Gut Check: Hans Törnblom, MD, on Gastroduodenal Disorders
Dr Törnblom reviews the revised criteria for gastroduodenal disorders with host Dr Brian Lacy as part of the overview of new Rome V guide for disorders of gut-brain interaction.
Brian Lacy, MD, is a professor of medicine at the Mayo Clinic in Jacksonville, Florida. Hans Törnblom, MD, is associate professor of gastroenterology at Sahlgrenska Academy, the University of Gothenberg. in Gothenberg, Sweden.
Clinical Practice Summary
Rome V Criteria for Gastroduodenal Disorders: Key Diagnostic and Treatment Updates
- Disorders of gut-brain interaction (DGBIs) affect about 40% of adults across 26 countries, with gastroduodenal disorders affecting >10%. Rome V recognizes 5 major categories: functional dyspepsia (FD), chronic nausea and vomiting disorders, excessive belching disorders, inability to belch syndrome, and rumination syndrome. FD prevalence is 7.2%.
- Functional dyspepsia management begins after addressing H. pylori and explaining the diagnosis, followed by small, frequent meals and avoidance of high-fat meals. If needed, a standard once-daily proton pump inhibitor (PPI) for 4–8 weeks is recommended. Persistent postprandial distress syndrome (PDS) may be treated with prokinetics or herbal preparations, while centrally acting neuromodulators can be considered for persistent PDS or epigastric pain syndrome (EPS).
- Other Rome V disorders have distinct clinical features and approaches: Cannabinoid hyperemesis syndrome (CHS) is associated with cannabis use >1 year and >4 times/day, with cessation recommended for ≥6 months or 3 emetic cycles. Inability to belch syndrome may be treated with upper esophageal sphincter Botox, while rumination syndrome, affecting 2.8% of adults, can be evaluated with combined esophageal impedance manometry when diagnosis is uncertain.
Transcript
Welcome to Gut Check, a podcast from the Gastroenterology Learning Network. My name is Brian Lacy. I'm a professor of medicine at the Mayo Clinic in Jacksonville, Florida. And I am absolutely delighted to be speaking today with Dr Hans Törnblom, Associate Professor of Gastroenterology in the Department of Molecular and Clinical Medicine Institute of Medicine, Sahlgrenska Academy, the University of Gothenberg in Gothenberg, Sweden.
Our podcast today focuses on one of the key content areas of the recently released Rome V criteria for disorders of gut-brain interaction, that of gastroduodenal disorders. And who better to have on the podcast today than Dr Törnblom, the lead author of the revised Rome V criteria for gastroduodenal disorders. So Dr Törnblom, welcome. Let's start simply by setting the stage for our listeners. What are disorders of gut-brain interaction, something we oftentimes refer to as DGBIs?
Dr Törnblom:
To start with, thank you, Brian, for inviting me. It's truly an honor to talk to you and your podcast followers. Your first question is a simple one but very important, or perhaps not simple, but very important. The DGBIs are a group of chronic gastrointestinal disorders in which symptoms arise from abnormal communication between the gastrointestinal tract and the brain, rather than from structural abnormalities, comparing with ulcer disease or tumors or readily identifiable biochemical markers otherwise. The DGBIs were previously known as functional gastrointestinal disorders, but the name was changed some 10 years ago to better reflect current scientific understanding that these conditions involve measurable disturbances in gut-brain signaling where people like you and I do research to find out what is it that are drivers for this abnormal gut-brain signaling.
Dr Lacy:
And when we think about the prevalence of DGBIs worldwide, how prevalent are they and how prevalent are the gastroduodenal disorders?
Dr Törnblom:
Yeah, I mean overall, what the DGBIs are surprisingly prevalent. They're very common and this has been extensively studied and described in the adult population during the recent years by the outcome of the Rome Foundation Global Epidemiology Study that was performed in 26 countries worldwide by using internet service. And overall, the prevalence for having at least one DGBI fulfilling criteria for that and not having signs of any other organic disease explaining it was 40% among adults. And the prevalence specifically of the gastroduodenal disorders was a bit more than 10%, 10 to 6% with functional dyspepsia being the most common.
Dr Lacy:
So that's an important topic—10% of the world's population have one of these gastroduodenal disorders, so an important topic for our listeners. So Hans, you mentioned the Rome Committee and the Rome Committee includes experts from around the world to help develop these criteria. What are the 5 major gastroduodenal disorders?
