So, I have no disclosures. My objectives are, we'll discuss the esophageal symptoms and what are some of the common etiologies for esophageal symptoms, what are the tools we have to evaluate these symptoms, then we'll move over to GERD, how do we differentiate between GERD and EOE, how do we diagnose GERD, how do we treat it, and then moving on a little bit, talking about EOE again, and distinguishing EOE from really what are the other disorders that we sometimes see, Zenker's, achalasia, and scleroderma. Here are some common esophageal symptoms, as you'll hear frequently through this talk, GERD, commonly heartburn and acid regurgitation, then dysphagia, the feeling of the food really lodging in the chest, this can be anywhere from the external notch area, mid-chest, or even lower chest area, it's not really specific where the food gets stuck. Then adenophagia, this is pain caused by or made worse by swallowing. And then globus is a common finding or symptom we see in the clinic, the feeling of a lump or fullness or even a choking sensation in the throat. And then lastly, water brush, this is excessive salivation, this is a response to a reflux. When I see patients in the office, I like to think or divide the symptoms, especially if they have dysphagia, to think about is this a structural abnormality, is there a narrowing, is this a sensory abnormality, or is it really a motility issue, and that's how I really try to sort this out through history. So structural abnormalities, this is usually when patients have solid food dysphagia, can be liquids but mostly solids, as you can see, there's some common etiologies, AOE is certainly high on the list, stricture from reflux, less commonly infectious esophagitis, can also be esophagitis from pills, and some rare dermatologic disorders, or even extensive compression on the esophagus. Then moving over to the motility disorders, this is when you can start seeing patients with both liquid and solid dysphagia, it's where you incorporate these esophageal function tests, you can see anywhere from, you know, achalasia, to aparistalsis, to spasm in the esophagus, and GERD can cause some dysmotility as well. And then I always talk to my patients about, you know, if there's no structural abnormality or a motility issue, then it certainly can be their esophagus having an abnormal sensory component. This is usually with a negative EGD, or it can be with a nonspecific esophageal motility disorder. And there certainly can be some overlap between these motility disorders and GERD. Talking about how do we evaluate, what are the tools of the trade, commonly used—and you'll hear more detail about this with Dr. Olson's talk later on—is a barium esophagram. This can be modified with a video swallow study, usually done with speech pathology. This can also be done with occupational therapy. And then the timed barium esophagram—I'll talk a little bit more about this later, where the radiologist timed the flow of barium at 1 minute, 2 minutes, and 5 minutes. Then we have endoscopy. This can be done with or without a Bravo test—we'll talk more about this later—esophageal manometry, the pH impedance test, endoflip, and esophageal emptying test. So how do we distinguish GERD from EOE? You know, the typical symptoms of GERD is heartburn or the substernal burning and regurgitation or the feeling or the cessation of movement of stomach contents into the chest, while EOE, typical symptoms, certainly they can have some heartburn, but it's generally dysphagia with a history of food polls and infection. GERD can cause dysphagia, though, and EOE can cause GERD. The thinking is that these eosinophil products relaxes the lower esophageal sphincter and can alter the motility of the esophagus. That's why folks with EOE can have GERD. Just again here, typical symptoms, specificity for GERD is about 62 to 90 percent regurgitation is most often after meals or when patients are bending over, working in the garden or when they lay down at bedtime. When we think what causes GERD, you know, it's going to be really anything from decreased salivation that doesn't buffer the acid to patients with esophageal motility disorders that doesn't clear the esophagus, acid out of the esophagus, to relaxation of the lower esophageal sphincter, or in patients with, you know, large anatomic defects, a large hiatal hernia, all the way to delayed gastric emptying, so these are all things to think about what is the possible factors that's involved in GERD. We commonly see these extra esophageal symptoms. They can be at times difficult to work through. Most commonly, they come with ENT complaints, throat clearing, sore throat, hoarseness, cough and globus, but they can also have some chest pain and asthma, and we'll talk about how to work through this on the later slides. What do we see from complications for GERD? Most common, peptic stricture, and also see some Schatzky's rings, bleeding or anemia, and then Barrett's as a precursor for esophageal adenocarcinoma. Endoscopy can be normal in patients