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Peritonitis is a serious complication of inflammatory-destructive diseases of the abdominal cavity, accompanied by pronounced local and general symptoms, the development of multiple organ failure. Mortality from peritonitis in gastroenterology is 20-30%, and in the most severe forms it reaches 40-50%.
Peritoneum (peritoneum) is formed by two serous sheets passing through each other - visceral and parietal, covering the internal organs and walls of the abdominal cavity. Peritoneum is a semipermeable, actively functioning membrane that performs many important functions: resorptive (absorption of exudate, products of lysis, bacteria, necrotic tissues); Exudative (discharge of serous fluid), barrier (mechanical and antimicrobial protection of the abdominal cavity), etc. The most important protective property of the peritoneum is its ability to distinguish inflammation in the abdominal cavity due to fibrous spikes and scars, as well as cellular and humoral mechanisms.
The etiologic link in peritonitis is a bacterial infection, in most cases represented by the nonspecific microflora of the gastrointestinal tract. It can be gram-negative (enterobacter, E. coli, Proteus, Pseudomonas aeruginosa) and Gram-positive (staphylococcus, streptococci) aerobes; Gram-negative (fusobacteria, bacteroides) and Gram-positive (eubacteria, clostridia, peptococci) anaerobes. In 60-80% of cases, peritonitis is caused by the association of microbes - more often with E. coli and staphylococcus. Less often the development of peritonitis is due to a specific microflora - gonococci, hemolytic streptococcus, pneumococci, mycobacteria tuberculosis. Therefore, to select a rational treatment of peritonitis, bacteriological sowing of the contents of the abdominal cavity with the sensitivity of the isolated microflora to antibacterial drugs is paramount.
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 lymphogenous, hematogenous or by fallopian tubes. Direct inflammation of the peritoneum can 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 experience secondary peritonitis, which develops as a result of childhood inflammatory diseases or abdominal injuries. Most often, peritonitis complicates the course of appendicitis (perforated, phlegmonous, gangrenous), perforated gastric ulcer or duodenum, pyosalpinx, rupture of the ovarian cyst, intestinal obstruction, infringement of the hernia, acute occlusion of mesenteric vessels, Crohn's disease, diverticulitis, phlegmonous gangrenous cholecystitis, Pancreatitis, pancreatic necrosis and other diseases.
Post-traumatic peritonitis develops due to closed and open injuries of the abdominal organs. The causes of postoperative peritonitis can be the failure of anastomoses, defects in ligation, mechanical damage to the peritoneum, intraoperative infection of the abdominal cavity, hemoperitoneum with inadequate hemostasis. Separately, there are carcinomatous, parasitic, granulomatous, rheumatoid peritonitis.
The etiology distinguishes 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, chyleic fluid). Abacterial peritonitis takes a rather rapid microbial character as a result of the attachment of infectious pathogens from the lumen of the digestive tract.
Depending on the nature of the peritoneal effusion, there are serous, fibrinous, hemorrhagic, bile, purulent, fecal, putrefactive peritonitis. According to the clinical course, peritonitis is divided into acute and chronic. Given the prevalence of lesions on the surface of the peritoneum, there are distinguished (local) and diffuse peritonitis. The variants of local peritonitis include subdiaphragmatic, appendicular, subheading, intestinal, pelvic abscesses. About diffuse peritonitis is said when the inflammation of the peritoneum has no tendency to limit and clear boundaries. By the degree of defeat of the peritoneum, diffuse peritonitis is divided into local (developing in one anatomical region, near the source of infection), common (covering several anatomical regions) and common (with total peritoneal injury).
In the development of peritonitis, it is customary to isolate the early phase (up to 12 hours), late (up to 3-5 days) and final (6 to 21 days from the onset of the disease). In accordance with pathogenetic changes, the reactive, toxic and terminal stages of peritonitis are distinguished. In the reactive stage of peritonitis (24 hours from the moment of injury of the peritoneum) there is a hyperergic reaction to irritation of the peritoneum; In this phase, local manifestations are most pronounced and general symptoms are less pronounced. 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), defensive-compensatory mechanisms are depleted, deep violations of the vital functions of the body develop.
