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Today we're honored to welcome

0:48

Dr. Giuseppe Bronticatelli for a lecture on MRI of focal

0:53

liver lesions with extracellular contrast agents.

0:57

Dr. Bronticatelli studied at the University of Palermo School

1:03

of Medicine and is currently a professor of radiology.

1:06

He has published several academic papers and

1:08

has received several awards.

1:11

At the end of the lecture, please join us

1:12

in a Q&A session where he will address any

1:14

questions you may have on today's topic.

1:17

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1:22

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at the bottom of your Zoom screen.

1:32

With that being said, we are ready to begin today's lecture.

1:36

Dr. Bronticatelli, please take it from here.

1:39

Thank you.

1:40

Thank you very much, Olivia.

1:42

Welcome everybody.

1:43

It is my great pleasure to be here with you today and to

1:47

talk to you, uh, on, um, on MRI of focal liver lesions.

1:53

I'm grateful to MRI Online for this possibility.

1:58

So my name is Giuseppe Bronticatelli from Palermo in Italy.

2:02

That's where I am right now.

2:04

And, uh, again, the topic of today's presentation

2:08

is MRI of focal liver lesions, and we will

2:13

focus on extracellular contrast agents.

2:16

So we all know that when we study liver lesions,

2:20

we can either use extracellular contrast agents

2:23

or hepatobiliary contrast agents.

2:25

Today, I would like to focus on extracellular contrast

2:29

agents, which are by far more widely used so far

2:36

in comparison to hepatobiliary contrast agents.

2:39

Hopefully, there will be the opportunity in the

2:41

future to discuss hepatobiliary contrast as well.

2:46

Okay.

2:46

So, um, when talking about liver lesions, I always

2:53

find it convenient to reason on what the, um,

2:59

origin of the liver lesions is and I'm trying to report on.

3:03

So, liver lesions can be divided based on the cell of origin.

3:08

So, in the liver, we can have lesions originating

3:13

from the hepatocytes, from the

3:15

cholangiocytes, or from mesenchymal cells.

3:19

So, let's start with the lesions

3:20

originating from the hepatocytes.

3:22

You see here they are listed here: focal nodular

3:26

hyperplasia, hepatocellular adenoma, and these are the two

3:31

that are more common in the non-cirrhotic liver.

3:34

We will get to that in a few minutes.

3:38

And then we have regenerative nodules,

3:39

dysplastic nodules, and hepatocellular carcinoma.

3:43

And these three are definitely

3:45

more common in the cirrhotic liver.

3:48

So, lesions originating from the hepatocytes.

3:53

Then, we have lesions originating from the mesenchymal

3:57

cells. By far, the most common is a hepatic hemangioma.

4:03

It can be either capillary or cavernous hemangioma.

4:07

And then we have less common lesions like

4:10

epithelioid hemangioendothelioma and angiosarcoma.

4:15

Again, originating from mesenchymal cells.

4:18

Uh, epitheloid angiomatosis a lesion that are, um,

4:23

that has, uh, um, uh, moderate potential oncologic potential.

4:29

Um, so patients with the epithelial angiomatosis can, can

4:33

live for many, many years, but with time, unfortunately,

4:37

this condition can, can lead to emphatic insufficiency.

4:42

And finally, we have cholangiocytes.

4:44

So, um, lesions originating from cholangiocytes.

4:48

So, hepatic cyst, of course, the most common.

4:52

And then, uh, biliary cystadenoma,

4:54

not very common, and cholangiocarcinoma.

4:57

So, these are the primary lesions of the liver,

5:02

then we can also have in the liver metastasis.

5:05

So, uh, any GI tumor can metastasize to the liver,

5:09

of course, uh, breast cancer can metastasize

5:12

to the liver, uh, lung cancer can metastasize

5:15

to the liver, uh, melanoma and so forth.

5:19

Now here, uh, is the spectrum of liver lesions that we can

5:23

encounter in the liver based on the cell of origin.

5:26

But now look at the, at the

5:28

brightness of, uh, of the writing.

5:31

In this, uh, in this slide you see that here I'm darkening.

5:36

Some of the lesions, some are, um, bright, some are

5:41

slightly darker.

5:42

Some are definitely darker.

5:44

And the darker they are, the less common they are.

5:48

So among them, mesenchymal cell lesions, epitheloid

5:52

angiomatosis, and angiosarcoma are very uncommon lesions.

5:58

Epitheloid angiomatosis or angiosarcoma are

5:01

lesions that we encounter maybe once a year,

5:04

or maybe once every two years in our practice.

6:08

And the same applies to, uh,

6:10

lesions originating from the, from cholangiocytes.

6:12

Um, biliary cystadenoma is very uncommon,

6:18

and cholangiocarcinoma is less

6:21

common in comparison to hepatic cyst.

6:23

Among the lesions originating from the

6:27

hepatocytes, I would say that adenoma is

6:30

definitely the least common among the ones

6:34

that are listed here.

6:36

Okay.

6:36

Now, what is also very important to remember before starting

6:41

to report your cases when you face a liver lesion is to

6:48

ask yourself, what type of patient am I reporting on?

6:52

Is this a patient with cirrhosis

6:55

or is this a non-cirrhotic patient?

6:57

And also, what is very important is also the age of

7:01

the patient because we know that some of these lesions

7:04

are more commonly found in young women, while some

7:09

other lesions are more commonly found in older men.

7:14

So, here, you see that, beside some of

7:18

these lesions, we see the shape of a liver.

7:22

This means a non-cirrhotic liver.

7:25

And so, as I was saying before, FNH or adenoma

7:30

among the lesions originating from the hepatocytes

7:33

are more common in the non-cirrhotic liver.

7:37

The lesions originating from the mesenchymal cells,

7:40

they are all more common in the non-cirrhotic liver.

7:43

As are metastases.

7:45

And so, the same applies for lesions originating from cholangiocytes.