Dr Törnblom:
Well, according to the Rome V classification, categorize these disorders into functional dyspepsia, which we subcategorize into postprandial distress syndrome and epigastric pain syndrome. Talk more about that later on. Chronic nausea and vomiting disorders, which are subcategorized into chronic nausea and vomiting syndrome, cyclic vomiting syndrome, and cannabinoid hyperemesis syndrome. Then we had the excessive belching disorders that are subcategorized into excessive gastric and supergastric belching. And then we had a new category when you belch too little, inability to belch syndrome. And finally rumination syndrome. So we have 1 new category defined in the Rome five criteria compared to the Rome IV criteria.
Dr Lacy:
Wonderful. Great overview. Thank you. So let's start with the most common gastroduodenal disorder that of functional dyspepsia. How common is this and how is it defined?
Dr Törnblom: Well, the prevalence of functional dyspepsia in the Rome Foundation Global Epidemiology study was 7.2%. And the definition of functional dyspepsia is based on having at least one of postprandial fullness, early satiation, epigastric pain, or epigastric burning, where there also needs to be a component of bothersome, having it to a bothersome extent during the last 3 months and with an onset of these at least 6 months before the diagnosis can be made. An add-on to the criteria is that there should be no evidence of structural systemic or metabolic disease that is likely to explain the symptoms as well.
Dr Lacy:
And that's an important point. Well, you made several great points, but one of them too is the chronicity of symptoms that this can't be just for a day or a week, but symptoms should have started at least 6 months ago and have been active in the last 3 months like many other Rome criteria.
And Hans, your committee used a lot of new data obtained since the last iteration of the Rome criteria 10 years ago to help refine the diagnosis of functional dyspepsia. And you revise the definitions of the 2 subcategories. You mentioned them before, postprandial distress syndrome and epigastric pain syndrome. Can you tell us how these definitions changed and why the new criteria might help clinicians and patients?
Dr Törnblom:
Well, yes. I mean, although functional dyspepsia remains the umbrella term in general, the subgroup's terminology PDS or EPS or both should preferentially be used. And that was stated already in the Rome IV criteria. In PDS, postprandial distress syndrome, bothersome postprandial fullness or early satiation of both remain the coronal symptoms. What is important is that other symptom triggered or worsened by the ingestion of a meal, for example, epigastric pain or burning, epigastric bloating, nausea, excessive belching may coexist. And if they do but are not the predominant symptoms, they are considered part of PDS. This what has been changed for the ROME V criteria. In the ROME IV criteria for EPS, it was stated that epigastric pain may occur after meals, postprandial epigastric pain, but that was more counted into the EPS subcategory alone, which created a problem with quite a big overlap between those 2 categories.
And this issue was set to be solved in the current criteria by specifying that postprandial—which is defined as within 2 hours of having a meal—epigastric pain in the presence of PDS symptoms should be characterized as PDS and not EPS. And I mean that can be motivated by studies showing that the meal related epigastric pain in PDS can respond to therapy with prokinetic agents similar to that in PDS, which is a clinically important difference.
Dr Törnblom:
And added to that you can say just to make things perhaps a bit confusing, but not I would say for the future we have provided also provisional criteria to dig in deeper to that. The provisional criteria for postprandial EPS, which is epigastric pain or epigastric burning that starts or get worse after meals in more than 50% of time and provisional criteria for meal-unrelated EPS, which are the rest, epigastric pain or epigastric burning that starts or gets worse after the meal in less than 50% of the time that we have defined this in order to have scientists digging into it and see if the relevance is there, if there is a need to subcategorize these symptom profiles or not, if it makes a clinical difference.
Dr Lacy:
And thank you so much for teasing that out. Very useful. And I think getting rid of that big overlap category will help streamline things.
Thinking a little bit about streamlining, although we could spend an hour just on this one topic alone, what is your simplified treatment algorithm for functional dyspepsia? How do you start treating a patient? Is it with a specific diet and then use an H2 block or a PPI or a prokinetic? Could you just simply lead us through your personalized pathway for an FD patient?
Dr Törnblom:
Yeah, of course. Try to keep it simple as well. You can say to start with during the diagnostic process, H. pylori can be considered as the cause of dyspeptic symptoms, not of FD, but of dyspeptic symptoms. You can say that H. pylori issue should be solved before you make the diagnosis of functional dyspepsia. So you can say that's part of the diagnostic process rather than the therapeutic process, even if it involves a therapeutic intervention for the symptoms of dyspepsia.
