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Show Notes
Pearl 1: Diagnosis and Empiric Therapy
- COPD label without spirometry is very common
- About 33% of patients are diagnosed empirically and do NOT receive spirometry
- You cannot diagnose COPD without spirometry
- “History and physical examination are poor predictors of airway obstruction and its severity” – Joint statement from 2011 from ACP, ACCP, ATS, and ERS
- 1 in 3 patients empirically diagnosed with COPD do NOT have airflow obstruction (AFO) on PFTs.
- Despite not having obstruction on PFTs, 1 in 4 patients who are empirically treated continue to be treated a year and a half later!
- A note on defining airflow obstruction (AFO):
- Historically (and currently, by GOLD), defined as post-bronchodilator FEV1/FVC < 0.7 or by FEV1 < 80% of predicted.
- However, there are concerns that this can ignore normal, age-associated decreases in FEV1/FVC and lead to overdiagnosis.
- The ERS/ATS are now recommending using the lower limit of normal (defined as the 5th percentile) to define AFO.
- Empiric initiation of maintenance inhalers for COPD generally shouldn’t be done
- However, in patients with radiographic evidence of emphysema/COPD and with symptoms consistent with the diagnosis, it’s probably ok to start maintenance inhalers so long as outpatient PFTs are ordered for confirmation
Pearl 2: The Initial Visit–Blood Work and Initial Treatment Choices
- Blood work in COPD:
- 1) Every new diagnosis of COPD should be checked for alpha-1-antitrypsin deficiency
- 2) Every COPD patient should have a CBC with diff checked at least once to look at their eosinophils. Specifically, do not interpret eosinophils when they’re taking systemic steroids or have an acute infection.
- The idea behind this is that COPD patients with higher eosinophils may have an allergic or inflammatory phenotype that an ICS will directly treat and therefore reduce exacerbations.
- Exact values differ between studies and individual’s practice patterns, but there’s evidence that peripheral eosinophils >100 cell/microL predicts
- a patient’s risk of exacerbation and
- More likely to respond to an ICS.
- Exact values differ between studies and individual’s practice patterns, but there’s evidence that peripheral eosinophils >100 cell/microL predicts
- On the other hand, patients without high eosinophils don’t have an inflammatory phenotype and so are only getting the risk for immunosuppression and pneumonia with ICS use.
- ICS use is associated with an increased risk of PNA
- Data supports that if eos are < 100, patients may have a higher rate of PNA and so at higher risk of harm from ICS use.
- The idea behind this is that COPD patients with higher eosinophils may have an allergic or inflammatory phenotype that an ICS will directly treat and therefore reduce exacerbations.
- Simplify inhalers by remembering that there are only 3 classes of medications:
- 1) Beta agonists
- Generally end with “-ol”
- E.g. formoterol, salmeterol
- 2) Muscarinic antagonists
- Generally end with “-ium”
- E.g. tiotropium, aclidinium, the umeclidinium
- 3) Inhaled corticosteroids
- Generally end with “-one”
- E.g., fluticasone, beclomethasone
- 1) Beta agonists
- The most widely used staging/grouping schema (see infographic) is described by GOLD, which uses a combination of spirometry, symptom burden, and history of exacerbations over the last year to determine grade and group.
- COPD grade informs prognosis
- COPD group informs initial therapy.
- Memorization of specific cutoffs isn’t necessary, and can be looked up.
- The way you assess symptom burden matters.
- COPD is more than a disease of breathlessness!
- Consider using a standardized instrument to assess your patients- a significant number of symptomatic patients will underreport dyspnea otherwise.
- The modified medical research council (mMRC) score has been used quite broadly due to its simplicity, but its use alone is now considered inadequate.
- The GOLD recommended mMRC cutoff of 2 may be too high/cause understaging.
- This matters because it can lead to under-treatment!
- GOLD recommends the COPD Assessment Test (CAT), which assesses symptoms across 8 different dimensions, for its wide availability, predictive utility, simplicity, sensitivity to difference in state, and its correlation with scores on more comprehensive but unwieldy measures like the St George’s Respiratory Questionnaire (SGRQ).
- For Group A and B, you can start with either a LAMA or a LABA.
- For Group C, LAMAs are recommended over LABAs because they are more effective in reducing exacerbation rates
- For Group D, start with a combination of LAMA/LABA or LAMA/ICS, if the patient has the inflammatory phenotype and has higher eosinophil count.
Pearl 3: Inhaler Devices
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- Studies have not identified a single device or delivery method to give superior control!
- This is true on a population level, but the individual patient in front of you may have reasons to benefit from one device type versus another.
- Patients make device use errors regardless of device type.
- Using different devices for rescue and maintenance inhalers worsens outcomes in both asthma and COPD–learning one technique is hard enough, and learning two is even harder.
- We haven’t gotten better at reducing error rates in the last half century!
- Utilize your interdisciplinary colleagues–pharmacists can be important teachers of inhaler technique for patients
- Studies have not identified a single device or delivery method to give superior control!
- Pressurized metered dose inhalers (pMDI)
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- These are the quintessential “inhalers” that most people think of when they hear the word inhaler.
- Medication is stored under pressure in the canister, and is released when the canister is pushed downward
- Pros:
- Familiarity
- They can be used with spacers and valved holding chambers (VHCs)–details of which are below
- Cons:
- These have to be shaken before each dose to ensure a consistent dose is delivered
- Requires coordination between pushing down and inhaling
- They need to be primed (IE, wasting doses) if the inhaler has not been used in a few days (or it may not deliver a consistent dose)
- Substantial amount of oropharyngeal drug deposition, which is inefficient and can cause side effects
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- Spacers and valved holding chambers (VHC):
-
- Spacers are basically just big reservoirs that you add on to the pMDI
- VHCs are basically spacers with a one way valve
- Why use spacers or valved holding chambers?
