HCC with arterioportal Shunt|TACE |68|Male
HCC with arterioportal Shunt|TACE |68|Male
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This is a good case of mine,

hes' a 68 year old male. He has alcohol cirrhosis and esophageal varices, he's not a prisoner. But he doesn't speak English, so just putting that out there. He's a child Pugh A5, he had a total bilirubin of 0.7 his AFP was 43

so not indicative, and his ECOG was 0-1 when he saw me for the first time in clinic and this is what his initial CT scan showed, to from my clinic, he had not been followed up appropriately and just came in with a belly ache and they noted this very large mast in his right hepatic lobe.

Further down you can see that the tumor extends more inferiority and you are getting a very avid enhancement of the portal vein and you can see there's some portal vein thrombosis in there. So the arrow is really pointing at what I was reading as an arterial portal shunt. So knowing that this is what you are going to face ahead of time

sort of can help you plan. So arterial portal shunting diagnosis can very often be made on multiphasic CT scans so you know I'm sure you all get those patients that come from an outside hospital with HCC diagnosis and they have one phase of imaging so it's really important to get that multi phase imaging

CT or MRI because you can make these diagnosis. So this group showed that about 15% of patients can be or actually have this and the diagnosis can be made on CT scan and then they just talked about where these arterial portal shunts are about half of them essential or 24 from a peripheral and then 22 of them are mix. So you can't really tell if they're central or peripheral on the CT

imaging. And then how severe are they, 35% are severe. Severe means that on that arterial phase imaging your portal vein is as bright as your aorta. And 41 or about moderate which is you know.

You can imagine what moderate is and then 24 are mild so you just saying it's within the peripheral areas. Interestingly about half of these patients that do have arterial portal shunting also have portal vein thrombus so even if you just have single phase image and you have portal vein thrombus you can sort of start thinking in your head that these patients may have an arterial portal shunt and they actually

went on to get hepatic and angiography, 22 of these patients went on to get hepatic and angiography and of those patients 86% had arterial portal shunting the author said that they probably all had it they just missed it on angiography. So what's the prevalence really there is not a lot of great data on there you see I went all the way back to 97 to see if I could

actually get a prevalence but overall arterial venous shunting. They said it was about 31%. If you had arterial portal shunting or arterial venous shunting of that, 31% of patients that HCC 92% had arterial portal shunting. So what's the treatment?

So as you can imagine we've all come up with creative things we've been at this meeting all week. And, you go into a room and you can imagine everyone's doing these different things. So, if you can find a single feeding vessel, a coil is a great choice

if you can find it. Glue, if you have a network of vessels and you don't think that glue is gonna get stuck proximally to prevent you from treating the tumor eventually. And particle embolization is a good option. You can use large particles if they don't cross over into the shunting

I had a patient that had a large, we'll get to them in a minute, but it was a very bad complication from outside the hospital. And the other thing is you can try lipidol based embolization and that's not well supported in literature but there are case reports talking about it.

So for my treatment planning, because he had portal vein thrombosis I decided that I was gonna go ahead and do a 190 based on the literature. And so, he showed up to the suites and we had planned for the shunt study. So the initial angiography you can see,

as soon as I'm seeing the arterial phase of imaging. And this is seconds after the injector goes. you can see filling that portal vein, the main portal vein.

And you can see, the filling defect within the main portal vein indicating that he had portal vein thrombus. So, this severe arterial portal shunting was noted. I couldn't find a single vessel, it's just this huge network of vessels that was supplying or communicating with

the portal vein I didn't think I could do glue because I was worried that the glue would embolize the proximal artery and I'll never be able to go back in treat it, and because the tumor was in the right hepatic lobe I just wanted to see is there, I have

had a pulmonary shunt as well as the ulterior portal shunt and so I went ahead and infused the MIA. The lung shunt fraction as is very typical was 20%. And so that brings us to hepatopulmonary shunting. How common is this?

Is it a prevalence of overall again arterial venous shunting is 31% and of those hepatopulmonary shunting is much less so it's 8% of those patients. And all patients with HCC they say the prevalence is about 2.4%. Again in my clinic it's probably much higher than that. So the typical shunting in HCC this is Ron Gaver's/g group who talked

about what's the prevalence based on lung shunt fractions they said about 56% of patients are gonna have no lung shunt fractions to less than 10%. 10 to 20% of lung shunt fraction you got 30% of patients with HCC and those higher lung shunt fractions are going to be 14% of your patients that you are treating.

So they also found that there is correlations how can you sort of predict this on imaging sometimes you can't see this hepatic pulmonary shunts on imaging so if you do have an infiltrate of tumor that was correlated with hepatic pulmonary shunting if you had greater than 50% hepatic tumor burden, if you had portal vein thrombosis or

portal vein compression so the tumor is actually pushing on the portal vein you are going to see a higher degree of hepatic pulmonary shunting. If you have arterial portal shunting that's interesting that also correlated with the hepatopulmonary shunting. And if your tumors are hypervascular,

all tumors are hypervascular so that's not gonna be very helpful again how do you treat this? So embolization again if you can see that single feeding vessel that's fantastic and you can do it again glue is possible particle and hepato-based embolization is also then reported. Systemic therapy with Sorafenib has some literature saying that

if you start patients on Sorafenib you can reduce the shunting, this is the case serious with couple of patients, that they showed that the mean shunt fraction in the patients was 26.5 prior to starting Sorafenib therapy, and post sorafenib therapy, went down

to 7.5. But again the time it takes to treat patients with Sorafenib to get those shunts to come down sometimes can be longer than the patient would survive otherwise. And what about if we do the Y90 what if we,

go ahead and do Y90 therapy is there real risk of radiation pneumonitis? So this is out rehabs group and he found that of his 403 patients now these are patients not only with a HCC but all comers 58 of those patients or 14% actually received greater than three gray accumulative lung dose and of those just so I wanted to highlight that HCC population

74% of those patients with those elevated or high lung shunt fractions were actually patients with HCC with sort of a similar to the data that I showed you earlier. And the mean shunt fraction in the HCC patients was 20% and the mean accumulative

of lung dose is 54 Gy to those patients and his report he had no cases of imaging or clinical real issue of pneumonitis. And so you can quote that to your patients that you know a very large series has shown that there's no risk of having any risk issues with the lungs other patients or other series have sort of talked about may be having radiation pneumonitis.

So really the things to consider when I was treating this patient are you have severe arterial portal shunting on the angiogram because we're seeing filling of that main portal vein and now he's also has a hepatic pulmonary shunt which is almost 20% and so do I go on to do Y90? With an arterial portal shunt you have to really think about where

the beads are gonna go so if they cross over into the main portal vein, where are they gonna lodge? So they are gonna lodge any where in the liver and we have started to do or what I've started to do is if you see these large arterial portal shunts you can do CT spect with your MAA and then you can see where the bead is gonna go because that really is a good indicator.

I had a patient a couple of weeks ago that we did that and it actually shunted to the contralateral lobe, so I felt why don't we just treat the whole liver except all of the beads would have got the contralateral lobe not the lobe where the tumor was. So I would have had an effective dose and I would have just cause atrophy of the wrong lobe of the liver.

So that sort of a trick you can think about. With hepatic pulmonary shunting you have to think about can I get a dose high enough to effectively treat the liver without having it just bypass around and go into lungs. And so if that's the case, do I have to worry about this cummulative/g

lung dose? Do I, do I not or can I do some sort of fancy technique in the end of my hepatic vein and do an occlusion during my Y90 administration to get those beads to lodge in, take out the balloon afterwards get an effective treatment.

And really, is it affectatious, do I go ahead and treat and is this gonna affect these patients, appropriately? So again, here's the image this huge tumor. Here's the shunt.

Here's my hepatopulmonary shunt. So, I'll bring my first team question up. [BLANK_AUDIO] So given the clinical and imaging characteristics below, how would you treat the tumor?

Anyone change the words from a monograph. So a, systemic chemotherapy, percutaneous ablation, c, full dose radioembolization d, conventional chemoembolization or e, reduced dose radioembolization.

[BLANK_AUDIO] Good answers. I love it. [LAUGH] I don't think there's a right answer. I chose the answer D,

conventional chemoembolization, and if we can go back to my slide. I said it was incorrect. You can do Sorafenib and I don't think that's the wrong answer it's just a matter of how long are you willing to wait and how often are you gonna re-image these patients to try to shut down their

shunts again. The studies showed that their follow up was up to 270 days, that's almost a year that the patients need to out to be able to get these shunts to shut down. You're never gonna ablate a tumor like this.

It's too big. C. I said is incorrect because the Y90 is gonna disperse throughout the entire liver unless of course you do that spect imaging and then you can sort of determine that it's really gonna go to where you want it to go. So I said I probably wouldn't just go ahead and treat the whole

liver if the patient's is cirrhotic. In the patient that has liver metastasis since they may be willing to or able to tolerate it just depending on how bad your patient's overall liver function is. I thought D was the correct choice,

patient is candidate for conventional chemoembolization. Cuz it really provides treatment while potentially reducing the shunts and allowing the future radioembolization. The other thing I like about lipidal based chemoembolization is you can see it.

So the shunts crosses over, you can see where it's going, so you know if it's going only to the left at the time we can see if it's going only to the right if you're not doing your pre Y90 ahead of time instead of beads where you sort of can't see where they're going and don't really have a good handle on it at the time.

And then C, they've talked about in a literature doing a load of stuff that guys at Stanford published trying to decrease your dosing when you do Y90 and they actually show that it had decreased efficacy of treatment. So that's probably not the best choice according to the literature that we have now.

So I went ahead and I proceeded with TACE I did the lipiodol based TACE. We don't have any support in Wisconsin I think that's probably universal in the United States these days. So I used Doxorubicin and mitomycin I mix my lipiodol thicker so it would get stuck into those blood

vessels so it would trap it so it wouldn't cross over into the portal veins so I did a two to one and sometimes I'll even do a three to one just to get that lipiodol thicken and sludging in instead of just crossing over into the portal vein,

and now embolized into the back end with 3 to 5 PVA. So this is what my angio looked like at the end. It was sort of shocking that we had shut down that shunt with the lipiodol based TACE. We always get CT scans the day following.

I would show you the picture but really, you can't appreciate where the lipiodol is because it's so defused throughout the entire liver, I thought this is never gonna work. I called the medical oncologist and I said can we start the Sorafenib?

And I told the patient and his family I didn't have very good hope that this was going to work but we were gonna try to take care of him. On follow up imaging about a month later, this is what it looked like so you can see that that huge mass is gone,

I thought I had the wrong patient. Study pulled up and then, did you scan the wrong patient? I looked at the other anatomical structures, those were his kidneys,

no, this is this guy. It really melted away that tumor. You can see some residual lipiodol there and he did have a residual viable tumor that you could see. His portal vein thrombus had melted away so that was no longer there and on the arterial phase imaging there was no longer any appreciable

or arterial coral shunting. So we decided why don't we go ahead and repeat the shunt study and see what's happened to the hepatopulmonary shunt and see if that was also effectively treated. This is the second study. I took these pictures and I told my fellow this was the most traumatic

case that I had ever seen in my life and everyone should go back and look at the pre-images because I've never seen this that you have zero arterial portal shunting after one session of TACE, is a very dramatic change in his imaging. I did a CT spin just to

see if I could figure out the distribution of was there anything going to that left hepatic lobe you can see this is residual viable tumor enhancing here and nothing is going to that left hepatic lobe again we did hepato pulmonary, a lung shunt fraction calculations and

it came down to 7.4%. We went on to do a Y90 radio embolization of the right hepatic artery and on seven month follow up the patient is disease free, he has no residual viable tumor he has no portal vein thrombus and he tells me that he prayed and I told him to tell me to whom he prayed

cuz I wanna give that to all of my other patients.

