All right. Thank you. That was absolutely fabulous. Let's see. I have a slightly different bent. My approach is to seek a mechanism based on what the patient tells me and what test results I have. I put this up yesterday. I'm going to focus on the transit part. This is the complement of symptoms that I query in these achalasia patients. This is the armamentarium. I look first. Very often in somebody with a transit symptom, I will do a flip at that first endoscopy. They're coming back with a transit symptom. I want to know diameter, distensibility index, and contractility. Those are the three elements from flip. Manometry, not as useful, but if you do a manometry, you want a provocative test. We'll look at that in a second. And I use a lot of barium in this setting. It's a challenge sometimes to get the right kind of barium. I usually beg the radiologist to at least stand the patient up after they've done it. It's tough to get them to do a full protocol, especially if they're being done at a peripheral center, but I try my best to get them to stand the patient up. Even if it's not a perfect timed upright study, you can tell something if they stand the patient up and the barium doesn't empty. I showed some of this yesterday. This is low-hanging fruit for me. If I go in there, I find candida, I'm going to treat it. If it is simple candida, I prefer topical stuff. I prefer nystatin or myselex. If it is more profound stuff, I will do fluconazole. I will sometimes send the refractory patients to infectious diseases because they have other medicines they can use. And part of candida is stasis, so you want to look for stasis and improve. Pile esophagitis, same thing. This is what I showed yesterday. This was from potassium in an achalasia patient, but the issue is not just the potassium, it's the stricture that you see, and that stricture needs to be dilated, right? And strictures can be part of reflux too. So if you see LA grade B or higher in these patients and you've started treatment or make a change in treatment, you should probably bring them back in two or three months because when the esophagitis heals up, you may end up with something like this. And this you can treat. We know how to treat these, all right? Once in a while, you'll have to monitor for Barrett's. This is a patient probably had some reflux before he developed achalasia and he has long segment Barrett's. I bring him back and biopsy him every two, three years. Okay, let's talk about a couple of cases here. This was a lady, 53-year-old with esophageal type dysphagia, chest pain, weight loss, and on the index endoscopy there, a little bit of candida, okay? So all of this is evidence, even before you get a manometry, that there is some problem with the esophageal emptying, okay? So I chose this case because all four of these elements complement your diagnosis that there is an obstructive process, okay? That was the manometry, okay? So there is an intact progression. The distal latency is borderline. But there is a prolonged contraction phase in the distal esophagus, okay? A prolonged contraction phase. And then there is this pressure compartmentalization. This is compartmentalization of pressure. When you see compartmentalization of pressure, it means that there is a problem with emptying. That is a surrogate marker for abnormal emptying, okay? A surrogate marker for abnormal emptying. So if you see that on a manometry study in a patient with dysphagia, you're probably dealing with some emptying issue, okay? And in this case, because of this prolonged contraction, okay, the DCI does not make it to hypercontractile here. But you see a pattern here where there is distal shift in contraction vigor, okay? So this is the second esophageal contractile segment. This is the third. You can see that there is a dominance of contraction in the distal contractile segment. And that is a version of a spastic process, okay? If this is much more profound, you will see a blob of contraction that includes both the second segment and the third segment. You guys know about the three contraction segments, right? The esophagus? No? Yes? No? So the three contraction segments are, oops, the three contraction segments are the skeletal muscle segment here. This is skeletal, not affected with achilles or spastic disorders. The second contraction segment, which is the pump for the esophagus. That is the part of the esophagus that has cholinergic dominant transmission. And that is the part that will augment if you have a mechanical obstruction. So if you have somebody with a tight stricture, tight fundoplication, if you look at the high-resolution manometry, you will see this segment to be prominent. The third segment has non-adrenergic, non-cholinergic dominance. It has a lot of inhibition because this is the part of the esophagus that contracts the last, right? So this part contracts the first. This part contracts the last. So you need maximal inhibition there. You need maximal inhibition, right? It is inhibition that times peristalsis. Inhibition also dampens contraction. So if inhibition is abnormal, if it is deficient, then you're going to have a more upright contraction segment sequence, meaning the swallow is going to be premature. You can have a more exaggerated contraction. And remember, abnormal inhibition is what drives incomplete relaxation of the lower esophageal sphincter, okay? So even though this does not fulfill all the characteristics of what you would call achalasia, this is a spastic disorder. Remember, the symptoms here tell you that there is an obstruction, okay? So when I teach my fellows, I tell them, I don't care what you call this. You can call it hypercontractile or EGJ outflow obstruction or type 3 achalasia. This is an obstructive