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乙二醇中毒后的多发性颅神经缺损

Multiple cranial nerve deficits after ethylene glycol poisoning.

作者信息

Spillane L, Roberts J R, Meyer A E

机构信息

Department of Emergency Medicine (Division of Toxicology), Mercy Catholic Medical Center, Philadelphia, Pennsylvania.

出版信息

Ann Emerg Med. 1991 Feb;20(2):208-10. doi: 10.1016/s0196-0644(05)81226-0.

Abstract

We report the cases of two patients who developed cranial nerve palsies after drinking ethylene glycol. A 33-year-old man developed multiple cranial nerve deficits nine days after the ingestion of ethylene glycol in a suicide attempt. Clinical findings included profound bilateral cranial nerve VII palsies and severe dysfunction of cranial nerves IX and X. The neuropathy occurred despite treatment with hemodialysis. The dysphagia completely cleared within two weeks, but at six months a severe bilateral cranial nerve VII dysfunction persisted. A 22-year-old man undergoing hemodialysis for ethylene glycol-induced renal failure developed bilateral cranial nerve VII dysfunction 14 days after ingestion. At a three-month follow-up, the patient demonstrated only moderate functional recovery. The etiology of the cranial nerve deficits is unknown but may be related to oxalate crystal deposition of ethylene glycol-induced pyridoxine dysfunction.

摘要

我们报告了两名饮用乙二醇后出现颅神经麻痹的患者病例。一名33岁男性在自杀未遂摄入乙二醇九天后出现多发性颅神经功能缺损。临床发现包括双侧严重的面神经(VII)麻痹以及舌咽神经(IX)和迷走神经(X)的严重功能障碍。尽管进行了血液透析治疗,但仍发生了神经病变。吞咽困难在两周内完全消除,但六个月时双侧严重的面神经功能障碍仍然存在。一名因乙二醇诱导的肾衰竭而接受血液透析的22岁男性在摄入乙二醇14天后出现双侧面神经功能障碍。在三个月的随访中,患者仅表现出中度功能恢复。颅神经功能缺损的病因尚不清楚,但可能与乙二醇诱导的吡哆醇功能障碍导致的草酸盐晶体沉积有关。

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