound toilet
 Antibiotics(penicillin or metronidazole)
Prophylaxis:
 Patient who have undergone previous active immunization within 5 years of time of injury require no further prophylaxis
 Patient with tetanus-prone wound who hv received their most recent booster injection more than 5 years before injured shud be administered a booster
dose of toxoid.
 Patient with non-tetanus-prone wound who hv received their most recent booster injection more than 10 years before injured shud be administered a
booster dose of toxoid.
 Patient who have not undergone prior immunization or without history of immunization shud be given 250-500 units of human antitatenus globulin at
one site n initial immunizing dose of toxoid administered at another site.
 Appropriate wound care(esp tetanus-prone wound)
190. Clostridial myonecrosis: epidemiology, etiology, pathogenesis, clinical picture

Epidemiology:
 Widely found in nature-soil n faeces

 Disease relevant to military n traumatic surgery, colorectal operations n anaerobic wound with necrotic or foreign material
 20-80% traumatic wounds contaminated w spores but gas gangrene remain rare w only 0.32%
Etiology: Cl. Perfringens, Cl.novyi, Cl.histolyticum, Cl.fallax, Cl.septicum, Cl.sordelli
Pathogenesis: The clostridia produce numerous toxins leading to clinical manifestations
Clinical picture:
Local features:
 Common clinical setting is a traumatic injury or postoperative wound after GIT surgery
 Sedden onset severe wound pain w rapid progress of signs
 Wound is under tension n between sutures the pouting edges exude a brownish n foul-smelling fluid
 Skin discolouration n bullae formation
 Crepitus –due to subcutaneous emphysema
General signs:
 Signs of intoxifications (raised pulse, diaphoresis)
 Pale skin colour
 Mental changes: anxiety, extremely alert followed by delirium or finally coma
 Change of body temp
 Systemic complications w circulatory collapse (drop of ABP), intravascular hemolysis followed by acute renal failure.
191. Clostridial myonecrosis: diagnosis, treatment, prophylaxis

Diagnosis:
- Characteristics of clinical findings
- Gram stain with specific bacteris n absence of WBC
- CT, plane X-ray (gas)
- Characteristics of tissues changes during surgery – pale or darkened cooked appearance (myconecrosis)
Treatment:
 Surgery -exposure of all muscles gp by long incisions, debridement n excision of all involved muscles, irrigation n wound draining. - Daily
reoperations.
 Medical therapy – antibacterial therapy (penicillin or clindamycin n metronidazole) –infusion detoxifications therapy. –hyperbaric oxygen. –use of
antiserum
Prophylaxis:
 All traumatic wound should be irrigated, n debrided of all dirt, foreign bodies n devitalized tissues followed by wound draining. Delayed closure is
preferred.
 Antibiotics prophylaxis necessary for biliary n colonic surgery as well as peripheral vascular diseases, contaminated traumas m gunshot wounds
 Correction of tissue perfusion
192. Necrotizing fasciitis epidemiology, etiology, pathogenesis, clinical picture

Epidemiology: Synergistic rapidly progressive bacterial infections spreading along fascial planes which is not caused by clostridia
Etiology: Mixed pattern of microorganisms: coliforms, staphylococci, Bacteroides spp. Anaerobis streptococci, pepto-streptococci.
Pathogenesis: Infections spread along fascial planes leading to vascular thrombosis n necrosis of involved tissues.
Clinical picture:
 Severe wound pain
 Signs of spreading inflammations –skin maybe normal, with crepitus, smell n discharge
 General signs of infection – tachycardia. Fever
193. Necrotizing fasciitis diagnosis, treatment, prophylaxis

Diagnosis:
 Presence of clinical pictures
 Initial wound small size
 Gram stain reveals multiple m/o
Treatment:
 Surgery – wide excision n laying open of affected tissues. Debridement must be extensive. Daily debridement necessary at post-operative period.
Patient who survive need barge areas of skin grafting.
 Medical therapy – wide-spectrum aitibiotic therapy (clindamycin plus aminoglycosides in high doses), aggressive circulatory supports, correction of
immune deficits (diabetes)
Prophylaxis: none
Tuberculosis of Bones and Joints
194. etiology of tuberculosis of bones and joints

Etiology: Mycobacterium tuberculosis (acid fast slow growing bacillus is spread by air-born infection)
195. 195) Pathology of tuberculosis of bones and joints

Pathogenesis: Primary focus→blood→synovial membrane (5%) or intraarticular bone of the hip (20%),knee (15-20%) or spine (40%)→destruction of
articular cartilage n adjacent bone.
196. clinical picture of spine, hip and knee tb

 systemic effect of the disease
 primary focus
 diseased joint(sweeling,wasting)
197. diagnosis of tuberculosis of bones and joints

 TB anamnesis
 Physical signs obtained during local examinations include: effusion(superficial joints), tenderness, position of ease, local colour n temp, movements
 Lab tests(ESR, Ley, RBC, Mountoux test)
 Instrumental investigation (chest X-ray, bone X-ray, arthroscopy(needle biopsy), arthrotomy with biopsy n histological examination)
 Bacteriology
 Differentiate w rheumatoid n infective arthritis, hemarthrosis, osteomyelitis.
198. treatment of tuberculosis of bones and joints

 Diet
 Medications- antiTB agents
 Triple therapy administered orally for at least 2-3 months(Rifampicin 600mg, Isoniszid 300mg, Pyrazinamide 1500-2000mg) followed by 6 months of
double therapy(Rifampicin 600mg n Isoniazid 300mg)
199. etiology and clinical features of cutaneous anthrax

Etiology:
 Bacillus Antracis is a gram positive aerobic rod very resistant to environment n antiseptics.
 It is an occupational disease of farmers n wool workers
Clinical features:
 Cutaneous form is common – called malignant pustula. The itching papule with induration is at the beginning. It suppurates n replaced by a black
slough. A browny, congested area of induration dev around site of infection
 Signs of toxemia – fever, malaise, vomiting
 Systemic infection may lead to septic shock
 Differentiate pustula with furuncle
200. Diagnosis and treatment of anthrax

Diagnosis: Smear n culture
Treatment: Penicillin G 2mln every 4 hours i.v
201. Etiology of actinomycosis

Etiology: Actinomyces is rarely gram positive branching filamentous microorganisms.
202. clinical picture of faciocervical, thoracic, and abdominal actinomycosis

Faciocervical:
 Commonly starts from carious tooth of lower jaw.
 Gums become indurated
 Nodules appear which soften n burst
 Overlying skin of face n neck becomes indurated n bluish in colour (ma reach bones)
 Forming abscess is caused by secondary infections, it burst thru the skin n sinuses follow
 Pain is uncommon
Thoracic:
 Lung n pleura maybe infected by aspiration of fungi or caused by spread fr the neck or diaphragm
 At advanced stage, chest wall(ribs) is involved forming multiple sinuses
 Pleural empyema is common
Abdominal:
 Ileocecal region usually affected
 Usual manifestations 3 weeks after appendectomy when the mass is palpable n soon wound begin to discharge forming sinuses
 Finally secondary fistula may dev
 Further spread might affect pelvic bones n vertebrae
203. diagnosis and treatment of actinomycosis

Diagnosis:
 Smear of pus with specific microorganisms.
 Laboratory signs of infections (leucocytosis and anemia are common)
Treatment:
 Penicillin G 10-20 mln daily during 2-4 weeks
 Surgery is done acc to common rules. Abscess must be incised n drained. Sometimes resections of involved organ (part of colon, lung) may be needed.
Case History
204. Case history assessment of subjective information

 Case history is a detailed account of the facts affecting the development or condition of a person or group under treatment or study, especially in
medicine, psychiatry, or psychology.
 In assessment of subjective information, we need to get the chief complaints, history of present disease (anamnesis morbi) and past health history
(anamnesis vitae).
 In chief complains, the detailed evaluation of basic complaints should be done thoroughly reflecting character, localization, irradiation, provoking and
relief factors, etc the additional complaints are examined briefly.
 The history of present disease is written as a story describing the development of complaints and signs of a disease. When was the first onset of
symptoms (commonly a pain), how the signs had developed, and according to patient’s opinion, what was the possible causes.
 In health history, childhood and youth diseases, information about past operations, drugs history, used of alcohol and tobacco, allergy history, family
history, hereditary disease, previous blood transfusions and gynecologic anamnesis if the patient is woman should be collected.
205. case history general inspection and system investigation

In general inspection, certain information are collected. They are general condition of the patient, consciousness, appearance of the patient according to
age, examination of the skin and mucus, nails, subcutaneous tissue, lymphatic, muscular system, joints and bones, examination of the neck mostly thyroid
gland with description of basic characteristics.
In system investigation, respiratory system, cardiovascular system, gastrointestinal system, genitourinary system, nervous system and locomotor system
are revealing. In every system, inspection, palpation, percussion and auscultation should be done. Note the abnormalities and the sounds.
206. case history assessment of the local status

Local status is described most thoroughly in case history. It described the body system which involved into the pathologic process. Check all the signs
using inspection, palpation, percussion and auscultation. For example, if a patient has hernia or appendicitis (which are referred to GIT system), the local
status is the GIT. So, GI system must be described at this section. Description of affected system is completely omitted at the examination of body
system.
207. case history laboratory examination at the diagnosis of surgical conditions.

Several tests are done to reveal the pathology. They are:
 Blood type, RH
 Blood for RW, AIDS, HBA

 Complete blood test (WBC, RBC, ESR)
 Blood chemistry
 Glucose level
 Urine analysis
 Stool analysis
 Sputum analysis
 Bleeding time, PT, aPPT, INR, platelet count, fibrinogen, D-dimer level, INR are used for evaluation of coagulation system
 Blood culture
 Culture of exudates with bacteriologic examination and assessment of sensitivity to antibiotics
 Biopsy (puncture, needle or excision biopsy)
208. case history instrumental examination at the diagnosis of surgical conditions

In instrumental examination, invasive and non-invasive methods are used. This including:
 X-ray examination (plane radiography or contrast series, for eg gastroscopy, barium enema, Cyctography, fistulography, etc)
 Angiography (arterio-, phlebo, -lymphography)
 Ultrasound examination
 Hand-held Doppeler, duplex scaning, colour mapping
 Endoscopic examination
 Perfusion scan, scintigraphy
 CT
 MRI
 Laparo-, thoracoscopy, diagnostic peritoneal lavage
 Laparocentesis, pericardiocentesis and other types of puncture
Arterial insufficiency
209. pathphysiology of acute and chronic arterial ischemia
(a) Chronic: It results from the gradual alteration of blood flow in artery leading to chronic impairment of organ perfusion (extremity).
1) Artherosclerosis:
Condition in which lumen of artery filled with fatty deposits(plague).symptoms occur only when a stenosis is higher than 60% of the arterial lumen.
Rough texture of plague causes platelets to clump together. Clot may form n reduce or interrupt blood supply to that area
2) Buergers disease:
Inflammation of the blood vessel associated with clot formation and fibrosis of the blood vessel wall. It affects primarily small arteries and veins of legs.
3)Raynaulds disease
Frequent at young female. Periodic constriction of the arteries that supply extremities. It is normally secondary to sclerodermia, lupus erythematosis,
rheumatoid arthritis, osteochondrosis, etc
4)Diabetes mellitus
Primarily affects nervous system (neuropathy). Arterial involvement is a common reason for gangrene of the limb
(b) Acute: It results from the sudden arrest of the blood flow in an otherwise normal artery leading to impairment of organ perfusion (extremity). It may
be caused by the following:
Thrombus-representing stationary clot tar suddenly forms on the surface of a changed vessel
Thromboembolus- clot traveling within blood stream till it reaches a vessel which size is to small to permit further passage of thromboembolus
Embolus- which is a moving mass (clot, particles of a solid or gas matter)traveling within blood stream.
When a thrombus forms an embolus reaches a blood vessel that is too small to permit its further passage, partial or total occlusion of blood flow thru the
occurs.
Loss of function develops within 4-6 hours, irreversible changes of ischemic tissues may occurs in 10 hours, and therefore it is an emergency condition
requiring early diagnosis and treatment.
210. Subjective and objective examination arterial disturbances
Subjective and objective examination of a patient is done according to general rules: chief complaints, present and past medical history, general
inspection and system assessment. Local status of peripheral vascular system.
(a) Inspection of peripheral vascular system of extremities for evidence of arterial insufficiency
(b) Palpation of peripheral vascular system of lower n upper extremities to reveal absence of pulsation, temperatures, tenderness, measurement of arterial
blood pressure at the arms, pulse rate and etc
(c) Auscultation of peripheral arteries reveals murmurs, vascular bruits,(carotid, subclavian, abdominal aorta, iliac, femoral arteries) etc
211. Laboratory examination at patients with arterial disturbances
Laboratory: changes in WBC, RBC, and blood chemistry are not specific
Specific tests: -cholesterol level n B-lipoprotein for atherosclerotic patients
-glucose level for diabetic patients
- PTT, PT, bleeding n clotting time, INR, platelet count should be assessed at most patients with vascular pathology.
-INR. Commercial prothrombin time (PT) reagents vary in their response to warfarin induced decreases in clotting factors. INR serves as reference point
to be able to compare results fm different labs
212. Instrumental examination at patients with arterial disturbances

(a)ECG to reveal cardiac abnormalities (exercise ECG with treadmill is more valuable)
(b)Hand held Doppler ultrasound :beam is sent to artery(blindly to anatomic location and projection of the vessel onto the skin).the reflected beam is
picked up by the receiver. Reflection of the beam by moving cells changes the frequency in the reflected beam.that frequency change may be converted
into an audiosignal. Therefore it may be used to access systolic pressure in small arteries.
(c)Ankle/brachial index (ABI): ratio of the systolic pressure of the arm to the arm. N=1.0, values below o.9 indicate degree of arterial obstruction. Value
less than 0.3 suggest necrosis. In the calcified arteries (diabetes) the pressure may falsely high due to incompressibility of arteries. ABI can be used to
access difference in arterial blood pressure between segments of a limb thereby giving indication of site of stenosis.
(d)Duplex scanning: uses B mode ultrasound to provide image of vessels. (Because ability of different type of tissue to reflect ultrasound beam. Doppler
ultrasound is used to isonate the imaged vessel (blood flow , size, etc)disadvantages-maybe confusing in some areas to distinguish artery n vein. Triplex is
duplex scanner with color adding.
(e)Pletismography: access changes in volume of a limb. Air filled cuff or special gauge systems are applied on an extremity to detect changes in volume
of a limb. Air filled cuff or special gauge systems are applied on an extremity to detect changes at size. Less accurate
(f)Rheovasography: abilty of structures to pass the current thru tissues depending on their filling with blood. N index =1.0.
(g)Treadmill: assessment of walking distance at claudication
(h)Thermometry, capillaroscopy, angioscopy: may also be used but less useful.
(i)Arteriography: cannulation of an artery followed by injection of a radiopaque solution into the arterial tree using seldinger technique. Precise
information is provide by this technique. It pocesses a risk of hematoma, thrombosis, arterial dissection and anaphylactic complications
213. Reasons and pathophysiology of chronic arterial ischemia.
Chronic: It results from the gradual alteration of blood flow in artery leading to chronic impairment of organ perfusion (extremity).
1) Artherosclerosis:
Condition in which lumen of artery filled with fatty deposits(plague).symptoms occur only when a stenosis is higher than 60% of the arterial lumen.
Rough texture of plague causes platelets to clump together. Clot may form n reduce or interrupt blood supply to that area
2) Buergers disease:
Inflammation of the blood vessel associated with clot formation and fibrosis of the blood vessel wall. It affects primarily small arteries and veins of legs.
3)Raynaulds disease
Frequent at young female. Periodic constriction of the arteries that supply extremities. It is normally secondary to sclerodermia, lupus erythematosis,
rheumatoid arthritis, osteochondrosis, etc
4)Diabetes mellitus
Primarily affects nervous system (neuropathy). Arterial involvement is a common reason for gangrene of the limb
Etiology: 1) artherosclerosis
2) Raynaulds disease
3) buergers disease
4) Diabetes mellitus
214. Clinical presentation of chronic arterial ischemia
Cramp like feeling at low extremities during walking and relieved by standing still. This sort of pain named intermittent claudication. Walking distance
must be evaluated. One or both extremities maybe involved depending on level of arterial block. Pain commonly located at posterior calf, thigh buttocks
(lerish syndrome).
At more advanced stage rest pain may develop .it is severe pain during rest made worst by lying down or elevation of the foot. Occurs at more advanced
age. Pain is worse at night and be relieved by hanging of the foot out of bed
Last stage of chronic arterial insufficiency is ulceration of the lower extremities and gangrene.
215. Classification of chronic arterial ischemia.

1st stage: asymptomatic stage(numbness and paresthesias)
2nd: intermittent claudication
3rd: critical ischemia (presence of rest pain, pregangrene state)
4th: gangrene
216. Diagnosis of chronic arterial ischemia
History of present disease: gradual onset and progression of symptoms (decrease of walking distance) maybe traced
Past health history: risk factor maybe found; smoking, hypodynamic, inherent predisposition, previous examination or treatment, etc
Objective examination: evidence of smoking; changes in lungs, clubbing of fingers maybe found, obesity, etc
Inspection: compare both legs for discolouration .location and and condition of dry gangrene with poor granulations have to be described, hair absence
and muscle wasting noted.
Palpation: temperature, movements are usually not effected, hyperesthesia only at severely ischemic extremity. Pulsation is assessed, compared maybe
localized aortoiliac, iliac, femoropoplitieal and distal obstruction. Diminution or absence of pulse. Venous refilling time (not more than 3sec)
Auscultation: For arterial bruits (most arteries should be isonated-femoral, abdominalaorta, supraclavicular, carotid, mesenteric, renal.
TECHNIQUE OF FUNCTIONAL TEST REVILING ARTERIAL ISCHEMIA

1) Ratshove’s maneuver
 Patient at supine position, bents his legs at knee and hip joint under 45°
 Patient is ask to flex and extend his ankle joints
 If patient has arterial insufficiency of low extremities a pain starts at the calf muscles during very 1st min of exercise
2) Samuel’s maneuver
 Same as Ratshov’s maneuver
 But if patients has severe arterial insufficiency of low extremities the skin of the foot become pale after 3-5 sec
3) Capillary refilling time / venous filling time / phenomenon of “pale spot”
 Patient at supine position
 By the index finger, doctor presses the nails / skin of examined toe
 Once the pressure has been released “a pale spot” disappear within 1-3 sec
 If patient has arterial insufficiency of low extremities the refilling times last longer than 5-10 sec
4) Oppel’s sign
 A purple discoloration of the foot skin develop after elevation of low extremities
5) Panchenko’s phenomenon
 A patients sits crossing one legs over the knee joints of another legs
 Appearance of numbness and paresthesia at the foot and tips of toes followed by the pain at the calf muscle suggest impairments of arterial blood
circulation
6) Alexaev’s maneuver
 Measurement of skin temperature at the space between 1st and 2nd toes is done using electrothermometer
 After that the patient is asks to walk a distance enough to produce pain at the calf muscle (intermittent claudication)
 After physical exertion a temperature of healthy person ↑ whereas the temperature of ischemic extremities falls approximately at 1-2°C
217. medical and surgical treatment of chronic arterial ischemia
(a)Medical therapy: risk factor modification

Exercise therapy
Antiplatelet therapy
Medical therapy at targeted symptoms
Modification of risk factors: smoking cessation, diabetes control, dyslipidemia management, hypertension control(bp <130/85mmhg)
Vasodilators (verapamil, isoxsuprine, cinnarizine, xanthinol nicotinate, cyclandelate)
Antiplatelet therapy(aspirin,clopidogrel, piridomole, vesseldue)
Treatment of claudication(pentoxiphylline,cilostazol,alprostan)
(b)Surgical treatment: revascularizatioin procedures

