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Why is ICU-acquired weakness an independent predictor of mortality? What role does muscular atrophy play in multi-organ failure? When we unnecessarily sacrifice muscles for other organs, how badly do we damage patients’ chances to survive and thrive? Jereon Molinger, MSc, brings eye-opening information to the discussion.
Episode Transcription
Kali Dayton 1:51
Now let’s talk about muscles. Like really talk about them. My understanding has been limited to muscles being vital for movement and quality of life. But what role does muscular atrophy play into multi organ failure?
What are all the contributing factors that lead to lethal muscle loss during critical illness?
This episode is the first of a few with Jeroen Molinger. I keep seeing in the literature that ICU acquired weakness is an independent factor of mortality. But I didn’t really understand why- until I started chatting with him. I have listened to his episodes a few times. Now. If this information is new for you, too, you may have to replay these as well.
Jeroen, thank you so much for coming on the show. I’ve been eager to talk to you and pick your brain about a lot of things. Can you tell us about who you are and your background? What’s led you to do all the wonderful research you’ve done?
Jeroen Molinger 2:52
Right? My name is Jeroen Molinger. I’m from the Netherlands, right now almost two and a half years here at Duke at the Department of Anesthesia and cardiology. My background is mainly in the clinical medical physiology.
The way I came about to come more interested in the ICU space was I did a lot of interesting stuff with elite athletes, where we did a lot of assessments based on their cardiopulmonary metabolic phenotype. And I saw that it’s kind of weird that we do so much cool stuff in athletes, but we don’t do that very well, in our rehabilitation patients are mainly looking at what relation of the ICU patients in the in the early phase.
So I was thinking, “Maybe we should treat our patients….” what become kind of my slogan is, “Treat our patients more like athletes.”- I think that will be better if we can also from a therapeutic point of view. So before entering the ICU, if you have elective surgery, can you somehow optimize them to make sure that if they have a stay in the ICU and making sure that it’s the best they can have and the shortest they can have and also be the shortest on the on the ventilator.
And also during this day, you have to optimize them, I think already from the admission they want. So the whole optimization part does not start upon discharge but automation start really upon admission of ICU. I think that’s the different kind of approach I’m having right here. What’s but I think you’re seeing here also in the US is that they have right now it’s kind of a kind of an “ad hoc stuff” that we’re doing in the ICU, we’ll see issues.
And we don’t have any clue how these issues came about regarding getting dysfunction, muscle wasting, cardiac failure, all that other stuff. But mainly if you combine all this complication or possible adverse effects, it’s all based on your mitochondrial function of the system right now. So also the medical function of the brain, looking at delirium, metabolic function or systemic metabolic function and metabolic function of the kidney is all based on “how can you be optimized?”
Because, if one organ does not show very well function, it’s already because it was already there, it’s not an ad hoc thing that was done in the ICU, you’re just showing it because you’re already prone to having issues. So coming from the Netherlands and they asked me to come out here at Duke. And we have a kind of a cool, I think research group over here or we collect all kinds of data. Non-invasively, using ultrasound is kind of a neat approach reducing muscle size.
So we’re able to drive muscle metabolic phenotyping in a non-invasive way, day by day. So we’re looking at muscle size, and also looking at glycogen content and looking at muscle for muscle fat infiltration. So that’s really where I see my kind of…bridging the gap between the athletic world where we already do that stuff. Then going to the more clinical space where we don’t do that stuff.
I kind of always think it’s kind of funny, but I think it’s kind of an insight. I think we’re still looking into the first days over here, and I think still also that dietitians and physical therapists do meet each other was mainly when one says, “Good morning”, one entering the ICU room and one leaving.
And I’m pretty sure everyone does the best they can in a job. But in a perfect world, that will never be the issue, because you’ll always be talking to a dietician, Western performance coach and extra physiologist to make sure that the nutritional dimension, and your training and recovery is aligned and is paradox.