So basically this is a 32-year-old male with Budd-Chiari syndrome,

in the setting of idiopathic hypercoagulable state. He's had a four variceal bleeds with EGD and banding each time. He also is on has refractory ascites and is on numerous diuretics. So here is a CT scan again showing the ascites here is thrombus within the main portal vein,

here is a little bit of contrast coming through coming up and then the left portal venous patent, the right is thrombosed. And there's actually a spontaneous portal vein to hepatic vein fistula here, a connection and the hepatic vein on the left comes back

and it connects up with this system here. Which drains down in to the IVC. So here are some chronic reconstruction showing this big this is how the hepatic veins sort of this is a venogram injected here showing the flow. So basically we were thinking what's the best way to decompress

this system again here is the thrombosed portal vein. We thought there is a pretty nice after examining all the different potential ways to go, percutenous approach here if we could just come from just the right up mid line here, we come down through

the portal vein into the IVC, that can give us a pretty nice outlet. One thing to be a little weary of and careful is, this is the hepatic artery here, so obviously that's something we want to avoid. We did the trans-splenic approach as we had discussed,

and this is our splenic venography showing the main portal vein here. This is a little deceptive because the thrombus is sort of an AP projection, so this is a very thin venogram here. And then going into the left portal vein the right portal vein as you can see is occluded.

And here it's just a lot of variceals this a later phase of the same run. Showing all these gastric variceals. Getting the catheter up a little further during the run you can see hepatic vein here, and that co relates very well to the emission

here. Prior to all these cases, again I think it's essential to have a really exquisite imaging and that really helps me determine where I'm gonna go, what I'm gonna do and I'm constantly referring back to the CT or the MR, I actually prefer CT,

it helps me see the venous flow a lot better and helps me plan these approaches. So I personally really dig good cross sectional imaging. We're able to use a little sharp needle recanalization, getting from here through this clot.

It wasn't as difficult as we thought it would be, we used the back end of a Benson/g and a 4 French Berenstein catheter, just sort of poked it then, just sort of went, and you can see we're in this right portal

venous clot here, some portal branches and then what we end up doing is placing a loop snare in this area. We have an arteriole catheter here for a couple of reasons. One is we did a celiac axis run and so much to that CT scan this is the hepatic artery that we see right over line like portal vein. So we put a microcatheter out and that is gonna be our no go zone,

so we see under fluoroscopy where to go and then we angle it to about 15-20 degrees and then we align everything up, here is our right portal vein snare. Here is our snare in the IVC, and here is our know go zone with

the artery. And here is our needle percutenously. We just sort of drop down into IVC. And so here is the lateral view. You can see the needle coming down, here is the snare around the

needle we snared it adequately. We got into the IVC again avoiding the hepatic artery. And then passing and 018 wire which we snared, and we we're able to do a series of exchanges, such that we got an 035 wire and catheter

up. And then out through the neck. We reversed the wire cuz we wanted the floppy part of the 035 wire to be in the portal venous system. We took the catheter out. So we just had the wire snared.

And then we pulled the wire and now we have access from the right IJ through the spline. [UNKNOWN] tract and then we place, in this case we decide to place self expanding stents,

not covered. We really didn't know what was gonna happen once we got into the IVC here so we didn't have anything overly occlusive. So we used a number of I think they were 10 by 60 stents, we ended up using three in series.

This is our run showing just a little bit of filling of these gastric varices. This is quite frankly the other trash from the other 018 wires we just sort of left that and excluded that. We got up into the varices and we placed an enhanced plaster here. The main reason we did this is because this was sort of new to us

we didn't know how long this was gonna stay open, and while we were there we felt we would at least take care of the varices. This is our final SMA run, showing brisk flow through this stent. Here's a follow up CT two days later,

here's the proximal part of the stent within the portal coming around and coming into the IVC. As you can see at this point, compared to where it was previously sort of going centrally sort of fell back and was more parallel.

We decided at this time not to really do anything and this is one of the things we thought it would be essential to have an open cell stent here. So this did not occlude fortunately, and didn't really retract any more than this.

In retrospect, maybe putting another stent in there to anchor it a little more going centrally pair would have been essential. So at three weeks and three months, we have follow up ultrasound on this dually/g patent. Here is a follow up MR at 28 months,

so this is the preprocedural CT scan shown in the abundant ascites going on here, no ascites, here is the stent. Here is the ultrasound at that time, widely patent stent, and clinically

the patients been without bleeding so much that they have been resumed on anti-coagulation with Coumadin through their primary care physician for their idiopathic hypercoagulable state and the patient has been off diuretics without recurrent ascites. So he is sort of living a normal life now, as much as he can live

with being on Coumadin any questions? >> That's kind of the amalgamation of three sophisticated techniques you got the the transsplenic technique, you got the dips going through the [UNKNOWN] and then you got the gun sight. So its a very cool case.

>> You add this sort of things on as you go along and then you can just throw them at one bucket, but I think that's why you said it's essential, being here at this talks and going to the different abstract presentations. It really helps build, I was telling Mr. White/g how you can do and how you can put these things together.

>> I think a nice thing also I think we're seeing in all this is the adoption of the splenic technique is you can do all sort of IMV SMV work now from now on. Instead of going transhepatically or whatever malformations or anything else rather than looking for many lapse and stuff it's just another way to get to that system it's pretty easy to get there.

Question? >> [INAUDIBLE] >> Louder. >> [INAUDIBLE] You think that might be easier? >> I have a mixed and probably biased feelings about that. I don't

I don't that. Look, there are some people that are excellent interventionalists that say this is a game changer to use IVIS to do with the TIPS. It's an extra procedure, it's more costs, this, that. I think those that, I think a lot of people,

yeah, I'm not sure. I'm not a big fan. I'll just leave it at that. >> This particular case, the cathet/g was very bulky. I think in a smaller cathet/g that's a great tool to have,

and like you point out can give more of an angled approach to the TIPS. But in this case, this was a huge cathet/g. It was like a left lobe. >> Yeah, absolutely. >> But people are using it

to extend your question, more people are now using it for routine TIPS. So I don't know what your thoughts are. You guys using it for every TIPS now? The big right portal vein?

Are you using IVUS, or? >> No. Not routinely.>> I guess we're all similarly. >> But I mean it's very center specific, the [UNKNOWN] Institute,

from what I understand that IVUS gets open for every case. [BLANK_AUDIO] >> [INAUDIBLE] >> I mean we're sort of restricted by sort of the angle with which we can come in, based on the ribs,

the bile, where the hepatic artery was. Where we're gonna be so we were sort of didn't have that much wiggle room in regards to how we were going to approach this overall to be honest with you. >> [INAUDIBLE] >> I'll just repeat, this,

we haven't been doing that the question is there any concern about ascites with respect to bleeding or other complications doing that on site?. >> So two things one in regards to what we do with the ascites pre-procedure I know he does not tap them, we usually tap them

mainly because it helps our anesthesia patients alot and so they just love the fact we're able to get some of this fluid off. Secondly we have a very low threshold for doing arteriography after some of these cases when we have multiple passes during the routine tips, we wanna go in transsplenic and it's really, it saved us a couple of times and it's a very,

I would, again have a very low threshold for doin arteriography because you will see some subtle bleeds. And often times you really don't even have to treat. I saw a very small pseudo once that I just sort of let go but I knew it was there. And I followed

it very closely and it went away, but there could be an argument to treat some of these as well. But we've had no issues regarding bleeding into the ascites afterwards, so no. >> Yeah, I'm a strong proponent of training the ascites at the time

of the tips and it's for several reasons. When you're making the portal passes the liver is less mobile it can be like bobbing for apples sometimes with a small really trophic cirrhotic liver. The second thing is, that acidic fluid causes a huge amount of radiation

scatter. So you and everybody in the room is getting a lot more scatter and because of that scatter factomy and the additional attenuation by the acidic fluid, it degrades your visualization. So you're needing to use more magnification and there by more radiation

and so on and its like a cycle. So I think you know some people are concerned that you can get post ascites circulatory issues and I think if you're replacing with albumen, for the higher volume taps, we leave in our ascites drain during the TIPS,

that has a big advantage as well, and a big disadvantage. The big advantage is that it's very reliable indicator of capsule perforation. The big disadvantage is that it's a very reliable indicator of capsule

perforation. >> Exactly. >> For me, for my rationale for not draining the ascites is that, it's purely anecdotal by my experience. I'm not sure it's a very well studied parameter in TIPS, pre or

post TIPS placement, but for me it's from experience. And I had a case in the past where we had drain, cuz we used to drain them right after fellowship. And then we drained five litres or so or whatever it was right

out of the belly just to make it easier, less scatter, better visualization. And there was an extra capsular puncture and the patient almost died because we had no intra-abdominal pressure to tampen down the capsular puncture. So we had to pump fluid,

five or six litres later he started to stabilize but he almost died. I know it's an end of one, but I've been doing this for 20 years now, and I like a nice tense belly. And I never thought I'd ever say that but I guess I like-

>> [LAUGH] We knew that about you. [LAUGH] Question. >> So your IVUS [INAUDIBLE] very C-Section [INAUDIBLE] and so it's always hard to get [INAUDIBLE] we don't have that in our institutions [INAUDIBLE] so what if I'm gonna use this from other guideline procedures, on that site. What about [INAUDIBLE]

>> Well, I mean you could go really old school, and I'm aging myself as well but for some of our early cases, we do transhepatically you'd use what clotted blood. One of my fellows on day one didn't realize why I had withdrawn that 20cc of blood to let if clot off,

by the time I was done with my transplant, cuz my case would take six to eight hours to that portal vein reconstruction. It takes six hours so if you just have some blood it will be clotted by the time you're done. I was looking for my blood and discarded it.

But you can do something like that but I don't if there is enough time in this case cuz using this is much faster. So much faster but Gelfoam, I get nervous with Gelfoam I've caused abcesses, again I've seen a couple of abcesses with Gelfoam, so I don't know. >> I use thrombin, really tight coil nest,

helps. We found that really densely, densely packed track of coils and that seems to be helpful as well. >> Tim is right, it's easy to get lazy with coils and you put something too big, and its not tightly packed enough and- >> You're tired,

it's the last stage of the case, the tips is open it's like high fives all around, and then you go, I'll just throw a couple of coils in there. >> That's the time is right,

that's the time when you're like, exhausted you wanna get out. But that's the time when you say okay I don't wanna make a basic mistake you know, I've worked out this hard, you don't wanna put a lazy coil in, spend the extra five minutes it's well worth it.

He's absolutely right you know you're a lady you wanna get out there and then you put a lazy coil in. >> You >>[INAUDIBLE] >> You've done that stick generally with ultrasound and so you have a sense of the transition from the splenic vein,

and the length fluoroscopically, you can see the splenic parenchyma >> You can use Dermabond if we don't have Frank and the neural glue, and I have used Gelfoam either as infectious risk, there's whole host of risks of getting off CT scan and having a colon infection because

they see some error in the spleen or even in the liver if you use it in the liver so you have to really make sure you notify turn to body imagers that hey, this is actually some error from Gelfoam. >> Question in the back? >> [INAUDIBLE] how do you deal with [INAUDIBLE]

>> Are you referring to TIPS created with wall stent or wall stented hepatic vein? >> [INAUDIBLE] TIPS, through that wall stent. >> I've done that in Budd Chiari where the Budd Chiari patient has been managed with hepatic vein wall stent and then that is occluded. I

have not, what you've described I haven't seen but it is possible to go through the interstitial wall stent and use a conventional TIPS kit, angle through that target your portal vein it's gonna be Budd Chiari so it's a long way down you know [UNKNOWN] Get down to your portal vein and then the radial force of the viatole/g actually with your predilation is actually fine.

