Good afternoon, everyone. It's 4 o'clock. Thank you so much, all of you, for being here. I am Marco Restrepo, and it's an honor for me to present the Controversies in Pneumonia, a Rapid-Fire Expert Panel Discussion. So I would like to ask you, all of you, to please go back to the chest up, okay? Because we want your participation during this session, okay? We want you to be part of the session. Today, what we would like you to do is, where it says here in the description, go show more, okay? And then it says, audience response pooling, okay? And what I'm going to ask you to favor is to please do not respond until the timer is on the slide, okay? In order for you to be counted on the responses. If you do it before, most likely we are not going to be able to see it. So the honor for me today is because I am here with great friends and all great experts in pneumonia. And we tried to put this panel, and I hope, I hope, that by the end of this session you give us some feedback, because this is the first time we are trying to do this thing. The way that we did it is we have three fantastic experts that I'm going to ask you to first introduce yourself. I'm going to start by saying that we have Dr. Barbara Jones. Thank you. Can you hear me? My name is Barbara Jones. I'm a pulmonary critical care physician at the Salt Lake City VA and University of Utah. I'm Christina Crothers. I'm a pulmonary critical care physician as well. I'm a section chief of pulmonary critical care and sleep at the VA Puget Sound and professor at the University of Washington. I'm Charles Delacruz. I'm one of the faculty at Yale University, adult pulmonary critical care physician and also at the West Haven VA. Very good. Do you guys have any conflict of interest that we need to know for the start of this session? I do not. No. Did you want us to mention the conflict? Okay. I will. Okay. Do you have any conflict? Okay. So we don't have any conflict of interest, and the four of us are part of the panel that is writing the newer version of the American Thoracic Society and Infectious Diseases Society of America Guidelines. Therefore, whatever we say here is not what the guidelines will say. At least we don't know yet because it has not been written. Dr. Barbara Jones is our chair, and we are part of the representative from the American Thoracic Society. So Dr. Barbara Jones, would you like to make a disclaimer that whatever we say here will be more of our own views of the literature? Yes, definitely. Not necessarily represented by the ATS or IDSA. Excellent. Thank you very much. So how is this going to work today? We have several cases, and what we want you to do is to write the answers on what you do on clinical practice, okay? And our panelists will do exactly the same. But the big difference compared to most of the other sessions with audience response is that most of the time we see just the responses by the audience, and then the panel experts will comment on the responses. But here, what I'm asking them to do, I assign them the same letters that you are going to be responding. I'm going to know what they answer, okay? And what I want to know is not so much about all the literature that they have read, all the knowledge that they have acquired, it's how much of what we learn that we have seen in papers is really applied to clinical practice. And in addition, your feedback as clinicians is going to help us better understand what clinicians think in clinical practice about how to apply these guidelines. So at the end of this session, we hope that by bringing clear cases, at the end of the day we don't know how clear they are for all of us, and the interpretation of the data will allow us to really practice better medicine, especially now that we are embarking into the community-acquired pneumonia season. So we try to really approach it from the three perspectives, the diagnosis, the treatment, and the prevention. So let's start with the first case. This is a 74-year-old man that is bedridden in a nursing home resident, arrives to the department, the permanency department with a chronic tracheostomy and a PEC2. He has a past medical history of ependymoma resection in 1993, complicated by cerebral ataxia, dementia, chronic respiratory failure, PTSD, gout, prior pseudomonas pneumonia, hypercholesterolemia, anemia, depression, dysphagia, dysphonia, and GERD. Welcome to the patients we see on a daily basis at the VA hospital. He presents with fever and tachycardia for one day. His physical exam reveals blood pressure of 77 over 50, heart rate 108, respiratory rate 24 per minute, and the saturation is 92% on three liters of oxygen by tracheal mask. He has decreased breath sounds on the right lung compared to the left with dullness and crackles. So the first case relates to biomarkers. And what we want to know is what test should we consider in this case, in addition to CBC, CHEM20, coagulation, and lactic acid, and ABGs? A, a C-reactive protein, and wait one second, B, procalcitonin, C-reactive protein and procalcitonin, and D, no biomarker test is needed. So I want to please ask you the favor to document your responses and you guys will show me. Okay, very good. So it looks like the controversy from the expert panel is not too much, and it looks like 50% of you answered that no biomarker test is needed. Okay, so no one seems that both, that procalcitonin, some of you, one-third thought that procalcitonin might be a biomarker that could be indicated here. C-reactive protein, almost no one, and both almost 18%. Okay, so Dr. Jones, tell us why no biomarker test is needed as half of the audience relates to this answer. That's a great question, and I would probably flip that to wondering how people here in this audience use procalcitonin. My experience with procalcitonin is that it's correlated with bacterial infection, but the evidence really doesn't support any binary classification yes or no. That doesn't necessarily mean it might not be helpful to give you some kind of pattern of a type of infection that you might be considering, but especially in patients that have multiple comorbidities, the host response is so poorly understood that, to me, the data that supports procalcitonin is so messy because we just really don't understand this molecule, and we don't really understand its function. It's really easy to characterize the structure of a molecule and to be able to measure it, and that was done in the 1980s, but we really still don't understand its function, and so there are always some scenarios where you have an overwhelming bacterial infection and the procalcitonin will be low. I always try to remember that procalcitonin is supposed to be representative of a host response, and whether or not your patient has a host response to an infection is really poorly understood. It's so complex that to use procalcitonin as a binary classifier of this is bacterial infection or it isn't doesn't seem to be useful to me, but I would love to hear how people