0:02

Hello and welcome to Noon Conferences hosted

0:04

by MRI Online. In response to the changes

0:07

happening around the world right now in

0:09

the shutting down of in-person events,

0:10

so you have to decide to provide free daily

0:12

noon conferences to all radiologists worldwide.

0:16

Today we are joined by Dr. Shanna A. Matalon.

0:18

She graduated magna cum laude from Boston University

0:21

School of Medicine and completed her radiology

0:24

residence and an abdominal imaging and intervention

0:27

fellowship from Brigham and Women's Hospital.

0:30

She serves as the Associate Program Director

0:31

of the Diagnostic Radiology Residency at

0:34

Brigham and Women's Hospital in charge of the

0:37

resident recruitment and innovative curricula.

0:39

She has received several teaching awards and was

0:41

the 2017 ACR Valerie P. Jackson Education Fellow.

0:45

Shanna's area of professional interests include

0:47

gastrointestinal imaging and medical education.

0:51

A reminder that there will be time at the

0:52

end of this hour for a Q and A session.

0:55

Please use the Q and A feature to

0:56

ask all questions and we'll get to as

0:57

many as we can before our time is up.

1:00

That being said, thank you so much

1:01

for joining us today, Dr. Matalon.

1:02

I'll let you take it from here.

1:04

Great.

1:05

Okay.

1:06

Um, so good afternoon, everyone.

1:07

Um, I wanted to start by just welcoming you here.

1:10

Thank you for joining me.

1:12

Um, I know this is a crazy time for everyone.

1:14

Um, so it's really nice that we get to

1:15

share, um, a little bit of what we do with

1:18

people from all over the country and

1:20

all over, presumably all over the world.

1:22

Um, so I'm really excited to be part of this platform.

1:25

Um, today I'm gonna be talking about Eovist MRI,

1:27

which, um, to me is the epitome of why we love MRI.

1:31

It's where we do the problem

1:33

solving for liver lesions.

1:34

Um, we really have to think through things.

1:36

We have to look at the clinical history.

1:38

Um, and I think it's a fun topic.

1:40

Um, I know we have all types of learners

1:42

here from beginners to probably more

1:44

experienced people who use Eovist all the time.

1:46

So I hope to have something for everyone.

1:48

Um, a little bit review for the more

1:49

experienced people and some new content, um,

1:52

for people who haven't used much Eovist MRI.

1:55

Um, so getting started, I have no disclosures.

1:58

Um, so my learning objectives will, um, review some

2:01

common indications for Eovist MRI, we'll recognize the

2:03

typical appearance of different liver lesions on Eovist

2:06

MRI, and we'll also describe some imaging pitfalls for

2:09

Eovist MRI so that you're ready to use this in practice.

2:12

So we'll start with the what.

2:14

So what is Eovist and how does it differ

2:16

from other MRI contrast agents?

2:19

Um, then we'll talk about how to use it.

2:21

So I'll just discuss some protocol

2:22

considerations and other things that we

2:24

need to keep in mind when we use Eovist MRI.

2:27

And then we'll talk about the why.

2:28

So what are the indications that we might select Eovist

2:31

MRI, and what are typical imaging appearance of liver

2:34

lesions, and how can we use it for biliary evaluation?

2:37

So we'll start with the what.

2:40

So when we are doing an MRI, we have

2:41

a lot of options for contrast agents.

2:44

The ones that we use most commonly in everyday

2:46

practice are the extracellular agents.

2:48

These are the ones that we inject into

2:49

the vein and go through the vascular

2:51

system and end up in the interstitium.

2:54

And then we have the hepatobiliary-specific

2:56

agents, um, and then we have combined

2:58

agents, which we'll get to in just a second.

3:00

So these are the ones that I'll focus on today.

3:04

So nearly all of our MRI contrast

3:06

agents are gadolinium-based.

3:07

Gadolinium is a rare earth metal

3:09

element, and interestingly, it's actually

3:11

highly toxic, um, to human bodies.

3:13

And so that's the reason that we have to chelate it

3:15

to other compounds so that it's safe for human use.

3:18

The reason it functions so well as a contrast

3:21

agent is because it's highly paramagnetic.

3:23

So what that means is that it becomes

3:25

temporarily magnetized when it's placed

3:27

in a magnetic field like an MRI scanner.

3:30

So interestingly, we're not actually seeing the

3:32

gadolinium itself on the MRI, but instead what we're

3:35

seeing is the effect it has on nearby water molecules.

3:39

So what we see is that in low concentrations, which is

3:41

the typical use that we have, we see T1 shortening

3:45

effects, which causes increased signal, high contrast.

3:47

That's why we use it for contrast.

3:49

On the other hand, if we have a very.

3:51

High concentration of gadolinium.

3:53

What might happen as we excrete gadolinium into

3:56

our urine, into our collecting system, we actually

3:59

have T2 shortening effects that dominate.

4:01

And so that's why if you see excreted gadolinium

4:04

in maybe the collecting system or in the urinary

4:07

bladder, we might see that layering with that T2,

4:10

um, shortening effect and that decreased signal.

4:14

So, as I mentioned, we have two main types of, um,

4:17

gadolinium contrast that we use on a daily basis.

4:19

We have our extracellular agents.

4:21

These go from the vascular compartment

4:23

into the interstitial, and these

4:24

are really our workhorse contrast.

4:26

This is what we use on a daily

4:27

basis all throughout the body.

4:29

But in abdomen, we have a special type

4:31

of agent called the hepatobiliary agent.

4:34

These agents are taken up by functioning hepatocytes

4:37

and excreted into bile, and so we can utilize

4:39

this to image the liver and the biliary tree.

4:42

You know, in a different way.

4:44

Um, but what's good to know is in the US at

4:47

least, we don't have any hepatobiliary-only agents.

4:50

Most of our agents are combined agents,

4:52

meaning they function both as an extracellular

4:54

agent and as hepatobiliary agents.

4:57

So we can use this to our advantage by, you

4:59

know, being able to do our standard

5:01

protocol for a liver, but then also getting

5:03

to do some hepatobiliary phase imaging.

5:07

Alright, so from now on, when I say hepatobiliary

5:10

contrast, I'm really talking about combined agents.

5:13

And in the US we have two main types that we use.

5:16

Although this talk will focus mostly on Eovist,

5:18

I think it's worth talking about both MultiHance

5:20

and Eovist and the differences between the

5:23

two and their overall features so that we can

5:25

understand why you would use one over the other.

5:28

And, um, other considerations that we need to

5:30

keep in mind when we use either of these agents.

5:33

Um, so we'll talk about each

5:34

of these features in turn.

5:36

So the first thing we're gonna talk about

5:38

is the hepatocyte uptake mechanism.

5:40

So both MultiHance and Eovist function the same way.

5:44

And they're taken up by the OATP receptor.

5:46

So this is a schematic of a hepatocyte cell.

5:48

We see all the membrane transporters,

5:50

and the OATP receptor is what takes in the

5:53

hepatobiliary agent or bile into the cell.

5:57

Um, they're competitive antagonists, meaning that the...

6:00

To the hepatocyte, they're exactly the

6:02

same, and so they compete against each

6:03

other for places on these transporters.

6:06

Once the bile or the contrast agent is within

6:09

the hepatocyte, it's usually excreted into the

6:12

bile canaliculus through the MRP2 transporter.

6:15

On the other hand, in rare circumstances, it

6:17

can also be effluxed out of the cell back into the

6:20

sinusoids through the MRP3/4 transporters.

6:23

So this is how, you know, bile is transported in

6:26

our body, as well as hepatocellular agents.

6:29

If a patient is cholestatic, so they have bile

6:32

everywhere, too much bile, then the hepatocyte

6:35

and the biliary tree gets overrun with bile.

6:38

And what ends up happening is the MRP

6:39

2 transporters are taken back up.

6:42

So they're downregulated, and the MRP

6:44

3 transporters are upregulated to

6:46

get rid of the bile, um, out of the cell.

6:49

So if we try to give these patients hepatobiliary

6:51

agents, although they might be able to get into

6:53

the cell through the OATP receptors, they can't get

6:56

excreted through the biliary tree like they should

6:58

be, and instead they're effluxed out of the cell.

7:01

So these contrast agents are not particularly

7:03

helpful in patients with elevated bilirubin.

7:05

So this is something to keep in mind when

7:07

we're deciding what type of contrast to use.

7:12

Alright, next, um, feature is dynamic imaging.

7:15

So as I mentioned, both of these contrast

7:17

agents are actually combined agents, so

7:19

they function as extracellular agents and

7:22

they function exactly the same way as our

7:24

typical extracellular contrast agents work.

