Good morning, everybody. Welcome to year six of Pardon the Disruption. I am your host, Dave Shulman. I have very few skills other than insulting people, and they figured this is the perfect job for that. Thank you all for joining us. For those of you in the audience who have not yet had a chance to grab one of the little thumbs up, thumbs down, please go ahead and grab one. Please do not hit each other with them, but they will be used to have you participate in the conversation. I am joined by a wonderful group of individuals. Some of you may recognize that we've changed the name of the session. I can't say it is because ESPN threatened to come at us, but that may have something to do with it. So we've now rebranded to Pardon the Disruption. And because we've done this for five years, we've now curated enough of a group of champions over time that we have a tournament of champions. So this is the best of the best. I would have said it was the best of the best, except one of them is joining us on the phone. So that person is not the best of the best, but is the second best or the third best of the best. Before we pardon the disruption, as always, we will pardon the introductions. So first, introducing on the far left of your view, the real deal Tar Heel hailing from Wake Forest University School of Medicine, nothing could be finer coming out of Carolina than Dr. Dave, row, row, row your boat. Dave, a round of applause, please, for our champion from year two. Introducing our, this is the only repeat champion we've had from years three and four, the General Patton from the borough of Manhattan, the beast from the Northeast hailing from Columbia University School of Medicine, Dr. Stop Look and Kristen Burkhardt. Round of applause for our double winner from years three and four. Joining us on the line and held up, hopefully you can hear him, we'll see as it goes on, he is our last year's champion, he's the current reigning PTI champion, the greater debater from the city of Decatur, using each date to teach great in the Peach State, hailing from my own institution, Emory, Dr. Andre, just wait until I'm holder. There he is. Round of applause. Hopefully he can hear you. And I would not be doing due diligence if I did not pay some homage to our wonderful late great Ben de Boisblanc in memoriam, original PTI champion, the big cheesy and the big easy, educational high water from the French quarter, hailing from LSU, Ben de Boisblanc, Sauvignon Blanc. Oh, wait. Oh, well, that's supposed to hear him talking, tell me he's not actually dead. Yeah, so for those of you who are worried, the sound was not working, but Ben is not actually deceased. Ben is just not able to join us this go around and sends his regrets. I was going to say he sends his good luck to the champions, but he does not. He said something saucy is exactly you'd imagine Ben to say. Also joining us for the first time on my direct right is Dr. David Bell sitting in for Dr. Alex Niven, although I'm told that smarter people than me have said you are no Dr. Alex Niven. So he nods because it's an inside joke. I promise that's less of an insult. They all have water to keep them refreshed. I have a combination of diet Mountain Dew with extra caffeine and mortar oil pulled in there. So we should be good to go for the rest of our competition. Quick review of the rules of engagement for the contestants. We're going to get to all of the topics we can. For most of the topics, I will select speakers in a random order. I ask them to keep their comments relatively short because we will move on and I do get bored quickly. We encourage volume, humor, and accuracy. I reserve the right to cut people off. I will do so using my patented America's Got Talent buzzer. I will cut them off for a multitude of reasons. Four points are available per topic, two for data, two for attitude. Points can be lost if you bore me or if somebody else comes at you strong. You're welcome to come at me. In fact, I encourage people to come at me. That's worth lots of points. But if you come at me, you better not miss. Back this year, audience participation. So again, please use those. If you hear something you like, go ahead and give them a green thumbs up. Thank you. You like this already. You like me. In the words of Sally Field, you like me. You really like me. If you don't like what you hear, go ahead and red thumbs down it. We'll take some points away. And then if you do want to tweet doing so, you can. Dr. Bell, to my right, will be following the hashtag, and we'll be having a debrief after the game. Contestants, are you ready? No. Dr. Holder, have you heard anything we've said at all? I'm definitely not ready. Definitely not ready, he says. All right. Well, we'll find out. All right. So it is go time. And I will start with the first topic with Dr. David Bowden. Is direct laryngoscopy in the intensive care unit dead, Dr. Bowden? You know, I think with the device trial, clearly, video laryngoscopy is the standard now and should be. But calling DL dead is sort of like Monty Python, I'm not dead yet. You know, and so I think that part of the problem with the device trial is there are so few of us left who use DL preferentially. And those operators were markedly underrepresented in the device trial. So almost everybody in the device trial was predominantly a VL person. I think VL is clearly better for early visualization and first pass success, perhaps. But DL in a very soiled airway, I think, is going to be your likely rescue device. Dr. Burkhart? So I'm going to say that very few of you left who can do the DL. That's an unfair advantage to throw out there, my friend. So first of all, I also trained on DL. And I'm going to say this is akin to the central line access, right, where I was like, I didn't have ultrasounds available when I was a resident or a fellow or when I first started. I used to tap out my thoracentesis, I used to go blind and stick Big Red. But I'm going to keep doing it because no ultrasound is going to replace my technique. But I think we are here. I think that rescue modes may be DL, but it may actually be bronchoscopy. And I don't know that... If you're that bad off, bronch ain't going to help you. Oh, I'm not sure about that. I think we do a lot of bronchs. I think we're better at the bronchs from that. I don't think DL is dead dead. I think DL in anesthesia has not been tested, right? So this was early ED residents