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Sinonasal Case Review - Vitamin C & D, Dr. David M Yousem (2-22-24)

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0:02

Hello and welcome to Case Crunch Rapid Case

0:04

Review for the core exam hosted by Medality.

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In this rapid-fire format, faculty will

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show key images and you'll respond with your

0:11

best choice via the live polling feature.

0:14

After a quick answer explanation, it's on to the next case.

0:18

You'll be able to access the recording of today's case

0:21

review and previous case reviews by creating a free account.

0:24

Questions will be covered at the end if time allows.

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Please remember to use the Q and A feature

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to submit your questions so we can get

0:31

to as many as we can before time is up.

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Without further ado, please enjoy this case review.

0:36

Thank you very much.

0:39

So, today we are going to go through

0:41

some multiple-choice questions

0:43

on sinonasal imaging unknown cases. I'd like

0:47

to have as much participation as I can from the

0:50

standpoint of the polling and the multiple choice

0:54

answers, and we'll see how you do.

0:57

So let's, uh, get going.

0:58

Just as a reminder, my mnemonic VITAMIN C and D refers

1:03

to vascular, infectious, traumatic, acquired, metabolic,

1:06

idiopathic, neoplastic, congenital, and drugs.

1:09

And those are the general categories of disease that

1:13

we see across the full spectrum of pathology in the

1:17

body. And in the sinonasal cavity, obviously, it's

1:20

going to be dominated by infectious etiologies,

1:23

inflammatory etiologies, and neoplastic etiologies.

1:26

So let's begin.

1:28

And, um, my disclosures.

1:31

I do have several books, um, published by

1:33

Elsevier, for which I receive royalties.

1:35

I do medical-legal expert witness work,

1:37

and I am, uh, one of the consultants

1:39

and speakers for MRI Online or Medality.

1:42

And yes, the fifth edition of Neuroradiology: The Core Requisites,

1:45

is coming out in March.

1:48

So, uh, go to the Elsevier site

1:50

or, um, Amazon, wherever you want.

1:52

All right, here's our first case.

1:55

So what we got here is the sagittal T1

1:59

weighted MR, the axial T2 weighted MR,

2:04

a post-gadolinium enhanced, uh, scan here.

2:08

And this is the FLAIR scan, so T1,

2:12

axial T2, FLAIR, and post-gadolinium.

2:16

This is with fat suppression, T1-weighted scan.

2:22

So what is the most likely diagnosis given the, given

2:25

these imaging findings? Do you think this is most likely a

2:28

squamous cell carcinoma, a mucus retention cyst, allergic

2:33

fungal sinusitis, inverted papilloma, or a schneiderian polyp?

2:39

So looking at the pathology that's being demonstrated,

2:43

what do you think the most likely diagnosis is?

2:45

If you think it's squamous cell carcinoma,

2:47

answer number one.

2:49

If you think it's a mucous

2:49

retention cyst, answer number two.

2:52

If you think it's allergic fungal sinusitis,

2:54

answer number three.

2:55

For inverted papilloma, you're gonna put number four.

2:58

And for a Schneiderian polyp, put number five.

3:03

So we're— um, got about 200 people on board

3:06

and we're going to, uh, see what the audience

3:13

recommend. So let's share results.

3:15

And it looks like 68% of the people, uh, answered

3:20

allergic fungal sinusitis, and indeed that is the correct

3:24

answer.

3:25

You notice that on the T1-weighted scan,

3:27

we have areas within the paranasal sinuses that are

3:29

bright on T1 as well as dark on T1. On T2,

3:33

the predominant abnormality here

3:35

is dark on T2 as well as flare.

3:38

In fact, you might think that this is aerated sinus

3:41

just looking at the T2, and then we get to the

3:44

post-GAD T1 and we see, no, that's not aeration.

3:47

That's very inspissated secretions or allergic

3:53

fungal mucin that is causing the very

3:56

low signal on the T2-weighted scan.

3:59

And you see also that the ethmoid sinus is opacified.

4:03

So remember that the signal intensity of the secretions in

4:08

the paranasal sinuses is dependent in part on the protein

4:12

concentration. This was beautiful work that was done

4:16

by the late Peter Som in the 1980s in which he aspirated—

4:20

he actually got the ENT doctors to aspirate sinus

4:24

secretions and then measure the protein concentration.

4:28

And what he showed was that this is signal intensity.

4:31

This is the T1, and this is the T2.

4:34

When you have low protein concentration,

4:36

effectively just fluid, it's gonna be dark on T1

4:40

and bright on T2.

4:41

However, as the protein concentration

4:44

increases, you notice the first thing that

4:46

happens is that the T1 becomes bright,

4:50

this is the iso-intense line here, becomes bright.

4:53

So you'll have a period where it's

4:55

bright on T1 and bright on T2.

4:58

But as those secretions get more and more mucinous

5:01

and less watery, you come to a point where

5:05

it's bright on T1, but now it's dark on T2.

5:10

And when it becomes a concretion, effectively like

5:12

a calcification, it's dark on T1 and T2.

5:16

So these are the graphs that you should

5:18

know about protein concentration.

5:20

And this also will pertain to things like craniopharyngiomas,

5:25

or pineal region cysts, or other things that have

5:28

high protein content, like colloid cysts, for example.

5:33

The things that are hyperdense on CT

5:35

but dark on T2 include blood products.

5:38

It's just like that.

5:40

Hyperproteinaceous secretions, fungus.

5:42

You may see that with osteomas or odontogenic lesions,

5:46

and indeed melanin, which may be bright on T1 and dark

5:50

on T2 from the melanin, is often hyperdense on CT in

5:54

part maybe because of—it may be hemorrhagic as well.

5:58

So this was a case of allergic fungal sinusitis, which

6:01

is not an aggressive, invasive type of fungal sinusitis.

6:07

Remember that we have five different varieties.

6:09

We have our non-invasive fungus ball or mycetoma.

6:13

It's usually in the maxillary sinus.

6:14

We have our non-invasive allergic fungal

6:17

sinusitis with the eosinophilia and the mucin.

6:22

Um, we have the acute invasive fungal sinusitis.

6:24

Those are usually the patients who have diabetic

6:27

ketoacidosis at presentation and are immune

6:30

compromised, and they may have mucor or aspergillus.

6:33

Then we have the chronic invasive

6:35

sinusitis, long-standing patients who have

6:38

chronic rhinosinusitis, and then this

6:40

unusual chronic granulomatous invasive fungal

6:43

sinusitis that is not usually seen in America,

6:46

but more commonly in Africa or Southeast Asia.

6:49

Here's another example on CT of a patient who

6:53

had allergic fungal sinusitis, and you see the

6:55

hyperdensity to those secretions, and there is some

6:59

bony dehiscence because of effectively like polyps.

7:02

It's remodeling the bone.

7:06

The five criteria for allergic fungal sinusitis:

7:08

Type 1 hypersensitivity, often seen with the

7:10

eosinophilia, nasal polyposis, CT findings of

7:14

opacification, eosinophilic mucin, and a positive fungal

7:19

stain without demonstration of invasion.

