Good morning. Good morning everybody. I'm going to start on time today because then it depends how the clock goes from now on. Welcome to our All That We Use Is Not Asthma, a base case approach. I have been asked to give you some reminders. So please remember that you can evaluate all the sessions through the mobile app and remember to do the evaluation after this session. All presenters are required to verbally disclose their financial relationship, so you will see that in all of our slides. All rights are reserved. The visual and audio content presented during this meeting is the exclusive property of CHESS. No personal recording of the content of this meeting are allowed. Please allow CHESS staff by keeping the aisles and the exits clear. Please silence all cell phones and pagers during the presentations. Please make room for attendees to have a seat by moving toward the center of the rows and leaving empty seats in the aisles for late comers. And then CME claiming will open Wednesday, October 11 at noon. This is a session that is using the audience response system, so please keep your phone handy and use the app for the audience response system questions. By finding the session in your schedule and clicking on the polling link at the bottom of the session details. There will also be a QR code that you can scan, and I am about to show you that one. So my name is Maria Velez. I'm one of the associate professors of the Pulmonary Department and Lung Transplant Department in UT Health San Antonio. And I'm going to be talking today about our first topic, which is expiratory central airway collapse, which comprises tracheomalacia and excessive dynamic airway collapse. This is the code that you can scan for the audience response system. If you haven't done it through the app, I'm going to give you a couple of seconds there. Okay, my introduction slide, and I have nothing to disclose relevant to this presentation. Okay, so at the end of this short talk, I really hope that you can think outside of the box and think about excessive dynamic airway collapse in patients who have difficult to control asthma, that you can describe the symptoms of this disease, that you can work it up and have an algorithm in your head for the treatment. So I'm going to start with a case presentation, and this was a 32-year-old healthy male who had been very active all his life and then started having decreased exercise tolerance, wheezing, specifically when exercising, and progressive dyspnea. He was seen by pulmonary, and they did the basic workup. Physical exam was normal. No wheezing, no stridor. PFT is completely normal. I don't have a picture because it was really unremarkable with a normal flow volume loop. He was initially treated empirically for asthma, and the therapy was escalated to triple therapy because his symptoms failed to improve with asthma therapy. He had a metacolin challenge test that was negative. He had a chest x-ray that was normal, a chest CT that was normal, and an echo that was not suggestive of pulmonary hypertension. He was also sent for evaluation by the ear, nose, and throat doctors, and he had no evidence of vocal cord dysfunction. So my first question for you is, what would you do next? And rather than being a right-wrong answer for this one, I just want to see what your algorithm is for difficult-to-control asthma. Okay. So in this case, the next step was he had an exercise bronchoscopy. He was seen in our military center. He had an exercise bronchoscopy. And these are the findings of his bronchoscopy. So as you can see, there's a marked decrease in the lumen of the airway during expiration. So he was diagnosed with excessive dynamic airway collapse of the distal trachea and bilateral menstruating bronchus. So what is expiratory central airway collapse? So this is an entity that comprises the diseases that decrease the lumen of the trachea. The first disease is tracheal bronchomalacia in which there is loss of the anterior wall of the trachea due to cartilage issues. And then there is excessive dynamic airway collapse. And then there is bowing of the posterior wall of the trachea into the lumen of the trachea, decreasing the lumen. They are usually paired together because they cause very similar symptoms. The diagnostic evaluation is similar, and then similar but not completely equal therapeutic approach. So why does this happen? Well, in the case of tracheal bronchomalacia, it's a destruction of the cartilage, either because you have ischemia due to infection or due to repetitive trauma or due to chronic inflammation. In the case of EDAC, it's an atrophy of the smooth muscle of the posterior wall of the trachea. And this happens due to changes in the interactions of the pleural pressures and the airway pressures in obstructive lung disease like COPD and asthma where there's air trapping, pooling on the airways and making that posterior wall more lax. So the classification, the most common classification is either congenital or acquired. In the congenital, you're gonna see the idiopathic giant trachea, Mounir, Kuhn, Erlens, Danlos. And then the acquired, which is the most common one that we're gonna see is common in patients with tracheostomy, patients after lung transplant, patients who have had surgery to the chest, chest trauma, chronic compression from a goiter, from a tumor, from a vascular abnormality, chronic inflammation, as in patients with cystic fibrosis who have chronic infections, or chronic inflammation for the cartilage itself in patients with elapsed polychondritis. As I told you, in EDAC patients with COPD, patients with asthma and air trapping, acid reflux, there's a big correlation between acid reflux, inflammation of the airway, predisposing patients to these entities. In health corticosteroids, by mechanism of ischemia of the airway, can increase the risk of both EDAC and tracheobronchomalacia. And then obesity and inhalation of fumes. So the classification can be based on the morphology, the appearance, the distribution, or the severity. So the location can be either proximal or distal, trachea, main stem bronchi, or either distal in the airway. The morphology, what you see with your bronchoscopy, is it present, is it the whole circumference of the airway, is it just restricted to one little segment, is it diffused through the airway? And the severity is important, because in healthy volunteers, you can have up to 70% collapse of the airway during forced exhalation. So in