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Link will be provided in the chat box.

0:32

Today, we are joined by

0:34

Dr. Benjamin Spilseth, one of our esteemed faculty

0:36

members who has also contributed essential mastery

0:39

series courses in gastrointestinal imaging, which

0:42

are available to MRI online premium members.

0:45

Both of which will be linked in the chat

0:46

box along with membership information.

0:49

Dr. Benjamin Spilseth is an Associate Professor of Radiology,

0:53

a Division Director of Abdominal Radiology at the University

0:56

of Minnesota, and Abdominal Imaging Fellowship Director.

1:00

He has published over 25 articles and book chapters

1:02

on abdominal and pelvic MRI, as well as being

1:05

a frequent presenter of lectures and workshops

1:07

at national societies including RSNA and SIR.

1:11

We truly appreciate him for joining us today

1:13

and being a part of our MRI online faculty.

1:16

A reminder that there will be a Q&A session at the end

1:19

of the lecture for any questions you may have for Dr. Spilseth.

1:23

Please use the Q&A chat feature to submit your questions.

1:25

We will get to as many as we can before our time is up.

1:28

With that being said, we welcome you.

1:30

1:30

Dr. Spilseth, please take it from here.

1:33

So, I'm Ben Spilseth.

1:34

I'm here at the University of Minnesota, and I'm

1:37

going to talk to you about Crohn's disease today.

1:42

So, first of all, this is an introductory talk.

1:46

It's going to be 40 minutes, and it's not enough

1:48

to get all the details, all the different

1:50

iterations you can see with Crohn's disease.

1:53

Um, as she just mentioned, I do have a more

1:57

fully detailed, um, case series

2:02

in the mastery series at MRI online.

2:05

If you want to check that out for more details, if you like

2:08

what you hear, or, um, you want some more experience working

2:11

with that, of course, um, that is a paid subscription piece.

2:14

So you'd have to pay for that, but, um,

2:17

but, uh, we'll, we'll get you kind of the,

2:19

the nuts and bolts of it with this talk.

2:21

So here, we're going to talk about the role of imaging,

2:24

some imaging techniques that we use for Crohn's disease.

2:27

And we'll also, um, talk about the key findings

2:32

and how to track severity, and then we'll do a

2:34

little bit of an intro to some of the advanced

2:36

topics that we talked about in the other series.

2:39

So we will get started here.

2:43

Um, so, you know, that's the

2:45

outline of what we're going to do.

2:46

Hopefully when we're all done, um, you, you're

2:48

not going to want to put me in that outline.

2:51

But if you do, there'll be a firing squad

2:53

of questions at the end of the series.

2:55

So you can go ahead and fire away at that time, or as we go

2:59

along, go ahead and enter your questions in the chat box and

3:02

we'll get to them as we go or towards the end of the time.

3:06

So Crohn's disease is

3:08

an idiopathic autoimmune disorder, and it

3:11

can involve any portion of the GI tract.

3:13

Um, it's typically a segmental, and, you know, as

3:16

you know, many cases have skipped lesions, so it can

3:20

involve anywhere from really the mouth to the anus.

3:23

Um, and oftentimes involves multiple regions.

3:27

Um, it's notably mostly in the terminal

3:29

ileum as, as kind of the classic location,

3:32

but any part of the bowel can be involved.

3:35

So why do we use, uh, radiology to image Crohn's?

3:39

You know, it's a good question because the

3:41

disease is often suspected or established with

3:43

direct visualization, colonoscopy, endoscopy,

3:46

um, can see Crohn's and make the diagnosis.

3:48

They can get biopsies, and the pathologist can oftentimes

3:52

diagnose the disease, but, and colonoscopy does remain

3:56

kind of the mainstay, uh, for disease monitoring.

3:59

But there are some reasons why we like imaging.

4:02

First of all, um, really getting the accurate diagnosis.

4:04

Sometimes you do need imaging to do that.

4:07

The big one is UC versus Crohn's.

4:09

On colonoscopy, there can be some overlap in how

4:12

they look and sometimes the pathologist can't

4:14

even tell on biopsy which one it's going to be.

4:18

Even experienced pathologists can have trouble

4:21

depending on what they're seeing on their slides.

4:23

So CT or MRI imaging is often needed

4:26

to exclude the small bowel involvement.

4:28

And that way, um, if it is small bowel, it

4:33

shouldn't be UC, it should be Crohn's disease.

4:35

This is also important because surgeons really hate

4:38

removing colons, um, in patients with a diagnosis

4:41

of UC when they really had Crohn's disease all

4:44

along because the outcomes are really poor.

4:46

If they do that, and they didn't know what they were getting

4:48

into, small bowel disease can be seen in over half of Crohn's

4:53

patients with a negative terminal ileum on ileocolonoscopy.

4:56

So sometimes they will do the colon and they'll see some

5:01

disease, but they think that the TI is not involved.

5:03

So they don't think there's small bowel disease.

5:04

Well, the truth is, they don't

5:06

know because they haven't seen it.

5:08

And so, um, doing MRI or CT is a great

5:11

way to view the rest of the small bowel.

5:15

Here's another reason why we do imaging

5:17

and that's monitoring the disease.

5:18

So after the disease has been established,

5:21

the gastroenterologists do need to track the severity

5:23

of inflammation and to monitor their treatment.

5:25

The symptoms that patients have don't really correlate

5:28

very well with what the actual disease activity is.

5:31

Um, they have to, you know, do counting

5:33

of stools and vague abdominal symptoms.

5:35

It can be.

5:36

It can be hard to really suss together how bad

5:39

their underlying disease is in these patients.

5:43

Capsule endoscopy is complimentary, but,

5:45

but CT and MRI are really getting widespread

5:47

use for monitoring Crohn's disease.

5:51

So we're going to start with, um,

5:53

talking about MRI and Crohn's disease.

5:55

And really it's all about technique.

5:58

And then it has to start with the

5:59

technique of how you do your exams.

6:00

If you don't get good MRIs, you can't give good

6:03

reports, you can't help the patients or your clinicians.

6:06

So we're going to spend a good

6:07

amount of time on the technique.

6:11

Part one of the technique is really the small bowel distention.

6:14

So when you do imaging, you have to give

6:18

the patient something to distend the bowel.

6:21

That way you can see the wall much better.

6:23

You can see if there's narrowing or strictures.

6:26

And if you don't get good distention,

6:27

you won't be able to see that.

6:29

So our protocol is we use three bottles

6:32

of, um, hyperosmolar agents.

6:34

So, Brexanolone, Volumin, there's other,

6:36

there's other ones out there.

6:38

And we usually do that over about 60 minutes.