and critical care fellows, right? And I think first pass success is important. But the other caveat is they use bougies in every single patient. And I think that's probably also assisting. Dr. Holder, you're third up on the issue. Anything you want to add to your competitor's discussion? So you may have to forgive me. I may not have heard everything that was said. But I think that the use of DL is kind of going the way of the dodo bird. And I'm actually one of those dodo birds, unfortunately, because I trained in the era before video laryngoscopy was so common. But I think certainly the newer literature, the more recent evidence, even from this year in the New England Journal, suggests that most people are going to do better with first pass with video laryngoscopy compared to DL, at least those who are being trained now and those who've been trained more recently. I mean, I'll have to sort of re-echo what you said, because I think you said this up front, right? Seventy-five percent of the prior intubations had been with DL for the majority of the people participating, right? So it also reflects that training environment. And I think, importantly, in the device trial, there was no difference between groups in severe complications between DL and VL. And I think it underscores the difficulty of using first pass success as an endpoint in any airway trial, because it's not patient-centered. Should we be training—we have at least one program director on the panel—should we be training current trainees in the art of direct laryngoscopy? I'm going to say we still do. I actually think that in our program, we really work to emphasize both video, but then when fellows have been comfortable with video, we push them to actually start doing some DL in that space as well, although it may start to move and change since the device trial came out. But that's still where we're at. All right. Lots of thumbs up for Dr. Burkhart. She's maxed out her points on this topic, unfortunately. All right. Let's move on to topic two. Dr. Holder, I'm going to go to you first on topic two. What is the current role for corticosteroids in critically ill pneumonia patients? Dr. Holder. So I think that there's a growing body of evidence to support that it is useful, but that it needs to be done relatively early in order to actually maximize that use. And I think that's the theme of most things that we're seeing in critical care. So if we're going to give it, we should give it early. That came across in the systematic review that came out, actually a couple of systematic reviews, one of which came out in CHESS. And the more recently, there was one in critical care that suggests the same. So I think, you know, really, again, it needs to be given early. And I think the two trials that seem to make that point the best are one that came out in intensive care, which showed no difference. And then the CAPE COD trial that seemed to show that there was a strong impact, particularly on death by day 28. And the difference between those two trials, for the most part, was just when it was given. In the first trial, it was given up to 72 hours from the time that patients were diagnosed. And in the CAPE COD trial, it was given within 24 hours. So again, I think, at least for severe CAP, the evidence seems to suggest that it should be given. Dr. Burkhardt. Yeah, I mean, I have to say, for me, severe CAP sort of just confirmed what I think we should be doing with severe pneumonia. So in those patients, in particular, when we sort of think about who this may actually benefit, we have a very sick intermediate care unit where a lot of patients are on high-flow nasal cannula and non-invasive. And that was the majority of that population. So I think only about 12% or 15% were actually had invasive mechanical ventilation. So starting steroids early, meeting that criteria for severe community-acquired pneumonia. The dose will someday be figured out. But right now, it's that hydrocortisone at 200, infused continuously, I believe, in that trial. And the decreased mortality, the decreased numbers of intubations, and the decreased new shock at 28 days, I think it's hard to say not to use it. We have to recognize people excluded in that trial were immunosuppressed, right? And we have a lot of centers that have transplant patients who are immunosuppressed. So it doesn't meet for that. But I do think that looking at the historical data suggestive there, this, to me, pretty much says, specifically in that patient population, and if that CRP is greater than 15, there may be even greater benefit for that. Bowdoin? Yeah. And I, you know, the DEQUIN trial published just recently in the New England Journal with 800 patients, cap. Steroids had a lower mortality. All the other trials that had no effect enrolled HCAP patients, HAP patients, and not very ill patients. So if you've got a critically ill, mechanically ventilated, high-flow oxygen patient with cap, yeah, steroids. All right. Dr. Burkhart, you're up next on topic three, just a touch of the flu. Should fludrocortisone be given to most or all patients receiving steroids for septic shock? I have to say, I do love the comment. The steroids in the ICU, I used to give a lecture to the fellows about the whole history going back to the 1950s and looking at. And we have lots of debates and debated for a very long time about the role of fludrocortisone, right? And when you look at it, it goes back to Anand's original paper, and Anand used fludrocort. Back in 2001, Corticus did not. There's a lot of hand-waving as to why there were differences, not differences, and approaches came out, adrenal came out. And again, they tend to show that the trials, both Anand's, that included fludrocort, had lower mortality, although the patient populations were different. But it's really hard to argue against the most recent sort of analysis from Bosch, thank you, where they looked at almost 90,000 people and getting hydrocortisone versus hydrocortisone plus fludrocortisone, and recognizing that almost 97% only got hydrocortisone, but of that 2.5% or whatever that got the fludrocort, the mortality was significantly lower, to the point where a number needed to treat to save a life was 29. So I think it's low risk to add fludrocortisone, doesn't make the most sense from a pharmacologic standpoint. Prior to this, we were not doing it, but we have moved to add fludrocort to hydrocort now. I'm