All right, we are at the start time, 1045, so even though I don't even know what time it is. I don't know if you feel like me. It feels like it's two in the afternoon or something. So welcome. This is session 4005, clinical mimickers, which I think is, having looked at the cases already, a great collection of things that I think, as clinicians, keep us on our toes and give us a chance to think about some differing presentations of diseases that maybe we've encountered personally. I think it'll be a fun discussion of these cases. We have four folks who will be presenting their cases to us today, and what I would just remind everybody is that all of the sessions, including this one, can be evaluated. If you have the CHESS mobile app, the team here at CHESS, we're always looking for your feedback on the program in general and on the sessions specifically. Just a reminder to each presenter, we are asking all presenters to verbally state their disclosures if present or if not present, you know, for your presentation. I'm also supposed to announce that all rights are reserved. The visual and audio content presented during this meeting is the exclusive property of CHESS. No personal recordings of the content of this meeting are allowed. Take that as you will. And they are going to also open CME claiming, which this session will also qualify for CME. Otherwise, with the kind of more boring stuff out of the way, thanks for being here. My name is Matthew Miles. I'm an associate professor of medicine at Wake Forest School of Medicine in Winston-Salem, North Carolina. I'm really privileged to get to moderate today. I love hearing the cases that have been presented at chest in the past, having been able to moderate several times before. It's always just fun to see the different things that are encountered in our field of practice, and I know that you'll enjoy these sessions as well. Otherwise, I look forward to turning the podium over and giving you all the time to speak. So our first presenter is going to be covering a pressing case of dyspnea. That's Zach Bauer coming to us. I don't have the listing here, but I believe. All righty, so as said, my name is Zach Bauer. I'm a pulmonary critical care fellow at Henry Ford Hospital in Detroit. I have no financial disclosures for this presentation. So I'm gonna be talking about a case in the pulmonary clinic. A 36-year-old woman came to see me without any prior cardiopulmonary history with exertional dyspnea. She was 28 weeks pregnant with a twin pregnancy at the time that she met me. Her symptoms began about two months prior, so about 20 weeks of her pregnancy. Had an associated dry cough that resolved on its own within a day or two, but her exertional symptoms persisted. She described these symptoms as feeling her heart rate go very fast when she's walking, and she had a little fitness band on that said her heart rate would go up to the 140s while walking about 50 to about 100 meters or so, or to the opening of a store, essentially from the parking lot. She had no associated fevers, sputum production, no sweats or weight loss, no wheezing or chest pain or pressure, no bleeding, no muscle aches, and no swelling. She saw her OB about this, and she got two courses of oral antibiotics directed towards CAP without any improvement in her symptoms and noted that actually her symptoms continued to slowly progress over time. Her medical history was significant for pancreatic cancer eight years prior to her presentations, for which her spleen and distal pancreas was removed. It had negative margins, she didn't receive any further therapy for that. She had two prior uncomplicated pregnancies without any issues of dyspnea. She was a never smoker, and she only took prenatal vitamins, including over-the-counters that were none. Her physical exam was mostly unremarkable. She had a gravid abdomen, as would be expected, and she had absent breath sounds over her posterior right lung field. Otherwise, her vitals were all normal, including her resting heart rate and saturations. Investigations of labs of her comprehensive metabolic profile, including a thyroid-stimulating hormone, were all normal. Her CBC was remarkable for a slightly elevated white blood cell count with a neutrophilic predominance. Her hemoglobin was close to eight, which was about 1.5 grams lower than what it was a few months prior. And then her platelet count was elevated to about 700. This is a representative chest X-ray that she had you could see significant findings where the elevation of her right heaving diaphragm was some adjacent airspace disease. And because of her persistent symptoms, she ended up getting CT imaging with IV contrast protocol for a pulmonary embolism study. There was no evidence of a pulmonary embolism, but I'd like to point your attention to the right atrium, which is very small, almost imperceptible here. And you can see on the axial cut, her liver looks a little