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Pathophysiology of Shock, Sepsis, and Organ Failure

  • Book
  • © 1993

Overview

Editors:
  1. Günther Schlag

    1. Ludwig-Boltzmann Institute for Experimental and Clinical Traumatology, Vienna, Austria

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  2. Heinz Redl

    1. Ludwig-Boltzmann Institute for Experimental and Clinical Traumatology, Vienna, Austria

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    You can also search for this editor in PubMed   Google Scholar

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Table of contents (76 chapters)

  1. Front Matter

    Pages I-XIX
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  2. Introduction: “Organ in Shock”, “Early Organ Failure”, “Late Organ Failure”

    1. Introduction: “Organ in Shock”, “Early Organ Failure”, “Late Organ Failure”

      • G. Schlag, H. Redl
      Pages 1-3

  3. Trauma, Shock and Development of the Organ in Shock and Early Organ Failure (SIRS)

    1. Front Matter

      Pages 5-5
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    2. Shock, Sepsis, and Multiple Organ Failure: The Result of Whole-Body Inflammation

      • R. J. A. Goris
      Pages 7-24

    3. The Role of Complement

      • M. Heideman, A. Bengtsson
      Pages 25-35

    4. Activation of Humoral Systems. The Role of Coagulation, Fibrinolysis, and the Plasma Kallikrein-Kinin System

      • A. O. Aasen, L. Buø
      Pages 36-45

    5. Proteinases

      • M. Jochum, W. Machleidt, H. Neuhof, H. Fritz
      Pages 46-60

    6. Cellular Mechanisms of Leukocyte Adhesion

      • Asrar B. Malik, Yan Wang
      Pages 61-78

    7. Eicosanoids in Trauma and Traumatic Shock

      • H. Neuhof
      Pages 79-91

    8. Radical Related Cell Injury

      • H. Redl, H. Gasser, S. Hallström, G. Schlag
      Pages 92-110

    9. Humoral Mechanisms

      • D. B. Hoyt, W. G. Junger, A. N. Ozkan
      Pages 111-130

    10. Monocyte and Lymphocyte Responses Following Trauma

      • R. Stephan, A. Ayala, I. H. Chaudry
      Pages 131-144

    11. Metabolic Response to Trauma

      • J. Arnold, D. Leinhardt, R. A. Little
      Pages 145-160

    12. Morphology of the Lung as a Consequence of Direct and Indirect Trauma

      • G. Schlag, H. Redl, J. Pretorius
      Pages 161-175

    13. Permeability Changes

      • M. Seyr, N. J. Mutz
      Pages 176-193

    14. Cardiac Function During Hypovolemia

      • D. L. Traber, J. Meyer, L. D. Traber
      Pages 194-199

    15. Cardiodepressant Factors

      • S. Hallström, B. Koidl, U. Müller, K. Werdan, G. Schlag
      Pages 200-214

    16. Response of the Macrocirculation

      • G. Gutierrez, S. D. Brown
      Pages 215-229

    17. Response of the Microcirculation: Tissue Oxygenation

      • G. I. J. M. Beerthuizen
      Pages 230-241

    18. Cardiovascular Function in Acute Burns

      • C. S. Cox Jr., D. L. Traber, J. B. Zwischenberger, D. N. Herndon
      Pages 242-256
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Keywords

About this book

In this book current knowledge of the pathophysiology of shock, sepsis and multi organ failure is presented. The rapid progress which has been made and the results achieved in intensive care medicine are based on sound basic research, which is duly reflected in these chapters. Multiorgan failure is the foremost cause of postoperative and posttraumatic death and many complex mechanisms are involved. Only with a good foundation of basic research can abnormalities in the physiological, biochemical, and morphological course of shock be recognized and the necessary conclusions for treatment drawn. Therapy must proceed from profound knowledge of the multi variant physiological events in order to influence shock, sepsis and organ failure. Although numerous possibilities for therapy have arisen from pharmaceutical research in recent years, they are beyond the scope of this book and are not discussed here. To gain a better understanding of the pathophysiological events it was necessary to examine and to describe different models that simulate and reproduce these events. Here we describe the causative agents (shock) and the consequences (sepsis, organ failure) in two main sections, divided on the basis of their pathophysiology.

Editors and Affiliations

  • Ludwig-Boltzmann Institute for Experimental and Clinical Traumatology, Vienna, Austria

    Günther Schlag, Heinz Redl

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