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Trauma, Sepsis, and Immune Defects

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Host Defense Dysfunction in Trauma, Shock and Sepsis

Abstract

Traumatic injury and burns remain a major cause of morbidity and mortality in the United States and despite modern techniques of resuscitation and intensive care and an ever increasing number of powerful and effective antibiotics nearly 80% of deaths that occur in trauma and burn patients more than 7 days after injury are caused by sepsis [1]. During the past 10 years the longstanding clinical assumption that host defenses against invading microorganisms were impaired following severe injury has become grounded in fact through the study of injured patients and appropriate animal models. Abnormalities in both specific and nonspecific mechanisms of defense against microorganisms have been described by a number of laboratories, including our own. Nonspecific mechanisms include function of polymorphonuclear [2–4] and mononuclear phagocytes [5–6], natural killer cells [7–9], and products of complement activation [10–13]. Specific defense mechanisms include antibody formation by B lymphocytes [14–16], direct microbial killing by T lymphocytes, and T lymphocyte activation of mononuclear phagocytes [17–19].

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Authors and Affiliations

  1. Harvard Medical School, Department of Surgery, Brigham and Women’s Hospital, 75 Francis St., Boston, MA, 02115, USA

    J. A. Mannick

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  1. J. A. Mannick
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Editors and Affiliations

  1. Dept. of Surgery, Ludwig-Maximilians-University Munich, Klinikum Großhadern Marchioninistr. 15, 8000, Munich 70, Germany

    Eugen Faist  & Friedrich W. Schildberg  & 

  2. Dept. of Surgery, McGill University, Room 510.34 687 Pine Avenue West, Montreal, Quebec, H3A 1A1, Canada

    Jonathan L. Meakins M.D., D.Sc.

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© 1993 Springer-Verlag, Berlin Heidelberg

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Mannick, J.A. (1993). Trauma, Sepsis, and Immune Defects. In: Faist, E., Meakins, J.L., Schildberg, F.W. (eds) Host Defense Dysfunction in Trauma, Shock and Sepsis. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-77405-8_2

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  • DOI: https://doi.org/10.1007/978-3-642-77405-8_2

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-77407-2

  • Online ISBN: 978-3-642-77405-8

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