Esophageal, tracheal and pulmonary parenchymal alterations in experimental esophageal atresia and tracheoesophageal fistula. A histological and morphometric study.

Pulmonary complications are among the most important causes of morbidity and mortality in neonates with esophageal atresia and tracheofistula. We aimed to investigate the possible causes of respiratory complications encountered in esophageal atresia (EA) and tracheoesophageal fistula (TEF) in an experimental model. Sprague-Dawley fetal rats treated with adriamycin were used for the experiment. Time mated pregnant rats were given 1.75 mg/kg of adriamicyn intraperitoneally on days 6-9 of gestation. The fetuses were sacrificed on day 21, weighed, and dissected under the surgical microscope. The animals were divided into four groups: (1) control group; (2) saline-injected group; (3) adriamycin-induced EA group, and (4) adriamycin administered but without development of EA. The lungs, esophagus, and trachea were excised and underwent histological examination. The mucosa of distal esophagus was thickened (p < 0.05); the submucosa was thinner (p < 0.05); and the muscular layer was thickened (p < 0.05) in fetuses with EA and TEF. In adriamycin-treated rats, in which EA and TEF developed, tracheal cartilage was loosened and formed into a D or C shape. The cartilage was fragmented into several segments on transverse sections in most fetuses. Alveolar septa were thin in lungs of fetus with EA and TEF (p < 0.05), without any fibrosis or evidence of parenchymal abnormality microscopically. Our findings suggest that respiratory complications may contribute to structural lesions in the trachea and particularly in the distal esophagus but not in the pulmonary parenchyma itself.