Recurrent Hepatocellular Carcinoma (Multifocal) | Radioembolization | 65 | Male
Recurrent Hepatocellular Carcinoma (Multifocal) | Radioembolization | 65 | Male
Recurrent Hepatocellular Carcinoma (Multifocal) | Radioembolization | 65 | Male
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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.

cholangiocarcinoma. She had a left hepatectomy and she now has a three centimeter recurrence

at the resection margin. She has good liver function, bilirubin is 0.8, child pugh A and good functional status, ECOG is zero. So, here's the tumor,

you can see the resection margin here and here's the three centimeter recurrence. So the options for treating this you could do ablation, bland embolization, Y90, now the location is not great for ablation, it's next to the IVC, next to the heart, so not a great ablation

candidate. In this particular case since it's sort of a hypovascular tumor, we decided to do Y90 and so they've had a left hepatectomy so they only have a right hepatic artery and on the angiogram, this is the right hepatic artery and it turns out that this tiny vessel

here is what's supplying the recurrence. So I spent a lot of time trying to get into this vessel and could not get into it so the question at this point is if I can't get into this vessel, should I embolize the entire remnant liver. I think you could potentially do it.

You don't wanna do it because there's gonna be a higher risk of liver failure, so what I ended up doing is protecting some of these off target branches by embolizing with gelfoam and then I delivered the Y90 to the right hepatic artery. You can see on the Bremsstrahlung

SPEC CT after delivering the Y90 that the tumor is right here at the resection margin so the Y90 got to the target and protected a lot of the off target liver. So the other question here is TheraSphere versus SIR-Spheres and in this particular case we're treating a small tumor, and it's

supplied by a very small vessel and one issue with SIR-Spheres is that it's less dose for particles but there are more particles, it's more embolic, and sometimes you reach stasis before you've delivered your entire dose. So for the small tumors supplied by small vessel, you might have

better success delivering your whole dose with TheraSphere which is gonna be less embolic. So in terms of comparing TheraSphere and SIR-Spheres, the way that I think about it is that if you're worried about reflux,

if you're worried about reaching stasis before delivering your entire dose, then that might push you more towards TheraSphere, also for portal vein thrombus, if you wanna be less embolic that might be another reason to use

TheraSphere. For SIR-Spheres it's lower dose per particle, more particles so if you have a large lesion and you feel like you need a lot of particles to cover the whole thing that might be a reason to use SIR-Spheres. In terms of indications,

TheraSphere has a humanitarian device exemption for HCC, SIR-Sphere is FDA approved for colorectal mets .At our hospital we're not particularly influenced by the indications. If your IRB for TheraSphere says you can only use HCC then of course that's gonna be a restriction.

Our IRB says that we can use TheraSphere to treat anything, so that doesn't restrict us. And then in terms of insurance approval, I have had some issues, if you're treating something unusual like if you're not treating HCC, neuroendocrine tumor or colorectal mass sometimes the insurance

company won't pay for it but if they are gonna pay for it I personally haven't had any issue where the insurance company said it will only pay for SIR-Spheres or will only pay for TheraSphere. >> For a long time Blue Cross had a national non payment policy for any kind of metastatic disease other than the tumors that Edd listed and they actually just reversed that policy recently.

So it used to be almost impossible to get approval. In fact when I would have conversations with patients about chemoembolization verses Y90, I just flipped to the back of their charts and look at their insurance cuz often that determine what they got. I mean in Philadelphia, it's either Blue Cross or Medicare and so depending upon who their insurance

coverage often that determined what therapy they could get paid for. But now they've Blue Cross is when they used change policy where they will cover therapy for any liver dominant not about any but most liver dominant metastases so breasts and things that they used

to not pay for. That's a big change. When you [INAUDIBLE] assume that the rest of the liver was gonna get [INAUDIBLE] kinda the same thing. >> Yeah. I just ordered it as a whole remnant liver dose, and then assumed

that I would just deliver it more selectively. >> So you're doing a segmentectomy? >> Right. Yeah. Yeah.

