Good afternoon, everyone. My name is Tiffany Kaiser. On behalf of myself and my co-moderator, Dawn Dresick, we'd like to welcome you to the Hepatology Associate SIG Program. This comprehensive session will provide an overview of key management considerations and review strategies for healthcare teams to overcome the challenges commonly faced when considering surgery in the cirrhotic population. Am I supposed to advance the slides? As I said, it'll be a comprehensive program, and it's going to include four talks with a panel discussion at the end. And within the talks, we're going to cover these objectives. We have four outstanding speakers joining us today. I'm going to introduce all of them now so we can go through each talk to make sure we have time for the panel discussion in the end. Our first speaker is Dawn Dresick, who's a hepatology nurse practitioner at Atrium Health Liver Care and Transplant in Greensboro, North Carolina, working in liver disease and liver transplantation for almost 20 years. She's a recipient of the ASLD NPPA Hepatology Associate Fellowship, the 2019 ASLD Mid-Career Hepatology Associate Scholar Award, member of Hepatology Associate Committee, Hepatology Associate SIG Committee, and the incoming vice chair of the Hepatology Associate SIG. Our second speaker will talk on surgical procedure considerations, Cori Burke. She's an FMP and AGNP Program Director at Loma Linda University School of Nursing and practices clinically at Loma Linda University Health Transplant Institute, where she serves as a clinical director at the Las Vegas campus. She's an ASLD Hepatology Associate Committee and is the 2022 Associate Course Director for the liver meeting. She is a recipient of the 2019 ASLD Mid-Career Hepatology Associate Scholar Award and is the 2021 American Society of Transplant Surgeons Advanced Transplant Provider. She received all degrees and training at the University of Pittsburgh and practiced at the Pittsburgh Medical Center in transplantation from 2008 to 2018. Our third speaker will talk to us on the Preoperative Medical Therapy Optimization, and it's Ho Chung Gillis. She worked at the Central Virginia Veterans Affair Medical Center in Richmond, Virginia, and serves as the Clinical Program Director for GI, the Hepatology Division Program Director for Liver Transplant and Assistant Director for GI Research at the McGuire Research Institute. And we'll finish with Georgene Smith talking on the Interoperative Considerations and Post-operative Recovery. She's a Surgical Physician Assistant at the Hospital of the University of Pennsylvania and has worked in transplant surgery for 15 years. She's an Associate Member of ASLD, member of ASTS, where she's on the Fellows Training Committee and Foundation Board, and former Chair of the Advanced Transplant Provider Committee and Inaugural Associate Counselor. Her main responsibility at Penn is Procurement Surgery and Training Fellows on the Procurement Procedure. So, we'll go ahead and get started. Dawn? Thank you, everyone, for coming, and thank you to the SIG and AASLD for inviting me to be here today. And my slides will come up in a second. I'm going to speak to you today on risk stratification of patients with cirrhosis who are potentially undergoing surgery and focus primarily on the predictive models that are available and what to kind of take into consideration as we're referring a patient, as we're asked as hepatology providers or potentially even GI providers to assess the surgical risk for someone planned for surgery. So my disclosures are here, none of which are relevant to this discussion. So we know patients with cirrhosis are at an increased risk for morbidity and mortality when they undergo procedures, and it's multifactorial why that is. There's a lot of changes that happen within the body related to cirrhosis that affect our body outside, that affect the body outside of the liver. We can see changes in hepatic metabolism, reduced synthetic function of the liver, changes in homostasis or hemostasis, changes in protein metabolism, risk for bleeding, nutritional deficits, neurologic impact, and all these do affect how a patient is going to survive through surgery as well as recovering after surgery. There were early studies published that reported a postoperative mortality as high as 67 percent in patients with cirrhosis, and a mortality for a cirrhotic undergoing surgery is anywhere between two to ten times higher than for those patients who are not cirrhotic. So when we talk about assessing somebody's surgical risk, the first thing we want to do is look at the factors that affect that risk, be able to take those factors and put them into some type of predictive model that can adequately and accurately assess what their post and perioperative risk may be for morbidity and mortality, so that we can then use that information for patient selection for a surgery procedure, so we can have shared decision making with the patient, informed consent of the patient because their risk may be beyond what are generally expected, and as well as how to modify patient risk both preoperatively and as well as management perioperative and postoperatively. So first we'll talk about risk factors that can affect these patients. So they're multifactorial again. We have risk factors that are related directly to their cirrhosis as well as surgery-related factors and patient-related factors. So particularly related to their cirrhosis, we spoke about this briefly, or I spoke about this briefly. Patients with cirrhosis are at a high risk of complications. Interestingly they have both thrombocytopenia and coagulopathy with elevated INR, however they're in a state where they have an increased risk for developing clot as well as an increased risk for bleeding. Their protein synthetic dysfunction impacts wound healing as well as delaying physical recovery if they're extremely frail. They're more susceptible to infection due to immune dysregulation and dysfunction. In cases of splenic vasoconstriction and vasodilation, they have decreased effective intravascular volume maintenance, so we can have difficulty with volume status as well as increased susceptibility to renal failure, as well as collateral circulation due to portal hypertension which can increase risk of bleeding, particularly with abdominal surgeries, as well as create some technical challenges in that setting. Directly related to the particular surgery, type of surgery is important. Is it an elective per surgery or is it an emergent surgery? So for patients undergoing emergent surgery, the risk of postoperative mortality is anywhere between four and ten times higher than for someone who's non-cirrhotic. Hepatobiliary procedures carry a higher risk than abdominal procedures which carry a higher risk than cardiothoracic procedures, but those three types of surgeries do have the highest risk. The longer a surgery takes, the longer their anesthetic time, the more likely they may be to have respiratory depression and issues with potential for postoperative pneumonia. As I said, they have a rebalanced homostasis or hemostasis, so patients may have thrombocytopenia but that doesn't necessarily mean they're at a higher risk for bleeding because even though their peripheral platelet count is low, that does not mean that they're at a higher risk for bleeding and that they're not going to coagulate. Where the surgery is performed is important. Is it a tertiary center or a transplant center or is it being done in a community hospital that may not have anesthesiologists on board who are familiar with managing these patients during surgery? If something does go sideways, is there a transplant there as a backup or are there surgeons and hepatologists there who can manage? And then also anesthetic agents are important as well. Some may have reduced hepatic clearance as well as other risks that can be associated with their cirrhosis. And then we have to look at patient-related risk factors. How old is the patient? Are they overweight? Are they actively drinking, which may be affecting their liver function? Are they using other drugs? Are they a smoker? That's going to affect pulmonary outcomes. We know you don't want a patient to quit smoking right before surgery because they're going to have worse outcomes than if they quit much prior to surgery. Their ASA class, their functional status, and do they have sarcopenia? Do they have muscle loss? Are they going to recover quickly? We're going to, in the ACLF clinical course on Friday, discuss this and how quickly patients with cirrhosis can lose muscle mass. Comorbid conditions like diabetes, high blood pressure, COPD, CHF, all of these things independent of cirrhosis will increase a patient's risk undergoing surgery, so we have to take that into consideration. The next thing we want to do is look at all of those risks and figure out how that affects the likelihood of postoperative morbidity and mortality, and we do that through predictive models. There are several predictive models that have been developed and studied. Many of these were not developed specifically for patients with cirrhosis. The earlier models that were cirrhosis-specific did not risk adjust for the type of surgery or the urgency of surgery. They don't always take portal hypertension into consideration. These are retrospective studies, which is important to note because we're looking at patients who did undergo surgery. That's not capturing those patients that were sent for assessment and automatically came to the point of, you know, we really don't think this person should proceed, so we're not capturing what additional risk those patients may have had. And some of these models are older, and do they hold up over time? A lot of things have changed over the years. We see from year to year at this meeting how quickly science changes, and is surgery techniques improving, is our management of these patients both perioperatively and postoperatively improving, and does that affect what the older models predict? So the NSQIP is a retrospective review that was developed looking at over 5 million surgeries from 874 hospitals between 2016 and 2020. There is an online calculator available. It's a patient-specific index that looks at 20 different patient predictors. Interestingly, the only cirrhosis-specific indicator is a CITES. It does incorporate the type of procedure that's being formed, and it's actually pulled up based on the procedure CPT score, and it predicts a 30-day postoperative risk of 18 potential complications, and you can easily pull this up online, and it's really interesting because it will map out whether specifically is that patient considered high, low, or moderate risk for each of those individual outcomes. And we also have the ASA system, which many of us know. If you've ever sent a patient for endoscopy or colonoscopy, it's right on the report when you get it back. The ASA score has been used for over 60 years, and it estimates perioperative risk. It's not looking at risk postoperatively after this patient comes out of the OR. Alone, it is not predictive of those outcomes for that reason. Interestingly, for patients with an ASA class V who have cirrhosis, so these are patients