Video Case Based Question & Answer Session: Upper GI (Esophagus, Stomach and Duodenum) Play Pause Volume Quality 720P 720P 576P Fullscreen Captions Transcript Chapters Slides Case Based Question & Answer Session: Upper GI (Esophagus, Stomach and Duodenum) Overview Upper GI (Esophagus, Stomach and Duodenum) Live webinar Q&A on 9/13, 6pm-7pm ET Yeah mm. Home Yeah. Yeah mm. Mhm. Mhm. Okay, well everybody welcome to the ninth annual Mount Sinai G. I. Hepatology board review uh for the second year this is a all zoom virtual event. Um and if you log onto the website you can see all of the lectures encompassing everything from esophagus to stomach to large bell to IBD to liver. All of those are available to you on the website. So I encourage you if you have not yet uh Access those videos. Each one is about 20 minutes or so. Nice, digestible snippet of one particular topic given by one of the Mount Sinai faculty. So again, thank you for joining us. This is the first of four live virtual Q. And a sessions that we will be having. Tonight's topic is esophagus, gastro duodenal gi bleeding and upper gi pathology. So any and I encourage you to ask questions and you can see on the bottom of your zoom screen there should be a cute and a box. Please feel free to type in any or question that you may have and we will direct them to the panelists to discuss. Any question may have I I promise you that somebody else probably has the same question and it will be a great way to begin some discussion um uh Without further ado we'll get started but first I do want to thank our sponsors for supporting this event. Uh and there should be a way that you can actually access our sponsors so you can see the amazing products that they have uh and to help support uh the educational program that we have for you this evening. Um So um if not for anything else, we'll get started just to get jumping in here. Um And I'm gonna start off with a case and a question just to begin the whole process for this evening. But again I please I encourage you panelists and attendees of course acts ask questions, be that the Q. And A button so we can get everything started here. But I figured we'd start with a case and so this is a celiac question. I hope I didn't give it away with their but you'll see it right from the get go. Okay So you are seeing a 25 year old woman with a past medical history of migraines and several upper respiratory infections in the last three years requiring antibiotics. She was sent to your office for newly diagnosed celiac disease. She was told to start a gluten free diet and to see you for further management, reviewing her records. You find the following. She has a five month history of Diarrhea stool studies have been negative. She is not taking any medications at this time. Her labs are notable for a positive I. G. A. Anti glade and antibody a negative I. G. A. Anti TTG antibody A positive H. L. A. D. Q. Two. An endoscopy was performed with small bowel biopsies shown on the left hand side. What is the next best step in management? Hey refer to a dietician to discuss a gluten free diet beat check and a missile antibody tigers. See check immunoglobulin levels. Di inquire about n said use or e screen for HIV. You will see a lot of these types of questions on the boards where they take a disease that we are very familiar with, but they are trying to get to you to understand some of the finer details of that process that may actually shed light on a different disease pattern that's actually presenting in a very similar way. So the answer here is c check immunoglobulin levels and the rationale behind that question, we'll pull up on the on the next slide but perhaps um Alex, see if you are available, perhaps sort of comment here about what the pathology is showing on the left hand side of the screen, Alexa, you're on mute. Can you hear me now? Sorry about that? I thought you can hear me right? Yeah, so this is a little bit of a difficult biopsy even for a pathologist. So like this this pathology picture actually deserves to be on the pathology boards because it's so hard. Um What's the first thing you have to recognize that this is from the intestines because it has goblet cells. All these white little round spots or goblet cells. So you're talking about the body from the bow and it has a village up on the top. So that's the small bowel. Um uh you should notice that there's all these little blue dots within the materials and they're not supposed to be there uh in that number, those are all lymphocytes. So what we're seeing here is intrepid phileo lymphocyte oh, sis which has actually a pretty broad differential, including including Celia. So by just by their presence, the lymphocytes in the film did not necessarily diagnosed celiac disease, but they bring up a whole differential including ceiling disease, including tropical screw bacterial overgrowth, certain medications um et cetera. The thing that's glaring about this biopsy is uh the absence of something and that's why it makes it particularly difficult because it's really hard to recognize something that's not there and what's not there is plasma. Um and I'm saying that it's difficult because of this magnification. I don't think you'll be able to recognize that there are planets out there if they if they had a larger magnification or they told you that the lamb inappropriate is relatively empty. Um then suddenly there might be something that you would recognize but based on an appropriate does not have enough to fund ourselves. And if you were to be given higher magnification, you can see that there's actually no clouds of Sils there at all. You might actually be given them. So you have to think about the differential diagnosis of interpretive and proceed doses, which is fairly broad plus the specific absence of plasma cells which narrows it down a lot and I guess I'll stop there. Um for questions or for, you know, somebody take it from there, a diagnosis, although in the pathology report would actually provide some clues as to what the absence of provinces mean. So, Alexis while we have you here for a moment, um I'd like to just get your input because frequently take small bowel biopsies and somebody we're questioning a potential diagnosis of celiac. Um we see as the gastroenterologist, a a litany of potential diagnoses that are placed into that the pathology report. Um so from from a gastroenterologist, what should we do when we see that information? Do you tend to give us a hint of what you think is going on? Or is it really is sometimes just too difficult to say what the underlying processes. So, if there is architectural distortion on top of the interpretation and acidosis, that makes celiac disease and they send it here more likely than the rest. So things like medications, tropical screw bacterial overgrowth or even autumn, I'm sorry, inflammatory