0:02

Hello and welcome to Case Crunch, rapid case

0:04

review for the core exam hosted by Medality.

0:07

In this rapid-fire format, faculty will show key images

0:10

along with a multiple-choice question, and you'll respond

0:13

with your best answer via the live polling feature.

0:17

After a quick answer explanation,

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it's on to the next case.

0:21

Today, we're honored to welcome

0:22

Dr. Claire for the GI board prep case review.

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Dr. Brookmeyer completed her radiology residency,

0:28

chief year, and body MR fellowship at Johns Hopkins.

0:32

She's on the faculty in the Body Division at

0:34

Johns Hopkins Department of Radiology

0:36

and also serves as the course director for the

0:38

medical student clinical electives in radiology.

0:41

Questions will be covered at the end if time allows.

0:43

So please remember to use the Q&A

0:45

feature to submit your questions.

0:47

With that, we are ready to begin today's board review.

0:50

Dr. Brookmeyer, please take it from here.

0:54

Hello, everyone.

0:56

My name is Claire Brookmeyer.

0:57

I am on the faculty at the Johns Hopkins

0:59

School of Medicine, and I am very excited

1:01

to present to you my GI board review.

1:04

So, our plan for the day

1:06

is to do a rapid-fire case review.

1:08

I want us to get through as many questions

1:10

as possible because more is more.

1:13

So, I'm going to give you a strategy

1:14

for getting through these questions.

1:16

I will present to you the question stem,

1:18

including the images, and I want you to try and

1:20

answer before looking at the answer choices.

1:23

This is a way to help you avoid getting distracted

1:26

by the distractors. Use everything on the images.

1:29

And then, please hold your questions to

1:31

the end, and I will stick around to answer

1:32

any questions regarding all the cases.

1:36

So, one question to get us warmed up—

1:39

are you a resident, an attending physician,

1:42

just here for the cases, or other?

1:54

All right, and I see most of us are here cramming

1:56

for the course, so this is the right time to do it.

1:58

All right, let's go ahead and

1:58

get started with our first case.

2:03

So, best diagnosis—so I'd like you to take a look

2:07

at the images, formulate what you think is going on,

2:15

and here are your answer choices.

2:27

All right, it looks like we have an even split

2:29

here between internal hernia and a volvulus.

2:32

So here, the best answer choice is a volvulus.

2:36

And really, the key here is identifying

2:37

that there is this mesenteric whorl.

2:40

So here, we have an acute closed

2:41

loop small bowel obstruction.

2:43

There is lack of enhancement of the involved bowel loop,

2:46

uh, of the walls of the involved bowel loop, indicating

2:49

that there is some degree of bowel ischemia.

2:52

And if this is acute, if this is acute,

2:54

this is truly a surgical emergency.

2:57

So, why are the other answers incorrect?

2:58

Well, partial small bowel obstruction

3:00

is an incomplete answer, and it really

3:01

doesn't account for the mesenteric whorl.

3:03

Same thing with the internal hernia.

3:05

While you can have a, um, a closed-loop small bowel

3:08

obstruction that results from an internal hernia,

3:11

those are typically much more sac-like,

3:12

with sort of a mushroom appearance, and really aren't

3:15

characterized so much by this mesenteric whorl here

3:17

that I've identified by this orange arrow.

3:20

Um, acute embolic mesenteric ischemia, while it

3:23

would account for the ischemic bowel, would not

3:25

account for this mesenteric whorl here in the middle.

3:30

Next question.

3:35

All right.

3:36

19-year-old male, previously healthy,

3:38

presenting with abdominal pain.

3:40

What is your best diagnosis?

3:44

I'm going to let this image stack scroll.

3:47

For a while, and then I'm also

3:48

going to give you sequential images.

3:54

Here are three sequential images

3:55

from that scrollable stack.

4:02

And here are your answer choices.

4:12

All right, looks like the majority of us did choose

4:14

the correct answer, which is a left peritoneal hernia.

4:17

So, really identified by this left upper quadrant, um,

4:20

sac of bowel, um, originating near the DJ junction.

4:26

So, why are the other answers incorrect?

4:28

Well, a right-sided peritoneal hernia would

4:30

really have the sac of bowel on the right side.

4:33

Peterson's space hernia is an acquired hernia after

4:36

a Roux-en-Y surgery, and I haven't shown you any

4:38

uh, post-surgical changes here in the abdomen.

4:40

And then the foramen of Winslow

4:43

hernia.

4:43

While it can also cause a loop or a sac

4:46

of small bowel on the left side of the

4:48

abdomen, you would expect to see bowel and

4:51

mesentery between the portal vein and the IVC.

4:54

That's the point of showing you this axial image here.

4:58

You can see that there's no mesentery or bowel

5:01

here between the portal vein and the IVC.

5:03

So that excludes a foramen of Winslow hernia.

5:06

So, you should really be able to

5:08

differentiate between these hernias.

5:10

The left periduodenal is much more

5:12

common and occurs at the DJ junction.

5:14

The right periduodenal is less common and is

5:17

typically associated with non-rotated bowel.

5:19

And then the foramen of Winslow hernia, which is

5:21

in fact a distractor for the left periduodenal,

5:24

really should be identified with mesentery

5:26

or bowel between the IVC and the portal vein.

