Advances and Challenges in PVR-TIPS for Portal Hypertension

Episode Transcript

Recorded live from Cook Medical and featuring leading experts in the field of interventional radiology discussing a wide range of IR-related topics. This is The Cook@ SIR Podcast Series.

Good day audience. I hope everyone is well. I’m Siobhan Flanagan, an associate professor at the University of Minnesota, where I’m an interventional radiologist who specializes in the management of portal hypertension among other entities. Thank you for tuning in for another Cook podcast. We enjoyed our first year last year at SIR and we’re here to continue the fun. It’s a cold winter day in Minnesota, but we’re going to bring the temperature up with some hot topics surrounding the clinical impact and more recent evolution of TIPS utilization. Today, I’m excited to be again joined by two esteemed colleagues. Steve Sauk is an associate professor of radiology for Mallinckrodt Institute of Radiology at Washington University School of Medicine in St. Louis. Steve brings with him a wide breadth of IR knowledge and experience. His interests are many but also include advanced portal venous endovascular treatments. He’s also passionate about educating our next generation of interventional radiologists.

Nassir Rostambeigi is here again as well. He’s an associate professor at the same institute, Mallinckrodt Institute of Radiology in St. Louis. His interests also include TIPS, prostate artery embolization, interventional oncology, and pulmonary embolism treatment. Previously, we discussed the expanding role of TIPS beyond refractory ascites and variceal bleeding at the SIR 2025 Cook podcast, and today we’re going to dive a bit deeper into PVR-TIPS, the impact of that procedure on patients, and we’ll even get into some M&M cases where we can share some significant learning points that we’ve all experienced in our lives. So, I’ll start off our discussion. We’ll start off with the post PVR-TIPS era, and I’ll just quickly review what we mean by that. PVR-TIPS stands for portal vein recanalization and transjugular intrahepatic portosystemic shunt creation. And our goal with these procedures is to reopen a portal vein that’s commonly chronically occluded, and we can take a number of approaches to get to the portal vein that’s occluded, most commonly a transsplenic approach, but we’ll get into approaches later.

But the goal is that the recanalization restores physiologic flow to the portal vein. And then of course the TIPS decompresses portal hypertension that we most commonly see in cirrhotic patients that in turn reduces risks of problems like variceal bleeding and ascites. But also more recently, it has become useful in making patients good surgical transplant candidates when previously maybe their portal vein occlusion excluded them from transplantation. So we’ll start off, I’ll ask Nassir. We talk about PVR-TIPS and we talk about something called the “impossible” TIPS. I’d love to hear your nutshell of what that means and why you think it’s more popular now than it was maybe 10 years ago.

Sure, I’ll start. Thank you very much for this beautiful introduction. So “impossible” TIPS and the fact that why we call it impossible, back in the day, was essentially with the concept of we want to have a patent portal vein so that we are able to create this TIPS from the portal vein to the hepatic veins. So early on, the patency of both hepatic and then portal venous end is been always the key concepts for the TIPS creation. And then whenever we didn’t have those, there was a little bit of a pause by the interventionalists for obvious reasons because there is no patent vessels to be able to create this shunt. On top of that, the patency becomes an issue when we don’t have patent inflow and patent outflow. And the portal vein thrombosis more and more became known and became something that comes to our clinic just because of the fact that we see more of these patients from more cirrhotic world as well as non-cirrhotic world.

And then more and more, this became more commonly seen in the clinics. So the concept of “impossible” TIPS gradually became something to think about because these patients now coming to our clinics with the ascites with the bleeding, so what do we do? And because of that, over and over, when we learned from the experience from big centers like Northwestern, we have expanded our armamentarium of creating these TIPS from impossible realm to the possibility by the fact that we are now able to recanalize the portal vein and then create the TIPS for the good outflow. The creation starts from whatever anatomy dictates. So when we have a patent SMV and a splenic vein as good inflows, and we are dealing with only partial thrombosis of the portal vein, those are really starting from the, so to speak, easy patients. Then we gradually can see the spectrum of patients to become really, really more complex with more complete occlusion of the entirety of the portal vein than extension into the SMV or in the cases of pancreatitis, for example, or chronic pancreatitis for example.

