Erfan Bashar
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Subarachnoid Haemorrhage

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Educational scope notice: This is a study note for medical students, not medical advice, diagnosis, or treatment guidance. Clinical management should follow local protocols and current guidelines.

Subarachnoid haemorrhage is bleeding into the space between the arachnoid and pia mater that normally holds cerebrospinal fluid. Blood spreads over the brain surface and bathes cortical structures and cranial nerves in irritant products. Rupture of a saccular (berry) aneurysm is the most common cause, and the defining symptom is a thunderclap headache reaching full intensity within seconds. Reported one-year mortality is high, near 50%, with a meaningful fraction of deaths occurring before hospital arrival.

Saccular aneurysms form at bifurcations where turbulent flow and shear stress thin the tunica media and fragment the elastic lamina over years. Reported locations in order of frequency are the anterior communicating artery at roughly 35–45%, the internal carotid territory including the posterior communicating artery near 30%, the middle cerebral artery bifurcation near 20–25%, and the posterior circulation near 10%. All sit around the Circle of Willis. Incidentally found aneurysms above roughly 2.5 mm are often considered for preventive treatment with surveillance for smaller ones. Arteriovenous malformations are a less common cause, and some bleeds remain cryptogenic.

Thunderclap, meningismus, and a localizing nerve sign

The presentation is sudden severe headache with nausea, vomiting, neck stiffness, and sometimes loss of consciousness. Headache severity and instant onset reflect blood under arterial pressure entering the subarachnoid space and irritating the meninges. Nuchal rigidity with Kernig and Brudzinski signs follows for the same reason: inflamed meninges resist stretching. Focal deficits are usually less prominent than in intracerebral bleeding because blood distributes around the brain rather than compressing one region.

One focal sign localizes. A posterior communicating artery aneurysm sits beside the third cranial nerve, and compression can produce ipsilateral ptosis, a down-and-out eye, and a dilated pupil. A third nerve palsy with severe headache points to that aneurysm until proven otherwise, and it can occasionally precede full rupture as a sentinel warning. Against meningitis, which also gives headache with neck stiffness, timing helps: subarachnoid bleeding is instantaneous and maximal at onset, while meningitis evolves over hours to days with fever.

Diagnosis in three steps

Non-contrast CT comes first and is highly sensitive in the acute phase: bright blood fills the basal cisterns, Sylvian fissures, and sulci where dark cerebrospinal fluid should be. The blood pattern can hint at the source, such as anterior interhemispheric blood with an anterior communicating aneurysm or Sylvian blood with a middle cerebral artery aneurysm.

When CT is negative but suspicion stays high, lumbar puncture follows. Bloody fluid that does not clear across tubes, with yellowish xanthochromia from hemoglobin breakdown persisting for days, confirms bleeding and cannot be explained by a traumatic tap alone. Modern CT has made this step uncommon but not obsolete.

Once bleeding is confirmed, CT angiography or digital subtraction angiography defines the aneurysm’s location, size, and shape for treatment planning.

Coiling and clipping

The ruptured aneurysm is evaluated and treated promptly, preferably within 24 hours, because acute rebleeding worsens mortality and outcome. Endovascular coiling is the usual first approach: a catheter reaches the aneurysm from femoral access and fills it with detachable coils, excluding it from the circulation without craniotomy. Surgical clipping through craniotomy, placing a clip across the aneurysm neck, remains necessary for shapes unsuited to coiling such as broad necks or branches arising at the base. Historical mortality was devastating, with the majority dead within a year; modern endovascular care has improved survival substantially although the condition remains life-threatening. Vasospasm with delayed ischemia, hydrocephalus, and rebleed timing are set out under complications (/notes/neurology/sah-complications/).

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