Video Diagnosis, Evaluation and Treatment of Bronchiectasis Evolving Strategies for Managing Exacerbations Play Pause Volume Quality 1080P 720P 576P Fullscreen Captions Transcript Chapters Slides Diagnosis, Evaluation and Treatment of Bronchiectasis Evolving Strategies for Managing Exacerbations Overview Welcome. I'm Patrick Flume. I'm a pulmonary physician at the Medical University of South Carolina in Charleston and welcome to this uh webinar on the diagnosis, evaluation and treatment of bronchiectasis. Uh This C M E certified webinar is provided jointly by the University of Massachusetts Medical School and C M E Education Resources and is supported by an educational grant from SMD Pharmaceuticals. So, what are we talking about when we're talking about bronchiectasis? So, bronchiectasis is a structural description of the airways. It's an abnormality in the airways in which the airways have become dilated. Now, there are two general mechanisms by which there can be bronchos, there can be pulmonary fibrosis which causes a pulling on the airways causing what we call a traction bronchos. In those cases, the disease is not really in the airways, it's in the inner, that's different from the condition we're going to be talking about in which the disease is in the airwaves in which there has been a morphological change of the airways causing this permanent dilation. It does have its own diagnostic code. Uh It has been classified as a rare disease in general. A rare disease. Are those conditions that occur fewer than 200,000 cases in the country. But what we have learned is that that prevalence of uh bronchiectasis has been increasing over time. Uh The most recent rates of, of the prevalence have been in the range of 566/100,000 persons. And that has been a substantial increase in the last 10 years now. Although some of this could be because there is an increased incidence of disease. More likely it's that people have it on their radar. Uh With the use of high resolution C T scanning, we are identifying more persons that have bronchiectasis. And I've shown you here three examples of pretty substantial uh bronch tadic features ranging from dilation of the airways to actual cystic changes uh that occur in the airways. There's a lot of heterogeneity of disease in the population with bronchia tosis. And that's for a variety of reasons. First is that there's a number of different ideologies. Uh The list of conditions that are known to cause bronchia or associate with bronchia is really quite long. And so, one of the key questions, when we first evaluate patients is trying to identify why they have the condition, there can be some clues as to how, what that definition may lead to. Uh For example, there are people who have very focal disease, which is a different ideology than those persons that have much more diffuse disease, which suggests more of a systemic uh condition. So, in focal disease, we can see that sometimes in which there has been a history of infection that caused injury to the airway such as a very bad pneumonia or perhaps a mycobacterial infection that caused an injury and did not fully repair. Or there might be some focal obstruction such as with a foreign body or um a mass of some sort that has included the airway and caused Broch to occur distally to that. And then when you think about the diffuse disease, this too can follow postinfection like that might happen with a severe measles infection or could be in the case of congenital disease. Uh cystic fibrosis would be a key example. Uh primary salary dyskinesias, it can occur in people that have immunodeficiency states. Uh They don't combat infection very well and are more vulnerable to development of infection. And then eventual bronchos also can occur in those that have autoimmune diseases. Um A B P A or allergic bronchopulmonary, aspergillosis is really an allergic asthma that has bronchiectasis as a feature and it's related to the fungi. Um but we also see it in things like rheumatoid arthritis or Schroen syndrome. We see it in persons that have inflammatory bowel diseases. And then another common uh feature that we see in these patients is aspiration and it really is a way in which they are introducing, not just injury to the airways, but also a pathway by which organisms can get down into the lower airways. This is oftentimes related um or found in persons that also describe symptoms of gastroesophageal reflux disease, not necessarily the heartburn, but the type of reflux that gets all the way up to the vocal cords. So there's symptoms that might involve the sinuses, uh the vocal cords and the like. Now, sometimes these things may be positive and in some cases, just a comorbid feature, but it becomes part of our overall evaluation of these patients. The is also great heterogeneity in terms of the radiologic severity. I've already talked about the differences between focal disease and diffused disease. But then there are people who have really very mild increases in the size of their airways. Whereas others have very, very serious disease with large expansion of the airways, oftentimes associated with increased airway wall