Mohamed Mujtaba, Al-Hillan Alsadiq, Flores Marcus, Kaunzinger Christian, Mushtaq Arman, Asif Arif, Hossain Mohammad
Department of Medicine, Jersey Shore University Medical Center, Hackensack Meridian Health, Neptune, NJ 07753, USA.
Gastroenterology Res. 2020 Feb;13(1):40-43. doi: 10.14740/gr1254. Epub 2020 Feb 1.
Hepatotoxicity caused by chronic oral amiodarone is well documented with around 15-20% incidence rate. However, acute liver failure due to intravenous (IV) amiodarone is rare clinical presentation with 3% incidence rate. Incidence of concomitant renal failure is even rarer. There is no full explanation for the underlying mechanism. Herein, we are presenting a rare case of concomitant acute hepatic failure and acute-on-chronic renal injury induced by use of IV amiodarone. A 67-year-old man with past medical history of coronary artery disease s/p coronary artery bypass graft (CABG), history of alcoholism, and chronic kidney disease stage 3 presented with chest pain for 1 week. In the emergency department (ED), he was found to have atrial flutter. Due to unresponsiveness to IV β-blocker and diltiazem, the patient was loaded with IV amiodarone and continued IV amiodarone drip. His liver function tests (LFTs) and renal functions at the time of administration of IV amiodarone were aspartate transaminase (AST) 176 (10 - 42 IU/L) and alanine transaminase (ALT) 208 (10 - 60 IU/L), international normalized ratio (INR) 1.39 (reference value 2 - 3), blood urea nitrogen (BUN) 37 (5 - 25 mg/dL), and creatinine 1.85. Sixteen hours later patient developed acute hepatic failure with AST 4,250 (reference value 10 - 42 IU/L), ALT 2,422 (10 - 60 IU/L), INR 2.28, and acute renal failure with creatinine of 3.2 mg/dL (0.44 - 1.0 mg/dL), and BUN of 44 mg/d (5 - 25 mg/dL). Patient was intubated due to acute hepatic encephalopathy and sent to intensive care unit (ICU). IV amiodarone was stopped immediately. All workup for other causes of acute hepatic failure came back negative. He was started on IV N-acetylcysteine and required hemodialysis for acute-on-chronic renal failure. LFTs peaked 72 h after discontinuation of amiodarone. Kidney functions started to improve 5 days after discontinuation of amiodarone and patient came off hemodialysis. Acute hepatic failure as result of IV amiodarone is a rare presentation; however, it has a high mortality. Risk factors include low ejection fraction, hepatic congestion and pre-existing hepatic dysfunction. No obvious underlying mechanism to this presentation has been fully explained. Acute renal failure can be associated with this presentation which is even rarer. Stopping IV amiodarone, administering N-acetylcysteine and good supportive care can lead to favorable outcome.
长期口服胺碘酮所致肝毒性已有充分记录，发病率约为15% - 20%。然而，静脉注射胺碘酮导致急性肝衰竭是一种罕见的临床表现，发病率为3%。合并肾衰竭的发生率甚至更低。目前对于其潜在机制尚无完整解释。在此，我们报告一例因静脉注射胺碘酮导致的罕见的急性肝衰竭合并急性慢性肾损伤病例。一名67岁男性，既往有冠状动脉疾病史，曾行冠状动脉旁路移植术（CABG），有酗酒史，慢性肾脏病3期，因胸痛1周就诊。在急诊科，发现他患有心房扑动。由于对静脉注射β受体阻滞剂和地尔硫䓬无反应，给予患者静脉注射胺碘酮负荷量并持续静脉滴注胺碘酮。静脉注射胺碘酮时他的肝功能检查（LFTs）和肾功能指标为：天冬氨酸转氨酶（AST）176（10 - 42 IU/L），丙氨酸转氨酶（ALT）208（10 - 60 IU/L），国际标准化比值（INR）1.39（参考值2 - 3），血尿素氮（BUN）37（5 - 25 mg/dL），肌酐1.85。16小时后，患者出现急性肝衰竭，AST为4250（参考值10 - 42 IU/L），ALT为2422（10 - 60 IU/L），INR为2.28，同时出现急性肾衰竭，肌酐为3.2 mg/dL（0.44 - 1.0 mg/dL），BUN为44 mg/d（5 - 25 mg/dL）。患者因急性肝性脑病插管并被送往重症监护病房（ICU）。立即停用静脉注射胺碘酮。针对急性肝衰竭其他病因的所有检查结果均为阴性。开始给予静脉注射N - 乙酰半胱氨酸，患者因急性慢性肾衰竭需要进行血液透析。停用胺碘酮72小时后LFTs达到峰值。停用胺碘酮5天后肾功能开始改善，患者停止血液透析。静脉注射胺碘酮导致急性肝衰竭是一种罕见的表现；然而，其死亡率很高。危险因素包括射血分数低、肝淤血和既往存在的肝功能障碍。目前对于这种表现尚无明显的潜在机制得到充分解释。急性肾衰竭可能与这种表现相关，这种情况更为罕见。停用静脉注射胺碘酮、给予N - 乙酰半胱氨酸并进行良好的支持治疗可带来良好的预后。