And I think we do that need to be doing far more better in the ICU. We have to treat our patients like athletes, but also treat them as as unique in the phenotype. So you have to tailor their specific needs on a day by day basis and nutritional needs wise and renumeration wise, and there’s a lot of stuff I think we need, we still need to talk and to see what we can do to.
And also I think one of the cool stuff you’ve shown already is to be able to have an early mobilization with the ventilator early on. So can you even really mobilize with a being on the vent already. So that’s a kind of a complete different ballgame. And if we can combine specific early mobilization with other assessments. We can do things using metabolic carts, using muscle metabolic imaging with ultrasound. So we can then drive far better and larger data sets which can help us tailor those specific needs for a patient. Which again, I think right now, it’s…. everyone does their utmost. Also here, you know, COVID, but I think we need to be more aligned. We literally need to talk. We don’t have to be multidisciplinary, we need to be interdisciplinary. And that’s a different, different thing.
Kali Dayton 7:39
Yeah. Yeah, that’s absolutely correct. And I am feeling a little bit silly because I structured the beginning of this podcast very specifically. And I went through each discipline of the team. And I had interviews with everyone but the dietitians, which is ridiculous, because we always have dietitians with us during rounds. And I don’t think I really understood what role nutrition plays in critical illness.
But I think that’s because I don’t think I really understood the role that muscle mass plays in critical illness. I worry about preserving it for quality of life for long term outcomes, but you had posted something on Twitter. It really got me interested led me to you about the role muscle loss plays during critical illness.
I think we forget that muscles are just a vital part of the body. We’re focused on perfusion- keeping the kidneys, the liver and everything going- perfused that we forget that muscles are essential for survival. So what all goes into muscle loss during the ICU? I talk a lot about deconditioning as far as not using the muscles, but you clued me into the other things that expedite the loss of muscles during critical illness.
Jeroen Molinger 9:00
No, absolutely. I think the the muscle itself is a very underestimated kind of an organ and organ system itself. People think that the muscle wasting or your your loss of muscle is all only heard for because you cannot move anymore. But there is just one very small part of the whole story. Because the muscle itself is one of your biggest metabolic organs.
It is an organ that has profound interaction with other organ systems like the heart, the liver, the kidney, the gut. So the ability to talk, it’s called “interorgan crosstalk”. So there are specific- they’re called “myokines”. They are some kind of cytokines that kind of…. there’s ability to secrete specific Myokine from the muscle into the bloodstream. Which then can make kind of a communication with the brain, with the liver, with the heart.
And that specific intern crosstalk has to be there. If they cannot talk to each other anymore, then the whole efficient metabolic system is gone. Because if you have a very fast muscle wasting huge or being happy metabolic or very high inflammation faced in the ICU. Then you have an instant kind of a, I say “inter-organ discourse”, I would even say they shout to each other, and after the shouting, because there is so much secretion. After the shouting will be silent, there will be no inter-organ discourse anymore.
So this to me is where we are, we’re seeing that the amount of muscle wasting you have is also correlated to cognitive function is also correlated to mitochondrial function of the kidneys. So API is also collected to muscle wasting itself. So if you want to make sure that your muscle quality, not only looking at muscle mass, but really looking at muscle quality itself. So your mitochrondiral biogenesis. So how we really efficient issue muscle, even during the resting phase in the ICU, being sedated and being on the vent- that’s essential for your for your outcome.
And, of course, looking at the system itself, looking at the body that the muscle of the lack, of course, by far the biggest ones. So those will be the ones you can train easily. But there are other stuff. Also, I think one of the muscles, we tend to forget is the diaphragm. It’s a skeletal muscle, which has fast and slow twitch fibers, that means that it’s a kind of a weird muscle that can be as a function be non-fatigue for 50%. So there’s 50% non-fatigue fibers and 50% fatiguing fibers.
