As we get started, I just want to go over a case to present to our faculty. This is an 84-year-old type 2 diabetes who presents with esophageal dysphagia and has had esophageal strictures, has undergone multiple endoscopies with dilations, mostly with balloon dilations being inflated up to about 10 millimeters every six to eight weeks without relief of symptoms. I should also add, even after dilation to 10 millimeters, the report suggests that the diagnostic endoscope was unable to be passed and the patient presents for further management. The stricture encountered is shown here in these endoscopic photos and measured about seven millimeters in diameter from about 20 centimeters to 29 centimeters from the incisors, was not traversed with a diagnostic endoscope but was traversed with an ultra-slim endoscope. Any thoughts on how you characterize this stricture? That's a great question, and since I'm a panelist, I think I don't know is not an appropriate answer. This looks to me fairly inflammatory. I don't see any obvious evidence of malignancy. It seems like it's been biopsied, so I think that you would have identified that. You know, this could be like a lymphocytic esophagitis. If biopsies haven't demonstrated that, maybe less likely it's that or eosinophilic esophagitis. I guess I would have a few questions or make some comments that if this patient has been maintained on high-dose PPI in between sessions, I don't think this is a peptic stricture, but I think certainly in terms of healing, mucosal healing in between dilations, it would be very important. It does look like if you compare the second and third pictures to the first that there has been incremental increase in the size of the lumen diameter. I think if I, so this is a refractory stricture. I think I would tend to bring this patient back sooner rather than every six to eight weeks to be a little more aggressive since the longer intervals have not been effective. I would use a polyvinyl, you know, wire-guided dilator in this setting. I would be very generous with steroid injections in this patient and, you know, I guess I would at least, if none of that is effective, I suppose I would at least consider an esophageal stent in this case. I would be a little bit concerned about pressure necrosis in this esophagus that already seems inflamed, but again, I think if the patient is on high-dose PPI, that might be an option, but I think what I would do first is make sure they're on high-dose PPI, make sure we're not dealing with some sort of inflammatory stricture such as lymphocytic colitis or, I mean, esophagitis or EOE, and get the patient on a little bit more aggressive dilation regimen. So, Dana, sorry, you mentioned several things and all excellent points, so can I sort of like maybe either you or Iko or Madhav just try to hone you into some specifics? So, your first comment was you do it sooner rather than later. What's that sooner? Is it every week? Is it every two weeks? Every three weeks? What do you do? I tend to do every two to four weeks because you do sometimes find that in between dilations, the stricture will sort of resume its original size, narrow back down, and so I think being a little more aggressive, particularly at this patient. Okay, so maybe a little less frequent than that, so maybe two weeks I think sounds good. Iko, I mean, this is pretty much like proximal mid-esophagus at 29 centimeters. I mean, it's not peptic stricture because, you know, the distal esophagus is probably normal. Why should we even give PPIs in this situation? I mean, I don't see any reason to give PPIs. Yeah, thanks, Prateek. So, a few comments. This is certainly a long stricture, so it would fit, I think, all Dana's comments about a complex stricture, severity-wise, it's refractory. A couple things to add to the differential. I think it doesn't have the EOE features here, other than, you know, long stricture, narrow caliber. It's in the differential, but I think Vanya would have told us if it was EOE. Lymphocytic esophagitis is certainly on the list, but an important one that I'm seeing more and more of is lichen planus, particularly in older women, and the pathology can overlap with lymphocytic esophagitis, and it causes mucosal sloughing. A couple other things. We didn't get a radiation history, but a radiation thing would have obviously been…that could present years after, you know, head and neck or thoracic radiation. We don't see any barrets, but, you know, long-circuit barrets could be associated with long strictures if there was a large hiatal hernia. And then the other thing is something called intramural pseudodiverticulosis, and I almost saw a hint of it there in the middle panel there, but these can be small little diverticula. They're pinhole-like diverticula, often in the proximal to mid-esophagus that are associated with high-grade proximal strictures. So those are other things to add to the differential. I think the thing that might change your management is lichen planus, because that can be managed with anti-inflammatory in combination with esophageal dilation. It can also account for refractory strictures. Steroids. I use a lot of intralesional steroids. It's a little bit difficult in something like this where it's a 9-sonometer stricture to literally deposit, but if there was a focal dominant, then, you know, steroids can certainly be helpful, and I agree completely with the comment