fact, to call this abnormal, you have to have more than 70% obliteration of the airway. And this happens 70 to 80%, mild, moderate, 90, and more than 90, we'd call it severe. So in our patient, you saw there's complete obliteration, it is severe. And this is our radiographic and bronchoscopic samples of each classification, each type. So the prevalence isn't clear, 10% of the general population, 20% of patients needing a bronchoscopy for any reason, and almost 40% of patients with COPD. And it's most common in patients more than 40%. The symptoms are dyspnea, which can be exertional, can be at rest if the patient is having any respiratory disease, any viral infection. Patients can have hemoptysis, and they have this characteristic barking cough. Then they can have a stridor or wheezing, which is usually expiratory zone. And then even in severe cases, this can progress to hypercapnic respiratory failure. So our next question is, what is the most common pattern found on pulmonary function tests? Okay. So obstruction is the most common finding, but I must say there's not one single PFT finding that is going to make you think about this diagnosis. As you can see, you can have obstruction, you can have restriction, as in our case in our patient, it was completely normal. So these are the pulmonary function test patterns that can make you think about excessive dynamic airway collapse. You can have this notch pattern, you can have a peak pattern with a low FEF max that drops really quickly, and you can have these oscillations of your flow volume curve again. You only see them in a minority of patients, and these are not pathopneumonic of the disease. So how do you diagnosis? So CT, very, very important. It is important to know that you have to order a dynamic airway CT. This is important because this CT is going to take images in inspiration and exhalation during tidal exhalation and respiration as well, so you can make the measurements. Because if you only do it during forced exhalation, this may not show what the patient is clinically having during tidal breathing. There's several places where you measure the airway of the lumen, and you can see those there. And if the airway of the lumen decreases more than 50% between inhalation and exhalation, you can call it abnormal. The goal starter is going to be bronchoscopy, ideally under minimal sedation, again, so you can give instructions to the patient, breathe normally, forced exhalation. You can change, are they sitting, are they laying down? So you can mimic when they are having the symptoms. Okay, so you can see here pictures of airway CT showing a very dramatic narrowing in the airway lumen during exhalation. And then you can see bronchoscopic findings are going to be corresponding to these findings. So the next question is, now you know what the diagnosis of your patient is, what do you do next? Oh, and that one didn't come. Okay, so most of you answered the right answer, which is try air positive pressure. So the first thing in all of these patients is treat the baseline disease. If the patient is obese, yes, they should lose weight. If the patient has severe acid reflux, you treat the acid reflux. Even if it's mild acid reflux, you should treat the acid reflux. If they have obstructive lung disease, they should be treated for obstructive lung disease. So airway clearance is very, very important in these patients because they have problem expectorating secretions. They do have recurring infections. So having them on pulmonary rehabilitation, breathing techniques, so the patient learns how to splint their airway open with balsalva are very, very important. However, if after that your patient continues to have symptoms, then you can try positive pressure. And then there's a very interesting article in which they put the patient with a mask, positive pressure, and they start titrating the pressure until the airway is splint open. And this usually happens between zero and five or seven of pressure. You don't need a lot. And the patients do experience significant improvement. The problem is, as you can imagine, the patients cannot have positive pressure all day long. So this works when they're having exacerbations. They work when they are in the hospital, but they're having symptoms, for example, with exercise, this doesn't really work. There is a mistake in this question. It should read a stent for excessive central airway collapse not tracheal ronchoplasty. So which of the following is correct regarding airway stent for ECAC? I'm gonna move through this one a little fast because I'm running short on time. So it helps to identify the patients who will benefit from airway surgery. So there's a trial of stenting of the airway in which you can use either self-expanding metallic stent, usually on cover, or you can use silicone stents. And these stents are left in place anywhere between one to two weeks. After 80% of patients are gonna experience very significant improvement of symptoms with the stent. If the patients improve with the stent, then you know that this patient is gonna benefit from airway stabilization. So this is basically used as a trial to see if the patient will benefit from surgery. There's some data on long-term stents, but this is not recommended due to the complications of the foreign body in the airway itself and it's for repeat procedures. So tracheal ronchoplasty is the surgery of choice. It basically stabilizes the posterior wall of the trachea. There's a mesh, a solid mesh, that is put behind the wall of the distal trachea, right, left, main stem, bronchi, and bronchus intermedius. And it basically decreases the bowing of the posterior wall, but it also reshapes the trachea when the cartilage is the problem. It improves quality of life, it improves performance. It may improve pulmonary function tests, but this data is conflicting. These are just some schematic pictures of how this surgery works. You can see the wall of the trachea being pulled back by this mesh. It's a complicated procedure. It's only supposed to be done in centers of expertise and it carries up to a 40% complication rate and a one to 3% mortality rate. So you really have to select the patients that are gonna benefit from this procedure because it's a big one. Other options would be terminal-terminal anastomosis, resection with anastomosis if it's really a small segment of the trachea that is abnormal, or you could do a tracheostomy in a T-tube if your abnormal