Intestinal Rehabilitation Webinar

Hello everyone. Hi, Doctors Michael Hamrath and Paul Wales. How are you? Hello, hello. Hello, good. Welcome everyone to the first webinar in intestinal rehabilitation with these two experts from Cincinnati Children's Hospital. Before we start, I'm going to say a few things. First of all, uh, we are going to discuss a case study, so. We have the case study in a button that it's in the left of your screen that says case study, so if you wanna read it again, you can press there. Um, it's going to be on for the whole webinar, so press it as many times as you want. Also, this is, uh, the idea is, is an interactive event, so we'll have the chat box. Please ask as many questions as you want, we are going to address them along the way, so please write, interact with us, we love that. And um finally, we are going to have a break at 3:50 p.m. so we can stretch our legs, grab some water, go to the restrooms, and then we'll come back with more about this webinar, OK? So now, I'm going to present or two experts of the day, we have Doctor Paul Wales. He's the actual surgical director of the Intentional Rehabilitation Center here at Cincinnati Children's, and Doctor Michael Hamrath, that he is the director of surgical Research. He's the director of the Center for Stem Cells and Organoid Medicine and the Center of Bariatric Research and Innovation also here at Cincinnati Children's. So, I'll let you do it, and everyone have fun and remember to write questions in the chat box. Well, welcome everybody. Um, Doctor Helmroth and I are very happy to be doing this today. Um, uh, what we thought we would do is start the day off by presenting a case and let the case act as the framework for, um, for the rest of this discussion. We can get into specifics about medical and, and surgical management and just global care of these patients in the context of a, of a, an actual patient. So, what I, what I'll start off with is just a very brief uh summary of a case that uh hopefully, you can see on your screen. And then that'll help, that'll initiate the conversation. So, Uh, this is, uh, actually a, a, a real case that had come to our center not that long ago. This is a, an 8 month old male that was born at term, who unfortunately suffered an intestinal, uh, volvulus, um, that was initially managed somewhere else and came to our center at 8 months for a second opinion regarding their care. Um, so, at birth, uh, the patient, uh, you know, he suffered, uh, evidence of abdominal, uh, distention and, uh, a neonatal bowel obstruction that required an emergency exploratory laparotomy, and a mid-gut volvulus was encountered. And, uh, the patient had a lads procedure and a resection. And unfortunately, lost a significant amount of, of small bowel, leaving 14 centimeters of jejunum. And uh the rest of the distal small bowel, cecum, and right colon were also removed. Uh, the baby was stable enough, it sounds like, at that first operation to tolerate reanastomosis. So had the 14 centimeters of jejunum anastomosis to the hepatic flexure, putting the bowel in continuity. By the time that we saw the patient, uh, at 8 months of age, this child was on, on parenteral nutrition for 22 hours a day, uh, receiving uh uh mixed composite lipid emulsion, uh, 3 days a week, averaging about 1.3 g per kilo of fat, 3 g per kilo of protein with, uh, glucose infusion rate of around 12, for total of about 115 mL per kilo and 78 calories per kilo. Enterally, the baby really wasn't tolerating anything by mouth at all and was uh receiving a small amount of elf-ammino uh formula through a G tube, uh, regular strength at 3 mLs an hour, uh, providing about 10 mLs per kilo per day and 6.8 calories per kilo per day. The child, uh, from a growth perspective was well below the 3rd percentile for both age and height. Um, And uh IV access had been established through a double lumen central venous catheter that was in the right femoral vein that was placed at the time of the original surgery. Patient had had one infectious episode uh related to the Lyme and typically has about 10 watery bowel movements a day and, and had fairly extensive perineal rash. And the only, only medications that the patient was receiving at the time that we saw them was, uh, was on, uh, loperamide or Imodium liquid at a dose of 0.2 mg three times a day and was on continuous metronidazole. 6 mg twice a day. So that's, that's, um, that's the patient. Uh, please feel free to reference that slide. Yeah, you can get it off your screen if you just wanna you need to refresh your memory with specifics about the case. But we thought that we would use that as a guide for our discussion. So, so this, we commonly get called for patients to be evaluated here, uh. This child, correct, you met in the office, right? So this was a patient whose family sought care and was capable of driving to Cincinnati. I recognize around the different people watching this that, you know, we're US centric and can talk about things, um, and every institution is different. But I wanna highlight a couple of things just to start. Um, when we get called and it's an 8 month old, you have to put it in the context of knowing the natural history of a child that had, uh, an intestinal catastrophe, and to recognize whether they're on track or not. And if there's things that you can support the patient at their local institution, particularly, many of these kids come from a long distance away. And there's many factors that play into uh reasons we think children need to be seen at centers with more experience, um, particularly the younger infant where time really plays a big role in the outcome of patients. Uh, the first couple of years of life, particularly the first year of life, is extremely valuable. And the point I want to make to start is that it's often more difficult when a patient is at your institution for a long period of time and they're not progressing, um, to recognize that there are underlying issues that need to be evaluated, um, that are often not thought of or, or overinterpreted or misinterpreted. So, I think it's important. Uh, to take a step back and start at the beginning to highlight why we think this child needs to be under, uh, center care like we have here in Cincinnati, and, um, what we would expect a typical patient who, um, had a similar episode of intestinal damage to be doing at 8 month old, and how the management we might have provided might um be a little different. And trying to, uh, try to optimize what uh can be the long-term outcome. So I think the first thing that, that I want to talk about was the fact that the child was full term. And I want Paul to, to, to kind of discuss um what our expectations are for intestinal length, and, and how the, uh, the, the child's um age influences a lot of the decision-making that we have. So that's a good point. So the thing, one key thing to, to acknowledge is that Young infants, babies, infants, and young children have tremendous gut growth potential. The gut grows for the first several years of life. Um, and that's why when we're, we're talking about residual bowel, it's really important to talk about it, not in absolute centimeters, as I did in this case, 14 centimeters. It's to talk about it in relationship to what is normal for a child of that age. So, a term baby uh will have 160 centimeters of small bowel, and by the time you're 5 years old, it, it almost triples, about 425 to 450 centimeters. So, when we got the history that this baby was born at term and um was left with 14 centimeters, that's about 10% of expected uh gut length uh for age. I think, you know, an example of, of the importance of this concept is, let's pretend we had a patient that, that had, you know, um, resection of bowel, was left with, we was, we took out, uh, we left the baby with 80 centimeters, a term that would represent 50% of expected gut length. If the child was 30 weeks gestation, and we, we left the patient with 80 centimeters, that would represent 80% of expected gut length cause a 30-weeker has 100 centimeters. And for an older child, like 2 or 3 years of age, it's really gonna represent about 20 to 25%. So, that's why it's really important that we don't, we don't talk about centimeters in, in the context of young children. We talk about it as a percentage. And so, we have about 10% of expected gut length. And I had mentioned in the case that basically, the bowel was anastomos of the hepatic flexure, which essentially represents about 75% of residual colon. So, we have 10% of small bowel, 75% of colon. So, an important observation that you have to remember is that if this child was truly malrotated, The duodenum actually is often involved in the measurement, whereas obviously with normal rotation, it's not. And that actually can represent, you know, 10 centimeters. So, the children that are malrotated that are measured to the pylorus, you have to keep that into account because the Sturgis data that Paul just recognized is really to the ligament right, right, Paul? Right. We don't typically include the duodenum in, in, that's correct, in the residual bowel measurements. So, it may be that this patient actually had a little bit less um than 10%. Um, it is important though, uh, to, to unders to understand the residual anatomy because it really feeds into prognosis as well. So, not only gut length, um, and we can probably get into a little bit more about this, about prognosis, uh, of who's gonna achieve enteral autonomy or not. But gut length, you know, always comes up as the number one variable in any series that looks at prognosis for enteral autonomy. Um, but you can have as low as 10% expected gut length and still achieve enteral autonomy if you have the majority of your colon in continuity. Um, so, this patient has 75% um of their large bowel and a, and in a publication that came out, I guess about 5 years ago. Patients that would fall into that quadrant, if you will, of less than 50% small bowel, but more than 50% large bowel, all, all comers in that group would have about a 56% probability of achieving enteral autonomy. So, it's not hopeless for this patient, but, um, you know, the median time in that, in that data to achieve enteral autonomy was about 4 to 5 years. So, I think the message is, is that the child's gonna require parenteral support for a long period of time. There is hope of getting off TPN, but it just kinda goes to the point that the child's gonna need really good management to not only promote adaptation, but to mitigate the complications of long-term TPN. So, one factor most people don't consider, but I believe is extremely important, is the fact that in a volvulus, especially a full-term child, usually, that child has been fed. The ability to have been fed initially at birth does a lot to promote the way our motility and our maturation processes occur in the GI tract. And so, unlike most vuluses, however, this baby's uh event occurred in utero. Um, and so, therefore, this baby's never been fed. When you look at the complic, the, the things leading to intestinal failure, Interestingly, the diagnosis that probably has the best prognosis with the least amount of bowel is neck. And neck is often, as you all know, happening after uh feeds have been initiated in the 2nd, 3rd week. Um, and we often see children with very small amounts of intestine. In neck that actually go on and do tremendously well, especially compared to others. Whereas in contrast, perhaps a kid with gastroschisis has more bowel, but those kids can do poorly, and certainly, the kids with gastroschisis and atresia fit into this really complicated, uh, you know, mixture. That is very different than the volvulus that happened in a baby that was, let's say, you know, 6 weeks old at, at home who comes in emergently. So, you really have to put into context the timing of when that, that does, and that's why you can't just call these kids shortcut. You have to remember what the etiology was and when it occurred, right. So, to, to add to that, the, you know, so the, the, you know, the factors associated with being able to, you know, achieve ventral autonomy, yes. Gut length is always an important variable. But