Well, thank you. It's a privilege to be here and to be presenting after all those great presentations. I'm going to try to hit some of the things that we haven't done and try to de-emphasize some of the things in my slides that we've already covered. So, these are my disclosures. So, what are we going to talk about today? Well, I want to talk about, you know, how do we monitor, why are we monitoring, and what are we looking for when we're feeding our internal patients? And so, you know, is the internal nutrition tolerated? To Dr. Patel's point, is it safe? I'm not doing, is it efficacious as much? Hopefully, we kind of believe in it if we're monitoring it this aggressively. And then, is it dosed appropriately? So, we're going to talk about both what to monitor and some of the evidence about what not to monitor. And I really want to emphasize some of the basics to start. So, I really want to emphasize the abdominal exam. You know, that's not as well, you know, yes, we write a daily progress note, yes, we put an abdominal exam in, but it's not often part of these discussions. And so, is the abdomen distended? Is it tympanic? And then, you know, the GI symptoms, what are the bowel movements? Is there frequency? What's the consistency of it? You know, and then certainly, is there nausea and vomiting? At my hospital, we often, the charting will say times one. Well, you know, did they spit up a little? Was it a big MSS event? I don't know. So, how can we monitor that more closely? I want to share with you, this is a schematic called the iFeed scoring system. It actually comes from the surgical literature. It's not specifically really about critical care, but I think it gives us a framework for how to think about this. And it's really, this is for orally fed patients thinking about when is it safe to feed. And it basically scores and takes into multiple accounts what, you know, are they already taking something? Are they feeling nauseated? Is it responsive to the treatment or is it refractory to the odansetron or whatever treatment you're doing? Is there MSS? Is it low volume? Is it bilious? Is it not bilious? Are they distended? And how long have they been ill? And so, they schematic it out into kind of normal or is there intolerance or is there true dysfunction? And I think, well, it's not validated for critical care. I see some ICU correlates in this. So, you know, clearly if you're a green light, advanced to full feeds, we're good to go. If we're in that yellow zone, a bit infant tolerance, that's kind of caution. You know, while it might be that's the person getting clear liquids if they're on oral, if it's enteral, that may be the one I'm holding at the trophic rate. I'm thinking about what else can I do? Add a promotility agent or move to post-pyloric feeding, something like that. And then, if we're in that high risk group, then, yeah, we're going to have to hold off. We're going to have to think about whether we need PN, whether the timing is going to be appropriate. I think that a lot of this slide has already been kind of covered, but certainly I want to individualize these decisions. You know, what does the GI tract look like? I think that feels, feeds into a lot of it. You know, what is the blood flow looking like? How is the liver functioning? The splanchnic blood flow? I think those are all key points. And we also talked about the mitochondria already. So, to the extent that we can think about those things, I would also mention specifically gut hypoxia, the upregulation of hypoxia-inducing factor one, HIF-1, that decreases the sodium and glucose co-transporter expression, decreases amino acid transport activity as well. So, you know, I think that the bottom line though is that if oxygen is lacking, our energy production is lacking, and it's a dangerous situation. Our nutrient may not be absorbed. It may not be effective. And so, these are where I want to be cautious. Now, everybody else has shown great evidence today. You're going to get a little bit of opinion from me. People always ask me, what is the cutoff for vasopressors? And I'm never able to answer that question. The folks that work with me, they all want me to give them a dose, you know. One, you know, whatever, point whatever, no feeding. It doesn't work like that. And I think that for me, I'm often looking for downtrending of lactate levels. I'm looking for downtrending of liver function test as two kind of key correlates of, you know, is there, you know, a certain, or sorry, normalization of lactate, not downtrending. Essentially, have we shifted completely away from anaerobic metabolism? If there is ongoing tissue hypoxia somewhere in the body causing an elevated lactate, certainly that concerns me in the context of mineral feeding. So, what else am I thinking about? Well, I'm thinking about refeeding syndrome and the risk for this. If you aren't familiar with this paper, I would refer you to the Aspen 2020 Refeeding Syndrome Consensus Statement. It's a very helpful document. It identifies both moderate and significant risk criteria and lays out kind of tables of essentially, you know, mostly severely malnourished patients are gonna be high risk, moderate, less so. And it helps us guide at which patients might be at risk for refeeding syndrome. And then, in the paper, I'm not gonna go through it in detail here, it spells out some of the practices of how we would intervene and minimize that risk in basic summary. You know, starting at a low rate, monitoring our electrolytes closely, advancing slowly, and I'd refer you to that paper for more detail. We also, I think, have really done a nice job talking about the assessment of energy expenditure using indirect calorimetry. And just, I would point out, we're really only about 30% of the time probably on target. So, I think there's a lot of