Podcasts about Procalcitonin

For this episode we are joined by EBM guru, Dr. Brian Locke, who deftly breaks down all of our statistics questions. Is half dose DOAC as good as full dose DOAC for preventing VTE, and does it reduce bleeding risk? Can procalcitonin reduce duration of antibiotics for infections without compromising mortality rates? Can LLMs like GPT-4 help physicians manage patients better? Can reinforcement learning models predict when to start vasopressin in patients with septic shock? What is the risk of resuming anticoagulation in patients with atrial fibrillation and prior intracerebral hemorrhage? Is high flow nasal cannula as good as non-invasive ventilation for different types of respiratory failure? We answer all these questions and more!Half Dose DOAC for Long Term VTE Prevention (RENOVE)Biomarker-Guided Antibiotic Duration (ADAPT-Sepsis)GPT-4 Assistance for Physician PerformanceOptimal Vasopressin Initiation for Septic Shock (OVISS)DOACs for A fib after ICH (PRESTIGE-AF)High Flow Nasal Cannula vs NIV for Respiratory Failure (RENOVATE)Music from Uppbeat (free for Creators!): https://uppbeat.io/t/soundroll/dope License code: NP8HLP5WKGKXFW2R

W jaki sposób sprawdzić, czy w organizmie toczy się stan zapalny, zwłaszcza ten przewlekły? To jedno z najczęstszych pytań, jakie dostaję – i nic dziwnego! Stan zapalny nie zawsze daje jednoznaczne objawy, a jego wykrycie może wymagać wykonania różnych badań. Jakie markery świadczą o obecności stanu zapalnego? Czym różni się CRP od OB i kiedy warto je zbadać? Czy da się określić stan zapalny w konkretnym miejscu w organizmie? W jaki sposób zbadać przewlekł stan zapalnym o niskim nasileniu? Na te i inne pytania odpowiem w dzisiejszym odcinku. Zachęcam Was do regularnych badań. A gdybyście chcieli skorzystać z domowego pobrania badań laboratoryjnych z krwi to ze stałym kodem DRKARABIN20 otrzymacie 20% zniżki na na badania laboratoryjne z pobraniem w domu #uCiebie z #uPacjenta. Kod działa przy zamówieniu powyżej 250 zł na wszystkie badania i pakiety. Możecie skorzystac z mojego autorskiego pakietu badań profilaktycznych “długoWITALNI”: https://upacjenta.pl/landing-page/pakiet-dlugowitalni lub innych dowolnych badań. A jeśli potrzebujecie konsultacji stylu życia i pomocy w interpretacji badań napisz do mnie na adres konsultacje@drkarabin.pl a wyślę Wam więcej szczegółów. Ten materiał nie stanowi zamiennika wizyty lekarskiej. Nie jest też poradą zdrowotną, ani nie służy do diagnozowania ani leczenia chorób. Materiał ma charakter wyłącznie edukacyjny. Autorka nie ponosi odpowiedzialności za sposób wykorzystania przedstawionych informacji. Piśmiennictwo do odcinka: van den Brink W. i wsp. Current and Future Nutritional Strategies to Modulate Inflammatory Dynamics in Metabolic Disorders. Front Nutr. 2019 Aug 26:6:129. Del Giudice M. i Gangestad S.W. Rethinking IL-6 and CRP: Why they are more than inflammatory biomarkers, and why it matters. Brain Behav Immun. 2018, 70, 61-75. Choroby wewnętrzne, pod redakcją Szczeklik A., Medycyna Praktyczna Kraków 2021 C-reactive protein concentrations as a marker of inflammation or infection for interpreting biomarkers of micronutrient status. Vitamin and Mineral Nutrition Information System. Geneva: World Health Organization; 2014 (WHO/NMH/NHD/EPG/14.7; http://apps.who.int/iris/bitstream/10665/133708/1/WHO_ NMH_NHD_EPG_14.7_eng.pdf?ua=1, accessed [date]) Dembińska-Kieć A. Diagnostyka laboratoryjna z elementami biochemii klinicznej Edra Urban & Partner 2021 Samsudin I. i Vasikaran S.D Clinical Utility and Measurement of Procalcitonin. Clin Biochem Rev. 2017 Apr; 38(2): 59–68. Jukic A. i wsp. Calprotectin: from biomarker to biological function. Gut 2021 Oct;70(10):1978-1988. O'Connor M.F. i wsp.To assess, to control, to exclude: Effects of biobehavioral factors on circulating inflammatory markers. Brain Behav Immun. 2009 Apr 21;23(7):887–897. 0:00 Intro  0:37 - Wstęp 02:20 - W jaki sposób zbadać stan zapalny? 04:10 - Białka ostrej fazy - czym są i jakie funkcje pełnią? 07:19 - Białko CRP - co to za marker i kiedy warto go badać? 10:10 - Czym jest wysokoczułe białko CRP? 12:14 - Jak różnicuje się zakażenia bakteryjne od  wirusowych na podstawie białka CRP? 14:26 - Jakie wady ma białko CRP jako marker stanu zapalnego? 15:54 - Czy OB jest dobrym markerem stanu zapalnego? 20:38 - Kiedy warto badać OB? 21:45 - CRP czy OB - który marker wybrać? 23:04 - Kontekstowe markery stanu zapalnego: Prokalcytonina - kiedy warto ją zbadać? 26:02 - Swoiste markery stanu zapalnego: Kalprotektyna - kiedy warto zbadać i w jaki sposób to robić? 29:20 - Przeciwciała - czy mogą wskazywać na stan zapalny? 32:33 - Czy w morfologii można zobaczyć stan zapalny? 34:16 - Jaki jest najlepszy sposób na badanie stanu zapalnego w organizmie? 36:33 - Jak zbadać przewlekły stan zapalny o niskim nasileniu? 40:57 - Wpływ allostazy na parametry krwi

0:16 Intro 2:29 Updated community-acquired pneumonia guidelines 5:41 Diagnostic tools for CAP following COVID-19 9:35 Procalcitonin levels as a biomarker 12:30 The CAP treatment algorithm 18:36 Best practices for antibiotic stewardship 20:40 New CAP therapies on the horizon 22:36 ACIP recommendations for vaccination 24:30 Remaining areas of CAP uncertainty 26:30 Final thoughts 27:25 Outro Featuring infectious disease expert Dr. Thomas File of Summa Health in Ohio, this episode delves into how community-acquired pneumonia has been affected by the COVID-19 pandemic. It additionally covers the role and importance of antibiotic stewardship and the concern of ‘superbugs' due to antimicrobial resistance. Want more Lungcast? Visit us at HCPLive.com/podcasts/lungcast or www.lung.org/professional-education/lungcast

2024 SCCM Congress: Tuesday Special Guests: Karen Berger, PharmD, FASHP, FCCM, BCCCP, BCPS Melanie Smith Condeni, PharmD, FCCM, BCPS, BCCCP Julie Farrar, PharmD, BCCCP Lama Nazer, PharmD, BCPS Joanna Stollings, PharmD, FCCP, FCCM, BCPS, BCCCP Andy Webb, PharmD, BCCCP 03:05: Star Research Presentation: “Effect of Antipsychotics on Agitation in ICU Delirium: Secondary Analysis of a Randomized Trial” featuring Joanna Stollings 10:43: Star Research Presentations: “Procalcitonin and Antimicrobial Utilization in Critically Ill Cancer Patients with Sepsis (PRO-CAN)” & “Diagnostic and Prognostic Value of Procalcitonin in Critically Ill Cancer Patients with Sepsis” featuring Lama Nazer 25:32: Clinical Pharmacy and Pharmacology (CPP) Year in Review presenter and moderator roundtable discussion featuring Karen Berger, Melanie Smith Condeni, Julie Farrar, and Andy Webb 2024 SCCM Congress website: https://congress2024.sccm.org PharmacyToDose.com  @PharmacyToDose  PharmacyToDose@Gmail.com Learn more about your ad choices. Visit megaphone.fm/adchoices

CHEST September 2023, Volume 164, Issue 3 Lisa Hessels, MD, joins CHEST Podcast Moderator, Dominique Pepper MD, to discuss use of a procalcitonin-guided antibiotic protocol to safely reduce the use of antibiotics in patients with a COVID-19 infection. DOI: https://doi.org/10.1016/j.chest.2023.04.032   Disclaimer: The purpose of this activity is to expand the reach of CHEST content through awareness, critique, and discussion. All articles have undergone peer review for methodologic rigor and audience relevance. Any views asserted are those of the speakers and are not endorsed by CHEST. Listeners should be aware that speakers' opinions may vary and are advised to read the full corresponding journal article(s) for complete context. This content should not be used as a basis for medical advice or treatment, nor should it substitute the judgment used by clinicians in the practice of evidence-based medicine.

On episode #32 of the Infectious Disease Puscast, Daniel and Sara review the infectious disease literature for the weeks of 6/21 – 7/4/23. Hosts: Daniel Griffin and Sara Dong Subscribe (free): Apple Podcasts, Google Podcasts, RSS, email Become a patron of Puscast! Links for this episode Clinical characteristics and outcomes among travelers with severe dengue (AIM) Phase 3 randomized trial of Bulevirtide in chronic hepatitis D (NEJM) Increased peripheral inflammation associated with structural brain changes and reduced blood flow in virologically controlled people with HIV (JID) Sustained viral suppression with dolutegravir monotherapy over 192 weeks in HIV patients (CID) Side-by-side comparative study of the immunogenicity of the intramuscular and intradermal rabies post-exposure prophylaxis regimens in suspected RABV exposed individuals (CID) Reliability of admission procalcitonin testing for capturing bacteremia across the sepsis spectrum (CCM) Early discontinuation of antibiotics in patients admitted with clinically suspected serious infection but negative cultures (OFID) Short-course therapy for urinary tract infections in children (JAMA) Autochthonous Leprosy in the United States (NEJM) Management of pediatric pneumonia (CID) Added value of (1,3)-β-D-glucan for the diagnosis of Invasive candidiasis in ICU patients (Infection) Selection for insecticide resistance can promote Plasmodium falciparum infection in Anopheles (PLOS Pathogens) Locally acquired malaria cases identified in the US (CDC) Nanoplasmonic amplification in microfluidics enables accelerated colorimetric quantification of nucleic acid biomarkers from pathogens (NN) Music is by Ronald Jenkees

In this episode, Marion Elligsen, BScPhm, MSc, RPh, ACPR; Keith S Kaye, MD, MPH; and Andrew Shorr, MD, MPH, MBA, discuss key considerations for selecting empiric antibiotic regimens in patients with HABP/VABP in the intensive care unit, including: The role of novel β-lactam/β-lactamase inhibitor combinationsUse of clinical predictions scores (eg, Drug Resistance in Pneumonia [DRIP] score) to predict risk for pneumonia caused by multidrug-resistant pathogensApplication of rapid diagnostic testing in critically ill patients with pneumonia, including current limitationsImplementation of advanced antibiograms and clinical prediction scoresClinical utility of biomarkers for pneumonia (eg, procalcitonin)Application of updated nosocomial pneumonia classifications in clinical practiceFaculty:Marion Elligsen, BScPhm, ​ MSc, RPh, ACPR​Practice-Based Researcher​Sunnybrook Research Institute​Antimicrobial Stewardship Pharmacy Lead​Department of Pharmacy​Sunnybrook Health Sciences Centre​Toronto, Ontario, Canada​Keith S. Kaye, MD, MPHChief  Division of Allergy, Immunology and Infectious DiseasesProfessor of MedicineRutgers Robert Wood Johnson Medical SchoolNew Brunswick, New JerseyAndrew Shorr, MD, MPH, MBA​Director​Pulmonary and Critical Care Medicine​Medstar Washington Hospital Center​Washington, DC​Content based on a CME program supported by an educational grant from Merck Sharp & Dohme Corp. Link to full program:https://bit.ly/3HaZpYwLink to downloadable slideset:https://bit.ly/3UxHoqr

Dr. Centor discusses the role of procalcitonin measurement with Dr. Joshua Stripling.

This is our last episode from the PHM 2022 National Conference in Orlando, Florida. For this episode we are recapping and summarizing one of the most attended lectures at the conference, "Procalcitonin: What is it Good For?" We were fortunate enough to be joined by all three presenters of this talk, Drs. Brittany Slagle, Rebecca Cantu and Sara Sanders from Arkansas Children's Hospital and the University of Arkansas. This episode does not have CME associated with it.   We hope you enjoyed these sessions from the PHM National Conference!

