Peritonitis stages of development and clinical picture. Peritonitis

– local or diffuse inflammation of the serous covering of the abdominal cavity – the peritoneum. Clinical signs of peritonitis include abdominal pain, muscle tension in the abdominal wall, nausea and vomiting, stool and gas retention, hyperthermia, and severe general condition. Diagnosis of peritonitis is based on medical history, identification of positive peritoneal symptoms, ultrasound, radiography, vaginal and rectal examinations, and laboratory tests. Treatment of peritonitis is always surgical (laparotomy, sanitation of the abdominal cavity) with adequate preoperative and postoperative antibacterial and detoxification therapy.

ICD-10

K65

General information

Peritonitis is a severe complication of inflammatory and destructive diseases of the abdominal organs, accompanied by severe local and general symptoms and the development of multiple organ failure. Mortality from peritonitis in gastroenterology is 20-30%, and in the most severe forms reaches 40-50%.

The peritoneum (peritoneum) is formed by two serous layers passing into each other - visceral and parietal, covering the internal organs and walls of the abdominal cavity. The peritoneum is a semi-permeable, actively functioning membrane that performs many important functions: resorptive (absorption of exudate, lysis products, bacteria, necrotic tissue); exudative (secretion of serous fluid), barrier (mechanical and antimicrobial protection of abdominal organs), etc. The most important protective property of the peritoneum is its ability to limit inflammation in the abdominal cavity due to fibrous adhesions and scars, as well as cellular and humoral mechanisms.

Causes of peritonitis

The etiological component of peritonitis is a bacterial infection, in most cases represented by nonspecific microflora of the gastrointestinal tract. These can be gram-negative (Enterobacter, Escherichia coli, Proteus, Pseudomonas aeruginosa) and gram-positive (staphylococci, streptococci) aerobes; gram-negative (fusobacteria, bacteroides) and gram-positive (eubacteria, clostridia, peptococci) anaerobes. In 60-80% of cases, peritonitis is caused by an association of microbes - most often Escherichia coli and staphylococcus. Less commonly, the development of peritonitis is caused by specific microflora - gonococci, hemolytic streptococcus, pneumococci, mycobacterium tuberculosis. Therefore, to select a rational treatment for peritonitis, bacteriological culture of the contents of the abdominal cavity with determination of the sensitivity of the isolated microflora to antibacterial drugs is of paramount importance.

In accordance with the etiology, primary (idiopathic) and secondary peritonitis are distinguished. Primary peritonitis is characterized by the penetration of microflora into the abdominal cavity by the lymphogenous, hematogenous route or through the fallopian tubes. Direct inflammation of the peritoneum may be associated with salpingitis, enterocolitis, tuberculosis of the kidneys or genitals. Primary peritonitis occurs infrequently - in 1-1.5% of cases.

In clinical practice, it is much more common to encounter secondary peritonitis that develops as a result of destructive inflammatory diseases or trauma to the abdominal cavity. Most often, peritonitis complicates the course of appendicitis (perforated, phlegmonous, gangrenous), perforated gastric or duodenal ulcer, pyosalpinx, rupture of an ovarian cyst, intestinal obstruction, strangulated hernia, acute occlusion of mesenteric vessels, Crohn's disease, diverticulitis, phlegmonous gangrene severe cholecystitis, pancreatitis, pancreatic necrosis and other diseases.

Based on etiology, a distinction is made between bacterial and abacterial (aseptic, toxic-chemical) peritonitis. The latter develop as a result of irritation of the peritoneum by aggressive non-infectious agents (bile, blood, gastric juice, pancreatic juice, urine, chylous fluid). Abacterial peritonitis quite quickly takes on a microbial character due to the addition of infectious pathogens from the lumen of the gastrointestinal tract.

Depending on the nature of the peritoneal effusion, serous, fibrinous, hemorrhagic, bile, purulent, fecal, putrefactive peritonitis are distinguished.

According to the clinical course, peritonitis is divided into acute and chronic. Taking into account the prevalence of the lesion on the surface of the peritoneum, limited (local) and diffuse peritonitis are distinguished. Variants of local peritonitis include subphrenic, appendicular, subhepatic, interintestinal, and pelvic abscesses. Diffuse peritonitis is spoken of when inflammation of the peritoneum does not tend to be limited and has no clear boundaries. According to the degree of damage to the peritoneum, diffuse peritonitis is divided into local (developing in one anatomical area, close to the source of infection), widespread (covering several anatomical areas) and general (with total damage to the peritoneum).

