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      Acute lung injury: how to stabilize a broken lung

      Critical Care
      Springer Nature

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          Has mortality from acute respiratory distress syndrome decreased over time?: A systematic review.

          It is commonly stated that mortality from acute respiratory distress syndrome (ARDS) and acute lung injury (ALI) is decreasing. To systematically review the literature assessing ARDS mortality over time and to determine patient- and study-level factors independently associated with mortality. We searched multiple databases (MEDLINE, EMBASE, CINAHL, Cochrane CENTRAL) for prospective observational studies or randomized controlled trials (RCTs) published during the period 1984 to 2006 that enrolled 50 or more patients with ALI/ARDS and reported mortality. We pooled mortality estimates using random-effects meta-analysis and examined mortality trends before and after 1994 (when a consensus definition of ALI/ARDS was published) and factors associated with mortality using meta-regression models. Of 4,966 studies, 89 met inclusion criteria (53 observational, 36 RCTs). There was a total of 18,900 patients (mean age 51.6 years; 39% female). Overall pooled weighted mortality was 44.3% (95% confidence interval [CI], 41.8-46.9). Mortality decreased with time in observational studies conducted before 1994; no temporal associations with mortality were demonstrated in RCTs (any time) or observational studies (after 1994). Pooled mortality from 1994 to 2006 was 44.0% (95% CI, 40.1-47.5) for observational studies, and 36.2% (95% CI, 32.1-40.5) for RCTs. Meta-regression identified study type (observational versus RCT, odds ratio, 1.36; 95% CI, 1.08-1.73) and patient age (odds ratio per additional 10 yr, 1.27; 95% CI, 1.07-1.50) as the only factors associated with mortality. A decrease in ARDS mortality was only seen in observational studies from 1984 to 1993. Mortality did not decrease between 1994 (when a consensus definition was published) and 2006, and is lower in RCTs than observational studies.
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            New directions in evidence-based policy research: a critical analysis of the literature

            Despite 40 years of research into evidence-based policy (EBP) and a continued drive from both policymakers and researchers to increase research uptake in policy, barriers to the use of evidence are persistently identified in the literature. However, it is not clear what explains this persistence – whether they represent real factors, or if they are artefacts of approaches used to study EBP. Based on an updated review, this paper analyses this literature to explain persistent barriers and facilitators. We critically describe the literature in terms of its theoretical underpinnings, definitions of ‘evidence’, methods, and underlying assumptions of research in the field, and aim to illuminate the EBP discourse by comparison with approaches from other fields. Much of the research in this area is theoretically naive, focusing primarily on the uptake of research evidence as opposed to evidence defined more broadly, and privileging academics’ research priorities over those of policymakers. Little empirical data analysing the processes or impact of evidence use in policy is available to inform researchers or decision-makers. EBP research often assumes that policymakers do not use evidence and that more evidence – meaning research evidence – use would benefit policymakers and populations. We argue that these assumptions are unsupported, biasing much of EBP research. The agenda of ‘getting evidence into policy’ has side-lined the empirical description and analysis of how research and policy actually interact in vivo. Rather than asking how research evidence can be made more influential, academics should aim to understand what influences and constitutes policy, and produce more critically and theoretically informed studies of decision-making. We question the main assumptions made by EBP researchers, explore the implications of doing so, and propose new directions for EBP research, and health policy.
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              Lung stress and strain during mechanical ventilation: any difference between statics and dynamics?

              Tidal volume (VT) and volume of gas caused by positive end-expiratory pressure (VPEEP) generate dynamic and static lung strains, respectively. Our aim was to clarify whether different combinations of dynamic and static strains, resulting in the same large global strain, constantly produce lung edema. Laboratory investigation. Animal unit. Twenty-eight healthy pigs. After lung computed tomography, 20 animals were ventilated for 54 hours at a global strain of 2.5, either entirely dynamic (VT 100% and VPEEP 0%), partly dynamic and partly static (VT 75-50% and VPEEP 25-50%), or mainly static (VT 25% and VPEEP 75%) and then killed. In eight other pigs (VT 25% and VPEEP 75%), VPEEP was abruptly zeroed after 36-54 hours and ventilation continued for 3 hours. Edema was diagnosed when final lung weight (balance) exceeded the initial weight (computed tomography). Mortality, lung mechanics, gas exchange, pulmonary histology, and inflammation were evaluated. All animals ventilated with entirely dynamic strain (VT 825±424 mL) developed pulmonary edema (lung weight from 334±38 to 658±99 g, p<0.01), whereas none of those ventilated with mainly static strain (VT 237±21 mL and VPEEP 906±114 mL, corresponding to 19±1 cm H2O of positive end-expiratory pressure) did (from 314±55 to 277±46 g, p=0.65). Animals ventilated with intermediate combinations finally had normal or largely increased lung weight. Smaller dynamic and larger static strains lowered mortality (p<0.01), derangement of lung mechanics (p<0.01), and arterial oxygenation (p<0.01), histological injury score (p=0.03), and bronchoalveolar interleukin-6 concentration (p<0.01). Removal of positive end-expiratory pressure did not result in abrupt increase in lung weight (from 336±36 to 351±77 g, p=0.51). Lung edema forms (possibly as an all-or-none response) depending not only on global strain but also on its components. Large static are less harmful than large dynamic strains, but not because the former merely counteracts fluid extravasation.
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                10.1186/s13054-018-2051-8

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