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Mentions: The patient was in acute distress for intense pain, fatigued and cachectic, with tense ascites. A central venous catheter was inserted and a paracentesis was performed. Ascitic fluid was orange-colored and cloudy (fig. 1), with marked leukocytosis, and bilirubin and amylase concentrations far exceeding the corresponding values measured on the same day in blood (table 1). The serum-ascites albumin gradient was 1.0 g/dl. The patient's condition was considered too poor to sustain an endoscopic retrograde cholangiopancreatography, proposed in order to identify and treat a biliary fistula. Antibiotics, parenteral nutrition, terlipressin and albumin were started intravenously, with initial improvement of renal function. Cultures of ascites and blood turned positive for E. coli. On a new abdominal CT, pancreas morphology was reported as normal, without pseudocysts or duct dilatation. On the 11th hospital day, however, the patient developed frank peritonism, associated with sudden deterioration of liver function tests. A plain film of the abdomen showed generalized bowel distension with fluid levels but no evidence of free peritoneal air. Surgical exploration documented biliary peritonitis with gallbladder perforation; a cholecystectomy was performed, and the gallbladder was sent for pathologic examination (fig. 2). No biliary stones were present in the biliary tract, including the gallbladder, and the anatomy of the extrahepatic biliary tree was intact. Ascitic fluid amylase concentration dropped to normal within few days from surgery, and the patient was discharged in fair condition 30 days after his admission. At the last follow-up visit, 10 months later, he had fully recovered his usual body weight, showed no physical or ultrasonographic signs of ascites, and had platelet count and liver function tests within the normal reference range.
Pancreatobiliary Reflux Resulting in Pancreatic Ascites and Choleperitoneum after Gallbladder Perforation
Bottom Line: Ten days later, at laparotomy, acalculous perforation of the gallbladder was identified.After cholecystectomy, amylase concentration in the ascitic fluid dropped within a few days to 40% of serum values; ascites disappeared within a few weeks.We conclude that in the presence of a perforated gallbladder, pancreatobiliary reflux was responsible for this unusual combination of choleperitoneum and pancreatic ascites, which we propose to call pancreatobiliary ascites.
Affiliation: Department of Clinical and Experimental Medicine, University of Eastern Piedmont 'A. Avogadro', Novara, Italy.
A 65-year-old man with chronic hepatitis C and no history of alcohol abuse was admitted to our liver unit for the recent development of massive ascites and presumed hepatorenal syndrome. In the preceding two weeks, he had received medical treatment for acute pancreatitis and cholecystitis. Abdominal paracentesis demonstrated a cloudy, orange peritoneal fluid, with total protein concentration 3.6 g/dl, serum-ascites albumin gradient 1.0 g/dl, and ratios of ascites-serum bilirubin and amylase approximately 8:1. Diagnostic imaging demonstrated no pancreatic pseudocysts. Ten days later, at laparotomy, acalculous perforation of the gallbladder was identified. After cholecystectomy, amylase concentration in the ascitic fluid dropped within a few days to 40% of serum values; ascites disappeared within a few weeks. We conclude that in the presence of a perforated gallbladder, pancreatobiliary reflux was responsible for this unusual combination of choleperitoneum and pancreatic ascites, which we propose to call pancreatobiliary ascites.