Thanks for inviting me. I'm going to be speaking today, get us started with talking about portal hypertension with talking about disease ideology, you know, pathogenesis and what medical management options are available for portal hypertension. So portal hypertension simply can be defined as a portal pressure gradient of five millimeters of mercury or higher. So that's the difference between the pressure in the portal veins and the hepatic veins. Now thinking about pathogenesis, let's go back to physics a little bit and recall Ohm's law, right? So pressure is flow times resistance. So anything that's going to increase blood flow will increase portal pressure and anything that's going to increase alpha resistance will increase portal hypertension. Portal hypertension causes can also be sort of divided into anatomical causes. You know, we have pre-hepatic causes of portal hypertension, conventionally referred to as left-sided portal hypertension. These are things like splenic vein thrombosis, portal vein thrombosis, congenital arteriovenous fistulas. Most common, however, are hepatic causes of portal hypertension in our practices in liver centers. You know, we see a lot of patients with cirrhosis. So, you know, sinusoidal causes of portal hypertension is anything that's infiltrative, anything that disrupts the architecture of the liver, such as cirrhosis. Some other subclassifications could be post-sinusoidal or pre-sinusoidal. Pre-sinusoidal is pretty much primary biliary cirrhosis. Post-sinusoidal, portal hypertension occurs in veno-occlusive disease. A lot of times in post-transplant patients. Post-hepatic causes could be alpha obstruction, most commonly butch-Chiari syndrome, which is hepatic venous thrombosis, or also IVC thrombosis or WEBS. Looking at our Ohm's law and looking at what can increase resistance causing portal hypertension, you know, there's obviously mechanical obstruction to flow in the sinusoids because the fibrosis that forms in cirrhosis. There's also a dynamic component, which is caused by active vascular or smooth muscle contraction and basically intrapathic vasoconstriction. This is due to numerous endothelial factors and also decreased nitric oxide availability. And that's resistance. And in terms of portal flow, there is mesenteric arterial vasodilatation. In most cirrhotic patients, which increase portal venous inflow, there's also increased nitric oxide production in the systemic circulation causing vasodilatation. Again, several, you know, sear stress and a lot of VEGF-type growth factors cause increased portal flow. Where is the clinical sequela? I often talk to patients in clinic, in consultation, talking about clinical sequela of this high-pressure system. So when you have a high-pressure system, you got to let go of the pressure somehow, and that's development of varices or portosystemic collaterals. You also get ascites, which is, you know, in cirrhotics, a combination of the hypoabuminemia or systemic arterial vasodilatation may have, and also the increased sinusoidal hydrostatic pressure. Hypersplenism, encephalopathy, hepatorenal syndrome, which often goes hands and hands with severe ascites, and portal gastropathy as well. You know, several portosystemic collateral pathways exist in the body. You know, in the lower esophagus, most commonly, you have the left gastric, left coronary vein causing esophageal varices. You have the splenic vein with the splenorenal shunt, usually an area where gastric varices develop, as you can see here. On the right, you can see a gastroesophageal variceal complex, and this is your left coronary vein. Other collateral pathways are in the superior mesenteric vein. Here's an SMV injection showing rectal varices. Sorry, an IMV injection showing rectal varices. Other areas of ectopic varices exist. This is an angiogram in a patient who had cirrhosis and colon cancer and actually had a stoma and developed bleeding stoma varices. You can see this SMV injection shows stoma varices with outflow into the iliac vein. And these typically pose some challenge to endoscopic treatment. Diagnosis of portal hypertension, you know, gold standard is, you know, invasive with a wedge hepatic venogram and with a gradient of five millimeters of mercury being considered diagnostic for portal hypertension. This can be done with, you know, free hepatic vein pressure measurement and wedge pressure measurement, which can be done by wedging a catheter into the venous branch or using a balloon occlutant catheter. The number five diagnosis portal hypertension, but 10 to 12 is when risk of variceal bleeding is high, and over 20 is a very extremely poor prognostic factor for patients who have acute variceal bleeding. A note of caution, patients who may have prehepatic causes of portal hypertension have reduced portal blood flow before they reach the sinusoid, so the wedge hepatic venous pressure may not actually reflect the portal pressure, and they tend to have normal wedge hepatic venous pressures. The wedge hepatic venous pressures, how well do they correlate with direct portal pressures? There's, you know, gastroenterologists who will stick a needle during endoscopy into the portal vein to get direct pressures. You know, several studies have looked at this. This is a study that pooled 11 studies and showed that it was a pretty accurate method of measuring actual portal pressure. Non-invasive methods of a diagnosis, the best validated method is elastography and platelet count. You