So, next up, we have Prakash Geowally from Washington University in St. Louis. He's going to talk to us about post-poem complications, how to identify and manage them. Thank you, Aziz. Welcome everybody. I'm an esophagologist. I don't do poems, but other people do poems on my behalf, on my patients. And my job for this talk is to try and explain to you how I troubleshoot patients who are symptomatic afterwards. The interventionist has done their job, they're off the case, and I want patients back to my care. All right? So these are my disclosures. And you can use this information in evaluation of practically any esophageal motor disorder that's been treated, or practically any achalasia that's been treated. I try to think about esophageal symptoms along the lines of perceptive, which the patient tells me they feel, or transit, which is a symptom that impedes the movement of food downwards, or a symptom that tells you something is coming up from below upwards. So dysphagia, regurgitation. And sometimes patients have other symptoms. So among the perceptive symptoms, these are the usual ones. Medinaphagia, chest pain, heartburn. These are the usual ones that patients complain about. And transit symptoms, dysphagia, obviously, regurgitation, and food impaction. These are the usual transit symptoms that a patient can claim up. And there are a couple of others. Some patients may have supraesophageal symptoms, they may have belching, and weight change. Now, you might think this is a laundry list that would apply to any patient that you see in clinic. That's true. And if you think about symptoms in this fashion, you're usually able to sort through any kind of patient that comes to your clinic. But the achalasia patient, the patient with motor disorder, spastic motor disorder that needs a pump, has a couple of other unique things that you need to remember. One, late stage achalasia is associated with esophageal hyposensitivity. Late stage achalasia, esophageal hyposensitivity. And that's part of what Joe was talking about. You can have significant esophagitis, and the patient may not feel it until they've developed a stricture later on. Some of these well-developed achalasia syndromes have an idiopathic chest pain syndrome associated with it. The actual ideology of that chest pain is not known. It's not necessarily reflux. And sometimes that pain requires a neuromodulator. I actually have one patient who continued to have that idiopathic pain even after an esophagectomy. And I've treated him with gabapentin for years. Amitriptyline gabapentin can sometimes help that idiopathic chest pain of achalasia. The third part is, there can be true esophageal visceral hypersensitivity in the spastic achalasias, the spastic syndromes. So when those spastic patients say they have chest pain, that might be a true visceral hypersensitivity, not the idiopathic pain. So those are the patients where if you distend a balloon in their esophagus, they're going to feel it at lower degrees of distention, all right? So let's start with the reflux spectrum. So this is the reflux spectrum here, conveniently colored for your focus here. Now if you look at POM data, this is the updated data from the European group, the JAMA study updated and presented at DDW. So they had 133 patients that were randomized to POM versus PD. And the study showed that POM was more effective than pneumatic dilation in dysphagia relief. And now it's out to five years. The JAMA paper is, I think, two years. This is a courtesy of the lead author, and of Orien Bredenoord from Amsterdam, the slide data. There was no difference in quality of life. The significant adverse events were both in the pneumatic dilation group. But look at the reflux information here. This is symptoms by GERT-Q. Granted, GERT-Q is not perfect. Symptoms by GERT-Q, seen more often with POM compared to pneumatic dilation. Significant esophagitis, not very frequent. Lower grades of esophagitis, that includes B. So A and B is the blue here. More frequent in POM compared to pneumatic dilation. And the third is PPI use, more frequent with POM compared to pneumatic dilation. Now, let's look at POM versus Heller myotomy. So as you might imagine, prolonged durable benefit in dysphagia at the cost of reflux was the conclusion from this, at least symptomatic reflux. This is POM versus laparoscopic Heller myotomy. This is the New England Journal paper that you've seen several times so far already this afternoon. Again, good treatment success, both arms, no difference in quality of life, a smattering of significant adverse events. Again, reflux symptoms, both groups. Pneumatic dilation has the least degree of symptomatic reflux of these three therapies that you have. Significant esophagitis, you can see some significant esophagitis. Significant meaning LA-grade C and D with both laparoscopic Heller myotomy and with POM. And PPI use, again, you can see here half the patients are on PPI. So there is a disconnect between the degree of PPI use, the degree of reflux symptoms reported by the patient, and the actual obvious esophagitis that you see when you endoscope these patients. And when you see esophagitis, much of the esophagitis is at the lower end of the LA-grade spectrum. And that is something that is well-established from these randomized studies. So what do you do when somebody has reflux symptoms? Well, you can start out with a PPI trial. You probably scope most of these patients. Some of these patients will remain on a PPI because when you try to stop the PPI after the procedure, it doesn't matter whether it's POM, pneumatic dilation, Heller, they will say they are symptomatic and they'll keep taking it. Now if at that initial EGD, whether you have done it on or off therapy, there is advanced grade esophagitis, so LA, C, or D, maybe even B. Well-defined B is good evidence for true reflux. If they have a long-segment biopsy-proven Barrett's mucosa or a peptic esophageal stricture, they have reflux. You're done