disorder for which there is a treatment, okay? This is the type of disorder that you can treat with one of these techniques. And these days, you can tailor the treatment. This is the perfect patient for a POM. Unfortunately, in 2014, there wasn't the availability of POM. Even if there was, the insurance was probably going to deny this. So this patient actually got a Heller. But this is the other part of evaluating the patient, doing a provocative study, okay? This is a rapid drink challenge. The patient was given 200 ml of water in the upright position, and you can see that there is pressurization in the esophageal body, okay? There's pressurization. The LES partly relaxes because there is some retained inhibition, okay? But there is pressurization, and there is incomplete inhibition in that there is contraction where they shouldn't be. That means that the inhibitory force that would determine lack of any peristalsis here, that is deficient. Again, it supports your clinical concept that this is a disorder of inhibition. This is a spastic disorder involving the smooth muscle esophagus, okay? And what we know today is when you have a spastic disorder involving the smooth muscle esophagus, you got to destroy the smooth muscle esophagus and the sphincter so that you protect the patient from having issues in the future. The contraction phase after multiple rapid swallows shows augmentation and a prolonged exaggerated contraction of the lower esophageal sphincter, okay? That tells you that even though your single swallows don't show a problem with the sphincter, the sphincter has the capacity to really clamp down, okay, in an obstructive fashion. Now, if all these things were not met, if I just saw the manometry and the patient said, oh, I can eat fine, I'm gaining weight, I just have an occasional chest pain episode, I will not send the patient for a POM procedure. You have to have all these elements in place, okay? That was the barrier, the initial barrier. And you can see the spastic segment down here. It does empty, but there is a prolonged spastic segment which correlates with what the manometry showed. It's like the idea of three strikes, okay? You have to have more than one test showing you the abnormal emptying before I will commit a patient for something irreversible. This patient met that, and this was the after picture. You can see that there is better emptying, and you can tell that this is not a timed upright study, but you can see that the fundus is nicely filled, which means that the barium from the esophagus is emptying after this person underwent their hell or maya. And then 2016, patient came back. They have food stuck in the middle of the chest if they try to eat solids, okay? And you get the drift here. So what's happening? Any thoughts? You can see a contractile segment that is kind of vertical in the mid-esophagus. And so this is an incomplete myotomy in the esophageal body, right? It's not a DGJ. It's an incomplete myotomy of the esophageal body. Now again, looking at the period between swallows is important. And this is between swallows. We're not doing anything. We're just getting the patient ready for a rapid ring challenge, and look what happened. A very intense prolonged contraction, okay? So this is probably the reason for the patient's symptom, right? When you see this manometry, this is probably the reason for the patient's ongoing symptoms. So what would you do? Yes? It would extend the myotomy. That is probably the right answer. Vani, you have any thoughts? Yeah, no. I think this is sort of that setup of having that spastic component only partially treated. And given all, I like your three strikes, you sort of have accumulated them already. If for any reason there was something that wasn't there, like for example, I would say in the setting of chest pain but not as much dysphagia, I might have done something like a Botox trial, because I do think that dysphagia is more predictable to treat. And when you have that obstructive component that you relieve, then you know it's going to get better. Chest pain, to me, is more elusive. And in these situations, sometimes you show up with patients who don't have as much dysphagia, but have more chest pain symptoms. And you don't quite know what's driving that, and whether or not cutting the muscle will alleviate the chest pain symptoms. And so I might do a little bit more trialing in that effort, but I feel like you sort of accumulated all your data. And that's the barium. And you can see that the myotomized segment at the bottom is starting to balloon a little bit. And the mid-segment in the soft-shelled body is closed here. And that's the segment that corresponds to this. In 2016, when somebody has already had a myotomy, it's tough to get a poem approved. And it's tough, at that time, it was tough to convince a person who was doing poem to go back and do this. So I endoscoped the patient, and that's what I saw in that closed segment. And I Botoxed it. And three months later, that segment's open, patient's happy as a clam. Six months, nine months later, symptoms come back. And that is when they underwent their completion poem. And later on, of course, she developed a stricture down at the esophagogastric junction. You can see the stricture in 2018. The extensibility index was wide open, diameter was 10. And this stricture was easily treated with balloon dilation, periodic balloon dilation. And the final barium, you don't see the spastic segment anymore. This is the supine picture. And on the upright picture, the barium empties very well. So what would be the long-term management for this? What would you tell this patient at this point? So this is 2022, just a few months ago. How would you continue this patient's