QD clinics on ILD - lessons from the Cliniic Save
"QD clinics on ILD - lessons from the Clinic; brought to during the "Rheum to Breathe" ILD campaign
Transcription
Welcome to ILDRA QD clinics. I'm doctor Brian England from the University of Nebraska in Omaha, Nebraska. Today's case is entitled be careful what you look for. Now our patient today is a 57 year old female with a history of right knee pain and a diagnosis of osteoarthritis. But she started developing hip, hand, ankle, and foot pain over the last few months.
This is accompanied by about one to two hours of morning stiffness. She's a former smoker, have one pack per day for fifteen years, but quit eight years ago. Today in clinic, she has a BMI of forty three kilograms or meter squared. She has a little fullness in her MCPs. Her lungs are clear to auscultation.
Her serologies return with a CCP greater than 300, her rheumatoid factor is four forty, and her CRP is 2.7 milligrams per deciliter. Radiographs of her hand show possible MCP erosions, and the patient started on methotrexate, which is escalated up to twenty milligrams by mouth weekly. Within a few months, the patient has really complete resolution of her articular symptoms. There's no synovitis detected on exam, and she's functioning well in life and work. She's doing so well, she decides that she's gonna participate in a research study where she undergoes a chest CT and pulmonary function test.
The chest CT shows mild ground glass attenuation in the bilateral lung basis on both supine and prone imaging. And pulmonary function tests show an FVC of seventy seven percent predicted and an FEV one of eighty two percent predicted. As part of that visit, she has detailed assessment of her respiratory symptoms, and she does admit to a bit of shortness of breath and dyspnea over of exertion over the past few weeks. Now based on these findings, this case actually gets reviewed in a multidisciplinary discussion between rheumatology and pulmonology. Ultimately, it's felt that these findings are nonspecific with the potential for these to be a drug reaction, early interstitial lung disease, or of another cause.
Because of this uncertainty, the methotrexate is discontinued and azathioprine has started in its place. Over the coming months, the patient's articular disease remains very well controlled. She notices a little subjective improvement in her symptoms. She's able to do a little more physically at work without trouble, and PFTs over one year later remain stable with her baseline assessment. In terms of imaging over time, unfortunately she develops COVID-nineteen pneumonia and those, changes obscure any of the initial changes that were seen.
So this case really highlights the point of what do we do when interstitial lung abnormalities are detected in a patient with rheumatoid arthritis? Now when we see findings of interstitial lung abnormalities such as reticulation, ground glass changes, one of the things that comes up right away is, is this RA interstitial lung disease? But other things on the differential include things like drug induced pneumonitis, particularly if a patient is on a medicine that we think of this frequently, such as methotrexate. And if that's the case, then the question comes up, well, what do you do with their current medications? Do you stop methotrexate in somebody who has incidentally detected interstitial lung abnormalities?
Some important things to consider in this situation is that not all interstitial lung abnormalities or restrictive PFT findings are evidence of RA interstitial lung disease. So we just talked about that differential including other things such as drug induced pneumonitis, but also infections or post infectious reticulation can also appear similarly. People who have fluid overload perhaps related to heart failure may have some of these similar changes. And then on PFTs, we can have other causes of restrictive lung disease such as obesity, other chest wall diseases. Another important point is that when we incidentally detect these interstitial lung abnormalities or ILA, that doesn't necessarily mean that treatment changes are required.
In some situations, after a detailed assessment of this patient, we might be able to keep them on their current therapies and just monitor them closely over time. But there are some things that the identification of an ILA does require in a patient with RA, and that is number one, we need to thoroughly assess this patient. We need to ask about respiratory symptoms such as shortness of breath, cough, dyspnea of exertion. We need to obtain pulmonary function tests to understand their pulmonary physiology. These should be complete PFTs with spirometry, lung volume, and diffusion capacity.
If available, it's always a great idea to have a multidisciplinary discussion with pulmonologist and with a radiologist to discuss the potential etiologies of these findings. After doing these assessments, we don't wanna stop and never assess them again, but rather these assessments should be part of their ongoing care so we can understand the trajectory of their imaging findings, their pulmonary physiology, and their symptoms. We need to target the risk factors that can predispose these abnormalities to worsen or impact their survival. So things like if they're a cigarette smoker, we need to talk to them about smoking cessation. If they're, exposed to other inhaled exposures, we need to mitigate those.