use it in the field and whether you use it as an initial empiric choice kind of support or whether you're using it for antimicrobial response. How would you use this in this patient? Dr. Jones, thank you very much, but no. This is a rapid fire, okay? Rapid fire means you need to answer quickly so that we can all process this thing. So, in other words, there are 40% of people that says that they are using procalcitonin, okay? So, the fact that 50% said no, it says, okay, 40% are using procalcitonin. The question is how? How are they using procalcitonin? So, this is some of the labs that this patient had. The patient had leukocytosis. The patient was anemic. The playlist, bless you. The patient was elevated and has bandemia. The patient was hypoxic, and there were minimal changes on the lactic acid. So, among all those 40% of the people that said somehow they will test for procalcitonin, the answer is, okay, for those of you that think that procalcitonin is valuable, A, start antibiotics, don't answer yet, okay, until we have this thing, start antibiotics if positive for more than 0.25, do not start antibiotics if negative, more than 0.25, start antibiotics no matter the test results, and do not order procalcitonin as it is not helpful. And we know this already from you of 50% that you already mentioned this. Okay, please answer the question now. Okay, great. Thank you very much. Okay, so 50% of you answered start antibiotics no matter the test results. Dr. Barbara Jones seems to be the only one of the two panel experts that we have here that seems to agree with most of you. The other panel experts believe that do not order procalcitonin as it is not helpful, as most of you responded earlier. So, oh, D, I'm sorry, C and D. But C and D as well. C and D, do not procalcitonin as it is not helpful. So, Dr. Barbara Jones said yes. So, then I would like to ask Dr. Crothers, so start antibiotics no matter the test results. So, you do not believe procalcitonin is good, and you do not believe the procalcitonin is going to help you, and you say you still need to order procalcitonin to antibiotics to these patients, is that right? Well, I guess I assumed the question meant we'd already gotten the procalcitonin test, so I was saying I would start antibiotics no matter what the test result was, because maybe my resident ordered it overnight. And so I think, you know, pneumonia is a clinical diagnosis, and so I think this patient clinically, I don't remember if we saw the chest X-ray or heard the chest X-ray result, but I'm assuming that it was a case of pneumonia for us, that he has a clinical diagnosis of pneumonia, and I would start antibiotics regardless of whether the procalcitonin is high or low. And maybe it would be useful to follow the procalcitonin if there was a question of prolonged antibiotics being needed or not. Okay. Dr. Veracruz, any comments? I mean, the concern is, like, if the procalcitonin is low or negative, and then they present this way, you don't typically want to withdraw antibiotics, right, because you already have enough evidence to show that you're kind of concerned about a bacterial pneumonia in this situation. So the guidelines say, do not order procalcitonin. Most of the people here are according to the guidelines. Second, they said, okay, even if you order the procalcitonin, you don't care too much because you need to start antibiotics. So it looks like both of the answers so far are consistent with the guidelines. Okay. The question is, for the people that ordered the procalcitonin, is the guidelines going to help you later on? And it looks like my residents ordered the procalcitonin at night, of course, and then we show up the next day, and the procalcitonin is 4.04. So let's see if all the other things, so flu A and flu B was negative and my resident nurse was positive. All the other parameters are the same. So the question here is, how do I identify the pathogen? You know, whether we need to use sputum gram stain and culture, and are we still ordering sputum gram stain and culture for these patients? So the question here is, A, yes, no, B. Very good. So the majority of you still believe that the Gram stain and culture is still useful in the care of these patients with community acquired pneumonia. So Dr. Crothers, would you like to say something? Because you were assigned to do some of the diagnostic methods with Dr. Maturski, that is also over there. And this is what the guidelines say. Yes, please do it, but particularly for patients with severe community acquired pneumonia. Is this patient severe enough for you to be able to be considered here? Has any of the risk factors for the multidrug-resistant pathogens, previous MRSA or pseudomonas aeruginosa, as we heard in this case, and prior hospitalization with parenteral antibiotics. So what do you think about this approach that seems that most of the people seem to be very consistent with what the guidelines have recommended? Yeah, I mean, I think he has risk factors for, well, he has severe pneumonia and he has risk factors for multidrug-resistant organisms with being in a, he's very debilitated. And I'm not sure if he's had recent healthcare contact and antibiotics in the last 90 days, but he does also have a MRSA and ARIS that's positive. So he would be somebody where you'd be considering empiric treatment of MRSA and pseudomonas given those factors. And so then getting the sputum gram stain can be helpful for you to know if you want to, you know, to know if you can deescalate therapy if those aren't positive. Would you like to make a comment about the tracheostomy side that he facilitates? Oh yeah, I forgot. He had a tracheostomy. He's definitely going to be more likely to be colonized also, though, with organisms. So the question would be, could you do something more than a sputum specimen in him? And it may be very difficult to just, I mean, you wouldn't be able to probably obtain an expectorated specimen. So whether we could get a sort of a tracheal aspirate. Excellent. So this is just part of the whole thing of a recent systematic review that shows that the sputum gram stain is still helpful with a very good potential specificity. The sensitivity is not as good for certain pathogens, but it's still helpful, despite that it is superly available in almost every single emergency department, that if you graduated as an infectious diseases doctor, if your hands by the end of the call was not blue, you didn't do your job correctly. Therefore, this is still a valuable method, and it seems like most of you are doing. Now the intriguing part of the story is this one, no? It is, should we order a viral or a pneumonia rapid panel these days, and are your hospitals really doing this? The answer is A, yes, B, no. Please document your answers, please. Goodness. Goodness. Okay, so one-third of you are not using the viral or the pneumonia rapid panel. Probably most of you are using some sort of some viral panel still. I don't know to what extent, but