7:54

However, some of these lesions,

8:02

left, can also be encountered in the cirrhotic liver.

8:06

You see focal nodular hyperplasia.

8:10

Very tiny number of cases can be encountered in cirrhosis.

8:15

Also, hemangioma is less common in

8:17

cirrhosis, but it can be encountered metastasis.

8:22

Maybe we see metastasis in the cirrhotic

8:25

liver two to three times per year.

8:28

And also, hepatic cyst.

8:31

They are less common in the cirrhotic liver.

8:36

As you can see, hepatocellular adenoma,

8:40

I did not put a cirrhotic liver image

8:43

because I've never seen a case in cirrhosis.

8:47

Simply, I've never seen a case.

8:49

Okay, what about the other lesions?

8:51

The other lesions, on the opposite, are

8:54

encountered more commonly in the cirrhotic liver.

8:59

So, regenerative nodule, dysplastic nodule, and

9:01

HCC, they are more common in the cirrhotic liver.

9:05

Cholangiocarcinoma is more common in the cirrhotic liver.

9:08

The cirrhotic liver puts these patients

9:11

at risk for cholangiocarcinoma.

9:16

However, also in this case, some of these lesions

9:20

can also be encountered in the non-cirrhotic liver.

9:23

Non-cirrhotic liver.

9:25

Let's take the example of hepatocellular carcinoma.

9:28

Hepatocellular carcinoma, in 85 percent of

9:32

cases, will be encountered in the cirrhotic liver.

9:36

However, there is a 15 percent of cases of

9:39

HCC that are found in the non-cirrhotic liver.

9:44

And these are typically much larger in comparison

9:49

to the ones that are found in the cirrhotic liver.

9:53

Cholangiocarcinoma, as I said before, the cirrhotic

9:56

liver puts these patients at risk for cholangiocarcinoma.

10:01

However, cholangiocarcinoma can also be

10:04

encountered in the non-cirrhotic liver.

10:09

Okay, so here we are, the first message.

10:13

The first message is that when we discuss liver

10:15

lesions before discussing their appearance on MRI,

10:20

we have to remember that their prevalence differs

10:25

among different lesions and is influenced by the

10:29

setting, which means cirrhotic versus non-cirrhotic.

10:34

And again, also by the age, let's

10:36

say focal nodular hyperplasia.

10:38

I've never seen it in patients, uh, above

10:42

60 years old, and the same applies for adenoma.

10:47

Okay.

10:49

So let's move on.

10:51

Now, when we discuss the MRI of focal liver

10:55

lesions, our goal is not only to

11:00

detect lesions, but also to characterize them.

11:05

So, do we need contrast agents to characterize lesions?

11:10

Well, in the very early days of MRI, uh, researchers,

11:14

uh, researchers thought that, uh, at some point we would

11:19

have, uh, MRI contrast agents, uh, would not be needed

11:24

any longer because the, the, the result, the contrast

11:28

resolution of the technique was so high that with the

11:32

other sequences, we would have had enough information.

11:36

And actually, that is partly true.

11:38

Because if you look at this

11:39

case, here you see six sequences.

11:42

You see in phase and out of phase, so dual sequences.

11:48

And here, already, we have one piece of information.

11:51

And the information is that there is signal loss

11:54

on out of phase in this lesion; the lesion is almost

11:59

invisible on in phase, and we see signal loss on out

12:03

of phase due to the presence of intracellular fat.

12:07

And this is already a very important piece of information

12:10

because it narrows our differential diagnosis only

12:15

to those lesions that can contain fat; and actually,

12:19

lesions that can contain fat are not actually so many.

12:23

All the hepatocellular lesions

12:25

can contain fat.

12:28

While the mesenchymal lesions or the cholangiocyte

12:32

lesions, so the ones originating from mesenchymal cells or

12:36

from cholangiocytes, they typically do not contain fat.

12:39

So you understand how much we can already

12:42

narrow our differential diagnosis due

12:45

to the, just with this single sequence.

12:49

Of course, there are other lesions

12:52

that can contain fat, but these are very less

12:55

frequent in comparison to hepatocellular lesions.

12:58

Let's say occasionally we can have fat in

13:01

idiopathic cysts, or occasionally we can have fat in

13:05

metastases; I would say specifically metastases

13:09

from liposarcoma, at least in my experience.

13:13

Okay.

13:14

And so this is how we, we start our protocol on MRI.

13:17

So in phase and out of phase.

13:19

Then, then we have the T2s.

13:22

And what message do we have here from the T2?

13:24

We see that the lesion is bright on T2.

13:29

So when we discuss the brightness on T2, we know that the

13:32

brightness can be very high, and usually this means

13:38

that the lesion is either a cyst or a hemangioma, although

13:44

uncommonly also some metastases can be very bright on T2.

13:50

Metastases from a mucinous primary carcinoma

13:54

or metastases from neuroendocrine tumors.

13:58

But apart from those, lesions are

14:02

more commonly moderately hyperintense on T2.

14:06

So less or the same intensity in comparison to the spleen.

14:12

And here you can see the spleen, and you

14:14

see that this lesion is, uh, less, um,

14:19

hyperintense in comparison to the spleen.

14:22

So since this lesion is not very bright, we can

14:25

exclude, uh, um, uh, a lesion containing fluid,

14:29

containing fluid, so we can exclude a cyst.

14:32

We can exclude reasonably a hemangioma.

14:34

So we, no, we are facing a solid lesion.

14:41

And then below you see that we have, uh, the

14:44

diffusion sequences, so B0, B150, and B600.

14:50

So you see that the lesion stays bright also

14:53

on a high B; uh, this lesion was dark on the ADC

14:58

map, and so we know that there is restricted diffusion.

15:04

And restricted diffusion means

15:06

that there is hypercellularity.

15:09

Be careful, restricted diffusion does not

15:12

necessarily mean that the lesion is malignant.

15:15

Focal nodular hyperplasia will show restricted diffusion.

