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Hello, and welcome to Noon Conference hosted by Modality.

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Noon Conference connects the global radiology community through free, live

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educational webinars that are accessible for all and is an opportunity to learn

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alongside top radiologists from around the world.

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Today, we are honored to welcome Dr.

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Roni Kamelath for a lecture entitled "CTE and MRE in the Evaluation of

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Crohn's Disease." Dr. Kamelath is an abdominal imager at

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the University of California Irvine Medical Center.

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His professional interests include oncological imaging and as well as resident and

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medical student education. At the end of the lecture, please

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join him in a Q&A session where he will address questions you may have on today's

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topic. Please remember to use that Q&A feature to submit your questions so

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we can get to as many as we can before time is up.

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

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Kamelath, please take it from here.

0:52

Hi, everyone. Thank you, Ashley, for that introduction.

0:55

So I'm going to talk about CT and MR enterography in the evaluation of Crohn's

0:59

disease today.

1:01

And,

1:02

yeah. So let's get started.

1:05

So I wanted to make this talk kind of clinically oriented.

1:08

I feel like as a radiologist, sometimes I'm in my reading room, and I get sort of

1:11

stuck in a silo where I'm

1:14

a little too focused or intensely focused on the imaging alone

1:17

without really thinking about how the imaging fits into the larger

1:21

enterprise of IBD management. So I kind of wanted to take a step

1:25

back and look at how CTE and MRE fit into the larger picture of IBD

1:29

management, and then by doing that, we can create reports which are relevant and

1:33

actionable for our gastroenterology and surgical colleagues.

1:37

So the outline of this talk,

1:39

I'm going to talk a little bit about the diagnostic and therapeutic approach to

1:42

Crohn's disease.

1:44

I'm going to talk about CTE and MRE protocols.

1:48

And then I'm going to talk a little bit about the IBD multidisciplinary conference

1:51

we have at our institution and talk about common clinical scenarios that

1:55

arise at that conference.

1:57

So I wanted to start with a little bit on the medical management of Crohn's

2:01

disease, and this isn't new information.

2:03

This is actually a slide I've had for at least a decade, but I think it's really

2:06

useful to help us understand how imaging kind of fits

2:10

into the larger picture. So kind of the old school model for

2:13

treatment of Crohn's disease, we can call the step-up model, where

2:17

you base your treatment decisions primarily on the patient's symptoms and

2:21

clinical status. So you start sort of conservatively with the small

2:25

guns, in this case salicylates, right, like sulfasalazine and

2:29

mesalamine. And based on the symptoms, you ramp up the treatment based

2:32

on how the patient is doing and how they're doing symptomatically.

2:37

And the problem with this approach is,

2:39

this significantly under treats or is associated with

2:43

delays in treatment in a significant number of patients who

2:47

have signs of active inflammation and markers of a

2:51

more morbid, complex disease course.

2:55

So now for the last few decades, gastroenterologists have had these

2:59

newer biologic therapies, which actually enable us to

3:03

change the disease course and not only alleviate symptoms.

3:06

And if you live in the United States, you've probably seen commercials for agents

3:10

like these, like

3:12

Stelara, for example, and Skyrizi, which are these biologic

3:16

agents, which can really help change the course of disease for patients with

3:20

signs of a morbid disease course. And in these patients, early

3:24

intervention is key. But this model sort of

3:27

relies on the identification of objective markers for high-risk

3:31

disease. Right. Not just symptoms, but these objective markers.

3:35

And that's when CTE and MRE and imaging in general becomes so important

3:39

for these patients.

3:41

So what are the objective markers for inflammation?

3:46

You can do blood tests like CRP or fecal calprotectin.

3:49

You can rely on endoscopic findings, and then, of course, imaging findings,

3:53

which are relevant to us, right? CT enterography, MR

3:56

enterography. And we can identify signs of active disease,

4:01

like ulceration. We can identify markers that really predict a

4:05

more complicated disease course, like penetrating or stricturing disease

4:08

or extra intestinal complications.

4:11

So the key point here is that the top-down model is enabled by the

4:15

introduction of these biologic therapies, which we've had for the last few

4:19

decades. And this model really relies upon the identification

4:23

of objective markers of inflammation.

4:25

Failure to identify these objective markers and just rely on

4:29

symptoms will result in a treatment delay or undertreatment of a significant number

4:33

of patients.

4:35

Okay. So here's an example. We had a patient at our institution who was a

4:38

69-year-old guy. He had a longstanding history of ileal Crohn's,

4:42

treated with just the salicylic acids, and he really had minimal

4:46

symptoms. He had a CT for some other reason,

4:51

and this is what it showed. I'll let it scroll for a second.

4:54

But you can see right away that he's got a lot of disease.

4:58

I'll let it scroll through, but you see this really abnormal bowel loop here with

5:01

these areas of narrowing and upstream dilation.

5:05

There's fecalization of contents in the bowel.

5:09

So this patient has multifocal strictures.

5:13

He has this fibrofatty proliferation in his central mesentery.

5:17

Here you can see there's a fistula between this ileal loop and the terminal ileum.

5:20

There's a stricture here. The terminal ileum looks abnormal.

5:23

There's a lot of circumferential wall thickening and submucosal fat deposition in

5:27

that TI.Okay.

5:31

So if you didn't catch the video, here are some still images from that same CT, and

5:34

here again, you can see circumferential wall thickening in this TI, an

5:38

enteroenteric fistula here with tethering of multiple bowel loops, and you'll

5:42

notice that there's stricturing disease with upstream dilation

5:46

of the bowel loops with fecalization of the contents. Right?

5:50

So both stricturing, fistulizing disease, very extensive disease.

5:53

We did an MRI, and it shows much of the same thing.

5:57

Again, we see this abnormal ileal loop here with these areas of

6:00

stricturing. There are skip lesions with upstream dilation and

6:04

fibrofatty proliferation. On these T2 weighted images from the MR

6:08

enterography shows some of the same sort of findings.

6:12

Here, you can see the hallmark findings of active inflammation.

6:15

Here's his terminal ileum on the top left image.

6:17

You can see that there's this increased T2 signal in the

6:21

wall, which indicates active inflammation, as well as

6:25

these more sort of low T2 signal areas,

6:29

which probably represents fibrosis within an enteroenteric fistula.

6:33

The patient also had diffusion restriction in the affected loops,

6:38

and diffusion restriction is a good marker of active inflammation,

6:42

not necessarily specific to Crohn's, but in this case, in a patient with

6:46

multiple other findings of Crohn's, it's very helpful. Okay.

6:50

So clinically, the patient had minimal symptoms.

6:52

He'd been treated a long time with just salicylates alone.

6:56

And again, this is a patient where the newer treatment model becomes

7:00

relevant, right? This is a patient who would qualify for biologic therapy.

7:04

The surgeon, when he saw the patient, was sort of surprised at how bad the

7:08

imaging looked when compared to the patient's symptoms.

