Well, I'm going to continue the trend here and see if I can rocket through this and get everybody to the reception, because I'm certain that many people can use it after a long day like this. In terms of what I had to do, there is a lot of redundancy with my talk this morning that I gave the panel, but it's nice to see that there are different people here. And I think what I'd like to do with this talk and when I was thinking about doing this was talk a little bit about some of the highs and lows that we've gone through with POEM and our physiologic explorations and discoveries that we were really excited about. Maybe we got a little too excited, and then we probably should have put the brakes on a few things. And then talk a little bit about the bomb, which people are probably going to get sick of me saying things about the bomb. But I think it's a really important thing that we're going to be dealing with for many years if we're not careful. These are my disclosures, and obviously keep in mind the Medtronic disclosure. So the cool thing was about seven or eight years ago when this started happening was that we had this beautiful synergy of we started to really understand the physiology a lot better because of the tools. And then we had this technique, POEM, that came around that right at the same time allowed us to be a lot more personalized and precise in how we would deal with these subtypes. We could actually define different variants of achalasia and think about taking each one of these subtypes and providing them with a precision care model. So this was really exciting. It was an exciting time in manometry, and believe me, manometry is not a really exciting field. And with that came the Chicago classification, and I have to say that from my take on it, I don't think 4.0 was that much of an incremental improvement in 3.0. I thought 3.0 was pretty good. I think we could have done a lot better job on a few of these particular disorders. In fact, we did nothing for spasm, essentially, and jackhammer other than say that you had to have symptoms of dysphagia. And if you had GERD, consider that it's not a real primary motor disorder. So outside of recognizing that HRM was somewhat flawed and that there was an issue with EGG outflow obstruction that we needed to use complementary testing, there really was not that huge an incremental improvement with that. So if you look at the achalasia subtypes from 3 to 4, it really didn't change much. In fact, we tried to make it a little bit different in the narrative around it, but essentially it's the same, the caveat being that we did recognize that the IRP in supine position alone was probably a mistake. We've known that for a really long time, but it took us 4.0 to bring that out, and that you really needed to be abnormal in both positions. And then obviously the recognition that EGG outflow obstruction was also an issue of artifact and that we had to add further testing. But there was a lot of really good stuff that came out of high-resolution manometry, and the subtypes really were an important thing. And I'll tell you, when we first recognized that this was this progression and we could really look at the natural history of the disease in terms of looking at a normal caliber esophagus and how it progressed to dilatation and sink trapping, and then we had this other variant that was spastic, that when you query these patients, half of the patients had a history of being on opioids. We started to think a little bit more outside the box in terms of what we could do. And for those of you who were here this morning, that's where I get to this issue of achalasia and making mistakes before you even start this whole process of POM. And a lot of this is the recognition that these diagnoses are not always achalasia or not always a primary motor abnormality. And I've seen so many people who get a POM for EGG outflow obstruction or jackhammer esophagus who had a small hiatal hernia that was the cause of the motility abnormality. And it's so obvious on the preoperative motility study, but because people were really excited about doing POM, they probably didn't care that much, to be honest. But then, you know, if you take someone with a small hiatal hernia and you take away their peristalsis and you create a bomb, they're in a lot of trouble. They're going to have a lot of complications, they're going to have severe reflux and significant bolus retention. So going back to that, though, I do think there was, you know, a lot of excitement about the recognition that we had this group of patients who were coming back to our clinics, you know, who had recurrent symptoms. And we could define that, yeah, you know, laparoscopic heller myotomy, pneumatic dilation didn't treat these people adequately. This was a type 3 patient who was treated with the lap heller, and they obviously were just converted to spasm and did a POM, turned this person into scleroderma esophagus, and they did quite well. And it was interesting because, you know, people with scleroderma esophagus typically don't do well, right? I mean, that's why they present with dysphasia and reflux. But because the wall of the esophagus in these particular patients still has some elastic recoil and some compliance to it, you know, they don't get as significant reflux as the patients with scleroderma, despite the fact that's what we're trying to target. And then we started to recognize that, you know, manometry, you know, missed a lot of things, which, you know, and I love this figure because, you know, if I looked at that top panel here, I don't think my mouse is working here. Oh, there