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Stones in the common bile duct (CBD) are either primary or secondary. Primary stones are formed de novo in the CBD as a result of bacterial action on phospholipid and bilirubin (see Chapter 134 ). Secondary stones, including cholesterol and pigment stones, are formed in the gallbladder and are passed into the CBD.
The prevalence of CBD stones varies depending on several factors. Along with stones in the gallbladder, choledocholithiasis is noted in 10% to 20% of patients with symptomatic gallstones. In addition, in the immediate postoperative period, almost 1% of cholecystectomy patients have a retained stone. The prevalence of concomitant CBD stones increases with advancing age. Hemolysis predisposes patients to black pigment stones. Bacterial or parasitic infection of the biliary tract, a foreign body in the duct (surgical sutures and clips), and juxtapapillary duodenal diverticula increase the prevalence of brown pigment stones. Ascaris infection is a rare cause of CBD stones in endemic areas. Anatomic abnormalities such as low entry of the cystic duct (<3.5 cm from ampulla) and sphincter of Oddi dysfunction predispose patients to CBD stones. Intrahepatic calcium bilirubinate stones (Oriental cholangiopathy) are noted in Japanese and Korean patients. An iatrogenic form of choledocholithiasis is the development of pigment stones (regardless of original type of gallstones) after endoscopic sphincterotomy, which permits bacterial colonization of the CBD, deconjugation of bilirubin, and formation of pigment stones.
In patients with intact gallbladder, the symptoms of choledocholithiasis and cholecystolithiasis are clinically similar, and the diagnosis of CBD stones cannot be made based solely on symptomatology. CBD stones may be asymptomatic for many years, or they may present with jaundice or with biliary colic, pancreatitis, or acute suppurative cholangitis ( Fig. 138.1 ). “Biliary colic,” a misnomer for the constant pain over the right upper quadrant, lasts for 30 minutes to several hours and is associated with nausea, vomiting, and diaphoresis but is not related to food intake. Prolonged obstruction for 4 to 5 years without therapy leads to biliary cirrhosis. Elevated serum bilirubin concentration (2 to 14 mg/dL) and elevated alkaline phosphatase levels indicate cholestasis.
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