S100B protein (S100B) has been described as a marker of brain injury. Various cytokines also increase in the cerebrospinal fluid (CSF) of patients with severe traumatic brain injury (TBI). Thus, we investigated early changes in the concentrations of CSF S100B and various cytokines after TBI and evaluated the relations of both S100B and cytokines to intracranial pressure (ICP) and prognosis. Twenty-three patients with severe TBI and a Glasgow Coma Scale score of 8 or less on admission were included in this study. CSF and serum samples were obtained on admission and at 6, 12, 24, 48, 72, and 96 h after injury. CSF concentrations of S100B and CSF and serum concentrations of five cytokines (IL-1beta, TNF-alpha, IL-6, IL-8, and IL-10) were measured and compared. The CSF S100B concentration was increased for 6 h after injury and decreased thereafter. The CSF concentrations of IL-6 and IL-8 peaked within 6 h after injury; other cytokines (IL-1beta, TNF-alpha, and IL-10) were elevated for 24 h after injury and gradually decreased thereafter. Peak CSF S100B concentrations correlated significantly with ICP determined at the time CSF samples were taken (r = 0.729, P < 0.0001). For the cytokines investigated, only the peak CSF IL-1beta concentration correlated significantly and positively with the peak CSF S100B concentration (r = 0.397, P < 0.005). Peak CSF concentrations of S100B (1649 +/- 415 microg/L, mean +/- SEM) and IL-1beta (16.5 +/- 3.3 pg/mL) in the 6 patients with high ICP were significantly higher than those (233 +/- 67 microg/L, 7.6 +/- 1.7 pg/mL, respectively) in the 17 patients with low ICP (P < 0.05). The CSF S100B concentration (1231 +/- 378 microg/L) in eight patients with an unfavorable outcome was significantly higher than that (267 +/- 108 microg/L) in 15 patients with a favorable outcome (P < 0.05). The CSF IL-1beta concentration (14.8 +/- 3.4 pg/mL) in eight patients with an unfavorable outcome tended to be higher than that (7.3 +/- 1.5 pg/mL) in 15 patients with a favorable outcome (P = 0.057). CSF concentrations of S100B and cytokines peak within 24 h after severe TBI and decrease gradually thereafter. CSF S100B and IL-1beta may be useful as predictors of outcome in cases of severe TBI.

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We studied cerebral blood flow (CBF) in the transition from the acute to the chronic phase of severe head injury in order to determine patterns of change in relation to neurological outcome. We measured CBF with stable xenon-enhanced computed tomography (Xe-CT) in 20 consecutive patients at 1, 2, 3, 4, and 6 weeks after severe head injury, and analyzed the relation between the pattern of change in CBF and neurological outcome at 6 months after injury. CBF values were significantly lower in the brain-injured patients than in 14 healthy volunteers, except at 3 weeks after injury, when CBF increased in the patients to a value that did not differ significantly from that in the normal volunteers. We therefore focused on the change in CBF at 3 weeks after injury. We separated the 20 brain-injured patients into two subgroups, of which the first (subgroup A) consisted of nine patients whose CBF had returned to normal by week 3 post-injury, while the second (subgroup B) consisted of 11 patients whose CBF was subnormal at week 3 post-injury. CBF was significantly higher in subgroup A than in subgroup B at 2 weeks post-injury (p < 0.05). CBF in subgroup B remained significantly lower than that in subgroup A throughout the study period. At 6 months post-injury, subgroup A had a significantly better neurological outcome than did subgroup B (p < 0.05). We conclude that patients whose CBF returns to normal at 2-3 weeks following severe traumatic brain injury after being abnormally low in the acute phase of injury can be expected to achieve a good neurological outcome.

The authors concluded that moderate hypothermia is not effective in improving clinical outcomes in severely head injured patients whose ICP remains higher than 40 mm Hg after treatment with mild hypothermia combined with conventional therapies.

We clarified the effect of exchange transfusion with liposome-encapsulated hemoglobin (neo red cells, NRCs) with low O₂ affinity (P₅₀O₂ = 50 mm Hg) on O₂ metabolism. Rabbits were randomly assigned to receive serial exchange transfusions with NRC (NRC group, n = 5), shed blood diluted 1:1 with saline (red blood cell (RBC) group, n = 5), or saline alone (plasma group, n = 4) under hemodynamic monitoring. Cardiac tamponade was then induced and successively reversed to determine relationships between O₂ consumption (VO₂) and O₂ delivery (DO₂) using the dual-line method. Mean values of Hb concentration after exchange transfusion were 5.7 (NRC), 6.0 (RBC), and 1.5 (plasma) g/dL. The plasma group could not even survive the initial exchange hemodilution due to a critical decrease in DO₂. The NRC, but not the RBC group, developed progressive metabolic acidosis and lactatemia, as well as increases in PaCO₂ and decreases in tissue PO₂ in skeletal muscle after exchange transfusion. Nonetheless, systemic O₂ uptake indices obtained from an analysis of the VO₂/DO₂ relationship in the NRC and RBC groups were comparable. These findings suggested that systemic O₂ uptake was maintained in rabbits after exchange transfusion with NRC, although progressive tissue hypoxia with systemic acidosis is indicative of inadequate peripheral circulation and insufficient aerobic metabolism during extended hemodilution in which 86% of the circulating blood is replaced.