as Doctor Helmras alluding to, the, the functional capacity, the underlying diagnosis of the bowel that remains often is, is also critically important. I mean, you, you know, you have, we all have patients that they may actually have the majority of their GI tract, but it just doesn't work very well. Um, So, other, other factors that are, that are involved, that are sort of important in addition to gut length and diagnosis, you know, age, we've discussed because of the impact of age on gut development. Um, the presence or absence of the ileocecal valve is often, lots of papers will quote the importance of the ICV. What do you think about that? So, to me, I believe the more important fact is the presence or absence of the distal small bowel or the ileum and even right colon. That can act as a reclamation of bile and get the inopathic circulation, as well as producing hormones and incretins like uh GLP-2 is in everyone's mind these days. But, you know, all the incretins, GLP-1 and, and even hormones like PYY are produced in the distal ileum that control motility and absorption of nutrients in the proximal bowel. And when they're lost, It's because the ileocecal valve is lost because that region was removed. And if you try to solely preserve an ileocecal valve in the face of not the best, uh, tissue, sometimes you end up causing more long-term problem. Problem. So, I think the, the thought of trying to preserve as much bowel and strategy to preserve predominantly the ileum as best you can, um, is something that we do, but it's not because of the ileocecal valve, it's because of, to me, the ileum, yeah. And then, uh, you know, added on to that is the colon and the, and the importance of the colon and continuity. And the colon has, you know, unique contributions. And, you know, if you've got a longer small bowel remnant, then, you know, the, a lot of the work is being done by the small bowel. But the shorter your small bowel remnant is, the colon takes on a much more important role. From a fluid absorption perspective, GLP2 um secretion. And the conversion of undigested carbohydrates into short chain fatty acids for energy salvage. So, the colon is really important. Um, to kinda touch on what you were sort of just alluding to, like, uh, as far as, you know, preserving bowel. So, Let's go back to, let's say this baby, the original, the original operation, yeah. So, the baby comes in, you know, the, you go to the operating room and you open the tummy and, and, you know, you find this disaster, you find this bowel that is, um, you know, ischemic, um, or, or has patchy necrosis, for instance. You know, and, and, you know, you're trying to, there's a general feeling to let's remove what's dead so that we can sort of reverse this septic response and get this baby better. But, uh, do you have any thoughts about that? Like, are there any other strategies? Did they do a primary anastomosis at birth? Yes. So, obviously, you know, we're mostly surgeons out there from what I can understand. You're gonna want us so healthy to healthy. So, you're gonna try to make sure that your edges are, are the best that they can. And recognizing little centimeters of bowel that you are trying to remove to get the best anastomosis have a lot of potential and certainly could be a lot in between. There's a few things that I think is important to remember. When the baby is first born, the GI tract hasn't colonized yet. And so, you know, in some situations like in a resia where you have a huge size mismatch, that's the time probably to tackle your anastomosis. I think it's, it's a safe, reasonable approach as long as the bowel is healthy. But it sounds like in this situation, the bowel wasn't healthy. And I think sometimes strategy at the first operation needs to be to be able to So, if the baby isn't an extremist, is to be able to provide a pathway forward that allows early interval feeding. And it's oftentimes, sometimes better to stage the idea that you're gonna put this back in continuity under more control that potentially allows you to salvage intestinal length that at the time, you aren't quite sure are is gonna survive. And here in Cincinnati, um, In a situation of overwhelming intestinal loss like here, um, the strategy for us is to, um, provide a control proximally that allows feeding to occur without the enteric stream going and to actually leave a lot of Questionable bowel later with the experience that many of that, many segments of bowel that are deemed to be non-usable actually in this population has a potential to heal and can really make a huge difference in the lifetime of this child, yeah. Uh, you know, the, the decisions that we make surgically at the beginning will have a lifelong impact on prognosis. And, um, I mean, uh, as Doctor Helmras saying, you know, it's, you know, we need source control. We need to control the proximal fecal flow. But if we can control that, divert that, and, and leave, even Islands of questionable bowel in there protected, a lot of that will come back. So people think this baby is gonna get really critically ill, and what we have found is that doesn't generally occur. So, common sense at the bedside is always required to make decisions, but trying to predict the future in intestinal failure tends to lead to increased loss of bowel. Um, and so, our recommendation here is And to you all is to consider maybe the fact the baby's stable, leaving in segments of bowel, um, with the idea that you're gonna go back at a later date. And because, as I mentioned, this child has never been fed, this was early and not colonized, um, you're gonna find that many of his bowel, even though you think it looks really sick, actually doesn't drive a process that leads this child to become, um, as dramatically ill as people would have predicted. OK. So, Why don't you tell the audience, I'll, I'll, I'll, I'll explain what we found in the OR, let's say, and you tell, you tell the audience what you would do in that context. So, uh, we're, we're operating on this baby and we find 14 centimeters, let's say it's 14 centimeters of, of jejunum that looks pink and healthy, um, after de-rotating the volvulus, and then we see. We see bowel that looks ischemic. There's some greenish areas, some areas that are patchy necrosis with, you know, some partial circumferential or even little islands of viable bowel of a few centimeters each, all the way down, uh, involving the rest of the small bowel, the cecum, and the ascending colon. And then everything else from the hepatic flexure onwards looks pink and healthy. So, so there's two things. You need to get proximal and distal approaches. So, if you're looking at 14 centimeters off of the stomach above, um, you all know that the output of a stoma there is gonna be quite challenging. And I believe that likely was in the consideration of the surgeon to do the anastomosis knowing that a proximal stoma is gonna be an issue. Um, What, what my thoughts would be at that point is that I wanna be able to provide this baby, a chance for early interval feeding. And I would, I would not typically want to place a stoma through the abdominal wall, um, in a baby because you're gonna lose a, a few centimeters at best, a bowel when you end up taking that back down. And, and managing the output can be quite challenging, and the complications of stomas can be quite hard. So what I typically would do is to place a retrograde tube. Into that jejunum and over sew it, so that it's controlled, and bring it out, um, and stand that up to the abdominal wall and bring it out um as a control bag. And we always talk about the best tube to do that with, and I can't tell you for sure what the best one is. The one I currently use is a Blake because it has multiple side, um, Creases that allow it to drain really well and less likely to get clogged like JP's can be. But the problem is, is that you can't pass a wire and change it later in interventional radiology if there are problems which seem to always happen. So, um, I do think that it's dealer's choice. I always put something in the stomach to be able to feed. Many times when the babies are, this is an older baby, but when they're really young and small, I will just put Uh, a feeding tube quickly through the, um, the skin into the stomach and just do a, a stem of the stomach up to the abdominal wall to get access. And often if there's intestine in a length, I will direct that tube out the pylorus and that can later be used as a way to start initiating feeds when the stomach doesn't empty and I'll use a, an NG repogo or similar to decompress the stomach. And so that allows the child to recover from surgery, resume, um, or start enteral feeds in a controlled way that doesn't require another procedure, um, and it gives you the time to wait. Now, the question about the distal bowel, given the way Paul described it, if I could do a target and I could put a tube in the distal bowel that would allow me to refeed, I would, but this doesn't sound like a situation where that's gonna be feasible. Um, if there are areas of necrosis, I might do a, a generalized repair, but not a very complicated one. Um, and, and I would park that bowel, and I would allow it to, um, to just have time to heal. And preferably, I would try to close the abdomen, um, primarily. Um, but I have a low threshold if I had to put an Alloderm in there. Um, If I felt like it was compromised. It doesn't sound like that would be this case. That tends to be more of the neck kid that has an overwhelming inflammatory situation and you don't feel like you can get the abdomen closed, um, safely. Um, and wound complications are more of an issue maybe in a neck kid than this kid would practically have. Um, um. Hi, um, here we have a question that if you can develop a little bit more, how you do the drainage, which one is better, and where do you place them, like to, to get a good drainage. That's a great question. Thanks for the first question. That was nice to have. So, you know, when you look at the abdomen. Um, remember, you never, I hate stomas in wounds, and I always like to place my drains, you know, in the bowel in a way that when we come back at surgery, that they're oriented. So, you know, in this situation where the bowel might be damaged, um, I don't like to mess with it a whole lot. And if I have tubes on both sides, I try to create them, um, you know, The bowel in the place that when we go back, they're set up where you don't have to go diving through everything and looking for them. That's more typically neck. Um, the refeeding tube is really nice because you can orient it and then you can, you can track it out away from a stoma or from another tube so that it can be managed at the bedside. So, when I look at the belly, there's gonna be a G tube. in the left upper quadrant. I probably have a transverse incision. This is gonna be a jejunal, uh, and it's often gonna be on the right side. And so it would probably be on the right side, and I would consider where it's gonna lie with my incision and where the, the, the, where I think the proximal edge of the bowel. The thing about the small bowel in this case is that what's gonna die mostly is the jejunum. The ileum actually gets retrograde blood supply from the ileocecal blood supply and will actually recover better, but I don't like to mess with it at all in the blood supply. So, I recognize in this case that Paul and I are gonna have to go back and find it, where in other cases, like an atresia, that was bad, I might be putting in another tube. And if I were to put that other tube in, it would probably go in on the left side. Reasonable to where the um incision is cause we're gonna use that for our second one. So, um there isn't a one. Thing, but you really wanna just think about your next surgery and set yourself up for success. And I think just thinking yourself through and like I said, the G tube, I'm not putting in a MICY or a formal G tube in a baby. It takes too long sometimes, but just a tube in the stomach, actually, the stomach heals and you can put a wire and dilate that to a G tube, actually in the NICU in most of the cases that we've ever done that. So, um, it doesn't really