7:11

He said the clinical history is surprising juxtaposed to the imaging.

7:15

The patient was offered surgery, bowel resection, but he elected

7:18

medical therapy with vedolizumab.

7:21

So that was a patient who was on long-term salicylate therapy, relatively

7:25

asymptomatic, but the imaging identified complicated disease

7:28

behavior, which wasn't clinically obvious.

7:31

Ongoing inflammation didn't correlate well with the patient's symptoms.

7:34

We did offer him surgery, but vedolizumab was started instead.

7:39

Okay. So let me talk about CTE and MRE.

7:42

And I want to start with a question just to understand my audience.

7:45

How many CTE or MRE studies do you interpret per month, would you say?

7:49

Just ballpark.

7:51

I'll give you a second to answer that.

7:59

Okay, so the majority of you said you interpret between zero and five

8:03

CTE or MREs a month. Some of you said five to 10.

8:07

The minority of you interpret 10 to 15 or greater than 15.

8:11

So very good.

8:15

So CTE and MRE, as you guys know, are sort of our

8:18

go-to imaging studies for the evaluation of Crohn's.

8:21

We use it for initial staging. We use it to help

8:25

us make decisions on when to start treatment and what sort of treatment to

8:29

start. We use it to look for complications, and

8:33

increasingly, we're using it to monitor response to therapy.

8:37

We have literature that shows that CTE and MRE does change

8:41

treatment plans, that

8:44

CTE and MRE makes findings that aren't necessarily clinically

8:48

suspected, particularly occult inflammation, fistulas, abscesses,

8:52

and strictures we can see easily on CTE and MRE.

8:56

Here are some papers which sort of bring home that point.

8:59

This was a study published back in 2012 where they looked

9:03

prospectively at 273 patients with Crohn's disease

9:06

undergoing an indicated CT enterography.

9:10

And in this study, CTE altered management plans in about 51% of

9:14

patients.

9:18

In some of the patients, in about 36% of the patients, the CTE helped

9:21

exclude Crohn's disease,

9:24

and in 24% of patients, the imaging

9:27

prompted medication changes. Here's another study.

9:30

This was published back in 2007, where a radiologist and a

9:34

gastroenterologist looked retrospectively at both the clinical data and then

9:38

the imaging data, and it turns out that CTE findings don't

9:42

correlate well with the clinical picture. Right?

9:45

There were lots of patients who had

9:49

strictures that the clinicians didn't suspect, and a number of

9:53

patients as well for whom there was a suspected stricture clinically,

9:57

but that didn't bear out on the CT enterography.

9:59

So CTE and MRE are very powerful at

10:03

finding things that may not be apparent on clinical assessment

10:07

alone.

10:08

So I'm going to talk a little bit about protocol considerations.

10:11

As you know, CTE have the benefits of being fast,

10:15

having a high spatial resolution, and being relatively insensitive to motion.

10:19

MRE does not require ionizing radiation, has better

10:23

soft tissue contrast, and one sort of unrecognized maybe

10:27

advantage is that it takes a long time, an MRE to do, and the sequences

10:31

are obtained at different time points, so you can sort of look at the bowel

10:34

dynamically to see

10:37

it at different time points.

10:40

CTE and MRE are probably equivalent in detecting small bowel

10:44

inflammation. CTE may be better at detecting mesenteric findings

10:48

of inflammation, while MRE may better identify

10:51

fibrosis. So if you're considering which exam

10:55

to do on your patient, consider CTE on a patient who's kind of acutely

10:59

sick, who may be septic and may require urgent intervention,

11:03

and also an older patient for whom radiation

11:07

exposure may not be as much of a concern.

11:10

Also consider CTE if this is the patient's first exam or if you're

11:14

trying to rule in any other disease process other than Crohn's disease,

11:18

if the patient has contraindications to MRI, and of course, every

11:21

imaging decision sort of depends on how the local expertise is at

11:25

your institution. Consider MRE if the patient has had a prior

11:29

CTE, particularly in young patients who may be more radiation sensitive,

11:33

and patients who are not quite as acutely ill, patients who are stable may be

11:36

better candidates for CT enterography.

11:39

Also, obviously, if patients are pregnant

11:41

or have an iodine allergy, MRE may be the way to

11:44

go.So at our institution,

11:48

we start with neutral oral contrast, right?

11:50

That's 20 to 30 Hounsfield units on CT enterography.

11:54

And at our institution, University of California, Irvine, we use Briza,

11:58

which is a solution of sorbitol and mannitol that's commercially available.

12:02

In my prior institution, we used Volumen, which is a very

12:06

low-density barium solution. But in any case, we keep the patient

12:10

NPO for about four to six hours, and we have the patient ingest

12:13

between one and one and a half liters of neutral contrast material

12:17

over 30 or 60 minutes. For CTEs, we

12:20

begin imaging about 45 to 70 minutes after

12:23

ingestion.

12:26

So it's a single-phase study with IV contrast

12:30

acquired in either the enteric phase, so 40 to 50 seconds, or the portal

12:34

venous phase.

12:36

Some institutions include coronal MIP images to evaluate the mesenteric

12:40

veins, which can be very helpful in identifying chronic mesenteric vein

12:44

thrombosis. The MRA protocol, we start similarly with

12:48

between a liter and a liter and a half of oral contrast, and many

12:51

institutions

12:53

divide that up so the patient ingests 200 to 500 milliliters immediately

12:57

prior to scanning to help better distend the stomach and proximal small bowel.

13:01

We use a paralytic agent. In the US, that's usually Glucagon,

13:05

which we give before diffusion-weighted and T1-weighted

13:09

post-contrast imaging.

13:12

So these are sort of the core

13:14

sequences for

13:16

any MR enterography examination.

13:18

So we start with axial and coronal T2-weighted fast spin echo images with and

13:22

without fat suppression. So that's single-shot fast spin echo images and

13:26

steady-state free procession images.

13:29

And the advantage of fat suppression is that it helps us better

13:33

identify bowel wall and mesenteric edema,

13:36

perienteric edema, and the detection of intramural fat is a little

13:40

easier on fat-suppressed images.

13:43

We also do post-contrast images, so axial and coronal

13:46

T1-weighted gradient echo images with fat suppression,

13:50

multiple dynamic post-contrast phases, usually in the coronal plane.

13:56

DWI should be performed if possible.

13:58

As I mentioned earlier,

14:00

increased DWI above background in a bowel loop is a

14:04

nonspecific finding of active enteritis.

14:08

In this setting of other findings of Crohn's disease, it can be very

14:12

helpful

14:14

to help lead your diagnostic confidence.

14:17

Every MR enterography

14:19

should include images which include the entire anal canal because a

14:22

significant percentage of Crohn's patients present with perianal disease,

14:26

often occult.

14:29

Okay. So that takes me to my second question.

14:33

At your institution, are IBD patients discussed in a

14:36

multidisciplinary conference?

