Category Archives: Hyper-acidity

Understanding infant pyloric stenosis (1)

PS book coverIn the previous two posts I have “translated” several parts of the larger share of the small book I have co-written with the emeritus Prof. Dr Ian Rogers, titled  The consequence and cause of pyloric stenosis of infancy: Two personal stories.  My co-author has addressed his section to the medical profession but gives much information that is of no small interest to many of us who have been touched by infant pyloric stenosis (“PS”).  It has certainly helped me to understand much more of the what, how and why of this rather enigmatic condition, something I have longed for ever since I became aware of the strange markings on my belly!

In this post I want to revisit (in more detail than my initial post) the first pages of Dr Rogers’ section, in which he writes about the function of the hormone gastrin in digestion.  He mentions that the Glasgow academics under whom he trained specialised in the physiology (working) of the stomach and intestines, clearly because duodenal ulcers were a major cause of illness at the time.

When Ian Rogers finished his surgical training in the early 1970s, it was known that –

  • Stomach01hyper- (or over-) acidity could be constitutional or acquired, and was the major cause of duodenal ulcers;
  • hydrochloric acid release is triggered by the vagus nerve and/or the hormone gastrin;
  • the upper (proximal or first) part of the stomach secretes the hydrochloric acid;
  • gastrin occurs in the mucosa (lining) of the distal (or end) part of the stomach;
  • food in the stomach causes chemical change which releases gastrin into the bloodstream and this as well as stomach activity triggers the release of acid into the stomach contents;
  • acid is essential to digestion as well as sterilising food;
  • normally, gastrin controls acidity, not allowing its level to become too high or low;
  • duodenal ulcers were thought to be caused by hyper-acidity, most common in anxious men; often this could be controlled by cutting the vagus nerve, and otherwise by a gastro-enterostomy (which involves more radical surgery).

It has only become known in more recent decades that Helicobacter pylori bacteria are also involved in hyper-acidity and cause some 80% of duodenal ulcers, and also that antibiotic treatment and/or suppression of vagus nerve activity with atropine could control acidity, almost eliminating the need for surgery to relieve gastric ulcers.

Although both men and women have rates of H. pylori infection that rise during their lives and are almost similar at age 70, the acid-secreting stomach cells are more numerous in adult men than women.

Thus there are some interesting parallels between patients with PS of infancy and those with gastric ulcers in adulthood –

  • a 5:1 male preponderance;
  • high acidity;
  • a good appetite;
  • other family members affected.

The above facts represent what was commonly known in the early 1970s when Ian Rogers completed his surgical training in London and returned to Glasgow.

In later pages Dr Rogers continues by describing the “clinical (observable) signs” of PS – as they give many clues to its cause.

  1. Peptic ulcer3it arises very early in a baby’s life;
  2. it affects many more boys than girls;
  3. it cures itself in time if the patient can be treated medically;
  4. it can have a strong family link;
  5. if the pyloric tumour is split surgically the swelling soon disappears;
  6. the swelling does not disappear if the blockage is surgically by-passed;
  7. the high acidity in the stomach cannot be explained as accumulation due to the pylorus being closed;
  8. survivors continue to secrete higher than usual acid;
  9. PS babies have a ravenous appetite;
  10. they are often first-born babies;
  11. some PS babies are found to have a superficial duodenal ulcer.

Despite these clear pointers, the medical community still finds the cause of PS a mystery more than 120 years after it was first fully described.

Dr Rogers then refers to the significant 1921 paper of the Scottish Dr John Thompson who observed that –

  • the “pyloric tumour” is in fact over-developed muscle;
  • PS is self-limiting (see #3 above);
  • PS can be managed with small feeds, daily stomach wash-outs, and if feeding has been unsuitable, with IV feeding;
  • there are 3 kinds of PS: the acute (with sudden and violent symptoms), ordinary, and very mild.

Thompson accepted the theory that PS is caused by a functional abnormality, referring to an 18th century anatomist who found that all muscles develop with use, but involuntary muscles (ones like the pylorus over which we have no control) more than others.  However, this theory was not further explored, even though PS occurs also in other mammals.