opportunity here. And when we're looking at our predictive equations, you know, we need to be continuously assessing our patients. Now, we don't have good guidelines for how often would we be doing this. Do we do this twice a week? Do we do this once a week? You know, the short answer is how often to do indirect calorimetry is an object of ongoing question. I think that this is a slide showing us how our predictive equations are particularly ineffective in obese patients. And while the Penn State modified equation that already came up probably has some of the best success, these are patients where we often are way off track. So, Aspen SCCM Guidelines 2016 recommended the use of indirect calorimetry. I needed to, for my organization, we really needed to come up with something kind of practical so we knew which patients are we going to do it on. We did not have the resource to do it everywhere. And so, we do it typically in patients who we think are going to be in the ICU more than seven days. So, we think that internal feeding is going to be continuing longer. We do it for the severe TBIs. We do it for the extremes of BMI, less than 20, greater than 40. We do it for the open abdomens, those who are on multiple vasopressors. And those, this one is a little bit up in the air, but, or a little undefined, but where we think they're going to be on internal nutrition long term. So, I would say that certainly somebody who's going to leave the ICU probably still on internal nutrition, maybe we don't expect them to recover the ability to take an oral diet. What about, you know, I talked about the abdominal exam as being one of the basics. I think this, I have a, would call on all of us to come back and really work on our input and output records. You know, too often, our tube feed pumps, you know, we set the rate, let's say 55 an hour, and then I just see in the INO chart, every hour they rate 55, 55, 55, as if it's, we all know that's not really happening. So, at our place, we, you know, we've got the tube feed interruptions, but we have a process where we clear the pump. So, just like often with IVs, at least that's what they call it locally, we clear the pump. So, actually, at the end of the shift, you're supposed to push the button on the pump, it'll tell you how much was infused, and since it was last cleared or reset, and write that number down. So, we have a true intake number. And of course, focus on minimizing the interruptions. And we're going to talk a little bit more about GRVs, but certainly try to minimize the use of those as one of your strategies. And I also want to talk, because I think it's kind of an orphan topic, protecting our interval access. So, we're going to talk about that a little bit. What about feeding strategies, if you're not hitting your target? So, one thing that we're doing is volume-based feeding. So, I don't know what the familiarity of the room is with it, but essentially, instead of saying an hourly goal rate, we're doing a protocol where we've set a goal rate for the day. So, this patient needs 1,500 milliliters of internal feeds in the next 24 hours, and we give the nurses empowerment and discretion to turn up the rate. So, if there's an interruption in the tube feeding for an hour, they go back and they recalculate, and they say, we've got 12 more hours to get in a liter, and then they recalculate their rate based on that. And so, that's been shown in multiple trials, both multiple randomized control trials and single-center applications to effectively increase calorie and protein delivery with typically no change in outcomes, no increase in nausea or vomiting. Typically, essentially, you're going to have periods where the rate is going a little higher to play catch-up. My experience primarily with this, where it's been super successful, was in a burn intensive care unit, but it's also part of our trauma care protocol. What about muscle? We've talked about that a little bit today, and I think ideally in the future we're going to be doing some monitoring. This is my food pun for the day. So, we want to better characterize the muscle of our patients. Just like we would grade a steak, we can grade the quality of the muscle in our patient. And so, just briefly, this on the left is a patient with a BMI of 25. He was a healthy CrossFit athlete. He had appendicitis, really muscular guy. It was actually really hard to operate on him because it was hard to even get into the abdomen. The next patient, bowel obstruction, BMI of 18, CD4 count in the 50s. We see very little muscle. I lost my pointer. But anyway, very little muscle, very kind of slit-like psoas muscles. The rectus muscles are there, but they're not well-defined. And then over here on the right, this is a woman with a BMI of 58 who was in a motor vehicle crash. All these patients came to me within about a month of each other. And look, her, while she has all the muscles, a lot of intramuscular fat. So, just, you know, we want to be the select cut of beef, not the prime cut. Sadly, I'm more on the prime side. But anyway, so how can we monitor this on a daily basis? Well, or not a daily, but regular in the ICU. Well, certainly a CT scan's great if we're getting frequent CTs. I think a lot of cancer research is really being pushed forward by this because there's a lot of serial CT imaging for staging and monitoring of cancer. But for our ICU patients, musculoskeletal ultrasound, and to some extent, there's a lot of interest in BIA, impedance analysis. But unfortunately, that's affected a lot by volume status. So also probably more relevant in standard hospital patients, but not so much in the ICU, although it's of interest. This paper, I just added it, it came out this month. It's a large meta-analysis, 52 trials, near over 3,000 patients. 