0:02

Hello and welcome to Case Crunch rapid case

0:04

review for the core exam hosted by Medality.

0:08

In this rapid-fire format, faculty will show

0:10

key images, and you'll respond with the most

0:12

likely diagnosis via the live polling feature.

0:15

After a quick answer explanation,

0:17

it's on to the next case.

0:19

You'll be able to access a recording of today's

0:21

case review and previous case reviews by creating

0:24

a free account using the link provided in the chat.

0:27

Today, we are honored to welcome Dr. Navid

0:29

Faraji for an MSK board prep case review.

0:32

Dr. Faraji is an MSK radiologist and passionate

0:35

educator at University Hospitals in Cleveland, Ohio.

0:38

He's the Director of Medical Education in the

0:40

Department of Radiology and Associate Program

0:42

Director of the Diagnostic Radiology Residency.

0:45

As well, he's an assistant professor in the

0:47

Division of MSK Radiology and is heavily involved

0:50

in educating medical students in radiologic anatomy.

0:54

Questions will be covered at the end if time allows.

0:56

Please remember to use the Q&A

0:58

feature to submit your questions.

1:00

And with that, we are ready

1:01

to begin today's board review.

1:03

Dr. Faraji, please take it from here.

1:06

So first things first, I'd like to get a gauge of

1:10

who we have here in the audience to take part in

1:14

this lovely occasion we are gathered here today.

1:16

So, um, if you wouldn't mind,

1:18

yeah, just answering this question.

1:20

Are you a resident, attending,

1:22

just here for the cases, or other?

1:36

Survey says, all right, 46%

1:39

residents and some other results.

1:41

All right, cool.

1:42

So, let's get this party started.

1:44

Um, as mentioned, I'm Navid Faragi, MSK rad

1:47

here in Case Western/University Hospitals.

1:51

I have nothing to disclose other than I just ate dinner,

1:54

and, um, hopefully, I don't have anything in my teeth.

1:58

So, let's get started.

1:59

I just want to preface this, is that I made

2:03

some of these questions somewhat challenging.

2:06

And because it is my impression that

2:09

this potential upcoming examination that

2:12

you may or may not have is not tailored

2:15

to assess whether you are good at memorizing

2:17

facts, but rather, can you differentiate pathology—

2:22

various types of pathology that may look similar?

2:24

And what sort of clues and information

2:26

can you use to differentiate those things?

2:27

So, we're gonna try to go through that together.

2:29

And, um, yeah, let's have at it.

2:32

Have at it.

2:33

Um, just a brief distribution of the

2:35

topics per the ABR guide, most recent

2:37

came out in 2021, that I could find at least.

2:40

Um, so we got 20 questions today, and it's gonna

2:42

be generally in this distribution, um, to,

2:46

to somewhat, uh, kind of mirror the examination.

2:52

Okay.

2:52

So, this is gonna be a multi-image question.

2:55

I'm gonna give you a moment to take a look.

2:56

See, look at this one.

2:59

Okay.

3:00

And I can zoom in on things, but take a look.

3:02

Maybe here's a closer view.

3:05

If needed.

3:12

Here are some more images.

3:14

And, you know, if I were you, I'd be asking

3:16

myself, what sequences am I looking at?

3:18

So I can better understand what's happening, right?

3:20

So, every time you take a case, you should be asking

3:23

yourself, what sequences you're looking at?

3:25

Because various sequences are going to

3:27

give you varying pieces of information.

3:29

We can see fluid is bright on this one.

3:31

Fluid is dark on this one.

3:32

There's some bright synovial

3:34

enhancement or hyperintense.

3:35

Synovial enhancement so we can infer from that information that this is

3:40

and this is a T2 fat-suppressed coronal image.

3:45

Okay, what is the most likely diagnosis?

4:00

All right.

4:00

52% of folks said Milwaukee

4:04

shoulder. Septic arthritis was close second at 33%.

4:07

90 00:04:09,089 --> 00:04:10,080 And, yeah, I would agree.

4:10

So, this is Milwaukee shoulder.

4:12

And the key is, if we go back to these images, you know,

4:14

septic arthritis could have a very similar appearance.

4:17

Um, but when you couple this with the radiographic

4:22

appearance of mineralization in the region of the

4:24

greater tuberosity/rotator cuff, you know, the

4:27

best answer is probably Milwaukee shoulder.

4:30

In my view, we can also see that there's loss

4:33

of articular cartilage, some destruction, and

4:35

flattening of the subchondral bone plate

4:37

loss of sphericity.

4:38

We also see some associated rotator cuff tearing.

4:40

I mean, you could see some of those

4:42

things in septic arthritis, but the, um,

4:46

mineralization in the region of the rotator

4:47

cuff would suggest Milwaukee shoulder.

4:51

Um, neuropathic arthropathy is a possibility,

4:56

but it tends to be a little bit more

4:57

destructive, and they might give you something

5:01

that leans you toward some cervical spine

5:03

disease and suggests a cervical spondylosis.

5:06

All of those entities could look very similar, and

5:08

they would hopefully, on a test, have to give you

5:10

some sort of clue to help you differentiate them.

5:13

On this particular question, that was the radiographic

5:15

appearance with some mineralization in the rotator cuff.

5:22

Okay.

5:25

Here's another radiograph.

5:30

What is the most likely clinical

5:33

history in this patient?

5:47

17-year-old weightlifter, 83%.

5:49

Okay, I guess I made this one too easy.

5:51

Um, yeah, well done, everybody.

5:53

So, um, the main imaging finding here is

5:57

that we have fraying of the distal clavicle.

6:00

We have resorption, subchondral resorptive changes,

6:03

loss of the subchondral bone plate definition.

6:06

And so here we can see this, uh, radiographic

6:09

appearance with some, you know, focal linear

6:12

hyperdensity, which is our subcortical bone,

6:14

and we can see that that definition is lost here.

6:16

And we can see these kinds of resorptive changes

6:19

that are isolated to the distal clavicle.

6:21

It looks like a relatively young patient, you know,

6:24

so these other questions, uh, other answer choices,

6:27

what, 17-year-old intermittent fever? Maybe that

6:29

would be like a JIA-type situation, but that

6:32

should probably involve both sides of the joint,

6:34

rather than one. Hyperuricemia would suggest gout,

6:38

um, and again, this is not a classic location for

6:41

gout, and there's no adjacent soft tissue prominence.

6:44

And again, it's also, it's not like a, um,

6:48

juxta-articular erosion, but rather it's subchondral.

6:51

17-year-old weightlifter, we can see some

6:53

distal clavicular osteolysis is the entity here.

