Fuad M. Baroody, MD, discusses Pediatric Obstructive Sleep Apnea.
[MUSIC PLAYING] DR. FUAD BAROODY: Hello, my name is Fuad Baroody, and I am a Professor of Otolaryngology, Head and Neck Surgery, otherwise known as Ear, Nose, and Throat, at University of Chicago Medicine Comer Children's Hospital. And I'm also part of the Department of Pediatrics. And my specialty is taking care of children with ear, nose and throat problems. And what I was going to share with you today is some thoughts and some teaching about pediatric obstructive sleep apnea, which is difficulty breathing in children while you are asleep due to obstruction. So if you look at an entity called sleep disorder breathing, it's a wide spectrum of problems. And it ranges from the child who just snores without any problems with drop in oxygen levels or high end-tidal CO2 or repeated arousal. So these are called primary snores. There are many kids who snore and have no other sequelae from that. Then we come to a secondary entity, which is called Upper Airway Resistance Syndrome, which is a slightly more severity entity. And these kids snore and work hard to breathe at night, and they do have repeated arousals but do not have hypoxia or hypercarbia. And finally you come to the full-fledged obstructive sleep apnea, which is snoring with apnea, intermittent hypoxia, hypercarbia, and repeated arousals. And if you look at the proportion of kids who have these entities, about 12% of children in the United States, probably throughout the world, will snore. And only 3% of those will have the full-fledged obstructive sleep apnea with the gas exchange abnormalities. So we will concentrate talking a little bit more about these children with obstructive sleep apnea in the next slides. How do these people present? They are snoring. They have their mouth open. And oftentimes not just at night, but when they come to your office during the day, they come with their mouth open. They're audible breathers. You can hear them breathe. When they're asleep, they seem to pause and get apneaic episodes where they pause and then compensate by a big breath afterwards. That leads to shallowing of their sleep, microarousals, and wake-ups at night. So these kids often will wake up at night. As a sequela of that, their sleep is fragmented, and they usually are not getting very restful sleep. And they tend to have issues during the day, or sequelae of obstructive sleep apnea. Some are sleepy, take multiple naps, get crabby towards the end of the day if they're not napping. Some are hyperactive. There's a strong association between ADHD-type behavior and obstructive sleep apnea. Some bed wet for reasons of bladder control that happens in correlation with sleep apnea. And rarely, but sometimes, we see children who have such severe obstructive sleep apnea from such a young age that they present with failure to thrive and growth retardation-- not very common this day and age, because parents usually bring these children to our attention earlier. A typical exam in children-- and please concentrate, those of you who take care of kids and grownups, that this is a different entity in kids. It has common elements with what we see in adults. But in kids, this is by and large an entity related to adenotonsillar hypertrophy. So children on physical exams typically have large tonsils and adenoids. You see the picture on the left has what we call 2+ tonsils. They're large and full. You see them on both sides of the uvula, but they're not touching each other or touching the uvula. If they touch the uvula, they'd be labeled as 3+ tonsils. And when they touch each other, we call them 4+ tonsils or kissing tonsils. And those are often what you see when you examine these children. Obesity is an important correlation in children with obstructive sleep apnea, especially the older kids. We see more and more these days children who struggle with sleep apnea and who potentially could have persistent sleep apnea even after adenoid tonsillectomy if they are obese, and kids who have neuromuscular disorders or craniofacial disorders, clearly those anatomical problems will play a role in obstructing the airway in addition to obstructive sleep apnea. But we'll concentrate on the run-of-the-mill, regular presentation of obstructive sleep apnea in kids. If we have doubts about the diagnosis and the tonsils are not that large, we sometimes will visualize the adenoids by obtaining a lateral neck fill. And this is an example of that. And you see, in this film, it's a black and white film, and air is the black air column. So you follow the tracheal air column. And then when it goes up towards the back of the nose, behind the soft palate, as is shown on the screen, you will see there's a complete obstruction of the nasopharyngeal airway. And thus, this is a reflection of very large adenoids. And this is a child who will walk into the office with mucus dripping out of their nose and their mouth hanging open, and they're breathing very noisy. And at night, they start snoring and having these interruptions. So a child like that would have a very typical clinical presentation. Polysomnography, or sleep study, in addition to the symptoms is the golden standard. We know very well that there is not a good correlation between parental observation and reporting of apneaic episodes and a polysomnogram. So very often, the parents will tell you, oh, my kid snores mildly, they do no stop. You do a polysomnogram, they turn out to have obstructive