it is. If I look at this top panel here, you know, this does look like probably achalasian evolution. You know, once that little focal contraction up there is gone, that would probably be a panosoptic pressurization. No big surprise that the esophagram looks like that and the flip looks like that. And the bottom panel in C, you know, that looks pretty normal. I mean, I'm not too worried about that and probably wouldn't even had to get the flip or the esophagram on that one. But that middle panel, if you look at that closely, you know, yeah, there's a little bit of pressurization, IRP is a little bit abnormal. But that peristaltic sequence is beautiful. That's very normal. You know, that's a normal DCI and it's propagation. But then if you look at the flip and the esophagram on that person, I mean, it looks like chaos. So we started to realize that, you know, manometry was not perfect and there were these patients that, you know, we may not appropriately address with the right surgical approach or endoscopic approach. And we started critically looking at a lot of the type 2 patients also. So this is some work that we just actually submitted for publications, actually under major revision. It's not accepted yet. But where we looked at type 2 variants. And you know, there's this idea that, you know, the pressure level on type 2 may give you some insight into what's going on. And it certainly looks that way. And you know, technically, all of these people would theoretically be called type 2 achalasia. But you know, I would probably say that the first two, A and B, are type 2 achalasia. The second two, C and D, are probably more likely spastic. And you know, you can generate that hypothesis based on the fact that these pressures are very high. And they do have some focal contractions. So these are patients that have an esophagus that can touch the catheter, can squeeze down and touch that catheter with the balloon, which is now the esophagus, and I call this the water balloon hypothesis, can squeeze it down and contract, even though those pressures are pretty high in the body. And you can look at those esophograms, and those look like spasm. You know, that's not type 2 achalasia. The other two, type 2 with some moderate dilatation, that probably will get better after you decompress them. So this is where my, I guess, journey with thinking about POEM and extending POEM started. And this is a success story. I'm going to start with a success story, and I'm going to start with a failure, finish with a failure. So this was a patient that I saw. This must be now like 10, 12 years ago. And she was the person that I coined the frame Jackhammer. So she was a young woman who came to see us, had significant chest pain, you know, just moved from Indiana to Chicago, under a lot of stress, was getting married, you know, just started a new job. So everybody thought she was crazy. So she kept coming into the emergency room with horrible chest pain, debilitating chest pain, couldn't go to work. And then they wound up in the psych ward. And they were diagnosed with somatization disorder. And you know, it was interesting because a medical student on the psychiatry service decided that he should get a manometer. And he said, you know, he was reading in his Washington Manual, whatever they read now, and you know, said, oh, this person has chest pain, their endoscopies were negative, she had stress tests were negative, she's like a marathon runner. And he convinced the psychiatry attending to call us up and we did a manometer. And that was her manometry there on the left. So you know, when we saw that, we're like, wow, you know, that's pretty abnormal. And that would have been considered at that time, Nutcracker, right? But the thing about Nutcracker is Nutcracker is one squeeze, right? So when you think about a Nutcracker, it's a squeeze. So I was sitting on a panel with Don Costello, and I'm like, that looks more like a jackhammer. And he laughed, he giggled. And I'm like, all right, that's what we're going to call it. And it was interesting, because I gave her sildenafil. And her symptoms went away completely. And her manometry looked beautiful. And she was happy. Her family was happy, because now they had their daughter back, and they didn't think she was crazy. And what happened was, was she started thinking about getting pregnant. And you know, I'd left her on sildenafil twice a day for a pretty long time. She wanted to stop the sildenafil. And then she developed that pattern right there. So that's kind of like an accordion. It almost looks like an accordion in the esophagus. And you know, so we were managing her, and we put her back on the sildenafil. And for some reason, she didn't respond. It was very odd, because she had such a good response to the sildenafil before. So she stopped it on her own, came back, and then had this pattern. So you know, she was actually in the hospital. She couldn't eat. You know, was on IV fluids, was basically barely getting down any soft food. And we eventually decided to do a poem on her. And we extended the poem the entire length. And she did phenomenal. No PPIs, doing well. And even to this day, she's still my patient, doing well, and is happy as a clam. So this, to me, was remarkable. I mean, these were patients that, you know, that we've had, that if you've done motility for long enough, that you've really struggled with these type of people. And to have this therapy work this well. And the only thing that I still, you know, really am a little bit pissed off at myself is, I didn't get tissue. It would have been nice to have the tissue there