So, we have several here. We probably will get through a couple of them, and there's some interactive parts just like the last one. So, feel free to shout things out. So, here's our first case. So, we have a 12-year-old male who presents for concern for poor growth. So, the mom is there, of course, with the patient, describes that he's a very slow eater, eats very carefully, no history of food impaction, no heartburn or acid reflux-type symptoms. They do note that he has some chronic nausea as well as some burping. Past medical history is important here, significant for asthma as well as seasonal allergies. And mom also notes that when he was younger, he used to vomit really easily, but over the last several years, that part has improved. So, what do you recommend next? Yeah. All right. So, I'm hearing endoscopy from everyone, right? Perfect. So, yes, that's correct. And what are you looking for on endoscopy? Exactly. So, you know, similar to adults, endoscopy is warranted in children as well. So, what we'll talk about in some of these slides is more of the spectrum of EOE and how symptomatology can be different or overlap between children and adults. And so, some of this we talked about in those natural history slides that Dr. Gonsalves reviewed this morning. So, some of that will be a refresher for you to see those slides again and really remember it well. So, in terms of the overall mean age of diagnosis, that runs in the 30s, usually for adults. But there is a peak that can occur in the pediatric population between 5 and 10 years. So, that's what these two peaks are showing in the diagram here. But typically, all comers were looking more in the 30s. And then, as I mentioned, the presentation can vary by age as well. So, in the really young children, infants, toddlers, they may present with some sort of feeding disorder. They can have vomiting, nonspecific abdominal pain or discomfort. And it's really more when you're getting into the later grade school and then adolescent age when they present a bit more like adults. So, that's when they're going to start coming in with dysphagia and food impactions, similar to what we see in our adult population. So, as I mentioned, natural history, you can have very nonspecific symptoms in kids. So, it's really important to look for EOE with nonspecific GI symptoms. And again, it's this hypothesis that Dr. Gonsalves reviewed nicely this morning. So, we talk about in the pediatric population that the Th2 pathway is causing inflammation. And then, over time, there's overlap with inflammation and stenosis. And then, this fibrostenotic pattern. And so, patients may not necessarily fit clearly in those phenotypes. But overall, that's the natural trajectory that we see for the current hypothesis. And this is a diagram you saw before as well. So, a lot of these cases are just really repeating information to make sure that you remember it and have it in your mind as you're helping with other physicians and patients. So, this is that same diagram looking at, over time, the risk of having stenosis. And EOE is going to double every 10 years. So, every decade, you're getting a doubling effect. So, that's pretty significant. And remember, this is the natural history for patients that aren't on treatment, right? So, this is just if they had a delay in diagnosis or they're not on any therapy. So, our goal when we see patients in clinic, as we said earlier, is to make sure we tell them about this and that our goal is to reduce the risk of this happening by giving them a treatment. Because patients will come in and they'll wonder, they're like, well, is my risk going to be related to having cancer or something of that nature? And thankfully, we aren't seeing that association, as you know, with EOE. However, we do tell them how our goal is to reduce the risk of food impaction, tears, as well as this trajectory here. So, this is another slide just to hit home again on the symptomatology so that we all remember it in terms of children in the red here versus adults. So, much more common to see the failure to thrive, vomiting, pain, heartburn, those types of symptoms. As you can see here on the bottom, dysphagia, much more common in the late adolescent and adult population. So, a typical pediatric patient with EOE. So, persistent reflux symptoms is very common. In addition, as I mentioned, vomiting. But, of course, in the later years, dysphagia and food impaction are still going to be important. And we keep telling you about this, but it's so important for us to ask our patients about these compensatory measures. They get really good at doing this. Just like our case earlier, we had that 20-year-old college student, but he's had the symptoms since he was in first grade. And that's very common for our patients. They learn to live with it. And so, it's really important to ask them, are they eating slowly? Does their family notice they're the last one to leave the table? Are they chewing carefully, cutting things up? All of those specific things are important. And then, when you're talking to the parents, when you have an infant or toddler, then you want to see what they're noticing. Do they notice that their child's gagging when they're trying to eat? Are they seeing a lot of vomiting or their child doesn't want to eat? So, thankfully, parents are very observant, so they can tell you symptoms as well. We've talked before about how there's a significant overlap between EOE and objective GERD, where they actually have both conditions. And that we can define. For