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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

so 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.

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.

So a brief clinical history. We have a 32 year old female who initially presented as a

transfer patient from an outside institution with hematemesis. She stated that after a dinner, she had a couple episodes of bloody vomiting, hematemesis which prompted an ED visit. She was initially started on Nexium and octreotide drip. And she underwent upper endoscopy at the outside institution,

which confirmed gastric variceal bleeding. However, they were not able to perform any kind of endoscopic intervention at that time. She was therefore transferred to our institution for a higher level of care. Briefly, there's her past medical history.

Wanna point out that she has a history of hypertriglyceridemia which led to necrotizing pancreatitis, which eventually led to a splenic vein thrombosis and formation of her isolated gastric varices. This diagnosis was initially made about three months prior to her presentation to our hospital. So here's kind of a summary. She had hypertriglyceridemia which led to necrotizing pancreatitis, which formed a pancreatic pseudocyst, which led to splenic vein thrombosis,

which led to isolated gastric varices, which then bled. So here's a couple of pictures of her EGD from the outside institution. Just wanna point out the highlighted texts there, this is directly from their report. Gastric varices were noted in the proximal stomach and fundus. There was new blood in the fundus. The exact point

of bleeding was unable to be localized. They sighted heavy clot burden. The likely source was the gastric varices, which is kinda obvious but they were not able to perform banding at that time. So upon arrival to our institution she was admitted to the medical ICU.

Her vital signs were initially stable. Hemoglobin and hematocrit on the day of her admission were 9.2 and 29.7. After 24 hours they trended down slightly to 7.5 and 24.2. However, her blood pressure did remain stable. She was placed on a transfusion protocol which she responded well

to, and her H&H did stabilize at about 8.0 and 25.0 over the next couple of days. On the second hospital day an abdominal CT scan was obtained and was compared to the scan from approximately three months ago. Again, the highlight of the findings were that the pancreatic tail pseudocysts, the splenic vein thrombosis and isolated gastric varices

were all stable. And importantly there was no portal vein- >> [COUGH] >> Or superior mesenteric vein thrombosis. So here's a couple of pictures of that CT scan. I just wanna point out here, if I can get the mouse over.

Here's the isolated gastric varices. Adjacent to the fundus of the stomach you can see the pancreatic tail pseudocyst here, which are budded and lied adjacent to the splenic hilum. And then you can actually see the distal head of the chronic splenic vein thrombosis.

And this thrombosis, like I said earlier, is at least three months old. [BLANK_AUDIO] Lost the ability to go to the next slide here. [BLANK_AUDIO] There we go. So general surgery was consulted to evaluate for possible splenectomy. They initially deferred any operative treatment.

They cited high operative morbidity and the adjacent pancreatic pseudocyst would be extremely difficult to navigate operatively. And so surgery made plans to follow-up in surgery clinic after discharge in about three months. Okay, there we go. So on hospital day three,

things changed for the worst, she became unstable. Her blood pressure dropped precipitously to 78/36. Heart rate rose to 140. Hemoglobin and hematocrit had trended down significantly to 6.4 and 20.2. A gastric lavage was performed bedside which revealed acute blood.

And so then therefore she was emergently intubated and sedated. They repeated the EGD, this time at our institution they saw a bleeding gastric varix. They were able to localize it and they were able to sclerose that with Sotradecol solution and that initially stabilized the patient.

Per the GI service definitive treatment for these bleeding gastric varices was strongly recommended due to the high likelihood of re-bleeding, and she actually re-bled while in the hospital. So surgery was called back in, and despite the high operative morbidity they decided to plan a splenoctomy the following day. I'll just kinda skip over these for the sake of time.

We were then brought in the next day on hospital day four, and we were initially brought in for splenic artery embolization prior to surgery to control intraoperative bleeding. Upon our initial evaluation she was still intubated and sedated in the medical ICU. Her blood pressure had stabilized to 103/61. Heart rate had dropped to 76.

She had no active signs of upper GI bleeding at that time, and her H&H had stabilized somewhat to 7.6 and 23.4. So after our initial evaluation we reviewed all the prior imaging and we recommended a splenic vein recanalization with angioplasty and stenting of the splenic vein, followed by balloon-occluded trans-catheter obliteration of the isolated gastric varices.

And if this procedure was unsuccessful, we would then just embolize the splenic artery in preparation for surgery. So, I took the patient to the Angiography Suite. These are the list of our procedures here. Just skip over that cause we'll get to the good stuff.

We initially accessed a portal vein branch via the right hepatic lobe under direct sonographic guidance. We used a 21 gauge GrebSet introducer system. We swapped that out for a 6 French 45 cm Ansel sheath and through that sheath we advanced a Pigtail flush catheter into the portal venous system and then performed venography.

