So, my first case is really—since this is an EOE course, it's an EOE case—it's been really well talked about throughout this course so far, so I'll go quite fast through the slides. Again, this is a 34-year-old Caucasian male who was in the emergency room for sudden onset ability to swallow water and even saliva while eating chicken. As resolved, he presents now to you in the office for evaluation. He has some heartburn, reflux twice a week, several years of occasional uncomfortable slow transfer of food, he has no weight loss, history for asthma, and childhood rhinitis. He does take over-the-counter histamine for his allergies, exam is normal, and then we move on to think about what are the causes for his dysphagia. Again, a little bit earlier, EOE is a high-end diagnosis, could also be a Schatzky's ring, peptic stricture, and less likely motility or the other differential diagnoses as listed. So, what do you think the next best step is in the care of this patient? CT chest, barium swallow, manometry, endoscopy, or a trial of a PPI for eight weeks. And I think in this case, you know, getting a diagnosis with endoscopy has been my first choice. Here, again, it's endoscopic findings that the histopathology showed about 60 eosinophils per hypoart field. What would you do next? Refer to allergy for skin testing, initiate a long-term elimination of eggs, fish, soy, nuts, corn, and legumes, perform a 24-hour pH impedance study, start him on a PPI trial, or a salvageal manometry. I think first choice for me would be a PPI trial. Patients come back after eight weeks, you question them whether he's taking his PPI, he's taking it twice daily at the appropriate time. He still has some dysphagia, but no heartburn. He performed another endoscopy, this time showing about 40 eosinophils per hypoart field. What would be the next best step? Start him on a topical steroid for two months and perform endoscopy. Again, avoidance of eggs, fish, soy, nuts, corn, and legumes, a pH impedance study, continue your mepresol twice daily, and perform an endosalvageal manometry. I think best choice would be at this time since he has dysphagia and still eosinophilic infiltrate would be a course of topical steroids. And then the point I want to bring over, this is a patient that is in remission after topical steroids, but still has dysphagia. In my practice, anyway, the role of esophagram, you can see here on the right is the tablet sticking at the endodystal esophagus. This dilation slide was very well discussed earlier, so I won't cover this again. A true or false dilation in EOA treats the underlying inflammation and should be used as a sole treatment. This is false. Reviewing the dilation slides again, can have up to a 92% symptomatic improvement. There's some thought that is really best reserved until you see effects after medical therapy. It really depends on how severe the patient's dysphagia is and if they have a narrow caliber esophagus. Dilation rate is low in the hands of a trained, well-trained endoscopist. Really counsel your patients regarding pain management after dilation as some patients will have, can have significant dysphagia symptoms, or sorry, pain symptoms after dilation. The goal for dilation is about 16 millimeters. Start low and go slow. Does not address the underlying disease. We'll skip over this. This, you know, you need symptoms, biopsy of 15 eosinophils or hyperfield or greater. Just showing some of the demographics and clinical features has been well discussed throughout the day today. Again, the endoscopic findings of stricture, rings, spheros, exudates, some can be normal, and then esophagram findings of a narrow caliber esophagus in some patients. Here's a slide about the overview of the treatment options again. And I want to take some time and pause at this algorithm we've put up here. This is a paper we wrote with Dr. Narneski last year and published, and it's really a good guide to keep if you're new to EOE is really to kind of follow this stepwise approach in treating EOE. As you can start in the top, you know, good history. Suspect in males more than females with solid food dysphagia, then you establish your diagnosis with endoscopy and biopsies. Then you really decide about the treatment that you want to pursue in this patient. High-dose PPI, eight weeks, assess the response to treatment by endoscopy, and then you can go down the pathway of the responder to the left and non-responder to the right and consider alternative treatment. So, it was really a good guide to keep on hand for a stepwise approach in treating EOE. But really, ultimately, treatment depends on the efficacy of the medication. What does patients really—what do they prefer? How severe are the disease? I tend to, in my practice, go to a topical steroid if they have significant narrowed and severe disease. What is the insurance coverage, and what are the resources for diet? Ultimately, it's a shared decision-making process between the provider and the patient. Moving on to case two, this is a 50-year-old female who presents with dysphagia that's progressive over the last four years. She reports a sense of pressure in her chest after solids and liquids, and over the last several months, regurgitates unadjusted solid food consumed several hours earlier. She denies any weight loss. She has no prior medical illness and has been prescribed Omeprazole, 40 milligrams twice daily to treat her symptoms. Physical exam is normal. So, if we look here, both solid and liquid dysphagia. What are the differential diagnoses