instance, if you have a patient who's on EOE therapy, endoscopically, the EREF score is zero. You biopsy carefully, systematic biopsies. The eosinophils are zero, but they're still having a lot of heartburn. And you get a pH study that measures objective acid reflux. So, there can be overlap with both. However, it gets more complicated, because they may just have EOE, but the EOE itself causes heartburn. So, there's also a high overlap for that. However, the heartburn may respond to the EOE treatment alone, even if it's not a proton pump inhibitor. So, sometimes it can be clinically complex for us to tease through the different symptoms and define exactly what conditions or overlap of conditions patients have. But we do the best we can with talking to them in clinic and doing various tests. This is a slide to talk about how our eating behaviors can really change. So, you know, when you're a younger infant toddler, their meal times are going to be a lot different, right, than the standard three meals and a snack that we have when we're older. So, they're going to be eating every few hours. If they're refusing food, it's really important, or their formula, or whatever it is, it's important to kind of observe those measures. And patients' parents are really good at doing that. And as I said, regardless of age, endoscopy is important for diagnosis. So, this is a similar schematic to what you've seen before for adults. So, clinical presentation suggests EOE, food refusal, vomiting, failure to thrive in infancy, dysphagia, food impaction in older children and adults. Then you get the upper endoscopy. You get your systematic biopsies, always targeting the areas that have the endoscopic features. Eosinophils are above 15. And then you have your diagnosis provided there isn't another reason, like inflammatory bowel disease or acid reflux that's driving the eosinophils. And as we all know, there's a lot of overlap with the atopic conditions as well. So, it's really important. So, we always in clinic ask our patients about that. I'll ask them about seasonal allergies, whether they're a pediatric patient or adult. We see more adult patients. So, for those patients, we're very thoughtful about, well, you may not have certain allergic or atopic conditions now. But I ask them in childhood, oh, did you have an inhaler? Did you have albuterol as a kid? Did you have wheezing? Oh, yeah. I grew out of that. But now you have EOE. So, you really, it's important to tease through those things with your patients to get a sense of what their other atopic conditions are or if there's current overlap, of course, when we're going to be using things like dupilumab. So, endoscopic appearance. So, a couple things. So, there is overlap. The EREF score is still used in the pediatric population. So, you're still going to look for those same features, the nice images that Dr. Gonzalves showed you this morning for diagnosis. The difference is really being in the stricture part of it. So, the rings and the actual stenosis, that may not be as prevalent in children because we're in that spectrum on the left side that we showed of the inflammatory pathway. But still, using the EREF score is important. And then histologically, things are going to look similar to what they do in adults in terms of a prominent eosinophilic infiltrate. So, things may be a little bit different in terms of the fibrotic component of it. But in terms of the eosinophils, it's very similar in terms of pathology. And so, here's another diagram showing that. So, you can see in terms of, at the bottom, the strictures and rings. Much more common in the blue that signifies adults there. So, hitting home again, what the endoscopic features look like. So, this is normal esophageal mucosa. It's a nice smooth lining. You can see the beautiful vascular pattern there with the red lines throughout. And then contrast this with eosinophilic esophagitis. So, very consistent rings there. You can see really nice exudates there, quite prominent. So, one important thing to note about that. So, we have patients that have these exudates. They're eosinophilic abscesses. But also, sometimes these exudates look like Canada esophagitis. So, when we're, you know, doing these procedures on our patients that are taking this wild topical steroids and they have a risk that's increased for Canada, it looks a lot like this. It looks like white spots just like that in the esophagus. So, when in doubt, we'll biopsy to really delineate, is this someone where we have to give them a yeast infection treatment or is this someone where it's strictly active EOE? So, we can delineate that under the microscope with the pathologist too. And then it's a little hard to see here, but there are some furrows too, but the rings are pretty prominent here. So, histology, same thing. So, on these stains, we have the bluish purple color and then all the pink in here is going to be the eosinophils. So, in terms of contrasting the management between children and adults, same things we just talked about. So, dilation in children is going to be less common. We're dealing with more of the inflammatory pathway. But certainly, if dilation needs to be done, particularly in the older children, that's still reasonable to do. We're just less likely to see that narrowing. Questions on the first case? Yeah, go ahead. When you see exudates and are trying to question is this candidiasis or exudates, I know endoscopically sometimes we do brushings of candidiasis. Can you see eosinophilia from just a