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ACUTE PURULENT INFECTION OF THE SEROUS CAVITIES, VESSELS, BONES, JOINTS. PUTREFACTIVE INFECTION
PURULENT INFLAMMATION OF THE SEROUS CAVITIES
Purulent meningitis — inflammation of the brain membranes caused by purulent microflora (staphylococcus, streptococcus, E.coli, pneumococcus). Purulent meningitis, as a rule, is a secondary process caused by penetration of microflora into the subarachnoidal space during traumas to the skull (fracture to the calvarium or basis) or during purulent diseases of the ear, nose and paranasal sinus, brain abscess burst. Hematogenous or lymphogenous bringing of the infection is less often observed.
Clinical picture. According to the course meningitis is divided into traumatic, otitic, hematogenous, lymphogenous. The disease symptoms are intolerable headaches, high temperature, rigidity of the occipital muscles, positive Kernig’s symptom, nausea, vomiting. Impairment of consciousness (inhibition) down to full loss is observed. The characteristic pose of the patient — lies on his side with legs pressed against the abdomen and the head leaned back. Hypertension of the skin sensitivity and increase in tendon reflexes are marked. Along with the changes in the blood (leukocytosis — left shift, increase in ESR) a big diagnostic value has the data from the spinal puncture: liquid flows out under high pressure (400–500 mmH2O) and contains a significant amount of protein, leukocytes, bacteria. The disease course is characterized by fast deterioration of the patient’s condition, growth of intoxication. Lethality is from 50 to 70%.
Treatment. The earlier treatment the more successful results. In the early stage, conservative therapy is indicated: repeated lumbar punctures, endolumbar antibiotic therapy. Along with antibiotics, antiseptics, sulfanilamides (preparations of metronidazole, dioxydine, etazol, sulfalen) are entered intravenously, intra-arterially. Surgical treatment provides an early exposure of the focus of the inflammatory process and removes purulent exudate (incision of the paranasal sinus, purulent mastoiditis, brain abscesses, and infected wounds of the skull).
Purulent pleurisy. Purulent pleurisy or pleural empyema — inflammation of the pleura caused by pyogenic infection (staphylococcus, streptococcus, pneumococcus, enterobacteria). As a rule, it is a secondary process. It develops during burst of the abscess of the lungs, pneumonia complicated by the abscess, traumas to the thorax, costal osteomyelitis. Less often the infection is brought by the hematogenous (sepsis, deep phlegmons, hematogenous osteomyelitis) or the lymphogenous way (appendicitis, cholecystitis, pancreatitis). There are different classifications of acute pleural empyema:
after the causative agent (staphylococcus, streptococcus, diplococcus, etc.);
after the location of pus (free — total, moderate, mild; sacculated — multichamber, one-chamber);
after the pathoanatomical characteristic (purulent, putrefactive);
after the clinical course (septic, severe, moderate, mild).
Clinical picture. Displays of purulent pleurisy accumulate on the attributes of the basic disease (pneumonia, abscess of the lungs, etc.). The clinical picture is characterized by the occurrence of strong stabbing pain in the thorax, which amplifies during cough and breathing. Increase in the body temperature up to 39–40°C, occurrence of dry cough, dyspnea, cyanosis of the skin. The patient takes a bent position; the damaged side is delayed during breathing; intercostal spaces are smoothed; vocal tremor is weakened. In the initial stages, pleural friction rubbing, diminished breath sounds are determined. With the accumulation of pus in the pleural cavity, the clinical picture becomes precise. With the help of percussion and auscultation, attributes, which specify the accumulation of liquid in the pleural cavity, the height of its level, and the shift of the mediastinum appear. The line of dullness in the back is usually higher, in front — lower (Damoiseau’s line). Higher than the dullness in the paravertebral zone, a clear pulmonary sound is determined (Garland’s triangle), which corresponds to the contour of the lung. With significant accumulation of liquid, the mediastinum shifts to the healthy side, which is determined as a blunt triangular form from below the vertebrae (Grocco—Rauchfuss’s triangle).
During radiological examination, homogeneous shadow of the pleural cavity, the level of liquid, and the shift of the mediastinum are determined, and with the presence of a putrefactive process — an air bubble above the liquid. The pleural puncture allows to determine the character of the exudate and conduct bacteriological research. During sacculated processes, thoracoscopy with following drainage of the accumulated pus is conducted for diagnosis sometimes.
Treatment is begun with therapy of the primary process (pneumonia, abscess of the lungs, etc.). All methods of treating empyema have the purpose of providing evacuation of the exudate, spreading the lungs and reducing intoxication. The methods of treatment are divided into closed and open. Closed: repeated punctures of the pleural cavity, entering drainage through a small puncture (cut) with constant aspiration of exudate. After removing the pus, washing with antibiotics the pleural cavity has negative pressure, which promotes the decomposition of the lungs. Constant aspiration of exudate can be carried out with the help of the Subbotin—Peters’s triampullary systems by or a water-jet vacuum pump. The pleural cavity is washed out with antiseptics (furacilin, dioxydine, chlorhexidin) with the following introduction of proteolytic enzymes (for the lysis of fibrin, dense pus) and antibiotics taking into account the sensitivity of microflora.
With the development of massive accretions (sacculated processes) and the presence of fibrin masses, the efficiency of the closed methods of treatment is not high. They resort to the open method — thoracotomy with wide opening of the pleural cavity, evacuation of pus and fibrin clots, liberation of the lungs from accretions (decortication), resections of the damaged segments or a part of the lung (with gangrene) with following pleural drainage. Along with surgical methods, detoxication of an organism (intra- and extracorporal methods), immune and antibiotic therapy (intravenous, endolymphatic introduction) are widely used.
Purulent pericarditis is a purulent inflammation of the pericardium, very seldom primary (tubercular, gonococcal), more often secondary. It develops as complication of the heart wound or as the result of lymphogenous bringing of infection during different diseases (purulent pleurisy, pulmonary abscess, rheumatism, scarlet fever, phlegmon, osteomyelitis). Causative agents: staphylococcus, streptococcus, tubercular bacillus, etc.
