Recurrent Ascites Following Laparoscopic Cholecystectomy: Can You Find the Cause?

Abstract

Purpose: Ascites following laparoscopic cholecystectomy has been described with potential etiologies to include iatrogenic biliary, lymphatic or ureteral disruption. However, this case involves recurrent inflammatory ascites following laparoscopic cholecystectomy without an obvious etiology despite extensive evaluation. Methods: A 36 year old female with a history of chronic hepatitis C was hospitalized at a tertiary referral center due to a one month history of recurrent ascites following laparoscopic cholecystectomy. She was diagnosed from an outside institution with chronic hepatitis C about three months prior. Liver biopsy was performed at that time and demonstrated stage 1-2 fibrosis. One month prior to her transfer to our hospital, she underwent elective cholecystectomy. Postoperatively, she developed significant ascites three days following her procedure. HIDA and abdominal ultrasound with Doppler did not demonstrate any biliary leak or abnormalities of the liver or portal system. Ascitic fluid analysis demonstrated WBC of 6200 (rare PMN, largely lymphocytic), serum-albumin gradient (SAAG) >1.1, and negative urea and fat analysis. She required multiple large volume paracenteses. Given her difficulties she presented to our institution. Results: Repeat ascitic fluid analysis demonstrated 4,700 nucleated cells/uL (83% lymphocytes), SAAG > 1.1, gram stain and culture negative, AFB negative, cytology negative, lipid analysis negative, and no evidence of bile. HIDA was repeated with no evidence of biliary leak. Abdominal ultrasound with Doppler analysis of the portal veins, splenic veins and hepatic veins was unremarkable and without evidence of portal hypertension. CT of the abdomen and pelvis was only notable for ascites. Transthoracic echocardiogram was negative with normal cardiac findings. Venogram with measurement of hepatic vein pressure gradient was unremarkable and without evidence of portal hypertension. Serologic testing with ANA, SPEP, beta-2-microglobulin, and CA-125 were negative. Re-evaluation of outside liver biopsy confirmed absence of cirrhosis. Surgical consultation was obtained and no intervention was recommended. The patient initially required multiple large volume paracenteses. She was started on diuretic regimen with spironolactone and furosemide and afterwards had significant improvement without requiring further paracentesis. Conclusion: Ascites following laparoscopic cholecystectomy has been described with iatrogenic causes being prominent. However, idiopathic postoperative inflammatory ascites has only had limited description in the literature. This case illustrates the complexity involved in these cases, but also supports the use of diuretic therapy in its treatment.