Episode 9: ARDS

Welcome to TVSA, the Burn Searcher in Critical Care Podcast, bringing you up to date, relevant content for the treatment of Crutically L Burn patients. Welcome back everybody to TVSA, the Burn Searcher in Critical Care Podcast. My name's Jake. We are back today to talk about arts and burn, right? Yeah, excellent. A very difficult pathological entity in any ICU and certainly no less than in the Burn ICU. As we're going to go through this, like we usually do, talk about definitions, talk about how we manage this, talk about some of the subtleties involved in burn care, and a little bit of how we both do it individually and any differences we may have and some big take home points. But as usual, I think out the gate, we need to have a good working definition of what arts is and how it's relevant to us. And so, I don't know, any thoughts out the gate? Well, it's my baby. I can tell you that much. This is what I love. Got the huge passion for it during COVID as many people did. Absolutely. And a lot of people who lost passion for it during COVID. But this is definitely my baby. And I have real babies. So this is, you should tell you how important that this is for me. And it is a little bit unfair to put this in the first 48 hours podcast. But I think for completeness sake and for how important it is and how difficult it is to manage, I think it fits well into this part of our series. So just talking about what it is, usually when I'm asked somebody what is arts, they say, "It's a cute respiratory distress syndrome." And I'm like, "That's not what I was asking." Or they'll give me the criteria of the definition of it. P-da-free, sure. Exactly. So what it really is, a cute respiratory distress syndrome is an acute diffuse inflammatory lung injury that is associated with a variety of etiologies. Those etiologies can be directly injuring to the lung or it can be indirectly. And so, as we talked about in our previous podcast, sometimes when you have a large inflammatory cascade, you get leaky vessels. When you get leaky vessels, they start to leak places, especially in smaller vessels. A lot of those are in your alveoli. So things that can cause a massive inflammatory cascade can have nothing to do with the lungs, whatsoever. And now you have ARDS. Things like that, pancreatitis, some of the worst arts I've ever seen in my life were from pancreatitis. Burns have been early on described in ARDS literature as a cause of ARDS. Cepsis, other things that cause a massive inflammatory cascade. And then there's the direct causes that are direct injuries to the lung. COVID is the one that we're all going to think about just because we're in 2026. Not that far away from it. Nomonias, any sort of toxic thing that you breed then. And then, you know, trolley is another sort of form of it that we think about as sort of indirect and direct both to the lungs. But a lot of different in the trauma world, there's contusions, things like that. Like injuries. Yeah, massive pulmonary contusions, phylesigments. So a lot of things that can cause this. But the actual definition of ARDS, because often people want to take management of ARDS into a normal pneumonia. And you have a low bar pneumonia and they're like, well, we should start pronating this person. Well, that's not somebody with ARDS. It's not really proven that that's going to help them. Right. And so the actual definition in diagnostic criteria is you start with the burlin criteria. And then we have now have a extra additions to the burlin criteria. Some people call burlin 2.0. I was published in 2024, getting more and more widely accepted. There are parts of it that I love. Some parts that I'm not a huge fan of. But there's parts of burlin criteria that I'm not a big fan of either. And so, you know, not everything's perfect for me. But the burlin criteria, there's a timing onset. So onset within the first seven days of whatever insult that's causing this massive inflammatory lung injury. I don't know how many people really use the timing portion of this. But what they definitely use is the imaging portion. You need to have bilateral opacities that are consistent with pulmonary edema on chest radiograph. That is not cardiogenic pulmonary edema. Non-cardiogenic pulmonary edema. And then you have all of this is under the assumption that you're on a PPA5, which is one of my problems with the burlin criteria. As if you have somebody on a PPA5, you are doing it incorrectly. And it's going to wildly change the numbers portion of this, which I also have a huge problem with, which is the PETA F ratios. And so, the PETA F ratios is a categorization of ARDS severity. And the reason it mostly still matters is because it has a mortality implication. But also because all these trials that we're going to talk about, that was their inclusion criteria. And so, it's kind of hard to just throw the baby out with the bath water and still be managing patients using things, using things that the trials that led to show that it improves ARDS is something that you don't really believe in. I will always rant against PA02 until the day I die, but it's important in this case. So a mild ARDS is a PETA F ratio, that's PA02 to FIO2 of 300 to 201. That has a mortality of 27% when the burlin criteria was created. Moderate PETA F ratio is 200 to 100. That has a 32% mortality. And then severe is less a PETA F ratio, less than 100. And that has a 45% mortality. Now the new global definitions of ARDS, like I said, published in 2024, adds a few different things to it. One of that is having non-invasive ventilation as part of this definition still. There's a few things that I personally got from COVID. Two big ones, one we're going to talk about later. But the other one is the respect for high flow nasal cannula. And so this definition now includes patients receiving high flow nasal cannula at greater than 30 liters a minute. And so that is now in the ARDS literature as somebody who can still be, have ARDS in there for, can benefit from treatment that we're going to go through below. The other thing is the oxygenation criteria. So like I said, the PETA F ratio less than 300, we can also use a saturation FIO2 of less than 315 when the Spo2 is less than 97%. This edition allows you just to use your pulse ox and you can do the simple math to show you where you're at and where you're heading down as you continue to treat ARDS. The other thing that adds is the imaging modalities. Adds in lung ultrasound. It's now sort of explicitly accepted as an imaging modality alongside chest radiographs in CT. Part of this was for more resource limited settings. I don't love it because I don't know how many resources don't have a chest x-ray. But if you do not have a chest x-ray, perhaps you're deployed downrange or something all you have as an ultrasound, you can still use it. You're probably in a bad way if you're that resource limited. It really strikes me as something that's beneficial for wilderness medicine, real true to your austere environments. I necessarily just necessarily resource poor environments because I would feel like chest radiography is rather ubiquitous at most places. Even in relative to your resource poor environments. Yeah, I'm surprised they added that. But they did. Yeah. Then obviously treatment for this is you're treating it underlying cause and we're going to get into all the management of it, not the treatment of it below. But I think first, can we talk about some data and some burn specifics that are associated with ARDS just to drive home why it's important for us to even talk about it in the burn podcast at all? Yeah, and I think a couple of takeaways to this. Burn in ARDS is it's heterogeneous for sure. But in the burn patient population, it carries a significant morbidity risk for patients. Their burn patients certainly are at a relatively high risk of developing ARDS. And further, there's a significant mortality benefit or a significant mortality risk for these patients that go on to develop ARDS in the burn population. All comers admitted to burn centers occurs anywhere from 2% to upwards of 15, 16, 17% of all burn