All right, good morning. Let me show you my case. There was years of struggle. Even though the poem was really helpful, I didn't know what to do for a while. And this is a 64 years old lady with dysphagia, weight loss, and chest pain. She had months of history of worsening dysphagia and some of the intermittent chest pain associated with weight loss. She couldn't eat much because of dysphagia, but the chest pain was some of the component. She was on oxycodone and fentanyl patch for back pain, so that kind of mud picture. And ECRS score at the time was 9, 3, 3, 1, 2. Dysphagia, regurgitation, chest pain, and weight loss in order. So at the outside institution, they saw the patient. They decided to do high-resolution manometry. And I don't have a complete picture. According to the report, the complete clearance was 20%. PAM pressurization is 70%. DCI was high. One time it's really high, more than 8,000, but mostly in 7,000. So it's not just the borderline. And IRP was 24, mildly increased. So the diagnosis from outside hospital was EGJ outflow obstruction. Do you agree, Prakash? My point about a study like this is it doesn't matter what you call it. There is exaggerated esophageal body contraction, and there is incomplete LES relaxation. So those two components you can see. So a DCI of 7,000 is not very far away from a DCI of 8,000. I do not differentiate those, because that is a contraction in the exaggerated realm, right? Your normal DCIs are going to be 2,000, 1,000. So 7,000 is at the high end even of the normal. So this person is developing features that are in the direction of a spastic esophagus with outflow obstruction. And I would be interested to see if that pressurization is between the contraction front and the EGJ. It probably is. If the IRP is 24 and you have that high a contraction, the person is probably compartmentalizing there, and that might be the mechanism for dysphagia. The opioid can do that. That could be an opioid effect. So the complete picture was not clear. The patient was referred to our esophageal specialist, and they decided to do an endoscopy. The sensibility index was really low, less than 1. It's almost like a kalasia. So they did the injection to the G-junction. It's 100 units. As a result, she actually improved symptoms. She recorded 40% improvement, but she had some still ongoing dysphagia and chest pain. So the esophageal group referred to me for a point. Like, I can decide what to do. So I asked for a repeat high-resource myelometry at Mayo Clinic. So here's the data. So it looks a little more different. It's complete clearance of 0%. Palm pressurization is 100%. I don't know why they called DCA NA, but they couldn't really measure it as soon. IRP, despite the Botox injection, was 40 mmHg, which is really high. The diagnosis was type 2 akalasia. Any comment? Well, I think this is not your typical type 2 akalasia. This is a spastic disorder that has been treated with Botox. That's how I would interpret this, because it has dampened the esophageal body contraction. So this DCI is going to be maybe 1,000, but you can't clearly measure it because there is compartmentalization. That's exactly what I was talking about. There is compartmentalization between that little bit of contraction in the middle of the esophagus and the EGJ. And clearly, there is a dominant outflow obstruction issue at the EGJ. So I think what you're seeing is a Botox effect that has impacted distal esophageal contraction and that's why you're seeing a little bit of proximal contraction, mid-esophageal contraction in that compartment. And just to say, when we're looking for panesophageal pressurization, we technically want to see it from the UES all the way down to the LES, which we're not seeing in this. But having said that, sometimes the computer will see that vertical swallow and read it as panesophageal pressurization. And so I think always double checking to see how the swallows are interpreted is important. If you're going to be a purist and follow the Chicago classification to the T, you would call this inconclusive EGJ outflow obstruction, according to Chicago 4.0. And you're going to want a barium or a flip. Now, you have a flip, but that was before the Botox. So I think that might be enough to make it conclusive EGJ outflow obstruction. I would say maybe opioid contributing, but, you know. I appreciate that. So esophagram, as you mentioned, was done. This is a slow transit across the G-junction. There's a spastic component after a while, and barium tabulate kind of stayed up. So should I do point? If so, how long should we cut? We shouldn't do it. Go ahead. I've asked this question before. Some of the opiates can cause spasm and can cause incomplete relaxation. Wouldn't you at least at first try to work with whoever their pain specialist is to try to decrease their dose and or wean them off before doing some sort of definitive therapy that they don't, in my limited