So it can have a huge amount of power, but very briefly, but also can elute amount of influence, but with a very slow power. So if we then look at ventilation, looking at mechanical ventilation, that’s completely off physiology, because your diaphragm will be used completely different than ever. And if you have muscle wasting on your diaphragm itself, is also a specific kind of wasting, which shows instantly will be seeing already four hours after intubation, that your muscle of diaphragm is already remodeling.
So if you’re able already to aim, because we know that that’s kind of weird, if you’re just looking at some of yourself, the diaphragm, diaphragm is connected to the psoas muscle. So all muscles are kind of connected with with facia, with connective tissue. So everything is is one specific kind of system, which works very well. And you have to understand from a biomechanical point of view, that the lack of support and also for a different type of diaphragmatic function.
So there’s a lot of stuff which we just don’t understand, I think when you’re really talking with an RT, or when you’re talking with a perfusionist, they have their specific core is ventilation or perfusion that way. They have no clue, for instance, that when you’re laying a patient on this side, and making a more extension of the hip, that diaphragm on that side will change a little bit in the length and potentially have a better length power curve. So the patient will be able to breathe easier. Just bioomechanics. It’s not perfusion is not gas. It’s just biomechanics. Yeah.
Kali Dayton 13:17
And some of the patients when you get them up to the chair, they’ll write on the board and say, “Oh, I can breathe so much better”.
Jeroen Molinger 13:25
Yeah, it’s just biomechanics, exactly. And also, what we’re seeing is just looking at architecture of the muscle. One of the things I always see in the first days, and I think that’s hard for also for nurses to to be very clear about this is that you have to make sure that the architecture of the muscle is preserved.
So if you have a leg that’s very external rotated, or internal rotated, that instantly changes the architecture of the leg, because the gravity still pulls the muscle down. So your femur, femur bone will be kind of a glide. They were gliding off on the medial side or the lateral side. So if you must have changed this from this position in it from the joint.
Even if it just stays the same side, but it just changes his position from the joint, your brain does not know anymore, where the specific muscle was, so your motor programs in your brain will not work anymore. So if you want to stand up, you cannot stand up anymore because the muscle has different kinds of properties right now. His length and his position in the leg is different than the brain doesn’t know anymore.
Kali Dayton 14:25
How long does that take to happen? Is this after a day after a week?
Jeroen Molinger 14:30
Yeah, yeah, and I think that will be happening I think already within 24 hours or so. Because we’re seeing right now if you being sedated and your resting membrane potential of the muscle decreases. You see already kind of a the atrophy is not based on the muscle size changes but just based on your your tone of the muscle decreases instantly. So you get a kind of a more sedden muscle in the middle for the muscle and the muscle will be far more eager to slide off to the medial side or the lateral side. That’s almost instant.
Kali Dayton 15:03
So much more sense because in the “Awake and Walking ICU”, we walk people shortly after intubation. Yeah, and in my mind, it was to preserve mass right so that they don’t atrophy. But you’re saying, the sooner you preserve that connection…
Jeroen Molinger 15:19
Motor learning is one of the first things you have to do, because when you learn the brain to reconnect in the muscle, again, that is the first and the fastest way of recovering. That kind of specific programming can be done easily, instantly. And it’s kind of cool, because if you’re, and those, those kind of microprograms are crossing. So you’re only using one leg, for instance, if you do a kind of a standing up with one leg, and the brain pads also be changed for the other leg, the other other brain part.
So it will be crossing the programs will be matched in the left and right. So you can even already train people just training them feeling them program making sure that if they train that the brain feels that they probably have section of the of the joint is there and that the brain knows right now you’re already 90 degrees flexion of the knee and your muscles over there. So you have to contract over this, this this are are all information that the brain needs to have to make sure that is able to contract that muscle in that speed in that place and the time.
Kali Dayton 16:25
And so we had a an interview with a young guy, he’s 30, he was a firefighter, extremely good shape, and extremely good shape. And he lost a lot of muscle mass. But by mass wise, he still should have been able to just get out of bed.