6:40

Um, some people do it, uh, quicker than that.

6:43

And the key is that these agents have things

6:45

like sorbitol, mannitol, sucralose, things that

6:48

actually suck fluid into the gut as it goes through

6:51

because they're, um, hyperosmolar.

6:54

And so if you just give a patient water, you'll get good

6:57

distention of the stomach and duodenum and probably some of

6:59

the proximal jejunum, but by the time it makes it to the ileum,

7:03

your distention is gone and it's,

7:05

and it's reabsorbed into the body.

7:07

This is, this will go all the way through the ileum into

7:09

the colon, and that's why we use these agents.

7:13

You can also give a glass of water right before

7:14

getting on the table, just to, um, distend that,

7:17

that more proximal bowel, that can be helpful.

7:21

To get your distention.

7:22

So after we get distention, we have

7:24

another problem we have to deal with.

7:25

And that's the fact that the bowel

7:27

is a muscle that moves around.

7:29

And so you do need to give some sort of peristaltic

7:31

agent. In the U.S., that's typically glucagon.

7:34

And we do that for MRI. CT is fast enough

7:37

that you don't necessarily need that.

7:39

So we don't administer it for that.

7:41

So, um, at the University of Minnesota, we

7:44

do a scout film, and then we give IV glucagon

7:47

in, um, two divided doses of 0.5 milligrams to spread it out a little more.

7:50

So we give it right, you know, as we start and

7:52

then we give it again, um, before we get contrast.

7:55

A lot of places will just do a single dose.

7:58

Um, there's other routes you can do.

8:00

IM glucagon.

8:04

You can do, um, sublingual glucagon, although

8:06

the results don't typically look as well, and

8:08

I think some literature says that that's not

8:10

as, not as good as the IV or IM, uh, options.

8:14

Another thing we do for peristalsis, we do

8:16

try to image our patients in prone imaging.

8:18

And so, um, when you do prone imaging, what

8:23

happens is your bowel wall, um, your bowel doesn't

8:27

move as much if you're laying on your stomach.

8:29

And additionally, um, you get your images in coronal

8:35

images in fewer slices because the diameters decrease.

8:41

And so we try to image patients

8:42

in prone if they can tolerate.

8:44

Now if they can't tolerate it, we don't want to do that.

8:46

Um, because if motion is an issue and if

8:51

they're uncomfortable and they can't tolerate

8:52

the scan, it doesn't do anybody any good.

8:54

So only in the patients that are able to lay

8:55

prone, we do try to do prone imaging when possible.

8:59

Here's an example of the problems with bowel peristalsis.

9:02

If you look at this image, you see a lot of blurriness.

9:05

You can see there's bowel in here, but you

9:07

can't really get a lot of details from that.

9:09

And that's because this patient didn't, uh, get

9:11

the glucagon, their bowel was moving too much.

9:14

Um, this is a contrast-enhanced sequence.

9:17

When we look at the steady-state precession,

9:19

which isn't as motion sensitive because it's so

9:21

fast, we can see there's actually a big diseased loop

9:24

of bowel right here in the middle of the abdomen

9:26

that was really hard to see on, on this exam.

9:28

So, um, if we had a better, um, we can get that

9:33

image, but we can't get all the other sequences.

9:34

We really like to get the T2s, the T1s, pre and

9:37

post contrast, um, if you have bowel motion.

9:43

All right, the third thing we're going to talk

9:44

about is the sequences and this is also key.

9:47

There's a lot of guidance on which sequences

9:50

to do and you can look up the protocols and

9:51

literature in a bunch of different areas.

9:54

I'll tell you how we do it, though.

9:55

We do T2-weighted sequences.

9:57

With and without fat saturation.

9:58

And then we do, um, a steady-state free precession,

10:02

whether you have FISP or Fiesta, depending on your scanner.

10:05

Diffusion-weighted imaging, I do think is important.

10:07

And we do that.

10:08

And then we do pre- and post-contrast.

10:10

And optionally, more and more places are

10:13

doing some delayed imaging to help diagnose

10:15

fibrosis, and we'll talk about that.

10:17

And then you can do cine images

10:18

as well before you get glucagon.

10:21

Those, that produces some really nice pretty pictures.

10:23

Um, the diagnostic importance is probably not that

10:26

much, but our gastroenterologists do really like that.

10:28

So we do, we do cine images here as well.

10:32

So to help you look at those sequences, I'm going

10:34

to quickly go through a case and show you what

10:36

the sequences look like and how we use them.

10:39

And so here, starting at the top, we do some T2 images,

10:44

we do a HASTE image on our Siemens scanner, which

10:48

is kind of a faster half Fourier transform sequence.

10:52

And the, and you want to get

10:53

feed on these enterography exams because even with

10:56

the glucagon, if your sequence is too

10:59

slow, you're still gonna get motion artifacts.

11:02

Um, what you'll see here is you can

11:03

really see the bowel well, pretty well.

11:05

You can see that there's fluid

11:07

distending the lumen of this bowel.

11:08

So they did a good job with their preparation.

11:11

And you can also get the sense that there's some, a

11:13

loop of bowel wall that a loop of bowel that's sticking

11:16

down here in the location of the terminal ileum.

11:18

Here's your ileum and here's your

11:21

cecum.

11:23

So we're going to take a closer look at this

11:25

area and then talk about the other sequences.

11:26

One thing you'll notice is that this area of the

11:28

wall does look a little brighter than the skeletal

11:31

muscle, so it looks like it may be edematous,

11:33

but we want to do some things to confirm that.

11:35

And the way we typically confirm edema and look at it

11:38

is use the other T2 sequence, the fat-saturated T2.

11:41

And when we look at this, you can again see that that

11:44

bowel wall is indeed brighter than the skeletal muscle.

11:48

And when you have that, you know there's,

11:49

there's true edema and that's a marker of

11:51

inflammation, um, typical of Crohn's disease.

11:55

Now this isn't a specific, uh, appearance.

11:59

It doesn't have to be Crohn's.

12:00

Other types of ileitis can cause this, but

12:02

Crohn's disease, um, when you see it in that

12:04

location, it should be at the top of your mind.

12:08

Um, we also do T2 weighted images in the

12:10

axial plane to give us another look at things.

12:13

So after we do T2, um, we, we do the true FISP, which

12:18

is a type of steady state free precession image.

12:21

And one of the real advantages of the true

12:22

FISP is that it's not motion sensitive.

12:24

So if the bowel is moving a bit, you're

12:27

still going to get good images here.

12:28

Another big advantage is that you can really see the

12:31

lumen really well, so you notice there's no artifacts

12:34

in the lumen of the bowel here, so if there was a polyp

12:36

or some sort of intraluminal defect, you're going to

12:39

see it here on your T2 sequences because it's moving.

