Pathophysiology of Concurrent Trauma and Exsanguination
Trauma continues to remain the leading cause of morbidity and mortality in the developed countries. Hemorrhage is the second most common cause of death after 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 after 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. The 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 traumaand bleeding from extensive tissue damage triggers a strong inflammatory response. Trauma to the head or to the pelvis is associated with significant mortality and morbidity particularly when accompanied by progressive or uncompressible hemorrhage. The 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 inflammatory response (SIR); and IV) Obligatory fluid shifts and failure of early fluid mobilization. These four pillars are inter-dependent and interact in a vicious circle pattern to determine the outcome from a traumatic exsanguination.
Obligatory fluids shifts occur during traumatic exsanguination due to the cellular ionic disequilibrium, and to the perturbations of the physiologic imbalance of the Starling forces that govern the trans-capillary fluid exchange [9,10]. Several mechanisms contribute to the cellular swelling. Depletion of cellular energy stores during traumatic exsanguination impairs the energy-dependent Na+-K+-ATPase function to eventually lead to Na+ accumulation and cellular swelling . Cellular swelling is also favored by the accumulation of extracellular K+ concentration, lactic academia and as seen in the brain by glutamate, which stimulates cationic receptors and subsequent accumulation of Na+, depolarization and uptake of Cl- [23-26].Remarkable Na+/H+ exchanger-mediated endothelial cell swelling was observed in intestinal capillaries in hemorrhagic shock [8-10]. This is presumably due to cytosolic acidosis from the increased PCO2 and the lactic acid build up from the anaerobic glycolysis, and from the effects of cytosolic acidification on the cell volume regulatory mechanisms.
In summary, the pathophysiology of concurrent trauma and exsanguinations consists of complex interactions at the molecular, cellular, and tissue levels of dysfunctions created by a cytosolic energy failure and sustained by ischemic hypoxia. These dysfunctions interact with each other in a cause-effect relationship and a vicious circle pattern to finally result in death from cardio-circulatory arrest.
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