Subarachnoid Haemorrhage: Complications

OVERVIEW

Important complications of SAH include:

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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