admissions are going to go on to develop ARDS. And certainly it's more prevalent and larger sicker burns. And I would go so far as to say larger deeper burns as well. Well, the deeper your burn, the deeper your burn, the more significant your pro and flimatory states can be driven by that. I think we see this anecdotally when you have somebody who's 20% superficial partial thickness and 20% full thickness. I mean, I think those are two different clinical entities when you see them right in front of you anecdotally. And art certainly, I don't think it's any different than that. Somebody who's got a larger deeper burn is going to be more at risk for arts. Specifically looking at the burn populations mechanically ventilated, a couple studies are out there that kind of look at incidents of arts. And when you're mechanically ventilated in burn patient, that risk of developing arts is 33 percent, upwards of 54 percent. In some trials, Nancy at all quotes up to 54 percent of all mechanically ventilated burn patients develop arts. And the mortality rates are also kind of all over the place. Numbers from 15 percent upwards of 42 percent. And so when you think about this, an incident rate that runs from 30 to 50 percent and the mortality rate that runs upwards of 30 percent and 40 percent, those numbers are higher than what you see in the Berlin criteria certainly. And again, I think that really speaks to the severity of the pulmonary injury that these large surface area burns get just from the hormonal response they have to these large surface area burns speaks to the systemic insult that these patients have. I think that there is, when you look at burn thickness, again, these full thickness burns are going to be more arduogenic for lack of a better term than some of its most superficial. Thanks, man. So good. Arduogenic. And got it here, folks. The other thing also to think about as well is, you know, we think oftentimes things that seem to go like a hand in glove inhalation injury, you must have a markedly high incidence of arduous social, the inhalational injury. And you know, as you do retrospective reviews of what inhalation injury causes, it certainly causes you to require more volume than you would otherwise based on your percent TBSA for your resuscitation. It certainly has a higher incidence, potentially, of other downstream systemic insults for these patients. But there's honestly mixed data about inhalation injury actually worsening your incidence of arduous social. And so in that setting, just because you have inhalation injury, it doesn't necessarily mean you're going to go on to develop arduous social. So there's just, there's mixed data behind that. So that's something else that also kind of confounds what arduous looks like in the burn population. Yeah, that seems so crazy to me that, you know, some of the papers I was reading and working out to this, like says inhalation injury might not be a risk factor at all. Isn't that wild? That I just, I can't fully accept this. I want to. But the timing of it is also very interesting of when this occurs. And I think it gets into somewhat of how we talked about in the burn resuscitation and where your fluid goes and what type of tissue gets more fluid or prognacious fluid in it first. So Car Tato at all showed that they had a large study and showed the majority of patients, 86% developed arduous in the first week post burn. And 43% of that were on post day three. And so we are kind of outside that 48 hours. And I wonder if that is because you have a patient on positive pressure in that, you know, if you think about like a hand, you, you, where that adema develops first is on the back part of the hand because that's where you have more lax tissue than on the front where you have less lax tissue. And so I wonder if you just being on positive pressure is giving enough pressure down to the alveoli that it doesn't allow more fluid to go in during the first 48 hours of that resuscitation while you have capillary leak elsewhere. Yeah, and actually it's interesting. I think it would also in preparation for this, this talk. I found some animal studies that showed that 24, 48 hours into those burn resuscitations, even though these patients, even though these large surface area burned animals were getting massive amounts of fluid. Every little of it was ending up in their pulmonary lymphatic vessels inside of their, their alveoli. They're getting no significant pulmonary demon that initial part of that resuscitation was only after their initial resuscitation when they started developing that. And again, it just, it kind of speaks to how different critical care is in the burn population. It's just the typical, the typical physiology responses that you'd anticipate for somebody with a huge pro-inflammatory burden, you'd anticipate them getting that fluid in their plural space in their alveoli in the interstitial. And you just don't see it in the initial burn resuscitation, which is interesting. Yeah. And I think it gives us, with that knowledge, it gives us the ability to possibly recruit long earlier than we would otherwise. So we're going to talk about how we're going to manage this. Because like I said, the treatment for this is remove the cause. But you can't remove a burn. You can't undo a burn. And so we got to manage it. And how do we manage it? So everybody talks about the piece of critical care, talks about the piece of ARDS. Listen guys, some other podcasts may give you three, four P's. All right, not the TBSA podcast. All the P's. We give you up to eight P's. Now listen, did I stretch some of these things to make them start with P? I did. And I, I don't apologize for it. No apologies. I don't apologize for it. All right. And so let's go through the different P's of how to manage ARDS. The number one, probably the most important. And it's not just most important because it is the most famous critical care trial ever and showed such a more mortality benefit. But it's also so important because every other trial and every other management strategy assumes that you are also following this. Right. It is the guidepost. It is the landmark. Yes. It's the shining city on a hill. So its protection is the thing that starts with P and it is ARDS net is specifically the trial that I'm talking about came out in 2000 and it's why we do low title volume ventilation in these patients. So you also sometimes hear it as ARMA. It ended up starting the ARDS net back then because it just got that popular. Originally it was called ARMA. It was a dual, dual trial with something called karma, which was for ketoconus all that it didn't work at all. It's going to worry about karma. But you may also hear it as ARMA. It's the same thing. Right. Kloquely, you to say ARDS net, you think about this trial. And so going back to the year 2000, the thought process behind this path of physiology is you have a bunch of fluid and a bunch of proteins going into your avioli. And so you need to push all those things out and have these big breaths. And so therefore you should have pretty big title volumes to try to improve your oxygenation and ventilation. Turns out that's probably a bad thing and it would seem to be completely heresy to us now. Right. But they compared 60Cs per gig of predicted body weight, predicted body weight is by height. Hight. Hight. Hight. And they had a goal plateau pressure of less than 30. And so what your plateau pressure, I don't know who all is listening to this, plateau pressure, you'll hear about peak pressures and plateau pressures. Peak pressure is where is all the pressure in the lung, plus where the air is moving. So trachea bronchials. And then the plateau pressure is the pressure all the way down to avioli itself. And so how you measure that on the vent, try not to make this event lecture. That is you stop the air from moving. So what do you do the inspiratory hole? So you decrease the resistance of your ventilator as well as your trachea bronchials. And therefore you get your plateau pressure. But. So with a goal plateau of pressure less than 30. And then they compared it against using title volumes of 12 