Introduction

Multiple organ failure remains a leading cause of mortality in intensive care units, with rates as high as 90 per cent, and therefore methods for preventing its development are crucial in the care of the critically ill patient. Major advances have been made in our understanding of the pathophysiology of multiple organ failure, leading to great hopes for new therapies. However, at present the best way of limiting the release of mediators is to identify and remove the cause (e.g. septic focus or devitalized tissue after trauma) and to avoid tissue hypoxia.

The importance of organ, particularly gut, hypoperfusion in the subsequent development of multiple organ failure makes optimal general resuscitation essential. Cornerstones of care include sufficient fluid replacement, adequate oxygenation with respiratory support where indicated, correction of anemia, use of vasopressors where necessary to restore perfusion pressure, and the maintenance of an adequate cardiac output. In addition to these general factors, support for individual failing organs may be required.

Multiple organ failure often starts with an episode of acute circulatory failure, not necessarily frank shock. In these conditions, the function of all organs is altered. Multiple organ failure sometimes appears to affect organs sequentially, starting with the lungs and followed by dysfunction of other organs. However, such a pattern may be related to our ability to diagnose organ dysfunction. For example, lung failure is identifiable early in its course (infiltrates on the chest radiograph and abnormal gas exchange) whereas liver dysfunction is usually recognized by an increase in bilirubin levels, which is a relatively late event. Gastrointestinal dysfunction is even more difficult to define. The likelihood of mortality is related to the number of affected organs and the degree of dysfunction, and can be assessed using various systems such as the Sepsis-related Organ Failure Assessment (SOFA) score.

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