Cerebral vasospasm following subarachnoid haemorrhage
Cerebral vasospasm following subarachnoid haemorrhage is a major complication of subarachnoid haemorrhage (SAH). It is overtaking rebleed as the major cause of mortality and morbidity in the subgroup of patients with SAH who reach hospital and receive medical care.
It is seen in 40-70% of SAH patients on vascular imaging, and becomes clinically apparent in 20-30% of patients, typically from the 4th to 10th day post bleed.
After decades of research the exact mechanism(s) responsible remain elusive although a number of candidate agents are demonstrated to play a role. These include:
- NO (nitrous oxide)
- endothelin 1
- thromboxane A2
- sphingosine 1-phosphate
Most likely the 'true' pathway involves multiple agents interacting with each other, both biochemically and via changes in gene expression, accounting for the delay of onset.
Oxyhaemoglobin, highest in concentration in arterial blood, appears to simultaneously up-regulate the expression of endothelin 1 (ET-1) and reduce the efficacy of NO.
This results in alteration of normal vascular tone, resulting in narrowing of the large vessels. Increasingly it is also becoming apparent that small caliber vessels which are in contact with CSF blood are narrowed also - down to 15 micrometers - far too small to be visualised on angiography, let alone CTA/MRA.
The result, if severe enough, is to reduce perfusion of brain parenchyma resulting in ischaemic symptoms, infarction, and its sequelae.
Treatment and prognosis
Aggressive, early and prophylactic treatment can markedly reduce the incidence of vasospasm, but often requires early securing of the ruptured aneurysm. Three main modalities are employed:
Triple H therapy
Haemodilution, Hypertension, Hypervolaemia to maintain adequate cerebral perfusion pressure is achieved with hydration and inotropes if necessary. This often requires admission to a neuroICU with central venous catheter and intracranial pressure (ICP) monitoring.
Calcium channel blockers
Nimodipine is the best known and most widely used calcium channel blocker, which dilate vessels especially leptomeningeal collateral.
In severe cases, intra-arterial therapy can be beneficial. Intra-arterial delivery of a calcium channel blocker such as Nimodipine or Verapamil has replaced previously used drugs such as Papaverine. They are administered by slow bolus injection into the relevant vascular territory via a standard diagnostic catheter, with careful monitoring of blood pressure. Treatment may need to be repeated daily for 3-5 days.
Balloon angioplasty is a more invasive neurointerventional technique requiring a guiding catheter and placement of an endovascular micro balloon over a guide wire across the affected segment. Expanding the balloon disrupts the smooth muscle fibres within the vessel wall. There is a risk of vessel dissection or rupture. Once treated the spasm does not usually reoccur.
Other experimental treatments include:
- intrathecal sodium nitroprusside
- mechanical (surgical) evacuation of subarachnoid blood
- intrathecal fibrinolytics
- 1. Thomas JE, Rosenwasser RH, Armonda RA et-al. Safety of intrathecal sodium nitroprusside for the treatment and prevention of refractory cerebral vasospasm and ischemia in humans. Stroke. 1999;30 (7): 1409-16. Stroke (link) - Pubmed citation
- 2. Onoue H, Tsutsui M, Smith L et-al. Expression and function of recombinant endothelial nitric oxide synthase gene in canine basilar artery after experimental subarachnoid hemorrhage. Stroke. 1998;29 (9): 1959-65. Stroke (link) - Pubmed citation
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- 5. Bevan JA, Bevan RD, Walters CL et-al. Functional changes in human pial arteries (300 to 900 micrometer ID] within 48 hours of aneurysmal subarachnoid hemorrhage. Stroke. 1998;29 (12): 2575-9. Stroke (link) - Pubmed citation
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- 7. Abruzzo T, Moran C, Blackham KA et-al. Invasive interventional management of post-hemorrhagic cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage. J Neurointerv Surg. 2012;4 (3): 169-77. doi:10.1136/neurintsurg-2011-010248 - Pubmed citation
Stroke and intracranial haemorrhage
stroke and intracranial haemorrhage
- general discussions
- scoring and classification systems
- by region
- hemispheric infarcts
- frontal lobe infarct
- parietal lobe infarct
- temporal lobe infarct
- occipital lobe infarct
- internal capsule infarct
- ataxic hemiparesis syndrome: MCA perforators or basilar artery perforators
- lacunar infarct
- thalamic infarct
- cerebellar infarct
- midbrain infarct
- pontine infarct
- medullary infarct
- acute spinal cord ischaemia syndrome
- hemispheric infarcts
- by vascular territory
- anterior cerebral artery infarct
- anterior choroidal artery infarct
- anterior inferior cerebellar artery infarct
- basilar artery infarct
- middle cerebral artery infarct
- posterior cerebral artery infarct
- posterior inferior cerebellar artery infarct
- superior cerebellar artery infarct
- basal ganglia haemorrhage
- cerebellar haemorrhage
- cerebral contusions
- CTA spot sign
- haemorrhagic venous infarct
- haemorrhagic transformation of an ischaemic infarct
- hypertensive intracranial haemorrhage
- intraventricular haemorrhage (IVH)
- lobar haemorrhage
- pontine haemorrhage
- remote cerebellar haemorrhage
- extra-axial haemorrhage
- extradural versus subdural haemorrhage
- extradural haemorrhage (EDH)
- intralaminar dural haemorrhage
- subdural haemorrhage (SDH)
- subarachnoid haemorrhage (SAH)
- intra-axial haemorrhage
- ischaemic stroke