12:42

You get flow voids, kind of like the carotid, because you

12:46

can't, uh, you don't image things after you excite them.

12:48

They actually move out of plane.

12:49

So you get these flow voids in your bowel.

12:51

That's normal.

12:52

Don't call these polyps.

12:53

This is just, um, because of the,

12:55

the way the sequence is obtained.

12:57

But on TruFISP, you don't get those.

12:58

So that's why we do that series.

13:00

Then, um, we do the pre and post contrast.

13:02

So this is our key sequence and

13:06

it's a little more motion sensitive.

13:08

Um, but when it turns out well, you

13:10

get a really good look at things.

13:11

We like to do several time frames.

13:13

So we do a pre-contrast and then we do post

13:15

contrast, and we can see right away this bowel loop

13:18

is enhancing more than the adjacent bowel loops.

13:21

So that's a marker that there's some sort of

13:23

disease there, and it's inflamed in this case.

13:26

This has early enhancement, as you can see on this earlier

13:28

time series, and so that's a marker of an acute inflammation.

13:32

And when you're trying to detect early enhancement, it's a

13:34

key to look at it in relation to adjacent bowel loops.

13:39

So this is ileum, so we want to

13:40

compare it to other loops of ileum.

13:42

And what we see is that this is clearly brighter,

13:44

in addition to being thicker than the other loops of

13:47

ileum, and that's clearly an indicator of disease.

13:50

You don't want to compare ileum to jejunum,

13:52

because jejunum always looks like this.

13:54

This is normal jejunum, and you can see it has

13:56

normal wall thickness and normal thickening, but

13:59

it does enhance a little more than the ileum.

14:01

Don't, don't be confused by that.

14:02

That's a normal finding.

14:04

Although I see it called a lot of times and people that

14:06

aren't familiar with, with MRI (Magnetic Resonance Imaging) as disease.

14:09

Uh, but this is, this is normal.

14:11

If you want to confirm that it's normal, sometimes

14:13

you can look at your T2 series and see just how

14:16

normal looking this is in terms of nice thin

14:19

walls with the normal valvulae kind of entities.

14:23

Okay.

14:24

That's the detection piece on post-contrast.

14:27

Um, we do the multiple phases, including

14:30

the delayed phase, which helps with fibrosis.

14:32

If you have more enhancement later, it suggests fibrosis,

14:36

and we'll talk more about that later in the talk.

14:38

And then we do an axial phase to get another look.

14:40

In this case, the axial phase is helpful because

14:42

it does look like it's irregular and there's some

14:44

mucosal abnormalities on this patient,

14:48

um, and some ulceration indicating more severe disease.

14:52

Last sequence we'll talk about is the diffusion series.

14:54

And for diffusion, what I really focus on

14:57

is that the highest B value of the diffusion images that you get.

15:00

And what you're looking for there is an

15:02

area of increased signal in the bowel.

15:06

And in this case, that just indicates disease.

15:09

It doesn't necessarily indicate whether it's

15:11

acute or chronic, um, but it does indicate disease

15:14

and it can be used for troubleshooting at times.

15:17

It's also good to find some adjacent lymph nodes,

15:19

which pop out as being very bright on the future.

15:23

Okay, so that is that.

15:26

Now we'll go back to the PowerPoint quick.

15:36

All right, so back to our slides, um, a couple more

15:39

examples of what Crohn's disease looks like on MRI.

15:42

So this is a separate patient with ileal Crohn's.

15:45

You'll see enhancement.

15:46

This time it's just the inner wall that's enhancing.

15:49

We don't want to call that mucosal enhancement necessarily

15:51

because oftentimes the mucosa is actually sloughed off.

15:55

Um, so it's not truly always a mucosal enhancement, but

15:58

it is enhancing and that is an indicator of disease.

16:02

Additionally, this is which indicates some bowel disease.

16:06

And then, um, it's also edematous as well.

16:11

Here's a more mild case.

16:12

And in this case, this is your terminal ileum here.

16:15

And what you'll see is the, um, the wall is a

16:19

little thick and then maybe a little edematous, but

16:21

it can be hard to differentiate that from just a

16:23

little bit more prominent, normal terminal ileum.

16:25

So you need your other sequences

16:27

in this, in this, uh, scenario.

16:29

Uh, when we look at our diffusion series here.

16:32

What we see is that that is bright.

16:33

So this is where I find diffusion probably the most

16:36

helpful is differentiating these mild cases of disease.

16:39

Is that really a disease segment of bowel

16:41

or is it just a contraction problem?

16:44

And in this case, because it's so much more

16:45

enhancing than adjacent bowel, I think we can be

16:48

very confident that this is abnormal terminal ileum.

16:51

Similarly, it does show some increased hyper,

16:54

hyper-enhancement on the post-contrast images.

16:57

And so this is indeed a disease segment of bowel.

17:01

Okay.

17:03

Jejunal Crohn's obviously can also occur.

17:06

This is a case with multifocal areas of skip

17:09

lesions, so here you can see some thickening here

17:11

and some enhancement, and then this part in the left

17:14

lower quadrant is also thickened and enhancing.

17:17

When we look at the axial series on the same patient

17:20

you can see this jejunum is very thick and enhancing,

17:23

and there's some edema on the fat-saturated

17:26

series as well, indicating acute disease.

17:32

So that's the basics of MRI.

17:34

We'll move to the basics of CT.

17:36

So for preparation on CT, it's not as complex.

17:39

It's the same oral prep as the MRI.

17:42

And we don't do all the series and we don't

17:44

have to mess with glucagon because it's so fast.

17:46

We just get a single late arterial or enteric

17:50

phase image, and that's because that's the

17:52

time when the bowel is enhancing the most.

17:54

So you want to do this a little earlier than your classic

17:57

portal venous phase we do for most abdominal imaging.

18:01

Uh, the findings in CT are very

18:03

similar and analogous to MRI.

18:04

You just don't have as much to look at.

18:06

You just have the single sequence, and what you're

18:08

looking for here is primarily enhancing wall, wall

18:11

thickening, and then inflammation surrounding the wall,

18:14

as well as the complications you may see with Crohn's.

18:17

Here again, this colon is diffusely involved.

18:19

It's too thick, it's enhancing, it's irregular, and

18:22

there's even some fluid around the colon indicating

18:25

some substantial inflammation of the bowel.

18:30

So now we've gotten through diagnosing, and now

18:32

we're going to talk about monitoring disease.

18:33

And the question is, you know, why do we need imaging to

18:36

monitor this if we can do symptoms and colonoscopy?

