Well, good morning, everybody. Thank you all for coming, for breathing uneasy airway infections. We have some, actually some very interesting talks that are going to be happening. So, very excited. My name is Casey Cable. I'm from VCU Health. My name is Subani Chandra. I'm from Columbia University in New York City. So, yeah, and we, so we're going to be giving the, we're going to give the title of the talks, and then ask each speaker to come up, introduce yourself, tell us where you're from, and it's going to be about eight minutes each with a couple minutes in between for switching up, and we're hoping for a question, one to two questions after each talk. So, if you guys have something, please, we would encourage that if you could come to the microphone so everyone can hear it, which would be, which would be amazing. I think that's about it. Yeah, we'll go in the order that this is listed. I have no idea how they picked that order, but it seems to serve our purpose, and sometimes it's tempting once you're done presenting to sort of go leave to the many things that you want to do, but it's really helpful to stay, listen, support. So, please try to do that as much as you can, understanding that you all have many responsibilities, but we are, it's a tight timeline, so I think we should get started. Yeah, let's go on, yeah, and please, this should be fun, fun, and easy. So, let's start with Lungs, Warts, and All. Keisha Porter for Current Policy. Good morning, everyone. Aloha. My name is Keisha Mahmood from Vardy Valley Medical Center, Midwestern University Entitlements in the Residency Program. All right. Oh, sorry. I have no disclosures. Okay. The objectives. We are going to see how our current pulmonary papillomatosis has a subclinical presentation. Appropriate intervention needs to be selected to prevent distance spread, and it carries certain risk, unquantifiable, but still definitive risk of malignant transformation. Pulmonary papillomatosis is a rare clinical entity with an obscure clinical presentation and a possible risk of malignant transformation. So this is a report of a 68-year-old gentleman who was referred to the pulmonary clinic because of chronic cough and shortness of breath. He presented the ENT with presumably secondary allergic rhinosinusitis, given the fact that he has been having that problem for the past 20 years. The vital signs were completely unremarkable at the presentation. Please ignore that heart rate of 53 for the purpose of this presentation. That is normal. Physical examination. Chest gut air entry, bilaterally vesicular breath sounds, nothing at all in the chest. So when he presented the ENT clinic with the chief complaint of cough and exertion of dyspnea, it was thought this was actually exacerbation of his allergic rhinosinusitis. Inhalers were tried, and other conservative management. Of course, don't ask a barber if you need a haircut. You see an ENT, you have some shortness of breath, he'll think this way. Symptoms persisted. Chest excrement obtained, which showed a diffuse paranormal density in the right middle lobe. This actually prompted the ENT to suspect something sinister is going on. So he obtained a chest CT and sent him to the pulmonary clinic. CT came back, it showed an opacification in the right middle lobe with some proximal tracheal extension. Initially, this was a, hmm, what is this? Is this some mucous debris? Possible. But hey, let's take a deeper look. MRI was obtained, which showed a significant abnormal enhancement of soft tissue in the upper infrascriptic area. PFTs, just a mild illustrative picture. The patient went on to have a bronchoscopy, which showed a friable white pinkish tissue in the bronchus intermedius, extending to the trachea. Biopsies were obtained, which showed a high-rate focal dysplasia, positive for HPV6 and 11. The patient was treated with a repeated cycle of bronchoscopy, which is now electrocuting an intra-additional cytoplasia. These are the pictures. I think this is the bronchus intermedius lesion. This is the partially obstructed tracheal lesion. I did not include the histological slides because of time constraints. So, a quick recap. HPV is a DNA virus with more than 200 serotypes. However, 6 and 11 express affinity for mucosal surfaces. Virus initially infect the basal layer of epithelium, actually the keratinocyte, and after doing that, it activates the EGFR pathway, encouraging a lot of proliferation. While concurrently, the proteins secreted by the virus, such as E6 and E7, deactivates the retinoblastoma and the P53 tumor suppressor genes. It has a bimodal representation. We have the numbers here. In adults, most of the lesions affect the vocal cord. This has spread down to the tracheo-bronchial tree across in, like, 2 to 5% by literature review, with an estimated subset of 1% going on to develop frank pulmonary parenchymal affectation. Initially, this disease was thought to be spread by sexually transmitted, but however, we are now coming to understand it's actually the activation of latent focus. That's actually what informed the topic, long words and all. Risk factors for distal spread include viral particle contamination during instrumentation. Hence, you need to select appropriate intervention. Initially, a couple of people were advocating use of laser, but laser has been