The gastric outlet obstruction due to the hypertrophic pylorus impairs emptying of gastric contents into the duodenum. As a consequence, all ingested food and gastric secretions can only exit via vomiting, which can be of a projectile nature. While the exact cause of the hypertrophy remains unknown, one study suggested that neonatal hyperacidity may be involved in the pathogenesis. This physiological explanation for the development of clinical<unk>  at around 4 weeks and its spontaneous long term cure without surgery if treated conservatively, has recently been further reviewed. Persistent vomiting results in loss of stomach acid (hydrochloric acid). The vomited material does not contain bile because the<unk>  obstruction prevents entry of duodenal contents (containing bile) into the stomach. The chloride loss results in a low blood chloride level which impairs the kidney's ability to excrete bicarbonate. This is the factor that prevents correction of the alkalosis leading to metabolic alkalosis. A secondary hyperaldosteronism develops due to the decreased blood volume. The high aldosterone levels causes the kidneys to avidly retain Na+ (to correct the intravascular volume depletion), and excrete increased amounts of K+ into the urine (resulting in a low blood level of potassium).The body's compensatory response to the metabolic alkalosis is hypoventilation resulting in an elevated arterial pCO2.
Pyloric stenosis
Gastroesophageal reflux disease
Retained antrum syndrome
Intussusception (medical disorder)
Gastric volvulus
Esophageal achalasia
Hiatal hernia
Atresia