heterogeneous. For comparison, this image was taken just after her pancreatic cancer was resected. And you can see the difference here. I'll go back between her right atrium on the axial cuts looks much compressed. As far as lung windows, you can see at the right lower lung field that there are some airspace disease, some consolidation. You'll have to trust me as we're not scrolling through, there's no endobronchial lesion seen on these images. So our differential, what was going on, we were mostly concerned about why this woman would have volume loss in her thorax as well as compression of her cardiac structures. And with her heterogeneous liver, we were concerned that that was causing compression of all these structures. There's no evidence of endobronchial obstruction on the CT scan, which made it less likely for us. And while this wouldn't explain those other CT findings, we were also querying whether she had either resistant or non-bacterial pneumonia or some aspiration event, or potentially her anemia was contributing to her dyspnea. So we'll go on to the further studies. We ended up getting an echocardiogram that confirmed their findings of the compression of her right atrium and vena cava, and then also pursued imaging via ultrasound and MRI of her liver that showed multiple liver masses. You can see here, it's bad when a pulmonologist can tell that the liver looks abnormal on imaging, but it definitely does. And unfortunately for her, a biopsy revealed metastatic pancreatic cancer to her liver. Which was a recurrence of her prior disease. So I think important teaching points for here is that by the third month, or the third trimester, up to three-fourths of women will experience dyspnea during their pregnancy, and that's in a normal pregnancy. So it's very difficult sometimes to tease out normal versus pathologic dyspnea. But it's very important because it affects both the mother and the fetus. I'd like to draw your attention to the graphs on the side here. She was about 20 weeks pregnant when her symptoms started. And you can see that cardiac output, stroke volume, and heart rates are all higher in these women. And we kind of postulated that by compression of her right-sided structures, that she likely couldn't increase her preload or stroke volume, and that probably led to her increased heart rate that she was experiencing causing her symptoms. So I'd like to just point out, don't forget about anatomic compression of cardiac or respiratory structures, because it's sometimes not as obvious, and it's easy to overlook. These are my references here. And I'd like to thank Dr. Debian for his assistance during this case presentation. That's all I have, thank you. No, don't leave, don't leave, don't leave. There's gonna be tons of questions. There's gonna be tons of questions. Okay, what questions, comments are there for Zach seeing a case like this? How did the patient do when they had to do this for her own health? She ended up getting chemotherapy. She did deliver her babies. I didn't look up how they did, because I'm not sure how that covers HIPAA and whatnot. But unfortunately she had multiple complications and she didn't. and respond to the chemotherapy like they expected. She's still alive, but dealing with multiple issues, essentially, yeah. Thank you, great, great question. I see what you did now with the title of the thing. Yeah. Oppressing Case of Dyspnea. You did it. Yeah. They didn't call that out. It's interesting that a mass. at this point in her pregnancy? She did, yes. And it was not commented on. I had spoken with her OB, and they had no idea about this. Yeah. Yeah, I mean, certainly a little higher than maybe they would be focused on. I would presume so, yeah. Yeah. All right, great. Well, thank you so much for your talk. Yeah, of course. Thank you. Thank you for your talk. OK. Our next presenter will be Katerina Bianova. And I'll go ahead and get her slides pulled up here. My name is Katarina Bianova, and I just graduated fellowship, so I'm a very early clinical instructor at UCSF, and I have nothing to disclose. We're going to go through the case details. I'm going to talk a little bit about plastic bronchitis, and then I'm going to go over some of these new, interesting, emerging treatment options. So straight on to the case. We have a 92-year-old woman. She has a history of GERD, multinodular goiter. She had tracheal compression and successful thyroidectomy in 2014. She also has history of diabetes and chronic rhinitis, and she's been followed in pulmonary clinic for persistent cough with cast expectoration and hemoptysis since 2018. She was known to the clinic before, but she just had occasional cough, mild dyspnea. And since 2018, she developed a subsequent progressive worsening of her symptoms. Her specific symptoms were cough with mucus plugs and small volume hemoptysis, which was usually worse at night, as well as dyspnea on exertion that was