Esophageal Disorders: Manometry, Belch, Rumination, Dysphagia, EoE | UCLA Digestive Diseases

this is the posse these are the guys who are going to be talking to you the first couple hours and our approach is going to be a little bit different and these guys are are members of the motility group the esophageal diseases group the functional bowel group they're all important cogs in our wheel so their names are up here we will talk about them as as they come up in the talk okay this is whenever i do this i always start out explaining what esophageal manometry is and how to think of it this catheter that you're looking at is in a high resolution esophageal manometry catheter the gold sort of bands here are impedance electrodes they're used to uh determine the the direction of flow in the esophagus the copper color those are pressure sensors they're 36 pressure sensors they're they're a centimeter apart this is the output this is a normal peristaltic sequence it looks daunting to most people but i want i want folks to think about this as in this way if if you're looking at this uh along the x axis is time along the y axis is position and up and down is amplitude so this is a composite of all 36 pressure sensors positioned one behind the next with the first one in the stomach the last one in the upper esophageal sphincter think of it in this way right like a mountain range and pressure is altitude basically now take this we can add color to the pressure profile and it looks it's beginning to look like that mountain that range of mountains now what i want you to do to understand what this manometry stuff is is think of yourself as as flying above the mountain range okay and when you do that or or rotate this image up so you're looking down on it you get this the top right bar is the upper esophageal sphincter at the the bar uh below is the lower esophageal sphincter and that diagonal band of color is uh the peristaltic pressure wave now bolus when we when we look at impedance we can look at the direction of a bolus a low impedance means that there's a liquid in the esophagus and these are two examples of the impedance dropping uh one is in a grade and that is a swallow and then there's one that's retrograde and that is a reflux event air we can also detect and in this way you can see that air can be tracked going into the esophagus or out of the esophagus okay so we can see a belch and sometimes we use this for this for impedance uh it the magenta color is where the bolus is and you can see in this case that it's been cleared by the esophagus okay our first case b is a uh 38 year old man he has a history of substernal burning excessive belching particularly after large meals uh or drinking beer as he is uh often doing and even after coffee he's had an upper endoscopy that was normal biopsies revealed one to two eosinophils per high power field consistent with esophagitis this is his esophageal manometry or excuse me this is his ph study and he has a ph below four which is the cut off for reflux events 16.3 percent of the time this is positive for acid reflux so he has reflux this is what his esophageal manometry looks like it's very different from that normal one this one is weak so it's ineffective esophageal motor function and this odd looking thing is actually a belch okay you can see that the lower esophageal sphincter or esophageal gastric junction opens at the bottom at the top the upper esophageal sphincter opens but there's no peristalsis and then you see where that little arrow is there's a little increase in pressure and that's actually gas moving from the stomach up the esophagus and out through the upper center now this this is called a transient alias relaxation it is triggered by distension of the stomach stimulation of the pharynx or cck cholecystokinin it is inhibited by nitric oxide synthase inhibitors atropine which is a cholinergic antagonist and lying down this is the mechanism one of the major mechanisms of reflux and this is how it works the stomach gets distended there is a neuron that is activated it's a vagal neuron it goes to the brain stem to an area called the nucleus tractus solitarius glutamate is released that activates an interneuron that goes to the dorsal motor nucleus of the vagus that activates another vagal efferent or motor neuron that goes into the myenteric plexus into the wall of the esophagus it stimulates the release of nitric oxide and that makes the sphincter relax and you get the belch so that's the mechanism we do have we don't use this medication very often it's baclofen baclofen turns out to be a very effective way to treat reflux uh if you look at this this is really a a good randomized a double-blind controlled trial looking at baclofen's effect the top two panels are the effect of back off and the bottom two panels are placebo and you can see that both the number of reflux events and the ph the number of a percentage time that the ph bill is below four is they're both improved uh by the baclofen common side effect need to be aware of it makes some people sleepy if that's the case it can't be used okay that's our belch case two es is a 52 year old anxious gentleman with an 18 month history of substernal dysphagia squeezing chest pain regurgitation of foamy fluid and undigested food he had an upper endoscopy that was normal except for seeing some foamy material in there he had biopsies that revealed one to two eosinophils per high powered field and he had an esophageal manometry and that esophageal manometry is here anybody have an idea what this might be how about the fellows any fellows what does it look like so do you see relaxation of the lower soft fuel sphincter yes or no shaking your heads no okay do you see peristalsis no okay so if the sphincter doesn't open and there's no peristalsis that is pretty much diagnostic of what somebody speak up echolasia so this i wasn't entirely sure with this guy so i gave him some botox he got better and then a few months later his symptoms came back so he had a heller myotomy and he did really well for a year and then in a year he came back and he was complaining now of frequent repetitive belches no dysphagia no chest pain no heartburn and no regurgitation so it doesn't really sound like achalasia right his endoscopy was negative he had a 48 hour ph study that was normal and he had an esophageal manometry and this esophageal manometry looks really weird doesn't it these aren't swallows they're something else and craig craig glickman is going to tell us what's going on here thanks dr conklin and thanks to the course coordinators for giving me an opportunity to speak today and to answer dr konkin's question this patient is having a repetitive super gastric belchers and i'm going to spend the next 10 minutes explaining exactly what a supergastric belch is so with the advent of 24 hour ph impedance studies and high resolution esophageal manometry we were able to diagnose a new kind of belch that is totally different to the gastric belch and it was called the supra gastric belch and the reason it was called supragastric is that it's above the stomach so everything with this belch really happens above the stomach so if you look at the image top left you can see that throughout this belching episode the low esophageal sphincter remains closed the first thing that happens is the diaphragm contracts and moves downwards this results in a negative intra-esophageal or negative intrathoracic pressure if you go to the image on the top right you can see that there's a pressure gradient of pressure differential between the higher atmospheric pressure and the mouth and the pharynx with the lower pressure in the esophagus and air will move from the mouth and the pharynx the atmospheric pressure to the lower pressure within the esophagus this happens through the open and relaxed upper esophageal sphincter the air flows down the esophagus it reaches the lower esophageal sphincter which has remained closed at all times and is immediately pushed forcefully back up the esophagus out through the upper esophageal sphincter out through the mouth so as you can see the stomach is by no way involved in this supergastric belch so this is a high resolution of software germanometry and they've superimposed in white ph impedance tracing and this and this explains the first mechanism of the supragastric belch where patients are air inhalers they actually suck air into the esophagus so the lower esophageal sphincter remains closed throughout air moves down the esophagus from the higher atmospheric pressure the mouth and the pharynx it moves into the esophagus and it is immediately forced back up out the esophagus and out through the mouth and you can see the red arrows point the direction that the air flows down the esophagus reaching the low esophageal sphincter and out through the mouth the white ph impeda ph impedance tracings show that gas or air causes an increase impedance as it moves down the esophagus and then as the air gas moves back up the esophagus the ph impedance tracing returns to baseline so this is by foreign away the most common mechanism uh that a supergastric belch occurs and it's through air inhalation it is important to remember that this is not a swallow there's no pharyngeal peristalsis there is no esophageal peristalsis and the lower esophageal sphincter the egj junction remains closed throughout this belching episode the second mechanism for a supragastric belch and this is way less common is air injection or air pushing and for this to happen there needs to be an increase within the pharynx so whatever can cause increase in the pharynx be a tense labial closure laryngeal movements base of tongue and pharyngeal contraction anything that causes an increased pressure in the soft in in the pharynx will push air down the esophagus it immediately reaches the low esophageal sphincter and then is pushed back out through the mouth and once again this is not a swallow there is no peristalsis in the esophagus so side by side looking at the impedance signatures of these two belches dr conklin mentioned the gastric belch where air begins in the stomach and it moves up the esophagus and out through the mouth that's the image on the left the ph and penis tracing on the left contrast that to the image on the right where air moves down the esophagus reaches the closed lower esophageal sphincter and then is immediately and rapidly pushed back out the esophagus and out through the mouth and this is the ph impedance tracing of a supragastric belch what are some of the cash characteristics of these super gastric belchers we initially believe and if you look at the top image on the right this patient has had a reflux episode and then immediately after that reflux episode there is a super gastric belt so what we believe is that maybe this supragastric belch is relieving the uncomfortable sensation of the acid reflux episode to begin with supragastric belching is completely voluntary and the patient has control over this but after some time it really becomes out of control and it almost becomes you know like a behavioral disorder patients can belch many hundred times per day and it can really interfere with their quality of life in the study that i'm going to refer to later the number of supergastric belches per 24-hour period range between 17 and 510 for 24 hours so you can see how this can really affect quality of life it can be repetitive can almost happen you know every five seconds and what we do know is that supergastric belching does not occur during speech and nor does it occur during singing and this is apparent when the patient is in your consulting room and when they talking to you they don't belch but the minute you as the doctor start talking to the patient and they're distracted then they go ahead and belch away so clearly supragastric belching lessened with distraction and then we know that supragastric belching does not occur during sleep and you can see the 24-hour impedance ph impedance tracing on the bottom during the day and waking hours you can see there's a lot of noise a lot of activity a lot of super