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Pyloric stenosis/muscle hypertrophy

Pyloric stenosis (PS) usually occurs and is diagnosed in the first few weeks of life, where the muscle at the outlet of the stomach hypertrophies in the newborn, and presents as projectile postprandial vomiting. The condition is much more frequent in those born with OA/TOF, at around 7.5% compared to 0.25% of the general population, a 30-fold increase. It is unclear if this is a result of the surgical repair of the OA or due to shared genetic aetiology. In infants with both conditions, this is often diagnosed late, due to the overlap in symptoms of PS and oesophageal strictures, severe reflux etc. (83)

Rarely, this may not be diagnosed until adulthood. While there are a number of causes of PS in adulthood, such as malignancy and gastric and duodenal ulceration, most authors on the subject regard idiopathic adult PS (which we are discussing here) to be a milder form and continuation of infantile PS. However, it can be made evident by inflammation or oedema in the area, eg due to GORD. (84–86)


  • Pain in the epigastrium.
  • Early fullness after meals and feeling full all the time.
  • Vomiting and nausea after eating.


  • Palpation of the abdomen does not usually show a mass, unlike in infantile PS.
  • Barium swallow and follow through shows markedly delayed gastric emptying.
  • Endoscopy shows a fixed narrowed pylorus with smooth border.


  • Surgery, including pyloromyotomy, partial gastrectomy and pyloroplasty, is usually the treatment of choice.
  • Endoscopic dilatation may also be considered, though recurrence is common. (84–86)

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