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口服和静脉给药引起的水合氯醛毒性。

Chloral hydrate toxicity from oral and intravenous administration.

作者信息

Sing K, Erickson T, Amitai Y, Hryhorczuk D

机构信息

Cook County Hospital/Toxikon Consortium, Chicago, Illinois, USA.

出版信息

J Toxicol Clin Toxicol. 1996;34(1):101-6. doi: 10.3109/15563659609020242.

Abstract

BACKGROUND

Overdose from enteric chloral hydrate results in cardiovascular and central nervous system symptoms.

CASE REPORTS

This case series compares and contrasts two cases of oral chloral hydrate overdose with two cases of accidental i.v. administration. Whereas ingestion of 219 mg/kg of chloral hydrate resulted in transient bigeminy, ingestion of up to 960 mg/kg caused torsades de pointes and ventricular fibrillation which were effectively treated with defibrillation and a beta blocker. I.V. administration in humans does not appear previously documented. Two cases of i.v. administration of a therapeutic chloral hydrate dose resulted in central nervous system depression and minimal local effects at the injection site.

CONCLUSIONS

Given the high bioavailability of oral chloral hydrate the major determinant of cardiotoxicity may be the dose rather than the route of administration. Cardiac arrhythmias due to chloral hydrate appear to be responsive to beta blocker therapy.

摘要

背景

肠溶性水合氯醛过量会导致心血管和中枢神经系统症状。

病例报告

本病例系列对两例口服水合氯醛过量病例与两例意外静脉注射病例进行了比较和对比。摄入219毫克/千克水合氯醛导致短暂性二联律,而摄入高达960毫克/千克则引起尖端扭转型室速和心室颤动,通过除颤和β受体阻滞剂有效治疗。此前未见人体静脉注射的文献记载。两例静脉注射治疗剂量水合氯醛导致中枢神经系统抑制,注射部位局部影响极小。

结论

鉴于口服水合氯醛的高生物利用度,心脏毒性的主要决定因素可能是剂量而非给药途径。水合氯醛所致心律失常似乎对β受体阻滞剂治疗有反应。

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