Overwhelming sepsis continues to be a major source of morbidity and mortality in patients who have sustained severe traumatic injury. Recently, much interest has been focused on the role of the peripheral blood neutrophil (PMN) in infections in these patients. Two surface receptors, CD11b (CR3) and CD16 (FcγRIII), are thought to participate in bacterial phagocytosis and are both present on >85% of normal PMNs. We have previously shown that cells that lack both of these receptors have markedly reduced phagocytic function. The purpose of this study was to determine the effect of severe trauma on the expression of these PMN receptors. Twenty severe trauma patients, age 19-70 years, presenting with an initial APACHE II score of ≥10 were arbitrarily divided into two groups to define severity of injury: Group A, initial APACHE II of 10-18 (n = 11) and Group B, initial APACHE II of 19-25 (n = 9). Blood was obtained on admission, on Day 3, and weekly thereafter. PMNs were stained with fluorochrome-labeled monoclonal antibodies directed against CD11b and CD16 and then analyzed by flow cytometry. Controls consisted of 14 normal adults, age 20-65 years. The percentage and absolute numbers of CD11b+/CD16+ PMNs were determined for each patient or control sample. ANOVA and multiple comparison of variables (P = 0.05) were performed for each week. Values for Group A were different from controls at Weeks 0, 1, and 3. Values for Group B were significantly lower than those of controls at all weeks. Group B showed significantly lower percentages of CD11b+/CD16+ PMNs than those obtained for Group A at weeks 0, 0.5, and 3. Group A patients had an initial mean percentage of CD11b+/CD16+ PMNs of 68% and an average late septic complication rate of 0.8 per patient. Group B patients had an initial mean percentage of CD11b+/CD16+ PMNs of 35% with an average of 3.3 late septic complications per patient. We conclude that after severe traumatic injury, the percentage of CD11b+/CD16+ PMNs is significantly decreased and is influenced by the severity of injury. The significantly reduced percentage of CD11b+/CD16+ PMNs in Group B as compared with Group A at Week 3 may possibly be explained by the increased incidence of septic complications seen in the more severely injured group at this time. © 1992.
