2024-03-20 07 Panel 5 Extra-Esophageal Reflux Laryngitis Laryngospasm Desaturation Bronchospasm

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Panel 5: Extra-Esophageal Reflux: Laryngitis, Laryngospasm, Desaturation, & Bronchospasm: What’s Related to What? Moderator: Matt Brigger (ENT), Speakers: Sari Acra (GI), Edgar Belteton (Pulm), Melissa Brooks (Anesthesia)

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>> Now without further ado, we’re going to get rolling here. So we’re going to be talking about a little bit something different. This is a very, very aero sort of subject right here, an extra esophageal reflex. So and let’s see, here’s your team. Notice we have Scott Rickert who unfortunately is not going to be able to join us today. We have Sariah Crete from Vanderbilt, Edgar Beltaton from Guatemala, and Melissa Brooks Peterson is here from University of Colorado. And unfortunately you are stuck with me as a stand-in for Scott Rickert. So basically I’ll be able to, I’ll spend a little bit of time along the way conveying what Scott, which is he could convey to everybody. So with that, to be able to talk about this whole idea, this concept of extra esophageal reflex and what it really means, and we’re going to start off with the most obvious person to start with, our gastroenterologist on the panel. So come on up and we’ll get rolling. >> Thank you, Matt. So and this presentation is mostly for the non-gastroenterologist, so I apologize if it’s a bit too simple for the GI folks out here. Thank you. Hopefully we’re going to go through all these objectives, but I’ll start off by just some basic definitions and a brief overview of the clinical spectrum of GERD and extra esophageal GERD. So GER or gastroesophageal reflux is what we consider to be physiologic reflux. It’s what most of you are having at the moment, a little bit of reflux after a nice meal, or what we often see in babies who are otherwise healthy and have some spit ups. Now when you add the D to it or GERD, D for disease, then it’s GR or gastroesophageal reflux with troublesome symptoms or complications. And in that realm GERD can be either acidic or non-acidic. Going on with the definitions, Barrett’s esophagus is where you have severe enough reflux to where you go from erosive esophagitis or erosions into intestinal metoplegia so that the lining of the esophagus becomes somewhat similar to the intestine. And that is often a precancerous condition. Erosive esophagitis or what we call EE is just that, erosions, and we’ll see some photos in the next slide. GERD or non-erosive reflux disease is what is the most common type of reflux that we see in children. So if you do an endoscopy, the scope itself will look normal to the naked eye. But when you take a biopsy, you might see histologic esophagitis. Or GERD could also be normal gross appearance but an abnormal pH impedance probe study. Extracepagia reflux is just that, reflux that is outside of the esophagus. And it has a subset called LPR or laryngeopharyngeal reflux. And that’s reflux-related laryngitis. And so on the far left, upper photo is a normal endoscopy or it could also be GERD or non-erosive reflux disease because they look the same. And again, like I said, this is the bulk of patients that we see with reflux. The middle panel represents erosive esophagitis and you can clearly see the erosions. And when erosive esophagitis is severe and consistent, then you get bad esophagus where you have a precancerous condition with intestinal metabolism of the lining. As you can see on the bottom right-hand side, the mucosa is completely more like of an intestine than a normal esophagus on the top right. One thing to remember also is that the more exposure you have to noxious gastric contents in your esophagus. So Barrett’s esophagus, more exposure. You actually have less pain. So you don’t have heartburn in these folks who have reached the degree of Barrett’s esophagus. And then, GERD, which is the normal, normal appearance may actually have more pain than somebody who has Barrett’s esophagus. So that’s important to keep in mind that sometimes there’s a discrepancy between the symptoms of heartburn and the actual pathology. And that also translates into that most children with extra esophageal reflux, 75% of them actually have no esophageal symptoms. And in a later slide, I’ll kind of mention why the airway may actually be more sensitive to acid than the esophagus. Therefore, the esophagus can handle a fair amount of reflux while the airway may not. There are many clinical symptoms of extra esophageal reflux. And you can divide them into infants and children. But they’re actually fairly similar or have a homologous component in children compared to infants. But so going through infants, regurgitation, wheezing, stridor, persisting cough, feeding difficulties, apnea, failure to thrive, recurrent croup, recurrent pneumonias, aspiration. On the older children, you can add dental erosions and bad breath or halitosis. I’m not going to comment too much on the airway findings because Matt will go over those. But there are a number of findings that may go along with reflux, also some conditions in the airway that may predispose to reflux, including laryngomalacia, et cetera. So what is the pathophysiology behind extra esophageal reflux? There are two theories. One