7:26

I put a little asterisk here for Eovist because

7:29

there's just slight differences, um, in the way that

7:32

we might perceive the dynamic imaging, and that's

7:34

something I'll get to in just a couple of minutes.

7:38

Okay.

7:38

The next thing is the excretion and

7:41

the timing of this hepatobiliary phase.

7:43

So MultiHance is only excreted through

7:45

the biliary tree, about 3 to 5%.

7:48

And so because of that, it takes longer

7:50

to achieve our hepatobiliary phase,

7:52

which occurs at about one to two hours.

7:55

On the other hand, about 50% of Eovist is excreted

7:58

through the biliary tree, and so we get our

8:00

hepatobiliary phase as early as 10 minutes,

8:03

but on average about 20 minutes, and it

8:05

usually persists for about 120 minutes or so.

8:08

So this window is a little bit more flexible

8:10

and it's much earlier than MultiHance.

8:13

All right, so with this in mind, now we'll talk

8:16

about how to use these agents, what we should

8:17

consider, uh, when we're making up our protocols.

8:21

So this is a standard MRI protocol at my institution.

8:24

I imagine, um, most are very similar,

8:26

um, for an extracellular contrast agent.

8:28

So we start with T2-weighted images.

8:31

Um, so this would include like a

8:32

coronal, an axial T2 fat sat.

8:35

Then we would get our T1 pre-contrast image.

8:37

This would include our in and out of phase,

8:39

um, our T1 pre-contrast with fat sat.

8:41

Then we would get our post-contrast

8:43

dynamics, our 30, 60 and 90-second

8:46

dynamic images. While we're waiting for our five

8:48

minute delay, we'll get our diffusion-weighted

8:50

images, and the whole exam is under 40 minutes.

8:54

If we were to use MultiHance, we could

8:56

do the exact same exam because it is an

8:58

extracellular agent, so we can get the

8:59

standard images that we would normally get.

9:01

But because the hepatobiliary phase takes one to two

9:04

hours, we can't just leave the patient on the scanner.

9:06

That's not a very efficient,

9:07

um, use of our scanner time.

9:10

And so we would have to take the patient

9:11

off the table, scan other patients, and then

9:14

bring the patient back one to two hours later

9:16

to get our hepatobiliary phase images.

9:18

So although this part of the scan may take

9:21

less than 40 minutes, there's a gap and then we

9:23

have to bring the patient back on the scanner,

9:25

which is not exactly efficient or logical.

9:29

Eovist,

9:29

on the other hand, we can just sort of

9:30

rearrange things so that we can make use of

9:33

the time and keep our exam under 40 minutes.

9:36

So what we would start with is the T1 pre-

9:39

contrast images, and then we would give our

9:41

Eovist. So we would get our dynamic phase images.

9:44

Um, then we could get our five-minute post-contrast

9:46

image, which is sometimes called the transition phase.

9:49

Then we would go back and get our T2-weighted

9:51

images, our diffusion-weighted images, and then we

9:54

can get our, um, hepatobiliary phase, um, in the, in

9:57

the three different planes that we would normally get.

9:59

And everything stays under 40 minutes.

10:01

So I told you earlier that in high concentrations

10:05

during excretion, that VUS, or gadolinium in

10:08

general, can cause T2 shortening effects.

10:11

So if we've given our contrast early, what happens

10:14

if we wanna do an MRCP where the contrast isn't

10:16

now being excreted through the biliary tree?

10:18

And that's what we're mostly interested in.

10:20

So if you are gonna do MRCP

10:22

images with VUS or with, um...

10:25

You're gonna wanna do it early before you give

10:27

contrast, because as we mentioned, contrast is

10:30

excreted through the biliary tree, and it could

10:32

obscure our visualization of the, um, biliary tree on

10:36

a T2, heavily T2-weighted image like an MRCP.

10:40

All right, for this exact reason.

10:42

So this is an example of the same patient

10:45

who's had both an, um, extracellular agent

10:47

protocol and a VUS protocol at my institution.

10:50

And I timed, I looked at, you know,

10:51

when the first series was acquired

10:53

to the last series on both studies.

10:55

Um, and it was 22 minutes versus 29 minutes.

10:57

So VUS is a little bit longer, but the patient

11:00

was still scheduled for 40-minute slots.

11:02

So as far as efficiency of our, um, MRI

11:04

scanner, um, this is nice and efficient.

11:08

Okay.

11:08

Moving on to the next feature and

11:10

consideration for how this affects our

11:12

imaging and our protocol is the dose.

11:14

So MultiHance is very similar to our other

11:17

extracellular agents, um, in that the doses, um, are

11:20

very similar, but VUS on the other hand, is only half

11:23

the volume, and it's only a quarter of the gadolinium.

11:26

So this is important for two reasons.

11:28

We'll first focus on the volume.

11:30

So because we're using a smaller volume,

11:32

this could lead to issues in bolus timing.

11:35

So the small volume makes for a potential

11:37

error in the timing for our dynamic images.

11:40

So some solutions that people have come up with

11:42

is to stretch the dose, meaning to decrease

11:45

the, um, injection rate from two milliliters

11:48

per second to one milliliter per second.

11:50

You can also dilute the dose in saline to make it 20

11:53

milliliters and keep it at the same injection rate.

11:56

Um, you can also consider that this might be an

11:58

even greater issue in children, given their great

12:00

variability in size and cardiovascular status.

12:03

So something to keep in mind.

12:06

The next thing has to do with the fact that the

12:08

VUS is only a quarter of the gadolinium content.

12:12

So what does this matter?

12:13

Right?

12:14

So this has to do with the contrast signal.

12:16

So we have the feature of T1 relaxivity,

12:19

basically like how bright will this be?

12:21

And actually MultiHance and VUS

12:23

are quite high.

12:24

If we look at the different rates of, um, T1

12:27

relaxivity of the different contrast agents, we can

12:30

see MultiHance and VUS are actually the highest.

12:32

But remember, VUS is only a quarter of the

12:34

amount of gadolinium and half the volume.

12:37

And so for that reason, although it may be one

12:39

of the brightest agents, it actually can appear

12:42

a little bit duller when we image the patients.

12:44

So let me show you a nice study

12:46

that, um, did this example.

12:48

Um, so this study looked at 13 healthy

12:50

patients and had them get both an extra,

12:53

uh, a VUS study and also a Magnevist study.

12:56

Magnevist is a type of extracellular contrast agent.

12:59

Then what they did was they had radiologists rate

13:01

how bright different structures were and how, how

13:04

good of, how good was the contrast, basically.

13:06

So they looked at things like the liver parenchyma,

13:08

the IVC, the portal vein, and the aorta.

13:11

So in the arterial phase, they found that

13:13

Magnevist significantly outperformed Eovist

13:16

as far as the signal intensity

13:18

of all of these structures. On the

13:20

portal venous phase, it was the same.

13:22

So as we can see here on this image, you know,

13:25

the contrast between the liver parenchyma

13:27

and the vessels is not so good, whereas

13:29

in Magnevist, the contrast is much better.

13:32

But at the equilibrium phase, now our contrast is

13:34

basically washed out of the vascular system, but it's

13:37

in the, um, but it persists in the liver parenchyma.

13:41

So we actually do have better contrast

13:43

now at the equilibrium phase, um, or the

13:45

hepatobiliary phase compared to, um, the Magnevist.

13:49

So this is one area where VUS is better,

13:53

but you can see that the images just look a

13:54

little dull, a little less bright for VUS.

13:57

So something to keep in mind.

13:59

There is something we can do in our

14:01

protocols to improve the brightness of

14:03

VUS, and that is changing the flip angle.

14:06

So this is an example of an FNH,

14:08

which we'll talk about more later.

14:10

Our standard flip angles for post-contrast

14:12

studies is about 10, um, about 10 degrees.

14:15

Um, we should change our flip angles

14:17

to between 20 to 35 degrees for our hepatobiliary

14:20

phase to bring out this bright signal.

14:22

So this is just a nice example.

14:24

Same patient, same lesion,

14:25

just two different flip angles.

14:27

Much, much brighter, more contrasty.

14:31

All right.

14:31

And then another interesting thing to know about

14:33

Eovist is that there's this phenomenon called

14:36

the transient arterial phase respiratory motion.

14:39

So we all hate when our MRIs come out like

14:41

this because it's basically non-diagnostic.

14:43

And this is something that happens in about,

14:46

uh, let's see, about 15% of patients, um, they

14:49

just get this transient feeling of dyspnea,

14:51

feeling like they can't catch their breath.

14:53

Um, and it happens in the arterial

14:55

phase that's right after the injection.

