XXXX /organ failure: the role of the activated macrophage as a metabolic regulator.

@entity1522 @entity295 @entity649 @entity26 @entity409 @entity1735 @entity2495 @entity1578 @entity519 @entity881 @entity204 @entity130
@entity881 continues as the main cause of @entity204 after burns, @entity130 and @entity295 . This clinical syndrome represents the transition from a hypermetabolic response to injury to a setting of clinical organ failures and @entity204 . Risk factors include: perfusion deficits, persistent foci of dead or injured tissue, an uncontrolled focus of infection, the presence of the @entity649 , persistent @entity2495 , and preexisting @entity409 . Once in the @entity881 , most treatment modalities become progressively ineffective, including: ventilation, antibiotics, nutrition, and surgery. The best treatment remains prevention with rapid control of the source and restoration of @entity26 transport. The response to injury involves alterations in physiology and in the metabolism of @entity1735 , fat and @entity1522 . These changes seem to reflect the modulation of the end-organs by the mediator systems activated in response to the stress stimulus. The transition from @entity2495 to organ failure appears to reflect the clinical appearance of @entity1578 . It is currently hypothesized that this @entity1578 represents a state of regulatory dysfunction induced by the activated hepatic macrophage, the Kupffer cell. This same process may also influence metabolic failure in other organs where this cell-cell regulation can occur, e.g. kidney, lung. The activation of these macrophages is hypothesized to represent the final stage of a series of continuous stimulating events, eg. @entity519 , endotoxin, bacteria, and gut translocated toxins. The precise monokine(s) responsible are not yet completely characterized. Treatment consists of the modalities outlined above and the employment of aggressive metabolic (nutritional) support.
