gms | German Medical Science

64. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

26. - 29. Mai 2013, Düsseldorf

No impact of sedatives on critical glucose metabolism in brain-injured patients: a microdialysis study

Meeting Abstract

  • Daniel N. Hertle - Neurochirurgie, Universitätsklinikum Heidelberg
  • Edgar Santos - Neurochirurgie, Universitätsklinikum Heidelberg
  • Anna M. Hagenston - Neurobiologie, Universitätsklinikum Heidelberg
  • Christine Dictus - Neurochirurgie, Universitätsklinikum Heidelberg
  • Daniel Haux - Neurochirurgie, Universitätsklinikum Heidelberg
  • Andreas W. Unterberg - Neurochirurgie, Universitätsklinikum Heidelberg
  • Oliver W. Sakowitz - Neurochirurgie, Universitätsklinikum Heidelberg

Deutsche Gesellschaft für Neurochirurgie. 64. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC). Düsseldorf, 26.-29.05.2013. Düsseldorf: German Medical Science GMS Publishing House; 2013. DocP 134

doi: 10.3205/13dgnc551, urn:nbn:de:0183-13dgnc5517

Veröffentlicht: 21. Mai 2013

© 2013 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: Sufficient glycolysis and cellular respiration are vital components for survival of neuronal tissue after brain injury. Critical glucose concentrations below 0.2 mmol/l lead to coma and neuronal death. Reduction of brain energy consumption is therefore a promising target for prevention from secondary brain damage. GABAergic sedatives are known to reduce glucose consumption of the healthy brain by up to 40%. Thus administration of sedatives was long thought to rescue tissue at risk from metabolic deterioration. But all clinical trials failed to demonstrate improved outcome. This is surprising since the beneficial effect of sedatives on brain metabolism seems obvious. We hypothesized the effect of sedatives to be missing under critical metabolic conditions. We undertook this study to investigate episodes of cerebral critical (<0.2 mmol/l) and non-critical (>0.2 mmol/l) brain glucose concentration and the correlation with analgesics, sedatives and outcome.

Method: In an explorative analysis we investigated 19 patients after acute brain injury. Cerebral glucose concentration was measured by bedside microdialysis (CMA 600, Kista, Sweden). We retrospectively analyzed the application of anesthetic drugs (ketamine, GABAergic drugs and opioids) and their correlation with glucose concentrations.

Results: The previously established level for critical (<0.2 mmol/l) brain glucose concentration was associated with increased glutamate concentrations and increased lactate/pyruvate ratio in the patient collective presented here. Non-critical extracellular glucose concentrations were associated with the application of midazolam (p<0.05). Ketamine administration was associated with a trend towards lower glucose concentrations (p<0.1). Critical glucose concentrations below 0.2 mmol/l, however, showed no correlation with any administration of sedatives.

Conclusions: Brain glucose concentrations below 0.2 mmol/L were associated with increased glutamate levels and lactate/pyruvate ratio, and thus seemed to be a good separator of critical and non critical brain glucose. Anesthetic drugs showed expected influence on non critical brain glucose metabolism. However, critical brain glucose concentrations could not be rescued by anesthetic drugs. This might explain why efforts to demonstrate beneficial effects of sedatives on neurological outcome failed in large clinical trials. A larger patient collective is needed to further investigate critical brain glucose metabolism.