Pyloric stenosis can often be avoided!

If you are a parent with a pyloric stenosis (“PS”) baby facing surgery, how much would you wish you could have avoided your child’s heart-rending sickness and surgery?

If you are alive today only because you had a Ramstedt operation for PS when you were a baby, how much would you hope you’ll never pass this on to any of your descendants?

If you had PS and still struggle with physical after-effects, your scar and/or mysterious emotional problems (although you are grateful to be here today), you’d most likely wish with some passion that you could have avoided some of what came with your PS.

If you have been though PS and surgery for it, whether as a parent or yourself as a baby, how much do you wish your doctor (or just anybody) could have helped you to understand the causes of PS better, and possibly have coached you or your parents through avoiding the surgery or reducing its possible traumatic effects?

Count me in!

I often dream of a world in which PS and other conditions are better understood, can increasingly be avoided, and in which infant surgery is more often unnecessary!  My hope is that one day soon medical research will consign to the dark and distant past the kind of infant surgery which traumatised my parents, me and countless others in a variety of ways and for life.

Although the surgical remedy for infantile hypertrophic pyloric stenosis (“PS”) is now a century old, research into the cause(s) and prevention of PS seems to have made very little obvious headway.  The numerous medical articles I have read skate around the edges of PS: they report on the statistics of its incidence and risks, the time taken by this or that surgical technique, the benefits of various anesthetics.  Jah-dee-yah-dee-yah!  But little or nothing about the cause(s) or prevention of PS.

But then, a few months ago I read an article that I found fascinating.

A senior Scottish paediatric surgeon, Dr Ian Munro Rogers, visiting professor of surgery at a Malaysian university, made some remarks on the cause of infant PS which bring together several well-known facts about this condition.  As happens in academia, the proponent of a significant paper or thesis must defend their findings.  However, while much of the medical world discusses its work behind university walls and in costly publications, Prof. Rogers’ thesis and its defence are freely available on the web.  Many of those you and other surgeons have helped thank you, sir!

The details of Prof. Rogers’ thesis and its discussion are too technical for me to understand fully, let alone explain here.  But the main arguments are clear and I want to pass them on…

If you can’t be bothered with the detail and just want the good news, go straight to the end of this post.

If you’d like to know more, follow the two links and read Dr Rogers’ article and the ensuing discussion.

Prof. Rogers observes that PS in babies usually follows a quite typical pattern: its incidence peaks about 3 weeks after birth, it affects mostly boys, it occurs often in the firstborn, it can often be cured medically as well as by the surgeon, there is often a family incidence, and the swelling disappears within weeks of the standard pyloromyotomy (muscle splitting) but not after a gastroenterostomy (that creates a bypass of the pyloric valve).

Dr Rogers mentions the 1941 discovery that a baby’s stomach acid level rises for a short time a few days after birth, the later discovery that the hormone gastrin in both mother and baby stimulates this spike, and that the pylorus contracts in the presence of such acidity.  In fact, adult PS can be managed by antacid medication.  The physiology (working) and biochemistry of our digestive tract involve the interaction of acid and alkaline hormones with our intake.  Milk is alkaline and stimulates gastrin and acid secretion, increasing the work and development of the pyloric muscle.  Experiments with rats and dogs have shown that excess gastrin and acidity can be linked to PS.

Hyper- (raised) acidity is the clear link with PS in both baby and adult humans and in animals.  And, Dr Rogers observes, people who had PS as babies have a higher incidence of peptic ulcer in later life, also involving hyperacidity.  Over-production of acid will often be an inherited trait, explaining why PS can be so strong in some families.  The antibiotic erythromycin is also known to stimulate the pyloric muscle, explaining why this drug has been linked with a 7-fold increase in the incidence of PS.  The article also recognises acidity as the culprit in the frequent link between infant PS and atresia (closing) of the esophagus (the passage from the throat to the stomach).

Recent studies have reported that a decrease in cot deaths came with a fall in infant PS cases.  Dr Rogers explains that the stomach empties faster when we lie on our back, reducing the passage’s exposure to acid.  The male 4 or 5:1 dominance of PS (and of duodenal ulcers) is also explained, as male babies have been found to have higher acid levels.

