Thank you so much, Caitlin, and a proper topic to talk about after lunch. I have no disclosures. So, the objectives are we're going to describe gastroesophageal reflux, what are the etiology of reflux, and how do we manage it? And then we'll touch, basically, on Barrett's esophagus and then the different treatment options we have for Barrett's with dysplasia. So, during the talk about GERD, we will cover what it is, you know, what are the complications we see with GERD, when do we test, and what are the testing options we have available, and lastly, how do we manage it? So, if we look at the studies, up to about 20% of patients have weekly heartburn. We can see a troublesome heartburn in about 6% of the population. GERD can really have impacts on quality of life, as evidenced by lower scores on the sleep scale and decreased work production. It tends to be equal in gender. We do see more esophagitis in males, those who are over 40, and smokers. Typical symptoms of heartburn and regurgitation, where heartburn is described as can be epigastric burning, but substantial burning mostly, usually moving up into the chest while regurgitation, and the other hand is stomach contents coming up into the chest, oftentimes in the mouth. This usually happens after meals, but can be when bending over or laying down for a meal. As you can see, the specificity of GERD is from 60 to 90%. We cannot always rely on symptoms alone to make a diagnosis of GERD. Common referral to my clinic, at least, is these atypical or extra-substantial symptoms. They can include anywhere from chest pain, asthma, and several ENT complaints, as listed below. GERD can be seen in asthmatics and can make asthma worse in anywhere up to 80 or 90% of patients. What causes GERD? GERD, it's really a complex disorder that's associated with several pathophysiological changes, leading to the breakdown of these esophageal defense mechanisms. It can be anywhere from decreased salivation that fails to buffer the acid in those patients with esophageal motility disorders, altered anatomy in patients with a hiatal hernia, all the way down to delayed gastric emptying. Those are all things to think about, and why do these patients have these symptoms? The contact of this gastric reflux to the esophageal epithelium can cause numerous complications. Most commonly, we see peptic stricture and Schatzky's ring, but others, as listed there, can be seen as well. So, when do we consider endoscopy in patients who have reflux? I would say, if they present with typical GERD symptoms, it's reasonable to start them on an empiric PPI trial. On the other hand, I would do endoscopy in atypical symptoms, especially those with longstanding history of symptoms, those over 50, and especially if they have alarm symptoms. This was covered yesterday, just a brief overview of the LA classifications of reflux esophagitis. Grade A is really minor reflux esophagitis. Some endoscopists will call this, and others would not, while grade D is the most severe esophagitis. Symptoms can be anywhere from dysphagia, chest pain, heartburn, or dynaphagia. The most common cause of esophagitis is obviously reflux, but I would like you to think about pill esophagitis, as well as certain infections that can cause esophagitis. What do we do with patients with esophagitis? It really depends on the grade of the esophagitis. My practice, I usually will start them on high-dose PPI twice daily for two months, and then decrease it to once daily if the reflux esophagitis is healed, and that's for grade B. With grade C and D, they really require an endoscopy, and that's really to rule out Barrett's, as they can have a Barrett esophagus underlying the grade C or D esophagitis. It's a Lyon consensus for GERD. You can diagnose GERD, and those with grade C or D esophagitis, if they have evidence of long-segment Barrett's, and those with distal esophageal acid exposure, that's greater than 6% when you do a pH monitor. So, when do we test for GERD? Testing for GERD can be done in atypical symptoms and those who do not respond to PPI therapy, and we will go over this in the next slide. So, here are the two different options for diagnosing GERD. Firstly, I would say if you see a patient in the clinic, and your question is whether they really have GERD, perhaps they referred for a cough or they have some mild typical symptoms, I would say the best test to consider is an endoscopy with a Bravo test. It could also do 24 pH impedance, but the preferred test would be a Bravo, ideally done 7 to 10 days off of PPI therapy. On the other hand, if you see a patient in the clinic that's on medical therapy, for GERD, and you wonder whether the ongoing symptoms are related to reflux, then a pH impedance study would be the best test. Here's an image of the Bravo capsule. You do require endoscopy. It's attached about 6 centimeters up from the gastroesophageal junction and suctioned and clipped into the superficial esophageal mucosa. It can be done for 48 hours up to 96 hours. It does increase the yield a bit if you go to 96. Patients are assigned a button they can push for mealtime, for when they have symptoms, and when they take their medication. It does provide us with a symptom correlation, which is quite helpful. On the other hand, there's a pH impedance study. It has a pH monitor in the stomach at about 5 centimeters proximal to the lower esophageal sphincter. This is generally done on PPI. And for about 24 hours, it can be uncomfortable. It alters their diet and sleep pattern. Here's just a summary of the Bravo and the pH impedance options. How do we manage GERD? Firstly, we'll start with lifestyle modifications. Recommend weight loss in those who are overweight, elevation of head of bed, 4 to 6 inches at least. Just sleeping on two pillows is not enough. They really need to elevate their whole upper body down from the hips up. There's a council on smoking sensation and limiting alcohol. In regards to diet, I generally ask patients to avoid their trigger foods. Otherwise, eat a balanced diet in moderation. PPI's are superior in healing esophagitis. Up to 90% has completed the treatment. PPI's are superior in healing esophagitis. Up to 90% has completed the treatment. And they also work better in treating symptoms. 