S5464 Refractory Ascites in Non-Cirrhotic Steatohepatitis: Diagnostic and Management Challenges

Introduction: Ascites typically presents as a complication of cirrhosis and portal hypertension; when cirrhosis is absent, the differential includes malignancy, infection, cardiac disease, nephrotic syndrome, and rarer hepatic or peritoneal conditions. We present a diagnostically complex case of persistent ascites in a young male with alcohol use disorder and biopsy-confirmed steatohepatitis without cirrhosis. Case Description/Methods: A 26-year-old man with alcohol use disorder was admitted following stab wounds and underwent exploratory laparotomy with cholecystectomy. Postoperatively, he developed kidney injury and diuretic-refractory ascites requiring frequent large-volume paracenteses. Ascitic fluid showed high protein, variable SAAG (low to high), negative cultures and cytology, and lymphocyte predominance without evidence of malignancy or lymphoma. Extensive workup was unrevealing: autoimmune and viral serologies, TB, and parasitic studies were negative. BNP was mildly elevated; thyroid studies revealed worsening hypothyroidism, though endocrinology thought myxedema ascites were unlikely. Norovirus was detected, but other infectious stool studies were negative. Serum ceruloplasmin and A1AT levels were normal. Imaging (ultrasound, computed tomography, HIDA scan) demonstrated large-volume ascites and fatty liver without cirrhosis or biliary leak. Echocardiography and cardiac catheterization revealed preserved EF and only mild post-capillary pulmonary hypertension. Two liver biopsies revealed advanced steatohepatitis with bridging fibrosis, but no cirrhosis. Repeat hepatic venous pressure gradient (HVPG) was normal, excluding portal hypertension. Despite aggressive diuretics and robust urine output, his ascites has persisted. Transjugular intrahepatic portosystemic shunt was ultimately deferred due to normal HVPG and portal pressures. A trial of resumed diuretics showed some benefit but limited by hypotension. Discussion: This case illustrates the diagnostic complexity of refractory ascites in the absence of cirrhosis. Findings suggest functional portal hypertension secondary to steatohepatitis or surgical decompensation, despite normal HVPG. SAAG variability may reflect inflammation or prior surgery, and HVPG may underestimate portal pressures in select contexts. Persistent ascites in such cases may require careful consideration of less desirable options such as peritoneal drains or peritoneovenous shunts. Ascites can precede histologic cirrhosis in advanced steatohepatitis. A multidisciplinary approach is essential in evaluating ascites of unclear etiology.