18:40

Well, we've talked a little bit about the problems

18:42

with symptoms, but also, um, there's another factor

18:46

to consider. For one thing, the decision to

18:49

change drugs depends a lot on disease activity, and

18:53

the drugs they use these days are very expensive.

18:56

The immunomodulator infliximab and rituximab, etc.

19:01

They can cost tens to hundreds

19:02

of thousands of dollars a year.

19:04

And so the cost of, you know, $1,500 MRI compared

19:09

to that makes it really cost-effective to get to

19:12

use it to get a really good diagnosis and understand

19:14

what's going on with the patient's disease to pick the

19:17

right drug or decide if they even need drugs at all.

19:21

Additionally, we want to monitor disease for the detection

19:24

of complications such as fistulae and abscesses, which

19:26

aren't always apparent clinically or may not be suspected.

19:30

And then for surgical planning, monitoring

19:33

disease, understanding the full extent

19:35

of disease activity is really critical.

19:38

So as we do disease monitoring, one of the

19:40

questions we want to answer is, is there

19:42

inflammation that's active here or fibrosis?

19:45

The reason is inflammation is

19:46

treated differently than fibrosis.

19:48

Inflammation can be treated with immunologics,

19:51

infliximab, etc., or steroids, whereas

19:54

fibrosis is typically treated first with diet.

19:56

So if you have strictures, adjusting your diet

20:00

may help you get through that, or surgery if that

20:03

is, um, unable to be managed with diet, and immuno

20:09

modulators don't have a role once you become fibrotic

20:12

because you're no longer actively causing disease.

20:16

It's more than the sequela of disease

20:18

that's already happened, and surgery is

20:20

really the best bet to finally cure that.

20:23

So how do we tell inflammation versus fibrosis?

20:26

It's a challenge.

20:27

And the truth is, it's almost always a mixture of

20:30

both inflammation and fibrosis in Crohn's disease.

20:33

But we can find the predominant component, and we

20:36

can see that the degree of inflammation goes up

20:38

or down over time as we monitor these patients.

20:41

So how do we do that?

20:43

Inflammation, first of all, has higher T2 signal.

20:47

Um, and as we talked about before, if the signal of

20:50

the bowel is greater than the skeletal muscle on T2

20:53

series, that's an indicator that there is inflammation.

20:56

Inflammation also has ulceration and

20:58

blurred margins, especially when it's

21:00

more severe, and that's highly specific.

21:03

In the fibrosis side, the signal is dependent

21:05

on the amount of acute component on T2 series.

21:09

And the ulceration and blurred margins are

21:10

also not predictive of the amount of fibrosis

21:13

because those are markers of acute inflammation.

21:16

We can also look at the enhancement.

21:17

So early enhancement that doesn't

21:19

increase indicates inflammation.

21:21

Whereas if you have these progressive

21:23

enhancements, that indicates fibrosis.

21:25

And this is where we kick in those seven-minute images.

21:27

That's why we do that.

21:29

If you see more enhancement at seven minutes,

21:31

you're gonna, um, you're gonna think fibrosis is

21:34

a major component of the disease you're seeing.

21:37

So there's a good paper.

21:38

This is kind of a busy slide, but there's a good

21:40

paper showing that what I just said, that if

21:43

you have over 25 percent of enhancement gain at

21:46

seven minutes, you're going to see, you're going

21:48

to see patients do have significant fibrosis.

21:51

And depending on the T2 signal and that

21:54

enhancement gain, you can actually place

21:56

patients in this kind of two-by-two chart

21:59

in terms of whether they have fibrosis or inflammation.

22:02

And as we look at that in a little more detail,

22:04

what you see is what the T2 signal that's

22:07

going to tell you your inflammation component.

22:09

So if you have normal T2 signal, then

22:12

you have low inflammation and you're

22:14

going to be up on this part of the chart.

22:16

Whereas if you have bright T2 signal, you're

22:17

going to have more inflammation, higher

22:19

inflammation, and that'll put you down here.

22:21

And the next step is to look at the enhancements.

22:23

So if you have normal enhancement, you're going to

22:26

have lower fibrosis and only inflammation or no fibro

22:31

or low inflammation, whereas if you have delayed

22:33

enhancement and you have fibrosis on top of inflammation

22:37

on the bottom or without inflammation on the top.

22:39

So using T2 signal enhancement, you can really

22:42

decide how much inflammation and fibrosis you have.

22:46

So let's do one example here.

22:48

And there's many more that we went through

22:49

in the, um, the other talk I've done for MRI

22:52

online, but here's a case of mixed disease.

22:55

So if we look at this case, first thing

22:57

we're going to do is look at our T2 series.

22:59

And what we see here is the wall is thick.

23:01

So there's a disease segment, but it's also

23:03

a little bit brighter than skeletal muscle.

23:05

So that indicates there's some inflammation

23:07

when we look at it on the fat images.

23:10

We need that's important because fat can also cause

23:13

this bright signal on the T2 series, and on the

23:15

fat-saturated series we see it remains brighter

23:18

than skeletal muscle, so that's true inflammation.

23:20

So there's inflammation in this loop

23:21

of bowel, but what about fibrosis?

23:24

For that, we look to our contrast.

23:26

We look at the early enhancement here, and we see

23:28

it's enhancing a little bit, but the enhancement

23:31

increases as we get to that seven-minute delayed series.

23:35

And with that increased enhancement,

23:37

um, that indicates some fibrosis.

23:40

Now in the literature, they measure

23:41

that enhancement in practicality.

23:43

If you just look at it and you

23:44

see that it's clearly enhancing,

23:46

substantially more on the delayed series,

23:49

then you can say that there's also a fibrotic.

23:53

Um, beyond acute, uh, beyond the type of

23:56

inflammation, there's a severity of inflammation.

23:59

And there's been a lot of research that's

24:00

gone into developing severity scores.

24:03

There's these, the MARIA score and

24:05

Nancy score and others out there.

24:07

Um, the MARIA score has been validated, but

24:09

it's probably too complex for clinical use.

24:13

That being said, I'm going to just talk briefly about it.

24:15

And the MARIA calculation is very complicated.

24:18

They do a lot of noise adjustments and they

24:20

do a multi-factor weighted calculation.

24:24

And nobody in clinical practice really does this, but we can

24:28

get some key components from what the research has shown

24:31

about the MARIA score in terms of how severe inflammation

24:34

is, and this is how I use it: I look for the factors in

24:38

the MARIA score that were important, and I talk about those

24:41

in my reports, and I can relay that to my gastroenterologist.

24:44

So for one thing, if there's edema

24:45

or not, that tells you whether there's

24:47

severe, the severity of inflammation.

24:50

And this is just a plus-minus.