is the reflux theory, which entails basically that the material being reflux from the stomach go all the way up and land in the airway causing direct inflammation. There is the other theory, which is the reflux theory, where reflux only happens to the distal esophagus. And then that stimulates a vagal response that leads to bronchoconstriction or asthma-like symptoms or chronic throat clearing. And there’s evidence in the literature to support both of these theories. Again, as I mentioned, the laryngeal mucosa seems to be much more sensitive than the esophagus to any gastric content exposure. And that’s been verified in animal models back in the early ’70s where they exposed gastric material and placed it into the airway of rabbits. And within seconds, the airway was severely inflamed, whereas it took about four or five hours to get the equivalent amount of inflammation in the esophagus. So there’s a difference between how the airway reacts and the GI system reacts, partly because of the lower expression of carbonic anhydrase in the airway epithelium, so less acid neutralization. Also, the pulmonary epithelium is much, much sensitive to pepsin exposure. And so there are known risk factors for GERD, and we pretty much know these, I think, as an aero-digestive community, but neurologic impairment is obviously one, repaired esophageal atresia, diaphragmatic hernias, chronic respiratory conditions. Laryngomalacia can act as a suction pump, obesity, and obviously also family history. Now, we don’t have actually numbers on the incidence of extra-physiogastrous, gastrous-physiogarrelia reflux. We have some estimates on GERD, and it varies between, you know, 2 to 10%. We do know that there’s a peak of reflux in infants at age 4 months, and most of them resolve by age 13, 14 months. But when you actually look at these kids who had reflux in infancy, the more severe ones actually will have another peak later on in life, and they will have an increased risk for vomiting, heartburn, and acid regurgitation compared to controls. We don’t have estimates on the prevalence of extra-physiogarrelia reflux, except from small case series and case reports. So, in many ways, the data you see here are amalgamated from about 15 different papers, but they may represent, and I think they do represent an overestimation of these. But nevertheless, they do show some associations. So, if you have reflux, there’s a chance that you may have sinusitis, otitis, dental erosions, asthma, pneumonia, bronchiectasis, and general respiratory symptoms. The reverse is also true. If you have a chronic respiratory condition, such as asthma, or apparent life-threatening events, or laryngotrichitis, then you’re more likely to have reflux associated. And the thing to remember is that, like I said, these are unproven. They’re not by controlled studies. So, I would not assume that anybody has extra-physiogarrelia reflux based on symptoms alone without considering other etiologies or trying to prove that they have reflux. So, how do we diagnose reflux? We have several — our exosophageal reflux, we have several tests. Clinical diagnosis, the clinical history may be helpful. For example, the timing of coughing in relationship to meal or having coughing at night. However, clinical history by itself is of modest sensitivity and specificity. The same thing for an empiric therapeutic trial of acid blockers. The placebo effect is high and the sensitivity and specificity is low. Our main tools are pH monitoring and impedance monitoring. And now, they’re combined together. They may give us an idea about the extent of reflux, how much time you spend on reflux, and also a correlation between the symptoms such as cough and a reflux event. Again, there’s an element of false negative with this test even though it’s our gold standard. Triple endoscopy is obviously helpful. On the EGD or endoscopy front though, it’s not helpful in diagnosing reflux that much. It’s more in excluding other conditions such as EOE. I’ll let my pulmonary and ENT colleagues comment some about the bronchoscopy findings. But they may offer some utility. And then from a radiological standpoint, the main test that might be helpful in evaluating for exosophageal reflux is like Dr. Torres mentioned and showed you some CT scans where you have bronchiectasis on a CT scan indicating chronic reflux. This is the impedance pH catheter. Every two black units are one unit where you measure electrical resistance between these two points. The red point is our pH meter. And so between these two points, we can actually measure electrical resistance as the food bolus moves, electrical resistance will change, and then you can tell whether it’s a swallow or a reflux event. And so this would be representative of a food bolus going in. The resistance actually drops because food or solid food is a conductive of electricity. And that would be a typical sort of food bolus. And we can determine then whether it’s a swallow or a reflux event. And we can correlate it with a symptom when the folks press on a symptom button. And finally, talking a little bit about medical management of GERD, we all know there are some nonmedical approaches. Medical approaches, principally proton pump inhibitor therapy, sometimes it changed in the way you feed or where you feed. So thickening the feeds in the — for