You can flare that up and out to the ostium of the hepatic vein. Have you seen that before? >> I have not seen that. I think what [UNKNOWN] was showing earlier. I think may be even coming percutaneously into the hepatic vein and coming out.

And then being able to switch back around. You can also use that approach. It can be difficult coming from above or straight through or trying to get adjacent to that. But if you got some forward pressure sort of create a stiff system.

Then you are more apt to be able to- >> That's what we do when we have clotted TIPS and you're trying to recanalize the clotted TIPS or whatever, we puncture the TIPS directly but at an up angle. Then you draw back up then you snare and then you pull your sheet back and then you can sort of drill back down.

>> Great I have to run to another meeting [INAUDIBLE] thank you. [BLANK_AUDIO]>> It's the same thing as the glue so you mix it with ThioDox/g and then you utilize it, it's the same exact thing [INAUDIBLE]

Okay. So this is a generally healthy 7-year old male with no significant

past medical/surgical history and with normal birth and development. He had a very vague history of "liver shunt" that was never followed up. And he was noted to be very hypoxic, having shortness of breath

while playing Tee Ball. His physical examination was unremarkable and he demonstrated normal growth and development. The concerns were seasonal and there was exercise induced asthma. He was placed on several medications. But he failed to show any improvement.

On follow-up appointment, the patient was noted to be very hypoxic, starting at 87% standing and 83% with minimal exhaustion. Chest 2 view was done at an outside institution so the image is not available unfortunately, but it demonstrated increased peripheral

interstitial markings. So with continued shortness of breath and no response to medication, high-resolution CT was recommended. And at the same time, ECHO was performed to rule out a pulmonary right-to-left

shunt. CT of the chest without contrast was negative and the ECHO demonstrated in intact arterial and ventricular septum. However, there was a positive bubble test were demonstrated a early filling of the left atrium only after 3 cardiac cycles diagnostic of right-to-left intrapulmonary shunt. With this positive ECHO result

and a vague history of a liver shunt, there was increasing concern for portopulmonary syndrome. So a CT of the chest, abdomen, and pelvis was performed. So the CT of the chest did not demonstrate any pulmonary AVM's, however it demonstrated an enlarged main pulmonary trunk as you

can see. The arteriole phase of the CTA of the athena pelvis did not demonstrate an early venous filling of the portal vasculature which would suggest arteriovenous fistula. However on the portal phase, I want you guys to focus right here, following

the right atrium cordially, you can see a large vascular structure, coursing through the liver, and connecting to the portal system. [BLANK_AUDIO] And splitting up, right here. And now the coronal reformat gives you the same thing,

gonna focus right here. Here is a large vascular system, structure connecting the portal to the systemic. To summarize, there was a portal systemic shunt in the branch

of the left portal vein extending through the liver, connecting to the dilated vascular structure which was then emptying into the hepatic vein and the inferior vena cava. Hepatic veins were isodense to portal vein suggestive of shunting. And the liver and spleen were fortunately unremarkable

otherwise. To confront the CT findings, a limited abdominal ultrasound was performed. And this demonstrated a largely focally ectatic left portal vein, which had internal turbulent venous flow and connecting to the left hepatic vein and finally draining into the IVC. His labs were fortunately unremarkable and his ammonia was within

normal limits for the patients weight and age. So the diagnosis was a congenital intrahepatic portosystemic shunt. So this is an abnormal intrahepatic connection between the branches of the portal vein and the hepatic vein. So normally, people would develop a sinusoids. The vitalline veins would develop a sinusoids. And as you see

right here, these would be the vitelline veins and these would develop sinusiods in a normal liver. And connected a sinus venosus. But in our patient, there was a lack of sinusoid formation resulting in a in a direct shunt.

So there're different types of congenital Portosystemic Shunt. Type 1 is the No Intrapathic portal flow which should be (congenital absence of portal vein or type I Abernethy malformation). So you can see the Splenic and the SMV directly draining into the IVC in type I A. Type I B, you will see the Splenic and the SMV coming together endangering into the IVC. Type II is a partial shunt with preserved hepatic portal flow (t

ype II Abernethy malformation). So you can see the splenic and SMV coming together forming the portal vein and going in through the liver and there is an extra hepatic shunt from the portal to the IVC as you see right there. And our patient was presenting with 2A which is a Fistula arising from the left portal vein and it can also be a right portal vein going to the systemic.

The other two are more rare. And IIb is a Fistula from the main portal vein. IIc is a mesenteric, gastric, splenic vein fistula to the systemic circulation. Portopulmonary syndrome at the exact mechanism is not really well known but its thought to be a combination of upregulation of nitric oxide and inability for the liver to metabolize vasoactive mediators.

So this is the normal alveolus. This is the abnormal alveolus receiving all the vasoactive mediators and nitric oxide. This will result in V/Q mismatch, diffusion limitation and shunting through the AVMs. These patients will often times present with cyanosis,

clubbing, polycythemia and impaired exercise, tolerance from hypoxemia. And serious complications include systemic embolizations, pulmonary hemorrhage or cerebral abscesses. So this was an unusual case of congenital intrahepatic portosystemic shunt where the patient presented with isolated

portopulmonary syndrome without clinical evidence of hepatic encephalopathy which is most commonly the presenting symptom. Although CTA of the chest did not a demonstrate a pulmonary AVM, ECHO findings were diagnostic. And the AVM's were most likely due to the shunt which was shunting the vasoactive mediators and the nitric oxide to the lungs directly. Despite the presence of a large shunt, the patients hepatic function

determined by LFs were well preserved. So the patient was soon admitted under transplant and I was consulted for possible minimally evasive intervention. So we could just be cowboys and just go and close this thing but there are a lot of questions that were not answered yet.

So we had to know how developed are the hepatic veins? How developed is the peripheral portal system in the rest of the liver? What is the pre-procedural direction and quantity of flow to the right liver lobe? Will be the change that portal pressures following occlusion and

will the patient be able to tolerate this. So we decided to obtain answers to this questions by performing a temporary occlusion of this shunt intraoperatively with a balloon. The back up plan was to consider liver transplantation if the patient was unable to tolerate it and if the hepatic veins and the intrahepatic portal system was poorly developed.

So this is the initial hepatic venogram, and in this pediatric patient, we chose the left IJ for stable intravascular sheath position in a 9-fr Pinnacle was placed. The right and middle hepatic veins were cannulated and a hepatic venogram was performed.

A free and wedge hepatic venogram demonstrated well developed right and middle hepatic veins. The shunt was then cannulated through the left hepatic vein with a coaxial 7-Fr, double angle 45 cm sheath for stability. Through this shunt, a 5-Fr

glide Cobra catheter was finally advanced into the main portal vein and a direct portovenogram was performed. And this demonstrated a small but patent right branch of the portal vein with hepatopetal flow and well developed intrahepatic portal branches were documented. We then performed occlusion

portogram by inflating a properly sized balloon in the shunt for 20 minutes. So, before the occlusion, we saw the gradient was 1 and after the occlusion for 20 minutes the gradient rose to 9. So the change was only eight, so decided to proceed with the shunt

occlusion. The shunt was closed with two 2nd generation 16 millimeter Amplatzer plugs, and the final venogram demonstrated a total occlusion of the shunt. He was admitted to PICU for post op monitoring. He was initially

on 2LNC but was weaned pretty quickly and saturating at 93 with ambulation without any problem. He was then downgraded to floor pretty quickly. And repeat ultrasound demonstrated complete occlusion of the previously demonstrated shunt with no residual shunting.

He had stable HGB and LFTs and he was discharged on post procedure day two in a stable condition. In the most recent follow up, we performed an ultrasound. There's no left portal veins in the region of the left portal vein. So, this is what we saw before,

left portal vein left hepatic vein, IVC, and now we see the implantser. Oh sorry. And in the critical note, he's doing well, he's in the 3rd grade now and he's enjoying playing baseball, and he has no shortness of breathe and he's thriving. And his lungs remain stable and notably his pneumonial level has actually gone down.

[BLANK_AUDIO] So to summarize, congenital intrahepatic portosystemic shunt is a very very congenital anomaly that can result in hepatic encephalopathy from increased ammenomia. Other complications include heart failure and fatty degeneration of the liver from luck of nutrition to the hepatic cells due to

reduced inflow. Portopulmonary syndrome is an uncommon complication resulting from congenital intrahepatic portosystemic shunt, is believed to be due to increased NO and vasoactive medators being shunt to the lungs. Congenital intrahepatic portosystemic shunt, can be differentiated from Abernethy malformation by the presence of an intrahepatic shunt versus an extrahepatic

from the portosystem to the systemic circulation. Our patient presented with a clinically symptomatic portopulmonary syndrome alone. And he had no signs of liver dysfunction and demonstrated sufficient blood supply to the liver parenchyma to proceed with the occlusion. And patient demonstrated almost immediate improvement in symptoms

and continues to be asymptomatic. Orthotopic liver transplantation may not be necessary to correct portopulmonary syndrome. And early occlusion of the shunt can serve as a minimally invasive option from IRs, for pediatric

patients who demonstrate noncirrhotic intrahepatic vascular abnormalities with early reversible pulmonary vasodilatation. Thank you for your

So first case is a 23 year old female on oral contraceptive pills. She presented, she works in finance, works at a desk all day, had

a recent travel to Europe about four weeks prior which we thought was probably not related to this particular incident. She was walking going to lunch near her work down in the Financial District and was going up an escalator, climbing some stairs and sink a pause/g found down, taken to our New York Lower Manhattan

Hospital. Relevant history, she had this one week insidious onset of progressive dyspnea and four days prior she remembers she can only do one minute on the treadmill, she's very active 23 year old. She runs, she does cycling classes, all these fitness type classes

which was pretty unusual for her. When she arrived at the Lower Manhattan Hospital this is some selected images of her CT so you can again appreciate the RV dilatation, no calipers necessary there. On the axial images you see some large volume thrombus within the main pulmonary arteries on either side in the coronal

view, you can see these are kind of extending from the main pulmonary arteries down into the lower branches on both sides. A little more history, so no relevant past medical history, she's not a smoker, no recent travel besides this four weeks ago which is probably not related,

no family history of thrombosis, her Troponin I was 0.2, BNP was 175 which is elevated in our institution. You can see her vitals here on the right. So her blood pressure 111 over 53, her heart rate is only 87, she's breathing at 20 a minute like everybody in the hospital, and her

SP02 is 99% on room air, her TT is very abnormal. So dilated RV, reduced function, severe TR, severe pulmonary hypertension measured by that tricuspid regurgitation jet and so the question now becomes, what do you do with

this patient? And a couple of issues that we have and probably most of you have when you're a big medical center and you're not just one hospital, what do you do with this patient? They're now at one of our affiliated institutions where maybe we don't have the expertise or the availability to bring them for

catheter directed lysis at that institution. Do we transfer this patient now from Lower Manhattan up to our main campus, do we give them systemic TPA at this Lower Manhattan Hospital because maybe there is an expertise or she's probably more of a stable submersive, so time is really on our side. So, go back a sec, I forgot to ask my important question here so,

she had a history of syncopy and lost her consciousness so, one important point you wanna make sure you re-stratify these patients and don't have a catastrophic event and so in everybody who loses consciousness at our institution we get a head CT just to make sure there isn't a bleed. So we got her head CT, we saw no bleeding and you'll trust me based on that

one image. All right, so I think this is the kind of best question that I get asked when we start to do these cases, how do you get into the PA and you've had I think four different ways to get into the pulmonary artery. Some people go in from the IJ approach, some people from the femoral approach, people use different catheters, pigtail catheters, copper catheter, some people float a swan,

we happen to use a modified grollman catheter and just for your entertainment pleasure, we have a clip of how we do that and there is some technique to do this when you are treating these patients and while this is playing I'll just kind of elaborate. I think at our institution we don't try to put this patients

under general anesthesia because the anesthesia comes with its own risk and all these patients are pre-load dependent. So once you induce these patients with anesthesia they are gonna loose their pre-load and we've had situations where these patients have become hypertensive and crash on table during induction of anesthesia because we've removed that pre-load on

them. And so we do this completely under local anesthesia and with our patients awake. And so for that reason I prefer to go into the groin where our patients are just more comfortable on the procedure and with that particular arrangement. We do two punctures into the right [INAUDIBLE] femoral vein if its open, if not we'll do the left [INAUDIBLE] femoral

vein both under ultrasound. As far as how you get this grollman catheter to go in where you needed to go. So the nice thing about the grollman is that it is a pigtail, so it's something that you can do your power injections, you don't have to do an extra exchange. When you come in you come in through the IVC and you get into the right atrium here and you

are gonna cross the valve, and then you take your modified grollman you start to rotate it posteriorly slowly as it kind of flicks across there over the valve. And then as you're seeing this kind of upward motion of that pigtail then you can advance it forward. And so if I just go back and just play this one more time,

you can see how this is right now sitting in the right atrium kind of slowly twisting it and you can see how it's having this kind of upward movement, enduring that upward movement just giving some gentle forward pressure as it kind of pops through the pulmonic valve, into the pulmonary artery.

