Peritonitis pathophysiology

Peritonitis Main Page
Patient Information
Overview
Causes
Classification Spontaneous Bacterial Peritonitis Secondary Peritonitis
Differential Diagnosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2]

• The main causes of peritonitis are the acute inflammation of the abdominal viscera, discontinuity and increased permeability of their walls, open and closed traumas of the abdomen with the damage of viscera followed by microbial contamination of peritoneal cavity.
• Despite the cause of peritonitis, the disease is characterized by a typical bacterial inflammation.
• Chronic peritonitis mainly caused by extraperitoneal (lungs, lymph nodes) tuberculosis, entering the peritoneal cavity through hematogenous way.
• Spontaneous bacterial peritonitis is thought to result from a combination of factors often related to Cirrhosis and preexisting ascites, such as:
• In patients with diseased liver and altered portal circulation a defect in the usual phagocytic activity results in the hematogenous spread of organisms
• prolonged bacteremia secondary to compromised host defenses
• Intrahepatic shunting of colonized blood and
• Defective bactericidal activity within the ascitic fluid. Contrary to earlier theories, transmucosal migration of bacteria from the gut to the ascitic fluid is no longer considered to play a major role in the etiology of SBP.
• With respect to compromised host defenses, patients with severe acute or chronic liver disease are often deficient in complement and may also have malfunctioning of the neutrophilic and reticuloendothelial systems.
• As for the significance of ascitic fluid proteins, it was demonstrated that cirrhotic patients with ascitic protein concentrations below 1 g/dL were 10 times more likely to develop SBP than individuals with higher concentrations. Additional studies have confirmed the validity of the ascitic fluid protein concentration as the best predictor of the first episode of SBP.

Secondary peritonitis

Bacteria and digestive enzymes act on the peritoneal serosal surface lead to enzymatic digestion and necrosis and an outpouring of serum protein and electrolytes from the blood to the cavity. There is formation of exudate rich in granulocytes, which may be diffuse or confined to an abscess. Systemically, there is paralysis of the bowel, hemoconcentration occurs, and alterations of the cardiac output due to the shift of fluids and later acidosis. Intrapulmonary shunting, hypo- or hypercapnia, hypoxemia, progressive azotemia, acute tubular necrosis, weight loss by protein consumption, fall of body temperature, loss of heat production, and exhaustion are other complications that may lead to the death of the patient, if the process is not interrupted.