G-tube fed kits may be helpful or feeding beyond the stomach into the jejunum would be another option. And very rarely surgical options. And the key take home points for treatment of exosophageal reflux is please do not empirically treat without trying to get proof or considering other diagnoses. And of all the tools that are out there available to a gastroenterologist, the pH impedance is the one that is most likely to be best at diagnosing exosophageal reflux and correlating it with symptoms. [ Applause ] So now we’ve established that reflux definitely occurs and definitely affects outside of the esophagus. So this is something that we’ve argued in the arrow circles for a long time. And so now we have proof he has said it, at least to some degree. So with that though, we’re going to talk about sort of the next place. And I’m going to have Dr. Belton come on up here and he’s going to talk to us about on the pulmonary side of things. [ Background Sounds ] [ Background Sounds ] [ Foreign Language Spoken ] [ Background Sounds ] — of history. Through history Aristotle has said, and when you speak about Aristotle, you say he doesn’t miss it. So you will tell me at the end, he did fail. He said what is current is always — comes always before than the potential, speaking about the chicken, I guess. And then history, Papineo Brookfield, a philosophy professor in London, says in the last year science has had thousands of changes and even so the conclusions are not final. But it seems that the egg comes before a chicken. For an egg to become a chicken, there you must have an egg before. So then the evolutionary theory changes and Professor Brookfield from the United Kingdom says the genetic change process in the species comes through the egg. So we have a little bit more clarity. Now, living aside philosophy and history, let’s speak about the extras of a geomanifestations of GERD. The extras of a geomanifestations that are relevant for us include three factors. One, chronic cough. Chronic cough is basic. The chronic cough is the daily consult of the pediatrician, especially when we work in pulmonology. Asthma is another of the very common diagnosis and chronic exponential syndrome is becoming an entity that is also very important. We’re getting acquainted with it, but that part we’re getting acquainted with is that we see a group of patients that don’t die anymore. These are the patients that come out of NICUs and sometimes parents receive them, not in the best conditions, neurological conditions of all, but they receive their children, they receive a problem actually and there is a longstanding medical problem. Many of these respiratory symptoms then appear and going back to what we just heard from another point of view, the gastroenterologic point of view, I will emphasize the pulmonary side too, serious reflex theory. If we go back to the anatomy of the process, we have the vagus and the brain stem. The vagus is throughout our body and has the characteristic of being gastropulmonary and gastrointestinal in its innervation. And if the vagus is affected, then the response will be bilateral on both sides. So we have to think that it is a tracheobronchus of ideal reflex. That’s how it is called, mediated by the vagus nerve and induced by reflex based in embryology, the same origin for the gastrointestinal and respiratory system. And due to that, there is a sharing of the vagus nerve. Now, if we go into the three pathologists mentioned, chronic coffers, it’s worthwhile for the neurologist in pediatrics, it’s important to define it. Chronic cough is vague, but the definition has changed and it’s always important to separate adults from children and being pediatricians, we have to differentiate between chronic cough for a child or an adult under 14 years of age. Over the four weeks is defined as chronic cough. The cutting point is four weeks. So chronic cough is attributable to an underlying problem. And then we have a chronic cough that can be identified after an evaluation. A cough without concrete characteristics. We need to understand the definitions to standardize the clinical approach. Different than what we say for adults, totally different. Acute cough is less than three weeks. Acute between three to eight. And chronic if over eight weeks. So we are speaking about timeframes that are totally different in adults and children. The origin is pulmonary, generally speaking. So asthma, prolonged bacterial bronchitis, and chronic suppurative pulmonary disease are the consequence of bronchitis. [ Speaking in Spanish ] [ Speaking in Spanish ] [ Speaking in Spanish ] [ Speaking in Spanish ] [ Speaking in Spanish ] [ Speaking in Spanish ] When there’s neurological damage, we have as an exception the primary evolution and the laryngeal disorders, trachea suffigial fistulas. So in the non-pulmonary etiology, especially the controverted for us, continue to be gastrosophageal reflux as the first possibility. Now looking for answers, we have to continue to mention our dear friend, Dr. Annie Chang. Over 10 years ago, she performs this carousal study where she tries to find cohort studies where Kronikoff has been mentioned in a series of studies. She brings together, she analyzes all these studies trying to find the etiology and they see Kronikoff in children. She does a systematic review based on key