bowel disease uh in the colon with upper gi manifestations particularly influence disease would only give you the interpret building uh interpreting those. And that's when we tend to give the whole differential. If it does have architectural distortion, then it really narrows it down to basically screw or some other entities like autoimmune disorders and the particular disorder which is here from here with the absolute classes. So, if all you're looking at is interpretations acidosis and the architecture is completely intact. We're really at a loss because we don't know if the patient has indeed, you know, we're usually not given all the labs in terms of the antibodies that are positive or the history of of a diet, you know, in terms of syria etcetera. So if there is no architectural distortion then everything is in play pretty much. And what's nice about these uh these board questions is that they provide all the information there. It's not like you're having an actual patient, your office who may not know to present you with some information that would become vital. So you can actually understand what's going on. Um and so pascal, correct me if I'm wrong. But when I look at this question, some things that immediately come to my mind as they comment on several upper respiratory infections over the last couple of years and look at the labs and what the story is telling me, Oh this is this is gonna be celiac. Then you look at the labs, okay, the Glee Aiden was positive but most importantly, the I G A T T. G. Was negative. And I think the important thing is when you see that in a question for on the boards, you should really think about, okay, what's in the differential diagnosis for somebody who's presenting these things presenting like a celiac like pattern correct. I think the biggest thing here was that there was a recurrent upper respiratory infections and so with the diarrheal syndrome and the recurrent upper respiratory infections, you want to think of other things like common variable immune deficiency or C. V. I. D. Which is where they were going here with regards to checking the immunoglobulin levels. Um In terms of that, I mean there will be low I G I G M N I. G will be low. Um The anti leading positivity here is kind of like trying to trip people up here because it's most likely a false positive tests in this situation because of its low sensitivity and specificity. Um that serological test is actually not even recommended anymore. And so you look at the TTG that's negative. And so that essentially you know, we'll have you roll out celiac in this particular situation. Um 30 to 40% of people can have a positive haplotype of H L A. D Q two and Q eight and so positive result does not necessarily indicative of disease. We know that in patients who are negative for this particular haplotype is a 99% chance they basically don't have celiac disease is a high um you know, negative test rate if it's negative and you basically don't have soviet if you don't have a genetic abnormalities. Um And so with here we're looking at again, big clincher here is that is recurrent upper respiratory problems. We have a patient that essentially has a negative T. G. Um They threw him and said use here. Uh and Alexi was right in terms of uh it's not unusual to see say intra epithelial impulse psychosis with and set and do vcenter apathy. But you would not see any atrophy if it's inside induced and so that pretty much takes that off of the differential here and then um HIV has nothing to do with this. So again it just kind of threw things in here to kind of trip people up which the boards love to do. I believe in the next slide, we have a little explanation for what we saw here. Um this this recording or this this broadcast will be recorded and will be available for review. Um And so what you can do is you can either choose to look at this right now or you can take a screenshot of it or whatever is easiest way for you to uh to review this. But again we will have all of these. Um This entire session will be available for you to review on the website after the broadcast. Um So to the attendees, please, any questions or concerns that come up uh This is your time. You have a wonderful set of panelists here who are ready and willing to answer all of your questions. Feel free at any point in time. Hit that Q. And a button and go ahead and ask us some questions Murray while while we're waiting. Maybe I can ask Alexa question that I bet some other people might be looking for which is just a quick reminder going all the way back to the first year of medical school or second year. Just a quick primer on how you evaluate the ville i when you're suspecting celiac disease. So maybe we can go back to the slide and Alex could could point that out for it because I think that would be really helpful. There's certainly inevitably going to be a small bowel biopsy on the boards every year. So it might be a great chance to just go back and look at that when you're evaluating each of the villas there to see if there's something wrong. The the I. L. S. Was a great point out but just if we can spend a minute on that. So um the first thing you would have is you would need is a very good very well oriented bias. So I think that they you know they would give you a little bit more low power so you can look out over the line. Um This one zooms in because they want you to also observe the interpretive Olympus. It's um and that's why it's it's uh uh it's it's more like close in and more high magnification. So you will need a bit of a lower magnification picture. Nazi over the line. Um So the villa are the things that are speaking out about the surface. So this little pointy thing on the top that that works a little bit. That's that's a village. And what you want to see is that the length of the villas about the surface is um as long or even a little bit longer than the crib which is the part of the perfume that goes down to the coast. So this in this case there's actually a little bit of villas blunting because in cases of what this disease is you get over architectural distortion. If you see a nice small bowel mucosa you would see all the bill like pretty much straight up and there will be as tall as the crips are deep and in fact in my building taller the ratio of the perfect rations 3-2. So you would sort of mentally decide whether with surfaces, everything that's about that imaginary line is the villas, everything that's below is a creek. And the ratio of the crips the crypt hype. I'm sorry but those hide quick. That should be approximately 3-2 and they should all be pretty slender. We have a question from the audience. The question is if the patient has a I. G. A deficiency is the negative IgG Iga Ttg a useful antibody to check uh in this patient. So pascal would you like to answer this question. Yeah so if we have a I. G. A