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What role does nutrition play in improving outcomes in the ICU? How can we help preserve muscle through appropriate nutrition during critical illness? Jeroen Molinger, MSc continues to upgrade our approach to critical care through exercise physiology.

 

Episode Transcription

Kali Dayton 0:28
In the ICU world, there is a new emphasis on ICU rehabilitation, which is extremely important because really, no one is going to leave the ICU at their baseline functional status yet. I hope this podcast also brings our attention to preservation how different sort of rehabilitation needs be or even simply survival if preservation of a muscular system was just as important as any other organ.

Last episode, we talked about how muscular atrophy contributes the inflammatory process, we need to be keenly aware of ways to preserve muscle mass and function. Starting the moment, patients come to us, this should be just as important as any other bundle. Mobility should be just as important as any antibiotic that we give.

This podcast is focused a lot on early mobility or better titled, “prompt walking”, yet the picture would not be complete without diving also into nutrition. They go hand in hand- and it is just as important. So Jeroen is back with us to continue to fill in the gaps head on. Thanks so much for coming back. And teaching us more. Today we’re gonna talk about nutrition. So Jeroen, tell us why nutrition is so important during critical illness.

Jeroen Molinger 2:26
Good question. I think it’s nutrition. And as always, a kind of thing that I think is not being very well understood in the intensive critical care world. Because think people think that they don’t need nutrition in the very first acute phase. And I think that’s partly due that we do not have or didn’t have the ability to assess it very well- what the patient’s nutritional status was.

We have, of course grading levels now, but that’s very hard to assess in real patient because whatever confounding factors surrounding it. We don’t have very well defined metabolic profile which gives more rise to nutritional status. What we’ll do now is that if you do not feed a patient very well, specifically in a second or third week, and on that the outcomes, current length of stay length on the ventilator or increases, there is a very well defined kind of malnutrition risk.

Which can be I think, somehow overcome where people already have tube feeds for so how can you make a very well tailored tube feed based on a patient being admitted to the ICU. Which, as of now, I think in most hospitals in the US is purely based on BMI and potentially age, and gender.

Which, if you really go for more depth in how that specifically defined the BMI, or the weights being defined, was just people ask to a DEXA scan or what the specific way was, before they were made in the ICU. So that’s a very weird kind of way looking at weight because the weight is going to vary upon discharge, admission, going through the ICU stay can change overall based on just our fluid loads, all the stuff. Which doesn’t really give a good insight in their overall lean body mass, muscle mass, fat mass, and maybe a potential whole body water.

So you have to assess patients how that changed from a body composition point of view on a day by day period. And also, again, combine that with- what are the particular nutritional needs on the specific day during the ICU stay. So the only way to assess that very well is – we have a lot of equations which can define the resting energy expenditure people have.

So you can have a kind of derivative of how many calories you’re going to need for a specific day, again, based on weight and gender and age. But that doesn’t give us the whole story and we just put out a article is going to be submitted where we try to show that using specific equations in the ICU in COVID patients that when you look at equations and then again, compare that with the golden standard that is index kilometer metabolic rate measurements, were you measuring a patient from the ventilator.

Where you’re measuring Vo2 and co2 from the patient, which then calculates for you the real resting energy expenditure value of the patient on that specific time. You see, that doesn’t match up. So overall, we tend to overestimate and or underestimate patients based on their nutritional needs. And over and under estimate is based on a specific phase they’re going through.

We put out an article, maybe I can send you also a link where you can put it in a podcast. In our COVID patients that we saw that the first week that kind of were kind of normal metabolic. So there they had their normal metabolic needs. Not very different from our normal patient we saw in the ICU.

But moving on from the second and third and fourth week, we saw a very high increase in metabolic rate. And metabolic rate increase was different between the people who were being obese, or being non obese. When you were obese, you see a very well increase upon I think, on the third and the fourth week. Then you see decrease again. That increase can be almost 200% of predicted. So you can have a patient being proned, having a BMI larger than 30, being paralyzed, still having a energy expenditure overall, or more than 3000 calories a day.

Kali Dayton 6:24
Why is that? What is contributing to that?

Jeroen Molinger 6:26
Yeah, that’s that’s a very good question. So one of the things we’re looking into right now, there, I think there is not one single answer to that one, I think there are different kinds of phenotypes in those patients who are in the ICU. If you have a more– again, I think in my in my my former podcast, I said to you that the Vo2 is being derived from cardiac output.

