Welcome to Bugs and Drugs in the ICU, a series of oral case reports. Thank you for coming today to learn from our case report presenters. I'll maybe ask somebody in the back of the room if you might close that door for us with a lot of hallway noise. My name is Megan Conroy. I'm at The Ohio State University and a member of the CHESS Training and Transitions Committee. My role here today is really just as moderator. So for all of our presenters today, I will be tasked with keeping you on time. You have eight minutes for each of your presentations and then we'll moderate about two minutes worth for questions. I will hold my hands up for you, two or one to let you know in time and be sitting right here. And with this, I welcome first Dr. Michelle Iguina to present Disseminated Persistent Mycobacterium Abscesses. Hi everyone, good morning. My name's Michelle Iguina. I'm currently an intensivist practicing out of West Palm Beach, Florida. And I'm gonna be presenting a case to you about disseminated persistent mycobacterium abscesses, cutaneous inoculation from a spider bite in an immunocompromised patient. And I have nothing to disclose. So today's objectives, we're just gonna focus on summarizing the associated challenges with not only identifying, but diagnosing non-tuberculous mycobacterium. And just for the sake of not getting tongue tied, I'll just refer to NTM infection moving forward. And understand the clinical importance of atypical NTM as extra pulmonary infectious pathogen, especially in the high risk patient population. So a little bit about our patient. She was a 75 year old female, and she came in complaining of bilateral lower extremity pain, and these violatious cutaneous nodules, and being progressively unable to ambulate. Important past medical history for her, she had rheumatoid arthritis on tocilizumab infusions, and chronic corticosteroids. On top of that, she was getting IVIG therapy from her rheumatologist recently. She did have known history of moderate persistent asthma on triple therapy, as well as Saba PRN and Singular Daily, and just some allergies there to note of cephalomides and iodine. Interestingly to note, she was hospitalized about one week ago, or one week prior to presentation for lower extremity cellulitis after a spider bite, for which she received IV vancomycin, and was sent home to complete a course of PO-daptomycin. So these are just some pictures of her physical exam. Hopefully you guys can appreciate them up there. Just interesting, impertinent positive. She was febrile. She was an obese lady with somewhat of a cushion-like appearance. She had rheumatoid deformities of her hands, and multiple lower extremity lesions, as you see in the photos, with shallow-based ulcerations, compromising essentially both lower extremities from the thighs all the way down to the calves and ankles. Just important imaging, just kind of a snapshot of her CT chest, just to show you guys that there were no nodules, cavitary lesions, or any kind of tree and bud opacities. And imaging of her lower extremity, she didn't have any lower extremity DVTs, and the CT of her lower extremities just showed symmetric subcutaneous edema without any gas or osseous involvement. So kind of stepping back, we have to take into consideration differential diagnosis for a rash in the immunocompromised patient. So 20% of immunocompromised hosts will develop skin lesions and fever. And for those of you who are like me, who haven't read up on our dermatological manifestations of disease recently, of course, common things being common, bacterial, things like staph, strep, of course, pseudomonas, especially in the immunocompromised patient, Vibrio, common in our cirrhotics and end-stage renal patients. Nocardia, you'll see disseminated disease with skin manifestations with underlying pulmonary disease, not the case in our patient. And then, of course, all the way at the bottom of the list, mycobacteria. Viral and fungal, we also have to keep in mind, especially when the patients are high-risk. So on day five of hospitalization, her blood cultures tested positive for M. abscessus complex and antimicrobial sensitivities remained pending. And at this point, Puritan in the lab, she was pancytopenic, elevated inflammatory markers, and we did obtain sputum cultures. Of course, as chest physicians thinking that this was maybe pulmonary disease disseminated, her sputum cultures were negative for acid phosphosylase. So ID was involved on this case, and we started her on IV amikacin, lenazolid, azithromycin, and IV meropenem, which was later deescalated to IV cefoxitin. Her blood cultures remained positive on day five, all the way through about two weeks, two weeks into her hospitalization. And even, unfortunately, she progressed to septic shock. She complicated with multi-organ failure, requiring intubation and ICU support. And unfortunately, the family decided to do palliative withdrawal of care, and the patient did expire. And even on her post-mortem blood cultures, because we continued to follow the case, despite having received maximal medical therapy, her blood cultures still remained positive for M. abscessus. So these were the sensitivities that came back much later, unfortunately, just showing that her amikacin was susceptible, cefoxitin showing intermediate susceptibility as well as imipenem, and then lenazolid also being susceptible. So just going into our discussion, non-tuberculous mycobacterium infection, or NTM, they're ubiquitous in our environment. They're found everywhere, soil, water. They even have