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60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit den Benelux-Ländern und Bulgarien

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

24. - 27.05.2009, Münster

Influence of sedatives and analgesics on spreading depolarisations in brain injured patients

Meeting Abstract

  • O. Sakowitz - Neurochirurgische Klinik, Universitätsklinikum Heidelberg, Heidelberg
  • D. Hertle - Neurochirurgische Klinik, Universitätsklinikum Heidelberg, Heidelberg
  • D. Haux - Neurochirurgische Klinik, Universitätsklinikum Heidelberg, Heidelberg
  • B. Orakcioglu - Neurochirurgische Klinik, Universitätsklinikum Heidelberg, Heidelberg
  • K. Kiening - Neurochirurgische Klinik, Universitätsklinikum Heidelberg, Heidelberg
  • A. Unterberg - Neurochirurgische Klinik, Universitätsklinikum Heidelberg, Heidelberg

Deutsche Gesellschaft für Neurochirurgie. 60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit den Benelux-Ländern und Bulgarien. Münster, 24.-27.05.2009. Düsseldorf: German Medical Science GMS Publishing House; 2009. DocMO.02-01

DOI: 10.3205/09dgnc001, URN: urn:nbn:de:0183-09dgnc0015

Veröffentlicht: 20. Mai 2009

© 2009 Sakowitz et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective: Spreading depolarisations (SD), characterized by large propagating slow potential changes, have been demonstrated in patients with brain injury using electrocorticography (EcoG). SDs occur early after brain injury while most patients are under sedation and analgesia. The influence of sedatives on electric brain activity is well known, but has not been well investigated for the condition of SDs. Therefore, we analyzed prospectively obtained data from the Cooperative Study on Brain Injury Depolarisations (COSBID) with regard to sedative and analgesic medication.

Methods: Multimodal cerebral monitoring was performed in a series of 26 patients undergoing emergency craniotomy. In addition to routine monitoring, patients had subdural 6-contact linear electrode strips (Wyler, 5/10 mm platinum; Ad-Tech Medical Instrument Corp., Racine, WI) placed adjacently to the injured cortex in a centrifugal orientation. We retrospectively analyzed the application of analgesia and sedation to correlate the results with the occurrence and frequency of CSDs. Odds ratios (O.R.) and 95%-confidence intervals were calculated in comparison to no sedation.

Results: We recorded a total of 392 events of SD. Of these, 274 SDs occurred under the influence of a sedative. Without sedation SDs occurred at an average ratio of 0.5 per hour. Deep sedation decreased the occurrence of SDs. Single components of the combined administration of several sedatives and analgesics were analyzed. With fentanyl, midazolam and/or propofol, SDs occurred at an average ratio of 0.1–0.2 per hour of sedation (O.R. 0.89, 0.65–1.23; 0.23, 0.16–0.32; 2.04, 1.47–2.83). The non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist S-ketamine extinguished SDs (O.R. 0.03, 0.01–0.08).

Conclusions: Sedatives and analgesics vary in their influence on the occurrence and frequency of SDs. Our findings suggest that SDs are blocked by the NMDA receptor antagonist ketamine. This may be of potential interest for future cerebroprotective trials in neurointensive care.