add. But a minute to the case. Um, and trying to do it later when everything is socked in often can be much more challenging, yeah. And it's a, it's a sort of line of thinking around, you, you don't have to get it all done in one operation, uh, especially for these kids with complex disease, complex anatomy. As Doctor Helmrath said earlier, you know, you want a roadmap for the future and a roadmap, a plan, and, and a realization that this may take more than one operation, and you're setting yourself up for the next stage. Um, So I think that's an important concept. It is. I think one of the things we always are learning and um one of the things that we found is that we were having issues with some wound complications in the NICU and that we would close our wounds in layers with typicallyvicro, um, And that you get some erythema, some redness, and, and whatnot. I think in the last year and a half, we just established doing some interrupted nylons and just putting a dressing on it here that has some erro form, which has some bismuth in it, um, and letting it be open to air. And, and wound complications are a major issue, and your point about where to put the tubes is a really good one, because When you have a stoma that gets necrosed, it prolapses, it retracts. You have an open wound that's been soiled with, um, with stool, um, it becomes a misery, and every one of us has lived that misery. The tubes, proximately, um, really control the skin extremely well. They, babies could easily be fed with a tube in the proximal jejunum. It's not gonna clog. Um, you're not gonna have the skin breakdown. You're not gonna lose the bowel by taking it off the abdominal wall. You're not gonna lose the abdominal wall musculature by making the stoma. Um, it has a lot of advantages to it that, um, That I think you should think about when it's proximal, when it becomes more a mid-small bowel distal stoma is the logical choice, um, but, uh, certainly at 14 centimeters in a non-rotated child, I would be putting a tube and I wouldn't be making a stoma because the other consideration there is, you know, and we've all experienced it, you know, you've got a patient with a stoma that's leaking and, um, skin is breaking down, and that might be forcing your hand. Uh, to have to do something surgically to revise or to re-operate maybe before you had intended or wanted to. Uh, so the tube approach really does work very nicely. Yeah, and, and even the interrupted nylons, um, avoids, and putting these kids back on antibiotics also is a setback. So, um, it, it has proven to be better than I even appreciated at the beginning. Um, it's a neat trick. So, um, before we move on from this sort of extensive necrosis thing, I just wanted to bring up the concept of the ethical consideration of this, right? Um, you know, I remember as a fellow, Um, Back in 1999, operating on babies in the middle of the night, and I know that there were babies that we probably opened and closed at that time that we probably would not do that now. Um, and this sort of ethical issue around the, what do you do in the setting of pannecrosis? And, um, is it the right thing to do, to resect and proceed, or should you move in the direction of comfort. So, I think that, that's a, Something that's important to just talk about. It is, and I mean, now we have the hindsight of having multiple children who present in those scenarios that are now running up and hugging us in clinic, um, to have the, the courage to know that the patient really should be the one driving the decision and not the, not the, the prediction of the NICU or the surgeon or other, um. Meaning that there are kids that have overwhelming gram-negative sepsis and, and they're gonna pass. I'm not sure surgery is gonna solve that problem one way or the other. When we do massive resections in these babies, we actually make them sicker. The solution that I just mentioned actually oftentimes is a lot less stressful than trying to go through and do a primary anastomosis and remove a bunch of bowel, which is far more stressful on the baby. Um, but it all comes back to, if you have a baby that, um, has segment of bowel and you choose what we talked about, and they're getting clinically ill, you have to make the decision to go in and remove it. Um, Or to watch it, when it's, that there's really nothing else to do. Taking out all the bowel when there's nothing left really is, is an end game. Um, the idea that that child's gonna go to transplant is almost never comes to fruition. That child, um, morbidity is Gonna be fairly profound, um, leaving the bowel in and letting the child declare themselves, meaning that, are they getting sicker, are they on oppressors, are they on high vent settings? Are they abdominal compartments in them where they're so edematous that you can't move them forward, um. is a scenario where the child's clinical course is dictating it. What I am trying to convey is that that doesn't happen nearly as much as one would have predicted. In fact, if you had to guess, it's far less than 10% of the time um that we see that happening. And, but it takes It takes conviction and it takes what is a team approach. And so, for a surgeon to make that decision requires that the neonatologists and others agree. And then the communication to the family is that the child's course is extremely critical and will be determined over the next hours based on how the baby does, as opposed to walking out and saying, your baby basically has no chance of survival, and we're just gonna let the baby pass and extubate, um, it's currently. Uh, I think, yeah, and I, I think you have to put it in the context of current modern-day outcomes as well. Like, you know, I'm getting older now, and, and back in 1999, mortality was pretty high and most of these kids would die of TPN liver disease or sepsis. If we look now, um, you know, the 5-year survival in most sort of larger intestinal rehab programs is over 90%. Um, even with bowel transplant, although not a perfect solution, still, the five-year survival is about 65%. So, from a survival basis, it's, those are not unreasonable numbers compared to some other diagnoses. Um, And then, you know, Dave Mercer actually did some nice work from his center in Nebraska where they did some quality of life studies looking at uh the patients themselves and how they felt about their situation and parental proxy. And in both cases, just to very quickly summarize, both the patients themselves and the parent proxies uh stated that their quality of life and what they, uh, their quality of life was, was exceeded significantly what they were led to believe it might be at the very beginning. So, um, coming from the patients themselves and their parents, and based on what we have in the literature, um, with survival data, It's in the modern era of management, it is a lot. It's very difficult to just open and close them. So yeah, um, sorry, we have a question here that How much the size, the age, the different, uh, patient that you have in front change your Outcomes, your, like your surgical technique to do an ostomy, to do a tube. How do you handle that depending on the patient? So, I would say the youngest patient we're gonna be operating on here is 23-ish weeks, 24 weeks, and they could be 550 600 400 g. Um. Those are honestly patients where um you're really wanting to control the situation in the least stressful way, and, and they're the ones that are gonna benefit most by these tube approaches that, you know, they can easily tolerate a 4 or 5 French tube. Uh, the operation is much Less, um, stressful on that baby. Um, their abdominal wall, as you know, doesn't have much, and so, um, bringing stomas out and stuff in that baby are the ones that are gonna be the biggest issue. It's, it's when they get bigger that I feel like you can become more aggressive with other things. In the, in the earlier the baby, the more the points I make a hold. Um, I was gonna just finish one other comment, and then we'll go back to age. But to me, and we're gotta, we gotta really talk about what we expect these babies to do, and that's what age is really gonna play. And it's gonna play into the conversation about when Paul and I started all this, our babies were passing away because of cholestasis and infections, and we were fighting time. And our surgeries, we really felt like if we couldn't get these kids on a significant amount of enteral nutrition, they were gonna die from these morbidities. Of, of the therapies of general nutrition and, and whatnot, which, frankly, doesn't happen. We can talk about why that doesn't happen today. But I just wanted to mention, you know, last, just this week, we had a boy come back who's 9.5 years old, who essentially was pannecrosis of his gut, um, and had multiple surgeries using the techniques that we talked about. And You know, he's still on PN, um, but he does get a third of his nutrition by, by tube feeds. But cognitively, he is in school, he is an active child. Um, he at the time had a, uh, an intraventricular head bleed, was on a vent, was septic, and Intellectually, he is thriving. And so, whereas most people would have predicted the outcome cognitively for that child, that's just not the case. And so, those are the cases that give me um the strength to make some of these decisions, because ultimately, they're the, they're the outcome that will validate and why we all became um people who want to take care of these babies. So I think probably the question here for you, Paul, is to start talking about what is the expectation and the management of this child's nutrition um in the post-operative period, and how would you expect things to progress forward and obviously, 3 cc's an hour at 8 months is not good. And when we see that, we always wonder about many things, and we're gonna end up talking about, those are the things you need to consider when you work up this kid. But what is the expectation? What would your expectation of this kid be from a PMEN standpoint? Had we, let's just say, did a primary anastomosis, cause that's what they did at birth. 14 centimeters to mid-transverse colon. Um, what would your expectation be on where that child should be at 1 month, 3 months, 6 months? Um, Well, there's gonna be the individual variability. Uh, you know, I think the overarching plan, the overarching principle is we want to, we want to deliver adequate nutrition to, to have normal growth within normal parameters. Ideally, that's central. But, uh, you know, as these kids are adapting, uh, they're gonna be either partially or totally parenterally dependent for at least some period of time. And we also, the other guiding principle is, as much as possible, we'd like to try to establish normal feeding behavior. Realizing that enteral nutrition is more than just uh nutrition. There's the whole social aspect and quality of life aspect that's important. And to get to your previous point about this race against time, And those, back in, you know, 20 years ago, it really was a race against time and we, we often would sort of not think about doing things like, you know, bolus or oral feeds because we're trying to feed the patient continuously thinking that we could get them off TPN faster. And there actually might be some truth to that. But now that we are much, much better at, at, at giving these babies, even with marginal anatomy, the time they need to, to meet their potential. It's not that same level of urgency. So, I think whatever feeding plan, especially in the term baby, whatever feeding plan we initiate, uh, we're gonna try to establish some oral feeds, um, pretty much from the beginning. Let the babies show us that they can't do it before we default to other forms of, of feeding. So, those are guiding principles, normal growth and trying to establish normal feeding behaviors. What do you think is gonna limit? The ability to feed this child. What are they gonna be the factors that, um, that limit what we're able to do and, and how we're gonna do, how we're gonna treat those. Yeah. So, some of that is gonna be related to, um, I mean, this, again, this is a term baby. So, so this baby, just by definition, that the fact that