So I will move forward now and talk a little bit more about the POM and GPOM procedures that were touched on earlier. I'm really going to focus on what as APPs we're seeing in clinic beforehand, the guidance we can provide our patients regarding these procedures, and then how we're going to care for them in the immediate post-op period, as well as down the road. So first I'll define the procedures. What are they? POM is peroral endoscopic myotomy. It is a minimally invasive endoscopic procedure that's developed for the treatment of achalasia. And GPOM is a gastric peroral endoscopic myotomy. And it's essentially an adapted POM for treatment of gastroparesis. So rather than targeting the lower esophageal sphincter with POM, GPOM is targeting the pylorus. And why as APP should we care about these procedures? Well, we, of course, will be seeing these patients in clinic initially. We'll need to recognize the symptoms of these diagnoses. We'll need to order and interpret the tests for them. And then we're also going to need to talk our patients through their treatment options. These are great treatment options for achalasia as well as gastroparesis, the risks, benefits, and then help follow up as well. So we'll start with achalasia and POM. Achalasia is an esophageal motility disorder. It's characterized by failure of the lower esophageal sphincter to relax, as well as impaired peristalsis. There are three subtypes, which I'll get to here in a moment. The pathophysiology involves degeneration of the myenteric plexus, leading to impaired relaxation of the LES. And this is thought to be possibly due to autoimmune response. Presenting symptoms, patients will often have dysphagia to both solids and liquids. They may complain of chest pain, regurgitation, as well as weight loss associated with these symptoms. Diagnosis, gold standard of diagnosis for ACG is high-resolution manometry. Endoscopy can also be useful. Oftentimes, you'll see retained saliva and then a puckering of the GE junction. Esophogram also can be useful in diagnosis, and you see that pathognomonic large dilated esophagus with that bird beak appearance along the lower esophageal sphincter. And then as I mentioned earlier, there are three subtypes based on the Chicago classification system. Type one is classic akalasia. This is characterized by essentially a tight lower esophageal sphincter and then not a much peristalsis or pressurization upstream. Type two is associated with that lower tight sphincter and then more of a building pressure, but not in a coordinated peristaltic wave. And then type three is spastic contractions and then premature distal esophageal contractions. And here's some endoscopic photos. There's that saliva pooling as well as that puckering of the GE junction, and then a nice esophogram to show that large dilated esophagus that goes down into the bird beak appearance there before entering the stomach. And a few more images of what the manometry for each subtype may look like. And then also the variety in the esophograms that you may see. You can see on that type three there, that's a really nice picture of how the spasticity can show up on the esophogram there. So management of akalasia, few routes to take here. Pharmacotherapy is actually our last resort. It's really reserved for patients that are unable to undergo procedures for whatever reason that might be. Treatments include calcium channel blockers, nitrates, anticholinergic therapies, terbutaline, theophylline, silzinophil. And then you have the more conventional endoscopic therapies which includes botulism toxin injection into the lower esophageal sphincter as well as pneumatic dilation. Of note when we're performing dilation with AGD, the pneumatic dilation for akalasia, patients are at a little bit higher risk for perforation with that. And then there's a surgical option of a Heller myotomy. Typically we see the highest success rate for this surgery in type two. And then the home procedures that we're here to discuss today. And I wanted to mention that there is a clinical scoring system, the Eckhart score. It looks at four key areas, four key symptoms of akalasia including dysphagia, regurgitation, chest pain and weight loss. And this is a great tool to evaluate with your patients before a recommended intervention is utilized and then after to really get an idea of how well they are doing before and after. So when we're talking about who should get POMS, type three akalasia has a great response rate to POMS. Patients that have had prior Heller myotomies as well as patients with prior obesity surgeries are all good candidates for POMS. Someone that might not be as good of a candidate is a patient that might be unable to tolerate general anesthesia. Patients with coagulopathies that are difficult to manage or patients that are on chronic anticoagulation that cannot be held. Patients that would be adverse to being on long-term PPI therapy as well as patients with gastroparesis. Here's some pictures. There's a video next that I have for you all to see but essentially there's that hypertonic the lower esophageal sphincter. They make that mucosal incision. They tunnel down into the submucosa, locate that area of high pressure, perform the myotomy