thickness, uh suggesting inflammation and infection cystic changes uh and can be rather progressive. Not all these patients are gonna have a reduction in lung function. Um but some will actually develop pretty severe obstructive airway disease. And then in terms of their symptoms, the way in which they present uh or their day to day symptoms can also be quite varied. Uh for example, cough is a very common symptom that we see in bronchiectasis. And in a person that has a persistent cough, that's unresponsive to more typical common therapies, bronchiectasis should fall in the differential and AC T scan should be performed. But we have patients who may have bronchiectasis discovered by imaging done for another purpose. Say, for example, lung cancer screening or uh calcium scoring uh of the heart and the radiologist identifies broncho and yet that person might be asymptomatic. This can range all the way to patients who have daily cough that can be quite uh problematic for them. Sputum production can range from none at all to actually frequent uh sputum. It can range from clear to perent secretions if there's infection and uh even the presence of blood. Uh and that can range from very scant all the way to massive heis systemic symptoms are not uncommon. Uh but some will have none. They won't complain of anything specifically and yet others are gonna complain about severe fatigue. Um just not able to do what they previously could do pulmonary exacerbations episodes in which there isn't a worsening of their symptoms, uh might not occur in many patients and in others, they might be rather frequent multiple times per year where intervention is warranted. And then I already had mentioned uh the impact on airways function and there will be many patients that will have very preserved lung function and yet others that might have pretty severe impairment, either a restrictive or obstructive uh phenomenon. So let's give you an example of one of our patients uh that we have followed um as an example of how we might evaluate and treat uh such a patient. So this was a 55 year old female who had, was been referred to our center for further evaluation, but she had a long history of known bronchiectasis. She also had a history of known esophageal reflux as well as a hiatal hernia. Demonstrated on imaging part of her evaluation showed a normal I G E level and her Aspergillus antibodies were um unremarkable suggesting this was not A B P A, her I G G level was normal suggesting this was not an immune deficiency. She also had been tested for uh cystic fibrosis screening with a sweat test and she had a normal study. Her symptoms were daily. She had a cough, productive of sputum but also suffered from frequent exacerbations. She was malnourished with a body mass index of only 16.3 and her lung function was impaired with an F E V. One of 42% of predicted and there was a history of feed and cultures that had been performed and they had grown pseudomonas serosa and testing for mycobacteria had been negative. She had some pretty remarkable findings on imaging and I've just given you three slices. And what you can see is that she has evidence of disease in it's bilateral, but it's also in the upper airways as well as the lower airways. So she has diffuse disease. There's a couple other features that we can see on here when we look at the, the thickness of the airway walls they're quite prominent in these, uh certainly that center stand, but also that on the left, you can see that he bronchular cuffing where the airway walls are quite thick. And again, it's not necessarily that the airway wall itself is thick, but it might mean that there is a lot of excess mucus or phlegm lining those airways similar density as the airway wall. And so to us, it suggests that there's significant inflammation and likely infection. There also is mucus plugging where you see the airway is completely excluded. Some of that can contribute to that reduction in lung function. So when we evaluate these patients, obviously, we have two principal questions, um why do they have the bronchia of trying to figure out the ideology? And then the second is, well, what are you gonna do about it? And in general, our goals of therapy are to relieve the symptoms that led to that diagnosis. Ideally, we'd like to prevent progression of her disease. And we'd also like to prevent complications of disease. And in that case, a very common complication are the pulmonary exacerbations. So what is a pulmonary exacerbation in general? It is a worsening of the airway or systemic symptoms that we can blame on the underlying condition that meaning it's not due to something else. There are a number of definitions that are out there. We have a consensus agreement as to the definition that we use in the conduct of research studies and that is a person who with brachia, who has a change in at least three key symptoms. And for a specific period of time, at least 48 hours, we're not focusing on just day to day variability, but that there is a persistent change and those key symptoms were cough. So an increase in cough or a more severe cough, looking at the quantity or