Pathogenesis of cholangitis in obstructive jaundice-revisited.

Obstructive jaundice produces a number of biochemical and physiologic alterations in the biliary tract. Acute cholangitis occurs in an infected, usually obstructed biliary system, at the level of the common bile duct. The most common cause of obstruction is stones. Bacterial reflux from the biliary tract to the systemic circulation is considered to be the primary etiologic factor in bacteremia and the development of sepsis in cholangitis. The main factors in the pathogenesis of acute cholangitis are biliary tract obstruction, elevated intraluminal pressure, and infection of bile. The bile is normally sterile. The route of infection may be ascending, hematogenous or by lymphatics. Bactibilia (presence of bacteria in the biliary tract) increases in the presence of biliary obstruction, particularly partial and in the presence of foreign bodies like stones. Obstruction produces local changes in the host defenses, both in chemotaxis and phagocytosis along with systemic changes. The absence of bile and secretary IgA from the gastrointestinal tract because of biliary obstruction produces changes in the bacterial flora, loss of mucosal integrity, decreased endotoxin inactivation and promotes bacterial overgrowth, portal bacteremia, endotoxemia and increased translocation of endotoxin (LPS) to the liver, resulting in sepsis and also serving to inhibit hepatic macrophage (Kupffer cell) function in these patients. Early intervention in relieving biliary decompression is imperative in restoring normal function of the Kupffer cells in the liver and to prevent functional alterations in the liver because of chronic obstruction and cholestasis and to decrease the postoperative morbidity and mortality.