they're term, unless there's a significant neurologic problem, Um, out of, right out of the gate, you know, already is in a position to try to, uh, have some success with, with oral, with oral feeding. A lot of the babies, as everyone in the audience knows that we treat, may be quite premature and, you know, unable to feed orally at that time and need to be tube-supported. Um, but I would argue, my personal bias would be, even if a patient needed to be tube-supported from the beginning, I would typically try to do that with bolus feeding. Um, rather than default to continuous feeding, let the baby fail the bolus feeding, uh, before going to, to, uh, continuous feeding. And what do you, what do you think causes these kids to fail the bolus feeding? Uh, sometimes, you know, initially, you know, when the bowels, when they, when they've had, uh, you know, a septic event or they're premature or an insult, there's, there's motility issues, delayed gastric emptying. Um, and they just don't tolerate food into the stomach. They have a large volume of gastric aspirates. And then, in that setting, actually, there's a tendency to, to, to, to be fearful and to not want to feed. And often, you know, our strategy here would be if, if the child failed a gastric approach, bolus and then continuous, then we would consider feeding beyond the stomach and decompressing the stomach uh through an NG uh but we would feed them beyond the stomach. And often, once you initiate those feeds beyond the stomach, Then the gastric emptying will improve. And, uh, and then they'll, they'll actually start to function better. So, we're getting ready for a break, but I think it's important, we'll, we'll leave it at this, is that it's really important to recognize that the failure to feed often is that the stomach isn't functioning, but the small bowel and colon will. And that using the small bowel and the colon is what makes the stomach work. And so, in, in cases where we haven't seen a progression on enteral feeds because of high gastric output, um, and poor gastric emptying, the solution is what Paul mentioned, and I'm alluded to it earlier by saying, when we put a tube in the stomach, I often direct it outside the stomach because It's not an uncommon problem. This child probably had gastric emptying problems because we commonly see that when the colon is being hit so quickly and distends, it sends signals back to the stomach not to empty as a mechanism of control. That's part of physiology. Um. So, uh, I would say I think we're taking a break now, but I think, think about the challenges that limit animal nutrition, and we'll, we'll come back at that. And any questions, please send them now, and we'll try to make this as productive for you all as we possibly can. Yeah. Yes, we have, um, some questions about. When to start feeding, how to feed, volume, and I think that's we, what we are going to do after the break, what we are going to talk about, so, just handle uh a little bit more to find the answer to that question, and we are going to address them. So, now we are jumping to a 10-minute break, um, so stretch your legs and wait for more of this intestinal rehab webinar. OK, everyone, welcome back to this first webinar, Industrial Rehabilitation. We are back from the break, um, and we are going to talk about how to feed, when to feed, volume, etc. So, just For you, as a reminder, please leave any questions in the chat box below, and if you wanna reread the case study, you have it in the right side of the screen. So, I'll leave you with the experts to keep this talk. All right. So, we, we, we spent, uh, a good part of the first half of this, today's webinar talking about really a lot of surgical considerations, OK? Now, I think you, It would be appropriate to transition and have a conversation, getting in more into the overall nutritional management and uh management of other potential comorbidities, um, and, in, in the context of our patient that was in the case study. So, yeah, yeah. So, why don't we, why don't we talk about nutrition. So, you know, overall, we were touched on it a little bit just before the break. Um, You know, and, and overall here, we have a patient that's gonna require At least, you know, it's gonna be definitely parenterally supported. We can talk about issues around that and what's appropriate. And then there's the enteral nutrition piece. Um, and just to remind everybody, uh, if we pull up the case very briefly. This child at 8 months of age. is on 22 hours of TPN receiving just over 1 g per kilo of a composite lipid emulsion, 3 g of protein, glucose infusion, uh, overall fluids are about 115 per kilo and 78 calories per kilo. And the enteral nutrition is regular strength alphamino, which is a formula that has a predominant MCT component in it being delivered at 3 cc's an hour, providing very little um nutritional support and nothing by mouth. Yeah, so that's what we're working with. So let's first talk about the formula. What obviously, formula of choice coming from the breast? Breast milk, always best. Breast milk. Um, yes, breast milk, not only for its nutritional, uh, benefits, obviously, but, uh, all the other goodies that are within the breast milk. There's growth factors in breast milk, as example, EGF, for instance. There's immunoglobulins in, in breast milk. These other factors, there's oligosaccharides in, in, in breast milk. A lot of these, these, um, these other growth factors and antibodies and such that are in the breast milk. Or have a, you know, a real positive effect on gut development. Uh, so, we will, we always default to breast milk if we have it available to us. Mhm. Um, there is a myriad of formulas out there, and regard in regard, depending on what jurisdiction, country you're living in, they're all gonna, they're all slightly different. But the, the principles are, you know, we have intact formulas, and we have either semi-elemental or elemental formulas. And uh yeah, 2 modules I think that are important to talk about are the protein module and the fat module. So, a lot of the formulas that we end up using, practically speaking, are, are formulas that are either semi-elemental or elemental with respect to the protein. So, they're either hydroxylated uh protein or free amino acid protein. Things like neocate, um, pyramino, uh, nuramigen, um, Elicare, alphamino, a lot of, they all have broken down, uh, protein module. So, let's talk about the protein module first. How relevant is it to have You know, uh, uh, free amino acid formula versus an intact protein. Uh, for feeding our babies, well, obviously, the thing you worry about is allergies and the kids that have had damage to their gut are more prone, like the neck kids to do that. And, um, obviously an elemental, uh, diet and, and single amino acids is gonna be the one that is least, uh, gonna give you that problem. And so the preference is to, is to try to avoid that. Um. And, and as Paul's gonna get to, I mean, the truth be told that this kid's never been fed and so you, and it doesn't have a lot of intestines. So we just wanna get the thing started in the safest and most efficient way. Um, and so starting at the, the bare bones, you know, single amino acilo is gonna be, you know, our generalized preference. Um, Yeah, yeah, what's interesting is, is, you know, if you look at, if you look at the physiology, even in the setting of ultra-short bowel syndrome, you know, protein absorption is probably the best maintained macronutrient as far as absorption. Um, and there's, there's also pre-clinical data in, in piglets, you know, that are fed free amino acid versus intact protein that really shows no difference when, when it comes to driving an adaptive response. Uh, protein absorption is pretty well maintained. And even in some human data that were, that was done, um, that we had written several years ago, these are patients that had a lengthening, lengthening procedure. When we looked at like protein absorption over time, even at baseline protein absorption was well maintained. So, the biggest benefit, if you will, of a, of a broken down protein module is regarding the allergy component. It's not so much from a um absorption, adaptation perspective. And, and you're gonna support this child's protein needs predominantly through the p.m. um, so really, it is getting them on a formula that they can tolerate and they can, uh, gently move forward with. Um, and so the option to concentrate and whatnot might be in the back of your mind, but you're so far away from that at the beginning. Meaning that I, I would venture to say volume tolerance is the key and, and not, not trying to push the calories early. I'm just trying to get the motility and the functional volume controlled, um, is key and making sure they're not having high stool output, high fluid losses, wound breakdown, rashes, um, emesis, um, are all the limiting factors. Yeah, so, yeah, what's gonna, what's, you know, we define tolerance from the top as reflux, vomiting, that kind of wretching, and tolerance from the bottom as diarrhea, stool volume. And that's what's gonna guide your progression. Yeah, so I, I, in the old days, and maybe you guys still do this, you know, everyone wants to know what are the reducing substances, and they actually, I think it's really helpful to know the cc per kilo out. And there's like some people that believe a number like 40 is a hard number to stop. Um, and, and I would tell you, it's probably not as, as rigid as we might have thought. Um. I like looking at the baby's overall, uh, hydration status, and CO2 on our chem 7 is a really good indicator. When they lose a lot of fluid, that CO2 will drop below 20. And I'm not sure if all of you have the same lab levels that we have, so I don't know how to correlate that to potentially other sites. But your CO2 is a really good measure of when you're about to go over the cliff and being able to feed too much. Um. And, and sometimes it's important to know when you start feeds, the outputs are very high, because the gut has never learned to reclaim fluid. And you will never teach the gut to work unless you give it nutrition to turn on those signals. It doesn't happen if you don't feed them. And so, oftentimes when you start feeding and the output goes up, people get scared and they stop. And you sometimes have to support these kids with fluid, initially, especially at 1 and 2 cc's, it's this high output. You need to kind of sit on your hands and hydrate the kid. You do not wanna stop feeds because you'll never induce the, the gut reclamation of fluid that's gonna prevent that high output in a week or so. Right. You don't get intestinal adaptation without enteral nutrition. It will not happen. Even if you start throwing meds like diglutatide, so GLP-2 analogs, they don't work unless there's enteral nutrition. So, I think that's a really good point. Um, especially in a case like this where you've got 14 centimeters, and people are afraid because they're afraid about high sid fluid, fluid losses. And so, they don't wanna progress any further. So, what, what I think is a, uh, a helpful strategy is, um, Not to include all of the fluid requirements in the TPN at the very beginning. When things are very acute and they're changing rapidly, um, it's less work for the team, frankly. If you write the TPN prescription to, to be its own entity, and you have replacement fluids that you can weigh in. That you can adjust up and down based on the patient's outputs. You can keep them uvolemic and keep their electrolytes normal. And you don't have to keep changing the TPN all the time. You let the patient's daily weight, their fluid balance, their, um, their, their, their CO2 level guide whether you're going to continue to advance the nutrition. And you don't wean the TPN if you're not actually gaining appropriate weight. It makes no sense to wean the TPN if the patient's weight is flatlined cause they're just gonna lose more weight. So, you need to be gaining appropriately, be in, uh, a positive fluid balance with, with an, with an adequate CO2 and, and before you think about weaning, weaning, uh, the TPN support. I think we got a question. Yeah, we, we have a lot of