know, cross-sectional imaging can also help identify sequelae such as varices and hypersplenism. A little bit about medical management. I'm just going to discuss the ASLD practice guidelines for, you know, risk stratification and management of portal hypertension and varices, as well as some ascites. For portal hypertension, any patient with cirrhosis should get a screening endoscopy. Anybody with, you know, a measured portal systemic gradient of five or higher should be screened with endoscopy. The risk of bleeding esophageal varices depends on the gradient, also on variceal diameter, you know, what's called endoscopic red signs and liver function. Once you have varices, the primary prophylaxis for variceal hemorrhage, first line is non-selected beta blockers. These produce mesenteric arterial vasoconstriction and basically decrease portal pressure. They've shown to be reduced the risk of bleeding from 25 to about 15%. Endoscopic variceal ligation also has comparable outcomes. According to ASLD, the recommended non-selected beta blockers, carvitolol, usually started at a dose of 6.25 milligrams a day. Other recommendations are lifestyle modification, you know, alcohol cessation and such, and treatment of underlying liver disease. Another note is patients who have, are found to have isolated gastric or ectopic varices. Even if non-bleeding is small, you should consider non-selected beta blockers in those and also investigate these patients for portal vein thrombosis as these can be a common cause of ectopic varices. In patients with high risk cardiofundal varices that are not bleeding but are greater than 10 millimeters in diameter or have red whale signs and have contraindication or intolerance to non-selected beta blockers, you can also do endoscopic glue injection. For acute variceal bleeding, once the patient bleeds, you know, resuscitation and ICU-level care is recommended. Initiate a vasoactive therapy in all patients with suspected variceal bleeding and this should continue for two to five days. Antimicrobial therapies also recommended for two to five days. Endoscopy within 12 hours, and we all know that should be probably done sooner than that. Once they've bled and treated, what can you do to prevent recurrent bleeding? You know, again, non-selected beta blockers have shown to reduce the relative risk of bleeding. Endoscopic variceal ligation also reduces the risk of re-bleeding in these patients. And TIPS is actually a reserve for salvage therapy for patients who've had repeat bleeding despite these measures. And finally, we'll just touch a little bit about medical management ascites, as we do see this quite often in the patients we see for portal hypertension. For ascites, you know, there's moderate sodium restriction, about two grams a day should be prescribed to basically all patients who can tolerate it. Fluid restriction is usually not indicated unless hyperendotremia is present. Diuretics are recommended in patients who have failed the sodium restriction, and typically you have fluorosamide or spironolactone, which is potassium sparing, but always remember diuretics, as you titrate them up, can have adverse effects such as hyperendotremia, hypokalemia, and renal impairment. Large volume paracentesis has also been shown to help manage ascites associated with portal hypertension. So in summary, you know, the pathogenesis of portal hypertension involves increased resistance and increased blood flow. If you look at that, you can kind of understand how, what different things can cause portal hypertension or make it worse. An understanding of the anatomical causes is important, especially when you're looking at left-sided portal hypertension or prehepatic portal hypertension to guide future therapy. Non-selective beta blockers and screening endoscopies are recommended for all patients who've had variceal bleeding or have a high clinical risk of variceal bleeding. Both have shown to reduce re-bleeding episodes. In terms of ascites for portal hypertension, medical management includes sodium restriction and diuresis as the mainstay. Thank you. I'm very excited to be here. This is a wonderful session with a lot of great talks, and we're going to kind of kick it off right where we left off, and we can kind of fly through some of these early slides. I think we kind of went over what is portal hypertension already sufficiently, but I think the big thing to remember is how much flow is going through the portal system, right? So normal portal blood flow is 700 to 1,000 milliliters per minute. So this is a lot going on, and a lot of what we're dealing with is cirrhosis that is causing this. So we already kind of went through this, so not going to go through it again, but it's important to remember that there's both intrahepatic and extrahepatic causes of portal hypertension, and those can be presinusoidal or post sinusoidal, and then the intrahepatic causes is the vast majority of what we're dealing with, so 95% of cases. So how does IR play a role? So we are really a key factor, but it's a multidisciplinary team that manages these patients. Usually gastroenterology, hepatology is involved. Surgery, this may be transplant surgery depending on the patient. It may be oncology, but we are really not out there alone, but we do have a lot of things that we can offer these patients. So if you kind of think about it, there's the TIPS, there's the RTOs, the ATOs, and then Denver shunt, and also stent placement. So TIPS, we all know what