brushing? Like, if the endoscopist doesn't get a biopsy and just does a brushing? No, we wouldn't. So, the brushing, that's going to go off to the microbiology lab. So, it's different than the surgical pathology lab that Dr. Saleria showed you. So, the brushing is just going to tell us if there's canna or another form of yeast in there. However, the surgical pathology, sometimes they stain and can see yeast. So, you can catch it the other way, but you're not going to see the eosinophils with the brush that we used for yeast. So, what I'll end up doing is I'll do brushing and biopsies to make sure that you're checking for both if we're not sure when we're visualizing endoscopically. And so, the other related thing to that, so then there's the cytosponge, though. So, the cytosponge is something we do in clinic where it's basically a little pill capsule attached to a string. It's like those animals you had in the bathtub as a kid where you wet the little pill and the dinosaur comes out. So, it's the same thing. So, basically, in clinic, our nurses give the patient the pill on a string. They swallow it, and then the acid in their stomach digests the little capsule on the pill. It opens up into a circular sponge, and then we pull the string up, and the sponge takes some of the epithelial layer off just superficially. As it comes out, it rubs on the lining of the esophagus, and that can measure the eosinophils. The sensitivity and specificity is not the same as the gold standard as biopsies, but it can be used, and we do sometimes use it. So, that's different than the brush that we use in endoscopy that's just brushing and physically taking off the little can of the yeast that's sitting on there. So, just another thing to keep separate. Yeah, great question. Other questions? Yeah, go ahead. Sorry, I don't know if I'm on there or not. So, the question about the brush, that's a really interesting one. There was a study that was done previously that looked at those brushing specifically, and you can get some of those eosinophil byproducts and even look at some of that eosinophil tissue, but that's really been done in just research modalities, but something that might eventually be developed. But yes, it has been looked at, but not done clinically. Great, thanks. I'm glad you knew about that. I have a quick question. It's interesting that dysphagia is required for the diagnosis of AOE, but it's one of the last symptoms to show up. Do you have a rationale behind that? Oh, you mean in terms of the young children versus older? I think that's just because they haven't had the fibrotic remodeling yet. So, when it's strictly the inflammation that's sitting there, they're more likely to have things like vomiting and a stomach ache kind of thing. Later, when they've had the actual inflammatory pathway sitting there long enough, we're getting the subepithelial fibrosis, we're getting the muscle rigidity deeper in the layers of the esophagus, and that's when the dysphagia is going to show up. However, the other part of that is they've had dysphagia likely for longer than we know, right, because they're compensating. So it's two parts. It takes time for the remodeling to happen, for the dysphagia to occur, but then they also may not present clinically to the doctor yet because they compensate once the dysphagia starts. So I think there's two parts to that. Anything else you wanted to add on that, Dr. Gonsalves? We may not have her. Okay, we'll keep going. Any other questions on that one? Yeah. The transnasal endoscopy, it has been used. So some people were asking about that yesterday. At Mayo, they were using it for a while in the adult esophageal clinic we're in, but they stopped using it before I came on staff three years ago, so mainly because adults wanted to undergo anesthesia. They didn't like it. But it has been used more in the pediatric population, and we were talking to some people about that, that I think Cincinnati Children's has done more work with that. As many of you know, the large research center for EOE with Seeger and everything. So I think there are some institutions doing it. At Mayo, we haven't been doing it as much. Yeah, sorry. When she said T&E, that's the transnasal endoscopy, so it's done while they're awake. So, Dr. Snyder, I'll just add something to that. We did try that at Northwestern as well. And I got to tell you, our patients were not so enthusiastic about doing it. Any time I described it to them, they would say, are you kidding me? You're going to put something in my nose and I'm awake? No, please give me the great medication. So I think it is something that maybe people have to adopt. It has been used pretty extensively in the pediatric group, and Lurie does many of these. And I think there's somewhat of a difference in terms of a fear and approach with general anesthesia in children versus some of the monitored anesthesia care that we do in adults. But we do have the capacity to do it at Northwestern. I just haven't been able to convince many people to do it. Other questions? Okay, we can go to the next case then. So this is a 16-year-old male. He presents to the emergency department with an acute food impaction. So typical fashion, he was at a barbecue and had a chicken sandwich, and then he felt it stuck that occurred about eight hours ago. And he reports that about once a year he experiences difficulty swallowing food, but assumes because he has eaten too fast, and often patients will tell us that. And usually he is able to clear it with sips of