[Continuous measurement of peripheral oxygen availability in skeletal muscle of patients with infection]

In patients with sepsis, a pathologic oxygen uptake supply dependence due to an oxygen extraction defect was suggested to result in tissue hypoxia--a hypothesis which is discussed controversially. In order to determine more directly whether the oxygen transport to tissue was reduced in patients with sepsis, the distribution of skeletal muscle pO2 was measured intermittently by polarographic needle electrodes in 28 patients with sepsis for 7 days. Comparison of intermittent with continuous measurements by pO2 catheters showed a close linear relation (r = 0.88; p < 0.001) and acceptable agreement. Therefore, continuous measurement of skeletal muscle pO2 by pO2 catheters can be used as an estimate of mean skeletal muscle pO2. Neither by intermittent nor by continuous measurements, skeletal muscle hypoxia was detected in patients with sepsis. In contrast, the skeletal muscle pO2 was statistically significantly higher on days with septic state (44.1 +/- 10.3 mm Hg) than on days with intermediate (30.1 +/- 8 mm Hg) and nonseptic (26.8 +/- 5.1 mm Hg) states. From our data we infer that the hypothesis of tissue hypoxia in sepsis must be questioned at least for the skeletal muscle. The increase of skeletal muscle pO2 in sepsis, however, suggested that oxygen utilization within skeletal muscle decreased the more severe the stage of sepsis was. A decreased oxygen utilization within tissue, which may result from a 'downregulation' of oxygen-dependent metabolic pathways, might account for a decreased oxygen extraction of peripheral tissue in sepsis.