a change in the sputum. Uh So looking at volume or its consistency, meaning it's become more thick sputum pence, um there actually is a color scheme, uh looking at the color of, of sputum that correlates with the probability of growing a pathogen. So you can imagine that a a patient that has clear sputum that they cough up is less likely to have any um pathogen grow in there compared to those patients that might have more yellow green or even brown sputum, breathlessness or reduction in their exercise tolerance, an increase in fatigue or malaise and certainly coughing up blood hemoptysis suggests that there's worse inflammation. But another critical part of the definition of exacerbation is that there was an intervention that the clinician determines that this change in their symptomatology warrants a therapy. And so the research definition looks at both the key symptoms as well as the intervention. Our treatment of Broch is uh first, I want to make clear that there are no medications or therapies that have been approved by regulatory authorities for the indication of bronchos. The exception to that is that we have a number of therapies that are specific for patients who have cystic fibrosis. But their disease is also bronchiectasis. And it's very common for clinicians to take those therapies to see if they might be effective in their other patients who have bronchiectasis for other ideologies. Certainly, we want to treat the underlying cause of the disease if we can. So for example, if they have an immune deficiency, then perhaps providing replacement antibody uh would be beneficial for their long term therapy, treating A B P A uh with uh steroids or antifungal therapies, we also want to treat the comorbid conditions, for example, esophageal reflux because they may be contributing to the progression of disease or these exacerbations. And then we want to target the essential aspects of what we believe to be the path of physiology of their disease. Historically, we have talked about the vicious cycle of disease in which uh all of these different ideologies of, of uh bronchiectases can be at play. And so if we start with an abnormal mucus uh clearance, the airway mucus clearance method is is defective, say like in cystic fibrosis, this then leads to a retention of airway mucus. It becomes a great environment for which bacteria can um reside and replicate. And so you end up with this chronic or persistent infection, the host responds with a neutrophil response that inflammation is trying to get rid of the bacteria but is also harmful to the airway, causing further injury, further destruction and distortion of the airways, further impairment of the mucolytic clearance. And you can see that the cycle persists. What we have subsequently learned is that any one of these features can promote the other. And so, for example, in those patients who have impaired mucosy clearance, not only does that create an environment that's ripe for infection, but also contributes to the persistence of these inflammatory materials that this inflammation has come into play. The cells have dumped their contents but you can't clear them out. And so that issue, the inflammation persists and it actually augments more inflammation that obstruction of the airway can cause more deformity of the airways. And I can talk about all these various combinations, how each of these contributes to it. And so we've now come to think of this more as a vortex and that we have to target each of these areas. In order to get control of the disease. We have a number of therapies that have been tried and are often used in our patients. I will put the caveat that these are generally therapies that have been studied and approved in the patients with cystic fibrosis have been used in patients with bronchitis due to other causes not necessarily successful as they are not had the labeled indication for those those conditions. And so this does not mean that these therapies are appropriate for everybody but they consist of airway clearance therapies using therapies to augment the clearance of this mucus. Since the normal mucus laid clearance pathways aren't ineffective. Using hypertonic saline nebuli into the airways to hydrate those secretions and promote cough and clearance using chronic macrolite antibiotics, using other suppressive antibiotics. Is there a role for inhaled bronchodilators and then corticosteroids because there is inflammation. So let's just take a look at each of these and, and what their potential role can be. So, airway clearance therapies are basically job one for the patient that has bronchiectasis and retention of airway mucus. So certainly those patients who cough up sputum, they should be on airway clearance therapies if they don't cough up much. But their C T scan demonstrates an increase of mucus retention because there are thickening of the airway walls or Mica's plugs. They are likely to benefit from airway clearance therapies. There are a number of, of approaches that one can take ranging from breathing techniques, percussion and postural drainage using devices. There is not one of these which is clearly