mils per gig of predicted body weight to a plateau pressure less than 50. Again, this seems insane to us. And that's because of how good this trial was, how much it just completely changed everything in critical care and ventilator management. And so in this, it had all the things that we really care about. The things we really care about in ARDS, critical care, vent management is mortality. It took your mortality 31% versus 40%. Ventilator free days also thing we care about. And then breathing without assistance by day 28 also had a statistically significant impact. And so again, there's going to be bigger, bigger bangs for our buck in the different trials and the different management strategies that we're going to talk about. But that's all assuming that you're also doing this. So where this becomes an issue in burn is that if you think about when you're decreasing your title volumes, then you know, in a patient that is hypermetabolic, when you're hypermetabolic, you're increasing your CO2. So title volume times respiratory rate is a minute ventilation. You're decreasing your minute ventilation on purpose by having this ventilator strategy. And a patient who is going to not be able to be produced. is gonna be producing more CO2 and you're not gonna be able to clear it as well. And so a big thing in the critical care world is we believe in this data so much and it's also, it's not just the one trial, this has been multiple trials that have confirmed this, that we allow something called permissive hypercapnia. And so permissive hypercapnia is, I don't really care how high their CO2 goes. It's the downstream effect of that CO2 that we actually care about, which is your pH. - Acidosis. - Yeah, so if you're getting a persistent acidosis because of this, maybe you're gonna have to change things up a bit. I know some intensivists that are like, keep it above seven. I don't go that far. I think keep it above 7.2. I'm okay having that level of acidemia, not acidosis. And that's the reason that is is because of how important and how much of a mortality benefit this has. So the problem with burn is that you're going to have those high PCO2s and so you're gonna have to adjust accordingly. And so you're doing the best you can. There's not a great amount of data for this. Outside of it just having some large burn center retrospective data showing that most burns they're using at least less than ACC's per gig of tidal volume, whether you have ARDS or not. And most of those patients it's doing well. And so I can't really tell you specifically that you're not gonna be able to do this in a burn patient but you should try and you should try to get as close as you can. - Yeah, I think that for, if you are ever outside of if you're doing some kind of novel ventilation strategy or you're doing non-invasive ventilation, you're doing something you had a patient who progressively is failing, failing, failing, and eventually is developing the VELP formal ARDS and whatever intervention you're doing at that time isn't working for you anymore. You gotta put them on ARDS and you gotta get them down and you gotta start decreasing that tidal volume as best you can. And there's all sorts of ways to deal with the CO2 problems whether it's liberalizing a little bit of the tidal volume, whether it's increasing your minim ventilation more. There are certainly some centers that would even say, hey, I need them to hold on, they're holding on to a whole lot of CO2 and I need to give them a little bit of bicarbonate. That's certainly something that I've seen a few places do before also while we're waiting for our kidneys to catch up. But yeah, the safe spot, the place to go for these patients that are having progressive ARDS that are not getting, but you gotta be thinking of low tidal volume ventilation. - Yeah, so moving on to the next P is perfusing or pain. - I like pain more because it's funnier. And so it might be the most interesting of all these Ps because we are the fluid docs. And so this really comes back from the fact trial, it's fluids in catheter trial in 2006. A few interesting things about this trial, A, it had a thousand patients, which if you don't read a lot of critical care literature and certainly burn care literature, that is a huge, enormous. - Huge. - Yeah. And so part of what, the other interesting part of this is they were titrating based off CVP, which is not really used anymore, and part of it was started from this trial. And it sort of led us to not taking CVP seriously, as well as not taking pulmonary catheters as seriously. - Totally. - It wasn't the dagger in the heart of the pulmonary catheter, but it sort of started us down that. And it was more of a confirmation of these are probably not great. - Right. - And they're probably not really changing anything. And so, shortly, what they did with these patients was, you know, this was also at a time when people had a higher resuscitation. This is not in the burn world. And so at the time, back with then, they said you got to swell to get well. And so they were given a lot, they would lean a lot more on fluids rather than pressers. We don't really do that in the critical care world as much, but in the burn world, we certainly lean on fluids. - Yeah, this is back in Rivers, Trial Days, right? Well, we're pushing patients off, Starling curves and everything else like that. - Oh, yeah. And so they had more to diarice than your standard critical care patient would. - A lot to give. - Yeah. But they diarized the hell out of people. You can look, if you wanna, if you're interested, you can go look at their tables of their 10 day diaresis. You're talking about, you know, over 200 of Lasix a day. And the big parts of it are not just the benefits of it, which didn't have a mortality benefit, but it did have us off the vent, ventilator free days, it had shorter mechanical ventilation duration. Also had less ICU, or more ICU free days, which is very important for lots of reasons. But the big part of it that I saw is it didn't have an increase in causing people to be dialysis dependent, which when you diarize somebody that hard, it's always a worry. Like am I diaricens somebody so bad that I'm giving them an AKI and I'm still going, and eventually they get an ischemic ATN and possibly become dialysis dependent. It didn't happen. So this is sort of where we get the dry lungs or happy lungs. And like you said, before mostards patients, they don't start having, or I'm sorry, most burn patients don't haveards in the first resuscitation when we're giving them a ton of fluids. That is very lucky in this case. Because it's around the same time that you would start your de-resuscitation normally that if you had ARDS, you would start de-resuscitating in the same way that you would in the fact trial. And so if you do have somebody who are having trouble with their kidneys, CRT is a possibility here, you can still bring, you know, you can de-resuscitate very well with that if they do go into ESRD from their burn. But one of the things that I wanna talk to you about 'cause you're more on the surgical side is how much are these dioresis in this aggressive dioresis strategy going to affect graphs? - Yeah, so I think that the, it's hard to take all these trials independently and be able to extrapolate what the implications are applying that trial to the burn population and all the heterogeneous things you gotta worry about. And like you mentioned, if you have this patient who in the first 48 hours has been resuscitated, well the next 48 hours hours 49 to 96, this patient is going to the operating room for de-breedment as well. And so, you know, when you put, if you're doing early grafting for a patient and doing a single stage surgical de-breedment and immediate grafting, these patients do have a lot of interstitial fluid that have to get rid of. And certainly as these patients are losing interstitial volume, you do worry about graphs. You worry about matrix application adherence. As again, what you would hate to do is put down a graft of some kind. And that graft shifts and moves a whole lot as this patient is losing a whole lot of fluid. Or you put down a sheet graft and this patient doesn't have any way to get that trapped fluid out of their interstitial, it's just pouring into their interstitial still. And all that can complicate, you know, your reconstructive algorithm for these patients. And the other thing I also think about with aggressive de-resuscitation strategies is one of the best ways to get patients de-resuscitating is to debris the dead skin off. Right. And as you give, as you debris dead skin off, that gives opportunities for the interstitial fluid to number one, weep out of wounds. But number two, the body is going to be in a less pro-inflammatory state by just getting the dead stuff off and keeping healthy stuff around. And that also kind of factors into what de-resuscitation looks like. 