Infant pyloric stenosis (“PS”) is a condition that may affect babies during their first months, and it is regarded as the most common life-threatening affliction of early infancy, affecting between 3 and 5 babies in every 1,000 in “Western” countries. It will usually starve the infant to death unless treated, either by surgery or medically.
In the previous 4 posts I have summarised the main points made by Dr Ian M Rogers in a recently published small book, The consequence and cause of pyloric stenosis of infancy: Two personal stories. Ian is a retired surgeon and professor of pediatric surgery, and his book enlarges on his argument in several medical articles which are based on a lifetime of observation, research and experience with PS.
Dr Rogers believes that the cause of PS is not a mystery, and that surgery is often not needed to remedy it.
This post continues a series and overviews the first three of Ian Rogers’ six conclusions, all based on the discoveries and facts which he has presented. I have outlined Dr Rogers’ book in lay terms to make it accessible and understandable for non-medically trained parents, PS survivors and others interested in this subject.
Having set out the information which I have covered (selectively) in the previous posts, Ian Rogers comments that in 1970 his career put a halt to his work on PS, but that he returned to it in the 1990s, when several basic questions called for answers he believed could be given.
1 What makes some babies develop IHPS when normal babies do not?
Without entering into the more complex areas of the medical science that Dr Ian visits and must be considered to answer this question more fully, “the bottom line” is that inherited hyperacidity would be an answer to this question that fits what we know, although some details remain to be discovered.
Dr Rogers mentions several other known facts that add support to this answer, even explaining why some babies develop PS well before the usual 3 weeks to 3 months “window”, and the well-known link between PS and “O” blood. Of course heredity as a key factor also explains the frequency of PS in certain families.
Babies with normal gastric acid secretion do not overwork the pylorus despite the raised levels of the hormone gastrin during the first post-natal weeks.
2 Why do male babies predominate?
The 4-5:1 male dominance of PS runs parallel to the incidence of gastric ulcers, well known to be linked with hyperacidity, and males having a more active parietal cell mass (PCM), the acid secreting part of the stomach.
Male babies have also been shown to secrete almost twice as much gastric acid as girls during their first 10 days.
3 Why self-cure with the passage of time?
Release of the hormone gastrin is at very high levels after birth, normally peaks at between 10 and 17 days, and then falls to the equivalent of adult levels at 3 – 4 months. In normal babies raised acid levels continue for about 4 weeks, thus protecting the baby from microbe attack. But in PS infants, while gastrin release starts to fall, acidity continues to rise and the sensing that normally allows the stomach to switch between acidity and alkalinity is overwhelmed.
Pyloromyotomy (the operation to remedy PS) disables the pyloric ring, immediately blocking its overwork and allowing normal peristalsis and acidity and alkalinity to return.
The traditional medical treatment of PS in babies and adults was based on the belief that the muscle was not hypertrophied (enlarged through overwork) but spasming, and cutting the vagus nerve and administering the anti-spasmodic drug atropine, combined with regular stomach washouts were used to reduce acidity and spasms.
Effectively, these measures (together with the relief of dehydration and the restoration of healthy blood chemistry) allow babies to survive until they are old enough to outlive the natural raised acidity levels of the first post-natal weeks.
Next post –
Dr Ian Rogers answers three other “obvious” questions about the character and “unknown” cause of PS.