去氨加压素诱发的严重低钠血症伴中央脑桥髓鞘溶解1例。

Tanzib Hossain, Marya Ghazipura, Vineet Reddy, Pedro J Rivera, Vikramjit Mukherjee
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引用次数: 6

摘要

去氨加压素是一种合成抗利尿激素类似物,用于治疗中心性尿囊症、血管性血友病等止血障碍和夜间遗尿。我们报告了一位69岁的男性患者,由于慢性多尿和夜尿被认为是由中央性尿囊性糖尿病引起的,他在接受每日两次10微克的鼻内降压素治疗期间出现了严重的低钠血症。治疗5个月后,患者出现进行性疲劳、厌食、头晕、虚弱、头晕、注意力下降和新发跌倒。治疗6个月后,患者因精神状态改变被送往急诊科,发现严重低钠血症,血清钠水平为96 mmol/L,低于治疗开始时的134 mmol/L。停用鼻内去氨加压素,患者住进重症监护室,在接下来的一周内,低钠血症逐渐纠正到132 mmol/L,每天从未增加超过8 mmol/L,并进行了仔细的液体管理。这包括输注超过11l的5%葡萄糖,以解释高尿量,在1天内达到峰值7.4 L。然而,尽管遵循了推荐的钠校正率,出院后患者的脑磁共振成像显示有脑桥中央髓鞘溶解的证据。尽管有这样的发现,患者最终还是恢复了他的基线精神状态,没有永久性的神经功能缺陷。
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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Desmopressin-Induced Severe Hyponatremia with Central Pontine Myelinolysis: A Case Report.

Desmopressin, a synthetic vasopressin analog, is used to treat central diabetes insipidus, hemostatic disorders such as von Willebrand's disease, and nocturnal enuresis. We present the case of a 69-year-old man who developed severe hyponatremia during treatment with intranasal desmopressin at 10 µg twice daily for chronic polyuria and nocturia thought to be due to central diabetes insipidus. After 5 months of therapy, the patient noticed progressive fatigue, anorexia, dizziness, weakness, light-headedness, decreased concentration, and new-onset falls. At 6 months of therapy, the patient was brought to the emergency department for altered mental status and was found to be severely hyponatremic with a serum sodium level of 96 mmol/L, down from a value of 134 mmol/L at the initiation of therapy. The intranasal desmopressin was discontinued and the patient was admitted to the intensive care unit where the hyponatremia was slowly corrected over the next week to 132 mmol/L, never increasing by more than 8 mmol/L a day, with careful fluid management. This included infusion of over 11 L of 5% dextrose to account for a high urine output, which peaked at 7.4 L in 1 day. However, while the recommended rate for sodium correction was followed, the patient's magnetic resonance imaging of the brain obtained after discharge displayed evidence of central pontine myelinolysis. Despite this finding, the patient eventually returned to his baseline mental status with no permanent neurologic deficits.

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