So we'll start, uh, this morning's first session with acute and acute recurrent pancreatitis, and I'll hand things over to Doctor Abu Haija. Great, we're very excited to be here. Um, thank you for everyone who's going to join us. Please keep the questions coming. Come up with your cases and debates. Um, we know that this is an underserved field in the pediatrics and even in adult pancreatology, so we're very excited. I think we can go ahead and start uh the first session, OK? So if I play this first slide, if we can show up the first slide. Perfect. So, the first session, I will um um help uh moderate with my colleagues, uh, Doctor Tom Linn and Doctor Andrew Trout, and hopefully we'll walk you through some of the bread and butter of acute pancreatitis and then move on to acute recurrent pancreatitis through case discussions. To start with some, uh, definitions, acute pancreatitis, we all know that based on the Atlantic criteria first established by Doctor Peter Banks and his colleagues and then later revised in 2012, um, requires two of the three criteria. So we need, uh, the clinical symptoms and exam that are consistent with pancreatitis. So the classic belly pain that is upper epigastric, sometimes nausea, vomiting, fussiness in the little toddlers or infants would qualify as a symptom. And then we need an elevation of serum amylase or lipase, at least 3 times the upper limit of normal. We always ask what is the normal range for the lab wherever we get the labs from, because not every lab runs the same ELISA test. Then 3 times the upper limit is diagnostic, and then findings on imaging. If any patients meets 2 out of these 3, then they have acute pancreatitis by definition. So it is an insult to the pancreas that leads to acute inflammatory cells, edema, and necrosis. We're very lucky that in the majority of cases in pediatric pancreatitis this is self-limited and reversible, and you would just have a one-time event and resolves completely. From the AGA, this is a nice demonstration of what happens. So an insult takes effect on the pancreas. It leads to zymogen activation. Then we have inflammatory mediators released, leads to ischemia, further ischemia and inflammation, and then necrosis and apoptosis. In the rare cases when we have severe pancreatitis, it actually leads to surges and multi-organ failure. So I'll start by a case and to show you a real case from our practice when a 9-year-old comes to the emergency department because he has this sharp, intense belly pain, he rated it 7 out of 10. It started kind of 2 days before coming, and he also has vomiting, and I showed the labs, so the amylase was 100. Our upper limit of normal in this institution is 109, and the lipase was 9800. And the upper limit is about 199 or 200, so Does he meet criteria for acute pancreatitis and based on what I showed you, we think he does, but moreover, um, we did get an ultrasound and I'll let Doctor Andrew Trout comment on what we saw in his ultrasound at that time. So this is a single transverse image from the ultrasound examination, and what this shows, I'm not showing a cine clip here, but what this shows, the yellow arrows here indicate the pancreas. It's a portion of the pancreas you're seeing is the midbody and out toward the tail of the pancreas. The splenichylum is over here on the right hand side of the image, and what we see is that the pancreas itself is swollen and thickened compared to what we normally see. The pancreas and then the surrounding tissues around the pancreas are also thickened and increased in echogenicity and that's what the blue arrows are indicating here anterior to the body and tail of the pancreas as well as to some degree here posterior to the tail of the pancreas and we like to use ultrasound as our initial imaging test in children where there's suspected uncomplicated acute pancreatitis and the value of ultrasound is that it. A radiation free modality. It gives you in general a reasonably good look at the pancreas. That said, it's a little bit limited in the setting where you are concerned about complications of pancreatitis. Yeah, can I ask a question? And by the way, absolutely tell me to shut up if I'm obstructing this conversation. Amylase and lipase, lipase more sensitive than amylase. I never, that's a great question. So the So it's not that the sensitivity is different early on, but amylase rises and normalizes much quicker than the lipase. So if you remember with the case, the kid presented two days prior. Having symptoms for almost 2 days, so that's what we commonly see. The MLAs might not be your best indicator. Got it. Um, lipase is more specific though. Um, so lipase half-life is about 7 days, but it's also more specific because it's mostly elevated if there's intestinal or pancreatic, um, things. MLAse could be due to appendicitis. I mean, as a surgeon, you probably know that. GYN things could cause that salivary, so MLAse is less specific for the pancreas, but I think this is classically what we see. Some people get a little bit confused. They're like, well, your amylase is not elevated. You probably don't have pancreatitis, and we knowing what I just presented, it's classic really for pancreatitis. Got it. And then for you, you obviously usually would go over to gallblad. Make sure there's no stones and evaluate the duct and all that stuff. Correct? Yeah, this was just a selected image from an exam because of what we're covering today for sure though, you want to rule out potential causes of that pancreatitis, gallstones, and obviously we're looking for those complications. They're not going to be fully characterized by ultrasound. You may need to go to CT, but at least it gives us an initial look. If we see a lot of fluid, if we see, you know, areas that look like necrosis, then we may consider going on to another modality at that point. Got it. Thanks. Yeah, but thank you for that question, Todd, because the ultrasound is really, that's the most helpful use of it. It's not really to document that the patient has pancreatitis or looking for complications. It's really looking if there's a biliary component. So if there is CBD dilation, then you would consider an ERCP early, or if there's gallstones, then that changes the whole management. Got it. So further on with the history, you know, this kid has been healthy, no family history of any diseases, no medications, no trauma. He might have had some flu-like symptoms, really nothing too impressive. So low grade fever, sore throat, and myalgias. And um I just want to cover in a couple of slides what is imaging in acute pancreatitis. Doctor Trout alluded to that earlier. Really the ultrasound should be the initial imaging for the reasons he mentioned. Um, it is used to confirm the diagnosis and also we screen for complications and identifying gallstones. CT is the image of choice if we're thinking about a complicated case. It is a much better modality to better visualize the necrosis and fluid collections, um, hemorrhage or masses. MRCP, it's, it's a very useful imaging tool we'll be showing through