7:23

Here, on the other hand, on an MRI with

7:25

bright on T1, this is, uh— turned

7:28

out to be a mycetoma fungus ball in the

7:31

right maxillary antrum, opacifying it.

7:34

This was one of the cases that I saw back when I

7:37

was a resident, in which the patient had severe

7:41

fungal invasive sinusitis with mucor mycosis.

7:45

And what you're seeing on this post-gadolinium

7:47

T1-weighted scan is opacification of the right cavernous

7:52

sinus, but absence of opacification in the left

7:56

cavernous sinus.

7:57

And if you look at the carotid artery here, faintly

8:00

seen, it's narrower than the normal right side.

8:04

It's got a little irregular margin.

8:05

So this patient had fungal sinusitis with invasion

8:08

of the cavernous sinus and thrombosis of the cavernous

8:11

sinus associated with vasculitis, and the neck scan

8:15

showed MCA infarction secondary to the left internal

8:19

carotid artery vasculitis from the invasive mucormycosis.

8:25

All right, next case, case number two.

8:28

Let's move on.

8:29

Here's the CT scan axial original

8:34

data, sagittal reconstruction, MRI

8:39

T1 post gad, MRI Axial T1 post gad.

8:45

So I'll give you a moment to look over the case.

8:49

CT and MRI with gad.

8:54

Most likely diagnosis for this entity.

8:56

Is this a mucocele?

8:59

Is this pott puffy tumor?

9:02

Is this a dermoid?

9:05

Is this nasal glioma, or is this a sebaceous cyst?

9:10

So the most likely diagnosis here, if you

9:12

think it's a mucocele, answer number

9:14

one, if you think it's pott puffy tumor,

9:16

number two, if you think it's

9:17

a dermoid, answer number three.

9:20

If you think it's nasal glioma, number

9:23

four, or a sebaceous cyst, number five.

9:27

So, let's see how the audience is doing here.

9:32

And I think we can end the poll because

9:34

there's an overwhelming— let's share that result—

9:37

overwhelming, uh, support for pott puffy tumor.

9:40

And that is indeed correct.

9:43

You have a patient who has a frontal

9:45

sinusitis with opacification.

9:47

There's a little divot here out of the frontal

9:50

sinus where the infection has entered the

9:54

soft tissues of the forehead, and obviously, this pott

9:58

puffy tumor was thought to initially be a tumor because

10:01

it was presenting as a soft tissue mass under the

10:03

skin, and the— let me give you a little history here.

10:09

All right.

10:09

Pott puffy tumor. Forehead edema, resulting

10:12

from osteomyelitis of the frontal bone

10:14

associated with a subperiosteal abscess.

10:17

First described by Sir Percival Pot

10:20

in 1768. Let me tell you, they did not have CT scans back

10:24

then, and that's why he thought it was a tumor rather

10:26

than the spread of infection from the frontal sinus.

10:30

And obviously, when he went to cut it open

10:32

and got that purulent stuff coming out.

10:35

Um, so you have rubor, tumor, calor, and dolor.

10:39

So redness, swelling, warmth, and the tumor

10:41

in this case is the observable swelling of

10:44

the forehead rather than to any neoplasm.

10:46

And it's a complication of frontal sinusitis.

10:49

So pott puffy tumor. We often call it, Pott's puffy tumor.

10:53

But the gentleman's name was Sir Percival Pott.

10:59

Frontal sinusitis,

11:00

um, is

11:02

an entity that may be associated with the infection

11:05

going superficially and creating a Pott puffy tumor.

11:09

But it could actually also extend intracranially,

11:13

where you may have an epidural abscess

11:15

developed from the infected frontal sinusitis.

11:18

You see that here.

11:19

If this collection dissects the sinus off of the

11:26

periosteum of the frontal bone, uh, it may actually cross.

11:31

The midline and any collection that's crossing the

11:34

midline, we assume is going to be an epidural, uh, abscess

11:38

or epidural, uh, hematoma, as the case may be with trauma.

11:43

So you may also see findings of meningitis.

11:47

So look at the flare scan, look at the CSF, is the.

11:51

CSF still suppressed on the flare scan, or

11:54

if it's not suppressed, that might imply

11:56

that there's meningitis associated with it.

11:58

Obviously, with this type of proximity to the superior

12:02

sagittal sinus, you may get sinus thrombosis and then

12:04

have a superimposed venous infarction on top of

12:08

the infection on top of the sinusitis, for example.

12:15

We're moving on to the next case.

12:16

This patient had previously had a medial antrostomy

12:21

for inflammatory disease, and what you're seeing is

12:24

this is the sagittal cyst T2-weighted scan.

12:28

This is the post-gadolinium T1-weighted scan.

12:32

This is the axial T2-weighted scan, and you

12:35

can see that we're going through this abnormality.

12:39

And then this is the ADC map.

12:42

Of the lesion.

12:44

So patient who had previously had surgery,

12:48

and you can see that the lesion in question

12:51

here that we're looking at is this area here.

12:58

The most ominous feature of this lesion is, what is it?

13:02

The dark signal on T2A imaging.

13:05

Is it the fact that it enhances?

13:07

Is it the low ADC?

13:09

Is it the eroded bone or is it

13:12

being bright on T2A scan?

13:14

So on the imaging features of this lesion,

13:17

which one kind of bothers you most?

13:19

Is it the dark signal on T2-weighted imaging?

13:22

Is it the presence of enhancing tissue?

13:25

Is it low on ADC?

13:28

Is it eroded bone or is it bright on the T2-weighted scan?

13:32

Which of these is the most ominous feature of this lesion?

13:39

Alright, T2 post-Gd T2 axial ADC map.

13:48

We got over a hundred responses,

13:50

so let's, uh, see what people said.

13:52

Okay.

13:52

So the answer to the question, um, by the

13:56

group is low ADC, and I would agree with that.

14:00

Um, I. The reason why I would

14:02

agree with that is dark on T2.

14:04

As you know, we just saw a case of allergic fungal

14:07

sinusitis that can occur within inspissated secretions.

14:11

It can occur with fungal sinusitis,

14:12

it can occur with osteomas.

14:14

I gave you all of those

14:15

differential diagnoses for enhancement.

14:18

So enhancement is important, and solid enhancement

14:21

is going to be a pretty good indicator that this

14:24

is neoplastic as opposed to an inflammatory.

14:28

Process.

14:29

So the fact that this tissue shows enhancement

14:32

is an ominous finding, low ADC, yes.

14:35

However, remember that just as epidermoids.

14:40

May have low ADC, and it's not

14:43

necessarily because of hypercellular tumor.

14:46

It's in part because of the concentration of protein

14:49

in the lesion or, or the content of the lesion.

14:52

Um, you may see inspissated secretions and things

14:55

with high protein that will have restricted

14:58

diffusion, eroded bone definitely, but a lot of

15:01

benign tumors, uh, benign conditions, including

15:04

mucoceles, including polyps, including, um.

15:09

You know, osteomas, those things can erode

15:12

the bone and yet be a benign condition,

15:14

right on T2 usually that's reassuring.

15:17

So that would be the least.

15:19

So given all of these findings, what do you

15:21

think the most likely diagnosis here is?

