A (1:53)

And just a reminder to post the hashtag MOPPA for Make America Paul again.

B (2:01)

This is going to be posting well after the fact that that is relevant question mark. We'll see how things go.

A (2:08)

No, I just want that to be an ongoing thing. Anyway.

B (2:10)

Great.

A (2:11)

On tonight's episode, a much needed update to asthma with a fantastic guest expert and longtime Curbsider now runs his own podcast, but Dr. Cyrus Askin will tell you more about him in a second. But pa, can you remind people what is it that we do on the Curbsiders? And can you introduce our co host for tonight?

C (2:34)

Sure.

B (2:35)

Matt we are the internal medicine podcast. We use expert interviews to bring you clinical pearls and practice changing knowledge. As you mentioned, we are joined by Dr. Paul Wertz, one of our newest wunderkins, one of the up and comers, hopefully one of my future replacements who did Yeoman's work, both writing the episode and then also co hosting with us. So Paul, how are you?

D (2:52)

I'm doing well. I don't know about all that, but happy to be here.

A (2:55)

And I should mention to the audience we are recording with two Pauls, so I'm going to call Paul Wirtz, I'm going to call you Wirtz. And Paul Williams, you've been here first, so we're just going to call you Paul. So Wirtz, can you please tell the audience about our wonderful guest?

D (3:10)

Of course. So we have a fantastic conversation with our guest, Dr. Cyrus Askin, who is a longtime beloved member of the Curbsiders family and a current pulmonary and critical care doctor. Cyrus is now serving as an internal medicine associate program director at an academic medical program in El Paso, Texas. He is the medical director of their intensive care unit and an assistant professor of medicine for the Uniformed Services University. He is also the co founder for Critical caretime, an intensive care podcast where he and his co host dive into the high stakes world of critical care medicine and discuss all things critical care. In this episode, he teaches us all about asthma and smart or mart therapy. So without further ado, let's get to it.

A (3:51)

And a reminder that this and most episodes will be available for CME for all health professionals through VCU Health at curbsiders.vcuhealth.org and if you haven't done so yet, sign up for our patreon@patreon.com curbsiders where you get twice monthly bonus episodes, ad free episodes and a whole bunch more patreon.com curbsiders okay, Cyrus, so the listeners have heard your bio, but they want to know what, what hobby or interest are you currently up to outside of medicine?

C (4:24)

Yeah, no, it's a great question and thank you guys so much for having me on as a guest. This is really exciting. It's sort of like this weird, like full circle experience that I've had with you guys. So I'm tremendously grateful.

A (4:35)

Yeah, it's like it's gotta be at least seven years, Cyrus, that you've been working with Curbsiders.

C (4:40)

Maybe longer, maybe eight or nine. I don't even, I lost track. You know, when time flies, when you're having fun. So. Yeah, so Hobby outside of medicine. So, you know, I've got a one child, one on the way, so that kind of keeps me pretty busy when I'm not at work. And I know, Matt, I know you're familiar with that life aside from that, so. I spend a good amount of time in the gym whenever I can. I've sort of, like, in this constant balance between lifting and cardio and, like, trying to figure out what works for me without causing all of my joints to spontaneously explode. Such as life. Right. For those of you that might be watching, I have this whiskey collection here, so I do enjoy a sip or two every now and again. The guitar, I still play from time to time when I have the opportunity. And then really the. The. My podcast, Critical Care time, which I really credit you guys to helping me, like, inspiring me to get that off the ground. That takes up a lot of my time, too. So between the kids, the gym, and all that good stuff, yeah, I. I stay pretty busy.

A (5:42)

My joke is that you, like, when people ask me if I play golf, I'm like, you're not allowed to play golf and have a podcast, so. Cyrus, do you play golf?

C (5:50)

I do not. Absolutely not. No way.

A (5:52)

Yeah.

C (5:53)

Yeah. I'd be sleeping on the couch if that were the case.

A (5:57)

Smart man.

B (5:58)

Let me channel Marc Maron. Cyrus, I may have even asked this before, but who's your guitar guy? Do you have a particular guitarist that you like a lot or that you're actually inspired by? I mean, I'm sure you have a list, but so I'm gonna narrow it down to a couple, if you're able to. I will always not to be sexy.

C (6:14)

No, no. I will always love Carlos Santana, and he's the one that kind of got me into Paul Reed Smith guitars because I just think they're so beautiful. The tone is amazing. That's like, something. I'd love to buy one again when. When my wife loosens the purse strings a little bit for me, so there's that, you know, Baby Cyrus.

B (6:35)

That's a good way to start.

C (6:36)

We're done. After two, we're done. Like, that's. Yeah. I can't. I can't. The transition from, like, man to man to zone defense is very scary to me. I'm not very fast, so that bothers me a lot. The other thing, the other guitarist who I. I really like, and I know this is maybe a bit of a polarizing answer, is John Mayer. I. I think he's a. A great acoustic guitarist, and I think his ability to improvise. I'VE heard him live a few times. It's, it's really amazing. I mean, I've listened to all the old band, like I love, you know, I love Guns and Roses and Slash. Like I love listening to Led Zeppelin, more contemporary. So the Mars Volt is actually probably my favorite band. And I think Cedric Bixler Zavala is like one of the most like amazing singers and Omar Rodriguez Lopez is like a phenomenal guitarist. So, yeah, my interests are like all over the place when it comes to music.

B (7:23)

But yeah, I don't think anyone's arguing that John Mayer is not a good guitarist. Maybe personality standpoint, you may not want to spend time with them, but the guy can play guitar.

C (7:32)

There you go.

B (7:32)

There you go.

C (7:32)

Yeah.

A (7:34)

All right. We're going to get Paul, Paul going on music here and we're never going to get to the cases. So I guess I think we should get to a case because I think we're going to run long otherwise. So, Paul Wurtz. Wirtz, will you read our first case from Cash like Memorial Hospital?

D (7:48)

Yes, I'd be happy to. So we've got Allie butyroll. She's a 32 year old woman who presents to your office for intermittent worsening cough and shortness of breath over the past year. She's establishing care as she recently moved here from across the country and began noticing symptoms shortly thereafter. She's also currently pregnant at 22 weeks gestation. She notes a remote history of mild childhood asthma, but nothing beyond elementary school age. Her mother has asthma, her sister has eczema and bad allergies. She states that the symptoms used to occur two to three times per month but now occur two to three times per week, especially at night. She also has accompanying allergy symptoms that started recently. She manages these with some over the counter cetirizine. She has tried a coworker's albuterol inhaler which helped her symptoms and is requesting one for herself. So in general, when you're talking to a new patient with potential asthma symptoms, I guess I'm interested in how do you conduct this interview and how do you elicit the specific triggers and things that you're that help you talk with patients about their potential asthma.

C (8:51)

So, Paul. Yeah, great. That's a great question, a great way to I think start the discussion. Yeah, I'd probably just give her the albuterol and send her on her way.

A (8:59)

That's my bit.

B (9:00)

Come on.

C (9:00)

Yeah, so no, there's, there's, obviously there's a lot to unpack here. It's like I said, it is a great case. So initially I think it's really, it's really important to start, I think with an open ended question. So a lot of times what I use in my clinic is, you know, hey, welcome to the pulmonary clinic. It's great to meet you. I'm Dr. Askin, what the heck are you doing in pulmonary today? You know, how can I help you? What's going on? And oftentimes that is a great sort of informal way of establishing rapport and getting your patient to share a lot of information that you would otherwise be asking kind of piece by piece. Now, depending on the situation, sometimes you don't get all of the information that you need. And so I'll start to ask certain elements of the history, get at certain elements. Now in this case, you've given a pretty classic story for someone that we call has allergic type asthma, classic asthma, high T2 or high T helper 2 type asthma, given the eczema, the family history, the association with allergies, et cetera, et cetera. And so with that all being said, I'd probably get at things like is there an environmental association? Hot versus cold, humid versus dry? Do you have worse symptoms when there are changes in climate, when the pollen count is high? Do you ever, like I know on my smartwatch you can look at the aqi and I follow that from time to time because I'm a nerdy pulmonologist. And so if you see an association between the air quality index and worsening symptoms, that could be a little bit of a suggestion that there could be something, something going on in areas where there's a lot of dust wildfires. So you know, here in Texas there could be dust storms. Obviously California has their, their issues with wildfires. So that, that could be a, something you want to know about kind of moving on from that. Other kind of big things to be would be like activity associations. So when you exercise, is that when you have symptoms, is it only when you exercise, is it worse when you exercise? If you exercise indoors versus outdoors, is there a difference? I'll often ask that. I'll ask, you know, you gave us that family history, which is awesome. But I'll often ask, you know, history of asthma, history of other lung diseases. And then a couple big things that I'll kind of close out with would be history of prematurity or history of quote unquote childhood asthma. So when it comes to prematurity, really what we're asking about is born prior to or at about 34 weeks. And the reason being is that we know that distal airway development, terminal airway development, surfactant production, all of those things don't really come to a head until later in the pregnancy. And in certain cases, in extreme cases, you can see bronchopulmonary dysplasia. You can also see folks that have, you know, they think back to their childhood, and they're like, yeah, I was always in and out of the hospital. Well, that can be related to, you know, some degree of immunodeficiency or immune dysfunction that a patient may have grown out of, or maybe not hard to say. Or maybe not hard to say, but it kind of depends on the case. So all of that, I think, goes into why I asked that particular question. And then finally, I asked that question about childhood asthma. So a lot of times, and especially you can see it in these folks that have a history of prematurity. Not always, but sometimes there's that association. They'll have this quote, unquote diagnosis of childhood asthma, which may or may not be rooted in spirometry. I think we'll get to that later. But they'll basically have symptoms consistent with asthma that abate as the patient gets older. Why? Because you see increased airway diameter, improvement in airway inflammation, or damage that may be reversed as the patient kind of continues to mature, especially if they're on ics. So if you start them on ICS or inhaled corticosteroid early, that may actually mitigate some of those inflammatory changes. We don't totally understand this idea of childhood asthma and why it disappears and why it can relapse. But that's definitely something I ask about as well.