6:57

We can see that there's distal clavicular marrow

6:59

edema, some loss of the definition of the subchondral

7:02

bone, and this can be seen in the setting of chronic,

7:05

repetitive microtrauma, which is commonly seen in

7:08

weightlifters, bench pressing, things like that.

7:11

In addition, someone who had a trauma to the

7:14

distal clavicle or acromioclavicular joint can have

7:17

disappearance subsequently in the subacute or chronic

7:21

phase rather than an acute, traumatic-like AC joint

7:24

sprain. If it's isolated to the distal clavicle,

7:26

it's most likely to be distal clavicular osteolysis.

7:29

Rib pain—some patients can get stress fractures

7:31

of the ribs or stress reaction, commonly seen

7:33

in swimmers, which we don't see on this image.

7:38

Okay, next question.

7:40

I'm just going to give you the big pic

7:42

here, and then we'll go to the smaller pic.

7:45

So, what is the most likely associated

7:47

additional imaging abnormality?

7:49

166 00:08:03,185 --> 00:08:07,444 Okay. 50% syndesmophytes, 29% MCP erosions,

8:07

and then Morel-Lavallée lesion at 14%.

8:11

So, okay, yeah, this one is, um, we can see that there's

8:15

bilateral greater trochanteric marrow edema, which is at

8:19

the insertion of our gluteal tendons, minimus and medius.

8:22

Um, similarly, we just see a little bit of

8:24

marrow edema of the acetabulum, um, here on

8:28

the left and maybe some minimal on the right.

8:30

But the main thing is that

8:32

these areas, um, of subinsertional

8:36

marrow edema is called enthesitis and can

8:39

be seen in, like, spondyloarthropathies, such as

8:42

ankylosing spondylitis or psoriasis,

8:46

um, or, you know, inflammatory bowel

8:49

disease-related arthropathies.

8:51

And so, you may see them at the ischial

8:53

tuberosities, at the origin of tendons.

8:55

You can see them at the lesser trochs, you can

8:57

see them at AIIS, or anywhere that a tendon is

9:00

originating or inserting, is called enthesitis.

9:03

And so, MCP erosions would most likely be

9:06

seen in the setting of rheumatoid

9:08

arthritis, is the classic, and is not

9:11

commonly associated, it's less commonly at least associated

9:13

with this finding of enthesitis.

9:16

And syndesmophytes is what we see here, where there

9:20

are thin, linear ossifications between

9:24

the intervertebral bodies, thought to be

9:27

ossification of the ALL (anterior longitudinal

9:29

ligament) and/or annulus fibrosus. They're not

9:32

big, bulky osteophytes like you might see in DISH.

9:35

So, multilevel bridging osteophytes is indicative

9:37

of diffuse idiopathic skeletal hyperostosis (DISH).

9:40

In this case, they're very thin and

9:43

most indicative of syndesmophytes, which is

9:45

what we might see in ankylosing spondylitis.

9:48

Morel-Lavallée lesion would be more of

9:51

a post-traumatic thing if we thought this person

9:53

had trauma and maybe they had a shearing injury

9:57

or a degloving injury from the, um, across the

10:00

myofascial plane, of the superficial myofascial plane.

10:03

You can get fluid collections there.

10:06

A classic scenario is someone

10:07

being tossed off a motorcycle.

10:09

So, that's the various pathologies that might

10:12

be associated with these answer choices.

10:15

And the best answer choice is syndesmophytes and

10:17

someone who might have ankylosing spondylitis.

10:19

Another thing they could show you is

10:20

like, you know, some of these patients

10:23

get other systemic manifestations.

10:25

So, ankylosing spondylitis patients can get apical fibrocystic

10:28

changes on a chest X-ray, for example, so just

10:32

be aware of, um, multisystem pathology that can

10:36

occur in these various patient presentations.

10:40

Okay, here is another case.

10:43

I put some arrows there because the imaging findings

10:46

are somewhat not conspicuous, so in order to avoid

10:50

any confusion, the arrows is where I'm suggesting

10:53

that there is abnormally increased T2 signal.

10:59

And so, arrows aren't here,

11:00

but again, it's here and here.

11:01

So, what is the most likely etiology?

11:17

Survey says.

11:18

Okay.

11:19

Nice.

11:20

All right.

11:21

So, relatively even distribution, which can mean

11:25

that this is a terrible question and that the

11:27

imaging findings aren't great, but, or it could

11:30

mean that it's a good, difficult question, I hope.

11:35

Um, but okay.

11:36

So, we see edema here in the infraspinatus

11:40

region.

11:41

Okay.

11:42

And in the deltoid.

11:44

All right.

11:44

Um, this is subscap. Again, supraspinatus, infraspinatus, teres minor.

11:45

245 00:11:49,220 --> 00:11:50,960 That's how I would separate these.

11:50

Um, and so this is anterior, this is posterior, supraspinatus,

11:54

infraspinatus, teres minor, subscap.

11:57

Okay.

11:58

And here's the deltoid, which

12:00

originates from the acromion process.

12:01

And we can see

12:03

edema that's relatively diffuse and not feathery.

12:06

Okay, so feathery edema is indicative of muscle

12:09

strains, but kind of diffuse-like edema that

12:13

doesn't seem to have fluid insinuating between

12:16

muscle fibers and stuff is most indicative of

12:18

denervation or subacute denervation change.

12:21

And so, you know, we can have various patterns

12:24

of denervation in the shoulder that can result

12:28

from various nerve distribution pathology, right?

12:30

So let's just take these one by one.

12:32

A cyst in the spinoglenoid notch.

12:35

Okay, or a cyst in the suprascapular notch.

12:38

Okay.

12:39

So both of these areas is where

12:41

the suprascapular nerve goes.

12:43

All right.

12:43

So the suprascapular nerve, proximally,

12:47

it can be impinged on the suprascapular

12:49

notch and then distally, in this general area,

12:51

is where the spinal glenoid notches.

12:54

Okay?

12:55

And so, at the level of the suprascapular

12:57

notch, because that's proximal, it has not yet

12:59

innervated the supraspinatus or infraspinatus.

13:02

Okay?

13:02

So, if there were a cyst there impinging the

13:05

suprascapular nerve and the suprascapular notch,

13:07

we would, suggest, we would expect to see

13:09

supraspinatus and infraspinatus denervation changes.

13:13

Um, so that's not the setting here because

13:16

we only see infraspinatus and deltoid.

13:19

So, spinal glenoid notch, the supraspinatus

13:22

is also—has already been innervated.

13:24

So, we would expect to see isolated infraspinatus

13:28

muscle edema or atrophy.