So once you reach the diagnosis of functional dyspepsia, I'm a fond supporter of that making and explaining diagnosis is actually the first and probably most important treatment step for most patients I would say. And for many patients, this is the only thing that will be needed. And furthermore, for those where more specific treatments are needed, this is a very difficult task to succeed in if you don't have a patient that is still reluctant about the diagnosis or not understanding what the diagnosis is.
But from that on, the next step that is recommended are dietary and lifestyle advice that should proceed pharmacotherapy. If you compare to the bowel disorders, the evidence base for the diet advice, for example, is not very strong. Simplified, you can say to advocate frequent small sized meal and perhaps avoiding high fats meal as a general recommendation. If that doesn't turn out to be sufficient, still a standard one's daily dose of PPIs during 4 to 8 weeks with discontinuation of therapy in case of insufficient improvement is the next step. You shouldn't use a dose escalation strategy in this instance if it doesn't help get off PPIs. If it helps, try to have it intermittently rather than continuously. We don't have any strong advice to say that it is better to use it in FD or in EPS or in PDS rather than it might be useful in both instances.
From here, the next step, there are slight differences if you compare PDS and EPS. And if having PDS, the first line or the treatment that should then be offered is prokinetic agents or herbal preparations. These are treatment interventions where the availability differs a lot around the world. But if you have first prokinetic agents like itopride, which is a combined D2 receptor antagonist and cholinesterase inhibitor, it is good evidence to say that it can reduce symptoms of PDS. The same goes for acotiamide, which is a cholinesterase inhibitor and antagonist at presynaptic muscarinic receptors also can reduce symptoms. And it's well tolerated and most effective. Particularly in the Eastern world, you can say that herbal therapies are very popular and there are decent evidence for treatments like using rikkunshito, peppermint oil, caraway oil, some Chinese herbal medicines as well. So that is next step level of use. But if you have EPS, there is no real support for using these prokinetics.
At this point of time for both EPS and PDS, if you haven't done an endoscopy, which is not needed from a clinical point of view, if you don't have alarm symptoms and are HP negative or eradicated, at this point of time, if there are considerations that you think it is needed either from this doctor's side to keep your confidence high that I'm treating the right disease or disorder or from the patient side, this is the place where we recommend that do an endoscopy before going on with what is next recommended, which are the centrally acting neuromodulators. Simplified, you can say that the 3 cyclic antidepressants can be used for pain and also for the postprandial fullness in functional dyspepsia. Mirtazapine for improved food intake tolerance and weight gain in situations where you lose weight due to food intolerance. And you can also use buspirone, which can be effective to reduce symptoms of early satiety through its effect on gastric accommodation.
If you are not successful at this point of treatment, this is where we can recommend at least considering a gastric emptying test before embarking on medication that only has evidence from studies of patients with delayed gastric emptying, and that is prucalopride or erythromycin. Importantly, if you have the dyspeptic symptoms predominating, our advice is to not change the diagnosis to gastroparesis, which in my opinion and many others is a different clinical setting. This is a diagnosis where there are epidemiologic data that differs quite extensively when it comes to, for example, the prognosis, which is totally benign in functional dyspepsia, but not so, for example, in idiopathic gastroparesis. So what we say is to then use the terminology of, for example, PDS with delayed gastric emptying time as an indicator of using, for example, erythromycin intermittently or prucalopride long-term if the patient improves by that.
And finally, if all fails, which happens, your primary aim will be to support those poor patients with refractory symptoms where nutritional needs will be in focus and also being the advocate to screen the patient that they don't develop other diseases just like anyone else— be their insurance that they can trust your diagnosis.
Dr Lacy:
Hans, that was perfect. To our listeners, that's something maybe to listen to a second time because there was such a wealth of knowledge there, so thank you.
So Hans, the next big category of gastroduodenal disorders is that of nausea and vomiting. And there are three key nausea and vomiting disorders. What are they and how can you distinguish them by symptoms or testing?
Dr Törnblom:
Well, the three disorders are chronic nausea vomiting syndrome, cyclic vomiting syndrome, and cannabinoid hyperemesis syndrome. And you either have cyclic symptoms with better periods in between or at least periods where you don't have that much symptoms even if you can have them, separating intense episodes of nausea and vomiting. If this is associated to prolonged, which we have defined now as more than 1year and excessive, which is defined as using it more than 4 times per day, cannabis use, then you can start talking about the risk of having a cannabinoid hyperemesis syndrome. The chronic nausea and vomiting syndrome is more characterized by having this relentless situation with nausea and/or vomiting—nausea more than twice per week, vomiting more than once per week without these cyclic characteristics.
