All right, I can do mine fast, because I think I'm supposed to be done by 8, right? That's all right. 20 minutes. I think we've got a tight schedule with everything going, so I'm just going to try to rocket through this. All right. What I was tasked to talk about in this discussion session was recurrent symptoms after treatment. How do I address these patients? And I think one of the things I just wanted to touch upon before we start is making mistakes before you even start this whole process. Not understanding the subtypes, potentially doing aggressive myotomy, whether it's laparoscopic heller myotomy, or potentially POEM on patients who may not need it. Not appreciating the anatomy, I think, is also extremely important. I think that's something that certainly does predict outcome probably better than anything. Not understanding the biomechanics of bolus transport, I think, is also another thing that plagues people when they're evaluating these people afterwards. And then the other one, psychological distress. And I think that's something that we have to be more appreciative of. So I'm going to rocket through this. The subtypes are really created in a way, to be honest, when we first started looking at this, to decipher what vigorous achalasia was. It was this idea that vigorous achalasia was this entity unto itself that in some studies had a great outcome, and in other studies had a really bad outcome. And how do you kind of reconcile that? So when I actually looked at those papers and looked at the patterns, I realized that the ones that did well had an isobaric pressurization pattern. And the ones where they actually did poorly had a very spastic, or not isobaric. And that really was the impetus for this. So probably one of the easiest things that I see in my clinic is the patients who had type 3 achalasia, who had something like a heller myotomy or a POEM, who comes in and still has spasm. So this is something that's very easy. This is a patient who I actually saw who had a laparoscopic heller myotomy by one of our surgeons many years ago, continued to have symptoms, just never came back. And when we repeated her manometry, she essentially now has distal spasm instead of having type 3 achalasia, did a POEM, and she did exceptionally well. Anatomy also extremely important when you're making your decisions of treatment. And it's really going to help you in terms of your follow and explain why patients are not doing well after a myotomy. This is actually a study that we did a little bit ago, which really highlighted the fact that regardless of what your DI is or your opening dynamics, really the thing at the end of the day that dominated bolus retention and symptom score was really this idea that anatomic deformity was a lot more important than actually the EGJDI in that concept. So my case presentation, like I said, I'm going to try to get through this in 5 or 10 minutes, is a 54-year-old woman who underwent a laparoscopic heller myotomy with a door in 2016. She now presents with one year of heartburn, chest pain, regurgitation, which has really progressed to liquid and solid dysphagia now. The key point in your history, though, is she initially did really well for a year. So for a year, she did exceptionally well, which probably means she had a pretty good myotomy. The people who never get better either have horrible anatomy to begin with, or they might have had an incomplete myotomy. But the people who really did great, gained a lot of weight, were happy, probably had a pretty good operation and a good outcome. And probably the reason why they're coming back now a year, two, three years later, especially in the context of laparoscopic heller myotomy with a door, is maybe a wrap complication or another complication. So that's kind of the point that I just wanted to make with this particular case presentation. And this is the algorithm that I use. And once again, I always joke around, if you see an algorithm like this, it means you don't know what you're doing. But I think this one I have a pretty decent handle on. And the point that I want to make on this particular slide is the importance of the time-barium esophagram. So when I see people in my clinical practice, and they come in with recurrent symptoms, especially if it's dysphagia, bland regurgitation, they're losing weight, they're regurgitating at night, the test that I do first is a time-barium esophagram. And we have a modified time-barium esophagram. So if we do a time-barium esophagram, and they swallow the barium, and it goes right through and it's gone, then they actually do a more formal esophagram and end with a barium tablet. So we have actually a very regimented time-barium esophagram that we worked with our radiologists to put together so that we could get the most information. And we start typically with this time-barium esophagram. And if they clear it, you obviously don't want to say, OK, everything's fine, because that's just liquid barium. You want to go through the process. You want to get good CINI images. You want to look at the anatomy of the EGJ. And then, of course, you want to do a barium tablet. Some people are lucky enough that their radiologist will actually do a marshmallow or a bread bolus. Ours will not, because they don't want to send someone to the ER with a food impaction. So in this algorithm, if their TBE