I would like to ask Dr. Barbara Jones, what is your opinion about utilizing this rapid test in the context of community-acquired pneumonia for this upcoming season? What do you think? Well, as we've seen with COVID now, viruses can surprise us. They can happen outside of the season, but definitely during the viral pneumonia season, that's a key time to really start, especially now it's October, really start testing for viruses. Because of COVID, we really don't know what the year is going to look like. All the other viruses are confused. Prior to COVID, that was even before the standard. Now, the bacterial molecular diagnostic tests, there is less evidence certainty around those. I'm curious, can I ask one question? Not even one question. I really want to know how many of you have those available to you. There's a lot of adoption, and we're really not sure how to use those. The problem is with all of these tests is we don't really have a great gold standard. Our microbiology testing is also flawed. How do you even assess these, kind of torch the biofire assays? How are they going to help us make better decisions in the clinical field? It's hard to know. I actually don't even have the torch assay or any of the biofire stuff available in my center, and so I don't have experience with them, and I don't use them. The viral panel, I am pretty diligent at getting. We just don't know what's going to happen with the viral seasons now. This is the difference between the viral panel and the pneumonia panel. Many hospitals, and here Dr. Barbara Jones can ask the question, how many people are utilizing the viral panel, the one that you can see here with the extended identification of viral pathogens, and how many of you, a big proportion of you are still using the viral panel, and how many of you are using the pneumonia panel? Some of you. Some of you have the pneumonia panel, but not too much. Let's take a look at what the experts have published in non-influenza viral pathogens. Recently, these doctors, including me here, just needed to make sure that SARS-CoV-2 is excluded, okay? These experts here said, suspected CABs should routinely diagnose and include nucleic acid-based testing or respiratory samples for viral pathogens. Now patients know, and inpatients, only a few of them. So Charles, what do we do here? Because this patient is not there, to my knowledge, or where is it? Yeah, I think the evidence for the use of these extended viral panels, it's clear the recommendation is for influenza during influenza season to do that. This recent guideline was for non-influenza viral diagnostics, and most of the literature has poor evidence. And it was felt by the panel, not important for outpatient use, right? But for inpatient, despite the lack of evidence, we felt that the patient with severe CAB, and also people with immunocompromised, we sort of suggested the use of these extended viral panel for several reasons. One, we know we have therapies now for COVID, and potentially RSV, and people with adenoviral infections, we have specific antivirals for that. It's also important for infection control during the winter season. And so those are the reasons why it was recommended by the panel. Again, we need more data, but I guess based on the severity of these hosts, I think that was recommended. So this excluded SARS-CoV-2. We just have been almost dealing with three years of SARS-CoV-2. So what do you think is the future, no? It seems like this data comes from the past, but we're now dealing with certainty that we have all these viral pathogens, and some of them may have these highly resistant bacteria. So what do we do with this? Yeah, so I think the debiophile bacteria, I think we need more data. I think part of the problem with that platform is the sensitivity is really high, and so it's hard to distinguish colonization, contamination from real pathogens. And I think as more people are using this sort of judicially in their hospital, but I think in thinking about how to use this as an antibiotic stewardship approaches, that may be one way of encouraging different hospitals to decrease the use of antibiotics. And then also, you need sort of a group of experts who can sort of say, this is a true pathogen for your patient. The danger is that using these highly sensitive platforms will increase the use of antibiotics, unless we do it appropriately. So Dr. de la Cruz, when the experts say, we need more data, is that we don't know? Or what do we need to do, no? Because these clinicians are dealing with this problem over the winter, and therefore, are we going to order it, or we are not going to order it? So what is the message here? Yeah, so I think for the viral diagnostic, definitely, we have to think about for these patient population, I think that you can see that the gram stain was quite important for the detection of bacterial infection, and I think still be the mainstay of recommendation at this point, as well as culture. Dr. Krodos, would you think that if you have it, you use it? If you don't have it, well, you cannot use it? Is that kind of the message here for them? Yeah, I mean, I think the struggle, right, is that you're going to detect organisms that are present by PCR, but aren't causing the pneumonia, and lead to increased antibiotic use and more resistance. And I think it's then, sort of, can we get at the question of load? Like, is there a quantitative cutoff that we can identify that, you know, sort of like 10 to the fourth colonies in the BAL, like that is, correlates with infection, what's the copy number? And actually, Rich Wunderink, I don't know if he's here, but he talked about an interesting paper at the Monday nosocomial pneumonia session that kind of did a Bayesian analysis of looking at the probability of infection, that actually, because of this problem, that we don't have a good gold standard to really know what's causing the infection, and it was interesting that the sort of, their conclusion was that potentially some of these PCR tests, they are actually maybe better than the culture. But again, we get to that question of what's the quantification that's going to identify pneumonia? Yes, sir. There's a protection for negative predictive value. Yes, yes. So we are trying to look at that in our investigation. Yeah, and he reported, and so the study, that study, I think some of the ones he showed had like 100% negative predictive value. So I think that is where it can be very useful. It's sort of peeling back those antibiotics, you know, good point. And the MRSA PCR really led the way for a lot of these other rapid molecular diagnostic tests, and we have more clinical experience with that, but that does have a really high negative predictive value and can help clinicians feel comfortable with holding. and the PCT, which you didn't really get. Only coronavirus, no bacteria. Have we looked elsewhere for an infection too? I mean, because he was hypotensive, had bantamia, then I'm wondering if