Alimentary tract duplications are uncommon. Gastric duplication accounts for only 3.8% of these duplications. The cause is not known, but faulty separation of the endoderm and notochord early in embryonal development is thought to be responsible. The anomaly occurs in twice as many female as male infants.
Alimentary tract duplications are uncommon. Gastric duplication accounts for only 3.8% of these duplications. The cause is not known, but faulty separation of the endoderm and notochord early in embryonal development is thought to be responsible. The anomaly occurs in twice as many female as male infants.
Gastric duplications vary in size and shape. Most are located along the greater curvature of the stomach or the posterior wall of the antrum (A and B). The clinical presentation depends on the size and location of the duplication and whether there is communication with the rest of the alimentary tract. Patients may be asymptomatic or present with an abdominal mass and symptoms of upper GI tract obstruction, such as nonbilious vomiting. Other presenting symptoms include failure to thrive, abdominal pain, and anemia.
Associated anomalies, which occur in about 50% of cases, include duplications of the esophagus, ileum, and colon; congenital heart disease; vertebral anomalies; diaphragmatic hernia; omphalocele; and malrotation of the bowel. An upper GI tract series usually reveals a filling defect of the stomach or compression of neighboring structures.
Ideally, gastric duplications are treated by total excision. This may not always be possible, however, since the duplication and the stomach usually share a common wall and blood supply. Wedge resection, antrectomy, and subtotal gastrectomy have been used.
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