Surgery
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Modern operating rooms are considered to be aseptic environments. The use of surgical mask, frequent air exchanges, and architectural barriers are used to reduce airborne microbial populations. Breaks in surgical technique, host contamination, or hematogenous seeding are suggested as causal factors in these infections. This study implicates contamination of the operating room air as an additional etiology of infection. ⋯ Gram-positive staphylococcal isolates were frequently isolated from air samples obtained throughout the operating room, including areas adjacent to the operative field. Nasopharyngeal shedding from person participating in the operation was identified as the source of many of these airborne contaminants. Failure of the traditional surgical mask to prevent microbial shedding is likely associated with an increased risk of perioperative contamination of biomedical implants, especially in procedures lasting longer than 90 minutes.
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The justification and preference for operative versus nonoperative management of hepatic injuries caused by blunt trauma remains ambiguous. This review assesses the outcome of operative and nonoperative management of liver injury after blunt trauma. ⋯ Selective management of liver injuries presented a low liver-related mortality rate. Low-grade injuries can be managed nonoperatively with excellent results. High-grade injuries can be managed nonoperatively, if operative intervention is not required for hemodynamic instability or associated injuries, with a low mortality. In these patients, adjunctive procedures will be required selectively for successful nonoperative management of high-grade liver injuries. High-grade injuries requiring operative management because of hemodynamic instability or concomitant injuries continue to have significantly higher mortality.
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Postinjury multiple organ failure (MOF) is a result of a dysfunctional inflammatory response to severe injury and shock. Acute lung injury is thought to promote further organ dysfunction by the systemic release of inflammatory mediators from injured lung tissue. Although clinical evidence supports this model, a clear understanding of the relationship between lung dysfunction and multiple organ failure has yet to be defined. We hypothesized that respiratory dysfunction is an early obligate event in the progression of postinjury MOF. ⋯ Postinjury respiratory dysfunction is an obligate event that precedes heart, liver, and kidney failure. The severity of other organ dysfunction is related directly to the severity of respiratory dysfunction. These data implicate lung dysfunction as central to the promotion of pathogenic inflammation and the development of postinjury MOF.
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Intraoperative parathyroid hormone (iPTH) testing often is used during minimally invasive parathyroidectomy for primary hyperparathyroidism (1 degrees HPT). However, several investigators report that these assays are not cost effective and do not improve outcomes significantly. ⋯ iPTH testing improves cure rates in patients undergoing minimally invasive parathyroidectomy. iPTH testing allowed intraoperative recognition and resection of additional hyperfunctioning parathyroids missed by preoperative imaging studies. Consequently, we strongly advocate the routine use of iPTH testing in patients who undergo minimally invasive parathyroidectomy for 1 degrees HPT.
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Vascular endothelial growth factor (VEGF) is a potent vascular mitogen that selectively stimulates vascular smooth muscle cell (VSMC) migration through an unknown mechanism while having no effect on VSMC proliferation. It is known that VSMC migration and proliferation are dependent on the second messenger Ca2+ and, in particular, mitogen-stimulated Ca2+ influx. We hypothesized that the selective effect of VEGF on VSMC migration versus proliferation was a result of differential VEGF-stimulated Ca2+ signaling pathways. ⋯ VEGF induces extracellular calcium influx but no intracellular calcium release in VSMCs. This lack of intracellular Ca2+ release stems from the inability of VEGF165 to activate the PLCgamma1 cascade and IP3 receptor-mediated Ca2+ release. The lack of PI3-K/Akt activation at these time points indicates a novel extracellular Ca2+ influx pathway sufficient to activate CaMKII. A paradigm relating extracellular Ca2+ influx to CaMKII activation and migration is suggested and may account for the selective effects of VEGF on VSMC migration.