title: Pathology of the adult respiratory distress syndrome.
abstract: Despite the wide range of insults that can lead to the development of ARDS, a common sequence of pathologic changes can be identified in the lung. These changes can be divided into three phases: the acute, or exudative, phase (up to 6 days), in which hyaline membranes are a characteristic feature; the subacute, or proliferative, phase (4 to 10 days), in which metaplasia of the alveolar lining cells and early evidence of fibrosis are seen; and the chronic phase (8 days and on), when organizing fibrosis is a major finding. Structural changes of chronic pulmonary hypertension are also found in the patients with ARDS of longer duration. The mechanism by which these pulmonary changes occur is unknown. Studies of experimental models of ARDS may offer the best opportunity to elucidate the mechanisms. For example, a single infusion of E. coli endotoxin into sheep mimics the pathophysiologic changes of ARDS, offering a model for study of the initial insult on the lung. In addition, animals exposed to high concentrations of oxygen also show morphologic changes similar to those seen in patients with ARDS. Whether the hyperoxia is responsible for such changes, or whether it potentiates the injury induced by some other insult, is not certain.
authors.affiliation: Pulmonary Circulation Center, Vanderbilt University School of Medicine, Nashville, Tennessee.
authors.forename: B
authors.initials: B
authors.lastname: Meyrick
mesh_terms: D000818:Animals; D001706:Biopsy; D001792:Blood Platelets / Q000502:physiology; D003167:Complement Activation; D006801:Humans; D007962:Leukocytes / Q000502:physiology; D008168:Lung / Q000473:pathology; D011651:Pulmonary Artery / Q000473:pathology; D011652:Pulmonary Circulation; D012128:Respiratory Distress Syndrome / Q000276:immunology / Q000473:pathology* / Q000503:physiopathology