So we get into the pulmonary artery and here's her initial pulmonary arteriogram we take. In all of our patients we take pulmonary artery pressures before we do our injections and basically my rule of thumb is anybody who has a peak systolic pulmonary artery pressure below 40, I'll inject at a rate of about 20 cc per second for a total volume of 25.

Once you get kind of in the 40 to 60 range, I drop that down, do 15 for 20 and then if they are above 60, then I drop it down even more and do ten for 15. And so just some practical aspects of how to get this pictures, and the reason for that is you don't really wanna overload the pulmonary arteriole system with more volume

and somebody who already has a high pressure in there. So her pulmonary pressures are obviously very elevated, peak systolic 59, on the right, peak systolic 68 on the left. This is a very surprising for a very young, healthy, active, woman. You can see the amount of clot burden on the screen.

She has this large thrombus here as well, some occlusive thrombus here in this lower lobe branch and you can see the tram tracking all around the thrombus here on the left side. What I tell everyone who does this with me at Cornell, not only

is it important to look at that initial pulmonary arteriogram and see if you can see tram tracking and sometimes it's better to look at it in DSA, sometimes it's easier to look at it unsubtracted, but more importantly it's probably the perfusion of the lung itself. So we always carry out our injections until

you see the aorta and at that time you can start to see perfusion of the lung parenchyma and you see these large perfusion defects on the right, the entire lower lobe is not perfused, same kinda thing is on the left. Big perfusion gaps, big perfusion defects.

So at this point, where do you place your catheters and how do you get there? What catheter combinations do you use? These are kind of the practical details and questions that we have so I'll just kinda answer each one of those individually. So I

like to have my sheaths all the way out in the main pulmonary artery crossing the pulmonic valve and the reason for that is there's a lot of pressure, the RV's dilated and this catheters if they are soft they are gonna tend to buckle in your RV, and you're gonna get a lot of arrhythmias over time. And you're gonna leave this catheters

in 12, 24 hours overnight and they are in the ICU, so you wanna be able to have a stable system that's not gonna back out by this buckling into the RV. So I use 7 French, 70 centimeter radio sheath that are nice and stiff and get them all the way out across pulmonic valve.

What was my other question? I forgot already. I always take my pictures at End inspiration, I think it spreads out the lung parenchyma, spreads out the vessels, allows you to

get the best appearance of the vessels as opposed to what we do basically everywhere else, if you're doing a liver embolization, you're gonna do it at End expiration rather than End inspiration. Again triangles, I'm sure we can probably argue on what gives you the best picture. I usually do ipsilateral obliques at 30 degrees,

I think that opens it up well for me and I'm able to do one injection to either side. And Access sites we talked about. So in this particular patient we put in Uni*Fuse catheters. Here we have them in both lower lobes.

Our protocol where we inject our patients 0.5 milligrams an hour through each side and we usually run it for 20 to 24 hours and a lot of that duration is based on our room availability. So if we can get them back sooner or later usually after about 24 hours, we can turn off the infusion at the bedside and just start running saline.

In the beginning of our experience we were bringing everybody back and doing follow-up pulmonary arteriograms, measuring repeat pressures, again like was said earlier, we've changed that policy to now basically at the bedside transdusing pressures from our infusion catheters

and pulling at the bedside. So here's her follow-up, pulmonary arteriogram, and you can see it's not perfect, there's still residual thrombus here in the right main pulmonary artery. However, pretty dramatic reduction in pulmonary artery pressures. Her peak systolic pressure

dropped by nearly 30. And again, to correspond that perfusion argument that really the perfusion of lung is so important. You can see how a lot of these perfusion defects that we saw previously

he has fibrosis. There's a little bit of ascites

so maybe portal hypertension and a five centimeter solitary HCC. The patient has good functional status, ECOG of zero. Meaning he's active, no activity restrictions and he has good liver function.

Billirubin 0.6 and Child Pugh A. So here's his tumor, five centimeter HCC in the right liver, exophytic hanging off the edge here, and he has possible portal hypertension. So the options to consider,

resection, transplant, embolization and ablation. So for resection, his liver function is normal, and the location of the tumor looks like it's a resectable location. So he's a potential candidate for resection.

For transplant, he has underlying liver disease, NASH, he has HCC, possible portal hypertension and its a solitary five centimeter HCC so he's within the long criteria so potentially a transplant candidate. So it's important to have this patient evaluated by surgery.

So we sent the patient to surgery and they said that because of the patient's comorbidity they didn't wanna operate, so that takes resection and transplant off the list and now we're left with embolization and ablation. So for a five centimeter tumor, that's sort of at the upper limits

of what you can completely ablate, so you could potentially ablate this. If the tumor was much larger than fivr centimeters we wouldn't be ablating it and we would just be embolizing the tumor. This large solitary tumor we could embolize it.

We would wanna do a selective embolization for a solitary tumor. So in this particular case we decided to both embolization and ablation just because the size is at the upper limits of what we can completely ablate so we wanted to do sort of a double kill where we embolize it and also ablate it. So the way we do that is we do it on the same day.

We embolize first and then we ablate. Here you can see we're trying to get selective. We're in a branch of the right hepatic artery it seems like we're covering the whole tumor and in this case we did the bland embolization after we do the bland embolization we get a non contrast CT while they're still on the procedure table to see the contrast retention

within the tumor. So this is important because you can see if you missed part of the tumor maybe you have to go out for a different branch in order to cover the entire tumor. And then we use this contrast retention as a target for placing our ablation probe and this just shows one of our ablation probes post ablation.

So the reason we do the embolization first is for two reasons, one is that the contrast retention gives you a nice target for placing your ablation probe and the other reason is that embolizing the hepatic artery reduces the profusion, takes away some of the heat sync and potentially

gives you a better ablation zone. >> Can you comment on the size particles you would have used for your bland embolization and also the type and number of ablation probes you used in a five centimeter lesion? >> Yeah, okay. So let me go through that.

So I have a couple of slides here on bland embolization. So Karen Brown did a randomized trial of bland embolization versus DEB-TACE for HCC and she saw that there was no difference in response or survival. So I think what this means is that the main mechanism for these procedures is tumor ischemia since adding the chemotherapy didn't

seem to make any difference. Now, there are some potential advantages of bland embolization which is you can embolize multiple times and the hepatic atrial tree stays the same. So Joe Erinjeri looked at patients who had at least five bland embolization procedures and found that 84% of them, there

was no change in the hepatic arterial tree. In the remaining 16% there was occlusion of fourth or fifth order branches. So I think if you did five conventional TAE procedures you might start to see some pruning of the arterial tree. Now in terms of our technique for bland embolization we start with 40 to 120 micron embospheres and the reason we start with these small particles is we think

that it gives better penetration of the tumor, more tumor necrosis to use smaller particles. But if we've used five syringes and we've still haven't gotten to stasis then we start to go to larger particles 100 to 300 micron embospheres.

And the reason is that when we first started dealing bland embolization, and we were just using the 40 to 120 micron, we actually had few patient deaths and on autopsy it turns out the particles were in the lungs, and in those cases , they receive

many, many syringes of the 40 to 120. So we tried to limit the amount of small particles that were use and of course if you're seeing hepatopulmonary shunting, or if you're embolizing a large dome lesion where there might be hepatopulmonary shunting or you're embolizing the phrenic artery,

then you might wanna just start with some larger particles 100 to 300. And in terms of the embolization end point, for a bland embolization we embolized stasis. So in this case we used two probes,

we probably could have used more but I think we got a pretty good response in this case. >> Can you comment on that probe you have in that picture is going to ablate some of the chest walls- >> Yeah. >> And muscles there. >> Exactly.

>> Do you not worry about that or what do you do? >> Yeah so sometimes we'll, it's not great we probably could have done hydrodissection, the other thing that we do sometimes is we'll use bupivacaine at the liver capsule for post procedure pain when we're abating things that are near the surface.

I mean, ideally if you can go through normal liver on your way to the lesion, that's preferable. But sometimes if you can't, we do end up going directly into the

lesion. >> And what type of microwave system were you using? Do you remember? >> This one I think was imprint, but I normally use the new wave system. >> Can we see a show of hands how many people in the audience

do bland embolization for HCC? How many, okay so nobody. How many people can still get your hands on and do a conventional TACE right now? So only a few so and so is everybody else doing drug-eluting beads then?

Raise your hands if your doing drug-eluting beads. Okay. >> [LAUGH] >> There's a bunch of people that I [INAUDIBLE] >> There's also Y90

[LAUGH] >> Assuming that you have Y90 you also do chemoembolization. All right. >> Okay. All right so- >> Can I make one comment on that one?

>> Sure yeah. >> So that lesion there's so many different options you can do for treatment and there's no evidence, great evidence, saying one is better than the other. So in my institution that would be specially given your ateriogram,

an excellent case for segmentectomy. A radiation segmentectomy. You can get a really good treatment there. >> You can also do a chemoembolization segmentectomy for about one third the price. >> [LAUGH]

>> And it works just as well. A couple of comments. I mean I love doing commission therapy so you were saying you might ablate up to five centimeters. I think that is generous. I mean I wouldn't really try ablation alone for a lesion over three

centimeters unless I had some contra indication of embolotherapy cuz really your failure rate goes up pretty dramatically for a tumors above three centimeters in size. So I think above three, there was a solitary lesion like this I would do exactly what I did which is combination therapy.

In our series for a combination therapy what we do chemoembolization with lipiodol and drugs. Day one, we mint them all overnight and bring them back the next day and use the lipiodol contrast which is retained the next day to help with the try and the CT works great, and then basically just lay a series of ablation probes and

you're not gonna ablate the whole thing thermally. But the idea is that you're gonna have an area that's thermally ablated then you're gonna have a large hyperthermic zone around your probes and the hyperthermia sort of just stick with the doxorubicins you get very intense doxorubicin binding to the tumor DNA, and get very very large kill zone.