water, coughing, different modalities to try to get it through. He is noticeably uncomfortable, but he is breathing well, and he's swallowing his saliva. Past medical history is significant for mild exercise-induced asthma, seasonal allergies. He doesn't have any drug allergies, that's NKDA there. Mild egg allergy though, no medications. And then on physical exam, he's thin, quiet. His heart is normal on exam. His abdomen is flat, normal in terms of pressing on it and palpation. He does have some mild eczema that's seen on his skin. So what would you recommend next? Chest X-ray, upper GI series, endoscopy, or administer Coca-Cola in the emergency department? Okay. So I'm hearing a lot of endoscopy among the giggles. I'm assuming you're laughing at the Coke. I will say this has been done in the emergency room quite a bit. But, yes, endoscopy is the correct answer, so strong work. So a typical pediatric patient with EOE. So as we talked about before, male predominance. We do see a lot of women with it, but three-to-one male predominance. Then atopic disease, so always asking about eczema, asthma, seasonal allergies. Forty percent of the population has seasonal allergies, so that's going to be quite common, but certainly the overlap in general with all of these is important. History of food allergies, family history of allergic or atopic conditions as well, or family history of EOE itself. And then sometimes we will see peripheral eosinophilia on CBC, so on our blood count panels. It depends on the patient. And often it can present at times where seasonal allergies flare up, so that's why we're saying in here spring or fall. So we know it's an allergic esophagitis. So, again, so hitting home on some of the points that we talked about in terms of the lectures this morning. So prevalence can vary. Dr. Gonzalez had that nice slide with the triangle where it showed globally a little bit broader in terms of what the prevalence was, and then she showed at the bottom, I think it was Sweden, that was 1 in 100 patients. So as she said, the sweet spot is probably somewhere in between all of that. So 35 to 100 per 100,000 patients. And as we know, the antigens are typically food, but environmental components can also play a role. We already know the most common ones, milk, soy, egg, wheat, nuts, and fish, but there are other ones including corn, legumes, certain meats, beef, pork, chicken, there's different ones, potatoes, other things that have been listed that aren't as common. And 50% of patients, as we know, can have atopic overlap, family history of atopic conditions. And, again, we've talked about these symptoms over and over again. Acid reflux type symptoms may or may not be overlap of objective acid reflux, dysphagia, and food impaction. And we always, as Dr. Gonzalez said, we like the beautiful pictures that we see with EOE, so we keep showing you these pictures over and over to enhance the points about the eREF score. So really nice for our train tracks up there in panel A, B. We have some lovely rings there, C, a combo, and some of the exudates, as well as narrowing that you can see in the bottom there. The histologic features once again. So when you see pink sticking out of the purple and blue, that's when you know you can see the eosinophils hanging out. So what does everyone want to do next with this patient? So are we going to advise a six-food elimination diet, start high-dose PPI, and then plan an endoscopy in two months, start high-dose PPI with no further endoscopic evaluation required, or start topI guess you could educate them on the elimination diet, but I feel like a 16-year-old boy is not going to be the most compliant. Yeah, you're bringing up a good point. So I'm hearing a 16-year-old boy may not be necessarily an ideal candidate for a six-food elimination diet. Excellent point. Other thoughts? Okay. So yeah, I'm hearing PPI and follow-up endoscopy. Okay. So this patient had already been symptomatic for a while. He's just felt like, oh, it's whenever I ate too fast, or he was compensating. So you're right. The six-food elimination diet would be maybe not the best thing for him. Okay. All right. So yes, I heard PPI and follow-up. So follow-up is key, right? Yeah. And I know you're working on our colleagues in many institutions to do this, so I know you're already on top of that. I've got a quick question. Yeah, go ahead. In some cases, I know some of the folks that I've talked to, they're already going straight to PPI and a steroid at the same time, if managed care will allow that, would you mind expanding your call? So my practice is not to do that. So there is some data that you can, so if they're on Swallowtopical steroids for pediatric patients, then you can add an adjunctive PPI if you need to. In the adult population, we tend to streamline to one therapy if we can, except for the caveat I talked about earlier today, where if they also have concomitant objective GERD and they're on Swallowtopical steroid, I try to get their EOE into remission with Swallowtopical steroid and then have them on a low-dose PPI for reflux management because you're, we couldn't do a two-for-one. When I can get a two-for-one, I prefer that. So I don't like starting two things at once because then when you biopsy, let's say they are in remission, well, what did it? You don't know. So that's what's tricky. So I prefer to objectively biopsy on a specific therapy, whether it's specific diet therapy or one medical therapy. So I'm guessing, so you're saying they're basically doing that to try to