15:18

Hepatocellular adenoma will show restricted diffusion.

15:22

But, uh, uh, and therefore the message is

15:28

that if we see a restricted

15:29

diffusion, there is hypercellularity.

15:33

We can get to the conclusion that the lesion is

15:35

malignant only by putting together the single pieces of

15:39

information coming from all the different sequences.

15:44

All right.

15:45

So, so far with all these sequences,

15:48

we certainly have several pieces of information.

15:51

However, we still need to inject contrast.

15:56

And so after acquiring these, uh, uh, sequences,

16:02

we typically move to the part of the MRI

16:05

examination where we inject the contrast.

16:07

And again, today we are focusing

16:10

on extracellular contrast agents.

16:13

So here we have the, uh, breath-hold 3D gradient

16:17

tackle with fat suppression technique sequence.

16:21

So here you see that this is a pre-contrast phase.

16:25

You see that there is fat suppression.

16:28

And then, uh, after we inject the hepatic arterial

16:32

phase, we acquire, after we inject the contrast,

16:35

sorry, we acquire the hepatic arterial phase,

16:40

typically 25 seconds after contrast injection.

16:43

And here you can see that we have

16:46

contrast; we already have contrast in the

16:48

portal vein, and that's how it should be.

16:51

So in a well-performed hepatic arterial

16:54

phase, it is a phase where you want to have

16:58

already contrast in the portal vein.

17:00

Okay.

17:02

We, you don't want to have contrast in the pancreatic phase, but

17:05

definitely you want to have contrast in the portal vein.

17:08

So after the pancreatic arterial phase, we typically

17:12

acquire the portal venous phase.

17:14

So here you see that the liver is brighter in comparison

17:17

to the pancreatic arterial phase because now the total

17:22

amount of contrast has arrived, uh, in the liver.

17:26

And so the liver is definitely brighter.

17:29

And then

17:30

we have the three minutes delayed phase,

17:35

the typical delayed phase, and we can acquire, if

17:40

we wish, uh, other sequences later based on our,

17:45

uh, on the need to acquire them based on

17:48

the type of lesions we are, uh, we are studying.

17:54

So in this case, you see that the

17:56

uh, ten minutes delayed phase was

18:00

now in this, uh, part of the examination that

18:04

post-contrast part of the examination, definitely

18:07

the arterial phase and the portal phase are the

18:10

sequences and the phases that define our lesions.

18:15

Because based on the lesion behavior on the

18:19

hepatic arterial phase and the portal venous

18:21

or three minutes delayed phase, this is how

18:25

we will characterize the lesions.

18:30

Okay.

18:30

So with these extracellular contrast agents, we can obtain

18:34

this multi-phasic approach, because you

18:38

see that we can acquire several phases after contrast

18:42

injection, and they give us information on vascularity.

18:46

So basically we can tell whether a lesion on

18:49

the hepatic arterial phase is hypervascular or not.

18:55

And also this type of contrast agent distributes

19:00

into first into the vessels and then into the interstitium.

19:05

The main difference with the hepatobiliary contrast

19:07

agent is that while the extracellular contrast

19:11

agents stay in the interstitium, the hepatobiliary

19:15

contrast agent, after they move into the interstitium,

19:21

they will be taken up by the hepatocytes.

19:24

And so the dynamics are different in

19:27

comparison to extracellular contrast agents.

19:30

Again, these are the agents that are more widely used.

19:35

And so, um, and, uh, and therefore it is

19:40

very important to know how to use them and

19:42

what type of information they can give us.

19:46

Okay, so after, after, uh, having talked about the origin

19:51

of liver lesions and the protocol of study on MRI, um,

19:57

and after having, uh, emphasized once again that the

20:02

multiphasic protocol is the cornerstone of liver imaging,

20:07

let me now move to the next slide that is the slide

20:11

that we will keep until the end of this presentation.

20:15

So here you see a sort of table or a grid, if you

20:19

wish, because we have columns and we have lines.

20:23

So let me write here in the first line, arterial and

20:30

venous, which stands for venous or portal venous.

20:34

And now we will see how different lesions will

20:38

behave based on their behavior again on the hepatic arterial

20:43

and portal venous phase.

20:46

So we can differentiate and characterize lesions based on

20:52

their behavior on hepatic arterial and portal venous phases.

20:57

Okay, so let's pretend that the first lesion we are

21:01

discussing is a lesion that does not make any changes,

21:06

does not show any changes on hepatic arterial phase.

21:11

And the same happens for the portal venous phase.

21:16

Let me show you an example.

21:19

Here we have a 49-year-old female

21:22

with HCV-related cirrhosis.

21:25

So in this CT, this is the pre-

21:28

contrast. Here is the pancreatic phase.

21:31

So I don't see anything abnormal.

21:34

Here is the portal venous phase.

21:37

And as we typically do in the cirrhotic liver, we

21:41

also acquire on CT, uh, a three minutes delayed phase.

21:45

And in the three minutes delayed phase,

21:47

what we notice is that there is this lace-

21:51

like pattern surrounding these nodules.

21:57

These entities, okay, so here, here is a lace-like pattern.

22:03

The same we see on MRI in the same patient.

22:07

You see that on pre-contrast, uh, uh, MRI,

22:10

uh, in this liver, there are several nodules.

22:15

The liver is divided into several smaller nodules.

22:18

On hepatic arterial phase, no enhancement is visible.

22:24

On portal venous phase, again, nothing is seen.

22:29

And therefore, these are regenerative or dysplastic nodules,

22:37

nodules that don't show an enhancement in the hepatic arterial

22:42

phase, don't show washout in the portal venous phase.

22:46

Therefore, in this, and we know they are there because

22:49

in, uh, on the three minutes delayed phase, we see that there is

22:53

this lace-like pattern of fibrosis surrounding the nodules.