85% of the time they were doing ultrasound measures, and they saw by ICU day 10, they had lost about 20% of their muscle mass. They were looking at rectus femoris, quadriceps, and biceps, like I said, primarily with ultrasound. So a nice paper to kind of summarize a lot of the recent data. My experience with ultrasound has been a little more mixed. When I took the medical students into the lab and we all learned how to do it, we were great. We could reproduce it on our standardized patients. But in the ICU environment, I've had trouble getting good reproducibility because of obesity, because of an edema, intramuscular fluid, variability in the compression that's applied with the ultrasound probe. So there's a lot to be worked out. I think that we're going to get better and better. And certainly, you know, I showed you those studies as well as these two. I mean, there's a lot of predictive value in the use of ultrasound. You know, right now I think we're more at the correlation stage, but we haven't been able to show a lot of impact of intervention, and hopefully we will in the future. Now certainly, while I just would kind of tickle the idea, you know, exercise I think is a key part of this story too, because we can only do so much to maintain muscle mass with protein delivery, but we also need to use the muscle, whether it's by active, you know, strategies or even passive strategies to use muscle. So I think, you know, continuing to be a lot in that arena. So I mentioned that I wanted to talk about monitoring the access. So, you know, do we have an adequate, appropriate flushing protocol in effect? Are we taking some precautions not to be flushing a medication that, for example, can't really be well-dissolved, can't be crushed effectively? You know, start talking to the nurses about what you might be using in your ICU that they have trouble dissolving, and maybe that might be the med that we need to look for an oral alternative, or sorry, a liquid alternative to, or some other strategy. And then also work on getting the team really comfortable with what the protocol is to save a tube if it clocks. You know, I don't want to hear about it the next day that it's been clogged all night. I need people to know what to do in the moment when it's clogging. Look at the tubes daily. Have a tube feeding declogging or tube declogging protocol. There's evidence out there that the mixture of pancreal lipase with bicarbonate is the most effective strategy. I've got the reference there for you for one way of doing it, to open the capsule of the creon, get the granules broken up, dissolved in bicarb, and that's how we do it, and it works pretty well. So, I'm frozen. Oh, there we go. You know, I mentioned, look at the access site. You know, how is the skin? Is the nose breaking down? Sometimes it's just re-taping or, you know, revising the bridal device, making sure it's not too tight around the septum. So, we want to take care of the skin. It's really a tragedy in the ICU if we lose our internal access because I can no longer have access to the nose because the wound care team is working on the ulcer that we gave them. So, we want to prevent our pulling, so particularly our G-tubes, our PEG tubes. You know, you may have some of these activity aprons, something that people can fidget with, so they won't fidget with their tube. That's another thing to do. So, for those of you who might not place internal tubes, you may be surprised to know that looser tubes are often better. We often see PEG tubes that are too tight. The skin, you know, we may see instances where they actually keep over-tightening the tube because, you know, it looks kind of loose. It looks kind of floppy. Maybe I should tighten it up. But that actually contributes to a wound. There's data going back, pretty old data, that a long, loose PEG tube track where it's mobile is associated with fewer complications than a tight PEG tube track. It's kind of counterintuitive because when you put a fresh PEG tube in, you'd think you'd want to kind of sandwich things together to get them to heal, but that's not the case. And what happens is, if the tube is over-tightened, you get both ulceration on the inside of the stomach, ulceration on the skin, and you can get what's called a buried bumper syndrome where the tube has migrated into the abdominal wall and may result in bleeding, loss of access, or even a peritonitis event. Yeah, so did I cheat? I got two jokes in. So what's our, you know, what about the tube feed diarrhea? So we're monitoring it. You know, typically it's a situation where we've been pounding the patient with stool softeners and laxatives, and now here we are. We have diarrhea. So step one, look at what we're doing. Make sure we stop all the stuff that's causing diarrhea. Then, this is just kind of my algorithm based on the guidelines, you know, make sure it's not an infectious cause. We can, you know, we may need to work that up. You could consider changing to a semi-alimental feed. If you think that that's going to help get a hydrolyzed protein, it'll be better absorbed, even though our standard recommendation is for the non-hydrolyzed. What about adding fiber? So there's evidence that adding a soluble fiber, you know, we could get a, it ferments into short-chain fatty acids. There's co-transport with water, and several trials that in the ICU setting that have shown reduced diarrhea output. And then finally, think about our antibiotics. Of course, we're all trying to do antibiotic stewardship, so, but certainly if there is an antibiotic that's not appropriate, let's stop it. And then the use of probiotics. So we talked a great talk about the microbiome earlier, and many people are surprised to see that there's grade A consensus data going back to 2005 for recommending either Saccharomyces boulardii or Lactobacillus GG for the reduction