not improved on COPD treatment. She had stable GERD on PPI therapy. She had a negative swallow evaluation, and she was following behavioral modifications. She had multiple hospitalizations between 2018 and 2022 and was treated for a combination of pneumonia, COPD exacerbation, and pulmonary edema. This is what her casts look like. These are just two of the many she has brought up over the years. But they were submitted for pathology, which came back as bronchial cast composed predominantly of fibrin and mucus, most consistent with plastic bronchitis, a cellular variant. We'll get back to that. In terms of other relevant history, past medical surgical history, there was nothing else to add. She was originally from Malaysia, but has had no occupational, behavioral, or other risk factors. All her relevant medications were things that we prescribed, so mucolytic therapy, COPD therapy, rhinitis therapy, GERD therapy, allergy meds. In terms of notable workup, she had PFTs back in 2014 and 2017 with mild obstruction and moderate diffusion impairment that were pretty stable between those two checks. She had autoimmune inflammatory labs and BMP checks multiple times that were unremarkable. And she had multiple sputum cultures that never grew anything. She had multiple CTs. Most of these were obtained during acute hospitalizations. But even so, with each hospitalization, we saw a progression of severity of her findings. And you can see that she had bilateral ground gloss opacities and consolidations. They were worse on the left with peribronchiolar densities and septal thickening. So we managed her symptoms essentially as a combination of all of these underlying pathologies. We felt that the mucolytic therapy was her optimal treatment for her version of plastic bronchitis, and then managed all of these other comorbidities. She actually was getting worse on these therapies. And she had a really hard time tolerating the mucolytic therapies in particular. We did a trial of azithromycin and prednisone with no clinical benefit. And given sort of the progression, her now need for oxygen, which she didn't need before, it was continuous on three liters, as well as poor appetite and weight loss. And we actually referred her to palliative care for symptom management given her advanced age and the steady clinical decline. And it was actually palliative care who came back to us. And we're like, well, should we consider alternative treatments for plastic bronchitis? Let's really dig into these case reports because this person, even though she's 92 years old, is otherwise pretty healthy. And this is her major complication. So a lot of credit goes to them for this case. Briefly about plastic bronchitis, this is a condition that's characterized by this expectoration of entire casts of the bronchial tree of various sizes. It can be acute, subacute, or chronic in presentation. And it can be caused by a number of different ideologies, including infectious processes like viral and bacterial infections, but also primary and secondary lymphatic abnormalities, hematologic conditions, silicosis, a couple of types of malignancies, and then post-cardiopulmonary interventions. In terms of management, if you suspect plastic bronchitis, if it's acute, it's important to provide supportive care and potentially you can do bronchoscopic extraction of the casts. In subacute chronic cases, you have a little more time. Regardless, it's important to obtain casts for pathologic examination because the content of the casts can determine what you do next. If they're infectious, you treat the infection. If they're eosinophilic, then you can focus down the path of asthma and fungal sensitization. And then if they're more of the mucinous, fibrous, or chylous cast presentation, so acellular variants, that's when you want to think about cardiac disease as a common potential predisposing factor, as well as lymphatic abnormalities. With this, you also want to think about what other contributing factors there are. Are there any of these, you know, did the patient have Kaposi's sarcoma? Is there any relevant surgical history or any exposures that potentially could be treatable or reversible? So are there any medication options? The answer is not really. I'm going to go back here just to highlight that for eosinophilic casts, for example, you can do inhaled corticosteroids and bronchodilators. With acute cases, people have tried using TPA or heparin to help break up some of the casts, but again, this is a short-term therapy. And then again, just airway clearance therapy. So there's really nothing targeted to the cast specifically, especially the acellular variant. So there's some literature, meaning one case study, that hypothesized that octreotides should have a benefit because it can decrease chyoproduction and lymphatic flow. They tried it on this specific patient and it did not work and has really not been tested in additional