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
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:
Reference:
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