'Cause I've certainly taken patients that, we're holding on to a whole lot of fluid. You take them to the operating room, you take a whole lot of dead tissue off, and they start diureasing. Autodirestis are really pouring out a lot of fluid once you get that pro-inflammatory insult off of them. These will be the dead skin. And so yeah, it makes you wonder with these significant resuscitations. Does aggressive diurestis have implications for graft-taken graft-filiberates? - Yeah, so I mean, I have seen people who especially have very healthy kidneys, they just reclaim all this third space fluid as soon as they're holding on to fluid again, and they just start autodirestine, maybe beyond what I would even want to do with a lase of stress. - Right. - And those guys really help you out. So you may be just autodirestine as well as diurestine via insensible losses, just from your wounds. - Right, I think it gets back to the, one of the hardest things to figure out is with burn patients is that any given time, what does this patient's volume status at? - Yeah. - It's like the heart, one of the hardest ICU questions to ask in burn is is this patient up, down, or right where there need to be? And then one hour later, are they up, down, or right where they need to be? It's a very difficult decision to make sometimes these patients. - Sometimes you just can't tell. I mean, I covered in everything. Sometimes you can't focus. It's doing a ruby-squb under water in the dark. So the next P is my favorite. - Absolutely. - I'll let you take this one. - So proning, guys, gotta talk about proning. Perseva is the trial, is the landmark trial, 2013. And this was the, this is one of those ones you gotta know. Like they're studying for, a critical care board. If you're a burgeoning intensivist and you want to learn more about how to manage arts patients regardless of burn ICU or any other ICU, Perseva is one of those that you just got to know. And the reason why it's because it's so beneficial and it works so good. And so Perseva, a European trial, French, as I recall, that took patients and said, what we're going to do is we're going to take these patients and we're going to have patients that are going to remain in the supine position and patients that we're going to randomize to pruning. And the supine patients would be put into a similar incumbent position and get all their measurements done every six hours and they would just remit and that was effectively standard of care for these patients. Head of bed elevation and just kind of hanging out in bed. The prune patients would be pruned for 16 hours or more. Okay, so it's not like the pruning is just a couple hours here there. It's 16 hours or more a day. It's spending the majority of their time lying on their belly. And it's repeated daily for a month, 28 days. And they would only be the pruning protocol only be ceased if they met a couple of endpoints. Number one improved oxygenation. This was defined as a pdf ratio greater than 150 with a peep less than 10 and a FiO2 of less than 60 for four hours after their last pruning session. Kind of showing that this patient can tolerate being in the supine position and no longer having to be pruned. The other thing would be a decreased pdf ratio after before two consecutive pruning sessions with a greater than 20% increase relative to the supine ratio. And the last thing is that they're having any complications during a pruning session that leads to its interruption. All those things would cause them to be taken out of the prune position. So if you put them prune and they coat or you put them prune and they have some other issue or you put them prune and they need a line becomes dislodged. All those things would cause them to need to be supinated. But otherwise they're spending the majority of their time every single day in the prune position. Their primary outcome they were looking at was what was their 28-day mortality. And guys you heard it here first. Their mortality got cut in half. Their mortality went from 33% in the standard care group. It's a 16% in the pruning group. I have no mathematician but that seems like half. That's incredible. Yeah. Like it's a huge, I mean it's so rare that we see numbers needed to treat that are in single digits. And the number needed to treat for this intervention is six. Where you could sit there and say if I just prune six patients I'm going to save one life. I mean if we could find that for anything else like it would be people would be getting Nobel prizes. It's just it's a huge intervention to a huge benefit. Also secondary outcomes it looked at all-cause mortality at 90 days, 41% died in the traditional care group and then 23% died at 9-day mark in the pruning group. Again it's statistically significant benefit at all-cause mortality at 90 days. Exhibition at 90 days statistically significant 65% versus 80%. I see you linked to stay significantly significantly significant at 24 and 26 days. Vinylator free days got cut from 14 days to 10 days. The 90-day ventilator rate was statistically significant at 57 to 43. All that being said it cannot be overemphasized how important pruning is in the management of our patients. Yeah I can't stop talking about this. So if you think about you know if you think about where your lungs are and how they move so for you know my 35 years much much older for you. I've been pulling air in. Now we have a definitive airway in and now we're shoving air in. So if you think about how your lungs are oriented there's more lung in the back than there is in the front roughly 40 to 40 in the front 60 in the back. So whenever you roll somebody over a few things happen you decrease the weight from your heart you decrease the weight from your abdominal organs but I think what's overlooked is that you are pushing air into a body. That air is going to go to the point of least resistance right and so if you think about how your ribs move. Most of your ribs the movement is in the front. You have the anterior excursion. I don't know if excursion is the right word but I think that sounded good. And so you don't have a lot of movement in the back and so if you're shoving air into somebody you are going to have more movement in the front from your ribs and therefore you're going to have that air go to the path of leasers distance to more front where it can't be used as well because there's more lung and more alveol in the back. You flip somebody over you have decreased that movement and so therefore you have a more of a homogenous amount of alveoli and more alveoli that are getting oxygen than you would otherwise. So I mean I know we're we're loving on this trial as much as possible but I personally think that pruning someone from a data standpoint is probably the most impactful thing we can do in the ICU. Absolutely. And to see when people don't. It just hurts me deeply. Crines my gears. I mean if you think about the metrics that ED docs have to go through and hunt very flimsy data and that you know that you could shut down a place and stop and you could have insurance companies and Medicare and Medicaid stop paying a place because they don't meet these metrics and they don't come close to the data that this has. I mean seat belts don't have that and you know this kind of data and it's illegal for us to not wear them. Exactly. I mean