sleep apnea. The reverse is true. Sometimes the parents come very worried about their child, telling you that they obstruct and they stop a lot. You do a sleep study, the sleep study is not that abnormal. So by and large, the golden standard of determining this diagnosis and making it, in addition to the clinical picture, is a polysomnogram. And there will be other talks on our website that will focus on the physiology of how you obtain a polysomnogram. For the purposes of my lecture, basically this gives you multiple channel monitoring of the child asleep. We look at the duration and efficiency of sleep. We look at EKG and EEG monitoring. And the EEG is very important to look at the stages of sleep and the arousals. We also look at obstructive apneas, complete cessation of breathing, and obstructive hypopneas, shallow breaths. We look at changes in pulse oximetry with hypoxia, which typically happens during the apneaic episodes. We look at arousals. And we look at hypercarbia, the physiologic changes. And these are reported. Typically they are read by our sleep experts. We have a pediatric sleep section here at Comer Children's Hospital, and they will look at report apnea-hypopnea index, which is the number of abnormal breaths per hour of sleep. They will also tell me how much this happens in REM sleep and they tell me how high the end-tidal carbon dioxide was and how low the saturations went. And all that report allows us to determine the severity of obstructive sleep apnea. And in general, for kids, again, the guidelines are different than in adults. Most experts agree that an index between one and five is considered mild obstructive sleep apnea, an index between five and 10 is considered moderate obstructive sleep apnea, and an index over 10 in a kid is considered severe obstructive sleep apnea. Now, who do we get a polysomnogram for? I am lucky to work in a place where we have a very strong sleep medicine section, pediatric. So there's easy availability of pediatric polysomnography. We have about two or three beds a night where we do pediatric sleep studies, and I can get a sleep study relatively quickly. As a tertiary referral, I see kids who are relatively complicated. But for people who are out in practice, these are recent guidelines from our Academy of Otolaryngology, Head and Neck Surgery, published in 2011, that looked at all the existing literature and tried to suggest when one should do a polysomnogram-- obese child, the child with a syndrome, Down Syndrome, craniofacial abnormality, neuromuscular disorders, sickle cell disease, mucopolysaccharidosis. All these will present with complicated sleep apnea and should get a polysomnogram. You should also get a polysomnogram if the history is not obvious. If a patient has big tonsils but the parents don't think they're snoring at all, you might want to get a polysomnogram, make sure we're not missing obstructive sleep apnea, especially if they have daytime sequelae that go along with sleep apnea-- for example, they're hyperactive, they're sleepy during the day, they're not doing well in school. Or if the tonsils are very small but the parents are very worried. Again, that's another reason to get an objective test, and that test is the polysomnogram. What are some sequelae of obstructive sleep apnea? Physiologic sequelae, recurrent hypoxia is the culprit. It leads to alveolar hypoventilation, carbon dioxide retention, and hypercarbia, with secondary pulmonary edema, pulmonary hypertension, and ultimately right heart failure. Luckily, we catch all those kids before they have these problems. But we've seen a few who will have all these issues because they don't present quickly enough. Other sequelae that are much more common and much more important on a quality of life perspective, it does affect the quality of life, it sometimes leads to failure to thrive, behavioral disturbances, attention deficit hyperactivity type issues are much more common in kids with sleep apnea than in normal controls. Excessive daytime sleepiness, poor learning, poor performance in school, bed wetting, and there's some data that's emerging about the presence of systemic inflammation in these kids, kids suggesting that this is not just a snoring, wake-up type problem, but it leads to systemic sequelae. This is an example of a study published in 2008 looking at quality of life by administering a questionnaire. The domains are on the legend on the right, and you can look at those at leisure. And when you look at the line at zero, to the left of the line suggests poorer quality of life in the child with obstructive sleep apnea compared to a healthy control. And what you see here is for almost all of those domains, the kids with obstructive sleep apnea have significantly worse quality of life than their healthy counterparts of similar age, matched for age and sex and others. This is a very nice study that was done while back but I think is very important that was done by Dr. David Gozal, who's the Chairman of Pediatrics here at our institution. And he looked at almost 300 children in first grade who were not doing well in school. So he picked a slightly biased group. He looked at the people who were performing in the lowest 10th percentile in grades in first grade. And then he administer questionnaires to look at snoring. And then the kids who had trouble, he did the equivalent of a sleep study, but he sent monitoring with them at home to look at transcutaneous carbon dioxide and pulse