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[一名患有高渗性高血糖状态的慢性酒精中毒患者在酒精戒断期间发生了中央桥脑髓鞘溶解症]

[Central pontine myelinolysis developed during alcohol withdrawal in a chronic alcoholic with hyperosmolar hyperglycemic state].

作者信息

Sakai Toshiyuki, Tomimoto Hidekazu

机构信息

Department of Neurology, Saiseikai Matsusaka General Hospital.

出版信息

Rinsho Shinkeigaku. 2014;54(2):116-23. doi: 10.5692/clinicalneurol.54.116.

DOI:10.5692/clinicalneurol.54.116
PMID:24583585
Abstract

We present a 46-year-old man with central pontine myelinolysis (CPM). He had been diagnosed with diabetes mellitus and chronic pancreatitis. He had drunk more than 1.2 l of Japanese sake daily for 20 years and more. He developed slight reduction of consciousness, dysarthria and truncal ataxia 7 days after he stopped drinking. The laboratory data on admission showed hyperosmolar hyperglycemic state, according to the following findings; glucose 1,058 mg/dl, serum osmolality 328 mOsm/l and serum sodium 119 mEq/l. According as administration of acetic Ringer's solution and insulin injection, the laboratory data 14 hours after admission showed glucose 235 mg/dl, serum osmolality 290 mOsm/l and serum sodium 131 mEq/l. The initial diffusion weighted images (DWI) on MRI revealed a small high signal intensity spot in the pons. The second DWI after 14 days revealed a trident-shaped hyperintensity in the pons that was compatible with CPM. His symptoms showed no remarkable changes, but susceptibility weighted images of MRI after 4 months revealed low signal intensity area in the CPM lesion that indicated pontine hemorrhage. We speculate that marked fluctuation of serum osmotic pressure associated with the rapid change of the serum glucose had a significant role in the pathogenesis of the present case. Therefore, we recommend gradual correction of serum glucose and serum osmolality to maintain less than 12 mEq/l/day as correction of chronic hyponatremia in to prevent and ameliorate pathologic condition of CPM.

摘要

我们报告一例46岁患有中枢桥脑髓鞘溶解症(CPM)的男性患者。他被诊断患有糖尿病和慢性胰腺炎。他有20多年每天饮用超过1.2升日本清酒的习惯。在他停止饮酒7天后,出现了意识轻度减退、构音障碍和躯干共济失调。入院时的实验室检查数据显示为高渗高血糖状态,具体表现如下:血糖1058mg/dl,血清渗透压328mOsm/l,血清钠119mEq/l。经给予醋酸林格液和胰岛素注射后,入院14小时后的实验室检查数据显示血糖235mg/dl,血清渗透压290mOsm/l,血清钠131mEq/l。MRI上最初的扩散加权成像(DWI)显示脑桥有一个小的高信号强度斑点。14天后的第二次DWI显示脑桥有一个三叉形高信号,符合CPM表现。他的症状没有明显变化,但4个月后的MRI磁敏感加权成像显示CPM病变区有低信号强度区域,提示脑桥出血。我们推测血清渗透压与血糖快速变化相关的显著波动在本病例的发病机制中起了重要作用。因此,我们建议像纠正慢性低钠血症一样,逐步纠正血糖和血清渗透压,使其每日纠正幅度维持在12mEq/l以下,以预防和改善CPM的病情。

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