prove at once that they're a PPI and steroid non-responder so that they can get dupilumab-approved faster? Is that what you're saying? I think it's advantageous. Oh, okay. So again, I think it's maybe going back more towards documentation and having it all filed. I'm not putting up to that factor of information where all of it is 100%. Yeah. Yeah, that process is not part of my practice and most of us. Dr. Mather can comment too, but no, I don't do that. Yeah, I agree with that because you don't know. Even if you then peel off one of the therapies in the future, then again, there's leading to more endoscopies. So I think doing it in a kind of standard step-up manner is what we have data on and that's probably the best, unless they have more systemic symptoms, then we can talk about other therapies directly. But you're right. If you're going to do it in managed care, you're not going to get that. Go ahead. PPI, he gave it the eight weeks, follow-up, endoscopy, it's still not working. Then what would the next step be, steroids and remove the PPI? Yeah. So if the PPI is not... So you're saying a histologic non-responder to PPI. So they took an adequate dose, they were compliant, they had a repeat endoscopy after eight weeks, biopsies are showing eosinophils 100 or whatever it is. So then I take them off the PPI, provided I didn't have a prior diagnosis of objective GERD that they need it for, take them off, and then you can start over. So you can do swallow topical steroids, you can do diet, or you could do dupilumab. So then it turns into a fresh discussion with the patient on which the risks and benefits of each pathway. And Dr. Goncalves may have another comment, I see her video popped up. Yeah. So I just wanted to add to that because I do things a little bit differently. So if that patient were to have that PPI on board for eight weeks and you don't see significant improvement, I don't stop the PPI at that point and switch to something else. I kind of build upon that. So if we're going to use the option of swallow topical corticosteroids, I will add the topical corticosteroids on top of the PPI and then do that follow-up endoscopy to see if they're in remission. Because the problem with just stopping the PPI is you're now introducing another whole confounder into the situation. We know that 25% of adults have reflux, we know that there's benefits to the PPI. It may have helped to a certain degree. So I don't swap one thing out for another. I will build upon that, get them in remission, and then ultimately try to taper off medications and pull things back. But I have found in my practice, at least, when we just swap one thing for the other, it becomes very confusing when patients are ultimately not in remission. And I'll give you an example, for instance, with dietary therapy, if someone is doing dietary therapy and they're not responding, sometimes we'll fold in that PPI and they may respond because we're getting rid of that GERD signal. We're seeing a lot of concomitant reflux in EOE in our patient population. So we kind of do things in a very algorithmic and built-up way. There's no perfect answer. And what you do with the PPI, does it depend on any of their symptomatic responses? So because I'll have patients that come in and they don't have any symptomatic response in addition to non-histologic responders for the PPI, so then I may not continue it if I switch to another therapy. Does that matter for your practice at all? Yeah, I mean, I would say that the majority of my patients do respond to some degree with the PPI. It's a very small percentage that will say, I did not feel a single bit better, and their histology and endoscopic change did not get any better. It may still be persisting, but I mean, again, there's just no right way to do any of this. This is really the art of medicine in terms of how to come about it in different ways. I think I try to do things in a very kind of algorithmic and systematic way, so that way I know everything I'm doing is making sense, at least to me and the patient. But there's no right way. I would say the majority of people that have started on PPI in my practice, they end up feeling better. And I think we saw all the mechanisms from Dr. Snyder's slide and why that is. There's decreased eotexin-3, there's improvement in some of those barrier genes, there's decreased acid, which can bathe out esophagus and cause irritation in a patient with EOE who already has a barrier defect. So there are a lot of benefits there. So that's why I keep it on, and then ultimately will try to pull it off, but really just trying to get them in remission quicker. And then the other caveat to mention when I talk about stopping PPI, so if they come in with high-dose PPI twice a day, I don't just have them stop the next day. I usually have them wean down. And there isn't, again, there's an art of medicine for this, too. There isn't an appropriate, necessary way to do it. But sometimes I'll have them do daily for a week, and then every other day for a week. It just depends, because some patients will get this kind of phenomenon of rebound acid when they come up. So depending on what dose they're on, I may not stop it immediately. But ultimately, I get them off of it. It just depends on what they come in with, too. And you're raising a really good point about the dosing of the PPI, because some people will get put on omeprazole 40 milligrams twice daily. And that's not actually the dosing that was used in the initial consensus guidelines. When we talk about