Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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Meta Analysis
Frequency and predictors of ventilator-associated pneumonia recurrence: a meta-analysis.
Large clinical series focusing on the risk factors associated with recurrence after the onset of an initial episode of ventilator-associated pneumonia (VAP) produced inconsistent results. A meta-analysis would be helpful to shed light on the issue. Our objective was to estimate the frequency of VAP recurrence and to identify risk factors associated with it. ⋯ There was also evidence, albeit inconsistent, that severity of illness at intensive care unit admission was associated with VAP recurrence. Recurrence involves almost one in four cases of VAP and is associated with acute lung injury/acute respiratory distress syndrome and shock, but not with first-episode causative pathogens. Recognition of these predictors may permit the timely implementation of measures to prevent recurrence of VAP.
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Severe burn causes a pronounced hypermetabolic response characterized by catabolism and extensive protein wasting. We recently found that this hypermetabolic state is driven by a severe inflammatory response. We characterized in detail the kinetics of serum levels of a panel of cytokines in a rat model, which may serve as reference for the development of therapeutic interventions applicable to humans. ⋯ Serum levels of TNF-alpha and vascular endothelial growth factor in burned rats were not found to be significantly different to controls. Burn causes a profound inflammatory response in rats. Specific cytokines known to increase in humans postburn such as IL-1 beta, IL-6, IL-10, MCP-1, and IL-8 (CINC-1, CINC-2, and CINC-3 in the rat) were also observed in our rat burn model, which now allows us to study new anti-inflammatory treatment options.
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Ischemic gut contributes to the development of sepsis and organ failure in critically ill patients. Toll-like receptors (TLRs) have been reported to mediate the pathophysiology of organ damage following ischemia/reperfusion (I/R) injury. We hypothesize that LPS, a ligand for TLR4, decreases mesenteric I/R injury-induced gut damage through tumor necrosis factor alpha (TNF-alpha) signaling. ⋯ Commensal depletion enhances I/R-induced gut damage. LPS prevents I/R-induced intestinal permeability, lipid peroxidation, and decrease in GSH level. Given that the preventive effect of LPS on I/R-induced gut damage and NF-kappaB activity of the intestine is abolished in Tnfrsf1a mice, we conclude that TLR ligand decreases mesenteric I/R injury-induced gut damage through TNF-alpha signaling.