who the surgery is life-threatening. If they do not have the need for surgery, it's life-threatening. If they do not have that surgery, their risk of dying is extremely high. For those patients with cirrhosis, the median survival is only two days, with a 90 percent mortality at 14 days and 100 percent mortality at 90 days, and that's important to consider because when we have this shared decision-making and we look at this risk, oftentimes in cirrhosis, we say, you don't go to the OR electively. So things like hernia repairs oftentimes will wait until it is an emergent procedure, and is that actually the right time to do it? Should we be looking at sending those patients to the OR sooner? And interestingly, in Georgine's world, and I did not know that this was even an ASA score, there is an ASA class VI, which are patients who are brain-dead and going to the OR for transplant, so I never knew that existed until I pulled up a new chart. The Child-Turkot-Pugh score was one of the first scores that were developed specifically for patients with cirrhosis, but not necessarily just looking at surgical procedures. It was developed in 1964 to identify patients who were at high risk for portal decompression interventions. It's been validated in portal cable shunt surgeries, TIPS procedure, as well as other major surgeries. It is a very nice score because it does not take a whole lot to come up with that score, although it is very subjective. If I had a patient and asked five different people who saw that patient whether they are a grade 1, 2, 3, or 4 encephalopathy or where their ascites fit along that line, you may get different answers. It also does not take portal hypertension into account. A lot of times, if I'm writing a CTP score out, I'll actually put, like, CTP-A plus portal hypertension because that is a known risk when we go into surgery. For abdominal surgery, mortality with CTP for somebody who's a Child-A is 10%, where if you take somebody who's a Child-C, that mortality can go as high as 70% to 80%. MELD score was developed to predict risk for patients undergoing TIPS procedure, and it's also been found to be a predictor of not only just overall survival, but also perioperative outcomes. It is based solely on liver synthetic function, so it takes that subjective piece out. However, in doing that, it does not look at portal hypertension, as well as hepatic decompensation. For those of us that work in transplant, we often have patients that are much sicker than their MELD score is telling us they are. It does not include surgery-specific risk. It's been demonstrated that for patients who have a MELD score below 16, that they have better outcomes, and that that risk does increase incrementally as that MELD score increases as well. It looks specifically at bilirubin, INR, and creatinine, and there's also now MELD-NA or MELD-sodium that incorporates sodium into that measure as well. The surgical risk assessment score that most of us are most familiar with right now is the Mayo Center Postoperative Mortality Risk Assessment score for patients with cirrhosis. And this was the first score that was the first predictive model that was developed specifically to identify the risk of patients who are undergoing cirrhosis. It was a retrospective study of about 700 or closer to 800 patients. It looked at patients who underwent abdominal cardiovascular and orthopedic surgeries. Interestingly, that study excluded the most common surgeries we see done or request it to be done in cirrhotic patients, such as appendectomy, hernia repair, and cholecystectomy. It did not stratify by the type of surgery other than general, it's abdominal, it's cardiovascular or orthopedic, and it didn't stratify by urgency either. And it excluded those ASA class V patients. So in those patients that needed to undergo hernia repair emergently, we're not capturing what a potential risk was there. And there is evidence that's come over time, and I'll talk about in a minute, that it may overestimate that risk now as things have progressed as far as the art of surgery. One of the nice things about the Mayo score is they actually define ASA class for our cirrhotic patients. So they have, and this is available on their website, and there's other, like mdcalc.com and such have these calculators readily available. But for patients who have compensated cirrhosis, they're considered an ASA 3. And if they have decompensations, they're an ASA 4. The other thing that the Mayo score doesn't take age as a factor. It looks at ASA, the MELD score, and also stratifies by type of liver disease. And I was playing with the Mayo score earlier today, and it's interesting how much, whether or not somebody is considered alcoholic or cholestatic liver disease versus viral or other liver disease, it can change that risk assessment. And we know patients don't always just have one chronic liver disease. You may see a patient that has both hep C and alcohol, or NASH and alcohol, and NASH doesn't really fall in there either. We can't, alcohol with cholestasis, you would think NASH to some degree is similar. So more recently, and the new kid on the block is the VocalPen Surgical Risk Score. This was published originally within the last two years. It was a dedicated risk assessment model that's been validated in patients with cirrhosis, and it used the VA's database to retrospectively look at over 4,000 patients who underwent surgery with cirrhosis. They looked at the types of surgery that were done, and you can see there the breakdown. It separated abdominal wall from abdominal surgery, vascular, major orthopedic. So we're looking at those patients that are requesting total knee replacement or total hip replacement, as well as chest and cardiac surgeries. And it also separated out vascular from chest and cardiac, which is nice. It looks at the risk of hepatic decompensation at 90 days, which is also very nice to know. It's great if I can tell a patient you're not likely to die in 30 days, but in 30 days you may now have encephalopathy, anesthesia, and other decompensation. So which models should be used? So this is a, I used a case, a 64-year-old female, hep C. She wants to have her knee replacement done. She is well compensated in the sense that she's never had ascites or variceal bleeding. She doesn't have encephalopathy, but when you look at her labs, she does have some lab derangement. Her INR is just above normal. Her billy's a little bit up, platelet count's a little bit down. She did have an EGD after hep C eradication and took grade one varicea, so she continues to have portal hypertension. And her history is significant for lung cancer. She's had a right lower lung lobectomy. She's got COPD, hypertension. She's still smoking, and she's overweight. So she's technically, and I apologize for my urine aside, she's probably an ASA 3, but with that history, you know, yes, death is not imminent for her, but that's a lot going on for somebody we're planning to do surgery on. By the Mayo risk score, it would estimate a 30-day risk of mortality at 8.9%, but when we look at the VocalPEN, her risk would only be .8%, and that is a really big discrepancy when we're trying to discuss this with a patient. So how do you decide, and how do these scores match up? So not only was the VocalPEN information published on its own, there's been another paper that supported it looking at the UCET score in two large health systems. And sensitivity and specificity, the VocalPEN and the Mayo score match up very closely, but when we look at actual outcome versus the predicted outcome, you can see in those bottom two graphs that the VocalPEN significantly outperforms the Mayo risk score when it comes to risk, predicted versus actual. And they did mention in their study that they feel that that's because of those changes in surgery and treatments and management that have impacted that. It's not a bad thing that that Mayo score is not performing as well as it did 10, 15 years ago. It's actually a sign that healthcare has changed and improving, and any of these models can't be a static model. We have to relook at these things over time. And on the left side of the slide for you, it's actually mapped out with calibration that the three scores that actually kind of map the best patient outcomes are going to be the VocalPEN, the MELD, and the MELD-sodium, with the MELD and MELD-sodium performing very closely. So how do we take this information and synthesize it to give the requesting surgeon or our patient an actual surgical risk assessment? So the first thing you want to do is you want to look at the patient that needs surgery. You want to look at that type of surgery. Is it emergent or elective? You want to look at their labs. You want to look at do they have any clinically significant portal hypertension? So that may be getting a fiber scan, doing an EGD, pressure measurements. Have they had decompensation now or in the past? Once a decompensated cirrhotic, always a decompensated cirrhotic, as far as I'm concerned. Their liver may be doing well now, but if we stress them with surgery, we've already had a stress test that their liver may not handle that stress. And then what other risk factors do they have? So from there, you kind of stratify it out. If they don't have any clinically significant portal hypertension, they're well compensated, and it's an elective surgery, they're good. They can proceed. If they do have any of those things, then you definitely want to do those surgical risk models. And in looking at those outcomes, are they a patient that you should have a discussion of the risk with the patient and between the patient and surgeon, risk modifications preoperatively. Should they be considered for transplant evaluation prior to surgery as a safety net, or should they just be evaluated for transplant? And then if it's emergent surgery, you also have to look at the futility when you're looking at risk versus benefit, discussion with the patient and family regarding their risk. And a lot of times, that may be the decision to avoid elective surgery. So again, for our 65-year-old patient, things are not always black and white. They're often gray. So depending which score you look at, if you look at her Mayo model, it's going to tell you that she should not have that elective surgery. But if you look at vocal pen, or you look at her CTP, or her MELD score, that risk is not as high. And that's where shared decision making comes in between a patient, their surgeon, and their hepatology provider. But I think, and we talked about at some of the sessions, motivational interviewing. For this patient, not having her knee surgery is affecting her quality of life and her ability to do the things that she wants to do. So it's that discussion, do you want to undergo that surgery knowing that risk, and how's that going to impact you? So takeaways, patients with cirrhosis are at increased risk. Their thorough evaluation is important so that you can predict their risk, so that you can have shared decision making. Remember that we don't clear patients for surgery. We provide a risk assessment. If I say I'm clearing somebody for surgery, I'm not taking into consideration the fact that this