management going forward? You've heard a lot of things from Vani. All of those things, this patient was recommended. Similar to that patient that Dr. Konda showed. Do they need to stay on a PPI? Yes, certainly. This person will be maintained on a PPI. The other thing I told this patient is don't gain weight. That was the other piece of advice I had for this patient. And I will probably look at her esophagus every couple to three years. I like to alternate a barium with an endoscopy. I probably will do it every two to three years. I will do one or the other if they are asymptomatic. If they are symptomatic, I'll probably start with an endoscopy. I also like to set them up to expect maybe a periodic balloon dilation and not to think it's a failure. And I just tell them, oh, you'll just need a touch-up balloon dilation every now and then knowing how scarred down it was. And then also that way they expect that. And if they wind up thinking that something didn't work, it's not that it didn't work. It's just, you know, it's like a tune-up. And so sort of getting them to understand that these endoscopies are part of their maintenance care and not that it didn't work is an important thing. And you can sort of set that groundwork going, you know, at the beginning saying, you know, you might need an endoscopy every couple of years with periodic balloon dilations. That's not a failure for that patient. It's just maintenance. So working with the expectations. I also just will say, going back a little bit to the importance of going in and doing that endoscopy and the balloon dilation. So if you get referred back or if you get referred someone that had a myotomy and they think that it's an incomplete myotomy and they're asking you to do a poem, but no one's done just a standard balloon dilation in that setting and a good, careful inspection, it's worth it to do that. I will say it's a simple thing. Just do it and make sure you get that off the table before, you know, sort of tunneling down and cutting the muscle. Yeah. And the other point about that endoscopy is best that you do it. You know, I've stopped relying on peripheral endoscopies because they don't always look at the esophagus. You know, you want to sit there and inflate the esophagus a little bit and see if there is any restrictive ring down there. If there is a restrictive ring, that's going to hold up solids. And it may not hold up liquids, but it will hold up solids. Yes. I was wondering, how did they perform the poem on this patient? Did they just cut the selective, like do a selective myotomy of the spastic segment? And did they use an anterior approach or posterior for that? No, I don't do poems. I'll just, because you know the patient, that's why I thought. Don't go past the previous Heller site. I didn't want them to go down below. So they're supposed to have only done it based on the measurements from this, let's see, measurements from this manometry. So they would not go below this level, and they'd start somewhere there. They probably did a posterior, I think. I do not know whether they went anterior or posterior. Yes. Since this course has started, we've talked about like blowing out myotomy. There was a mention today that if you stay anterior or posterior to, and not laterally, the chances of forming a diverticulum and so forth are less. And we've switched concepts from going long to short in order to address this thing. But based on all these manometry findings, it seems like the proximal segment that we have left behind that still has the capacity to contract is creating all of these issues. So going from long to short, is that the wrong approach, rather than going from long to even longer, where you target the entire smooth muscle in case of type 2 achalasia? Because nothing is wrong, nothing is right. The right answer is individualize it to each patient, okay? If you have a type 1 achalasia, you know it's type 1, there is no need to fillet it open. Just cut the sphincter. If it is type 2 without a spastic element, however you discover or not discover spasm, there is no need to fillet it open. And for the most part, in those types of achalasia, you don't want to make a half-ass palm. It can't be just the distal esophagus. And I tell that to my surgeons, too. Don't go up higher than you need to into the esophagus just because you can't. That is the recipe for disaster. So in some of these instances, it's much better to create, if you're not sure, create a scleroderma-like pattern because that can be easily managed rather than these retained spastic elements. I think manometry with provocative maneuvers and barium is quite useful in making some of these determinants. And then in those situations where you do have a spastic element, so type 3, then you do do the long, complete myotomy. So then you still are committing to that long myotomy and you want to make sure you capture all of the spastic component. And then I think the curveball is the type 2 with the element of spasm, which it's true. It's like if you find it or not find it. I think that this is where I do find the endoflip helpful because that's where I find it all the time when I find it, but I have a very specific practice where I see a lot of those. But I think that it's still, if you don't need to go long, then you go short. And then if there is elements of spasm, then you go long and always individualize and then monitor the patient. Don't say that we cut it, you're cured and you're done. We have to follow it. So we do yearly, again, alternating esophogram or endoscopy, but I do the same if they're symptomatic, then go to endoscopy. And watch for any evidence of progression of disease, concern for some sort of bowing out or early forming diverticulum or residual