aggressive belches but during the period of sleep for six to eight hours it's quiet there's no super aggressive belching so it's really a chicken and egg scenario and that does the acid reflux episode cause the supragastric belch or does the supragastric belch lead to acid reflux and we do know that 40 to 50 percent of patients with acid reflux belch and we also know that the majority of these belchers are super gastric rather than gastric belching pprs we know are excellent for acid reflux but we really don't know their role in treating supragastric belching and these these three questions need to be answered does the belch inducer reflux episode does the belch actually relieve the reflux episode or is the acid reflux actually causing the belch so if you look at these two ph uh ph impedance tracings we give the two scenarios side by side so on the left the patient first has a supragastric belch and this is immediately followed by an acid reflux so could you say that this supragastric belch is causing the acid reflux unclear if you look at the ph impedance on the right the patient has an acid reflux episode the ph in the distal esophagus is low and then immediately after the patient has a supragastric belt so you can almost imagine that in response to this uncomfortable acid reflux sensation the patient tries to relieve the sensation with the supragastric belch this study came out of the united kingdom in 2015 and it was one of the first studies to really look at super gastric belching in terms of its prevalence and its association with acid reflux and esophageal hypermotility so what they did to begin with is they got 40 healthy volunteers who were all asymptomatic and all these volunteers underwent 24-hour impedance and high resolution to suffer germanometry and what they found was that even in these normal asymptomatic patients they still had supragastric belching with a range of between 0 and 15. so they used the 95th percentile which was 13 supragastric vouchers per 24 hours and they said that in this study anyone with more than 13 super gastric vouchers per 24 hours was regarded as excessive so when looking at the study they analyzed almost 3 000 patients retrospectively between 2010 and 2013 they looked at all their ph impedance and esophageal manometry recordings and what they found in the math works out perfectly is that 100 patients had supragastric belching episodes and by that they mean more than 13 supragastric belches per 24-hour period and this gave them a prevalence of 3.4 percent so with the math being great you know 95 patients out of 100 that's 95 presented with typical acid reflux symptoms 86 out of 186 percent actually reported excessive belching but only 50 said that belching was the predominant complaint so the other 50 percent thought that you know other symptoms they might have had with a predominant complaint and in this study what's surprising is that 5 of patients five out of a hundred um had excessive supragastric belching and isolation which means uh they had no associated abdominal pain acid reflux or dyspepsia so if you look at the results and just briefly those patients with acid reflux in and what i mean by that those patients with increased acid exposure time those patients had more supragastric belching episodes and secondly those patients with hypomotility so an esophagus that contracts ineffectively those patients also had increased supragastric belching episodes compared to patients with normal motility and if you look at the bar graph those patients with normal motility have way less super gastric belching episodes than those with hypomotility so the conclusion from the study is that patients with acid reflux and esophageal hypermotility have increased supergastric belching episodes and what they did say that increased belching episode increased belching is really a symptom in isolation it's normally associated with other gi symptoms so we're able to diagnose super gastric belching you know we obviously need to treat it and originally and there was excitement in using baclofen as a way of treating supragastric belching and this study looked at 12 patients they were studied for one week before baclofen and then they were studied for one week on baclofen at a dose of 10 milligrams three times a day uh interesting to note there was only 12 patients in the study um and only two of those patients actually com complained of supragastric belching as their predominant symptom we know that baclofen is a gaba beta agonist and we know that this is believed to decrease transient lower esophageal sphincter relaxation but what's interesting to know is that patients with supragastric belching they don't have transient lower suffuri sphincter relaxation so it's really unclear if baclofen does help exactly how it's helping it may actually be a placebo effect and in the study you can see that those patients on baclofen they had far less supergastric vouchers than when they weren't on baclofen if anyone has ever tried to place a patient on baclofen we know that there's many intolerable side effects sedation drowsiness and it's really difficult to up titrate the dose so um clearly we need other treatment modalities for treating supergastric belching um so what do we have available in our homematerium uh our psychology colleagues are able to perform cognitive behavioral therapy we are able to make use of abdominal breathing exercises maybe as a distraction mechanism to decrease the supragastric belching episodes but lastly there's been some excitement in speech therapy and at this point i'd like to hand over to my colleague lisa bolden who's going to explain how speech therapy can help a patient with supragastric belly thank you thanks craig so our next speaker you just heard her name lisa is one of our speech language pathologists we work very closely with the folks in in speech language pathology she has an interest a new interest in uh supragastric belching and therapy from the point of view of a speech pathologist thank you all right so i bet most of you didn't expect to see a speech pathologist here at a gi conference so why a speech pathologist if you think about it speech pathologists for years have taught people who have had laryngectomies how to speak using esophageal speech so the thought is if we can teach someone how to talk using esophageal speech we can teach them how to not use a supragastric belch so our program is based on five studies that are available in the literature and if you'd like those references please contact me after but we've taken the best of what's available in all the projects that we've read about there are four primary components the first one is explaining the supragastric belch we have in speech the advantage of spending about 50 minutes with a patient so that allows us to go in depth in explanation we help create self-awareness we teach rescue breathing and then most importantly we help our patients generalize this into the real world so explaining the supragastric belch we go through and differentiate the gastric from the supragastric belt we explain the manometry and impedance results we solicit the patient's thought as to what the trigger is and we assign homework to develop a belching diary creating self-awareness so the first step is to be aware of the preceding gi sensation is it abdominal distension is it pressure in the chest is it pressure rising through the chest we develop self-awareness of injection and inhalation the two methods that you heard about from dr gluckman to get air into the esophagus and we use the mirror and video we teach rescue breathing and this is um this is the hallmark of what is successful for these patients and we have the patient place their tongue on the alveolar ridge which is the bony ridge right behind the front teeth they gently part their lips and they feel the air flowing in and out we focus attention on the ribs and abdomen we focus on the air flow fully filling and fully emptying and we will have them inspire and expire to account this is not with the mouth wide open in this position because that would just be trading one unusual behavior for another but rather it's subtle so it just looks natural and then we help them generalize develop a hierarchy of situations based on information from their diaries we plan and rehearse and we apply it in the real world we then rate on a visual analog scale and i hope is that large enough for you to see about how bothered the patient is by their super gastric belching how bothered others are how much it impacts them socially and professionally and how much control they feel they have over their belt gene so first case is um a 61 year old female who came to see me and you can see that her belching was the preceding event for it was her diagnosis of cancer and the loss of her beloved dog and what was so so moving about her story is that she is a veterinary surgeon and so the loss of her dog was just it was devastating to her you can see up above the results of her gi testing and i'll give you a second to look at that and here she is and let's see if i hit this if we'll play now you're going to notice that our patient has injection as her primary method which is a less common method of getting air into the esophagus so this is a great chance to have to see that okay linda go ahead and all right so could you see that the tight labial seal the larynx moving up and down and then this is her after treatment so well i guess this is a condition that i've been experiencing for approximately a year and a half now that has been gradually subsiding with treatment i'm substantially improved at this point it's gone from barely tolerable to very tolerable and no longer has a significant effect on my everyday life and i really appreciate her willingness to let us use the videos not all of our super gastric belching patient will allow that so her visual analog scale which is a really good way to assess progress um without an invasive procedure and you can see her initial ratings were high 325 out of 500. after treatment 55 out of 500. so again 325 55. so good improvement there um and that's what we can offer in speech therapy for your patients with supragastric balcine thank you [Applause] thanks that was great show of hands how many of you have seen this in your clinic and wondered what the heck to do i'm i'm assuming everybody right yeah all right uh that was great next case is a i'll present 23 year old college student with a history of regurgitation into the mouth during and after meals no nausea wretching dysphagia heartburn cough or weight loss endoscopy is normal upper gi is normal and this is the esophageal monometry now we showed you what's normal and this this one certainly has normal peristalsis but there's something else happening here there's a big pressure that's going up the esophagus starts in the stomach and goes up the esophagus before the swallow happens and remember i said we could watch where the bolus is going with this magenta so there's some the material that's in the stomach is moving up with that positive pressure wave lisa you're up what what in the heck is this you know it sounds like this patient truly has regurgitation because just come on up here there you go since there's no preceding symptoms of retching or nausea and you know based on clinic clinical history alone you might think in clinic oh does this patient have really bad reflux or something else but i think the esophageal manometry really helped to clarify that this is consistent with rumination syndrome which i will talk about in the next 10 minutes so we're going to talk about the epidemiology pathophysiology clinical symptoms diagnosis and treatment for rumination syndrome the epidemiology for rumination syndrome is not totally clear we don't really have a great idea of the in true incidence and prevalence but in the literature the prevalence has been reported to be between somewhere between 0.8 percent to 10.6 percent in community samples we also know in certain patient populations like patients with eating disorders or fibromyalgia that prevalence can be as high as seven to eight