• H P Friedl and O Trentz.
• Departement Chirurgie, Universitätsspital Zürich, Schweiz.
• Unfallchirurgie. 1992 Apr 1; 18 (2): 64-8.

AbstractMultiple organ failure (MOF) following major trauma occurs in response to perfusion deficits, a persistent inflammatory focus, or a persistent focus of dead and/or injured tissue. Several pathophysiologic aspects are considered relevant to current clinical practice. Their application in settings of trauma and surgical sepsis reduces overall mortality and incidence of multiple organ failure. With regard to the pathophysiologic background (I) microcirculatory resuscitation, (II) source control, and (III) metabolic support appear to be important therapeutic principles. (I) Microcirculatory Resuscitation: Since time is a critical factor in damage control, resuscitation and restoration of microvascular perfusion needs to occur as soon as possible if multiple system organ failure is to be avoided during the later time course. (II) Source control: The best treatment for multiorgan failure appears to be prevention. With early, aggressive control or removal of risk factors for multiple organ failure, namely early surgical intervention for control of hemorrhage, control of potential septic sources, decompression, and early fracture stabilization reductions in the incidence and mortality of MOF have been observed. Metabolic support: Malnutrition appears to be an important cofactor in morbidity and mortality. (III) Metabolic support needs to be started early and prior to the phenomenon of nitrogen retention during the hypermetabolic state of multiple organ failure.

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