0:02

Hello and welcome to Case Crunch Rapid Case

0:04

Review for the core exam hosted by Medality.

0:08

In this rapid fire format, faculty will

0:10

show key images along with a multiple-choice

0:12

question, and you'll respond with your

0:14

best answer via the live polling feature.

0:17

After a quick answer explanation,

0:19

it's onto the next case.

0:21

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

0:23

review and previous case reviews by creating a free

0:26

account using the link provided in the chat.

0:29

Today, we're honored to welcome Dr. Melissa Carroll

0:31

for a thoracic imaging board prep case review.

0:34

Dr. Carroll is an assistant professor in the Department

0:36

of Radiology at the University of Kansas Medical

0:39

Center, specializing in cardiothoracic imaging.

0:43

She completed her diagnostic radiology

0:45

residency at the University of Kansas School of

0:47

Medicine and cardiothoracic imaging fellowship

0:50

at University of Wisconsin in Madison.

0:52

She's passionate about resident and medical student

0:54

education and mentorship, and we're thrilled.

0:56

She's here today to lead this case review.

0:59

Questions will be covered at the end if time allows.

1:02

So please remember to use the Q and

1:03

A feature to submit your questions.

1:06

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

1:08

Dr. Carroll, please take it from here.

1:11

Hi everyone.

1:12

Thank you so much for joining me today.

1:14

Um, we're gonna try and get through about

1:16

25 thoracic imaging cases, um, that will

1:20

hopefully touch on a lot of, um, high-yield

1:22

topics for your Core Exam that's coming up.

1:26

Um, and then hopefully we'll have a few minutes

1:28

at the end, um, for any questions that come up.

1:31

Um, like the introduction said, I'm Melissa Carroll.

1:34

I'm an assistant professor of cardiothoracic radiology

1:37

at the University of Kansas, um, in Kansas City, Kansas.

1:41

Um, and again, thank you for joining us.

1:43

Um, I have no disclosures.

1:47

So our first quick little question, um, I

1:50

just wanna learn who all is here with us.

1:52

So, um, are you a resident that's

1:55

taking the Core next month?

1:56

Are you an attending physician?

1:58

Are you just here for the cases?

2:00

Maybe you're just a resident trying to gain some

2:02

extra studying, um, or any other possibility.

2:15

Okay, perfect.

2:16

So it looks like about 60% of you

2:19

are residents taking the exam.

2:20

Um, and then we got a few others that are

2:23

just here for the cases and then a couple

2:24

attending physicians, so that's great.

2:27

Okay, let's get started with case number one.

2:31

Um, so I will give you, um, a brief little, um, history

2:36

of the patient, um, and then show you some images and

2:40

then a multiple choice question on the next slide.

2:42

So this first case is a 41-year-old female, um,

2:46

that's presenting for evaluation of dyspnea.

2:51

So we've got coronal and axial CT images of the lungs.

2:57

I'll give you guys a couple of seconds to look

3:00

at these.

3:04

So think about what your differential diagnosis

3:06

would be, how you would describe the findings.

3:14

So what is the most likely diagnosis?

3:17

A. Usual interstitial pneumonia.

3:20

B. Nonspecific interstitial pneumonia.

3:23

C. Acute interstitial pneumonia or organizing pneumonia.

3:36

Okay, so 60% said NSIP.

3:41

That's correct.

3:44

Go to the next slide here.

3:48

So nonspecific interstitial pneumonia.

3:50

This is a common type of

3:51

fibrosing interstitial pneumonia.

3:54

Typically, we have basal predominant ground glass

3:57

opacities that are in this per bronchial or more

4:00

central distribution than what we see with UIP.

4:03

Um, you typically have a little more traction,

4:06

bronchiectasis than we see with UIP.

4:10

Um, and then plus or minus subpleural sparing.

4:12

This can be really specific for NSIP and can

4:15

be very helpful, but is not always the case.

4:17

Um, I think most people quote about 60% of the

4:20

time that you'll see the subpleural sparing.

