Hey, everybody. Thanks for tuning in to Palm Peeps. We are very excited today to be joining you with another episode. We haven't done one of these in a little while. We're getting a preliminary fellows case file today. These are one of our favorite episode types that Monty and I get to record and meet fellows and program directors from across the country. So we're very excited to be back with you and take you through
a really interesting case. But before we do that, as always, join with my partner in crime, Christina Montanor. Christina, how's it going? Hey, Ferb. Good morning. Doing great. Glad to be back with you. I feel, like, haven't seen you in a few weeks, so this is always the best part of my week. So excited to be back. And as you said with another Fellow's case files, I feel like we've had some new initiatives for 2025 including our guideline series, which have been fantastic.
But the Fellow's case files remain one of my favorite episodes that we do because we get to hear from fantastic educators, trainees from across the country. So really excited today to be virtually visiting Rutgers University and Robert Wood Johnson Medical School, which I have not visited personally, but I still think for if we're gonna go on a summer road trip in a bus and Yeah. Visit all the Fellowes case files that we've done. So I still think we're gonna make
that happen. A %. A bus or Winnebago, we'll have to we'll have to decide on the best mode of transport for us. Exactly. But really excited to get started today, and we have two guests today, and I have the honor of introducing our first guest. We have doctor Khalil Elgarib. Khalil completed his residency training at Northwell at Staten Island University Hospital program and is currently a first year fellow at Rutgers Robert Wood
Johnson Medical School. And Khalil reached out to us with a fantastic case that I'm really excited for us to go through today and such an honor to have you on the show today. Welcome to Palm Peeps, Khalil. Thank you for the introduction, Christina. I'm a big fan of the show and I'm thrilled to be here. Yeah. Thank you. We're thrilled to have you, and thanks for listening, certainly.
Next, we have doctor Sabia Hussain. Sabia completed her residency training at Robert Wood Johnson Medical School and her fellowship training in pulmonary and critical care at Columbia Presbyterian Medical Center in New York, where I did my fellowship. So we're bonded for life by that. She is currently a professor of medicine, and the program director for the pulmonary critical care medicine fellowship program. Thanks for coming on the show. Oh, thanks so much for having me. I'm really excited.
Wonderful. Excited to have you and walk through some really great teaching points with us today. As our quick disclaimer, just a reminder, the podcast is not meant to be used for medical advice, and the views we expressed today do not reflect the opinions or policies of our respective employers. The case we'll present today is HIPAA compliant, and some details might have been changed to protect the privacy of our patient. But let's go ahead and dive into the
case. Khalil, you as I said, you this was your brainstorming and great educational feature that you wanted to share on the show today. So why don't you go ahead and tell us about the patient that you met and how they initially presented? This is a patient that we met a couple of years ago in the clinic. It's a 28 year old male patient with a past medical history of Asperger's syndrome and IgA nephropathy who presents to the emergency department for shortness
of breath and cough. The caregiver reports that the patient has been having dry cough and dyspnea ambulation, progressing for the past three months prior to the presentation to the ED. The patient didn't have any wheezing, no chest pain, no palpitations, or any constitutional symptoms. The patient's medications were van stropin and oxcarbazepine, and his social history is mainly notable for questionable black mold exposure in the apartment where he resides.
Great. So thanks so much for sharing that, Felil. And I say fairly common pulmonary visit, at least from a complaint standpoint and chief complaint that we're hearing, although in a much typically younger patient than we probably see on average. So, Dave, I would love for you to share how you'd start your diagnostic reasoning approach for the specific patient. Yeah. Absolutely. This is something we've talked about a lot on the show about critical thinking
and diagnostic reasoning. I think we everybody uses variety of modalities to think about a new patient, and it's important to have some metacognition about that. And so I think the common ones that people use are diagnostic schemas and illness scripts. You hear about some symptoms. You're trying to fit them into a pattern that you recognize, and then you're trying to go down based on different likelihoods, different parts of that sort of flow diagram.