debating if I should give a point to Bowdoin for giving you that, or if I take a point away from Bowdoin. I would have gotten there. I might have been having a word-finding difficulty issue. It was there. I was just needing to read through the little lines of my brain. It's not a question of whether you would have gotten there, it's a question of whether I should respect helping your opponent or to punish him for helping his opponent, and I'm inclined to do the latter, but I'm just going to give you a warning for now, a yellow card. I don't give a shit. Dr. Holder, you're up next. Should fludrocortisone be given to most of our patients receiving steroids for shock? For me, it's like, meh. That's all you have to say is, meh? Well, I'll elaborate. So the evidence for me isn't as compelling. I kind of treat it like when I talk to my kids, like, if you like it, I love it, when my residents might want to give it, especially for those who may have a severe septic shock. But I think the APOC study is probably the best, or the one that seems to come to mind, at least more recently, that talks about this. The problem with that study is that it didn't look at hydrocortisone by itself versus hydrocortisone plus fludrocortisone. So, I mean, if you really wanted to test it, then that would be the way to go. But for me, the steroid question, it kind of feels like the conversations I've had with my wife for like 10 or 11 years, and it's like, we haven't really come to a resolution on this. So we're going to agree to disagree, and if you love it, I love it. If you don't, so be it. But I think that the APOC trial is issues with generalizability, because those patients were so super sick. So how do we know what actually was the thing that improved mortality in that group? And I think, you know, the fragility index in that study was super poor. I mean, it was something like three, you know, which suggests to me that maybe it's really the luck of the draw on the patients that they recruited. Can I just ask you a question? A number needed to treat a 29 for a low-risk medication like fludrocortisone, is it really worth dissecting all that other data? Yeah, it's cheap, no side effects, virtually, orally administered. It's probably the only cheap medicine we have in the ICU. And we've been discussing steroids and septic shock for 100 years, or at least 50, since I've been in the lab. Holder, I'm going to let you back. Lots of green thumbs. All right. Holder, go ahead. Back to you. That's kind of why I say, if you like it, I love it. I see very little downside, you know, because like everyone said, it is cheap. I think, what, a 0.1 of fludrocortisone is like $225 a day, something like that. But again, the question here is not whether or not it's safe, but whether it's efficacious. And for me, it hasn't really borne out in literature. There's still questions, let's put it like that. But for me, I don't even know if I want to even answer those questions just because of the amount of patients you probably need to recruit for a study like that, and also the risk-benefit. All right. Let's move over to the physiology section of our discussion today. Dr. Boaten, you're going to be up first, and maybe you should drive. Must we strive for a driving pressure of less than 15 centimeters of water in all mechanically ventilated patients? I won't say all, but I think it's a reasonable place to start, and better than tidal volume of less than six. I mean, people forget that in the original ARJNET trial, the only people that benefited from low tidal volume were those with compliances less than 45, 47 in that range. And that driving pressure less than 15 helps obviate that, and I think it's a decent place to start. We don't know what the number is. I mean, I don't know whether it's 10, 12, 14, but I think it's a good place to start. Dr. Holder, should we strive for driving of less than 15 in our mechanically ventilated patients? I'm sorry. Can you repeat the question? One last time. Yes. Must we strive for driving pressure of less than 15 centimeters of water in all mechanically ventilated patients? Again, I think that the evidence seems to suggest that, and it's based on sound physiologic principles, it's a surrogate for volumetric strain. And if we decrease that, then we're probably going to decrease the likelihood of a ventilator-induced lung injury, at least based on where the evidence is going. And again, I agree with the prior comment that we don't really know what that magic number is, and maybe there is no magic number. Maybe it's variable, depending on the patient. But I think that the principle is there. Okay. Dr. Burkhardt. I mean, I think I actually am going to say, I first think it's important for us to focus on doing lung protective ventilation, sticking with our ARDSNET protocol at that 6 cc per kilogram or less of predictive body weight, and keeping an eye on your driving pressure, right? So if my driving pressure is high in that space, I will go down, and I will try and keep it into that less than 15. So I'm not just a driving pressure less than 15, and I'm not just an ARDSNET sort of box person, but I look at both, right? And in critical care medicine, I think we need to. We don't know what the perfect plateau pressure is, right? Probably less than 25. Actually, we've seen that you actually have improved mortality as you go down. So I think looking at everything in our toolbox and using everything as opposed to anchoring on one thing, physiology is super important, but also having some large evidence-based studies showing that this results in improved outcomes, I think is important. So I think the combination of the two is actually where we need to go. I feel like we have consensus on this issue, and I hate consensus, so let's move on. I know. I'm sorry. Don't apologize. Okay. No apologizing. No apologizing. Yeah. Schulman. No apologizing. We can talk about title volume. How about we talk about the PEEP table? So should we, is it time for us to ditch the ARDSNET PEEP table, Dr. Burkhardt? I'm going to ask how many people in the room, show of hands, actually use the ARDSNET high PEEP table on a regular basis? Green arrow if you use it, red arrow if you don't. Right? Overwhelmingly, no. So I'm going to say that routine use of the ARDSNET high PEEP table has already fallen way out of favor. I do think there are some patients, right, when we talk about people with elevated