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由于大剂量拉莫三嗪过量,严重的钠通道阻断和心血管衰竭。

Severe sodium channel blockade and cardiovascular collapse due to a massive lamotrigine overdose.

机构信息

University of California San Diego, Division of Medical Toxicology, 200 West Arbor Drive, MC 8925, San Diego, CA 92103-8925, United States.

出版信息

Clin Toxicol (Phila). 2011 Nov;49(9):854-7. doi: 10.3109/15563650.2011.617307. Epub 2011 Oct 5.

DOI:10.3109/15563650.2011.617307
PMID:21972916
Abstract

BACKGROUND

Cardiac arrest due to lamotrigine (LTG) has been reported after co-ingestion with bupropion, but severe sodium channel blockade in the absence of other toxins has not been described. We report a case of cardiac arrest and status epilepticus following a massive LTG overdose.

CASE REPORT

A 48 year-old female was brought to the ED with seizure-like activity subsequent to ingesting 7.5 g of LTG. Vital signs were HR 131, BP 107/68, T 99.4°F, RR 16. She was intubated in the ED for a low GCS. Initial ECG demonstrated a narrow-complex normal sinus rhythm, and her labs were unremarkable. Three hours after intubation she developed status epilepticus, and a pulseless wide-complex tachycardia. She was aggressively resuscitated during which time pulses were periodically reestablished, but lost each time seizures recurred. She was not stabilized until the convulsions were terminated with vecuronium. Her post-resuscitation ECG demonstrated a junctional tachycardia with a 3 mm R-wave in aVR. The LTG level was 74.7 mcg/ml (therapeutic: 3-14 mcg/ml). Comprehensive LC-MS/MS drug screen was negative for all screened compounds.

DISCUSSION

This is the first report of cardiovascular collapse due to LTG with the highest drug concentration to date.

CONCLUSION

The degree of neurologic and cardiovascular toxicity seen in this case are novel and illustrate the potential for severe sodium channel blockade after massive LTG poisonings. Drug levels are not clinically relevant in the acute setting due to the time delay in obtaining results, and recurrent seizure activity may be the only clinical finding that precedes severe cardiac toxicity.

摘要

背景

在与安非他酮共同摄入后,已有报道称拉莫三嗪(LTG)引起心脏骤停,但尚未描述在没有其他毒素的情况下严重的钠通道阻断。我们报告了一例因大剂量 LTG 过量摄入导致心脏骤停和癫痫持续状态的病例。

病例报告

一名 48 岁女性因摄入 7.5 克 LTG 后出现癫痫样活动而被送往急诊室。生命体征为 HR 131,BP 107/68,T 99.4°F,RR 16。她在急诊室因低 GCS 被插管。初始心电图显示为窄复合正常窦性节律,实验室检查无异常。插管后 3 小时,她出现癫痫持续状态和无脉宽复合心动过速。在她被积极复苏期间,脉搏周期性地恢复,但每次癫痫发作时都会失去脉搏。直到使用维库溴铵终止抽搐后,她才得以稳定。她复苏后的心电图显示为交界性心动过速,aVR 中的 3 毫米 R 波。LTG 水平为 74.7 mcg/ml(治疗范围:3-14 mcg/ml)。综合 LC-MS/MS 药物筛选对所有筛选化合物均呈阴性。

讨论

这是迄今为止报道的第一个因 LTG 引起心血管崩溃的病例,且药物浓度最高。

结论

本例中所见的神经和心血管毒性程度是新颖的,表明在大剂量 LTG 中毒后存在严重的钠通道阻断的可能性。由于获得结果的时间延迟,药物水平在急性情况下并不具有临床相关性,并且反复的癫痫发作活动可能是先于严重心脏毒性的唯一临床发现。

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