antibiotics and sepsis don't have these kind of numbers. Right. And so I personally we talk about like no misses. I personally think that not pruning somebody is a no miss. Agreed. And I think that you know the other thing that I got from COVID was pruning whether you have a tube or not you do better. Whether you're on nasal cannula, high flow or intubated. Yeah. I mean we saw I mean while saw those the pictures of the patient who was completely awake has a high flow nasal cannula laying on the belly. Yeah. Like in their stepdown bed all day long board de tears but during COVID. And yeah I mean it's interesting. It's one thing that came to me during COVID was everybody always kind of treated anecdotally I would say my experience pre-COVID was do everything possible not to prone this patient because prone to this patient is so difficult and you got to get the line sorted. And it's so can't we just try some parolytics? Can we just try some flow land? Like do we really need a pruning? Like that was always the institution of pushback and you always had to be like yes we're going to prone the patient. You got to prone the patient. And then here with when COVID came on everybody all of a sudden got on board the pruning. It was like we had pruning teams and we're doing the pruning thing all day long and yeah pruning is pruning is great. And I say all that because in burn I think there's a little bit of that pushback that you still get sometimes with pruning patients. Yeah. Why do you think that is? Listen. We do a lot of intensive care for these patients. These patients have multi-hour dressing changes. These patients have a lot of line maintenance because they got lines coming out of everything. Every tube that can every tube that can go in a hole is in a hole somewhere. They've got donor sites that need to be maintained. They've got fresh graph sites we don't want to share. All those things really complicates the nursing care that's been given to this patient hour by hour. And despite that I think that when with the benefit of ProCIVA being 16 hours in the prone position it becomes incumbent upon the entire multi-disciplinary care team to critically think about how are we going to get this patient prone for 16 hours? How are we going to lump cares together? And how are we going to plan our post-operative dressing plans? How are we going to plan our takedowns? How are we going to plan the trips to the operating? How are we going to plan all this around the need that this patient ultimately has to get through their arts pathology? We're just getting a prone for 16 hours a day. Right? And so that becomes a bit of a tug of war that needs to be sorted out across multidisciplinary team to lump those cares together, to limit interventions that can stay prone as long as they possibly can. Yeah. But honestly I think the juice is worth the squeeze for all those problems and those are problems. I think that it doesn't really matter. I think that it's something we have to do because there's so much data. It just works too good not to do it. And lean on that as one of your first interventions and other things that you're bailing out the leak you can do with all the other stuff. Yeah. So the next pee is peep, positive end or end expatory pressure, almost at end organ pressure, positive end expatory pressure. I mean I'll just quickly say high peep is better than low peep. Yeah. And I think it's a very similar reason as to what we talked about before is these patients have that active capillary leak. I think these patients more than most patients that go into ADS have more recruitable lung. So there's no like there's some I mean the SECM has six RCTs that are pretty big that tell you high peeps better than low peep. The probably the most famous is alveoli. I personally believe it's the express trial. I like how they go up on their peep until they meet that 30 of plateau pressure and you just keep going up until you get there because we know above 30 is dangerous from from Ard's net and we know that higher peep is better. And so I tend to like that but the take on point for this is high peep is better. And I think something that also anecdotally I see with peep that becomes that becomes important for Ard's and also in burn patients. You know this our patient population has changed since our arts arts that first came out in 1999 and how rivers was being done in the in the 90s. You know we have a much higher incidence of obesity of yes of central obesity pushing up against diaphragms good point and I think that we have a real problem and I see these days where we are I estrogenically targeting lower peeps and they need to be and you can't overemphasize that these patients that have again as we have larger and larger patients these patients really need a lot of peep to overcome all that weight that's been pushed up against diaphragm and I think that the thing in the burn population is these patients also are walking around at a dry weight of 70 80 100 kills whatever it is and you've during the during the burnization have given them leaders of IV fluid that they're holding on to and their weight can be significantly higher than their bodies used to and all those things really speak to the need to target an aggressively high-peep to really improve your oxygenation and not slowly walk that up right so what's another pee we can talk about paralysis yeah let's walk through it so putting patients on a Cicerochic churrim drip is the other is the other thing that we can do for patients and the idea behind this is to increase vent compliance it's to decrease the amount of resistance in the chest wall in the airways to really allow more laminar flow and hopefully improve your oxygenation because of that and when it first came out part of the other thing that they were thinking is it decreases your VO2 right you know the thought processes could be true that you paralyzed somebody and they're not using their muscles anymore and therefore that oxygen can go somewhere else where it needs to go yeah exactly two big trials to walk through first one accuracy this took arts patients put them a gave him sedation and either gave them Cicerochic churrim or placebo and then it assessed their 90-day mortality rates and what they found was a statistically significant decrease in mortality on Cicerochic churrim versus placebo 31% to 40% so 10% decrease number needed to treat 11 p value 0.04 there are some there are some issues with with the study the main things that we worry about with these patients is that by giving them all paralytics you know we do worry about you know I see you critical illness poly neuropathy we do worry about you know if you don't have adequate enough sedation on board then you have a patient who might be a arousin not a depress of you know negative four negative four but you could have somebody who's a little bit more awake than you would otherwise without appropriate neurological monitoring and patients that are paralyzed and awake that is a horrible horrible state to be in and so ICU PTSD rates are certainly problem and then post ICU syndrome also can be associated with this and certainly you know the 2016's Raging Substance Campaign said that you could consider neuromuscular blockade for patients with arts from sepsis with a pdf ratio less than 150 but I mean this remains a weak recommendation for these patients with that there was some there was some impetus to say well hey maybe we should be using Cicerochic churrim more in these patients and that led the the rose trial those investigators to come together and retest acurusis that a much larger study these more typical modern protocols they also assess 90 mortality and with it they found no difference between Cicerochic churrim and placebo and they said that you know they're more tally great for these patients is 42% all comers and the 42.5% all comers in the treatment arm and then 42.8% in the placebo arm they did notice that there's a higher critical illness a critical illness neuropathy and the Cicerochic churrim patients and they also noticed that they had more serious adverse events and more serious cardiovascular