I am Momina Amjad, I'm a PGY3, I am resident at Albany Medical Center, and I'm presenting for my colleague, Dr. Maryam Fez. So her case was, that was toxic to your lungs, exposure associated lung disease, specifically for daptomycin-induced esophageal pneumonia, and I have no disclosures. So the objectives to this lesson are to understand that daptomycin-induced AAP is an under-recognized healthcare complication. Just to elaborate on the pathophysiology, daptomycin is proposed to bind to human surfactants causing damage to pulmonary epithelium and cytokine-induced inflammation, leading to acute esophageal pneumonia. And typically, the association usually presents within two to three weeks of daptomycin therapy. And then in our case, I'll elaborate on this further, but eosinophilia was prominent in the BAL sample, and one of the classic FDA diagnostic criteria is that after you, to save daptomycin therapy, that you should see some improvement, and we saw that. So, daptomycin supports can be adjunctive to help in acute eosinophilic pneumonia as they cause eosinophilic apoptosis, and then it's important to timely recognize this entity and treat eosinophilic pneumonia. So the patient was a 77-year-old male. He presented with two weeks of progressive dyspnea, cough, seven-pound weight loss in the last two months, and malaise, low-grade fevers. He was recently hospitalized for osteomyelitis caused by MRSA bacteremia, and he was currently on week three of IV daptomycin therapy. He was receiving 900 milligrams IV daily. His vitals were significant for respiratory rate of 24, temperature of 101.1 Fahrenheit, so low-grade fever, and he was also satting 96% on three liters per minute of oxygen in nasal cannula. His physical exam was significant for bronchi in the right lung field and fine crackles in bilateral lower lungs. So workup of any eosinophilic pneumonia is usually aimed at ruling out other infectious causes, as the presentation could look very similar. So we did the basic sort of CBC metabolic panel, lactic acid, ProCal, and then the infectious panel included respiratory viral panel, sputum cultures, blood cultures, and Legionella antigen in the urine. We also obtained a chest X-ray and a CAT scan, and then finally we did a bronchoscopy with a BAL. So this patient's labs were significant for a white count of 11.9 with an absolute eosinophilic count of 1.8, and elevated inflammatory markers, his CRP and ESR were both elevated. Lactic acid was 2.32, and ProCal was 0.29. And then the rest of the infectious workup was negative. This was his chest X-ray. We can see some right-sided infiltrates and also some trace bilateral pleural effusions. Moving on to his CAT scan, we can see some non-segmental distribution of airspace consolidation with a peripheral predominance on the right side and a little bit on the left. We can also see some intralobular and septal thickening, and there are some centrilobular nodules. These are findings classically associated with acute eosinophilic pneumonia that are typically seen. And at this stage, you know, before doing the BAL, the team was considering various differentials, including MRSA pneumonia itself, other community-acquired pneumonia, CHF exacerbation. Those are all possibilities with this case. So they proceeded to do the BAL, and this is what showed 57 eosinophils, which was suggestive of acute eosinophilic pneumonia, as well as no other infectious. There was no other organism that grew on the cultures, the Gram stain and AFB. All the other infectious etiologies were negative. So at this point in time, they diagnosed the patient with acute eosinophilic pneumonia because of the daptomycin-induced injury. And essentially, the FDA has the diagnostic criteria includes fever, dyspnea, exposure to daptomycin, and bilateral lung infilt, or some sort of chest infiltrates in the patient met all those criteria. So he initially was started on a broad empiric therapy for pneumonia when he first came to the hospital, and his daptomycin was being continued for MRSA osteomyelitis. At this point in time, they discontinued all antibiotics, and especially the daptomycin was stopped, and it was replaced with linezolid for the treatment of MRSA osteomyelitis. He was started on 60 milligrams oral of prednisone daily, and this two days after these interventions, after stopping the daptomycin and starting the prednisone, his dyspnea and his respiratory distress significantly improved, as well as his peripheral eosinophilia. And so this was the case that we took care of. I'm happy to take any questions. Yes? How long was the patient on DAPCO? He was on it for three weeks. So he was supposed to be on it for four weeks. This was week three. How long did he have to be on prednisone? So he had to be on it for four weeks, and then a taper, like a slow taper of five milligrams per week after that. So he was on the 60 mg dose for that long. Can you mention on the BAL, 57 eosinophils, was that like the count of eosinophils, or 57% eosinophils? So from what I could piece together, I think it was the count, but I think the details were that this was still more than 25% of the entire BAL. you know, purposes of treating MRSA and pneumonia, you don't typically use daptomycin because it wouldn't penetrate the tissue. I do think that