the talk today, you know, through really the whole course, the uses of MRCP and different indications. What I would like to say is that we get calls often. So the kid has acute pancreatitis. Do you want an MRCP? That's really not the first imaging modality that I want to think about in the. acute attack event, the edema tends to obscure ductal anatomy, so it's not the most helpful if you're looking for ductal irregularities or even anatomic things, and we usually leave the MRCP for workup of these kinds of biliary and pancreatic ductal issues. Talking about pain and we're very lucky that the way we managed even acute pancreatitis and Doctor Ken Goldschneider will elaborate more on management of chronic pancreatitis, which you know the hallmark of the disease is pain. He helped us like I will show later in the order set um. Incorporate what is best management for acute pancreatitis, and we really build it based on the sparse evidence that we have available. So what I would like to highlight from this slide is that there is no data on what is optimal management. Even the studies in adults have not identified a superior medication in acute pancreatitis, and don't be shy of using opioids actually. If you use them in in the right patient and right setting, even in acute pancreatitis, you could actually advance feeds and improve the outcomes and send them home earlier. Um, however, you know, we don't want to use too much because there are newer medications that could really help um what we call narcotics sparing or opioid sparing medications in pediatrics, and we really need more trials on those. So we're going to talk about the nuts and bolts of management, OK? You get a patient, what are you going to do? Are you going to feed them? Are you going to admit them? Are you going to send them home? What IV fluids? This is supposed to be open to discussion, so feel free to send your input and points as we're going through, but I'll start with a poll question. So for how long would you keep the patients with mild pancreatitis, and really the patient that I just presented is mild. It's mild because there was no evidence of pancreatic complications and because the kid did not have systemic inflammatory response syndromes or signs of multi-organ failure. So that's really the majority of pediatric pancreatitis. Would you keep them NPO for the 1st 11 to 3 days? Would you keep them NPO until their lipase and amylase normalize, so checking them every day until they're normalized? Would you keep them NPO until their pain is gone, or NPA until they're off narcotics? Or do you allow your patients to eat immediately and you don't keep them NPO? So I will come back to that question in about a few seconds and we'll get your polling answers to show on the screen in a few slides. So nutrition is very, very important, and actually the more we know about it, the more I'm intrigued about how you should tailor specific nutrition therapies to mild pancreatitis versus severe pancreatitis. The data is very convincing that. You need to start it early, and early means really within 24 to 72 hours, and it's been proven. There is no debate. It is associated with more favorable outcomes, and it's all the reasons that I mention here. It helps maintain that gut barrier function, inhibits bacteria translocation. The gut is very inflamed and leaky at that time. It actually lowers the incidence of systemic inflammatory response, hence avoids having severe complications of pancreatitis. I will just show one meta analysis because this is the strongest level of evidence we could have. This was in 2012 where they compared TPN, so total parenteral nutrition versus enteral nutrition, in the predicted severe acute pancreatitis, and enteral really was associated with better outcomes in terms of decreased organ failure and surgical intervention rate. And these are forest plots. So it again shows that um the for mortality, the analysis favored enteral nutrition and for infections, the analysis favored enteral nutrition. So very strong evidence from pooled analysis from different studies that if you have even the predicted severe, go ahead and allow nutrition. So let's see the responses and how people responded to the poll question. So I can tell you that right now it's about 30% mark. If you can pull up question one, topic one, question one. So it's divided three ways between NPO for the 1st 24 to 72 hours is where most people wrote um and that was before you gave your answer uh and then um I allow my yeah uh no that's not the right one Mark that's not the right uh and then uh the other people were divided between um. NPO until their pain is improved or gone, which was my answer. That's what I was, and, and so I already I've learned three things which I'm gonna tell you and then, um, NPO until they're off narcotics was another uh common answer. So can I ask you a question? So, so far I've learned that I was always afraid of opioids, so that's something I don't need to be afraid of anymore. I thought it's gonna cause, make the pancreas worse because the sphincter vos spasm. No good data. It's what I just data. It's really conflicting. That's an important key point to. Send out to the OK. Second thing is, oh, and a new person just answered another one NPO until their lipase and amylase normalize, which is what I see a lot. I think the majority tends to do that, yeah, until pain is improved or lipase and amylase, so OK. In other words, they cooled down the pancreas. They cooled down. That's what I always thought, right? This is why this is so great for me. Everybody's afraid of aggravating the pancreas, right, right? That's right. So what about we keep getting new answers now. So what about how do you feed them? You said enteral nutrition. They're going to throw it right out. Yeah. So what do you do? I, I, I think I'll show you in a second how we incorporated standardized. Every mild pancreatitis case gets the standard management. We made it easy on providers hospital-wide, you know, we are 659 beds or almost 700 beds with the expansion, so it was very, very important to standardize how we manage the cases. These patients are under HMO floors, um, trauma, and obviously that's a different case in some aspects because if the duct is not in continuity then you probably can't feed them, but. Cardiac kids, GI, general peds, so they go all over and it was very important just to say allow the kids to eat. They're going to self-regulate and I'll show you the data in a second, but that was the most easy one. We haven't gone to feed them aggressively now when you get into the severe. They're probably not going to be able to eat, and that's where the art comes to use some internal nutrition mode to really expedite the healing without tipping things over, OK, and so you're going to show us this algorithm on how you, I'll, I'll show you some things from our electronic medical record of how we make it easy and provide. To order the standardized management, but this could be again orders on papers elsewhere. This could be used in any other electronic medical