• Paul Vespa, Robert Boonyaputthikul, David L McArthur, Chad Miller, Maria Etchepare, Marvin Bergsneider, Thomas Glenn, Neil Martin, and David Hovda.
• UCLA Division of Neurosurgery, Los Angeles, CA, and Barrows Neurologic Institute, Phoenix, AZ, USA.
• Crit. Care Med. 2006 Mar 1;34(3):850-6.

ObjectiveTo determine that intensive glycemic control does not reduce microdialysis glucose concentration brain metabolism of glucose.DesignProspective monitoring followed by retrospective data analysis of cerebral microdialysis and global brain metabolism.SettingSingle center, academic neurointensive care unit.PatientsForty-seven moderate to severe traumatic brain injury patients.InterventionsA nonrandomized, consecutive design was used for glycemic control with loose insulin (n=33) for the initial 2 yrs or intensive insulin therapy (n=14) for the last year.Measurements And Main ResultsIn 14 patients treated with intensive insulin therapy, there was a reduction in microdialysis glucose by 70% of baseline concentration compared with a 15% reduction in 33 patients treated with a loose insulin protocol. Despite this reduction in microdialysis glucose, the global metabolic rate of glucose did not change. However, intensive insulin therapy was associated with increased incidence of microdialysis markers of cellular distress, namely elevated glutamate (38+/-37% vs. 10+/-17%, p<.01), elevated lactate/pyruvate ratio (38+/-37% vs. 19+/-26%, p<.03) and low glucose (26+/-17% vs. 11+/-15%, p<.05, and increased global oxygen extraction fraction. Mortality was similar in the intensive and loose insulin treatment groups (14% vs. 15%, p=.9), as was 6-month clinical outcome (p=.3).ConclusionsIntensive insulin therapy results in a net reduction in microdialysis glucose and an increase in microdialysis glutamate and lactate/pyruvate without conveying a functional outcome advantage.

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