percent and historically rumination syndrome was described more in children or in adults with developmental delay although now it's really recognized as a clinical disorder unrelated to mental status or age um so the pathogenesis for rumination syndrome is also not completely understood but this is kind of um an overview of what we think is going on we really think that rumination syndrome is a habit that the body kind of forms in relation to food so i want you to focus your attention to the middle of the slide there under the primary pathway and you can see basically after the patient eats food they usually get some sort of premonitory urge so they usually feel some sort of sensation in the esophagus or abdomen that then triggers a habitual abdominal wall contraction that then causes material from the stomach to come up into the esophagus and this process of regurgitation basically temporarily resolves this premonitory urge for basically providing kind of a positive feedback onto this loop and patients can then re-true and re-swallow or spit out the food now if you focus your attention to the right side of the slide you will see that there are also secondary psychological mechanisms that contribute to this process so patients can have learned associations between the abdominal wall contractions and certain cues like for example certain food triggers or like specific activities that are not necessarily always related to food some patients also have very low tolerance for these premonitory urges so it further pushes them to develop this behavior some people also have body image issues that basically helps to drive this behavior so for example some patients will actually spit up their regurgitated food in an attempt to lose weight and you know some people actually do find the taste of the regurgitant pleasant and they find this rumination process actually soothing so again further reinforces this behavior so now if you look on the left side of the slide you will see that there are also secondary path of physiologic mechanisms that contribute to this behavior so some patients will have belching that proceeds or happens around this same time as the rumination event and some for some people the rumination event is preceded by acid reflux as well so rumination syndrome is really characterized by recurrent postprandial and effortless regurgitation so really no wretching and i think in clinic it's really important to differentiate whether your patient truly has symptoms of regurgitation or vomiting or reflux you know those are different things to different people but regurgitation is really no effort no wretching vomiting oftentimes is associated with nausea i so rumination syndrome symptoms can oftentimes be confused or you know be mistaken for other conditions because a lot of the symptoms can sound similar so i'm going to go over here just some of the typical symptoms for each of these disorders there are exceptions to these ex to these symptoms but basically rumination syndrome generally happens after every meal or with every meal usually happens soon after eating within an hour the regurgitant often lacks a sour bitter or acidic taste and tastes similar to recently ingested food because it's a behavioral issue again you usually don't have symptoms when sleeping and it can cause weight loss in up to 40 of patients and usually rumination syndrome does not cause electrolyte disturbances dental erosions malnutrition or esophagitis gerd on the other hand can happen when someone's sleeping they usually have more heartburn that's reported and generally it does not cause weight loss gastroparesis is oftentimes associated with nausea or wretching happens usually the you know the vomiting or things coming up usually happens later after eating by more than an hour and the food that comes up is usually no longer recognizable when regurgitated and it doesn't necessarily happen with every meal and the other thing you know the symptoms of eating disorder is very variable so i'm not going to go into the details here but i do think it's a really important diagnosis to keep on your differential when you see someone with prominent regurgitation or vomiting rumination syndrome is classified by both the room 4 criteria and dsm-5 i'm going to just focus on the room 4 since i think we're all more familiar with that in order to meet the criteria you really have to have persistent or recurrent regurgitation of recently ingested food into the mouth with subsequent spitting or remastication and swallowing and regurgitation is not preceded by wretching these criteria have to be fulfilled for at least three months with symptom onset at least six months before diagnosis and other these are some of the other characteristics that further support the diagnosis so effortless regurgitation events are usually not preceded by nausea regurgitant contains recognizable food which may have a pleasant taste and the process tends to cease when the regurgitated material becomes acidic and really we can diagnose rumination syndrome based on clinical history alone but we can also diagnose it on esophageal high resolution impedance manometry so as you can see in this manometry photo here this is a rumination event and it starts out with increased gastric pressure so the patient is doing a valsalva maneuver this then generates this retrograde pressure wave so that liquid bowl is coming up into the esophagus and that's that's followed soon after by a swallow and you can see on this impedance tracing here basically the liquid bowl is coming up and then being swallowed back down into the stomach and in one study postprandial gastric pressurizations of more than 30 milligram millimeters of mercury was actually a hundred percent specific for rumination syndrome there are actually three subtypes for rumination syndrome um so this is a picture of uh of the manometry and the four white lines that you see are the impedance tracings that overly it so there's primary rumination which is a rumination event that's not preceded by any leading event there's secondary rumination which is where the rumination event is preceded by a reflex event so as you can see in this manometry the lower esophageal sphincter relaxes the impedance drop some liquid comes up and this is followed by the rumination event and then the third type is supragastric rumination so that's where the rumination event is preceded by a super gastric vouch and as you can see here you see that inflow of air on the manometry correlating with the rise in impedance shortly before the rumination event in terms of treatment for rumination syndrome patient education and reassurance is really important and in clinic i often find that just even showing them the manometry picture and going over with them what is happening physiologically is very helpful for them first line therapy is really diaphragmatic breathing which our next speaker will talk to you more about but you can do biofeedback therapy with high resolution manometry or electromyography other non-diaphragmatic breathing related treatment include cognitive behavioral therapy you want to make sure to treat any comorbid psychological disorder like anxiety baclofen has also been looked at for rumination and as we know it suppresses the transient low esophageal sphincter relaxation so they have done randomized control crossover study this is a small study with 20 patients and it did show significant improvement in rumination events increase in the lower esophageal sphincter pressure and a decrease in the number of transient lower esophageal sphincter relaxation not really reported in adults but the two case reports in the pediatric patient population showed that having them chew gum soon after they eat can also reduce rumination events other things have been looked at for treatment of rumination syndrome but hasn't been as effective for treating it so neuromodulators we often use to treat comorbid disorders of gut brain interaction like ibs but it hasn't really been shown to be effective for treatment of rumination syndrome alone other things like acid-suppressing medications prokinetics anti-medics have also unfortunately not been shown to be effective in retrospective studies and surgeries such as fundamlycation there's really no data to support long-term effect so really not currently recommended so in summary rumination syndrome can be diagnosed with clinical history alone or esophageal manometry it's important to clarify with your patients what their true symptoms are whether it's regurgitation or vomiting or reflux first line treatment is really patient education and diaphragmatic breathing and if that's not effective you can do diaphragmatic breathing with biofeedback if available or cognitive behavioral therapy or using baclofen and it's also important to treat any comorbid psychological disorder thank you thanks lisa that's really good um i was just thinking while while you were talking and when when we do manometries on these folks to identify these unusual kind of belching things or rumination we actually don't do what most labs do and what we do is we have the patient in all these cases sit at we do the manometry and then we have the patient just relax or we actually feed them something and then leave them in the room by themselves for a while and we tell them to push the button on the recording device uh when they have the symptom it's it's really important to do that kind of thing when uh when looking for these unusual belching uh phenomenon okay so now our next speaker is suzanne smith she is an integrative health nurse who works in the motility group and uh the functional group she's going to talk to us about her approach to uh treatment of rumination syndrome probably the uh a little editorial aside this is probably the best way to manage these patients good morning everybody so i'm going to talk about why diaphragmatic breathing is indicated for rumination syndrome talk about evidence to support its efficacy touch on psychosocial factors and then give some pointers to how to teach your patients diaphragmatic breathing so here's a picture of the diaphragm and as you know there's the esophageal hiatus right here which is made up of the right crust of the diaphragm and this right crust acts as a physiological barrier so it keeps food from coming up from the stomach into the esophagus so as dr lynn mentioned it's not completely understood rumination but what we do know is there's this unintentional contraction of the abdominal muscles which leads to a cascade of events so increased intra-abdominal pressure increased intragastric pressure the lower esophageal sphincter relaxes and that and there's voluntary relaxation of that right crust that i showed you and this creates a pressure gradient which allows food to move up into the esophagus but in contrast to that when you look at the physiology of diaphragmatic breathing it does the opposite so as we when we breathe in diaphragmatically when we inhale this increases the activity the diaphragm moves down it contracts and flattens this relaxes the abdominal muscles this reduces postprandial gastric pressure and increases the ge junction pressure which does not allow this gradient to occur and we can see this on manometry here so you already saw you already saw the manometry of rumination this here is that valsalva maneuver and where the star where the arrows are and where the stars are this is the in the gradient where the bolus moves effortlessly up this is diaphragmatic breathing under manometry and i think this is pretty amazing see how this just keeps the contents of the bolus where it needs to be in the stomach so i want to talk about some evidence for diaphragmatic breathing for rumination syndrome so there's been various studies that have been done some without biofeedback and some with biofeedback so these two were done without the first study 15 adolescents and adults it was an open label study and as you can see they had a good responder rate 66 percent of symptoms were resolved 20 percent had a 50 reduction the second study this is the largest retrospective study