4:23

Um, NSIP can be idiopathic, but commonly

4:27

it's associated with an underlying

4:28

connective tissue or autoimmune disease.

4:31

Um, sometimes this could be the first presenting symptom

4:35

or presenting finding in a patient with an autoimmune

4:37

disorder, particularly like myositis syndromes.

4:40

Um, so keep this in the back of your mind.

4:43

If you see a patient come in through the

4:44

ED and they have this type of appearance,

4:47

um, throw out there that this could be an

4:50

underlying autoimmune disorder causing this.

4:54

Okay, case number two.

4:56

This is a 3-year-old male with recurrent pneumonias.

5:00

I'll give you a few seconds to look at these images.

5:13

Okay.

5:13

So name a common imaging finding associated with

5:17

the underlying diagnosis, hypertrophy, bronchial

5:20

arteries, lower, lobe predominant bronchiectasis,

5:23

calcified lymph nodes, or pulmonary emboli.

5:35

Okay, good.

5:37

All right.

5:37

The answer here is hypertrophied bronchial arteries.

5:42

So this is a case of cystic fibrosis.

5:45

Um, you can see, I'll go back to this first slide here.

5:48

Um, a classic imaging appearance on chest

5:52

radiograph of upper, lobe predominant bronchiectasis,

5:55

um, causing architectural distortion.

5:58

Then you can see the CT correlate, where again,

6:01

we've got, um, bronchiectasis, some areas of

6:04

consolidation and really severe architectural

6:07

distortion, um, most pronounced in the upper lobes.

6:12

So, um, hypertrophied bronchial arteries are a finding

6:15

that you may see in a patient with cystic fibrosis.

6:19

Um, so CF is an autosomal recessive disorder

6:22

from the CF, from mutations in the CF transmembrane

6:25

conductance regulator or the CFTR gene,

6:28

um, which regulates chloride transport.

6:31

So this, uh, this affects the thickness and viscosity

6:34

of, um, of secretions in the lungs, um, and can lead

6:39

to chronic airway destruction and recurrent infections.

6:42

So classically we see bronchi wall thickening,

6:44

bronchiectasis, um, and it's most severe in the upper

6:48

lobes, which is kind of your key finding here to

6:51

differentiate from other, um, other lung diseases.

6:55

Um, and then those chronic bronchial injuries

6:58

is what leads to hypertrophy or bronchial angiogenesis

7:01

and vascular hypertrophy of those bronchial arteries.

7:05

This image here shows the bronchial, an

7:07

example of a hypertrophied bronchial artery.

7:09

Your bronchial arteries are what extend from the descending

7:12

aorta to the hilum and supply the hilar structures.

7:16

Um, they supply them with vascularity.

7:19

Um, they usually come off around T5, T6.

7:23

Um, so again, this is a nice example of a

7:26

hypertrophied bronchial artery in the setting of CF.

7:32

Okay, case number three.

7:34

So this is a 28-year-old CTIC male with cough,

7:38

fever, and small purple papules on his arms.

7:43

So look at the radiograph.

7:44

Think about how you would

7:45

dictate this if you were on call.

7:48

What would be your differential and your findings?

7:56

So hopefully in your mind you're thinking

7:58

something like, there's irregular kind of

8:01

perihilar predominant opacities and nodularity,

8:06

with relative sparing of the periphery.

8:11

And we've got CT, uh, coronal and axial images.

8:15

And the question is, what is the diagnosis?

8:19

Is this pneumocystis pneumonia, sarcoidosis?

8:23

Strep pneumonia, or Kaposi's sarcoma?

8:26

Sarcoma.

8:37

Perfect.

8:38

Yeah.

8:38

So most people chose Kaposi's sarcoma.

8:41

Great.

8:43

So the key here is really in this, this question stem.

8:46

If I didn't give you the small purple papules

8:48

on the arm, your differential would be a little

8:50

bit wider, but this tips you off that this

8:53

may be an HIV patient with Kaposi's sarcoma.