14:43

Okay, so 36% of you said yes, IBD patients are discussed in a

14:47

multidisciplinary conference. And I'm surprised that it's

14:51

that much. That kind of warms my heart because I think these are really

14:55

helpful for patient management.

14:58

So at our institution,

15:01

we do meet monthly for an IBD multidisciplinary conference,

15:05

and the reason for that, the rationale for that, are that surgeons and

15:08

gastroenterologists have more and more tools at their disposal.

15:12

Treatment for Crohn's disease is truly individualized now, and

15:16

patients really benefit from a multidisciplinary discussion of their care.

15:20

I'm sort of sensitive to the fact that this requires a

15:23

significant

15:25

time commitment from the surgeons, gastroenterologists, and radiologists, but I

15:29

really do think that the patients do benefit from this

15:32

discussion.

15:35

So for the rest of the talk, I'm going to talk about our IBD conference and

15:38

particularly common clinical scenarios that arise in

15:42

conference, common questions that the radiologists are asked at the conference,

15:47

and how we deal with them.

15:49

Okay. So question number one, is there active inflammation?

15:53

This is probably the most common and broadest question that we get asked.

15:58

So that brings me to my next question, and this one has multiple

16:02

correct answers, so please select all correct answers.

16:05

What imaging findings,

16:08

on MRI mostly, correlate with active inflammation?

16:13

So the choices are bowel wall thickening,

16:16

low T2 signal in the bowel wall, bowel wall enhancement, diffusion

16:19

restriction, mesenteric lymphadenopathy, and a mesenteric comb sign.

16:28

Okay, very good. So

16:32

good job. Bowel wall thickening, yes, definitely.

16:35

70% of you got that right. Low T2 signal in the bowel wall is actually

16:39

not a finding of active inflammation.

16:40

You actually want to see high T2 signal in the bowel wall.

16:44

Bowel wall enhancement, that's correct.

16:46

So hyper enhancement of the bowel wall relative to the other adjacent bowel

16:50

loops is a sign of active inflammation. Diffusion restriction as well.

16:54

Mesenteric lymphadenopathy can be seen with both active and chronic

16:57

disease, but it tends to be more

17:00

florid with active disease. And then the mesenteric comb sign or

17:03

vasorectal engorgement is a

17:06

helpful sign, which correlates well with active inflammation. So very good.

17:11

Here are some

17:12

cases of patients with active Crohn's disease.

17:14

So this is a patient with active terminal ileitis related to Crohn's

17:18

disease, and you can see the terminal ileum.

17:21

So the bowel wall should be less than three millimeters thick in an

17:25

adequately distended small bowel.

17:27

So we consider anything greater than three millimeters to be bowel wall thickening.

17:32

Three to five millimeters is considered mild, five to 10 millimeters is considered

17:35

moderate, and greater than 10 millimeters is considered severe.

17:39

So the degree of bowel wall thickening correlates well with the degree of active

17:42

inflammation.

17:44

And this patient also has some other findingsAssociated with active

17:47

inflammation, right? You see this high T2 signal in the bowel wall.

17:51

You see these prominent mesenteric lymph

17:54

nodes, and maybe you see some proliferation of the mesenteric fat of this ileal

17:58

mesentery. You can see this terminal ileal loop is kind of separated from the other

18:03

ileal loops.

18:05

Here are some other findings of active inflammation in the same patient.

18:08

So you can see persistent small bowel wall thickening in the terminal ileum with

18:12

hyper enhancement. And then you can see, again, diffusion restriction, which is a

18:16

helpful adjunct marker of active inflammation.

18:20

Here's a patient with a CT enterography, and here you can see this

18:24

bilaminar enhancement, moderate bowel wall thickening, and you can see this

18:28

is a nice example of the mesenteric comb sign, right?

18:31

Someone thought this looked like a comb, where you have

18:36

engorgement of the vasa recta, which looked like the teeth of a comb.

18:39

So this is a very helpful finding for active inflammation.

18:44

So that brings me to the next question. We saw a case of bilaminar enhancement.

18:47

So what bowel wall enhancement pattern is most specific for

18:51

Crohn's enteritis? And this has one single-choice correct answer.

19:01

Okay, I might have misled you.

19:04

So, the majority of you said bilaminar mural enhancement.

19:07

Actually, the most specific bowel enhancement pattern is asymmetric

19:11

enhancement, and that's the most specific for Crohn's disease.

19:14

The other choices, bilaminar enhancement, trilaminar enhancement, and then

19:18

homogenous symmetric mural enhancement, are definitely

19:21

findings that you can see with active Crohn's, but are also less specific.

19:25

You can see them with other forms of enteritis.

19:29

Here's an example of this asymmetric enhancement that I was talking about.

19:33

So this brings home the point that Crohn's is not

19:37

only asymmetric in the X direction, so along the length

19:41

of the bowel wall, because we're all sort of familiar with skip lesions in Crohn's.

19:45

But Crohn's also tends to affect the mesenteric side of the bowel more so than the

19:49

anti-mesenteric side, right?

19:52

So very often, you see this specific enhancement pattern of

19:55

enhancement along the mesenteric side, and eventually you get sort of

19:59

scarring and shortening of that mesenteric side, which results in this

20:02

pseudo-sacculation appearance of the anti-mesenteric side.

20:06

So you can see this sort of lobulated appearance of the anti-mesenteric side, which

20:09

is also a sort of specific sign of Crohn's enteritis.

20:13

And if you're old school and you like small bowel follow-through

20:17

examinations, this is an example of that.

20:19

A patient with Crohn's terminal ileitis, and he or she

20:23

had this sort of straightening along the mesenteric edge with this

20:26

pseudo-sacculation appearance of the anti-mesenteric

20:30

border. Probably also some fibrofatty

20:34

proliferation here because this terminal ileal loop is separated from the other

20:38

bowel loops. Here's another example I got from the literature.

20:41

This is a RadioGraphics article from 2020, where you see this

20:45

asymmetric enhancement along the

20:48

mesenteric border, as well as pseudo-sacculation along the anti-mesenteric

20:52

border. And here's another example from the same article.

20:55

Again, thickening and hyper enhancement along the mesenteric border,

20:59

and you can see early sort of pseudo-sacculation along the anti-mesenteric

21:03

border.

21:06

Here's some other sort of imaging patterns, features, I

21:10

guess, of patients with active Crohn's ileitis.

21:12

This is a patient who's had a

21:14

ileocecal resection for Crohn's, and you can see that

21:18

this patient has active ileitis, where there's circumferential wall

21:22

thickening, increased T2 signal in the bowel wall.

21:25

And then this patient has this sort of trilaminar enhancement

21:29

pattern. You can see maybe that there are some prominent mesenteric lymph nodes as

21:32

well. So, all sort of helpful findings of active inflammation.

21:36

This patient also did have some increased diffusion restriction in the

21:40

bowel wall.

21:41

Here's another patient. You can see this is a nice example of a comb sign with vasa

21:45

recta engorgement. You have nice sort of prominent

21:49

hyper enhancement of this inflamed loop.