5:31

All right, next case. Best diagnosis?

5:36

Look at everything on the images, formulate your plan.

5:42

And here are your answer choices.

5:53

All right, looks like we have a pretty even spread.

5:55

Uh, the correct answer here is a femoral hernia.

5:59

So, the key to distinguishing between, uh,

6:01

the femoral hernia and the inguinal hernia

6:03

is really where the inguinal ligament is.

6:04

So, femoral hernias occur, uh, medial to

6:07

the femoral vessels, which this one is.

6:09

So, here are the femoral vessels,

6:10

and then here's the neck of the hernia.

6:13

Importantly, it is inferior and

6:14

posterior to the inguinal ligament.

6:16

So, the inguinal ligament,

6:19

I've identified here by these yellow arrows.

6:22

And you can see that as we move from anterior

6:24

to posterior through these sequential

6:25

slices, the hernia neck is posterior to the inguinal ligament.

6:31

These are much more likely to incarcerate

6:33

because they have a narrow neck.

6:36

So, why are the other answers incorrect?

6:37

Well, the obturator hernia originates

6:39

between the pectineus and obturator, and it's

6:41

usually associated with pelvic floor laxity.

6:43

These are a lot easier to see on axial images.

6:46

And then the inguinal hernias—the neck of the

6:48

hernia is superior to the inguinal ligament.

6:52

So, because this is such an important distinguish,

6:55

an important thing to distinguish, I've brought

6:57

up a companion case of an inguinal hernia.

6:59

Here, you can see that the neck of the hernia

7:02

originates superior to the inguinal ligament,

7:05

which I've identified here by the yellow arrows.

7:07

In contrast to the case that we had,

7:09

where the neck of the hernia is posterior.

7:12

Okay. It's an important distinction here.

7:17

Alright, next case. Best diagnosis?

7:20

Take a look at all of the images.

7:23

Formulate your thoughts.

7:29

And here are your answer choices.

7:40

Alright, perfect.

7:40

Everyone here got scleroderma?

7:42

Scleroderma is, in fact, the correct answer.

7:45

So, scleroderma in the gut is really identified by

7:48

impaired gut motility, so you can have a patulous,

7:51

fluid-filled esophagus, and then things that look like

7:53

obstructions because of the impaired gut motility.

7:56

So, a pseudo-SMA syndrome, where the proximal

7:58

duodenum is dilated, and then a pseudo-obstruction,

8:01

where there's diffuse dilation of the bowel.

8:04

If you see interstitial lung disease at

8:06

the lung bases, that's a nice tip-off that

8:08

you're probably dealing with scleroderma.

8:09

So...

8:12

So, why are the other answers incorrect?

8:13

Well, celiac disease on CT is really identified

8:16

by dilated bowel and, on fluoroscopy,

8:19

byt the jejunal and ileal fold reversal.

8:20

Eosinophilic enteritis really, um, identified by

8:24

diffuse bowel wall thickening, and it's quite rare.

8:27

And then adhesive small bowel obstruction

8:28

really wouldn't explain the esophageal

8:30

and lung findings that I gave to you.

9:55

Next case.

9:59

Take a look at the images.

10:08

And here are your answer choices.

10:18

This was part one of the question.

10:19

We're going to move on to part

10:20

two before we go over the answers.

10:26

All right.

10:27

Here's the follow-up question.

10:37

Good.

10:38

All right.

10:39

So we will go over the answer choices.

10:41

So the best diagnosis here was toxic

10:43

megacolon, and the majority of you chose that.

10:45

So, toxic megacolon, really identified by this complete

10:48

loss of haustra, and the mucosal irregularity here.

10:51

And so, these tiny little pseudopolyps—

10:53

that’s from the mucosa, that’s ischemic, and it's dying,

10:56

and it's starting to slough off into the lumen.

10:59

And it’s part of this pattern

11:00

of this marked colonic dilation.

11:03

So, why are the other answer

11:04

choices here incorrect?

11:06

Well, large bowel obstruction and Ogilvie's

11:08

syndrome, while they can cause dilated

11:09

colon, really wouldn’t explain the loss

11:11

of haustra and the mucosal changes.

11:14

Ulcerative colitis, when it's uncomplicated,

11:16

really shouldn’t have this much colonic dilation

11:18

and also would not have these mucosal changes.

11:24

And then for the follow-up question, the correct answer here

11:26

was to discuss with the team that it is contraindicated.

11:29

That is the correct answer,

11:29

and that's what the majority of you chose.

11:31

Remember that in toxic megacolon, enema is

11:33

contraindicated because there's a risk of perforation.

11:35

That colon is, uh, that colonic wall is dead,

11:39

and ischemic, and, um, can risk perforating.

11:41

And in fact, if you look closely at this

11:44

image, at the yellow arrows here, you can see

11:46

that this patient had actually already perforated,

11:48

and there's a little bit of pneumoperitoneum.

11:53

Next case. This is a scrollable stack of images,

11:58

so I'm going to let it play for a while, and then

12:00

I'm going to give you sequential images as well.

12:03

So I'll let this play.

12:13

And here are your sequential images if you

12:15

were to be able to scroll through them.

