Metabolic changes during impending and manifest cerebral hypoxia in traumatic brain injury

Abstract

The objective was to measure metabolic changes monitored by bedside microdialysis during impending and manifest hypoxia in traumatic brain injury. In 41 patients, a PtiO₂-catheter (Licox; 1/min) was placed into non-lesioned frontal white matter together with a microdialysis catheter (CMA, hourly). Data were analysed for identification of episodes of impending (PtiO₂ < 10 - 15 mmHg > 5 min) and manifest cerebral hypoxia (PtiO₂ < 10 mmHg, > 5 min). In 69% of patients hypoxic episodes occurred, most frequently associated with hyperventilation (p < 0.001). During impending hypoxia, glutamate was increased (p = 0.03), while the energy metabolites remained stable. Manifest hypoxia was reflected by significant increases of glutamate (p = 0.007) and lactate (p = 0.044), but normal lactate-pyruvate ratios. We conclude that hyperventilation had a potential adverse effect on cerebral metabolism and was most frequently associated with cerebral hypoxia. A PtiO₂ < 10 mmHg can induce metabolic changes with increase of glutamate and lactate. The presence of anaerobic cerebral metabolism probably depends on duration and severity of the hypoxic episode.

• Brain Tissue-PO2
• Cerebral Metabolism
• Cerebral Oxygenation
• Hypoxia
• Ischaemia
• Microdialysis
• Multimodal Monitoring
• Severe Head Injury