24:51

Is there, is there, is there not edema? More edema?

24:54

If there is edema, then that's indicated

24:56

there's some disease, at least.

24:58

Um, next thing I look at is ulceration.

25:00

So in this case, you see this

25:02

ulcerated component right here.

25:05

There's an irregularity in the wall.

25:07

Sometimes you'll see it on the T2 series.

25:09

Sometimes it'll be on the delayed series.

25:14

Or the contrast series, et cetera.

25:17

But whatever you see it best, if you see an

25:18

irregularity in the wall, you can call that ulceration.

25:21

And that indicates pretty severe

25:23

disease, severe inflammation.

25:25

That's the most, um, the most telling

25:28

factor of severe inflammatory disease.

25:32

The MARIA score also includes

25:33

wall thickness, which is helpful.

25:35

So if you're, you know, getting to five, six, um,

25:38

millimeters, you've got a really thickened wall.

25:40

Um, those are more severe disease cases.

25:43

And then you can, the early enhancement intensity

25:46

is also, um, is also a marker of inflammation.

25:50

And so if you have a lot of early enhancement,

25:54

that indicates more inflammation, and in the

25:57

MARIA score you measure that with our lives, etc.

26:00

And you use the brightest area, and in practice, you just

26:03

look at it and say if it's really bright and enhancing

26:06

in portions, it's probably more inflammation than if it wasn't.

26:10

And the last thing is the length. So MARIA doesn't directly

26:13

look at length, but we've shown independently

26:16

that length is a significant factor in

26:18

the degree of severity of Crohn's disease.

26:21

And so I try to report out the length of segments involved

26:24

to indicate severity and to monitor, but also to help the

26:28

gastroenterologist understand where the disease is in case

26:30

they can see it or in case surgery is needed to fix it.

26:35

Um, so that's severity.

26:36

Next, we're going to talk about the complications.

26:38

So, complicated disease is managed differently, so we want

26:42

to find things like fistulae, sinus tracts, and strictures.

26:45

And those can be hard to see or think about clinically,

26:48

but on imaging, we often are very helpful to the

26:51

clinicians in treating these patients that have them.

26:56

Uh, they can be found with CT or MRI,

26:59

and I'll talk a little bit about that.

27:02

So to understand these complications, you have to understand

27:05

that Crohn's disease is a transmural inflammatory disease.

27:09

And, um, because the whole bowel wall can get diseased,

27:12

then you can have strictures and fistulas and, and,

27:16

and problems from that so-called penetrating disease.

27:19

If you've broken through that bowel wall, they call

27:21

it penetrating disease, and now you're in a different

27:23

classification and a more severe type of Crohn's disease.

27:29

So there's, um, there's a kind of a

27:32

progression that Crohn's patients go through,

27:34

and I'm going to talk quickly about that.

27:36

So first of all, they can get strictures

27:38

because of the transmural inflammation.

27:40

It starts out as inflammation, and then over time it gets

27:45

either fibrotic or inflamed and narrows the lumen.

27:49

And once you've narrowed the lumen, eventually,

27:52

something's got to happen, and one of the most

27:54

common things is proximal dilation.

27:57

So as we're reading cases, when we see this narrow lumen

28:00

and proximal dilation, we can call that a stricture.

28:03

Be confident and slam dunk, say, you know, there's

28:05

a stricture here, especially on MRI where we

28:08

have multiple time points showing that narrowing.

28:11

If all we have is the narrowing and we don't have

28:13

the proximal dilation, we can't be as confident.

28:15

There's a, there's clearly a stricture because

28:17

it functionally may still be fine.

28:19

Um, and so this, we may have to hedge a little bit and say

28:22

that there's a possible stricture or something of that sort.

28:26

Once you've got, so here's an

28:27

example of an inflammatory stricture.

28:29

You can see, um, long segment. In this case, it could be

28:32

long or short, but this one's a longer segment, very

28:35

narrow lumen, and then proximal you've got some dilation.

28:38

You can see probably better here the degree that there is

28:40

clearly dilation proximal to that segment, and so this is

28:44

clearly a stricture, and that should be managed as such.

28:49

From strictures, you can develop fistulas, and it has to

28:52

do with not just the transmural inflammation but also

28:55

the fact that approximately that stricture that we get

28:58

pressure build-up, and that has to be released somewhere.

29:01

Ideally, it would go through the stricture, but sometimes

29:03

it goes through the weakened wall, and you get

29:07

fistulas or sinus tracts that develop or abscesses.

29:11

And so, this can be seen in the setting

29:13

of the proximal dilation or not.

29:15

Oftentimes, if you've developed the fistula, you no

29:17

longer have that proximal dilation because the, um,

29:21

the contents of the bowel have gone through,

29:25

they just haven't gone where you want them to.

29:28

So fistulas have a very characteristic appearance on Crohn's

29:31

patients, and that's because they're chronic, they're

29:34

chronic processes, and they often have a lot of scarring

29:37

and architectural distortion, and they basically stop

29:40

sucking all the bowel or other organs in the region towards it.

29:44

And so they have this kind of asterisk shape.

29:46

And if you see here, you can see this is a number of

29:50

segments of bowel that have been sucked together, and

29:52

centrally there's a little bit of anitis, and they're

29:54

all kind of tethered with this asterisk-shaped fistula.

29:57

This is a T2 series; you can also

29:59

see it on the post-contrast series.

30:02

Post-contrast here, T2, and they all kind of have this

30:04

nice little asterisk look to them, which is, I think,

30:07

very helpful in finding these fistulas, which often do

30:10

get mixed, I've noticed in private practice, um,

30:13

but people who just aren't used to seeing them.

30:18

So, um, finding strictures and fistulas brings

30:21

us to surgery, and, um, there are a couple

30:24

reasons why you might do surgery for Crohn's.

30:26

One is for the failure of medical management.

30:28

So, if there's no active inflammation to treat, but

30:31

there's fibrosis and the patient's still having symptoms,

30:33

sometimes surgery may be the only answer.

30:36

Or if the active inflammation is just no longer responding

30:39

to the medication, they've thrown the kitchen sink at it.

30:41

You can't get it better.

30:42

Sometimes they'll try to do surgery,

30:44

but there's also, um, if you have severe

30:47

stricturing or fistulae, those are other reasons

30:50

why the surgeon may need to be getting involved.

30:53

So when the surgeon does get involved, they often, the most

30:55

common thing is to do a hemicolectomy, taking the portion

30:58

of the right colon terminal ileum and then creating a new

31:02

terminal ileum or neo-terminal ileum with the terminal

31:05

ileum now connecting to the ascending colon somewhere.