deficiency. Usually the lab will reflexively check I. G. T. T. G. And so the fact that it's deficient. You're not going to be able to detect any antibodies that are being made against it uh in that sense. So our lab essentially kicks it off to T. G. I. G. Which would be the next best thing to check any other questions or concerns about celiac. And again on the website pascal has a wonderful talk about celiac where she goes into all of the details that you need to know. Just not just for the board but also for clinical practice but please feel free to have any questions. This is the time to uh bring it to our attention. Okay perhaps we'll move on to another case. Um So this is a good related question. A 29 year old woman has heartburn and acid regurgitation several times a week. E. G. D. Is completely normal. No Heidel hernia is seen. A ph study demonstrates acid exposure time of 7%. Barium swallow demonstrates significant reflux among patients with non erosive reflux disease. Which of the following factors predicts symptom improvement with proton pump inhibitor therapy. A abnormal barium swallow. Be symptom of regurgitation. See esophagitis on biopsy D abnormal ph study And E. Or e no evidence of high it'll hernia. So the uh we'll get the answer and then we'll have perhaps um mike if you have a moment perhaps you can dive into this question and talk about some of the ins and outs here uh the answer here is going to be d an abnormal ph study. So mike let me hear your thoughts about what you think is going on here and what the rationale is behind this. Yeah. So the again there are a lot of hints in the in the question stem and then you get a question that is completely separate from the case and this is the this is the joy of the A. B. I am right. Um And and unfortunately that's sort of how it goes. But let's look at both parts of the question stem just to think a little bit about things. So The first question, the first part is 29 year old woman. Alright. Not normally typically somebody that would jump into your office with the stereotypical gastroesophageal reflux disease like a 56 year old obese male, right? Where you're you're sort of thinking okay right down the pipe 29 year old woman with good sounds like it could be set up for something kind of funky but they have typical symptoms of reflux heartburn and regurgitation. And if you watch the lecture that's that's law loaded for you. We talk about a typical and typical symptoms of reflux. The frequency is again very important several times a week versus here and there suggests the severity of the disease. Um And then they sort of throw you a little curveball E. G. D. Completely normal. Great but you have to remember that 70 to 80% of patients with clinically significant reflux disease are nerds they have non erosive reflux disease. And so this really doesn't exclude or include anything for you and the lack of Ohio oh honey. Again not not unsurprising. And a good patient especially a young woman. Now the key thing right? A ph study demonstrates asset exposure time of 7%. You're going to see numbers all over the place. But anything over the 56% number is really suggesting a positive study where there isn't debate. So 7% definitely lands in the abnormal area. That certainly sounds like it's out of whack for overall reflux and a barium Asafa graham demonstrating significant reflux. And this gets to answer a um it's great that it shows significant reflux but it's just a small component in time and it doesn't tell you over time whether or not you just happen to catch a freak reflux episode or if this is a common occurrence for the patient. So we can't really use that to predict the same way that we can the quantitative reflux testing that suggested an answer. D and that's why a is no good compared to d. Regurgitation is a symptom that is very unlikely to respond to proton pump inhibitor theory therapy which is the question that's actually being asked because a volume regurgitate er a volume reflux. Er It's the amount of reflux that's causing the symptoms and or tissue damaged. Not necessarily the acidity of it. And so of all the symptoms out there and of the typical symptoms regurgitation is less likely to respond just by making reflux ate less acidic. And that's why uh that's not a good answer. Their Asafa Ghitis on biopsy can be non specific. Um And again if it's not a severe arose of esophagitis in the L. A. Classification. Now we've really moved to C. And D. Grades of esophagitis being clinically relevant compared to A. And now be being lumped more with A. Than in the past where it was lumped more with C. And D. Doesn't necessarily predict anything. And you can see a sausage itis on biopsy for multiple different reasons and not just good and the lack of a hiatus hernia. Um Doesn't really tell you a whole lot about response to PP. I. Therapy. There's just no no knowledge nothing in the literature that really links those and that's why I. D. Is the best answer here. Thank you mike. That was a wonderfully detailed answer. Um I have a question for you. If this 29 year old woman came into your office, would you have performed an E. G. D. On this patient? So that's a that's a great question. And the initial presentation would probably say um no because you don't have any red flags or at least were not presented with any here and so an empirical PP. I. Trial would be reasonable. Um But as we all know in and regular everyday practice, chances are they're coming to you because their primary care doctor or larry, the cable guy is convinced them to take a pee pee. I empirically and they didn't get fully better. And so that's why they're in your office. So um failure of a. P. P. I. In this in this patient um You know depending especially with typical symptoms might lead you to look to see is there something going out else going on here? But in E. G. May not be as helpful as something for example like in a salvageable manama tree test. Uh In addition to the quantitative reflux testing again here, depending on their response to a P. P. I. Trial as I talk about in the lecture. Um That may guide you as to what kind of quantitative testing you might want to do to rule in or to rule out excess gastroesophageal reflux and are you are muted? I just got emailed a question um about would you consider a gastric emptying study in this patient? If all above was normal. So, gastro Priestesses, One of those things that I think is very much under diagnosed when we're considering a diagnosis of GERD? Um And it is certainly a not so uncommon cause that of exacerbation of gastroesophageal reflux leading to it being symptomatic or causing tissue damage. Um But if everything here were normal including the quantitative acid uh the quantitative reflux testing. Indeed it would be very unlikely that Asafa google symptoms of heartburn and acid regurgitation would be