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Cellular and mediator mechanisms that contribute to lung injury in the acute respiratory distress syndrome

  • Herbert Y. Reynolds
Chapter
Part of the Developments in Critical Care Medicine and Anaesthesiology book series (DCCA, volume 1)

Abstract

Acute respiratory failure may develop after diffuse injury to the alveolar-capillary membrane in human and mammalian lungs following a variety of direct insults to airways or after severe systemic injury or disease. The clinical syndrome in adults usually features a latent period after the inciting event before the pathologic sequence is recognizable and progressive respiratory distress ensues; once in progress the severity of lung injury may vary, but mortality from the syndrome is appreciable in most reports. The disease entity is not new, although the current coinage — adult respiratory distress syndrome — is recent [3], and the outpouring of related research publications underscores the contemporary importance of this affliction. The designation, adult respiratory distress syndrome (ARDS), which distinguishes this syndrome from the pathologic changes found in infant hyalin membrane lung disease, conveys a dynamic interaction of clinical, radiographic, and physiologic parameters in the affected patient that mirror pathologic changes thought to be occurring in lung tissue. ARDS imparts an urgency and seriousness in its progression that automatically elicit ominous concern among the patient’s family and medical care personnel because of the morality that the diagnosis portends. It is probable that this type of lung failure was first recognized with reasonable frequency in combat casualties during World War II (1940–45). The combination of advanced surgical methods, intravenous replacement therapy plus rapid removal of the severely wounded to high-technology medical facilities salvaged many soldiers, often suffering hemodynamic shock, with greater success than ever before on battlefield circumstances.

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© Springer Science+Business Media Dordrecht 1982

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  • Herbert Y. Reynolds

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