31:10

And after we do that, we still end up

31:13

getting imaging to look for recurrence from

31:15

time to time because symptoms can recur.

31:17

It's a chronic condition that can relapse after surgery.

31:21

When they do have recurrence, it can occur anywhere, but

31:23

most commonly the anastomosis is seen, or if it's a patient

31:27

with an ostomy, that's another common site of recurrence.

31:31

It can be difficult to distinguish a mild post

31:34

operative inflammation, which isn't necessarily Crohn's

31:36

disease, from a true recurrence, and we have to look

31:39

at the severity to really make that distinction.

31:41

So here's an example of a recurrence.

31:43

This patient had a right hemicolectomy.

31:46

Here's the ascending colon, and here's the new terminal

31:50

ileum, and what you can see is that neo-terminal

31:52

ileum is a bit thickened, connecting up to there.

31:55

It's a bit enhancing.

31:56

And the degree of thickening and enhancing is,

31:59

is more than we'd expect postoperatively.

32:02

And so we would call that, uh, uh, some recurrent Crohn's

32:04

at that site, which can be verified on colonoscopy.

32:09

A couple more things before we're done here.

32:11

Um, one is to talk about the classic

32:13

question of is it Crohn's or is it UC?

32:16

So, um, there's some things that we've all learned in

32:18

medical school about this, and we'll go through that as

32:21

well as some other things that we can see on imaging.

32:23

So Crohn's does have the skip lesions, so it's not

32:25

confluent, whereas ulcerative colitis typically

32:28

classically starts at the anus and goes up

32:31

from there confluent. It may involve

32:35

portions of the colon or the entire

32:36

colon, and maybe the terminal ileum.

32:40

Crohn's can go from mouth to anus, whereas UC

32:43

is typically isolated to the colon, as we said.

32:46

Crohn's is transmural, which is why you get

32:48

fistulas and abscesses, whereas UC doesn't.

32:51

So, uh, you shouldn't expect to see the fistula and

32:54

abscess complications of UC in a typical patient.

32:58

Because it doesn't involve the whole wall,

32:59

it just involves more of the mucosal surface.

33:02

And that's why we see that.

33:05

Uh, also important to know that they both do

33:08

predispose to adenocarcinoma, so keep that in

33:10

your mind if you see masses forming or adenopathy

33:13

that's out of proportion to the inflammation.

33:16

And they both do have extraintestinal

33:17

manifestations, which we'll talk about next.

33:20

So Crohn's, especially colonic Crohn's,

33:23

and UC both have extraintestinal problems.

33:26

So, um, you can have musculoskeletal issues,

33:29

typically called, you know, seronegative spondyloarthropathy

33:32

that can involve the spine, can involve the SI

33:35

joints with an asymmetric inflammatory process.

33:38

And we see that in our MRN geography.

33:40

And so if you see over-enhancement of those

33:43

SI joints, don't forget that these patients

33:45

are at risk for that spondyloarthropathy and

33:48

we need to let the clinicians know about that.

33:51

PSC, primary sclerosing cholangitis, is another one.

33:55

It's typically seen with UC but can

33:56

also be seen in Crohn's disease.

33:58

And then along with that comes cholangiocarcinoma.

34:01

You can get stones and portal

34:03

vein thrombosis is another thing.

34:05

And especially in the acute stage,

34:07

keep your eye on that portal vein.

34:09

Make sure that you're looking at it to see

34:11

if there's thrombus because that can happen.

34:14

The skin findings are something we don't need

34:17

to worry about as radiologists, but can happen

34:19

and is important to know about, as well as some

34:21

ocular findings with episcleritis and scleritis.

34:25

PSC warrants a little bit more talk.

34:27

Um, so most PSC patients do have IBD.

34:31

So 75 percent of them have UC, 5 to 10 percent have Crohn's.

34:37

About 80, um, 15 to 20 percent that don't have IBD.

34:42

But that being said, PSC is uncommon in IBD patients.

34:45

So you can read a hundred, um, a hundred Crohn's patients,

34:49

and you'd only expect to see two patients that actually

34:51

have PSC. Nevertheless, we do want to look at it.

34:55

Cause that's a, that's still relative

34:57

to the population, a high rate of PSC.

34:59

So make sure you're looking in the liver,

35:01

looking for those peripheral areas of dilated

35:04

ducts or enhancement of the biliary tree.

35:07

If you see that, those could be early markers

35:09

of PSC, and that's very important for everyone

35:11

to know about before it gets too advanced.

35:15

So, uh, CT or MRI, um, what,

35:19

what can both detect on Crohn's?

35:21

Why would you choose one or the other?

35:23

Well, first of all, they both can detect inflammation.

35:25

They both are pretty good for fistulas and abscesses.

35:29

So I would be confident using both of them.

35:31

Strictures, you can see it on both, but I would

35:34

say MRI, because you get the multiple time points,

35:36

does have an advantage for evaluation of strictures

35:39

if that's what you know you're trying to solve.

35:42

But there's still reasons to choose

35:43

CT, so why would you choose that?

35:45

Well, it's much faster, it's available for emergencies,

35:48

whereas MRI can take a lot longer and it requires

35:51

a detailed protocol, and it's not available everywhere.

35:55

CT is more straightforward than MRI, and it's obviously

35:58

less expensive than MRI, although MRI, as I said

36:02

before, is cost-effective relative to no imaging.

36:07

Spatial resolution is probably a little

36:08

better on CT, but it's adequate on MRI.

36:11

And then you can have some error artifacts that can

36:13

cause problems on MRI that aren't an issue with CT.

36:17

What about MRI?

36:17

Why would you choose MRI?

36:19

Well, one big thing is there's no radiation, right?

36:22

Um, CT is high radiation, and that's especially

36:24

important for young Crohn's disease patients who may get

36:27

imaged, you know, half a dozen times a year for years.

36:30

Um, if you're getting radiation with each

36:32

one of those, that can affect you long term.

36:34

And so I really would like to see

36:37

MRI being used in those patients.

36:39

It gives you multiple time points on MRI,

36:41

which can be especially helpful for strictures.

36:45

You get really good soft tissue contrast, and you

36:48

can get more information from the T2 series,

36:51

the diffusion series, et cetera, which can help you

36:53

differentiate that acute and chronic inflammation.

36:56

So here's a nice case showing the

36:58

advantage of the multiple phases.

36:59

Any of you who've read CT have seen this before

37:02

when you have basically an intussusception

37:04

in the small bowel in the upper abdomen.

37:06

Sometimes it can be pretty, um, pretty significant

37:09

and you may need to talk about it in your report.

37:13

Well, in this case, you see a loop of bowel that's

37:16

intussuscepted into another loop of small bowel.

