Microdialysate concentration changes do not provide sufficient information to evaluate metabolic effects of lactate supplementation in brain-injured patients.
Cerebral microdialysis is a widely used clinical tool for monitoring extracellular concentrations of selected metabolites after brain injury and to guide neurocritical care. Extracellular glucose levels and lactate/pyruvate ratios have high diagnostic value because they can detect hypoglycemia and deficits in oxidative metabolism, respectively. In addition, patterns of metabolite concentrations can distinguish between ischemia and mitochondrial dysfunction, and are helpful to choose and evaluate therapy. Increased intracranial pressure can be life-threatening after brain injury, and hypertonic solutions are commonly used for pressure reduction. Recent reports have advocated use of hypertonic sodium lactate, based on claims that it is glucose sparing and provides an oxidative fuel for injured brain. However, changes in extracellular concentrations in microdialysate are not evidence that a rise in extracellular glucose level is beneficial or that lactate is metabolized and improves neuroenergetics. The increase in glucose concentration may reflect inhibition of glycolysis, glycogenolysis, and pentose phosphate shunt pathway fluxes by lactate flooding in patients with mitochondrial dysfunction. In such cases, lactate will not be metabolizable and lactate flooding may be harmful. More rigorous approaches are required to evaluate metabolic and physiological effects of administration of hypertonic sodium lactate to brain-injured patients.
Department of Neurology, University of Arkansas for Medical Sciences, Little Rock, AR, USA, and Department of Cell Biology and Physiology, University of New Mexico, Albuquerque, NM, USA gadienel@uams.edu.
Gerald A
GA
Dienel
Department of Radiology and Biomedical Imaging, Magnetic Resonance Research Center, Yale University School of Medicine, New Haven, CT, USA.
Douglas L
DL
Rothman
Department of Neurosurgery, Lund University Hospital, Lund, Sweden, and Department of Neurosurgery, Odense University Hospital, Odense, Denmark.
Carl-Henrik
CH
Nordström
D001921:Brain / Q000378:metabolism*; D000070642:Brain Injuries, Traumatic / Q000378:metabolism* / Q000628:therapy; D003422:Critical Care; D004734:Energy Metabolism; D005947:Glucose / Q000378:metabolism; D006801:Humans; D019344:Lactic Acid / Q000008:administration & dosage / Q000378:metabolism* / Q000627:therapeutic use*; D017551:Microdialysis; D010100:Oxygen / Q000378:metabolism; D019289:Pyruvic Acid / Q000378:metabolism; D012680:Sensitivity and Specificity
D019344:Lactic Acid; D019289:Pyruvic Acid; D005947:Glucose; D010100:Oxygen
Cerebral microdialysis; brain metabolism; glucose; lactate supplementation; traumatic brain injury