15:24

Is this a squamous cell carcinoma?

15:25

Is this an inverted papilloma?

15:27

Is this melanoma, is it lymphoma or is it fungus?

15:31

So our lesion is here, uh, relatively dark

15:34

on the T2, showing contrast enhancement.

15:38

Dark on T2, a little bit of obstructed

15:40

secretions and low on ADC. Mep, what

15:43

do you think the most likely diagnosis is?

15:45

Is it squamous cell carcinoma?

15:47

Is it inverted papilloma?

15:49

Is it melanoma?

15:50

Is it lymphoma or fungus?

15:52

So, uh, number one for squamous cell carcinoma.

15:54

Number two for inverted papilloma, three for melanoma, four

15:58

for lymphoma, and five that there's a fungus among us.

16:03

See what people say here.

16:06

So let's, uh, share some results and we have a

16:11

mixture of, um, different suggestions including

16:15

squamous cell carcinoma, lymphoma, inverted papilloma,

16:18

not so much melanoma and not so much fungus.

16:21

So I think that's reasonable.

16:23

All three, the squamous cell carcinoma, inverted papilloma

16:25

and lymphoma may look this way if you're going with the

16:29

most likely diagnosis by the numbers, the most likely.

16:34

Cancer of the paranasal sinuses

16:36

is squamous cell carcinoma.

16:38

So that would be the best diagnosis here.

16:41

It's not a particularly good location for

16:44

inverted papilloma, which usually occurs along

16:47

the, uh, common wall between the maxillary

16:50

sinus and the nasal cavity, or along the.

16:54

Septum plume.

16:56

This area, which is effectively in the

16:58

ethmoid sinus, is not the best location

17:01

for an inverted papilloma, not classic.

17:05

So our answers are low, A, D, C,

17:10

and squamous cell carcinoma by numbers.

17:13

It looks like there's some, I got some chat things.

17:16

Let's see.

17:16

Um, immer, no, not for me.

17:18

Okay.

17:20

No questions at the moment.

17:23

Question and answer.

17:24

What is a Schneiderian polyp?

17:26

Schneiderian polyps are, uh, types of polyps

17:29

that are included with inverted papilloma and

17:32

it refers to the histopathologic features.

17:36

And, um, I'll move forward

17:39

because they ask about the next.

17:40

I. The answers.

17:42

All right, so here is a graph that you see

17:45

from head and neck surgery in oncology.

17:48

Justin Jain Shaw, who's from Memorial Sloan Kettering.

17:52

And you notice that the most common of the

17:54

cancers of the, uh, nasal cavity and paranasal

17:57

sinuses are, is indeed squamous cell carcinoma.

18:01

And then we have this kind of other category

18:03

which are undifferentiated cancers.

18:06

We have melanoma, which is the pink.

18:08

Here, minor salivary gland tumors, et cetera.

18:11

And, um, the sinonasal undifferentiated carcinoma,

18:15

uh, one of the more aggressive of the sinonasal cancers.

18:19

All these kind of look alike except for melanoma,

18:22

which hopefully you'll see as bright on T1

18:25

if it has enough melanin content within it.

18:28

Aesthetic neuroblastomas are the ones that are usually

18:31

in the upper nasal cavity and ethmoid sinus and

18:33

cribriform plate that grow most frequently intracranial.

18:37

And the characteristic feature of that is the

18:39

peripheral cyst associated with the anesthesia that

18:43

happens with other cancers, but the highest

18:46

rate is with aesthetic neuroblastomas, or what

18:49

we sometimes use the term olfactory neuroblastomas.

18:54

Here's the 80% rule.

18:56

80% of.

18:58

Sinus cancers occur in the maxillary antrum.

19:01

Of those 80%, 40% are squamous cell carcinoma, of those 80%

19:04

erode bone, and 80% have a history of chronic sinusitis.

19:08

Moving on to the next case,

19:14

CT scan.

19:15

Axial raw data, coronal reconstruction,

19:22

least likely diagnosis.

19:26

One.

19:27

Granulomatosis with polyangiitis.

19:29

Number two.

19:30

Fungal.

19:31

Sinusitis.

19:32

Number three, cocaine.

19:33

Abuser.

19:34

Number four.

19:35

Syphilis.

19:37

Number five.

19:37

Klebsiella.

19:39

So

19:41

for this imaging finding that you're seeing,

19:44

what is the least likely diagnosis, if you think

19:48

it's granulomatosis with polyangiitis, GPA, number one.

19:54

If you think it's fungal sinusitis, put number two.

19:56

If you think it's a cocaine abuser, put number three.

19:59

If you think it's syphilis, put number four.

20:01

And if you think it's Klebsiella, put number five.

20:07

Okay,

20:09

so let's, uh, share the results, and, um.

20:15

The correct answer here is fungal sinusitis,

20:18

which I guess is the second most common answer here.

20:21

Klebsiella is one of the bacteria that

20:25

will collapse your nasal septum.

20:28

So the finding here is nasal septal perforation.

20:31

Erosion and you have all that soft tissue.

20:34

So in yesteryear, we would often use the term

20:38

Wegener's, but now we're using granulomatosis with polyangiitis.

20:41

That's a pretty frequent cause, um, of

20:45

demonstration of sinus involvement by Wegener's.

20:50

Fungal sinusitis doesn't often cause.

20:53

Septal perforation; cocaine abuser in East Baltimore

20:57

at Johns Hopkins is probably the most common thing.

20:59

And we probably have around a 10 to 20%

21:02

rate of patients that you're reading their

21:04

trauma head CT or motor vehicle collision.

21:07

And you see nasal septal perforation.

21:09

So cocaine or other drugs, um, syphilis, uh, saddle

21:14

nose deformity associated with syphilis and leprosy.

21:19

Those are known causes as well.

21:23

So the correct answer was fungal sinusitis.

21:26

This is another one of the entities that can lead to an ominous sinusitis as well as inflammation in the orbit.

21:34

So Wegener's also may have inflammation in the

21:39

orbit associated with a nasal septal perforation.

21:42

When you put those two together, you

21:44

will come up with granulomatosis with polyangiitis, as well

21:48

as sarcoidosis as another of the etiologies.

21:51

It can occur after trauma.

21:53

It can occur with a nasal septal hematoma that

21:56

erodes the bone, so there's lots of differential

22:01

diagnosis for nasal septal perforation here.

22:03

I have a relatively large listing.

22:06

Remember I talk about

22:09

Vitamin C and D, vascular, infectious, traumatic,

22:12

acquired metabolic, osteopathic, neoplastic, and drug.

22:14

And here we have our trauma, causes.

22:16

We have inflammatory causes, lots of those collagen,

22:19

vascular disease, infectious causes, syphilis, et cetera.

22:23

Uh, you know, is that CCI is not listed here, but

22:28

it is one, it does mention fungal, but that's the

22:31

aggressive fungal infections, neoplasms, carcinoma,

22:34

T-cell lymphomas, and then all these toxic.

22:38

Etiologies.

22:41

Alright.

22:43

I wanna make a point here that on this case you

22:46

saw that there was some dehiscence along the lamina

22:50

papyracea and when I am reading a sinus CT where

22:56

I know the patient is going to surgery or is about.