done 54 patients now the age of these patients were from 5 to 20 years old so they were a much younger population but they still had a pretty good responder rate 30 percent had symptom resolution 56 percent had symptom improvement and 13 had no improvement so in this study they also did other behavioral treatments such as relaxation training progressive muscle relaxation but i also want to point out that 16 of these people had psychological comorbidities so then there's diaphragmatic breathing with biofeedback so in this first study what they did is they used emg to teach the patient's diaphragmatic breathing in three sessions and then they had them go home and practice for five minutes before and after meals they had a 70 reduction in their symptoms after only 20 days and this improvement was sustained at six months four patients did not improve and to note they had psychological comorbidities and then this same group decided to do a randomized placebo-controlled trial with the same treatment but they used oral simethicone after each meal as the control and the results as you can see seventy four percent reduction compared with only one percent with a simethicone they had them continue to practice for six months and they had further reduction in their symptoms so at a patient visit i think it's really important to assess the patient's understanding of the diagnosis many of these patients have waited years to get a diagnosis they've been to seen many doctors and had many tests so i want to make sure that we are reassuring them that we know what they have and that we can work together to treat it i also want to know what other presentation of symptoms so they can apply the diaphragmatic breathing most effectively and then also assess psychosocial factors so educating them discussing the reason for diaphragmatic breathing talking about the physiology showing them manometry readings and demonstrating the breeding and practicing making sure they really understand how to do it correctly and offering guidance so i want to touch on the psychosocial factors briefly because there's a significant impact on these patients quality of life and daily functioning so the things that are important to assess are what is the impact on their individual quality of life what life stressors are happening because oftentimes these episodes start with a stressor so what are they having things that are stressing them that are driving this mechanism any presence of avoidance behaviors do they not like to eat with friends or eat out what are their worries and fears and what are their expectations of treatment and this is important to assess because you want to evaluate should we get a gi health psychologist involved in their care so teaching diaphragmatic breathing i always have people lie down on the exam table first because the body relax and most people actually start breathing from their diaphragm that way i can have them know that the body already knows how to do this and then we enhance it after that once the proper technique is demonstrated it's important to have them sit up they really need to learn this sitting up because this is when their symptoms occur 10 to 30 minutes after ingesting meals so i'm gonna tomorrow i'm actually going to be demonstrating diaphragmatic breathing we're all going to practice together so i'm just briefly going to go over the steps now so what you want to do is you want to have them place one hand on the chest and one hand below the ribs and this is kind of just to cue them then you have them take their normal breath and you have them understand you know as lisa was talking about self-awareness how are they breathing normally and then what you do is you teach them diaphragmatic breathing so you have them breathe in through the mouth and you what they're doing is keeping the chest motionless and only letting the abdominal muscles work so as they breathe in the diaphragm comes down and this abdominal muscles relax and then they breathe out through the mouth and you just have them continue to practice this until they demonstrate proper technique diaphragmatic breathing as you saw on the manometry is incompatible with this abdominal wall contraction which is what's driving their symptoms so when do you have them practice breathing for rumination well it depends on their sensory feeling each patient is different if they don't know when they're having their symptoms or they're not that clear about it have them keep a journal this also builds that self-awareness the goal is to retrain them with the breathing so we want this to start coming up unconsciously after they eat instead of having their abdominal muscles contract so it's best to have them practice before during and after meals for five minutes and after each episode of regurgitation but what's really important is to have them get this down so practice it when they're not eating so doing it regularly on on a daily basis so for severe symptoms we want them to practice for five minutes three to five times throughout each meal with 10 minutes in between so just some things to consider when you're teaching people breathing it may be awkward for some patients especially patients who have anxiety so you want to think about should i be referring them to someone who can spend more time with them really have them get this technique down body images image issues can come up when you're breathing in and your abdominal muscles are relaxing and coming out this makes some people feel very uncomfortable so you need to address this in the office when you're teaching them have them wear loose clothing when they're practicing and if refractory consider other comorbidities and treat any secondary psychological comorbidities is really important and interdisciplinary team is important to the care of a patient with rumination so thank you [Applause] all right so very good okay next case mt is a 16 year old complaining of dysphagia he had episodic vomiting at six months of age after uh intake of any solid foods this this uh contin started after uh he was taking formula it triggers for his uh vomiting where things like fatty foods ice cream cheese and milk uh he was treated as is everybody who has this kind of symptom with famotidine and it did not improve he had a 24 hour ph study done the ph was below 4 6.3 percent of the time and normal is less than 5.6 percent of the time so he had a little bit of reflux but not a lot his gastric emptying study however was quite abnormal uh he should have had greater than 50 emptying at um 90 minutes he had an upper gi that was normal with a small amount of fluid in the stomach at age three and a half he had a nissan fundoplication he had lo interestingly he had large lamb lads bands coursing between the duodenum these and the liver these were divided as any surgeon would do in this situation it did not improve his symptoms in any way he continued gagging and wretching with eating his current symptoms when we saw him uh he was taking an hour to eat every meal at the least uh he had epigastric discomfort like something being stuck uh when he put food actually when he just put food into his mouth he would have the symptom uh he then started to chew and he would chew very slowly and as he was chewing and swallowing he would chew more and more slowly he actually had a fear of eating and was worried about swallowing he would not go out in public to eat and he was avoiding his friends his mother reported that earlier in life he was at camp and he got a tick and the tick was turning his head over and over this was treated successfully with cbt so here is his endoscopy and what you see here is a normal esophagus and a fungal plication that looks intact it does not look too tight does everybody agree with that okay biopsies did not reveal eosinophilic esophagitis he had a barium swallow [Music] basically normal and he actually swallowed some solid material and it passed through without any difficulty here's his esophageal monometry and you can see that he has adequate peristalsis the lower esophageal sphincter opens appropriately so this is not a motility abnormality that we could define and in fact we couldn't find anything any physiological reason for this young guy to have dysphagia so christina christina is christina gentilly is one of she is our gi psychologist she has been a great addition to the division has helped a lot of people in in situations like this where we can't find a pathophysiological problem and uh they have some kind of funny stories so she's gonna talk to you about how this young man was taken care of by her okay so when the patient presented to to gi health psychology he had a lot of significant anxiety and worry about his anxiety about his um esophageal sensations as dr conklin mentioned he had concerns about his ability to swallow and he had significant fear of choking and he tended to have a lot of anticipatory anxiety especially at dinner he described dinner as being his most problematic meal when he tended to have the most bothersome symptoms and what we started to see was there that there was this pattern between with him managing his anxiety through safety and avoidance behaviors and what this included were things on that dr conklin described excessive chewing prolonged eating at meals skipping meals and avoiding certain food items and also associated with his distress was that he had a lot of different psychosocial stressors related to academics and his athletic performance and what we saw was that these stressors tended to build throughout the day and he didn't really have any good coping skills or stress management skills in place to help him regulate those and i'll talk about that more in a moment as a pre-treatment measure he completed the esophageal hypervigilance and anxiety scale this is a measure that was developed by taft and colleagues at northwestern university in chicago and you can see his scores listed above and it ranges on a scale from zero to 60 with higher higher scores more indicative indicative of the construct that is being being measured symptom anxiety subscale looks at the cognitive mechanisms associated with symptom anxiety so this idea of catastrophizing where um patients are likely to then awfulize their symptoms saying you know this is horrible and feeling very helpless with their ability to control or manage the symptoms and the hyper vigilance looking at this behavioral pattern of selectively attending to those sensations and monitoring and detecting any variance in change and since dinner was his most problematic we just looked at in terms of over the last seven days how how often were you experiencing uh these dysphagia episodes and he endorsed six out of the seven so i wanted to present then a biopsychosocial formulation to help us understand how gi health psychology can be used to help a patient like this and by the time he approached dinner there were two things at play that happened as i mentioned he had significant stress related to school and academics and this stress basically built built up but throughout the day and by the time he got to dinner he was very um aroused his he had a lot of autonomic activity at the same time there was a lot of anticipatory anxiety about dinner he approached dinner with dread and was making these faulty predictions about him having some sort of adverse outcome and this ultimately resulted in a few things him becoming very hyper vigilant to any changes that he was experiencing at the moment he started to notice any changes in his esophage in his esophagus he started to have um these faulty threat appraisals where he started to have more catastrophic thinking he you would endorse thoughts about oh my gosh this is going to be another uh you know issue i'm not going to finish eating my food i don't feel normal and he would have this perceived loss of control and this ultimately then set off an interacting relationship between his his thoughts what he was saying to himself his emotions and this fear-based physiological response where we see increased autonomic arousal and as we all know that can also worsen esophageal and gut