0:00

Once again, we go right to the SAGE.

0:03

Easy-peasy.

0:04

Everybody knows how to look at a lateral

0:06

conventional radiograph, so why not?

0:09

We've got two sagittals.

0:11

I think we'll take one other projection.

0:15

Let's take an axial T2, since it's

0:17

available, and we have no other sagittals.

0:20

So we have a proton, actually a T2, with a T of 68.

0:26

I'm not thrilled with that TE.

0:27

12 00:00:28,400 --> 00:00:30,410 I'd either like it to be 40 or a hundred.

0:30

This is kind of a no man's land, but okay.

0:33

It's a T2 with fat suppression.

0:36

It's a T1 without fat suppression.

0:39

It's a T2 without fat suppression.

0:41

That's scroll.

0:45

We talked about erosions.

0:47

That could be central or

0:49

marginal or para-articular.

0:52

So-called pressure erosions.

0:56

These pressure erosions can be quite large.

0:59

They're due to increased intra-articular pressure.

1:03

They produce a scalloped, yet well-

1:06

defined sclerotic border, and they are

1:09

a cardinal feature of this diagnosis.

1:12

Here's another set of pressure

1:14

erosions in the subtalar space.

1:19

A couple of other features of this, this

1:22

abnormality, um, one feature besides the

1:26

distention and the pressure erosions.

1:29

Is the signal.

1:31

The signal is very low on

1:33

everything except the T1.

1:37

It's very low on the T2.

1:38

It's very low on the PD spur.

1:42

And they failed to give you a gradient

1:44

echo, which would have been lovely.

1:47

This is just another fat suppression sequence.

1:50

And the reason a gradient echo would have

1:52

been lovely because when you go from a

1:54

spin echo to a gradient echo, and you have

2:00

something that has blood or iron in it, which

2:03

this does, That blood or iron is going to

2:05

get much darker, and it's going to distort

2:08

the tissues, and that's known as blooming.

2:12

But this case is so grotesque and

2:14

obvious that you don't need that.

2:18

There's not too many things inside

2:21

a joint that are going to be black.

2:23

Let's talk about a few of them.

2:25

Air.

2:26

This isn't black enough for air.

2:28

Plus, it's got stuff in it.

2:29

It's gray on the T1.

2:31

Air is black.

2:32

Flow.

2:33

Flow is either going to be black

2:35

or white depending upon the speed.

2:37

These things aren't tubular.

2:40

Metal.

2:41

That's a possibility, but that would

2:43

be a lot of metal in the joint.

2:45

How does metal get into a joint?

2:47

From a joint replacement.

2:49

That's called metalosis or aseptic

2:50

lymphovascular-associated lesions.

2:54

Some of which are metal-containing.

2:57

So metal is out clinically.

3:01

Blood.

3:02

You could have a hemorrhage, but

3:04

a hemorrhage is going to have some

3:06

methemoglobin associated with it.

3:09

I don't see any methemoglobin, but I do see some

3:12

high signal, which is corticated right there.

3:17

And that is a focal area of osteochondromatosis,

3:21

part of this metaplastic process right here.

3:25

What's another cause of intra-articular blood?

3:29

Hemophilia.

3:31

Probably one you hadn't thought of.

3:33

They get big pseudotumors.

3:35

They're notorious for producing pressure erosions.

3:38

They usually bleed in one locus.

3:40

We don't see it as much today because of the

3:42

skill and training of our rheumatologists and

3:45

internists in dealing with factor VIII deficiency.

3:49

So it's uncommon.

3:51

It also tends to be in one

3:52

quadrant, not in multiple quadrants.

3:56

Usually, the patients are so uncomfortable that

3:59

it gets addressed in the single quadrant that

4:01

it's in. They get factor eight, and if it's a

4:04

big enough pseudotumor, it will get excised.

4:07

Here we have a patient where the process is

4:09

slowly, slowly, slowly progressed in more than

4:13

one compartment. It's posterior, it's anterior,

4:16

it's subtalar, and if we look coronally, it is

4:19

lateral, sorry, it is lateral, and to a lesser

4:22

extent, it is It is medial, not so much medial.

4:27

So the diagnosis here is pigmented villonodular

4:32

synovitis, and it's the diffuse type.