this is, but it's kind of fun to think back as to where it originally happened, right? So this came from, the whole idea came from an inadvertent puncture of the portal branch during a transhepatic cholangiogram in the 1960s. It has clearly evolved a ton, and now we're placing these new controlled expansion stent grafts. So you see you have kind of the two centimeters of uncovered, and we now can dilate up that stent to the desired eight to ten. So what are the indications? We kind of touched on this before. This is a lovely endoscopic image showing blood in the stomach, a varicea in the red whale sign, right? So those nice little red dots, something I never hope I ever have to see as an IR, because I don't want to be scoping them. But these patients come to us when they have acute variceal bleeding that is not able to be treated endoscopically. So these are going to be your patients that are crashing, coming into the IR suite. There's also evidence to support early TIPS for patients that are at high risk of re-bleeding, and the re-bleeding risk can be as high as 50 to 60 percent in these patients. And then for patients with refractory ascites who failed medical therapy. So important when you're thinking about TIPS, if you're seeing these patients electively, how do you work them up? So you're going to want pre-procedural imaging. This should include cross-sectional imaging with CT or MR, plus or minus ultrasound. Sometimes if you have a question, need to evaluate flow, you may want the ultrasound as well. A clinic visit is really key because you need to discuss the risks and benefits and figure out, A, you know, are they a good candidate? And B, is this something that they want, right? A lot of these patients are going to be on medications for life, lactulose afterwards, and you need to really kind of have a sense, they have to understand what they're walking into. And then do they need a pre-op anesthesia evaluation? We suggest an echo in anyone that has a cardiac history or is elderly because you're going to be increasing the blood flow to the right heart, and you want to make sure that you're not putting someone in a situation where you're trying to help them and actually making something else worse. So contraindications, absolute contraindications, severe elevated right heart pressure, pulmonary hypertension, CHF, severe encephalopathy. We used to shy away from encephalopathy a little bit more, and we're now a little bit better at treating it medically, so it's no longer kind of a concrete, you can never do a TIPS on someone with a history of encephalopathy, but it's something you really need to kind of dig into. Uncorrectable bleeding diathesis, active infection, obviously you don't want to place a stent in someone with active infection, and unrelieved biliary obstruction because you're going to end up going through that. So moving on, we're going to kind of fly through these because there are a bunch of different options, the RTOs. So these are your BRTO, your C, your CARTO, and your PARTO. So BRTO is your original balloon occlusion, occluded retrograde transvenous obliteration, where an occlusion balloon was placed in the gastroenal shunt and sclerosin injected. Then a prolonged balloon occlusion, hours, sometimes 24 hours with patient monitored in the ICU, was performed to allow for the sclerosin to kind of seal off those varices, and then you take the balloon down and don't leave anything, right? So as you can imagine, you can't just inject the sclerosin and then let it fly into the systemic venous circulation. This has largely been kind of gone out of favor with CARTO and PARTO, where it's a very similar procedure, but you're using coils to assist or plugs to assist that outflow so that you are no longer having to leave that balloon and monitor the patient for hours. So indications, bleeding gastric or ectopic varices. This is an alternate treatment to TIPS, and in some ways you can think of it as less invasive because it's a venous access, but you still have to remember you're dealing with varices, which can be very fragile, and the patient needs to have favorable anatomy. So they have to have a gastro renal shunt that you can catheterize. Contraindications, sepsis, splenic vein or portal vein thrombosis. If you all of a sudden are occluding their only outflow, you can really put that patient into a lot of issues and have them have uncontrolled portal hypertension or bleeding elsewhere. Uncontrollable esophageal variceal bleeding, this really is not going to treat that. Lack of a catheterizable shunt, or a large volume of ascites is kind of a relative contraindication, but these patients may need a sequential TIPS to manage because as you can imagine if you're shutting down the shunt, you're increasing the flow to the liver and may actually worsen their underlying portal hypertension. So considerations, high MELD is not a contraindication like TIPS. You're going to increase the portal flow to the liver, which can increase your portal hypertension. Close follow-up is necessary. They need endoscopic evaluation because they may develop varices due to this worsening portal hypertension, and they may need subsequent TIPS as definitive treatment. So the ATOS, or antegrade obliteration of varices. So access is key for this. This can be done in multiple different ways. It can be percutaneous, that can be trans-splenic, trans-hepatic, or don't forget to look for those nice juicy umbilical veins that can kind of dump you