We’ll see splenic vein thrombosis and occlusion as well. And then what I’m trying to say is that as the complexity gets worse, obviously the possibility of creating these TIPS becomes less and less, but with more experience, we are seeing that it’s actually possible to find a solution in a lot of these patients by having a very careful evaluation of the anatomy, establishing a good inflow, having a safe access into either SMV inflow or a splenic vein inflow via transsplenic access. And then after recanalizing our main portal vein, then creating our TIPS, and then move on to establishing the main inflow and establishing a patent TIPS. So the bottom line is that we want to have a good understanding of the anatomy and then move on safely.

Let’s talk about that, and thank you again for the introduction, Siobhan and thank you Cook for having us. What happened to these patients before PVR-TIPS was done? I mean, portal veins have been occluded since the first alcoholic beverage was created or the first virus of hepatitis was ever out there. What happened to these patients do you think? Again, talking broadly speaking, I mean, it’s not like this pathology just came out of the blue in the past decade.

I think, Steve, it’s a great question, and I think a lot of patients were just bound to chronic medical management and procedural management, like endoscopic management of varices, for their lifetime. I think that patients were— At some point in time, banding becomes an impossibility. There’s enough scarring in the esophagus that there’s not even anything that can be grasped endoscopically anymore for effective banding. I think those patients eventually would have their bleeds, and they would be catastrophic bleeds for patients who perhaps were eliminated from transplant consideration because of their portal vein occlusion. They died of their cirrhosis, and I think chronic medical management and early death was the case for most of these patients.

So would it be fair to say that you think that the description and the popularity of this procedure is increasing longevity and improving quality of life for some, I guess?

I think both of those are an absolute yes.

Yeah, absolutely. As well as the transplant candidacy and bringing a lot of difference for these patients as far as their lifestyle goes, as well as the possible future procedure goes.

So even as residents, however long that was– I don’t want to state our ages, but I’m sure it was at least 10 years ago. Do we feel like even as residents in surgery or medicine, we saw these catastrophic variceal bleeds and their portal veins were occluded and people weren’t as gung-ho about doing the TIPS—the “impossible” TIPS—at that time, we saw these patients just go into hospice or into comfort care? I mean, I’m just talking out loud now. I’m not sure if you guys have experienced that.

I can say for myself, I experienced as an intern a cirrhotic variceal bleed that led to a patient dying on my clinical service. We all got out of ward services after our first year of training, but that was one experience for me that really stuck in my mind. And I think back then it wasn’t a refusal or people weren’t thinking of TIPS, at least from an IR perspective. I think there just wasn’t a lot of data on using TIPS for all the indications that we see it used for today. It’s a procedure that was rare during my first fellowship year, and over time at my current position, I mean, we’ve seen the number of TIPS that we do per year more than triple. So the more we all do these procedures and the more positive patient outcomes that have been witnessed in our respective institutions, the more the referrals happen and the more willingness there is from other clinical teams to consider this as a therapeutic option for their patients.

Excellent point. Exactly. As we are proving safety of these and gaining experience and showing that how effective is this, it’s definitely showing its impact. One other thing that, Steve, that you brought a very nice point that, so what was happening to these patients? And that’s a great question, and I think some of these patients were getting other sort of interventions that, for example, partial splenic embolization, to control this bleed or some sort of getting access into the transsplenic variceal embolization in sense of gastric varices from the splenic vein origin when we have portal vein occlusion, sort of like other things that people used to do to temporize the situation. Some of them I have seen, remember that I saw it in my residency that was just not exactly completely helping the patient, but temporizing the situation a little bit.

Interesting. How did, Siobhan, you said you almost tripled the number of TIPS. Again, the focus isn’t necessarily on the number of procedures, but the patients that you’re helping. I’m curious to know how did you do that and what kind of approach did you to take to almost, is it marketing or is it demonstrating outcomes?