21:51

And on the T2 weighted image on your left, you can see that there is bowel

21:55

wall thickening and this increased T2 signal in the bowel

21:58

wall. Here's the axial images on the same patient, where

22:02

you see some of the same findings. Bowel wall thickening, increased T2

22:06

signal, and then diffusion restriction in the bowel wall.

22:09

I just wanted to show the six-month follow-up for that patient.

22:11

It was kind of interesting because you can see that some of the increased

22:15

intramural edema on the T2 weighted images sort of has gone away on the

22:19

six-month follow-up, and this patient started to develop this sort of

22:22

pseudo-sacculated appearance.

22:25

Yeah. This is the patient I showed you earlier with that severe disease,

22:29

and you can see he also has findings of active inflammation, right?

22:32

You can see this high T2 signal in the bowel wall, diffusion restriction,

22:36

with a more sort of fibrotic T2 dark appearance in

22:40

this

22:42

enteroenteric fistula.

22:45

Ulceration, if you do see it, is a very helpful sign, and it is

22:49

associated with severe active inflammation.

22:52

So ulceration is a focal defect in the inner

22:56

luminal wall of the bowel that fills with either

23:00

contrast or fluid. And if you do see it, sometimes

23:04

I find it helpful to look down the barrel of the bowel wall on

23:08

multiplanar reformats, and that can help me see ulceration.

23:12

Here's another example from that same RadioGraphics article showing

23:16

ulceration. And you can see that these bowel loops are quite

23:20

actively inflamed, quite severely inflamed.

23:23

So other findings that aren't necessarily so strongly associated with active

23:26

inflammation. Mesenteric vein thrombosis

23:29

can be acute or chronic. Acute mesenteric

23:34

vein thrombosis is characterized by a centrally located thrombus in the

23:38

mesenteric veins and expansion of the vein.

23:41

Once the thrombus becomes more chronic, you just sort of

23:45

see narrowing of the vein and you see the development of prominent mesenteric

23:49

collaterals like are shown in the arrowheads on this

23:52

example.Here's another example, and this

23:56

shows why it's helpful to get coronal MIPs on your CT

23:59

enterographies. But you can see narrowing of the mesenteric

24:02

veins as well as these sort of

24:05

dilated venous collaterals, which can help clue you into the diagnosis

24:09

of chronic mesenteric vein thrombosis.

24:11

The thrombosed mesenteric veins usually follow the anatomic

24:15

distribution of the inflamed bowel loops.

24:18

So that may be helpful.

24:20

Another finding, fibrofatty proliferation usually occurs on the mesenteric

24:24

side of the bowel, although it can be circumferential.

24:28

And this just refers to the proliferation of mesenteric fat around

24:32

an inflamed bowel loop. And it sort of becomes

24:35

apparent on CT enterography and MR enterography because the inflamed bowel

24:39

loop is sort of separated, pulled away from its neighbors.

24:45

Here's another example of fibrofatty proliferation.

24:47

Here's an inflamed jejunal loop in the left hemi-abdomen, and you can

24:51

see that it's sort of separated. It's pushed away from the other bowel loops

24:54

because of the fibrofatty proliferation.

24:58

So just to sum up, acute disease versus chronic or fibrotic disease.

25:02

Bowel wall thickening is more severe in acute disease.

25:05

Bowel wall enhancement is more brisk and more prominent in acute disease,

25:09

less so in chronic and fibrotic disease.

25:12

Bowel wall T2 signal tends to be hyperintense on MR images in

25:16

acute disease, whereas it's more iso or hypointense

25:20

with chronic or fibrotic disease.

25:22

And ulceration, if you do see it, is a helpful finding of severe active

25:26

inflammation.

25:28

Lymphadenopathy is more prominent with acute disease, less prominent with chronic

25:32

disease. Vasorectal engorgement or that comb sign that we showed

25:36

is more prominent with acute disease, less so with chronic or fibrotic disease.

25:40

So as I said, as a key point, active inflammation as identified on

25:44

imaging is an important marker. It helps

25:47

inform the decision to start treatment, escalate treatment, and to assess

25:51

response.

25:53

So the next question:

25:55

Is my patient getting any better? So, after the patient has

25:59

been initiated on biologic therapies, the gastroenterologist will also

26:03

often get an MRE or CT enterography to assess treatment

26:07

response. So I'm going to show you a case.

26:10

This is a 67-year-old lady who was at our institution with longstanding ileal

26:14

Crohn's disease. This was her MR enterography from

26:17

2017. You can see that she has moderate bowel wall thickening in her

26:21

terminal ileum, as well as some intramural edema.

26:25

On the post-contrast images, sort of gives you the same sort of picture where you

26:29

see circumferential wall thickening of the terminal ileum with hyperenhancement.

26:33

So she had a colonoscopy. We saw this linear

26:36

ulceration in the terminal ileum, and they did some biopsies, which are chronic

26:40

active ileitis.

26:42

So the patient was started on ustekinumab,

26:45

and this is her follow-up MRI. And you can see that the wall

26:49

thickening of the terminal ileum right here has completely resolved.

26:53

This is essentially a normal

26:55

TI. There's no wall thickening. There's no hyperenhancement as such.

26:59

So I would say that the imaging findings have completely resolved.

27:04

And then the endoscopic findings bear that out as well.

27:07

The TI

27:09

was examined at about the same time as the imaging, and it was basically normal

27:13

ileal mucosa. So this is a patient who had complete

27:17

resolution of her inflammatory findings on imaging, and she did well and continues

27:21

on ustekinumab.

27:24

So that sort of brings me to the subject of what are our treatment

27:27

goals when

27:30

putting patients on these biologic therapies, right?

27:33

The historical standard has been endoscopic remission, the complete resolution of

27:37

findings on endoscopy. But endoscopy obviously is invasive, and

27:41

it has the disadvantage of only being able to assess the mucosa.

27:44

Imaging has the advantage of being non-invasive, obviously, but also

27:48

being able to look at the entire bowel wall, not just the mucosa, as well

27:52

as the sort of mesenteric findings associated with Crohn's.

27:56

So that's given rise to a concept called deep remission or

28:00

transmural remission, which is what we're going for when we treat these patients.

28:04

This is sort of the ideal. Patients with transmural remission,

28:08

more so than patients with just clinical remission, have a reduced need for

28:13

future steroids, hospitalizations, and future surgical interventions.

28:17

So when you're assessing a patient for treatment response,

28:21

the findings of active inflammation can resolve completely like they did in this

28:25

patient, but radiologists should also be attuned to the fact that

28:30

response may just be partial, and patients may have partial

28:34

resolution of their findings. So look for a decrease in severity of the

28:38

findings within the affected bowel segment, look for an evolution to

28:41

shorter and patchier areas of involvement, and then look for residual

28:45

findings such as intramural fat deposition, scarring, or

28:49

pseudosacculation, which can help you sort of identify the

28:53

evolution and improvement in the patient's picture.