In the development of peritonitis, it is customary to distinguish the early phase (up to 12 hours), late (up to 3-5 days) and final (from 6 to 21 days from the onset of the disease). In accordance with pathogenetic changes, reactive, toxic and terminal stages of peritonitis are distinguished. In the reactive stage of peritonitis (24 hours from the moment of damage to the peritoneum), a hyperergic reaction to irritation of the peritoneum is noted; During this phase, local manifestations are most pronounced and general symptoms are less pronounced. The toxic stage of peritonitis (from 4 to 72 hours) is characterized by an increase in intoxication (endotoxic shock), intensification and predominance of general reactions. In the terminal stage of peritonitis (after 72 hours), protective and compensatory mechanisms are depleted, and profound disturbances in the vital functions of the body develop.

Symptoms of peritonitis

In the reactive period of peritonitis, abdominal pain is noted, the localization and intensity of which is determined by the cause of inflammation of the peritoneum. Initially, the pain has a clear localization in the area of the source of inflammation; may radiate to the shoulder or supraclavicular region due to irritation of the nerve endings of the diaphragm by purulent-inflammatory exudate. Gradually, the pain spreads throughout the abdomen, becomes unremitting, and loses its clear localization. In the terminal period, due to paralysis of the nerve endings of the peritoneum, the pain syndrome becomes less intense.

Characteristic symptoms of peritonitis are nausea and vomiting of gastric contents, which in the initial stage occur reflexively. In later stages of peritonitis, the vomiting reaction is caused by intestinal paresis; an admixture of bile appears in the vomit, followed by intestinal contents (fecal vomiting). Due to severe endotoxicosis, paralytic intestinal obstruction develops, clinically manifested by stool retention and failure to pass gases.

With peritonitis, even in the earliest stages, the patient’s appearance attracts attention: a pained expression on the face, adynamia, pale skin, cold sweat, acrocyanosis. The patient takes a forced position to relieve pain - often on his side or back with his legs tucked to his stomach. Breathing becomes shallow, the temperature is elevated, hypotension is noted, tachycardia is 120-140 beats. per minute, not corresponding to low-grade fever.

In the terminal stage of peritonitis, the patient's condition becomes extremely serious: consciousness is confused, sometimes euphoria is observed, facial features become sharpened, the skin and mucous membranes are pale with an icteric or cyanotic tint, the tongue is dry and coated with a dark coating. The abdomen is swollen, palpation is not painful, and “deathly silence” is heard on auscultation.

Diagnostics

Palpation examination of the abdomen reveals positive peritoneal symptoms: Shchetkin-Blumberg, Voskresensky, Medel, Bernstein. Percussion of the abdomen during peritonitis is characterized by dullness of sound, which indicates effusion in the free abdominal cavity; The auscultatory picture suggests a decrease or absence of bowel sounds; the symptoms of “deathly silence”, “falling drop”, “splashing noise” are heard. Rectal and vaginal examination for peritonitis allows one to suspect inflammation of the pelvic peritoneum (pelvioperitonitis), the presence of exudate or blood in the pouch of Douglas.

Changes in the general blood test during peritonitis (leukocytosis, neutrophilia, increased ESR) indicate purulent intoxication. Laparocentesis (puncture of the abdominal cavity) and diagnostic laparoscopy are indicated in cases that are unclear for diagnosis and allow us to judge the cause and nature of peritonitis.

Treatment of peritonitis

Detection of peritonitis serves as the basis for emergency surgical intervention. Therapeutic tactics for peritonitis depend on its cause, however, in all cases, the same algorithm is followed during the operation: laparotomy is indicated, isolation or removal of the source of peritonitis, intra- and postoperative sanitation of the abdominal cavity, and decompression of the small intestine.

The surgical approach for peritonitis is a median laparotomy, which provides visualization and reach of all parts of the abdominal cavity. Elimination of the source of peritonitis may include suturing the perforation, appendectomy, colostomy, resection of a necrotic section of the intestine, etc. All reconstructive interventions are postponed to a later date. For intraoperative sanitation of the abdominal cavity, solutions cooled to +4-6°C are used in a volume of 8-10 liters. Decompression of the small intestine is achieved by inserting a nasogastrointestinal tube (nasointestinal intubation); Drainage of the colon is performed through the anus. The operation for peritonitis is completed by installing vinyl chloride drains into the abdominal cavity for aspiration of exudate and intraperitoneal administration of antibiotics.

Postoperative management of patients with peritonitis includes infusion and antibacterial therapy, prescription of immunocorrectors, transfusion of leukocytes, intravenous administration of ozonized solutions, etc. For antimicrobial therapy of peritonitis, a combination of cephalosporins, aminoglycosides and metronidazole is more often used, providing an effect on the entire spectrum of possible pathogens.