If you're a parent, you've probably had this experience many times: Your young child has a high fever, and maybe a sore throat, but you don't know exactly what's wrong. Is it a bacterial infection, in which case an antibiotic might help? Or is it a viral infection, in which case, you just have to wait it out? The symptoms of bacterial and viral infections are often the same, and most of the time, even a doctor can't tell the difference. Viral infections are more common, but sometimes, the doctor will prescribe an antibiotic anyway, if only to help the parents feel like they're doing something to help. But what if doctors didn't have to guess anymore? What if there were a fast, easy blood test that a doctor could run in their own office to look for biomarkers that discriminate between bacterial and viral infections? Well, that's the seemingly simple problem that a company called MeMed has been working on solving for 13 years now. Recently MeMed's first testing product got approval from the FDA, and now the company is finally beginning to roll out it out commercially in the US. And here today to tell us more about how it got built, how artificial intelligence fits into this picture, and how rapid diagnosis could change the practice of medicine, is MeMed's co-founder and CEO, Eran Eden.Please rate and review The Harry Glorikian Show on Apple Podcasts! Here's how to do that from an iPhone, iPad, or iPod touch:1. Open the Podcasts app on your iPhone, iPad, or Mac. 2. Navigate to The Harry Glorikian Show podcast. You can find it by searching for it or selecting it from your library. Just note that you'll have to go to the series page which shows all the episodes, not just the page for a single episode.3. Scroll down to find the subhead titled "Ratings & Reviews."4. Under one of the highlighted reviews, select "Write a Review."5. Next, select a star rating at the top — you have the option of choosing between one and five stars. 6. Using the text box at the top, write a title for your review. Then, in the lower text box, write your review. Your review can be up to 300 words long.7. Once you've finished, select "Send" or "Save" in the top-right corner. 8. If you've never left a podcast review before, enter a nickname. Your nickname will be displayed next to any reviews you leave from here on out. 9. After selecting a nickname, tap OK. Your review may not be immediately visible.That's it! Thanks so much.TranscriptHarry Glorikian: Hello. I'm Harry Glorikian, and this is The Harry Glorikian Show, where we explore how technology is changing everything we know about healthcare.If you're a parent, you've probably had this experience many times: Your young child has a high fever, and maybe a sore throat, but you don't know exactly what's wrong. Is it a bacterial infection, in which case an antibiotic might help?Or is it a viral infection, in which case, you just have to wait it out?The symptoms of bacterial and viral infections are often the same, and most of the time, even a doctor can't tell the difference.Viral infections are more common, but sometimes, the doctor will prescribe an antibiotic anyway, if only to help the parents feel like they're doing something to help.But what if doctors didn't have to guess anymore? What if there were a fast, easy blood test that a doctor could run in their own office to look for biomarkers that discriminate between bacterial and viral infections?Well, that's the seemingly simple problem that a company called MeMed has been working on solving for 13 years now. Recently MeMed's first testing product got approval from the FDA, and now the company is finally beginning to roll out it out commercially in the US.And here today to tell us more about how it got built, how artificial intelligence fits into this picture, and how rapid diagnosis could change the practice of medicine, is MeMed's co-founder and CEO, Eran Eden.MeMed has a growing office in Boston, but I reached him at the company's first office in Haifa, Israel.Harry Glorikian: Eran, welcome to the show.Eran Eden: Thank you very much for having me.Harry Glorikian: It's great to have you here, I know that there's a significant time difference, so I appreciate like but it still looks like it's really bright and shiny out there right now. So what time is it in in Israel right now?Eran Eden: Five o'clock in the evening,Harry Glorikian: It's five o'clock. All right. Well, you guys have a lot more sun than we do anyway because we're in the middle of winter, but absolutely.Eran Eden: So this, here, is actually full of people as well. So yeah, you don't stop innovation as five o'clock in the evening.Harry Glorikian: So, you know, I was looking at your background and I mean, it's really it's interesting. It's diverse. You have a degree in biology, computer science, systems biology. You were first job was in computer vision data and analysis. But then all of a sudden you wound up starting a company that builds sensors and software for infectious disease. Like, how did you end up down this path, and do you feel like everything that you were doing until you got here was preparing you for it?Eran Eden: Well, I think... A great question. So I think, on the face of it, it obviously the background in data science, as you know, in molecular biology, obviously all of that relates to what we're doing is part of our day to day and it is a good starting point. But in reality, there's a very big gap between what I was trained to do and today, my every day, day to day activity. I would say that probably the most important training that I got during my days at the Weizmann Institute has got less to do with differential equations or molecular biology, and it was more about a story that my mentor, Professor Uri Alon, told me when I was three years into the PhD, about three years into the PhD, he asked me, Am I already in the cloud? He said what? And he said, are you in the cloud? I said, Well, what is the cloud? He said, Well, every PhD, every scientist, when you start your PhD, you know, you have you go you go and read the latest papers in Science and in Nature and you see how somebody starts at Point A, makes a hypothesis about point B and then take the straight line from A to B, and then you say, OK, I'm going to do the same thing and you start at Point A, the known. You shoot for the unknown and you start going and suddenly you hit a roadblock. And then you hit another one and another one. At a certain point, you'd really lose direction, which he called the cloud. You're in the cloud. And then if you have enough perseverance and luck, you find a point C which is not exactly where you thought you're going to end. You go there with, you know, your last energy. And if you're lucky enough, then you publish another paper about how you started at point A, went to point C and connected between the two dots with a straight line. And then you have another generation of PhDs that are asking themselves, Well, why am I the only one that's struggling? And that lesson about how to be in the cloud, how to deal with uncertainty, to deal with failure and still move on. That is probably more important in the training that I got to become an entrepreneur and CEO of a company than any specific scientific knowledge.Harry Glorikian: Ok. Yeah, no, I mean, trial and error, dusting yourself off, getting up and moving forward is, you know, my wife calls me crazy when I keep doing it, but I think you have to be a little on the edge to constantly keep repeating and being willing to fail and then stand up and then move on. Maybe it's a, I think I was reading a paper recently that said forgetting quickly is evolutionary, you know, a positive trait so that you forget what happened, that wasn't good and you keep moving forward. So. But let's talk about your company, MeMed, like you started that in, I believe, it was 2009. And what was your founding vision? I mean, if you can talk about what you and your co-founder did when you came up with this idea, I think you were both studying at the Technion at the time?Eran Eden: Yeah, so so he was studying at the Technion, M.D., Ph.D. I was studying at the Weizmann Institute and Data Science and Biology. And frankly, I would love to tell you a story about a vision, but it started with a game. I don't think we had the presumptions to have really something that would grow to what MeMed actually became today. It was playing. We both have had different reasons first of all for doing this. I can say that from my my end, it was probably a pretty big gap between the places, the caliber of where we were able to publish high impact journals. And when I was looking at myself in the mirror and I was asking myself, Is this actually going to have an impact on real patients? I couldn't really see the connection. There's another reason why I decided to found MeMed or co-found MeMed. That's probably off topic for today. We can take this on a beer some time when we meet face to face. But so it's first of all, it didn't start with a vision. It started with a scratch wanting to apply a some of the know how that we had had in converting between molecular immunology and data science, and to try to solve big, ugly problems that don't have a good solution in 21st century medicine and trying to find something pragmatic now rather than having it a eureka moment. You know, some pioneers describe a eureka moment where suddenly you have the best and coolest idea in vision. For us, it was darkness for almost a year rather than the eureka moment. It is was more like an evolutionary process. Trial and error. We tried a bunch of solutions to problems that didn't really exist until eventually we came up with what we want to work with, but again was no, no eureka, and the way that it actually started was again, Kfir was coming from from med school talking about this problem of of AMR, antimicrobial resistance and the problem of distinguishing between bacterial infections and given our different backgrounds, we said that's interesting. How can we apply immunology and then science to try to solve that, and then at that point, we formulated what was to become MeMed's vision. And MeMed is based on a very simple premise, a very simple idea. Our immune systems have evolved to tell us what's going on our bodies and all we do at MeMed is we listen to the immune response with biochemical sensors and machine learning and what have you. And we use that to translate or decode the immune system into insights that can potentially transform the way that we manage patients with acute infections and inflammatory disorders. The first problem we went after, because that's a very lofty goal, was potentially the most prevalent clinical indication on the face of this planet. A child with sniffles. Our elderly patients that coughs. Come to the doc, they have a fever. As a parent, you're many times hysterical, you're asking yourself, is it a bacterial infection or bowel infection. If it's a bacterium, antibiotics. It's a viral infection, chicken soup. And we said, Well, what if we can harness the immune system? What if we could measure or listen to the immune system in real time and use that to try to aid clinicians to tackle this seemingly simple problem? So the vision was listening to the immune response. In the first embodiment of the first problem we went after is this huge intractable problem, B versus V versus. Bacterial versus viral infection. To treat or not to treat.Harry Glorikian: Yeah, I mean, you know, it's funny, you say simple, and I've worked in this area for a long time and now not simple, not simple, but I've been watching dozens of companies over time try and tackle this problem, and everybody always comes at it and says, Yep, we should be able to do it. And I'm like, OK, that's a big hill, you know, to go and try and die on so. But you got FDA approval for your device in the U.S., and I want to talk about that later. But it did take 13 years. Like to, you know which parts of the process turned out to be harder or slower than you thought it would be?Eran Eden: Before I answer that, I just want a minor correction. I didn't say it's simple. I said it's a seemingly simple problem. In reality, it's an extremely difficult problem to go after. I think some of the most the biggest challenges that we have can be phrased in a very simple manner. But as you alluded to, yeah, it's an intractable problem. Bacterial and viral infections are often clinically indistinguishable. And it took us over a decade to take this from my idea on a napkin and grandmother's kitchen. That's where we found with no garage, it was Grandmother's Kitchen to what is considered a landmark FDA clearance that I think many folks did not believe we're going to be able to get this because it required so many innovations, not only on the technological side, but also on the regulatory side. And when you ask why only a decade? I think it's, we're very lucky that it took us only a decade and it sounds there, let's not call them challenge. Let's call it problems. Challenges is something I always envy the people that have challenges. We have problems with immune, and we work every day to solve those problems, right? So. So there's many problems or hurdles you have to go through. So there's first of all, you have to overcome some pretty big research issues, where do you find these hypothetical molecules of the immune response that go after bacteria and viruses. So research, then you learn the hard way.Eran Eden: The research is very different from development, and development is very different than product, and product is very, very, very different than manufacturing, and manufacturing is very different than regular regulation, and regulation is very different than reimbursement in marketing, which is a very different than commercial, et cetera, et cetera. So it's not good, it's not enough to excel in one thing. You have to really reinvent the wheel on several things, and as a company and as a team, reinvent yourself, and that's probably one of the biggest challenge, probably your biggest impediment to progress is yourself and your team because you might be an excellent data scientist, but you have to talk with the clinician. You might be an excellent clinician, but you have to talk the language of the molecular immunology. You might be very versed in all these three, but it's still not product and it's still not the graphical user interface. And how is that connected to manufacturing and really creating a culture or a team that can combine these seemingly very diverse elements within a small company. That is a very, very daunting and big task, and again, we frankly failed on multiple avenues there. We had to go back, we were in the cloud and we had to reinvent point C again and again and again. So, you know, we were in a very far position that we are today that we thought we were going to be at this stage.Harry Glorikian: So I'm going to ask at some point, you know, after this whole interview is I'm going to encourage you to write the next IVD book because everything you said is absolutely the way that I've seen it over time is, you know, having to bring all these pieces together is not trivial in our world. But let's step back here for a second for everybody that's listening, right? Talk a little bit about basic immune system biology and the, you know, technology behind your diagnostic system. So if someone presents with an inflammatory response, why is it so hard for doctors to destroying distinguish between the bacterial and viral infection?Eran Eden: Because bacterial and viral infections are clinically indistinguishable and you don't have to be an M.D. to to understand this. Intuitively, we know our kids so well. But still, you know, when they have a fever or runny nose, you know, we know that it's 80 percent, 85 percent a viral infection. But what if? What if there's a lingering bacterial infection? And it just it turns out that because of the clinical manifestation is very similar. It's really hard to figure it out. Not only children, also adults with suspected LRTI or a fever without sores, and even when we apply modern, I would say diagnostics, there's still a big gap that remains. So for example, when as a scientific community or a clinical community, when we approach this problem, we have tools at our disposal. A rapid strep test. A rapid influenza tests. Multiplex PCR. In today's world, I think everybody, even my grandmother is talking to me about the difference between rapid antigen tests suddenly becomes a really interesting topic over, you know, weekend dinners, culture. So there's technologies out there. And going back to your question, why is it still, why is there still a gap? And we've identified several things. The first one is probably the most trouble is time to results. Many of the clinical encounters, you want to have the solution here and now where whereas that technology that we have often provide solutions in hours and even days, and that's not always good.Eran Eden: That's one hurdle. Not the biggest one. The second one is that many times the infection site is inaccessible. Take, for example, otitis media, an ear infection or sinusitis or bronchitis or pneumonia. It's really hard to reach the infection side and therefore identify the pathogen. It's one in four patients in the most prevalent disease on Earth. That's really hard. Third, even if you use the best, most broad technology diagnostics to try to identify the bug, say a multiplex PCR. In more than 50 percent, five, zero percent of the cases, you're not be able to put your hands on any microorganism, but you still, as a clinician, have to make a decision. And lastly, there's the issue of colonization. So even if you're lucky, the infection that is readily accessible and you do get some sort of a virus, for example, that you detect, say, for example, an influenza or or let's take a rhinovirus, the rhinovirus is very prevalent in children. That's a problem. It's very prevalent in children. Even if you take seemingly healthy children in a very high percentage of those children, they're going to have a rhinovirus. So mere detection does not apply causality. All this complexity is sunk into this few minutes that the clinician basically needs to make a decision, and it's a really hard dilemma because it's hard to know to distinguish between the two and the ramifications could be quite significant.Harry Glorikian: So I know the answer to the question, but I'm going to ask it so you can explain it is: So who cares? I mean, I know that it's ineffective to treat a viral infection with antibiotics and that only you know, that only work against a bacteria, but you know. We've been doing a trial and error, so what's the downside of doing that?Eran Eden: So it's actually a pretty deep, it's a very deep question because there are several layers. You're right, this sometimes people actually say there's several layers to answering because the first one is, well, if you treat erroneously, with antibiotics, antibiotics, because of this uncertainty, there's a lot of antibiotics overuse that one of the consequences of this it drives anti microbial resistance, which basically means that the drugs don't work anymore. And if we continue on that path, we will potentially lose modern medicine because if you lose the potency of antibiotics, you cannot treat infants when they have an infection. Or an oncology patient that would succumb to a parasitic infection, or even yet have your wisdom tooth pulled out, because antibiotics won't be effective. And there's several quite influential studies that came out in the last few years. The last one actually in The Lancet came out two weeks ago portraying a world without antibiotics, which is, you know, we're seeing right now the consequences of COVID SARS-CoV2. Some might argue it's not a smaller problem. So that's and it has both clinical and health economic consequences. According to Jim O'Neill, over $100 billion by 2050 in lost GDP.Eran Eden: And. And it's a big number, right? It's a really, really big number. And maybe, maybe it's overly inflated and maybe it's conservative, but it's a big problem. The issue is that nobody cares. Sometimes the individual doesn't care because the doctor, right now, when he has a patient in front of him, he doesn't think about the masses. He thinks about the patient. So you might ask, well, what the doctor care. Why does the patient care? And it turns out that there is an angle on the personal level as well, not only the societal level. If you give erroneous antibiotics, you can drive anaphylactic responses. You can drive allergies, which have a toll. But then there's another element that people are less aware of. In addition to overuse, there's also simultaneously underuse. One in five patients that have a bacterial infection are not receiving antibiotics in time. There's much less publication on that. But it is a reality. And that also has consequences, including prolonged disease, duration and sometimes even morbidity and mortality. So it's a really delicate equation, right? You don't treat. And you don't want to get ... some countries overtreat, some undertreat. And again, at the end of the day, the day to day, it does have ramifications both from the patient and on the doctor.Harry Glorikian: You know, if we could accurately treat people right, I think there would be a whole host of issues that could get solved and a whole host of issues that wouldn't emerge because of overtreatment or treating the wrong people that you know, we could spend hours over a beer discussing the microbiome and allergies and all sorts of other consequences of doing this. [musical interlude]Harry Glorikian: Let's pause the conversation for a minute to talk about one small but important thing you can do, to help keep the podcast going. And that's leave a rating and a review for the show on Apple Podcasts.All you have to do is open the Apple Podcasts app on your smartphone, search for The Harry Glorikian Show, and scroll down to the Ratings & Reviews section. Tap the stars to rate the show, and then tap the link that says Write a Review to leave your comments. It'll only take a minute, but you'll be doing a lot to help other listeners discover the show.And one more thing. If you like the interviews we do here on the show I know you'll like my new book, The Future You: How Artificial Intelligence Can Help You Get Healthier, Stress Less, and Live Longer.It's a friendly and accessible tour of all the ways today's information technologies are helping us diagnose diseases faster, treat them more precisely, and create personalized diet and exercise programs to prevent them in the first place.The book is now available in print and ebook formats. Just go to Amazon or Barnes & Noble and search for The Future You by Harry Glorikian.And now, back to the show.[musical interlude]Harry Glorikian: So your system, which is, I love, is a basic blood test, right? So the MeMed BV looks at three immune system proteins in the blood: TRAIL, IP 10 and CRP. So how are these proteins related to infection and how can measuring their levels tell you about the nature of the infection?Eran Eden: Ok, so. Each one of those proteins that you just mentioned plays a critical role in the immune response to different invaders, bacteria and viruses. What's special about this particular trio, is that they work really well as a team. Maybe if you take a step backward to identify them, we had to run for about four years what is arguably the largest prospective proteomic study ever to be conducted of the human response to acute infections. And start with a host of multiple tens of thousand proteins bioinfomatically and then down-select this eventually to three. And these three, while none of them is perfect in itself, they cover one another's blind spots. So let's go one level deeper. When we went on this, one of the things where we were surprised to find out that is a clinical community, we've been obsessed with the bacterial side of the equation. Every biomarker that you have in 21st century medicine, 20th and 21st century medicine, has been mostly predominantly upregulated in bacterial infection. Procalcitonin: bacterial infections, CRP: bacterial infections, white blood count: bacterial infections, absolute neutrophil count, which we use as part of routine day to day care: bacterial infections. What about the viral side of the equation? We couldn't find one that was used or cleared by FDA as part of 21st century medicine. The last. The reason the FDA cleared us, we actually just cleared the first viral protein ever to be cleared by FDA. And so we went on this fishing expedition and four years into the process, again, this was 2009-2013. We identified this trio. TRAIL Is a protein that shoots up in your bloodstream when you have a viral infection, whether it's a common influenza A, influenza B, parainfluenza or corona, and it has this very unique property that it goes down when you have a bacterial infection, why nobody really understands the reason. But it really creates a very dramatic full change because of this up and down type of a response. And the story there, there's a lot of interesting stories around TRAIL, but one of the ways mechanisms by which it does that it causes the cells that are infected by viruses to commit apoptosis. Cells suicide. And by that, protect the brethren cells. So that's one of the mechanisms that the body is using.Eran Eden: The second one is called IP 10, which is an interferon. This protein basically shoots up in your bloodstream if you have a general infection, and more so if you have a viral infection. It recently got a lot of headlines in the context of SARS-CoV-2 and hyperactivity of the immune response. It's also associated with lung injury, but a really interesting biomarker that plays a critical role there in clearance of infections. The third one is called C-reactive protein, that's been around for about 40 years. Goes up in bacterial. And the nice thing about them? They work as a team. So as I said, they're not perfect. So take, for example, CRP. It's reasonably OK after 48 hours. But because it takes it to about 48 hours to reach maximum level, but in the early phases, you have a blind spot. Whereas TRAIL, at time of symptom onset, it's already differentiated, so they cover one another. By the way, we didn't identify this. The computer identified that. This is a lot of insights that we had in hindsight when we were looking.Harry Glorikian: Yeah, that was going to be my next question, which is. You know, the the heart of the show is always like, you know, artificial intelligence and its whole basket of tools and biology. So how does machine learning come into this process? Is there some corpus of training data that shows that certain levels of these three proteins correlate? Or can you tell us, you know, how you developed that part of the system?Eran Eden: Absolutely. And I think again, I was teaching a machine learning at the Weizmann Institute over a decade ago before it was a sexy topic. You know, people are using the term machine learning and data science so often so frequent. I think what's important to say is that machine learning is part of the component technology, but there's hardcore immunology and molecular biology. So it's not just one technology that we're, you know, it's a it's a very high entry barrier because of that and adds to the complexity. So that's one thing, just to put machine learning in context. Where machine learning plays an important role here is two places: in the development and in the final product. In the development, there's a process of how do you find the optimal team of biomarkers that would give you the the best performance? And over there, there's a lot of activities around using publicly available data sets and and proprietary data sets and data analysis and statistical analysis and feature selection and find the right models, et cetera, et cetera, coming up with what is the right model. Some of these are more conventional tests. Some of these are more cutting edge tests in the final product. It basically uses what's called a supervised learning approach, which basically means the following. Imagine every problem in here, I'm going to be a little bit technical here. Imagine you have, let's say one feature. Say a viral biomarker. TRAIL. High levels, viruses, low levels, bacteria. You find some sort of cutoff that separates between the two. It was the most informative biomarker that we found.Eran Eden: Is it good? It's reasonably good, but there's no perfect biomarkers out there. We don't have them, nor do we believe they exist. Nor do we believe in unicorns, even though my daughter is trying to continually persuade me that there is one. Then you add another biomarker to that. Imagine that you have right now a two dimensional grid. And now suddenly, every patient is met this two dimensional coordinates and you have a cloud of bacterial and the cloud of viruses. And you find a line that separates the two. And then a third dimension and a fourth and so forth and so on. And eventually, the problem becomes how can I find this type of plane or hyper surface that separates between the cloud of bacteria and the cloud of viruses? This is the essence of the machine learning and the way you go about this. You train give it a lot of patients, a lot of data, and then you train the system. And the more data you have, the smarter it becomes. The same principle applies for doing diagnostics in oncology, span detection, computer vision and what have you. It's the same underlying, often similar underlying principles to try to solve many of these problems. So hopefully I was able to to simplify and somewhat exaggerate how this is actually working and where the AI plays here.Harry Glorikian: So what's that accuracy rate of the diagnosis from your system? And is there are certain things, let's say it's good at in certain things, it's maybe not so good at?Harry Glorikian: Yeah, absolutely. So so if you look at the overarching population, if you look at our pivotal FDA study, the AUC, the area under the operating curve, the entire population was 0.9 to 0.97 across different cohorts, which is considered very high. So that's the short answer. The more we see deeper level, it's there's obviously nuances across different populations. One of the things you have to show is what happens in children versus adults. Upper respiratory tract infections, lower respiratory tract infections, et cetera, et cetera. So we've shown a relatively consistent and robust response. That's how the system was developed. But there are, for example, certain viruses that we know that we perform less accurate. For example, adenoviruses. Adenoviruses are notoriously hard to to treat well. By the way, they're one of the most prevalent, for example, viruses in children, why? Because the immune response looks like a bacterial infection. For many, many reasons. So white blood count is going to be elevated. Procalcitonin is going to be elevated, CRP is going to be elevated and we're often going to overtreat with antibiotics. So if you look at our performance in that particular sub-cohort, our performance drops somewhat from, you know, a 0.90-something to maybe 0.89, but that's actually one of the viruses that we see the most added value because compared to standard of care, it's many times close to flipping a coin.Eran Eden: So even though our performance is eroded in this particular virus. The standard of care in this particular situation is particularly challenged, and it's almost 0.5, 06. so that's one example. There's multiple examples. We can study the immune response to pathogens again for almost a decade now. This is just one interesting anecdote. And I think just connecting this to the who cares question that you had. So here's an interesting case that we had a few weeks ago. A child, young, three years old, coming to a major medical center, not really sure if it's a bacterial or viral. Ran a PCR, came positive for adenoviruses and it looked a little bit bacterial. But yeah, OK. Adenovirus explains everything. Released home. Got a 99 score. 99 probability of bacterial infection. So they start to do additional follow up and then it eventually turned out to be a bacterial axis in the spinal cord of that particular child. It had to be mechanically removed. This is a very dramatic case. This is one of those potentially underused cases that could be very dramatic. This is very rare. It doesn't happen often. But again, it's hard. It's really, really tricky to distinguish between infections and we added this right now, this is how everything maps together to the adenoviruses and and to why we think this could be helpful.Harry Glorikian: So, you know, like I said earlier in the show, you know, you got FDA approval and granted 510K clearance back in September, which congratulations, that's a huge step. But you know, for everybody listening, what Gates does, does that open for you. What's the pathway to getting the device out into the market?Eran Eden: So as you said, first of all, you have to get the clearance, which I think took us almost five years working with FDA. FDA, by the way, we've worked with them extremely collaboratively and they've been instrumental in helping us form and shape, what's the methodology to actually prove something. We didn't talk about this? But how do you prove that absence or presence of bacterial viral infection in the absence of a true gold standard? So let's put that thing aside. We were able to work with FDA and come up with a methodology to do that. So now, what is required to take it to the next step? There's several things. The first one you need, and we didn't talk about this, you need a way to measure those biomarkers. You need a platform. Right, one of the challenges that we had is that in the early days, none of the big strategic players, the Roches, the Abbotts, the DiaSorins of the world were willing to bet on this because the risk were so high, as you alluded to in the beginning, the graveyard. And nobody got FDA clearance, so they basically they wouldn't. They were not willing to bet on us today. Some of them become partners and we're working with them. So it's, you know, there's been great development. But at that time, it was really hard. The platform is also challenged because some of the proteins are picograms, some are nanogram and some are micro per mil, which poses again the challenge from a technological perspective. Again, not going too much into the technology side, but we've been able to come up with a technology or a platform that can actually measure multiple proteins across almost a six to nine order of magnitude range. And so you have to have a platform and can do that in about 15 minutes right now, serum working in whole blood.Eran Eden: The second thing you need, you need obviously manufacturing capability, which is again, a different story, you have to manufacture the cartridge. The third thing you need is building the clinical evidence beyond, I mean, FDA's great, but you have to create what's called a clinical utility, real world evidence, what have you, working with peers. Work with partners or with clinicians working the societies. Publishing. Building a commercial team which we're right now established commercial team in the U.S. So there's multiple things. And probably last but not least, this is too big of a challenge to go at it by yourself. You need to have partners. Whether it's governments, the U.S. Department of Defense, the European Commission have funded this heavily and have been amazing partners, whether it's strategic partners, you can take it by yourself versus vs not one market. It's markets. You have patients in the wards and the EDs and the urgent care physicians' offices, retail clinics. No single player has enough of a presence in one platform that covers it all. So again, we've announced about a year ago, you know, the first partnership with DiasSorin, which has today almost a thousand installed installed across Europe and the US in these large automated immunoassay machines. And that's covering certain parts of the market that are overlapping or, sorry, that are complementary where we're going at. So that's a little bit of what needs to be done. But again, it's changing the boundaries of what what we've been doing so far, and that's always a it's always a challenge, but also an opportunity.Harry Glorikian: So you guys raised I believe it was $93 million, if I remember the number correctly, in new funding, which sort of really adds to the firepower of being able to take that next step, but. You know, can you can you envision a future where we get a solid diagnosis and an appropriate treatment plan, you know, quickly while you're in the doctor's office?Eran Eden: Oh, yeah.Harry Glorikian: That was the shortest answer you've given yet.Eran Eden: I think you can be much more radical. I think there's several things that are happening. There's two major discontinuities. There's a technological discontinuity. There's a regulatory discontinuity. And I'll actually add another one, which is there's a psychological discontinuity. The technology that we can do today that we have today, the tip of our fingers can do can provide so much valuable information that can help make better decisions. The regulatory framework has changed because of COVID, it's basically shattered a lot of things. And from a psychological perspective, I think there's a push to polarization, right? Both decentralization and centralization at the same time. And so I definitely see that happening. I think we can take this several step further. How can we take it from physician's office, also retail clinics and even further? And that will take time, obviously, because we're dealing here with some pretty, pretty deep questions. But I think the world across multiple fields and this is not different than anything else. I think it's definitely going in that direction.Harry Glorikian: Yeah, no, I mean, I was going to, you know, looking at what you've created and, you know, obviously first getting everybody on board, but then seeing how it can be deployed at a CVS or something like that, it could drum, you know, you could have a dramatic impact on how we manage patients. The whole antibiotic dynamic and maybe even relieving stress on the system so that, you know, it doesn't get overwhelmed by what your system may be able to sort of help get to a much faster, much more accurate answer too.Eran Eden: I wanted to say relieving stress from stressed mothers and fathers. But yeah, I agree with you also, relief. And by the way, as you start going from more centralized to decentralized, there's obviously additional workflow challenges. How do you make this simpler? There's regulatory bars that you have to meet. How do you go from a mod complex to a clear waived test that can actually go to those directions so that there's we still have we have work, there's work, work to be done. But I think we've been able to potentially break a glass ceiling in terms of getting the clearance. And now I think with that, there's going to be additional innovation that will come in both by us and others who are entering the space.Harry Glorikian: So. Just slightly moving to one side is like, how has MeMed responded to say, COVID-19? I think you guys have developed a test that runs on your platform and predicts how severe the infection will be. How does that test work? Did your previous work, you know, and also did your previous work like on the platform prep you for this virus? Just curious how it works and how you got there?Eran Eden: Absolutely so. So it always starts with the clinical question. I mean, many of us are technophiles, but at the end of the day it's about solving a real problem. And the problem here is the following. You have see SARS-CoV-2 positive patient presenting to the ED. And one of the questions that we have in mind is whether that patient is going to deteriorate or not. Do we escalate treatment or not? And it's a real question, right? And the more you know, the more stress the system is feeling because, you know, because of the the peak of a pandemic, the more important that is. So we said, Well, how can we harness the technology? Is the framework that we created host response in general, right? The biomarkers we've developed, the platform that we have, the Biobank and what have you. And so and how can we take a process that maybe took 10 years and now collapsed into something maybe that's 10 months? How do you get a 10 X? And and first of all, with amazing partners around the globe, you start running huge clinical studies to basically collect patient samples. We also use again information from the public domains, our own repositories, our own previous data because from many perspectives. Sars-cov-2 is very interesting, but guess what? Similar to SARS and to other types of severe viruses, there's differences, but also commonalities.Eran Eden: So we use a lot of the bioinformatics, the previous data samples. Current data samples. The know how and the platform that's readily available right now. They can measure basically anything to collapse this and develop. This is probably just got clearance in Europe that basically allows to take a snapshot, the main response again in real time. Give you a risk stratification regarding the probability of a patient to experience severe outcome defined as ICU level of care and mortality within two weeks. Again, it's only clear right now in Europe, not cleared in the U.S. and we view this also as a stepping stone going beyond just COVID severity to a general severity signature. So what you do, both B versus V and severity, what if you could do it in the same cartridge or what have you? So I think what's what's really interesting, we build here this core technology. We went after one big problem, B versus V, but now that you have that, you're like a child in a candy store. There's many more things that you can do. And rather than taking you a decade, you can start to collapsing things because there's a lot of there's a lot of. Resources that you can now leverage or platform that you can leverage, so that's a story around MeMed and COVID severity.Harry Glorikian: Yeah, platforms are wonderful in that way, right, that I like a platform more than I like, like a, you know, sharpshooter bullet, from an investment perspective. Thinking about it that way. But so. You recently got COVID. We were supposed to talk like over a week ago, and I, you know, we had to postpone it. Did you use the test on yourself? I mean, if you did, like did it work the way you thought it was going to?Eran Eden: Yeah, so so yeah, I got my I got it from my daughter. We went on a trip and five out of five family members got infected. So yes, it was at least from our small experiment. It was very infectious. We got the Omicron. Actually we didn't have symptoms, apart from the fact that I think it just jacked up the energy level of my kids. So before we talk about running around the house and thank God, you know, my wife didn't didn't kill any one of them. So there's no casualties from this, from this infection. So because we didn't have symptoms, we didn't go to the ED. It was not relevant. You have to have SARS-CoV-2 symptoms. So in that case, no, no, no need. I mean, we were pretty much hunky dory. But what I can tell you is that on the B versus V. Again, it's potentially bacterial and viral infections are potentially the most prevalent indication in children. And my children, those little incubators of bacteria and viruses, are no exception. So I had a chance to use the technology on my kids many, many times, including last time was about a month and a half ago, and my eldest daughter, who is four, before going to a business trip. And my wife is asking, is it a bacterial infection? I said, I don't know. She spits on me. The shoemaker is going barefoot. So we ran it. It was a viral infection. No antibiotics. Went back to school. So and I got a lot of brownie points with my wife and my mother in law, which is obviously always very, very strategic.Harry Glorikian: That's that's a good one. That's always helpful. Exactly.Eran Eden: So we're actually using this quite often in our families as well. And it's very very gratifying.Harry Glorikian: Interesting. Excellent. So now you guys are, you know, I believe you have an office in Haifa, which I remember as being beautiful and hilly and wonderful food, and then you have Boston. You know. What are the strengths of being in these two locations. What happens in Boston that can't happen in Haifa and vice versa?Eran Eden: Well, again, we're going after a global problem and you have to have a global team to have a global perspective. Whatever you have in San Francisco today, you have tomorrow in Shanghai and the day after that in Tel Aviv. So you have to look at this from a global perspective, number one. Number two, since the US is the primary market, as I said, we have to build a very significant presence in the U.S.. Why specifically Boston? Very talented pool of, a pool of talent that's very wide in the domain. There's a big overlap in terms of hours between Boston and Tel Aviv, so you can grow one unified team. And that's basically, that's where we're basically building our U.S. headquarter. And the team is quite complementary. Again, we've we've recruited by now roughly 25 to 30 folks, folks with a very strong background, both IBD, Troy Battelle, formerly Thermo Fisher, who's buying commercial for microbiology in the Americas. Fred, who is running Corp Dev, from bioMérieux. Again, another large multinational, Jim Kathrein was former head of sales for BioFire. Again, not sure if your audience is familiar with but and so forth and so on.Eran Eden: And Will Harris was running our marketing global marketing, is ex-Amazon and then before that, 15 years in IBD. So it's really bring here a blend of, we call this affectionately an anti disciplinary team. We don't care about disciplines, we care about solving big, ugly problems. So you have to bring the IBD experts with the clinicians, with the folks and the big data science side or in the molecular immunology and the manufacturing. And nobody knows, single location has all the know how, no single location has the recipe because frankly, we're doing here something new. There is no real tech like this. And so bringing those this pool of talent, I think has really helped us, propels us moving forward. And it is the bridge to be able to to launch in the U.S., a U.S. very focused, commercially marketing product where a lot of the I would say more of the molecular immunology data science team is more in Israel. I'm simplifying and exaggerating. That's some of the team.Harry Glorikian: So the last funding round, was that the argument to the investors, like we need to hire these types of people to help blow this out? What was what was the rationale for that last round?Eran Eden: So, so basically three things. Number one, commercialization. U.S. Europe, Israel. That's our initial focus and then the rest of the world. Second is product pipeline, so we talked about bacterial versus viral infection and a bit about COVID severity. But what would you do if you had a blank canvas and these platforms to go after the new response to measure the immune response? What additional big problems would you go after? So it turns out that there's some pretty interesting stuff in. We're working on additional activities. So that's the second thing product pipeline. And the third thing is a scaling manufacturing. So as I think people have a new appreciation for manufacturing and supply chain during COVID times, it's a really big topic and critical for success. So this these are the three major elements that we raise the funds for.Harry Glorikian: No sounds I've I've been I've seen this rodeo a few times, so yes, I understand completely. So, well, you know, especially because I come from the diagnostic world and I can't wish you enough success because we need more products like this out on the market to help us manage patients and help give physicians better information so that they can make better decisions, right? More informed decisions than just, you know, looking at a patient and trying to figure out what's going on. So I wish you incredible success and I'm, you know, great. Great to have you on the show.Eran Eden: Thank you so much for for the kind invitation. Enjoyed our discussion.Harry Glorikian: Thanks.Harry Glorikian: That's it for this week's episode. You can find a full transcript of this episode as well as the full archive of episodes of The Harry Glorikian Show and MoneyBall Medicine at our website. Just go to glorikian.com and click on the tab Podcasts.I'd like to thank our listeners for boosting The Harry Glorikian Show into the top three percent of global podcasts.If you want to be sure to get every new episode of the show automatically, be sure to open Apple Podcasts or your favorite podcast player and hit follow or subscribe. Don't forget to leave us a rating and review on Apple Podcasts. And we always love to hear from listeners on Twitter, where you can find me at hglorikian.Thanks for listening, stay healthy, and be sure to tune in two weeks from now for our next interview.

