病例报告:评估职业性1,2-二氯乙烷暴露引起的中毒性脑病:磁共振成像的贡献。

IF 4.6 Q2 TOXICOLOGY
Frontiers in toxicology Pub Date : 2025-06-25 eCollection Date: 2025-01-01 DOI:10.3389/ftox.2025.1557995
Jieru Wang, Tianzi Jian, Guangcai Yu, Baotian Kan, Wei Li, Xiangdong Jian
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引用次数: 0

摘要

背景:1,2-二氯乙烷是一种常用的工业溶剂。急性或亚急性职业性接触可引起中毒性脑病;然而,脑成像的长期变化并不经常被记录下来。病例介绍:一名39岁女性在涂胶9天后出现头晕和健忘。休息7天后,她的症状明显好转。然而,恢复工作3天后,她返回时出现头晕、头痛和焦虑。脑磁共振成像(MRI)显示小脑齿状核、基底节区和双侧脑白质广泛水肿和弥漫性异常信号。给予丹参酚酸注射液、异甘草酸镁及神经营养治疗。入院两周后,除轻度行走不协调外,患者症状明显改善。异常MRI信号的范围与先前的发现一致。她第二天就出院了。3天后头痛加重。计算机断层扫描显示弥漫性脑水肿。尽管用甘露醇治疗,她的头痛迅速恶化,并伴有恶心、呕吐、高血压、心动过缓和呼吸困难,最终导致昏迷。后续MRI显示与前次扫描相似,只是表观扩散系数(ADC)序列由低信号变为高信号。核磁共振检查后不久,她出现呼吸骤停。不幸的是,由于严重的脑损伤和感染,她在初次入院32天后死亡。结论:职业性暴露于1,2-二氯乙烷可导致中毒性脑病,表现为弥漫性进行性脑水肿。该病例表明,脑成像结果可能并不总是与患者的临床状况相关,因此仔细监测是必不可少的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Case Report: Evaluating toxic encephalopathy from occupational 1,2-dichloroethane exposure: magnetic resonance imaging contributions.

Case Report: Evaluating toxic encephalopathy from occupational 1,2-dichloroethane exposure: magnetic resonance imaging contributions.

Case Report: Evaluating toxic encephalopathy from occupational 1,2-dichloroethane exposure: magnetic resonance imaging contributions.

Case Report: Evaluating toxic encephalopathy from occupational 1,2-dichloroethane exposure: magnetic resonance imaging contributions.

Background: 1,2-Dichloroethane is a commonly used industrial solvent. Acute or subacute occupational exposure can cause toxic encephalopathy; however, long-term changes in brain imaging are not frequently documented.

Case presentation: A 39-year-old woman developed dizziness and forgetfulness 9 days after performing glue coating. Her symptoms improved significantly after a 7-day break from work. However, after resuming work for 3 days, she returned with dizziness, headache, and anxiety. Brain magnetic resonance imaging (MRI) showed extensive edema and diffuse abnormal signal intensities in the cerebellar dentate nucleus, basal ganglia, and bilateral cerebral white matter. She was treated with salvianolate injection, magnesium isoglycyrrhizinate, and neurotrophic therapy. Two weeks after admission, her symptoms improved significantly, except for mild uncoordinated walking. The range of abnormal MRI signals remained consistent with previous findings. She was discharged the following day. She experienced worsened headache 3 days later. Computed tomography revealed diffuse cerebral edema. Despite treatment with mannitol, her headache rapidly worsened and was accompanied by nausea, vomiting, hypertension, bradycardia, and dyspnea, ultimately leading to unconsciousness. Follow-up MRI showed findings similar to the previous scan, except that the apparent diffusion coefficient (ADC) sequence had changed from hypointense to hyperintense. Shortly after the MRI examination, she experienced respiratory arrest. Unfortunately, she died 32 days after her initial admission due to severe cerebral injury and infection.

Conclusion: Occupational exposure to 1,2-dichloroethane can lead to toxic encephalopathy, presenting as diffuse progressive cerebral edema. This case shows that brain imaging findings may not always correlate with the patient's clinical condition, so careful monitoring is essential.

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