13:31

So, suprascapular notches—

13:33

again, it's more proximal.

13:34

You'd see supra and infra, spinal glenoid notch

13:36

is more deltoid, is more distal on—

13:38

I'm sorry.

13:39

It's more distal.

13:40

So, the supraspinatus has already been innervated, and

13:44

infraspinatus would have the denervation change.

13:46

Fibrous bands in the quadrilateral or

13:48

quadrangular space is in this general area.

13:51

That's where your axillary nerve is, and the axillary

13:54

nerve innervates the deltoid and the teres minor.

13:57

But we're saying teres minor is spared here.

14:00

And therefore, the best answer is the brachial

14:03

plexitis, which is also known as Parsonage-Turner

14:07

syndrome, which is—I'm not sure what causes it.

14:09

It's thought to be post-viral, similar to Bell's palsy,

14:12

where basically you have multifocal denervation changes

14:17

that does not match a single nerve distribution.

14:21

So, since we have deltoid and infraspinatus here,

14:24

it doesn't match the nerve distribution and part of

14:27

the heterogeneity of the answers may be

14:29

because it's not the best imaging example,

14:32

but that's why I tried to give you the arrows.

14:33

So, hopefully, at least going through this

14:35

process together has provided you with some

14:37

informative, uh, feedback to get this answer

14:41

right on a future patient or examination.

14:46

Brachial plexitis.

14:48

Okay, here's another patient.

14:52

One clue, um, on the examination is that

14:57

if they're giving a specific MRI sequence

15:00

that highlights specific types of tissue,

15:03

the abnormality is likely to be, you know, more

15:08

indicative of a pathology involving that tissue.

15:12

But don't let that lead you astray.

15:14

Just look at the pictures.

15:15

Tell me what you think.

15:29

Survey says: Osseous middle subtalar coalition.

15:33

Well done, team.

15:35

Okay.

15:35

Better question.

15:37

So, one, we can see that this is at least the fat

15:40

sensitive sequence, probably T1, because we don't see

15:43

any bright fluid signal intensity within the joint.

15:46

And we can see that this is our talus, and this

15:49

is our calcaneus, and then there is continuity

15:52

of the marrow between the calcaneus and the

15:54

talus, uh, indicative of a subtalar coalition.

15:58

Here, we can see the sustentaculum tali, also

16:01

continuous with the talus marrow, and similarly here.

16:05

Um, we can see the talus and calcaneus

16:07

with continuity of the marrow there.

16:08

That is indicative of an osseous

16:10

coalition in the subtalar region.

16:13

And then the next part of the question is kind of

16:15

saying, do you know the anatomy of the subtalar joint?

16:18

And this is where the middle facet of the subtalar

16:20

joint would be, which is the most common area

16:23

for these coalitions to arise.

16:26

The posterior facet is a little bit more

16:27

posterior and not depicted well here.

16:29

Similarly, the anterior facet is not depicted

16:31

well here, but on a sagittal plane, it would

16:33

be in this general area where the anterior process

16:35

of the calcaneus is, which we don't see.

16:37

So, this question is supposed to test, um,

16:40

whether you can identify continuity of the

16:42

marrow between two bony structures and then

16:44

also, um, identify the subtalar anatomy.

16:51

And subtalar joint is the same thing

16:53

as saying the talocalcaneal joint.

16:56

And here's what this would look

16:57

like in radiographic appearance.

16:58

We can see the talar beaking, and we can see our

17:01

C sign, which is continuity of this talar dome.

17:06

And then this region, sustentaculum tali.

17:09

And then we can see that there's continuity,

17:11

um, here, which usually there is some disruption

17:15

and lucency in this region, but this is

17:16

continuous and looks like a backward C.

17:22

Okay, next question.

17:24

Next patient.

17:27

This is a hip.

17:31

What is the next best step in management?

17:45

Contralateral imaging.

17:48

I had a typo, but I fixed it.

17:50

Um, so here it is.

17:51

Yes, contralateral imaging would be the answer choice.

17:55

We can see here that here's the femur,

17:58

and we can see in the lateral cortex.

18:00

If we trace it down, that there is this cortical bump,

18:02

and you can even hallucinate a little bit of lucency there.

18:05

If I zoom in,

18:07

maybe there's a linear lucency, and that is

18:08

indicative of a bisphosphonate-associated fracture.

18:13

Um, and these can be commonly bilateral.

18:15

So we see here in that same patient

18:18

that there is bilateral fractures

18:21

associated with bisphosphonate use. And—

18:24

Key thing here is you don't want to pay—

18:26

you don't have to fix one side, have the patient

18:27

walk out of the hospital,

18:29

and then fracture through the other side.

18:30

So we need to suggest this.

18:32

Usually, these will get prophylactically fixed

18:35

with an intramedullary nail due to the, uh,

18:40

morbidity and mortality associated with femoral

18:42

fractures in this patient age population.

18:46

One of these days, um, they are going to

18:51

ask, instead of bisphosphonate, I think

18:54

they're going to ask about another drug,

18:56

that can cause this, um, which is denosumab.

19:00

Um, so that is another drug that can cause this.

19:04

It is used for similar purposes,

19:07

um, but it can also, yeah, cause the

19:10

same thing, just a different, um, path—

19:13

pathway in causing this abnormality.

19:15

So, denosumab is another possible, um, answer choice

19:21

if they ask you about drugs that can cause this.

19:24

Okay.

19:25

This is a wrist.

19:27

So if you're ever taking case conference at, um,

19:30

your hospital, your residency program, always

19:32

start like, what views, what is the anatomy?

19:35

What is the modality? That gives you time

19:37

to think about what you want to say next.

19:39

But these are the easiest, low-hanging fruits,

19:41

and it's actually a good thing to

19:42

get in the habit of starting with.

19:46

So you can really—particularly when you

19:47

get to M.R.—you can start figuring out

19:50

what these sequences are showing you.

19:52

So I highly recommend that.

19:54

Okay.

19:56

Damage of which structure can result

19:58

in the given radiographic abnormality?

20:14

Survey says scapholunate ligament

20:17

or lunotriquetral ligament.

20:19

Okay, that is correct.

20:21

Scapholunate ligament is the answer.

20:23

One, we can see widening of the scapholunate

20:25

interval, also known as the Terry-Thomas sign, who

20:28

was a British comedian, I'm told, although I'd never

20:30

heard of him until I became a radiology resident.

20:34

I think

20:35

more accurately, we should use the, at least,

20:37

more modern-day should be the Michael Strahan

20:39

sign, who is the next most popular person

20:42

I know with a gap tooth in his front teeth.