28:58

When you look at a stricture, look for a greater than 50% improvement in

29:02

the luminal narrowing, prestenotic dilatation, and wall thickening of the

29:05

stricture.

29:07

So there exist scoring systems, which I won't talk much

29:12

about because I don't use them that much in my clinical practice.

29:16

But the MARIE score is probably the most famous, and this is used a lot in

29:20

clinical trials. So the MARIE score is the magnetic resonance index of

29:23

activity, and it takes into account wall thickness, intramural edema

29:27

enhancement, and ulceration. And you can sort of punch it into a

29:31

formula and come up with a number that you can compare or follow over time

29:35

to decide how severe the patient's inflammation is.

29:39

And if you're interested, there are online calculators that can help you come up

29:41

with MARIE scores. There are also other scores which we use.

29:45

There's a simplified MARIE score, which is a bit easier to use, and a Clairmont

29:48

score, which is used with CT enterography.

29:52

Okay. So CT enterography and MR enterography allow

29:56

us to target transmural remission as a treatment goal,

30:00

and achieving transmural remission leads to improved patient

30:03

outcomes.Okay. So that brings me to my next question.

30:08

Do you see a stricture?

30:11

So greater than 50% of patients with Crohn's disease will develop

30:15

strictures. Most of these will require an endoscopic or surgical

30:18

intervention.

30:20

So my next audience response question is going to be about this patient.

30:24

So take a look at this MR enterography.

30:26

So on your left, there's some coronal T2 weighted images, and I'm

30:30

interested in what you think about this bowel wall segment, which I'm

30:34

indicating with the white arrows.

30:36

On your right are the coronal T1 weighted post-contrast images.

30:41

So in your report, what do you call this?

30:43

Would you call this a stricture, a probable stricture, or normal bowel with

30:47

peristalsis?

30:54

Okay. So 52% of you would call it a stricture, 41%

30:58

of you would call it a probable stricture, 8% of you would call it a normal bowel

31:02

with peristalsis. That's good because these are challenging cases.

31:05

So let's look at this case. So here's a long ileal

31:09

segment with wall thickening, luminal narrowing.

31:13

An important observation is this upstream bowel here, which is dilated,

31:17

and it's dilated up to a caliber of 4.5 centimeters,

31:21

and that persists across multiple time points over

31:24

multiple series.

31:27

So the Society of Abdominal Radiology has recently

31:31

issued some guidance on what to call a stricture.

31:35

And the definition of a stricture according to that recent paper in

31:38

radiology is a stricture is a small bowel segment with wall thickening,

31:42

luminal narrowing, and upstream dilation of greater than two and a half

31:46

centimeters.

31:47

And if you see that, you see this fixed luminal narrowing, wall thickening,

31:51

with upstream dilation of 2.5 centimeters, then you can call that a stricture.

31:56

The other portion of the definition is if the

31:59

endoscopic passage has been attempted and failed in association with luminal

32:03

narrowing and wall thickening, even if there is no upstream dilation, you can call

32:07

that a stricture. And in this case, luminal narrowing is a diameter

32:11

reduction of greater than 50% compared with the normal

32:14

adjacent bowel. So in this case, I would call this a definite stricture.

32:18

You have luminal narrowing, upstream dilation greater than 2.5

32:22

centimeters.

32:24

How about this case? This is another case we saw.

32:27

Here you have a patient with terminal ileitis. It looks active.

32:32

You have this segment with luminal narrowing, but I don't think the upstream bowel

32:37

is quite 2.5 centimeters. It looks a little less than that.

32:41

But it is persistent. This luminal narrowing is persistent over multiple time

32:45

points. So what would you call this?

32:48

Stricture, probable stricture, or normal bowel with

32:51

peristalsis?

32:57

Yeah. So the majority of you said probable stricture, and I think that's

33:01

correct.

33:02

So let's look at this. Again, you see wall thickening, luminal narrowing greater

33:06

than 50% narrower than the adjacent bowel loop.

33:09

You don't see the persistent, the upstream bowel dilatation greater than 2.5

33:13

centimeters.

33:15

It's not as clear how to describe these sort of findings.

33:20

Recently, the Society of Abdominal Radiology has issued some guidance and

33:24

suggests that we call these probable strictures to help more

33:27

quickly identify patients with this stricturing phenotype of disease

33:31

who may have this more complicated disease course and may require

33:35

more urgent intervention, rather than dismissing this as just

33:39

purely inflammatory.

33:41

So probable stricture is what we would call this.

33:44

Here's another example of a probable stricture, this time taken from that

33:47

Radiographics article, where you see focal luminal narrowing,

33:52

but no real upstream dilation.

33:55

Here's another. Here, I'm just showing examples of strictures.

33:59

This looks like a fibrosenotic stricture in this jejunal loop in the left

34:02

hemiaбdomen. You see this significant bowel wall thickening, quite a bit of

34:07

luminal narrowing, and then upstream dilation of the proximal jejunum.

34:11

So this, I would have no qualms calling this a stricture.

34:16

Here's another example in a 15-year-old patient where you have luminal narrowing,

34:19

upstream dilation. This is a case I'm not

34:23

particularly proud of. This was a patient who underwent a CT enterography,

34:27

and you can see it looks like he's got

34:29

strictures related to Crohn's disease, right?

34:32

He's got these sort of multifocal areas of luminal narrowing with upstream bowel

34:36

dilation here, here, and it looks like they're skip lesions, as you

34:39

might appreciate, with multifocal areas of upstream

34:43

dilation. Unfortunately, we didn't recognize this, or we didn't

34:47

specifically say stricture

34:49

on our report.

34:51

We did point out the active inflammation, but here you can see the coronal images

34:55

here with luminal narrowing and upstream dilation.

34:57

And unfortunately, this patient was given an endoscopic video

35:01

capsule, which became impacted at one of the strictures.

35:04

So that was not ideal. That may have been prevented if we could have

35:08

identified the strictures more clearly.

35:11

Okay. So when you see a stricture,

35:15

there's a couple things that are important to describe to help out the radiologist,

35:19

or rather the gastroenterologists and the surgeons.

35:21

Is there active inflammation present?

35:24

Has the patient had prior bowel resections?

35:27

Because your surgical options for strictures are either a stricture

35:30

resection or a strictureplasty, which tends to preserve the

35:34

bowel in patients who have concern for short gut

35:38

syndrome.

35:39

Is the stricture endoscopically accessible?

35:43

So at our institution, they do dilation of many of these strictures,

35:48

but there's a limit as to how far from the ileocecal valve they can reach.

35:53

And then also describe the length of the stricture.

35:57

At our institution, at least, our endoscopic balloons are five centimeters

36:01

long, and the gastroenterologists want to completely traverse the

36:05

stricture with the balloon. So for a stricture to be

36:08

endoscopically accessible and amenable to

36:11

endoscopic treatment, the stricture should be less than

36:15

five centimeters long,

36:16

ideally.Remember

36:20

to describe whether there's upstream disease present, because obviously it doesn't

36:24

help if you dilate a stricture if you have a high-grade stricture proximal to it.