Dr Rogers has now laid the foundations for his conclusions about the cause of PS, and in the next post we’ll see how what he has been mentioned in these three posts applies to gastrin, hyper-acidity and PS in the newborn.

Finding the cause of infant pyloric stenosis

In the previous post I passed on something of the first part of a book in which the retired pediatric surgeon and emeritus professor Ian Rogers reviews what he has learnt about infant pyloric stenosis (“PS”) over a lifetime of interest and work with this condition.  This book, The consequence and cause of pyloric stenosis of infancy: Two personal stories, was a joint effort: in the first 20 pages I told something of “My Story”.

Communication04Dr Rogers continues his account, touching on a large number of medical facts and research findings that together have shaped his well-based and considered understanding of what causes PS.  To me they read a bit like a criminal case: What can we say immediately? Where and what are the clues? How do we put it all together to make a case that will stick?

Those with medical training and knowledge should refer to the book, as here I can only glean some of its main lines and those that can be explained in brief to the interested general reader.

Under the heading, My journey, Prof. Ian Rogers tells how his journey started when he found a 1941 article which documented the gastric acidity in newborn breast-fed babies.  It must be remembered that gastrin, the hormone that controls stomach acidity, was not identified until many years later.

In 1941 a researcher (Dr R A Miller) reported finding that babies’ stomach acidity was neutral at birth, probably  due to the swallowing of alkaline amniotic fluid, then rose very rapidly to an extreme level, and returned to normal levels after some 10 days, and the difference between minimum and maximum acidity also fell: clearly the baby’s body was taking control.  Miller concluded that the mother transmits a chemical to the infant to explain this pattern.

It is known that when birth is induced with the drug syntocinon the baby’s gastrin levels are not those of the spontaneously born child, probably because syntocinon affects the gastrin transfer.  It is now known that the mother’s placenta has a high level of gastrin at birth, and that rising gastrin levels parallel rising stomach acidity in babies from Day 4.

Ian Rogers then mentions several more points made by Dr Miller –

  • When acid enters the duodenum the pylorus contracts; antacid medication is therefore effective in treating some cases of adult PS.
  • When food enters the stomach several stages of relaxation occur, involving different parts of the stomach, various digestive movements, and preventing excessive discomfort.  The contraction and relaxation of the pylorus are integrated with this complex feeding process.
  • Repeated feeding results in repeated pyloric contraction, and this is amplified not only by hyperacidity but also by incompletely digested food and a stressed mother repeatedly feeding a desperately hungry baby.
  • More specifically in babies, milk accumulating behind a closed outlet increases alkalinity and the stretching of that part of the stomach, both triggering the release of gastrin and thus acid.  In addition to this, some people inherit their stomach walls secreting more acid than normal.  Dr Rogers proposes that it is the combination of high acid secretion, repeated pyloric contraction causing muscle over-work and over-development (hypertrophy) as well as further increasing gastrin levels, and too frequent feeding that together are the cause of PS.
  • When the pylorus of rats was artificially narrowed, it was found that the secretion of gastrin increased.

Dr Rogers then found the work of Dr John Dodge, who produced PS in 28% and gastric-duodenal ulcers in 16% of the puppies of 20 bitches injected with a synthetic form of gastrin.  It is known that gastrin crosses the canine placenta, increasing the gastrin level in her pups.

  • It is noted that the over-worked and over-developed pyloric muscle is also essential to PS: when it is divided it shrinks to its normal size, but when it is bypassed it does not.  But a working muscle does not usually over-develop: something else is causing this.
  • Cell studies of the pyloric tumour have confirmed that over-work causes the over-development of the pylorus of PS babies, and that no other abnormality causes the tumour.
  • Pregnant mothers and babies who take the macrolide antibiotic erythromycin see a 7-fold increase in the incidence of PS.  Macrolides increase the activity of the part of the stomach that is closest to the pylorus, as well as contracting the pylorus.
  • Another gastro-intestinal hormone, motilin, stimulates the emptying of the stomach.  It is believed to be linked with PS and may stimulate pyloric contraction; however the role of motilin is still incompletely understood.

Next post – some clinical aspects of pyloric stenosis

Are infant pyloric stenosis and gastric ulcers linked?

