The etiology of tracheal mucosal injury in proximal esophageal atresia plus distal tracheoesophageal fistula: an animal study

Abstract

Tracheal mucosal damage has been reported in autopsy specimens of cases with proximal esophageal atresia and distal tracheoesophageal fistula (EA-TEF) (Gross classification type C). Such changes have not been reported for isolated EA (Gross classification type A). Our hypothesis is that passage of amniotic fluid (AF) through fistula via larynx and trachea may damage tracheal mucosa. An experimental study was conducted to investigate this hypothesis in the Adriamycin-induced EA-TEF model. In the first stage of the study, we tested whether the fetuses with EA-TEF associated with pyloric atresia cannot swallow AF whereas the fetuses EA-TEF without intestinal atresia can swallow AF. Carbon solution was injected into the AF for this purpose. In the second stage of study, at the 21st day of their gestation, fetuses were extirpated and dissected under microscope. In both stages, fetuses were divided into four groups as control, fetuses without tracheoesophageal abnormalities, fetuses with EA-TEF only, fetuses with pyloric atresia associated with EA-TEF. Lungs and tracheas of the all fetuses were removed for histopathological examination. While carbon particles were present in the trachea, stomachs of the fetuses without tracheoesophageal anomalies, with EA-TEF only and control fetuses, carbon particles were absent in both trachea and stomachs of the fetuses with pyloric atresia associated with EA-TEF. Histopatological examination of the tracheal mucosa showed damage throughout the trachea in the fetuses with EA-TEF only group. Tracheal mucosa was found to be normal in other groups. Bronchial mucosa and lung tissues were found to be normal in all groups. Amniotic fluid swallowed through the TEF causes histopathological changes in the tracheal mucosa of the fetuses with EA-TEF only group. These findings may also contribute to the development of new fetal treatment modalities.