superior to the other, but what we have is a tool kit that we can use with our patients to find out which one is best suited for the individual patient because the one that they will do is likely to be the one that's best for them. Secondly, some of these are far more portable than others. And so if we're trying to find something that's conducive to a busy lifestyle. Perhaps one that involves travel, some of these devices might be uh better suited for, for packing and carrying with them. It is very helpful if you have a talented respiratory therapist who can help coach your patients and find the method that is most suited to them. Um We see patients very frequently who have been given a device but yet never got proper coaching uh for the device. So um there are a number of these uh choices that one uh should consider in their patients with AIS. Now, what about trying to treat the impaired mucosil clearance and a strategy that has been used most commonly is hypertonic saline. Now, this really sort of came to to the head and the cystic fibrosis patients with the belief that we could uh perhaps um replete the airway surface liquid and restore the balance. So the CIA could do their job. What we have since learned is that that can happen, but it's very transient. And so the impact of using hypertonic saline is not likely to restoration of the airway surface liquid, but very likely related to um changing the nature of the phlegm hydrating those secretions. So perhaps they are more fluid but also promoting cough uh and clearance. And so what you can see in the left panel was a typical dose finding study in which cystic fibrosis patients were exposed to um uh varying concentrations of hypertonic sailing and what you can see is that at the higher concentrations of sailing, there was an improvement in the clearance from the airways in terms of measuring iron particles that have been uh inhaled and looking at their clearance to the proximal airways. But for the most part, that clearance, the differences that you see in those concentrations all happens in that first hour, the slope of those lines after that time are all pretty much the same. It's ok that it's working only for the short term to try to clear this out. This is about lung hygiene, trying to help clear these secretions out. And so when you look at the panel on the right, looking at a variety of therapies in bronchiectasis patients and comparing the outcomes, whether you're doing air weight clearance uh alone using uh a bronchodilator like tribute using normal sailing or 0.9% to 7%. What you can see is that the sputum weight is greater. When you use the hypertonic saline, the improvement in their symptoms is greater. And even though it didn't have much change in the lung function, remember that many of these patients, it's not going to to change much. Um but it can be a very, very effective therapy. Now, when we start our patients on hypertonic sailing, we inform them that some people, it is the best thing that's happened to them. They really feel like they clear their airways out and yet there will be some people who think that we're Satan, um, this can be irritating to the airwaves for some people. It should cause cough and that's ok. A little bit of cough is fine because you're trying to clear these secretions. We are not looking for them to develop a bronchospasm or have a sense of chest tightness or be coughing all day long. Uh And in some of those patients, you can mitigate those symptoms with, uh and treat pretreatment with inhaled bronchodilator. But we just have to be cautious about how we coach our patients in terms of their expectations. What about macrolides for Broch? So, macrolides are a very interesting antibiotic. And in the setting of bronchos, you will hear people talk about their benefits as an anti-inflammatory. And there are in fact data to support an a mechanism of macrolides at reducing inflammatory mediators. But the truth is is we don't know how they're working in terms of the mechanism of action in our bronchia patients. What we do know from a number of studies is that in the proper patient population, when you put them on chronic therapy with a macrolide, their outcomes are better. Uh This is exactly heightened in patients who have pseudomonas. And generally speaking, we don't think of the macrolides as an effective antibiotic against pseudomonas. Um but there could be other bacteria, it is an antibiotic. But nonetheless, there are two key trials. The Bless trial and the bat trial that looked at the the use of macrolides over a long period of time. And if you're looking at the bless trial on the left, comparing Erythromycin to placebo, looking at exacerbation rates over that time, you see that those curves begin to diverge. Uh And so there is a lower incidence of cumulative exacerbations in the treated group. And you see similar effects in the bat trial which compared azithromycin to a placebo. And you see there's about a 30% reduction in exacerbations over that time. And so you can also see an improvement in symptomatology in terms of cough. But really, this is a therapy which is appropriate for patients