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