oximetry, not a full-fledged study. And then the kids who were found to have the equivalent of sleep apnea, the parents were informed. And some of those parents took care of their kids, which means they took them to an ENT like me, and they ended up removing their tonsils and adenoids. And there's a portion of parents who did not act on this. And then he followed these kids the year before intervention and the year after intervention and looked at their grades in first grade and second grade, and I'll show you the data in a minute. This is the questionnaire response. Look at the questionnaire score. The higher the score, the worse the problems with breathing at night. And when you see in the first two columns, the NT and the TR refer to the group who had the most severe symptoms. These are the kids with documented obstructive sleep apnea. And the NT is the non-treated group, and the TR is the treated group. And you see that both have equivalent severity of symptoms during sleep. If you look at the kids who had primary snoring-- so these are kids who snored and scored at about a six on the questionnaire but did not have any gas exchange abnormalities. So the equivalent of a sleep study at home was essentially normal. And you had a bunch of kids who also were not performing well in school who were fine and did not have snoring problems. And these are called the controls. And then what you will see in this slide is very striking in my mind and very interesting, in that such a soft parameter as school grade, you could see a significant change after intervention like that. And let me walk you through that. To the left is the first graders, to the right is when these kids became in second grade, and we're looking at actual school grade. And the group that is black is the group that had sleep apnea and was treated. And you see among the four groups, this is the only group that had a significant improvement in their grades after resolution of their obstructive sleep apnea. The other three groups were the sleep apnea not treated, the snorers, and the controls. And you'll see the lighter bars, they all stayed exactly the same in second grade. And thus, they were not improved. A very compelling study. It's true that this does not affect every kid, and this was a biased population of the worst performers, but it's food for thought. So keep that in mind if a child is struggling in school and has symptoms of obstructive sleep apnea. There could be something there that we could make better. Inattention, hyperactivity, and sleep disorder breathing, there's lots of literature which I will not go over. But in general, people know that habitual snorers, almost 22% of them, will have hyperactivity as measured by a hyperactivity index, HI more than 60, which denotes hyperactive behavior. In patients who don't snore all the time, only 12% had a hyperactive pattern of behavior. So more hyperactivity in kids who tend to have breathing problems during sleep. This is bed wetting-- a quick slide to show you. I'll walk you through this. This is a bunch of kids with presenting to a sleep lab to get a sleep study. And then there was a questionnaire asking, how often do you bed wet? These were all kids that were relatively older, so they should have been dry by now. And first of all, let's look at the x-axis. The x-axis says RDI, and RDI is the Respiratory Disturbance Index. Remember, less than 1 is essentially normal, 1 to 5, is mild, 5 to 15 is moderate to severe, and more than 15 is pretty severe obstructive sleep apnea. And these were the number of kids, 44, 46, 42, and 28 in each group. And each of the bars-- the dark bar is any bed wetting episode, and the light bars are frequent bed wettings. And what you see in this graph is the percentage of subjects with any type of bed wetting, including frequent. And you see that the worse the sleep apnea as you progress towards the right, you see worsening of severity or the number of kids who had bed wetting. So good correlation, like a dose response curve, between the frequency of bed wetting and the severity of obstructive sleep apnea. Again, we see that frequently in clinic. This is again from Dr. Gozal's group, who has a tremendous amount of research in the field of obstructive sleep apnea. This is sort of a speculative slide as to what are the changes that lead to systemic inflammation in the child with obstructive sleep apnea. If you look at pediatric sleep apnea, arousals, hypoxemia, and changes intrathoracic pressure to compensate for the obstruction, this leads to systemic inflammation. There are levels of IL-6 that are measured that are higher in these kids. CRP, the same, leads to oxidative stress and potential increase in reactive oxygen species. And sympathetic activation with all the changes that it entails from the physiology of the heart. And that can potentially in the future lead to potential problems in atherogenesis, hypertension, left ventricular remodeling. And more and more work is being done to elucidate these in kids. We know a little bit more about these effects in grown ups. We're learning more in kids as the research is done. Now, how do we treat these kids? Many doctors in practice will think, if they're very mild, we can try medical therapy. And indeed, there is medical therapy that is fit for the mild child. And this is an example of fluticasone, which is an intranasal steroid. It has been shown to shrink adenoids in other studies. And this is an example where if you look at a group