case reports. So there's very little data on it, but some theoretical benefit. Serolimus is the one that was reported in really just a couple of case reports. When we were looking, as you know, it's an mTOR inhibitor and the mechanism of action is thought to be inhibition of abnormal smooth muscle cell proliferation that can cause some of the lymphatic leakage. The data really comes from management of chylothorax in patients with LAM, where serolimus was shown to have a benefit. And so the gold trough that you could use or that we chose to use based on this very limited data was the one based on LAM data, which is five to 15 nanograms per milliliter. One thing to keep in mind is that serolimus can also impair lymphatic drainage and lymphangiogenesis and can cause lymphedema in certain patients, and that's data from the transplant literature. Our patient did undergo an MRI lymphangiogram, and as you can see, all the bright areas are essentially areas of lymphatic spillage, mostly into the left, but also on the right. And she had evidence of discontinuity, cystic dilation, and then again, leakage into the mediastinal, peribronchial, and intrabronchial spaces. So a lot of the peribronchial or thickening that we were seeing on CT, in retrospect, we think that this is actually lymphatics that we were seeing that were causing that thickening. So our patient, we started her on a low-fat diet. One thing I didn't mention is, again, with chylis effusions, we decrease lymphatic flow by putting patients on a low-fat diet. We tried the same approach here. We started her on serolimus about a couple of weeks later. She weaned herself off the low-fat diet very quickly, didn't enjoy it, was already eating pretty healthy, but continued the serolimus. And miraculously, within a month, she was off oxygen, off her medications, with minimal symptoms, doing really well. The only complication that she's had so far was that her diabetes control is a little worse. Her A1C before was about six. It's about 8.4 now. It's mostly treated with dietary modifications. It's managed by her PCP. Because she had the lymphangiogram, she was considered a candidate for a thoracic duct embolization, but she declined, again, given that she was doing so much better clinically already on the rapamycin and given her advanced age. As of today, she's been on serolimus for over a year, and she has been doing well. And in fact, she's now the caregiver of her prior caregiver. In terms of take-home points, I'm just gonna leave them out there. I think the point of this case was really to highlight sort of a novel use Thank you very much for presenting that interesting case. What questions are there for Dr. Bianova, or comments, please? that I think one thing that stood out to me, as you rightly highlighted, the incredible value that the palliative care team has brought for this patient. It's almost like sort of the peak use or the peak benefit of the palliative care intervention to say the symptoms led to a reconciliation. I could speak from some experience that we've had at our institution with this. The ligation can sometimes be used itself as a treatment for chylothorax, depending on the nature, but again, is not in any way 100% effective for that, and so I think that the data is too limited for us to draw great conclusions. This patient certainly did very well, you know, from our experience, and I'm sure yours as well, in treating patients with LAM with sirolimus. Those who aren't familiar, the trough levels listed here are dramatically lower than the trough levels pursued for solid organ transplantation, and so patients were able to tolerate these lower doses of sirolimus typically very well, and so it seems like a symptom-focused approach worked very well for this patient in this case. All right, thank you so much again for your presentation. All right, next we'll hear from Dr. Ellen Han. I'll bring her presentation up. Ellen's coming to us from Tulane. Hello, thank you for having me. This is Master of Disguise Pulmonary Vein Stenosis. My name is Ellen Han, I'm an internal medicine resident at Tulane and I have no financial disclosures. Today we're gonna talk about the signs and symptoms of pulmonary vein stenosis and how to diagnose and treat it. Our patient is a 62 year old man with a history of atrial fibrillation. He had three ablations between the years of 2020 and 2022. He also had newly diagnosed right heart failure in the previous six months from this presentation as well as hypertension. Other relevant history, he does have a significant travel history as a paratrooper throughout the US and Asia. So he actually presented with a three month history of hemoptysis, pleuritic chest pain, night sweats, weight loss and shortness of breath. As you can see here, he presented to the ED multiple times before this presentation and had multiple CT scans. You can see here he had migrating ground glass opacities changing in