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62. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit der Polnischen Gesellschaft für Neurochirurgen (PNCH)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

07. - 11. Mai 2011, Hamburg

Impact of sedation on glucose metabolism in brain-injured patients: a microdialysis study

Meeting Abstract

  • D. Hertle - Neurochirurgische Klinik, Universitätsklinikum Heidelberg
  • E. Santos - Neurochirurgische Klinik, Universitätsklinikum Heidelberg
  • D. Haux - Neurochirurgische Klinik, Universitätsklinikum Heidelberg
  • K.L. Kiening - Neurochirurgische Klinik, Universitätsklinikum Heidelberg
  • A. Unterberg - Neurochirurgische Klinik, Universitätsklinikum Heidelberg
  • O.W. Sakowitz - Neurochirurgische Klinik, Universitätsklinikum Heidelberg

Deutsche Gesellschaft für Neurochirurgie. Polnische Gesellschaft für Neurochirurgen. 62. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Polnischen Gesellschaft für Neurochirurgen (PNCH). Hamburg, 07.-11.05.2011. Düsseldorf: German Medical Science GMS Publishing House; 2011. DocMO.06.02

doi: 10.3205/11dgnc030, urn:nbn:de:0183-11dgnc0309

Veröffentlicht: 28. April 2011

© 2011 Hertle et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen ( Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.



Objective: Glucose and oxygen are key components for cellular respiration and critical for neuronal survival. Low concentrations of glucose cause coma and neuronal death. Energy consumption of the acutely injured brain is one of the targets for neuroprotection and prevention from secondary brain damage. Among other treatments analgesics and sedatives are thought to reduce energy consumption – especially the NMDA receptor antagonist ketamine and GABAergic drugs or opioids to a lesser extend. We undertook this study to investigate brain and blood glucose concentrations and their correlation with analgesics, sedatives and outcome.

Methods: Blood and brain glucose were measured in 19 acutely brain-injured patients. In this first analysis a total of 564 hourly paired measurements were investigated. We retrospectively analyzed the application of sedatives in their correlation with glucose concentrations and eGOS after 6 months. We focused on ketamine, cumulative GABAergic drugs (midazolam and propofol weighted 10:1) and cumulative opioids (sufentanil, remifentanil, fentanyl and morphine 710:457:71:1). Analysis of variances (ANOVA) was performed.

Results: Serum glucose concentrations above 50 mg/dl and relative brain glucose levels above 0.5 correlated well (Pearson r 0.3, 95% CI 0.2 to 0.4). To compensate for variations in systemic blood glucose we calculated the ratio of brain glucose/blood glucose (QGLUC). QGLUC under influence of ketamine, GABAergic and opioids were categorized as to have occurred under "no sedation", "low sedation" and "deep sedation". High levels but not low levels of ketamine correlated with decreased QGLUC (p < 0.05). In contrast GABAergic drugs correlated in a dose dependent manner and increased measured QGLUC (p < 0.05). Opioids had similar dose dependent effects. Survival was correlated with lower levels of QGLUC (p < 0.05).

Conclusions: Normal and elevated blood and brain glucose levels correlated well. High doses of ketamine correlated with lower QGLUC, GABAergic drugs and opioids increased measured QGLUC in a dose dependent manner. On the assumption that local brain perfusion remained unchanged, this could relate to changes in the cerebral metabolic rate of glucose (i.e. increased with high-dose ketamine, dose-dependently decreased with all others).