to really see what was going on. Because frankly, I don't think any of us really know what the pathogenesis of this disorder is. So let's go to one of my failures here. So this was a woman, 44 years old, who presented with two to three years of heartburn, chest pain, regurgitation. Progressed to liquid and solid. You know, once again, we heard, originally diagnosed with GERD. You know, of course, everyone with a esophageal problem has GERD. But was losing significant weight and no response to PPI, and pretty severe sleep disturbances to regurgitation. I mean, she said she would wake up and have stains on the pillow. She was a little bit heavy. You know, BMI was 36.4. Medications are really not. She was on some NSAIDs. But otherwise, just in a lot of distress. So this was her manometry. And you know, this looks pretty abnormal. And the one thing I want to kind of discuss a little bit is that, you know, this is a patient with jackhammer, hypercontractile esophagus. But every single swallow was actually abnormal. And if you actually scale this appropriately, it almost looks like intrinsic to the contraction. There's just a chaotic kind of peak going down the esophagus. So this is almost like spasm, but spasm with kind of a normal latency and an IRP that was kind of borderline. But this was her esophagram. So I mean, technically, people with hypercontractile esophagus and nutcracker should have a normal esophagram because they have normal propagation. But she had obstructive features. You know, I mean, it was pretty clear that she had spasm and her EGJ was tight. So we did a poem. Now granted, this was, you know, a while ago before we were, you know, doing our more tailored approaches for everybody. And we still had a little bit of debate in our group. You know, there were some people who thought these people should always get a tailored and other people, because if they have normal peristalsis, and it's not a spastic disorder, they should get a standard poem. And so that's what this person had, she had a standard poem. And I was against this. And I was, I think this person should get an extended, but they did this and she was fine. And she was so happy. Everything was great. So this is how this progressed. So in 2013, she was good, looked really great, no bolus retention. And then 2017, started having some weird symptoms, hiccups, dysphagia, had this little pocket there. And in 2018, her symptoms started getting worse. And she was pretty much back to where she was when we initially saw her before that poem. So this is what her flip looked like. And I want to try to sneak through here, because I want to get you guys to the reception, because I know I could use a beer. But she had this really distinct pattern here. And you know, you could clearly see that she was blowing out that area of her esophagus. And that was kind of right in that area where that pocket was, which we now call the bomb. And you know, one of the things that was interesting was that although her LES looked pretty good on all of our other studies in manometry, she did spasm. It was very reactive. And we see this in some of these patients, especially the spastic and the hypercontractile people that even though you may treat their myotomy or you may treat their LES with the myotomy quite well, even after the procedure, even though it looks great at baseline, every now and then they spasm down, and they cause a little bit of an obstruction. So now put that in contrast to this person, so her initial manometry. So this is another patient with this pattern here, and you can clearly see that there is a little bit of hypercontraction, but really good multiple rapid swallow. And then you can see in this person here, you know, this doesn't look as bad. But then when you do the multiple rapid swallow, you see this kind of weird contraction there, and you do the rapid drink challenge. So I'm flying through this a little faster because I know Prakash just kind of went through this. But it's really important to do a really good manometric evaluation. It's really important to look at the stuff in between the swallows, because this person is grossly abnormal. So this is a person that kind of a mild jackhammer pattern, a mild hypercontractile pattern. But this rapid drink challenge, I mean, that's obstructive. So there's a big difference between, you know, the run-of-the-mill jackhammer hypercontractile and the jackhammer that actually has an obstructive pattern. So getting back to our patient here, you know, this is someone who, when we went back and kind of looked at her, you know, that was in a very good multiple rapid swallow. And once again, you have to get those swallows within two to three seconds. And she had a little bit of spacing there. But there was something definitely different there that we probably, you know, would have appreciated a little bit better. But the bottom line here is, is that this person got an inadequate myotomy, meaning that she didn't extend far enough into her body. And we literally created a scenario where she had a functional obstruction at her crura. And she was contracting in a very strong way above it. And we literally, it was almost an experimental model to create a bomb. And she hasn't done very well. I'll tell you that right now. And she's essentially looking still. We've been trying to kind of temporize her. But she's probably going to make the decision to get an esophagectomy. But it gets back to this jackhammer problem. Because I think these are the really difficult cases. And I see these people referred all the time. And I'll tell you, if you are going to get a poem in our