there's something else going on in addition to like a urinary tract infection. Yeah, and there's also a question about the source of the airway specimen, right, where there's a big debate about tracheal aspirates versus deeper sampling of the lungs. I know others feel that sort of a deeper BAL or mini-BAL might be a better approach to really answer and sample the lung, you know, to see true infections versus colonization, for example. But I would like to build on the question that Dr. Matevsky just made. Why? Because we hear all the time, no, in pharmacy, the police, the pharmacy police from the antimicrobial stewardship follow you throughout the hospital and say, okay, this patient has a procalcitonin 0.1, is hypotensive, and is in the ICU with dystracheostomy, and we cannot find anything else other than rhinovirus. So should we stop antibiotics at the time, or what do you guys think? Barb, what do you think? I wouldn't, and the reason is that I really don't trust my diagnostic tests as well enough, and my patient is really sick, right? Now, I study antimicrobial use and the psychology of that, and it is this justifying interventions because your patient's sick is tricky, right? And one of the things, you know, people talk about risk of badness and then your threshold at which risk of badness, you know, you should try to treat your patient. But it is important to always remember that the patients who are at risk of an omission, you know, are also at risk of harm from your antibiotics. So the people who are at highest risk of an antibiotic failure from a resistant organism, they're also at the highest risk of developing kidney injury from your vancomycin. So I don't take that lightly, but I do think that a patient with a history of pseudomonas colonization, assuming that there's an infiltrate on the x-ray and the patient's hypotensive, I don't trust a negative microbiology sample to really help me, you know, stop antibiotics. I think that this person would probably in my ICU get at least a five-day course. Yeah, I think the information would allow us to start narrowing, but at the same time balance empiric coverage for what you're worried about, right? In this case, probably a lung infection that is severe. So not to like just stop it altogether, but shorten the course, covering enough, narrowing the spectrum, ruling out MRSA, ruling out pseudomonas, for example, based on your organisms, rather than broader antibiotics. I think the goal is to really tailor, but at the same time cover for the patient. Good luck with antimicrobial stewardship team. Yeah, very good. So in other words, you do one medicine for your mother and another one for your mother-in-law, no? Okay, so now let's move on to whether you guys are using the MRSA swab at the beginning, yes or no? So MRSA swab, patients with community acquired pneumonia, is this part of your practice? You guys work in the VA. That's okay. Because we always get the MRSA swab. Okay, so 92% of all of you are collecting MRSA in the swab. Okay, sounds good. So Dr. Crawley, what do you think about this response that it seems that the majority are utilizing the MRSA in the swab, and if you collect it and it's positive, what do you do? And if it is negative, what do you do? Well, I think it depends on the severity of the pneumonia, for one. Well, if the MRSA swab's positive and the patient has severe pneumonia, I would cover them for MRSA, probably with vancomycin, or potentially lenazolid. If the MRSA swab were negative and the pneumonia was severe, I think then you could still think about do they have additional risk factors, have they been exposed in the prior 90 days, and if they're in septic shock, maybe in that point covering. But if they're MRSA negative and not severe, I would withhold coverage of MRSA and kind of wait the culture results. Very good. Anyone will do something different, or we're all in agreement? To me, this patient in my ICU, if this was a patient of mine, I would probably start with the pseudomonal coverage, and I think I would feel pretty comfortable holding MRSA coverage because my suspicion that he has a recurrent pseudomonal infection would be sufficiently high. Even if the MRSA nurse is positive? Yeah, that doesn't have a very high positive predictive value, so I don't use that to rule in a patient. So if I have a patient that's been historically colonized by pseudomonas but has never had an MRSA infection in the past, I think that I would use that more. Very good. Anyone disagree? Okay, so it looks like now after this study and after several others suggested and after three years of COVID-19, it looks like most of these pathogens are viruses. And so far we only had treatment for influenza. Now Charles mentioned that there is some coming data on RSV and of course from SARS-CoV-2. But what should we do now, these days, when we find another coronavirus or adenovirus? Should we really start considering, no, this is only a viral pneumonia, we don't need any antibiotics here? What do you guys think? Well, one of the things that I like about this study is that this is using clinically available but aggressive diagnostic tests. And it is important to highlight that there are a lot of co-detections. And I use the word co-detection rather than co-infection because this does not measure the host response whatsoever. So we still have these microbiology molecular diagnostic tests, things that will identify potential pathogens, but we're really just detecting. And then hopefully around the corner we have some newer diagnostic tests that will help us characterize the host response. But we haven't really integrated them into reliable tests that combine things for us. But one thing to really point out here is that for adults hospitalized with community-acquired pneumonia, there is a large number of patients who have a viral infection but have a co-detection of a virus and a bacteria at the same time. So that gives us pause a little bit to the approach that we start to see, especially with halfway through COVID. We started to see people de-adopt antibiotics for patients with COVID. Really clear case, really great story for just a strict viral pneumonia. And people were being pretty comfortable about not using antibiotics if they didn't have any evidence of other pneumonia that was bacterial. So how do we go forward? Do people feel more comfortable now de-adopting antibiotics for non-COVID viral infection? Hard to know. I think it's very important though to remember that there are a lot of patients that were viral and bacterial pathogens are detected when they're aggressively looking for it. But here is the question that Dr. Maturski brought up earlier. If the procalcitonin is there and the procalcitonin is low and you happen to find one of these viral pathogens, will the procalcitonin allow you to make the decision to really remove antibiotics? What do you think? Because then you guys say no procalcitonin, trash the procalcitonin and then at the end of the