In the treatment of peritonitis, the use of extracorporeal detoxification methods (hemosorption, lymphosorption, hemodialysis) is effective

Since most peritonitis is secondary, their prevention requires timely identification and treatment of the underlying pathology - appendicitis, gastric ulcers, pancreatitis, cholecystitis, etc. Prevention of postoperative peritonitis includes adequate hemostasis, sanitation of the abdominal cavity, and checking the integrity of anastomoses during abdominal operations.

Sources of peritonitis are:

Vermiform appendix (30-65%) - appendicitis: perforated, phlegmonous, gangrenous;

Stomach and duodenum (7-14%) - perforated ulcer, cancer perforation, gastric phlegmon, foreign bodies, etc.;

Female genital organs (3 - 12%) - salpingo-oophoritis, endometritis, pyosalpinx, rupture of ovarian cysts, gonorrhea, tuberculosis;

Intestines (3 - 5%) - obstruction, strangulated hernia, thrombosis of mesenteric vessels, perforation of typhoid ulcers, perforation of ulcers due to colitis, tuberculosis, Crohn's disease, diverticula;

Gallbladder (10 - 12%) - cholecystitis: gangrenous, perforated, phlegmonous, sweaty biliary peritonitis without perforation;

Pancreas (1%) - pancreatitis, pancreatic necrosis.

Postoperative peritonitis accounts for 1% of all peritonitis. Rarely occurring peritonitis occurs with abscesses of the liver and spleen, cystitis, suppuration of chylous ascites, breakthrough paranephritis, pleurisy, some urological diseases and others.

In some cases, the root cause of peritonitis cannot be determined even at autopsy; such peritonitis is called cryptogenic.

It is generally accepted to divide peritonitis according to the prevalence of the inflammatory process, since the severity of the disease depends on this. Based on the generally accepted division of the abdominal cavity into nine anatomical regions (hypochondrium, epigastrium, mesogastrium, hypogastrium, umbilical, pubic, etc.), widespread and local forms of the disease are distinguished. Peritonitis is considered:

local, if it is localized in no more than two of the nine anatomical regions of the abdominal cavity,

in all other cases, peritonitis is designated as widespread.

in turn, among local peritonitis there are:

unlimited and limited forms. In the latter case, we are talking about abdominal abscesses. Common peritonitis is divided into diffuse (the inflammatory process occupies from two to five anatomical areas) and diffuse (more than five anatomical areas).

During acute purulent peritonitis, several stages (phases) are distinguished. The classification of peritonitis by phases (stages), proposed by I. I. Grekov (1952), was based on the time factor:

early stage - up to 12 hours,

late - 3 - 5 days

final - 6 - 21 days from the moment of illness.

However, in practical work there is a significant difference in the dynamics of the pathological process depending on the individual characteristics of the organism, the causes and conditions for the development of peritonitis.

The identification of stages (phases) of peritonitis depending on mobilization, inhibition of protective mechanisms, and the presence or absence of intestinal paralysis seems overly general, precluding the possibility of developing sufficiently convincing clinical criteria.

The most appropriate classification of peritonitis is considered to be separating reactive, toxic and terminal phases (Simonyan K. S., 1971). The advantage of this classification is the desire to link the severity of clinical manifestations with the pathogenetic mechanisms of peritonitis.

Characteristics of the stages of the disease of acute purulent peritonitis are as follows:

reactive (first 24 hours) - the stage of maximum local manifestations and less pronounced general manifestations;

toxic (24 - 72 hours) - the stage of subsidence of local manifestations and the prevalence of general reactions typical of intoxication;

terminal (over 72 hours) - a stage of deep intoxication on the verge of reversibility.

Experimental and clinical data of many authors, including the results of studies carried out by I. A. Eryukhin et al., have led to the belief that the pathogenetic essence of the transition from the reactive phase of peritonitis to the toxic phase consists in breaking through the biological barriers that inhibit endogenous intoxication (including primarily include the liver, peritoneum, and intestinal wall), the transition to the terminal phase of peritonitis is determined by the depletion of protective and compensatory mechanisms.

The need for an objective assessment of the results of research work on the problem of acute widespread purulent peritonitis, the complexity of diagnosis and determination of optimal surgical tactics in the treatment of this category of patients, the most severe in terms of clinical course and consequences, and other factors determine the special significance of the problem of developing a generally accepted classification of peritonitis. The modern clinical classification should provide real assistance to the practical surgeon in timely diagnosis of the disease, carrying out therapeutic measures, incl. choosing optimal surgical tactics that are adequate in scope. Unfortunately, the proposed and existing classifications do not solve these problems. So, classification of peritonitis according to etiological principle(combined, staphylococcal, streptococcal, etc.) are extremely cumbersome due to the multitude of pathogens and their associations, do not contain data on the localization of the lesion, its prevalence, features of clinical manifestations, etc.