A (12:46)

Yeah, and we're gonna get to the Th2 high and low asthma at some point. But let's just. I mean, this person seems to have asthma, like, pretty good story for it. Childhood asthma, family history of allergies. It sounds like maybe moving environments kind of re triggered it. But when we talked to Dr. Blagev, and this was, like, 400 episodes ago, Cyrus, I think you were part of probably the planning or the recording of that episode.

C (13:14)

Yes, indeed.

A (13:15)

She mentioned that she feels like you could probably get away with not doing spirometry because it's not always available. So where are we at with that these days in making the diagnosis of Asthma? Is spirometry 100% necessary? And I was surprised to see peak flow, peak expiratory flow testing even mentioned in the genome guideline.

C (13:33)

Well, I would say that the guidelines and kind of best practices would Definitely support using spirometry. If not spirometry, you would use that peak exploratory flow. And we can sort of touch on that here in a moment. What I would say is that I think in certain situations, depending on patient factors, institutional factors, et cetera, there may be a place for empiric therapy with corticosteroids, inhaled corticosteroids, as sort of a diagnostic and therapeutic approach. Now that is not the standard of care and I want to be very clear on that. But you know, I've done it before and maybe that's me evoking the like. I'm a pulmonologist, I hear what this patient is saying. The patient doesn't have any like employment related implicate issues here. So for example, if you're in the armed forces, if you are in like let's say certain public services, fire, ems, police, there may be a requirement for you to have a solid diagnosis, a bonafide diagnosis with objective data. For a lot of my patients that is not necessarily the case. And so it's like, well, risks versus benefits. We tried to do spirometry a couple times and you coughed too much or you weren't able to actually complete the test per ATS standards. Let's just go ahead and see how you do with some inhale pluticasone and go from there. Those are rare cases, I will say otherwise, we're really using spirometry and then in some occasional circumstances we'll use peak exploratory.

B (15:08)

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A (18:01)

Paul, what are you seeing in your practice?

B (18:05)

Yeah, I was going to go back to actually our case stem. So for this patient, it's funny because in our script, we're like, well, this is obviously asthma. And I'm like, I could see a world where I think this is allergic rhinitis. And the patient's short of breath because she's 22 weeks pregnant and has restrictive lung disease from gravid abdomen. And so I.

C (18:21)

So, like.

B (18:22)

So maybe obviously asthma, maybe not. But I think sometimes it's not totally clear. But to your question, Matt, I don't see the PFTs ordered consistently in part because I feel like we've had them all come back normal, which is not surprising much of the time. And that doesn't tell us that the patient does not have asthma. So it gets a little bit sort of sticky from that standpoint. So I guess that would be the question I would have for Cyrus, probably. I would imagine you would do pulmonary function testing after this patient delivers, just so the water's not too muddy. But then also, what do we do with normal results then?

C (18:50)

Okay, perfect. So, first and foremost, you mentioned that this patient is pregnant. That rule of thirds that we learned, you know, eons ago is. Is still relevant. So that kind of idea of a third of folks with asthma get worse, a third get better, a third stay the same. That is still kind of what I teach my residents. That's still kind of our general understanding. So. So that may be why these symptoms are coming to a head. Or it could be the fact that this patient has dilutional anemia and a gravid uterus and, you know, et cetera, et cetera. Recognize that this idea of just dyspnea, that the.

A (19:23)

The.

C (19:24)

The differential for dyspnea is massively huge and involves, like, all of the organ systems from the integument all the way to the heart. Right. So with that being said, if we assume this patient might have asthma, then you could go ahead and get spirometry. There's not a reason why you couldn't get spirometry in a patient that is 22 weeks pregnant. But as you said, the results may be skewed by the fact that they're. They may have restrictive pattern on their PFTs, depending on how gravid they are, you know, etc. Etc. But I would say, in general, if we take a step back and say, okay, take pregnancy out of the equation, how do we approach this patient from a pulmonary function testing standpoint? Well, as you alluded to, Paul, normal pulmonary function tests in a patient who's not terribly symptomatic on that day when they come to see you, it tells me Nothing. You may see if you order spirometry with bronchodilator. And the idea there is like, I don't care whether or not they have obstruction. I want you to do a bronchodilator challenge and see if they have that change that could be helpful. If that's not helpful, you may see and this is very sensitive but totally not specific and not guideline driven. But in my practice, if I look at that peak FEF, so the forced exploratory flow 75 to 25, that'll kind of show you medium airway evidence of medium airway disease potentially. So basically what you're looking at is how well does air escape from those medium sized airways and if there's a limitation and a big bronchodilator change in those medium sized to small sized airways that may be indicative of asthma potentially. All that is to say, oh, go ahead, Matt, did you have a question?

A (21:09)

No, I just, I've seen people point to that on PFTs and say even more general than asthma. Just say this patient could have small airways disease, which I guess is like could. I had to look up what that is. Could be asthma or COPD, some issue with the small like less than 2 millimeter airways or something.

C (21:28)

Right, right. Yeah. So that could be seen in like a bronchiolitis or it could be seen in bronchiectasis that's affecting the really smaller airways. Because we recognize, you know, bronchiectasis is also a obstructed lung disease. A lot of people forget that they're okay, so COPD and asthma, but bronchiectasis can be too. And then there's of course overlap. But that's just, that's something that I do, something that I was taught when I was in training. You can look at that. But really I wouldn't say, oh well, their FEF 25, 75 is reduced, so they have asthma and they have a bronchodilator response. So they definitely have asthma. No, I would look at other tests. So if they have a normal spiral with BD or spirometry with bronchodilator, then I'm going to be looking at my provocative tests or evocative tests. And so your direct bronchopopagation test, typically that's done, is a methacholine challenge test. And in fact, in my practice I've kind of jumped to doing those very early. In fact, I'll often do those right away because based on availability of spirometry it can be, it can take a while to Get Spyro, see the patient or talk to them again, then order the meth and then we have to fit them in the schedule. When I order a methacholine, I get baseline spirometry and then I get a graded test with increasing doses of methacholine and then I kind of get a pretty good answer. I mean, your, your methacholine is a tremendously sensitive test. It's not very specific, but it's tremendously sensitive. I want to say upwards of 95%, maybe 98% of memory serves, don't quote me on that, but it's quite, quite high. Or I may get an exercise challenge test. You know, if that's kind of consistent with the patient's symptoms, I might get them both. And then there are plenty of other tests we can sort of talk about, but basically to sort of answer the question, yes, every once in a while I'll make a quote, unquote clinical diagnosis. I really hate doing that. I really try to avoid doing that. There are so many other things that can look like asthma. So I think it's really, really important to do that spirometric testing. And if you are in a resource limited environment and all you have is access to exploratory flows, sure, you can do that. But the trick is you've got to get multiple readings in the morning and in the evening over like a two week period and compare that to what will be predicted based upon the patient's demographics. And you can MD Calc has like a little calculator you can use to come up with that.

A (23:51)

So to recap a little bit, basically when someone with asthma, let's just say asthma, and they have no symptoms on that day, they might have a normal spirometry. But if we did a bronchodilator response, maybe we would see something that might capture a couple more patients or help us make the diagnosis correct. And then you said you could look at this FEF 25, 75 and is that reduced, Is there a bronchodilator response there? That could be a clue, but maybe not what we hinge our whole diagnosis on. And then you said that what you like to do, just for practical purposes, to save a patient a trip and is do baseline spirometry. So spirometry probably with the bronchodilator, then they do the methacholine challenge where they step up how much they're getting and you see if you can induce symptoms.