actually shown to encourage spread. Some of the clinical features of this disease you see are harshness, wheezing, which our patient had, dyspnea, and hemoptysis. Of course, you need CT and bronchoscopy for definitive diagnosis. The treatment is micro-debriding and the interrelation to Sidofovir. While Sidofovir was tried on animal models, it shows a dose-response relationship. However, in human models, no. No such luck. With micro-debridement, you cannot actually get rid of all the HPV because this keeps recurring. It's a gift that keeps on giving. In conclusion, this is a rare disease with a subtle clinical presentation and non-specific features that requires multiple intervention and monitoring for possible monogamous transformation. Thank you. Questions? Nice case. Do we have any questions from the audience? It's a quiet group. Oh, yes, please. Can you speak into the microphone? I think it is being recorded. Thank you. Just curious about the follow-up. Did this recur or we haven't gotten there yet? No. It keeps recurring, actually. After every six weeks, this patient has six to 12 weeks, he gets repeated broncs and debridement with additional Sidofovir. Thank you. Great question. That was my question. Did they have any HPV anywhere else on their body, and did they have immunosuppression or anything like that? I didn't quite get the question. Did you find that they had any HPV lesions elsewhere on the body? And did they have any history of immunosuppression? Sorry, two questions. No. The patient has no history of immunosuppression and no other lesions in the body. Interesting. So for, like, CT diagnosis, is it a CT chest that's the best choice of imaging? Because it was interesting in your case that it didn't, like, show up in the CT, and you had to end up pursuing an MRI to get the diagnosis. Yes. So CT chest, as the first step, it did show. But one of the radiological, but you know how sometimes when you look at images in CT, especially chest CT, if you don't do a high-res, you look at it. There's always this margin where one can, is it this or that? So to actually reach a definitive diagnosis, I would agree with you. The MRI could have been an overkill. But we did obtain it, which actually gave us quite a definitive picture of what we're dealing with. Thanks. Awesome. Great questions. Thank you all. Okay. Interesting case. Thank you. Up next is going to be… Oh, you can introduce yourself. Hey, guys. My name's Sivantur. I'm a third-year resident at Corwell Health West in Grand Rapids, Michigan. I'm getting up for I.T. help as though I'm generally not the I.T. help. So, I think it's like, you need to move it down to the bottom. Oh, the bottom right. Oh, is that what it is? Oh, I apologize. There we go. It's just hiding. Oh, there it is. Perfect. Okay. Can we duplicate it, can we do that? Let me stop your time. You won't have your notes. Oh, I don't need it. Is everybody okay with that, if you don't have presenter view on that? I mean, it might just be this presentation. Because you said the last one worked out, right? Interesting case and interesting IT. Alright, well, I appreciate everyone's patience. It's just an interesting session. Alright, well, again, I'm Saban, I'm a third-year resident at Corwell Health West in Grand Rapids, Michigan. It's a case of endobronchial histoplasmosis. I also worked on it with two attending physicians, Dr. Bilal Bangish and then Dr. Gustavo Cumbo. And we all have no disclosures. So, just getting to the patient case, it's a 34-year-old female that presented to our PCP. She was complaining at the time about having a one-month history of nonproductive cough and fatigue. And she also was experiencing a 20-pound weight loss over the last four months. Some pertinent past medical history is that she had polycystic ovarian syndrome and then she also had hypertension. So, upon presentation to our PCP, he had obtained just vitals. Everything was within normal limits as far as her vitals are concerned, pretty unremarkable. And then also her physical exam as well was unremarkable. She started an initial laboratory workup. White blood cell count was within normal limits. He also pursued an autoimmune workup at the time, which ANA was negative and then the rheumatoid factor titers were also within normal limits. Did see that she had some elevated inflammatory markers. So, her CRP was mildly elevated at 20. ESR was mildly elevated at 48. And then he just also threw on a quantifier on just to rule out latent TB given that she had had this cough and then she had the weight loss as well. She did not have hemoptysis or anything like that and didn't have any risk factors, no recent history of travel and no workplace risks either. So, just given that this patient was having pretty much a subacute one-month history of cough and then also had weight loss, he just pursued imaging. So, they started with a chest x-ray, which if you can see right there, it's kind of hard to see, but there's this 3.1 centimeter right upper lobe opacity which is pretty suspicious for a mass. So, then they obtained a follow-up CT scan. In this CT scan now you can see much more clearly that we have this 3.1 centimeter peripheral right upper lobe mass. You can also and you'll be able to see it more on the next CT scan, but there's also some pretty significant mediastinal