PTBA(precutaneous transluminal balloon angioplasty): catheter with inflateable balloon is inserted into lumen of an artery and inflated at the narrow
area.most effective for short stenosis,esp at iliac artery.
Intraluminal stent may be placed after ballon dilation.laser evaporation of the plague may be accomplished.
Artherosclerotic narrowing of aortic bifurcation. Aortobifemoral graft to bypass stenosis. It is used to by pass obstructed area. Human umbilical vein
graft. Politetrafluorethylene graft, Dacron bifurcation graft.
Endarectomy and angioplasty(evacuation of the plague thru an arteriotomy). Occlusive diseases below the popliteal artery regarded as unconstructive.
Microvascular surgery maybe done bypass the tibial vessel. Amputation is the last procedure at inoperable patient with 3-4 stage of disease.
218. reasons and pathophysiology of acute arterial ischemia
It results from the sudden arrest of the blood flow in an otherwise normal artery leading to impairment of organ perfusion (extremity). It may be caused
by the following:
Thrombus-representing stationary clot tar suddenly forms on the surface of a changed vessel
Thromboembolus- clot traveling within blood stream till it reaches a vessel which size is to small to permit further passage of thromboembolus
Embolus- which is a moving mass (clot, particles of a solid or gas matter)traveling within blood stream.
When a thrombus forms an embolus reaches a blood vessel that is too small to permit its further passage, partial or total occlusion of blood flow thru the
occurs.
Loss of function develops within 4-6 hours, irreversible changes of ischemic tissues may occurs in 10 hours, and therefore it is an emergency condition
requiring early diagnosis and treatment.
Etiology:
mitral stenosis, myocardial, endocarditis, aneurysms, arrhythias, artherosclerosis, complete disruption of an artery, arterial ligation ,tourniquet application
219. clinical presentation of acute arterial ischemia
Complaints: according to stage of ischemia

Classification (fontain’s): 1st stage- numbness and paresthesia, pain unbearable
2nd stage- paresis, paralysis
3rd stage- superficial muscle compartment edema, deep muscle compartment edema, total muscle compartment edema
4th stage- gangrene
220. Classification of acute arterial ischemia
Classification (fontain’s): 1st stage- numbness and paresthesia, pain unbearable

2nd stage- paresis, paralysis

3rd stage- superficial muscle compartment edema, deep muscle compartment edema, total muscle compartment edema
4th stage- gangrene
221. Diagnosis of acute arterial ischemia
History of present complaints (anamnesis morbi): onset of symptom is sudden, without any signs of low extremities disease (claudication)
Past medical history: search of source of embolus (heart abnormalities, arrhythmias, artificial valve, etc)
Objective examination:may be found some evidence of heart pathology(changes in heart sounds, arrhythmias, clubbing etc)
Local status: a) inspection- both legs are compared for signs of discolouration or gangrene.absence of hair, muscle condition(wasting) noticed ,commonly
not changed in acute process
b)palpation- affected part is usually cold, movements are affected depending of the stage,change of sensation (fm 2nd stage), inability to move toes or full
extremity. Palpation is commonly painful, muscle compartment edema is presented as muscle stiffness (fm 3rd stage).pulsation is assessed, compared, may
be localized obstruction(according to localization of embolus).venous refilling time is prolonged
c) auscultation- for arterial bruits (usually absent because blocked artery was normal before embolization)
TECHNIQUE OF FUNCTIONAL TEST REVILING ARTERIAL ISCHEMIA

a. Ratshove’s maneuver
i. Patient at supine position, bents his legs at knee and hip joint under 45°
ii. Patient is ask to flex and extend his ankle joints
iii. If patient has arterial insufficiency of low extremities a pain starts at the calf muscles during very 1st min of exercise
b. Samuel’s maneuver
i. Same as Ratshov’s maneuver
ii. But if patients has severe arterial insufficiency of low extremities the skin of the foot become pale after 3-5 sec
c. Capillary refilling time / venous filling time / phenomenon of “pale spot”
i. Patient at supine position
ii. By the index finger, doctor presses the nails / skin of examined toe
iii. Once the pressure has been released “a pale spot” disappear within 1-3 sec
iv. If patient has arterial insufficiency of low extremities the refilling times last longer than 5-10 sec
d. Oppel’s sign
i. A purple discoloration of the foot skin develop after elevation of low extremities
e. Panchenko’s phenomenon
i. A patients sits crossing one legs over the knee joints of another legs
ii. Appearance of numbness and paresthesia at the foot and tips of toes followed by the pain at the calf muscle suggest impairments of arterial blood
circulation
f. Alexaev’s maneuver
i. Measurement of skin temperature at the space between 1st and 2nd toes is done using electrothermometer
ii. After that the patient is asks to walk a distance enough to produce pain at the calf muscle (intermittent claudication)
iii. After physical exertion a temperature of healthy person ↑ whereas the temperature of ischemic extremities falls approximately at 1-2°C
222. medical and surgical treatment of acute arterial ischemia

Medical
heparin i.v 10.000IE(to limit propagation of the thrombus)
Vasodilating drug (papaverin 4ml)
Narcotic analgesics (promedol 2ml)
Dimedrol 2ml (antihistamine drug) to accelerate anesthetic effect. Give parele to infusion therapy.
Intraarterial thrombolysis- if ischemia not severe and time available. Urokinase or tPA streptokinase, Tpa (thrombolytic agents) infused via
catheter .streptokinase 5.000U per hour , usually during 48 hrs(effect assessed by arteriography)
Surgery considered if medical treatment not effective

Intraarterial thrombolysis andembolectomy done at 1st to 2nd stage of acute ischemia. due to irreversible changes of tissue after 3rd stage, restoration of
blood flow is contraindicated(may lead to dev of renal failure caused by products of tissue degradation).Therefore amputation is the only option done at
3rd-4th stage if acute ischemia.
Venous and Lymphatic Insufficiency

223. etiology of venous blood flow disturbances
Etiology of primary varicose veins:-

-pregnancy
-obesity
-inherent predisposition
-excessive physical exertions
-occupation(long periods of standing)
Etiology and pathology of a secondary varicose veins:-the cause is a DVT

After DVT the deep veins are blocked by the thrombus interfering with normal blood outflow.
Etiology of Superficial thrombophlebitis

- thrombophlebitis (varicothrombophlebitis);
- thrombophlebitis migrants (as a systemic manifestation of the malignant process anywhere at the body);
- polycitemia;
- Burger's disease;
- thrombophlebitis after vein cannulation
Etiology of DVT
1) Damage to the venous wall (e.g. inflammation, trauma, pelvic surgery, central lines)
2) Change (decrease) in flow due to immobility (surgery, neurologic patients), local pressure (cast).
3) Blood hypercoagulability (e.g. malignancy, protein C deficiency, protein S deficiency, antithrombin deficiency, pregnancy/postpartum, surgical
operation)
Etiology of Chronic venous insufficiency

may be caused by two major reasons: varicose disease which is responsible for development of primary varicose veins, and postthrombotic (PTS)
syndrome which is responsible for development of secondary varicose veins. The rule which one should always remember is that varicose disease is
commonly characterized be excessive varicose of superficial veins and few trophic changes, whereas a distinctive features of PTS are the extensive
trophic changes and only moderate varicose of superficial veins.
224. pathophysiology of venous insufficiency
Acute venous insufficiency is caused by 2 reasons:

A deep vein thrombosis (DVT) / thrombophlebitis (deep)
B. thrombophlebitis of superficial vein (superficial)
 Thrombophlebitis represents condition in which the venous lumen is blocked by thrombus formed due to some reasons.
o So it may be considered as a complication of another disease.
o Two types of thrombophlebitis are recognized: superficial and deep (depending on affected venous system) ones.
o Thrombophlebitis is different of phlebothrombosis.
o The first one is usually accompanied by prominent clinical picture of inflammation and rarely complicated by thromboembolism
Chronic venous insufficiency may be caused by two major reasons:

o varicose disease which is responsible for development of primary varicose veins The rule which one should always remember is that varicose disease
is commonly characterized be excessive varicose of superficial veins and few trophic changes
o postthrombotic (PTS) syndrome which is responsible for development of secondary varicose veins, a distinctive features of PTS are the extensive
trophic changes and only moderate varicose of superficial veins.
225. subjective and objective examination of patients with venous disturbances
Refer to “THE FEATURES OF EXAMINATION OF SURGICAL PATIENT”

Page29-34
226. Classification of varicose veins and chronic venous insufficiency
Degrees of chronic venous insufficiency:

1st degree: transient limb edema and presence of superficial varicose veins.
2nd degree: constant edema, presence of superficial varicose veins, evidence of trophic changes (hyperpigmentation, lipodermatosclerosis).
3rd degree: all aforementioned plus acute trophic ulcer.
Varicose Veins: primary (essential) and secondary (varicose form of postthrombophlebitic syndrome [PTPS])
227. Laboratory and instrumental examination at patients with venous disturbances
Special diagnostic tools:-

Laboratory-changes in WBC, RBC, blood chemistry are commonly not specific
More specific….PTT, PT, bleeding and clotting time, INR, platelet count-should not be assessed at most patients with vascular pathology.
Instrumental:-
Hand-held Doppler US
-characteristic sound (waveforms) like a soft wind sound(above large veins-cava iliac, femoral, popliteal) phasic to respiration. Above small veins due to
low speed of low blood flow the signal sometimes is difficult to pick up. So the low speed of blood flow may be increased by special maneuvers: distal or
proximal compression of the muscles to squeeze out the blood.
Antithrombitic Agents:-
Anticoagulant:delay/prevent clot formation and extension (heparin, coumadin)
Antiplatelets drugs:interfere with platelet activity(ASA)
Thrombolytic agents plasmonogen activators) dissolve existing thrombi (Tpa,streptokinase)
DUS
1)May be avaluated the patency of the veins (the blood flow is registered)and conclusions about the level of venous conclusions about level of venous
blockage (thrombosis)can be made;
2)presence of venous reflux (the blood is at opposite side to normal one,in normal circumstances the blood reflux is absent or no longer than( 0.5second)
can be found,thereby ythe conclusion about condition of venous valves can be made.
Dupplex Scanning:_
A duplex scanner uses B-mode US to provide an image of vessels (because of ability of different tissues to reflect the US beam. A second type of US
beam(Doppler US)is than used to onsonate the image vessels(detailed information about BF and size…)
Triplex diagnosis of the venous thrombosis

is based on detecting an incompressibility of the vein and absence of the blood flow in it. Duplex scanning is almost the best investigation technique; it is
not invasive but highly investigator-dependent (experience of the doctor).
Pletismography
A probe is attached to the skin to assess venous filling of the surface venules by measuring light transmission of the skin (photopletismography). The
filling of these vessels reflects the pressure in the superficial veins of the legs. In patients with venous incompetence the veins fill by venous reflux giving
fast refilling times. Air pletismography assesses the changes in volume of a limb (the amount of the blood at the skin). Air filled cuff (air
pletismography) or rubber measuring strip (strain gauge pletismography) are applied on an extremity to detect changes of the size. The principle of the
diagnosis is the following. Once a patient at the horizontal position, his veins are emptied, after that a patient is asked to assume upright posture. In
normal circumstances the changes in the extremity's volume are minimal. If the valves of the low extremity are insufficient the blood flows back
(downwards, blood reflux) with stagnation, so the changes in the extremity's volume are more prompt and pronounced. But, there is some difficulties if
the deep or superficial venous system are responsible for blood reflux.
Phlebography (venography):
injection of a radiopaque solution into the venous tree (is used in investigation of the deep venous system). Two techniques are used:
a) ascending, when the contrast is injected via the catheter into the medial plantar vein. The tourniquet should be above the ankle to compress the
superficial veins preventing the contrast to enter superficial venous system. Technique is used to reveal the parts of stenosis or occlusion of the deep veins
by tracking the flow of the radiopaque agent upward through main venous conduits. Localization of the stenosis or obstruction are noticed
b) descending, when the contrast is injected via the catheter placed into the femoral vein. Than a patient is asked to fulfil the Valsalva's test to trigger the
venous reflux. The extend and intensity of the venous reflux are noticed. Most precise information is obtained with venography, but it is invasive,
possesses the risk of hematoma, infection, thrombosis, anaphylaxis. Venography is especially useful planning intervention on the deep veins at patients
with PTS and if the Duplex scan fails to solve all diagnostic questions.
Venous pressure measurement. It is always higher if a patient has pooling of venous blood at low extremities due to some diseases of venous system. It is
rarely used, invasive, and more important for scientific investigations
228. Etiology and pathogenesis of varicose disease

Pathogenesis:
It is due to the valve incompetent and leads to venous stasis, congestion, edema and thrombosis. It is also abnormally dilated, tortuous, elongated veins
produced by increased intraluminal pressure and by loss of support of vessels wall.
Etiology of primary varicose veins:-

-pregnancy
-obesity
-inherent predisposition
-excessive physical exertions
-occupation(long periods of standing)
Etiology and pathology of a secondary varicose veins:-the cause is a DVT

After DVT the deep veins are blocked by the thrombus interfering with normal blood outflow.
229. varicose disease: Clinical presentation, laboratory and instrumental diagnostic methods
Complaints: tiredness, aching, tingling, edema (usually unilateral, appears at the end of the day), night cramps. (almost always the symptoms are
alleviated by the night rest), and unpleasantly appearing varicose veins.
At the most advanced stage the trophic ulcer may develop (very rare).
Local status (peripheral VS):

a) inspection: both low extremities in upright position are examined. Picture depends on the stage of condition. May be present only moderately dilated
tortures veins of the medial aspect of the thigh or calf (if the GSV is involved, 85% of cases) or at the posterior aspect of the calf only (if the LSV is
involved, 15% of cases). At advanced cases dilation of veins is more prominent, edema may be present (pitching), calf and thigh may be affected, skin is
not changed above varicositis. Later the changes of the skin are obvious (hyperpigmentation at the medial aspect of the low third of the calf), and at most
advanced cases in rare situations a patient is presented with trophic ulcer at the characteristic location (at the area of the hyperpigmentation with poor
granulation, and superficial round shape.
b) palpation: veins are compressible, usually painless. Cough impulse is + (the fingers are placed at the projection of the SFJ - 1,5 cm medially to femoral
pulsation, and a patient is asked to cough. The tips of fingers should feel the wave of blood reflux due to excessive abdominal pressure produced by
cough). The test reveals insufficiency of the SFJ. Also the palpation of the medial aspect of the calf is done to find fascial defects and insufficiency of the
perforators. Pulsation of arteries must be assessed in order not to overlook the pathology of arterial system (sometime the complaints are confused with
intermittent claudication). Special tests include (Trendelenburg 's, etc.).
Special diagnostic facilities

Laboratory: as usually, are commonly normal.
Instrumental: Duplex scanning or hand-held Doppler ultrasound are usually enough to plan surgery (extend of the reflux), venography is rarely used, only
for ambivocal cases.
230. varicose disease: medical and surgical treatment
- Avoid severe physical exertions to lower limbs

- Cool showers, swimming, elevation of the extremity
- Elastic compressive stockings or bandages;
- Venotonic drugs - detralex;
Least invasive treatment results in best cosmetic results but only possible at the early stages of disease.
- Microsclerotherapy
- Sclerotherapy
- Radiofrequency endovenous obliteration
- Laser endovenous obliteration
Sclerotherapy
Injection of a sclerosing agent (polidocanol, sodium tetradecilsulphate, etc.) into the vein leads to sclerosis of the vein.
Surgical Treatment of superficial varicose - Stages

 Crossectomy (flash ligation of the SFJ with all tributaries).
 Stripping (removal) of the stem of the GSV (or LSV) and ligation of all tributary veins
 Stab avulsion is used for varicose changed branches
 Ligation of perforators (if present)
231. Superficial thrombophlebitis etiology and pathogenesis clinical presentation, diagnostic methods and treatment.
Clinical Picture
Varicothrombophlebitis is a nonmicrobial inflammation.
Complaints: usually sudden onset with development of pain, hyperemia, and moderate swelling at the previously painless varicose veins. Subfebrile
temperature is common.
At patients with Burger's disease or malignant process the veins are not changed by varicose process, but inflammed.
Present ant past medical history: usually a patient has long history of varicose disease; risk factors may be found.
General inspection and system assessment: Is commonly without features. May be found signs of malignancy (if thrombophlebitis is caused by
neoplasm) or arterial ischemia (at patients with Burger's disease).
Local status:
Inspection: presence of varicose veins, hyperemia of the skin above them, moderate swelling, other signs of varicose disease are possible (skin kolor
change, etc.);
Palpation: tenderness above thrombosed varicose veins, they are incompressible and not deflated at horizontal position. The level of thrombosis is
difficult to predict clinically, approximately extends till the level of tenderness.
Special diagnostic facilities:

Laboratory: signs of inflammation are possible, changes are not diagnostic.
Instrumental: Duplex or Doppler US to establish the level, localization, and extend of thrombosis (veins are not compressible and blood flow is not
registered).
Treatment:
If the superficiall thrombophlebitis is at the level of midthigh there is a high risk of progression of thrombosis upwards and extension to the deep veins
and possible dislodgment which is followed by pulmonary embolism. Surgery is necessary to prevent further propagation of the thrombus and usually it is
limited by SFJ ligation (crossectomy).
Medical treatment
 The patient is bedridden with legs elevated to reduce edema and possibility of thromboembolism.
 Elastic bandages or stockingsare used.
 Direct anticoagulant – conventional heparin (5 000 IU administered 6 times a day subcutaneously or i.v. constantly;
or low molecular weight heparin (LMWH) - fraxiparin, enoxaparin, etc. two times daily subcutaneously. PTT has to be increased to 2 times higher of
original; INR has to be increased till 2,5 – 3.
 Nonsteroidal antiinflammatory drugs (NSAID)- diclofenac, ibuprofen, etc.
 Spasmolytics – papaverine, etc.
 Enzymes – trypsin, haemotrypsin
 Application of heparin-containing ointment topically
 Local novocaine block – Mixture of heparin, prednisolon, enzyme, and novocaine.
232. Deep vein thrombosis: etiology and pathogenesis, clinical presentation
Etiology and pathogenesis

operation)
Clinical Presentation
Patient's complaints:
sudden unilateral swelling of low extremity (rarely a subclavian deep vein thrombosis may be present). Pain is dull, constant at the n/v bundle;
subfebrille temperature.
Present ant past medical history:
possible reason of DVT. Any causative factors like drug history, family history, previous surgery and infection may be found. If there is no any obvious
reason, the search should be oriented on possible malignancy (GIT, respiratory, etc.).
General inspection and system assessment
may reveal obesity, malignancy (if the last is a cause of DVT), etc.
Local status
inspection:
swelling (unilateral). The color of the skin is usually normal (pale at case of phlegmasia alba dolens and bluish at case of Phlegmasia cerulea dolens).
Superficial veins may be dilated due to collateral flow of the blood via superficial venous system. The level of the DVT can be suspected depending on
the extend of edema. Edema of all the extremity is characteristic to ilio-femoral DVT, whereas the edema of the calf suggests DVT at the calf veins.
palpation:
there is a hot skin (cold at Phlegmasia alba dolens) and tenderness at the posterior surface of the calf or/and medial aspect of the thigh (depends on an
extend of thrombosis). Pulsation of arteries is difficult to feel due to swelling.
Phlegmasia cerulea dolens as well as phlegmasia alba dolens are the possible complications of DVT with progress of symptoms, necroses of the skin,
arterial spasm, and sometime fatal outcome
Functional tests
Signs of deep venous thrombophlebitis
 1. Homan's sign. Dorsiflection of the foot by a doctor stresses the soleus muscle that compresses thrombosed veins of the examined low extremity
leading to pain at the posterior calf.
 2. Mozese's sign. Tenderness during palpation of the examined extremity at the projection of the neuro-vascular bundle at the posterior calf, medial
surface of the thigh, and groin region is present at the case of DVT. Localization of the pain is influenced by the level of DVT.
 3. Opit's sign. The inflatable cuff is placed at the thigh region. It is inflated reaching the sufficient pressure to compress deep veins, approximately till
100 mm of mercury. The arteries are not compressed. Pain suggests the DVT.
 4. Bischard's sign. Palpation of a neuro-vascular bundle behind a medial malleolus results in pain if the posterior tibial veins are thrombosed.
 5. Valsalva sign. A patient is asked to take and hold deep breath. Increased intraabdominal pressure extends to deep veins. Appearance of the pain
suggests the DVT.
233. Deep vein thrombosis: laboratory and instrumental diagnostic methods, treatment
a) laboratory: complete blood test, PTT, PT, INR, bleeding time, platelet count are to be assessed
b) instrumental:
 1) Hand-held Doppler ultrasound;
 3) Duplex scanning with color mapping of blood flow (triplex);
 5) Phlebography (venography);
Medical treatment
 The patient is bedridden with legs elevated to reduce edema and possibility of thromboembolism.
 Elastic bandages or stockings are used.
 Direct anticoagulant – conventional heparin (5 000 IU administered 6 times a day subcutaneously or i.v. constantly;
or low molecular weight heparin (LMWH) - fraxiparin, enoxaparin, etc. two times daily subcutaneously. PTT has to be increased to 2 times higher of
original; INR has to be increased till 2,5 – 3.
 Nonsteroidal antiinflammatory drugs (NSAID)- diclofenac, ibuprofen, etc.
 Spasmolytics – papaverine, etc.
 Enzymes – trypsin, haemotrypsin
 Application of heparin-containing ointment topically
234. Subclavian vein thrombosis: etiology and pathogenesis, clinical presentation
Etiology and pathogenesis

operation)
Clinical presentation
Patient's complaints:
Sudden unilateral swelling of upper extremity (rarely a subclavian deep vein thrombosis may be present). Pain is dull, constant at the n/v bundle;
subfebrille temperature.
Present ant past medical history:
possible reason of DVT. Any causative factors like drug history, family history, previous surgery and infection may be found. If there is no any obvious
reason, the search should be oriented on possible malignancy (GIT, respiratory, etc.).
General inspection and system assessment
may reveal obesity, malignancy (if the last is a cause of DVT), etc.
Local status
inspection:
Swelling (unilateral). The color of the skin is usually normal. Superficial veins may be dilated due to collateral flow of the blood via superficial venous
system. Edema on the shoulder and neck area.
palpation:
There is a hot skin and tenderness. Pulsation of arteries is difficult to feel due to swelling.
235. Lymphatic insufficiency: etiology and pathogenesis, classification
Classification
Congenital (primary)
 Hypoplasia
 Aplasia
Acquired (secondary)
 Trauma or surgical removal of lymphatics
 Repeated acute infections
 Chronic infections: elephantiasis, erysipelas, fungy, Tbc, etc.
 Advanced malignant disease
236. Lymphatic insufficiency: clinical presentation, diagnostic methods, treatment