segment is pretty high and you can bypass it with a tube. And this should be my last slide. So future therapies that we can look to. I think the most interesting one here is the use of laser and APC. And the way this is being used is by burning to say something about the posterior wall of the trachea. So thermal therapies are applied to create some sort of scarring that will give rigidity to that posterior wall of the trachea in hopes that the symptoms are gonna improve. And there's very interesting studies on this area. This is, if you're gonna go back to this presentation, I think this is a very nice algorithm basically telling you, you see this, your patient is asymptomatic, forget about it, you don't need to worry about it. If your patient is symptomatic, treat the primary disease. And then if you treat the primary disease and your patient is still having symptoms, consider an stenting trial followed by surgery. Okay, so for our patient, I just wanna tell you that he had a stent, he did great, he was referred to surgery, he had tracheal bronchoplasty and he's doing excellent with resolution of all his symptoms. So I hope that by this presentation you think about this disease when you have a patient with difficult to control asthma and you have formulated an algorithm on what to do when you suspect this disease. And thank you Dr. Velas for this invitation. So, you know, we talk about what's our sort of, what do we most enjoy taking care of, is right, our patients with chronic cough and then I put inducible eryngeal obstruction right next to it, it's a challenging diagnosis but once you recognize it and treat it, it's really rewarding. So I just wanna cover in the next 10, 15 minutes really how I approach it and walk you through some of the recent advances. But just a word of caution, this is really an evidence-free zone and it's not, there's really not a lot, you know, a lot of it is really art and not science. So just keep that in mind and that should give us just such enormous respect for our speech pathology colleagues because they all, they truly are practicing personalized medicine here. So these are my disclosures, I have no relevant disclosures for this talk. Let's start with a patient who's 29 years old, she has poorly controlled asthma. So she does have history of asthma that was diagnosed in childhood and had been really minimally symptomatic, well-controlled until two years ago when she started experiencing symptoms and her symptoms were acute onset, cough, chest tightness and shortness of breath, rarely wheezing and so much so, these episodes were so distressing for her, she presented to the ED twice and both times she received steroids and only felt partially better. The triggers, these are key, her triggers were cigarette smoke, any strong scents, so just keep that in mind if you have somebody who tells you particularly, there's a particular brand of a perfume or a deodorant that bothers them that should raise the flag for inducible orange oil obstruction and then intense exercise and she's already treated with a high-dose inhaled steroid and long-acting beta agonist and her exam's really unremarkable, she's got good air movement, she's not obese and this is her chest x-ray, looks pretty normal. Spirometry, just looking at numbers, also looks normal, normal FEV1-FBC ratio, no bronchodilator response, exhaled nitric oxide levels low, eight parts per billion, so less than 25 parts per billion but keep in mind she's on a high-dose inhaled steroid so we just have to interpret it in that context. Normal IgE, negative allergy testing and low blood use on a full count of 100 cells per microliter and then we get the spirometry, so always, right, what do we tell our fellows? Don't look just at the numbers, look at the full volume loop, so there you have it in the inspiratory limb, there's flattening consistently and I was concerned about inducible orange oil obstruction. So what is inducible orange oil obstruction or ILO? It's an inappropriate transient reversible narrowing of the larynx, has been called many names, vocal cord dysfunction, paradoxical vocal full motion but really the correct term now that is being used is inducible orange oil obstruction, the VCD sort of had a pejorative connotation to it plus also VCD-PVFM suggests that the problem is only at the glottis level at the vocal cords but we know now that there's a significant supraglottic contribution as well and ILO can occur spontaneously or in response to these triggers that we mentioned and as I mentioned can be glottic, supraglottic or both. This is sort of your classic, you know, medical school understanding of a VCD where you have during inspiration, you have a closed vocal cord with that diamond-shaped chink at the back. The prevalence varies about four to 6% in general population 50% of patients with chronic cough probably have it and then 30% in asthma. So it's commonly a mimic and also can be a comorbidity and if it's a comorbidity in somebody with asthma, we really can't get them well controlled until we address and treat this condition and it is associated with significant increase in morbidity and healthcare utilization, 40% increase in healthcare utilization in patients with asthma if ILO is coexisting and because it's consistently, there's a consistent pattern of under-recognition, misdiagnosis, delayed diagnosis and that culminates in potentially harmful treatment with IV steroids. How many in this room have had patient with ILO intubated? And what happens, you know, the airway pressures as soon as we intubate them are normal so you kind of, that's sort of, but why does it even get to that whether they require intubation? And a lot of times these patients get confused for anaphylaxis and end up with epinephrine injection so there's a lot of harm that can be done to these patients if it's not recognized. And the pathophysiology is complex. Larynx itself is such a complex structure and my intent to put that figure there is not to walk you through every muscle and, you know, I don't understand it that well, I'm a pulmonologist, but the thought is that there's laxity inherent in the larynx and then this airflow movement in and out causes pressure changes that can exacerbate ILO. Also, the posterior crico-retinoid muscle contributes to that supra-glottic-like closure. It can be hyper, you know, active or malfunctioning. There's some altered laryngeal sensitivity and then comorbidities play a role as well. And when I