Dr. Brett Fortune and Dr. Steven Sauk discuss the management of patients with chronic non-malignant ascites and how a multidisciplinary approach can help enhance treatment options and quality of life. Join faculty during webinar to discuss management of patients wiht chronic nonmalignant ascites and how a multidisciplinary approach can help enhance treatment options and quality of life.
Greetings colleagues. I am Donna Watson, a senior clinical manager in the advanced team of the BD peripheral intervention. On behalf of BDP I, it is my pleasure to welcome you to this webinar multidisciplinary strategies for the chronic care of patients with non malignant ascites building and ascites management practice as the moderator. It is my privilege to introduce the faculty. Doctor Fortune is the medical Director of the liver transplant program and Associate Professor of Medicine at Montefiore Einstein in the Bronx New York. His clinical focus centers on providing care for patients with advanced liver disease and those who have or will need a liver transplant. Doctor Sock is an Associate professor of interventional radiology. He currently practices at the uh Malin Institute of Radiology at Washington University in Saint Louis for a more detailed bio. Please review the respective bios listed in the program. These include each speaker's disclaimers. Additionally, we have a list of commonly used abbreviations and their meanings that will be used throughout the program. The agenda this evening will include starting with a patient presentation, a review of pathophysiology of non malignant ascites as cites management team models and at the very end, we will take questions and answers. So on your screen, uh to the left, please fill in any questions that you may have throughout the program. And we will answer as many of these as we can uh following the formal presentation. So at this point, I would like to turn it over to Doctor Fortune and again, enjoy the program. Great. Thank you very much for that kind introduction and, and kind invitation to participate this evening and thank you to the audience for joining us. Uh We're going to start off this uh discussion tonight uh reviewing a case presentation which will be a 75 year old female next slide. Uh The chief complaint is a 75 year old female patient with what we call metabolic dysfunction associated sto hepatitis, formerly known as nash uh cirrhosis who presents to the PC PS office for abdominal distention related to ascites and was referred to interventional radiology for a paracentesis on physical examination. The abdomen was distended, nontender and otherwise well appearing uh female. Her medications consisted of furosemide, 40 mg twice a day, spiral lactone, 25 mg once a day, lactulose, uh three times a day, rifAXIMin twice a day and other medications listed below including diabetes medication, reflux medication and blood pressure medication. Next slide due to advanced age and other comorbidities, the patient was deemed not to be a liver transplant candidate. Uh and therefore proceeded with the paracentesis. Uh due to her abdominal distention. When she was found to have ascites, it did show a serum albumin ascites gradient of greater than 1.1. There was no evidence of a spontaneous bacterial peritonitis. Um There was uh evidence of significant uh liver dysfunction including a cra uh uh Bir Rubin of 9.4 um A meld of 28 and also had significant renal dysfunction with a creatinine of 1.6. She did have a work up including a, a two dimensional echocardiogram which showed normal right and left heart function. She did proceed with an upper endoscopy with grade two esophageal varices. And it also had cross sectional imaging with cat scan, uh showing cirrhosis, uh patent portal veins and hepatic veins and a moderate to large ascites next slide. So as we start with this case, I would like to first start off with kind of where we know on the natural history of chronic liver disease because we do know that the staging of their disease is quite relevant. First, you start off with uh chronic liver disease and then next quote for and then whatever ongoing insult, whether it's alcohol use metabolic syndrome, including diabetes, hypertension, hyperlipidemia, um increase uh central opacity uh with elevated BM I active viral hepatitis, whether it's hepatis B or C or autoimmune disease. There is an ongoing progression to development of cirrhosis. And with that, you start off with a compensated state, meaning that you don't have any clinical manifestations of cirrhosis. However, when you develop uh uh the event of varicel hemorrhage, uh ascites hepatic encephalopathy, you're now deemed in decompensated cirrhosis. And this is relevant because of the significant increase in morte short term mortality. Um However, there's even another stage of decompensation, what we call further decompensated cirrhosis. And these are patients that develop multiple phases of decompensation and can in fact have significant uh liver dysfunction and significant features of portal hypertension, including peril rebleeding, refractory sites, hyponatraemia, uh pater renal syndrome and an acute inflammatory state, uh which involves organ dysfunction called acute on chronic liver failure. This obviously carries extremely high short term mortality and without a liver transplant, uh would be deemed a high likelihood of fatality with this. Uh I also wanna mention the importance of the competing risk for uh liver cancer or pilar carcinoma throughout these stages of advanced fibrosis. What we'll do today is focus on the term refractory ascites. Next four, which as I stated earlier carries median survival of well under two years. Whereas compensated cirrhosis carries uh me uh median survival of well over a decade. Excellent. OK. When you was with the