caused by gas delayed gastric emptying if it's not leading to excess reflux. So in a patient where all of this looked normal, we'd be having to consider a diagnosis of a functional to sort of like visceral hypersensitivity syndrome where a normal amount of reflux is causing the symptoms and a trial of neural modulator therapy would probably be indicated uh Perhaps mike or berry can sort of chime in here. But what would be your threshold in this patient who's having symptoms? Now? We don't get a clear answer here based on this questions them about whether they're on a P. P. I. Or not. But what would be your threshold to even do a functional test the ph or manama to test and when would you consider that to be appropriate there? You want to take that first. Um Basically the abnormal ph study was done, it would be interesting to know whether how much was upright and how much was supine. The number 7% makes it is abnormal but it's not highly abnormal. Most of the patients we see 10 15% if we're contemplating surgery. So I think there may still be an element of functional heartburn in this patient even though she has a normal or abnormal ph studies. So I would not rush to manama tree without dysplasia or any other symptoms. Yeah I think that's an important comment, right. That that the diagnosis of visceral hypersensitivity or a functional disorder here functional heartburn is a diagnosis of exclusion. We don't have a test to confirm it. So we've really got to rule out other things going on and it would be appropriate to treat GERD if you see it there. But uh you know, that's that's just an important that there is no definitive test. Um And ari do you want me to answer the question that came up in the Q. And A. There? Yes. So if if everyone can't read out, I will say it out loud, doesn't A. P. P. I. Reduced volume of gastric contents and therefore wouldn't reduce regurgitation. So this is one of those great debates in the esophagus ology world. And there's certainly two camps. One camp says absolutely the less acid you secrete, the less fluid should be there to bounce around in your stomach and flow retrograde into the esophagus. Uh And then the other group says, well, you know, there might you might secrete a little bit less fluid. But overall the amount of gastric secretion that is non acid. Um And plus the amount that you eat and swallow um is going to stay about the same. And so actually when you look at Quantitative reflux testing with 24 hour impedance, catheter on or off P. P. I. The number of reflux events and most patients doesn't change a whole heck of a lot what changes is the acidity of the P. P. I. Is effective. Um And so that second camp sort of says you don't you might get a mild decrease in the number of reflux events but overall it doesn't change a whole heck of a lot. So if you're a volume regurgitate er the reflux they may be less caustic if you remove the acid but you're still prone to developing the damage coming from the pepes in and the bile and all the other constituents of that reflux. Eight. And in fact there are emerging studies that barrett's esophagus forms not necessarily only as a result of acid exposure in the distal esophagus but that bile can be a contributing factor in the pathogenesis. Uh Another question was emailed um If this patient had a normal endoscopy would you consider by up seeing at the time to rule out e perhaps Mirena can chime in here? So again man and this woman comes into you, she's having symptoms. Endoscopy is normal. Do you buy ups here and perhaps you are biased? But would you biopsy her to look for E. O. E. Yes. So um thank you ready for the question. Um So the I would look for symptoms of this vision this patient. So um before I would assume it's just heartburn and acid regurgitation. So it's important uh with patients to find out if they have any behavioral feeding modifications um Where you would ask them if they have trouble swallowing, let me tell you know. And then you find out that they eat funny korin co which means you know they're taking time to chew. They would eat only the soft part of the meat they throw out dressed. Um They always have to have a drink with them um when they're sitting for dinner etcetera etcetera. And uh and I do talk about that in my recorded talk. So um if there's any hint of that and now we have this aphasia uh the endoscopy is normal. I think I'm there I would take biopsies. Yes I am biased. But I guess this is an important part when patients coming on P. P. I. You know, nowadays as um mike mentioned, most patients are being treated with PP. I. When they come and see us. So if they are still um symptomatic despite PP. I definitely that is a um indication for biopsies. Um Now more interestingly sometimes even in the absence of dysplasia, we have a young woman here um if there's really no obvious risk factor for reflux that would be the patient that would be missed. And drug with PP. I. Therapy and her symptoms are actually only symptoms in that case they're more likely. So um young females they are more likely to have non specific symptoms of E. O. E. Than a typical male with the O. E. So yes I would look into that and biopsy her about I would say up to 10% of e. Um in the adult more than that in the pediatric population but in the adult up to 10% or so could have normal endoscopy grossly. And then you will see the essentials on biopsy. So as mike as you mentioned she's she's not the classic patient that comes into your office thinking about GERD or acid reflux. So if any G. D. Is being performed, do you take that opportunity to say well I'm here I'm gonna biopsy and rule out another process. Um maybe that wasn't the case a couple years ago. But I think more and more of us are doing that now. Has that sort of taken over. Is that common? Do you think in in everyday practice? Yeah. I think I think that has moved in that direction. And I think as we learn more about uh essentially gastrointestinal disorders or Egypt's that go beyond eosinophilic esophagitis but involved the stomach and the intestines as well that patients we've learned that patients are not particularly good at giving us precise symptoms that zoom in on those diagnoses. And so if you're going in with someone where you're just Not getting clear guidance. Uh and this is your chance to take some samples in there. You know there's very little downside to doing that. But it may give you some clarity. Um and so absolutely would think about that. I would add in a 29 year old woman um that you have to think about some congenital issues like underlying uh weak sphincter or an anatomical abnormality of some kind that may predispose them to having um reflux that is presenting at an early age. We don't know about this woman's BMI or or concurrent medical problems. But do they have autoimmune disease? And could they have an underlying the esophageal