8:57

So this is a low-grade mesenchymal neoplasm of blood

9:00

and lymphatic vessels, um, that can affect the skin and

9:04

also disseminate disease, which can affect the lungs.

9:07

And it's primarily in patients with HIV.

9:10

Um, so you get these classic flame-shaped nodules

9:14

in this peri-bronchovascular central distribution.

9:19

Um, you can also get some ground glass opacities,

9:21

some interlobar septal thickening or fissure thickening,

9:25

um, sometimes lymphadenopathy and pleural effusion.

9:27

So don't let those, if you see those extra

9:29

findings, don't let that throw you off

9:31

from what the underlying diagnosis is.

9:33

Um.

9:35

But having this history of a patient with

9:36

HIV and that rash is gonna be your big clue

9:40

to, um, placing this as Kaposi's sarcoma.

9:45

Okay, case number four.

9:47

This is a 38-year-old male with shortness of breath.

9:51

So we've got axial and coronal CT images of the lungs.

10:04

Some keys to taking some of these cases,

10:07

uh, particularly when you're given

10:08

a coronal or a sagittal view of the lungs.

10:10

Always look at that cranial-caudal

10:12

distribution of what the abnormality is.

10:18

Okay, so what is the next best step

10:20

in management for this patient?

10:23

Is it percutaneous biopsy, bronchoalveolar lavage?

10:27

Should we get a PET CT or smoking cessation?

10:40

Okay, so we had a few people say

10:43

bronchoalveolar lavage, and then most people

10:45

saying smoking cessation, so that's great.

10:51

So this is pulmonary Langerhans'

10:52

cell histiocytosis, or PLCH.

10:55

You'll hear it abbreviated pretty frequently.

10:58

Um, so this occurs in smokers, um, and

11:03

it appears as upper lobe predominant

11:06

small nodules and bizarre-shaped cysts.

11:10

So if you look on the CT image, you can see

11:12

this little irregular cystic space here.

11:16

Um, that's a classic looking PLCH cyst.

11:19

Um, sometimes you'll hear people

11:20

say like the cheerio-shaped cyst.

11:23

Um, so be on the lookout for the, for

11:25

buzzwords like that bizarre-shaped or

11:28

cheerio-shaped cyst in the upper lobes.

11:31

Um, classically the costophrenic

11:33

angles in these patients are spared.

11:35

Um, so the upper lobes can look really busy

11:37

with all these nodules and cystic spaces,

11:39

and then the bases look completely clean.

11:43

Um, so this is caused by the, um, per

11:46

bronchial proliferation of Langerhans cell

11:48

histiocytosis, um, which form these stellate

11:52

cells around the airways, which then, um, enlarge

11:56

and cavitate, forming these thick-walled cysts.

11:58

So this is why you see kind of this

12:01

differing, differing, um, imaging

12:03

appearance with the nodules and the cysts.

12:06

Um, it's the same mechanism, just in different

12:08

time points of the hypertrophy of the

12:12

cells and then forming into cavitary spaces.

12:16

Um, so these irregular and stellate nodules that

12:20

can be one to ten millimeters in size.

12:24

Um, and again, the cysts can vary

12:26

much in size and shape.

12:28

They can have thin or thick-walled, um.

12:32

Over time, you can get this burned-out appearance of

12:35

PLCH, um, where a lot of the kind of cystic spaces

12:39

and nodules are less apparent and you are kind of left

12:42

with more of a reticular pattern in the lung apices.

12:46

Um, so if you ever see that in a smoker, go back

12:49

and look at some of their previous imaging, you may

12:51

find a more classic appearance years previously.

12:55

Um, and then the main treatment

12:57

for this is just smoking cessation.

12:59

Um, a lot of patients, um, will have complete reversal

13:03

of these findings, um, after they stop smoking.

13:09

Okay.

13:09

Case number five.

13:11

This is a 54-year-old female with

13:14

mild dyspnea for three months.

13:24

Okay.