So the potential of the tissue to utilize oxygen in the peripheral tissue like muscle, like the gut, like the kidney in the brain. And of course, also the heart, there is a kind of tendency that someone has a very high cardiac output. And then if I were to low ability to utilize oxygen, extract oxygen in the peripheral tissue, or the other way around.

You can ask yourself- why do you see a very high cardiac output?- And that high cardiac output can be, for listeners that know those numbers- they have a cardiac index of 9.1 or 9.2. So there’s almost 25 liters or 30 liters per minute. Those are numbers we normally see in healthy volunteers just running up in a very high intense kind of exercise.

They do that in a 24/7 being proned, being sedated, paralyzed, and on the vent. So you can imagine it’s a very high rate in the heart itself. And one of the habitus we have is that the inability to enter oxygen from peripheral tissue can only be overcome when you have a higher flow.

So there’s still a need, there is a demand for more oxygen, because you’re in the inflammatory state. So your lymphocytes you’ve got everything needs more oxygen to extract from, but if you have a less oxygen, so your mitochondria is not that very, it’s very poorly functioning all the way to get around this. More -More perfusion more.

On top of it, you mentioned last episode that propofol inhibits mitochondrial function, right. So we have these COVID patients on very high doses of propofol, so even less function, and that causes what were you saying?

That causes literally, I think, already a kind of potential, strain on the heart. Because if you have mitochondrial dysfunction, so impairment of extraction of oxygen from peripheral tissue, the only way to meet the demand that the system is having is high flow. The higher flow that the system can only be done.

So you’re already giving is kind of a weird kind of circle we’re living in. So, the medication you give to be sedated, is also the medication that give rise to this specific phenotype. Again, that is the question we try to answer, becuase it’s not for everyone. Not everyone responds that this way to propofol.

So we’re trying to figure it out. Which one does? Is it specifically for a very well defined patient group in ICU or the ice group by betas by population is that a population that shelter specific kind of interact with this saw specifics in our COVID population like fasciculations. So these are kind of a low Motor Neurone Disease, which also give part to a higher perfusion of the specific muscle.

So and again, this is all specific to COVID. And I’m talking about COVID, because it it shows such a very domestic difference than are called our classic ARDS patient or our classic sepsis patient, which shows that motor organs are being right now being impaired not only the lung, or the pulmonary system.

So have you studied normal ARDS patients, or other patients in different phases of critical illness and how does that compare to these COVID patients as far as how their nutritional needs change?

Yes, we have in depth before in our COVID adult population, which showed a very, very well defined hypermetabolic phase, which we have not seen yet in our classic ARDS and our classic sepsis patients We’re still try to find out what was the reason why there is a specific hypermetabolic face because we saw on the first week of kind of a normalized metabolic rate based on their normal equations based on reference values. And in the second, third or fourth week, depending on being obese, yes or no is not. We saw an increase till 200% and up.

So that’s a very high number, which, which shows that there is a increased metabolic need, you can ask ourselves- why is there a increased metabolic need in the second or third or fourth week upon the ICU stay? Even if you are being sedated, paralyzed, proned, and ventilated- which you think that the system itself should be completely down.

So why is there such a high need? I think there are different kinds of scenarios and kind of storytelling over here, I think. So there is not just one silver bullet that tells the whole story. What we saw was, that again, if you have a high BMI, you have a different metabolic phenotype a different metabolic rate in the second, third and fourth week, than when you have a normal BMI.

So 30 or lower. What we saw was the highest were the obese- that be had in the third and fourth week, around 200% of their predicted metabolic needs. So again, you’re looking at numbers at around 3500 calories a day. Those are huge numbers, if we just tried to cheeky to do to find local better with our normal, healthy volunteer if compared with us.

If you want to have a total caloric needs or kind of burned day 4500, we have to do some major work, we have to have a specific imagine if you’re able to burn 1000 calories in a normal year have 2000 for just for one day, you have to do some serious, some serious work to get that done. That’s two hours on a big night on a gym, on the bike and all that stuff.

So imagine, again, a patient COVID intubated, sedated, paralyzed, prone and ventilated as the same number. And if you got a little bit more in depth, especially patient, I’m seeing that the big difference we’re seeing this patient is the how the amount of cardiac output took for human heart rate is defined versus their ability or inability to extract oxygen from peripheral tissue. So we have patients who had no more extraction values, who had normal correct outputs, all the way under normal cardiac output with very high spectral values and still came up with a very high view to that’s a kind of a number of what you want to see.

