Multiple organ failure syndrome.

Abstract

Tissue injury, whether from infection, blood or volume loss, trauma, or inflammation such as pancreatitis, induces local and systemic responses. The systemic responses include shock, reperfusion, systemic inflammation (hypermetabolism) with primary organ dysfunction, and secondary organ dysfunction that either becomes progressive and leads to death or from which the patient recovers and enters into a period of prolonged rehabilitation. Each of these responses has its pathogenesis and treatments that are appropriate and effective. The research indicates that the responses may contribute to the development of cell and organ injury and to progressive multiple organ failure syndrome and death, particularly in the case of the systemic inflammatory response. Current therapy is designed to rapidly remove the cause of injury, resuscitate the microcirculation, and institute nutrition therapy to prevent single and generalized nutrient deficiencies and promote repair and healing. Newer therapies are designed to modulate the inflammatory response itself to minimize its injury potential and promote tissue repair and recovery of the patient. Genetic regulation of metabolism is also a pathogenetic mechanism. Its role in these responses is just starting to be understood--new therapies will need to await this understanding. Once the patient begins to recover, rehabilitation tends to be long and problematic. Nonetheless, significant survival rates are now occurring, with continued improvements expected in response to the newer therapeutic approaches. Planned rehabilitation thus becomes an important component of effective recovery. Professionals trained in critical care and well versed in cellular and molecular biology provide the milieu within which continued improvements in prevention, therapy, and outcome will continue to occur.