- 1) They slow down the drug particles and reduce particle size, which decreases oropharyngeal deposition
- 2) Both (though more so with VHCs) start to decouple pushing down on the canister and inhalation by holding the drug inside the reservoir
- NOTE: Even though there’s a reservoir, patients should only use one puff at a time—using more puffs greatly reduces the fraction of the dose that is inhaled (IE 2 puffs at once is less than 1 puff followed by another puff).
- Dry powder inhalers (DPI)
- These create an aerosol by drawing air through a dose of powdered medication
- Pros
- You do not need to coordinate pushing down with inhaling!
- These devices often have a dose-counter within them
- Cons
- You have to be able to generate a sufficient inspiratory flow to aerosolize the drug
- There aren’t hard and fast rules about when a patient won’t be able to do this, but more severe emphysema or hyperinflation on imaging can be signs to be cautious of this device type
- Up to ⅓ of patients after a COPD exacerbation have peak inspiratory flow rates < 60 L/min
- Humidity can make the powder clump, making it harder to aerosolize the drug–decreasing the lung deposition and increasing oropharyngeal deposition
- Single dose capsules can protect against this, but then have to be loaded individually per dose
- You have to be able to generate a sufficient inspiratory flow to aerosolize the drug
- Soft mist inhalers (SMI)
- SMIs are devices that are shaped like tubes that work by having the patient twist part of the inhaler and then push a button that releases an aerosolized mist
- Pros
- Dose delivery does not depend on inspiratory flow
- No need to shake (though you should prime them if you haven’t used them in a while)
- The mist moves slower and lasts longer than pMDIs, which leads to more lung and less oropharyngeal deposition
- The slower mist means patients have longer to inhale, decreasing the urgency of coordinating working the inhaler with inhalation
- These devices also usually have a dose counter built into them
- Cons
- They still require coordination of working the inhaler and inhalation
- The patient usually has to load a cartridge the first time they use it
- Not all medications are available in this format
- These can be more expensive because they are newer
Pearl 4: Inhaled Steroids and Inhaler Escalation
- Every visit should have a review of symptoms, exacerbations, and inhaler technique.
- Gold recommends annual spirometry to monitor for rapid disease progression
- It can also be useful to monitor other measurements of lung function/gas exchange such as functional capacity via a 6MWT, as this helps prognosticate
- Try and de-escalate inhaled steroids if you can–there is evidence of a dose dependent risk of systemic side effects with inhaled steroids!
- GOLD recommends considering de-escalating from an ICS if they develop pneumonia, if it doesn’t decrease their exacerbation frequency, or if there wasn’t an appropriate indication for the ICS in the first place (IE, to reduce exacerbation frequency in someone with high eosinophils).
- Be aware that some patients can have more exacerbations when their inhaled steroid is decreased, so this should be done carefully and with close follow up.
- Generally speaking, this should be done gradually over an extended period of time
- Be aware that some patients can have more exacerbations when their inhaled steroid is decreased, so this should be done carefully and with close follow up.
- Other inhaled medications are not adjusted via GOLD group. They are adjusted based on the specific issue being targeted: dyspnea or exacerbations. Gold has algorithms for both.
- To simplify, add either a LAMA or LABA (whatever the patient isn’t already taking) so they are on combination therapy. And think about inhaled steroids if they have high eosinophils and frequent exacerbations.
- If they are already on a combination of inhalers and are still short of breath, check their technique. If this isn’t the issue, try adjusting the inhaler device or specific drug within that class they’re inhaling (EG, a different LABA).
- Finally, as part of management of refractory COPD with frequent exacerbation there are roflumilast and other PDE4 inhibitors. These are for patients with an FEV1 < 50%, and are generally only prescribed for severe COPD and most patients will not be on them.
- Pulmonary rehab is incredibly important–it raises quality of life, reduces readmissions, and lowers mortality.
- It is so effective that the Cochrane review recommended against further studies of its effectiveness.
- Accessibility can be an issue, but there is essentially no reason not to refer a patient. It’s just like ordering outpatient physical therapy.
Pearl 5: Communication, Palliative Care, and End of Life Care in COPD
- Communication about COPD is analogous to communication about other serious illnesses like CHF or cancer.
- The mortality rate post-hospitalization for COPD exacerbations is very high: the one year mortality ranges from 23% (post-floor admission) to 35% (post-ICU admission). The 5 year mortality rate post-hospitalization is about 50%.
- Exacerbations can often be a good trigger to talk about GOC and values with patients
- Prognosticating is hard! The classic teaching is that COPD is a disease with a gradual decline in function punctuated by acute exacerbations, but in fact progression can be very heterogeneous
- Patient death is often unanticipated by loved ones and caregivers
- BODE index:
- This stands for BMI, Obstruction, Dyspnea, and Exercise, and is a composite score that is a better predictor of subsequent survival than any individual component (and than many other scores).
- These are quantified using % predicted FEV1, mMRC score, and 6 minute walk distance.
- BODE scores give an estimate of 4 year survival.
- GOLD recommends that, where possible, a scoring system like BODE be used a few months after discharge from a COPD exacerbation to assess prognosis
- It’s important to discuss what quality of life and functional status things are non-negotiable early and often with a phased introduction of supportive/palliative care because our patients are going to get sicker and their functional status will almost certainly decline.