And thinking about that consciously is that sort of type two slow thinking. We do it very unconsciously while we're gathering information in the clinic, that sort of type one rapid reasoning response. And this is a very common complaint. As you said, we're thinking about a patient who's coming in with cough, and then we wanna amend just that basic presentation with some info that will change the likelihoods of diagnosis. So those have to do with the chief complaint, the substrate, predisposing
conditions, and exposures. As you said, this is a relatively younger patient. We don't have any history of smoking or things like that lead us down a different pathway, and we're thinking about what sounds like a progressive chronic dry cough. And so if we were thinking about that, the most common reasons for that in The United States are GERD, postnasal drip, cough variant asthma. There's actually an excellent review article that just came out in the
New England Journal on chronic refractory cough. It was a really great read and definitely good for any pulmonary provider or fellow to read about. But I think the key thing that helps me distinguish how I'm gonna approach this patient is that he's also having dyspnea on exertion.
Exertion. And so cough in isolation and a dry cough in isolation is very different than a cough with dyspnea on exertion because now I'm starting to think a little bit more about the lung parenchyma, about airways disease that's reaching a level that's affecting the patient's ability to exert themselves. I'm starting to really think about if that cough is reflecting some more progressive pulmonary process.
And then one thing of interest that the patient brought up, and this is not uncommon, is that they talked about a possible exposure to mold. And so I think mold is a broad bucket term, hot term for most people, like in the public. And so you'll often get a patient that comes up and says, I was told I have mold or there's mold in the workplace, and they're a little bit worried about that. And it certainly
should affect our thinking some. So, Sabi, I was wondering if you could tell us how you think about your diagnostic reasoning and what changes about it when a patient mentions a mold exposure. Yeah. Thanks so much, Dave. Yeah. I think that there's a lot of things that when you have a patient that comes in that's having progressive symptoms and dyspnea, especially as you were saying, this younger age population, you really do have to think about, like, exposure.
And and so this individual tells you a little bit about mold and mold exposure. So that's like puts your thinking caps on and figuring out, like, what does this mean? And as mold is, like, all around us, it's ubiquitous. It's in the indoor and the outdoor environment. And in majority of cases, most humans and and mold coexist. Like, they don't have any issues or problems
that are going on. But then there are individuals that this mold could then re lead to other things like allergic rhinitis, complications of allergic asthma. And then less frequently, these moles can result in atopic conditions such as allergic bronchopulmonary, astragelosis, and allergic fungal rhinosinusitis. Rarely do they present as, maybe in this instance, as hypersensitivity pneumonitis, and that really would be something that's high semi differential right now in this individual. And so
you think about, like, exposures. So sometimes, like, occupational exposure that can cause these kinds of hypersensitivity and pneumonitis symptoms. And so we do try to figure out exactly how much exposure that individual is happening is having. Is that exposure continuing? And all those kinds of things does go into, will we take this mold exposure seriously? That's really great. Hey. I think you bring up some great points so that we have to think about this. It puts it at
the forefront of our mind. That being said, most of the time, these things are mild exposures, and there might be something else going on, so we don't just hone in on that. And then I think you also hit the nail ahead of figuring out how significant and real and continuous this exposure is. Is this something the person can get away from? And there are a variety of different ways to do that, including having somebody even go out to a patient's work or home to try to understand what's going on.
So these are things we'll have in the back of our head as we continue to hear more about the patient. So, Kahlil, can you move us forward in case? Tell us a little bit about the patient's exam. Sure. In the EDE, the patient was hemodynamically stable, but his pulse ox was around 91% on room air. His, examination was mainly notable for crackles in the right upper and lower lung fields as well as in the left upper lung fields.