patient, for example, had a lung resection. So all I'm doing is providing a risk from a hepatology perspective. Risk models should not replace clinical judgment. It is important to know exactly what the patient is. Again, these models often did not include patients, or these models did not evaluate and take into consideration those patients who are automatically deemed not a candidate for surgery. And informed consent with the patient is important as well. So with that, I'm going to invite up Cori Burke. And she is going to talk to you about procedure-specific considerations. Thank you, Dawn. And thank you to both of you for inviting me to speak today, as well as the Hepatology Associates SIG, and as always, the AASLD for their continued support of Hepatology Associates, particularly APPs. So Dawn laid some beautiful groundwork for me to build on. And so I'm going to talk about procedure-specific risk stratification in cirrhosis. These are my disclosures, not really relevant today. How many of you have a patient that looks like this? Everyone. Awesome. You're in the right room. How many of you have had a patient that looked like this sneak off, get that hernia repaired, and die? Almost everyone in the room. So it's good we're here. Why do patients with cirrhosis die after surgery? Well, if you asked a surgeon, they'd say bleeding, right? They have all those messy collaterals to deal with, all those coagulopathies. If you'd ask an anesthesiologist, they'd say, well, like the perioperative events, like hypotension, right? Cirrhosis character is hypotensive at baseline. Of course, having liver disease, they're at increased risk of sepsis. There's administration of hepatotoxic drugs. But if you ask the hepatology providers in this room, you know that it's hepatic decompensation. That's what we're actually worried about in surgery. As Dawn mentioned, there is the magnitude of risk. And she really covered, she did a great job covering the type and severity of liver disease, as well as the type of anesthesia. My talk specifically is going to talk about the type of surgical procedure. And ironically, I put a cataract surgery here, because I don't know about you guys, but I get clearance form after clearance form for cataract surgeries, yet my patients will go off and get a colectomy without me ever hearing about it, right? But pretty much, eventually in your career, you're going to be approached about every type of procedure. We all know the contraindications to elective and semi-urgent surgeries and liver disease. Many acute hepatitis, decompensated disease, child PUC, mild over 15, severe coagulopathy, and severe extrahepatic complications. So going into the specific procedures, I kind of divided these into two categories. Major risk, and really the risk is liver failure and further hepatic decompensation versus minor risk, which in these cases, we do worry about bleeding. That's really the main complication. So I'm going to talk about surgeries, primarily hepatic resection, right? Because when you have a cirrhotic liver and you go taking out pieces of it, and it wasn't doing so hot to begin with, you can get into trouble real quick. I'm going to talk about cardiac, because that's also a huge risk to undergo for patients with cirrhosis, as well as any abdominal surgery, as Dawn had said in her talk as well. I have cholecystectomy highlighted here, because in a patient without cirrhosis, that's kind of a benign elective procedure that happens a lot in the US, right? But when you have cirrhosis, due to the location, a lot of things can technically go wrong in that area. Also, hernia repair, the bane of our existence, bariatric surgeries, orthopedic surgeries, and even though TIPS is not a surgery, per se, I did put it in this column of major risk. More minor procedures, dental work, which I say that with a caveat, because some dental work will not be so minor in patients with cirrhosis, especially if their platelet count is quite low, then also paracentesis, endoscopies, cataract surgery, and skin biopsies, the stuff that we're seeing our patients go through regularly. So to start off with hepatic resection, in a cirrhotic liver, at least 40% future liver remnant is required in cirrhosis, at least. And at that point, they still better be pretty compensated and without portal hypertension. They even need more FLR if they have NASH, right? If they have over 30% steatosis, you don't have a lot of healthy liver tissue to work with, because a lot of it's fat, so you need more than 40% FLR. And this is usually calculated by IR, and some places even send it out to do this, and you work with the surgeon on determining FLR. As far as the mortality rates, they can be quite high. Perioperatively, it's 3% to 16%, but that's dependent on minor versus major hepatectomy. And then post-op, it's up to 60% mortality in these patients. Of course, with clinically significant portal hypertension, we know that there's an increased risk of decompensation, as well as increased three- and five-year mortality. My take-home for you from this slide is that if they have an elevated total bilirubin and a significant degree of portal hypertension, it's an automatic no. Don't waste the HCC patient's time by sending them to surgery, and they're waiting, and the tumor's growing, only for them to say, I'm not going to do this surgery. So that's when we need to consider alternatives to hepatic resection, particularly for HCC, right? So surgical regional therapies, ablation, TACE. Now that the results of Y90 are so good, TACE is kind of falling by the wayside. Liver transplant, and then, of course, systemic therapy, which have also made significant advances in the past few years. Moving on to cardiac surgery, we know that this is an increased risk of mortality in cirrhosis, but we're also seeing an increased need for this, right? Because of all of the increased NASH and metabolic syndrome in the country. So compared to other surgical procedures, this is a quite high mortality risk. Child Pew A, it's about 5%, so not too bad. Child Pew B, 35%, but once you get to Child Pew C, it's up to 70% mortality. We see this particularly with CABG and valve replacement, and mortality gets worse the longer the patient's on cardiopulmonary bypass, right? Because you're having these huge hemodynamic shifts in an already hemodynamically unstable patient, and it also exacerbates underlying coagulopathies. And that's not to mention the post-op anticoagulation to boot that presents additional challenges. And this is a photo of Off Pump, and these patients just tend to do better with that type of cardiac surgery. But we do have cardiac surgery alternatives as well. So we have the minimally invasive techniques such as PCI, valvuloplasty, TAVR, and then also in some instances, you can actually do cardiac surgery immediately prior to transplant. If you can get all of your surgeons above and below the diaphragm to play nice in the sandbox and you have a cardiac surgeon that's willing to pop into the OR right before the transplant, this can work, and it does work. We've done this in quite a few instances at Loma Linda. Abdominal surgery, another high-risk area. So gastric resection and colectomy, any of these big bowel resections, have the highest complication rates in decompensated cirrhosis. Portal hypertension puts the patients more at risk for bleeding, not only because of the coagulopathies, but because of all of those collaterals in the abdomen, and then also just huge risk of developing post-oposites. Obviously the surgery's done in decompensated patients when there's cancer involved, right? But if they're coming to you to discuss colectomy for diverticulosis, that might be a different conversation that you may want to guide them toward as far as looking at medical management rather than going to the OR for a colectomy. Mortality rate here up to 26%, and like all surgeries, lap mortality lower than open. And then we have cholecystectomy, and just having cirrhosis at baseline, there's an increased susceptibility to gallstones. And so if a patient has symptomatic gallstones, laparoscopic surgery can be tolerated in cirrhotic patients if their child Pue A, if their MELD is less than 13, and if there is no portal hypertension. These patients actually can do quite well. However, a lot of the patients, child Pue B and C, and if they're decompensated, we need to consider alternatives to a cholecystectomy, and that can include percutaneous cholecystostomy, which is a quite morbid procedure. So I usually do cystic duct stent, or the newest technology, the Axios gallbladder drainage, and you can see you can kind of pull the two lumen together with that metal stent, and that's done via EUS. Now everybody's favorite topic, do we do elective hernia repair and decompensated cirrhosis? And if you would have asked me years ago, I probably would have not written caution on the sign. I would have written no in really big letters, right, because that's what the practice guidelines used to say, no elective hernia repair and decompensated cirrhosis. But now it's kind of a more proceed with caution feel, right, and this leads to the highly debated hernia repair. So looking at elective hernia repairs, I mean, I still urge everyone to think twice if, you know, the patient has low albumin, if the patient is a higher MELD, if the patient has refractory ascites, these are all, like, reasons to not proceed with an elective hernia repair. But if this is going to happen, it's important on the part of the hepatology provider to aggressively control ascites, because otherwise, if that ascites keeps coming back, the wound's going to de-hiss, it's never going to heal, and the hernia is going to recur, and then you're back to where you started, right, and you put the patient through all of that for what. It's also maybe prudent to consider a TIPS if you do go the route of hernia repair. And then there's also the school of thought of why repair this electively, is the juice worth the squeeze, and, you know, we only would do this if it's emergent, if the hernia becomes incarcerated, right? But we know that that is associated with higher mortality. So, you know, on the other side of that same coin, that begs the question of, like, should we actually be doing this more electively, knowing that the mortality rate is so high when it's an emergent repair? I have my own opinions on that, but I'll let you decide on yours. So if you do decide to go to TIPS, these are some tips for ordering a TIPS, right? So as Dawn mentioned, the MELD before transplant, right, the MELD was originally was a predictor of mortality and TIPS. So higher the MELD, the worse a patient's going to do with a TIPS, right? So MELD over 20, do not pass go, do not do that TIPS. MELD under 20 and MELD under 16 being the best outcomes, as Dawn's slide said, you know, you want to get a CT for a roadmap, so IR knows exactly what to expect with those collaterals when they get in there. You want to get an echocardiogram, right, because if you don't, you may send the patient into right-sided heart failure if you kind of come upon something unexpected there. And then if you're doing the TIPS for ascites, the kidneys need to work, otherwise the