sensations and then these maintaining factors with behavioral avoidance so either skipping foods or using these safety behaviors to manage the distress with the meal as well as this catastrophic misinterpretation of these signals or rather sensations so i wanted just to provide a general overview of treatment we did two things we did esophage esophageal hypnosis which is an evidence-based brain gut uh psychological treatment we emphasize that in the beginning portion which is you can see is shaded in blue the gray boxes indicate areas that were more of a less focus of treatment the later half of treatment we decided to include then gi focused cognitive behavioral therapy to tackle some of this fear and anxiety and avoidance around food and i'm going to go into more details about these these treatment modalities tomorrow but as a general overview with esophageal hypnosis it's a form of medical hypnosis so usually when i present this to patients i have to correct some of these myths and let them know this is nothing like you know what you might see on los in las vegas or on tv it's a form of helping you achieve a very very deep and focused state of relaxation and in doing so we use different different ways of helping the patient achieve this deep state of relaxation we're using things such as diaphragmatic breathing as suzanne has discussed progressive muscle relaxation and we're also pulling in imagery and the imagery is connected to these esophageal sensations and so we're using calming and soothing imagery to help the patient uh correct any um any ways in which he's misperceiving the these sensations so when we pull in the hypnotic suggestions which are verbal repetitions we're helping his brain begin to start down regulating pain processing and unpleasant sensations so we're trying to alter the perceptual experience and with our hypnotic suggestions we want them to be uniquely tailored to the patient so for him since he was endorsing significant fear with swallowing it was important then to hone in on this and with these suggestions like as i mentioned we're pulling in imagery so for example more and more you begin to feel confident in your esophagus ability to function in a steady flow natural rhythm imagining fluid flowing down like like a gently flowing stream so we want the patient to begin to feel this in their body see it in their mind with the imagery and we're using language to help develop this positive association to their to their sensations so we did this about four times he came in to to session we would do the hypnosis and he was he received a recording to practice at home and he was encouraged or encouraged to practice most days per week but his teenage boy so we had to encourage him and reinforce the importance but it was important because he saw when he wasn't practicing he started to have more of these unpleasant sensations return so once he developed mastery with this we decided to move on to more of a gi cognitive behavioral approach and with this aspect of treatment we did a few things we did exposure based treatment and we included cognitive therapies with exposure we worked together to identify his most feared foods and food items that he's been avoiding for a significant period of time and he would bring these into clinic so my office smelled uh very delicious actually we had french toast burgers pizza and he would practice eating these as he was using different skills uh behavioral and cognitive skills to manage that distress and as he learned that he could eat eat these food items with not having this adverse prediction this adverse outcome he started to gain a sense of control and what this did was it served to help disconfirm that faulty belief he had about his symptoms and this fear that he might choke and there's going to be some sort of horrific consequence and he would go home he would also practice these exposures at home and what we saw was then between session habituation and what this essentially means was that between each visit that fear and anxiety began to decline with the cognitive interventions we were tackling how the the faulty appraisals that he was saying to himself so how he was approaching his sensations and also how he was approaching stress because as i mentioned earlier he had a lot of stress that would build up by build up throughout the day and by the time he got to dinner it would basically just boil over so he learned how to de-catastrophize which mean which means instead of looking at the worst case scenario can we help you find some sort of balance in terms of finding a more realistic outcome and should there be a problem how can we help you use some flexible problem solving skills to manage and navigate that that situation so we essentially wanted to help promote some self-efficacy with this patient with mindfulness of thoughts we wanted him to also begin to recognize when he was starting to make these faulty threats or threat appraisals about his sensations and symptoms and take a non-judgmental stance allowing them to come and go where he's not buying into them and becoming hooked and basically thrown off his course of life so that he could re-engage with things that bring him joy and what he values and he would practice those skills as well at home so by at the conclusion of treatment we he recompleted his uh the esophageal measure and what we saw then was a general decrease in scores across the board um so as you can see his total score went down as did the the subscale for anxiety and in hyper vigilance although he still presented with some symptom related anxiety it was not as bothersome he was better able to manage because what he learned that was a very very important point was that he needed to practice skills throughout the day whether it was how he was talking to himself how he was approaching stress related to school or the stress related to these bothersome sensations and use these skills to help lower arousal so that by the time he got to dinner he was able to have eat more foods that he enjoyed and i want to just bring our attention down then to that last item in terms of the frequency of dysphagia episodes when he came in he reported he experienced these six times over the last seven days at dinner and at the end of treatment he reported zero and i he also was self-monitoring this and mom also agreed that she hasn't seen this uh even occurring for the last two weeks um so with this he was able to reintroduce more foods he was eating french toast he was actually eating probably what we would see of an average teenage boy and he was really excited because he didn't feel hung as hungry anymore so the big take-home point then for him was he needs to practice and he needs to also develop self-awareness of when his anxiety is starting to intensify and where his key vulnerabilities are with his stressors thank you thanks a lot she has really changed the the practice uh in in our gi division there's no question about that so d.o 52 year old woman with chest pain she had solid food dysphagia starting in her 20s and she had her first food impaction in her 30s her dysphagia was felt in the suprasternal notch so right here worse with bread meat and potatoes she did not have heartburn nausea vomiting or melanoma so with that history uh fellows what would you think eoe okay good thought so she was in libya with her husband she was eating a chopped salad and she said she felt an explosion in her chest odd symptom right it was followed by severe chest pain she went into the hospital there she was told that it was her gallbladder she had cholecystitis fortunately her husband who was an oil guy was a bright guy and he said i don't think that sounds right she was flown to malta where a diagnosis of esophageal perforation was made she was treated with antibiotics tpn and a chest tube no surgery pretty amazing after six weeks she returned to the u.s and continued to have dysphagia now i'd say she's lucky right so this was her manometry uh as part of our our studies to evaluate her dysphagia like one of our other patients the esophageal gastric er junction is not opening so the lower esophageal sphincter is not relaxing and there's pan-esophageal pressurization that is there's a simultaneous pressure wave that goes up and down the entire esophagus and it's associated with swallowing so this looks like echolasia and it looks like type 2 acolysia right with panasoftial pressurization so she actually was referred to me by a thoracic surgeon i should have said that sooner and when he saw this he said ah i need to do a heller myotomy. can you see this is it is that pretty clear so i s i also got a barium swallow on her and this is the barium swallow you see anything funny about this so i saw these rings in the esophagus and i said to him no don't don't operate on her just yet let me scope her first and so i did and this is what we saw so what's the diagnosis just endoscopically eoe those are the biopsies and sure enough she had lots and lots of eosinophils so the diagnosis was eosinophilic esophagitis showing you that eosinophilic esophagitis can present manometrically in a number of ways including looking like echolasia so kevin i promised you not to torture you on the on the stage but uh i'm going to ask you what what are the medical therapies that we can use now in the treatment of eosinophilic esophagitis so historically or recent history was that the first line therapy is double-dose ppi uh as is mentioned in the first line there uh although the most recent uh guidelines coming from europe actually say that that doesn't have to be the case um so really the main medical options are ppi and topical steroids whether it's using an inhaler like fluticasone um and swallowing it instead or taking uh budesonide the rest fuels that are used for nebulizer and mixing them with usually it's been sucralose although other media can be used to make a viscous solution that can have a better coating effect there's evidence to suggest that either one can be used first although in this case given how high up it looked like there was those rings and given the severity of it i probably would have started with steroids first fair enough so as you can see she refused steroids so we're in this situation where her the proton pump inhibitors did not help and she's not going to take steroids for whatever reason the question is is there anything else we can do nancy this is nancy jaffe she's one of our gi dietitians another person who's made a big difference in the practice is there anything else we can do for this guy you jeff so i have the honor to speak on uh some of the current research that we're seeing with elimination diets in cenophilic esophagitis and i'm also really excited to talk about the new model that we've created at ucla to work with this group of patients and how we're going about utilizing the diet research that we've had so before we go into the research on eoe i thought we should first define what an elimination diet is so historically speaking an elimination diet is a procedure used to identify foods that we think are causing an adverse effect in a patient and what we do is we remove all of these suspected foods and then we exclude them for a while and then we bring them back and i think it's really important that we add a couple of elements to that historic definition we need to be very specific about the foods that we're choosing so this isn't just what food but what food components what food composition what element are we trying to get to and you'll understand more of what i mean by that as i move through my talk we also want to make sure that this is done for a set period of time so elimination diets are not meant to be long-term solutions they're not meant to be the diet for the rest of the patient's life so there are actually three very specific phases that we want to make sure we hit when we do an elimination style diet with a patient we want to start with what's called the elimination phase which is when we remove all of those specific food and food components that we think might be triggering for a patient after that we want