is normal, and it looks great, and their esophagram looks normal, there's no evidence of obstruction, there's great emptying, then I start thinking, OK, this is probably GERD. I will have tried an empiric trial of PPI, specifically if they have reflux-like symptoms. But these are now relegated to people who may only have regurgitation, dysphagia-like symptoms. So if it's normal, I'll start thinking more GERD, and I'll likely do an endoscopy right off the bat. But if their TBE is abnormal, in those particular instances, I do an EGD with FLIP. And you see there plus minus HRM? I rarely schedule the patient for an HRM anymore, because it really doesn't help me. I think really what I'm trying to go in there and see is, is there really severe esophagitis, a mechanical problem, stricture? Is there a hernia of the rap? Or is there truly a tight EGJ? And the thing that's going to tell me that is going to be the FLIP in this particular case. One quick question. Will the chronic narcotics she's taking, Norco, affect your readings at all? I mean, once again, you're using it in the context of the patient. If someone has achalasia, then the Norco is not going to get them to a worse achalasia. It's already kind of destroyed the enteric neurons at that particular point. So it's not going to make anything worse at that. Because it's a qualitative defect in the latency. So certainly, when I do my EGD and FLIP, if everything is normal, I'm thinking, well, maybe this could be functional or more stress. But of course, if I see that there's something on the esophagram, like a bomb, I'll certainly address that. But typically, if it's persistent during that particular endoscopy, I can actually do a pneumatic dilation right then and there. So if I'm doing that, I've got them scheduled. I typically schedule the patient so I'll have access to fluoro. I do an EGD. I do the FLIP. If it's tight, I can do either an ESO FLIP. To be honest, I still prefer the Boston Scientific microvasive balloons. I'll typically do a pneumatic right then and there, recheck them, and see if I've made some headway there. But if it looks like spasm, those are some of the few patients that I may get a manometry on. But typically, I will have had the preoperative manometry, which makes me less inclined or at least more informed as to what this might be. The one thing I want to say is, just as an aside, the ECKRT score is horrible. The ECKRT score was never validated as a PRO to be used for patients and to monitor outcome. And in fact, the first study to look at validation of the ECKRT score was a study we did. And we actually showed that it's not very good. It actually barely meets criteria in terms of reproducibility, reliability, all of these important psychometric measures that tell you whether or not a PRO is good. And I will tell you that using the ECKRT score of 3 as kind of this benchmark is ridiculous. Because in my practice, I mean, that means you could have symptoms every day. That's not a good outcome. So if you really want to say that someone's doing well using the ECKRT score, you should expect a score no greater. I mean, how we look at it, it's less than 2. So we want to see an absolute good outcome. People gaining weight, sleeping through the night, I mean, all of these things that are really important to patients' quality of life, as opposed to just asking them this very simplistic questionnaire that doesn't really have clinical relevance, to be quite honest. But we do. We use it. And this is what is in every single research study. So lo and behold, this is what her esophagram looked like in 2016. So she was seen, actually, just to preface this, she was at an outside hospital. And this is what they saw. They thought she had an incomplete myotomy. So they went ahead, and they did a pneumatic dilation. She did not respond. They did another laparoscopic Heller myotomy. She did not respond. They did a poem, and she did not respond. And this is all throughout that year. And in 2017, she still sat there with this same esophagram. So just to tweak the audience here, and this is another reason why I don't think these tests are all that helpful, does anyone want to give me the read on her manometry here? What do you guys think about this manometry? I know I'm trying to get through this fast, sorry. So is this consistent with an incomplete myotomy, spasm? So you see this manometry. So do you think the catheter is in the abdomen? What do you think about the position? So this is a really bad manometry. I'll tell you that right here. So this is probably the end of her career. You can see there's no pressure inversion here. She's actually breathing in. So there's really no gastric. And what happened with this particular patient, because of her anatomic abnormality, it was almost impossible to get her catheter into her abdomen without actually endoscopic placement. So when she had this manometry, then outside. So they actually kept thinking this was an incomplete myotomy because of this band here. So it was read as an incomplete myotomy, high IRP. I don't know how they could get a high IRP when they really have no gastric component there. So it goes back to this, that manometry in this situation can be very difficult for patients, especially if it's not placed endoscopically. And many times, it's not all that helpful. There's a lot of contact