Create an account and get 3 free clips per day.
Is It Cured? MR And Angiographic Imaging After Treatment With Radiopaque Embolizing Agents (Onyx)
Is It Cured? MR And Angiographic Imaging After Treatment With Radiopaque Embolizing Agents (Onyx)
42 vials of EVOHAdditional 17 vials of EVOHan AVPanatomyangiographyarterialAVMavmscoilscontrastcuredembolizationenhancedfeedersferromagneticimageimaginginjectionmissedoccludedoverlayphaseproximalradiopaqueresultshuntingsome coilstemporalTherapeutic / Diagnosticvenousvesselvials

- Thanks, I appreciate the invitation. MR imaging of vascular malformations poses some challenges primarily related to the heterogeneous spectrum of the lesions. The primary distinction to be made with imaging is between low flow and high flow abnormalities. This distinction, however, can often be made clinically

and so the real value in MR is in determining the malformation extent and the associated involvement of adjacent normal structures. The basic MR evaluation of vascular malformations should of course be multiplanar in two or three orthogonal planes, and in each of those planes,

there should be T1 and T2 weighted imaging. There's some debate about the value of contrast-enhanced scans. Certainly contrast-enhanced scanning will show things like arteriovenous shunting and lesion perfusion, but mostly the value of contrast-enhanced scanning

is in making the diagnosis of the abnormality rather than in guiding specific treatment. So let's talk about the various imaging sequences and go through a few examples. On T1 weighted images, we see the anatomy of the limb or of the area in question quite clearly.

But what you notice is that there's a signal similarity between the normal tissues and the adjacent malformation, such that they blend together. That means that assessment of lesion extent is poor on T1 weighted images. Now this is in distinction from T2 weighted imaging

where malformation images tend to stand out quite dramatically from the adjacent surrounding normal tissue, making assessment of lesion extent quite good, with the following caveat that on these bright water-type sequences, edema, when present, especially in high-flow lesions

or in low-flow lesions following embolization, it can result in overestimation of lesion extent. Many people routinely include contrast-enhanced imaging for malformation evaluation. I think it's probably not necessary and doesn't actually provide that much

additional information beyond making the actual diagnosis. Now that said, that's to be distinguished from dynamic time resolved imaging, which is a newer type of contrast-enhanced imaging using faster acquisition. It has what's called a higher temporal resolution and we can clearly differentiate

inflow arteries from draining veins and this can be valuable in treatment planning as well. Here we see pre- and post-contrast images and you'll notice that on the post-contrast images, there's slightly better visualization of the malformation, but the difference between the two is really modest

and probably not clinically relevant. Now that's to be distinguished from time resolved imaging, which will allow us to see arterial, parenchymal, and venous phases, and these can be stitched together to create a movie that really does look quite a bit like a catheter-based angiogram.

The difference between high and low flow malformations is primarily made based on structural characteristics, rather than MR signal abnormalities. So, low flow lesions will usually have minimal mass effect. Here we see signal abnormality with almost no mass effect. When a mass is present, it sometimes has

hamartomatous stromal elements that look like septations running through the mass. When a mass is not present, the lesion tends to be pretty infiltrative. Without any mass effect, sometimes the degree of infiltration is amazingly intimate, as in, case like this.

When we see phleboliths, which are routinely identified on radiographic images, we have confidence that we're dealing with a low flow lesion. But in fact, MRI imaging can identify phleboliths pretty consistently, and here you see they appear as rounder, oval, low signal images

on all imaging sequences, and of course, they don't enhance. Now, these findings are in distinction to high flow lesions, which demonstrate no well-defined mass ever, and in fact, if you see a well-defined mass it should make you think that you're dealing with a tumor rather than a malformation.

But they will demonstrate characteristics of enlarged feeding arteries, enlarged draining veins, and these infiltrative masses will often be riven through with multiple flow voids, and the degree of infiltration can be really, pretty impressive.

There are some signal characteristic differences between the various malformations. It's a long and involved topic, and probably something that doesn't make sense to go into here at this point, but I think the utility of MR in vascular malformations is primarily related to defining the anatomic

characteristics of the malformation, assessing what normal structures are involved or immediately adjacent, and this allows us to mitigate risk and plan the procedures. Now this is different from post-treatment evaluation of MRI, where there's definitely differences between how low flow and high flow lesions respond.

In low flow images, post-embolization we see significant signal changes. In high flow lesions, post-embolization we see anatomic changes. One important caveat to remember is when imaging and malformation within three months of an embolization,

it can be difficult to interpret related to the post-embolization inflammatory reaction. So on T1 weighted imaging post-embolization, we see bright signal, representing thrombus is the treated area as opposed to lack of bright signal, in the non-treated area.

