J Trauma
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With rising health care costs, methods to decrease length of hospital stay without compromising care are necessary. One area that extends length of stay in trauma patients is inpatient anticoagulation to a therapeutic international normalized ratio. The 1998 American College of Chest Physicians guidelines recommend thromboprophylaxis with low-molecular-weight heparin (LMWH) and oral warfarin in this population. The LMWH Expedited Anticoagulation Program (LEAP) was created with the following goals: to decrease the number of inpatient warfarin days and to reduce overall number of hospital days. ⋯ LEAP has successfully decreased the number of inpatient days on warfarin and total hospital days for trauma patients requiring deep venous thrombosis prophylaxis. These results have substantially decreased health care costs and increased available hospital beds in this era of high hospital occupancy.
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Splanchnic hypoperfusion is believed to be central in the pathogenesis of hemorrhagic shock-induced acute respiratory distress syndrome and multiple organ failure. Our previous work focused on the portal circulation as the conduit for gut-derived mediators of acute respiratory distress syndrome. Our current focus is the proinflammatory effects of postshock mesenteric lymph. We hypothesize that postshock lymph induces neutrophil (PMN)-mediated endothelial cell damage in an intercellular adhesion molecule-1 (ICAM-1)-dependent fashion, and devised a two-insult model to test this hypothesis. ⋯ Postshock mesenteric lymph activates endothelial cells for increased ICAM-1 expression and PMN adherence. Furthermore, postshock lymph acts as an inciting event in a two-event in vitro model of PMN-mediated endothelial cell injury. These findings further substantiate the key mechanistic role of mesenteric lymph in hemorrhagic shock-induced acute lung injury and suggest that ICAM-1 expression is pivotal in the two-event model of multiple organ failure.