From Hepatitis A to Acute Liver Failure in a Resource-Limited Setting: A Case Report

• HAV can rarely progress from acute hepatitis to acute liver failure. • Worsening INR with encephalopathy should prompt urgent reassessment. • Serial monitoring was key to recognizing formal ALF. • Supportive care and NAC may stabilize early non-acetaminophen ALF Hepatitis A virus (HAV) infection is usually self-limited, but a minority of cases progress to acute liver failure (ALF), particularly in resource-limited settings. We report a previously healthy 19-year-old woman who presented with 20 days of jaundice, dark urine, and hepatic encephalopathy. Baseline tests showed total bilirubin 18.3 mg/dL, AST 281 U/L, ALT 341 U/L, INR 1.23, and positive anti-HAV IgM/IgG. Although she did not meet formal ALF criteria at presentation, within 72 hours she progressed to ALF, with bilirubin rising to 28 mg/dL, INR to 1.8, and ammonia to 140 µg/dL; ultrasonography revealed hepatomegaly. In the absence of liver transplantation or continuous renal replacement therapy, a resource-adapted supportive bundle was implemented, including intravenous N-acetylcysteine, vitamin K, neuroprotection, glucose control, early enteral nutrition, conservative transfusion, and infection surveillance. Clinical and biochemical parameters improved, and she was discharged after approximately 4 weeks with recovery on follow-up. This case highlights early warning signs and the feasibility of a structured non-transplant management pathway for HAV-associated ALF in constrained settings.