Some 40 years ago, one of my uncles had surgery for a gastric ulcer.  When he visited us I found that his scar from that operation was not unlike mine from pyloric stenosis (PS) surgery when I was a newborn.  But little did I think there might be much more of a connection.

In the first sections of his part of the book to which I devoted last week’s post, and which Dr Ian Rogers and I have co-written, Ian lays the foundations for understanding the link between infant PS and a duodenal ulcer.  Here is the first part of my summary of Dr Rogers’ comprehensive report – for the medically untrained (and isn’t that most of us reading this?)  And do get a copy of our book if you’re interested in more details.

This is information I want everybody with an interest in PS to have!

Personal history, gastrin and acid

Rogers Ian frcs frcp (Small)When Scottish medical student Ian Rogers graduated and started his work in 1970, duodenal ulcers (DU) were common and dangerous, and related research was prominent.  At that time it had become well-known that the ulcers were caused by over-acidity in the stomach which was triggered by the hormone gastrin, the release of which was in turn caused by food reducing the acidity of the stomach.  When acidity rises, the release of gastrin stops, and thus balance is maintained.

It was also known that DU patients produced more gastrin than usual after a meal (especially when the gastric acid had scarred the stomach’s outlet or pyloric passage), that males produced more gastrin than females, and that 5 male DU patients presented for every one female.  It was found that the vagus nerve (the hunger messenger) also raised gastrin secretion.  In those days the role of Helicobacter pylori (or H. pylori) bacteria and the possibility of antacid treatment were unrecognised, and surgery was the accepted answer to a DU: the vagus nerve was immobilised and/or the lower part of the stomach was removed.

Because the drug atropine blocks the vagus nerve it was used to test whether a vagotomy would be effective in reducing stomach acidity.

All the above classical features of a DU are similar to those of infant pyloric stenosis (PS), including what was already described in 1921 as the PS baby’s “voracious appetite”: being ravenously hungry immediately after vomiting (not normal behaviour after bringing up a meal!).

The important role of the bacterium Helicobacter pylori was not yet recognised in 1970: it has infected 80% of DU patients, creating an alkaline environment in the lower stomach to protect itself from acid and also stimulating acidity.

Ian Rogers lists 11 telling clues about babies who present with PS, and yet the cause of the condition remains (it is claimed by most) unknown today.


In 1921 Dr John Thompson reviewed what was then known and done about PS – the details are most significant but too many to detail here.  Most importantly he (1) identified 3 common levels of PS, the acute, the ordinary and the very mild, and (2) reported on how PS could often be managed medically (and without surgery).

Dr Thompson also mentioned two theories about the cause of PS: (1) that is was caused by an abnormality of the pylorus, and (2) that the pylorus was being stimulated to malfunction.  He favoured the 2nd theory, citing the work of an 18th century anatomist on what causes muscles to hypertrophy (over develop).

Next:  My journey 

PS book coverWhenever I asked my parents about the weird marks on my stomach their answer was limited to “A doctor did that because you were a little bit sick when you were a baby”.  Yikes, I hoped I wouldn’t get “a little bit sick” ever again.  So as a child and ever since, I’ve been in the hunt for a better answer.  But apart from one-paragraph entries about pyloric stenosis in encyclopedias and medical handbooks, there was nothing.  So in recent years I’ve been passing on what I’ve learnt about PS issues by blogging (“Surviving Infant Surgery”).  And when the British professor of pediatric surgery Dr Ian M Rogers invited me to contribute “My Story” to a small book he was publishing about his conclusion after a lifetime of work – that all the symptoms of PS agree with it being caused by over-production by mother and baby of a gastric hormone, the result was: “The consequence and cause of infant pyloric stenosis: two personal stories”.  I hope that this modest book will go viral and make it onto many bookshop, library, and doctors’ shelves.  Interested PSers, parents and others can find out more about the book by googling for the title – and get a copy if you have a spare €24 for a medically priced publication – lol.  Anything I get will go to medical research into the diseases of infancy.

Understanding adult peptic ulcers and infant pyloric stenosis

As a boy I remember my heart churning and racing when I overheard my parents talking about my namesake uncle in the Netherlands having a peptic ulcer and facing surgery for this.

