Tag Archives: Ian M Rogers

Reflecting on my 70th

Birthdays and anniversaries are times for celebration, and reaching “three-score years and ten” years is certainly worth a big three cheers! But they are important for reflection as well.

150926-25 sml

Renmark Reunion September 2015

Gratitude to God and to the most important people in my life over these 70 years are features I’d like to be emblematic of me.  I am still surrounded with so many loving and kind people, I have enjoyed wonderful peace and excellent health, and my contribution in several circles is still wanted and apparently appreciated.

Ten days ago Helen and I gathered to celebrate my 70th birthday with our 4 children, their spouses and our 11 beautiful grandchildren.  A wonderful 5 days . . .

October 6th is ten days after my birth-day and  marks the 70th anniversary of the life-saving surgery I had in the Netherlands.  I would not be writing this but for that day in my life!

Together with the country of my birth and background, my weary and expecting parents were struggling to emerge from the ordeal of World War 2.  And then I arrived, their long-awaited first child, but soon clearly defective: scary, uncontrollable and life-endangering vomiting (infant pyloric stenosis – “PS”).  And these were times when medical science was pretty rough and ready by today’s standards and when people didn’t dwell on what they’d rather forget.

Pic 12

Mother with me – October 1945

So October 6th marks what I now realise was the gift of a new and wonderful second start in life, but also the beginning of a life-shaping journey of exploration and discovery – outside of me and within.

Outside, my parents were unwilling or unable to answer my reasonable questions about the 10 cm scar on my belly, and this drove me to look for information elsewhere.  But until the advent of the web, this search yielded only cold textbook medical data about PS and the then 33 year old surgical fix for the condition.  And explanations of my deeper issues were nowhere to be found: there were no pointers to where these might be unearthed and no ways of identifying people who could help me to realise (as I do now) that my pain was by no means wacky.

Book coverWithin, I was tormented with private pain from the dawn of my self-consciousness until recent years.  Even now I am still working to piece my private pain-puzzle together, although the web has given me access to much information, clarification and to networking with fellow-survivors, all of which has enabled me to receive and share much healing.  Since 2012 I have blogged about my journey, and in 2014 a pediatric surgeon friend and I published a small book, in which he explained what many still regard as the elusive cause of PS and I outlined my personal experience of this condition. It so happens (in Australia at least) that October 6 falls in “Mental Health Week” – and my own story has certainly helped me to feel a sense of identity with people challenged by mental health issues.

Time changes things!  The past 70 years have taught us the value of openness in the home, the importance of both listening and speaking for healing, of collaboration in achieving goals, and (by no means least) we have learnt much about trauma.

70 years have also brought huge changes to surgical technique and to holistic care in the hospital and home.  Time seems to have done less to change the unhelpful attitudes of some in the medical profession – but that’s due to human nature being far from perfect.

What do these changes (and their lack in some respects) mean?

120327-07-WgHcThe kind of trauma symptoms I struggled with is rare among more recent PS survivors.  Their surgical scars are sometimes almost indiscernible, usually tidy and very rarely as gnarly.  Affected children’s and their parents’ questions are typically answered much more fully and sympathetically, and the children are helped to understand, “own” and even feel pride about their story.

As I see it, I have discerned this is the growth in myself.  I am indeed a survivor from a bygone era of medical practice and parenting, and my scar is an exhibit of mid-20th century surgery.  I know it’s not socially correct for a cultured older gentleman like me to proudly show off his scar as an 8 year old lad might… but I’m catching up on lost joys and enjoying it!

Advertisements

Understanding infant pyloric stenosis (Conclusions)

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

The reason for this series of posts?

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

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

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

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

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

4   Why is PS more frequent in the first born?

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

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

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

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

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

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

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

Dr Rogers mentions two possible reasons.

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

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

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

Other lines of enquiry

1   Genetics

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

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

2   Chemistry of the pylorus

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

3   Infection

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

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

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

Conclusion

Dr Rogers sums up:

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

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

The future

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

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

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

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

Understanding infant pyloric stenosis (3)

Infant pyloric stenosis (“PS”) is a condition that may affect babies during their first months, and it is regarded as the most common life-threatening affliction of early infancy, affecting between 3 and 5 babies in every 1,000 in “Western” countries.  It will usually starve the infant to death unless treated, either by surgery or medically.

ponderStrangely, we are usually told that the cause of this malady is unknown.  But is it really?

In the previous 4 posts I have summarised the main points made by Dr Ian M Rogers in a recently published small book, The consequence and cause of pyloric stenosis of infancy: Two personal stories.  Ian is a retired surgeon and professor of pediatric surgery, and his book enlarges on his argument in several medical articles which are based on a lifetime of observation, research and experience with PS.

Dr Rogers believes that the cause of PS is not a mystery, and that surgery is often not needed to remedy it.

This post continues a series and overviews the first three of Ian Rogers’ six conclusions, all based on the discoveries and facts which he has presented.  I have outlined Dr Rogers’ book in lay terms to make it accessible and understandable for non-medically trained parents, PS survivors and others interested in this subject.

Having set out the information which I have covered (selectively) in the previous posts, Ian Rogers comments that in 1970 his career put a halt to his work on PS, but that he returned to it in the 1990s, when several basic questions called for answers he believed could be given.

1   What makes some babies develop IHPS when normal babies do not?

Without entering into the more complex areas of the medical science that Dr Ian visits and must be considered to answer this question more fully, “the bottom line” is that inherited hyperacidity would be an answer to this question that fits what we know, although some details remain to be discovered.

Dr Rogers mentions several other known facts that add support to this answer, even explaining why some babies develop PS well before the usual 3 weeks to 3 months “window”, and the well-known link between PS and “O” blood.  Of course heredity as a key factor also explains the frequency of PS in certain families.

Babies with normal gastric acid secretion do not overwork the pylorus despite the raised levels of the hormone gastrin during the first post-natal weeks.

2   Why do male babies predominate?

Male dominance1The 4-5:1 male dominance of PS runs parallel to the incidence of gastric ulcers, well known to be linked with hyperacidity, and males having a more active parietal cell mass (PCM), the acid secreting part of the stomach.

Male babies have also been shown to secrete almost twice as much gastric acid as girls during their first 10 days.

3   Why self-cure with the passage of time?

Release of the hormone gastrin is at very high levels after birth, normally peaks at between 10 and 17 days, and then falls to the equivalent of adult levels at 3 – 4 months.  In normal babies raised acid levels continue for about 4 weeks, thus protecting the baby from microbe attack.  But in PS infants, while gastrin release starts to fall, acidity continues to rise and the sensing that normally allows the stomach to switch between acidity and alkalinity is overwhelmed.

Pyloromyotomy (the operation to remedy PS) disables the pyloric ring, immediately blocking its overwork and allowing normal peristalsis and acidity and alkalinity to return.

The traditional medical treatment of PS in babies and adults was based on the belief that the muscle was not hypertrophied (enlarged through overwork) but spasming, and cutting the vagus nerve and administering the anti-spasmodic drug atropine, combined with regular stomach washouts were used to reduce acidity and spasms.

Effectively, these measures (together with the relief of dehydration and the restoration of healthy blood chemistry) allow babies to survive until they are old enough to outlive the natural raised acidity levels of the first post-natal weeks.

Next post –
Dr Ian Rogers answers three other “obvious” questions about the character and “unknown” cause of PS.

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.

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.

History

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.