22:59

So if we go back to our master slide, here we write

23:04

interpretation, and therefore we know that if there

23:09

are nodules, but these don't take contrast in the

23:14

hepatic arterial phase, and they don't show, you

23:16

know, washout in the portal venous phase, these

23:20

are either regenerative or dysplastic nodules.

23:24

Actually, regenerative nodules, they will

23:26

show this behavior 100 percent of the time.

23:29

We know that in some cases, high-grade

23:33

dysplastic nodules can be hypervascular, but

23:36

this typically occurs in 3 percent of the cases.

23:39

So, basically, they will not show an enhancement.

23:43

Now here we have smiling faces, and this

23:46

refers to the regenerative nodules because

23:49

regenerative nodules are benign entities.

23:51

They are not dysplastic.

23:53

However, dysplastic nodules, we have learned from our

23:59

pathologists that they can be divided into low-grade that

24:03

are considered benign and high-grade dysplastic nodules.

24:06

Now high-grade dysplastic nodules

24:11

are considered premalignant.

24:14

They can evolve into early HCC and then into HCC.

24:19

So that is why here we have a yellow

24:21

face rather than a green face.

24:25

Okay, so let's move on to the second line.

24:28

Let's now pretend that we have a lesion that does

24:31

not show any enhancement, but then on the venous

24:34

phase, we suddenly see that it becomes hypo-

24:40

vascular in comparison to the surrounding liver.

24:44

Let's see an example.

24:45

Again, we have a patient with cirrhosis, a man, 53 years old.

24:52

Here is the pre-contrast phase.

24:55

Honestly, I don't see much.

24:58

Here is the pancreatic phase.

25:00

You remember in the master slide, in the hepatic arterial

25:03

phase, there was a line, meaning that there was no enhancement.

25:07

And actually, I don't see enhancement in this image at all.

25:12

Then if I show you the portal venous phase, now I do see

25:18

a lesion that is hypo-intense in

25:22

comparison to the surrounding liver.

25:25

So this explains why we had a narrow

25:30

pointing south in the master slide.

25:34

And now my question to you is, in a cirrhotic

25:37

liver, what is the meaning of such a finding?

25:40

What could this be?

25:44

This is a hypovascular HCC.

25:48

So it would be easy if all HCC would show

25:52

up as an enhancing lesion with washout.

25:55

Unfortunately, the smaller the HCC is, the less

26:01

common it is that we will find a typical enhancement factor.

26:06

What we know is that, uh, when lesions

26:09

are smaller than three centimeters,

26:12

10 to 15 percent of HCC will be hypovascular.

26:18

Again, it means that they will not show enhancement in

26:21

the hepatic arterial phase, but they will be visible

26:25

as hypo-intense in comparison to the surrounding

26:29

liver on either portal venous or delayed phase.

26:34

So remember, this is very important.

26:38

10 to 15 percent of hepatocellular

26:41

carcinoma will be hypovascular.

26:45

Okay, now let's move from the cirrhotic

26:50

liver to the non-cirrhotic liver.

26:52

Here is another example of a lesion that is

26:56

almost invisible on the hepatic arterial phase.

26:59

Here we have a hepatic arterial phase,

27:01

and be careful, there is a lesion.

27:04

However, the lesion is not this one.

27:07

This is, of course, the ghost artifact from the aorta that

27:13

is seen here, but it's hard to see a lesion in this liver.

27:21

Only when I show you the portal venous phase,

27:25

the venous phase, you see that this black arrow

27:28

is pointing to a lesion that is now visible.

27:33

And this is actually a metastasis from colorectal carcinoma.

27:37

And, uh, we know that metastases can be

27:42

divided into hypervascular and hypovascular.

27:47

In this case, we are seeing a hypovascular

27:52

metastasis, as it typically happens from any

27:56

metastasis originating from the GI tract.

28:00

These metastases will not show an enhancement

28:02

typically on the hepatic arterial phase; they will

28:05

be much more visible on the portal

28:08

venous phase because the surrounding liver

28:11

enhances more in comparison to the lesion.

28:16

So, remember this tip: the majority

28:20

of metastases are hypovascular.

28:23

Occasionally, metastases can be hypervascular

28:26

from renal cell or neuroendocrine tumors,

28:30

but the majority of them will be hypovascular.

28:34

Okay, so we go back to the master slide.

28:36

So how do we interpret this finding?

28:40

No enhancement on the hepatic arterial

28:41

phase and hypointensity on the venous phase.

28:45

As we have just discussed, this can either be hepatocellular

28:49

carcinoma, those 10 to 15 percent of HCC that are hypovascular

28:54

and that may become hypervascular, and

28:59

then metastasis, as we have just seen in the case of

29:03

colorectal carcinoma metastasizing to the liver.

29:06

So here, after the green face and the yellow face, we have

29:11

a red face because these are definitely malignant lesions.

29:17

Okay, so these two categories of lesions are lesions

29:22

that do not show enhancement on the hepatic arterial phase and

29:26

are either invisible or hypo-intense on the venous phase.

29:33

So this is the category of hypovascular

29:37

lesions, and we've listed here a few.

29:41

Let's keep moving.

29:43

So let's now pretend that we have a lesion that enhances on

29:46

the hepatic arterial phase and then stays bright on the venous phase.

29:52

Here is a case, an example of a 49-year-old man.

29:57

So, here we have a pre-contrast; there

30:00

is a lesion that is clearly hyper-intense

30:03

in comparison to the surrounding liver.

30:06

And on the hepatic arterial phase, this lesion

30:08

is quite bright, so it clearly enhances

30:13

more in comparison to the surrounding liver.

30:17

And then, on the portal venous phase, the lesion stays

30:22

bright, so the enhancement is visible on the hepatic arterial

30:26

phase and keeps being visible on the portal venous phase.

30:32

And actually, a three minutes delayed phase

30:34

was also performed, and the lesion is still

30:37

visible on the three minutes delayed phase.