20:45

Uh, we can see that there's widening of the scapholunate

20:47

interval, there's proximal migration of the capitate,

20:50

and it's beginning to insinuate between these two

20:53

bones, and that is called a SLAC wrist deformity,

20:56

which stands for scapholunate advanced collapse.

20:59

The lateral view, we can see that there's

21:02

beginning to have some dorsal tilt of the lunate, which is

21:05

indicative of—so this is the reminiscence of the lunate.

21:07

Its half-moon shape,, it should be facing straight up,

21:10

but here, it's tilted dorsally.

21:12

And that's indicative of dorsal

21:13

intercalated segmental instability.

21:17

Um, the scapholunate angle should

21:20

be between thirty and sixty.

21:22

Um, and—

21:24

So, the thing to know is that the lunate is

21:27

an innocent bystander in all of this, okay?

21:29

It does whatever the scapholunate and

21:31

lunotriquetral ligaments make it do.

21:34

The lunotriquetral ligament is

21:35

rarely torn, but it can be torn.

21:37

Um, so if the scapholunate ligament is

21:40

torn here, which I agree with you guys

21:42

if that's the answer, then what happens?

21:44

So, the lunotriquetral ligament forces predominate.

21:48

And so we can infer from that information that

21:50

the lunotriquetral ligament causes dorsal, um—

21:55

dorsal, uh, effect on the lunate, so it tilts

21:59

dorsally when the scapholunate ligament is torn.

22:01

In contrast, if the scapholunate ligament is

22:03

intact and the lunotriquetral ligament is torn, the

22:06

the lunate starts to tilt volarly, um, because of that

22:10

traction, and that's called volar

22:12

intercalated segmental instability, or VISI.

22:15

So, the biomechanics here is that the

22:17

lunate just does whatever it's told.

22:19

Um, and whichever of these two is

22:23

intact is going to be the predominating force.

22:27

Um, the other one that's torn

22:28

is going to lose its effect.

22:29

But when everything is intact, then it sits

22:32

neutrally in its upward position like a good lunate.

22:36

Um, TFCC is a little meniscoid or

22:38

fibrocartilaginous structure here that

22:40

cushions the ulna against the carpus.

22:43

It can be torn, sending off ulnar-positive

22:45

variance, let's say an ulnocarpal impaction.

22:48

Um, but not in this particular case.

22:56

This is one of my favorite cases of all time,

23:00

except for one that I had recently that has a similar

23:02

pathology, but I didn't put it in the presentation.

23:06

Here's images.

23:11

Okay.

23:12

What are the abnormalities on the images

23:14

associated with which structure?

23:29

Nice.

23:29

Okay, great.

23:32

4% got it right.

23:33

And I feel like this is just a tough question,

23:36

um, but not a bad question. We're gonna talk about it.

23:39

Right.

23:39

So.

23:40

Right.

23:41

This is the, um, Guyon's canal, right?

23:44

So, um, where we have the ulnar artery, we have

23:47

the ulnar nerve and paired veins in that region.

23:51

And in this case, we see a T2 hyperintense

23:53

mass in the region of, uh, I guess it's a

23:58

little bit distal to Guyon's canal, but,

24:00

um, we see this mass and it has a peripheral low

24:04

signal intensity rim, and the key here

24:08

to differentiate all of these three

24:09

structures are in this region.

24:11

Um, all of these, you know, the median

24:13

nerve is in the carpal tunnel, so it

24:14

would not be in this particular area.

24:17

Um, it's probably right here, but

24:18

sorry for the poor image quality.

24:20

But the key here is that this mass has this

24:24

artifact going in and out of the plane of the image.

24:27

We can see it here,

24:28

nicely associated with this mass.

24:31

And here it is less conspicuous, but the low signal

24:35

intensity tubular structure going into this mass,

24:38

both on the sagittal and coronal planes, also

24:41

suggests an association with an artery and flow void.

24:44

And then the pulsation artifact really confirms

24:46

that this is a pulsatile arterial structure.

24:49

And so this is a pseudoaneurysm of the ulnar artery,

24:53

also known as hypothenar hammer syndrome. And the

24:56

clinical history might be a construction worker or

24:59

someone who works with their hands, with like a chronic

25:01

repetitive traumatic injury to that wrist region,

25:05

can cause an ulnar artery pseudoaneurysm, also known as

25:08

hypothenar hammer. You may say this is an IR case, but

25:12

I saw it as a musculoskeletal radiologist, and so do

25:15

not ignore artifacts that give you information.

25:18

And so, if you're having trouble with a question, just see

25:21

if there's any piece of information that you may be

25:24

missing, and it might be an artifact that can help you.

25:27

I just saw a case where there was a patient who had

25:30

a big femoral hematoma, um, and they were wondering

25:34

if it was like a neoplasm, a hemorrhagic neoplasm.

25:38

But it happened to be that there was the same pulsatile

25:40

artifact in there, embedded in this hematoma.

25:43

There was a big—there was a pseudoaneurysm

25:44

resulting from the surgical fixation.

25:47

So, um, yeah, do not forget about artifacts to

25:49

help you differentiate various types of pathology.

25:52

And in this case, anatomy.

25:58

Here's what you might see—an ultrasound or yin-

26:00

yang sign and a to-and-fro flow on spectral

26:03

Doppler due to turbulent flow within that structure.

26:06

Alright, we're halfway there.

26:09

Um, I think that's a song.

26:13

Okay, here is the images.

26:17

Here's a positive arrow sign in

26:18

case you can't see the abnormality.

26:20

I windowed it heavily and I gave an arrow,

26:22

but don't expect that on the test.

26:24

But hopefully, that'll give you a better image.

26:28

Which examination would be useful for confirmation?

26:43

Survey says MRI wrist.

26:46

Agree.

26:47

So we can see that there's sclerosis of the

26:49

lunate. Incidentally—or not so incidentally—

26:52

there's ulnar negative variance, which has an

26:55

association with this particular pathology.

26:57

Not everybody, most people with ulnar

26:59

negative variants are not going to have,

27:01

um, osteonecrosis of the lunate, a.k.a. Kienbock's disease.

27:03

569 00:27:03,485 --> 00:27:03,495

27:03

571 00:27:05,015 --> 00:27:08,159 Um, but there is some sort of association

27:08

between Kienbock's and ulnar negative variance.

27:10

We can see on the MRI, we would expect to see T2

27:13

hyperintensity, which is nonspecific, but it's

27:16

the relatively confluent loss of T1 signal that

27:19

is most indicative of osteonecrosis of the lunate.

27:22

Similar findings if they give you a scaphoid

27:24

fracture, for example, the proximal pole.