contractile activity that might be dysfunctional. And the other point to remember here is to understand how patients empty their esophagus with these three achalasia subtypes, okay? Because these patients are not bottoming out with their weight right away, right? They may lose 20, 30 pounds, but they're not losing 100 pounds, right? And that's because they can empty their esophagus, depending on what the consistency of the food is. Does anybody know how type 1 achalasia empties their esophagus? No. They do it by certain thoracic positions, right? They develop mechanisms of UES contraction against a closed chest and alternating with breathing. So they develop their own method of increasing intraesophageal, intrathoracic, really, pressure because the esophagus itself has no tongue. That's how type 1 empties, right? Type 2 empties with longitudinal muscle contraction. That's why you don't want to mess with longitudinal muscles in type 2. They pull up the esophagus and they compartmentalize. And that interbolus pressure actually serves to empty because if the interbolus pressure, that pressurization, is higher than the closing pressure of the LES, that's how they empty, okay? Type 3 achalasia and EGJ outflow obstruction, there is only segmental compartmentalization. There is no panesophageal compartmentalization. So the part that is not segmented is actually empty. And that's the reason why you can have type 3 achalasia with hardly any weight loss. And EGJ outflow obstruction, the same. So if you remember those mechanisms of weight loss, mechanisms of esophageal emptying, sometimes it helps understand which part needs to be addressed in each type of achalasia. And I believe you had a question there? When you're doing these Botox trials in anticipation of a poem, if the patient benefits down the line, do you do anything particular with your placement of your quadrants to preserve a tunnel down the line? Or you just have faith that your endoscopist can deal with whatever they come across? I inject Botox into the contracting segment. I have never believed that Botox makes a surgical or an endoscopic intervention, you know, completely impossible or very difficult. It can make it a little inconvenient. But if you need that information to ensure the patient moves to the next step, you do it as best you can. So it's usually 100 units you inject in the 20 or 25 unit aliquots circumferentially into the spastic area. I do. And I work with a variety of different teams, including one where a thoracic surgeon and I, we actually work together during the poems. And each person has different versions of doing posterior or anterior. So depending on which person might be the person doing the myotomy, I might avoid the left upper quadrant versus the right upper quadrant versus the right lower quadrant. And it's not that Botox makes it impossible, but I feel like it holds the blue less long or the methylene blue sort of dissipates faster. And so I think it does make a slight difference. Yeah. I mean, I've done a lot of post Botox patients and it does make it more difficult. It definitely does create more fibrosis, particularly around the junction, which can cause problems with bleeding and also just expanding the tunnel enough to, you know, there's a risk of mucosal damage. So I work with an esophagologist on all my cases too, and she knows that I prefer posterior. So for cases where you could do like selective sparing, she spares that quadrant. And then in cases where I'm doing a trial, particularly spastic components, where I'm not sure that a myotomy is the right decision when they only are presenting with chest pain and they don't have dysphagia, those are my ones I might consider a Botox trial first. And it's a longer segment. I might, I like to mix in a total of six cc's, just to say it out loud, six cc's, non-bacterial static saline, gentle roll, not shake, keep it cold. That's how you keep your Botox active. And I do a total of six cc's, and I do half cc aliquots if I'm going a longer segment. And I am a little bit more comfortable going deeper in the LES at the bottom, but once I start going into areas of mediastinal structure, I probably err on the side of shallower, just because I don't want to hit anything else. And so I probably am more shallow when I go proximally, just to say that out loud. Thank you. All right, very good. So patient, so this is this, let's go to the next one. So this is a 75-year-old lady, dysphagia, Eckert of seven, that's your initial endoscopy. You can see here that the IRP is 24, it was consistently higher than 20 in most of the swallows, but intact peristalsis in the esophageal body, so nice, intact peristalsis. This is what the manometry, I'm sorry, endoscopy looked like. You can see a puckered, enclosed LES that doesn't open easily to air insufflation, okay? So it's important to sit there and insufflate air, and if you see this pattern that persists, that is probably a true obstructive element, and that was the barium. And you can see that the barium doesn't empty very well. A pre-poem flip, you see the DI was low, diameter 5, intact esophageal body, but spastic contractions. And so this person underwent a poem that destroyed the entire contractile element here, okay? And post-poem, the patient was having chest pain, not much dysphagia, chest pain, okay? The original symptom was dysphagia. Now the symptom is chest pain. Eckert of three. Eckert is not the greatest way of looking at this, but that three came from chest pain and not from dysphagia. Important to look through the actual scoring here. And that was the post-POM endoscopy. You can see the EGJ is open compared to the previous study. A little bit of reflux. You can see a little erosion there. DI of 4.7, diameter