C (24:38)

Well, so typically what happens is they'll come in, they'll just blow a baseline.

A (24:43)

Yeah.

C (24:44)

And That'll be kind of their spirometry. You can't, unfortunately, give them bronchodilator at that time because it's going to ruin your methacholine.

A (24:52)

Okay. So.

C (24:53)

So you have to start. You basically roll right into the methacholine. And the way that the respiratory therapists will do that is they. They follow the ATS protocol, giving increasing doses of methacholine. And then they're going to be looking for a drop, like either the appearance of obstruction or a drop in FEV1. There's kind of like some variation in terms of what kind of a drop you're looking for based upon, like the institution, for example. Like, you know, if you're again in. Well, I'll just leave it at that. But basically you're going to look for a drop in FEV1 and then you're going to give that person bronchodilator and see if they have. They should have reversibility. They should reverse at that point. And that. That's how I. That's how I use the method.

A (25:31)

Okay. Yeah, great. And then with the peak flow, which is kind of our peak expiratory flow, as our last resort, you'd get them a bunch of readings morning and night, because, you know, when I've done them at bedside, you get variation from reading to reading, and then you would sort of compare them to what you would expect for someone that age and that size. And. And then we can kind of look at the charts to see if they would meet criteria or not.

C (25:53)

Okay, that's essentially right. Yeah. You're going to be looking for basically two weeks worth of data, and you want to see greater than 10% of.10% variability, assuming technique is right. But, like, you're not going to. I mean, I don't know about you, but I'm not going to be there in the morning, in the evening for two weeks.

A (26:08)

Paul moves in with all his data for two weeks.

B (26:10)

Really dedicated Dr. Cyrus.

C (26:12)

Yeah, I know, I'm a slacker. Yeah, so. But. So that's why it's, like, really not ideal. But I think the takeaway for this is, although Gina and pulmonologists agree that the gold standard in what should be pursued is objective diagnosis, I mean, if you're relying on a peak expiratory flow, then the threshold for starting empiric inhaled corticosteroids is pretty low. So I think that then feeds into the idea of, okay, if the patient's really symptomatic and you think it's asthma, probably as Long as they're doing good techniques, swishing and spitting after use, et cetera, they're probably not gonna take a big hit from a trial of something like a fluticasone or a budesonide. But again, gold standard is testing, and that testing should be spirometry.

A (26:58)

Okay, so let's say we've done spirometry. We're in a good situation. We've done spirometry. We've observed a bronchodilator response. We didn't have to do the methacholine challenge. And she has symptoms that we think are compatible. So we're thinking this is asthma. So I guess. Paul Williams, I'm going to ask you because I don't want to jump the gun. Are we ready to talk about treatment, or do we have more diagnostic questions?

B (27:22)

Thank you for asking. Yeah, actually, I was hoping I'd get a chance to jump in here and ask. Cyrus, would you mind talking to us a little bit about staging? So we've made the diagnosis, and I know the treatment depends on stage, at least sort of. Back when Matt and I were residents, there was this mild intermittent concept, which may or may not germane. And then you throw in albuterol at the end. You'd escalate therapy if you were actually paying attention, asking about symptoms. But can you. Can you talk us what the current guidelines tell us about staging, what we're to do with that information before we start treatment?

C (27:49)

Yeah. So I think I also learned this idea of, like, mild, mild intermittent, persistent, et cetera. And I'll be honest with you guys, and maybe this is just because I'm lazy and a bad doctor, but I don't really use those terms a lot. I kind of just try to get a feel for, like, I really focus on more patient centered language and patient centered. Like, the patient experience, I guess, which maybe sounds kind of. Kind of fluffy, but I think it's really important. So if the patient's, like, always symptomatic and waking up at night with symptoms, and you can sort of elicit this through the asthma control test, like you can use an asthma control test, which we may talk about a little later. But basically it's a questionnaire that you can use even in someone who you think could have asthma, but you don't know. And so if they're. If their score is really low and you're thinking, okay, they might have asthma, or you make the. Let's say in this case, like, you have this biometry. Yeah, they have asthma and their score is really low, that's probably more of what I would use to say, okay, maybe I need to start this patient at step two or step three versus step one. Um, and we could talk about what that means in a moment. But. So I don't really like hem and haw or agonize over, like calling it moderate intermittent mod or whatever that I don't even think that's a thing. But moderate, persistent or whatever. I just kind of look at like, yeah, I was like, that's not a thing. I was like, I just kind of focus on persistent, intermittent. Yeah, they're persistently intermittent and moderately severe. Um, but I really just focus on trying to understand how bad are their symptoms, how much is it affecting that patient on a day to day basis? Is this episodic to the extent where there's like the potential for trigger mitigation, trigger avoidance? Is this not. And so I kind of have to go with a treatment that's going to be targeted around the trigger, or is this like, yeah, the person's got symptoms pretty often and it's kind of life limiting and impactful. We're going to be a little more aggressive. And that's kind of to an extent where practice patterns are going to vary. But in general, that's how I kind of like three buckets would be like. Does the patient have symptoms? Only in certain circumstances. Does the patient always have symptoms, but they're fairly mild in nature based on ACT score or my kind of general gestalt? Or is this person pretty much always short of breath and they're not able to play with their kids, really take care of business at home, they're having issues at work, et cetera. That's how I sort of approach it. I just find that to be a little bit more practical.

A (30:09)

I like it. I can remember that. And I guess, should we talk about the ACT score? Like, do we have enough information to score hers, or do you need spirometry data for that? I have not used that score before.

B (30:22)

No.

C (30:23)

So the act. So the asthma control test is super effective. I would encourage everyone to use it. The nice thing is there are a million different pronouns that you could just hand your patient or have your nurse or MSA or whomever give the patient that while they're waiting to see you, and then you'll get it back. So just in a nutshell, it's basically you get scores from 5 to 25, where a score of 19 to 25 would indicate well controlled asthma. Anything less than 19 would be not well controlled or perhaps even poorly controlled asthma. And the Five questions that are rated on a five point scale include frequency of shortness of breath over the last month, limitations on daily activities, frequency of asthma symptoms at night, how often are you using a rescue inhaler, and then finally, what is your sort of assessment of your own asthma control? So you'll take one out of five for all of those, sum it up and you'll get an answer. As you can imagine, that's also great to report longitudinally. So like when I see a patient in clinic, if I have an index ACT score, I can then kind of track them over time and use that to guide do I step up, do I step down? Am I totally off the mark? So that's how I use it.

A (31:29)

Beautiful. Okay, so for somebody that, let's say they have an AXE score of, I guess let's start with greater than 19, so it's 20 to 25 range. Let's give her. So it's on the more mild end. I guess that means maybe she's doing better at this time. What might you start at as your first step in therapy?

C (31:52)

Yeah, so I think the first question is, okay, is this an ACT score? That is, how accurate is this? Like sometimes what I found is sometimes patients will underreport symptoms too. So if someone's in my clinic for asthma or for shortness of breath but their ACT score is like 24, then I'm like, oh, well, hold on, like there's some discordance here. And so then I have to kind of tease through that a little bit more. But let's say, you know, this is a good day and you push them a little bit more and you're like, okay, yeah, you've got a good ACT score, but you are reasonably symptomatic and I think we should start treatment. You know, the data for inhaled corticosteroids preventing progression is not the most robust data in the galaxy. So we know that it helps reduce inflammation, we know that it does have an impact. But how do you quantify that impact? What is that impact? It's much, I guess, less significant to the patient on a day to day basis than how is it going to improve my symptoms? And that's where you get a lot of bang for your buck, is symptoms control. So with that being said, a patient like this who's like, yeah, my act's pretty good, but really, you know, I do notice when I'm exercising, that's really when I have symptoms, that's when I might use the as needed reliever therapy. And so really, for the most part that's going to be Budesonide for Motorol in inhaler form. And I'm going to have patients take, you know, two puffs of that with symptoms whenever they have symptoms. That's one approach, another approach. And I'm not sure that this is explicitly stated in the guidelines, but many of us do. This would be. If patient knows that their group exercise class is going to trigger their symptoms, I'll say, hey, 15 minutes prior, go ahead and take that budesonide formoterol, two puffs before you, you exert yourself and then you can take another couple puffs later if you do have symptoms and just go at it that way. So long as a patient's keeping under 12 puffs, 10 to 12 puffs, 12 is the absolute max in a 24 hour period. There should not be any issue there because it's really Limited by the 4 Motorola dose, by the long acting beta agonist.

A (33:55)

Yeah. And maybe we should talk about. Because this is, you know, Cyrus, we've talked about this on the show. This came the Gina guidelines back in 2019 started to talk about this and we talked about the Sigma trials which I just have to, as an aside, if you have middle school children, everybody says like what the Sigma all the time. And there's all these like, I don't know if Sigma's good or bad, but the middle. It's in this like lingo that these, these kids have. And I just thought it was funny when I was looking back that the, I didn't remember these were called the Sigma trials. So. Yeah, anyway, for what it's worth. So Budesonide for Motorol, why is that the reliever? Because I'm still seeing a ton of people on albuterol.

