Contents
Introduction
This is bleeding into the subarachnoid space.
The classical sign is a sudden onset intense headache (“feel like I’ve been hit on the back of the head Doc”).
The bleeding occurs as the result of rupture of aneurysm (80%) and AV malformations (15%). In the remainder of cases, no cause can be identified.
- Trauma is also a major cause, but is not considered true SAH.
Epidemiology and Aetiology
- Incidence is about 8 per 100 000
- Risk factors
- ↑BP
- Smoking
- Known aneurysm – Or disease that causes aneurysm – e.g. polycystic kidney disease, co-arctation of the aorta, Ehlers-Danlos Syndrome
- Family history – increases risk by 3-5x
Signs and Symptoms
- Sudden onset severe headache, often at the back of the head
- Neck stiffness – Kernig’s sign may be present after 6 hours (due to chemical meningitis), or in massive bleeds it may occur sooner due to herniation of the cerebellar tonsils (due to raised ICP).
- Sometimes the chemical meningitis can cause vomiting and extensor plantar responses after 24hrs
- Impaired consciousness (drowsiness / coma) – usually occurs very shortly after the onset of symptoms, but can occur several hours later.
- Cranial nerve signs
- Hemiplegia
- CNS deficits can become permanent within minutes. If it lasts more than several hours it is highly unlikely to ever resolve.
- Sentinel headache – is experienced by about 6% of patients, and is a prodromal headache thought to be the result of a small leak before rupture of an aneurysm or malformation.
Classification
|
Grade
|
Signs
|
Mortality (%)
|
|
I
|
None
|
0
|
|
II
|
Neck stiffness, cranial nerve lesions
|
11
|
|
III
|
± Drowsiness
|
37
|
|
IV
|
± Hemiplegia
|
71
|
|
V
|
Prolonged coma
|
100
|
Prognosis
- Overall mortality is 35-50%
- About 30% die within a few days, and another 10-15% within a few weeks.
- Most patients die within 1 month
- After 1 month, 90% of patients will survive >1 year
- Prognosis is worse with aneurysm, better with AMV, and best when no lesion is detected (presumably the lesion was small, and has healed in these instances).
Pathology
- The period of haemorrhage is actually very short – and it normally stops bleeding by itself.
- After the initial haemorrhage, patients are at risk from vasospasm. This can causes ischaemia, which can result in secondary brain damage and further neurological signs.
- 25% of patients will have signs of TIA / stroke after SAH as a result of vasospasm
- Brain oedema and risk of vasospasm is greater between 72hrs and 10 days
- Secondary acute hydrocephalus often occurs
- Re-bleeding is VERY COMMON and usually occurs within 7 days. The risk thereafter is about 3% / year
Investigations
Diagnosis is by CT, or if this is normal with a high sense of suspicion, CSF.
CT – is able to detect >90% of lesions within 48 hours of onset of symptoms.
- Often star shaped lesion on CT – or the blood fills in giral patterns around the brain the ventricles
- If CT is negative, but SAH is highly suspected, consider :
Lumbar puncture – contraindicated in raised ICP – so be careful! – Several features:
- Blood – detected via the presence of bilirubin. Previously, people would use the level of RBCs as an indicator, however, it is unreliable to use the rule: if blood remains constant in 3 separate samples = SAH, if blood declines = tap trauma.
- Xanthochromia – yellow appearance of CSF if it is left to stand for a few hours
Treatment
- Get specialist help! – call the Medical Registrar, the Neurosurgeon on call, and depending on GCS, call the anaesthetist. (Patients are unable to maintain a competant airway at GCS <8)
- Stablise the patient haemodynamically
- Many patients require ICU treatment
- Neurosurgical interventions are limited, but in severe cases, a drain may be placed.
- After the acute presentation, the patient may have their aneurysm clipped or coiled to prevent further bleeds