Clinical presentation
 Stage 1
o Bouts of fever accompanied by pain, headache, malaise
o Lymph node tend to be hard and tender
o Lymphatic vessels are tender and show erythema along their course
o Lymphaitis extend from proximal to distal limb segment
o Inflammation of spermatic cord and axillary lymph node → lymphangitis
o Simultaneously, ulticaria-like rash with pruritis
o
 Stage 2
o Temporary edema becomes more persistent and regional lymph node are enlarged
o Progressive enlargement, coarsening, corrugation and fissuring of the skin and subcutaneous tissue with warty superficial excrescences develop
gradually, causing irreversible “elephantiasis” with vascular rupture
o chyluria and chylous effusion
 Stage 3
o Elephantiasis of the lower limb and scrotum and occasionally upper limb, breast and vulva
Diagnosis: clinical data, history of disease - may find long anamnesis, gradual onset, family history (congenital), etc.
Invasive diagnostic tools:

Lymphography: Obstructive lymphedema of the right leg following radiotherapy and hysterectomy for carcinoma of the cervix
Treatment
 Medical:
- change of lifestyle: elevation of the extremity, elastic compressive stockings or bandages;
- etiologic treatment (antibiotics for infections, antiparasitic drags for filariasis, etc.)
- lymphotonic drags: detralex, etc.
 Surgical:
- 1st group: lympho-venous anastomoses (nastamosing of lymphatics with veins);
- 2nd group: removal of pathologically changed subcutaneous tissue;
General Trauma
237. Soft tissue contusion: reason, clinical presentation, treatment
Contusion of soft tissues is characterized by pain, edema, and bruising as a result of laceration of small vessels of the skin and subcutaneous tissue.
Trauma to underlying structures must be presumed requiring further investigation. Neurologic or vascular abnormalities may arise as a result of trauma
leading to motor or sensitivity dysfunction.
A closed blunt injury may result in a bruise or contusion. There is bleeding into the tissue and visible discoloration.where the amount of bleeding is
sufficient to create a localized collection in the tissues, this is described as a haematoma.
Initially, this will be fluid, but it will clot within minutes or hours. Later, after a few days, the haematoma will again liquefy. There is a danger of
secondary infection.
The patient should be advised that the time required for bruising to clear is extremely variable, and in some individuals, discoloration may persist for
months.
A haematoma should be evacuated by open surgery if it is large or causing pressure effects (such as intracranial). Alternatively, it can be aspirated by a
large-bore needle if it is smaller or in a cosmetically sensitive site. It maybe necessary to wait for several days until the haematoma has liquefied and to
perform repeated aspirations.
Appropriate antiseptic precaution must always be used. A haematoma will generally be reabsorbed without scarring but there maybe persistent tethering
of the skin.
238. Crush-syndrome: etiopathogenesis, clinical picture, diagnosis and treatment
It is a condition caused by prolonged compression and crashing of soft tissue (mainly muscles) resulting in characteristic local and general pathologic
changes in the body developing during and after release of compression.
Pathogenesis:
Compressionacute arterial ischemia (compression of arteries, pain is followed by angiospasm, hypovolemia)
Release of compressionreperfusion injury (edema of muscle compartments, compartment syndrome and ischemic muscle necrosis)
resorption of toxins from necrotic tissuesendotoxicosismultiple organ failure
Clinical pictures and diagnosis
(1) Early Period

(a)General:
signs of traumatic shock with characteristic hemodynamic changes

(b)Local:
Initially the skin is worm, PA on arteries is present. Further an edema increases, skin necroses appear and signs of compartment syndrome develop (acute
arterial ischemia)
(2) Second Period

Is characterized by signs of ARF and poliorganic failure characteristic clinical and laboratory picture with progress of fluid-electrolyte disorders and
intoxication
Local changes are less important and characterized by edema and local septic complications
(3) Late Period

It is accompanied by necrosis and sequestration of dead muscles, purulent complications, muscles and joint constructures.
Treatment
- elastic bandaging (to decrease postischemic edema)

- aggressive antishock and detoxication therapy
- treatment of ARF, anemia, hypoproteinemia, etc
- early surgery is indicated at case pf steadily progressing edema and development of life-threatening ARF
- without aforementioned indications a surgical procedure is done only after demarcation of necrotiozed tissue
- early surgery: fasciotomy, is done to decompress compartment pressure
- postoperative wound is managed according to common rules of untidy wound care preventing accumulation of necrotic tissue, etc
- external fixation is useful if patient has coexisting fracture
239. Ligament sprain and rapture: etiology, clinical picture, diagnosis and treatment
-ligament is broken into two.

Clinical picture
is the same but accompanied by. Pain provoked by movements in the joint, localized tenderness. Joint’s instability found during local examination Bone
percussion is painless. Local swelling and bruising are common.
Treatment: first 24-48 hours- ice or chemical cold pack elevation, elastic bandage, after two days heat may be used, NSAID, no weight bearing,
removable splint or light cast, progressive active exercises after healing. Immobilization is necessary. Suture is done only at some type of rupture
(arthroscopic suture of the cruciate ligament of the knee)
240. tendon and muscles disruption: etiology, clinical picture, diagnosis and treatment.
Retraction of ends (muscle contraction). Because of the gap the healing does not occur leading to impaired function. The active movements are lost,
passive movements may be painful. Localized tenderness.
Rapture of the insertion of the quadriceps muscle into the patella
241. Joints dislocation: definition, clinical picture, diagnosis treatment
Dislocation is a complete displacement of the joint ends of bones in relation to each other; it will be noted that partial dislocation may also occur.
Clicking sound when the dislocation has occurred. Pain and tenderness, edema and bruising, hemarthrosis, loss of normal joint shape. The joint area looks
like the hollow. The extremity may be shortened and loses its normal axis.
-Closed joint reduction. Commonly reduction is done under i.v sedation. Local anaesthesia is done into joints cavity (20 ml 1% lidocaine). Always assess
neurovascular status.
-Shoulder joint dislocation. Matson’s method is shown using two wrapped sheets. Tractions and contratraction are applied over a period of several
minutes, which should reduce the dislocation with a click. After reduction a shoulder immobilizer is necessary at position of internal rotation and
adduction. X-ray confirms reduction.
-The arm hangs free off the table with appropriate weights (approximately 5kg) attached at the wrist (Stimon’s method). Usually it takes 20-30 minutes to
achieve reduction. Dzhanelidze’s method uses force produced by doctors weight.
Motais and Kocher’s methods of shoulder reduction
-Kocher’s method of reduction of dislocated hip. An assistant stands on the side and steadies the pelvis. Traction is applied in the line of the femur.
Reduction is achieved with a clunk and is confirmed by radiology.
-Closed reduction of a radial head. The physician holds the patients injured hand ia a hand-shake position.
IMMOBILIZATION AFTER REDUCTION OF DISLOCATION

POSITIONING USED TO IMMOBILIZE A BODY PART
-Ankle/foot: 90° angle between foot and leg. Neutral eversion/inversion.

-Knee: 15-20° flexion
-Shoulder: resting at the side of the body
-Elbow: 90° angle between forearm and arm. Neutral pronation/suppination.
-Wrist: Neutral pronation/suppination, 20-30° wrist extension
-Thimb: wrist position as above. Thumb in 45° abduction, 30° flexion
-Metacarpals, MCP joint, proximal phalanges: wrist position as above, MCP joint in 90° flexion, DIP and PIP joints in a full extension
-IP joints middle/distal phalanx: full extension at IP joints.
-Splint padding is done to entire area to be splinted. Evenly, circular fashion at least 2 layers with extra over bony prominences.
-Fiberglass (prefabricated splints can be measured and cut)/ plaster (10-15 layers): generally immobilize one joint above and one joint below injury.
-The splint is applied to the soft roll (after water dippening). Hold the bandage in desired position until splint hardens (5-10 min with fiberglass, 10-15
min with plaster)
-Posterior elbow splint (above) and sugar tong forearm and wrist injuries. Note: the splint reaches the level of MCP joints.
-Commercial sling. The elbow is fixed at 90° angle. With the arm resting across the chest the wrist is elevated higher than the elbow with the thumb
pointing upward.
-Ulnar gutter splint is used for 4th – 5ht metacarpal or phalanx injuries. Radial gutter splint is used for 2nd – 3rd metacarpal or fingers injuries.
-Long leg splint is used for knee and tibia injuries (it consist of two splints for additional stability)
-Ankle splint is used isolated ankle injuries (it consist of two splints).
242. Joints dislocation: diagnosis, methods and principles of treatment (similar as 242)
Clicking sound when the dislocation has occurred. Pain and tenderness, edema and bruising, hemarthrosis, loss of normal joint shape. The joint area looks
like the hollow. The extremity may be shortened and loses its normal axis.
-Closed joint reduction. Commonly reduction is done under i.v sedation. Local anaesthesia is done into joints cavity (20 ml 1% lidocaine). Always assess
neurovascular status.
-Shoulder joint dislocation. Matson’s method is shown using two wrapped sheets. Tractions and contratraction are applied over a period of several
minutes, which should reduce the dislocation with a click. After reduction a shoulder immobilizer is necessary at position of internal rotation and
adduction. X-ray confirms reduction.
-The arm hangs free off the table with appropriate weights (approximately 5kg) attached at the wrist (Stimon’s method). Usually it takes 20-30 minutes to
achieve reduction. Dzhanelidze’s method uses force produced by doctors weight.
Motais and Kocher’s methods of shoulder reduction
-Kocher’s method of reduction of dislocated hip. An assistant stands on the side and steadies the pelvis. Traction is applied in the line of the femur.
Reduction is achieved with a clunk and is confirmed by radiology.
-Closed reduction of a radial head. The physician holds the patients injured hand ia a hand-shake position.
IMMOBILIZATION AFTER REDUCTION OF DISLOCATION

POSITIONING USED TO IMMOBILIZE A BODY PART
-Ankle/foot: 90° angle between foot and leg. Neutral eversion/inversion.

-Knee: 15-20° flexion

-Shoulder: resting at the side of the body
-Elbow: 90° angle between forearm and arm. Neutral pronation/suppination.
-Wrist: Neutral pronation/suppination, 20-30° wrist extension
-Thimb: wrist position as above. Thumb in 45° abduction, 30° flexion
-Metacarpals, MCP joint, proximal phalanges: wrist position as above, MCP joint in 90° flexion, DIP and PIP joints in a full extension
-IP joints middle/distal phalanx: full extension at IP joints.
-Splint padding is done to entire area to be splinted. Evenly, circular fashion at least 2 layers with extra over bony prominences.
-Fiberglass (prefabricated splints can be measured and cut)/ plaster (10-15 layers): generally immobilize one joint above and one joint below injury.
-The splint is applied to the soft roll (after water dippening). Hold the bandage in desired position until splint hardens (5-10 min with fiberglass, 10-15
min with plaster)
-Posterior elbow splint (above) and sugar tong forearm and wrist injuries. Note: the splint reaches the level of MCP joints.
-Commercial sling. The elbow is fixed at 90° angle. With the arm resting across the chest the wrist is elevated higher than the elbow with the thumb
pointing upward.
-Ulnar gutter splint is used for 4th – 5ht metacarpal or phalanx injuries. Radial gutter splint is used for 2nd – 3rd metacarpal or fingers injuries.
-Long leg splint is used for knee and tibia injuries (it consist of two splints for additional stability)
-Ankle splint is used isolated ankle injuries (it consist of two splints).
243. Fractures: mechanism of injury, fracture healing
a) formation of hematoma
b) after 1 week osteoblast start to from as the clot retracts
c) after 3 weeks a procallus begins to form and stabilize the fracture
d) from 6 to 12 weeks a callus forms with bone cells
e) in 3 to 4 months osteoblast begin to remodel the fracture site
f) with normal apposition the bone will be completely remodeled in 12months.
244. Fractures: clinical presentation, diagnosis
Clinical signs:
- relative signs: local tenderness, swelling, and brusing deviation of extremity’s axis, disturbance of function of extremity
- Absolute signs: (pathognomonic) to fracture: exposure of the bone fragments or obvious protrusion of bone fragments under the intact skin, pathologic
mobility, bone crepitation, and radiologic signs of fracture.
- Fracture of extremity: peripheral blood circulation and nervous function must be examined (physical examination or using additional tools)
245. Fractures: classifications, general treatment of a patient
Classification:
(a) Congenital & attained
(b) Closed & opened (with injury of skin)
(c) Complete & incomplete (with injury of periosteum)
(d)According to the line of fractures: transverse, oblique (spiral), compression, comminuted, impacted
(e) According to the presence of displacement of parts of a bone: with displacement or without displacement
(f) diaphysial, epiphysial, metaphysical
(g) single & multiple
(h) ordinary & combined (associated with another type of trauma: burn, rupture of spleen etc)
(i) non-complicated and complicated (shock, injuries of internal organs, injuries of vessels & nerves, fatty embolism, osteomyelitis, sepsis)
General management:
General management
-ABC approach
-Correction of blood loss and shock (pelvic fracture may lead to approximately 2 L blood loss)
-Pain: splintage and analgesics
-Coexisting injuries are treated according to priority plane
-Tetanus toxoid and AB (for open fractures)
-Splintage is done at the scene of injury (to reduce pain and additional trauma due to displacement of bone fragment)
-Buck’s traction may be used for hip fractures until surgery is performed.
Scheme for fracture management (local management)
- Define fracture
- Detect complication
- Does the fracture need reduction?
- Is the fracture stable or unstable?
- How can the fracture be stabilized?
- Does the fracture need immobilization and for how long?
- How can the patient best be reached rehabilitated?
Possible method of fracture treatment

-protection alone
-immobilize with external splint without reduction

-closed reduction (manipulation or traction) followed by immobilization with external splint traction:
-open reduction and external fixation
-excision of fractured fragment and prosthetic replacement.
Treatment of open failure.
The aim of surgery is convert open fracture to closed one. Tetanus toxoid and AB are considered. Wound irrigation. An open fracture of the tibia at the
initial operation.
Dissection and excision of tissue as well as lavage with copious of fluid (by a jet lavage system). Surgery is finished by closure of wound.
Distal superficial femoral artery traumatized at the site of fracture of the diatl third of the femur. Blood supply is restored parallel to open reduction of
fracture.
Restoration of bone integrity (methods of fracture reduction)
-Gravity methods: collar and cuff, “hanging cast”

-Closed manipulation
-Traction (fixed or sliding)
-Operation
Fracture reduction using
-Gravity reduction U-slab with collar and cuff sling.

-Fracture reduction using skeletal and skin traction (fixed or sliding)
Methods of stabilization of fractures (immobilization of the fracture)
-External splint: a) plaster of paris or plastic cast, b) external fixation

-Internal splint (screws, plate, nail)
-Continuous traction: a) “hanging cast”, b) fixed or sliding traction (skin or skeletal)
246. Fractures: types of fracture’s reduction
-Gravity reduction U-slab with collar and cuff sling.

-Fracture reduction using skeletal and skin traction (fixed or sliding)
247. Fractures: types of fracture’s stabilization
-External splint: a) plaster of paris or plastic cast, b) external fixation

-Internal splint (screws, plate, nail)
-Continuous traction: a) “hanging cast”, b) fixed or sliding traction (skin or skeletal)
248. Fractures: causes of delayed union, complications of fractures
Causes of delayed and nonunion of fractures

- Compound fractures
- Severe initial injury
- Infection
- Soft tissue interposition
- Poor blood supply
- Inadequate immobilization
- Osteoporosis
- Pathological fracture
- Distraction
- Nutritional disorders (malnutrition, vit D deficit)
- Metabolic disorders (uremia, hyperparathyroidism)
- Drugs (steroids, cytotoxic drugs)
Complications:
Local (nerve, arterial injury followed by acute arterial ischemia, acute compartment syndrome (edema of muscle compartment)
Early: skin necrosis, gas gangrene, DVT, infections, embolism
Late: joint stiffness, osteomylitis, pseudoarthrosis, deformed union.
Head, Thorax and Abdominal Trauma
249. classification of trauma patients according to urgency
Categories f injury :
1. Exigent
These are the most life-threatening conditions, requiring instantaneous intervention(e.g. complete airway obstruction)
2. Emergency
Those condition requiring immediate intervention over period of few minutes.
3. Urgent
Those condition requiring intervention within the 1st hour.(e.g fracture and dislocation)
4. Deferrable
Those condition that may or may not immediately apparent but will subsequently require treatment.(e.g.urethral disruption)
250. steps in initial resuscitation of trauma patients: airway patency and breathing
Airway :
1) removal of debris
2) chin lift or jaw thrust( to pull out the toungue forward)

-jaw thrust maneuver : 2 hands are placed on the mandibular rami and pushed anteriorly,
thus opening the airway.
-Chin-lift maneuver : The tip of fingers are placed beneath the patients chin and the jaw is
Lifted anteriorly while the mouth is open by drawing down on the
Lower lip with the thumb of the same hand.
3) Endotracheal or nasotracheal intubation is required at patients with severe head injury ,profound shock
4) Surgical Cricothyroidotomy : by needle cricothyroidotomy with jet insufflation to improve oxygenation
5) Tracheostomy
Breathing (ventilation):
If there is decrease respiratory drive or unstable chest wall an assisted ventilation is neccesary
Assisted ventilation may be done using Ambu Bag or with mechanical ventilator.
Common reason for ineffective ventilation after intubation :

o Malposition of endotracheal tube
o Pneumothorax
Example :Tension pnemothorax (depression of the chest by needle catheter 2nd ICS on midclavicular line must be done at seen of accident
o Hemothorax
251. steps in initial resuscitation of trauma patients: circulation maintenance
Possible control of bleeding preceeds :

o Placement of IV lines
Minimum 2 IV lines should be placed percutaneously or with venous cutdown
or with Internal jugular( Subclavian) vein cannulation.
o Compressive dressing
o Tourniquet
o Placement of pneumatic anti-shock garment (pelvic injury)
o Fluid resuscitation :
Begin with 1000ml bolus of Lactate Ringer. Response to therapy is monitored
by skin perfusion, urine output or CVP.
252. trauma patients: neurological assessment
A brief examination to determine :

a) Level of consciousness ( Glasgow Coma Scale)
b) Pupillary condition
Size ,equality, response to light must be checked
Example ; Dilation of pupil more than 1mm = severe brain injury
c) Movement of extremities ( paralysis)
Lateralised extremity weakness
253. trauma patients: definitive diagnosis, priority plane for further management
Definitive diagnosis : Reexamine the patient completely( diagnosing other injuries).