36:29

Take into account whether this is an anastomotic stricture, a stricture occurring

36:32

at a prior bowel resection, or a naive stricture, because that'll

36:36

affect how the patient is managed.

36:39

Look carefully for penetrating disease because strictures are associated

36:43

with penetrating disease. And then obviously look for signs of cancer,

36:47

severe bowel wall thickening, nodularity,

36:50

signs that may suggest that there's something more sinister going

36:54

on. So this is a patient, this is a 35-year-old

36:58

patient with longstanding stricturing ileocolonic Crohn's disease.

37:02

He'd had multiple prior surgeries and has nightly bloating symptoms, and this is

37:06

his MR enterography. I know these images are a little bit blurry, but the

37:10

patient has had an ileocecal resection.

37:12

And then I'm pointing here with this red arrow to the neoterminal ileum,

37:16

and you can see there's a real short segment where there's this tight sort of

37:19

narrowing right at the neoterminal ileum.

37:21

And they did an endoscopy, and you can see that they

37:24

advanced the scope right to the ileocolonic anastomosis, which was

37:28

strictured with a little small clean-based ulcer, and they were unable to

37:31

transverse it even with a pediatric scope.

37:35

So they took a balloon. It was a short segment stricture, as you saw, and they were

37:39

able to traverse it and did some serial balloon dilation.

37:42

And then the post-dilation image looks a little better.

37:45

There was a mucosal rent with a larger lumen,

37:49

but it still wasn't ideal.

37:52

But it did allow the scope to pass.

37:56

So this patient did well for a while, but unfortunately did recur with his

38:00

symptoms of nightly bloating. So the patient ultimately went for

38:04

a repeat small bowel resection, where they found patchy, active chronic

38:08

ileitis with focal ulceration.

38:11

So that was a nice example. So,

38:13

that was the definition of a small bowel stricture.

38:15

And remember, the SAR has recently given guidance on what to call a stricture

38:19

versus a probable stricture. And treatment of strictures is variable,

38:23

so it's important to describe the length, the location,

38:27

the association with any prior anastomosis, and the presence of

38:31

associated penetrating disease.

38:35

Okay. So question four.

38:38

Is this stricture, when you see it, is it more inflammatory or fibrotic?

38:42

And the gastroenterologists are interested in this question because, in theory,

38:46

inflammatory strictures are maybe more amenable to medical therapy alone,

38:50

whereas a fibrotic stricture may be less so, and

38:54

you're thinking about maybe this patient will require surgery.

38:58

I have a patient here. This was a 39-year-old lady

39:01

diagnosed with ileocolic Crohn's nine years earlier, and she's had

39:05

multiple prior treatments, Asacol, adalimumab, steroid tapers, and

39:09

infliximab.

39:11

The patient has had a bunch of recent ED visits for abdominal pain and rectal

39:15

bleeding, and this is her MR enterography.

39:19

And you can see, so here's the terminal ileum here, and you can see this sort of

39:22

tight narrowing right at the TI. But then you can also see this

39:26

sort of longer abnormal segment of distal ileum more

39:30

proximally. And you can see there's some wall thickening, but the wall

39:34

isn't that thick, and the signal in the bowel wall, it's kind of

39:38

dark. It's not really the intramural edema that we're used to seeing with active

39:42

inflammation. So we ended up calling it long segment fibrostenotic disease

39:45

involving the distal and terminal ileum.

39:48

There you go.

39:51

On the post-contrast images, you do have enhancement, but it's not sort of the

39:55

florid enhancement that we saw with some of the earlier cases.

39:58

Not much of a comb sign, not much of a

40:01

mesenteric engorgement. And there's no real

40:06

diffusion restriction in that involved a bowel loop above background.

40:11

When they scoped the patient, they had a tight sort of narrowing right at the TI

40:15

due to pinpoint stricturing of the TI associated with some extensive ulceration

40:19

right at the entrance to the terminal ileum.

40:22

So,

40:25

this is kind of a patient where it looks like she has more of a chronic disease

40:28

pattern, but there are also some signs of active inflammation.

40:32

The patient failed multiple types of medical therapy, and she has frequent

40:36

ER visits with bloating and abdominal pain.

40:38

So the patient eventually progressed to bowel resection.

40:41

And on the path,

40:43

you kind of get this impression that there's this combination, right, of both

40:46

active and chronic inflammation.

40:47

There's patchy, moderate to severe chronic enteritis with ulceration, fibrosis,

40:51

transmural inflammation, and granulomas.

40:54

So again, the gastroenterologists are very interested

40:58

in the question of whether a stricture is predominantly active or fibrotic.

41:03

And it's important to sort of tell them what the signs are and

41:07

what we think. But usually, active inflammation and

41:10

fibrosis

41:12

coexist, and in practice, it's sort of difficult to give them a binary

41:16

answer. So, the decision on how to manage will

41:20

rely on both sort of clinical and imaging findings.

41:25

Okay, so next question.

41:28

Are there any other signs of penetrating disease?

41:33

Pardon me. So,

41:35

penetrating disease in Crohn's disease, when associated

41:39

with small bowel inflammation, penetrating disease is fairly

41:42

specific for Crohn's disease. You don't usually see it with other forms of

41:46

chronic enteritis. And when I say penetrating disease, I'm

41:50

referring to enteroenteric fistulas, sinus tracts,

41:54

perianal fistulas, which are thought to be pathophysiologically different from

41:57

enteroenteric fistulas, inflammatory masses, and abscesses and

42:01

perforation.

42:03

So here I'm going to ask you a question about this case on the right of the

42:07

slide. The asterisk or star sign shown here is a sign of

42:11

what complication?

42:13

Okay,

42:20

good. So 62% of you said enteroenteric fistula, and that's correct.

42:24

So let's take a lookSo here's that patient.

42:27

So you can see a nice asterisk or star where multiple

42:31

ileal loops and also it looks like a colonic loop are sort of pulled

42:35

together by the inflammatory

42:39

process. And there's tethering. There's a pointy appearance of the bowel loops,

42:43

and you have this star in the center, which represents a complex enteroenteric

42:46

fistula. This is referred to the star sign.

42:49

Keep in mind that with complex fistulizing disease like this, this is

42:53

very highly associated with strictures. Right?

42:56

So,

42:57

sort of carefully look at the surrounding bowel for

43:01

signs of upstream dilation, fecalization that

43:04

will

43:06

clue you in that there's stricturing disease.

43:09

This patient I showed you earlier with also fistulizing disease.

43:13

Here's an enteroenteric fistula here.

43:15

There's upstream dilation of the more proximal bowel loops with

43:19

fecalization here. So here, I would say, not only

43:23

is there complex enteroenteric fistula, but there's evidence of stricturing with

43:27

upstream dilation. Also, keep in mind that

43:32

fistulas upstream can sometimes

43:35

decompress the more distal bowel,

43:39

and so

43:41

a

43:42

stricture may not be associated with as much upstream dilation.

