gms | German Medical Science

68th Annual Meeting of the German Society of Neurosurgery (DGNC)
7th Joint Meeting with the British Neurosurgical Society (SBNS)

German Society of Neurosurgery (DGNC)

14 - 17 May 2017, Magdeburg

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Does the interruption of nimodipine administration lead to delayed cerebral ischemia in patients with aneurysmal subarachnoid hemorrhage?

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  • Silvia Hernandez Duran - Universitätsmedizin Göttingen, Klinik für Neurochirurgie, Göttingen, Deutschland
  • Dorothee Mielke - Universitätsmedizin Göttingen, Klinik und Poliklinik für Neurochirurgie, Göttingen, Deutschland
  • Veit Rohde - Universitätsmedizin Göttingen, Klinik und Poliklinik für Neurochirurgie, Göttingen, Deutschland
  • Vesna Malinova - Universitätsmedizin Göttingen, Klinik und Poliklinik für Neurochirurgie, Göttingen, Deutschland

Deutsche Gesellschaft für Neurochirurgie. Society of British Neurological Surgeons. 68. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), 7. Joint Meeting mit der Society of British Neurological Surgeons (SBNS). Magdeburg, 14.-17.05.2017. Düsseldorf: German Medical Science GMS Publishing House; 2017. DocDI.27.04

doi: 10.3205/17dgnc341, urn:nbn:de:0183-17dgnc3418

Published: June 9, 2017

© 2017 Hernandez Duran et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.

Outline

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Objective: Nimodipine is routinely used for vasospasm prophylaxis and thus for prevention of delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH). Hypotension due to vasodilatation can be a side effect of nimodipine. Catecholamines are then applied to maintain mean arterial pressure and cerebral perfusion. In case of DCI, catecholamines are also used to induce hypertension as part of the triple-H therapy. The high need for catecholamines and associated side effects could lead to an interruption of nimodipine. The aim of this study was to evaluate the interaction between the administration of nimodipine and catecholamines, and to investigate its impact on the incidence of DCI.

Methods: We gathered data concerning nimodipine and norepinephrine administration in patients with aSAH admitted to our center from January 2012 to October 2015 and performed a retrospective analysis. In all patients, nimodipine was started on day 1 after aSAH. In case of hypotension and need of more than 10µg/h norepinephrine, nimodipine was stopped. The incidence of DCI, infarction and vasospasm diagnosed by transcranial Doppler sonography (TCD) was also collected. Bivariate correlation analysis was performed using the Spearman’s rho (ρ). For statistical analysis, IBM® SPSS® Statistics Version 21 was used.

Results: A total of 170 patients, 106/170 (62%) females and 64/170 (38%) males, with aSAH were included in the study. Mean age was 54 years (range: 25 – 90). In sum, 90/170 (53%) had nimodipine interruption, while noradrenaline was administered in 94/170 (55%) of patients. DCI, infarction, and TCD-vasospasm were seen in 85/170 (50%), 42/170 (25%), and 66/170 (39%) of cases, respectively. A positive, statistically significant correlation was found between nimodipine interruption and norepinephrine administration (ρ 0.442, p<0.001). Additionally, a positive correlation was found between nimodipine discontinuation and DCI (ρ 0.431, p<0.001), infarction (ρ 0.254, p=0.001), and TCD-vasospasm (ρ .385, p<0.001).

Conclusion: Our analysis reveals a higher incidence of DCI, infarction, and vasospasm in patients with aSAH when nimodipine is interrupted. Nimodipine interruption also correlated with norepinephrine administration. Future studies with a larger patient population are needed to evaluate the appropriate norepinephrine cut-off at which nimodipine should be discontinued.