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Context: Current laboratory parameters provide limited information about the prognosis of severely injured patients; therefore, novel laboratory parameters are needed.Materials and methods: We compared the morphological parameters of neutrophils and lymphocytes, and white blood cell (WBC) differential count between survivors and nonsurvivors within 7 days after admission. Multiple logistic regression analysis was conducted to identify independent prognostic factors for 7-day in-hospital mortality.Results: Neutrophil cell size was significantly different between survivors and nonsurvivors (p= 0.04), whereas WBC count and differential were not significantly different. Multiple logistic regression showed that neutrophil cell size was a significant predictor of poor outcome.Conclusions: Neutrophil cell size at admission is a prognostic factor for 7-day in-hospital mortality in severely injured trauma patients, whereas conventional WBC count and differential have no prognostic value.

Systemic inflammation results in release of refractory neutrophils which can cause susceptibility to infections and activates differentiated neutrophils, which can mediate tissue damage. Neutrophils play an important role in host defense. However, deregulation of neutrophils contributes to tissue damage in severe systemic inflammation. In contrast to complications mediated by an overactive neutrophil compartment, severe systemic inflammation is a risk factor for development of immune suppression and as a result, infectious complications. The role of neutrophils in this clinical paradox is poorly understood, and in this study, we tested whether this paradox could be explained by distinct neutrophil subsets and their functionality. We studied the circulating neutrophil compartment immediately after induction of systemic inflammation by administering 2 ng/kg Escherichia coliLPS i.v. to healthy volunteers. Neutrophils were phenotyped by expression of membrane receptors visualized by flow cytometry, capacity to interact with fluorescently labeled microbes, and activation of the NADPH‐oxidase by oxidation of Amplex Red and dihydrorhodamine. After induction of systemic inflammation, expression of membrane receptors on neutrophils, such as CXCR1 and ‐2 (IL‐8Rs), C5aR, FcγRII, and TLR4, was decreased. Neutrophils were also refractory to fMLF‐induced up‐regulation of membrane receptors, and suppression of antimicrobial function was shown by decreased interaction with Staphylococcus epidermis. Simultaneously, activation of circulating neutrophils was demonstrated by a threefold increase in release of ROS. The paradoxical phenotype can be explained by the selective priming of the respiratory burst. In contrast, newly released, CD16dimbanded neutrophils display decreased antimicrobial function. We conclude that systemic inflammation leads to a functionally heterogeneous neutrophil compartment, in which newly released refractory neutrophils can cause susceptibility to infections, and activated, differentiated neutrophils can mediate tissue damage.

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