been colonized in hospital water supplies. They can cause a myriad of clinical syndromes and disease, typically in what we're most commonly known for, pulmonary involvement, of course, but they can cause superficial lymphadenitis, especially in the pediatric population. Skin and soft tissue infections, which we'll focus on today, after usually direct inoculation after trauma, surgery, sometimes there's been case reports of pedicure salons kind of harvesting in their tubs and stuff, and disseminated disease being definitely most common in the HIV-AIDS population, as we would assume, but definitely in patients who have underlying immunologic disease, hematologic malignancy, and other immunocompromised states. Determining disease incidence and prevalence is very challenging because NTM is not a reportable disease by the CDC because it's not contagious, so we don't really know how frequent it is out there, and our index of suspicion should be high. Diagnostic challenges, from the pulmonary disease standpoint, we know that we should have kind of the triad of clinical radiologic and microbiologic evidence to diagnose, but when we're talking about extrapulmonary disease, sterile collection and isolation of the organism from an affected site is diagnostic. Unfortunately, in our patient, her course was so rapidly progressive that we never really got like a skin biopsy, which probably would have been the best thing for her, or from a diagnostic perspective, but just her clinical course really didn't allow us to do that. And I put in quotations, rapidly growing NTM, because it really is not, it's really not rapid, compared to its slower-growing partners, but takes seven days on culture to test positive, so there's usually, and can be a delay in diagnosis, which therefore delays treatment. So you have an AFB positive that shows NTM, now what do you do? And the most important thing is that you speciate out these organisms, because treatment depends on it, because what you worry about is antimicrobial, inducible resistance, especially in amikacin, and your macrolides. A high index of suspicion is necessary for a timely diagnosis. This was a retrospective case series where we looked at 63 patients with confirmed rapid-growing microbacterial soft tissue infections, and it took 86 days on average, from onset of symptoms to culture positive. M. abscessus was typically found in patients that were older, immunocompromised, and especially multiple lesions, 62% of those patients versus 11% were shown to be definite M. abscessus infection. It's rare, it carries a poor prognosis, fatal in an immunocompromised patient. Keep in mind if you see a patient that has these kind of violacious purple skin nodules, they follow kind of this lymphatic, you know, ascending presentation, just try to keep it in the back of your mind, especially if these patients are immunocompromised, because it is a manifestation of immunologic defect. And in conclusion, our patient, she was highly susceptible because of her acquired immunodeficiency, having RA and being on corticosteroids, even after minor skin trauma after a spider bite, this is our first, to our knowledge, the first reported case of an M. abscessus bacteria from a spider bite, and systemic mycobacterium infection in the immunocompromised patient with suspicious skin findings should definitely warrant the proper workup in the right clinical setting. Next, I welcome Dr. Rahid Mohamed to present a case of severe disseminated monkeypox. Hello, everybody. So today we're gonna be talking about a case of severe disseminated monkeypox in an immunosuppressed non-vaccinated patient. First death report in New York City. My name is Rahid Mohamed. I am a critical care fellow at the Mount Sinai Hospital in Manhattan, New York. I have no financial or any other disclosures relevant to this presentation. So for our objectives today, we're gonna be talking about monkeypox, how it presents, how it's managed, and then really focus on some of the complications that can arise, some of which are not common to us. So the case, this is a 53-year-old African-American gentleman with a history of renal disease who underwent transplant in early 2022, had complications, notably BK viremia, later that year, who then presented in October of 2022 for back pain and the skin rash that had been going on and progressing for about a week. The patient did report to us that he recently moved in with his son who suffers, who has a diagnosis of untreated HIV-AIDS, and per the patient, the son did have an onset of this identical rash months prior to this patient's presentation but never saw any medical attention. So regarding our patient, vital signs, patient was afebrile, was a little bit tachycardic, but notably on physical examination, there were these centrally umbilicated pustules, notably on the face, neck, trunk, upper back, and extremities. In these images here, you see the described lesions in the middle of the face here to the nose bridge and then on the right side of the neck. Again, raised centrally umbilicated lesions with some hyperpigmentation there in the center. Again, here we see these same lesions on the upper back and the upper interior chest, and notably, these lesions all look to be in the same stage of healing, which is important regarding this case. So when we see centrally umbilicated lesions, a short differential that came to our mind in the ICU was, of course, molluscum, chiral disease, given the fact that this is a renal disease patient, cryptococcus, and then monkeypox came to our mind. And the reason