institution, and you have a jackhammer pattern, you know, we do everything we can to disprove that that is a primary motility disorder, so that you don't get an inappropriate myotomy. Because if you find the right patients, they do great. But I will tell you that 90% of the people that present with hypercontractile esophagus are just like normal variants. They have GERD or a small hernia. But yet, we see these people all the time who come to our referral practice who get, you know, tailored myotomy. And now you've just destroyed this person's esophagus, literally destroyed it for no reason. So I think it's really important to think about this. And we'll go as far as doing a deep muscle biopsy in some of these patients. I've had Aziz do that for me a couple of times. And it swayed me from not doing or not sending that person for a poem because they had no evidence of any kind of neuromyogenic architectural defect, just some fibrosis. And there's really no reason that that person should have gotten better. And we've just watched them, and they just kind of stayed the same. But in our practice, we are very, very conservative when it comes to this group. So this is kind of the algorithm that I've kind of put together in my mind for these jackhammer patients. So I really want to see, if we're going to do something for somebody, I want to see that, one, they have obstruction. You know, that's a big thing. If I see someone jackhammer and they have an obstruction, I feel a lot more comfortable sending that person for a poem because I know that they have an abnormality of transit because of an obstruction that you can probably treat pretty effectively. Now that being said, do I think you need to extend the myotomy for everybody? No. In fact, Iko Hirano, one of my partners, asked a very good question yesterday. What do you do with the person who has kind of a jackhammer pattern, who has a normal latency interval, but clearly has an obstruction on a salvagram and flip, and looks like their IRP is pretty normal on a menopause? Those people, we look to do a tailored, a short tailored in those patients, even though historically we talked about doing extended poems in all those patients. And really the ones that get extended poems are usually the ones that actually have more of a spastic feature to it. And if we see something spastic, we'll extend it. But the other thing that's important is that, you know, I like to see that there's concordance between their manometry improvement on sildenafil and their symptoms. So if I see that someone tells me that their symptoms are still the same, but yet I give them sildenafil and their manometry is completely normal and their esophagram is completely normal, I'm going to be very nervous about sending that person for an extended poem or a poem or any treatment that's addressing their motility. So I mean, this is not perfect, but I certainly think that if there's discordance between manometric findings and symptoms after an aggressive trial sildenafil, I get very nervous. And in those patients, I start sending those people for behavioral modification. So a lot of the other nightmares that you run into are pretty straightforward. I will tell you, panel D there, no one makes that better. So don't feel bad if you do a poem on this, if you do a lap Heller with a myotomy and you do pneumonics on it. That's impossible to make better. The key is to find people before that happens. And we saw this great case of this 92-year-old woman in the panels this morning who presented with her first presentation of achalasia, was essentially a nosebleed that led to clots filling up her esophagus. There are people out there who live with achalasia their entire life and never come to see us. They just get used to doing weird things when they eat. But if people are symptomatic and you can cast them early, you want to prevent D. C2 is not so great. But what I want to talk about is A and B. Those are findings that I think are going to be very problematic over the next few years. I'm going to skip this slide. But before I go to that, I also want to get back to FLIP. Because although I'm telling you that manometry is not perfect, FLIP is also something that you have to be very careful with. We're in the same era of FLIP that we were in probably 2006 with high-resolution manometry, where there were a lot of us who were pretty big proponents of it. And there were a lot of people who were doubting it. I will tell you right now, I joked about this at DDW. The same people who were stomping on high-resolution manometry catheters when I would debate them at DDW, saying that high-resolution manometry was nothing, it's not a better mousetrap, now are the same people who are literally defending it with their life, saying that FLIP is horrible and they're stomping on FLIP catheters. So I mean, people fear change. And I think when you're bringing something that's disruptive, you have to look at all of the problems with that technology. And these are just some examples here. Because these particular cases, if you look on the left, there's an interesting phenomenon. If you look at old radiology textbooks, those guys used to do some crazy stuff to people during esophagrams. Like they'd hang them upside down. They'd jump on their belly. I mean, they did a lot of weird stuff. But one of the tests that is still done that I think is kind of important that we as gastroenterologists kind of make fun of is when they do the abdominal compression. Because they're looking for reflux. And yeah, it doesn't matter if they reflux during that, because most people would. I don't think it's a