We have quite a few questions that we can get to in the chat, so we'll start right off here. We'll first start with Samit. This question is about the diagnosis of going from compensated to decompensated cirrhosis. Once a patient advances to that diagnosis of decompensated state, can they go back to having a more compensated cirrhosis? Thanks for the question. I do think that if we're good about treating the underlying disease and controlling patients' symptoms, you can classify them back as compensated. The scoring systems that we use, particularly the Child's Pew that breaks down into A, B, and C, Child's Pew A is is considered compensated. The situations where I've seen this are particularly patients with alcoholic liver disease who you're able to really drive home that importance of alcohol abstinence, and they are able to successfully do that. They're successful to comply with recommendations such as the 2-gram sodium diet if they've had an issue with ascites. If you've managed their varices, but really treating that underlying disease, I have seen patients that really become very well compensated despite being on the verge of mortality in the hospital. It takes a lot of initiative both from the physician and from the patient, but I do think patients can go back to a compensated state with those interventions. Great. In regards to EGD screening for esophageal varices or any type of varices, I suppose, how often would you recommend repeat EGD after variceal banding or if the patient's on appropriate beta blocker therapy? That's a great question, too, and a little bit of nuance there. I guess it depends on whether they've had variceal bleeding or not, but in patients, for instance, who you've done just endoscopic screening, they've never had variceal bleeding, and your decision up front is to use the beta blocker. There's actually no specific recommendation for repeat endoscopy surveillance that I'm aware of as long as you're titrating that beta blocker to goal heart rate therapy. If you do choose to undergo the variceal band ligation process and you do get to a point where those varices are eradicated endoscopically, then typically we'll do initially annual surveillance, but then also, again, consider whether or not their underlying disease is adequately managed. Have they reached a compensated state? You could theoretically go out to every two years. We typically don't go longer than that. Most of our patients are on annual surveillance. Great. Thank you. Sarah, do you know what it is about the GLP-1 medications that cause acute pancreatitis? I do not know why. I don't know either. It's actually pretty infrequent, but yes, it can happen. I've seen it happen a couple times in patients who have been on GLP-1s, or at least we presume it's related to that. I don't know the exact mechanism though. I'm not sure either. I don't know if we know. Another question for you, Sarah. Let's see here. If you have a patient that has abdominal pain that's consistent with acute pancreatitis and has that lipase three times greater than upper limits of normal, would you necessarily order imaging? I think this person's trying to tease out, would you get an ultrasound, an X-ray? Would you go straight to CT? What would prompt you to get further imaging? Yeah, that's a great question. So in a patient who has that classic abdominal pain, who has a lipase elevation, and that really is diagnostic of acute pancreatitis alone, you don't need any further imaging to diagnose acute pancreatitis. Imaging will be helpful though if you are trying to parse out why. And so if they, particularly if they have elevated LFTs, or if this is their first episode, I would get an abdominal ultrasound looking to say, what does their common bile duct look like? Do they have stones? Do they have a gallbladder full of stones? If they have like a rigid abdomen, I would maybe consider a free air series. I don't typically do a CAT scan in these patients unless I'm worried about other potential complications. It doesn't add much in the setting of acute pancreatitis. It shows us that they have peripancreatic edema, which we expect anyway. Yeah. So, Neat, would you recommend re-tapping on day three in the setting of SPP to track improvement? That's a good question. This is something I know has been discussed and has maybe been recommended to consider. We don't routinely re-tap on day three unless, for instance, we're concerned that the patient's not improving after a diagnosis of SPP. If a patient is actually having a good course in terms of improvement with management, with appropriate management of SPP up front, we don't routinely re-tap them on day three, although I know that there have been some recommendations to consider that to ensure that the nutricidic count is decreasing. But in practice, we don't routinely do that. Can you review the use of non-selective beta blockers to prevent decompensation for patients with low platelets and high KPA on FibroScan? Yeah, that's also a great question. Traditionally, we've been using non-selective beta blockers once you've had a diagnosis of varices, but there is some literature in the hepatology journals basically supporting the use of non-selective beta blockers for patients with thrombocytopenia and very high KPA levels on transient elastography. From what my understanding is that if the VCT score, the