Jeroen Molinger 16:42
Right.
Kali Dayton 16:42
And yet he struggled during that recovery. So that makes more sense that all that communication had been severed or altered.
Jeroen Molinger 16:52
And you kind of even even what we’re seeing already is that the you know, your vesicles that are your muscle fibers, they have a specific angulation in the muscle. And it’s the angulation changes. So if there are if there is less stone angulation changes and then it’ll be more horizontal. So then the torque but you can drift by your muscle. Normally when this is a angulation of the muscle, you have this bone here bone.
Now you change it over here more horizontal when you pull on the leg, it will not give you that force anymore. So yeah, efficient way of collecting power through a specific muscle fiber is gone this instantly.
Propofol is one of the biggest issues over here. Propofol has that kind of this kind of instant effect on the muscle, apart from being also very toxic for mitochondria, but from a resting membrane potential of the leg will change. Mainly only losing in the slow twitch fibers.
Kali Dayton 17:48
Why does it do this? Why does propofol do that to the muscles?
Jeroen Molinger 17:51
It does specifically on the sodium potassium channels, it has this effect. We’ve seen that mainly in a kind of a weird way in the intermediate muscle. That the muscle, the knee rectus femorus, for most muscle that’s a very deep muscle. Normally you cannot see it and I think it’s still one of the muscles most underestimated because this muscle you cannot biopsy because you have to go through the rectus femoris to biopsy it. So nobody will do that.
And in the world of muscle histology, is kind of, when you cannot biopsy it, it is not there. So we don’t we don’t talk about it. And imagingvis one of the things and ultrasounds one of the things where you can easily look at a specific muscle and even with muscle ultrasound, you can even see the angulation. And you can calculate the angulation of muscle fiber.
And we saw that intermediate muscle is mainly a very slow twitch muscle is a muscle that is a primary driver. And as a muscle that tends to increase your tension inside the overall muscle itself where you need to have movement, it can be easily instant movement based on your morth muscle so that there is an instant tone over there.
And if that tone decreases, then we’ve seen already and that was only in the active more intermediate muscle, then we see that the the change of the diet, the extent of fasiculation is more horizontal and you can have more flattened muscle. And maybe I can think you can agree on the outside. Everyone in the end ends up being a pancake on the ICU. The muscles will be a pancake.
Kali Dayton 19:19
Well, outside of the “Awake and Walking ICU”.
Jeroen Molinger 19:22
Exactly. That’s what we wanted to move. Yeah, if you’re not walking, when you’re not mobilizing, the you get a pancake also looking at the… if you’re looking at the top of the muscle you can see muscle on the left on the medial side and also on the lateral side. And you can see the bone in the middle.
Kali Dayton 19:36
Yeah.
Jeroen Molinger 19:38
And that is really based on the rest the muscle but this is all being kind of wasted away but also being forced because of gravity to one side or the other side.
Kali Dayton 19:48
No matter how you position a patient in bed. And so propofol disrupts mitochondrial function and sodium channels…
Jeroen Molinger 19:57
Sodium channels. Membrane potential changes. Yeah Yeah,
Kali Dayton 20:00
So we love propofol. I say “we” as an ICU community, because it’s “short-acting”, quote, unquote, which I completely dispute, depending on your body habitus. And it’s deliritious but I didn’t appreciate how much it affects the muscles. And we just, “we”, as an ICU community, just crank it up and think it’s totally benign. Because we’re unaware of what it’s really doing. And I focus on the brain- what it does to the brain, the delirium…. Yeah, but you’re saying that it is toxic for the muscles.
Jeroen Molinger 20:34
Toxicu for the muscles, toxic for the mitochondria, also. So yeah, yeah, definitely. And and I think we still need to find out. And I think one of the questions we have and also the question we have in our research group is: we see potential, or our patients are more susceptible to this kind of toxic effects of propofol, some are not. So there is a kind of responsiveness or an unresponsiveness to the toxicity of propofol.