We need to talk to them about optimizing physical activity levels. Then finally, when we detect an ILA, we also need to make sure that there weren't other findings on that CT scan we need to act on. So other incidental findings of particular interest are lung nodules because patients with ILA are at higher risk of developing lung cancer. So those are the things that we absolutely need to do to really understand and monitor this disease over time. The things we may need to do require making treatment changes.
But again, remember that not all ILAs are definitely RAILD. Keep your differential open. So thanks for joining me to discuss this case.
Hello, everyone. I'm Richard Conway from Dublin, Ireland, and this is, QD Clinics from RheumNow. And today's case is that of rapidly progressive, rheumatoid arthritis interstitial lung disease or not. So this is the case of a 60 year old lady. She's been attending my rheumatology clinic for the last ten years.
She is an ex smoker. She has seropositive rheumatoid arthritis, strongly positive for rheumatoid factor and CCP antibody. So she is currently on treatment with methotrexate and adalimumab. And we have been lining her up in the clinic to switch over from the adalimumab to tocilizumab because she has not been controlled. So her disease activity has been high.
Her C. Dye at her most recent visit was 25. Her DAS 28 CRP is 5.4. So we had this plan to change her. We haven't changed her yet because she had some life things going on and wanted to delay treatment change.
So that plan has been there for about two months and hasn't happened yet. And I am surprised then to get a call from our intensive care unit. And they tell me that this patient of mine has been admitted into them. And she come in initially through the emergency department. She's had a three to four week history of progressive dyspnea, which has culminated in her emergency department visit, a day or two on the ward, and she deteriorated further and has ended up in the intensive care unit, intubated and ventilated due to this pulmonary process.
She's had a chest x-ray and a CT scan done, and they show widespread pulmonary infiltrates with interstitial changes really throughout both lung fields. And they've called me and said to me that this lady has rapidly progressive rheumatoid arthritis interstitial lung disease. What do we do here? So that is the question. What do we do in a case like this?
I can tell from the way our intensivists are talking that they are keen for us to go ahead and start treating her autoimmune process. Maybe give her some methylbritinolone, maybe some rituximab, cyclophosphamide, something to address this perceived autoimmune process. I think it's always important to take a step back here. And that's what we did in this case. We said that, yes, absolutely, this would be RI ILD that has rapidly developed and progressed, but that would be slightly unusual in somebody, yes, who's had high disease activity, but hasn't previously had interstitial lung disease and has had rheumatoid for quite a bit of time.
And in some ways, it's not necessarily the type of patient we might be more worried about getting rapidly progressive lung disease in, which usually be older men who have relatively new onset disease. So we don't have a trajectory of the disease process over time, you know, are still smoking. And that is not the case here. So a woman, ex smoker, she's had disease for ten years or more. So we look at her imaging and she really does have a lot of changes.
Her lung fields on CT are, there's no normal lung there. It's interstitial changes everywhere on the lung fields. And again, that could be seen with rapidly progressive rheumatoid lung disease, but would be a little bit unusual as a presentation. The other thing we note on this lady is that she does have quite a bit of herpes simplex around her mouth and nose. Again, a sign that somebody is sick, potentially immunosuppressed, not unusual in an ICU patient, but work nudging.
So our recommendation here was this before we do anything else and mush in with more immunosuppressive medicines, we should make sure that there's not something else going on. So we stop recurrent immunosuppression is one thing. And then do a bronchoscopy and some serum looking for potentially other infectious processes that could be at play here. So I know as rheumatologists, we are relatively wary of this, and Pneumocystis jirovecii is always one that stands out to us and is in our minds. But there are multiple other pathogens that could be at play here as well.
And the other non infectious cause potentially is diffuse alveolar haemorrhage, unusual in rheumatoid arthritis, but can be seen in some of her other diseases. So this lady has her bronchoscopy. There's no blood staining of the sputum and bronchial or vage on that. We send it away to be cultured. No signs of pneumocystis on it.
But actually what comes back on her serum is that her CMV titers are absolutely through the roof. So we felt that actually this lady probably had cytomegalovirus pneumonia. So viral opportunistic pneumonia from reactivation of the virus in the setting of immunosuppression. And then why would that happen? That was a bit odd in the setting of somebody who's a TNF inhibitor and methotrexate, yes, immunosuppressive, but something that we wouldn't consider overly so.
And that brings us back to what was happening before she came in. She was due to switch, but hadn't switched due to life events. And she'd had some course of steroids from us, and then also had some further course of steroids from her primary care, unknown to us in the interim. And these repeated use of oral glucocorticoids, it is a cumulative thing. It does increase the risk over time.
