CEimpact Podcast
Acute Pancreatitis
Join us as we discuss new guidelines from the American College of Gastroenterology for the management of acute pancreatitis.
The GameChanger
New guidelines from the ACG address changes in treatment and management of acute pancreatitis.
Host
Geoff Wall, PharmD, BCPS, FCCP, BCGP
Professor of Pharmacy Practice, Drake University
Internal Medicine/Critical Care, UnityPoint Health
Reference
The American Journal of Gastroenterology
Drug-Induced Acute Pancreatitis: An Evidence-Based Classification
Pharmacist Members, REDEEM YOUR CPE HERE!
Not a member? Get a Pharmacist Membership & earn CE for GameChangers Podcast episodes! (30 mins/episode)
CPE Information
Learning Objectives
Upon successful completion of this knowledge-based activity, participants should be able to:
1. Discuss changes Review the American College of Gastroenterology guidelines for the management of acute pancreatitis.
2. Discuss changes in treatment of acute pancreatitis.
0.05 CEU/0.5 Hr
UAN: 0107-0000-24-175-H01-P
Initial release date: 05/20/2024
Expiration date: 05/20/2025
Additional CPE details can be found here.
Join us as we discuss new guidelines from the American College of Gastroenterology for the management of acute pancreatitis.
The GameChanger
New guidelines from the ACG address changes in treatment and management of acute pancreatitis.
Host
Geoff Wall, PharmD, BCPS, FCCP, BCGP
Professor of Pharmacy Practice, Drake University
Internal Medicine/Critical Care, UnityPoint Health
Reference
The American Journal of Gastroenterology
Drug-Induced Acute Pancreatitis: An Evidence-Based Classification
Pharmacist Members, REDEEM YOUR CPE HERE!
Not a member? Get a Pharmacist Membership & earn CE for GameChangers Podcast episodes! (30 mins/episode)
CPE Information
Learning Objectives
Upon successful completion of this knowledge-based activity, participants should be able to:
1. Discuss changes Review the American College of Gastroenterology guidelines for the management of acute pancreatitis.
2. Discuss changes in treatment of acute pancreatitis.
0.05 CEU/0.5 Hr
UAN: 0107-0000-24-175-H01-P
Initial release date: 05/20/2024
Expiration date: 05/20/2025
Additional CPE details can be found here.
Hey, ce Plan members from CE Impact. This is Game Changers. With me today is our resident clinical conversation expert, jeff Wall. Good morning, jeff Good morning. How are you today?
Speaker 2:Not too bad, not too bad.
Speaker 1:Good, good. Well, before we get started, I actually have a fun fact to share. This episode is being released on May 20th, so if you're listening on the day it's released, it's Monday, may 20th. And did you know, Jeff, that our first Game Changers podcast was released almost exactly four years ago, on May 22nd 2020?
Speaker 2:Wow, yeah, I, I, I did not know that and and I I'm sure the the number of podcasts then that were on COVID, compared to the podcast now that are on COVID, where, where, where it's probably a little bit different. But yeah, no, it's, it's been. That's good to hear. It's been four years and I think, I think, I mean certainly I've heard from people who listen to the podcast, have gotten back to me email in person and stuff that I think a lot of people do find this informative and helpful, you know, and they're able to translate all this stuff to the bedside and apparently I'm not incredibly irritating, so that's, that's always nice too. So yeah.
Speaker 1:Not even close to irritating. So I mean, maybe the only irritating thing is people can't listen on 1.5.
Speaker 2:Yeah, yeah, that's yeah, that's definitely heard that from several people. They say that this is literally the only podcast. They can't listen to it at faster speeds because I talk too fast. It's okay, it makes it interesting, so I love it.
Speaker 1:And funny that you say that. So the first podcast was on hypercoagulability in COVID. So we started in the middle of COVID and I, which is ironic, because last week our topic was COVID too. So here we are still talking about it four years later not today.
Speaker 2:Yes, no, no, yeah.