Because then you see there is a metabolic phase going on. Something in the system is using more energy, like just the immune system cause you’re having or an inflammatory phase. But all around just kind of weird when you have a low extraction value, and a very high cardiac output, which then because it be multiplied shows very high for you to which combined with tissue to give high resting energy expenditure outcome give rise to a phenotype that is being laying down. And the only way for the system to compensate for it less restriction is more flow in the system.

And the more flow in the system is just gaining in your stroke for you, or heart rate in increasing your cardiac output. And this kind of the story that we’re telling right now and also for my my colleagues at Duke heart. And we do a lot of stuff in the cath lab that we’re seeing is the hardest kind of weird kind of organ, I will potentially see them that their heart is just a slave of the cell. It only strikes and responds to differences from a cellular level in the peripheral tissue.

So if there is an expression of bone in the tissue on way for the heart to compensate that is in high flow, try to somehow compensate for the high demand that there still is again, and we talked about before in our first episode that one of the things that we see in our patients that have very high adverse effects and organ failures is that they have the inability to utilize fats very well. And that was mainly what we’re talking about the skeletal muscle.

But that’s again, that’s not the whole story. Mitochondria are all over the place. There are no lymphocytes there are in our kidneys there are in our gut there in our brain, but also in our hearts. And the heart muscle itself. The cardiomyocytes is a very weird kind of muscle because it’s one of the muscles that is most adaptive to changes, it’s a muscle that’s kind of a garbage muscle, if you throw elected to it, it lost lactate. If you throw ketosis, it lost ketones, it can utilize anything more than once. Because from a evolutionary perspective, that’s kind of phase four, because that’s a very, it is the organ that shows perfusion, that is the demanding organ for perfusion.

So you have to be sure, next to the brain that the brain is being perfused. So make sure that that system is always working no matter what. But if you have patients who have this kind of issues, they also have the ability to utilize fats in their hearts, they have an ability to utilize lactates in the hearts and ketones in the hearts. And that in turn, give rise to a heart failure. So the idea being different, more rigid heart or more effective heart in the sense that it cannot cope with the demand is getting, and you still haven’t patience, that is a high strain on the heart that the heart cannot cope.

Because there is a flow demand because there’s a higher view to demand based on the information state. But the heart is still impaired. And somehow you get compensation, get the compensation throughout their stay. And we all know that one of the major complications you can have any ICU was not organ failure. And another organ failure is kind of a kind of a safety way of the system to make sure, again, from an evolutionary perspective, that the brain in the heart always is being refused. So if you have issues with procuring a system, make sure that he just closed systems off, to make sure that the high demand systems are still be able to provision refused.

And then making the whole circle back again to where is nutritious or important is that nutrition is one of the micronutrients that that you can somehow trick the system with, because there is still in demand in high inflammation or inflammatory state. Because there is a demand for you to know anyway to give you to to a system is to utilize it with substrates like lipids and carbohydrates again, so you have to make sure and I’m not talking about protein at all, still, because there’s a third step. Protein is also a source of to be utilized as a as an energy on an energy level. Those are also building blocks for the system to make sure that your protein buildup is also being there, because you try one of the easiest thing for the muscle or for the system to use as muscle is the amino acid pool.

Because the muscle in rest is just an amino acid pool for the system to be used for energy. That’s why you get wasted. And somehow we just don’t know is that even if you get that, that is again, looking to the back, look back again, amino acids is very easy for the system to use. So if you have an impairment of neutralization of lipids, then your family from easily being pushed to your protein to your muscle protein, which in turn give muscle wasting. And then we have the third circle with the My Accounts, you’re not able to see Americans anymore, because the most a very high metabolic profile organ, which talks with all kinds of other organs like the brain, like the gut, and the kidney, which they don’t talk anymore. And then you have kind of a constant looping, which ends up with nausea organ failure in the end.

So in the context of ensuring that patients maintain functionality and that they’re able to maintain muscle mass. If we don’t give them the right kind of nutrition…. it contributes the multi organ dysfunction, right?

Right. Yeah, no, I think if you if you’re going to see and of course, one of the course of you’re showing already that we are able to mobilize patients very early on even with on a vent. If you’re looking at how would you define what is needed from a muscle perspective- on the muscle level and cellular level, which will trigger the system. Building muscle, you have two specific triggers.