of kids with documented obstructive sleep apnea, and the y-axis shows you the apnea-hypopnea index, the number of stops per hour, and on average they both start at about 11 to 12 stops an hour, which is sort of the mild end of the severe spectrum, and you look at pretreatment, post-treatment-- this was six weeks of the typical recommended doses in children, which is one puff in each nostril one time a day, then what you see is that the group who had treatment in the dark circles dropped their apnea-hypopnea index. Didn't bring it to zero, but brought it down significantly. And this was P equals 0.04. And the placebo group actually increased their number or stayed about the same. This is very good for mild obstructive sleep apnea. If you have very severe obstructive sleep apnea, your index is 20 or 30, we see many kids like that, I don't waste my time with medical therapy. The typical treatment for those kids is removal of the tonsils and the adenoids, which is still standard of care to treat sleep apnea in children. This is another anti-inflammatory. Again, remember, I talked to you about systemic inflammation. Leukotrienes are some of the substances that are found to be important in the inflammation, in allergy, in asthma, and from this study by Dr. Gozal's group in obstructive sleep apnea in children. And in this group, what they did is to, proof of concept, they obtained tonsils from children with obstructive sleep apnea, SA, or recurrent tonsillitis, or recurrent infection, RI, on the x-axis of these graphs. And they looked for receptors for the leukotrienes to see if there was actually any truth that these leukotrienes could be important in the pathophysiology of the disease. And indeed, there were more receptors, both receptor 1 and receptor 2, in the kids with sleep apnea compared to the kids with recurrent tonsillitis. And this was at the site, at their tonsils. Because of that study, then it became reasonable to see, if we use a leukotrienes receptor antagonist, the typical one that's used most often is montelukast, will we see an improvement in sleep apnea? And that study was done very recently, published out of Israel in 2012, randomized, placebo-controlled, double blind study in 46 kids with mild obstructive sleep apnea. They were given the medicine montelukast, which is a leukotriene receptor antagonist, for 12 weeks. And they had sleep studies before and after. And these are the results. The left panel shows the obstructive apnea index. The right panel shows basically the size of the adenoids. And if you look at the montelukast group, there was a significant drop in both apnea-hypopnea index and the size of the adenoids with montelukast therapy, whereas there was no significant difference or change in the placebo group. And these were statistically significant differences, as you see at the top of both graphs. So this is, again, something that is available to us to treat mild disease. Notice, look at the indices on the left picture. Pre, there were about 3.5 stops an hour. Again, the kids who stops 50 times an hour or 20 times an hour, I wouldn't waste my time with these treatments. Now, what do we do surgically? The treatment that is time honored for the treatment for the treatment of obstructive sleep apnea in kids is andenotonsillectomy, or removal of the tonsils and the adenoids. And for curiosity, I looked at four studies here to show you comparative effect size of medical versus surgical. Look at the left panel as medical therapy. The top study is the fluticasone study. The bottom study is the montelukast study that I just showed you. You see an effect size of about 40%. So there's about a 40% reduction. And you start with much less severe obstructive sleep apnea. Look at the baseline numbers. The index was 10.7 in the fluticasone study and six in the montelukast, so mild to moderate obstructive sleep apnea. Look at-- these are two studies. That's one I published, our group published, not too long ago, looking at kids under three. And the study below is a study published by Dr. Bhattacharjee, who is here in our Peds section also, in our Peds Sleep Division. And his study was in older kids. And you see the effect size of adenotonsillectomy in these children is in the range of about 80%. So it was almost double, the effect size of medical therapy. And if you look at the baseline apnea-hypopnea index, these kids had more severe obstructive sleep apnea. In the top study, the index was 34. In the lower study, the index was 18. Let me walk you through these two studies so you look firsthand at the efficacy of adenotonsillectomy, and not only about the efficacy but information that we have gleaned now that not everybody does perfectly after adenotonsillectomy. Everybody improves, but some people have persistent obstructive sleep apnea. This is-- do we admit patients after adenotonsillectomy? Again, the guidelines suggest that the patients are very young. If they have very severe obstructive sleep apnea, if they desat a lot, we do admit them. And we tend to a admit them routinely. And the more severe we keep in stepdown or the Pediatric Intensive Care Unit overnight, and they usually do very well. How do we manage pain? This is something for those of you who might see patients post-adenotonsillectomy. This is very important. That has been a recent development over the past year or two that has altered how we manage these children. In 2013, the FDA sent out a warning that says in a recommendation that there