Jugular venous oxygen saturation (SjvO(2)) measures the balance betwee
n cerebral oxygen delivery and cerebral oxygen consumption. Abnormalit
ies that increase oxygen consumption (e.g., fever or seizures) or that
decrease oxygen delivery (e.g., increased ICP, hypotension, hypoxia,
hypocapnia, or anemia) can decrease SjvO(2). Measuring SjvO(2) continu
ously in the ICU in 177 patients with severe head injury, jugular veno
us desaturation (SjvO(2) < 50%) was identified at least once in 39% of
the patients. Approximately half of the episodes of desaturation were
due to intracranial hypertension and half were due to systemic causes
. The occurrence of one or more episodes of desaturation was strongly
associated with a poor outcome, suggesting that the reduction in oxyge
n delivery identified with the SjvO(2) monitoring contributed to the n
eurological injury. In the operating room, jugular venous desaturation
was identified in 6 of 8 patients who were monitored during emergency
evacuation of a traumatic intracranial hematoma. The lowest SjvO(2) o
bserved was 28%. In all 8 cases, the SjvO(2) increased, from 47 +/- 10
% to 63 +/- 5% after evacuation of the hematoma. Additional data suppo
rting the hypothesis that these secondary insults identified with the
SjvO(2) monitoring contribute to the patient's neurological injury com
e from measurement of the extracellular concentrations of lactate and
excitatory amino acids in the brain using microdialysis. Lactate conce
ntration increased from 0.9 +/- 0.3 to 2.4 +/- 0.5 mu mol/L and glutam
ate increased from 11.5 +/- 8.5 to 55.0 +/- 10.4 mu mol/L during 8 epi
sodes of jugular venous desaturation in 7 of 22 patients monitored wit
h microdialysis. SjvO(2) identifies global reductions in cerebral oxyg
enation due to a variety of causes, and is useful as a monitor for sec
ondary insults in patients with severe head injury.