Drs. Jennifer Lee and Temara Hajjat talked to Dr. Mercedes Martinez, a Professor of Pediatrics and Pediatric Gastroenterologist and Transplant Hepatologist from Columbia University, about diagnosing and managing pediatric patients with portal hypertension and esophageal varices.
Learning Objectives:
Produced by: Temara Hajjat
This episode is eligible for CME credit! Once you have listened to the episode, click this link to claim your credit. Credit is available to NASPGHAN members (if you are not a member, you should probably sign up). And thank you to the NASPGHAN Professional Education Committee for their review!
Links for this episode:
***
This episode is eligible for CME credit! Once you have listened to the episode, click this link to claim your credit. Credit is available to NASPGHAN members (if you are not a member, you should probably sign up). And thank you to the NASPGHAN Professional Education Committee for their review!
As always, the discussion, views, and recommendations in this podcast are the sole responsibility of the hosts and guests and are subject to change over time with advances in the field.
Check out our merch website!
Follow us on Twitter, Facebook and Instagram for all the latest news and upcoming episodes.
Click here to support the show.
Drs. Jennifer Lee and Temara Hajjat talked to Dr. Mercedes Martinez, a Professor of Pediatrics and Pediatric Gastroenterologist and Transplant Hepatologist from Columbia University, about diagnosing and managing pediatric patients with portal hypertension and esophageal varices.
Learning Objectives:
Produced by: Temara Hajjat
This episode is eligible for CME credit! Once you have listened to the episode, click this link to claim your credit. Credit is available to NASPGHAN members (if you are not a member, you should probably sign up). And thank you to the NASPGHAN Professional Education Committee for their review!
Links for this episode:
***
This episode is eligible for CME credit! Once you have listened to the episode, click this link to claim your credit. Credit is available to NASPGHAN members (if you are not a member, you should probably sign up). And thank you to the NASPGHAN Professional Education Committee for their review!
As always, the discussion, views, and recommendations in this podcast are the sole responsibility of the hosts and guests and are subject to change over time with advances in the field.
Check out our merch website!
Follow us on Twitter, Facebook and Instagram for all the latest news and upcoming episodes.
Click here to support the show.
Welcome to another episode of Bowel Sounds, the Pediatric GI podcast, the official podcast of the North American Society for Pediatric Gastroenterology, hepatology and Nutrition, or NASPEGAN. My name is Jen Lee, pediatric Gastroenterologist at Nationwide Children's Hospital, and I'm joined today by Dr Tamara Hajat from Cincinnati Children's. Hey Tamara, hey John.
Speaker 2:How's it going?
Speaker 1:Good, Good, good good. So it's almost the fall. Tell me some about your summer plans.
Speaker 2:So every year for my birthday I go to Seattle, and this year my goal is to go to Olympic Park. I was going to go to Alaska on a cruise, but I was like that might be too much planning in my brain. I don't have a lot of brain space right now to plan a big trip like that, so maybe next year, if you have any tips for me on how to plan my Alaska trip, let me know on Twitter. I'd appreciate that.
Speaker 1:I've actually been to Alaska. Totally recommend it, highly recommend, didn't do a cruise, but would highly recommend going.
Speaker 2:Yeah, I think Peter went to Alaska as well, but he did a cruise. So I'll probably sit you both down during NASPEGAN and ask you about Alaska on a cruise and not on a cruise. So I'll decide then yeah, how are you?
Speaker 1:Let's do that. I'm doing great. We are hoping to go to the beach this summer, which I think would be totally doable. We usually go to Myrtle Beach in the summertime.
Speaker 2:Oh, I've heard of it. I've heard of it. It's nice. I've never been there.
Speaker 1:It's okay. If you are a college student looking for spring break. That's typically like a go-to spot for a lot of college kids, but we usually stay in the more retirement area, a little bit more low key.
Speaker 2:Yeah, anyway, and our guest today is from one of my favorite cities in the world, new York City.
Speaker 1:Yeah, but she's actually a former surgeon who is now a pediatric gastroenterologist, dr Mercedes Martinez. So she's a professor of pediatrics and medicine and the medical director for intestinal transplant as well as pediatric abdominal organ transplant at New York Presbyterian. And she is joining us today to talk about a really cool but also a little bit scary topic portal hypertension and variceal bleeding.
Speaker 2:Yeah, she gives us a lot of great information about portal hypertension, the pathophysiology kind of the background, what to look for and how to manage it, and also variceal bleeding and managing it, kind of one-it's bleeding and preventative care. So it's a great episode. You should definitely take some notes because it's a very thorough episode. It's great.
Speaker 1:Yes, love it All right. Well, we hope you enjoy it as much as we did. Ready.
Speaker 2:On to the show.
Speaker 1:Dr Martinez, thank you so much for joining us on this episode of Bowel Sounds today.
Speaker 3:Thank you for the invitation and extremely honored to be here. I'm very excited to be able to talk with you guys about this topic that is very close to my heart.
Speaker 1:Good, and this is our first time meeting. So for our listeners and for me, who has never met you before, how would you describe yourself in one sentence?
Speaker 3:Well, I will say that an optimistic and self-confident person who loves my family and work extremely hard to serve my patients and the community. I function as a task oriented, goal-driven and over-committed person.
Speaker 1:That's pretty cool, that's pretty great.
Speaker 3:I know.
Speaker 1:I think we can relate to that over-committed and task-driven.
Speaker 2:So you are in Columbia University, which is in the great New York City. I love the city. I like to go there as much as I can Tell us, if somebody were to visit the city, what is one great restaurant that they need to try, or one thing, or maybe multiple things that they need to go to and try that you can't find on Google?
Speaker 3:Well, I don't know if I know very, maybe adventures with restaurants, and maybe the place that I go the most and I would recommend to everybody to go at least one is Ellie Island and the Statue of Liberty. And this is all over the world. But I think that I have my personal perspective of this. I think that for the vast majority of immigrants, ellie's Island was truly the island of hope for generations, and when you go there and see the pictures and testimonial of those earlier rivals, with nothing in desperation, and see how many of these people became very prominent social and cultural or economical in this country, that is something that resonate with me very, very close. I think that when people go there, they must accept and realize that the history of this country is the history of immigrants.
Speaker 3:When I go to the island, I go there maybe more than I should, but it's only a reminder of when I arrived to this country 25 years ago with no financial support, unable to speak the language, scared and concerned what is going to happen? And you know, it's just. It brings me back to those thoughts and how I was scared but at the same time I was eager to learn and to work hard and to achieve my dreams of becoming a doctor in this country again, again, over optimistic and overachiever. But when I go there, I just relate to those moments and I really feel like it's a great place to go, at least once in your lifetime.