body mass index that have a lot of sort of pressure and chest wall that they benefit, and they end up looking more like a high PEEP sort of strategy in that group, but I do not use the high PEEP strategy. I'll give you an extra point for audience participation, Dr. Burkhardt, just so you know. Bowdoin. The high PEEP table is not saying you can't ever use high PEEP, but using it routinely is a mistake. I think if you look at, for example, Tregyani's articles, God, they're five, six years old now, small numbers, looking at people with hyperinflation, 30% of the patients were hyperinflated on the low PEEP table because they weren't paying close attention to driving pressure and other elements. Dave, I'm going to ask you to get a little closer to the mic just so Dr. Holder can hear just in case. Thank you. Oh, okay. I think the size data, BAL, IL-1, IL-6, TNF-alpha, were all higher in patients with hyperinflation, and 30% of the patients were hyperinflated on low PEEP table because you've got some normal lung units that even at low PEEP can be overinflated, and I think that's where driving pressure plus low tidal volumes, you've got to think about what you're doing to the considerable portion of relatively normal lung. Wait. Can I get ... I want to get some clarification before I go to Dr. Holder. Is it high PEEP you want to abandon, or is it just the routine use of the table? Is it that the specific use of the table is problematic? You like the principle but not the actual table, or do you think that the table represents something that we should not be routinely doing? I think it's the routine use. I think PEEP needs to be titrated to the individual patient. Obese patients are going to take a higher level of PEEP. They have a high intrapleural pressure. It'll take more PEEP to overcome that, but to say, oh, everybody gets the high PEEP table, I think you're making a mistake. I actually think the majority of obese patients are under PEEPed, truthfully, in most units. I agree. You're coming out against the higher PEEP table, the low PEEP table, all PEEP tables? No, no, no. I said high PEEP table, so I start at the low PEEP table, and I understand that it may be too high in some people. I think that's the important thing, is that it's not this is mana from heaven, that this is what we have to use, especially as you get up to FIO2s of 0.6 and 0.7, where you can get even the low PEEP table to 12 and 15 of PEEP, and in some people, that's too much. I'm going to go to Dr. Holder on this. The question from the audience was, should we abandon the low and the high PEEP table, or is it simply the high that we're throwing our eggs at? Your thoughts, sir? So, you know, this is, like, with many of these questions, I feel like we're asking the wrong question, like, really, you know, the issue to me is why not titrate it based on the patient's need? And I think I'm sounding like I'm beating a dead horse here, but I think it's a very true principle. You know, I have two kids. One of them is hyper, and both of them, neither of them like to do homework. One of them is super hyper, the other one sits down quietly, but gets easily distracted in her own mind. And the way that I try to get them to refocus is going to be very different because I'm dealing with two different people, and I feel like, you know, if that simple example is true for such a scenario, then why can't it be true for complicated syndromes that are heterogeneous in patients who respond differently and have different pathophysiology? I mean, I think, you know, we can't really oversimplify this. So using either of those strategies, low or high PEEP, for me is starting to get archaic. We really need to tailor it to the physiology. I've got a follow-up question for Dr. Holder. So if we're not using oxygenation to drive the determination of PEEP, what parameters are you going to use? So I think oxygenation is definitely one of the big ones, right? But I think my point is just, you know, when we're determining whether or not we have adequate – well, actually, it's on the flip side, actually. When we're talking about the harm that we're doing by the PEEP and whatever strategy we're using, that's what I'm talking about. So if we're going to use a low PEEP strategy, we may not be – or rather, a high PEEP strategy, we may be giving too much therapy and potentially causing hemodynamic compromise in those who are at risk. So I think that's really where I think what I'm talking about really plays a role. So I don't disagree with the parameters that we're using, but it's more so we can't apply a one-size-fits-all approach to everybody. I'm going to say that I feel we are incredibly hard-pressed as a community to say we're not going to use a table to guide PEEP and ARDS. The vast majority of critical care happens out in community hospitals, doesn't have expert physiologists looking at the ventilators. We have to have a place for everybody to start at separate centers or places who really want to sit there. And if you're at the bedside 24-7 – it's my interns at an RT at night, it's not me at the bedside 24-7 – tweaking this based on all these different parameters. So I think that we have to recognize that data's not perfect and that each individual is going to be different and that there are certainly some people that are definitely not going to fall under the table, but to just say we don't need a table to help manage patients with ARDS I think is a bad decision for the community at large. So I'm not saying necessarily we don't need the table. What I'm saying is that if we have better ways of doing things and we have the resources to do them, then why not do it? Yeah, the problem is we don't know the better ways. Obviously right now there's a trial for esophageal balloon, and I kind of like that idea, but it's never been shown to be – Wait, how many esophageal balloon trials have we done? A tiny little trial. A tiny little trial. I realize that. We should be making balloon animals out of these things we've done so many times. The physiologist in me says, ooh, that's appealing, but it'll probably be a negative trial. And I think, by the way, this – I'm sorry, I apologize if I'm talking over someone. I can't quite hear you. We got you. We're running it. Go ahead, Holder. Okay. No, I was simply going to say, you know, to the point that was made before, this is where clinical trials are helpful. And if we try that