day maybe maybe it is working for some of us. What's going on? This is one of the reasons why in the viral statement that we talked about before that we didn't recommend widespread use of the viral panel in patients is because there isn't that data showing that if patients have a virus detected and don't have a bacterial copathogen detected that we can safely stop antibiotics. There was not very much data that antibiotic use was changed at all in the current studies that have come out. And that's where I think we're all feeling uncomfortable with knowing is it safe to stop, yes or no? Do we know from prospectively collected data that particularly with these tests implemented really at the point of care at the bedside where it could make a difference in antibiotic administration, not getting the results 48 hours later type of thing. In English it means you stop antibiotics or not? So I think I would assess kind of for other infections if there's nothing else apparent and I guess I haven't seen his chest x-ray still. So demanding. But I guess I would stop his antibiotics. I'm assuming he has just a little patchy infiltrate. Very, very good. So before we show you the x-ray let's go on to this question. What should be our approach regarding the imaging, diagnostic testing? Should we just do x-rays only? Should we just do the long ultrasound, of course compared to the x-ray? Or should we just do chest CTs as some of us have read these papers? Or should we just use the UK approach for patients that are not very sick that they don't do an x-ray, they just do a C-reactive protein that you trash from the first question, no? So what do you guys do? Let's go on answering this question. Chest x-ray, long ultrasound, chest CT. Let's see how many people are really using long ultrasound here in this room. So chest x-ray, very good. Long ultrasound, chest CT, C-reactive protein. So it looks like all of us except 3% of the believers in long ultrasound, 8% of the chest CT that probably will not do first the initial chest CT but they think the confirmation of the chest CT is the way to go. But the most of you definitely do not like any biomarker whatsoever in the world. And then the majority like the chest x-ray. So we have this very several systematic reviews trying to compare these things just suggesting that the sensitivity may be not as good but when you look at the ultrasound it's much better than the x-ray, the specificity is much better and the area under the curve is good. So in reality during COVID-19 we started to see all these papers on long ultrasound. So Charles, what do you think we need to do with the long ultrasound? Is this something that only the youngsters are doing this these days, they love it? Is this something that will allow us really to follow the patients constantly or is this just the newest fashion and then you guys want to stay with the chest x-ray? Well I think the data is pretty convincing and so I think a lot of this is generational gaps based on people's comfort and so I think the older generations try to avoid it because they're not as comfortable with these procedures and that's why you're seeing the results. But the data is the data at the end of the day and the beauty of sometimes these ultrasound, there's probably some dynamic changes too over time like an x-ray can and an x-ray you can see the numbers are not great and so I think I foresee that over the years we will do more and more of this but the community and the practitioners need to start adapting this before we can get more real-time data. Yes. That's a great comment. Would you like Mark to comment about the operator dependence of this test and your ability to really identify what you're supposed to be testing? Doesn't it depend on the operators? Yes. And the person holding the probe and Marcos would not allow me to answer E to all these questions but my E is it depends. All of these questions, it depends. If I am in a clinic in the Himalaya, I'm going to use lung ultrasound. If I have a really highly trained POCUS emergency department physician and a patient that doesn't have insurance, then that would be totally appropriate to diagnose pneumonia I think with a lung ultrasound. A lot of us here practice in tertiary 1A hospitals, large highly complex hospitals. We have rapid chest radiograph and chest CT which people trust and trust is actually really important. To be able to communicate to other clinicians, to have a paper trail, EHR documentation of lung ultrasound that's bedside is actually one of the other challenges of adoption. We don't have a good place to put it where people can see it if you're doing POCUS in the emergency department. But it is coming around the corner. So I actually do think that as people become more comfortable with it and we become more trustful and we have really high quality training which currently is a little patchy in POCUS, then I think people will start to trust it and it may be a real huge game changer in diagnosis for patients in the ER. Okay guys, but don't forget that nowadays everyone could really bring the iPhone and really can make the diagnosis right directly in the office and now we're wanting everyone to get an x-ray somewhere else. So for follow-up, for the pleural space, for paranumonic pleural effusions, these kind of trends, I think they might be important for us to really consider and this is why if you are very well trained maybe you may trust your data a little bit more and the documentation will be great. So finally the x-ray. This is definitely at least do you think this is a pneumonia, Dr. Brothers, or what do you think? Looks pretty convincing. Very convincing. There may also be some effusion. Some effusion, exactly. So this is an admission. Here is the prior chest x-ray. So definitely this has changed on this patient with a tracheostomy. Look at the CT scan so I'm going to tell you very briefly and the patient had a chest tube for the paranumonic pleural effusion. So if you have to guess what will be the pathogen that is the most likely pathogen that we are going to identify in this patient with the risk factors that we mentioned, with all the antibiotics that you suggested we needed to really be looking at knowing that you guys carry the viral panels that you do not recommend but you do and then that you don't like. What do you think it's going to be? What do you think is the pathogen that is likely to occur here? A gram-negative bacteria. Most likely pseudomonas with the prior exposure. Very, very good. Do you think? Strep pneumo and staph aureus are also common causes of pleural effusions. Strep pneumo and pleural effusions. Pseudomonas isn't necessarily very good at a pleural infection. So 36 hours post-presentation. These are the laboratory from the pleural space. We have glucose less than 10, pH 6.9, LDH in the pleural space more than 1,000, the protein, the serum, and the protein ratio is 1.48 and the majority were segments, although the sample was clotted and