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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

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 puncturecontraindicated 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

References

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