27:27

If it had confluent T1 hypointense signal, that would

27:30

suggest avascular necrosis because, as we know,

27:33

the perfusion or the arterial structures that feed

27:37

the scaphoid go from the distal pole proximally, and

27:40

so if you have a waist fracture, you have loss of

27:43

the blood flow to the proximal pole, and that

27:46

can lead to avascular necrosis, which would appear

27:49

similar, just in a different bone in a different case.

27:53

Here's that CFCC we talked about.

27:56

And so, MRI would be confirmatory.

27:59

CT is not going to add much value.

28:00

It's just going to show you it's sclerotic.

28:02

Yes, if it is, it can help,

28:03

but it's not super sensitive.

28:05

Bone scan—not super useful in this particular case.

28:09

Bone age—not particularly useful in this case.

28:15

Okay.

28:16

Hands.

28:22

What is the best treatment for this pattern of disease?

28:38

Survey says 64%

28:40

And says/conservative— 24% DMARDs and

28:45

biologics— 12% Nobody wants to do distal

28:47

interphalangeal arthroplasty for some reason.

28:50

I don't know why.

28:52

Um, but okay, that is correct.

28:54

64% of you got this correct and

28:56

said, um, so let's just talk about general

29:00

diagnosis of hand X-rays when it comes

29:03

to arthritis. Things you want to—

29:05

you want to have a systematic approach.

29:07

My approach is like, what is the distribution, right?

29:10

Is it distal?

29:11

Is it proximal?

29:12

Is it in a classic distribution for osteoarthritis?

29:15

And I would say, in this case, it is a

29:16

classic distribution for osteoarthritis.

29:18

One, we can see some triscaphe and first carpal

29:20

metacarpal degenerative change with productive changes,

29:22

a little bit of sclerosis, and joint space narrowing.

29:25

That's indicative of osteoarthritis.

29:27

Then we can also see the second most

29:28

involved joints of the D.I.P.s—2nd,

29:31

3rd here, and the 2nd, 3rd, and 5th here.

29:36

So, distal interphalangeal, and CMC, and triscaphe—

29:39

very commonly involved joints for osteoarthritis.

29:43

You didn't have to know this here, but we can see

29:46

that there's central erosions, which is our, uh,

29:50

gull-wing deformity here of the 5th D.I.P., for

29:54

example. 2nd D.I.P. here shows it quite nicely.

29:57

So, that combination of central erosion and peripheral

30:02

osteophyte formation and productive change is most

30:05

consistent with erosive osteoarthritis, which is

30:08

generally treated conservatively or with NSAIDs.

30:10

DMARDs and biologics might be given for rheumatoid

30:13

arthritis or other inflammatory arthropathies.

30:17

Rheumatoid arthritis, we kind of touched on

30:18

before, but mostly it's the MCPs and other

30:21

common areas. The ulnar erosions, either the

30:24

styloid process or of the fovea, for example.

30:28

Um, so you want to take a quick look if you're

30:32

about to call something negative or you're

30:33

not sure what's going on. Take a look at the

30:34

ulna; you may see some subtle erosions there.

30:37

Um, so we talked about distribution as one thing, right?

30:40

So MCPs would be more proximal. Diseases are more

30:43

likely to be rheumatoid. But then the other

30:45

thing is, like, is it predominantly productive,

30:48

is it predominantly erosive, or is it both?

30:51

Okay, because that's going to help.

30:52

There's a couple of things that can give you a

30:54

combination of productive and erosive changes.

30:56

One is this.

30:57

The other is psoriatic arthritis.

30:59

Psoriatic arthritis can give you this

31:01

fuzzy periosteal reaction of the DIPs.

31:04

Um, and it can also give you some erosions,

31:07

and it can be markedly destructive.

31:08

You can have ankylosis in psoriatic arthritis.

31:12

I mean, technically, anything can happen

31:13

to anybody, but that is the classic.

31:17

If the patient reads the books, so the two, like, mixed

31:19

productive and erosive ones would be, um,

31:23

uh, this erosive osteoarthritis and psoriatic

31:26

arthritis. But the distribution of psoriatic

31:27

probably might spare the CMCs and triscaphe.

31:31

You might have this fluffy periosteal reaction,

31:33

you might see ankylosis, and you're not going to see

31:35

this gull-wing deformity either because the central

31:38

erosions is classic in erosive osteoarthritis.

31:40

But the pencil-in-cup deformity would be more psoriatic,

31:43

for example, where there's more, like, pointy

31:46

distal or middle phalanges than cupping

31:48

of the distal phalanx.

31:52

Okay, there's a bunch more findings

31:53

associated with those things.

31:55

You can look them up on the interwebs.

31:58

Like this case, relatively subtle but real.

32:04

What is the most likely

32:05

underlying laboratory abnormality?

32:11

That is not actually how I say "laboratory," but

32:15

sometimes I just like to keep it interesting.

32:30

Survey says increased serum PTH.

32:34

Increased ESR, CRP would be the next choice—

32:36

19% and 14% decreased serum PTH.

32:38

So this one would be increased serum PTH.

32:41

I was going for hyperparathyroidism.

32:44

Um, and...

32:46

We can see here that there is relative

32:49

lucency of the ischial tuberosities.

32:52

Inferiorly, they're kind of ragged and indistinct,

32:54

and we don't see, like, a nice cortical margin.

32:57

Similarly, the pubic symphysis is not well seen.

33:00

Similarly, many of you may have perceived that

33:02

the SI joints were relatively wide and indistinct. Um.

33:08

There's a little bit of lucency

33:09

of the femoral heads bilaterally.

33:11

And then the iliac wings, um, also

33:15

relatively—or crest—relatively radiolucent.

33:18

And so this sub-insertional

33:22

resorptive change, or sub, um...

33:26

Subarticular resorptive change, can be

33:29

seen in subligamentous resorptive change.

33:31

All those things can be seen in hyperparathyroidism.

33:34

Um, so increased serum PTH was

33:36

the answer I was going for.

33:38

Increased ESR and CRP is possible if we were just going

33:41

for something like sacroiliitis, but it's unlikely to affect all

33:45

these various areas if it's inflammatory arthropathy.

33:49

Increased WBCs would maybe be seen in

33:51

the setting of, um, like infection.

33:53

But again, this is multifocal, like

33:56

subchondral, subligamentous, subtendinous,

33:59

resorptive changes, which can be seen in

34:01

hyperparathyroidism and decreased serum PTH.

34:03

The clue here is there's two

34:04

answers that contradict each other.

34:06

So it's likely that one of them is correct.

