脑卒中患者低钠血症的诊断和管理分步指南。

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
Fotios Barkas, Georgia Anastasiou, George Liamis, Haralampos Milionis
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引用次数: 2

摘要

低钠血症在卒中患者中很常见,并与不良结局和死亡风险增加有关。本文综述了脑卒中患者低钠血症的潜在原因,并为低钠血症的诊断和治疗提供了一个彻底的算法。伴随疾病和治疗,如糖尿病、慢性肾病和心力衰竭,以及利尿剂、抗抑郁药和质子泵抑制剂是社区低钠血症的最常见原因。在急性中风的情况下,低钠血症的出现可能是由于给药低渗溶液和药物(即。甘露醇和抗癫痫药),溶质摄入不足,感染,以及卒中相关疾病或并发症,如抗利尿激素分泌不当综合征,脑盐消耗综合征和继发性肾上腺功能不全。诊断的第一步是区分低渗性和非低渗性低钠血症,低渗性低钠血症通常是由高血糖或近期服用甘露醇引起的卒中患者。测定尿渗透压、尿钠水平和尿容量状态是鉴别低渗性低钠血症的以下步骤。值得注意的是,特定参数,如尿酸和尿素排泄分数,以及血浆copeptin浓度,可能进一步提高诊断率。治疗选择是基于低钠血症的持续时间和症状。在急性或症状性低钠血症的情况下,建议使用高渗盐水。低血容量性慢性低钠血症用等渗溶液治疗。虽然液体限制仍然是其他形式的慢性低钠血症的一线治疗,但增加肾脏游离水排泄的治疗可能是必要的。循环利尿剂和尿素在卒中患者中起到这一作用,而钠-葡萄糖转运蛋白-2抑制剂似乎是一种有希望的治疗方法。然而,目前尚不清楚钠水平的适当恢复是否能改善这类患者的预后。需要随机试验来比较卒中患者低钠血症的治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

A step-by-step guide for the diagnosis and management of hyponatraemia in patients with stroke.

A step-by-step guide for the diagnosis and management of hyponatraemia in patients with stroke.

A step-by-step guide for the diagnosis and management of hyponatraemia in patients with stroke.

A step-by-step guide for the diagnosis and management of hyponatraemia in patients with stroke.

Hyponatraemia is common in patients with stroke and associated with adverse outcomes and increased mortality risk. The present review presents the underlying causes and provides a thorough algorithm for the diagnosis and management of hyponatraemia in stroke patients. Concomitant diseases and therapies, such as diabetes, chronic kidney disease and heart failure, along with diuretics, antidepressants and proton pump inhibitors are the most common causes of hyponatraemia in community. In the setting of acute stroke, the emergence of hyponatraemia might be attributed to the administration of hypotonic solutions and drugs (ie. mannitol and antiepileptics), poor solute intake, infections, as well as stroke-related conditions or complications, such as the syndrome of inappropriate secretion of antidiuretic hormone, cerebral salt wasting syndrome and secondary adrenal insufficiency. Diagnostically, the initial step is to differentiate hypotonic from non-hypotonic hyponatraemia, usually caused by hyperglycaemia or recent mannitol administration in patients with stroke. Determining urine osmolality, urine sodium level and volume status are the following steps in the differentiation of hypotonic hyponatraemia. Of note, specific parameters, such as fractional uric acid and urea excretion, along with plasma copeptin concentration, may further improve the diagnostic yield. Therapeutic options are based on the duration and symptoms of hyponatremia. In the case of acute or symptomatic hyponatraemia, hypertonic saline administration is recommended. Hypovolaemic chronic hyponatremia is treated with isotonic solution administration. Although fluid restriction remains the first-line treatment for the rest forms of chronic hyponatraemia, therapies increasing renal free water excretion may be necessary. Loop diuretics and urea serve this purpose in patients with stroke, whereas sodium-glucose transport protein-2 inhibitors appear to be a promising therapy. Nevertheless, it is yet unclear whether the appropriate restoration of sodium level improves outcomes in such patients. Randomized trials designed to compare therapeutic strategies in managing hyponatraemia in patients with stroke are required.

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CiteScore
7.20
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