So here is a different one, a larger HCC with satellite lesions, so 65 year old male,

no known liver disease. He was on statins and his LFTs were off so they did some testing and then they found this bilobar HCC and biopsy was performed cuz he doesn't have underlying liver disease to confirm HCC. So there is the lesion, it was 15.9 centimeters on MR but on CT 10.9 centimeters and there is satellite lesions bilobar

but there was no vascular invasion. So technically he is BCLC B but I wouldn't TACE this or bland embo it because I would feel like it would require multiple, multiple, multiple treatments and it'd have a huge post-embolic syndrome. So, I talked to them about Y90,

I talked to them about sorafenib and then Jefferson we have this STOP-HCC trial which combines sorafenib and Y90. Would you guys have thought about chemo? >> Sure. There's no reason not to.

I know why you'd think they would get terrible post-embolization syndrome because there's no correlation with tumor burden and post embolization. The only thing that affects the severity in duration of post embolization syndrome is whether you get the gallbladder or not. Nothing else matters. So that wouldn't put me off.

I would just give the patient the option of going either way. >> So STOP-HCC trial it's for unresectable HCC. It's Y90 plus sorafenib or sorafenib alone. We discussed this with the patient, he was agreeable. And this wasn't done in multidisciplinary clinic so, the hepatologist, the oncologist and I

all three of us go in at the same time to talk to the patient about all the options and so I do the planning arteriogram and there is supply from the left hepatic artery, the anterior right hepatic artery and the posterior right hepatic artery, line spread function is 5%. So the first treatment I treat the entire right hepatic lobe, I

use 220 gigabecquerel on extended shelf life vials and that's probably the maximum I use in one area, so I did that. A month later brought him back and did the left hepatic artery and then 2.5 weeks later, he starts sorafenib. [BLANK_AUDIO]

And the other thing I wanna show you is only using 124 Gy, I tend to go a little higher now but for that protocol I go with 120. >> Do you wanna talk a little bit more about your treatment days and obviously it makes sense to use extended shelf life glass spheres with patients with high tumor burden for more spheres

and coverage. But what are your days that you will treat and how do you decide if you'll do a patient on a Thursday or a Friday with TheraSphere. >> It depends for me, on the planning day, how super selective I can get, I can get very super selective and the flow,

between how super selective I can and how the flow is, if the flow is little, not as brisk and I'm very super selective, I probably would just treat on a Tuesday or Wednesday but if I'm treating like a whole anterior, whole

posterior or whole left, I tend to use extended shelf life and there is usually really good flow. Also I might use non extended shelf life if there is a vessel nearby that I'm concerned about. For TheraSpheres I tend not to,

my threshold for coiling is much lower than SIR-Spheres but I will coil if something is close by as well. So in this patient, because of the protocol and the STOP-HCC trial, we get CTs every eight weeks.

Pre treatment 10.9 by CT, AFP was 11.4. The second treatment day, the AFP is actually rose to 17 but one month followup, the lesion's already shrinking, 7.6 centimeters, AFP's dropping.

Six month follow up, continuing improvement. Now he is 13 months out and things are truly good and he is tolerating even though. With the trial they actually start with the high dose of sorafenib. He's tolerating it well and doing well but I think usually they dose escalate the sorafenib but not for the trial.

>> He's lucky he got randomized to Y90. >> That's my biggest fear of it, but I think that's the problem with the study is recruitment. Because if it was probably slightly smaller, I would be like, no I'm just gonna go into Y90 right away and then start with sorafenib.

That's why the trial isn't doing that well because we all wanna Y90 everything. Not everything but appropriate things. >> Well, more importantly is we don't wanna just put people on sorafenib and get liver directed therapy which is why a lot of people wouldn't refuse to

be on that study. >> Yeah, and part of it is if they start progressing on sorafenib and their function is okay they come back to us. >> Anybody else participating in that trial here in the audience? No.

>> I think it will take a while to recruit because of the [INAUDIBLE]

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.

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.

of plants and this is not a transplant case I apologize for that one infraction but it's related to our portal biliary case and it's one you probably should see. This is a patient with pancreatic cancer, a biliary drain in place

over a period of time. You can see that there's a tumor right at the hepatic hilum here and again the patient comes to the ER with gross blood distending the bag and unstable hemoglobin is exceedingly low in the 4's. And comes to us and this time it's not HAT so the patient does have a hepatic artery.