Speaker 2:That is so beautiful. I think a lot of our listeners can in some way relate to what you're saying, so we kind of really truly appreciate you sharing with us your journey to becoming a very successful hepatologist. It resonates with me a little bit because my journey is probably a little bit similar to yours.
Speaker 1:And speaking of hepatology, before we get into our topic today, will you just walk us through how did you end up becoming a hepatologist?
Speaker 3:Well, like everything in my life, my journey is a little different than other people. I wish that I could tell you a pathology was my dream. I always wanted to be a pathologist, but in reality, my early encounters with patients with significant liver disease was not very inspiring. During my medical school in Cuba and early during my career I didn't know if many of you know I was a general surgeon in Cuba.
Speaker 2:Oh wow. We didn't know that, whoa.
Speaker 3:So you know patients can. To me with GI bleeds in the emergency room end state liver disease, cirrhotic the resources that were very limited. Then I would place a lot of Blackmore tubes. Many of you even don't know what that is, but I did a lot of those balloons placement to stop the suffrage of viruses from bleeding. We did chun surgeries with high mortality because patients have very advanced liver disease.
Speaker 3:That was really in the Blackburner, something that maybe I was interested but not very passionate about because the outcomes are not that great. But it's when I came to Columbia University in New York, presbyterian, to do my fellowship when I really fell in love with the collaborative team associated with the liver center for liver disease and transplantation. That includes surgical medical specialties that care for children with liver disease with dedication, compassion. They change the life of these kids. They care with these kids with the most advanced clinical innovations and scientific progress. They provide sophisticated medicine and surgical technologies, resulting in excellent outcomes, so different from my experience before. Here we can assess the patient, we can assess the severity of the disease and we can apply new technologies. We can do a liver transplant, which is something that I never saw before I came to Columbia. Then my journey really started here, and I guess I fell in love and never left.
Speaker 2:That's amazing, which makes you the perfect guest for our topic today, which is we're going to talk about portal hypertension, varices and variceal bleeding in kids. So portal hypertension, which is an increased pressure is in portal venous blood, often, but not always, is caused by cirrhosis. So we're going to start with some definitions. What is portal hypertension and what are the clinical signs and symptoms that one might see in somebody who has portal hypertension?
Speaker 3:Portal hypertension is the main driver of complications in patients with advanced liver disease and it also could be the first manifestation of a liver disease that has been burning for many years. And there are also some cases when the patient doesn't have cirrhosis, doesn't have advanced liver disease, and those are classified as non-cirrhotic portal hypertension. Therefore, in pediatric, the majority of these patients are patients with portal venous blood. But let me start. Maybe this definition is a little technical. Cirrhotic portal hypertension is defined by values of hepatic venous pressure gradient of more than five millimeters of mercury. Maybe many of you said, wow, what is that? We take care of patient with portal hypertension, but this is why we are here. Yes, it's new.
Speaker 3:Then this hepatic pressure gradient is the difference between the wish-occluded hepatic venous pressure and the free hepatic venous pressure. How do we get these pressures? Oh, this is an invasive procedure and this is maybe where many people are not very familiar with that in pediatric, but it's very widely used in adults. Then the way that this is done through a transjugular approach, you get a catheter that advances to the hepatic veins and measure the pressure of the hepatic veins and then you advance this catheter a little bit more and wish the catheter very close at the end of the hepatic veins or you inflate a balloon and get the pressure on the other side. So doing this too is what we call the hepatic venous pressure gradient and live a number more than five millimeters of mercury is diagnosis of portal hypertension. But really clinical portal hypertension, you see, when this number is more than 10. We are very aware of the difficulties of getting this test done in pediatrics children's needs sedation. The catheters are small. Maybe it's not a lot of expertise to do this in children's and this is what we don't talk about, these values very much. But in adults it's really used to make clinical decisions to evaluate response to therapy. For example, a decrease of the portal pressure to less than 10 decrease the risk of complications. If you see a decrease of the portal gradient less than by 20 percent is a good response to treatment, then all these things are used to really guide therapy.
Speaker 3:But it's in basis and for many of us portal hypertension is based on a clinical, laboratory and radiological data. Then clinically you see this patient that comes to you most likely have the stigmata of liver disease. If the patient have advances, roses, you can see a splenomegaly collaterals in the abdomen, acitis Laboratory. You see, thrombocytopenia is made the most relevant value. You can see some leukopenia in more advances case. This is why many of our patients end in hematology for many years before they come to see us. Then, radiologically we will see the collaterals or we see vascular thrombosis. You can use a wide variety of radiological studies, from ultrasound to CT scan to MRIs. It's a full spectrum of evaluation.
Speaker 1:Wow. I mean, there's so many different approaches here and it can be so challenging. So I think for this particular episode, we're going to kind of talk through a case, just because I think there's just so many variables and I think that might help direct our discussion. So, say, we have a child who has autoimmune hepatitis, but we don't know if they have portal hypertension. They've never had varicellar bleeding. They're about 12 years old, which is a typical age we may see. And so what approach do you have for screening for portal hypertension, knowing all of these challenges that you just mentioned, and screening for varices, cirrhosis, and does this approach change based on the underlying etiology of chronic liver disease or the patient age?
Speaker 3:Well, the diagnosis of cirrhosis is histologically. You have a biopsy that shows you that you have cirrhosis and if this is a new patient that has a new diagnosis, you might have that in front of you and you could say this patient has cirrhosis or not. But let's say that is a patient that you have been treating for six years with autoimmune hepatitis. It's very different of a patient with, for example, biliary atresia, because autoimmune hepatitis if you are treating the patient well, it shouldn't develop portal hypertension. The patient shouldn't have advanced liver disease. When the patient with biliary atresia that was born already with cirrhotic liver, depending on how the evolution of the disease goes, the patient might have progression of the disease Clinically. You see the patient in front of you. This patient has a splenomegaly. This patient has colaterals right there. This patient very likely have portal hypertension. But those are the most advanced cases. You might want to learn that this patient have portal hypertension or have some progression of the fibrosis before that. And, as we said, liver biopsy is invasive and nobody wants to do very often. Then playlacone is something easy that you can see. The playlacones are low. You can start thinking this patient might have portal hypertension. And one thing that I want to mention the lack of clinical findings doesn't exclude portal hypertension. Then there are patients that have portal hypertension and you don't find any of these. It's a spenomegaly or a cytosine. Then it's kind of a difficult to assess. Then the playlacone is great, it's easy, it's available to you but doesn't correlate very well with the hepatic venous gradient.