here? If we think about liquid and solid dysphagia, malignancy is certainly always on the differential. Can be a peptic stricture, less likely with liquid dysphagia. EOE is in the differential, Schatzky's ring is too, but less likely again with liquid dysphagia. Infectious esophagitis, medication-induced, and likely a motility disorder given liquid and solid dysphagia. What is the next best choice? Barium esophagram, wireless pH study of PPI therapy, upper endoscopy, or change her PPI from Omeprazole to esomeprazole for eight weeks. I think my choice would be barium esophagram, upper endoscopy is certainly another option too. You perform an esophagram, the radiologist gives you some measurements at one and two minutes. They say a standing column of barium about 21.3 centimeters, and at five minutes it only decreased to about 17 centimeters. Given these findings, you pursue an endoscopy. You then receive a call from the endoscopist with the endoscopy showing a dilated esophagus that has retained secretions. What is the next most appropriate step? Perform esophageal biopsies, perform esophageal dilation, send patient for a high-resolution esophageal manometry, or a CT scan of the chest. And I think the next best choice is to perform an esophageal manometry. Here's the manometry results that you get after that was completed. The lower esophageal sphincter shows abnormal relaxation reflected by an IRP, or integrated relaxation pressure of 19.1 millimeters of mercury, total of 10 swallows were evaluated of which 100% were failed, and showing some pan-esophageal pressurizations. Total impression was achalasia type 2 per the Chicago 4 classification. So achalasia is the loss of these neurons in the myoenteric plexus of the esophagus. It really results in an aperistaltic esophagus and the failure of the lower esophageal sphincter to relax. Generally develops slowly over years, can affect really young to older adults. Think about achalasia related to tumor and those patients with rapid onset of symptoms, weight loss, especially with advanced age. Tumor they present generally solid and liquid dysphagia. They can have regurgitation of retained material. Really any time after they eat or when they lay recumbent, ask about symptoms at night. Are they finding liquid or food on the pillow? Some have to induce vomiting, a majority have difficulty to belt, likely related to a tight lower esophageal sphincter. Some can have substernal chest pain, and oftentimes you can have patients with hiccups, likely related to a distended esophagus. Here's an image of a normal esophageal manometry, the top bar, the red, and you can see there's a break where it's blue, that's the relaxation of the upper esophageal sphincter. Then you can see a nice even swallow going through to the right, and then the bottom line is a break where the blue and the green separates, that's where the lower esophageal sphincter relaxes. Here are the subtypes of achalasia, on the top is type 1 achalasia, this is also called classic achalasia. There's aperesthalosis and the failure of the lower esophageal sphincter to relax. Type 2 is similar to type 1, but you can see some panesophageal pressurization. And then type 3 is more of a spastic achalasia, you can see that high-pressure zone and the distal esophagus with failure of the sphincter to relax. Esophagum, what you can commonly see is typically called bird speaking of the esophagus, barium filling the esophagus, as well as a dilated esophagus. Upper endoscopy can be normal, oftentimes some endoscopists will describe a popping sensation as they traverse the lower esophageal sphincter. You can see it retains secretions, food, dilated esophageal lumen, again important to have a good retroflex view of endoscopy to rule out a mass at the G-junction. And think about peroneoplastic phenomenon in those with lung cancer, as these can present as a pseudo-achalasia. Moving on to some treatments of achalasia, botulinum toxin injection is an option. This is usually reserved in my practice to patients that are not candidates for more definitive therapy, those with more comorbidities. About 100 units of Botox was injected in four quadrants at the lower esophageal sphincter. And this can certainly be repeated, but the effects become less with repeated Botox injections. Next is pneumatic dilation. The balloons generally start at 30 millimeters, can be 35 or 40 millimeter balloons. This can be a primary treatment for achalasia, but I generally reserve this as a rescue option in patients that had a heller myotomy or a POAM. Next is laparoscopic myotomy with partial funnel application. This is done laparoscopically through about four to five incisions in the abdomen. The esophagus—the myotomy is done onto the esophagus, and then a partial funnel application is performed to help with reflux. Then peroral endoscopic myotomy or POAM, the submucosal tunnel is made in the esophagus, and then a myotomy is performed and extended about two to three centimeters onto the gastric cardia. This slide looks at the treatment efficacy and achalasia subtypes. For type 3, POAM is preferred as you can ask the procedure list to make a longer myotomy, but type 1 and type 2 laparoscopic myotomy and POAM is equally effective. Here's an image of an esophageal pre-POAM and then post-POAM day one. You can see there's good emptying and there's some faint lines there with the—showing the clips in the esophagus that close the myotomy incision. And to counsel patients regarding follow-up, I generally ask patients to return about three months