The clinical significance and reliability of self-reported smoking status in patients with intracranial aneurysms: a review.

OBJECTIVE

Here we present a review of the pathophysiology of tobacco smoking on intracranial aneurysms, self-reported smoking status in these patients, screening tools and assays available for assessing active nicotine use, means of impacting smoking cessation rates, and the potential impact of smoking cessation on risk of rupture and recurrence of treated intracranial aneurysms.

METHODS

A literature search using PubMed was done to identify all English language studies relating to tobacco use and intracranial aneurysms, smoking and subarachnoid hemorrhage, nicotine breakdown products, and smoking cessation in neurosurgery. Results from the studies were reviewed and summarized.

RESULTS

Tobacco use is an independent risk factor for formation, growth, and rupture of intracranial aneurysms. The pathogenesis of aneurysm formation is complex, and related to increased wall shear stress, endothelial dysfunction, atherosclerosis, and altered gene regulation. Furthermore 80% of all aneurysmal ruptures occur in patients who have used tobacco products. It is suboptimal to rely on self-reported smoking status in order to determine patient risk. Use of objective metrics for ongoing tobacco use may be indicated in selected patients, and may increase smoking cessation rates in these patients. A variety of laboratory and point-of-care tests are available for measurement of nicotine and nicotine breakdown products. Most assays in clinical practice measure the nicotine breakdown product cotinine, which constitutes 75% of nicotine metabolites excreted in the urine and has a substantial half-life of 16h, compared to nicotine's 2-h half-life. With proper identification, an astute physician may be able to assist in smoking cessation and foster improved patient care. By following recommended guidelines and prescribing pharmaceutical aid, a patient has a 2.5 times greater chance of smoking cessation compared with attempting to stop without physician assistance.

CONCLUSIONS

Smoking increases risk for intracranial aneurysm formation, rupture, re-rupture and need for re-treatment. Measurement of nicotine breakdown products may have clinical utility in the management of patients with intracranial aneurysms. Smoking cessation interventions may be effective, and use of established smoking cessation tools use may lead to improved clinical outcomes in these patients. The effects of smoking cessation efforts on smoking cessation and intracranial aneurysm outcomes is a fertile field for future investigation.