(628) Association With SSRI/SNRI Use and Incident Hyponatremia After Aneurysmal Subarachnoid Hemorrhage

Introduction: Hyponatremia is common following subarachnoid hemorrhage (SAH) and is associated with increased risk of vasospasm and delayed cerebral ischemia (DCI). Risk factors for post-SAH hyponatremia are poorly defined; however, selective serotonin reuptake inhibitors (SSRIs) and selective norepinephrine reuptake inhibitors (SNRIs) are associated with hyponatremia. This study assessed whether pre-admission SSRIs/SNRIs increased risk of hyponatremia after SAH.

Methods: This was a single-center retrospective study at a comprehensive stroke center. Patients were included if they were admitted for nontraumatic SAH (aneurysmal, perimesencephalic, or angiography-negative) and were excluded if they died within 24 hours of presentation or were hyponatremic on admission. The primary endpoint was the rate of hyponatremia between patients on and not on SSRIs/SNRIs pre-admission. Key secondary endpoints included incidence of vasospasm, DCI, and rebleeding, time to hyponatremia, and discharge modified Rankin scale between groups.

Results: 292 patients were included; 49 patients were prescribed an SSRI or SNRI prior to admission. Of those included, most patients had a Hunt and Hess score of 1 or 2, and 45% of patients had anterior aneurysms. 11% and 26% of patients had perimesencephalic and CTA-negative SAH respectively. The incidence of clinically significant hyponatremia occurred in 37% of patients prescribed SSRIs/SNRIs compared to 30% of patients not on SSRIs/SNRIs (OR 1.35; 95% CI, 0.70-2.55). The time to incident hyponatremia was consistent between groups (6.0 days vs. 5.5 days; p = 0.80), and there were similar rates of rebleeding (4.1% vs. 5.4%; p > 0.99) and delayed cerebral ischemia (12% vs. 14%; p = 0.80). There was an insignificant trend towards increased incidence of vasospasm in the SSRI/SNRI cohort (33% vs. 21%; p = 0.065).

Conclusions: Pre-admission SSRI/SNRI utilization was not associated with hyponatremia or secondary endpoints including vasospasm, DCI, or rebleeding. This study suggests serotonergic therapies are not a significant risk factor for clinically relevant complications after SAH.