S5272 Hemostasis With Fully Covered Self-Expanding Bare Metal Stent as a Bridge to Liver Transplantation in a Patient With Acute Liver Injury and Hemodynamically Unstable Hemobilia

Introduction: Hemobilia is an uncommon but important etiology of upper gastrointestinal bleeding presenting with jaundice, right upper quadrant abdominal pain and gastrointestinal hemorrhage. The source may be arterial or venous caused by iatrogenic, traumatic, neoplastic, inflammatory, infectious, and vascular etiologies. Rarely, hemobilia may occur due to portal hypertensive biliopathy secondary to varices in the bile duct. Case Description: A 49-year-old man presented with jaundice, abdominal pain and melena. He was admitted for acute liver injury secondary to alcoholic hepatitis complicated by portal hypertension, ascites with hepatorenal syndrome and portal venous thrombosis with a MELD score of 41. He was evaluated and listed for liver transplant. This was precluded by acute hematochezia and shock requiring multiple blood transfusions and vasopressor support. Upper endoscopy demonstrated hemobilia. Labs were notable for hemoglobin 7.6, platelet count 49,000, and INR 2.3. Interventional Radiology was consulted for transcatheter arterial embolization (TAE), but non-invasive imaging supported variceal bleeding in the distal bile duct due to portal hypertensive biliopathy rather than arterial bleeding. A TIPS procedure was considered but determined to be too risky in the setting of his clinical instability. Endoscopic retrograde cholangiopancreatography (ERCP) was performed with placement of 1 fully covered self-expandable metal stent (FCSEMS) into the common bile duct, achieving hemostasis and clinical stability. He underwent liver transplantation with successful duct-to-duct biliary anastomosis. The stent was removed 2 days later without further hemobilia. Discussion: Treatment goals in hemobilia are hemostasis and maintenance of bile flow. TAE is becoming the gold standard for treatment of persistent arterial hemobilia in hemodynamically unstable patients. Endoscopic biliary stent placement is the initial therapy for venous hemobilia in hemodynamically stable patients. TAE would have been therapeutically ineffective in our patient due to the venous source of bleeding. Moreover, given the presence of a thrombosed portal vein, TAE could have led to significant hepatic ischemia. Though palliative biliary stenting for portal biliopathy has been reported previously, the success of ERCP with FCSEMS in our patient highlights the use of FCSEMS as a bridge to liver transplantation in patients with hemodynamically unstable hemobilia secondary to portal biliopathy.