high-dose PPI, we're talking about the dosing that heals erosive esophagitis. So that's 20 milligrams of omeprazole twice daily, or the equivalent of omeprazole 40 milligrams once daily. So that's also the right thing. If they're coming on really high doses of PPI, it's totally reasonable to bring them down to that treatment dose. One last thing I'm going to add, but I agree with everything that you both have said, that sometimes in our referral centers, the patient has gone to another GI, and now we're at the second or third opinion. So usually, they're already on a PPI by the time they're getting an endoscopy. So that's the other caveat for having added rudescinide and PPI when you get the initial diagnosis of EOE. So I don't know if that's pertinent to your community doctors, but I feel like I'm hardly sometimes doing that to initiate the PPI. They've already taken it over the counter or have gone to another, like a PCP or somebody else. So here we have options for clinical management. So as we talked about, there's a lot of overlap between the pediatric population and adults for this in terms of PPIs, swallow topical steroids, and then dietary exclusions, as well as the endoscopic dilations. It's just that strictures are less prevalent in the pediatric population. Here's an important point, though, a big difference. So obviously, with these shared decision-making discussions that we've been talking about with patients the whole time, they're particularly tailored for patients with parents if you're dealing with a pediatric population. So it's really important to involve the parents so that they understand exactly what the risks and benefits are. Sometimes you'll have scenarios we've all alluded to where we're taking care of the child and the parent in the same family because there's localization with families. And so sometimes you'll have parents that are very educated because they already have EOE or someone else in the family does. But certainly taking that time to make sure that parents have a good understanding of particularly even the risks with the medications and other therapies, it's important to really build that relationship with them too. So PPI responsiveness, again, pediatric population responsive to PPI like we talked about. We talked about these mechanisms. Some may be related to the anti-sacratory reflux overlap effects, others directly that eotaxin three-pathway blockage that we talked about. So here's more examples. So three different patients, teenagers as well as in their 20s. We'll start with this first one. So we have a 14-year-old that comes in, main presentation. They're a little bit younger. They presented with abdominal pain, have environmental allergies, treatment, one on Omeprazole 10 twice a day, eosinophils go from 37 to 1. So these are nice examples of PPI responders in younger individuals. Endoscopic dilation as I showed you early, very safe and also safe in the pediatric population. The dreaded risk we always think about as I noted this morning is perforation. And again, low risk, I told you 0.4% for that pooled grouping from the adult population. We're looking at that similar here, 0.1 to 0.3%. So really it's effective but also safe for patients and making sure patients understand that is really important. This is reiterating the same thing that I just mentioned. So goals of dilation, again, similar. So typically we like to get patients above 15 millimeters if we can. So a normal esophagus is 20, 25 millimeters wide. We're not trying to get that far with EOE. We just need them above 15 and even a little bit above 15 is ideal. If we can get them to 18, that's helpful. We don't need to get them to over 20 millimeters. But we want to get them to that critical threshold where it really helps their symptomatology. And as I mentioned, we don't want to go too far and cause a perforation initially. So that's why we go very slowly. If they need serial dilations, that's very reasonable to do. Patients typically are going to prefer another procedure than a complication, right. Of course they're okay with doing another procedure if it means we're doing it in a safe manner. And so yes, there are patients that are lost to follow-up. But in general, most patients are comfortable coming back knowing that we're doing things systematically and safely. And as I said this morning, chest pain is very common, 50-75% of patients. Soreness there is going to happen for those first few days. It's really important to let them know ahead of time about that so that they don't get scared if that symptom happens. And so I always talk to them about that. Types of dilators, same concept. The bougie, the long tubes, or the balloons, there's really no difference. It depends on the endoscopist. Here's another nice example. You can see the balloon. So the top one, you see how narrowed the lumen is there. This is what the balloon looks like when it comes out of the channel from the scope before it's inflated. And then we inflate it. And then at the bottom here, you can see on this bottom right section, that's the nice moderate mucosal disruption. That's our goal to help our patient. So we've also mentioned a couple times about FLIP. So Functional Lumen Imaging Probe, so basically Northwestern, Dr. Gonzalez's group is really the pioneer group on FLIP. And so basically what it's looking at is what you can see here is the length of the esophagus on an X-ray. So the patient's head is up here. And then their stomach's down here. And so this is a probe that's being placed through