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| AuthorNezam H Afdhal, MD, FRCPI | Section EditorsSanjiv Chopra, MDStephen B Calderwood, MD | Deputy EditorAnne C Travis, MD, MSc |
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Acute cholangitis is a clinical syndrome characterized by fever, jaundice, and abdominal pain that develops as a result of stasis and infection in the biliary tract. Cholangitis was first described by Charcot as a serious and life-threatening illness; however, it is now recognized that the severity can range from mild to life-threatening [1].
The clinical features and therapy of acute cholangitis will be reviewed here. The etiologic agents, clinical features, and management options are quite different in patients with AIDS and are discussed separately. (See appropriate topic reviews).
Acute cholangitis is caused primarily by bacterial infection. The organisms typically ascend from the duodenum; hematogenous spread from the portal vein is a rare source of infection [2].
The most important predisposing factor for acute cholangitis is biliary obstruction and stasis secondary to biliary calculi or benign stricture (picture 1). Chronic biliary obstruction raises the intrabiliary pressure, a central pathogenetic event in the development of acute cholangitis. High pressure promotes the migration of bacteria from the portal circulation into the biliary tract and subsequent colonization. It also favors migration of bacteria from bile into the systemic circulation, resulting in a higher incidence of septicemia [2]. One study, for example, demonstrated a significant correlation between biliary and serum levels of endotoxins and the clinical severity of acute cholangitis [3].
In addition, increased biliary pressure adversely affects a number of host defense mechanisms including [2]:
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