Speaker 1:Yeah, well, we have thousands of listeners now, um, so I think that's really cool. This has been one of the more fun things that we do, I feel like, and I feel like it's really a great way to learn. I am always learning from you and from all of our guests, so thanks for sticking with us and celebrating our four-year anniversary. It's exciting, yeah.
Speaker 2:I agree, and it's been fun for me too, and you know it forces me to learn too. You know we're doing, we're doing research for the pod and you know I've got to, I got to dive in and, yeah, no better way than to teach it Exactly, Correct, Yep.
Speaker 1:So yeah, Well, um start, let's teach us today Um we're talking about the management of acute pancreatitis. So I'm going to let you, uh, let you take it away.
Speaker 2:Sounds like a plan. So so, yeah, this is. This is one for my inpatient homies, as it were. So today we're going to be talking about the brand new American College of Gastroenterology guidelines for the treatment of acute pancreatitis. Again, for the inpatient pharmacists listening, inpatient providers listening, I, you know, I know, we all know this is something we see all the time. I don't think that there's too often on one of my services that I don't have at least one patient with acute pancreatitis. I currently have one poor gentleman on my service with this and you know, again, it just you know, we see this literally all the time. So it's always nice when ACG decides to update these guidelines.
Speaker 2:It's it's been a few years, I think, pre-pandemic, speaking of pandemic. Pre-pandemic was when the last set of guidelines came out and there's been a couple of new things. There's, you know, I think this is a set of this is a disease state where you know a lot of times we don't wait for the guidelines. I think there's a lot of disease states where nobody really jumps until you know, until the guidelines are released. You know, septic shocks, I think, a good example where you know there may be a study or two that shows.
Speaker 2:Well, maybe we could do this, maybe we could do that. But I think everybody kind of waits until the society of critical care medicine comes out with their guidelines and then they move or they don't move. This is not that case, I think. When new studies come out that suggest you know, this works, this doesn't. It seems to be adopted relatively quick, and maybe it's just because it's such a common disease state and because it is a deadly disease state. So I was glad to see these updates and so the guidelines are pretty much standard to the American College of Gastroenterology guidelines.
Speaker 2:They bring in a series of experts and they have a medical librarian come with them. They ask a number of questions in PICO format. They then do an intensive literature search. They grade the evidence using the grade process, from very high things like meta-analyses or randomized control trials, all the way down to case reports and retrospective studies. And then they either recommend something which means you probably should do it, they suggest something which means, more often than not, you should use it, or they recommend again something which means you should do it. And again, this is the same for, I think, pretty much all their guidelines. They note that again, this is pretty common about 300,000 admissions annually in the United States for acute pancreatitis. 300,000 admissions annually in the United States for acute pancreatitis. So that ends up being a million patient days at a cost of over $2.5 billion.
Speaker 2:And they note that the incidence of acute pancreatitis is increasing, probably because of the increase in alcohol abuse which is number one cause, but also because of the obesity epidemic, because one of the issues that comes with the obesity epidemic is gallstones and gallstone pancreatitis is the number two cause and there's some interesting new data that they talk about that I was certainly unaware of. When it comes to the treatment and diagnosis of pancreatitis that we'll be talking about coming along here, the case fatality rate, I think, is generally decreased, but it's still a deadly disease Somewhere. Around 10,000 people die every year in the United States due to acute pancreatitis and it's usually not the pancreatitis itself, it's usually the overwhelming inflammatory sequelae. So organ failure, septic shock, ards, which I've seen many times, dic, which I've seen several times. So I mean that's what usually ends up killing the patients. But it all starts with starts with pancreatitis and even if you take all that away, about 20% of patients who have acute pancreatitis go on to develop chronic pancreatitis. And again, for both inpatient and outpatient clinicians, they know this is it's one of the most frustrating diseases to treat for both the patients and the clinician, because these patients have terrible abdominal pain, they have serious nutritional problems and it just it's extremely difficult to treat these patients. So if we can prevent the development of chronic pancreatitis by treating acute pancreatitis appropriately. I think that's that's something to think about as well.