It’s in part demonstrating outcomes, but even before the demonstrating outcomes, we have a multidisciplinary liver tumor team that consists of hepatology liver transplant, IR, et cetera, et cetera. And we had a few young hepatologists come in out of training who were experiencing and recognizing positive data on using TIPS for controlling refractory ascites and refractory hepatic hydrothorax. When those two indications were recognized as reasons to place TIPS, our referrals just started to explode. And then, of course, there’s the transplantation prospects for patients, patients who previously weren’t transplant candidates.

Northwestern published their data, and really at that point in time, that was a trigger point I think for some of our surgeons who understood the potential utility to really say, “This is an institution that had a large number of patients undergo this procedure, the mortality and morbidity rate of that procedure was very low, and their outcomes for an end-to-end portal anastomosis were good.” Meaning they didn’t have the long-term data with their first publications, but they did have the data showing that these patients underwent an end-to-end portal anastomosis, which based on surgical literature, we know that’s going to be the best outcome for long-term portal patency post transplant.

And that’s a nice, we can transition to talking about cirrhotics versus non-cirrhotics and what are we really treating in each of these group of patients? What do you think, Steve? Do you want to chime in about non-cirrhotics and what is the goal in them?

I think that’s what we’re– Yeah, I think that’s a good way to categorize it. I think when we talk about what are we treating exactly. Is this a variceal bleed situation? Is this postprandial pain? And we’re not really dealing with transplant status in the non-cirrhotics. The liver tissue is healthy. These are people with JAK2, polycythemia vera, pancreatitis, pancreatic cancer, even post-surgical or androgenic causes, even umbilical venous catheters for pediatric populations. So I guess the question really, I guess when I approach a non-cirrhotic is what am I trying to treat? Not the picture. We’re not trying to make a vein appear just for the sake of a magic trick, but we’re trying to treat a symptom. If we’re treating varices, then the whole purpose of the reconstruction with the PVR-TIPS plus whatever stent into the SMV or splenic vein is meant to decompress the varices.

And now if I’m going for postprandial pain, varices and patient doesn’t have that bad of a varices burden, then I’m not going to really concentrate so much on decompressing all the collaterals that we see on the CT. But I’ll just be focusing on how do I relieve the intestines? How do I get the mesentery to calm down? And that may involve extending a stent from the TIPS into the SMV. I think then when we deal with prognosis, I don’t know because that’s where I struggle with, especially with the varices, because you put a big stent in there, you got to put them on anticoagulation because of their hypercoagulability either from their JAK2 mutation or from their cancer, but then they just bled from their varices. So that’s totally paradoxical. Now, I’m starting to talk in digression. So sorry, I didn’t go back to your question. How do I approach a non-cirrhotic? I think it’s always about the symptom to me. If someone’s asymptomatic, I don’t do anything.

That was going to be my question, Steve, because that’s where I really struggle. There’s a patient that– I think our institution is recognized what we can do with these occlusions, and we’re seeing more referrals for patients who found to have an occlusion, but they haven’t had a complication yet. They haven’t had a GI bleed yet. Maybe they see some varices on the endoscopy, but they haven’t bled. They’re not a high grade, they’re not going to bleed. How do you manage those referrals?

I say we need to have a portal tract trial. You’re hitting it on the nail. What is the risk long-term of these patients if we treat with catheter therapies or if we don’t? That was the ATTRACT trial. If someone has an acute DVT, is intervening going to prevent post-thrombotic syndrome? And the short answer was not so much. I mean, it helps with the acute symptoms and shortens acute symptoms. And so I think what you’re alluding to is that, well, if someone has an occluded portal vein now, do I intervene now even though they’re not symptomatic so that I could prevent the equivalent of a post-thrombotic syndrome of the liver, which might be postprandial pain, which might be varices. So again, that was a long-winded answer that didn’t really answer your question. I don’t know. And that’s why I am more conservative in just saying I need a symptom to treat, otherwise I can’t get myself to put the patient through the risk of the procedure.

I was just going to say in general with you on that, I think it’s really hard to talk about the procedure and the risk and all the post-procedure care and imaging, everything that they have to go through, without having a symptom. And then you have the patient ask you, “Well, I varices now. What if these enlarge and I bleed later?” That’s really where I get into thinking more than I used to think about approaching those patients. But in general, I agree on your assessment on that.