34:09

And in this case, it's increased serum PTH—

34:11

could be primary, could be secondary, depending

34:13

on the patient and their clinical situation.

34:21

I like this case too, actually.

34:26

Okay, these images are not on the next slide.

34:28

So really look at them.

34:30

There's a thing here.

34:32

There's a thing here.

34:34

This looks like some sort of ghost cartoon character,

34:37

but not relevant to the examination here. Here.

34:43

Look at everything else too.

34:44

Maybe there's hidden clues on the image.

34:48

Here's the next image.

34:50

This is a radiograph that's a few months later.

34:53

This is a GRE from the initial MRI.

34:57

Scout.

34:57

GRE Scout.

35:00

I'm kidding.

35:11

Conservative management.

35:12

Well done.

35:13

70% of you, um, got it correct.

35:17

And so, yeah.

35:18

So the answer we were going for

35:20

here is myositis ossificans.

35:23

Okay, so if we look at the MRI, which is the

35:26

way this patient presented initially.

35:27

We see this T2 hyperintense mass within

35:31

the anterior hip musculature, let's say.

35:34

It does kind of have this low signal intensity

35:36

rim, which is confirmed on this gradient echo scan,

35:39

that there's this peripheral low signal intensity,

35:42

which can suggest peripheral mineralization.

35:45

Similarly, the initial radiograph shows this hazy

35:47

mineralization here in this general area, and we can

35:51

see subsequently on the follow-up radiograph that this

35:55

tends to have trabecular markings, maybe some peripheral

35:59

cortication, and begins to resemble mature bone.

36:04

And that's indicative of myositis ossificans, and you

36:07

know, the alternative diagnosis, which is more sinister,

36:11

would be an extraskeletal osteosarcoma if you thought

36:14

this was osteoid matrix. But classically, extraskeletal

36:17

osteosarcoma tends to have central mineralization

36:20

first and then peripherally will mineralize.

36:23

It shouldn't ossify; it would be more

36:24

dense without a trabecular kind of pattern.

36:28

And then the other clue here is this

36:29

patient is an obvious, like, bone former.

36:32

Sometimes patients who are HO formers—it's kind of

36:34

like keloids, for example—some people are

36:37

just more predisposed to having HO or MO and being

36:41

inflammatory bone formers when they're traumatized.

36:44

We can see this AIIS and rectus femoris

36:47

tendon have ossified from prior trauma, which

36:50

can be, you know, clue here in this particular instance.

36:54

Um, so these things would be radiation, neoadjuvant,

36:58

systemic therapy—could be treated— use to treat,

37:01

um, sinister neoplastic etiologies like

37:04

extraskeletal osteosarcoma—whereas conservative

37:06

management, um, for myositis ossificans.

37:09

You don't want to biopsy MO because it can

37:13

look like osteosarcoma histopathologically.

37:16

And you put your, um, you put your pathologist

37:19

in a tricky situation, and, you know, it's not

37:22

unheard of for folks to have had, um, kind of

37:26

amputations and more aggressive surgeries for

37:29

MO that was biopsied and thought to be osteosarcoma.

37:33

So, biopsy would not be a good next

37:36

best step for this particular patient.

37:37

I think follow-up imaging, if you think

37:40

it's likely MO, would be the next best step.

37:47

Okay.

37:50

Here we are.

37:54

The imaging findings are most likely related to

38:09

chronic renal failure.

38:11

Love that for you guys.

38:12

So actually, many of these choices are

38:14

possible answer choices, but the best answer

38:18

choice is, in fact, chronic renal failure.

38:20

So, what we see is large areas of T2 hyperintense

38:25

signal with maybe some layering hypointensity.

38:28

We can see on the CT, corresponding CT

38:31

that there's these large areas of globular

38:35

mineralization periarticular distribution.

38:37

And that's most in keeping with metastatic

38:41

calcification or tumoral calcinosis.

38:43

In my quick Google search,

38:45

there's preferred terminology.

38:48

Metastatic calcification is more broad, whereas

38:50

tumoral calcinosis is supposed to primarily be used

38:53

in patients who have milk-alkali syndrome.

38:56

But in this case, you're given a CT.

38:58

Coronal CT slice, and we can see the kidneys have these

39:01

multifocal cysts bilaterally, which can suggest end-stage

39:05

renal disease, and they're somewhat atrophied.

39:08

So, that's kind of what I was going for as the best answer

39:10

choice in this instance—chronic renal failure.

39:14

Um, so I guess the point I want to give

39:16

you here, even if this question wasn't

39:18

the most ideal one, is that on the test,

39:22

if you are in a situation, again,

39:24

I'm not an ABR exam writer.

39:27

I'm just a dude who took the boards, whatever, seven

39:29

years ago or something like that—six years ago.

39:32

Um, but, you know, they're not

39:35

really always testing facts.

39:37

Okay, fact recognition.

39:39

They also want to see, like,

39:40

can you think like a radiologist?

39:42

And radiologists are responsible

39:44

for everything on the image.

39:45

And if there's multiple correct answer choices to you,

39:50

I would highly recommend a second look at

39:52

the image to see if there are any pieces

39:55

of information that you may be missing.

39:56

And in this case, you know, it's windowed.

39:58

It's tricky because it's windowed for the bones, right?

40:01

But you can still see some solid organs and see if

40:03

there's any additional information that you may be

40:06

missing that can help you point to the best answer.

40:09

And this one, I was going to

40:11

go with chronic renal failure.

40:13

It seems like many of you agree,

40:15

hopefully for the same reason.

40:19

Okay.

40:20

Here is an AP and lateral of the knee.

40:27

What is the most likely diagnosis?

40:31

This was just a first-order

40:32

question, not second in this case.

40:47

Nice.

40:47

Okay.

40:48

What is the most likely diagnosis?

40:54

A couple of folks thought

40:56

maybe chondrosarcoma or chondroblastoma.

41:00

And I think those are reasonable.

41:02

And let's talk about why

41:03

giant cell tumor of bone is the best choice.

41:05

Okay.

41:06

So, similar to hands, you know, I

41:08

have an approach to these things.

41:10

And for me, first thing is first,

41:13

what is the patient's age?

41:15

Are they skeletally mature or skeletally immature?

41:17

Do not expect them to give you

41:19

that information on a test.

41:20

If you can ascertain it by the image,

41:22

we can see the physeal plates are closed.

41:24

This is a skeletally mature patient.

41:27

The next thing: Is it a metaphyseal,

41:29

diaphyseal, or epiphyseal lesion?

