S5751 IV Amiodarone-Induced Acute Liver Failure: A Case Highlighting Rapid Hepatic Decompensation

Introduction: Amiodarone is a widely used antiarrhythmic agent associated with both chronic and acute hepatotoxicity. Long-term use can cause asymptomatic elevations in liver enzymes in 15%–50% of patients, with about 1% developing clinically significant hepatitis or cirrhosis annually. While chronic damage is linked to drug accumulation, rare cases of intravenous (IV) amiodarone induced acute liver failure (ALF), characterized by rapid hepatocellular injury. Case Description/Methods: A 62-year-old man with atrial fibrillation, severe systolic heart failure (EF 23%), pulmonary hypertension, chronic kidney disease stage IIIb, and multiple comorbidities received IV amiodarone (total 2,250 mg) for rate control. Within 34 hours, he developed massive elevations in transaminases (aspartate aminotransferase 7,396 U/L, alanine aminotransferase 4,122 U/L), coagulopathy (international normalized ratio 8.3), and hyperammonemia (158 μmol/L), consistent with ALF. Viral and autoimmune causes were excluded. Imaging including ultrasound and computed tomography abdomen revealed hepatic steatosis without biliary obstruction. Supportive care included N-acetylcysteine, lactulose, and rifaximin. Liver function improved after discontinuation, demonstrating a drug-induced pattern. Discussion: IV amiodarone-related ALF is rare but potentially fatal. Risk factors include high cumulative doses (>900 mg), advanced age, pre-existing liver or renal disease, and concomitant hepatotoxic medications. Diagnosis often relies on rapid onset, marked enzyme elevations (>50× ULN), improvement after stopping, and exclusion of other causes. This case met all criteria per the American College of Gastroenterology guidelines. Regular liver monitoring—initially at baseline, then every 4 hours during infusion in high-risk patients—is crucial for early detection. Prompt drug discontinuation at the first signs of hepatotoxicity can prevent progression to fulminant failure, improving patient outcomes. N-acetylcysteine may provide hepatoprotective effects in amiodarone-induced liver injury by enhancing glutathione levels, and although its role is not well-defined, its use is reasonable due to potential benefit and low risk.