right into the portal system and be a great conduit to get in there and embolize. You can also do this trans-jugular, I like to say TIPS style, without leaving a TIPS, right? So you perform it just the way you would a TIPS, but you don't necessarily have to leave it. So indications, this can treat esophageal gastric or ectopic varices. You can do large afferent shunts and high flow varices, and this can be done alone or in conjunction with TIPS. This is good for gastrofemundal varices without a gastro-renal shunt. You can actually get to them. And it's also something you can consider in a patient with a high MELD that's actively bleeding but is not a transplant candidate yet, but maybe in the future to kind of temporize them to see if you can get them onto that transplant list. But that should definitely be a multidisciplinary discussion, not something you're going off on your own. So considerations, again, you're going to increase portal flow through the liver by shutting down the shunt, right? So this is when you do it kind of solo without placing a TIPS. So you may want to leave that TIPS or do a sequential TIPS. And again, high MELD is not a contraindication. Contraindication to sepsis, portal vader splenic vein thrombosis precluding your access to the varices, and coagulopathy. So Denver shunts. So this is a radiograph of a Denver shunt. This is a peritoneal venous shunt that's used to treat complications of portal hypertension, so really ascites. This does not treat the underlying portal hypertension, but is a good option for patients with large volume ascites that are not a transplant or a TIPS candidate. This can be done percutaneously or placed surgically, and kind of institutionally depends on the practice there. But it's good to be aware of that this is something that IRs can offer to their patients and can manage. Contraindications are coagulopathy, SBP, or active infection. Obviously, you don't want to be shunting this peritoneal fluid into the blood system if it's actively infected. End-stage renal disease on dialysis, hemorrhagic ascites, or prior abdominal surgery with adhesions and septations, you're going to have a really difficult time kind of actually actively draining that ascites. And morbid obesity, as this becomes very difficult not only to place it, but the patient actually has to physically push that pump against their rib cage in order to pump the ascites. And if they can't feel that and can't palpate it, they're going to be unable to actually do that. So finally, portal vein and splenic vein stents. This isn't something that we always think about when we're thinking about portal hypertension interventions, but I think it's something that it's really important because we can actually make a big difference and really help a lot of these patients. So this is indicated for treatment of portal hypertension due to obstruction of the inflow. So again, we already kind of touched on the synestral portal hypertension or left-sided portal hypertension. But this is usually due to obstruction of the splenic vein and can often be related to pancreatic pathology. The causes can be benign. So it can be pancreatitis, as I mentioned. It can be appendicitis that's causing collections and then compression or post-surgical adhesions, but can also be malignant. Your access, again, it's going to depend on where your occlusion is and where you want to place the stent. But it can be transsplenic, transhepatic, again, through the umbilical vein, although be careful with that if you want to make sure that your stent will actually track where you want to go. Or transjugular is another great option for this. So consideration, you want to think about where you're placing the stent. So the location of the stenosis, you want to make sure that you're going to have enough inline flow so that the stent will actually stay open. Closure of your access is really important kind of with any of our percutaneous portal hypertension interventions. You want to think about getting sufficient hemostasis. A lot of these patients are somewhat coagulopathic, so you can see this is an ultrasound and then radiograph of a plug being placed in a transhepatic access. And then when you're stenting these patients, do they need anticoagulation posts to keep that stent open? So in conclusion, portal hypertension can cause significant morbidity and mortality. A multidisciplinary team is key to the management of these patients, but IR has a lot of options for interventions, and you can really individualize your care based on patient presentation, clinical status, and imaging. Thank you. We're going to talk about some advances in tips and dips in access and guidance. The post-procedural management, we'll touch on, but it's not going to be as big of a focus just because some of it's being covered by some of my other colleagues today. So looking at this talk, really what we're going to get into is looking at some indirect portal data and access techniques, looking at some of the direct portal data and access techniques, some closure techniques, and then finally, some technical tips and some of the data along the way. Now, I put this first slide up because if you look at what we're looking at in 2024 on access techniques and decision-making, what it comes down to is there's a lot of ways to do this, and there's a lot of ways that are very safe to do this. I would pick what you're comfortable with and stick with that. And there are a lot of really good