about the, you know, when you've got a refractory stricture like this, think about going back early, not waiting, you know, a month or two, going back at, you know, two to three weeks even. One other comment, because for age of 84, you know, a little bit more morbidity, you've got to worry about complications, but also check her teeth, because a lot of older people start to lose their teeth, and that might help her a lot. You might have to not be as aggressive with dilation if you can get her, you know, if to make sure that her dentition's intact, just to find a more conservative way to manage her. Okay, so, Iko, you didn't answer the question about PPIs. Oh, sorry about that. You answered everything else, but that's great. You know, you know, in something like this where it's, you've got an older person, again, the morbidity, I think you throw in a lot of things, and I think I would often use PPI. If there's a hernia, I would definitely do it. Any hint that there could be some reflux as a component, this is certainly not purely a peptic structure, but in this refractory situation, I think PPI, probably in combination with some anti-inflammatory, particularly if you see an inflammatory component, if there's anything, suggest lichen plantus. And one other comment about lichen plantus is that the pathology often does not help you, because the mucosal biopsies are not sufficient to make a diagnosis. So, it takes a high index of suspicion. It takes the endoscopic features, mucosal sloughing and erosions, and the, you know, the appearance of the structure to really think about lichen plantus, which really can modify the way you approach it. So, Dana, real quick, you mentioned steroids. After how many dilations would you go to steroids? So, is it two dilations, three dilations, or is it based on, like, individual patient and characteristics? So, when do you decide to do that, Dana? You know, I'm not sure there's any evidence specifically about that. My particular practice, I think if I've dilated somebody more than twice, excuse me, more than twice, and especially if I don't feel like I'm making great progress with each dilation, that maybe I'm taking two steps forward and one step back, I'm going to go to steroid injection fairly early on. There's really, as best as I can tell, there's no downside, and, you know, it might help. Thank you. So, during this particular session, dilated 33 French with a Bougie dilator and injected with steroids and biopsied again. Previous biopsies did not show evidence of malignancy or eosinophilic esophagitis, and this time we also added, in addition to histology, which was unrevealing for EOE malignancy or infection, we also added studies for immunofluorescence, looking for lichen planus, because sometimes those lymphocytic features are difficult to tell on histology, and making a diagnosis of lichen planus specifically on histology is difficult. We're looking for these IgG deposits on immunofluorescence, which were negative, and we repeated on subsequent endoscopies, biopsies, and immunofluorescence again. Again, these were unrevealing during those serial dilations and did take into account the recommendations of the panel of going sooner before spacing out as well. But in addition to that, any next steps for this refractory stricture, now that you know the biopsies have been inconclusive, do you still think that lichen planus is an option, or there's no evidence of radiation and no history of lye ingestion? Yeah, since you mentioned the immunohistochemical, the fluorescent staining, the other thing we've got to mention is Bullis disease. Bullis pemphigoid, secretitial pemphigoid, can also cause proximal strictures, although usually they're oral cutaneous. The other thing about lichen planus, you know, we typically think of it with oral lesions or vaginal lesions, but there have been many series where 40% of patients with lichen planus or esophageal lichen planus have no cutaneous or oral manifestations, so it can be very difficult to recognize. And I do look for the endoscopic features. It's these characteristic linear erosions that accompany these strictures that can be very helpful to distinguish it from other causes. Great. And we actually sent the patient for an oral examination as well as a dermatologist. No other lesions were found. We did suspect lichen planus. We started with topical steroids and did serial dilations and were able to keep him above 13, 14 for a little bit and pulled him off. He sort of tapered off the viscous budesonide and then he closed back down. We started back from square one and had to get back up to, you know, being able to keep his lumen caliber up where he's eating and drinking, you know, without any issues. We did actually explore other issues for immunosuppression for lichen planus, which was suspected even though our studies were not diagnostic, but he, given his comorbidities and age, opted to just sort of keep current. He just wanted to keep things the way they were. But I appreciate all of the discussion on the panel about this case. Navani, did you, so how many times have the biopsies been done, like twice, thrice in this individual? I think one of the key messages here is that, you know, we need to also continue following the biopsies and taking as many, because just one set may not be enough at one go around to make a diagnosis. Yeah. And we've repeated them three times. And I