and right hilar lymphadenopathy as well. So, right here you can see more clearly just the mediastinal lymphadenopathy and then also the right hilar lymphadenopathy. At this time, concern for just this patient having some sort of non-resolving pneumonia, this patient having sarcoidosis with her age, TB kind of still on the differential, but really the main thing people were thinking was that this was some sort of malignancy that this patient was experiencing. So, with the workup, they proceeded with pulmonology at this time, now took over, proceeded with EBUS, with BAL, and right upper lobe endobronchial biopsy. This is just the diagraphic schema of the endobronchial ultrasound with BAL, and also they did transbronchial lymph node biopsy. It was, I believe, 4R11R and, sorry, 4R11R and then 11L were the lymph nodes that were biopsied. And then this is just the picture that you can appreciate of the right upper lobe endobronchial mass that they had appreciated, which they had biopsied. So, going to really the pathology, cytology, and lab workup from this EBUS and this BAL and the endobronchial biopsy that they had obtained, fine needle aspiration of the 4R11R and 11L lymph nodes, they were negative for malignancy, but they did demonstrate necrotizing granulomatous inflammation. There was a BAL of the right upper lobe that had a negative infectious workup, including for fungal organisms at this time. Really, the main kind of diagnosis came once the right upper lobe biopsy came back and that was consistent with necrotizing granulomatous inflammation. And then that also found fungal organisms consistent with histoplasmosis species. This patient had GMS staining, which is essentially the gold standard for how you diagnose histoplasmosis, wanting to see ovoid, essentially fungal species on cytology or pathology, I should say. They had also, ID had gotten involved at this time and they had just done some additional workup. So they had looked at serum and urine antigens. Those were both negative. They had, again, just wanted to be sure for TB. So just to rule it out, they had sent to AFB culture and smear, but they did find that this patient had elevated histoplasmosis antibody titers, kind of consistent at this time right now with a subacute histoplasmosis presentation. And these are just essentially the smears, which, again, you can kind of appreciate that these ovoid fungal species, I'm not a pathologist by any means, but this is what I was told were the histoplasmosis species. So this patient was started on iatroconazole and had some pretty significant improvement in her symptoms, the cough, weight loss, fatigue, all had pretty much improved pretty significantly at this time. At about three months, she did end up having repeat imaging of her, both her chest and her abdomen and pelvis. So there you can appreciate that, this one is hard to see, but the peripheral right upper lobe lesion has decreased in size, and that does lead more towards the diagnosis of endobronchial histoplasmosis. There was a bit of a hiccup, and this is kind of hard to see, but I did point it out right there. There were these hypo-enhancing splenic lesions that this patient had. Really they were more scattered kind of all throughout the spleen francuma, but this in particular kind of threw a bit of a hiccup, because now there was a concern of whether or not this was disseminated histoplasmosis. I.D. was pretty sure that it wasn't, just because this patient was pretty, she was pretty overall hemodynamically stable. She wasn't, you know, certainly as sick as you would expect with disseminated histoplasmosis, and she didn't have any immunosuppression or any risk factors for it, but still, just given that she was having these splenic lesions, there was at least a concern, because she was on nitroconazole at the time, not amfotericin B. And then again, just with the repeat imaging, you can see that she does still have pretty significant mediastinal and right hilar lymphadenopathy that you can appreciate on the CT of her chest. This time, there was still a lingering concern for malignancy in this patient, so they did go ahead and do a PET CT. Again, like I was saying, the differentials at this time were endobronchial histoplasmosis, disseminated histoplasmosis, and lymphoperliferative malignancy. The PET CT scan was really what ended up towards the diagnosis of endobronchial histoplasmosis, because there was hypermetabolism that was really consistent with a histoplasmosis infection. There were no other sites of abnormal hypermetabolism, and there were no splenic lesions appreciated on this PET CT, which that kind of was a bit of a red herring to some degree. So just kind of talking a little bit about endobronchial histoplasmosis results from a calcified lymph node that's perforating the bronchial wall that results in an erosive endobronchial lesion. You see this typically in the right upper lobe, right main stem, and the bronchus intermedius, just given the high concentration of lymph nodes our patient had in the right upper lobe. And then it's frequently mistaken as malignancy. This is what we were thinking the majority of the time with this patient. And it does usually present with hemoptysis. This patient particularly didn't have hemoptysis, but that's usually thought to just being erosion of the bronchial