Monitoring of cerebral oxygenation in patients with severe head injuries: Brain tissue PO2 versus jugular vein oxygen saturation

Monitoring of cerebral oxygenation is considered to re of great importance in minimizing secondary hypoxic and ischemic brain damage following severe head injury. Although the threshold for cerebral hypoxia in jugular bulb oximetry (measurement of O-2 saturation in the jugular vein (SjvO(2))) is generally accepted to be 50% oxygen saturation, a comparable value in brain tissue PO2 (PtiO(2)) monitoring, a new method for direct assessment of PO2 in the cerebral white matter, has not yet been established. Hence, the purpose of this study was to compare brain PtiO(2) with SjvO(2) in severely head injured patients during phases of reduced cerebral perfusion pressure (CPP) to define a threshold in brain PtiO(2) monitoring. In addition, the safety and data quality of both SjvO(2) and brain PtiO(2) monitoring were studied. In 15 patients with severe head injuries, SjvO(2) and brain PtiO(2) were monitored simultaneously. For brain PtiO(2) monitoring a polarographic microcatheter was inserted in the frontal cerebral white matter, whereas for SjvO(2) measurements were obtained by using a fiberoptic catheter placed in the jugular bulb. Intracranial pressure was monitored by means of an intraparenchymal catheter. Mean arterial blood pressure, CPP, end-tidal CO2, and arterial oxygen saturation (pulse oximetry) were continuously recorded. All data were simultaneously stored and analyzed using a multimodal computer system. For specific analysis, phases of marked deterioration in systemic blood pressure and consecutive reductions in CPP were investigated. There were no complications that could be attributed to the PtiO(2) catheters, that is, no intracranial bleeding or infection. The ''time of good data quality'' was 95% in brain PtiO(2) compared to 43% in SjvO(2); PtiO(2) monitoring could be performed twice as long as SjvO(2) monitoring. During marked decreases in CPP, SjvO(2) and brain PtiO(2) correlated closely. A significant second-order regression curve of SjvO(2) versus brain PtiO(2) (p < 0.01) was plotted. At a threshold of 50% in SjvO(2), brain PtiO(2) was found to be within the range of 3 to 12 mm Hg, with a regression curve ''best fit'' value of 8.5 mm Hg. There was a close correlation between CPP and oxygenation parameters (PtiO(2) and SjvO(2)) when CPP fell below a breakpoint of 60 mm Hg, suggesting intact cerebral autoregulation in most patients. This study demonstrates that monitoring brain PtiO(2) is a safe, reliable, and sensitive diagnostic method to follow cerebral oxygenation. In comparison to SjvO(2), PtiO(2) is more suitable for long-term monitoring. It can be used to minimize episodes of secondary cerebral maloxygenation after severe head injury and may, hopefully, improve the outcome in severely head injured patients.