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西酞普兰过量:尖端扭转型室性心动过速(TdP)伴心脏骤停的延迟表现。

Citalopram overdose: late presentation of torsades de pointes (TdP) with cardiac arrest.

作者信息

Tarabar Asim F, Hoffman Robert S, Nelson Lewis

机构信息

Yale University School of Medicine, New Haven, CT, USA.

出版信息

J Med Toxicol. 2008 Jun;4(2):101-5. doi: 10.1007/BF03160963.

Abstract

INTRODUCTION

Citalopram overdose may produce bradycardia, QT prolongation, and torsades de pointes (TdP). A cardiotoxic metabolite may be responsible for the delayed onset of cardiotoxicity. Although some authorities recommend a minimum of 24 hours of observation following citalopram overdose, a recent analysis suggested that dysrhythmias rarely occur beyond 13 hours post-ingestion. We present a case of citalopram overdose with a substantially delayed onset of cardiac toxicity.

CASE REPORT

A 36-year-old woman complained of shakiness, numbness in the arms, and palpitations that began approximately 32 hours after ingesting 50 (20-mg) tablets of citalopram. Her initial vital signs were: blood pressure, 84/44 mmHg; pulse, 102-150/minute; respirations, 17/min; temperature, 99.3 degrees F (37.3 degrees C). Her initial ECG showed sinus rhythm with a prolonged corrected QT interval (572 msec) with paroxysmal, self-limited runs of wide-complex tachycardia that appeared multifocal in nature. Approximately 20 minutes after presentation, she experienced self-terminating TdP, with transient hypotension and loss of consciousness. Her serum citalopram concentration (33 hours post-ingestion) was 477 ng/mL (therapeutic: 40-110 ng/mL); desmethylcitalopram concentration was 123.2 ng/mL (therapeutic: 14-40 ng/mL). She was treated with magnesium and lidocaine, and her corrected QT interval remained abnormal for 24 hours after presentation.

DISCUSSION

Citalopram overdose can produce life-threatening cardiac toxicity with a clinical onset that may be delayed beyond a routine observation period of 6 hours. Once the QT interval is prolonged, it seems prudent to prolong the observation period.

摘要

引言

西酞普兰过量可能导致心动过缓、QT间期延长和尖端扭转型室速(TdP)。一种心脏毒性代谢产物可能是心脏毒性延迟发作的原因。尽管一些权威机构建议西酞普兰过量后至少观察24小时,但最近的一项分析表明,心律失常很少在摄入后13小时以上发生。我们报告一例西酞普兰过量导致心脏毒性显著延迟发作的病例。

病例报告

一名36岁女性在服用50片(每片20毫克)西酞普兰后约32小时出现手抖、手臂麻木和心悸症状。她的初始生命体征为:血压84/44 mmHg;脉搏102 - 150次/分钟;呼吸17次/分钟;体温99.3华氏度(37.3摄氏度)。她的初始心电图显示窦性心律,校正QT间期延长(572毫秒),伴有阵发性、自限性的宽QRS波心动过速,呈多灶性。就诊后约20分钟,她出现了自行终止的TdP,伴有短暂性低血压和意识丧失。她摄入西酞普兰33小时后的血清浓度为477 ng/mL(治疗浓度:40 - 110 ng/mL);去甲基西酞普兰浓度为123.2 ng/mL(治疗浓度:14 - 40 ng/mL)。她接受了镁剂和利多卡因治疗,就诊后24小时内校正QT间期仍异常。

讨论

西酞普兰过量可导致危及生命的心脏毒性,临床发作可能延迟至常规6小时观察期之后。一旦QT间期延长,延长观察期似乎是谨慎之举。

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