and then ultimately end up closing that mucosal incision with these clips here. And like I said, there's a video here I can play for you. And Sam, I'm also having a hard time with the video play. If you could play that for me. So here they're making that initial injection, inserting some fluid to kind of help beef that up in order to perform that. So as far as post-home protocols, it's a little bit center dependent on whether the patient will stay for a night for observation or go home. I think most centers are keeping patients for observation, but some are moving towards that same day discharge. So patients should be counseled to expect to stay the night in the hospital. When they wake up, they can expect to have some chest pain. I have some patients that wake up and say, I feel fine and don't need any type of pain medications. Others do require medications as strong as IV Dilaudid to manage their chest pain. And it's not necessarily an indication of a procedure gone wrong or an adverse event. It's just some people have more pain. Typically, I tell patients that this resolves within about 24 to 48 hours. It's very rare that I need to send patients home with oral opiates. Patients have to remain strict in PO until their esophagram, which oftentimes is next day. So that can be uncomfortable for patients. They should be expecting that. And then there is a post-procedure diet, which again, varies a little bit from center to center, but it is essentially a liquid to soft food diet for up to a week. Sometimes when I tell patients they have to be on a liquid diet for five, seven days, they look at me like I have six heads. So it's good for them to know this going in and have these expectations. Oftentimes we'll recommend prophylactic antibiotics for three days, and then they'll need to be on a PPI for at least three months after a procedure, possibly lifelong. We would want to repeat that Ecker score in clinic at the three-month visit, and frequently we'll recommend repeating an EGD at three to six months following the poem. So for the ASGE, there's, you know, with every procedure, a lot of risks. I think a lot of these risks are something that is often managed during the procedure, and notably, generally do not have adverse long-term sequelae. And most of these, most serious, the serious adverse event rate for POM is less than 0.5%. So it's overall a very safe and well-tolerated procedure. If there is an issue at the time of the procedure itself, most often we are able to manage that endoscopically, either at the same time of the poem, or should there be a concern for an ongoing leak on the esophagram the next day, it also is something that oftentimes we can manage by bringing that patient back to endoscopy lab, and it doesn't necessarily mean they would have to move on to a surgical intervention or IR drains. And there's the study, so if you're in clinic and someone says, well, should I get a heller myotomy? Should I be getting a POM? What's the data? There was this study in the New England Journal of Medicine that compared POM and heller myotomy. It had a two-year follow-up, primary outcomes were based on the effort score, and it showed that the clinical success rate of both POM and heller myotomy are very similar. But notably, it did show that reflex esophagitis is more common in patients after POM than heller myotomy, which is why we need to counsel our patients that there is a chance that they could require lifelong PPI therapy. So POM versus heller myotomy, POM is minimally invasive. It is a rapid recovery. Most people are discharged less than 24 hours after they've come into the endoscopy lab. You can tailor the length of the myotomy. It's durable, and overall there are less complications. But as I mentioned earlier, we know that that risk of GERD is higher. So pulling it all together, we look at all of our treatment options. We know that both POM and heller myotomy are more effective than pneumatic dilation. We know that POM and heller myotomy neither are more effective than the other. Pneumatic dilation was significantly less likely to lead to adverse events. Heller myotomy was least likely to lead to GERD. Pneumatic dilation is least likely to lead to erosive esophagitis, and POM was least likely to lead to perforation, need for surgery, serious AEs, and need for re-intervention. So which of these candidates would be the best candidate for POM? Would it be a 45-year-old with type 2 achalasia and no prior surgical history, an 83-year-old patient with type 2 achalasia on lifeline plavix for a recent STEMI with BCI, a 65-year-old patient with type 1 achalasia and multiple prior episodes of Botox injection, or a 24-year-old patient who has intermittent reflux symptoms? And the answer is A. So as I mentioned earlier, we know that type 3 achalasia is best treated with a POM. And then one other thing for us to think about as APPs and to confer with our physician colleagues that might be performing these procedures is patients that have had multiple rounds of Botox may make that procedure more technically challenging. So that is something to consider as well. All right, moving on to gastroparesis. It's an NG POM. So gastroparesis is a chronic GI disorder characterized by delayed