monkeypox came to our mind was because we were aware of the presentation that monkeypox can, the way monkeypox can present. And classically, monkeypox can affect face, trunk, extremities, and anogenital regions. In our patient, face, trunk, extremities were mostly affected. The rash can be painful, it can be itchy, especially if crusting occurs or once crusting occurs. Usually, you have a few lesions, but you can have several hundreds, although more than 20 is not typical. And this is the important part. Lesions are generally in the same stage of healing. And in this next slide, it depicts the classic progression for monkeypox, which again, I don't know if many intensivists are aware of this, but earlier on, the lesions can appear as macules, non-raised. They then can raise and become pustules within several days, eventually turn into vesicles, and then pustules here towards five to seven days. Again, you see the centrally umbilicated raised lesions. Later on, the lesions could fall off, scab over, and leave areas of hyperpigmentation. And our patient, again, was presenting with these raised pustular lesions with centrally umbilicated marks. So since monkeypox can present along the spectrum, the differential must be broad, so it shouldn't be limited to just those four diagnoses that we mentioned. So you should consider all of these diagnoses, especially in somebody who's immunosuppressed. And we did, and we'll talk about the workup that we sent. And we're not gonna go into all of these diagnoses, of course, but according to the CDC, you should suspect monkeypox if somebody presents with a lesion that could fall along that spectrum who also has greater than one of these findings within 21 days of the rash onset. So if you've had contact with somebody who's high-risk, or if you've had contact with somebody who has a similar rash that could be monkeypox, if you've traveled to a country endemic to monkeypox, or if you've had contact with an African endemic animal, whether live or dead, for instance, a lab personnel. So our patient specifically did have contact with somebody who had a similar rash, and that person was also considered a high-risk patient, knowing that he was undiagnosed, untreated HIV AIDS. So regarding our patient's clinical course, the patient did have a profound leukocytosis with the bandemia, notably also anemic thrombocytopenic, did have a transaminitis, two to one ALT to AST, without significant evidence of hemolysis. And then while in the ED, the patient actually experienced acute hematemesis, and a lot of focus was placed on that. MTP was initiated, GI was consulted for possible endoscopy, and the patient was admitted to the transplant ICU. Again, he was a kidney transplant patient. Monkeypox was suspected, proper precautions, including contact respiratory precautions were ordered, and then dermatology and infectious disease were consulted, and we immediately called the CDC, and we sent out a monkeypox PCR, which was sent from skin sample. We started the patient on empiric antibiotics, antivirals, and then per the CDC, tecovirumat was initiated as well. These are some of the additional viral tests that were sent. Again, as stated earlier, the differential must be broad, and somebody such as this who presents as sick as he was. And then these are some of the non-viral tests that we sent, including histoplasma, aspergillus, and cryptococcus. So on the following day, the patient did go for an upper endoscopy, which showed numerous rays and friable lesions throughout the esophagus and the stomach. Unfortunately, no endoscopic interventions or biopsies were performed due to the friability and high risk for hemorrhage. So regarding the findings, serologic and skin testing did come back positive for monkeypox virus PCR. Serologic testing was also positive for CMV, BK virus, and EBV, but skin testing was negative for these organisms, and we sent a smear that didn't show any evidence of parasites. No bacteria grew on blood cultures, and then fungal and opportunistic testing was otherwise negative. Our patient's outcome, he did decompensate, septic shock, respiratory failure, did get intubated, developed liver, kidney failure, some multi-organ failure, and then within days had a cardiac arrest, PEA arrest, and then subsequently passed away. The case was transferred to a medical examiner for autopsy, which did confirm disseminated monkeypox lesions in the esophagus and stomachs, and biopsies of these lesions were negative for CMV or BK virus, which actually confirmed our suspicion of monkeypox. So our main discussion points, monkeypox can disseminate, especially in immunosuppressed patients, and several complications can include sepsis, hematologic abnormalities, so in our patient, there was anemia, there was thrombocytopenia. Those are documented in the literature, as is organ failure, but this was the first case of hematemesis from monkeypox-induced esophageal gastric lesions. And in patients who present high risk, who have such a hemorrhagic shock with lesions, the possibility for rapid decompensation is possible, even if you promptly start appropriate treatment. In this case, we believe that we did. So in conclusion, this is the first death from monkeypox reported in New York City, and the first disseminated case resulting in hematemesis and hemorrhagic shock from esophageal and gastric lesions. And the main takeaway for everybody listening is clinicians must be aware of the potential for fulminant monkeypox in any high-risk patient who develops rash and gastrointestinal bleeding. And