Bacteremia and Sepsis

  • James M. Herman
  • William J. Curry
  • Edward G. Paul


Bacteremia indicates the presence of viable bacteria in the circulatory blood and is usually defined clinically as positive blood cultures.1 A cascade of local and systemic regulatory mechanisms exist to protect against endothelial damage caused by a variety of nonspecific insults. The systemic inflammatory response syndrome (SIRS) denotes clinical response to endothelial damage including two or more of the following: (1) temperature higher than 38°C or lower than 36°C; (2) respiratory rate more than 20 breaths per minute or a PCO2 less than 32 mm Hg; (3) pulse higher than 90 beats per minute, or (4) white blood cell count more than 12.0 × 109/L or less than 4.0 × 109/L or more than 10% immature neutrophils. When the clinical insult is a documented infection, sepsis is present. As counterregulatory mechanisms fail, endothelial damage progresses leading to severe sepsis (previously the sepsis syndrome), which includes hypotension and hypoperfusion manifested by lactic acidosis, oliguria, or altered mental status. Finally, septic shock occurs when hypotension and hypoperfusion abnormalities persist despite adequate fluid resuscitation.2,3


Septic Shock Severe Sepsis Systemic Inflammatory Response Syndrome Lactic Acidosis Endothelial Damage 
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  1. 1.
    Bone RC. Sepsis, the sepsis syndrome, multi-organ failure: a plea for comparable definitions. Ann Intern Med 1991;114: 332–3.PubMedCrossRefGoogle Scholar
  2. 2.
    Rangel-Frausto MS, Pittet D, Costigan M, Hwang T, Davis CS, Wenzel RP. The natural history of the systemic inflammatory response syndrome (SIRS). JAMA 1995;273:117–23.PubMedCrossRefGoogle Scholar
  3. 3.
    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 1992;20:864–75.CrossRefGoogle Scholar
  4. 4.
    Mortality patterns—United States, 1992. MMWR 1994;43: 916–20.Google Scholar
  5. 5.
    Pinner RW, Teutsch SM, Simonsen L, et al. Trends in infectious diseases mortality in the United States. JAMA 1996; 275:189–93.PubMedCrossRefGoogle Scholar
  6. 6.
    Conboy K, Welage LS, Walawander CA, et al. Sepsis syndrome and associated sequelae in patients at high risk for gram-negative sepsis. Pharmacotherapy 1995;15:66–77.PubMedGoogle Scholar
  7. 7.
    Bone RC. The pathogenesis of sepsis. Ann Intern Med 1991; 115:457–69.PubMedCrossRefGoogle Scholar
  8. 8.
    Van der Poll T, Lowery SF. Tumor necrosis factor in sepsis: mediator of multiple organ failure or essential part of host defense? Shock 1995;3:1–12.PubMedGoogle Scholar
  9. 9.
    Rackow EC, Astiz ME. Pathophysiology and treatment of septic shock. JAMA 1991;226:548–59.CrossRefGoogle Scholar
  10. 10.
    Barriere SL, Ognibene FP, Summer WR, Young LS. Septic shock: beyond antibiotics. Patient Care 1991;25:95–109.Google Scholar
  11. 11.
    Gross PA, Barrett TL, Dellinger EP, et al. Quality standard for the treatment of bacteremia. Clin Infect Dis 1994;18: 428–30.PubMedCrossRefGoogle Scholar
  12. 12.
    Warren HS, Danner RL, Munford RS. Anti-endotoxin monoclonal antibodies. N Engl J Med 1992;326:1153–6.PubMedCrossRefGoogle Scholar
  13. 13.
    Ertel W, Scholl FA, Gallati H, Bonaccio M, Schildberg F, Trentz O. Increased release of soluble tumor necrosis factor receptors into blood during clinical sepsis. Arch Surg 1994; 129:1330–7.PubMedCrossRefGoogle Scholar
  14. 14.
    Fujishima S, Aikawa H. Neutrophil-mediated tissue injury and its modulation. Intensive Care Med 1995;21:277–85.PubMedCrossRefGoogle Scholar
  15. 15.
    Kaplan SL. Bacteremia and endotoxin shock. In: Feigin RD, Cherry JD, editors. Textbook of pediatric infectious diseases. Philadelphia: Saunders, 1992:863–75.Google Scholar
  16. 16.
    Grubb NS, Lyle S, Brodie JH, et al. Clinical guidelines and primary care: management of infants and children 0 to 36 months of age with fever without source. J Am Board Fam Pract 1995;8:114–19.PubMedGoogle Scholar
  17. 17.
    McCarthy PL, Sharpe MR, Spiessel SZ. Observation scales to identify serious illness in febrile children. Pediatrics 1982; 70:802–9.PubMedGoogle Scholar
  18. 18.
    Barlett J. Management of opportunistic infections and miscellaneous conditions. In: Medical management of HIV infection. Glenview, IL: Physician & Scientists, 1994:61–86.Google Scholar
  19. 19.
    Pearson HA. Sickle cell diseases: diagnosis and management in infancy and childhood. Pediatr Rev 1987;9:121–30.PubMedCrossRefGoogle Scholar
  20. 20.
    Minard G, Kudsk KA. Effect of route of feeding on the incidence of septic complications in critically ill patients. Semin Respir Infect 1994;9:228–31.PubMedGoogle Scholar
  21. 21.
    Moore FA, Feliciano DV, Andrassy RJ, et al. Early enteral feeding, compared with parenteral, reduces postoperative septic complications: the results of a meta-analysis. Ann Surg 1992;216:172–83.PubMedCrossRefGoogle Scholar
  22. 22.
    Salzman MB, Rubin LG. Intravenous catheter-related infections. Adv Pediatr Infect Dis 1995;10:337–68.PubMedGoogle Scholar
  23. 23.
    Plouffe JF, Brieman RF, Facklam RR. Bacteremia with Streptococcus pneumoniae: implications for therapy and prevention. JAMA 1996;275:194–8.PubMedCrossRefGoogle Scholar
  24. 24.
    Barker GJ, Call SK, Gamis AS. Oral care with vancomycin paste for reduction in incidence of alpha hemolytic streptococcal sepsis. J Pediatr Hematol Oncol 1995;17:151–5.PubMedCrossRefGoogle Scholar

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© Springer Science+Business Media New York 1998

Authors and Affiliations

  • James M. Herman
  • William J. Curry
  • Edward G. Paul

There are no affiliations available

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