this, you know, as far as acute ozone and like pneumonia is a concern, daptomycin is sort of one of the more common agents that's associated with it. And I actually don't know the answer as to how, if it doesn't penetrate, why it would cause this injury associated with the surfactant. But I think the surfactant also metabolizes daptomycin, and that's one of the reasons why we don't use it for treatment for lung disorders, or lung pneumonias. Or something like that. All right, does anyone else have any other questions? All right, well, thank you very much. Thank you. It was a great presentation. All right, our next presenter is Dr. Jared Hilton, talking about diffuse alveolar hemorrhage from electronic cigarette use, a rare manifestation of an increasingly common disease. Awesome. Hello, everyone. I'm Jared. I'm a second year fellow at the University of Utah. I'm going to present, hopefully, an interesting case of DAH for you guys. That's me. I have no financial disclosures. We'll just roll through the objectives real quick. Just present a case of DAH, talk about evaluate for a second, and then I'd like to touch on the pathophysiology. I think it's always a little fascinating to think about, even though there's a bunch of gray areas. A lot of text. I'll go kind of quick. She was 47. Main history was suboptimally controlled diabetes. She's had a result in CKD. And then this past history, about three years ago, of pulmonary mucor, that she had resection antifungals that had been stable and in remission for all intents and purposes. She came in a couple of weeks of kind of hard-to-quantify hemoptysis. Not a ton. She had maybe a tablespoon of blood every other day, sometimes a teaspoon. But otherwise, she felt really well. She had no extra pulmonary manifestations. Didn't even really endure shortness of breath, just this hemoptysis. And then socially, she used to smoke, but she had recently transitioned to vaping nicotine. And she obtained the vape liquid through a resident at her living facility. She was currently living in a women's shelter. She had a distant history of some inhalants, cocaine and methamphetamine, but nothing for several years. And then nothing that popped up on labs and stuff. Quickly, her medical history. Mostly type 1 diabetes. This mucor I mentioned that was like multiple years ago. Around that time, she had a bunch of other things. Our patients come in sick, they have PEs and CVAs, all that stuff, but kind of distant. And then quick medication scroll through. Notably, no real anticoagulants other than just aspirin, and then kind of usual things treating her bipolar neuropathy and her diabetes. Hopefully, this will work. This is a video of our viewer. Great. Quality maybe suffers. So scrolling down her chest, this was obtained in the ER. You have kind of diffused bilateral kind of ground glass and consolidated opacities down in that right lobe that popped up. Doesn't look like I'm able to go back and forth on it. But if you want to scroll through it again, there's a kind of a chronic appearance scar in the bottom. And then there's maybe a little bit of pleural sparing that you can appreciate kind of in the upper lobes. So she got admitted to the pulmonary service. And in summary, we did a large DAH workup. And we'll talk about the bronchoscopy in a second. But vitally, four liters of oxygen, which was new for her, but otherwise was great. Her exam, just crackles in her lungs, no joints, pain, rashes, anything new. Then her workup was quite normal as well. Her coagulation cascade, UA, drug screen, and then all kind of the autoimmune and inflammatory things were negative. Did a bronchoscopy. This was at the end of my third year of residency. So they didn't let me touch the bronchoscope, but I was present. Otherwise, it looked OK. The airways looked great. Didn't see any localized bleeding, but had progressively bloody aliquots on her BAL. And then had an echo, which was largely normal. She had some improved tricuspid regurgitation, but it was not quantifiable. So she was in the hospital for about five days. We actually didn't touch her with anything. We didn't give her steroids or antibiotics or diuretics or anything, because she was overall doing well. We had rheumatology and nephrology weigh in just to make sure there wasn't a GN or some other autoimmune process going on. And since she was doing so well, we actually just repeated the CT before we made any treatment decisions. Hopefully, this plays. And it's not normal still, but it's markedly better, right? Just a five-day difference. And you can see that scar in the right lower lobe as well. So she had markedly improved. And kind of floating around in the case report literature was some diffuse alveolar hemorrhage associated with EVI, so that was sort of what we'd pinned it on with a largely negative workup. She was supposed to follow up in Palm Clinic, never did. But I've been stalking her in Epic, and she's doing well and has had no recurrences. And at least of her note, she stopped vaping and stuff. So we thought that was probably the most likely ideology. I think I just touched, I have a couple minutes, it looks like. So just touching briefly on EVALI, Utah was kind of on the leading edge of it. We had a lot of cases relative to our population. But generally, respiratory