Today we're joined by repeat guest Dr. James Neuenshwander, Attending Physician and Research Director for Genesis Healthcare System and Adjunct Associate Professor at The Ohio State University Medical Center. We usually discuss topics around potassium and things of that nature with Dr. Neuenschwander, but this week we discuss Procalcitonin with differentiation between bacterial and viral and its role in emergency medicine. Dr. Neuenschwander indicated that he has relationships that could be perceived by some as real or apparent conflicts of interest as they pertain to Procalcitonin. He is a speaker and consultant for Thermo Fisher and a consultant for Ortho Clinical Diagnostics.

Dr. Centor discusses the use of procalcitonin in the diagnosis of pneumonia with Dr. David Gilbert.

Dr. David Gilbert, Professor of Medicine at Oregon Health Sciences University, presents an update on the use of procalcitonin as a diagnostic marker. Dr. Gilbert emphasizes the role of procalcitonin in three main clinical sydromes: Community acquired pneumonia, Sepsis, and COVID-19 Pneumonia.

Dr. Ebell and Dr. Wilkes discuss the POEM titled ' In-office procalcitonin testing can lead to less antibiotic prescribing '

This week Kate, Mark, Henry and John talk about measuring temps in kids, implantable monitors to diagnose afib, procalcitonin in primary care, and HPV based cervical cancer screening

David F. Gaieski, MD, Associate Professor, Emergency Medicine, Jefferson University Hospitals, Philadelphia, interviews Daniel Feinstein, MD, FACP, ACRP-PI, Medical Director, Critical Care, Novant Health, about the outcomes and benefits associated with the use of syndromic PCR testing and procalcitonin in the emergency department for patients with suspected and confirmed respiratory infections such as community-acquired pneumonia and COVID-19. Opinions expressed in this podcast are not necessarily those of bioMérieux, Inc.

HOST I am Marc Davis, PA-C who graduated from Hahnemann University in Philadelphia and have over twenty years of clinical and didactic experience. I taught at Hahnemann University, Philadelphia College of Osteopathic Medicine, and Nova Southeastern University. I practiced nephrology and internal medicine for eighteen years, cardiology for two years, and currently, I am practicing critical care medicine. I studied genomics at Stanford University and was the Officer In Charge of a medical unit in the U.S. ARMY. This podcast is dedicated to all licensed healthcare professionals who serve patients among the various sick wards. DISCLAIMER The content herein at 'My Grand Rounds' is mine alone and does not reflect the opinions or values of my employer. The podcast ‘My Grand Rounds' is intended to provide medical education for licensed healthcare professionals. The podcast ‘My Grand Rounds' is not intended to provide or be taken by patients as medical advice. Knowledge and best practice in the field of medicine are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their safety and the safety of others, including parties for whom they have a professional responsibility. Concerning any drug or pharmaceutical products identified, listeners are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method, and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein at 'My Grand Rounds.' FAIR USE POLICY The podcast, ‘My Grand Rounds' may contain copyrighted material the use of which has not always been specifically authorized by the copyright owner. All rights are reserved by their respective owners. In accordance with the Non-Profit mission of the podcast, ‘My Grand Rounds,' it is believed the use of this content helps fulfill the intention of copyright law to stimulate creativity for the enrichment of the general public and does not “supersede the objects” of the original for profit. The aim of the podcast, ‘My Grand Rounds' is to advance the knowledge and progress of medicine through comment, education, or the addition of something new in a transformative work, in accordance with - Fair Use Law, Title 17, United States Code, Section 107. The material on the podcast, ‘My Grand Rounds' is distributed without profit to those who have expressed a prior interest in receiving the included information for research and educational purposes. If you wish to use copyrighted material from the podcast, ‘My Grand Rounds' for a purpose of your own that goes beyond the ‘Fair Use' Law, you must obtain permission from the copyright owner. SOURCE(S) Source(s) will be verbalized during each podcast episode.

David F. Gaieski, MD, Associate Professor, Emergency Medicine, Jefferson University Hospitals, Philadelphia, interviews Charles B. Cairns, MD, the Walter H. and Leonore Annenberg Dean of the College of Medicine, Senior Vice President for Medical Affairs, and Professor of Medicine and Emergency Medicine at Drexel University, about the new potential for care utilizing host response biomarkers, pathogen identification and surveillance as well as newly published research. Opinions expressed in this podcast are not necessarily those of bioMérieux, Inc

Katarzyna Pawlak, social media editor, talks to Alexandre Nuzzo about his recent findings from a prospective study about the role of serum procalcitonin in patients with acetaminophen poisoning.

Jana sucht nach belegen für die Hypothese, "Erkältung" hätte was mit Kälte zu tun. Ob sie fündig wird? Jan Hendrik Oltrogge-Abiry berichtet, wie er zur Leitlinien-Arbeit kam und antwortet auf Fragen zur DEGAM-S3-Leitlinie "Halsschmerzen" Ilja ärgert sich über Platz 5 seiner Top Ten Medis

David F. Gaieski, MD, Associate Professor, Emergency Medicine, Jefferson University Hospitals, Philadelphia, interviews Michael R. Broyles, BSPharm, RPh, PD, PharmD, Director of Clinical Pharmacy and Laboratory Services, Five Rivers Medical Center, Arkansas, about the advantages of using procalcitonin and data analytics for emergency physicians. Opinions expressed in this podcast are not necessarily those of bioMérieux, Inc.

Welcome to the second episode of the A.M. Labs podcast! We tackle procalcitonin and its use in lower respiratory tract infections. We learned a lot and hope you do too! Email us at amlabspodcast@gmail.com with any thoughts or questions! For show notes and transcripts visit www.amlabspodcast.com

On today's episode, Holly Ledyard, MD, MS is joined by Ryan Maves, MD, FCCP, FCCM, FIDSA to discuss his recent article, "Procalcitonin Is Not an Adequate Tool for Antimicrobial De-Escalation in Sepsis."   NCS offers free CE credits for the NCS Podcast Series episodes. Listen to any of the posted episodes, complete a five question survey, and claim your credits here! Credits are available for physicians, pharmacists, nurses, and non-physicians. The NCS Podcast is the official podcast of the Neurocritical Care Society. Our senior producer is Bonnie Rossow. Our host is Fawaz Almufti, and our production staff includes Tareq Saad Almaghrabi, Andrew Bauerschmidt, Leonid Groysman, Atul Kalanuria, Lauren Koffman, Kassi Kronfeld, Holly Ledyard, Lindsay Marchetti, Alexandra Reynolds, Lucia Rivera Lara, Jon Rosenberg, Jason Siegel, Zachary Threlkeld, Teddy Youn, and Chris Zammit. Our administrative staff includes Bonnie Rossow. Music by Mohan Kottapally.

Today we are doing double duty: podcasting and parenting.  Fortunately our babies were well-behaved.  We talk about three trials for semaglutide and weight loss and a new 4 level pre-test probability rule for diagnosing PE.  We also talk about a retrospective study of cefazolin vs nafcillin for epidural abscess, a ferritin/procalcitonin ratio for differentiating bacterial from COVID pneumonia, and a new randomized controlled trial of intermediate thromboprophylaxis for ICU patients with COVID19.  Check it out! Semaglutide for Weight Loss (STEP 1)Semaglutide for Weight Loss in Diabetics (STEP 2)Semaglutide + Intensive Calorie Restriction for Weight Loss (STEP 3)4PEPS for Pulmonary EmbolismNafcillin vs Cefazolin for Epidural AbscessFerritin/Procalcitonin Ratio for COVID-19 vs Bacterial PneumoniaIntermediate Thromboprophylaxis for COVID-19 (INSPIRATION) Music from https://filmmusic.io"Sneaky Snitch" by Kevin MacLeod (https://incompetech.com)License: CC BY (http://creativecommons.org/licenses/by/4.0/) Hall of the Mountain King Kevin MacLeod (incompetech.com)Licensed under Creative Commons: By Attribution 3.0 Licensehttp://creativecommons.org/licenses/by/3.0/

Quick Summary Prognostic Value of Serum Procalcitonin Levels in Patients with Febrile Neutropenia A review of an article from JEM regarding the use of serum procalcitonin with or without MASCC score in patients with febrile neutropenia.

15 glorious minutes dedicated to pediatrics' hottest new biomarker: procalcitonin. Don't forget to check out the articles discussed in this episode - full source lists can be found on mdnotified.com.

