Shock lung and diffuse alveolar damage pathological and pathogenetic considerations

Abstract

Diffuse alveolar damage may be caused by any one or more of a large number of injurious agents. While the etiology may be diverse, the pathology is relatively uniform ranging from an acute exudative phase characterized by protein-rich interstitial and alveolar edema, through to a reactive subacute proliferative phase characterized by interstitial fibroplasia and collagenization together with granular pneumocyte hyperplasia. Interstitial inflammation is a variable feature and of course mixed exudative and proliferative features are common. In the clinically overt adult respiratory distress syndrome, the mortality is formidable. The pathogenesis is damage to endothelial cells and membranous pneumocytes. This may be caused by direct chemical action or indirectly through the mediation of oxidizing free radicles or leukotrienes. In diffuse alveolar damage associated with shock, recent work suggests mediation of the cellular injury via complement activation following tissue injury, with the major pathology being due to lysosomal enzyme damage from phagocytes chemotactically attracted to the lung. Etiological factors in diffuse alveolar damage are numerous and details of appropriate primary therapy are therefore diverse. The pathogenesis and pathology are however relatively uniform, calling for uniform supportive therapeutic measures of the clinical adult respiratory distress syndrome.