portal pathophysiology of the uh uh of the development of ascites from portal hypertension, it all starts with the foundation of having cirrhosis and because of this, with those fibrotic bands and nodular regenerative nodules, you get increase of enteropathy resistance. Uh This leads due to se several uh mechanisms of developing increased portal inflow and therefore increasing your portal pressure, which leads to this portal or sinusoidal hypertension uh due to the body trying to compensate for this increasing portal hypertension. Uh you end up getting significant splenic and systemic vasodilation, usually related to nitric oxide and other um uh uh endogenous uh vaso um uh dilator uh hormones and this leads to a decrease in the effect of arterial blood volume, particularly to the kidneys. And with that, you get activation of some neuro hormonal systems, including the rant alg uh angiotensin aldosterone system, the sympathetic nervous system, as well as the anti diuretic hormone release. And this leads to the listed uh complications below including severe sodium retention and fluid retention, thus development of ascites um as well as over overt uh water retention due to excessive use of anti diuretic hormone, which leads to hypernatremia and then extreme vaso uh constriction in the kidneys due to uh multiple um effects that lead to or can lead to acute kidney injury, but specifically for a paternal syndrome. And with that next, for uh we're starting to learn that there's some other important uh interactions related to our, our gut microbiome, as well as our innate immunity and how our body handles inflammation. So as we have different changes in our, in our gut, uh particularly pathologic bacteria, we tend to get uh gut translocation, which leads to more endotoxemia or other inter and and cytokine release, which worsens the the vasodilation system and even further decreases the arterial blood volume and leading to more complications as well as some other molecular patterns, whether it's damage associated or patho uh path pathogens associated molecular patterns. And this increases oxidative stress of the endothelium and worsens the microcirculation. And with that on top of inflammation of multiple types, whether it's infection related or toxin injury or some other um insult, this can further exacerbate these manifestations that all come from uh portal hypertension as its origin. Next slide. Furthermore, we're learning that cardiac compensation, particularly the hyperdynamic state that occurs during these uh stages of cirrhosis. Um e eventually you lose those compensatory mechanisms and you're no longer able to maintain adequate perfusion. Your mean arterial blood pressure is bottom out and basically uh this further exacerbates as well forward sla excellent. So I will hand over to doctor Sock um to review the Ascites management treatment model or team. Thank you, Doctor Fortune. Um Sorry if my screen looks like it's a little blurry just because my computer decided just to restart right now. So I'm on my phone. Um So, um anyways, uh it is definitely apparent these days that they are essentially kind of one of many models how asides is managed. And I'm gonna present basically two major models that exist in this country and how interventional radiology interfaces with subspecialist GIS uh or the lack thereof. And so this first slide here is gonna probably represent most of us who are in academics, when you have a subspecialized G I and hepatologist available, who can help partner in managing the society's patients. And so the typical kind of referral pattern is the primary care physician. The general G I or the er, or hospitalist will consult a subspecialist G I or hepatologist to evaluate a patient with ascites. This is kind of a quote pretransplant evaluation H and P social assessment labs, imaging and managing the the the aside start with starting with diet modifications and medications. The referral to IR is typically that of if an intervention is needed such as a paracentesis or thoracentesis or something else, that's when the patient is referred to IR. And so um the role of IR in this type of model is more that of a kind of a AAA procedural list placement of the tips, placement of a perineal venous stunt tunnel peritoneal catheter or anything else. What we do in interventional radiology is we check the work up and ensure that this is uh is uh not only feasible but also um certainly also indicated as per the subspecialist G I. And if this is indicated and that this is feasible, then whatever more pretesting may be needed, such as more imaging, more recent labs, uh we will go ahead and, and order for those, then we will of course arrange for the procedure, discuss the patient with the patient about the risk and benefits of these types of procedures w whether it be just a paracentesis or tips or Perito venous shunt. And uh when it is uh finished, the patient is either returned to the subspecialist G I or hepatologist, postprocedure or uh the, the IR and the hepatologist uh continues to manage and, and, and collaborate together to manage these patients. Um Can we go on to the next slide, please? So, before we continue on to the second model, I'd like to uh ask the audience to identify your profession, whether you're a G I physician PC P, registered nurse, advanced practice providers such as a physician associate or nurse practitioner or other. Uh please uh continue with um answering those polls if you haven't already and uh as people are filling that out, um so far it looks like uh in our audience today, um we have 84% who are other, which I assume are uh people uh who are working with BD or barred advanced practice providers about 13% G I physicians, about 2%. Um And at, at this time, uh there are no PC PS or registered nurses here today. Why