Classification by V. S. Savelyev, B. R. Gelfond provides for the identification of the following forms of peritonitis: serous-fibrinous, fibrinous-purulent, purulent, fecal, biliary, hemorrhagic, chemical peritonitis. This classification is attractive for its ability to differentiate the pathogenetic and prognostic significance of the components of the abdominal contents - exudate, pus, bile, etc., which is very important when choosing adequate surgical tactics.

An extremely important classification feature of peritonitis is its prevalence. Based on an assessment of the practical significance of various classifications of peritonitis, a clear belief has emerged that the most important is to distinguish two main forms of peritonitis: local and widespread (Kuzin M.I., 1986; Gostishchev V.K. et al., 1992, etc.). Other definitions - diffuse, general, total, etc. - do not have clear clinical and morphological characteristics and are rarely used. This approach is very important for determining surgical tactics. So, if the diagnosis of “extensive peritonitis” involves performing a wide median laparotomy, removing the source of peritonitis and performing a complete sanitation of the abdominal cavity, then

Rice. 8.3. Abdomen areas:

1 – regio epigastrico; 2 – regio hypogastrica sinistra; 3 – regio umbilicalis; 4 – regio lateralis sinistro; 5 – regio Inguinalis sinistra; 6 – regio pubica; 7 – regio Inguinalis dextro; 8 – regio lateralis dextra; 9 – regio hypogastrica dextra

local peritonitis provides for the need and possibility of sanitation of only the local focus. By widespread peritonitis, most surgeons understand the involvement of three or more conventionally designated areas of the abdominal cavity in the inflammatory process; local peritonitis, as a rule, is limited to the area of infection or traumatic injury, in which leakage of abdominal contents into other areas is possible, most often into the right iliac (Fig. 8.3). However, local peritonitis can be clearly demarcated or undemarcated, which is the leading factor in determining surgical tactics.

The most widespread in clinical practice is classification of peritonitis according to the severity of clinical manifestations, proposed by K. S. Simonin, developed at the Institute of Emergency Medicine named after. N.V. Sklifosovsky, which provides for the allocation reactive, toxic and terminal phases peritonitis.

The classification according to the severity of the clinical course has undergone changes after the introduction of the concept of “abdominal sepsis” into clinical practice (Savelyev V. S. et al., 1999) and its clinical classification adopted in Chicago in 1991 (Bone R. S.). The appearance of multiple organ failure syndrome (MODS) in accordance with this classification is defined as severe sepsis, and the development of uncontrolled arterial hypotension below 90 mm Hg. A. is assessed as terminal sepsis - the stage of infectious-toxic shock. Thus, in recent years, instead of classification according to the severity of the clinical course depending on the phase of peritonitis (reactive, toxic, terminal), distribution of the disease by phases: peritonitis with the absence of sepsis, peritoneal sepsis, severe peritoneal sepsis, infectious-toxic shock.

In recent years, it has become increasingly common in Western medical literature. division of peritonitis into primary, secondary and tertiary. Primary peritonitis is proposed to include peritonitis that occurs as a result of hematogenous translocation of microorganisms into the abdominal cavity from other organs (tuberculous peritonitis, ascites-peritonitis, etc.). The category of secondary peritonitis includes several of their varieties: peritonitis caused by perforation or inflammatory destruction of the abdominal organs, postoperative, post-traumatic peritonitis. The term “tertiary peritonitis” refers to those sluggish forms of the disease that arise and develop without pronounced clinical signs in weakened patients with secondary peritonitis during intensive therapy, usually accompanied by immunosuppression, which keeps surgeons from active surgical tactics. When deciding on an operation in the abdominal cavity, against the background of a dull peritoneum without pronounced inflammatory changes, multiple interloop abscesses, purulent or serous-purulent exudate, and fibrinous layers are revealed.

The final classification sign of peritonitis is the separation of complicated (intra-abdominal complications - abscesses, phlegmon of retroperitoneal tissue, etc., and extra-abdominal complications, developing as a result of hematogenous spread of infection - pneumonia, bacterial endocarditis, etc.) and uncomplicated peritonitis.

In recent years, an improved and somewhat abbreviated classification of acute peritonitis has been proposed for practical use, adopted by the joint Plenum of the problem commissions “Emergency Surgery” and “Purulent Surgery” M3 of Russia, Moscow, 1999, according to which peritonitis is distinguished:

I. According to the prevalence of the process:

1. Local.
2. Common:

■ diffuse (goes beyond the inflammation and spreads to adjacent areas);

■ general (applies to large areas or the entire peritoneum).

