Abstract

Following subarachnoid hemorrhage, hyperglycemia is strongly associated with complications and with impaired neurological recovery. Targeted insulin therapy for glycemic control might, on the contrary, have harmful effects by causing too low cerebral glucose levels. The study published by Schlenk and colleagues in the previous issue of Critical Care shows that insulin caused a significant decrease in the interstitial cerebral glucose concentration although the blood glucose level remained unaffected. Since several studies utilizing various analytical techniques have shown that cerebral blood flow and cerebral glucose uptake and metabolism are insulin-independent processes, the observation remains unexplained.

Highlights

  • The study published by Schlenk and colleagues in the previous issue of Critical Care was initiated by clinical experience that, after subarachnoid hemorrhage, hyperglycemia is strongly associated with complications and impaired neurological recovery

  • Utilizing intracerebral microdialysis and bedside biochemical monitoring, Schlenk and colleagues made the unexpected observation that insulin caused a significant decrease in the interstitial cerebral glucose concentration the blood glucose level remained unaffected [1]

  • The intracerebral glucose concentration obtained from microdialysis reflects the balance between transport of the substrate into the tissue and its intracellular consumption

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Summary

Introduction

The study published by Schlenk and colleagues in the previous issue of Critical Care was initiated by clinical experience that, after subarachnoid hemorrhage, hyperglycemia is strongly associated with complications and impaired neurological recovery. Utilizing intracerebral microdialysis and bedside biochemical monitoring, Schlenk and colleagues made the unexpected observation that insulin caused a significant decrease in the interstitial cerebral glucose concentration the blood glucose level remained unaffected [1]. Since glucose is the main – or sole – substrate for cerebral energy metabolism under normal conditions, the possibility of measuring the glucose interstitial concentration is of obvious clinical interest.

Results
Conclusion

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