with GERD symptoms, but you can see inflammation of the esophagus, as you see to the right, this is called esophagitis. We'll talk about degrading in the coming slides. Symptoms can be dysphagia, chest pain, typical heartburn or adenophagia. Most common causes of esophagitis is reflux, commonly caused by significant reflux, mostly at night. Less commonly is infectious causes, and then we also can see some medications causing pale esophagitis. This is a picture of the Los Angeles classifications of reflux esophagitis, so when the endoscopist really look at the distal esophagus, and they can measure the breaks in the mucosa, and that's how they classify them in grade A, B, C, or D. Grade A is usually minor GERD. Grade C and D is the severe reflux esophagitis. In practice, Pearl here, to follow up patients with grade C and D esophagitis, to really make sure the esophagitis is healed, this is after you put them on a twice-daily high-dose PPI for at least eight weeks, to really rule out embarrassed esophagus. Generally, in my practice, if the esophagitis has healed, I will place them down onto a morning dose of PPI, usually indefinitely, as they will have recurrence of esophagitis if they come off. Now we're thinking about diagnostics. If you see a patient in your office with some GERD symptoms, you have a couple choices here, and this is what I really like to think about. If the patient comes with some symptoms and they are sometimes atypical or they didn't respond to the reflux medicine they've been taking, really say, well, does the patient have reflux? Best option for testing here is a 48-hour Bravo test. You can push this out to 96 hours. This has to be done off of medicine, ideally about seven to 10 days prior to the Bravo, and they can take H2 blockers up to two to three days before the Bravo. Second question, if you see a patient with symptoms that are not responding to PPI therapy or any other GERD-related therapy, you wonder sometimes if the symptoms are related to GERD. Then it's best to think about a 24-hour pH testing on therapy. This is an image of the Bravo pH system. It's usually the small green device on the picture here is placed endoscopically. It's clipped and suctioned into the esophagus about six centimeters proximal to the lower esophageal sphincter. They have this monitoring pack that they have to carry close to their chest, and they usually can be assigned a button for symptoms. The Bravo can be done 48 hours up to 96 hours. It's generally better tolerated, but it cannot measure non-acid reflux. Next is ambulatory pH impedance study. In my practice, we always do manometry beforehand to really get a good measurement in where the esophageal sphincter is so they can get accurate placement of the pH impedance catheter. In contrast to Bravo, pH impedance can measure acid and non-acid, but it can be uncomfortable. It really can alter a patient's diet. They can have a runny nose, and it can be artifact-prone. There are some folks that we see with erosive esophagitis with a normal pH impedance study. Again, they can be assigned a button for symptoms, so we will look for symptom correlation. For example, if they have chest pain, they can push the button, and we can see if this is acid or non-acid related. Again, mostly patients on PPI therapy. How do we manage GERD? Really going back to the basics, lifestyle modifications, aggressive weight loss attempt in folks that are overweight or obese, elevation of the head of bed, I say usually 4 to 6 inches. Oftentimes patients will say that they do elevate their head, but if you really ask them, it's only on pillows. Pillows are not enough. There are some long wedges available that goes down to the hips, but ideally if they can put their head on the bed on blocks, that works the best. It works the best for nocturnal symptoms. Then avoiding meals. In other studies, it showed 2 to 3 hours, and patients with severe GERD, you can ask them to avoid a meal up to 4 hours. Sometimes it can be very difficult as patients will be hungry when they go into bed. And then avoiding their trigger foods. If they eat a certain food and they get heartburn, then I generally ask them to avoid that certain food. I generally don't recommend patients remove all, quotation, acid type of foods, as studies does not recommend that. Moving on to management, PPIs are superior in symptom resolution as well as healing the esophagitis. Best taken half an hour to an hour before meals on an empty stomach. Okay for patients to drink coffee, but they really have to make sure they chew and swallow food to activate these PPIs. If they forget to take them, then it's okay to take, but they will lose some value of the PPI. In patients with non-erosive esophagitis, you can certainly consider on-demand therapy or even consider H2 blockers. Those with erosive esophagitis will usually require indefinite therapy, as they will have recurrence if you stop the therapy. And then thinking about surgery, Nissin front application is the gold standard. There are some other