And what we found is in solitary HCC is up to eight centimeters in size, we had 80% complete kill, by combining chemoembolization with mostly RFA in that era and that for metastatic disease, we would do tumors up to six centimeters in size of the combined therapy and

we have 70% complete kill for mets up to six centimeters in size, so I think it's a very great strategy for solitary tumors that are too big to ablate alone. Question in the back. >> Do you ever take longer or do you find the synergistic effect works better or sooner I mean so do you wait a month or two for the lesion

to shrink to make it more [INAUDIBLE] >> I don't, I mean there are people who do wait a week or two after their chemoembolization before they ablate. I don't cuz A, I want to get advantage of the high drug levels, they're still there to get the synergistic effect with the hyperthemia and also it's just practical since I'm admitting my patients

anyway so I just bring them down, first case the next morning do the ablation and they can still go home the next day. That way they don't have to come back to the hospital for a secondary outpatient procedure. But there are some people who do delay, whereas there are some

people who do it the other way around, they ablate first, and then chemoembolize, for whatever is left and there is a different rationale for doing it that way. And in general that also works fairly well. Logistically it doesn't make sense in my practice since I may meet them for

the chemoembolizations. Also if you look at animal studies where they've looked at sequencing, you get a higher volume of kill if you chemoembolize first and ablate second. So that's why I do what I do. Question?

>> Do you use alcohol? >> We do use alcohol sometimes, it's a little big for alcohol, usually we're using alcohol in smaller lesions like a couple of centimeters. You could try it, I think you're gonna get a better ablation for

a big lesion with some sort of thermal ablation. >> Again sort of the same thing the efficacy of picking as ethanol injection, on average it's similar to heat ablation but you have to do multiple procedures to get the entire tumor cuz it just doesn't diffuse well enough whereas heat will get everything. I actually had a very interesting conversation with someone this

week who said I don't know why you guys bought all the expensive stuff, I just do my chemoembolizations with alcohol and lepiodol. For segmental or sub-segmental especially doing alcohol ablation transarteriorly works great, there is actually a pretty substantial Asian literature on this, I don't know we never do it, and it gets rid of the whole

drug particle issue. You're basically doing an embolization segmentectomy with ethanol which if you're again segmental or less, works great, it's very cheap.

So my case is kind of reiterate some of the same points. So the first case is a 65 old male, HCV cirrhosis, newly diagnosed HCC potential liver transplant candidate. It's not working? So a look at the liver status as well as

the performance status, get the lab, look at the CT, so he's beyond milan, there is 4.5 centimeter segment five LIRADS five lesion, and a 2.6 centimeter segment five lesion as well.

So then I see the patient in clinic and I have a discussion with them of kind of like what Mike was saying, of between what the options are and what the benefits and risks are of each one of them, and so there is no good randomized control trial comparing

these. So I go over some of the retrospective trials that are out there. So I talk to them how there's no difference in the survival. [BLANK_AUDIO] I talk about how there's no difference in the survival with the patients and then if there are a transplant candidate I talk about how a retrospective

study showed that the downstaging rate from t3 to t2, was better with Y90 that TACE. Time to response also shown to be better with Y90. Time to progression better with Y90. Looking at pathologic response and explants, two separate papers but at the same institution show that Y90 was a little better.

Toxicity profile also has shown again retrospectively Y90 a little bit better. >> Not really. >> So looking at TACE, I talked to them about why TACE and it's kinda of what Mike was saying that you can get them to treatment faster, potentially.

It depends where you are so at North Western we could, see them in clinic one week and the next week treat. Not only do the full study and treat them the same day. At Jefferson I can't do that. That was one of the biggest shocks when I first got there.

I have to wait about two weeks to get insurance approval then I have to do the full study. I'm not allowed to be the authorized user so I have to wait for Radhoc/g to figure out the dosing. It takes another two weeks to get the dose. So it takes a month till I can treat the patient versus TACE I can

do the next day. So I talk about that with my patients and TACE shorter time to evaluation results, so it's embolic and on imaging we look at enhancement. So TACE, one month out you can tell whether you need to go back in or not Y90. Sometimes you can tell,

and I'll show an example of that, but generally I usually get an imaging at one month and then another one in three to four months, and it's that second imaging that I go off of whether I needed the treatment more. And then I also talk about micro-embolic versus macro-embolic so it's all theoretical but I feel like if I do Y90 first I may still

preserve the vasculature to be able to do more TACE later. Do you guys have any comments on any of that? >> Well just that I mean the whole the idea of who goes first is, a little bit of a myth in that some people say why should you do Y90 first coz with chemoembolization shall

block the vessels. Well, if you do chemoembolization first the tumor grows, then there's obviously there's arteries to treat and the Y90 will get in there and we actually went and looked retrospectively the bunch of patients we treated with Y90 who either had or did not have prior chembolization. There is absolutely no difference in dose delivery

between the two groups and no difference in tumor response between the two groups. So you really can't go on either order, and you're not comprising anything. >> So I went with Y90 in the patient, after discussion agreed.

So just a little about how I do it. So I give some peri-procedure medications. Before treatment they're on protonix a week before and then four weeks after, and I send them home with zofran and oxycodone. So in terms of catheters that I use, I use different catheters

for planning versus treatment. For guiding catheters there is a lot of different things you can use, I generally use a Simmons one. For planning treatments, I want something short and higher flow so that I can get good contrast delivery and see things well,

so I tend to use the 110 2.8 F Progreat. When training I did the Renegrade Hi-Flow but if I wanna coil I don't wanna use the 2.8 F microcatheter so I use the 2.4 F catheter if I can predict that I'm gonna coil something. And then for treatment I want something that's longer with a smaller

diameter so that I don't just rush in Y90, it might just be theoretic but to decrease the risk of reflex I tend to use a 130 Maestro for that. Do you guys put things in that order or is that just my OCD? [LAUGH]

>> OCD >> OCD [LAUGH] It's also the North Western way. [LAUGH] So this is that treatment, you can see that the lesion, I didn't

see the smaller lesion, this is the planning arteriogram but the bigger lesion was treated, was supplied by both mainly the posterior branch but a little bit of the anterior branch. And I do a lot of cone beam CT,

I'm a cone beam CT junkie, I do it in my pre-planning and on my treatment days. So I got in and decided I need treat both, line spred function was 6.15. And so on the same day I treated both with two separate vials, and

I like to use extended shelf life in my mind it's still less embolic than SIR-Spheres but you get better coverage within the tumor especially if it's something that's very hypervascular. And so based on the volumes I did 18 Gigabecquerel vials, that's a relatively large amount of beads to segment six, seven and then a smaller one to the other

one, but that was based on volume, not based on how much the tumor is getting covered. >> So then one month out, no viability in the tumor and it's 4.1 centimeters.

So we started the transplant evaluation. And then nine moths out, they started, the tumor got smaller but then there started being some LIRADS three lesions. >> They developed the ascites. >> And they developed ascites, yes. Which you don't know whether it's the Y90 or whether it's the natural

progression of the cirrhosis, could be a combination. But unfortunately at 12 months, multifocal bilobar HCC and distant mets so, this kinda shows for down staging why some people think that there needs to be a waiting period. Because something that's bigger might be more aggressive but something that big is not necessarily more

aggressive so, if you can find those ones that aren't, then they can do well in transplant but those ones are aggressive then you've weeded them out, so that's how we do it so unless there is a question.

Here's a companion case.

So take a look at this. This is a young female. She had a large subcarinal mass. And then she went for a VATS biopsy. And then started getting uncontrollable hemorrhage. So take a look at this. First, I read diagnostic too and I read chest. Try to think first in your head, where you think this might be.

This is a contrast and hair study. Big, solitary subcarinal mass in a 26-year-old woman. She goes in for a biopsy. They've uncontrollable bleeding. She gets sent then to us, to just basically try to control the bleeding. Now look at how vascular this is.

You could tell by it's location, that it's gonna really get a lot of supply off the bronchial arteries. And then you could see nicely, the enhancement, just from the CT, and how that correlates really well with the bronchial anatomy. We embolize the hairs/g one. And then here's another artery, how big that is, and it's showing nicely the perfusion.

We embolized it, for the goal of just stopping the emerging hemoptysis that was occurring. This is a case of Castleman's disease, angiofollicular lymph node hyperplasia. But turns out over time, this thing started to shrink, and we followed it every six

months. She was on and off some of these different therapies, you can have from it, but over time this did go down, so. That may in your mind think, well. hey, we do a lot of embolization for liver tumors. Can you do embolization for lung cancers or tumors in the

chest? So some groups have written that up. I don't have any first hand experience with it. But a group has looked at RFA with bronchial artery chemoembolization, right? So they've/g a chemoembolization they do in RFA.

Now the other question is, which artery do you put the key find? Here's another group, and they looked at transpulmonary chemoembolization, where they gave mitomycin C and iodized oil with particles through the pulmonary artery.

So these are all things maybe you wanna consider. If you have a research interest in it too, that's definitely not widely accepted, but people are looking at those things as well. I mentioned getting a CT, I really think it's useful.

We're so used to having a lot of pre procedural imaging, that it can really help you during your procedures. You might identify pathology that's not seen on chest X-ray or bronchoscopy. They may help you identify interstitial lung disease, and the location. So the group looked at how helpful that was. And it was quite helpful to have high rise CT.

The benefits of getting a CTA, it might help you show the bronchial artery number. As we talked, there's a lot of variability about bronchial artery anatomy, the location, the orientation.

Maybe there's an AVM. Maybe there's alternative suppliers. Maybe there's an aneurysm, they're rare. So it's just, it's really helpful to know before you go in there, how it looks. So when you get a CT, and then you know exactly

kinda, how are things supposed to look on my angiogram, when I get in there, and is it covering the right area? So if the patient's stable enough, I strongly recommend getting an angiogram. There's a study looking at the evaluation, a bedside evaluation with CT on that, and it really helped lateralize and localize these cases.

And then also modified treatment in some cases. The other thing I like is, sometimes especially when, if you're doing patient set, the more for cancer than bronchiectasis, the bronchial arteries aren't really that hypotrophied, and it can

be a little bit difficult to get into them. I like having the anatomy ahead of time. And then I know what type of catheter I'm gonna use. And I know a little bit, what angle everything's gonna be coming at. So I can have a little bit of a game plan beforehand. When you see it's really pointed, more superiorly, than we

can choose the right type of reverse care of catheter, you get in there. So it's really, it just really helps a lot. And so, just to, we're gonna move on from bronchial artery embolization to some of the other embolotherapies in the chest.

But just remember that massive hemoptysis is commonly seen with bronchitis. When you have massive hemoptysis, it's most commonly associated with bronchitis or bronchiectasis. And even though it's not really a first line treatment, it has a good safety profile, and success rate for malignancy. And recurrent hemoptysis,

be prepared for it, and then that might affect what you're gonna use to treat it. The sources of bleeding is typically the bronchial arteries. The preprocedure CT is extremely helpful for planning. Beware of rapid

shunting to the systemic veins. You could consider coils or just using larger particles to close the shunt in larger cases. I've one companion case, cuz I have a little

And non functioning patients asymptomatic. He had pancreatectomy, splenectomy and metastasectomy and he was doing okay for about a year and then mets start grow in the liver

so he was referred to us. Overall labs looked great, chromogranin A is a little high, bilobar disease including a dominant lesion 8.7 centimeter lesion segment five. No mets anywhere, negative octreotide scans, he wasn't on anything else.

So discussion with patient about the different options and what Bill said earlier about holding off Y90, is a valid point but I did not, I did Y90 first. >> [LAUGH] >> Just so I'm just giving you guys information,

if they have actual symptoms, what we we do. I think it's a little aggressive. Some literature says just give sandostatin 150 sub Q before. I don't know what you guys do for this but this is what we do at Jeferson.

>> I give 500 micrograms of sandostatin sub Q, the morning of the procedure. >> Morning. >> We do 200 sub Q. >> So this is similar to what Ed had on SIR-Spheres versus TheraSphere.

SIR-Spheres is the full pre marketing approval for colorectal mets. TheraSpheres is this humanitarian device exemption for HCC so you do need an IRB for that and you can get an IRB just for HCC or an IRB that's primary and secondary liver disease. And I think the biggest thing down here is each bead of TheraSphere, each bead has much more activity than a SIR-Sphere.

