Chapter 61: Post-Injury Inflammation and Organ Dysfunction

HISTORICAL PERSPECTIVE: EVOLVING CONCEPTS ON THE PATHOGENESIS OF MULTIPLE ORGAN FAILURE

Our increasing ability to keep severely injured patients alive eventually created a new clinical syndrome known as post-injury multiple organ failure (MOF). As advances in prehospital and acute hospital care conquered “the golden hour”; the trimodal distribution of trauma deaths described in the 1970s and 1980s slowly flattened its first mode and MOF emerged as the leading cause of late trauma death.^1,2,3

Much of the advances in the treatment of trauma and shock have been stimulated by military experience (see Chapter 13)⁴ and refined by research in civilian trauma centers. In World War I, soldiers’ death on the battlefield was initially attributed to toxins released by dead or dying tissue (Table 61-1).⁵ Cannon et al, via observations on the battlefield in 1917, expanded this concept to question the role of hypovolemia; however, it was not until the 1930s that Blalock et al established that reduced circulating blood volume was the dominant cause of shock and mortality.⁶ Casualties in World War II were initially resuscitated with freeze-dried plasma and later with stored whole 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, prompt 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 the addition of 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 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, and was named 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