12:18

You will be able to manipulate how fast you

12:20

scroll if you're given a stack on the exam.

12:33

And here are your answer choices.

12:44

All right, looks like the majority of

12:45

you chose the correct answer,

12:46

which is, in fact, Meckel's diverticulitis.

12:48

Remember, this is a omphalomesenteric duct remnant.

12:51

Complications in adults—think much

12:53

more about small bowel obstruction and

12:55

diverticulitis, less likely bleeding.

12:57

And then, of course, the rule of twos

12:58

that is always harped on—2 percent of the

13:00

population, 2 feet from the ileocecal valve,

13:03

and it's usually symptomatic before age 2.

13:07

So, follow-up question to this.

13:11

What is the next best step?

13:21

All right, looks like the correct answer eked out.

13:25

The next best step here is a surgical consult.

13:28

Well, I think some of us gut-react,

13:30

and we go to the free pertechnetate scan.

13:32

Remember that this free pertechnetate scan

13:33

is a distractor, and it's really to evaluate

13:35

for a gastrointestinal bleeding source.

13:38

It's only going to be 60%

13:39

positive predictive value in adults.

13:41

This patient's problem is

13:43

predominantly the diverticulitis.

13:45

And so, just like appendicitis,

13:47

it needs a surgical consult.

13:49

We haven't said anything about this patient bleeding.

13:51

We just know that this diverticulum is inflamed.

13:57

All right, next case.

13:58

Best diagnosis?

14:02

Formulate your thoughts.

14:09

Here are your answer choices.

14:19

All right, 100% correct.

14:21

I love it.

14:22

Uh, so the correct answer here is,

14:24

in fact, epiploic appendagitis.

14:26

And you can see that there is this small, ovoid fat

14:29

density here arising from the descending colon.

14:32

Um, and you have a central dot sign, um,

14:35

which corresponds to this thrombosed vascular pedicle.

14:38

When you see this central dot sign, it is

14:40

really pathognomonic for epiploic appendagitis.

14:43

So, the real infarct.

14:45

And so, you should be able to tell

14:46

the difference between these two.

14:47

Epiploic appendagitis happens in the

14:49

descending colon, the rectosigmoid.

14:51

The fat density is smaller.

14:52

It's in the one to three-centimeter range.

14:55

Ovoid, and again, when you see that central dot sign,

14:57

you know right away it's epiploic appendagitis.

14:59

In contrast, an omental infarct is

15:01

much more likely to be right-sided.

15:02

They are much larger.

15:04

They are typically less well-defined.

15:05

And depending on the size and how much necrosis

15:07

is going on, you can get central liquefaction,

15:10

like I've shown you in this example here.

15:14

All right, next case.

15:20

I'm going to let this CineStack scroll for a

15:22

minute, and then I will also give you still images.

15:33

Here are your still images.

15:43

And here are your answer choices.

15:54

All right, we're going to move on

15:56

to Part 2 of this question.

16:01

What is this patient at increased risk of?

16:04

And here are your answer choices.

16:05

Read all of the answer choices.

16:16

All right.

16:17

So, answer— the correct answer to

16:19

Part 1 of this question is ulcerative

16:20

colitis, which the majority of people got.

16:23

This is a really nice example of that lead

16:26

pipe colon that we are often taught about.

16:28

So, chronic repeated inflammation of the colon leads to

16:32

this featureless pattern with complete loss of haustra.

16:35

You can also see neural fat deposition in some cases.

16:39

It tends to involve the entire

16:40

colon, and especially the rectum.

16:42

And so, here I've given you arrows pointing out

16:44

this lead pipe appearance of the colon.

16:49

So, what is this patient at increased risk of?

16:51

They're at increased risk for both

16:52

toxic megacolon and colorectal cancer.

16:55

This is a friendly reminder to

16:56

read all of your answer choices.

16:59

So, why is perianal fistula incorrect?

17:01

That is a much more typical finding in

17:02

Crohn's disease, and that's because Crohn's is

17:05

transmural, and so it has more fistulization.

17:09

And also, ulcerative colitis, while it tends to involve

17:12

the entire colon, typically spares the anal canal.

17:18

Moving on to our next case. Best diagnosis—take a

17:23

look at the images, including this scrolling image.

17:30

I'm going to let it play for a while

17:31

before I give you your answer choices.

17:45

All right, and here are your answer choices.

17:56

Perfect.

17:56

It looks like the majority of people got the

17:58

answer correct, which is, in fact, a marginal ulcer.

18:01

So, the key here is identifying that there's lots of

18:04

inflammation in this patient who is post-gastric bypass,

18:07

and the inflammation is all at the gastrojejunostomy.

18:10

So, this happens when gastric acid crosses the

18:13

GJ and enters the jejunum, and it makes the

18:15

jejunum really angry and inflamed because it's

18:17

not used to receiving all of that acidic fluid.

18:20

And so, here you can see that there is wall

18:22

thickening, and surrounding fat stranding, and

18:25

outpouching here at the gastrojejunostomy.

18:28

So, why are the other cases incorrect?

18:30

Well, while these are all other

18:31

complications of a gastric bypass, they don't

18:35

apply—they don't fit these imaging patterns.