to bring them through what's either called the reintroduction or the challenge phase where we're actually challenging the assumption did those foods actually help and if they did which ones of the specific foods that we removed actually were causing the problem and then from there we can move into what's called a maintenance phase and this is where we take the data that we've collected from the other two phases and we actually create a long-term intervention that hopefully does not decrease quality of life in our patients especially in the case of a dietitian we're talking about food and food is very pleasurable and it's very social and we want to make sure that we take those elements into consideration when we're working with this patient population so how did we come up with the elimination diet so basically this all started with dr albert rowe who was the chief of allergy at the university of california medical center in san francisco and he actually wrote a paper that you can see there in the 1940s where he first started talking about the need of these elimination diets to work with allergic patients we then had another study that came out by an australian group in the 1970s where they actually started to put into detail the different steps we should be using for an exclusion diet and this actually helped to set up some of the double blind placebo control trials that we use in allergy today and nowadays elimination diets are used by all sorts of different types of practitioners and mainly they're used to look for different types of food allergies and possibly food sensitivities and the most important part of that type of elimination diet is that we're removing what's called the six leading allergens so that includes dairy soy tree nuts which includes peanuts fish which include seafood addicts and wheat so you may hear it called the top eight allergens just so you know the top eight and the six are the exact same thing it's whether we pull out peanuts from tree nuts and seafood from fish identical in this case we're going to be talking about them as the six foods so where did the research start with eosinophilic esophagitis so the first study that was really done with this cohort of patients was done in the late 1990s by the pediatric group at johns hopkins medical center and what they did is they took patients who were refractory to other types of medical intervention and they put them on a hypoallergenic elemental formula to remove all of the proteins from the diet since we know that proteins are usually the most allergic part of the specific foods that we're worried about these patients were only allowed to have clear liquids and they were allowed on occasion to have corn and apples again this was a pediatric population so that was for those who could actually chew and what they found is that when patients were put on this elemental diet for six weeks just to point out this was a small study there were only 10 patients on it but while they were going through the um elimination part where they were on the formula eight out of the ten patients had significant reduction in their symptoms so they were feeling almost completely better two of them actually had full remission of their symptoms and when they went in and they actually did an endoscopy they found that the um essential count was reduced to the point of remission in over half of the subjects and that the median rate for improvement was actually about three weeks and that in order to see maximum it was about six weeks so this is how we started to learn about time frames and what time frames we should be thinking about when we're looking at diet intervention for this patient population but of course putting patients on an elimination or sorry an elemental diet for the rest of their life is not a good option right we don't want to do this to our patients and especially adults are not going to be wanting to follow suit with that so other groups started to look at the elimination diet and so this was one of the first studies in 2006 to look at the six food elimination diet and what was great is they compared it to that exact same formula that the other group had used so they found this hypoallergenic formula they gave the elemental exclusion diet to half of the cohort in this case it was 25 children and then the other 35 children were actually placed on the six food elimination diet for six weeks and what they found is that about uh 74 of the children who were placed on the six food elimination diet had clinical remission of uh their eosinophilic esophagitis under endoscopy and that was compared to 88 percent in the elemental group so yes the elemental group won out but not by that big a margin and the six foot elimination diet is a much better tolerated protocol the other thing that came out of this research is that we started to see which foods were the most common problems in this patient population and what we saw was that milk overwhelmingly was the biggest issue followed by wheat eggs and soy so another group went well what if we actually start to look at adults and we start to figure out if maybe the food for food elimination diet would be enough do we really have to remove all six food triggers from the diet so what this group did in spain was they had six week four food elimination diet it was a multi-center study because it was in spain they decided to remove all mammalian milk not just cow's milk all gluten grains not just wheat and then legumes as well as soy and eggs and what they found is in their 52 adults that participated in the study 54 of them achieved both symptomatic and um histological remission of their symptoms and what was great is they then took the patients who did not respond to the forefood elimination diet and they gave them an option of going on to the six food elimination diet and with that option they were then able to rescue 31 of those non-responders so we ended up with quite a significant number of the patients who had a clinical and histological remission and again we're seeing which foods tend to be the most problematic even in the six food elimination diet group milk eggs wheat and soy tends to be the big triggers and again milk overwhelmingly is the largest problem in this patient population so i wanted to show you one more study there's actually quite a few studies on eoe i just wanted to show you the ones that really really focused on to help come up with our protocol at ucla so that same group that we just saw in spain who did that for food elimination diet they then ask the question well do you need four food could you do two food so do we need a two food a four food or a six food elimination diet what will give us the best results and in this case they went big they got 14 different centers six week protocol everyone was started on the two food elimination diet if they failed the two food they were then increased to the for food if they failed the four food they were increased to the six food and you can see the results that they got so on the two food elimination diet they were able to achieve remission in 43 of the patients and what they found is yes they had a teenage cohort so that's what they mean by the pediatric population it was actually teenagers but they found there was no difference between the pediatric population and the adult population they responded identical to this intervention and again we found that dairy and wheat biggest triggers for those patients who did not do well on the two food and were stepped up to the four food and the six food we ended up with 60 and 79 remission both of symptoms and of um their uh histology so this is pretty impressive results um one thing that we learned from this study is that if a patient is put on a two food or four food strategy before they are moved to the six food we might be able to save up to 20 to 30 percent of the endoscopic procedures necessary and that might be a question you're asking is how many endoscopies does it take to actually figure this out and we're about to show you what it takes so what we've decided to do at ucla is to start with a for food elimination diet and then we can always step up to the six food elimination diet if a patient has a very strong allergic history we may start them at a six food elimination diet or if they have already a good sense that milk and wheat are their big triggers we may even choose to step it down and start at a two food but we always go for a six week intervention during that first elimination phase which is followed up by endoscopy to make sure that we achieve less than 15 eosinophils per high-powered field clinical remission and then we can start the reintroduction phase if a patient does not achieve that outcome then of course they're going to be stepped up to the next intervention and diet or of course they can consider other treatment options so i don't want to go too in depth in this but i wanted you to have this information in your slides so that you could be thinking about the types of foods that are necessary to remove for the for food elimination diet and this is actually where a team approach is really important in having your dietitian available we're lucky at ucla to have three gi dietitians now who are able to work with our patient population so that we make sure we're rooting out any problem foods that might otherwise not be noticed so for instance not everyone thinks that there's they need to look at their salami to see if it actually has milk protein in it which by the way a lot of them do so this is something that the dietitian can do with the patients um we also know things like you don't have to worry about soy lepicin or soybean oil they don't contain the allergenic protein so patients don't have to freak out every time they see soy lethosa on a packaged food that would otherwise be safe also we don't require patients to go gluten-free but we may recommend that they use gluten-free oats during the elimination phase because oats can be very highly cross-contaminated and so there could be enough wheat in there to potentially cause um the problem that we're we're trying to assess for of course if we put the patient on a six food elimination diet we include or exclude everything that was on the previous slide and then of course we have to take out the nuts and the fish as well so how do we create success with our patient population we need to make sure that we're giving them very clear identifiable foods that they need to remove and foods that they need to keep in the diet we want to offer them grocery lists with lots of brands we need to make sure that we find the foods that are most important to them and that we find them good pleasurable alternatives because they're going to be on this diet for a while and we do not want to decrease their quality of life any more than is necessary hopefully we can really find a lot of good options for them and there are there are so many good alternative products out there nowaday we do a lot of meal planning and meal strategizing and then we also help to create realistic attainable goals and expectations so that they have an understanding of how long it takes for symptoms to start to be reduced what we can expect with percentage-wise from the endoscopies and how long the process potentially could be so the next part is that we want to go over a challenge phase so this is probably the most complicated part of the intervention so if a patient successfully makes it through the elimination phase they're having both clinical and histological remission of their symptoms what we do is we bring two foods back at a time for each of two weeks for the least reactive foods and then for the most reactive foods we do them one at a time for each of two weeks and if there are symptoms which usually can start occurring within about five days of adding the food back in we may actually need to speed up the timeline or we may need to have them pull back on eating that food until closer to the next scheduled endoscopy in order to make sure that we're not basically torturing our patient right we don't want them to be suffering needlessly we just