The Gut-Origin Septic States

  • J. R. Border
Conference paper


The gut contains sufficient bacteria and toxins to kill the host millions of times over. In normal life these toxic entities are confined to the gut by processes dependent upon food ingestion, defecation, the interactions of the gut associated lymphoid tissue and the systemic immune system, and the function of various valves such as the glottis and gastro esophageal junction. Food ingestion stimulates salivary gland secretion, stomach digestion, biliary tract secretions, replication of enterocytes, mucous secretion, and growth of commensal bacteria. Secretory IgA is delivered to the lumen of the gut by the salivary gland, biliary tract secretions and in mucous. Secretory IgA binds to bacteria and thus prevents binding of the bacteria to the enterocyte in preparation for penetration. The gut mucosa wall is continually renewed by a process of cell and mucous shedding which also aids in preventing bacterial binding and penetration. Finally, commensal bacteria bind to the enterocytes where they consume available nutrients, prevent pathogenic bacteria binding, and release metabolites toxic to pathogenic bacteria. It is the growth of commensal bacteria that is the primary factor that prevents growth of pathogenic bacteria in the gut.


Injury Severity Score Positive Blood Culture Commensal Bacterium Septic State Original Injury 
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.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Riska EB, Von Bonsdorff H, Hakkinen S, Jaroma H, Kiviluoto O, Paavilainen T (1976) Prevention of fat embolism by early internal fixation of fractures in patients with multiple injuries. Injury 6: 110–116CrossRefGoogle Scholar
  2. 2.
    Riska E, Von Bonsdorff H, Hakkinen S (1977) Primary operative fixation of long bone fractures in patients with multiple injuries. J Trauma 17: 111–121PubMedCrossRefGoogle Scholar
  3. 3.
    Wolff G, Dittman M, Ruedi T, Allgower M (1978) Koordination von Chirurgie und Intensivmedizin zur Vermeidung der posttraumatischen respiratorischen Insuffizienz. Unfallheilkunde 81: 425–442PubMedGoogle Scholar
  4. 4.
    Goris R, Gimbrere J, Van Niekerk J, Schoots F, Booy L (1982) Early osteosynthesis and prophylactic mechanical ventilation in the multiple trauma patient. J Trauma 22: 895–903PubMedCrossRefGoogle Scholar
  5. 5.
    Meek R, Vivoda E, Crichton A (1981) A comparison of mortality in patients with multiple injuries according to the method of fracture treatment. J Bone Joint Surg [Br] (63 b): 465Google Scholar
  6. 6.
    Meek R, Vivoda E, Pirani S (1986) Comparison of mortality of patients with multiple injuries according to type of fracture treatment: a retrospective age and injury matched series. Injury 17: 2–4PubMedCrossRefGoogle Scholar
  7. 7.
    Johnson KD, Cadami A, Seibert G (1985) Incidence of adult respiratory distress syndrome in patients with multiple musculoskeletal injuries. J Trauma 25: 375–385PubMedCrossRefGoogle Scholar
  8. 8.
    Bone L, Johnson K, Weigett J (1989) Prospective randomized study of early versus delayed femoral fracture stabilization. J Bone Joint SurgGoogle Scholar
  9. 9.
    Lozman J, Deno C, Feusetel P, Hewell J, Stratton H, Sedraush N, Detton R, Fortune J, Shah D (1986) Pulmonary and cardiovascular consequences of immediate fixation or conservative management of long bone fractures. Arch Surg 121: 992–1000PubMedCrossRefGoogle Scholar
  10. 10.