with that, I'd like to thank you all, and don't forget to evaluate the session in the app. Next, I invite Dr. Dishant Shah to share a case of anicteric leptospirosis. Hi, everyone, I'm a second-year Palm Creek fellow at Westchester Medical Center, and I'm here to present a case of anicteric leptospirosis present against ARDS. I do not have any disclosures. Okay, so leptospirosis is a spirochetal zoonotic disease. Estimated worldwide incidence is more than one million cases. But it is mainly endemic to like South, Southeast Asia, Oceania, Caribbean, and parts of sub-Saharan Africa and Latin America. We don't see a lot of cases in the U.S., and I think that's why, I mean, there's one of, something that I wanted to present. So less than 150 cases are reported annually in the U.S., and outbreaks have occurred in Florida, Puerto Rico, U.S. Virgin Islands, and here in Hawaii, especially after heavy rainfall and flooding in urban areas. So there's a picture from 2000 Eco Adventure Multisport Race that was held in the Malaysian Borneo, and more than, like close to 40% of the people develop leptospirosis during this event. So our patient is a 50-year-old female with pre-diabetes hyperlipidemia who presented with, who presented to the emergency department for abdominal pain and poor oral intake. And she denied any nausea, vomiting, diarrhea, constipation, melanin, hematochysia, cough, shortness of breath, chest pain, fever, or any kind of weight loss. Initial vital signs, she was hypotensive, borderline tachycardic, not febrile, and a 95% saturation on room air. She received three liters of lactated ringers for hypotension, and her blood pressure did not really improve a lot, so hence she was started on low-dose presses and broad-spectrum antibiotics for possible septic shock. Because this patient came in with abdominal pain, that's why we got a, okay, before that, so labs, mild leukocytosis, thrombocytopenia, creatinine was four, we did not know the baseline creatinine at that point in time. Pilirubin was 1.2, MAG was low, lactate was 5.1. And COVID, flu, and RSV were negative. Because this patient presented with abdominal pain, patient got a, I mean ideally should have gotten only like abdomen, CT abdomen and pelvis, but then for some reason also got a CT chest. And this is what, this is what the CT chest showed. It basically revealed like bilateral ground-glass opacities and reticulonodular opacities. Because the patient was not getting better on like low-dose presses, that's why a center line was placed. Shortly after this, patient started developing shortness of breath, respiratory distress, and had to be intubated for respiratory failure. And this is the chest X-ray post-intubation. So if you look at it, I mean, center line is there on the right side, but the pneumothorax is on the left. And of note, there were attempts made on the left side to place a center line, which were unsuccessful. This is, so a chest tube was placed on the left side, as you can see over here. And then the remaining results, basically respiratory PCR later showed positive for rhinovirus and enterovirus. After intubation, PF ratio was 110. Initiated on lung protective ventilation, patient was paralyzed, prone, and the presser requirements at this time included Levo 20 and vasopressin. Patient was also started on stress-steroids. PF ratio improved, patient was continued to be paralyzed, patient was not prone on the next day. Urinalysis, urine culture were negative. Blood culture from day one showed as epidermidis, and leptospira antibody and PCR were sent just because of local high prevalence in one of these hospitals in the Bronx. As you can see, chest X-ray continued to worsen, but PF ratios were slightly stable-ish. Patient was off paralysis, shock was getting better, and blood culture is negative, and urine legionella was negative. Despite this, patient was initially started on, like, vanc, cefepime, and doxycycline, and we continued doxycycline at this point in time because of suspicion for leptospirosis. Levo requirements continued to come down. By day two, we did not really isolate anything from respiratory or blood cultures. That's why a decision was made to perform bedside flexible bronchoscopy, and when we performed a BL of the right lower lobe, we basically found diffused alveolar hemorrhage. That's why patient was started on pulse-toe steroids for possible vasculitis, and autoimmune panel were sent. PF ratios continued to get better. Patient was off paralysis, and now just after one day we do this, now the respiratory culture started growing MRSA, and the BL culture also grew GPC, which eventually grew MRSA. On day six, patient was extubated to high-flow nasal cannula. Leptospira IgM came out to be positive on day seven. Patient was transitioned to room air on day 10. Throughout the course, patient received 14 days of vancomycin, doxycycline was continued for 10 days, cefepime initially, and once the Leptospira IgM was back, the patient was switched to cefaraxone, and then ultimately discharged on day 14. This is in summary, basically, as described, you know, day one, basically, patient was intubated. Chest tube was placed. By day four, we figured that patient had DAH. Day seven, chest tube was removed, and patient was discharged. Of note, if you look at steroids, patient got three days of streptosteroids, hydrocortisone, 50 milligrams Q6, and pulse dose for another three days, 500 methylprednisolone for three days. So there are two known forms of leptospirosis, ecteric and anecteric, and pulmonary manifestation is