that have frequent exacerbations. And that's what you're trying to improve caveat to. This is that many of our patients are vulnerable to infection with mycobacterium, especially with mycobacterium avium complex. In those patients, macrolides would be a key part of a treatment regimen um if they needed it. And so what we do not want to do is select out resistance to macrolides. And so, whereas we would not treat mycobacterial infections with monotherapy with a macrolide, we we would not want to ignore the possibility of N T M infection in these patients. So, in those patients in whom you think they might be a candidate for macrolite therapy, it is prudent to get some baseline cultures to ensure there are no mycobacteria, but also to monitor those cultures over time because they could acquire mycobacteria. Um and then you would consider withdrawing therapy. What about infection in general? Uh I advocate uh for surveillance cultures. I think it's important to know what bacteria or other pathogens might be present in your patients over time. Um When you find them at the beginning, looking at that microbiology, cultures for bacteria, fungi and mycobacteria are important. Um but then also to monitor over time because they may acquire a new infection and give you an opportunity for an earlier intervention. So for example, the opportunities for the treatment of infection might include prophylaxis in general. This is not recommended. We have not come to a strategy where we are prophylaxing against any type of pathogen. Um eradication of a new pathogen. This has been done in the cystic fibrosis population where we have had rig rigorous surveillance programs, looking for new evidence of pseudomonas and then treating those patients with inhaled antibiotics to try and eradicate the infection and delay the time to persistent infection in the airways. We have some recent evidence that this does result in long term benefit. Um Pseudomonas has been determined to be a difficult pathogen in the C F population. Um So similar strategies are being tested in the bronchia population. But the only way you would know if there is a new pathogen is if you are doing surveillance cultures in those patients who have persistent infection, you could use suppressive antibiotics either through systemic uh oral therapy or by topical, inhaled therapy. And then of course, if they have an acute exacerbation, then having knowledge of what organisms they have will help you choose the appropriate antibiotics to treat that acute event. So I wanna talk a little bit more about antibiotic suppression. So a aerosolized antibiotics for bronchus is this has been standard of care therapy in the cystic fibrosis population. Um I've already mentioned eradication strategies but, but the development of inhaled toro mycin uh back in the nineties really cemented our approach to using chronic suppressive therapy to try and prevent progression of disease and prevent exacerbations because of the success in the C F population. This strategy has been used in other patients who have bronchiectasis and grow pathogens such as pseudomonas. It has been tried with toy, it has been tried with ace Triam closin and in all of those trials, they failed, they failed in, in terms of being able to prove the benefit that would lead to a labeled indication for bronchiectasis. Um And yet it is a strategy that we use in many of our clinics because we have affirmative findings in other studies. There has been a lot of work looking at clinical phenotypes of bronchiectasis and there are a few that uh really sort of have have come out and, and one is the group that's chronically infected with pseudomonas, AOA. Um obviously, it's not just that they grow pseudomonas, they grow it persistently, it has been associated with worse quality of life and increased risk of exacerbations, increased likelihood of hospitalizations. And actually, in some prognostic models is associated with mortality. There also is a group of the frequent exacerbators that these are patients that have at least three events a year, very strong predictor of future events. And so in those patients that have frequent exacerbations and in those that have pseudomonas, this idea of trying to find some other way to suppress uh in infection in these patients certainly remains attractive in our own center. We did a post hoc analysis of our clinical data and what we looked at were those patients that we had on inhaled antibiotics and compared them to a matched cohort of patients that we did not have un inhaled uh antibiotics. Now, obviously, this is a um biased uh analysis of the data. Um but what you can see in there are some critical differences between those two groups. So in the table, if you compare those treated to those untreated, the likelihood of them having frequent exacerbations is much greater in those patients that we treated. Now, what I mean by that is that they were having those exacerbations prior to the onset of therapy. And if you look at the curve, the the figure on the right in those patients, you can see the number of exacerbations before we started treatment in the blue and after we