Navaneethan U, Jayanthi V, Mohan P
Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
Minerva Gastroenterol Dietol. 2011 Mar;57(1):97-104.
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.
梗阻性黄疸会在胆道产生一系列生化和生理改变。急性胆管炎发生于通常被阻塞的、受感染的胆道系统，位于胆总管水平。最常见的梗阻原因是结石。胆道细菌反流至体循环被认为是菌血症及胆管炎中脓毒症发生的主要病因。急性胆管炎发病机制的主要因素是胆道梗阻、管腔内压力升高及胆汁感染。胆汁通常是无菌的。感染途径可能是上行性、血源性或经淋巴管。在存在胆道梗阻尤其是部分梗阻以及存在结石等异物的情况下，胆道细菌感染（胆道内存在细菌）会增加。梗阻会导致宿主防御机制出现局部变化，包括趋化作用和吞噬作用，同时伴有全身变化。由于胆道梗阻，胃肠道内胆汁和分泌型IgA缺失，会导致细菌菌群改变、黏膜完整性丧失、内毒素失活减少，并促进细菌过度生长、门静脉菌血症、内毒素血症以及内毒素（脂多糖）向肝脏的易位增加，从而导致脓毒症，还会抑制这些患者肝脏巨噬细胞（库普弗细胞）的功能。早期进行胆道减压干预对于恢复肝脏库普弗细胞的正常功能、预防因慢性梗阻和胆汁淤积导致的肝脏功能改变以及降低术后发病率和死亡率至关重要。