Speaker 3:Then we have been created over the years to try to generate more tools, and one tool that has been used for many years and it has been actually validated in pediatric there are few reports is the apricot, is the AST to playlet ratio index. The problem with the apricot is that there are different numbers that we give to this and you just divided the AST of the patient by a normal value that is considered 40 by the playlacone. It's kind of a math involved. And then the problem is that the sensitivity and specificity of this apricot is only in the 70, 72, 77 percent. Then you meet a lot of patients that you might want to identify or you might think that the patient might have portal hypertension. When they don't, then this is not a very good way, but at least it's something that we have to use in these patients.
Speaker 3:More recently there are new techniques that have been developed, for example, the ability to assess delivery stiffness. Stiffness is a physical property of the liver, influenced by the amount of liver fibrosis content, and these have represented a major advance in the field of hepatology. We can measure delivery stiffness. Or also there is a new technology called sonorelastography that gives you also numbers have proved there be significant indiscriminated patients with and without clinical, significant portal hypertension. For example, adults very clear have defined that a patient with a liver stiffness of more than 20 kilopascals and a playlick on less than 150, half is an strong indicator for portal hypertension. The problem is that we don't have those specific values in children. There are new people have been working very hard in the last few years to develop these values, but still there is a lot of difference in the technologies that is using the tool.
Speaker 3:Maybe the the lastography that I have in my hospital is different than your lastographies and we don't have thousands of children in any given hospital to do these tests. Then we need to be collaborative, we need to have multi-centers. All these and all these are things that are cumbersome. For example, the lastography shouldn't be the same for a six-month-old or a 20-year-old, then a patient that is overweight. We have a big problem with a population that we take care of very frequently, for example, the fontan patient.
Speaker 3:The fontan patient, fontan associated liver disease these patients, regardless of the amount of scar tissue they have a very an increased stiffness. Then we have these problems and many of these parameters really don't correlate very well with the things described in the literature. What I would usually do is perform serials of these lastographies in this patient and we can see how they change over time and we are using the patients of their own control. This is not very scientific, but if I see that the stiffness is increasing, I get concern about those patients.
Speaker 3:The other thing that is maybe more recently also is the splint stiffness. This is a new technology and people feel like it because the splint is more related to the portal hypertension. It might be a better parameter to define portal hypertension. There is a lot of things in the pipeline. There are some laboratory tests that you can use, the fibrochure, then a lot of things that are out there. Many of those are not validated in pediatric, but I think that you can draw some conclusions and try to use it in your patients if you don't want to be doing liver biopsies or endoscopies. That are maybe the way that you really can assess these problems.
Speaker 2:Absolutely so. That was a great kind of overview of how to diagnose a patient with portal hypertension and the different avenues to look into. So, for example, our 12-year-old patient has some sign of possible kind of varices, or esophageal varices in particular, I guess. Focusing on esophageal varices, when would you consider screening for them In any primary prevention methods, for example endoscopically or medically? Would you do to prevent bleeding from happening?
Speaker 3:That is an excellent question.
Speaker 3:The clinical presentation of portal hypertension in the form of baristial hemorrhage is very dramatic and it changed the life of patients. You are traveling and your child has a baristial bleeding. I have patients showing the ED the day of their birthday, that they're celebrating their birthday and they start with hematomesis. Then you can imagine. This is very dramatic and also maybe the first symptom of then recognizing that they have a liver disease. They didn't know that anything is going on. There is really also associated with morbidity and mortality. There is a lot of adult data for many years that I think that 20, 30 years ago they reported 20, 30% mortality in the management of this when this patient is presented with baristial bleeding, and it has been an extraordinary effort over the years for people to have an algorithm on how to treat these patients. There are hundreds of clinical trials in adults, including thousands of patients that they have been following different ways to try to determine what is the right thing to take care of these kids. The problem is we don't have that in pediatric. There are no evidence-based recommendation for primary prophylaxis in the management of children with baristial bleeding and if you are not going to do primary prophylaxis, then you are just going to scope the patient until the parent, you have barisis and you may bleed. It's worth doing the endoscopy if you are not going to do anything. It's a little bit difficult and then adopting the recommendation based on adult's experience maybe not be in the best interest in the children's.
Speaker 3:You see there was a publication a couple of years ago from the Children's Network. They report about 630 children that they follow over. I think that was 10 years or so and this is patient with biliary atresia. The risk of baristial bleeding at five years was 12.5%, Very low, and this is 600 children. This is as good as it gets for us in pediatric. And then from that 12.5% of children that bled, nobody died. Then the question is is it really worth to put these patients through endoscopies and all this if they don't carry any mortality? 12% of those children that bled went to liver transplant and it drives. You know that when you get there the patient is at the edge of something big. Then that is one question. On the other hand, if you look at a publication by Dr Molly Stone and collaborators I think that was two years ago she looked at the FIS database. It's a pediatric health system database and she looked at about 3,000 kids with portal hypertension and this is a conglomerate of about 50 pediatric hospitals in the country I can imagine that that might be one of the best 50 pediatric hospitals in the country that they collaborate to do that and about half of those kids bled in a period of years about 1,500, I think of 1,200. And in that cohort there is 7% mortality during the admission and 20% mortality overall. Then when you look at these numbers you say wow, it's not Arbena.
Speaker 3:And then I think that it's just the mix of how you want to look at the problem. Then here at Columbia we are scrimmed for varices, we are scrimmed for a portal hypertension and we try to eradicate the varices. I don't know if that is the right thing to do, but this is what we do here and this is what I want to put into examples because I don't want people to get the idea this is what they should do. But when you get these patients that were on vacation in New York and they have a paracelblit one of my patients was vacationing during Christmas break in Colorado in an area that the closest pediatric hospital was three hours away, and he has a variceal bleed those things really get close to home for you and you want to prevent that from happening and for that reason I think that maybe screening is important.
Speaker 3:Then the adults screen and also the prophylax, what it calls primary prophylaxis. The backbone of primary prophylaxis for adults is non-selective beta blockers and these non-selective beta blockers we know that they have B1, other energetic blockade that address a decreased the portal flow through decreasing the cardiac output and a beta 2 blockade that decrease the portal flow through the splamming vasoconstriction. Very important. Most of the effects are based on the beta 2 blockade. I don't know if any of you have star patients on beta blockade but that involves that the patient have to come to your office every week to check the heart rate and you want to decrease the heart rate by 20% and sometimes it's very difficult and you get to very high dose and you stop there. But then you see the effects of the varicose decreasing and I have done that many, many times and I have done that in the past, I do that less now.