would say periodically I will repeat them again. Not always doing the immunofluorescence every time, but I've also just repeated regular histology as well. And I've had other cases where I might've not picked up the lichen planus until the fourth or fifth, you know, set. And so I do periodically repeat that. I think at the beginning, maybe there's so much inflammatory necrosis and debris that they're not picking it up. And so sometimes maybe we have a chance of being more diagnostic later, but it's poor yield and often inclusive and challenging. So Iko, since you brought up this diagnosis, so are you satisfied with this or would you, let's just assume that this was, you know, this individual was maybe 10 years younger and you still want it to go after a diagnosis. I mean, three sets of biopsies, are you happy with that? And would you continue managing this as somebody who potentially may have that, or would you keep repeating it every time this individual comes back for a dilation? I mean, how do you approach these? You know, again, I find often probably half the time the biopsies were not helpful. We rely too much that our pathologist is going to give us the answer, but remember it's often interface inflammation that they're looking for this between the squamous epithelium and the lamina propia and our standard biopsies, unless you're going to get, you know, you start using deeper biopsy techniques, you're not going to get that interface. Probably you might get it if you're lucky 30% of the time, so you don't pick up that, and so I think it's very tricky. I think it really gets down to your clinical suspicion, ruling out other things that are, you know, other causes, approximate structures, and then looking for those endoscopic characteristics, these linear erosions. Again, the mucosal sloughing can be very characteristic and help you clue in, because often you just get back nonspecific inflammation or lymphocytes and everyone jumps on the lymphocytic aphagitis bandwagon, but I think Vani had a clinical suspicion there's something on the pathology that led her to use budesonide. It's usually what I start with, either fluticasone or budesonide, but, you know, I think there's mixed results from the topical steroids, and I often have to resort to immunosuppression, but I, you know, understand the concerns about that in an 84-year-old, and again, I'd ask about the teeth. Could this be like burnt-out EOE in which you're not seeing the eosinophils? I mean, your treatment strategy appears to be very similar. I mean, you're starting with oral steroids, so EOE, lichen planus, I mean, lymphocytic aphagitis. I mean, it sounds like we have these different terminologies, but the treatment appears to be very similar. It's similar to a certain point, right? After you don't go to things like rituxan and methotrexate and tacrolimus with EOE, at least I haven't heard of people using that potent systemic immunosuppression to date. We're using biologics now, but not global immunosuppression. So, I think first line, certainly topical steroids, you could say use it for either, but I think there's limited efficacy for topical steroids for lichen planus. There's a series from Mayo Clinic, Jeff Alexander and Dave Kaska published on it, that there was some efficacy, but I think it's limited. Great. And we have questions from our audience as well. The first one I will ask is, how can we reliably exclude proximal esophageal stricture greater than 10 millimeters without doing a savory dilation of patient with dysphagia? Any tips? Okay. I'm sorry. Can you say that again? Sure. How can we reliably exclude proximal esophageal strictures that are greater than 10 millimeters without doing a savory dilation in a patient who presents with dysphagia? So, how do you recognize a proximal esophageal stricture when the scope is passed essentially? There might be a stricture. What are tricks that you might do during an endoscopic examination? I mean, I think that's a fair point. I think, you know, in patients with solid food dysphagia, you know, just common things are common. So, rings and peptic strictures are just going to be much more common than a proximal stricture, which would generally be a web. Or if you, you know, if you think about the causes of proximal strictures, it's generally going to be a web or EOE. And so, if it's EOE, you're presumably going to have other features of that. And if you suspect that, you'll identify that on your pathology. Now, if it's a web, I mean, it should really demonstrate itself on endoscopy. So, I'm not sure I can think of a condition that would cause a occult upper esophageal stricture. Okay. And Dana, just along those lines, either you or Madhav can answer this. What's the dose of steroids that you use for injection? And then also a more practical one is do you inject before the dilation or after the dilation? So, I use, we have vials of Triamcinolone that are 40 milligrams per ml and we dilute it into five mls. And I prefer to do the injection after the dilation because I prefer to target it to the actual mucosal tear, because to me, that's the narrowest part of the stricture. And that's the one we want to be more aggressive, the area that we want to be more aggressive with. So, I dilate first and then I go back and inspect. And I might inject two different areas. I might only inject one area. It kind of depends. I usually inject at least a cc into