C (34:36)

Yeah. And you'll probably continue to see that because it's like so ingrained in textbooks and folks just learn that that is the approach. And really at this point we have very good data to suggest that it really shouldn't be the approach. So the data for Budesoni and for Motorol in combination really goes back decades. That's the data that sort of demonstrated efficacy, but it really wasn't until recently. And that was Sigma 1, Sigma 2 and Novel Start. Those are three studies which I'm sure we can link to in the show notes. But those are three studies that sort of solidified the utility of Budesonide and Formoterol in combination as being a quote unquote superior option for asthmatics. Why is it superior? Because it provides reliable and pretty impressive symptom control. There's a statistically significant reduction in exacerbations. And if you're using it especially as kind of on an as needed basis, you're getting those benefits at a lower dose of corticosteroids. Now some of the data is a bit conflicting in that if you have someone on maintenance therapy, they have better control than as needed, which kind of makes sense. We know that inhaled corticosteroid is a cornerstone of asthma therapy. If someone's taking it all the time, yeah, they're probably gonna have less airway inflammation, but the downside is of course they're gonna be on more inhaled steroid. And so your risks of really thrush and really that's the big one, is thrush, maybe other cavities, et cetera, that might be higher. But then I think to get to the other element of that question is are all long acting beta agonists created equal? Are all short acting beta agonists created equal? The answer is definitively no. So for motorol is special in the sense that you get short acting benefits of the short acting benefits of let's say an albuterol with the long acting benefits of a lava. So it's really got kind of a dual mechanism. You get onset of relief within typically five to 10 minutes and then it's going to last up to 12 hours. It really kind of depends on what's going on with the patient, what their trigger situation is, etc. But that's why we really like it. That's why it works in the way that is suggested by gina. That is the smart or single maintenance and reliever therapy approach to asthma management.

A (36:56)

Yeah, love it. And you know, it comes up all the time on boards questions and you know, mix app and what have you. But I still find when I'm talking to trainees that a lot of them have not yet been taught this when they're coming through medical school. Paul, I don't know if that's your Paul Williams, I don't know if that's your experience as well.

B (37:15)

It does not seem largely changed. The practice does not seem changed from 10 years ago, to be honest with you. It feels like it just has not caught up with the current guidelines and there's a lot of inertia I'm seeing as well where someone is on the Saba and you're like, well probably we should actually update this to a more evidence based inhaler. And people are like, I'll talk to him about that next time. So there just seems like a general lack of enthusiasm. I Can't really explain, but it's what you're fighting against, Dr. Haskins.

C (37:38)

Well, and the thing is like, it may be more convenient, it may be faster to not bring it up, but you're really doing a patient a disservice. So we know that patients have more exacerbations and more severe exacerbations when they're on SABA monotherapy. That's not cool. And we also know that tachyphylaxis is a significant issue, also similarly uncool. So you give a patient a medication that makes them feel better, what are they going to do? They're going to use it more and more. But the sad thing of it is we see this on the inpatient side a lot of the times when we're using short acting BRCA dilators for asthma exacerbations. The law of diminishing returns. It's like, it's really bad with like donuts and then it's like almost as bad with beta agonists. So it's very real. Right. And so that's why I think that the GINA guidelines, in their infinite wisdom, and I mean that in a, in a true way like those, those guidelines make a lot of sense and that's really what we should be following. I don't. Unless you are in a, a truly resource limited environment. And I, I think that's gotta be a place where you're like reliant on peak exploratory flows to make the diagnosis or you're just kind of assuming people have asthma. Okay, maybe, maybe there's a place for it if you are using albuterol in addition to another inhaled corticosteroid other than, let's say budesonide, maybe you're using fluticasone and then as needed, albuterol on top of that. Oh, okay, that may be okay. Or you're doing sort of a, a similar approach where you're using maybe fluticasone and albuterol in the same way that you might use budesonide formoterol. So sort of this like a few times a day as needed sort of approach. Okay, fine, there's, there's a, there's a place for, for albuterol. But I, I mean to be fair, sometimes it is like you're prying away a security blanket from a patient. It's like you don't need this anymore. You don't need this anymore. But I, I just take the time to explain this is why. And right there you, there you have it.

A (39:31)

Yeah, I think the other Tricky part about this is the cost, because Budesonide for Motorol is not always affordable to patients. So, yes, I'm still seeing a lot patients on fluticasone Salmeterol, which. And Salmeterol is. It takes two hours or so, the onset, from what I recall. So it's definitely not five minutes. And so they take that one, they feel nothing for two hours and they take their albuterol, they feel something right away. So it just reinforces that, that's why they like that one. And that's why it's almost like if you can get them on for Motorol from the start, that seems to be the better way to go.

C (40:08)

Very true. It's dangerous too. Right. Because for exactly that reason you described is they'll be on the appropriate controller or inappropriate controller, if that's your strategy. They don't feel anything from it. They feel something from the albuterol and like, I don't really need this one. I'll just. This is, this is my. This is the money maker right here. This is the one I need because it makes me feel better. And so I think that just gets back to taking time to explain the method behind the madness and why we do it the way we do it and then good follow up and all that.

A (40:36)

Paul Williams I'm going to make. Here's my analogy. It's like when someone starts taking Ativan for anxiety and then you try to put them on an ssri.

C (40:44)

Yeah. Good luck.

A (40:45)

You're like, I promise this is going to help control your symptoms in the long term. They're like, that one makes me feel something. That one I didn't. You know, maybe they felt nausea or some like, bad side effect, but they.

B (40:57)

Yeah, no, I think that's a great analogy.

A (40:59)

It's tough.

C (41:00)

Foreign.

B (41:04)

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A (42:46)

Wirtz what's next? How are we doing here on this? I know we have a lot to get to, but I feel like, like we're, we're making, we're covering some ground. What's next?

D (42:56)

No, I think this has been great. Can you talk a little bit about the Mandela trial and how we think about ics, albuterol and then also just like when do you start with the mart therapy versus just the reliever alone.

C (43:08)

Okay, great. So I'll start with the second question if I may. So. And then I'll talk about mandala. So when do I start maintenance and reliever therapy? Really? There's kind of two cases. I think I'll say that. So in someone who perhaps under reports their symptoms and says oh, they're just with exercise and I sort of start them on as needed, trigger targeted therapy and then I find out that they're maybe not as well controlled as I had hoped, then I might transition that person to mart or smart therapy, depending on if you are a fan of five or four letters, I guess. But. But yeah. And so the way that looks for me is, and this might be helpful to the listeners is I say okay, you're take two puffs in the morning, two puffs in the evening and then you have another kind of six to eight puffs to use over the course of the day. To sort of manage symptoms as they come up. If someone's using 10 to 12 puffs a day every day, that's worrisome to me. And that would indicate there's something going on. But the flip side of that coin is, okay, how are they taking it? Are they just like grabbing the inhaler, shoving it in their mouth and kind of puff, puff, and that's that, or are they doing it deliberately? What does deliberate look like? Well, for me, it's, I give patients a spacer and I'm a reasonable person too, so I'll usually give the person two inhalers, one that they can at least carry in their pocket, recognizing that they may not have room for a spacer. So they may just use that one as needed without it. But the maintenance doses, I want them to really take that with a spacer. And the idea there is it's going to force the patient to take a slow, deep inhalation. It's going to allow medication to collect in the collecting chamber and then be distributed to the lungs rather than to the back of the throat. That's another thing I see a lot of is like they coat the back of their throat. They don't get it actually into the airways. And they're like, why isn't it working? And why do I have thrush? Well, boom, boom. And so. And then there's like the brushing teeth, swish and spit after use, all of that. So I go through all that upright big breath, all that good stuff. And so, yeah, so that's kind of how I, how I educate patients and how I go from as needed to mart or smart therapy.

A (45:10)

And we're talking about the same agent Budesonide for Motorol. It's just, instead of just the as needed reliever therapy, they're, they're doing the, the maintenance dose like you said. And can you talk about the steroid dose with that? Like the two puffs versus one puff? Because, you know, I guess it depends on which because there's usually a couple different strengths of inhaler.