neuroendoscopic procedures around, including the LYNX and the TÜV procedure, but really surgery is reserved as a last resort for patients and those that have failed medical therapy. And surgery really works best in patients with typical symptoms, those that if you've given a PPI and they're like, I really feel better, it's treating my heartburn. Patients that had an abnormal pH testing, so you've proven they have reflux. And those with significant erosive esophagitis and you give them a medical therapy and they just really don't respond. Then again, we also have the cohort of patients with large tidal hernias, paraseptural hernias, and those who have aspiration from non-acid reflux. Surgery works, usually most patients are symptom-free at one year, about 60% will be back on medical therapy at about 10 years. I usually counsel my patients regarding surgery. Some can have dysphagia, that's usually early. Most will have inability to vomit. And there's a significant amount of patients that will have gas, bloat syndrome. So really counsel your patients regarding all the treatment options for GERD, what side effect profiles we have for surgery so they can make an informed decision. And going to atypical symptoms, these are, as previously discussed, the ENT symptoms. It's important to really rule in or rule out GERD here by either a BRAVO or a pH impedance study as these patients will have a poor response to reflux surgery. Then depending on where you are, refer them to the other specialties for evaluation and treat other causes. And then when I have a talk with my patients, we really weigh out the options, how to treat their GERD. Is an H2 blocker enough? If that's the case, if they don't have erosive esophagitis, I think that's a good option. Then moving on to PPI with potential potential side effects and then balancing that with a fundamentation. So just have a good discussion between all the treatment options for GERD. PPIs are certainly a controversial topic, but what do we do with long-term PPI? We really use those that control their symptoms and stop the PPI if that's not needed. Consider the use of H2 blockers. There's really no guidelines for laboratory testing. If patients are concerned, you can really consider creatinine yearly, B12, and magnesium every three to five years. These are not very common, but I have seen some low magnesium that's directly related to an increased dose in PPI in one of my patients. But again, no recommendations for testing. We'll move on to a question here. You have a 42-year-old man that presents for a consultation regarding GERD. He has heartburn symptoms two to three times a week, usually gets this after meals, and he has some regurgitation of acid on rare occasions. He is used for monitoring 20 milligrams once daily with partial improvement in his heartburn symptoms. His weight is up 20 pounds. He has no dysphagia or non-cardiac chest pain. His exam looks good. What is the most appropriate next step for a patient? Should we increase the thermodyname to 20 milligrams twice daily, initiate patient on an empiric PPI trial, perform endoscopy, or perform barium esophagram? Best option here, I think, is a PPI trial. If we look at the guidelines and we look at the question, patient has typical GERD symptom. He can make a diagnosis of GERD based on the typical symptoms, and an empiric trial of PPI is a good choice. Barium esophagram is not used to diagnose GERD. We will oftentimes see that the radiologist described a reflux during the barium esophagram, but this is not diagnostic for GERD. Over-endoscopy, in this case, not needed in the absence of alarm symptoms, and when we think about PPIs, they are superior when compared to H2 blockers in treating both symptoms and esophagitis. Second question here, you have a 55-year-old overweight male, 20-year history of GERD. He's in your office. He has breakthrough heart symptoms twice a week over the last six months. He has a dynaphagia with solid foods. You do an endoscopy on him, and it shows grade C esophagitis. There's no weight loss. He's taking Omeprazole 20 milligrams once daily in the morning. He's a smoker, and the exam is unremarkable. What is the most appropriate next step for this patient? Do we increase the Omeprazole to 40 milligrams twice daily and do not perform an endoscopy as long as his symptoms are under control? Do we increase the Omeprazole to 40 milligrams twice daily and repeat endoscopy in eight weeks? Do we perform a pH impedance test or a barium esophagram? This option here for me is to increase the Omeprazole to 40 milligrams twice daily and perform an endoscopy in eight to 12 weeks. Again, looking at the guideline, we are thinking about the risk factors for Barrett's esophagus here. Male, Caucasian, over 50, long-standing history of GERD, obesity, and smoking, those are all the risk factors for screening for Barrett's. Last question here, 51-year-old female is referred for hoarseness and cough. He saw his local ENT, and he was told that he has GERD based on laryngoscopy, and this is a