motility disorder? As a result of that? I would caution our our audience as they take the boards. Be careful and look for those subtle clues. Um Just like we talked about with the patient with presume celiac that didn't really have celiac necessarily there. Look for those subtle findings that may point you in a different direction for a related disorder. That isn't the one that is the first that comes to your mind. Okay, that was great discussion. Thank you everybody. Uh any other questions that come up uh that you want to ask us? Please feel free. This is your time to uh make use of the wonderful panel panelists in front of you. Um anything no matter how small or big or anything we're happy to answer any questions. So please take a take advantage of us being here. Um So here is the answer again. Uh feel free to take a screenshot again. This recording, this broadcast will be recorded and so you can access it again on the website, but I think we should uh mike had a nice little transition, We'll go to the next question. Uh Well this is a good question to the next one is as a nice segway. But for question number two, which of the following is most likely to respond to a trial of PP. I. Therapy regurgitation, Non cardiac chest pain, chronic cough globe ist sensation or hoarseness. Would any of the panelists like to stab at this question? Sure. I'll be happy to start at this. Well, I mean it's a great question because all of these may respond to P. P. I. So I look at it almost which ones won't respond that well. And if you look at all the LPR ones which are C. D. Any chronic off Wallabies and hoarseness. A lot of times the E and T. Docks will be giving double those PPS for these conditions. They come see you because you're not getting better and they're saying, what do we do? So right off the bat, LPR is not one of these conditions that are gonna respond most likely the PPS. In fact, most of the time they won't more than 50% of the times they won't. So then if we look at regurgitation and then non cardiac chest pain is mike said, regurgitation tends to be more of a volume issue as opposed to ph acid or non acid, which also then leads us to be non cardiac chest pain. And so that certainly would be an answer that I would choose. In fact, if you switch the question around and said if you have a patient with non cardiac chest pain, how would you treat that patient? You would start off right with PP therapy. So uh in numerous ways right off I would say that non cardiac chest pain would be most likely to respond the L. P. R. S. Of chronic cough globus and hoarseness rarely respond even a double dose. And it would make sense in these cases to do a 24 hour ph probe off medicine to actually ascertain that reflux may not or ask the reports may not be the answer here and it's very nicely put out. And it was a great way to go through the question sort of they're asking a question what's not the right answer. Uh And so as you nicely put C. D. And E. Are those symptoms of our LPR. And I think it was actually a recent clinical trial that showed that people don't really do much for those symptoms at all. And so we should probably be moving away from using those medications as front line as opposed to doing further investigation. Um and then the next slide is again, it's an explanation uh for this answer. Feel free to take a screenshot or if you want to uh relive this hour, feel free to watch us again after the webinar. Uh we can move on to the next question unless any of the attendees have any questions or concerns about any of the information that has been provided or anything else that you want to bring up. Uh so far. Okay, well, we'll start with question three. While you're thinking of good questions to ask us a 40 year old male presents to your office with regurgitation. A common theme here. Regurgitation. He initially presented six months prior with heartburn and regurgitation E G. D. At initial presentation demonstrated L. A C. A. Savage itis. He was started on P P I. B. I. D. With improvement in heartburn. But ongoing regurgitation repeat E G. D demonstrates a three centimeter high. It'll hernia complete resolution of esophagitis and no barrett's esophagus. What is the next best step in evaluation? Hey, gastric emptying study be barium swallow, see endoscopic ultrasound, D, esophageal manama tree or E ph impedance on PP. So again, we are really harping on regurgitation here today. Uh And so any of the panels like to take a stab and what your thought processes for this question. Go ahead. Mike, you're the regurgitation expert. Well, you know, it's it's this is an interesting question because the actual clinical management versus what's what's on the boards here. Uh Maybe two different answers and it depends on the practicality of your approach versus the academic approach here and you know, there are a couple of factors that are very important here. The typical symptoms of heartburn and regurgitation has already pointed out in the question stem the grade C a savage itis that was seen, again feeling relatively definitive for reflux esophagitis being made as an accurate diagnosis there. Um and the resolution of the heartburn on PP. I. Um is helpful. The hiatus hernia obviously also helpful and seeing that resolution of the esophagitis, which really makes you feel like you've hit the right diagnosis there with GERD. In evaluating them further, you've got to decide, well, what is it that you need to know about the patient at this point in time? Um, they're not presenting with symptoms of gastro praecis and you've gotten clinical improvement to some degree with only an esophageal symptoms reported to you. So it's a gastric emptying study to rule out Gastro Parisse is going to give you bang for the buck here. Probably not. We talked before about the value of an Asafa graham um in in patients and its its sensitivity and and uh and its accuracy and diagnosing good, not as good as quantitative testing um that we have available. So that's probably going to fall down your list and endoscopic ultrasound here. I'm not sure what you're the US sing. So you have to think about that, but it probably means it's going to be this is an easy one because they needed five answer choices and you could probably pull that off um manama tree here um would be interesting from a practical standpoint if you've decided that a patient who's young who had significant grade C. Esophagitis and has a hiatus hernia. That's only going to grow potentially with time should just go off to surgery. You can make an argument. You don't need quantitative reflex testing. You prove that they have endoscopic lee a reason to have anti reflux uh intervention anatomically. So you need the manama treat appropriately. And following the A. C. G. Guidelines evaluate this patient's peristalsis prior to an atomic intervention. So that sounds great