30:40

So how do we call this behavior?

30:42

How do we define this behavior, this lesion in this case?

30:47

This is what we call a persistent pattern.

30:50

So we have an enhancing lesion in the portal venous

30:53

phase, and then on later phases, there is still an

30:58

enhancement visible on the portal venous and delayed phases.

31:03

So this is what we call the persistent pattern.

31:11

And what is this lesion?

31:12

This lesion is a flesh-filled hemangioma.

31:15

So we know that hemangiomas can be either cavernous

31:19

or they can be flesh-filled or capillary.

31:23

This is a typical example of a capillary hemangioma

31:29

that enhances vividly on the hepatic arterial phase and

31:34

stays bright also on the portal venous and delayed phases.

31:42

Let me show you another example of a persistent pattern.

31:44

Here we have another liver.

31:47

There is more than one lesion in this liver.

31:50

Let's focus on this one right now.

31:53

So this lesion enhances on the hepatic arterial phase.

31:57

This is a non-cirrhotic liver.

32:00

This is a young woman, and on the portal venous phase, you

32:04

see that the lesion shows persistent enhancement

32:08

on the portal venous phase that

32:12

actually persists also on the three minutes delayed phase.

32:18

and is still slightly visible on the five minutes.

32:22

What is another type of lesion that stays bright

32:25

and shows persistent enhancement on the portal venous

32:28

and three minutes and also sometimes five minutes?

32:32

It's an inflammatory adenoma.

32:36

This type of adenoma has sinusoids

32:40

that are dilated within the lesion.

32:43

And so the contrast will stay longer there

32:47

and will justify this persistent enhancement.

32:52

So we go back to our master slide.

32:54

So we are discussing enhancing lesions that show

32:57

persistent enhancement on the hepatic arterial phase

33:00

that show persistent enhancement on the venous phase.

33:04

And we've seen examples of capillary

33:05

hemangiomas and inflammatory adenomas.

33:10

So the green is for the hemangioma.

33:13

The yellow is for the inflammatory adenoma, because

33:17

unfortunately, this lesion can sometimes cause

33:23

complications. In the case of inflammatory adenoma,

33:26

what might occur sometimes is bleeding, especially

33:31

if the lesion is larger than five centimeters.

33:35

Let's move to another row below.

33:38

So, again, we are discussing enhancing

33:41

lesions in the hepatic arterial phase.

33:43

However, now, this lesion becomes invisible on the venous phase.

33:50

How come?

33:51

Let's see an example.

33:52

Here you see that we have a lesion that is slightly lower

33:58

in intensity in comparison to the surrounding liver.

34:01

The lesion then shows strong and homogeneous

34:05

enhancement on the hepatic arterial phase and then is

34:09

invisible on the portal venous and three minutes delayed phase.

34:14

This is a non-cirrhotic liver, and I know that the

34:16

majority of you have already guessed what this is.

34:20

This is a typical example of a fade pattern of enhancement

34:26

that disappears on the portal venous and delayed phases.

34:30

You see, the lesion would be invisible.

34:32

So if we hadn't shown, if we hadn't seen the hepatic

34:35

arterial phase, and again, most of you I'm sure have guessed

34:40

that this is a typical example of focal nodular hyperplasia.

34:44

So the typical findings are strong and homogeneous

34:48

enhancement on the hepatic arterial phase with a fade pattern

34:53

on the portal venous and three minutes delayed phases.

34:58

So, whenever in a non-cirrhotic liver,

35:01

I find homogeneous enhancement in the

35:03

hepatic arterial phase in lesions larger

35:07

than three centimeters, I know this is benign.

35:12

The meaning of this enhancement pattern is benign.

35:15

And actually, this is a sign that was described almost

35:19

15 years ago now by the group of Claude Sirlin in San Diego.

35:24

Homogeneous enhancement larger than

35:25

three centimeters equals benign.

35:27

Benignity.

35:29

Here is another example.

35:31

You see that in this hepatic arterial

35:33

phase, we have an area of hypervascularity.

35:37

Here it is, that is quite homogeneous,

35:40

and on later phases, it disappears.

35:44

This is another example of a fade pattern.

35:48

This is now in cirrhosis, and this is a

35:51

typical example of a perfusion disorder.

35:54

So, areas of enhancement seen in the hepatic arterial

35:58

phase only that disappear in the portal venous phase.

36:03

And here is another example of a fade pattern in cirrhosis.

36:06

Now we have a lesion that enhances on the hepatic arterial

36:09

phase that fades toward isointensity on the portal venous

36:16

and delayed phases.

36:19

As I said before, FNH is practically

36:23

non-existent in the cirrhotic liver.

36:27

And so whenever we see an enhancing lesion

36:29

in a cirrhotic liver, we have to rule out HCC.

36:34

And actually, that's what it is in this case.

36:36

This was a hepatocellular carcinoma.

36:40

So earlier we saw an example of an HCC that was

36:44

hypovascular, so no enhancement in the hepatic arterial phase.

36:49

But hypointensity on later phases.

36:52

Now we are seeing the other type of atypical HCC.

36:59

So an HCC that enhances on the hepatic arterial phase but fades

37:05

toward isointensity on the portal venous and delayed phases.

37:12

So again, the smaller the HCC, the

37:16

less common it will be to have the typical

37:21

vascular pattern of enhancement and washout.

37:25

The smaller the HCC, the more common it will be that we

37:31

will see either enhancing HCC with no washout, as in this

37:37

case, or HCC that will not enhance on the hepatic arterial

37:41

phase and show hypointensity on the later phases, as in

37:45

the case we saw before that we defined as hypovascular HCC.

37:50

So we move again to the master slide.

37:54

Here we write "fade pattern," and we've seen examples of FNH.

37:59

Perfusion disorders.

38:01

And here you see the green phase, because

38:03

these are benign entities, but also HCC.

38:07

We've just seen an example of HCC showing enhancement

38:10

with no washout, but also metastases can have

38:14

this behavior with enhancement and no washout.

