J Trauma
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Hypercoagulability is a major source of morbidity and mortality after injury. A resuscitation regimen that modulates this coagulopathy may prove beneficial. We sought to evaluate the effects of lactated Ringer's (LR) solution and Hextend on the resuscitation of uncontrolled hemorrhagic shock. ⋯ Modulation and restoration of normal coagulation is critical in the management of trauma patients. The patient's coagulation profile might determine the type of fluid to be used at various times during their course. Thrombelastography is superior to routine coagulation assays for the detection of a hypercoagulable state. Resuscitation with Hextend results in a decreased fluid requirement and attenuation of hypercoagulability after injury without increased blood loss.
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"Off-label" use of human coagulation factor VIIa (FVIIa) is presently restricted to patients in extremis at our institution. Although bleeding will diminish in most patients, some will still die early as a result of irreversible shock and/or rebleeding. Futile administration of FVIIa significantly increases the economic burden of this expensive therapy and therefore limits its availability. On the basis of both human and in vitro studies, profound acidosis may be expected to predict lack of response. In addition, the depth of hemorrhagic shock, as defined by the degree of hypoperfusion over a given period of time, may be predictive of failure of FVIIa administration. We hypothesized that retrospective review of FVIIa use would identify variables associated with clinical futility. ⋯ Profound acidosis and coagulopathy may predict failure of FVIIa therapy. Depth of hemorrhagic shock, as described by the RTS, was also associated with futile administration. These variables should be considered as potential contraindications to the use of FVIIa. Earlier administration of FVIIa, before the development of massive blood loss and severe shock, may increase the rate of clinical response.
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To investigate whether multiple imputation (MI) of missing Glasgow Coma Scale (GCS) values generates more accurate GCS frequency distributions and less biased parameter estimates in logistic regression models predicting mortality than the standard procedure of excluding observations with missing GCS values. ⋯ MI is a valid solution to the problem of missing GCS data in trauma research. It allows the conservation of precious data observations and leads to unbiased estimates in consequent analyses. Analyses, which exclude observations with missing GCS data, provide biased results.
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Alcohol-related injuries comprise a large percentage of injuries in the United States. As the impact of these injuries on society increases, a well-functioning trauma system becomes increasingly important. ⋯ Further, evidence supports the effectiveness of brief intervention programs to reduce alcohol-related injuries and demonstrates that trauma centers can improve patient outcomes by integrating them into care. Although many obstacles have inhibited progress and made implementing preventive interventions a difficult task, economic constraints are among the biggest challenges to implementing intervention programs as part of routine trauma care.
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In sepsis, activation of inflammatory cells and excessive production of proinflammatory cytokines leads to tissue injury, multiple organ failure, and death. We postulated that attenuation but not complete abrogation of hyperinflammation is of clinical benefit in sepsis. Because pentoxifylline (PTX) is known to decrease tumor necrosis factor (TNF)-alpha production and to increase anti-inflammatory cytokine synthesis, we tested the hypothesis that PTX treatment would change the pro- and anti-inflammatory balance and decrease mortality in a murine model of acute endotoxemia. In addition, we investigated the effects of PTX on nuclear factor (NK)-kappaB activation using lipopolysaccharide (LPS)-stimulated human peripheral blood mononuclear cells (PBMCs) as a model. ⋯ PTX enhances anti-inflammatory activity and decreases mortality in acute endotoxemia. PTX may be an important adjunct to therapies aiming to modulate the inflammatory response in sepsis.