13:24

What is the next step in management?

13:27

Should we biopsy, bronchoalveolar,

13:29

lavage, PET CT, or smoking cessation?

13:33

So same options as before.

13:44

Perfect.

13:45

So most of you, the majority of you said

13:47

bronchoalveolar lavage, which is completely correct.

13:51

Move to the next slide.

13:54

So this is pulmonary alveolar proteinosis or PAP.

13:59

Um, you get accumulation of surfactant-like

14:01

material in the alveoli and the terminal bronchioles.

14:04

Um, it's either from deficient surfactant

14:07

protein or impaired function of the

14:08

G-M-C-S-F, um, often from autoantibodies.

14:12

So the etiology of this, most

14:15

of the time it's idiopathic.

14:17

Um, and then.

14:19

Otherwise it, it could be secondary to something else.

14:21

So like an inhalational injury, a lot of times it

14:24

could be from an underlying autoimmune disorder,

14:27

hence the autoantibodies to G-M-C-S-F, um, or there

14:31

could be an underlying hematologic malignancy.

14:34

And then rarely, this can be PAP can be congenital.

14:39

Um, so typically patients will have

14:42

kind of chronic cough over a few months.

14:44

They'll have a similar imaging appearance to

14:46

what we're seeing on the, on the CT imaging,

14:49

um, with ground glass opacities and superimposed

14:53

reticulation or that crazy paving appearance.

14:56

Um, it's named after, um, pavers

14:59

like this down here on the bottom.

15:01

Um, so think about that, that crazy paving appearance.

15:05

You classically have areas of geographically

15:07

spared lung, so you have kind of a sharp demarcation

15:11

between the ground glass opacities

15:14

and just relatively normal lung adjacent to it.

15:17

Um, the patients that have this are

15:19

usually young to middle age, um, and it

15:21

does have an association with smoking.

15:24

Um, and again, the treatment

15:25

is bronchoalveolar lavage.

15:28

Um, a lot of these, they go in, they wash out the

15:31

lungs, get all this, um, junk out of the lungs,

15:34

and a lot of the patients never have a recurrence.

15:37

Um, and that occasionally some patients can, but for

15:40

a lot of them this, um, is curative to undergo BAL.

15:46

All right, case number six 42-year-old

15:50

female with progressive dyspnea.

16:03

Okay, so what is a common finding associated with the

16:06

underlying diagnosis that these images are showing?

16:11

A kylothorax effusion, calcified lung

16:13

nodules, mediastinal lymphadenopathy.

16:17

Bone lesions.

16:27

Okay, perfect.

16:29

So the answer here is chylous effusion.

16:31

You can even see down here in the CT image.

16:34

That this patient has an effusion down here.

16:37

So this is lymphangioleiomyomatosis.

16:41

Um, this is from the proliferation of

16:44

neoplastic smooth muscle-like cells.

16:46

You can get sporadic LAM or LAM

16:48

associated with tuberous sclerosis.

16:51

Um, so remember that for boards, that

16:52

association. Um, sporadically, most commonly

16:56

occurs in women of childbearing age.

16:59

And the CT appearance looks similar to this.

17:02

This is again, when you have it, when they're

17:04

giving you a cranial or a coronal CT image.

17:07

Look at that cranial-caudal distribution.

17:09

And you can see we have relative diffuse

17:11

distribution of these thin-walled lung cysts.

17:15

And they're, they're pretty similar in size.

17:17

They're pretty uniform.

17:18

And again, diffusely distributed.

17:21

You can also get some ground

17:22

glass opacities from hemorrhage.

17:24

You can get some septal thickening.

17:26

You can get hemo- or pneumothorax.

17:29

You can see here this patient has a small

17:30

pneumothorax, probably from one of these

17:32

cysts that ruptured to the pleural space.

17:35

Um, lymphadenopathy and then renal.

17:37

Renal AMLs are the other associations to think of.

17:41

And then again, pleural effusions, which most likely

17:45

if they sampled the fluid would be chylous fluid.