In the reactive period of peritonitis, abdominal pain is noted, the localization and intensity of which are determined by the cause of inflammation of the peritoneum. Initially, the pain has a clear localization in the source of inflammation; Can irradiate into the shoulder or supraclavicular area due to irritation of the nerve endings of the diaphragm with a purulent-inflammatory exudate. Gradually, the pain spreads all over the stomach, become unfloppy, lose clear localization. In the terminal period, due to the paralysis of the nerve endings of the peritoneum, the pain syndrome becomes less intense. Symptoms of peritonitis are nausea and vomiting of gastric contents, which in the initial stage appear reflexively. In later terms, peritonitis, an emetic reaction is caused by intestinal paresis; In vomit masses there is an admixture of bile, then - the contents of the intestine (fecal vomiting). Due to pronounced endotoxicosis, paralytic intestinal obstruction develops, clinically manifested by stool retention and non-removal of gases.
With peritonitis, even at the earliest stage, the external appearance of the patient attracts attention: a painful facial expression, adynamia, pallor of the skin, cold sweat, acrocyanosis. The patient takes a forced position, relieving the pain - more often on the side or back with legs clamped to the abdomen. Breathing becomes superficial, fever is elevated, hypotension is noted, tachycardia 120-140 ud. In minutes, not corresponding to the subfebrile condition. In the terminal stage of peritonitis, the patient's condition becomes extremely difficult: consciousness is confused, euphoria is sometimes observed, facial features are sharpened, the skin and mucous pale with icteric or cyanotic shade, the tongue is dry, covered with a dark bloom. The abdomen is swollen, with palpation is not very painful, and "grave silence" is heard at auscultation.
Palpatory study of the abdomen reveals positive peritoneal symptoms: Shchetkin-Blumberg, Voskresensky, Medel, Bernstein. Percussion of the abdomen with peritonitis is characterized by blunting sound, which indicates swelling in the free abdominal cavity; The auscultural picture allows you to talk about the decrease or absence of intestinal noises, listen to the symptom of "deathly silence", "falling drops", "noise of splashing". Rectal and vaginal examination with peritonitis allows to suspect inflammation of pelvic peritoneum (pelvioperitonitis), the presence of exudate or blood in the Douglas space. Survey radiography of the abdominal cavity with peritonitis, caused by perforation of hollow organs, indicates the presence of free gas (symptom "sickle") under the dome of the diaphragm; In the intestinal obstruction the Clauber cups are found. Indirect radiographic signs of peritonitis are high standing and limited excursion of the dome of the diaphragm, the presence of effusion in the pleural sinuses. Free fluid in the abdominal cavity can be determined by ultrasound.
Changes in the general analysis of blood in peritonitis (leukocytosis, neutrophilia, increased ESR) indicate purulent intoxication. Laparocentesis (abdominal puncture) and diagnostic laparoscopy are indicated in cases unclear for diagnosis and allow one to judge the cause and nature of peritonitis.
The detection of peritonitis is the basis for emergency surgical intervention. The therapeutic tactics for peritonitis depends on its cause, but in all cases, during the operation, the same algorithm is followed: the performance of laparotomy, isolation or removal of the source of peritonitis, intra- and postoperative sanation of the abdominal cavity, ensuring the decompression of the small intestine. Operative access for peritonitis is median laparotomy, which provides visualization and reach of all parts of the abdominal cavity. Elimination of the source of peritonitis may include perforation suturing, appendectomy, colostomy, resection of the necrotic bowel area, etc. All reconstructive interventions are postponed to a later date. For intraoperative sanation of the abdominal cavity, solutions cooled to + 4-6 ° C in a volume of 8-10 liters are used. Decompression of the small intestine is provided by installing the nasogastrointestinal probe; The colon is drained through the anus. Surgery for peritonitis is completed by installing in the abdominal cavity of chlorovinyl drains for aspiration of exudate and intraperitoneal administration of antibiotics.
Postoperative management of patients with peritonitis includes infusion and antibacterial therapy, the appointment of immunocorrectors, transfusion of leukocyte mass, intravenous administration of ozonized solutions, etc. For antimicrobial therapy of peritonitis, a combination of cephalosporins, aminoglycosides and metronidazole is often used, which provides the effect on the entire spectrum of possible pathogens.
In the treatment of peritonitis, the use of extracorporeal detoxification methods (hemosorption, plasmapheresis, lymphosorption, hemodialysis, enterosorption, etc.), hyperbaric oxygenation, UFO of blood, VLOK is effective.
In order to stimulate peristalsis and restore the functions of the gastrointestinal tract, the appointment of anticholinesterase drugs (neostigmine), ganglion blockers (dimecolonium iodide, benzohexonium), anticholinergic agents (atropine), potassium preparations, physiotherapy (intestinal stimulation, diadynamotherapy).