Advertisement

Sepsis pp 1-14 | Cite as

Physiopathology of Sepsis

  • Marco A. Perafán

Abstract

Infection occurs in 15% to 40% of admissions to the intensive care unit (ICU); mortality ranges from 10% to 80%. The EPIC (European prevalence of infection in intensive care) European study, with 10,038 patients, found that 21% of patients enter intensive care: 65% with pneumonia, 17% with urinary infection, and 12% with bacteremia. The most frequently found germs were the following: enterobacteria (34%), Staphylococcus aureus (30%), and Pseudomonas aeruginosa (30%). The risk factors observed in the study were the following: prolonged stay, mechanical ventilation, trauma, central venous catheter, and urinary catheter. Only 50% of blood growths were positive in sepsis patients.1

Keywords

Tumor Necrosis Factor Nitric Oxide Septic Shock Severe Sepsis Right Ventricle 
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.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Humphreys H, Willatts S, Vincent J. Pathogenesis of infection in the intensive care unit. In: Humphreys H, Willatts S, Vincent J., eds. Intensive Care Infections. London: WB Saunders, 2000: 3–17.Google Scholar
  2. 2.
    Das U. Critical advances in septicemia and septic shock. Crit Care 2000; 4: 290–6s.PubMedCrossRefGoogle Scholar
  3. 3.
    Ely E. New evolutions in understanding and managing patients with sepsis. Medscape Crit Care Treatment Updates. 2000;www.medscape.com.Google Scholar
  4. 4.
    Shaw H. Understanding sepsis: New findings, new theories. Medscape Crit Care. 1999; www.medscape.com.Google Scholar
  5. 5.
    Hotchkiss R, Karl I. The pathophysiology and treatment of sepsis. N Engl J Med 2003; 348: 138–50.PubMedCrossRefGoogle Scholar
  6. 6.
    Vincent J, De Backer D. Pathophysiology of septic shock. Adv Sepsis 2001; 1: 87–92.Google Scholar
  7. 7.
    Casey L. Immunologic response to infection and its role in septic shock. Sepsis and septic shock. Crit Care Clin 2000; 16: 193–213.CrossRefGoogle Scholar
  8. 8.
    Opal S, Huber C. Bench-to-bedside review: toll-like receptors and their role in septic shock. Crit Care 2002; 6: 125–36.PubMedCrossRefGoogle Scholar
  9. 9.
    Sessler C, Shepherd W. New concepts in sepsis. Curr Opin Crit Care 2002; 8: 465–72.PubMedCrossRefGoogle Scholar
  10. 10.
    Tobin M. Sepsis and shock. Year in review. Am J Respir Crit Care Med 2003; 167: 298–300.Google Scholar
  11. 11.
    Visvanathan K, Zabriskie J. The role of bacterial superantigens in sepsis and treatment implications. Curr Opin Crit Care 2000; 6: 312–6.CrossRefGoogle Scholar
  12. 12.
    De Jonge E, et al. Coagulation abnormalities in sepsis. Curr Opin Crit Care 2000; 6: 317–22.CrossRefGoogle Scholar
  13. 13.
    Balk R, Goyette R. Multiple organ dysfunction syndrome in patients with severe sepsis: more than just inflammation. International Congress and Symposium series 249. London: Royal Society of Medicine Press Limited, 2002: 39–60.Google Scholar
  14. 14.
    Singh S, Winlove C, Evans T. Microvascular permeability in experimental sepsis. In: Vincent J, ed. Yearbook Intensive Care Emergency Med. Berlin: Springer, 2000: 80–92.Google Scholar
  15. 15.
    Neviere R, Sibbald W. Microvascular alterations in sepsis. Sepsis 2001; 4: 81–8.CrossRefGoogle Scholar
  16. 16.
    Hiltebrand L, et al. Distribution of microcirculatory blood flow in multiple splanchnic organs in septic shock. Crit Care Med 2000; 28: 3233–41.PubMedCrossRefGoogle Scholar
  17. 17.
    Tham L, Martin C, Sibbald W. Intestinal microcirculation: Changes in sepsis and effect of vasoactive manipulation. In: Vincent J, ed. Yearbook Intensive Care Emerg Med. Berlin: Springer, 2000: 72–9.Google Scholar
  18. 18.
    Groeneveld J, et al. Regional differences in vascular reactivity in sepsis and endotoxemia. In: Vincent J, ed. Yearbook Intensive Care Emerg. Med. Berlin: Springer, 2001: 221–32.Google Scholar
  19. 19.
    Preiser J. Role of nitric oxide in cardiovascular alterations. Sepsis 2001; 4: 99–109.CrossRefGoogle Scholar
  20. 20.
    Vallet B. Vascular nitric oxide during sepsis: From deficiency to overproduction. Adv Sepsis 2001; 1: 52–57.Google Scholar
  21. 21.
    Martin C, et al. High adenosine plasma concentration as a prognostic index for outcome in patients with septic shock. Crit Care Med 2000; 28: 3198–202.PubMedCrossRefGoogle Scholar
  22. 22.
    Landry D, Oliver J. The pathogenesis of vasodilatory shock. N Engl J Med 2001; 345: 588–95.PubMedCrossRefGoogle Scholar
  23. 23.
    Kumar A, Harry C, Parrillo J. Myocardial dysfunction in septic shock. Crit Care Clin 2000; 16: 251–80.PubMedCrossRefGoogle Scholar
  24. 24.
    Dhainaut J, Cariou A, Laurent I. Myocardial dysfunction in sepsis. Sepsis 2001; 4: 89–97.CrossRefGoogle Scholar
  25. 25.
    Kumar A, Harry C, Parrillo J. Myocardial dysfunction in septic shock. J Cardiothorac Vasc Anesth 2001; 15: 364–76.PubMedCrossRefGoogle Scholar
  26. 26.
    Krishnagopalan S, Kumar A, et al. Myocardial dysfunction in the patient with sepsis. Curr Opin Crit Care 2002; 8: 376–88.PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 2004

Authors and Affiliations

  • Marco A. Perafán

There are no affiliations available

Personalised recommendations