18:37

So, afferent loop syndrome is a type of

18:38

small bowel obstruction in the right upper

18:40

quadrant involving the afferent loop.

18:42

Gastro-gastric fistula is really identified

18:44

by fluid, or if you're lucky enough to have

18:46

given oral contrast in the excluded stomach.

18:48

These patients typically have weight gain.

18:51

And then, a GJ stomal stenosis—you might think of that

18:53

as a bowel obstruction involving the gastric remnant.

18:57

So, you'd expect to see a dilated

18:58

gastric remnant and a dilated esophagus.

19:04

All right.

19:05

This is the same patient as the last case,

19:08

but two weeks later. What is your best diagnosis?

19:13

Take a look at the images. Form your thoughts.

19:22

And here are your answer choices.

19:32

Perfect.

19:33

And the majority chose the correct

19:34

answer, which is a pyogenic abscess.

19:37

So, here we can see that there's this, um,

19:40

coalescing intrahepatic collection, and if you're

19:43

lucky, you can see a double target sign, either

19:45

involving the entire rim of the collection or,

19:47

in this case, just the posterior margin,

19:49

and that's really indicative of a pyogenic abscess.

19:52

So, what is the double target?

19:53

Well, I zoomed in here, and I'm really showing the

19:56

double target here, just along the posterior margin.

19:59

That's when there's central necrosis,

20:00

this enhancing rim of granulation tissue,

20:04

and then perilesional inflammatory edema.

20:06

So, that makes up your double target.

20:09

Okay.

20:11

Next case.

20:14

Take a look at the images and formulate your thoughts.

20:23

And here are your answer choices.

20:33

Use everything on the images.

20:38

All right.

20:39

All right.

20:39

Looks like we were a little more

20:40

evenly split here between sclerosing peritonitis

20:43

and pseudomyxoma peritonei.

20:45

The correct answer here is sclerosing peritonitis.

20:49

So, the key here is identifying

20:51

these sheet-like peritoneal calcifications.

20:55

What this is really getting at is what's the

20:56

differential for sheet-like peritoneal calcifications.

20:59

You could think about prior bacterial peritonitis,

21:02

chronic peritoneal dialysis, and sort of what goes

21:05

along with that is secondary hyperparathyroidism.

21:07

So, the key here is really to use

21:09

everything that's on the images.

21:10

So, this patient's native kidneys are really atrophic.

21:13

You can infer that they are on dialysis.

21:17

So, sheet-like peritoneal calcs, very

21:18

characteristic of sclerosing peritonitis.

21:23

So, the other answer choices—why are they incorrect?

21:25

Well, let's talk about pseudomyxoma

21:26

peritonei since that was the distractor here.

21:28

You really want to think much

21:29

more about scalloped margins.

21:31

You typically don't see this degree of sheet-like

21:34

peritoneal calcs, especially if it's prior to treatment.

21:37

So, that would be highly unusual.

21:39

The other answer choices—peritoneal mesothelioma,

21:42

you'd be much more likely to see masses or cysts,

21:45

not so much the peritoneal calcifications,

21:48

and the diffuse ascites, and then peritoneal

21:50

carcinomatosis, you'd be much more likely

21:52

to see omental caking or nodules.

21:54

Um, really the identifying feature

21:56

here is these sheet-like peritoneal calcs.

22:03

Alright, next case.

22:05

Formulate your thoughts.

22:14

And here are your answer choices.

22:23

Alright, looks like we, uh,

22:26

were also not quite sure here.

22:27

Um, so the correct answer here is littoral cell angiomas.

22:30

These were half proven.

22:32

So, what this is really getting at

22:34

is, um, what's your differential for

22:36

multiple hypoenhancing splenic lesions?

22:38

Well, you think about things like METS, sarcoid,

22:41

um, and then you get down to these, um, other benign

22:43

things like littoral cell angiomas, um, and peliosis.

22:47

So, why are the other answers incorrect?

22:50

Well, splenic infarcts—the morphology here is wrong.

22:52

Those tend to be more wedge-shaped and subcapsular.

22:55

These are much more intraparenchymal.

22:56

Echinococcal cysts.

22:58

The APR would really need to show you these,

23:01

like, clearly defined daughter cysts in order

23:03

for you to confidently make that diagnosis,

23:05

and I have not pictured them here for you.

23:07

And then post-traumatic pseudocysts—these are true

23:09

cysts, they don't have any intralesional enhancement.

23:12

On these images, you can clearly see that,

23:14

um, this lesion is taking up contrast between

23:16

the arterial and the venous phase, and so this

23:19

definitely has some, um, internal vascularity to it.

23:25

Alright.

23:26

Best diagnosis.

23:29

Take a look at these images.

23:36

And here are your answer choices.

23:46

So, it looks like we also had an even split here.

23:49

So, um, when I'm dealing with an MR case that has

23:54

multiple images, I start by identifying each sequence.

23:59

So here we have a T2 coronal, a T1 fat-sat

24:03

pre-contrast, and then a T1 post-contrast subtraction image.

24:08

So we can see that we've got some T2 shading and

24:11

some intrinsic T1 hyperintensity within this lesion.

24:14

This combination of signal between T1 and T2

24:18

is very characteristic for blood products.

24:20

You could think of that just like

24:21

you would for an endometrioma.