think about laryngeal sensitivity, in addition to ILO, there are a few other things that happen in the larynx and often these patients who present with this problem will have some or the other of the others, right? So chronic cough, muscle tension dystonia, which on laryngoscopies can be evaluated, and then this globus feeling, this globus pharyngeus is commonly seen. And then these are the exacerbating factors, some of which we've already covered, environmental exposures, viral infection. Laryngopharyngeal reflux is a big one and commonly seen on laryngoscopy. And just like in any disease, there's increasing recognition of heterogeneity and multiple phenotypes of ILO are now emerging. So the classic inducible laryngeal obstruction is that mimic of asthma that we just discussed, but often patients who have lung disease, especially asthma, will have comorbid inducible laryngeal obstruction. EILO, or excise-induced laryngeal obstruction, is actually a very well-characterized phenomenon that is, we see it in adolescents, high school, college, young adults, basically athletes, you know, like track, they run track and then I had one patient who would do well in practice runs, but during their actual race, they would develop this. This can be really distressing to them. And then incident-associated ILO, which came to light a little bit more in the setting of COVID vaccination, where patients would present to the ED because they think they're having an anaphylactic reaction, but it's really more the anxiety associated with it driving this. And then we think the cough-associated ILO may be another evolving phenotype. So the clinical features, I think a lot of it, which we've already covered. The things that raised this concern for me is if somebody has very rapid onset. So it's a rapid onset, rapid offset. Usually triggers, you know, if it's smoke, perfume, chemicals, laundry detergent. It is often inspiratory, so I usually ask them, do you have more trouble breathing in than out? And they'll say breathing in, but it's not, it can be both. And then exercise-induced laryngeal obstruction, how to separate it from exercise-induced bronchoconstriction is this loud, sort of stridorous, high-pitched sound that develops, usually at the maximal intensity exercise, while EIB is more after the exercise is done or towards the end of a very prolonged exercise. And there are some screening questions available. The one we use in our clinic is the Pittsburgh Vocal Cord Dysfunction Index, so Pittsburgh VCD Index. It's really easy, four-item questionnaire. And, you know, you get actually, if there's no wheezing, you get a high score. So that just, that was one of the things that was validated. A lot of these patients don't complain of wheeze, but they'll complain of chest tightness, upper chest tightness, throat tightness, shortness of breath, and then cough ends up often being, it starts with cough, like when they're around these triggers, often cough is what starts that. And then this EILDI was just published last year, so just a questionnaire that's now available for exercise-induced laryngeal obstruction. So how do we diagnose, you know, you maintain a high degree of suspicion, you use these questionnaires, you look at that flow volume loop, and then laryngoscopy, and then I'll talk a little bit about this dynamic CT of the larynx that I think is going to become one of the tools. But the most important thing is that it's most informative to perform a diagnostic test when patient is symptomatic. Oftentimes, if they're not having symptoms, the diagnosis will not be confirmed, you just have to then go with your high clinical suspicion. I don't think there's any harm. If you suspect and you can't confirm, I still think there's value in referring them to your speech pathologist colleagues. Respiratory retraining is not, you know, there's minimal risk associated with it. We love our spirometry, right? Like, we are pulmonologists, most of us, PFTs is what we do, but diagnostic precision of the flow volume loop is really low, and often it'll be normal if they're asymptomatic, does not correlate well with laryngoscopy, and it's not always suggestive of ILO suboptimal effort, if it's poor coaching, if it's a poor inspiratory effort, that can do it, so I always look at all the loops and all the trials to show that if there's consistent flattening of that inspiratory limb, then I think it's a concern. Laryngoscopy with provocation is the gold standard, and up until last year, we did not have a consensus on how to diagnose, but last year, this paper in Jackie, it was a Delphi consensus statement for diagnosing ILOs, if you have further interest, certainly please review it, but greater than 50% closure on inspiration is considered abnormal, and right here, this is during an inspiration, what a normal vocal cord should look like. This here, you see this anterior closure with posterior, that small chink, and this actually is that posterior cricarotenoid sort of coming together, so this is more the supraglottic inducible angioabstruction that I just mentioned, and we've had, you know, our laryngologist will do a provocation, and if a patient has something that they react to, they'll have them bring that in and do a provocation and try and reproduce this. If you see somebody like this out in the field, please don't make fun of them, they're undergoing continuous laryngoscopy, so continuous laryngoscopy during exercise is a thing, there are some centers that do it, it's basically you, you know, anchor the laryngoscope, it's sitting right above the vocal cords, and you can do it in your facility setting, but now there's actually validation for doing this in the field test as well, so patients are experiencing it, because often the challenge, and we see that with CPET as well, that especially in patients who are very athletic, it's really hard to get them to exercise at that maximal level, so if you do an in-the-field test, you can try and reproduce it, and that's a little bit better. This is a dynamic CT of the larynx, it's a low-dose CT, there's increasing, I'll tell you, this is very exciting to be able to have another imaging procedure that can help with diagnosing inducible angioabstruction, but this is really data from two large case series, and here, this is the laryngoscopic image, correlation with that, this is an axial scan, and this data, this particular group, this is that virtual sort of reconstruction, anteroposterior of the