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Endotoxaemia in Multiple Organ Failure: A Secondary Role for SDD?

  • G. Ramsay
Part of the Update in Intensive Care and Emergency Medicine book series (UICM, volume 7)

Abstract

The final common pathway which leads to a fatal outcome in the majority of non-surviving patients within an intensive care unit (ICU) is multiple organ failure (MOF). This is true regardless of whether the patients are suffering from multiple trauma, burns, or postoperative sepsis. Infection is present in virtually all critically ill patients who go on to develop multiple organ failure, and the incidence of acquired infection within ICUs is extremely high. The infection rate of patients whose stay in intensive care exceeds 5 days can be as high as 80% [1–3]. Until recently, it was widely believed that infection, particularly recurrent infection, was responsible for initiating the MOF syndrome. This was a not unreasonable hypothesis since up to 80% of late deaths in trauma and 75% of all deaths in burn patients are related to infection. However, the results of a recent study have laid open to question the hypothesis that there is a causal link between recurrent: infection and MOF. In the Western Infirmary, Glasgow, an SDD regime was recently applied, as part of a trial, to all patients admitted to a single ICU [4]. In that study, SDD resulted in a reduction in secondary infection from 24% to 10%, these results included a sixfold reduction in secondary pneumonia. Despite this, the mortality rate in the SDD group was identical to that in the control group. Patients in the SDD group still died of MOF, but in the absence of infection. These results suggest that the previously observed link between infection and MOF was not a causal one. An alternative hypothesis for. the pathogenesis of MOF in these patients is that endotoxin, particularly endotoxin of endogenous source, is the trigger [5].

Keywords

Kupffer Cell Multiple Organ Failure Obstructive Jaundice Lower Gastrointestinal Tract Selective Decontamination 
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.
    Thorp JM, Richards WG, Telfer ABM (1979) A survey of infection in an intensive care unit. Anaesthesia 34: 643PubMedCrossRefGoogle Scholar
  2. 2.
    Northey D, Adess ML, Hartsock JM et al (1974) Microbiologie surveillance in a surgical intensive care unit. Surg Gynecol Obstet 139: 321PubMedGoogle Scholar
  3. 3.
    Stoutenbeek C, van Saene HKF, Miranda DR et al (1984) The effect of selective decontamination of the digestive tract on colonisation and infection rate in multiple trauma patients. Int Care Med 10: 185CrossRefGoogle Scholar
  4. 4.
    Ledingham IMcA, Alcock SR, Eastaway AT et al (1988) Triple regimen of selective decontamination of the digestive tract, systemic cefotaxime and microbiological surveillance for prevention of acquired infection in intensive care. Lancet 1: 785PubMedCrossRefGoogle Scholar
  5. 5.
    Ramsay G, Ledingham IMcA (in press) Management of multiple organ failure, control of the microbial environment. In: Cerra F, Bihari D (eds) New horizons textbook of critical care medicine. SCCM, Los Angeles (in press)Google Scholar
  6. 6.
    Ledingham IMcA, McCartney AC, Ramsay G, Wright (1988) Endotoxins as mediators. Prog Clin Biol Res 264: 125PubMedGoogle Scholar
  7. 7.
    Ramsay G, Newman PM, McCartney AC, Ledingham IMcA (1988) Endotoxaemia in multiple organ failure due to sepsis. Prog Clin Biol Res 272: 237PubMedGoogle Scholar
  8. 8.
    McCartney AC, Piotrowicz BI, Edlin S, Ledingham IMcA (1988) Measurement of endotoxin in the acute phase of septic shock. Prog Clin Biol Res 272: 225PubMedGoogle Scholar
  9. 9.
    Tracey KJ, Lowrie SF, Cerami A (1987) Physiological responses to hectin. In: Tumour necrosis factor and related cytotoxins, Ciba Foundation Symposium No. 131. Wiley, Chichester, pp 88Google Scholar
  10. 10.
    Natanson C (in press) Microbial toxins. In: Cerra F, Bihari D (eds) New horizon textbook of critical care medicine. SCCM, Los AngelesGoogle Scholar
  11. 11.
    Fine J (1984) The bacterial factor in traumatic shock. In: Page IM, Corcoran AG (eds). American Lecture Series, Thomas, IllinoisGoogle Scholar
  12. 12.
    Pardy BJ, Spencer RC, Dudley HAF (1977) Hepatic reticuloendothelial protection against bacteraemia in experimental haemorrhagic shock. Surgery 81: 193PubMedGoogle Scholar
  13. 13.
    Jacob AI, Goldberg PT, Bloom N, Degenshein GA, Kozinn PJ (1977) Endotoxin and bacteria in portal blood. Gastroenterol 72: 1268Google Scholar
  14. 14.
    Wellman W, Fink PC, Vernier F et al (1986) Endotoxaemia in active Krohns disease. Treatment with whole gut irrigation and 5-aminosalicylic. Gut 27: 814CrossRefGoogle Scholar
  15. 15.
    Bailey ME (1976) Endotoxin, bile salts and renal function in obstructive jaundice. Br J Surg 63: 774PubMedCrossRefGoogle Scholar
  16. 16.
    Cahill CJ (1983) Prevention of post-operative renal failure in patients with obstructive jaundice — the role of bile salts. Br J Surg 70: 590PubMedCrossRefGoogle Scholar
  17. 17.
    Pain JA, Bailey ME (1986) Experimental and clinical study of lactulose in obstructive jaundice. Br J Surg 73: 775PubMedCrossRefGoogle Scholar
  18. 18.
    Gilmour DG, Aitkenhead AR, Hothersall A et al (1980) The effect of hypovolaemia on colon blood flow in the dog. Br J Surg 67: 82PubMedCrossRefGoogle Scholar
  19. 19.
    Rayner R, McLean LD, Grim E (1960) Intestinal tissue capillary blood flow in shock due to endotoxin. Circ Res 8: 1212PubMedGoogle Scholar
  20. 20.
    Banks JG, Fowlis AK, Ledingham IMcA et al (1982) Liver function in septic shock. J Clin Pathol 35: 1249PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1989

Authors and Affiliations

  • G. Ramsay

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