1. Examination is done in a head to toe manner.
o Shape of the skull (may indicate intracranial hemorrhage)
o Neck (injury of the spinal chord)
o Chest ( to reveal hemothorax,pnemothorax ,pericardial tamponade)
o Abdomen (intraabdominal haemorrhage)
o Extremities ( to reveal fracture)
2. Obtaining and collecting data from laboratory and radiologic test

3. Placement of additional lines,cathether( nasogastric and foley) and
monitoring device.
Priority plane for further management

When the patient is oxygenating , ventilating and perfusing adequately a priority plan should be established for subsequent treatment.
Example : In case of multiple trauma, we must treat the more life-threatening injuries (severe trauma, intracranial hematoma) to less threatening ( fracture
of toe )
254. mechanism of primary and secondary brain injury???
255. initial resuscitation of a patient sustained head injury
Initial resuscitation : 1) Airway patency ( Chinlift,jaw thurst,endotracheal intubation)

2) Breathing (Ambu bag or mechanical ventilator)
3) Circulation
(Stop bleeding by using tourniquet , compressive bandage,elevation
of the injured area and infusion therapy)
4) Assesment of CNS (neck must be secured with cervical collar)
Consists of examination of :
1) conciousness ( GCS )
2) lateralized weakness of upper and lower ext.
3) pupillary function(size ,equality,response to light)
256. neurological assessment of a patient sustained head injury
A brief examination to determine :

a) Level of consciousness ( Glasgow Coma Scale)
b) Pupillary condition
Size ,equality, response to light must be checked

Example ; Dilation of pupil more than 1mm = severe brain injury
c) Movement of extremities ( paralysis)
Lateralised extremity weakness
257. diagnosis of the brain injury, medical and surgical treatment
Diagnosis of brain injury:

Inspection :
 Bruising,
 scalp laceration with or without skull damage,
 open wound with exposed brain,
 depressed skull fracture,
 Blood or CSF in nose or ear
 Bruising around the eyes (Panda sign :bilateral periorbital hematoma in pt with a fracture of anterior cranial fossa)
 Bruising over the mastoid bone suggests a basilar skull fracture
 Observation of zygomatic arches and maxillary bones for evalution of degree of skull damage
Absolute clinical symptoms of facial bone damage :

 Depressions
 Deformaties
 Facial assymtery caused by bone displacement
 Parasthesia
 Numbness
 Restricted movement
 Deformaties of jaw
 Pathologic unusual increase in mobility
 Abnormal bite
Meningeal signs:
 Brudzinski’s sign : with patient in recumbent position, place hands behind patients head and flex the neck forward until the chin touches the chest if
possible. Note the resistance of pain. Watch also for flexion of patients hips and knees in reaction to maneuver. Pain in the neck and resistance to flexion
suggest subarachnoidal hemorrhage.
 Kernig’s sign : flex one of the patients legs at hip and knee and then straighten the knee. Note resistance of pain. Resistance to straightening the knee
and pain in the lower back and posterior thigh suggest subarachnoidal hemorrhage.
Instrumental investigation( definitive diagnosis)

 Craniography and cervical spine x-ray : skull and vertebral fractures
 CT scan or MRI : for pt with depressed skull fracture,neurologic focal signs and coma
 Echoencephalography
 Electroencephalography
 Reoencephalograpy
 Carotid angiography,lumbar puncture,skull trephination(emergency burr holes)
*lumbar puncture should be avoided as it causes ‘coning’ of brain stem
Medical treatment :
All measures oriented towards prevention of possible brain edema

o Diuretics (mannitol 1g per kg,IV)
o Hyperventilation
o Fowler’s position
o Maintainence of normal circulating volume
o Monitoring of intracranial pressure
o Steroids are not used
Surgical treatment :
 Placement of exploratory burr holes at the same side with dilated pupil or CT data
 Craniotomy : the cuts between burr holes are made using Gigli saw which is passed between
burrholes using the malleable saw guide.
 Creation of bone flap and evacuation of epidural hematoma after craniectomy
258. brain concussion: clinical picture, diagnosis, and treatment

Clinical picture:  Signs are resolved 3-5 days

 Regain consciousness completely after trauma ( GCS = 15 points )
 Loss of consciousness few seconds to few minutes Diagnosis :
 Drowsiness  Craniography : to exclude skull fracture
 Irritable and patient may not know where he is  CT scan : absence of any changes
 Dizziness
 Single vomiting Treatment:
 Diaphoresis  Monitoring
 Sleep disturbance  Bed rest(5-7 days)
 Headache  Sedative and antihistamine drugs
 Unsteady gait  Vasodilators
 Vital functions are not changed  Nootropic agents
 Neurological status : light horizontal nystagmus
259. brain contusion: clinical picture, diagnosis, and treatment
Clinical picture :
 Frequently associated with skull fracture and may be intracranial hemorrhage
 All signs of brain concussion ( refer to 258)
 Always accompanied by signs of areas involved ( Eg. Occipital region = disturbance of vision)
 Degrees of brain contusion :
a) mild degree:
o loss of consciousness up to 10 minutes
o retrograde and antegrade amnesia
o vomiting several times
o vital functions are not changed
o neurologic status lightly changed ( eg. Clonic nystagmus and meningeal sign)
o signs are resolved within 2-3 weeks
b) moderate degree:
o loss of consciousness 10 minutes to few hours
o pronounced retrograde and antegrade amnesia
o repeated vomiting
o temporary alteration of vital function( low BP,weak and rapid PR,shallow respiration,pale cold skin)
o neurologic status :more changes(nystagmus ,meningeal sign,muscle tone, focal symptoms, speech abnormalities)
o signs resolved within 3-5 weeks
c) severe degree :
o loss of consciousness several hours to several weeks
o alteration of vital function ( low BP, bradycardia, shallow arrhythmic respiration)
o marked hyperthermia
o neurologic status ; paresis of extremities
o subarachnoidal haemorrhage is common
o decorticate or decerebrate posturing,coma state prolonged
Diagnosis:
 Craniography : to reveal skull fracture
 CT scan : to reveal brusing of brain tissue and area of heterogenous high brain density
due to mass of fluid , clotted blood and distructed brain tissue
Treatment of mild diffuse brain injury :

o Bed rest
o Sedatives
o Antihistamine drugs
o Vasodilators
o Nootropic agents
o Monitoring
o Antibiotics for open trauma with CSF
260. skull fractures: classification and clinical picture??????????????????
Classification :??????????????????????
Focal brain injury
Brain compression due to ICH:
It results frm tearing of a meningeal vessel. Commonly associated with skull fracture. Enlarging ICH is characterized by life-threatening rise of clinical
signs of neurologic impairment. It may develop after some period of time after trauma or immediately after it.
Enlarging ICH must be suspected if during continuos monitoring a patient develops:

 Progressive decrease of GCS score by 3 or more points
 Presence of lateralized weakness
 Enlargement of one pupil (usually the largest pupil is at the side of ICH)
There are 2 types of intracranial hematomas: epidural and subdural
Pathology of intracranial hematoma:

Characteristic clinical pic is caused by the following pathologic changes:
1. Acute extradural hematoma. Impaction of opposite crus against the opposite rim of the tentorial opening.
2. displacement of the inner edge of the temporal lobe descending into the tentorial opening.
Diagnosis of ICH: CT or MRI
261. skull fractures: diagnosis and treatment depending on the type???
262. complications of head trauma
o infection complications (encephalitis, meningitis, brain abscess, etc)

o posttraumatic skull defects may require acrylic or titanic cranioplasty
o Hydrocephalus. If persist the ventriculoperitoneal shunt may be placed. Brain atrophy.
o CS fistula: otorrhoea, rhinorrhoea. In the majority of cases the leak will have stopped at 48 hrs.
o Psychologic dysfunction (dizziness, irritability, neck pain)
o Chronic ICH
o IC foreign bodies
o Epilepsy
o Vegetative dysfunction
o Curling’s ulcer with hematemesis
263. initial management of patients sustained severe thorax trauma
 Approach to severe chest trauma: A → B → C

 Complaints vary depending on type of injury. Dyspnea and chest pain are common.
 History of trauma and progress in patient’s condition
 Local status:
o inspection: skin injuries, bruising, shape of the chest, intercostals spaces, expansion, RR, etc.
o palpation: presence and site of tenderness, elasticity, and vocal resonance
o percussion: percussion note (dullness, resonance, hyperresonance, tympany), diaphragmatic excursion, etc.
o auscultation: breath sounds (crackles, wheezes, and rubs)
264. rib fracture: clinical picture, diagnosis and treatment
Clinical picture:
 Complaints: pain on inspiration
 Examination of the chest:
o sparing of the affected part during respiration.
o Signs of soft tissue damage are common
o Local tenderness, and occasionally crepitation and ecchymoses
o Rib fracture may be accompanied by damage into pleura, lung tissue, or other mediastinal organs by bone fragments.
o Crepitations (subcutaneous emphysema) felt by palpation of chest wall suggests injury to the pleura and lung
o Hemoptysis and lung bleeding are the evidence of lung tissue injury
Diagnosis :
Plane chest X-ray
Treatment:
Treatment of single rib fracture:
o Rest
o Analgesics
o IC nerve blocks can be done
o Ovoid restrictive dressing
265. flail chest: mechanism of development, clinical picture, diagnosis and treatment
Mechanism of development:
Unilateral fracture of four or more ribs ant and post or bilateral ant or costochondral fracture of 4 or 5 ribs will produce instability (paradoxical respiratory
motion of the chest segment). It results in severe hypoventilation.
Clinical picture :
 During inspiration, ribs retract on abdomen
 Paradoxical movement of chest segment
 Respiratory insufficiency
Diagnosis:
 Plane chest x-ray
Treatment:
 An assisted ventilation is necessary (several weeks)
 Serial intercostal rib blocks
 Open fixation is rarely done.( Eg. Internal fixation screw)
 At the scene of incident, endotracheal tube placement and assisted ventilation is started until ribs are restored
266. pneumothorax: etiology, pathophysiology, clinical picture
Etiology:
 Subpleural TB cavern or lung abscess
 Bullae rupture in emphysema, asthma
 Chest injury
 Iatrogenic pneumothorax
Definition ; collection of air in the pleural cavity
Pathophysiology :
Depends on the types of pneumothorax:

 Open penumothorax :
Air enters through opening in chest which have penetrated lungs during expiration and inspiration. Pressure in the pleural cavity and atmosphere are the
same
 Closed pneumothorax :
Air enters pleural cavity through opening in the lungs and then accumulates in the chest.
 Tension pnemothorax:
Layers of the thoracic wall form a valve so that air enters on inspiration but can not exit on expiration. Air pressure builds up and compresses the lung.
Clinical picture:
 Complaints: pain and dyspnea

 Physical examination: respiratory sys
o Inspection: high RR, unequal expansion, bulging of ICS
o Palpation: decreased or absent vocal fremitus
o Percussion: hyperresonant note. Displacement of the heart and arch of aorta towards the opposite side.
o Auscultation: absence of breath sounds
267. )pneumothorax: types, pathophysiology of different types
Types and Pathophysiology :
According to mechanism:
 Open penumothorax :
Persistent communication between the outside and the pleural space that allows outside air
to enter the pleural space,causing the lung to collapse.
Air enters through opening in chest which have penetrated lungs during expiration and inspiration. Pressure in the pleural cavity and atmosphere are the
same
 Closed pneumothorax :
Air enters pleural cavity through opening in the lungs and then accumulates in the chest.
The chest wall becomes airtight after penetration.
 Tension pnemothorax:
A check valve mechanism in a bronchoplueral fistula allows air to enter but not leave the pleural space, causing pressure in the space to rise above
atmospheric pressure.
According to etiology :
 Traumatic pnemothorax:
1. Penetrating chest wound, by a thoracocentesis needle, fractured rib or knife.
2. Ruptured bronchus or perforated oesophagus
3. Active TB or other infectious granuloma
4. Pulmonary barotraumas(patient on mechanical ventilator)
 Spontaneous pneumothorax(no antecedent trauma)

1. Primary :occurs in a previously healthy patient. Most occur without exertion or during diving.
2. Secondary :occurs in patients with extensive underlying pulmonary disease
 Induced pnemothorax:
Air may be used to replace fluid as a prelude to thoracoscopy or rarely for x-ray.
268. pneumothorax: diagnosis and treatment
Diagnosis :

o Palpation: decreased or absent vocal fremitus
o Percussion: hyperresonant note. Displacement of the heart and arch of aorta towards the opposite side.
o Auscultation: absence of breath sounds
 Instrumental: Plane AP chest x-ray: thin line visible caused by visceral pleura.No vessels are seen
beyond this line and the line is curved.
Treatment:
 Needle aspiration of the air from the pleural cavity (no continuous leak of air into the pleural cavity) is done after control of the sucking wound.
Aspiration is done by large syringe. Further chest X-ray is done.
 Continuous collection of pleural air requires placement of the chest tube (using ant tube thoracostomy)
 First-aid for open and tension pneumothorax:
Treatment of sucking chest wound. On inspiration, the dressing seals the wound, preventing the
entry of air; on expiration, trapped air is able to escape through the 152ntapped section of the dressing
269. hemothorax: etiology, pathophysiology, clinical picture
Definition : Collection of the blood in the pleural cavity
Etiology :
 Aortic aneurysm rupture
 Injury of chest and lung.
 Bleeding from thoracic wall (ICS) or adjacent thoracic organs.
 Surgical manipulations
 Diseases of lung and pleura (TB,tumour..etc)
Pathophysiology:
Hemothorax can be divided into:

 Mild : blood is only accumulated in the pleural sinus of pleural cavity
 Moderate: blood can reach the scapula angles
 Severe: pleural cavity full with blood
Owing to the anticoagulant properties the blood that has accumulated in the pleural cavity is not generally inclined to clotting except for the catastrophic
bleeding.
Clinical picture:
 Vital signs : universely changed
o Palpation: normal vocal fremitus
o Percussion: dull note over fluid. Displacement of the heart and arch of aorta towards the opposite side.
o Auscultation; absence of breath sound over fluid.
270. hemothorax: diagnosis and treatment
Diagnosis:
 Vital signs : universely changed

o Palpation: normal vocal fremitus
o Percussion: dull note over fluid. Displacement of the heart and arch of aorta towards the opposite side.
o Auscultation; absence of breath sound over fluid.
 Plane X-ray of chest.
 US, CT, MRI may detect free pleural fluid
 Invasive tools: thoracocentesis
Laboratory diagnosis : Signs of bleeding (anemia)
Treatment:
 Placement of the chest drain (evacuation of the blood).Stop of bleeding is indicated by low amount of blood drained and appearance of lung
expansion.
 Thoracotomy is done to control major bleeding
 For hemopneumothorax, may require placement of 1 or 2 chest tubes.
271. pneumohemothorax: etiology, pathophysiology, clinical picture
Etiology :
272. pneumohemothorax: diagnosis and treatment
273. penetrating chest injuries: initial management
Chest trauma may also be accompanied by damage to other mediastinal organs: aorta, diaphragm, etc
Lung contusion
 A multiple rib fracture is accompanied by some degree of lung contusion. Fluid and blood frm ruptured pulmonary vessels enter the alveoli and
produce localized airway obstruction.
 Physical examination has low value.
o Auscultation – diminished breath sounds, multiple crackles, or wheezing.
o Percussion – some degree of dullness.
 Chest radiograph: patchy consolidation in lungs.
Atelectasis of the whole lung is characterized by decrease of chest’s size, whole lung collapsed producing white X-ray shadow. Atelectasis may affect one
lobe, or even lung’s segment. Radiologic pic shows triangular white shadow with the apex oriented towards pulmonary root.
274. cardiac tamponade: etiology and pathophysiology, clinical picture, diagnosis, treatment
Etiology:
o Penetrating injury within the parasternal region.
Pathophysiology:
Cross section through the heart causes accumulation of blood in the pericardial sac. The accumulated blood will compress the heart. Filling of heart will
decrease, cardiac output and blood pressure decrease, CVP increase and dilated jugular vein due to high volume of blood in vena cava.
Clinical picture:
o Complaints: chast pain and dyspnea

o Signs (Beck’s triad): low arterial BP
o Inspection: dilation of jugular veins (rise of CVP)
o Palpation: weak and rapid pulse
o Percussion: Dilation of the heart dullness
o Auscultation: muffled heart sounds.
Diagnosis:
o Plane chest X-ray (increased round heart shape)

o US, CT, MRI may detect pericardial fluid
o Invasive tools: pericardiocentesis
Treatment:
o Pericardiocentesis is used with diagnostic aim and to relief the cardiac tamponade.
o Treatment may require emergency thoracotomy to control bleeding.
275. pathophysiology and anatomical features kidney trauma
Pathophysiology:
Anatomical features:
Types of renal trauma:

a) Subscapular hematoma
b) Laceration
c) Avulsion of one pole
d) Avulsion of vascular pedicle
276. kidney trauma: etiology, clinical picture, diagnosis, treatment
Etiology: o CT scan
 Blows or falls to the loin o Arteriography
 Crushing injury to the abdomen
Treatment:
Conservative approach is common:
Clinical picture: o Bed rest
o Local pain o Analgesics
o Bruising o Prophylactic antibiotics
o Tenderness o Monitoring patients conditions( vital signs)
o Hematuria
Surgery for expanding hematoma
Diagnosis: o Midline laparotomy
o Urine analysis o Nephrectomy
o IV urogram o Nephrostomy
o US
277. anatomical features and pathophysiology of intra- and extraperitoneal bladder rupture
a) Intraperitoneal rupture :
Anatomical features:
Intraperitoneal rupture of the bladder with intraperitoneal extravasation of urine.
Pathopysiology:
Contamination of abdominal cavity by urine and leads to development of peritonitis
b) Extrapertioneal rupture:
Anatomical feature:
Extrapertoneal rupture of the bladder with extraperitoneal extravasation of urine
Pathopysiology:
Rupture of bladder with escape of urine but not into the abdominal cavity.Thus no peritonitis
278. intraperitoneal rupture: etiology, clinical picture
Etiology:
Abdominal trauma (Fall, kick), surgery
Clinical picture:
 Complaints ;sudden hypogastric pain, absence of desire to micturate.Abdominal pain.high body temperature,vomiting.(signs of peritonitis are delayed)
 History of presenting complaints : history of trauma
 Physical examination: signs of hypovlemia(vital signs)
 Examination of GIT : Abdominal tenderness,rigidity followed by distension(signs of peritonitis
delayed)
Shifting dullness
Rectal examination: bulging
279. intraperitoneal bladder rupture: diagnosis, treatment
Diagnosis:
 Plane abdominal radiograph

 IV urography
 US,CTscan to find abdominal fluid
 Invasive tools
Treatment:
Surgical treatment stages:
 Low midline laparatomy
 Cleansing of the cavity
 Suturing of the rupture
 Placement of suprapubic and urethral catheters
 Wound suturing
280. extraperitoneal bladder rupture: etiology, clinical picture, diagnosis, treatment
Etiology:
 Pelvic fracture
Clinical picture:
 Pain
 Bruising
 Dullness above umbilical line( percussion)
 Rectal exam: too high position of prostate
Diagnosis:
 Plane radiograpy of pelvic bones: if significant displacementis present the chance is very high
 Ascending urethrogram
Treatment:
 Cystostomy: For posterior urethral disruption with healing in 8 months
 Percutaneous suprapubic cystostomy: for long term evacuation of urine
 Urethroplasty: If stricture has formed
281. etiology and mechanism of rupture of the urethra

Etiology:
 Pelvic fracture = for membranous urethra
 Blow to the perineum= for bulbar urethra
Mechanism:
282. rupture of the membranous urethra: etiology, clinical picture, diagnosis, treatment
Etiology:
 Pelvic rupture
Clinical picture:
 Pain
 Bruising
 Rectal exam: too high position of prostate
Diagnosis:
Treatment:
 Cystostomy: For posterior urethral disruption with healing in 8 months
 Percutaneous suprapubic cystostomy: for long term evacuation of urine
 Urethroplasty: If stricture has formed
283. rupture of the bulbar urethra: etiology, clinical picture, diagnosis, treatment
Etiology:
 Blow to the perineum
Clinical picture:
 Signs of retention of urine
 Perineal hematoma
 Bleeding from external urinary meatus