TIPS isn't going to work, right? Just some things to remember with TIPS. So bariatric surgery, if the patient's non-cirrhotic and has NAFLD, NASH, giddy up, do it, right, because then they may not even become cirrhotic. But if they are cirrhotic, we are seeing that bariatric surgery is well-tolerated if it's a sleeve gastrectomy, if it's done by an experienced surgeon, if it's done at a high-volume bariatric center, and it's done in compensated cirrhosis with no portal hypertension. Now in some instances, this has been performed at the time of liver transplant. And then orthopedic surgery as well, and I feel like this is another one that as clinicians we get nagged about, because patients really want elective joint replacement, right? And I personally don't recommend it to the patients, and I remind them that there's a two-fold risk in hepatic decompensation within 90 days after that surgery. As far as fracture repair, that becomes a little bit more necessary, and arthroscopic surgeries are less risky, as well as joint washouts and things like that. And then tooth extractions. So this is a personally somber topic for me, because I've had not one but two patients die from tooth extractions. And these patients can look quite good, and when they go to the oral surgeon, if the patient doesn't disclose that they have cirrhosis, their platelet count can still be very low with a clinically significant degree of portal hypertension, right? So unknowingly, they could do an outpatient extraction, seemingly be doing fine, get sent home, and then bleed to death in their sleep, right? So platelets above 80, you're probably fine, right? Just proceed with caution. Platelets above 100, even better. But once the platelets get down below 80, that's where patients can get into trouble with this seemingly benign procedure, right? So I always recommend that this is done in the inpatient setting with platelets transfusing during the extraction, or the patient be put on a TPO agonist prior to the extractions. Now more minor procedures, as I said, endoscopy, paracentesis, cataract surgery, skin biopsy, all of the other dental stuff, like cleanings and root canals and all that, just some management pearls. These are low risk in most patients with cirrhosis. INR is not a predictor of bleeding, but platelets are. So the platelets ideally should be over 50. Every clinician in every center kind of has their own protocol and comfort level as far as platelet counts. But a good rule of thumb, just for all intents and purposes, is 50. And if it's any lower than that, administer a TPO agonist. So key takeaways, obviously I'm going to show you the vocal PEN score, because this is the only predictive model that takes into account the actual surgical procedure, and the link is there if you're unfamiliar. But again, just risk stratification versus clearance. Is anybody ever really clear for surgery? I don't have cirrhosis, and I'm probably, when you think about it existentially, not clear for surgery. So you want to think risk stratification. And sometimes it helps with these scores to have that objectivity, that actual number that you can put in your note, put in your documentation, use that number when you collaborate with the surgeon or the other physician. A number can mean a lot to patients as far as their risk of death, right? And then also just getting down to the crux of risk versus benefit, and finding out why does this patient actually want the surgery? How do they think it's going to change their life? How will it actually change their life? And then just collaborative management. So calling the surgeon, calling the referring provider, actually having those discussions, not using the patient as the middleman, not using the notes that you think are going to get to the provider, but your MA never faxed, things like that. And then lastly, patient education. I just look back at my own practice, and I think of those hernia repairs, and I think of those dental procedures, and my patient education patterns have looked a lot different since those times. And so just really making patients their own advocate and truly the last stop before they may be put into a situation that could be bad for them. So hopefully you took something away from this. Thank you so much for listening. And next we're going to talk about pre-op optimization with Ho-Chunk Gillis. Questions after. Thank you. Okay. So for patients with cirrhosis that need surgery, you want to just optimize them. So it's done. Oh, it's the mouse. Oops. Okay. That's not my talk. But Georgine can go first if she wants. It's the preoperative medical therapy? Oh, Gillis. Gillis. Okay. Okay. So I think Don and Corey has created a great landscape to essentially optimize these patients so that if they require surgery, it's done under, you know, elective conditions. Okay. I have no disclosures, and here are the objectives. So I'm going to start with a real case. It's Mr. B. He's a 6-year-old male with hep C cirrhosis, compensated. He achieved a SVR back in 2018. He comes to you for a follow-up appointment. This is a new patient for you and reports worsening peripheral edema, increased abdominal girth, and new umbilical hernia. He reports fatigue, poor appetite, has limited mobility because of his edema. He denies any history of confusion or melanoma. He has no history of cystitis or encephalopathy, so previously compensated. He's married. He's retired. He smokes. He dabbles a little bit in marijuana and is a social drinker. He also has comorbidities of metabolic liver disease, so hypertension, hyperlipidemia, diabetes, and probably one of the reasons why his cirrhosis can be progressing because even though you treated his hep C, he has other risk factors for other liver disease. His meds include hydrochlorothiazine, an ACE inhibitor, metformin, and also atorvastatin. And here are his labs. Essentially, his MELD is 16 with a CTP7B, and his hemoglobin A1c is 8.7. His BMI is 25, but again, he's gained weight, no more intensive. Otherwise, he has poor dentition. He does not have any ictus. He has reduced breast sounds at the right base, mild ascites, reducible umbilical hernia, and no obvious, but he does, you can see that there's a fluid wave and no asterixes. He had an EGD at the time of his diagnosis of cirrhosis a year ago, which showed no varices, and he had an ultrasound three months ago that showed nodularity but no lesions or ascites. So what do you do? So when there's clinically apparent new onset of ascites, you should get a differential, you should do a diagnostic paracentesis to get the differential, and it's based on the protein content and the serum ascites albumin gradient. So in a cirrhotic ascites, you expect a low protein, high sag ascites. And so low protein, meaning anything less than 2.5 grams per deciliter. High sag, meaning greater than 1.1. So we did an ultrasound, which showed a model ascites. We removed two liters and also did fluid characteristics. His serum albumin was 2.8. Fluid analysis showed no SVP, albumin 1.6, and a total protein count of 2.0. So as you can see, he has a low protein and a sag of 1.2, which is greater than 1.1. And his ascites has been confirmed to be from portal hypertension. So what are you going to do? So you know that this patient was a prior compensated, but now a hep C cirrhotic that achieved SVR with a new onset of ascites because it's been confirmed by the low protein and high sag ascites. So as far as medical treatment, the mainstay is really diuretics. But you want to enforce that they are restricting salt. You don't really need to restrict free water unless there was severely hyponatremic. And you want to make sure that these patients have adequate protein. The other thing, too, because of his limited mobility, it's important that we get maybe our physical therapy partners so that we can increase their mobility and increase muscle mass. But the main treatment for ascites is diuretics. So we do a combination of a distal tubular diuretic and also a loop diuretic. And for refractory ascites, large volume paracentesis. But remember to use albumin to prevent post-paracentesis circular dysfunction. And then, of course, tips may be required. So the plan is reinforce a low sodium diet, less than two grams per day. I started furosemide, step one diuretics of 40 milligrams daily with aldactone, 100 milligrams daily. Are there other medication changes that you might want to do? So you may want to obviously discontinue the HCTZ and stop the ACE inhibitor because hypotension to avoid hypotension in a patient that is cirrhotic plus having ascites. So the question is, we get this asked all the time because liver transplantation is a surgery unless it's an elective if it's a live donor. But when should patients be considered for liver transplantation? And simply, the answer is when the prognosis with transplant is better than without it. And because liver transplantation is the only treatment that can reverse cirrhosis and its pathophysiological consequences. So what is minimal listing criteria? Anyone with a MELD score consistently above 14, without a MELD exception, decompensation. So this patient has new onset ascites. So you're going to start thinking about, does this patient need a liver transplantation? Liver mass is suspicious for early HCC. And then other MELD exception cases because in these cases, the MELD does not predict their overall mortality. So this is a comprehensive list that's required in a liver transplantation. But I think the four most important elements is a social work evaluation, a psychosocial evaluation, an echocardiogram because you want to make sure, one, you could see what the EF is, but also rule out significant PA systolic pressure. And then you want to do at least a three-phase or a multi-phase CT or MRI to look at the hepatic anatomy and also make sure that they don't have liver cancer. So you know that these are his current barriers. He's a social drinker, and even though he is cirrhotic, he does smoke THC. And he is a current smoker. And then you have his sarcopenia and frailty. But even if you have some barriers, these are potentially modifiable variables. So you want to work on that. Don't defer the evaluation. Continue to work them up so while you can address some of these barriers. So I'm not really going to go into because I think Corey and Don talked about managing coagulopathy. And as Corey mentioned, paracentesis is low risk. He does need dental extractions, but that could be a high risk in this patient. Repeat colonoscopy. Interestingly, if it needs polypectomy, it's considered a high risk. And then also cardiac cath, which is diagnostic, is low. But if he needs a PCI, it's high. So you want to determine the procedural risk does require collaboration because we also have to understand the expertise of the specialist that may be doing the procedure. And identify and correct modifiable risk factors for bleeding. Again, there's low evidence for pre-procedure correction for thrombocytopenia. I'm not a big fan of the TPO agonist, but they're there if you need it because I think it's more cosmetic. And then INR should not be used to determine pre-procedural risk because as you know, FFP is associated with