of 15, so a little bit of narrowing there. No contractility. What do we do? Amplitory pH like Bravo, maybe? What will you do with the result? This is the thing about ordering a test. You need to know what you're going to do with the results. What are you going to do with the result? I don't know for sure, but I'm trying to rule out whether the chest pain is secondary to reflux post-POM. I'm trying to prove that that's the etiology. I guess you could try a PPI trial and see if they improve, and not before you do that. And so potentially just PPI and see how they do would be an alternative. My thing about ordering tests is that you need to know what you're going to do if it's negative. You need to know what you're going to do if it's positive. And you need to know what you're going to do if it's equivocal. From a PPI standpoint, in all three of those situations, I'm going to leave this person on a PPI. So the Bravo is not going to tell me whether to start a PPI or not to start a PPI. With the EGJ that looks like this with a few erosions there, I'm not going to believe that I won't use a PPI in somebody with a borderline AAT. And now if you're looking for reflux symptom association, what would you do if it's positive? And what would you do if it's not positive? I'm not at the point where I'm going to intervene from an invasive procedure on this person. So a test is probably not going to tell me what to do next. So this is the type of situation where an empiric trial and talking a little bit more to the patient is probably going to get me there. Because the original symptom is gone. And it's replaced by a sensation, a perceptive symptom. And the perceptive symptoms, if you remember my talk from yesterday, the top of the list is reflux. So I'm going to treat as if this person has reflux. Below that is reflux hypersensitivity. Remember the change that has happened with the palm, with the palm procedure, is that now the person is refluxing gastric content into the esophagus. Maybe they're feeling that, right? Maybe they're feeling that. Maybe it's the volume that they're feeling, not just the acidic nature. You treat the acidic nature with a PPI, but you're not treating the volume with PPI. PPIs don't treat that. So if you follow those concepts, this is an hierarchical therapeutic trial patient. She's 70-some. I don't really want to send her for a fundoplication or TIF or anything like that. And I want to try and manage this medically. So instead of putting her through another test, remember, if that pain is a functional pain, doing tests will try to, doing more tests will kind of make the patient believe there is something I haven't yet found. I want to tell her, this is what I think your symptoms are coming from. We have created reflux here. We're going to treat it. And we've probably created a situation where the esophagus is responding to reflux with chest pain. Because her pattern, I didn't tell you that, but her pattern of chest pain was postprandial in the middle of the night. It was happening three or four times a week, and lasting 30 seconds to five, 10 minutes at a time. But it was distressing for her. When she had it, she was uncomfortable. And so in a patient like this, my usual approach is to make sure there is no retention. And clearly, there is no retention of barium. The chest pain is not a surrogate for incomplete emptying. OK? It's not a surrogate for incomplete emptying. And the EGJ, with the flip findings, you can see that there is a little bit of a stricture there. I will treat that if the patient has significant dysphagia. And indeed, this patient got a couple of dilations. But this is a person who would benefit from a neuromodulator, OK, in addition to a PPI. So PPI alone, there was some improvement that didn't go away. I put the patient on gabapentin, OK? And the reason I chose gabapentin is gabapentin has been shown to be useful in idiopathic pain of achalasia. Achalasia patients can have idiopathic pain. She didn't have a shred of anxiety. She was just frustrated with a symptom, but she didn't have a background. She's 75 years old. She didn't have a background of anxiety or depression. So I didn't really want to pull out the duloxetines and the buspirones in this person. And I didn't want to really give her a tricyclic. She's 70-some years old. I gave her 100 of gabapentin at night. The nighttime pain improved. She still had a few episodes. I got her to take another dose in the morning. So on twice a day, gabapentin and PPI, she's happy as a clam, OK? So functional symptoms can coexist, but it's important to assess bolus retention. I'm not going to go through this. You've seen the slides from yesterday. But important to make sure that the esophagus empties. Chest pain can sometimes be a surrogate for incomplete emptying. It can be a surrogate for dysphagia if it is postprandial, even though it's a perceptive symptom. And this is the part where doing one of these studies does correlate a little bit with manometry. But FLIP is very good, too. This is the original study that Pandolfino published in 2013. The original use of FLIP was not to diagnose achalasia, but to diagnose, to identify patients who had an incomplete response. And when the EGJ looked like that after this was pneumatic dilation, the pneumatic dilation, if the EGJ looked like an untreated achalasia, that meant that you needed to dilate more, OK? So that was their original study. And using a provocative maneuver, you can see the difference between good emptying and incomplete emptying with the rapid drink challenge. Very useful to have impedance and useful to look at the IRP. If the IRP during the rapid drink challenge is less than 10, a timed upright is going to show emptying. In most instances, it's