So here's a couple of pictures of our initial pictures. There's our Pigtail flush catheter there showing patency of the portal vein and superior mesenteric vein. We were able to get a 5 French Kumpe/g catheter into the distal aspect

of the splenic vein and did a contrast run which obviously confirmed the absence of the splenic vein due to chronic thrombosis. We probed and probed and probed here in the splenic vein for a very long time, and we used a 5 French guiding catheter, actually a Kumpe/g catheter, and a 0.035 hydrophilic guidewire. And we were able to reach the proximal aspect of the splenic vein

here. And we were actually doing pretty well to this point but then we encountered a very significant roadblock here, which was kinda disappointing because it was so far proximal. So we utilized multiple different techniques but none of them were successful. [BLANK_AUDIO]

[INAUDIBLE] So we decided to change our game plan a little bit. We wanted to map out the splenic venous drainage pathway in a physiologic fashion, so we actually we had the foresight to do this beginning with the case, we had the groin already prepped.

We accessed the common femoral artery, ultimately we accessed the ciliac atery with a 6 French C2 catheter. And we then performed celiac trunk angiography and we carried that up to the venous phase, primarily to highlight the venous drainage pathway of the splenic parenchyma. I have a movie in the next slide but just real quickly, just wanna point out that here's our splenic hilar veins which are very close to the tip of our hydrophilic guidewire here, so we weren't too far away.

We were pretty close and it made us happy. [BLANK_AUDIO] Still having trouble. Okay so here's the angiographic run. The injection is from the C2 catheter here at the celiac trunk. And again, just to highlight the fact that all the splenic venous

drainage is 100% via these isolated gastric varices up here near the fundus of the stomach. And we were able to see the veins of the splenic hilum here very close to our catheter tip. So, at this point we obtained trans-splenic venous access,

under ultrasound guidance. We used the same GrebSet micro-introducer system. Through the sheath we performed splenic venography and placed a 6 French pinnacle sheath. We advanced a Fogarty balloon catheter and we inflated it just proximal

to the gastric varices. And then we performed balloon-occluded venography of the spleen through the pinnacle sheath with the balloon inflated. So here's our run. This is our run through the GrebSet introducer sheath. This is our first

real good look of the nature of the isolated gastric varices, they're very large, very voluminous. And, clearly, no drainage via the splenic vein. Here's our run with the Fogarty inflated. This run is through the sheath, this is our trans-splenic sheath

right here. Again it highlights the veins of the splenic hilum which again are very close to the tip of our wire. And again all drainage is kind of backflowed through these gastric varices here. No drainage to the splenic vein. Here's some still pictures for

you in case you missed any of the highlights there. Again the isolated gastric varices and the veins in the splenic hilum which are nice and mapped up for us very nicely there. So at this point we employed the gun-sight technique and we had used this technique before with a lot of success. Usually in the setting of a TIPS procedure,

never in this setting but we knew it worked. It was originally described by Dr Richter and Dr Haskal in the 90s, again in the TIPS literature. I do have an animation slide after these couple of slides, so just kinda bear with me here for a second.

We deployed 2 0.035 Amplatz Gooseneck snares, one on either side. One in the proximal splenic vein via the trans-hepatic access and the other in the splenic vein hilum via the trans-splenic access. We then took a 21 gauge needle,

again our GrebSet needle. We advanced that percutaneously through each snare loop via an anterior abdominal approach, and we had to align each snare loop to where they were overlapping. And so it took a little while to get the detector just right. But once we got that it was fairly easy to advance that needle through

those two snare loops. And then once we confirmed in orthogonal views that we had that needle through each snare loop, we advanced the microwire through the needle and then removed the needle. So then we cinched down each snare loop to capture the microwire. And then the snare that was originating from the trans-hepatic access

was retracted, which then retracted the snare from the trans-splenic access across the occluded segment of the splenic vein. And then the snare catheter was then advanced over this narrow wire across the splenic vein. And we were able to actually advance that through the trans-hepatic sheath to externally. And then it was easy just to exchange that snare wire for an 0.035

stiff guidewire. We used an 0.035 Rosen wire in this case. And then once that was achieved we had resulted in successful through-and-through access across the occluded splenic vein segment. So here's a couple of pictures of this. Unfortunately this part of the procedure we had a high level of focus and we didn't save any angiographic or fluoroscopic images, so

I had to kind of draw it out here but bear with me. There's our occlusion and it kind of blowed up there for you a little bit. There's our 2 0.035 implants Gooseneck snares with our GrebSet needle through it. Again with a detector those snare loops were actually overlapping to RI/g so we were able to see exactly down the barrel or the gun-sight technique.