questions. The main idea was to evaluate the most frequent etiologies of Kronikoff. They had the following questions. Are the more frequent etiologies different from those in adults? Are the more frequent etiologies, do they depend on the age or the environment? Are there environmental aspects altering Kronikoff in children? Or is it the age also? Sleep obstructive apnea causes Kronikoff in children? And then they decided that the etiology in children is different than in adults for the three questions answered. And there you have the answers. I won’t read them. It’s a wonderful study that gives us the context of Kronikoff in the pediatric age. And three, four years afterwards, another study on Kronikoff, specifically gastrosophageal reflex in children. And she says recently that the same group publishes another study. Four publications were reviewed for questions one, for question two, two, four, three. No publications were found. And the question said, children that do not have gastrointestinal symptoms should use a perical treatment. And the answer, the answer is in children under 14 years with Kronikoff without pulmonary pathology, we recommend not to use medications for gastric fragile disease like regurgitation, positions, epigastric pain or stomach pain in older children. Well, little by little answers are obtained. But the conclusion of the study is that we need to be more cautious with the indiscriminate use of medications for the management of reflux because the benefit so far is a big question mark. Asthma is a disease. Now we’ll leave aside Kronikoff and we will speak about asthma. And asthma is one of the most frequent diseases in children. Nothing new for all the audience. Prevalence, 11.7 in children, 13.4 in adolescents, 5.8 million in the United States have been diagnosed in 2020. The coexistence with GERD is more frequent than what we thought. The presence of asthma increases the chances of GERD in 2.8 percent. Children that do not improve, you must check adherence to treatment if there is poor, if there is still poor response, other causes of the pulmonary symptomology have to be assessed. So there is a pathophysiological relationship between asthma and GERD. But we have to be very careful in doing precise diagnosis not to try to benefit patients with drugs or medications that finally won’t be really beneficial. The physiological relationship, cough increases intra-abdominal pressure, this is what we believe, which increases the pressure. Air entrapment causes a descent of the diaphragm. Hyperinsufflation alters the relationship between the pleural part and the gastroesophageal junction. There is an increase in the negative intracephagial area and some specific drugs also help to increase the presence of reflux. This is quite a large study in Chinese population. Big studies can be carried out, bidirectional, where the authors have the hypothesis that there’s a bidirectional association between GERD and asthma in children. And this goes in the two directions. So they do two longitudinal studies with figures of patients, 86,000 asthma patients and 86,000 controls. And the results are not very conclusive. Asthma increases the risk of GERD and in turn GERD increases the risk of asthma in children. Well, both go hand in hand. And I think that it could be an interesting conclusion. In this study, and I won’t bore you with more studies in this control, case studies, all the patients evaluated from 96 to 2,000 in the Texas Children’s Hospital of Houston were evaluated. And patients with reflux have more risk of presenting asthma as compared with those that do not have the reflux disease. Management of asthma reflux, the patient with asthma moderate to severe wheezing at night. Suggestive symptoms of reflux disease has seated irritations indicated to do a therapeutic test of four to eight weeks with the PPIs. And if the patient has no symptoms, it is not recommended to use PPIs in children with asthma without symptoms of reflux disease. But some patients can present silent reflux disease. It is reasonable to do tests in patients with nighttime pressure or use of asteroids. And finally, and very quickly, I’m going to speak about chronic pulmonary aspiration syndrome. This syndrome is given by a dysfunction of swallowing aspiration of saliva and GERD. And it seems that the reflux happens in almost 6% of cases. The predominance of pneumonia three times more. This is the pathophysiology of what is recognized as the chronic syndrome. As you can see, there is a perfect relationship as far as the phageal function, airway function. If that perfect relationship is broken, we start to see problems of microaspiration of gastric content. Esophageal clearing does not happen properly, so we have the vocal folds affected. The microaspiration of acid leads to inflammation and bronchoconstriction. Weak acid, now it is very fashionable to speak about bronchospiration of weak acid and reflux of acid with pH under 4. Broncholvular lavage of these microaspirations present concentrations of epithelial cells with bronchial hyperresponsiveness. Bio-acids and pepsin are, together with the growth factor, transform TGFV through a kinase protein activated by metagen P38 dependent on the growth factor and connective tissue. This leads to cell damage cytokines, leukotrienes, thromboxanes, and the whole