but it's probably not the right answer because it sounds too logical. Um And might be how you actually practice ph impedance testing on PP. I will tell you whether or not you've been able to control the patient's reflux which if you're deciding do they have truly refractory reflux? That's the cause of their regurgitation. Um You know do you feel that much better about taking them in? So it's very easy to narrow it down to D. N. A. And you're probably gonna overthink this question. Um And that's why um now you've seen the practical and the academic answers. R. DNE respectively and that's why he is there because it's the academic answer which is study the heck out of this patient. But from a practical standpoint you should know that the manama tree would take you to the right outcome for the patient. It just doesn't answer the question ultimately which is why do they have refractory regurgitation. We can infer that clinically. But that testing uh e will tell you whether or not they truly have excess reflux, or is this a hypersensitivity or other issue that may be causing persistence of symptoms pathology. So as a follow up, if you are concerned that this could be um a hypersensitive esophagus, visceral hypersensitivity, would you want to know that information before you would send the patient for a surgical evaluation? A great question and again, where the art of medicine and the science of medicine sort of come at odds with each other because you already have enough objective evidence with the grade C. Esophagitis and the three centimeter hiatus hernia to take the patient to an anti reflux and atomic intervention. So you don't need more than that. And as I said, visceral hypersensitivity is a diagnosis of exclusion. And so the best way to treat volume regurgitation is to stop the volume regurgitation which would be an an atomic intervention including high it'll hernia repair. But in this case, uh you know what they're essentially saying is if you do quantitative reflux testing on P. P. I. The acid is well controlled and the number of reflux events are reasonable. And the symptom correlate, particularly if the symptom correlation to a normal number of reflux events is good. It would increase the likelihood that you've got a visceral hypersensitivity process of play. And the patient may benefit from non acid reduction interventions such as a neural modulator. Actually I have a question. Hello, I have a question for mike. So, in the differential, wouldn't even though the patient has established a soft mastitis with rumination syndrome being the differential and which would be the better test to evaluate for. That would be phenomena tree. Or I thought you'd get a pretty good sense of that with the impedance study. Yeah. You know, that's that's a great, that's a great question is, you know, the manama tree would certainly be helpful there. I guess what they didn't describe was the classic effortless regurgitation and re swallowing. That would be the hallmark of what I would expect on the boards to see for a patient where they want to move you in the direction of rumination syndrome, and oftentimes those patients don't have the heartburn that's presented in here. Um so again, I I love the idea of manama tree. This is a patient, I would do a manama tree on because I'd be setting up a 40 year old who's going to hopefully have, you know, a half century of life to live God willing, uh you know, it's going to need an intervention other than just throwing medicine at it. Um there's just going to be kind of a band aid to the primary process. Um and I think if they had said effortless regurgitation or regurgitation and re swallowing or regurgitation and re chewing. I would very much be thinking about what dr Weiss said there in terms of of of working that up for room in asia. Do you have any thoughts on that one? Comment here would be that you'd want to soften your manama tree with impedance because you can only pick up illumination with the impedance cats that are not with the mana metric catheter. So if d said the stoppage of geometry slash impedance and there was a question of effortless vomiting or regurgitation then that might be the test is mike mentioned but rarely nowadays do we just do manama tree alone? We always have impedance which gives us a lot of information especially about ineffective contractions. Yeah. Great. Any other questions or concerns? Anyone of the attendees have any thoughts or anything they want to bring up to the panelists? Okay again here is the explanation behind this answer again. Uh Take a moment. Uh take a screenshot or wherever is easiest. Uh And amount will move on to the next question. Okay we'll talk about some motility. A 37 year old gentleman with a past medical history of longstanding heartburn was seen in your office. His pp therapy was recently increased from once a day to twice a day and h two blockers were added at bedtime. He denies other symptoms. He has been adherent to his GERD diet. He is considering coming off of the medications and going for surgery? E. G. D. Has revealed a small Heidel hernia and normal distal esophageal biopsies. Wireless ph study off medication showed a percent time with ph less than four it was 8% and a damn easter score of 22. What should be done prior to a Nissen fund application in this patient. Again we've discussed some of these but perhaps I will lead them to the panelists to decide what they think is the best uh test prior to a fund application in this patient. And every panelists care to take a stab at this one so we can start and then mike and finished. Um I think the last sentence would be what should be done prior to this. And granted the patient has abnormal ph parameters of the meister Of greater than 20 or 22 normal. Should be 14.7 or less. Clearly documents the patient is reflux. The question really is in my mind. What kind of surgery you're going to do? Okay? Are you gonna do to pay are you going to to a fullness in And actually mike and I had a similar patient. We went back and forth on who had some dysplasia prior to the nissen. And so the manama tree had actually revealed an abnormality of ineffective parasol tick function. So certainly a is my answer right off the bat be a cat scan of the chest and that really doesn't help you PPE should be done prior to meals or not after. The patient doesn't have dysplasia. So I'm not so sure I wouldn't do an endoscopy if it has unless it has never been done and there's no evidence that the patient has. You know we so political person would not be it. But manama tree is very important within penis to try to get an idea whether there's a good parasitology function prior to the procedure and if not in this and there are other procedures out there whether it's links procedure or tips procedure what have you and you certainly want to know what the mana metric characteristics