Acute Liver and Renal Failure : A rare adverse effect of intravenous amiodarone Robin Paudel1, Saurav Suman1, Prerna Dogra1, Saurav Acharya1, Jyoti Matta1 Authors’ Affiliation: 1: JERSEY CITY MEDICAL CENTER, JERSEY CITY, NJ Introduction 24 hours. Patient manifested acute liver failure and also acute renal failure that required emergent dialysis. Amiodarone was discontinued and a detailed work up ruled out any other possible etiology behind liver and renal failure. Patient was monitored in the hospital for 5 days for downward trend of LFT and creatinine and was discharged home with arrangements for further follow-up plans. After 1 month, oral amiodarone was started and patient tolerated well with follow up lab work at 6 months showing normal values. mechanisms are ischemic liver injury5 secondary to relative hypotension in the setting of congestive hepatopathy, E-ferol syndrome6 or carido-renal syndrome causing renal failure. Irrespective of the etiology, acute toxicity of IV amiodarone is a distinctly different entity from the chronic toxicities of oral amiodarone, and we support the recommendation not to withhold the potentially lifesaving oral amiodarone after the patient has an acute toxicity due to IV amiodarone. Oral amiodarone can be safely started once the liver enzymes normalize, although further monitoring of the liver enzymes is recommended once the patient is started on oral amiodarone. Limited knowledge about the mechanism behind acute liver and renal failure secondary to intravenous amiodarone always puts a physician in a dilemma whether to start a potentially live saving medication once the acute effect has resolved or to withhold it altogether owing to the adverse effects exclusively seen with the intravenous(IV) form. We report an unusual case of acute liver and renal failure within 24 hours of initiation of IV amiodarone which reversed after discontinuation of the medication. Case Presentation References 65 years old male with past medical history of CAD s/p CABG, ischemic cardiomyopathy s/p AICD, HTN, dyslipidemia presented with c/o multiple AICD shocks. Lab works at presentation were within normal limits. AICD interrogation showed 16 episodes of Ventricular Tachycardias with 10 episodes of appropriate AICD firing. Patient was loaded with IV amiodarone and was started on amiodarone drip. The patient received the medications for total Discussion Lewis JH, Ranard RC, Caruso A, et al. Amiodarone hepatotoxicity: prevalence and clinicopathologic correlations among 104 patients. Hepatology. 1989;9(5):679-85. http://livertox.nlm.nih.gov/Amiodarone.htm Rätz Bravo AE, Drewe J, Schlienger RG, Krähenbühl S, Pargger H, Ummenhofer W. Hepatotoxicity during rapid intravenous loading with amiodarone: Description of three cases and review of the literature. Crit Care Med. 2005;33(1):128-34; discussion 245-6. Chan ALF, Hsieh HJ, Hsieh Y-A, Lin S-J. Fatal amiodarone-induced hepatotoxicity: a case report and literature review. Int J Clin Pharmacol Ther. 2008;46(2):96-101 Gluck N, Fried M, Porat R. Acute amiodarone liver toxicity likely due to ischemic hepatitis. Isr Med Assoc J. 2011;13(12):748-52. Rhodes A, Eastwood JB, Smith SA. Early acute hepatitis with parenteral amiodarone: a toxic effect of the vehicle? Gut. 1993;34(4):565-6. Amiodarone is an antiarrhythmic drug highly effective against a wide spectrum of ventricular tachyarrhythmias. Amiodarone is notoriously known to cause various adverse effects including but not limited to liver toxicity, hypo or hyper thyroidism, QT prolongation, AV block, severe hypotension, ARDS, cardiogenic shock, pulmonary fibrosis and visual disturbance1, 2. While most of the known toxic effects of amiodarone is seen on prolonged oral use, for reasons unknown, few of the rare side effects that include acute liver failure, cardiac arrest, ARDS, renal injury and hypotension are almost exclusively seen with the IV administration of amiodarone and not with oral loading or maintenance dosing of amiodarone3,4. The most widely accepted