And here is a little animation. So we deploy our Gooseneck snares on either side of the occlusion. There goes our 21 gauge needle right through each snare loop, and then once we confirm access we send the microwire down and remove the needle. And then as the needle is removed we cinch down on either side of that wire with our snare

loops, and then we pull from the trans-hepatic side through. And that's how we achieved the through-and-through access. So once we had access we felt like we had accomplished something significant there. We then performed balloon angioplasty of the splenic vein. Initially we pre-dilated with a 6mm Mustang

balloon, and then we deployed a 9mm self-expanding bare-metal stent across this lesion. And we-post dilated that utilizing an 8mm balloon. So the diameter of the stent now is eight millimeters. We then repeated the venography through the trans-splenic sheath which demonstrated successful recanalization and importantly brisk outflow through the portal vein.

Here's a couple of pictures of this showing the balloon up. That's a six by ten, followed by the deployment of the stent there post-dilated to eight. And here's our run which shows patency of that stent with a patent outflow. And here's a movie showing that.

So at this point, this is a critical point in our procedure. We're happy with ourselves that we were able to recanalize the splenic vein nicely. However, we were disappointed that we did see a lot of outflow via the isolated gastric varices, and we were concerned with two things at this point.

We obviously didn't want her to re-bleed, and we're also concerned with the patency of maintaining a good flow through that stent to maintain patency of that stent. So we elected to proceed. We then repeated the run from the celiac artery through the C2 catheter.

Again, we noted that the gastric varices were found to supply significant outflow from the splenic parenchyma, despite recanalization of the splenic vein. And so at that point we elected to go ahead and proceed with balloon-occluded trans-catheter obliteration of the gastric varices. And here's a good picture showing that most of that outflow will

still be at the gastric varices even though we have some outflow via the stent right here. So we re-advanced our Fogarty into the splenic vein outflow tract and inflated it and performed venography through the Fogarty. And we were paying close attention here to the volume of contrast that we injected so that we would have an idea of how much sclerosant we

needed to use. Here's a still image of this which shows that these isolated gastric varices just like before are very large and very difficult to deal with. So we utilized Sotradecol solution with lipiodol foam. At our at our institution, Scott and White,

we do a 3:2:1 ratio. Being, three parts air, two parts Sotradecol and one part lipiodol. We then followed this up with placing a total of 4 6mm Nester coils right there in the outflow tract.

And then performed venography after all that, which did demonstrate successful exclusion of the gastric varices, with dominant outflow now via the splenic vein stent. However, this injection here was via the trans-splenic sheath, so it's not exactly physiologic.

And this just kind of shows what we saw. Nice widely patent stent, good outflow and exclusion of the gastric varices there with our coil pack right here in the trunk. We then had the problem of closing our access in the spleen. We did that with Gelfoam.

So we injected Gelfoam on our way out and that closed nicely. And then we performed a celiac run mainly to take a look at the physiologic drainage of the spleen from an arterial run, but also to make sure that we didn't have any extravasation in the

splenic parenchyma from where our sheath was. And we noted that the splenic vein was nice and widely patent after a parenchymal drainage. There was some flow through the varices, but really only the top, maybe 10, 15% of the spleen was draining through the varices. We considered that a success. And here is our run,

which shows good flow through the splenic vein there through the stent. A little bit of flow through the gastric varices, but very minimal compared to our first runs at the beginning of the case. Again I'll kinda skip these. So briefly, clinically she did very well.

We did place her on a Heparin drip for three days and prescribed Plavix 75 mg a day for a total two months. We felt safe in doing this. She did not have any chronic liver disease, she was not

a TIPS patients so placing her on antiplatelet therapy was we felt okay. We were mainly concerned with the patency of that stent. So we went in and did that, she required no further blood cell transfusions. Her H&H stabilized and rose to 8.1 and 24.2 on the second day after intervention. She was actually extubated the next day, which was great. She had no further episodes of GI bleeding. And importantly

general surgery cancelled their planned splenectomy, so we were able to save her from a potentially very morbid operation there. And she was discharged four days later following the intervention. So our follow-up was to obtain CAT scans at one and six months, and evaluate those scans for patency of the stent. And on both scans the stent remained widely patent, and most importantly there have

been no recurrent GI bleeds since we've done this. And the GI followed up with her in clinic and actually repeated an upper endoscopy, and there are no, according to their note, they noted that the gastric varices were quote unquote barely perceptible. So they had decompressed significantly following intervention.

Here's a picture from her CT scan at six months following the intervention. It's a portal venous contrast phase imaging which shows that, I don't have a movie of this, but it does show that the stent, there is a patency of that stent up to six months.