Speaker 2:So you know, diving right into the guidelines, they spend a significant amount of time talking about the diagnosis of acute pancreatitis and there's not a whole lot new here. I think most people who deal with this you know see that. You know, basically it's established by two of the three criteria they have to have abdominal pain that's consistent with the disease, a serum, amylase or lipase greater than three times the upper limit of normal, and then characteristic findings from abdominal imaging, either a CT scan, a right upper quadrant ultrasound, something along those lines. They do note, interestingly, that abdominal pain is not always severe in patients with acute pancreatitis. Sometimes it's actually fairly mild and I may not even mention it. They may say, oh yeah, I got a little bit of discomfort there, but it's not too bad. That's not been my experience. Usually people end up in the hospital because they have severe, uh, abdominal pain. So I thought that was. That was kind of interesting, um, you know.
Speaker 2:So, uh, they note that of course lipase is the test of choice and, again, all clinicians know that amylase just isn't sensitive or specific enough. They also note though I haven't seen this done in a long time. You shouldn't follow serum lipases. When I came out of school, 8 million years ago, when dinosaurs roamed the earth, you know we would follow serum lipases to see if patients were getting better, and there really is. You know there's no correlation to that, so don't do it, just use it to establish the diagnoses. Keep in mind, too, the lipases can be elevated by other things. Dka is the one that kind of jumps to my mind where you're going to see a significant increase in certain lipase.
Speaker 2:They do suggest that in all patients and this is one of the new recommendations that in all patients with pancreatitis even if you have a fairly good idea that, for example, is alcoholic pancreatitis that all patients with pancreatitis, that all patients with a pancreatitis should receive an abdominal ultrasound to evaluate for any biliary component and I've seen that done. Certainly, but not universally. If somebody comes in with a long history of pancreatitis or long history of alcoholism, excuse me, and this is their second, third bout of pancreatitis we usually don't get a right of a quadrant ultrasound to see if they've got gallstones. It's like oh, you have pain, you have the alcoholism, that's why you have pancreatitis. So that's pretty new and the reason they do that is some new evidence suggests that, uh, um, we miss a biliary component of acute pancreatitis even when there's another cause, and that again, I was unaware of that and and and so that's that's. That's kind of a new thing that that pretty much everybody who gets admitted to the hospital with pancreatitis. Even if you're pretty sure of the cause, you should go ahead and get right over quadrant. They know that there are other causes besides alcoholism and biliary pancreatitis hypertriglyceridemia. If you can't find another, another cause should be checkedactic triglyceride should be checked and if the levels above 1,000 milligrams per deciliter, that might well be your cause. Certainly I've seen overwhelming hypertriglyceridemia-induced pancreatitis with triglycerides in the tens of thousands.
Speaker 2:I'll never forget and I tell this story all the time. A lot of my students I'll never forget and I tell this story all the time. A lot of my students and residents know this Years ago we had a patient who had hypostragalus rademia pancreatitis, had a hypostragalus radium level of 20,000. And they drew blood initially from the patient and with that kind of lipid in the blood, the blood didn't look red, the blood literally looked like a strawberry smoothie and we were passing this vial of blood around and it was just completely gobsmacking. I was like how has this guy not had a stroke? I mean, that doesn't even look like blood. You know, it was one of the most bizarre things I've seen in 30 years of being a pharmacist. So it was. It was pretty weird.
Speaker 2:The other problem with hypertriglyceridemic pancreatitis is that evidence is pretty clear that outcomes are worse, people do worse. Mortality is higher in patients with hypertriglyceridemia than they do from, say, alcoholism or gallstones, and so you do want to aggressively treat those patients. They don't go too much into detail on that, but this is definitely where plasmapheresis can play a role and, you know, sometimes I think we pull the trigger on that a little late. You know we, we, you know well, gee, let's see how they do with with. You know insulin infusions and and, and you know the regular treatment for pancreatitis. I would argue that, you know, especially if somebody has severe acute pancreatitis in the ICU and they have, you know, triglycerides above a thousand and you don't have another cause, I would, I would be sooner than later to start a plasmapheresis on those patients because of the higher incidence of mortality associated with them.
