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苯二氮䓬类药物过量后急性致死性缺氧后白质脑病:一例病例报告及文献综述

Acute fatal posthypoxic leukoencephalopathy following benzodiazepine overdose: a case report and review of the literature.

作者信息

Aljarallah Salman, Al-Hussain Fawaz

机构信息

Department of Medicine, King Khalid University Hospital, College of Medicine, King Saud University, Riyadh, Saudi Arabia.

出版信息

BMC Neurol. 2015 Apr 30;15:69. doi: 10.1186/s12883-015-0320-6.

DOI:10.1186/s12883-015-0320-6
PMID:25925073
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4418099/
Abstract

BACKGROUND

Among the rare neurological complications of substances of abuse is the selective cerebral white matter injury (leukoencephalopathy). Of which, the syndrome of delayed post hypoxic encephalopathy (DPHL) that follows an acute drug overdose, in addition to "chasing the dragon" toxicity which results from chronic heroin vapor inhalation remain the most commonly described syndromes of toxic leukoencephalopathy. These syndromes are reported in association with opioid use. There are very few cases in the literature that described leukoencephalopathy following benzodiazepines, especially with an acute and progressive course. In this paper, we present a patient who developed an acute severe fatal leukoencephalopathy following hypoxic coma and systemic shock induced by benzodiazepine overdose.

CASE PRESENTATION

A 19-year-old male was found comatose at home and brought to hospital in a deep coma, shock, hypoxia, and acidosis. Brain magnetic resonant imaging (MRI) revealed a strikingly selective white matter injury early in the course of the disease. The patient remained in a comatose state with no signs of neurologic recovery until he died few weeks later following an increase in the brain edema and herniation.

CONCLUSION

Toxic leukoencephalopathy can occur acutely following an overdose of benzodiazepine and respiratory failure. This is unlike the usual cases of toxic leukoencephalopathy where there is a period of lucidity between the overdose and the development of white matter disease. Unfortunately, this syndrome remains of an unclear pathophysiology and with no successful treatment.

摘要

背景

滥用物质导致的罕见神经并发症中包括选择性脑白质损伤(白质脑病)。其中,急性药物过量后出现的迟发性缺氧性脑病综合征(DPHL),以及慢性吸入海洛因蒸气导致的“追龙”毒性,仍是最常描述的中毒性白质脑病综合征。这些综合征与阿片类药物使用有关。文献中很少有描述苯二氮䓬类药物导致白质脑病的病例,尤其是急性和进行性病程的。在本文中,我们报告了一名患者,在苯二氮䓬类药物过量导致缺氧性昏迷和全身休克后,发生了急性严重致命性白质脑病。

病例介绍

一名19岁男性在家中被发现昏迷,被送至医院时处于深度昏迷、休克、缺氧和酸中毒状态。脑部磁共振成像(MRI)显示在疾病早期有明显的选择性白质损伤。患者一直处于昏迷状态,没有神经功能恢复的迹象,直到几周后因脑水肿和脑疝加重而死亡。

结论

苯二氮䓬类药物过量和呼吸衰竭后可急性发生中毒性白质脑病。这与中毒性白质脑病的常见病例不同,后者在过量用药和白质疾病发生之间有一段清醒期。不幸的是,这种综合征的病理生理学仍不清楚,且没有成功的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8851/4418099/70afc6ab4050/12883_2015_320_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8851/4418099/83d03af31753/12883_2015_320_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8851/4418099/c51ad70736fc/12883_2015_320_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8851/4418099/70afc6ab4050/12883_2015_320_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8851/4418099/83d03af31753/12883_2015_320_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8851/4418099/c51ad70736fc/12883_2015_320_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8851/4418099/70afc6ab4050/12883_2015_320_Fig3_HTML.jpg

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