So that gives you the difference, so for the same radiation you have way less beads of TheraSpheres than SIR-Spheres. And also when I look at my doses is although the dose symmetry is a little different, the

doses are much higher with TheraSpheres than SIR-Spheres even though it's less embolic. But again there is no study comparing one or the other, I really wanna do it but I have to get everyone on board [LAUGH]

So I do a planning arteriogram, and I coil the SIR-Spheres and I coil the GDA and the right gastric, it's a little more embolic than TheraSpheres. And I do left hepatic artery and right hepatic artery, and they

both go into tumor. Line spread function 3.1. So, I bring them back. First treatment I do, most of the diseases on the right, so I do this right sided treatment,

a month later bring back and do the left sided treatment. [BLANK_AUDIO] And since June 2014 he hasn't gotten any other treatments, the tumor marker gone down, size initially went up and now starting

to go down. He's currently asymptomatic and we're just watching every couple of months or more. >> It's one of the interesting diseases where if you look at the treatment guidelines for embolization of NET mets.

Basically embolization is indicative for progressive or symptomatic NETs and all the treatment guidelines basically say you can embolize any of the four possible modalities. There is no recommendation among which one you should use, and it's also if you look at the practice survey that Ron Gulper/g published in 2012, was like 260 radiologists and they asked like what agent do

you use for which kind of hepatic benignancy, NETs was the only one that was evenly divided among the four, everything else there was a strong bias toward either Y90 or chemoembolization. So we really don't know what is best we just presented a multi-centered retrospective study from 7 major US centers here about 150 patients

who have been treated however they were treated. So basically about a third were bland embolization, about a third were conventional chemoembolization, about a third were Y90. And there weren't really differences in terms of tumor control or

survival outcomes among the four in the sort of retrospective assessment. The only things that way matter were tumor grade and tumor burden. And that was basically base net information for the RedNet study which is a perspective randomized trial of the three embolic techniques that's gonna be starting later this year that, hopefully, will

tease out whether one really is different from the rest or not. But right now you can do whatever you want. >> Except well, do you wanna maybe talk about drug-eluting beads in neuroendocrine? Do you guys, do you do drug-eluting beads at all in neuroendocrine tumors?

There's concern that there may be an increased risk of bile duct injuries. I think the data is kinda weak but basically there are some reports of increased bile duct injuries especially neuroendocrine patients with drug-eluting beads. So we occasionally do it when we run out of our ability to get powder doxorubicin.

Sometimes we don't have a choice when we use it. But I think patients need to be informed when there's that situation going on. So we talk to the patients about it. >> Especially three single institution papers that suggested that an increase that happen to be

injury in NETs patients getting DEBs. And if you sort of pull all the patients of those three studies together, the incidence s about 20%, 25%. But, there's just those three papers, no one else has actually reported it and obviously a quarter of the country is using it. And you don't exactly see people refer to it as a big problem then

some of them meeting here said they went back analyzed all the data to present at this meeting hoping to support that concept and found actually that it wasn't true at all. So, one of things that we're looking at the RedNeck studies is when their arms is drug eluting beads is very early safety analysis to see if this is really a true phenomenon,

or whether this is some random single institution misleading retrospective's papers and it remains to be determined but there's definitely some concern because of those papers.

So, lets just start with like a basic case such as this. This is a guy with multifocal hypervascular tumors which was diagnostic of hepatocellula carcinoma. You can see Bilovar disease and he's got kind of labs that many

of us see in the mid-range overall chop UA. And so we chose to do chemoembolization. And I'm gonna just go through the basics of how we do chemoembolization. So, this is our initial workup. They usually get evaluated in a multidisplinary liver tumor board or I'd say about 50% of the patients just get a direct referral to IR instead.

So we do an initial outpatient consultation, get cross sectional imaging, labs, tumor markers, stage them. This is an example. I just kind of did a screenshot of our pre-procedural order set.

It constitutes of IV fluids, some steroids and antibiotics. And obviously antibiotics are different depending on your institution and in terms of your existence flora. So if you are getting this started at your own practice it's important to talk to your pharmacists and talk to infectious disease to find out what antibiotics are most appropriate in our specific

setting. Okay, so this is my basic template of how I do a liver angiogram. And I used to do a lot of abdominally aortogram just kinda with a multi-side hole flash catheter. I've gone away from that just because our arterial phase CT, or MRs

I find reasonable enough to where I don't feel I need an abdominal aortogram. So if I have the baseline imaging which has a really bad arterial phase then I might still do an abdominal aortogram but otherwise I'll skip that. And so, I'll typically first go to the SMA,

and I'll talk a little bit about my catheter selection. I tend to do a slow, long run and that's to extend it out into the portal venous phase to look for portal vein thrombosis. Obviously we're also looking for variance such as replace right hepatic artery etc.

And then I put the notation as to what my flow rates are. So my SMA run is a 3 for 30. And I find that this gets good antegrade flow, with minimal amount of reflux into the aorta.

So this is my ciliac run. I typically do a 4 for 15, then again this is a patient with standard branching anatomy. So in terms of catheter selection, I typically get arterial access with a five French sheath. And I know there's a big push to do radial access. We haven't moved

over to radial access much. Have you guys done much move your practice over to radial? We haven't. Anybody in the audience primarily doing radial access. >> A loud No. [CROSSTALK]

>> As all of you know there's a lot of radial access talks here. So I'm not gonna belabor the point about femoral verse radial. But we are traditionalist. I think that the one thing in livers if you are gonna do a lot of CRM CT, if you're gonna do radial you have to figure out a good way to coordinate

that. So that's one challenge. My personal preference is to use a 5 French 65 cm Simmons-1. And this is how I learned in fellowship. But I find that compared to a SOS, the AP diameter on a Simmons-1 is much fatter so it sits on the the back of the aorta.

So the nose sits well in the mesenteric vessels. It doesn't bounce out when you do your angiogram. So there's almost no contrast that refluxes down into the aorta. The key thing is forming a Simmons. There's a Cope suture technique and you can just search this on YouTube if you haven't heard of it or look in a Coffin/g or Balgy's/g

textbook. And I typical just position this at the branch vessel origin instead of just driving it out into the common hepatic, right hepatic, left hepatic etc. In rare cases I will use a 4 French C 2. But my go-to is a Simmons 1 on almost every case, so I just basically

tell the techs open it on the the table as they are prepping. What do you guys typically use? >> Cobra for us. >> Cobra for you? Okay. I use Mickles. Mickles? So a 100 cm? So that means like a 110 cm microcatheter is probably too short.

>> Yeah we use high, about 130s. >> 130s? Okay >> I think, what I mean you trained with me. >> So you brain washed me. >> I like your approach to the case. But I think that many people probably here,

how many people are using SOS Omni for this? Raise your hand. Most people are using reverse curve catheter? Raise your hand. So most are using Cobra's catheter, is that correct then?

>> Don't you think we can discuss that from the CT? If you have a celiac access that goes down then you need a Simmons one which is very convenient. If it goes up or goes straight Cobra is really sufficient. >> I use Simmons for all of them. Despite that.

It sits pretty well. Everybody has their preference, I think that's interesting but I don't know if makes a big difference. I think what makes a big difference is when you have large hypervascular tumors. Maybe be it's people with a lot of ascites and you need better imaging.

Cause then you can get your Cobra catheter out into the hepatic atrial tree and get some more robust runs. I think when you have, in those situations microcatheters often aren't enough. But I think otherwise it's sort of a dealers choice.

>> Right. We use a common hepatic run and using a Cobra so we can get really good pictures of the hepatic arteries. >> So John when you are doing that though, let's you have a guy who's been on Avastin four weeks ago right? And then you shove a Cobra out there. Are you having any cases of a lot of spasm,

dissection anything like that? Because we have seen that and- >> Very rare. That doesn't happen too often with us and the other catheter that we like, actually I like a lot is the RH catheter or Rosch Hepatic. They use a lot of that in Asia.

>> Any other suggestions? Any one else have a better idea? No? Okay. >> But I think one the interesting things as you sort of alluded to it, when you use a shorter catheter, Cobras can be shorter. The Simmons

when you order a special Simmons at 65 you can use shorter micro catheters. Because I think there's an advantage from an imaging stand point, the shorter microcatheters. When you use a 100 cm catheter you use a bare catheter like SOS or Mickleson you have to use longer microcatheters to get out into the liver.

And that's similar with the radial access, you would have longer microcatheters. It is dependent on that. There are equations that govern that principle. But I have seen when go to longer microcatheters, I don't often times don't get as good as imaging which is important in some of

these air piece we do. So I'd like to you a shorter base catheter when possible. >> I think like if we've done comparisons within patients comparing like Prowler 110 verses a Prowler 150 and there is a, even though the PSI ratings are the same.

There's a remarkable difference in terms of the flow dynamics, in terms of the image quality of a 110 compared to 150. So that's become our preference, at least to use 65 cm which is nice and short and will fit with several inches outside

the sheath. In this case we did celiac. Let's see if this plays. Oh, it's playing up there. Okay. So if you recall we had bilobar tumors. And so this is a Progreat 2.8 French selective catherization of the left.

And you can see kind of infiltrative tumor on the left. And then we switched over to the right. So my initial plan was to treat the right side, and he has multifocal tumor on the right.

So in this case I elected to actually treat the left first just because he had infiltrative tumor. So I went back to the left and did a TACE there and then brought him back for a TACE on the right side. I won't discuss the details of how we do chemoembolization. There's

plenty of other workshops for that. But just real briefly in terms of this- >> Do you wanna talk a little bit about, you mentioned a microcatheter, one or two- >> Yeah >> You've mentioned a Prowler and-

>> And I'm gonna go over that. I'll bring that up, yeah. Okay, so this is our real brief screenshot about post-procedure order set. Again standard nursing stuff like vital signs post-op check etc diet.

And then again we have a standard antibiotics that we use in our hospital and then we kind of have this mishmash of different types of pain meds, steroids and antinausea stuff. So we just kind of have this blank very standardized order steps for basically every patient. Bob mentioned in terms of microcatheters selection. I think their

is a large debate about this. And this is what we stock. I look at it as three categories, like large small and super small. The large one's we use probably for 90% of our work, these are the 2.8 French distal outer diameters.

We mostly stop the Progreat mostly because we have good contracting on with Terumo. Again as disclosure I don't have any relationship with any of these companies. This are great for diagnostic angiograms and lobar treatments. I personally don't like them for really selective super selective

sub-segmental treatments. Any case with glue or onyx, I find that the dead space in a Renegade Hi-Flo or Progreat is really high. So putting onyx of NBCA through these catheters can be a little challenging. And then moving down to the small microcatheters, this is probably

our other 15% of cases, the 2.3 French distal outer diameter. My personal preference is the Prowler plus. These are great for coil embolization because your ID is around 0.021 so it fits an 018 coil really well. Great for sentimental infusions but the diagnostic angiograms are

obviously not as good because your PSI is limited. The super small once we use I would say rarely. This are for like ultra segmental sub-segmental infusions. So I'll use this in probably about maybe 2 or 3% of cases at most. They are great for really small vessels.

Any case with glue or onyx they work wonderfully. If you are gonna do particles, we use this, I use a curve tip Excelsior SL10 for our prostrate artery embolizations. And so if we inject 1 to 300 micron embosphers we just have to dilute it like crazy. And it will still go, you just have to have it diluted.

The diagnostic component of these catheters are terrible so your diagnostic angiography is almost, is borderline useless. So that's one thing to keep in mind. I just listed the more well-selling brands. There's obviously a ton of different manufacturers which you can see down at the exhibit booths. Any preferences for you guys?

>>We do. We have the same practice. We start with 2.8 and when needed we switch to angulated or smaller diameter if needed, for the right gastric for instance. >> John?