mucosa by the histoplasmosis. And the diagnosis requires tissue biopsy with GMS staining, demonstrating histoplasmosis. Really the take-home message from this presentation is though while endobronchial histoplasmosis is rare, it should remain on the differential diagnosis of obstructing endobronchial lesions even in the absence of hemoptysis. References. Thank you. Questions? Applause Applause Yeah. Was the bronchoscopy repeated after treating histo? No, just the first time they just developed bronchial mucosa. Because she was getting better, you were seeing the lesions getting smaller, so we didn't really see any inclination. And she overall, like I say, she was feeling a little bit better after we started on hydroconzole. Thank you. Hey, I've got a random question. So with the FNA, was that sent for staining at all or would you expect that to have a positive? That one, I believe, was not sent for staining. The biopsy, the mass, that was what was sent for staining. I saw that. Okay. I'm just personally curious if that would have shown something. You wouldn't expect it because it's pretty, I mean, yeah, with that anopathy is usually pretty consistent with histo, but I don't think that was sent. Okay. And just in case. Applause All right, good morning, everyone. I'm Keetana Seeley, and I bring greetings from Delaware. Thankful to CHESS and the organizers for this opportunity for all of us to share our work. Thankful to my co-authors as well. One of our co-residents is also here supporting me, and all of us have no disclosures. We'll talk about how we managed a cricoid abscess, and briefly after that, we'll review its incidence, pathophysiology, and management as well. We had a 31-year-old female who came in with progressive strida, and her symptoms initially began as a sore throat, but an upper respiratory tract infection that never got better. And over two months, she ended up in the ER, unfortunately, with respiratory distress. On exam, she had strida in the neck and a clear chest to auscultation. Important medical history to note here is she's got multiple sclerosis, and she has dysphagia from the MS. Exactly two months ago, she was started on ocrelizumab infusions for her MS. We can all see the X-ray here, a lot of prevertebral edema, and the arrows pointing to the subglottic narrowing of the trachea. Here's a CT neck, which showed complete obstruction at the laryngeal level, and we could also see a small hypodense, you know, circular lesion where the arrow's pointing. In this situation, we did not want to give her any general anesthesia, compromise whatever airway she had, patency that she had left, and the best decision here was to, you know, send her to the OR and have her undergo an awake tracheostomy. Once the airway was stabilized, she underwent a direct laryngoscopy, and the first picture is a small exophytic lesion that was biopsied to show a pyogenic granuloma. The second picture, the arrow points to where the surgeon performed a blind biopsy and a fine needle aspiration that returned purulent bloody fluid. At this point, we weren't sure if it was a mass or if it was an abscess. Honestly, we weren't sure what was going on. Many weeks later, the culture came back positive for Fusobacterium nucleatum, and we also sent a lot of inflammatory workup because she was a young female coming in with a history of autoimmune disease, which is MS, and she also had type 1 DM, but we wanted to rule out more inflammatory causes or any vasculitis that could have contributed to subglottic stenosis and laryngeal infections. Pathology was also benign, so we knew that this wasn't cancer, and even her clinical presentation was unlikely to be cancer because it all developed over a span of two months. We treated her with a four-week course of amoxicillin and clavulinate, and a post-treatment direct laryngoscopy showed complete resolution of the disease. She had fantastic vocal cord mobility as well, and she was safely decannulated. So cricoid abscesses, extremely rare, especially nowadays in the post-antibiotic era, and back in the day, yes, tuberculosis, TB, syphilis, or even extension of upper airway infections caused them, but according to our literature review, there was an article that was published in 1931 that reported less than 50 cases, and nowadays in the post-antibiotic era, it's mostly immunocompromised or any history of instrumentation, either intubation or nasogastric tube placements that can predispose patients to cricoid abscesses. Repeated mucosal damage, perichondritis, and poor blood supply could have led to the abscess formation, and in our patient, the MS, the dysphagia, and the immunocompromised was a perfect storm. However, that was definitely not number one on our differentials. Best imaging modality would be a CT NEC with contrast if your patient is stable enough or once you stabilize the airway. Once you perform your non-invasive imaging, you can move on to your invasive imaging, which is a direct laryngoscopy, direct visualization that will help us appreciate the structures, the anatomy, perform biopsies, and aspiration like in our patient. Airway management obviously takes precedence, and the most important thing that we all learned in this case was the coordination between ER, palm crit, ENT, everybody coming to a decision even though time