C (45:33)

Yeah. So if memory serves, like 80 and 160 are the common doses that at least I've seen. And so depending on how symptomatic I think the patient is, that might indicate whether I start them on the higher dose or the lower dose. If you're a purist and you're following Gina guidelines, you're gonna start at the low dose and give yourself room to work up. But the reality is, especially recognize that things are a little biased from my standpoint. Cause Oftentimes a patient has been seen already and then they're coming to me and, and maybe their symptoms have brewed in the background, things have gotten worse. So I'm a little bit more inclined, I think, than, than, you know, my colleagues in general, internal medicine, family medicine, whatever, to start someone at a higher treatment dose and then step them down because I want to, like, get them kind of on the straight and narrow and then I'll move them back. But that's generally how I look at it and how I'll dose it. And again, the, you know, that 10 to 12 puffs, that's really limited by the lava elements because we know that high doses of lava can have cardiac side effects. That's why we don't do like lava monotherapy. That's like a. No, no, we really do it in concert with, with inhaled corticosteroids. So I, I guess I'll pause there. Does that kind of answer that first element of the question? Is there anything else that you wanted me to get to on that?

D (46:44)

No, I think that that's perfect.

C (46:47)

Okay, so then the other question is. So the Mandala trial. So really, the Mandala trial is a pretty recent study. It really concluded that the combination of albuterol and budesonide used kind of as needed, significantly reduced the risk of severe asthma exacerbations compared to albuterol alone in patients with moderate to severe asthma. And so that kind of dual therapy that was provided is kind of a more effective option for symptom relief while while also reducing the need for systemic corticosteroids. But all that is to say, like, we kind of knew that. Like, we knew that budesonide and formoterol did that. And now we know that albuterol and budesonide do that as well. But I mean, we knew that even back in 2004, 2001, that that combination was a good one. But here we are talking about albuterol, which we've already discussed is like kind of an inferior drug to formoterol. And so I guess I don't really see an indication for that agent. Again, it's an industry sponsored trial. A lot of these trials are industry sponsored. So, you know, that kind of, you can, we could debate the merits of that all day long. But yeah, I don't really, really see an indication for it. And there are no head to head studies that I'm aware of. I actually searched this. There's no air head to head study looking at like albuterol and budesonide and formoterol and Budesonide, which one's better? And I don't even know if you'll ever see that, to be honest.

A (48:03)

Yeah. And, Cyrus, if I may, I mean, if. If the person won't give up their albuterol, you'd be like, all right, fine, I'm just going to give you albuterol, but this it ha. You're going to sneak in the budestonide on them. I don't know, Paul. That's like. Paul Williams. Can you see that working maybe as like a 100%?

B (48:18)

Because I think the idea is to not be in there unprotected without the inflammation being reduced by the corticosteroid. So, like, however you get them, there is. Yeah. I'm kind of with Siren, so that.

A (48:26)

That might, you know, maybe that's going to help us, but it's probably expensive at this point, so I think so.

C (48:32)

I mean, you're right. Jedi mind tricks, to an extent is like, what are you going to do to get this person who's clinging to, like, their security blanket? Sure. Seems that's. That's reasonable. I think, like, at my shop and a lot of other shops, you're not going to really have a choice, like, you're going to do one or the other based on what's available to you on your formulary or what insurance is going to pay for. I just think physiologically and pharmacologically, if I had my druthers, I don't really see a great place for that combination without.

A (49:02)

Can I mention the step down. So let's say we did put her on March therapy, the two puffs am, two puffs pm. And then she was using six to eight puffs as needed. And part of what I was reading, they were mentioning, and this was something from Journal Watch, they were mentioning that a lot of the efficacy of inhaled corticosteroids, like, is achieved at low doses. So going up, you sort of have diminishing returns. And they were saying that the high doses are associated with more side effects. And it might be as much as comparable as like, taking 5 milligrams of prednisone a day if you do it over the long term.

C (49:37)

Yeah.

A (49:37)

So that you mentioned stepping down. Is that. Is that why we step down, because of that risk with steroids? Like, and I even heard adrenal insufficiency as a risk.

C (49:45)

Yeah. I mean, I think that systemic side effects from inhaled corticosteroid that I have picked up on in my practice and recognize I'm relatively junior compared to my colleagues. So just in my own experience, I haven't seen much of that. I certainly see more of the local reactions. Um, so again, thrush, cavities, et cetera, people just don't, you know, maybe don't. It doesn't agree with them or what have you. Um, but I think you're, you're absolutely right. The data would support exactly what you said. And so my thought is, well, every patient, I say this like on rounds all the time in the ICU and when I have folks in my clinic, every patient is at the end of the day an n of 1. And so some patients are going to respond better than others to different doses. I think that there is a time and place to start the higher dose. But if I get the patient, if I start the patient on a higher dose of inhaled corticosteroid and like, man, I'm loving life, everything's great, then really it is incumbent upon us to try them at a lower dose for those reasons that you described. The classic approach to step up, and this is kind of what's indicated in gina, is to try a higher dose of the, of the inhaled hailed corticosteroid to see if you just haven't kind of hit what that patient needs. But again, you may see diminishing returns there, and that may kind of indicate you need to broaden your horizons and try something else. Hit the problem from a different angle.

A (51:10)

Paul Williams, what questions do you have about treatment here?

B (51:16)

I feel like I'm in a fairly good place from the inhaler therapies. I did want to ask actually about Montelukast. I just de escalated. I feel like I've never started it and I'm much more likely to actually take it off of medication list. But I would like to hear your approach as a pulmonologist and someone who deals with asthma much more than I do. When you use it, how you use it and what you might actually who might be right for.

C (51:41)

Yeah, so I think that there's sort of data for and against the use of Montelukast. When I trained, it was commonly used as an adjunct. So typically like your typical allergic asthmatic type patient might be on a, an antihistamine such as cetirizine. They might be on back in the day, they might be on fluticasone, salmeterol. That's, that's what a lot of my patients were on Now. Now you're butesigned for Motorol and then you'd often see they're on Montelukast too. So a leukotriene receptor antagonist. So there is some benefit, like I said. So it's beneficial in reducing symptoms and exacerbations in certain populations. And those populations are really allergic asthma, perhaps those with exercise induced bronchoconstriction, and even those with aspirin sensitive asthma, which is like another subset of asthma, which is probably outside the scope of this discussion. But there are groups where it is effective. It can be a helpful steroid sparing agent. So it can kind of, because it's reducing exacerbations, can reduce the need for oral corticosteroids and then it is an oral drug too, so it makes it kind of easier to take. And I did come across something that suggested it might have a benefit as monotherapy, which was crazy to me in cough variant asthma. And if we get to phenotypes, maybe we'll talk about that. But generally for the folks that are listening here, I would say it's seen and used as an adjunct, primarily in allergic type asthma. The physiology and pharmacology makes sense in that regard. Now, what is the data against Montelukast? Well, the big thing that's come up recently is this black box warning. And specifically it's neuropsychiatric side effects. So depression, anxiety, sleep disturbance, and really the most worrisome thing would be suicidal ideation. And so that's really where the black box warning came from. That being said, I did a little bit more digging and there was a 2023 meta analysis of 59 publications that really suggested that sleep disturbances and anxiety are seen. But the other concerns, particularly the suicidal ideation, was didn't really, um, didn't really appear, didn't really bear fruit, that, that concept. When they looked at these 59 studies in this meta analysis. So all that is to say, when I talk to patients about Montelukast, I still bring it up. Of course, I say, you know, there is this potential more likely to be. It's, it's most likely that you're gonna have no issues. It's possible that you could have some issues with anxiety or sleep disturbance and there is a slight risk that you could have suicidal ideation. And I talk about that and I say, okay, have you had behavioral health concerns in the past? You know, and I really have a very open and honest discussion. And so I would say that with Montelukast, the question is always, is the juice worth the squeeze? I think if someone has allergic type asthma and they're kind of already on, let's say, smart therapy, they're already on an agent like a Cetirizine, you've perhaps already gone down the road of specific allergy testing, maybe allergy immunotherapy. Then perhaps in that same breath you might want to add something like a Montelukast.

A (54:47)

Okay, that's, that's a great answer. Thank you. That's, that's very clear. Yeah, we talked about that with Dr. Fadugba, Paul. Right. On our recent, recent episode on rhinitis as well. And she was, she said she was cautious about that. Yeah. And unless people have asthma, she's an end allergy. She's usually not using it.

B (55:06)

That's right.

C (55:06)

Yeah.

B (55:06)

There is not a role for allergic rhinitis exclusively. But with patients with asthma, then you.

C (55:11)

Might consider, and I've never used it like that either.

A (55:13)

So any other therapies or non pharmacologic things that we should be thinking about for our patient here? Like let's say we decided not to give her Montelukast, but anything else that we would think about doing?