4:35

So what types of pigmented

4:36

villonodular synovitis do you have?

4:39

You got focal, which is also known as

4:43

localized giant cell tumor of tendon sheath.

4:45

Same thing.

4:46

It's a synonym.

4:48

Then you have diffuse, where it's everywhere.

4:52

That's this case.

4:54

Then you have multifocal, where you

4:57

have nodules, but they're discrete

4:59

nodules in more than one quadrant.

5:02

And then you have non-pigmented villonodular

5:07

synovitis or villonodular synovitis.

5:11

And that is a tricky one.

5:14

It looks like this on the T1, but doesn't have

5:16

this degree of dark signal intensity on the water

5:20

weighted sequences because it's maybe not devoid

5:23

of hemosiderin, but has very scant hemosiderin,

5:26

which can only be seen on the gradient echo image.

5:30

Now, pigmented villonodular synovitis falls

5:33

into the family of synovial metaplasias.

5:36

So there can be some overlap.

5:39

There is a heredofamilial predilection for this

5:43

condition, but it is not discreetly inherited.

5:47

In other words, family members who

5:49

have had it, the risk of another

5:50

family member having it is increased.

5:53

But nobody knows what factors cause it, although

5:57

friction and a certain subgroup of the population

6:00

is believed to be the underlying etiology.

6:04

So let's talk about the synovial metaplasias.

6:07

We've got pigmented villonodular synovitis,

6:13

and the subtypes of villonodular synovitis

6:15

that we gave you earlier, all four of them.

6:18

So there'll be four of those.

6:20

Then we've got synovial chondromatosis,

6:26

and those are usually round objects

6:28

that look more like cartilage.

6:30

They are not pigmented and do not

6:32

give you this dark signal intensity,

6:34

and they don't give you blooming.

6:37

Then you've got ossified synovial

6:40

chondromatosis, where you have the same

6:43

thing as SC, but they have marrow in them.

6:46

I showed you one.

6:47

Ossicle that was mixed in with

6:50

the PVNS, that little white object

6:53

with the ring of cortex around it.

6:57

Then you've got lipoma arborescens, where

7:00

you have intraarticular fatty proliferation.

7:05

And then one more, you've got

7:06

synovial hemangiomatous proliferation.

7:10

So that's actually one, two, three, four, five,

7:15

and then four subtypes of, uh, villonodular

7:19

synovitis or pigmented villonodular synovitis.

7:22

Okay.

7:23

Um, one, one other parting note on,

7:25

on synovial metaplegia is anywhere.

7:27

There are two, two treatments.

7:30

Well, actually, there are three treatments

7:32

for synovial metaplastic disease.

7:34

One, the most advanced grotesque

7:38

treatment is to resect the joint.

7:41

In other words, do a hip replacement.

7:43

I've, I've, I've done that in 20

7:45

year-olds who had very severe PVNS

7:47

and they have done, done terrific.

7:50

Um, another treatment, which

7:53

is less invasive, invasive,

7:55

is to go in and do a synovectomy.

7:58

To do that, you need to map out

8:00

where the PVNS is for the surgeon.

8:02

It's lateral, it's subtalar, it's posterior

8:05

and to a lesser extent it's medial.

8:07

So you, you are the mapper, uh,

8:10

for that surgical procedure.

8:12

And then you can also use a beta emitter

8:14

and put that in the joint ligament.

8:16

And, uh, you know, that can be done

8:18

by an interventional radiologist

8:20

or an orthopedic surgeon.

8:21

Musculoskeletal radiologists.

8:23

It's just putting a needle in the joint and making

8:25

sure your beta emitter gets into the right place.

8:28

That's the least common therapy

8:30

and the least invasive of all.

8:35

Would gout be a reasonable differential

8:37

diagnosis with juxta-articular erosions?

8:40

It would, but not in this case.

8:42

The signal intensity of gout is not this black.

8:46

It's not this dark.

8:48

Um, it also happens to be a woman.

8:51

So, you know, you don't see gout that

8:53

often in women, but this very, very dark

8:55

signal is not characteristic of gout.

8:58

Gout tends to be intermediate, more

9:00

close to the signal intensity of

9:02

muscle, and that's also true for TOFI.

9:06

Too dark for gout.

9:09

Wrong gender.