14:57

And so one study looked at patients, um,

14:59

prospectively by evaluating them and asking

15:01

them after a study whether they experienced any

15:05

symptoms, and then also having radiologists rate

15:07

the level of motion on the arterial phase scans.

15:10

And what they found was that with VUS compared

15:12

to MultiHance, there was a significant

15:14

increase in the amount of patients reporting

15:16

dyspnea and also the amount of motion artifact

15:19

in the arterial phase.

15:21

So this is something that's important to keep in mind.

15:23

'Cause as we'll talk about later in

15:24

this talk, we often use VUS to evaluate

15:27

arterially hyperenhancing lesions.

15:29

And if arterial phase is full of

15:31

motion, that could somewhat degrade

15:32

our ability to evaluate those lesions.

15:35

So it's not, um, most of the patients,

15:37

but it is a significant percentage of

15:39

patients that have that phenomenon.

15:42

Okay.

15:42

And then the all-important question is,

15:44

well, is there a big difference in price?

15:46

You know, we don't wanna rack up our cost to our

15:48

patients, our cost to the hospital unnecessarily.

15:51

And the main answer is yes, VUS is a little bit

15:54

more expensive, but it's not a lot more expensive.

15:56

At least at my institution. I know costs

15:58

can be different in different places.

16:00

Um, but as I said, we can use the same time

16:02

slot, so it's just as efficient for our MRI time.

16:05

The overall cost of the MRI scan is the same.

16:09

The main difference is the price of the contrast.

16:11

So at my institution, we pay about $3 per

16:14

milliliter of standard, um, gadolinium contrast.

16:17

We pay $13 per milliliter of VUS, but remember now

16:20

we are only using half the volume of VUS, so it...

16:24

It out a little bit.

16:25

So, you know, the overall total cost of

16:27

contrast is about, you know, 50 plus dollars

16:30

more for a VUS scan compared to a liver

16:32

MRI.

16:34

All right.

16:35

And then the last thing that I think is

16:36

all on our minds is, of course, safety.

16:38

We wanna do what's right by our patients and

16:40

make sure that we are selecting safe contrast.

16:43

So, you know, in general, gadolinium contrast

16:45

are pretty well tolerated by patients.

16:46

Very few adverse events, very few allergies.

16:49

Um, you know, the most common problem is NSF,

16:52

which is quite rare and, you know, not really seen

16:55

nowadays. But nephrogenic systemic fibrosis,

16:57

we're much more careful about screening our

16:59

patients for renal dysfunction and using, um,

17:01

agents that are less likely to cause this.

17:04

Um, but in 2016, the gadolinium deposition

17:06

disease, GDD, sort of came around.

17:09

It was this new proposed pathology.

17:11

You know, it's been long known that gadolinium

17:13

deposits in different parts of the body — the

17:15

bone, the kidneys, the brain — um, but since

17:18

2016, there has been this proposal that certain

17:21

types of sort of vague subjective symptoms like

17:24

peripheral neuropathy, headache, clouded mentation,

17:28

joint stiffness — all these things — they might

17:30

comprise this gadolinium deposition disease.

17:33

You know, there hasn't been any clear

17:35

studies that have, like, clearly correlated

17:37

these vague symptoms with gadolinium.

17:39

Um, but it is something that's

17:41

on everyone's mind these days.

17:42

A lot of, um, press and a lot of

17:44

patient interest in this issue.

17:46

Um, so I think it's something

17:48

that we have to pay attention to.

17:49

Studies have shown that the non-ionic linear

17:53

contrast agents are more likely to deposit than the

17:56

ionic linear contrast agents, which is what VUS is.

17:59

And then those are more likely than the macrocyclic.

18:02

So macrocyclic is considered the

18:04

safest — the least likely to deposit.

18:06

And then VUS is sort of in this middle category.

18:10

So this was a really nice retrospective study that

18:12

was, um, basically — or sorry — a meta-analysis that

18:15

looked at all the recent retrospective studies.

18:17

And I know you can't read any

18:18

of this content, which is fine.

18:19

This column is the linear, um, non-ionics.

18:23

This column is the, uh, linear

18:25

ionics, which VUS is in this column.

18:28

And this column is macrocyclic.

18:30

The dark green colors are non-confounded

18:32

studies — so studies where patients only received

18:35

that specific contrast agent and not other ones.

18:38

Um, and the red — sorry,

18:40

dark red and dark green are

18:41

both, um, non-confounded studies.

18:44

And so there were only, at this time, three studies

18:47

that had looked at VUS and two of them showed

18:49

no increased deposition in the dentate nucleus,

18:52

whereas one did.

18:53

So, you know, I think the jury is

18:55

still out as to whether or not VUS

18:56

is, um, a significant depositor.

18:59

Um, and even if it does deposit, it's

19:01

still unclear whether this illness really

19:03

results from gadolinium deposition or not.

19:06

Um, very controversial, but I think

19:08

something worth talking about.

19:10

Okay, so now we'll move on to the more fun part of

19:12

the talk, which is looking at the radiology images.

19:15

Um, so we'll start with the why.

19:16

So what are the different indications

19:18

that we might select VUS for?

19:22

So the first thing we're gonna talk

19:23

about is lesion characterization.

19:27

So I mentioned that VUS is taken up by

19:29

hepatocytes and excreted by the biliary tree.

19:31

So this contrast agent will be especially helpful

19:34

when we're trying to identify lesions that

19:36

come from hepatocytes over the biliary tree.

19:39

And so, um, most of those lesions, if we think

19:42

about it, tend to be arterially hyperenhancing.

19:44

So if things like focal nodular hyperplasia or

19:46

FNH, we have adenomas, we have HCCs, and then we have

19:50

other things that live in the liver like hemangiomas.

19:52

So these are the things that

19:53

we'll focus on for the next

19:55

couple of minutes, um, and we'll talk about

19:57

how to differentiate these two using VUS.

20:00

Um, and the key again is that these are

20:01

basically all arterially, uh, hyperenhancing masses.

20:06

All right.

20:06

So we'll start with FNH because I think

20:08

when most people think VUS, they think FNH.

20:11

So it's the second most common

20:13

primary liver lesion in adults.

20:15

And it's basically just hepatocytes

20:16

with abnormally organized biliary tree.

20:19

And it's thought to be secondary

20:20

to a vascular malformation.

20:22

Um, basically FNHs are, you know, considered

20:25

stealth lesions, which means they look and act

20:27

like liver, except that they're arterial hyper-

20:29

enhancing, likely due to that vascular malformation.

20:32

And because they look and act like liver and have

20:35

biliary tree within it, they retain VUS at 20 minutes.

20:38

So they're usually either isointense or

20:40

hyperintense relative to the liver parenchyma.

20:43

And then there are some rare subtypes that can

20:45

actually show a peripheral rim of hyperintensity.

20:48

So I'll show you what that looks like as well.

20:50

And then it's important to remember, you

20:51

know, we always think FNH has a scar.

20:54

Um, the central scar, although usually

20:56

is enhancing on a delayed image with

20:58

FNH, um, does not enhance with VUS.

21:01

So just 'cause you don't see the central scar

21:03

enhance with VUS, I don't want you to worry, and

21:05

I don't want you to think that it's not an FNH.

21:07

So I'll show you some examples.

21:10

This is a really important diagnosis

21:12

that we make prospectively.

21:13

We shouldn't be sending these patients for

21:15

biopsies unnecessarily, or God forbid, a liver

21:17

resection or something that really isn't necessary.

21:20

So we want to be able to make this an imaging

21:23

diagnosis, not a pathologic diagnosis.

21:26

All right, so I'm gonna show you a couple of cases of

21:28

FNH, both in the wild and also from the literature.

21:31

So this is a very classic FNH.

21:33

So on T2 we see that the mass itself is pretty

21:36

much isointense to the adjacent liver parenchyma.

21:39

And we see our T2 hyperintense

21:40

scar. Pre-contrast, again, stealthy.

21:43

It's blending into the adjacent liver parenchyma.

21:45

We see our scar. Here it is arterially hyperenhancing.

21:49

By the portal venous phase, it's isointense

21:52

to the adjacent liver parenchyma, and with

21:54

VUS at the hepatobiliary phase at 20 minutes,

21:57

again, it's isointense to the adjacent liver

21:59

parenchyma. And notice that the scar never enhanced.

22:03

This patient also happened to have

22:06

um, an MRI with an extracellular agent.

22:08

And so we see on this coronal image that the

22:11

central scar did enhance at five minutes.

22:14

So again, the scar will not

22:15

enhance with VUS, and that's normal.

22:17

Not a reason to raise the possibility

22:19

of it being anything else.