II. By the nature of the exudate:

1. Serous.
2. Serous-fibrinous.
3. Purulent.

General clinical classification, designed to systematize the main factors of the pathological process in peritonitis and largely determine differential diagnostic and therapeutic tactics, may be the following:

By etiological factor:

■ primary(spontaneous peritonitis in children and adults, specific);

■ secondary(caused by perforation and destruction of abdominal organs, postoperative, post-traumatic);

■ tertiary(persistent, sluggish).

By prevalence:

■ delimited(infiltrate or abscess);

■ unrestricted:

■ local (occupies less than B of 9 anatomical regions of the abdominal cavity);

■ widespread (occupies B and more anatomical areas of the abdominal cavity).

According to the nature of the pathological content

■ peritoneal cavity:

■ serous;

■ serous-fibrinous;

■ fibrinous-purulent;

■ purulent;

■ fecal;

■ hemorrhagic;

■ chemical.

According to the microbiological factor:

■ nonspecific – caused by microorganisms of the gastrointestinal tract:

■ aerobic gram-negative (Escherichia coli or Pseudomonas aeruginosa, Proteus, Klebsiella, Enterobacter);

■ aerobic gram-positive (staphylococcus, streptococcus);

■ anaerobic gram-negative (bacteroides, fusobacteria); anaerobic gram-positive (clostridia, eubacteria, lactobacilli, peptostreptococci, leptococci);

■ specific(gonococci, hemolytic streptococcus, mycobacterium tuberculosis).

According to the severity of general clinical manifestations:

■ absence of signs of sepsis;

■ sepsis;

■ severe sepsis(presence of multiple organ failure, indicating the volume and degree of multiple organ dysfunction);

■ infectious-toxic shock.

According to the presence and nature of complications:

■ intra-abdominal;

■ wound infection;

■ infection of the upper and lower respiratory tract (tracheobronchitis, nosocomial pneumonia);

■ angiogenic infection;

■ urinary tract infection.

Classification of peritonitis

At local peritonitis, the inflammatory process is localized around the affected organ and can be limited or unlimited. Common peritonitis is divided into diffuse(inflammation of the peritoneum spreads beyond the affected organ, but covers less than two “floors” of the abdominal cavity), spilled(almost the entire peritoneum is affected) and general or total

by phase- reactive, toxic, multiple organ failure (terminal).

according to clinical flow- acute, subacute or sluggish, chronic or specific.

By the nature of the exudate- serous, purulent, hemorrhagic, bile, urinary, fecal.

Postoperative peritonitis is divided into primary and secondary. Primary may be a consequence of the neglect of the primary pathological process and, even more so, if the source of infection of the abdominal cavity is not eliminated, and also when, during the initial intervention, the abdominal cavity is poorly sanitized and inadequately drained. In such a situation, the patient's condition progressively worsens. Secondary postoperative peritonitis is clinically manifested by a sudden sharp deterioration in the patient’s condition due to the development of an intra-abdominal catastrophe.

The causative agent of peritonitis is usually a mixed microflora

clinics peritonitis should begin with a description of its classic symptoms: it is necessary to emphasize the dynamics of symptoms as peritonitis progresses. Peritoneal irritation is easier to identify by performing a digital examination of the rectum. The role of auxiliary research methods for the early recognition of peritonitis and developed purulent complications is great. First of all, a detailed clinical blood test is prescribed. An X-ray examination is carried out with the mandatory participation of the attending physician: it consists of a polypositional examination of the abdominal and thoracic cavity. Signs of peritonitis are bloating of the stomach, intestines, swelling of their walls and mucous membranes, blurred contours, the presence of fluid in the intestinal lumen and in the free abdominal cavity. When diagnosing postoperative peritonitis, contrast research methods are also used: attention is drawn to the high position of the dome of the diaphragm, limitation of its mobility, the presence of effusion in the pleural cavity, and disc-shaped atelectasis. Sonography also allows you to detect free fluid in the abdominal cavity, abscesses, and infiltrates. Laparoscopy makes it possible not only to recognize peritonitis, but also to clarify its cause and prevalence.

Preoperative preparation necessary in the toxic phase and, especially, in the phase of multiple organ failure, and should be aimed at restoring the volume of circulating blood, correcting the disturbed electrolyte balance, improving the rheological properties of the blood, and detoxification. .

The method of choice for pain relief is endotracheal anesthesia.

