Endoscopic management of a spontaneous gallbladder perforation and bile leak.

A 53-year-old man with a past medical history of alcoholic liver disease complicated by esophageal varices, ascites, hepatic hydrothorax, and hepatic encephalopathy presented to a local community hospital with 10-day history of abdominal pain. His pain was 10/10 in intensity, constant, worse in the supine position, increasing on the dependant side of the abdomen (when lying on the left side, the pain worse on left and vice versa), and improved in the upright position. The pain was not worsened by food and was not associated with fevers, chills, nausea or chest pain. He also reported shortness of breath and diarrhea, but denied rectal bleeding. When he was admitted to the local hospital, his white blood cell (WBC) count was 15,000/mm, predominantly bands and neutrophils. Because of concern for spontaneous bacterial peritonitis, empiric antibiotics were started and a nasogastric tube was placed. An abdominal ultrasound revealed a cirrhotic liver and a contracted gallbladder with mild gallbladder wall thickening. There was insufficient ascites to perform a diagnostic paracentesis. An abdominal radiograph series was negative for free air. Over the next 24 h, his pain continued to worsen and there was intermittent abdominal distention. A computed tomography (CT) of the abdomen and pelvis revealed a nodular liver capsule consistent with cirrhosis and large volume ascites (Fig. 1a). The gallbladder was contracted around dependent radio-opaque calculi (arrow, Fig. 1a). Two radio-opaque calcified structures in pelvis (arrow, Fig. 1b) consistent with gallstones with associated free fluid in pelvis were also seen. He was transferred to our institution. The patient’s past medical history was significant for alcoholic cirrhosis, and he had been on the liver transplant list. He also had a history of an incarcerated umbilical hernia that was repaired in 2008, as well as cholelithiasis. Upon transfer he was receiving piperacillin and tazobactam, vancomycin, ondansetron, pantoprazole, lactulose and hydromorphone as needed. He had no known drug allergies. He was single and did not smoke tobacco. The patient had discontinued alcohol use in 2008, and had no history of illicit drug use. Family history was negative. On physical examination, his vital signs were stable. The patient appeared to be in no acute distress with icteric conjunctiva and a nasogastric tube in place. There were decreased breath sounds bilaterally with a diffusely distended abdomen with tenderness to palpation in all quadrants. There was shifting dullness and a fluid wave consistent with ascites, but no guarding or rebound. The patient had scrotal and lower extremity edema but no asterixis. The patient had a WBC count of 10,300/mm, hematocrit 27.2%, mean corpuscular volume 84.7, platelet count 86,000/ mm, sodium 136 mmol/L, carbon dioxide 19 mmol/L, blood urea nitrogen 42 mg/dL, creatinine 1.5 mg/dL, albumin 3.1 g/dL, total bilirubin 8.3 mg/dL, alkaline phosphatase 130 U/L, aspartate aminotransferase 37 U/L, alanine aminotransferase 29 U/L, and international normalized ratio for C. Munroe (&) G. Triadafilopoulos J. Van Dam G. Lutchman Division of Gastroenterology and Hepatology, Department of Medicine, Stanford University School of Medicine, Stanford University Medical Center, 300 Pasteur Drive, Always Building, Rm M211, Stanford, CA 94305-5187, USA e-mail: camunroe@stanford.edu