very unusual to have a timed upright that is abnormal with good emptying on a rapid drink challenge. I talked about this yesterday, so I'm going to skip through this. And I'm going to show you a patient's description of their achalasia. I think this is very telling. I'm very much into listening to patients. And this was a patient of mine that we have seen since the mid-'90s. I met him first when I was a fellow. And recently, we had the opportunity to write a review on achalasia for Nature Reviews. And they wanted a patient perspective. So I asked him to write a piece. And this is what he wrote. And it's very interesting reading, because he reported that he felt his chest really, really uncomfortable. He calls it food stuck like beating a drum vigorously, as his description, that he could not quiet or stop. And he went through the usual steps that patients with achalasia go through. Somebody thinks it's reflux. And then somebody else thinks it's all in their head, that this is a functional issue. It is only after he underwent these objective tests, and he was one of the earlier patients who underwent water-perfused high-resolution manometry in our institution. So we started doing that in 1995. So he was one of the earlier patients with true high-resolution manometry. He was diagnosed with achalasia. But he would go to the ER with chest pain. And they'd think he was a drug seeker. So Ray Klaus wrote him a letter that he could take to the ER if he went to the ER with chest pain, so that they'd give him an opioid. Because at that time, he was having his episodes of idiopathic pain once in a while. So fast-forward to 2009. He's had two myotomies. The first one was unsuccessful. He had a second one. And this is his esophagus in 2009. It's starting to become sigmoid. By 2009, Ray has already passed, and I'm seeing him regularly in my clinic. I used to see him intermittently. I used to share patients with Ray Klaus. And I started talking to him about getting an esophagectomy. Because I will show you his esophagus. I used to balloon dilate him once in a while. But there was retained food in a part of the esophagus that was not necessarily going to empty regardless of physician. You see that? That's the LES. Doesn't matter how open this is. This is probably not going to empty, even in the upright position. And so ultimately, he agreed in 2012, he underwent an esophagectomy with gastric pull-up. So sometimes it takes these patients a little bit of work to get to the point where they agree to an esophagectomy. And this was his comment about that process. So in the mid-2000s, this is after two myotomies and a few years later, he started having issues again. And he was pushing food down by drinking a ton of water. So he was about 20 years, I think, in the mid-2000s, a little more than that, 22, 23 years. And he came to me and he told me, I can't date anyone. Because when I go to a restaurant, I got to pee all the time because I'm drinking so much water. It's just a deal breaker, right? So that was his complaint at that time. And he compared his esophagus as, I don't know if it's written in there, like a flat tire folding on itself. I think that's a very nice description of a dilated esophagus. But after his esophagectomy, he's leading a more normal life. He still can't eat normally, right, after an esophagectomy, still have to be upright. But he can at least get foods he likes down. So that's a story about esophagectomy. And it's important to recognize that when the esophagus starts getting into that sigmoid shape, that it's probably coming, especially for a younger patient. It's either going to be esophagectomy or you're going to enterally feed them. You may try another myotomy. You may try another pneumatic dilation, trying to reduce the resistance to flow across the EGJ. But when the esophagus becomes sigmoid, and especially if they start having pneumonias, they start aspirating, you have to pull the plug. And my experience is it takes anywhere from six months to a year for a patient to accept that, accept the fact that you're going to have to send them to an esophagectomy. You probably have to do it before the top segment of the esophagus dilates, because that's where they're going to anastomose the stomach to. The surgeons have gotten a lot of experience with cancer surgery in doing these, you know, cancer for esophageal cancer surgery, in doing these esophagogastric conduits. And you know, there are problems with the conduit, it doesn't necessarily always empty very well. But the surgeons have gotten much, much better at managing these, and it's well worth having the patient talk to somebody who's had one of these, either in the context of achalasia or in the context of esophageal cancer. So I have a small following of patients who I keep track of, and I usually have my other patients talk to these patients if they're going for an esophagectomy. Any questions about this end-stage achalasia part? I think the sump effects and stigmoidization is really challenging. And sometimes what we've done is just done an esophobe, just to see if they improve at all, to know whether it's worth doing anything. Because if they don't improve after that, then I don't think that doing a poem is going to be helpful. So again, sort of trialing things just to see if they're going to get better. And developing that relationship with the surgeon upfront is also helpful, because it's not cancer. So it's not like you walk in, there's no choice. I mean, you basically are going to have the surgery if you can be a surgical candidate. This is an elective procedure, and it does take some time, and it does take some acceptance of the surgery. And so I think not waiting until the very last moment, but starting that relationship