24:23

You can see that there's no intralesional enhancement.

24:26

You also notice that the stomach and

24:28

the proximal duodenum are quite dilated.

24:30

So, the correct answer here is a duodenal hematoma.

24:33

So, causes of duodenal hematoma—blunt abdominal

24:36

injuries is by far the most common, although it can

24:38

also be caused by an underlying coagulopathy.

24:40

Nearly a third of these cases present with proximal

24:43

small bowel obstruction, like this case did.

24:46

It's typically associated with

24:47

other solid organ injuries.

24:49

Um, this particular, uh, patient, um,

24:52

had dropped a barbell on his stomach.

24:55

So, um...

24:58

The ABR can show you common things like duodenal hematomas

25:02

in uncommon ways, for example, on an MRI.

25:05

Um, but just remember to break it down by, um,

25:09

each sequence and then really, um, think about,

25:12

you know, what blood looks like on, um, on an MRI.

25:19

All right.

25:20

Next case—best diagnosis.

25:22

Use all of the images. Formulate your thoughts.

25:31

And here are your answer choices.

25:41

Alright, and the majority chose the correct

25:43

answer here, which is, in fact, pseudocirrhosis.

25:46

So, this happens after treatment of diffuse

25:48

liver metastases, typically with breast cancer.

25:51

Um, and you get hepatic capsular

25:53

retraction and fibrosis.

25:54

Um, and these patients may or may not have,

25:56

uh, clinical evidence of liver failure.

25:59

So, why not the other answer choices?

26:01

Well, really, the only distractor here is cirrhosis,

26:04

and it might have a very similar appearance to this

26:07

post-treatment scan, but it wouldn't fit with the

26:09

history, and I've given you the pre-treatment imaging.

26:11

It really wouldn't, um, explain the

26:12

diffuse, um, FDG-avid hepatic uptake.

26:17

All right, next case.

26:21

You can just go ahead with the answer choices.

26:32

All right, it looks like the majority of you

26:33

did, in fact, choose the correct answer choice,

26:36

which is primary sclerosing cholangitis.

26:39

You can see that there is both

26:40

intrahepatic and extrahepatic biliary ductal dilation, and stricturing,

26:45

very characteristic of PSC.

26:48

That's why the other answer choice is incorrect,

26:50

while primary biliary cirrhosis really only affects

26:53

the intrahepatic ducts. AIDS cholangiopathy,

26:56

while it can involve both the intra-

26:58

and extrahepatic ducts, really occurs in very sick individuals,

27:01

people who have a CD4 count less than 100.

27:03

It does not fit the history I've given you.

27:06

And also, um, tends to have

27:08

papillary stenosis, which I have not pictured here.

27:11

Recurrent pyogenic cholangitis, really

27:14

identified by really dilated intrahepatic

27:16

ducts with filling defects from stones,

27:18

again, which I have not pictured here.

27:22

So, pertaining to this patient,

27:23

here's a follow-up question.

27:26

What are they at increased risk for?

27:29

Read all of your answer choices.

27:39

All right, looks like the majority chose the right

27:41

answer here, which is A, B, and C, meaning cirrhosis,

27:44

cholangiocarcinoma, and gallbladder carcinoma.

27:47

So, I think we are all very much aware of the

27:50

increased risk of cirrhosis and cholangiocarcinoma.

27:52

We see that on a day-to-day basis.

27:55

These patients have a 400 times increased risk

27:57

of cholangiocarcinoma compared to the general population.

28:00

Sometimes, we forget about their

28:01

increased risk of gallbladder cancer.

28:03

They have a lifetime risk of about 3% to 14%,

28:06

which is about 10 times that of the general population.

28:08

So, this patient is at risk for all of these things.

28:16

All right, next case. I'm going

28:18

to give you sequential images.

28:23

What is your best diagnosis here?

28:34

All right, 100% got the right

28:36

answer here, which is, in fact, aspiration.

28:38

What I have given you is basically a

28:40

bronchogram—just massive aspiration.

28:43

You can see that, um, the airways here at the

28:46

lung bases are actually really dilated and

28:47

bronchiectatic, and so this patient's probably

28:49

been chronically aspirating for a while.

28:56

All right, best diagnosis.

29:10

All right.

29:10

The majority here got the correct

29:11

answer, which is, in fact, lymphoma.

29:14

So, when in the mesentery, you're going

29:15

to look for it to encase the vessel.

29:17

So, you can see here that there's

29:18

all this lymphadenopathy that's

29:20

working its way around the vessels.

29:22

That's the sandwich sign.

29:24

And then, also in the retroperitoneum, it will encase

29:27

the aorta and IVC and lift it off of the spine.

29:30

So, very characteristic appearance for lymphoma.

29:39

Next case.

29:41

Look at all of your images.

29:52

It looks like the majority here did get the correct

29:54

answer, which is a lymphangioma, identified by this

29:59

low-density fluid signal mass that is

30:03

conforming and insinuating around the

30:05

existing structures. On ultrasound,

30:08

it has this really characteristic honeycomb appearance,

30:10

and they can be both intraperitoneal or extraperitoneal.