Clinical picture. Attributes of general intoxication and phenomena connected with the difficult work of the heart as the result of the accumulation of inflammatory secretion in the cardiac sac. High temperature, facial cyanosis, swelling of cervical veins are marked. The patient is disturbed with pain of compressing character behind the sternum, dyspnea, and attacks of palpitation. The patient takes a compelled position (semi-sitting). With percussion the heart borderlines are dilated. With auscultation in the early stages — pericardial friction rub, and with the presence of exudate — acute dullness of the cardiac tones. Radiological exam reveals an intensive triangular enlargement of the cardiac shadow with the disappearance of the weist of the heart. An auxiliary method of diagnosis is the exploratory puncture of the pericardium. The intoxication phenomena, changes in the blood (left shift leukocytosis, increase in ESR) join early. Lethality is high because of complications (cardiac weakness as the result of adhesions between the myocardium and pericardium, sepsis).
Treatment. With the help of a functional bed, the patient is put in a semi-sitting position; cardiac substances, antibiotics, antiseptics are given. There are two methods of local treatment: conservativesurgical (repeated punctures of the pericardium to remove the pus) and surgical (pericardiotomy). For conducting the puncture of the pericardium, today the safest is the Marfan’s method (a needle is injected near the basis of the xiphoid process to the left at the place of junction with the cartilage of the VII rib). The pus is aspirated from the pericardium and antibiotics are entered (semisynthetic penicillins, cephalosporins). With the absence of effect after carrying out 3–4 punctures and the deterioration in the patient’s condition they resort to pericardiotomy — openning of the cardiac sac and creation of a constant drainage of the pus. With adhesive pericarditis and the development of the stone heart phenomena, pericardectomy (resection of the pericardium) is indicated.
Purulent peritonitis — inflammation of the serous covers of the abdominal cavity, caused by diverse microflora (E. coli, staphylococci, streptococci, pneumococci, mixed infection). Peritonitis, as a rule, is a secondary process, which develops as a complication of diseases of the abdominal organs (pyesis, gangrene, perforation) or their wounds, as well as the result of infection of the abdominal cavity during surgery. Less often the infection penetrates the abdominal cavity hematogenously or lymphogenously.
Peritonitis is divided:
after the aetiology: E.coli, staphylococcus, streptococcus, mixed,and also nonspecific and specific (tubercular);
after the mechanism of occurrence: perforational, traumatic,postoperative, hematogenous, cryptogenic;
after the type of exudate: serous, serous-fibrinous, purulent, putrefactive;
after the prevalence of the process: local (limited), diffuse(spread), general;
after the phase of the process: reactive phase (1st day), toxicphase (2nd–5th day), terminal phase (after the 5th day); 6) after the clinical displays: acute and chronic.
Local peritonitis is damage to a certain area of the peritoneum with restriction from free abdominal cavity by adhesions, accretions, internal organs. Diffuse (spread) peritonitis is characterized by the spreading of the process into the abdominal cavity without precise borders, affecting different parts of the abdominal cavity. General peritonitis is an inflammatory process of the entire abdominal cover.
Clinical picture. Taking into account secondary peritonitis, attributes of the disease, as a rule, accumulate on the clinic of the primary process. The very first attribute is pain in the stomach, intensity of which can be different: dull, gradually increasing, and during perforation of a hollow organ — acute, knife-like. Localization of the pain can be different and depends upon the prevalence of the process (appendicitis, cholecystitis). During diffuse or general peritonitis, the pain spreads onto the anterior abdominal wall and becomes constant. These attributes of peritoneal irritation appear early: nausea, vomiting, swelling of the stomach, pressure of abdominal muscles, Shchotkin—Bluberg’s symptom. The given symptoms are characterized by pain increase during palpation of the stomach, at the moment of sharp lifting the hands from the abdominal wall. Strain of the stomach muscles is a very typical symptom that appears already on the initial phase of peritonitis. With local processes, it is determined above the center of damage, during diffuse and poured peritonitis — on the whole anterior abdominal wall. Expressiveness is different, including “disk-shaped belly” with perforation of hollow organs.
Spread forms of peritonitis are characterized by paresis of the GIT that appears as a decrease or full absence of peristalsis, meteorism, swelling of the belly, retention of gases and urination. Vomiting in the initial phase is characterized by stagnant contents, and in the terminal — faecal. Effusion appears in the abdominal cavity, especially with spread forms, which appears during percussion (dull sound in the sloping areas) and palpation (fluctuation with significant amount of free liquid). In the aged patients, signs of peritonitis are frequently vague. For specification of the diagnosis, additional methods of inspection are applied: radiological, ultrasonic, “searching” catheter method during laparocentesy, laparoscopy, endoscopy. With peritonitis, endotoxicosis is observed too early, the basic pathogenetic moment of which is adsorption of a significant amount of metabolism toxic products, microbic toxins into the blood from the abdominal cavity. Endotoxicosis grows progressively in time, starting from the 2nd day of the disease, and is the main cause of high lethality (in the terminal stage — up to 60%). Endotoxicosis causes significant infringement of the function of vital organs: the heart (pronounced tachycardia of 100–140 per minute, hypotension, decrease in the color index, acrocyanosis), the lungs (dyspnea, stagnant pneumonia, hypostasis of the lungs), the liver (hepatopathy, parenchymatous jaundice phenomena), the kidneys (nephropathy, oliguria, anuria, uraemia), the brain (encephalopathy, headaches, sopor, intoxication delirium). Because vomiting in the terminal stage, significant infringement of the acid-base condition (metabolic acidosis), desiccation are observed.
The patient’s appearance in the terminal stage, described by Hyppocrates, is very characteristic. The patient takes a compelled position, bent at the knee and hip joints. Features of the face are sharp, hollow eyes, grey skin, dry mucous, dry tongue with fur. The abdomen does not participate in respiration. Peritonitis can be complicated by the development of sepsis, the formation of abscesses of the abdominal cavity (subphrenic, subhepatic, interintestinal), eventration of the intestines, intestinal fistula, which considerably influence the outcome of the disease. Nevertheless, the principal cause for high lethality (with spread forms of peritonitis) is endotoxicosis with the development of multiple organ failure syndrome (MOFS).
Treatment. If diagnosis of peritonitis is confirmed, the patient is subject to emergency surgical treatment (within 2–3 h). Contraindications to the operation: pre-agonal condition with acute haemodynamic infringements. The peritonitis treatment should be complex and include the following actions: liquidation of the source of peritonitis and action on the microflora; endotoxicosis therapy.