experience, they don't typically do as well as people that have, like, you know, typical achalasia. But I don't, again, I'm just thinking out loud. Well, at our institution, we try to ask them to just wean it off, and if they can, we'll try to do the manometry again. But more than we want to see, it's failed. They cannot wean off. They refuse. They have a reason to take pain medication. So I want to hear what you think. See, my approach with these patients is to let them earn their myotin, right? And a few sessions in the office with a lot of discussion about what's going to happen if we do one option versus another option. So first, you'll have to understand what do opioids do to the gut, okay? So you have to start with that. What do opioids do to the gut? They make the sphincters more spastic. So it happens in the anal sphincter. It happens in the sphincter of OD. It happens in the lower esophageal sphincter. In the esophageal body, it makes the contractions more premature and spastic, okay, more exaggerated as well as premature. So it seems like the esophageal elements are fulfilled here. The other thing that opioids do is it makes the bowel hypersensitive. Pain transmission, pain is transmitted preferentially to the brain, right? So over time, visceral pain worsens with opioids. So if this person has an alternate trigger for esophageal sensation, then they're going to have post-treatment pain as well as reflux-induced pain. So I would bring this person to the office, and I would say, are you okay with 40 to 60 percent symptom improvement with Botox, right? And see if they're comfortable with that. And the other thing that I try to assess is what is the duration of benefit of the Botox. When we started using Botox in the 90s, we did a series at that time, and we found that if you did a second one at three months, you get incremental benefit. It's only the multiple Botox over a number of years that you lose efficacy. You may get additional benefit out of a second one. But I think the part that you really need to establish here is that the patient might have improvement in a transit symptom at the cost of perceptive symptoms. And that might provoke her to take more opioids, and over time, that's going to make her even worse. So, you know, somebody like this, there probably needs to be some neuromodulator in the mix, which may hopefully reduce opiate doses. There is new data from Vanderbilt that suggests that Tramadol has the least detrimental effect on esophageal spasticity. So if they're an oxycodone or one of the more potent ones, you know, switching them down to Tramadol could be an option. Trying to get the primary doc to understand the bad effects of long-term Botox on the gut, you know, long-term opioids on the gut. It's not just up top. You know, they have delayed gastric emptying. They have delayed colonic emptying. So I think it requires a more comprehensive, you know, educational element to the referring doctor before we do something to the esophagus. And for me, that process takes six months to a year before it. You know, it's only recently that I've been relenting, and especially if the esophagus is dilating, and relenting and saying, okay, do something permanent, because I don't see a way out of them getting off the opioids. Some patients will understand and try to temper, but, you know, some patients will write horrible things about me on Google. What about gastric emptying? That's a good question. It comes afterwards, but I'll give you it was normal. So to give her credit, she came off a fentanyl patch, but she continued on oxycodone. And from my esophageal specialist, number one is that the sensibility is really low. Manometry is more consistent with achalasia, responding to Botox. With those, we decide to give a more durable response with one procedure. So how long should we cut? That's another question. I think this is one way you should fillet it open, top to bottom. Yes. Otherwise, you're going to run into problems. I agree. I think there's some spastic components hidden there. Okay. So I did a short myotomy. The reason is that she responded fairly well to the disruption of the LES, so I would give her a chance to declare that she needs a much longer myotomy before we complete the esophageal myotomy for the whole length. So five centimeter myotomy, two centimeter cardiac, she did well. Within a month, she started to have more chest pain, responding to nitroglycerin. At three months surveillance, the echo score was six. It's not that great, but it's an improvement. Dysphagia improves so much because its value is one from three. High-resolution manometry, significantly lower IRP, but still a little bit elevated. DCI is 2121 in the spastic segment. And the esophageal looks actually good. And endoscopy, there's no esophagitis, open GEJ. The distensibility, for some reason, it was seven, but about 2.6 to 3.2. So it seemed to be responding fairly well to the point procedure