Causes of Subarachnoid Hemorrhage
Ruptured intracranial aneurysm is the overwhelming cause of subarachnoid hemorrhage, accounting for 85% of all spontaneous cases, with the remaining 15% due to non-aneurysmal causes including perimesencephalic hemorrhage, vascular malformations, and rare etiologies. 1, 2
Primary Etiologies
Aneurysmal Causes (85% of cases)
Ruptured saccular (berry) aneurysms are responsible for 70-85% of all non-traumatic SAH, arising from the larger conducting arteries at the base of the brain, particularly in the anterior circulation. 1, 3
Aneurysms most commonly rupture at the anterior communicating artery, posterior communicating artery, and middle cerebral artery bifurcations, with anterior circulation locations being most frequent (approximately 65% of fatal aneurysms). 4, 5
The majority of fatal aneurysms are small (<5mm in diameter), challenging the assumption that only large aneurysms rupture—in one autopsy series, 73% of fatal aneurysms measured less than 5mm. 5
Non-Aneurysmal Causes (15% of cases)
Perimesencephalic SAH accounts for approximately 10% of cases, characterized by blood restricted to perimesencephalic cisterns with negative angiography, likely caused by small venous or capillary ruptures not detectable on conventional imaging. 1
Cerebral amyloid angiopathy and reversible cerebral vasoconstriction syndrome are rare causes of non-traumatic diffuse SAH. 1
Other uncommon causes include vascular malformations, neoplasia, and hematological disorders, which must be ruled out when aneurysm is not identified. 5
Major Risk Factors
Modifiable Risk Factors
Cigarette smoking is the most significant modifiable risk factor, with current smokers having substantially elevated risk in multivariable analyses. 4, 6
Hypertension independently increases SAH risk and is present in the majority of patients, though the direct relationship remains somewhat uncertain. 4, 2, 6
Heavy alcohol use (not moderate consumption) is an independent risk factor, with population-attributable risk analyses showing substantial contribution to SAH burden. 4, 6
Sympathomimetic drug use, particularly cocaine and phenylpropanolamine, has been implicated as a cause of SAH, with cocaine-related SAH occurring in younger patients. 4
Non-Modifiable Risk Factors
Female sex confers 1.24 times higher incidence than males (lower than previous estimates of 1.6), with a sex-age effect showing higher incidence in younger men (25-45 years), women between 55-85 years, and men >85 years. 4
Age is a critical factor, with incidence increasing with age and typical average onset at 50 years; SAH is relatively uncommon in children (0.18-2.0 per 100,000). 4
Race and ethnicity influence risk, with Blacks and Hispanics having higher incidence than white Americans. 4
Genetic and Familial Factors
Family history of SAH or intracranial aneurysm is an independent risk factor, particularly when 2 or more first-degree relatives are affected, conferring a relative risk of 4.2. 4, 6
Autosomal dominant polycystic kidney disease and type IV Ehlers-Danlos syndrome are genetic syndromes with substantially increased SAH risk. 4
Previous SAH carries a 1-2% annual rate of new aneurysm formation, with patients having multiple aneurysms being particularly susceptible. 4
Aneurysm-Specific Risk Factors
Symptomatic aneurysms, larger size (though most ruptures occur in small aneurysms), and posterior circulation location (posterior communicating artery or vertebrobasilar system) increase rupture risk. 4
Anterior circulation aneurysms appear more prone to rupture in patients <55 years of age, while posterior communicating aneurysms rupture more frequently in men. 4
Common Pitfalls
Do not assume that only large aneurysms rupture—the majority of fatal aneurysms are actually small (<5mm), making size alone an unreliable predictor. 5
Recognize that diabetes does not appear to be a risk factor for SAH, contrary to its role in other cerebrovascular diseases. 4
Be aware that low body mass index has been associated with increased SAH risk in multivariable analyses, though this may be confounded by smoking. 6
Understand that even in families with genetic susceptibility, smoking cessation, hypertension treatment, and reduced alcohol intake may substantially decrease SAH risk. 6