23:01

Or has gone to surgery.

23:03

There's four critical areas of dehiscence that

23:06

you might want to look at and put in your reports.

23:09

The four critical areas of dehiscence are the

23:12

lamina papyracea, as you see here along the medial

23:16

orbital wall because if it's dehiscent and the

23:19

surgeon is going in to clean up that ethmoid sinus,

23:23

there is that possibility that they would perforate

23:25

into the orbit and lead to an orbital hematoma.

23:28

Second is the cribriform plate.

23:30

Here you see a defect in the cribriform plate.

23:32

In fact, this patient actually has a

23:34

meningocele that's extending intracranial.

23:37

So post-op, if they take down the middle turbinate,

23:41

remember that the middle turbinate has a connection.

23:45

To the cribriform plate as well,

23:47

as to the lateral orbital wall.

23:48

And if they're removing the middle turbinate, there's a

23:51

chance that in that removal, they lead to a cribriform

23:55

plate or a lamina papyracea, basal lamella, uh, injury

24:00

to the medial orbital wall or the, or the skull base.

24:04

And that.

24:05

Potentially it could be a source of CSF leakage,

24:07

but it also, if it's dehiscent, could lead to the next

24:11

time they operate, uh, potential intracranial

24:14

perforation, the optic nerve and canal.

24:16

It's interesting how often you will see that the

24:20

optic nerve at the optic canal has no bone around it

24:26

in the sphenoid sinus and, and or posterior ethmoid

24:29

region, depending upon whether you have an anterior cell.

24:32

So.

24:33

I often will comment on the dehiscence of the

24:37

wall of the optic nerve if they are contemplating

24:40

surgery with endoscopic removal and more and more that's

24:43

usually, uh, associated with, um, cell tumors

24:48

or pituitary adenoma resection, for example.

24:51

And then finally, the carotid canal.

24:52

So here we have the descending carotid canal.

24:55

You can see the enhancing carotid artery.

24:57

There's no bone overlying it again.

25:01

At our institution, they will do a 3D reconstruction,

25:06

3D data set of the paranasal sinuses prior

25:10

to pituitary adenoma surgery because they

25:14

want to know where the carotid arteries are.

25:17

With the potential for injury if they're doing

25:20

an endoscopic removal of a pituitary adenoma.

25:22

So they wanna see the walls of the carotid

25:26

arteries and actually then also the

25:28

tumor's relationship to the carotid artery.

25:30

So these are the four things you might

25:32

wanna think about adding to your report.

25:34

When you look at a sinus case that's either about

25:37

to be operated on or has previously been operated.

25:42

Okay, let's move on.

25:43

Uh, next case, most likely diagnosis,

25:53

CT scan, axial and coronal reconstruction.

25:56

Most likely diagnosis is this, most likely an antrochoanal polyp.

26:01

Is this most likely a mucus retention cyst?

26:04

Is this most likely allergic fungal sinusitis?

26:07

Is it inverted papilloma, or is

26:09

the old Schneiderian polyp once again?

26:12

So if you think it's an intracranial

26:14

polyp, you'll put number one.

26:16

If you think it's a mucus retention cyst, you'll put

26:18

number two. If you think it's allergic fungal sinusitis,

26:21

number three. If you think it's an

26:23

inverted papilloma, put number four.

26:25

And if you think it's a Schneiderian polyp, put number five.

26:33

All right.

26:34

Tricky case.

26:37

Um, so most people put antrochoanal polyp, and

26:41

that is not the correct answer, although

26:45

this looks exactly like an antrochoanal polyp.

26:48

So why, why is this not an antrochoanal polyp?

26:52

Um.

26:52

The density of this lesion is what should give you

26:56

pause there.

26:57

This is not like a typical polyp.

27:00

Polyps generally are lower density on the CT scan.

27:03

They may even be fluid density.

27:05

Remember that mucus retention cysts and polyps of the

27:08

maxillary antrum often are very liquidy and low density.

27:14

The key here to this case was

27:16

that this looks like hyperdense.

27:19

Here's the mucosa.

27:22

Here peripherally that is less dense.

27:26

This was histopathologically, an inverted papilloma,

27:29

so that was the second most common answer.

27:31

So very good to those people.

27:33

The antrochoanal polyp, as you see here,

27:36

more likely to be a low density lesion, but it

27:39

does go through the osteum of the maxillary sinus.

27:43

Usually, we say it's the inferior osteum or the accessory

27:46

osteum, but it does then project into the nasal cavity.

27:50

That's sort of the choanal portion of it, and then it

27:53

can even project back into the nasopharyngeal airway.

27:57

Posteriorly.

27:58

So from here, it may project posteriorly

28:02

as a nasopharyngeal soft tissue mass.

28:05

In this case, again, look for a lower

28:07

density to suggest that it's an antrochoanal

28:10

polyp as opposed to the inverted papilloma.

28:14

Here is the, an inverted papilloma, as I mentioned.

28:16

It usually forms along the common wall of

28:20

the maxillary antrum and the nasal cavity,

28:23

and from there it can grow into the maxillary

28:25

sinus or into the nasal cavity, or both.

28:28

Here you see a little bit more growth into the

28:30

nasal cavity than into the maxillary antrum.

28:33

It will show solid enhancement,

28:35

not peripheral enhancement.

28:37

Peripheral enhancement, more common with

28:39

the antial polyp, not solid enhancement.

28:43

You can see that intermediate signal

28:45

intensity on the T2-weighted scan.

28:49

There are two features of inverted papilloma

28:52

that we say are relatively pathognomonic

28:56

to suggest that specific diagnosis.

28:59

One is this little bony bar upon

29:03

which the tumor may be fixed.

29:05

So if you see that hypostatic bone.

29:10

The tumor seems to be centered

29:12

around that hypostatic area.

29:16

That would be an indicator for an inverted papilloma.

29:20

Again, usually the common wall between

29:22

the maxillary antrum and the nasal

29:25

cavity, or along the midline nasal septum.

29:32

The other feature that we say is.

29:34

Relatively pathognomonic for an inverted

29:37

papilloma is this cerebriform.

29:39

Look to it, it, it has almost a look like gyriform and osseous

29:44

within it that you see here, or gray and white matter.

29:48

And you can see the enhancement, uh, as, as you see here.

29:51

Maybe this is the cortex and this is the

29:53

underlying white matter that imaging.

29:58

Pattern is more typical of inverted

30:02

papilloma than anything else.

30:04

Now that said, we always worry with inverted papilloma

30:07

because there is that high rate of concurrence of squamous

30:10

cell carcinoma and about 15%, so these tumors are resected

30:17

in their entirety and with a margin because of the worry

30:21

that there may be underlying squamous cell carcinoma.

30:25

Unfortunately, the squamous cell carcinoma

30:27

has the same relative imaging features

30:31

as that, um, of the inverted papilloma.

30:34

So it's not as if you can look at this and

30:35

say, oh, this is, um, you know, this one has

30:38

squamous cell versus this one that does not.

30:45

Okay.

30:46

Next case, question six, most likely diagnosis.

