Tag Archives: hyper-acidity

Pyloric stenosis can be for adults too

Infant pyloric stenosis (“PS”) is not well-known in the general community.  Many of those who have been affected by it had never heard of it before.  But today far, far fewer people know anything about the adult form of PS.  As I will explain below, this is (in large part) a measure of the tremendous progress that medical science has been made in this area.

The stories of adult PSers vary even more than those about the infant form of the condition.  Some may find that hard to believe but it’s true!

When did problems start?
What happened?
What did the doctor say and do?
Did it work?
What happened then?
What choices did you face?
How are you doing now?

Think about it:  for adults there are many more variables than a baby might have: diet, wellness, lifestyle, age and stage of life…

However, the basic cause of all PS seems to be the same: high gastric acidity.  And one of the symptoms is usually the same: vomiting that is often severe and possibly (especially in infants) life-threatening.  But unlike babies with PS, adults usually find that with the loss of weight and wellness come pain, bloating, food intolerances, and reflux.  These are usually not a problem for the hungry but (at first) happy infant PS spitter.

In the infant disease, the high gastric acid level over-stimulates the pylorus (the circular muscle valve at the stomach’s exit), causing it to thicken, toughen and choke the muscle’s ability to relax and pass food.

Adult PS is also caused by high acidity, and often also by a virus, Helicobacter pylori, which has the nasty habit of stimulating acid secretion.  The acid erodes the stomach lining and creates conditions which enable the virus to trigger the eruption of gastric ulcers, which then scar as they heal, so thickening the walls of the stomach and pylorus, ultimately narrowing and blocking the stomach outlet.  If left untreated these ulcers can also give rise to stomach cancer.

These differences do not affect the name of the condition: “pyloric stenosis” means a “narrowing” of the pylorus (which means “gate”).  The term “hypertrophic” means “enlargement” and is only used of the infant form.  The effect of PS, whether in its infant or adult form, is also the same: the narrowing of the stomach’s exit ring muscle, causing vomiting and a reduction of food throughput, and thus starvation.

The difference in the development of the two forms of PS explains why the relatively simple “fixes” for infant PS (medication or surgery to relax the pyloric ring) do not relieve the adult form.  The PS baby’s problem is the thickening of the pyloric passage’s muscular outer layers, whereas the adult’s scarring, narrowing and blockage occur inside the pylorus or at the antrum, the tapered (narrowing) part of the stomach closest to the pylorus.

Adult PSers suffer from a range of symptoms including vomiting, reflux, pain, lack of appetite, and inability to maintain body weight.  The adult patients’ general practice doctors and GI specialists will try various treatments, starting with drugs to kill the virus infection and reduce acidity, and then relaxant medication and repeated stretching (“dilation”) to widen the pylorus.  Dilation is often repeated several times but is hardly ever successful as a long-term remedy. Sooner or later the patient usually decides to continue to one or more of a short list of surgical remedies, all of which are more severe and often less effective than the rather simple pyloromyotomy which is the usual surgery of choice for infants.


The simplest surgical remedy is pyloroplasty, a technique that was modified to become the pyloromyotomy which has usually remedied infant PS since Ramstedt’s accidental discovery in 1912.  Ramstedt discovered that it was not necessary to stitch the cut pylorus after he’d split it to relieve the enlarged muscle. He left the gaping pylorus wound to heal by itself in time.

[Select an image to enlarge it if you wish.]



But very sometimes the infant pylorus will not stay open for various reasons, and then a surgeon may return to the pyloroplasty: here the pylorus is split down to the mucosa or inner lining lengthwise (as in a pyloromyotomy); in a pyloroplasty the split muscle is then stitched closed across the pylorus, thus forcing it to stay open.  But because the adult pylorus is often scarred (thickened and hardened) by ulceration, it is often not in a fit condition to be modified.


The second option is commonly adopted: gastroenterostomy is a bypass of the pylorus by joining the duodenum to the stomach.  This removes the pyloric “gate” between the two which understandably has an effect on digestion.  Dietary changes and smaller, more frequent meals are necessary and often the “dumping syndrome” becomes part of daily living, as the body struggles to maintain a regular and appropriate source of energy.  Gastroparesis is a fairly common problem after gastric surgery: damage and interference cause the nerves and muscles of the region to stop working as they should.

So adult PS is more complex in its causes, symptoms, and available treatments.  And all these several treatment options are far from assured of success, as our gastric passage is easily unsettled and has a mind of its own: it is part of a complex network of different and linked organs and chemical input and processes.  Moreover, like any worker our abdominal organs can protest against being handled with less than good skill by working more slowly or sometimes a complete stop-work.  Medication and especially surgery can be quite successful or can result in unwanted and significant continuing physical side-effects.  Some “survivors” are pleased with the results of their choice, and others find they have to “adjust”, sometimes struggling to do so.

“Major adjustment” is thankfully something that is needed by only a very small minority of infant PS survivors.

Scared_DoctorDespite the dismissive words and comforting promises of pediatric surgeons, infant PSers also run a risk of a short list of abdominal and other complaints, some of them after their early surgery and then possibly also in later life.  Remember that the pyloromyotomy does not deal with the baby’s high gastric acidity.  One of the long-term risks is reflux and developing gastric ulcers – and as a result the adult form of PS.  Deja-vu!