great reflux test. But you know what it is. It's a great test for seeing a subtle hernia that's reducible. And those hernias can be problematic. So this is actually a great example of someone had pretty significant dysphagia. And if you looked at that FLIP up there, it kind of looks more like achalasia than it does normal. And if you look at that manometry, the manometry looks kind of normal there. And I will tell you that this person was one of the first people that made me start thinking about this problem with FLIP, where there is a group of patients that look like achalasia on FLIP that are not. I mean, they look classic sometimes. And they have these spastic features. And if you only do FLIP on some of these people and you see some of these spastic features where the lower esophageal sphincter contracts really hard or it lifts up, be very careful. Because those patients tend to have a small little hernia or some laxity there that can be causing this. And in these particular examples, you can see that, at least in the other persons that are reducible, this person over here, there's definitely some motility abnormality here. You know, you can see that the manometry looks kind of borderline abnormal, but pretty normal. But look at that esophagram on that person, developing these little ticks, pretty spastic looking. And the FLIP looks this spastic reactive pattern. It's not perfect. We don't know what's going on with these patients. But it's not achalasia. A lot of these patients actually have pretty normal looking peristalsis. But yet they have pretty abnormal looking esophagrams. In fact, these are two people have epiphrenic diverticulum. So when you see these kind of weird patterns on FLIP, I will tell you that I don't really know what they are. They're definitely not normal, but they're also definitely not achalasia. So I think treating these people right now, the same way we treat achalasia is probably a mistake until we get a little bit more information. Because most of these people, outside of the ones that actually have epiphrenic diverticulum, because if they have an epiphrenic diverticulum, you're going to repair that, and you're going to do a myotomy below it. Because if you don't, the diverticulum is going to come back. Outside of the people who have an abnormal esophagram, I'm not going to do much, and I'm going to watch this. In fact, the person on the left, I'm still watching. She's actually not that bad off. She's got a little dysphagia, so we're just kind of watching her. And it's interesting, her diverticulum hasn't grown. So just really important to think about the fact that when you see these patients, you know, one test can fool you. But when you get the three of them together, they kind of give you a little bit better idea. And what they do is they often prevent you from making a mistake instead of actually pushing you towards that. So, getting back to the bomb. This is going to be a big problem. I think in five years, ten years, we're going to see a rash. Because I will tell you that I think the referral practices that I talk with are kind of the canaries, right? The canaries in the mines. We're starting to see these people pop up. And, you know, we're seeing one or two a week in our practice. And I talk to other referral doctors who have seen them over and over. And really what this is, this is a perfect storm. You know, we've been doing these myotomies that have literally been creating this because it literally is an experimental model to develop a diverticulum. And this is a little cartoon just to kind of explain that. And really when you look at it, you know, the esophagus in achilles is like a water balloon, right? It's like a balloon, it's filled with liquid and air. And really the way it empties in type two is you see these non-occluding contractions that can happen anywhere in the esophagus. They don't have to happen up top and go down. It can just happen in the middle. If you have a water balloon, you squeeze it in the middle, but you don't squeeze it all the way down, the top and the bottom bow out. They pressurize. And if it pressurizes enough to overwhelm the lower satsal sphincter, you can empty. And that's why patients who have type two achalasia tend to not lose that much weight yet, right? They lose weight when they become type one. So when you do a long myotomy, and I call them long, a standard myotomy is long myotomy. You go six centimeters into that beautiful esophageal body and you destroy it, you create a defect that at first is elastic, but eventually after repetitive stretching will eventually become plastic. And this will lead to something called the bomb. And, you know, it's pretty simple. So we have this thing that we've created. This was the first version of it. It was our virtual esophagus. And it was a spring model esophagus that we based on, you know, just flip data, input data, high resolution manometry data. And subsequently after using some AI techniques and physics hybrid machine learning, we've now developed something that looks a little bit more like the esophagus and it actually functions quite well. And we can play around with this thing here and we can actually have it tell us whether or not certain things will happen. Let me see if I can get this guy to work. So we can actually query it and have it just sit there. And honestly, these things take like two months of just the computer running nonstop, but it'll actually tell you what's gonna happen based on operations now. So if you wrap the EGJ too tight with a fundoplication, use a Lynx ring with, you know, 12 beads instead of 14 beads you can actually