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在心脏骤停前启动静脉-动脉体外膜肺氧合成功治疗确诊的严重安非他酮心脏毒性。

Successful Treatment of Confirmed Severe Bupropion Cardiotoxicity With Veno-Arterial Extracorporeal Membrane Oxygenation Initiation Prior to Cardiac Arrest.

作者信息

Pires Kyle D, Bloom Joshua, Golob Stephanie, Sahagún Barbara E, Greco Allison A, Chebolu Esha, Yang Jenny, Ting Peter, Postelnicu Radu, Soetanto Vanessa, Joseph Leian, Bangalore Sripal, Hall Sylvie F, Biary Rana, Hoffman Robert S, Park David S, Alviar Carlos L, Harari Rafael, Smith Silas W, Su Mark K

机构信息

Division of Medical Toxicology, Ronald O. Perelman Department of Emergency Medicine, New York University Grossman School of Medicine, New York, USA.

New York City Poison Center, New York City Department of Health and Mental Hygiene, New York, USA.

出版信息

Cureus. 2024 Feb 7;16(2):e53768. doi: 10.7759/cureus.53768. eCollection 2024 Feb.

Abstract

Bupropion is a substituted cathinone (β-keto amphetamine) norepinephrine/dopamine reuptake inhibitor andnoncompetitive nicotinic acetylcholine receptor antagonist that is frequently used to treat major depressive disorder. Bupropion overdose can cause neurotoxicity and cardiotoxicity, the latter of which is thought to be secondary to gap junction inhibition and ion channel blockade. We report a patient with a confirmed bupropion ingestion causing severe cardiotoxicity, for whom prophylactic veno-arterial extracorporeal membrane oxygenation (ECMO) was successfully implemented. The patient was placed on the ECMO circuit several hours before he experienced multiple episodes of hemodynamically unstable ventricular tachycardia, which were treated with multiple rounds of electrical defibrillation and terminated after administration of lidocaine. Despite a neurological examination notable for fixed and dilated pupils after ECMO cannulation, the patient completely recovered without neurological deficits. Multiple bupropion and hydroxybupropion concentrations were obtained and appear to correlate with electrocardiogram interval widening and toxicity.

摘要

安非他酮是一种取代卡西酮(β-酮安非他明),为去甲肾上腺素/多巴胺再摄取抑制剂和非竞争性烟碱型乙酰胆碱受体拮抗剂,常用于治疗重度抑郁症。安非他酮过量可导致神经毒性和心脏毒性,后者被认为是间隙连接抑制和离子通道阻断的继发结果。我们报告了1例确诊摄入安非他酮导致严重心脏毒性的患者,对其成功实施了预防性静脉-动脉体外膜肺氧合(ECMO)。该患者在经历多次血流动力学不稳定的室性心动过速前数小时被接入ECMO回路,这些室性心动过速经多轮电除颤治疗,并在给予利多卡因后终止。尽管在ECMO插管后神经系统检查显示瞳孔固定且散大,但患者完全康复,无神经功能缺损。检测了多次安非他酮和羟基安非他酮浓度,其似乎与心电图间期增宽及毒性相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2227/10922220/47db31f97ebd/cureus-0016-00000053768-i01.jpg

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