Objective: In order to obtain direct evidence for tissue hypoxia in pa
tients with sepsis oxygen, partial pressure was measured within skelet
al muscle. Furthermore, serial intermittent and continuous measurement
s of skeletal muscle Po-2 in patients with sepsis were used to find ou
t whether skeletal muscle oxygenation may change in the course of seps
is and depends on the severity of sepsis. Design: Prospective study. S
etting: Intensive care unit of a university hospital. Patients: Intens
ive care patients (n = 98) with sepsis (group 1, n = 39; group 4, n =
28), limited infection (group 2, n = 16), and cardiogenic shock (group
3, n = 15). Interventions: Pulmonary artery catheterization; standard
antibiotic therapy and volume replacement. Measurements and Main Resu
lts: Skeletal muscle Po-2 was determined by polarographic needle elect
rodes or cathether probes. In patients with sepsis (n = 67), no eviden
ce for skeletal muscle hypoxia was obtained from the Po-2 distribution
within biceps muscle. Mean skeletal muscle Po-2 was increased in pati
ents with sepsis (group 1, 48 torr [6.4 kPa]) compared with patients w
ith limited infection (group 2, 28 torr [3.7 kPa]), p < .001) and with
patients with cardiogenic shock (group 3, 22 torr [2.9 kPa], p < .001
). Serial measurements of the Po-2 distribution during seven consecuti
ve days in another 28 patients (group 4) with sepsis showed that a mor
e severe degree of sepsis was associated with an increase of mean skel
etal muscle (p < .001). These results were confirmed by continuous mea
surements of mean skeletal muscle Po-2. using Po-2 catheters. Conclusi
ons: In patients with sepsis, oxygen transport to skeletal muscle was
not critically reduced. Serial intermittent and continuous measurement
s of skeletal muscle Po-2 showed that skeletal muscle Po-2 increased i
n relation to the severity of the stage of sepsis. Our findings sugges
t that oxygen utilization within skeletal muscle decreased with deteri
oration of sepsis, thereby increasing skeletal muscle Po-2.