In non-pronounced diagnostic cases before the operation it is not recommended to apply drugs, antiemetic substances, siphon and cleansing clysters, which can worsen the patient’s condition. Operative help mostly consists of median laparotomy, which allows examining the abdominal organs for revealing and liquidating the source of peritonitis (suturing the perforating ulcers, appendectomy, removing the biliary bladder, etc.). After liquidating the source of widespread forms of peritonitis, they remove the exudate and wash the abdominal cavity with antiseptic solutions. The operation is completed with introducing through certain counterapertures into the abdominal wall polyvinylchloride (rubber) drainages to the areas of possible exudate accumulation (subphrenic or subhepatic space, right and left iliac sites, pelvic cavity). The wound median is sutured tightly. In pronounced cases of peritonitis, they apply open management of the median wound with liquid sutures (laparostomy), which gives an opportunity for dynamic control over the process condition in the abdominal cavity.
With limited peritonitis after removing the exudate, peritoneal lavage is not conducted in order not to entail spreading the infection into the abdominal cavity. Thus the cellular inflammation is drained. With general peritonitis in the postoperative period for reduction of intoxication and infecting the abdominal cavity, many surgeons apply constant or fractional washing of the abdomen with antiseptic solutions (peritoneal dialysis). The entering of antiseptics is conducted through top drainages, and the removing — through lower ones (5–10 l of solution).
Liquidating the intestinal paresis has great value when fighting endotoxicosis. With the purpose of liquidating the paresis they apply medicamentous (neostigmine methylsulfate, eserin, kalymin, pituitrin, etc.) and intestinal electric stimulation, warming the abdomen (solux), hypertonic clysters. In order to reduce the paresis and intoxications they remove the contents of the GIT (intestinal decompression). Intestinal decompression is carried out by introducing perforating one- and two-opened tubes (2–3 m in length) through the mouth to the level of the empty intestines. It is usually carried out during the operation. With progressive peritonitis, operative ways of intestinal decompression are used (enterostomy, appendicostomy, colostomy).
In order to influence the abdominal microflora, they apply antiseptics (dioxydine, chlorhexidine, dimexide, biseptol) and antibiotics with taking into account the microflora sensitivity (polysynthetic penicillin, aminoglycosides, cephalosporin). The way of introduction is intraperitoneal, intravenous, intraarterial, endolymphatic. For endotoxicosis correction and with the purpose to normalize homeostasis, besides of peritoneal irrigation and dialysis, they apply intracorporal detoxification: forced diuresis (lazex, manitol), haemoinfusion and endolymphatic detoxification (haemodes, polymisin formation, albumine), enterosorption (sorbents, carbovit), and intravascular laser irradiation of the blood. With deep forms of endotoxicosis with hepatic and renal insufficiency, extracorporal methods of detoxification are indicated: ultra-violet irradiation of the blood, lymphosorption, haemosorption, plasmosorption, plasmapheresis, emodialysis, haemofiltration, hyperbaric oxygenation. With widespread forms taking into account infringements to the immune status and the development of secondary immunodeficiency, they apply replaceable immunotherapy (fresh-citrate donor blood, gamma-globulin, hyperimmune plasma, leukomass) and immunity stimulators (decaris, daucifon, thymalin, T-activinum, timogen, myelopeptide).
Phlebitis, thrombophlebitis. Phlebitis is an inflammation of the venous wall, during the phenomena thrombogenesis is called thrombophlebitis.
Aetiology and pathogenesis. It is caused by diverse microorganisms, more often staphylococci. Damage to the venous wall can occur during the presence of neighboring inflammatory processes (erysipelas, phlegmon) or the infection is brought through the blood or lymph by the unleashed cells. Change in the vascular wall, chemical compound of the blood, delay in blood circulation and infringement of the coagulation system have crucial importance.
More often the veins of the lower extremities are affected. Thrombophlebitis is observed twice as often in women. First inflammatory infiltration of the vascular wall, which results in vascular spasms, occurs. It, in turn, promotes the delay of blood circulation, and the formation of a blood clot. The spasm, thrombosis of the veins results in the increase in pressure in the veins and capillaries that causes an increase in vascular permeability and hypostasis of the extremities.
Clinical picture. Thrombophlebitis of the deep and hypodermic veins is distinguished. By the clinical course: acute, subacute and chronic stages of thrombophlebitis.
Acute thrombophlebitis of the deep veins of the hip is characterized by strong pain along the way of the vascular bunch, increase in temperature (39–40°C ), and the development of hypostasis of the extremity. The skin on the sick extremity is shiny with a cyanochroic marble shade, cold to the touch as compared to the healthy one. As a result of spasm in the main arteries, the pulse on the damaged extremity is absent or less than on the healthy one. During acute thrombophlebitis of the hypodermic veins, pronounced morbidity along the veins, hyperemia of the skin as a cord or separate inflammatory infiltrations are marked. Acute thrombophlebitis can transform into purulent one with the occurrence of numerous abscesses and phlegmons by the damage course, deterioration in the general condition (fever, intoxication), in case of an abscess burst into the blood system septicopyemia arises. More often acute thrombophlebitis transforms into subacute or chronic forms. Thus, the general condition suffers a little, infiltration is determined along the veins, with loading — morbidity and hypostasis of the legs.
After thrombophlebitis course, chronic venous insufficiency develops (hypostasis of the shin and feet, etc.), joined by trophic failure (dryness and pealing of the skin, varicose ulcers). It is especially necessary to allocate migrating thrombophlebitis (Buerger’s disease) during which mainly the superficial veins of the upper and lower extremities are involved. The process is frequently accompanied by endarteritis. Mainly young men are affected. The general condition suffers a little. Along the superficial veins, less-painful nodules appear with hyperemia of the skin and swelling. The process can last for years, periodically recurring.
Treatment for thrombophlebitis, basically, is conservative. Therapy should be directed on decreasing the hypercoagulation phenomena, acting on blood clots and improving microcirculation of tissue. With this purpose they apply anticoagulants of direct and indirect actions (heparin, dicumarin, phenilin, syncumar), thrombolytic means (streptokinase, fibrinolysin, trypsin, chymotrypsin, thrombolytin), preparations which improve microcirculation and reduce aggregation of erythrocytes, thrombocytes (rheopolyglucin, haemodes, haemplasmin, trental).
With the acute process, the patient is appointed strict bed regimen with raised legs, warm and physiotherapy (solux, UV irradiation), ointment bandages on the damaged legs during the formation of a blood clot. With unsuccessful conservative therapy (ascending septic thrombophlebitis in varicose veins), they resort to surgical treatment. Legation, incision of veins along the veins with removing the damaged area (venectomy), removing a blood clot (thrombectomy), transplantation and plastic operations on the veins belong to surgical treatment. With limited purulent thrombophlebitis, incisions with opening the vein are applied and treating by the type of purulent wound or removing the damaged vein.