Optimal access for widespread peritonitis - midline laparotomy. Local approaches are used for local peritonitis. It is necessary to dwell on the approaches used to open abscesses - subdiaphragmatic, interloop, and Douglas space.

The purpose of surgical intervention is to eliminate the source of peritonitis, thoroughly sanitize and drain the abdominal cavity.

Lung abscess Under acute (simple) lung abscess understand purulent or putrefactive melting of necrotic areas of lung tissue, most often within one segment with the formation of one or more cavities filled with pus and surrounded by perifocal inflammatory infiltration of lung tissue. The purulent cavity in the lung is most often delimited from unaffected areas by a pyogenic capsule. Acute abscesses and gangrene of the lungs are most often caused by staphylococcus, gram-negative microbial flora and non-clostridial forms of anaerobic infection. Depending on the routes of penetration of microbial flora into the lung parenchyma and the cause with which the onset of the inflammatory process is associated, abscesses and gangrene of the lungs are divided into bronchogenic (aspiration, post-pneumonic and obstructive), hematogenous-embolic and traumatic. However, in all cases, the occurrence of the disease is determined by the combination and interaction three factors:

1. Acute infectious inflammatory process in the pulmonary parenchyma;

2. Impaired blood supply and necrosis of lung tissue;

3. Impaired bronchial patency in the area of inflammation and necrosis.

Main mechanism the development of the pathological process in most cases of acute abscesses and gangrene of the lungs is a spiratory y. For the occurrence of the disease, not only aspiration of the infected material is necessary, but also its persistent fixation in the bronchi in conditions of reduced or absent their cleansing function and cough reflex, which are the most important protective mechanism.

Clinical picture. suddenly: against the background of complete well-being, chills, an increase in body temperature to 38-39 C, malaise, and dull pain in the chest occur. Often the patient accurately names the date and even the hour when signs of the disease appeared.

The patient's condition immediately becomes serious. Tachycardia and tachypnea, hyperemia of the facial skin are detected. It may soon appear dry. Less common wet cough.

involvement of two or more segments of the lungs in the process: shortening of the percussion sound over the affected area of the lung, weakening of respiratory sounds and crepitant rales. Blood tests show neutrophilic leukocytosis, a shift in the leukocyte count to the left, and an increase in ESR. On radiographs in the initial phase of the disease, inflammatory infiltration of the lung tissue without clear boundaries is determined, the intensity and prevalence of which may subsequently increase.

signs of severe purulent intoxication: increasing weakness, sweating, lack of appetite, loss of body weight, the appearance and increase of anemia, increased leukocytosis and a shift in the leukocyte formula, tachycardia, high temperature with hectic ranges. Due to the involvement of the pleural layers in the inflammatory process, pain increases significantly, especially with deep breathing.

In typical cases first phase of purulent-necrotic melting of the lung continues for 6-8 days, and then there is a breakthrough of the abscess into the bronchi. From this moment on, we can conditionally distinguish the second phase - phase of open pulmonary abscess. The leading clinical symptom of this period is the release of purulent or putrefactive sputum, which may contain an admixture of blood. When settled in a vessel, the sputum is divided into three layers. Detritus accumulates thickly at the bottom, above it there is a layer of turbid liquid (pus) and foamy mucus is located on the surface. In the sputum you can see small pulmonary sequesters, and microscopic examination reveals large quantities of leukocytes, elastic fibers, cholesterol, fatty acids and a variety of microflora.

After the abscess begins to empty through the draining bronchus, the patient’s condition improves: body temperature decreases, appetite appears, and leukocytosis decreases. Physical data change: the area of shortening of the percussion sound decreases, symptoms of a cavity in the lung appear. During an X-ray examination at this time, against the background of inflammatory infiltration of the lung tissue, an abscess cavity with a horizontal fluid level is usually clearly visible.

Diagnosis radiography of destruction cavities, most often with a horizontal fluid level and perifocal inflammatory infiltration of the lung tissue. Superexposed images or tomograms help detect decay cavities in the lungs. Pulmonary sequestration is diagnosed using tomography.

Treatment.. After spontaneous opening of the abscess into the lumen of the bronchus, the simplest and most effective method of drainage is postural drainage. Swelling of the bronchial mucosa can be reduced by local use of bronchodilators (ephedrine, novodrine, naphthyzine) and antibiotics (morphocycline, monomycin, ristomycin, etc.) in the form of aerosols.

bronchoscopic sanitation of the tracheobronchial tree is indicated.

empty the abscess through chest wall. To do this, under local anesthesia, either repeated punctures of the abscess cavity with a thick needle are performed, or continuous drainage is carried out using a catheter passed through a trocar (thoracentesis). The drainage installed in the abscess cavity is sutured to the skin, connected to a vacuum apparatus, and the abscess is periodically washed with antiseptic solutions and antibiotics. From operational methods the simplest is pneumotomy, which is indicated when other methods of emptying the abscess from purulent-necrotic contents are unsuccessful. Pneumotomy can be performed under general anesthesia or local anesthesia. The abscess in the lung is opened and drained after thoracotomy and subperiosteal resection of fragments of one or two ribs.

