What causes pyloric stenosis in babies and what does this mean for the way it is treated?
In my previous post I reviewed the first part of a recent open-access medical journal article by Prof Dr Ian M Rogers, a senior practising and teaching pediatric surgeon. It supported his theory and belief after a lifetime of work that infant hypertrophic pyloric stenosis (PS) is chiefly caused by over-acidity in the baby’s stomach during its first weeks or months.
The hyperacidity theory satisfies all the features of PS and the requirements for its development, most of them familiar to anybody who has been involved with PS; Dr Rogers listed these in his article and I mentioned them at the close of my previous post.
The hyperacidity theory is based on the discovery that PS babies have inherited the ability to produce much more gastric (stomach) acid than is in the normal range for babies of similar age, and that this additional secretion affects the pyloric muscle. The difference is not evident when the stomach is at rest, but the acidity is “hugely” higher when the stomach empties and it remains high when measured a week after surgery, so that it is clearly not caused by build-up in a blocked stomach.
Dr Rogers mentions some supporting evidence for this theory:
- Of 200 babies half were treated medically rather than by prompt surgery. The therapies used included gastric wash-outs, cautious feeding, and the administration of atropine, all to reduce gastric acidity, and the long-term cure rates achieved under both treatment regimes were similar. The same doctor performed both treatments, the mortality rate of each group of 100 was 1%, and neither group had recurrences.
- Any baby who is of PS-vulnerable age who vomits persistently and is alkalotic is diagnosed with PS, as the condition causes the loss of substantially more acid than in non-PS babies.
- Experiments with dogs have resulted in 25% of puppies developing PS after their mothers were injected with pentagastrin before labour, and even more when the puppies themselves were injected after their birth. This also shows that in dogs at least maternal gastrin crosses the placenta and increases gastrin secretion in the foetus.
- PS shows the same male/female sex ratio as duodenal ulcer in adults, a condition known to be due to hyperacidity.
- Blood group O is over-represented among both those who suffer from PS and from duodenal ulcer.
Hyperacidity which occurs after 4 – 6 weeks of age is unlikely to produce a pyloric tumour since the hormonal feedback from the duodenum will have become established, and the normal pyloric widening with age will also make pyloric obstruction less likely. See the diagrams.
The histochemical theories do not explain the timing of PS, and the infection theory has insufficient support, both as explained in the earlier post.
Dr Ian Rogers also discusses the effect of acid and repeated contraction on the pyloric muscle, and the role of the hormone motolin, which stimulates muscular activity in the stomach. This section is more technically specialised, based as it is on bio-chemistry, and I ask that those interested read Dr Rogers’ document in full.
Prof. Rogers sums up his argument as follows:
The Primary Hyperacidity Theory explains all the classical and less well known clinical observations. It explains the male predominance, the self-cure with time, the typical presentation at 4 weeks of age, the familial (genetic) inheritance and the increased incidence of hyperacid disease in adulthood. It explains the complete cure by sphincter division and the good response to antacid measures which result from standard medical treatment at the critical time.
How can Dr Rogers’ writing help those who have suffered from PS or whose baby may suffer from it?
- Parents are far too often told that the cause of their baby’s PS is unknown and that surgery is the only sure remedy. Dr Ian Rogers’ theory, his open publication and advocacy of it, the weight of the evidence he has gathered that supports the Hyperacidity Theory, and the consequences of all this have demonstrated that the cause of PS can in fact be understood beyond reasonable doubt.
- In light of the data cited by Dr Rogers –
- the incidence of PS can be reduced by addressing one or more of the causative factors he identifies;
- the need for PS surgery can be significantly reduced by early recognition, diagnosis and treatment by any of the medical treatment options mentioned above;
- parents can be reassured that medical treatment is in many cases just as safe and effective as surgery, besides being far less stressful and non-invasive ;
- parents who have a PS history themselves or in their family can be empowered to eliminate or reduce the possibility of their children developing PS or needing surgical treatment for it.
- Those who have been afflicted with PS in their infancy and live with any of the long-term effects of this condition and/or its surgical treatment can now understand what caused their problem and be better informed and aware of how these effects can be minimised and perhaps eliminated in future generations.
Knowledge is power! For much of my life I have been unable to discover much about the PS which has had such an effect on my inner life. Now that I know and understand the answers to almost all the questions I have had, I am quickly coming to peace, acceptance and even gratitude. I hope that my posting about these matters enables me to help others looking for answers to similar questions, and keen to reduce the PS statistics and the discomfort of both present and future PS survivors.