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首页> 外文期刊>The Journal of pharmacy technology: jPT : official publication of the Association of Pharmacy Technicians >Hypermanganesemia-Induced Cerebral Toxicity Mimicking an Acute Ischemic Stroke: A Case Report and Review of Overlapping Pathologies
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Hypermanganesemia-Induced Cerebral Toxicity Mimicking an Acute Ischemic Stroke: A Case Report and Review of Overlapping Pathologies

机译：高锰血症诱导的脑毒性模仿急性缺血性脑卒中：案例报告和重叠病理的审查

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Objective: To review and consider risk factors associated with the accumulation of and toxicity from manganese in patients receiving total parenteral nutrition (TPN). Case Summary: A 66-year-old female presented to the emergency department with right facial and arm weakness that initiated 1 hour prior to admission. Past medical history includes oral cancer with chronic aspiration and gastroparesis secondary to chemotherapy, TPN for 9 months, and a previous episode of right facial and arm parasthesias due to hypertensive emergency 4 years prior. The patient was assigned a National Institutes of Health Stroke Scale score of 6, cleared of an intracranial hemorrhage on imaging, and was administered tPA (tissue plasminogen activator) for an acute ischemic stroke after managing her hypertension to <185/110 mm Hg. Resolution of symptoms occurred within 24 hours. A magnetic resonance imaging of the patient’s brain 24-hours post-tPA indicated an increased signal density in the globus pallidus, which in turn is linked with encephalopathy and has been described as a marker for hypermanganesemia. Discussion: Manganese is an essential trace element with a critical role in numerous physiologic functions. Though readily obtained from dietary sources and rarely causing issue, manganese provided to patients via TPN may result in toxicities. Though the presentation of neurotoxicities associated with TPN-delivered manganese has been previously documented, the clinical presentation of toxicity has never mimicked an acute ischemic stroke. Conclusion: Though an evaluation of overlapping pathologies is warranted, this patient’s clinical presentation of manganese toxicity mimicked an acute ischemic stroke and resulted in the administration of a fibrinolytic. A more comprehensive appreciation of the implications of trace elements is demanded of clinicians.
机译：目的：回顾和考虑与接受全胃肠外营养（TPN）的患者中锰的积累和毒性相关的危险因素。病例总结：一名66岁女性在入院前1小时因右侧面部和手臂无力入院。既往病史包括口腔癌伴慢性误吸和化疗后胃轻瘫，TPN治疗9个月，以及4年前因高血压急症而发生的右面部和手臂感觉异常。该患者的美国国立卫生研究院卒中量表评分为6分，在影像学检查中清除了颅内出血，并在将高血压控制在<185/110毫米汞柱后，对急性缺血性卒中给予tPA（组织纤溶酶原激活剂）。症状在24小时内消失。tPA后24小时患者大脑的磁共振成像显示苍白球内的信号密度增加，这反过来又与脑病有关，并被描述为高锰血症的标志物。讨论：锰是一种必需的微量元素，在许多生理功能中起着关键作用。虽然很容易从饮食来源获得，很少引起问题，但通过TPN提供给患者的锰可能会导致毒性。尽管TPN释放的锰相关神经毒性的表现之前已有文献记载，但毒性的临床表现从未模拟急性缺血性中风。结论：尽管有必要对重叠的病理学进行评估，但该患者锰中毒的临床表现类似于急性缺血性中风，并导致服用纤溶药物。临床医生需要更全面地了解微量元素的含义。

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