Introduction/Purpose Cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage (aSAH) is associated with increased morbidity and mortality. Previous reports indicate severe hemorrhage, tobacco use, and hypertension as risk factors for vasospasm following aSAH. This study evaluates the effects of cocaine on the incidence, severity, and treatability of vasospasm in aSAH patients.

Materials and Methods A retrospective chart review was conducted on all patients admitted with non-traumatic SAH at Temple University Hospital between 2014–2023. All patients with a confirmed aneurysm on digital subtraction angiography (DSA) and admission urine drug screen (UDS) were included in analyses. Patients were separated into two groups, those with positive cocaine use and controls. Demographic data including sex, race, and age, in addition to past medical history, Hunt Hess (HH) scores, modified Fisher scores (mFS), and UDS results were collected. DSAs were reviewed and vasospasm was graded on a scale of 1 to 3 using the visual classification system from Merkel et al. (2022). Analyses were performed using Prism 10. A P-value of 0.05 was set as statistically significant.

Results A total of 225 patients with non-traumatic SAH were identified, of which 75 met the inclusion criteria with a mean patient age of 53, HH score of 3.26, and mFS of 2.47. Mean age, HH score, and mFS did not vary significantly between groups. Internal carotid artery (ICA) segment aneurysms were the most frequent suspected ruptured aneurysm. The majority of aneurysms were treated with coil embolization. The primary outcome demonstrated a strong correlation between a positive UDS for cocaine and risk of radiographic vasospasm (OR=12.5, 95% CI:2.04–244, p=0.02). Additionally, cocaine users were 1.06-fold more likely to have vasospasm requiring treatment (p=0.0219). This correlation persisted with multivariate analyses controlling for both sex (OR=6.63, p=0.0273) and tobacco use (OR=6.309, p=0.0254). Cocaine use was not associated with increased radiographic severity (β=0.005, 95% CI: -0.75 to 0.77, p=0.99) or refractory vasospasm requiring multiple treatments (β=0.25, 95% CI: -1.08 to 1.57, p=0.71). Secondary outcomes showed association between age, gender, and tobacco use, and vasospasm risk. Age was found to be correlated with vasospasm incidence in an unimodal distribution with peak incidence occurring at 50. Female sex was also associated with a higher risk of vasospasm. Tobacco use was statistically associated with a higher grade of vasospasm compared to non-tobacco users, with a mean difference of 0.794 (p=0.0319). No other substances screened for on UDS were associated with vasospasm.

Conclusion Our findings demonstrate a substantial and statistically significant increase in the odds of developing cerebral vasospasm following aSAH associated with cocaine use. Additionally, our study showed an increased frequency of vasospasm in female aSAH patients and was congruent with existing literature suggesting a decrease in vasospasm risk with age and an increased risk of vasospasm associated with tobacco use.

Disclosures A. Rao: None. S. Ricci: None. T. Hannah: None. E. Graves: None. E. Quach: None. K. Erkmen: None. R. Almefty: None.