Journal of the American College of Surgeons
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Some authors have stated that virtually all patients with penetrating colon injuries can be safely managed with primary repair. The purpose of this study is to test the applicability of this statement to all trauma patients by evaluating a protocol of liberal primary repair applied to a group of patients at high risk of septic complications. ⋯ On the basis of these data and the relative infrequency of patients in prospective randomized trials with destructive colon injuries, we believe there is still room for consideration of fecal diversion in patients in high-risk categories with destructive colon injuries requiring resection.
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Neutrophil infiltration is a characteristic feature of the hepatic injury associated with prolonged hypotension. Previous work has already stressed the important contribution of neutrophil-endothelial cell interactions in the organ injury seen after hemorrhagic shock. Single-blockade strategies using monoclonal antibodies (MAbs) against either selectin or integrin receptors have been demonstrated to be effective in limiting the tissue inflammatory response observed in this clinical disorder. One unexplored topic is the additive effect(s) and the potential antiinflammatory properties of the combined blocking of P-selectin plus beta2-integrin in the liver inflammatory response after uncontrolled hemorrhagic shock in rats. ⋯ These results indicate that dual-blockade strategies aimed at P-selectin and beta-integrin provided a protective effect in the liver inflammatory response after uncontrolled hemorrhagic shock in rats. Although dual blockade was more effective than either individual blockade alone, questions remain about the possible redundancy in the inflammatory adhesion pathways after this clinical condition.
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The side effects of acute elevations in intraabdominal pressure (IAP) are related to a multifactorial etiology. Previous studies have reported that acute elevations in IAP produce an immediate increase in intracranial pressure (ICP). This study was designed to analyze the reasons for increased ICP during acute elevations of IAP and to determine the combined effects of IAP and changes in ventilation indices on ICP and hemodynamic indices. ⋯ Acutely increased IAP displaces the diaphragm cranially, narrowing the IVC and increasing intrathoracic pressure. This increases CVP and increases ICP by venous stasis and increased pressure in the sagittal sinus with decreased resorption of cerebrospinal fluid. Hemodynamic changes are directly related to the rise in ICP. Hypoventilation and hypercarbia significantly increase ICP when compared with hyperventilation and hypocarbia. Hyperventilation does not significantly decrease ICP during acute elevations of IAP.