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Acute lung injury

Dhruv Parekh, Rachel C Dancer and David R Thickett
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DOI: https://doi.org/10.7861/clinmedicine.11-6-615
Clin Med December 2011
Dhruv Parekh
Centre for Translational Inflammation Research, School of Clinical and Experimental Medicine, University of Birmingham
Roles: Research fellow
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Rachel C Dancer
Centre for Translational Inflammation Research, School of Clinical and Experimental Medicine, University of Birmingham
Roles: Clinical lecturer
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David R Thickett
Centre for Translational Inflammation Research, School of Clinical and Experimental Medicine, University of Birmingham
Roles: Reader in respiratory medicine
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  • For correspondence: d.thickett@bham.ac.uk
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    Fig 1.

    (a) The normal alveolus (left) and the injured alveolus (right) in the acute phase of acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS); (b) mechanisms important in the resolution of ALI and ARDS. ATPase = adenosine triphosphatase; ENaC = epithelial sodium channel; IL = interleukin; MIF = macrophage inhibitory factor; PAF = platelet activating factor; TNF = tumour necrosis factor. Reproduced with permission from the New England Journal of Medicine.9

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Acute lung injury
Dhruv Parekh, Rachel C Dancer, David R Thickett
Clinical Medicine Dec 2011, 11 (6) 615-618; DOI: 10.7861/clinmedicine.11-6-615

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Acute lung injury
Dhruv Parekh, Rachel C Dancer, David R Thickett
Clinical Medicine Dec 2011, 11 (6) 615-618; DOI: 10.7861/clinmedicine.11-6-615
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  • Article
    • Historical background
    • Definitions
    • Incidence
    • Clinical risk factors for acute lung injury
    • Pathophysiology
    • Clinical evaluation
    • Initial management of cases
    • Protective ventilation
    • Fluid management
    • Non-conventional ventilation
    • Failed pharmacological therapies for acute lung injury
    • The future
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