One is just the building blocks itself, like protein amino acids, and the second one is the most important one, you have to have an anabolic trigger. system need to be triggered to make the system anabolic. And the reason that trigger right being for being anabolic, is exercise. Exercise is a trigger of the muscle. When you’re when you’re doing exercise, and then putting on the protein on top. There’s a trigger for the system to build muscle protein.

Kali Dayton 19:33
And preserve it, correct?

Jeroen Molinger 19:35
And preserve it. Correct. To maintain it. Yeah. You cannot do with just one you cannot do just only exercise. You can do only protein because that’s going to work. You have building blocks, but you have no people who can build it. And you can of course have a trigger for anabolic when you have not the building blocks. You can’t build anything.

Which is also fascinating to me because we talk a lot about personalizing and optimizing care for each patient and their individual needs. So, doing mobility as far as what they can tolerate what they’re able to do, as quick as they can do it. But I feel it’s silly that I hadn’t discussed nutrition more promptly, because apparently this is a really big deal.

Absolutely, yeah.

Kali Dayton 20:17
And so when patients don’t have, well, first of all- when do you recommend starting nutrition? Because I think sometimes patients can sit in our ICUs for days without getting nutrition started. And one of the first things that we do in the “Awake and walkign ICU” is we drop the feeding tube as soon as someone’s intubated, or even often on high flow, and we start nutrition. But what would you recommend from a nutrition standpoint as far as promptly starting here?

Jeroen Molinger 20:40
Yeah, there are two, I think two very, is very important points. You mentioned here, a point you mentioned here, one of the points is seen as the constant frustration that dietitians. Also I’m seeing when people going from the ICU to the floor, is that people tend to think that their tube feed is not necessary again if they have any potential in eating themselves.

There is a large study done is the starvation trial in the…. just after the second world war, here in the US. For a specific population of people that were healthy volunteers that were giving up to say what starvation does to your system. They were being starved, I think around I’m not sure exactly the numbers, I think, even not that low, but 1000 kilograms for three months.

To see how that specific phenotype and then the men and then after a few months, they are going to eat again. And they looked up, what is the nutritional needs to get the normal metabolic and muscle health back again, before they get the starvation for three months. They needed around more than the double of the need for a year, to go back what they were three months before.

Kali Dayton 21:54
So they needed twice as much food for a year….

Jeroen Molinger 21:57
But you can never ever eat that. You cannot ask for a patient on the floor, kust getting off the ICU, was able to eat and have half a potato to think, “Alright, we’re there. Because you can eat.”- No, never, ever. Maybe even maybe even in the home kind of environment you started to put it.

Well, now that makes me think about how quickly I’ve had feeding tubes removed on patients after they’re extubated. And once they pass a small without how quickly we remove it. Because no one wants a feeding tube, it’s so uncomfortable, it’s annoying, and it’s a sign of progress. So you’re excited to get it out for the way you just want them to feel free.

Absolutely, I would definitely get it to keep it there. And kind of the cool thing that you can do with it, you can give bolus. So if you’re looking at athletes, there is a kind of an anabolic window when you’re doing your mobilization when a muscle is the most sensitive in gaining muscle protein synthesis. That’s just after your exercise 45 minutes if you exercise if you then give them a specific high protein bolus, that is the reason why the muscle is triggered.

And being anabolic triggered and gaining muscle mass. So make that that window work for you in using the specific bolus feeding. Because, again, going back to the nutrition tube feeds, it’s kind of weird that people are doing 24 hour dribble into your stomach of feeds. It’s ridiculous.

And we talked about this before. We love our jujunal tubes. Yeah, that makes us feel better. Like they’re not going to aspirate. So how safe is it to feed patients, especially in the prone gastrically? What have studies shown?

Yeah, you know, also a good question. I think that’s also one of the kind of the paradigm still needs to be needs to be needs to be very well cleared up. Right now. There is no evidence that you have stomach issues or high secretion or a no…. not at all.

Kali Dayton 23:57
No aspiration?

Jeroen Molinger 23:58
No aspiration at all. Because the thing is, when you’re looking at the stomach works….. Also, again, from an exercise perspective, the stomach works the stomach emptying works, not with droplets. Emptying works when you have a 200 mls coming to your stomach just to trigger the stomach to be to empty. Are you ready to a dropper? dropper? Then you get….

more gastroparesis?

Well, yeah, yeah.

Kali Dayton 24:24
And what about patients with GERD or undiagnosed esophogeal sphincter problems?