Although my parents would never tell me much about the kanji-like scar on my belly from an infant pyloric stenosis operation and didn’t tell me much about my uncle’s problem, I immediately sensed some kinship.  It was obvious that I had also had a stomach operation… maybe my uncle Fred and I would have similar scars?  Migration to Australia had taken my family half a world away from our Dutch relatives so I assumed I’d never find out.  In the 1950s people didn’t talk about such personal and medical matters, and they certainly didn’t post “selfies” on Facebook.

However, two decades later my uncle visited us in Australia and during a hot summer day’s outing my young family together with my parents and Dutch uncle and aunt enjoyed a swim… and I had confirmation at last!  Despite the usual male body hair I had a glimpse of my uncle’s similar vertical scar.  (It looked tidier and a lot smaller than mine!)  Of course I kept my deeply unloved scar hidden and didn’t dare to talk: I was too choked with shame and other emotions.  Besides this, I was around age 30 and my uncle was 43 years older than me, and I’d come to know him as a friendly but very distinguished man.

I treasured but filed the link away and thought little more about it until 30 years later…

Genes baby1When I started researching PS and related issues on the web in 1997, I soon learnt that sometimes there is a genetic element causing it, and that although a family link is not discovered in the majority of cases, five genetic loci have been identified as having possible links with the development of PS.

I have not heard of anyone else on either side of my family tree having PS and this suggests that there is no clear genetic factor in my story.  There are a few other recognized risk factors which do apply to me: male, firstborn, Caucasian, and maternal stress make a substantial list.

But more recently I discovered a small number of medical journal articles reporting infant PS and peptic ulcers occurring in adulthood in the same families.  Contact me for links if some case stories would be of interest.

Peptic ulcer3And then my web searches yielded a 2007 article written by a retired professor, Dr Ian M Rogers – and since added to by an interview and another article.  Dr Rogers has proposed hyperacidity as the key cause of PS and as the consistently demonstrable link between virtually all that we know about the symptoms and incidence of PS.  His theory also argues that hyperacidity explains why in some families PS can occur in babies and gastric ulcers in adults.

A search of the web will show that Dr Rogers and others have been studying the link between gastric acidity and PS since at least the 1970s and that Dr Rogers’ thinking and knowledge of this have been developing throughout his professional life.  Again, contact me for links if you are interested.

Peptic ulcers of the stomach, pylorus and duodenum are now a very much reduced threat thanks to the discovery that the presence of a bacterium, Helicobacter pylori, was usually needed to develop an ulcer from hyperacidity.  H. pylori is now treated with antibiotics in most or many cases, avoiding the need for a surgical remedy.

This gives me a new line to explore when I reconnect (as planned) with my Dutch relatives in 2014: apart from my uncle’s peptic ulcer is there evidence of hyperacidity or even PS in my Dutch family?

Some readers may be more than interested in building a similar knowledge of their genetic legacy!

The answers to this line of information will help my family and other present and future generations to –

  • better understand the risk profile of their family members,
  • simplify and speed up the diagnosis and management of PS in infants and of hyperacidity and its possible damage in adults, and
  • reduce the likelihood of PS developing to the extent that surgery is considered or recommended for babies, whether actually necessary or not.

The more we know and understand about PS and its related issues, the more we can do to manage it with less cost, upheaval and trauma for baby and parents alike.

The cause of pyloric stenosis revisited

Prof. Dr Ian M Rogers has had a strong interest in infant pyloric stenosis (“PS”) throughout his long career in the practice and teaching of paediatrics and paediatric surgery.

A year ago I posted an overview in two parts of one of Prof. Rogers’ articles on the essential cause of PS.  His interest in this and a friend’s blog projects to publicize some of the patient issues around infant surgery and PS in particular has been a tremendous encouragement.  So also his willing and generous help in getting some of the benefits of his lifetime of knowledge and work onto the computer screens of those interested and affected.

Some months ago Dr Rogers wrote another article, The whole Story of Pyloric Stenosis, on this subject.  I have not found it published online, but it should be of great interest to all specialist paediatricians and to some of those personally affected by PS; this is why I am so grateful I can overview it here.