Diagnosis:
Treatment:
 Percutaneous suprapubic cystostomy
 Prophylactic antibiotic
 Surgical repair of the complete disruption of the urethra is done using urethroplasty
284. Blunt injuries of the parenchimal abdominal organ: etiology, clinical picture
Etiology:
 Spleen and liver injury
Clinical picture:
 Complaints: abdominal pain
 History of presenting complaints:necessary to obtain
 Inspection:thoracic pattern of bleeding,sign of changing posture
 Auscultation: decrease bowel sound(paralytic ileus)
 Palpation: tenderness and muscle guarding,rebound tenderness(moderate),Zegeser’s (phrenic) and Kehr’s signs are possible
 Percussion:Mendel sign is positive, shifting dullness due to large volume of fluid in the abdomen
 Rectal examination: blood at the retrovesical pouch
 Vital signs: universely changed due to bleeding
285. Blunt injuries of the parenchimal abdominal organ: laboratory and instrumental diagnosis
Signs of inflammation & hypovolemia
 Leukocytosis with shift to the left
 Anemia
 ESR increase
 Non invasive tools: US,CT,MRI to detect free abdominal fluid and to visualize damage tot the
Parenchymal organ
 Invasive tools; Culdocentesis, paracentesis,diagnostic peritoneal lavage,video assisted
Laparoscopy,laparocentesis
286. Blunt injuries of the parenchimal abdominal organ: medical and surgical treatment
Medical treatment:
 Control of bleeding
 Replenishment of lost blood( fresh frozen plasma,packed RBC)
Surgical Treatment
 Splenectomy
 Viable omental pack to manage a fractured liver
 Spleen injury managed by wrapping with polyglycolic acid woven mesh
 Spleen repaired with pledgets composed of gelatin sponge wrapped in oxidized cellulose
287. Blunt injuries of the hollow abdominal organ: etiology, clinical picture
Etiology:
 Gut trauma
Clinical picture:
 Complaints: abdominal pain,high body temperature,vomiting
 History presenting complaints: trauma
 Vital signs: signs of hypovolemiat
 Inspection : wound on the abdomen,thoracic breathing
 Auscultation :absence of bowel sounds (paralytic ileus)
 Palpation: tenderness, muscle guarding, rebound tenderness
 Percussion: mendel sign positive,shifting dullness due large amt of fluid in abdomen
 Rectal and vaginal examination : tenderness
288. Blunt injuries of the hollow abdominal organ: laboratory and instrumental diagnosis
Laboratory diagnosis:  Signs of inflammation and hypovolemia

i. Leucocytosis with shift to the left Instrumental diagnosis

ii. Presence of C-reactive protein  Plane abdominal x-ray
iii. Increase ESR  US,CT,MRI to detect free abdominal fluid
iv. Increase Hematocrit  Invasive tools: culdocentesis,paracentesis,diagnostic peritoneal
v. Increase specific gravity of urine lavage,video assisted
Laparoscopy
289. Blunt injuries of the hollow abdominal organ: medical and surgical treatment
Medical treatment:
 Control of source of peritoneal soiling.(Requires exploration and treatment of damged part)
 Correction of infection by antibiotics ( Metronidazole,aminoglycosides,cephalosporin 3rd generation,clindamycin)
 Correction of hypovolemia(lactate ringer solution,D5W,etc)
 GIT decompression using nasogastric tube
 Oxygen supplementation
 Analgesia
Surgical treatment:
 Resection of part of the intestine and reanastomoses of both ends
 Resection of part of the bowel and reanastomoses of both ends
 Stomach injury: repair by excision of wound edges and suturing of the wound
Principles and stages of surgery:

 Wide midline laparatomy
 Exploration of intraabdominal organs
 Treatment of injured organ
 Cleansing and draining of peritoneal cavity
 Suturing of surgical wound
Thermal Injuries
290. definition and pathophysiology of the burn
Definition :
Burn is the loss of integrity of the skin, loss of body temperature, loss of proteins, loss of fuid and electrolyte, and ingress of the foreign materials and
inavasion of microbes.
Pathophysiologic changes at the body

Hypoproteinemia due to colloid-free fluids and loss of plasma,must be replaced with colloid fluid(albumin 5%)
GIT : paralytic ileus if there is >25% of TSBA
Increase of Hematocrit due to loss of fluid and increase in vascular permeability which is caused by heat, humoral factors liberated from damaged tissues
and cytokines are produced by activated leukocytes (histamine from mast cell, arachidonic acid metabolites like thomboxane A2 and leukotrienes,
substance P, activated proteases, products of complement activation, lysosomal enzymes, oxygen radical)
291. evaluation of the involved surface area of the burn
Extend of injury (the surface and depth of injury) is necessary to guide fluid resuscitation and plan the care.
The rule of nines:-
 palm = 1%
 Head (face) =9 %
 Anterior surface of trunk = 18%
 Posteterior surface of trunk = 18%
 Upper limbs(each) =9 %
 Lower limbs(each) = 9%
 Genital area =1%
292. evaluation of the burn's depth
Depth of injury :-
1. Partial thickness burn
Subdivided into - superficial
-deep
2. Full thickness of burn
Partial thickness burn

Partial thickness burn involves the outer layer of the skin and may extend to the dermis.(first and second degree burn). Manifestations :-
 Blistering
 Skin is red and moist
 Painful to touch
 Sensation is intact
Clinical differentiation of superficial and deep partial thickness burn is difficult. It is done according to the length of time it takes to heal, and by using
laser Doppler flowmetry.
Superficial partial thickness burn should heal within 2 weeks with minimal cosmetic and fiunctional consequences.
Deep partial thickness burn takes 3 weeks to reepithelize with cosmetic deformity and disturbance in function. Skin grafting will improve the outcome
and is preferred approach in this depth if injury.
Full thickness wound

Full thickness wound, all dermis is destroyed with following manifestation.:-
 Leathery
 White or charred
 Dry
 Insensate
During healing a contraction occurs decreasing the area but leading to poor cosmetic result and joint stiffness.Except for small surface area wounds, full
thicknes wound should be either excised and grafted with the patient’s skin.
293. chemical burns: etiology, mechanism of injury, diagnosis, and management
Etiology:
Ingestion of chemical agent leads to esophageal injury later consequences include dvplmt of strictures. Besides local effects, chemical agent may also
exert systemic effects (esp. phenol and mustard gas). Alkali tend to penetrate deeper into tissues than acid.
Mech of injury :
Chemical burns case denaturation of proteins.
Diagnosis :
Diagnosis is made based on the degree of injury which depends on :
 Time exposure
 Strength of the agent
 Solubility of the agent in tissue
Management :
Irrigation with normal saline or tap water for as long as 6h.
294. electric injury: etiology, mechanism of injury, diagnosis, and management
Etiology :
???
Mechanism of injury :
Electrical current passes thru the path of least resistance between the entrance and exit point (nerve and blood vessels). In the local area of injury,
subcutaneous tissue, muscles and bone may be injured.
Diagnosis :
Injury of the heart arrhythmia or cardiac arrest. Resuscitation may be initiated immediately with ECG monitoring.
At the small point of contact, the skin is charred. It may overlie extensive areas of devitalized muscles. Liberation of myoglobin may cause acute renal
failure. Renal biopsy of a patient who had rhabdomyolysis and myoglobinuric acute renal disease. Coarse eosinophilic casts of myoglobin are evident in
tubular lumen.
Management :
Edema formation in injured tissue beneath fascia may compromise blood supply.Fasciotomy should be performed.
Fluid resuscitation as in burned patients.

The first 24 hour administration of crystalloid solutions, The amount is based on patients’ response to resuscitation. Administered solution should
maintain a normal:
 BP
 HR
 UO( 1 ml/kg/h or 30-50ml/kg)
 Mean arterial BP at 60mm Hg
 Blood lactate level
Goodwin formula : 3ml/kg per % of the body surface area burned.

Parkland formula : 4 ml/ kg/% of burn surface of LR
Second 24 hour administration of colloid containing solution.
Evaporative loss (25+% of burned area) multiplied by total body surface area in meter square (100%). This formula is used for fluid replacement for the
following days.
295. inhalation injury: etiology and pathophysiology, diagnosis and management
Etiology :
Aldehyde, carbon monoxide, cyanide
Pathophysiology:
Erythema, edema, blistering, ulceration, and soughing in the airway followed by endobronchial cast and obstruction of the bronchiole. Injury of the
mucocilliary mechanism causes obstruction and accumulation of the necrotic debris.Poor ventilation and ground for infection.(70% within a week of
injury ).
Diagnosis :
Diagnosis based on the history, signs, and symptoms. Assume inhalation injury in :
 Injury in closed space

 Has burn above clavicle
 Singeing of nasal vibrissae
 Hoarseness
 Carbonaceous sputum
Management :
Airway evaluation using flexible bronchoscopy. It confirms diagnosis and helps to insert and endobronchial tube if necessary.
Therapy is not specific (the injury is not quantified by testing-x-ray, respiratory tests are not helpful).
 Aggressive pulmonary toilet

 Use if mucolytics
 Early identification and treatment of infection
 Prophylaxis with Abc is not used
 Steroids are no benefits and are potentially harmful.
 Nasotracheal suctioning to clear the upper airway. If frequent suctioning is required a soft rubber nasopharyngeal trumpet maybe placed to minimize
trauma.
 Carbon monoxide poisoning treated with administration of 100% oxygen
 An endotracheal tube for patients with inhalation injury.
296. severe burns: first aid, initial fluid resuscitation, initial wound care
First aid :
At scene of injury :
 remove patient from heat
 extinguish burning cloth
 Remove from electrical contact
 Ice or cold water soaks within 10 minutes to decrease pain (burns <25% of TSBA) and reduce tissue heat content
CPR and iv lines if necessary for patients with cardiac irregularity, massive blood loss as coexisting trauma and if the transport takes longer than 30 min.
Initial fluid resuscitation :

The first 24 hour administration of crystalloid solutions, The amount is based on patients’ response to resuscitation. Administered solution should
maintain a normal:
 BP
 HR
 UO( 1 ml/kg/h or 30-50ml/kg)
 Mean arterial BP at 60mm Hg
 Blood lactate level
Goodwin formula : 3ml/kg per % of the body surface area burned.

Parkland formula : 4 ml/ kg/% of burn surface of LR
Second 24 hour administration of colloid containing solution.

Evaporative loss (25+% of burned area) multiplied by total body surface area in meter square (100%). This formula is used for fluid replacement for the
following days.
Resuscitation :
 IV fluid replenishment thru venous cannulation

 Cathether in the bladder for patients with >20% burn
 Nasogastric tube to decompress the dilated stomach
 Patients wrapped in clead sheets or blankets
 Resuscitative fluids must be warmed
 Burn-injured extremities must be elevated above the level of heart
Initial wound care :

Burned areas :
 Small blisters must be left intact

 Debridement and application of topical agents for larger blisters and full thickness burn
297. temporary and permanent coverage of burn wound: reasons, types
Temporary coverage of burn wound by using temporary skin substitutes:-
 allograft skin from cadavers (can be used for no longer than 7days)
-free of jaundice, cutaneous malignancy and viral disease
 synthetic membrane (Biobrand, Silastic)

 Autologus keratinocytes
 Skin substitutes : Integra artificial skin, Alloderm
 Pig skin, Biograne, Transcyte
Permanent coverage of burn wound:-
Excision and closure of wound are done when the patients have been stabilized 3-4 days after injury.
 Tangential excision until viable tissue

 Excision of the wound to the level of fascia especially for deep full thickness burn and infected.However cosmetic result is poor and lymphatic
drainage is impaired.
Consider skin donor sites or skin grafting at patients with deep partial and full thickness burns >40%.
Autograft:-
i. If there is sufficient donor sites, split thickness or full thickness graft are used.
ii. If donor sites are limited, autograft can be expanded.(Mesh grafts). Mashing increases the are of the skin graft.
Mesh graft allows blood and exudates to escape thus minimizing hematoma.
Reasons???/
298. circumferential burns, prognosis and rehabilitation
Circumferential burn
A full thickness burn injury possess a risk of compression and compromise of blood flow:-
 elevate extremity to reduce edema

 evaluate hourly for signs of vascular compromise (pallor, pain, parasthesia, paralysis)
 Doppler examination
Prognosis
Risk scoring system in which one point is given for each of
 Burn size greater than 40% of TSBA

 Age >60 years old
 Presence of inhalation injury
Mortality rate
 0.3% with no risk factors
 3% with one risk factor
 33% with two risk factors
 90% with three factors
The system does not consider preexisting pathology, stratification of age and extent of injury
Rehabilitation
I. Escharotomy
An incision done thru the eschar. If escharotomy doesn’t restore blood flow a fasciotomy is required.
II. Pressure garment
The treatment of hypertrophic scar with pressure garment. A typical example of active hypertropic scarring following a full thickness scald. Pressure
garment is worn continuously for 14 months and the scar matured with reduced contracture formation.
III. Z-plasty is used to relief scar contracture.

IV. Fish-tail incision and graft method of releasing broad contracture.
299. complications of burns: types, diagnosis, prophylaxis and treatment
I. Infection complication. Open wound infection with cellulitis
Diagnosis with the help of following clinical picture :

 Localized pain
 Tenderness
 Swelling or heat at the affected area
 Systemic signs of infection : Fever , leukocytosis and leukemia
 Signs of lymphangitis, lymphadenitis or both
Prophylaxis : ???Changing dressing everyday and follow all aseptic rules.
Treatment: Change in local wound care, more frequent dressing change and administration of systemic Abc.
II. Pneumonia as a complication of inhalation injury. Development of respiratory distress syndrome is possible.
Diagnosis : Chest x-ray, gram-staining of sputum
Prophylaxis : ??
Treatment :
 Initiation of empirical Abc therapy,
 specific antimicrobials after culture
 Respiratory support with volume-cycled ventilators in case of pulmonary failure
III. Suppurative thrombophlebitis

It is due to colonization of venous cathether especially central with bacteria.
Diagnosis :
Clinical presentation such as persistent fever and bacteremia. Diagnosis is confirmed by aspiration of purulent material from the affected vein.
Prophylaxis :
i.v cathether should be changed once a week
Treatment :
Consist of excision of the involved vein to the point that the vessel is normal where bleeding is encountered.
IV. Gastrointestinal complication .

Occurrence of acute ulceration of stomach and duodenum (Curling’s disease) is possible,
Diagnosis :??
Prophylaxis :??
Treatment: When a paralytic ileus is present, an antacide is instilled thru nasogastric tube.After return of GI motility, antacid is administered orally.
Nasogastric tube should be removed as soon as GI motility has restored.
Tetanus prophylaxis by evaluating patient’ss immunization status :

 Burned patients who have undergone previous active immunization within 5 years of time of injury require no further prophylaxis.
 Patients who have received their most recent booster injection > 5years before injury should be administered a booster dose of toxoid.
 Patients who have not undergone prior immunization or without history of immunization should be given 250-500 units of human antitetanus globulin
at one site and initial immunizing dose of toxoid administered at another site.
300. frostbite: etiology and pathophysiology of injury, classification
Etiology :
a) Poor clothing during winter months
b) Acute alcoholism
c) Psychiatric illness
Pathophysiology of injury:
Freezing of tissue, damage by tissue ice crystallization, cellular dehydration, and microvascular occlusion.
Classification of depth of frostbite :
i. First degree : Hyperemia and edema

ii. Second degree : Hyperemia and edema with vesicle formation(partial thickness burn ), cutaneous sensation is intact.
iii. Third degree : Necrosis of entire skin thickness, formed vesicle much smaller than those with second degree frostbite.
iv. Fourth degree : Full thickness necrosis of the skin and extend into underlying muscle and bone.
301. frostbite: clinical presentation medical and surgical treatment
Clinical presentation according to classification of depth of frostbite :
i. First degree : Hyperemia and edema

ii. Second degree : Hyperemia and edema with vesicle formation(partial thickness burn ), cutaneous sensation is intact.
iii. Third degree : Necrosis of entire skin thickness, formed vesicle much smaller than those with second degree frostbite.
iv. Fourth degree : Full thickness necrosis of the skin and extend into underlying muscle and bone.
After thawing
Mild injury
Capillary flow restores. Area is red and warm with throbbing pain( arterial pulsation), sensation and motor function return. Large vesicles appear within
few hours, filled with straw-colored fluid. Most of these changes resolve 1-2 weeks with little or no tissue loss.
Severe injury
Capillary flow is never restored(arteriovenous shunting), the injured area is cold and deep red. Patient is still able to move the distal part. Extensive edema
may persist for months. Eventually the non-viable skin and deep structure demarcate and mummify.
Determination of tissue viability is impossible during the first several weeks following injury and often can be made only after gangrenous tissue has
demarcated and sloughed.
Medical treatment
 Remove constricting clothes Local care to prevent infection

 Wrap in warm blanket  Vesicles are left intact (not leaking and intact)
 Give hot fluids  Bed rest
 Rewarming (40 c 20 to 30 min)  Wounds are exposed to air
 Foot cradle
 Lamb wool’s is inserted between affected digits
 Cleansed daily with Abc solution in whirlpool bath
 Use of pressure dressing is contraindicated
Surgical treatment
Surgery is delayed until clear demarcation.
1. Wet gangrene requires immediate surgical removal of the source of sepsis.

2. Tetanus prophylaxis is based on the patient’s prior immunization status.
3. Antibiotics is indicated when infection is evident.
4. If large volume of tissue has been frozen and there is massive fluid loss may require i.v fluid resuscitation.
5. Chronic frostbite : Hyperhydrosis, parasthesia, cool extremities, cold sensitivity, and edema. Surgical division of segment sympathetic trunk provide
long term relief.
Oncology
302. Definition and classification of the cancer
It is a group of diseases caused by unregular growth and spread of neoplastic cells
Classification:
(1)Benign
Eg: Fibroma, adenoma, lipoma
(2)Malignant
Eg: Fibrosarcoma, adenosarcoma, liposarcoma
303. Characteristic of premalignant states, screening tests for malignant tumors
Premalignant slates
•Atrophic gaitritu
• Polypus
• Diverticulum
• Leukoplakia
• Metaplasia
• etc.
Basic principle
• most tumors have been present for one to ten years before they become clinically evident;
• asymptomatic cancer detected by screening tests generally has a better prognosis (hen symptomatic one.
Basing on these principles a number of screening tests for cancer has been elaborated.
• mamonography (annually after age 40-50);

• stool for occult blood and digital rectal examination (annually after age 50);
• smear of the cervix (every three years after two negative tests done year apart).
• some laboratory tests identifying so-called tumor markers: •y-fetoproteins occur in various neoplasms, etc.
304. Epidemiology and comparative characteristic of benign and malignant tumors
Signs Benign Malignant

Atypism Tissue (chaotic arrangement) Tissue + cellular
(enlarged, different size, shape, color, many mitosis)
Type of Growth Expansive growth (node-like) Infiltrative or invasive growth
->well described with differentiated borders ->diffused, no borders
Preserved basal membrane preserved destroyed
Capsule present absent
Growth slow rapid
305. General and specific signs of malignant tumors
General signs of malignancy (so-called syndrome of minor signs)

• malaise
• Change of test (rejection of meat)
• Apathy
• Discomfort
• Inexplicable toss of body weight
• Debilitation
• Inexplicable anemia
• Long lasting inexplicable sub febrile body temperature
Specific signs are determined by exact localization of the tumor
Esophagus- dysphasia (difficulties with swallowing).