- There is not a wrong time to do ACP or talk to your patients about their values. This isn’t just about yes or no procedural questions, but about getting to know the person you’re talking to.
- Outpatient palliative care can be a limited resource, so do not be afraid to do this yourself!
Transcript
Pearl 1: Diagnosis and Initial Clinical Assessment
Luke: So let’s start with a case we’ve all met—you’ve got a middle aged patient who smoked for 10 years or so in the past. They’ve got a cough, some dyspnea on exertion. So they get empirically diagnosed with COPD and given some inhalers.
Dr. Saukkonen: I do see a fair number of people who have been labeled with COPD. Um, and, and as you said, it’s not really clear that that’s what their diagnosis is. I think it’s tempting to label someone as having COPD, if they have respiratory symptoms and they have a smoking history
Luke: What really surprised me while working on this episode was just how common this actually is—depending on the study you look at, about 33% of patients get labeled with COPD without ever having spirometry!
Shreya: Yicks! and thats a big yicks – especially if we go back to the two things to actually diagnose COPD: you need 1) the symptoms like dyspnea, sputum production, wheezing and #2, you need airflow obstruction on spirometry without an alternate explanation
Ali: Just a quick point on the obstruction on PFTs, we often use FEV1/FVC of 0.7 cut off but there’s new guidelines to instead use the 5th percentile, or lower limit of normal bc it might better address systemic misinterpretation for women, children and older adults.
Shreya: Thats really neat that we redefining cutoffs based on what might be normal for different types of people. Ok so for those patients who do end up getting spirometry with that COPD label, I’m curious how many actually have obstruction on their PFTs?
Luke: One study I was looking into found only 62% of patients labeled and even treated for COPD actually had obstruction on their PFTs!
Shreya: Wow, so about 1 in 3 were getting treated for something they didn’t have
Ali: I am actually not surprised by that number. I’ve seen a decent amount of patients with an impressive smoking history who actually have no evidence of COPD.
Luke: What’s wild to me is that some studies found even after the spirometry didn’t show obstruction, 1 in 4 patients were STILL getting treated for COPD a year and a half later.
Shreya: Oh man—that’s a long time to be using daily inhalers for something you don’t have.
Ali: And not only that but it actually really worries me that we could be treating someone for COPD that they don’t have then there could be something else that’s really concerning that we’re missing.
Dr. Saukkonen: Maybe they’ll have some other smoking related lung disease, respiratory bronchiolitis, interstitial lung disease, Langerhans cell histiocytosis, or maybe they’ll have congestive heart failure, or maybe they’ll have lung cancer, or maybe they’ll have something completely unrelated.
Dr. Saukkonen: There are days where it seems like everyone has reflux until proven otherwise, which can often, uh, contribute to cough wheezing and if they are refluxing and actually regurgitating and aspirating, that can certainly contribute to respiratory problems. There are other days when it seems like everyone has oral pharyngeal aspiration until proven otherwise. So, especially as people get older, things don’t work the way they used to.
Ali: Yeah i feel a lot of what we do in pulmonary clinic is helping to say “it’s not the lungs” causing the dyspnea
Shreya: So guys help me out, how do we go about all the patients coming in with labels of COPD without ever having had spirometry. Should we not be starting empiric COPD inhalers?
Dr. Saukkonen: “I think it makes a little bit of a difference, um, what the clinical situation is at the time with the patient, if you’re seeing somebody in the emergency room or in the hospital who, um, is having some kind of acute respiratory crisis, you treat for what you think is going on, you can treat them theoretically and you worry about the details later, but it is really important to, um, to try to nail down the diagnosis
Ali: I would think of it the same way you would a presumed heart failure exacerbation. If someone has never had a cardiac workup but their presentation to the hospital seems consistent with a CHF exacerbation then of course you’re going to give them diuretics, but you would never empirically start them on beta blockers or ACE-Is without getting an echo. Similarly with presumed COPD, you can treat empirically in the acute setting but I would be cautious about continuing maintenance inhalers without having spirometry.
Luke: On the other hand, as one of our peer-reviewers, Dr Jamie Betancourt, pointed out, so many inpatients end up getting a chest CT for one reason or another, and we may see radiographic evidence of emphysema. In that case–symptoms that sound like COPD and imaging evidence of it–it’s probably ok to start maintenance inhalers and order outpatient PFTs for confirmation.
Shreya: im glad you brought that up. it comes up all the time! So luke—why don’t we recap pearl 1
Luke: So, while it is ok to treat an acute respiratory issue empirically as COPD, make sure you do your due diligence the next time you see someone with COPD in their one liner, who’s on maintenance therapy, and who hasn’t had spirometry–advocate for them to get PFTs! It can really clarify if obstruction is actually causing their symptoms.
Pearl 2: The Initial Visit–Blood Work, Staging, and Initial Treatment Choices
Shreya: So say we finally got our patient to get a spirometry and there is, in fact, evidence of obstruction –we ruled out other conditions of obstruction. What are the next steps?
Ali: Well there’s some bloodwork to do!
Shreya: What bloodwork? That is definitely something I am not jumping to in COPD
Ali: One that I actually learned recently is that you should check everyone with COPD just once for alpha-1-antitrypsin deficiency because it’s something that we can treat and we treat it differently.
Shreya: Yep not something I routinely do or chart review if its been done in the past
Ali: The one people seem to think of more commonly is to check CBC with diff at least once to look at their eosinophils.
