熱傷受傷時における肺変化に関する病理学的研究

Abstract

A remarkable progress in clinical therapeutic aspects on the thermal burns has been made recently. Preventions of the infections and subsequent septic shock with Gramnegative bacilli have been achieved by virtue of silver sulfadiazine or mafenide acetate cream. It is, however, noteworthy that the prolongation of the life eventually lead to cause the serious complication of respiratory impairment. The patho-physiological analysis of the respiratory impairment is rather scanty. Cooper, Tepliz and Foley described the morphological changes of the lungs in the case of the thermal burns. But the pathological changes mentioned above await further analysis. From this viewpoint, author has studied the changes of the alveolar cells of the lungs in the case of experimentally induced severe thermal burns, adult rabbits of both sexes were as materials. Their back hair was shaved and thermal burns were produced after Sternberg's method. The animals were divided into two groups. The first group was permitted free access to water and diet. The second group was treated topically with mafenide acetate cream once a day or more. They were sacrificed 3 hrs., 1 day, 3 days, 7 days and 14 days after the burn was induced by the nembutal injection and small cubic pieces of the lungs were quickly removed and pre-fixed in 2% glutar-aldehyde and rinsed in propylene oxide and embedded in Epon 812. After polymerized by heat, ultra-thin sections of greysh-white interference color were cut with the ultramicrotomes. An observation was made after uranyl acetate and lead hydroxide double stain, Dermer's tricornplex flocculation method, ruthenium red and PAM staining procedures. At the early stages in both groups, the alveolar lining layer was destroyed in disintegration and fragmentation, and subsequent decrease and loss of the osmiophilic bodies in the type II alveolar cells were encountered. The alveolar septum also shows swelling and edema as well as the endothelial cell hyperplasia of the vasculature. In the late stages, focal desquamation of the alveolar cells and focal edema were seen. The disintegration and fragmentation of the alveolar lining layer as well as the phospholipid were also confirmed, suggesting that the decreased pulmonary surfactant materials may be related to the respiratory impairment.