The hardest part is right now how to find out and mainly- Can we non invasively find out?- Because the only way to do it very well, from a muscle point of view is doing a muscle biopsy, but as always kind of hard to do. Still looking into potential other imaging modalitie which can use. What we’re seeing right now, specifically we saw in our COVID, of course, is very specific population. The software is remember, we have very high propofol uses in that population also.
It’s a very specific knowledge changes. And also, again, in the intermedius muscle, we saw mainly fasciculations. So those are first case are kind of low motor neuron disorders, which I saw only in the very subcohort of my all COVID population. So imagine if you have a…. almost a kind of neurologic disorder, which we don’t know if it’s based on COVID alone, or COVID and on top of propofol. Then also being being prone for having a specific phenotype and that responsiveness of propofol…
Kali Dayton 22:06
and paralyzed…
Jeroen Molinger 22:08
and paralyzed. Yeah, yeah. The potential be seeing is, again, again, it’s one of the stuff, we’re still going to strike out on a peer review. But that could potentially be the explanation when people have so many issues afterwards. Because if there is cognitive dysfunction, but also overall fatigue, and you have a lower motor neuron disease behind it, that can be an explanation of the “long-haul”, or the “long COVID” that we’re seeing right now.
And I only saw the very niche COVID populations being intubated. And that’s very well and well defined, because you’re not stuck with them. Imagine those people on the floor, or very, very sick at home, which we just didn’t know about. So there’s a lot of stuff there. Yeah, I’m just gonna define that.
Kali Dayton 22:53
And along the same lines, you mentioned the hypermetabolic state during critical illness. Can you tell us more about what happens when someone is incredibly inflamed or what contributes to the metabolic state, as well as other things that contribute to muscle loss?
Jeroen Molinger 23:07
We published an article, John Whittle, I, and the whole Paul Wischmeyer, and the whol COVID team. We saw a very specific kind of phenotype in these COVID patients. When we were measuring metabolic or metabolic rate driven by inflammation. So we put a metabolic cart on a patient and we’re measuring VO2, VC2, and ventilation. And we can calculate the amount of calories they’re burning on that specific timeframe. So you can calculate over 24 hours.
So you have a kind of a insight in how much kilocalories they’re burning day by day, and you have kind of normal reference values based on your length and your weight. Normally, you have very information base. Many our ARDS patient, for instance, you have a very defined inflammation phase in the first week or so. Again, in the first acute phase, you have the acute phase itself, you have a early and the late onset kind of a phase.
So you have a hypermetabolic and kind of leaving off and then you go back again to kind of a more normal metabolic, maybe even hypometabolic phase. In COVID, it was completely different, besides a normal metabolic phase in the first week, and the second, third and fourth week. Based on your BMI, we saw a very high metabolic phase. High metabolic means you’re above your 100% predicted value.
So and maybe we have to get a little bit in depth of physiology, but it’s because RE is based on your Vo2, so your oxygen consumption of that specific time. And Vo2 is being calculated, you can of course measured the mouth, which we do. We can also calculate based on your, your cardiac output, you’re stoke volume and your heart rate, and your arterial venous oxygen difference. So your oxygen consumption from the peripheral tissue tissue like you’ve got like your brain, like your heart.
The thing is what we just don’t know….. And that’s also one of the articles that’s coming up right now… is that can we somehow see that people were…. I saw, for instance, patients that were being sedated being proned, still had a cardiac index of 9.1. So from a cardiac point of view, and they had Vo2s around five 600 ml/minute. This is actually very high, not high we normally have to do when you’re running. But from a cardiac point of view, we have a stroke volume of 125 liters or so… and the cardiac output is 25 liters or so. That’s when you’re running. Those recording outputs that sustain when you’re running.