Shreya: Eos?! I’m surprised to hear that too. What’s the thinking behind eos in COPD?
Dr. Saukkonen: “The movement in COPD in terms of treatment now is much more linked to phenotypes, you know, so are you a frequent exacerbator? Do you have high eosinophil levels or do you have an asthma-COPD overlap syndrome? These are all sort of clinical phenotypes that are probably dictating therapy a little bit more
Shreya: That was Dr. Dr. Schwartzstein, Chief of the Division of Pulmonary, Critical Care, and Sleep Medicine at Beth Israel Deaconess Medical Center and Professor of Medicine at Harvard Medical School.
Ali: the idea here being that people with a higher eosinophil count might have an allergic or inflammatory phenotype and the inhaled corticosteroid, or as we’ll being referring to ICS, will directly treat this and therefore reduce exacerbations
Shreya: Ah nice but then why isn’t everyone on ICS?
Ali: Well if you don’t have high eosinophils then they don’t have an inflammatory phenotype and then an ICS will just result in immunosuppression and an increased risk of pneumonia.
Shreya: Ah good old weighing risks and benefits rears its head again! so we have use inhaled steroid cautiously only in the inflammatory phenotype. So what sorts of esoinphil values should we be looking at for clue us this person may be more of an inflammatory phenotype?
Luke: Exact values differ between studies and individual’s practice patterns varies — some people use a threshold of 300 or 400, but there’s evidence that peripheral eosinophils >100 cell/microL predicts a patient’s risk of exacerbation and that they will likely respond to an ICS. And if the eos are < 100, the patient may have a higher rate of PNA with an inhaled steroid
Ali: One pro tip is to make sure you’re not checking the eos when the patient on systemic steroids because that will make the eos go down and could mask their true eosinophil level
Shreya: Yes thats a good one, blood work ordered. Now, how do I start thinking of treatment? There are so many different options for inhalers
Ali: It’s so much easier once you realize there are actually only 3 classes of medications! There are beta agonists, muscarinic antagonists, corticosteroids, and that’s it! So when we’re talking about initial therapy and inhalers, all you have to remember are those 3 drug classes – beta agonists, muscarinic antagonists, and corticosteroids.
Shreya: I used to feel fuzzy about which ones are which but once I made the connection that all the long-acting muscarinic antagonist inhalers or the LAMAs end with -ium (these are the tiotropium, aclidinium, the umeclidinium) and all the inhaled steroids end with -one (these are the fluticasone, beclomethasone (BECK-lomethasone)) and the last one is the long-acting beta agonist have an end of -ol.. so examples of LABAs are formoterol and salmeterol
Luke: Ok, lets move on which patients get which combination of those 3 types of meds
Ali: To do that, you are gonna go to GOLD staging. The long and the short of this is that patients are given a grade which is defined by FEV1 and informs prognosis and then they’re given a group which informs initial inhaler choice
Shreya: Take a look at the awesome 2×2 table by GOLD that we will link in our show notes but its basically categorizing patients as group A, B, C, D based on # and severity of the exacerbation and symptom burden
Luke: And to quantify their symptom burden, it may be tempting to use the mMRC–one of the two tools GOLD recommends–since it’s only 1 question asking at what level of exertion someone feels dyspneic. But this actually leads to understaging and undertreating because patients often downplay their shortness of breath!
Ali: Exactly, and it can be helpful to look at the 2×2 table to guide you, but in practice it’s actually pretty simple. If your pt has NOT been hospitalized in the last year, so group, A or B, you’re going to be starting with only one inhaled medication, either a beta agonist or a muscarinic antagonist
Luke: Yeah this is because both LABAs and LAMAs are good meds, shown to improve lung function, SOB and exacerbation rates so you can reach for either one of them for patients in group A or B
Ali: But then when we jump to group C, these people have had 1 or more exacerbations leading to a hospitalization, and so for these people, LAMAs were more effective in reducing exacerbation so LAMAs are recommended over LABAs in group C patients
Shreya: I’m hearing a lot of LAMAs and LABAs and I know it’s only two different medications we’re talking about here, but still seems like a lot of variability in terms of what you can do
Ali: That is true! But what you’ll notice is that LAMAs are an option as initial therapy for all three of these groups, A, B, and C so to make my life easy, I almost always prescribe a LAMA as initial therapy for these patients
Shreya: Ok, that makes things a bit simpler! And what about group D?
Luke: Group D is your patients who have the highest symptom burden and frequent or severe exacerbations. For these patients, you are going to want to start with a combination of two inhaled meds.
Ali: Yeah bringing back to our earlier point, the Group D patients that have high eos, you can choose LABA/ICS BUT if they don’t have high eos then you can start with LAMA/LABA.
Shreya: this is clicking a bit more! Ok, Luke, can you summarize this pearl for us?
Luke: Definitely! When you’re first seeing a COPD patient make sure to screen for A1AT deficiency once, especially in a young person or someone without significant smoking history. And check their eosinophils, especially when they are not on steroids. Initial choice of inhalers is based on which GOLD group they fall into, and the group is determined by the # and severity of exacerbations in the last year and their symptom burden.