GI and constitutional symptoms. Imaging can look like a lot of things, typically organizing pneumonia in mixed central alveolar nodules, kind of an HP pattern. And then you can also see diffuse alveolar damage and AEP and exogenous lipoid pneumonia patterns as well. So in summary, it can look like anything. And then on pathology, you usually get organized pneumonia, DAD, or this fibrinous pneumonia back. This was the outbreak before the outbreak. This is just a graph of cases. Around 2019, they actually stopped reporting in February 2020. We can talk about that pop-up here in a little bit. I thought vaping's interesting, because it's more than just smoking. There's these competitions dedicated to it. And I actually was watching some YouTube videos about people who do tricks. It's actually kind of cool. Not that I would get into it. But I tried to look up, it's like a cigarette smoking competition. There's nothing like that. But people are building these devices, modeling them, using different things to have different smoke characteristics, more smoke, that sort of thing. So it's a little bit different from exposure, I think, than just our standard tobacco and nicotine. So quickly on the pathophysiology, the oils they use is some combination of a deliverant oil. And then you can add in different things like nicotine, THC, whatever you choose. The initial outbreak, you could say, of eValley was largely attributed to this vitamin E acetate. And the table here on the right, the details aren't important. But it was kind of the NEGM paper linking the two. They found vitamin E in most of the cases of eValley on BAL. And then on the left is just a picture from a paper where they aerosolized vitamin E acetates to rats or mice. I can't remember which one. But on the left, kind of healthy control airway. And on the right, you can see all that inflammatory badness up there. And it's a little unclear exactly what the pathophysiology is. You can see vitamin E acetate down below. That rightmost picture sort of looks a little bit like it could fit into surfactant with the dipalmitoyl phosphatidylcholine. So is it just an interaction with surfactant? You're surfactant causing lung injury? Or vitamin E is normally in phospholipid bilayers. So is there some interaction going on there causing the lung damage? And then the other two kind of additives, propylene glycol and vegetable glycerin, they're the other kind of two big oils. They're like food safe, but we don't know how they aerosolize. And then down here, that graph shows that as you increase the concentration of, I believe that one was vegetable glycerin, it showed interactions with the surface tension of these membranes. So they probably even have an effect as well. Not to mention, you're heating these things up. And then who knows what you get when you heat them up as well. So on the top left, that is the glycerol heated up. It breaks down into formaldehyde and acetaldehyde, which are, as we all know, bad. And then I circled this acrolein. That's actually a blistering agent that was used in World War II in the trenches. So those things are happening in your lungs when you vape. And then on the bottom, the vitamin E turns into this ketene gas, which is actually a pulmonary toxin. And they've looked at studies in animals that it causes death by pulmonary edema. And then obviously, all the other things they're putting into it, nicotine, there's flavoring chemicals, other oils. And then there's going to be changes and people modding things. So even though the vitamin E is out of the main formulations, there's still other things that would be causing issues. And that's it. We're right at eight minutes, I think. So happy to take questions. Thank you. You know I have seen two cases of people that one was from out like ordering online from like Silk Road or one of those places and another one was like getting it from like a friend who made their own like homebrew sort of oils. So yeah that's tough you know there's definitely more regulations on the actual vaping industry now after kind of the valley outbreak and such but yeah when you're getting it from somewhere else you really don't know what you're getting which makes it really difficult to know. Yeah. Yeah yeah I didn't put in much about treatment and stuff but you know steroids are kind of in the you know we don't haven't really had robust trials to say you know if they're beneficial versus other things but at least that seems to be standard of care yeah yeah she had done so well we said well let's not rock the boat by any means. Yeah, I don't know off the top of my head. You know, I imagine it's probably some complex, you know, interplay between someone's, you know, genetics and development and then, like, all the other medical problems they have. But I didn't come across the specific things. Cool, thanks. All right, next up is Dr. Dale Smith, talking about PAP secondary to Everolimus. All right, hello, I'm Dr. Smith. I'm one of the third-year fellows at the University of Kansas. My case is on pulmonary ulnar prognosis secondary to Everolimus. So here's the crazy paving that we've all seen on Google Images a couple times. That's me, nothing to disclose. So lesson objected. So we're going to discuss the case first, then we're going to