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Spontaneous intracranial arterial bleeds into the subarachnoid space.
15 per 100,000 per year. Accounts for 5–10% of cerebrovascular disease.
In most cases spontaneous subarachnoid haemorrhage results from an underlying lesion:
· Saccular (berry aneurysms), 85%
· Arteriovenous malformations, 10%
· No lesion found, 5%
Saccular or berry aneurysms arise due to defects in the internal elastic lamina of arteries and occur in 2% of the population. They may be multiple, and tend to occur at junctions of arteries on the circle of Willis or with its adjacent branches. Common sites include the anterior communicating artery, the posterior communicating artery and the middle cerebral artery. Most are idiopathic, but they are associated with diseases such as arteritis, coarctation of the aorta, Marfan’s syndrome and adult polycystic kidney disease.
Arteriovenous malformations (AVM) are developmental abnormalities of blood vessels.
Sudden onset of a very severe headache, often followed by vomiting and/or loss of consciousness. There are signs of meningeal irritation with neck stiffness and a positive Kernig’s sign (pain in back on flexing the hip). Neurological signs, papilloedema and retinal haemorrhages may be present.
A layer of blood is present over the brain in the subarachnoid space and in the cerebrospinal fluid.
The blood acts as an irritant, causing vascular spasm leading to further ischaemia, infarction and cerebral oedema. It also interferes with CSF resorption, causing hydrocephalus which may be acute or chronic.
CT brain scanning will demonstrate the bleed in most cases, but is falsely negative in up to 15% (less >8 hours after onset), therefore a lumbar puncture to demonstrate the presence of blood in the CSF space may be required. To differentiate from a ‘bloody tap’, i.e. trauma from the spinal tap needle, xanthochromia (yellowness of the CSF due to blood pigments) is looked for. It appears 12 hours post SAH, and may persist for 1–2 weeks.
If the patient is suitable for surgical intervention, carotid and vertebral angiography is used to demonstrate the site of the aneurysm or AVM.
i. Patients should be resuscitated as necessary.
ii. Oral nimodipine (a calcium-channel blocker) has been shown to reduce mortality. It is thought to work by reducing vascular spasm. Severe hypertension may need to be controlled but hypotension must be avoided to prevent further loss of perfusion pressure, so patients are kept well hydrated with intravenous saline.
iii. In suitable patients surgical or radiological intervention for aneurysms takes place a few days later in a neurosurgical centre:
· The neck of the aneurysm is clipped, and in some cases the aneurysm is wrapped in gauze to induce a fibrous reaction.
· An alternative method is to obliterate the lumen of the aneurysm by intraarterial embolisation using metallic coils.
iv. AVMs can be treated with microembolism or focal radiotherapy.
50% of patients with a subarachnoid haemorrhage die prior to or soon after arrival In hospital, and a further 10– 20% die in the first few weeks from rebleeding. Without intervention the risk of rebleeding is 30% in the following year from a berry aneurysm, 10% for AVMs.
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