OVERVIEW
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:
NEUROLOGICAL DETERIORATION
- metabolic causes (GOPETCO)
- drugs
- seizures (think re-bleed), consider non-convulsive status epilepticus (NCSE) in coma
- intracranial hypertension
- Hydrocephalus
- re-bleeding
SEIZURES
- 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
HYPONATREMIA (<135 mmol/L)
- 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 conivaptam, can use fludrocortisone and hypertonic saline
CARDIAC COMPLICATIONS
- 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, arryhthmias, trop rise, myocardial dysfunction
RE-BLEEDING
- 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’s
- anti-fibrinolytic agents decrease rebleeding -> but increase vasospasm and hydrocephalus (not used now)
HYDROCEPHALUS
- 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.
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