the left upper lobe every time we got a scan. He also had lymphadenopathy that was pretty diffuse along the chest that did have increased uptake and PET scan as well as some cavitary lesions. On one of these presentations, he did get a bronchoscopy. As you can see here, the mucosa is very erythematous. He had very engorged veins as well. He did actually have significant bleeding like about 200 CCs of blood loss during this bronchoscopy. So on this presentation, he was hemodynamically stable on room air. As you can see here, his labs are pretty unremarkable actually. We did find this time a new DVT on his right leg and we got another CTA of the chest. It still had the ground glass opacities, the cavitary lesions, the lymphadenopathy in a different location, of course. But he now had a large left-sided PE with some right heart strain. And I do have a video, let's see. Kind of scrolling through, you can see, especially in this left upper lobe, the opacities here and how they're different from the previous scans. We also got a VQ scan to further characterize the PE, and you can see absent perfusion of the entire left lung here. During our workup, we also found that he had worsening right heart failure and worsening pulmonary hypertension on right heart cath. So our differential was pretty broad at this point. Obviously, he had this new large PE, although he was very stable. Malignancy was at the top of our list with these new clots, with the increased uptake on PET scan. And we were concerned maybe something was compressing vasculature in his chest. However, we couldn't rule out any sort of like vasculitis infection, especially with his travel history. Maybe he had some sort of odd fungal infection going on. And then kind of in the back of our mind was his ablation history as well. So our workup was pretty unremarkable as well. We got all sorts of blood work that was negative for vasculitis, no rheumatologic process, no infectious process going on. We repeated the bronchoscopy, cytology was negative, cultures were negative, pathology was inconclusive, showing mostly hemorrhage and inflammation. And then we decided to get a TEE with the input of cardiology, which showed left superior vein stenosis, likely from his ablation history. So that gave us our diagnosis on that imaging. And his case was actually so severe that he had to have a thoracotomy for surgical repair of his pulmonary vein, as well as a pulmonary artery and arterectomy. So kind of bringing this back to why all these symptoms happen, AFib is very common. We know that. We see it all the time. And radiofrequency ablations are also becoming increasingly more common because they have great symptom improvement. And however, some patients do need to have multiple, which we see all the time. Complications are usually pretty rare, less than 5%. I think we think of more like perforations, tamponade, effusions, and that kind of stuff. Pulmonary vein stenosis is very uncommon. Used to be more common in the past when ablations were pretty new, but at this point, it's rarely seen. Usually, if patients have pulmonary vein stenosis from an ablation, since ablations are usually around those pulmonary veins, usually they've had more than one. The rates of severe stenosis, like our patient, are extremely rare, 0.3 to 3.4%. Usually, they'll have shortness of breath and cough, more rarely like our patient, chest pain and hemoptysis. Usually presents within weeks to up to a year after their last ablation. And it's very misdiagnosed. As you can see from the imaging, it looks much more like pneumonia or some sort of malignancy. The best way to diagnose pulmonary vein stenosis is a CTA at the chest, and you need to time the contrast for the pulmonary veins. You can also do an MRI as well with contrast, or a TEE like we did, looking at the flow velocity. The best treatment is usually reserved for symptomatic patients only. You want to do percutaneous stenting, which is far superior than the balloon. Restenosis of the stent is about 10%, balloon is 70%. And if severe like our patient, they may need a thoracotomy or even lobectomy. There's very little research about pulmonary vein stenosis and how often it occurs. In this advice trial from Canada in 2020, they found mild to moderate stenosis in about 20% of patients, but they did not have any data on what happened with those mild to moderate asymptomatic patients afterwards. And this is definitely something we should look into in the future. You know, the question comes up if we should consider screening people after ablations. Although it's uncommon, pulmonary vein stenosis is extremely life-threatening. Our patient actually now is on the heart transplant evaluation list because he had re-stenosis of his veins. So the right heart failure was very extreme from his case. Some institutions do screen, but very few, and they don't have much data on what to do with that screening information, especially