Subarachnoid Haemorrhage: Complications


Important complications of SAH include:

  • Neurological deterioration
  • Seizures
  • Hyponatremia
  • Cardiac complications
  • Re-bleeding
  • Vasospasm

Oli Flower discusses complications of aneurysmal SAH in this PK SMACC talk:


  • metabolic causes (COATPEGS)
  • drugs
  • seizures (think re-bleed), consider non-convulsive status epilepticus (NCSE) in coma
  • intracranial hypertension
  • Hydrocephalus
  • re-bleeding


  • suspect re-bleed
  • risk factors for seizures: MCA, clots, infarction, clipping, poor grade
  • suspect NCSE in coma
  • NCSE is associated with poor prognosis, other seizures unclear
  • phenytoin for 3 days is as effective as 7 days
  • no evidence for one AED over another
  • levitracetam increasingly used, as phenytoin associated with worse cognitive outcomes


  • 30-50% of cases
  • days 3-14
  • SIADH and cerebral salt wasting are most common (see CCC entry on this) – both cause hypotonic hyponatremia and high urinary sodium
  • SIADH is euvolemic and CSW is hypovolemic, but both may coexist
  • avoid fluid restriction, strict fluid status monitoring, avoid conivaptan, can use fludrocortisone and hypertonic saline


  • due to cardiac effects of sympathetic outflow and catecholamine release
  • dysrhythmias (35%)
  • troponin (35%)
  • RWMA on Echo (25%)
  • neurogenic stress cardiomyopathy (12% of deaths) — chest pain, SOB, arrhythmias, trop rise, myocardial dysfunction


  • 1-3% of aSAH
  • associated with poorer prognosis: 12-fold increase in disability at 3 months
  • risk factors: degree of aneurysm occlusion after treatment, aneurysm size,poor grade (coiling a risk factor in only one study)
  • avoid hypertension
  • avoid decreases in ICP
  • sedation in the agitated
  • no coughing or Valsalva
  • antifibrinolytic agents decrease rebleeding -> but increase vasospasm and hydrocephalus (not used now)


  • obstruction of CSF flow by blood (acute) or impaired reabsorption at arachnoid granualtions (chronic)
  • diversion indicated in: deteriorating LOC and enlarging ventricles on CTEVD (risk of ventriculitis after 3 days), may need VP shunt chronically
  • Risk factors: IVH, posterior circulation aneurysm, elderly, hyponatremia, low inital GCS, HTN, treatment with anti-fibrinolytics
  • weaning EVD over 24h and routine fenestration of lamina terminalis does not decrease need for VP shunt

VASOSPASM (see CCC entry on vasospasm in SAH)

  • prevention: removal of SAH at surgery, nimodipine, maintenance of euvolaemia, avoiding hypotension
  • monitoring: clinical, transcranial Doppler, 4 vessel angio, CTA/MRI, EEG, SPECT/PET, microdialysis catheters
  • treatment: haemodynamic augmentation to reverse neurological deficits, endovascular treatment (balloon angioplasty, papaverine, nicardipine), investigational therapies
  • because of the disparity between vasospasm on trans-cranial Doppler, angio and what happens clinically there is disagreement about how aggressively vasospasm should be treated.

References and Links


CCC 700 6

Critical Care


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