approach and it doesn't work, or if it's no better than the approaches that we're using right now, then of course, yeah, we should keep it simple. But we just don't have an answer to that question yet. Does any of the audience want to see any more esophageal balloon trials out of curiosity? I'd love a thumbs up or thumbs down on that. Both of them. I have to take a point away. Dave, come on, man. Come on. Come on. We're not. No. All right. Next topic. Holder. You're up first. So when someone's suffering from a biscuit overdose, how do you decide how much peep to use? I'm going to move on to the next topic. Pick your poison, Dr. Holder. Pick your poison. Dr. Holder, you're gonna be up first on this. What is the best initial fluid for volume resuscitation? I'll be curious to see if my emergency medicine trained intensivist feels differently than an internal medicine trained intensivist. So Dr. Holder, best initial fluid for volume resuscitation. I still say 20 to 30 cc's per kilo. Well, what fluid would you choose? Oh, what fluid? Oh, well, based on more recent evidence, LR, or whatever balanced crystalloid you may have, you know, in your shop. Anybody else voting? Lactated ringers? The first thing the nurse hands you is what you start with. Doesn't matter. And then you change to balanced crystalloid. And you know what? And you know what? If you're only resuscitating for a couple liters and you're stopping at 30 cc's per kilo, it probably doesn't matter, right? But I think if you have access to it, then you should use it. Yeah, I mean, I think balanced crystalloids, right? If you look at the SMART trial, it sort of showed that for the post hoc analysis of sepsis patients mortality was lower. And does it mean there's lower mortality with balanced crystalloids? I don't know. But does it mean it's probably safe to use? Yes. And so based on all of the sort of trials and the work leading up to it, I think for us it's the right choice to use balanced crystalloids. Again, maybe has a benefit. Certainly doesn't have a harm. It doesn't appear. For those of you in the audience who are interested, Dr. Bowden is pulling together a trial for esophageal balloons to determine the answer to this question. So if you're interested in participating, please come see him after the session. All right, Dave, you're gonna go up first this time. Hold your water. Should we minimize early fluid resuscitation in sepsis in favor of more aggressive vasopressor use? Hell if I know. I mean, I think that there's this concept that more fluid is required, and we've tended to go, well, less fluid is equally good. But most of the trials looking at fluid minimization already had patients resuscitated with about 30 mLs per kilo. And there's even a study in academic emergency medicine this past year that looked at patients with heart failure in sepsis, and those that got less than 30 mLs per kilo had a higher mortality even with heart failure. So I think initially, you gotta give them fluid. After that, vasopressor, and I'm not saying you can't start both simultaneously, but you may use the volume. Dr. Burkhart. It depends, right? So I'm gonna go the opposite of my comment about the ARDS trial, right? So, and using tables. I actually think we really don't know with volume. I think initial resuscitation is really important. Too much, you don't want people 20 kilos overloaded, which we would see, right? But also under resuscitation, I'm gonna quote the great Laura E. Evans on her debate last year at CHEST where she was debating fluid resuscitation, and she said, I don't know about you, but I don't miss digital ischemia and lost limbs, right? So volume is important, and we need to keep an eye on all those parameters. And if we pivot to using just pressors, we are gonna go back to seeing a lot more digital ischemia. Dr. Holder, so are we too aggressively pushing fluid should we use more vasopressors early? I think that, you know, based on the more recent trials that come out, it doesn't seem like it makes a difference. If we're looking specifically at just carb, you know, just gun size fits all, lots of fluid or very little fluid. I think what for me decides that is, believe it or not, just logistics. So if we decide to start pressors early with the intention of withholding fluid, then you're gonna have a lot more patients ending up in your ICU and particularly if you have if you have limited bed availability or limited ICU beds, I think this may become logistics issues as well. So I think as long as we're, from my perspective, what I think as long as we're mindful of the fact that giving too much fluids will have untoward effects later on and also if we're using some way of assessing whether or not they're fluid responsive early on, then I think that to me that's the better approach rather than saying I'm just gonna restrict versus give liberally. But I certainly don't withhold fluids if patients are fluid responsive even early on for a lot of reasons, including Dyspo. Yeah, I guess I'm a little uncomfortable that we have good tools for fluid responsiveness, you know, that intermittent tools don't appear to work, flow-directed tools appear to work better, and so I think in most instances you're not going to have a continuous flow-directed tool available to you initially. So 30 mLs per kilo as a start. After that, don't give them fluid if they don't need it. Agreed, and I and I'll just sort of say that I think looking for tissue perfusion, looking for tissue sort of injury and organ injury is an important part of it. I also think that we have fluid, we have tools to help us if someone's be fluid responsive, but I'm not aware of any patient-centered mortality or outcome data on those tools. Dr. Burkart, I did give you an extra point for quoting Dr. Evans from last year. All right, next topic. Dr. Burkart, you're up first. Cool hand Luke. Are we done with TTM? Is this for out-of-hospital arrests? This is where I get to be the controversial person in the audience. So I will tell you, I don't think we are, right, and we can go through all of TTM-1 and TTM-2 and quote all the data, but if you look at the TTM-2 trial, right, that most recent targeted temperature management, 90% of the out-of-hospital arrests were witnessed. 