Understanding infant pyloric stenosis (Conclusions)

In the previous few posts I have overviewed and “translated” in some detail the major and professional medical section of a small book recently published by Dr Ian M Rogers and myself, with the descriptive title, The consequence and cause of pyloric stenosis of infancy: Two personal stories.

The reason for this series of posts?

At least some of the survivors of infant pyloric stenosis (“PS”) and their parents will be interested to know and understand this condition better, as we keep being told that “we still don’t know what causes it”.

Let’s face it, “knowledge is power”, and how many parents don’t wish they knew more about PS when they are suddenly and horribly faced with it?  What causes this?  What can and should I do?  How do I look after my sick baby when I feel the doctor fobs me off? Can my beautiful baby avoid surgery for this? What are the possible short- and long-term side effects?

Although I have never had a child with PS, I had it as a baby and wish I had known what I know now much, much earlier.  In the past this was virtually impossible, but the power of the web has changed this completely.

True, there are still some areas that are not fully understood, but it’s also true that drawing on a lifetime’s work with PS, the retired professor Ian Rogers is able to give us a clear and (it seems to me) compelling explanation of what does in fact cause PS.  The fact that he has written his part of the book using a lot of medical language must not keep his knowledgeable and compelling explanations and rich insights from those of us most affected by PS!

In this the last post of this series, I look at the last three of 6 questions which are often regarded as summing up the mysteries of PS, but which can in fact be answered in the light of Ian Rogers’ discussion of the discoveries that together explain PS.

4   Why is PS more frequent in the first born?

first-time-mom2First-born babies are cared for by cared for by first-time mothers.  PS babies are hungry and vigorous, ravenously hungry (at first), and unusually, the condition does not leave them feeling nauseous but immediately voraciously hungry for more.  Understandably but tragically, this gives the stomach and the acid-caused work-enlarged pyloric muscle no rest; an experienced mother will be more inclined to give feeding a break.

Mention is made of a 1962 article by Dr N M Jacoby, who compared two groups of 100 babies treated medically and surgically for PS, with one baby (only) of each group dying.  Of the medically treated children, Jacoby stresses the importance of (1) relative under-feeding, (2) the drug involved (atropine) being carefully used in relation to body weight, and (3) regular stomach washouts.  Two of these cautions can be linked to the hyper-acidity theory.

It is often mentioned that PS occurs far less frequently in under-developed countries: this also fits the theory, although more factors may be involved.

5   Why does pyloromyotomy, and not gastro-enterostomy, cause the tumour to disappear?

There are reports about 52 year old patients whose pylorus was found to be still enlarged after a gastro-enterostomy surgery in infancy to overcome PS; after pyloromyotomy the pylorus returns to its normal condition after several weeks.

Unlike gastro-enterostomy, pyloromyotomy disables the muscle ring and widens the opening temporarily, which breaks the cycle of its becoming enlarged by overwork.  Gastro-enterostomy was used before pyloromyotomy was discovered and is still used occasionally: it by-passes the pylorus which removes the immediate feeding problem but the pylorus continues to be over-stimulated by an over-acidic stomach.

6   Why does PS present at around 3-4 weeks of age?

Dr Rogers mentions two possible reasons.

It could take some weeks for higher than usual acidity to enlarge the pylorus sufficiently to make a clear diagnosis of PS possible.  But if this were so, we could expect other problems caused by hyper-acidity to arise at this time – and they don’t.

More likely is that the switching mechanism between alkalinity and acidity is more immature than usual during the first weeks.

In evolutionary terms, the benefits of the normal high acidity in a baby during the first weeks (incl. guarding against microbial attack as mentioned earlier) outweigh the negative of a few babies with hyper-acidity having problems!

Other lines of enquiry

1   Genetics

genetics1Genetic studies have shown that more than one gene is involved in PS, and that the condition is multifactorial: it can be caused by any one or more of several factors.  This is confirmed by studies of identical twins who are more likely to share PS than non-identical twins or siblings but far from always.

It has been found that PS infants tend to have higher birth weight, and (anecdotally) they may also become more athletic!

2   Chemistry of the pylorus

Prof. Rogers gives three reasons why the reports of chemical abnormalities of the pyloric muscle (the presence of growth factors and the absence of other chemicals) are theoretically attractive but do not stand up to scrutiny.

3   Infection

The analysis of swabs taken from the nose and throat of babies have shown no abnormality in PS babies.

A previous post has mentioned links between hyperacidity in PS babies and in adults infected with a stomach bug, Helicobacter pylorus, which can trigger gastro-duodenal ulcers.  But several studies of PS infants have not discovered any H. pylorus infection.

Dr Rogers remarks how strange it is that none of these studies links the hyperacidity triggered by a H pylorus infection with the hyperacidity that is part of PS.  Strange indeed!

Conclusion

Dr Rogers sums up:

Constitutional hyperacidity coupled with developmental hyperacidity begets pyloric contractions which begets work hypertrophy which begets IHPS.  IHPS begets further hyperacidity, and so on.
Maternal anxiety in the novice mother means that the hungry but vomiting baby is frequently fed with more pyloric contractions and more work hypertrophy – and a bigger tumour.

Wryly, he adds that it seems there is nothing new under the sun, and that “we are almost back where we started”.  In 1921 Dr J Thompson already proposed that the pylorus spasming and overdeveloping through over-work were the cause of PS, and still earlier, in 1903 Dr W Freund had suggested that excess hydrochloric acidity was a key factor.

The future

Dr Rogers urges that his theory is “perfectly testable”.

  • It is well known that PS babies’ serious loss of acid through their vomiting must be remedied before surgery, as their alkalosis (excess alkaline in the body) causes dangerous hazards during and after the operation.
  • ranitidine01Adults similarly affected by vomiting and acid loss are quickly and effectively treated with drugs to reduce the excessive release of acid.
  • Successful medical treatment of babies with PS is regularly reported: intravenous atropine is used to rapidly reduce the size of the pyloric tumour while the malnutrition and chemical imbalance are corrected.
  • Surgical treatment is now more prompt with a drug (cimetidine) that rapidly corrects alkalosis.  The author mentions an as yet unpublished report that this drug when given to mild cases made surgery unnecessary in 16 of 17 cases.
  • Another powerful acid blocking drug, Ranitidine, has also proved to be very effective in avoiding surgery when PS is recognized early; it should also be useful when surgery is not safe or accessible.  Dr Rogers then briefly outlines several other avenues of treating PS safely and medically.

He concludes his comments on considering non-surgical treatment by adding:

Such a pre-operative strategy with babies with IHPS is long overdue. It should not come as a surprise if we find that such temporary treatment promotes a lasting cure. 

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