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Adult respiratory distress syndrome: problems and progress.

Introduction The Adult Respiratory Distress Syndrome (ARDS) has been extensively described in human studies as a complex collection of clinical events that result as a sequelae of massive lung injury (1, 2). Since it was first conceptualized in 1967, it has become apparent that ARDS represents the final common pathway of a variety of different and frequently unrelated assaults to the lung. The triad of features, hypoxemia, decreased lung compliance, and pulmonary infiltrations, is now well recognized, and it is estimated that 150,000 cases occur yearly in the U.S. Despite greater sophistication in methods of respiratory support, the mortality remains greater than 60070. Care today of these patients remains supportive very much as it was when ARDS was first recognized as a clinical entity. Attempts to better define the complex pathophysiologic series of events has resulted in the development of many experimental animal models for lung injury, each of which has contributed to our understanding of the syndrome. Unfortunately, all too often these models fall short of mimicking the constellation of physiologic and radiologic consequences of acute lung injury in the human. The exact mechanism of that injury, its amplifiers and modifiers, remains speculative, and this has led to a high degree of frustration among clinicians and basic scientists alike, and has resulted in scientific conferences designed to help elucidate and unravel the many mysteries surrounding ARDS. The purpose of this commentary is to briefly summarize one of these conferences that was held in Dallas, Texas, on June 27-28, 1985. The deliberations of 30 scientists in attendance who are listed at the end of this report redefined the state of our thinking about both experimental and human ARDS.