>>I'd start with a good 5 French runs and then once I need to get selective I use 2.3 French Prowler plus and a Fathom wire. And for me, in my hands, I can get into any artery with that combination. [CROSSTALK]. >>You kind of skip the Progreat/Renegade Hi-Flo and then

just go from base catheter- >> Go base to - >> Small. >> I skip the whole large microcatheters. >> Just to be a little bit of a devil's advocate. Again, I don't have a horse in the race here and there are a lot of microcatheters.

Probably people in the room are using microcatheters that aren't listed here. But the Prowler plus, again it goes back to we all have our own contracts but that's about twice as expensive as these other catheters listed. >>I only open one catheter instead of two.

>> I couldn't tell you the last time I opened two. But in the imaging it's not very good. You said okay diagnostic angiography. But I think that it's actually relatively poor diagnostic angiography with the Prowler plus. I get it, you're doing your big runs is with your different practice.

You're putting in your 4 or 5 French catheter out into the common or proper hepatic. But it's just something to take into consideration. It depends on how distal and selective you're going to be. But some of these other microcatheters will tract just as well as a Prowler.

>> Is it through your post-op procedure,orders, post-procedure orders, do you admit your patients anymore or do you admit some or none-? >> You mean for chemoembolization? >> Yeah. >> We admit probably 25% right now. Again it's a practice variation.

I think that all of that is probably local and depending on your patient population. Honestly I admit that the guys who want that free dinner, the crappy hospital food. So most of them we're doing as out patients.

Any other, I mean does anyone have any other thoughts on microcatheter selection, how they do it so that we can all benefit from that? Cause I think there's a lot of debate here and there's obviously no right answer. >> Does anyone use the nitinal hypotube high pressure microcatheters that you can put 1200 PSI through an 021?

>>So that's the direction [CROSSTALK]. >>Correct. >> Some people see it as a nice hybrid between the two, they can do better imaging and then if they have coil work to do, they can

engage their coils with less chance for buckling etc. And get into smaller vessels. Just something to consider. >> I think the bottom line is no matter what liver therapy you're doing or if you're trying to embolize something in the liver otherwise is to get good imaging.

And there different ways to do it. There's a trade off between being able to get good imaging, and it tracking in different things so there's a wide variety. One thing you didn't bring up is microwires

I don't know- [CROSSTALK] >> That's right. No, no I didn't bring that up but it's something we can talk about. But real quick are people doing routine coil embolization through the high-flow catheters, through 2.8 French? >> Yeah.

>> Yeah? Any issues are you guys getting? Because the ID is big right. So it's like an 027 so you have a lot of dead space. Any time I know I'm gonna coil a GDA I tend to go down, I down size. >> It depends which coil you use actually.

If you use Concerto for instance it will be trapped within the lumen. So it's not ideal for this kind of microcath, but if you go for the other companies, the Cook coils it works well, so no issues

with that. >> Well it depends if your putting a detachable coil versus a, and if you're going to push it in, if you're going to puff to get it in. >> And I guess that was more referring to let's say a pushable

fibered 018. Right, so where you're basically pushing it out with a 018 wire pusher. At least we've had issues with, you get that coil wire overlap,

so that's why we've routinely kind of gone to the 2.3 French if we're gonna do a lot of pushable coil work. So any other thoughts from anyone on how they do it? >> Okay, Bob you mentioned something about wires. You have a wire preference? >> Well, I typically, I'm really partial to the double angle Glide GT wire,

a Terumo wire. I like it. It's a short angle on it but it selects a lot of branches I don't use it if patient has been on chemotherapy and I'm worried about it will get stuck on one little branches, and you can cause some vasospasm etc.

If I need to shaper wire, currently I'm using the Fathom which is Bosche Scientific. It's usually my shapeable wire of choice. And again when I'm worried about vessels I'm worried about, it's something really straight, a falciform for instance, I wanna get there far out there. I'll use a Headliner 90 wire.

>> And were similar, we use I think Fathom for half the work and then we'll use an 014 Synchro for matching it up with the smaller microcatheters. Those are very shapeable. And very soft and atraumatic, so kind of a similar concept. John any,

>> I usually start with a Fathom and it's the opposite, I use the double angle GT once I've trouble selecting. >> Anything else? >> We use Progreat so there's a guide wire inside. So we solve most of the problems and when we have issues I use the same Terumo double angulation,

mainly for right gastric. Because it's really well angulated and you can't go backwards. >> Okay. >>If people are not familiar with these catheters, I think they

exhibit hall is open. A lot of these companies have all of these wires and these catheters. It be be good to just go through it and look at them. >> Anyone have suggestions on good wire-catheter combinations that we can all use?

>> What size Fathom do you use? Do you use the 016 or 014? >> Our preference is to use an 016 with the large microcatheters, I think there's a little better fit. The 014 with a 2.8 French has a bigger mismatch. So even when you're able to get out there there's sometimes a little

more hesitancy in pushing your microcatheter over it. Believe it or not the 016 is just a little smoother. I use a Fathom 016 and then if I'm gonna use the Prowler or an Excelsior we'll go with an 014 Syncro >> Another cheap wire I use is a Runthrough.

That's like $80. 014 wire, it's shapeable. >> Is it transcend? >> Yeah. >> Guide wire, very cheap as well. >> Still doesn't make up for

your Prowler plus but okay, >> To drive a Mercedes or an Audi. >> And I work at a state institution so I couldn't care less how much that cost, so we just run up the bill on everybody.

So this is a different patient, there's actually, I'll tell you

the end story of this one. But solitary HCC within Milan, 63 year old male, history of a renal transplant and he may be a potential dual liver renal transplant patient. So on a seeming clinic he has a solitary 4.1 centimeter lesion near

the dome, and he has no mets so I always check for that as well. So treatment goal here is bridging to transplant, so I have a similar discussion of chemoembolization versus Y90. You could also talk about bland embolization, I tend to do bland embolization for extrahepatic vessels. So I go through the same

conversation, similar conversation. This guy is with renal insufficiency, renal transplant so I just put up here my renal sparing protocol, how I try to I know a lot of them might be theoretical help prevent contrast-induced nephropathy.

And another comment I wanna make is, he's got in multi hands MRIs, even though his GFR is less than 30, and so the odds comments on nephrogenic systemic fibrosis are related to older garmenia/g products and

with multi hands for example there aren't any known cases of nephrogenic systemic fibrosis. And my MRI radiologists are comfortable giving contrast so I had a discussion with a patient, basically just what I told you and they do fine with this. So this is the planning arteriogram and you can see that the segment

three, two and four. I can pass segment three but I couldn't get up and over into four because of the angle so I decided to treat two and four. Line spread function is a little higher, 10.3 but I also noticed this area, in my cone beam and on my arteriogram that was not there.

So right off the bat, I knew that it's like getting something from the phrenic but I was really worried about his kidney so I didn't actually go and investigate although in retrospect I would have, you'll see [LAUGH] So then I go in and give the Y90 and again you can see

that area. [BLANK_AUDIO] So one month out most of the tumor is dead except for the same area that I saw on my planning arteriogram and I can follow the inferior phrenic artery, the right inferior phrenic artery is these arrows, all the way up to the tumor to that area. So instead of waiting another two three months,

which is what I normally do for Y90, I decided to go back in. And I found the inferior phrenic and I saw the tumor and I did bland embolization. I used 100 to 300 micron embospheres stasis.

>> What would you have done if this patient didn't have renal failure and you saw that tumor and you recognized that there's extrahepatic supply when you're doing your pre Y90 mapping study, how would you do that? >> So I would try to do some redistribution so I probably would have gone into the inferior phrenic then and bland embolized at that point, hoping

to redistribute either on that day or the treatment day and deliver the Y90 hoping to get everything from the left hepatic artery. >> What would guys do? >> Well, I think we would probably do point down on treatment of the phrenic and hepatic artery. >> Would you do the same? >> There's a pre transplant patient so we had one patient go to the

OR, hot many years ago, and the resulting chaos was such that we don't do Y90 in pre transplant patients anymore. >> At all? >> At all. I guess if you guys just de-list them and then put them back on the list, but they don't wanna do that so basically we just don't use Y90 in our bridging patients.

Even though normally times over a year for HCC, every now and then, someone gets lucky. So just to avoid that problem we just don't do it. >> If we can tell prospectively from the imaging that the patient has a phrenic supply at the time of the pre Y90 we sometimes will

do actual chemoembolization of the phrenic suply at the time of the shunt study as well, just because I think the duration of response is better than bland embolization, but I think if you figure that out ahead of time you're better off doing at

the time of it. Obviously in this case you had reasons why you didn't do it right away because of the renal failure. >> How are the symptoms if you do the phrenic with chemo? >>They get shoulder pain but it goes away. >> Okay.

>> Yeah. [BLANK_AUDIO] >> All right. So, one month following the bland embo it was still viable in that same area so I got him back again [LAUGH] poor guy.

I decided to do convectional chemo to the left hepatic artery and this is my pre-procedure and post-procedure medications, based off of the pen protocol. Not everyone gives antibiotics, I don't know if you guys do.

I'm the only one at Jefferson that does, my colleagues do not. And with patients with renal failure actually with him I only gave zosyn the one dose because of his renal insufficiency. And then the catheters I wanna use a higher flow catheter

to get a good dose of chemo in. So then you come back and you can actually see this this little vessel here going up to that area, cone beam shows that well. I get a post treatment CT, not everyone does that, especially when

you're first starting off is really helpful for future treatment planning if you can see how much of your tumor got picked up everything, or you can do a cone beam at the end as well. And then one month following, no viability, four months following,

still no viability, decrease in size and I actually got an email today saying he just got transplanted so that's good. >> Yeah. >> [LAUGH]

This is a 51 year old man with HCV cirrhosis and a right hepatic lobe HCC which is recurrent after RFA 10 months prior. This is the arterial phase from his CT scan. You can see recurrent enhancing tumor around the ablation site, kinda nodular tumor on both lateral aspects of the abrasion site.

We've prescribed conventional TACE. We use triple therapeutic cocktail in this case and you can see the right hepatic angiogram showing multifocal disease, the patient underwent an uneventful therapy here. However given the multifocal disease he was brought back for multiple rounds of therapy. You can see this is a repeat TACE

five months later. Now we're starting to see some vessel abnormalities. Slight vessel attenuation in the right hepatic artery, again repeat TACE six months after that you can start to see multifocal vessel attenuation, vessel occlusion with an abrupt cutoff. And now one

month after that again lots of occlusions, lots of attenuation that completely obliterated right hepatic arterial system 13 months later. So this is a guy who has arterial injury or arterial occlusion related to TACE. This is not a complication per say but I think this is part of the natural history of multiple local-regional

therapies with embolic type treatments. The incidence spans anywhere from about 10 to 50%. You can get loss of vascular patency when TACE is performed to stasis or near stasis endpoint in a good percentage of cases. And I think most people take this to be related to caustic chemotherapy and embolics precipitating the hepatic injury. And obviously the

major consequence is loss of future access for local-regional therapy. It's been described for multiple chemotherapy drugs and embolic agents. And obviously what you're looking for here is attenuation, stenosis,

slow flow or occlusion in the vascular bed that you're treating. I don't think there's any real way to avoid this if you're gonna do multiple local-regional therapies, although you can consider embolizing to a substasis angiographic endpoint, use of temporary

embolic agents. And some practitioners will advocate bland particle embolization in this case, stating that there's a reduced rate of arterial occlusion, although I'm not necessarily certain that we know this for sure. From a management standpoint, I think this is a permanent event.

If one wants to pursue local-regional therapy you can consider looking for parasitized extra hepatic blood supply to HCC's in particular. However, I think at this point, systemic therapy is a pretty good option.