record that the other institutions use. I've shared it with a lot of other institutions and I found it very helpful. I would love it. Yeah, sure, you've got to pay money though. I know fair enough, fair enough. So we answered the poll question really. The answers were within the realm of what people were doing before we start a standardized management 3 years ago, OK. Um, Again, um, to Todd's question, NG feed versus NJ feeds, uh, really the majority of the studies shows different, um, sorry, no difference, so same outcomes. Um, the duration of hospital stay and mortality were very similar, and this is, for instance, one small randomized trial with even severe acute pancreatitis. NG and NJ similar outcomes. So if you can feed with NG, there's probably not much added benefit from inserting the NJ under floro, and sometimes these are difficult cases and going that route. This is the first in design, and that's why I show it. In 2007 was the concept when do not. Rest the pancreas came about and this is a study from Ekerwal and colleagues where they really just simple in design, randomized 60 adult patients, allowed 30 of them to eat on admission, and kept 30 of them NPO on admission and really the NPO was the classic method they managed the patients. Guess what they found? They found that you could feed without increased abdominal pain, so you're going to wait on feeding your patients until their pain is gone, but their pain is going to be the same whether you feed them or not, and that's what the study showed. Um, and then the main outcome actually that they showed a difference, which is a big thing for hospitals right now, especially with the healthcare reform and everything that we're going through in this era, they decreased the length of stay by 2 days in the group that ate earlier, so that was very, very beneficial. If I show that to my hospital, they would love me too, and everybody who hears us, I'm sure patients would love it. It's a very important patient related outcome. So 2 days earlier discharge in the group that 8, same pain scores in both groups, and no harmful events. So we replicated that in kids and this was just published actually late in 2015. I just allowed the kids to eat like I mentioned and 38 admissions, mild pancreatitis. We have shown that we could do that in kids, that early nutrition is safe, feasible, and is not associated with pain outcomes. In fact, The patients who received feeds and the patients who were NPO had similar pain scores. These are patients who were evaluated multiple times per day, almost every 4 hours, subjectively and objectively by pain scores, and they really had similar scoring assessment. And then we really wanted to look at whether fat intake, so we start the patient on feeds, we say low fat diet. Again, that's another thing that. Has been planted in our heads and I've been looking on the evidence and if anybody from the audience has a great point on that, please fill in to call or send us your thoughts. Um, I haven't found a good evidence for the low fat. However, we know that fat stimulates lipase and we don't want to increase lipase, but at least from this pilot analysis that we did, we showed that the ones who had, um, so if I want to show here. The lowest pain scores, this is the pain score on the X axis, were actually the ones who ate the most fat. I just don't get that. It's, it's a myth. It's a surprise, but it actually decreases pain. It's, it's, it's probably that they're ready to eat more. They self-regulate again, so they eat more and they order a burger by their 2nd or 3rd day, and then you feel, OK, you're ready to go home. Um, does fat intake increase the length of stay? Um, so we looked at the total hospital stay and really it didn't affect the length of stay. Um, I think we probably talked enough from a nutrition standpoint. I don't know if there are questions we need to cover, but from there I would jump to the IV fluids, which is again a very important aspect from the moment the patient hits the ER, what are you gonna do? And we know that sometimes our surgical colleagues love the LR and GI colleagues love the normal saline, and that's another debate too. Before we jump to IV fluids, there was a comment from the audience regarding emesis. Patient presents with emesis and pancreatitis. You know, I think we need to be clear that we're not force feeding the kids. We're not pushing feeds in the face of ongoing emesis. I agree. I agree. So again with our pain order sets that Dr. Goldschneider helped us build, we have. Narcotics pairing medications and I, I probably should change the name, right? I should say opioids pairing. OK, um, so we use IV Tylenol, we use ibuprofen, we use, um, things that allow the gut to move better, so do not delay gastric emptying and things and pancreatitis itself could cause ileus, so those medications help not have ileus, but we also keep them comfortable with Zofran and things like that, so. All right, another poll question is coming. So what would you choose as the IV fluid of choice for administration, um, when you start the patients with acute pancreatitis, um, on any IV fluids? Would you not use IV fluids? Would you have normal saline bolus followed by 1 time maintenance D5NS? Would you have normal saline bolus followed by 1 time maintenance LR? Would you have normal saline bolus followed by. You know, kind of higher than maintenance, so more than 1.5 maintenance of D5NS or bolus followed by more than 1.5 LR. So I'll come back to the question in a little bit, um. So the adult studies showed that aggressive resuscitation is associated with improved outcomes, and these are retrospective studies, but they really defined the early aggressive as they calculated what is the 72 hour fluid volume for a patient, and if the patient got more than a third of that in the first day, it was counted as aggressive. Two studies at least showed beneficial event. Benefits, so it was associated with reduced mortality and the early fluid resuscitation was associated with reduced incidence of SERS and organ failure at 72 hours. Here I show the graph that shows the SERS and organ failure decreased at 72 hours in the group that got aggressive resuscitation. By the way, in the late resuscitation group in total they got more than what the earlier resuscitation group got. So that puts the pressure that really you've got a window and it's a 24 hours and if you don't interject then probably you lost your window and more than 85% of patients really got normal saline and then another small study showed the benefits of LR and actually there is another one that was presented at DDW this year that again showed. Benefits of LR. Again, this study is 40 patients from 2011. The abstract from Spain this year, I believe it was from Spain, was 40 patients. So they used LR versus normal saline and they used a goal directed management where they aggressively resuscitated until the urine output was at 3 mL per kilo per hour. Um, and the results showed that early resuscitation with LR did lead to reduced inflammation with certain