Abstract
Since its description 30 years ago [1], the acute respiratory distress syndrome (ARDS) has remained a very topical issue for intensivists, with a large literature ranging from the molecular basis of the disease and underlying physiology to the quality of life of survivors. Despite recent advances, the mortality of this syndrome remains 40 to 50% [2, 3]. Part of the difficulty in developing effective therapies is the heterogeneous nature of the disease and its complex pathophysiology. For the most part, the literature on the management of ARDS seems to converge on two basic principles: 1) preventing further injury improves outcomes; and 2) basic initial management strategies have a larger impact on outcome than ‘salvage’ therapies. To a certain extent, these concepts are reflected in the results of all the trials carried out to date. This is not surprising. ARDS is not a disease but a syndrome, characterized by a severe localized inflammatory reaction. Most patients who die with this syndrome do not die from their local disease (pulmonary hypoxemia), but rather they succumb to a systemic inflammatory reaction that ultimately leads to diffuse organ failure. Consequently, it makes sense conceptually that all the approaches directed towards preventing loss of pulmonary compartmentalization of the inflammatory reaction could improve patient outcome, versus salvage therapies that are instituted later in the course of the disease — the proverbial “horse is out of the barn” concept. This idea underscores the fundamental importance of early recognition and appropriate aggressive management of the ARDS patient.
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dos Santos, C.C., Slutsky, A.S. (2002). Advances in ARDS: How do they Impact Bedside Management?. In: Vincent, JL. (eds) Intensive Care Medicine. Springer, New York, NY. https://doi.org/10.1007/978-1-4757-5551-0_30
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DOI: https://doi.org/10.1007/978-1-4757-5551-0_30
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