Galankina I E, Permiakov N K
Arkh Patol. 1983;45(1):12-7.
Morphological, including electron microscopical, dynamics of multiply recurrent pulmonary edema in myocardial infarction at intervals of 2 to 35 days is presented. The macroscopical picture of the lesion at that resembles croupous pneumonia. Microscopically, release of large disperse proteins and precipitation of fibrin in alveolar lumens, erythrocyte stasis in capillaries, and lipid vacuoles in their lumens are observed. Subsequently, the fibrin exudate in alveolis undergoes organization and carnification. In diffuse lesions this may cause acute respiratory insufficiency. Pathogenesis and morphogenesis of pulmonary changes as well as their importance in tanatogenesis are discussed. The patterns of changes in the lungs in recurrent edema allowed the authors to classify them as a new kind of pathology of intensive therapy caused by prolongation of the terminal condition.