Abstract

The prevention of multiple organ failure (MOF) represents a major problem in intensive care medicine. Great progress has been made in the immediate resuscitation of the acutely ill patient in the areas of fluid and drug management, emergency surgical management, and technical support so that patients can be maintained alive beyond this acute phase. Yet not uncommonly, even when the resuscitation appears adequate, some patients develop complications, including acute renal failure, acute respiratory failure related to adult respiratory distress syndrome, unexplained alterations in liver blood tests, or unexplained confusion or altered mentation. Once MOF develops, the prognosis is grim in all cases. Although it remains possible to support the individual failing organs for some time, the process then appears irreversible. The focus should therefore be placed on the prevention of MOF, and this approach must be based on the understanding of its development. Because all tissues are involved in this process, to base the prevention of MOF on each individual organ would be naive. A common pathophysiologic basis must be sought to account for the cellular dysfunction of all organs. Patients who develop MOF frequently develop signs of sepsis such as fever, tachycardia, tachypnea, or hypotension. Yet the documentation of an infection is often not possible. The release of inflammatory mediators has been incriminated in this process.’ The gut could be involved, because the ischemic gastrointestinal mucosa could become permeable to bacteria and their products that could then be released into the circulation.2 In these situations progressing to sepsis and MOF, cardiac output is usually normal or increased, so that the adequacy of cardiac function has usually been assumed. However, recent findings force a reevaluation of this assumption.

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