22:22

Okay.

22:22

Another example of the scar not enhancing with VUS.

22:26

It's a very small, subtle FNH.

22:28

Here in the right hepatic lobe, we can see the

22:30

linear T2 bright scar. With an extracellular agent,

22:34

we can see that the scar did enhance at five minutes.

22:36

But with VUS, although the lesion

22:38

itself is isointense to the adjacent

22:40

liver, the scar did not enhance.

22:44

Okay, so we, you know, we always

22:46

think of FNH as matching the adjacent liver.

22:48

It's a stealth lesion.

22:50

But what about if we have a background of fatty liver?

22:52

This confuses things quite a bit, right?

22:54

So we have, um, a patient with

22:56

fatty liver. T2 fat out,

22:58

we can already see that the

22:59

liver seems to be dropping out.

23:00

And then on the in and out

23:01

of phase we see, like, diffuse

23:03

pretty marked signal dropout.

23:04

So fat everywhere.

23:06

Um, this mass is arterially hyper-

23:08

enhancing relative to the adjacent liver.

23:10

But again, remember the adjacent liver's always

23:12

gonna show diminished signal because of that fat.

23:15

And then on portal venous phase, again, there's

23:17

a pretty stark difference between the amount of

23:19

enhancement of this lesion and the, um, and the, uh...

23:24

parenchyma.

23:25

So this was initially called a probable adenoma,

23:27

um, from my, from my friend's outside institution.

23:31

And the patient underwent a biopsy,

23:33

and this was a path-proven FNH.

23:35

Unfortunately, the surgeon did not

23:37

believe the, um, the biopsy results.

23:40

And so we suggested, or radiologist suggested,

23:42

getting an Eovist study, which very nicely

23:44

showed the persistent enhancement and actually

23:47

hyperenhancement of this mass relative

23:49

to the liver parenchyma at 20 minutes.

23:52

So this is a nice example of an FNH.

23:56

Okay, so this is, um, a sort of unusual but not

23:58

totally uncommon pattern that we can see with FNHs.

24:01

So I wanted to show it because if we see this

24:03

in real life, again, we don't wanna be confused.

24:06

So this is a pattern that occurs in about

24:08

15% of patients where the central portion

24:11

is similar background to the liver at

24:13

hepatobiliary phase at 20 minutes, but

24:16

the peripheral portion is hyperenhancing.

24:19

Um, so this is thought to be related to, you know,

24:21

a greater amount of that OATP transporter in the

24:24

periphery of the lesion relative to the center part.

24:26

So that periphery is taking in more Eovist and

24:29

holding onto more Eovist than the center part.

24:32

Then one other interesting thing that I learned

24:34

in the literature was that people can also develop

24:37

FNHs after receiving certain types of chemotherapy.

24:41

Um, so this was an example, um, of a

24:43

multi-institutional case report of 14 patients

24:45

who had received oxaliplatin for GI malignancy.

24:49

Um, oxaliplatin is often used in pancreatic and also,

24:52

um, colorectal cancer, um, part of FOLFOX or FOLFIRI.

24:56

And, um,

24:57

interestingly, the average interval

24:59

time, um, from treatment completion to

25:01

the new lesions was about four years.

25:03

So these can pop up a little bit

25:04

later, more removed from treatment.

25:07

So it's always, you know, good to

25:08

keep this in the back of your head.

25:09

I don't know how commonly you'll

25:11

see this in clinical practice.

25:12

Um, but it would be nice if we could

25:14

avoid biopsying these patients if we

25:15

see something that looks like this.

25:19

Okay, so moving on to adenoma.

25:21

Unlike FNH, adenoma is made of hepatocytes only.

25:24

It does not have any bile ducts.

25:26

So we would think that adenomas don't retain

25:29

Eovist 'cause they're not gonna be excreting into

25:31

the biliary tree as we would see with FNH.

25:34

Um, but we'll get to in a second

25:36

that some actually do retain Eovist.

25:38

And there are four different subtypes.

25:40

And of course they all have different

25:41

imaging features, which can sort

25:42

of complicate things a little bit.

25:44

But we're gonna work through how we can

25:46

differentiate, um, all these different subtypes

25:49

and how we can differentiate them from FNH.

25:51

And this is also an important diagnosis to make

25:53

confidently, or at least to raise the possibility

25:56

of, because some adenomas have increased risk

25:59

of hemorrhage and also malignant transformation.

26:01

So we don't wanna just send these patients off

26:03

into the world without follow-up, um, you know,

26:06

or without potential resection if they need it.

26:09

So this small study found that up to 25% of

26:12

the adenomas in their study cohort actually

26:15

did have hepatobiliary uptake, which seems like

26:17

a lot more than I've ever seen in practice.

26:19

And probably most of you have

26:20

never seen that many in practice.

26:22

Um, but I do think it's worth mentioning that

26:25

the inflammatory and the β-catenin subtypes

26:27

were the only ones that showed some retention.

26:30

Um.

26:31

So unfortunately, these are the two subtypes that

26:34

have the highest rate of malignant transformation.

26:35

So we certainly don't wanna be calling these FNHs.

26:38

So why do adenomas sometimes

26:40

take up Eovist and hold onto it?

26:42

And so it has to do with the fact that some

26:44

of these subtypes have higher levels of OATP,

26:47

meaning they're bringing more of the, um,

26:49

hepatobiliary agent into the hepatocyte, but

26:52

they have decreased levels of MRP3.

26:54

That was the transporter that effluxes the

26:57

contrast out of the hepatocyte.

26:59

So that means that they have more uptake at 20

27:01

minutes 'cause it's just sitting in the hepatocyte.

27:06

All right.

27:07

Um, so how can we tell the difference?

27:08

Now, I've probably scared you. You're worried that

27:10

you've called all these adenomas FNHs.

27:13

I wanna reassure you that there are a lot

27:15

of features that differentiate these two.

27:17

So the first is the central scar.

27:19

Um, no hepatocellular adenomas

27:21

were shown to have a central scar,

27:23

whereas, you know, many FNHs do. If we

27:26

look for signal dropout fat, FNHs are

27:29

very unlikely to have any fat within them.

27:31

Whereas we know certain subtypes of adenomas

27:33

do have quite a bit of fat within them.

27:35

If we look at the arterial phase of contrast,

27:38

you know, we always think of FNHs as

27:39

having marked arterial hyperenhancement.

27:41

90% of them do, whereas the adenomas,

27:45

you know, most of them have mild

27:47

arterial enhancement, um, not marked.

27:49

And so this is another way we can differentiate.

27:52

If we look at the portal venous phase

27:53

enhancement, again, FNH should be isointense

27:56

or hyperintense to the adjacent liver, whereas

27:59

adenomas tend to be a little bit hypointense.

28:01

Um, more so than, um, FNH.

28:04

If we look at late dynamic phase of

28:06

contrast enhancement, same thing.

28:09

The FNH should blend into the liver, iso or

28:11

hyperintense, whereas the adenomas tend to be hypo

28:14

intense, have started to wash out their contrast.

28:17

And then again, if we look at hepatobiliary phase

28:19

imaging, the majority of adenomas do not retain Eovist.

28:23

In this study, they found only 7%, which was

28:25

fewer than the study that I showed you before.

28:28

So again, if you, you know, consider all of these

28:31

different features, we should be able to differentiate

28:33

adenoma from FNH pretty confidently, and that way

28:36

we're not biopsying these patients unnecessarily.

28:40

So now how do we have high sensitivity or high

28:43

specificity and feel confident in our interpretations?

28:46

So if we see a central scar or a strong

28:49

arterial hyperenhancement, or isointensity or

28:52

hyperintensity on the hepatobiliary phase, these

28:54

are all features that are highly specific for FNH.

28:57

And if we see more than one of these features,

28:59

then it's very specific and we can feel very

29:01

confident in our diagnosis. For adenoma,

29:04

on the other hand, if we see intrafat

29:06

signal dropout on that out-of-phase imaging,

29:08

hypointensity on the late dynamics, or

29:10

hypointensity on the hepatobiliary phase,

29:12

again, all highly specific for adenoma,

29:15

and if we see multiple of these features,

29:17

we can feel even more confident.

29:19

So this is sort of how I think of this in my

29:21

brain when I'm seeing a case like this. You know,

29:23

if it looks and smells like an FNH, I just call

29:26

it an FNH, and that's the end of the workup.

29:28

If there's one minor feature that doesn't quite

29:30

feel right, doesn't really look like an FNH,

29:33

there's something that's not quite right about it,

29:35

just recommend some imaging follow-up.