uncommon in the ecteric form, and not typically described in the anecteric form. And I'd also mentioned bilirubin, which is normal. So this, our patient was really an anecteric form of leptospirosis. And to the best of our knowledge, this is the first reported case of ARDS in the United States. And despite the pulmonary complication had high mortality rates in general, our patient did fine. And of note, this patient also had hypomagnesemia, which is like a classic finding that is found in leptospirosis. And we could not really, I mean, we kept repeating magnesium and we could not really figure out what was, we, or any other reason for hypomagnesemia. So maybe this was just all leptospirosis. So transmission pathway, basically, mammals and environmental, environment like soil and water are predominantly reservoirs. Usually rodents are asymptomatic and other mammals are symptomatic. And the infection could be transmitted to humans through any of these sources. As I mentioned, two forms, anecteric and ecteric. Anecteric initially presents as acute phase, which is mainly flu-like syndrome. And then immune phase has aseptic meningitis and uveitis. And the ecteric form classically has liver failure, kidney failure, and fever. And as I mentioned, these patients could also have DAH and ARDS. This is conjunctival suffusion, so if you look at it, it doesn't really have any exudates, so it's not really conjunctivitis, and there's dilated blood vessels. So diagnosis, it's really compatible febrile illness. Mainly, the main thing is PCR and or positive serologic testing, differential diagnosis, sepsis, vasculitis, pulmonary syndrome, and other malaria, dengue, typhus, typhoid. Treatment includes doxycycline and azithromycin for seven days. Severe cases, we can do doxy versus third-generation cephalosporin. Corticosteroids don't really have a well-proven role, but they can be used as an adjunct. And yeah, so pretty much. I mean, usually, leptospirosis with pulmonary involvement has very bad prognosis, but because we were able to diagnose it earlier, I think this patient is just fine. Next, I welcome Dr. Eric Carnevale to present a case of pneumorhachis, pneumoperitoneum, pneumo-retroperitoneum, say that three times fast. All right, good morning, everyone. Yeah, so the title of my presentation is Pneumorhachis, Pneumoretroperitoneum, Pneumoperitoneum, and Pneumominiosteinum, an unusual presentation of cannabinoid hyperemesis syndrome in a young, healthy patient. My name's Eric Carnevale. I'm a second-year internal medicine resident at Case Western in Ohio, and I have nothing to disclose. So kind of just some general lesson objectives here. I'm just gonna present an unusual case, highlighting mainly the imaging findings of this patient, which were the most impressive of the case, just bring some awareness to a rare but potentially fatal consequence of cannabinoid hyperemesis syndrome, and then kind of just briefly touch on some implication associated with cannabis legalization and kind of public use trends in the United States. So kind of just starting off with some history. It was a 19-year-old Caucasian male presented to an outside hospital ED for severe nausea, vomiting, and abdominal pain that had been going on for the past two days. He reported daily heavy cannabis use for the past multiple years. He also reported that kind of warm showers and warm baths kind of relieved the symptoms temporarily for him. These were, this was the initial physical exam at the outside hospital before he kind of came to us, highlighting mainly just the crepitus that can be felt along the bilateral upper anterior wall, kind of extending into the upper anterior or posterior neck and extending down the back. He also had some mild diffuse tenderness in all abdominal quadrants and was tachycardic, but otherwise, exam was kind of unremarkable from that standpoint. These were the initial labs at the outside hospital ED, mainly noting a profound AKI in a young patient with a normal creatinine, as well as a profound leukocytosis of 26.4,000. The imaging was obtained at the outside hospital, mainly in the form of a CT head and neck, as well as a CT chest, abdomen, and pelvis. So the kind of first stack that I'll show you is a sagittal view, kind of highlighting the neck. I'm not sure if you're able to see the cursor on here, but mainly you can see subcutaneous air under the jaw when it progresses as well as into the paraspinal musculature. I'm not sure if I can rewind it so you can see it again, but the air, if you want to focus on the spinal canal, air in the epidural space itself, that's called pneumorhachis. That was a new term that I had to learn, actually, for this, so pretty extensive, as you can see. The next stack is an axial view of the chest, kind of also highlighting the parasternal air kind of escaping down the back, as well as air in the upper anterior chest wall. And then as we scroll down a little bit further, you can see kind of subcutaneous air in the anterior, middle, and posterior medastinum area. This one's a little bit longer, so I won't look at it the whole way, but I couldn't be using the laser pointer. The third and kind of final stack is a CT abdomen and pelvis sagittal view. This is where you can kind of see the air in the, you'll see it kind of pop up here in the peritoneal space, in the retroperitoneal space behind the kidney, and then you can kind of see it in this paraspinal musculature, and then also within the spinal cord all the way down to the lumbar space. This was all done at the outside hospital. They also