Dr Lacy:
One question that comes up all the time is about cannabinoid hyperemesis syndrome, sometimes what we call CHS. How long is it necessary to stop cannabis for a patient to improve if that's the underlying diagnosis?
Dr Törnblom:
Million dollar question. Well, as we have defined it now as well, what you can read from literature and expert experience, if you call it that way, what we are recommending now is that the cessation of at least 6 months or 3 typical emetic cycles. The second part is if the cycles are shorter than 2 months in between or short cycles in between, that is also you can think of it even earlier than 6 months cessation.
Dr Lacy:
Hans, you mentioned that belching is a common problem for many patients and certainly many patients with disorders of gut-brain interaction and excessive belching is now broken down into supragastric belching and gastric belching. How do you tease these 2 disorders out in terms of symptoms and does the treatment for these 2 disorders vary?
Dr Törnblom:
Well, to start with gastric belching, I mean that is something that we all experience and experience from time to time as a normal physiological reflex that is triggered by distension of the proximal stomach, which results in a transient relaxation of the lower esophageal sphincter and the eructation of air from the stomach. On the contrary, if you have supergastric belching, the air does not originate from the stomach, but it's either sucked or less commonly injected into the esophagus from the pharynx and then expelled immediately thereafter, which means that it hasn't been entering the stomach at all. And the characteristics of this, I think most of us, once you've seen a patient with supragastric belching, you can easily identify it from the clinical characteristics with repeated bouts of belching, where distraction tends to reduce the frequency of belching, whereas driving attention to it, discussing it with the patient, quite often results in an increase in the belching frequency.
From this, the treatment of these 2 disorders differs. I mean, these are not the most well investigated situations and there are a lot of opinions about this, but when it comes to gastric belching, probably dietary and behavioral modifications are important. If you are keen on chewing gum, if you are using sweets that slowly are sucked on in your mouth, and if you're drinking a lot of carbonated beverages or eating yourself full before stopping, you probably need to change those treatments, these behaviors. When it comes to supergastric belching, I think one of the most important things is to make patient aware of the mechanism. Sometimes you can do that also by having an investigation with pH impedance monitoring in those patients where you yourself are hesitating or the patient doesn't believe you. It's quite intuitively shown by sitting down with the patient with the impedance curve and showing what is going on.
Making them aware of this sometimes is enough for them to stop their behaviors. They recognize what is triggering in what they're doing. Otherwise, there are dates on speech therapy, cognitive behavioral therapy. And also what I often use is to tell about tricks that if you feel that, okay, now I'm in a situation where I really don't want to belch, and you know that is a risk for belching. Try to stay with your mouth open. It's very difficult to swallow air without closing your mouth. Or if you're sitting in a meeting and sitting with a pencil or something like that, put it in your mouth, bite on it, do something that doesn't look too odd, that prohibits you from having your mouth closed and being able to start this behavioral swallowing and getting it quickly up again from your esophagus.
Dr Lacy:
Wonderful. We call that the pencil trick here. It's funny, you and I have not discussed this before, but it can be very effective for many patients. So
Dr Törnblom:
You look smart as well when you're doing that.
Dr Lacy:
Exactly. Not too hard gently biting out on that clean pencil. You're right. So you mentioned that the Rome V Committee on Gastroduodenal Disorders added a new category, inability to belch syndrome. How common is this and why does it occur?
Dr Törnblom:
Well, actually I have a figure that I can't share with you yet that will be presented in a publication that will appear very soon, which is another epidemiological study based on Rome V criteria. What I can tell is that it is not that uncommon, so it seems to be reasonable that we define it now. The mechanism in patients with the inability to belch syndrome is related to that gas that enters the esophagus after a lower esophageal sphincter relaxation fails to elicit this upper esophageal sphincter relaxation. Rather leads to what we define as a common cavity pressurization that air is entrapped between two close sphincters and oscillates in between and creates this sensation of being unable to belch. It ends by a secondary peristalsis that clears the air into the stomach again, that is a peristaltic wave that is not triggered by pharyngeal activity, rather by the distension of the esophagus.
And apart from the sensation of not being able to belch, there are also varying degrees of descriptions in relation to this inability to have a sensation of chest pain or odd, funny gurgling noises in the chest, bloating flatulence and epigastric pain that can be reported. And I think in many of us who has some experience in this, it's quite common that these patients have a lot of overlap with other gastrointestinal or extraintestinal symptoms or characteristics as well.
