Endoscopic Management of Biliary Complications After Liver Transplantation

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Risk factors for biliary complications

There are several known risk factors for the development of biliary complications after LT. Hepatic artery thrombosis can lead to complex hilar strictures as the blood supply to the bile ducts is solely via the hepatic artery. There are several technical factors during surgery that can lead to biliary problems and these include excessive dissection of periductal tissue during procurement, excessive use of electrocautery for biliary duct bleeding control in both donor and recipient, and tension

Living-donor liver transplantation as a risk factor for biliary complications

Living-donor liver transplantation (LDLT) has been associated with a higher rate of bile leaks than in deceased-donor transplantation: 31.8% versus 10.2%, respectively.19 Factors that are associated significantly with increased biliary leaks are a donor with 3 or more bile ducts, a recipient diagnosis of hepatitis C, and the experience of the transplant center at performing LDLT. Once a center has performed more than 40 LDLTs, the incidence of biliary strictures and biliary leaks decreases

Diagnostic approach

Although occasionally patients will have nonspecific symptoms (fever and anorexia), right upper quadrant abdominal pain (especially with bile leaks), pruritus, jaundice, or bile ascites, a biliary complication usually is first suspected in asymptomatic LT recipients who have elevations of serum bilirubin, alkaline phosphatase, and/or gamma-glutamyl transferase (GGT) levels. Absence of pain does not exclude a biliary leak (exposure of the peritoneum and other visceral structures to bile usually

Etiology and types of biliary strictures

Bile duct strictures occur in 4% to 13% of patients after deceased-donor LT and account for approximately 40% of all biliary complications after LT.1, 2, 3, 4, 5, 6, 10, 11, 32 Higher incidences are found in reports with longer follow-up.10 The mean time from LT to diagnosis of strictures has been reported to be approximately 2 months.33 Strictures that occur early after LT are mostly attributable to technical problems, whereas late strictures are mainly attributable to vascular insufficiency

Biliary leaks

The incidence of biliary leaks after LT ranges between 2% and 25%.1, 2, 3, 4, 5, 6, 46, 47 Bile leaks can occur from the anastomosis, the cystic duct remnant, the T-tube tract, or (in the case of living donor LT) from the cut surface of the liver. Many bile leaks can be resolved nonoperatively with early intervention.1, 2, 3, 4, 5, 6, 46

When there is a low suspicion of a biliary leak, a radionucleotide scan has reasonable accuracy at noninvasive detection of a bile leak.48 ERC, though, is the

Biliary stones, sludge, and casts

Biliary filling defects occur in approximately 5% of patients after liver transplantation.47 These filling defects can be caused by gallstones, sludge, debris, blood clots, casts, or migrated stents; as many as 70% of such defects are caused by stones.5, 9 Management is similar to the nontransplant setting (with sphincterotomy and balloon or basket extraction) with the caveat that in the presence of immunosuppressive agents, patients can have a rapid clinical decline. Patients can present with

Sphincter of Oddi dysfunction

The sphincter of Oddi is a muscular structure that encompasses the confluence of the distal common bile duct and the pancreatic duct as they penetrate the wall of the duodenum. The term sphincter of Oddi dysfunction (SOD) has been used to describe a clinical syndrome of biliary or pancreatic obstruction related to mechanical or functional abnormalities of the sphincter of Oddi. It is postulated that in the posttransplant setting, denervation of the common bile duct in the ampullary region

Summary

Biliary complications are common in recipients of deceased-donor and live-donor liver transplants and can occur in up to 9% of donors as well. These complications include biliary strictures, bile leaks, biliary obstruction (with stones, sludge, or casts), and sphincter of Oddi dysfunction. Given the frequency of these complications and the risk for significant impact on the transplanted organ, the transplant team needs to work closely with endoscopists and interventional radiologists to treat

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      NABSs were first identified in liver transplantation following hepatic artery thrombosis, which caused the biliary tree to become ischemic, leading to a diffuse ischaemic cholangiopathy and intraductal cast formation [25,26]. Today ischemic injury to the biliary epithelium remains the most common cause of NASBS [7] and in addition to hepatic artery thrombosis or stenosis can be caused by long cold or warm ischemic times, grafts which are donated after cardiac death (DCD) or where there has been a significant reperfusion injury or inadvertent damage to the peribiliary vasculature [1,25,27]. Other causes of a NABS include an immunologically-induced or a cytotoxic injury [1,25,27].

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