So, Christina, can you tell us how this exam would influence your thinking? Sure. Thanks so much, Khalil. I think here, it's really important, the pulse ox that you mentioned as well as the physical exam findings. So I'd like to go ahead and first talk about the ninety one percent on room air. Right? This is atypical for a 28 year old at rest, Something that I would consider to be abnormal and would really probably have our head head scratching. Something's going on
here. I think we'll definitely wanna get a gas, and this would be a patient who's has, be I would be concerned about having exertional hypoxemia. So if we were able to get an ambulatory sat on him, this would be a patient that I would definitely consider that in. But really starting to think about with this 91% on room air honing in on the diagnosis and the etiologies of hypoxemia. So I think with that adding to that are is a physical exam
finding. So you said there's crackles scattered throughout. And while we say sometimes you can say dry versus wet crackles, the physical exam, I think, is somewhat not the best at distinguishing between those two etiologies. Well, I think using our exam, knowing an abnormality, trying to figure out what diagnostic test would be appropriate to order and what we anticipate
to show on that diagnostic test. But I think when we're really saying, like, we we feel like we hear a wet crackle, I tend to correlate that with more of an alveolar filling process, whereas I hear, like, dry or fine crackles or even, like, the Velcro crackles, sometimes that's commonly used for terminology, I would correlate that more with a pringable process. So I think either one is definitely concerning in this patient and lines up with the
relative hypoxemia that we're seeing. And I think to think about because you think as we're seeing someone very early on in the course, there's gonna be a lot of tests that are ordered, but this is a patient, and when I work with trainees, would really like to say, based off our physical exam and based off the current diagnostic testing that we have, like, what do we anticipate we're going to find on x diagnostic test? As opposed to say, let's wait to see what the
CT shows. It's based off this. I think the CT show is going to show either alveolar filling process here. I if we were to get PFTs on this patient who has a pulse ox at 91% on room air at rest, we'd probably be concerned that there's some diffusion capacity, so probably an impairment in DLCO. So just another way to start to frame what diagnostic test we wanna select and what we anticipate to see based off the limited but great data that you've presented so far.
And I'm sure this patient did have some additional workup done. So, Khalil, any did the patient get a an ABG in any other labs that you wanna share at this time? Yeah. Of course. So the patient the labs were ordered, including a CBC with DIF and a complete metabolic profile. TMP and the CBC was with were with the normal limits, but an ABG on Lumiere was mainly notable for a pH of 7.38, a p c o two of 34, a p o two of 55, and a bicarbonate level on the metabolic profile that was of 20.
Thanks, Khalil. This is super helpful. As Christina was mentioning, we are thinking about etiologies of hypoxemia now interestingly because he's not hypoxemic by standard criteria, but I think we all know that twenty one percent ninety one percent for a 28 year old in room air would be abnormal. And this gives us that same indication. The PO two is 55. It lines up pretty nicely with us. And so my first sort of step on this is if you have a patient, they have shortness of breath, is
to calculate an AA gradient. And this is a perfect patient to do that in. They're not that sick where a lot of the factors are gonna be changing in the AA gradient. They're on room air, and they're a young patient where we have good expected normal values. And I think all of everyone will reach back and remember their equation, but f I o two times atmospheric pressure minus water pressure, which in our standard, we can simplify down to one fifty minus p c o two over 0.8.
That is giving us our sort of metabolic ratio and profile. And that gives us an estimation of their alveolar oxygen content. And then we're subtracting from that, our p a o two. And for this patient, we get a gradient of 50, which is certainly well above the normal expected for someone who's this age, which would be in the 10 to 20 range. And so now we have hypoxemia. We have hypoxemia at rest. And so we could do other things like giving oxygen, trying to see
how that changes. But we are really starting to worry here now about a BQ mismatch or sort of shunt situation. DLCO obviously can do this as well, but it very unusual for a 28 year old to have relative hypoxemia and the elevated gradient at rest, just from DLCO. We'd really think about exertion as driving that. And then because you gave us a metabolic profile, we can also think about the acid base status. We see in this that there's a little bit of a metabolic
acidosis with some respiratory compensation. So that's just something for us to think about as we're gonna keep approaching this patient. So now our our differential that had started as that dry cough, then maybe dry cough or dyspnea, is now a little bit more focused on hypoxemia and crackles. And so we can assume that we're gonna explain those other findings by explaining this one and kinda move forward the case from that.
