Decreased soluble adhesion molecule L-selectin plasma concentrations after major trauma.

BACKGROUND

Binding of the leukocyte glycoprotein L-selectin to ligands expressed by activated endothelium directs leukocyte recruitment to areas of acute inflammation. Sequestration by activated microvascular endothelium has been proposed to explain the low plasma concentrations of soluble L-selectin (sCD62L) observed early in patients with acute respiratory distress syndrome. We hypothesized that inflammatory endothelial activation may occur in trauma patients, leading to decreased sCD62L plasma concentrations.

METHODS

This study was a prospective analysis of sCD62L plasma concentrations in patients with isolated head injuries and multiple trauma patients without head injuries admitted to two tertiary-level intensive care units. sCD62L plasma concentrations were determined in 18 consecutive adult patients with isolated moderate and severe head injuries and in 13 multiple trauma patients without head injuries immediately upon admission to the intensive care unit and then daily for up to 10 days after trauma.

RESULTS

Compared with healthy adult controls (n=22), patient sCD62L plasma concentrations were significantly decreased upon admission (5.7+/-1.6 vs. 11.0+/-1.7 pmol/mL; p < 0.001). In all patients, sCD62L concentrations remained depressed throughout the study period. sCD62L concentrations did not differ significantly between patients with isolated head injuries and multiple trauma patients without head injuries, although repeated-measures analysis of variance showed significantly more depressed sCD62L concentrations associated with severe (n=14) compared with moderate head injuries (n=4) during the study period (p < 0.05).

CONCLUSION

Patients with major trauma present with a significant reduction of sCD62L plasma concentrations within the first 12 hours after trauma and during subsequent intensive care. This finding suggests widespread microvascular endothelial activation after trauma, which may be associated with increased neutrophil extravasation.