And if somebody is constantly getting pulses or tapers of these to control active disease, there is a risk there. So that is today's QD clinic. And our learning point from today is keep an open mind. Don't always presume it is the rheumatic disease that is causing the problem. Tune into RheumNow for more from QD Clinics.
Hi, I'm Doctor. Janet Pope reporting at RheumNow. You can follow me on Twitter at JanetBurdope. And welcome to QD Clinic, a case that could be your patient. So this could be a patient with shortness of breath.
So let's dive right in. This is a 74 year old man. He has SEER positive RA and he has extra articular manifestations, nodules, and subluxations with joint damage. Unfortunately, he was a fifty pack year smoker, but he quit after having an MI when he was 70 years old. He's a retired high school teacher.
He's on methotrexate, folic acid, and multiple cardiac meds. However, he's also known to have chronic obstructive lung disease and he's on a puffer that's a combo of a long acting beta agonist and also an anti muscarinic inhaler. He has not needed steroids or antibiotics for his COPD. Now he is an exerciser, fortunately. So former smoker, he walks 10,000 steps a day because when he had his MI at age 70, he changed everything, stopped smoking, started walking regularly.
He did undergo cardiac rehab and he knows to continue doing that. He's never needed oxygen therapy. Now, just as an aside, when I have a patient who has obstructive lung disease and RA as a for instance, I do really look at vaccinations. So this fellow's vaccinations, he is a retired school teacher and he's very forthright in keeping records. And he tells me and shows me that since he had his MI at age 70, every year he gets the annual over 65 year old flu shot.
He did get his Prevnar twenty. He had had Pneumovax before, but was able to get Prevnar twenty because he is immune suppressed and he doesn't wanna have a super infection. And he did get the RSV vaccine. Now, he has come to me though with the known COPD and he says he's more short of breath. He's not coming in because of that.
It was a routine follow-up for his rheumatoid arthritis. So when I auscultated, I heard bilateral basal crackles. And I look back in my notes because I do make a habit of listening at the bases in every patient. And if you do it on everyone, you may as well, you can find things and you can record it and then you know if there's a change. So that's a little clinical pearl.
Listening to the bases is where the money's at for most of our patients for ILD. So here's what I would do working this guy up. I would do a chest x-ray, not because I'm wondering about ILD initially, because I am wondering about that, but is there something like a bilateral pneumonia? I would consider if warranted his oxygen saturation at rest or with activity, I would order an HRCT scan. So he had an HRCT scan and it was a bit complicated and I did review it with the radiologist.
So he had a mixed NSIP and UIP type changes. So some honeycombing. He has emphysema as before, no significant bronchiectasis and fortunately no pulmonary nodules. I also did PFTs and they were a mixed pattern. He had the known obstructive pattern and he also had a restrictive superimposed.
So what are a couple pearls? I don't want you to know how to read every PFT and I certainly don't know how to read PFTs. I just have a little bit of a sense about it because of running a large CTD practice. So obstructive, you're looking at FEV1 over FVC and the ratio should be reduced, less than 0.7. But if it's restrictive, there would be reduced TLC, quite a markedly reduced DLCO often because it's parenchymal with the ILD.
And you can also look at residual volume if you want, which would be elevated because of the obstructive lung disease. So what are we gonna think about? We're going to look for other reasons for fibrotic or interstitial changes. So as a for instance, if this guy had amiodarone with a fib treatment, I would wonder about a drug effect. Of course, I am wondering if this is rheumatoid arthritis, but I would also look for eosinophilia, which could be a drug effect.
So peripheral eosinophils on the differential. I'd look for low grade infection, the atypicals, if he had sputum and fevers, if it was warranted. Things like Legionella are usually more acute, but post COVID he could have had COVID and then had chronic ILD changes. Mycoplasma pneumonia is usually acute, but it could be subacute. It can be bilateral and atypical mycobacteria.
So there's a lot of things to think about. He could also be more short of breath because of sleep apnea. So these things sort of come into my mind, and I think it's really important that we need a systematic approach and you can listen to some of the other modules in our CTD ILD unit and become more systematic in assessing your patients. So the bottom line is a mixed pattern is quite common. In rheumatoid arthritis with RAILD, about half of those patients, maybe a quarter to a half will also have emphysema because smoking is a risk for RA, RA ILD and for emphysema.
But even in non smokers that can occur. In systemic sclerosis, about a fifth of patients with ILD from scleroderma will also have emphysema and a bit less so in the other CTDs. The final thing, if you really wanna be keen about this is this can be called CPFE in CTD. So it's a combined pulmonary, both fibrotic or ILD and emphysema. But I don't think we have to worry about the names as much as really trying to diagnose and get the right treatment for the patient.