Med research1Dr Rogers restates some of the research and conclusions reported on in his 2012 article, but the 2013 report is not as readily accessible to the general reader.  Rather, it very much (and appropriately) addresses his colleagues.  The 2013 essay again reflects Dr Rogers’ career-long interest in IHPS and the progress of his and others’ research, discoveries and reports on hyperacidity as the cause of IHPS.

The article necessarily includes a lot of the language of bio-chemistry and reasoning and refutation on this basis.  I found this interesting, but without help much of it was hard to understand, let alone assess.

Dr Rogers has been very generous with his time and help, giving me a quick lesson in the biology of the stomach and making detailed corrective explanations to several parts of my first draft.  He has kindly added some more explanatory notes to make this post as clear as possible.

So I am now able to pass on the main points of significance to those who like me are interested in the causes and treatment of PS, as well as Dr Rogers’ answers to several of my questions.  This means this post is now quite lengthy, but those interested will be happy to read on!

In his email to me Dr Rogers first gave this most helpful explanation of how the stomach works; this helps us understand what happens when PS develops.

When you eat and food enters the stomach a chemical is released from the lining cells of the stomach into the blood stream.  It is called gastrin.  It is an internal messenger or hormone, and rises naturally during feeding and passes into the circulation when the stomach is distended and alkaline.

Gastrin circulates and causes other cells in the stomach lining to secrete acid: these cells are called parietal cells.

bub w bottle1The stomach contents then become acid – and this acidity stops the secretion of acid since gastrin secretion is switched off when the stomach becomes acid.  It is called a negative feed-back mechanism and you will see that acid secretion is controlled and extreme hyperacidity or hypoacidity (i.e., lower than normal acidity) are avoided by this mechanism.  If acidity falls, gastrin rises and if it rises, gastrin falls.  Hence acidity is under control.

Acid causes the pyloric sphincter to contract; if there is undue acidity the sphincter contracts frequently and, as with any exercising muscle, it becomes stronger and larger – resulting in the narrowing of the exit passage, i.e. pyloric stenosis.

That is all the physiology you need to know!

Prof. Rogers starts his article by mentioning that as far back as 1972 he was interested and became involved in the then recent discovery that the excessive release of the hormone gastrin is responsible for stimulating high levels of acid in the stomach which causes the pylorus to overwork, enlarge, and close to the passage of food.  His team discovered however that gastrin is not passed on to any great extent from mother to baby, but rises to very high levels about 4 weeks after birth.  This is the time when most PS develops.  Let me again allow Dr Rogers to explain this in more detail –

Miller in 1947 thought that the observed wave of neonatal hyperacidity might be due to a chemical being transferred from mother to baby at the time of birth.  Naturally I thought of maternal gastrin and that is why I measured blood gastrins in mother and baby – on day 1 and day 4.

[I found that] baby gastrins were higher than fasting maternal gastrins at the time of birth (on Day 1).  On Day 4, the fasting baby gastrins were several times higher than those in fasting normal adults.  (Because gastrins do not last long in the body (a short half-life of 17 minutes) it was presumed that Day 4 must be coming from the baby – and since a low level on Day 1 meant a low level on Day 4, the baby gastrin at Day 1 etc (they were individually statistically related) was likely to also be largely baby in origin.  We did not prove that gastrin did not transfer from Mother to baby.  It might for example be concentrated in the placenta before being transferred.  (Maternal transfer has been clearly shown to occur in the dog!)

The peak gastrin level has not been clearly shown but the experiments of Rodgers and MacGuigan strongly suggest the peak at around 15-17 days.  Acidity in NORMAL babies peaks at around that time.

I have suggested that in NORMAL babies the negative feed-back takes time to mature — this would not matter in babies with the normal number of parietal cells – but in those with a super-normal number of parietal cells, dangerous hyperacidity (leading to pyloric stenosis) would occur before the feed-back is established, at the best guess time of around 4 weeks.

In his main article Dr Rogers wrote –

We concluded that neonatal gastrin secretion was present at birth and became greatly increased by Day 4… the rising gastrin should be considered as an independent primary phenomenon causing acid secretion.