30:13

Lymphoma, mesothelioma, and nodal mets are

30:16

incorrect because those would be much more likely

30:18

to be solid in appearance and have much more

30:21

enhancement on post-contrast CT.

30:30

All right, next case.

30:41

So, we have an even split, but the

30:42

majority did eke out the correct answer

30:44

here, which is a serous cystadenoma.

30:48

So, these are typically honeycomb

30:50

or microcystic in appearance.

30:52

On a contrast-enhanced CT, those really

30:54

tiny honeycombs or microcysts, they can

30:57

look kind of solid around the periphery.

31:00

But on a T2 sequence, you can clearly see

31:04

that these are, in fact, just tiny little cysts with

31:07

these very thin, fine septations throughout it.

31:10

Very occasionally, they can

31:11

be oligocystic or polycystic.

31:13

What I've given here is the much

31:14

more classic microcystic.

31:17

The tip-off here that this is a serous cystadenoma,

31:20

is this central stellate calcification. Ansd so, you can

31:23

see even on the T2 that there's this architecture

31:27

forming here towards this central stellate process.

31:30

And on the CT, you can see that it's all calcification.

31:33

So, when you see this morphology and

31:36

this architecture, it's a very characteristic

31:38

appearance for a serous cystadenoma.

31:41

Mucinous cystic neoplasm is much more likely to

31:43

be unilocular or just a few large cysts.

31:48

A pancreatic neuroendocrine tumor, you'd really

31:50

need to show some sort of hypervascularity

31:51

to confidently make this diagnosis.

31:54

And a SPEN, while they can have calcifications,

31:57

really, this architecture with a central stellate

32:01

calcifications is much more characteristic of a serous cystadenoma.

32:08

Next case.

32:12

Use all of the images.

32:23

All right, looks like the majority did get to the

32:25

correct answer, which is a focal nodular hyperplasia.

32:29

So, as I mentioned earlier, when I'm dealing with these

32:32

questions that have multiple sequences or images,

32:35

I start by identifying each one that I'm looking at.

32:38

So, here we've got a T2.

32:39

We can see that there's a central

32:42

T2-hyperintense scar in the middle, but the,

32:44

the parenchyma of this

32:46

lesion is actually, like, very subtly T2 bright.

32:49

Barely above background liver.

32:52

On this out-of-phase image, which we identify by this

32:55

India ink artifact, there's no intralesional fat in it.

32:59

Here, we have an arterial phase image where

33:00

we see that the majority of it is really

33:02

hypervascular, except for this central scar.

33:05

And then, this is an EOVIST scan, so this is

33:07

a hepatobiliary phase. You can tell because

33:09

there is some retained

33:11

contrast here in the intrahepatic bile ducts.

33:13

You can see that there is uptake

33:15

slightly above that of background liver.

33:18

So, FNH lesions, you can think of them as

33:20

stealth lesions because they're almost

33:22

isointense on T1, T2, and venous phase imaging.

33:26

What tips them off is if you're lucky enough to

33:28

get this central scar, which is T2 bright and has

33:30

very delayed enhancement. And then, the majority of

33:32

the lesion is arterial enhancing, and then there's

33:34

persistent uptake similar to or above that of

33:37

background liver on the delayed hepatobiliary phase.

33:43

Hemangiomas are characterized by peripheral

33:46

discontinuous nodular enhancement,

33:49

and poorly differentiated HCCs and

33:50

metastases really shouldn't have this

33:53

persistent uptake on the hepatobiliary phase.

34:00

All right, next case.

34:02

Best finding, best diagnosis for

34:05

the finding at the yellow arrow.

34:07

Use all of your images.

34:18

All right, looks like the majority of

34:19

you got to the correct answer.

34:21

So, this is in fact a dropped gallstone.

34:26

All right, this is in fact a dropped gallstone.

34:29

So we can see that there is this punctate

34:31

hyperdensity here along the hepatic capsule in

34:33

this patient who has, in fact, had a cholecystectomy.

34:37

This punctate hyperdensity is intrinsically

34:40

T1 bright, so this is a T1 FAT SAT sequence.

34:44

And then, this is a subtraction image.

34:47

You can tell because the fat is almost all the way dark,

34:49

but there is still contrast in the vessels, and you can

34:52

see that there is no enhancement within this lesion.

34:55

So, this is consistent with a dropped gallstone.

34:57

So, when you see this intrinsic T1 hyperintensity,

35:01

that really helps you narrow your differential.

35:03

So you want to think about

35:04

intrinsically T1 bright stuff.

35:05

So, things like subacute blood, cholesterol—like

35:09

cholesterol gallstones, melanin, and proteinaceous debris.

35:14

So dropped gallstones, they tend to

35:15

occur along the hepatic capsule, as well

35:17

as dependent areas in the abdomen.

35:18

So, along the hepatorenal

35:19

recess or the pericolic gutters.

35:22

This is a case of an uncomplicated gallstone, but

35:25

they can develop some pretty significant complications,

35:27

including inflammation, abscess, and fistula.

35:32

Good job on this case, guys.

35:34

Let's do the next one.

35:39

Read all of your answer choices.

35:50

All right.

35:51

And it looks like the majority of patients did,

35:53

or the majority of students did, in fact, get to

35:56

the correct answer, which is "any of the above."

