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61st Annual Meeting of the German Society of Neurosurgery (DGNC) as part of the Neurowoche 2010
Joint Meeting with the Brazilian Society of Neurosurgery on the 20 September 2010

German Society of Neurosurgery (DGNC)

21 - 25 September 2010, Mannheim

Dynamics in the influence of sedatives on spreading depolarizations in patients after acute brain injury

Meeting Abstract

  • Daniel Hertle - Neurochirurgische Klinik, Universitätsklinikum Heidelberg, Deutschland
  • Jed Hartings - UC Neuroscience Institute, Department of Neurosurgery, University of Cincinnati, Ohio, USA
  • Jens Dreier - Neurologische Klinik, Charité – Universitätsmedizin Berlin, Deutschland
  • Anthony Strong - King's College London, Department of Clinical Neurosciences, London, United Kingdom
  • Andreas Unterberg - Neurochirurgische Klinik, Universitätsklinikum Heidelberg, Deutschland
  • Oliver Sakowitz - Neurochirurgische Klinik, Universitätsklinikum Heidelberg, Deutschland
  • COSBID group

Deutsche Gesellschaft für Neurochirurgie. 61. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC) im Rahmen der Neurowoche 2010. Mannheim, 21.-25.09.2010. Düsseldorf: German Medical Science GMS Publishing House; 2010. DocV1599

DOI: 10.3205/10dgnc074, URN: urn:nbn:de:0183-10dgnc0746

Published: September 16, 2010

© 2010 Hertle et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.


Outline

Text

Objective: Spreading Depolarizations (SD) are frequently recorded in proximity of cortical injury sites. Most patients with severe brain injury are under sedation and analgesia. The influence of sedatives on electric brain activity is well known, but has not been investigated for SDs in brain-injured patients where dynamical changes might occur during several days of intensive care treatment.

Methods: Electrocorticography (ECoG) using linear subdural electrode strips was performed in 81 patients with acute brain injury. In this preliminary analysis of an ongoing international multicenter observational study (Co-Operative Study on Brain-Injury Depolarizations, COSBID), we retrospectively analyzed the occurrence and frequency of SDs in times of analgesia and sedation. All applications of sedatives (midazolam, fentanyl, propofol, sufentanil, S-ketamine and morphine) were logged and correlated. Time-windows after brain injury were arbitrarily defined as acute = 0–24 h, subacute = 25–72 h, delayed = 73 h–9 d and late >9 d phase.

Results: A total of 836 SD were recorded. Of these 477 occurred under the influence of a sedative. Total recording time and number of SDs were stable from day 2 to day 9 with a ratio ranging from 8 to 13. Single components of the combined administration of several sedatives were analyzed according to predefined time-windows. The noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist S-ketamine most effectively extinguished SDs, irrespective of the timing. Sufentanil also decreased the occurrence of SDs with an odds ratio (OR) of 0,6 and 95% confidence interval (95%CI) of 0,4 to 0,8.

Most profound dynamic changes in the impact of sedatives on SDs were seen between subacute to delayed phases after injury. Midazolam (OR 0,6 95%CI 0,5–0,8), fentanyl (OR 0,8 95%CI 0,6–0,97) and morphine (OR 0,4 95%CI 0,3–0,6) reduced the occurrence of SDs during delayed phase after injury, but showed no or opposite effects in the subacute phase (midazolam; OR 2,2 95%CI 1,5–3,2; fentanyl: OR 1,7 95%CI 1,2–2,6; morphine: OR 1,0 95%CI 0,7–1,5).

Conclusions: Sedatives have a strong influence on the occurrence and frequency of SDs. Our findings suggest that sedatives may differentially affect SDs during subacute and delayed phases after brain injury. This is of potential interest for the understanding of the phenomenon per-se and may affect future use of analgesic and sedative drugs in acutely brain-injured patients.