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67. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit der Koreanischen Gesellschaft für Neurochirurgie (KNS)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

12. - 15. Juni 2016, Frankfurt am Main

Isoflurane improves cerebral oxygenation after severe aneurysmal subarachnoid hemorrhage

Meeting Abstract

  • Michael Reiner - Zentrum für Neurochirurgie, Klinik für Allgemeine Neurochirurgie, Universitätsklinikum Köln, Germany
  • André Schulte - Zentrum für Neurochirurgie, Klinik für Allgemeine Neurochirurgie, Universitätsklinikum Köln, Germany
  • Roland Goldbrunner - Zentrum für Neurochirurgie, Klinik für Allgemeine Neurochirurgie, Universitätsklinikum Köln, Germany
  • Gerrit Brinker - Zentrum für Neurochirurgie, Klinik für Allgemeine Neurochirurgie, Universitätsklinikum Köln, Germany

Deutsche Gesellschaft für Neurochirurgie. 67. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), 1. Joint Meeting mit der Koreanischen Gesellschaft für Neurochirurgie (KNS). Frankfurt am Main, 12.-15.06.2016. Düsseldorf: German Medical Science GMS Publishing House; 2016. DocMI.14.06

doi: 10.3205/16dgnc317, urn:nbn:de:0183-16dgnc3171

Veröffentlicht: 8. Juni 2016

© 2016 Reiner et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe http://creativecommons.org/licenses/by/4.0/.


Gliederung

Text

Objective: Data from sedated and ventilated Neuro-ICU patients suffering from aneurysmal subarachnoid hemorrhage (SAH) suggest that volatile anesthetics might have beneficial effects on cerebral oxygenation and neuroprotection. The aim of this retrospective study was to analyze the impact of isoflurane on critically ill patients after subarachnoid hemorrhage in a multimodal monitoring setting.

Method: Seven ICU patients after SAH with standard i.v. sedation and continuous multimodal monitoring (MM) were additionally treated with isoflurane (MAC 0.6-1.2). Two patients were WFNS grade II and five in grade IV & V on admission. MM included at least intracranial pressure (ICP), intraparenchymal O2 saturation (PbrO2) and a 2-channel near-infrared-spectoscopy monitor (NIRS). All patients were treated with external CSF drainages. MM was performed for 8-20 days (median 13 days), isoflurane sedation lasted from 3 to 10 days (median 7 days) and started between day 7 and 13 after the hemorrhage (median 9 days). In a post-hoc analysis the isoflurane effect on cerebral oxygen saturation in a short-term (1-5h) and long-term interval (6-12h) was assessed. At 6 month follow-up, modified Rankin Score (mRS) was documented.

Results: A significant rise of cerebral oxygenation parameters recorded by the invasive PbrO2-probe as well as by non-invasive NIRS was observed during application of isoflurane. 12 hours after initiating the isoflurane administration PbrO2 was still significantly elevated with a mean of 6,73 ± 4,18 mmHg above baseline (p=0,014*). The NIRS tissue oxygenation index increased by a mean of 5,05 ± 2,84 % (p=0,007*). A consistent correlation between NIRS values and the established PbrO2-monitoring was observed. ICP was slightly elevated (mean 2,23 mmHg ± 2,12; p=0,016*) while the mean arterial pressure decreased by 7,62 mmHg (± 16,56). Therefore, vasopressor therapy had to be adjusted. mRS ranged between 4 and 5 at 6-month follow-up (median: 5).

Conclusions: The data indicate that additional isoflurane treatment of patients after SAH is able to significantly improve critical cerebral oxygenation for at least 12 hours with acceptable side effects. The combination of lowered cerebral oxygen demand with effective vasodilatation induced by isoflurane might be a strategy to avoid delayed cerebral ischemia after SAH and should be tested prospectively in a larger series.