C (55:28)

Yeah, there's a couple things that we want to consider perhaps with this patient, but again, maybe with a more generic patient, the pregnancy element makes it a bit challenging in the sense that some things may not be feasible. We're often very sensitive to the fact that we're taking care of a patient and a second patient. And so I do think that that makes us a little more concerned about the interventions, particularly pharmacological and also recognizing that maybe some of these non pharmacological interventions may not be feasible. That all being said, things that I would consider if they have more severe obesity, we definitely want to counsel and facilitate with respect to obesity, risks of obesity and then weight loss. And in this day and age, in my mind that may even be, you know, having that, looking into a, a GLP1 agent, if that's appropriate for that patient. Even like surgical weight loss for sort of like a more extreme step. Obviously you're going to start with your classic approaches to calorie restriction, increase activity. But the reality is, and I don't want to get on the soapbox, we know that obesity is a lot more complicated than stop eating and go exercise. It's a much, much more complicated disease than that. I know it's heavily stigmatized. And then when folks have shortness of breath, that even contributes more so I think to some of the biopsychosocial aspects of their obesity. So it's just really, to me that's a very important thing. I spend a lot of time talking to my patients about that and trying to help motivate them. And to me, none of the tools are off the table. So that's a big thing. We really have good data to suggest asthma control is more challenging in the setting of obesity. Exacerbations are more frequent in the setting of obesity. So I'll get off my stop box and then move on. So as far as exercise goes, that's another big thing, irrespective of this obesity discussion. But this is kind of an important one. So you'll hear a lot of folks say, oh, I've exercise induced asthma, or I have asthma because of my exercise. Well, that is like the worst thing. It just kills me on the inside when I hear that. So if you look at the quad AI guidelines, which is kind of the allergy immunology version of gina, and if you talk to folks in the field that have been doing this a lot, I will often refer to exercise as a trigger and say you have asthma with an exertional trigger. But I'm very particular to not say, oh, you have exercise induced asthma. So that they don't leave my office and they go, I just need to stop exercising. Then my asthma will go away. Because we know that the reality is the reverse. Like you want your patients to improve their musculoskeletal strength, their neuromuscular efficiency, their obviously cardiopulmonary function, all of those things are going to help their asthma control. We don't want them to stop exercising, so that's important.

A (58:16)

So we convince them. We have to reinforce the fact that just because you have asthma doesn't mean you can't exercise. We should be able to get you to be able to exercise.

C (58:25)

That's the goal. The goal is to facilitate exercise and normalcy. That's one of the sort of triggers that to me is non negotiable. It's like we have to find a way to get you to exercise. We may have to change what that looks like for you. It may not be like, you know, sprinting intervals in the middle of a, of a dust storm in, when it's hot and humid. Like maybe we have to get you, you know, on a bike indoors or something like that, you know, different options. So that's, that's kind of that other soapbox that I'll, I'll, I'll, I'll step off of. As I'm stepping off, I'll say consider pulmonary rehab in these folks too. So if, if they're, maybe if they need some encouragement, they need some support pulmonary Rehab is a good option. Last couple of things I'll mention. So trigger removal, if possible. And this can be helpful. Like this could be a place where a subspecialist can help because they can really maybe drill down what the triggers are. They can do maybe a more in depth history. They could also explore the possibility of occupational type asthma and maybe work through that element. But definitely trigger removal whenever possible. I often will have my patients journal when they have symptoms and like, then they bring it back to me and they're like, oh, yeah. So I had symptoms in this scenario seven times. Like, oh, well, maybe we should not do that. And then finally. And this is kind of pharmacologic, so I'm sorry, but I have to put this in. So vaccines. So flu and Covid for sure. Rsv, now that it's available in kind of the appropriate patient, pneumonia in the appropriate patient, those vaccines can really help because that's gonna help reduce other potential insults to a patient.

A (59:55)

Yeah. And the pneumonia vaccines, even for patients under. They just lowered the age to 50. But even, even patients under 50 should get a pneumonia vaccine if they have asthma, right?

B (60:08)

Yeah. Cyrus, you alluded to this earlier. I don't want to escape this case without kind of coming back to it and talking about it. It's a concept I was super unfamiliar with, this idea of sort of phenotypes and asthma and what you do with them. So you talked about like high T2 and type 2s and I nodded wisely because that's what I do when I don't know what someone's talking about. So could you.

C (60:26)

Me too. Me too.

B (60:27)

Could you educate. Educate me a dumb, dumb, simple country doc and sort of what those phenotypes are and sort of how they might actually impact your management.

C (60:34)

Yeah. If I may, let me briefly introduce some of the. Introduce. Scratch the surface on some of the more advanced concepts in therapy because that's really going to dovetail with the phenotypes. So all that is to say, once you've done your smart therapy and a patient needs more, that's really when things get confusing and probably when I would recommend for most folks to refer to a pulmonologist, if they haven't already, because. Because of this idea of phenotyping. So again, to set the stage, there are a lot of options for therapy beyond your inhaled corticosteroid and long acting beta agonist. Do you put this person on an anti muscarinic agent? Do you put them on omalizumab? Do you put them on One of these, like a benralizumab, a dupilumab, et cetera, like all these omabs, it gets pretty confusing. So that's really where your phenotyping can play a role. So typically what we'll do if it hasn't already been done, is we'll obtain kind of a panel of testing. So if for whatever reason you want to set up your patient for success, like go way above and beyond before you send them to us. You might get a CBC with differential to look really for an eosinophil count, a C reactive protein. You could get immunoglobulins, really specifically IgE, but you could check a full panel. You could consider getting a fungal precipitins, although you could also leave that to us. That's really looking for allergic bronchopulmonary aspergillosis primarily, which can be a situation where asthma doesn't really respond the way you expect. It's because they have an underlying fungal infection. Imaging, so chest X ray, if it hasn't been done, high resolution CT scan, allergy testing, and then even things if you really want to go crazy, like anca, bnp, echo, all of those things. So those are, those are all things that can help us with our phenotyping. If you haven't ordered them, no sweat, I'll take care of it. So you get those things, you've got a patient that's like not really responding well. That's when we get into the phenotypes. And so the phenotypes, essentially you've got your classic allergic asthma. That's going to be your high T2 or your type 2. This is usually going to be your most easily recognizable. In a case like the one that we talked about earlier, got this family history, you've got some eczema going on, allergic rhinitis, maybe some food allergies. That's again your classic kind of high T2 or type 2 asthma. You might get an induced sputum that has elevated eosinophils on the sputum sample. That's something that we would do potentially and just briefly because I can't not talk about the physiology here. Essentially you're just talking about high or pathologic elevation in T helper 2 cell count relative to the other cell lines, which results in increased production of IL4, IL5 and IL13, which can sort of like add fuel to the cytokine fire, which coincidentally are the targets for the biologics that we would be using. And so that's why again, getting that testing can be helpful. Moving on. You've got your kind of low T2 asthma. So these are folks. When you do all your testing, you might send them for allergy testing, et cetera. Nothing really comes back positive. But they have bonafide asthma. The thing to know there is those folks are often harder to treat. The response to inhaled corticosteroids is often not as impressive as you'd want it to be. And really these are the folks for whom a lot of the biologics are not. Are not a good option. There's kind of the new one that came out recently. It's like tech Millimab or something, I can't remember. I remember the brand name, but. But there's the new one that came out which is really for like low or high T2. It's basically works on a different part of the. It works like upstream of those agents, if memory serves. So that would really be the option for those folks. And why again, phenotyping is helpful.

A (64:16)

Is it tazepellumab?

C (64:18)

Yes. Tesapellumab? Yes. Sorry, that's the only one I remember.

B (64:22)

Obviously. Cyrus, this is embarrassing for.

C (64:25)

I'm embarrassed.

A (64:26)

We basically tied both arms behind your back by saying we couldn't say brand names. So that one in particular.

C (64:33)

That one in particular, like it's a. It's a pretty memorable brand name. But. But yeah, so. So as I remove my foot from my mouth, that one is. Is really your option for those low T2 cases. And then briefly I'll talk about the others. So cough variant or cough persistent asthma. So these are folks who don't have necessarily shortness of breath, but they have cough as a, as a principal symptom. Again, maybe Monte Lucas could be more helpful in these folks. But. But typically we're treating them similarly. And then you've got this idea of adult onset asthma which basically we kind of treat those folks like regular asthmatics based on other elements of their history. And then finally you have this asthma with persistent airflow limitation. Is that asthma COPD overlap or acos? I don't know. It depends on the patient's history. Those are folks. If they skew further towards the COPD side of the house, you might put them more readily on a long acting muscarinic antagonist. And then finally there's this asthma with obesity which is considered its own phenotype. But really that gets back to what I was talking about earlier. So I think that does a pretty good job of talking about the phenotypes in the Context of the biologics and the other therapeutic options. I hope that's helpful.

A (65:42)

Yeah, that's great. I mean, maybe a standing ovation for that rapid recap. Paul Williams, any other questions about that? Is that.

B (65:50)

No, that's very helpful. And you know, I just want to sound smart when I'm talking to my specialist. Cyrus. I feel like that at least gets me, gets me started. But I'll probably not be ordering these sensitive panels. I will leave that to the pros.