43:46

So if you do have a fistula, and you think a stricture may be present, it's fair to

43:50

say, a stricture is likely present.

43:53

Here's another nice example taken from online, and this

43:57

is a nice example of a star or an asterisk sign with these tethering of

44:01

the bowel loops in a star in the mesentery representing

44:05

these complex enteroenteric fistulas.

44:09

Here's an image taken from that Radiographics article,

44:12

again, showing the star sign and enteroenteric fistulas.

44:17

My next question is about this case,

44:21

so

44:22

particularly this finding here.

44:24

What's the preferred term, according to the Society of Abdominal Radiology,

44:28

for this structure indicated by the red arrows?

44:37

Yeah, very good. So 64% use an inflammatory mass, and that's correct.

44:40

That is the current guidance, right?

44:42

So, an inflammatory mass is dense

44:46

mesenteric inflammation related to penetrating

44:50

disease adjacent to a severely inflamed small bowel loop.

44:54

And we used to call these phlegmons, but the term phlegmon is probably

44:58

discouraged now because of potential ambiguity about whether a

45:01

drainable collection exists. So,

45:05

again, the Society of Abdominal Radiology

45:08

suggests using the term inflammatory mass instead.

45:11

And again, this is another finding of penetrating disease.

45:14

So generally speaking, penetrating disease and Crohn's disease have a

45:18

poorer prognosis. They have a more morbid disease

45:21

course. They're more likely to have surgically

45:24

complex disease. And again, penetrating disease is highly associated

45:28

with stricture. So carefully scrutinize the associated bowel for evidence

45:32

of strictures, and keep in mind there may not be as much upstream dilation as you

45:36

would otherwise expect. Here's a nice example of that taken

45:40

from online with a patient with an enteroenteric

45:43

fistula here on this image on the left between two ileal

45:47

loops, and you can see there's also luminal narrowing and upstream dilation

45:51

of the more proximal bowel loop. So this is a stricture

45:55

associated with penetrating disease.

45:57

This is also a nice example of the fact that strictures or rather fistulas when

46:01

they do arise from a stricture tend to arise from the

46:05

proximal portion of the stricture. So look closely if you do see a stricture.

46:09

Look at the proximal end of that stricture to see if there's any evidence of

46:13

a sinus tract inflammatory mass fistula that could indicate

46:17

superimposed penetrating disease.

46:21

So identification of penetrating disease, fistula abscess, inflammatory mass,

46:25

or perforation is important because it portends a more morbid disease course.

46:30

Okay. Question number six. Does this patient need surgery?

46:34

And I kind of added this a little bit facetiously because obviously

46:38

radiologists can't answer this question by themselves.

46:41

This is a question that has to be answered by the surgeons, but we can give them

46:45

information that can help inform this decision.

46:48

So

46:50

the mainstay of therapy for Crohn's disease is medical, but half of patients

46:54

will require at least one surgical procedure due to complications or

46:57

refractory symptoms despite medical management.

47:00

Indications for surgery usually are fistula perforation,

47:04

abscess, or stricturing disease.

47:06

And obviously, patients with

47:11

superimposed cancer will require surgery as well.

47:15

So typically, historically, the indications for surgery have

47:19

been refractory disease, disease that is not improving despite

47:23

maximal medical management. I'll tell you that in

47:26

2017 in "The Lancet," there was a big trial called the Lyric Trial,

47:31

which looked at patients

47:35

with limited disease. And in this trial, they came to the conclusion

47:38

that actually upfront resection in patients with limited

47:42

disease, limited to just the terminal ileum, less than 40 centimeters,

47:46

non-penetrating, non-stricturing ileocecal Crohn's disease.

47:50

So upfront resection may be a reasonable option in this

47:54

patient rather than starting with medical management.

47:57

And this approach of upfront surgery isn't pursued that much in

48:01

the US, at least at our institution.

48:03

But from what I understand, more so in Europe, they do follow this

48:08

guideline. And like I said, this study was

48:11

published in 2017, so now we have 10-year data sort

48:15

of

48:17

supporting these findings.So this is a patient that we had

48:21

where that became relevant. So this is a young guy, he was 33.

48:24

He had a history of testicular cancer, status post-orchectomy and adjuvant

48:27

chemo. So we actually were doing this CT just for staging of his

48:31

testicular cancer, and we actually did notice, oh, look at this terminal ileum.

48:36

There's quite a bit of wall thickening, and he kind of has this pseudossaculated

48:39

appearance, which is sort of very typical for Crohn's disease, even though he

48:43

didn't have a history of that diagnosis.

48:46

So we recommended an MR enterography, which showed sort of the same thing, sort of

48:50

active inflammatory changes of this TI,

48:53

pseudossacculation of the anti-mesenteric side.

48:56

So they eventually did a scope, and this is the terminal ileum.

48:59

They saw mild ulceration and inflammation of the TI, and the remaining small bowel

49:03

and colon were not involved.

49:06

So the pathology showed acute ileitis with focal erosion.

49:10

So this patient

49:11

got a presumptive diagnosis of Crohn's disease.

49:14

So this patient was actually nervous about

49:18

biologics because of his history of testicular cancer, so didn't want to do that.

49:22

So we actually offered him primary surgery according to the LYRIC data.

49:26

He ended up just sort of wanting

49:29

surveillance, but that would've been a reasonable option in this

49:33

patient.

49:36

Okay. So

49:38

in conclusion, the introduction of the new biologic therapies that we've had over

49:42

the past two decades has really shifted Crohn's management from a step-up to

49:46

a top-down approach. And this newish approach

49:50

really sort of

49:53

puts objective markers of inflammation front and center, both to

49:56

stage the disease, to decide what the treatment should be, and

50:00

to monitor treatment response. So clinically relevant reports

50:04

will identify active inflammation, identify strictures and other

50:07

complications, guide treatment of active disease and complications, and then

50:11

assess treatment response.

50:14

So the last thing I did want to share with you, two articles that I find very

50:18

useful, in day-to-day practice, in sort of

50:23

creating my reports. This one was Bruining et al., published in

50:26

2018. And these are the consensus recommendations for

50:30

evaluation of CTE and MRE in patients with Crohn's disease.

50:34

This is really helpful. It's kind of a long article, but even if you just look at

50:38

the pictures, I find it really sort of useful.

50:41

The other paper that I wanted to share with you is this one.

50:44

This was published in 2020, and this is "Small bowel Crohn's disease at CT

50:48

and MR enterography." This is an imaging atlas and glossary of terms.

50:52

Again, if you don't read the article, but you just look at the images and the

50:55

captions, I find it really helpful.

50:58

And that's all I have. Thank you so much.

51:01

Thank you so much for that awesome lecture and case review.

51:04

We've got some questions in that Q&A box if you're able to pop that open.

51:09

Oh.