29:37

If you see more than one minor feature

29:39

or any major feature that really doesn't

29:41

fit for an FNH, you know, say it's hypo-

29:43

hypoenhancing at the hepatobiliary phase,

29:46

then consider whether they need a

29:47

surgical consultation and/or a biopsy.

29:51

All right.

29:52

So a couple of examples, um, from the

29:53

literature and from my institution.

29:55

Um, this is just like a no-brainer, classic adenoma.

29:58

I don't think anyone here would be

29:59

confused about this being, um, an FNH.

30:02

Um, but fortunately this patient has both

30:04

an FNH and an adenoma, so we can look at

30:06

them simultaneously on the same slice.

30:08

So on the T2, the FNH is basically invisible.

30:10

You can't even see it.

30:12

And the adenoma is T2 bright.

30:13

Again, an FNH would never be this T2 bright.

30:16

It would be very unusual unless

30:17

you had a severe fatty liver.

30:19

On the pre-contrast, again, the FNH is very hard

30:23

to see, whereas the adenoma blends in with the liver.

30:26

So that might be a little bit confusing, I

30:27

guess. Arterial phase, they're both sort of

30:30

equally hyperenhancing. By portal venous phase,

30:33

again, I think they're both sort of about the

30:35

same, um, as far as like their relative enhancement

30:38

to the adjacent parenchyma, but by five minutes,

30:40

the FNH is really holding onto its contrast.

30:43

It might even be a little hyperintense relative

30:45

to the adjacent parenchyma, but this adenoma

30:47

is starting to wash out. And by 20 minutes,

30:50

there's no contrast left in this adenoma.

30:52

And the FNH is holding onto contrast.

30:54

So I think, you know, we can look at all the

30:56

different features and recognize that this is

30:57

clearly not an FNH between the T2 contrast and

31:00

the 20-minute phase, and even at the five minutes.

31:03

Um, whereas this, it's matching

31:05

an FNH in every way.

31:08

All right.

31:09

Um, another example, I think, of

31:11

a more straightforward adenoma.

31:13

Um, unlikely to be confused

31:14

for an FNH. We have this T2,

31:16

um, kind of hard to see.

31:19

So in this, in this way, it might be,

31:20

initially you might think, oh, is this an FNH?

31:22

Here it's blending into adjacent liver parenchyma.

31:25

The T1 also is blending in a little bit as well.

31:28

But on the in and out of phase, we

31:29

see clearly that there's some fat,

31:32

um, both surrounding the mass and also within

31:34

the mass, which is very unusual for FNH.

31:37

The arterial enhancement is really not as

31:39

marked as we would like to see for an FNH, and

31:41

by five minutes it has started to wash out.

31:44

So again, really no confusion here.

31:45

Enough features of an adenoma that

31:47

we would not confuse it for an FNH.

31:50

This lesion,

31:51

on the other hand, I could see why

31:52

people might confuse this for an FNH.

31:54

So this actually was a beta-catenin

31:56

subtype adenoma, but I think

31:58

in many ways it looks like an FNH.

32:00

So it's quite large.

32:01

I've never seen an FNH this big, but it

32:03

certainly could happen, and it seems iso-

32:06

intense on the pre-contrast arterial phase.

32:08

Very bright, a little bit heterogeneous,

32:10

you know, wondering, is this a central scar?

32:13

On the portal venous phase, again, the

32:15

parenchyma and the mass seem to be hypo-

32:17

intense, and at the 20-minute Eovist, it is iso-

32:20

intense relative to the adjacent parenchyma.

32:23

Um, the scar does not enhance.

32:25

But again, we wouldn't expect any

32:26

FNH scar to enhance with Eovist.

32:29

But if I told you the history, which was that

32:31

this was a bodybuilder and personal trainer with

32:33

seven years of testosterone and other steroid

32:35

use, then you might start to think adenoma.

32:38

And you know, the fact that the size doesn't really

32:40

fit, and the clinical history doesn't really fit.

32:42

This turned out to be biopsy-proven

32:43

beta-catenin subtype adenoma.

32:46

So this is one of the more confusing cases

32:48

where I think the clinical history, um, and

32:50

sort of it not quite feeling like an FNH,

32:52

the size doesn't quite look right,

32:54

the size of the central scar.

32:56

Some of these features, um, help you

32:58

to distinguish between. All right, so

33:02

moving on to hepatocellular carcinoma.

33:04

Um, this is the most common primary malignancy.

33:07

It occurs in certain types of patients,

33:08

who are at risk—patients with chronic

33:10

hepatitis or cirrhosis from other reasons.

33:13

Um, so we generally use LI-RADS in these patients,

33:16

which is our imaging and reporting system.

33:18

And LI-RADS does not specify whether you should use an

33:21

extracellular agent or hepatobiliary combined agent.

33:24

Um, there are certain features that can help you.

33:27

Um, there are certain features—ancillary features—

33:29

that we can use hepatobiliary for, but it's

33:32

important to know that they're not specific for HCC.

33:35

So our overall evaluation for major

33:37

features is the same whether we use

33:39

extracellular agent or hepatobiliary agent.

33:42

And it's also important to keep in mind that about 10

33:44

to 15% of HCCs can actually hold onto Eovist as well.

33:49

And so this might confuse us

33:50

rather than help us in the end.

33:53

So the ancillary features that we can use for, um,

33:57

hepatobiliary agents are, um, favoring malignancy

34:00

in general, but again, not specific to HCC, are

34:03

transitional or hepatobiliary phase hypointensity.

34:06

So this is what we would expect

34:08

really any non-liver lesion to—

34:11

any non-hepatocyte or biliary lesion to do.

34:14

Um, and that can help us bump up our LI-RADS

34:17

scoring, but we can't go from a LI-RADS 4

34:20

to a LI-RADS 5 based on ancillary features.

34:22

So that's something important to keep in mind.

34:24

And then there's one ancillary feature that

34:26

favors it being a benign lesion, which

34:28

is the hepatobiliary phase isointensity.

34:31

And for that, we are able to bump down.

34:33

So it's worth thinking about whether you

34:35

would want to use ancillary features, um,

34:37

in your LI-RADS assessment because it is

34:39

possible to bump up or bump down

34:41

a lesion, but again, it's not necessary.

34:44

You can use whichever contrast agent

34:45

you feel more comfortable with.

34:47

Um, so just a straightforward case of, uh,

34:50

HCC from the literature, like a very classic

34:52

HCC, um, using hepatobiliary phase contrast.

34:56

We see at the late arterial phase our typical

34:58

hyperenhancement. By portal venous phase,

35:00

we have washout and a capsule, so this

35:02

is a LI-RADS 5. Ancillary features here,

35:04

not really important, but we do have the

35:06

ancillary feature of hypoenhancement at the

35:08

hepatobiliary phase. But this remains a LI-RADS 5

35:11

no matter what. So very straightforward.

35:15

On the other hand, this was an example

35:16

from my institution that I thought

35:17

was a little bit more confusing.

35:19

So this was a patient at risk for HCC undergoing

35:22

screening, and we have our T2 fat sat.

35:24

We see a very faint T2 hyper-

35:26

enhanced kind of lobulated lesion.

35:28

It's much more apparent on

35:29

the diffusion-weighted images.

35:31

And then we have our arterial, portal venous phase,

35:33

and then our hepatobiliary phase shown here.

35:36

It was arterial hyperenhancing.

35:38

Portions of it appear to wash out.

35:40

Not quite sure we see a capsule though.

35:42

And then on the hepatobiliary phase, you know,

35:44

some parts of it are isointense to the

35:47

adjacent liver, and parts of it appear washed out.

35:50

So is this just some sort of weird, you

35:52

know, fatty change with perfusion change?

35:55

Well, the patient had an elevated AFP.

35:57

This turned out to be a LI-RADS 5 based

36:00

on arterial and portal venous phase.

36:02

The hepatobiliary phase wasn't convincing

36:03

enough to bump it down to a LI-RADS

36:06

4, and this was treated as an HCC.

36:11

All right.

36:11

And then just one quick word about

36:12

fibrolamellar HCC versus FNH.

36:14

Because I remember when I was a resident,

36:16

I was always very confused about how

36:18

to differentiate these two things.

36:19

Um, even though I think in real life it's

36:22

a little bit easier to differentiate, um, there

36:24

are some overlapping features in the, you know, in

36:26

the literature—that they both have a central scar.

36:28

They both tend to be arterially hyperenhancing.

36:31

Um.

36:32

Fibrolamellar HCCs can sometimes show some hepatobiliary

36:35

phase enhancement, but they usually are hypo-

36:38

enhancing relative to the background liver.