    Seibel R, LaDuca J, Hassett J, Babikian G, Mills B, Border D, Border J (1985) Blunt multiple trauma (ISS 36), femur traction, and the pulmonary failure septic state. Ann Surg 202: 283–295PubMedCrossRefGoogle Scholar
  11. 11.
    Border JR (1982) Trauma and sepsis. In: Worth MH (ed) Principles and practice of trauma care. Williams and Wilkins, Baltimore, pp 330–388Google Scholar
  12. 12.
    Alexander JW, Macmillan BG, Stinnet JD, Ogle G, Bozian R, Fischer JE, Oakes J, Morris M, Krummnel R (1980) Beneficial effects of aggressive protein feeding in severely burned children. Ann Surg 192: 505–518PubMedCrossRefGoogle Scholar
  13. 13.
    Antonacci A, Cowles S, Reaves L (1984) The role of nutrition in immunologic function. Infect Surg 3: 590–597Google Scholar
  14. 14.
    Border J, Hassett J, LaDuca J, Seibel R, Steinberg S, Mills B, Losi P, Border D (1987) The gut origin of septic states in blunt multiple trauma (ISS = 40) in the I.C.U. Ann Surg 206: 427–448PubMedCrossRefGoogle Scholar
  15. 15.
    Border J (1988) Hypothesis: Sepsis, multiple systems organ failure, and the macrophage. Arch Surg 123: 285–287PubMedCrossRefGoogle Scholar
  16. 16.
    Marshall J, Meakins J, Christou N (1988) Small bowel bacterial overgrowth and systemic immunosuppression in a rat model of intra-abdominal sepsis. Program Society University Surgeons, San Antonio, 11–13 Feb, 1988, p 62Google Scholar
  17. 17.
    Alverdy J, Sang Chi H, Sheldon G (1985) The effect of parenteral nutrition on gastro-intestinal immunity: the importance of enteral stimulation. Ann Surg 202: 681–685PubMedCrossRefGoogle Scholar
  18. 18.
    Alverdy J, Aoyes E, Moss G (1988) Total parenteral nutrition promotes bacterial translocation from the gut. Program Society University Surgeons, San Antonio, 11–13 Feb, 1988, p 23Google Scholar
  19. 19.
    Deitch E, Bridges W, Baker J, Jing W, Berg R, Granger N (1988) Hemorrhagic shock induced bacterial translocation is reduced by blocking xanthine oxidase activity. Program Society University Surgeons, San Antonio, 11–13 Feb, 1988, p 24Google Scholar
  20. 20.
    O’Dwyer S, Michie H, Zeigler T, Reohaug A, Smith R, Wilmore D (1988) A single dose of endotoxin increases intestinal permeability in man. Program Surgical Infection Society, San Francisco, 5–6 May, 1988Google Scholar
  21. 21.
    Zeigler T, O’Dwyer S, Demling R, Smith R, Wilmore D (1988) Increased intestinal permeability associated with infection in burn patients. Program Surgical Infection Society, San Francisco, 5–6 May, 1988Google Scholar
  22. 22.
    Dunn D, Priest B, Condie R (1988) Protective effect of polyclonal and monoclonal antibodies directed against endotoxin during experimental sepsis. Program Surgical Infection Society, San Francisco, 5–6 May, 1988Google Scholar
  23. 23.
    Jacobs D, Evans G, Smith R, Wilmore D (1988) Combined effect of glutamine and epidermal growth factor (EGF) on G.I. mucosal cellularity. Program Society University Surgeons, San Antonio, 11–13 Feb, 1988, p 51Google Scholar
  24. 24.
    Mochiguki H, Trocki O, Dominioni L, Brackett K, Jaffe S, Alexander J (1984) Mechanism of prevention of postburn hypermetabolism and catabolism by early enteral feeding. Ann Surg 200: 297–310CrossRefGoogle Scholar
  25. 25.
    Arita H, Agle C, Alexander J (1988) Continuous administration of low dose endotoxin through the portal vein induces hypometabolism in guinea pigs. Program Surgical Infection Society, San Francisco, 5–6 May, 1988Google Scholar

Copyright information

© Springer-Verlag, Berlin Heidelberg 1989

Authors and Affiliations

  • J. R. Border

There are no affiliations available

Personalised recommendations