transfusion-related complications with no proven benefits. So really, no specific cutoffs. I think you need to approach them in an individualized fashion. So I think nutrition is something that we could really improve in our patients. We have a dietician. I strongly recommend dietary assessment for supplementation and also to improve their nutritional state. You want to make sure, because of the catabolic state of cirrhosis, to ensure that they get enough calories and adequate protein. The literature says the ideal goal is 1.2 to 1.5 grams per kilo per day. But the goals may be higher if the patients are more critically ill. And the timing of meals are very important. You want to, again, avoid fasting states and be mindful when you're doing the liver transplant workup, all these procedures, to minimize prolonged NPO status. Because you want to restrict NPO status as little as you can. You don't want them to not eat something greater than four hours. So the timing is also important, so you want to encourage them. It's small but frequent meals. And it's amazing how many cirrhotics eat soup, which is tons of salt. But anyway, early breakfast is encouraged, and also a nighttime snack. You want to replace vitamins if indicated. Vitamin D is something that's underscored, and also magnesium and zinc. But also, I think we have to make sure that we tell our patients to drink lots of coffee. So as you remember, back to Mr. B, he had an EGD a year ago. When do you repeat the EGD? Because he had no varices a year ago. And you want to do an endoscopy to screen for varices and determine the need for primary prophylaxis. So with any new decompensation, a repeat EGD. Because he has clinically evidence of portal hypertension, right? So you want to repeat the EGD. And you want to start primary prophylaxis with large varices. Now, there are guidance that if platelet counts are greater than 150, and the fiber scan is less than 20, that you may defer an EGD. And to the right on the table are the management for moderate to large varices by based on non-selective beta blockers versus CAR-beta law versus endoscopic variceal ligation. So we repeat an EGD on Mr. B. And we find that he had no varices a year ago. He has now grade 2 medium varices, but there are no red whale signs. So again, treatment for primary prophylaxis. And sometimes it's patient preference, but really didn't see anything targetable for EVL. So we decided to treat that. Because he preferred the medication route, we initiated CAR-beta law. CAR-beta law is different than the traditional non-selective beta blockers. Because for propranolol and natal law, you want to do a target heart rate between 55 and 60. Whereas on CAR-beta law, you want to titrate to a max of 12.5 milligrams. But you want to maintain their systolic blood pressure for greater than 90. So we started at 3.125 milligrams BID and titrated up. So he continues to develop refractory ascites. And he needs probably an umbilical hernia repair. Because if you notice in the picture, he's starting to develop scabs. His skin is very friable over that umbilical hernia area. And he's developing these scabs that you worry about rupture. So despite moderate sodium restriction, dose escalation of diuretics, he continued to have refractory. Now he's got diuretic intractable ascites. And so we switched him to the main therapy. We tried to maintain him on a good dose of diuretics if possible. But now you're going to do more large volume paracentesis. He requires this every one to two weeks. And we have to give him albumin replacement. Now his total protein and ascites is less than 1.5. So you want to start thinking, does he require antibiotic prophylaxis? So the guidelines do support in a very low protein ascites to start. But you have to balance the risk versus benefit. Because there is a lot of multi-drug resistant species out there. And we did recommend tips. But the patient was reluctant initially. But he's thinking about it. And he finally agreed. And so we were trying to schedule that. So a lot of electrolyte abnormalities in cirrhosis, particular hyponatremia. But it's also secondary to some of the diuretic treatment that we use to manage their ascites. But hyponatremia, remember, is also an independent prognostic indicator for poor survival if they have significant hyponatremia. It is very common due to loop diuretics. There's no specific management if asymptomatic between 125 and 135. You may want to consider fluid restriction in less than 125. And you may want to give albumin for severe hyponatremia less than 120. Hypokalemia, again, associated with loop diuretics. And then you have hyperkalemia that's common with aldosterone antagonists. So if you see hypokalemia or hyperkalemia, you can kind of dose adjust the diuretic that's causing. So you may have to increase the aldactone if they have hypokalemia, instead of increasing in a stepwise fashion with furosemide. But one of the things that happens is that we see in the setting of refractory ascites, you're going to develop AKI, which is defined as the rise of creatinine, at least 0.3 milligrams per deciliter in 48 hours. So again, you want to avoid all potential nephrotoxic medication, especially NSAIDs, ACE inhibitors, and ARBs. But non-selective beta-blockers do not need to be discontinued unless hypotensive. But if they can't tolerate the non-selective beta-blocker or Carvedilol, you want to switch them back, or switch them to endoscopic varicella ligation for primary prophylaxis to prevent bleeding. So going back to Mr. B, he presents to the AD with altermental status. He's alert and oriented times one. He's now jaundiced, has asterexis. He has 10 societies, but afebrile. He has no significant abdominal tenderness. His umbilical hernia is larger, but reducible. But again, these areas are even worse. And now, his melanin was 16, now 28. So you all know about hepatic encephalopathy. It's a reversible impairment of neurologic function caused by portosystemic shunting and or advanced liver disease. So there are many precipitating factors for HD. You want to rule out GI hemorrhage. You want to rule out electrolyte imbalance. You want to rule out malignancy and also infections. And when you approach HE treatment, it's usually in a four-pronged approach. You want to initiate care with patients that present with altered consciousness. You want to explore alternative causes of AMS. You want to identify the precipitating factors and treat them, and also commence early an empiric hepatic encephalopathy treatment, which initially starts with lactulose. You're trying to get a goal of two to three bowel movements. You have to escalate the lactulose every one to two hours until you achieve your target. And then you may have to add rifaximin for secondary prophylaxis. And again, just a reminder, no role for ammonia testing. So what happened to Mr. B? You had to admit him to the ICU because, again, he's alert and orient I-1. You want to do close observation, but maybe he may require protection of the airway. You perform the diagnostic paracentesis because he has an elevated creatinine because now his MELD was 28, which revealed SPP, which is a PMN count, greater than 250. You treated him with antibiotics and albumin. You stopped the non-selective beta blocker because due to hypotension and added minadrinactreatide. But then his kidney function gets worse. He developed AKI-HRS type 1. He started requiring CRT. His MELD is 40, but luckily, you already completed majority of his liver transplant evaluation. So we were able to successfully list him, and he was transplanted. But stories don't end like this all the time. So again, just really quickly, I know you've probably seen this slide, but I love this slide. It's a portal vein. It describes the 10 elements of cirrhosis management and optimizing your patient. And also, the key takeaways is that cirrhosis care is complex and best managed using a multidisciplinary approach. Optimization in patients with cirrhosis prior to surgery should focus really on arresting liver damage, treating the symptoms, and reducing its complications. An elective surgery best performed after a patient's overall condition is optimized, especially including the nutritional status. But you always want to try to prefer an elective approach versus a margin one due to the risk of post-operative mortality. Thank you. I'm going to invite up Georgine Smith. She's going to discuss preoperative and perioperative risk management. Thank you, Dawn, for inviting me to speak. Dawn used to work with us at UPenn, so it was always nice to make some connections with old family members or former family members. And also, I would like to thank the ASLD for having me an opportunity to speak. This is the first time I've spoken here, so I really appreciate the opportunity. No disclosures. So Corey and Ho-Chang, as well as Dawn, have gone over a lot of the information. So I'm going to hopefully bring it all together for everyone, but a lot of this is going to be a bit duplicate. But certainly, since it's duplicated, we're all doing the same practice and managing our patients appropriately when we're trying to take them to the OR. My key takeaways is things to consider when you try to reduce and or eliminate the morbidity, mortality in cirrhotic patients when you're taking them to the OR. This talk is focused around everything else except transplant, because certainly with transplant, hopefully we're giving them the cure, and a lot of these horrible things that are happening to them while they're waiting for transplant will be alleviated. So like everyone else, we're going to talk about a patient. This patient came to us in eval clinic for consideration for transplant. He's 57, history of alcohol. He has encephalopathy and ascites. He's got hypertension, some diabetes. He's a little bit obese, has bipolar disorder. He's got a very complex abdomen, gunshot wound back in 95, bunch of surgeries, and he just had an inguinal hernia repair. He came to us, I guess, a couple of months after that. Alcohol was diagnosed in August of 20. He presented with encephalopathy. He was found down in his home. He's been managed appropriately with diuretics and lactulose. During his admission, he was found to have ascites, and he had just one paracentesis of two liters, so that's not so bad. He was discharged to inpatient, and he's been abstinent from alcohol since then. And then less than a year later, he came back. He had an SBO, went to the emergency room. They were fortunately able to decompress it, but he was advised to seek repair of his hernia. So he comes to us for transplant consideration in the setting of extensive hernia repair, and his MELD at that time was 10. So he would drink a pint of vodka every day, and he had prior hospitalizations for alcohol withdrawal. And we're managing him in probably similar to where you would manage with some folic acid. He's got some Lasix and spironolactone, lactulose, and meprazole. Give him some Miralax, venlaxafine, as well as zyfaxan and quetiapine. These are his labs when we saw him in clinic. Nothing really bad. His albumin is a little bit there, almost there. His billy's a little bit elevated. INR, okay, we're not really concerned