38:19

So in these cases, we have a red phase.

38:25

Let's move on.

38:26

Again, we are in the category of enhancing

38:30

lesions that may show washout in the venous phase.

38:36

Here is an example: pre-contrast T1, hepatic

38:39

arterial phase, portal venous, and delayed phase.

38:44

So this is a...

38:47

Again, an example of an enhancing

38:49

lesion that will show washout.

38:53

And this is a typical, a very typical

38:56

example of HCC showing this washout pattern.

39:01

You see the enhancement, you see

39:03

the washout, and you see the capsule.

39:05

So on this MRI, we have all the typical criteria

39:09

for HCC: enhancement, washout, and capsule.

39:16

So here we write "washout," and we know that this behavior is

39:21

typical for HCC, but also metastases can show this behavior.

39:32

So, in the first two lines, we had

39:35

discussed the hypovascular lesions.

39:39

That can be divided based on their behavior

39:42

on the venous phase, either invisible or hyper.

39:47

And here we have grouped together the hypervascular

39:54

lesions. You see, they enhance in all cases,

39:57

what differentiates them is their behavior on

40:02

the venous phase, because some of them show persistent

40:04

enhancement, some of them will show a

40:08

fade pattern, and some of them will show washout.

40:12

So, not only is the hepatic arterial phase very

40:16

important, but in order to characterize our lesions,

40:19

we rely a lot on their behavior on the portal venous phase.

40:25

To emphasize this point, let me show you these

40:29

two different patients: upper row and lower row.

40:32

In the upper row, we have a cirrhotic

40:37

patient with an enhancing lesion.

40:40

And in the lower row, we have a different

40:42

cirrhotic patient with an enhancing lesion.

40:44

What we know is that whenever we have

40:47

an enhancing lesion in cirrhosis,

40:50

HCC must be ruled out.

40:53

Now, this is a very small lesion, and the smaller the

40:57

lesion is, the less probable it is that it is an HCC.

41:01

However, how can we tell whether either of these is an HCC?

41:07

In the first case, the lesion shows a persistent enhancement

41:12

pattern of enhancement.

41:15

And we know that a persistent pattern

41:17

of enhancement equals hemangioma.

41:21

Hemangioma is not as common in the cirrhotic liver,

41:24

it's not as common in the cirrhotic liver as

41:27

in the non-cirrhotic liver, but occasionally we

41:30

can encounter hemangiomas in the cirrhotic liver.

41:33

And this is an example.

41:35

Look at the lower row.

41:36

Enhancing lesion, however, on the venous and

41:40

delayed phases, the lesion shows washout.

41:43

And so here we have the typical findings for HCC.

41:49

In a cirrhotic liver, a lesion that

41:50

shows enhancement and washout equals HCC.

41:54

So here we understand how important the venous

41:58

phase is in order to characterize those lesions

42:02

that show enhancement in the hepatic arterial phase.

42:07

Finally, in the last line, I want to briefly

42:12

discuss a different type of enhancement that

42:15

we call rim enhancement.

42:19

So here we have a rim pattern of enhancement

42:24

that will typically stay also in the later phases.

42:28

Let me show you this example.

42:30

Here we have a cirrhotic patient.

42:32

This is pre-contrast.

42:33

This is the hepatic arterial phase.

42:36

Now, just disregard this area.

42:39

This is just an area of perfusion disorder.

42:42

Please focus your attention on this observation here.

42:46

You see that there is a ring pattern of enhancement

42:49

that is also recognizable on the portal venous phase.

42:53

And actually, this is a cholangiocarcinoma occurring in

42:58

cirrhosis.

42:59

And the ring pattern of enhancement can be

43:01

encountered in cholangiocarcinoma both in

43:03

the cirrhotic and in the non-cirrhotic liver.

43:06

Let me show you another case.

43:08

This is a 45-year-old female with rectal carcinoma.

43:13

Now, what we said before is that metastases

43:17

originating from the GI tract are typically hypovascular,

43:23

and that's actually how I would define this lesion

43:26

because the majority of the lesion is hypovascular.

43:30

However, what is peculiar about this lesion is that we

43:34

see some sort of enhancement in the peripheral part of

43:40

the lesion, which is actually where the viable tumor is.

43:44

So the neoangiogenesis is able only to

43:48

vascularize the peripheral part of the lesion.

43:51

That's why we call this type of

43:53

enhancement a rim pattern of enhancement.

43:56

Now, if you look, however, on the portal venous,

44:00

three minutes and five minutes delayed phase, what is

44:04

interesting is that the part of the lesion that showed

44:09

enhancement on the hepatic arterial phase now shows

44:13

washout on the delayed phase.

44:17

And this is a finding that we define as peripheral washout

44:25

that can be observed either in metastases, typically

44:29

from colorectal carcinoma, or sometimes observed also

44:34

in breast carcinoma, but also in cholangiocarcinoma.

44:38

So, peripheral washout pattern.

44:43

Okay, so the ring pattern of enhancement

44:46

observed in the hepatic arterial and portal venous

44:49

phases that sometimes on later phases can also

44:54

convert itself into a peripheral washout pattern will

44:58

be observed in cholangiocarcinoma and in metastases.

45:03

And again, here you see the red phase.

45:06

Okay, so this leads me now toward

45:09

the conclusion of this presentation.

45:12

So we've seen different types of liver lesions.

45:16

We have divided them based on their cell of origin.

45:20

So some of them originate from hepatocytes, some others

45:24

from mesenchymal cells, some others from cholangiocytes,

45:28

and then we have the secondary lesions, the metastases.

45:31

And we have seen that some of them are more

45:36

common in the cirrhotic liver, some others are less common,

45:40

more common in the non-cirrhotic liver.

45:43

And finally, we have seen in this table with

45:49

different columns and different lines that based on

45:52

their behavior on hepatic arterial and venous phases, we

45:56

can divide lesions into hypovascular and hypervascular.