after either a helical myotomy or a POAM. We get an ECHR score. We talk about reflux symptoms. We get a time-varying esophagram endoscopy with endoflip and do a Bravo to evaluate for reflux. And then yearly, really up to clinical judgment, consider time-varying esophagram with endoscopy. You can alternate these every other year or even extend follow-up if a patient's based on their clinical response. Moving on to case 3, this is a 42-year-old female who has several-month history of heartburn and acid regurgitation. Heartburn is described as substernal burning happening about three to four times a week, typically after meals and when supine. In addition, she complains of nocturnal acid regurgitation occurring about twice weekly. She has no dysphagia or weight loss. She has been treated with over-the-counter twice-daily PPI without improvement in her symptoms. A barium esophagram is performed and an episode of reflux is noticed to the thoracic inlet. To a female with some typical symptoms, no response to PPI, what is the most appropriate next step? Refer for surgical funnification, perform an esophageal manometry, increase PPI to two times daily high dose, perform a 48-hour Bravo study off of medication, or initiate low-dose tricyclic antidepressant. Given typical symptoms without response to PPI, it's best to get objective evidence of reflux with a 48-hour Bravo. It certainly can be done with a pH impedance study on therapy, off the therapy, but Bravo is my preferred choice. This is coming out of the guideline. In patients for whom the diagnosis of GERD is suspected but not clear and endoscopy shows no objective evidence of GERD, we recommend reflux monitoring be performed off therapy to establish the diagnosis. HG is a normal 48-hour Bravo study off of PPI shows a positive study. This abnormal esophageal acid exposure in the upright and supine positions on day one and two and the symptom correlation for heartburn was good. No reflux, esophagitis, positive pH study off of PPI, what would you do next? Refer for surgical funnification, perform an esophageal manometry, start high-dose twice daily PPI, initiate low-dose tricyclic antidepressant. I think a good choice would be really to bump up and give them a good course of high-dose twice daily PPI since she was only on over-the-counter dose. Patients return several weeks later with only mild improvement and her GERD symptoms, what would you do next? Patients return several weeks later with only mild improvement and her GERD symptoms, what would you do next? Refer for surgical funnification, esophageal manometry with pH impedance study on PPI, consider alternative PPI or initiate the low-dose tricyclic antidepressant. You certainly can consider alternative PPI, but I think from my standpoint really seeing what's going on if there's symptom correlation and if she has non-acid or acid reflux with the pH impedance study on therapy. Looking at the guideline again, we recommend esophageal impedance pH monitoring be performed on PPIs for patients with established diagnosis of GERD whose symptoms have not responded adequately to twice daily PPI therapy. This is a slide that I found interesting if we think about, you know, which PPI to start first. They have taken the omeprazole equivalent, so if you can see here 20 milligrams of pantoprazole is only equivalent to about 4.5 milligrams of omeprazole. Lansoprazole 15 milligram is very close to the omeprazole equivalent. Esomeprazole 20 milligrams, it's about 32 milligrams of omeprazole and robeprazole 20 milligrams is equivalent to about 36 milligrams of omeprazole. Just a helpful slide to have. I generally will start with omeprazole then move on to an axiom then robeprazole or even dexalant if that's covered, but that's just my personal preference. So, what do we do with refractory GERD? You know, ask about document compliance. Are they taking the PPI at the right time before meals? Are they eating something? Are they doing lifestyle modifications? You can consider H2 blockers for bedtime or evening symptoms. Consider switching to a CYP-independent PPI. Consider PCAPs and really ask about the lifestyle modifications. Evaluate patients for hiatal hernia or hypertensive lower esophageal sphincter and delayed gastric emptying and then for those folks that you can't heal their esophagitis or they have persistent acid or non-acid reflux, especially those with aspiration, you can send for a consideration of anti-reflux surgery. Here's an algorithmic approach to evaluation of GERD. I will just leave this for you as a resource. It kind of guides you through the process to consider as you work out patients for GERD. Amateur pH study off of PPI, if that's normal, then the likelihood of GERD is low. Consider functional heartburn or hypersensitivity, wherever it's a positive pH study, likelihood of GERD is high, and it'll give you some options to work through as we discussed in the previous slides. Moving on to case four. This is a 74-year-old female who has presented with acute onset of dynaphagia and dysphagia. A history of hyperlipidemia, hypertension, and hyperkalemia. She takes rosuvastatin, metoprolol, a multivitamin, and a potassium pill. You do an esophagram and you find this not quite distal, but this quite tight esophageal stricture. So, we think about, you know, that differential is what we could consider here. You do an endoscopy and it shows this discrete alterations with normal surrounding mucosa. Thinking about dynaphagia, common to be a pill esophagitis, but can also be HSV or Crohn's