In this week's episode guest Jeff Schunk, MD, FAAP and host Paul Wirkus, MD, FAAP discuss Procalcitonin's role in identifying infection and the relevance of a CPM. Next week we will be answering your questions. You can reach us at questions@vcurb.com.

On this episode, we are joined by PGY-1 resident Dr. Sharon Yousif-Dickow, PharmD to discuss the possible value of procalcitonin in antimicrobial stewardship. We give a brief review of the basic science behind procalcitonin. We also review its current place in the treatment of sepsis and other infections. Let us know about your personal experience with procalcitonin! Thanks for listening! If you want to support the podcast, check out our Patreon account. Subscribers will have access to all previous and new pharmacotherapy lectures as well as downloadable Power Point slides for each lecture. You can find our account at the website below:  www.patreon.com/corconsultrx If you have any questions for Cole or me, reach out to us on any of the following: Text - 415-943-6116 Mike - mcorvino@corconsultrx.com Cole - cswanson@corconsultrx.com Instagram and other social media platforms - @corconsultrx This podcast reviews current evidence-based medicine and pharmacy treatment options. This podcast is intended to be used for educational purposes only and is intended for healthcare professionals and students. This podcast is not for patients and not intended as advice or treatment.

This week's episode features author Torbjørn Omland and Senior Guest Editor Vera Bittner as they discuss the artile "Growth Differentiation Factor-15 Provides Prognostic Information Superior to Established Cardiovascular and Inflammatory Biomarkers in Unselected Patients Hospitalized with COVID-19." TRANSCRIPT BELOW: Dr. Carolyn Lam: Welcome to Circulation on the Run, your weekly podcast summary, and backstage pass to the journal and its editors. We are your co-hosts, I'm Dr. Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore. Dr. Greg Hundley: I'm Dr. Greg Hundley, Director of the Pauley Heart Center at VCU Health in Richmond, Virginia. Well, Carolyn our feature this week gets into inflammatory biomarkers in patients that have been hospitalized with COVID-19, but before we get to that, how about we grab a cup of coffee and work through some of the papers in the issue. Would you like to go first? Dr. Carolyn Lam: Absolutely. With both the coffee and the papers. So great, for this first paper, have you thought about concentric versus eccentric cardiac hypertrophy? We traditionally associate them with pressure versus volume overload respectively in cardiovascular disease, both though conferring an increased risk of heart failure. These contrasting forms of hypertrophy are characterized by asymmetric growth of the cardiac myocytes in mainly width or length respectively. However, the molecular mechanisms determining myocyte preferential growth in width versus length remain poorly understood. Dr. Carolyn Lam: That is until today's paper, and it is from Dr. Kapiloff from Stanford University, and Dr. Rosenfeld from UCSD, School of Medicine and their colleagues, and what they did was used primary adult rat ventricular myocytes, as well as Adeno associated virus mediated gene delivery in mice, to define a regulatory pathway controlling pathological myocyte hypertrophy, and they found that asymmetric cardiac myocyte hypertrophy is modulated by serum response factor phosphorylation, constituting an epigenomic switch balancing the growth in width versus length of adult ventricular myocytes In vitro, and In vivo. Dr. Carolyn Lam: Serum response factor phosphorylation was bi-directionally regulated at signalosomes organized by the scaffold protein muscle, A kinase anchoring protein beta. This newly identified molecular switch controlled a transcriptional program responsible for modulating changes in cardiomyocyte morphology that occurs secondary to pathological stressors. Dr. Greg Hundley: Very nice, Carolyn. So switches controlling this transcriptional program. Tell us a little bit, and bring us back to the clinical relevance of this and starting with that concentric versus eccentric hypertrophy? Dr. Carolyn Lam: I thought you may ask. The identification of a molecular mechanism regulating that asymmetric cardiomyocyte growth, really provides a new target for the inhibition of pathological cardiac hypertrophy. Studies in mice using these Adeno associated virus based gene therapies to modulate that signalosome, really provided proof of concept for translational potential in the treatment of pathological cardiac remodeling and prevention of heart failure. Dr. Greg Hundley: Oh, wow. Very nice, Carolyn. Well, my first paper comes to us from Professor Dirk Westermann from Hamburg, and focuses on cardiogenic shock patients, and veno-arterial ECMO, the results from the international multicenter cohort study. So Carolyn this study evaluated data from 686 consecutive patients with cardiogenic shock treated with VA ECMO with or without left ventricular unloading using an Impella, and they conducted this at 16 tertiary care centers across four countries. They examined the association between left ventricular unloading and 30 day mortality. Dr. Carolyn Lam: Huh, so what did they find? Dr. Greg Hundley: Okay. Carolyn. Well, left ventricular unloading was used in 337 of the 686 patients enrolled, and after propensity matching 255 patients with left ventricular unloading were compared with the 255 patients without left ventricular unloading. In the match cohort, left ventricular unloading was associated with lower 30 day mortality without differences in the various subgroups. However, complications occurred more frequently in patients with left ventricular unloading, like severe bleeding, which happened in 38.4% versus only 17.9% in those without unloading. There was also access-related ischemia and renal replacement therapy. Dr. Greg Hundley: So Carolyn, the take-home message from this International multi-center cohort study, is that left ventricular unloading is associated with lower mortality, and cardiogenic shock patients treated with VA ECMO, despite higher complication rates. In the absence of randomized trial data these findings support the use of left ventricular unloading and cardiogenic shock patients treated with VA ECMO, and call for further validation, ideally in a randomized controlled trial. Dr. Carolyn Lam: Very nice. Well for my next paper, Greg, it's all about desmin. Now we know that mutations in the human desmin gene caused myopathies and cardiomyopathies. Well, today's authors, Dr. Hermann and Schroeder from University Hospital Erlangen in Germany and Dr. Lilienbaum from University of Paris and France and their colleagues, report an adolescent patient who underwent cardiac transplantation, due to restrictive cardiomyopathy caused by a heterozygous R406W desmin mutation. Sections of the explanted heart were analyzed with antibodies specific to 406W-desmin, and to intercalated disc proteins. Effects of this mutation on the molecular properties of desmin were then addressed by cell transfection and In vitro assembly experiments. They further generated these desmin mutation knock-in mice haboring the orthologous form of the human, R406W-desmin. Dr. Greg Hundley: So Carolyn, what did they find? Dr. Carolyn Lam: Well, they demonstrated a novel pathomechanism in which cardiotoxic R406W-desmin, could adapt dual functional status with the abilities to integrate into the indogenous intermediate filament network, and to cause formation a protein aggregates. This R406W-desmin modified the extra sarcomeric cytoskeleton, such that desmin filaments were not anchored to desmosomes anymore. Thereby destroying the structural, and functional integrity of intercalated discs. Dr. Greg Hundley: What are the clinical implications? Dr. Carolyn Lam: Well, since these cardiotoxic desmin mutations could affect the integrity of intercalated discs, thereby inducing conduction defects and malignant arrhythmias, they suggest early implantation of pacemaker, or cardioverter defibrillator devices, may be considered to prevent certain cardiac death in patients with these mutations. Furthermore, state-of-the-art basic molecular risk stratification of desmin mutations may encompass a multidisciplinary experimental approach as exemplified by the approach taken here, which comprises assessment of the tissue pathology in conjunction with genome analysis and desmin assembly studies as well as patient mimicking cell and animal models for the In vivo validation of these mutations. Dr. Greg Hundley: Well, fantastic, Carolyn. Well, my next paper comes to us from Dr. Ravi Shah from the Massachusetts General Hospital. This study evaluated 2,330 white and black young adults, average age of 32 years, in the Coronary Artery Risk Development in Young Adults, or the cardiac study, to identify metabolite profiles associated with an adverse cardiovascular disease phenom that included, myocardial structure and function, fitness, vascular calcification, and then also mechanisms, and other cardiovascular outcomes that would occur over the next two decades. Statistical learning methods, including elastic nets and principal component analysis, and Cox regression generated parsimonious metabolite based risk scores, validated in over 1800 individuals in the Framingham Heart Study. Dr. Carolyn Lam: Wow. What did they show, Greg? Wow, that's a lot of work. Dr. Greg Hundley: Yeah. So Carolyn, the authors found two multiparametric metabolite-based scores linked independently to vascular, and myocardial health. With metabolites included in each score specifying microbial metabolism, hepatic steatosis, oxidative stress, nitric oxide modulation, and finally collagen metabolism. Over nearly 25 year median follow-up, and cardia, this metabolite based vascular score, and the myocardial score, and the third and fourth decade of life were associated with clinical cardiovascular disease. Importantly, the authors replicated these findings in 1,898 individuals in the Framingham Heart Study followed over two decades, such that young adults with poor metabolite based health scores had higher hazard ratios of future cardiovascular disease related events. Dr. Carolyn Lam: Oh wow. Greg, what an elegant study with both development and validation cohort evaluating the metabolome. Dr. Greg Hundley: Yes. Carolyn. So metabolic signatures of myocardial, and vascular health in young adulthood specify known novel pathways of metabolic dysfunction, relevant to cardiovascular disease associated with outcomes in two independent cohorts. So these data suggests that efforts to include precision measures of metabolic health in risk stratification to interrupt cardiovascular disease at an early at stage, are warranted. Dr. Carolyn Lam: Wow. So interesting. Other very interesting articles in today's issue, there's an In Depth article by Dr. Angiolillo entitled, “The Antithrombotic Therapy for Atherosclerotic Cardiovascular Disease Risk Mitigation in Patients with Coronary Artery Disease and Diabetes.” There's also Research Letters, one by Dr. Sultan on, “The Longterm Outcomes of Primary Cardiac Lymphoma” and one by Dr. Wang on, “Loss of Phosphatase and Tensin Homolog Promotes Cardiomyocyte Proliferation and Cardiac Repair Following Myocardial Infarction.” Dr. Greg Hundley: Great, Carolyn. Well, I've got a couple other articles in this issue as well. One is by Professor Ganesan Karthikeyan who has an On My Mind piece entitled an “Alternative Hypothesis to explain Disease Progression in Rheumatic Heart Disease.” Dr. Stuart Chen has an ECG challenge entitled, “Alternating QRS Duration and a Normal T-waves. What is the mechanism?” Then finally, Carolyn, a series of Letters to the Editor, one by Dr. Peterzan and the other by Dr. Mehmood regarding the prior published article, entitled “Cardiac Energetics in Patients with Aortic Stenosis and Preserved Ejection Fraction.” Well, Carolyn, how about we get onto that feature article and learn more about inflammatory biomarkers in hospitalized patients with COVID-19? Dr. Carolyn Lam: Yes. Let's go. Greg. Biomarkers are really playing an increasingly important role in cardiovascular disease, and even in the current COVID 19 pandemic, there's been a lot of news about how biomarkers such as traponin may be prognostic, and in fact, we're all wondering about maybe even newer biomarkers. In fact, today's feature discussion does bring to light one of the newest, and in fact, this is the first publication on the role of Growth Differentiation Factor 15 or GDF-15 in COVID-19. We're so pleased to be discussing this with the corresponding author, Dr. Torbjørn Omland from University of Oslo, in Norway, as well as our senior guest editor, Dr. Vera Bittner from University of Alabama at Birmingham. So welcome both. Tobjorn, could you tell us a little bit about GDF-15 and what made you look at it, and what did you find? Dr. Torbjørn Omland: Yeah, so GDF-15, that's a very interesting biomarker. It's considered a biomarker of biological aging cellular stress, and perhaps also the inflammation, and tests being studied within the cardiovascular field for some years now, and it has been shown to be a strong prognostic indicator across the cardiovascular spectrum, actually. So it is a new biomarker in one sense, but there are some data already in the cardiovascular field. Dr. Carolyn Lam: Not in COVID. So this is the first study to really look at its prognostic value in COVID 19. So congratulations Torbjorn, and if I may also to the first author, Dr. Peter Meer, a good friend as well, but please, could you tell us about your study and what you found? Dr. Torbjørn Omland: Yes. So when the COVID pandemic hit Norway in the spring, we thought that we should plan a prospective biomarker study. So we had to really fast track approval by the IRB and so forth, and we're able to actually cover most of the patients that were hospitalized in our hospital, Akershus University hospital, which is right outside of Oslo, and it's a pretty large hospital by Norwegian standards. It covers about 11% of the Norwegian population. Dr. Torbjørn Omland: So in that period, when we were including, we had 136 patients hospitalized with confirmed COVID 19, and we have biobank bank samples from 123 of these, and then there have been reports from retrospective studies, first from China, that seemed to suggest that markers like cardiac troponin, Anti-Troponin T, and Ferritin were associated with outcome, but those studies were prone to selection bias in that the measurements were performed in the most sick patients. So in this study we included all patients and then we thought we should examine a broad panel of biomarkers, and that included Interleukin 6, CRP, Procalcitonin, Ferritin, and the D-dimer Cardiac troponin, and N-terminal pro B, and GDF-15. Dr. Carolyn Lam: Wow. Thank you, Torbjorn. Even before you carry on with the results, can I just say having visited your hospital in pre-COVID days, I can only imagine what a work of love this was to do it prospectively. Any particular experiences to talk about, to get a fast-track even in the midst of to perform a well done prospective study, that must have taken a lot. Dr. Torbjørn Omland: Yes. But it's also interesting in that the whole sort of ablation on Norway was very much into this from the highest political level. Also, the decision that the older research on COVID should be prepared to retire, then the IRB had an eight hour and deadline for them to approve or not approve the study. So that's went surprisingly smoothly, I must say. Dr. Carolyn Lam: Wow, that's great. So what did you find? Dr. Torbjørn Omland: Yeah, so we found that among these biomarkers, several seem to predict outcome, and the primary end point of this study was to combined end-point of the hospitalization in the ICU, or death. We found that also markers like cardio traponin, BNP, ferritin, and the D-dimer and so forth, in univariable analysis, were very associated with outcome, but when we perform a more comprehensive, mostly variable modeling, then the prognostic value of some of these markers disappeared. In contrast, for GDF-15, it seemed to perform very strongly, both on the baseline sample, and interestingly also it increased in those reaching the primary end-point during the hospitalization. So it provided a very strong and independent information also when we adjusted for clinical risk scores, like the NEWS score. So that was a very pleasant surprise to see that there was one marker that's actually performed so well. The other marker that's also performed well was Ferritin. Dr. Carolyn Lam: Very interesting, and so the new score being the National Early Warning Score. Thank you. Verra, I really love to bring in your thoughts. I mean, could you take us behind the scenes with the editors? What did you think when you saw this paper? Dr. Vera Bittner: As you know, I mean, a lot of journals have been inundated by COVID papers, and so this one stuck out to us, because it's the first time that we had seen that anybody linked GDF-15 to a COVID population, even though it has been out in the literature for ACS, and in my prognostication, and in a healthy populations, and in chronic coronary disease populations, heart failure, and so on. So this is the first time that we've seen it applied there. Dr. Vera Bittner: Then I would echo some of the things that Torbjorn said, that we were also impressed, that it was prospective, because when you look at some of the other biomarker studies, what was prognostic in one with then not shake out the other one, because either different variables were included in the models, because the population's differed. So to have something that was representative of the population that was actually admitted to this, Norwegian Academic Hospital, stood out to us. So we're excited to get this paper basically for circulation, and hope that it also will be impetus for future research. Dr. Carolyn Lam: Thank you so much for sharing that end for helping us publish such a beautiful paper. Did you have some questions for two of your own? Dr. Vera Bittner: Yeah. So what stuck out to me is that you had this a whole crew of biomarkers, and then when you looked ultimately at the final model, there were two that were standing out, that was ferritin, and it was the GDF-15, and then when I looked at your graph, it looks like not only did these biomarkers measure different contrasts, but their time-course also seemed to be different, and so I was just wondering whether you had thought about, maybe using these to joint the model outcome, and whether we might even be able to get more information that way. Dr. Torbjørn Omland: I think that's an excellent suggestion, and as you correctly pointed out, they do have different sort of profiles and ferritin being an acute phase reactant, having various sort of dramatic early rise whereas we see that GDF-15 increased progressively during the course of hospitalization in the most severe patients. I think when combining them, is actually a great IMT that we should look further into. Dr. Carolyn Lam: Very nice. Torbjorn, if I could, I've got a couple of questions too. So 123 patients, 35 of whom had the primary outcome, right? So that may be sort of seen as, is this too small? and they're all hospitalized patients. So could I ask, what do you predict maybe seen in a larger population or outside of Norway or in a non-hospitalized population? Dr. Torbjørn Omland: So as you say, we were early with this report, but since it was submitted, there has been a couple of smaller studies that seemed to confirm our results. So that is reassuring, but of course we would like to have studied this in logical patients. We are in touch with the other biobank samples that could possibly confirm the data. So that's one obvious step. Then it's very interesting, as you say, could we sort of expand this to also apply to non-hospitalized patients? I think that it would be a very interesting hypothesis to test, and I think there's still a pretty good rationale for this. Dr. Torbjørn Omland: It's interesting that the insoluble group actually showed a correlation that when the soluble ST2 concentrations and GDF-15. So there might be that those with more susceptibility to COVID infections, actually, I thought that, that is actually reflected by GDF-15 concentrations, but the challenge is how to sort of get a representative non-hospitalized population, but interestingly, I was approached by some of the hospital staff that actually are in contact with general practitioners, and wanted sort of implement this test also for this group. Dr. Carolyn Lam: So Verra, we're really grateful that Allan Jaffe was working with you in managing this beautiful paper, and if you don't mind me cheekily paraphrasing that you said you might channel him, if you could, what would the channeled Allan Jaffe perhaps say about what's needed in this whole biomarkers fear in COVID-19? Dr. Vera Bittner: Hopefully, many. A channeling element is obviously difficult, because he is such an incredible expert on biomarkers that I can't even pretend to be able to see, that you might be thinking, but it seems to me that one thing that we could all agree on is that it would be really exciting if something like the: get with the guidelines COVID registry, could decide to measure this marker perspectively in the participating hospitals, for example. Dr. Vera Bittner: Then be able to look at this in a much, much larger population. I mean, especially with different ethnic backgrounds as well. I mean, I noticed actually to my surprise that, this Norwegian study how to fairly high proportion of Asians in the sample, but that may not be the ethnic distribution that we might see in different regions of the US, or different regions of the world. So it would be really nice to incorporate the measurement of this biomarker in much larger datasets. So things can be explored a bit further. Dr. Carolyn Lam: That's excellent, and Torbjorn, if you could channel Allan. What would you say? Dr. Torbjørn Omland: That's a difficult path, but absolutely just to me what Verra said. Then I think the importance of prospective studies in the COVID biomarker field, I think is our at most importance. Dr. Carolyn Lam: I think on behalf of both Torbjorn and I, and in fact everyone in circulation. Thank you, Verra for the amazing work that you and your team do for circulation as well. Thank you so much for making the time to share your thoughts today and thank you for that beautiful, beautiful paper both of you. Thank you. (singing). Listeners you've been listening to Circulation on the Run. Thank you for joining us from Greg and I. Don't forget to tune in again next week. Dr. Greg Hundley: This program is copyright, the American Heart Association 2020.  

