History and exam

Key diagnostic factors

common

headache

Most important clue to diagnosis when described as sudden, severe, or "worst ever."[37] Around 10% to 43% of patients experience a sentinel headache in the 3 months prior to SAH.[2]

photophobia

Eye pain with exposure to light.

loss of consciousness

On admission, up to two-thirds of people with SAH have a depressed level of consciousness, half of whom are in a coma.[40]​

uncommon

third cranial nerve palsy

The presence of third cranial nerve palsy can be very useful and specific, as it typically signals the presence of a posterior communicating artery aneurysm compressing the ipsilateral third cranial nerve. Given their proximity to the third cranial nerve, aneurysms arising from the superior cerebellar artery or posterior cerebral artery can result in the same.

Other diagnostic factors

common

age >50 years

Average age between 50 and 55 years.[1][11][12]

female sex

After the sixth decade, women are affected 1.6 times more than men.[80]

black people

When adjusted for age and sex, in the US the incidence of aSAH is greater in black patients (15.4) compared with that in non-Hispanic white patients (9.9) and other races and ethnicities.[81]

nausea/vomiting

Seen in majority of patients with SAH but nonspecific.[82][83]

altered mental status

Common but nonspecific.[82]

uncommon

meningismus

A clue to diagnosis only when associated with sudden, severe headache.

unilateral or bilateral sixth cranial nerve palsies

This indicates increased intracranial pressure. Nonspecific.[84]

intraocular hemorrhage

Intraocular hemorrhages are seen in 10% to 40% of patients with SAH.[43] Intraocular hemorrhages cause visual loss in the affected eye. This is associated with worse prognosis and increased mortality.[43]​​

focal neurologic deficits

Focal neurologic deficits reflect presence of mass effect from subdural or parenchymal hematomas.[82] Independently associated with higher in-hospital mortality rates and severe disability at discharge.[85]​​

seizures

Seizures occur in around 1% to 10% of patients with SAH.[86][87][88]

Risk factors

strong

hypertension

Hypertension is an important risk factor (relative risk is 2.8) and is potentially modifiable.[26][29][30][31][32][33][34]

smoking

Smoking is one of the most important potentially modifiable risk factors.[26][30][31][32][33][34][35]​​ Relative risk is 1.9.[10][11]

family history

First-degree relatives of patients with SAH have a 4% prevalence of harboring cerebral aneurysms and a three-fold to seven-fold increased risk of having SAH than the general population.[15][34] The risk is highest when the affected relative is a sibling.[29] Population studies of aneurysmal SAH have demonstrated that 9% to 14% of patients with a SAH have a family history of SAH in a first-degree relative.[25]

Having two or more first-degree relatives with SAH has a relative risk of SAH of 6.6.[15] Patients who have two or more first-degree relatives with SAH are potential candidates for aneurysm screening.[25][29]

autosomal dominant polycystic kidney disease (ADPKD)

ADPKD is an important risk factor (relative risk is 4.4).[29] One-quarter of patients with ADPKD have aneurysms at autopsy, and 2% to 8% of patients with aneurysms have ADPKD.[36]

Individuals with ADPKD are potential candidates for aneurysm screening.[25][29]

weak

alcohol use

The relationship of SAH to excessive alcohol use is less robust than that of hypertension or smoking.[30][31][34][35]​​

cocaine use

The relationship of SAH to cocaine use is less robust than that of hypertension or smoking.

Marfan syndrome

Connective tissue disorder with an increased risk for aneurysmal formation and SAH.[36]

Ehlers-Danlos syndrome

Connective tissue disorder with an increased risk for aneurysmal formation and SAH.[36]

pseudoxanthoma elasticum

Connective tissue disorder with an increased risk for aneurysmal formation and SAH.[36]

neurofibromatosis type I

Connective tissue disorder with an increased risk for aneurysmal formation and SAH.[36]

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