are of the paris topic function and also of the L. E. S. To making sure that that's functioning well and that you don't have an elevated I. R. P. Because of other things that may be going on. Like what are your thoughts? Don't totally agree with you. Barry. I think they you know it's important to recognize that in the the A. C. G. Guidelines. Uh It said the last good guidelines to come out there being revised now but I suspect they will say the same thing which is don't send a patient for anti reflux surgery until you've done a manama tree a high resolution esophageal manama tree to assess the peristalsis because it's a sin to send a patient for a nissen if they have weak peristalsis and you trade a reflux problem for a swallowing problem and that's where you really want to do this as a preemptive strike to make sure you're getting the right wrap as dr Jackson said. Um and also realizing that patients are presenting subjective symptoms. You have a lot of objective data here which certainly is confirmatory for reflux. Um But if you had a little bit less data and the question stem uh it's very reasonable to say in the setting even of esophagitis that we need to rule out an elevated relaxation pressure of the lower sphincter that's causing retention of esophageal contents and we're getting related uh savage itis as a result of that that's not really coming from gastroesophageal reflux but intra esophageal retention and reflux. And that would definitely be the case if the patient we're on narcotics. Everything nowadays uh when it comes from an almond tree, narcotics raises the I. R. P. And as soon as you see patients on a narcotic apt to think of an elevated I. R. P. And what you're gonna do about it, obviously stopping the medication ski. But it may be augmenting or causing problems with intra stoppage of reflux. As mike mentioned. I would not be surprised if there was a question on the boards with a manama tree finding that looked like a kel asia or a significant peristaltic abnormality. Like a non relaxation of the lower esophageal sphincter. And in the question stem it says that there are opioids on board and the right answer. And let me know if you agree would be to try and lean the patient off the opioids and restudy before you sent them for a um Iata me of any kind or intervened on that manama tree result. Great question. Um It's about endo flip. What is the role of endo flip? An evaluation of dysplasia? You are the end of flip men? Well I would say the short answer for the boards is it's in evolution and they probably shouldn't be asking you about it or won't be asking you about it and if they do it's probably not a question that will count. Um So don't worry too much about it at this stage. Um It's evolving. It's it's really primary use right now is to look at the relaxation of the lower esophageal sphincter. The low, the last, latest version of the Chicago classification of motility disorders. Version four point that came out earlier this year. Um says that manama tree should suggest the diagnosis of eg junction outflow obstruction. Which should not confirm it. That you need a confirmatory test like the endo flip which is impedance, planetary testing or in Asafa graham or some other objective test demonstrating an obstruction, functional obstruction or otherwise at the esophageal gastric junction. Um And so that's really where it's primary evolving uses. The latest version of the technology is able to assess um into some degree although without the quantitative approach. Parasol tick function in the esophagus but it's a not a natural peristalsis, the patient is asleep and they're under sedation and you're triggering um a sort of parasol tick response by dilating up of this balloon or filling this balloon with sailing inside the esophagus and seeing how the the esophageal um uh tissue is reacting to um that distention. Um So it's not the same as doing a manama tree upright. People are trying to extrapolate so that we don't have to place a large trans nasal catheter while the patient is a week and really gets upset with us but we're not there yet. Where where endo flip can replace um manama tree. So if you see something that says uh you don't need to do in manama tree. If you've done an endo flip at this point the answer to that is that's an incorrect choice. Um I have one more uh We have another question that we have prepared but another question just came into the email. Um And I'll direct this to to dr weiss. Uh It's about H. Pylori. And the question is do we still need to treat H. Pylori so dr weiss feel free to take what you want. But I think I think the underlying question is we've seen a lot of patients they have refractory H. Pylori. And so I guess I'll rephrase the question somewhat is you have a patient is refractory H. Pylori. Do you continue have to continue going down for eradication or do at some point time. You just say you know what you got it? We'll just sort of watch and wait and see how things progress Just before you get to the refractory question. I think if we look at the position papers and Houston Consensus from 2018 and everything that David Graham saying, he thinks absolutely everybody should be treated for H. Pylori. Uh you know, the academic position is that it's a disease that should be treated. So in the real world, of course we know that the vast majority of people will live and die from something else and have H. Pylori, even though it is a designated as a carcinogen by the World Health Association and major cause of peptic ulcer disease and cancer. Um But the question really what you're saying is, yes, sometimes you just can't get rid of it at this point in time. Um If you don't adequately treated for the first time and the patient develops resistance or they've already got multiple drug resistance is which is not uncommon in the Western society, especially when people have previously been treated with antibiotics for upper respiratory disease and prior antibiotic exposure has been shown to make it much less likely that you respond to that antibiotic in the future? If you need a bridge by lorry. So when the real world is, you know, what do we do when you can't get rid of the H. Pylori and say you've done all the exotic regimens, you've done the high dose of amoxicillin. You've done the Tallahassee and the refresh button and the reality is we at this point we really can't sometimes you just have to make that decision that you have to live with it and have the discussion with the patient. Look, it is a risk factor for various diseases but it can't be gotten rid of at this point and we'll just have to monitor you and monitoring. There's no guidelines so that it can be if you're concerned that at high risk for gastric cancer because they've been tested on meta play asia following them a little bit more closely. If they've got refractory peptic