of the distal myotomy. No reflux. So far, so good. Things continues. She continues to have just chest discomfort. She started taking Xanax, nitroglycerin. And eight months later, she was diagnosed with hypothyroidism. So the TSAs were really low. She was treated with methamazole. The hoarseness came on. She thought it was an allergy, but we started PPI and it continued, although there's no reflux on the PH study. And because of the chest pain, I sent her to cardiologist. She has a high-risk factor. She has a strong family history of coronary artery disease and stroke, but stresses was negative. So for now, it's cleared. At two years, she continued on and off coming back to me, and there's no dysphagia. She feels great from that aspect. But she has a regurgitation. Some things come back, and chest pain still comes up on and off, and she cannot gain weight. The soft gram shows still delayed transit of barium. It's not going through quickly. So there's a question. The IRP was somewhat high. Did I not complete myotomy? That was one of the concerns. EGD was done. The endoflip contradict. The desensitability index was 6 and 7, which is almost like reflux value. So what's going on? I think she's developing a bum. She's developing a bum. That is the classic symptom, the classic finding of a bum there. If you look at the soft gram endoflip, that makes more sense. The high-resolution manometry was repeated. This is what you see. The IRP was coming down to almost normal. 100% pump pressurization is unchanged. Body is normal, normal, and the DCI was somewhat in the middle. So there's a concern about unrelaxing GE junction. So I did the Botox. Guess what? Symptom improved, and barium actually started to pass through well. So is it the incomplete myotomy? It's possible. How do you explain chest pain? What's regurgitation? Is it coming from the poor transit? She continued to have chest pain. This is over the three years course, so bear with me. She went to the emergency room here and there outside the hospital so many times. Four months after the Botox injection, she was diagnosed with non-STEMI. She had ST change, woke up, showed patent coronary, as she had before. So the diagnosis was Takotsubo cardiomyopathy at the outside hospital. She was studied on beta-blocker aspirin, but continued to have chest pain, so I added long-acting nitrile. It's a nightmare. I just don't know. Did I do something wrong, or she's having trouble with the achalasia? At the loss, I repeated manometry again. This is pretty much similar findings. Esophagram looks great. Everything goes through. However, there's some contraction here that's correlated with the manometry. But since we were not so sure, we continued to medically manage. So this was not a bone yet, or it may not be bone forever. Eight months later, she came back to Mayo ER because she went to the other side of the emergency room. They said, you have to go back. We don't know what she had. Go back to Mayo ER. So she came back, and again, ruled out cardiac cause. So what should we do? Amrita, what would you do? How often does she have chest pain? Pretty much every day. Every day. So I think this is the point where she's manifesting increased hypersensitivity, very likely. She's probably retaining in that segment that has been myotomized. I would treat her medically for now, where she doesn't have dysphagia, but I would put her on a neuromodulator of some sort. Neuromodulator? So the pain suppressing neuromodulators in this setting, you have a few options. You can do a tricyclic, but clearly there is an anxiety component. She's been using Xanax, so you're probably better off using duloxetine or venlafaxine. Both of those are very good for pain suppression and anxiety suppression, because anxiety will make the pain worse. And during the pain episodes, I usually have them use topical lidocaine, so GI cocktail with lidocaine during pain episodes. And daily titrating doses, probably duloxetine better tolerated than venlafaxine. So starting at 30, going up to 60 twice a day would be the highest. Interesting. We haven't done that, so we decided to inject Botox to the segments of the spasm. We did 200 units in a spiral shape around 28 to 33. Remember that I did a seven centimeter of me from 34 down, so just avoided that area. Her score went down. It's now 33. She feels fantastic. She gained weight. Chest pain eventually disappeared. Now we have somewhat proved that she is developing dysplastic disorder. So first, as you mentioned, I should have cut the whole thing, but that's why I said I hate you. Reducing mechanism. So it will reduce sensation as well. So it's not unusual to have this result. Interesting. Well, as you expected, the Botox effect faded away. Two and a half months, started having chest pain. So after discussing options, I offer a second point. First one is anterior, so I went to posterior. So that's the video. You see, this is above the spasm. Then this