This free iTunes segment is just one tiny snippet of the fully-loaded 3-hour monthly Primary Care RAP show. Earn CME on your commute while getting the latest practice-changing primary care information: journal article breakdowns, evidence-based topic reviews, critical guideline updates, conversations with experts, and so much more. Sign up for the full show at  hippoed.com/PCRAPPOD We have been waiting and waiting and waiting for the new community acquired guidelines. And here they are! Infectious Diseases expert Devang Patel,MD joins Matt DeLaney, MD and Neda Frayha, MD for a conversation on CAP in general and the new guidelines in specific. Pearls: The latest guidelines for community acquired pneumonia now includes amoxicillin or doxycycline for 5-7 days as first-line treatment given the rising rates of macrolide resistance and less emphasis on coverage of atypical pneumonia pathogens.   Review of pathophysiology: Lower respiratory tract often preceded by an upper respiratory tract infection, that inhibits ability to clear mucus and pathogens invade the lungs Other risk factors: Smoking Elderly Immune compromise (ie: infection, steroids, cancer) Pathogens: Typical - strep pneumo, haemophilus, staph aureus Atypical (more common) - influenza, parainfluenza, mycoplasma, chlamydia pneumoniae, legionella, coccidioidomycosis (in the southwest) EPIC Study (2015) - study to determine pneumonia pathogens using all the tools we have available (culture, PCR) 62% no pathogen detected 22% viral - most were rhinovirus which does not cause lower respiratory tract infections but predisposes to pneumonia Strep pneumonia was the number one bacterial pathogen Bottomline: we still don’t know what causes most pneumonias but just that our patients get better with antibiotics Differentiating between typical v. atypical pneumonias - there’s no good way to know viral versus bacterial → default is to treat as bacterial pneumonia with antibiotics Diagnosis: Clinical features (cough, fever, sputum production, pleuritic chest pain, crackles) Guidelines recommend a chest x-ray For outpatient uncomplicated pneumonia, don’t get blood or sputum cultures For severe cases (those with risk factors for multidrug resistance, MRSA, or pseudomonas) you still want to get blood and sputum cultures Pearls: No more healthcare-associated pneumonia Emphasis on CURB-65 to assess severity of who does NOT need to be admitted Procalcitonin is NOT endorsed as a way to determine who gets antibiotics and who doesn’t Treatment: Increasing strep pneumo resistance to macrolides so no more monotherapy with macrolide (azithromycin) unless resistance is less than 20% in the area First-line in non-hospitalized adult is amoxicillin or doxycycline for 5-7 days Steroids recommended not use but may be considered in septic shock Commentary from Dr. Patel (ID specialist): Not a major change in practice other than to consider not covering atypicals in an otherwise healthy person   REFERENCES: Metlay JP, Waterer GW, Long AC, et al on behalf of the American Thoracic Society and Infectious Diseases Society of America. Diagnosis and Treatment of Adults with Community-Acquired Pneumonia. An Official Clinical Practice Guideline of the American Thoracic Society and Infectious Diseases Society of America. Am J Respir Crit Care Med. 2019 Oct 1;200(7):e45-e67. doi: 10.1164/rccm.201908-1581ST. https://www.atsjournals.org/doi/10.1164/rccm.201908-1581ST  Jain S, Self WH, Wunderink RG, et al for the CDC EPIC Study Team. Community-acquired pneumonia requiring hospitalization among U.S. adults. N Engl J Med 2015; 373:415-427. Postma DF, van Werkhoven CH, van Elden LJR, et al for the CAP-START Study Group. Antibiotic treatment strategies for community-acquired pneumonia in adults. N Engl J Med 2015; 372:1312-1323.

Procalcitonin testing on admission seems to be a valuable piece of information for early risk assessment and ruling out bacterial co-infection in COVID-19 patients.

Procalcitonin testing on admission seems to be a valuable piece of information for early risk assessment and ruling out bacterial co-infection in COVID-19 patients.

David F. Gaieski, MD, Associate Professor, Emergency Medicine, Jefferson University Hospitals, Philadelphia, interviews Charles B. Cairns, MD, the Walter H. and Leonore Annenberg Dean of the College of Medicine, Senior Vice President for Medical Affairs, and Professor of Medicine and Emergency Medicine at Drexel University. Sponsored by bioMérieux, Inc.

In this episode, Eric and Joe do a deep dive on sepsis with Dr. Rob Stenstrom, Sepsis and Infections Lead for the EM Network. They discuss the most practical definition of sepsis in the ED and which diagnostic score to use. They find the bottom line on serum lactate, fluid treatment, and blood cultures and antibiotic timing. Rob answers questions on which pressor to use, central access timing, and the status of novel therapies. Plus, is there a genetic predisposition to developing sepsis?Sepsis Stats1 in 18 deaths in Canada involve Sepsis30% of Canadians hospitalized with sepsis die within 1 month.Related linksSepsis and Septic Shock – DiagnosisSepsis with Hypotension and Septic Shock – TreatmentSepsis without Hypotension – TreatmentPediatric Septic Shock ManagementEM Network Sepsis and Soft Tissue Infections Research ProgramEnd of Shift HostsEric AngusEric Angus is an emergency physician and trauma team leader at Lions Gate Hospital. He is married with 15-year-old twins. His nonmedical interests include origami, meditation, mountain biking, skiing, rock climbing, just generally being outside, and drinking wine. He has a diploma in mountain medicine and volunteers for ski patrol and the North Shore Rescue team. He is an ATLS instructor. He dabbles in stoicism and Buddhist philosophies.Joe HaegertJoe Haegert practices emergency and trauma medicine at the Royal Columbian Hospital in New Westminster, British Columbia. He is a talented teacher, engaging speaker, and devoted clinician. He lives in South Surrey with his wife Sandy and managed to raise three children without much incident. Known for his unflagging enthusiasm, Joe enjoys all aspects of the outdoors and recently has taken to turning wooden burls into all manner of bowls and tables.DisclaimerThe discussion within the End of Shift podcast may be graphic, and some listeners may find the language and content disturbing. The views and opinions expressed in this podcast are those of the participants and do not necessarily reflect the official policy or position of the BC Emergency Medicine Network.

David F. Gaieski, MD, Associate Professor, Emergency Medicine, Jefferson University Hospitals, Philadelphia, interviews Daniel Feinstein, MD, Adult Intensivist and Clinical Associate Professor, Medicine, University of North Carolina. He has extensive research in antibiotic administration and is a pioneer in antibiotic stewardship and sepsis care. Sponsored by bioMérieux, Inc.

David F. Gaieski, MD, Associate Professor, Emergency Medicine, Jefferson University Hospitals, Philadelphia, interviews Robert Balk, MD, Associate Chief Medical Officer, Critical Care, and Director, Division of Pulmonary, Critical Care, and Sleep Medicine, Rush University Medical Center, Chicago. Sponsored by bioMérieux, Inc.

Dieses Mal haben wir gleich 4, hoffentlich interessante, Beiträge für euch. Die Themen von Folge 13 sind: ACILS ( Advanced Critical Illness Life Support ), Blutkulturen, adipöse Pat.im Schockraum und Procalcitonin.

In this episode, we right some wrongs. As we said in the beginning, given the fast pace we were bound to be wrong, and will be again. 1) New paradigm for COVID-19 patients 2) Procalcitonin: not as good as we thought 3) Malignant atelectasis and the crashing hypoxemia 4)SARS-COV-2 & DIC 5) Awake Proning / CPAP / Vent Splitting / Extubation 6) Ethical dilemmas

David F. Gaieski, MD, Associate Professor, Emergency Medicine, Jefferson University Hospitals, Philadelphia, interviews Devendra N. Amin, MD, Medical Director of Critical Care Services, Medical/Surgical ICU and Neurocritical Care ICU at Morton Plant Hospital, Clearwater, FL, about the importance of PCT protocol adherence to optimize antimicrobial stewardship. Sponsored by bioMérieux, Inc.

COVID-19:  Troponin, Abx, Chloroquine, X-rays, Rationing Tests, Public Health Responsibilities Rob Orman MD and Rick Pescatore DO   In this episode I speak with Dr. Rick Pescatore, Chief Physician for Preparedness for the state of Delaware and a front-line emergency physician.  While the general topic is the COVID-19 pandemic, specific issues discussed include: triage decisions, X-rays, troponin, what to do when there’s limited testing ability, antibiotics, chloroquine, viable strategies for managing homeless populations, and more.  Let’s go.   We’re in this strange time of limited testing capacity (due to insufficient swabs, testing kits, universal transport media, lab equipment, etc.)  with an exploding infection. If you are working in an area where COVID is rampant and you can only test a select population, what is the highest yield?    When you have a dearth of tests, they need to be rationed.   Patients who come in in respiratory distress and with obvious upper and lower respiratory illness need to be assumed to have COVID until proven otherwise. The decision has to move away from identifying who is at risk for deterioration or for having the disease and needs to move toward identifying who is at risk for infecting others. This is a constantly evolving process and recommendations will change.  But FOR NOW, when tests are limited, Rick recommends we use those tests to mitigate disease spread.  DO NOT TEST:  the asymptomatic or the mildly symptomatic. DO TEST:  hospitalized patients with respiratory illness, symptomatic people who are likely to put others at risk (health care workers, mass transit drivers, law enforcement officers, firefighters, EMS providers.  As emergency physicians, it’s incumbent upon us to not forget about our differential diagnosis.  We don’t want to focus so much on COVID that we miss pulmonary emboli and other life-threatening causes of respiratory distress.   Are there specific symptoms that can identify who is more likely to deteriorate?  The only sign or symptom that seems to have any discriminatory capability for severe disease is a patient complaint of shortness of breath.   Other risk possible factors:  males, elderly, diabetics.   Tent management Who should get a chest x-ray?    Have a low threshold for CXR in those with chest pain, SOB, severe cough, rhonchi, and/or rales.  We must remember, however, that the Chinese data showed that the overwhelming majority of patients had radiographic findings whether or not they had severe disease.   When should we send patients to the ED for further testing (CBC, ECG, troponin, other labs) and advanced treatment?   Lacking evidence to guide us, we rely on our gestalt to separate the sick from the not sick. If there’s any concern about myocarditis, ED evaluation is mandatory. Pneumonia severity scoring tools can be helpful to guide disposition.   Should we give antibiotics to the “not so sick” patient with infiltrate(s) on x-ray?   Yes. Azithromycin is the antibiotic of choice due to its antibacterial and immunomodulatory properties.   What about hydroxychloroquine or chloroquine?   There is limited but justifiable data showing that implementation of one of these agents may be effective at stopping viral replication. Dosing recommendations are all over the map, but many suggest a 400 mg loading dose followed by 2oo mg bid for the duration of the illness. Studies in California are looking at hydroxychloroquine for prophylaxis for providers.  These drugs have few side effects and are not at this time a limited resource.  Both azithro and chloroquine are QTc prolonging   Once a patient is triaged from the tent to the ED, what is the inflection point for admission to the hospital and what work-up should be initiated?   Many who are identified to be sick enough to come into the ED are going to require hospitalization. Labs should include:  CBC, BMP, troponin, CRP, and procalcitonin.  Troponin elevation has been found more common in non-survivors and those with critical illness CRP is one of several inflammatory markers that, when elevated, can indicate cytokine storm. This subset of patients has a prognosis of severe disease with different avenues of treatment. Procalcitonin has been used in China to help determine when antibiotics can be stopped.   What should be the disposition for homeless patients with suspected COVID who do not meet admission criteria based on their clinical severity?   These patients are going to need assistance from the public health infrastructure of the state or region. There will need to be structures (tents, buildings, etc.) dedicated to house these patients. The general public will soon recognize what we have known for ages:  the social safety net of the ED and of the hospital cannot continue to weather the strain of the social service failures that are prevalent throughout the nation.   Troponin in COVID ACC Update on Troponin and BNP March 18 Link ACC Cardiologist’s Perspective Treating COVID in China Link   Chen C, Chen C, Yan JT, Zhou N, Zhao JP, Wang DW. Analysis of myocardial injury in patients with COVID-19 and association between concomitant cardiovascular diseases and severity of COVID-19.  Zhonghua Xin Xue Guan Bing Za  Zhi. 2020 Mar 6;48(0)PMID: 32141280. Full text link (Google with translate to english)   Zhou F, Yu T, Du R, Fan G, Liu Y, Liu Z, Xiang J, Wang Y, Song B, Gu X, Guan L, Wei Y, Li H, Wu X, Xu J, Tu S, Zhang Y, Chen H, Cao B. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet. 2020 Mar 11. PMID: 32171076. Full Text Link   Azithro plus Chloroquine  Gautret et al. (2020) Hydroxychloroquine and azithromycin as a treatment of  COVID‐19: results of an open‐label non‐randomized clinical trial. International Journal of  Antimicrobial Agents – In Press 17 March 2020 Full Text Link   Editor-in-Chief:  Rob Orman, MD Associate Editor: Melissa Orman, MD

We have been waiting and waiting and waiting for the new community acquired guidelines. And here they are! Infectious Diseases expert Dr. Devang Patel, MD joins Matt DeLaney, MD, FACEP, FAAEM and Neda Frayha, MD for a conversation on CAP in general and the new guidelines in specific. For more incredible segments like this, subscribe to PC:RAP today. You'll never miss a moment of the program and earn 42 hours of CME per year.  Pearls: The latest guidelines for community acquired pneumonia now includes amoxicillin or doxycycline for 5-7 days as first-line treatment given the rising rates of macrolide resistance and less emphasis on coverage of atypical pneumonia pathogens. Review of pathophysiology: Lower respiratory tract often preceded by an upper respiratory tract infection, that inhibits ability to clear mucus and pathogens invade the lungs Other risk factors: Smoking Elderly Immune compromise (ie: infection, steroids, cancer) Pathogens: Typical - strep pneumo, haemophilus, staph aureus Atypical (more common) - influenza, parainfluenza, mycoplasma, chlamydia pneumoniae, legionella, coccidioidomycosis (in the southwest) EPIC Study (2015) - study to determine pneumonia pathogens using all the tools we have available (culture, PCR) 62% no pathogen detected 22% viral - most were rhinovirus which does not cause lower respiratory tract infections but predisposes to pneumonia Strep pneumonia was the number one bacterial pathogen Bottomline: we still don’t know what causes most pneumonias but just that our patients get better with antibiotics Differentiating between typical v. atypical pneumonias - there’s no good way to know viral versus bacterial → default is to treat as bacterial pneumonia with antibiotics Diagnosis: Clinical features (cough, fever, sputum production, pleuritic chest pain, crackles) Guidelines recommend a chest x-ray For outpatient uncomplicated pneumonia, don’t get blood or sputum cultures For severe cases (those with risk factors for multidrug resistance, MRSA, or pseudomonas) you still want to get blood and sputum cultures Pearls: No more healthcare-associated pneumonia Emphasis on CURB-65 to assess severity of who does NOT need to be admitted Procalcitonin is NOT endorsed as a way to determine who gets antibiotics and who doesn’t Treatment: Increasing strep pneumo resistance to macrolides so no more monotherapy with macrolide (azithromycin) unless resistance is less than 20% in the area First-line in non-hospitalized adult is amoxicillin or doxycycline for 5-7 days Steroids recommended not use but may be considered in septic shock Commentary from Dr. Patel (ID specialist): Not a major change in practice other than to consider not covering atypicals in an otherwise healthy person   REFERENCES: Metlay JP, Waterer GW, Long AC, et al on behalf of the American Thoracic Society and Infectious Diseases Society of America. Diagnosis and Treatment of Adults with Community-Acquired Pneumonia. An Official Clinical Practice Guideline of the American Thoracic Society and Infectious Diseases Society of America. Am J Respir Crit Care Med. 2019 Oct 1;200(7):e45-e67. doi: 10.1164/rccm.201908-1581ST. https://www.atsjournals.org/doi/10.1164/rccm.201908-1581ST  Jain S, Self WH, Wunderink RG, et al for the CDC EPIC Study Team. Community-acquired pneumonia requiring hospitalization among U.S. adults. N Engl J Med 2015; 373:415-427. Postma DF, van Werkhoven CH, van Elden LJR, et al for the CAP-START Study Group. Antibiotic treatment strategies for community-acquired pneumonia in adults. N Engl J Med 2015; 372:1312-1323.

Matthew DeLaney, MD  and Rick Pescatore, DO discuss the new IDSA updates regarding the diagnosis, disposition and treatment of patients with possible community acquired pneumonia. There is so much more to Urgent Care RAP each month? Click Here to hear more of what you need to be ready each day and we'll toss in 42 CME hours per year to boot. Pearls: When considering influenza, patients should be tested using NAAT rather than diagnosed clinically. Patients with test proven influenza and infiltrates on CXR should receive oseltamivir, regardless of duration of symptoms, in addition to appropriate antibiotics Patients should be risk stratified using a clinical decision tool, preferably PSI/PORT score,  to determine who is likely to benefit most from hospital admission. Procalcitonin is no longer recommended in the initial evaluation of patients with possible pneumonia.  At the end of 2019, the American Thoracic Society (ATS) and the Infectious Disease Society of America (IDSA) released the first update of the treatment guidelines for community acquired pneumonia (CAP) in >10 years.  IDSA now recommends more routine testing for influenza using nucleic acid amplification testing (NAAT) for influenza because of enhanced sensitivity of NAAT compared to older antigen based testing (>90% vs. ~50% sensitivity).  The IDSA now recommends that patients with test proven influenza and an infiltrate on CXR receive oseltamivir (regardless of duration of symptoms) in addition to appropriate antibiotics. 30% of deaths from influenza come from bacterial co-infection.  IDSA recommends risk stratifying patients with a Pneumonia Severity Index (PSI)/PORT score and recommends against relying heavily on a CURB-65 score to determine which patients will benefit from hospitalization.  Several questions on the PSI rely on lab testing which may not be available in UC, however, the parameters give guidance to factors associated with higher risk of adverse outcomes in patients with pneumonia. https://www.mdcalc.com/psi-port-score-pneumonia-severity-index-cap Clinical gestalt and assessment are also critical. Patients who appear ill and/or show signs of respiratory distress should be referred immediately to an ED. The guidelines also discuss major and minor criteria suggesting need for ICU admission including need for intubation, hypotension, tachypnea, and multilobar infiltrates. Multilobar pneumonia is a concerning finding and an independent predictor of poor outcome.  All patients with multilobar pneumonia should be referred to an ED for further evaluation. These guidelines suggest that, based on the low quality of evidence supporting utility, procalcitonin is no longer recommended in the diagnosis or treatment of CAP. There may be some limited utility in specific patients (mostly hospital inpatients) however, so this test is probably not going away, but having access to PCT testing from UC shouldn’t be a priority.    References: Metlay JP, et al. Diagnosis and Treatment of Adults with Community-acquired Pneumonia. An Official Clinical Practice Guideline of the American Thoracic Society and Infectious Diseases Society of America. Am J Respir Crit Care Med. 2019 Oct 1;200(7):e45-e67. doi: 10.1164/rccm.201908-1581ST. PubMed PMID: 31573350 https://www.thennt.com/nnt/corticosteroids-treating-pneumonia/ Eliakim-Raz N, et al. Empiric antibiotic coverage of atypical pathogens for community-acquired pneumonia in hospitalized adults. Cochrane Database Syst Rev.  2012 Sep 12;(9):CD004418. doi: 10.1002/14651858.CD004418.pub4. Review.PubMed PMID: 22972070.