And this gentleman actually was prescribed sorafenib after his hepatic arterial loss. He underwent 7 total TACEs to both lobes and he expired more than 3 years after his first TACE, so he actually did pretty good for his tumor burden. Any questions or thoughts about this case?

>> [INAUDIBLE] >> We usually aim for complete tumor devascularization and maintenance of antegrade flow in the treated vascular bed. Given that he had so many TACEs I can't promise you that that was the case for every single procedure but that's our usual approach to these chemoembolizations. >> Has anybody got a question?

[INAUDIBLE] The question is, what's the threshold for switching modalities, if we start to see such changes after multiple TACEs. And the answer is it's probably operator preference again, I'll put that to the

to the group here. Would you guys switch modalities if you started to see arterial abnormalities in the treated vascular bed after some TACE procedures? >> I think some of it depends on your response. I'm not sure with this patient I wouldn't have gone right to Y90 you know multifocal

disease or bilobar disease or PVT is typically when I would go to a Y90 initially instead of TACE. If I could mention one thing about the temporary agent. In the past we used to use that in all patients, right, rather

than lipiodol, you kinda chase it with gel foam and I think, to be perfectly honest it didn't work. You see just as many cases like this with the temporary agent as you would. Because it's three weeks to three months generally in terms of

with gel foam particles when these things are gonna recanalize. So by then you're already persositizing it and frankly I just don't think work and it hurt very badly. >> Not to make this too complicated, we can all snicker but we started radioembolization obviously at North Western but for other reasons is because of this.

Some of these patients get many treatments over the course. You had seven TACE procedures here and we know in general with radioembolization, we can repeat the therapy. So we tend to do radial embolization if we decide that it's not working or there's early progression or we've reached radiation dose limits, then we do chemoembolization.

It's anecdotal that's the way we kinda run it now. In this particular patient you had seven time points. If you noticed that the vessels are starting to go away you know in the back of your mind that there may be a point that you're not gonna be able to do any more therapies. You could consider

going into something else such as radioembolization at that point but it's a little bit convoluted by the fact that there's evidence that doing repeated TACEs is better than doing TACE in one session and you wonder why did you do seven, is it not working. It didn't seem like you're doing

a lot of different segments, it was all re-occuring in the same spot so. >> I think it's a great point and I think it's one worth considering in a case like this. What I will say is we typically practice on demand therapy so this

gentleman actually having a response at each time point but then recurrence and repeat TACE. So I think to Bob's point, the therapy that we were applying was working although we were having kind of collateral damage

effects here. >> Who would have started with conventional TACE here? Who would have started with Y90? Who would have started with line/g embo/g? Cerefolin? Guess mostly Y90. You guys aren't answering much by the way.

this was actually a trainee case. This was a woman with a very small left hepatic lobe tumor, some

variant anatomy with a gastrohepatic trunk. You can see TACE was prescribed and you can see the gastric branches on the left hepatic trunk arteriogram. And actually this was late in the year, the trainee was by himself in the case and

he mistook the gastric fundal blush as tumor, didn't notice the left draining left gastric vein. Usually you would anticipate from liver to see hepatic venous drainage and began to get his catheter in a more selective position and give chemotherapy to the gastric fundus.

At that point I came by the room said, whoa! Let's stop, we re-positioned the catheter, stopped injecting the chemotherapy, advanced the catheter, saw the true enhancing tumor and applied treatment,

nice chemotherapy uptake. And in this case the patient actually did pretty nicely, no abdominal pain, nausea, vomiting, tolerated oral intake, after TACE without issue and she was discharged home. We added a PPI for her but she remained asymptomatic,

and a nice result at one month.>> So was whoa the only thing that you actually said when you- >> [LAUGH] I like to take it easy on these guys

yeah. >> [INAUDIBLE] >> Sometimes it's nice to know you can get away with I guess right? >> [INAUDIBLE] That was the procedure that had happened to the patient in the past for that patient. So that's a good point perhaps the patient had recruited

vessels from the hepatic circulation to supply that previously embolized location. So that's an astute observation there. >> Why are you treating those [INAUDIBLE] >> The question is why are we even treating those with TACE, can

you->> [INAUDIBLE] >> The hepatic tumor in case one? Either one of them, I guess that's an institutional and personal preference and there's a lot of options for us. At our institution we use all three forms of therapy but in these

particular cases. The operator had selected conventional TACE which I think is appropriate for parenchymal lesions like we saw in those two cases. Yeah question >> [INAUDIBLE] >> Well that-

>> [INAUDIBLE] >> We won't get too lost in the weeds on answering those types of questions but nonetheless, patient did pretty well. I wanna briefly overview non-target embolization, incidence is pretty low. It can span from anything from colocentesis,

pancreatitis, all sort of lesions, and the severity can be related to the embolic load size and collateral perfusion. We see high attenuation chemotherapy on CT, might not be able to see it on MR.

And we talked about some avoidance techniques, careful angiographic review, selective therapy, cone beam CT for real time therapeutic monitoring. You can embolize vessels or use cold packs to avoid non-target to superficial structures and consider vasodilation of treatment beds with things like

Nitroglycerine and then there's some specialty catheters obviously. For management I think subclinical cases can be observed. We use PPIs in our second case to help prevent EGI symptoms and symptomatic improvement to improve patient comfort and then escalation is needed.

All right so next case, this is a 72 year old man, with HCV cirrhosis, he has a large HCC with portal vein and hepatic vein tumor thrombus. He has good liver function, bilirubin is 0.4, child pugh A but he has very poor functional status,

ECOG is 2. So here's his tumor, here's the HCC, here's the portal vein thrombus, this is enhancing so it's tumor thrombus and here's the hepatic vein tumor thrombus, so when we see an HCC with portal vein thrombus this sort of tends to make

us wanna do Y90. Just because if you are doing a bland embolization and you are shutting down the hepatic artery and the portal vein is also out then that could increase your risk of a liver infarct or liver failure in you are embolizing a large piece of liver.

So, even in the setting of main portal vein thrombosis if the patient is child pugh A. You can still potentially do radioembolization. So the portal vein thrombus pushes us more towards Y90. The other issue for this patient is his poor functional status. So we saw this before, we also get an ECOG on all of our patients,

ECOG zero means that they are active no restrictions. ECOG one they are walking around and doing some stuff but not fully active. ECOG two, they are walking around but not doing much around the house. ECOG three they are mostly in bed or in a chair and ECOG four they're

are completely disabled. So for me, for bland embolization I usually use a cut off ECOG of up to one, and then for Y90, I'll go up to an ECOG of two. And I think its just because the Y90 is a little better tolerated. It's done as an out patient procedure.

There's less post embolization syndrome. So for someone with border line functional status, Y90 might be better tolerated. So in terms of Y90 versus bland embolization the Y90 of course is done as an outpatient,

but you have to do the mapping and order the dose first. So if you have a tumor that's growing quickly and you wanna treat it immediately and it's a tumor that could potentially respond to bland embolization, that might push you towards bland embolization because you'll be able to treat them immediately.

Of course the bland embolization has more post embolization syndrome and they're getting admitted for the most part, Y90 is more expensive and in terms of what we're treating, for the most part bland embolization we're using on hypervascular tumors like HCC,

neuroendocrine tumor, melanoma and then Y90 were using on we're using on hypovascular tumors like colorectal liver metastases. And of course the Y90 we can treat the main portal vein thrombus if they have good liver function. So in this case because of the functional status and the portal vein tumor thrombus we did Y90, treated the right hepatic artery and got a good response. >> So what was the shunt in this case? >> I think it was under 10% I don't remember the exact number. >> Right, you wanna talk a little bit about how you handle higher shunt fractions and people who have vascular invasion? >> Yeah, so the shunt fraction is greater than 20, you could reduce the dose or you could just not treat them and do bland embolization instead. >> You ever put him on sorafenib and redo their shunt study? >> I personally have not done that, have you seen good results with that? >> I've never done it either but other people have, and said if you put on sorafenib for a month and then redo their shunt study that the shunt fraction will go down after the entire androgenic therapy. >> You can also do bland embolization or TACE and then redo a post study and see what the shunt value, it usually goes down as well.

>> I would just add that there's not an absolute cut off for shunts or 20% is high but that doesn't mean you can't treat the patient, you have to do the volumetrics and dosimetry and if the patient doesn't have COPD or something where you're worried about you can go up to the maximum lung dose, and if you're getting a therapeutic

dose into the tumor at the maximal lung dose, you can still treat people with 20 to 25% shunt fractions as long as. I have a lady whose got really bad COPD and has had 22% shunt and I decided not to do Y90 on her cuz she had hepatic vein invasion, and we're trying

other things first and then come back to it, but there is no magic number you have to plug in the numbers and see what you can get and usually we just go up the maximal lung dose and you can still get a therapeutic dose in the tumor. >> I think that I can comment on,

I think you frequently here this philosophy that patients with microvascular invasion sort of get Y90 versus chemoembolization because somehow the smaller reactor microspheres will get into the tumor thrombus better, but that's basically marketing as far as I know, there is no real

data to support that concept. I think if you are doing lipiodol based chemoembolization the liquid emulsion will go right in the tumor, I mean it's an arterialized tumor thrombus and you'll see the lipiodol uptake in the tumor thrombus. You could actually get complete responses in the tumor thrombus to conventional hepatomized chemoembolization.

So, you know, there are other factors that might tip you between re-embolization, chemoembolization but I don't think vascular invasion is really one that should play into it. The other comment i'll make is one of the comments you said was in deciding between the two, whether you want a quick response or not might influence your decision but the other person in the room is the patient,

and you should ask the patient what they want cuz maybe what the patient wants as a quick response, as opposed to what you want. And so what I tell patients is for the average patient with no big factors that the medical benefit and

the medical risk of chemoembolization or embolization is the same. You don't know how it will work on that patient, but on average they work similarly well and they're similarly safe assuming that there's no other mitigating factors, I can tell them can be quick and sick or you can be slow and glow.

It's up to you. You can pick your poison. We'll start with whichever you want, I'm happy to do it, and if it works well, we'll stick with it and if it doesn't work well we can still do the other one.

You haven't burned any bridges. I hear a lot of people say, oh I told them to get Y90 cuz I they won't get sick. I said, how do you know that's what they want? Most patient want their cancer dead and frankly if they have a little

pain and nausea and in the hospital overnight, it's worth it to them to know that tomorrow the cancer is dead as opposed to getting Y90 a month from now and waiting three more months to find out it didn't work. So, patient preference does come into play.

It's not only a medical decision, in most patients it's really a patient preference decision in terms of quality of life issues and for some patients the quality of life has improved knowing that cancer has been treated as opposed to knowing they'll be done as an out patient.

>> Yeah, so we also do bland embo in the setting of segmental portal vein thrombus. >> How many people have Y90 programs at their institution? Raise your hands. Okay, so far less than half, and how many people have glass microspheres, and how many people have resin microspheres?

Some people don't have either. >> [LAUGH] >> I don't know what the other option is. >> Maybe we have both but we just follow regulatory guidelines and doing it since we are training program so our HCC patients get TheraSphere

under the HDE and all our meths get stratospheres but we basically just do that cuz we have it and we wanna train the fellows in both, and it's compliant to do it that way so we can do it [INAUDIBLE ] >> Same thing although I'm working on getting an IRB to use TheraSpheres for primary and secondary.

>> So we have both and we have an umbrella IRB that allows us treat any patient with either of the devices and we pick the device based on the tumor, the characteristics of tumor burden and sort of patient characteristics with regard to the capacitance in the blood vessel like a metastatic cholorectal patient who's had tons of chemotherapy and has really beat up blood vessels.

We may have had a hard time getting an adequate dose in with resin so we use glass in that patient, so we don't really pay attention to the label indications so we do it on patient's characteristics. >> You decide after? >> After the shunt study,

yeah, we decide after the shunt study.

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