references looking at this. In the next eight to 10 minutes, we're not going to cover everything. But the one piece of it that I would say is this table probably covers 99% of the things you need to know to basically do any tips from beginning to end. So the other question that people always ask me is kind of what's in my toolbox. This is what I have my technologists prep and know so that these are the pieces of equipment that we have available in the event that we're going anything from basic to advanced for some of these procedures. And as the prior speaker alluded to, get good imaging. If you look at what our colleagues are recommending for us, many of our friends in oncology, hepatology, they're still living in an era where they think that an ultrasound is enough for us in the era of 2024 tips imaging. I tell everybody they should get an ultrasound. They should also get a triple phase contrast enhanced CT. And so how do I approach cases when I'm doing this? I plan and I have a backup plan. I like to get the neck prepped and a full abdominal prep. Obviously, we're going to get right internal jugular access, transvisceral access if it's needed. And if we're planning to use ice or some of the IVUS imaging guidance, I'll either get a second right IJ access or femoral access. And ultimately, you need to have an exit strategy, particularly if you're going to be using transvisceral access techniques. So if you look at this first case, really what you want to start with is the basics. And that's by knowing the vein. And so I always show this case anytime I give tips talks, particularly to my residents. And this is a nice axial coronal MRI image showing your right middle and left hepatic vein. And the piece of it that I like to point out is that the middle and the right can look eerily similar to each other. And so before I even start the tips, most of the patients that we get referred in from some of my colleagues from other centers, oftentimes for whatever reason, because of visualization or whatever, ultimately, the reason that the tips was unsuccessful is they never realized they were either in the middle hepatic vein, and they thought they were in the right, or they were in the right hepatic vein, and they thought they were in the middle. So ultrasound or a good lateral image can oftentimes really help you out with this. You can see the amplot's wire there in the right hepatic vein. The lateral image, you can see that image with the catheter going posteriorly. From there, we'll go to indirect portography, where you have a wedged catheter placed in the hepatic vein. And you can use the other dilute CO2, or sorry, dilute iodinated contrast, or CO2, to get a nice image of the portal vein. This is kind of an indirect or non-invasive technique. I like to do this in both the AP and the RAO view, so that you know what you're targeting, and you can triangulate to where you need to be. We get access into the portal vein, and then you measure your stent diameter and length, and then finally, you're going to leave your tips behind. So what's the key point from the case? Number one, understanding the hepatic vein anatomy is absolutely critical to these cases. Portography is still a very powerful tool, even in the age of ice. And if you're going to do it, you want to be making sure you're doing a gentle injection, so you don't get capsular rupture along the way. So now looking at the next case, this is a 55-year-old diminutive right lobe and right hepatic vein. We've been asked to do a shunt on this patient. Here, you can see on that left image from that groin, we have an ice catheter coming up. And then on the right video, you can see the needle going directly from the hepatic vein right into the portal vein. So the advantage of ice is, obviously, you get very beautiful imaging. This is on the first puncture. You can see that we immediately have access into the portal vein. We're measuring our stent and then leaving the stent behind to create the tips. So when you look at ice, obviously, a lot of people talk about this. There is an increasing amount of data being presented for the advantages of using ice for tips and complicated tips patients. I will say at BI, while this is a tool that I use, it's probably not the thing that I use most often. Lots of data to support reduced fluoroscopy time. There's a suggestion of decreased capsular punctures with utilizing this technique. There are still questions. Do you need a second operator for many of these cases? What's the cost? Is it worth it? And ultimately, is it affecting the clinical outcome by implementing something like intracardiac echo in these patients? The other thing that I like to point out is there are studies out of Asia demonstrating that you have pretty similar results using transudominal ultrasound, where you have a second operator using transudominal ultrasound to guide the needle puncture of your primary operator. So moving through, this is a third case. This is a 65-year-old with cirrhosis, portal vein thrombosis, who's being evaluated for transplant. In this case, you have an axial and a coronal image showing complete occlusion at the main portal vein confluence, large coronary vein there, pointed out, with cavernous transformation. So what we're going to look at here is how are you going to access into the thrombosis system? And this is really where you get into some of these transvisceral access techniques. Depending on your imaging, we usually prefer either a splenic vein