questions, so I'm going to try to uh summarize them. But basically, what they're asking is, when you start feeding, um, You start with breast milk. If you don't have breast milk, what do you use? And if we need to supplement that with something else to create a healthy growing in these patients. So, as, as we sort of alluded, we're gonna start with breast milk. We have the, we have the privilege of having donor breast milk here, which I recognize is a, is a gift that everyone doesn't have. And then, if that's not the case, we're gonna start with an elemental diet. And, and I can give you a brand name, but, you know, I really think an elemental diet, um, EleCare or whatever, um, is, is the right choice at 20K cal. Um, And we're gonna start that. Generally speaking, um, we're gonna start, um, it depends on the underlying condition, but, you know, 10 ccs per kilo per day is a reasonable one. The premature kids, we're gonna start much slower, and we're gonna try to get, we have a small baby feeding protocol that we've established here where the early moves are, have been dictated out. Um, and they're really about, um, a 3-day basis at the beginning, um, based on a 10 cc per kilo today starting with. Um, and it's often gonna be given through a tube, even though Paul says as much as you want oral, that's really has to be introduced once you've established the fact that the GI tract works. So the first feeds are almost predominantly not gonna be given to A new baby that's never been eaten by mouth. It's gonna always start by a tube, but you're gonna always try to consider if you're doing that as a bolus, you're gonna be able to transition. And this baby, um, you know, I think we would have likely, uh, waited to see GI function, making sure that there wasn't a high output and has recovered from the surgery, which will often be the first week. And then we would start this child, uh, what was it, we don't know what the kid's weight was at birth, but I'm assuming 3 kg because full term. Um, so this kid would have gotten, you know, wouldn't be starting, you know, start off something like 5 cc's an hour, yeah, or Q3, Q3, yeah, um, so I think, you know, the, as Doctor Helmer said, the brands of formulas, you know, vary by jurisdiction, but, um. In spite of what I said before about, you know, whether a free amino acid formula is, you know, totally necessary or not, by convention, it does appear to be what we default to after breast milk. I think the more important factor, frankly, is the, the fat module. Um, and it's very interesting because back in the old days, if you look at, uh, Neocate, which was a really popular formula, it's a free amino acid formula, it used to be 95% long chain fat, 5% MCT, and then they, nutritia changed the formulation, probably about 10 years ago, uh, uh, and they made it 30% MCT. So, they increased the MCT component. And many of the other formula companies have kind of done the same thing. And There's this, there's this feeling out there that especially in the setting of short bowel syndrome, that an MCT fat is better tolerated, better absorbed, because it's, it's not, it's absorbed directly through into the bloodstream and not through the lymphatic system like long chain fat. So, it's easier to absorb. Um, But I would argue that uh long chain fat is the preferred module rather than MCT. And, you know, what I sort of refer to it as is the, the Dominican Republic factor in the sense that If any of you have gone to the Caribbean and sipped on too many pina coladas, you might notice that your stool gets a little loose, right? And that would be the MCT in the coconut milk of your beverage that's having an impact. And so, there's actually some good uh pre-clinical data in animals that, you know, is oldish data. It's coming, you know, from the mid-nineties, um, showing that there was a nice study done in, in rats where Where they were fed, uh, MCT. Some rats were fed MCT, some were fed long chain fat. They cannulated the portal vein and the, uh, mesenteric lymphatics, and they measured the amount of fat in the, in the bloodstream and in the lymphatics. And what they They found was both the MCT and the LCT were present in the lymphatics. About more than 50% were recovered in the lymphatics. Only like 1% of both fats were found in the bloodstream. So, the, the point being that, even though it was, it's MCT that was being fed, the majority of MCT is actually absorbed through the lymphatics and not the bloodstream. So, we're not getting the effect that we actually think we are. The other thing with MCT is that it does not stimulate GLP-2 release the way LCT, uh, long chain fat does. Long chain fat is a much stronger stimulus for GLP-2 release, and that's what we want when we're trying to drive adaptation. MCT doesn't do that. In other pre-clinical models with MCT versus LCT in animals, we see, um, less, uh, less sucrase activity, um, uh, leucine absorption. Uh, is lower in the animals that were fed MCT compared to LCT. So, you don't seem to get the same adaptive drive. And then in some human studies, MCT was shown to, uh, decrease transit time. Uh, it, so, transit speed increases with, uh, with MCT compared to LCT. The, the cycling time between the MMC cycle, uh, complexes is shorter. Um, when you feed someone long chain fat, it puts them into like a fed motility state compared to MCT that doesn't. So, you get rapid transit, that might explain the diarrhea, um, and you don't get the same adaptive drive. So, we prefer a formula that is predominant long chain fat. Um, and that, that may sound counter, you know, counterculture, but that's, that's our feeling. And, uh, so, in our setting here in Cincinnati, that would be a formula like Elicare, which is, um, it's a, it's a, it's a free amino acid formula, but it's, it's got the predominance of long chain fat, less MCT as opposed to alpha-amino, which this patient uh comes to us on. And so, when we look at a patient like this who's got 10 stools a day and perineal rash, um, You know, some of that may be related to what we're feeding this baby. Uh, and, and so, that would be a, a change that we would think about making is to change that formula. So, when we go back to where we were, uh, in the discussion about How to move forward and stuff. The volume that the child has, you know, is determined at the bedside with the neonatologist. So, you know, 120, 130 cc per kilo per day. Um, and what you're gonna find is that you're gonna be limited by how much volume you're able Able to give if you go 1 to 1 because the nutritional content of enteral nutrition will never outduel PN um, at best, it's 2/3, and it's actually far less than that. Um, so as you're pushing your enteral nutrition, we asked about supplementation. The time, the, the thing I might supplement and consider in this patient earlier than later, which is the only one is if you're giving breast milk, the protein levels certainly can be lower, and you can easily and safely add protein to breast milk, which I think is reasonable. But concentrating on other things is not really the first line that we go at. Um, as you start to feed the child, there's gonna be increased losses that you have to take into consideration and remind your neonatologist to potentially liberalize you from 130, 140 per kilo to 160, sometimes 180 per kilo, that allows you to get parental nutrition, um, to grow the child healthy, but to continue to slowly advance your internal nutrition. And what Paul and I really believe that you should not just go up 1 cc in animal nutrition and down 1 c in PN. It seems logical, but you'll end up finding that you're gonna restrict the calories if you do that. What you wanna do is you wanna look at the growth of the child, not the weight of the child, but the growth of the child linearly in the head. Because if the head's growing and the baby's growing linearly, they're using the protein, and they're taking, and you can then go up on your EN and go down on your PN. If they're not growing, You need to really focus on healthy growth. And then, particularly if we know, we put tubes in like we started talking about, and the question's gonna be, when do you go back to surgery? And that's when the child is growing well, the liver is stable. Um, when you're in a position where You can do that and that could be within six-ish weeks. It could be longer if it's not limiting your ability to go forward. If you're able to keep feeding the child, there's no rush to get back to surgery as long as you are growing in a healthy way and to do so is really managing. Volume. So, let's talk about um TPN. OK. OK. Smoth was what this child on. Should every kid be on Smoth? Uh, I think, you know, in the current, no, I don't think that's absolutely necessary. I think, um, you know, so SM, uh, in my previous institution in Canada, we, it became available to us in 2013. And at that time, we said, Any, um, any term baby or older child that came in would get intralipid, which is our standard soybean-based lipid emulsion, um, out of the gate. Um, if they required, um, TPN longer than 2 weeks, then you would, we would consider switching them over to SMO. Any preterm baby that came in would get SMO, um, initially, right, from, from the beginning. That has since, that had since morphed and, and basically, SMOth became the default lipid emulsion in my previous institution, uh, basically for every patient in the hospital. Um, for preterm babies, SMO is not the ideal lipid emulsion, but it's kind of the best we have. There is some ongoing research and development into newer lipid emulsions. Um, the, the deficit with, with Smoth is that it doesn't have enough arachidonic acid in it. Um, and arachidonic acid is really important for brain, uh, for brain development. So, Um, the, there is a concern, I guess, smoth's been available down here in the US for about, uh, for a couple of years, really. And there's this increasing feeling that smoth may be associated with essential fatty acid deficiency, which, which we just published a paper on this, uh, recently, which I would say in the, those reports of, uh, that suggest essential fatty acid deficiency, most of them are case reports where moth was dose restricted. Um, those, the, this whole discussion about alternative lipid strategies, 11 strategy to deal with the TPN liver disease is to dose restrict. Uh, you dose restrict anybody with any type of fat, their cholestasis will get better. Uh, the other strategy is to change composition, and that's where newer novel lipid emulsions like Smoth or like Omegavin, for instance, um, you know, in the setting of Omegavin, it's actually both lipid restriction and composition change. But dose restriction will cure cholestasis, no question. What we want is, yes, we wanna protect the liver, but we want to ensure normal growth. And the problem with lipid dose restriction or even the use, the very liberal use of, of Omegavin. Which as sole lipid source at 1 g per kilo, is you are dose restricting. You are, you are losing calories and you do have to make that up somehow if, uh, and that would, that would mean that you have to increase the glucose, uh, infusion rate to try to compensate for the caloric loss. That will, yes, protect your liver, but SMO, I would argue, which can be delivered at Conventional lipid doses, you know, 2 2.5 3 g per kilo, um, not only protects your liver, but it also provides more balanced nutrition to, to allow better growth. So this patient comes to us on Basically 1.3 g per kilo of, of smoth and this child really has no, no appreciable enteral nutrition. Yeah, so, so one concern would be is that this child is at risk of developing essential fatty acid acid deficiency. If you look at that case, this patient's only getting 115 mLs per kilo in the setting of 10 bowel movements a day. And only what did I say, 78 calories per kilo, um, and is well below the growth curve. So the, this child's TPN management, you know, needs the child probably needs more volume, he needs more calories. Um, so clinically, how do you see essential fatty acid deficiency and, and are you sending off trying to tetrane ratios or what are you doing? That's a great question. I mean, it's