Peritonitis: causes and pathogenesis

Causes of peritonitis

The main cause of the disease is microbial invasion.

The latter in gynecological patients is principally possible 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 ablation in the abdominal cavity - an extremely rare form of peritonitis in girls or girls. Pathogens - hemolytic streptococcus, pneumococcus, associative flora.
2. Progression of acute purulent inflammation (ascending way of infection):
   • Specific purulent salpingitis - pelvioperitonitis - peritonitis (pathogens - gonococcus in association with STI, sometimes anaerobes).
   • Obstetric peritonitis due to progression of the endometritis: endometritis - endomyometritis - panmetritis - peritonitis (pathogens - associative flora with predominance of gram-negative and anaerobic) or as an option: endomyometritis - purulent salpingoophoritis - pelvic peritonitis - peritonitis (pathogens - gonococcus in association with anaerobes).
   • Peritonitis due to criminal interventions: endometritis - endomyometritis - panmetritis - peritonitis (pathogens - associative flora with prevalence of anaerobic).
   • Peritonitis after caesarean section (direct infection of the peritoneum during surgery or due to insufficiency of the sutures on the uterus). Pathogens are an associative flora with a predominance of gram-negative flora.
3. Infection of the abdominal cavity in the presence of a chronic suppurative focus in the abdominal cavity.
   • Perforation or rupture of the encapsulated abscess into the free abdominal cavity - rupture of pyosalpinx, pyovar, purulent tubo-ovarian formation, extragenital abscesses. Pathogens - associative flora (anaerobic and gram-negative), less often gram-positive.
   • Perforation or rupture of encysted abscess in patients with delayed complications of caesarean section (formation of secondary inconsistency of sutures on the uterus and other purulent foci against the background of endometriometritis) is the rupture of purulent tubo-ovarian formation, extragenital abscesses, and 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 difficult - with the disintegration of tissues, the formation of isolated purulent foci and the frequent development of pelvic thrombophlebitis and sepsis - anaerobic peritonitis is caused by B. Fragilis, P. Melannogenicus and other bacteroides.

Mandatory components of peritonitis in the initial stage are hyperemia of the peritoneum and the formation of fibrinous overlays on it. The latter serve as the main site for the concentration of microbial flora.

The leading role in the pathogenesis of peritonitis is intoxication due to the action of the decay products of bacteria (toxins), tissue proteases, biogenic amines, and hypovolemia and paresis of the stomach and intestines.

Together with reflex effects toxic substances of bacterial origin increase the permeability of capillaries and lead to the formation of inflammatory exudate. Loss of fluid can reach 50% of the whole extracellular fluid of the body (up to 7-8 L) by moving it to 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 the disturbance of microcirculation, which in many ways contribute to the development and deepening of hypovolemia.

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

With the progression of peritonitis and the growth of intoxication, the liver, which is the main barrier to toxins, gradually loses its antitoxic function, and the growing changes are aggravated by metabolic disturbances in the liver and other organs. In this regard, the fight against intoxication is one of the main tasks in the treatment of peritonitis.

A special role in the pathogenesis of peritonitis belongs to the functional obstruction of the gastrointestinal tract. There are several mechanisms for its development. The main one is neural-reflex inhibition, which occurs when the peritoneum is irritated by the type of viscer-visceral reflexes and reactions of the central nervous system. In the future, the intestinal motility is further inhibited by toxic effects on both the central nervous system and the nerve and muscular apparatus of the intestine. At various stages of development and course of peritonitis, the state of the gastrointestinal tract is also affected by violations of electrolyte balance and acid-base state, since hypokalemia and acidosis significantly reduce the contractile capacity of the muscular wall of the intestine.

With functional intestinal obstruction, full nutrition is impossible, which aggravates all kinds of metabolic processes, causes vitamin deficiency, dehydration, electrolyte balance disturbance, adrenal and enzymatic systems. The development and flow of peritonitis is always associated with large losses of the body protein. Especially large losses of albumin.