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3 fractors determine the pathogeneis of the SBP:
Bacterial overgrowth in cirrhotic patients: Secondary to decreased intestinal motility and frequent use of PPIs in this population of patients. Defensive intestinal barrier in the Both secretory and physical barriers are defective in cirrhotic patients: (1) Decreased immunity: both local and systemic immunity are decreased.
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A. Bacterial overgrowth:
Intestinal mobility decreses with cirrhosis. Increased symapathetic drive and oxidant stress are believed to be the reasons for the decreased mobility. Also, cirrhotic patients administer PPIs more frequently than other populations. The diminished intestinal mobility makes the intestinal contents more stagnant and allows the bacterial contents to flourish and overgrow and thus predisposes to cirrhosis. (2)
B. Increased bowel permeability: Normally .. the intestinal mucosa is impermeable using 2 lines of defence.(1) Secretory componenet which physical component. Both are affected with the development of cirrhosis.
Secretory defense mechanism is composed of mucins, immunoglobulins and bile salts. Bile salts is protective through preventing adherence and internalization of bacteria. Bile acids are decreased in cirrhosis partly due to decreased secretion from diseased liver and partly from increased conjugation by the flourishing intestinal flora. This gives bacteria easier access through the mucosa.
Physical componenet is the intestinal epithelium itself. Intestinal musosa is more permeable as a result of Increased oxidant stress. NO proinflammatory cytokines Increased intercellular spaces as a result of vasodilation, edema from portal hypertension.
Decreased local and systemic immune responses: Kupffer cells (local macrophages of the liver) normally contribute in eradicating infection with neutrophils. But as a rsult of the extrahepatic porto-systemic shunts, bacteria in the circulation do not come in contact with these cells. And as a result of defective liver secretory functions, complement levels decrease (in serum and ascitic fluid) and the neutrophils seems to have qualitative deficiencies.
Bacteria that translocates are carried through lymphatics. It can reach to the ascitic fluid either through the circulation then through the liver it can have access to the peritoneal cavity. Another way is through rupture of the lymphatic vessel carrying the contaminated lymph under pressure from the portal hypertension and the increased lymph content.