the, the clinical evidence of essential fatty acid deficiency happens late. And it's, it's not always easy to detect clinically. You can see problems with wound healing, problems with hair, uh, skin rashes, um, sores around the mouth, um, those kinds of clinical findings, uh, which, you know, you can imagine in a complex patient may not, they may be more subtle or, and, and harder to pick up. Uh, so, the clinical features are late features. The, um, biochemically, the, the, the strategy really should be to send off a lipid panel, um, and not just, not just look at the, at the triene tetrine ratio, um, the TT ratio. The TT ratio was, was really developed when we were using soybean lipids. You have to realize that the TT ratio is gonna be influenced by the composition of the lipid that you're delivering. So, um, when, when, um, when we are deficient in arachidonic acid, we're gonna see a drop in the, in the denominator of that, of that ratio. And we're gonna see the, when essential fatty acids are deficient, we're gonna see the desaturase enzymes work on oleic acid, uh, to lengthen those, and that's gonna increase your, the numerator, um, of your, of your ratio. And so, uh, depending on the method of measurement, um, a number greater than 0.2 is often referred, is thought to be essential fatty acid deficiency. But if you're giving someone a lipid like smoth, they have a higher content of oleic acid in smoth just because of its composition. They may not have meat acid production, but they have a higher level of oleic acid that's being metabolized, so that's gonna increase your numerator. And you may misinterpret that as essential fatty acid deficiency. Um, so, it's really important when you look at the TT ratio that you're looking at, you should have a derangement of both the numerator and the denominator, not just one over the other. It should be both. Um, to really reflect a true essential fatty acid deficiency. We, we actually recently published a paper on this. It's in JPE. It just came out in the last few months that explains this point. We looked at patients that were pretty much exclusively PN supported for several years and looked at their essential fatty acid profiles and basically showed that those patients, none of them were all on small Exclusively had any essential fatty acid deficiency. But just to summarize, cause, you know, obviously I think take home, I don't feel comfortable with small less than 2, 2.1 per kilo and 2.5 per kilo. So this dose is too low, but you're not gonna really see the clinical manifestations at 8 months yet. But, but the, the damages are ongoing. And so you really just have to pay attention to making sure that you're providing uh the right lipids and, and other nutrients um that you should be thinking about in high stoma outputs are gonna be things like zinc. That are often low and are associated with low alkaline phosphatase. Um, if you look at it, at your just biochemical profiles in these kids, um, and that will associate with some of the rashes that we see. And so making sure your PN has appropriate micronutrients in it. Um, all the things that we do see, those are things that we do see in the NICU. The essential fatty acid deficiency, um, I don't believe I've seen it clinically manifest, but I've seen it biochemically manifest, um, in this age group. Yeah, I think you just need to provide, uh, lipids should be, it should, in a normal person, it should comprise somewhere between 20 to 35% of overall calories. And so when you write your TPN prescription, your lipid modules should sort of fit into that proportion to be healthy. You got a question. Yes, we have, um, a couple of questions. Um, how do you, you're asking like how do you handle the electrolytes like sodium in the TPN? Like, do you use urine sodium? Do you use, um, The blood sodium or how do you address that that's a great question. I'm glad whoever asked that asked that because we were gonna segue into that. Um, I was gonna ask Doctor Helmerth that question. Um, awesome. We use, we use urine lights a lot to help guide us. Number one, It's, you, you can, there's several reasons for it. Number one, the, what happens in the urine is, it's actually, uh, you get, it's a more responsive assessment of what's really going on in the body more than the serum. There's quicker changes in the urine before you see changes in the serum. So, that's one advantage to it. Number 2, you can, you can assess what's going on in the body without having to draw more blood work. So, when we're tweaking the knobs and making adjustments, we will often look at the impact on the urine lights. When you look at the literature on urine sodium, um, most articles talk about a, a spot using a measured urine sodium, and anything greater than 30, uh, is considered to be OK. Uh, our approach here is to not only look at the sodium, but to also look at the potassium and we include the chloride as well. We usually throw in an osmoality as well. So we, we're looking at the concentrating ability of the kidney. But you wanna look at the relationship of the sodium with the potassium. What you wanna see is that the sodium in the urine is higher than the potassium. This is a baby that has reasonable, a patient that has reasonable renal function, not on diuretics. OK. So, you wanna see the sodium higher than the potassium. If the potassium flips higher than the sodium, that tells you that this patient is sodium depleted, volume depleted, and they've now turned on their, their renin angiotensin aldosterone axis. The body is trying to preserve sodium. So, typically, the picture is, if you were to measure serum and urine lights simultaneously, the serum sodium might be 139, let's say 140, 139, it's normal. You're measuring the, the urine sodium. As this patient is losing salt, that urine sodium might go from, let's say, 50 or whatever, down to 40, down to 30. And that serum sodium is actually maintaining itself quite normal. And the urine sodium is dropping faster. Once that urine sodium drops low, and then, then the serum's gonna follow later, that's gonna lag behind. So, the urine is much more uh responsive. So that's why we, we follow that, but we follow it also in relationship to the potassium. The other caveat I wanna mention here, the strategy that we use is we do a lot of pre-hookup blood work. If you think about our normal conventional practice, people get TPN often, even if it's cycled, it's usually overnight. And we measure blood work in the morning. That is the period, that's the time in the day when the person is the most hydrated typically than they're gonna be. They're probably not eating as much. The losses are less, and they've been on infusion all night. So, you look at the blood work in the morning and you get this false sense of security like the patient is doing really well. When we're making fluid changes and we're contemplating whether to, to increase someone's uh window on their TPN, we will measure blood work pre-hookup. So, let's say they're cycled off for 4 to 6 hours and we're thinking about extending that, we will draw the blood at, at the hook-up time. That is the time of the day where they are theoretically the most dehydrated that they're gonna be. They, they hook up in the afternoon, by the way. So they're gonna, they've been off the pump, they've been off the pump for 4 to 6 hours or whatever it is. Um, and depending on what they're taking in ly. You know, may or may not be that much or whatever, that's where they're gonna be the most dehydrated. And it's really helpful data. You, if you were to check it in some patients, the same patient, blood work in the morning, blood work pre-hookup on the same day, you might see a very different picture. And that's a very helpful strategy to help guide whether it's safe to extend their window time or to wean TPN fluids. So, to go back to the question, if, if the sodium, we check a weekly urine, unless we want something else, but typically, it's on a weekly basis. And if, if the sodium is less than 30, we're gonna add sodium to the child. If the child's able to take EN, my Preference is to add 1 to 2 million equivalents of sodium per day to the feeds because it increases the ability to take up sugars and protein, meaning that you need sodium to take up these uh nutrients in the lumen of the bowel. Um, you can adjust it with PN and the question whether that's the same is controversial and, and I'm just telling you my preference. If The potassium is over the sodium, the child's dehydrated. You need to provide more fluid to that child. So that child's needing some boluss and some background fluid, um, because the child's getting dehydrated, and that also may be reflective in the CO2, but certainly, an elevated K means you need to do something about providing extra fluid for that child. Mhm. Awesome. Thank you for that. And also, people are asking, what about the high output in the ostomies? Like, how do you handle the high output in ileostomies or jejunostomies? Do you do something different? Do you analyze that? Do you do refeeding? Um, what, how do you handle that? So, high output, if you can feed it, that's an, that's an ideal way and why we like to place tubes. Um, so certainly, if, if the child has a refeeding ability and um is in a stable situation, we will start refeeding them at a, at a standard, um, that we'll advance. And again, that usually starts at 10 ccs per kilo, and then we'll go up. And, and actually, we, we can feed back a fair amount more. Um, it's often given over a pump, but I believe you could also do. With the bolus because it's usually well accommodated. But let's say that's not the case, which is often the case, and you have high stoma. Again, I look at the wound. Is the wound OK? Are you keeping the bag on? Uh, what's the CO2 of the baby? Are the baby hydrated? Is the baby growing? And if that's the case, um, oftentimes I don't let the output number overwhelm me. Um, Uh, many times, it will get better, as we alluded to, by allowing the bowel to have nutrition. If the baby's only starting on nutrition and we're at, let's say, 5 cc's per hour, it's different than if the kid's on 65 and the stomal output jumps way high. Um, there are different scenarios and there's different things you think about, uh, in them. And then, um, the only thing I'll say before we forget is the established stoma that starts to have high output is often the first sign of a stricture, um, and it's oftentimes missed that as the bowel starts to have a stricture, it's contracting and the output is the first sign that goes. Up, but again, that's kind of downstream. Um, Paul, can you talk about the things that you try to do to manage output, maybe pharmacokinetics and, and other motility stuff. So when you're assessing your patients, um, and they have high output, you know, some of that just may be just bad luck related to their underlying gut function. But sometimes it's, it's the therapies that we've implemented that are impacting the output, so. From a diet perspective, is the patient taking in the source of, uh, of simple carbohydrates. Like in an older child, they might be, you know, taking in juices or fruits or, you know, uh, sugar, monosaccharide sources from cookies, candies, muffins, things like that, that might be driving osmotic losses. The other important thing to remember is medications is often a source of carb of simple carbohydrates. And if you look at the case, what I mentioned there was that this patient's getting loperamide liquid. Um, at 0.2 mg three times a day and, and Flagyl liquid. Um, now, we can talk about the dosing of those medications, but the fact that they're both liquid implies that it's, it's very common that a lot of the meds have a carbohydrate carrier. Um, and that is driving some of the losses. So, part of your initial assessment is to sort of think about all of these things that might drive gut losses, um, in addition to just their underlying diagnosis. You know, it's, I think it might be easy to think, well, the kid's got 14 centimeters, therefore, it's definitely gonna have high output. But we may be contributing to that by what, A, what we're feeding, and the kind of meds that we're