Speaker 3:The biggest concern is what happened when one of these kids on beta blockade bleed. Young children's response to hyperbolemia is mainly with increased heart rate. They don't increase the stroke volume that much. If this kid is beta blockade, they don't have the capacity to respond with tachycardia and maybe a small amount of bleeding can cause shock in this case. And for that reason is that many people don't feel like the risk outweigh the benefits or the benefits outweigh the risk in this patient population, because they depend on that heart rate and we are nervous. This is a patient at high risk for bleeding and now I'm going to do beta blockade.
Speaker 3:There is other things that people do. That is called pre-primary prophylaxis. This is the prevention of the progression of the varices. Then you endoscopy someone and the varices are small. You can start in on beta blockade. Those patients are at lower risk of bleeding and the beta blockers can prevent the progression of the varices.
Speaker 3:The problem is we don't know. Most of these studies in adults were done on patients with hepatitis C. That was a progressive disease. Now there are studies done in adults on patients with NASH. Many of the studies were done with alcoholic cirrhosis. Those are progressive disease but we don't know if, for example, in the area of Tricia patient the disease is progressing or is it static or is it regressing, then what will be the value of starting this pre-primary prophylaxis? We don't know if the portal hypertension is getting worse, then all these dilemmas in pediatric are very difficult.
Speaker 3:I want to, at the end, touch on the endoscopic ligation.
Speaker 3:That is the second method for this primary prophylaxis. This is what we do. There was a recent publication maybe 2017, or that recent anymore from France, dr Duchesne collaborators in Paris. They look at their experience. It was a 15-year cohort. They look at our close to 200 patients and they did prevention prophylaxis in one group and no in the other group. This is not randomized this is not but the study demonstrated that the patients are under when primary prophylaxis did much better, have less mortality and less complications that the patient that didn't receive the primary prophylaxis. They also felt a small group of patients felt the primary prophylaxis and those were patients that they started banding late. It was also very interesting in this study they did sclerotherapy for prophylaxis, which I will never advocate. I will never advocate I think that sclerotherapy carries a lot of complications that I will not advocate to do sclerotherapy for primary prophylaxis, but this team in France did it and the conclusion of the study is that all patients should receive primary prophylaxis to prevent morbidity and mortality.
Speaker 1:Were those pediatric patients? I may have missed that. Yeah, those are pediatric patients. Oh, they were pediatrics. Oh, interesting, all these are pediatric patients.
Speaker 3:That is the largest cohort that I have seen reported in pediatric patients.
Speaker 2:And the primary prophylaxis they use is medicine, ligation and sclerotherapy. No, they use only sclerotherapy.
Speaker 3:Just sclerotherapy and they didn't use any ligation and many people are scared of using beta blockers.
Speaker 1:So I just want to kind of move on a little bit to our patients. So say we did or did not do this and she's actually coming into the ER with an acute bleed. Say we're the fellow and I always make this joke because all fellows do this but they say, hey, let me call my attending and call you right back, but can you walk us through your process of that initial assessment and stabilization? And how do you make the determination of hey, it's the middle of the night on Christmas night, we need to go in tonight, versus doing medication stabilization and maybe going to the OR at a different time?
Speaker 3:The first thing that you need to do is assess the patient and see the hemodynamical stability of the patient. You need to assess the patient. You need to resuscitate the patient if they are hemodynamical or unstable. The goal of the resuscitation is to preserve tissue perfusion. Then you will start with whatever you have in hands. If the patient is hemodynamically stable and you might not need to give normal saline or albumin right away, it might be better to just give blood and remember this patient with portal hypertension. They most of the time don't handle fluids very well. They might have some subclinical acitis or they might have clinical acitis. And now you are giving more volume to this patient. That is a problem. But this is the third thing is to assess the patient. Maybe the patient know that they have liver disease, but they may not. And if they know that they have liver disease, I don't put an NG down for the GI bleed. I just start with lab blood work and resuscitation and some medication. Let me walk you through about the resuscitation first and what is the kind of blood products that I use and how much. Much is no better here. Then don't try to just give two units of blood or three units of blood. You need to make the patient hemodynamically stable with the minimum amount of blood products that you can, and actually the aim of the hemoglobin is six to eight. You don't want a hemoglobin of 10. And the problem is the more volume you give to these kids, maybe they stop. Sometimes they bleed and they stop. But if you give a lot of volume and you increase the blood pressure then they bleed again and what you want is to keep this patient stable, or nylon, then you will be able to stop them in the morning. Or you want to transfer the patient from one hospital to the other. You don't want this patient bleeding in route. Then minimum resuscitation to keep hemodynamic stability. Goal of hemoglobin seven to eight.
Speaker 3:Then CBC, liver tests, biochemical profile, coagulation profile, type on a screen because you need to give the blood products and an ammonia level, and we will talk about why all these are important. The liver test you want to know is how is the liver of these patients? You don't know this patient, you just met them. You want to know what is the bilirubin. What are the liver tests? Sometimes just for having. If they have an underlying liver disease and they have a low blood pressure, the liver tests may elevate something that we call as not a chock liver. The biochemical profile is relevant because you want to make sure this patient is not hyponatrimic. Hyponatrimic patients are sicker than you think. They can go down very fast when the electrolytes are not right. And then the coagulation profile.
Speaker 3:This is maybe one of the biggest problems that we have because we order, but then I don't think that we should correct coagulopathy. First of all, the conventional coagulation tests that we do here proton beam time, inr, ptt really they do not reflect the hemostatic status of the patient. They don't reflect the risk of bleeding from the patient Patient with advanced liver disease as an elevated INR and PTT. But they also have a low protein S and protein C that are antithrombotic factors. Then the balance here, what we do in the emergency room, really doesn't correlate. Then you shouldn't correct those numbers and remember the body's ability is to do portal hypertension, not due to the coagulopathy. Then you need to try to control the portal hypertension and not the coagulopathy. There is also then given FFP. It's not recommended for this patient.
