The epidemiology of critical illness is not well defined. There are several reasons for this. First, at present there are no universally agreed definitions of organ system failure which adequately describe severity independent of therapy. Second, the risk factors which determine susceptibility to critical illness are poorly understood. Third, multiple organ failure is a syndrome, not a disease, and there are likely to be many mechanisms involved. Fourth, in any individual there is a complex interaction between the degree of homeostatic reserve, the severity, site, and multiplicity of the precipitating insult(s), and the specificity and timing of treatment, all of which will influence the appearance of organ system dysfunction. However, certain characteristic patterns may be observed, and it is the development of secondary, or remote, organ failures following initial resuscitation from an acute physiological disturbance, such as trauma or surgery, which has excited the greatest interest.

A characteristic pattern is the multiple trauma patient who is fluid resuscitated, taken to the operating room for fracture stabilization, and then develops progressive organ system dysfunction during the ensuing days in the intensive care unit (ICU), with a systemic inflammatory response which resembles sepsis and is often associated with microbial colonization or infection at different sites, particularly the lungs. In one study ( Sauaia,efal 1995), over 60 per cent of late trauma deaths were a consequence of multiple organ failure. This pattern of an initial insult, usually involving hypovolemic or hypodynamic shock ('ebb phase'), followed later by multiple organ failure and a state that looks like the response to infection ('flow phase') encouraged earlier investigators to assume that organ failures were caused in some way by micro-organisms or their products. While this may be so, there is growing evidence that microbial colonization is a consequence, and not necessarily the cause, of organ failures. Two mechanisms at least are considered to be fundamental to this process: tissue hypoxia and activation of the immunoinflammatory cascade, producing a systemic inflammatory response and cellular injury.

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