This post is the 4th in a straight series in which I have overviewed the section of a book in which the retired Scottish professor of paediatrics, Dr Ian Rogers, recounts what he has learnt from a lifetime of the observation and study of infant pyloric stenosis (“IPS”).
How digestion works
Dr Rogers describes the process of digestion that occurs in the stomach. He describes the stomach as having two parts, each with a distinct structure and function, and the stomach’s three stage role in digestion. During these stages the pylorus contracts and relaxes, early to allow fine and easily processed food to pass, after which the stomach continues grinding and breaking down the coarser food to chyme (or pulp) before the pylorus allows it to pass. He concludes that the contraction of the pyloric ring muscle is associated with feeding.
This raises the question: how would this process work in a baby? Dr Rogers points out that –
- Milk in the stomach raises alkalinity which triggers the secretion of gastrin and acid. This in turn activates the pylorus, and if acid secretion is higher or feeding is in greater quantity and/or more frequent than usual, then the pyloric muscle is overworked and over-develops.
- Artificially narrowing the pylorus in rats stimulates the development of the stomach’s acid secreting lining, thereby increasing even more the stimulation of the pylorus.
- Studies have shown that gastrin-induced hyper-acidity is indeed a symptom of IPS.
- In 1976 Dr J A Dodge reported that he had generated PS in 28% of 84 puppies after injecting 20 bitches with a synthetic form of gastrin; it is known that gastrin crosses a dog’s placenta and stimulates acid secretion. Still more puppies developed PS when they were injected after birth.
Dr Rogers concludes from this that the pyloric muscle is clearly the culprit.
- Disable the pylorus by splitting the muscle and its enlargement soon disappears; bypass it (which the gastroenterostomy operation does) and the enlargement remains.
- This also shows that although the gastric hyperacidity may be hereditary, the cause of IPS is not a hereditary tendency for the pylorus to be enlarged.
- The only cause of pylorus enlargement that has been found is repeated contraction.
- Pathological study has found no abnormality in the tumour tissue.
- The erythromycin phenomenon also confirms this conclusion. Erythromycin is a macrolide antibiotic widely used to treat bacterial infections, but when taken during pregnancy or by a newborn it has been found to cause a 7-fold increase in the incidence of IPS. This group of antibiotics works like the hormone motilin which increases stomach activity and contractions of the pylorus when the stomach should be empty after it has done its work: an empty duodenum (as with IPS) releases motilin. Some details of the function of motilin are not yet fully understood.
Other indicators – clinical aspects
- IPS is normally recognized by a doctor using the standard test meal for a baby who is vomiting profusely without bile in the vomitus: gentle palpation (feeling while stroking) will reveal the swollen pylorus (the “pyloric olive”) in some 80% of cases, and peristaltic waves can be seen moving from left to right.
- Adults with a duodenal ulcer caused by hyper-acidity can be treated by ranitidine (or in the past by atropine sulphate), a drug that blocks the release of acid, thus raising the alkalinity of the stomach contents. This suggests the possibility of also managing IPS by using a drug that reduces the secretion of acid in the digestion process.
- As mentioned, a baby who inherits a high gastric acidity added to the raised acidity levels normal in early infancy can develop uncontrolled hyperacidity which will over-work and over-develop the pylorus. A first-time and understandably anxious mother who continually re-feeds an obviously hungry baby will amplify what happens.
- A decline in both IPS and sudden infant death syndrome (SIDS) in babies who sleep on their back has recently been reported in Sweden. The back sleeping position results in feeds moving with gravity, making gastric emptying easier and faster: this would also seem to confirm hyperacidity as the cause of IPS.
In the next post, we follow Dr Rogers as he applies the information in these four posts to the classic characteristics of PS in babies.