ABSTRACT
Surgery for esophageal atresia (EA) is widely regarded as one of the greatest milestones in newborn surgery. Embryology and molecular genetic studies have yielded fascinating insight into the etiology of EA and tracheoesophageal fistula (TEF), with many important contributions emerging from animal models sharing striking similarity to the human phenotype. EA and TEF are more common in twin pregnancies. Exposure to teratogenic drugs during pregnancy has been implicated; these include thalidomide, progesterone, and estrogens. Significant contributions to understanding the embryology and genetic control of foregut development have evolved from laboratory research involving animal models of EA and TEF. Antenatal diagnosis of EA should theoretically reduce the likelihood of inadvertent newborn feeding and aspiration pneumonitis. The incidence of anastomotic leak following repair of EA and TEF ranges from 11" to 21". This is usually manifested by pneumothorax and salivary drainage from the chest drain.