36:41

Um, whereas FNHs should be at least

36:43

iso-, if not hyperenhancing, relative

36:46

to the background liver. And fibrolamellar

36:48

HCCs tend to be more T2 hyperintense,

36:51

T1, and heterogeneous compared to FNHs.

36:54

So there's, again, enough features to differentiate

36:56

these two that I don't think that we should

36:58

be confused, um, by the differential here.

37:02

Okay.

37:02

And then the last lesion I want to mention is

37:04

hemangiomas, mainly 'cause we just see them so

37:06

frequently and we're so used to their classic

37:08

appearance that I don't want Eovist imaging of

37:11

a hemangioma to confuse anyone and to make

37:13

you think that it looks like something else.

37:15

Um, so they are our most common liver lesion.

37:17

They're basically just blood-filled

37:18

vascular cavities of varying size.

37:21

And when we do dynamic contrast enhancement,

37:23

we see that peripheral nodular discontinuous

37:25

enhancement of the lesion, sort of

37:27

filling in, um, from the outside in.

37:30

We are classically thought to

37:32

that these should match the blood pool.

37:34

But remember, with Eovist, things are excreted

37:36

a little bit differently, and so the

37:38

blood pool changes as we get later in our

37:40

exam and we do our hepatobiliary phase.

37:43

And because in the hepatobiliary phase, all the blood

37:46

pool is washed out, it will not persist as is.

37:49

The enhancement will not persist on the hepatobiliary

37:52

phase, which is something we're used to looking

37:54

for on the delayed phase of extracellular agents.

37:57

Um, so this is just a nice

37:58

classic example to show you that.

38:00

So we see T2 bright lesion gets

38:02

brighter on the T2 fat sat, which is

38:04

another classic feature of hemangiomas.

38:06

And then on the dynamic contrast enhancement, we see

38:09

that peripheral nodular discontinuous enhancement.

38:12

But remember, at five minutes

38:14

we're starting to see washout of the vascular system.

38:17

But keep in mind, it matches the adjacent IVC,

38:20

so it does still match the blood pool, even though

38:22

there's not much contrast left in the blood pool, and

38:25

by 20 minutes, again, it matches the adjacent IVC.

38:28

No contrast left in it, but neither

38:30

is there any contrast left in the IVC.

38:32

So since this is just basically a vascular lesion,

38:35

it should match the vasculature at all phases.

38:39

Okay, so moving on to lesion detection.

38:41

This is just a quickie.

38:43

Um, but basically, Eovist MRI is considered to be the

38:46

most sensitive type of test to find liver lesions.

38:49

So definitely better than

38:51

CT, better than a standard MRI, which

38:54

is about equivalent to an FDG-PET.

38:55

Keeping in mind that there are some size

38:57

limitations with FDG-PET.

38:59

Um, but this is the most sensitive, and detection

39:02

of lesions is especially important in certain

39:04

malignancies like colorectal cancer, where

39:07

oligometastatic disease is considered curable.

39:09

So we wouldn't want the surgeon to leave behind

39:11

any small lesions because we miss them on imaging.

39:13

We need to be able to point out to the surgeon

39:16

exactly where the lesions are so they can

39:17

wedge them out or perform the resection.

39:21

So this was an example from my institution, a patient

39:23

with, um, colon cancer who was having staging done.

39:26

And we saw this small ill-defined hypodense lesion.

39:29

Didn't really look like anything

39:30

benign, but hard to tell on a CT scan.

39:33

And so we recommended an MRI with Eovist because

39:36

yes, we wanna characterize this, but we also

39:38

wanna make sure that there are no other lesions

39:40

elsewhere because if this was a metastasis,

39:42

this was this patient's only metastasis, and so

39:45

they're potentially curable if this was resected.

39:49

So we did our MRI, and we see our lesion here on

39:53

the hepatobiliary phase, but we also see another

39:55

lesion here, and we see another lesion here.

39:59

And it's important to note that these

40:01

lesions were not seen on any other sequences,

40:03

not even diffusion-weighted imaging.

40:05

So the hepatobiliary phase is very

40:07

important in these patients before resection

40:09

to make sure we don't miss anything.

40:11

And fortunately, all these lesions were very

40:12

peripheral and easy for the surgeon to wedge out.

40:17

Okay.

40:18

All right.

40:19

And then moving on to our last topic, I'll

40:21

be brief so we have time for questions,

40:23

is how to evaluate the biliary tree.

40:25

So the benefit of Eovist compared to other types

40:27

of biliary imaging is that we can evaluate in

40:30

a non-invasive way both the anatomy and the

40:32

functional, um, functionality of the biliary tree.

40:36

So we'll start with, um, living liver donors.

40:40

So, um, living liver donors have a not

40:43

insignificant frequency of biliary complications.

40:47

Um, so somewhere between 2 and 32%,

40:50

the average in most studies is about 7%.

40:52

So it's not a huge number, but it's not insignificant.

40:55

And if you were giving your liver as a donor, I think

40:57

you would wanna make sure that you did everything

40:59

you could to reduce your potential complications.

41:02

And the most common complications are bile leaks

41:04

and strictures, which are not insignificant.

41:07

About 40% of the population

41:09

has biliary anatomy variants.

41:10

So I think that's something that's important to keep

41:13

in mind is that it's our job to tell the surgeon what

41:15

they're going to encounter so that they don't mess up

41:17

the anastomosis or cause a leak or cause a stricture.

41:21

Um, so this study, excuse me.

41:23

This study looked at 42 patients who

41:26

had both a standard MRCP and also

41:29

an MRCP in the hepatobiliary phase.

41:31

Basically looking at excreted

41:32

contrast in the biliary tree.

41:34

And they did a subjective scoring

41:36

visualization of the different ducts.

41:38

And what they found was that the hepatobiliary

41:40

phase was actually beneficial compared to

41:42

the MRCP for certain parts of the biliary

41:44

tree that included the cystic duct, the left

41:46

hepatic duct, and the right second order ducts.

41:49

Whereas there was no significant difference

41:51

in several of the other ducts, like the

41:52

CBD, the right hepatic duct, and some of the

41:54

other second and third order hepatic ducts.

41:57

So this was an example from their article

42:00

that I thought just nicely illustrated the

42:01

difference between MRCP and hepatobiliary phase.

42:04

So here we see a patient who has a type six variant.

42:08

So we can see the, um, segment two and

42:10

segment three ducts insert directly

42:12

on the common bile duct, which both

42:14

studies show nicely. But we see this right

42:17

posterior branch, um, inserting onto the common

42:20

bile duct only on the hepatobiliary phase images.

42:23

Um, we don't see it at all on the MRCP images,

42:25

so just something to keep in mind that maybe if

42:28

you're going to do one, you might as well do the

42:30

other to make sure that you see everything clearly.

42:33

We can also use, um, Eovist or hepatobiliary

42:36

contrast to assess biliary obstruction.

42:39

So not only can we identify the point of

42:41

obstruction, but we can also identify whether

42:43

the obstruction is clinically significant.

42:45

Is there any excretion through the point

42:47

of obstruction or is everything held up?

42:50

Remember though that, um, hepatobiliary phase

42:53

studies can be limited in patients with very high

42:55

bilirubin because of that competitive antagonist,

42:58

um, relationship between the contrast agent and bile.

43:02

So this is really better for patients

43:03

with mildly elevated bilirubin compared

43:05

to markedly elevated bilirubin.

43:08

And so this study looked at.

43:10

Um, Eovist MRI or Eovist MRCP,

43:13

compared to standard MRCP.

43:14

And then all patients had some sort of reference

43:16

standard, whether it was an ERCP, um, PTC, or

43:19

intraoperative cholangiography, and they found

43:22

that the overall accuracy for the evaluation

43:24

of the significance of the biliary obstruction,

43:27

whether it was a complete, a partial, or

43:29

really not obstructing at all, increased

43:31

from 60 to 91% when they added the Eovist

43:34

portion of the study. And the radiologists'

43:36

confidence also increased when they

43:38

added the Eovist portion of the study.

43:40

So this was just a nice example

43:41

from the, from their study.

43:43

Um, looking at a patient who has had a, um,

43:46

hepatic or choledochojejunostomy, and the

43:50

MRCP image, because of overlying structures, was

43:52

not clear whether there was a narrowing here.

43:54

There was.

43:55

A little bit of upstream biliary prominence, but we

43:57

can see nicely on the hepatobiliary phase that this,

44:00

um, contrast is being excreted into that choledochojejunostomy,

44:03

and there was no significant stricture here.

44:08

Um, another example here is a patient who has

44:10

status post cholecystectomy, who's had some

44:12

incidental, um, biliary ductal dilatation.