17:48

So remember that association with LAM, chylous effusions.

17:54

Okay, case number seven.

17:55

This is a 73-year-old male with chronic dry cough.

18:03

So think about how, what descriptors you would use

18:06

to descr— to, um, to describe this on a CT image.

18:13

Okay.

18:13

So what is the CT pattern of fibrosis?

18:17

Probable UIP, UIP, organizing pneumonia,

18:22

or non-specific interstitial pneumonia.

18:33

Okay.

18:33

Okay.

18:34

So we're about 50-50 between probable UIP and UIP.

18:39

Okay.

18:40

So the key here is identifying this area of

18:44

honeycombing down here, and probably some, some

18:47

single layers of honeycombing, um, down here

18:50

in the lower lobes, but particularly out here.

18:53

So UIP and probable UIP.

18:57

Are similar in appearance other than the fact,

19:01

other than there being the presence of honeycombing.

19:03

And that pushes us into the UIP pattern.

19:06

So UIP, idiopathic pulmonary fibrosis.

19:11

Um, the UIP describes a histologic finding

19:16

that we correlate with CT imaging findings,

19:21

um, to allow or to prevent the patient from

19:23

having to undergo a surgical lung biopsy.

19:26

So we can be, um, about 80 to 90% sure that

19:30

the patient, if they had a lung biopsy, would

19:33

have a UIP pattern if we can say it on, on CT.

19:37

So again, you should see this basal predominant

19:40

reticulation, some mild traction bronchiectasis,

19:44

maybe some ground-glass opacities, but

19:46

should not be the predominant feature.

19:48

And then bronchiectasis and bronchiectasis.

19:51

And then the key feature, again, for UIP versus

19:55

probable UIP is the presence of honeycombing.

19:59

There's been kind of some changes in our

20:02

definition of honeycombing over the years.

20:04

Classically, we talked about two to three rows of

20:07

clustered small cystic spaces with shared walls.

20:11

Um, the newer thought of bronchiectasis is

20:14

that really these are dilated distal airways.

20:18

Um, because on pathology, we see that

20:19

they have bronchial epithelium in them.

20:22

Um, so really a thin layer or a single layer

20:25

of honeycombing could exist, but it's incredibly

20:28

difficult or impossible for us to tell the

20:30

difference between that and paraseptal emphysema.

20:33

So it's really useful for us to see the stacked

20:35

thin-walled cyst and use that classic definition.

20:39

Um, so again, this area here would, would

20:42

push us into that UIP pattern rather

20:44

than calling this a probable UIP.

20:47

Um, UIP in the setting of idiopathic pulmonary

20:51

fibrosis, or IPF, is most common in older males.

20:55

So you have a really high pretest probability

20:58

just knowing the age and sex of your

20:59

patient before you're even reading the CT.

21:02

So always look at the demographics of your patient

21:05

on these interstitial lung disease cases, um,

21:08

because that will really help kind of guide what

21:11

your pretest probability should be for

21:14

the different imaging features of fibrosis.

21:20

Okay, case number eight, male.

21:22

Patient with heart failure.

21:32

What is the most likely etiology

21:34

for the abnormality shown?

21:36

Is it iatrogenic?

21:38

Is it acquired post-infectious,

21:40

acquired post-traumatic, or congenital?

21:52

Okay, good.

21:52

We are a little bit split, but most

21:54

people did choose congenital, perfect.

21:59

So this is congenital pulmonic valve stenosis.

22:03

So you classically get the stenotic valve with obstruction of the right ventricular

22:08

outflow tract, and it dilates the main

22:10

pulmonary trunk and the left pulmonary artery.

22:12

So just that direction of you

22:16

can imagine a stenotic flow.

22:18

Jet just directed this direction

22:20

towards the left pulmonary artery.

22:23

So it preferentially dilates the left pulmonary

22:26

artery, rather than the right pulmonary artery.

22:29

So that's your key to recognizing this as pulmonic

22:32

valve stenosis, which is most commonly congenital.