Speaker 3:And at the same time there is no evidence that the platelet count of the fibrinogen level correlate with the risk of failure to control bleeding or re-bleeding. Patients bleed because they have high portal hypertension. Patients re-bleed because you didn't take care of the portal hypertension. You didn't do, you banned it, but new collaterals developed and they bleed again. However, if you have a patient and you cannot control the bleeding and you are in the OR and you have been big trouble with bleeding and maybe those patients might require some kind of products, because volume is always a concern, ffp might not be ideal.
Speaker 3:There is a new product that I don't know why not many people know about that. It's something called K-centra. It's a protein-being complex concentrate. It's a concentrate of the vitamin K-dependent and this is called K-centra, vitamin K-dependent factors. It's factor 2, 7, 9, and 10. And they also have protein S and protein C. Very small volume. This is the few ccs can control the coagulopathy, can normalize that INR. Then this is something that you can do.
Speaker 3:The other problem is what are those patients that come with a acute bariceal bleed and they are on anticoagulation? Some patients with anesthetic liver disease that might have a portal ventrombosis or has some other coagulable disorders might be an anticoagulation. There is no question that you should stop the anticoagulation, but for how long? Each have to be individualized? This is when you need to call your hematology friends and say help me here, for how long I can stop it? The patient is bleeding. Once I control the bleeding, one can bring them back. I think that vitamin K is something that everybody gives to these patients because it's easy and if they have a coagulopathy from vitamin K deficiency, that help us. It's always better. I'd rather scop somebody with an INR of 1 than with an INR of 3. But that means that I need to give 500 ccs of FFP and not going to do it Then this is the balance risk benefit and what I want to achieve.
Speaker 3:The other portion that is very important is antibiotic prophylaxis. This is an integral part of the therapy for patients with bariceal bleed, for those patients with advanced liver disease, and I will say this might has been the most relevant change in the management of patient with bariceal bleed in the last 30 or 40 years. Many years ago patients came with bariceal bleed. They didn't get antibiotic. They develop SVP. It's a patient in the ICU, their cytosys there. We gave fluid. We didn't think about the patient is not responded. People didn't think about sepsis, because SVP is no flourish sepsis. They don't have a lot of fever, they don't have a lot of peritoneal signs and for these patients that are coming with bleed, the translocation is there, then antibiotics must be there and the other part is encephalopathy.
Speaker 3:Bloating the GI tract is a big load of protein and they become encephalopathy. You see patients coming with GI bleed totally encephalopathy. You need to intubate them and you think this patient needs to go for transplant. Can even they bridge to transplant? And once you stop the bleeding and you clean the GI tract they wake up. Keep that in mind that you need to treat the hyperammonemia.
Speaker 3:And then the last but not least, the medication that is my favorite is optiotide, because it keep me home.
Speaker 3:Optiotide is a somatostatin analog that decrease the inflow of blood to the portal system by constricting the splanic arterioles and significantly reducing intravartiscial pressure. Then when we give optiotide to the patient we can weigh six, seven, eight, nine hours to come under the endoscopy and we can stay home. Optiotide usually in pediatric patient is a way base. We start with two micrograms per kilo bolus and then go with one or two micrograms per kilo per hour in fusion and in adults or older kids the maximum dose is like 50 or 100 micrograms bolus and 50 micrograms per hour in fusion and most patients actually do very well they stabilize.
Speaker 3:You have time to make them hemodynamically stable and scoped them in the morning Very rare we have to come in the middle of the night and that is for the patient that maybe you thought that you can. If the patient came at 1 pm and you think that you can leave it for tomorrow, that is a mistake. Try to get that patient stabilize and scoping before you go home because so many hours later you might not get the same thing. But you need time to stabilize the patient and usually the optiotide and the blood products help.
Speaker 1:How about use of proton pump inhibitors? Is that something that you do in addition to octriotide? Have you ever used it instead of? Is octriotide for everybody?
Speaker 3:For portal hypertension is octriotide. Actually, proton pun inhibitors are not recommended. If the patients come with a GI bleed and you are not sure that this is a bariceal bleed and this is maybe something that we also should talk about that many patients with esophageal varices that present with a bleed they might not be bleeding from the esophageal varices Then if they are bleeding from the doodenal ulcer they might benefit from PPIs, but the PPIs after then. If I start the patient which I start the patients on that, I usually start PPI bolus. It's not enough lines to have blood, I have fluids, the octriotide drip is a priority and then the PPIs. The PPIs I use it.
Speaker 3:Once I scoped the patient If I didn't fire an ulcer the only thing that we found is varices, then you know, still you keep the patients on PPI because the reflux of the acid in that varice that you like it, that eventually become an ulcer, then that acid reflux can cause bleeding in the next couple of weeks. But you shouldn't keep these patients on very long-term PPI. Actually, some adults literature recommend stopping once you diagnose that this is just a variceal bleed because of the risk for aspiration pneumonia, the risk for clostridium-difficile infection and colitis on this patient population. Then many of the adults recommend stopping the PPI after the endoscopy proof that this is a variceal bleed.
Speaker 2:That's very important to know because I think everybody's thought process would be okay just start them on PPI and octereotide, but it's good to know the risks and benefits of the medications that you're using. So overnight the patients stabilize octereotide your best friend was used to stabilize the patient and you come in first thing in the morning, 7.30 am, to scope the patient. Can you walk us through what you bring to the OR and then what you're looking for in terms of the scope, kind of the location of varices, the grade, the wheels, and how would you decide on which method to use to stop the bleeding or prevent further bleeding?
Speaker 3:First of all, you are scoping this patient but you don't know what you're going to find. You think that the patient has variceal bleeding but, as I said before, you might find other things and you should bring all the tools that you have to take care of a bleeding. You need to use your banding device, use a scleral device, your clips, your loops, your sprays. You bring everything with you because you are going to evaluate the patient first and then decide what you need. Then you have to bring your whole bleeding basket, everything in there. I'm going to tell you this if you want to remember something about scoping a GI bleeding from this discussion is this part If the patient doesn't have a contraindication before you take this patient to the OR. If an erythromycin infusion 20, 30 minutes before the OR, if erythromycin to this patient. Sometimes they forget and we are just pushing the patient out of the ICU and we just push the erythromycin there. Erythromycin is a prokinetic and when this by the patient that get anesthesia and you enter the scope, you will find zero blood in the stomach. The most difficult part of a GI bleeder is to see where the patient is bleeding from and to find the source. Once you find the source. Most of us can handle anything else but find it. When you get to the stomach and the stomach is full of blood and you spend two hours or three hours if you're clearing that blood clot, then erythromycin is fantastic. It works. 90% of the time you go in and there is no blood in the stomach and you see the blood clots in the Dino, they really the erythromycin, push it out. Then. This is the first consideration. The second consideration is stop to anesthesia. Most pediatric anesthesiologists intubate everyone, but sometimes once in a while. If, depending on which institution you practice, adult anesthesiologists don't intubate everyone for endoscopy, then this patient that is bleeding and is vomiting blood should have an airway protection. Then that is the most safe safety first, very safe that this patient should be intubated. And then I don't use even if the baby is a small baby, I don't use neonatal scopes for this. These are prestigious when you need big channels to flush to, to intervene, then I use a regular pediatric scope or an adult scope all the time for GI bleeders. Even if there are small babies, I don't think that you need to use this neonatal scope. Then I advance the scope and I perform a full endoscopy.