This is our injection of the biliary drain so again are we done? No. [LAUGH] looks like a good injection and everything looks fine but the guy almost exsanguinated a number of times. So make sure you inject everything that could potentially supply the hepaticojejunostomy in the liver, this is a SMA injection so

nothing there, right? This is a celiac injection. Remember the strain goes in over here into a duct but the tumor's here. So it looks a little funny there and given that this patient almost died a couple of times it looks pretty benign.

So again, are we done? No. Pull this over wire so you're not tapping out the bleed and then reinject the artery, we'll do that, still nothing. So are we done? Get a little closer all the way up to our catheter inject,

still nothing, pull it back 2 millimeters, [BLANK_AUDIO] Boom! And then patient immediately unstable, tachycardiac, starting to drop blood pressure on the table. So what's the next step?

People say embolization, no, it's put the catheter back in immediately and a larger bar if you have to, think fast, so do that and in this case embolize the entire hepatic artery. This is not a transplant so if the patient can tolerate that,

fine. And then just to illustrate another point about covered stents so really short bile ducts with hepatic jejunostomy, you know you have wall flexes I think they are four centimeter, the length is

the shortest one, this patient needed that for the tumor, that was placed and this is a follow up, it's down here, so it got fired out and then replaced by a standard roll stent. All tubes and wires removed,

the patient tube free at three months so just a couple of standard logistical points there and that's it for me. Thanks for the attention. >> [APPLAUSE]

So this is a case, this is a male, 75-years-old with lung cancer in

the left lower lobe, and he's getting chemo and radiation. And then starts to develop massive hemoptysis. He's too unstable for bronchoscopy. So he gets sent to us. And here we go, here's a big mass. It's very near the mainstem bronchus bifurcation. So we go right to our bronchial embolization which shows bronchial artery, and the blush that you get from the tumor there. And then we go ahead and

embolize it. And it was successful. We do this usually with moderate sedation, as I'm sure most of you do. After the procedure though, in the holding room, he developed altered mental status. He gets a full work up. And it turns out he get's a small stroke, likely related to our procedure.

A lot of different ways that you could think this might have happened, maybe at some point when, if we were working up in the arch, something could have happened. But I wanna show you some cases, and alert you to some things that might happen that could cause this. So one is shunting. Now we didn't really see it that well, on that

bronchial artery embolization, I showed there in the left. But here's a different case, patient with chronic lung disease. And here we're doing an embolization in the bronchial. And you can clearly see the pulmonary venous drainage, and how easily using particles that would go through. So when you guys see shunts, like Charles,

what do you do if you're doing one of these, then you see a pretty obviously shunt like that, how do you proceed? >> I'm sure you'll serve it with large particles. >> Large particles. And Bill how about you? >> Yeah, so I was gonna ask you. What did you use in that first case? What's-

>> The first case, 700, 900 microns embosphere. So the bigger ones, and that still was an issue. So that's a good point. So some people say, if you use larger particles, it'll probably close the shunt, I mean you save. But others have advocated trying to close the

shunt, or just using coils approximately. We'll talk a little bit about difference in using coils and particles there. In this case we used coils. Here's another case where you can see the drainage pretty well. >> One of them, [INAUDIBLE AUDIO] particle and ATR, bring them together [INAUDIBLE AUDIO] in common cases.

>> Yeah, if you're comfortable using glue, I mean this would be a great instance for that. You could get embolization, and then you wouldn't have to worry about necessarily these small particles getting through.

So just to quickly review massive hemoptysis. The exact definition varies in literature. Most people use about 300 cc over 24 hours. And the mortality results from asphyxiation, rather than just a blood a loss and exsanguination. The management mostly, these patients, if they're unstable, they get ICU support, bronchoscopy/intubation,

and then they try to get them to us. You don't wanna wait too long. When they're more stable then they get a work up like that. So mostly you're gonna be doing these for bronchiectasis, TB, chronic lung diseases, but

lung cancer and other tumors can account for hemoptysis. And bronchial artery embolization in these cases, is still a really viable alternative to treat these. The sources of bleeding is usually the bronchioles, but the pulmonary arteries and nonbronchial systemic arteries can cause a sort/g. In malignancy

