J Trauma
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Intra-abdominal hypertension and abdominal compartment syndrome cause significant morbidity and mortality in surgical and trauma patients. Maintenance of intravascular preload and use of open abdomen techniques are essential. The accuracy of pulmonary artery occlusion pressure (PAOP) and central venous pressure (CVP) in patients with intra-abdominal hypertension has been questioned. ⋯ RVEDVI is superior to PAOP and CVP as an estimate of preload status in patients with an open abdomen.
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Immune responses are markedly depressed very early after the onset of hemorrhage. Furthermore, endothelial cell dysfunction occurs after trauma-hemorrhage and may contribute to alterations in immune function. Recent studies have shown that administration of L-arginine restores the depressed organ blood flow, probably because of the provision of substrate for constitutive nitric oxide synthase. It remains unknown, however, whether administration of L-arginine would have any salutary effect on the depressed macrophage function after trauma-hemorrhage. ⋯ L-Arginine administration after trauma-hemorrhage significantly improves the depressed macrophage function, presumably by decreasing the increased plasma IL-6 levels and improving organ blood flow. Early enhancement of the depressed constitutive nitric oxide synthase activity by provision of L-arginine after trauma-hemorrhage, therefore, represents a novel and safe approach for improving the depressed immune function and decreasing plasma IL-6 levels under such conditions.
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We conducted this study to determine whether the dry fibrin sealant dressing (DFSD) would stop bleeding from a grade V liver injury and to evaluate the effects of leaving the absorbable DFSD in survival animals. ⋯ In this model of grade V liver injury, blood loss with the DFSD was 51% of that observed with standard gauze packing (not statistically different). Initial survival data revealed no complications attributable to the fibrin dressing. DFSD may provide simple, rapid, and definitive hemorrhage control in life-threatening liver injuries without the need for reoperation.
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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.