Peritonitis - Causes and Pathogenesis

Causes of peritonitis

The main cause of the disease is microbial invasion.

The latter is fundamentally possible in gynecological patients due to the action of three mechanisms:

1. Hematogenous or lymphogenous infection of the peritoneum - the so-called idiopathic peritonitis without a focus of pus or destruction in the abdominal cavity - an extremely rare form of peritonitis in girls or young women. Pathogens - hemolytic streptococcus, pneumococcus, associative flora.
2. Progression of acute purulent inflammation (ascending route of infection):
   • Specific purulent salpingitis - pelvic peritonitis - peritonitis (pathogens - gonococcus in association with STIs, sometimes anaerobes).
   • Obstetric peritonitis due to the progression of endometritis: endometritis - endomyometritis - panmetritis - peritonitis (pathogens - associative flora with a predominance of gram-negative and anaerobic) or, alternatively: endomyometritis - purulent salpingo-oophoritis - pelvic peritonitis - peritonitis (pathogens - gonococcus in association with anaerobes).
   • Peritonitis due to criminal interventions: endometritis - endomyometritis - panmetritis - peritonitis (pathogens - associative flora with a predominance of anaerobic).
   • Peritonitis after cesarean section (direct infection of the peritoneum during surgery or due to failure of the sutures on the uterus). Pathogens - associative flora with a predominance of gram-negative.
3. Infection of the abdominal cavity in the presence of a chronic purulent focus in the abdominal cavity.
   • Perforation or rupture of an encapsulated abscess into the free abdominal cavity - rupture of pyosalpinx, pyovarium, purulent tubo-ovarian formation, extragenital abscesses. Pathogens - associative flora (anaerobic and gram-negative), less often gram-positive.
   • Perforation or rupture of an encapsulated abscess in patients with delayed complications of cesarean section (formation of secondary uterine suture failure and other purulent foci against the background of endometritis) - rupture of a purulent tubo-ovarian formation, extragenital abscesses, abscess of the Douglas space. Pathogens - associative flora with a predominance of gram-negative and anaerobic.

[ 1 ], [ 2 ], [ 3 ], [ 4 ], [ 5 ], [ 6 ]

Pathogenesis of peritonitis

The most severe form of anaerobic peritonitis is caused by B. fragilis, P. melannogenicus and other bacteroids, with tissue breakdown, formation of isolated purulent foci and frequent development of pelvic thrombophlebitis and sepsis.

The obligatory components of peritonitis in the initial stage are hyperemia of the peritoneum and the formation of fibrinous deposits on it. The latter serve as the main place of concentration of microbial flora.

The leading role in the pathogenesis of peritonitis is played by intoxication caused by the action of bacterial decay products (toxins), tissue proteases, biogenic amines, as well as hypovolemia and paresis of the stomach and intestines.

Together with reflex effects, toxic substances of bacterial origin increase capillary permeability and lead to the formation of inflammatory exudate. Fluid losses can reach 50% of the total extracellular fluid of the body (up to 7-8 l) due to its movement into the abdominal organs, as well as deposition and sequestration in the vessels of the abdominal cavity. Hypovolemia is one of the main pathogenetic links of diffuse peritonitis. Another important link is microcirculation disorders, which largely contribute to the development and deepening of hypovolemia.

Further increase in intoxication during peritonitis and growth of protein losses (hypo- and dysproteinemia) lead to deepening of microcirculatory disorders. If at the first stages of these disorders protein and fluid pass from tissues into the bloodstream, then during decompensation the reverse movement occurs. This is facilitated by increasing aggregation of formed elements, capillary thrombosis and accumulation of substances that expand blood vessels (histamine, serotonin), which further increase the permeability of vascular walls. Central hemodynamic indicators do not fully reflect the state of peripheral circulation. A noticeable change in arterial pressure and cardiac index often occurs when irreversible phenomena occur in the microcirculation system.

As peritonitis progresses and intoxication increases, the liver, which is the main barrier to toxins, gradually loses its antitoxic function, and the increasing changes are aggravated by metabolic disturbances in the liver itself and other organs. In this regard, combating intoxication is one of the main tasks in treating peritonitis.

A special role in the pathogenesis of peritonitis belongs to the functional obstruction of the gastrointestinal tract. Several mechanisms of its development are distinguished. The main one is neuroreflex inhibition, which occurs when the peritoneum is irritated by the type of viscero-visceral reflexes and reactions of the central nervous system. In the future, intestinal motility is additionally suppressed as a result of toxic effects both on the central nervous system and on the intestine's own nervous and muscular apparatus. At various stages of the development and course of peritonitis, the state of the gastrointestinal tract is also affected by disturbances in electrolyte balance and acid-base balance, since hypokalemia and acidosis significantly reduce the contractility of the intestinal muscular wall.

Functional intestinal obstruction makes proper nutrition impossible, which aggravates all types of metabolic processes, causes vitamin deficiency, dehydration, electrolyte imbalance, adrenal and enzymatic systems. The development and course of peritonitis is always associated with large protein losses by the body. Albumin losses are especially large.