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The Systemic Inflammatory Response Syndrome (SIRS)

  • R. C. Bone
Part of the Update in Intensive Care and Emergency Medicine book series (UICM, volume 19)

Abstract

Sepsis and multiple organ failure remain as important causes of mortality and morbidity in hospitals around the world today, despite the innovative techniques that have been developed to deal with these illnesses and the vast body of knowledge accumulated regarding its causes and pathogenesis. Over the last decade, basic science researchers have determined that the systemic inflammatory response syndrome (SIRS) and a number of related clinical entities actually represent different phases and severities of a single pathologic dysfunction. This dysfunction affects the pathways of inflammation, a complex response that is normally beneficial in assisting the host to fight infecting pathogens. It is for this reason that the term sepsis — meaning a systemic infection — came into being: the adverse condition of sepsis was almost always associated with the presence of invading bacteria. The problem with this definition was that infection could not always be found when sepsis occurred; riot only was infection simply not seen in some cases, but it could also be associated with certain other, non-infective states, such as fat embolism, burns, and trauma. With this and other discoveries about the pathogenesis of sepsis, it became apparent to researchers and clinicians that the old concepts and terminology regarding sepsis were not accurate. In order to develop a new terminology that complemented the new discoveries about the pathophysiology of sepsis, the American College of Chest Physicians/Society of Critical Care Medicine held a consensus conference on the terminology and medical treatment of sepsis [1]. The updated terminology for sepsis and its sequelae are presented in Table 1.

Keywords

Septic Shock Systemic Inflammatory Response Syndrome Hageman Factor Basic Science Researcher Endogenous Tumor Necrosis Factor 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    Bone RC, Balk RA, Cerra FB, et al (1992) Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Chest 101: 1644–1655PubMedCrossRefGoogle Scholar
  2. 2.
    Suffredini AF, Fromm RE, Parker MM, et al (1989) The cardiovascular response of normal humans to the administration of endotoxin. N Engl J Med 321: 280–287PubMedCrossRefGoogle Scholar
  3. 3.
    Wolff SM (1973) Biologic effects of bacterial endotoxins in man. J Infect Dis 128 (Suppl): 251–264CrossRefGoogle Scholar
  4. 4.
    Nies AS, Forsyth RP, Williams HE, Melmon KL (1968) Contribution of kinins to endotoxin shock in unanesthetized rhesus monkeys. Circ Res 22: 155–164PubMedGoogle Scholar
  5. 5.
    Young LS (1990) Gram-negative sepsis. In: Mandell GL, Douglas RG Jr, Bennett JE (eds) Principles and Practice of Infectious Diseases, 3rd Edition. Churchill Livingstone, New York, pp 611–636Google Scholar
  6. 6.
    Kreger BE, Craven DE, McCabe WR (1980) Gram-negative bacteremia. IV. Re-evaluation of clinical features and treatment in 612 patients. Am J Med 68: 344–355PubMedCrossRefGoogle Scholar
  7. 7.
    Treadwell TL (1988) Gram-negative bacteremia: The current setting. Hosp Pract July: 117–123Google Scholar
  8. 8.
    International Antimicrobial Therapy Project Group of the European Organization for Research and Treatment of Cancer (1983) Combination of amikacin and carbenicillin with or without cefazolin as empirical treatment of febrile neutropenic patients. J Clin Oncol 1: 597–603Google Scholar
  9. 9.
    Packman MI, Rackow C (1983) Optimum left heart filling pressure during fluid resuscitation of patients with hypovolemic and septic shock. Crit Care Med 11: 165–169PubMedCrossRefGoogle Scholar
  10. 10.
    The Veterans Administration Systemic Sepsis Cooperative Study Group (1987) Effect of high-dose glucocorticoid therapy on mortality in patients with clinical signs of systemic sepsis. N Engl J Med 317: 659–665CrossRefGoogle Scholar
  11. 11.
    Sprung CL, Caralis PV, Marcial EH, et al (1984) The effects of high-dose corticosteroids in patients with septic shock: A prospective, controlled study. N Engl J Med 311: 1137–1143PubMedCrossRefGoogle Scholar
  12. 12.
    Schumer W (1976) Steroids in the treatment of clinical septic shock. Ann Surg 184: 333–341PubMedCrossRefGoogle Scholar
  13. 13.
    Rackow EC, Astiz ME (1991) Pathophysiology and treatment of septic shock. JAMA 266: 548–554PubMedCrossRefGoogle Scholar
  14. 14.
    Greenman RL, Schein RMH, Martin MA, et al and the XONA Sepsis Study Group (1991) A controlled clinical trial of E5 murine monoclonal IgM antibody to endotoxin in the treatment of gram-negative sepsis. JAMA 266: 1097–1102PubMedCrossRefGoogle Scholar
  15. 15.
    Ziegler EJ, Fisher CJ, Sprung CL, et al (1991) Treatment of gram-negative bacteremia and septic shock with a HA-1A human monoclonal antibody against endotoxin. N Engl J Med 324: 429–436PubMedCrossRefGoogle Scholar
  16. 16.
    Bone RC (1991) Monoclonal antibodies to endotoxin: New allies against sepsis? JAMA 266: 1125–1126PubMedCrossRefGoogle Scholar
  17. 17.
    Bone RC, Balk RA, Cerra FB, et al (1992) American College of Chest Physicians/ Society of Critical Care Medicine Consensus Conference: Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med 20: 864–874CrossRefGoogle Scholar
  18. 18.
    Bone RC (1991) The pathogenesis of sepsis. Ann Int Med 115: 457–469PubMedGoogle Scholar

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© Springer-Verlag Berlin Heidelberg 1995

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  • R. C. Bone

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