A 57-year-old male presented with acute epigastric pain and decreased urine output. The pain was mild-to-moderate in severity, intermittent, with occasional vomiting. There was no radiation of pain, and the patient had little relief with analgesics. The patient had decreased urine output over the past 24 h. He was a chronic smoker. There was no past history of diabetes mellitus, hypertension, or tuberculosis. There was no past surgical history. On examination, there was mild pallor. Mild tenderness was elicited in the right upper quadrant. Hemogram revealed a low platelet count (14,000/mul). There was mild elevation of liver enzymes [aspartate transaminase (AST) 87 IU/l, alanine transaminase (ALT) 95 IU/l, alkaline phosphatase 198 IU/l] and serum bilirubin (1.5 mg/dl). Renal function tests were within normal range.
Abdominal USG (iU22 x MATRIX, Philips, Best, Netherlands) revealed echogenic contents within gallbladder (GB) lumen. Common bile duct (CBD) was prominent (8 mm). There was no intrahepatic biliary radical (IHBR) dilatation and the pancreas was normal. A magnetic resonance cholangiography (MAGNETOM  Aera, Siemens, Erlangen, Germany) was performed that revealed mild dilatation of CBD and intrahepatic biliary radicles [Figure 1]. No filling defects were noted within the CBD. GB was normal. There was worsening of the abdominal pain over the ensuing few days associated with progressive elevation of conjugated bilirubin (7.5 mg/dl). Endoscopic retrograde cholangiography (ERCP) was performed. There was blood ooze seen at the papilla. However, cholangiogram did not reveal any filling defects. A naso-biliary drainage (NBD) tube was placed which resulted in decline of conjugated bilirubin to 4.4 mg/dl. Cholangiogram was performed through the NBD after 1 week, which revealed filling defects within the GB and CBD suggestive of blood clots.
Patient continued to deteriorate with a falling hemoglobin suggesting ongoing hemobilia. A vascular cause [pseudoaneurysm or arteriovenous (AV) malformation] was suspected and computed tomography (CT) angiography (SOMATOM  Definition Flash, Siemens, Erlangen, Germany) and digital subtraction angiography (Allura Xper FD 10, Best, Netherlands) was performed. The vascular causes were ruled out. Finally, an exploratory laparotomy was performed. Cholecystectomy and CBD exploration was performed. No calculus or mass was detected within the CBD. Intraoperative cholangioscopy, however, revealed unhealthy mucosa at the confluence that was biopsied. A T-tube was left in situ to achieve continuous drainage. Subsequently, there was no hemobilia. Histopathologic examination of the tissue revealed only inflammation. There was improvement in patient's condition with falling levels in serum bilirubin. However, 4 weeks later, there was mild rise in the serum bilirubin as well as alkaline phosphatase.
A T-tube cholangiogram was performed. There were filling defects within the proximal CBD with no opacification of IHBR suggestive of an inflammatory stricture at or just beyond the confluence [Figure 2]. Cholangioplasty was planned through the T-tube tract under conscious sedation. A 0.035'' guidewire was passed into the left ductal system across the stricture at the confluence. After removal of the T-tube, a 7F 35 cm sheath was inserted over the wire and advanced into the biliary tree. Balloon dilatation was performed using a 10 mm diameter by 40 mm long angioplasty balloon (Advance , ATB PTA dilatation catheter; Cook  Medical, Bloomington, IN, USA), inflated for 10 min. We also did cholangioplasty of the lower end of CBD as filling defects were seen in the proximal CBD on the T-tube cholangiogram suggesting distal stasis. Repeat balloon dilatation of the hilar stricture was done after 3 weeks. A temporary external drainage tube [12F percutaneous transhepatic biliary drainage catheter (PTBD catheter)] was placed with its tip just across the stricture, after each session of cholangioplasty. Cholangiography via the biliary catheter following the procedure revealed good opacification of the entire biliary tree [Figure 3]. The external biliary drainage catheter was finally removed 3 weeks after the second session of cholangioplasty. The procedure was successful, with no complications. Patient was followed with serial evaluation of serum bilirubin, alkaline phosphatase, and ultrasound examinations. At the last follow-up, i.e. 7 months after the procedure, the patient was asymptomatic.