Stimulation of inflammatory markers after blunt trauma

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Abstract
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 measurements. Conclusion: These data show that markers of inflammation are specifically stimulated by trauma even when ARDS and MOFS do not occur. The CD11b receptor on PMNs may be useful in screening patients destined to develop post-traumatic sepsis.