inflammatory chain. Well, a couple of years ago, we learned a lot about it in TILUKIN-1, tumor necrosis factor and IL-8 are also stimulated and there is a loss of the architecture of the parenchyma with collagen deposition. This very small aspiration that could be happening every day in that patient could lead to fibrosis and bronchiolitis of riturans, which is the role of the pediatrician, the pneumologist, those who work in this area. Well, right now, you have to intervene in this big chain of that algorithm of the whole team that is being managed by the patient who is having chronic pneumopathy. The role of CURD in the pathogenesis of respiratory conditions of the lower airway. The variety of methodologies used makes it difficult to interpret the outcomes. That is the big problem when we try and find analysis from different studies. Different variables are used. The absence of a standardized definition for respiratory symptoms is another big disadvantage. Absence of time relationship between the onset of signs and symptoms, and signs and symptoms of CURD. Absence of representative control group. Also, it’s a risk factor for aspiration, the presence of CURD. Treatment, I want to add on this. Treatment of reflux is done by the gastroenterologist, and he knows much more than we do. And these are just two more slides. I think the take-home messages are as frequent causes of chronic cough are asthma, bacteria and viruses, nonspecific cough, CURD, and the upper airway cough syndrome are controversial causes in children. You have to consider treatment for chronic cough as symptoms of CURD in patients with clear symptomatology and pathologic tests for CURD. The treatment only with gastric acid suppressors. It shouldn’t be used as treatment for chronic cough. It’s difficult to prove cause-effect relationship between asthma and reflux. However, the evidence suggests that they share a complex mechanism that could be reciprocal. The treatment of CURD in patients with asthma must be considered when they present moderate to severe asthma with symptoms of CURD. If they have asthma that is steroid dependent, if they have symptoms that start at night, and in those that have excluded other specific symptomatologies. Finally, the chronic pulmonary aspiration syndrome happens in children with underlying medical conditions. The treatment of this chronic aspiration syndrome has to be started with medical conservative measures and only scaled up to surgical procedures in some cases. Due to the complexity presented by a patient with suspicion of lung symptoms, they have to be assessed and treated by a multidisciplinary team. It is ideal to have diagnostic evidence to guide the treatment to be performed and you have to avoid using unnecessary medication because of the adverse events that we all know they can cause. And these are thanks from Children of Guatemala for all of you. [Applause] All right, excellent. Thank you so much, Edgar. So now the case builds. So we know the reflux is a thing out there. We know that it definitely causes these problems. We know that it affects the lungs. We have pathophysiology. It may be all circumstantial evidence, but the circumstances are getting closer and closer. So now we get to the crossroads here and the ENT perspective. If there’s anyone who knows about circumstantial evidence, it’s us. We have definitely got circumstantial evidence down. So what about it? You know, this kind of in between. So we know, at least we say we know, that we know extra self-geo-reflux affects the airway because at the end of the day, very much as Christopher related, early on when aero-digestive programs are coming together in Cincinnati, we had airway reconstructions that certainly were not failing because of our surgical technique. We know that’s not the reason. So it’s got to be some sort of pathophysiology. So when we think about the airway and swallowing and how this all comes together, we think of this common innervation. Certainly the common innervation will make sense that we have where reflux is going to be affecting the airway because clearly it’s making its way down to the lungs. So somehow between this coordination, taking the fact that we know that without this overlap between the two areas, we need to be able to understand really how do we make sense of all this and who are the risk factors. And we’ve talked about this as far as we go through here, risk factors for — but from our standpoint, when we look at it, we look at kids from a breathing standpoint, whether it’s kids who are having these ALTIs and we’re getting called about that to assess the larynx or if it’s because we’re about to undergo an airway reconstruction or worse yet, you failed one. So as was mentioned before, we know that the laryngeal mucosa is more sensitive than the esophageal mucosa. So therefore it makes sense. Whether you do the reflux theory or the reflux theory of the manifestations of extra esophageal reflux, we know that the laryngeal mucosa is different. So that gets us into, well, how do you link this stuff? Well, we know that when we take these different pieces and puzzles and we come across this place where this intersection occurs, we talk about the symptoms. And so certainly, Laryngomalacia, we’ve been pointing at that for years. And I think the beauty of these — of our programs as we