Please follow us for the other reporting we'll be doing this month. Thank you.
This is accompanied by about one to two hours of morning stiffness. She's a former smoker, have one pack per day for fifteen years, but quit eight years ago. Today in clinic, she has a BMI of forty three kilograms or meter squared. She has a little fullness in her MCPs. Her lungs are clear to auscultation.
Her serologies return with a CCP greater than 300, her rheumatoid factor is four forty, and her CRP is 2.7 milligrams per deciliter. Radiographs of her hand show possible MCP erosions, and the patient started on methotrexate, which is escalated up to twenty milligrams by mouth weekly. Within a few months, the patient has really complete resolution of her articular symptoms. There's no synovitis detected on exam, and she's functioning well in life and work. She's doing so well, she decides that she's gonna participate in a research study where she undergoes a chest CT and pulmonary function test.
The chest CT shows mild ground glass attenuation in the bilateral lung basis on both supine and prone imaging. And pulmonary function tests show an FVC of seventy seven percent predicted and an FEV one of eighty two percent predicted. As part of that visit, she has detailed assessment of her respiratory symptoms, and she does admit to a bit of shortness of breath and dyspnea over of exertion over the past few weeks. Now based on these findings, this case actually gets reviewed in a multidisciplinary discussion between rheumatology and pulmonology. Ultimately, it's felt that these findings are nonspecific with the potential for these to be a drug reaction, early interstitial lung disease, or of another cause.
Because of this uncertainty, the methotrexate is discontinued and azathioprine has started in its place. Over the coming months, the patient's articular disease remains very well controlled. She notices a little subjective improvement in her symptoms. She's able to do a little more physically at work without trouble, and PFTs over one year later remain stable with her baseline assessment. In terms of imaging over time, unfortunately she develops COVID-nineteen pneumonia and those, changes obscure any of the initial changes that were seen.
So this case really highlights the point of what do we do when interstitial lung abnormalities are detected in a patient with rheumatoid arthritis? Now when we see findings of interstitial lung abnormalities such as reticulation, ground glass changes, one of the things that comes up right away is, is this RA interstitial lung disease? But other things on the differential include things like drug induced pneumonitis, particularly if a patient is on a medicine that we think of this frequently, such as methotrexate. And if that's the case, then the question comes up, well, what do you do with their current medications? Do you stop methotrexate in somebody who has incidentally detected interstitial lung abnormalities?
Some important things to consider in this situation is that not all interstitial lung abnormalities or restrictive PFT findings are evidence of RA interstitial lung disease. So we just talked about that differential including other things such as drug induced pneumonitis, but also infections or post infectious reticulation can also appear similarly. People who have fluid overload perhaps related to heart failure may have some of these similar changes. And then on PFTs, we can have other causes of restrictive lung disease such as obesity, other chest wall diseases. Another important point is that when we incidentally detect these interstitial lung abnormalities or ILA, that doesn't necessarily mean that treatment changes are required.
In some situations, after a detailed assessment of this patient, we might be able to keep them on their current therapies and just monitor them closely over time. But there are some things that the identification of an ILA does require in a patient with RA, and that is number one, we need to thoroughly assess this patient. We need to ask about respiratory symptoms such as shortness of breath, cough, dyspnea of exertion. We need to obtain pulmonary function tests to understand their pulmonary physiology. These should be complete PFTs with spirometry, lung volume, and diffusion capacity.
If available, it's always a great idea to have a multidisciplinary discussion with pulmonologist and with a radiologist to discuss the potential etiologies of these findings. After doing these assessments, we don't wanna stop and never assess them again, but rather these assessments should be part of their ongoing care so we can understand the trajectory of their imaging findings, their pulmonary physiology, and their symptoms. We need to target the risk factors that can predispose these abnormalities to worsen or impact their survival. So things like if they're a cigarette smoker, we need to talk to them about smoking cessation. If they're, exposed to other inhaled exposures, we need to mitigate those.
We need to talk to them about optimizing physical activity levels. Then finally, when we detect an ILA, we also need to make sure that there weren't other findings on that CT scan we need to act on. So other incidental findings of particular interest are lung nodules because patients with ILA are at higher risk of developing lung cancer. So those are the things that we absolutely need to do to really understand and monitor this disease over time. The things we may need to do require making treatment changes.