maybe a little different. Usually hemoptysis occurs cuz of local necrosis in vessel inflammation, rather than a direct tumor invasion of an artery. And obviously we're talking about embolotherapy. But the interventional bronchoscopy's based on what's locally available, have a lot of

toys to play with too with this. We looked at bronchial artery embolization for malignant hemoptysis, so lung cancer patients. And it's very similar to looking at bronchial artery embolization for all commas/g cystic fibrosis, or patients with bronchiectasis. You have good technical success rate,

low complication rate, but the recurrence rate is relatively high, and so you might need to go back in. The mortality rate is high. Another- >> Have you heard times where, you showed that case when you quoted coil, and where we saw us some shunting, have you heard cases where you quoted coil incision, and you heard/g in your access- >> Yeah, yes we have.

And that's the main hesitation we always have about using a coil. It's like you feel safe at that time, but you know this patient will probably come back. And the chances of you getting back through there are tough, and then you've got to look for other arteries that feed it. Another group looked at as

well, where they had a good technical success rate, but had a high recurrence rate. This is all commas. And the other thing that's interesting to look at, the embolic material look at, it's all over. Even the same groups are using combination of gelatin and PVA,

some glues out there, coils. So I think there is a lot of different options out there for you. And it's a memory of a good clinical success rate, but your recurrence rate is gonna be a little bit higher.

So these are some of the complications that we mentioned, the CNS complication. One other thing is the anatomy, and the bronchial artery anatomy, it can be variable. Mostly we're gonna be looking in the descending aorta around like

T5, T6. Now remember the bronchial arteries also supply the visceral pleura, great vessel vasa vasorum, mediastinum, middle third of the esophagus. There's an abstract in one of the other sessions, a group from Asia, they made a point to look for the esophageal artery to

try to embolize that, from lower lobe branches that they were doing. A lot of these are, the remaining 20% are gonna be from either thoracic or abdominal branches. And then the bronchial venous return is via the pulmonary veins. But there is some minor drainage to the SVC, the azygos etc.

But you shouldn't see the rapid shunting. You should see like in a normal angiogram, the venous phase come a little later, not a direct thing. So, here's just some other drawings to show nicely the anatomy. And there's a lot of variabilities, especially when patients have

advanced lung disease, and you get a lot of neovascularity. And then you eventually can develop nonsystemic bronchial feeders like the internal mammary, branches of subclivian, the inferior phrenic artery, these can all feed there. So

just wanted to ask my co-presenters, when we get a case of bronchial artery embolization, we usually identify the bronchial arteries, embolize those, and then if we're happy with that, we're done, and we don't go on a hunt for other arteries.

Do you guys do something similar or do you try to be more complete when you first start? >> In general, we do something, somewhat a better case of my presentation, where we'll show when we do go for other arteries. But usually if the bronchial looks like it's covering the distribution throughout then we'll keep them coming/g. >> Yeah, Phil/g. >> Yeah, I think if it's a first time case, we hit the bronchioles first, and see how the patient responds. There are some patients that are coming back multiple

times. And we know when we absolutely look for some of these transportal collaterals. And especially like you just said is, if the person with perfused lung disease, and if the area they're bleeding from isn't really being perfused in the bronchioles, then I think that makes us fulfill- >> Right. >> Or something- >> Good. So the bronchial artery anatomy, a lot of this comes to a relatively old cadaver study, but these are the main variance of the bronchial artery anatomy. This is the most common. We have an intercostobronchial trunk, and then two left bronchials. But just be aware that there's a lot

of variance of this. And I really like to have a CT scan before hemorrhage. Mostly it's patients where will have, and in cases with hypertrophy bronchial artery, you can usually pick them off the aorta, and I'll show you some cases. So the goal is really to get a durable occlusion without affecting

the capillary bed. There's really no single embolic agent that has shown clear superiority. Most people use particle embolics. The dogma is that metallic coils should be avoided, because you only get a proximal occlusion, you kinda burn your bridge, and then collateral pathways develop. I put a couple of asterisks there. I was at a session

where the group from Pittsburgh showed that using coils, they were using them mostly because of shunts, and they had good outcomes with that. So we'll have to see how that goes. Gelfoam, liquid embolics has also been reported.