A (66:00)

Yeah, but I think the CBC with dif, the crp, the ige, you know, I'll probably order that. The fungal test.

B (66:08)

That way lies madness. Watto, I don't. You're just, you're asking for trouble.

A (66:10)

It's going to come back abnormal.

B (66:12)

And then what are you doing?

A (66:12)

I guess it depends, you know, Or I might reach out to the pulmonologist and ask if, if they have an appointment in a month or two, I might ask if they want me to do any of this testing ahead of time, depending, depending on your relationship, but it can be more efficient for the person.

C (66:26)

One thing I'll also just mention here is like this was a lot of information to go through and for folks that are caring for the broad spectrum of the human condition, it's a lot to remember. The GINA guidelines are really great for this. It does spell that stuff out. And so actually if you go to page 144, it talks a lot about the biologics specifically. So if your patient is on one, you can get some information on there. And then there's also a portion where they actually have it color coded. So it's like there's green and there's blue charts and text. One portion is for your sort of primary care, the other portion is for your specialist. And so if you're ever like lost or trying to figure out like where to draw the line, it's such a great resource.

B (67:04)

Yeah.

A (67:05)

Okay, so I think we need to go on to the next case. Wirtz, can you read that for us?

D (67:12)

Yeah, absolutely. So it seems like you've just been doing a terrible job because a few months later you see this patient back in your clinic for a hospital follow up visit. After a recent hospitalization for an asthma exacerbation. This is her third exacerbation this year. Each episode typically resolves with steroids and nebulizer therapy. She normally takes a medium dose ICS format inhaler, two puffs twice daily, and as needed, she feels she never quite returned to her baseline since hospital discharge two weeks ago. And continues to have cough and shortness of breath with exertion. She's also been using her inhaler more frequently for rescue purposes, often two to three times per day. On physical exam, you notice she is breathing 23 times per minute and wheezing is noted. She looks mildly uncomfortable but not fatigued. So what factors are you paying attention to when deciding on sending this patient to the ED versus a outpatient approach?

C (68:05)

So again, I will start this discussion with the caveat of the patient is pregnant. So like, my threshold to send that person to the ED or bring them into the hospital is going to be extremely low. Mostly out of, again, just my overall concern, like I don't know where this patient is ultimately going to end up. And I think like obsing them for a day or two and treating them under my kind of watchful eye or someone else's watchful eye is maybe safer in a patient like this or perhaps one that's a little bit sicker. 23 times a minute is a decent respiratory rate. But if you're on the fence for this lady or for another patient, there are a couple of tools that you can use. So getting back to that discussion we had on peak expiratory flow, so this is really where that is helpful. I don't think I've ever used it for diagnosis, but that's because I don't work in a resource limited setting. However, if you obtain a PEF in a patient who you're diagnosing or whatever, and you know what their, their PEF is on, on the best day, so their peak exploratory flow, their peff, you know what that is on their best day, you can then look and be like, oh, well, can you do, can you do it for me here in clinic and see what they do? Now this is super nerdy, but there is up to like a 20% variability depending on the device that you use. So there is that consideration. But if the person's PEP is like, great, and then today it's just in the toilet, that's probably not good. I think we can assume that that's probably real. So that's one thing. So like, if it's 40, 50% of what it should be, that's not great. If the patient has underlying comorbidities, structural lung disease, et cetera, that's going to move the needle for me towards like admit versus treat at home. A lot of times I'll talk to patients over the phone, so I won't actually have the benefit of seeing them. That's also going to make me more likely to bring the person in just because I can't see them. But even more so if they're like four or five, you know, word sentences, huffing and puffing on the phone, struggling to breathe. Like, I had a call like this just a couple weeks ago, and I was like, ma', am, you sound awful. Like, you need. Do you want me to call you an ambulance right now? I'm going to call you an ambulance right now. And she's like, no, no, no. My colleague is right here. I promise. She's taking me right to the local er And I was like, I'm going to call you back in five minutes. If you're not on the way or at the er, I'm going to call you an ambulance. And then so she. So that was. You know, those situations, they do arise, and that was pretty stressful. But. But, yeah, if they sound terrible over the phone, I don't mess with that. Like, they're going. They're going to get someone to lay eyes on them. If I'm wrong, cool. If I'm cavalier about it, then it's not cool because they could be an extremist, and that's not. That's not okay. And so, yeah, I mean, I think that's. That's kind of how I look at it, Cyrus.

A (70:46)

So you don't just give them antibiotics over the phone and tell them to call it a day?

C (70:49)

Yeah, I actually. I send them to their nearest procedure clinic and get a PICC line and I start them on, like a carbaped them.

A (70:56)

There you go.

C (70:57)

To make sure that I'm not missing anything. No, so that's a. That's a great point. So I was going to. Because there's a few different places we can take this. It's like asthma action plans, you know, home treatment approach, et cetera. So I guess what I'll say is for. For a treatment approach, if I may talk about treating briefly to your point, Matt, we really don't use antibiotics in exacerbations of asthma. Classically. If there is something else going on, if we think this person has a pneumonia, you know, if they're like febrile with a muco purulent cough and they had sick contacts. Okay, sure. You know, that's. That's enough for me. But. But generally speaking, there isn't a lot of utility for antibiotics that don't conflate that with azithromycin that we might use for asthma therapy as an adjunct, just like Montelukast. So we can use it as an immunomodulator in certain patients. There's actually pretty good data for that. This is more like acute exacerbation. Put them on antibiotics, yes or no? They've got to have symptoms that are consistent with. With really like an infection, best I can tell.

A (71:59)

Yeah. Like it. It has nothing to do with the asthma. It has to do with what infection they have. Whether or not you give an antibiotic. It's not like COPD where you. You count the cardinal symptoms, and if they have two or three, then you. You treat. Okay.

C (72:11)

Yes. I mean, it's. Yeah, in. I guess the way that I would approach it for listeners is in clpd, you should ask yourself, why am I not going to give this person antibiotics and asthma? You should ask yourself, why should I give this person antibiotics? And I think if you approach it that way, really both disease processes, you'll probably end up at the right answer most of the time, which is the best we can do. And then otherwise, things I'll do for a patient at home is, you know, increase their dose of their, you know, smart therapy, perhaps, or tell them to take it more frequently, potentially have them use their nebulizer if they have, like, nebulized, but nebulized album uterol. You know, for folks who are having a little bit of a harder time, perhaps more frail individuals, that can help sort of take the negative inspiratory force element out of the equation. So if you're really constricted, sometimes it can be hard to generate enough force to actually get the medicine in your lungs, whereas a nebulizer can be a more passive process. So that could be something you can do. And then of course, there's the, like, 40 to 60 pred that you could do for five days, typically, maybe a few more if you're thinking this person, for whatever reason, would benefit from from 7 or 10, although the standard is usually 5 days of 40 to 60 of oral prednisone for folks that you think are good enough to send home or good enough to keep at home with a phone. Follow up in 24 to 48 hours.

A (73:26)

Paul Williams, are you writing asthma action plans as America's pcp?

B (73:30)

Not as often as I should, if I'm being honest with myself and our listeners, but it's something I should get more in the habit of doing.

A (73:37)

Yeah. So, Cyrus, can you talk us through that?

C (73:40)

I mean, I feel like a man. I feel like a fraud because I'm kind of with Paul on this one. I don't use them as Often as I probably should, but recognize that my patients have pretty good access to me, so they just call me if something happens and then I can help them out. And the other thing I'll say before we get to that is just a plug for our colleagues in the er. Our colleagues in the ER are so good at treating asthma when those folks show up that I rarely see the inpatient asthma. So you've got this combination of, like, a really great security blanket to fall back on and patients that have good access. I probably don't use them as often as I should. That being said, for many of you guys that are working in the community, it's actually pretty helpful. So. So what is it? It's basically like, this is what to do if you're feeling short of breath and if you're, you know, if your symptoms are starting to get the better of you. So the way it works is, is typically you'll see these charts, and I guess our colleagues in pediatrics are probably better about using these, but the charts are very similar. There's like a green, a yellow and a red. So like a stop light or whatever the green is typically going to be. If you're at 100 to 80% of your best or your predicted PEF, 80 to 50% would put you in a yellow category, or caution, if you will, and then less than 50% puts you in the red or kind of warning category. So the way that I typically would approach this, so if someone's calling me on the phone and they're sort of in that yellow zone, so if they're in the green zone, it's like, okay, well, this is that variability that you might see in someone from day to day. There's nothing to really do about that necessarily, or really by definition, there's not a lot to do with that. If someone's in that yellow zone, it's like, okay, well, I'm going to talk to them, I'm going to ask them questions, I'm going to assess them, make sure they're actually in the yellow zone. And then I might have them take more of that Budesonide for Motorol. I might have them switch to nebulized therapies. And again, the key is like, do, act, follow up, or, sorry, I should say assess, act, follow up. So what do you think they need? Have them do whatever it is you think is appropriate and then follow up in 24 to 48 hours. That may be systemic steroids. It kind of depends on what I'm. What I'm hearing from them. Also, I may just have that person come to the clinic in a day or two. So I'm not as concerned, like, this person needs something stat. But that's usually my approach. And a lot of times this will be written out. The idea of the action plan is like, they're not calling me for guidance. They're calling me to say, hey, I felt bad. I checked my PEF. My PEF is like 60% of my best. A couple of weeks ago, I was at 100%. And so I started doing A, B, and C. If this is someone who I've known for a while, I might give them prednisone to have at home and they might be like, yeah. And I started taking my prednisone too. So that really, like, it empowers the patient. It provides some element of self efficacy. It also, like, frankly, makes your life a little easier because you already have a plan to fall back on. So that's usually how that works. And then if they're in the red zone, I. E. They're less than 50%, you could have them mess around with home therapies. And you're probably. What I would probably do, practically speaking, is I would do everything I would do for the yellow zone. I would. I would like necessarily, oh, hello, Kitty. I would like, definitely start the patient on. On. On their steroid or tell them to start it. And I would tell them to come to the ER and be evaluated in the er. That's typically what I'm doing. Because again, if that patient is. If I'm over calling it, that's fine. If I'm under calling it and they come in with like, hypoxemic respiratory failure, I lose a lot of doctor points. And more importantly, they may not be doing so hot. And that's not cool.