and CRP markers compared to normal saline. So both groups got the same rate. One got LR and one got NS. And here brings the question of should we all use LR? Again, this is one study. So let's see the poll question, um, responses on that, um. Yeah, so, um, can you pull up, uh, topic one question two. Almost 60% said that normal sailing bowls followed by 1.5 times maintenance of LR. The other two responses were normal sailing followed by 1.5 maintenance of D5 normal saline, and um. By let's see, this one is 11 times maintenance of LR. So but it looks like the majority are saying 1.5 LR. I, I agree. So the majority is aware of the evidence of aggressive resuscitation. That's really great and I think the LR remains. Kind of debatable. I know that there are centers that strictly shifted to LR versus we, for instance, have not shifted yet because there's no studies in pediatrics, um, but it's a very intriguing concept to be studied further. But we all agree on the aggressive resuscitation. So I'm just gonna show you snapshots of our order set. Um, do you get your surgeons involved early in these patients? Are these usually managed by you guys and then you call them if there's a problem, um. I think Dr. Lin has a very good experience on the gallstone pancreatitis, and mostly those, the gallstone and the trauma related are the ones we get surgery involved. So if you want to comment on that, Tom, right, so it, it does really very much focus on the, the likely probable etiology of the pancreatitis. If it is trauma or if it is highly suspicious for gallstone pancreatitis, um, we will involve our surgeons and, and Jamie Nathan, um, early in the course of, of that patient's hospitalization. Um, there definitely are other possibilities to and other considerations to involve them as well, um, including, um, uh, necrotic pancreatitis too as well. That's right, and so early involvement of our surg surgical colleagues is very important. OK, so I'll show you in brief. I'm not gonna be able to cover the whole order set, but just to show you how we standardize things in the management, we really built it into making it user friendly and incorporated the best evidence in management into um we use Epic and this is not, you know, a presentation about Epic, so we use their permission to get these slides up, um, so. For the vital signs, for instance, we want them to be checked, checked very often the 1st 2 days, including pulse ox checks, because when we aggressively resuscitate, there are some evidence that shows that you could actually flood the lungs and result in pulmonary edema and SERS by itself could do that. So we really are very watching. We're watching for this and we want the nurses to be aware of those complications um again, nursing orders that they notify if there's decreased breathing, for instance, decreased urine output, because we want to use some goal directed management for the IV fluids um in terms of diet, there's all kinds of options and even if the physician, for instance, wanted to use the. NPO, they could go and click these boxes we check for them already though what we think is best practice, which is Start your patients on a clear liquid diet, and it's really a progressive transitional diet, so they start on a clear liquid diet. If it's tolerated within 6 hours, the patient is ready to order regular diet foraged food, and the nurses would give them the menu and they would just eat. We would not force them to eat if by the day 2 or 3 they're not eating, then we discuss internal feeding options. For IV fluids, we just add education points with the red that the evidence shows that the outcomes are better with aggressive resuscitation. We really defaulted our management to D5NS since we're using higher rates. We didn't want people to use half an S, so hypotonic solutions with the higher rates. So back to our patients, um, we did kind of use that standard way of management that we use in the institution and mainly when we divide the patients to who got. You know, NPO and low IV fluids, NPO and high IV fluids and early PO and low IV fluids, early PO and high IV fluids, this is really a study when we studied 201 patients, we really showed that in terms of developing severe pancreatitis or even the associated outcomes, about 35% of the NPO and low IV fluids group could develop severe pancreatitis. Versus the ones who ate early and got aggressive resuscitation had a 4.2% association with severe pancreatitis. For that reason, really, our patient got 1.5 maintenance D5 normal saline over the first day, was eating and drinking, while by the next day we sent him home with oral as needed PRN medications after 52 hours of admission. The classic story, since we're talking about diseased pancreas, it can't be that easy, right? So he came back five months later, same patients with the same symptoms, and this time his lipase is even higher. It's 20,000 international units per liter. He also had other labs that could suggest that this is a severe course. He had a YPC that is elevated, albumin that is low, and a CRP that is high. So we got an ultrasound and you probably see that also in your own institutions and we see it too. I mean when the patients are not NPO enough time and I don't know Andrew if you want to comment why sometimes we get the non-specific findings or not adequate to comment, but this is really what we got. We didn't see anything on his pancreas. I mean unfortunately the pancreas can be a little bit difficult to see sometimes. Especially in larger patients and as you say, in patients that are NPO, if you've got a stomach full of gas or if you have an ileus because there's a real inflammatory process going on, all that bowel gas can really affect the penetration of the ultrasound waves and make the pancreas non-visible. Additionally, if there's just a massive inflammatory process, all the inflammation can obscure the normal tissue planes and what we normally expect to see. Sometimes we can still sort of make a call and say, well this looks bad. We need to do something more like we're talking about before ultrasound as an initial assessment, screening test, and then recommend moving on to something more definitive like CT that gives us a good look at the anatomy and the adjacent structures. Absolutely, and I think I really have to say we're very blessed here that sometimes we don't see it. The radiology colleagues help us get the patient back to an ultrasound. If that's still kind of a needed study, we give the patient a few hours and then repeat it. So this patient, we admitted him, we used the orders set, we allowed him to eat. He wasn't really eating. He couldn't eat. He said, I can't. I have no appetite. He was really sicker looking every day. On hospital day number 4, he was having tachypnia, so increased respiratory rate, severe belly pain. So day 4 is really not a time we like to see the patients taking this course. So what would you do next for this child? He's really not expected to have the classic recovery from acute pancreatitis, where you get an ultrasound, MRCP, CT scan, or