identify risk factors that should make you more concerned about this being a possibility in a patient. And then we're going to talk about comorbid infections and then management of respiratory failure if it gets to that point. So all this is kind of bulleted, but anyway, so it's a 56-year-old with ESRD status post transplant in 2020. His post-transplant course was complicated by CMV colitis. He also had a history of HFREF prior to that status post ICD. And then in the post-transplant course, he started on Everolimus, thinking that it would work better for him. And then he presented in early 2022, what turned out to be a long hospitalization with respiratory failure after being persistently positive for COVID-19. There were a lot of factors that went into different possible differential diagnoses in him, but underwent a BAL with 20% eosinophilia. And there was concern about Everolimus pneumonitis and possibly organizing pneumonia secondary to COVID-19. So eventually over his course, he had worsening respiratory failure despite steroids and diuresis. He had a repeat cryptococcus antigen later on in the hospitalization, which returned positive after initial one was negative. And then eventually he underwent a VATS and a WEDGER section, which found PAP and cryptococcus. Ultimately, he underwent a VV ECMO to facilitate a whole lung lavage with significant improvement in symptoms. He was intubated post the VATS and WEDGER section and was able to be exubated the next day after the whole lung lavage. So this is a representative cut of the initial CT that he came in with. And so just kind of diffuse ground glass, but also there may be some hints of interlobular septal thickening that you can see in there. So this is 10 to 14 days, I think, into his case, where you see more prominent interlobular septal thickening. And then you also see a worsening consolidated process in the left lower limb. This is from the surgical lung biopsy. And then you can see the periodic acid shift or PAS positive in the left side. And then here you can see the fungal yeast forms with the mucoid capsules and clear halos over on that right side. And then this is a mucocarmine stain demonstrating encapsulated cryptococcus bodies. This is the obligatory whole lung lavage gradient. So talking about secondary pulmonary aldehyde prosthenosis. So it's a problem, more general PAP, is a surfactant production versus clearance issue. It can have an invalid presentation, so slowly over definitely weeks to months. And then the incidence is pretty rare. And then even more rare within that group is secondary PAP, which is only about 4% of cases. Most of those are going to be related to hematologic malignancies, but they can also be associated with infections, and in this case, drug-related to everolimus, especially in the post-transplant setting. So immune deficiencies and toxic inhalations have also been related. And then the mortality is higher in secondary PAP. So in general, PAP was first reported in 1958. A breakthrough kind of came in 1994 when they looked at GM-CSF knockout mice and suggested that this was a possible pathogenesis for PAP. And then in 2009, they took PAP patient-derived autoantibodies to GM-CSF and transferred it to a non-human primate, resulting in PAP. So and then for diagnosis and treatment of secondary pulmonary aldehyde prosthenosis. So usually it can be diagnosed with a BAL. In this case, the BAL fluid was tannish, but because of the more consolidated process, it was thought to be more related to purulence. And so it also can be diagnosed with transbronchial lung biopsy, and then less often requires a surgical lung biopsy. And of course, on the BAL, or on pathology, you're going to see the periodic acid shift. And then for the treatment of it, specifically for secondary pulmonary aldehyde prosthenosis, you want to treat the underlying cause, which would be hematologic malignancy or discontinuing the drug. Or if it's related to an infection, you'd want to treat that. Whole lung lavage is the mainstay of treatment, but more recently, they've been using inhaled and subcutaneous GM-CSF for those patients who are more likely to be autoimmune, which means that they would have GM-CSF autoantibodies. And that's my presentation. Any questions? So, in regards to the diagnosis, how did you all differentiate from the drug-induced etiologies versus COVID and Kripakakl? Yeah, so in this case, it's not completely clear. I think we arrived on Everolimus, but there were a lot of possible etiologies. I mean, Kripakakl itself has been related to PAP, and so that could have been a culprit. And then, yeah, actually, I didn't show this because it was already kind of complicated, but he actually also had some NTM in the pathology as well, which has been linked to it. All right, our next presenter is going to be Dr. Arash Safavi, Excipient Induced Lung Injury from Total Parenteral Nutrition. Hello, thank you for joining me in this session entitled Excipient Induced Lung Injury from TPN. My name is Arash Safavi. I'm a PGY2, it's overwhelming to see my own picture, PGY2 anesthesiology resident at Cedars-Sinai in Los Angeles, and I have nothing to disclose, unfortunately. So my lesson objectives today will be to give you a brief overview of excipient lung injury by kind of going