J Trauma
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Despite recent advances in the management of severe hepatic injuries, the operative mortality rate of grade V hepatic injuries still ranges from 67% to 80%. Grade V hepatic injuries involving the retrohepatic cava or main hepatic veins are almost always lethal, especially those from blunt trauma. The purpose of this study is to understand the risk factors determining operative mortality in grade V blunt hepatic trauma, and to try to improve the surgical management of these injuries. ⋯ Initial base deficit and total intraoperative blood loss were the significant factors that determined operative mortality after grade V blunt hepatic trauma. We suggest that prompt resuscitation and expeditious and appropriate surgical management, to control operative blood loss, is the only way to reduce operative mortality in patients with grade V blunt hepatic trauma.
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Comparative Study
Effect of rate and inspiratory flow on ventilator-induced lung injury.
We examined the effects of decreasing respiratory rate (RR) at variable inspiratory times (It) and reducing inspiratory flow on the development of ventilator-induced lung injury. ⋯ High-pressure ventilation for 6 hours using conventional flow patterns produces severe lung injury, irrespective of RR or It. Reduction of inspiratory flow at similar PIP provides pulmonary protection.
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Comparative Study
Characteristics of infection and leukocyte count in severely head-injured patients treated with mild hypothermia.
This study was designed to characterize the infectious complications and kinetics of leukocyte count in severely head-injured patients treated with mild hypothermia. ⋯ Infectious complications were more severe and leukocyte counts were lower in patients treated with mild hypothermia, who also had the highest initial intracranial pressures, than in patients treated with conventional therapies. Measures against increased susceptibility to infection and leukocyte suppression should be explored.
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No previous studies have examined actions of adenosine or related compounds after blunt chest trauma, but we have shown that the prototype adenosine-regulating agent, acadesine (aminoimidazole carboxamide ribonucleotide [AICAR]), has multiple favorable anti-inflammatory actions after other forms of trauma, ischemia, hemorrhage, and sepsis; and that a progressive inflammatory response in the contralateral (uninjured) lung after unilateral blunt chest trauma is caused (in part) by activation and sequestration of circulating leukocytes (white blood cells [WBCs]). Thus, we hypothesized that AICAR would ameliorate WBC-dependent, secondary pathophysiologic changes after blunt chest trauma. ⋯ Pretreatment with AICAR before experimental pulmonary contusion ameliorates the trauma-induced destruction of the alveolar capillary membrane, and attenuates the delayed secondary injury in the contralateral uninjured lung, by a mechanism that may be independent of leukocytes. Endogenous adenosine could have a role in the pathophysiologic response after blunt chest injury, with potential sites of action including the endothelium and alveolar macrophage. Adenosine-regulating agents may have therapeutic potential after blunt chest injury, but further studies are needed in clinically relevant models, with administration begun at the time of resuscitation.