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Peritonitis indicates inflammation of the peritoneal layer in the abdominal cavity that arises when local mediator cascades are activated by different factors. Depending on the pathogenesis, it can be classified into three types: primary, secondary or tertiary peritonitis – each of them considered a separate clinical entity.
Peritoneal mesothelial cells are not inactive cells, but play essential roles in peritoneal homeostasis and synthesize a plethora of cytokines, growth factors, proteases and matrix proteins. Peritonitis causes severe injury to those cells, peritoneal host defense as a whole, as well as the maintenance of the peritoneal membrane structure.
There is a principal, surgically pertinent causal problem in most forms of peritonitis that is related to abdominal sepsis. Nevertheless, peritonitis is inhomogeneous in regards to its cause, pathophysiology and severity, thus every single case necessitates a meticulous approach.
The pathogenesis of primary or spontaneous bacterial peritonitis is related to altered host defenses observed in end-stage liver disease, deficient ascitic fluid antibacterial activity, overgrowth of microorganisms, as well as bacterial translocation from the intestinal lumen to mesenteric lymph nodes.
The gram-negative aerobic bacteria are the major factor in the development of spontaneous bacterial peritonitis (most notably Escherichia coli and Klebsiella pneumoniae), but Staphylococcus aureus and other gram-positive bacteria are being considered as emerging agents causing this inflammation. Anaerobes and microaerophilic organisms are still infrequently reported.
In prepubescent girls, primary peritonitis is apparently a result of an ascending genital infection, which can be confirmed by the finding of bacterium Streptococcus pneumoniae in vaginal secretions and peritoneal fluid. In this age group, alkaline vaginal secretions do not sufficiently inhibit growth of bacteria in comparison to postpubescent females with acidic secretions.
Although the number of bacteria present in an episode of spontaneous bacterial peritonitis is usually very low, they excite an intense inflammatory response. That leads to a dramatic increase in the concentrations of polymorphonuclear leukocytes and inflammatory cytokines within the ascitic fluid.
The ascitic total protein has been shown as a predictive tool, therefore the risk for the development of this type of peritonitis is higher when there is less than 1 g/dL of total protein. Other described risk factors are serum bilirubin concentration above 2.5 mg/dL, variceal bleeding, and a prior episode of spontaneous bacterial peritonitis.
Secondary peritonitis arises as a result of an inflammatory process in the peritoneal cavity secondary to inflammation, perforation, or gangrene of an intra-abdominal or retroperitoneal structure. Some of the more common causes include appendicitis, pancreatitis, diverticulitis, acute cholecystitis and perforated peptic ulcer.
Other nonbacterial causes of peritonitis include leakage of the blood into the peritoneal cavity due to a rupture of a tubal pregnancy, ovarian cyst or aneurysmal vessel. As blood is highly irritating to the peritoneum, it may cause abdominal pain akin to septic peritonitis.
Aseptic peritonitis may also be caused if a sterile foreign body is inadvertently left in the peritoneal cavity after surgery (for example, surgical sponges, instruments or starch from surgical gloves). This condition can also be a complication of certain systemic diseases such as porphyria, systemic lupus erythematosus or Familial Mediterranean fever.
Tertiary peritonitis is defined as the persistence or recurrence of intra-abdominal infection following ostensibly adequate therapy of primary or secondary peritonitis. This type of the inflammation of the peritoneum is associated with higher mortality than secondary peritonitis.
Age of the patient, malnutrition, underlying etiology of peritonitis and presence of multidrug resistant microorganisms are some of the risk factor that predispose to the development of tertiary peritonitis. In this type of peritonitis opportunistic and nosocomial facultative pathogenic bacteria (but also fungi) predominate as the main microbial causes.