with testing. You don't need to prove reflux anymore. You can move into the realm of managing reflux. If they do not have this kind of conclusive evidence for reflux and the patient is symptomatic enough that you are not getting them better with simple medical management of reflux, that's the point where you need to decide if reflux exists so that you can further optimize treatment. And this is true for patients in any scenario, not necessarily post-POM. And you have these options of testing these patients. So how do you decide whether you're going to do a wireless monitoring versus a catheter-based monitoring? There are positives and negatives for either. And there are a couple of direction-related information that you need to understand. Perceptive symptoms, generally, a wireless study is reasonable. The exception is if the esophagus is massively dilated, you'll have trouble getting a BRAVA to attach, a wireless pH monitor to attach. But if somebody has a perceptive symptom, you have a narrow esophagus that is not massively dilated, and you're trying to rule in or rule out reflux for a heartburn or chest pain symptom, it might come up when somebody has chest pain, you're not getting better with the PPI, and you are on the fence as to what you're going to do next. That might be a situation where you do a wireless pH monitor. Again, remember the caveat. Getting it to attach in a dilated esophagus, not always great. Catheter-based pH monitoring, great for these belchers and for the people with regurgitation if you need to prove something here. The caveat there is baseline impedance is really, really low in a dilated esophagus. You will barely see reflux episodes. So you really have to alter your range if you're going to find reflux episodes. Now, you might see stasis in the esophagus. You might see these long pH drifts without reflux episodes. That means that there is stasis. That doesn't mean that the acid is coming up at a higher degree from the stomach. It might mean that in certain positions, refluxed acid or ingested acid doesn't clear out of the esophagus. And clearance is never perfect after any kind of achalasia, especially if the esophagus starts dilating. Now, if patients have evidence of reflux and their symptoms persist, now you are in a position where you'll have to decide, does this patient need some other treatment option beyond your medical mannequin? That's where a pH impedance study on PPI is going to be useful. For me, the pretest likelihood is generally high for reflux in patients who have undergone a POM procedure. But it's not so high that I will use an algorithmic approach. I will still use a personalized approach. I will still try to understand what I'm going to do with a positive result, what I'm going to do with a negative result, and what am I going to do with an equivocal result. Without that information, you really should not order a test. I don't do a test just because. The only test I would do just because in somebody who has had a POM is an upper endoscopy at some point during the follow-up, sometime between three and six months. Joe said three. Somewhere in that range, it's reasonable to do one, preferably off PPI if they're asymptomatic. So how would you treat? What adjunctive therapies do you have? You can use antacid with alginate. You can get this as Gaviscon Advanced from Amazon.com. There is a new preparation called Reflux Gourmet. And the nice thing about alginate is you can use it instead of a PPI. You can use it before PPI. You can use it along with PPI. Generally, in patients with infrequent, you can use antacids alone. You can use antacids with lidocaine. In infrequent symptoms, that might be adequate. In patients with an acid pocket, not so relevant in somebody who's undergone a POM. But if they have a little hernia, if they've had a little hiatus separation after a hell or myotomy, for instance, it might be relevant. In patients with persisting symptoms, you can add it onto a PPI. What about sucral fate? There is only evidence for rosifasciitis. Pregnancy is the other situation. Probably not relevant here that you use sucral fate in place of acid suppression. But in the absence of erosion or damage to the lining, there is no good data that sucral fate does anything. I actually hesitate to use sucral fate because it can actually bind medicines that the patients might need and render them ineffective, just like cholecystermine can if it's taken with medicines. So you have to be careful about that. You don't want medicines, heart medicines or antidepressants or something like that, not to be effective because you are throwing caraphate at the patient. The medicine is really not meant to be used in a non-erosive setting. So these are some of the adjunctive therapies, nocturnal H2RA, maybe short-term benefit baclofen in the post-POM setting, probably not very useful. And also mycosal protective agents, useful here. So the usual algorithm for reflux management still applies in the post-POM patient, acid manipulation. A couple of other points about PPI optimization. Make sure they are dosed 30 to 60 minutes before meals. Increasing dosing to twice a day may be more effective than giving them a lot of dosing at one time, so separating it out. Switching to a more potent PPI. So there is an hierarchy of PPI. And unfortunately, even though a lot of physicians try to switch patients from other PPIs to pentoprazole, pentoprazole is the weakest of the PPIs. Ribeprazole is the strongest, just from a bioavailability and efficacy point of view. So you can go up the ladder. And sometimes you can talk insurance companies into allowing like dexalant or Asifix in these patients. Remember that the presence of affective disorders, irritable bowel syndrome, and affective central disorders, anxiety and depression, increases visceral perception and increases the patient's perception of heartburn if they have reflux. So when they say my PPI is not working, it might mean I'm feeling refluxed, even