title: Low extracellular (ECF) glucose affects the neurochemical profile in severe head-injured patients.
abstract: Glucose (Gluc) is the main energy source for the brain. After severe head-injury energy demand is massively increased and supply is often decreased. In pilot microdialysis studies, many patients with severe head-injury had undetectable glucose concentrations, probably reflecting changes in metabolism and/or reduced supply. We therefore investigated whether patients with low ECF glucose (criterion: < 50 microM for > or = 5 hrs), LOWgluc, differ from patients with higher glucose levels (NORMALgluc) We also tested the interrelationships between other parameters such as lactate, glutamate, K+, brain O2 and CO2, ICP, CPP, and CBF in these two groups. We found that patients with low ECF glucose, LOWgluc, have significantly lower lactate concentrations than patients with "normal" glucose, NORMALgluc, levels do. Spearman correlations between glucose and most other parameters were similar in both patient groups. However, glutamate correlated positively with glucose, lactate, brain CO2 and negatively with brain O2 in the NORMALgluc patient group, whereas glutamate did not significantly correlate with any of these parameters in the LOWgluc group. There was also no correlation between outcome and the dialysate glucose. The results indicate that low ECF glucose is almost always present in severe head-injury. Moreover, the lack of correlation between low glucose and outcome, however, suggests that other energy substrates, such as lactate, are important after TBI.
authors.affiliation: Medical College of Virginia, Division of Neurosurgery, Richmond, USA.
authors.forename: B
authors.initials: B
authors.lastname: Alessandri
authors.forename: M
authors.initials: M
authors.lastname: Reinert
authors.forename: H F
authors.initials: HF
authors.lastname: Young
authors.forename: R
authors.initials: R
authors.lastname: Bullock
mesh_terms: D001786:Blood Glucose / Q000378:metabolism*; D001921:Brain / Q000098:blood supply / Q000503:physiopathology; D001929:Brain Edema / Q000503:physiopathology* / Q000628:therapy; D001930:Brain Injuries / Q000401:mortality / Q000503:physiopathology* / Q000628:therapy; D002245:Carbon Dioxide / Q000378:metabolism; D003422:Critical Care; D004734:Energy Metabolism / Q000502:physiology*; D005110:Extracellular Space / Q000378:metabolism*; D006801:Humans; D007427:Intracranial Pressure / Q000502:physiology; D019344:Lactic Acid / Q000378:metabolism; D008991:Monitoring, Physiologic; D010101:Oxygen Consumption / Q000502:physiology; D011379:Prognosis; D014882:Water-Electrolyte Balance / Q000502:physiology
chemical_list: D001786:Blood Glucose; D002245:Carbon Dioxide; D019344:Lactic Acid