80% of them had bystander CPR, very few comorbidities. They have a really aggressive pre-hospital care where that was performed. That does not reflect my patient population, and so I do respect the neurointensivists at my institution. They are incredibly smart and very invested in this field, and we have stuck actually with 33 if tolerates and if not 36. Part of it is that I think we really need to be a little more precise. It's a heterogeneous group of people that are coming in without a hospital cardiac arrest. There's some small studies that show that more severe cerebral injury is actually better at 33. If you have moderate cerebral injury, you're probably better at 36, right, so just grouping everybody together the way we do with COPD, right, like let's separate out what does this look like. We need early phenotypes. We need to figure out what those groups look like, and there is some data that's coming out that appears that 36 may actually be less than 30, and maybe it's we're not being as aggressive with controlling for fevers, right, so I think the key thing, no matter what you do, there is targeted temperature management, right. You can't let people be febrile for those first 72 hours, and then you have to decide on that case-by-case basis, but we still do 33. Dr. Holder, is TTM for out-of-hospital cardiac arrest still a thing? It absolutely is still a thing. I think for all the reasons that were mentioned before, you know, I think we may make an argue about, you know, or at least discuss what the best target is, and I think, you know, perhaps the best target may be different for different people, but I think no one would disagree with the fact that we need to ensure that patients don't go, don't become hyper, so like, because of all the untoward complications that can happen from that. Bowden? Yeah, and I hate to agree, but I think, importantly, there's a post hoc analysis TTM trial looking at the in-hospital arrests, and the in-hospital arrests did better at 33, and I think it reflects a sicker population, a different population, and I think this underscores what Kristen said, that if you've got a bad brain injury, cooler is better. Sorry, one other thing I was going to add, at least with respect to the TTM-2 trial, I also don't know if, you know, in terms of talking specifically about the temperature we use, I don't know if we can completely extrapolate that to the U.S. population. That was done in Europe, where I believe, I think, 90% of the patients... I'm gonna say that's what I said. I'm gonna say that's what I said. All right, let's move on, just a tiny fib. We'll let Dr. Bowden go first. Patients, this is a new topic, we haven't tackled this one before, I don't think. Do patients with new onset AFib in the IC require anticoagulation, and if not, which ones do you think do require anticoagulation? So we'll start with Dave Bowden. Oh gee, no, I don't think patients in the ICU who have atrial fib need routine anticoagulation. For one thing, most of them will resolve their atrial fibrillation by the time they go home. There's been a nice study looking at adoxaban in patients with, quote, high rate atrial events in outpatients, but a large study, and the folks with adoxaban did not have lower rates of stroke, but had higher rates of severe bleeding, which is only going to be a bigger problem in the ICU. So I think that that routine anticoagulation of AFib patients who did not have AFib beforehand is a mistake in the vast majority of patients. Are there patients who do? So agreed, so new onset, we're not gonna deal with the chronic ones, new onset, are there patients you would anticoagulate? So if they're still on AFib by the time they're ready to go home, I think I've got to at least talk to them about the fact that you have a higher risk of bleeding, and I'm not entirely sure I'm gonna reduce your risk. Not for the duration of intensive care stay, right. Dr. Burkhardt. Yeah, I agree, which I also try not to. I think that the data that we that we know for improved outcomes with anticoagulation and AFib are looking at one-year outcomes, and in the ICU the risk of bleeding and complications from that far outweighs the benefits. I think the patients that I would consider using anticoagulation for new onset AFib is that if they actually had clot somewhere in there. Dr. Holder, are there patients that you would anticoagulate with new onset atrial fibrillation in the ICU? The only ones I would give serious consideration to are patients who, you know, had some kind of cerebral vascular event sort of relative to the ICU hospitalization. So if they're in the ICU for a stroke, or they were in the ICU for a stroke and it's been a few days and, you know, they're they're showing signs of AFib, I would consider anticoagulating those patients, you know, of course once neurology, you know, neurology service feels that it's... You agree? Would you, so a patient with stroke symptoms? No, because we have data on that. We have data on early anticoagulation of stroke with AFib and later anticoagulation with AFib, and there is no difference and it may be safer, and it depends upon the severity of the stroke, the high severity strokes. You may need to anticoagulate a little bit earlier. And that's what I'm talking about, right? So if the patient's in the ICU for a stroke, chances are it's a pretty significant stroke. If it was the incident event that brought them there. Yeah, it does depend upon how interventionalists take care of their post-interventionalist patients, and if they're in there for the first 24 hours or 48, you might still see them, and the temptation from our cardiologists and people is, oh, put them on anticoagulation. Tristi, thoughts on this one? No, I mean, I stand by, I tend to not anticoagulate my new AFib in the ICU. I've seen too many ICHs. I also just want to thank the incredibly strong arm hold of this phone that's been going on for the last 30 minutes. I'm very impressed. He's an army man. All right, moving on to the next topic, Dr. Burkhart, you go first. I can hold the phone up as well. All right, next topic. Bleeding is fundamental, for those of you who are old enough to remember that reference. Dr. Burkhart, what is the optimal management of anti-platelet drug-associated ICH? And I've listed a panoply of options here that I'll read for Dr. Holder's benefit. DDAVP, tranexamic acid, avoidance of platelet transfusions. Dr. Burkhart. Okay, so I guess I would say the only thing that I know we shouldn't do is give platelets, unless their platelet counts less than 50,000 and that hasn't been studied, right? So