don't we move on to the next slide, please? The next is uh to identify a practice type uh for those who are uh practitioners. Uh Are we in an academic hos uh an academic institution, hospital based institution or uh an outpatient lab? And currently, it looks like about 44% of us are working in a hospital based uh practice, 44% in an academic practice. And about 11% of us working in a solely outpatient type practice. Can we move on to the next slide, please? And so um the reason why this is interesting to know is essentially that the the summary is that there isn't a subspecialist G I managing people with perhaps alcohol associated liver disease. For instance, mortality is also uh affected. What does this mean? There are studies, there is a study that demonstrates that the geographic density was significantly associated with lower asso uh alcohol associated liver disease um mortality when compared to other places that have higher densities of uh subspecialist gis, essentially having a hepatologist or subspecialist G I uh reduces mortality in, in populations uh um associated with alcohol associated liver disease. And so it would be important for us to certainly recruit and create more hepatologists in this world. However, since that is not the case, uh this next slide is starting to discuss, well, what do we do then? In the meantime, um in these in these populations where you don't have a such specialist G I or hepatologist nearby to help manage the asides empower is the keyword, empower those who are managing the patients to formulate treatment plans. Um Can we go back to the previous slide, please? So, um in general, the IR group, those who are doing these Paris and T CS and seeing these patients weekly are probably one of the most um valuable practitioners. Seeing these patients where poor is developed. If any further tests or workups are needed in the management of their sides. Say you need to get up sodium or potassium or a urine sodium potassium. Uh check their creatinine, check uh their medication uh lists well, the patients coming in for a paracentesis every week, we can certainly run tests and workups tied with the paracentesis. And of course, the IR should aim to feel comfortable in managing the candidacy of these patients for other interventions. So, if we're thinking of tips, uh maybe we need to get uh more updated cross sectional imaging or uh we're thinking about a perit neo venous shunt, refer for an endoscopy if needed and certainly in both cases, refer uh for a two D echo or in certain practices, cardiac clearance if needed. Next slide, please. And so when you look at a AAA picture like this, I know this, this table looks a little stretched out. But um how many of us who are practicing? Sees see this a patient who literally comes in. If you open up their uh electronic medical record, you pull up their procedures and literally just see a stack of Paris and T CS over and over and over again, almost to no end to me. This breaks my heart. This is almost something like there's there something needs to change in this patient but of course, a lot of patients don't realize that there is something more that can be done. Um And those who are seeing these patients, whether we're midlevels or we uh M DS are certainly in a unique position to improve these patients quality of life. And so, um where I've diagrammed here is now the interventional radiologist in a place that doesn't have specialist subspecialist gis or hepatologists might be the quarterback to then say, you know what? Hey, I'm gonna help manage your diuretics. Oh, hey, wait a minute. I, I, I'd like to get you a two D echo. I'd like to get you a referral for an endoscopy and kind of be the person who, who sort of a point as a serves as a point person um for these patients tumbling through getting Paris and T um every week. And so this could be the MD or it could be the midlevels um kind of anecdotally. I mean, a practice that manages not only a sort of a satellite uh community hospital but also the academic hospital. Um It is certainly teachable and certainly doable to manage these patients diuretics as interventional radiologists uh when a hepatologist is not necessarily available. Um And that is something that I think Doctor Fortune will be talking in the next slide here. Yes. Thank you, Doctor Salk. And, and uh so when you look at the management of non malignant ascites from portal hypertension, um First, you wanna confirm it is truly from portal hypertension. And that can be done with a diagnostic paracentesis, sending the fluid for studies showing that the serum albumin and ascites albumin gradient is greater than 1.1 to confirm the presence of poor hypertension. And obviously further confirming with a total protein uh showing that it's related to cirrhosis and not heart failure. And then also ruling out uh spontaneous bacterial peritonitis with uh cell count, including the differential to look for the poly uh rose coco albumin levels. Um With that um if it's early stage ascites, you can initiate medical therapy. But the one thing that I want to make sure that we highlight uh as a quality care in index is to anyone with a always consider liver transplant referral. Um As uh the development of cities is a significant uh marker reflection point of decreased survival and liver transplantation should be considered regardless of meld score. Um uh uh threshold. Uh with that with medical management. If they uh mean arterial blood pressure or systolic pressure is acceptable, you can initiate uh curvet AOL or some non sys uh nonselective beta blocker. Uh assuming they have an endoscopy that shows uh vices um as well as um a um highlight through with a dietician on sodium restricted diet, ideally trying to stay within a 2 to 2.5 g sodium uh diet per day. Um add the diuretics which