A Diagnostic Dilemma of New Onset Ascites

Abstract

Introduction: Successful treatment of ascites depends on identifying the correct cause, since some non-hepatic causes of ascites, such as peritoneal carcinomatosis, do not respond to diuretic therapy. We present an interesting case of new onset ascites involving a delayed diagnosis as well as the multidisciplinary approach for resolution of the diagnosis. Case Report: A 40-year-old man presented with abdominal distension, vomiting, fever, and 20-lb weight loss. A diagnostic paracentesis performed at an OSH excluded SBP and patient was transferred to us for further management. USG suggested a large amount of ascites and cirrhotic morphology of liver but a normal-sized spleen and normal portal flow. The CBD was non-dilated at 3 mm. Initial labs revealed total bilirubin 2.3 mg/dL, direct bilirubin 1.1 mg/dL, AST 22 U/L, ALT 39 U/L, ALP 450 U/L, and GGT 65 U/L. A therapeutic paracentesis was performed revealing dark brown fluid. Further history revealed the patient underwent laparoscopic cholecystectomy for biliary dyskinesia 2 months prior. Ascitic fluid bilirubin was obtained and was elevated at 17.4 mg/dL. HIDA scan revealed a large confined area medial to the liver with extension into the stomach area, and CT confirmed the biloma. During ERCP the guide wire was unable to be advanced into the CBD and no contrast was found proximal to this area of resistance and hence procedure was aborted. A percutaneous transhepatic cholangiography (PTC) was performed, which revealed marked leakage of contrast into the peritoneum with poor opacification of biliary tree, confirmatory of bile leak due to CBD injury. Subhepatic and intrahepatic drains were placed for decompression of bile for 1 month's time. Discussion: Initial SAAG of 15.5 g/L reported from OSH generated a differential list of cirrhotic ascites, cardiac ascites, and Budd-Chiari syndrome. However, clinical, laboratory, and radiological findings did not support any of these. Removal of dark brown peritoneal fluid raised a possibility of a biliary leak, which was later confirmed with high bilirubin and CT/HIDA imaging. With the emergence of the ERCP and PTC, the management of bile leaks has evolved away from the patient returning to surgery. Endoscopic internal stenting is currently the procedure of choice for treating bile duct leaks with a therapeutic response, with cessation of bile extravasation in 70-95% of cases within a period of 1-7 days. PTC is often used when intrahepatic bile duct injuries are unable to be accessed by the retrograde route, as with this patient. This interesting case of new onset ascites involves discussion of misleading factors for delayed diagnosis and emphasizes a multidisciplinary approach for resolution of the diagnosis and its management.