ERCP, and this is a poll question. So please go ahead and submit your thoughts, um. And I'll just give you 2 seconds and then I'll show you which image modality we chose or procedure we chose for him. OK, Doctor Trout. So this is a selected CT or image from a CT scan in this patient and again. Like we just said, this is a patient now at this point that we think that there's something more severe going on, and so CT is our test of choice here at this institution and should be your test of choice in those patients where you think there's complications going on. It really does give the best appearance or the best image or view of the lay of the land in terms of identifying complications, identifying effects on other structures, identifying issues that would potentially lead to surgical consultation or involvement of other experts. And what this CT image shows here, so there's an extensive inflammatory process in the belly here. The blue arrows show inflammation in the mesenteric and omental fat all around the pancreas. The pancreas is markedly enlarged and very abnormal in contour. The tissue planes around the pancreas are clearly abnormal, and the yellow arrow there is indicating an area of. Enhancement in the head and insonate process of the pancreas and when we see absent enhancement like that, that's highly concerning for necrosis within the pancreas. And so that's the diagnosis or the concern that we raised here. There is a small amount of ascites over here in the left hemi abdomen as well, which is a common thing that we see, or acute fluid in these cases of pancreatitis. OK, that's great. So, um, before I show you the answers of the poll question, we do have a question from, uh, um, Doctor Alex Bondo, and the question is, is there any role in the modern era for using Ransom's criteria to predict mortality in pediatric pancreatitis? That's a great, great question. Um, we currently do not apply ransoms directly to kids for the different, um, causes and limitations. You can start with age first, right? Um, the. The studies that try to do that earlier are really, they started in 2002, um, I believe with the Midwest study, so University of Cincinnati was part of it and um they applied that into kids. It was promising initially. It required 48 hours to be completed, but then when it was validated with further studies, it didn't pan out to be as sensitive and specific as they hoped. Later on, actually, there are some other studies that showed that maybe you could use lipase as a marker within the 1st 24 hours, and we just finished our study that talked about using prognostication markers on admission to predict severity. Some of the ransom's elements are in there and some different ones are are are there too. So what we predicted using from our tool are mainly white blood cells. Count, albumin value, and lipase on admission, and those together in a formula could predict severity in almost 70% of the patients. Still needs to be optimized, but at least that's a promising direction we're going. OK, so good, keep the good questions coming. So let's show the answer to our poll question. I'm interested to see what the audience chose to do for this patient. Oh good. So it sounds like the majority chose the CT scan and then even before you gave the answer, yeah, yeah, that's awesome. And then MRCP 20% and ultrasound looks like people would repeat it in 20%, um. The ultrasound for necrosis, it's probably not your best choice, don't you think, Dr. Trout? In a patient that you think has complications or has a particularly severe presentation, yes, maybe you could, if it's been 4 days, you could do another ultrasound to see if there's something there, but the high likelihood is you're going to have to go to a CT. And as we said earlier in the presentation, while MRCP does provide. Ductal anatomy in the setting of an acute attack like this, the ductal anatomy can be obscured, and so the added value of MRCP is not so much in the acute setting like this. And as everybody knows, an MR takes dramatically longer than a CT scan does. And in these patients that can be sick and uncomfortable, asking them to lie on an MR scanner for 40 minutes can be a little problematic. One quick point about the CT exam in terms of how to protocol or order. Those exams, we simply do a portal venous phase. We don't do a multi phase in the initial assessment of these pancreas, these patients. You're not in general in pediatric patients looking for masses where there's added value of having both the arterial and the portal venous phase. We're really looking for those complications venous thrombosis, necrosis, acute fluid collections, those sorts of things. We do try to get oral contrast on board in these patients. The main reason for that. is to help separate fluid-filled loops of bowel from fluid collections or acute fluid collections or developing collections in and around the pancreas. That said, if you have a sick patient who really cannot handle the oral contrast, you can get a lot of information without the oral contrast. And so that's not a deal breaker in my opinion in terms of how to do the CT in these patients. That sounds reasonable. So what should we do for this patient next? I mean, we diagnosed that. The patient has complicated pancreatitis with a possible necrosis and those kind of small tiny fluid collections. Would we just do observant management? Would we go ahead and drain it using EU US guided procedures? Would we consult interventional radiology for drainage? Use antibiotics, would we feed or not feed, and these are really the valid questions that go in our minds whenever we face these situations. So a few highlights again and to make it as high yield as possible from this and definitely keep the debates coming. The patient is afebrile. I don't think this is an infected necrosis, so we did not start antibiotics. Juginal feeds were started because this patient could not tolerate anything in his stomach, and as clinical course improved, he was actually then allowed to do PO and he was eating by the end of the 10th day of his hospitalization. So to highlight antibiotics and acute pancreatitis, which is another hot topic, really we want to use them for mild. And in a case like this one, even when we had signs of severe, unless it's infected necrosis, we probably would not have a strong evidence to use it. And when we think about antibiotics, usually Emipenem or 3rd generation cephalosporins are the good initial choices again based on the evidence that we have out there. So his attack really, I would say resolved with conservative management, but we categorized him as having acute recurrent pancreatitis, and all the inflammation cooled down three months later. And this is his MRI 3 months later. Looks pretty good, huh? Yeah, the MRI, um, I got 2 images here from the MRI. Both are fluid sensitive sequences. There's a coronal image there on the left side and an axial image there on the right side. And again, now you have a patient who's cooled down, and now's the. Where you can use MRI to assess for pancreatic