Nimodipine



Nimodipine

  • Lipophilic dihydropyridine Ca++ antagonist.
  • Improves outcome after SAH ( reduced incidence & severity of cerebral ischaemia).
  • Moderate cerebral vasodilation not thought to be mechanism of action.
  • Mainly limits intracellular Ca++ influx and so reduces ischaemic damage.
  • Good PO absorption.

Indications

  • SAH Significantly better prognosis.
  • 60% of SAH die (in 6 month) if no Neurosurgery i.e. delayed ischaemia.
  • Delayed ischaemia = confusion, level conc. ± localizing signs.
  • Spasm generally on day 2-3 (max spasm frequency on day 6-8).

Causes of cerebral ischaemia post SAH

Cerebral Art Narrowing

Vasospasm, thrombosis, embolism from aneurysmal clot, atheroma, tentorial herniation compressing post cerebral art, antifibrinolytic therapy

Hypotension

Antihypertensive drugs, arrhythmia, low cardiac output, medullary compression

Hypovolaemia

Dehydration, hyponatraemia

High ICP

Rebleed, hydrocephalus, IC haematoma, cerebral hyperaemia/oedema, giant aneurysm

Metabolic

Hyperglycaemia, epilepsy

ABG abnormal

Hypoxia, hypercapnia

Evidence

Latest nimodipine trial = BRANT (Br Aneurysmal Nimo Trial)

  • Nimodipine 60mg 4 hourly - cerebral ischaemia = 22%.
  • Placebo - cerebral ischaemia = 33%.
  • Poor outcomes 4-0% lower in Nimodipine group.
  • Higher doses no better.

Head injury

  • No improvement.

Stroke - TRUST study

  • 1215 patients = no indication for Nimodipine use.

Cognitive impairment

  • Some studies show trend improvement in dementia.

VF

  • No improvement .

Adverse Rxns

  • Small ↓ BP (mild).
  • Flushing.
  • Occasional jaundice.

Content by Dr Íomhar O' Sullivan 12/06/2007. Last review Dr ÍOS 16/09/19