was of the essence. Incision and drainage, systemic antibiotics, like treating any other abscess, and if your patient has long-term complications like vocal cord dysfunction or airway stenosis, treatments are, they range from endoscopic procedures to surgical treatments, and that is too much to talk about in eight minutes. However, she didn't have any complications. She did really well. I'd like to leave you all with three take-home points. Precoated abscesses are extremely rare. However, if your patient is immunocompromised, if your patient had some history of recent instrumentation, keep it on your differentials. Maybe not number one, but if you have no other answers, definitely think about it, and airway management is top priority. We stabilize, and then we can go through our differentials. Last but not the least, prompt treatment can avoid long-term complications. Here are all my references. It was hard because I couldn't find the number as to how many precoated abscesses, but all it said was rare. These are some really good references, guys, and thank you all. I'm happy to take questions. Questions? Did the patient, was she just diagnosed with MS two months prior to this? That's actually a good question. She had relapsing-remitting MS, and long story short, no. She was, she had MS for a long time, and we just couldn't find a good regimen for her. Ultimately, it was acralizumab. Do you know how was she getting these infusions, via which type of line? Oh, I don't know the line, but to my knowledge, it was a petrol IV, and this was once every six months. Okay. That's to the extent of my knowledge. Thank you. You know, it's always interesting and nerve-wracking when you have these critical airways that are so narrow, and you made fantastic points about airway management sort of being primary and not giving this patient general anesthesia, so it would be helpful if you could elaborate a little bit about what are the options, like what are the things for airway management in somebody like this that you were worried about? So, no general anesthesia, because when they lose muscle tone, and they're laying flat, and that little one or two millimeter airway gets compromised. Flexible laryngoscopy is interesting, depending on how deep they can see, because laryngoscopy typically won't go past the vocal cord, and percutaneous tracheostomy, in the OR, tracheostomy. Are there any? I mean, I can't really think. If you don't want to intubate this patient from above, that's probably going to be very difficult. I don't know, Casey, if you can think of other options for airway management in a situation like this. I might not even be able to get a bougie down, so no, I'd be worried. One comment that our otolaryngologist made was, if it's a polyp, or if it's, at least if we know what it is, we could try passing it in a very small, narrow tube. However, the airway trach was the best approach for her. Yeah, I think these are really dicey, because it handles it really, really well. My other quick question was, how often can these be polymicrobial, do you know? Because a lot of, like, neck soft tissue infections sometimes tend to be. Yes. Great. That's a great question. So most of the, so they did a literature review of all the cases that were reported, which were spontaneous laryngeal abscesses, and not an extension of other deep neck abscesses. And most of the time, they were, it varied. There was no strict pattern as to, you know, it's usually orophlora, or it's pseudomonas, et cetera. However, it varied a lot, because the population was all immunocompromised. And back in the day, it was TB, so it was a little bit more consistent. But nowadays, there's no strict pattern. Yeah. Good question. Great. All right. Thank you. Oh, OK. There we go. We're good. Yeah. Awesome. Hi, everyone. Thanks for attending. It's another endobronchial infection. It's this time endobronchial TB, secondary to direct lymph node invasion. My name is Anton Kamel. I'm one of the second-year residents, intern medicine in Brown. And I have nothing to disclose. The objectives for today, I will go through a case presentation about endobronchial TB. We speak about the definition, the pathogenesis, possible complication, and some evidence of possible adjunct therapy. So our case was a 20-year-old male with no previous medical history, who just came with four-week history of fever, chills, and no other symptoms, no weight loss. He wasn't a smoker. He doesn't drink. There was no sexual history. He wasn't active. And there was no family history of cancer or any lung disease. He visited his home country. He was from West Africa, visited a couple of times in the last year. And on exam, he was febrile to 103. Otherwise, he was hemodynamically stable. And the physical exam was only remarkable for some cachexia, but everything else was unremarkable. And for the labs, CRP was 55. Otherwise, he had extensive workup, infectious workup, cultures, viral panels, including COVID, and everything was negative. He had some also autoimmune workup, also was negative. He received also two courses of antibiotic over the four-week period, but also it wasn't helpful. And his chest X-ray initially was unremarkable. So as a case of fever of unknown origin, he was admitted. And he started to have images. And initial CT chest showed, as you can