artifact because they're tortuous. So it's often not very helpful. So then when we saw her, we did a flip. And during her flip, it appeared that she had some sporadic little chaotic contractions that were up in the top of the proximal esophagus that were really not very contributory. But her EGJ opened up pretty well. I mean, she actually, during the second laparoscopic helomyelin, I failed to let you know, they took down her door for what it's worth. But still, her EGJ opened up quite well. And that's why I show this plot here, that if you fulfill criteria in this range here, meaning that your DI is very low, less than two, and your opening diameters are less than 12, and you're having persistent symptoms post-treatment, you have retention, there's probably some efficacy or some effectiveness of doing something at the EGJ, like a pneumatic dilation or a POM. If you're in this range, and you have a barium column of 12, 15 centimeters up in your chest, you're in a lot of trouble, because your EGJ is open. And treating the EGJ at that point is not going to do anything for that patient. So our surgeons really like the flip, because if we tell them that this person is in this range, these are people that will need an esophagectomy. But if we see people in this range, they often would like us down in the red area. They often would like us to try at least a pneumatic dilation or attempt at another myotomy at that particular point. So we use this actual graph a lot to kind of pinpoint where people sit. Once again, going back to the anatomy. If they have D here, it's no big surprise that this person didn't get better, right? But probably the more important people are these people in A and B. I apologize, I don't think those are that easy to read back there. But A is kind of the start of this bomb, this blown-out myotomy. And then actually B is actually a true, complete blown-out myotomy. And it depends on where the person had their myotomy, whether it's anterior or posterior, that's where it'll occur. And once that occurs, that completely destroys the biomechanical principles of fluid dynamic emptying in the esophagus. So in essence, when you see this particular slide set here, this is what we found. And when we went back retrospectively, and a lot of these cases are actually at Northwestern, these are cases that we did standard myotomies on, laparoscopic heller myotomies, and we went back and looked at this, this is a real phenomenon, this blown-out myotomy. Because what happens here is that this pocket doesn't allow recoil to actually allow the pressure that's generating the esophagus to open up the esophagal gastric junction. And it was interesting because we never saw this with pneumatic dilation. So it never occurred with pneumatic dilation, which in our mind made even more sense because you're just affecting the lower esophageal sphincter, and you're not creating this defect in the lower esophagus. So when we looked at this, there were definitely some predictors whether or not they had type 3A kalasia, whether laparoscopic heller myotomy with a door had a higher prevalence. And really, this is the biomechanics behind it. So remember, this is like, I call this, you know, some people call it the pump gun hypothesis. That's wrong because it's not really a pump gun. It's actually a water balloon. So you can think of the esophagus, especially in type 2A kalasia or even type 1A kalasia, as a balloon that's filled with water. And the only way it can empty is if the pressure in the esophagus is greater than the pressure at the EGJ. Now, there are some fancy biomechanical principles because they're perpendicular forces that you need to consider. But the long and short of it is if your esophageal pressures are 5 and your intergastric pressures are 8 to 10, you're not going to empty, right? So you need to generate some pressure gradient in order to open the EGJ and then overcome the gastric gradient. And that's what we see in type 2A kalasia. You see a water balloon being squeezed, almost like a hand squeezing it, it pressurizes, and then it opens the esophagal gastric junction. Well, what happens when you do a long myotomy? You have a defect there. And where is that pressure going to be transmitted? It's going to be transmitted into that zone of weakness. And eventually, there is a mechanical strain stress phenomenon that occurs where you go from an elastic tissue to a plastic tissue. And what happens in the bomb early on, what you see is you see in the elastic phase where they actually blow up during the time-bearing esophagram. You see it, and then it resolves. And then eventually, it turns into this plastic where it doesn't resolve. And when you scope these patients, you see this big pocket there. When you do esophagrams, the barium just sits there, and the food just sits in that particular pocket. So we went back and did. We have a virtual esophagus that lives on a server that we can tweak. We can actually do a myotomy of any length we want on it. We can change the outflow obstruction. We can give it a wrap. We can take the wrap down. And in that, this simulation, after it worked on this for three months, it essentially came back and said that the standard myotomies that we do at laparoscopic helomyotomy in POM are completely flawed and will inevitably lead to a bomb pattern in most patients given enough