Introductory Chapter: Biliary Tree

Abstract

Biliary stones are formed as a result of failure to maintain biliary solutes (primarily, cholesterol and calcium salts) in a soluble state. The pathogenesis is multifactorial and involves cholesterol supersaturation, crystal nucleation, and gallbladder dysmotility. The vast majority of patients are asymptomatic, often discovered at laparotomy or during abdominal imaging. Over time, asymptomatic gallstones can progress to symptomatic disease. Prophylactic cholecystectomy is not generally indicated in patients with asymptomatic gallstones. Prophylactic cholecystectomy is considered for children with gallstones, patients with sickle cell disease (as cholecystitis can precipitate a crisis with substantial operative risks), and large gallstones (>2.5 cm), porcelain gallbladder (calcified gallbladder wall). Acute cholecystitis results from a stone impaction at the gallbladder-cystic duct junction. The extent and the progression of inflammation are related to the duration and degree of obstruction. In severe cases, this process can lead to ischemia and necrosis of the gallbladder wall. More frequently, the gallstone is dislodged, and the inflammation gradually resolves. Intrahepatic stones are more prevalent in Asia. They are associated with prolonged partial BD obstruction, as in sclerosing cholangitis, benign and malignant biliary strictures, choledochal cysts, and biliary parasites. Mirizzi syndrome is a form of obstructive jaundice, first described by Mirizzi in 1948, caused