larynx, and you can see there's a laryngeal obstruction here, and what they then did is they actually did, they made this sort of motion curve, so right here is time, over here is the ratio of laryngeal diameter to the tracheal diameter, and then this is inspiration, expiration, this is the median, this is the lower limit of normal, and as you can see, patient with laryngeal obstruction was much below that, so this actually is a cool technology, hopefully we'll see more, we just need more studies to validate the test. What about forced oscillometry, or impulse oscillometry? So there was a very small case series that came out in 2013, where they looked at six patients, three of them had laryngoscopy-confirmed inducible laryngeal obstruction, and they showed that during inspiration, the impedance waves were very high, so there was a lot of fluctuation, and this actually got us excited, and our former fellow, who's now our colleague, Patrick Donahue, decided to look at it, to see if we could use oscillometry and compare, and try and separate asthma from inducible laryngeal obstruction, and we were disappointed, because we actually did not find a signal that was classic, specific for ILO, and he's gonna be talking more about ILO later today, so please, to see if that session is of interest to you, but what we found was that there were variables that were measures of small airway obstruction in asthma that correlated, but there was nothing that was specific. The inducible laryngeal obstruction patients, that group was closer to healthy controls, so there may be more to come on this, but certainly not, nothing, there was no great signal that we would say we could do this in the office setting, and say, hey, this patient has inducible laryngeal obstruction. Management, it's multidisciplinary, again, no randomized controlled trials, respiratory retraining is really the key, and I just put that here, because we asked our speech pathologist, okay, when we're seeing this patient in clinic, what is the rescue breathing strategies? Until they can get to see, what can we tell them? And there isn't one. You know, sometimes they have them use a straw to breathe in and out, and that sort of aborts the attack. Otherwise, this sort of smell the rose and blow out the candle can be used. So the systematic review that was published, actually also last year, suggested that most of the studies were observational and case-series, but it did suggest that there was a positive signal and undergoing respiratory retraining was associated with 60% reduction in healthcare utilization in these patients. And then strategies to reduce laryngeal irritation, which is treat laryngopharyngeal reflux, hydration, avoid phonotraumatic behavior. But we still need a lot. A lot needs to be done. We need more accurate diagnostic criteria. We need validated screening tools. Phenotypes need to be validated. And then we really need some randomized controlled trials to see what really works and what are the standardized respiratory retraining approaches that can be used. So for our patient, you know, I referred her to our laryngologist, speech pathologist. They found LPR, treated laryngopharyngeal reflux, and then underwent speech pathology, the respiratory retraining. And it's not always 100%. She's not completely asymptomatic, but significantly improved, and certainly no ED visit. She's learned to recognize upper from lower obstruction. So thank you for your attention, and it's my pleasure now to introduce our next speaker, Dr. Audra Schwalk, who will talk to us about nonmalignant central airway obstruction. Thank you to everyone for showing up today so early for our session. So I'm an interventional pulmonologist at UT Southwestern, and I have my contact information up here because I was asked to talk to you about nonmalignant airway obstruction in 15 minutes, which I can probably spend four or five hours talking about that, so I'm happy to connect, you know, kind of outside of the conference or even outside the room to talk about it in more detail. This is my disclosure slide. I was on an advisory board for AMBU, but that's not relevant to this talk. And if you haven't already scanned the QR code, I do have some questions in a case throughout the talk just to keep us kind of actively engaged in thinking about the topic. So go ahead, and I'll give you a few seconds just to scan that. I think there's another opportunity for each question as well. Okay. So throughout the talk, I'm just going to give a general overview of nonmalignant airway obstruction, particularly in regard to patient symptoms, how we should work up these patients when we have a suspicion. We'll review briefly some classification systems for central airway obstruction as well as potential etiologies and then very briefly go through an algorithm for how to manage this because it does really vary depending on the etiology, so we'll just have a general overview at the end. So I think an in-depth knowledge of airway anatomy is important for any chest practitioner, but particularly when we're talking about central airway obstruction. So in the first couple slides, I just want to review that. The average length of the trachea is about 10 to 13 centimeters. We know it's made up of 18 to 22 D-shaped cartilaginous rings. It's about 3 millimeters in thickness, and the diameter of the trachea in particular varies depending on whether we have a male or female patient, but it ranges anywhere from 14 to 20 millimeters. And I have this picture here on the right hand of the slide just to kind of remind us of something we all know, but that's that the airway is in close proximity to the thyroid, the great vessels, other mediastinal structures, and this is important because these things can contribute to nonmalignant airway obstruction and malignant for that matter. So, you know, as we go further out in the airways, more distally the airway lumen diameter decreases in size. Again, it varies depending on whether we have a male or female patient and also depending on whether we're talking about the left or the right main stem bronchus. So the right main stem tends to be a little bit larger than the left. Now, not every patient with a reduction in the size of their airway lumen will become symptomatic from central airway obstruction. So oftentimes at least a 50% reduction in the size of the lumen is required for many patients to develop symptoms. And certainly this varies, and we'll talk about that