cloudy. Okay. And you end up growing gram-positive coccine chains that it was streptococcus pneumonia. So pneumococcus still? Patients from nursing homes? We always thought that these might say pseudomonas. How come this happened? What do you think? Well, one thing I always like to remember is that community-acquired pathogens can be nosocomial spread. So actually, you know, you can get influenza in the hospital. You can get strep in the hospital. So these are actually important pathogens to keep in mind and common things being common, especially with an effusion. It's not too surprising. I would have had personally a few hours of decision regret with my vancomycin with this patient. Kind of wringing my hands. Probably would have been started by the resident overnight. Okay. The interesting thing is the sputum sample that you guys recommended at the beginning showed these other two gram negatives, no? The providencia stuartii and pseudomonas aeruginosa. So now we have three pathogens in the same host. So what do you guys think? Christina, what do you think? Were there any quantitative cultures on the sputum or was this just overall? Overall. High growth. It just makes it, I think, a little confusing because he has a tracheostomy and so still kind of coming back to the question of is this colonization? And so now that we have strep pneumo in his pleural space, I'm more thinking that these could be colonizers, I guess. What do you think, Charles? It's hard to know. Given severity of the patient clinically, it's kind of hard to ignore some of these positive results. And so I think in the beginning I would cover at least what these organisms are showing in the different sites and then see how the patient responds to therapy given how sick the person is. But that way you're almost halfway to a seven-day course of antibiotics. Okay. The good thing is that in the blood and in the sputum, on another sample, grew streptococcus pneumoniae. So bottom line here is we wanted to really show you in a real case that this is not as straightforward as we all believe. Let's go to the second case. 66-year-old man presents to the emergency department with fever, chills, night sweats, cough, and yellow productive sputum for three days. Symptoms worsening has now shortness of breath and confusion. His past medical history of hypertension managed with amlodipine, dysphagia, and hyperlipidemia treated with astatine. On physical exam is tachycardic, tachypneic, febrile, blood pressure 110 over 65, long exam, right lower lobe crackles. The lab showed leukocytosis, 5% bands, BUN 28, creatinine 1.2, and his x-ray confirms a right lower lobe bronchoalveolar infiltrate. Okay. So where do we need to take care of this patient? So I'm going to allow Dr. Barbara Jones who is to answer as soon as we get this one so she can get prepared. Should we send the patient home? Should we put it on an observation unit? Should we put the patient on the war service or should we put this patient in the ICU setting? So most of you answer that you will put this patient on a ward service. Some of you will put him in observation, and a few of you will put him in the ICU or send the patient home. Okay. So, Dr. Jones, why should we deal with this, and what is your approach? Well, to me, clinically, the first, the biggest warning flag for this patient was his confusion. So, confusion is very highly related to mortality, and it's one of these things that the more we rely on things like electronic health record, adapted predictive models, which I love. If you lack these kind of gestalt-y, more mental status assessments, these things that you actually pick up at the bedside, if you lack those in your models, you're going to miss patients who are really sick. And so, this is a person I was worried about, and this would be an E for me, because it actually- An E, maybe. So, you don't know what to do with this patient. To me, he was a little borderline, too. A few things made me worried about, you know, does he actually need pretty intensive monitoring? It might be somebody that you want, the ER physician, to let you know how he looks in a couple of hours after resuscitation or after the antibiotics are started. He definitely looks like, you know, a ward patient. There aren't any severe pneumonia criteria. He doesn't have, you know, I think he's got a single infiltrate. He didn't have any really concerning end organ damage besides the confusion. And so, that would be something to really pay attention to. Anyone agrees or disagrees? So, anyone will add something? No. So, those things that they talk about, CURV-65, poor score, do you guys care about it? Do you do it, or this is just, I see the patient, he looks a little bit sick, let's put it on the ward, or what do you guys do? How many of you are doing the CURV-65? On a regular basis? On a regular basis in the emergency department? Is that true? You have to go to confession, or this is true? True. So, how many of you are doing CURV-65 in the emergency department on a regular decision to really make this, put this patient? Two. And, poor score, PSI score? PSI score, so, oh my goodness, so, all the data, all the data, all the data published from Utah about all these things, what's going on? No one is doing this thing, why? How do you see that? And, it's okay. I think that's pretty much every emergency physician, yeah, every emergency physician I talk to, they say, well, yeah, I use the CURV-65, and they say, well, actually, I kind of just sort of eyeball the CURV-65, and I know it is the components, right, and one of the things I like to think about with the severity assessment tools is, you know, after about five features, you really are slowing an ER physician down if you're asking them to impute, you know, the PSI is just kind of unusable. It's 22 features. A busy emergency department clinician is not going to be able to do that, but this is where computers could help, you know, so, if you have embedded tools that actually are helping calculate these in the background, they can augment, you know, the clinician's ability to assess a patient. Does it really help a clinician assess a patient? I'm not sure, but one of the things that I think is really important with the severity assessment is it helps us communicate, and so people know what PSI is, and they know what CURV-65 is. These are classic kind of heuristics, and so people actually do trust these scores because they are very well validated and, you know, suggested by guidelines, so when you are trying to, as the ER physician would say, sell a patient to your ICU or your hospital ward, having the data that backs up, you know, what their score is actually does really help communication. So, actually, I see these more as communication tools rather than decision tools. Okay, but this patient has three parameters, no? Tachybnic, has the BUN that is elevated, and he's confused, so this is the kind of things that probably could help in the emergency department to really identify