Abstract

INTRODUCTION: Hepatotoxicity caused by chronic oral amiodarone is well documented with around 15–20%. However, acute liver failure due to intravenous Amiodarone is rare clinical presentation with 3% incidence rate. Incidence of concomitant renal failure is even more rare. There is no full explanation for the underlying mechanism. CASE DESCRIPTION/METHODS: 67-year-old male with PMH of CAD s/p coronary artery bypass graft, CKD, presented with chest pain for one week. In the ED, he was found to have atrial flutter. Due to unresponsiveness to IV beta blocker and Diltiazem, patient was loaded with IV Amiodarone and continued IV Amiodarone drip. 16 hours later patient developed acute hepatic failure with AST 4250 (10-42 IU/L), ALT 2422 (10-60 IU/L), INR 2.28 (2-3 conventional anticoagulation), acute renal failure with creatinine of 3.2 mg/dl (0.44-1.0 mg/dl), BUN of 44 mg/d (5-25 mg/dl). Patient was intubated due to acute hepatic encephalopathy. IV Amiodarone was stopped immediately. All workup for other causes of acute hepatic failure came back negative. He was started on intravenous N-Acetyl cysteine and required hemodialysis for acute renal failure. LFTs peaked 72 hours after discontinuation of Amiodarone. Kidney functions improved 5 days after discontinuation of amiodarone and hemodialysis stopped. DISCUSSION: Acute hepatic failure due to intravenous amiodarone is extremely rare with incidence of 3%. The underlying mechanism is still not fully understood. However, a case–control retrospective study argues that hepatotoxicity due to intravenous amiodarone cannot be differentiated from ischemic hepatitis from concomitant hypotension. Intravenous amiodarone is formulated with polysorbate 80 as a solubilizer, which has been shown to induce hypotension. In this case, patient had a stable blood pressure when amiodarone was started. Intravenous (IV) amiodarone toxicity can raise AST/ALT up to 100–200-fold (AST of 21000 and ALT of 9020 in our case) within a day of infusion which then reverses quickly after discontinuation of amiodarone. In this case, liver function tests increased after 26 hours of starting intravenous amiodarone and peaked after 72 hours of stopping the infusion. All cases of acute liver failure due amiodarone didn't survive except for one case. The most common cause of death is encephalopathy. Administration of N-Acetylcysteine was administered is associated with good outcome. Incidence of concomitant renal failure is extremely rare. It is caused by concomitant acute tubular necrosis.

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