35:58

So, what this question is getting at is,

36:00

what is your differential for linitis plastica?

36:03

So, here we can see that the stomach wall is

36:06

diffusely thickened, and we've got complete

36:08

loss of the normal gastric fold pattern.

36:10

So, this is very characteristic of linitis plastica.

36:14

So, what can cause linitis plastica?

36:17

Well, you can have a primary adenocarcinoma, like a

36:19

signet ring cell carcinoma, lymphoma, or metastases,

36:24

especially from breast, can cause this appearance.

36:27

So, any of these things can cause a linitis

36:30

plastica appearance, and you just needed

36:31

to recognize this, this, um, appearance.

36:40

All right, next case.

36:41

This is part one.

36:44

There will be two parts.

36:56

It looks like we have an even split.

36:59

Let's do the second part.

37:01

And then we will come back and

37:02

talk about the correct answer.

37:15

Good.

37:15

Okay.

37:17

So, let's talk about the correct answer to the first one.

37:19

So, this post-liver transplant ultrasound.

37:22

So, let's look at what we are actually presented with.

37:27

So, we are given the prior exam,

37:29

which was four days post-transplant.

37:31

You can see on this exam, we did have a normal or a

37:36

nearly normal arterial waveform where we have a clear

37:38

systolic peak tapering off towards end-diastole.

37:43

On the current exam, which is two days later,

37:45

or six days post-transplant, you can see that

37:48

we've lost that normal arterial waveform.

37:51

That is a very concerning finding in the early post-

37:53

operative period, and you must interrogate that quickly.

37:58

So, really what you're left with is, um,

38:00

a CT angiography or an MR angiography.

38:03

And between those two options, a CT angiography

38:05

is much faster, um, and is, um, much more

38:08

practical for a very sick post-transplant patient.

38:11

It is inappropriate to wait 24 hours on this exam.

38:15

Um, this is clearly a change and a

38:17

loss of a normal arterial waveform.

38:18

And that is very concerning, um,

38:20

for acute arterial pathology.

38:22

Do not leave this alone.

38:24

Um, if you do no further follow-up,

38:27

um, you really haven't interrogated

38:29

what's going on with the artery.

38:33

So, here I've given you the CT angiography.

38:37

And this shows that there is, um,

38:39

an early hepatic artery thrombosis.

38:40

So, you can see that there is a

38:41

cutoff of the celiac artery here.

38:45

And then you can even see that there's

38:47

really no, um, contrast-enhanced vasculature,

38:51

no contrast-enhanced artery, um, anywhere

38:53

along the length of the porta hepatis here.

38:56

Early hepatic artery thrombosis is really the most

38:58

feared complication because it has a very high

39:00

morbidity and mortality in the early postoperative

39:02

appearance— in the early postoperative period.

39:05

So, in ultrasound, you're really looking

39:07

for this loss of waveform, like I showed

39:09

you in the first part of this case.

39:12

So, typically, it starts out with a high resistive

39:13

index, which can be really hard to differentiate

39:16

from just, like, early postoperative edema,

39:18

but then it progresses to slow flow and parvus tardus,

39:21

and eventually loss of flow, which is what we

39:23

were seeing on that six-day post-op ultrasound.

39:28

So the next steps, depending on your

39:30

institution, will either be CT angio,

39:34

catheter angio, or straight to surgery.

39:36

That depends on the clinical picture

39:38

and your institutional practice.

39:44

All right, next case.

39:47

Oh, I wanted to show you one quick thing.

39:48

So one of the distractors here is a late

39:50

hepatic artery thrombosis. Um, it doesn't fit the

39:52

early post-op time period that I've given you.

39:54

And also, um, this often develops,

39:56

um, slowly and over time.

39:58

And so you'd be much more likely to see

39:59

collateral vessels, which we don't see here.

40:05

All right.

40:08

Next case.

40:10

Take a close look at the image.

40:21

All right.

40:21

Looks like the majority of

40:22

people got this answer correct.

40:24

Um, so the correct answer here

40:26

is gastroesophageal reflux.

40:27

This is a case of feline esophagus, and that's really

40:31

where you get this very striped appearance with these

40:33

very thin, one- to two-millimeter circumferential folds

40:36

that involve the lower, um, two-thirds of the esophagus.

40:39

And they're very transient when you

40:41

are, um, doing fluoroscopy in real time.

40:45

Uh, these are associated with gastroesophageal reflux.

40:49

So are the other answers incorrect?

40:50

Well, CMV is really identified by large, flat ulcers.

40:54

Candida has these discrete, small, shaggy plaques.

40:57

And then scleroderma has this, um, distal dilation

41:00

and poor emptying of the lower esophagus.

41:06

All right.

41:06

Next case.

41:09

Best diagnosis for the CT finding at the arrow.

41:20

All right.

41:21

It looks like we had sort of an— we weren't sure here.

41:24

Um, so, uh, the correct answer

41:26

here is actually focal fat, and so,

41:31

um, I've given you an in-phase and out-of-phase

41:33

sequence, and you can see that there's, um,

41:34

loss of the signal here between the in-phase

41:37

and the out-of-phase, and that accounts for

41:39

the hypodensity that's in the pancreatic head.