transient elastography score, FibroScan score is above 25 in combination with thrombocytopenia, there is good evidence now to show empiric use of non-selective beta blockers to reduce portal hypertension. And then one more for you, Smeet, and then I'll give you a break. When do you add junk rifaximin? So this individual has gotten kind of varying advice, but do you initiate it with the initial hepatic encephalopathy episode or only if subsequent episodes occur despite lactulose? We usually try to use lactulose first line and assess the patient's response to the lactulose before adding rifaximin. The primary limitation to the rifaximin is the cost prohibitive nature of it. And so even in an initial presentation, if lactulose is insufficient, yes, we may add rifaximin pretty early. But a lot of times we will hold off on that because we're limited by patient access in the outpatient setting. But at least I haven't used it first line before trying lactulose. That actually addresses another question. Do you have any alternatives if rifaximin is cost prohibitive? Oh, unfortunately, not that I've seen or not that I've used in practice apart from considering the zinc deficiency in nutrition. I'm not sure if others have in their practice beyond rifaximin. Lactulose and zinc is the only other ones that we use. Right. Sarah, this person was asking, how do you interpret if the fecal elastase and the fecal fat is discordant? So if you have a normal fecal fat, but a high fecal elastase or vice versa? Yeah. So if you have a normal fecal elastase and a high fecal fat, I'm still thinking malabsorption, but I'm thinking potential causes of malabsorption that maybe are not pancreatic related. So these could be patients who have gastric bypass. They could be patients who have issues with small intestinal absorption. So I would kind of go that route. Remember, the pancreatic elastases is only so good. It's not perfect. And so it's still possible that you'd get some improvement from pancreatic enzymes, especially if you do have other features and evidence of chronic pancreatitis. But certainly look into other causes of malabsorption in that case. This individual had a question about if pancreatic enzymes are difficult to get approved and if they are expensive. Yeah, that's a great question. So this is like the rifaximin of liver disease. They can be expensive. Insurance kind of dictates which one I use, to be honest. To me, they're all the same as long as we're dosing them appropriately based on units of lipase. But they can be cost prohibitive. Most of the companies have really good patient assistance programs. And so even if they don't technically qualify on paper, I always suggest putting an application in and seeing if you can help get some copayment reduction on them. They are the only ones that are regulated. There are some over the counter that you can get from like nutrition stores that are digestive enzymes. It's not really quite the same thing. They certainly are not regulated through the FDA. It's hard to recommend those and to dose them equivalent. The other issue with them is that they're porcine. So if people, for religious reasons or otherwise, are not able to have any of those products, that makes it really challenging to prescribe them as well. I'm going to stick with you, Sarah, because we have a few other questions on these. Let's see here. I think there was one question regarding how long patients can safely stay on these enzymes. And then do you have any recommendations for monitoring and management? Yeah, so patients can stay on them indefinitely and they likely will need to. If you're starting them because they have exocrine pancreatic insufficiency, unless it's in like right around a course of acute pancreatitis where you're going to get some improvement back, I don't typically expect that they're going to be able to come off of them. The best way to monitor them is actually clinically. So I wouldn't expect that their pancreatic fecal elastase is going to change, right? So that's a stool test that's really looking at an enzyme that's produced by the pancreas. Taking enzyme supplemental is not going to change your pancreatic ability to produce fecal elastase. So I don't think that that's going to be helpful in any way. The benefit of that means that if they're already on enzymes and you're still kind of working through the diagnosis, you can check your pancreatic elastase and it's not affected by the enzymes. If it's low, it's low. And it's not that the enzymes aren't working, it just means they're not producing it. You could monitor it with fecal fat. But again, compliance is a really big issue and it could give you a falsely low result if they're not collecting all of their stool in that time period. So typically I just go off of symptoms. I go off of what's their weight loss look like? Are they still getting postprandial bloating? Are they able to eat and drink a little bit better? And then more subjectively from the patients, how frequent are their bowel movements and are they getting any form to them? Thank you. And then one more, does pancreatic enzyme replacement theory influence blood glucose in patients that have EPI and concurrent diabetes? It does not, no. Okay. Sumit, would you put a patient on beta blockers for varices if they are seen on imaging prior to endoscopic screening? Good question