see what the effects would be on that particular person's esophagus because you can input that data. You can input their manometry data, you can input their flip data and get a pretty good idea of what's going on. And with that, you can play around with this, you can do all cool stuff with this. You can strip out the mucosa, you can create eosinophilic esophagitis and you could look at all these different patterns. And really in doing this in a very simple mathematical way, we actually show that if you're doing six centimeters, six centimeter esophageal body myotomies, you will eventually create a bomb. And even if you do a very good myotomy because there is a functional obstruction at the coral diaphragm. And if there is any evidence of contraction, I will tell you when I first started talking to people about bombs and how they would do with myotomy and POM, I told people at EGG outflow obstruction, no, you're gonna do great because your esophageal body is still strong, it's good, you're gonna do fine. Those are the people that develop bombs the worst because you deliver the most volume into that defect. So as we've gone through this, we basically asked this supercomputer virtual esophagus, what's the best operation for someone with type 2 achalasia and essentially told us it was a short myotomy that was non-transmural and not to have any type of anti-reflux procedure with it. So that's kind of not what we're doing now in many centers. A lot of centers are doing them transmural. I don't know why people do transmural myotomies in these patients. The longitudinal muscle has nothing to do with this pathogenesis. There's no reason to destroy it, it didn't hurt you. It's not hurting the patient. It's providing a little bit of a buffer. And I understand that maybe getting into that, you feel like you've done a really good myotomy, but we have tools that you can use during the procedure to show that you've done an adequate myotomy, but certainly doing a long myotomy is something that I think is gonna be very detrimental to patients. So this is just an example I showed this morning of another patient, just a bomb. And what's curious about this patient is if you look at that manometry in the bottom, it's a horrible manometry. But some of these patients, it's very difficult. They have the bomb, that catheter's gonna get coiled, it's gonna bow. This is a patient who they thought had an incomplete myotomy because of this pressure band down here. But that's a very poorly placed manometry. And that is probably just a bend artifact and you can't really even see the gastric compartment. So it's really hard to see what's going on there. But on the flip, you could clearly see in this person that her EGJ opened pretty well. I don't think you can read that, but the pressures are very low and she was able to get to almost a normal diameter with very low pressure. So it wasn't an incomplete myotomy, despite the fact that I think she had like three other different types of myotomies in between. And she's probably looking at also an esophagectomy at this point because there's really no way to deal with that. But I do think this is where a flip can be very helpful. Because if you do a good evaluation, you measure the EGJ distensibility index and the maximal diameter, you will see that there's really not much more you can do with further myotomy in these people. And I know Prakash showed this picture, but if you're in this blue range or this greenish range with these blue dots up there, you know, if that's where you're at post myotomy, there's nothing more you can do for that person. That's a pretty normal looking result where the people you're gonna help are the people that are in the red. So in the end, because I want you guys to get to the reception, I'm gonna finish here and just say that, you know, POM is a great procedure. And there's a lot of excitement about it. Everybody wants to do it. And I applaud that. But I would say that we're still in a learning phase, and we're gonna make mistakes. And the key is to recognize mistakes right away and start to correct them. Instead of, you know, trying to hunker down and say, this is how we've done it for so many years, we're gonna keep doing that. When something is so logical in terms of explaining why it's wrong, when you have computers telling you it's wrong, when you have your eyesight telling you it's wrong, I can't put together a 10-year paper for you yet, right? I'll do that in 10 years and come back and say, this is why this happened, but I can't do that right now. So my little soapbox thing for this particular meeting is to basically say, be careful. Think about extending those myotomies and why you're doing it. Don't destroy something that is working or something that's, you know, intact if you don't have to, because then you're gonna run into problems. So with that, I'm gonna stop because I definitely want people to get a beer and it's 5.50, right? So, question? Sorry, this question may not sound intelligent, but a bomb. Believe me, people say that about me all the time. So I understand what you meant by short myotomy for type two. And then would that mean that if you don't extend the myotomy enough in a type three, you would also run into a bomb phenomenon? Yeah, so the people who are more prone to, I rocketed through that, when Joe Triggs looked at that data. And yeah, so, you know, type three EGJ outflow obstruction patients who still have an intact contraction. Because remember, it's like you're squeezing it up here and they have a functional obstruction here. So when you squeeze here, it bows out. And then what happens just