disease. And immunocompromised patients consider CMV, HIV, and those who are taking checkpoint inhibitors. This is a case of pill esophagitis. This patient actually was hospitalized for hyperkalemia, was given her potassium supplement, and barely sat up straight on the bed to take it, and that got stuck causing that tight stricture on the esophagram. These are the most common offenders when we think about prescriptions that can cause pill esophagitis. Really, any prescription can cause it, but you can see it commonly in tetracycline, especially used in treatment—treatments for—sorry, for adolescents taking treatments for acne, NSAIDs, potassium, alendronate, but even vitamin C. So, what are the risk factors? Really taking their pills with inadequate liquids, taking a handful of pills at a time, laying down shortly after taking their pills if patients are dehydrated and taking pills shortly before bed, and these are all things to counsel your patients on. How do we manage these? Most heal spontaneously. Obviously, stop the offending medication or switch it to a liquid formulation. You can dilate these strictures. You can set a carafate and do not take pills less than 30 minutes before lying down. This is my final case. This is a 56-year-old Caucasian male as referred for difficulty swallowing. He has a two-month history of food hanging up in his mid-chest region. His symptoms have gotten worse, and he has now to really chew his food well before swallowing, but swallows liquids without any difficulty. He has about 15-pound weight loss. He has hypertension. Take lisinopril and over the counter omeprazole for heartburn, history of smoking, physical exam shows an increased or elevated BMI, and what do you think about differentials here? Obviously, malignancy is high in a differential. It certainly can be a peptic stricture, eosinophilic esophagitis, Schatzky's ring. What will we do next in the care of this patient? Do a CT of the chest, barium swallow, high-resolution manometry, endoscopy, or a trial of PPI. If we're thinking about the red flag symptoms, weight loss, dysphagia, endoscopy would be the next best choice. Endoscopy shows his mass and showing adenocarcinoma. Looking at esophageal cancer, the two common types is squamous cell cancer. This is usually found in the middle and upper third of the esophagus. There's a strong association between tobacco and alcohol. And then second is adenocarcinoma. This is usually distal esophagus. This association between untreated reflux and perits, progressing from low to high grade dysplasia and eventually cancer. Risk factors is tobacco, obesity, non-Hispanic, white race, male, age over 50, and a family history when we think about adenocarcinoma, while squamous cell carcinoma risk factors are tobacco, alcohol, among others. This slide is just showing the progression from perits to adenocarcinoma. See the normal lining of this squamous cells of the esophagus, then turning into these goblet cells or perits esophagus with low grade dysplasia, high grade, and can go into invasive cancer. Symptoms early can be really no symptoms. Later symptoms are dysphagia and weight loss, less commonly bleeding from an ulcerative mass, chest pain, cough, aspiration, and hoarseness. How do we stage esophageal cancer? I usually will counsel patients about obviously a diagnostic endoscopy, then a CT of the chest, abdomen, and pelvis, a PET CT, and endoscopic ultrasound. And treatment is really dependent on the stage of the cancer. This is a slide I like to show my patients between the different T-stagings of the esophageal cancer. If it's early T1, consider referral to an endoscopy for consideration of endoscopic resection. But if it's T1B and beyond, generally we'll need referral to surgery plus, minus chemotherapy and radiation consults. What's the role of the endoscopy in adenocarcinoma? Obviously we get a tissue diagnosis. We evaluate the extent of the tumor. How far does it come up? What's the exact location on the retroflex view? And as earlier discussed, it may play a role in resecting early cancer and can be used for stenting or placement of feeding tubes for palliation. A CT scan, given intravenous contrast, it can detect the local extent of the tumor as well as lymph nodes. Look for liver metastasis. It helps us with the M-staging. Then PET scan, tumors have high metabolic activity and also helpful in detection of M-stage. What's the algorithm for a workup of esophageal adenocarcinoma? Endoscopic ultrasound, CT chest, abdomen, pelvis, generally meet back with the patient. If T1A, consider endoscopic therapy, T1B, endoscopic therapy, then meet with the surgeon for consideration of esophagectomy. If it's T2, T3, then generally endoscopic therapy is not an option. You would refer them for a surgical consult, medical and radiation oncology. Folks with T4 disease generally will be referred to medical oncology as well as radiation oncology. Again, dysphagia, history is important. Ask about solid, liquid, or both. Where does the food get stuck? Is it in the sternal notch, lower chest? Is it progressive, non-progressive? Do they have weight loss? Ask about heartburn. Sometimes ask about medications they take, if they have any atopy or other systemic diseases. Just again, the tools of the trade for evaluating dysphagia, bariomassalagram modified with speech, timed bariomasswallow, endoscopy, manometry, and endoflip, as we discussed earlier.

eosinophilic esophagitis

dysphagia

endoscopy

proton pump inhibitors

achalasia

esophageal adenocarcinoma

shared decision-making