and I haven't actually considered that previously. We have traditionally used the endoscopic features of varices. Now you'll frequently see varices on imaging, but they don't actually manifest with endoscopic findings, or their minimal endoscopic findings, grade one varices or none. So I haven't considered beta blockers just based off of imaging results. I'd be interested to know how those imaging findings correlate with some of those elevated transgeny elastography scores. And if there is a correlation there, maybe that is something we need to consider, but that's not something that I've done in practice previously. Okay. And have you seen BRTO be used for varices treatment before? For gastric varices, yes, as an alternative to tips. And this is where the expertise of your IR colleagues comes into come to play in terms of what they feel comfortable doing and whether or not that's an alternative option. I have not seen it for other processes, however. And what are your thoughts on non-selective beta blockers with those who have been diagnosed and treated for SBP? That's something I did not touch on during the talk, but beta blockers have been shown to increase the risk of SBP. And so in patients who have been diagnosed with SBP, we do recommend stopping their beta blocker and avoiding beta blocker therapy. Thank you. Sarah, what have you seen for patients that have pancreatic divism that have recurrent acute pancreatitis? What therapeutic options do we have for them? PD stenting, pancreatectomy, what do you think works best there? Yeah, so I think typically patients will have a minor pancreatic duct sphincterotomy and stenting potentially with dilation. They do well with that. Sometimes it will take a couple stents. They may do well for a period of time and then it may become stenotic over time and years later they may require it again. But usually that would be the treatment of choice. I have not seen a patient who has required surgery or anything above that. Do you see that patients with chronic pancreatitis have consistently elevated light pace levels? That's a great question and the answer is sometimes. So sometimes they're at this like low grade chronic elevation and sometimes you'll actually check them and they'll be low and they'll never mount a really high response even when they're having acute exacerbation of pain. There's a phenomenon or concept of pancreas burnout where you've had so many episodes of acute pancreatitis or you've developed so much fibrosis and scar tissue that instead of mounting that high light pace during these acute and chronic episodes, their enzymes always stay low. So certainly it's possible to see a low grade elevation. I wouldn't expect to see it three times the upper limit of normal unless it's acute and chronic, but they may always just live in like the 60s for example, or you may see a patient that just has a low level of 15 no matter what and it stays there. Even if you see CT evidence of acute and chronic, they may still have a low light pace. I think it's really important to talk to our patients about that, but also it's a good opportunity to educate other people. So sometimes I still have patients that will come into the emergency room, have a documented history of chronic pancreatitis, and they'll have an acute flare of symptoms. Maybe they have acute and chronic, but their light pace level never changes and they're told, you know, your light pace is low, it's not going up, you can go home. You still should treat them as pancreatitis. That's a good point. When evaluating chronic pancreatitis with diagnostic imaging, we have the Rosemont criteria for EUS and Cambridge for ERCP. If you weren't aware of any criteria that we use for CT or MRCP? I am not aware of any formal criteria. I don't know if Sumit, do you know? Not from cross-sectional imaging that I'm aware of, no. We certainly look for the pancreatic calcifications, the duct irregularity, pancreatic fluid collections, but I don't know that there's a criteria like there is for EUS. And then one more for the chronic pancreatitis. Looks like patients, can patients stay on GLP-1 with a history of chronic pain, or would you discontinue that? Yeah, you know, if they have stable symptoms, I do clear them to go on it and stay on it. With a discussion, obviously, to say a small number of patients will get acute pancreatitis with us. I don't have enough information or a way for me to predict how you're going to respond to it. I don't think it's necessarily a contraindication though. If they start to have acute exacerbations and I can't find another reason, then I do have the conversation with the PCP or endocrinologist or whoever started it to start to kind of explore, could it be related to the medication? It's really tough because when it's potentially medication induced, we don't have a test for that per se. Yeah. Risk benefit kind of discussions. Absolutely. So, Meet, at what point does the risk of hepatic encephalopathy with tips become worth it for refractory ascites? I think basically the question is when should we start moving towards tips? What kind of pushes us towards that? Yeah, this is a great point in terms of having to individualize for your patients. If the patient's never had any symptoms of hepatic encephalopathy, but they're really suffering from their refractory ascites needing frequent