Normal babies can manage the normal early acidity spike, but infants whose unusually high acidity overworks their pylorus would die unless their muscle’s over-activity and over-development can be controlled.  This can be done by reducing the acid level with medication, by regular stomach wash-outs (“lavage”), or by disabling the muscle surgically, allowing the stomach’s hyperacidity to drain naturally down the gastric tract.

Prof. Rogers’ model also explains why on average PS affects more first-born babies.  Inexperienced and anxious mothers are more likely to over-feed and less likely to consider resting their baby’s stomach.  And mothers of PS babies find that, unlike our feelings after bringing up a meal, their vomiting seems to invigorate them: they are immediately hungry for more.  Because their vomiting is caused by a “mechanical” problem and not a “bug”, PS babies don’t feel sick and become more and more demanding of food – until starvation’s effects set in and they become lethargic and sleepy, a serious danger signal.

The theory also explains why PS occurs more among Caucasians (whites) and least in the undeveloped countries.  Where mothers and babies have tended to be less well-nourished, maternal and babies’ energy and breastfeeding are slower, making mothers less inclined to keep “topping up baby”, and reducing the baby’s intake and level of nutrition – and acid stimulation of the pylorus.

Medical and surgical treatments of PS have been found to be equally effective because both reduce the pyloric muscle’s workload and gastric acid secretion.  Gastroenterostomy bypasses the problem, and interestingly, the pylorus has been found to remain swollen even 40 years after this surgical technique!

Prof. Rogers also finds significant that although PS is more common in identical twins than in unidentical ones, the incidence of both identical twins being affected is still below 50%.  This fits with the established recognition that there are various factors and several different genes involved in who has PS.

How can we who have been affected PS in the past benefit?  Very little, of course.  However, everything I have learnt about this condition and its treatment has helped me: I no longer feel a freak with a strange scar and strange symptoms of trauma.  I now know my story and its historical context, and understanding the trauma that resulted helps me to manage it.

For those who are concerned about their own or a child’s PS being passed on to future children, Prof. Rogers’ insights are gold.

Because PS is multi-factored, it and remedial surgery cannot always be avoided.  But Dr Rogers has shown that many of the PS risk factors that have been identified in the past may well be linked with hyper-acidity in the baby’s stomach.  By being aware of many of the possible ways in which hyper-acidity in the stomach can be managed, I believe I can have a well-founded hope that the incidence and severity of PS and its treatment and long-term effects can be greatly reduced.

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12 thoughts on “Pyloric stenosis can often be avoided!

  1. wendy williams

    Reading this post, my mouth was agape in amazement, shock, and astonishment. I may have gotten the answer to a question that I’ve been asking consciously for over ten years and more subconsciously, for my whole life. I think, Fred, you’ve found the gold, indeed! I haven’t yet read the article–next up–but the fact that this doctor’s theory poses logical explanations of all the variables–the high incidence of ps in first born babies, in males, etc. And the erythromycin connection–WOW! Recently, I yet again posed the question to my dentist (a new one): Why do I have a dot of white on each front tooth and why have my teeth always been yellowish? He told me that I must have ingested Erythromycin as a child. This answer was new. My dentist during childhood told my mother that I didn’t get enough Vitamin C as a baby. I thought that strange, for my brother’s teeth were perfectly white, and I’m sure my mother carried out much the same feeding regimen with him as with me. Well, here you are, Fred, solving this mystery. Perhaps my mother had high gastric acidity while pregnant with me and was prescribed Erythromycin. If this drug makes the pylorus hyperactive and can render it dysfunctional, voila!–the answer to the age-old question! I truly, truly think you’re onto something here and will get back to you, probably in an email, soon after I finish ingesting (pun intended) the research. I can’t begin to describe my feeling right now. It’s one of thrill, elation, relief, and astonishment!

    Reply
  2. Fred Vanderbom Post author

    Thanks Wendy for another enthusiastic and heartfelt response: your words almost jump out off my screen! Every time I read Prof. Rogers’ reflections I am thrilled too by the masterly way he fits together so many pieces of the PS puzzle! The web address with the debate on his theory is also well worth a read: it takes nothing away from his conclusions after a lifetime of observation and research.
    It’s such a joy for me to pass this kind of material on in language I hope will make it more accessible to people like us.
    Btw, erythromycin was once given routinely to pregnant women and babies at risk of rubella (German measles) infection: I took it myself some years ago (without a second bout of PS!).
    Prof. Rogers’ paper has been available in academia since 2006 but I’ve come across no traces of it other than what I’ve mentioned. It certainly is “gold” to anyone with PS in their history or genes.