41:43

And we go back and we look at this T2

41:45

sequence and really see there's not really any

41:47

pancreatic parenchymal or peripancreatic edema here.

41:51

Um, and there is preserved, um, normal

41:53

intrinsic T1 signal hyperintensity

41:56

in this part of the pancreatic head.

41:57

So groove pancreatitis, autoimmune pancreatitis, and

42:01

pancreatic adenocarcinoma would not fit that appearance.

42:04

For autoimmune pancreatitis, groove

42:06

pancreatitis, you really expect to see some

42:08

T2 signal, and pancreatic adenocarcinoma,

42:11

you'd expect to see loss of

42:12

the normal T1 hyperintensity.

42:15

But the in-phase and out-of-phase images here really

42:17

seal the deal, particularly this area here

42:19

where you can see that there's loss of signal.

42:29

All right, next case.

42:31

Best diagnosis.

42:41

All right, looks like the majority

42:42

here did get the correct answer.

42:44

And so that is von Hippel-Lindau, um,

42:50

uh, von Hippel-Lindau.

42:51

So VHL in the abdomen.

42:52

Think about pancreatic and hepatic cysts.

42:55

In particular, this nearly complete cystic replacement

42:58

of the pancreas is very characteristic of VHL.

43:01

You can also get pancreatic serous cystadenomas,

43:03

pancreatic neuroendocrine tumors, and renal cell

43:06

carcinomas, which I've shown you here. I've given you

43:08

a picture of a mixed cystic and solid enhancing, uh,

43:11

renal mass, um, to help sort of tip us off that

43:14

we are dealing with a syndrome here of VHL rather than

43:17

other, uh, other types of isolated pancreatic cysts.

43:28

All right.

43:29

Best diagnosis in this patient with

43:32

a remote history of gastric sleeve.

43:44

All right.

43:44

Looks like the majority did get this correct.

43:46

So this is a case of atrophic gastritis.

43:49

You can see that there is complete

43:50

loss of the normal gastric folds.

43:53

When you see this complete loss of normal gastric folds,

43:55

there's really two things you want to think about.

43:57

A late-stage atrophic gastritis,

44:00

as well as linitis plastica.

44:02

So why are the other answers incorrect?

44:04

Well, while this tubular configuration is, um, is

44:09

characteristic of a post-gastric sleeve patient,

44:12

you should have normal gastric

44:14

folds, even after a gastric sleeve.

44:16

This patient does not have normal gastric folds.

44:19

Zollinger-Ellison syndrome

44:21

should have hyperplastic folds.

44:24

This patient's folds are completely gone.

44:26

And then a gastric stricture, while a known

44:27

complication of a gastric sleeve, is not pictured

44:30

here. Usually, that's, um, a short segment

44:32

involving the mid or distal pouch.

44:37

So this brings us to the end.

44:38

Here's a quick summary of all the diagnoses

44:40

that we have seen, um, and I've given you a

44:43

pretty, uh, wide-ranging distribution across

44:46

the gastrointestinal imaging, um, mimicking the

44:50

distribution that the ABR has for their blueprints.

44:53

I'm going to stick around to go over any questions

44:55

that you have about any of the cases that we've seen.

44:57

I hope that this was useful and that you got

44:59

to see a lot of different types of cases.

45:03

Thank you very much for joining.

45:05

And please give feedback on this session.

45:07

Thank you.

45:09

Thank you so much, Dr. Brickmeyer.

45:10

901 00:45:10,480 --> 00:45:11,550 That was great.

45:11

You got through so many cases.

45:14

Um, if people have questions, please go

45:15

ahead and put those into the Q& A box.

45:18

And I think there's one in there already.

45:20

Could you please repeat the MR pattern for blood?

45:23

Sure.

45:25

So, um, so think about an endometrioma, right?

45:28

Subacute blood, you're going to see intrinsic

45:30

T1 hyperintensity and, like this, T2 shading.

45:33

So that's exactly what's going on here.

45:35

T1 bright, mild T2 shading.

45:40

It's like an endometrioma, but

45:41

it's, it's in the duodenum.

45:43

And it's just because it's a hematoma.

45:45

And so this is a process that happens

45:46

as the blood starts to break down.

45:48

And so it's part of a sort of subacute process.

45:53

So, T1 hyperintensity—please have a differential

45:55

ready to go for intrinsically T1 bright stuff.

45:58

Subacute blood, cholesterol,

46:01

melanin, proteinaceous debris.

46:06

You covered everything then.

46:07

No questions.

46:09

Sounds good.

46:09

All right.

46:10

Well, please fill out feedback on this session.

46:12

Um, and thank you very much for attending.

46:14

Thank you so much, Dr. Brookmeyer, and for everyone

46:17

else for participating and attending, of course.

46:19

Um, you can access the recording of today's case review.

46:23

We will be sending that via email in a couple of days,

46:25

so be on the lookout for that.

46:27

Be sure to join us Wednesday,

46:28

May 8th, with Dr. Judy Squires.

46:30

She'll lead us in a rapid review

46:31

of pediatric imaging cases.

46:33

You can register for that on our website,

46:36

or in that email we'll send, or follow social

46:39

media for updates on future case reviews.

46:42

Thanks again for learning with us,

46:43

and we will see you soon.