ductal anomalies or other things that might be predisposing to the cases of pancreatitis or to the pancreatitis events and what I'm showing with the blue arrows there in the in the figure is the body of the pancreas. The duct is a little bit prominent. It's this. White stripe, sorry, I'm I'm having trouble seeing my area. There we go. It's this white stripe running down through the body of the pancreas here. It's a little bit prominent. Generally in a in a healthy pancreas you're not going to see the duct that well, and there is some atrophy and irregularity of the contour of the pancreas related to these prior attacks, but we're not seeing findings here that we would by imaging consider diagnosis diagnostic for chronic pancreatitis. Right, and we really use MRI MRCP quite a bit in the workup of acute recurrent. Um, so what is acute recurrent pancreatitis for definition purposes, for the sake of studies and research, um, the Inspire Group, which is the International Study Group for pediatric pancreatitis in Search for a cure, led by Doctor Aliyah Uchin, the University of Iowa. Gathered together the first time in 2009 and then later in 2012 we came up with definitions. What is acute recurrent pancreatitis in kids? So we said for the sake of consistency it is at least two distinct episodes and you need to have complete resolution of pain and a one month pain free interval between the episodes. Or if you have normalization. Of the enzyme between them with complete resolution of pain within less than 1 month, then that is diagnostic as well. Exclusion, of course, if there is a pseudocyst, then it doesn't qualify as acute recurrent pancreatitis until the cysts resolved. So the patient really recovered for 5 months and then presented with another attack. So in that case we have a very specific workup for acute pancreatitis that is. We think about inflammatory causes like IBD and celiac disease. We work them up for systemic illnesses and mitochondrial diseases, um, cystic fibrosis, metabolic conditions that predispose patients to acute recurrence like triglyceride elevation, calcium and kidney disease, anatomic, and that's the reason why we get an MRCP, possibly an ERCP. And Dr. Tomlin will cover that through cases next here in a minute and then a genetic workup. The 4 genes that I listed here are the most common genes, and I will cover that more in the topic that comes in this session too. And then um it's really a very comprehensive workup, but we're trying to find causes that could be treatable or not treatable for the patients, but it's very, very important for counseling. When can I interrupt you? You can right now because I'm giving the podium to Dr. Lin so much. So we got, so, so just tell me when to slow down here. So first of all, question from Mira Mennon. Mira says the lipids thing. Can we go back to the lipids thing? Enteral lipids. You said there's really no data to show that it really is worth. What about the parenteral lipids? That shouldn't be a problem either, right? Yeah, when we use TPN. Um, so you want to use some nutrition, right? Let's say in severe pancreatitis we absolutely fail. We have patients where we fail, so Enal is better. We fail to even place an NJ because of how complex the pancreas is and the fluid collections, or there's complete duct disruption or whatnot. So we use TPN in certain situations, but rarely we use intralipids with them. So Mira, now that you've heard this conversation, I want you to answer in the chat. Would you now reconsider using TPN as your standard and maybe move to Entro? I'm curious if that would change your management. For me, I have a lot to bring back to my institution. Um, I hope you're writing a review article on all these things because I'm like tweeting like crazy here of all these new things I've just learned, so there are a few, but maybe we should update it. Uh, we'll, we'll help you if you want, if you want us to do the dirty work for you. All right, so the, the second question is, um, I noticed in your patient you did NJ feeds, so you still do it even though you found that it doesn't make a difference, so. NJ versus NG, no added benefit to the NJ compared to the NG, right? The classic teaching was get past the past the envelope batter. We, we don't believe that's the case from the evidence, but this patient really could not tolerate feeds in his stomach, so we advanced, right, yep, yeah, and because we believe with severe pancreatitis, even the nutrition has added value, we still fed him kind of um with an NJ, OK. Um, would you let them eat by mouth if they could tolerate it? OK, yeah, even in the severe if they can tolerate it, low fat diet or no, you just give them whatever they want. Honestly, we, we allow them to eat whatever they want. They usually don't choose the high fat diet the first day or two anyway. Yeah, got it. The questions are piling in here, but, uh, so. Talk to me through this is one thing I never understood. uh, how do I know when to get an aspiration of the pancreas to rule out septic versus non-septic necrosis? What's your indicator to know when to do that step? If you see necrosis, do you do it all the time or only if they start getting really septic? I think it's a very interesting question. We could get a doctor pancreas. Great. So how do you know when to only when needed. I've always struggled with that. That, that, that is, um, uh, classically the, you know, a very challenging question, um, you know, uh, you really, you can very much be opening a can of worms if you're starting to stick things into the pancreas. Um, I can tell you that I, I think we've had, um, the need for one in the last 10 years, one necrosectomy for, for, you know, necro truly. Awful necrotizing pancreatitis, uh, you know, clinical decompensation can be caused by a variety of circumstances. Um, you know, we're always quick to, to point at, you know, continued fevers, you know, do we stick a needle in the pancreas, you know, in the absence of true significant clinical deterioration, we, we really avoid, avoid sticking needles in the pancreas, sticking drains. Um, you'll see later on in the sessions we have had, uh, on occasion to stick drains into certain places to deal with clinical decompensation. Um, but we are loath, loath to intervene. Then can I take you through this, so this patient has, you get it, he doesn't get better, you get your CAT scan, you show necrosis. Uh, we don't know if it's sterile or we don't know if it's sterile necrosis or not. Do you just start antibiotics because you don't know? Do you wait for them to clinically deteriorate? Why even bother getting the aspiration if you think it is? Just start the antibiotics? Is that if that patient had a fever, I think I would start the antibiotics. You think inflammatory antibiotics, I think empiric antibiotics would probably have a short threshold or a low threshold for starting them, assuming it's infected, but you know there's all, you know, there is a little risk, you know, you stick a needle into a collection that may be sterile, and then you have the risk