Critical care medicine
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Critical care medicine · Aug 2011
Review Meta AnalysisSubglottic secretion drainage for the prevention of ventilator-associated pneumonia: a systematic review and meta-analysis.
Aspiration of secretions containing bacterial pathogens into the lower respiratory tract is the main cause of ventilator-associated pneumonia. Endotracheal tubes with subglottic secretion drainage can potentially reduce this and, therefore, the incidence of ventilator-associated pneumonia. New evidence on subglottic secretion drainage as a preventive measure for ventilator-associated pneumonia has been recently published and to consider the evidence in totality, we conducted an updated systematic review and meta-analysis. ⋯ In those at risk for ventilator-associated pneumonia, the use of endotracheal tubes with subglottic secretion drainage is effective for the prevention of ventilator-associated pneumonia and may be associated with reduced duration of mechanical ventilation and intensive care unit length of stay.
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Critical care medicine · Aug 2011
Multicenter Study Comparative StudyRed cell distribution width and all-cause mortality in critically ill patients.
Red cell distribution width is a predictor of mortality in the general population. The prevalence of increased red cell distribution width and its significance in the intensive care unit are unknown. The objective of this study was to investigate the association between red cell distribution width at the initiation of critical care and all cause mortality. ⋯ Red cell distribution width is a robust predictor of the risk of all-cause patient mortality and bloodstream infection in the critically ill. Red cell distribution width is commonly measured, inexpensive, and widely available and may reflect overall inflammation, oxidative stress, or arterial underfilling in the critically ill.
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Critical care medicine · Aug 2011
Comparative StudyDifferential ex vivo and in vivo endotoxin tolerance kinetics following human endotoxemia.
Endotoxin (lipopolysaccharide) tolerance is characterized by a transient refractory state to a subsequent lipopolysaccharide challenge. Following human endotoxemia, ex vivo tolerance of circulating leukocytes to lipopolysaccharide resolves within 24 hrs. However, the duration of in vivo tolerance, assumed to be primarily mediated by tissue-resident macrophages, is unknown. DESIGN, SETTING, SUBJECTS, AND INTERVENTIONS: Clinical experimental study in 16 healthy male volunteers at an intensive care research unit. To compare ex vivo and in vivo tolerance kinetics, whole blood from healthy volunteers was stimulated with lipopolysaccharide before, 4 hrs after, and 1, 2, 3, and 4 wks following in vivo endotoxin (2 ng/kg; lipopolysaccharide derived from Escherichia coli O:113) administration. Furthermore, we compared the inflammatory response during two subsequent endotoxemia experiments in healthy volunteers with an interval of 2 wks. The cytokines tumor necrosis factor-α, interleukin-6, interleukin-10, interleukin-1 receptor antagonist, and transforming growth factor-β were measured. ⋯ While ex vivo lipopolysaccharide tolerance quickly resolves, in vivo lipopolysaccharide tolerance persists for at least 2 wks. These findings strengthen the notion that the in vivo response to lipopolysaccharide is mediated by tissue-resident macrophages and that ex vivo stimulation does not accurately reflect the in vivo innate immune response. Intervention studies utilizing the human endotoxemia model should be performed using parallel groups rather than a crossover design.
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Critical care medicine · Aug 2011
Editorial Comment Comparative StudyPrediction is very difficult, especially about the future-Niels Bohr.