Pathophysiology of Concurrent Trauma and Exsanguination.
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Trauma continues to remain the leading cause of morbidity and mortality in the developed countries. Hemorrhage is the second most common cause of death DÑ–er trauma, only outnumbered by traumatic brain injury. Exsanguinating hemorrhage is the most common cause of mortality in the first hour of arrival to a trauma center and accounts for almost half of deaths in the first 24 h. In addition, about 20-40% of trauma deaths that occur DÑ–er hospital admission usually involve massive hemorrhage, in which death is potentially preventable. Although the resuscitation protocols and management strategies for resuscitation of patients with exsanguinating hemorrhage have evolved in the past two decades, mortality among these patients remains high. Ðe type and site of injury are detrimental to the pathophysiology and to the outcome of traumatic exsanguination. While a penetrating injury rapidly provokes hypovolemia and its sequel, a blunt trauma and bleeding from extensive tissue damage triggers a strong inflDmmDtory response. Trauma to the head or to the pelvis is associated with significDnt mortality and morbidity particularly when accompanied by progressive or uncompressible hemorrhage. Ðe pathophysiology of traumatic exsanguination encompasses four major pillars: I) Profound depletions of cellular energy stores; II) Progressive end-organ vasoconstriction and hypo-perfusion; III) Exaggerated systemic inflDmmDtory response (SIR); and IV) Obligatory fluid shiÑ–s and failure of early fluid mobilization. Ðese four pillars are interdependent and interact in a vicious circle pattern to determine the outcome from a traumatic exsanguination.
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