like anything, when you stretch and you stretch and you stretch, you know, you tend to remodel. And you see this go from, you know, elastic to plastic. And when it gets to plastic, and plastic doesn't, in biomechanics, it doesn't just mean stiff. It means that it won't have hysteresis. It won't go back to its normal shape. And that's really what happens with these patients. And then so as a follow up to that, if you have a type three patient, when you're trying to tailor the myotomy, are you trying to tailor it to the entire spastic segment or at the CDP point? Or like, I don't know exactly where you kind of are trying to tailor it to. If they truly have a type three pattern and it is spastic, right? And you know, you see it, it's clear. Almost every swallow is abnormal. Then yes, then extend it the entire length of that spastic segment. You know, we do see some people though, even though you do that, and I know Vani does it on FLIP. Sometimes FLIP actually unmasks some of these areas that are hyper contractile and spastic that you might've missed with just the high resolution manometry, especially in some of these type two people. Because the type two people have this kind of, it's not buried spasm, because the spasm is actually on top. It's actually encasing it, but it actually is missed spasm in those particular patients. So you have to be careful. But you know what, if you notice it early and you catch it and people are symptomatic and you know, at your follow-up at six to 12 months, you're probably in that window where you can fix it. And you can just go back in and just extend the poem. A question from the virtual audience. When you're, just to sort of really define short myotomy, are you talking four centimeters above plus the two into the cardia, or are you shortening the cardia? Can you just define exactly what you mean? Yeah, so I'm gonna have the expert define it. So how would you define it, Aziz? Because that's who I send them to, to get it. Three centimeters of the esophagus, okay, and one centimeter in the cardia. Which can be kind of hard to define, but try to shorten it up. To be honest, I don't really care how long you go in the cardia. You know, at least from the BOM perspective, it doesn't really matter. Certainly it might matter in terms of reflux and position of where you put the, where you decide to have your trajectory for the poem, but in terms of the BOM, the cardia component's not gonna contribute to it. It's really the body part. Another question for the jackhammer esophagus. What are you seeing with LES sparing versus non-sparing in the myotomy? So LES sparing versus, yeah, so you know, I think if you're gonna do anything, I'm not gonna spare the LES. The LES has gotta go away. Because what do you know about diverticulum? If you repair a diverticulum and you don't do a myotomy below it, that diverticulum's gonna come back. So you know, I do not think that you should spare the LES in that scenario. I think if anything, you gotta make that decision to go all the way down. But if they have beautiful peristalsis and you feel pretty comfortable that there's not spasm there, you could make the case of just doing an LES myotomy, a short myotomy in those people. Because if they're still sweeping that bolus down, you know, they're gonna empty pretty well with an LES that's gonna open up. So that's why I say, I don't think, jackhammer's a very heterogeneous group. And I don't think we have a really good understanding of the pathogenesis behind it and why this entity is very different than the other entities. So that's why I think if you're doing poems on these patients, get pathology, get tissue. And even if you don't, you know, use it now, just get it so that people can look at it later. I think a lot of these people have dense fibrosis in there. There's also this thought that there might be an eosinophilic or a mast cell disease state that's giving us this, you know, which theoretically would respond to a better therapy, you know, targeting that. So I think we're at a point where, I mean, we've got a really great technique that treats these patients very well. You know, I've made mistakes because, you know, I get excited about treating patients and offering a new technology with a new diagnostic. But then you take a step back when you see, wow, you know, this person is not doing well. And I still have a few of my early type two patients who I, you're gonna do great, you know, and they develop horrible bombs. And I'm, you know, it's devastating to see that because these people are young and they're healthy. And, you know, I might've missed it. I keep kicking myself. Why didn't I do a pneumatic on those people? You know, but, you know, we don't really know. Not everybody gets a bomb, right? Sometimes things are just bad luck. Sometimes there's an angulation at the EGJ. Maybe their career is a little bit tighter. Those are the things we need to figure out, you know, and maybe, you know, five years of data will give that to us. But I think in the meantime, I would be, you know, if someone asked me, if someone asked me five years ago, what, and if I had type two achalasia, what I would get, I would get a pneumatic dilation. If someone asked me today, I would get a tailored myotomy by Aziz. So it's a pretty good endorsement. Yeah. And maybe I should say Eric and Ezra too. So Eric and Ezra, I'd get a tailored myotomy from my guys in Northwestern. Any other questions? You guys don't want to get a beer? All right, good. Thank you very much. Thank you.

POEM

achalasia

myotomy length

type 2 achalasia

type 3 achalasia

risks

cruroplasty

hiatal hernias