And so for the interest of time, I've got about 30 seconds but I'll just kind of fly through this. Basically what the main teaching points are is that we did have a interdisciplinary approach. We had four different services involved in this patient's care. And we were able to definitely treat the isolated gastric varices in order to prevent life threatening

bleeding, and simultaneously save this patient, this young patient, 32 year old patient from a potentially morbid splenectomy. The gun-sight technique is a technique that we don't use too often, but we

do employ it from time to time. We were very happy with Dr Richter and Dr Haskal who first talked about this in the 90s and gotten us out of a lot of jams since then. And kind of just words there, here's my references. And then obviously coming from Texas we love the gun-sight technique so

[LAUGH] we try to employ it whenever possible. And thank you very much. >> [APPLAUSE] >>

So the first case that I present pretty typical patient hepatitis C virus herpes carcinoma won't deliver the point this isn't a tumor board. We decided to do radioembolization I know it comes as a surprise to most of you, but the patient was a good candidate for such.

They weren't a candidate for surgery because of their coma [INAUDIBLE] Particularly their PAD. And you can see here they have this tumor here in the posterior right hepatic lobe. Now one of things that we've been doing more recently over the last several years is trying to do

radioembolization on the same day. So we bring these patients in we map, we do the long shunting and then we treat. We've ordered a dose ahead of time for this went ahead to order

a post right hepatic lobe dose and be ready to treat these patient. So this is what I was going to do here, and this is just a slide we published this concept in a few patients back in 2014 in JVIR, and it takes us about two and a half hours room time. Now we've done probably about a 100 patients and again it's about

two and a half hours of room time to do this whole process. So when they go to nuclear mess/g and they just get the player imaging for long shunting and we move along so it's a relatively quick procedure but this is a replaced anatomy here, and you could see the replaced right hepatic artery. We deliver the MAA and as we can see we get to see the hyper vascular

muscle, but hard to see [INAUDIBLE] But we can see it here and we can do Cone-Beam to show that. But as the patient so then what we do is we map things out and again there is the Cone-Beam CT. We are happy with that [INAUDIBLE]

We inject the MAA the patient. I take the catheters out I leave the sheath in, the patient goes up to NUCS med and comes back. And here's the NUCS med scan we actually did some spect imaging on that, but when they came back here is the angiogram and this is something this patient didn't get shot in, that's not a bullet but that's something we all dread seeing in our patients.

So this artery has thrombosed. I'm still to this day not exactly certain why I don't think it was from the MAA I took the catheters out. I didn't leave the catheter in the hepatic artery when I did this, but what would you do here, Chuck? What are your thoughts?

You bring them back another day put them on plavix or how do you manage this? >> [INAUDIBLE] [BLANK_AUDIO] >> Thanks. Yeah I think sometimes it's better to live to fight another day

I do think that often times when we get ourselves in a situation like this, we feel badly about it and we tend to wanna try and push things too hard on the same day, and then you just end up getting yourself in bigger trouble. So yeah I think I would probably stop for the day even though it's a dose that you're worried about wasting I don't think that should

come in the decision and I'd probably put him on antiplatelet agents to see if contrary indication to anticoagulation how bad is- >> He does not know. >> Yeah. I'm not sure about anything other than antiplatelet agent but I'd definitely stop at this point.

>> Any comments to that [INAUDIBLE] Run? >> I tend to be relatively conservative when I encounter this sort of event as well. So I agree with Chuck. I'd probably put the patient in an antiplatelet agent,

forego the dose for the day unfortunately and probably come back another day. If the vessel has not reopened you're likely to be able to still treat bi-collateral's so I'd wait it out. >> I guess I would just try to see whether I can pass a wire beyond

there. If it's easy then I might go ahead and angioplasty and see whether it opens up. If it's difficult then I would back off and bring the patient back. >> [INAUDIBLE] Stop now and [INAUDIBLE] Keep going. [INAUDIBLE]

>> Rusty you would keep going. What would you do? >> I'd try to use some water [INAUDIBLE] [INAUDIBLE] [INAUDIBLE] >> So what I ultimately decided to do was to do just that as you can see the imaging here,

it seemed over the course of a few minutes of repeating the angiogram giving a little bit nitroglycerin knowing that that's not gonna help anything upfront, but certainly not getting any better so I did administer TPA and I ended up giving 14 milligrams total, I gave it in 2 to