using. So, those would be some simple things initially to, what can you modify. And often by doing Diet modification, changing meds to tablets. We tend to use more tablets, things like that. That can often have a really positive impact on, on output. The other thing too is, is solid food. Babies, you know, children do better with solids, and that's why it's so imperative that you establish early good oral feeding skills. So, even if it's really non-nutrient in those first several months because the child's either not connected or has a very short gut. As long as they learn how to eat and to swallow, then you can introduce purees and solids at the age-appropriate time. And this kid comes to us at 8 months of age, and they have an oral aversion because, you know, no one wanted to feed them because they only have 14 centimeters, so they're trickling in, you know, 3 meals an hour. So, this kid never learned how to eat. This child would be better served if he was able to take purees off a spoon. Uh, the, the, the, then you can introduce complex carbohydrates like the starches, you know, rices, potato, pasta, green beans, yes, green beans, things like that, that, that help bind you, right? So diet is a really good management strategy for high output. Beyond that, we do have some um medications that we, we do use. So we do use loperamide or Imodium. Um, we, we would use the tablets. We don't use the liquid. Often, the liquid will drive further diarrhea, as I mentioned. And the dose really is, um, you can use up to like 1 mg per kilo per day up until like a maximum of, of 18 mg per day or, or let's say 6 mg 3 times a day. So, if you look at this patient at 8 months of age, Um, who, I didn't give you the weight specifically, but it was like just over, it's about 6.5 kg. This patient's getting 0.2 mg three times a day. So, he's getting 0.6 mg total a day. So, it's basically homeopathic, uh, dosing. So, we do have an option there. As, as one of our strategies, we could increase the loperamide dose as a way of trying to drop, drop some of the stool losses. Other drugs that are available for hypersecretion would include clonidine. Um, clonidine, you know, you, if you're gonna use clonidine, I have had some mixed success with clonidine. Uh, you have to type, we usually will initiate it in a hospital setting because of its impact on, on, uh, blood pressure. And really, you just need to titrate up the dose, uh, using your blood pressure as, as a metric, uh, of, of, you know, as a threshold. But it does, it does work in, in some patients. Octreotide is a, is another medication that helps with hypersecretion. from the GI tract by impacting splenik blood flow. We don't tend to use it much at all because it's, it's the big, you know, GI tract inhibitor. And it can accelerate cholestasis cholestasis. Uh, we don't tend to use it that often. And then, there's, uh, PPI. PPI, yes, there's, um, acid suppression. In the first, probably 6, 12 months of life after massive resection, people are hypergastronemic because of loss of the, of hormonal feedback. Um, so they tend to be hypergastronemic with increased acid production with rapid gastric emptying. And so, you have a high acid load that leaves the stomach quickly and that can have, uh, that can also make your abs your, uh, accentuate your malabsorption. Uh, because of that as causing enteritis, etc. And so, often these patients will require a PPI to decrease, uh, not only gastric acid production, but gastric fluid production to allow enteral, uh, tolerance. How about? Pein is a good strategy, um. We have, sorry. We have a couple of questions about loperamine and, and cholestyramine, like the comparison, which one you prefer, and if it is safe to give these medications to Patients younger than 2 months. Uh, loperamide, yeah. Yes. Um, I, I think loperamide's definitely safe to, to give. And, you know, we will use it, you know, intermediate to long-term as, as required. Um, I don't have too much concern about loperamide, frankly. Cholestyramine, there's a lot of places that, that like to use it very liberally. It's just never been a major part of my practice. We use it occasionally here, but we don't use it a lot. Um, You know, and, uh, the, you know, the, theoretically, you're binding, you're binding some of these bile acids that aren't being reabsorbed because there's no ileum, and, uh, and that's, that's gonna help decrease some of the colitis that might happen as a result of having these undigested bile acids enter the colon. So it may help with some of the, the diarrhea. It's just a, it's a medication that I just haven't tended to use much personally. It's certainly, I mean, if you're having a bad rash, cholestyramine in your rash formula can certainly help, and, and that's one thought, but that's the rare cause that we use it. We also see people do ursodiol and stuff, which, those are all resins. And if you don't have an ileum, you don't absorb them. So, they're off on something cause they're worried about their cholestasis and, and providing that in the absence of an ileum doesn't make sense to me. And um, And they actually increase stool output. Um, honestly, I think this kid at this low amount of interval feeds, the way to control the output is to actually provide the child some fiber, um, in some kind of a sense to both drive adaptation and to start to, um, form some bulking, um, and they're not just getting enough of it, uh, into the kiddo. So the, the soluble pectin is a great option for that. Um, oatmeal in an older child is another option. Um, green bananas works really well. But, uh, the pectin, you know, we haven't really, we don't tend to use it in patients that have no colon and continuity. Uh, you really want the benefit of the colon and continuity. It's the delivery of that soluble fiber into the colon, and you're leveraging the, uh, metabolism from the colonic flora. To convert that into short chain fatty acids. And uh, it improves water absorption and it's a source of energy absorption. And, and the last thing to mention is antibiotic use. Um, you'll often have a child that was doing OK and they'll get a brief course of antibiotics for Lyme infection or other, and they will have a lot of high output stoma, and that's just re-establishing the microbiome. This child was on a background of an antibiotic, which often, often can also contribute to um the fact that the short chain fatty acids and fiber that stimulate the colon to function as a nutrient source in short gut need bacteria. And so, half of this child's gut is colon, and it's not being provided the, the Substances because the the microbiome that it needs to create them are being inhibited by the antibiotic. And so the antibiotic uses, especially when you're trying to get the colon to help you, can, can actually drive high stomalos. And this patient, you'll see on the, on the history, uh, it was on basically continuous metronidazole, um. You know, didn't really have. What sounded like profound bacterial overgrowth that they were treating empirically with, with, with Flagyl. Um, was just sort of on it all the time. And, uh, so it's very well, what we, we stopped that antibiotic when we saw the patient just cause for the reasons that Doctor Helmroth was mentioning. So, if a child has anaerobic overgrowth, they're gonna have a lot of gas. Um, you might be seeing some Lyme infections and high stool outputs. Certainly, I think the child that you have to be careful on is the older one that's eating sugar, that can get dlactic acidosis and presents drunk or in a, in an obtundant state. Um, and that's really restricting the sugars more than it is the antibiotics, but sometimes you have to do both. Um, oftentimes, You know, doing such a broad-spectrum anaerobic approach, um, can get you into trouble. And uh most of the kids with just 14 centimeters are, are not your bacterial overgrowth kids. Um, and so what you define as bacterial overgrowth class Basically it is by an aspirin, but I'm not sure that really counts when you only have 14 centimeters. So clinically, if you start something, you should have a stop in mind or at least criteria. Leaving a child on the antibiotic prolonged is definitely not a good idea. Yeah. Uh, just one brief comment about the venous axis in this patient. They came to us with a, uh, line, a double lumen line in the right femoral vein. Not because there was no other sites, but that, because that's just where they put it at the time of the original sort of emergency surgery. And, you know, it's just not an ideal location for an infant who's trying to learn how to crawl and to, you know, eventually stand and walk and poop and poop all, all over the dressing. So, you know, again, one of the recommendations was to move. We don't like taking out lines that function, but, you know, getting it out of the groin in this patient was a recommendation. And also going to a single lumen catheter. As opposed to a double lumen cavity. And so remember, we used to be running against the clock. Now we're not, and our really biggest hurdle is the kid that doesn't have vascular access when they're older, and, and burning that bridge is something that we really have to be aware of, um, and when to place lines and to place them in sites that are capable. And one of the things that happens in a toddler is they pull. And so, the kid that keeps pulling their line out and is active, you don't wanna put them in the, you wanna actually tunnel them to places they can't reach. And, and so strategies to the placement of lines for care and for trauma that can happen uh at that age need to be considered. That's just a routine part of our, our program. Um-hum. So, one thing we haven't talked about that, that, that sort of also Uh, is part of like fluid management, fluid losses, is, is the role of taglutide. Yeah, well, so let's get to the second. Let's first go back cause this kid's at 8 months and so obviously taglutide would just be starting, and we've, we, when we get a kid like this who's not on the amount of feeds that I would expect, this kid really needs to be admitted, and we need to observe the feeding. This is not an outpatient type of a situation. And I would tell you that when we have kids in other NICUs that we send in that aren't meeting uh their goals, uh, whether they're gastroschisis or atresia, they're only on a couple of cc's. They've done an outside upper GI or BE that says everything is open, and they're labeled as motility problems. They more than not end up having a mechanical problem, when they're not meeting the needs. It's really hard to understand which child is gonna have a motility problem early and not. And I can't specifically tell you, but you need to like do things like post-gastrically feed these kids slow and assess them. When things don't add up and contrast studies don't um show us anything, sometimes the, the solution is to look. Um, and it's amazing that I can't remember a case where we don't find something. And so, to settle for the child as a dysmotility, not moving forward, um, is something that, um, really takes exclusion of a lot of things, and that's where having experience, um, And watching the child. I mentioned at the beginning, we see this child at 8 months and it's striking where this kid's not, but in our own hands, when a child's not progressing, you, you forget that they've been here for 3 and 4 months and not moving forward. And here, we have weekly conferences and we, we have outside people talking about it, it kind of reminds you to look at the big picture, and are we progressing like we expect? Because when they're not, it's, it's oftentimes something that we actually can do something about. And I think that's intestinal failure surgery, not bowel lengthening stuff. I think it's identifying and putting things together in a way that function, um, and oftentimes, these kids are, their anastomosis are to the animessenteric side, and that's beyond this conversation. We've had a podcast on that, but, um, it's really making sure as a surgeon, you're putting the kid in the best situation to move forward. Yeah, especially if they've got pain associated with feeding and stuff. Yeah, um, but they're 8 months, so. It's