Cigarette smoke (CS) contains several carcinogens known to initiate and promote tumorigenesis and metastasis. Because various genes that mediate carcinogenesis and tumorigenesis are regulated by nuclear factor kappa-B (NF-kappaB), Anto et al., postulated that the effects of CS must be mediated through activation of this transcription factor 1).
To improve the understanding of the impact of smoking on long-term outcomes after coil embolization of intracranial aneurysms, Brinjikji et al. studied a consecutive contemporary series of patients treated at their institution. The aims of this study were to determine whether smoking is an independent risk factor for aneurysm recurrence and retreatment after endovascular coiling.
All patients who had received an intrasaccular coil embolization of an intracranial aneurysm, who had undergone a follow-up imaging exam at least 6 months later, and whose smoking history had been recorded from January 2005 through December 2012 were included in this study. Patients were stratified according to smoking status into 3 groups: 1) never a smoker, 2) current smoker (smoked at the time of treatment), and 3) former smoker (quit smoking before treatment). The 2 primary outcomes studied were aneurysm recurrence and aneurysm retreatment after treatment for endovascular aneurysms. Kruskal-Wallis and chi-square tests were used to test statistical significance of differences in the rates of aneurysm recurrence, retreatment, or of both among the 3 groups. A multivariate logistic regression analysis controlling for smoking status and for several characteristics of the aneurysm was also performed.
In total, 384 patients with a combined total of 411 aneurysms were included in this study. The aneurysm recurrence rate was not significantly associated with smoking: both former smokers (OR 1.00, 95% CI 0.61-1.65; p = 0.99) and current smokers (OR 0.58, 95% CI 0.31-1.09; p = 0.09) had odds of recurrence that were similar to those who were never smokers. Former smokers (OR 0.78, 95% CI 0.46-1.35; p = 0.38) had odds of retreatment similar to those of never smokers, and current smokers had a lower odds of undergoing retreatment (OR 0.44, 95% CI 0.21-0.91; p = 0.03) than never smokers. Moreover, an analysis adjusting for aneurysm rupture, diameter, and initial occlusion showed that former smokers (OR 0.65, 95% CI 0.33-1.28; p = 0.21) and current smokers (OR 1.04, 95% CI 0.60-1.81; p = 0.88) had odds of aneurysm recurrence similar to those who were never smokers. Adjusting the analysis for aneurysm rupture, diameter, and occlusion showed that both former smokers (OR 0.49, 95% CI 0.23-1.05; p = 0.07) and current smokers (OR 0.82, 95% CI 0.46-1.46; p = 0.50) had odds of retreatment similar to those of patients who were never smokers.
The results show that smoking was not an independent risk factor for aneurysm recurrence and aneurysm retreatment among patients receiving endovascular treatment for intracranial aneurysms at the authors' institution. Nonetheless, patients with intracranial aneurysms should continue to be counseled about the risks of tobacco smoking 7).
Tobacco use were not significantly associated with poor outcome after aneurysmal subarachnoid hemorrhage 8).
Previously established risk factors such as hypertension and smoking were identified as the most prevalent comorbidities, with disparity between subgroups, particularly women and African Americans 9).
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 subarachnoid hemorrhage (aSAH). Although Krishnamurthy et al. 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 result 10).
Only 8 studies have investigated the incidence and epidemiology of aneurysmal subarachnoid hemorrhage (aSAH) in the United States. This is the first investigation in Indiana, which has some of the highest rates of tobacco smoking and obesity in the nation. The authors prospectively identified 441 consecutive patients with aSAH from 2005 to 2010 at 2 hospitals where the majority of cases are treated. Incidence calculations were based on US Census populations. Epidemiologic variables included demography; risk factors; Hunt and Hess scale; Fisher grade; number, location, and size of aneurysms; treatment type; and complications. Overall incidence was 21.8 per 100,000 population. Incidence was higher in women, increased with age, and did not vary by race. One third to half of patients were hypertensive and/or smoked cigarettes at the time of ictus. Variations by count were partially explained by Health Factor and Morbidity Rankings. Complications varied by treatment. These findings deviate from estimates that 6-16 per 100,000 people in the United States will develop aSAH and are double the incidence in a Minnesota population between 1945 and 1974. The results also deviate from the worldwide estimate of 9.0 aSAHs per 100,000 person-years. The predictive value of variations in Health Factor and Morbidity Rankings implicates the importance of future research on multivariate biopsychosocial causation of aSAH 11).
Very low birth weight (VLBW) infants (< 1500 gm), cocaine-exposed infants were at increased risk of intraventricular hemorrhage, were more likely to be placed outside maternal care, and had higher incidences of cognitive and motor delays at follow-up. Cocaine-using women were also more likely to use other drugs, especially alcohol, marijuana, and tobacco 12).
In a analysis, intraventricular hemorrhage and tobacco use were associated with symptomatic vasospasm 13).
Tobacco use and a history of diabetes mellitus were associated with vasospasm 14).
CT-evident SAH, left ventricular hypertrophy (LVH), cigarette smoking, and hypertension are associated with vasospasm. In smokers or hypertensive patients, premorbid LVH appears to predict much more severe vasospasm 15).
Cocaine users were younger than control, and were more likely to smoke tobacco, drink alcohol, and have renal dysfunction 16).
There are limited scientific data on the impact of smoking on patient-reported outcomes following minimally invasive spine surgery.
Nonsmokers experienced a significantly larger improvement at 1 year following microdecompression for LSS compared to smokers. Smokers were less likely to achieve a minimal clinically important difference. However, it should be emphasized that considerable improvement also was found among smokers 18).
Considering sex, smoking and heavy works as predictors of recurrent lumbar disc herniation (LDH), surgeons should advice their patients to limit hard work and put away smoking especially in tall and male ones to prevent LDH recurrence 19).
Smoking was the strongest predictor of reoperation in patients who had undergone single level laminectomy, multilevel laminectomy, or reoperation for progression of spinal degeneration. These findings suggest that smokers have worse outcomes of lumbar decompression than nonsmokers 20).
In postlaminectomy pseudomeningocele a retrospective analyses of six cases was made including: clinical signs and symptoms, radiological findings, and possible therapeutic modalities.
In every case, there was a palpable fluctuating mass under the surgical scar, sensory loss in both low extremity, and limited leg raising; moreover, heel tapping produced pain. Also, every patient had a history of long standing cigarette smoking and multiple spinal surgeries. Radiologically dural saccular or tubular structures were noted at myelograms, magnetic resonance imaging, or computed axial tomography scan, usually at the site of the surgery. In one patient with metallic devices, diagnosis was made by ultrasound 21).
Compensation claims and smoking had very significant adverse impacts on both employment and pain results despite high fusion rates, particularly in patients under the age of 55 years 22).
Cotinine, a main metabolite of nicotine, has harmful effects on SCI via GFAP and CNP expression. The findings of the present study support the hypothesis that tobacco causes neuronal degeneration via cotinine 23).
Exposure of nonsmoking pregnant women to environmental tobacco smoke (ETS) is associated with a number of adverse perinatal outcomes including lower birthweight, smaller head circumference and stillbirth, as well as shorter birth length. This information is important for women, their families and healthcare providers, and reinforces the continued need for increased public policy and education on prevention of exposure to ETS 24).