over a brief clinical case we encountered while I was an intern on the Palm Service at Cedars. There are some typical and kind of well-known causes of EILI, and this was a less common presentation. So to dive right into our case here, our patient was a 51-year-old female. She had a history of short gut syndrome, secondary to abdominal trauma as a child, and for this reason she was on chronic TPN. She also had a history of chronic regional pain syndrome following multiple surgeries, and at this point of her presentation was pretty well controlled on ketamine and with aid of a spinal cord stimulator. She presented to the ED at an outside hospital, so not our institution, with a month of cough and progressive dyspnea on exertion. Her initial presentation at the outside hospital, labs were notable for leukocytosis and a mildly elevated lactate to 3-9. Her blood cultures eventually went on to demonstrate gram-positive bacteremia, gram-positive rods, and then she had imaging that demonstrated diffuse central lobular nodules, and she had an echocardiogram with an estimated PA pressure of 47 millimeters mercury. Her CTA was negative for PE, which was one of their leading suspicions at the time. What was most concerning about her presentation at that outside hospital was that she had been there previously about five months prior, and this was a new diagnosis of pulmonary hypertension because they previously didn't see it on echo. She was transferred to our facility at that point for consideration of a lung biopsy and then to further work her up for the etiology of this new diffuse bronchiolitis and pulmonary hypertension. And before they transferred her, she was initiated on broad-spectrum antibiotics and supportive therapy. So now upon arrival to our facility, this is three days after her original presentation, her lactate and leukocytosis had largely normalized. Notably she did have a ProCal elevation to 4.8 and a C-reactive protein of 79. Her initial respiratory virus panel as well as Legionella, Cocci, Crypto, Aspergillus slabs were all negative on workup. So several causes of interstitial lung disease were considered in the differential diagnosis, including infectious agents, hypersensitivity, pneumonitis, silicosis, and bronchiolitis. However, this patient denied any kind of occupational travel, exposure history. Her infectious workup was negative, as we discussed previously. We did a right heart catheterization that showed mild pulmonary hypertension, pulmonary artery hypertension, and her CT again demonstrated similar findings to the outside hospital as seen in Figure 1. She also had, a week after her presentation to our hospital, an interval scan, which showed now superimposed ground glass opacities, which we can see in Figure 2. Let's see if this works for us. Okay, so here's a video of the original CT upon arrival to our facility. As you can see, there are central lobular nodules diffusely throughout the bilateral lung fields. So her sputum exam was not diagnostic, and the next thing we did was a bronchoscopy with a transbronchial biopsy. There weren't any infectious agents found in the biopsy, but macrophages were identified containing polarizable crystalline materials, and there was a granulomatous reaction with giant cells seen surrounding the areas of the foreign material. They were birefringent under polarized light, and the location of the foreign body deposition was kind of consistent with intravenous route of induction, introduction. The microscopic findings on biopsy were pretty consistent with excipient lung injury. This is classically associated with injection of crushed oral tablets, tablets such as narcotics and stimulants, and excipients are, by definition, the not pharmaceutically active fillers, binders, compounds that are formulated into medications. Some examples are microcrystalline cellulose and talc. And then when these excipient-containing medications are abused or injected intravenously, they wind up deposited into the pulmonary vasculature with subsequent angiogranulatomous reaction, which can cause micronodules, microemboli, and can potentiate hypoxia and pulmonary hypertension similar to what we saw in our patient. The very first cases of EILI were seen in individuals who had heroin dependency and were maintained on methadone. They would kind of crush up the methadone and inject it to get a quicker high. And then ritalin lung is the term for basal predominant panlopular emphysema caused by injecting talc-containing methylphenidate, which we can see in the coronal CT on the left, and biopsy from the same lung shows birefringent talc deposits on the right. And these figures are from a 2014 Journal of Radiology paper. So since we had our diagnosis, our first consideration was, could this patient who has a PIC with central axis, this history of chronic pain, and opiate use be crushing and injecting her medications? It was a logical assumption, but after talking with her extensively, we had a lower suspicion for this. Notably, her pain was well-controlled on her current regimen. She was not being prescribed any parenteral opiates for quite some time, given her ketamine spinal cord stimulator were pretty sufficiently controlling her pain, and neither for us nor the previous hospital, she wasn't exhibiting any signs