Speaker 3:I assess for the Udenol ulcers, gastric varices gave for the hypertension, gastropathy, esophageal varices, and you know, you go in, you see the varices, but you unless you see that the varices bleeding right there, and most of the time you don't see that these days because the octrotide held, decreasing that pressure in the varices and the varices are not bleeding at the time that you go there and for that reason sometimes you feel like the varices is not big enough. This is not the varices that I think that the patient bled for, because usually the varices are very big and these are not All. These varices might have been decompressed by the bleeding or it might be decompressed by the octrotide. Then these are things to keep in mind. If you don't find any other source of bleeding, banding that varices or sclerosis in their varices, don't leave the patient without doing an intervention. I get referred very often. We discovered we didn't think that the varices were big enough and we didn't do anything and then the patient bled a week after, no reason to do that, and then the best area where you assess the severity of the varices is the distalisophagus and this is where you are going to start therapy.
Speaker 3:I don't think that I'm going to talk here about the different classification of the severity of a gel varices. There are many classifications. There is the pac-wear classification, the dog-radi classification, the Japanese research society classification. There is no need for that. I really think that you need to describe in your procedure what you saw. You need to assess the size of the varices and the science that can tell you that there was risk that these varices are going to bleed soon or they bled, and these are these red patches or a strip on the top of the varices. It's a sign of increased risk for bleeding. They are called red signs or the red-well signs and when you see those, those varices next to be banding before you leave that patient's body, sometimes I think that they are small varices on top of the varices, because there are small vessels on top of that big vessel and those are the vessels that bleed and that right there tells you that the severity of the portal hypertension. Then you remove the scope because you went in with the scope with no attachment.
Speaker 3:The best method for me to control varices is banding. Variceal bleeding or to do primary prophylaxis is banding. The problem is that the banding device is very large and you cannot pass through the throat of the baby very often, mainly if they are intubated, and then you want to pass this device. It's almost impossible. I think that I have passed it in people that are a year old. It's a lot of negotiation with anesthesiologists. The fluid to decrease the size of the balloon in the tracheal tube is sometimes it's just better to do the scleral. If you think that the patient is not big enough to accommodate the banding device For the scleral, you just go through the channel with an either and a scleral.
Speaker 3:You can do inject directly into the varice or even parts of a gel injection. Sometimes people are very scared of injecting the scleral gene in the varice and when you inject they bleed. You are going to cause bleeding, but don't panic. You did also already something to stop that bleeding, that is, injecting the sclerosin agent. Go to the next varice and sclerosin, the next one and go to the next, and by that time the first one is stop bleeding. The second time, the second one is stop bleeding. And this is sclerosis of varices, injecting on the varice and it's very easy, but it's not a recommended method. Really, these sclerosis can cause ulcerations, can cause problems, can record ulcerations in the sofagos, can cause esophageal structures.
Speaker 3:It's not ideal, then the ideal method is banding and for the banding you remove the scope because the scope and you put the banding attachment. There are different types of banding devices. I recommend that people become familiar with one, mainly when you don't do many of these, become familiar with one. And how to assemble the bander devices is sometimes the most stressful part. People don't know how to put it together and you don't have to put it together, otherwise it would not function. Inside the patient you misfire, you get a lot of problems and once you do the suction and you have to release, bleeding happen. Then make sure that attachment is placed appropriately in the scope. You go inside again. All of a sudden you see that it's more difficult to pass the scope because now you have a bigger attachment on the tip of the scope and you have decreased visibility because the attachment with all the bands are at the tip of the scope. Then your visibility decreased significantly. That's what you need to do in the scope before and do all the assessment without the attachment.
Speaker 3:Once you are in the stomach, I put it back into the sofagos and I kind of know already which varices I'm going to ban first. I put that in my head. When I go with the regular scope, and then I go to that, I put the device on top of the varices and I do suction. When you do suction, the varix comes to you. You move the device and fire. Many people are very nervous and think one on fire, I let this go.
Speaker 3:I think that this is the number one reason why many people misfire the bands.
Speaker 3:I tell the fellows when they are doing this first time, once you deploy that you feel that the band is there, count one, two, three and then you blow air. By doing that you are sure that the band is in place. If you do the band, deploy it and you pull out too fast, you might pull out before the band can appropriately place into the esophageal varices and that's it. You do that again and again and again until you see that you eradicate the varices. Most of the time, after you put two or three very distally, most of the proximal varices disappear. It's like a miracle happened All these varices that were here. Now they are not here anymore because you stopped the blood from coming through. Things that you tell the patient when you do the banding is sometimes they have some chestiness If you band too high. This is the other thing. Don't get very excited and place too many bands, because if you band above the maybe half of the esophagus, the patient gets very much pain and is very uncomfortable. Then try to do the distal banding first.
Speaker 2:So there was a great overview about how to approach a patient after they're stabilized during the endoscopy. So the patient has been stabilized, went to the OR. You did some banding and stopped the variceal bleeding. The most common question asked by the nursing team and by the family and possibly the fellows, is when can we advance feats? When can the patient start eating and drinking? Post-procedure and once the patient is stabilized and gets to go home, is there anything that you would do to prevent recurrent variceal bleeding?
Speaker 3:Well, I think that the most important thing is you did the procedure where sometimes these patients reblead Very rare what sometimes happens. The other thing is you are given octrotide to this patient, you are decreasing the blood flow to the intestine. Then these two things maybe dictate when you are going to let the patient bleed, when you do these procedures on the outpatient basis, that they come for follow-up of this banding. They go home. I let them eat the same day. I think that the biggest issues when they are bleeding, I want to make sure that the bleeding is stopped and I don't have to take them back to the OR After banding I recommend, and after escalator, a soft mechanical diet as soon as the patient can tolerate, and that's it. They get this soft mechanical diet and for seven days I tell them that they can have bleeding, maybe three or four days after the banding, because when those bandings fall off an ulcer can form in that area and they can have the bleeding.
