A disorder of the antropyloric gastric junction affecting infants and manifesting as an exceptionally thick musculature causing gastric outlet obstruction is familiar as infantile pyloric stenosis (IHPS). Usually the neonates are born with no clinical symptoms. Nevertheless, in the post natal period, a non-bilious, vigorous, “projectile” vomiting ensues. Emaciation result from the gastric outlet obstruction terminating in death in untreated cases. Palpation of the thickened pylorus or “olive” is the mainstay of clinical evaluation. Precise abdominal palpation is contingent to determinants such as the investigator’s judgement, gastric distension and a sedated infant. With inconclusive clinical exponents, selective, contemporary imaging establishes the diagnosis. In infants with hypertrophic pyloric stenosis, the pyloric ring is undetectable as a clear segregation between the capacious pyloric antrum and the duodenal cap. A variable conduit (1.5 cm to 2.0 cm) analogous to the pyloric canal is visualized, dividing the dilatable segment of the pyloric antrum from the duodenal cap. Muscular hypertrophy defines the groove which deftly transforms from the usual 1 mm of the distensible pyloric antrum to a 3 mm or up to 6 mm thickness in the expansive, archaic, hypertrophied pyloric canal. The lumen of the pyloric canal ranges from 3 mm to 6 mm owing to a compressed, superfluous and protuberant gastric antral mucosa. The mucosa, characteristically on endoscopy, appears as a nipple like projection resembling a cauliflower. Clinical Exposition is contingent to the duration of the disease. Early symptoms enunciate a classic projectile non bilious vomiting. The extensive emesis, on account of superimposed gastritis, is composed of blood tinged gastric contents Initially intermittent, the emesis becomes continual, subsequent to each intake. The infant displays an insatiable appetite, because of insufficient nutrition, notwithstanding a gastric distension. Malnutrition can aggravate the reduced functioning of hepatic glucoronyl transferase and induce indirect hyperbilirubinemia (1-2%). Gastric emesis triggers the sodium /potassium depletion and diminished hydrochloric acid terminating in a hypocholeremic alkalosis

With Regards,
Sara Giselle
Associate Managing Editor
Global  Journal of Digestive Diseases