though it is not acidic. So PPI response is lower in patients who have these affective disorders. So it might mean that the PPI is doing what it should, but the patient is viscerally receptive. What about using alternative pharmacotherapy? This might be available, penoprazan PCABS might be available in the US later this year or next year. And there is data, good data, that there is some gain in healing of advanced grade esophagitis with PCABS as compared to lensoprazole in this setting, especially in the maintenance phase. This was the Asian study. And this was the US study, the maintenance phase that was reported at DDW this year. Again, this was designed as a non-inferiority study. But when they looked at their maintenance data, healing of advanced grade esophagitis and relief of heartburn in the maintenance phase was better with PCABS compared to PPIs. So there may be advantages over PPIs. So the potential scenarios here with reflux symptoms, obviously reflux, but reflux hypersensitivity, patients feeling reflux more, sometimes you get these belchers. Supragastric belching is a situation where air is brought into the esophagus and belched out of the esophagus. And sometimes that is a reactive phenomenon, a response to an esophageal symptom, an unconscious response to food not moving through. So they develop this compensatory mechanism to fill the esophagus so that they can push the food through. But that compensatory mechanism persists even after you've resolved their obstruction. And so you may have to send them for cognitive therapy or diaphragmatic breathing or some of the other conventional treatments for these belchers. And obviously, these patients can have overlap of other functional syndromes as well. Can you do anything about reflux or reducing the potential for reflux? You know, Aziz has this data on the short form, and I quite like this as a potential option to reduce the likelihood of reflux with the more classic achalasia subtype. So if you have type 2 or type 1, you don't really need to fillet the body of the esophagus. And I like this idea. Obviously, this is preliminary data. This is just one of their slides from their DDW presentation. And then you've heard about the POM plus fundoplication. People have done TIFs afterwards. Again, you have to be selective. Why do it preemptively? Because only half the patients generally develop reflux, and a very small proportion of those need to move past PPI. So this is the data from one of the reports that I could find, a recent one. Generally, their conclusion was that it works. Symptoms go down. Severe symptoms improve. PPI use improves if you do a TIF. But I would say do it when you really need to. And the hierarchy of getting there is failure to either heal esophagitis or improve symptoms that you have confirmed with impedance pH monitoring on PPI. Partial fundoplication would work. There is no reason why it wouldn't work in volume regurgitators. There's little data in the post-POM setting, but this has been used in the helper myotomy setting. POM-F, it sounds a little cowboy to me. But this is one of those procedures where during the POM procedure, the endoscope is made to exit the body of the stomach. The fundus is grasped and pulled across to form a fundoplication. Again, my position with this, and this is data on a retrospective series of 25 cases. My position with this is you're doing 50% of this in people who are not going to reflux. You're creating a situation when maybe it may not have been needed in half the patients. I like to go in a systematic approach. If somebody has a problem, then you solve it. You don't try to solve problems when the incidence is not massively high. Okay, let's go to the transit side. You generally start the evaluation of transit symptoms with endoscopy. It's not uncommon to see this. This can account for some transit and some perceptive symptoms and some nonspecific symptoms. If you find this, you want to treat it. If it is minor, I like to use topical stuff, myselx or nystatin. Sometimes you have to leave patients on some prophylactic dosage. Bile esophagitis. Again, if there is an issue with the opening, a strictured opening, this is from potassium. NSAIDs can do it. There are several medicines that are associated. Doxycycline is particularly bad. You have to make sure that any existing strictures are treated. This is esophagitis with stricture. That's another stricture. Again, these things can be picked up very easily with that first endoscopy. Once in a while, you'll run into Barrett's. This patient probably had preexisting Barrett's. I did not see him until after he had his poem, but he had long-segment Barrett's esophagus. Clearly, you want to monitor these patients. Beyond that, the next step is to decide, is there bolus retention? In this particular series, there is no bolus retention. This is not from poem, by the way. This is from patients who underwent pneumatic dilation. You can see that the retention in a timed upright barium completely went away when the patient was stood up after they underwent the pneumatic dilation. Not so in this case. Barium is very useful after therapy of achalasia. In my opinion, much more useful than manometry. It can correlate with manometry, but it gives you a very good idea. Then the other option you have is FLIP. FLIP gives you a very good idea about not just an incomplete myotomy. In other words, not just a muscular issue, but it can also give you diameters if there is a stricture, subtle stricture. If you were going to do a manometry, I would not rely on the supine IRP alone. I would challenge the esophagus with a rapid drink challenge, 200 ml of fluid in the upright position. You can see a positive A, negative B. There is a very good correlate with the IRP during the rapid drink challenge, especially if you take a threshold of 10. A threshold of 10 will actually tell you if the number is higher than 10, it is likely that a timed barium esophogram is going to show barium