or a transhepatic access to the portal vein system. At BI, what I usually prefer is a splenic access. I find that this works quite well. And so I use a 21-gauge needle, which you can see on the left, to get right into the splenic vein. I use an 018 wire to get across the vein, across the needle into the vein. And then before upsizing anything, I actually just use the inner portion of an acustic to make sure I actually have vascular access. Once that's done, we go ahead and dilate to a six-french sheath and get a nice portogram. And then we can use that to do the work you need to do to ultimately create your tips. So in this case, we crossed over through the occluded segment of the portal vein. And the teaching point here, because this is talking about access techniques, is you can either use a balloon or a snare at this point to really give you easy access into the portal system from your right internal jugular access. So we targeted the balloon. You can see the balloon rupturing, got through and through access, and ultimately left tip spine for this patient. So when you look at transvisceral access, transplenic and transhepatic access are both pretty well studied at this point. Very similar safety profiles. The real key point, though, is if you're going to do this, you need to have an exit strategy so that you know what you're doing. And you can keep the patient nice and safe. For certain cases, I'll only use a 21-gauge needle and an 0.8-inch wire, and that's enough. For other cases, you're going to need to dilate to a seven-french sheath. So I like to use track closure with gel foam pledges. I clamp the sheath and use those rolled pledges, where I'm cutting the strips of gel foam very thin, rolling them right on my hand. I clamp the sheath, and then what you, oops, sorry about that, so once the sheath is clamped, what you can see is I'm just loading gel foam pledges right into that clamped sheath, using that dilator as a pusher to load the sheath completely. Once I feel that that's adequate, I'll ultimately just push the gel foam out using the pusher until I see that amplot swire right about at the level of the rib cage. And you'll see that coming into focus right about now. And then I essentially just unsheath the pledges like a filter. And then on that right image, you can see the gel foam tracked on the spleen. And so again, when you're looking at track closure, multiple published techniques are out there. 205 patients, 105 with gel foam, 54 microcoils. They all work. Pick a one that works for you and get good at it. That's my advice for you. So final case we're going to show you, this is a 56-year-old male, atherosclerosis, portal pulmonary syndrome, utilizing transplenic access to get into that thrombosed vein. We got a nice portogram here. And now because of the difficulties in access, we have a snare in the right hepatic vein, snare in the portal vein. And you can see that we're using a 20-gauge Chiba needle to cross through the snares and ultimately get through and through access. Once the through and through access is obtained, then you can ultimately leave your tips behind and do whatever work that you're ultimately going to need to do. So this is a nice example of the gun sight technique. This is percutaneous access through the target in the portal in the hepatic vein to overcome challenging access scenarios. This is a nice tool to have in your toolbox. There are several studies on this being published out there. I would warn you that some of the recent studies that have shown some concern for bleeding complications with this. So you want to make sure you have an exit strategy if you're going to be doing this. So in conclusion, what I would say is good cross-sectional imaging is going to guide your plan and your decision-making strategies when it comes to these tips procedures. If you're going to plan trans-visceral access, you absolutely need a closure strategy. And ultimately, what I would say is alternatives to indirect portography are essential as you get into some of the more advanced techniques. Thank you very much. Yep. Management of portacist epistemic shots, everything but tips. And so a little bit, there's going to be a little bit of overlap between what Claire spoke about earlier. So again, not to belabor this just to keep us on time a little bit, we sort of went over the sort of the causes of portal hypertension. The point of this slide really is to make sure that your whatever intervention you're going to do sort of fits what the patient needs. So don't do embolization for patients with SIDs and or pain when they eat. We talked a little bit about this, about the balloon occluded retrograde transvenous obliteration. And as Claire spoke about earlier, you know, can make your esophageal varices worse, but can make your encephalopathy better. This is sort of our way of doing it. We like to put in a 10 French tip sheet up from the groin into the shunt and get into the shunt that way. And then what we like to do is use if we can, we use one of those neuro balloon occlusion sheets, which allows us to then occlude the shunt and then give us gives us a six French channel to work through so we can go up through that. We can put coils and plugs through there. There are different ways of doing it. Some people will put the plug first and then work next to the plug and holding it in place and then do the embolization. We tend to just use the balloon, go up, inject the foam, sclerose the veins, and then just sort