OBJECT: The authors evaluated the use of bedside cerebral online microdialysis for the detection of impending and present cerebral hypoxia in patients who had sustained traumatic brain injury. METHODS: Thirty-five severely head injured patients (with Glasgow Coma Scale scores < or = 8) were studied. Patients underwent continuous brain tissue PO2 (PtiO2) monitoring. The PtiO2 catheter was placed into the unaffected frontal white matter within 32.2 hours postinjury (range 7-48 hours). The microdialysis catheter was placed close to the PtiO2 probe via a 2- or 3-way skull screw that was connected to a pump and perfused with Ringer's solution at 0.3 microl/minute. The microdialysis samples were collected hourly and analyzed at the bedside for glucose, lactate, lactate-pyruvate ratio, and glutamate. Data were analyzed for identification of episodes of impending (PtiO2 10-15 mm, Hg > 5-minute duration) and present cerebral hypoxia (PtiO2 10 mm Hg, > 5-minute duration). In 62% of the patients hypoxic episodes occurred and were most frequently associated with hyperventilation (p < 0.001). During impending hypoxia, extracellular glutamate concentrations were increased (p = 0.006) whereas energy metabolites remained stable. During cerebral hypoxia, the extracellular glutamate (p < 0.001) and lactate (p = 0.001) concentrations were significantly higher than during normal oxygenation, whereas the lactate-pyruvate ratio was only slightly increased (p = 0.088, not significant). CONCLUSIONS: The authors conclude that a PtiO2 below 10 mm Hg is critical to induce metabolic changes seen during hypoxia/ischemia. Early markers of cerebral hypoxia are increased levels of glutamate and lactate. Regional hypoxia is not always associated with anaerobic cerebral metabolism. In the future, this technology of bedside monitoring may allow optimization of the treatment of severely head injured patients.
OBJECT: The authors evaluated the use of bedside cerebral online microdialysis for the detection of impending and present cerebral hypoxia in patients who had sustained traumatic brain injury. METHODS: Thirty-five severely head injured patients (with Glasgow Coma Scale scores < or = 8) were studied. Patients underwent continuous brain tissue PO2 (PtiO2) monitoring. The PtiO2 catheter was placed into the unaffected frontal white matter within 32.2 hours postinjury (range 7-48 hours). The microdialysis catheter was placed close to the PtiO2 probe via a 2- or 3-way skull screw that was connected to a pump and perfused with Ringer's solution at 0.3 microl/minute. The microdialysis samples were collected hourly and analyzed at the bedside for glucose, lactate, lactate-pyruvate ratio, and glutamate. Data were analyzed for identification of episodes of impending (PtiO2 10-15 mm, Hg > 5-minute duration) and present cerebral hypoxia (PtiO2 10 mm Hg, > 5-minute duration). In 62% of the patientshypoxic episodes occurred and were most frequently associated with hyperventilation (p < 0.001). During impending hypoxia, extracellular glutamate concentrations were increased (p = 0.006) whereas energy metabolites remained stable. During cerebral hypoxia, the extracellular glutamate (p < 0.001) and lactate (p = 0.001) concentrations were significantly higher than during normal oxygenation, whereas the lactate-pyruvate ratio was only slightly increased (p = 0.088, not significant). CONCLUSIONS: The authors conclude that a PtiO2 below 10 mm Hg is critical to induce metabolic changes seen during hypoxia/ischemia. Early markers of cerebral hypoxia are increased levels of glutamate and lactate. Regional hypoxia is not always associated with anaerobic cerebral metabolism. In the future, this technology of bedside monitoring may allow optimization of the treatment of severely head injured patients.