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.