On T2 weighted images, where the malformation generally appears bright, post-embolization we see dark areas in the treated zoned, representing scar. I personally prefer evaluating these with T2 weighted images. I think the distinction between treated and

untreated is greater and more consistent. Another example, scar forming, T2 weighted images. Again, I think the distinction is pretty clear. Although, contrast-enhancement isn't all that valuable in pre-treatment planning. Actually, can I get this video to go?

There we go. Although contrast-enhanced scanning isn't generally valuable in pre-treatment planning, there can be some utility in post-treatment evaluations. Specifically, dynamic time-resolved imaging or virtual angiography can be applicable to high flow malformations.

As you can see here, when the post-treatment evaluation and assessment of residual arteriovenous stunting is an important end point. Thank you. (applauding) - [Announcer] Any questions from the audience?

I think it's important to note, you mentioned the importance of T2 weighted imaging. And it is crucial, particularly for venous and lymphatic, or mixed lesions. But I think it's also important to state with T2 imaging, that you have to have fat suppression,

'cause fat also has bright signal and can be confused with malformation. - [Scott] Yeah, exactly, and there's really a broad range of T2 weighted images. What we rely on mostly is this short towen version recovery which,

- [Announcer] Now that's different, yeah. - [Mark] Yeah that's going to be. - I was going to write next. - [Mark] Yeah, so the, T2 fat suppressed images are, of course, critical, and should be obtained in every plane. We actually also obtain stir imaging in every plane. Yes, question?

- [Audience Member] So is the T2 full, (mumbling) what time do you need. - [Mark] I'm sorry, can you repeat that? - [Audience Member] What time do you need to continue to use of a full of T2 for (mumbling) - [Mark] Well, it depends on what you're looking for.

If you're trying to assess for complications, you can image any time. But, the challenge in interpreting is that the diagnostic radiologist won't necessarily know exactly where you've treated, and the lesion may appear abnormal in ways that aren't understood.

So, as the interventionalist who's doing the procedure, you really need to sit with the radiologist and help them understand what you did within that short timeframe. Now, if you're talking about imaging after three months, it's much easier to interpret signal changes have moderated, and that post-embolization inflammatory

phase has resolved. - [Audience Member] After two or three months? - [Mark] After three months, yeah. - [Announcer] Okay, thank you so much. - [Mark] Thank you.

- Is it cured or not if you have a radiopaque embolization agent, and you are doing some x-rays, there may be problems. How to go forward, it's not the mouse here? Maybe this, this one? Ah, I see. Okay, what are radiopaque embolization agents?

Basically, you have glue, NBCA and EVOH, like Onyx, Squid, or PHIL. And they, all of them are radiopaque and they are liquid, and they can overlay the result of your embolization. And we start with MR-Angiography and the most important basic fact here

is that you have to use time resolved, contrast enhanced MR imaging. It's not worthwhile to do this with time of flight or phase contrast or anything without contrast because you need that contrast and you need a high temporal resolution

meaning many, many sequences as a follow-up. And you need a large field of view, because after treatment, there can be recruiting feeders from very remote sites. And how do you image the result of an embolization in DSA in contrast angiography?

You know this old thing with high, hot, helluva lot? Of course you need a very proximal injection site. You need a high injection rate and you need enough contrast, otherwise you will say, okay, this AVM is cured, but it isn't. And the most important thing is,

don't show me any arterial phase AVM images and tell me that you cured this AVM. You need to go to a late parenchymal phase or most important, you need to go to a venous phase. And if you see any early venous shunting, this AVM is not cured.

So you're overestimating the result of your embolization. So here's an example. This is a huge abdominal AVM and this is, you have to image high, because you see a lot of arterial feeders there and even see the inferior mesenteric artery

contributing to this AVM and you see where the arrow is, there is the pigtail catheter up there. Did I miss a feeder, yes. I missed a feeder, you have to go very high up, it was even feeding through the renal arteries, this AVM. So never underestimate a big AVM.

So what are the special issues with DSA imaging in AVMs? First of all, it's a flow-passive thing. Remaining where the point of injection and it's like blood contrast. It will flow through the point of the least resistance, but it will never show you the whole extent of the AVM.

So you really have to inject very proximal with a high flow rate, and if you control your results, you have to wait and to do and a real follow-up is not at the end of the embolization session. You always have to do it later because after extensive embolization session,

like it does, it takes hours. You always will have vessel spasm, and you will have a thrombotic component which shows you an occluded vessel. But wait, a couple of days, it will always recanalize. We're dealing with AVMs here.