retention. You can see the performance characteristics. This is data from Italy, the Italian group. This is useful if the IRP is below 10. In other words, it helps you not move it to a more invasive therapy because the esophagus is not going to be retaining barium. You can probably treat the patient with symptomatic adjustments in how they eat. The value of FLIP, this is data from Dusty and John Panofino's group. If you look at HRM, supine IRP more than 15 being abnormal, and FLIP reduced opening. Reduced opening means an EGJ distensibility index of less than 2 and a small diameter less than 16. You will see that in people with poor outcomes, both are going to be abnormal in a proportion. In people with good outcomes, both are going to be normal in almost everybody. The combination of HRM and FLIP can detect most patients with an emptying issue. The point about the emptying issue is that FLIP complements HRM. The emptying issue can be both an incomplete myotomy and a structural issue like a stricture. What do you do in that setting? This was a series from the Europeans where they followed up symptomatic dysphagia after a poem with pneumatic dilation, Heller, and re-poem. You don't need to read the various numbers, but the response was best symptomatically with the repeat poem. Again, the fact that some patients respond to one therapy and others respond to another means that you have to individualize management. There's no one size fits all with this. The predictors for a symptomatic, suboptimal symptomatic outcome, the only one that they found was female gender. For transit symptoms, incomplete myotomy is the one that most people worry about, but it's more likely that the other ones here, stricture, mucosal inflammation, functional, are going to be more common. Then finally, let's briefly talk about blown out myotomy. Blown out myotomy is a situation where the weakness created by the myotomy of any kind in this esophagus becomes ballooned out or becomes accentuated with the formation of a pseudodiverticulum, especially if there is intact contraction upstream and there is some resistance to flow downstream. You can get this after a poem. You can get this after Heller myotomy when the myotomy extends up. That's another reason why I like this idea of making the myotomy as short as possible. What happens is that weak area highlighted in red here in the third image starts ballooning out. Unfortunately, when it gets to a very large size, there isn't a whole lot you can do. That's the blown out myotomy segment. You can try and reduce resistance distal to this by doing another poem or pneumatic dilation or Heller myotomy. You can carry some patients through, but eventually, this is a situation where that segment may need to be cut out. That segment may need an esophagectomy. This is from the Northwestern paper. The likelihood of a blown out myotomy was higher with type III achalasia, and it took a little while to build up, is what this table says, for the most part. It is not an early thing. Other issues that come up with achalasia, massive esophageal dilation, sigmoid esophagus. Sometimes you can retreat the esophagogastric junction. Eventually, you may need either the esophagus out or enteral feeding. Esophageal cancer, not very common. Once in a while, you'll find a patient. I try to endoscope my achalasia patients at least once every second or third year overall. And finally, I want to leave you with a little thought from my side about not overdoing PONG. In this era of getting a FLIP study on patients, you have to be a little careful about FLIP. FLIP was originally studied to look at what's called esophageal reactivity in patients with functional disease. And the property of measuring cross-sectional area was what was very useful for that. Reactivity means a change in lumen diameter when you distend a balloon. If you distend a balloon, the muscle responds by contracting or can respond by contracting. And it turns out that patients with a functional syndrome like chest pain react more than a normal esophagus. And here, the solid bar is the functional group, non-cardiac chest pain. And there is a direct correlation between pain sensitivity and amplitude of contraction. So the higher the amplitude of contraction, the more the pain sensitivity. The more the patient feels the pain with less degree of esophageal stimulation. So think about these patterns when you see these exaggerated contractions in FLIP. You got to be absolutely sure that what you are seeing here is not a reactive contraction, that this is the native esophageal pattern that is causing transit. What is going to help you is that the reactive patient is going to complain of chest pain. The reactive patient is not going to complain of dysphagia. So be very, very careful about doing something permanent to somebody's esophagus when they have chest pain. So if they have chest pain as a symptom, you want to rule out reflux. You want to treat them with neuromodulators. If they have dysphagia as a symptom, you want to make absolutely sure that the symptom is related to disturbed bolus transit. If you're not sure, treat them with a neuromodulator. It's only if you are sure that there is an abnormal bolus transit. Think barium. Barium is very useful here, solid bolus. Only then would you want to go ahead and cut the person, because you can do harm by doing a myotomy. So reflux, transit symptoms, you have these long-term outcomes that are less desirable. All of these apply to the postponed patient. Weight change. Some patients gain a lot of weight, and that changes the physiology of the esophagogastric junction. It is reasonable to discuss this. You can have weight increase as well as weight decrease with achalasia. The increase may be a problem sometimes, because the dynamics may change. And that's really all I have. Happy to answer any questions anybody might have.

achalasia

esophageal motor disorders

complications

symptoms

treatments

reflux symptoms

transit issues