46:02

And the hypervascular lesions can be subdivided into those

46:07

lesions showing persistent enhancement, fade, and washout.

46:13

So let me conclude with this final slide.

46:18

So four tips, four points to bring back home.

46:21

Prevalence differs among different

46:23

lesions and is influenced by the setting.

46:26

Again, cirrhosis versus non-cirrhotic liver.

46:31

FNH is more common in the non-cirrhotic liver.

46:34

HCC is more common in the cirrhotic liver.

46:38

Number two, the multiphasic protocol

46:40

is the cornerstone of liver imaging.

46:43

So you should always acquire a pre-contrast

46:47

hepatic arterial, portal venous, three minutes,

46:50

and based on the type of lesions you are studying,

46:53

you might consider also acquiring later phases.

46:58

Number three, as I said before, lesions can

47:01

be divided based on their behavior on the hepatic

47:05

arterial phase into hypervascular and hypovascular.

47:10

Again, examples of hypervascular lesions

47:14

are FNH, inflammatory adenoma, capillary

47:18

hemangioma, and most hepatocellular carcinomas.

47:23

But we know that some hepatocellular carcinomas can also

47:27

be hypovascular, and also the majority of metastases

47:31

will be hypovascular on the hepatic arterial phase.

47:35

And finally, hypervascular lesions can have

47:38

different patterns of enhancement on the venous phase.

47:42

So, the venous phase is important in order to

47:47

subdivide these lesions into persistent

47:50

patterns, fade patterns, and washout patterns.

47:55

And this is the end of my presentation.

47:58

And now I will be happy to take any questions.

48:03

Let me see if there are any.

48:05

So let me, first of all, thank you for your attention

48:10

throughout this almost 15 minutes. I see that we have

48:15

had 160 participants steady throughout the presentation,

48:19

so thank you for participating and for staying with us.

48:23

Okay, so let me.

48:24

Let me read some of these questions.

48:28

So the first one, what will be the enhancement

48:30

pattern of high-grade dysplastic nodules?

48:33

Now, dysplastic nodules are typically small lesions.

48:37

They are very uncommonly larger

48:40

than one centimeter and a half.

48:43

So if they enhance, they will have

48:47

some sort of homogeneous enhancement.

48:49

The enhancement of these dysplastic nodules is never

48:52

as strong as that of capillary hemangiomas.

48:55

It's more a type of moderate enhancement, but since

48:58

the lesion is small, it will be quite homogeneous.

49:02

Here is another question.

49:04

Is there overlap?

49:06

And the question comes from Daya.

49:08

Thank you, Daya, for this question.

49:09

Is there overlap, uh, overlap between focal

49:13

nodular hyperplasia and fibrolamellar HCC?

49:17

How to differentiate?

49:18

Thank you, Daya, for this question because this gives me

49:21

the opportunity to discuss briefly fibrolamellar HCC, which

49:24

is something I hadn't done in my presentation.

49:28

Okay, differences.

49:30

First of all, FNH will show both of

49:34

them similarities and differences.

49:36

Similarities: both of them are

49:38

hypervascular on the hepatic arterial phase.

49:41

However, FNH will show a type of

49:44

enhancement that is strong and homogeneous.

49:47

Fibrolamellar HCC might show strong

49:50

enhancement, but it's never homogeneous.

49:52

It's more a heterogeneous pattern of enhancement.

49:57

Another similarity is that both of them have a central scar.

50:01

However, the scar has differences because in FNH, the scar

50:06

will typically be hyperintense on T2 while it will be hypointense on T2

50:13

in fibrolamellar HCC. If you do

50:18

CT, in two-thirds of the cases you will encounter

50:22

stellate calcifications that would be very,

50:26

very uncommon in focal nodular hyperplasia.

50:29

I've seen just one case of

50:31

calcifications in focal nodular hyperplasia.

50:35

What else should be remembered? In two-thirds of the

50:38

cases of fibrolamellar HCC, there will be lymph nodes.

50:41

FNH patients will never have lymph

50:43

nodes because FNH is a benign entity.

50:46

And what else?

50:46

Fibrolamellar HCC typically occurs in

50:51

people in the first decades of life.

50:53

So it's uncommon after 30, 35 years old.

50:58

FNH is also found in young individuals, but it can be

51:02

encountered also until 50 years old.

51:08

Most importantly, what you should

51:10

remember is that FNH is a benign lesion.

51:13

And does not degenerate into fibrolamellar HCC.

51:17

So FNH is not a pre-neoplastic lesion.

51:21

Whenever I see FNH in a CT or

51:24

MRI report, this is a benign lesion.

51:28

You should leave it alone.

51:29

No follow-up is needed.

51:33

Let's move on.

51:35

How to differentiate HCC and metastasis

51:37

in cirrhotic liver if both show washout?

51:40

Okay, actually, it is true that HCC will show washout

51:45

while not necessarily metastasis will show washout.

51:49

What I mean is that, typically, metastasis

51:54

will show a ring pattern of enhancement on

51:58

the hepatic arterial phase, while typical HCC

52:01

will not show a ring pattern of enhancement.

52:03

Now, there can be some HCC that might present

52:06

with a ring pattern of enhancement, and that is

52:08

why in the LI-RADS system, we call these LI-RADS M,

52:13

because these have the same possibility of being

52:17

either HCC, cholangiocarcinoma, or metastasis.

52:21

Metastasis.

52:22

So to summarize, metastasis in cirrhotic liver

52:25

will typically present with a ring pattern of enhancement.

52:30

HCC will typically present with a

52:33

non-ring pattern of enhancement.

52:35

HCC will typically show washout

52:39

for metastasis in cirrhotic liver.

52:41

Washout is less common in comparison

52:44

to metastasis in the non-cirrhotic liver.

52:46

What is really the key finding

52:49

is the ring pattern of enhancement.