Lymphangitis is a secondary inflammation of the lymphatic vessels, which occurs as a complication of pyoinflammatory diseases (furuncule, anthrax, abscess, phlegmon, panaritium, infected wound). Causative agents: staphylococci, streptococci, E. coli, proteus. Microorganisms from the inflammation focus penetrate into the lymphatic capillaries and farther with the lymph flow — into larger lymphatic vessels and lymph nodes.
Clinical picture appears locally (pain, local rise in temperature, swelling, reddening) and generally (fever, headache, sweating, general weakness, increased leukocytosis). Local displays depend upon the type of the vessel. With reticular lymphangitis, pronounced hyperemia of the skin, similar to erysipelatous but without precise borders is marked. With stem lymphangitis — hyperemia as separate strips from the inflammation focus to the regional lymph node zone. The lymph nodes are affected early in the process — regional lymphangitis occurs. Complications: phlegmon, abscess, thrombophlebitis, sepsis.
Treatment should be directed on the liquidation of the primary focus (lancing of abscesses, drainage). A damaged leg is in a raised position, sometimes immobilized. Antibiotic therapy is appointed with taking into account the kind of microflora and its sensitivity.
Lymphadenitis — inflammation of the lymph nodes occurring as a complication of different purulent diseases and specific infections (tuberculosis, actinomycosis, plague, etc.).
Acute and chronic, specific and nonspecific lymphadenitis are distinguished. The infection gets from purulent or specific cells through the lymphatic or blood vessels to the lymph nodes. The primary process is seldom observed during wounds or infected lymph node. Depending upon the exudate character, it can be serous, haemorrhagic, fibrinous, or purulent. Purulent processes result in the destruction of node’s tissue and transition of the inflammation to the surrounding tissue with the development of adenophlegmon.
Clinical picture for nonspecific lymphadenitis is characterized by painfulness and increase in the lymph nodes, headaches, weakness, indisposition, and rise in the body temperature. In the initial stages, pain in the regional lymph nodes, which are dense, painful, not adhered with the surrounding tissue, is marked; and the skin above them is not changed.
With destructive processes (purulent form) the pain has an acute character; the skin above the lymph nodes is hyperemic; the nodes merge together and with the surrounding tissue. With an adenophlegmon, dense infiltrations with softening cells are determined. Intoxication phenomena join: fever, tachycardia, headache, weakness. With putrefactive adenophlegmon, in the damage zone crepitation is determined during palpation.
Complications: thrombophlebitis, spreading of pus onto the areolar tissue with the development of phlegmons (retroperitoneal, mediastinitis, etc.), purulent fistulae, sepsis.
Treatment depends upon the phase of the process. In the initial stages (infiltration) treatment is conservative: rest, antibiotic therapy taking into account the microflora, treatment of the basic focus of infection (cutting abscesses, phlegmons, drainage), dry heat (ultra high waves, solux, warming compresses). With abscess lymphadenitis — surgical treatment (cutting the abscess or adenophlegmon with following drainage and treatment like for purulent wounds). The treatment for specific lymphadenitis is determined by specific therapy of the basic disease (tuberculosis, actinomycosis).
Bursitis is inflammation of the mucous sacs. Mucous sacs are limited connective tissue sacs, covered with endothelium, which produces sinovial liquid. Bursas form in many places, but basically on areas of continuous pressure and skin friction, fascia, muscles, and bone protrusions. Causative agents of purulent bursitis are more often staphylococci and streptococci, less often specific bursitis (gonococcal, tubercular, pneumococcal). The infection penetrates by the lymphogenous or hematogenous way. More often purulent inflammations of the mucous sacs of the ulnar, humeral and knee joints are observed. Generally, it is explained by the patient’s profession (miners, engravers, carriers, etc.) and constant trauma of the mucous sacs.
Clinical picture consists of systematic and local symptoms. The occurrence of painful swelling according to the location of the mucous sacs, swelling and local increase in temperature is evidence of bursitis. Along with the local signs of purulent bursitis, a rise in temperature and leukocytosis, weakness occur. The diagnosis of bursitis is not complex with superficial localization of mucous sacs. It is necessary to distinguish bursitis from arthritis: with bursitis movements in the joints are kept. With chronic bursitis, the bursa is filled with serous contents; the walls of the bursa are sharply thickened.
Treatment. In the initial stages of the disease for exudate resorption they apply dry heat, ultra high waves, bandages with Vishnevsky ointment, immobilize the leg. With pyesis, a puncture with sucking out the pus and antibiotics introduction are carried out. With unsuccessful therapy, the sacs are cut open; they delete the pus and further treat as a purulent wound. With chronic bursitis, remove the mucous sacs without incision its opening.
Tendovaginitis is inflammation of the tendinous sheath. Causative agents (staphylococci, mixed flora) penetrate during wounds or as the result of inflammation spreading from the surrounding tissue.
Clinical picture. Tendovaginitis is characterized by the occurrence of pain, inflammatory infiltration by the course of the tendinous sheath. To reduce pain, the patient fixes the extremity (finger) in a half-bent position. Hyperemia of the skin above the damaged area, rise in temperature are observed. If the process progresses as a result of vascular constrictions which nourish the tendon, necrosis of the tendons can develop; purulent fistulae form.
Treatment. In the initial stages rest, immobilization, application of antibiotics and physiotherapy (ultra high waves, solux, magnetotherapy) are indicated. With the development of pyesis, the suppurative focus is opened with following washing and drainage.
Arthritis is inflammation of the joint.
Aetiology. Arthritis can result from different reasons. Such kinds of arthritis are distinguished: traumatic, infectious, dystrophic, endocrine, anaphylactic. More often purulent arthritis, the causative agents of which (staphylococci, pneumococci, enterobacteria) penetrate into the joint during a trauma or from other cells (osteomyelitis, phlegmon), less often with the hematogenous way with sepsis, thrombophlebitis.
Clinical picture depends upon the morphological changes in the joint. First serous or fibrinous synovitis, which can further turn into panarthritis and phlegmon of the articulate capsule, develops. The process can spread to the next bones with the occurrence of osteoarthritis (purulent fistula, sequestrations). Local symptoms: pain, swelling. The compelled position of the extremity depends upon the reflex muscular contraction. The extremity is fixed in such position (half-bent, retracted, pronation, etc.), during which the capacity of the joint is maximal. As a result of an increase in exudate, the contours of the joint are smoothed, there is fluctuation. With damage to the knee joint, balloting patellar is determined. Reddening, swelling of the skin, local rise in temperature on the damaged joint are observed. With dry forms (fibrinous), deforming arthrosis, ankylosis of the joints can develop. With purulent osteoarthritis, the articulate ligaments and cartilages are damaged, therefore incomplete dislocations and full dislocations can occur. The systematic intoxication phenomena appear (fever, encephalopathy, delirium). Frequently hematosepsis or septicopyemia develops.