come together is that we understand that maybe an otolaryngologist is throwing reflux medication at noisy breathing is maybe not the way to go, but still it’s done and something that we do on a regular basis. So then it’s trying to understand that. And I think we’ve gone down the road before many, many times of trying to look at it. And I think that when we take the expertise that’s been stated already as we go through, we know that there’s this, well, the larynx looks red. Well, if I change my video parameters, I can make it look even redder and then I have a better explanation. We — ADEEM is in the eye of the beholder for so many of these things. We also know that the way that the larynx develops over time, that when we start trying to balance this out, we find that while we bring all these parts together at this crossroads, still at the end of the day, there is something going on here. And I think that’s really where it takes this coordination between everyone working together. And so when we say that we take these laryngoscopy findings, these bronchoscopy findings, and we tie it all together, we use it with the information we get from the pH probes. We use it with the information that we get from doing a broncho — BALs and working our way towards coming up with a comprehensive plan for these kids. I think it’s really important that we realize that as we step back and look at the entire picture, when we talk about the things that are most concerning from the otolaryngologist site, particularly from the airway surgeon side, it’s seeing that we’re really concerned about how this comes together and manifests from a healing standpoint. And I really think that while the evidence is not high quality, it’s not out there, there are certainly the protocols that we work through together to try to come up with some sort of a way to prevent this. And I think that’s really where this whole group comes together. And I want to make sure that we have time for our cases, so what we’ll do is we’re going to keep moving along here. But we’re going to come back to this common theme where the reflex is certainly playing a role in the care of these children. But at the end of the day, while the information — while the data is circumstantial, it’s really important to how we move through. And with that, Melissa is going to come and talk to us about the idea for the perspective of the anesthesiologist. [ Applause ] >> He did a very nice job reading Scott Rickert’s mind from halfway down the world. So I’m back, your anesthesiologist. The chicken versus the egg question is an interesting one, particularly for me, because when we evaluate kids for reflux, I really care the most about getting them through the case that we are asked to do safely. But frequently, the reason why — oh, this is my favorite cartoon, by the way. This is from Curious George Gets a Job. You should all check it out. It has a very good description of an inhaled induction of anesthesia. So the chicken or the egg question is really curious to me because a lot of the reasons and times that I anesthetize a baby is because we’re asking those questions. And so we don’t know what’s going on, but the kid is coming to the operating room for a procedure to help us determine what’s happening or to possibly treat the effects of extra esophageal reflux. And so I really spend a fair amount of time trying to just sort kids into scary and not scary. I’m pretty simplistic, but scary to me, either aero patients or patients who have a broken elbow who need it pinned, a toddler or a child who regurgitates regularly, like actual food in the mouth regurgitation, a child who has a vomitous taste in the mouth at night or in the morning. One of my three kids can pretty clearly describe that. He has EOE, and he also gets reflux symptoms from his EOE. Anyone having an open airway procedure with lengthy time or multiple steps, not because they have reflux, but because I’m worried about anything that’s in their stomach, including saliva from being nervous coming up into their esophagus and into their airway while the thing is wide open and they anesthetize and they lose all tone of sphincters. And then any patient with either delayed gastric emptying or a chronically full GI tract for one reason or another, short gut syndrome, all sorts of other GI issues. Things that aren’t scary to me, these won’t surprise you, the fake baby GERD I referred to earlier, kind of that pendulum swing of all babies used to be on PPIs, now we kind of hope no babies are on PPIs until they prove themselves. Any baby who is not scary, who has some pulmonary manifestations or like a casual diagnosis of GERD, so I’ll frequently in aero clinic ask families, GERD is listed on the patient’s problem list, but how did that diagnosis come about? When were they diagnosed? Were they put on medication or were they reassured that their baby had normal baby reflux, but it still ended up in the chart? So, an in-person assessment of those questions to me is important. I can’t really do that on a day where I have 12 healthy ortho cases in the operating room, but with complex kids, especially in an aero digestive setting, it’s important to me to figure out if we think that this is food or refluxate that I’m going to come across under anesthesia. And then to have that conversation with our team about what