events as well for these patients and so in the setting of rows you kind of see that applying neuromuscular blockade early in modern arts care maybe non-beneficial or potentially even harmful for patients that have modern to severe arts the one thing to think about in the burn population when you think about a pair of paralysis to treat patients that have arts is that these patients you know we talk a lot about the neuro humor a humoral response to response to burn it's a systemic problem to fix multiple organ systems one of those organ systems certainly is surgical nutrition and muscle strength and catabolism you know we're going to talk about this more in future podcasts certainly but patients that have such a high catabolic rate are going to use up a lot of lean muscle to get through their burn insult and if you take somebody who's already at risk for deconditioning take somebody's already at risk for significant weakness from their burn and then you also paralyze them out the gate for long periods of time they really have a significant risk of having a significant neuropathy their ability to actually move their body functionally rehab participate in their rehab it's going to be problematic for them and the lesser using those joints less using those muscle groups that's going to really increase your risk for things like contractures and things like that as well and so it can really put somebody in a significant long-term rehabilitation hold that climb out of by arbitrarily putting them on on a paralytic early potentially and so there's there's issues with that yeah I'm I try to avoid yeah we're gonna get through what we do at the end but I try to avoid based off of this one interesting thing with accuracy is one of the things that that made them redo this was not strict adherence to arts network calls so right we just keep going back to the same thing over and over but yeah I mean sure if you're sink if you're to sink run us to the vent and I need to get all these other things going that I know is going to help you okay putting you on on some paralytic to get those going I think is fine but I think we need to be cognizant of as soon as you can take it off you should great personally would I agree so the next P is one of those ones I stretched because it's not it's prednisone but it's not prednisone because it's Dexamethasone but you know what Dexamethasone doesn't start with P and so there I'm not going to talk about the mediree protocol because it was a bit of a mess but I am going to talk about Dexa ARDS so this was a trial that came out in 2020 this did not involve COVID patients it just happened to come out in 2020 so all the all the patients that were involved were not before COVID had existed so the intervention was Dexamethone 20 IV daily days one through five some context for this that is a monster dose in a population that at the time people thought that steroids killed everybody who had ARDS and most of that came from the flu data in the 1990s and so this was somewhat heresy I mean the recovery trial people in COVID they gave 10 milligrams of Dexamethasone and that was heresy right these guys gave 20 they one through five and then 10 milligrams day six through 10 and they was discontinued upon excavation if you didn't get past that 10 or are you expated before day 10 and so the thought process behind this is that you have this massive inflammatory cascade that leads you to get into these leaky vessels and cause all this extravization of fluid into the lungs and giving somebody a monster dose of steroids maybe stops that inflammatory cascade was sort of the thought process behind this and so this also had a statistically significant all cores mortality benefit it is yeah I think it was only 220 patients which like we said pretty standard for critical care trials that we were not cardiologists with you know framing ham studies that go on for years and years with millions of patients also gave you a ventilator free days that it was a statistically significant benefit duration of mechanical ventilation both at and then duration of mechanical ventilation at 60 days what's very interesting is is that there was no difference between the two groups of infection rate and hyperglycemia the hyperglycemia makes me is more surprising to me than the infection rate but the infection rate is also surprising as well and so sort of the downstream effects that we worry about with with these that this dose of of so some of the downstream effects that we worry about with these patients in this level of steroid it didn't really show which was surprising and so I do use this I realize it's one trial but I think it was important enough that I think giving it a shot is worthwhile this has a big problem with the burn population and it's graphs right so steroids and graphs don't mix very well correct and so I have done this in the past where I was had a patient heading towards ECMO and I was like look we got to try everything here and I put that 20 milligrams of dexamethasone on and her graphs especially on her hands suddenly didn't look so great for a long period of time and occupational therapists are coming up to me like why is that why do your hands look so bad I'm like I don't know I did know I was lying. Right. And so that is a worry here. Totally. And so you do have to have a living body for your grafts to live is sort of the how I have my excuse for this. But it is an extra consideration in our world versus every other world. Right. And certainly I'm not aware of any randomized controlled trials where you just you take large surface area burn patients and you graft them and you give them half of them mega doses of steroids and they're happy to give no like that that that data doesn't as an exist. I don't think that would fly. I don't know how it fly either. But you're right at some point in time when the when the house is burning down around you to use a burn analogy here, you got to be able to put the fire out and like if you have graft loss because of that then that may very well be a reasonable thing. Now the one thing I always had to get a keep in mind is you know ultimately what could be the thing that's driving your arch response. That negress as well. And so I think that when you think about using high dose steroids in the burn population, that just needs to be a nuanced decision to kind of all shareholders have an opinion about real time because you're right if if arts is progressing and you got problems like we got to pull it out the stop so you have to be alive to making the use by your graft loss. So the next P is pulmonary vasodialaiders. So a few different ones inhaled nitric oxide and then the two process cyclans with the leachery and flow land. I will say every there's not burn data obviously in this but every other scenario that this has been studied and this has been studied a lot. Flow land leachery and inhaled nitric oxide in every pathophysiology that I've ever seen are equivalent. So we will talk about them as if they are the same thing. This is inhaled vasodilators. You do not want to give that through an IV because that's going to worsen a lot of things. But basically this is like especially inhaled nitric oxide has been studied and studied and studied. They keep trying to make fetch work as a mean girls reference. And all it shows is it increases your oxygenation, just that number. It changes nothing else. ICU days, vent free days, anything along those lines. Certainly not a mortality benefit. It just changes that number. Now there is data and inhalation injury with burns and it basically showed the exact same thing. Just because I want to bring some burn literature into this and because it's so lacking. It showed the exact same thing. All it does is increase that number. And so I have used this in the past as I'm getting on to something else and getting on to things that I know are going to be better to increase somebody's oxygenation, which is the understanding that I need to take it off. It is a little harder to get off once you have it on. And so if you need some extra oxygenation to get you to one of these other peas