got a GI esophogram that didn't show any esophageal or pharyngeal contrast extravasation, so they kind of hinted at a presumed upper oropharyngeal lesion. So I just included these in case the videos didn't work when I got here, but I'm just planning ahead. Kind of just talking about the hospital course. So he was transferred to our ICU where I saw him in consultation with thoracic surgery and otolaryngology. He was treated conservatively with IV vancomycin, IV piperacillin tezovactam, and IV fluconazole for presumed kind of mediastinous with this pretty significant leukocytosis. And he performed a direct video laryngoscopy as well as a repeat esophogram that also just didn't reveal any sort of sign of kind of the source of the lesion. Luckily, he kind of just improved on his own after 48 hours of observation and supportive care within the ICU. His creatinine significantly improved and his leukocytosis resolved, and he was able to be transferred to the floor after 48 hours of observation. And of course, he was counseled on the importance of a complete sensation from marijuana. Kind of just diving into the discussion associated with cannabinoid hyperemesis syndrome used as mainly an extension of cyclical vulmonary syndrome, of course, with the caveat of having kind of chronic and heavy cannabis consumption. Currently, there's 38 states that permit cannabis for medical use and 23 states that have it for recreational use. The Rome IV diagnostic criteria is kind of used to help aid diagnosis of it. It was used or developed mainly for cyclical vulmonary syndrome and kind of has this stereotypical symptoms that present for the past three months. The episodes can last between a day to like less than a week and then you'll have these periods of kind of normalcy between the episodes. Obviously, with the caveat of having the chronic cannabis use as well. There's a few different kind of proposed mechanisms that I came across like in the literature kind of trying to figure out the exact mechanism of this. The first one associated with barotrauma, rupturing the alveolar septa, mainly it was used as a hypothesis for explaining pneumomediastinum in which the breathing techniques to use in the inhalation of marijuana kind of create pressure gradients within the alveolar septa causing rupture and the air can kind of dissect along the perivascular sheets and peribronchial sheets into the mediastinum. But this one really explained the pneumoperitoneum or pneumoretroperitoneum or pneumorhachis that we saw in our patients. So the second kind of mechanism obviously is kind of associated with the Boerheave syndrome in which there's direct rupture in the esophagus or oropharynx kind of leading to air escaping everywhere it shouldn't be. To our knowledge, this was the first case having air in all four of those chambers. I'm not gonna say it again. But there were a few cases associated with cannabinoid hyperemesis syndrome with pneumoperitoneum, pneumoretroperitoneum and then two cases that showed air within the spinal canal itself. Looking at some like ED, like hospitalization and ED visits specifically in Colorado which is what I came across. So cannabis was legalized in Colorado I believe in 2012. So these studies were kind of completed before two years before and then two years after that kind of looking at emergency department visits associated with nausea and vomiting not necessarily cannabinoid hyperemesis syndrome itself but it found like an increase of 40,000 visits between 2010 and then 2014 within those time periods. And then it showed an increase in about 300 hospitalizations associated with that. Nausea and vomiting and kind of cannabis being the presumed underlying factor for that driver in Colorado itself. So just an interesting kind of tidbit and just for us to be aware. Luckily this patient had a good outcome and didn't develop any mediastinitis or anything else associated with that. So I think that's everything I have. These are my references. Thank you all for listening. Does anyone have any questions? Next we have Dr. Mohamed Arian on phenobarbital, ultimate antitussive. Hi, my name is Mohamed Arian. I'm a ICU hospitalist out in Wenatchee. I'm gonna be presenting a case about a patient with refractory coughing that led to multiple intubations and us scratching our head about what to do next. I have no disclosures. So it's a 45-year-old gentleman presented with a three-day history of a cough and nasal congestion. He presented to his primary care provider initially and diagnosed him with a viral URI and he was prescribed some oral steroids and sent home. Symptom progressed over the next 24, 48 hours to the point that his wife called EMS. EMS arrived and found him to be in a state of severe distress, diaphoretic, and they elected to intubate him. Of note, they report when they intubated him with DL that he had swollen, vocal cords appear swollen to them. Past medical history of relevance is he had COVID back about a year ago with severe ARDS requiring intubation and then subsequently had two episodes of oropharyngeal swelling and bilateral vocal cord paralysis that was attributed as a sequelae of COVID-19. They required intubation, tracheostomy, and then he was decannulated within a month. This is all occurring a year prior to this presentation. He had an extensive workup in the ED. Physical exam was really unremarkable, vital signs as well. CBC, BMP, chest X-ray, pro-calc stone, and CRP, everything was unremarkable except for a viral PCR panel that showed human metanumovirus and a cell that's hypercapnic