if they're asymptomatic. We don't really have any guidelines to tell us when to intervene and when not to. So the takeaways for this case is to consider pulmonary vein stenosis in patients with AFib, especially if they have these constellation of symptoms and abnormal imaging that doesn't seem to be adding up. You want to get the CT or MRI with the contrast time to the pulmonary veins to make the diagnosis. And percutaneous stenting is the preferred method of treatment if not severe enough that you would need a thoracotomy. And I really think more research would be critical to see how often this is happening and how many asymptomatic patients are progressing to symptomatic. I just want to give a shout-out to my mentors. Thank you so much, Dr. Becknell and Dr. Aguilar, as well as Dr. Farrell and Espinoza. And thank you for having me. Thank you, Dr. Hahn. Our next presenter, Dr. Pravan Mahadevan. I'm sorry, I'm going to say your last name incorrectly. Mahadevan. Mahadevan. Thank you very much for coming to speak to us and going to show us another very interesting case, and I won't take any more of your time. Please join us. Thank you all for having me. So, I'll be talking about an interesting case of bronchobiliary fistula. So, my name is Pranav Mahadevan. I'm a medicine resident over at Memorial Health University. That's over in Savannah, Georgia, and I have nothing to disclose today. So, this case, I'll be going over some of the risk factors for the formation of bronchobiliary fistula. In our case, I'll try to go over some of the diagnostic clues that pointed us towards this diagnosis, and then I'll just briefly touch on some of the conservative versus surgical management. So, by way of background, when I say bronchobiliary fistula, I'm talking about an abnormal connection between the biliary tree and the bronchial airways. Some of the most common etiologies identified in the literature would be something like hepatic tumors or biliary tract obstructions. And so, there are some other more unusual cases involving maybe trauma or pancreatitis or iatrogenic. So, this makes bronchobiliary fistulas particularly hard to diagnose and does require a high index of suspicion given its rarity. And the management of this condition is not universally agreed upon and certainly involves the efforts of many subspecialties, GIs, surgical, et cetera. So, I'll just jump into the case here. This is a 28-year-old female presented with one-week history of shortness of breath and production of cough-productive yellow sputum. So, our first diagnostic clue here is her past medical history, which is notable for hepatic angiosarcoma, status post-presection. That was about six months prior to presentation. Following this, it was complicated by a bile leak that required stenting. And then, she was followed by medical oncology and started on chemotherapy. She was actually on her third cycle when she initially presented to us. And then, in terms of her hospital course, she was pretty sick. She had high fevers, high white count. She was pretty floridly septic. She required intubation due to deteriorating respiratory status on the day of admission. Immediately following that, we went ahead and did bronchoscopy. And that showed localization of these thick, purulent, yellowish secretions to the right, middle, and lower lobes. So, that was sort of another clue as to sort of what might've been going on. And then, we also got CT imaging that showed bilateral ground-glass opacities and significantly a large mass over the right hepatic lobe. And I'll briefly show this over here, some representative slices from the CT, which the radiology read as like a large 11 by 7 by 10 centimeter cystic, peripherally calcified mass over the right hepatic lobe. There is some right hemidiaphragm elevation as well. And so, in terms of our initial differentials, mainly revolved around the sepsis. She, you know, most likely had some bacteremia going on. As for the source, prior to the CT, we probably would've just said community-acquired pneumonia. And then, this, you know, mass concerning for a liver abscess. Was this a manifestation of recurrence, sort of metastatic disease? We're not completely sure about this. So, but the first thing to kind of start off with in terms of treatment was just broad-spectrum antibiotics. We had seen some blood cultures. They're positive for strep angiognosis, somewhat atypical organism. And the most concerning feature, of course, is this liver abscess that was going on. So, we went ahead and aspirated that. And those cultures did grow positive for staph angiognosis and enterococcus. That's confirming, essentially, the source of the infection. So, following that, she did do well on her treatments, but she did have a persistent leukocytosis. Her respiratory requirements did decrease enough that we were able to extubate her about five days later. She did, unfortunately, have continued copious