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

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.

Detection of secondary insults by brain tissue pO2 and bedside microdialysis in severe head injury.

We evaluated bedside cerebral on-line microdialysis for early detection of cerebral hypoxia in patients with traumatic brain injury. 24 severely head injured patients (Glasgow Coma Score < or = 8) were studied. Patients underwent continuous brain tissue PO2 (PtiO2) monitoring using the LICOX (GMS mbH, Germany) microcatheter device. The catheter was placed into the non-lesioned frontal white matter within 32.2 (7-48) hrs post injury. The microdialysis catheter (CMA 100, Sweden) was placed close to the PtiO2 probe via a 2- or 3-way skull screw, connected to a pump and perfused with Ringer solution (0.3 microliter/min). The microdialysis samples were collected hourly and analyzed at the bedside for glucose, lactate, lactate-pyruvate-ratio and glutamate (CMA 600, Sweden). We identified 252 episodes of impending hypoxia (PtiO2 < 15 mm Hg; 11,810 minutes) and 38 episodes of cerebral hypoxia (PtiO2 < 10 mm Hg; 1996 minutes). Before cerebral hypoxia, glucose decreased significantly. Glutamate was unchanged when no hypoxia or impending hypoxia occurred but increased 3-4 fold before a hypoxic episode appeared. We conclude that early metabolic detection of cerebral hypoxia before a critical decrease in brain tissue PtiO2 is seen and possibly allows earlier changes in treatment (e.g. reduction of hyperventilation therapy).

Bedside microdialysis for early detection of cerebral hypoxia in traumatic brain injury.

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.