Jeroen Molinger 24:29
Yeah, good question. I think we I think it’s sometimes you just have to see our works and maybe it can, of course the bolus is also you can go from 50 mils to 200 mils, it’s it’s up to you and to see how it goes. Maybe you can have a kind of a graded kind of bolus to look how to how to look at a dose. As for now there are there is not clear evidence that it shows being having adverse effects at all.

There’s a big study I think done right now in the UK, by Daniel Baer from the CC PhD, it’s a dietitian PhD, as he showed already that there is no issue at all in doing a bolus. And I think right now as net only looking at safety from bolus perspective, I, the second step will be how can you integrate bolus feeding, with mobilization?

And again, going back to my first log on this, you have to treat your patients like athletes, right? So how can we somehow combine nutritional knowledge and mobilization knowledge or exercise knowledge and training knowledge for PT together? And then making sure you have the building blocks? That’s for the nutrition? And we have the anabolic trigger? This would be for PT and nourish to go.

And how much would that change outcomes?

I think it would change Immensely. Immensely.

What do we know about malnutrition in the ICU? And how that impacts outcomes when we are delaying feeding patients? We don’t feed them enough. We feed them too much. How does that impact?

We just the thing is right now, there we were, I think the it’s now becoming more and more of a science that we see because we were able there were not large trials, able to use the metabolic carts. Which we then show what what’s really there. What is the real need of a patient? Right now at Duke, we are we having a couple of trials running in COVID. We are starting also a clinical service using metabolic carts.

And then you see, because if you only use your equations, you don’t know, you have no clue if you’re using the right numbers, because you have no reference value where you can compare with, right? So and now we see that we don’t do a good job at all, because our equation doesn’t match up. Anyway. And you can ask yourself, “Okay, okay, what 500 calories, plus or minus? What does that do to the system? If I give somebody 1500 or 2000? What does it matter?”

I think it matters a lot. Mainly if you’re overfeeding patients. Underfeeding, of course is on a muscle wasting perspective and issue. Overfeeding is an issue, just based on your co2. If you have a larger sheet to breathe out, you have a larger driven co2 ventilation. So from a ventilator perspective, that’s not good. Because you’re having a very high respiratory drive.

Kali Dayton 27:09
Right.

Jeroen Molinger 27:10
You don’t want to have a patient when you already have a specific issues with diaphragmatic dysfunction of other stuff. You want to make sure there is not a very high respiratory drive over there. So you have to keep the co2 levels low. Because they also have not the ability to force the co2 out through the breath, right? So there is definitely a need for not underfeeding or overfeeding a patient.

But part of outcomes, I think, the only way to really look into it is that there are now new devices coming into the market that are very easy to be used can be used sideways to the ventilator. And those numbers coming out right now. And that shows that that we’re not doing a very good job at all at using the equations.

And we’re not doing a good job using the equations or the equations aren’t appropriate for our patients.

Sorry, yeah, the equations are not appropriate right now. They are not very appropriate for the issue space. There are some that are matching up a little bit. But again, one of the things you cannot use, you cannot utilize, you can come up with the equations is number of RQ, or the RER numbrer.

That’s the equation number, that’s a number that is a ratio between your Vo2 and Vc02. So let’s say, kind of a proxy of your substitutions. So if you have larger than 0.85, then you are more in carbohydrates, or you’re smaller than 0.8, then you’re more in the lipids and more in the protein kind of usage.

So that gave rise and that is one of the things on the articles right now we are submitting that the our RER number is also predictive of a length of stay. So if you’re on admission, or your first measurement after your intubation is already predictive of your outcome.

So if you have…. if the first day of intubation and you show in high RER number, so you show a very high carbohydrate utilization number, or you show a low number. More lipids than in the first step, you’re more willing, you’re having a lower length of stay. It’s kind of a weird thing, because in our ward patients, it’s the other way around.

So if you’re not in the ICU is the other way around. When you have a low RER number, so you have no high ability to utilize fat’s in rest. That’s a good thing. In the ICU, first day after ventilation, that’s a different story, because we’ll be seeing is one of the first things that happens is insulin resistance. And insulin resistance goes instantly into an inability to utilize carbohydrates. If you can overcome that resistance, you can still utilize carbohydrates and you packaged very well. So that makes a high RER number, and that shows a more efficient kind of metabolic profile. You’re able to switch very easily to carbohydrates.

You mentioned last episode, the propofol contributes to insulin resistance.

Yeah. From a mitochondrial function perspective, that’s one way, but also the lipids.

So when we have patients on high dose of propofol, or any propofol period, how could that impact their nutritional needs?

