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Hello and welcome to Case Crunch Rapid Case

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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

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best choice via the live polling feature.

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

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

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review and previous case reviews by creating a free account.

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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

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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

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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

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64:23

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64:25

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64:27

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