Gastric outlet obstruction and in particular, pyloric stenosis, is relatively common in developing countries. Acute clinical presentation is often the manifestation of biochemical and electrolyte changes. The presence of metabolic alkalosis in combination with acute renal failure should alarm us to the possibility of adult pyloric stenosis. We report a case of adult pyloric stenosis that presented as acute renal failure and discuss its pathophysiology.
Sixty seven infants were admitted over a 10-year period from 1972 to 1981: 50 males and 17 females. A higher incidence of hypertrophic pyloric stenosis exists in West Malaysia than was previously recognised. However, it remains at less than one tenth of the Western figures. Among the three major races, the condition was commonest in Indians and least in Malays. Most cases presented between the ages of 3 to 8 weeks. Prolonged history of vomiting of more than 3 weeks occurred in 43.3 percent cases, usually among Malay and Indian patients. All patients were treated surgically with 1 death (1.5 percent). The usual postoperative complication was vomiting which occurred in 22.4 percent. Early presentation, adequate preoperative resuscitation and improved anaesthetic techniques can further reduce this mortality and morbidity.
The cause of pyloric stenosis of infancy (PS) is at present unknown. A theory of causation is proposed which is consistent with all the known clinical features of this condition. It is based on the knowledge that PS babies are hypersecretors of acid which pre-dates the development of PS and is an inherited constitutional feature. This acidity will become temporarily and dangerously high due to an insensitivity of the negative feed-back between gastrin and gastric acidy within the first few weeks of life. Normal babies who have inherited normal acidity will also experience peak acid secretions at that time but will be much less acid than babies destined to develop PS. Acid entering the duodenum causes contraction of the pyloric sphincter. Hyperacidity will naturally lead to repeated pyloric sphincter contractions and sphincter hypertrophy. Inappropriate repeated feeding of the vomiting PS baby by a first-time overanxious mother to her ever hungry baby, by provoking feed related sphincter contraction is considered to play a significant part in pathogenesis. Should the baby with PS survive beyond the age of around 6weeks, the matured negative feed-back between gastrin and acid will ensure that dangerous hyperacidity is kept in check. This coupled with the natural pyloric canal widening with age, will lead then to an long lasting cure. This theory explains satisfactorily all the known and hitherto unexplained features of this condition.
Foveolar cell hyperplasia (FCH) has been reported as a rare cause of persistent gastric outlet obstruction in patients with infantile hypertrophic pyloric stenosis (IHPS), which, if present, requires excision of the gastric foveolar folds to resolve the persistent obstruction. This is a review of patients with IHPS diagnosed on abdominal ultrasound to determine the incidence of FCH in IHPS and to evaluate whether it has a causal role in postoperative vomiting following pyloromyotomy for IHPS.
The incidence of congenital hypertrophic pyloric stenosis among 141,215 Chinese, Malay and Indian live births in Singapore from 1972 to 1974 was determined. The incidence per 100,000 live births among these ethnic groups are: Chinese 21.2, Malay 9.7 and Indian 35.0. Pyloric stenosis is not absent although rare in oriental babies.
Development of infantile hypertrophic pyloric stenosis during postoperative period in EA with TEF is rare. Postoperative vomiting or feeding intolerance in EA is more common which is due to esophageal stricture, gastroesophageal reflux and esophageal dysmotility. A typical case of IHPS also presents with non-bilious projectile vomiting at around 3-4 weeks of life. The diagnosis of infantile hypertrophic pyloric stenosis in this subset is usually delayed because of its rarity. We report a case of IHPS in postoperative EA and emphasize on high index of suspicion to avoid any delay in diagnosis with its metabolic consequences.