Speaker 3:The other thing that we prescribe is a medication called sucrafate. We are familiar with that and we prescribe that three or four times a day to provide like a coating substance on top of that ulcers to prevent the bleeding. But totally normal activity. They can do everything that they want, no limitations. They can go back to school and then to prevent the bleeding you can do two things. You need to eradicate the viruses, which doesn't happen, as I told you. You put three or four bands and you don't see more viruses there, but they will come back. And then you need to do these every three to four weeks until totally eradication. And once you eradicate the virus, that means that they came back and you don't see any virus. You call them back in six months because they can come back, or you can call them back in a year. That's why many people advocate to use beta blockers that might be preventing the development of new viruses. Depending on the patient, you might need to talk about doing tips or doing other interventional procedures to prevent the recurrent of the bleeding.
Speaker 1:So just to clarify, because we mentioned primary prophylaxis and the beta blockers having some concern what is your approach to using these beta blockers for the secondary prophylaxis? So you've banded them, we don't have any more. Would you use it in that instance?
Speaker 3:Well, I don't think so. I try to, but there are patients that I kid banded and the viruses coming back. Then that patient is now. I know that this patient have viruses. Remember we talk about primary prophylaxis when we didn't know if the viruses are going to progress. We didn't know the liver disease. I still have the same concern that if these patients bleed they might not have the appropriate heart rate response. But in selective patients you really want to prevent these viruses from coming back. You are scoping them very often, every three to six months. Then they might not get to the point of developing very large viruses that they bleed. That might be the only difference that you are scoping them frequently, but I still have the same concern.
Speaker 1:Yeah, no, that definitely makes sense. And then you even mentioned a shunt just to kind of take us way back. You talked about how the most common reason that we'll see with the portal hypertension is often extra hepatic. Our case has been mostly intra hepatic, but either way we can potentially have recurrent bleeding. So if you have someone who does have this recurrent bleeding, can you walk us through that timing of referral for surgery and what that looks like?
Speaker 3:Well, I think that it goes back again to assess the patient. If I have a patient with recurrent esophageal variceal bleeding and it's a cirrhotic patient, we are at this stage of the compensating portal hypertension. This might be an indication for transplant. But let's say that this patient is not that cirrhotic or it's a patient that have extra hepatic portal hypertension and even in certain patients, biliary atresia. Patients are stable for years and they are growing well and they have perfect synthetic functions.
Speaker 3:Sometimes people decide to send this patient for a shunt. Then the surgery will be transplant. For those patients that have very advanced liver disease and they have a compensated portal hypertension, that will be the surgery. But for patients that might have a better synthetic function and deliver diseases in advance or have maybe portal hypertension due to portal vein thrombosis or non-cynrotic portal hypertension, those patients benefit from shunt and actually the management of patients with portal vein thrombosis. The recommendation is this patient have portal vein thrombosis and have varices, to just send them to a surgeon Don't even bother to try to eradicate the varix and then to a surgeon that is expert in these procedures and they can perform something called a mesentery cleft, portal vein bypass or mesorection. The benefit of this is that you are bringing the blood flow back to the liver. The surgeon will create a bypass between the superior mesentery vein and the intrahepatic vein. Then you are bypassing the portal vein and you bring the blood flow back to the liver.
Speaker 3:Having a portal vein thrombosis is not very healthy for the liver and when you do this bypass the liver benefit from that and that's why this patient should get this shunt. Or it's a new technique by interventional radiology where they attend recanalization of the portal vein with a placement of the tips, and these are vascular interventional procedures. This is for the mesorection For patients with non-serotic portal hypertension that don't have a normal liver. Then the shunt that is ideal it will be a distal splenorinal shunt. It's a shunt between the left renal vein and the splenic vein. This way you dvA some of the blood and the collaterals that the spleen is bringing to the stomach and the esophagus to the left renal vein but still preserve the blood flow from the superior mesentery vein to the liver.
Speaker 3:There are many other type of shunts that are central shunts that are not really recommended in pediatric because they carry a high risk of worsening liver disease, hyperamonemia. Then I will say when we talk in pediatric my three preferred surgical procedures for portal hypertension are transplants, mesorection or distal splenorinal shunt. But the mesorection only work if the liver is healthy. This is for patients with normal liver, parenchyma and portal vein thrombosis.
Speaker 1:I see. So there's really a lot that goes into this decision making, and it's another one of those situations where you do share decision making with the surgeon, and I can see how it's important to have someone with a lot of experience in this area.
Speaker 3:Yeah, I think that these decisions have to be made at a center with a multidisciplinary approach, a center where you have interventional radiology that offer your input. You have the surgeons. Usually there are the transplant surgeons, the one that the most of the expert is doing this, and a hepatologist that we can speak about the patient's liver health status. It's really worth to get this patient to surgery. We know that he will need a transplant in the next three, four years and I will not recommend this chance if I think that the patient will need a transplant in the next couple of years and definitely is contraindicated. If the patient have elevatability rubin impersonation that patient needs a transplant, that patient cannot offer surgery.
Speaker 1:Yeah, no, that makes sense. And if you're practicing in a smaller center or a rural site who maybe doesn't have access to this, would you recommend then a pretty early referral to a larger center that has all of these resources?
Speaker 3:Yeah, I think that these patients with pediatric patients, adult patients, are different because there are so many of them and there is so many expertise by the regular gastroenterologists to manage this patient. Pediatric gastroenterology in a center with our hepatologists and the expertise of interventional radiology shouldn't be managing these patients. Children's are very compressed. We don't have large database or multi-center trials or large trials that you can read and get the knowledge from that. I hope that we can get there. But today we practice based on the experience that we have and I have to tell you we take care of a lot of these kids here in New York at the Children's Hospital, new York Presbyterian, but in other hospitals you see one patient every two, three years. You don't have expertise to handle this patient. Then they should refer to a center of expertise.
Speaker 1:Well, and the science is changing so much. So, if we start to look towards the future, what do you see as the main changes that are coming in the next 10 years or so?