Dr Lacy:
That's a good teaching point. The way I think about it is these DGBIs, they travel in groups. So it's not uncommon to have somebody with this inability to belch with dyspepsia and IBS as overlap. So let's say you see that patient in clinic and they really describe these uncomfortable symptoms because they can't belch. How do you treat that patient?
Dr Törnblom:
The currently best established treatment approach consists of injection of Botox in the upper esophageal sphincter. And I think in most instances or almost exclusively, this should be performed by an ENT specialist with target injection to the upper esophageal sphincter by knowledge of anatomical landmarks and the tools of doing that as well. Some use confirmatory electromyography while doing it, others don't. The precise responder rate and the long-term outcome of Botox injection is still unclear, but it seems to last for at least 6 months in most patients and the sustained remission also seems to occur. It would be interesting to see what the literature will show in 10 years’ time when it comes to this. If it's something similar to the dyssynergic defecation, but in the other end of the GI tract, that we're trying to find a way to relieve the tension there. There's probably also behavioral part of it and things that is related to reactions to other GI symptoms or psychological symptoms.
Dr Lacy:
Well, this is how we advance science. We pin something down, we start investigating it and we'll find out more in the future. And we'll keep an eye out for your new publication, one of many. Lastly, as we kind of wind down here, the fifth gastroduodenal disorder is rumination syndrome. If you could just briefly tell us how common it is, how you make the diagnosis of rumination syndrome, and how do you treat it?
Dr Törnblom:
Well, it is quite common actually, and it's definitely more common that I guess both you and I were taught when we were medical students a long time ago, where it was mostly described in patients with cognitive problems and so on. But once more through the Rome Foundation global epidemiology study, we ended up with showing that 2.8% of the adult population had these symptoms— a recurrent seemingly effortless regurgitation of recently ingested food into the mouth with subsequent oral expulsion or swallowing that was not preceded by retching and nausea. And the absence of these nausea and retching characteristics are important clues in the differentiation from vomiting. And this can be quite tricky to tease out when meeting with a patient. Is it vomiting or is it rumination? And it can also be difficult to differentiate the rumination syndrome from regurgitation in the context of gastroesophageal reflux disease. It can be challenging, particularly in patients with associated heartburn.
It should also be differentiated than from mimetic conditions like gastroparesis. In the latter, vomiting typically occurs later in the postprandial period than if you compare it to rumination, which comes in closer relation to when swallowing the food. And if you are in trouble in trying to tease out these mechanisms, additional evaluations will be needed. And for this, the combined esophageal impedance manometry is the gold standard where you perform it with a meal provocation test where you with an impedance signal and then a pressure tracer can see the characteristics of reflux-like event happening by an active contraction that creates an intraabdominal pressurization that precedes the reflux of gastric content.
Dr Lacy:
I like your teaching point. It's the absence of nausea and people just describe this kind of movement up and oftentimes they then reswallow it and reswallowing becomes bitter then they stop that behavior. So Hans, this has been an amazing discussion. Any last comments for our listeners?
Dr Törnblom:
Well, I agree with you. I've had a good time. It's been a great experience. My last comment is probably more a general one to all of us who meet patients where you suspect them to have a DGBI and this goes for primary care physicians up to expert gastroenterologist. I would say trust your clinical experience in identifying a DGBI. Check guidelines for wise clinical decisions about what is needed to confirm this diagnosis and also communicate with the patient that actually recognizes this as with high certainty being a DGBI when you order the tests or investigations. And also tell that the normal outcome of this will confirm—it will not show nothing. I tell my medical student if a test or an investigation shows nothing, you have probably not done it because it always show normal or abnormal or some gray zone. So read up on current knowledge of pathophysiological mechanism and find ways to explain it in lay terminology.
These are basic things that I think will do the trick in the majority of patients that seek healthcare to understand what they're having and the reasons why it can be like this, even if we don't have the ability to show the mechanism or measure the mechanism other than in just a few instances, some of them which we have discussed today.
Dr Lacy:
Two more great teaching points. Part of our job is to educate our patients and to reassure them and of course to try to make them feel better, but great teaching points. So Dr. Törnbloom, again, I had a great time, so thank you. Thank you for lending your expertise on this important topic to our listeners on Apple, Spotify, and other streaming networks. I'm Brian Lacy, a professor of medicine at the Mayo Clinic in Jacksonville, Florida. Our guest today was Dr Hans Törnblom, associate professor of gastroenterology at the University of Gothenberg in Gothenberg, Sweden. I hope you found this just as enjoyable as I did. I know I learned an awful lot today. I look forward to having you join us on future Gut Check podcasts. Stay well.
