Abstract

Esophageal atresia (EA) is a relatively common congenital anomaly of the gastrointestinal tract, with a prevalence of approximately 1 in 5000 to 1 in 3000 neonates. Since 1939, when the first surgical repair of this once-fatal condition was performed, survival rates of uncomplicated cases without associated anomalies have steadily risen and today can reach 100%1. Approximately half of the cases present with other malformations, which may include cardiac, other gastrointestinal, genitourinary, or skeletal anomalies (Table 1)2–4; chromosomal anomaly is found in 8–10%2,3. EA has been classed into five types, whose prognosis depends on the type of lesion, the presence of associated structural and/or chromosomal anomalies, and expeditious referral to a tertiary care center for initiation of surgical repair. Prenatally, esophageal atresia is often suspected with the diagnosis of polyhydramnios and small or absent fetal stomach, with or without intrauterine growth restriction (IUGR). Shulman et al. employed a systematic approach to two-dimensional (2D) ultrasound scanning of the fetal thorax to identify the blind pouch characteristic of the

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