harder at 8 months, but you got there. OK, so going back to the lines, people are asking, which line do you prefer, which side, sizes and uh lumen amount and why? So, um, I think I would start out, uh, typically, traditionally, we use predominantly, uh, let's talk about line type, silicone versus polyurethane. Traditionally, we use almost exclusively silicone lines. Um, now, there's been a general move in many institutions to move towards polyurethane lines because they don't break as easy. The trade-off between silicone and polyurethane is silicone is more supple, it's easier to coil and to dress, but the poly, and the polyurethane lines are, are, they resist breakage more, but they're stiffer and they tend to kink. And I actually think my anecdotal experiences, they actually dislodge more because you can't coil them and dress them. In many patients, more of the weight and the traction is actually on the entry site. Um, and I, I think there's more dislodgement. Um, the, the use of ethanol locks historically, you know, we, we would only use ethanol in a silicone line. Uh, and that's why in our population, silicone was sort of the preferred line. When you actually look at the data around ethanol and catheter type, it is true that there is some decrease in tensile strength and elasticity in, uh, polyurethane lines that are, you know, soaked in ethanol. Um, but the, the forces required to snap that line, even though there is some diminish in strength, are well exceed normal, you know, normal stresses that, you know, humans will, you know, expose their line to. So, it, it's almost clinically irrelevant. And, and, and many centers that have transitioned to polyurethane, I mean, uh, they, those centers still use ethanol, even in a polyurethane line. Now that ethanol's become much harder to get and much more expensive and many centers can't access it anymore, that's becoming a non-issue. And there's a new catheter lock solution that's on the horizon. It's actually available in Canada, Europe, and Australia already. It's licensed for children called Kitelock, which is a 4% tetrosodium EDTA solution, um, which is antimicrobial, anti-fibrinolytic, and thrombolytic. And it not only, you know, prevents infection, but it prevents occlusions because it, it degrades the biofilm. Once there's an FDA trial starting in the United States this year, um, and hopefully, that'll become licensed in the United States in the next, you know, probably 2 years, I'm hoping. Um, and that will mitigate any concern about catheter type cause you can use kite lock in a polyurethane or a silicone catheter. As far as lumens, we, you know, like the almost exclusively, our patient population has single lumen lines. The more lumens you have, the higher the rate of potential infection. So, I can't think of I think we have one patient that has a double lumen line. mine because I'm a softy, he's not, uh, but almost exclusively single lumen lines. From, from, uh, infection risk perspective, as, as far as, uh, location, uh, left subclavian would be, would be the preference. Uh, it's, it's comfortable on the chest below the clavicle. It's, it's a nice straight shot down, and you often will leave the catheter a little bit long, frankly, for patients that are gonna require very long IV access. So we, all of our trainees now do right IJ. And they like right-eye jays. The reason I don't as much is that you tunnel it over the clavicle. These are lines that should last a long time, but also, as Paul said, the left lets you have the most length before they outgrow it. Um, and so it gives you that extra length, so you, you don't end up with it in the central, like the innominate or up high, um, uh. We usually, most of our babies have PICC lines. We usually, the infants less than 10 kg are gonna get a 4.2 single, and then above 10, here, it's typically a 6 French single lumen, but that's size dependent, but you can actually get these kids through on a 6 French, uh, well into the The, uh, before their 10th birthday. So, you know, you don't need to put a big hunk in line. In fact, you don't want to. Um, sometimes when I'm on the, the borderline, I like, I'll put a 6 French line in sometimes just cause I want it to be the line that the kid has for a while, um, and again, my preference is left. Yeah. And percutaneous access, um, I think most of the majority of centers do it that way anyway, as opposed to cutdowns and, and, you know, it's all about trying to preserve IV access. Kids aren't getting listed for transplant anymore really as much because of liver problems. IV access is the number one indication. You know, we've, we've shifted down the road a little bit. We used to have a population of infants that were dying of liver failure, would get listed, you know, somewhere between 1 or 2 years of age or whatever, and they'd be listed for a combined graft, liver, bowel, because they were dying of liver failure. Now, we see a population of older patients, 89, 1011 years old, who have livers that are healthy, but have no IV access. And they're now getting listed for, you know, an isolated bowel because their liver is, is, is OK, but they've lost their IV access. So, Being very thoughtful about um placement and trying to preserve catheters, trying to salvage catheters, even in the setting of, of, of infection. You don't have to pull a line out just because there's a bacteremia. Even with the traditional You know, the three organisms that, you know, traditionally, we would pull a line out, Staph aureus, Pseudomonas, and fungus. Um, Uh, especially Staph aureus, uh, you can often salvage the catheter, um, using either a longer course of, of antibiotics with, uh, like a lock solution, an ethanol lock solution done as a therapeutic maneuver where you lock the line for 24 hours. Um, as a way of trying to sterilize the catheter and then a longer course of therapy, maybe 3 weeks, you can salvage about 50% of catheters that have staph aureus and not have to pull the catheter. So, Trying to salvage catheters when it's safe and reasonable. Obviously, if the patient's, you know, you know, hypotensive and symptomatic, you, you wanna get the catheter out. And before the question, talk about anticoagulation. So, um, You know, the risk of IV of venous loss is significant, as I mentioned. Um, our practice in Toronto before I came to Cincinnati was to use enoxaparin. After, if someone developed a clot and they had a, they had a therapeutic, uh, course of, of anticoagulation, um, we would continue prophylactic, um, usually enoxaparin for the time, duration that the person had the line. Now, that could be years or that could be forever depending on the diagnosis, and you're poking this kid every day. And we did not know if that was a good idea or not. We just kinda made it up. We did a, a study with the, with Seattle Children's several years ago, where their protocol was to treat for 12 weeks and then stop treatment. And we, we compared outcomes between that protocol and our protocol. We looked at what was the rate of secondary thrombosis between the two protocols, and we found actually like to our surprise too, a significantly lower rate of secondary thrombosis in the patients that had ongoing uh prophylactic, prophylaxis. And so that, that was our program, that protocol that we had in Toronto. Um, I, I, I feel very strongly about prophylaxis in the setting of thrombosis. I, I think it's, I think it's important. I, I appreciate the fact that, you know, you're giving a baby a needle or a child a needle every day. Um, and if that child is also on tiglutatide, uh, they're getting another needle every day, that's potentially two needles. There, there are some, there's some early work looking at oral anticoagulation, uh, not Coumadin, but, um, um, uh, what do you call it, uh, I'm blanking on the name. Oh, I'm blanking on the name, but, um, oral anticrivarivarivaspirin, rivaspirin. Um, as an oral agent, because it's absorbed in the very proximal jejunum, and most of our kids have a jejunum. Um, and that might be a more, a more, uh, you know, acceptable modality for families, but that has yet to be studied. Question. Awesome. Now, actually, we are wrapping up this, so I wanna ask you five take-home points about this webinar because we are 5 minutes to 5, and I want you to give us like a summary of what you talked because it was a lot and we have to remember this. Well, I guess I'll take over. I guess, you know, there's, we've talked about a lot, and I think let's go back to the patient. I think the key is, is that this patient's not thriving at 8 months, and they need to be in the center. You need to evaluate that patient and you need to recognize that they aren't following on the natural history curve that you would expect. We really didn't get into what that natural history curve is, um, but that, there's so many ways we're gonna help that child, not just vascular access and feeding, whether that child has an underlying condition to get that kid on. Glutide is to actually provide dental nutrition because at this amount taglutide will not work. So I think the key there is is that know who you need to see and if you're a smaller center you're not getting referred to they live in your hospital and, and have a have a meeting that you schedule with your colleagues and review your patients and look at their. Progress and then come at a monthly rate, see if you're making progress because the ones that are not are the ones that have in your program is gonna really, really help and as you start to identify them, you're gonna start to find that other places will send you patients. Um, and then as far as, you know, take home from the newborn, there's too many things to take, um. I think feel free to email Paul and I questions, and, and we will help you address the specific questions because this is not like many situations that we can just tell you if and then because it's very, the nuances of intestinal failure are many, and many people hear what we say about one thing and apply it to another, and we'll say no. So, um, if you wanna just have our opinion, we're happy to respond to emails anytime. Feel free to do that. Yeah. Awesome. Basic, uh, just these patients are complex, uh, they're challenging. It's, it's great to manage them as part of a team so that you get the benefit of everyone's expertise cause there's like too much to know for one person. Um, as a, as a program, as a care provider, you're, you have a two-pronged approach. Um, the first prong is promoting adaptation, promoting optimizing gut function, which you're gonna do using nutritional strategies, pharmacologic strategies, and surgical strategies. And the other prong is trying to mitigate the complications of long-term TPN, liver disease, infection, vascular loss, renal dysfunction, bone problems, all that kind of stuff. And really try to, even though the patient's complex, try to give this kid, uh, try to normalize life as much as possible around eating behavior and really a focus on quality of life. Simplify the plan. Um, so that this child's, you know, because the parents are the, are, are eyes and ears and hands at home. And, you know, you can do anything in a hospital, but it needs to be sustainable at home for the family. And we see a lot of families burn out after, uh, several years. So, you have to be pragmatic. Thanks for spending time with us today. Yeah, thanks everyone for joining. Remember, to all the attendees, you will receive a survey through email, so please reply it because we love to hear your feedback uh for the next time that we do this. And if you want, as um Doctor Humbrath said, if you wanna email them, remember you have a button in the bottom right um of the screen where you can email even Doctor Wales or Doctor Hamrath. And remember that this webinar, it's going to be posted in the Stay Current app and in the Globalcast web page for you to see it as many times as you want and to share it with people that couldn't join us today. So thank you very much for joining us. Thank you to the doctors for sharing all of your knowledge, and I hope we see you next time in the next industrial rehabilitation webinar. Thanks very much for everybody.