of introducing infection, and then once you have infected necrosis. Things can can really deteriorate so this would be one of those things that you're taught that's in the books that's on the boards, but I don't see anyone really doing it that often. It's just treat with your your brain more than, yeah, OK, um, what is this here? Yeah, OK, as you might suspect that there's a, there's this extreme limited amount of evidence as it relates to best management of necrotic pancreatitis in kids. um, now for adults there's more evidence and there's growing evidence in terms of being more aggressive, especially. From an endoscopic standpoint for necrostectomy, endoscopic necrosectomy, um, and that evidence actually is showing very good positive outcomes in that regard. Now there's do you do that for endoscopic or endo endoscopic, endoscopic, yeah, so that's via endoscopic ultrasound actually transmural. So you, you do a gas you open the stomach into the pancreas that that's already almost like a pseudocyst where it's right, right, right, very, very similar to that. So, so you, um, uh, enter the cavity of necrotic cavity, and then there's, uh, the bridement of that from an endoscopic standpoint and, and obviously that can also be accomplished from a surgical standpoint too as well. But, um, depending on the, the, uh, other comorbidities of the patients and how stable they are, one option might be better than the other. But again, pediatric wise that. Evidence is extremely limited. Have you done that here? We have not. We have not. Fortunately we haven't had any patients that we still want to avoid it. We still want to. I don't want, because to think that we're, you know, endoscopically draining a bunch of pancreatic acute pancreat, you know, pancreatic fluid collection. So do you use MR after secretin stem at this point? I think they're talking about back when the case when the patient sort of got worse, right, so we're gonna talk a little later in the second session actually about how we do our exams with Secretin um we're still sort of feeling this out a little bit again this is one of those areas where. There's not great data in pediatric patients about the added value of Secretin. In fact, if you look at the adult literature, the, the, the data is a little bit iffy there in terms of the added value of the use of secretin. There's a lot of case theories and anecdotes and things like that about an improving visualization of ductal anomalies, but when you have, it's. Often in the chronic pancreatitic patients or the acute recurrence that we're doing these MR exams and they've had enough attacks that generally the ducts dilated and you can see it without secretin, but I'm not going to categorically say no to it again they're still we're still feeling out the evidence and trying to to figure out exactly how to proceed. OK, all right, so, uh, Enrique, I hope that answered your question. Um, question between, uh, is there a relationship between BMI of a child and recurrent pancreatitis? Has that ever been studied? That's interesting. That's actually our next abstract that we submitted to World Congress. Wow. Where did that question come from? That came from Mira Mennon. OK, good job. So actually we have a prospective acute pancreatitis registry. We follow kids from the first attack onwards, and it's almost 3 years old now, and one of the first abstracts that we're very excited about is showing that the increased weight percentile for AIDS patients during the first attack. Not really the BMI, and I'll I'll, I'll tell you why, um, does predict recurrence. Now we think that there is some evidence too that the higher BMI does um kind of predict uh severity. We haven't proved that yet in the US population, but there's enough um in um outside the world studies that higher BMI predicts severe pancreatitis course even in adults and in kids. Um, the BMI didn't pan to be the case maybe because. Our patient sample was 85, the ones we looked at, but also it had a wide variation. We had heavy patients on both ends, so the ones who did not develop recurrence and the ones who developed recurrence, and also we had the thin population, but the weight percentile for age was a predictor. So great question. Next thing, so I have, for, by the way, Mira Mennon, after I asked her, she said. She definitely learned the point that you made and now she's gonna move to enteral nutrition. I will too, yeah, you've made a big impact. Um, the question about, uh, I have a question. The antibiotics that you would use, I know you, I think you said immipenem, Emipenem or cephalosporins based on that one study, OK, yep, OK, yep, cool, uh. I think that's good, so we're, we can keep going. That sounds good. Great, um, so moving on, uh, one of the topics that we wanted to, to cover, um, to some degree was, um, ERCP management in, in the setting of acute slash acute recurrent pancreatitis. And so as we know, there's been a trend towards when ERCP was first introduced, um, back in the 1970s that it was purely a diagnostic modality, and as time has gone by, it's evolved from a diagnostic, um, to a more therapeutic, uh, modality and Because of the advances that we've had with our radiology colleagues and their, their, uh, their capabilities of, of, um, identifying abnormalities just from a radiologic non-invasive standpoint and so I, I wanted to go over to one case first that'll somewhat demonstrate, uh, one of the, the patients that we had. And so this is a 15 year old male with cerebral palsy. He has a history of encephalopathy with epilepsy. Um, he's also G tube feeding dependent um because of his, uh, his disability, um, and so one month prior he had, when he presented to us, one month prior he had a spinal fusion surgery for his scoliosis. Um, his presenting symptoms to us were G tubilius drainage, abdominal distention, and some, uh, component of abdominal pain, abdominal discomfort. Um, his initial imaging because of his presentation and because of his, uh, some limitation due to his disability, um, he did have a CT scan, um, as well as a an ultrasound early on in the course of his presentation, and there were abnormalities that, that we, um, that were identified that we'll get, um, over to the next slide, um, from a biochemical standpoint, um, he was found to have elevations in his serum lipase and amylase, um, with normal liver function tests. So just quickly, here are two images from this patient's CT, and this case shows the value that CT gives in these very complex cases and in these complex patients. What you have on the left there is an axial image and on the right, a coronal image in this patient, so you can see there's spinal hardware in place. There's a severe scoliotic curvature. All of these elements make it difficult to get a good ultrasound. Yellow arrows indicate the pancreas, which because the patient's anatomy is shifted off to the left side there and what you can see is right in the midbody of the pancreas there's a fluid collection that's replacing a large chunk of the pancreas. There's essentially normal pancreas