Article
Continuous intra-arterial nimodipine infusion as treatment for cerebral vasospasm – what are the key factors for successful treatment?
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Authors
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Sylvia Bele
- Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Regensburg, Germany
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Judith Scheitzach
- Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Regensburg, Germany
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Andreas Hochreiter
- Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Regensburg, Germany
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Alexander Brawanski
- Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Regensburg, Germany
| Published: | June 8, 2016 |
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Outline
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Objective: Severe cerebral vasospasm (CV) still remains a leading cause of mortality and morbidity after aneurysmatic subarachnoid hemorrhage (aSAH). Continuous intra-arterial nimodipine infusion (CIAN) is a successful treatment option for patients suffering from CV. But what are the key components for a successful CIAN therapy?
Method: Data of 23 CIAN treated patients were analyzed with regard to the implementation time-point of multimodal neuromonitoring (MMN) and data integration into clincial decisions by the neurointensivist. Outcome was analyzed at discharge and 6 months after the SAH using the Glasgow Outcome Score (GOS) and CT-scans screened for infarctions.
Results: Nineteen patients showed favorable outcome (GOS 4-5) and 4 patients remained in the unfavorable outcome group. In those 4 patients MMN was implemented unilaterally according to the highest TCD values at beginning of CV. When TCD values started to rise on the non-monitored side, bilateral PbtO2 monitoring was installed. In 3 of this patients, the additional PbtO2 values were 2 ± 4 mmHg and could not be elevated despite maximum HH-therapy. Angiography was again performed and in all cases a second or third catheter was introduced and CIAN continued. Ct scans of those 3 patients showed multiple infarctions at discharge despite CIAN therapy. In contrast, patients with good outcome mostly were bilaterally monitored at very early time points and monitoring data were taken seriously by the intensive care doctor in charge. Dropping in PbtO2 always led to imminent TCD controls, further diagnostics and potential repeat or expansion of CIAN therapy, if necessary.
Conclusions: A delay in bilateral MMN might facilitate delayed ischemic neurological deficits due to CV since CIAN might not be successful since started too late. In contrast, relapses of CV after CIAN stop could be detected efficiently with bilateral neuromonitoring if the values were taken properly into account. We believe that early bilateral installment of neuromonitoring is crucial for successful treatment of patients with severe CV.