So DSA imaging in AVMs is always overestimating your result because you have this vessel spams and you have this thrombosis. And of course, if you have a radiopaque embolization agent, you can have some obscuring overlaying effect,

so this can be a problem as well, but it's not that much of a problem, because you're not looking at the, sort of nidus, you're looking is there any early venous return. And if there is any venous early shunting, the AVM is not occluded.

So here's a, that's a huge, with an AVM in this ten year old boy. You can see the heart, it's showing a grade four AVM. And this is after 42 vials of Onyx in this patient. And some outflow coils, you see them down there. And that's the venous phase DSA.

Is it occluded or not? It's very difficult. I thought maybe it's occluded, but I was not sure. And I did an MR-angio two weeks later, and as you see, it's not occluded. But the DSA, I wasn't very sure.

In the MRA, I am sure it's not occluded, so you have to add 17 more vials there. You see the DSA, is it occluded or not? You don't see any venous return, it was occluded. MR angiography is clearly showing you a result in this patient.

So why is MR angiography better than DSA in controlling the result of your embolization? Of course, it's all this blah blah, noninvasive, but you have no issues with late phase venous imaging because you can image as long as you want.

As compared to DSA, where it costs you some radiation and things like that. The field of view is normally in a good MR scanner. It's bigger than you have available in your angio suite. So that's better for even very distant feeders. And of course, you don't have any overlay

with radiopaque embolization material here. So, from my point of view, DSA is nice, and MRA is better to control the result of AVM embolization. Thank you. (audience applauds)

- [Moderator] Any questions? I thought your examples, yes? - [Bob] No, no, go ahead. - [Moderator] I thought your examples were very good at showing the MR occlusion. And those were in the type 3A, 3B,

AVMs with venous aneurysms, which are large. All the type four infiltrator forms, they can be missed on MR. Type 2A nidal forms can be missed on MR. And direct fistulas might be missed on MR depending on size. What is your opinion of that?

- [Walter] I think if we are talking about high temporal, spacial resolution, dynamic, contrast enhanced MR angiography. When all the rest doesn't matter, it's a waste of time to do a TOF or a phase contrast. And you always see if you have a high temporal resolution,

like five seconds, four seconds, you can even go to three seconds. You always see the early return, so you can't overlook any AVM, but it the fistula or be it a very small, that was formerly known as small vessel type AVM

and things like that, you can't overlook it, because you see the early return. Maybe you don't have the spacial resolution to see very tiny vessels, but you see there is an AVM, and you can't overlook it. If you use this technique.

- [Moderator] Bob? - [Bob] No, that was my question as well, the various types and so on with these radiopaque agents. - [Walter] Yeah, but it's not for classification. My talk was about follow-ups, so... - [Moderator] Well, that's what we're talking too,

follow-up to see if it's there or not. - [Audience Member] I have one question, when you're looking at MR in a setting like this, where coils are present, presumably these are all ferromagnetic and are going to cause all sorts of artifact,

how do you deal with that? - [Walter] Well, you know, most of the coils, nowadays, the coils are not any ferromagnetic coils. Of course, they make some issues with local artifacts, but to see whether there is some AVM left or not,

it's totally unimportant. Of course, you have in gradient echo sequences, you have local artifact with ferromagnetic material. Again, with normal coils, some signal loss. But if you don't want to see

the subtle anatomy of the AVM, you want to see if there an AVM left, is there shunting left or not, so there is no problem. - [Moderator] Well, it is a problem, being that with the focal artifact,

even on platinum or other coils that have minimal effect, within it, you cannot see anything. - [Walter] Yes, but I don't want to see the angi anatomy of tiny residual nidus, I want to see whether there is shunting left or not. And if there is no shunting left, the AVM is gone.

- [Moderator] Thank you very much.

- Now I want to talk about, as Chrissy mentioned AVM Classification System and it's treatment implication to achieve cure. How do I put forward? Okay, no disclosures. So there are already AVM Classification Systems. One is the well-known Houdart classification

for CNS lesions, and the other one is quite similar to the description to the Houdart lesion, the Cho Do classification of peripheral AVM's. But what do we expect from a good classification system? We expect that it gives us also a guide how to treat with a high rate of cure,

also for complex lesions. So the Yakes Classification System was introduced in 2014, and it's basically a further refinement of the previous classification systems, but it adds other features. As for example, a new description of

a new entity, Type IV AVM's with a new angioarchitecture, it defines the nidus, and especially a value is that it shows you the treatment strategy that should be applied according to angioarchitecture to treat the lesion. It's based on the use of ethanol and coils,

and it's also based on the long experience of his describer, Wayne Yakes. So the Yakes Classification System is also applicable to the very complex lesions, and we start with the Type I AVM, which is the most simple, direct

