Subarchnoid haemorrhage

Subarachnoid haemorrhage accounts for approximately 5% of CVAs
Outcome depends on the degree of neurological deficit
The lower the GCS on presentation the worse the prognosis
70% are due Berry aneurysms
10% are due to arteriovenous malformations
10% are due to hypertension
5% are idiopathic

Pathology of Berry aneurysms

Aneurysms are found in 8% of individuals at post mortem
They are thin walled saccular aneurysms found at arterial bifurcations
Occur due to turbulent flow and damage to internal elastic lamina
Commonest site of aneurysms are:
- Posterior communicating artery 30%
- Anterior communicating artery 25%
- Middle cerebral artery 25%
Estimated to have a population prevalence of 1.5%
Most remain asymptomatic but they are a common cause of sudden death

Clinical features

Classic presentation is with a sudden onset of severe headache
Often assocaited with nausea, vomiting, photophobia and neck stiffness
Neurological symptoms and signs may be present
Level of consciousness may be reduced
Fundoscopy may show subhyoid haemorrhages
The clinical course is unpredictable
Overall mortality is approximately 40%
Many patients die before reaching hospital

Investigations

Diagnosis can often be confirmed by an early CT
Has a sensitivity of 90% if performed within the first 24 hours
Sensitivity reduced to 50% by 72 hours as blood is reabsorbed
CT may also identify source of haemorrhage
If diagnosis is on doubt then lumbar puncture may be indicated
Will show uniform blood-staining of CSF and xanthochromia
Cerebral angiography will identify site of an aneurysm
15% of aneurysms are multiple

Complications

The major complications are:
- Rebleeding
- Delayed ischaemic neurological deficit
- Hydrocephalus
Risk of rebleed is 4% at 24 hours, 25% at 2 weeks and 60% at 6 months
Rebleeding is associated with a 60% mortality
Delayed ischaemic neurological deficit (DIND) is due to intense vasospasm
Treatment is by maintaining cerebral perfusion with adequate hydration
Calcium channel blocks may also be useful
Hydrocephalus results from impaired CSF reabsorption through arachnoid villi
10% of patients will require CSF diversion or shunting

Management

In patients fit for surgery the aneurysm should be clipped at craniotomy
Aim is clip neck of aneurysm whilst maintaining flow in native vessel
May also be embolised endovascularly with platinum coils
Timing of intervention is controversial
Vasospasm usually greatest at 5 days
Surgery traditionally deferred until 10 days after the initial bleed
Patients may die as a result of rebleed during this period
Early surgery may be associated with reduced mortality and no increased morbidity

Bibliography

Edlow J A, Caplan L R. Avoiding pitfalls with the diagnosis of subarachnoid haemorrhage. N Engl J Med 2000; 342: 29-36.

Feigin V L, Rinkel G J, Algra A, van Gijn J. Circulatory volume expansion for aneurysmal subarachnoid haemorrhage. Cochrane Database Syst Rev 2000; 2: CD000483.

Feigin V L, Rinkel G J, Algra A, Vermeulen M, van Gijn J. Calcium antagonists for aneurysmal subarachnoid haemorrhage. Cochrane Database Syst Rev 2000; 2: CD000277.