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创伤性脑损伤后持续性抗利尿激素分泌异常综合征

Persistent syndrome of inappropriate antidiuretic hormone secretion following traumatic brain injury.

作者信息

Dick Michael, Catford Sarah R, Kumareswaran Kavita, Hamblin Peter Shane, Topliss Duncan J

机构信息

Faculty of Medical and Health Sciences, The University of Auckland , 85 Park Road, Grafton, Auckland , New Zealand.

Department of Endocrinology and Diabetes, The Alfred Hospital , Commercial Road, Melbourne, Victoria, 3004 , Australia.

出版信息

Endocrinol Diabetes Metab Case Rep. 2015;2015:150070. doi: 10.1530/EDM-15-0070. Epub 2015 Aug 27.

Abstract

UNLABELLED

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) can occur following traumatic brain injury (TBI), but is usually transient. There are very few case reports describing chronic SIADH and all resolved within 12 months, except for one case complicated by meningo-encephalitis. Persistent symptomatic hyponatremia due to chronic SIADH was present for 4 years following a TBI in a previously well 32-year-old man. Hyponatremia consistent with SIADH initially occurred in the immediate period following a high-speed motorbike accident in 2010. There were associated complications of post-traumatic amnesia and mild cognitive deficits. Normalization of serum sodium was achieved initially with fluid restriction. However, this was not sustained and he subsequently required a permanent 1.2 l restriction to maintain near normal sodium levels. Multiple episodes of acute symptomatic hyponatremia requiring hospitalization occurred over the following years when he repeatedly stopped the fluid restriction. Given the ongoing nature of his hyponatremia and difficulties complying with strict fluid restriction, demeclocycline was commenced in 2014. Normal sodium levels without fluid restriction have been maintained for 6 months since starting demeclocycline. This case illustrates an important long-term effect of TBI, the challenges of complying with permanent fluid restrictions and the potential role of demeclocycline in patients with chronic hyponatremia due to SIADH.

LEARNING POINTS

Hyponatraemia due to SIADH commonly occurs after TBI, but is usually mild and transient.Chronic hyponatraemia due to SIADH following TBI is a rare but important complication.It likely results from damage to the pituitary stalk or posterior pituitary causing inappropriate non-osmotic hypersecretion of ADH.First line management of SIADH is generally fluid restriction, but hypertonic saline may be required in severe cases. Adherence to long-term fluid restriction is challenging. Other options include oral urea, vasopressin receptor antagonists and demeclocycline.While effective, oral urea is poorly tolerated and vasopressin receptor antagonists are currently not licensed for use in Australia or the USA beyond 30 days due to insufficient long-term safety data and specific concerns of hepatotoxicity.Demeclocycline is an effective, well-tolerated and safe option for management of chronic hyponatraemia due to SIADH.

摘要

未标注

抗利尿激素分泌不当综合征(SIADH)可发生于创伤性脑损伤(TBI)后,但通常是短暂的。描述慢性SIADH的病例报告非常少,除了1例合并脑膜脑炎的病例外,所有病例均在12个月内得到缓解。一名32岁既往健康的男性在TBI后因慢性SIADH出现持续性症状性低钠血症长达4年。与SIADH相符的低钠血症最初发生在2010年一次高速摩托车事故后的即刻。伴有创伤后遗忘和轻度认知缺陷等并发症。最初通过限液使血清钠恢复正常。然而,这一效果未能持续,随后他需要永久性限制1.2升液体摄入以维持接近正常的钠水平。在接下来的几年里,当他多次停止限液时,发生了多次需要住院治疗的急性症状性低钠血症发作。鉴于其低钠血症的持续性以及严格限液的困难,2014年开始使用地美环素。自开始使用地美环素以来,在不限液的情况下钠水平正常已维持了6个月。该病例说明了TBI的一项重要长期影响、遵守永久性液体限制的挑战以及地美环素在因SIADH导致慢性低钠血症患者中的潜在作用。

学习要点

SIADH导致的低钠血症常见于TBI后,但通常较轻且短暂。TBI后因SIADH导致的慢性低钠血症是一种罕见但重要的并发症。它可能是由于垂体柄或垂体后叶受损导致抗利尿激素不适当的非渗透性分泌过多引起的。SIADH的一线治疗通常是限液,但严重病例可能需要高渗盐水。坚持长期限液具有挑战性。其他选择包括口服尿素、血管加压素受体拮抗剂和地美环素。虽然口服尿素有效,但耐受性差,并且由于长期安全性数据不足以及对肝毒性的特殊担忧,血管加压素受体拮抗剂目前在澳大利亚或美国使用超过30天未获许可。地美环素是治疗因SIADH导致的慢性低钠血症的一种有效、耐受性良好且安全的选择。

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Clinical practice guideline on diagnosis and treatment of hyponatraemia.临床实践指南:低钠血症的诊断与治疗。
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Am J Med Sci. 2008 May;335(5):390-3. doi: 10.1097/MAJ.0b013e318149e6f1.
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Ann Intern Med. 2001 Nov 20;135(10):932-3. doi: 10.7326/0003-4819-135-10-200111200-00027.
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