I'll talk about in a sec and then, or if they have mi mild to large ascites off start. You're welcome to do a one time large volume parasites with the use of albumin um particularly in the setting of greater than 5 L uh to help uh treat these patients once you initiate diuretic therapy, um obviously, in the, you know, outpatient setting, um you can initiate typically uh between 2040 mg of uh furosemide and uh anywhere from 50 to 100 mg of spinal lactone. Um as the synergistic effect seems to be very effective as well as having potassium homos stasis. When you increase the doses, uh you may see uh some uh whether it's dose dependent effects or perhaps um harmful uh changes uh forward slide or slide. If you can, there we go. Um And with that, if you start to see an increase in their um re um creatinine uh or decrease in their sodium, you do have to worry about development of intolerance to these diuretics and it kind of inhibits you from being able to maximize their diuresis. And and sometimes you may lead into if you forward the slide, uh what we call recurrent or uh uh in. So, in this case, refractory sites where you're unable, even with proper sodium restrictions and uh intolerance to the diuretics, you are uh now um LVP dependent um in addition, forward slide for those that do not develop renal dysfunction or hyperemia. However, go to maximum level of medications assuming again that their dietary restrictions of sodium is appropriate. Uh There can be a part where uh in a very rare uh circumstance where you can have diuretic resistance, which is another category of river factory ascites and LVP dependence. Again, this carries extremely high short term mortality and is really important to capture uh early in in a transplant pathway. Um or some type of other intervention uh for site. And uh one of those interventions may be uh tips uh transjugular opic portal systemic shunt. Uh This has gained a lot of uh headway in the last few years. With the development of very high graded uh literature including randomized control trials. It's mostly been indicated in the setting of both rescue and uh preemptively uh control of beal or portal hypertensive related bleeding. Uh In addition, now to uh recurrent and refractory C uh with significant uh transplant free survival benefit in selected patients. Uh It does require certain selection criteria though it does require adequate liver reserve. Um uh therefore, for those patients that have higher meld scores, it it could be which uh the meld was originally uh coined for a prediction of 90 days survival after it tips. Uh It's important to make sure they have adequate liver reserve to uh to handle that acute ischemic uh adjustment with the tips placement. Uh It's very important to have some type of uh caregiver system at home as these patients that live by themselves can be very dangerous in the setting of, of hepatic encephalopathy that uh not having someone present uh to capture and maybe preemptively manage to, to prevent that uh readmission for hepatic encephalopathy. It's, it's really helpful to have caregiver at home. Having adequate cardiac function is a must, whether it's a um adequate ejection fracture on the left ventricle or also uh avoiding any high right sided uh pressures including pulmonary hypertension and having favorable of anatomy, including uh patency of vessels or avoiding uh malignancies. Uh As you can see here, contra or relative contraindications include the poor liver reserve, which is typically represented by the meld score. Although we do not advocate for any significant meld thresholds. Uh The risk of of a complication does increase as the meld increases. Uh as I mentioned earlier, right, heart failure is a contraindication as we can um exacerbate that with the tips. Uh And obviously, for those that have uncontrollable uh paddy encephalopathy prior to the uh tips placement, uh we would advocate not to do that uh uh in those patients. However, having a one time uh or medical control of paic encephalopathy is not a contrary indication. Uh as it says here, Tips is an effective therapy for both recurrent and refractory ascites and select patients. And there are some uh selective criteria here, although it can be a case by case basis. Next slide. So again, when we talk about management as I mentioned earlier um when we have uh declared refractory uh sites. Uh Again, it's really important to talk about what's their candidacy for liver transplant. And if you're unsure, always contact your local liver transplant center next for uh and if they are a candidate for it, um then proceed to uh initiate the transplant evaluation next four. And if they're not a candidate, can they be a tips candidate as either a bridge or a destination therapy to control their poor hypertension and their ascites. And for those that are in the transplant pathway, if, if they're uh looking at a long uh wait time uh while they're awaiting a liver transplant, it might be uh something to think about as a bridge to transplant of using uh uh tips to uh to manage these patients as they do have an improved transplant, free survival and select cases. Um Again, if you're a trip, uh tips candidate, you can be considered for tips if you're not. Uh one thing that we will discuss uh a little bit more detail later with doctor Salk is to talk about the um uh are they a a peritoneal Venus uh shunt uh candidate with PD curve? Uh next for. And if they uh we'll talk about the selection criteria for that in a sec. And if they are proceed with uh considering uh shunt again and select patients, and if not also uh proceed with either serial large volume parasites or if they're um uh select uh patient uh and uh per patient and, and provider uh decision. Uh We'll also talk about a little bit more about the peritoneal catheter. In this