When they’re still, laying down, proned, being sedated…. So there is something going on over there being hypermetabolic. So the the heart itself has a huge train. Someone tries to compensate for the lower perfusion or the lower extraction of oxygen in the peripheral tissue. The only way for the system to do that, if you have lower section of oxygen is higher flow. This makes sure that you have a high flow of the system. And if you have a percentage of restriction, just make the flow bigger, so the sort of restriction is higher. So you get more extraction and essentially more perfusion in your peripheral tissue.
So that’s what the hypermetabolic phase kind of invokes is that it is a higher Vo2 consumption. But we don’t know is where does it come from? When we do an exercise test. And measuring Vo2, we know for sure, as many muscle because we’re driving muscle, because there is some specific stress going on. Right now basically is laying down, being sedated, is being prone. So it’s a more mitochondrial function for measuring all over systemic mitochondrial function.
Measuring respiration of mitochondria, you don’t know which mitochondria, you don’t know which- the brain or it’s more the gut, or is it more the heart or is mixed with the muscle? So inflammation itself can come over and over. So immune response is very defined- very high. And in ARDS is more in the first week, and then in the COVID, we saw more in a second and third week. And the third hypermetabolic phase is defined, of course, you have more need of your caloric needs.
So there’s kind of also discussion, what do you should do? Should you also give more calories? And how will you define the calories itself? Based on micro net nutrients, so looking at more lipids or looking at more carbs? And then the whole question again, that’s the kind of ship we’re in right now is… I’m always talking about systemic metabolic mitochondrial dysfunction.
And one of the things we’re seeing right now patients they have also made, mainly for muscle point of view, a inability to utilize fats. So your switch from fats, carbohydrates, and fats again, that’s impaired right now. So if you have a system that can only utilize carbohydrates in the system right now,
Kali Dayton 28:01
That’s what you need to give.
Jeroen Molinger 28:02
Yeah, they need to give but then you have another issue. You are insulin resistant.
So you can’t utilize carbohydrates from it also being pushed back to lipids, which you cannot do. So then you have an overall metabolic dysfunction, which can cannot utilize any substrates. But there is a demand, because there is inflammation. So the tissue needs to be added to use extra oxygen. So there’s a lot of stuff.
How do you define that specific… Can you can you somehow kind of hack, or kind of tweak the system in this way? If you actually give them carbohydrates, they cannot use carbohydrate. You get some lipids, they cannot utilize lipids, anymore. So if you look at propofol, it’s also kind of a weird way, because there’s a lot of lipids in it. If you give them a high lipid load, the only way but what happens then the accumulates lipids inside the muscle, or inside the organ. That in itself give rise to insulin resistance.
Kali Dayton 29:04
So you propofol contributes to insulin resistance?
Jeroen Molinger 29:07
In the end, when you’re not able, …. when you, Yeah, when you have an accumulation of fat because you’re in enable to utilize that fat, especially propofol, accumulates in the muscle. Then you have muscle insulin resistance, which is kind of weird. We are already kind of building some resistance with our own stuff. And we’re doing we get some insulin. So we have a kind of weird kind of a circle over here.
Kali Dayton 29:32
So that’s a third way in which propofol is not helpful to muscles.
Jeroen Molinger 29:36
No. No.
Kali Dayton 29:38
I had I didn’t know that. Wow.
Jeroen Molinger 29:41
So… and there is this potential way. And this kind of a we’re also coming from coming back from the athlete world, is when you have a patient- and again, you can argue potentially, which we don’t know yet, but in our view is that the people vulnerable for that kind of affection of COVID being intubated, potentially being prone, having an impaired systemic mitochondrial function. Because, if you cannot utilize a natutal immune response, and the immune cells itself has mitochondria, so your mitochondrial function itself also drives your immune function.
If you have an inability to utilize substrates, then you’re kind of in the middle, because your oxygen is needed, but you cannot give it because you cannot utilize any substrates. To bypass that system is using ketosis. So if you use ketosis, you bypass the cycle. You can give instant kind of back to making people instantly going into ketosis, ketosis state, which normally only can be done when you have a ketogenic diet, which also is one of the potential ways of doing is that you’re lowering carbohydrates. Even for children, and going and kind of pushing them to ketogenic or go to etc, count to ketones.
