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      Acute lung injury: how to stabilize a broken lung

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          Abstract

          The pathophysiology of acute respiratory distress syndrome (ARDS) results in heterogeneous lung collapse, edema-flooded airways and unstable alveoli. These pathologic alterations in alveolar mechanics (i.e. dynamic change in alveolar size and shape with each breath) predispose the lung to secondary ventilator-induced lung injury (VILI). It is our viewpoint that the acutely injured lung can be recruited and stabilized with a mechanical breath until it heals, much like casting a broken bone until it mends. If the lung can be “casted” with a mechanical breath, VILI could be prevented and ARDS incidence significantly reduced.

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          Most cited references51

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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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                Author and article information

                Contributors
                niemang@upstate.edu
                pla@xmxmail.com
                315.464.1696 , satalinj@upstate.edu
                wilcokai@upstate.edu
                kolliscm@upstate.edu
                mmadden@intensivecareonline.com
                aiashh@upstate.edu
                blairs@upstate.edu
                louis.gatto@cortland.edu
                nmh@xmxmail.com
                Journal
                Crit Care
                Critical Care
                BioMed Central (London )
                1364-8535
                1466-609X
                24 May 2018
                24 May 2018
                2018
                : 22
                : 136
                Affiliations
                [1 ]ISNI 0000 0000 9159 4457, GRID grid.411023.5, Department of Surgery, , SUNY Upstate Medical University, ; 750 E. Adams Street, Syracuse, NY 13210 USA
                [2 ]ISNI 0000 0000 9340 0716, GRID grid.264266.2, Department of Biological Sciences, , SUNY Cortland, ; Cortland, NY USA
                [3 ]ISNI 0000 0001 2175 4264, GRID grid.411024.2, Department of Trauma Critical Care Medicine, , R Adams Cowley Shock Trauma Center, University of Maryland School of Medicine, ; Baltimore, MD USA
                Article
                2051
                10.1186/s13054-018-2051-8
                5968707
                29793554
                3abf330d-e16d-43dd-b929-1ed803637688
                © The Author(s). 2018

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/100000050, National Heart, Lung, and Blood Institute;
                Award ID: R01 HL131143
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                © The Author(s) 2018

                Emergency medicine & Trauma
                acute lung injury,injurious mechanical ventilation,tcav protocol

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