Speaker 2:The other thing in my world when I see that is that, you know, obviously anyone who has triglycerides that high, you know I make sure their blood sugars are in control if they have diabetes, but even so they probably should be on you know when, when they recover you diabetes, but even so they probably should be on you know when, when they recover. You know fibrate therapy, fish oil I'm usually pretty aggressive about, about treating, you know, trying to keep their triglycerides above, below 500, because they've already demonstrated that they're going to have pancreatitis. So the other question that I get asked a lot about, of course, is drug induced pancreatitis and they know that that a lot of drugs get attributed to druguced pancreatitis based on case reports.
Speaker 2:Or you know, you know something. You know my cousin's, friend's, brother's, sister's, you know, friend had, you know this, you know, had pancreatitis and they were on this drug. They note that there was a very recent classification scheme and review that some authors did that took a look at causation of drug-induced pancreatitis based on a classification system. And if you're an inpatient clinician, I would recommend and we'll have a link to this in the show notes because it's free for the taking on the internet a nice elegant classification system about a causality where they start off with class one drugs where there's high quality of evidence for causation of acute pancreatitis, usually from randomized control clinical trials, all the way down to class four where it's basically just a few case reports. And they note that you know, probably you know class four drugs. You know you might be able to say that it causes it, but I think you're kind of hard pressed to say that for sure, whereas in you know class one, two and three. I think you can at least suggest that, yeah, this might be the cause of everything else fails of those drugs.
Speaker 2:It's worth note you know that the class one drugs. The big one that I've certainly seen in my career is azathioprine and six mercaptopurine. Both of them are well known to cause pancreatitis. And so there are class one, class two drugs, ace inhibitors, which again I've seen in my practice, as well as DPP-4 inhibitors and GLP-1 agonists. Keep in mind they know that the GLP-1 agonists, the reason for pancreatitis in those patients may well be that with the rapid weight loss you see with those drugs that you do develop gallstones and that increases your risk of pancreatitis. So that might well be it. The immune checkpoint inhibitors, where you know basically those drugs for cancer cause every itis, right. So pneumonitis and pancreatitis and hepatitis, you know if it's an itis those drugs basically cause it. Ssris were listed as a class two and I have don't think I've ever seen or recommended or suggested that SSRIs were a cause of acute pancreatitis. But they note that there is moderate quality of causation in acute pancreatitis of SSRIs I had not known that before.
Speaker 2:And so I was. I was kind of interested in that Metronidazole and valproic acid were all class two as well. Everything else kind of falls away at that point. The only two other surprises I saw in this, in this classification scheme, is Bactrim or trimethoprim. Sulfapoxazole was a class 3B, which is basically, you know, low level of evidence.
Speaker 2:I was taught that Bactrim is one of the most common causes of drug-induced pancreatitis, so that kind of surprised me. And the same with hydrochlorothiazide. Again, thiazide, as I was taught, is one of the more common cases of drug-induced pancreatitis. They actually classify that as stage four. So I guess I'm going to be saying now that that you know someone has acute pancreatitis, we can't figure out a reason why and they're on thiazides. It certainly, I guess could be, but I the evidence does not really suggest a causative factor there.
Speaker 2:So again, some some surprises there and again especially for the pharmacist listening a study or basically a review that I think is definitely worth taking a look at because I had not seen that. So, and then you know they. The other thing they talk about, that that is, is relatively new, is that there's growing evidence that suggests that tiny gallstones, what are called microlithiasis, are the cause of eratogenic acute pancreatitis. In most of patients who have not, they've not found an etiology and they note that even on imaging it might be very, very difficult to see these teeny tiny stones.