case, the periton uh peritoneal catheter next slide and then always uh determine that uh uh consideration for liver transplant is a dynamic um status. So patients that may not be initially, candidates always can be reconsidered in the future. That's something that I try to highlight to referral uh referring doctors. And I, we hope to highlight that uh throughout the discussion tonight, that it's always relevant every time you have a, a point uh contact with the patient always reassess can they or can they not be a transplant candidate because things can change? And it's important to not just deem them, not a candidate at the beginning and never reconsider throughout their course because uh it's often that some of the barriers may have been uh mitigated next slide. So we're gonna move on to talking about the management using the PD curve uh to manage society in those patients that uh we feel are not uh adequate transplant candidates um and may or may not be adequate uh trans uh um tips candidates. Um And uh with that, uh I I if you're not familiar, the PD curve is a shunt between the peritoneal cavity and this and uh connection to the central veins using a silicone coated tube with a uh unidirectional valve four. And with that, we'll get a little more detail with, uh, Doctor Sock. Thank you. Um, the BD curve is, it was called the Denver shunt, which, by the way, it wasn't because it was from Colorado. I think it was a, it was the name of the physician by Doctor Denver. And also, uh, it was called the Right, the Levine Shunt back in 19 fifties. Um, and so a lot of people when they hear the word Denver shunt or per Neo Venus shunt, it usually causes pause. Um My dad is a surgeon. He retired, but I talked to him about the Denver shunt and he said that was, it was, it was a back in the day, a lot of it was fraught with some issues. Um And the reason why I'm talking about this is that since then, a lot of more has been understood, not only about patient selection for the Denver Shun or now called the BD curve, but also the device itself has been modified to adjust to a lot of the issues that um that existed back in the 19 fifties. So what do I mean by that? And so this slide is talking to us about a study that was really good, I thought in 2008 um that mentions that uh there was a couple more exclusion criteria that should be considered in patients who are not tipped candidates. Perhaps they have the their male score is way too high or perhaps their, their encephalopathy is way too under, um, out of control. They mentioned that the exclusion of patients with a history of varico bleeding should be considered. And before the shunt gets placed to drain as much of the asides as possible. And so when most of us think about installing these Perito venous shunts are now the BD curve, we think, well, the patient has like 10 L of asides in their abdomen and we just install a catheter and just let all 10 L unleash itself into, into the circulation. Um And so that's not what we do. Uh And that shouldn't be done. And a couple other issues occurred back in 1950 when this, when the shunt first got developed, people developed pulmonary edema, meaning fluid in their lungs. People developed AAA ton of this complication called D IC disseminated in intervascular coagulopathy, which basically means you're kind of sort of clotting and bleeding at the same time. And all of your clotting factors start to disappear in your body. The shunt were getting occluded actually relatively frequently. Um And people were bleeding. And the study in 2008, I thought was very interesting because after they started to notice that they were select, after selecting patients who uh did not have a history of uh grade three or four varices or any kind of recent varices. And they started putting these in patients uh without that type of bleeding history, their bleeding rate dropped dramatically and of course, by uh draining out of the aside before you install the shunts, the risk of pulmonary edema or fluid in the lungs almost dropped to zero. Um And the risk of D IC, which is that blood blood clotting disorder, you know, that clots and bleeds at the same time, that also reduces when you quote, wash out the abdomen, meaning you pull out all the ascites. You put in a, a sterile, warm sterile saline back in the abdomen and then drain that s that sterile saline back out. You're kind of washing the abdomen by doing that. The risk of D IC also was sort of started to be uh started. It was noticed to decrease as well and lastly pump education. Um A lot of people think you put in this shunt and you, you say see you later, I hope you have good life. No, no, no. These patients need to actually be very vigilant about pumping it, not because it's necessary to push the fluid from the abdomen into the circulation. But by pumping it, if the shunt isn't being pumped, it can clot up with crystals or clot a little bit. And so if you ask the patients to pump it to 20 times in the morning and 20 times at night, the risk of shunt delusion also started to decrease this daily pumping education actually reduces the risk of shunt delusion and of course, uh patient selection, um grade zero, grade one vises are optimal candidates. Grade two, you start to think a little bit, you know, I think uh it's still doable. Um and uh can be performed in patients with grade two vars, but once they're grade three or 41 should really pause and, and, and consider other options for the asides next slide, please. So for those of us who, who do interventions and for those of us who are in, who are at least um familiar with interventions, I describe the BD curve as basically a catheter in the abdomen that tunnels into the skin and is attached to this internally placed pumping chamber which is not battery operated. It is basically