Bowel- change of bowel habits (irregularity), change of stool's
Consistency or composition.
Skin • sore that does not heal, change of papilloma (appearance of
Pain, enlargement, inflammation).
Breast - thickening or lump in the breast, nipple discharge, edema.
Lungs - cough or hoarseness.
Bladder- hemaniria, urinary retention, etc.
306. Staging of cancer: TNM classification, patient’s clinical groups (Gastric CA)
Staging of gastric cancer (TNM)
Stage definition
T0 No evidence of primary tumor
TIS In situ tumor limited to mucosa
T1 Tumor limited by mucosa or sub mucosa
T2 Tumors to but not thru the serous
T3 Tumor through the seruosa but not into adjacent organs
T4 Tumors into adjacent organs (direct extension)
N1 Only per gastric within 3cm from the primary tumors
N2 Only regional lymph nodes more then 3cm from primary tumors but removable surgically
N3 Others intra abdominal lymph nodes involvement
N4 Other INTRA ABDOMINAL LYMPH NODE involvement

M0. Not distant
M1 Distance present (to umbilicus ,duglaspouch, krukenbergs, virchow’s)
GROUPING OF PATIENTS
Group 1
a) Suspicion to presence of a cancer Group 3
b) Premalignant state Patient after surgery (completely cured)
Group 2 Group 4
a) Undergo to surgical treatment Inoperable patients
b) Undergo to any other type of treatment
307. Types of cancer treatment, types of biopsy
Types of cancer treatment

 Surgical
 Radiation
 Chemotherapy
 Immunotherapy
Choice of therapy
Disease, stage, histological grade, patient’s age, concomitant diseases, intention of
therapy (cure versus palliation)
1. Surgery and radiation: treatment of primary tumor and the regional lymph nodes
2. Chemotherapy and immunothearpy are used to affect distant areas of spread
3. Multimodality therapy uses the advantages of each therapy
4. Adjuvant therapy is a systemic therapy used after local control of tumor (resection) who are at high risk of microscopic disease extension.
Principles of a surgical treatment

 Dissection through uninvolved tissues
 Minimal manipulations
 Early vessels ligation
 Removal of lymphatic drainage in continuity with the tumor
Chemotherapy
1 Cytostatics affect cellular mitosis: ciclophosphan, vincristin, etc.
2. Antimetbolites:
a) affecting the synthesis of purins (mecaptopurin)
b) affecting the synthesis of enzymes (fluoruracil) transformation of folic acid (metotrexate)
3. Antineoplastic antibiotics: actinomycin D,etc.
Radiation therapy
may be used intracavity
Immunotherapy
either tries to promote the body's own immune surveillance (activating T lymphocytes) or tries to direct antibodies against tumor antigens.
Physical agents
hyperthermia and cryotherapy attempt to selectively kill more thermally sensitive neoplastic cells.
*The problem with all treatments other than surgery is that they are never 100% selective for the neoplastic cells, and normal cells are injured.
Types of biopsy
Incision biopsy, needle aspiration biopsy, smear biopsy, operational biopsy
308. Examination of the patient with malignancy: complaints, anamnesis, and general examination
Examination of a patient
Patient's complaint* (pain is infrequent)

History)' of presenting complaints (progress, previous treatment,etc.
Past medical history (occupational hazards, contact with physical
or chemical cancerogcns, genetics I predisposition, etc. Any former
surgical operations (to (real malignancy), etc.
General examination and system investigation. At an advanced
cases the patient is exhausted, with dry, pale, and grayish skin
color, cachexia, etc. Attention is given to any changes of the skin
and mucous membranes. An areas of a thyroid gland, mammary
glands, and lymphatic nodes are inspected and thoroughly

palpated. A rectal or vaginal examinations may be necessary to
detect a tumor of that areas.
Local status includes thorough investigation of involved system
Superficially located tumor - local description.
The found mass is thoroughly described

Inspection: presence of mass, change of skin colour sewelling discharge localization size
Palpation :shape consistency tenderness pulsation ,mobility
May be found coesixting . Condition of peripheral lymph nodes is evaluated by palpation,
This investigation may give preliminary conclusion about whether the tumor is benign 0r malignant one.
Benign: incapsulated,smooth soft mobile not tender
Malignant: clear border uneven surface is un even consistency is firm mobility is limited and palpation is tender.region lymphatic nodes
309. Examination of the patient with malignancy: Laboratory investigation, instrumental investigation
Laboratory examination:
It may show signs of low grade inflammation, anemia, disproteinemia hyper coagulation, etc.
Instrumental examination
-Radiologic (X-ray) examination: plane and contrast radiography,tomography, angiography, lymphographyh /tomography, etc.
-Imaging studies: ultrasound, CT, MRI.
-Radioisotope investigation (scintigraphy).
-Endoscopy. flexible or rigid sigmoidoscopy, colonoscopy, branchoscopy, etc. ''
-More invasive techniques may be used if the diagnosis is difficult or tissue biopsy is required: laparoscopy (video assisted),
thoracoscopy, diagnostic thoracotomy, diagnostic laparotomy, etc.
-A found tumor must be morphologically verified. It is achievedusing the following possible methods of biopsy: aspiration,
needle,incisional , or excisional one.
310. General principles of surgical treatment, chemotherapy of the cancer
Principles of a surgical treatment

 Dissection through uninvolved tissues
 Minimal manipulations
 Early vessels ligation
 Removal of lymphatic drainage in continuity with the tumor
Chemotherapy
1 Cytostatics affect cellular mitosis: ciclophosphan, vincristin, etc.
2. Antimetbolites:
a) affecting the synthesis of purins (mecaptopurin)
b) affecting the synthesis of enzymes (fluoruracil) transformation of folic acid (metotrexate)
3. Antineoplastic antibiotics: actinomycin D,etc.
General Principles of Transplantation and Plastic Surgery
311. immunologic aspects and role of transplantation, classification
Transplantation is a surgical procedure that involves the removal of an organ from one individual and placing it in another who has markedly impaired
function of this organ. If successful; it is the best treatment option for chronic organ failure.
Each cell carries its own original series of membrane proteins that are necessary to identify itself:
 MHC, example HLA A,B,C,DP,DG,DR
 Unique cell surface
Types of immunity:
 Cellular,
Determined by T-lymphocytes provide host defensive mechanisms against viruses and so on but are also responsible for rejection of grafts
 Humoral,
Provided by B-lymphocytes that produce antibodies.
According to origin, immunity types are:
 Natural- nonspecific, innate, not acquired thru antigen contact
 Acquired- can be of 2 forms:
o Active- after contact with antigen, body responds with specific antibody production for that specific antigen. The immunity lasts longer despite having
a long time to form
o Passive- these antibodies are formed in another body due to exposure to an antigen. These antibodies are then separated and introduced to another host.
Since this host isn’t exposed to the antigen, it is called passive.
Classification of organ transplantation:

 Auto graft (skin graft)
 Isograft (syngenic graft)
 Allograft(homograft)
 Heterograft(xenograft)
Graft rejection often occurs in allograft and it can be minimized by matching for the MHC and HLA
312. types of donors: characteristic, storage of organs
Types of donors:
 living related donors
 cadaver donors
 living unrelated donors
Living related donors, the donor genotypes are more compatible and can either be perfectly histocompatible or half histocompatible. Perfect
histocompatiblilty occurs in siblings, while half histocompatibility occurs in parent child relationships.
However the donor has to have a good history, free of illness, malignancy and other disorders. Of course, the organ functionality has to be normal too. If
malignancy or any active infection is detected, it is totally CONTRAINDICATED!
Cadaver donors are usually young and healthy individuals who suffered an irreversible brain injury. Common candidates are: intracranial hemorrhages,
trauma, suicide, and brain trauma.
 GCS = 3points
 Isoelectric EEG
 Absence of intracranial blood flow
 Visual evidence of cerebral tissue damage
To store the organs, special machine perfusion is used. For example, kidneys are placed in a chamber and continuously perfused by pulsatile flow via the
renal arteries with chilled preservation solution. They are preserved up to 48hours by cold storage in ice with no perfusion using a concentrated KCl
solution or with pulsatile perfusion using plasma like solution. An additional surface cooling with iced saline packs is necessary. Heart can be stored up to
5 hours, liver and pancreas up to 12 hours.
313. technique of different organ transplantation, classification depending on the site of transplantation
renal transplantation:
for incision, either right sided or left sided approach may be used. The right internal iliac artery is anastomosed end to end to the donor renal artery.
Alternativly, the donor renal artery on a patch of aorta is anastomosed to the side of proximal external iliac artery. The donor renal vein is usually
anastomosed end to side to the external iliac vein.
Urinary tract reconstruction:
The urinary tract is reconstructed, by passing the ureter through a posterior bladder wall tunnel and anastomosing to the mucosa. Reconstruction with
extra vesicular ureteroneocystostomy involves reanastomosing the donor ureter to the bladder mucosa through a small myotomy in the anterior bladder
wall.
Pancreas excision:
If liver is not used for transplantation, the pancreato-duodenal graft can be excised with an aortic patch.
Liver transplantation:
Incision is done. Hepatectomy without the use of bypass done, by dividing the hepatic artery and bile duct and applying 2 clamps on the inferior vena
cava and the portal vein before the removal of liver. During the anhepatic phase of transplantation, the venovenous bypass is done, by inserting a canulla
to the IVC and the portal vein, and the blood is returned to the jugular veins and the superior vena cava via a centrifugal pump. Finally anastomosis of
new liver done.
NOTE: technique is generally the same, patient given general anesthesia, prepping and dreppign of the area and then incision introduced, and vessels
clamped and target organ is removed and new organ is reanastamosed. For vital organs during the period of removal, a special bypass circuit is used.
Classification of transplantation according to site:

 homotopic/ortotopic- position into same position as diseased organ (for kidney,liver,heart,lung)
 heterotopic- (pancreas, kidney), organs in another anatomic region
314. prevention of graft rejection, complications after organ transplantation
The following criteria must be satisfied:-

 Kidney must be less than 60 years and without contraindication

 Heart less than 50 years.
 ABO compatibility
 Rh compatibility
 HLA (human leukocyte Antigen) – most important A locus (30 function)
 Cross matching should be done for all those stated above.
 If completely compatible, rate of survival 90%
 ½ matched antigen, rate of survival 60%
Also to minimize the tissue rejection, besides good matching mentioned above, we administer immune suppressants. examples are:
 Cyclosporins
 Prednisone
 Azathiprine
 Orthoclone
 Antilymphocytic globuline
Complications:
 Rejection, maybe acute(3months) or chronic
 Infections
 malignancy
due to steroid therapy, the following complications occur:
 aseptic necrosis of hip or knee
 obesity and cushingoid features
 hypertension,hyperglycemia,osteoporosis
 poor wound healing,peptic ulcers
315. postoperative scar: principles of good cosmetic results
post-operative is present after any surgery is performed. However it can be minimized, if the incision before operation is performed along the Langer’s
lines and the dissection is made as minimal as possible. Monofilament suture materials should be preferred to the braided sutures. Removal of sutures
must be as quick as possible,
 face, 3-5days
 abdominal, 1-10days
 low extremities,10-14days
For big wounds, we use secondary method of healing, if no infection present, the wound is closed by:
 secondary suturing
 skin graft placement in area of significant size and that woud not be healed in 2 -3 weeks
 skin flap is used in areas of poor blood supply and absent of padding
316. classification of suture material and types of placement
Suture materials:
 absorbable
o organic- catgut
o synthetic-polyglactin, polyglycolic acid, poliglecaprone, polyglyconate
 non-absorbable
o organic-silk, cotton
o synthetic-nylon, polypropylen, Dacron
Types of closure:
 simple interrupted
 vertical mattress sutures
 horizontal mattress sutures
 subcuticular sutures(interrupted & non-interupted)
 continuous over and over sutures
317. Skin grafts: definition, types
Skin graft is defined as a segment of the epidermis and dermis that has been detached from its native supply of blood to be transferred to another area of
the body. The blood supply now is provided by diffusion of nutrients from the recipient’s bed.
Types of skin grafts:

 Split thickness- maybe thin, medium, and thick harvested using a dermatome from abdomen, buttocks , thigh
 Full thickness- contains epidermis and dermis without subcutaneous fat. However it requires the closure of the donor site(via primary closure or
grafting).this graft is harvested using the free hand technique
 Meshed grafts- when graft added with several holes for stretching and inflow of fluids under graft
318. characteristic of full-thickness and split-thickness skin graft

See number 7(previous question)
319. Flaps: definition, classification of flaps depending on the surgical technique
Flaps are segments of skin and subcutaneous tissue that are moved from one part of the body, either retaining or transplanting their vascular supply. It is
useful for healing and for covering defects that require padding. They are used in poorly vascularised beds with the best functional and cosmetic results.
Flaps are used to close defects too large for primary closure and where skin grafting is inadequate. It may also be sued to cover exposed BRAIN, blood
vessels, bone and joint surfaces, and wound of poor vascularity. Please note that the vascularity of the transferred tissue is maintained through the nutrient
vessels present in themselves. The pedicle of flap maybe attached (random flap or axial flap) to its origin or be divided during transfer and reanastomosed
to recipient vessels using microvascular surgery.
According to surgical technique, flaps are classified as:

 Advancement flap: o Transitional flap
o Single pedicle advancement  Simple transposition flap
o V-Y and Y-V flap  Bilobed flap
o Bipedicle flap  Rhomboid flap
 Pivot flaps  Z-plasty
o Rotational flap  Interpolation/island flap
*Also can be classified as free, pediculated, distant and direct
320. classification of flaps depending on blood supply
according to blood supply:

 random flap- survive on perforating blood vessels extending from dermalsubdermal plexus(from musculocutaneous perforators). Such flaps are limited
in length and rare always pedicled
 axial flap- receive their blood supply from specific defined blood vessel longitudinally oriented within the flap. The tissue composition of the flap
varies.
o Latissimus dorsi flap
o Deltpectoral flap
o Groin flap
o Radial forearm flap
321. types of random and axial flap plasty

see number 7(previous question)
322. fasciocutaneous and musculocutaneous flaps, free flaps – characteristic
According to tissue composition, flaps are classified into: random, fasciocutaneous, arterial, and musculocutaneous
Musculocutaneous flaps are classified by the type of blood supply ( 5types )
Areas for rising of fasciocutanous flaps usually in deltoid region, arm, forearm, thigh, legs etc. and for musculocutaneous flaps, they are taken from
trapezious, latisimus dorsi, abdominal muscles,gastrocnemius, sternocleidomastoiedeus etc.
Free flaps are used but they require special microvascular technique and they pocess a high number of complications.any axial flap can actually be
detached and transferred as a free flap using the microvascular technique. ( side to side micro vascular anastomosis)
General Principles of Malformation Surgery

323. etiology of congenital malformations
Malformations result form a primary structural defect that is caused by a localized error of morphogenesis.
Ethilogy:
 intrauterine factors o age of patients
o position of fetus o idiopathic
o trauma in uterus
 environmental factors according to the system involved it may be:
o infection during pregnancy  cardiovascular
o ionizing radiation  respiratory
o pollution  musculoskeletal
o drugs  urologic
o hereditary predisposition  GIT
o alcohol and smoking  CNS
 Etc.
324. congenital dislocation of the hip: pathology, clinical picture, diagnosis and treatment
the acetabulum Is shallow and has a more vertical orientation than a normal one.
Diagnosis is made by:

 clinical examination
o barlow’s sign(hip in full adduction)
o ortolani’s sign(hip in full abduction)
 asymmetry of gluteal folds, shortening of extremity
 limp or waddling when the baby starts to walk/crawl
 plane pelvic X-ray, arthrogram, MRI
Treatment:
Conservatively, a special position is maintained by braces, splints, use of harness,etc. for 3 to 6 months. Open reduction is done if its too late to be treated
by conservative way.
325. clubfoot: pathology, clinical picture, diagnosis and treatment
aka talipes equinovarus, it is a complex deformity, the patient has the following features, ankle plantar flexion, inversion of the foot, adduction of the
forefoot, and internal rotation of the tibia
diagnosis is usually made by the base of the clinical presentation itseld and also X-Ray.
Treatment :
 medical- stretching, strapping, serial splintage, special boots
 surgical- release of tendon, resection of bone of foot floor
326. wryneck: pathology, clinical picture, diagnosis and treatment
caused by trauma of the fetus in the uterus or during diffivult delivery
hypertension of the sternocleidomastoid muscle of one side causing the head to tilt to the affected side. Hence the clinical picture is the persons neck
being tilted to one side at all times.
Treatment:
 medical- stretching exercise and braces
 surgical- division of muscle
327. flat foot and knee deformities: pathology, clinical picture, diagnosis and treatment
In flat foot, the patient’s feet are totally flat on the ground without the normal arch at the floor of the feet. In knee deformities, we see either genu
varum( bow leg, or outward bowing of the legs) or genu valgum(knock knee, or inward bowing of the legs) usually it is physiologic for 3-8 years.it is
usually due to rickets and skeletal dysplasia.
Clinical picture:-
 flat foot:
o tiredness of the foot during walking
o the characteristic foot visible
 genu valgum and genu varum
o the characteristic appearance of the knees which are bowing outwards or inwards
diagnosis is based on the appearace and clinical examination
treatement:
 flat foot- arch supports (special ortho[pedic shoes)
 knee deformities- use long leg braces or corrective osteostomy needed if its too late.
328. accessory neck rib: pathology, clinical picture, diagnosis and treatment
accessory ribs arise from C7
clinically presentation may vary, usually there is a lump of tenderness, vascular symtoms might be present and also nerve pressure symptoms
diagnosis is based on plane chest x-ray
treatment is by sling and exercise scalenotomy or removal of the cervical rib is also done in severe cases.
329. spina bifida: types, pathology, clinical picture, diagnosis and treatment
it is caused by the failure of fusion of vertebral structures
forms:
 spina bifida aerta- the neural tube opens without skin coverage through a defect in the posterior vertebral arch. CSF leakage occurs and high risk of
meningitis
 spina bifida cystica- skin covers the spinal defect which may contain CSF. This is meningocele, if there is neural tissue withing the sa, its called
myelomeningocele
 spina bifida occulta- no protrusion of spinal cord or meninges and on the skin may be various skin changes
diagnosisi is based on US, MRI plane X-Ray, alpha feto protein is usually present in CSF in amniotic fluid or use an antenatal US before delivery
treatment is medical or surgical and varies depending on the individual and type of spina bifida
330. deformities of the thorax, congenital defects of the skull
can be due to heart and the common complaints are palpitation, dyspnea, exhaustion, fatigue, intolerance to little physical exercise, weakness
in physical examination we see cytanosis or clubbing, abnormalities in growth, systolic murmur and gallop rhythm, signs of congestivce heart failure with
hepatomegaly etc.
examples are :
 patent arterial duct
 coarctation of aorta
 ventricular septal defect
331. cleft lip: types, pathology, clinical presentation, diagnosis and treatment
generally can be:

 complete- joined with anterior nose
 incomplete- not joined to nose
 unilateral- only one side involved
 bilateral- involved in both sides
clinical presentation are inability to feed and breathing problems
diagnosis is based in physical examination

treatment is usually by suregery, the baby heals perfectly fine and almost absent of scars
332. cleft palate: types, pathology, clinical presentation, diagnosis and treatment
cleft of primary palate:

unilateral,bilateral, median
ceft of secondary palate:

complete, incomplete, submucous
cleft of both primary and secondary:

unilateral, median, bilateral
diagnosis is critical and can be observed
immediately after birth , ter wud be breathing problems and feeding problems. If untreated leads to otitis media, hearing deficit, speech problems from
airflow problems, dental problems, facial growth
treatment is surgery by making incision and excision of the plate, then suturing it with tension that reduces the width of the palatal cleft.
333. coarctation of the aorta: pathology, clinical presentation, diagnosis and treatment
it is due to aortic stenoosis and is manifested by left ventricular hypertrophywith hypertension proximal to site of aortic stenosis and hypotension at site
distally to it.
In patients, we see epstaxis or nose bleeds, headaches, and increased blood pressure in higer extremities and insufficient circulation at the lower
extremities.
Diagnosis is based on chest X-Rays and it revelas notching of artery at lower margin of rib, also aortogram and CT can be used.
Treatment is by percutaneus balloon dilation , and also we can use resection and reanastomosis of the coarctation.
334. patent ductus arteriosus: pathology, clinical presentation, diagnosis and treatment
its due to communication of aourta directly to the pulmonary artery, hence abnormal blood flow occurs.
Upon examination we see cyanosis and clubbing if larger ducts are involved, continous machine murmur at left 2nd intercoastal space, in X-ray we see
enlarged heart and enlarged pulmonary artery size and increased pulmonary vasculature, ECG shows left ventricular strain, echocardiography can be
used, and cardiac catheterization is used,
Treatment is by percuateus insertion of umbrella occlusive device and thoracostomy and ligation of ductus arteriosus
335. ventricular septal defect: pathology, clinical presentation, diagnosis and treatment
the magnitude of the shunt is determined by the relative difference between the pulmonary and systemic vascular resistances. Conoventricular and
perimembranous are the most common types reqiring surgical repair.
Clinical picture would be poor feeding, frequent resp tract infections, dyspnea and exertion, easy fatigueability
To diagnose, use Chest x ray, Echo CG, cardiac catheterization
Treatment is only surgical closure of the defect.
336. hypospadia: pathology, clinical presentation, diagnosis and treatment
the external meatus opens on underside of penis or perineum. Penis is curved and inferior aspect of prepuce is poorly developed “hooded prepuce”
treatment is by different types of skin plasty with repair of the urethra.
337. epispadia: pathology, clinical presentation, diagnosis and treatment
groove on dorsal aspect of the penis extending from the urethral meatus, its uncommon has various deree of severity, leads problems to ejaculation and
urination. Treatment is surgery
338. cryptorchism: pathology, clinical presentation, diagnosis and treatment
testis doesn’t descend and is arrested in certain parts. It maybe in intraabdominal, inguinal canal, or superficial inguinal pouch
may cause sterility if both testis involved and pain in trauma. Malignancy is possible, and the patient experiences a lot of psychological problems.
Diagnosis is made on basis of US, laparoscopy
Treatment is called orchidopoxy to descend testis to normal position.
339. Hirschprung's disease: pathology, clinical presentation, diagnosis and treatment
Due to failure of neuroblast that form the myenteric plexus to migrate. This abnormality causes intestinal obstruction in neonates. Rare, and the locations
vary. Significant stenosis may cause immediate signs of acute bowel obstruction.in mild constrictions ter is constipation, and hypertrophy of the area of
bowel above the stenosis
Diagnosis is based on coloscopy, sigmoidoscopy, biopsy of the ganglion, and by barium enema
340. pyloric stenosis: pathology, clinical picture, diagnosis and treatment
Caused by anrtal muscular hypertrophy and mostly affects male babies. Symptoms are hypovolemic changes and poor nutrition, non bilious vomiting,
metabolic alkalosis, hypokaliemia
Diagnosis is by palpation of lump in abdomen, US, barium swallow, endoscopy
Treatment is by Ramstedt’s operation
General Principles of Parasitic Surgery
341. Echinococcosis: life span, pathology and classification of hydatid disease