time. And that's really what I think we're seeing in these particular patients. We're seeing bombs where these myotomy sites are blowing out. It is not an issue of incomplete myotomy. I actually think that a lot of patients that I've diagnosed with incomplete myotomy 10 years ago actually had bombs. And they didn't get better, and they wound up getting esophagectomies. And now we've gone back, and we've appreciated the fact that we've probably overcalled incomplete myotomy. So in the end, this is really a biomechanical problem that we need to address. And the way I think we're going to address this is by actually being really precision and personalized in the approach. And Iko brought up a comment yesterday that I didn't get to address at the meeting about jackhammer esophagus. And I'm going to touch upon a mistake I made as a clinician in the cases later on in the day. But there are differences in jackhammer esophagus. It's a very heterogeneous group. And there is a group that actually has very nice peristalsis. And by cutting into that peristaltic muscle and getting rid of that, you're actually doing a disservice to the patient. And you're actually setting them up for a bomb. So we'll talk a little bit more about that this afternoon. I don't want to take too much of that. But I do think in many of these cases now, we need to rethink this myotomy length. We've known for years that the high-pressure zone is only 2 to 3 centimeters. So the idea that we're doing 9 centimeters myotomies on these patients is ridiculous. It defies what we know about physiology. And it actually sets people up for this bomb. And we probably diagnose at Northwestern now at least one to two cases of bomb a week. Now, granted, we're a referral center for redos. But this is a very common problem. And I think if we don't address this upfront, we're going to be seeing a lot more of these cases. So I'm going to stop here, because the time issues I know we've gone way over. But anyway, be cognizant of the bomb. The surgeons hated that. But I think the endoscopists should hate that. Because I think we're causing more of them than the surgeons now. And the bottom line is that an esophagram is probably your best tool to follow up patients after they don't do well with a laparoscopic helomyotomy or a POM. Any questions for Dr. Panofino? Yeah, John. Yeah. I mean, conceptually, the surgeons cannot do a long myotomy simply because they cannot for anatomical reasons. With POM, we can. If what you're saying is the main driving force, a too long of myotomy, you should not see it with Heller myotomy. But we do. So I mean, I'm not sure just a short myotomy will solve the problem. So if you look at the Heller myotomies that most surgeons do, they actually extend quite high, 6 centimeters up into the chest. And in fact, I've been at meetings where we've talked about the benefit of POM versus laparoscopic Heller myotomy. And the surgeons always say, we can go up as high as 10 centimeters pretty easily. We can mobilize things quite well. And that was interesting that you can clearly see. And I think when you look back at these, that POM starts at the extent of the myotomy. You see this little ridge there. And you can clearly see that that's probably the proximal extent of the myotomy in those particular patients. So it's a problem with laparoscopic Heller myotomy. And I think probably the door fundoplasty creates a functional obstruction that's very mild, but enough that drives that bowing out of the lumen. And if it keeps doing that, repetitively does that over and over, you will eventually progress to losing those elastic recoil properties and develop some plasticity in that wall. I mean, because that makes sense, the door contributing to blown out myotomy. Because this is a disaster when it happens. And if we can do something about it, it's a how about the typical curve of the esophagus traversing the diaphragm is from right to left. And bone usually forms on the right hand side. Can we do something about the position of our myotomy to avoid that if we go really anterior? I mean, truly at 12 o'clock position? Yeah, I think it's interesting because I think the most important thing is just being short and short enough that you're really not into the body. The question is, yes, the hiatus can also give you a functional obstruction in doing that. The one thing I am careful about is that when you look at the hill grade and flap valve one or two, and you see that beautiful flap, you don't want to destroy that flap during the poem. So if there's a way to preserve the flap and then shorten it and actually keep it away from that particular area, I think that would probably be the best way to go. But what position of myotomy will accomplish that in your mind? Well, I think the anterior is going to destroy the flap valve. So I tend to think that the posterior would be a better route to go because then you're preserving the flap valve and you're actually dealing with that tailored component of it. So I think that this, that right there would be what I would consider my optimal myotomy where I'm not destroying that beautiful flap valve over here. And I'm just cutting it here and therefore relieving that pressure without destroying the beautiful anatomy of hill. Thank you.

recurrent symptoms

achalasia

subtypes

anatomy

biomechanics

psychological distress