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Prevention of delayed cerebral ischaemia

Last reviewed dd mmm yyyy. Last edited dd mmm yyyy

Authoring team

There is a compelling precedent for prophylaxis after SAH; up to 25% of patients with a ruptured aneurysm develop cerebral ischaemia between 5 to 14 days after the initial bleed.

The pathogenesis is complex and not fully understood. Narrowing of the arteries around the base of the brain is a necessary but insufficient factor.

Nimodipine is a calcium antagonist that reduces the influx of calcium in the smooth muscle cell through the blockage of the voltage-operated calcium channels

  • may lead to reduced vascular smooth muscle constriction and a decrease in the release of vasoactive substances from endothelium and platelets
  • has also been hypothesized that nimodipine may have direct neuroprotective properties
  • many previous studies have proved the efficacy of prophylactic oral or intravenous nimodipine in reducing the evidence of cerebral infarction and improving outcomes after SAH

Nimodipine, in a dose of 60 mg orally every 4 hours or by nasogastric tube, reduced the incidence of cerebral ischaemia by one third (1)

Intra-arterial nimodipine is used in SAH to reduce risk of cerebral ischaemia (2,3).

Hypertension during the acute stage should generally be left untreated as it is probably a compensatory response to maintain cerebral perfusion.

Plasma volume must be maintained - at least 3 litres of fluid per day with iv fluids to supplement oral intake.

NICE note:

  • consider enteral nimodipine for people with a confirmed subarachnoid haemorrhage
  • only use intravenous nimodipine within a specialist setting and if enteral treatment is not suitable.

Reference:


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