Document Type


Publication Date



Maine Medical Center, Medical Education, Maine Medical Center Research Institute, Critical Care

MeSH Headings

Humans, Hyponatremia, Subarachnoid Hemorrhage, AVP protein, human, Neurophysins, Vasopressins


Background Aneurysmal subarachnoid hemorrhage (aSAH) is complicated by delayed cerebral ischemia (DCI) in approximately 30% of patients. Vasopressin (AVP) is used to induce hypertension to treat delayed cerebral ischemia (DCI). Prior literature is inconsistent regarding risk of hyponatremia with AVP during DCI and SAH. We report 5 patients who experienced AVP-induced hyponatremia, which may be especially detrimental to patients with SAH and review the literature regarding this controversial area.

Case series Case 1: A 51-year-old woman developed DCI on day 8 after coiling a left MCA aneurysm. AVP was initiated due to tachycardia with norepinephrine. Sodium dropped from 143 to 127 mEq/L in 26 hours, back to 143 mEq/L in 15 hours of stopping AVP. Case 2: A 57-year-old woman developed DCI on day 4 after coiling an anterior communicating artery aneurysm; symptoms improved after norepinephrine and intrarterial nicardipine, but recurred requiring induced hypertension. Ventricular tachycardia developed on day 10, AVP was substituted, and sodium dropped from 139 to 129 mEq/L in 130hours. AVP was stopped, sodium climbed to 131 mEq/L at 6 hours and 140 mEq/L at 12 hours. Case 3: A 68-year-old woman developed DCI on day 4 after coiling left posterior inferior cerebellar artery and basilar tip aneurysms. Phenylephrine and intrarterial verapamil improved her symptoms, but norepinephrine and AVP were added to induce hypertension. Sodium dropped from 140 to 124 mEq/L in 22hours. AVP was stopped, and sodium increased to 129 mEq/L at 3 hours and 141 mEq/L at 18 hours. Case 4: A 51-year-old woman developed DCI on day 5 after coiling an anterior communicating artery aneurysm. Phenylephrine and norepinephrine were added to induce hypertension but were changed to AVP due to tachycardia. Sodium dropped from 140 to 130 mEq/L after 12 hours. AVP was stopped and sodium increased to 144 mEq/L at 24 hours. Case 5: A 62-year-old woman developed DCI on day 5 after coiling right middle cerebral artery aneurysm. Norepinephrine was started to increase blood pressure but soon required addition of AVP to maintain target blood pressure with stable sodium over two days. However on day 10, with readministration of AVP, sodium dropped from 145 to 129 after 35 hours. AVP was stopped and sodium increased to 139 mEq/L at 20 hours.

Discussion/Conclusion This case series supplements 2 prior reports of AVP use during SAH with conflicting results. Muehlschlegel (Neurocrit Care 2007) reported similar sodium changes among 24 patients receiving AVP versus phenylephrine. Marr (Neurocrit Care 2017) noted greater sodium decreases in 19 patients with AVP compared to 22 with other vasopressors. AVP administration for DCI during SAH may precipitate the rapid development of significant hyponatremia, which quickly corrects when AVP is stopped. In both series including ours, there is a predilection for female gender among those developing hyponatremia. Our study is the only study to replicate the AVP hyponatremia data reported by Marr in 2017.


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