B (77:08)

Yeah. You anticipated a question I had, which I had, and I. It makes for any catchphrase. I'm not sure how entirely true it is, but someone who once told me that if a patient with asthma presents the ER for an exacerbation, that's a failure of outpatient care, and actually talked about this idea of having courses of antibiotics. Not antibiotics, forgive me, steroids to take at home for sort of these moderate, moderate exacerbations. So I was going to ask what your practices are on that, but you answered that perfectly. Thank you.

A (77:32)

I was going to say to the audience, Cyrus said, hello, Kitty because Paul's cat jumped on the back of Paul's chair, which happens every time we record.

B (77:40)

No, that's just a weird verbal tic Cyrus has. He just says hello Kitty from time to time.

C (77:43)

Yeah, it's just, it's.

B (77:45)

We usually fix it in post.

A (77:46)

I think I just saw your cat jump into the litter robot, Paul.

B (77:51)

You did not.

C (77:52)

When you go, you got to go. You got to go. Yeah, I get that.

A (77:55)

Okay. All right. Well, have we done it, guys? Are we at the end of this thing? Do we have more to go through? I think we talked about our asthma action plan. We talked about when we might. That most people with asthma are not going to need antibiotics unless they have a separate infectious thing going on. Talked about giving 40 to 60 of prednisone, usually for five days. Anything else that we're going to be doing for an exacerbation?

C (78:24)

I mean, there's a ton that we could talk about at another time, you know, for more, like, inpatient, focused stuff. If you do get to that point. I don't. I think that's outside of the scope of this discussion. So I. I think we're probably pretty good.

A (78:35)

Yeah. Wirtz, what do you think? Anything else that we're missing here?

D (78:40)

I think this has been fantastic.

A (78:42)

All right, so let's go to some take home points, Cyrus, knowing we're leaving some stuff on the table, maybe an inpatient episode or an asthma COPD overlap or something in the future. But we have plenty of time to have you back.

C (78:56)

We do. Not going anywhere.

A (78:58)

What are some take home points you want people to remember?

C (79:01)

Yeah. So I think first and foremost is, you know, many, many diagnoses are clinical diagnoses. Asthma really shouldn't be a clinical diagnosis in most cases, like solely a clinical diagnosis. So, yes, you should suspect asthma if a person's presentation is consistent with asthma, but really it's a diagnosis that should be supported by spirometric values. And if spirometry is not consistent with asthma, and you've also done perhaps a provocative test, like a methacholine challenge test, and you're still not getting the results that you would think are consistent with asthma. I think that it's incumbent upon the clinician to start looking at other diagnoses before empiric therapy for asthma. You'll miss things like inducible laryngeal obstruction or vocal cord dysfunction. You'll miss cardiac disease. You'll miss perhaps other structural lung diseases by treating empirically for asthma. So I think that's probably if. If people take anything away from this, it's that do not fall back on the, oh, this person has shortness of breath. Let's give them an albuterol inhaler? No, there's a lot more to it than that. It's a lot more nuanced. I think that dovetails nicely with the idea of like only under rare circumstances should you be really writing for an albuterol inhaler in 2024. I think there is a time and place for it, but that time and place is kind of like warfarin, like the, the, the like indications are fewer and further between. I would say similarly that's, that's true for albuterol monotherapy. So that, that's probably one other take home point. And then I think, you know, really the other two big ones would be for exacerbations have a pretty low threshold to lay eyes on that patient or have that patient seen because really folks shouldn't be exacerbating a lot once they're at steady state. Um, that's gonna help make sure the patient is safe, but also make sure you're not missing an alternative diagnosis. Who's to say that you're, you know, 63 year old with asthma didn't just manifest their first episode of acute decompensated heart failure. Like you may not be able to tell that over the phone. And then finally I would say I like to think we're pretty friendly in the world of pulmonary medicine, so please like let us help. I will be like fully transparent and say at least in my station in life it can be a bit frustrating. When I read consultant, it's like dyspnea is the assessment or problem plan is referred to pulmonary and like literally nothing has been done. But I think if you've tried to do something for that patient and maybe gotten some baseline spirometry and checked a lab or something along those lines and you're kind of stumped, then by all means, please let us help. Part of that too is it's hard for us to help if we're seeing a patient with absolutely nothing in the background that's been done. And we want to try to help people efficiently. You know, your patient's time is very valuable. A lot of times they're waiting for the appointment, they're waiting to see me or whomever. And so just I think being mindful of all that is helpful. But I guess those are my kind of four big take home points.

A (82:12)

There's no way that's a Paul Williams consult coming to you. That patient's going to be wrapped up.

B (82:17)

Nicely done, the progress is going to be sparse. It's going to be maybe something about like athletes foot or something. And they'll just show up on your doorstep and Godspeed and good luck.

C (82:24)

I did the open lung biopsy in my clinic and you know the darndest thing, I still couldn't figure out what's going on. So. Yeah.

A (82:30)

All right, well, thank you so much, Cyrus. We will fade into the outro. All right. And actually, no, before we fade into the outro, check out Critical Care Time. What are you waiting for? Subscribe, give it a five star review. Anything, Cyrus. Where can they find that?

C (82:47)

Thanks. Yeah, no, I appreciate it, Matt. So, yeah, like I said, Critical Care Time wouldn't exist if not for the Curbsiders. And I mean that whole. And so I appreciate the opportunity to, to represent us and, and also to join the team again for this. So we're on Instagram, we're on X. Our website is www.criticalcaretime.com. we're really the podcast for everyone who cares for the critically ill. So it's really not just for intensivists. In fact, we're really focused more on early career physicians, nursing staff, respiratory therapists, etc, all of those folks that really make critical care possible. We've had our release shockingly, in my opinion, shockingly successful first couple years. We're really excited about it. Myself and my co host Nick Mark are loving every second of it. And so yeah, please check us out on your favorite podcast app or on YouTube. Whatever works for you, works for us.

B (83:37)

This has been another episode of the Curb Siders bringing you a little knowledge food for your brain hole. I'm Shine Palwirtz. Yummy. No pressure.

A (83:46)

He didn't want to say it.

C (83:48)

Yep.

B (83:48)

No, just forced him into it. And the look of shame on his face is really worth the whole effort. Still hungry for more. Join our Patreon and get all of our episodes ad free plus twice monthly bonus episodes at patreon.com curbsiders. You can find our show notes at the curbsiders.com and sign up for emailing us to get our weekly show notes in your inbox. This includes our Curbsiders Digest which recaps the latest practice changing articles, guidelines and news in internal medicine.

A (84:08)

And we're committed to high value practice changing knowledge. So we want your feedback. Email us ataskCURBSIDERS gmail.com Please subscribe, rate and review the show wherever you listen. YouTube, Spotify, Apple Podcasts. A reminder that this and most episodes is a bit are available for CME for all health professionals through VCU Health at curbsiders.vcuhealth.org A special thanks to our writer and producer for this episode, Dr. Paul Wertz, and to our whole Curbsiders team. Our technical production is done by Podpaste. Elizabeth Proto runs our social media. Jen Watto runs our Patreon. Chris the Chumanchu moderates our discord. Stuart Brigham composed our theme music. And with all that, I have been Dr. Matthew Frank Watto.

D (84:50)

I've been Dr. Paul Wertz, and, as.

B (84:52)

Always, remain Dr. Paul Nelson Williams. Thank you and goodbye.

C (85:04)

Sam.