Shreya: And summarizing the initial inhaler option, you can prescribe a LAMA as initial therapy for any of the groups! but for group D you’ll usually prescribe a combination with either LAMA/LABA, but if they have the high eos/ inflammatory phenotype, reach LABA/inhaled steroid combo
Ali: Just one caveat to clarify is that if you have a patient who has low eos but is having frequent or severe exacerbations, then you CAN consider ICS in these patients to see if it can reduce their exacerbations. This can be helpful to loop in a pulmonologist
S: ok so sounds like it gets a bit more nuanced if it is a patient with exacerbations and honestly sometimes we might NOT have a reliable eosinophil count when they were off of systemic steroids to go by so that’s when you may wanna weigh pros and cons and see how the patient does
Pearl 3: Inhaler Devices
Luke: Ok, so now we’ve decided on the initial meds we want to prescribe our patient. You open up the medical record to write the prescriptions and suddenly a wall of words like handihaler, diskus, ellipta, MDI, respimat, and respiclick fill the screen.
Shreya: Oh jeez–I feel I’ve actually woken up with mind trying click through this exact section of the EMR and feeling lost at which is the right inhaler device to click. It can be really tempting to just prescribe the first inhaler device–it’s all the same drug right? But come to think of it, does this device we choose even matter? Is one superior for COPD outcomes?
Luke: Not really! I was pretty surprised to learn that studies have not identified any single device or delivery method to give superior disease control!
Ali: Yeah on a population level there doesn’t seem to be a difference, but its an entirely different story when you’re talking about the individual patient in front of you.
Dr. Schwartzstein: So I think the biggest mistake that we make is we give them the inhaler. We sort of tell them how to use it, but we don’t actually watch them use it. We don’t, you know, critique them and, and help them with that.
Luke: And what frustrates me is that we know that a lot of patients struggle to use their inhalers, and despite that rates of proper use haven’t gotten any better over the last half century
Dr. Saukkonen: I do ask patients to demonstrate how they take their inhaler, and sometimes they’ll tell you, oh, I’ve been doing this for years. I know what I’m doing. And so then, and then they demonstrate completely the wrong technique. So they will be exhaling while the mist is coming out of the device. And you can see the mist floating up around their face as they exhale. So then I say, well, let me give you a few pointers. So I explain why and how to do it. So I explain why and how to do it. So it’s, um, not everybody necessarily needs a spacer. And I, I think it’s also very important to review inhaler technique. And I’ve had people who once you show them and explain to them how it’s supposed to be done, they come back and say, you know what that stuff really works?
Ali: Dr. Saukkonen also had one other practical tip that I want to make sure we share with listeners that applies to all inhaler devices
Dr. Saukkonen : You squeeze then breathe and then hold your breath for a good 5 or 10 seconds. And the reason you’re holding your breath is so that the mist settles down and sticks to the walls of the airway. So it gets absorbed. If you, if you just inhale and exhale, then the medicine goes in and goes out and doesn’t do anybody any good.
Ali: I have some patients in my clinic who are like “you want me to hold my breath for 10 seconds??” good joke, but you know it’s good for them to know and do the best they can.
Shreya: My motto #something is better than nothing! Why don’t we delve into the different inhaler devices we should choose from and what we need to educate our patients about each
Ali: YesI You know as a first year fellow my program had a pharmacist do a demonstration of all the different inhalers for us. I was surprised by how many different delivery systems there are and how confusing they are and I genuinely had no idea how to use half of them.
Shreya: that makes me feel a lot better about my sweats when i get to that inhaler device page in the EMR
Luke: Ok, so there are 3 big buckets of inhalers. The first are pressurized metered dose inhalers, or pMDIs. Generally speaking, if a med you’re prescribing has “HFA” after it there’s a good chance it’s a pMDI
Shreya: Yes, I’ve definitely seen lots of HFA before! I’m not sure what it means or it was used with a pressurized metered dose inhalers
Luke: It stands for hydrofluoroalkane–which is just the propellant a lot of these use. An advantage of these is familiarity–even though TV and movies show them being used wrong most of the time, this is what your patient will think of when you tell them they need an inhaler.
Ali: In counseling our patients with pMDIs, we need to make sure they shake before each dose to ensure you get a consistent dose. If you haven’t used it in a few days you need to prime it by pumping it a couple of times before you use it to make sure you get a consistent dose.
Shreya: Good to know! [pause] so what are some of the cons with pMDIs?
Ali: With pMDI, one of the challenges is the patient has to coordinate pressing down on the canister and inhaling and unfortunately if they don’t do this, a lot of the drug can stay in the oropharynx and NOT get into the lungs, which is wasteful, but can also cause side effects like funny taste or throat irritation.
Luke: And for this reason,pMDIs are often given with a separate prescription for a spacer or holding chamber
Shreya: spacers and holding chambers…How exactly do spacers or holding chambers help with the drug in pMDI get into the lungs?
Luke: Spacers are basically just big reservoirs that you add on to the end of a pressurized metered dose inhaler, and valved holding chambers are basically just spacers with a one way valve inside.
Ali: So there’s a couple benefits but the main reason we use them is to slow down and reduce the size of drug particles
Dr. Saukkonen: One of the benefits of the spacer is that, that the larger particles that offer that without a spacer would get deposited in your oropharynx causing the dysphonia on the thrush. They, they fall out in the spacer. So only the three micron particles go down to your alveoli, those get inhaled into your lungs.
Shreya: Oh interesting so if spacers and chambers are slowing practicals down and only allowing smaller ones to go through, in theory less drugs get stuck in the oropharynx there should be less side effect like thrush
Ali: Right! Another reason we use these and this true for spacers too, but even more so with valved holding chambers, is that the patient then has a bit more time so that they don’t need to perfectly time their breath with pushing down on the canister.
S: Sounds like a win!