respiratory failure and a pH of 7.3. He was diagnosed with severe post-viral cough syndrome and he was, ENT was consoled and he was admitted to the ICU on steroids, six milligrams every six hours. ENT came, they did their direct laryngoscope, no more appearing vocal cord, no subglottic stenosis, and patient was extubated several hours after the procedure. Immediately afterwards, he had an intractable cough with severe desaturation and hypoxemia. He ended up needing to be re-intubated within four hours given the degree of saturations and inability to bring it up. ENT came in again, they did another direct laryngoscope, where the bronchoscopy, removing the ET tube and looking around and then placing it back in and everything was negative. So we added gabapentin, continued the steroids, and the plan was continue for another 48 hours and then extubate. Of course, the patient extubated himself a couple hours before the 48-hour mark. Immediately afterwards, again, he had intractable cough, but this time he was holding saturation with four liters of humidified air. And over the next 24 hours, he did progress to astritis sound and became encephalopathic with an ABG done again, demonstrating hypercapnia with a CO2 of 62 and a pH of 7.27. He became somnolent and he ended up being intubated again overnight. Overall, this is his third intubation. So steroids and gabapentin were continued, workup again, what this time was unremarkable, except now the respiratory culture is going to MSSA and you're starting a Cetrax and had a little bit discussion with ENT, the pharmacist and pulmonology as well, and we decided let's extubate on low-dose hydromorphone drip with a dexmedetomidine drip and also start viscose lidocaine. He was extubated again 24 hours later. Again, persistent intractable cough, but again, he was holding his own with four liters of supplemental oxygen, but he was still kind of distressed, but not significantly serious. Over the next 24, 48 hours, and this is when I came on, we switched to viscose lidocaine to nebulize. We started albuterol. We also started something with morphine. Then we did a trial of diazepam pushes, lorazepam pushes, and midazepam pushes, and with the last one being actually the one that offered some relief for a little bit, but didn't really last that long. And we also put him on non-invasive positive pressure ventilation. Of course, we did the obligatory CT scan, which was largely unremarkable. I'm gonna just post it up here for you. He had progressive symptoms over the next 24 hours, multiple desaturation. Again, diaphoresis can never really have an answer to any questions. Visibly distressed and minimal benefit at this point, noted from any medications that we're giving. So now what? We had another talk. Again, pulled the whole crew together, ENT, pulmonology, ICU pharmacy, and reevaluated diagnosis, thinking recurrent and allergenal nerve irritation. What are the pathophysiology process of vagal neuropathy? And this is kind of presenting like not really a chronic cough, but it's still less than two weeks, so an acute cough. But in review of literature, Gabby Penton has been proven to be efficacious. And it has a peak effect two hours and half-life of seven hours, but he's on and off, intubated and extubated. And every time we extubate him, we can't really give him anything, can't tolerate a nasogastric tube, we can't swallow anything, which is already evident by his MSSA, which was likely aspiration. So we tried to figure out what is the closest mechanism to Gabby Penton that we could do intravenously. And we decided on phenobarbital. From a mechanism point of view, they all kind of work on Gabby. We already tried benzos and Gabby Penton, and then phenobarbital kind of had a similar mechanism. Dosing-wise, we implemented, we used a phenobarbital for alcohol withdrawal protocol at our facility, so we kind of decided on one of the PRN doses, which is 130 to 260 milligrams. And then the idea was to give more if he started, if there was no effect or there was some improvement noted. Within 10 minutes of giving IV phenobarbital dose, he had improvement within 10 minutes, and at a two-hour mark, completely stopped coughing. To the point, speech therapy came. They evaluated him. It was clear that he was talking in full sentences. We watched him for another 24 hours in the ICU, downgraded him another 24 hours on the floor, and he had no recurrence of the cough. Discharged him on 300 milligrams three times a day, and we referred him to a specialist in Wenatchee. So take-home point is, if you have a patient with refractory coughing that you have to intubate multiple times, consider phenobarbital. But of course, this needs to be reproduced without confounding medications, and also study for the optimal dosing at that point. And that's it. Thank you. And to close us out, I invite Dr. May Abdullah. Well, thank you very much for attending this session. I find my title's a mouthful, so I put a picture to describe. I don't know whoever watched Brain on Fire. This is exactly, my patient had the same disease. So my name is May Abdullah. I'm a first-year pulmonary critical care fellow at St. Louis University Hospital in Missouri. I have no financial interest to disclose, and my objective to this presentation is to really hopefully achieve that, identify the impact of the pharmacological features of orfenadrine drug in patient with NMD, autoimmune receptor encephalitis, and discuss the impact of orfenadrine dose reduction and or withdrawal, and really cultivate the culture of practice mindful