75% in PPI and only about 50% in H2 blockers. It's important to counsel patients to take it about 30 to 60 minutes before their meals. And that's for most PPI's. In patients with non-erosive esophagitis, you can consider on-demand therapy. While those with erosive esophagitis will usually require indefinite therapy as they will recur when you stop it. Moving on to surgery, I usually counsel my patients that surgery is really reserved as the last option if everything else fails. Laparoscopic adenosine funnel application is the gold standard for treating GERD surgically. There are some other options including magnetic sphincter augmentation, or LINCS, and transoral incisionless funnel application, or TIF. Consider a referral to surgery in those with significant erosive esophagitis despite maximal medical therapy, and those with non-acid reflux in the setting of a large hiatal hernia, especially with aspiration, or a paraseptural hernia with obstructive symptoms. Make sure you assess their esophageal motility by manometry before referral to surgery as this will determine if they need a partial or a full wrap. Surgery does work best on those patients that have a response to PPI, those with typical symptoms, and those with abnormal pH testing. And we'll talk about the Barrett's later, but there's studies that show that anti-reflux surgery does not prevent progression of Barrett's to cancer, and those who are reluctant to take PPIs. When considering surgery for GERD, it's really important to counsel patients on the potential side effects. Most do well in about a year, but about 60% of patients require medical therapy at 10 years. Dysphagia can be a common symptom, but that's mostly seen early after anti-reflux surgery. Most patients will have the ability to vomit, and several patients will have gas, bloat syndrome. Another big topic that I see in my clinic is how do we manage these atypical symptoms. Oftentimes, I get a referral for a cough, and the question is, is GERD contributing or the cause? These patients really will need some sort of objective testing to either rule in or rule out GERD. Otherwise, a referral to ENT, pulmonary ENT, or allergy can be done. So what should we do with long-term PPI? Really use the lowest dose that's required to treat their symptoms. If you start them on twice-a-day therapy, consider decreasing to once-a-day therapy, and even low-dose once-a-day therapy, as long as it's controlled their symptoms. And stop it when it's not needed. You can consider H2 blocker therapy. We don't really have societal recommendations for laboratory testing. If you have a patient that's quite worried about the potential side effects of PPI, you can consider a yearly creatinine level, a B12, a magnesium every three years, and a CBC every two years. In my practice, I've seen one patient with a decreased or low magnesium, but this is very rare. We'll move on to a case. This is a 51-year-old female referred to mutual hoarseness and cough. She was told by her local ENT that she had GERD based on her laryngoscopy. She doesn't have any typical GERD symptoms. She's not on a PPI. What is the most appropriate next step? Refer a patient to ENT for a repeat laryngoscopy. Start them on a PPI trial or refer to endoscopy. Refer a patient for antireflux surgery if she does not respond to PPI and refer for endoscopy with BRAVA pH monitoring. So I think the best answer here is to really get objective evidence as we talked about earlier. Atypical symptoms really rule in or rule out GERD here. If you look at the guideline for gastrointestinal reflux disease, there's a good statement there on that we cannot make a diagnosis of GERD just based on laryngoscopy. PPI trials are recommended to treat extra esophageal symptoms in patients with typical GERD. Upper endoscopy is not used as a means to establish GERD-related chronic cough or laryngitis. And surgery, as alluded to earlier, is not recommended on those who do not respond to PPI therapy specifically for these extra esophageal symptoms. So clinical pearls for GERD. Remember to do endoscopy for red flag symptoms. PPI works best as compared to H-blocker therapy. I generally use H2 blocker for patients with nocturnal symptoms. Be sure to use the lowest dose PPI that's needed to control their symptoms. Remember to repeat endoscopy in 8 to 12 weeks in patients with grade C or D esophagitis. And that's just to rule out their esophagus. One application works best in typical GERD and those who have a response to PPI therapy. We only pursue surgery if medical and lifestyle therapy fails. And for risk factors for these PPI, careful combination of antibiotics and PPI prevents C. diff and caution international travelers on PPI to prevent gastroenteritis. And really have a good discussion regarding all the options for treatment of GERD with your patient. Lifestyle versus H2 blocker versus PPI. Moving on to Barrett's esophagus. Here's a definition. So it's really the extension of this salmon colored or stomach colored tissue into the esophagus. And the biopsies have to confirm intestinal pleasure. So important point to make here is you really need both to make a diagnosis of Barrett's. Here's the picture on the left showing the extension of the stomach tissue into the esophagus. And with this intestinal pleasure on the right side. Oftentimes, we see referrals for Barrett's esophagus. And I look at the outside endoscopy report and I see a notation made of the biopsy of the irregular Z line. Again, the Barrett's is a little bit larger than the biopsy of the irregular Z line. Again, the Barrett's tissue should be a centimeter or greater in the esophagus before it should be biopsied. There is a study that was done on intestinal