or not normal, but preserved pancreatic tissue on either side of that collection. But nothing around that collection that looks like preserved pancreatic tissue, so that looks like an area of necrosis or walled off necrosis at this point. The asterisk in both of the images demonstrate the extensive ascites and fluid that has accumulated due to the inflammatory process in the pancreas. So, um, his, his, his recovery was rather prolonged, and, and during his, uh, extended hospitalization, his lipase peaked, um, even higher than it was at the time of presentation, um, and he was, um, also, it was difficult to advance his enroll fees despite the fact that he already had ro access via his gastrostomy. Um, so, um, I believe it was, uh, one or perhaps even 2 weeks into his hospitalization with his slow recovery that we repeated his ultrasound. And I just said this is a complex case and ultrasound can be a little bit difficult in these cases, but once you've got a lay of the land with CT and you know what you're looking for, you can use ultrasound in these patients to sort of target and look at those areas of interest and again though, if you see something that has changed dramatically or if you're just not getting a good sense of things, you may need to go back. To cross sectional imaging, CT or MRI, depending on the patient and the exact situation, but ultrasound can be a good modality to follow patients serially over time. It's easier on the patients. There's the lack of ionizing radiation, and what the ultrasound showed in this patient was that that fluid collection, the peripancreatic or intrapancreatic fluid collection, was increasing in size on the follow-up ultrasound. So moving to our next poll question, uh, what would be the next best course of action that, uh, individuals, if they were confronted with this patient and his, his, uh, clinical progression or lack of progression, how would you, uh, decide on approaching him next? So number 1 would be either watchful waiting with supportive medical management, um, and continuing what we're attempting to do. Uh, number 2, endoscopic intervention with endoscopic ultrasound. 3, ERCP, or 4, surgical intervention. So we'll come back to this poll question. Uh, so what we opted to do based on his, his, um, his findings and increased, uh, fluid collection, um, we opted to actually go forward with ERCP. And so here's his first fluoroscopic imaging image, uh, that is a, uh, a scalp film before we do anything. And, and as I had mentioned, um, he had a recent one month prior, uh, spinal fusion surgery and so it was a little bit challenging to actually, um, identify and, and visualize, um, the normal ductal structures that we typically want to see. From the ERCP standpoint with those rods in place, but it, uh, we were able to accomplish what we needed to. And so here's his next fluoroscopic image, as you can see on the, on the image on the left, he does have contrast filling in his gallbladder and a cystic duct. Um, there was no apparent abnormality, um, uh, or any type of pathology from his biliary tree standpoint, but, um, secondary contrast injection and, and, uh, opacification of his pancreatic duct, we see with the two yellow arrows there's a blush of contrast extravasation. Uh, in the midbody, um, almost at the mid and at the body tail junction and further down towards the tail there's also an, uh, an additional extravasation with the yellow arrow, uh, to the far right, um, uh, documenting his, uh, his pancreatic duct leak. So, um. I don't have an image here, but, uh, what we opted to do at at that time in terms of therapeutic endoscopic therapy was, um, perform a pancreatic sphincterotomy as well as a pancreatic duct stent placement, um, to really allow the flow of his pancreatic juices to the path of least resistance with hopes that it would resolve the, the, um, the defect that he has in his duct. So this is his repeat ERCP 4 or 5 weeks later and the removal of his pancreatic duct stent and, and, um. Fortunately for him, he had a very positive successful outcome from his endoscopic ERCP intervention and so we see that his duct is a little bit tortuous like it had been before, but more importantly, his extravasation towards the tail as well as that blush of contrast that was in the body is no longer present. So again, the part of the decision to go forward with the ERCP was based on his clinical suspicion. Um, for a pancreatic duct league as well as, uh, more importantly, um, whether or not you have, uh, such, uh, the, the type of expertise that you have at your your particular institution, and so, um, if you're at a pediatric institution. Um, there is a growing number of pediatric gastroenterologists, um, uh, becoming skilled in, uh, performing ERCP, um, and so if you, if there is, uh, that readily availability, perhaps that would be one of the options that someone would choose to go on, um, to early, earlier rather than later with the understanding that, um, again the goal is to hopefully be therapeutic and given the, uh, invasive nature of, um, ERCP and the, the potential that it might exacerbate someone's pancreatitis. I think the poll question is ready to be shown, the responses. Mark, can we display a nice way to wrap up our first session. Actually a good mix. It is a good mix. Yeah, it is a good mix if I see correctly, it's a watchful waiting and supportive, um, measures is 44% and then 33% endoscopic intervention with ERCP, um, so people are a little more shy to do the ERCP and then, um, endoscopic with an EUS actually. At 22% and none chose surgery. Good. Sounds good. Yeah, don't you think we can wrap up our first one and this way we could just introduce the next session for the chronic pancreatitis? Yeah, my question is though, the reason people would shy away from ERCP, I'm assuming is that their fear of worsening the pancreatitis or. Uh, likely that that's the scenario. And so it's a balance of high, uh, what's your clinical suspicion suspicion and what do you anticipate that you're gonna encounter at the time of ERCP with the hopes that you would be capable of resolving that. And so it wasn't 100% clear in this particular case that the ERCP was the best option. Um, the watchful waiting, um, that, that the pollers, um. Several pollers actually chose, um, we chose not to do that because it was more of an extension of what we already had attempted to do in terms of a conservative approach and also there was that particular option of continuing that wasn't necessarily acceptable for the family as well. Got it. OK. And in the setting of a patient with an enlarging collection, I mean, he's already showing himself to some degree potentially be failing watchful waiting, right? Correct. That is correct. OK, sounds good. Well, thank you guys for um allowing us to introduce this very interesting discussions on acute and acute recurrent pancreatitis. I think we will take a 5 or 10 minutes break. How much are we allowed? 55 minutes break and then we'll um start the chronic pancreatitis stuff. Sounds great. All right, thank you. See you in 5.
