Subarachnoid Haemorrhage: Complications

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 (COATPEGS)
  • 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

HYPONATRAEMIA (<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 conivaptan, 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, arrhythmias, 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
  • antifibrinolytic 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.

CCC Neurocritical Care Series

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at The Alfred ICU, where he is Deputy Director (Education). He is a Clinical Adjunct Associate Professor at Monash University, the Lead for the  Clinician Educator Incubator programme, and a CICM First Part Examiner.

He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives. He was one of the founders of the FOAM movement (Free Open-Access Medical education) has been recognised for his contributions to education with awards from ANZICS, ANZAHPE, and ACEM.

His one great achievement is being the father of three amazing children.

On Bluesky, he is @precordialthump.bsky.social and on the site that Elon has screwed up, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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