pleasure of the G junction that can be seen in about 20% of the population. And the risk of developing high grade or cancer is low in the studies they done. None of the patients progressed to high grade or cancer. This slide just shows the progression. You see normal G junction with Z line, the Barrett's esophagus and lower high grade and cancer. Here are some older studies looking at the progression of Barrett's to esophageal adenocarcinoma. So no dysplasia, the risks about 0.1 to 0.3. And to put this in other terms, if you take 100 patients and you follow them for 10 years, about 3 will get cancer. So a very low risk. So when we evaluate patients in the clinic, consider risk factors for Barrett's esophagus. Those include caucasian male, over 50, history of GERD, central obesity and smoking. As mentioned earlier in my esophagitis slides, it's important to screen for Barrett's after treatment of esophagitis as up to about 15% of patients with erosive esophagitis can have Barrett's found on subsequent endoscopy. Here are some current guidelines on Barrett's that you can review. I tend to follow the ACG because that's what my practice do here. These are generally guidelines. When there is multiple guidelines, that's a suggestion there's not enough evidence to manage the disease. So understand that it underscores that clinical medicine is really important not to rely on protocols. When making decisions regarding treatment of Barrett's with dysplasia, it's important to counsel patients regarding the benefits and risks before making a decision regarding endoscopic therapy. Understanding the degree of dysplasia makes a difference. Here, as when they have high grade dysplasia, we tend to push more for endoscopic therapy as compared to when they have low grade dysplasia. Take-home point is just to have a good discussion and understanding from the patient that they know what they are signing up for. It's a basic algorithm for Barrett's and I will touch more on this on my later slides. Moving on to endoscopic therapies, we have options for a radiofrequency ablation, cryoablation, and then endoscopic mucosal resection and submucosal dissection. So treatment options, endoscopic therapies, ablation, the whole goal is to get rid of the Barrett's with metaplasia or with dysplasia and to reduce the risk of esophageal adenocarcinoma. Endoscopic resection can help us classify the T staging and can also tell you degree of differentiation if there's lymphovascular invasion present and it can be curative. So RFA is basically a heating of the Barrett's tissue to a point of evaporation coagulation. The neosquamous cells will grow over that area. Average treatment really depends on the length of the Barrett's segment. In my practice, we do it about every three months until all the Barrett's is ablated. Here's an image of a 90 degree RFA catheter to the left is the Barrett's tissue and to the right after it's ablated. Here's an image of the balloon pre-treatment to the left and after treatment to the right. Complications, the most common complication I see are the highest risk of complication as a risk but there's also, sorry, strict information about perforation and bleeding can also be seen. Patients are given clear diet instructions what to follow for after ablation. Cryotherapy is used in Barrett's generally in my clinic and those folks that are resistant to RFA but can be used in some with a palliation and bulky tumors or those who are proximal disease can be delivered via the spray as well as the balloon device. I was wondering if we can play this video for me and start it. Here we go. Do I have control over it? Can you skip to 40 please? So here's just the imaging of the inside the balloon with a cryo catheter and the therapy applied coming up. And the catheter is just turned and the rest of the Barrett segment is done. Can we skip to two minutes please? Here's an image of post-treatment. Moving on to EMR, this is generally reserved for lesions that are less than two centimeters. Again, it would give us the status of the deep margin if there's any lymphobascular invasion or if there's a deeper invasion into the esophagus wall. Similar to the RFA, there is some risk of strict deformation, bleeding, and perforation. Images of the EMR to the top left is where the lesion is marked. Moving on to the right, it's injected and sucked up into the cap that's on the scope, banded, and then resected. And you can see the right bottom is the area after it's been resected. ESD, we tend to focus on ESD with lesions that are greater than two centimeters where the whole lesion can be removed in one piece. There is a greater risk of strict deformation, but it really depends on the size of the resection. These can be treated with dilation and steroid injection. Some of these patients are observed overnight in the hospital, but we are moving them as an outpatient procedure. The lesion is injected to the top left, the esophagus and incision is made, and to the right is the area that's resected. A summary slide for Barrett's. If there's no dysplasia, we recommend that you follow up with biopsies every three to five years. The new updated guideline in 2022, as you see I've referenced below, if the Barrett segment is less than three centimeters, you can do endoscopy in five years. If it's greater than three centimeters, it's three years. It's really difficult to convince patients to go to five years. We'll see how the future holds with this recombination. Indefinite for dysplasia, I treat these patients with high dose PPI, repeat their endoscopy in three to six months, and then this generally will go back to a nondysplastic biopsy results. If they continue to be indefinite for dysplasia, especially if they're multifocal, then you would consider referring for ablation, or you treat them like, you surveil them like low grade dysplasia on the right. And that's all I have. Thank you.

GERD

Barrett's esophagus

heartburn

diagnosis

treatment

esophageal adenocarcinoma