see here, some necrotic mediastinal lymph nodes, subcranial lymph node in the gastrointestinal window, and then chest window and the lung window had multiple nodule of aerospace disease, some ground glass opacities, middle lobe, and the right lower lobe. So he had some sputum. So sputum was collected and sent for AFB smear TB PCR that came positive. And he had indeterminate sensitivity to rifampicin. So as a case of pulmonary TB, he was started on the first line right regimen for two months initially, and then continued on rifampicin and isoniazid for four more months. He had a follow-up sputum sample that were negative for TB, but the patient continued to be symptomatic. He continued to have fever. He started actually to lose weight. And he also started to have more and more productive cough of yellowish to blue sputum. So he had a follow-up in the clinic when CT chest was repeated. And if you can see here, he started to have multiple necrotic other lymph nodes. And the subclinical lymph node that we had showed some. airways or bronchi. As you can see here, actually it looked more necrotic also than the previous one. So he was referred for flexible bronchoscopy and excuse me for the bad quality of the image, but if you can see here they had right and left. like yellowish, grayish, endobronchial lesion or tumor-like lesion. So he had bronchial wash that was sent for TB workup and he had endobronchial biopsies from actually both right and left endobronchial lesions. So the TB-PCR came back positive also for TB and the lesion showed necrotizing granulomatous inflammation. So he was labeled as endobronchial TB case secondary to direct invasion of subcranial TB lymphadenitis. And he was started on a second line anti-TB medication for six more months with improvement in his symptoms and radiological evidence and also a follow-up repeat sputum sample for AB was negative. So if I wanna discuss endobronchial TB, it was defined as it's a tuberculous infection of the trichobronchial tree with both microbial and histopathological evidence. And there are different, so most of the cases that were reported were actually like long time ago before the availability of the anti-TB medications. We don't see that more often now, but the common mechanisms that were suggested is that most likely it can be from direct extension from adjacent parenchyma most of the time. And many cases also were reported from implantation of the organism from the infected sputum that the patient is coughing up his like infected phlegm but will have some TB like implant in the airway causing the endobronchial TB. And some also in disseminated TB, especially you can have just hematogenous dissemination. In some cases also like you can have just endobronchial TB without clear evidence of parenchyma TB. And all of them, the pathological process and all the reported like these three steps. So mainly the procedure starts like from inside out or from invasion of the mucosa, submucosa, causing some ulceration, granulomas or some tuberculosis nodules. But here in our case, it was the opposite. It was from outside going inward and I'll discuss this. So there are different appearance of endobronchial TB and by bronchoscopy. Some of them and most of them can be just like non-specific inflammation with high premia swelling and many cases like showing some just nodular inflammation. Some ulceration can happen, some tumors or fibrostenotic lesions can be seen like in our case. And mainly fibrostenotic lesions are like the next step that can happen if the patient is not treated. As we see here, endobronchial TB can also result from lymph node erosion into the bronchus. If that happened, as in our case, it was reported to be like a grayish yellowish mass, same like what we had in the picture. And for complication of endobronchial TB can cause hemorrhage, granulation, tissue fistula, which were one of the things that we were worried if our patient had, with like patient that would be coughing like the case is material from the lymph node itself up. And in later stages, the patient can have stenosis and airway obstruction. And it was reported that even after starting treatment, if the patient has endobronchial TB, that can worsen with like the healing process causing some fibrosis, getting things worse. Treatment is mainly treatment of TB, but there were some adjunct therapy that were reported before and discussed. Mainly, as I said, the evidence is long time ago, but I looked for some newer evidence. And there were some cases about adjunct corticosteroid therapy, inhaled corticosteroid therapy that was discussed. Some cases reported that it worked, some cases said that it didn't really matter and that were different. So there was one prospective study that actually didn't show, it didn't influence outcome. There were some also cases from Japan that discussed adjunct aerosolized streptomycin and steroids together. They discussed that and they found it worked for ulcerative endobronchial TB, and it led to like a faster healing process. And also they studied that also for a patient with bronchial stenosis, secondary endobronchial TB, and they found that it resulted in a better outcome in regarding the range of stenosis. But that take-home message, and I think the most important thing is that early diagnosis, choosing the