4 milligram boluses at a time, and things did open up some. As time went on and as I gave more it seemed to open up and I didn't know if this was going to be a process where if I waited longer it was gonna re-thrombose or not, or I should give more. One of my colleagues came walking through and said, what are you

doing? He's gonna have a hemorrhagic stroke or something. It's just one of those things that you think you're doing the right thing and you're wondering if you should've just stopped, I mean my first thought was I bring him back potentially and then as I'm doing this he's getting

better I'm feeling pretty confident and then at the back of my mind that's the last thing I wanna do I certainly haven't fully worked this patient up for TPA, but didn't have any obvious contrary indications so at this point I did Cone-Beam CT, and I was getting a chunk of the tumor so I actually delivered the dose. In terms of trying to treat this and here the patient is in one month follow up,

and you can see there's a reasonable response, there's certainly some component of it that's still enhancing that was being profused prior to this process so I brought the patient back actually not for radioembolization thinking that this is an ideal location

for a phrenic artery. So when I brought the patient back here certainly there's right inferior phrenic artery profusion, and I was able to do just blunt embolization to that component of it and got a good response as three months following treatment but I think that it added complexity I had to do another procedure for the patient, and we'll see how

robust the response is over time if there's a difference between the component that was blunt embolized and radioembolized. But again I'm not exactly certain, I haven't had this happen in many patients, how I've changed my practice is I still do the same day Y90's but I don't catheterize the segmental branches anymore

on the planning part, I will just do a low bar, do a Cone-Beam CT, inject the MAA, take everything out and come back then I will do the selective or segmental catheterizations, I don't know what's from our original catheterization,

or there's some other process. [BLANK_AUDIO] And there's the pre and the follow up as it stands we're probably about five months out from treatment now. Any comments, questions? >> Why did you choose, other than the fact that you're [INAUDIBLE] Why did you choose Y90 here instead either chemo embo or [INAUDIBLE]

>> Well I'll turn the question and ask you why you would choose chemoembolization, blind embolization, or ablation, there's certainly are a lot of different factors at play. Our evidence with radiation segmentectomy is pretty robust in terms of getting histologic, pathologic necrosis.

I understand why ablation can be good this is an extro phytic tumor, there is a patient that we didn't want to put under, we put patients under a generalized seizure for ablations not everybody does but he had enough risk factors with his triple A e.t.c. that it was not something

we were gonna consider, so ablation from that stand point is a little bit bigger than I like to ablate, certainly people ablate bigger tumors you can consider combination therapies, but the ablation factor with the anesthesia weren't going to do in terms of it's not a tumor border or things like that but in terms of what intra

arteriole therapy is best certainly there can be discussion but we favor proforal solitary tumor prefers segmentectomy radiation. [BLANK_AUDIO]

epithelioid hemangioendothelioma very rare. This is a 64 year old female she had a recent history of breast cancer and then followed by lymphoma and then she had a follow up PET probably a year out after her lymphoma was treated they showed no FDG avid lesions but

four months later there were multiple bilobar FDG avid lesions. She was referred to surgery for laporoscopic evaluation, possibly ablation and resection. They did a biopsy and it showed hemangioendothelioma so they

closed her up and sent her our way. [BLANK_AUDIO] So this is five months after the PET so nine months after no, the PET was negative. And so she was asymptomatic, ECOG zero,

labs looked okay. No mets anywhere. So then I was with the task of what are treatment options and there really isn't that much for hemangioendothelioma. Liver transplantation seems to be the main stage treatment for it, for hepatic hemangioendothelioma.

Unfortunately she had breast cancer and lymphoma recently so she's not a candidate. In terms of going doing a literature review on transarterial therapy. There's a few case reports of doxorubicin based chemoembolization with up to the seven years survival with that. There's not much of anything about radioembolization or radio

sensitivity of these lesions. And then targeted molecular therapies are just starting to evolve including one that's a merck inhibitor that's used for melanoma. So me and the oncologist saw the patient together and we talked about all these things with her and she decided to go with Y90 first, I talked about TACE versus Y90 and I said there is no data saying

to do one or the other so let's try Y90. So, of course people with odd diseases also have odd anatomy [LAUGH]. So her common hepatic trifurcated into the GDA, a small little origin that went into the lateral left hepatic artery and the right hepatic artery, and a separate branch that was the

medial left hepatic artery and the right gastric. So, on the planing day I embolize the GDA and the right gastric. And, first treatment I treat her entire right hepatic lobe. Second tumor are two separate bios, I went into the lateral and media left hepatic arteries.

[BLANK_AUDIO] So, one month following she had increased size and number of lesions. Some of the larger lesions had necrosis and well this is treatment effect or she progressed between, it could be multiple things.

Treatment effect, she progress after treatment or she progress between the pre treatment scan and post treatment scan. Again I try to get a pre treatment scan within one month of treatment, to avoid that compounding factor. But in five months she had decrease in her lesions so things were looking good.

The first nine to eight months there was two lesions, so the rest were stable or slightly decreased the two lesions on the right that we're growing. So this seems to be an aggressive tumor because it popped up in four months and even within like two months it looked like it had grown.