each mucosal tear, cc and a half. I generally tend to use the whole five mls. But I do target the mucosal tears. No, completely agree. I do the same. If it's a long stricture, then sometimes like I try to use in eight different areas, like 0.5 ml. But again, I agree with Dana. And then here's a question for any of the panelists. How, when we do these dilations, we always are concerned about complications. We intend the mucosal tear, but we don't want a perforation. Can you discuss what you're looking for to differentiate between a mucosal tear from a perforation? Yeah, well, I mentioned even you know, when I'm using balloon dilators, which is what I tend to use for any, you know, fairly simple structure, I'll usually go look in between inflating the balloon to the different sizes. And once I achieve a mucosal tear, what I'll tend to do is look at it very closely. And I use my water jet function to wash away the water so that I can see the tissue at the base of the tear. And, you know, just to assure myself that I'm not, you know, seeing a black hole, for example, that I'm seeing, you know, usually what you're going to be seeing are the fibers of the muscularis mucosa, you know, most likely that, you know, you're not seeing any fat or you're not seeing a hole that you can't see the bottom of that kind of thing. So I, I inspect it really closely and a real use copious irrigation to make sure I can see the actual base of the tear. Okay. And then maybe Madhav for patients within, by the way, I appreciate we have two other esophageal experts who are online. One is Roy Wong and Vivek and I just wanted to say hello to them and thank you for their comments as well, both of them EGD masters as well. So question to Madhav is you go in a patient with reflux comes in with dysphagia and you find a rose of esophagitis at the GE junction, let's say grade C, you know, do you go ahead and dilate that patient because he or she has dysphagia or would you prefer to hold off and treat with PPIs first? What's your approach? Yes. Generally, if they have, you know, non-significant stenosis, ideal strategy would be to heal all the inflammation. So if they have a significant stenosis to the point where they have, you know, significant dysphagia and you are not able to pass the adult gastroscope, then doing some dilation would be helpful to relieve their dysphagia and reduce hospitalization, et cetera. But ideally you would want to treat that first. And also in refractory cases, I want to highlight another point that what I generally ask patients regarding their persistent smoking, alcohol use, but also component of pill-induced esophagitis, because many times there might be two overlapping issues. One is peptic stricture. And because of that, they are not able to swallow their pill or that they are swallowing a pill, which is associated with a pill-induced esophagitis. So something to consider in refractory cases. And another question from the audience, do you avoid dilation with esophagitis in which degree? Any degree or severe LA grade C or LA grade D? I again would generally treat that medically and bring the patient back. And I even tell the patient if they have a pretty significant stricture that, you know, this is sort of a, again, this is sort of a chronic condition and you may be seeing me, you know, several times. So I feel like it's safer to treat the inflammation and, you know, see them back to obviously check on healing of the inflammation. And then if they continue to have dysphagia after the inflammation is healed, then to do a dilation at that time. And any specifics on post dilation care management in terms of medications and diet after dilation? Well, as I mentioned, if you think it's anything even remotely acid related, or maybe even if it's not, I'm pretty generous with PPIs at least until the next follow-up, but, you know, treat them medically if you think there's any kind of acid reflux component to the stricture. And as I mentioned, if it seems to be a fairly significant stricture, I generally suggest that they modify their diet and particularly avoid bread and dry bread and meat. Because if anything is going to get stuck, that's what, you know, meat's going to get stuck. And so I suggest that they avoid anything but ground meat. Okay. Iko, I know you're typing this or perhaps you already have, but just in the last few minutes, since you and Vani were, you know, hammering on this lichen planus diagnosis, which who knows whether it's true or not, but anyway, Iko, your approach to a patient like this, let's say, I know you've typed it, but just for the rest of the audience, if you want to just end up with that as what's your approach to a patient like this, let's say you've given steroids, doesn't help, what's your next step? Yeah. So, again, I'll start with either Budesonide or Fluticasone. There is a series from Mayo that described their Budesonide experience. They did push the dose up to even three milligrams twice a day, which I am a little bit reticent to use long-term because I think you can run into systemic absorption. And then if it's from there, I've tried hydroxychloroquine, very limited success, tried methotrexate, very limited success. And I've been using more that Joel Richter published a very nice series in the Red Journal. It's his case experience. It's not a controlled study at all, but he's been using a lot of tacrolimus with apparent