the mouth. So it's a little bit different than the manometry probe that we were showing you. So the manometry probe that we showed you, that's done while the patient is awake in a motility lab with a nurse, where they're placing it through the nose into the esophagus and stomach. And then they're asked to swallow different liquids and solids in different positions while they're awake. So this is occurring during a propofol sedated endoscopy through the mouth. It's basically a catheter that has impedance sensors and a pressure sensor. And so it's measuring diameter and pressure in the esophagus. And the bag that's on it, it looks kind of like a sandwich baggie. And it's not dilating like the balloons that I just showed you. So it's not dilating, it's measuring. So it's this very flimsy compliant bag. And what we do is once we place it through the mouth into the esophagus, we want to get it with a few of the leads at the bottom of it into the stomach. It's hard to see here because we aren't showing the full thing. But basically, this is the whole pipe system of the esophagus, and the stomach would be down here. And what we're doing is we're sequentially increasing the volume that's in that bag. So we'll start at 30 milliliters, 40, 50, 60, 70. And as we increase the volume, there's a pressure sensor that's measured there and diameter. So in EOE, basically, we're trying to measure the narrowest diameter. Once we get to a certain peak pressure, that's the distensibility plateau. So basically, it's just a surrogate measure for the diameter in the esophagus. And so this is being used and studied more and more in EOE. And I know you all are looking at that now in terms of dupilumab and response rates with distensibility. So treatments, same things that we talked about, PPI, topical steroids. It's really important for us to avoid systemic steroids if we can in our pediatric patients as well as our adults. If they really had to be used, it would need to be in a very particular scenario with significant disease that couldn't be treated any other way and would just be a short course. But it's very rare for us to do that. And so this is more data showing you in the pediatric population, the similar viscous budesonides are effective. So you're seeing the drop in symptoms as well as the drop in the eosinophils. Questions? I think we have a couple more minutes on this one. And then we'll go to Dr. Goncalves' patient case. Questions? Yeah. Hi. Just a quick question about FLIP. I always pictured it going through the scope, but it doesn't go through the channel at all? Do you use the scope at all to introduce it or is the scope removed? It depends on your practice. So there are ways. So yeah. So there's different ways to do it. One, you can place it blindly. So you don't have to have the scope in at all. It can be sitting on the table next to you. And so the catheter, you just are standing in front of the patient and pushing it through their mouth in. And then on the actual device, kind of that picture that I was showing you with the yellow, you can see how far. And we can tell if the distal sensors got into the stomach. So you can do it that way. But you can also do it with endoscopic guidance, where you have the scope in there at the same time. The actual FLIP device is not going through the scope channel the way like our forceps and our snare and everything do. It's just next door. But you can also have the endoscopy scope in there just to guide you visually. So in our institution, we place a lot of them blindly. But it just depends on what kind of esophagus we're dealing with. In EOE, if they don't have a really tight stricture, you should be able to. The time where it gets a little trickier for me is actually with our achalasia patients, because they're the ones that have that really tight sphincter below, right? So sometimes the little flimsy catheter at the bottom of the FLIP doesn't want to get through. So sometimes I'll have to use a little snare on the scope, attach it, and kind of wiggle it through. So there's all different techniques. It's whatever the endoscopist is comfortable with. But the FLIP does not go through the scope channel. And I will add one more thing to that, and that's a really nice description of FLIP. Our protocol at Northwestern, and we do a lot of these endoFLIPs, is we actually do go in and directly visualize the placement of the catheter into the esophagus. And primarily because some of our patients are going through what's called monitored anesthesia care, so it's a deeper sedation. And so they don't have the same gag or cough reflex. And sometimes if you're doing it blindly, the catheter can go in the airway. So we do go in and watch it go down into the esophagus. Definitely, as Dr. Snyder pointed out, in cases of achalasia where you have a big, floppy esophagus, it is required to go down. We can kind of wiggle and jiggle it through the esophagus and into the stomach. So every single catheter is done kind of under direct guidance at Northwestern. Do you have patients who have a normalized eosinophil count but have persistent endoscopic findings? And how do you manage that? Do you continue down your treatment algorithm and escalate therapy? Or do you think they're slow responders and just continue to watch? Or do you then look at endoFLIP and mucosal impedance or find another way to measure success of treatment? So those are usually patients where I'm dilating them. It's usually more related to fibrostenosis. So the inflammatory pathway is controlled. So