that actually work and actually change things. It is a reasonable thought. Yeah, I think that applying it in an effort to improve oxygenation certainly worthwhile. But the data is certainly not there to suggest you should be doing this at the expense of say proning a patient. Yeah, for sure. So now let's get to your baby, which it doesn't start with pee, but it has a pee in it. It does have a pee in it, and that's correct. Yeah, so go ahead. So we can't have a talk about arts without having conversation with APRV. We can. You know, I think when you think about pulling out all the stops for patients, being an intensivist in the burn ICU, it's going to require you to not just be limited to one tool on the ventilator that you can use. And I certainly agree that for the majority of patients, putting them on a ventilator, if they have arts, putting them on and doing arts net style ventilation is going to get you through a lot of, a lot of arts problems. I will say though that I think there is certainly a role for APRV. And I really lean on the two Zao trials 2017 and 2025 that showed that using APRV has a mortality benefit compared to low tide of ion ventilation. APRV, automated pressure leads to ventilation is a ventilator mode that kind of does a little bit of the opposite of what low tide of ion ventilation is doing. The goal of APRV is you give these patients a pressure-cycled mode of ventilation. You give them a significant amount of driving pressure and you hold them at a higher, at a higher P high than you would normally, 24 centimeters of water. Give them pressure support on top of that and allow them to have breaths on the plateau portion of your, of your respiratory cycle. And then you take them from a high, a P high of say 24 centimeters of water and you drop them down to zero or five centimeters of water to wildly de-recruit them. And you do it over a very short interval in time. So you have your ID ratio is inverse. So you're doing inverse ratio ventilation where you're spending the majority of the time in the respiratory phase at your P high and very little at your, at your respiratory phase at your P low or your P. And I like this in the burn population where a couple reasons. One, applying it early, like in extrapolating from the Jau-Data would certainly suggest that there's a mortality benefit by applying it early compared to low tide of ion ventilation. The other thing is you really maintain your critical space when you do APRV. Patients can, compared to low tide of ion ventilation, they obtain a PAO2 to FIO2 ratio that's much higher. They get expated faster and they have better oxygenation indices. The other thing that I really like APRV for in the burn population is in inhalational injuries. And I say that because the biggest problem with inhalational injuries is all this detritus that builds up in the airways. You get cast, you get slough, you get mucus. You get all this stuff that's in the airways and needs to be cleared. One of the benefits of APRV is when you significantly fill somebody's lungs up and then deer creep them very quickly and fill it back up again. You're effectively coughing. That's the same thing that you do with a cough. You fill your lungs over the air, you force a whole lot of it out and you fill it up again as you cough. And so, you know, frequently, you find an inhalational injury patient that you're doing frequent bronchoscopy and a lot of interventions, try to clear these castles stuff out. APRV is coughing 10, 12, 14 times a minute as you cycle through your APRV. You cycle to really push all these secretions stuff out of the LVLant, out of the distal bronchules into the main airways. So you can suction up much easier with your end line suction. And you know, probably a further conversation about APRV and fully going into the two's out trials, maybe something we can do and a little bit of a pro-con debate into the future. But I do think that the take home that I would offer for people when they think about using other forms of ventilation is that while whichever mode that your shop uses, whether it's early application of APRV or whether it's arts and that style of ventilation at the gate, you got to be more than a one-trip pony on the ventilator. And knowing which patients would be would benefit from one form versus the other, as an example, with APRV patients that have significant obstructive pathology in their lungs coming in, bad CUP deers, they won't tolerate APRV, they don't have a lung and an expatory phase to fully deer-cute their lungs and you're going to have a significant auto-peat problem very, very quickly on APRV. You got to know which interventions use for the right patient. And so for me, I really like APRV and I like APRV out the gate for lots of patients, especially in the institutional injuries. Yeah, now I give you crap just ingest because you love it so much. And I do. I'm a middle child and I can't allow that. So no, listen, the Zao at all the 2017 trial, even though it was single center, was pretty convincing from almost every metric. Right. I haven't read the larger trial in 2025. I know it came out in chests just a few months ago, right? Yeah, yeah. Maybe in August. Oh, let me. I don't know. But my biggest thing with APRV, well, a few things, is if you're going to be an APRV guy and a center, you need to have everybody on board with this. Oh, a thousand percent. Because everything you know about vents and all the settings are completely different. So you go from, you know, FIO2P title volume and which one am I missing? PIP, a little rest of your inventory. You go from that, which everybody understands, to pressure, which throws everybody for a little bit. Yeah, so P high, which is pressure high, pressure low, which is the low part, and then your timing intervals at those two things. You also have FIO2. But that completely changes all your, what you understand about vents. Right. And so you do have to have everybody on board with that and everybody has to understand that. Because I know we talked about in the breathing podcast before of like, well, you know, I love it. And so I'm going to start it on it. Patients doing great. Night guy comes in. He knows nothing about it, turns it back, and you didn't do anybody any good at that point. So it'd be no different than if you worked in an environment that didn't understand Perseva and you prone a patient and then they're prone for two hours. The night shift shows up and they supinate them, keep them supinal night long. Like we're not doing anybody any favors. If the system isn't built to be able to deliver that kind of care. I would lose my mind. I absolutely. I'm just flipping tables. Yeah. left on right. And then the other aspect that's specific to burn is you do sometimes with this mode risk ventilation, which you do have an increase in PCO2 with your hyper metabolism. And usually that is more in the early forms of your burn resuscitation. So you might be okay at that point that you might start somebody on APRV for ARDS if that's what you're doing it for. And I will say for me because of the CO2 retention risk, whether I'm doing low-tuttle ventilation or not, but especially for my APRV patients, you do need to have the ability to check your ABGs a little bit more frequently, I feel like. Good point. For me, I certainly think that the evidence is pretty clear that titration of your FIO2 should not be based on serial ABGs. Those serial ABGs, it's additional cost with no benefit for a lot of the should I go from an FIO2 of 40 to 39. Like you don't need a ABG to do that. You should just be going off SPO2 for all these things. I certainly think that's rather settled at this point in time. The one thing though that is important, those understand the patient's been a biolic status from CO2 perspective. And so when I put a patient on APRV, I'll send that first blood gas off and I'll get an idea of what their starting pH is, what their starting CO2 is. I generally wait an hour and I'll send a second one after starting after an hour, just to see where their CO2 like trajectory is. If they go from pH of 7.32 to a pH of 7.22, I'll probably check