But again, remember that not all ILAs are definitely RAILD. Keep your differential open. So thanks for joining me to discuss this case.
Hello, everyone. I'm Richard Conway from Dublin, Ireland, and this is, QD Clinics from RheumNow. And today's case is that of rapidly progressive, rheumatoid arthritis interstitial lung disease or not. So this is the case of a 60 year old lady. She's been attending my rheumatology clinic for the last ten years.
She is an ex smoker. She has seropositive rheumatoid arthritis, strongly positive for rheumatoid factor and CCP antibody. So she is currently on treatment with methotrexate and adalimumab. And we have been lining her up in the clinic to switch over from the adalimumab to tocilizumab because she has not been controlled. So her disease activity has been high.
Her C. Dye at her most recent visit was 25. Her DAS 28 CRP is 5.4. So we had this plan to change her. We haven't changed her yet because she had some life things going on and wanted to delay treatment change.
So that plan has been there for about two months and hasn't happened yet. And I am surprised then to get a call from our intensive care unit. And they tell me that this patient of mine has been admitted into them. And she come in initially through the emergency department. She's had a three to four week history of progressive dyspnea, which has culminated in her emergency department visit, a day or two on the ward, and she deteriorated further and has ended up in the intensive care unit, intubated and ventilated due to this pulmonary process.
She's had a chest x-ray and a CT scan done, and they show widespread pulmonary infiltrates with interstitial changes really throughout both lung fields. And they've called me and said to me that this lady has rapidly progressive rheumatoid arthritis interstitial lung disease. What do we do here? So that is the question. What do we do in a case like this?
I can tell from the way our intensivists are talking that they are keen for us to go ahead and start treating her autoimmune process. Maybe give her some methylbritinolone, maybe some rituximab, cyclophosphamide, something to address this perceived autoimmune process. I think it's always important to take a step back here. And that's what we did in this case. We said that, yes, absolutely, this would be RI ILD that has rapidly developed and progressed, but that would be slightly unusual in somebody, yes, who's had high disease activity, but hasn't previously had interstitial lung disease and has had rheumatoid for quite a bit of time.
And in some ways, it's not necessarily the type of patient we might be more worried about getting rapidly progressive lung disease in, which usually be older men who have relatively new onset disease. So we don't have a trajectory of the disease process over time, you know, are still smoking. And that is not the case here. So a woman, ex smoker, she's had disease for ten years or more. So we look at her imaging and she really does have a lot of changes.
Her lung fields on CT are, there's no normal lung there. It's interstitial changes everywhere on the lung fields. And again, that could be seen with rapidly progressive rheumatoid lung disease, but would be a little bit unusual as a presentation. The other thing we note on this lady is that she does have quite a bit of herpes simplex around her mouth and nose. Again, a sign that somebody is sick, potentially immunosuppressed, not unusual in an ICU patient, but work nudging.
So our recommendation here was this before we do anything else and mush in with more immunosuppressive medicines, we should make sure that there's not something else going on. So we stop recurrent immunosuppression is one thing. And then do a bronchoscopy and some serum looking for potentially other infectious processes that could be at play here. So I know as rheumatologists, we are relatively wary of this, and Pneumocystis jirovecii is always one that stands out to us and is in our minds. But there are multiple other pathogens that could be at play here as well.
And the other non infectious cause potentially is diffuse alveolar haemorrhage, unusual in rheumatoid arthritis, but can be seen in some of her other diseases. So this lady has her bronchoscopy. There's no blood staining of the sputum and bronchial or vage on that. We send it away to be cultured. No signs of pneumocystis on it.
But actually what comes back on her serum is that her CMV titers are absolutely through the roof. So we felt that actually this lady probably had cytomegalovirus pneumonia. So viral opportunistic pneumonia from reactivation of the virus in the setting of immunosuppression. And then why would that happen? That was a bit odd in the setting of somebody who's a TNF inhibitor and methotrexate, yes, immunosuppressive, but something that we wouldn't consider overly so.
And that brings us back to what was happening before she came in. She was due to switch, but hadn't switched due to life events. And she'd had some course of steroids from us, and then also had some further course of steroids from her primary care, unknown to us in the interim. And these repeated use of oral glucocorticoids, it is a cumulative thing. It does increase the risk over time.
And if somebody is constantly getting pulses or tapers of these to control active disease, there is a risk there. So that is today's QD clinic. And our learning point from today is keep an open mind. Don't always presume it is the rheumatic disease that is causing the problem. Tune into RheumNow for more from QD Clinics.