    Reply
  3. wendy williams

    In your post, you state: “And it’s well-known that PS babies’ vomiting means they are invigorated and always hungry. This also explains why PS occurs more among Caucasians and less in the undeveloped countries.” Can you explain further? I don’t understand the connection. Why are Caucasian babies more likely to get PS?

    Reply
  4. Fred Vanderbom Post author

    Mea culpa! Thanks for raising this, Wendy. Dr Rogers is really making two separate links, and I have edited my post to make this clear and explain these connections: I trust they are now clear.

    Reply
    1. wendy williams

      Thanks, Fred. I got clearer after reading the medical article, but it’s great to include the clarification in the post. You have a wonderful way of making the complex clear and easy to understand.

      Reply
  5. Pingback: Is infant pyloric stenosis linked other conditions? « Stories from the Survivors of early Surgery

  6. Pingback: Infant pyloric stenosis – some theories about its cause « Stories from the Survivors of early Surgery

  7. Micki Freels

    I found this article very interesting for several reasons. In 1980 my only son died having only gained a little over 4 pounds in the four months of his life. He had constant tummy aches and vomited just about everything. He aspirated in his sleep and they put it off to crib death which we never quite believed. Fast forward several years and my nephew has a son born constantly hungry, constantly with the tummy ache, and constantly vomiting. The doctors diagnosed him with PS, did the surgery and he is a fine young man now. This year my grandson was born. Constantly crying, hungry, tummy aching, and vomiting, he was almost at failure to thrive by the time of his diagnosis and surgery. He is doing much better now. What I know is that I can’t seem to help make the connection that all three of these boys from the same basic family line were all born face up: sunny side up babies they call them. Now can anyone explain that?

    Reply
  8. Fred Vanderbom Post author

    Micki, your Comment touches me deeply, as my wife and I also had a son in that same year, and because of my PS history and his frequent vomiting we were very much alert. We were grateful it was diagnosed as an allergy issue.
    With your family history since 1980 you may well conclude that your son like his later relatives had PS, and feel angry and sad that he was not given more careful diagnosis. In the distant past more babies died after “failure to thrive” but that should not have happened in the later 20th century in a country with good medical training.
    Thank you for alerting our readers to the very real danger and tragic results of PS being misdiagnosed.

    Reply
  9. Ika

    Hello Fred, I’m Ika (25) from Indonesia. My baby was born 29 Sept 2015. On 22 oct 2015, he do surgery for his PS. I’m afraid and confuse before. Because, my family and my husband family never know anything about Ps. Yes.. Ps puzzle.. I feel guilty because my baby’s surgeon doctor say: your baby PS is caused by me. Because I eat something that we dont know what. But, Alhamdulillah.. All praises to Allah. My baby is 5 months old. And he is 8.3kg already. Thanks to your article that opened my mind. (Sorry, if my grammar is wrong).

    Reply
    1. Fred Vanderbom Post author

      Hello Ika,
      Thank you very much for your Comment. Your English is much, much better that my Behasa Indonesia. My wife and I followed Indonesian lessons for a year, but that was many years ago. We are glad that we could visit your beautiful country several times (Java, Bali, Kupang NTT), and everyone was very welcoming and helpful although we could speak only English and Dutch.
      I am sorry that your doctor said what he said to you, because (1) it is not true and (2) mothers often feel anxious and even guilty when their baby gets sick. I am very glad that your son is now growing well, thank to Allah – and your good care for him!
      It is true that a mother can add to the risk of her baby having PS – but only in ways she does not realise or want: her husband’s or her own inheritance or genes, stress, taking antibiotics, smoking. It is still not correct to let a mother think PS is her fault.
      When people write that articles in my blog helped them, I am thankful to Allah also. It is sad that so many people tell me their doctor or surgeon said things that upset them, or were not correct. One of the things I hope for is that this and other information on the web will help parents, doctors and PS patients.
      Greetings from me in Australia.

      Reply
    2. Wendy

      Hi Fred,I tried to comment or reply but Worpress wanted me to confirm a bunch of info, including my password which I don’t have for some reason. Wendy

      Reply

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