gms | German Medical Science

59th Annual Meeting of the German Society of Neurosurgery (DGNC)
3rd Joint Meeting with the Italian Neurosurgical Society (SINch)

German Society of Neurosurgery (DGNC)

1 - 4 June 2008, Würzburg

Role of hyperglycemia and insulin treatment for cerebral metabolism in aneurysmal SAH

Einfluss von Hyperglykämie und Insulin aus den Hirnstoffwechsel bei aneurysmatischer Subarachnoidalblutung

Meeting Abstract

  • corresponding author D. Graetz - Klinik für Neurochirurgie, Charité - Universitätsmedizin Berlin, Campus Virchow Klinikum, Berlin
  • A. Nagel - Klinik für Neurochirurgie, Charité - Universitätsmedizin Berlin, Campus Virchow Klinikum, Berlin
  • F. Schlenk - Klinik für Neurochirurgie, Charité - Universitätsmedizin Berlin, Campus Virchow Klinikum, Berlin
  • A. S. Sarrafzadeh - Klinik für Neurochirurgie, Charité - Universitätsmedizin Berlin, Campus Virchow Klinikum, Berlin

Deutsche Gesellschaft für Neurochirurgie. Società Italiana di Neurochirurgia. 59. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), 3. Joint Meeting mit der Italienischen Gesellschaft für Neurochirurgie (SINch). Würzburg, 01.-04.06.2008. Düsseldorf: German Medical Science GMS Publishing House; 2008. DocP 064

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dgnc2008/08dgnc333.shtml

Published: May 30, 2008

© 2008 Graetz et al.
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Outline

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Objective: To determine whether hyperglycemia or insulin treatment exert detrimental effects via cerebral metabolism, and to illuminate the effects of high/low cerebral glucose in aneurysmal subarachnoid hemorrhage (SAH) patients.

Methods: Prospective study of 31 SAH patients during intensive care. A microdialysis catheter was inserted into the vascular territory of the aneurysm after clipping, microdialysates were analyzed hourly for 10 days after SAH. Hyperglycemic blood glucose levels (>140 mg/dL) were treated with intravenous insulin. A period of 12 hrs after onset of insulin infusion was studied for changes in cerebral metabolism.

Results: Hyperglycemia was more frequent in patients presenting ischemic deficits (p<0.01) and was reflected in higher glycerol concentrations (p=0.04). Episodes of low or high cerebral glucose occurred independently of blood glucose levels. In contrast to high cerebral glucose, low cerebral glucose was associated with severe cellular distress (increase in lactate/pyruvate ratio, glutamate, glycerol; p≤0.01) and unfavorable outcome (p<0.001). 24 patients were treated with intravenous insulin. Though blood glucose remained stable after insulin onset, insulin induced a significant decrease in cerebral extracellular glucose starting at 3 hours after onset (p<0.05). Glycerol tended towards higher values at the end of the observation period, possibly reflecting cellular distress following insulin infusion.

Conclusions: As hyperglycemia was not related to high cerebral glucose, the association of adverse outcome with hyperglycemia seems not to be mediated by cerebral glucose metabolism. Low cerebral glucose was associated with severe metabolic distress and unfavorable outcome. Insulin infusion induced a decrease in cerebral glucose and a slight increase in glycerol though blood glucose remained normal. Future studies might detect relevant metabolic derangements when insulin treatment starts at low cerebral glucose levels. Optimizing cerebral glucose might present a target for therapy in SAH patients.