correct regimen based on sensitivity if you need, would reduce the complication. There were also some reports of like intraluminar injection of steroids, but also the evidence is still lacking and we don't have much evidence. That's it, thank you. Thank you. Questions? I was wondering if you found anything in your literature review that endobronchial tuberculosis was more likely to be resistant to first-line treatment for TB. That's an interesting question. So nothing much about resistance. Most of the cases were like late start of treatment of TB, but I didn't find that everything. I bring greetings from Abu Dhabi, very close to your place. What is the indication for the second-line drugs in this case? Was he resistant to the first-line anti-tuberculosis medication, number one? Number two, what is the prevalence of endobrongial tuberculosis in this country? You mean in the U.S.? So I've seen this patient outside the U.S., I've seen him in the Middle East. Well, I heard that. My question is, what is the incident? Because the literature says that way back in the year 1943 in West Virginia, 15% of them were diagnosed to have endobrongial tuberculosis on a bronchoscopy, 40% were found at autopsy, that was in 1943, pre-ATD era. I don't know what it is now. Thank you for the question. So for the first question, actually I will start with the second question. So most of the evidence, as I said, was a long time ago, as you were saying, also the prevalence I've seen sometimes approaching, in other countries, approaching 40% even more. That was before 1960. Currently we don't see that more often, and I didn't find current studies, nothing I think in the U.S. that showed any prevalence numbers regarding endobronchial TB. And the first question about the second line, anti-TB. So the sensitivity of Thompson was indeterminate in the beginning, and the patient received initial ripe regimen for two months, and then it continued six months. And then after that, he continued even till 12 months with no response. So at 12 months, it was a multidisciplinary discussion. We thought that maybe it is the resistance of the anti-TB regimen that led to the progression of his TB. Hello everyone, we're going to switch gears a little bit from endobronchial infections to a case of disseminated cryptococcus. I cannot take full credit for this title, my medical student is much more creative than I am and came up with this very interesting title. My name is Rachel Mullins, I am a first year fellow at the University of Mississippi Medical Center and I have no financial disclosures. So today my objectives are to tell you about my case of a patient with disseminated cryptococcus. We're going to discuss the pathogenesis and common presentations and what might could have changed my patient's outcome. So the classic infection of cryptococcus occurs after inhaling of spores of the fungus into the lungs, this classically causes a pneumonitis picture and then depending on the patient's immune status it will either disseminate or resolve. The pulmonary and CNS systems are the most common systems involved with disseminated cryptococcus. Chest radiographic findings are classically pulmonary nodules with immunocompetent hosts and then in immunocompromised hosts we have adenopathy and also larger nodules or masses. And before I go on, the skin findings that I'm going to talk about in this case are an uncommon presentation of disseminated cryptococcus, especially in the outpatient setting. So as far as the... In the emergency department, our sign out from the ER was the patient, you know, came in, was encephalopathic, not protecting his airway, mildly hypoxic, so was intubated. They performed an initial workup that included an HIV antibody antigen that was positive, an elevated creatinine, pretty significant, 4.7 and potassium and 5.7 and lactate 7.3. Because of the encephalopathy, they, of course, obtained imaging of his head, which was unremarkable, and they started IV fluids and broad spectrum antibiotics. They then called us for admission. When we went to evaluate the patient, of course, he couldn't give us any history, so we spoke with his family. They told us that about four months ago, he was referred to The dermatology office thought that maybe the differential would include molluscum, conigiosum, prurigo, nodularis, and monocupox. The biopsy that was obtained at the clinic was obtained about a month after his initial presentation to that clinic. Our workup on admission included respiratory cultures and a lumbar puncture. Because of his HIV status, obviously we were very concerned about immunocompromised hosts and opportunistic infection. We didn't have the information about the biopsy results from the dermatologist until a few days later. So the opening pressure on the LP was elevated to 28. Respiratory cultures, of course, showed the cryptococcus neophormans. We started him on amphotericin therapy. So, we perform serial lumbar puncture. but you can see bilaterally. in a compromised state with multiple infections. vasopressor requirements and ventilator requirements. if you don't know differently even if you don't think that they have obvious risk factors. You know we discussed that the common systems that are involved or What questions do you guys have? Was the MSSA, and then I think there was a bunch