And one thing to add to this, and also makes it a more clear how complex is decision-making, is the CT findings of possible bowel ischemia, patient having some abdominal pain or postprandial pain, but we can’t really pinpoint that to occlusion or it could be both that plus for example, a chronic pancreatitis that patient has. That abdominal pain and postprandial pain could be having a complex etiology and that makes it still a dilemma that we need more data.

It’s funny you mentioned that. I had the reverse of what you talked about. Someone was referred for decompression of these varices prior to a cholecystectomy because the pain was not to be related to biliary colic. And then we did the whole PVR-TIPS, we decompressed the system, got the varices to go away, and then the patient’s pain got better. And so they didn’t get the cholecystectomy anyways. The surgeon wasn’t happy, but I mean, I was like, “Well, we treated the patient.” And I’m just kidding. He was happy, of course. But it obviated a future surgery even though the intent was to make the surgery more possible.

And that brings another question for me. We see that from time to time. How often are you guys seeing those referrals for recanalization to make an abdominal surgery possible?

Yep, I had one of those, and it made it possible. But did I have a clinical trial to support me that, that if it didn’t do it? I don’t have level one evidence, but it makes sense.

And Nassir, was it to reduce inadvertent incision of a varices and cause intraoperative bleeding? Was that the reason for their request?

Yes, correct. That was the case.

And we’re seeing that at our institution. I think the non-cirrhotics are really where our harder decisions are made. But let’s transition into talking about about cirrhotics. Nassir, when you’re treating these patients, in general, what are you trying to treat and what’s your approach with cirrhotic patients?

And really nicely, I agree that it’s easier because now we are dealing with a patient who has liver disease. So, right off the bat, if the patient is a liver transplant candidate, that should be the goal. And multidisciplinary decision making is more important than ever to talk about the pros and cons of intervening here. And so like you mentioned, Siobhan. So, these patients, if they are going to the transplant route and they don’t have a portal vein patency and they have some level of portal vein thrombosis occlusion, they’re going to be having more mortality and they’re going to be having more recurrent PVT after transplant. So, having an end-to-end portal vein anastomosis is a key here and is very valuable. So, historically, these patients are always going to be poor candidates for transplant if they don’t have portal vein patency, and making a non-physiologic portal vein flow like it’s been historically described as having any sort of cable anastomoses or right renal vein anastomoses, those are not favorable because of all sorts of morbidities accompanied with them.

So if you want to have a physiologic inflow for the portal vein for the liver transplant, maintaining it an end-to-end anastomosis is the key. And to achieve that, we should be able– we need to have a PVR-TIPS done, and that has shown by the data now. And more data is needed, but based on the data that we have from Northwestern, definitely we have seen that they were able to have a very high rate: 96% of the patients who got into transplant, they were able to have an end-to-end anastomosis, which is fantastic. And then also, they also showed that their survival was more than three years when they were able to achieve that. So, that’s really amazing, and it shows the fact that this is going to be very helpful.

Over and over, when we can achieve this safely among the different institutions, I think that the data will prove it to itself that this will be something that can be used in all the different institutions, even though there is a little bit of resistance, there’s a little bit of a learning curve, there’s a little bit of back and forth with the transplant surgeons that we are all aware of. It’s a different dynamic in different institutions, in terms of how we should look at these data. And I think it’s just mainly because of the fact that the surgeons are having a certain mindset that probably needs more patients and more data and more multi-institutional studies to show that this is really working and this is safe in experienced hands. So, that’s one, plus probably historically, they were able to do jump grafts and interposition grafts, and even though the data shows that the end-to-end anastomosis is better, maybe the trust is not there yet that the PVR-TIPS will give them the end-to-end anastomosis option and that should be the key to pursue before sending these patients to liver transplant. Long answer. What do you think?

Well, I can give you our institutional perspective and there’s been a change for us over the years, too. And similar to hepatologists coming from other practices, newer practices, they’re more open to the procedure because they’ve had experience with it. Same thing for our surgeons.