So based on the abnormal exam, based on that abnormal gas exchange, I'm sure that this patient is going to get some imaging. So we will post all the images from this case so everybody can follow along and review. But, Cleo, maybe you can walk us through the imaging studies. Yeah. They did a chest x-ray on this patient in the ED, which showed patchy bilateral infiltrates without any specific regional or lower predilection.
There were no associated mediastinal abnormalities or any pleural effusions. So these opacities seem not to be interstitial, but seem to be to represent actually airspace disease. The list of differential diagnosis that the EDI attendings were thinking of seems to be broad, but at least we can narrow it down to alveolar processes rather than interstitial ones.
Among the more common alveolar etologies is pneumonia, might be multifocal in this case, but can also include aspiration, tuberculosis, sarcoidosis, certain types of cancers, either primary, pulmonary, or metastatic disease to the lung. So, again, we have various differentials that we might be thinking of in front of this clinical case. Thanks, Kaleo. And I think those are really great differentials
to think about. Right? And probably an exercise that you could do is list the differentials, and then as you get more aliquots of information, you can move those differentials up and down based off the data and kind of the pretest probability. So I agree. I think that the differential for this patient is still broad. We're still keeping in mind this potential mold exposure.
And probably some of these that you said, an ammonia process, if this has been more of a subacute three month process going on, like, I that can't completely rule that out, but would probably start to put some rearrange those in certain instances just to to see. So I would probably move infectious down lower on my list of differentials. But great ones great differentials that that we have so far. And love for you to tell us and walk us through what happened next for this patient.
As you mentioned, infectious etiologies of the presentation might be less probable, but the ED physicians mainly addressed it as a possible multifocal community acquired pneumonia. And since the patient has a good social support, mainly his mother at home, he was discharged on empiric antibiotics with an outpatient pulmonary clinic follow-up in a week. However, the patient presented to the ED five days later with worsening symptoms and with a cough that has now a blood tinged sputum.
Thanks so much, Cliff, for taking this through. Yeah. I think that that your explanation is really right that maybe we have some signs of not being quite sure of infection. That being said, we do this all the time. Like, if common things being common, we have to still consider it, and the low risk of an antibiotic course plays in. But this is an important thing that comes up as what are we calling community acquired pneumonia? What when are we starting to put on our hat to think about some
other things? Seems like he still has something lingering, could have some superimposed infection at this point. But, Sabia, I was hoping you could walk us through CAP. We see and we treat really often, but there's always this range of certainty. Sometimes it's super obvious, and sometimes it's a little subtle. And just hoping you can talk us through how you think about this diagnosis and what do you think about it relative to this case?
Yeah. Thanks so much. Yeah. I think that Kalia was really right on in terms of you know, in fact, your CDology seems a little bit less likely, but I mean, being in the ER with all these patients that come through, I don't blame them for saying, okay. Maybe you have something superimposed right now. Let's make sure we take care of this,
and then we'll see. But most of the time when you're talking about, like, a community acquired pneumonia, we really, you have to have a constellation of symptoms like fevers, along with the shortness of breath, maybe having x-ray findings as so as, like, an alobar consolidation. Although you can have these alveolar kind of infiltrates that can give you this picture of multifocal pneumonia. Atypical pneumonia is all those kinds of things, and there's ground glass opacities that can happen.
And then oftentimes, you give them antibiotics, and then the pneumonia resolves. In this instance, it didn't seem that's what happened is this person comes back to the emergency room with ongoing symptoms. And in patients who have who are immunocompromised, it's really important to give them antibiotics. And I don't know how much of this he does have, like, an IgA kind of nephropathy. Does this make him somewhat much more symptom much more likely to have atypical kind of presentation?
And so something to think about in this instance. Totally. And I I think the the we talked a lot about the diagnostic process. I like to kinda show flow diagrams, but then also say the flow diagrams are still just a probability. Right? And you always have to factor in the prevalence in the population. But then we sometimes don't always do the same really rigorous thought process, the treatment process.