Team up with the authors of the JAMA Medicine series on Medical Overuse, Dr. Dan Morgan @dr_dmorgan (University of Maryland) and Dr. Deborah Korenstein @DKorenstein (Memorial Sloan Kettering). We discuss procalcitonin (again!), the dangers of incidentalomas, risks of chest CT for lung cancer screening, the easiest place to get antibiotics for a viral infection, and why not to treat subclinical hypothyroidism despite guidelines. Trying to find ways to shed the fat off of some common medical practices? Look no further.  ACP members can claim CME-MOC credit at https://www.acponline.org/curbsiders (CME goes live at 0900 ET on the episode’s release date).  Show Notes | Subscribe | Spotify | Schwag! | Top Picks | Mailing List | thecurbsiders@gmail.com Credits Written and Produced by: Justin Berk, MD MPH MBA Infographic: Justin Berk, MD MPH MBA Cover Art: Matthew Watto MD, FACP Hosts: Stuart Brigham MD; Matthew Watto MD, FACP; Paul Williams MD, FACP    Editor: Molly Heublein MD, Matthew Watto MD, FACP, Emi Okamoto MD (written materials); Clair Morgan of Nodderly.com (audio) Guest:  Daniel Morgan MD, Deborah Korenstein MD, FACP Time Stamps 00:00 Intro, disclaimer, guest bios 04:45 Guest one-liners Picks of the Week*: The Fifth Season is part of The Broken Earth Trilogy by NK Jemisen; The Great Believers: A Novel by Rebecca Makkai; A Constellation of Viral Phenomena by Anthony Marra 09:22 Best advice 11:18 Defining Medical Overuse and defining categories 19:20 Procalcitonin testing for pneumonia 27:42 Imaging and incidentalomas 37:38 Lung cancer screening CT scan; the Bach model 46:25 Urgent care and antibiotic prescriptions for viral illnesses 52:43 Subclinical hypothyroidism 58:32 Take home points 61:00 Outro and Stuart tells us about his knee pain *The Curbsiders participates in the Amazon Services LLC Associates Program, an affiliate advertising program designed to provide a means for sites to earn advertising commissions by linking to Amazon. Simply put, if you click on my Amazon.com links and buy something we earn a (very) small commission, yet you don’t pay any extra. Goal Listeners will consider 5 of the top articles from 2018 that demonstrate signs of medical overuse that seem to offer more harm than benefit to patients. Learning objectives After listening to this episode listeners will…   Define medical overuse Discuss recent data about the utility of procalcitonin for antibiotic stewardship in respiratory infections. Recall the frequency incidentalomas on imaging and which modalities are associated with the highest risk. Identify the differences in benefits of annual lung cancer screening with CT based on baseline risk Recall the lack of evidence for treatment of asymptomatic subclinical hypothyroidism Describe the locations that are associated with more antibiotic prescriptions for viral infections. Disclosures Dr. Morgan and Dr. Korenstein report no relevant financial disclosures. The Curbsiders report no relevant financial disclosures.  Citation Morgan D, Korenstein D, Berk J, Williams PN, Brigham SK, Watto MF. “#189 Medical Overuse”. The Curbsiders Internal Medicine Podcast. https://thecurbsiders.com/episode-list. December 23, 2019.

The Spiro Podcast is written for health care specialists that practice pulmonary, critical care and/or sleep medicine. We cover a broad range of subjects from the newest recommendations for your clinic to pending diagnostic and therapeutic options for your patients that are on the horizon. From time to time we will interview thought leaders in our specialty with our two-minute elevator pitch and are going to be sharing how certain long term clinical trials are going in the United States and Abroad. So subscribe now to The Spiro Podcast so you can help your patients while being the most informed.

CHEST 2019 Recap Part 2 featuring random pearls and highlights from #CHEST2019 in New Orleans including: tips for addressing futile end-of-life care, bleeding in the ICU, DOAC reversal agents, use of procalcitonin and monocyte distribution width to identify sepsis, vitamin C for sepsis treatment, small particles and lung cancer risk, augmented reality/virtual learning, and tech as a teaching tool. Special thanks to Dr. Bill Kelly and his team at CHEST (@accpchest) for their hospitality.  Full show notes available at https://thecurbsiders.com/episode-list. Join our mailing list and receive a PDF copy of our show notes every Monday. Rate us on iTunes, recommend a guest or topic and give feedback at thecurbsiders@gmail.com. Credits Written, produced, and co-hosted by: Sarah Phoebe Roberts MPH; Paul Williams MD, FACP; Stuart Brigham MD; Matthew Watto MD, FACP Edited by: Matthew Watto MD, FACP Special Guests: Nina Maouelainin DO, MBA (@lungsolutions); Erin Narewski DO, FCCP (@erinnarewski); Chidinma Chima-Melton MD, FCCP (@LABritishLady), Kim Fabyan MD (@kfabsMD) Time Stamps 00:00 Pun, Disclaimer, Intro 03:58 Dr Erin Narewski on end of life conversations 13:30 Bleeding in the ICU 15:40 DOACs and reversal agents 18:40 Dr Chidinma Chima-Melton on ICU visiting hours 22:50 Vitamin C use in the ICU, Stuart’s Vitamin C rant 29:22 Monocyte distribution width for identifying patients with sepsis 30:55 Sarah Phoebe Roberts on Procalcitonin and CRP for sepsis 39:36 Dr Nina on technological innovations in MedEd: Virtual bronchoscopy; Dropping a computer in a remote village 46:49 Sarah Phoebe Roberts on Small particles and lung cancer risk 54:48 Outro Citation Narewski E, Chima-Melton C, Maouelainin N, Roberts SP, Williams P, Brigham S, Fayban K, Watto MF. “CHEST 2019 Recap Part 2”. The Curbsiders Internal Medicine Podcast https://thecurbsiders.com/episode-list. October 30, 2019.

In this podcast, Kevin Downes, MD, discusses procalcitonin as a marker for sepsis, how a procalcitonin test fares among other diagnostic tests, and how this testing can guide antibiotic stewardship. More at: www.consultant360.com/infectious-diseases

The EMGuideWire Team is visited by a prior crew member, Russell Trigonis, MD! Join them as they discuss how the patient diagnosed with Sepsis in your ED has their care continued in the ICU! Pearls Start pressors with IVF (30-40cc/kg). NE at 7mcg/min peripherally can always be stopped, but better earlier than later. Increase NE until at 20mcg/min, if still hypotensive, then add a 2nd pressor like Vasopressin at 0.03units/min and 100mg Hydrocortisone Q8h. Start antibiotics early and identify source. CXR, US lungs/abd, UA, CT abd should all be considered.  Procalcitonin is helpful for stopping abx. Doesn’t change ED treatment. Don’t order Vitamin C or thiamine in ED. -Travis Barlock, MD

Dr Kimberly Manning joins to discuss imposter syndrome, how vacations affect health, and an update on the pneumonia vaccine, PCV13. Plus, hot takes on the dangers of vaping, and using procalcitonin and CRP to determine need for antibiotics.  Howdy, gentle listeners! It’s that special time of year when the school doors reopen, classrooms are awash in ‘new pencil’ smell, and FOAMed fans grab their trays and head to the cafeteria for some tasty knowledge food. Rest assured your Curbsiders friends have saved you a seat at the lunch table for this very special September 2019 episode!  Today we are joined by Dr. Kimberly Manning MD, FACP, FAAP, who is an Associate Professor of Medicine at Emory University School of Medicine. Dr. Manning authors a blog (“Reflections of a Grady Doctor”) that was named in 2010 by ‘O’ The Oprah Magazine as one of “four top medical blogs you should read.” She can also be found on Twitter, @gradydoctor. Thanks for listening! Full show notes at https://thecurbsiders.com/episode-list. Rate us on iTunes, recommend a guest or topic and give feedback at thecurbsiders@gmail.com. Credits  Written and Produced by: Sarah Phoebe Roberts MPH, Christopher Chiu MD, FACP, FAAP Hosts: Matthew Watto MD, FACP; Sarah Phoebe Roberts MPH, Paul Williams MD, FACP; and Christopher Chiu MD, FACP, FAAP Editor: Christopher Chiu MD, FACP, FAAP; Emi Okamoto MD Cover-Art: Christopher Chiu MD, FACP, FAAP Guest: Kimberly Manning MD, FACP, FAAP Time stamps 00:00 Introduction/Disclaimer 03:15 Guest bio 05:00 Getting to know Dr. Manning 11:05 Picks of the week*: Reflections of a Grady Doctor, Dr. Kimberly Manning’s Blog; To Kill a Mockingbird by Harper Lee, audiobook narrated by Sissy Spacek; LeVar Burton Reads, a podcast; Aziz Ansari Right Now (comedy special) and Master of None (TV show); Garfield Minus Garfield, an existential take on a classic comic; Clue, the 1985 movie 17:15 Paul’s vaping update (CDC media statement) 20:10 Procalcitonin, CRP and antibiotic prescription for COPD exacerbation 24:30 Pneumococcal conjugate vaccine 30:00 Imposter syndrome 49:00 Vacation time and metabolic syndrome 57:00 Wrap-up and outro *The Curbsiders participates in the Amazon Services LLC Associates Program, an affiliate advertising program designed to provide a means for sites to earn advertising commissions by linking to Amazon. Simply put, if you click on my Amazon.com links and buy something we earn a (very) small commission, yet you don’t pay any extra.

Speakers: - Tom File, MD, MSc, MACP, FIDSA, FCCP - Shira Doron, MD, FIDSA - Moderator: Whitney Buckel, PharmD Summary: Procalcitonin has been shown in numerous trials to reduce unnecessary antibiotic use associated with sepsis and respiratory infections and is a diagnostic tool that antibiotic stewardship programs can use to improve antibiotic use. This episode discussed the role of procalcitonin in antibiotic stewardship programs and examples of intervention to improve the use of procalcitonin.

In this episode we discuss the elements of documenting a patient's decision-making capacity, pearls from the last month of ERcast, our new newsletter, and Carl Sagan's Pale Blue Dot.   Links from this episode Sign up for the ERcast newsletter HERE THIS is the newsletter discussed in today's podcast If you want to learn more about the full on, full cowbell, full BAFERD, total ERcast experience, Click Here In case the links above don't work URL for newsletter discussed in this podcast: https://mailchi.mp/hippoed/some-things-just-dont-work-on-a-podcast-2090489 URL for newsletter signup: https://mailchi.mp/hippoed/ercastnewsletter

Eric Yeager, MD Travis Neill, PA-C, MMS Assistant Medical Director - Vivage References: Cedric Daubin, "Procalcitonin algorithm to guide initial antibiotic therapy in acute exacerbations of COPD admitted to the ICU: a randomized multicenter study", Springer, 2018 Eosinophilic inflammation in COPD: prevalence and clinical characteristics", Agora Research Letters Travis Neill, COPD Pearls" PA-C, 8/1/19 Anthony W Huckle, et. al.,"Prophylactic Antibiotic Use in COPD and the Potential Anti-Inflammatory Activities of Antibiotics", Respiratory Care, May, 2018 Yaeger, Abx in COPD working document

Hello from Seattle! We are at the PHM National Conference and one of the most popular talks was the "Review of Is it Bacterial or Not? When to use Procalcitonin". It was standing room only. The speakers were kind enough to talk with us today to summarize their talk for anyone who missed it.  Our special guests are Drs. Rusty McCulloh and Marie Wang. There is no CME associated with this episode. 

In this episode of Critical Matters, we discuss the role of procalcitonin as a biomarker in lower respiratory tract infections and sepsis. Our guest is Dr. David Huang, the primary investigator in the recently published Procalcitonin-Guided Use of Antibiotics for Lower Respiratory Tract Infections (ProACT) clinical trial. He discusses lessons learned from this very important study and offers insight into the use of procalcitonin in clinical practice. ADDITIONAL RESOURCES: Procalcitonin-Guided Use of Antibiotics for Lower Respiratory Tract Infections (ProACT) clinical trial: https://bit.ly/2BTZNsf A meta-analysis evaluating the effect of procalcitonin-guided treatment on mortality in acute respiratory infections: https://bit.ly/2Un6Lgz FDA Executive Summary on Procalcitonin assay: https://bit.ly/2EiBN4r BOOKS MENTIONED IN THIS EPISODE: 7 Habits of Highly Effective People by Stephen R. Covey: https://amzn.to/2Ss0mPq Partners of the Heart by Vivien Thomas: https://amzn.to/2QC6vLP

Dominique Pepper, MD, and Andre C. Kalil, MD, MPH, join CHEST Podcast Editor, D. Kyle Hogarth, MD, FCCP, to discuss the serial procalcitonin measurement for antibiotic de-escalation and discontinuation.

2-Minute Tip — Remove Filler Words   Filler or crutch words are the bane of many a speaker’s existence. The ums, ahs, likes, verys, you knows, and more clutter up our talks and conversation so much we don’t even notice them. They waste time, annoy the audience and distract from your message. So get rid of them.   Easier said than done.   One technique is to have a friend or colleague listen to you practice your talk and ring a bell every time they hear a filler word. Once you actually know you are using them in real time, it becomes easier to eliminate them and relish the power of silence   Post Tip Discussion — Meet John Rohe   One of the terms you hear in the training field (and likely other education related fields as well) is the “sage on the stage.”   In describes the lecture format in many education contexts. The wise experts stands on the stage at the front of the room and imparts knowledge on to the lucky audience members. It’s one way communication, and it has its place, but can have a certain amount of arrogance associated with it.   Bio   John Rohe is a speaker who eschews the lectern and the stage. He a speaker and trainer in both the commercial and ecclesiastical fields, and one of themes that comes through in the episode is the importance of humility with your audience.   John’s experience ranges from start-ups to established multi-billion dollar enterprises. John launched the cardiac marker proBNP for Roche Diagnostics and the first personalized health (test and drug) for osteoarthritis for Roche Pharma, Roche Diagnostics and GSK.   ​ He also internationalized sales for RPS, revived sales of Procalcitonin for Thermo Fisher, grew Alere’s PT/INR home testing from $9 million to $25 million in 1 year and boosted equipment service contracts for BD.   ​ John has taken products from R&D through FDA clearance and achieved CMS and other third-party reimbursement. He has implemented user friendly CRMs and automated quoting systems, and he integrated marketing collateral with sales force access. He has also been responsible for developing and implementing automated quoting and contracting systems.     John’ Speaker Evaluation Checklist   Are they using filler words? Do they appear to be knowledgeable about the material? Are they speaking to the audience? Are they looking down at their notes? Are they reading slides to me? Are they moving around? Are they actively engaged with the audience?   Kirkpatrick Levels of Training Evaluation   How do the learners feel about their training experience? How effectively did the learners acquire new skills or knowledge? How effectively did the learners apply what they learned in training? How effectively did the training ultimately meet its goals for the organization?   You can read more about the Kirkpatrick framework here. It’s a fascinating mental exercise.   Links   Hycap Consulting http://hycapconsulting.org John’s Email John.rohe@hycap.org John on LinkedIn https://www.linkedin.com/in/johnrohe1/ John on Twitter https://twitter.com/johnrohe Kirkpatrick Model https://www.kirkpatrickpartners.com/Our-Philosophy/The-Kirkpatrick-Model Servant  Leadership with Lyle Tard http://2MinuteTalkTips.com/ServantLeader Caring and Connection with Richard Kauffman http://2MinuteTalkTips.com/Richard   Call To Action Check out the work John is doing at Hycap.org Share this episode with another speaker or trainer by giving the link http://2MinuteTalkTips.com/JohnRohe Don’t get best…get better   2-Minute Talk Tips is the public speaking podcast that help you become a more effective speaker in as little as 2 minutes a week.

Dr. Gllava reviews the value of the procalcitonin laboratory test as an inflammatory marker useful in making treatment decisions in infectious diseases patients. First, she introduces the idea of a biomarker: a laboratory assay that is useful in detecting inflammatory states. She then explains the advantages and disadvantages of procalcitonin as an ideal biomarker. Dr. Gllava goes on to describe the current recommendations for the use of procalcitonin in specific infectious conditions and reviews the body of scientific evidence for its use. Lastly, she reviews how hospitals can utilize procalcitonin-based algorithms to improve clinical care and promote antimicrobial stewardship.

Ranjit Deshpande, MD, and Simon W. Lam, PharmD, MS, BCPS, BCCCP, FCCM, discuss procalcitonin guidance during different phases of antibiotics management in patients admitted to intensive care units.

Ranjit Deshpande, MD, and Simon W. Lam, PharmD, MS, BCPS, BCCCP, FCCM, discuss procalcitonin guidance during different phases of antibiotics management in patients admitted to intensive care units.

Author: Michael Hunt, MD Educational Pearls: As many as 20% of women in assisted living have asymptomatic bacteriuria This can present a diagnostic conundrum when seeing these patients in the emergency department, particularly for altered mental status and deciding whether to treat True diagnosis of UTI in the emergency department is difficult as true diagnoses required culture results and repeated positive samples Procalcitonin is an emerging biomarker that may be helpful in determining the presence of infection References: Cortes-Penfield NW, Trautner BW, Jump RLP. Urinary Tract Infection and Asymptomatic Bacteriuria in Older Adults. Infect Dis Clin North Am. 2017 Dec;31(4):673-688. doi: 10.1016/j.idc.2017.07.002. Review. PubMed PMID: 29079155; PubMed Central PMCID: PMC5802407. Huang DT, Angus DC, Chang CH, Doi Y, Fine MJ, Kellum JA, Peck-Palmer OM, Pike F, Weissfeld LA, Yabes J, Yealy DM; ProACT Investigators.. Design and rationale of the Procalcitonin Antibiotic Consensus Trial (ProACT), a multicenter randomized trial of procalcitonin antibiotic guidance in lower respiratory tract infection. BMC Emerg Med. 2017 Aug 29;17(1):25. doi: 10.1186/s12873-017-0138-1. PubMed PMID: 28851296; PubMed Central PMCID: PMC5576372. Summarized by Erik Verzemnieks, MD

Ludwig H. Lin, MD, and Philipp Schuetz, MD, discuss procalcitonin and how it impacts treatment of sepsis.

Ludwig H. Lin, MD, and Philipp Schuetz, MD, discuss procalcitonin and how it impacts treatment of sepsis.

