J Trauma
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Postinjury neutrophil (PMN) priming identifies the injured patient at risk for the subsequent development of multiple organ failure (MOF). PMN priming has previously been shown to cause enhanced release of proteases and superoxide. PMNs, however, are a rich source of proinflammatory cytokines, such as interleukin (IL)-8 and tumor necrosis factor (TNF), which have been implicated in the development of MOF. PMNs also make IL-1ra, which is an anti-inflammatory cytokine that inhibits IL-1. It is our hypothesis that postinjury PMNs are primed for increased stimulated release of the proinflammatory cytokines IL-8 and TNF but not the anti-inflammatory cytokine IL-1ra. ⋯ After injury, PMNs are primed for proinflammatory cytokine release in addition to superoxide and elastase. This augmented release of IL-8 and TNF may be involved in the subsequent development of organ dysfunction and ultimately MOF.
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The extent to which severely injured patients receive definitive care at trauma centers is determined by the accuracy of prehospital major trauma criteria in predicting severe injuries and by the level of compliance with these triage instructions by prehospital providers. This study was conducted to evaluate the level of compliance with triage criteria in an established trauma system. ⋯ The majority of patients meeting prehospital major trauma criteria were transported to designated trauma centers. Patients meeting only physiology criteria, however, were much less likely to be transported to trauma centers, and there was a differentially low compliance for elderly trauma patients meeting physiology criteria alone. The causes and consequences of lower compliance with triage instructions for the elderly population deserve further investigation.
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Although rapid fluid resuscitation continues to be an important component of the initial therapy for trauma patients, it remains unknown whether the rate of fluid administration after trauma-hemorrhage has any deleterious or beneficial effects on immunity. ⋯ These results suggest that a slower rate of fluid resuscitation after trauma-hemorrhage leads to a faster restoration of the depressed cell-mediated immunity, whereas rapid fluid resuscitation produces a prolonged depression of immune responses. In view of this, we propose that a prospective clinical study of this type must be performed in a select group of trauma patients to determine whether or not a slower rate of fluid resuscitation also improves immune responses in trauma patients.