But again, you only can go towards ketones, when you have the ability to utilize fats, which they cannot do. So you have kind of a weird kind of… in the middle. But when you’re giving them oral ketones, instantly, then that’s kind of a shift that the brain and the gut and the kidney and mainly also the heart can use instantly. So you give, literally the system, the centers they use without interfering with the impairment they have. So the mitochondria, for your immune system, can be used in your hacking of the mitochondria been used for using different kind of stuff.
Again, that is not standard of care yet, we are still looking into that specific use because it’s just ketones… is just a food supplement. It’s not medication. It’s not it’s kind of a vitmaminD, or wherever. So we’re looking at utilization of that specific intervention. And if it is in the first week, because we show hyper and hyper and hypo metabolic states and people, the question only is, is it hypermetabolic or hypometabolic?
Based on just their, just in a kind of a…lower-state, or you’re just not able to use oxygen. If they’re able to use oxygen itself, then we have to help them. And in a way, looking at multi organ failure is kind of a way of think makes sense. It’s kind of a way of struggling from the body to get into kind of a hibernation phase. Because if you want to make sure that the the the most important organs in the system, like your heart and like your, like your brain preserve, and you already have a low mitochondrial function, just shut down the system and have poor mitochondria function. And that’s the reason why you get API, that’s when you get that stuff.
Kali Dayton 33:02
So when muscles break down, they atrophy, due to all the factors we’ve discussed.
Jeroen Molinger 33:07
Yeah.
Kali Dayton 33:08
It expedites the immune response, right? So you get even in a hyperinflammatory state. So COVID is already an inflammatory disease. So when we sedate people, leave them in bed, and don’t nourish them properly, we expedite or we aggravate this inflammatory process that’s already going on.
Jeroen Molinger 33:30
Exactly. Yeah.
Kali Dayton 33:31
That I do not know. And so, I mean, I mean, there’s no way to really know, but some patients develop renal failure, some people, some don’t. And it seems to be almost random or spontaneous with COVID. But could it be aggravated by this mitochondrial dysfunction that we’ve created?
Jeroen Molinger 33:51
Exactly, exactly, yeah. Maybe maybe some, I think, I think somebody is already prone. In the whole… from admission, sometimes we push patients to a level that the system cannot cope with it anymore, and it just shuts down. And what I tried to find out is, Can we somehow dissect it? Can we somehow predict the specific phenotype? That I know, if you push this guy this way, this will be his reaction. This one is very prone to having an AKI, because of this and this and this.
So, we have to find out more. That will be of course, not a very easy task, but I think it shows that we have to be far more…. looking at uniqueness of the system itself. We have to assess on a day by day basis that of course takes time and takes effort. What I was taught to advocate for is that we have to have a kind of a task force- a mobilization, nutrition, respiration kind of task force where the RT the dietitian, Nurse Practitioner and a PA.
Everyone is somehow involved in having a specific kind of discussion in how to pursue early mobilization, combination with potential changes in ventilation stuff, or changes in medication and all With the foremost first focus is we have to make sure that our focus and our goal upon admission is to quality of life to patient after they’re discharged from the ICU.
I think if you work in the ICU, you’re tend to be only looking at “Wow, we did it, he is discharged from the ICU”. But that is just the beginning of that specific life or non-life. So going back to what always Paul says is “We have to create survivors not victims”.
I think we tend to not look at the outcome. Again, if you have output, we are fine, the ECMO did well. Right. But sometimes you have to see patients after ECMO and see what kind of scars they have in their neck.