ulcer disease, you can't get rid of it. And of course um you have to treat them in a long term antacid uh the you know, before H. Pylori was quote unquote discovered but you know, marshall um right on the crest of that, there had just been a whole slew of Publications on long term use of H two blockers in recurrent peptic ulcer disease. So we know historically that if you have to you can create somebody with peptic ulcer reason. H Pylori with a long term H two blocker and have very good success and we don't seem to have the same issues of H pylori. I mean with H two blockers that we do all the theoretical concerns with proton pump inhibitors and you know, for those people in between. They have family histories or you know, just have general concerns and animals or dyspepsia. You know at this point, you just have to make that decision that you have to quote unquote live with H. Pylori in the future. Of course, the Holy Grail we're hoping for is better tips, biology. Uh molecular diagnostics will help us figure out the sensitivities of these drugs because as you know, in the guidelines that always says you should try and culture and sensitivity. But in my professional experience, I've had zero success rate doing that. So the idea is to get rid of it. There are several good regiments out there, I think hopefully in the next year. But at present the japanese uh quote unquote potassium competitive proton pump inhibitor well which seems to be much more effective. And there's also um and the japanese trials have been trying to have much higher rates of eradication of H pylori. I think there was a meta analysis from Graeme in last week's last month's Gastro that talked about that. So there will be a future, better therapies and be hopefully better molecular diagnostics to help us refine our antibiotic use in the future. But for now, yeah, I think if you made a reasonable effort and you can't get rid of after two or three times, then you can have that discussion with the patient budget. They're just going to keep it for now and be observed very uh difficult patient populations and we all have a subset of our patients who just, we just can't, you can't get rid of it. Um so we have about four minutes left. So we do find other question, but if there's anybody from the attendees who want to send in a question, this is your time um about anything again related to the upper gi tract esophagus stomach. Do a damn. We we are here, we are willing and able to answer your questions. Feel free to use again that Q. And a button or or shoot me an email. A couple of people send me emails. Um But otherwise I'll throw up the last question and again, if we have time to to review it in detail. Great. But we have about three minutes left in our session. Uh So briefly A 65 year old woman with past medical history of rain odds. Uh Wait before we go on a last minute question, somebody wants to discuss the role of anti spas Maddox. Um So anti spasmodic that that that's a big sort of generality. There's a lot of uses for anti spasmodic. Um Anyone in the pen I want to talk about use of anti spasmodic for upper G. I. Um uh scenarios for example, for people with GERD, is there any role for anti spasmodic? Sor dyspepsia? Any role for for using anti spasmodic in this uh for upper G. I. Uh reasoning real quick if the esophagitis improved with PP. I. Therapy, what additional information? Oh no I'm sorry this is uh so again roll of anti spasmodic, would anyone like to jump in? Well I'll just say in terms of dyspepsia the guidelines do actually in the algorithm. Probably the most effective medication for non ulcer dyspepsia is um a trip line though. I don't know if we would consider that Monica as much as a neural modulator but definitely a role for am a tripling in non ulcer dyspepsia. I agree. And I think for the fellows who are who are part of being comfortable with using these medications in G. I. Uh is uh imperative in your training because otherwise you're gonna become an attending one day and you and writing that prescription is a little frightening using something that you're not familiar with. Uh and they've become a mainstay with managing uh dyspepsia and other functional disorders of the gi tract. Um There's another question here regarding back to another question. If the esophagitis. So on a patient with gert cassava is improved with PP. I. Therapy. What additional information would a ph study actually give you? Um I think Dr. Smith you you you nicely answered this before but perhaps you can just briefly recap in the 33 seconds that we have remaining in our session. Yeah. So uh if you've got L. A. Grade C. Or D. That improves with P. P. I. That's helpful in in confirming a diagnosis of GERD what you're looking for is to see um with the quantitative testing on pp. I what's going on with the acid control and the number of reflux events especially if the patient is respond is reporting regurgitation. Um You're looking to see do you have reflux that is quantitatively uncontrolled or you have good control and therefore you're more likely to have that component of visceral hypersensitivity if all of the quantitative parameters are normal. Thank you. Were at the end of the hour that went by shockingly fast. Um Thank you to all the panelists for providing your expertise. Thank you for the attendees for bearing with us and and asking great questions. Thank you for our sponsors as always for supporting us what we can have this educational event and I encourage all the attendees to on your zoom you should be able to access uh those the people who support us please feel free. They have wonderful things that they can offer to help support not just our educational programs but also your education and your practice. Again, thank you so so very much. Uh and uh feel free to email each individual panelists if you have any other questions or concerns. We are more than happy to to help and educate as we go through. Not just in the board of course but that's why we're here. Um And stay tuned for the following monday uh for our discussion of small bowel. Uh And then the monday after that is colon including I. B. D. And then the monday after that we will discuss all things liver. Uh so again, thank you attendees and panelists. And uh, it was a wonderful event. Take care. Have a wonderful evening. Thank you. Published September 23, 2021 Created by Featured Faculty Ari Grinspan, MD Assistant Professor in the Department of Medicine (Gastroenterology) and the Director of the GI Microbial TherapeuticsMount Sinai Health System View full profile Pascale White, MD Assistant Professor of Medicine (Gastroenterology)Director, Gastroenterology Clinic View full profile Douglas Dieterich, MD Director, Institute of Liver MedicineMount Sinai Health SystemIcahn School of Medicine at Mount SinaiProfessor, Medicine (Liver Diseases) View full profile