And so it may just be worth having some treatment to take a question off the table, especially if that treatment is low risk tolerated short in duration. And as you say, when you see sort of these types of cases in the emergency department, I think with an infiltrate on imaging and some hypoxemia is maybe the better part of valor to even try to treat it and see what happens. And then take your next steps from there. Yeah. And especially because he's, like, relatively young.
So you're you're like, sweating your eyes. I think that if he was older, it will be a very different kind of process. Yeah. Or immunocompromised, like you indicated. Yeah. It might change things a little bit as well. Yeah. Totally agree. So, Kahlil, when this patient came back then with worsening symptoms, right, I think this, as I maybe talked about earlier, alluded to, just you have the ability to reassess and renew your diagnostic differential in the diagnostic process.
So I'd love for you to walk us through what happened next and what were the initial thoughts on his representation. Yeah. They reassessed the patient in the ED, and they repeated an x-ray. It showed a similar appearance to the one done on the first presentation a couple of days prior.
And for to advance in the diagnostic process, a CT scan of the chest was done, which showed diffuse ground glass opacities with, again, no specific location predilection, no consolidation, no mediastinal or hyaloid lymphadenopathy, and there was no pleural disease. Great. And I think I think the CT scan is definitely helpful and indicated in here. And and I'd love and I know in a minute you'll talk us through a little bit more of
the diagnostic reasoning. But before this, I wanted to just resummarize the case because I think this is gonna be a case that you will continue to see throughout the remainder of your fellowship and probably a case that a lot of our listeners today have had the opportunity to treat and work up as well. But just to briefly summarize, young man with a past medical history notable for Asperger's and social history notable for mold exposure,
who's presenting with chronic worse who sorry. Who's presenting with a chronic worsening cough and dyspnea, now progressing to small volume hemoptysis, who's found to have relative hypoxemia on room air with an elevate with an elevated AA gradient and scattered GGO nodules on CT scan. So, Kahlil, could you share with our listeners how you would approach this diagnostically?
Thank you, Christina, for the summary. So at this point, our diagnostic process will be based on the findings of the CAT scan and the temporality of the symptoms. Having ground glass opacities means that the process is most likely to be alveolar. Again, differentials remain broad, but the underlying cause seems to be a subacute one that tends to be chronic. Infectious etiologies are less likely in front of this alveolitis.
And in the setting of exposure to black mold, hypersensitivity pneumonitis like doctor Sabia, doctor Hassan actually mentioned, was high on offered on our different differential. At this point, blood and sputum cultures returned negative, and we decided to proceed with the diagnostic bronchoscopy and the BAL. We performed the BD bronchoscopy, and the fluid that came back was turbid, and cell count was about 9,000, predominantly neutrophilic.
Later on, AFB, respiratory, and fungal cultures came back negative. We also performed a hypersensitivity pneumonitis panel that came back positive for high titers of antibodies against, and be patient with me over here, Oreobacidium pululans, which is a fungus frequently found in black mold. Patient. That was perfect. I'm glad I don't have to try to pronounce that. But this is great. I love the way
that you're approaching this case. We seem to have a patient that had a few things that could be pointing towards hypersensitivity pneumonitis, and so we're gonna be aggressive in that workup. And so I think sending the lab panel to adjust our pretest probability is gonna be really helpful. I also think, like, a bronchoscopy at this point just makes a lot of sense. Right? Patients come back, failed one course of antibiotics, gram last opacity, small volume hemoptysis.