So, let’s get real now. So, we want to talk about something that it’s not easy to talk about, but I think we all alluded to these, that these are sick patients. These patients have lots of comorbidities to start with, cirrhotics or non-cirrhotics have their own nuances. But we are dealing with a population of patients who have a very niche diagnosis. They have a thrombocytopenia, they have coagulopathy, and yet we are going to do a very involved procedure in them. So, no matter how experienced we are, unless we are God, we are going to have some bad days and bad complications, and let’s talk about those. And let’s see if we can have some candid conversation about them and have some input about what we have learned from a bad unpleasant experience that we had in the past, and we can discuss it. Obviously, having this is going to be very helpful but not easy, but usually having these conversations are really elucidating for our future.

It’s also going to be a nice therapy session, at least for me, so I could use any mental health tips as well after discussing it.

One thing I’ll say is that I’ll have an early-on career case to talk about, and I’ll tell you that the M&Ms don’t go away even with PVR-TIPS. My first really bad experience with the PVR-TIPS was actually in a non-cirrhotic patient with a portal and SMV occlusion. He had a gastric bypass, and sometime in that post-operative frame developed clot. He had intestinal angina from it, essentially from his venous hypertension, his outflow obstruction. So, he underwent a TIPS and a portal, superior mesenteric vein recanalization and TIPS placement. Procedure went great. He had progressed some of his thrombus down his SMV, so that was a trigger to start him on anticoagulation. And he came from one of the Dakotas, went back out, discharged back out to the community, and then came back several weeks later with a subtherapeutic INR and catastrophic diffuse thrombosis and could never recover the patency that he had before.

Regardless of the number of procedures, he actually sadly was admitted for about a week or so before he made it to our institution. So, we learned about that complication for him late, and that really inspired in us having a more of a multidisciplinary approach to managing these patients. I know we wanted– that it’s an important part of all of our practice, but that triggered us to involve hematology in the care of these patients. And when patients need anticoagulation after their procedure, they’re going to see a hematologist at our institution, they’re going to be tightly monitored and controlled.

What would’ve changed do you think, if you could do it over again? What medicine, I guess, would you mind even?

So he was put on warfarin, and that was what he was on after they had diagnosed his thrombosis. And I think, for him, something faster acting– I’m more of a Lovenox® proponent, at least in the first month after recanalization. It’s just more reliably therapeutic in patients as long as they don’t have renal insufficiency, and you don’t have to worry about your diet as a patient and throwing off the efficacy of warfarin, for example. So that is something that I would’ve have reconsidered, and that’s my approach now for patients is Lovenox in that first one to two months post procedure just because they may be coming back for an intervention sooner than later, too. So, that’s our habit. But also the habit is hematology is involved, and they’re going to look at the complete patient. They will know more factors about this patient that would contribute to a specific anticoagulation selection than I could possibly know.

Just touching on that too, I 100% agree. It’s not just even anticoagulation, might I add. It’s about whatever other medicine they’ll need to treat the substrate problem. I mean, I was treating a JAK2 mutation patient, polycythemia vera, a central thrombocytosis-type patient, and they need Jakafi®, they need Pegasys®, these medicines that I don’t really know how to manage or by no means am I comfortable using. I had a similar case of someone who, because of insurance reasons, couldn’t take the medicines she needed for her essential thrombocytosis. And despite my managing her Xarelto®, I think I had her on, her platelets just went into the millions still. And the platelets won and the whole thing shut down. And I had a similar experience as you were describing, Siobhan, and I don’t think I– In retrospect, I think I should have engaged in hematology a little bit more when I started to wonder why the platelets just kept skyrocketing after the procedure.

What do you think about antiplatelets in these patients and dual antiplatelets?

I think that’s a big unknown.

I agree.

I do peripheral vascular work, too, and I’m a very strong proponent of antiplatelet therapy. So, if you’re going to put more than a TIPS, and you’re going to extend it with a stent, you have to be on antiplatelet. I mean, you just have to, and I’ll start with Plavix® straight from the get-go in addition to whatever anticoagulant of choice and then graduate that down to a baby aspirin after. I feel like the flow is really good after many months of follow-up scans, but that’s just me.