Treatment depends upon the process phase, type of exudate. In the initial stages, they apply extremity immobilization, physiotherapy (ultra high waves, solux, ionophoresis, magnetotherapy), punctures of the joint with the introduction of antibiotics into the cavity. With the development of purulent arthritis, incision the joint (arthrotomy) and washings with antiseptics are administered. Further, washing the joint with antibiotics and antiseptics (dioxydine, chlorhexidine, dimexide) are indicated. Antibiotic therapy, haemotransfusion and protein blood substitutes, desintoxication with therapy during the development of endotoxicosis and sepsis (hyperbaric oxygenation, haemosorption, plasmapheresis, etc.) add to it.
With the destruction of the bones’ articulate ends and with the absence of effect from the applied treatment they carry out a resection of the joint with the creation of ankylosis. With threat to the patient’s life in case of sepsis, panarthritis with extensive destructions in the joint, amputation of the extremity is performed.
Osteomyelitis is inflammation of the bone tissue that covers all the bone elements (bone marrow, compact layer, periosteum). Depending upon the causative agents of osteomyelitis are divided into nonspecific (caused by pyogenic microflora) and specific (syphilitic, tubercular, brucellosis). The infection can penetrate hematogenously or exogenously. Depending upon the ways of penetration osteomyelitis is distinguished as hematogenous and non-hematogenous.
Non-hematogenous osteomyelitis is subdivided into: traumatic; gunshot; osteomyelitis, which occurs during the spread of purulent inflammation to the bone from adjacent tissues or organs.
According to the clinical course: acute, chronic, primary-chronic, atypical forms of osteomyelitis are distinguished.
Each form of osteomyelitis has prominent features of the clinical course.
Pathological anatomy — changes in the bone during osteomyelitis can begin in the bone marrow, less often — internal layers of the periosteum. Hyperemia, hypostasis of the bone marrow, development of phlegmon causes the penetration of an infection into the compact layer of the bone and periosteum. With the development of purulent infiltration of the periosteum and sub-periosteum abscesses, the nutrition of the bone is sharply broken, resulting in necrosis and rejection of bone areas (sequestration). Bone sequestration is located in the sequestral cavities where there are products of autolysis, pus. Pus from the sequestral cavities, sub-periosteum abscesses, destroying the periosteum, can go between muscles, forming phlegmons, soft tissue abscesses, spreading to the next joint. With pus breaking out the fistula such ducts form through which pieces of dead bone, purulent secretion discharge. Extensive necrosis of the bone tissue can result in pathological fractures. With the development of sequestration and fistula, the process turns into the chronic form; its duration depends upon the size of the bone area rejected.
Parallel to the destruction processes, bone regeneration as osteoblastic processes (thickening of the periosteum, bone tissue, obliteration of the bone marrow cavity) occurs.
Acute haematogenous osteomyelitis is observed more often in children and teenagers. It is caused by pyogenic microbes. The damage covers mainly long tubular bones (hip, humeral, tibia). The infection from the primary cell (furuncule, anthrax, carious teeth, tonsillitis, phlegmon, panaritium, etc.) is carried by the blood current to the bone marrow where it causes inflammation.
The following factors play a role in the development of osteomyelitis:
Peculiarities of blood supply to bones in children.
Biological and immune features of the organism.
For the diaphysis the main type of blood supply is characteristic, metaphysis and epiphysis have independent arterial systems like intertwined network of fine vessels and capillaries.
A number of theories of the pathogenesis of hematogenous osteomyelitis exist.
The Lexer’s theory (1894), taking into account the features of blood supply of tubular bones in children, explains the development of osteomyelitis as the result of embolism from the branches of the metaphysic arteries with bacterial emboli from the primary cell. But, the value of the organism’s reactance is completely ignored.
S. M. Derezhanov (1940) proved that osteomyelitis develops only in sensibilized organisms and has the course of hyperergic inflammation. Products of protein disintegration, infectious diseases, etc. can cause organism’s sensitization. Favorable factors for the development of osteomyelitis can be avitaminosis, exhaustion, previous infections, trauma to the bone.
Clinical picture. Depending upon the speed of development of the pathological process, clinical displays and prevalence of local purulent foci, according to the Krasnobayev’s classification, three forms of hematogenous osteomyelitis are distinguished: toxic; septicopyemic; local.
With the toxic form, the phenomena of septic intoxication prevail. The process has a lightning course, causes the patient’s death frequently before any changes. The consciousness is confused, delirium, symptoms of irritation of the brain membranes, fever (39°C and higher), headache, vomiting. The person is pale; eyes are sunken; lips and mucous are cyanotic; the skin is dry with an icteric shade. Hypotension, tachycardia, dyspnea, bronchopneumonia phenomena are observed.
With septicopyemic form, local purulent-destructive changes quickly occur; there are different foci in different bones at the same time; pyemic cells can appear in other organs and tissues (the lungs, the liver). With the local form, during the first days of the disease, intoxication symptoms (fever, weakness, headache, nausea, vomiting, increased leukocytosis) are accompanied by pain in the legs, which are insignificant in the onset of the disease. The localization is difficult to find, only with the development (1–2 days) of hypostasis of local tissue, infiltration of the skin the site of the greatest painfulness by palpation can be determined. Heel or elbow palpation causes strong pain on the damaged site. The extremity is in a compelled half-bent position. At the end of the first week in the center of the painful swelling the skin becomes crimson, there is fluctuation; a sub-periosteal abscess, an intermuscular phlegmon form. The intermuscular phlegmon can independently break through with the formation of fistula. With the grave course, a phlegmon results in purulent arthritis, periarticulary phlegmon and sepsis.
An early radiological symptom of osteomyelitis is the symptom of the pealing periosteum — a thin linear shadow, above the shadow of the cortical layer of the bone. Changes in the metaphysis appear radiologically as a darkening of the bone structure; osteoporosis phenomena (different sites of thinning and condensing). The typical radiological picture (presence of sequestral cavities, sequestrations, fistula) appears on the second month of the disease. In order to determine the diagnosis, bone puncture, osteomedulography, fistulography are applied.