Here's a case of, I have asterisks again, but why surgery or just ligating something very approximately doesn't work. This patient had a clip right here. So it did absolutely nothing, right? It just finds a way around there. So it's just too proximal an embolization. You need to get in

there with particles to do it. Here is a patient that had a lung transplant on the left, and in the native fibrotic doing so. When you get called in, the bleeding from the right, to take care of that. And then they don't transplant the bronchi artery. They don't reanastomos/g that. These things find their way to this transplanted lung, over

the bronchial artery there. So it's just amazing how much collateralization can occur, and you just need to be cognizant on that. The other thing people talk about, we talked about a stroke, or other CNS complications of bronchial artery embolization, is

the spinal cord influx. So people are worried about the anterior spinal artery. Just to review some of the anatomy. It courses along the ventral surface of the cord. And you get a bunch of these segmental medullary arteries along the entire course. And it has this classic hairpin configuration.

Now the most prominent of these is the artery of Adamkiewicz. It's usually gonna be lower than where you're looking. So remember, we're gonna be in the T4 to 6 range usually for our bronchioles, but this is gonna be a little bit lower. Though a small percentage maybe off the intercostobronchial trunk.

I don't see these a lot. Here's what it looks like, just off an intercostal, the classic hairpin appearance. You could see it's a little bit lower than we'd be looking at. Here's another classic hairpin occurrence.

I very rarely see it. A fellow then, he went to California, his first week of practice, he said, oh look at my first bronchial artery embolization, and he did see it there. So in these cases, there are a few options. You could be pretty conservative, and basically not treat it.

Some people say, you can go beyond the spinal artery, and try to embolize it, and be very careful about getting any reflux, which is what we usually try to do. You could maybe try to use coils as well in that case. But you just have to be aware of it,

you gotta look for it, and just make sure that you don't have that complication, when you go ahead. >> You can coil the origin of it. And then use particles for your [INAUDIBLE AUDIO]. >> Okay, yeah, so that's a good point. You could coil it near the

origin, then protect that, and then get your particles to there. And then the coiling at the origin won't cause an influx, cuz you're not causing ischemia there.

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.

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 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]

So our second case, 65-year old female, HBV, cirrhosis, minimally elevated AFP. Previous ablation. No, sorry. This is just inside a large nodule that was growing, and there is a I think a 1 cm-ish

hypervascular nodule within the larger lower attenuation area. And it's seen best I think on the coronal image down on the left there, the little hypervascular dot. So enlarging low attenuation lesion in segment VI, it's a 1.1 cm hypervascular nodule. So it's the classic nodule within the nodule. It does have washout. So, how would you guys approach?

[BLANK_AUDIO] I go back? >> So how long was this follow up in this patient? >> I think we, I can't remember exactly- >> Okay. >> But I know it is new. This nodule, the hypervascular nodule is new.

>> And it's been enlarging? >> Well, from nothing to now a hypervascular with washout. So I think that pushes us into the larynx 5. >> Right. Without going through the entire series, first things first we wanna make sure that it's not a vascular issue from the previous ablation. >> No. >> Once we've cleared that,

and this is a 1.1 cm nodule in this particular patient, and if it's enlarging on the second follow up. One of the options would be to re-ablate, and do a biopsy frozen at the same time with the coaxial system, and if it is positive or not, we just go ahead and ablate it and do a track ablation out of that time. That's one option.

>> You mentioned this was ablated before. >> It's not a previous ablation- >> It's not. It's not, yeah. Because you mentioned and then you say no. So number one, the whole thing is an HCC, it's not just the one 1.1. It's all HCC. If not all HCC, it's almost HCC, meaning it's such a high grade dysplasia that you really need to take care of the whole

thing. Because this is nodule in nodule is typical, and I think so the mass is clearly like 4cm here or so, right? So what I think, so that being said, just to clarify because you've mentioned the ablation that's why Raj was, yeah I think looking at that answer, that would be like what has been left behind. So this could be a combo case I think, in

the right- >> You would the whole thing? >> In the right way, which means to do ablation first. >> [LAUGH] >> Followed by injection of, followed by transcriptive

therapy. This is the like a kind of alternate protocol that we developed. Actually I understand that if you do TACE in the first place, you have a nice picture to target the ablation. But as I said before, especially if you use different modalities, an ultrasound or whatever, you don't really need that. And particularly for this patient that is not prominently upper

vascular, doing the ablation in the first place will create the hyperemia and the upper vascularity that would then potentially facilitate the effect of the combo therapy. So that can be an option. I think that the whole lesion should be treated as an HCC, so the goal should be to ablate the whole thing.