about that. But ultimately, giving him a MELD score of 13. So that's a little bit higher than when he was originally calculated. And I win the prize for the best hernia picture. And this is impressive. So obviously, he's got a complex belly, and these were his hernias. This is what it looked like with CT. You can see the defect. And so, as always, with cirrhosis, we've got changes of portal hypertension. This was a diagnosis on his CT. No neoplasms, and it wasn't a triple-phase study. He's got some, had an SBO, likely to the adhesions, and clearly multiple ventral hernias. So when we're considering taking someone to the OR, the thing that everyone is concerned about is the portal hypertension. And with cirrhosis, certainly there's reduced blood flow to the liver. In surgery, you're gonna have continued hemodynamic shifts due to the vasoactive properties of anesthesia, as well as blood loss. So ultimately, you can end up with a hypoxic injury to the liver and hepatic decompensation, and that's not gonna work for your patient who walked into the hospital. And as we know, portal hypertension increases hypoxemia tissue injury. So the reason I included this CT here is to note the spleen is almost as large as the liver. You can certainly see the cirrhosis with the liver. I just included this slide just to briefly go over. We know the etiologies of cirrhosis and the complications that it leads to. And those are some of the things that I'm gonna talk about today in regards to taking these patients to the OR. But certainly we have ascites, we have SBP. You're gonna get some GI bleeds. Encephalopathy, hepato-renal, hepato-pulmonary, as well as hepatocellular carcinoma. These are all things that come with cirrhosis and indeed have to be managed while you're managing the patient in the OR. So I'm gonna talk about the VOCAL study as well. So this seems the one that's very popular. And I'm really proud of our institution with my colleagues there who developed the VOCAL study. So they changed some of the variations of some of the previous studies. So we're looking at age, albumin, bili, platelet count, BMI greater than 30, NAFLD, yes or no. The ASA score is the anesthesia score that's dealing with complications. If it's an emergent surgery, yes or no, and the type of surgery. So as Corrie had mentioned, she went over great detail, the different types of surgery. And this study also uses the different types of surgery as well as their degree of difficulties. And that's how you classify the patients when you're using this VOCAL study. And the ASA classifications, if we have mild systemic disease, severe systemic disease, or severe enough that it's gonna be a constant threat to the patient's life. So with our patient, Mr. Very Complex Hernia, put these values in. It's a really, I don't know if you guys have ever used it, but it's a really great tool. It's very easy to use. You just put the numbers in, you get your scores out, and it gives you some really strong information to go coincide with what you're already thinking in regards to managing your patient. So this is what our patient came up with. In 30 days, postoperative mortality would be 0.6%, and in 190 days would be 1.8%. So we thought it was reasonable for this gentleman to go and have his extremely complex hernia repaired. And in some of the reference material that I was looking up, there are a number of different studies done, and Jon had pointed out some other studies done when you're trying to evaluate your patient and stratify them for the risk of taking them to the OR when they have cirrhosis. But a lot of it is gonna be dependent upon your technical expertise, your knowing the patient, and the way that your practice is managing the patient. So there really aren't any formal guidelines, which is certainly good for us and beneficial for us as practitioners. So I'll talk about some of the things that we're concerned about when we're in the OR. This is outside of transplant. Of course, we know with portal hypertension, as we all have mentioned here, that you have the portal vessels directly connecting to the systemic circulation that's bypassing the liver. So therefore, we have this portal hypertension that's wreaking havoc. And one of the things that we're doing, when we're in the OR and you're trying to take care of your patient, you've got these collaterals. These things are big and they're mean, and they're going to bleed. You have the large inter-abdominal varices. Also, you can bleed in the splanchnic system into the thoracic and the peritoneal cavities. This photo is showing caput medusa. I'm not sure if any of you've seen patients with this in the clinic, but that's giving you a sign like there is badness. It's got a reasonable umbilical hernia here as well. But that's something, when we're in the OR and you know that you've got all these collaterals and all these badness is happening, you better have some suture ready. You better have someone that's going to be able to help you get in and out of the OR because it can be very, very dangerous for your patient. So as we talk about bleeding, of course, thrombocytopenia, that's one of the horrible things, one of the many horrible things that we have to manage with cirrhosis. And Dawn had mentioned the imbalances in regards to the PT, PTT, and the INR. You really can't rely on those values because they're not going to display exactly what's going on with your patients while your patients are susceptible to bleeding. As Dawn had mentioned, your patients are also susceptible to clotting. So you've got your platelets aren't working quite as well, you know, providing your primary hemostasis. You know, the generation of cross-linking of fibrin is going to challenge your coagulation there. Abnormal fibrinolysis, so these, you know, it's interfering with clot dissolution. So all these things are going on all at the same time. You also, you don't have a good deal of platelet production. Platelets are all going to be clogged up in the spleen. That's why obviously you get, you know, with these huge spleens. And talking to some of my anesthesia colleagues, they're not going to do a spinal or an epidural because of the propensity of bleeding with these patients. Ascites, portal hypertension, yeah, equals ascites. So recurrent ascites that Dawn had mentioned is going to cause problems with your wound. You're going to dehisc, it's going to be tough to get your wound together. So you want to make sure when you're doing your repairs that you really, really make it tight so you don't have any leakage of just fluid. Also, ascites is going to interfere with pulmonary function. As you know, your patients, they've got the sarcopenia because ascites is pushing their stomach up, but it's also pushing their lungs up. So these are things that they're going to delay with your lungs recovering. You have your risk of pulmonary aspiration because your lungs are getting crunched up as well as ultimately leading to atelectasis. Hydrothorax, some of your patients certainly have hydrothorax because there's some little leaky spots there in the diaphragm. So that's going to give you some problem, again, with the portal hypertension and the fluid overload. So we're going to do a pre-op paracentesis, give some albumin and move forward as quickly as we can. Talking to my anesthesia colleagues, they're going to do a rapid sequence induction. So they're trying to eliminate the time of intubation. So they're going to give the induction drugs and intubate them right away. They don't want to spend a lot of time bagging the patient, adding air to the lungs because it's not going to really go anywhere because you've got all this fluid with the ascites if you haven't gotten it out. And the ascites, again, becomes one of your big problems when you're trying to get your patient safely in and out of the OR. As I mentioned with the wound, you want to make sure you're closing your wound very tightly. We've talked about protein synthetic dysfunction. So your patient's going to be malnourished and sarcopenic. So that's going to interfere with wound healing. And it makes it difficult for the patient to recover. And obviously, they have a bit of decompensation already on board. Medications, because a lot of medications are processed through the liver, you want to be careful with what you're going to use. You want to give your opioids in lower doses over a longer period of time. You don't want to give too much at once of anything because it's going to take a longer time to metabolize through this liver. Keep in mind, they're not transplanted yet. And also, you have decreased hepatic clearance. So again, mentioned, you don't want any drugs that are going to go through the liver if you can avoid it. Hepatorenal syndrome, we're all certainly familiar with that. Hypoperfusion, just because of the vasodilation, as Dawn had mentioned, in the splanchnic circulation. So you really want to get your patients in and out of that OR as fast as you can. And I did a lot of phone calls and asked some of my former fellows, hey, how are you guys managing these patients? What are you doing? And everyone's like, make sure you have a lot of suture up and get them in and out as quick as you can. Some of our colleagues are saying if they're cirrhotic and they need a lap coli, nope, we're not even doing a lap coli. Our center's a lot more aggressive. We will do it accordingly when we calculate through the vocal study. And one other thing to consider is when you're considering your patients for surgery in the setting of cirrhosis, you want to make sure that the persons that are doing the surgery have done it before. So we're referring all of our patients to a particular general surgeon. And I guess they do okay. Then we don't see them coming back and you're listed as status 1A. So I think we're choosing appropriately together as a team. But that's something, in the readings that I've done, a lot of the determination is the hands, the surgical hands. And if they've done it before and they think they can do it again, then you certainly have a great chance of getting your patients safely out of the OR. And of course, blood pressure. We all know, as Ho-Chung had mentioned, we're not using a lot of the beta blockers and a lot of the blood pressure meds that they probably were on before they, starting with the cirrhosis and the portal hypertension, because you're already dealing with hyperperfusion and you have hyperperfusion to this liver. So this is a liver that's not getting transplanted yet. It's still got to make it through. So you want to make sure that anesthesia is aware and you're choosing anesthesia that's familiar with managing these patients. So I always feel like our anesthesia team, they can smell when that calcium is getting low or high. I don't know how they do it. And it's probably just from practice. But they're really sneaky and good about it. But they're also balancing the fluid. How much, how little. You can't give too much, can't give too little. And so it seems like so far we've been really good with the sweet spot of maintaining these patients. But a lot of times they'll say, you know, we've got this patient and they've got this nasty hernia that's being repaired