Multiple organ dysfunction syndrome in critical surgical illness.
BACKGROUND
Multiple organ dysfunction syndrome (MODS) is the leading cause of death in surgical patients and in trauma patients who survive the first 24 h. First observed systematically among Vietnam War-era battle casualties who began to survive previously fatal injuries owing to improved evacuation, triage, and resuscitation, only to develop catastrophic manifestations of organ failure never before seen, the syndrome was recognized formally in 1975 as "multiple organ failure." Ensuing observations and investigations, undertaken in large part by surgeon-scientists, have refined our current understanding of MODS, yielding better outcomes.


METHODS
Review and synthesis of pertinent literature with personal observations and recollections of the senior investigator.


RESULTS
The MODS is now recognized as a continuum of physiologic derangements, rather than an all-or-nothing phenomenon. The most common precipitant appears to be ischemia-reperfusion injury, although severe sepsis also is commonplace. Descriptive biology has enhanced the understanding of the pathogenesis and outcomes of MODS, although the therapy is largely supportive, making prevention of paramount importance. Measures such as drotrecogin alfa (activated), intensive insulin therapy, corticosteroids, and low tidal volume ventilation may be effective.


CONCLUSIONS
Although current treatment of MODS remains primarily supportive, the mortality rate appears to be decreasing. Appreciation of the interrelations between the inflammatory and coagulation systems provides hope in the battle against this frequent, elusive, deadly, and costly syndrome.
Barie
Philip S
PS
Department of Surgery, Weill Cornell Medical College, New York, New York, USA. pbarie@med.cornell.edu
Hydo
Lynn J
LJ
Pieracci
Fredric M
FM
Shou
Jian
J
Eachempati
Soumitra R
SR
D016638:Critical Illness; D006801:Humans; D009102:Multiple Organ Failure / Q000209:etiology / Q000503:physiopathology; D011183:Postoperative Complications / Q000209:etiology / Q000503:physiopathology; D013577:Syndrome