of coil or plug on our on our way out. This patient happened to get a CT scan afterwards. We don't typically get a CT scan afterwards, but you can see the the foam in the varices and everything looks good. You can also do it for ectopic varices. I'll be honest, it doesn't come up very often. It's sort of like one or two cases that we've seen as a patient with duodenal varices. It was misdiagnosed as a duodenal AVM and they started poking at it and made it bleed. It was actually varices, duodenal varices. We were actually able to get into sort of the right gonadal vein, put in a balloon from above, inject foam and then sort of plug our way plug our way out. You can do an integrated as well. We call it balloon occlusion, but it doesn't actually we don't really use a balloon that often. You can do it for gastric, small bowel varices, rectal varices and stomal varices and was actually originally described for esophageal varices, although we don't really do it that often for esophageal varices. This is a patient with rectal varices again, typically for these, just because the angle is easier, will come from a trans-hepatic approach. You can see a huge IMV going down and then going into this sort of nest of rectal varices. Typically, we'll put a balloon Fogarty. We've done this in different ways. We put a plug in and snuck past the plug just depends on the size of the IMV. We'll inject foam. We tend to use a Tessari method of making the foam. We'll tend also to mix it with lipidol just to make it a little bit more viscous. I don't know if it works better or not, but that sort of just helps us make it a little bit more viscous and you sort of inject the foam that way. So this is actually probably the more interesting part of the talk. So in patients with really complex porta-mesenceric occlusion, PVR tips is not always feasible or may not be advisable. The length of occlusion may be too long. So typically, we'll try to get the best or most robust amount of inflow, which would typically be the splenic vein. But especially if the splenic vein is really thrombosed or occluded too far into the splenic hilum, that may not necessarily be a feasible option. Patients who had previous splenectomy, obviously can't use that as an inflow. Transplant, the anatomy is a little bit messed up, especially in people who've had isolated left lobe liver transplant. You can't necessarily reconstruct and do a tips. It's not necessarily always as advisable. There are surgical options, but they are limited. There's a SIGURA procedure. There's not a lot of people that do them and do them well. But it does still, even in the patient, people who do them, they still portends a significant morbidity. It's really only used to treat left-sided portal hypertension, so esophageal or gastric varices. It will not work for ascites or ectopic varices if they have rectal varices or varices in the small bowel. Surgical shunt, obviously carries significant morbidity and mortality. It also may not be feasible. They really need to tie to the main SMV. Sometimes they can do an enlarged ileocolic vein, but that's really tricky and they don't like doing it. So that's really where they're at. And then last but not least is the multivisceral transplant. It obviously carries a very significant morbidity and mortality, up towards a 50% at two years. It's also difficulty, there's difficulty in posting these patients, because a lot of these patients, their livers are normal. They have a plumbing problem, not a liver problem. And so they have to get posted like a liver. And if their liver function is normal, it's hard to get them in appropriate points and score to get them. So they typically have to wait to a point where they are so sick that their liver is failing. And then they're really too sick for a multivisceral at that point. So percutaneous mesenchymal shunts were first described by Nyman et al to the Stanford group back in 1996. They used a combination of CT and fluoro to create a connection between the main trunk of the SMV and the IVC. This is not always feasible in every patient, because you may not have a main trunk of an SMV, or the target vein may be too small. Also, sometimes the target mesenteric vein and the IVC don't line up. And there also may be structures in the way, so bowel, artery, and pancreas. You don't want to go through the pancreas. So how we do this, we do them all, obviously, under GA. We have to have the devices ready to go. So we sort of pre-plan what stents we want, so we don't want to leave the hole that we create when we balloon open that tract open for too long, so we're ready to move and get everything going. So covered stents, snares, wires, we typically will have arterial access, one, to help decrease anesthesia time, so they can use that as an A-line. Also, we can do our imaging through that as well. Balloons, but really balloon only as big as you need for the covered stent. You want to keep the stent as short as possible, so you don't want super long shunts dragged way up into the IVC. And what we tend to do is bridge them with self-expanding stents to help anchor them, because your mesentery is going to move up and down, your IVC is going to be fixed, we sort of fear that the stent is going to ratchet itself out. So this is a case from about two years ago, a 21-year-old girl, OLT, for biliary atresia 20 years prior, extropatic vein, portal vein occlusion, Roo varices. She'd gone through, actually, multiple different interventions in trying