one another hour, but if they go from 7.32 to 7.28, that's a pretty gentle titration. I'm willing to tolerate that. I think the other thing also that comes along with me and my approach to how much CO2 I'm willing to buy really depends on where that pH starts settling out. As you mentioned, acidosis different than acidemia. I'll tolerate a fair amount of acidemia in these patients. I generally say 7.15 is when I start getting antsy about it and 7.1, I'm pretty much taking them off of APRV at that level. And certainly as that pH of a downtrend significantly, I'm increasing my pressure support on the breaths to try to get a little bit more minimization in there. Maybe I'm decreasing my p-high in an effort to get more tidal volume in there. Actually, I'm increasing p-high in order to get a little more tidal volume in there. But I'm doing all these things in an effort to get off that CO2. The 7.1 thing in my mind really stems from the physiologic effects of vasoactive medications at that level of a pH. 50% of your pressures that you give are immediately inactivated at a pH of 7.10. Certainly at 6.8, 6.9, 0% of your pressures are working at that point. But there's also centers that when they look at APRV patients, they'll sit there and say, I'll tolerate down to 7.2, 7.15, and at 7.15, not only am I changing the parameters of my ventilator catch-up, in an effort to keep them on APRV to optimize their oxygenation, if they're having that bit of a big of an oxygenation issue. They're starting bicarb drips on these patients in order to do with the metabolic consequences of their added CO2. So I say all that because the approach to APRV, there's not a standardized approach. The institutional specific experience of APRV really dictates with that. You can apply this ventilator mode for patients. But keep an eye out. Maybe the next 5 to 10 years, we'll see some significant trials about it. We'll see if it's got more ubiquitous uses or not. You guys can't see, but he's grinning so big right now. So great. APRV. So we got to talk about our last pee, and we're not really going to talk about it. Because we would do disservice. It deserves its own podcast, but it's peripheral oxygenation, which is ECMO. Pannulas? Pannulas? No, that's nothing. peripheral oxygenation works. peripheral oxygenation works very well. I think it deserves its own podcast. It's a big discussion, and there's so much to talk about in it that I think we shouldn't do at the end of a pretty long podcast. So I think we can get into how we do it, that portion. And I think what I teach people up front about ARDS is there are some things that you can do the second you sniff out ARDS. I see that chest x-ray. I look at that P to F ratio. I look at how they're doing on the vent. I know it's ARDS. I can immediately go over to the vent, find out how tall they are, you know, calculate my six CCs per KG of ideal body weight. With them on that, I usually do volume control because I can set that directly, and I know exactly the volume breath that they give that I'm the vent's giving. And then I can immediately go up on the peep, and I can go up on that peep, and what I do is I do what the express trial does. I go up on that peep until my plateau pressure is 30, because I know higher peep is lower peep, and I know above 30 is harmful. And then at that point, I can think about peep or perfusion, and I can going forward, I am going to either have a equal fluid goal or slightly negative fluid goal with Lasix. And then all these other things, we can start to talk about more. You know, if things aren't working, I'm looking at steroids, I'm looking at giving Dexametha Zone. I rarely if ever, I'm giving a pulmonary vasodial later. And then if I need to get somebody's synchronous on the vent to get myself to all these parameters that I want, that I know we're going to help, I will paralyze somebody for a short amount of time with the understanding that I want to take it off as soon as I can. Yeah. And then certainly pruning. Oh, right. Yeah. That's the goes that saying. Yeah. It goes without saying, but we shouldn't stop saying absolutely, absolutely. And you know, I will echo everything that Luke said, you know, my first approach to these patients generally, if I have a patient with arches, I'm going to trial them on APRV early at the gate to see how recruitable I can get these patients. And then if APRV fails, I'm immediately going to arches and that at that point in time. And I agree, early pruning for these patients, if your 48 hours into their arches experience and their pdf ratio is not improving, and it's persistently 150 or less, I'm doing pruning within 48 hours of that diagnosis. In addition of prednisone and appropriate selected patients. And then again, that getting the appropriate mean area pressure of these of the peep and conventional mode ventilation or these of the PI on an inverse ratio of ventilation is critical for these patients. And I think with that, we should probably walk through our big take on points for people for summary. First take on point for me that I would bring up is protection. Protecting those lungs and lung ventilation strategies needs to be the default answer for patients that are failing on arches. The second thing for these patients to talk about is peeing for these patients. Again, getting that residual pulmonary edema off as much as possible to really get your active diaries to send these patients. Pruning, we've said it so many times, but pruning is going to give you that mortality benefit you're looking for. And then targeting that higher peep are also big learning points. Yeah, then the other things that's more consider rather than a must are the paralysis, I think considering paralysis with the understanding that you are going to eat those issues on the back end. And then prednisone, which is not prednisone, it's dexamethasone, but it doesn't have a good therapy. The anti-inflammatory effects may mitigate the early exudated phase of arDS with the understanding, especially in the berm world and grafting and wounds, you are going to eat those problems on the back end. And then pulmonary viso dilators really if it needs to get you to something better. And then taking that off whenever you get to something better I think is important. Absolutely. Absolutely. Well, I think this is a really great third view. I think also we're missing things we're going to talk about. I don't think so. Like you said, I think ECMO deserves a stone podcast. A pump. Maybe that could be a pump. Put them on pump. I don't know. The next time guys I know we got done doing arts today, we're going to stay in the poem system. Next time we're going to talk about inhalation injury and management strategies for that. Everybody loves it. Everybody loves it. Well, everybody thanks for tuning in. Really appreciate it. My name is Jake. My name is Luke. I'm talking about some stuff next week on inhalation injury. Thanks everybody. See you guys. Thank you very much for joining us. If you enjoyed this episode, please help us by subscribing to the podcast and leaving a five star review on whichever podcast platform you listen to a song. Also, please check out our website social media accounts. We can be found at our website at tvsapod.com. You can also find us at xan@tvsapod. Lastly, if there's a topic you'd like us to discuss for our question you have, please email us at [email protected]. We would like to thank VelocityTX, this podcast would not be possible without their support. VelocityTX is a world-class innovation campus, accelerating breakthroughs from startups to industry leaders with a special focus on military medical innovation located in San Antonio, Texas. To learn more, visit VelocityTX.org. tvsa is a podcast for educational and entertainment purposes only. It is not intended to diagnose, treat, or offer patient-specific advice. Please see your doctor for personalized medical advice. The views expressed in this podcast are the those of the participants only, and do not reflect the official policy or position of the Department of Defense, the United States Army, or the United States Government.