early, and having them being able to meet with the surgeon multiple times, really understand what life after esophagectomy looks like, what the pros and cons of doing it, not doing it are, is an important decision that involves a lot of thought and time. And so making that connection early is helpful. And it doesn't matter how you treat the patient, what option you've offered them, this might need to be an option to be brought up if the esophagus gets sigmoid, because it can. Some people have that phenotype, but they end up with a type 1 achalasia that is sigmoid. Not every patient develops this, but the ones that do are miserable. So repeat disruption, esophagectomy, entrophy, these are the options. I talk to them about these three options when I meet with the patient. And once in a while, you'll run into esophageal cancer. I've seen one case of squamous. I've not seen any adenoma. But again, if you see a suspicious bump in the esophagus, not just the stasis changes, it's worth biopsy. I have one more case. Should we do that? Yep. Okay. So this was another patient of mine, mid-70s, man. Right? His symptom was dysphagia. I don't have his records on the screen, but he was in the high single digits, so 8, 9, 10, somewhere in that range. And you can see, this is what I meant by merging of the contraction segments. You can see that the second segment and third segment are merged together in this big glob of contraction. So this is a hypercontractile segment in the esophagus. Right? And most of these patients have an obstructive element if they have dysphagia as their symptom. Sometimes you can see this in somebody with zero symptoms. One of my fellows had this pattern when we were doing healthy normals. He had a hypercontractile esophagus with zero symptoms. You don't treat that. Sometimes these patients have chest pain. And exaggerated contraction can be a marker for esophageal hypersensitivity. You're going to make them worse if you intervene on them, because then you'll have reflux as an additional trigger or noxious trigger for chest pain. So you've got to be careful about that. This person had an obstructive pressure compartmentalization with bread. You can see this is pressurization in front of the contraction. Okay? And what this tells me is that this contraction element here is gripping the food and holding it so that you have the pressure impression of compartmentalization there. That is the part that FLIP can demonstrate. It can demonstrate that obstructive element, even in disorders where the IRP may look normal. Actually, the IRP is not normal here. You're just not seeing the LES, because the LES has moved up here. And this part is the LES during the contraction. And here, when the contraction has gone away, the LES comes back to its original place. You're measuring the IRP here. Here, all you have is the diaphragm during this exaggerated contraction. It's just pulled up, usually by the longitudinal muscles into the chest, as this exaggerated contraction happens. Okay? And that's where FLIP can be useful. So if you have somebody with dysphagia in this setting, and the FLIP shows a low distensibility index, that's the person who might benefit from having a POM procedure being done. And this was the patient's esophagogram pre-POM. And you can see that the FLIP showed a very low DI and vigorous body contractions, low diameter. That is his post. Unfortunately, they didn't do a long enough POM in this. Even though I had asked them to look at the manometry and go as high as they could, they didn't. But the initial studies are looking all right. But then he's starting to develop a blowout at the bottom, because the middle part of the esophagus is still contracting. You can see that this part is starting to blow out. Okay? And this part is still contracting right here. So this is a person with blown-out myotomy. You can see that the EGJ looks all right. This is the blown-out segment. You can see pills and liquid refluxed material in there. So he has both regurgitation and a sensation of food sitting in the distal esophagus. You really have no solution for that other than a distal esophagectomy and a pull-up, a gastric pull-up. So he's not quite there with getting that. Okay? So this is a blown-out myotomy. I'm not going to spend too much time showing this, because John Panolfino addressed this in great detail yesterday. But it's actually a weakness. I don't quite agree with what was said this morning about that you can't have this if you do anterior-posterior poem. I've seen it with anterior-posterior poem. This can happen. You know, the esophagus is very dynamic. It isn't just fixed in that position. And the part that is weak finds a way to go to the weakest part that will accept a dilation. So you will see it laterally, regardless of where it's done. And there is no good solution for this other than taking out that segment. Okay? It develops after a period of time. It's not right away. And you saw in my patient that it took several years for the dilated segment to develop. Okay? And this is what the Chicago group showed as well. Their average time, the median time, was 52 months, which is a decent duration of time, more so with type 3 achalasia. I will leave you with one word of caution about evaluating these patients and jumping to poem. Okay? John Panolfino finally has started talking about this. I debated him regarding this. It was an ASG-sponsored session. I think you were there, Vani. I think you were there. And, you know, this is what keeps me awake at night. When you distend a balloon in the esophagus, remember, flip is balloon. When you distend a balloon in the esophagus, if the patient has a reactive esophagus, the esophagus is going to want to squeeze the