Speaker 2:And because of that they actually recommend, and again, this is new that for a second episode of acute pancreatitis with no identifiable cause in patients fit for surgery, even if you don't have imaging evidence of gallstones or biliary sludge, they recommend performing a cholecystectomy. So so basically, you know, if you have a second bout, that you should probably consider having your gallbladder re-engaged and I was again, I had not heard that that was pretty surprising. And again they. It's just that they, they've noted that that even in patients who have pancreatitis of another etiology.
Speaker 2:These microstones, which again are very hard to see on imaging, can play a role, and they note that there was a study that was published just a couple of years ago that looked in patients who had, after pancreatitis, had undergone cholecystectomy versus those who didn't, and found a significant reduction in recurrent pancreatitis in those patients, even if they had normal gallbladders, even if they didn't see stones or anything along those lines, and the number needed to treat was pretty impressive. Her treat was five and so again, I had not heard that. That's not something that I see a whole lot, and so that's that's something that I think is is, is is definitely worth thinking about in patients is you know, this is the second admission for pancreatitis, even if their wide upper quadrant is normal. Do you consider getting surgery involved and having them take a look and see what's going on? Basically, so they note that severe, acute pancreatitis, as I pointed out earlier, you know, is associated with all sorts of badness. Unfortunately, there is no easy early way to tell who's going to develop severe versus mild pancreatitis. Level of abdominal pain doesn't do it. Ct imaging doesn't do it, you know. So you know, and unfortunately they've tried to come up with different and various schemes, looking at, you know, laboratory values and the physical exam, and nothing has really come up with it. They of course note that in organ failure patients who have acute kidney injury, acute liver injury or ARDS, they're obviously by definition going to have severe acute pancreatitis. They know that gastrointestinal bleeding is often missed in patients with acute pancreatitis, which I mean I've certainly seen before but I never really connected the dots that GI bleeding be a sequelae of acute pancreatitis. So that was kind of interesting.
Speaker 2:So then we move on to treatment, which of course is my ballywick. You know, again, when dinosaurs roamed the earth and I was in school, it was beat into my head that the treatment for acute pancreatitis is fluids, fluids, fluids, fluids, fluids, and then when you're done, give them more fluids. And that again there's been some shift there. I mean, certainly intravenous fluid resuscitation is still, of course, the cornerstone of therapy for acute pancreatitis. The reason, of course, is that patients who have acute pancreatitis have marked endothelial injury, they have increased vascular permeability, and so that leads to a third spacing of fluids, at least an intravascular depletion, which then of course leads to hypovolemia and organ damage. So you know, aggressive fluid resuscitation is still the cornerstone of therapy and, as many people know, the shift has been away from normal saline into lactated ringers. You know again, not just for this but septic shock and just about every other disease state where you need aggressive resuscitation that lactated ringers is now preferred to normal saline and resuscitation and early aggressive hydration.
Speaker 2:There's been several benefits shown to LR, which includes a decreased risk of acute kidney injury, better electrolyte balance. They found that in laboratory studies that LR actually decreases systemic inflammation. I was unaware of that. It also provides calcium that binds ionically with fatty acids that are associated with severe disease and pancreatitis, and that lactate is in the ringers. Lactate has also been shown to reduce pancreatic injury in animals animal models. So again, kind of interesting. But then the second question and this is something that again it's kind of brand new is how much? Because again, you know we used to just blast people. I mean, even today I think we just blast people with, you know, 250, 300, 500 mils an hour of LR, and so you know the question is, you know, do you need that much? You know the thought's always been well, you know, if I fluid overload them I can always diarrhea some later.