like a, a one way valve. I call it like a whoopee cushion in there. Basically that prevents any fluid from going backwards into the chamber. And then the ca the venous catheter tunnels through the skin just like a port and enters into the right internal jugular vein and then terminates in the superior vena arial junction or the or the right atrium. And so essentially a beauty curve equals pert plus port fused together next slide. So um indications for use, I it's not just for non malignant societies, even though that's the topic of our discussion today, it is indicated for both malignant and non malignant. Now, the whole malignant societies uh discussion certainly happy to answer any questions related to that afterwards, but, um, certainly indicated for that. What's interesting is the Kyle Society's indication. A lot of people wonder. Well, is that natural? And it's actually 100% natural because the way Kyle normally drains is through the th thoracic duct and drains into the Venus circulation in all of our bodies. And so AAA VD curve is sort of like an artificial conduit for performing a very physiologic transport of Kyle into the circulation. Um It is indicated for those who are not responding to standard medical management and not candidates. Uh for portal venus shunting, it is designed to control fluid accumulation and may reduce the need for reintervention and gives the patient back the ability to perform daily activity, uh activities of daily living in the comfort of their home. As an aside also some of the earlier studies um back in the eighties and the seventies looked at patients muscle mass by just measuring how much nitrogen they have in their body. And those who had shunt, uh BD curves are back then called the Denver shunt. Placed patients got more muscular. I'm not talking about like bodybuilding muscles, but they gained actual muscle mass because this fluid that normally was getting drained out, pulled out every week by a paracentesis was staying in their body. And these patients also noticed quite a bit more energy, which is important, especially uh either whether they're a future liver transplant candidate or not where we're looking for quality of life here. And if these patients are tied to a hospital every or, or, or a lab or an office that does Paris and T CS every week, you can't really do much more than otherwise schedule their appointment every week to get a needle put into the abdomen just to pull out the asides, they can enjoy traveling, they can enjoy playing with their Children or their grandchildren and also have the energy to do so. Um It is contraindicated in patients with peritonitis. So obviously, if there's an infection in the abdomen, you don't wanna introduce that into a shunt and put that into the circulation, renal failure with no plans of dialysis is the reason is that you're putting fluid back into the circulation. If someone's not planning to get that ultra filtrated out of their body, then you're putting quite a bit more fluid into the circulation, decompensated heart or respiratory failure or severe pulmonary hypertension, the extra fluid that's going into a heart can actually stress it out even further. The existing D IC. And as I mentioned before, uh this last contraindication is quite important. History of grade three or four varices or recent variceal bleeding is a contraindication for the BD curve. Next slide, please. So say that the patient is identified uh and one is placed the main things to monitor the patients for afterwards are D IC, pulmonary edema aside, leakage and infection. And so uh uh not on the side, uh there are ways to help kind of compensate for each of these um issues. And uh we'll actually talk about one of them or two of them in the next slide. Can we go to the next slide, please? So D IC again, D IC is that, you know, clotting and bleeding disorder at the same time. And uh after I placed BD CURVES, I admit the patient overnight for observation and I draw Q six labs, I measure their platelets, I measure the fibrinogen, their inr and their P TT. And this is meant to monitor for subclinical signs of D IC before they presented the clinical symptoms of bleeding or, or clotting. And so um a vast majority of the time after performing the aside, removing the aside and washing the patient out and putting in the Denver uh the BD curve and then um watching the patient, they all do fine. A very small subset of patients when I start to see the fibrinogen starts to decrease quite a bit or the playlists are starting to drop and the inr is starting to increase. And I think that this patient might develop clinical signs of D IC, I'd like to um intervene before it gets to that point. And so essentially what we want to do is temporarily shut the shunt down without actually exp planting it in these situations. What you can do is make an incision over the peritoneal insertion site, then essentially capture the peritoneal venus and deliver part of that shunt to the surface, tie a 20 nylon or silk suture, basically toy off the lumen and then reinsert it and then close the insertion site and the skin uh with absorbable sutures and glue. And this of course, would stop the shunt from working, but at least you're avoiding a potentially uh uh symptomatic D IC situation. Um Then we can talk if there's questions about what to do next. I mean, are we just gonna leave a tied off shunt in the patron or not? I'm happy to answer that um at the end of the presentation. Um but for instance, if say that someone is still doing poorly for XY and Z reasons and you need to explant the shunt. Well, it's kind of like ex planting a port. It's relatively simple. You make an incision over that pump pocket, access the pump chamber and you literally just remove it. It's all silicone, so it all slides out very fast. Um And