we really think is going on and what we’re going after and what we’re interested in looking at for whatever study the child is signed up for. And then I think more about the, sorry my GI friends, but the end organ about what I’m the most responsible for managing and what gives me the most headache on the recovery room side is pulmonary risk stratification for these patients. So, again scary and not scary sorting. Patients who live on a lot of oxygen, either asleep or awake, scare me because if they also have reflux or an aspiration event, the likelihood that I’m going to return them to their former state is quite low without an adventure through the ICU or the floor being admitted where I would have previously expected them to be able to go home. Especially if they have severe pulmonary manifestations of their reflux, like indirect evidence, multiple pneumonias, they’re always admitted when they get a cold, like kids should be able to get a cold and not end up in the hospital, or that they’re having frank witness to aspiration events, which is the rarity. I always also like to do an in-person assessment of the impact of what this potential reflux is on their pulmonary status, get an idea of what their baseline is when well and when ill. And then integrate that plan with the whole team. I referred to earlier the CT scan or not CT scan plan with our pulmonologists, and I think we can really only get the right studies under anesthetic conditions if your anesthesiologist understands what you’re looking for and what’s going on with the whole patient. It’s a reasonable conversation probably for happy hour later about where should we do this risk stratification and modification, and I think the answer is it depends. I think for aero-digestive patients I hope that with time I will make a strong case for assessment in your aero-digestive clinic given the complexity of our patients. I think it’s important also for especially our complex kids to avoid the day of negotiation and frustration. Like if I feel like a kid has a full stomach or is GJ fed and got their J tube feeds up until two hours before because oh gosh they’re going through the J, they’re not in the G, I’m like that can’t possibly be true because you put a GJ in for a reason. The day of negotiations and frustrations especially for complex aero kids we avoid by seeing the kids ahead of time. So it is a thousand percent possible to accomplish assessment of extra esophageal reflux or the absence of or the question mark if that’s what you’re diagnosing and how to risk stratify and care for patients if you have a team that backs you and like Emily DeBoer said you find your people. So I, we’re going to skip this slide. We’ve talked about triple endoscopy. Options for managing kids with suspected severe reflux is to have an anesthesiologist that can address changing the order of the cases. So in kids who we know have full stomachs reflux, delayed gastric emptying and are sitting ducts for a massive and frightening aspiration event we will frequently change the order of our procedures meaning we do an inhaled induction, let ENT take a very quick look at the airway and the subglottis and the trachea knowing that time is aspiration and then we will secure the airway and make unfortunately our pulmonologist then scope through the endotracheal tube to kind of triage what our most important information is. But you can’t have an anesthesiologist that’s ready to do that unless they understand the patient and the plan from a team standpoint. Also, one thing, we’re going to skip through all these. The last thing I will say is that we do all kinds of funky stuff in the operating room for totally different types of surgeries including for example, pyloric stenosis where we have this, it’s actually oddly enough scientifically like studied phenomenon of awake suctioning a baby with a gigantic NG tube prior to the induction of anesthesia when they have pyloric stenosis because we know that they have hundreds of cc’s of gastric contents and usually all formula even though they’ve been MPO for usually about 24 hours. So we do this multiple pass suctioning thing where we have the baby sit up and then we lay the baby on one side and we suction with this big hose and then we lay them on the other side and then sometimes we tip them the other way and it’s kind of this multi planar multiple pass suctioning. The kids hate us, they scream bloody murder but they have an empty stomach when they go to sleep. So in the worst case of scenarios we can approach it like that. That’s a little extreme but it works, it works like charm. Knock on wood never had a baby aspirate after or for a pyloric so that evil suctioning works. Take home lessons for me especially when you’re managing potential aspiration in the question of extra esophageal reflux, I’ve said it again, I’ll say it forever, find a champion. The people in this picture below are some of our aero champions at Children’s. When your champion speaks up like if I’m massive NG tube suctioning a aero baby it’s for a reason like I don’t do it just for fun. So listen when your champion speaks up and also be flexible and be trusting which are two things I think we’re pretty terrible at in the operating room so consider it. That’s it. Let’s do some cases. Yes? Yeah, that’s it. Thank you. [Applause] All right. Well, so