should be no codeine after tonsillectomy for children. And the reason for that is as follows-- this is interesting. I think everybody should know that. Between 1969 and 2012, there were 10 deaths and three overdoses identified in children treated with codeine. Eight out of the 13 occurred in children after their tonsils and adenoids were removed-- big deal. A lot of these kids had disastrous outcomes like death, which is sort of inexcusable if we can avoid it, because this is a simple procedure that's supposed to take care of a benign, relatively simple problem. And the last thing you want is for a child, God forbid, to die from a procedure like that. So this was 8 out of 13 kids-- although in a large span of time. But death in a child who's otherwise healthy and just snores with sleep apnea is sort of a disastrous outcome. So the FDA generated a boxed warning, and it is the strongest warning. It is now added to labels. And it recommends no use of codeine for postoperative pain management in children who undergo adenotonsillectomy. Why is that? What happens to codeine after you ingest it is it's using the cytochrome system in the liver. It's metabolized to morphine. And we know for a fact that children with obstructive sleep apnea are much more sensitive, their respiratory drive is much more sensitive, to morphine than kids without obstructive sleep apnea. There's good data to support that. So if they see a lot of morphine, they are much more likely to have respiratory problems and respiratory distress and potentially respiratory arrest. Now, why do some people have it, some people not? Come to find out, there are genetic variations in the metabolism of codeine in the body that varies between different people and different ethnicities. And the people who have two non-functional alleles of that gene are poor metabolizes. These are the people you give codeine to and they do not get good control of pain, because it's never metabolized appropriately to morphine. You have one or two functional allele children who will have extensive metabolism. You get reasonable conversion, good control, but potential respiratory side effects. And patients with amplified active genes but duplicated alleles will have ultra-rapid. They're called the ultra-rapid metabolizers of codeine. So you give them codeine PO, they metabolize it very quickly into morphine. And that dose of morphine is usually high enough that it could cause respiratory arrest in these children, and thus the disastrous outcomes. About 7% to 10% of whites have poor metabolism, and about 1% to 7% of whites and more than 25% of African descent Ethiopians, which potentially could be the same in African Americans in the United States, have gene duplication, ultra-rapid metabolizers. So that's the rationale for not using codeine in any child who's undergoing adenotonsillectomy, specifically for obstructive sleep apnea. I think in a way, FDA couldn't recommend that you genotype the patient to figure out whether they'd respond well or not well, so across the board they prevented it, because the potential disastrous outcome is just too disastrous. So what we do for pain management after adenotonsillectomy, which we've been doing for the past couple of years, is I medicate every three hours when the patient is awake, and we vary between acetaminophen and ibuprofen. And we alternate the doses. And there are good studies that show that there's really no increase of a bleeding risk with ibuprofen in these children. So we've been able to manage very well with this pain control regimen. Now, what happens after adenotonsillectomy? Do these kids get better? The answer is yes. This is improved quality of life, six to 16 months after adenotonsillectomy in these children. Everything to the right of that line at zero is an improvement, and they do improve. What happens to their behavior? This is a study that shows multiple indices of hyperactive behavior, baseline and postoperatively, and you see a significant improvement in all these parameters after adenotonsillectomy in these children. So the hyperactive behavior improves-- not in everybody, but as a group, everybody moves favorably in that parameter. And if you look at kids with bed wetting, this is an observational study of patients who were snorers, underwent adenotonsillectomy. 35% of them had bed wetting at the time of surgery. And after surgery, almost 63% reported complete relief of nocturnal enuresis, NE, 4% reported partial relief, and a third had no change. So that's what I tell my patients when we discuss adenotonsillectomy. There's a good 2/3 chance that the child will do better after adenotonsillectomy and resolution of obstructive sleep apnea. Now, the more recent information that's come up in the past-- like, when I started practicing, we used to take the tonsils and the adenoids out, parents would come after surgery and be very happy, the child stopped snoring, they're very quiet, sleep was better, that was the end of it. We've come to find out, if you repeat a sleep study in some of these children, they do have persistent obstructive sleep apnea, and we're much more aware of that, and we're looking at more and more of these children right now. This is the study that I told you. This is Dr. Bhattacharjee's study, who's here in Pediatric Sleep Medicine. He looked at a multicenter study from around the country, 578 children who had a sleep study before tonsils and adenoids removed, a sleep study later. And typically sleep studies