of drug-seeking behavior or symptoms of withdrawal. So in discussing with our pathologists and pharmacists, there were a few instances in literature to suggest that there was a possibility of calcium phosphate precipitation as a product of the TPN that she had been on. This would be the potential excipient. And we ultimately reformulated her TPN without calcium, and over the next two weeks, her respiratory status improved. She was discharged. And a key takeaway from this case for us was that whenever there are unexplained pulmonary symptoms to consider all external inputs, including common excipients and less common ones like TPN, and of course, the importance of multidisciplinary approach. My reference is, and thank you so much. I'm happy to take any questions. All right. Our next presenter is Dr. Laura Glassman, who's presenting a unique case of acute respiratory distress syndrome from the Sleepy Chicken Challenge. I had to look that one up. We'll get into it. Yes. Okay. Hi, everyone. My name is Laura Glassman. I'm one of the third-year pulmonary and critical care fellows at UCLA and the West L.A. VA. And I'll be presenting a unique case of acute respiratory distress syndrome from the Sleepy Chicken Challenge, a viral trend gone afoul. That was my favorite part. So here's my information, and I have nothing to disclose. So we'll kind of be focusing on a few things here. Inhalational injuries are an uncommon but probably overlooked cause of ARDS, and therefore kind of a comprehensive history is crucial in the diagnosis and treatment of acute lung injury. And then that really, especially after COVID, that providers need to be aware of these kind of viral trends and the negative health impacts they may have on our patients. So we'll start off with our case. This is a 61-year-old male. He has a history of active tobacco use, about 50 pack years, reported COPD, though no supporting PFTs on file here, and polysubstance abuse, who presented with three days of progressive nonproductive cough and dyspnea. Here are his vital signs in the emergency room. Really notable, he was very hypoxic. His saturations were 70% on room air when he came in, and his respiratory rate was 20 or higher. His physical exam shown here, really just wanted to point out some significance for the pulmonary exam. He had bilateral crackles, decreased breath sounds at the bases with kind of faint wheezing in all fields. His left arm was in a cast from a motorcycle accident about a week ago, and a little bit of lower extremity edema. But otherwise, the rest of the exam and the review of symptoms was otherwise unremarkable. Here are his initial labs shown here. He had a leukocytosis that was neutrophil predominant, a BMP-CMP that was largely normal, and then a VBG that was 7.438, which is abnormal in someone breathing so rapidly, as well as an elevated BNP. Here is his X-ray gotten first. Just really showed bilateral airspace opacities, maybe a little left lower lobe effusion, as well as you can kind of see thickening of kind of the fissures, especially on the right side. And then hopefully his, this is a CT scan. He did get a CTPA, which showed no pulmonary embolism. And then you can kind of see here, he has bilateral, more upper-low predominant patchy areas of ground glass in the upper lobes, middle lobe. And then you can kind of see the development of a left lower lobe kind of consolidation, as well as smaller consolidations in tree and buds, but really within the whole right lobe. This will kind of go back up. So his clinical course, he really decompensated in the emergency room. He was tachypneic. Now he was developing hypercapnic respiratory failure as well, despite kind of escalating bypass and levels of support. So they did intubate him down in the emergency room. You can see here initially it was kind of requiring near-maximal ventilator settings, which an FiO2 of 100%. A post-intubation ABG did show a P to F ratio of about 80. So our initial differential diagnosis after he was then admitted to the MICU, he didn't meet criteria for severe ARDS at that point with that P to F ratio. So it could have been done to infection, maybe aspiration, or vasculitis, given his kind of recent drug use. Diffuse alveolar hemorrhage, given his nonspecific imaging. Acute interstitial pneumonia, kind of given his rapid progression. Cardiogenic pulmonary edema with that elevated BNP and kind of lower extremity edema. We didn't know his cardiac status at that time. A valley, which we heard a little bit about. And then, you know, seemed unlikely with all of his parenchymal disease, but given the kind of recent motor vehicle accident, couldn't rule out a fat embolism as well. So he was started on empiric antibiotics, and on admission to the MICU, underwent a broad infectious and autoimmune workup, which cultures, serologies, all were unremarkable. He had a TTE that showed really a relatively preserved cardiac function, no significant ventricular or valvular issues, no PFO. And then repeat ABGs were still, you know, pretty borderline, and P to F was 100, so still severe. So at that point, kind of given our concern for severe ARDS of unknown etiology, he was paralyzed and prone, and was initially kind of responsive with a PDF ratio of 150 immediately after being prone. So we did kind of