Speaker 3:I think the changes has to come from data. We need to get data and I'm very, very excited that Dr Benjamin Snyder from Texas Children has organized an international multi-center pediatric portal hypertension registry. He started about two years ago. There are several centers already participating. We are one of those centers. Then we are just collecting retrospective data and people say it's retrospective, but this is the data that we need. To make sure that agencies, mainly the NIH, understand the need to study this, understand the need to support prospective data collection, understand the need for us to have a thousand patients with portal hypertension and then different etiologies that we can stratify and do clinical trials and apply new medications. I think that this is very, very important and then very excited about this registry.
Speaker 3:The other thing is new medications that has been approved. For example, terlibresin is a medication that has been used in Europe for a year. They don't use optretide, they use terlibresin for these GI bleeds. It's not approved in this country, but it has been recently approved for the treatment of hepatoreal syndrome in adults. Then I hope that this will follow through with that. Eventually we'll get approved also for the management of patients with GI bleed, and we didn't talk about other complications of patients with GI bleed, like hepatorenal syndrome, acute kidney injury. That can happen, all the things that could happen in these patients. Enterlibresin is a drug that is promising and I hope that we can get approved for pediatric.
Speaker 3:The other thing is development of predictive models. I really think that we need to stratify portal hypertension in different categories and these models for example, most of these prognostic models that has been done. All these algorithms of treatment that were developed 15 and 20 years ago in adults were developed on patients with hepatitis C. Guess what? Those patients don't exist anymore because they're cured and we don't know if we can apply that to patients with a fatty liver. We don't know if we can apply that with patients with autoimmune hepatitis that will be responding to treatment and getting better. Then I think that developing predictive models based on the theology of portal hypertension is important.
Speaker 3:And the other thing that is very exciting is the new interventional radiology techniques that are our best friends. They can do things that we cannot. For example, this technique and that is the balloon occluded retrograde transvenous obliteration of gastric varices. It's something that has changed the way that we manage gastric varices. Many of these patients there was a point that they needed to go to surgery. And now interventional radiologists if they have a spontaneous splenary nodule they go for a procedure and is one or two hours procedures and they go home and they are very successful. Then the re-analysation of the portal vein their interventional radiology is the field that will be an ally for us on taking care of this patient and treating this patient and I think that they have a lot to offer and it will bring a lot to the table for us to take care of the patients.
Speaker 1:I love that so much coming in the future for this patient population, and you do bring up a good point. I think this is one of our only episodes so far where we've talked about portal hypertension, but we definitely need to have some additional ones to talk about some of these details in the future. This is a newer question we've been asking for those who you know. We've talked about so much and you've already mentioned a couple key things for us to remember, but if you could summarize what are the top three takeaway points that you would like all of our listeners to remember from this episode?
Speaker 3:Well, I think, first of all, children are not small adults. The theology of liver disease is different, the ability to modify the progression of liver disease is different and the tools that we have is different. We cannot do banding in a three-month old and the way that we approach that patient is going to be different. Then the number two is the complexity of this patient. You need to understand the expertise that is required to take care of this patient and this go back to the question that you asked me before. You need a multidisciplinary team. You need a critical care team, an anesthesia team, surgeons, gi, interventional radiologists with expertise in this particular area. You don't have that in your center Refer the patient, stabilize the patient and send it to a center that can take care of that.
Speaker 3:The other thing is we need to develop data. We need to collect data. We need to stratify patients based on severity of disease and etiology of the portal hypertension and identify those patients that need treatment. How we are going to set and going to scope you, because you need a varecial ligation, getting to that point that I know you're selling the idea and taking you to the OR to scope you and see what you have, and I need to scope to any patients to find one that I can intervene. I really think that we need to get to that point to develop those models. Also, we need to develop effective treatment for the prevention of the varecial bleeding in children. That we don't have because the beta blockers are still scary and we are very scared to use it Pharmacotherapy that prevent the progression of the viruses in children.
Speaker 1:All right If Dr Snyder from Texas Children's is listening. You have a lot of work to do with all of this multi-center data that you're collecting. Dr Martinez, thank you so, so, so much for spending this time with us. If you've looked back on your long career, what has been your most valuable advice that people have given to you, and what advice do you give to our listeners?
Speaker 3:Well, I think that the most valuable advice came from my mother. Very early on, she told me you need to go to school, you need to study. My mother only finished sixth grade. My father only finished 11th grade. They were not well educated, but they knew that education was the way to bring us forward and the only way that we can be successful in our life and in our career. And then she also told me but when you go to school, try to choose something that you like and enjoy, because this is what you are going to be doing for the rest of your life. And these two things are very valuable for me, and it came from her, and she is, you know, my biggest advisor still today. She also is very bossy, but it's my mom. What can I do?
Speaker 1:I love that. My mom used to say you're either going to be working with your brain or you'll have to work with your hands and feet, and so you know studying is such an important thing.
Speaker 3:And then to the listeners I said people that are listening already have gotten an education and this is what they are here, and I think that the focus should be on advancing the field. We should be curious and we need to get involved and establish collaborations and answer relevant questions. It doesn't matter how difficult the question is today, you need to kind of peel it like you're peeling an onion. The question is in the center of that onion. The answer is there. You need to peel it one at a time and go through different phases of the investigation or the research. Engaging people, engaging collaboration, whether it is to improve the diagnosis and management of portal hypertension in children or any other disorder of your interest. The days go by, the years go by and the only thing that is relevant is what you contribute to your patients, to your society. And if you don't get involved and be curious and maybe the questions are not coming to you, then help others answer the question. If those people put the question out there and call you to be a collaborator, do that.
Speaker 1:That is so true. Well, dr Martinez, thank you so so, so much for joining us today.
Speaker 3:I want to thank you all the listeners. I hope that you enjoy and you'll know something from our discussion.
Speaker 2:Well, that was a great episode. Thanks to Dr Martinez for joining us today, for sharing her wisdom and knowledge on portal hypertension and management of various Cs and various CO bleeding. And, if you don't already, be sure to follow us on Twitter, instagram at at Bowel Sounds and Facebook at at PediatricsGi podcast for the latest news and updates on upcoming episodes.
Speaker 1:And if you like what you heard and want to support the podcast, it would really help us out if you did one or all of the following three things Tell a person about the podcast, leave a review on Apple podcast to help others discover it, and on the Buzzsprout page. You can also support the show by making a donation to the NASPGEN Foundation. You can get there at wwwNASPGANorg. The money you donate helps support some of the amazing things that the Foundation is doing, including supporting pediatric GI research and public education programs.
Speaker 2:And, as always, the discussion, views and recommendations of this podcast are the sole responsibility of the host and guests and our subject to change with advances in the field. Thank you all for listening Until next time. Ta ta for now.