41:32

And we can see on the lateral view that

41:34

there is involvement of the epiphyseal bone,

41:37

uh, extends to the articular surface,

41:40

which is classic for giant cell tumors of bone.

41:43

Um, and so we have a radiolucent lesion with marked

41:48

endosteal scalloping and thinning of the cortex.

41:51

Um, there's no real matrix, right?

41:54

So the next thing is, like, is there a matrix?

41:56

Is it chondroid?

41:57

Is it osteoid?

41:58

Or is there no matrix?

42:00

I guess you could hallucinate and say, like,

42:01

there's some curvilinear stuff in here.

42:03

Maybe that's a chondroid matrix.

42:06

But an enchondroma generally is

42:08

not going to appear like this.

42:09

They're not usually epiphyseal and

42:12

don't abut the articular surface.

42:13

They're more common in the hands and

42:15

wrists, but they can be seen in any parts.

42:17

Usually, they're going to have a curvilinear

42:19

matrix, um, suggestive of a chondroid matrix.

42:22

They can have some endosteal scalloping,

42:24

but usually don't have marked endosteal scalloping.

42:27

The other, um, so, geode—there's not really any

42:29

osteoarthritis here, maybe some minimal, but—

42:31

so you're not going to see a random geode in a patient who

42:33

doesn't have pronounced osteoarthritis, most likely.

42:36

Chondroblastoma is usually an epiphyseal lesion

42:40

in a skeletally immature patient, and it can be

42:42

markedly inflammatory, um, but this is a skeletally

42:46

mature patient, so not likely to be chondroblastoma.

42:49

Chondrosarcoma tends to happen in very old patients,

42:52

um, malignant degeneration of an enchondroma.

42:56

You might see endosteal scalloping greater

42:58

than 50%, but like this, cortical

43:00

breakthrough or soft tissue mass.

43:02

Um, but this patient doesn't look that old,

43:04

and you don't have any history that suggests

43:06

this was previously an enchondroma,

43:08

although it's not an unreasonable answer choice.

43:11

Um, so the best choice here is

43:13

giant cell tumor of the bone.

43:16

Uh, if you were in person, I would

43:17

ask you, is it benign or malignant?

43:19

Hopefully, you would say it's benign.

43:21

I would ask you,

43:22

can it metastasize, though?

43:24

And it can—sometimes, rare cases

43:26

can metastasize to the lungs.

43:28

Um, so, giant cell tumor of the bone—again, epiphyseal lesions,

43:33

articular surface extension, um, middle age, usually

43:37

thirties or twenties, um, people who have closed

43:41

growth plates. It can be markedly, um—it's usually

43:45

well-circumscribed, and it can really thin the bone.

43:48

Um, and it's generally benign, but it can metastasize.

43:52

That's the best choice here.

43:55

Okay, moving on.

43:57

What is the most likely complication

44:00

based on the above images?

44:04

Did not correct this one.

44:18

Arthrofibrosis.

44:20

Okay, great.

44:21

Seventy-four percent of you got it correct.

44:22

We can see we are presented with an axial T2 fluid

44:26

sensitive sequence, or a T2 fat-suppressed sequence.

44:30

And we are presented with the

44:31

sagittal proton density sequence.

44:33

Why is this not a sagittal T1?

44:35

We can see a little blip of joint fluid

44:38

in here, which is not hypointense.

44:40

It is actually hyperintense or

44:41

intermediate signal intensity.

44:43

We can see that there's an anterior cruciate

44:45

ligament reconstruction and can, in some instances,

44:48

be too far anterior or too far posterior.

44:51

If it's too far anterior,

44:52

you can get what's called roof impingement,

44:54

where the ACL graft is impinged upon

44:57

by the intercondylar notch roof.

44:59

If it's too far posterior, it can result in persistent

45:02

insufficiency of the anterior cruciate ligament.

45:05

Here, though, we see this big, um, focus of

45:08

nodular signal in the deep aspect of Hoffa's

45:11

fat pad pattern in the intercondylar region.

45:13

On the axials,

45:14

we see it as this U-shaped structure.

45:17

And if you were putting in an arthroscope here,

45:19

it might look like an eyeball staring back at you,

45:22

which is our Cyclops lesion or arthrofibrosis.

45:25

Patients can present with an incomplete

45:27

ability to extend their knee,

45:29

or pain, loss of ROM after, you know,

45:33

post-op physical therapy and all that.

45:35

So, arthrofibrosis is the question.

45:37

You can, uh, if the patient is persistently

45:39

symptomatic, they may go in and resect some of this

45:42

tissue to allow the patient to extend more fully.

45:48

Adhesions? It's possible, but not—

45:51

nothing in this case to suggest that.

45:59

What is the most likely diagnosis?

46:01

Spondyloarthropathy.

46:16

Okay, all right, so let's talk about it.

46:20

Secondary hyperpara was a close second, so we do see

46:23

here that there is sclerosis of the sacroiliac joints.

46:28

Um, it tends to be on the CT. We can see

46:31

it relatively isolated to the iliac side of

46:33

the joint, and the sacral side is not

46:37

as involved here, if at all.

46:40

We can see a relatively normal peripheral margin

46:42

of the sacrum, whereas the resorptive change in

46:45

this case is mostly on the iliac side, okay, which

46:50

is one way to differentiate sacroiliitis versus,

46:54

um, you know, subchondral resorptive changes or

46:59

subarticular resorptive changes and that.

47:02

And similarly, or to another case before,

47:06

this right kidney is looking super atrophic,

47:09

and the left kidney is a little bit atrophic.

47:11

So these are actually resorptive changes

47:14

in the setting of secondary hyperparathyroidism.

47:17

Um, and that's what I was going

47:19

for in this particular case.

47:21

More.

47:21

The two clues are that it's relatively isolated

47:25

to the iliac side of the bone, which is more

47:28

indicative of, you know, resorptive changes

47:31

rather than erosions related to sacroiliitis.

47:34

Um, and then the kidney. Uh, and the other

47:38

question I have—there's an axial CT of the kidneys

47:41

that confirms, uh, you know, an abdominal window

47:44

that they're small and atrophic, but I wanted to

47:46

make it a little bit more challenging for you.

47:48

So again, use everything on the image.

47:50

And then again, that this is isolated to the iliac

47:53

side is more indicative of secondary hyperparathyroidism.

47:55

Spondyloarthropathy could have a similar

47:58

appearance, um, but probably not the best

48:01

answer for the aforementioned reasons.

48:03

RA, not a really common presentation for RA, and

48:04

insufficiency fractures would be more in the sacrum.

