Subarachnoid Hemorrhage: Overview & Pathophysiology
Subarachnoid hemorrhage (SAH) is bleeding into the subarachnoid space between the arachnoid and pia. Most spontaneous cases are caused by a ruptured intracranial aneurysm, and the disease is defined as much by its complications — rebleeding, delayed cerebral ischemia, hydrocephalus — as by the initial bleed. This overview covers epidemiology, causes, risk factors, and pathophysiology. For grading scales see Grading Scales, and for diagnosis see Diagnosis & Initial Assessment.
Bottom Line: SAH Overview
- ~5% of strokes but disproportionately lethal — roughly a third die (including sudden pre-hospital death) and a third are left disabled; it strikes a younger population (peak 40–60) with a female predominance.
- ~80–85% are aneurysmal (ruptured saccular "berry" aneurysm at a circle-of-Willis branch point); a benign perimesencephalic non-aneurysmal pattern accounts for ~10%.
- Dominant modifiable risks: hypertension, smoking, heavy alcohol; key non-modifiable: family history, ADPKD, and connective-tissue disorders.
- Three time-defined complications drive outcome: early rebleeding (first hours–days), delayed cerebral ischemia / vasospasm (days 4–14), and hydrocephalus, plus hyponatremia and cardiopulmonary effects.
1. Epidemiology & Burden
Aneurysmal SAH has an incidence of roughly 6–9 per 100,000 person-years and accounts for about 5% of all strokes. Despite advances in securing aneurysms and managing complications, case fatality remains high — approximately one-third die (a substantial fraction before reaching hospital), one-third survive with disability, and one-third achieve a good recovery. Unlike most strokes, SAH affects a relatively young population (peak incidence 40–60 years) and is more common in women, giving it a high burden of lost productive life-years.
2. Causes
- Aneurysmal (~80–85%) — rupture of a saccular intracranial aneurysm; the cause that drives the classic management pathway.
- Perimesencephalic non-aneurysmal (~10%) — blood confined around the midbrain/prepontine cisterns with a negative angiogram; a benign course with very low rebleed and vasospasm risk.
- Other — arteriovenous malformation, dural arteriovenous fistula, intracranial arterial dissection, reversible cerebral vasoconstriction syndrome (RCVS), mycotic aneurysm, vasculitis, and coagulopathy.
(Traumatic SAH — the most common cause of subarachnoid blood overall — is a distinct entity managed in the trauma setting.)
3. Intracranial Aneurysms
Most ruptured aneurysms are saccular ("berry") aneurysms arising at arterial branch points of the circle of Willis, where hemodynamic shear stress is greatest. Common locations:
- Anterior communicating artery (ACOM) — the most common site.
- Posterior communicating artery (PCOM) — may present with a painful third-nerve palsy.
- Middle cerebral artery (MCA) bifurcation.
- Basilar apex and other posterior-circulation sites (higher rupture risk for a given size).
Rupture risk rises with aneurysm size, posterior-circulation location, prior SAH, and patient factors (captured by tools such as the PHASES score for unruptured aneurysms).
4. Risk Factors
| Modifiable | Non-modifiable |
|---|---|
| Hypertension | Female sex |
| Cigarette smoking (strongest modifiable risk) | Family history (≥2 affected first-degree relatives) |
| Heavy alcohol use | ADPKD (autosomal dominant polycystic kidney disease) |
| Sympathomimetic drugs (cocaine) | Connective-tissue disorders (e.g., vascular Ehlers-Danlos) |
| — | Prior SAH / known aneurysm |
5. Pathophysiology & Complications
At rupture, arterial blood under pressure floods the subarachnoid space, causing an abrupt spike in intracranial pressure that can transiently arrest cerebral perfusion — the basis of early brain injury (EBI) and the sudden loss of consciousness or death seen in severe cases. The subsequent course is dominated by time-defined complications:
Rebleeding
Re-rupture of an unsecured aneurysm carries very high mortality and is most likely in the first 24–72 hours. This is the rationale for early aneurysm securing (clipping or coiling) and short-term measures to control blood pressure and avoid sudden surges — see Clipping vs. Coiling.
Vasospasm & delayed cerebral ischemia (DCI)
Beginning around day 4 and peaking at days 7–10, large-vessel narrowing (angiographic vasospasm) and a broader process of delayed cerebral ischemia threaten new infarction. DCI is now understood to be multifactorial — not solely large-artery spasm, but also microcirculatory dysfunction, microthrombosis, and cortical spreading depolarization. It is the leading cause of preventable morbidity in survivors of the initial bleed — see Vasospasm & DCI.
Hydrocephalus
Acute (obstructive) hydrocephalus arises when blood impairs CSF flow through the ventricular system, often requiring an external ventricular drain; a subset later develop chronic communicating hydrocephalus from impaired CSF resorption, requiring shunting.
Systemic complications
- Hyponatremia — common, from cerebral salt wasting or SIADH.
- Cardiopulmonary — neurogenic stunned myocardium / Takotsubo cardiomyopathy and neurogenic pulmonary edema from a catecholamine surge.
- Seizures.
References
- Hoh BL, et al. 2023 Guideline for the Management of Patients With Aneurysmal Subarachnoid Hemorrhage. Stroke. 2023;54(7):e314–e370.
- Macdonald RL, Schweizer TA. Spontaneous subarachnoid haemorrhage. Lancet. 2017;389(10069):655–666.
- Claassen J, Park S. Spontaneous subarachnoid haemorrhage. Lancet. 2022;400(10355):846–862.
- Greving JP, et al. Development of the PHASES score for prediction of risk of rupture of intracranial aneurysms. Lancet Neurol. 2014;13(1):59–66.
