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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

lady with progressive worsening headache and altered mental status. And her blood pressure was very severe 239/132. She's had a very poor GCS score

that was continuing to get worse. And here is that blood pattern that I just talked with you about. A star pattern hemorrhage which we recognize a sub- arachnoid hemorrhage. When we did a CTA we found this bifurcation aneurysm at the

left MCA. So we went ahead and here is the aneurysm. And if you're used to looking at this we can appreciate that this aneurysm has multiple compartments. This double density here is a bubble on the anterior aspect of this aneurysm. This double

density behind this blood vessel is another pouch of this aneurysm behind this blood vessel. So we went ahead and put coils in the aneurysm and excluded it from circulation. So we can do that for

Excellent. Thank you. Thank you to the AVIR for having me today. So just a show of hands before we get started here. How many people here work in or exposed to the neurointerventional space. Very good and how many of you have been exposed to flow diversion for aneurysm

treatment. And how many of you have actually seen a flow diverter or a flow diverter case. Ok good. So today we're going to talk about flow diversion and for those of you that don't know flow diversion it

is the newest technology that we have available to treat cerebral aneurysms. So today we're going to talk about kind of how the technology flow diversion came to be what it is and kind of some of the applications and pitfalls that we have

with flow diversion today. So for those you didn't hear didn't hear the introduction. My name is John Gaughen. I'm an interventional neuroradiologist and the Director of the neurointerventional surgery service at Sentara Martha

Jefferson Hospital. I have several disclosures I take money from device companies with out any regard. The majority of money I take is for teaching purposes proctoring purposes. One of the devices that I do proctor is the

Pipeline device which is the only flow diverter that is FDA approved in the United States. There are several flow diverters used worldwide. A couple of which are now undergoing the FDA trials to become FDA-approved. But when we use the

term flow diverter in the American jargon we're really using flow diversion and Pipeline because that's the way the clinically relevant flow diverter. So you'll hear those terms maybe interchangeably in the talks because all

the devices that are shown here are Pipeline devices from Medtronic. So today we're going to talk about a brief history we're going to a device overview of clinical review and then we're going to look at the literature briefly very

briefly and then we're going to show some cases. So anybody know who this is

do have a strokes. They didn't come to you in proper time. Is there something that we can do to prevent their strokes? That's called medicines. That what we normally do. But there's some patients where you see

that the carotid arteries are still pretty narrow. It may have contributed to their stroke maybe they're outside the time window for you to be able to treat them with these. But now you know you have an

opportunity to treat the carotid disease it doesn't cause another stroke. That was the case that you have in front of you. A 72 year old man who came in with weakness in the left side couldn't see had slurred speech. He

unfortunately came a day after. So we couldn't offer him anything other than medical management. But a month later he came back so that he could have the carotid artery addressed. You can see on that picture that's a reconstructed

picture that shows the narrowing of the blood vessel with the arrow. There's hardly any flow across that narrowing. And the 2D reconstruction here with the coronal picture show that there is a huge atherosclerotic buildup to the point

where there is no flow. And the key to treat this is no small undertaking. Because if you go ahead and you angioplasty that atherosclerotic lesion you can actually send all the debris upstairs.

You could say that you could use a distal protection device but you would have to get through that narrowing. And when you do that you're going to dislodge all the debris upstairs. So in this case we wound up using a proximal flow arrest

device so that when you go ahead and do the angioplasty and lay the stent there is no forward flow to shower all that emboli. And that's exactly what we did. So here is the before and with that degree of stenosis the very next picture

shows you how much blood flow is going to the brain. (Thank you so much) So this is the narrowing. With that narrowing this is all the brain that this blood vessel is able to supply. The brain is starving for oxygen. Once we did the

procedure and you can see the outline of the stent here that looks like a very nice result. What does the brain look like. This branch wasn't even seen before. These branches were not even seen before. Now they're all open. So again there are

things that we might be able to do provided that the patient comes to us in a reasonably timely fashion to treat them from very their ischemic stroke and prevent the future risk of a stroke. So I'm going to

Randomized trials... I'm not going to go

through all those that we looked at... but here are a couple of big ones. So ACT 1 was a interesting trial in the fact that it was done on acceptable risk patients. And I hate the term low risk because if you have a carotid lesion you're not low

risk for anything. So acceptable risk for surgery patients. And the bottom line is CAS - carotid stenting - clearly established as a safe and effective procedure. And I think the shift really was away now from and that's why we're here today

talking away from carotid stent vs and endarterectomy. But can we actually optimize carotid stent outcomes. So can we pick the right patients to do carotid to offer carotid stenting to. And here's the composite endpoint for years not

statistically significant obviously between CAS and CEA. But remember again composite endpoints in all of the stroke in all the carotid stent trials include stroke death and myocardial infarction. Because if you take the MI picturing

out of it carotid endarterectomy is clearly a... excuse me... if you take the MI out of it carotid endarterectomy clearly has a lower stroke risk. So the other big trial was CREST. Looking at again

endarterectomy vs stenting and here again is your composite endpoint of death stroke or MI not statistically significant 5.2 vs 4.5. Primary endpoints equivalent. But again all strokes at 30 days were significantly

higher in carotid stent cases. And that continued out to 4 years. So equivalent if again if you add MI into it. But again this is now a technology that continues to improve and the progression of EPD or embolic protection devices has gone

from distal protection... so here and you know there's seven or eight of these filters now available... to proximal protection. This is a big device that you have to get in and occlude the common carotid

artery so you have no antegrade flow as your protection. And then what is the newest and I suspect is probably going to stay transcervical access with flow reversal which were going to talk a little bit about. Again to show

you the embolic risk is the big issue. And there is a 2x peri-procedural stroke rate for transfemoral CAS when you compare to carotid endarterectomy. So if you look at stroke 4% in the

transfemoral CAS group. 2.3% in the CEA group. And the peri- procedural stroke in patients that are over 75 look what happens here and we're going to talk about why. So the in the endarterectomy group a little bit

higher but not much but in the stent group goes up very significantly. And here's the the bottom line day 0 stroke is the culprit. If you make it through the procedure without a stroke you're probably not going to have one or

a very low risk and not much different than endarterectomy. But here's the issue so its procedural embolic strokes that were trying to avoid. So how do we

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