Brown Induration of the Lung

BROWN INDURATION OF THE LUNG, brown induration of the lungs, induratio fusca pulmunum, occurs as a result of prolonged venous blood congestion in the lesser circulation; most commonly observed in valvular defects of the left heart, where stenosis of the left atrioventricular opening must be placed in the first place. In addition, the cause of venous blood congestion in the lung may be prolonged muscular insufficiency (functional) of the heart of degenerative or cardiosclerotic origin. Macroscopically, brown induration of the lung is marked by a uniform thickening of the lung tissue and a yellowish-rust or brownish coloration of the latter. In a strongly pronounced case, this rusty coloration may have a patchy character and coincides with the anatomical pattern of the lobular structure of the lungs. The induration of the lung tissue (as seen below) is associated with the thickening of the connective tissue stroma of the lung, and the rusty-brownish coloration is associated with a significant deposition of pigment of hemoglobinogenic origin (hemosiderin). Microscopically in the lung in these cases one finds narrowing of the alveolar lumens and thickening of the alveolar septa. The capillary network is stretched, overfilled with blood, and protrudes into the alveolar lumen [see separate table (vol. III, pp. 531-532), fig. 2]. In the alveolar cavities one finds desquamated alveolar epithelium containing varying amounts of granular yellowish-brown pigment (hemosiderin) and erythrocytes. The latter are also found in a free state in the alveolar cavities; some of them stain well, while others, devoid of hemoglobin, turn into weakly staining erythrocyte "shadows." The alveolar epithelium is often completely packed with hemosiderin; it then has large dimensions (macrophages). In such patients, these cells are easily detected in the sputum; they are known under the designation of "heart cells" or "mitral cells" (Herzfehlerzellen). Cells with hemosiderin can in places completely fill the alveolar lumens and give a "rusty patchiness." The draining lymphatic vessels and lymph glands contain a lot of hemosiderin. — Pathogenesis. The pathogenesis of this condition is simple and entirely connected with the stagnation of venous blood in the lungs, thanks to which small hemorrhages (diapedesis) of erythrocytes into the alveolar cavity occur. The latter are engulfed by the alveolar epithelium and disintegrate, and the hemoglobin turns into the iron-containing pigment hemosiderin (as a product of intracellular processing of hemoglobin). Part of the freely lying erythrocytes in the alveolar cavity lose hemoglobin (hemolyze) and disintegrate. The same venous congestion leads to chronic pulmonary edema and proliferation, sclerosis of the connective tissue stroma of the lung. By means of the reaction for iron (Prussian blue), one can easily detect these deposits of hemosiderin in the lung. Along with this, with the indicated reaction, impregnation of the elastic stroma of the lung and its vessels with colloidal iron is often detected, which indicates the release at times of a significant amount of iron during extracellular hemolysis of erythrocytes in the lung. This impregnation is unstable, and apparently, in the future, the colloidal iron is removed from the lung by the lymph and blood circulation.