of antibiotic-associated diarrhea. In the final moments here, also exocrine pancreatic insufficiency. This is an emerging thing. You know, certainly we know that patients with pancreatitis or chronic pancreatitis or post-pancreatic surgery may be at risk, but this is a study from China published in 2013 that didn't necessarily get widely circulated, but they looked at over 500 patients, found that about 50% of their ICU patients, it was a pretty sick population, had low fecal elastase levels, 18% of which were severe, and those correlated with shock, sepsis, post-cardiac arrest, lactic acidosis, things like that. So certainly something also to be aware of, especially if there's signs of steatorrhea. In the final moment, what not to monitor? Well, I mentioned GRVs. So do they matter? So, you know, this is kind of the paper that changed it all, 2013 JAMA. They, using GRVs versus no GRVs, well look, intolerance went up because more patients vomited or had their tube feeds interrupted. Vomiting went up significantly. In a way, I would argue that's somewhat clinically significant. I mean, I don't want to be vomiting, but at the end of the day, the pneumonia rates were not statistically up. The delivering calories were the same. The mortality was the same. So no significant change in the outcomes when they eliminated residuals. So over the years, there's been kind of a creep, and if we are going to do residuals, what would that cutoff be? And so whether you thought it was going to be 200, 250, 400, now the last real big trial from Montejo in Spain, 500, still, despite raising that threshold to 500, complications were less. Volume delivery was better. So, you know, I think we have good evidence that if we're going to do it, let's do 500. Well, why are we doing it? Well, we're trying to prevent aspiration. Interestingly, aspiration is quite common. There's data looking for markers. So every four hours, they suction the tracheal aspirate. They put microspheres in the tube feed. Twenty-two percent of the time on any single suction of the airway, they found a microsphere. So there was some evidence that something from the tube feeds had gone into the lungs. Likewise, 31 percent of the time, there was some pepsin in the lung. So aspiration is occurring, like, all the time. And over three-quarters of the patients at some point during their ICU stay got some, had some aspiration. But is it clinically significant? So that's our key point there. And we don't recommend using blue dye. I'm now a minute over, so I'm going to wrap it up. But modifying our risk, of course, we know the standard strategies. I'll just share with you kind of my approach to it. Some of this is evidence-based. Some of it's more Gestalt-based. But if I get GRVs above 250, I start, or demonstrate a nausea or vomiting, not that I'm looking for the GRVs, but the nurses are happy to report them to me. You know, or if we have some other reason we suspect delayed gastric emptying, I start thinking about a pro-kinetic agent or going post-pyloric. And then I've kind of got my risk there, kind of a feel for if I have a higher-risk patient. You know, maybe it's that they have high vent settings, that an aspiration event is going to kill them. Maybe it's that they have low GSCS, so they're probably not going to protect their airway. Or they came in, we already knew they had dysphagia, or they have a chronic neurodevelopmental disease. Or my favorite is when they let me know that the secretions look like tube feeds. And I never know what to do with that. But I think, you know, these are patients where we need to do something different, intervene before it's too late. So Reglan, certainly it's effective. Multiple meta-analyses have showed it's beneficial. If you're worried about prolonged QT, spread the infusion out to 30 minutes rather than a push. And that's been shown to reduce the risk of arrhythmia. The Synergy Erythromycin plus metoclopramide is more effective than either alone, so don't be afraid to use both. In the final moment, another thing not to monitor. Albumin and prealbumin. Please don't call them the nutrition labs anymore. I get that so often. So what is going on? So when there's inflammation, interleukin-6 upregulates the liver. The production of the liver shifts away from the standard things like albumin and prealbumin and toward inflammatory things. C-reactive protein complement, serum albumin proteins, and so fibrinogen. So that shift is key, and that's why those drop. So we know that they decline. They also go out into that third space, where they actually function as an antioxidant. So where does that leave us? Well, they're markers of nutrition risk. They tell us, hey, these patients are sicker. Now we're, of course, struggling with, are these people that need more protein, like Dr. Harabi talked about? We need to figure that out. But certainly nutrition risk is probably an important predictor. We also know that these correlate directly with Apache scores. So as those levels are falling, Apache scores are rising. This is kind of a confusing graph, but that's what that means. But what do they tell us? Why would we ever monitor them? Well, normalization probably means that inflammation is better, the nutrition risk is down, maybe our patients transition to anabolism. All of these are kind of questions yet to be answered. And we know that as the albumin goes up, the CRP goes down. It's a beautiful relationship, very clear. And we know also that delivering extra feeding does not treat the prealbumin levels. So another reason that it's not the nutrition lab that we so often have treated it. So with that, I thank you for attending. I'm excited to hear your questions and discussion.

internal nutrition

ICU patients

iFeed scoring system

abdominal exams

muscle mass monitoring

tube feed diarrhea