Purpose: A 51-year-old female with chronic hepatitis C underwent orthotopic liver transplantation with bile duct-to-bile duct anastomosis. Her surgery was complicated by native hepatic artery dissection that was repaired using a supra-celiac conduit. Initial post-operative liver ultrasound showed elevated hepatic artery indices, this improved on repeat ultrasound on post-operative day (POD) 4. Bile ducts were normal caliber, however liver chemistries remained elevated (aspartate aminotransferase 6 times the upper limit of normal, alanine aminotransferase 3 times the upper limit of normal, alkaline phoshatase 445 IU/L, direct bilirubin 2.6 mg/dl). On POD 4, endoscopic retrograde cholangiogram revealed mild stenosis at the biliary anastomosis. An 8.5 French 10 cm plastic biliary stent was placed traversing the anastomosis. Liver chemistries began to normalize after 6 days. Patient later developed significant ascites and underwent paracentesis on POD 15. Culture of ascitic fluid grew enterococcus which was treated with intravenous vancomycin. The patient developed worsening ascites and abdominal pain. On POD 17, repeat paracentesis revealed bilious appearing fluid; ascitic bilirubin level was 34.3 mg/dl. Patient was taken emergently for surgical repair of bile leak and presumed bile duct disruption; however, the biliary system was intact. Exploration disclosed a 1 cm defect in the lateral wall of the second duodenum, just opposite the major papilla and the biliary stent. The duodenal defect was repaired with an omental patch. Patient improved and was discharged home after 10 days. Eight weeks later, endoscopy showed a normal appearing duodenum. At ERCP the biliary stent was removed. Cholangiogram showed moderate stenosis at the biliary anastomosis. The anastomosis was dilated with a 6 mm dilating balloon. A shorter plastic stent, 10 French 7 cm, was placed in the bile duct across the anastomosis. This case demonstrates a biliary prosthesis perforating through the small intestine, presenting with bilious ascites. The stent served as a conduit for bile to drain directly into the abdominal cavity. We suspect that the use of immunosuppressive therapy, a requisite after organ transplant, may have lead to increased fragility of the intestinal wall. It is plausible that the perforation resulted from endoscope trauma during the ERCP, though one might expect such an injury to be apparent earlier in her course. CT scans 2 and 10 days after the initial ERCP showed the distal end of biliary stent did approximate the lateral duodenal wall, though perforation was not apparent. Perhaps the use of a shorter stent or single pigtail design would prevent this complication in the early post-transplant setting.