want to find the answers that we're looking for so when i said the least reactive foods what i meant is if you're on a for food elimination diet we're starting with soy and eggs and if you're on a six food you start with fish and nuts and we always want to make sure that we're using a very pure form of the food so if a patient is going to do nuts we don't want them to do something that also contains wheat or contains eggs it needs to be just pure nut butter or just a handful of nuts and there really aren't great guidelines for how many of these foods what the dosing is that we need to use so what we're doing is we're starting at about you know 20 nuts or one tablespoon of a nut butter one egg per day one glass of soy milk so we're starting with just nice round numbers a good amount enough that it really should cause a reaction excuse me if they're willing to stay with that dose for those two weeks the most reactive foods as we mentioned are milk and wheat so we want to make sure that we choose very very pure forms of these and we can be a hard one because wheat is often mixed with some of our other allergens so choosing just a wheat pasta or like a saltine cracker might be your best way to go i also wanted to point out so you may have noticed in some of the studies that they removed all mammalian milk which included goat and sheep milk and they removed all gluten containing grains there have been several studies in the u.s including one by goncalves and his group in 2012 and another one in 2017 where they actually looked at a u.s population and they found that it was unnecessary to remove all gluten and all mammalian milk in our population and it's in part because in spain they eat a lot of legumes and they drink a lot of other types of mammal milk we don't really have that issue here in the u.s and so we can really focus on cow's dairy products and we can really focus on just weed as our source so i hope you can see this okay it's a really complex matrix that our esophageal group has come up with and it was based on not only the research that you saw but we also did a deep dive into what other academic universities are doing across the country and this is what we came up with so basically just to orient you um the yellow that you're looking at are endoscopies the blue is when a food is being reintroduced and red is when there is reaction so basic example of how this algorithm works is a patient will be put on this is the for food elimination diet for six weeks they would then have the endoscopy endoscopy hopefully showing remission then they would add soy in for two weeks hopefully there's no symptoms and they're able to then bring in eggs for two weeks after those two introductions they then go in for their next endoscopy if they are continuing to be in remission they get to move on to the next set of food challenges if they unfortunately had recurrence of their symptoms it means we've added in one of their trigger foods so again we pull out the most likely culprit and we have them then do kind of like a washout challenge for six weeks so as you can imagine this can take some time and it's really important that we're doing an individualized approach for our patients because we have to consider factors such as medical indication risk benefit discussions insurance coverages and patient preferences but we've got a really good team as you can see including an amazing nurse practitioner sonia who's in the room who really helps us to coordinate care and make sure that we're doing the best we can for our patients and then you can see the six food gets even more complicated so we all have um laminated copies of this in our offices that we can actually use with our patients to help them understand the process and how we're going to go through getting them through the process so the last part is the maintenance phase which of course is when we've finally gone through all of these endoscopies we've hopefully figured out the one or two food triggers that are the offending agent for them and we're now able to bring back everything that was not a problem and only focus in on those trigger foods from there we want to make sure we create adequacy and balance in the diet so again this is where having a dietitian as part of your team is really important we want to make sure that if we've removed something that has key nutrients such as dairy products we want to make sure we're giving those k nutrients such as possibly calcium vitamin d maybe zinc back into the diet in other forms and that we're alerting the patient to that we also want to make sure we supplement appropriately if necessary and then of course it's important that the patient continue to follow up with their physician so as a reminder diet is an option with your patients considering whether the two four or six food elimination diet is appropriate for your facility and your patient population is really important and making sure that you've got the staff that you need in order to accommodate these patients this is a complicated protocol but we've done it how many times about four times i think together and we've had some really good success rates and the patients have really actually been grateful to have options that they feel like they have some say and some control over when you actually hit on what those core triggers are and they get to move on with life and not have to go through this process anymore you're actually giving them a lot of self-confidence and you're giving them a lot of their life back so thank you thank you nancy so kevin i'm going to pick on you again so during this protocol this thing that we do how do you assess success of the therapy well ideally it would be great if we could just assess based on symptoms the problem is is that people and i've seen this um just recently uh people can say that they feel so much better yet when we do the endoscopy there's still quite a amount of esophageal eosinophilia so you really have and of course while we want people to feel well we want to make sure that we're actually doing them justice and also knowing what exactly are the triggers so really the endoscopy is the key in taking additional tissue samples to confirm that there is an uh improvement in that inflammation yeah i think that's a very important point the if there are too many eosinophils in there they're going to end up with fibrosis and all of the problems associated with that so it's really important to make sure well okay another question for you what what's your goal with therapy so the goal of therapy is to well ideally eliminate dysphagia completely but really allow patients to have a normal quality of life with regard to the foods that they're eating or can eat especially if they do endeavor on the food elimination diet understanding though that because this condition does involve more than just the esophageal mucosa and there can be some minor motility abnormalities as well they might still have symptoms but improving quality of life so especially for the young folks who avoid eating in social situations with their friends because it just takes them two hours to finish the meal that everyone else is finishing in 20 minutes uh we really want to improve that aspect of their lives so do you um do you have a target for the number of eosinophils research studies say the complete remission is less than five eosinophils um if they have less than 15 eosinophils per high power field and symptomatically they're doing better i'm fine with that okay that's great so i'll get back to you in just a sec we have we have only two questions so we have time if people want to shout out after these things so christina of course so our our patient with dysphagia you got him all better how often do the symptoms come back what's the rate at which they fail over time it depends um it it's dependent upon if the patient's continuing to practice those skills at home so for each patient there's going to be a degree of variance especially if there's any psychiatric comorbidity such as a pre-existing anxiety or a depression we do see from the research um some studies saying at least six months to one year remission but again it's it's very very dependent on is this patient practicing how adherent are they with their routine practice are they fully engaging in it um with this patient he since he had that fear of eating um that was another aspect of treatment that we hadn't had to manage so being able to continue to build those skills so they just become more routine and automatic so another question does the insurance cover the behavioral therapies very good and complicated question as well um so i use the health and behavior cpt codes and the so when i submit my bill i use the primary medical diagnosis or so for him the functional dysphagia the other codes are the psychotherapy cpt codes with those the psychologists would be diagnosing a like for example a major depressive disorder or generalized anxiety disorder we do see that patients have coverage using the health and behavior codes however there's some arguing with insurance panels having to go back and forth to to uh verify the coverage but generally speaking we've seen patients have the coverage with the health behavior codes yeah that's an important point actually all right so craig and kevin so what's the we're gonna i'm gonna ask you guys to talk about the role of biologicals in the treatment of eoe i seem to remember that there was one a few years ago was anti-il5 that worked great as long as it wasn't a controlled trial and when it was a controlled trial didn't work at all are there other things on the horizon so there are other immunomodulators or antibody type treatments however as jeff you mentioned they're really mainly uncontrolled trials and they were really designed for other reasons the problem here is that although il5 does seem to be increased in patients with eoe it just doesn't seem to work well when it's put to the test in a more controlled uh experimental setting um i've personally never had to use it we've i've always found something uh to help the patients that's let's just say more in the traditional or standard practice there's also an anti-ige antibody but because this isn't an ige mediated disease it's not surprising that it hasn't been helpful everything else is just too infantile right now to say that it has a real promise yeah i think that's right it's we don't have the data yet to support the use of of these drugs in eosinophilic esophagitis i think that's pretty much true okay go ahead in terms of the steroids there are there is work on an alternative to inhaled fluticasone or uh you know udecinadas like a slurry because you can imagine with the inhaled particle zone the majority is going to go into the lungs and it's really difficult to swallow that and with the slurry of budesta night you know how does that actually you know stick and attach to the esophagus so they're looking at oral dispose dissolvable steroid formulations as an alternative to buddha night or flutica yeah there's one i think there's one in europe that's a capsule that you put in your mouth and it slowly dissolves and gives it time in the esophagus so if you were going to make a slurry how would you go about doing that basically you take the budesinar dress bill that's um one or two you know point five or one milligram you need to take it twice a day you need to mix it up with some sort of viscous agent i've heard honey kevin you mentioned sucralose basically you just want to kind of make a slurry and then you want the patient to swallow it and almost use it like a lotion on this on the esophagus but what's important is once they take this budestinite slurry they shouldn't eat uh food or drink any liquids for about 30 minutes because it's like it's almost like putting lotion on your hands and then washing your hands immediately right after so uh if you take this butanol slurry no food or drink 30 minutes um after taking it just to add to what craig said um first of all i tell people do it after breakfast and then also before bedtime because why not make it longer than 30 minutes just in