amounts of what now appeared to be like bilious-appearing sputum. So, this is really sort of the other clue, you know, despite all of our therapy, broad-spectrum antibiotics, and pulmonary hygiene, et cetera, she was still having what we considered, at this point, to be bilioptosis. So, we were concerned, you know, whether this liver abscess and these bronchoscopy findings that were localizing to the right lower lobe were connected. And so, given our concern for reaccumulation of fluid, we went ahead and just did a repeat CT scan, and we did a DNA separation. So, this, if you can see on the right side, did confirm our findings that there was actually a defect in the right hemidiaphragm that allowed communication of this abscess with the bronchial airways. So, that, you know, essentially confirmed our diagnosis, and then at this point, we involved GI services, surgical services, and so they recommended going ahead and doing a DNA separation over this abscess, and following that, our patient did have significant improvement in her bilioptosis and respiratory status. We don't have a hepatobiliary program, so we went ahead and transferred her back to where she had her initial hepatectomy. And then, just to kind of summarize the rest of her hospital course, she did have GI services over there, attempted some multiple biliary stenting, but unfortunately did not control this fluid reaccumulation, and ultimately required cardiothoracic surgery to perform a thoracotomy, and they did an intercostal muscle flap with a fistula repair. All right, so what can we sort of learn about this case? First off, you know, bronchobiliary fistula is itself a rare entity. This case actually highlights a somewhat atypical presentation. I mentioned before that in the literature, most of the cases, you know, the vast majority really are related to the hepatic tumors, whether they may be primary or secondary or biliary obstruction, but there are some other unusual sort of presentations, and this is one of them. We felt that our patient's liver abscess following the hepatectomy probably contributed to this formation where she had some local inflammation around the area and caused some erosion into the diaphragm, ultimately. Some of these, some of this pathophysiology is not, you know, fully understood, but what we can identify are some of the risk factors, including hepatobiliary tumors, previous ablation procedures, especially with the rise of ablation procedures for hepatic tumors now, trauma, surgery, local infection, and some of the processes and factors that contribute to this are biliary tree pressure and local inflammation, and so as in our case, you know, really the pathognomonic feature would be bilioptosis, but that may not be immediately recognized, as was in our case. We, you know, that yellowish sputum, we just kind of chalked up to purulence, but there were some of the clues out there that I alluded to in terms of figuring this out. I mean, our bronchoscopy findings did show that yellowish purulence sputum in the right lower lobe that we were able to localize, and she still had bilioptosis following extubation, and she did have that prior hepatectomy, and all those things kind of pointed us towards bronchobiliary fistula, and some of the typical diagnostic modalities would be just CT, MRCP, ERCP, et cetera, and just briefly on the treatments, conservative treatments listed on the right there, if we're thinking about medical therapy, we see that somatostatin analogs, trietide, et cetera, supportive therapy, and orthostatic positioning, but I will say, you know, rarely has this been used effectively to manage these symptoms, and more often than not, we'll have to do some type of procedure. Minimally invasive procedures include percutaneous or endoscopic biliary drainage, and then, you know, definitive treatment will usually be achieved surgically. As in our case, she required a thoracotomy and fistula repair, ultimately. So sort of take-home points here and conclusions. So we had patients with a history of the hepatic angiosarcoma, sinus puss resection, and formation of the hepatic abscess that's put her at risk. Given those kind of peripheral calcifications, that was likely going on for quite a while, and so we felt that that was contributing to the fistula formation, and we can diagnose this. We go ahead and drain the abscess and do some serial imaging, and that'll confirm, hopefully, on imaging that we have a fistula. And then treatment-wise, despite the attempts of GI with multiple biliary stents, we were not able to control her symptoms, so ultimately required a thoracotomy with fistula repair. Another option would be a pulmonary lobectomy as well. So I hope that was an interesting case. Okay, thank you, Dr. Ladovan. Thank you all. Thank you.

clinical cases

dyspnea

metastatic pancreatic cancer

plastic bronchitis

pulmonary vein stenosis

atrial fibrillation

bronchobiliary fistula