Vasopressin-Induced Hyponatremia in Patients With Aneurysmal Subarachnoid Hemorrhage: A Case Series and Literature Review

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Journal of pharmacy practice

MeSH Headings

Humans; Female; Male; Subarachnoid Hemorrhage (complications, drug therapy); Hyponatremia (chemically induced, diagnosis); Vasopressins; Sodium; Treatment Outcome


Vasopressin may be administered to treat vasospasm following aneurysmal subarachnoid hemorrhage (aSAH). The objectives of this study were to describe five cases of suspected vasopressin-induced hyponatremia after aSAH and to review the literature. Single-center, observational case series of intensive care unit (ICU) patients. Ten-bed neurological ICU at Maine Medical Center in Portland, Maine. Convenience sample of patients with aSAH treated with a vasopressin for symptomatic, radiologically confirmed vasospasm. A total of five patients were included in the case series with a median age of 57 (51, 65) years and all were women. The median Glasgow coma scale score was 15 (11, 15) on admission, and the Hunt and Hess scale score was 3, (3, 4). All patients were treated with endovascular coiling of their aneurysm. Vasopressin was administered to treat symptomatic, radiographically confirmed vasospasm on median post-bleed day (PBD) 10 (10, 15) at a fixed-dose of .03 units/min. Serum sodium at baseline was 140 (140, 144) mEq/L and decreased to 129 (126, 129) mEq/L within 26 (17, 83) hours of vasopressin initiation for a median change of -16 (-10, -16) mEq/L. Serum sodium returned to baseline within 18 (14, 22) hours of stopping the infusion. Vasopressin use in vasospasm after aSAH may be associated with clinically significant hyponatremia within 24 hours of starting the infusion. Hyponatremia appears to resolve within 24 hours of stopping the infusion. Additional study in a larger sample size is needed to determine if a causal relationship exist.

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