Stimulation of inflammatory markers after blunt trauma.

Background Inflammatory mediators are released after trauma and may be related to the pathogenesis of sepsis. A prospective combined study of the pattern of release of an inflammatory mediator, interleukin (IL) 6, leucocyte activation (polymorphonuclear leucocyte (PMN) CD11b receptor expression and plasma elastase-α1 proteinase inhibitor complex (E–α1PI)) and soluble endothelial adhesion molecule expression (soluble E-selectin (sE-selectin) and soluble intracellular adhesion molecule 1 (sICAM-1)) was performed in patients suffering blunt trauma without adult respiratory distress syndrome (ARDS) or multiple organ failure syndrome (MOFS). Methods Thirty-one patients with a mean Injury Severity Score (ISS) of 14 (range 9–57) were studied. Venous blood samples were collected within 6 h of injury and then at 1, 3, 5 and 7 days. Leucocyte CD11b expression was quantified by flow cytometry. Serum IL-6, plasma E–α1PI, sE-selectin and sICAM-1 were measured by enzyme-linked immunosorbent assay. Results Serum IL-6, CD11b expression and E–α1PI levels were significantly raised above control values (P<0·0001) on admission, slowly returning towards control values over the study period (median IL-6, 140 pg/ml versus undetectable; CD11b, 14·8 versus 6·4 mean channel fluorescence units; E–α1 PI, 208 versus 52 μg/l). The sICAM-1 level rose to a median of 539 ng/ml at 5 days (control 243 ng/ml). The median sE-selectin level also progressively increased to a maximum level of 80 ng/ml at 5 days (control 49 ng/ml). Eleven patients developed postoperative sepsis. Significant differences in CD11b expression were seen at days 3, 5 and 7 and in E–α1 PI at 6 h, 24 h and 3 days in patients who subsequently developed sepsis (P<0·05). Severe injury (ISS 16 or greater) was associated with significantly greater responses in these... [ABSTRACT FROM AUTHOR]