Yeah, no. And Steve, we’ve thought about this in patients who have more extensive occlusions, usually SMV extension of thrombus. I think those patients, we’ve really thought about throwing the kitchen sink at the problem just in the hopes of keeping things open. Nassir, what’s your experience with the antiplatelet?

I have a case that I was going to share a little bit later, but I can share it probably now. I, early experience, we needed PVR-TIPS on a non-cirrhotic that actually came in because of GI bleed. Unfortunately, this guy had a splenic occlusion, SMV occlusion, and portal vein occlusion, so very challenging, but transsplenic access, PVR-TIPS went just fantastic. No problem. Day two, he was very good, out of ICU, ready to be discharged. We did start him on dual antiplatelets, so aspirin and Plavix plus anticoagulation. And unfortunately, he started having hemoperitonium, and hemoperitonium, so remained undiagnosed, so to speak, because he was doing well until he didn’t. And when they imaged him and they called us late, they also said that his TIPS is down because gradually they stopped all of his anticoagulants and antiplatelets on the day two.

So, unfortunately, before us being able to intervene upon him, he passed very quickly. And it’s a trade-off of having them on multiple antiplatelet anticoagulants versus not, and having just one agent, then monitoring them carefully. Plus having the hematology on board is also very important. So, I think at the end what I learned was that probably dual antiplatelets to begin with—if we are not extending to the SMV and we are just doing a PVR-TIPS—is my go-to to just have them on anticoagulants and one antiplatelet. And then getting imaging, non-cirrhotic, yeah, and getting imaging earlier than just waiting for the team to get that for us so that we are able to diagnose what’s going on as soon as possible.

So you’re saying triple therapy. You’re saying anticoagulant, Plavix, and aspirin post procedure?

Yeah, I’m not opponent of that. What do you think?

I think that’s a little, it depends on the case, it depends on the flow. I think we reconstruct the SMV or the splenic vein and you inject and you’re like the flow contrast is sitting in the stent then yeah, I would agree. I’m like, we got to keep it open somehow and not let it shut down. Or if, I’m curious to know what you guys would do in a case where you don’t have an SMV trunk or a splenic vein trunk and all you have are second-order veins, like jejunal branches or splenic hilum branches, do you stent into those? Those are lower flow, the inflow is not as good as a nice juicy SMV or splenic vein. Yeah, I might consider triple therapy, but then also at the same time, I’m like, “How did I get this to reconstruct if I went transsplenic or SMV? I’m not going to throw triple therapy post-op day zero and have them bleed into their abdomen either.” I think I would do the same in the legs world as well. Triple therapies, that’s a lot. It makes me nervous.

I would agree.

And if the flow is poor enough, what does adding the antiplatelet agent do for the situation?

I would agree. Yeah, if you have, I think flow, flow flow, it’s really important to have a good inflow, good outflow and–

Did you all ever stent into a second-order vein? If you didn’t have a trunk.

Like an SMV.

That, my nightmare index case as a newer staff was exactly that, and it didn’t stay open.

And if you had, and that was for an SMV branch or if that was stenting into a splenic vein branch?

So, he had bifurcated system where there was a opening of the splenic vein at midline, then a stent down the SMV. And it wasn’t a second-order vein, but it almost acted like in a second-order vein in the SMV because he had losted so much of his peripheral SMV to thrombosis that there wasn’t a whole lot of inflow coming into that SMV.

So you double barreled the stents into the portal vein?

Yeah.

Gotcha. And now, would you just choose one over the other now?

I would choose one over the other, and I choose the splenic vein every time. That is going to keep the TIPS open, because of the flow. And I think that a lot of these non-cirrhotic patients wind up having a parallel circulation. I don’t know if you guys have noticed this, but you have the splenic flow that typically will go right into your TIPS, but then depending on where your occlusion occurred, and if it does involve some of the SMV, you wind up having these duodenal collaterals that wind up going into the liver and connecting those two systems for me in a good number of patients has never been possible, and I just let it go. And they seem to do fine.

Do you do covered stents then when you’re stenting splenic, too?

No. I always use uncovered stent. Were you asking covered versus uncovered?

Correct.

Yeah, I always do.

Just uncovered.

Yeah, uncovered.