Speaker 2:A recent study and we actually reviewed this in a journal club in my hospital, I think, last year that looked at moderate intravenous hydration in the first 24 to 48 hours compared to aggressive hydration, may actually have equal outcomes and cause much less fluid overload and things like that. And so they noted that in patients with mild to moderate pancreatitis. So these people weren't super severe, weren't in the ICU, stuff like that. They noted that an initial resuscitation rate of 1.5 mils per kilogram of body weight per hour is where you should be starting. And again, so 100 kilograms person, that's 150 mils an hour, much less than I have seen in aggressive resuscitation in these patients. However, they note that if the person looks hypovolemic right, you know they've been throwing up a lot, et cetera, et cetera that you can bolus them with 10 mils per kilogram but then start at this kind of more conservative dosing approach With severe disease.
Speaker 2:The study that they reference in the guidelines don't really talk about that. They, you know, say that those patients still might require more aggressive resuscitation, but they also note that there's a window for that and if you don't complete your resuscitation goals in that first 24 hours, that resuscitation aggressively after that point has no benefit. And so they are actually pretty pointed in the guidelines talking about that. When someone comes in and you suspect severe acute pancreatitis, you know the key is to really hit them hard in that first 24 hours and then at that point you can probably back them off because you're probably not getting any benefit. And again, they they note that that goal clinicians often miss, the goal of failing to provide adequate hydration during the initial 24 hours, when it is most important. So again, I think that the key there is that a mild to moderate pancreatitis, that that we don't need to hit them with as many fluids as we used to and that it will probably decrease fluid overload and the need for diuresis.
Speaker 2:But, if they have severe pancreatitis, hit them hard in that first 24 hours and then then you can kind of back off after that. They note that, that that antibiotics and this isn't really a big change from the last set of guidelines are not usually recommended in these patients. And that's always a tricky piece. Again, the clinicians inpatient clinicians, listening know and they've all been in this situation before where you know patient comes and they look septic because you know pancreatitis basically is the perfect example of the SERS criteria, the systemic inflammatory criteria without a bacterial infection. Right, the reason that they have the SERS criteria is not because they're infected, it's because of this overwhelming inflammatory response of pancreatitis. And so the you know the immediate, you know knee jerk response is oh, we better start on antibiotics.
Speaker 2:And they know that in the last 10 or 15 years there's been a shift away from automatically using empiric antibiotics on all these patients and I think we've done a better job at my hospital of not immediately hitting these guys with zosyn or anything along those lines. But they note that even in patients with with, with necrosis on their imaging again, it used to be very common that we would hit these guys and and there was a bad, not very well done study in the 1990s and suggested that carbapenems were the treatment of choice for necrotic pancreatitis. There's really no evidence suggesting that it's any better than other. You know broad spectrum, you know beta-lactamase inhibitors. I mean really you need to cover gram negatives and anaerobes, like you wouldn't any inter-abdominal infection. So I mean you ceftriaxone and metronidazole would be perfectly fine, I think in most of these patients.
Speaker 1:But in any event.
Speaker 2:They know that, that you know necrosis does not automatically mean antibiotics.
Speaker 2:And so things get really tricky then, because it's like, at what point do you pull the trigger on antibiotics? And they know that there unfortunately is no easy test to say, okay, this person now has bacterial infection, unless they have something like positive blood cultures or things like that, not even fever, you know, because, again, acute pancreatitis can cause fever. So they just basically recommend that if the patient has positive cultures, particularly positive blood cultures, that antibiotics are reasonable. And they do actually recommend, if the patient can tolerate the procedure, fine needle aspiration of an infected necrotic pancreas to try and get an idea of the bugs that are leaded. I've rarely seen that done, at least in my hospital. But again, just to reiterate that antibiotics are usually not necessary to pancreatitis, even if they look like they have sepsis. Keep in mind that pancreatitis in and of itself will cause that SERS criteria.
Speaker 2:The other big change in the guidelines, and this is something that we've initiated in my hospital, but I have to admit there's been some resistance and fortunately I've got a couple of especially my intensivists who are champions on this. And you know, again, the idea is about nutrition and there's been a couple of big shifts talking about nutrition and pancreatitis Again. A million years ago, when I came out of school, we started these guys immediately on TPN as soon as they got diagnosed with, with with pancreatitis, and then when they were able to eat, we we converted them over to to oral and and basically the whole point was you never gave anything by mouth to someone with pancreatitis, no food, because that would cause the pancreas to release more pancreatic enzymes and make things worse, et cetera, et cetera. There's now the evidence that suggests that and even today.