>> So let me now get our approach, which is of course exactly the opposite. But that's okay, there is a reason for it. It's not that we are just doing that to disagree with the Italian approach. >> It's the Miami approach. Before I- >> That's fine. >> Before I moved there.

>> Before you were there? >> Yes, before I was there. >> These Miami people, they're very south. But- >> If I can tell you that Raj told me, his percentage of local recurrence with the combo, with microwave followed by the duct TACE. Guess how much?

>> 8%. >> 0. >> [LAUGH] >> Anyway so, I have a question for you. It looks to me, first of all before I say why we do it differently and how, it looks to me that the right liver and especially the posterior sector is small.

It looks like there is left hypertrophy. Is the portal vein patent? >> Yes. >> Or is it invaded? >> No, it's patent. >> Because it looks to me that, that right liver is a little small, which is a picture you see if there is invasion of the portal vein. >> No. This is a classic patient here who's Asian, who has a left lobe caudate hypertrophy splenomegaly related to HBV and

cirrhosis. >> Okay, so Riccardo and Raj like to do the ablation first, and then they use the hyperemia to give their TACE or drug-eluting beads. And that makes sense because they use chemotherapy in those beads and in the TACE, and they think the chemotherapy works. So in our approach, we don't think that chemotherapy adds anything

to the mix. We believe that it's only bland embolization enough to treat this tumor. And as a matter of fact again, we just published a JCO paper in January, showing that there is no difference between drug-eluting beads and there was no difference, Riccardo. >> There was a difference that was not significant. >> Well, okay, fine. So we don't believe there is a significant difference

between, in small particles versus small particles with doxorubicin. And therefore we think that de-vascularizing the tumor before will actually allow us to get a better ablation zone with better tumor kill, less viable tumor left behind. >> But that's not endovascular/g. >> No, I understand. I understand. I'm just saying the rationale on why we do it differently. In this

particular case, I'm not sure how big it is. If it is over 6 or 7, you may just do embolization, I don't know. But if it's 4, we'll definitely do to a kill or 5 definitely. And just to reiterate on this. I think from our institution and others it has been proven, at least in matched patients with resection, that segmentectomy is not better, but combination of intra-arterial

therapy with ablation. And I believe it was up to 7 cm at least from our cohort, and I think if I'm not mistaken, you may correct me if I'm wrong, I think it's up to 8 cm from other series. Which you can argue the 8 cm that you can do combined treatment, but at least the data so far, and again they're not randomized trials, but they at least match. And it seems that the only difference in mortality

or in survival of the patients was the occluded state at least in our series, or the Child cirrhosis level in others. So it was really the level of disease, the only factor that affected outcomes. >> And I just want to just clarify because we're all like kidding a bit. I've nothing against a combo in which you do your TACE first and

then the ablation. You probably can also do the other way round. And this particular case because it's not prominent hypervascular I would really, let's say go a little bit more aligning toward the other way for that reason. >> Okay. >> Fred,

do you wanna? >> I didn't want to convert this into a TACE, bland versus loaded discussion, since we are an ablation panel. But to Riccardo's point, the only thing we haven't done so far is publish that data and it is gonna come out, and I hope it's not dismissed the way you just dismissed it at a 0% low.

>> [LAUGH] >> So, >> 0% is almost like perfection. >> [LAUGH] Yeah.