arterial to venous connection without nidus. So Type I is the simplest lesion and it's very common in the lung or in the kidney. Here we have a Type I AVM come from the aortic bifurcation draining into the paralumbar venous plexus,

and to get access, selective cauterization of the AVM is needed to define the transition point from the arterial side to the venous side, and to treat. So what is the approach to treat this? It's basically a mechanical approach, occluding

the lesion and the transition point, using mechanical devices, which can be coils or also other devices. For example, plugs or balloons. In small lesions, it can also be occluded using ethanol, but to mainly in larger lesions,

mechanical devices are needed for cure. Type II is the common and typical AVM which describes nidus, which comes from

multiple in-flow arteries and is drained by multiple veins. So this structure, as you can see here, can be, very, very dense, with multiple tangled fistulaes. And the way to break this AVM down is mainly that you get more selective views, so you want to get selective views

on the separate compartments to treat. So what are the treatment options? As you can see here, this is a very selective view of one compartment, and this can be treated using ethanol, which can be applied

by a superselective transcatheter arterial approach, where you try to get as far as possible to the nidus. Or if tangled vessels are not allowing transcatheter access, direct puncture of the feeding arteries immediately proximal to the nidus can be done to apply ethanol. What is the difference between Type IIa and IIb?

IIb has the same in-flow pattern as Type a, but it has a different out-flow pattern, with a large vein aneurysm. It's crucial to distinguish that the nidus precedes this venous aneurysm. So here you can see a nice example for Type IIb AVM.

This is a preview of the pelvis, we can here now see, in a lateral view, that the nidus fills the vein aneurysm and precedes this venous aneurysm. So how can this lesion be accessed? Of course, direct puncture is a safe way

to detect the lesion from the venous side. So blocking the outflow with coils, and possibly also ethanol after the flow is reduced to reflux into the fistulaes. It's a safe approach from the venous side for these large vein aneurysm lesions,

but also superselective transcatheter arterial approach to the nidus is able to achieve cure by placing ethanol into the nidus, but has to be directly in front of the nidus to spare nutrient arteries.

Type IIIa has also multiple in-flow arteries, but the nidus is inside the vein aneurysm wall. So the nidus doesn't precede the lesion, but it's in the vein wall. So where should this AVM be treated?

And you can see a very nice example here. This is a Type IIIa with a single out-flow vein, of the aneurysm vein, and this is a direct puncture of the vein, and you can see quite well that this vein aneurysm has just one single out-flow. So by blocking this out-flow vein,

the nidus is blocked too. Also ethanol can be applied after the flow was reduced again to reflux into the fistulas inside the vein aneurysm wall. And here you can see that by packing a dense packing with coils, the lesion is cured.

So direct puncture again from the venous side in this venous aneurysm venous predominant lesion. Type IIIb, the difference here is again, the out-flow pattern. So we have multiple in-flow arteries, the fistulaes are again in the vein aneurysm.

Which makes it even more difficult to treat this lesion, is that it has multiple out-flow veins and the nidus can also precede into these or move into these out-flow veins. So the dense packing of the aneurysm might have to be extended into the out-flow veins.

So what you can see here is an example. Again you need a more selective view, but you can already see the vein aneurysm, which can be targeted by direct puncture. And again here, the system applies. Placing coils and dense packing of the vein aneurysm,

and possibly also of the out-flow veins, can cure the lesion. This is the angiogram showing cure of this complex AVM IIIb. Type IV is a very new entity which was not described

in any other classification system as of yet. So what is so special about this Type IV AVM is it has multiple arteries and arterioles that form innumerable AV fistulaes, but these fistulaes infiltrate the tissue. And I'm going to specify this entity in a separate talk,

so I'm not going too much into details here. But treatment strategy of course, is also direct puncture here, and in case possible to achieve transarterial access very close to the nidus transarterial approach is also possible. But there are specific considerations, for example

50/50 mixture of alcohol, I'm going to specify this in a later talk. And here you can see some examples of this micro-fistulae in Type IV AVM infiltrative type. This is a new entity described. So the conclusion is that the Yakes Classification System

is based on the angioarchitecture of AVM's and on hemodynamic features. So it offers you a clear definition here the nidus is located, and where to deliver alcohol in a safe way to cure even complex AVM's.

Thank you very much.

Disclaimer: Content and materials on Medlantis are provided for educational purposes only, and are intended for use by medical professionals, not to be used self-diagnosis or self-treatment. It is not intended as, nor should it be, a substitute for independent professional medical care. Medical practitioners must make their own independent assessment before suggesting a diagnosis or recommending or instituting a course of treatment. The content and materials on Medlantis should not in any way be seen as a replacement for consultation with colleagues or other sources, or as a substitute for conventional training and study.