I'm putting them through serial dilations until I get them above that 15 to 18 millimeter mark that helps them. Dr. Gonzalez, are you using, because Northwestern does the most with FLIP with this, are you guys using FLIP for that at all? We're not doing that as much in that scenario. Yeah. I mean, I think to go back to the question in terms of what is still active. So if that patient had a lot of endoscopic activity, meaning they're having a lot of exudates, a lot of furring, a lot of edema, then I still think that patient has active EOE. I think we know the limitation of the eosinophil count, and sometimes that can be not as accurate. So even if I have normal eosinophils but their esophagus looks like that, I have not met my endpoint. And sometimes that could be because those esophagus, those eosinophils were degranulated and that's why they're not picking it up. You can do some fancy stains through the Mayo Clinic looking at eosinophilic peroxidized staining to try and pick up on that. But I would still think you want to escalate therapy to treat that patient. In terms of the endoflip, where that endoflip can come into play is let's just say you have a patient that you think doesn't have stricturing, they're still having really bad dysphagia, sometimes that you think that you have healed their esophagus, their eosinophils are quiet, their endoscopic EREF scores are normal, that's when I think the flip can be very, very helpful. Because one, it can help understand if there's any subtle strictures that we've missed. But more importantly, it helps to understand the motility, because sometimes these patients are having persistent symptoms, maybe because they have ineffective esophageal motility. They have some type of esophageal spasm that's happening, which can be seen in EOE. So it can uncover that. We aren't doing flips routinely on every EOE patient, but that's a good role for endoflip. Thank you. The other thing we do is we do a lot of esophograms, I think maybe a bit more than some other institutions do because we have an EOE protocol where the radiologist designed it so they go in this right-sided position that helps with magnifying errors and it measures essentially the narrowest diameter and the max diameter so we can try to visualize some of those subtle strictures that we miss as endoscopists like we talked about before. So that plus flip are two ways that we're trying to detect those subtle strictures. And then Dr. Goncalves brought up the other good point. So if we're dealing with rings and strictures, that's one thing. But if we're really just dealing with a bunch of edema and exudates in there is the EREF score that's still present, it's patchy, right? So maybe the biopsies just weren't in the right spot. So that's something we're always telling our fellows to make sure you're targeting. Target that furrow, target that exudate to make sure we're not missing it. Other questions? So, I think it depends on the institution, community, academic, or referral centers. A lot of dysphagia patients will end up in ENT. Often it can be because the patient may not be able to articulate what their exact symptoms are, right? They're just pointing to their throat or they feel something in their throat or they have the globus sensation where something's always sitting in the throat that may not be related to actual swallowing. So there's a lot of overlap between the ENT and the esophageal clinic where we see them first and we send them to the ENT or the reverse. So I do think there is a lot of overlap that happens there, but hopefully eventually we get the patient to the right place. And it's not just for EOE patients. A lot of it's for acid reflux patients because they can present with nonspecific symptoms that aren't related to the esophagus, like are they having aspiration or do they have a hoarse voice? So they may come to us or go to ENT first and then we have to objectively define with pH testing, is it GERD that's driving the extra esophageal symptom or not? Same thing with asthma. We have to figure out is the reflux driving the asthma because they're having micro-aspiration. So there's a lot of overlap. So we don't order them very much. So a lot of those patients, it depends what institution you're at, most of the patients by the time they come to me, they've already had someone locally that checked the PFTs. So we're just talking about the pulmonary function testing. So I don't order that as much. And then the other overlap we have with ENT is they'll go to ENT or us with dysphagia and it's actually an oropharyngeal cancer. And so sometimes we'll pick up the ENT cancer in our clinic and then send them to ENT or the reverse where they go to ENT, have their oropharyngeal cancer treated with surgery and radiation and then they get a refractory proximal esophageal stricture and they come to us because we can't dilate weakly forever. So they come to us and we teach them self-dilation where they pass a similar version of the Bougie like I showed you in the photos. We teach them how to train themselves. It's not actually dilating the proximal stricture, it's just maintaining the opening after the endoscopies so that they don't have to get anesthesia and endoscopies every week. Good question. All right. I think we're at time now to move on to the last session that we're going to do with Dr. Gonsalves with the patient experience.

eosinophilic esophagitis

pediatric EOE

endoscopy

symptomatology

treatment options

FLIP tool

shared decision-making

multidisciplinary approach