30:52

So we have, uh, axial CT and a coronal CT.

30:58

You see that, um, contrast was administered here.

31:07

What do we got here?

31:08

Do we have orbital cellulitis?

31:11

Periorbital cellulitis, post-septal

31:15

cellulitis, periosteal abscess,

31:19

or none of the above.

31:21

So this case, what are we looking at?

31:24

Are we looking at orbital cellulitis?

31:27

Are we looking at periorbital cellulitis?

31:29

Are we looking at post-septal cellulitis?

31:33

Are we looking at a perio-, subperiosteal

31:35

abscess, or none of the above?

31:42

All right, so we're moving right along here.

31:49

Let's see.

31:50

So, uh, 66% of people put subperiosteal abscess,

31:55

and that is, ding, ding, ding, the correct answer.

31:58

Let's go back to the original images.

32:00

So most of the cases of inflammation of the orbit

32:05

occur secondary to things around the lids, bites,

32:09

or, you know, uh, lacrimal problems, et cetera.

32:14

Lytic.

32:16

Things in the forehead, et cetera, and sinusitis.

32:20

And with sinusitis, it's most commonly the ethmoid

32:24

sinus that has that ability to spread to the orbit.

32:30

Why is that so? Um, you see this a

32:32

lot with kids because there are areas of

32:35

dehiscence along the lateral wall of the...

32:39

Ethmoid sinus, and even in adults, it occurs.

32:43

And if you think of the, um, lamina papyracea, the

32:48

medial orbital wall of the orbit being that thin,

32:51

that we would call it paper-thin, um, you

32:57

might expect that along those channels that have

33:00

vessels going into it, that you might have, um, a

33:04

route for spread from ethmoid sinusitis to the orbit.

33:09

Additionally, remember that we have the anterior

33:12

ethmoid artery and the posterior ethmoid artery that

33:15

enter the, um, that go between the orbit and the

33:20

ethmoid sinus through those areas of vascular channels

33:24

that communicate between the sinus and the orbit.

33:28

So here we have this collection.

33:31

You notice that it's displacing the medial rectus muscle.

33:34

The superior oblique muscle is enlarged

33:36

compared to the normal superior oblique muscle.

33:39

And we have this low-density collection

33:41

here, and that is accounting for here.

33:44

This is probably the medial rectus

33:46

muscle, and this is the collection.

33:50

With these collections,

33:52

we call them subperiosteal

33:54

abscesses, even if we do not see...

33:58

Peripheral enhancement.

33:59

So this is one of the locations that we would

34:02

still use the term abscess, even though on

34:04

the post-contrast scan you don't see a walled

34:06

off, um, collection with peripheral enhancement.

34:12

Most of the time nowadays, these lesions are

34:17

treated with, um, intravenous antibiotics

34:21

and close observation in the hospital.

34:25

And if it does not.

34:26

Quickly resolve, then they usually are going

34:30

to treat the sinus disease endoscopically and

34:34

try to address the primary source infection that's

34:38

causing this problem with the sinus disease.

34:43

When I was a resident and before

34:45

endoscopic sinus surgery was, um,

34:48

so popular.

34:49

Um, they would go medially along here and

34:52

under the periosteum and try to drain these

34:55

surgically, but that's not, this is no longer

34:59

primarily a surgical orbital procedure.

35:04

It's, let's, let's give, you know, high-dose intravenous

35:08

antibiotics, see how the patient does, if they've improved,

35:11

continuing them as an outpatient on oral antibiotics.

35:15

If they don't improve rapidly, then consider

35:18

endoscopic sinus surgery to reduce

35:21

the infection in the ethmoid sinus.

35:24

Generally, the ENT docs don't like operating when

35:29

there's active acute sinusitis because of the potential

35:33

for spread by virtue of their surgical procedure.

35:39

Okay, so this was a, um, subperiosteal abscess, uh, note

35:44

that post-septal cellulitis and orbital cellulitis are the

35:48

same entity, the inflammation that gets into the orbit.

35:52

Uh.

35:52

Here's an example.

35:53

Post-septal cellulitis on the left side

35:55

with infiltration of the orbital fat.

35:57

You notice that the orbital fat on the left side is

36:00

more dense than the orbital fat on the right side.

36:02

There's all kinds of episcleritis

36:03

that's happening here as well.

36:06

Here's a collection that you see superior

36:09

subperiosteal abscess in this orbital septum.

36:13

All the diagrams always show it on a sagittal scan.

36:17

What we usually, um.

36:19

Want to see.

36:20

It is in an axial plane, and this is the

36:24

demonstration of the orbital septum, in this

36:26

case, inflammation of the orbital septum.

36:28

Still called, um, periorbital.

36:32

Cellulitis.

36:32

Here we have the collection of the subperiosteal

36:35

abscess from the ethmoid sinusitis, but here's

36:38

the normal septal tissues that you see here and here.

36:43

Orbital septum.

36:47

There is a classification for

36:51

the degrees of orbital infection.

36:55

We have the Chandler classification.

36:58

Uh, number one is preseptal cellulitis, what we call

37:02

the periorbital cellulitis, postseptal cellulitis

37:05

or orbital cellulitis, a subperiosteal abscess.

37:08

So this was a case of grade three Chandler classification.

37:13

Uh.

37:14

Four is actual orbital abscess, where the

37:17

lesion is in the intraconal space, for example.

37:20

And then as an example of that Mucor mycosis case, we have

37:25

cavernous sinus inflammation and/or thrombophlebitis.

37:29

So I'm just gonna refer to the question here.

37:31

In your practice, do you proceed to MR with

37:33

contrast for cases of suspected inverted papilloma

37:37

on unenhanced CT or inject contrast on CT?

37:40

Uh, we're going with MRI, um, mainly because there is that

37:43

potential for perineural spread of tumor back through the.

37:49

Tegopalatine fossa as well as intracranial

37:52

spread, and both of those are much

37:54

better seen on post-GA MR than with CT.

37:57

So it's pretty rare for us to do a contrast

38:00

enhanced CT for neoplasms or for suspected

38:04

intracranial spread of an infection.

38:06

Can you have orbital subperiosteal

38:09

abscess without concurrent?

38:11

Orbital cellulitis.

38:13

In general, what you see is the infiltrate, uh,

38:16

the infiltration and edema of the intraconal fat

38:20

associated with the, um, the subperiosteal abscess.

38:24

So most of the time you get this infiltration of the fat.

38:28

So it is, um, you know, it is with concurrent, um,

38:34

orbital cellulitis, but with a Chandler, oops, the

38:37

Chandler classification, we would call it grade three.

38:42

Alright, moving on to the next case.

38:47

Here we have, uh, CIS imaging, T2

38:49

weighted high-resolution imaging.

38:51

This is the traditional coronal T2-weighted

38:55

scan, post-GAD T1 SAG scan, the axial T

39:01

2-weighted imaging and a post-GAD axial scan.

39:05

So here we have a, um, child and we have.

39:11

T2-weighted imaging, high-resolution as

39:13

well as post-gadolinium enhanced scans.

39:19

What term should not be used for

39:23

this lesion should not be used.