Treatment depends upon the stage of the process. In the infiltration stage (up to 2 months) basically, conservative therapy is applied: immobilization, antibiotics (semisynthetic penicillin, aminoglycosides, cephalosporins), sulfanilamides, antiseptics (nitrofurane, metronidazole). Antibiotics are entered intramuscularly, intraarterially (regional perfusion), intraosseously, subperiostally. Subperiostal or intrabone introduction of antibiotics is carried out by micropunching the bone with the help of special needles and microirrigators, which enable the creation of high concentrations of antibiotics in the center of the damage, as well as at the same time, delete the pus and wash out the wound. With grave cases, they apply trepanation of the bone with the following washing out. In progressive cases with the presence of phlegmons, they are opened with the following continuous washing out with antibiotics and antiseptics.
Radical operations (sequestrotomy) are performed in the chronic period with precise restriction of the sequestration. A difficult task for the surgeon after sequestrotomy (removal of dead tissue, incision of the sinus tracts) is the liquidation of the residual cavity in the bone. There are about 60 methods of liquidation of sequestral cavities in the bones (sealing with paraffin, plastic, preserved cartilaginous tissue, bone alo- and autotransplantation, etc.). However, the majority of them are ineffective.
Methods with the application of transplants with blood vessel are effective. Recent years autotransplantation of bone-muscle-skin orifice has become very effective with the help of microvascular technique.
Non-hematogenous osteomyelitis. They include traumatic, gunshot, post-operative osteosynthesis, during the inflammation spread to the bone from the surrounding tissue (for example, with phlegmon). The infection is brought by the exogenous way from the environment. Many factors play a role in the incidence of traumatic osteomyelitis: degree of pollution of soft tissue and bone fragments, late primary surgical processing, organism’s reactance, microflora’s virulence, character of fracture (detrital).
Clinical picture. The development of osteomyelitis is usually preceded by the trauma (fracture) with the phenomena of soft tissue and infected wounds with pyesis within the next few days (rise in temperature, deterioration in the general condition). Occurrence of pain repeatedly on the fracture site or on the whole extremity testifies to the development of osteomyelitis. Thus, hyperemia of the skin, hypostasis of soft tissue, and significant purulent secretion from the wound are observed. The formation of purulent fistulae on the fracture site gives basis to suspect the development of osteomyelitis. Radiological changes arise a while after the trauma: osteoporosis, small cavities with soft sequestrations, usuration of the ends of the bone fragments. With gunshot osteomyelitis foreign objects are found (bullets, fraction, splinters from shells). Restriction of the destructive changes of bones only in the zone of the bone fracture is characteristic. The peculiarity of traumatic osteomyelitis in contrast to hematogenous is less pronounced systematic phenomena as a result of the nonunion of fragments; an artificial joint frequently forms. The acute period turns into the chronic with the formation of a purulent fistula with little secretion.
Treatment of non-hematogenous osteomyelitis is carried out by the same principles as for hematogenous. Surgical treatment is indicated to remove sequestrations, necrotic bone fragments, foreign objects, opening purulent fistulae. With the presence of a fracture which hasn’t not healed and osteomyelitis an economical freshening of the bone fragments with their repositioning is conducted. The method of immobilization of fragments is extrafocal compression osteosynthesis. With the inefficiency of treatment of the basic joint after the liquidation of osteomyelitis, resection of the bone is carried out within the limits of healthy tissue with simultaneous autotransplantation of the bone.
Primary-chronic osteomyelitis. These are rare forms of hematogenous osteomyelitis during which the disease from the very onset has an atypical course and appears in the chronic form. Atypical forms are Brodie’s abscess, Garre′’s sclerosing osteomyelitis, Ollier’s albuminous osteomyelitis.
Brodie’s abscess is a version of subacute hematogenous osteomyelitis. It is characterized by dull whining pains in the legs, especially at night. Radiologically in the spongy layer of a bone near the joint a round cavity appears. When incision an abscess filled with pus with little virulent microbes is found. Treatment is surgical: bone trepanation, removing the pus with the following sealing of the cavity in the bone.
Garre′’s sclerosing osteomyelitis begins subacute, with typical night pains in the legs, moderate rise in temperature and leukocytosis. The peculiar feature of the process is a sharply pronounced progressing sclerosis of the damaged bone and small sites of colliquation of the bone tissue. As a result of sclerosis, the diaphysis thickens spindle-shaped, the bone marrow cannel is completely sclerous. Treatment basically is conservative: antibiotics (lincomycine, semisynthetic penicillin), physiotherapy (electrophoresis with trypsin, ultra high waves, mud applications, and baths).
Ollier’s albuminous osteomyelitis is caused by little virulent microflora (streptococcus, staphylococcus). The disease has a subacute course with minor alterations (small infiltration of soft tissue with non-pronounced hyperemia of the skin). The peculiarity of this form is the following: serous liquid rich in mucin accumulates in the osteomyelitis focus instead of pus. The languid course sometimes is complicated with destruction of the skin with the formation of sequestrations or secondary infection.
Treatment is surgical (cutting the focus, currettage of the granulations).
Panaritium is purulent inflammation of the tissue on the fingers. The causative agents: staphylococcus and mixed flora, which penetrate into the tissue through fine traumas (injections), foreign objects (prickle, splinters of glass), after manicures. According to the anatomic principle the following classification of panaritium is distinguished: cutaneous panaritium, subcutaneous panaritium, tendovaginitis (tendon), articular panaritium, subungual panaritium, paraungual panaritium, nail-wall panaritium, bony panaritium, pandactylitis.
Cutaneous panaritium is the result of microtraumas, located under the epidermis both on the palmar and back surface of the fingers, within the limits of one phalanx. Characteristic: formation of purulent blisters with pealing of the epidermis and local hyperemia of the skin. Pains are not strong, the clinical course is favorable, without pronounced general phenomena. Treatment: surgical. Exfoliated epidermis is incised, and panaritium is treated as a purulent wound. In the initial stage, they apply spirit compresses, hot baths.
Subcutaneous panaritium is the most often form of panaritium with overwhelming damage to the palmar surface of the fingers. Because of the features of structure of the hypodermic tissue of the palm (cavernous) it tends to quickly transit into the bony form. Clinically it appears as two phases: infiltration and abscess. Infiltration appears within the limits of one phalanx. Pain is pulsating, pulling, hyperemia of the skin is non-pronounced; the patients protect the finger. In the abscess phase, fluctuation is difficult to find because the connective tissue membranes in the hypodermic tissue limit the spreading of the process on the periphery. The character of pain helps to find it (constant, pulsating which deprives the patient of rest and sleep). With compression of the vessels, purulent exudate disrupts blood circulation; therefore dry necrosis of the hypodermic tissue is possible.