on the next few slides, but for the trachea in particular, the airway needs to be about 8 millimeters or less for people to start having some symptoms on exertion, and even smaller than that for them to have symptoms at rest. So because such a dramatic decrease in the size of the airway lumen has to occur for many patients to even have symptoms and seek further evaluation, many patients will present in respiratory distress. Now certainly I think this number may change over time because we're getting so many CT scans for other things that we may incidentally find this, but that may be one benefit of doing the CT scans. So what kind of symptoms do patients with airway obstruction have? Well, oftentimes very general symptoms. That's why we're including it in this talk. They may be misdiagnosed as having other conditions, treated for those conditions, and then found to be refractory. So things like dyspnea, intractable cough, recurrent infections. Strider certainly makes you think about central airway obstruction, and they may have wheezing. So these are just general pulmonary symptoms. But the symptoms that patients have will vary depending on their underlying cardiopulmonary reserve. Someone with significant emphysema, heart failure, other things, may not tolerate an airway lumen that's as small as someone, like the case that we may talk about here, that doesn't have any underlying comorbidities. And the symptoms that someone has also depends on what we call obstruction-related factors, which we'll talk a little bit more about. Where is the obstruction? How severe is it? How much of the airway is involved? And how quickly did it develop? So when we have a suspicion that someone may have airway obstruction, asking detailed questions about when they develop the symptoms can give us a lot of information. You know, acute onset, they may have foreign body aspiration. And believe it or not, not every person remembers that they aspirated something. But that can give you some information. It could be they have a mucus plug at an area of small airway lumen and they really can't generate the force or the air movement to cough it out, and they have worsened symptoms acutely. Or if you make the patients go back and really think about when did they start becoming dyspneic? When did they develop this cough? Then over days, weeks, months, and sometimes even further back, they may start to recognize that they've really just been adjusting what they've been doing over time and that their symptoms have been going on for much longer, and that makes you start thinking about tumors and other things like that because there are certainly a number of nonmalignant tumors that can cause significant symptoms. Or in patients that have either been diagnosed with a systemic disorder or you make a diagnosis of central airway obstruction, they may have systemic signs of other things like relapsing polychondritis, which I have an example of that later. And I almost hate to even talk about this last point here because I think we probably all wanted to come to CHESS in Hawaii and have no one bring up COVID-19. But unfortunately, it's important to talk about because we're really seeing an uptick in the number of patients with post-intubation and post-tracheostomy tracheal stenosis. We had so many patients with ARDS that required prolonged intubation, and so these patients may be doing well. You may say, okay, it's time to go ahead and decannulate these patients, and then they acutely or subacutely have symptoms after the tracheostomy has been removed. And it's important not to just attribute these symptoms to deconditioning or the parenchymal abnormalities they have, but they may have central airway obstruction because of that. So I have a case here and some questions throughout the talk. So our patient is a 30-year-old female. She presents with progressive dyspnea for a pretty long time, about a year. She also has an intermittent nonproductive cough, episodes of wheezing with exertion, and also sometimes at rest. Only has a history of hypertension, said someone diagnosed her with asthma about nine months prior with a normal pulmonary function test, and she's been using her albuterol inhaler frequently without significant relief. She's also using her ICS Lava Montelukast and then had some other workup for asthma before she came. Physical exam was relatively unremarkable, just mild tachycardia, diffuse wheezing, both on inspiration and expiration, and it really sounded more like Strider. So we got a chest X-ray, right? Let's see if there's any abnormalities, and you can see there's no significant abnormalities on this X-ray. So she had been treated with multiple courses of antibiotics, steroids over the most recent few months, said she was regularly using these inhalers but still having these symptoms. We did a PFT, and she just had mild blunting of the inspiratory and expiratory loops that was otherwise normal. So what is the next best step in the evaluation and management of this patient's symptoms? Do we want to prescribe a long steroid taper, adjust the frequency of the breathing treatments, get a chest CT to look for other abnormalities, or just go directly to a bronchoscopy because of what we're thinking? Okay, so most of you chose to obtain a chest CT to evaluate for abnormalities, which is what we recommend. We chose A or B, which no one did. We just really exposed the patient to potential side effects of the medications while not really affecting her symptoms. And bronchoscopy can certainly be considered, and it's in the algorithm for evaluation and management of these patients. But as someone who's stable and we have the ability to get a CT to really get prepared for what we may experience during the procedure, that's usually recommended. So as we said before, I mean, bread and butter, you know, tests that we get is a pulmonary function test. So anyone who presents with some sort of respiratory complaint, it can be helpful. So if you have one of these characteristic flow volume loops here, it can give you a lot of information, you know, increase your suspicion for having airway obstruction. But I want you to take a few things away from this slide, that the airway lumen often has to be significantly narrowed before you'll even see one of these abnormalities on the flow volume loop. And just because a patient has a normal PFT or spirometry does not mean that they definitely don't have central airway obstruction. So if there's an