began treatment in the red. So yes, they're still having exacerbations, but there is a marked shift to the left of fewer events and even uh a a proportion of those patients that did not have any further exacerbations. Now, this should make perfect sense to everybody that if your patient is on your other therapies and still having exacerbations, it makes perfect sense to add yet one more novel approach to treatment. And if your patients not having those events, then why would you add more therapy? But contrast that to the two of the studies that looked at inhaled a triam. And what you see is that the larger proportion of patients that had no events or just one event in the previous year and um a much smaller proportion of patients that had more frequent events. So it's very difficult to improve upon uh a complication that they're not having in our group. The treated patients were more likely to have pseudomonas. There was a very high proportion of those patients who were on chronic macrolite therapy and hypertonic Saline compare that to what was seen in those um clinical trials. It was a pretty low rate of using those therapies. So you have to question about whether they were the appropriate patients to be enrolled in a trial. So in my book, there, there is a a niche uh for inhaled antibiotics in the appropriate uh patient population. How do we treat pulmonary exacerbations? Well, uh obviously this is an increase in symptoms. So we amp up our chronic therapies. So we increase their effort with air weight clearance. This could be changing the therapy, it could be increasing the duration of that therapy or its frequency. In many cases, they will get systemic antibiotics, could be oral if the organism is, has an antibiotic that would work there. Otherwise, it's likely to be intravenous in the right patient population corticosteroids might be of benefit, especially in those patients that have steroid responsive disease like A B P A, possibly a role uh for bronchodilators in those patients as well. Finally, we want to treat the complicating factors that might, you know, make their management of their disease more difficult. Again, we talked about treating the underlying causes, treating exacerbating comorbidities like esophageal reflux, but really focus on nutrition, especially in those patients who are malnourished with a low body mass index. Vaccination is encouraged in these patients and we refer a lot of patients for participation in pulmonary rehabilitation. So, nonetheless, our patients continue to have symptoms, they continue to have exacerbations. We don't have specific therapy. So what where are we where it is on the horizon? So even though they may not be labeled indications for therapy, we do have therapies that target the clearance of airway material and the phlegm and also infectious pathogens. But we don't nearly have therapies that specifically target the inflammation. Cortico steroids are appropriate only in some the macrolides. We've talked about whether they truly are functioning as a um immune modulator um or as an antibiotic is not clear. But the other thing that we know about these patients is that they have a neutrophil predominant inflammatory process in the airways. They have excess neutrophils and they persist in the airways in many patients, especially those with frequent exacerbations. The neutrophil amount quantity is excessive. The products that these neutrophils release are also injurious to the airways. And there are a number of these protein um se proteases that are important. But the one that we focus on the most is neutrophil elastase. You find very high levels of velocity in those patients that have pseudomonas origins. You find very high levels in those patients that have frequent exacerbations. So that could give us a strategy of trying to address this aspect of pathophysiology. So one approach might be let's just prevent neutrophils from getting into the space. The problem with that approach is that neutrophils are good that you, you need them to combat infection. So we can't risk having a therapy which is too good at blocking neutrophil migration uh and entering into the airway. What about trying to either down regulate or reduce in some way the quantity of neutrophil elastase in the airways. And there have been a number of strategies that have been discussed for this. Um One is to use neutrophil elastase inhibitors. Uh ALPH one and a Trippin is, is a product that does uh inhibit neutrophil ass ase. And the challenge there is being able to get a sufficient quantity of product into the airway to combat that amount of neutrophil elastase. But there is a novel approach that we are investigating now and this is about intubation inhibition of dipey peptid ase one. So DPP one is a normal enzyme. It uh cleaves the end terminal dipeptide of the cerium proteases essentially activating these proteases as they're being packaged into the neutrophil. And this happens in the uh bone marrow. So, there actually is a genetic condition in which this enzyme is lacking. Uh but uh we have now discovered and developed inhibitors of DPP one and developed them for clinical