were six to eight weeks after surgery. These are the kids. Their average age-- if you look at their numbers, look at what I'm pointing out, their apnea-hypopnea index went from 18 to four after surgery, a significant drop. So as a group, everybody improves. But four is not perfect. Zero would be ideal. And if you looked at their oxygen, the last, at the bottom, their drop was, at worse, at 80% preoperatively, and at worst postoperatively, jumped up to 86%, very good improvement. These were statistically significant changes. Now, who were the people who were more likely to have persistent disease postoperatively? These were older kids, age seven and older, kids with obesity-- huge risk factor for persistent sleep apnea after adenotonsillectomy-- kids with asthma, and kids who had a very severe sleep apnea prior to surgery, even if they were not overweight. So in our counseling now for patients who are undergoing this procedure, I tell the parents, if the kid's overweight, I tell them, we have to repeat the sleep study. There's a high chance that a child might have persistent. We will help, or else I wouldn't even touch the child surgically. But there is a chance that they will have persistent disease after surgery. Kids who have very severe sleep apnea at the beginning we also investigate with a postoperative sleep study. So that's important information that we did not know before. And if you look at outcomes, if you were religious enough and you wanted the apnea-hypopnea index to be less than one, then only 27% of people achieved that outcome. But if you said, if they're down to mild, I'm happy, then 80% did resolve basically to under five. And I told you, the higher risk were kids that were older, obese, and non-obese with severe obstructive sleep apnea or asthma, so keep an eye on these children and consider sending them back after surgery if they're still not doing too well. This is our study that we published last year in the otolaryngology literature. I looked at 70 children. We operated over, I think, a seven or eight year span on 283 kids under age three with documented obstructive sleep apnea. 70 of those we had sleep study after surgery, and we reviewed that information in retrospective fashion. It has some limitations. Ideally we should have everybody gets a sleep study. But it's expensive, it takes time to get on, and the kids who looked perfect I didn't sort of do it at the time. I will be more likely to do it now because of what I know. So this is our study published in JAMA. And what you look at here is we're looking at pre- and postoperative polysomnogram on these kids. Concentrate on the apnea-hypopnea index, which is the third row down. You'll see that they went from 34 to five-- a significant, important magnitude change, 80%, as I showed you before-- and statistically significant also. Also look at severity of obstructive sleep apnea-- none, mild, moderate, and severe, in the last four lines. And what you see is preoperatively, nobody had no sleep apnea. Everybody had either mild, moderate, or more frequently, severe. So most of these kids have more than 10 per hour stops. These are young children. And you see postoperatively, this reverses. So you have many more that have no sleep apnea, many more that have mild, and many fewer kids that have severe obstructive sleep apnea. And those numbers are on that screen. If you look at their apnea-hypopnea index individual data, everybody drops except maybe one child that went in the wrong direction. But almost all of these 70 kids had an improvement in the numbers. Not perfect, because as you see, there were many that still had an index above zero after surgery. If you looked at the percentages, AHI under one, complete resolution, 41%. If you consider one to five acceptable, 80% resolution, similar to the data I showed you on the older kids with Dr. Bhattacharjee's study. Again, we looked at what was it preoperatively that predicted persistent disease after surgery. And the only thing that predicted was severity of disease preoperatively. In these kids, obesity was not an issue because they were very young. We really did not have obese two-year-old or one-year-olds as a group. So what you look at is if you look at residual obstructive sleep apnea, yes in the column on the left, and no on in the column on the right, and compare their preoperative polysomnogram data, you'll see that the kids who had persistent sleep apnea post surgery had a much higher apnea-hypopnea index, 55, compared to the kids who were more likely to resolve, who had an apnea-hypopnea index of 29. And that was a significant difference. So severity of sleep study preoperatively in those young children predicted postoperative persistence of disease. And now I routinely will screen them postoperatively with a polysomnogram if they have severe obstructive sleep apnea. Now, what can we do for these kids with persistent sleep apnea? I have to tell you, we now have a multidisciplinary team, which includes my colleague, Dr. Bandla from sleep medicine, myself, we have colleagues from orofacial, to try to handle these children. It's difficult. The best benefit you get after adenotonsillectomy, and then you get incremental small benefits. It's very vexing, especially to take care of the obese children. But we do have a multidisciplinary team, and we always try to help them. And this is an example of where you double up the anti-inflammatory therapies. M is for montelukast, B is for budesonide, another