of other infections, was that all kind of nosocomial in nature, where it was like after it was already? It was. Yes, yes. He was hospitalized for about two and a half to three weeks. All of that happened after the fact, probably seven to 10 days in. The initial problem was the disseminated crypto and the prolonged hospitalization. I see, as you all know, we get all sorts of other infections, especially in immunocompromised patients. That happened later. After you've known that he was HIV positive, did we start the antiretroviral? That's a great question. That was a long discussion with our infection disease doctors. The consensus was to try to get a hold on the infection initially with the amphotericin B, amplicitazine. I think we did start antiviral therapy, I think it was towards the end of the first week. Any other questions? Good question. Yes. Okay, thank you guys. Thank you. All right, well, good morning, everyone. My name is Hassan. I'm a third year in telemedicine at UT San Antonio, and I'm presenting today a case that I work on with my fellows and my faculty about cryptogenic or cryptococcus neoforminus tracheitis. I think it was good that we discussed the disseminated cryptococcus, and now we're going into more airway cryptococcus. So I have no financial disclosures, and to start, also, I think Rachel already discussed it very well, like the life cycle of cryptococcus. It's usually inhaled by spores, resides in the lung, can present as a focal pneumonitis that can be asymptomatic or depend on the inoculum and the immune status of the patient. It can also present as disseminated, and it can also be multisystemic and involve the nervous system and the pulmonary. Speaking of the pulmonary cryptococcus, it can present as multiple radiographic presentation. I have some pictures here about different manifestations of cryptococcus, and as we can see, it can present as a small nodule. It can also present as a large nodule as well, sometimes like multiple nodules, sometimes like just a focal pneumonia-like picture, and can also be a mixed picture of multiple nodules and focal consolidation, kind of like a focal pneumonia-like picture. But what was interesting about our case is that it's like an endobronchial lesion that is very rarely reported of cryptococcus. So to start about our case, it's a 75-year-old male who has a history of COPD, presented with shortness of breath, wheezing, and he was diagnosed as exacerbation of COPD. But in our review of the system, he mentioned that he was also complaining of an intentional weight loss, fatigue, and also complaining of a headache that's also kind of new for him. So in the ED, he ended up getting a CT chest, which was significant for the way that his trachea looked. As we can see, it's like more thickened and more irregular shape. So by that time, we were discussing how can we approach that, and the decision was to go with a bronchoscopy of that. And I have some pictures here of his bronchoscopy, and as we can see, it's very well erythematous and inflamed and with a lot of flakes-like lesions in the main carina and extending also to the left main bronchus. So what ended up happening is that we got biopsies from these lesions and sampled that, and it turned back positive for Cryptococcus neoformis. These are some pictures of how the pathology could look like, and as we can see, it's usually encapsulated, multiple shape, and as we also can see here, it's usually a narrow base budding, which is characteristic for Cryptococcus neoformis. Because he was complaining of chronic headache, also we wanted to exclude more disseminated or more Cryptococcal meningoencephalitis, we ended up getting an LP that turned back negative for the culture. It showed mildly elevated opening pressure, but with the discussion with our ID team, we decided to start him on fluoconazole for 12 months without induction, and likely follow-up imaging and bronchoscopy showed complete resolution of his lesions, as also the patient was reporting that his symptoms got much better. So a quick discussion about our case is usually endobronchial fungal lesions are rare, and it's mostly occurring in immune-compromised patients, and it's more like with aspergillus cases that I found in the literature review. And as we kind of mentioned and talked about, that radiological presentation can be varied with the pulmonary Cryptococcus, it can present as malignancy-like picture, pneumonia, or also can mimic tuberculosis. So it's important to keep it in our differential for lesions that are not as common, because usually I put here like our differential diagnosis of endobronchial lesions, and it's usually divided as benign lesions and malignant lesions. So it's like mesenchymal, or like soft tissue and bones-related, or it could be malignant in nature. But also keeping the differential with the infectious etiologies is really important, as we saw with the other cases that was presented today. Infection should be in our differential. And here are my references, and thank you everyone for being here. I know it's really hard to stay away from Hawaii and the beach and be here, so thank you for coming. I appreciate it. Thanks so much.

cryptococcal infection

trachea

shortness of breath

wheezing

weight loss

fatigue

headache

fluconazole treatment

endobronchial lesions