37:18

And you can see it on the post-contrast image

37:20

as well as this fat-saturated T2 series.

37:23

However, when we look at our regular T2

37:26

series done at a different time, it's not there.

37:29

And that indicates it's clearly a transient phenomenon.

37:32

It's of no clinical significance and probably

37:34

doesn't even need to be included in our report.

37:39

What about barium?

37:39

Barium used to be the mainstay of looking at Crohn's

37:42

disease, and small bowel follow-through can be helpful,

37:46

especially nowadays, if you're looking to characterize

37:50

or visualize fistulas, it can be used for that.

37:52

It's a dynamic imaging technique, so like MRI, but even

37:57

better, it can help you understand what's going on

38:01

with strictures in real time.

38:02

How severe are they and how functional are they?

38:04

Are they really restricting the flow of luminal materials?

38:09

Um, the problems are that it's just insensitive

38:11

for inflammation, especially mild inflammation,

38:14

and it's not as, as you, um, used currently.

38:18

So here's an example.

38:19

This is the same patient with a CT and a small

38:22

bowel follow-through. In the small bowel follow-through,

38:23

you can see there's a diseased segment of bowel here.

38:25

You can even see there's maybe a little

38:27

bit of erosion into the wall,

38:30

but you can't really tell how severe it is.

38:32

Whereas with CT, you get a lot more information,

38:34

and with MRI, you get even more still.

38:37

And so it's really gone to the wayside for the

38:40

most part now that MR enterography has taken hold.

38:44

So my recommendations on imaging are to

38:46

use CT or MRI for initial evaluation.

38:49

Either one, it really depends more

38:50

on the urgency and the setting.

38:52

If you're in the ER, and you're

38:54

questioning Crohn's, uh, I think CT is

38:56

totally reasonable, especially the first time.

38:59

However, when you're following it up, MRI

39:02

is typically recommended, especially for the younger

39:04

patients because of the radiation issues, but also

39:06

because you get a lot more information out of it.

39:09

If you're looking for strictures, start with MRI.

39:11

And consider barium if you need it.

39:13

And then for perianal disease, which is a whole

39:16

nother topic, MRI is really excellent for that.

39:19

And we actually have a whole nother course on perianal

39:21

disease, which we're not going to get into today, but it's

39:23

available, um, on the series on MRI online.

39:28

And then don't forget about barium

39:29

for troubleshooting from time to time.

39:31

It does come in handy.

39:33

So that's the basic stuff.

39:35

Um, we're not going to get too much into some of the

39:37

advanced topics we talk about in the full series.

39:40

Um, but in the advanced topics, we're talking more about,

39:43

you know, really using the up-to-date nomenclature.

39:46

Um, this is a great paper out of gastroenterology in

39:49

2018 from Dave Bruning at the Mayo Clinic, who's a

39:52

gastroenterologist along with a bunch of excellent

39:55

radiologists at the Society of Abdominal Radiology.

39:58

And, um, in this paper, they talk about

40:03

the types of patterns of enhancement and what the

40:05

indications or what the implications of that are

40:08

and how to identify those, as well as, you know,

40:11

the importance of wall thickening and what it means.

40:13

And, you know, we talked a bit about edema and

40:17

strictures, but it gives a little more detail

40:19

on how to handle, how to phrase things when you

40:22

have with or without upstream dilation, etc.

40:25

And then, um, characterization of the different

40:28

types of fistulas and what those things mean.

40:32

Um, so we get into that more in the other talk.

40:35

Additionally, we talked more about the Crohn's reporting.

40:37

So, you know, you want to include all the relevant

40:40

factors we talked about today, as well as ideally

40:43

some of the nomenclature that's in that other paper.

40:46

And this is best done if you can set up a

40:49

template that includes all the information,

40:51

and they do include one in that paper.

40:53

Everyone.

40:53

Which we walked through a little bit with some modifications

40:56

in that, in that other series, um, in which I, I try to

40:59

use that, that way of thinking when I dictate my cases.

41:04

So in conclusion, imaging is critical for

41:06

diagnosing and monitoring Crohn's disease.

41:09

CT is fast and accurate, but MRI has its

41:12

role and can give you more information.

41:15

And recognizing disease is the first step.

41:18

Monitoring is important, and detailed reports are key to

41:21

really help your gastroenterologist with monitoring disease.

41:26

So thanks for your attention, and we

41:27

will go to some questions at this point.

41:30

Great, thank you so much for sharing your

41:32

lecture with us today and for contributing your

41:34

Mastery Series courses that give radiologists a

41:36

shoulder-to-shoulder view of your reading skills.

41:38

At this time, we will open the floor

41:40

for any questions from our audience.

41:42

So we do have two in the Q&A, and then we have one

41:45

in the chat, so we'll begin with the one in the chat

41:47

just so we can get it out of the way.

41:50

So they were wondering if there are any hints to distinguish

41:53

early tumors, such as lymphoma or, oh, I don't know,

41:58

carcinoma versus severe inflammation on chronic disease.

42:01

Should we suggest potential malignancy in cases with high

42:03

degree of thickness and no changes despite treatment?

42:06

Yeah.

42:06

So, um, that can be a challenge.

42:09

Um, and the, um, the best thing is to

42:13

really understand what's happened over time.

42:15

And so oftentimes, ideally, you'll have those patients

42:18

that have been monitored over time, and if you get a one

42:21

shot, it can be a challenge, but if you've seen them over

42:23

time, um, you get a better sense, and then you correspond

42:27

with your, your, um, gastroenterologist and see what,

42:30

you know, what are they seeing, what have they seen,

42:32

because these patients have had colonoscopy or endoscopy.

42:36

And, um, if, so if it's in the colon or if it's in the

42:39

terminal ileum, they can typically look at it, um, and if

42:41

you're worried about it, you can, you can suggest that.

42:44

The real challenge is the, the mid small bowel stuff,

42:47

which is harder to get to, and you don't want to

42:49

go digging in there unless you absolutely have to.

42:53

So some things you can look for,

42:54

first of all, is the adenopathy.

42:56

You know, metastatic lymph nodes

42:58

have a different appearance.

42:59

They can be necrotic, they can look

43:00

irregular, they can be kind of ugly.

43:02

Uh, you do have reactive adenopathy

43:04

typically with Crohn's disease.

43:05

But when it starts to get really large or

43:07

really ugly looking, that's when I start to

43:10

talk about adenocarcinoma.

43:12

Um, the more nodular types of enhancement or, you

43:15

know, nodular, um, projections out of the wall,

43:18

uh, or into the lumen, those types of things can,

43:21

can be, um, more concerning for adenocarcinoma.

43:25

Uh, diffuse wall thickening.