continue that for kind of the 16 hours. But at this point, our differential, we still didn't really know what was causing his issues. We kind of had to work through a lot of infectious workup. We had an echo that didn't show anything significantly cardiogenic. And so we went back and asked his partner if anything unusual or abnormal had been going on. And so she told us that he had been following the TikTok trend of, quote, boiling chicken in NyQuil and inhaling the fumes, which shown here is the Sleepy Chicken Challenge, where they kind of baste the chicken in NyQuil, put it over the stove, and then put their head over it to kind of get in all those NyQuil fumes into their lungs. And then I think they eat it too, though at that point, kind of seems they've had most of the effect. Fortunately, for our gentleman, he really did respond to proning within three days. So by day three, you know, his ABG showed a P to F of greater than 200. So we discontinued paralytics and proning at that time. Still was requiring a significant amount of ventilator support, but less certainly than when he came in. Hospital nine, day nine, he was extubated to high-flow nasal cannula and actually weaned to room air the next day and then completed an empiric course of antibiotics, though really nothing had turned up from our cultures. And then actually hospital day 15, he was discharged back to his inpatient rehab facility to continue his treatment there. So really a great turnaround. So kind of, you know, our lungs are really one of the few organs that are constantly in contact with the external environment. And so inhalational injuries are really relevant to kind of when you're taking care of these patients. There are many things, like I said, in the environment our patients kind of are exposed to, or even chemicals from occupational, you know, jobs like diacetyl, if you remember the popcorn lung, as well as, you know, chlorine and other chemical exposures that can kind of, you know, affect our patients. Inhalational injury, there's kind of two hypotheses to what causes it. There's kind of, you know, hypothesis one, which is really the kind of direct cytotoxic chemical in inhalation, which, you know, causes cellular necrosis, neutrophilic inflammation and kind of affects normal lung homeostasis. But there's also this kind of two-hit phenomenon where, you know, patients who smoke or have regular chemical exposure, you know, alters the kind of homeostasis in their lungs. And so it makes it like at the baseline that they're kind of in this pro-inflammatory state. And then when a new chemical exposure comes along that normally would be well-tolerated because the lungs at baseline are a little bit dysregulated, this can cause this whole inflammatory cascade that can kind of lead to lung injury and ARDS. And then after inhalational injuries, you know, ARDS develops kind of relatively quickly within three days. And so that was kind of the time course we also saw with this patient. I just wanted to point out that after inhalational injury, you know, the biggest risk to these patients is actually also infection. And this is really taken from the burn literature. But in burn patients who had inhalational injuries, about 40% of them developed pneumonia within that initial hospital stay compared to about 8% of patients without inhalational injuries. So it's kind of a significant risk factor, which you think probably ended up happening with this patient here. And that's due to, as we said, kind of a dysregulated immune response that probably occurs after the injury itself, as well as kind of, you know, altered, you know, mucosa and surfactant production and transport that we know protects the lungs at their baseline from infections. Kind of last, you know, to sum up to our knowledge, this is the first reported case of ARDS, secondary to the NyQuil inhalation during the sleepy chicken trend. The FDA did kind of come out with a warning against this practice due to risks of inhalational injury, though ARDS was not specifically mentioned. There's this hypothesis that the injury is caused from, you know, inhalation of dextromorphin, which is similar to heroin, which we know can cause injury, but the exact mechanism isn't exactly known. And then just last, being aware that, you know, social media trends, especially after COVID and now, really kind of have bad or negative health effects, you know, on patients of all ages. I kind of think of more like the tween or the young kid who's kind of more at risk for this, but about 20% of TikTok users are above the age of 18. So it's something that we should be aware as we take care of patients of all ages. All right. Here are my references, and I'm happy to answer any questions. Or if anyone's brave enough to tell us if they tried the challenge. So we were supposed, is Dr. Taifair here? All right, I think then he was supposed to be our last speaker, but I don't think he's here. So that concludes our session. Thank you so much. Don't forget to evaluate on the app. And thanks for our speakers, and congratulations for presenting. Thank you.

pulmonary medicine

case presentations

daptomycin-induced lung injury

PAP secondary to Everolimus

excipient-induced lung injury

TPN

acute respiratory distress syndrome

Sleepy Chicken Challenge