investigation. So this is not about reducing neutrophils. This is about uh essentially taking bullets out of the gun, reducing the quantity of neutrophil elastase that those neutrophils have available to them. This has been studied um in uh clinical trials. Um This is a phase two study of a DPP one inhibitor in which a little more over 250 adults were randomized to a six month study uh compared to placebo comparing two doses of a DPP one inhibitor. Um to be in the study, these were adult patients who had a daily symptoms of cough and sputum production and a history of at least two exacerbations in the previous year. And what you can see on this slide is the quantity of neutrophil elastase that was found in the sputum. And you can see it's relatively stable quantity in the placebo group. But there is a reduction uh at the two different dose levels during the treatment study, the phase of the study which then increased upon taking away uh the study drug. So it looks in terms of the mechanism of action that it is in fact reducing neutrophil elastase. But what you want to know is what the impact was on the primary end point, which is looking at reduction in exacerbations. And so what you can see here is that in the duration of the study, there is a reduction in the frequency of events uh for both doses of this DPP one inhibitor. This was very promising it. Now this particular product is now in a phase three study. Uh but there is another uh similar agent in the same class that is currently being investigated in a phase two study. So these are very promising results that we look forward to uh as giving us perhaps yet another opportunity uh to treat our patients with bronchiectasis. So let's go back to our patient that we presented at the early part of this presentation. Um Remember, our goals of treatment are to treat the underlying uh symptoms that she has. So she was having a daily cough and sputum production, frequent exacerbation. So our goals of treatment will be to try and reduce that cough, reduce the inflammation and try to prevent these events, these exacerbations. And I've given you some additional information that gives us a number of opportunities that we can take in terms of her disease management. So obviously, she has a daily cough and speed and production. So, airway clearance therapy is essential in this patient. She would be an excellent candidate for a trial of hypertonic saline. In our clinic, we would start at 3% if that's tolerated. Well, we have the opportunity to increasing that up to 7%. Um She has um been sputum cultures which have grown pseudomonas and cultures that have shown no evidence of um mycobacterium. And so chronic macrolite therapy is also an option in this particular patient. And we would continue to monitor um her uh cultures to make sure that there isn't development or acquisition of mycobacteria while on treatment. But because of the presence of pseudomonas and the frequent exacerbations, she would also be a candidate for aerosolized antibiotics. She we know that she has reflux. And so we talk about gird management. Many of these patients are put on acid suppressants. And so a proton pump inhibitor um that doesn't stop reflux. It changes the nature of what the reflux that comes up. And although it may be that the acid component really is the problem, we have to focus on other um conservative measures to try and reduce the complications of reflux. So, elevation of the head of the bed, um this can be done with pillows but better to elevate the the frame of the bed just a few inches to try to make a difference. There, smaller meals rather than larger meals don't eat right before going to bed. Um, try to reduce carbonated drinks because that increases the pressure in the stomach. And a key question that we ask in our patients is how much caffeine they take in because caffeine can weaken that distill esophageal sphincter. And so if we can create some changes in their, their life, that might help her body mass index is low. So we really need to focus on nutrition, try to get her um weight up. Also, we talk about vaccination and pulmonary rehabilitation. Obviously, we're not going to give her all of these all at the same time, but we can develop a strategy and tailor it to her particular um needs. And so I'm gonna conclude uh Broch is a condition that may have a common descriptive feature that is the dilated airways, but it has a very heterogeneous set of ideologies of severity and clinical presentation. And so even though we have a common term of bronchiectasis, our approach to treatment will vary based upon that particular patient's presentation. So a careful evaluation can inform your treatment decisions. So having a knowledge of the actual ideology and those complicating factors will inform those treatment decisions. As I said, the treatment should be personalized based upon those symptoms, the severity of disease and the resources available to that patient. And obviously, our treatment goals are to reduce the symptoms, prevent progression of disease and prevent pulmonary exacerbations. So with that, I thank you. Published March 31, 2023 Created by