22:35

You can get acquired pulmonic valve stenosis,

22:39

usually from rheumatic heart disease,

22:41

maybe carcinoid, maybe endocarditis.

22:43

But congenital is gonna be the most common cause.

22:46

Okay.

22:51

Okay.

22:51

Case number nine: 54-year-old male with

22:54

pre-op imaging for a valve repair.

23:05

What is the diagnosis?

23:07

Congenital lobar hyperplasia, A BPS,

23:10

bronchial atresia, or sequestration?

23:22

Okay, so we're a little bit split here

23:24

with some people choosing congenital lobar

23:25

hyperplasia, but most of us still choosing

23:28

bronchial atresia, which is the correct answer.

23:33

So bronchial atresia, this most

23:35

commonly occurs in the left upper lobe.

23:38

You can think about putting your hand

23:39

over your heart for the Pledge of Allegiance

23:41

to try and remember left upper lobe.

23:44

So it's congenital atresia of a

23:47

segmental subsegmental or lobe-bar bronchus.

23:51

So you end up with this tubular branching

23:53

opacified structure that if we were able to

23:56

scroll through this and follow it back, we

23:58

could tell that it's running alongside arteries.

24:01

So we know that it's a dilated airway, but it does

24:04

not connect back with the tracheal bronchial tree.

24:08

It's commonly asymptomatic

24:10

and just found incidentally.

24:12

But you're gonna look for that branching

24:15

tubular mucosal with the hyperlucent lung from

24:19

air that's trapped in there and can't get out,

24:21

and no connection to the tracheal bronchial tree.

24:24

And that will help you identify, uh, bronchial atresia.

24:28

And again, most common in the left upper lobe.

24:33

Case number 10.

24:34

This is a 64-year-old female

24:36

with fatigue and weight loss.

24:44

What is the most common primary pre-vascular anterior

24:47

mediastinal neoplasm: DMMC, carcinoma, thymoma,

24:51

germ cell tumor, or nerve shell, nerve sheath tumor.

24:54

Excuse me.

25:05

Okay, perfect.

25:05

Most of you chose thymoma.

25:07

Um, I know I helped you out by giving you the images.

25:11

You very well could just be asked a

25:12

question like this with no images.

25:14

So, um.

25:17

Keep that in mind.

25:18

You've gotta know kind of what's the most

25:20

common tumor in the mediastinum, posterior

25:22

mediastinum, um, primary tumor of the heart.

25:25

All those things can come up on exams.

25:28

Um, but if we look here, you can see that

25:31

there's this lobulated, pre-vascular mass.

25:35

Um, and then this patient actually has drop metastases.

25:38

So you can see some pleural nodularity

25:40

down here in the lower right hemothorax.

25:43

Um, so nice classic imaging appearances

25:46

of a thymoma, um, and drop mets.

25:49

So thymoma is the most common primary

25:52

anterior mediastinal neoplasm.

25:54

Um, they're considered malignant 'cause

25:56

they can metastasize at any stage.

25:58

Um, usually, like I said, it's a pre-

26:00

vascular mass with smoother, ovulated margins.

26:03

You don't usually have other lymphadenopathy like

26:06

you would if this were lymphoma, for example.

25:09

I. Um, and then we call it an invasive

26:12

thymoma when there's local invasion or

26:14

pleural nodules, such as these drop mets.

26:17

Um, and then as particularly with

26:20

pre-vascular mediastinal masses, it's

26:22

helpful to know the age of your patient.

26:23

So this is most common in the

26:25

fifth to sixth decades of life.

26:27

If we're talking about a younger patient,

26:29

um, germ cell tumor is probably gonna be higher on

26:32

your list, but has a different imaging appearance.

26:34

Usually they're more heterogeneous masses, um, sometimes

26:37

with calcification, sometimes with fat attenuation.

26:41

Um, but use your patient demographics as as clues to

26:46

kind of help you narrow down your answer choices also.