You could think about trying to do other empiric treatments, but we just have to know what's going on. And bronchoscopy with cell count, interestingly, is part of getting cultures really helpful for ruling out infections and especially helps us with atypical infections. Like, we're gonna set it AFP. We're gonna have a broader respiratory panel. But, cell count itself can be in the workup of some of our interstitial lung diseases and our hypersensitivity
pneumonitis as well. Okay. So this patient now, we have a bunch of things that are pointing towards hypersensitivity. We have a presentation that's consistent, subacute to chronic, progressive, cough, and hypoxemia. We have ground glass opacities on the CAT scan, and we'll post it for you all to see, but with features that may think of make us think about hypersensitivity and pneumonitis. To say some of these explicitly, I think we'll talk about it, but there are different
patterns we can see. We can see more upper lobe distributions and hypersensitivity pneumonitis. We can see more air trapping and things like that in association with our ground load, our GGOs. We also have a known mold exposure by history, and this is now also confirmed based on an antibody profile. So obviously this is raising it really high. There are some things that are not quite classic. The B a L B and PMN predominant is not what we classically read about.
We really think about lymphocyte predominant in the, in the HP process. So we'll just take those things into consideration. So clearly you are taking care of this patient, your fellow, I'm sure, very industrious about reading about all of these possibilities. So can you tell us a little bit more about the diagnosis of HP and how one comes to that diagnosis? Sure. Let me start first with a quick definition.
Hypersensitivity pneumonitis is a complex ILD caused by exposure to an inhaled antigen with many phases, extending from self limiting disease to relapsing or progressive inflammatory disease to chronic fibrotic disease resembling IPF. We categorize patients now as having nonfibrotic or fibrotic HP. We used to say that patients might be having acute versus subacute versus chronic HP, but we were forgetting about this definition.
And the high resolution CT scan of the chest plays a key role here in the diagnostic process. Early disease manifests with ground glass nodules distributed across all lung zones. This inflammation leads to small airway narrowing, causing lobular air trapping. Sometimes this process might create what we call a three density pattern, which is a combination of normal appearing globules, ground class opacities, and globules of decreased density and vessel size.
And this CT pattern is highly specific to HP. Later in the process, signs of fibrosis might appear, combining reticular abnormalities, traction bronchiectasis, loss of lobular volume, and honeycombing. PFTs, if performed, would show a restrictive pattern, and the BAL is usually done on these patients. Cell count would show high WBC count like you mentioned, Dave, but differential might be mixed.
It might be neutrophilic or lymphocytic predominant and tends to be lymphocytic predominant actually in later stages. Other work of that what we might be doing is specific serum IgG tests that can be valuable to pursue suspicious exposures or point toward an as yet undetected exposure. But there is a lack of well defined predicted values for specific IgGs, and the tests cannot really differentiate between sensitization and disease.
So it is mainly a combination of suggestive history and exposures, imaging features, and some labs that would lead us toward a diagnosis of HP. Thanks so much, Khalil. That was just a great summary of what learners should expect when they're thinking about this in imaging and history findings that are so important. And I think such a great teaching pearl that you also included was really this new terminology used to classify hypersensitivity pneumonitis, which is now nonfibrotic or fibrotic.
So glad that you brought that up. And for you in training and for others listening today, can I can now have that framework as well? So coming wanna come back to our case, though. So did you feel that at this point that this was a a concrete diagnosis? Were you a % confident on it? Or were there any other diagnostics that you and or the team felt needed to be pursued? Mhmm. So there was still an uncertainty regarding the diagnosis of HB in this case.
We opted then to pursue a long biopsy via VATS, and a sampling of the middle and right lower lobes showed small airways with mild chronic inflammation of the epithelium and submucosa, occasional entraepithelial eosinophils and neutrophils, mild smooth muscle hypertrophy, and mild submucosal fibrosis. Also, on the pathology, there were several poorly formed non necrotizing granulomas and occasional giant multinucleated cells adjacent to the small airways, as well as in the interstitium.
Thanks, Cleo. And I'm sure, in this case, right, I think the decision to do some of these more advanced diagnostics, right, the bronchoscopy, the vats, probably having a multidisciplinary team, a lot of people probably thinking about what makes sense for this patient. So thank you thank you for sharing that, and thank you for sharing the the pathology as well. I and I think that this
is gonna be important for trainees. I feel like some of this is gonna be it's kinda like board questions that you're writing for yourself, Khalil, in the future and for those listening. But there are a number of things on the biopsy that make the diagnosis of HP more likely. A couple things that you mentioned, right, the small airway diseases with some air trapping on a background of mild chronic
inflammation is really gets my attention. There's also some non nepotizing, as you said, poorly formed granulomas, some giant cells, and mononuclear infiltrates. And there are multiple pulmonary diseases that can have granulomas, though, so it is important for us to think about what process is here, which other disease manifestations that we can eliminate, and those that are gonna still remain at the high highest on our differential.
