Pathology

SAH usually results from rupture of an intracranial aneurysm into the subarachnoid space, the space between the pia mater covering the brain and the dura mater lining the skull (Fig. 1a). These aneurysms, usually found on the circle of Willis (Fig. 1b), are usually saccular but may be fusiform. About 5% of SAH is caused by bleeding from an arteriovenous malformation (AVM).

Fig. 1 Pathology of subarachnoid haemorrhage. (a) Aneurysms occur in the subarachnoid space, deep to the arachnoid mater and dura mater. The arrows indicate the direction of a bleed: may be intracerebral as well as subarachnoid. (b) Most aneurysms occur in the circle of Willis.

The pathogenesis of intracranial aneurysms is uncertain. Proposed mechanisms include congenital defects in the muscular layer or acquired degenerative changes in the internal elastic lamina. Rarely they occur after trauma or infective emboli. Asymptomatic aneurysms occur in 2–5% of the population.

Aneurysmal rupture may lead to an intracerebral haemorrhage as well as subarachnoid haemorrhage and this intracerebral haemorrhage can produce focal neurological deficits depending on its site. Large subarachnoid bleeds can interfere with CSF reabsorption and produce hydrocephalus.

Clinical features

The classical presentation of SAH is:

a sudden severe headache – ‘as if hit by a bat’

transient loss of consciousness

vomiting

neck stiffness and sometimes focal neurological signs.

It is important to realize that, while this is the classical presentation of SAH, not every patient has all these features. Sometimes the diagnosis of SAH is more difficult and up to 50% of patients are incorrectly diagnosed initially.

About a sixth of patients with SAH will die before reaching hospital. On arrival in hospital, about a third are drowsy and 20% are stuporous or in coma. In those who can give a history, almost all have had sudden severe headaches; rarely, it can come on slightly more slowly. Most patients have generalized headaches and occasionally it is localized. Fifty per cent of patients have had some loss of consciousness. Neck stiffness is found in about two-thirds of patients and localizing signs in 40% (motor deficits 15%, aphasia 15%, hemianopia 10%, sensory disturbances 5%).

A 3rd nerve palsy with pupillary involvement is occasionally seen and is of particular significance, indicating enlargement or rupture of a posterior communicating artery aneurysm. Such patients need urgent referral to a neurosurgical unit and investigation to try to prevent aneurysmal rupture. In an unconscious patient, a 3rd nerve palsy can also occur with uncal herniation due to raised intracranial pressure. A 6th nerve palsy can occur as a false localizing sign due to hydrocephalus. Ophthalmoscopy can occasionally reveal subhyaloid haemorrhage.

Hypertension occurs in about 50% of patients. About a third of patients who present with SAH have had another sudden severe headache in the weeks prior to their presentation. This probably represents a smaller bleed from which they have recovered.