39:24

Uh, talencephalocele, sino with mortal ceal,

39:29

meningocele, basal cephalic, or none of the above.

39:34

They're all good.

39:35

So which of these is the inappropriate term?

39:39

For this lesion, would it be central encephalocele,

39:43

ethmoidal cephaloceles, meningocele,

39:47

basal cephalic, or none of the above?

39:51

They all apply to this lesion.

39:57

Okay, so for this case, um, the key here

40:01

is the difference between TAL and Basal.

40:05

And the distinction is that the basal

40:07

cephaloceles, obviously base of the skull

40:11

are generally invisible to the naked eye too.

40:16

Observation externally.

40:19

Al cephaloceles are ones that protrude beyond

40:23

the skull such that you see them like the

40:29

puffy tumor in the forehead, et cetera.

40:31

And those are usually nasal ethmoidal cephaloceles

40:35

that will project through the foramen and seek

40:39

other pathways and project as a visible

40:45

to the naked eye lesion.

40:47

So that's TAL as opposed to basal,

40:50

where it's invisible to you.

40:51

So the correct answer here is that this should not,

40:54

this is not TAL, no one would be able to tell

40:57

what's going on despite the huge size of this lesion.

41:01

And this was indeed a, um, congenital,

41:05

um, a congenital, uh, encephalocele.

41:08

Now, the term cephaloceles is kind of a, you know, um,

41:14

indistinct, let's say, um, usually we want to know whether

41:18

the ceil contains meninges and fluid and/or brain tissue.

41:24

So, depending upon whether you think this

41:27

is purely meninges and fluid, you might use the

41:30

term meningocele. If you think that there is indeed.

41:34

Brain tissue, brain matter,

41:35

that's herniating through as well.

41:38

You would use the term encephalocele, and if

41:41

it's both the meninges, the fluid, and the brain

41:44

tissue, we would use the term meningoencephalocele.

41:48

The sloppy term or the, or the lazy term

41:52

would just be encephalocele, which

41:54

you're not making that distinction now.

41:57

Um, let me just see whether I can, um.

42:02

Go with the answer in the chat.

42:05

Do you think that this, um, cephalic e is congenital?

42:11

If you think it's a congenital lesion, please answer

42:15

yes in the chat. If you think that it, no, it's.

42:20

Developmental or secondary to operative or

42:23

trauma or other defect in the skull base?

42:27

You would answer no.

42:28

So just in the chat, if you think this is congenital,

42:31

say yes.

42:32

If you think no, this, this is, um, you know,

42:34

developmental or post-op or other cause, say no.

42:40

So I'm looking in the chat and there's a lot

42:42

of yeses and that is indeed the correct answer.

42:46

And one of the reasons why you know it's the

42:48

correct answer is you may have noticed that there's

42:50

missing portions of the splenium, of the corpus

42:53

callosum and the rostrum of the corpus callosum

42:56

identifying other congenital lesions that would

42:59

suggest that this is a congenital encephalocele.

43:03

Here is that CT scan where I was saying that

43:05

there was absence of the cribriform plate.

43:07

And look at this.

43:09

Same patient, brain tissue and fluid

43:12

and meninges assumed to be present.

43:16

Meningoencephalocele.

43:18

Through the cribriform plate.

43:20

This was a post-op patient who had

43:23

a defect in the cribriform plate.

43:25

This is a different patient, T1-weighted scan.

43:28

Notice the puckering of the brain tissue

43:31

towards this gap in the cribriform plate.

43:34

Post-gadolinium, a little bit of an,

43:36

uh, enhancement of inflammatory change.

43:40

This is actually the collection here and

43:43

here and where the collection is in the

43:46

brain tissue is you don't see the, um.

43:48

You don't see the, uh, enhancement.

43:52

So cephaloceles are a cause, uh, potential cause of

43:55

CSF rhinorrhea and, um, as you see here, congenital

44:01

most common occipital associated with potentially

44:04

are Chiari malformations, post-op, post-trauma.

44:09

Sometimes idiopathic intracranial hypertension

44:12

or pseudotumor cerebri may be associated

44:14

with cephaloceles and meningocele.

44:18

Um, you all, that's why we look at the Meles

44:20

cave region to see where that's associated.

44:23

And some tumors also may cause,

44:26

um, CSF rhinorrhea and/or seal.

44:30

Okay, next case.

44:35

CT scan.

44:35

We have a coronal recon.

44:37

Coronal reconstruction from the axial data.

44:39

And here's the axial scan. Most likely diagnosis here

44:43

Is this a mucus seal?

44:45

Is this a mucus retention cyst?

44:47

Is it silent sinus syndrome?

44:49

Is it a hypoplastic maxillary antrum, or is it a polyp?

44:55

So given, uh, question number eight is.

44:59

Is this a mucus seal?

45:00

If so, answer number one.

45:02

If you think it's a mucus retention

45:03

cyst, we're gonna answer number two if

45:05

you think it's a silent sinus syndrome.

45:07

Number three.

45:08

Number four, for hypoplastic maxillary sinus.

45:11

And number five, a polyp.

45:13

So obviously the abnormality

45:16

is in the left maxillary sinus.

45:20

How did the audience do on this case?

45:24

All right, so 73% of y'all went with silent sinus

45:28

syndrome, and that is indeed the correct answer.

45:31

Why is this not just a hypoplastic maxillary sinus?

45:36

Well, the imaging findings that you note, no doubt, are

45:39

the puckering inward of the posterior lateral wall of the

45:42

maxillary sinus associated with the proliferation of the

45:45

fat, and usually the floor of the orbit ipsilateral is.

45:54

Depressed.

45:55

And the common clinical finding here is

45:59

enophthalmos because everything's getting

46:02

sucked in, and the globe actually, um,

46:06

becomes more inwardly displaced as the sinus is.

46:10

Uh.

46:11

Progressively decreasing in volume.

46:13

So this is a source of enophthalmos

46:16

and, uh, chronic sinusitis.

46:18

This, on the other hand, is a patient

46:20

who has a hypoplastic maxillary antrum.

46:24

You notice in this case that the walls of the

46:27

maxillary bone are actually thickened, associated

46:31

with that hypoplastic maxillary antrum, and

46:35

the floor of the orbit is not depressed.

46:37

Here's another.

46:39

Hypoplastic left maxillary antrum.

46:42

Uh, although this is bone window, you see

46:44

that there's no proliferation of the fat that

46:47

is associated with silent sinus syndrome.

46:49

So silent sinus syndrome.

46:51

Usually you see complete

46:52

opacification of the maxillary antrum.

46:55

This was a little bit unusual in that it wasn't

46:57

completely opacified, and we call it also the

47:01

ectatic sinus as it kind of collapses on itself.

47:06

And, um, this is a manifestation of chronic sinusitis

47:10

with reduced pressure leading to the walls collapsing

47:14

inward and compensatory enlargement of the perianal fat.

47:19

So silent sinus syndrome, usually with an opacified sinus.

47:26

Okay, we're going to end on this one.

47:27

It's, um.

47:29

Sort of a classic case, and I wanted to show

47:31

it in the, uh, session SAG T one-way scan.