by general surgery, who certainly is experienced. And like, okay, we're going to see this patient in a couple of weeks getting a transplant because we're not sure if this patient is really going to go through. And a lot of the decompensations you're not going to see right away. I mean, you're going to get them out of the OR, absolutely. And you're going to get them home. But a lot of decompensations can happen as long, far out as 90 days after they've had these elective surgeries. We talk about HCC resection. Those debates go on way too long when you're in patient selection. Like, are we going to resect them? Are we not going to resect them? You know, and everyone is weighing in because this can be really dangerous for your patients. So you've got jaundice and ascites, you know, and that's obviously already bad. And most of these, as I mentioned, these deaths occur, you know, or complications occur 90 days post-op. But one of the things that some people are doing we're not doing in our institution is portal vein embolism. It can reduce your mortality. And what they've found is that it can initiate the hypertrophy of the remaining remnant of the liver. So these are some things to consider. So when you're talking about your patients, you know, as Ho-Chung mentioned, you know, have, you know, frank conversations. Some of the things in surgery that we're not worried about, as some of the others are worried about, like social work, like, you know, we're not as concerned about social work. We want to make sure our patients are going to make it, you know, to the OR if, you know, if they need a transplant. So going back to my patient, he didn't get his hernia repaired, I don't know, like he was all fired up about it, and then, you know, because he had just come out of the hospital after having the SBO, so he didn't get it repaired, and he was fine. And then, just this year, so like a year later, he's back for transplant re-eval because he didn't get the hernia repaired. He's still doing fine, he still needs the hernia repaired, and hopefully, you know, he can stay away from an elective hernia repair, certainly out of the ER, desperately needing a hernia repair, but we've listed him in the event that that hernia, you know, doesn't do so well. So these are my references, and I thank you for your attention. I'd like to invite Ho-Chung and Corey to come up for our panel discussion. So if anybody has questions, if you can come up to the microphone, and we have a couple, I think, online as well. We'll start here with Patrick. Thanks very much, and thanks to all of you guys, great talks, fantastic talks, everybody. This kind of, I guess, is a question probably for the whole panel, because I think everybody all kind of have their opinion on this. Okay. Okay, is that better? Okay. So what is the approach, or what is each of yours approach to a patient hernia repair, say umbilical hernia repair, that's already had a TIPS put in for ascites, actually developed ascites after a previous hernia repair that was done in an emergent setting, but now has a TIPS. TIPS is open, doing fine, so they're well compensated now because they have a TIPS, but now has another hernia they want to get repaired. So I have so many questions, right? And that's the thing, is that it's like, it's the gray area, like is the TIPS functioning? Do they not have any more ascites anymore? What's their INR? What's their bilirubin? How big is the hernia? Who's the surgeon? Are they at an academic medical center, right? Like these are all of my things. Is he on the transplant list? Right, right, because it's like any one of those things could blow the deal, you know? So it's like that's where you really, really have to think broadly about like what this patient's outcome could be and like literally play every single scenario out. And then also see like how badly does that patient, like some patients will tell you, like I don't care if I die, I need this repaired. And that's very different from someone who just kind of wants it repaired because otherwise they have to wear a Kim Kardashian waist trainer all the time, you know? So I'm going to say smaller umbilical hernias scare me more than the bigger ones, okay? Because they tend to be the ones that become more incarcerated. So again, you're trying to avoid, a lot of this is, you know, risk stratification, risk prevention, trying to eliminate and treat everything that you can. But with smaller ones, after tips, the other thing is you may want to do another repeat pressure gradient because they, even though it's patent, it may not be wide enough. So you might have to get like either double barotips or something like that. Because really, if they're having ascites after tips and you do an umbilical hernia, you have to aggressively tap them. You know, I see these patients once a week, sometimes twice a week. I don't like to tap patients more than once a week, but you might have to tap them more frequently to get that volume because allow that to heal, okay? And hopefully the smaller ones, the surgeons, and the surgeon is so important, so that they could try to do it in a very minimally invasive approach. Because a lot of surgeons that don't know what they're doing, like the larger ones, they put mesh. You don't want to put foreign objects in a cirrhotic belly. So it's, again, it's, but sometimes a lot of things are outside of your control. And I think we're all control freaks, and that's probably why we are cringing at this point, so. I think a lot of different institutions obviously get different information. We're going to list them and, you know, cross our fingers and, you know, hepatology, you know, colleagues, good luck. And we're ready for the OR. I'm going to actually take it a little bit in a different direction. As far as looking at the patient as a whole, what's their nutritional status? I mean, if they are severely sarcopenic, their nutrition is horrible, are they taking in too much sodium? Because it is truly a vicious cycle, that when these patients are muscle wasted and they're not eating well, they're breaking down more skeletal muscle, they're going to have more encephalopathy, they're going to have more ascites accumulation because their protein is so poor. So, what else can we do in the meantime to help optimize this patient? I have seen patients in similar situations where they're not a candidate for either repeat hernia repair at the time, or they're not doing well in general. They're not a candidate for initial hernia repair, but we're able to try and get things under better control, and sometimes you can. So, occasionally we have to look beyond the surgery piece. And to Ho-Chung's presentation earlier, how can we optimize these patients as a whole? Thank you. One second. Before we come to you in the room, we're going to take one of the questions that was in the chat. It's for Ho-Chung. Can you elaborate on why you recommend for the patient to drink coffee in your case? Oh, well, there's a lot of data protection of coffee, especially in decreasing the risk of HCC because you already have patients with decompensated cirrhosis. So, there's a lot of emerging data that was presented here. I didn't attend a lot of it, but there's a tremendous amount of health benefit in drinking three to four cups of coffee, probably without sugar and the cream because, again, my patient had a hemoglobin A1C of 8.7, so that's probably not going to help them. But I feel also it's something that I could tell my patient to do, but there is a lot of evolving data about coffee. Thank you. Okay. Go ahead, please. I'm Professor Angeli from Italy. My question is related to the mini-invasive abdominal surgery for minor hepatic resection. So, do you think that we can go beyond the actual concern about portal hypertension and serum bilirubin? Yeah, in certain situations. I mean, as you said, I believe everything's not black and white. Like, have I had a patient had a tiny little bit taken off because they had a minimally elevated bilirubin and, like, very minor portal hypertension? Have I seen it done? Has it been successful? Yes. But I think we all need to just be prudent, knowing the overall mortality risks, and just not take that decision lightly and have that decision made by a multidisciplinary team, have radiology calculate FLR. Like, just, I think, you know, I think it's possible, yes, of course, but... So, yeah, and I think we have to be very judicious with the organs that we transplant for HCC, right? So, there are a lot of allocation changes now with, you know, the concentric circle being at the donor hospital instead of the transplant center. A lot of surgeons can do, you know, minimally invasive segmentectomies very, very well, but I think that is very dependent on the skill of your hepatobiliary surgeon. And so, you know, sometimes we are pushing the envelope because the question is that, you know, when we apply for mild exception for HCC, you know, you have to pretty much attest, are they resectable, you know, candidates, right? You have to say that no, or it's not applicable, that, you know, they're not resection candidates. But I think that we do have to push the envelope because our patients are waiting longer and longer, even with a mild exception, because, you know, there's no mild calculated anymore. The medium mild, the transplant minus three points. And the longer that they wait, you know, they also can longer the wait that they can become beyond Milan where they're, you know, they're no longer a transplant candidate. But we have excellent hepatobiliary surgeons. I think we're exploring, you know, segmentectomies, very precise wedge resections. The other thing too is not just we could do laparoscopic. So, you know, they have like guided, you know, ultrasound ablation intraoperatively. So we are using more of those techniques as well, especially in the dome of the liver where they're very difficult to get to. And so it's really about, but not everybody has that access to those specialized, you know, hepatobiliary surgeons. And so, and then the risk becomes, you know, what's their risk of recurrence after resection where they're going to have to go into, you know, where they really need a transplant anyway. And, but that is a highly debated, but it's something that we should consider. And you have to know what your transplant and your transplant landscape is at your center that you're working with too. And also keep in the back of your mind that like, is this patient ultimately a transplant candidate if it hits the fan? You know what I mean? So that's always the question. If they're not, we're pretty more aggressive with first section. Right, right. Because that's a period of option. Right, of course. But it's like if something were to go wrong, if more was taken out than originally thought or, you know. But also if it's a chip shot, if it's an exophytic lesion, you can get it out laparoscopically and all's good. Yeah. I think too, that's where the knowledge at the center and the surgeons come in and where you have it done as well. Hi. Hi. This is Filippo Scapi from Italy. One question about, I would like you to focus just a while on the concept of significant portal hypertension, clinical