gastric emptying and absence of mechanical obstruction. The pathophysiology involves neuromuscular dysfunction of the stomach due to a variety of etiologies, including diabetes, post-surgical complications, as well as idiopathic causes. Presenting symptoms typically include postprandial fullness, nausea, vomiting, upper abdominal pain, early satiety, bloating, and some patients may tell you that these symptoms seem to get worse as the day progresses. Mainstay of diagnosis is a gastric emptying scan as well as EGD. Oftentimes on EGD, you'll see retained food in the stomach. EGD is also very useful in this diagnosis because it helps rule out any obstructive lesions that might be leading to delayed gastric emptying. And then much like the Eckert scar for akalasia, there's the gastroparesis cardinal symptom index, which is another clinical tool that can be used to assess the severity of gastroparesis based on the patient's ratings of symptoms and subcategories of nausea and vomiting, postprandial fullness, and early satiety and bloating. So, the opposite is true of gastroparesis from akalasia. Typically, we try medical management and dietary management before we'll try more aggressive interventions. So, dietary modifications include eating multiple small-volume meals, prokinetic agents, Reglan or metoclopramide is our first-line agent, but you may also try domperidone, erythromycin, anti-emetics, to help just control the symptom of nausea. And then there's the interventional, more aggressive therapies, including a feeding tube placement. Oftentimes, you would look at doing a PEG-J so they could use the G-port for venting, and then the J-port for nutrition, G-POM, pyloreumotomy, and then pyloric Botox as well. There are other surgical interventions that can be considered, such as certain gastrectomies, but those are, I think, a little bit less common for management of gastroparesis. So, when we're talking about patients for G-POM, good candidates, ideally, they have A1c of less than 10. They should have failed medication management, at least one, but possibly two. This is effective for patients with prior surgery, idiopathic causes, as well as diabetes. And then, as I mentioned earlier, we would like an EGD as part of the workup to exclude any mechanical obstructions. We want to be cautious in patients on chronic opiates, and this is a good general rule of thumb for any patient we're working with for gastroparesis. We want to avoid opiates as much as possible, patients unable to tolerate anesthesia, and similarly, patients with uncontrolled coagulopathies, and then patients that are on chronic blood thinners that cannot be held. Very similar pictures here regarding the processes for the G-POM as the POM. It's just that we're performing it in a different location and on a different muscle. So, it's further down into the stomach. We tunnel down and perform that myotomy on the pylorus. So, post-G-POM protocol, again, this is location-dependent, center-dependent, but likely patients will be looking at overnight stay in the hospital. They can also have abdominal pain and chest pain, usually worse within that first 24-hour period. Another strict NPO until the upper GI series is obtained the next day to rule out any type of leak. Similar liquid diet with slow advancement, prophylactic antibiotics for three days as well as a PPI for eight weeks to help that mucosotomy site heal. Typically, we'd like to repeat that GCSI score after the procedure at the three-month visit and then also repeat a gastric emptying scan one to three months after the G-POM. Risk profile for the G-POM ranges overall risk from 6.2 to 14%. Again, most of these are very mild and self-limited, including abdominal pain, bleeding, capnoparetinium, perforation, gastric ulceration, and there's a theoretical complication of dumping syndrome. I don't think I've ever seen that, though. It would be very low risk. When we look at the effects of a G-POM versus surgical pyloroplasty, there's this meta-analysis that evaluated 11 studies, and they defined clinical success both by looking at the GSCI as well as the gastric emptying studies. They found that they both are about equally as effective as the other with a similar adverse event profile, G-POM notably with a shorter hospital stay. G-POM is safe and effective management for medically refractory gastroparesis. G-POM versus surgical pyloroplasty are similarly efficacious with similar overall AE profile. G-POMs often offer a shorter length of hospital stay, and most adverse events associated with the G-POM are mild and self-limited. Generally speaking, patients are going to need to be accessed to a tertiary care center or at least a major city to get either G-POM or POM performed. They're both newer procedures that show promise in treating GI motility disorders. There needs to be ongoing research regarding long-term efficacy for both procedures. They are both safe and effective. Really, where our job as APPs come in, pre-procedure counseling, expectation setting is key, and then, of course, providing appropriate follow-up for these patients. With that, I will hand it back over to Dr. Call.

POM

GPOM

achalasia

gastroparesis

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