some people that are at risk, so I think this is something that we need to consider because sometimes with this regard, some of the variables, just looking at them, and if we have something in a platform, may be more helpful. Okay, now, how do we treat these patients? Do we treat them with vancocefepime and Acetro, vancopeptazone and Acetro, ceftriaxone and Acetro, or amsulbactam and Acetro? I'm really interested about this question. I might actually change it up a little. Okay, so most of you answered ceftriaxone and Acetro. The second one is vancopeptazone and Acetro, and vancocefepime and Acetromycin, okay. This one is hard to swallow, no? Because if you really go to hospitals on this particular patient with those characteristics, with dysphagia and all that kind of stuff, most of the time it's almost, almost vancomycin plus something else, no? So Charles, what do we do here? Well, I think, you know, a lot of the information we have here suggests that it's a communicord pneumonia, and so from the case information, there's not enough to know, there's a risk for MRSA or a risk for pseudomonas for this patient, and so therefore, you know, I think communicord pneumonia coverage at least would be sufficient for this patient. Okay, so you don't think that the history of dysphagia is good enough to really say, because all my residents believe that everyone is aspirating even during rounds. So they are covering for all the anaerobes all the time. So this is what the guidelines kind of recommend, but should we really cover anaerobes, yes or no? Because the guy had this aspiration with potential aspiration, we don't know, dysphagia. So please answer whether we need to do, because some of you choose ceftriaxone plus acetone, that it does not really cover. So the majority of you believe that we do not need to cover anaerobes. So why we use Piptezo every single day on everyone? So Dr. Crothers, what do you think about this thing? Is this something that we really truly do, or we just answered the test very well here? Well, maybe we're all good test takers, but I mean, I think all pneumonia is some type, it's some form of aspiration, right? It's the gradient, though, of like, is it a micro aspiration versus really a macro aspiration? And I think my practice is more to cover anaerobes if there's really been a macro aspiration event and I think somebody has a pneumonia, not just an aspiration pneumonitis. So you think ceftriaxone and acetone are good enough for patients that are aspirating even with a presence like that? I would say, well, I mean, I didn't get a sense that his dysphagia was all that severe and I didn't get a history of, you know, a really significant aspiration event. So I think I would start with that and also it didn't look like he had, you know, an abscess on his chest x-ray. So I think I would start with ceftriaxone as a throw and see how he's responding. If there's, if he's deteriorating or showing kind of signs of cavitation or something, then I might, you know, and see what the cultures are change to having anaerobic coverage. Very good. So most of you answered no. The guidelines say no. I'm going to have to leave this here because I only have 10 minutes to close this session and I have some potential questions that I wanted to really discuss. But the day three, the patient, he seems to be getting better. Less cough, less yellow production, no confusion, no shortness of breath, everything got better. Bands, BUN got better. What will we do next? Continue with cefepine and acetone. Change to levofloxacin, change to amoxicillin clavulanic acid to complete the course or stop antibiotics. So we're talking about day three. Where's E? Yeah, right? Where is E? You guys practice other medicine, no? Not the one that is provided. So, what are your answers, experts? Please. Okay. Oh, I haven't done this. I apologize. It's all my bad, my bad. We are really decided here, so continue with Cefepim and Acetro, some of you decided to continue. Change to levofloxacin, change to amoxicillin, clavulanic, stop antibiotics 11%. Okay guys, so what do we do with this clear course of decisions? Anyone believe that this patient has clinical stability according to the guidelines? This patient has no longer of this, of getting better, but you still want to continue antibiotics, so the majority of you, except 11%, decided to continue antibiotics on this patient. The guidelines recommend no less than five days. The majority of the people do five to seven days. Now the duration of antibiotics has been challenged with this randomized control trial that tried to show that there is no difference in the different groups no matter what. So what do we do with this data? Are we going to stop antibiotics, do we have the guts, or do we really say, no, no, no, I'm going to still do it in at least five days, or seven, or for how long? Chuck? I think it's an interesting study. I think it still needs sort of validation and additional studies to confirm this, but it does suggest that you don't need a really prolonged course like we've used to in the past. So I think I'm still comfortable with the five days until more data. Okay, anyone disagree? So no one will stop antibiotics on day three except for those 11 heroes here in the audience. Yeah, I mean, it's certainly tempting to because he's clinically stable. I think we have all gotten burned with one study that's come out showing things, but I think this is not the only one that's suggesting that three days of antibiotics may be enough. I do try to keep in mind the generalizability of my population to these studies, and I think I remember this one being pretty low mortality rate. For the patients that are hospitalized on the ward in that hospital, similar to my patients in my hospital, it may be different. And so that is one thing I try to really keep in mind. So I would be more comfortable with the five day so far, again, kind of with not wanting to be burned by one or two RCTs. Okay, so the message here is be careful, no? Because everything that is published may look very, very beautiful, but maybe one may not be enough and maybe may not fully, fully apply to your literature. So be careful on this one. However, in the United States, we do treat patients for 10 days. So even the problem is not even three days or five days. These guys talk about five days, but the people are using 9.5 days in hospitalized patients. So be careful on this because moving from nine to seven, that will be a big thing for all of us. Even moving from seven to five will be a bigger, bigger thing. Okay, so I don't know if in five minutes we will be able to discuss this case, but I'm going to try to do my best. 57-year-old woman arrives to the emergency department with fever, nasal congestion, shortness of breath, has past medical history of diabetes, treated with metformin, prior COVID-19 disease and depression. Physical exam 80 over 50, heart rate 118, respiratory rate 32, SpO2 90% on 10 liters of oxygen by nasal