balloon. Okay? Generally, there is contraction upstream of any distending force and relaxation distally. When you don't see that distal relaxation, there is a problem with the relaxation. That's why the DI is low when you can't open the EGJ. Okay? But the initial use of impedance planimetry was to look at esophageal reactivity, to look at the contraction in response to balloon dilation. This was done by Satish Rao in 1996. Hans Gregersen was the one who developed this technology. But he looked at impedance planimetry with cross-sectional area. And he looked at the reactivity, which is a change in that cross-sectional area, in response to steady distension. Remember, that's what we do with flip, steady distension. Right? And he showed that, it doesn't show very well, but the non-cardiac chest pain patients, not dysphagia, chest pain patients had very high reactivity. Non-cardiac chest pain is a functional esophageal disorder from esophageal hypersensitivity and hyperreactivity. Okay? All these functional disorders have a hypersensitivity component and a reactivity component. Right? Irritable bowel syndrome, hypersensitivity equals pain, reactivity equals constipation or diarrhea. Functional dyspepsia, hypersensitivity equals pain and discomfort, reactivity equals sensation of bloating, nausea, vomiting. In the esophagus, hypersensitivity equals chest pain or heartburn, reactivity equals contraction, vigorous contraction. You don't see it unless you distend a balloon. And the original studies that looked at atypical chest pain demonstrated that at very, very low levels of balloon distension, 5 mL, 7 mL, the patients developed crushing chest pain. That's because of hypersensitivity and reactivity. Right? So he showed, Satish Rao showed that there was increased reactivity compared to healthy controls in patients with non-cardiac chest pain. There is very good data showing that the higher the contraction amplitude, the higher the sensitivity. So the patients are more sensitive and more reactive if their contraction amplitude is high, especially in the context of pain as a symptom. Okay? And now look at these flip patterns. You have to be very, very careful that this is an obstructive pattern from some other test, not flip, some other test that tells you that the bolus is not moving through before you cut. Because if you cut this patient, now you have reflux, retrograde movement of gastric content as an additional noxious trigger for somebody who was already hypersensitive in the first place. Okay? So I will leave you with that. That is my thought-provoking element. I just want to add to that. It's really interesting because I am enamored with this as a disclaimer. And I think that it's true that chest pain only patients you have to really take with a whole different view. And then it's also having multiple studies point the correct direction. And if not, really considering all the trials of everything you have available to you that's not reversible first. So I echo that. Thank you. I think I have my algorithm here. This is my algorithm. This is my algorithm. I showed this and this is from Ray from years before flip was even a thing. Yeah. Right? So if you have a spastic motor process and no alternative explanation for symptoms, if the symptom is chest pain or perceptive dominant, the most common mechanism is reflux. Half of these will have reflux as a mechanism. If you don't see reflux, it is just plain visceral hypersensitivity. Treat with an antidepressant. If the patient's symptom is transit, first decide if the symptom is linked to abnormal bolus transit. How do you do that? Barium. Use marshmallow or barium tablet in addition to liquid barium. Do a rapid drink challenge with your high resolution manometry. Sit and wait in the esophagus and see if you can see an obstructive element. If the answer to that is no, you cannot prove that. Don't do something to the esophagus. Give the patient something. Give the patient a pill. If the chest pain is infrequent, GI cocktail PRN. If the symptom is more frequent, I usually start with a neuromodulator trial, but those are some of the patients. Sometimes we use other kinds of treatments like cognitive therapy, hypnotherapy, and things like that. If their symptom can be linked to disturbed bolus transit, those are the smooth muscle relaxants, the balloon trial, the Botox trial, the myotomy. You just have to remember that the patients who get to that myotomy phase will be a small number compared to the patients who have these spastic processes. So you can't look at high resolution manometry without context and say, oh, I see a jack hammer pattern or type 3 achalasia or EGJ outflow obstruction. This is a person I'm going to work up for a myotomy. No. It should be, I see this. Maybe I need to know what their symptom is. Maybe I need to see them in the office. Or working with a multidisciplinary team, or we work together as a group all the time to go through these trials. I think just taking your time. I always tell patients small steps in the right direction are better than big steps in the wrong direction. Because I have a long list of my spastic, especially chest pain, predominant patients as well. So just encouraging those small steps. And my fellow who had hypercontractile esophagus completely destroyed my normal patient, normal healthy volunteer, asymptomatic healthy volunteer cohort. He has had no symptoms. He's a successful gastroenterologist 15 years down the road now here in the Chicago suburbs. So he's doing zero symptoms. He has hypercontractile esophagus. Asymptomatic. Completely asymptomatic. Thank you.

achalasia

management

diagnostic tests

treatment options

dysphagia

chest pain

surgical intervention

patient expectations

comprehensive overview