once again surprising that in the aero discussions that we all have a lot to say and I think that’s really kind of just goes to show as we’ve shown during the course of this day that there are a lot of different things to be said about these really complex subjects. So right now we’re coming down to the end of the time for this session. I want to go ahead and take see if we have any questions out there. Burning questions. We do have a case that we could go through otherwise. Extra esophageal reflux we answered everything. Perfect. Thank you very much for excellent talks. I’m Chetan Pandit from Sydney. I’m a respiratory physician. We look after quite a few patients with Tiofisciula. I have a couple of questions. So my first question is the Tiofisciula patients they also have esophageal dysmotility in addition to the stricture. So at any stage do you consider using a prokinetic drug? That’s my first question. And second question is if they are on PPI how long do you leave them on PPI? So I rarely use motility agents in esophageal atresia patients because most often they don’t work. So they’re usually at the tail end of the therapies that we try. And then with regard to PPI therapy that’s the problem of doing empiric treatment. I see kids who have been on PPI therapy for three, four years with no discernible improvement in their respiratory symptoms or they’re just still on the medicine. And so whenever I get a patient like that I might take them off the PPI and actually do a pH impedance probe study to document that do they actually have reflux or not. Great. Thank you. Thanks. I think that’s such a good point too like trying to think about this because we do run into this and whether you have pH impedance at your disposal or not is having this idea of being able to really be able to test. And I think while we talk about all the circumstantial evidence you do have to have something to sort of base off of. Olaf. Sorry. Looks like Dr. Jennings had a question. Thank you. [Spanish] You said somebody translate that. [Spanish] Okay. [Spanish] Management. I mean that’s the most difficult part of treatment because there is no medical, pharmaceutical treatment for that except if there is an underlying motility disorder in the stomach then that might work. It also depends on the age group. So if we’re talking about an infant who is apneic at age two months because of reflux then the management and it’s usually nonacid reflux at that point because their food is buffering their acid. Then the management in that scenario would be to actually treat them by feeding them post-biolarically so that we’re actually not exposing them to that much of a volume. Time for one more question. You mentioned esophageal dysmotility in the esophageal atresia kids. All of them have some form of esophageal dysmotility but I would like to bring up the point that there are a spectrum of dysmotility all the way from a rigid tube to a completely flaccid esophagus to different types of contractions and sometimes the upper segment has a different motility in the lower segment and sometimes there’s a strict in the middle. The esophageal function in esophageal atresia children who’s been repaired is exceedingly complicated. So when we say they have esophageal reflux, they have dysmotility, it just admits there’s a problem. I would make the plea to really understand the problem both from how the esophagus is working, for instance, almost all of them have a cricophagous muscle that will close and pressurize the esophagus but whether it goes down and how it goes down needs to be understood. In addition, a great number of them have some form of gastric pull-up where the GE junction is above the diaphragm, above that pressure zone so it’s not going to work so now you can have kind of reflux and many times when the pediatric surgeon is repairing the esophageal atresia, he’ll injure the right vagus nerve, completely unintentional of course, and now you may have pyloric dysfunction, you may have gastric emptying problems and that’s going to worsen transition of fluids from the stomach up into the esophagus. What I’m trying to say is it’s really complicated and it needs to be really understood and your group, these aero-digestive groups are really one of the sources that we can understand this and make progress. And final comment just so I can throw a little nuclear bomb in the middle of everybody. The aero-digestive groups are great but you’re missing the experience of the pediatric thoracic surgeons. Like this comment I just made, every time you guys lecture I want to talk for an hour about things I could improve upon. I would ask that the aero-digestive groups start considering incorporating pediatric thoracic surgeon in your diagnosis, your treatment and in your follow-up. There’s only a handful of us, there’s maybe eight of us, I don’t know how Jason, but we would love to start giving you our experience and help teach you and build your own pediatric thoracic surgeons in your practices. Perfect, it’s exactly what aero is about and I think that comment really kind of seals it all together on how it is not an exclusive type society, this is inclusive of everyone we can and we need to figure out these problems. And so with that I think we’ll move on to the next plenary lecture, the first and only. [Applause][APPLAUSE] (audience