Research

Brain metabolism is significantly impaired at blood glucose below 6 mM and brain glucose below 1 mM in patients with severe traumatic brain injury

Roman Meierhans^1†, Markus Béchir^1†, Silke Ludwig¹, Jutta Sommerfeld¹, Giovanna Brandi^1,2, Christoph Haberthür³, Reto Stocker¹ and John F Stover^1*

• * Corresponding author: John F Stover john.stover@access.unizh.ch

• † Equal contributors

Author Affiliations

¹ Surgical Intensive Care, University Hospital Zürich, Rämistrasse 100, 8091 Zürich, Switzerland

² Ospedale Maggiore Policlinico Milano, Via Francesco Sforza, 28, I-20122 Milano, Italy

³ Surgical Intensive Care, Luzerner Kantonsspital, 6000 Luzern 16, Switzerland

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Critical Care 2010, 14:R13 doi:10.1186/cc8869

Published: 8 February 2010

Abstract

Introduction

The optimal blood glucose target following severe traumatic brain injury (TBI) must be defined. Cerebral microdialysis was used to investigate the influence of arterial blood and brain glucose on cerebral glucose, lactate, pyruvate, glutamate, and calculated indices of downstream metabolism.

Methods

In twenty TBI patients, microdialysis catheters inserted in the edematous frontal lobe were dialyzed at 1 μl/min, collecting samples at 60 minute intervals. Occult metabolic alterations were determined by calculating the lactate- pyruvate (L/P), lactate- glucose (L/Glc), and lactate- glutamate (L/Glu) ratios.

Results

Brain glucose was influenced by arterial blood glucose. Elevated L/P and L/Glc were significantly reduced at brain glucose above 1 mM, reaching lowest values at blood and brain glucose levels between 6-9 mM (P < 0.001). Lowest cerebral glutamate was measured at brain glucose 3-5 mM with a significant increase at brain glucose below 3 mM and above 6 mM. While L/Glu was significantly increased at low brain glucose levels, it was significantly decreased at brain glucose above 5 mM (P < 0.001). Insulin administration increased brain glutamate at low brain glucose, but prevented increase in L/Glu.

Conclusions

Arterial blood glucose levels appear to be optimal at 6-9 mM. While low brain glucose levels below 1 mM are detrimental, elevated brain glucose are to be targeted despite increased brain glutamate at brain glucose >5 mM. Pathogenity of elevated glutamate appears to be relativized by L/Glu and suggests to exclude insulin- induced brain injury.