frequent referral that I oftentimes see. He doesn't have any typical GERD symptoms. She's not on a PPI. What is the most appropriate next step? Refer to ENT for a repeat laryngoscopy. Start patient on a PPI trial and refer to endoscopy. Refer patient for antireflux surgery if she does not respond to PPI therapy, and refer for endoscopy with Bravo pH monitoring. This is atypical symptoms, extraesophageal symptoms, not responding to therapy usually, and no typical GERD symptoms. to do is an endoscopy with a Bravo to establish the diagnosis of GERD. Looking at the guideline again, at the bottom, reflux monitoring should be considered before a PPI trial in patients with extraesophageal symptoms who do not have typical GERD symptoms. Some clinical pearls for GERD, the pathophysiology as discussed here in that earlier slide is multifactorial. Be sure that patients are on the lowest dose of PPI to treat their symptoms. Remember to repeat endoscopy in 8 to 12 weeks in patients with grade C or higher esophagitis. Quantification works best in those with typical GERD and those who respond to medical therapy. Regarding side effects, the only two things I really counsel my patients on is careful combination of antibiotics and PPI to prevent C. difficile and caution international travelers on PPI to prevent gastroenteritis. Some complications, this again, and the treatment options really dictated by the symptoms, absence or presence of esophagitis. Then moving on to EOE, as you've heard earlier, it's a chronic immune antigen mediated disease. It really makes the esophagus narrow and sticky, usually seen in young adults, and the diagnosis require symptoms, endoscopy with biopsy showing greater than 15 eosinophils per hypert field, as well as a sophagram. When do we consider the diagnosis of EOE? Those in adults, the symptoms of dysphagia, food impaction, can also have some heartburn and chest pain, and important to really ask about eating behaviors, and more about this in the next slides, and atopic history, and ask about emergency room visits for food bowls and patients. And children have some symptoms listed there, and we'll hear more about this later from our pediatric colleagues. When you take a history in a patient that presents for dysphagia, it's important to ask questions about these adaptive behaviors, as oftentimes patients with EOE will really get used to their symptoms and adapt as they eat. So ask if you're a slow eater, are you the last one to finish at the table? This can be commonly seen. Do you avoid certain foods, stringy meats, breads? How much liquids do you drink with your meal? As you can sometimes find patients really taking a bite and then taking a sip of water to get their food down, do you prefer to focus on soft foods? Do we avoid going out to eat as if you're afraid for a food bowl's impaction? Endoscopic findings, as Dr. Novesky has earlier alluded to, to the right top, you can see some furrows, exudates, and edema. Endoscopy can be normal in some cases. On a esophagram, you can sometimes see a small caliber esophagus with rings. And then also stricture can be present. Diagnosing an EOE esophagram is helpful to distinguish between, is this an EOE stricture or a GERD-related stricture? It really helps us to see where is the location of the stricture. If it's a distal stricture, this can be likely a GERD stricture. An EOE can sometimes see a diffuse narrowing. It can also help to assess for changes that's not seen on EGD and can help with planning your dilation as the endoscopist can refer to the esophagram before planning dilation. In GERD, you can likely see a distal stricture or a Schatzky's ring, idle hernia, or parasophageal hernia. Here are some signs of EOE on an esophagram. To the left is a narrow caliber esophagus, and middle picture shows this ring or corrugated appearance sometimes called, and then the picture on the right is a tablet hanging up in the proximal esophagus. That's generally a 13-millimeter tablet that's used. We in doing endoscopy, signs for GERD can be esophagitis as earlier discussed. You can see some peptic strictures. Here's a nice image of a Schatzky's ring endoscopic and esophagram image. Why do we do esophagram in EOE? We know that EGD may be fairly unremarkable to detect to diffuse esophageal narrowing in EOE. This study has demonstrated that EGD failed to detect luminal narrowing to less than 13 millimeters in over 70% of cases in the EOE cohort. Esophagram has been shown to be useful tool in evaluating of EOE patients and is routinely employed in my practice in initial evaluation to rule out a significant esophageal narrowing, which may be contributing to dysphagia. This is not an EOE picture, but this is just an image to the left showing you a stricture comparing the endoscopy image to the right. Here's a quick slide about treatment. I will not go into detail about this. Again, PPI, topical steroid, food elimination diet, and the pill map. Best to start patient on only one treatment and assess response before moving on to a second