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Cerebral vasospasm

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  • Causes permanent neurological deficit or death in approx 12% of those who develop severe vasospasm.
  • Clinically detectable in 25- 40% between 4-12th day. Peak incidence around 6th-8th day but can occur up to 14th day.
  • Most reliable predictor of patients likely to develop vasospasm is amount and distribution of blood on CT. Thick layers of blood in basal cisterns associated with high risk, blood in Sylvian fissure intermediate and lobar haematomas and interhemispheric blood low risk.
  • Vasospasm usually develops over hrs or days.
  • Typically associated with gradual, progressive decline in neurological status.
  • Headache, fever and leukocytosis often present and may herald onset before neurological deterioration.
  • May last for several days to weeks.
  • Diagnosis based on time of onset (days 4-9), rate of development (over hours) of neurological deficits (decreased level of consciousness preceding focal deficits) and exclusion of other causes (eg rebleeding, hydrocephalus, hypoxia, hyponatraemia, cerebral oedema and ICH).
  • Doppler measurement of cerebral blood flow velocity not a reliable method of detecting vasospasm
  • Angiographic evidence of vasospasm in 40-70% of patients between day 4-12 following SAH
  • Appears to be two types of vasospasm: early and late. Late is difficult to treat

Pathogenesis of vasospasm

  • may be an inflammatory response. More common in patients with SIRS
  • appears to be the result of prolonged smooth muscle contraction mediated by oxyhaemoglobin either through a direct effect on muscle fibres or through indirect mechanisms such as the release of vasoactive substances from the arterial wall or the production of free radicals and lipid peroxides.
  • Postulated mechanism would be mediated by production of free anion radicals, which in turn, inactivate NO and increase the activity of lipid peroxidises.
  • The result is an increase in protein kinase C with release of intracellular calcium.
  • Superoxide radicals also increase the formation of eicosansoids and alter the balance between dilator PGI2 and constrictor PGE2, in favour of vasoconstriction though a calcium/calmodulin mechanism.
  • Eventually endothelin release not countered by NO production may contribute to vasospasm. (Endothelin antagonists have been used successfully in animal studies to reverse chronic vasospasm).
  • Prolonged contraction of the arterial smooth muscle musculature may lead to secondary morphological changes usually taking the form of intimal hyperplasia or subendothelial fibrosis of the vessel wall.
  • Structural vessel wall abnormalities including leucocyte, red cell, and macrophage infiltration are prominent and responsible for lumen size reduction. Degenerative changes of endothelium, smooth muscle proliferation and collagen deposition produce and increase in wall thickness.
  • Thus, structural changes, which were previously thought to be a major cause of luminal narrowing, are now considered delayed and non-specific responses to cerebral vasospasm appearing after its resolution.

Other theories

  • Impairment of normal vasodilatation
  • Mechanical compression by clot
  • Proliferative vasculopathy

Management of vasospasm

  • nimodipine improves outcome although does not affect vasospasm

HHH therapy

  • used after definitive treatment of aneurysm
  • aim is to increase CO and BP using initially fluid and then adding vasoactive drugs as required.
  • use fluids to aim for haemodilution (and hypertension; see below) haematocrit of 0.3-0.4 (it has been shown that cerebral oxygen transport is constant for haematocrits in this range) so in haemodilution will improve blood rheology
  • no consensus concerning to which level of BP and cardiac output should be increased
    • different values have been suggested including attaining a CI of between 3.5 and 6 ml/min/m2, a PCWP of 12-14mmHg and a systolic BP ranging from 150-240 mmHg, or expecting a 10-20 mmHg MAP increase from baseline.
  • despite the lack of large randomised trials, evidence from small series suggests this approach may decrease morbidity and mortality (level of evidence III to V, grade C recommendation).
  • no data to support this therapy in the situation of asymptomatic spasm detected on Doppler or angiography.
  • cerebral infarction should be excluded prior to instituting hypertensive therapy as it may increase the risk of haemorrhage into an area of infarction
  • hypervolaemia may produce a brisk diuresis and antidiuretics and/or mineralocorticoids may be useful
  • the endpoint of treatment is two fold:
    • resolution of symptoms
    • avoidance of complications
  • use of HHH therapy is controversial and not of proven value although it is recommended by the Stroke Council of the American Heart Association for the prevention and treatment of ischaemic complications from vasospasm. The optimal inotrope, degree of hypertension and degree of hypervolaemia have not been determined.
  • Hypervolaemia is reported to produce transient improvement in 80-90% of cases and permanent improvement in 60%.
  • Complications of hypervolaemia include
    • pulmonary oedema (7-26%)
    • cerebral haemorrhagic infarction
    • electrolyte imbalance
    • complications related to insertion of monitoring devices.
  • hypovolaemia is probably associated with an increased risk of delayed ischaemic deficit and should be avoided

Endovascular therapy for vasospasm

  • balloon angioplasty or intra-arterial injection of vasodilators can improve neurologic symptoms when aggressive medical therapy has failed or when its complications have ensued (level of evidence III to V, grade C).
  • proximal vasospasm, which occurs more often (70%), can be treated by percutaneous transluminal angioplasty, and distal vasospasm is treated by injection of dilator agents.
  • PTA is very effective while papaverine injection at a rate of 120 mg/30 min is not always effective for distal diffuse spasm.
  • effects of papaverine are transient, angiographic improvement is not necessarily accompanied by clinical improvement and, moreover, papaverine tends to dilate less spastic vessels ( because of the poor blood flow to the severely spastic ones) producing a steal.
  • papaverine can also cause spasm if the concentration is low. Adverse effects:
    • dose related hypotension
    • convulsions - probably related to the low pH of the injected solution.
    • mydriasis, unilateral blindness, arrhythmias and respiratory arrest.
  • Other classes of vasodilators have been used, and experimentally, endothelin antagonists and magnesium sulphate have shown promise.

 

 

©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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