44:15

The MRCP image shows a focal stricture here, and

44:18

the upstream dilatation, but on the hepatobiliary

44:20

phase, again, although there is a focal stricture

44:22

there and some upstream dilatation, we do see some

44:25

of the contrast being excreted into the duodenum.

44:28

And so we know that this is

44:29

only a partial obstruction.

44:31

And then primary sclerosing cholangitis,

44:33

um, is another thing that we can evaluate

44:35

with the, um, hepatobiliary phase contrast.

44:38

It's really thought to be complementary.

44:40

One is not necessarily better than the other.

44:42

Um, and interestingly, the Eovist MRCP

44:45

does not perform as well for

44:47

visualization of the peripheral ducts.

44:49

And so this is an example of a patient with MRCP.

44:51

We have our ERCP — sorry, PSC. We have in our

44:55

ERCP images here. We have our standard, um, MRCP

45:00

image here, and then we have hepatobiliary

45:02

phase axial and coronal images here.

45:04

And so although we don't see the biliary tree

45:06

as clearly, we don't see the stricturing and

45:08

the beading like we do with these two images.

45:11

We do see that the peripheral ducts are excreting the

45:15

hepatobiliary contrast, and so we can give them some

45:17

functional information about the biliary excretion.

45:21

Alright, um, I'm gonna skip this just so we can

45:23

get to our last topic before question and answers.

45:26

Um, so the last thing to think

45:27

about is using Eovist for bile leak.

45:30

Although, um, HIDA scans are classically

45:32

the best, um, study — you know, the gold

45:34

standard study to look for bile leak —

45:35

the nice thing about an Eovist MRI is that we

45:37

get a lot of anatomic information as well

45:40

as the functional information about a leak.

45:42

Um, so it increases sensitivity, um.

45:45

But it ha— you know, but, um, and it also

45:47

increases our ability to anatomically

45:49

localize where the bile leak is coming from.

45:52

So this was an example from my institution.

45:54

Um, this was a patient who had a perihepatic

45:56

fluid collection along the dependent portion of

45:59

the right hepatic lobe after cholecystectomy.

46:01

And so it was suspected clinically

46:03

that this might have been a bile leak.

46:05

We did our MRI. Again, we see our T

46:07

two bright multilobulated collection.

46:10

And then on the post-contrast, we started to see at

46:12

60 minutes — or sorry, at 20 minutes — we started to

46:15

see contrast being excreted into this collection.

46:18

But by— you know, we weren't quite

46:20

sure if we saw clearly enough the leak.

46:22

And so we removed the patient from the scanner

46:24

and brought him back later for a 60-minute study.

46:27

We can see more contrast and then we can see

46:29

some contrast, um, leaking into the biliary tree.

46:34

Um, this was another example from the literature.

46:36

Um, again, similar bile leak, um,

46:38

in a hepatic wedge resection.

46:39

So we see T two hyperintense

46:41

collection in the, um, surgical bed.

46:44

On the hepatobiliary phase,

46:45

we can see a little bit of, um, extravasated

46:48

hepatobiliary phase contrast, and

46:49

then correlate finding on the ERCP.

46:53

All right, so I know that was a whirlwind

46:54

of information in about 45 minutes.

46:57

Um, so things I want you to take home.

46:59

So the what — so Eovist is a gadolinium-based

47:02

contrast agent and it functions both as an

47:04

extracellular agent so we can get our dynamic

47:06

phase contrast images and our hepatobiliary phase.

47:09

But remember that it competes with bile and so it

47:12

has decreased uptake in patients with cholestasis.

47:14

So not a good idea to use if their

47:16

total bilirubin is greater than five.

47:19

The how.

47:19

Remember that we wanna rearrange our protocol a

47:21

little bit so that we can do VUS in under 40 minutes.

47:25

If you're going to get an MRCP image as

47:27

well, make sure to do it before contrast

47:29

to reduce some artifacts from that T2

47:31

shortening effect from that concentrated, um,

47:34

gadolinium being excreted in the biliary tree.

47:37

Remember the issues relating to VUS having

47:40

a smaller dose and a smaller volume.

47:42

Um, we have issues with bolus timing

47:44

and also maybe some decreased signal,

47:46

um, especially in the arterial phase.

47:48

And then remember that we can sometimes get

47:50

motion artifacts from that arterial phase too.

47:53

And then the why, the most common reason,

47:55

um, you know, lesion characterization,

47:57

especially arterially enhancing lesions.

48:00

Um, also very important lesion detection in patients

48:02

with oligometastatic cancer who may be curable.

48:05

And anyone with biliary pathology — great

48:07

for anatomy and functional assessment.

48:10

So I just wanna acknowledge a couple

48:11

of people who helped me with this talk.

48:14

And thank you for your attention.

48:17

Perfect.

48:17

Thank you so much.

48:18

Before we move into the Q and A, I

48:20

just wanted to thank everyone for

48:21

participating in this noon conference today.

48:23

A reminder that this conference will be made

48:25

available on demand on mionline.com, in

48:27

addition to all previous noon conferences.

48:30

And tomorrow we'll be joined by Dr. Navita

48:32

Agarwal for a noon conference on functional and

48:34

structural anatomy of the human cerebellum.

48:36

Dr. Lon, if you want to open up the Q and A

48:38

feature, I'll let you take it again from here.

48:40

Great.

48:41

Okay, so I see Q and A, so I'll just go, I think

48:44

down the line and, um, we'll, we'll go to about one

48:47

o'clock and if there's anything left unanswered, I'm

48:49

more than happy to answer questions offline as well.

48:51

Um, so first question is, um, so does Eovist as a

48:54

combined agent cause central scar in FNH to enhance

48:58

early, but then not enhance during equilibrium phase?

49:01

And the answer.

49:02

At least as far as I know is that with

49:04

Eovist, the central scar will never enhance.

49:07

Um, whereas with, um, other extracellular

49:09

agents or even with Multihance, the

49:11

central scar enhances in a delayed fashion.

49:14

Again, I think somehow relating to it going

49:16

into the interstitium, I don't quite understand

49:19

or know why it doesn't enhance with Eovist.

49:21

But, um, studies have always shown

49:23

you know, that it has never enhanced with

49:25

Eovist. Um, so I hope that's helpful.

49:28

Um, the next question, as you mentioned, adenomas have

49:32

mild enhancement and hypo intensity on hepatobiliary

49:35

phase, then more likely to be adenoma versus FNH.

49:39

But does it confound for possibility of HCC?

49:41

And that's a great question. And I think,

49:44

adenomas and HCC often have a lot of the

49:46

same imaging features, especially that

49:48

washout and the sort of capsule that we

49:50

sometimes see with either HCC or adenomas.

49:52

And so here the clinical

49:54

history is the most important.

49:55

Does the patient have any risk factors for HCC?

49:58

Any, you know, known cirrhosis or

50:00

chronic liver disease, um, or any

50:02

chronic hepatitis without cirrhosis?

50:05

Um, those are, I think.

50:06

Probably the best ways to differentiate

50:08

between an adenoma and an HCC.

50:10

But you know, again, if you're not sure, and

50:12

it looks and acts like an HCC, get a biopsy.

50:16

Um, and that'll give you the differential,

50:17

whether it's an adenoma or an HCC.

50:20

Um, the next question is, what imaging follow-up

50:23

would you use if FNH had atypical imaging features?

50:27

You know, to me, I think comparing apples

50:29

to apples is easier than apples to oranges.

50:31

So if you've done an Eovist MRI, presumably you

50:34

would have, if you think something is an FNH,

50:37

then I would just do an Eovist MRI as follow-up.

50:39

Um, unless there's some reason that

50:42

the patient can't get VUS, or there's

50:44

some other issue, but I think, you know,

50:46

comparing the same type of study is the

50:48

best way to, um, to follow up patients.

50:51

Um, compare the case with the, uh, the, uh,

50:55

beta-catenin adenoma and the bodybuilder.

50:57

How to differentiate confidently, uh,

50:59

confidently from FNH or fibro-ML or HCC?

51:02

I think that's a great question.

51:03

I'm not sure that that, um, case

51:06

could be diagnosed prospectively.

51:08

Um, I think a biopsy probably was necessary, but I

51:11

think, you know, we would wanna hesitate from just

51:13

calling it an FNH and sending the patient on their

51:16

way. I think including in the differential, you know,

51:20

beta-catenin adenoma, fibro-ML, or HCC and FNH is

51:24

reasonable, and then going forward with the biopsy.

51:28

How do you choose extracellular versus

51:30

hepatobiliary before knowing the diagnosis?

51:33

Is hepatobiliary a default for all MRI?

51:35

Um, great question.

