S5764 Severe Acute Hepatitis A Leading to Liver Transplantation: A Case of Fulminant Hepatic Failure

Introduction: Acute hepatitis A virus (HAV) infection typically presents with nonspecific symptoms such as nausea, vomiting, anorexia, and jaundice. Although generally self-limited, HAV infection can rarely progress to fulminant hepatic failure, especially in patients with underlying hepatic conditions. Here we present a case of severe fulminant hepatitis A necessitating liver transplantation. Case Description/Methods: A 61-year-old man with a history of resolved hepatitis B presented with a 5-day history of anorexia, nausea, vomiting, jaundice, and fever (38.6°C). He denied use of acetaminophen, herbal supplements, alcohol, or recreational drugs. Physical examination revealed scleral icterus, jaundice, and asterixis, though the patient remained oriented. Laboratory findings demonstrated severe hepatocellular injury (aspartate aminotransferase 7268 U/L, alanine aminotransferase [ALT] 6,997 U/L), progressive hyperbilirubinemia (total bilirubin initially 4.0 mg/dL), significant coagulopathy (international normalized ratio [INR] 3.1), and lactic acidosis of 5.7. Ultrasound findings were normal, ruling out biliary obstruction or chronic liver abnormalities. Diagnostic evaluation confirmed acute hepatitis A (positive HAV IgM), excluding other chronic and acute viral hepatitides and metabolic or autoimmune liver disorders. Severe disease progression was evidenced by rapid deterioration, worsening encephalopathy, ascites formation, and failure to respond adequately to medical management including N-acetylcysteine, lactulose, and rifaximin. His liver function continued to deteriorate significantly, as indicated by persistently elevated transaminases (ALT >2000), increasing bilirubin levels (peaking at 17.1 mg/dL), lactate of 9.7, and worsening coagulopathy (INR >11) despite medical therapy. Consequently, he was urgently listed and subsequently underwent deceased donor liver transplantation on hospital day 7. Postoperatively, the patient experienced transient delirium, acute pancreatitis, bacterial pneumonia, and peripancreatic fluid collections, managed effectively with supportive care and antimicrobial therapy. Immunosuppression therapy with tacrolimus, mycophenolate, and steroids was initiated, leading to gradual normalization of hepatic function. Discussion: This case highlights the potential severity of acute hepatitis A infection leading to acute liver failure, underscoring the importance of prompt recognition and management, especially in patients with previous hepatic conditions. Emergent liver transplantation remains a critical and life-saving intervention for fulminant hepatitis A.