How about in a pancreatitis patient? So I’ll preface that with my admission of guilt of treating a patient with pancreatitis with the PVR-TIPS. The PVR-TIPS connected a non-covered stent into the splenic vein, but it was someone with chronic pancreatitis but had pseudocysts that were being drained by cyst gastrostomy. And long story short, my theory is the patient leaked pancreas juice into the stents. Fortunately it went into the liver, I think because we found intrahepatic portal venous clot. That was really painful. Not like, oh, it’s painful for a day. It was out of proportionately painful for the patient, and eventually it subsided with antibiotics, pain medicines, but I had almost had a heart attack for about a week trying to figure out what’s causing this patient so much pain every day.

And then there was another case that I did with pancreatitis, someone who had an insane Whipple and had all sorts of anatomical distortion from radiation in the pancreas that happened before the surgery ultimately leading to a biliary portal fistula. And it’s a nightmare because the patient’s either getting septic from the fistula, it’s basically causing intestinal flora to seed the liver or bleeding because the stents in the portal venous system’s leaking into the biliary system and causing GI bleed. And so anyways, this is a grand admission of my M&M, but I’m curious back to the stent choice. Siobhan or Nassir, have you guys– What do you think about covered stents? Why not use a covered stent?

In a scenario like that, Steve, I wouldn’t– As long as you’re not covering something critical like SMV drainage into a main portal vein. I mean, I think a covered stent’s really reasonable in that situation. And pancreatitis patients, you mentioned them, they’re the hardest ones to manage. I think for all these recanalization patients that we’ve done at our institution, they’ve been really tricky. Making sure, as best you can, they’re out of that pancreatitis flare before you’re intervening if you can help that because active pancreatitis, I mean, I’ve seen a portal biliary fistula as well. I think I’ve talked about that before. And it was something that wasn’t recognized on a CT or an MRI. The guy was relieved from his– He didn’t have an active or acute pancreatitis going on, doing reasonably well, had a lot of biliary interventions three months before his procedure, three to four months before his procedure, and did the recanalization and TIPS for him.

He had intractable abdominal pain. It was intestinal angina basically, and he died two to three days after of sepsis. And he had a portobiliary fistula, and it wasn’t mean, it was at the periphery of the liver– but how did we know? Looking back, this guy had a million ERCPs, and on a couple of those studies, you can see it if you review the images, but it wasn’t recognized by the endoscopist who did the ERCP either. And you can see it in the portal– Yeah, you can see it flowing into the peripheral portal vein.

I’m surprised you even have the videos for that. Normally it’s just like a snapshot, like a fluoro will see.

Yeah, yeah. Our complex endoscopists tend to do a lot of video and clip storing.

Was there any transhepatic percutaneous access on that patient along the way? No?

No. No. It was transsplenic to get it done, and that one was he just got septic and they couldn’t, he succumbed to his sepsis.

That’s scary. I saw a case where someone else had done a PVR-TIPS plus splenic vein stent a decade prior to me seeing the patient, everything all clotted off, and God knows how long. The patient moved out of state and came back. And then I tried to recanalize the occluded TIPS plus splenic vein stent. I got through the stents, but I couldn’t get through the TIPS, and after an hour of flailing, I gave up, and then I just aspirated the clot. I thought I was just going to get out clot, and I aspirated bile while I was in the splenic vein stent, which was really bizarre.

And I had the ERCP guy, I just asked, “Can you please do an ERCP, send up a spy glass, show me that this stent has eroded into the bile duct.” And sure enough, I have a photo of that. You could see the splenic vein stent eroded into the bile duct, which may be the reason why the whole thing clotted, and if I had opened everything back up, the patient probably would’ve died because of a thrombus. And so it was a good thing I failed, I guess, in some respects,

And not to scare the audience off on pancreatitis patients, but they’re complicated and there’s a lot that goes into their management. And I know we talked about multidisciplinary teams and how important that is in our practice. I don’t know if you two want to touch upon that at all.