So, back to the clinic and talked to her about chemoembolization. >> I think that the concept of sort of pseudo progression that you show here were basically because the lesions become necrotic. They become easier to see on MRCT and that's something that is difficult I think for some of our diagnostic radiology colleagues to get

a handle on. It's hard for anybody. I think you know its hard to know sometimes whether there's true progression or pseudo progression, and it's just something to make sure that when you're discussing what's going on with the patient,

with medical and college tell people that sometimes the things that are called progression certainly after Y90 especially are not necessarily progression. >> Yeah. In fact mainly we don't image it one month after because they always

look worse at one month. I think that's just a very very misleading scan, unless its gonna change what you do next, I wouldn't do that scan. >> So the reason we do it,

I went back to Riod/g a lot and asked him why, it was mainly because that's what BTG recommends and what our IRB says. So when I talk to patients about it I tell them it's because I'm looking to see places I didn't treat if anything grew there. And I need to treat that,

but that one month one is definitely controversial whether you need it or not. And so I went back to the right and I did unconventional chemoembolization and that's how I do it. I continued to be symptomatic but at one month there's bilobar bar progression so I don't think the chemoembolization helped her

much. I saw her back in the clinic and said, I don't think it's worth doing your left side at this time, let's see what oncology can offer you cuz I knew there was that melanoma treatment with Trametinib so right now the oncologists decided to just hold off treatment for now,

they're just monitoring but I think soon she's gonna start Trametinib [INAUDIBLE] And hopefully we'll keep following her and see how things are going. >> It's a terrible disease, I mean nothing really works very well for this. >> We got a little bit of stability. That's my last case.

>> Good. We have other ten minutes if want, any questions about anything we talked about or other aspects. Sir? >> Can you talk about the dose and the shelf life thing?

>> So the glass microspheres are manufactured on Sundays and you order a dose based on your treatment days. So if you treat a patient on a Wednesday in particular, you're trying to target 120 grade to the right lobe for example you'll have let's say 5 GBq vial.

And if you treat the same patient tying to get the same dose on a Friday or it might be a 10 GBq vial. And if you wait for the extended shelf life which was manufactured the Sunday before, and you treat that on that patient on a Monday, it might be a 15 or a 20 GBq vial so the number of spheres increases as you go through the week. And then you can treat with an extended

shelf life that was on a Monday or Tuesday, for example, that was done the week before and it's all a matter of trying to get the tumor coverage hopefully that wanna get to. When you're trying to hit that sweet spot of having the right number of spheres to cover the tumor and get the right

therapeutic dose in the patient and so the TheraSpheres really the regular shelf life stuff is really hot. And then you have the extend the shelf life using it the next week, it's sort of in the middle and then SIR-Sphere, the resin microspheres are on the other end of the spectrum and we sort of do the same thing.

We mix and match based on the patients tumor burden, how vascular they are, the tumors are, what the flow is like, all that kind of stuff and trying to figure it out. It's something that gives you a lot of flexibility and everything

but we almost never give glass microspheres on Tuesdays, Wednesdays or Thursdays. We're treating almost all those people on Fridays, Mondays and Tuesdays. And in the middle of the week we're doing SIR-Sphere cases on Tuesdays, Wednesdays,

Thursdays, cuz we have both, so does that make sense? >> It's crystal clear. >> What's that? No. >> So basically you're trying to nail the dose and you're trying to

[INAUDIBLE] >> There's more spheres, the longer you wait out in the week, to get this, cuz each sphere has the same specific activity and it's decaying from the time it's manufactured.

So on a Friday, to get the dose you need, you need to give a lot more spheres on a Wednesday, right? So, on Friday we're giving, it might be a vial that has twice as

many spheres than versus the one you were treating on a Wednesday. So if the patient has a large tumor burden we wanna have more spheres to try to cover everything. If a patient has, if you're doing a raise in segmentectomy and you got a really hypovascular tumor it doesn't matter, right?

There all these spheres that are gonna go in the tumor, and you're gonna kill it. It's gonna be fine. But if you're treating larger volumes, larger tumors, hypovascular

tumors, that kind of stuff, it does matter, probably. We don't have a great data but it does matter how many spheres you're giving to the patient to try to cover the territory. Does that make sense? >>Yeah, I got it.

Okay, Derrick. >> I have two questions, first do you always do Y90 [INAUDIBLE] >> We generally don't alter the target dose based on the type of tumor but certainly based on sometimes patient characteristics or liver hepatic reserve

or something like that, I don't know what you guys do. [SOUND] >> I base it basically on hepatic reserve and how big of an area so if it's a small area, even if the bilirubin's a

little higher, I'm gonna t lean towards rad/g segmentectomy if I think they can tolerate that little area going away, kinda like what a surgeon does for whether they can resect something or not, how aggressive to be.