So now that everybody else has given you their opinion, let me just tell you how it is here. >> [LAUGH] >> You notice how our panel, nobody has strong opinions about anything. We're a bunch of low toasts/g up here. So our philosophy is a little bit

different than Riccardo's and Raj's, and may be a little closer to Costi's, but still there's some differences. So first of all, when we think about combination therapies, virtually any combination of anything is probably better than monotherapy alone for larger and mid-sized tumors. So I think that's the first thing. We tend to treat with conventional

TACE. We do it 2 weeks or so before we do the ablation, and there's two reasons why we do that. Number one is that there was a interesting animal study by Nahum/g Goldberg a number of years ago, looking at the order of embolization and ablation. And it turns out if you do the embolization first, you tend to get

larger ablation zones, than the other way around. Now that was in normal animals and this is in tumors, and so that's a little bit, you know how it applies, I don't know. So that's number one. Number two is that if you use conventional TACE with ethiodol, the background liver clears, mostly the ethiodol, after a couple of weeks. And so

when you do your ablation, it's really easy to see where your margins are. And you can see the tumor, you can see the margins and you know exactly what you got. So those are the main reasons why we do that. We tend to use chemoembolization. It's just been the standard, not planned, but that's been our considered way for a long time.

>> So, entirely different for us. We follow these extremely closely, so we don't go after, I think it's potentially a different patient population. We don't treat the part that's not hypervascular, it's that part what's stable. So we don't feel like that part's the part to treat, so we wouldn't. But we would follow that up, and we would treat the part that we, and the Europeans or the Asians or Canadians in the audience, we

do use Definity or other ultrasound contrast agents. So we use that to approach this lesion and within that, the top images are the pre and the bottom images are the post. And the beauty of that is we can continue to give as many doses as you need. You place the needle in, and we use just a standard ablation. Needle goes in, and we do a standard ablation using the standard protocols.

And that's our post-ablation images afterwards, and we will continue to follow. >> Great. >> Yep, that's good. >> Okay, thanks Steve. You're gonna have to click through the images. >> Okay. >> With this image you show the rationale for the combo later because what was not hypervascular is now surrounded by an unseen ring,

and you would be able to deliver some beads and chemotherapy. Of course, we don't know in this case that you really had an excellent ablation, but not margin. So if you want the margin in a lesion that is really above a certain size, it's gonna be difficult to get it with a single modality. That's something that I think we need to acknowledge as a practical limitation because

theoretically you can do multiple overlapping, but in reality I don't believe that this is really very common.

so this is a 65 year old man with insulinoma, and liver metastases and he's symptomatic. He has episodes of hyporglycemia requiring IV dextrose and here's what the CT looks like. You can see multiple hypervascular lesions. For neuroendocrine tumor, we're typically doing at our hospital

we're doing bland embolization and they're typically lobar embolizations because it's typically a multi focal tumor. So in this case we're treating the right hepatic artery and if you look at the follow up, this is six months post embolization. So if we compare initially,

we have these large tumors. Six months post, you can see they're smaller, they're non enhancing, so pretty good result. And then two years later you can see he starts to develop some new enhancing lesions, some new metastasis but it's very small,

it's slow growing, he's asymptomatic so we actually did not re-embolize at this point. We continued to follow him, and then four years post embolization they're still slowly growing,

he's still asymptomatic but at this point he has a decent volume of disease so at this point we re-embolized. So the point of this case is that when you have a small volume of slow growing neuroendocrine tumor you don't have to re-embolize the recurrences immediately.

So in this case if we re-embolized him every time there's a little bit of recurrent enhancement, we could potentially be embolizing him every six months. And then we'd have eight embolizations in four years and his liver would be pretty beat up at that point.

So we tend to wait until the tumor starts growing, they have more volume or they become asymptomatic before we retreat. >> Now it's most likely that this guy has a mesothelioma that he was not being treated with embolotherapy isolation. So you wanna comment on what other medical therapies this patient

would have been on during that four years? >> Yeah. So he was on octreotide, I don't think they actually resected his primary. But the primary was stable on the follow up scans. >> Okay.

So it's a little unusual just to have an insulinoma that stayed stable on, just cuz it's a with a grade one tumor, insulinomas tend to be more aggressive, so this is the kind of thing where I totally agree with your approach in terms of embolization, the big concern neurocan tumors is you're gonna

run out of bullets and then they're gonna die from pre hepatic tumor and you won't be able to embolize them again. So I completely agree with stringing out as long as possible between cycles of embolization, so you don't burn all your arteries. And the same thing applies to Y90,

they can only get Y90 maybe a couple times. I have two patients I've done three cycles, but they were three years apart in neuro endocrin patients, and their liver function