significant portal hypertension. Okay. You, when you have a patient with ascites, when you have a patient with viruses, it's okay. This patient has a clinical significant portal hypertension. But in patient with cirrhosis, without any evidence, clear-cut sign of portal hypertension, how you suggest to evaluate the presence of portal hypertension in this setting? I'm referring, for example, to the setting of patient undergoing liver resection. So, the actual easel guideline tells you that you have a small nodule. You can go to end portal hypertension. You have a moderate risk of the compensation. But the moderate risk goes from 3% to 6% to 35%. So, you have a huge range to rely on the indication to go ahead with resection. So, I would, I just, I would just. Well, I think with smaller lesions, it's, you know, if you have a solitary small lesion, there's actually good, you know, data that, you know, radiofrequency ablation or microwave ablation, you know, is probably as good as, you know, a resection, right? But, because small tumors, especially less than two centimeters, if you're pretty, you know, convinced of it. You know, we have a lot of tools in the United States. So, we have fiber scans. We have shear waves. We have many non-invasive ways. But, you know, hepatic, you know, wedge gradients, I think is, venous gradients is important because, you know, when they have clinically, it's different between if they have a HVPG of less than 10, right, versus that 12 mark, right? And so, I think as far as resection or HCC treatment, you know, when we, I mean, I run our liver tumor board, you know, we want to also make sure that they have the best curative option. Sometimes it may have to be resection, right? And so, but in those situations, you got to make sure that you have a downstream backup plan. So, you don't want to treat these less than two centimeter lesions that don't meet the OPTN criteria for a mild exception for HCC. And then, you go ahead and resect them, and then they have complications. You have no backup plan. In that situation, I would probably let that lesion grow to two centimeters, right? And then, you know, and possibly work them up for transplantation. And then, if they have a hepatectomy, I, for all patients, they're undergoing a hepatectomy, I do a liver transplant evaluation. Because if they're, if they're not liver transplant candidates or they're not good surgical candidates, the question is going to be, why are you going to put them through surgery when we have other things that we can offer them in the toolbox? But, you know, others. So, you mentioned virus in that as well, and I think that's an important thing to take into consideration. Because now, with being able to eradicate hep C, we're seeing a lot of patients who have a history of cirrhosis that may go on to develop a liver cancer. And do they, are they truly cirrhotic, for one? We know most patients with hep C that develop an HCC are cirrhotic, but not all of them. And in those situations, is there clinically significant portal hypertension? So, I had a patient recently in that exact situation, and she had, you know, one CT that showed a nodular contour, one two weeks later that didn't. So, it creates these gray areas. She had no splenomegaly, but has thrombocytopenia. But has had thrombocytopenia for 30 years. So, is it related to her liver? And what we did in her case is we actually, we did a transjug, well, we biopsied a guided biopsy, targeted biopsy of the liver lesion. Because if she wasn't cirrhotic, then what is this lesion? And at the same time, we did a transjugular biopsy to get random liver to see, is this cirrhosis? And did portal pressure measurements at the same time. She wound up, in her case, not being cirrhotic. She is great, I'm sorry, I take that back. She is F3, F4, no clinically significant portal hypertension. The plan is we are going to do a right lobe devascularization to see left hepatic lobe hypertrophy. We're going to tase her in the interim, and then do a right lobe resection, ideally in the near future. Another option that is becoming more and more considered, and I believe it was presented at this meeting, is xenotransplant for some of these patients as well, which is a whole other ballgame that's opening up to us. So I think that target of clinically significant portal hypertension is kind of a gray area as far as, you know, we know if somebody's fiber scan is greater than 20, and they have less than a platelet count less than 150, then technically that's clinically significant portal hypertension. But what can we do to mitigate those risks? Because as Ho-Chung said, you know, HCC is an indication for transplant. It is becoming a harder target to hit for a lot of these patients. And I feel like, yeah. The other thing is consider the age. If your patient's 70, and you're going to wait until they're 73, you know, to be transplanted, and you're transplanting at Mel-G, you know that's really not going to happen for your patient. You know, you're going to have to go ahead, you know, and hopefully, you know, with that billy, still be able to manage the patient. And risk-benefit-futility discussion with the patient. And with the surgeon. I mean, there are surgeons, I'm not saying transplant surgeons, but different surgeons have different comfort level with different risk. I mean, I can tell an orthopedic surgeon that, you know, this patient has a 60 percent risk of decompensation, and they're going to go and do a shoulder, thank you, whatever to their shoulder. And then the patient calls me three weeks later like, oh, my, you know, I've gained 15 pounds. Well, duh, we had this discussion. So, there also needs to be a risk-benefit and risk-comfortability discussion between surgeons and patients. Yeah, I think I'm seeing more of our pedobiliary surgeons that would previously say no way to resection if the platelet count was like around 100,000, but they don't even blink anymore with that. So, they push the limits and, you know, they're pretty comfortable with platelet counts like, you know, nothing less than like 70,000, 75,000. So, it's pretty amazing, I think, you know, advances in surgical techniques. I think, you know, that's really what, you know, Don and Georgina was talking about when they looked at older predictive models, too. So, I think this is a real testament to, like, the expertise that, you know, we're or improved expertise in handling these patients. And it's not just HPV surgeons, our transplant surgeons are taken to the OR as well. Yeah, I've noticed that as well. And that's why I just, I think bringing it back to multidisciplinary care and just having everybody weigh in on their piece of the pie is, like, really the best way to make those decisions. Thank you very much. And there was another question that came through the web portal that I did want to make sure we address. So, two things. One, there was a mention about PEG instead of lactulose for hospitalized patients with encephalopathy. We know that patients, particularly if they have severe encephalopathy and are abundant on a vent, that PEG may be better for those patients because it's less gas producing, so it's not restricting lung expansion. But the second question, to some degree in regards to encephalopathy, is why we don't recommend checking ammonia levels. And I will let Ho-Chung answer that. However, it was mentioned in the chat about patients with known encephalopathy grade four, which a lot of times these may be patients who are acute liver failure patients. And that's a different situation than what we're speaking about with patients with known chronic liver disease and encephalopathy. And I'll let Ho-Chung talk about that so I don't get on my soapbox about ammonia screening. We all have it. I manage liver transplant. I just don't check ammonia because hepatic encephalopathy is really truly a clinical diagnosis, right? It has no particular value. You don't titrate lactulose based on the ammonia levels. Majority of the ammonia specimens in the United States are performed in venous samples, and it's not really as accurate as if you have, like, the machine, you're doing the arterial sample at the bedside, and you're calculating ammonia. But that's just, you know, it's a very artificial setting. When we're using venous samples, it sits in the lab for one to two hours, and then you get your ammonia level. I think the absence of ammonia, if you do check it, so I had a patient that just would not wake up, but it just didn't fit with the clinical picture, right? We're doing all the things. We've scanned his head like a gajillion times. It's important to make sure that you also scan their bellies because they could have a portosystemic shunt that, you know, could be easily embolized, and that's another discussion. But so it was just a conundrum, and so we checked the ammonia level, and it was negative. So I think in that situation, when you have a very perplexed case, it's a better negative. So the fact that it wasn't elevated, he still, I mean, he just wasn't waking up. We just didn't understand, and so if something else was going on, we ultimately did not transplant him because, you know, if he's not going to wake up, he doesn't have signs of hepatic encephalopathy. I just don't think that transplantation would have benefited. So in that situation, ammonia was helpful, and when it was a negative but not a positive. I think, too, I think all of us have had, up here, have had patients who, you know, primary care or hospital is trying to be helpful. They get out of the hospital, and they're getting their blood drawn every week and getting ammonia drawn, and then I'm getting calls from the PCP that their ammonia is 35, and it was, you know, 15 last week, and it's like, please stop. And patients have access to their portal, and they see the big H as in high, and then they call you and say, my ammonia is elevated. And they're freaking out about it, and, you know, you have to treat encephalopathy based on symptoms. I have had patients with an ammonia level of 60 who are abundant and ventilated because they can't protect their own airway, and I've had patients sit in my office with an ammonia level of 200, and you wouldn't even know they were encephalopathic. It's impacted by how long the tourniquet is on. It's impacted by when they ate, what they ate. It is a good tool if you have somebody coming into the ER with no known history who has mental status changes and acute liver failure, but in general, chronic liver disease, it's actually in the guidelines. It says, do not check serum ammonia for management of encephalopathy. Again, clinical diagnosis, they're flapping. That's all I need to know. I always ask. I use the patient's spouse as the ammonia level. How many times did you have to repeat yourself? We're at the 3.30 mark a little bit after. I'd like to thank everybody for attending the session, and a special thanks again to our wonderful speakers today. Thank you.

management considerations

strategies

healthcare teams

surgery

patients

cirrhosis

risk stratification

predictive models

patient optimization

liver transplantation criteria

multidisciplinary approach

individualized patient care

comprehensive approach