The relationship of soluble adhesion molecule concentrations in systemic and jugular venous serum to injury severity and outcome after traumatic brain injury.
Adhesion molecules control the migration of leukocytes into tissue after injury. This may result in further cellular damage. We hypothesized that altered serum concentrations of soluble intercellular adhesion molecule (sICAM)-1 and soluble L-selectin (sL-selectin) after traumatic brain injury would correlate with injury severity and neurological outcome. We investigated serum concentrations of sICAM-1 and sL-selectin in 22 patients with traumatic brain injury admitted to the intensive care unit. The Glasgow Coma Scale (GCS) score and Injury Severity Score were recorded. Paired arterial and jugular venous blood samples were taken on admission and 24, 48, and 96 h after injury. Mean systemic and jugular venous concentrations of sICAM-1 were normal on admission but became significantly increased by 96 h (P = 0.018). sL-selectin concentrations of injured patients were markedly below those of controls at all time points (P < 0.001). There were no significant differences between jugular venous and arterial concentrations of either sICAM-1 or sL-selectin. Serum sICAM-1 was significantly related to neurological outcome (P < 0.001) and to the GCS score (P < 0.001). These changes in adhesion molecule expression after acute brain injury may be important in the pathophysiology of secondary injury. The highly significant relationship between serum sICAM-1 and neurological outcome suggests that the inflammatory response to injury may be detrimental. Drugs that antagonize the actions of the adhesion molecules may have a role in therapy after traumatic brain injury.


CONCLUSIONS
This observational study shows that there is a strong association between soluble intercellular adhesion molecule-1 in serum and poor neurological outcome after traumatic brain injury. This suggests that inflammation after brain injury may worsen the prognosis and that therapies directed against this inflammation may prove useful.
McKeating
E G
EG
Department of Anaesthetics, University of Edinburgh, Western General Hospital, Scotland. Grant.McKeating@ed.ac.uk
Andrews
P J
PJ
Mascia
L
L
D000293:Adolescent; D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D001930:Brain Injuries / Q000097:blood* / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D002634:Chemotaxis, Leukocyte; D003422:Critical Care; D005260:Female; D005500:Follow-Up Studies; D015600:Glasgow Coma Scale; D006801:Humans; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors / Q000097:blood; D015601:Injury Severity Score; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood*; D007601:Jugular Veins; D019041:L-Selectin / Q000097:blood*; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D009460:Neurologic Examination; D011379:Prognosis; D016896:Treatment Outcome
D000893:Anti-Inflammatory Agents; D018836:Inflammation Mediators; D018799:Intercellular Adhesion Molecule-1; D019041:L-Selectin