But there’s also good news.  Today, thanks to effective and modern surgery, deaths from infant PS are almost nil.  And adults will find that with antibiotic treatment, H. pylori infection is usually quite easily dealt with, and so gastric ulcers and related surgery peaked in the 1970s and are now far less common.

Some personal observations are indicative despite being anecdotal rather than based on a careful study.  Adult gastric ulcers and PS used to be quite common but the only person I have ever known with it in 70+ years was one of my uncles – possibly a family linkage there?

Contrast this with the 8 or so infant PS patients and survivors I have known of or met.

The reader may discover similar figures!

Another measure is Facebook: following its PS Groups for 10 or so years I have logged 1,020 infant PS survivors but “just” 56 adults struggling with the condition of adulthood (several of tham after having survived infant PS).

The medical journal The Gut published an article in 2011 titled, The scars of time: the disappearance of surgery for pyloric stenosis – referring to the virtual disappearance of the adult form of PS, usually caused by peptic ulcer disease.

If medical science had made similar progress in reducing the incidence of infant PS, many parents and survivors would really party!

For readers who have stories or questions about adult (or infant) PS and its treatment and who use Facebook, I can recommend its “closed” Pyloric Stenosis Support Group which includes more than 50 members who have experienced and have posted (in great variety) about their adult form of PS.  (Any Facebook subscriber can find a “closed” Facebook Group, but it cannot be opened and read only by those who have joined that Group.)

Understanding infant pyloric stenosis (2)

This post is the 4th in a straight series in which I have overviewed the section of a book in which the retired Scottish professor of paediatrics, Dr Ian Rogers, recounts what he has learnt from a lifetime of the observation and study of infant pyloric stenosis (“IPS”).

How digestion works

Dr Rogers describes the process of digestion that occurs in the stomach.  He describes the stomach as having two parts, each with a distinct structure and function, and the stomach’s three stage role in digestion.  During these stages the pylorus contracts and relaxes, early to allow fine and easily processed food to pass, after which the stomach continues grinding and breaking down the coarser food to chyme (or pulp) before the pylorus allows it to pass.  He concludes that the contraction of the pyloric ring muscle is associated with feeding.

This raises the question: how would this process work in a baby?  Dr Rogers points out that –

  • Milk in the stomach raises alkalinity which triggers the secretion of gastrin and acid.  This in turn activates the pylorus, and if acid secretion is higher or feeding is in greater quantity and/or more frequent than usual, then the pyloric muscle is overworked and over-develops.
    IHPS causation - I Rogers
  • Artificially narrowing the pylorus in rats stimulates the development of the stomach’s acid secreting lining, thereby increasing even more the stimulation of the pylorus.
  • Studies have shown that gastrin-induced hyper-acidity is indeed a symptom of IPS.
  • In 1976 Dr J A Dodge reported that he had generated PS in 28% of 84 puppies after injecting 20 bitches with a synthetic form of gastrin; it is known that gastrin crosses a dog’s placenta and stimulates acid secretion.  Still more puppies developed PS when they were injected after birth.

Dr Rogers concludes from this that the pyloric muscle is clearly the culprit.

  • Gastroenterostomy03Disable the pylorus by splitting the muscle and its enlargement soon disappears; bypass it (which the gastroenterostomy operation does) and the enlargement remains.
  • This also shows that although the gastric hyperacidity may be hereditary, the cause of IPS is not a hereditary tendency for the pylorus to be enlarged.
  • The only cause of pylorus enlargement that has been found is repeated contraction.
  • Pathological study has found no abnormality in the tumour tissue.
  • The erythromycin phenomenon also confirms this conclusion.  Erythromycin is a macrolide antibiotic widely used to treat bacterial infections, but when taken during pregnancy or by a newborn it has been found to cause a 7-fold increase in the incidence of IPS.  This group of antibiotics works like the hormone motilin which increases stomach activity and contractions of the pylorus when the stomach should be empty after it has done its work: an empty duodenum (as with IPS) releases motilin.  Some details of the function of motilin are not yet fully understood.

Other indicators – clinical aspects

  • Diagn palp.jpgIPS is normally recognized by a doctor using the standard test meal for a baby who is vomiting profusely without bile in the vomitus:  gentle palpation (feeling while stroking) will reveal the swollen pylorus (the “pyloric olive”) in some 80% of cases, and peristaltic waves can be seen moving from left to right.
  • Adults with a duodenal ulcer caused by hyper-acidity can be treated by ranitidine (or in the past by atropine sulphate), a drug that blocks the release of acid, thus raising the alkalinity of the stomach contents.  This suggests the possibility of also managing IPS by using a drug that reduces the secretion of acid in the digestion process.
  • As mentioned, a baby who inherits a high gastric acidity added to the raised acidity levels normal in early infancy can develop uncontrolled hyperacidity which will over-work and over-develop the pylorus.  A first-time and understandably anxious mother who continually re-feeds an obviously hungry baby will amplify what happens.
  • A decline in both IPS and sudden infant death syndrome (SIDS) in babies who sleep on their back has recently been reported in Sweden.  The back sleeping position results in feeds moving with gravity, making gastric emptying easier and faster: this would also seem to confirm hyperacidity as the cause of IPS.

In the next post, we follow Dr Rogers as he applies the information in these four posts to the classic characteristics of PS in babies.

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.

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.