So, Sabija, I'm wondering if you can share with us how you think about granulomas on a lung biopsy. Yeah. Thanks so much, Christina. Granulomas is sometimes the bane of our existence, but we actually often get CAT scans that have these tiny little nodules that come back as granulomas. What does it mean? And so I think this is a great case to go through some of that, as most granulomas are caused by infectious etiologies, either fungal or mycobacterium.
And remember when you do have granulomas that you do have to make sure that those are ruled out. So you have to make sure that those stains are done, the AFB stains, and then fungal skin stains are done, and those are negative, and that you're watching out for those cultures, which may take time. So it may take six weeks until those cultures have come back to definitively say that this is a noninfectious etiology.
And so you have your infectious, as I said, your mycobacterium as well as your fungal, then then you have your noninfectious etiologies of granulomatous diseases such as Wegenerous, granulomatosis, the hypersensitivity pneumonitis that we're entertaining in this instance, hot tub, lung disease, as well as aspiration pneumonia. Sarcoid is also something that we look at.
Remember, sarcoidosis is a disease of exclusion, meaning that you have to exclude every other ideology before you say this person has sarcoid. Now one of the things that you guys were talking about was like this, how do the granulomas look like? Are they tight? Are they loose? What's going on? And that really does help you differentiate between different ideologies.
So when you're having, like, loosely formed granulomas in the background where you're having these inflammatory infectious inflammatory processes, you're gonna think more along the lines of hypersensitivity pneumonitis. Whereas if you're having really nice tight granulomas, then you're thinking more along the lines of sarcoid as something as the ideology of your patients underlying lung disease.
So remember that hypersensitivity pneumonitis has this triad of findings that we all have been going through a little bit of. These poorly formed granulomas, and you're having this inflammatory and then also multilucleated giant cells as part of your pathological findings. Thank you for walking through that for us. I think this is as you said, sometimes granulomas or biopsy results can be confusing for
us. And and the presence of granuloma is great because we have something we have to act upon, but it can be difficult at times to to delve through. And so it's really helpful to have a framework. As you indicated with this sort of triad for HP, the pathologist can often say this is very likely to be HP, but that's not always the case. We often think of biopsy and pathology as the goldest of gold
standards in medicine, and it definitely is. I'm not I think it's always so helpful to have the information. But often the pathologist can just tell you what they see, and that doesn't always tell you what the diagnosis is. Like you said, no pathologist is going to write this is sarcoid based on this biopsy, but if they have these non necrotizing granulomas and big mediastinal lymphadenopathy and they're the right demographic and everything else has been ruled out, we know that helps
make us a diagnosis. So it's really helpful to look at slides, read through reports, and then think about how we integrate that knowledge into making a final diagnosis for our patient. So with all of that and our high pretest probability by the time of biopsy and then our consistent biopsy results, seems like we have a good solid diagnosis of HP for
this patient. We are gonna do a whole episode on the treatment of HP coming up, so I don't wanna dive too much into it, but I do wanna hear a little bit about and the wrap up of our case. So, Kahlil, can you tell us about the basic tenants of treatment for HP and how this patient was treated and responded? Sure. The mainstay of treatment is antigen avoidance and removal of the offending agents. Steroid therapy is debatable in the management of HP, but has been used in severe cases.