If their bili is between two and three I tend to go 120 and lower, but if it's between one and two I tend to go like 140, 150 or do radiation segmentectomy so it's like how much can their liver tolerated and there's no specific science to it,

but that's how I base it off of how much volume I'm treating and what the liver function

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

So with that introduction, I'm gonna show you one quick case and then turn the podium over. And my question to the panel and maybe to the audience is, how the heck do you ablate this? If you look at it, this is a 3 cm exophytic HCC in the back of the left lobe of the liver, and on the axial images it looks like

it shouldn't be too much of a problem. It is in a location that again looks very reasonable for ablation until you look at the coronal images, and this both exophytic and protruding on the stomach. So let me ask my panel a little bit about, how you would approach this? Raj, is this a IRE case? How do you approach this? >> The fact that it's exophytic and it's so close to the stomach would

be one of the reasons where we can potentially look at using IRE. But what I need to know more about is whether we would have, looking at approximate size of this, it's about 3 cm. So we're going to need at least three, if not four needles to bracket the tumor with IRE. So we need to make sure that we do have an adequate window,

and a safe path. I see there are some varices anteriorly and maybe some vessels. So if there is a path to get those needles safely, yes that would be one of the options. >> When you're talking to the patients, what would you quote as how, what's your likelihood you're gonna get this, assuming there's a safe window? How do you counsel the patients about that?

>> About IRE? >> Yeah. >> Okay. So when we think IRE is an option for a patient, all of them are seen in our clinic. And we discuss all the treatment options, and why we think that IRE would be a good option. And we

also explain the off-label use of the technology and that's documented in our clinic notes, and the reason we give them is also the advantages. Since it's predominantly a non-femoral technique, and you're able to go close to critical structures and do that safely, and we've done that in many, many patients so we're comfortable recommending it. But with IRE, you also have to look at other situations with the patients'

clinical history. If a patient has a history of cardiac arrhythmias or a patient has history of a pacemaker, so even though the technology may be the best one, the patient will not be a candidate for the procedure. And also, the access is very critical with IRE, you wanna make sure that you have a safe window. So these are all the things that we make sure we discuss with the patient, and once we explain

the rationale for why we are picking the technology, most of our patients have been comfortable. And it's actually even in our tumor board at this point, we've been using it for five years now. Whether it's liver or colorectal, if our surgeons and oncologists see a lesion which is close to critical structures then they will say, this an IRE case.

>> Fantastic. Costi? >> Well I would certainly not do IRE on this lesion, and I'm sure Raj answered IRE just because you ask him. I'm sure he wouldn't choose as IRE as

the first option for this lesion. Just for the people here to know that, that's not our recommendation. So first of all, we are looking at a case that you showed us a hypervascular subcapsular lesion.

And it looks like it's a patient, by the way for the disclosure everybody know, I've never seen this case before. It's the first time I've seen it, so it's no cheating. So all of us, none of us has seen each other's cases, right? I think you guys should know that, so it's really fresh ideas what you see. >> But I meant for everybody to see them ahead of time, but these guys are

such slackers. Nobody said anything till the last minute, okay? So I just wanna make sure everybody knows where the fault lies, so go ahead. >> No problem. So having said that, so this looks like a patient with HCC and cirrhosis with, as Raj said, varices. We see recanalization of the umbilical vein here. So this is a patient that probably has

advanced underlying chronic liver disease and cirrhosis. So number one question for me here, okay so we have an HCC by EASL criteria most likely here. Again, we can talk about a lot of things, but one thing that I wanna make sure is that there is no other tumor, that this is a solitary lesion.

>> It is. >> It is. And I would raise the question that in my practice, it's not rare that we think it's a solitary lesion and when we do an angiogram, we see other vascular nodules. Having said that, this is also a lesion that it seems to be over 2 cm. >> Yep.

>> It's probably 3 cm. So it's not the straightforward Barcelona Guideline 2 cm nodule ablation only can treat necessarily. So in my practice, most likely we would do a dual approach, arteriography, super-selective embolization if this is the only lesion. Bland particles because we just published a randomized control trial with Karen Brown as the first author in JCO. That showed that there is no real difference

between bland embolization versus drug-eluting beads with doxo. And so that would be our primary approach at Sloan. We would embolize this and offer ablation in the same sitting under general anaesthesia. We do have combined rooms that we can do that. I understand you may not have them everywhere. But with cone beam CT, most of you have the capability of using ultrasound or cone

beam CT to put a needle after embolization. After the embolization you can see this lesion very well, not unlike what you see it with contrast. So it makes your targeting very easily. What modality would you use to ablate once you embolize? I think it can be operator's choice. I don't think there is much difference, but you have to immobilize the stomach if you're gonna do thermal ablation. If you

think that you did a perfect embolization, I don't think there is much argument not to use even absolute ethanol, like the old fashion. I see Dr. Solbiati in the room. So we can go to the original teaching that this is an HCC, and you can really embolize it and even give ethanol if you have issues. But if you wanna use thermal ablation, any one

of them is fine as long as you immobilize the stomach. >> Okay, and do you usually use D5 for that, or- >> I'm sorry? >> Normal saline, air, what? How do you immobilize the stomach? >> I dilute contrast, water-diluted contrast.

