Is MOF an outcome parameter or a transient, adaptive state in critical illness?

The term 'multiorgan failure' (MOF) carries the negative connotation of major homeostatic breakdown and severe malfunction. However, this traditional paradigm may not be necessarily accurate. This review will investigate the rationale for no longer considering MOF to be simply a 'failed' pathophysiological state.

Multiorgan failure is characterized by a hypometabolic, immunodepressed state with clinical and biochemical evidence of decreased functioning of the body's organ systems. Notwithstanding these findings, evidence for cell death is scarce and organ recovery is frequently the rule in surviving patients without pre-existing organ disease. Decreased mitochondrial activity appears to play a key role in the processes underlying MOF, both as a victim and a player. Reduced ATP production will compromise normal metabolic functioning. To protect itself from dying, the cell may adapt by decreasing its metabolic rate, and this is clinically manifest as organ dysfunction. Mitochondrial modulation may thus represent an important therapeutic target.

The concept of MOF could be revisited as a transient state of metabolic shutdown analogous to hibernation. Avoiding the detrimental effects of inappropriate and counter-adaptive iatrogenic interventions is an important cornerstone of therapeutic management.