we do know that on the patch trial there was increased mortality by giving platelets in patients with ICH. There is some data with DDAVP that it actually slows the expansion of the intracranial hemorrhage. The problem is most of that expansion happens in the first three to four hours when I talk to our neurointensivists, and getting DDAVP on board in time to prevent that is challenging, although that is the recommendation for it. And then tranexamic acid has mixed results, right? There's been no mortality benefit. One trial has shown a decrease in ICH. One trial showed no change, so I think there needs to be more work in this space. So I guess I will stand by the strongest thing that we can say is please do not give platelets to people on antiplatelets with an ICH unless they've had recent neurosurgical neurosurgery or their platelet counts are less than 50. Dr. Holder, what's the optimal management of antiplatelet drug associated ICH? So I think for me, I was trying to break this down because it depends a lot on whether or not we're talking about traumatic versus non-traumatic, right? Because at least the literature with respect to platelet transfusions for that is very different. Traumatic, it's absolutely not indicated and should not be done. In the non-traumatic, at least based on at least one systematic review from a couple of years ago, there may be benefit potentially, although admittedly the confidence interval crossed one. But so I think platelets, there may be a role potentially. For a DDAVP, it's also unclear. You know, just there's been small studies that have looked at this and, you know, they're sort of all over the place with respect to that. Actually, I'm gonna have to say, I'm sorry to interrupt, but I am not aware of data that, the data I know for platelets is an increased mortality at three months. So I'm not sure how we can say that, and that was a large trial, that was in Lancet. How, where's the data for giving platelets in non-traumatic ICH? I'm sorry, I can't hear the comment. So we'll repeat. Question about, question about the Lancet trial suggesting increased mortality with platelet transfusions and should we really take perhaps a smaller study, less robust over, over that? That was your challenger's challenge. Well, I was just talking about a summary that came out three years ago in the neurosurgery, the world neurosurgery. So I mean, when that, when, when that particular systematic review of meta-analysis was done, particularly in non-traumatic intracranial hemorrhage, there was, at worst, no benefit, but it seemed to favor platelet transfusions. Dave, anything you want to add? I mean, platelet transfusions are probably the most evil transfusions we give in the ICU. The most evil transfusions we can give, that says a lot. More infection, more adverse events, you know, unless you've got reasonable evidence that it's going to help, don't give them. I will give you a point for the hyperbole of the most evil transfusions, because that's going to be, that's the forum that goes into the PTD quote book, is the most evil transfusions you can give. All right, let's go with, voting first on this one, two gentlemen of corona. This is a little bit more philosophical. There is no right answer, but let's wax a little philosophical. What are the most important, let's just say one, what's the most important lesson that we've learned from our COVID experience in the last three years that we can try to use proactively? Stick with what we know. I think we were so eager to grab at any case report, any pre-print that said, ooh, there's a signal here, and six months later, you know, oops, it didn't work. You know, and I think we all want to do something, but sometimes the appropriate thing is, don't do something, just stand there. Let me dive further into that. Who do you blame for the missteps? Is that intentional misinformation? Is that? No, it's our eagerness to attribute benefit to what we did. You know, that we all think that we're good, and well, we tried this, and our patients got better. It must have been because of that, ignoring the fact that most humans get better on their own, and probably more safely if we just leave them alone and support what we can. I have to echo that. I have to say, having been in New York City during the pandemic and the first surge, we had a lot of uncertainty, and I sat there at the bedside and had a lot of distress of having equal clinical equipoise for saying, I want to give steroids, but should I hold steroids, or I want to give the tool as a map, or should we hold this, and like, where are our studies, where are our trials, and they were just being thrown out there and pushed out through initiatives, and as the person on the ground at the bedside, like, that was tough, and so I think that's one lens. I think the thing that I found interesting in our community, how easily people gave up, basically, lung protective ventilation, and I'm gonna say I'm proud of our institution. If you look at our publication in Lancet, at our first 200-plus people, when we had 300 patients on ventilators and a single day in a unit that actually, in a hospital, only has 115 ICU beds, our mean was six cc's per kilo, and we stuck with it, but I think that's really hard to do with a lot of uncertainty, but I think that's... Point of order, were you a co-author on that reference that you just mentioned? I'm sorry? You mentioned a reference. I was not, but one of my fellows was, and he totally rocked it. We do have a formal policy here on pardon the disruption that if you self-reference, you get a yellow card. I did not self-reference, but I did reference my incredibly awesome, now attending, Matt Cummings, who is a fellow. It was a reference to the institution and not a personal reference, so you will not earn the yellow card for that borderline transgression. Can I add another lesson learned, though, besides this lens? Please do, yes. I think the other lesson learned that we, as a society, I think social determinants of health really need to be a priority, and in the ICU, it was so evident to see that inequity in that space, and so I think it's a call to arms to all of us to really say, even though I work in the ICU, what happens outside those doors affects the patients' lives that come into my unit. Dr. Holder, what would you bring forward as the most important lesson we've learned from COVID that we can try to implement