Is caused by E. granulossus and E. multiocularis
Life span:
 Embryonated egs from dog feces ingested by man and sheep
 Eggs hatch in upper small intestine
 Oncosphere emerges and with the aid of their hooklets, they penetrate the small intestine wall and enter the portal circulation
 The liver is the most usual resting place,although other organs can also be involved. Maturation takes several months and a “hydatid cyst” containing
an outer acellular membrane and a germinal layer from which protoceleces are produced is formed.
 The definitive host, usually a dog is infected by consuming the hydatid cyst in an infected sheep
 Each protoscolex can produce an adult worm in the dog
Pathology:
The embryo begins to grow in the liver into a larva and forms cystic structure with 3 layers. Outer layer is by host tissue itself. This causes presence of a
central avascular area (cyst) with hypervascular rim(halo). The middle layer is acellular, the innermost germinal layer is the living parasite and gives rise
to a number of protoscolices.this ayer may invaginate to form daughter cysts. Cytic form of hydatid disease is differentiated from alveolar form of the
disease by the appearance of the cyst.
Classification:
Classificationn if disease is either by E. granulosus the cystic form of disease or E. multiocularis the alveolar form
The cyst itself maybe calcified or uncalcified
342. Echinococcosis: clinical presentation, diagnosis, medical and surgical treatment
 Asymptomatic stage
 Clinical symptopmatic
o Pain
o Hepatomegaly
 Complication stage
o Secondary infection of the cyst
o Cholangitis leading to jaundice fever and pain
o Anaphylactic shock
o Obstruction of bile duct and mechanical jaundice
In advanced cases, there is sever abdominal distention with multiple cysts in it and there is massive pleural effusion.
In some atypical cases, te hydatid cyst may be located in lungs, bones muscles brain etc.
Diagnostic principles:
By clinical data,
By lab diagnosis, we find eosinophilia, casoni’sskin test, serological test(complement fixation,indirect IFT,haemaglutination test)
By instrumental,
US,CT,angiography,endosopic retrograde cholangiopancreatography
Treatment:
Medically,
Abendazole 4 tablets daily, percutaneous aspiration followed by injection of scolicidal agent
Surgical,
Approach done through cist, or maybe done by meticulous separation of the entire cyst, liver resection also indicated at times, scolicidal agesnt are
used frequently to prevent abdominal contamination with protoscolices
343. Filariasis: etiology, routes of contamination and life span, pathologic changes in the body
Cause by F. sanguineus hominis aka W. bancrofti
The life cycle:

 Larva is introduced into the dermis via the bite of an anopheles or culex mosquito.
 Migration to regional lymph nodes
 Maturation of adult male and female nematodes takes place in afferent lymph vessels
 Widespread dissemination of microfilariea produced by mature female
 Appearance of microfilariae in peripheral lood
 Then a fresh mosquito bites and sucks blood of the infected individual
 Microfilariae penetrates the mosquito’s intestine and then migrates to the thoracic flight wing muscles,here the infectious larva migrates to the mouth
parts are produced
Fever, elephantiasis, hydrocele, ascitis,chylous fistulas on the scrotum etc
344. Filariasis: clinical presentation of complications, diagnosis, medical and surgical treatment
Fever, elephantiasis, hydrocele, ascitis,chylous fistulas on the scrotum etc.
Diagnosis:
By clinical data, see mosquito bites any suspicion, complains history or lymphatic
By lab, see nocturnal blood smear because the microfilaria is present only at night or resting state of patient,also eosinophylia
By instrumental,Lymphangiography
Treatment:
Medical,
Banocide (diethyl carbamazine citrate) , elevation of extremity elastic compressive stockings or bandages for leg oedema and suspensory bandages for
orchidis, antibiotics for secondary infections, lymphtonic drugs
Surgical,
Removal of pathologically staind elephantoid subcutaneous tissue
345. Ascariasis: etiology, routes of contamination and life span, pathologic changes in the body
A.Lumbricoides is most common helmith. Infection is specific to human and direct transmission is impossible.
Life cycle:
Humans are infected by eating food conraminated by mature ova. The released larva migrate through the intestinal wall and are carried into the lungs.
Clinical presentations:
Pulmonary symptoms, or maybe asymptomatic, heavy infection results in colic symptoms in children and peptic ulcer like in adult. With heavy
infestation, worms may cause intestinal obstruction, volvulus. General signs are abdominal pain, multiple vomiting absence of stiool., abdominal
distention, tenderness and radiologic features.
346. Ascariasis: clinical presentation of complications, diagnosis, medical and surgical treatment
Clinical picture look above.
Please note, ascaris infection can be complicated with the following:
 Worms enter the common bile duct and obstruct it
o Treat with antispasmolytics, extracton of worm by the ampoule of vater by endoscopic retrograde cholangiopancreatography
 Perforation of intestinal wall and causing secondary peritonitis
o Wide midline laparotomy
o Exploration of intraabdominal organs
o Treat perforated organ
o Cleansing and draining of peritoneal cavity

o Suturing of surgical wound
Diagnosis:
Radiologic exam may show worms and characteristic eggs in feces.
Treatment:
Pyrantal pamoate, mebendazole
Surgically, for bowel obstruction, treatment consist of laparotomy, resection of part of the intestine and reanastamos with both ends. Enterotomy and
removal of ball of worms. Ascaris associated appendicitis is treated like normal appendicitis.
347. Amoebiasis: etiology, routes of contamination and life span, pathologic changes in the body
Due to E. histolytica
Life cycle:
 Cyst containing 4 nuclei and a central karyosome is ingested via contaminated food or water and swallowed
 Excystation occurs in small intestine due to digestive enzymes and 8 mobile trophozoites are liberated
 Trophozoites ingests RBC and also can depart from its life cycle and go to other organs like liver, it commits suicide if it does this
 Encycment occurs in colonic lumen, it is complete when all 4 nuclei are presend and the chromotoidal bars disappear. Cyst is passed out through feces
and can remain viable for up to 1 month
Pathologic changes are in intestine, the E.histolytica is presented by either cyst or mobile trophozoite. The parasite may invade wall of the colon leading
to amoebic ulcer. The ulcer is limited by muscular layer. There is signs of colitis, abdominal tenderness without peritoneal irritation. Severe cases include
multiple stool mass with blood and mucous , fever vomiting and abdominal tenderness are common
348. Amoebiasis: clinical presentation of complications, diagnosis, medical and surgical treatment
Ulcer may penetrate deeper and perforate bowel wall. Perforation of intestinal wall results in secondaty peritonitis. Clinical findings are abdominal
pain, body T increase, vomiting and hypocolemia. GIT examination shows thoracic breating, paralytic illeys, muscle guarding, and rebound tenderness
Diagnosis:
Lab, leucocytosis, maybe anemia, stool exam for amoeba and cysts serological test.
Instrumental, US, CT, endoscopy
For peritonitis,Lab changes show severe inflammation and hypovolemia, H-ray, US, CT, MRI may detect free abdominal fluid. By invasive ethods like
culdocentesis, paracentesis, diagnostic peritoneal lavage and video assisted laparascopy may be done in hard DS cases.
Treatment:
Medically, metronidazole, percutaneous aspiration
For peritonitis,Wide midline laparatomy, exploration of intraabdominal organs, treatment of perforated organ by sururing and resection, cleansing and
draining of the peritoneal cavity, suturing of surgical wound, antiparasitic agent for post operative treatement.
349. Paragonimiasis: etiology, routes of contamination and life span, pathologic changes in the body
Due to paragonimus westermani and is aka fluke worm(flatworm). The definitive hosts are human and others are carnivores(reservoir)
Organ of affection is the lungs
It passes from the git wall into the free abdominal cavity and then penetrates to the diaphragm and enters the lung parnechyme, sometimes the brain and
becomes encapsulated
Fecal oral transmission
350. Paragonimiasis: clinical presentation of complications, diagnosis, medical and surgical treatment
Clinical picture:
 Enteritis,acute hepatitis, acute abdomen
 Lung signs
 Low grade fever, dry cough, hemoptysis, pleuritic chest pain,dyspnoea, weakness, weight loss, signs of bronchopneumonia, headache,
anorexia,vomiting.
 Brain localztion causes meningeal signs
Lab. Diagnosis, is by detection of characteristic eggs in sputum, leucocytosois, eosinophilia, serological tests, chest X-ray with patchy infiltrates
Treatment:
 Medical
o Praziquantel
o Bithinol
 Surgical
o Only indicated wen drug therapy ineffective, and chronic stage of illness. It includes thoracotomy and removal of the parasite by resection of the lungs
351. Fascioliasis: etiology, routes of contamination and life span, pathologic changes in the body
F.hepatica is a treamatode affecting the liver and bile ducts. Infestation results from ingestion of encysted cercaria in water or water vegetables.
Life cycle:
The eggs passed out In the feces of definitive hosts mature in water and inside each egg a ciliated miracidium develops. On escaping from the egg, the
miracidium finds its way to its suitale intermediate host. Inside the lymph spaces of the molluscan host, the miracidium passes through the stages
Pathologic changes:
F.hepatica, passes from GIT and penetrates liver capsule. In the liver the fluke maturates and may stay in the gallbladder or biliary tree for years. Can
cause cholecistitis, cholangitis, obstructive jaundice, and liver abscess.
352. Fascioliasis: clinical presentation of complications, diagnosis, medical and surgical treatment
High fever,headache, anorexia, vomiting, liver enlargement , tenderness at upper right quadrant, anemia, leucoytosis, eosinophilia, g-globulinaemia, raise
the liver enzymes, eggs in feces, serologic tests
Diagnosis:
Diagnosis is not specific, usually obtained during surgery.
Treatment:
Bithinol, Emetine hydrochloric
353. Opisthorchiasis: etiology, routes of contamination and life span, pathologic changes in the body
Caused by O. felineus , Clonorchis sinesis is responsible for clonorchiasis. The last is endemic in area of japan, korea, china, Taiwan, and asia. Both of
them are identical clinically and epidemiologically.
O.felineus passes from the duodenum into the common bile duct through the ampoule of Vater ascending into bile capillaries where it matures and remain
throughout its life for years of shedding eggs.
Pathological changes in hepatocytes, causes hepatic changes, and hepatic fibrosis followed by chronice hepatic failure, acute pancreatitis also possible
due to entering into the pancreatic duct by fluke.
354. Opisthorchiasis: clinical presentation of complications, diagnosis, medical and surgical treatment
 Low grade fever
 Liver enlargement, tenderness at right upper quadrant
 Diagnosis is hard, but can be by following lab changes:
o Leucocytosis,eosinophila, ALT
o Characteristic eggs in feces
o Serologic tests
Treatment : praziquantel
Pre- and Postoperative period
355. definitions of preoperative and intraoperative period, postanesthesia period

 pre-op period: time btwn patient admission to hospital and start of operation
 intra-op period: time of patient btwn start and end of operation
 post anesthesia period: period of 24 hr post-op (early post-op) in which patient recovers from anesthesia treatment.
356. classification of surgical conditions according to urgency

1. emergency: op done immediately(within sev mins) eg;airway obstruction,ruture of vessels n internal organs.
2. Urgent: op done withn several days
3. Elective: op done at time convenient for surgeon n patient
357. classification of indications and contraindications to surgical operations

INDICATIONS TO SURGERY
4. life saving: emergencies
5. absolute (delay can be life threatening) eg; malignant tumor,pyloric stenosis

6. relative (optional surgery) eg; varicose veins of lower extremities,benign tumour
CONTRAINDICATION TO SURGERY
7. recent myocardial infarction
8. stroke
9. shock ( except hemorrhagic shock)
10. relative contraindications: Congestive heart failure,arhythmia,bronchial asthma,respiratory insufficiency,severe cachexia,anemia ,diabetes mellitus
358. features of patient's examination before elective and emergency surgery

Preoperative investigation (elective surgery)
 to make diagnosis, define contraindications ,urgency n type of op & min post-op risk
 done at out patient basis (before admission)
1. Clinical exam
 subjective(complains ,history) n objective exam (gen inspection,sys review,local status)
2. Lab tests
 hematological(RBC,WBC)& biochemical screens(albumin,creatin),glucose lvl,urinealisis,bl typing,serum sample for transfusion cross match,check
for hepatitis,HIV
3. Instrumental
 ECG and chest radiography in elderly receiving gen anesthesia for all but minor surgery
Preparation for emergency surgery:

correction of a shock according to general rules,
signs:
 dry mucous membrane,low bp(if bp low than 70 do not operate),l
 ow cvp(if cvs negative dun operate),
 low uo,
 hypotension
surgeons hands preparation with right sequences of washing

-gowning & gloving by scrub nurse
-prepping & dreppin(sterile drapes used to c over area that surrounds operation field)
Anesthetic monitoring devices

-cardiac monitoring device(heart rate,arterial and cvp,pulse oxymetry and body tempreture)
-Respiratory monitoring devices(respiratory parameters,including spirograph and volatile agent concentration)
359. preoperative preparation: consent to surgery, skin preparation, elimination, food and fluids
Consent for surgery and anesthesia

 -informed consent shud be taken before any sedation.
 -surgeon must explain surgical procedures and discuss potential sequrlae
Skin preparation-shave (moist or dry)
Elimination
 -rectum~ due to anesthesia rectum will dilate
 Stomach~ fasting min 6 hrs or else do stomach lavage
 Bladder~ for unable patient use folley catheter
 Valueables, attire, prostheses(dentures) shud be removed to prevent airway obstruction,mouth care and grooming
Food and fluid intake shud be limited(6 hrs fm food and 4 hrs fm fluids)
360. preoperative medication: used medicines, importance

Preop drugs
 oral short acting benzodiazepine given – reduce anxiety
 opiod analgesic (promedrol 2% 1 ml given) -2 hrs before surgery
 anticholinergic agents(atropine 0.1% 1 ml given to reduce respiratory and oral secretion) - 30 mins before surg-
 antihistaminic drug given (dimedrol 1% 1ml) given to enchance promedrol
 antiemetic maybe given (cerucal)
361. Same question as No. 358

362. degrees and assessment of surgical and anesthetic risk
ASSESMENT OF SURGICAL AND ANESTHETIC RISK
1) gen condition
 satisfactory
 moderate severity
 critical
 terminal
2) extent of surgery
 superficial operation-0.5 point
 more complex superficial op on the viscera-1 point
 prolonged traumatological,oncological,urologic op-1.5 point

 cardiac and major vascular surgeries,major reconstructive and oncological op -2 points
 complex cardiac surgery using artificial circulation ,transplantation surgery-2.5 points
3) anesthetic technique
 local anesthesia -0.5
 regional anesthesia(i.v or inhalation)-1 point
 standard combined anetsthesia-1.5
 combined anesthesia with controlled hypotension ,hypothermia,etc-2
 combineed anesthesia with artificial circulation9heart lung bypass),intensive care and resuscitation-2.5 points
summation of points:
1. 1st degree(minimal risk)-1.5
2. 2nd degree (moderate risk)-2-3 points
3. 3rd degree(significant risk)-3.5 -5
4. 4th degree(high risk)-5.5-8
5. 5th degree(extremely high risk)-8.5-11
363. intraoperative period: draping and prepping

o prepping and draping is important to prepare the operation site by proper antimicrobial regimes and techniques, making it less possible for a bacterial
invasion.
o Prepping: application of povidone iodine upon surgical area, as an antimicrobial agent
o Draping: sterile drapes are used to cover areas that surround operation field
364. role of nurses and anesthesiologic team

nurses: r valuable assistants to the surgeon:
1) pass surgical instruments, solutions etc to surgeon during a procedure
2) to manage surgical waste
3) to prepare the patient before entering operation theatre
4) main way of communication of the surgeon to other departments of the hospital during the operation
5) responsible for patient care post-op
6) fiilling up patient details, tending to patient needs.
anesthesiologist: needed alongside the surgeon to ensure smooth sailing of the operation:
1) responsible for administration of pre-op anesthesia
2) checking vitals of patient during an operation
3) maintain effifacy of peri-op anesthesia
4) observe patient recovering from anesthesia, post-anesthesia
5) responsible for pain management post-op
365. surgical operation: stages and types of surgery, monitoring

CLASSIFICATION OF SURGICAL OP
 radiative and palliative
 one stage and multistage
 simultaneous op
 microsurgical op
 endoscopic op
 roengenoendovascular surgery
 miniinvasive op
Stages of surgery
 Surgical access
 Surgical maneuver
 Closure of operative wound
Recovery fm general anesthesia
 supervised by nursing staff in area equipped with resuscitation and adequate monitoring devices.anesthetis shud be available
 for seriously ill patient,intensive care unit may be necessary until condition is stable
366. postanesthesia period: duration, patient's surveillance, monitoring

duration: during first 24h after surgery (may be said as early post-operative period)
patient surveillance : vital signs are taken at frequent intervals, assessment of general condition, inspection of dressing, surgical drainage tubes drains IV
lines.
Monitoring: pulse rate, resp. rate, BP
367. postoperative hemorrhage: types, etiology, clinical picture, diagnosis, treatment

types:
1) according to vessel: artery, venous, capillary
2) according to time of appearance: primary, reactionary, secondary
3) according to localization: internal, external
etiology:
1) primary hemorrhage: occurs at time of injury or operation
2) reactionary hemorrhage: follows primary hemorrhage within 24 hours (usu. 4.-6 hrs)
 due to slipping of a ligature
 dislodgement of clot
 cessation of reflex vagus spasm
3) secondary hemorrhage: occurs after 7-14 days

 due to infections
 sloughing of part of the wall of an artery
clinical picture:
1) signs: skin pallor, diaphoresis, facial cyanosis, weak & fast pulse, tachypnoea (chyeyne-stokes)
2) severe cases: decrease BP
3) symptoms: headache, dryness of skin n mucosa, nausea, blurred vision, malaise.
*severity and presence of symptoms depends on degree of bleeding.
diagnosis:
1) labs: full blood count – RBC, Hb, Ht, specific blood gravity
2) progressive fall in venous blood pressure: heart x receiving enuff blood due to decreased circulatory volume. ( measured using cathether from median
cubital/long saphena magna and measured at sup/inf vena cve)
3)special diagnostics: diagnostic punctures (hemothorox, hemoperitoneum, hemathrosis), endoscopy (GIT hemorrhage), Xrays, US, CT scans.
4) evaluation of clinical symptoms and signs to assess severity of blood loss.
treatment:
1) return patient to surgery for eliminate source of hemorrhage
2) pressure and packing: first aid treatment to stop and control bleeding
3) infusion therapy: FFP, packed RBC, cryo ppt,
4) oxygen therapy
5) drugs to increase vessel tone (vasopressors) – ONLY AFTER STABILIZATION OF CIRCULATORY VOLUME!
6) steroids: increase myocardial contractility & counteract peripheral vascular spasm (use only when indicated)
7) proper positioning of patient post-op and bed-rest
368. shock at the postoperative period: etiology, diagnosis, treatment

etiology: hypovolemia due to hemorrhage,
diagnosis: assessment of clinical picture, vitals: BP, PR, RR. (lab tests are often to slow to give exact results)
 Pale, clammy skin
 Delayed capillary refill
 Alteration of consciousness (mental changes)
 Tachypnea
 Tachycardia
 Low BP
 Oligo- or even anuria
treatment:
 expand bld volume
 control ongoing bld loss

 treatment of shock varies and often depends on the cause, if known-plasma expanders, parenteral fluids, oxygen, medication-adrenergics.
369. hypoxia at the postoperative period: etiology, diagnosis, treatment

etiology: inadequate supply of oxygen to recuperating patient due to: mechanical obstruction of upper resp. tract, or due to technical problems e.g.
ventilators not working properly
diagnosis: cyanosis and dyspnea
treatment: in uncounsious clients the tougue can fall back and cause obstruction the nasopharyx,pull the jaw low and insert an oropharyngeal airway,or
place the patient in side lying position.if indicated,positive-pressure ventilation can be applied with mechanical ventilat
370. vomiting at the postoperative period: etiology, treatment

etiology:
1) reflex vomiting due to recovery from general anesthesia
2) vomiting due to oro-pharynx intubation
treatment:
1) anti emetics
2) prevent the patient from aspiration or inhaling the vomits into the lungs.keep the suction machine at the bedside
3) if there is no evidence of complications and the client is fully recovered from anesthesia,patient can be returned to the unit.summarize the clients
recovery in clients chart.
371. recovery period: duration, patient's surveillance

duration: after postanesthesia period i.e. after first 24 hours after surgery until discharge of patient (can be said as the late post-operative period)
patient’s surveillance: should be closely monitored by hospital staff i.e. nurses, doctors and anesthesiologist. Vital signs should be monitored closely.
Look out for signs of post-op complications e.g. hemorrhage, shock, hypoxia etc. proper pain management should also be administered whenever needed
372. hypostatic pneumonia: etiology, clinical picture, diagnosis, prophylaxis

etiology:
1) accumulation of unexpelled mucus from patient resp. tract which promotes bacterial growth
2) nosocomial infections (secondary infection) due to weakened immune system of post-op patients
3) people at risk: patients with presenting chronic resp. diseases, the elderly
CP: fever, cough with sputum, dyspnea, malaise
D(x): spirometry, laboratory sputum exams (signs of microbial prescense), wbc count (signs of infection), X-rays
prophylaxis:
1) mucus suction from nose and mouth (in unconscious or unable patients)
2) encourage patients to cough and deep-breathe
3) change patient’s position every 2 hours