is more spastic area happens. I'm ready to cut, by the way. Then at 12 o'clock, this is the entry site from previous point. And here's myotomy site. This one down to G junction. The G junction actually looks really nice. I did a posterior approach, the hybrid knife, I-type. Injection was done, and longitudinal cutting was done with endo-cut. And then trimming was done to the side. And you practice those things. There's only one learner at the one station, so you can do anterior-posterior myotomy. My student completed both of them and closed it up. So this is a typical entry. So once you trim it, inject the fluid at the distal end, trim a little bit on the side. That will make it much easier to go into the semicolon space. I'm using endo-cut because I don't see much blood vessels. So it's much cleaner to cut with a cut current. So this is a semicolon layer. Muscle is pretty thin. This is five minutes. I put the speed because I don't want you to think that I'm going crazy fast, right and left. So continue on to trace the muscle. I do left and right because the channel is on the left. So if you go left to right, you can see what you're going to cut. And this patient doesn't have much of the fibrosis despite one time of injection of the Botox. Norio, do you prefer that lighter color? I do. Because in the lab it's so dark, but the blue is not necessary. It's a slight blue like this color. This one is maybe a little too light, but I prefer lighter because I can see the vessel much easier. This is just to show that you can go rotate so that you can do the up and down motion rather than the rotation. So from here, I can do the big knob from lower and upper as you cut. And this is down angle. And from here, push in and the up angle or actually down angle. And stay on to the muscle. The tunnel is created. I prefer narrower tunnel nowadays to reduce the risk of bone. That's my theory. At first, I continue down to the longitudinal muscle. I don't move around. And now I can see the longitudinal muscle, insert the knife and do this. Here, I insert the knife a little more and pull towards the lumen and the cut. Sometimes the patient breathes, so you have to time it. And continue on to insert the knife, go forward. And from here, I can see the muscle. I don't move around. And now I can see the longitudinal muscle. Continue on to insert the knife, go forward. The spastic segment is always difficult to just maintain the lumen. So if that's the case, I talk to the left, pull back the knife a little bit more so that I can push the semicozal to the side. And use more of a scope. I also wanted to show you this maneuver because we tend to just push the knife out. Then you just try, when you cut, you just accidentally go to the opposite wall, especially it's collapsing lumen. Am I going over time? Very much, right? Any questions about technique? This is after the myotomy. Larry, can you just describe maybe for the audience how you estimate your depth until you get to the longitudinal muscle for your selective myotomy? How are you estimating how much each cut? Are you just doing a slight tap on the pedal? Initial cut. Yeah, it's just tap, tap, tap with the end cut, with the stain onto the muscle. It just kind of keeps separating. And until I see the longitudinal muscle, I just keep tapping on it. I don't move around. So the clip is, clip closed. But if there's no question, I go to the outcome. The symptom improved significantly. She's super happy. First time I achieved this success. Aker scored two. She's gaining weight. High resolution manometry showed much reduced pressure in the center and the body. Not negative, but somehow they couldn't go into the G-junction. DCI was 2,000, 3,000 range. It's now 566. Esophagram showed smooth passage. But as Prakash said, I start to be a little worried about this segment. So now I keep in mind that her LES may be incompletely cut. I could have cut the LES at the last point procedure, but I'll just keep watching. I can do additional point posteriorly because I didn't go through all to the G-junction. Remember, I just only cut the mid-esophageal body. So repeat point is possible. She's so far doing well. And outcome is great. But I should have cut whole thing at the beginning. But I couldn't with the type 2 akalasia diagnosis. Go ahead. So from my experience, if you do anterior myelotomy for long segment, you have potential to spiral. And Haru was talking about try to avoid to the side because the side is the weakest point, especially epiphrenic diverticulum typically goes to the right because there's much less pressure in there. So if you spiral to the right during the myelotomy, then you probably create bone. So for me, it's just a posterior myelotomy makes sense for long segment because there's lots of supportive structures to avoid the bone for the future. Great. Thank you so much.

dysphagia

weight loss

chest pain

esophagitis

gastroesophageal junction

achalasia