Cholangitis pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Overview
Pathophysiology
The presence of gallstones alone predisposes to bacterial colonization. 70% of patients with gallstones will have bacteria in the bile while normal bile is usually sterile. CBD have a higher probability of infection. 80% of stones can be culture positive.
The source of biliary infection is usually ascending from the duodenum or jejunum and less commonly direct hematogenous seeding of the portal system. In the presence of obstruction, the small bowel becomes colonized with colonic flora. The common organisms are E.coli, Klebsiella, Enterococcus, Enterobacter, Proteus. Anaerobes (Strep, Bacteroides, Clostridia) can be found particularly in the elderly. Higher incidence of Pseudomonas in those who have been instrumented. Broad spectrum antibiotics to cover Gram negatives including Pseudomonas, Enterococcus and anaerobes are needed up front. Cephalosporins should not be used as monotherapy. Ciprofloxacin has been shown in one study to be as effective as monotherapy despite poor coverage for anaerobes and EC.
The most common causes of biliary obstruction are biliary calculi, benign stricture or malignant neoplasms. Benign strictures are caused by primary sclerosing cholangitis, ischemic cholangitis, iatrogenic biliary tract injury, congenital disease and infection. Chronic inflammation predisposed to the development of cholangiocarcinoma. Extraluminal obstruction can occur from pancreatic cancer or pseudocyst, lymphoma, hepatoma, metastatic disease or ampullary cancer.
Biliary obstruction leads to elevated biliary pressures, favoring migration of bacteria into the portal circulation and bile. As pressures increase hepatocyte secretion is impaired and bacteria move into the lymphatics and systemic circulation.