then you close the incisions with absorbable sutures. And I recommend also doing a paracentesis at that time because the tunnels and the the connection between the perineal access site and your port, the the reservoir pocket um are still communicating and uh asides can leak out. So you gotta start scheduling those Paris and T CS right away after the, the shunt is explanted. Next slide, please, pulmonary edema. Um You consider aggressive diuretic management um for those who are still responsive to diuretics, uh if the patient is starting to develop D SATS and not really oxygenating well or feeling uh short of breath and certainly including the shunt, just like as I mentioned before can be performed. Um Kind of as another aside thing, if someone doesn't want to necessarily go into the peritoneal um limb and try to tie it off that way. One kind of very temporary measure you can do is pinch the, the catheter near the collarbone. Um and basically throw a knot uh with a zero silk suture around it and try to t uh tie it off temporarily then too. Um in cases of isolated pulmonary edema, um that may result from catheter migration. Basically, um you just have to uh or then not pulmonary edema from skin edema. If the patient is starting to develop all sorts of skin edema around the perineal access site, um all the penetration should be insured to be inside the cavity. If one side hole is sticking into the skin and the rest of the side holes are in the cavity, um then that would be a reason why the patient is starting to leak asides into the sub QE tissues. You basically have to rest stick the peritoneal site something closer such that all the all the side holes are inside the peritoneal cavity. Um If there is a sinus fluid leakage immediately o include the shunt if there's, um, if there's a concern that this might be infected, uh, follow, uh, the patients, uh, basically with, uh, antibiotics. Um, I typically just provide antibiotic for skin flora. Uh, and once we feel like in any possible infection is cleared, you could basically reopen the, the shunt if you've occluded it. Um, and then of course, infection, it depends on how severe the infection is. If it's something quite severe such as bacteremia, it's kinda like a port situation. You may have to explant it completely. If it's just a skin site, you try to manage that with antibiotics only. Uh Next slide, please. So, um, following Doctor Fortune's uh pathway here, if someone is not a candidate for BD curve, say for instance, their functional status is really low, I mean, they're just bedridden and they're not really long for this world unfortunately anymore. Or um, if they already have a pretty bad coagulopathy that we don't feel like would be uh trans fusible. Um These are patients that could benefit from either a large volume pais and T CS or perit catheters. Um Next slide, please. Essentially, these patients are pretty, they're pretty sick. They're too deep, they're too decompensated for tips. They're too decompensated for an ASI uh BD curve. These are patients who are almost headed towards hospice if not already in hospice. Next slide, please. So, uh talking about the pretext catheter, if we will move on to the next slide. Um the pert catheter is the first and only tunnel catheter that is indicated for the drainage of malignant and non malignant societies. Um And, uh essentially as this picture shows it's a catheter that's tunneled into the skin and, and, and connects into the perineal cavity. And the tube itself can be connected to a vacuum container so that the patients can drain their asides at home, uh, whenever they want as often as they think, uh and their uh interventional radiologist or hepatologist feel is necessary. Um uh without having to go to the hospital and get uh poked for a paracentesis. Next slide, it is indicated for in long term drainage of symptomatic recurrent and malignant or nonmalignant cities that don't respond to medical management and for the palliation of symptoms related to recurrent asides. Um it is for the non malignant population limited to those who are intolerant or resistant to maximum medical therapy, refractory to large volume Paris and T CS and are not candidates for what we mentioned before the tips or the BD curve. And for it is indicated for adults only, we uh return back to our initial case presentation of our uh 75 year old woman with uh mass cirrhosis who presented to our primary care doctor's uh office for the worsening Ascites and was referred for Pair Andes, as I mentioned earlier, uh proceeded with medical management, uh was found to be diuretic intolerant with the increased creatinine. Uh was not deemed the tips candidate due to the high meld um was then assessed for a peritoneal catheter system with the pera infection risk family not quite ready for hospice. Uh She was still requiring routine persis coming in weekly for taps and it was felt after discussions to proceed with the PD curve aside shunt uh candidacy. So, next slide uh and just to uh conclude hopefully over the last 45 minutes, we've been able to kind of discuss uh the current understanding and pathophysiology of uh of a nonmalignant societies, particularly related to portal hypertension and cirrhosis. Uh We wanted to kind of go over the current algorithm paradigm management uh including uh initial uh candidacy evaluation for liver transplant. We wanted to talk about kind of the benefits of how patients uh with their caregivers who manage their aside uh whether that's with tips or with these other uh devices such as the PD curve and the Periton X catheter. We wanted to talk about the management of C that can achieve together with those uh as discussed by doctor. So how it can really be an ascites management team, including our interventional he uh radiologists, gastrologist, primary