Methylene blue for treating toxic encephalopathy due to acute nickel poisoning: A case report.

Rajathadri Hosur Ravikumar, Sayan Nath, Javed Ahsan Quadri, Sulagna Bhattacharjee
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Abstract

Background: Acute nickel poisoning is a rare clinical entity with no established management guidelines. Diagnosis is often delayed by non-specific clinical presentations that can mimic other common toxidromes, such as organophosphate poisoning.

Case summary: A female in her late twenties presented with a Glasgow Coma Scale of 3, profound hypotension, miosis, and hypersalivation following intentional ingestion of an unlabeled toilet cleaner. Initial management for suspected cholinergic toxidrome and corrosive ingestion failed to achieve clinical stability. The patient developed refractory vasoplegic shock and went into a deep coma. Magnetic resonance imaging revealed cytotoxic lesions of the corpus callosum, suggesting toxic encephalopathy. Comprehensive toxicological screening by inductively coupled plasma mass spectrometry confirmed severe nickel toxicity with significantly elevated levels in the blood, urine, and cerebrospinal fluid (55.5 μg/L). Methylene blue, initially administered as a rescue therapy for vasoplegic shock, was associated with a paradoxical spike in urinary nickel excretion (from 8.8 μg/L to 51.9 μg/L) and a rapid decline in serum levels. This biochemical "washout" coincided with dramatic neurological recovery from Glasgow Coma Scale of 3 to 15 within 72 hours.

Conclusion: Early comprehensive toxicological screening is essential in patients with suspected poisoning by unknown substances. In this case, nickel toxicity was confirmed by prompt screening. In the absence of standard treatment protocols in rare poisoning cases, treatment is largely supportive. The apparent clinical benefit of methylene blue-mediated nickel clearance in this case remains speculative.

亚甲基蓝治疗急性镍中毒致中毒性脑病1例。
背景:急性镍中毒是一种罕见的临床疾病,目前尚无明确的治疗指南。诊断常常因非特异性临床表现而延迟,这些临床表现可能模仿其他常见的毒副反应,如有机磷中毒。病例总结:一名20多岁的女性,格拉斯哥昏迷评分为3分,故意摄入未标记的厕所清洁剂后,出现深度低血压、呼吸急促和唾液过多。初步处理怀疑胆碱能中毒和腐蚀性摄入未能达到临床稳定。患者发生难治性血管截瘫性休克并进入深度昏迷。核磁共振显示胼胝体细胞毒性病变,提示中毒性脑病。通过电感耦合血浆质谱综合毒理学筛查证实镍严重毒性,血液、尿液和脑脊液中镍含量显著升高(55.5 μg/L)。亚甲基蓝最初是作为血管截瘫性休克的一种抢救疗法,与尿镍排泄的异常峰值(从8.8 μg/L到51.9 μg/L)和血清水平的迅速下降有关。这种生化“冲洗”与72小时内从格拉斯哥昏迷等级3到15的显著神经恢复相吻合。结论:对疑似未知物质中毒患者进行早期综合毒理学筛查是必要的。在这种情况下,镍毒性是通过及时筛选确认的。在罕见中毒病例缺乏标准治疗方案的情况下,治疗基本上是支持性的。在这种情况下,亚甲基蓝介导的镍清除的明显临床益处仍然是推测性的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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