Abstract WP203: Subarachnoid Hemorrhage and Long-Term Stroke Risk After Traumatic Brain Injury

Abstract

Background: Recent studies suggest that traumatic brain injury (TBI) is a risk factor for subsequent ischemic stroke, even years after the initial insult. The mechanisms of the association remain unclear. Hypothesis: The presence of traumatic subarachnoid hemorrhage (tSAH) may mediate the effect of TBI on long-term stroke risk, as it has previously been linked to short-term vasospasm and delayed cerebral ischemia. Methods: Using administrative claims data, we conducted a retrospective cohort study of acute care hospitalizations. Patients discharged with a first-recorded diagnosis of tSAH were followed for a primary diagnosis of stroke. They were matched to patients with TBI but no tSAH, based on age, sex, race, insurance status, income, admission year, coronary heart disease, hypertension, diabetes, congestive heart failure, peripheral vascular disease, chronic kidney disease, chronic obstructive pulmonary disease, atrial fibrillation, alcohol abuse, and tobacco use. Cox proportional hazards modeling was used to assess the association between tSAH and stroke while adjusting for covariates. Results: We identified 34,302 patients with TBI (17,151 patients with tSAH matched to 17,151 patients with non-tSAH TBI) who were followed for a mean of 3.2 ± 1.8 years. Overall, 481 of 34,302 patients with TBI (1.40%; 95% confidence interval [CI], 1.28-1.53%) experienced an ischemic stroke after discharge. There was no significant difference in stroke risk between those with tSAH (1.92%; 95% CI, 1.61-2.27%) as compared to no tSAH (2.08%; 95% CI, 1.78-2.44%). The same pattern was found in adjusted analyzes (hazard ratio [HR[, 0.86; 95% CI 0.70-1.06). This held true even when the group was stratified by age group or by proxies of TBI severity such as mechanical ventilation or discharge disposition during the index hospitalization for TBI. Conclusion: Recent data shows a protracted risk of ischemic stroke following TBI. Our findings do not support a role of vasospasm from tSAH in mediating this association. Further study is required to elucidate the mechanisms of long-term increased stroke risk after TBI