Pyloric stenosis

Pyloric stenosis is a narrowing of the opening from the stomach to the first part of the small intestine (the pylorus). Symptoms include projectile vomiting without the presence of bile. This most often occurs after the baby is fed. The typical age that symptoms become obvious is two to twelve weeks old.

The cause of pyloric stenosis is unclear. Risk factors in babies include birth by cesarean section, preterm birth, bottle feeding, and being firstborn. The diagnosis may be made by feeling an olive-shaped mass in the baby's abdomen. This is often confirmed with ultrasound.

Treatment initially begins by correcting dehydration and electrolyte problems. This is then typically followed by surgery, although some treat the condition without surgery by using atropine. Results are generally good in both the short term and the long term.

About one to two per 1,000 babies are affected, and males are affected about four times more often than females. The condition is very rare in adults. The first description of pyloric stenosis was in 1888, with surgical management first carried out in 1912 by Conrad Ramstedt. Before surgical treatment, most babies with pyloric stenosis died.

Babies with this condition usually present any time in the first weeks to 6 months of life with progressively worsening vomiting. It is more likely to affect the first-born with males more commonly than females at a ratio of 4 to 1. The vomiting is often described as non-bile stained ("non bilious") and "projectile vomiting", because it is more forceful than the usual spitting up (gastroesophageal reflux) seen at this age. Some infants present with poor feeding and weight loss but others demonstrate normal weight gain. Dehydration may occur which causes a baby to cry without having tears and to produce less wet or dirty diapers due to not urinating for hours or for a few days. Symptoms usually begin between 3 and 12 weeks of age. Findings include epigastric fullness with visible peristalsis in the upper abdomen from the infant's left to right. Constant hunger, belching, and colic are other possible signs that the baby is unable to eat properly.

Rarely, infantile pyloric stenosis can occur as an autosomal dominant condition. It is uncertain whether it is a congenital anatomic narrowing or a functional hypertrophy of the pyloric sphincter muscle.^{[citation needed]}

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 pyloric stenosis 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 pyloric 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.