abnormality present that's characteristic, it can increase your suspicion and prompt you to do further evaluation. But if it's not there, then you can't completely rule it out. So chest X-ray, just as in our patient, you know, it's kind of part of our algorithm for working at people with a respiratory complaint, low radiation. But oftentimes it's not helpful for identifying central airway obstruction. So CT is really the standard imaging modality. It can, one, tell us does the patient have central airway obstruction, where is it, how much of the airway is involved, do we have post-obstructive changes, and it can help give some information about vascular structures and things, which is important when we start doing bronchoscopies and interventions. And so I put these images here on the slide to show a different case, but you glance at the chest X-ray, there's nothing really abnormal, but this CT scan was taken from the same patient, and you can see subglottic stenosis with an airway of less than 5 millimeters. So we did, you know, do what all of you all wanted to do and get the CT scan on our patient, which revealed thinning of the cartilaginous rings looks like a tracheal web, kind of in the proximal trachea and significant narrowing. So based on the chest CT findings, what do we think is the next best step in the management of this patient? Do we want to continue current therapies, perform a bronchoscopy for urgent evaluation, refer her for surgery, or just repeat the chest CT, you know, since she's on an outpatient basis and doing okay? Okay, so yes, A is the right answer, and some people wanted to refer her for surgery, and that's certainly in the algorithm that we'll talk about. So bronchoscopy is essential for assessing the airway. You know, when you have an abnormal CT scan, it can give you some information, but it doesn't always tell you, you know, exactly what the underlying cause is many times, and you can also get information about dynamic airway collapse and changes. So like that top picture there was a patient I had with relapsing polychondritis. Had abnormal spirometry, significant symptoms. CT scan showed some collapse, but this was during bronchoscopy with significant left main stem malacia because of his underlying condition. So whether or not we're going to perform flexible versus rigid really depends on, you know, your expertise, what you have available, what is the safest at your institution, but I wanted to highlight that, you know, if you have critical airway stenosis and even, you know, gentle trauma of the airway can cause significant edema, acute airway closure, so you need to make sure that, you know, you're prepared to manage any complications that may happen during assessment. So bronchoscopy gives us many things when we're talking about nonmalignant airway obstruction, particularly these things, which we're going to briefly talk about here. So nonmalignant airway obstruction can be caused by a wide variety of things, and so for the sake of time, because I'm already going to steal some time from Phil, I don't have time to go into all of these in detail, but you can see inflammation, infection, other things can contribute to nonmalignant central airway obstruction, and there's not a lot of epidemiologic data, but post-intubation, post-tracheotomy, tracheal stenosis, foreign body, and then tracheobronchomalacia are some of the more common conditions. So when we perform bronchoscopy or even using CT scan, we categorize airway obstruction into one of three categories, and this is important not just for documentation purposes, but also for intervention purposes. So endoluminal, obviously there's an abnormality in the airway, and this can be things like hematoma, foreign body, and then extraluminal, there's compression of the airway from the outside, like significant lymphadenopathy, or mixed, which is a combination of both, obviously, and we see that more commonly with malignant than nonmalignant. And the treatment is different. We may do tumor debulking for endoluminal or stenting or other interventions for extraluminal depending on the actual etiology. So when we talk about stenosis in particular, like we suspect our patient has, we further categorize it into simple versus complex, and the difference really lies in the length of the airway that's involved and whether or not the cartilage has been affected, but complex stenosis responds less favorably to bronchoscopic interventions compared to simple stenosis. Now there are multiple classification systems for stenosis in particular. I mention the FriTag system here just because it is applicable to the main stem bronchi and the bronchus intermedius as well, where many of the other classification systems only pertain to the larynx and the trachea, but it categorizes it by type, degree, location, and so it helps us to standardize things just a little bit. And it also classifies it based on the dominant type of structural stenosis. And so these images were taken from the article, and I think it's just really good to kind of show the different types of stenosis that a patient can have. So we did perform a bronchoscopy on our patient and found proximal tracheal stenosis with an airway lumen that was less than 5 millimeters by the time she actually showed up for the bronchoscopy. And so it made it a little challenging to advance the bronchoscope and perform further intervention or evaluation during that procedure. So based on these findings, what do we think should be done next? Should we refer the patient for surgery at this point without any intervention? Should we refer her to oncology based on what we saw? Do we abort the procedure, or do we perform an intervention for tracheal stenosis during the procedure, or do we just go ahead and repeat the scan? Okay, for the sake of time, I'll go. So we perform an intervention for tracheal stenosis. So that is what we did, performed radial incisions and balloon dilation and then just forceps removal of this granulation tissue. She had some airway torsion but significant post-obstructive malacia, which is not uncommon in patients with severe stenosis like this. Unfortunately, she kept having recurrent stenosis, and because she was otherwise healthy, she was sent for surgical resection and did well. So in the last two slides here, I just have an algorithm for how to manage and evaluate patients. If they're stable, like my patient, you can go through that algorithm of getting the CT