We dive deeper into the world of Procalcitonin and help explain what it’s all about, when you should order it and its clinical significance. See more and read attributions at pulmcast.com

Disclaimer: This is the unedited transcript of the podcast. Please excuse any typos. Jeff:  Welcome back to Emplify, the podcast corollary to EB Medicine’s Emergency Medicine Practice. I’m Jeff Nusbaum, and I’m back with my co-host, Nachi Gupta. This month, we’ll be talking Updates and Controversies in the Early Management of Sepsis and Septic Shock. We have a special  episode for you this month… We’ve brought Dr. Jeremy Rose, one of the peer reviewers, and a sepsis expert, on with us to talk through the content this month. Jeremy: Dr. Jeremy Rose here. Thanks for having me in on this conversation.  I’m always happy to talk about this topic because it’s clearly important.  There’s a great deal of confusion around sepsis and I hope that in the next couple minutes we can clarify things in a way that really help your average front line doc trying to get it right. Nachi: So Dr. Rose, before we get started, tell us a bit about your background and your interest in sepsis… Jeremy: I’m the Assistant Medical Director and Sepsis Chair at Mount Sinai Beth Israel in Manhattan.  For those listening, my hospital probably looks a little bit like yours.  We’re busy, interesting, and just a little rough around the edges.  We like it that way.  More importantly, though, we mirror the national averages regarding sepsis.  Roughly half of in-hospital mortality is associated with septic  in some fashion.  Pretty incredible when you think about it.  Half. Jeff:  Sepsis chair... clearly this is an important topic if it warrants it’s own chair at a major hospital in NYC. But getting back to the article this month. This month’s issue was authored by Faheem Guirgis, Laurent Page Black, and Elizabeth DeVos of the University of Florida, Department of Emergency Medicine. Nachi: And it was peer reviewed by Michael Allison, Assistant Director of the Adult ICU at Saint Agnes Hospital, and Jeremy Rose and Eric Steinberg of Mount Sinai Beth Israel. Jeff: So as well all know Sepsis is bread and butter emergency medicine, but, what is sepsis?  It seems that every month or so we have a new guideline, bundle, definition, or whatever… I think it’s best to start with the basics -  At its core, sepsis is a dysregulated response to infection that can be life-threatening. Nachi: Right and it’s the combined inflammatory with immunosuppressive features of sepsis that lead to the devastating organ dysfunction and even death. Optimal management of septic patients has been a source of intense research, stemming from the landmark study by Rivers in 2001. Jeremy, can you give us a little historical context there? Jeremy: Rivers was a real pioneer.  He found a 16% mortality reduction with randomization to an early aggressive care bundle.  Amazing work.  That being said, many components of that bundle have since been disregarded.  For example, Manny Rivers would measure CVP in all of his patients, something we rarely do. Nachi: Not to cut you off and steal your thunder there, but we’ll get to the most recent updates in management shortly. Let’s first talk definitions and terminology, and specifically, diagnosis, which is definitely a big elephant in the room. As Jeff mentioned a few minutes ago, diagnostic criteria have undergone so so so many changes. Jeff: Yes it has! 1991 marked the first standardized definition.  Then in 2001, sepsis-2 was introduced.  In 2014, the Society of Critical Care Medicine and the European Society of Intensive Care Medicine started a task force, and by 2016, updated definitions were out again! Sepsis-3!! A lot of this came after the realization that SIRS was just too broad and was overly sensitive and non-specific. Jeremy, why don’t you take us through Sepsis 3. Jeremy: So just to back up a little and frame this: Here’s the fundamental problem:  As we likes to say, “there’s no troponin for sepsis.”  And if you look at our patients, we tend not to miss the hypotensive, tachycardic, febrile patient.  We know they’re septic.  But how do we find the ones who don’t look as sick.  Frequently elderly, possibly with normal-ish vitals and no fever.  Those can be a lot harder to spot, but they may indeed be septic.  Also, for research purposes we have to have a common definition, so Sepsis 3 came up with something called the SOFA score. The problem with the SOFA score is that its difficult to perform in the ED.  It has parameters like bilirubin that often aren’t available when we want to screen out very sick patients.  Fortunately there is the abridged version qSOFA, which identifies non-icu patients who are at high risk of inpatient mortality. So here it is, and if you get one thing from this episode, this is it: There are ONLY 3 criteria to the qSOFA.  3 Criteria. RR > 22; AMS; SBP 2. So quite a few changes! Jeff: And Jeremy, sticky topic coming up here. Center for Medicare and Medicaid Services (or CMS) quality measures - They haven’t really caught on to and adapted to Sepsis-3 yet, have they? Jeremy:  The CMS mandate is based on the presence of SIRS criteria. Sepsis 3 is based on SOFA.  This is definitely confusing.  Part of the challenge in discussing this topic is separating out the QI guidelines from what is actually relevant to patient care based on the latest evidence-based medicine. Nachi: That seems fair.  We’re really going to put you in an uncomfortable spot for a second and push you here Jeremy. Do you have any insight into why CMS isn’t interested in following the mountains of research that have led to sepsis-3? Is there a reason they are sticking to their current criteria? Jeremy:  I think some of it is the slow pace of bureaucracy and the time that it takes to develop a consensus on management.  Even if we can agree on who is septic, it’s really hard, if not impossible to link the care to a pay-for-performance metric which is what CMS ultimately would like to see.  That’s not how Sepsis-3, or for that matter, SIRS, was designed to be used.  You’re trying to take a tool which was originally designed for research and mold them into a tool used for pay for performance. Nachi: What a struggle. The CMS metrics are slightly different from the 2001 sepsis guidelines also. Take a look at Table 2 of the article for a quick comparison of sepsis-3, 2001 sepsis, and cms side-by-side. And for those on twitter, we’ll be sure to tweet this table out too for your review. Jeff: With so many different scores and definitions, I think that adequately sets the stage for the challenge this month’s authors faced coming up with real evidenced based guidelines. Nachi: Oh absolutely.  And to make matters worse - this is a HUGE problem. We’re talking up to 850,000 ED visits annually in the US, and 19 million cases worldwide. Compounding this, sepsis results in death in approximately 1 out of 4 cases. Not only is it lethal, it is also very costly -- 17 billion dollars per year in the US alone! Jeff: And don’t forget importantly the 30-day hospital readmission rate. Sepsis is coming in at a higher readmission rate and cost per admission than acute MI, CHF, COPD, and PNA. Nachi: Let’s speak briefly on the etiology and pathophysiology of sepsis: we all know that sepsis is due to local infections that then become systemic. Previously, it was believed that the bacterial infection itself was the cause of the clinical syndrome of sepsis. However, we now know now that the syndrome of sepsis is due to the inflammatory and immunosuppressive mediators that were triggered by the infection. Normal immune regulatory safeguards fail and this leads to the syndrome. And interestingly, several studies have shown that critically ill septic patients experience reactivations of specific viruses that were previously limited to patients with severe immunosuppression. Jeff: Definitely something to look out for in your critically ill septic patients.  We should talk  briefly about the most common inciting infections that lead to sepsis. In order, these are: pneumonia, intra-abdominal infections, and urinary tract infections. No surprises there! Nachi: Yeah, that basically parallels my own experience, so that’s reassuring!  That takes us to our next potentially controversial topic - blood cultures.  Jeremy - we’re going to punt this one back to you Jeremy: This is another interesting topic that has received plenty of attention.   CMS loves blood cultures.  It’s an easy metric to track.  That doesn’t mean they’re always helpful.  We looked at our patients with lactates between 2.1 and 4.0 which had “severe sepsis.”  These patients were normotensive though, In other words, the ones that aren’t that sick.  We found that blood cultures are useful about 20% of the time.  That’s not bad.  So what do we do? We draw cultures before pushing antibiotics.  Is that helpful? Sometimes yes, does it waste money?  Debatable.  Does it help us meet our metrics, yes. Jeff: And I think that gets at the crux of the problem here: we don’t want to delay antibiotics on anybody, but we must balance this with the potential harm of further increasing the drug resistant bacterial population via sound antibiotic stewardship.  Remember also that there is a broad differential for sepsis, with several “sepsis mimics”. To name a few, we have PE, MI, CHF, acute pulmonary edema, DKA, thyroid storm, GI bleeds, drug intoxications, and withdrawal syndromes, just to name a few.  In case that wasn’t enough check out Table 3 of the article. Nachi:  And we already mentioned the leading causes of sepsis, that’s pneumonia, intra abdominal infections, and uti’s. But remember the source can be anywhere. Be sure to also think of pyelonephritis, central line associated bloodstream infections, prosthetics, endocarditis, necrotizing fasciitis, and meningitis. Jeff:  I don’t think we need to dwell on this much longer - basically the differential is huge.  Let’s move on to my favorite section - prehospital care. Jeremy: 20 pages of evidenced based recommendations and your favorite is the prehospital section, what’s up with that? Jeff: I’m an EMS fellow, what can I say… Anyway, on to my favorite section -- prehospital care.  This is always a hot topic because the prehospital period is a special opportunity to get early interventions in for septic patients  as 40 - 70% of all severe sepsis hospitalizations arrive via EMS. Nachi: And in one study taking place in a large metropolitan area, prehospital care time was over 45 minutes, and less than  37% arrived with IV access. Of course, these numbers would vary significantly based on where you practice. Jeff: So get this -- one study showed that out-of-hospital shock index and respiratory rate were highly predictive of ICU admission. So clearly early recognition and therapy may play a role here. Another study, however, showed knowledge gaps by advanced EMS providers in diagnosis and management of sepsis. And yet another study showed that only 18 to 21% of confirmed septic patients were suspected of having sepsis by EMS. Out of hospital fluids were started in only half of patients with severe sepsis. In essence, there is likely a strong role here for pre hospital protocols for identifying and treating sepsis. Nachi: In terms of pre hospital treatments though, prehospital IV fluids haven’t been shown to improve mortality, but have been associated with shorter hospital stays. Prehospital sepsis protocols have been described, but in general more research is needed in this area. Jeff: While prehospital care hasn’t yet been shown to improve the prognosis of septic patients, those presenting via EMS do have shorter delays to initiation of antibiotics, IV fluids, and early care bundles. EMS should focus primarily on stabilizing vital signs and providing efficient transport. If it’s possible to establish an IV and initiate fluids without delaying transport, EMS should do that as well. Nachi: And of course, oxygen for the hypoxic patients! Moving on to history and physical for your presumed septic patient. Jeremy, what are the big hitting things here that you always ask and check for, and that you make sure your residents are doing? Jeremy:  After ABC’s and glucose, AMS is really important, it’s in the QSOFA SCORE.  Unfortunately, this can be hard in many septic patients where they’re baseline mental status is less than perfect.  The other thing is to try and find the source.  Finding the source lets you make wise choices about therapy. Jeff:  Great point about the mental status - so many of our older population have an altered baseline, but recognizing changes from that baseline is key. Nachi:  Absolutely, with that in mind, let’s talk diagnostic studies, especially lactate.  Where I trained, basically everybody was getting a lactate, even tired looking residents seemed to be having their lactates checked, and trust me, they weren’t looking that good... Jeremy:  Brace yourself: lactate is really important in septic patients.  That being said, not every cause of elevated lactate is sepsis.  There is this animal called Type B lactic acidosis can come from numerous drugs like albuterol. Just because you see elevated lactate doesn’t mean you can forget about the other causes.  That being said, we know that patients with sepsis do better when they clear lactate. Jeff: Seems like the evidence is definitely in favor of serial lactate testing… Jeremy: For sure.  At least until you have a reasonable trend towards improvement.  We know lactate clearers do better.  We’ve looked at our own lactate numbers.  Interestingly, the takeoff point for sepsis seems to be around 2.5.  Meaning that patients with altered vitals and lactates above 2.5 tend to do worse.  But, there is a broad ddx to elevated lactate.   What is true, though, is that lactate is a marker for badness.  If your patient’s lactate is rising, yours should be too. Nachi: I bet I’m a “lactate clearer”. I may add “lactate clearer to my CV,” sounds impressive.  But I digress…  Next up we have Procalcitonin.   Since procalcitonin becomes elevated in those with bacterial infections, intuitively, this should be a valuable marker to assess in potentially septic patients.  Unfortunately procalcitonin lacks negative predictive value so most literature supports its use in diagnosing pulmonary infections and for antibiotic de-escalation. Jeff: Good to know, I’ve seen it being used a lot more recently and wondered how evidence based this test was. Jeremy:  Honestly, I don’t see Procalcitonin changing ED management at the moment.  If you’re   waiting for Procalcitonin to start antibiotics or fluids, you’re waiting too long. Nachi: Moving on, let’s talk imaging.  Based on current studies, the authors recommend focused imaging only.  In addition, they also note that our good friend, the point of care ultrasound, likely plays a role, as in one study, POCUS demonstrated a 25% improvement in sensitivity from clinical impression alone. Jeremy:  I think there are two ways POCUS comes in.  One, lung ultrasound can be really useful to find that occult pneumonia or differentiating pneumonia from CHF.   Two, your ultrasound is your best tool for assessing volume status.  I try to look at the IVC of all my septic patients and echo them when possible. Nachi: Right.  So now we’ve examined, drawn labs and cultures, checked a lactate, may be obtained imaging… next up we should probably start treating the patient. Whether you like it or not, we have to discuss CMS. Jeremy: Just to clarify before we start.  CMS defines “severe sepsis” as SIRS + infection with a lactate of 2.1-4.0. Septic shock is SIRS + infection with hypotension or a lactate > 4.0. That’s where we’re at. Jeff:  Good point.  Back to treatment: within the first 3 hours, for any patient with sepsis and septic shock, you must measure a lactate, obtain 2 sets of blood cultures, administer antibiotics, and give an isotonic fluid challenge with 30 cc/kg to patients with hypotension or a lactate greater than 4.   Then, within the first 6 hours, you must apply vasopressors to achieve a MAP of at least 65, re-assess volume status and perfusion, and remeasure a lactate. Nachi: This begs the question - are these recommendations evidenced based? Jeremy…. Jeremy: I’m so glad you asked that . Let’s start with fluids. Patient’s need adequate fluid resuscitation.  Interestingly there are 3 large RCT’s, PROMISE, PROCESS and ARISE,  that compared a Rivers type bundle to usual care.  Surprisingly, they showed no difference.  But when your drill down into these 3 trials, you see that “the usual care,” now generally includes at least 2 liters of fluid. Jeff: Ok, so it seems that there is some pretty good data to support a rapid fluid challenge of at least 30 cc/kg.  But how do we determine who needs more fluids and how much more they need.  There must be an endpoint to all of this? Jeremy: Another million dollar question. 30cc/kg is probably a good place to start.  How much is too much?  I think we need to be smart about our fluids.  Some patients will need less and some will need much more.  So, I remind my resident’s to be smart about fluids.  Sono an IVC, trend a lactate, follow a urine output, do a passive leg raise, even check JVP.  I mean just because you haven’t seen a unicorn doesns’t mean they’re not real.  Do something to monitor volume status. Nachi: Very important. Put your ultrasound skills to work here. They’ll only improve as you practice more.  Jeff, let’s get started on the ever important topic of antibiotics. Jeff: Sounds good.  Current guidelines recommend that broad spectrum antibiotics be administered within the first hour of presentation for those with sepsis or septic shock, ideally with blood cultures being drawn beforehand. In one study, every hour of delayed abx administration was associated with an 8% increase in mortality.  Since this 2006 study, other studies have had mixed results - with studies showing increased odds of death with delays in abx administration and others showing only a benefit in those with septic shock with or without hypotension with no benefit to those without shock. Nachi:  In terms of antibiotic coverage - you need to consider the site of infection, local resistance patterns, the presence of immunosuppression, and the patient’s age and comorbidities.  Table 5 of the article is very thorough and should be kept as a quick reference. Jeremy do you have any specific recommendations for our listeners on how we should approach antibiotic usage in the septic patient? Jeremy: I like to think about antibiotics a little more simply than referencing a table.  I ask a couple questions.  Does my patient need MRSA coverage ?  Does my patient need Pseudomonal coverage?  If the answer is no and no, then narrow your coverage.  You don’t necessarily have to use a bunch of Vanco, or a big gun antipseudomonal like Pip/tazo.  Also, have a look at your local antibiogram.  I can’t tell you how many times this changes prescribing habits for even things like simple UTIs.  I’m going to stray into some controversial territory here. The benefits of sepsis protocols are measured one patient at a time, but the harms are only measured in the aggregate.  What does that mean?  CMS metrics have caused us to  use to use more broad spectrum antibiotics.  As a result, we’re seeing more resistance.  My resident’s tell me to make it easy, give em VZ (that’s vanco/zosyn) and it kills me.   Every time you put a Z-pack into the world a pneumococcus gets it’s wings. So think more about your antibiotics, and know your local biograms. Jeff: That’s a great way to think about it, I fear I’ve given a lot of pneumococci wings during my training…  Next we’re on to vasopressors.  The data is pretty clear on this one - norepinephrine is the recommended first line vasopressor for septic shock.  In numerous trials comparing Norepi to dopamine, NE was far superior, with dopamine increasing arrhythmias in one trial and associated with an increased risk of death as compared to NE in another trial. Jeremy:  So here’s a question I get all the time: How can I give Norepi without a central line.  Let’s use Dopamine, its safe peripherally.  Ok, so follow that through.  We’re going to give a drug to increase blood pressure by constricting blood vessels, but don’t worry, it’s safe peripherally.  What does that mean?  It means it doesn’t work!!  It doesn’t give much blood pressaure.  Dopamine is a lousy pressor.  It causes a lot of tachycardia, which is not what you want in failing septic hearts.  So what do we do if we don’t have a central line?   We start norepi peripherally into a large bore IV for the time it takes us to get a central line.  That’s where the evidence is.  There’s a mortality benefit to NE over dopaine in septic shock. Jeff:  Right, this month’s authors note peripheral pressors may be safe for brief periods in settings with close monitoring.  While this is commonplace in some hospitals, others haven’t yet jumped on that bandwagon. I think it’s important to mention that this is becoming more and more commonplace, even in the prehospital realm.  With the service I fly for, we routinely start peripheral vasopressors without hesitation.  But this isn’t limited to the air.  Many ground 911 services have also adopted peripheral vasopressors in a variety of settings. Nachi: I’m sure there are many trials to come in the future documenting their safety profile, but moving on to the next pressor to discuss... vasopressin. This should be your second line vasopressor for septic shock.  In the VASST trial, low-dose vasopressin was found to be noninferior to NE.  In other trials, vasopressin also appeared to show a potential benefit in those with AKI and sepsis, although the subsequent VANISH trial (perhaps the best name for a clinical trial so far) failed to demonstrate a benefit to vasopressin titration with regard to renal outcomes in septic shock. Vasopressin has also been shown to reduce NE dosing when administered at a fixed dose of 0.03-0.04 units/min. Jeff: Next we have epinephrine.  In one study epinephrine and NE were equivalent in achieving MAP goals in ICU patients with shock, however several of those receiving epi developed marked tachycardia, lactic acidosis, or an increased insulin requirement.  The increasing lactic acidosis could confound the trending of lactates, so in those requiring inotropy in addition to some peripheral squeeze - the authors recommend adding dobutamine to norepinephrine instead of starting epinephrine. Although, keep in mind, this can lead to some hypotension so remember to start at low doses. Nachi: Phenylephrine, a pure alpha adrenergic agent, is next and should be considered neither first nor second line, but it may have a role as a push dose agent while preparing other vasoactive agents. Jeff: And lastly, we have angiotensin 2.  One recent 2017 study examining the role of angiotensin 2 in those with septic shock already on 0.2 mcg/kg/min of NE found that those receiving AT2 had significant improvements in MAPs as well as cardiovascular SOFA score at 48h with no difference in mortality.  Unfortunately, these benefits do not come without risk as AT2 may increase risk of arterial and venous thrombosis and potentially thromboembolism.  Clearly, one study isn’t enough to change practice, but it’s certainly food for thought. Nachi: So that wraps up vasopressors. Jeremy, we’re on to corticosteroids -- another hotly debated topic. When do you give steroids in sepsis? Jeremy:  Hmmm steroids, this is an age old question.  No study has clearly supported the blanket use of steroids in septic shock. Several like CORTICUS and ADRENAL showed no difference.  I will use hydrocortisone for pressor refractory shock. Meaning, you’ve tried everything else, so you might as well try.  Also, I do tend to avoid Etomidate, given the possibility of adrenal suppression and that there are several other induction agents, notably Ketamine  that don’t have this problem. Jeff: Those trials are certainly important, thanks for bringing them up - Especially with all the FOAM content out there, it’s incredibly important to look back at the data to understand where certain recommendations are coming from.   Anyway… one quick note on blood transfusions before we move on to special populations - Although part of the original early goal directed therapy, thanks to data from the TRISS trial which showed no difference in outcomes with a transfusion goal of 7 vs 9, transfusions are reserved for those with a hbg of less than 7. Jeremy:  One population we should make sure to mention and be careful with is end stage liver disease.  In the ER, we tend to miss SBP alot.  Mostly because these patients have lots of reasons to be sick and they already have elevated lactate because of their deceased clearance.  My practice is to give a dose of Ceftriaxone and sent a diagnostic tap to patients who are sick and have ascites. Nachi: Alright Jeremy, let’s talk controversies in sepsis. We’re giving you all the big questions this month! Jeremy:  We’ve already talked about fluids and how much to give.  Just a reminder that a history of CHF doesn’t preclude proper fluid resuscitation.  I think broad spectrum antibiotics for relatively well patients is a big controversy.  Our national rates of antibiotic resistance are terrible, and yet we’re using more antibiotics all the time.  There are very few if any antibiotics coming down the pharma pipeline and we’re going to have to face the music eventually.  Finally, we need national metrics that mirror clinical evidnece.  Protocols should be a tool and not a crutch.  You know what’s best for the patient in front of you, so don’t let metrics or protocols make you do things you think are not in your patient’s best interest. Nachi: So how do you escape the hospital protocols and CMS and do what’s best for your patient without “getting in trouble”? Jeremy: Here’s how I deal with it as the one who reads and QI’s all of our sepsis charts. I tell my colleagues to do what’s right, and if you need to deviate from the protocol tell me why.  As long as you can explain your decision, I’ll support it.  Explaining your thinking is good clinical practice and is good medico-legal practice. CMS has been unable to link these metric  to payment, simply because no hospital can meet them with any regularity.  It’s important that we advocate for our patients or nothing will change. Make them respect you for the highly educated professional that you are, and your patients will ultimately benefit. Jeff: Preach!! And before we close out with disposition, there are a few new therapies and trials on the horizon to keep a lookout for. The RACE trail examined the role of L-carinitine.  The VICTAS trial is looking at vitamin C, thiamine, and steroids in sepsis.  The CLOVERS trial is looking at early vasopressors vs a crystalloid liberal strategy.  And lastly, IL-7 is also being investigated.  All really cool stuff that could change how we manage sepsis in the future.. Nachi  A few quick notes on disposition before we close this episode out.  Certainly not all patients meeting SIRS require admission, but many do.  Those with qSOFA of 2 or higher represent a sick population and an ICU admission should be considered.   Even for those with a qSOFA of 1 but a lacate over 2 -- they have a mortality approaching that of patients with a qSOFA of 2.  Be careful just sending a patient who is on the fence to the floor because several studies have demonstrated that patients who are later upgraded have worse outcomes. Jeff: That’s in line with the general themes we’ve laid out today - definitely better to start early with aggressive care rather than play catch up later.  Jeremy - in 30 seconds or less, what are the most salient points in the management of sepsis that you would like our listeners to take with them from this episode. Jeremy:  Here are my take aways: qSOFA, RR, AMS SBP < 100 Norepi, not Dopamine - it doesn’t work! Be smart about fluids!! Be smarter about antibiotic use! You are the best advocate for your patient, despite what anyone else says! Jeff: Excellent, so that wraps up the October 2018 episode of Emplify. A big thanks to Jeremy Rose for joining us. Jeremy: Thank you for having me!!! It was great talking with you. Nachi: For our listeners -- additional materials are available on our website for Emergency Medicine Practice subscribers. If you’re not a subscriber, consider joining today. You can find out more at www.ebmedicine.net/subscribe. Subscribers get in-depth articles on hundreds of emergency medicine topics, concise summaries of the articles, calculators and risk scores, and CME credits. You’ll also get enhanced access to the podcast, including the images and tables mentioned. You can find everything you need to know at ebmedicine.net/subscribe. Jeff: And the address for this month’s credit is ebmedicine.net/E1018, so head over there to get your CME credit.  As always, the ding sound  you heard throughout the episode corresponds to the answers to the CME questions. Nachi: Lastly, be sure to find us on iTunes and rate us or leave comments there. You can also email us directly at emplify@ebmedicine.net with any comments or suggestions. Talk to you next month!

