3181 Intravenous Amiodarone: An Uncommon Culprit of Reversible Hyper-Acute Liver Injury

Abstract

INTRODUCTION: Amiodarone is a commonly used anti-arrhythmic agent and it is important that physicians are familiar with the toxicity profile. We are reporting a case of intravenous (IV) amiodarone induced hyper-acute liver injury. CASE DESCRIPTION/METHODS: 62-year-old man with history of atrial fibrillation, non-ischemic cardiomyopathy and tobacco abuse, was admitted with atrial fibrillation and rapid ventricular response related to medication non-adherence. Patient was given IV amiodarone (total of 1050 mg) over 24-hour period, following which patient developed marked elevation of aspartate aminotransferase/AST (4021 U/L) and alanine aminotransferase/ALT (3000 U/L) with mild elevation of alkaline phosphatase/ALP (218 U/L) and total bilirubin (2.0 mg/dL). International Normalized Ratio (INR) - 5.3. Viral hepatitis panel, acetaminophen and drug toxicology screen - negative. Ceruloplasmin – normal. Ultrasound abdomen – normal liver and CBD diameter 4 mm. Portal venous duplex – no thrombosis. Patient denied use of over the counter medications or herbal supplements. No hypotensive episodes or evidence of cardiogenic shock. Due to the temporal relationship between the use of intravenous amiodarone and the development of liver injury, amiodarone-induced liver injury was suspected. Amiodarone was immediately discontinued and patient was given IV N-acetylcysteine (NAC). 24 hours later, AST fell by 50% to 2167 U/L. Liver enzymes continued to decrease and on day 4 (day of discharge), AST and ALT levels were 212 U/L and 929 U/L. After the liver enzymes normalized, our patient was started on oral amiodarone without recurrence of liver injury. DISCUSSION: IV amiodarone is typically used as a short-term therapy for various arrhythmias and is primarily eliminated by biliary excretion. Acute hepatitis due to parenteral therapy is extremely rare and can develop within 1 day of administration. Amiodarone should be immediately discontinued in those cases. The different mechanisms suspected to cause acute liver toxicity due to IV amiodarone are ischemic liver injury due to relative hypotension, hypersensitivity reaction, toxicity of the vehicle (polysorbate-80), and idiosyncratic toxicity. Limited evidence is available about the use of NAC in amiodarone induced liver injury.