Radical operations for acute suppuration of the lungs (lobectomy, bilobectomy, pneumonectomy) are classified as complex and dangerous. They are fraught with the occurrence of various complications (empyema, bronchial fistula, pericarditis, etc.).

. LUNG GANGRENE Lung gangrene- this is a purulent-putrefactive decay of a necrotic lobe or the entire lung, not separated from the surrounding tissue by a delimiting capsule and having a tendency to progress, which usually causes an extremely difficult general condition of the patient.

The development of pulmonary suppuration of the gangrene type is characterized by severe manifestations of intoxication and the rapid course of a purulent-destructive process.

In typical cases, pulmonary gangrene begins acutely, with a sharp rise in temperature, stunning chills, chest pain and severe intoxication. Early on, a putrid smell appears when breathing and a cough with a large amount of fetid, foamy, dirty gray or dirty brown (due to the admixture of hematoidin) sputum. With gangrene of the lung, the sputum is divided into three layers: the upper layer is mucopurulent, foamy, the middle layer is serous, liquid, brown in color, and the lower layer consists of scraps of lung tissue and purulent plugs of Dietrich. Despite profuse coughing up of sputum, there is no improvement in the condition of patients with gangrene of the lungs. Repeated chills in combination with hectic fever and increasing intoxication indicate the spread of the process to new areas of the lung.

In some cases, gangrene of the lungs develops slowly, without a clear clinical picture, which is typical for some forms of anaerobic destruction and with a decrease in the general reactivity of the patient due to immunodeficiency.

There are no specific physical signs of pulmonary gangrene. Over the affected lung, there is pain in the chest due to the early involvement of the pleura in the inflammatory process and a dull pulmonary sound upon percussion; Auscultation reveals bronchial breathing, moist rales of various sizes, and pleural friction noise. On the part of the cardiovascular system, tachycardia is pronounced, blood pressure is reduced..

In g emogram pronounced changes are noted - high leukocytosis, a sharp shift in the leukocyte formula to the left, toxic granularity of neutrophils, anemia appears early, and with further progression of lung gangrene, leuko- and lymphopenia develops, often aneosinophilia.

X-ray examination in the initial stage of pulmonary gangrene reveals massive inhomogeneous shading of a significant area of lung tissue- usually a lobe or two lobes of the lung

Radiologically, rapid negative dynamics of the disease are noted - the appearance of multiple cavities of destruction in the lungs, in the largest of them sequestration of the lung tissue is determined, exudative pleurisy will join early

For widespread gangrene of the lung, pneumonectomy is usually performed.

Etiological characteristics:

· primary;
· secondary;
· tertiary.
- Prevalence:
- · local: limited, unlimited;
- widespread (spilled).
- Character of the exudate:
· serous-fibrinous;
· fibrinous-purulent;
· purulent;
fecal
· bile;
· hemorrhagic;
· chemical.
- Process flow phase:
· absence of sepsis;
· sepsis;
· severe sepsis;
· septic (infectious-toxic) shock.

The classification is based on the identification of three etiological categories of primary, secondary, and tertiary peritonitis.

Primary peritonitis (1-5%) is considered to be forms of the disease in which the inflammatory process develops without compromising the integrity of the hollow organs, and peritonitis is the result of spontaneous hematogenous dissemination of microorganisms into the peritoneal cover or translocation of a specific monoinfection from other organs. As a type of primary peritonitis, spontaneous peritonitis in children, spontaneous peritonitis in adults and tuberculous peritonitis are distinguished. Pathogens are usually represented by monoinfection.

· “Spontaneous” peritonitis in children occurs in the neonatal period or at the age of 4-5 years. In the latter case, the presence of systemic diseases (lupus erythematosus) or nephrotic syndrome may be a predisposing factor.
· Spontaneous peritonitis in adults often develops after drainage of ascites caused by cirrhosis of the liver, as well as with prolonged use of a catheter for peritoneal dialysis. This form also includes peritonitis, which develops in women due to the translocation of bacteria into the abdominal cavity from the vagina through the fallopian tubes.
· Tuberculous peritonitis is a consequence of hematogenous infection of the peritoneum with specific intestinal lesions, as well as with tuberculous salpingitis and tuberculous nephritis.

