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

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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 ≤ 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 μl/minute. The microdialysis samples were collected hourly and analyzed at the bedside for glucose, lactate, lactate–pyruvate 5-minute 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 hypox-ia, 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.

Abbreviations used in this paper:CPP = cerebral perfusion pressure; ECF = extracellular fluid; etCO2 = end tidal CO2; ICP = intra-cranial pressure; MABP = mean arterial blood pressure; PtiO2 = brain tissue partial pressure of oxygen; SjVO2 = jugular venous oxygen saturation.

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 ≤ 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 μl/minute. The microdialysis samples were collected hourly and analyzed at the bedside for glucose, lactate, lactate–pyruvate 5-minute 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 hypox-ia, 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.

Abbreviations used in this paper:CPP = cerebral perfusion pressure; ECF = extracellular fluid; etCO2 = end tidal CO2; ICP = intra-cranial pressure; MABP = mean arterial blood pressure; PtiO2 = brain tissue partial pressure of oxygen; SjVO2 = jugular venous oxygen saturation.

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Contributor Notes

Address reprint requests to: Asita S. Sarrafzadeh, M.D., Department of Neurosurgery, Charité Campus Virchow Medical Center, Humboldt University of Berlin, Augustenburger Platz 1, 13353
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