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Better Late Than Never?

Christian Brun-Buisson, MD; Laurent Brochard, MD

JAMA. 1998;280:182-183.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

The annual incidence of acute respiratory distress syndrome (ARDS) has been estimated at 150000 cases in the United States.¹ Although its outcome may have improved in the past 2 decades,^2-3 ARDS remains associated with a very high mortality, ranging from 35% to 65% of affected patients.^{2, 4} Severe hypoxemia (ie, an oxygenation ratio of PaO₂ to fraction of inspired oxygen [FIO₂] of <200) is the hallmark of the syndrome,¹ but most fatalities result from associated conditions, especially multiple organ failure and sepsis, and less commonly from intractable respiratory failure.²

Acute lung injury and ARDS are characterized by increased permeability of the alveolocapillary membrane, whether caused by direct lung injury, such as pulmonary infection, or indirect lung injury, such as observed in severe sepsis or a host of other nonpulmonary conditions. Extensive research efforts have explored the pathophysiology of cellular pathways and biochemical derangements occurring . . . [Full Text of this Article]

From the Service de Réanimation Médicale (Drs Brun-Buisson and Brochard) and the Institut National de la Santé et de la Recherche Médicale (INSERM) U492 (Dr Brochard), Hôpital Henri Mondor, AP-HP, and Université Paris-XII, Créteil, France.

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