Dr. Saukkonen: “You attach your inhaler to one end of the spacer and the other end of the spacer you put in your mouth. So you can squeeze–the mist goes into the spacer. Then when you’re good and ready, then you can inhale. You inhale nice and slowly, then you hold your breath again. With the mist, settle down.
Luke: Ok, let’s move on to the next type of inhaler–dry powder inhalers, or DPIs. These are really common–if you’re ever prescribed a Diskus, Ellipta, or Handihaler, or an inhaler your patient loads with a capsule, you’ve prescribed a DPI!
Shreya: Oh those sound so different that I just assumed they were different devices so i’m really glad you clarified that
Luke: You would think! And there are some differences between brand names, but they all basically work the same way. With DPIs, the medication is stored as a powder and the device aerosolizes it when the patient inhales by drawing the air through the powder.
Some good things going for DPIs are that you don’t need to coordinate pushing anything with inhalation! You just take a puff.
Ali: Its great that they dont have to coordinate pushing on the inhaler and taking a breath BUT using these can be challenging for some patients because they really need to be able to generate enough negative inspiratory flow to be able to actually aerosolize the drug to get it into their lungs.
Shreya: Is there a rule of thumb to know that my patient won’t be able to generate enough inspiratory flow for a DPI?
Luke: I’d been wondering the same thing! I asked Dr. Schwartzstein, and he said there isn’t a hard and fast rule but that he starts to worry about DPIs when they have more severe emphysema or hyperinflation on imaging. More specifically, up to 1/3 of patients after a COPD exacerbation have peak inspiratory flow rates < 60 L/min so DPIs may not be optimal inhaler device for them.
Ali: Great point! the last issue to be aware of for DPIs is that humidity can actually make the powder clump so the particle size becomes larger and then more gets deposited in the mouth rather than reaching the lungs.
Luke: They do make single-dose capsules (what you’ll see called “Handihaler” devices) that help protect against humidity causing clumping, but then you have to load the inhaler with a capsule each time you want to use it!
Shreya: Ah of course–no free lunch with inhalers
Luke: Exactly, let’s move on now to the last type of inhaler device –the soft mist inhaler, or SMI. This is a newer technology you’ll see labeled as a “Respimat”.
SMIs are devices that are shaped like tubes that work by having the patient twist part of the inhaler and then push a button that releases an aerosolized mist
Shreya: Hah, hence the soft mist name
Luke: Right! And there are some pros of SMIs because of this. First, unlike dry powder inhalers, soft mist inhalers don’t depend on your patient’s inspiratory flow.
Ali: Also, the slower mist means that patients still have to coordinate their breath somewhat with pressing the button, but unlike with the pMDIs it doesn’t need to be *perfectly *coordinated.
Luke: The mist actually moves more slowly and lasts a few seconds longer than with a pMDIs, which leads to more drug in the lung and less in the oropharynx.
Shreya: Ok, so soft mist inhalers seem pretty great. I’m almost sold. Any drawbacks?
Ali: Maybe not quite drawbacks but something to be aware of is that because they’re a newer technology, not all types of COPD medications are available in soft mist inhaler devices. They can be a bit more expensive, too.
Shreya: hah still no free lunch! As one of our peer reviewer Dr. Nick Mark said, the best inhaler device is the one that the patient can actually take and afford e.g which ones their insurance covers. Luke, I feel like we’ve covered a ton of ground here, i think we can use a good recap
Luke: Some big takeaways with metered dose inhalers, or pMDIS, include making sure your patient gets a consistent dose by shaking it before using and wasting a puff first if they haven’t used it in a while. And make sure they’re timing pressing down and inhaling well. This last part is where ordering a spacer or valved holding chamber can come in handy so the drug really reaches the lung and patients don’t have to think as much about when they are inhaling.
Shreya: With dry powder inhalers like the Diskus, Ellipta, or Handihaler we have to make sure the patient can generate enough a breath to aerosolize the powder and not to store in humid area, the real benefit is that they don’t have to time pressing it and time taking a breath and just as an FYI if you are ordering a handihaler, the patient has to be able to physically able put in a pill into the canister every time they use it
Ali: And finally, Soft mist inhalers can get more drug in the lungs and less in the oropharynx, and give patients slightly more time to inhale after releasing the med. The only real drawback here is that they’re a bit newer so they can be more expensive and not every drug is available in this form.
Luke: And with all of these, make sure your patient is holding their breath for 5-10 seconds after a puff to give them the best shot at getting these meds into their lungs
Ali: And the last, we didn’t mention this fully before but in addition to counseling the patient yourself you can ask your patients to ask the pharmacist to go over again how to use the inhalers
Shreya: That was a humbling blintspot for me – i didnt know all pharmacists, not just the hospital ones but even the retail pharmacists are all trained to teach patients how to use inhalers
Ali: Patients really appreciate hearing it from me and then again with the pharmacists! So utilize your interprofessional colleagues!
Pearl 4: Inhaled Steroids and Inhaler Escalation
Shreya: Ok, so we’ve diagnosed our patient, decided what initial meds should be, we picked an inhaler device and we reviewed its technique with them. Fast forward time, they’re coming back to see us in the clinic. What else should I do or prep the patient about in the follow up visit?
Ali: GOLD recommends repeating spirometry annually to monitor for rapid disease progression so making sure they plugged in to get their annual spirometry.
