Marr Nancy, Yu Jessica, Kutsogiannis Demetrios J, Mahmoud Sherif Hanafy
Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, AB, Canada.
Division of Critical Care Medicine, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada.
Neurocrit Care. 2017 Apr;26(2):182-190. doi: 10.1007/s12028-016-0300-8.
Vasopressin is one of the vasopressors used to augment blood pressure in subarachnoid hemorrhage (SAH) patients with clinically significant vasospasm. The purpose of the present study was to determine whether the administration of vasopressin to a population of SAH patients was an independent predictor of developing hyponatremia.
A retrospective review on the health records of 106 patients admitted to the University of Alberta Hospital Neurosciences ICU, Edmonton AB, Canada, with SAH from June 2013 to December 2015 was conducted. Serum sodium changes in patients receiving vasoactive drugs were compared. In addition, independent predictors for hyponatremia (Na < 135 mmol/L) were determined using a multivariate logistic regression model.
Patients treated with vasopressin in addition to other vasoactive drugs had significantly higher sodium changes compared to those treated with other vasoactive drugs (-4.7 ± 6 vs -0.1 ± 2.4 mmol/L, respectively, p value 0.001). Hyponatremia occurred in 14 patients (70 %) treated with vasopressin, 10 patients (44 %) treated with vasoactive drugs other than vasopressin (p value 0.081), and 24 patients (38 %) who did not receive any vasoactive drug (p value 0.013). In multivariate logistic regression analysis, when adjusting for disease severity, age, sex, aneurysm location, and treatment, vasopressin was associated with hyponatremia (OR 3.58, 95 % CI, 1.02-12.5, p value 0.046).
The results of the present study suggest that hyponatremia may be more common in SAH patients treated with exogenous vasopressin compared to those who did not receive it. Serum sodium should be monitored closely when vasopressin is being used in the SAH population. Further studies are needed to confirm the effect of exogenous vasopressin on serum sodium levels in SAH populations.
血管加压素是用于提高患有具有临床显著血管痉挛的蛛网膜下腔出血（SAH）患者血压的血管升压药之一。本研究的目的是确定对SAH患者群体给予血管加压素是否是发生低钠血症的独立预测因素。
对2013年6月至2015年12月入住加拿大艾伯塔省埃德蒙顿市阿尔伯塔大学医院神经科学重症监护病房的106例SAH患者的健康记录进行回顾性研究。比较接受血管活性药物治疗患者的血清钠变化。此外，使用多因素逻辑回归模型确定低钠血症（Na < 135 mmol/L）的独立预测因素。
与接受其他血管活性药物治疗的患者相比，除其他血管活性药物外还接受血管加压素治疗的患者钠变化显著更高（分别为-4.7 ± 6与-0.1 ± 2.4 mmol/L，p值0.001）。14例（70%）接受血管加压素治疗的患者发生低钠血症，10例（44%）接受除血管加压素外的血管活性药物治疗的患者发生低钠血症（p值0.081），24例（38%）未接受任何血管活性药物治疗的患者发生低钠血症（p值0.013）。在多因素逻辑回归分析中，在调整疾病严重程度、年龄、性别、动脉瘤位置和治疗后，血管加压素与低钠血症相关（比值比3.58，95%置信区间，1.02 - 12.5，p值0.046）。
本研究结果表明，与未接受外源性血管加压素治疗的SAH患者相比，接受外源性血管加压素治疗的SAH患者低钠血症可能更常见。在SAH人群中使用血管加压素时应密切监测血清钠。需要进一步研究以证实外源性血管加压素对SAH人群血清钠水平的影响。