intranasal steroid. This was an open label study performed by the Gozal group also that shows you in kids with persistent sleep apnea, if you give both these anti-inflammatories together, for the column on the left, you will drop the apnea-hypopnea index from about a four on average to about a 0.5, which is pretty good. But if you're starting with a 10 and a 20, again, the efficacy of these drugs is limited. You see the kids on the right who were not treated stayed the same. Now, what else do we do? CPAP is treatment of choice for adults. Compliance is harder in children, so we struggle with that. Dr. Bandla has a CPAP clinic that he follows these kids in and gets feedback. He has a psychologist who works with them to try to enhance compliance with CPAP. Supplemental oxygen sometimes. As far as surgery, we do sleep endoscopies, which I will show you in a second, and we look for residual areas of trouble. And we sometimes identify palatal problems, base of tongue problems, lingual tonsils, floppy voice box, and all these we sometimes address surgically. Sleep endoscopy is performed in conjunction with our sedation team, who's based at Comers Children's Hospital also, and we sedate these children with the help of Dr. Fagan, who's the leader of the team. And we induce sleep with Presinex and propofol, given intravenously. And we give them topical anesthesia applied intranasally. And then we put a small scope when they're sleeping on their back and look at the abnormalities. When you look at a schematic of the airway, these abnormalities come in different regions. You could have congested turbinates. That's the nasal part of the obstruction. You could look at the back of the nose and see recurrent adenoids. You could look at the palate itself and see a very floppy palate, which could be targeted with the trimming. You could after that at the base of the tongue, and the base of the tongue could be large, especially in children with Down Syndrome. And so there are some procedures to address that. You could also look at the lingual tonsils, which are right at the vallecula, right above the epiglottis, could push the epiglottis down. And removing those could make the situation better. You could also look at laryngomalacia. The same entity we described for younger children is sometimes seen. A floppy airway is seen in children with persistent sleep apnea. Sometimes shaving the redundant sloppiness with a laser could be beneficial. And in kids who have a very small jaw, sometimes moving the jaw forward in conjunction with a plastic surgery team could help the situation. Remember, the jaw issues are not that common. The most common are long redundant palate, recurrent adenoids, nasal congestion, and lingual tonsils, and the floppy larynx. The lingual tonsillectomy is our surgical way of addressing these lingual tonsils. This is an example from a study from Stanford, looking at persistent polysomnogram proven obstructive sleep apnea despite adenotonsillectomy. They had sleep endoscopy, were found to have large lingual tonsils, and then they underwent a lingual tonsillectomy and underwent a polysomnogram after surgery. This is an example of a child in the operating room with endoscope in the mouth looking at those lingual tonsils. You see on the picture on the right, the endotracheal tube is at the bottom of the picture. The uvula is also seen to the left of the screen at the bottom. And at the top of the screen, you see those two big lingual tonsils. And they're at the level of the epiglottis, right above it. And they can push the epiglottis over the larynx when the patient is sleeping, especially if they're on their back. And what we do is use Coblation to shave these. We can't resect them like we do a tonsillectomy. We just flatten them down. We lower the mound basically with this Coblation technology. We do it very safely, all through the mouth. And now that it's been ablated, you can finally see the epiglottis. And you can see how that could improve the breathing. And in that data from that study, the index dropped from 14 to eight-- not perfect, but again, some improvement in these children. Supraglottoplasty is an example where you trim. This is an example where a child was breathing, and when they took a deep breath, you see the collapse over the voice box in the picture on the right. And you can come and trim those structures with a laser and decrease the collapse, and again, create a small incremental improvement in their obstructive sleep apnea. In general, it is important to recognize that sleep apnea is a very common problem in children. It leads to significant daytime sequelae, although not life-threatening, but important for functioning and quality of life. And one should keep that in mind and recognize this entity. The majority of kids will be documented by polysomnography, and the majority will do very well after removal of the tonsils and the adenoids, unless they have very mild disease, in which case we try medical therapy. We are recognizing residual obstructive sleep apnea after adenotonsillectomy, and we have a multidisciplinary group to try to address these patients. We do a sleep endoscopy to evaluate potential areas of residual obstruction. If surgery is to be offered, we offer it. If not, then CPAP is what is done to try to help them. And our team consists of otolaryngology, sleep medicine, sedation service, and pediatric intensive care to take care of the difficult patients. And I thank you for your attention.