Treatment. In the infiltration phase treatment is conservative: antibiotics, sulfanilamides, physiotherapy (hot baths, spirit compresses). In the abscess phase, the abscesses are opened with Klapp’s linear-lateral incisions, which are conducted on the edge of the lateral and palm surfaces of the finger within the limits of the phalanx. The incisions are connected among themselves with the help of a hypodermic tunnel by incision the tendinous membranes. It enables the opening of all abscesses. The incisions are drained with a rubber strip (but not gauze drainage) for sufficient outflow of the pus and prevention of the sticking of skin wounds and formation of another abscess. On the nail, incision of an abscess is conducted with a sticklike cut.
The incision used earlier as “fish jaws” is not desirable, because it damages the nerve endings, and tactile sensitivity is lost. The incision of abscesses can be carried out under narcosis or under local anaesthesia according to Oberst—Lukashevich. In the postoperative period — treatment is like for purulent wound (local antibiotics, antiseptics, proteolytic enzymes, ultra high waves, UV irradiation).
Paronychia — inflammation of the nail wall, which occurs with microtraumas (agnails, damage during a manicure). Reddening, swelling, and painfulness of the nail wall are typical. When pressing on the nail, pus discharges from under the edge of the nail wall. Frequently the process proceeds long without a pronounced reaction.
Treatment is conservative in the initial stage: baths, spirit compresses. With the accumulation of pus, under block anaesthesia, wedge-shaped, P-like pair of lateral incisions on the back surface of the nail (depending upon the localization) are conducted.
Subungual panaritium — develops when foreign objects (thorns) get in the nail bed, as a result of punctured wounds or pyesis of hyponychial hematomas. The development of purulent inflammation under the nail is characteristic. It is accompanied by pulsating pain, visible accumulation of pus under the nail plate. With the rupture of pus to the outside it can form purulent fistula. Treatment: surgical. With located forms of subungual panaritium it is necessary to limit the resection of the nail plate. With complete exfoliating of the nail plate, the latter is removed with the purpose of draining the suppurative focus and treating the purulent wound.
Tendinous panaritium (tendovaginitis) usually arises secondary as a complication of subungual panaritium with unsuccessful therapy. It is characterized by a deterioration in the general condition, occurrence of pulsating pain on the whole finger, uniform hypostasis of the tissue on the finger from smooth interphalanx sulcus. The finger looks like sausage, in a half-bent position. An attempt to unbend the finger causes sharp pain, during bending the pain abates. It is one of the characteristic symptoms. Dangerous tendovaginitis are on the 1st and 5th fingers, because of the possible drift of the infection onto the forearm, occurrence of V-like phlegmons. Treatment in the initial stage consists in puncturing the tendinous vaginas for draining the exudate and introduction of antibiotics. If inefficient, it is necessary to resort to an urgent operation. A delay concerning the operation is dangerous, because the tendon, deprived of blood as a result of compression of the vessels with exudate, quickly perishes. Thus the flexing function of the finger will be lost, though it is possible to stop the inflammatory process. Incision of the inflammatory cell is conducted with Klapp’s incisions on the anterior-lateral surface of the finger with the following drainage with rubber drainages and treatment with local antiseptics.
Bony panaritium is osteomyelitis of the phalanxes occurs as the result of wrong or late treatment of subcutaneous panaritium. With small incisions of subcutaneous panaritium, preconditions for deep infection spreading to the finger bone are created. The pain is dull, constant; the pus discharge from the wound does not stop, sometimes with fine bone sequestrations. The phalanx thickens clubshaped, sharply painful during palpation; the function of the hand is reduced. On the roentgenogram osteoporosis, destruction and sequestration of the phalanxes are found.
Treatment: a combination of antibiotic therapy (local and systematic) and surgical. Wide lateral incisions according to Klapp and the removal of necrotic hypodermic tissue with the rubber drainage are conducted. In grave cases, they remove the large sequestrations.
Articular panaritium occurs as a complication of subcutaneous or bony panaritium. Sometimes, it is the consequence of the infection bringing from wounds to the joints. Strong pains which amplify during bending the finger are typical. The joint is spindle-shaped, hypostasis and hyperemia of tissue are most of all pronounced on the posterior surface of the finger. Joint puncture reveales a muddy liquid. During grave cases destruction of the capsule and pathological dislocation are possible. Purulent fistulae form. There is destruction of the articular surfaces on roentgenograms. Treatment in the initial stage: joint puncture, liquidation of exudate and introduction of antibiotics. Immobilization of the finger is indicated. With the presence of pus in the joint, arthrotomy with two parallel incisions with the following draining and washing are done. Sometimes amputation of the finger with destruction of the joint and significant destruction of the bones is conducted.
Pandactylitis is a purulent inflammation of all tissues of the finger. Frequently, it is the result of the wrong treatment of bony, articular and tendinous panaritium. The disease develops gradually. The clinical picture consists of combination of all kinds of purulent damage to the finger. It has a severe course; it is accompanied by pronounced intoxication (headache, fever and leukocytosis), regional lymphadenitis. Pain in the finger is intolerable. The finger is sharply thickened, deformed, dark blue-crimson. The inflammation occurs with dry or damp necrosis. There are multiple purulent fistulae with grey granulations. With the presence of virulent infections, the inflammation frequently spreads to the hand.
Treatment is surgical (wide lateral incisions according to Klapp). It is necessary to try to save the fingers though, as a rule, with panaritium the finger contracture develops. For the prevention of the generalization of the infection, they resort to exarticulation of the finger.
PUTREFACTIVE (PUTRID) WOUND INFECTION
Aetiology. The putrefactive infection develops only in the wound where there is dead tissues, which are subject to putrifactive disintegration as a result of vital activity the putrefactive bacteria. Complications can occur from extensive severe wounds of the soft tissue, open fractures, gunshot wounds, and bed sores. The putrefactive infection seldom occurs independently; usually it joins Claustrid anaerobic or aerobic infection. Non-Claustrid anaerobic putrefactive infection is caused by: bacteroid, peptococcus, fusobacteria that generally saprofited on the mucous membrane of the GIT, respiratory ways, and female genitals.
Today the idea is established that 90% of surgical infections have an endogenous origin. As the most part of normal microflora are anaerobes, the anaerobic and mixed (anaerobic-aerobic) infections make up one of the most significant categories of pyoinflammatory diseases. An especially big role they play in surgery of diseases and complications in stomatologic, thoracic, abdominal, gynaecologic clinics and with certain infections of soft tissues. Experience testifies that the majority of infections which take place with the participation of anaerobes are not monomicrobic. More often they are caused by the association of anaerobes or the combination of anaerobes with aerobes (Staphylococci, E.coli).