Our paper was the first time that neonatal hypergastrinaemia (i.e., high blood levels of gastrin) had been documented.  It has now been confirmed many times.

Our hypothesis then was that a self-perpetuating process would have begun in which hypergastrinaemia, by causing hyperacidity, would induce pyloric contractions; pyloric sphincter work hypertrophy and eventually IHPS.  Babies destined to develop IHPS would self-select by starting out with an acid secreting ability at the top end of normal.

We found that basal acid secretion rates were greatly increased in the IHPS babies… This was the first time that hypersecretion (i.e., a higher than normal level of acid secretion) had been shown to be associated with IHPS.  Many others have confirmed hyperacidity and hypersecretion of acid.

Mum w baby me 1945This conclusion of Dr Rogers would seem to give the lie to my understanding (based on much earlier medical articles) that my mother’s stressful condition in 1945 may have triggered my PS.  A friend reports (see a Comment with this post) that Dr. Robert Sapolsky has done extensive research and concluded that stress hormones of the mother do affect the baby in utero.  I will pass on Dr Rogers’ comments to me on this subject in another post soon.

Dr Rogers comments that this finding agrees with all the features of PS and its effective treatment.  (For details of this see my previous posts.)  He adds that both the surgical and medical (with the atropine family of drugs and reduced feeding) treatments of PS both allow acid to leave the stomach, thereby greatly reducing gastric acidity and allowing the pylorus to resume its normal size and functioning.

He adds something that is significant for many who have had PS surgery as babies –

Long term analyses have repeatedly found evidence of clinical hyperacidity in adult survivors – either from the need for duodenal ulcer surgery or for anti-acid treatment.  Hypersecretion of acid must surely have a major part to play.

This will be of interest to many, as one of the most common (but often dismissed) complaints of PSers is of reflux (GERD) and other gastric discomfort.

The report then addresses three remaining questions –

  1. What is the specific cause of neonatal hypergastrinaemia?
  2. When does developmental neonatal hypergastrinaemia subside?
  3. Why is the presentation (and by implication, hypersecretion of acid) provoked so often at around 4 weeks of age?

He offers some considerations, and I pass on this emailed comment –

…the basic problem leading to PS is the inheritance of a larger than normal number of parietal cells (parietal cell mass PCM) — hence when stimulated by normal levels of gastrin there is a hyperacid state which is uncontrolled within the 2-3 weeks after birth due to an immature feedback process.  The further week necessary for maternal concern to lead to admission is likely to lead to a common presentation at 4 weeks.

Thickening of the pylorus has in itself been found to stimulate acid secretion: the process once begun has an element of fatal self-perpetuation unless there is surgical or medical intervention.

Mother and baby3I asked Dr Rogers why a sizeable minority of babies have PS surgery well before the most common age of 4-6 weeks.  I have read of a very few babies going to surgery only days after their birth, and I had my operation when just 10 days old.  He explained –

Earlier occurrences may be due to this process starting earlier — for example, there are an increased incidence and earlier presentation in babies whose gullet (oesophagus) is not open (oesophageal atresia).  The stomach is not alkalinized by swallowed saliva in these babies, hence – as far as acidity is concerned, they hit the ground running!  You are correct in citing the additional effect of pyloric stenosis itself for any reason, causing further acid secretion.  Gastrin is also secreted when the gastric antrum is distended due to a narrowed exit.

Finally, Prof. Rogers in his article makes some practical recommendations.

Because gastric acid secretion has been shown to be the main factor in the development of PS, babies who secrete high levels are most at risk.  How do we manage this risk?  Dr Rogers writes –

Medical control of acid secretion is now easy and safe and very effective.  We ought to use it – especially when pediatric surgical expertise is not available.  Medical treatment at present with atropine and controlled underfeeding with gastric washouts does reduce acidity and does produce enduring cures despite the temporary treatment.

He adds that the cause and character of duodenal ulcers in adults is similar to those of infant PS, and that medical treatment of duodenal ulcers is highly successful… so why, Prof. Rogers asks, should PS not be treated in a similar way?

Note:  Readers interested in obtaining a copy of Dr Ian M Rogers’ report including detailed references should request this in an email to the owner of this blog (see the About  page at top).

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.