Kali Dayton 35:59
And that’s something we discuss a lot that’s really unfortunate about our system here in the United States is that as soon as someone’s traipse, and they’ve been settings are down enough, then they can be sent to LTACH. And so the critical care world does not have to address it. I don’t think people realize how long it takes. And the mortality rates after the ICU, that could have been prevented by what we do in the ICU. And even just what you’ve explained and told me reaffirms, but it changes my perspective of when someone initially is admitted to the ICU. As far as how quickly we start nutrition, what kind of nutrition we do. I am so sorry, to all the dietitians, I should have done an episode because… apparently you guys have a lot to teach us.
Jeroen Molinger 36:45
No, no, no, I think they are central. As RT and PT are. But they have to work together. You have to somehow work in a way that you can….. And again, I think it’s um, it’s kind of weird way to push it. But I think when people are being admitted to the ICU, that is their Olympic Games, they want to reach the gold medal. So we are that team.
We are the performance coaches, we are the nutritionist, we are their all…. there surrounding it. And they will make we want to make sure they get their golden medal. And that has to be there this be our goal instead of just going with the flow somehow. And that kind of a weird way to say, but I think we need to be far more focused on life after ICU instead of the ICU itself.
Kali Dayton 37:33
I could not agree more. And no trainer is gonna sa, “Just kick your feet up for the next couple of weeks. And then then we’ll go hit a race.”
Jeroen Molinger 37:40
Yeah,
Kali Dayton 37:41
That’s not training. And that’s not…
Jeroen Molinger 37:43
that’s not how it goes. No, no, no,
Kali Dayton 37:44
That’s not how you create survivors.. That’s how you create “victims”, as you say.
Jeroen Molinger 37:50
Yeah, exactly, exactly. Because what we’re seeing right now we know that the mortality rate in ICU has dropped significantly in the the last 10 years or so. But most people are dying at home, seven, eight months after admission.
Kali Dayton 38:06
And what was that all for, besides prolonging suffering?
Jeroen Molinger 38:10
Yeah
Kali Dayton 38:10
And how much would that change at the moment someone rolled in, we said, “This is a human, this is a person, this is their, this is what they do for work. This is what they need their body for.” And appreciated the muscular system, as much as we do the kidneys and the heart and the lungs…. and implemented all this research that you’re doing, into actual practice.
But I, I was unaware of a lot of these principles, I didn’t realize how much muscle loss or wasting or atrophy contributes to multi-organ failure. I had no idea.
Jeroen Molinger 38:45
Absolutely
Kali Dayton 38:46
I’m obsessed with this stuff. And I didn’t know. So how much that would that change our approach to all of everything we do? How much more would we hesitate and dread sedating people instead of running to the propofol, if we knew that we were essentially kind of killing them with it.
Jeroen Molinger 39:05
I think we’re kind of it’s kind of the way, people are scared to change. And they know what they have right now when they are afraid that something will happen somehow. And yeah, I think we just need to make sure we have our dedicated team in knowing that you can have a lesson really is also when you have complex cases, you have to you have to make sure your are your interaction with your, your, your colleagues or healthcare professionals. And talking about everyone has a specific knowledge base, and we need to know far more from each other, I think, to have a better understanding which is important for this specific patient. And right now, the thing the knowledge base is not being shared. There are a lot of knowledge basis, but not shared once.
Kali Dayton 39:51
We have standardized practices that really impede us from doing personalized and optimized care for our patients. And so we just had to cut the cord and actually hear from people like you that provides such a different perspective and insight, and I’m excited for the episodes coming up.
Jeroen Molinger 40:09
Oh, definitely. Yep. Yeah, we have so much more to talk about.
Kali Dayton 40:14
Thank you so much. And if the listeners have any questions for Jeroen, we can talk about on Instagram and we’ll address the next episode. Thanks so much.
Transcribed by https://otter.ai
References:
Whittle, J., Molinger, J., MacLeod, D., Haines, K., & Wischmeyer, P. (2020). Persistent hypermetabolism and longitudinal energy expenditure in critically ill patients with COVID-19. Critical Care Medicine, 24(581). https://ccforum.biomedcentral.com/articles/10.1186/s13054-020-03286-7
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