Vasospasm in Subarachnoid Haemorrhage

Reviewed and revised 1 September 2014



  • vasospasm is dynamic narrowing of vessels due to a radiological diagnosis
  • delayed neurological deterioration (DND) is clinically detected neurological deterioration after stabilisation that is not due to re-bleeding, may be due to multiple other causes
  • delayed cerebral ischaemia (DCI) is any neurological deterioration >1 hour that presumed due to ischemia, and other causes excluded
  • aneurysmal subarachnoid haemorrhage (aSAH)


  • vasospasm occurs in up to 70% of aSAH
  • 3-15d, most frequently 7-10d, resolves spontaneously at 21d
  • DCI is the most important secondary cause of deterioration following SAH (occurs in about 30%)
  • early vasospasm occurs in 10%, associated with poor grade but not delayed vasospasm; independent poor prognostic indicator

Oli Flower discusses vasospasm following aneurysmal SAH in this PK SMACC-talk:


Summary of options for prevention, monitoring and treatment

  • 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.



  • best predicted by radiological grade (e.g. Fisher, Classen)
  • amount of blood and location
  • thick basal cistern blood and blood in lateral ventricles

Other risk factors include:

  • poor clinical grade
  • prolonged coma after aneurysm rupture
  • age <50y
  • smoker
  • hypertension
  • hyperglycemia
  • cocaine use
  • genetics

No difference between clipping and coiling


  • oxyHb contacts intraluminal wall of vessel
  • calcium dependent and independent pathways
  • free radical mechanisms
  • imbalance in vasoactive agents: NO, endothelin, arachidonic acid
  • neuronal mechanisms leading to increased vascular tone, endothelial tone and apoptosis


  • serial clinical examination (poor sensitivity if low clinical grade)
  • DSA is gold standard (also allows treatment) > CTA and MRA > TCD for large vessels only
  • Perfusion imaging may supersede DSA

Experimental methods

  • continuous EEG
  • brain tissue oxygenation monitoring
  • cerebral microdialysis catheters

See Monitoring in Subarachnoid Haemorrhage


Drug Therapy


  • calcium channel antagonist that has is known to have some selectivity for the cerebral circulation
  • used in cerebral aneurysm surgery to decrease perioperative vasospasm associated with blood in the cranium and also from perioperative handling/disruption of cerebral blood vessels during clipping (after a rupture of a berry aneurysm)
  • high risk time is between 4-10 days after clipping of the aneurysm
  • goal = to decrease neurological deficits that develop as a result of distal infarction of brain from site of vasospasm
  • should be commenced within 96 hours of subarachnoid haemorrhage
  • may be given PO, IV or intra-arterially (at angiography)
  • dose: PO 60mg Q4 hourly or IV 0.1-1mcg/kg/min
  • continuation of dose for 5-14 days in established vasospasm (IV) or else 3 weeks (PO)
  • predicting those patients who will get vasospasm is very difficult so invariably all patients are started on it post-operatively during elective surgery
  • has been shown to decrease morbidity surrounding aneurysm surgery but not mortality
  • data indicating decrease in morbidity has been documented for patients receiving PO or N/G nimodipine rather than IV – so some centres administer this via N/G tube placement in patient who can not reliably swallow
  • useful in prophylaxis
  • exact mechanism unknown — no convincing evidence that it affects vasospasm or DCI; only proven treatment for improving aSAH outcomes
  • side effects; hypotension, flushing
  • some patients do not develop vasospasm but everyone is treated because of uncertainty about those that will and won’t develop this complication

Nicardipine & AT877

  • both reduce vasospasm but do not improve outcome

Haemodynamic therapies

  • target euvolemia with isotonic crystalloid, avoid hypovolemia
  • target hypertension titrated to clinical response
  • HHH therapy is not currently recommended


  • correct hypovolaemia
  • belief that patients need a supraphysiological blood volume and thus preload to help increased perfusion to the vasospastic arteries.
  • no good data to support hypervolaemia over euvolaemia
  • harm may be produced in patients who are unable to deal with large fluid boluses.


  • evidence that works both based on clinical response (reversible neurology with an increase in BP) and published studies
  • it is unclear whether hypertension, cardiac output or volume expansion is the best therapy
  • the goal MAP should the titrated against clinical response to MAP elevation
  • aneurysm must be secured first!


  • the proposed mechanism is that a decreased haematocrit increases laminar flow through the vasospastic vessel by the decrease in blood viscosity
  • it is often not specifically targeted as hypervolaemia induces a degree of haemodilution
  • no good data to support it use
  • only indicated if coexistent polycythemia

Endoluminal Therapy

Early Coiling

  • good data that improves mortality but manipulation of vessel though to predispose to vasopasm
  • ISAT trial = RCT of neurosurgical clipping vs endovascular coiling – coiling ruptured aneurysms @ 1 year follow up
  • not all aneurysms can be coiled

Balloon Angioplasty

  • good data that sequential treatment with angioplasty does increase flow through the vasospastic area -> dilation is seen at the time of the angiogram
  • ? data on mortality and morbidity
  • associated risks are inherent


  • macroscopic evidence of dilation seen at the time
  • ? data on mortality on morbidity

Investigational Therapies

Studied in animal models, no hard clinical evidence, no RCTs

  • Statins – continue statins if patient is already on; phase 3 study in progress (STASH)
  • Intra-cisternal thrombolytics such as tPa and urokinase, intrathecal urokinase
  • early cisternal washout during operative repair
  • Endothelin 1 antagonists
  • Magnesium – no benefit in Phase 3 studies (e.g. MASH-II)

References and Links

CCC 700 6

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

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

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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