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Attributable risk of common and rare determinants of subarachnoid hemorrhage
Y M Ruigrok1, E Buskens, G J Rinkel
1Department of Neurology, University Medical Center Utrecht (Netherlands). ij.m.ruigrok@neuro.azu.nl
Insights
Alcohol consumption, smoking, and hypertension are major contributors to subarachnoid hemorrhage (SAH) incidence. Addressing these modifiable risk factors offers the most significant potential for reducing SAH occurrence in the general population.
Area of Science:
- Epidemiology
- Public Health
- Neurology
Background:
- Subarachnoid hemorrhage (SAH) is a critical neurological condition with several identified risk factors.
- Understanding the population-level impact of these risk factors is crucial for effective prevention strategies.
Purpose of the Study:
- To quantify the population attributable risks (PAR) of established risk factors for subarachnoid hemorrhage (SAH).
- To identify the most impactful modifiable risk factors for SAH in the general population.
Main Methods:
- Literature review to gather relative risks and prevalence data for SAH risk factors.
- Calculation of population attributable risks (PAR) based on retrieved data.
Main Results:
- Heavy alcohol consumption (>300 g/wk) accounted for 21% of SAH cases, moderate consumption (100-299 g/wk) for 11%, and smoking for 20%.
- Hypertension contributed to 17% of SAH cases, a positive family history to 11%, and autosomal dominant polycystic kidney disease (ADPKD) to 0.3%.
Conclusions:
- Targeting modifiable factors like alcohol consumption, smoking, and hypertension can significantly reduce SAH incidence.
- Screening for familial SAH provides a modest reduction, highlighting the greater impact of lifestyle modifications.
Background And Purpose:
Smoking, hypertension, alcohol consumption, autosomal dominant polycystic kidney disease (ADPKD), and positive family history for subarachnoid hemorrhage (SAH) are well-known risk factors for SAH. For effective prevention, knowledge about the contribution of these risk factors to the overall occurrence of SAH in the general population is pivotal. We therefore investigated the population attributable risks of the risk factors for SAH.
Methods:
We retrieved the relative risk and prevalence of established risk factors for SAH from the literature and calculated the population attributable risks of these risk factors.
Results:
Drinking alcohol 100 to 299 g/wk accounted for 11% of the cases of SAH, drinking alcohol >/=300 g/wk accounted for 21%, and smoking accounted for 20%. An additional 17% of the cases could be attributed to hypertension, 11% to a positive family history for SAH, and 0.3% to ADPKD.
Conclusions:
Screening and preventive treatment of patients with familial preponderance of SAH alone will cause a modest reduction of the incidence of SAH in the general population. Further reduction can be achieved by reducing the prevalence of the modifiable risk factors alcohol consumption, smoking, and hypertension.