51:37

So I would say the majority of our E

51:38

of S studies are done after a patient's

51:41

already had some other type of study.

51:43

So, you know, in rare circumstances

51:45

they've had a CT and something looks kind

51:48

of like an FNH, um, you know, that it's

51:50

arterial enhancing, or we're seeing a very

51:53

subtle lesion on the portal venous phase

51:55

that we think is probably an FNH, then

51:57

we might recommend going straight to Eovist.

51:59

But in most circumstances, patients have had

52:02

some other extracellular agent MRI, where

52:04

there's a lesion that's maybe indeterminate.

52:07

And we recommend getting Eovist as

52:09

the follow-up study to confirm whether

52:11

something might be an FNH or other.

52:14

Um, and then the only other example I can think

52:16

of where we would go straight to Eovist is in

52:19

that case where I showed you patients potentially

52:21

being evaluated for a liver resection, um, for

52:24

oligometastatic disease. Um, in those patients, I

52:27

would definitely go straight to Eovist because you

52:29

want to be able to identify all the liver lesions.

52:32

And as we saw from, um, my slide, which was

52:35

referencing another study, Eovist MRI is significantly

52:38

more sensitive than other gadolinium MRIs.

52:43

Um, next question.

52:46

What about well-differentiated HCC where we might see

52:48

homogeneous Eovist uptake, um, from Athens, Greece?

52:51

Thank you.

52:52

That's pretty cool.

52:53

Um, so, uh, that's, that's a great issue.

52:56

So for me, that's one of the reasons why I

52:58

personally don't, and, and my institution, we

53:00

generally don't use Eovist for, um, HCC LI-RADS workup.

53:04

Again, there's LI-RADS doesn't specify

53:06

which one you might wanna use, and

53:08

some people really like to use Eovist.

53:10

I think it's a matter of comfort level.

53:12

I tend, I tend to be someone who does not use

53:14

many ancillary features in my LI-RADS assessment.

53:17

Um, it's again optional for the radiologists

53:19

whether they want to use ancillary features or not.

53:22

Um, and again, no ancillary feature can

53:24

ever bump a patient up to a LI-RADS 5.

53:26

So I tend to, um, err on the side of just

53:29

using major features and we tend to use just

53:31

extracellular agents for our LI-RADS workups.

53:35

Um.

53:37

Another question is, is HIDA scan more accurate

53:40

than contrast-enhanced MRI regarding biliary leak?

53:43

You know, I think that HIDA scan is very sensitive.

53:46

Um, but I think it's not as

53:48

good for anatomic localization.

53:50

So I think, you know, if you're evaluating

53:52

a biliary leak for something straightforward,

53:54

where you know where the biliary leak is

53:55

probably coming from, so for example,

53:57

patient after sort of an uncomplicated

53:59

cholecystectomy, gallbladder comes right off.

54:02

They clamp at the cystic duct.

54:04

If they're having a leak, you know it's

54:05

coming from the cystic duct most likely.

54:07

Um, so in that case, I'm not

54:09

sure that an MRI is necessary.

54:10

But if you have a more complicated, um, story,

54:14

you know, some sort of complicated liver resection,

54:16

or a very complicated cholecystectomy, then it

54:19

might make sense to do the MRI so that you can

54:21

get some more anatomic information, even though

54:23

you might have slightly decreased sensitivity.

54:27

Um, at what GFR do you not

54:29

administer hepatobiliary agents?

54:31

So for us, this is the same rule

54:33

really, um, for all, all gadolinium

54:35

contrast agents, which is a GFR of 30.

54:38

Um, at my institution we also have gadoxetate disodium

54:40

available, which, um, has not yet shown to

54:43

have any, um, any cases of NSF in

54:47

patients with less than, uh, less than 30 GFR.

54:50

We still do consent

54:51

all those patients, um, make sure that

54:52

they understand the potential risks.

54:54

Um, so for Eovist, I would still use the GFR of 30.

54:58

Um, is there any difference in the scan parameter

55:02

for post-contrast dynamics in hepatobiliary phase?

55:04

Um, yeah, that's a great question.

55:05

So I did have the one slide that showed

55:08

the FNH at the dome of the liver with a

55:10

flip angle of 10 degrees versus a flip

55:13

angle of, I think it was 20 or 30 degrees.

55:16

And, um, we should be changing the flip angle for

55:18

hepatobiliary phase images to about 25, 20 to 35, I

55:22

believe, um, to sort of optimize the contrast there.

55:27

Um, how will we differentiate between HCC and adenoma?

55:31

I think we already addressed that.

55:33

Um, let's see.

55:37

How to differentiate primary HCC

55:39

from hypervascular mets on MRI?

55:41

That's a good question.

55:42

So again, you know, one, does the patient

55:45

have risk factors for HCC? And then two,

55:48

um, where do they fall in the RADS spectrum?

55:50

So there are features—

55:52

that, you know, ancillary features

55:54

that, again, are more likely to suggest

55:55

malignancy but are not specific for HCC,

55:58

things like targetoid-type enhancement.

56:00

Um, so if we see any of those features, we may want

56:04

to decrease our LI-RADS using the ancillary features.

56:07

Again, if they have other, you know, history

56:09

of having a hypervascular primary malignancy—

56:12

definitely something to consider.

56:14

And in those patients, a biopsy might

56:16

be necessary for treatment planning,

56:17

whereas in the standard patient who's at risk for

56:19

HCC and has no known primary malignancy, we can

56:22

go off the RADS and treat them without biopsy.

56:26

Um.

56:28

When will you use Eovist for liver surgery planning?

56:31

We mainly use it in patients who

56:33

are going to, um, who are potentially

56:36

curable by having their liver resection.

56:39

So, um, and so the main one I can

56:42

think of is colorectal cancer, but

56:43

there are probably others as well.

56:45

Um, and so, you know, our surgeons at our institution

56:49

are very good about knowing when they wanna order an

56:51

Eovist. So fortunately we don't have to necessarily

56:54

recommend it to them at this point, but it's always

56:56

something to keep in mind when you're protocoling.

56:59

Um, what about the green HCC in which

57:03

lesions appear hyper in biliary phases?

57:07

Um.

57:08

I think you're talking about the HCCs

57:11

that, um, hold on to the Eovist, and again,

57:14

those I think can be more confusing.

57:16

Fortunately, they tend to be slightly

57:18

better prognostic, um, prognostically

57:21

for the patient, although we would

57:22

certainly not want to miss one of those.

57:24

You know, for this reason, that's one of

57:26

the main reasons I don't really use Eovist

57:28

for evaluating, um, LI-RADS HCC screening.

57:32

But, um, that feature makes

57:35

it a little bit more confusing, but

57:37

even if it does hold onto contrast,

57:39

again, that's an ancillary feature favoring benignity,

57:42

and it would just bump down your LI-RADS if you choose to use it.

57:45

Again, if your clinical suspicion and your imaging

57:48

suspicion for HCC is high enough, you can leave

57:52

your LI-RADS score based on major features.

57:56

All right.

57:56

Let's do maybe one or two more

57:58

questions before one o'clock.

58:00

Um, do you screen for GFR, um, for gadoxetate and Eovist?

58:03

And we do, yes.

58:04

And do you give for GFR below 30?

58:07

And in that case, we would probably use gadoteridol.

58:09

Um, again, we use, um, we would

58:12

consent the patient for that as well.

58:15

Um.

58:16

Wondering what the downside to using Eovist

58:18

compared to regular agent all the time?

58:20

So I think the major downside is:

58:22

one, the contrast is not as bright,

58:24

things are just a little duller on Eovist; two,

58:27

you have that potential for having that

58:29

respiratory motion artifact in the arterial

58:32

phase, which is often a very important phase;

58:34

and three, it is more expensive.

58:36

Um, so if you don't need to use it, then we should

58:39

probably be using the cheaper option.

58:42

Um, okay.

58:43

I think I'll leave it at that, but if anyone

58:45

has any lingering questions, I'm happy to

58:47

share my email address and answer them offline.

58:52

Perfect.

58:52

As we, uh, bring this to a close today,

58:54

I just wanted to thank you so much,

58:55

Dr. Matalon, for your time today.

58:57

And thanks to all of you for

58:58

participating in this noon conference.

58:59

Again, this noon conference will be made available

59:01

on demand on mriline.com within the next 24 hours,

59:06

in addition to all the other previous noon

59:08

conferences on the website. Please follow

59:10

us on social media and for reminders

59:12

on upcoming noon conferences.

59:15

Thank you so much again, and have a wonderful day.

59:18

Great, thank you.

59:18

Thanks everyone.

59:19

Have a nice day.