43:27

I typically don't start thinking about it because you can

43:30

have really severe wall thickening with Crohn's disease.

43:33

And so, um, you need something more

43:35

than just wall thickening, um, to, to

43:38

to make that diagnosis.

43:39

Maybe if the wall thickening has gotten

43:41

worse over time, um, that sort of thing.

43:44

That's when you may think about it, despite it, like

43:47

they're on immunologics and most of it's improving,

43:49

but some area of wall thickening is getting worse.

43:51

That's a time you might think of it.

43:53

Um, lymphoma is a bit different, you know, for

43:56

lymphoma, I think it's a little easier to make

44:00

that differential, and the things you're looking for

44:02

there are more like the classic aneurysmal dilation.

44:06

So, if you have a really thick wall, but the

44:08

lumen isn't narrowed, then I'm starting to think

44:10

about small bowel lymphoma or large bowel lymphoma.

44:13

Often, usually, you'll have the kind of bulky

44:17

adenopathy as well. You know, true isolated bowel

44:20

lymphoma is pretty rare, and it's typically more

44:24

of that non-aneurysmal or aneurysmal dilation look.

44:27

And so, I find that helpful to make that

44:29

differentiation, but it can be a challenge for sure.

44:32

Okay.

44:32

We have another one.

44:33

Um, how to differentiate between edema and wall thickness?

44:38

So, they are really two different things.

44:39

Um, edema, you're looking at the, um,

44:44

for edema, you're looking at the signal.

44:47

So, edema is, how bright is it?

44:49

And in a case where you have

44:52

edema, what you're going to

44:55

do is compare it to the skeletal muscle.

44:57

And I'm just trying to go back

44:59

and find our edema slides here.

45:01

But, um,

45:04

here, you can see that this wall

45:06

is brighter than the muscle here.

45:10

And so, it's either fat or edema.

45:12

And so, when we look at our fat-saturated

45:14

series, if it's dark, then that means it's fat.

45:17

If it's bright, that means it's edema.

45:19

And so, that's how we make that distinction.

45:22

For wall thickness, we're just measuring the wall, and if

45:25

it's more than two or three millimeters, it's thickened.

45:27

And that doesn't necessarily indicate

45:30

an acute or chronic disease, but

45:33

it does indicate a diseased segment of bowel.

45:37

All right.

45:38

Uh, what's the best imaging feature to

45:40

define active disease?

45:43

Well, if you see ulceration, that's the best indicator.

45:47

Or if you see haziness

45:50

in the fat outside the bowel wall.

45:53

Sometimes, it looks blurry, especially

45:55

on your post-contrast images.

45:57

If you see one of those

45:59

two things, you can be very confident.

46:01

There's pretty extensive active disease.

46:03

Um, beyond that, you're looking for edema, and that

46:08

may indicate milder disease, but it does

46:11

suggest there's active disease if you have edema.

46:15

The enhancement of the wall itself is not as reliable

46:18

for indicating the activity of the inflammation.

46:22

So I try not to look at that as much as

46:24

those other factors that I just mentioned.

46:27

Thank you.

46:28

Why, in fibrosis, is the enhancement progressive?

46:32

So, throughout the body, when you have

46:34

scarring, you get progressive enhancement.

46:37

If you think about cholangiocarcinoma,

46:40

that's known to be more of a scarring-type malignancy.

46:43

And what you'll see is delayed enhancement

46:45

with cholangiocarcinoma.

46:48

It's the same with a desmoid-type tumor.

46:49

They enhance more later.

46:52

And it has to do with the fact that it's

46:54

not a hypervascular tumor or a hypervascular

46:57

process with a lot of edema and inflammation.

46:59

Instead, the contrast accumulates

47:02

over time in the areas of scar tissue.

47:05

And so, that's why we see it in Crohn's

47:07

disease, just like we see it elsewhere in the

47:09

body, as a delayed enhancement for fibrosis.

47:15

Thank you.

47:15

We have another one in the chat.

47:16

How do you approach enhancing bowel wall that

47:18

is not thickened and only mildly distended?

47:22

So, if you don't have a

47:26

diagnosis, there are two different situations.

47:28

One is if you know they have Crohn's, and the other

47:29

is if you're seeing it and don't know the cause.

47:32

It's an unknown case, basically,

47:34

and you're not sure what it is.

47:35

If that's the case and you just have

47:37

enhancement, it's very nonspecific.

47:40

It could be Crohn's, or any sort of

47:42

ileitis or inflammatory process, or infectious process.

47:46

But if you see it enhancing more

47:50

than adjacent bowel loops, then it is abnormal.

47:53

You need to call it some sort of

47:56

ileitis or colitis, but it's mild.

48:00

And the differential is much broader for that.

48:02

And so, you're not going to be able

48:05

to tell exactly what's going on necessarily.

48:07

You can just point to the fact that

48:08

there's some inflammation there.

48:11

All right, thank you so much.

48:13

We're going to leave it open for a few more seconds

48:15

before we give our final remarks.

48:20

We have another one.

48:21

It's, uh, Crohn's versus TB in the cecum and terminal ileum (TI).

48:26

Would you look at—oh goodness, I don't want to—

48:31

Yeah, so, um, Crohn's versus TB.

48:34

I mean, in Minnesota, that's not a very common differential.

48:38

And if you're in other parts of the

48:39

world, that certainly is more common.

48:42

So honestly, if you're in the cecum, the advantage

48:49

is that the next step is going to be a colonoscopy

48:53

if it's an unknown disease process. In the U.S.,

48:56

you're going to go to colonoscopy as the next step.

48:59

And they'll be able to tell a lot if it's Crohn's or,

49:03

or, um, TB, or some sort of malignancy in the cecum.

49:08

And so, really, our job in that scenario is really

49:11

just to get them to colonoscopy as the next step.

49:14

All right, thank you so much.

49:16

We're going to leave it open for

49:17

a few additional seconds.

49:20

There are some thank-yous and some praises

49:22

about your presentation in the chat.

49:25

Okay, we're going to leave it open for additional seconds.

49:30

All right, perfect.

49:34

So, as we bring our time together

49:35

to a close, I want to thank

49:36

Dr. Spilseth for this lecture, and thanks to all

49:38

for participating in our noon conference.

49:40

A reminder that you can access the recording of

49:42

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49:44

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49:48

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49:50

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49:58

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50:00

at the URL in the chat box.

50:02

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50:04

Thursday, February 10th at 12 p.m.

50:05

Eastern time for a lecture on renal transplants

50:07

Doppler ultrasound evaluation.

50:10

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50:12

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50:15

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50:18

Thanks again and have a lovely day.

50:20

Thanks.