case there can be the potential for increased contact time the other thing is because oral thrush is probably the number one side effect i tell patients you know within five minutes after they've either used the fluticasone inhaler or the oral viscous pedesta night just take a little water gargle swish and then spit that out just to get the additional residue out of the oropharynx all right any other questions bennett sure so the the question was to discuss just the role for dilation i've i've talked about this at previous conferences but i didn't want to sound like a broken record this time but it is a good point you know dilation actually does have i in my opinion an important role for treating the fibrostenotic form of eosinophilic esophagitis um we know that below a diameter of 12 millimeters patients are much more likely to have food impaction uh and much more significant and frequent dysphagia and in fact patients who are complaining of near daily dysphagia i can almost guarantee that they're going to have a significant stenosis so with regard to dilation just real briefly i prefer the balloon uh over the uh boujee dilator i'm comfortable using the bougie but the problem with eoe sometimes is that there can be multiple strictures of varying uh degrees and so it's going to be a lot more onerous tasks to start really small and then you maybe only can dilate one stricture in a given setting which is the most uh significant one but when you you dilate it with the balloon you you get to see you can actually look through the balloon while it's inflated if you just put a little uh water from the lens rinse to serve as an interface you can actually see most of the time when the mucosal tear occurs and that's a good stopping point because once you've gotten the tear going beyond that is just going to increase the risk for uh perforation the other thing is to have a really good working relationship with the nurse or tech who's inflating the balloon this is not like a shot ski ring you don't want to inflate the balloon too quickly that's an increased risk for causing more transmural damage once you reach that point of mucosal tear you're really done and then depending on how much you've gotten them dilated if you want to do the dilation protocol uh the evidence from joel richter suggests getting up to 17 millimeters or 16 and a half depending if you're using the balloon or the bougie the studies show that if you use that as just monotherapy patients can go for one to two years before they develop recurrent dysphagia but again it doesn't treat the underlying inflammation so and as much as i enjoy doing the dilations if the patient is willing to take some kind of therapy i think that it's best to do that as well it also for patients who have very significant stenosis even if i do an initial dilation i like to have them on either steroid or ppi because in a way it almost softens up the stricture so to speak it takes away the inflammatory component it might actually make the the stenosis less significant such that either you don't have to dilate uh or you can actually get to a higher level of dilation or you can do more in one sitting so i think it's a great option um but it again just like everything else whether it's diet or the different medications or dilation it really does need to be individualized and the patients just need to understand their options and it is very safe there's negligible increased risk of perforation the worst uh or highest rate of perforation that's been described as 0.3 whereas we typically think of the overall risk as less than 0.1 percent for just a standard egd all right any yeah shout out um so uh so i i'll also let nancy um talk about this as well but um the literature is actually suggests that it's a very poor predictive value for allergy testing um there was like one kid's study that suggested maybe a 50 correlation but really it's closer to about 15 percent and so typically it's there's not really much of a role for allergy testing when guiding food elimination um i'll let nancy comment anything more but i do want to just make a plug that our dietitians are great and this is actually a big commitment and patients need to understand what's involved so that if they're going to commit to it they commit to it right so their services have been invaluable and when it comes to that food elimination protocol they're way more important than the gastroenterologist thanks kevin so um in terms of allergy 100 agree the research really doesn't confirm that we should be automatically sending these eoe patients to an allergist what can be helpful is if there are already other allergens that we should be aware of so we've had patients who came in with a known shellfish allergy or a known legume allergy and that might help us to determine what type of eoe protocol we should be doing and what form of the elimination diet we should be doing so that's how that can help us but otherwise it's not it doesn't seem like it's necessary to involve the allergist otherwise anything else yeah what's the question so i i believe the question and please correct me if i'm wrong if if this is an allergy issue why aren't we finding out what the allergy is well i think probably that i mean the pathogenesis of eosinophilic esophagitis is allergy and we we all agree on that yeah i think i hope i'm answering the question correctly it is an allergy but it's a different uh immune mediating process than say the way uh food allergy testing is done with an allergist they whether it's skin prick or patch testing or even serum ige levels for different types of allergy triggers that's not how eoe works so that's why there is such poor correlation um i mean they can get it done and it you know it just doesn't seem to help uh lead to a more likely uh source for the trigger or triggers and also if a patient has an ige mediated true food allergy they're usually going to have upper respiratory symptoms that are going to occur within 30 to 30 minutes to two hours after a meal this is not necessarily the pattern we see with eoe it's a building up effect correct and so they may eat something eat something be fine and then boom they're having their dysphasia episodes so we can talk with the patient about the differences so that they can understand how those different pathways work and what types of symptoms we would expect to see and why an allergy test may or may not be necessary in their case so my personal belief is and i think the literature supports this is that aerophagia if it exists is exceedingly rare so the vast by far the vast majority of patients who have these this belching disorder this repetitive rapid belching that is almost universally uh supragastric belching and not aerophagia the symptoms you get from aerophagia really are you know you're swallowing nitrogen the nitrogen is getting into the gut and they get bloated it's not so much that they're belching yeah that's exactly right it's this is relatively newly understood um and we have we have to start thinking in terms of supragastric belch rather than aerophagia do you think you don't see any pharyngeal or esophageal peristalsis so it's not swallowing air it's sucking or pushing in the air so that's the distinction manometrically the speech the speech pathology community they use this as a way to teach uh esophageal speech for a long time yes the supragastric balcine is a way to teach teach esophageal speech we don't do that so much anymore because now we create a puncture between the trachea and the esophagus known as the tracheoesophageal puncture and we insert a prosthesis in there and that now is how our laryngectomies learn to talk right yes be truthful i'm not quite aware of studies looking at that and you know i'm going to assume it's done by way of endoscopy i'm not familiar with it though so i don't want to answer incorrectly and the one that i've seen was looking specifically for food sensitivities and irritable bowel syndrome um and i think it's it's being studied but it's nowhere near prime time yeah that's okay was it in this was it the squamous mucosa that was that had the eosinophils in it okay so that's you guys want to weigh in anybody so really so i guess couple points here if number one when you're trying to diagnose eosinophilic esophagitis you really want biopsies from two levels and that should both be in the esophagus and not specifically at the esophageal gastric junction in in this particular case if it sounds like it's in the stomach side of that z line i don't think that i would in any way say that this fits with the eosinophilic esophagitis or would raise much suspicion for me um most likely i would say that this it's probably related to a reflux effect because it's right at the egj yeah great but just to say there are other yeah sonophilic conditions that affect the gi tract other than esophagus the so-called egypts eosinophilic gastrointestinal diseases so you can get esinophelic gastritis you can get eosinophilic enteritis you can get eosinophilic colitis and we don't have the numbers like we do for eoe in terms of more than 15 less than 15 but you can get essentially disorders involving you know the stomach the duodenum and the colon separate to eoe yeah and in some places it gets really murky like the colon who knows what the right number is for a eosinophilic colitis because there are lots of eosinophils there anyway right yeah anything else so those are three absolutely correct absolutely correct anything else so i think i'll speak first we see people who have other things including uh just reflux and they get some of them get subtle furrowing like you'd see in eoe there are some of them who get what's called a feline esophagus which is really not the same thing as the rings that you see with eosinophilic esophagitis it's it's really contraction of the muscularis mucosa causing tiny little ridges that come and go when you're doing the endoscopy anybody else yeah just to add i mean there are there's a differential um for esophageal eosinophilia and especially in someone who wasn't necessarily experiencing prolonged symptoms so they came back and really without any change one thing to consider is maybe some medication that they might have been taking again don't know the full history but that would be something else it's i'd say pretty rare for eoe to just resolve on its own um so whether it's changing diet or avoiding a medication or you know um to lead to resolution of the eosinophilia something should have changed yeah anything else way in the back i'm sorry guys we're right at the we're right at the end of our time so so i've been seeing a lot of these types of conditions with regurge etc with chronic marijuana use it's on the rise here in california but elsewhere as well have you noticed more of these conditions where like in california because of the marijuana use the overeating eating too quickly eating at night i mean you guys can weigh in but personally i haven't i've seen a lot of patients who a lot of patients here like you said use marijuana and i have not seen an association with an increase in regurgitation or rumination or of these other behaviors i mean clearly you see something akin to cyclic vomiting syndrome in those patients that that's true those um or you know you can have the um cannabinoid associated hyperemesis those other conditions you know can be on the rise but in terms of like belching rumination behaviors i have not seen a rise in the prevalence of that yeah i haven't either maybe it's just my patient population anything else back there no so these guys will be happy to answer your questions at the break here uh this group has made a big difference in our practice of gastroenterology in in westwood and in other places where we have uh practices and we can't live without them so thanks guys [Applause] [Music] you

Channel: UCLA Health

Views: 32,057

Keywords: digestive diseases, gastroenterology, kevin ghassemi md, jeffrey conklin md, craig gluckman md, nancee jaffee rd, .lisa lin md, esophageal disorders

Id: yD7EUwcPUhg

Length: 116min 8sec (6968 seconds)

Published: Thu Jul 30 2020