3199 Acute Decompensation of Cirrhosis Complicated by Simultaneous Portal Vein Thrombosis and Hepatocellular Carcinoma

Abstract

INTRODUCTION: Prognostic factors differ significantly between those with compensated and decompensated cirrhosis. We present the case of a patient with decompensated cirrhosis who was found to have portal vein thrombosis and hepatocellular carcinoma simultaneously. CASE DESCRIPTION/METHODS: 68 year old Indian male with history of alcohol abuse, liver cirrhosis and gastroesophageal varices (GOV) type 2, presents with 4 days of diffuse abdominal pain, abdominal distension, fatigue and mild shortness of breath. Collateral information included recent episodes of confusion. Physical exam showed moderate abdominal distension with shifting dullness and diffuse tenderness. Patient was oriented only to person and space. Laboratory examination showed AST 166 U/L, ALT 58 U/L, total bilirubin 20 mg/dL, Ammonia 43 ummol/L and AFP 6.8 ng/mL. CT scan of the abdomen revealed heterogeneous nodular liver with enhancing nodule in the right hepatic lobe measuring 1.8 cm; portal hypertension, paraesophageal varices, and moderate intrabdominal ascites. Portal vein thrombosis (PVT) of intrahepatic portion was noted. Abdominal ultrasound was consistent with advanced cirrhosis and common bile duct (CBD) dilatation of 1.2 cm. Abdominal MRI and MRCP were performed, confirming liver lesion. Ascitic fluid analysis ruled out spontaneous bacterial peritonitis. CT- guided biopsy of hepatic lesion confirmed Hepatocellular Carcinoma (HCC). Patient underwent successful Transarterial Chemoembolization (TACE) of right hepatic tumor and was eventually discharged and followed by Gastroenterology as outpatient. DISCUSSION: Literature review stipulate that in the compensated patients, factors related to the tumor in HCC would be more important, whereas in the decompensated patient, both liver and tumor related factors would be important. However, the number of studies is too small to be conclusive, particularly regarding patients with mostly decompensated cirrhosis and those with non-advanced tumor stage. When it comes to PVT as a predictor of prognosis and mortality in patients with decompensated cirrhosis, recent studies strengthen the idea that PVT simply arises in the context of severe liver failure, and does not significantly worsen hepatic function. In our case, the simultaneous finding of PVT and HCC in setting of decompensation may be indicative of dismal outcome. The significance of HCC and PVT as predictors of prognosis and mortality, should be better evaluated in cirrhotic patients in compensated versus decompensated states independently.