52:53

Thank you, Patricia, for your kind comments.

52:57

Um, and also thank you to Mustafa for

53:01

his question on HCC and metastasis.

53:06

Let's move on.

53:09

Okay.

53:09

What will be the enhancement pattern in a

53:14

hepatic adenomas other than the inflammatory variant?

53:17

And this question comes from Dean P.

53:20

Senior.

53:22

Now, this is another important question.

53:25

Thank you.

53:26

Now let me tell you that until 2006 life was

53:30

easier because we just said hepatocellular adenomas.

53:34

From 2000 and on, with the articles published

53:38

by the groups of Valery Vilgrain and the groups

53:41

of Jessica Zucman Rossi in Bordeaux, we have

53:46

learned that different types of adenomas exist.

53:51

Now, to answer briefly, apart

53:54

from the inflammatory pattern that will show

53:59

persistent enhancement on the hepatic arterial

54:01

phase and persistent enhancement on later phases.

54:05

We can also have the HNF1 alpha adenomas

54:08

that typically contain a large amount of fat,

54:12

and therefore typically do not show a strong

54:16

enhancement pattern on the hepatic arterial phase.

54:18

They might be hypovascular on the hepatic arterial phase.

54:22

And then there is the beta-catenin variant that can

54:25

simulate HCC because they will show enhancement and washout.

54:29

And actually, this is the category of adenomas

54:31

that can degenerate more commonly into HCC.

54:36

Okay, next question from Mohammed Gasseb.

54:39

How to differentiate between a small

54:41

HCC with lack of washout and hemangioma?

54:44

And the answer is the following.

54:47

HCC will show a fade pattern.

54:50

So we have an enhancing lesion, but then it's

54:52

invisible on the portal venous and delayed phase,

54:55

while hemangioma will show a persistent pattern.

54:58

So typically we will see an enhancing lesion with a persistent

55:02

pattern of enhancement on the portal venous and delayed phase.

55:09

Okay.

55:10

Another question by Kausar.

55:13

Will radiologists, can radiologists, um, are radiologists

55:17

able to diagnose HCC based on the enhancement pattern?

55:22

Can enhancement pattern replace the tissue diagnosis?

55:26

And actually, the answer is yes.

55:29

What we know is that HCC is the only

55:33

tumor for which there are accepted guidelines.

55:38

Based on which, if we have a typical enhancement

55:41

pattern of enhancement and washout, this patient

55:45

can proceed to treatment, either RFA ablation,

55:49

microwave ablation, resection, or

55:53

transplantation without the need for a tissue diagnosis.

55:59

Okay, another question still from Kausar.

56:03

What is persistent enhancement?

56:06

Will it have the same Hounsfield unit or can it be

56:10

a little less, like on the RTL phase?

56:13

It's 150, it's 80.

56:16

Now, honestly, when you perform a CT or MRI,

56:19

you can either do quantitative imaging

56:22

so you measure with Hounsfield units or qualitative imaging.

56:26

What we mostly see is qualitative imaging.

56:28

So I define a persistent pattern of enhancement as any lesion that

56:32

in the portal venous or delayed phase shows, uh, brighter,

56:37

is brighter in comparison to the surrounding liver.

56:41

If I'm able to see that lesion as brighter

56:43

in comparison to the surrounding liver,

56:45

that is a persistent pattern of enhancement to me.

56:50

Okay, another question.

56:54

What multi-phase protocol can you recommend

56:57

for the characterization of these lesions?

57:01

Okay, now the multi-phasic protocol is different

57:04

based on whether you do CT or MRI.

57:08

On CT, we use the bolus tracking technique and we,

57:12

we consider, um, what we do is that, um, at 18

57:19

seconds, we wait for, uh, actually after we

57:26

reach the peak of enhancement in the arterial phase, we wait 18

57:29

seconds for the portal venous phase, and 40 seconds

57:33

more for the portal venous space. And basically on

57:37

MRI, the timing is quite similar, so you want to have

57:42

your hepatic arterial phase performed at approximately

57:45

25 to 30 seconds after contrast injection.

57:49

And you want to have your portal venous phase

57:52

35 seconds after the hepatic arterial phase.

57:57

Okay.

57:57

Another question by RT Gupta.

58:00

Do I use LI-RADS in my practice?

58:03

Yes, I do that.

58:04

I do report on LI-RADS in my cirrhotic patients.

58:08

Another question.

58:10

How to differentiate FNH

58:12

from HCC that doesn't show washout?

58:15

Again, FNH only in the non-cirrhotic

58:17

liver, HCC mostly in the cirrhotic liver.

58:20

So if we have a lesion in a non-cirrhotic liver

58:24

that shows strong and homogeneous

58:26

enhancement and a fade pattern, that's FNH and not HCC.

58:31

If you have an HCC in a non-cirrhotic liver,

58:33

it will be a heterogeneous pattern of enhancement.

58:38

Does FNH increase in size?

58:40

Yes, it does.

58:41

It can increase in size.

58:43

Benign lesions can either increase or decrease in size.

58:47

Um, okay.

58:50

We would have other questions, but I promised to

58:52

Olivia and to the excellent staff of MRI Online that

58:55

I would stop after one hour.

58:58

So it's seven o'clock

59:00

for your time, and therefore, again, it was my

59:04

great pleasure to spend this hour with you to

59:07

lecture on one of my favorite topics, and right of

59:10

focal evolution with extracellular conversation.

59:13

Again, thank you so much for participating.

59:16

And for contributing to this

59:19

presentation with your interesting questions.

59:23

Thank you so much for that great talk.

59:24

I learned a lot, and thanks to all for

59:26

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59:29

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Dr. Azita Khorsandi on thyroid

59:59

international recommendations online.

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You can register for that lecture at MRIonline.

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com and follow us on social media at The MRI Online

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for updates and reminders on upcoming noon conferences.

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Thanks again, and have a great day.