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)


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].


Kupffer Cell Multiple Organ Failure Obstructive Jaundice Lower Gastrointestinal Tract Selective Decontamination 
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© Springer-Verlag Berlin Heidelberg 1989

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  • G. Ramsay

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