Dr. Schwartzstein: I think the biggest one is missing their reduction in activity as a sign that they’re doing fine. In other words, they come and say, I’m, I’m kinda like I was before. And uh, you know, don’t get too short of breath at home and so on and so forth. But what you have missed is they’re doing less and less and less
Dr. Saukkonen: I love to take my patients for a walk for a couple of, for the patient’s benefit and for mine, um, they say sitting is the new smoking. So, uh, you know, if I, if I don’t take my patients for a walk, then I sit. So, so I go get my patients from the waiting room. I bring them back to the office, I have them. So I walk with them, I see what they can do, or if they’ve already been put in the room, I take them for a walk. I standardize my walk. So, so I’ll, and I’ll make a notation in the chart, walking from the waiting room to the, to the exam room.
Dr. Saukkonen : (28:26)
I find it very, very helpful to check oxygen saturation at rest and with walking
Dr. Saukkonen : (29:28)
And if I do that every time, then I’ll get a sense over time.
Ali: Exactly and also in the follow-up visits we should really be thinking if we can titrate down or stop some meds, especially the ICS. There is dose dependent risk with inhaled steroids!
Dr. Saukkonen: “One caveat about inhaled corticosteroids, um, is that people often get put on the highest dose or the medium dose just to try to get them feeling better, which is great. And then part of what I do, uh, is to, um, always look for ways to reduce the inhaled corticosteroids, if possible… (43:29) because over time you do see people who develop more uh bruising of the skin, increased risk of a cataract and glaucoma. Sometimes people, especially with diabetes, will have an elevation of their blood sugar, blood pressure will be up. All kinds of things like that…
Dr. Saukkonen : Occasionally you’ll see someone who develops actually adrenal, uh, iatrogenic adrenal suppression from the chronic. And what corticosteroids, if they’ve been on say fluticasone, uh, 500 micrograms, you know, with the, the, uh, twice a day
Shreya: Wow–I’m surprised to hear about systemic effects of just inhaled steroids! So maybe our default “things are going well” shouldn’t be to just continue ICS, but things going well for a patient should trigger de-escalating.
Ali: Another time I am decreasing steroids is if someone is coming in to my clinic and they’re having pneumonia or are still having exacerbations on the ICS then I’m like ok, this isn’t helping, maybe hurting, I really need to start down-titrating this.
Luke: Just remember that when you are de-escalating inhaled steroids, you really need to keep a close eye if they start having more exacerbations.
Ali: Yeah, and the WISDOM trial in NEJM from 2014 helped us understand how. Basically, with patients who are on triple therapy who you want to wean off their ICS, you should go gradually–like going from high dose to medium then lose dose over a 12 week period to mitigate the risk of exacerbation with de-escalation
Shreya: wow I feel like we are so bad about this — maybe it’s a knowledge gap issue. With heart failure meds I feel like I get up all in there with titrating, discontinuing but don’t do that in COPD.
Ali: you are not alone in that!
Shreya: What about uptitrating or down titrating LAMA and LABAs? How do we change the inhaler regimen?
Ali: most pts are started on a one agent, LABA or LAMA, and if they are still SOB or having more exacerbations, then you can add whatever they aren’t on so that they are on combination therapy with a LAMA/LABA.
Shreya: So with LAMAs/LABA you are not titrating up and down doses like you do with inhaled steriods?
Ali: Nope with LAMA/LABAs, its you usually just one dose (unless new formularies come out!) so if symptoms aren’t controlled on, you are reaching for another agent
Luke: And then of course if your patient has high eosinophils and lots of exacerbations, think about adding inhaled steroids to have them on triple therapy with LAMA/LABA/ICS
Shreya: OK, that actually seems simple enough
Luke: The last thing I’d say is that if your patient is still short of breath and already on combo inhalers–and you’ve checked they’re using them correctly– watch them use their inhaler and see there are any pointers you can give from pearl 3 OR you can try changing the inhaler device itself
Shreya: ah a little switchu- whether its placebo or easier technique for them, its worth a try and definitely gonna keep that in my bag pocket
One last thing that comes up in follow up visits or in the hospital is patients will ask me about pulmonary rehab and I say “sure! That’s great if your insurance covers it!” but I have to admit, I have a pretty superficial understanding of what pulmonary rehab is
Dr. Saukkonen: Pulmonary rehab can be so helpful for many people who are limited by their breathing. So there’s education, there’s physical training, it’s a social experience, gets people out of the house.
Dr. Schwartzstein: Rehab does more than just increase your cardiovascular capacity. It also gives you strategies, pursed lip breathing. It gives you the confidence that when you say, oh, I’m short of breath.
Dr. Schwartzstein: There’s nothing like having the therapist there saying, by the way, your saturation is fine, you look fine
Ali: Pulmonary rehab is the best! I just have to give a quick plug because this is one of the most effective but least utilized interventions for COPD. There was this metanalysis when pulm rehab was started after COPD exacerbation, they had better quality of life, they didn’t have as many readmission and what I was most impressed by is that they had a better mortality.
Luke: And in a bit of a mic drop, the Cochrane Review found that it was so effective that they said in the paper “it is our opinion that additional RCTS…are not warranted.” I don’t know about y’all but I can’t remember the last time I heard that!
Shreya: Yeah me either that is snarky and bold
Luke: Alright, so to recap pearl 4: get annual spirometry to track disease progression.
Luke: And, if you find your patient SOB or having exacerbation, reach for the combo LAMA/LABA
Ali:Or triple LAMA/LABA/ICS if they are more the inflammatory phenotype and high eosinophils initially.