51:09

It might be at the bottom of your Zoom right now.

51:13

This one?

51:14

The little question mark.

51:17

Oh, I'm sorry. I don't see a question mark.

51:22

Ah, here. I see. Okay.

51:25

"Have you thought about colorizing your DWI images to pick up increased signal?" I

51:29

haven't thought about it. That's a good idea.

51:31

But I'm sorry, I don't have

51:34

experience with that.

51:36

But it's an interesting idea. I'd like--

51:39

yeah, I'd want to look into that more.

51:43

"Can you share reporting formats or checklists for MR CT

51:46

enterography?" Yeah, so if you look at that Bruining article that I shared,

51:50

that was published in 2018. It's called "Consensus

51:54

recommendations for

51:56

the evaluation of MR and CT enterography." That

52:00

has

52:01

both a checklist and sort of a suggested reporting

52:05

template, which we use at our institution and we find quite helpful.

52:10

"Please show the slide of the table of findings of active versus chronic

52:14

disease."

52:15

I will do that in one s-- let's actually go to that real

52:18

quick. So again, findings associated with

52:22

acute disease. Oops. So again, bowel wall

52:26

thickening tends to be more severe with acute disease, less severe with

52:29

chronic and fibrotic disease. Bowel wall enhancement tends to be more

52:33

brisk and more prominent with active disease as opposed to chronic or fibrotic

52:37

disease. Bowel wall T2 signal, the signal is

52:41

hyperintense in the bowel wall,

52:43

with active disease and isohypointense with fibrosanotic or chronic

52:47

disease.

52:49

And ulceration, again, when you do see it, is a very helpful finding of

52:52

severe active inflammation. Other findings,

52:56

lymphadenopathy tends to be more prominent with acute disease, less prominent with

53:00

chronic or fibrotic disease. Vasorectal engorgement, the so-called

53:04

comb sign, tends to be more prominent with acute disease, less prominent

53:08

with chronic or fibrotic disease.

53:12

So I hope that was helpful.

53:15

"How do you differentiate stricture from malignancy?" That's a really good

53:18

question. Anytime you see a stricture in the colon, you should think

53:22

cancer first probably.

53:24

So that should, if you see bowel wall thickening and a stricture in

53:28

the colon, probably aggressively recommend endoscopic

53:32

evaluation. Small bowel, probably trickier.

53:37

Crohn's strictures tend to be probably longer, more diffuse,

53:41

less nodular,

53:44

associated with a more upstream dilation, although that can be variable.

53:50

And if the patient has other signs of malignancy clinically, this

53:54

is something that

53:56

they have to evaluate. But in my experience, strictures in

54:00

Crohn's disease tend to be kind of longer and then sort of more diffuse and

54:03

circumferential, not as nodular and irregular as

54:07

malignancy strictures.

54:09

"Do you ever see spontaneous improvement of Crohn's disease without treatment?"

54:12

Yes, we do see that.

54:14

Not as much in our patient population as we are a tertiary

54:18

referral center. But we do sometimes see

54:20

that.How to distinguish normal diffusion

54:24

restriction versus pathologic restriction in small bowel and colon.

54:28

Yeah, that's a good question. Diffusion restriction, as you know, can be very

54:33

sensitive to

54:35

artifacts like gas in the bowel wall, for example, or motion.

54:40

My best advice to you is to look for diffusion restriction

54:44

in the bowel wall segment that has other signs of active inflammation.

54:48

And if you see diffusion restriction

54:50

that's higher than it is in the surrounding non-inflamed

54:54

bowel loops that can help increase your confidence.

54:58

How to get qualitative images, 1.5 versus 3Ts.

55:02

Are there tricks to prevent motion blurring?

55:05

That's a good question, and it's probably more involved

55:09

than I can answer. We use

55:13

3T for our MR enterographies.

55:17

Tricks to prevent motion blurring.

55:19

Timing of the glucagon administration may be helpful

55:23

if

55:25

it's administered prior to the DWI and

55:29

T1 weighted images, which are more motion sensitive, that can

55:33

sometimes help you prevent blurring.

55:35

Obviously, using an anti-peristaltic agent

55:40

can be helpful. Also,

55:44

I'm sort of sensitive to the fact that our MRE protocol is very

55:48

long. So for our protocol, there's an hour

55:51

of table time, which in patients with back pain or have difficulty

55:55

lying flat, can be a real problem to stay still.

55:58

So shortening the

56:02

protocol to sort of the most important sequences can sometimes be helpful.

56:08

Once again, can you please say the difference between fibrotic and inflammatory

56:11

disease? We did go over that slide.

56:14

Did you mention residual functional lumen in stricture?

56:24

Did I mention residual or functional lumen?

56:26

I will mention the length of the stricture.

56:30

As far as the functionality of it, I don't mention

56:34

that,

56:35

if I understand your question correctly.

56:41

How to distinguish fistula versus sinus tract that does not yet perforate into the

56:44

neighboring small bowel. It can be

56:48

tricky. I just follow the tract

56:52

to see if it does terminate, and sometimes I'm sort of forced to say probable

56:56

stricture versus sinus tract.

56:59

Any confusion of diagnosing appendicitis and Crohn's disease, how to

57:03

differentiate between

57:05

surgical and non-surgical disease?

57:08

Yeah. So

57:11

sometimes there is

57:14

difficulty in distinguishing appendicitis from Crohn's disease.

57:18

My experience has been

57:20

in Crohn's disease, patients with

57:23

secondary appendiceal inflammation, usually

57:27

the inflammatory process will appear to be centered around the terminal

57:31

ileum rather than the appendix, and the appendix will be sort of peripherally

57:35

involved, whereas

57:37

in primary appendicitis caused by appendiceal obstruction, that inflammatory

57:41

process is really centered around the appendix.

57:44

What other non-bowel signs can be seen in Crohn's?

57:47

These are things that I actually didn't talk about that sort of were outside the

57:50

scope. But remember,

57:53

always look in MR enterography for signs of sacroiliitis,

57:58

primary sclerosing cholangitis with a beaded appearance of the intrahepatic

58:02

bile ducts.

58:03

And then

58:05

other bone findings. Avascular necrosis can be seen in patients with Crohn's.

58:10

So yeah, those are the ones that are, I guess the more

58:14

common ones we talk about.

58:18

More non-specific ones, cholelithiasis, nephrolithiasis, are more prevalent

58:22

in patients with inflammatory bowel disease.

58:26

And I think that's it.

58:29

Yeah. You really got through a lot of questions. Thank you so much.

58:34

Appreciate you being here for this presentation.

58:38

For sure.

58:38

Really appreciate it. Thank you. And thanks for everyone else for participating in

58:42

today's noon conference. You can access a recording of it and all our

58:46

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58:49

replay later today.

58:51

Be sure to join us next week, Thursday, May 21st at

58:55

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58:59

"The Aging Human Spine." You can register for that at medallity.com and follow us

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59:06

Thanks again for learning with us and have a great day.