was preserved, that's pretty rare. So, all these patients eventually get to the point where you can't embolize them any more and they die from liver recurrence and I hate it when that happens. So, it is good to string it out, but I think it's also important that you manage these patients with

a neurocan tumor board or at least some collaborative fashion because there are lots of great drugs in neuroendocrin tumors that either stabilize or sort of reduce disease. So an insulinoma patient like this I want a similar who they often respond pretty well to everolimus although that's more of a antistatic agent if can tolelrate everolimus and then CAPTEM

which is an oral chemoptherapy combination cytotoxic actually has about a 60% response rate. So I have one of my insulinoma patients now where I really have embolized her so many times, I'm getting nervous that I'm running out of bullets and she also is very sensitive to her insulin levels

going up. Tends to do things like pass out and crash her car, so we put her on CAPTEM and it's been like two years now and she has no symptoms and no measurable disease. So you're not working in isolation, here you wanna working in a

team and you wanna figure out what's part of the auto medicine in neuroendocrin patients as when to integrate your liver directed therapies with your systemic therapies, and kinda who goes next and one nice thing to do is actually ask someone you can kinda pass the ball back and forth,

so you can dream for a while, give him to a med unc/g for a while, and they can pass them back to you for a while, and you can sort of maximize the length of your benefit. Does anyone have any comment on how you do this? >> I agree, I think the tricky thing is

as you guys were already talking about is when do you pull the trigger? The asymptomatic, I mean if the patient is symptomatic it's easy but the asymptomatic slowly progressive neuroendocrine patient, when do you actually jump back in and make that decision to treat and I agree it's pretty difficult.

We have these discussions at tumor board. If they have significant progression like you see here like we would generally jump back in and I wouldn't wanna wait for this patient to progress even more even though they're asymptomatic but we regularly see people referred in from community oncologists that have waited on the asymptomatic neuroendocrine patient until they

have such bulky disease they're getting capsular pain biliary obstruction and you don't wanna wait that long. So we see that mistake made a lot so you can definitely be too aggressive and you can definitely be too conservative, try to find a sweet spot in the middle. >> Yeah, this is definitely a pitfall in neuroendocrine

patients because they've aggressed so slowly, and I got burned on a number of these earlier in my career when I was sort of foolish and did what Bill which is saw asyptomatic normal liver functions and decided to wait. And the problem is that the imaging will often underestimate the amount of disease infiltration and because it infiltrates so slowly,

the LTs will be normal and then you finally pull the trigger when they have over 50% tumor burden and they die of liver failure and then an autopsy what you find is they actually have 90 % tumor burden you just couldn't see it on your imaging. So you don't really wanna let it go that long and there are various cut points that predict worse outcomes, but generally for sure around

50% patients who have an over 50% tumor burden, have worse survival. But actually have worse tumor control after embolotherapy than patients if you treat them before they get to 50% tumor burden so you don't wanna wait that long. The other pitfall you see is because they progress so slowly, if

you're scaning them every three months or even every six months, they'll often get a scan that's red and stable because they only compare it to the prior scan. And often you have to go back a year or two to actually see that they've actually had the 20% growth that would be progression by this criteria. So, you know you can get a load

on this false sense of stability when in fact they are growing slowly, you just have to kinda visual, I always look at the pictures myself and for the nets I always pull up pictures from a year or two years previously, and often what you will see is there is actually real progression going on but the diagnostic wiz/g will never say

that. >> One other comment about Y90 in these patients and we talked about this a few weeks ago but there is a little bit concern in the neuroendocrine community about delayed sort of laid toxicity from Y90. And I think in a colorectal patient who probably doesn't have a very good

five year survival, using Y90 is great and we have good data for that in the salvage setting but in a neuroendocrin patient who might live 10 or 15 or 20 years with their disease, I think we have to really carefully think about when we integrate Y90 in these patients and whether or not there is potential for delayed toxicity from liver fibrosis from Y90. And especially now that most of these patients

are gonna be getting a bunch of systemic agents which ten years ago they wouldn't have been getting now they are getting a bunch of biologic agents and targeted agents and I've had a couple of patients that have gotten liver fibrosis after Y90 and it's a horrible outcome from Y90. So we for that reason use chemoembolization for first line in the low grade neuroendocrine patient and Y90

only if they don't respond to chemoembolization.

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