Secondary peritonitis is the most common category; it combines several types of peritonitis.

- Peritonitis caused by perforation and destruction of abdominal organs.
- Postoperative peritonitis.
- Post-traumatic peritonitis:
due to closed (blunt) abdominal trauma;
due to penetrating abdominal wounds.

Postoperative peritonitis is considered separately from post-traumatic peritonitis, although surgery is also an injury. The fact is that during the operation, the degree of negative consequences of tissue damage is significantly reduced by improving surgical techniques and instruments, and the body’s reaction to damage is leveled out by multicomponent anesthesia.

Tertiary peritonitis is particularly difficult to diagnose and treat. This term refers to inflammation of the peritoneum, which is of a “recurrent” nature, sometimes referred to as “persistent” or “recurrent” peritonitis. It usually develops in the postoperative period in patients (or wounded, victims) who have survived extreme, critical situations, and who have a pronounced depletion of anti-infective defense mechanisms. The course of such peritonitis is characterized by a blurred clinical picture, possible multiple organ dysfunction and the manifestation of endotoxicosis refractory to therapy. The main risk factors for the development of tertiary peritonitis are considered to be malnutrition (exhaustion) of the patient, a decrease in the concentration of albumin in plasma, the presence of problematic pathogens, usually resistant to most antibiotics used, and developing organ failure.

The main difference between secondary and tertiary peritonitis is that the clinical picture of secondary peritonitis is caused by the body’s protective reaction in the form of the release of a large number of pro-inflammatory cytokines in response to the entry of an infectious agent and the developing destructive process in one of the sections of the abdominal cavity. While tertiary peritonitis, according to most authors, is considered as the inability of the patient’s body to form an adequate response at the systemic and local levels as a result of the prevalence of anti-inflammatory cytokines (as a result of depletion of the pro-inflammatory pool of cytokines) in response to a developing infectious process in the abdominal cavity. During surgery, it is not always possible to determine the source of tertiary peritonitis.

In practical terms, the division of peritonitis into local and widespread (spread) can be considered fundamentally important. In this case, local peritonitis is divided into limited (inflammatory infiltrate, abscess) and unlimited, when the process is localized only in one of the peritoneal pockets. If with local peritonitis, starting from the access, along with eliminating the source, the task is reduced to sanitation of only the affected area with measures taken to prevent the spread of the process, then with widespread peritonitis, extensive sanitation is required, often with repeated lavage of the abdominal cavity.

The clinical course of peritonitis and the appropriate treatment tactics depend on the nature of the inflammatory exudate and pathological impurities coming from the hollow organs of the abdomen. The characteristics of exudates listed in the classification (serous-fibrinous, fibrinous-purulent, purulent) cover the main types of peritonitis used by practical surgeons with a focus on this classification principle when making a postoperative diagnosis.

The list of characteristics depending on pathological impurities (fecal, bile, hemorrhagic and chemical peritonitis) also includes important components that determine qualitative differences in the clinical course of peritonitis and affect the prognosis. Therefore, they are usually indicated in the postoperative diagnosis. The diagnosis of fecal peritonitis is made when there is significant contamination of the exudate with the contents of the colon or ileum.

This pathological admixture portends a severe clinical course due to the abundant entry of anaerobic and gram-negative microflora into the exudate, which is a nutritious protein medium. An admixture of uninfected bile can cause a short-term chemical irritant effect on the peritoneum, after adaptation to which the inflammatory process in the abdominal cavity may not progress for a relatively long time (up to several weeks) until secondary infection of the exudate occurs. Hemorrhagic peritonitis (when blood spilled into the abdominal cavity is mixed with the exudate) is associated with the danger of rapid colonization of microflora in conditions of an enriched nutrient medium (blood) and a thermostable regime characteristic of the internal environments of the body.

Finally, it is appropriate to talk about chemical peritonitis in the early stages of uninfected pancreatic necrosis or perforation of gastroduodenal ulcers. Aggressive chemical impurities contribute to the early clinical manifestation of this form of peritonitis, which results in early operations (for perforated ulcers) or removal of exudate during laparoscopic revision (for destructive peritonitis), and this in turn creates more favorable conditions for effective treatment.

After the introduction of the concept of “abdominal sepsis” into the domestic literature in recent years, it has become possible with sufficient certainty to distinguish between the phases of development of the pathological process during peritonitis, depending on the presence of signs of sepsis and its severity.

In addition to the indicated characteristics of peritonitis, the clinical diagnosis should first indicate its nosological cause (the underlying disease).