47:36

This is an MRA that was performed

47:41

because of the suspicion of an aneurysm.

47:45

And this is a T2-weighted.

47:46

This is actually a HASTE image 'cause the

47:49

patient was moving all over the place.

47:51

But, uh, subtly one MRA and HASTE image.

47:59

Is this most likely a mucus seal?

48:02

Is it a thromboaneurysm?

48:05

Is it a schwannoma?

48:07

Is it an epidermoid, or is it none of the above?

48:11

So this lesion that we're seeing here, is this

48:13

most likely a mucosal, a thromboaneurysm, a

48:18

schwannoma, an epidermoid, or none of the above.

48:27

Final case, so this is a petrous apex.

48:31

Case, and the petrous apex is very

48:33

much like the paranasal sinuses.

48:35

So I thought it was okay for me to put it in here in

48:39

a sinus talk, and the petrous apex may be pneumatized,

48:43

it may not be pneumatized. When it's pneumatized,

48:46

um, it has the potential for petrous apex, for petrous

48:51

apex mucus seals, and for an inflammatory reaction.

48:56

From bleeding, that leads to a giant cell reaction

49:00

and what we, uh, will call a cholesterol granuloma.

49:05

So the correct answer here is none of the above.

49:07

This is an example of a cholesterol

49:10

granuloma, which is typically bright on T1.

49:14

Maybe bright or dark on T2, depending upon

49:16

the protein/blood/CHO content of it.

49:21

You see, uh, here on the T1, it's in

49:24

the petrous apex, it expands the petrous apex.

49:28

So you see that here.

49:30

The differential diagnosis is, is all

49:33

of these a mucus seal of the apex?

49:38

Could look just like this as well, and it's

49:42

in the differential diagnosis, but cholesterol

49:44

granulomas are much more common, and they're

49:47

more heterogeneous, particularly on T2-weighted

49:50

scanning. Most of the time with mucus seals,

49:53

it's uniform signal intensity throughout the mucus seal.

49:57

Here, you've got a little bright area, you've got a little

50:00

darky, you've got a little peripheral rim here of black.

50:03

Is that hemosiderin, or is that the bone that's

50:07

pretty typical of a cholesterol

50:08

granuloma, not so much a mucus seal.

50:11

The reason why we have the MRA is to exclude a thrombo

50:14

aneurysm because your petrous carotid artery courses right

50:18

by here, and if you have a partially thromboaneurysm,

50:22

you could have signal intensity that looks like blood

50:26

products that will simulate a cholesterol granuloma

50:29

in this case, right on T1, and it may be any.

50:33

Any signal intensity on the T2, remember that

50:36

thromboaneurysms may have that same layering effect.

50:41

Laminated appearance that you can see with a cholesterol

50:45

granuloma, therefore could simulate that as well.

50:49

Not likely gonna be a schwannoma,

50:50

not in the petrous apex epidermoid.

50:52

So that's fair.

50:54

Right?

50:54

Because they may be bright on T1s.

50:57

The so-called white epidermoids.

50:59

Most of them are dark on T, on T1.

51:03

Um, and look kind of like dirty CSF on the.

51:07

On the, uh, flare.

51:09

Most of them, however, are very bright on the

51:11

T2, so this signal intensity would argue

51:14

against an epidermoid of the petrous apex.

51:17

Epidermoids can occur anywhere

51:18

in these bones, so it's fair.

51:20

Again, we would hopefully have a diffusion-weighted

51:23

scan, which might help us remember, however, that

51:25

diffusion-weighted scans in the presence of hemorrhage.

51:28

It got very confusing to interpret because

51:31

it looks bright and it may look like it

51:33

has dark ADC, but it's really not.

51:35

It's, you know, blood products can do that.

51:38

So, um, in this case, the correct answer

51:41

was none of the above because this was a

51:43

cholesterol granuloma of the petrous apex.

51:46

So, at this juncture, I am happy to

51:52

answer any and all questions about.

51:55

Sinus Imaging.

51:57

Uh, I will put in a couple of plugs if you don't mind.

52:00

Um, and that is, uh, on our MRI online modality

52:05

website, you have a case bank of 100 brain, 100 spine

52:13

and 100 head and neck cases with multiple choice

52:16

questions that I've created as part of an effort to.

52:21

Have MRI online as, as one of your sites that you go

52:24

to for case, uh, for case review, for board review.

52:27

So if you, you know, are a little shaky in your neuro,

52:30

um, come see me at Johns Hopkins or alternatively go

52:35

to MRI online and they have material there and, um,

52:38

they are building a larger and larger, uh, case bank

52:42

with multiple choice questions to simulate the boards.

52:46

And, uh, that's probably gonna be it.

52:48

Appropriate for the next couple years until we

52:49

return to the oral board format with, uh, Hotze.

52:56

So, um, I'm gonna go to the Q and A and

53:01

see where there are any questions for me?

53:03

Okay.

53:04

Questions and answers.

53:05

Excellent.

53:05

Uh, question.

53:07

Can susceptibility imaging help in the

53:09

diagnosis of cholesterol granuloma?

53:13

So most of the time.

53:17

The blood products or the brightness is bright on T

53:21

one and bright on T1 is methemoglobin and met.

53:26

Hemoglobin does not have proton relaxation enhancement

53:31

unless it's in the extra, uh, in the intracellular form.

53:35

So remember that in order to see susceptibility

53:39

artifact, you have to have a difference on

53:41

the signal intensity or, or the iron content.

53:46

Inside the cell versus outside the cell or

53:49

inside the brain versus in the extracellular space.

53:52

So if the blood products are bright on T1 and

53:55

bright on T2, that's the extracellular hemoglobin

53:58

phase where you have proton-electron dipole dipole

54:01

direction, but you do not have proton relaxation

54:04

enhancement, which is the T2 shortening effect.

54:06

So just a quick review of hemorrhage.

54:10

Methemoglobin has.

54:14

Proton-electron dipole dipole interaction, which leads to

54:17

T1 shortening, which makes it bright on a T1-weighted

54:20

scan, having blood intracellular and not extracellular.

54:25

It leads to a bar magnet effect of the difference

54:29

in charge between in the cell versus outside

54:31

the cell, which leads to proton relaxation

54:33

enhancement, which leads to T2 shortening.

54:35

Once you have cellular lysis and it's

54:37

extracellular and hemoglobin, you no

54:40

longer have proton relaxation enhancement.

54:42

It's no longer dark on T2, and that's why it is.

54:44

Bright on T2 from water content.

54:47

So a little digression there

54:50

into hemorrhage, but appropriate.

54:52

Um, hey, what do Circle of Willis

54:55

and your background stand for?

54:57

COW?

54:58

Um, Circle of Willis, I think.

55:00

And that was the MRA.

55:02

I think it's the picture of your cows

55:03

behind you, Dr. Oh, my cow's behind me.

55:06

People wanna know about my cows.

55:07

Those are bulls.

55:08

And this is my, uh, Picasso lithograph.

55:12

And, uh, if you wanna read about it, you can

55:15

call, you can look up, uh, Picasso's bulls, but

55:19

effectively what I've interpreted as to be is

55:21

that this is the progression of Picasso's artwork

55:25

going from initially charcoal drawings to.

