Abstract
Introduction The adult respiratory distress syndrome (ARDS) represents a final common pathway of injury due to a large variety of massive, often unrelated, insults to the lung (Table 1). For example, the injury may be a consequence of direct pulmonary damage such as aspiration ofgastric contents or pulmonary contusion or the result of a systemic process such as sepsis or cardiopulmonary bypass. Acute respiratory distress as a consequence of trauma, burms, sepsis and long surgical procedures was described by Moon in 1936. He suggested a direct injury to pulmonary capillary endothelium and plasma extravasation causing pulmonary oedema. More recently, ARDS was described as a distinct clinical entity with many causes (Ashbaugh et al., 1967). cies are present in both syndromes but are a consequence of diffuse lung injury in ARDS, in contrast to a deficiency as a primary aetiology in the infant respiratory distress syndrome. A debate has raged for several years concerning the appropriateness of the present title ARDS. One camp claims that lumping all of the different causes (Table 1) of ARDS together is crucial as the pathophysiology and management is almost always similar regardless of course. Another group passionately argues that we should split ARDS into specific syndromes for each cause. The latter stresses that future insight into mechanisms may lead to specific differences in treatment. We believe that this argument is moot. Lumping helps to identify the remarkable similarities among patients with ARDS while splitting is impor-
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