Unlike in asthma, the overall benefits of inhaled steroids in COPD are more marginal and the incidence of side effects is higher so titrate down the ICS if they are having pneumonia or exacerbation or if they’ve been really well controlled for a long time
And, if you find your patient SOB or having exacerbation, reach for the combo LAMA/LABA
Ali:Or triple LAMA/LABA/ICS if they are more the inflammatory phenotype and high eosinophils initially.
Shreya: And last but not least, my big takeaway is to get more of my patients to pulmonary rehab! Its just ordering outpatient PT for patients, which i imagine has accessibility issues but worth the try
Pearl 5: Communication, Palliative Care, and End of Life Care in COPD
Shreya: I’m so grateful we went over the trajectory of COPD mgmt from initial inhalers to device choices to titration and that’s all great from straight medication perspective but that does not mean much if we don’t communicate to our patients about the lifelong illness that COPD is
Dr. Omlor: “When you break the bad news to somebody that they have COPD, you have to think about it the same way as telling someone they have cancer. And understanding that in that first visit they’re likely not absorbing a lot of information… For COPD, the biggest thing for them to hear is that this is a disease that they’ll have for the rest of their life. It is a disease that is going to progress and only get worse over time, and that we have no treatments to cure or stop the progression of the disease… The biggest thing thing to really make sure in those first couple of visits that people hear and understand, because I think that’s the framework on which the rest of the discussions build”
Luke: And that was Dr. Rebecca Omlor, a geriatrics and palliative medicine trained doctor in Winston Salem, NC.
Ali: I think COPD is similar to heart failure in this, in that we don’t often hear that diagnosis and think of their mortality. In both cases, they come in for exacerbations, they get treated, they get better to some extent, but their mortality is really high. So in the same way cancer sets off mortality alarm bells, a patient being admitted with a COPD exacerbation should really get us thinking about their mortality risk.
Luke: There is a shockingly high mortality rate post-hospitalization for a COPD exacerbation. The one year mortality ranges from 23% (if admitted to the floor) to 35% (if admitted to the ICU)!
Shreya: Wow, that is pretty high.
Ali: I know, I’ll be honest that even though I see these patients regularly in clinic and in the hospital, I also find those numbers shocking and it’s a great reminder that a COPD exacerbation, whether treated inpatient or outpatient, can often be a good trigger to talk about overall goals of care.
Dr. Omlor: “if you have someone who’s never experienced a COPD exacerbation, has never been in the hospital or been in the ICU on a ventilator and really trying to explain to them what that’s like is going to be difficult, even with a picture. And so thinking that you’re going to have this like really great conversation upfront about whether somebody wants to be intubated or not, it’s probably not going to work out the way you’re hoping it would.”
Luke: One thing that can help in painting a picture for patients, with the caveat that we are not good at prognosticating and this is just an estimate, is the BODE index, which gives an estimate of 4 year survival.
Ali: It’s definitely not an end all be all, but GOLD recommends that, where possible, a scoring system like BODE be used a few months after discharge from a COPD exacerbation to assess your patient’s prognosis
Shreya: I do find it helpful to give numbers: “You have a 25% or 50% chance of survival after 4 years.” But it’s a 4 year survival estimate. Is there something to give us a sense of when someone’s truly at the end of their life?
Dr. Omlor: “We don’t have any really good tools for people who are within 6 months of death”
Ali: What we can try to do is get sense of a person’s functional status with iADLs and ADLs, which can guide some of her conversations
Dr. Schwartzstein: The, the issue in my mind isn’t you’re gonna be on the ventilator forever. The issue is will you be restored to the present level of activity that you have now? There was a study years ago in the Annals of Internal Medicine. It was a small study, 100 to 150 patients, as I remember, but they looked at people who had been on a ventilator for more than three or four days—not real long times on the ventilator. These are all bad COPD patients. And only 10% of them got back to the level of function afterwards that they had before they had the acute illness.
Luke: You know, this blew my mind. 90% of ppl that you have intubated will NOT return to their previous level of function
Dr. Schwartzstein: Now that may be okay. They may just, you know, adapt to that new level. But it’s important to say, how happy are you with your present level of function? And if you couldn’t do A, B, or C, the things that you do now, is that consistent with what you view as a valuable existence for you? Is that consistent with how you live your life and what you wanna do for the time that you have left? And if they say no, if I couldn’t do those three things, I’d just as soon not have you prolong my life.
Luke: Ok then, summarizing our last pearl here: COPD is a disease with a shockingly high mortality and a really significant symptom burden. Prognosticating is hard, but we can use the BODE index to estimate a patient’s 4 year survival. Advanced care planning is not a procedural yes or no question. Try to understand your patients’ values, in particular ask them what is an acceptable functional status for them knowing that things will most likely get worse
Outro
Shreya: And that’s a wrap for today’s episode! If you found this episode helpful, please share with your team and colleagues and give it a rating on Apple podcasts or whatever podcast app you use! It really does help people find us! Tweet us and leave a comment on our website, or on instagram or facebook page.
Ali: Thank you to Dr. Jamie Betancourt, Dr. Nick Mark and Dr. Laskshman Swamy for reviewing this episode. Thank you also to Daksh Bhatia for audio editing and to Dr. Michelle Lo for the accompanying graphic.
Luke: This episode was made as part of the Digital Education Track at BIDMC–thank you to all the educators and mentors for their wisdom and guidance, in particular Drs. Shreya Trivedi, Adam Rodman, and Chris Smith.
Shreya: As always, we love hearing feedback. Email us at hello@coreimpodcast.com. Opinions expressed are our own and do not represent the opinions of any affiliated institutions.
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Tags: medications, pulmonary