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 [22].  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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