paracentesis, I think it is an important consideration. But you have to recognize, obviously, that there are risks associated with tips and one of the major consequences of tips could be exacerbations of encephalopathy. And so, if they've had a history of recurrent hospitalizations for encephalopathy, if they have difficulty controlling their encephalopathy, those would be considered relative contraindications to tips. So, it's an important discussion and obviously tips has its own significant morbidity with it. So, sometimes it's picking the lesser of two evils or stuck between a rock and a hard place. But these are individual conversations to have with the patient, with the family, understanding what their baseline, you know, risk is. And I don't know that there's a great way to estimate or predict that. But if they're really suffering from their ascites, it's balancing the two. Is SPP determined by PNMs or total neutrophil count? And can you explain the difference? We use the absolute neutrophil count. So, I guess the total neutrophil count greater than 250 is the threshold that's used for the diagnosis of SPP. I guess the PNMs meaning, oh, I guess the total white cell count. So, it's the neutrophil count that we use for the threshold for 250 for the diagnosis of SPP. Okay. Let's see here. When surveilling pancreatic cysts, what imaging would be best? MRI or MRI abdomen with MRCP? Or I guess RCT could also be included in there. Yeah, that's a great question. So, you know, I look at CT and MRI as kind of being comparable. My preference for surveillance is generally MRI just because of the lack of radiation exposure, the safety of it. As long as the patient can sit still and you get good images and they don't have contraindications like cochlear impacts or, you know, non-MRI compliant pacemakers or something like that. Whether or not we do an MRCP with it, I think it depends. So, if you have a pancreatic cyst and you're kind of trying to differentiate it, I think an MRCP can be helpful when you're looking to say, does it communicate with the main pancreatic duct? So, something like an IPMN. If it's a clear pancreatic cyst like a pseudocyst or if it's a cyst that's outside that doesn't communicate with the pancreatic duct, you already know that. I don't typically add the MRCP. But for IPMNs, I do like it or if I'm trying to differentiate it, remember that one of those high-risk stigmata worrisome features is main pancreatic duct dilation. So, we want to make sure that we're getting a good look at that particularly for the IPMNs. And then I think kind of this is a technical terminology question as well since we're talking about imaging the pancreas. Is the distal portion of the pancreatic duct in the head or the tail? Which one's distal and proximal? That's a great question. And actually using distal and proximal and pancreatic duct is kind of a big no-no. And so, it's preferred to use upstream and downstream. And so, the upstream is the portion of the duct that's going towards the pancreatic tail, downstream towards the pancreatic head. And that would be a better way of differentiating. It is a great question. It can be confusing. So, how would you differentiate acute alcohol liver disease or hepatitis for cirrhosis? Yeah, this is great. And sometimes it is hard to distinguish what the difference is. So, cirrhosis is obviously the chronic manifestations of alcoholic liver disease. Whereas I think what you're alluding to is acute alcoholic hepatitis and whether or not there is truly underlying cirrhosis at the time of the diagnosis. And it's important to understand that sometimes patients even in the setting of acute alcoholic liver disease can develop almost manifestations of almost an acute portal hypertension without underlying cirrhosis. So, a lot of times we'll have to kind of wait and see how their course is afterwards, how much of that corrects with just treatment of the acute alcoholic hepatitis. But from what I understand, it seems a majority of these patients when they are presenting with acute alcoholic hepatitis do at least have advanced fibrosis if not cirrhosis underlying. And so, the long-term management and follow-up after the acute alcoholic hepatitis will guide how you treat them in terms of their long-term management of potentially cirrhosis. So, some of those portal hypertensive type manifestations will correct with just alcohol abstinence and management of the acute flare. But many times that is their first presentation as a decompensation from cirrhosis. Thank you. Then one last question, what's the benefit of octreotide? So, octreotide has been shown to improve hemostasis results in variceal bleeding at day five compared with I think placebo was the major study that was published on that. So, it's really hemostasis by reducing spiky resistance, spiky blood flow and improving hemostasis results that way similar to along the lines of beta blockers. But in the acute setting, octreotide is favored. Okay. All right. Yeah. Those were great questions. Lots of engagement. Those were amazing topics. Like I said, real heavy hitters. So, with that, we actually came up to our break time right on time. Look at us. Everybody will take a quick, let's see here, about 15-minute break and resume promptly here at 10.25 central time.

hepatology

cirrhosis

pancreatitis

beta blockers

Child-Pugh

TIPS