for the future? So I think one of the big things is the fact that is how partisan views and politics seem to get into things, and being mindful, especially now that we're in this era where things like treatments can get politicized, understanding how we can interact with the public in a more meaningful way so that we can affect the change that we want to see to improve outcomes. I think how we do that is, of course, a very, very open question, but I think that this is really, in my mind, a new era in health care where we're seeing this pervasive misinformation that's being transmitted across social media. One thing I did want to go back to, though, I do want to push back a bit on the, you know, going with what we know in the sense of, you know, when it came to the thing that's most analogous to COVID is sepsis. And, you know, we didn't really know about how well steroids would work based on its history with sepsis, septic shock notwithstanding. And even that has sort of been in this way. And also, anti-immunomodulatory therapies. I mean, if we went with what we knew based on our experience with sepsis, then we wouldn't have come out with, you know, we wouldn't have these oxygen inhibitors that actually improve mortality in patients who had severe COVID. So I think that certainly it should have been tempered, and we probably should have had a little more thought in terms of things that got published, particularly earlier on in the pandemic. But I do want to push back on that. The fact that this did teach us a valuable lesson about the fact that maybe there are certain aspects of sepsis that we didn't quite know, and COVID helped bring that out. I just want to say, I think that we needed to study it. Because we had an opportunity with, unfortunately, thousands and thousands of patients with very similar, if not almost identical, presentations. And we were throwing medications and drugs at them left and right with no system or process, no coordination. If you want to take lesson number three, learn from COVID. Like we broke down the walls in our own institution, but yet there's small hospitals outside who couldn't manage their patients. We didn't work collaboratively very well in that space. And again, having been in it, we were all just trying to get through it, and I get that. But I think we actually probably caused harm by throwing a lot of things at people early on. Pushing publications out, this rush to be the first to publish this, sort of to get their name on a paper and put information out, is also, I think, something that we as a community have to reflect upon. And I think if we learned anything, we needed to have a plan. You know, most of our hospitals just don't have good plans for surge, or the supplies to handle a surge. And unless we actually plan for it, it'll fall apart when it happens. Dr. Holder, I'm gonna give you the last word before we move on to the last topic. No, I certainly agree with the points of not trying to rush, especially if it's self-serving, to try to get a major publication out of this. But I do challenge us that we should try to think outside of the box when new challenges come across us, so that we can come up with new solutions. I'm gonna take host prerogative. Time for one more topic. I'm gonna jump to the last one, because it's one I want to discuss, which I think is super interesting. Is it time to consider a critical care residency to increase the pool of providers? So one of the potential barriers to intensive care from a training standpoint is, right now you have to do anesthesia first, you have to do surgery first, you have to do internal medicine first, you have to do neurology first. Is it time to consider a two to three year dedicated residency to decrease the amount of time and training individuals have to have to pursue a career in critical care, to try to increase that pool and lower the barrier of attendance? I'm going to start with Dr. Holder on this one. What are your thoughts on this matter? I'm sorry, I didn't hear the full question. Time for a standalone critical care residency program, and not go through a core pathway like internal medicine, emergency medicine, or anesthesia, surgery. So, I don't necessarily fully agree with that. I do believe that there's value in the various specialties that we have that make up critical care. I trained in a multidisciplinary critical care program, and I learned, even though, you know, I'm EM and medicine trained, but I learned a ton from my anesthesia colleagues, from my surgical colleagues, and had we not had those unique experiences in our specialties, then we wouldn't have had that kind of cross-pollination. So, I'm going to take, probably, I might take, this might be a unique perspective, but I do believe that there's value in having it be a subspecialty within another specialty. Thanks. Dr. Bowden, your thoughts on this matter? Yeah. I'm not confident that shortening the training time will necessarily increase the number of people in critical care effectively. I haven't seen any survey for that or anything like that, and I would tend to doubt it, but I agree with Audrey that having different perspectives coming into the unit, provided you actually listen to each other, is very useful because it makes you think about alternative approaches. Dr. Burkhart, final words on this topic. Final words. I think this is a complicated topic and a complicated question. I'll start off by saying I don't agree with the idea of just going straight into a critical care residency, and my lens is actually from a program director, but also from somebody who has worked in an ICU for now just a few years, as I tell the interns. There's a lot that goes into being a critical care physician, so there's that foundational knowledge that you have to come in with, right, whether it's from anesthesia, emergency medicine, or internal medicine. There is a lot of that, and so I personally, at this point in my career, I feel like I need to really think about how I'm going to do this, and how I'm going to do it. I think it's important to think about how I'm going to do this, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do it, and how I'm going to do

debate

standalone critical care residency program

increase pool of providers

dedicated residency

time and training

accessibility

multidisciplinary approach

subsidiary within specialties

different perspectives and expertise