Abstract
Abstract
OBJECTIVE
The association between smoking and intracranial aneurysms is now well recognized. However, the relationship between tobacco use and outcome after aneurysmal subarachnoid hemorrhage (SAH) is not as well understood and published results are contradictory. The purpose of this study is to examine the degree to which the amount of tobacco exposure/dose impacts delayed neurological deterioration and overall clinical outcome after aneurysmal SAH.
METHODS
We reviewed our retrospective database of patients with aneurysmal SAH. We assessed the impact of four independent tobacco variables: smoker (ever smoked), current smoker (actively smoking within the past yr and with at least a 10 pack per yr history of smoking), long-term smoker (at least a 20 pack per yr history), and salient (combination of current and long-term) smoker as well as tobacco dose (categorized according to number of packs per yr) on two outcome variables, delayed neurological deterioration and dichotomized Glasgow Outcome Scale score. Covariates included in the analysis were age, sex, Hunt and Hess grade, Fisher grade, and medical comorbidities. Stepwise elimination with logistic regression was used to arrive at a final multivariate model for each outcome and independent tobacco variable in the presence of covariates.
RESULTS
A total of 320 patients were analyzed. As expected, Hunt and Hess grade was a significant predictor of both delayed neurological deterioration and clinical outcome. Tobacco use (smoker variable) showed an independent association with the development of delayed neurological deterioration (P = 0.0409; odds ratio, 1.78; 95% confidence interval, 1.02–3.08). In addition, patients who were long-term or current smokers (salient smoker variable) showed a trend toward a slightly stronger association with the occurrence of delayed neurological deterioration (P = 0.0229; odds ratio, 1.85; 95% confidence interval, 1.09–3.14). No tobacco use variable was associated with clinical outcome (Glasgow Outcome Scale) in the multivariate analysis.
CONCLUSION
The duration and timing of tobacco use, rather than the dose of tobacco per se, seem to be risk factors for delayed neurological deterioration after aneurysmal SAH. Although we did not find an association between tobacco use and overall clinical outcome after aneurysmal SAH, these results suggest that the distribution of various patterns of tobacco use within a given data set may influence the overall results.