Speaker 2:I do definitely see where the practices. You don't give them anything to eat until their pain is essentially gone and then you can start oral feeding and usually start from like a clear liquid diet and then kind of slowly move, move your way up and see how they tolerate it. So you don't start them off with a cheeseburger and fries. You know you start them off with with something pretty easy. But it's been noticed that it's been noted that that in in the last 10 years studies have suggested that that may not be the right thing to do, because feeding is good. Feeding, oral feeding, maintains gut integrity. It prevents translocation of bacteria from the gut lumen into the necrospancreatic tissue, which theoretically then decreases the risk of infection. So the traditional you know, let's not give them anything by mouth until basically they have no pain anymore has really kind of fallen by the wayside. And they note that early oral feeding 24, 48, 72 hours, without waiting for the pain to receive, or if you're following, pancreatic enzymes which you shouldn't normalizing they note that in fact early oral feeding does not seem to be harmful and in fact may actually be helpful in these patients, and I mean as long as, again, they have bowel sounds present, they don't have significant nausea, vomiting any ileus, obviously those things would certainly stop. They stop you from feeding somebody orally. They know that system.
Speaker 2:Several systematic reviews and meta-analyses have highlighted the benefit of early oral feeding in these patients, despite the all types of pancreatitis mild, moderate, severe, without and they also note that advancing the diet solely from clear liquids to a low-fat diet is not necessary. And so you know, what they suggest in the new guidelines is that you really should consider early oral feeding with a low-fat, solid diet, which is going to be safe. Compared to liquid diets, it provides more calories and is actually probably a good thing. So you know again, you know that that's a. That's a big shift away from what I was certainly taught and I think up until the last couple of years was easily done. And really the trigger whether you should start a diet on these patients is literally are they hungry? They say to you I'm hungry, I'd like to eat. It is reasonable to go ahead and start them on oral feedings and again, a low fat, solid diet if they can, you know, swallow is certainly reasonable to do so again that's.
Speaker 2:That's a big shift and I big paradigm shift and I suspect will take a while for it to kind of, you know, settle in as the standard of care In patients who have, you know, severe acute pancreatitis, who are in or septic, or, and they, they basically can't tolerate regular oral feedings. Again, they know that TPN is not recommended anymore. The pendulum has completely swung the other way, away from from TPN. That, if at all possible, once the patient basically has an ileus or a small bowel obstruction or something along those lines, that if you feed entrally versus parenterally you have a decrease in infectious complications, organ failure and mortality. So again, very different from what was taught when I came out of school. They note that continuous infusion tube feeds are preferred over cyclic or bolus admissions and that if the patient doesn't tolerate traditional tube feeds preferred over cyclic or bolus admissions, and that if the patient doesn't tolerate traditional tube feeds, enteral formulas, that it's reasonable to use small peptide-based medium chain triglyceride oil formulas that may improve tolerance.
Speaker 2:The last piece about nutrition is that you know, even though we've been using more enteral routes, that the thought was if we can place a feeding tube past the ligament of tr. Uh, that, uh, the thought was if we can place a feeding tube past the ligament of trites, where so basically it passes the, the point where the pancreas would would release new pancreatic enzymes. That would be preferred Um and and they note that. However, you know that that's kind of fallen. I wouldn't say it's disfavorable, but there's been, uh, several small studies and a recent systematic review that suggests that nasogastric feeding so basically the way we would feed everybody else who required enteral feeding, is basically just as effective as nasojejunal feeding.