>> Okay. >> So one 1 to 10 or even less, 5% okay. Riccardo, what are your thoughts? >> Yeah, I also have a couple of comments. So first of all, I'm not sure that, that's gonna be our recommendation. As Costi said, each one of us will tell a different story, that I can guarantee. So

I have three points for this patient. Number one is that we need to trust the imaging for staging. So if I do an optimized CT or an MRI and the lesion is a solitary one, it's not that I do an angiography just because that could be that once I remember I saw additional spots that were missed by CT or an MRI. So CT or an MRI are the staging techniques, and

then of course nothing is perfect. Number two, the liver function. Here I definitely endorse what Costi said, that treatment should be, in a patient with cirrhosis and HCC, should be truly tailored to that patient needs. So, is this patient likely going to die for this HCC or not? Because every time I do like a systematic review, as I did

for instance for TACE last month, I still find Child C patients, decompensated patients who will never ever have any clinical benefit from any treatment. So I think this is a key discussion because even the way you treat can change, and you can be more aggressive or less aggressive depending on what you wanna achieve. Third point

is this would be like the unablatable lesion if you go next door to some other workshop, right? And this would be the unablatable lesion that it would be ideal for, I don't know, radiation segmentectomy for instance?>> [LAUGH] >> So really ablatable and non-ablatable, I think is like resectable and unresectable. So it's something that I think it really has to do with how the expertise is in place. I think you can probably

use any technique on this lesion. And now that we are in Miami, it's true that Raj is always carrying the IRE machine, >> [LAUGH] >> In the room, so I would be tempted to do that. But I would definitely, I would definitely have no restriction in doing

the ablation. The combo, Costi, I always endorse the combo, but I would do this on like on 3.5, or 4 cm. >> Yeah.

Steve, what are your thoughts? >> Okay, well I have another opinion. >> [LAUGH] >> We're very fortunate here at VGH where we work very closely with our hepatobiliary surgeons, with our tumor board. So this case, we don't see uncommonly. We see a lot of HCCs and this would be a typical, and I have the benefit

of every single ablation that occurs in our hospital we're involved in. So whether it's liver in the OR, anywhere, we do them. So in this case for access, we almost certainly would do a MIS access, and then separate the stomach away from the liver margin. And then we would go in and ablate it under direct visualization with the MIS, and we would

place a probe. >> Okay, that was a quite a potpourri of opinions. It goes to show that there's a lot of art here and sometimes not so much science, right? [LAUGH]

Raj, you have another solution? >> I just wanna add that, your comment about what people do not know about me, just to carry on with what Riccardo said. The popular opinion is that anything and everything I touch has to go to IRE, >> [LAUGH]

>> But the truth of the matter is that I do all ablations and IRE, and we end up doing more thermal ablations than IRE in our site. So that's probably something that most people may not know. >> [LAUGH] >> Okay. Yeah, and that's interesting because Riccardo was recommending against combination therapy, but if I recall correctly, you published

the first paper in the world on combination therapy. So he's running away from his past as well. >> No. No, it's just a matter of size. I say the size. I say 3 cm would be frankly, would be exactly the threshold. So I'm not

going away, but I recognize that the need for a combo in, let's say in the 90s where we were combining with ethanol, or in the 2000s where we were combining with RFA can change because ablation is changing. So it's not that we were combining just because we wanted to do that, but because frankly ablation modalities were largely

suboptimal compared with what we are today. >> Yeah, we'll do most tumors up to 3 cm without ever thinking about a combination. 3 to 4, we're starting to think about it, over 4 for sure. Okay, so we took a slightly different tact here. And we looked at this and looked at this, and Grant Schmit at Mayo had described an interesting technique to move bowel away from tumors

like this, and he calls it the Leverage Technique. And so we put a blunt tip needle down between the duodenum and the lesion and actually torqued it and pulled it away, and then ablated this thing right down the barrel. So it's a really neat technique. Grant, I don't know if you're in the room, but hopefully he's publishing this some time soon. It's a little bit scary when you're doing

this. You can see we torqued the duodenum, but it worked out great in this case, and I think I had a nine-month follow up there. Okay, with that I think Steve you're up next, and we'll have some more cases and more opinions.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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