Nimodipine
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, ischaemic oedema, giant aneurysm |
Metabolic |
Hyperglycaemia, epilepsy |
ABG abnormal |
Hypoxia, hypercapnia |
- 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
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 Nimo 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
- Tiny fall in BP Headache (mild)
- Flushing
- Occasional jaundice
