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Gastric Outlet Obstruction

Complete obstruction involving the gastric outlet is a rare condition usually due to antral or pyloric atre-sia, although it may be caused by extrinsic pressure from congenital peritoneal bands or by annular pancreatic tissue in the gastric wall. Antral or pyloric atresia accounts for less than 1% of all congenital intestinal obstructions. The condition is thought to be due to localized vascular occlusion in fetal life (Okoye et al. 2000). It is usually produced by a membranous diaphragm in which only the mucosa is involved. An association with epidermolysis bul-losa letalis has been described (Toma et al. 2002). It is unknown whether the association is on the basis of a causative effect on the antropyloric mucosa, or whether it is due to a genetic linkage (Dolan et al. 1993). The predominant symptom is vomiting within the first hours after birth, the vomits being free of bile. The absence of bile in the vomits indicates that the obstruction is above the ampulla of Vater. A plain radiograph of the abdomen shows distension of the stomach proximal to the obstruction and absence of air in the small bowel and colon, resulting in the characteristic "single bubble" image (Rathaus et al. 1992) (Fig. 1.1). When a single bubble is observed, examination with contrast material is unnecessary and most patients are taken directly to surgery. The membranous atresia may perforate after birth, leaving variable degrees of stenosis. In these cases, plain radiography will show distension of the stomach and some air in the small bowel depending upon the degree of obstruction (Bell et al. 1977).

Pyloric stenosis may lead to obstruction of the lumen and usually presents beyond the neonatal period. However, it has been diagnosed in utero and can be seen in the neonatal period after administration of prostaglandin E to infants with ductus-dependent congenital heart disease. The stenosis is produced by central foveolar hyperplasia. On sonography, mucosal thickening often with polypoid or lobular appearance is observed, different from the muscular thickening observed in hypertrophic pyloric stenosis (Peled et al. 1992; Babyn et al. 1995) (Fig. 1.2).

Fig. 1.1a,b. Pyloric atresia. Anteroposterior (a) and lateral (b) plain abdominal radiograph in a newborn infant that shows distension of the stomach (st) and absence of air in the small bowel and colon, resulting in the characteristic "single bubble" image b a

Fig. 1.1a,b. Pyloric atresia. Anteroposterior (a) and lateral (b) plain abdominal radiograph in a newborn infant that shows distension of the stomach (st) and absence of air in the small bowel and colon, resulting in the characteristic "single bubble" image

Fig. 1.2a,b. Prostaglandin therapy-induced gastric outlet obstruction. Neonate with ductus-dependent congenital heart disease treated with prostaglandin E to maintain ductus patency. a Longitudinal US scan through the pyloric channel shows mucosal thickening (M), and a thin muscular layer (arrows), different from the muscular thickening seen in hypertrophic pyloric stenosis. b Axial scan through the gastric antrum reveals markedly hypertrophic mucosa (arrows) and an undulating appearance. The thickness of the muscular layer of the gastric wall is normal (arrowheads)

Fig. 1.2a,b. Prostaglandin therapy-induced gastric outlet obstruction. Neonate with ductus-dependent congenital heart disease treated with prostaglandin E to maintain ductus patency. a Longitudinal US scan through the pyloric channel shows mucosal thickening (M), and a thin muscular layer (arrows), different from the muscular thickening seen in hypertrophic pyloric stenosis. b Axial scan through the gastric antrum reveals markedly hypertrophic mucosa (arrows) and an undulating appearance. The thickness of the muscular layer of the gastric wall is normal (arrowheads)

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