Hi, I'm Doctor. Janet Pope reporting at RheumNow. You can follow me on Twitter at JanetBurdope. And welcome to QD Clinic, a case that could be your patient. So this could be a patient with shortness of breath.
So let's dive right in. This is a 74 year old man. He has SEER positive RA and he has extra articular manifestations, nodules, and subluxations with joint damage. Unfortunately, he was a fifty pack year smoker, but he quit after having an MI when he was 70 years old. He's a retired high school teacher.
He's on methotrexate, folic acid, and multiple cardiac meds. However, he's also known to have chronic obstructive lung disease and he's on a puffer that's a combo of a long acting beta agonist and also an anti muscarinic inhaler. He has not needed steroids or antibiotics for his COPD. Now he is an exerciser, fortunately. So former smoker, he walks 10,000 steps a day because when he had his MI at age 70, he changed everything, stopped smoking, started walking regularly.
He did undergo cardiac rehab and he knows to continue doing that. He's never needed oxygen therapy. Now, just as an aside, when I have a patient who has obstructive lung disease and RA as a for instance, I do really look at vaccinations. So this fellow's vaccinations, he is a retired school teacher and he's very forthright in keeping records. And he tells me and shows me that since he had his MI at age 70, every year he gets the annual over 65 year old flu shot.
He did get his Prevnar twenty. He had had Pneumovax before, but was able to get Prevnar twenty because he is immune suppressed and he doesn't wanna have a super infection. And he did get the RSV vaccine. Now, he has come to me though with the known COPD and he says he's more short of breath. He's not coming in because of that.
It was a routine follow-up for his rheumatoid arthritis. So when I auscultated, I heard bilateral basal crackles. And I look back in my notes because I do make a habit of listening at the bases in every patient. And if you do it on everyone, you may as well, you can find things and you can record it and then you know if there's a change. So that's a little clinical pearl.
Listening to the bases is where the money's at for most of our patients for ILD. So here's what I would do working this guy up. I would do a chest x-ray, not because I'm wondering about ILD initially, because I am wondering about that, but is there something like a bilateral pneumonia? I would consider if warranted his oxygen saturation at rest or with activity, I would order an HRCT scan. So he had an HRCT scan and it was a bit complicated and I did review it with the radiologist.
So he had a mixed NSIP and UIP type changes. So some honeycombing. He has emphysema as before, no significant bronchiectasis and fortunately no pulmonary nodules. I also did PFTs and they were a mixed pattern. He had the known obstructive pattern and he also had a restrictive superimposed.
So what are a couple pearls? I don't want you to know how to read every PFT and I certainly don't know how to read PFTs. I just have a little bit of a sense about it because of running a large CTD practice. So obstructive, you're looking at FEV1 over FVC and the ratio should be reduced, less than 0.7. But if it's restrictive, there would be reduced TLC, quite a markedly reduced DLCO often because it's parenchymal with the ILD.
And you can also look at residual volume if you want, which would be elevated because of the obstructive lung disease. So what are we gonna think about? We're going to look for other reasons for fibrotic or interstitial changes. So as a for instance, if this guy had amiodarone with a fib treatment, I would wonder about a drug effect. Of course, I am wondering if this is rheumatoid arthritis, but I would also look for eosinophilia, which could be a drug effect.
So peripheral eosinophils on the differential. I'd look for low grade infection, the atypicals, if he had sputum and fevers, if it was warranted. Things like Legionella are usually more acute, but post COVID he could have had COVID and then had chronic ILD changes. Mycoplasma pneumonia is usually acute, but it could be subacute. It can be bilateral and atypical mycobacteria.
So there's a lot of things to think about. He could also be more short of breath because of sleep apnea. So these things sort of come into my mind, and I think it's really important that we need a systematic approach and you can listen to some of the other modules in our CTD ILD unit and become more systematic in assessing your patients. So the bottom line is a mixed pattern is quite common. In rheumatoid arthritis with RAILD, about half of those patients, maybe a quarter to a half will also have emphysema because smoking is a risk for RA, RA ILD and for emphysema.
But even in non smokers that can occur. In systemic sclerosis, about a fifth of patients with ILD from scleroderma will also have emphysema and a bit less so in the other CTDs. The final thing, if you really wanna be keen about this is this can be called CPFE in CTD. So it's a combined pulmonary, both fibrotic or ILD and emphysema. But I don't think we have to worry about the names as much as really trying to diagnose and get the right treatment for the patient.
Please follow us for the other reporting we'll be doing this month. Thank you.
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