48:09

We'd see vertically oriented areas of irregularity or

48:12

sclerosis, which could suggest insufficiency fractures,

48:16

either bilateral. On a nuclear medicine bone scan,

48:21

you might see your Honda sign, which is focal hyper

48:24

metabolic activity in the H-shaped distribution.

48:27

Um, we could suggest insufficiency fractures.

48:34

Okay.

48:37

What is the most likely diagnosis?

48:51

96%. Yeah, that is correct.

48:54

This is a meniscal flounce.

48:56

It is just a little bit of, um, hypermobility

48:59

of lateral meniscal tissue that results in this.

49:02

You know, kind of an undulating appearance. It is not

49:06

pathologic. It is not more prone to tearing. There's

49:08

no other consequence to this except for knowing that

49:12

it is a variant that is not pathologic, so you don't

49:16

want to call this a tear. This is a meniscal flounce.

49:27

What is the most likely associated serum abnormality?

49:29

Elevated ALK

49:42

Phos, that is correct.

49:45

Elevated PTH and decreased vitamin D

49:47

were the other options that people chose.

49:49

This is indicative of Paget's disease.

49:52

We can see trabecular coarsening.

49:55

We can actually partially see in the femur.

49:56

Here are similar findings.

49:58

Thickening of the cortex.

49:59

We can see trabecular coarsening as well.

50:02

And this is most indicative of polyostotic

50:05

Paget's disease, which is actually the

50:06

most common relative to monostotic Paget's

50:09

disease. In people with Paget's disease,

50:11

the most common abnormality of the serum would

50:14

be elevated alkaline phosphatase, elevated PTH.

50:19

Thank you.

50:19

It could be seen in hyperparathyroidism, rickets,

50:24

decreased vitamin D deficiency, and then

50:29

inflammatory arthropathy. Elevated ESR, CRP, are pretty

50:33

nonspecific. It can be an infection and other

50:35

reasons, but this was Paget's disease. Again,

50:38

trabecular coarsening, cortical thickening,

50:41

most indicative of Paget's disease of the bone.

50:48

Here's another.

50:49

Manifestation of Paget's disease.

50:51

You can see this kind of blade of grass appearance with

50:54

a bevel or sharp edge here that can be indicative of

50:58

Paget's disease in the leading edge of the osteolysis.

51:03

Same patient as we saw on the CT. We can see that

51:06

on the MR. If they want to be funny and make it

51:10

somewhat challenging, potentially they can show

51:12

you these linear trabecular coarsening or cortical

51:14

thickening on the MRI with preservation of the marrow.

51:21

Okay.

51:22

A new question.

51:26

What imaging finding is not depicted?

51:40

Survey says

51:44

sinus tract or involucrum.

51:48

Okay.

51:49

So here, um, the answer is sinus tract.

51:53

Okay.

51:53

So we can see in the distal radius, there's this area

51:55

of lucency, which corresponds to this area of fluid

52:00

signal intensity on this fluid-sensitive sequence.

52:03

We can see that there's a full-thickness disruption

52:05

of the cortex here at the volar aspect of the

52:07

radius, and that's most indicative of a cloaca.

52:12

A sinus tract would be if the fluid signal, um,

52:15

extended to the skin surface, uh, and that would

52:18

suggest a sinus tract. Intraosseous abscess is present.

52:21

This is a Brodie's abscess, and the involucrum is the

52:25

sclerosis and increased cortical bone formation,

52:28

which we can more easily see on the lateral view.

52:31

There's all this productive cortical change and

52:33

excess additional bone formation as a reactive change.

52:37

The sequestrum, which was not an answer choice, would

52:41

be if there was a little island of sequestered dead,

52:45

necrotic bone within the center of this involucrum.

52:48

That would be most indicative of a sequestrum.

52:50

And all of these findings amount

52:53

to chronic osteomyelitis.

52:56

This is what you might see in chronic osteomyelitis.

53:01

Yeah, so we have a Brodie's abscess, we have

53:04

a cloaca, we have a, you know, soft tissue

53:06

extension of fluid. We do not have a sinus tract.

53:09

We do have an involucrum, which is this excess bone

53:12

formation, and then, uh, we do have the cloaca.

53:16

No sequestrum, but that was not an answer choice.

53:21

Okay, and last but not least, on this momentous occasion.

53:27

What is the most likely diagnosis?

53:42

Survey says melorheostosis, and that is correct.

53:46

We can see this kind of dripping candle wax appearance

53:49

of sclerotic bone here of the second metatarsal.

53:53

You can even maybe see if the second or the intermediate

53:56

cuneiform and is most indicative of melorheostosis.

54:00

Albright's and Bruck syndrome are like of hands and

54:02

feet, where you get multiple enchondromas.

54:05

Thing in the foot.

54:05

You can also have associated, um, you

54:08

know, vascular malformations, vascular lesions.

54:13

Um, and one of these two is more

54:15

associated with malignant degeneration.

54:17

I think of enchondromas.

54:19

I don't want to give you a black pearl,

54:20

so I would encourage you to look it up.

54:22

Multiple familial exostosis is if there was

54:24

multiple osteochondromas, which we don't see.

54:28

Osteochondromas should have cortical

54:31

medullary continuity, a cartilage cap.

54:33

Remember, osteochondromas can degenerate into

54:37

chondrosarcoma, generally in an older population,

54:40

and if that cartilage cap is too thick—some

54:42

literature suggests 15, some literature suggests

54:45

20 millimeters—anyways, here nor there in

54:48

this particular case, but it's factoids to be

54:51

familiar with for future patient care purposes.

54:55

So that brings us to the end of this, um,

54:59

evening, and I appreciate everybody's time.

55:01

Hopefully, you found this to be useful,

55:02

even if the cases weren't ideal.

55:04

Hopefully, the thought process and going through, um,

55:08

things that you should be considering when you're going

55:09

through these cases, um, in real life and on the test.

55:13

Again, we're testing to see how your thought process is

55:18

as a radiologist, not necessarily how well you can

55:22

remember, memorize stuff—a little bit of both, probably.

55:25

So, thank you.

55:26

And I'll let the, uh, modality

55:28

team take it home from here.

55:31

Well, thank you, Dr. Farajii,

55:32

for that awesome case review.

55:34

That was great.

55:35

And for everyone else

55:37

participating, we really appreciate it.

55:39

Be sure to join us Monday, April 8th, for

55:43

another one of these with Dr. Erin Gomez.

55:45

She'll lead us in a rapid review of GU cases.

55:49

You can register for it at the link

55:50

provided in the chat and follow us on social

55:53

media for updates on future case reviews.

55:56

Thank you so much again for learning with us.

55:57

Good luck on the boards, and we hope to see you soon.