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啤酒狂饮所致重度低钠血症继发中央桥脑髓鞘溶解症

Severe hyponatraemia secondary to beer potomania complicated by central pontine myelinolysis.

作者信息

Kelly J, Wassif W, Mitchard J, Gardner W N

机构信息

Department of Healthcare for the Elderly, King's College Hospital, London, UK.

出版信息

Int J Clin Pract. 1998 Nov-Dec;52(8):585-7.

Abstract

A case of severe hyponatraemia in a 56-year-old male alcohol misuser secondary to beer potomania is presented. In view of severe volume depletion and the patient's inability to drink, normal saline was cautiously infused. Despite initial improvement, he subsequently deteriorated neurologically. Magnetic resonance imaging demonstrated the classical lesion of central pontine myelinolysis (CPM). The rate of correction of plasma sodium was within limits normally considered safe. Beer potomania should be considered as a cause of hyponatraemia in alcohol misusers. Recognition is important as the electrolyte imbalance repairs simply with cessation of alcohol intake and institution of normal diet. Correction of chronic hyponatraemia by infusion of normal or hypertonic saline should not be attempted unless life-threatening neurological complications supervene. When the balance of risks favours correction, caution should be exercised, as CPM may occur. Although a rate of correction of plasma sodium of up to 10 mM per 24-hour period has been associated with a low risk of precipitating CPM, this case illustrates that a completely safe rate of correction probably cannot be defined.

摘要

本文报告了一例56岁男性酒精滥用者因啤酒狂饮症继发严重低钠血症的病例。鉴于严重的容量耗竭以及患者无法饮水,谨慎输注了生理盐水。尽管最初有所改善,但他随后出现神经功能恶化。磁共振成像显示了典型的桥脑中央髓鞘溶解症(CPM)病变。血浆钠的纠正速率在通常认为安全的范围内。啤酒狂饮症应被视为酒精滥用者低钠血症的一个病因。认识到这一点很重要,因为停止饮酒并恢复正常饮食后,电解质失衡即可简单纠正。除非出现危及生命的神经并发症,否则不应尝试通过输注生理盐水或高渗盐水来纠正慢性低钠血症。当风险平衡有利于纠正时,应谨慎行事,因为可能会发生CPM。虽然每24小时血浆钠纠正速率高达10 mM与引发CPM的低风险相关,但该病例表明可能无法确定完全安全的纠正速率。

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