to manage this through either BATO, which didn't really work, because those varices were actually feeding her portal veins, because it was around the Roo, and then even tried a bear claw at some point, and that also didn't work and just actually made things a lot worse. So her liver functions normal, they don't really have a good shunt, a surgical option for her. They'd actually ligated her IVC during the transplant. So we said it does theoretically line up to where the IVC should be, so we reconstructed the IVC first, and then basically our plan was to use the coronary vein as the conduit to connect the mesenteric system. We come transplenic. Again, I tend to keep everything small here. We didn't actually put a sheath in, we just use the Accu-Stick. It's a four French sheath, so we'll just go right through the Accu-Stick. We'll put a four French Glycath up into the coronary vein, which a 10 millimeter loop snare will fit through. So we'll put the 10 millimeter loop snare through that, line it up, go right through, we sort of gunslide our way right through those two. So again, just don't really care what's in between the needle, the abdominal wall, and our gunslide, but we care about what's between the two snares, so we just sort of go bombs away with that. Snare wires out, cross, balloon, measure our lengths. I don't know if it projects very well here, but you can see basically a VBX to bridge the gap, and then sort of another small self-expanding stent to anchor it. This is actually just to show you what her SMA angiogram looked like before. You don't really see anything going through. You can see things going through collaterals. Hopefully this will play. Yep, there we go. This is the SMA angiogram immediately post-procedure, showing brisk flow through the shunt. And this is just the end of the splenic angiogram, again, showing the splenic veins not jailed out as well. We do an ultrasound follow-up. Usually, this is actually about six months post. You can see it very clearly on the ultrasound. Everything's open. She's doing well. She's actually, we stopped the DOAC because she doesn't really have a hypercoagulable problem, but she's about two years out and doing well. I'm not going to go through this, but basically a 30-year old Jehovah's Witness, bad porta mesenteric thrombosis. People at an outside hospital tried to do some stuff, didn't really work. They did a partial splenic embolization, which sort of jailed us out a little bit. She had bad porta mesenteric occlusion here. And then basically, because of VIRTRAC2, she needs to be on anticoagulation, but she has bleeding duodenal varices. She couldn't even tolerate aspirin when she came to us. She would continue to bleed. And so we tried some things. It didn't really work. So we're like, OK, let's try to do this here. So this is the SMA angiogram showing the flow. So again, part of the reason for doing this as well is to see which direction the flow is going in. You want to make sure that your shunt is pointing in the right direction. But this is the vein we're going to use right here. And this is the line from the jugular vein over here. So again, this is a triple loop snare from the IVC side. This is the vein we're going to use. Luckily, she was actually fairly thin, so we were able to just use transabdominal ultrasound. So we find the SMV branch that we want, turn the ultrasound until we see the IVC snare, and then just poke a needle through both using a 20-gauge NRAD needle. We used an 018 Glidewear Advantage, pulled it out, snared it through and through axis. Ultimately, we were able to then reverse that, push a 4-French glide cap into the mesenteric vein here. This is just a rosin jammed up into the mesenteric vein. This is a 7-French sheath from above, then the VBX to cross the gap, and then a self-expanding stent to keep everything from ratcheting out later on. And this is the SMA angiogram post. And you can see there's flow now going through the shunt. Sorry. And this is an ultrasound. She's actually two years post as well, because they actually happened about a week apart. And she's doing well, tolerating full-dose AC. I'm going to go through this case just to show you another example, basically bad porta-mesenteric occlusion. Here, what we did is we actually found a vein to stick percutaneously. We couldn't see this vein under ultrasound, so we found a smaller vein that we could stick and use that to image to line everything up. And again, did the music cable shunt this way. I'm going to skip this. So anyways, she's actually 11 years out. So she's actually done considerably well. The pain in our experience has been quite good with these, considering we're really not tying named mesenteric veins to the IVC. And our patients have done well. So in conclusion, I think patients with appropriate selection, you can use various techniques to use percutaneous music cable shunts can be recreated. I think the shunts can be recreated two collateral veins, the ones that typically wouldn't be justifiable for a surgical shunt. You just got to make sure they're large enough and have a long enough runway to land the stents appropriately. Again, our patency has been good. And I think for symptomatic, for patients with bleeding symptoms, shunts may not always be necessary. You can sometimes get away with a BRTO and a BATO. Thanks.

portal hypertension

causes

clinical management

interventional procedures

liver cirrhosis

variceal bleeding

TIPS

multidisciplinary approach