treatment option. Comparing GERD versus EOE. So main symptoms in GERD are usually a heartburn and regurgitation, can also have dysphagia if they have a peptic stricture. Contrast EOE dysphagia with a history of food bowls infection. Age can be middle adult in GERD and children and young adult in EOE. Ethiology in GERD is usually reflux, and EOE is immune and antigen mediated. Endoscopic findings in GERD, some can be normal. You can see reflux, sepagitis, strictures, and even Barrett's. And EOE, there's evidence of edema, rings, exudates, strictures, and ferros. On esophagram, it can be normal, there can be evidence of a hiatal hernia, can see a distal esophageal stricture, and EOE, you can oftentimes see a diffuse stricture or some corrugated appearance of the esophagus. pH testing, usually positive in GERD, can be positive or negative in EOE. On histology, usually less than 7 eosinophils, and GERD EOE is greater than 15. Treatment for GERD, lifestyle modifications, antacids, H2 receptor antagonist, and PPIs. Treatment in EOE, as discussed earlier, PPI, steroids, food elimination diet, and diplomab. How do we distinguish EOE from other esophageal disorder? I think dysphagia history is very important. You should have an idea of what is the patient having when you take the history. Try to establish if this is a mechanical issue or a motility issue or both. Where does food get stuck? Upper esophagus or throat or lower distal thirds. Sorry. If it's a mechanical issue, this is usually solid food and pills. The size of the bite does matter. Can feel individual bites get stuck. Patients can usually wash it down with liquids. It happens episodic. A good question to ask if they can continue to eat their meal after the food passes. That's usually a mechanical issue or sometimes patients will regurgitate. It can happen when patients are not concentrating on chewing at a party or when they're standing up or in a hurry to eat. Usually happening at the first few bites of the meal. Patients are usually hungry and take bigger bites and don't chew as well. Contrast if it's a dysmotility issue. Ask about liquids and solid dysphagia. This could start with solids. The symptoms are usually consistent. They have more regurgitation. Sometimes contaminated beverages can make it better or sometimes will help. It's not often the first bite. It usually will happen later in the meal, mid or end meal. Patients cannot continue their meal after they regurgitate. They really give up eating more easily. Just thinking about some other causes of dysphagia. It's a esophageal Zinker's diverticulum. It's an out-pouching at the level of the cricopharyngeus. Generally seen in males more than females. Usually in the seventh or eighth decade of life. Symptoms can be aspiration, halitosis, regurgitation, fullness in the neck. Oftentimes patients can allude to pushing on their neck one side or the other to help with the dysphagia. They can have some gurgling in the throat. Moving on to some esophageal motility disorders. I'll go through a case study later this afternoon. Achalasia, nutcracker, esophageal spasm, and scleroderma. Achalasia is loss of these neurons and the main plexus of the esophagus. It really results in aparistosis of the esophagus and the lower esophageal sphincter does not relax. Generally develops slowly over years. Can affect really young to older adults. Think about an achalasia related to tumor if you see a patient with relatively rapid onset of symptoms and significant weight loss. It's generally solid and liquid dysphagia. They can have frequent regurgitation. Ask about nocturnal symptoms if they wake up with liquid or food on the pillow. Some patients will need to induce vomiting. Majority have difficulty belching likely related to the tight lower esophageal sphincter. Some can have some substantial chest pain and some can have hiccups possibly due to distention of the esophagus. Here's an image of an esophogram diagnosing achalasia. Common findings can be dilated esophagus, barium filled, and a bird's beak appearance of the lower esophageal sphincter. Moving on to scleroderma. Patients can have this crest variant where there's a esophageal dysfunction. On exam you can see some sclerodactyly telangtasias. They can have Raynaud's. A diagnosis can be done on ANA that's nonspecific or anti-syndrome antibody. Most patients will have aparistalsis in the esophagus as well as a relaxed lower esophageal sphincter. They can have significant heartburn. Unfortunately there's no specific treatment for motility disorder in patients with scleroderma or for achalasia in that matter. You can dilate them if they develop a peptic sphincter. Typically a response on twice daily PPI. I have some patients on PPI-TID. Consider treatment of gastroparesis if they have it. Fundamentation is contraindicated because high rates of dysphagia and the setting of dysmotile esophagus. And that's all I have. Thank you.

GERD

Eosinophilic Esophagitis

esophageal symptoms

dysphagia

endoscopy

proton pump inhibitors

achalasia