Here, the patient switched apartments, so supposedly, he's no longer exposed to mold. And we also started him on prednisone forty milligram every day for a month with a slow taper over the next six months. Patient improved symptomatically, and the HS x-ray done six months after we first saw him showed resolution of the previously described infiltrates. That's awesome. Delgrad, he responded. And I cannot
stress enough the importance of antigen avoidance. This is not always possible, but it's very difficult to treat a patient if they can't change their exposure at all, even with medications, just because they already have this underlying and then continuous process going on. This is a really amazing case. We're very excited we got to do another fellow's case files, and we thank you guys both for
being here. We love building this network and getting to know trainees and program directors across the country, and we're excited to induct Rutgers University and Robert Wood Johnson Medical Center into that network. And so we'd love for each of you just to highlight what you love about being there, but about your education and about the program, and we're all ears. So, Kilo, why don't we start with you? So what I really like about my training here at Rutgers Robert Wood Johnson Medical School
is the supervised autonomy that I get. Also, we do encounter a lot of complex cases inside the ICU that we have to manage. Even if we have to manage them autonomously inside the ICU, as well as the diversity of cases that we encounter in the pulmonary clinic. Yeah. We're seeing the best of both worlds, if I would say, in the outpatient clopidmonary clinic and the inpatient ICU setting. That's great. That's wonderful. Flavia, anything to add? Yeah. Echo what Khalil was saying. It's really
fun being at Rutgers. I know we're, like, between New York City and and Philadelphia, so we get a lot of diverse cases here. And it's really fun to teach in this environment, and Rutgers seems like it's, like, taking over the entire state. So I think that in that kind of environment, we get a lot of very diverse case case loads. We actually recently had the the Mexican consulate next door, so we're getting a lot of it was from throughout the world, like this hot bodge of individuals.
So we get a lot of different disease processes. Wow. That's really interesting. Yeah. The people in New Jersey, thank you for their extensive network that's being built. I'm sure. I know. That sounds fantastic. Sounds like a, yeah, training program with really diverse patient care, fantastic education, and what seems like a really supportive environment. So glad to have you on. And for those listening today, think of this as a potential future fellowship home for you.
And as we end our case today, I know we like to wrap up each case with a takeaway point. I think mine today is I'm just gonna say relisten to Khalil talk about and define HP, but I really like to get how you mentioned we're moving towards this fibrotic, non fibrotic characterization of hypersensitivity pneumonitis. And I think you also mentioned the triple density sign, which can sometimes be seen with with HP.
So just making sure learners remember that and can their diagnosis and, clinical reasoning when looking at a patient together. Farf, what about you? Yeah. Yeah. I think we have a radiology rounds on the triple density side. We'll repost it so people can take a look.
I'll build on that. I think Khalil mentioned something that's really helpful to consider is that there's this acute to chronic, non fibrotic to fibrotic spectrum of HP, and some of the classic features we think about are really more in that chronic HP populations. That BAL lymphocytic predominant is a lot from the ILD literature, maybe a more chronic population, maybe some more fibrosis, but can have a neutrophil predominance early on
in disease probably like this patient did. So I'll take that teaching point away. Awesome. Kaleel, what about you? My teaching point is that high resolution CT scan remains the initial standard to diagnose HP like you guys highlighted prior. And we now use less lung biopsy to establish the diagnosis of HP. Great. And, Sabia? I think and I I'd bring it back to the very beginning. I think that a very good his history. I always tell my
fellows, like, concentrate on the history. The patient will give you his diagnosis or her diagnosis. So I think that this idea that he had ongoing symptoms, the fact that they had the mold exposure, that hypersensitivity in humanitis just in the very beginning would have been higher higher in my differential. And I think we don't emphasize it enough, like, really hone down, get exposure history, be really meticulous about those kinds of things is really important in taking care of your patients.
Yeah. Absolutely. Yeah. If patient told you what he had right away, I have black mold in my apartment. I love that. All right. Thank you both so much for joining us. We love doing these episodes. Thank you all for listening in. Make sure that you like and review wherever you're listening to your podcast and tune in two weeks for our next episode. This episode was written, produced, edited by myself and Christina Montemayor and music's original music by Eric Rogers. And we'll see you next time.
See you next time. Thank you. Thanks.