55:28

Uh, realism and then he converts

55:31

to cubism over the course of time.

55:33

This is more cubic cubism.

55:35

And then if you look over here, he got really

55:38

minimalistic at the end and he just did line drawings.

55:41

So this is the sort of the history of

55:43

Picasso's interpretation and how he drew bulls.

55:48

And this is Picasso's, uh, signature right here.

55:50

So, okay.

55:52

What do the cow in the background please?

55:54

Could you explain the features the surgeon

55:56

needs to know in our sinonasal CT reports?

55:59

Okay, so, um.

56:02

As I said, most of the time, the surgeon needs to

56:04

know whether or not there are any areas of dehiscence.

56:07

The endoscopic sinus surgery nowadays is

56:10

basically a medial antrostomy with removal of

56:13

the uncinate process and a potential ethmoidectomy.

56:17

The vast majority of the surgeries, they will sometimes

56:20

go into the sphenoid sinus recess and relieve.

56:23

Obstruction for the sphenoid sinus

56:25

and posterior ethmoid sinuses.

56:27

So that said, the main thing are the areas of dehiscence

56:31

around the ethmoid sinus that potentially could be the

56:34

cribriform plate superiorly and the lamina papyracea.

56:40

Laterally.

56:41

It's only if they're going into the sinonasal

56:43

ethmoidal recesses that you would worry about those

56:46

dehiscence in the carotid artery or the optic nerve.

56:48

Now, the other things that they want to know

56:51

is, is the ATE process opposed or attached

56:56

to the orbital floor or medial orbital wall?

57:00

There are.

57:01

Times when that occurs.

57:04

And if they're going to remove that ATE process and do

57:08

the medial antrostomy, and they rip that.

57:12

ATE process and pull on it.

57:14

Then they're pulling on the orbital floor or the

57:16

medial orbital wall, and you can have that dehiscence

57:19

and then bleeding into the orbit, orbital hematoma.

57:22

So they wanna know about the ATE process, whether

57:25

it's just hanging free as it does 90% of the time, or

57:29

is it bending over to the orbital floor or even to

57:33

the medial orbital wall of the lamina, um, aia.

57:37

So those are the main things they wanna know.

57:41

Explain question two again.

57:43

Oh my God.

57:44

Um, Ashley, can you go back to question two?

57:47

I don't remember which one that was.

57:50

Okay, yeah.

57:50

Well, she's doing that.

57:51

Are there any particular aspects of the

57:53

bone involvement in sinonasal pathology that

57:55

are specific or should guide our diagnosis?

60:28

For all those of you who have these questions

60:30

and would like a little bit more definition,

60:33

um, I did create a Sino Nasal Mastery course.

60:37

It's, uh, between two and three

60:39

hours, gets into more of the.

60:42

Inflammatory disease and the sinusitis and the O

60:45

osteo complex, et cetera, with examples of all these

60:49

different types of cells, the, you know, the Haller

60:52

cell, which is the maxillary ethmoidal cell below

60:54

the orbit, um, and the named cells, so to

60:59

speak, and how to distinguish them most of the time.

61:04

The surgeons nowadays are doing a

61:05

relatively minimalistic surgery.

61:08

They're just trying to open the osteomeatal unit,

61:11

so the atelectasis process is taken down; that allows the

61:15

infundibulum in the middle meatus to drain more easily.

61:19

Sometimes they're doing the partial

61:21

ethmoidectomy, not all the time.

61:24

Um, and

61:26

they're just trying to open the channels.

61:28

Same thing with the frontal, with the morton recess.

61:30

They're just trying to open that up for frontal sinus so

61:32

it will drain properly because the more what they found is

61:35

the more they operate and the more they take out, the

61:39

more likely you've screwed up the mucociliary clearance

61:43

that normally pushes the mucus in the appropriate

61:47

location back in the back of the throat, and then we go.

61:53

And we swallow it down.

61:56

So that's actually the best way, you know, the natural

61:59

way that mucociliary clearance goes, it passes it

62:02

back to the pharynx for us to swallow it down.

62:05

If you do too much of this operation, you ruin all the

62:08

cilia and everything, then it's all distorted and you

62:10

have chronic sinusitis because it's not draining properly.

62:13

So a little bit more minimalistic about

62:15

functional endoscopic sinus surgery these days.

62:19

Um, please, can you explain exactly what we have to

62:21

look for, anterior ethmoidal artery in our report, so

62:23

I don't even report on the anterior ethmoidal artery.

62:26

Anyone who's doing sinus surgery endoscopically

62:29

should be able to identify the anterior

62:33

and ethmoid and posterior ethmoidal air.

62:35

Um, communications.

62:37

Um, it's that little triangular thing that you see.

62:40

Again, I did describe this in my Mastery Series course.

62:44

It's the little triangular opening to the.

62:47

Uh, to the ethmoid air cells, um,

62:51

that you'll see on the coronal CT scan.

62:55

That is the potential source of an

62:58

orbital hematoma if they nail it.

63:00

But, uh.

63:01

Orbital hematomas are incredibly uncommon

63:04

nowadays with endoscopic sinus surgery.

63:06

Everyone knows the anatomy.

63:08

They do 3D to guide them most often, and so

63:12

they know where the carotid artery is, the up

63:15

optic nerve, the anterior ethmoidal artery.

63:18

So it's pretty rare to, to nail that.

63:20

Uh, please gimme have to.

63:22

Okay.

63:23

Uh, question number two.

63:24

What was question number two?

63:26

Uh, something that was about hot puffy tumor.

63:29

Uh.

63:30

Oh, pott’s puffy tumor.

63:31

So pott’s puffy tumor.

63:32

As you saw in that specific case, you saw a

63:34

defect that was in the frontal sinus leading

63:37

to the scalp, and it was a large inflammatory.

63:40

Process, not a tumor that occurs in the scalp and

63:44

then presents as a soft tissue mass in the frontal

63:48

region, and most commonly from frontal sinusitis.

63:51

When you have pott’s puffy tumor, you always

63:53

have to worry about potential intracranial

63:55

complications, which would include meningitis,

63:58

sinus thrombosis, and an epidural abscess.

64:05

I think that's it.

64:06

Dr. Uim.

64:07

Yeah, I think so.

64:09

Well, thank you so much for the case review

64:11

and for answering all those questions you got.

64:12

We appreciate it.

64:14

Thank you so much for this case review and for

64:16

everyone in the audience for participating,

64:18

be sure to join us for upcoming webinars.

64:20

You can register for those@modality.com

64:23

and follow us on social media for updates

64:25

on future lectures and case reviews.

64:27

Thanks again for learning with us and we'll see you soon.

Report

Faculty

David M Yousem, MD, MBA

Professor of Radiology, Vice Chairman and Associate Dean

Johns Hopkins University

Tags

Vascular Imaging

Pediatrics

Nuclear Medicine

Neuroradiology

Musculoskeletal (MSK)

Interventional

Head and Neck

Genitourinary (GU)

Gastrointestinal (GI)

Chest

Cardiac

Breast

Body

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