success. And I've been using more tacrolimus now, especially when they don't respond to steroids, but I prefer steroids because of safety. But when going to systemic, I'm using more tacro than other systemic therapies. Dilation approach is similar to EOE. It's conservative. I often can't get to target diameters of 16 with severe like implant. It's just often trying to get to 12 or 13 because of the severity of the disease. And there's another question from the vague, any role for thalidomide? For like implant, I haven't used it. I don't know if anyone else on the panel has used thalidomide. I know it's used for crowns for a while and other things, but I haven't seen it used in a long time. And anyone, Dr. Wong asked if anyone would want to do pH monitoring in this patient. I think it's more of a practical thing, right? Is perhaps you can answer that as in a tight stricture, like where would you place, you know? Yeah, there's, I mean, you could place a pH catheter, but I would say that it was a proximal stricture. The distal esophagus, which I didn't show pictures of was not nearly as involved and looked more spared. And the G-junction was more spared. And so I did not have a high suspicion of reflux. Having said that the patient was on PPI therapies in the past, and I continued that just to keep anything, to get any help I could get in this situation. Another thing that is just popping up now is the consideration of self-dilation, which has been reported and been successful, certainly in a motivated patient. I tend to consider it as an option more in calmer, less inflamed, less complex strictures. But does anyone on the panel have more experience with self-dilations in general that they want to comment on? No, I think one of your points well taken. So to, I mean, Roy's point is, you know, very valid one that I think we don't utilize it enough, but I think the case that you showed, I'd say that in a complex stricture, I'd try avoiding it, you know, just because of the risk of complication. But if you had a patient with a simple stricture, peptic stricture, or even, you know, radiation strictures, which are simple and respond to dilation, I think it's an underutilized technique, but, you know, I don't know if others, maybe Iko or Dana, you want to add to that before we wrap up? I just, I haven't really approached too many patients about it, and I just haven't had much success in terms of patient buy-in, you know, about it. And if it's performed, it's, you know, generally performed with Maloney dilators, which as it turns out, we don't even keep in our unit anymore. So no, it's not really... Dana just likes endoscopy too much, so that's why she doesn't... I guess so. Iko? No, it's interesting. I think the, you know, the older experienced esophagologist, Roy Wong and Joel and others are very comfortable with Maloney's, and I think even Mike Paisley is still using, but most of us have shifted to wire-guided. Maloney is a very different technique. It's blind passage, there's no wire. I think there's a safety issue a little bit for those who are not as experienced with placing them blindly, and if there's complex anatomy, if there's a large hernia, any concern about diverticula, I would not recommend blind passage. So I think most people have shifted to wire-guided, but there's still, you know, a very limited role for Maloney, you know, self-Boucher dilation. Quickly, last point, just to kind of go back to Roy Wong's question. So I have encountered some issues where I thought the stricture is related to ongoing acid reflux, and I was about to confirm if they are controlled on PPR or not, and somehow both patients had nascence from duplication in past, and they had hiatal hernia, and before proceeding to a PH study, I actually checked for gastric emptying study, which turned out to be positive in both of them. So in addition to confirming PPR adherence and other factors before probably kind of doing acid reflux testing, one would be to confirm if they have any delayed gastric emptying, which might be useful to alter their diet because they are not responding. And second point was that in one patient at least, I changed their PPR because the pharmacogenetic profile, you know, the data is pretty strong, although we don't have any existing guideline of changing PPR to what and not, but changing to ribiparazole sometimes, which has a different way of, you know, metabolism in the liver, might be helpful to kind of, you know, heal the stricture, and then you can, you know, treat it better. Yeah, I think those are good points, you know, especially if this was a distal dominant stricture and you had some erosions or a hiatal hernia, there's more suspicion for peptic etiology than you'd want to be aggressive at working up any causal refractory reflux, but in this case, it's really a proximal dominant stricture. It's a nine centimeter long stricture. I think the likelihood of refractory GERD, you know, playing a substantial role is small, but it's not unreasonable. You know, obviously Bravo would be out. The Bravo probably wouldn't even stick to that fibrotic stricture, but a catheter might work. Thank you for such an excellent discussion for our first session. We are going to take a 10 minute break, and we will resume at, it'd be 1040 central time, and please join us back. Thank you.

panel of experts

type 2 diabetes

esophageal dysphagia

strictures

endoscopies

dilations