Benign biliary strictures are the result of surgical (including liver transplantation) anastomosis or injury in about 95% of cases. The remainder of cases are caused by blunt external injury to the abdomen, pancreatitis, IgG4-related disease, erosion of the duct by a gallstone, or prior endoscopic sphincterotomy.
Signs of injury to the duct may or may not be recognized in the immediate postoperative period. If complete occlusion has occurred, jaundice will develop rapidly; more often, however, a tear has been made accidentally in the duct, and the earliest manifestation of injury may be excessive or prolonged loss of bile from the surgical drains. Bile leakage resulting in a bile collection (biloma) may predispose to localized infection, which in turn accentuates scar formation and the ultimate development of a fibrous stricture (eFigure 16–54).
Cholangiogram shows postoperative bile duct stricture. (Reproduced, with permission, from American Gastroenterological Association, Bethesda, Maryland.)
Cholangitis is the most common complication of stricture. Typically, the patient experiences episodes of pain, fever, chills, and jaundice within a few weeks to months after cholecystectomy. Physical findings may include jaundice during an acute attack of cholangitis and right upper quadrant abdominal tenderness. Serum alkaline phosphatase is usually elevated. Hyperbilirubinemia is variable, fluctuating during exacerbations and usually remaining in the range of 5–10 mg/dL (85.5–171 mcmol/L). Blood cultures may be positive during an acute episode of cholangitis. Secondary biliary cirrhosis will inevitably develop if a stricture is not treated.
MRCP or multidetector CT is valuable in demonstrating the stricture and outlining the anatomy. ERCP is the first-line interventional approach and permits biopsy and cytologic specimens to exclude malignancy (in conjunction with EUS-guided fine-needle aspiration, an even more sensitive test for distal bile duct malignancy), sphincterotomy to allow a bile leak to close, and dilation (often repeated) and stent placement, thereby avoiding surgical repair in some cases. When ERCP is unsuccessful, dilation of a stricture may be accomplished by PTC or under EUS guidance. Placement of multiple plastic stents appears to be more effective than placement of a single stent. The use of fully-covered self-expanding metal stents, which are more easily removed endoscopically than uncovered metal stents, as well as bioabsorbable stents, is an alternative to use of plastic stents and requires fewer ERCPs to achieve stricture resolution; stent migration may occur in 10% of cases. Uncovered metal stents, which often cannot be removed endoscopically, are generally avoided in benign strictures unless life expectancy is less than 2 years. Strictures related to chronic pancreatitis are more difficult than postsurgical strictures to treat endoscopically and may be best managed with a temporary covered metal stent. Following liver transplantation, endoscopic management is more successful for anastomotic than for nonanastomotic strictures. Results for nonanastomotic strictures may be improved with repeated dilations or the use of multiple plastic stents. Biliary strictures after live liver donor liver transplantation, particularly in patients with a late-onset (after 24 weeks) stricture or with intrahepatic biliary dilatation, are also challenging and require aggressive endoscopic therapy; in addition, the risk of post-ERCP pancreatitis appears to be increased.
When malignancy cannot be excluded with certainty, additional endoscopic diagnostic approaches may be considered—if available—including intraductal ultrasonography, peroral cholangioscopy, confocal laser endomicroscopy, and fluorescence in situ hybridization. Differentiation from cholangiocarcinoma may ultimately require surgical exploration in 20% of cases. Operative treatment of a stricture frequently necessitates performance of an end-to-end ductal repair, choledochojejunostomy, or hepaticojejunostomy to reestablish bile flow into the intestine.