care providers. Uh We're all here for our patients and we're very excited to continue to work together to improve the care uh for these patients that are in great need. And with that, we will conclude and move on to our uh question and answer and thank you for your time. So looks like maybe there's a, a question already. Um The question asked is after how many repeat Paris and T CS would you recommend chronic drainage? I can go first if you don't mind. Um, ok, so, um, basically someone who's coming in for uh at least uh two large volume Paris and T CS within a couple of months, I start thinking already that we need to do something uh more for that patient. I think um the Vino two and Brett can certainly talk about that more um kind of highlight something. Um I think even a little bit more of more kind of quote aggressive um uh in regards to that, but personally, I wanna see that they get at least two within three months. But that's, that's kind of more uh loose, I think. Yeah. So a a absolutely doctor. So uh when we did our initiative uh with uh both Bovino seven now, uh which is uh for those that don't know, that's our consensus conference, uh international conference held in Italy every five years to talk about kind of uh uh outcomes related to portal hypertension and its complications. Uh We with the recent increased data related to uh preempts tips. Uh we have learned that basically after uh whether it's two sequential large volume parasites within three months, or we've actually found that three liver, uh large volume parasites within 12 months is actually uh enough to consider or tips candidacy. Uh This is of course, under the assumption that uh they're not having ongoing alcohol use or other insults uh to the liver, uh which does make it a little complicated when we're dealing with uh some of the acute alcohol liver injury. Uh But uh basically, yes, uh we've had some increasing data showing that can, can be uh considered if they require three or more uh para uh therapeutic uh large volume parasites in a, in a year span. Uh Regarding the other uh criteria, I think it again gets to what we were talking about with patient selection. Uh and uh patient uh consideration, happy to take the next question. I think uh there's another question saying which study from 2008, I believe that's referring to a um a slide where I was talking about the, the changes um within the BD curve or back then in 2008 called the Denver Shunt. Um This was in JVIR, the Journal of Vascular Interventional Radiology. Um And I can't, don't quote me on this. I it was, it was one of the, the um the East Coast Universities. Uh Again, I don't want to miss miss, say it. So, um anyways, uh the primary author was Doctor Wan Won. Um and it was a study of probably, I think over 20 patients. Yeah. See here, I'll read the next question. How do you determine under ultrasound when draining prior to implanting the shunt that you have drained enough or not enough, uh, determining this by how much the patient typically drains weekly, quantifying how much you have drained into vacuum balls. Uh, so doctors, I'll leave this up to you. Uh, about how much do you think you need to drain prior to implanting the PD shunt? Um, in short, all of it. Um, so you, you basically drain the aside dry. Um, at my current institution we attach in the kit that comes with the BD curve. It comes with its own catheter. It's kind of, it's almost like a plex, but without the, with the cuff, it's essentially a tube that we put into the asides and I attach it to a, like a stronger vacuum and I literally go until it stops or until it's starting to just pull in air from the outside. And that's when I say, OK, we're, we drained it all completely. So, in short, you want the aside, completely dry? That's a good question. So there was a question about how about using the PD curve on a patient on dialysis? Um, yeah, this is, um, I laugh because this is a very good question and I, I wish I had a much stronger answer other than that, um, one patient I've tried this on, um, I had them get dialyzed instead of three days, three days a week a week. I changed them to four days a week and they did fine. Um, now how much someone gets, uh, removed during dialysis? Depends on a lot of factors. If they're hypotensive still, they can't get removed as much as someone who is, uh, normal tensive. And so, can it be done when someone is on dialysis? Well, it depends on, are they compliant with dialysis? Are they making all their appointments? Is our blood pressure gonna handle a full dialysis session? Um, it's, it's a, it's a tough one. That's a very patient specific uh question. But uh it's a very good question. I, I would probably favor making sure to uh uh go to a center with a lot of experience and, and more than likely uh would probably refrain from use would be my opinion. Um In, in addition, one thing I do wanna add is for those that have ascites. Uh Please don't let your uh inter individual radiologist or, or nephrologist convince you to do peritoneal dialysis because uh of the extremely high risk for peritonitis uh in these patients with cirrhosis. So, uh it may seem like an, a simple way to do dialysis because they already have ascites, but there's an extraordinarily high rate of peritonitis and uh uh so would not advocate for that. Um ok. Well, with that, I think we're are uh closing in on our uh last minute of the session. Um Thank you. Uh very much. I think we are planning if you could scan this QR code. Uh this will be an opportunity to give us some uh feedback about the session and your other thoughts. And we hope you uh en enjoyed the discussion and we appreciate your attention and thank you again for joining us uh this evening and have a great rest of the week.
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