Curbsiders’ Journal Club features rapid summary and critical appraisal of recent articles and news stories in internal medicine by The Curbsiders. This month’s topics include: asthma, maintenance versus as needed inhaler use, procalcitonin, Pneumocystis pneumonia prophylaxis, colon cancer screening, smoking cessation, cannabis and cognitive impairment, LDL cholesterol and mortality, plus some medical podcast recommendations. Over the last month, we have developed a list of more than 40 interesting articles and news stories that we have been feeding our own brain holes. From this list we have plucked a select few that we really wanted to highlight and share with you. Join our mailing list to receive a PDF copy of our show notes every Monday! And hey, while you’re here, consider rating us on iTunes and leaving a review. The Curbsiders thank you! We are also on Facebook, Instagram, and Twitter: @thecurbsiders. Credits: Written by: Christopher J Chiu MD, Sarah Phoebe Roberts MPH Producers: Christopher J Chiu MD, Sarah Phoebe Roberts MPH Hosts: Christopher J Chiu MD, Stuart Brigham MD, Paul Williams MD, and Matthew Watto MD Editor: Matthew Watto MD Time Stamps: 00:00 Announcements 00:20 Disclaimer 01:00 Intro to Curbsiders Journal Club 03:07 Mild asthma and as needed versus maintenance inhaler use 09:50 Smoking cessation, e-cigarettes, and financial incentives 17:23 Pneumocystis pneumonia prophylaxis 22:18 Cannabis and cognitive impairment 26:15 Colorectal cancer screening update by American Cancer Society 30:37 Procalcitonin for lower respiratory tract infections in the ED 37:29 Cholesterol, baseline LDL-C, mortality and cardiovascular events 41:01 Incorrect symbology and some podcast recommendations 46:22 Outro Tags: asthma, maintenance, inhaler, procalcitonin, Pneumocystis, pcp, pneumonia, prophylaxis, colon, cancer, screening, crc, smoking, cessation, marijuana, cannabis, cognitive impairment, LDL, cholesterol, mortality, cardiovascular, podcast, assistant, care, doctor, education, family, FOAM, FOAMim, FOAMed, health, hospitalist, hospital, internal, internist, meded, medical, medicine, nurse, practitioner, professional, primary, physician, resident, student

Controversies in diagnosing meningitis by Rhonda Cadena

In the edition of the Ercast journal club thrombectomy in pts with delayed stroke presentation shows promise beware behavioral changes after procedural sedation kids with isolated linear skull fractures have a good short term prognosis procalcitonin may help decrease abx use in respiratory infections steroids in mild sore throat help... a little   Registration for ConCert (the big board recertification exam we take once a decade) has opened. If this is your year to take the exam, there's only one place to go for board review.   The DAWN Trial Nogueira, Raul G., et al. "Thrombectomy 6 to 24 hours after stroke with a mismatch between deficit and infarct." New England Journal of Medicine 378.1 (2017). PMID:29129157 What happens when thrombectomy is done when last normal was over 6 hours ago? 206 patients with occlusion of the intracranial internal carotid artery, middle cerebral artery, or both these were patients excluded from TPA because of time from onset or they had persistent occlusion despite TPA Pts had to get either perfusion CT or diffusion weighted MRI to see if there was salvageable brain (there had to be) 107 got thrombectomy and 99 didn't. 90 day functional independence: 49% thombectomy vs 13 % controls No significant difference in symptomatic intracranial hemorrhage or 90 day mortality Trial stopped early because of superiority of thrombectomy Majority of patients were wake up strokes, a group we've had pretty much nothing to offer previously Industry sponsored, many conflicts of interest   Rob's take-This trial uses salvageable brain as a determinant of treatment which makes sense as these are the patents who may actually benefit from reperfusion. This purports to speak for the patient 6-24 hours, but from what I can tell, treatment was heavily skewed toward those with time from last normal 16 hours and under, so it doesn't really tell us much about 24 hours. I will be consulting stroke centers with this patient cohort. Adam's take- Impressive. I like that this is tissue based, not time based.     Skull Fractures in Kids Bressan, Silvia, et al. "A Systematic Review and Meta-Analysis of the Management and Outcomes of Isolated Skull Fractures in Children." Annals of emergency medicine (2017). PMID: 29174834  Are pediatric patients with isolated skull fractures at increased risk for short term adverse events? Pool of 21 studies, over 6,000 kids with isolated skull fractures. One required emergency neurosurgery, none died. All kids had CT scan or MRI to exclude intracranial injury 6 out of 570 had bleeding on a second scan and zero had surgery. The incidence of delayed hemorrhage is super low and even those with bleeding didn't need an intervention. Unless there is a change, you don't need to rescan.   Author take home: "Children with isolated skull fractures were at extremely low risk for emergency neurosurgery or death, but were frequently hospitalized. Clinically stable children with an isolated skull fracture may be considered for outpatient management in the absence of other clinical concerns." Rob's take-An otherwise well appearing child with isolated skull fracture has an excellent short term neurosurgical prognosis and probably don't need hospitalization based on the skull fracture alone Adam's take-Open and shut case. One kid out of over 6,000 is pretty good odds and that one patient got meningeal repair.     Procalcitonin is dead. Long live procalcitonin Schuetz, Philipp, et al. "Effect of procalcitonin-guided antibiotic treatment on mortality in acute respiratory infections: a patient level meta-analysis." The Lancet Infectious Diseases 18.1 (2018): 95-107. PMID: 29037960 Over 6,000 patients with respiratory infections Decision to give antibiotics based on procalcitioin level Primary endpoints: Mortality, treatment failure Secondary endpoints: Antibiotic use No significant difference in death, treatment failure, ICU length of stay Antitiocis initiated 86% controls, 70% procalcitonin guided and  shorter duration of abx using procalcitonin as the guide Fewer Abx side effects with procalcitonin guided therapy   Adam's take-This is not a lifesaving study, this is a safety study. The point is, can you safely withhold antibiotics from people? This study says you can, based on procalc level in a patient with respiratory infection. The scenario I envision is someone with CHF, COPD, fever, and coughing. If the procalc is low, I don't have to add a horrendous quinolone to your 25 other meds, you can take tessalon perles and do better. I'm going to keep one more abx prescription out of the pool and it's not going to harm the patient. This is a noniferiory trial to me. Prescribing fewer antibiotics is a worthwhile goal to me. We know that using procalcitonin for that purpose works and this study says it is safe.   Steroids for sore throat Little, Paul, et al. "Effect of oral Dexamethasone without immediate antibiotics vs placebo on acute sore throats in adults: a randomized clinical trial." JAMA 317.15 (2017): 1535-1543. PMID: 28418482 RCT of 576 adults with sore throat not requiring immediate abx. Treated with either steroid or placebo Most afebrile and did not have pus on tonsils Results: Symptoms better at 48 hours (but not 24) with dexamethasone   Rob's take- Set the expecation that it will take 48 hours to start feeling better if giving steroids. That being said,  I don't think that steroids are worth it in most mild sore throat patients. NSAIDS, tea, and time Adam's take- A cofounder for me was that 14% of the dexamethasone and 19% of no dex group had strep, a confounder I don't like. Steroids probably work a little, they're probably safe, but they're not amazing   The Brain Does Not Love Ketamine as Much as You Do Pearce, Jean I., et al. "Behavioral Changes in Children After Emergency Department Procedural Sedation." Academic Emergency Medicine (2017). PMID: 28992364  82 kids received ketamine for procedures in the ED Most had forearm fracutres Most had analgesia before procedure 22% with negative behaviors changes after discharge. Anxiety, aggression, withdrawal, sleep anxiety, separation anxiety Higher odd of this happening in kids anxious before procedure, nonwhite   Rob's take- ketamine is an excellent drug, but can have lasting effects. Also, it's not totally benign, one patient had over 30 seconds of apnea. Still one of our best options, but discuss with parents the post discharge behavioral changes that might occur Adam's take- I don't think this is a study about ketamine at all. This says nothing about ketamine, this talks about procedural sedation. There is a long history of research about general anesthesia that shows a similar pattern- post op kids have behoaboiral disturbance a week after and the kids who come into the OR have worse outcomes, and if you treat the anxiety before the procedure, they have better outcomes.This could have been propofol nitrous, whatever. The kids who start out anxious pre-procduere have a much higher incidence of behavioral disturbance post procedure.In my opinion, this study shows that anxious kids are more likely to be disrupted by this experience than non-anxious kids. I am going to give a lot more versed. Maybe this is the versed indication that works with ketamine.

Conquer community acquired pneumonia and avoid misdiagnosis with tips from Dr. Robert Centor, Professor Emeritus University of Alabama and newly appointed Chair of Medicine at Kashlak Memorial Hospital. We discuss diagnosis, misdiagnosis, procalcitonin, steroids for severe pneumonia, pneumonia severity index versus CURB-65, and how to determine antibiotic choice and duration. Special thanks to Correspondents Neela Bhajandas (cohost), Justin Berk and Bryan Brown who all contributed several articles, resources, and questions to prep for this show. Cover image by Dr Kate Grant paintscientific.com. Full show notes available at http://thecurbsiders.com/podcast Join our mailing list and receive a PDF copy of our show notes every Monday. Rate us on iTunes, recommend a guest or topic and give feedback at thecurbsiders@gmail.com. Time Stamps 00:00 Intro 02:38 Brief bio for Dr Centor 04:22 Picks of the week with Dr Centor 11:27 Clinical case of suspected pneumonia 12:30 Brief history of community acquired pneumonia 14:40 Misdiagnosis rates are high 16:18 Defining diagnostic criteria for pneumonia 18:50 Chest x rays and pneumonia 22:18 Illness scripts teaching about pneumonia 23:41 Ubiquitous misunderstanding of pneumonia definition 25:26 History and physical exam tips from Dr Centor 27:19 Further testing for pneumonia, PSI, CURB-65 32:50 Procalcitonin discussed 38:10 Antibiotic choice discussed with Dr Bhajandas 41:15 Safety considerations for various antibiotics 43:38 Use of high dose amoxicillin 44:45 Dr Centor’s antibiotic preferences, and some thoughts on blood and sputum cultures 46:55 Dangers of fluoroquinolones 48:25 Antibiotic duration 51:40 HCAP is no longer a thing and how to assess risk for drug resistant organisms 55:42 Corticosteroids for pneumonia 60:25 Inpatient antibiotic choices 62:00 Dr Centor’s take home points 62:45 Dr Centor becomes Chair of Kashlak Memorial 65:38 Outro Tags: pneumonia, community, acquired, cap, antibiotic, duration, diagnosis, misdiagnosis, strep, cough, procalcitonin, steroids, fluoroquinolones, azithromycin, drug, resistant, mdro, illness, assistant, care, education, doctor, family, foam, foamed, health, hospitalist, hospital, internal, internist, nurse, meded, medical, medicine, practitioner, professional, primary, physician, resident, student

Sepsis is a life-threatening condition associated with significant mortality and healthcare cost.  There is increasing evidence supporting the use procalcitonin as a biomarker for diagnosis of bacterial sepsis and as a guide to discontinue antibiotic therapy.  However, concerns about the efficacy, safety, and availability of procalcitonin exist.  A Q&A article in the September 2017 issue of Clinical Chemistry asked experts with different roles in this field to share their thoughts on the challenges of procalcitonin-guided diagnosis and antibiotic therapy. 

Role of Procalcitonin in Guiding Antibiotic Therapy Author Tasadaq Fazili discusses with Pamela Hsieh, Assistant Editor for AJHP, current clinical use of procalcitonin in guiding antibiotic therapy as well as future areas of research. The article under discussion appears in the December 1, 2012, issue of AJHP. For more information visit www.ajhp.org.

Use of Procalcitonin (PCT) for the diagnosis of infection has been studied extensively with conflicting results, in part because of the many different populations and clinical syndromes studied.

The role of procalcitonin (PCT) plasma levels as a diagnostic tool for intensive care patients has been intensively investigated during the past years. In particular for recognition of bacterial infections, PCT levels have been shown to be superior to other clinical and biochemical markers. Furthermore, some very recent studies show that in patients with lower respiratory tract infections PCT guided antibiotic therapy reduces antibiotic use and thereby may also reduce duration of stay of patients in hospital and thus cut hospitalisation costs. However, various studies indicate that the value of PCT as a prognostic marker is limited because of false positive or negative values. Despite these limitations PCT plasma levels are currently measured in intensive care units. The present study summarises the possible clinical uses of this lab marker as a diagnostic tool for the assessment of critically of ill patients.

Thu, 11 Nov 2010 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/12309/ https://edoc.ub.uni-muenchen.de/12309/1/Yilmaz_Yesim.pdf Yilmaz, Yesim ddc:610, ddc:600, Medizinische Fakult

Discussion of glucose control in type 2 diabetes.

Serum levels of interleukin 6 (IL-6), procalcitonin (PCT), and C-reactive protein (CRP) were measured in 38 critically ill patients immediately after an increase in body temperature above 38.3 degrees C. Ten healthy controls were also included for comparison. The onset of fever was accompanied by elevated circulating levels of all the 3 markers in comparison to healthy control subjects. However, only IL-6 levels were significantly higher (p

Patienten mit chronischer Niereninsuffizienz sind einem erhöhten Infektionsrisiko ausgesetzt. Durch unterschiedliche Entzümndungsreaktionen im Organismus (durch Hämodialyse, Autoimmunerkrankung, Abstossungsreaktion) kann es schwierig sein, eine bakterielle Infektion von einem anderen Entzündungszustand abzugrenzen. Procalcitonin (PCT), ein neuer Parameter zur Diagnostik bakterieller Infektionen, zeigte sich in der vorliegenden Studie durch eine eingeschränkte Nierenfunkton nicht beeinfliusst. Lediglich die Hämodialyse bewirkte einen leichten Anstieg des Parametes. Bei systemischer bakterieller Infektion liess sich, unabhängig von der Grunderkrankung der Patienten, eine vermehrte Freisetzung von PCT nachweisen. Bei Patienten mit Autoimmunerkrankung wurden erhöhte PCT-Werte nur gefunden, wenn zusätzlich eine bakterielle Infektion bestand. Im Gegensatz dazu konnte bei autoimmunerkrankten Patienten ein kontinuierlich erhöhtes CRP beobachtet werden. PCT erwies sich als ein nützlicher Parameter für eine frühzeitige Diagnose und die Verlaufskontrolle von bakteriellen Infektionen und deren Therapie bei Patienen mit renalen Erkrankungen.

Sat, 1 Jan 2000 12:00:00 +0100 https://epub.ub.uni-muenchen.de/16614/1/10_1159_000045570.pdf Schiffl, Helmut; Held, Eckhard; Sitter, Thomas; Burchardi, Christian; Schmidt, Martin ddc:610, Medizin