Intraventricular nicardipine

Local application of calcium channel blockers provides the advantage of bypassing systemic side-effects, in particular hypotension. Different types and routes of application have been studied. One such application method is via a pre-existing external ventricular drain inserted for CSF drainage and intracranial pressure monitoring. In a retrospective analysis, intraventricular nicardipine 4 mg every 8–12 h significantly reduced mean CBF velocities in the middle and anterior cerebral arteries of patients with clinical vasospasm 1).

The effect persisted over a 24 h period. This was a pilot trial examining sonographic vasospasm as a surrogate outcome parameter. The authors gave no insights into the use of additional rescue therapy, clinical outcome, or the incidence of vasospasm-related infarctions 2).

Surgical exposure of the aneurysm and the surrounding vessels most prone to vasospasm development allows the topical application of prophylactic vasodilatory agents. In this context, the most commonly studied drug is nicardipine applied via nicardipine implants. These offer the possibility of releasing the drug for up to 2 weeks in a controlled fashion. This is naturally applicable only in patients treated by surgical clipping, and effects on the contralateral side may not be as distinct. In a Japanese series, a low incidence of DIND was seen in Fisher grade 3 aSAH patients who were treated by surgical clipping and nicardipine 4 mg slow-release pellet implantation 3).

In a controlled trial of Fisher grade 3 haemorrhages, a group treated by surgical clipping and nicardipine pallet implantation alongside the exposed vessels was compared with a coiling and a clipping, without nicardipine group.

The nicardipine group showed the lowest incidence of cerebral infarction and a better 1 yr outcome measured by mRS 4).

Intraventricular injection of nicardipine was examined in one trial to treat TCD-diagnosed vasospasm. In this retrospective case–control study, intraventricular nicardipine was able to lower the mean flow velocity significantly in patients with suspected vasospasm 5).

However, this effect was observed only in the right-sided middle cerebral artery (P=0.041). No significant difference in clinical outcomes as measured by the mRS or GOS was seen between the treatment and control group after 30 and 90 days. This study had shortcomings, and both groups were not well matched for GCS and Fisher grade 6).


1)
Webb A, Kolenda J, Martin K, Wright W, Samuels O. The effect of intraventricular administration of nicardipine on mean cerebral blood flow velocity measured by transcranial Doppler in the treatment of vasospasm following aneurysmal subarachnoid hemorrhage. Neurocrit Care. 2010 Apr;12(2):159-64. doi: 10.1007/s12028-009-9307-8. PubMed PMID: 20012709.
2) , 6)
Veldeman M, Höllig A, Clusmann H, Stevanovic A, Rossaint R, Coburn M. Delayed cerebral ischaemia prevention and treatment after aneurysmal subarachnoid haemorrhage: a systematic review. Br J Anaesth. 2016 Jul;117(1):17-40. doi: 10.1093/bja/aew095. Epub 2016 May 8. Review. PubMed PMID: 27160932; PubMed Central PMCID: PMC4913393.
3)
Kasuya H. Clinical trial of nicardipine prolonged-release implants for preventing cerebral vasospasm: multicenter cooperative study in Tokyo. Acta Neurochir Suppl. 2011;110(Pt 2):165-7. doi: 10.1007/978-3-7091-0356-2_30. PubMed PMID: 21125465.
4)
Schneider UC, Dreher S, Hoffmann KT, Schmiedek P, Kasuya H, Vajkoczy P. The use of nicardipine prolonged release implants (NPRI) in microsurgical clipping after aneurysmal subarachnoid haemorrhage: comparison with endovascular treatment. Acta Neurochir (Wien). 2011 Nov;153(11):2119-25. doi: 10.1007/s00701-011-1129-8. Epub 2011 Aug 21. PubMed PMID: 21858650.
5)
Lu N, Jackson D, Luke S, Festic E, Hanel RA, Freeman WD. Intraventricular nicardipine for aneurysmal subarachnoid hemorrhage related vasospasm: assessment of 90 days outcome. Neurocrit Care. 2012 Jun;16(3):368-75. doi: 10.1007/s12028-011-9659-8. PubMed PMID: 22160865.
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