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. 1999 Sep;27(9):1965-73.
doi: 10.1097/00003246-199909000-00041.

Extracellular lactate and glucose alterations in the brain after head injury measured by microdialysis

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Extracellular lactate and glucose alterations in the brain after head injury measured by microdialysis

J C Goodman et al. Crit Care Med. 1999 Sep.

Abstract

Objective: To study cerebral glucose and lactate metabolism in head-injured patients using microdialysis.

Design: Prospective, nonrandomized, clinical study.

Setting: Neurosurgical intensive care unit in a university-affiliated county hospital.

Patients: One hundred twenty-six head-injured patients.

Interventions: Cerebral cortical neurochemical monitoring using microdialysis coupled with systemic hemodynamic and oxygenation monitoring, measurement of cerebral perfusion pressure and intracranial pressure, and measurement of global cerebral oxygenation using jugular venous oxygen saturation in all 126 patients. In selected cases, cerebral blood flow was also measured using cortical thermodilution probes in 33 patients, and regional cerebral oxygenation was measured using PO2 probes in 65 patients.

Measurements and main results: Elevated extracellular lactate, reduced glucose, and an elevated lactate/glucose ratio were observed with cerebral hypoxia and ischemia. Elevated lactate and an increased lactate/glucose ratio strongly correlated with death. Other more subtle alterations of lactate and glucose were seen early after injury that may reflect compensatory alterations in cerebral metabolism.

Conclusions: Clinical neurochemical monitoring of glucose and lactate levels in the extracellular space of the cerebral cortex is technically feasible and provides insight into the bioenergetic status of the brain. Increased lactate and decreased glucose, indicating accelerated glycolysis, commonly occurred with cerebral ischemia or hypoxia, and increased anaerobic glycolysis in this setting is associated with a poor outcome.

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Comment in

  • Lactate and traumatic brain injury.
    Marion DW. Marion DW. Crit Care Med. 1999 Sep;27(9):2063-4. doi: 10.1097/00003246-199909000-00077. Crit Care Med. 1999. PMID: 10507661 No abstract available.

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