pause before making changes in medication, especially with transitioning ICU team one week to next. So I'm gonna start with a case, which is my case. She is a 13-year-old African-American female. She had no past medical history. She came in with two weeks of headache, confusion, unusual behavior like doing things, standing out in the rain, saying things like doesn't make any sense, mumbling her words. Apparently, she was seen in outside hospital with the same symptoms, had a workup done that was negative. So when she came to our hospital, she was initially admitted to the general pediatric floor. However, one day after, she had decompensation rather quickly and was transitioned to the pediatric ICU. Her vitals initially was really unremarkable, and in terms of physical examination, she had a progressive decline in mentation, dyskinetic movement with her orofacial muscles and the limbs. She was a physic and dysarthric. She had bilateral clonus and brisk patellar tendon reflux and really was not able to follow commands. Therefore, she was intubated for airway protection at the time. Her initial workup did really show, was unremarkable overall, CBC, CMP, utox, was all under-revealing. And then we had underwent like a lumbar puncture for her, which did show increase of the titer of her NMDA receptor and lymphocytic pleocytosis. She had an MRI that did show basal ganglia, enhancement of the anterior cardiac nucleus, and she had a CT abdomen that did show 4.3 centimeter of the ovarian teratoma on the right side, for which she underwent a oophrectomy, the right oophrectomy. And clinical course, she basically was intubated and trached chronically, had underwent, it's not working, okay. She was treated with plasmapheresis for that, as well as high dose of corticosteroids, IVIG, rituximab. However, despite all these treatments, she had a cardiac arrest that precipitated by bradycardia while in prosthodox. I couldn't figure any better way of describing this kinetic movement, but it was just like a jigsaw kind of doll. Everything's moving uncontrollably, and which resulted in bleeding that induced by self-inflicted trauma like in massive transfusion. And she had a feeding intolerance requiring to be on TPN due to pneumatosis intestinalis. So these are all the multiple medication that was used only to just manage her movement disorder, as well as increased muscle tone. And that included gabapentin, baclofen, carpenazepine, clonidine, tramadol, clozapine, and orfenadrine, which is a central muscle relaxant. This is a scale that's actually, I adopted it from the American Association of Psychiatric Pharmacists that's used in patients who started dyskinesia to assess the progress of their movement while on treatment. So we kind of used this, we adopted this for her to be able to follow her progress while she was on those medication. So this is like a graph on the y-axis. You'll see the score up there. When initially admitted, she had a score of 36, and towards the end of November, she had almost zero, like three down while on specifically tramadol. As you see here with overlapping the drugs, the specific two medication that I really want to highlight here, the tramadol and orfenadrine. Tramadol actually had a non-competitive NMDA receptor. Antagonists work differently. However, orfenadrine also had a non-competitive NMDA receptor entity. So she used it for up until beginning of December, and that was her movement was all managed. However, she had the increased muscle tone. She started on orfenadrine at the time, and then abruptly was changed, dose reduction from 120, the doses here on the y-axis, to 30 because of the intolerance to PL. She had switched to IV drugs, and you can see within three, four days, she had worsening of the dyskinetic movement, specifically the orofacial ones. So, and if we know that this tramadol has a short half-life, it's about six hours compared to orfenadrine, which is about 12 to 14 hours. So it can't be the tramadol that she had caused the triggers for her symptoms. So this is just a brief description of how orfenadrine works. It's just, it's a central muscle relaxant, a chemical structure exactly like Benadryl with a methane group. It does block the histamine receptors. It also blocks the non-competitive NMD receptors, as well as anti-cholinergic and anti-spasmodic, and the outcome is alleviating dyskinesia. On the other hand, tramadol, as we all know, it's an opioid mu-receptor that inhibit the ascending pain pathway, as well as descending through the norepinephrine and serotonin reuptake inhibitor, as well as non-competitive NMD receptor, specifically the unit GLU-N2B. And the way how it works, it reduce clustering and internalization of the receptor, and therefore attenuation of the dyskinesia, sorry. So in conclusion, take-home messages here is really that worsening of dyskinesia related to my patient with NMDA receptor autoimmune encephalitis was successfully managed by identifying and treating the withdrawal itself by actually resuming the drug and slowly weaning off over about a week. And then it is really imperative to cautiously wean orphenogene-like drugs to minimize the side effects. And to this date, I don't think there is any specific recommendation exists to prevent withdrawal from orphenogene. With that, I would thank you all, and don't forget to evaluate. Thank you.

disseminated mycobacterium abscesses

immunocompromised patient

monkeypox infection

immunosuppressed patient

anicteric leptospirosis

severe coughing

autoimmune receptor encephalitis

diagnosis challenges