We’re seeing that there is a potential…. what we’re seeing is there’s a shift of substrates. So you see an inability to utilize fats anymore. But it’s kind of weird, because propofol is also full of lipids. So you’re also feeding them or lipid somewhere, it’s not a feeding that you’re giving, but just the medium in which propofol is built on. But also you have a issue that for mitochondrial level, the respiration is just lower, so you have a lower ability to extract oxygen for mitochondrial level.

So and again, we are just starting off to see that somehow evolves, because it’s not on everyone.

Kali Dayton 31:03
Right,

Jeroen Molinger 31:04
…and there is some specific and…. there’s always the hardest part doing clinical research in the ICU space, is that in ARDS, sepsis, and COVID patients, we don’t have any reference stories of them before. We’re seeing them upon admission. That’s that’s our first potential measurement.

…and oftentimes they come malnourished at baseline.

Yeah, yeah, there’s a lot of stuff that you just don’t know, if we have… and that’s stuff we’re doing right now. If you have a unique cardiothoracic ICU, or you have the surgery ICU when you have patients that already have elective surgery. So you already have potential assessment before the surgery, then you have comparison datasets.

We’re still looking at our trauma surgery patients, because those are numbers, our F traumas from from from car crashes, or from from gunshots. Then we have patients who are very young, which we know they should have have a very or not very bad metabolic profile, right. So then we can follow that up in the ICU and see how that goes. But that are very specific. Those are from gunshots, open belly victims, so they are having open belly in the ICU. That’s a whole other story, because you have issues with the dynamics and fluid dynamics in a stomach.

That gives rise to all different kinds of variables. But still, again, we have to have a better understanding in how Metabolic profiling is changing over time, in each specific population in the ICU, and driven on that specific outcomes given than their metabolic needs, nutritional needs, and the ability or inability to exercise. Because I think you can always exercise but the next question will be can we can we tailor exercise? Is is just walking? Should we walk and rest and walk?

There’s another kind of protocols you can think about and how should we deal with this? What is the outcome? And we can see this specific patient is more responsive to training and nutrition than this one is. Can you talk about…. we know in the in the event world we have overreaching and overtraining. Can you do? For my atomic perspective, in a patient who has very poor autonomic function? If you’re in the ICU, how much can you stress a patient out? And can we define how much you can stress a patient? Is it intensity? Is it volume? Or is it combined? Is it rest or non rest?

So there’s a lot of stuff which we already knew already using in our athletes, which somehow has to come back to our patients. But it still has to be driven by objective measurements and mainly by non invasive ones using sensor data. And that’s what we’re doing right now, we have a lot of sensor data here, which we can measuring perfusion we can measure in oxidation, profile of patients, in rest and also doing exercises you know.

So we try and have a far better insight in that as a number and when we do a electrometry measurement in a patient on day three where we have a 2500 kcals a day number more, what are the trends? How does the Vo2 trends over time? What does the VC02 trend over time? When you add on next to the metabolic cards also imaging. Right now we have the ability to use ultrasound on the bedside- point of care ultrasound. We began measuring muscle mass, we can measure in body composition, we can measuring the amount of glycogen in the muscle, we can measuring the amount of fat infiltration inside the muscle- just using non invasive point of care portable ultrasound devices

I think next episode we’re gonna have to dive into that big time because that is complete news to me but credibly interesting and I think it will be very valuable. It sounds like the future of critical care.

Oh, absolutely. I think one of the worst my always says and I think I think agreeing with everyone the stethoscope for the for the physicians is right now then the ultrasound probe for dieticians, because why dietitians struggle with right now and even also Pts, I think, struggle with is: how do I define my outcomes?

I know the mobilization is, is good. But how good is it? When is it good? When is it not good? When should I change it? And the same with nutrition? We don’t have any specifics where we can on a day by day basis, on the bedside, noninvasive, assess a patient, and based on those assessments, tailor our specific needs for this patient,

Kali Dayton 35:39
Right? We titrate all sorts of things in the ICU. Except for nutrition. I mean, we titrate their rate, so not always dependent on exactly what they specifically need. Well, as I said, we’re gonna dive into how we can better utilize dietitians, physical therapists and our upcoming technology.

Jeroen Molinger 35:56
Absolutely,

Kali Dayton 35:56
Jeroen, thank you so much for bringing in the muscles into our multiorgan picture of the ICU. Thanks so much. Talk to you next time.

Transcribed by https://otter.ai

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