Speaker 2:So I mean again, if you can do NJ placement, that's reasonable. But they note that that's more difficult to do, that NG tube feeding is far easier and allows you to start feeding the patient a lot quicker. So they don't come right out and say it's absolutely recommended, but they note that NG tube feeding may be preferred and the fear of activating the pancreas and releasing more enzymes doesn't seem to be a reality. So the final thing that is not in the guidelines but I'll talk just a bit about is pain control, cause of course these patients do have a lot of pain and um, uh, you know, uh, I think you know, I, what I'm I'm seeing at least in my practice and certainly when I've talked to other colleagues, is, you know, as as kind of an outgrowth of, of our, our response to the opioid epidemic we've.
Speaker 2:We've really, really pulled back on using opioids on these patients and you know, yes, we'll give them some PRN stuff and and and all that stuff and then that, then that's fine. But I, I I definitely seen a fear of of using opioids for acute pancreatitis and I just don't think that's warranted. I think that acute pancreatitis is is is very painful. I think that it is absolutely reasonable to use opioids in these patients.
Speaker 2:Yes, you are going to put them at increased risk for ileus because you know, opioids cause pancreatitis or, I'm sorry, opioids cause constipation and so, yeah, I mean that's a bad thing, but I just don't think, I don't think it's ethical, I don't think it's the right thing to do to not be aggressive at pain control in these patients. Certainly, you can use adjunctive therapy and stuff like that, but you know, opioids really should be the mainstay of therapy for acute pancreatitis. Now, yes, you know, sending them home on a hundred Vicodin or or things along those lines, yeah, I wouldn't do that, certainly, but but I think in the while they've got really bad pain. I think this is. We should not withhold opioids in these patients because of some fear of addiction or something like that.
Speaker 1:This is an acute syndrome.
Speaker 2:It's very painful, and I think the right thing to do is treat these patients aggressively. So, that's the new guidelines, jen. It's, you know, again, a couple of new things and a couple of things that have really, you know, changed the paradigm and how we treat these patients. I'm fortunate in my hospital that we're doing some of this stuff. Fortunately because I have a couple of physician champions. But it'll be interesting to see where we go with this as time goes on.
Speaker 1:Yeah, absolutely, jeff. That is such a great topic and I appreciate your pain comments because you know we've done so much on pain management and I think everyone is so scared to. You know prescribe opioids and use those, but you know. Your comment about the ethics of that and the true pain and what's really important in these patients I think is a really good comment.
Speaker 2:So I just, you know it's I, you know I again, I'm not, I'm not, I, I nobody wants to go back to the mid nineties, you know, I mean, and I get that, you know, and. But like so many things in medicine, when something terrible happens, the pendulum swings all the way back the other way and I think we've overcompensated now and and you know, you know I, I think it is. You know, again, this is a very painful disease. I would be very aggressive about treating these patients.
Speaker 1:Yeah, and you know, we have to remember what those indications were for you know it was. The fact that we overused was was a whole different conversation. So yeah really great point to end on Such a good topic. I think it was a great way to celebrate our four year Game Changers anniversary so thank you, thank you.
Speaker 1:Our goal with this podcast is to have clinical conversations that keep you curious and up to date with drug therapy topics. We all need continued education to stay sharp, and our listeners tell us that hearing these quick topics and these deep dives that we do quickly each week, that Dr Waldo does such a fabulous job and all the guests that we bring on, is a game changer for their education and practice. So, if you agree with that, we would ask that, in honor of our anniversary, you share it with a friend or two or three this week. We 'd really appreciate your support as we head into year five of our weekly podcast CE. It would truly help us grow and continue to bring these important topics to you. So thank you again, jeff Wall, for sticking with us for these four years, and helping us grow this.
Speaker 1:I think we both had a vision when we started, and I think we've achieved that, so it'll be exciting to see what happens next.
Speaker 2:I agree. Thank you, Jen.
Speaker 1:Yeah, so fun With that. That's it for this week. So if you are a CE plan member, be sure to claim your CE credit for this episode by logging in at ceimpactcom, and if not, if you're just here for the education, we appreciate that as well. As always, have a great week and keep learning. We'll talk to you next week.