scan, performing the bronchoscopy for further workup. If they're unstable, you have to stabilize the patient first, using heliox, potentially intubation, and then going through the algorithm for management or transfer to a center that can manage patients. So this is the only treatment algorithm here that I have. It focuses on bronchoscopy just to show you, depending on the underlying etiology, the options that we have. But surgical resection can play a significant role in the care of some of these patients, and often it's a multidisciplinary approach. So as we mentioned earlier, tracheostomy, Montgomery T-tube, can be used in many of these patients, either if they're not surgical candidates or as a bridge to surgery, or sometimes for airway remodeling after. And for those patients with systemic disorders, like relapsing polychondritis or sarcoidosis, things like that, they may require systemic therapies as well. So just to summarize, I hope that some of the main things you've taken away from this talk are that if someone is diagnosed with a common condition like asthma and they're just not responding appropriately, that further evaluation is warranted. There's a wide variety of things that can cause this, and even young patients can be affected. So CT scan and then bronchoscopy and further treatment is warranted in these patients. Thank you. So I'd like to introduce Dr. Ong, who will be talking to us about foreign body aspiration. Good morning. Thank you for waking up so early to see us. I call this the surprise because this is what usually happens when you have a case like this. So I'm an interventional palm and lung transplant in San Antonio. Those are my disclosures in the slides, and we've already done the QR code earlier today. That's the objective. So let's start with the case. We have a 50-year-old man, mild persistent asthma since childhood, lifetime non-smoker, who has been maintained on ICS and LAMA and Montelukast and albuterol as needed. And the patient is coming for complaints of persistent dyspnea, chest pain, and cough with yellow sputum for three months. The patient has had at least two or three courses of repeated antibiotic and steroid treatment on physical exam. The patient was found to have coarse breath sounds, bronchi, no wheezing, crackles, or clubbing. PFT shows airflow obstruction, FEV1 of 34% with no bronchodilator responsiveness. There's severe hyperinflation, as you can see. The chest X-ray was completely normal. However, when we did the chest CT, there's an arrow sign on the left main stem. So for our first ARS question, what would you do? We'd say this is just mucus, this is just uncontrolled asthma, there's something in the airway, and this is a tumor. So that's what we did. Of course, the topic of the session is foreign body. So upon further investigation, apparently, around when the symptoms started, the patient was chewing on a coffee straw and coughed severely afterwards, and that's all. And so what would you do? All right, so the classical teaching is that for foreign body you should be doing a rigid bronchoscopy. However, that's really not, doesn't reflect current practice anymore. In children it is still recommended to do rigid bronchoscopies just because the working channel of the pediatric bronchoscopes are quite small and so rigid bronchoscopies are recommended for children. However, for adults, the accessibility of various tools for us makes it possible for us to do, remove foreign bodies with excellent success rate as you can see on the table. And, you know, we have cryoprobes and things like that to remove foreign bodies. So these are just a few of the tools. There's a basket that, you know, is basically two loops at right angles to each other, put the foreign body inside and there's another retrieval net that was just recently available that's also for your, used to remove foreign bodies. And so we did a rigid bronchoscopy just because we have it in our center. We found this sort of necrotic looking substance in the left main stem and we basically just removed it with the forceps, which was the coffee straw. And so post-bronchoscopy the patient had marked improvement in his functional status and actually came off inhaled corticosteroids and only required as needed albuterol. And so this highlights the fact that even the GOLD initiative recommends CT of the chest and bronchoscopy for patients with difficult to control asthma. However, it's to remember that some of us think that, oh, there has to be a history of aspiration, but not all foreign body aspirations are acute. And the diagnosis is actually frequently delayed in adults compared to pediatrics because the acute aspiration episode may not be recalled by the patient. And this is a retrospective study of patients with foreign body aspiration. Around 7% actually were asymptomatic. Only 20 less than, in the meantime between the aspiration and bronchoscopy was around 77 hours to as much as 173 hours. And actually the event of aspiration is not known in more than a quarter of cases. And chest x-ray was only abnormal in 62% of cases. And so the sensitivity of your chest x-ray is actually not very good for foreign bodies. And 50% of patients with foreign body do not have a contributing history. And 20% of children are given medications such as inhaled steroids before being found to have foreign bodies. And these delays to diagnosis can lead to recurring infections and chronic symptoms and can be mistaken for asthma and bronchiectasis can actually develop many years after an unrecognized foreign body. In fact, there's an animal study that shows that animals develop bronchiectasis only after two to eight weeks of introduction of foreign bodies to the bronchial tree. And resolution after you remove the foreign body has been described, but surgery may be necessary to remove the bronchiectatic segment. Other long-term consequences include strictures, infections, and other inflammatory polyps. And so in conclusion, this is a short presentation, chest imaging may be indicated as part of the workup with severe difficult-to-control asthma, which may involve a bronchoscopy, depending on the findings. Chest x-ray has a low sensitivity for foreign body. And so you may need to do a chest CT to rule out foreign bodies. Thank you.

non-malignant central airway obstruction

tracheobronchomalacia

inducible oranchole obstruction

foreign body aspiration

wheezing

difficulty breathing

dyspnea

coughing

difficult-to-control asthma