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      Isolated blunt chest injury leads to transient activation of circulating neutrophils

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          Abstract

          Introduction

          The acute respiratory distress syndrome (ARDS) is a severe and frequently seen complication in multi-trauma patients. ARDS is caused by an excessive innate immune response with a clear role for neutrophils. As ARDS is more frequently seen in trauma patients with chest injury, we investigated the influence of chest injury on the systemic neutrophil response and the development of ARDS.

          Materials and methods

          Thirteen patients with isolated blunt chest injury [abbreviated injury score (AIS) 2–5] were included. To avoid systemic inflammation caused by tissue damage outside the thorax, injuries to other regions than the chest did not exceed an AIS of 2. At 3, 9 and 24 h after injury, the expression of circulating activating molecules on neutrophils and levels of circulating interleukine (IL)-6 were determined. Blood samples from eight healthy volunteers were used as control.

          Results

          Blunt chest injury resulted in the activation of circulating neutrophils, as characterized by a decreased expression of l-selectin (CD62L), CXCR2 (CD182b) and C5aR (CD88) compared to control ( p < 0.05). Expression of l-selectin, CXCR2 and C5aR was partially restored at 24 h after injury. In addition, the mean expression of FcγRIII (CD16) dropped ( p < 0.001), indicating the recruitment of young neutrophils into the circulation. IL-6 levels increased to a maximum mean concentration of 86 ± 31 pg/ml at 24 h postinjury. None of the patients developed ARDS.

          Conclusion

          Blunt chest trauma caused a systemic inflammatory reaction with transient activation of neutrophils and mobilization of young neutrophils into the circulation. Isolated chest injury, however, was not abundant enough to cause ARDS, so a second hit appears crucial.

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          Most cited references 28

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          APACHE II: a severity of disease classification system.

          This paper presents the form and validation results of APACHE II, a severity of disease classification system. APACHE II uses a point score based upon initial values of 12 routine physiologic measurements, age, and previous health status to provide a general measure of severity of disease. An increasing score (range 0 to 71) was closely correlated with the subsequent risk of hospital death for 5815 intensive care admissions from 13 hospitals. This relationship was also found for many common diseases. When APACHE II scores are combined with an accurate description of disease, they can prognostically stratify acutely ill patients and assist investigators comparing the success of new or differing forms of therapy. This scoring index can be used to evaluate the use of hospital resources and compare the efficacy of intensive care in different hospitals or over time.
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            The injury severity score: a method for describing patients with multiple injuries and evaluating emergency care.

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              Tissue injury in inflammation. Oxidants, proteinases, and cationic proteins.

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                Author and article information

                Contributors
                088-75590882 , L.P.H.Leenen@umcutrecht.nl
                Journal
                Eur J Trauma Emerg Surg
                European Journal of Trauma and Emergency Surgery
                Springer-Verlag (Berlin/Heidelberg )
                1863-9933
                1863-9941
                27 July 2010
                27 July 2010
                April 2011
                : 37
                : 2
                : 177-184
                Affiliations
                [1 ]Department of Surgery/Traumatology, University Medical Centre Utrecht, PO Box 85500, 3508 GA Utrecht, The Netherlands
                [2 ]Department of Respiratory Medicine, University Medical Centre Utrecht, Utrecht, The Netherlands
                Article
                41
                10.1007/s00068-010-0041-x
                3150797
                21837259
                © The Author(s) 2010
                Categories
                Original Article
                Custom metadata
                © Springer-Verlag 2011

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