Clinical picture. Putrefactive infection is independently observed rather seldom, usually it joins an already advanced anaerobic or purulent (aerobic) infection. Hence, the clinical picture of the wound complications is not frequently clear and merges with the clinical picture of anaerobic or purulent infection. Among the general symptoms, it is necessary to distinguish the following: oppression of mentality, drowsiness, decrease in appetite, development of anemia. The occurrence of sudden repeated fever is an early general sign of putrefactive disintegration in the wound. The major and constant attribute is the presence of sharp unpleasant odour of exudate. A bad odour is predetermined by flying sulphurous compounds (hydrogen sulphide, methyl mercaptan, methyl thiomethane) — products for the vital activity of putrefactive bacteria. The second attribute of anaerobic damage is putrefactive character of the wound. The center of damage contains dead tissues as unstructured detritis with a grey or grey-green color, sometimes with black or brown sites. These cells seldom have a cavity form, limited to correct contours, more often they have a chimerical form or fill intertissue cracks.
The color of the exudate also has peculiarities. It is usually graygreen, quite often brown. The coloring is not homogeneous; it contains small droplets of fat. With big accumulation of pus in the tissue, the exudate, as a rule, is liquid, but with damage to the muscles it is scanty, which diffusely impregnates tissues. With aerobic suppuration the pus has dense consistency, more often yellow or white color, homogeneous, without an odour. A characteristic attribute of anaerobic infections is gas formation.
The reason for gas formation is that during anaerobic metabolism, hydrogen, nitrogen, methane, which dissolve badly in water release. Gas formation causes crepitation during palpation of the damaged site, the presence of gas blisters in the exudate.
In differential diagnosis, radiological methods of research have great value. With putrefactive infection, the level of gas formation is low. In contrast to it with gas (claustridial) gangrene, gas spreads quickly, immense beyond the limits of the wound and into the muscular layer. Dirty-green spots appear at a significant distance from the wound on the skin as a result of haemolysis. In the initial stage when the putrefactive infection joins, during examination of the wound frequently it is impossible to find the presence of hypostasis, crepitation, gas formation, purulent swelling. External attributes of damage to tissue frequently do not correspond to extensive deep damages — hyperemia of the skin may be absent, which does not induce the surgeon to well-timed and extensive surgical operation of the focus of injury. Dry and dead tissue, the occurrence of a dirty-green or brown film, discharge of muddy exudate with a small amount of gas blisters, the presence of an awful (ichorous) odour from the wound — characteristic attributes of the adding putrefactive infection. The putrefactive infection spreads onto the hypodermic tissue, then onto the interfascial spaces, causing necrosis of the fascia, muscles, and tendons. The development of a putrefactive infection in the wound can have three clinical forms (P. M. Napalkov):
1) with the prevalence of shock phenomena; 2) with a rough progressing course; З) with a vague course.
The first two forms run have the phenomena of significant general intoxication (fever, chills, decrease in arterial pressure, encephalopathy, and the development of renal and hepatic insufficiency).
The diagnosis of putrefactive infection should be based upon the features of clinical and microbiological diagnosis of the exudate. The causative agents are not frequently determined by routine methods of bacteriological investigation. Bacteroids quickly perish with the presence of oxygen, the material for exam is to be taken with caution and urgently delivered to the laboratory. It is not allowed to contact the material with oxygen. The growth of the bacteroids on nutrient mediums is slow; the answer comes in 72 h and more. Microscopy of native material (exudate smears, stained by Gram) and gas chromatography belong to the simple and fast ways of identifying anaerobes. The method of gas chromatography is based upon the chromatographic definition of specific chemical substances of anaerobes vital activity products (volatile fatty acids: propionic, valerian, capron and others).
The treatment for putrefactive infections should consists of the following:
а) creation of grave conditions for the development of microflora (removal of dead tissues, wide drainage of the abscesses, antibacterial therapy);
detoxification therapy (methods of intra- and extracorporal detoxication);
correction of homeostasis and immune status of the organism(correction of systematic and organ infringements, immune therapy and immune correction).
With the presence of a putrefactive infection in the wound, they remove the damaged tissues. As a result of the anatomic localization, prevalence and other features of an infection, the achievement of radical results (removing the damaged tissue) is not always possible. In such cases, the operation has a palliative character and consists of a wide incision of the suppurative focus, removal of the necrotic tissues, draining the wound with the purpose of removing the exudate and local acting upon the microflora with different antiseptic substances. For prophylaxis of spreading putrefactive process onto the healthy tissue limiting incisions are performed.
The irrigation or constant perfusion of wounds with solutions of hydrogen peroxide, potassium permanganate, and sodium hypochlorite is expedient in the treatment of anaerobic infections. Sodium hypochlorite is prepared before use by electrolysis with a 0.9% solution of sodium chloride. Hydrophilic ointments on polyethylene oxide basis (levosin, levomacol, dihydroxycol, maphenid, sulfamilon) are very effective. Ointments on a hydrophylic base provide good adsorption of exudate and fast clearing of the wound. They apply hyperbaric oxygenation, but in some cases (with the presence of aerotolerance) a decrease in the effect of this method is observed.
The majority of bacteroids are resistant to antibiotics, therefore antibiotic therapy is necessary to carry out under obligatory control of the antibioticogram. Chemotherapy of putrefactive infection consists of effective antibiotics (thienam, lincomycin, rifampicin), preparations of metroimidazole (metronidazole, metragil, tinidasol).
The complex of measures on correcting homeostasis and detoxification should be determined individually for each patient according to the clinical course (rough septic course or languid, vague).
With a rough septic course, they begin with intracorporal methods of detoxication: haemoinfusion and endolymphatic therapies (introduction of haemodes, neoheamodes, albumin with disaggregants against a background of forced diuresis). They apply UV-irradiation, applicational sorption (placing carbon fibrous sorbents, immobilized enzymes in combination with antibiotics on the wound). With the development of the phenomena of hepatic insufficiency they use haemosorption, lymphosorption, plasmapheresis, plasmosorption.
In case of renal insufficiency, the method of choice is haemodialysis, haemodiafiltration.
Correction of immune status infringements with a putrefactive infection (especially with the development of septicopyemia) consists of transfusion of fresh-stabilized blood and the application of artificial (decaris) or natural immune correctors (thactivin, thymalin, thymogen).