cannula is now switched to high flow nasal cannula, 60 liters per minute on an FiO2 70%. She has decreased breath sounds on bilateral lung basis with crackles. The chest x-ray shows bilateral pulmonary diffuse infiltrates. This lab showed that the white blood cell count is 15,000. The hemoglobin is 8.3, hematocrit 31, platelet count 20,000. The lymphocyte count absolute is 1.5. The segment is 85%. Bands are 3%. Ionizer is fine, she's hypoxemic with a little bit of CO2 retention. All the other labs with a BUN might be elevated, albumin low. Respiratory panel is negative, MRSA in nurse is positive, Legionella antigen is negative, blood cultures are negative times two, sputum cultures are negative times two. This question relates to a patient that is sick. And the question here right now is, should we use systemic corticosteroids in those patients with community acquired pneumonia, all pneumonia comers, okay? So please answer whether you believe we should be doing systemic corticosteroids for patients that look this sick, or we should not be doing systemic corticosteroids when these patients are this sick. So the majority of you will not use corticosteroids, but I'm very surprised about 22% of you that believe that we should be doing corticosteroids in these patients. I'm going to follow with the second question saying, if the test shows that it's positive, will you be doing systemic corticosteroids? So SARS-CoV-2 positive, yes or no, whether you are going to use systemic corticosteroids? Is there a C on this one? Oh no, come on. She's on my flow. She had COVID already. No, but she's a fellow. Okay. So the majority of you will use corticosteroids in a SARS-CoV-2. What if the test is positive for influenza? Patient is the same sick, what are we going to do about influenza testing? Yes corticosteroids systemically or no? Very good. Thank you very much. Guys. Can I be a little blasphemous for the first one? Aye, aye, aye. No. Okay. So the majority said no corticosteroids and 13% are doing this one. So it is a little bit lower than the 22%. So now you start to reflect on your decision at the beginning. Maybe you change your mind here because how are you going to know which is the pathogen that you're dealing with? Okay, guys. So we need to conclude here. Very important. Corticosteroids, systemic corticosteroids. Patients are sick, severe community acquired pneumonia. I don't know the pathogen that people say no. I know the pathogen is COVID-19 that people say yes. I know it's influenza that people say no. What do I do in clinical practice? So short answers. Please, please, please go ahead. What do you think Charles? I think there's a lot of data for the SARS-CoV-2 and steroids, a certain population, a phase of the illness. Definitely, right now, no for community acquired pneumonia or influenza. I think the types of steroids used like dextromethazone might be important. Those studies need to be done. Potential use of CRP could be helpful for the other studies. But right now, only for SARS-CoV-2. Only for SARS-CoV-2. No matter how high is the CRP, no matter how inflamed the person is, no matter if your mother is the one in that bed and is on a high IL-6 with a high CRP, with bilateral pulmonary infiltrates, and he happens to have a bacterial pneumonia, you would not give corticosteroids. No. Only to mother-in-law. Not right now. Not right now. I think I would, actually. You would? Maybe in that group that has, she didn't have a very high CRP. What do you mean? The mother or the mother-in-law, you would? Potentially either, but I think in somebody who has a very high CRP, there is data saying that in that group, maybe we can at least prevent progression of illness, and we might have earlier resolution of infection. And so you wouldn't be going outside of the data to use it in that population, but then applying it to the population that is less inflamed, has a lower CRP, is helpful. does not show as much benefit and would have a greater risk of complications of corticosteroids. Very good. Barb, would you change anything? No, no, no, maybe. Yes or no? Would you change anything? So this lady, I'm just going to be blasphemous and say even if she had SARS-CoV, I might not give it to her. Because all of that data, the evidence that supports SARS-CoV, was done in an unvaccinated population. And she had a prior infection with COVID. And so this year, if we repeated the RCT, the recovery trial, in COVID-19 now, now that we have a vaccinated population or exposed population, we may see something very different. I think that all of this is so interesting because it points to the fact that we have a heterogeneity. Barb, it's 5 o'clock, so finish, finish quickly. Because you're reminding me that every single time my mother-in-law gets sick, I'm going to send it to you. You're not going to give corticosteroids to anyone. Okay, so basically we got this study that shows, yes, in people that are on oxygen, very sick, be careful with the hyperglycemia. But here is the most recent community aquanumonia of all these VA comparative trials that show no good with methylprednisolone. Okay, just recently published. So now what? If we're going to do it, like Christina said, we're going to do it, are you going to use dexamethasone or methylprednisolone? If you are not going to do it, well, you don't have to answer this question. But if you're going to do it, dexamethasone, yes, dose, and for how long? Okay, no, no, we're talking about patients. Yeah, I mean, SARS-CoV-2 would be dexamethasone for the recovery trial. Okay. And I have to say, I do not remember right now the TORAS study. What dose of? I think TORAS is 500 methylprednisolone, I think. Methylprednisolone, but not dexamethasone. But higher dose. Okay, so commit, commit. What antibiotic? No, you're going to write the order. So I'm going to say if their CRP was over 150, I'd use the TORAS protocol. TORAS protocol. Methylprednisolone. Oh, my goodness. Okay, Charles, what do you think? For bacterial pneumonia. This is easy. No medicine is easy. Yeah, I think right now I wouldn't probably use it. You're going to use it. I will not use it. You will not use it on community aquanumonia. You only will use it on SARS-CoV-2. Okay, guys, so you can see how challenging this story is. And if the patient is on ARDS, are you guys going to use it? No. No? No? Not right now. Okay, so no corticosteroids for ARDS patients from pneumonia. Only maybe if SARS-CoV-2, except BARP. Okay? But all the others, that's great. So I'm just going to end up here because I'm two minutes past the hour. We would like to thank you all for your time. Please, if you have any questions, please come by and ask us those questions. But thank you so much and have a great rest of the meeting. Thank you for the panelists and all of you.

controversies

pneumonia management

biomarker tests

antibiotic choice

viral panels

duration of treatment

systemic corticosteroids

procalcitonin

severe cases

individualized decision-making