4) intermittent positive-pressure breathing is performed 2 or more times perday
5) mechanical ventilator delivering oxygen + medication (treatment mainly)
373. postoperative atelectasis: etiology, clinical picture, diagnosis, prophylaxis;

etiology:
1) accumulation of unexpelled mucus from patient resp. tract – resulting in obstruction of bronchus
2) post-pulmonary operation
3) people at risk: patients with presenting chronic resp. diseases, the elderly
CP: unconsciousness, immobility, failure to cough, cannot deep breathe
D(x): spirometry, CT scan, Xray
prophylaxis:
1) mucus suction from nose and mouth (in unconscious or unable patients)
2) encourage patients to cough and deep-breathe
3) change patient’s position every 2 hours
4) intermittent positive-pressure breathing is performed 2 or more times perday
5) mechanical ventilator delivering oxygen + medication (treatment mainly)
374. postoperative upper GIT bleeding: etiology, clinical picture, diagnosis, prophylaxis and treatment
etiology: reflux esophagitis, ruptured esophageal varices, iatrogenic injury causing damage to the esophageal mucosa (due to complications of gastric
tubes or endoscopy, esophagoscope),
clinical picture: pain, signs of blood loss (pallor, nausea, weakness), hematemesis, heartburn, secondary anemia
diagnosis:
1) labs: rbc count, hb, ht
2) endoscopy
3) xrays
prophylaxis
1) proper handling of diagnostic apparatus which passes thru the upper git
2) thorough diagnostics of the upper git to rule out possible causes of bleeding: Mallory weiss tears, esophageal varices
treatment
1) etiologic treatment: fixing the cause of bleeding
2) reinfusion therapy wherever needed
375. paralytic ileus and constipation: etiology, clinical picture, diagnosis, prophylaxis and treatment;
paralytic illeus (post operative variety) – maybe local or general, maybe accompanied by infection.
etiology :
1) failure of neuromuscular mechanism in Auerbach (myenteric) and Meissner (submucous) plexuses
2) This condition may be prolonged if there is hypoproteinemia, or latent renal failure, or if gastrointestinal suction is continued beyond the point at
which effective bowel sounds have returned
3) Complication of laparostomy
4) Hypokalemic paralytic illeus: low potassium may cause ileus (disbalance of electrolyte in pre-op patient)
5) Formation of adhesions around loops of intestines following abdominal surgery
6) Infective paralytic illeus: due to peritonitis or post-op infections of abdominal surgery
clinical picture: abdominal distension due to accumulation of gas and fluid in intestine,abdominal pain, vomiting, absent or high “tinkling” bowel
sounds, failure to pass flatus.
Diagnosis:
1) no bowel sounds on auscultation
2) no peristalsis
3) increased pulse rate
4) respiratory distress due to abdominal distention
5) palpation: rigidity
6) x-ray: air-fluid levels in intestinal loops
prohylaxis
1) routine NG suction
2) withholding fluids by mouth after laparotomy until normal bowel sounds and/or passage of flatus returns
3) maintenance of electrolyte balance pre-op (and shuld be continued post-op as well)
treatment
1) etiologic treatment: remove causative factor
2) decompression of GIT: using NG tube /cleansing enema/rectal tube
3) avoid peristalsis-stimulating drugs: the main treatment aim is to REST the GIT, not to STIMULATE it.
Constipation: inability to pass stools easily/ at all.

Etiology: solid food, inactivity, diet, narcotic analgesics
Clinical picture: pain in passing stools, blood in stools, abd discomfort, signs of intoxication
Diagnosis: us, xray (see hard stools in colon)
Prophylaxis: ambulation, walking, change of position, some dietary limits (with hi amt of fibres, vege oils,laxatives)
Treatment: cleansing enema. To relieve gas: rectal tube for 20 mins.
376. control of postoperative pain: types, medicines, complications, duration

types, medicines: Analgesics may be used to relieve pain :-
o narcotic – morphine,meridipine(Demerol)
o non narcotic – aspirin,naproxen, ibuprofen (group of nsaids)
Precautions
-morphine depresses respiration
-Meperidin – decrease BP:
-the pain may be caused by the incision and other coexist disorders or complication – take measures to control it;
Duration: There is no set limit on how long after surgery narcotic analgesics are made (it depend on the type,extend of surgery and on the client)
377. postoperative DVT: etiology, clinical picture, diagnosis, prophylaxis and treatment
etiology
1) major surgeries (hi-risk) – orthopedic surgeries, pelvic, hip, low extremity surgeries/trauma.
2) patient factor: history of DVT/pulmonary embolism, over 40 yrs old, on oral contraceptives
clinical picture: swelling, pain, redness, dilated superficial veins, low grade fever
diagnosis
1) duplex scan
2) Doppler US
prophylaxis:
1) early mobilization
2) low-dose SC heparin
3) compression stockings
treatment
1) medications: thrombolytics
2) embolectomy
378. postoperative pulmonary embolism: etiology, clinical picture, diagnosis, prophylaxis and treatment
etiology:
1) dislodgement of venous thrombi usu. From lower extremities’ veins (after surgery on lower extremity veins)
2) fat embolus from multiple trauma (surgical iatrogenic injury)
3) tumor embolus (attempt to remove tumors e.g. renal carcinoma)
4) amniotic fluid emboli (post-partum complication)
clinical picture:
1) pleurisy + pleuritic pain
2) hemoptysis
3) chest pain
4) acute Shortness of Breath (SoB)
5) R-heart failure – raised CVP, tachycardia, low CO,
6) Patient prefers to lie down flat (severe cases)
Diagnosis
1) instrumental: US, CT, Xray, angiography
2) blood gas analysis: low Po2, PCo2
prophylaxis:
4) early mobilization
5) low-dose SC heparin
6) compression stockings
treatment
1) small emboli: systemic heparinisation, then oral-anticoags (warfarin). For recurrent emboli: inferior vena caval filter
2) large emboli: thrombolytic agents to increase RV filling, Oxygen admin thru face mask, IV heparin, pulmonary embolectomy
379. postoperative fever: etiology, approach in diagnosis and management

etiology aseptic inflammation,intake(absorbtion of blood and other).a significant rise in temperature may indicate infection
diagnosis: err...thermometer? oh yes – and also check for possibilities of infection (signs of other infection maybe a contaminate wound + pus, do WBC
count to confirm diagnosis.
Management
1) etiologic treatment: find cause of infection and do sumthing abt it
2) symptomatic treatment: antibiotics, antipyretics
380. removal of skin stitches: time frame
381. postoperative fluid volume deficit: etiology, clinical picture, diagnosis, prophylaxis and treatment
(hypovolemia)
etiology: npo restriction, intra-op bleeding causing fluid loss, insensible git, resp. losses, 3rd space sequestration of fluid.
Clinical picture: dry mucus membranes
Diagnosis: blood count (Ht increased), urine output, assessment of clinical picture
Prophylaxis & Treatment: proper fluid management
382. postoperative fluid volume excess: etiology, clinical picture, diagnosis, prophylaxis and treatment
(hypervolemia)
etio: renal failure, CHF, high sodium intake, excessive parenteral admin or oral intake of large amt of water (rapid admin of NS)
clinical picture: peripheral edema. In severe cases ascitis n pulm. Edema may devt.
Diagnosis: assessment of clinical picture, TBC.

Prophylaxis & treatment: proper fluid management
383. Nutrition of patients after GIT surgery

Assessment of nutritional status:-
1. history and physical examnation-weight loss,anorexia,vomiting,diarrhea,edema and ascitis
2. laboratory markers-serum proteins(N=65-85g/l)
3. nutrional requirements: most patients at rest require 25-35 Kcal/kg/day=3.000kkcal
4. stress significantly increases those values,by fever ,infections,burns,surgery,trauma.
5. nutrional supplementation is necessary for those in whom the surgery may delay oral intake for at least 7-10 days
384. reasons and prophylaxis of impaired postoperative wound healing

Skin integrity and activity
o Delayed healing is possible at some patients(poor blood supply)
o Symptoms of impaired circulation: swelling,coldness,absence of pulse,pallor or mottling.
o Ambulatory activity often are started shortly after surgery.if the patient confined to bed there is a risk of skin breakdown(bed sores),especially in
elderly and debilitated patients.
Prevention:-
-earlyy ambulation,meticulous skin care, frequent change of patients position.
When change dressing moisten the area with saline( because the gauze has adhered to tissue)
Care or postoperative wound

Montgomery straps allow access for changing a dressing without removing and reappling tape each time
385. wound disruption: types, reasons, prophylaxis and management

Post operative wound disruption
Dehiscence
Evisceration
o These complications most likely to occur between the 6th and 8th post operative days
Predisposing factors
o Malnutrition
o Defecting suturing
o Strain of the wound: coughing,sneezing, hiccupping
o Extensive obesity
o Infection
Diagnosis can be done during inspection of the wound. Measures-place the patient in complete rest and place sterile dreesing moistened with saline over
the produting organs. Closure of the wounds may require surgical operation.
386. postoperative urine retention: etiology, clinical picture, diagnosis, prophylaxis and treatment
etiology: urination disturbances frequently arise after abdominal(lower) and pelvic region surgery and caused by operative trauma
clinical picture: restlessness ,pain in the lower abdomen ;
diagnosis: distension of the area just above the symphysis pubis.
387. postoperative wound infection: etiology, clinical picture, diagnosis, prophylaxis and treatment
etiology
1) inadequate sterilization and disinfection measured carried out pre-op
2) failure to maintain sterile conditions throughout the operation
3) failure to admin protective dose of antibiotics to pre-op patient
4) failure to maintain adequate anti-microbial regime post-op
clinical picture: signs of infection and inflammation
1) general: fever, malaise, weakness
2) local: hyperemia, inflammation, swelling, exudation+pus, pain
diagnosis
1) full blood count: leucosytosis, increased ESR
2) microbiological study of pus – determine which causative agent
prophylaxis
1) adequate hygiene and preventive measures pre, peri and post operations.
Treatment
1) surgical: cleansing, debridement (wherever applicable)
2) medical: antibiotics (depending on which causative agent)
388. management of tubes and drainages: types, care and monitoring

tubes and drainages:

1) drainage tubes: foley catheters, rubber tubes for fluid drainage from operation sites etc
2) feeding tubes: NG tube, percutaneous endoscopic gastrostomy tube etc
care:
1. proper cleaning and necessary measures to prevent bacterial contamination
2. changing of tubes accordingly: not to be attached longer than the time limit indicated.
3. proper drainage placement so as to not be a hazard to anybody i.e. to patient, medical personnel
4. rate of administration fluids should be constant and suitable as to not cause any complications
monitoring: monitor signs of infection, changes in blood composition, local signs of irritation (site of tube entry), and vitals as well (RR,BP,PR)
389. central venous catheter complications: care and monitoring

complications:
1) air embolism
2) pneumothorax
3) injury to vena subclavia, brachial plexus
4) infection, septicemia
care:
- proper care to prevent bacterial contamination
- careful execution of cathether placement – prevent unwanted injuries
monitoring: not sure – but its supposed to be diagnostic measures to rule out the complications.
390. aspiration pneumonia: etiology, clinical picture, diagnosis, prophylaxis

etiology:
1) post-op vomiting (due to recovery from anesthesia), then aspirated into lungs with microbes
2) complication of Oro-enteric tubes
clinical picture: dyspnoea, cough, fever, pain in chest (sometimes),
diagnosis: xrays, laboratory sputum tests
prophylaxis:
- avoid oro-enteric tubes (use NG tubes wherever possible)
- prevent aspiration of vomitus (dunno how.)
391. reasons of malnutrition, assessment of nutritional status

reasons of malnutrition:
1) preoperative malnutrition: due to starvation or to a failure of digestion –
 difficulty in obtaining food (poverty)
 difficulty in swallowing food (dysphagia)
 difficulty in retaining swallowed food (vomiting)
 self-neglect (elderly, anorexics, alcoholics)
2) postoperative malnutrtition: transient nature due to short period of starvation and stress reaction to trauma
3) hypercatabolic state: in cases of severe sepsis (subphrenic abcess), severe trauma (burns), sever disturbances of major viscera (pancreatitis) – all of
them causing accelerated breakdown of tissue proteins
assessment of nutritional status:
weighing of body weight: BMI should be assessed
upper arm circumference: feeding is indicated in males if <25 cm, females if <23cm.
triceps skinfold thickness: minimum in females 13mm, males 10 mm
serum albumin levels: should be no less than 35g/l
lymphocyte count: less than 1500/mm3 indicates impaired cellular defence mech.
candida skin test: (-)ve reaction indicates impaired cell defence mech
nitrogen balance studies: must be (+) Nitrogen balance (anabolism tissue synthesis)
392. caloric and nutritive requirements, need for nutritional support

caloric and nutritive requirements:
 a healthy diet is needed with all the necessary amt of carbs, fats, proteins, vitamins, minerals, trace elements and water.
 Energy: provided by carbs and fats. Energy requirements depend on each individual needs and conditions
 Nitrogen requirements: necessary to keep a (+) Nitrogen balance (intake of 35-40g of protein per day for a normal healthy person. Hypercatabolics
need 3-4X more of this amt)
 Vitamins:
o Vit B & C = wound healing, collagen formation
o Vit B12 (500 microgram IM weekly)= given to patients with low levels of this vitamins
o Folate (3-6 mg IM daily) = esp. for those on parenteral nutrition
o Vit K (5-10 mg IM weekly)= enhances anticoagulative powers, reduces bleeding tendency
o Citamin ADEK = reduced in absence of bile, steatorhhea
o Vitamin A (5000 IU/week) = helps increase anti-tumor effect of cyclophosamide (for tumor patients
need for nutritional support
post-op patients sometimes need nutritional support especially when suffering from malnutrition or else complications such as poor wound healing
manifest as:
 wound dehiscence,
 leaking anastamoses of bowel,

 delayed callus formation,
 disordered coagulation,
 reduced enzyme synthesis,
 impaired oxidative metabolism of drugs by liver,
 immunological depression + increases susceptibility to infection
 decreased tolerance to radiotherapy and cytotoxic chemotherapy
indications for nutritional support are:
1) pre-op nutritional depletion
2) post-op complications: illeus more than 4 days, sepsis, fistula formation
3) massive bowel resection
4) management of: pancreatitis, malapsorption syndromes, colitis, entereitis, pyloric stenosis
5) anorexia nervosa
6) burns
7) malignancy
8) renal failure
9) hepatic failure.
393. enteral nutrition: types, advantages, disadvantages, indications, and complications.

Types: enteral nutritional support may be provided via:-
a) oro-enteric route
b) naso-enteric tube
c) direct enteric routes(gastro,jejunostomy)
Advantages: provides natural way of nutrition for the body i.e. thru the GIT (will stimulate usage of GIT and its more natural for the body to assimilate
food)
Disadvantages contrindications to enteral feeding
 mesenteric ischemia
 bowel obstruction
 intra-abdominal sepsis
 necrotizing pancretitis
 high output GI fistula
Indications
b) intact functional gastro-enteral tract
c) unable to eat
d) sever oropharingeal,facial trauma

e) swallowing abnormalities
f) oral or upper GI obstruction
complication
 placement of tube into trachea,bronchus
 intraabdominal injury during placemaent of gastro, jejunostomy
 aspiration
394. parenteral nutrition: indications, contraindications, advantages, disadvantages, and complications

indications: when other forms of nutrition is contraindicated or unavailable due to circumstances e.g. major GIT surgery
contraindications: affection of veins, coagulation problems in the patient,
advantages:
 the only way of nutrition where other forms of nutrition support are contraindicated
 management of both nutritional and fluid need of patients through one IV line
disadvantages
 venous access need to be changed often to prevent clotting onto tube
 not a natural way of nutrition for the body
 changes ph of blood
complications
1) thromboplebitis
2) thrombus formation
3) infection at site of insertion of tubes.
395. option of solutions for parenteral feeding, general scheme
TOTAL PARENTERAL NUTRITION

 indicated in patients who require nutritional support when GIT is not available or nonfunctional
A. protein solutions
B. dextrose solutions (D40W)
C. fat emulsions(10% - 20% solution iv lipids)
guidelines:
1. calculate volume requirements
2. calculate total daily calorific needs

3. determine % of proteins carbs n lipids
4. add electrolytes n trace elements
 if renal insuff. Is present proteins shuld be limited (to improve nitrogen balance)
 with liver disease – rich in branched chains amino acids (to be metab. By skeletal muscle) and low in aromatic aa’s (bcoz they burden liver: metab in
liver)

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Suggested Answers for General Surgery Final Examination 2008 1

Non Operative Surgical Techniques

3. Arterial access: indications and contraindications, procedure, complications

Preference of the arteries: Radial → Ulnar → Femoral → Dorsalis pedis → Axillary;

Procedure (E.g. Radial artery cannulation)

Complications: ischemic digits (remove the catheter), thrombosis, septic complications.

Swan Ganz Cathether (pulmonary artery catheter)

Contraindications: vein thrombosis, severe pulmonary hypertension, coagulopathy, ongoing sepsis.

Localization of the catheter should be confirmed by X-ray at least once daily.

Intraaortic balloon pump counterpulsation (IABPC).

Procedure: IABPC insertion.

5. Bladder puncture and laparocentesis: indications and contraindications, procedure, complication

Contraindications: skin infection, previous abdominal surgery (adhesions), pregnancy, coagulopathy.

7. Pericardiocentesis: indications and contraindications, procedure, complications

b) Post coronary bypass surgery because of risk of injury to grafts.

8. Thoracentesis and thoracostomy: indications and contraindications, procedure, complications

Thoracentesis is used to evacuate an effusion from the pleural cavity :

Complications: intercostal vessel damage (hemothorax), pneumothorax, lung injury.

Antisepsis and Asepsis

Types of closed drains

New cephalosporins (fourth generation) : cefepime, cefpirome.

Generally they are administered 2 times a day, 3 times in severe cases

Initial systemic antibacterial therapy

Risk patients: Advanced age, malnutrition, preexisting diseases.

In administering an antibiotic, we need to consider these factors:

Development of drug resistance.

Measures oriented on reduction of possibility of preoperative cross-infection

Measures oriented on reduction of possibility of cross-infection in theatre

I. Sterilization of reusable surgical instruments, dressing materials, etc.

II. Surgeon’s hands preparation (scrubbing)

III. Operation site.

12. Sterilization (complete characteristics of all stages and types.)

I. Preparation of materials (cleaning).

Solution A: perhydrol – 20g; washing detergent – 5; water 975 ml;

d) Instruments were used to operate a patient with anaerobic infection:

Arrangement and package for sterilization

Self-keeping of sterilized materials.

Gowning and Gloving

Gowning by own self Gowning by scrub nurse

Prepping and drepping

14. Common disinfectant and antiseptic agents: general characteristic.

15. Hemorrhage: Pathophysiologic changes, classifications, clinical picture

Pathophysiologic changes that occur are:

ii. According to area of bleeding – Internal, External

In Class I hemorrhage, In Class II hemorrhage In Class III hemorrhage

Class I Class II Class III

Treatment is oriented on achieving 2 primary goals

17. Hemorrhage: Replenishment of circulating volume

18. External and internal hemorrhage: Clinical picture

19. Hemoperitoneum: Etiology, Clinical picture, Diagnosis

Auscultation: Decreased bowel sounds (Paralytic ileus)

20. Hemothorax: Etiology, Clinical picture, Diagnosis

21. Hemopericardium: Etiology, Clinical picture, Diagnosis Diagnosis can be established by

22. Hemarthrosis and hematoma: Clinical picture, Diagnosis

23. Temporary and permanent methods of hemostasis.

Mechanical methods  Vascular anastomoses.

Chemical and biological methods  Cryoprecipitate, fibrinogen

 Concentrated definitive factors are used at states of deficiency of  Trasilol (biologic)

Coagulation disturbances of surgical patients