I think really we touched upon the fact that we want to have a close relationship with transplant surgeons also emphasizing hepatology, hematology. Really, these complex patients need a lot of smart minds in the field so that they have very good decision-making for these patients. Totally agree with that. We can’t really underestimate the amount of importance that all of these different specialties will have for these complex patients. Any final thoughts about PVR-TIPS? One thing that I want to just briefly touch upon is the access and the fact that SMV access and percutaneous SMV access under ultrasound is really feasible after evaluation of the CT findings. And I had a little bit of bad experience with transhepatic access and just the bleeding from the liver surface that I have really shifted towards using SMV access and obviously transsplenic, but if the transsplenic is not possible, SMV access is really, I think is a very viable option definitely above transhepatic.

That’s interesting. I wouldn’t guess that based on– And we’re all bound by our experience to a degree. I have yet to do a direct SMV access for any of my cases. We work really closely with our transplant surgeons and they provide surgical access for us. Bring out a small bowel loop and you just catheterize one of those anti-mesenteric branches with gel coat up it to a sheath and away you go. And then at the end, there’s a controlled surgical closure of that vein access site.

You can do so much more beyond that, I think if you have that ability. That’s amazing, Siobhan. I’m thinking about you could revascularize SMAs, not just SMVs. You can do a lot if you have a lap-assisted approach. Wow, that’s amazing.

But I get the allure of us doing our own access into the SMV. We know we have the skills to do it. At some point, I guess I’m going to have to try to get comfortable. One of you guys is going to have to come up and show me.

I would love to come up just in general. I’m not sure I would be considered an expert in that though. But yeah, thank you. I think we’re heading towards the conclusion and I just wanted to first thank our listeners for making it this far. If you’ve made it to this far, we just want to thank you for listening to our conversation. We really want to also thank Cook for hosting this. Before we conclude, just in summary, we talked about the PVR-TIPS. Hopefully this conversation made it a little bit more real to our listeners. Talked about not only indications and the interplay of different disciplines, but also we talked about some of our successes and failures. And I think at the end, maybe Siobhan, Nassir and I, we can– I would love to hear just two or three pearls, not pills, pearls, to offer our listeners just to come away with. What are two or three pieces of advice for those who are performing these procedures that you’ve learned in your experiences? Maybe Siobhan, you’d like to go first.

Okay. The first thing I’ll say is have a solid indication for doing it. Know the disease process. Understand why that occlusion happened. If you don’t have a reason, there’s got to be an undiagnosed hypercoagulable disorder and figuring out what caused it, but more importantly, how to manage these patients, hinges on that multidisciplinary team.

Totally agree. Multidisciplinary team decision-making is the key. Having constant conversations with the surgeons and hepatology. And then we touched upon the technical nuances of SMV access. I think these are areas that we need to evolve more and use more, and I think more data is needed, but definitely in experience they seem to be very safe. Plus a future research: We have a lot of gap on post-procedural care and post-procedural anticoagulation, antiplatelet regimens that I think that future directions will be able to show us in the future research.

Awesome. Two takeaways I’ve learned over the past few years is pneumobilia. When you see any sort of infection or colonization of the liver, be very careful and considered even prophylactic and post-procedure antibiotics. I think that once there’s gas in the bile ducts from either Whipple anatomy or a stent in the CBD, the TIPS graft can get infected. The bacteria are going to be in the tiny, tiny, tiny bile ductules, and we end up crossing that when you perform a PVR-TIPS.

Secondly, just anecdotally, I feel like a DIPS to maintain patency. If you’re going to do a long stent, like a TIPS plus SMV stent or a TIPS plus splenic vein stent, if you do a TIPS, you have the angle of hepatic vein and the diaphragm that’s going to create more resistance and more reason for the whole system to clot off. But if you have a DIPS, and if you do it carefully successfully, the stent length is shorter, your outflow is better. And I’ve noticed some of these patients with the PVR-DIPS, they do really well, and they don’t really require much antiplatelet anticoagulation after about a year. But again, this is just anecdotal. Definitely not supported by any data by whatsoever. Any last comments, Siobhan, Nassir before we close?

Not for me. Just thanks to the audience for sticking with us for a long conversation and to Cook for making these things happen.

Thank you all.

Thank you guys.

Thanks.

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