Our increasing ability to keep severely injured trauma patients alive resulted in the clinical syndrome called postinjury multiple organ failure (MOF). As advances in prehospital and acute hospital care conquered “the golden hour” and the trimodal distribution of trauma deaths described in the 1970s and 1980s slowly flattened its first mode, MOF emerged as the leading cause of late trauma death.1–3
Much of advance in the treatment of trauma and shock has been stimulated by military experience.4 In World War I, soldiers’ death on battle was initially attributed to toxins released by dead or dying tissue (Table 61-1).5 Cannon et al, via their observations on the battlefield in 1917, expanded this concept to question the role of hypovolemia; however, it was not until the 1930s that reduced circulating blood volume was recognized as the cause of shock and mortality.6 Casualties in World War II were initially resuscitated with plasma and later with blood. This continued in Korea where blood and plasma were administered until blood pressure returned to normal. In addition to rapid transport for definitive care in field medical units, blood and plasma resuscitation improved battlefield survival but resulted in late deaths due to oliguric renal failure. In the 1960s, Shires et al. proposed that extracellular fluid deficits (third space losses) compounded traumatic shock and demonstrated in animals that survival improved with balanced salt solutions.7 Consequently, crystalloid resuscitation was added to blood and plasma resuscitation in the Vietnam War and resuscitation end points focused on maintaining adequate urine output. Helicopter evacuation also enabled rapid transport of casualties and the overall mortality rate decreased. Although late deaths from renal failure declined, a new entity termed “shock lung” emerged as the primary cause of late deaths.5 This new disorder became recognized in civilian trauma centers as the adult respiratory distress syndrome (ARDS).8 In the 1970s, subsequent improvements in advanced organ support such as mechanical ventilation (MV), vasoactive drugs, total parenteral nutrition, and hemodialysis armed physicians with better treatment to sustain the critically ill. Death from isolated pulmonary failure became rare, and a new syndrome of “multiple, progressive, or sequential systems failure” was recognized.9
Table 61-1 Historical Perspective of Postinjury Multiple Organ Failure |Favorite Table|Download (.pdf)
Table 61-1 Historical Perspective of Postinjury Multiple Organ Failure
|Time Period||Proposed Etiology||Interventions||Clinical Patterns|
|World War I||Wound toxins||Undefined||Cardiac failure|
|World War II||↓ Blood volume||Resuscitate to normal SBP||Renal failure|
|Vietnam War||↓ Blood volume||Resuscitate to normal urine output||Respiratory failure|
|↓ Extracellular fluid||Crystalloid resuscitation|
|Mid-1970s||Shock||Advanced organ support||Multiple organ failure|
|Advanced age sepsis|
|Early 1880s||Uncontrolled infection||Prevent and treat septic complications||Infectious models|
|Late 1980s||Systemic inflammation||Control inciting event||Inflammatory models|
|Bacterial translocation||Attenuate early inflammation|
|1990s||SIRS/CARS||Improved resuscitation end points||Dysfunctional inflammation|
|Avoid secondary events|
|2000 to present||Cellular and subcellular ...|
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