26:50

Okay, case number 1140. 2-year-old male with cough.

26:56

So you have four CT images here.

26:58

The two on the bottom are MIP images,

27:00

so maximum intensity projection images.

27:04

So it gives us a kind of a thick slab of volume average,

27:08

um, to kind of see structures a little bit more clearly.

27:13

This image over here is a minute—or a

27:15

minimum intensity projection image.

27:18

Um, so it's bringing out the lowest attenuation pixels

27:22

and combining volume averaging into a thicker slice.

27:27

So what is the diagnosis?

27:30

Congenital lobar hyperplasia, bronchial atresia, intra

27:33

lobar sequestration, or extra lobar sequestration.

27:46

So we're split about 50-50 between intra

27:49

lobar and extra lobar sequestration.

27:52

Okay, so let's go over these images.

27:55

So this axial CT image, you can see that this

27:58

area of hyperlucent lung, kind of similar

28:01

to what we saw with bronchial atresia, right?

28:03

Um, and then the MIP image just brings that area of air

28:07

trapping, um, out, makes it a little more prominent.

28:10

And then the key to this case is recognizing that you've

28:14

got this extra vessel here coming off the descending

28:18

aorta, and you can see it right down here, and it's

28:21

going up to supply that portion of the left lower lobe.

28:26

And you can see that there's no discrete, um,

28:30

pleural lining or separation between this portion

28:34

of the lung and the rest of the left lower lobe.

28:37

Making it most likely an intralobar

28:39

sequestration rather than an extralobar.

28:42

Um, in addition, the intralobar sequestrations, they're

28:45

more common—around 75% versus 25% as extralobar.

28:51

So when we say intralobar, we're saying

28:53

that it shares visceral pleura of the

28:55

affected lobe, so it's part of that lobe.

28:58

Um, extralobar is just supernumerary lung

29:02

tissue that's covered by its own separate pleura.

29:05

Um, and that's less common.

29:07

So, uh, sequestration—there's no communication with

29:11

the tracheobronchial tree, similar to bronchial

29:13

atresia, but it also has systemic arterial supply.

29:18

So most commonly we see this in the left lower lobe,

29:21

and you see the systemic arterial supply coming

29:24

from the descending aorta, just like in this case.

29:27

Um, sometimes the, um, the portion

29:32

of the lung can have a variable appearance.

29:34

It can be consolidated or mass-like.

29:36

It can have cystic spaces or fluid spaces, or just

29:40

hyperlucent lung, or a combination of all of those.

29:43

So it can look very heterogeneous and it does not

29:46

always look, um, as clean and simple as this case.

29:50

So intra-lobar sequestration.

29:54

Okay, case number 12.

29:55

We have a 65-year-old male with fever and cough.

30:00

So we have a frontal chest radiograph

30:03

and then an axial CT image.

30:10

Okay, what is the CT imaging sign?

30:13

Halo sign, reverse halo sign, air

30:16

crescent sign, or comet tail sign.

30:28

Okay, perfect.

30:29

So most of you chose the reverse halo sign.

30:31

A few of you chose halo sign.

30:33

Um, so we'll kind of go over the differences of that.

30:38

So this is the reverse halo sign.

30:40

This is kind of a specific case of the reverse

30:43

halo sign, sometimes referred to as the bird's

30:46

nest sign, where it's one big area of peripheral

30:49

consolidation and central ground glass and

30:52

the setting of mucormycosis infection.

30:55

So mucor is an opportunistic

30:57

infection caused by a fungi.

31:00

Um, you can have nodules, masses, consolidation.

31:03

Um, you can have the ground glass halo from hemorrhage

31:08

or this reverse halo, um, the central ground glass.

31:12

Um, it reflects infarct or

31:15

hemorrhage from the vessel thrombus.

31:18

Um, so mucor is kind of interesting in that,

31:21

um, it has this component of angioinvasion and

31:24

can it, it can even be difficult to culture it.

31:27

Um.

31:28

So it, it often needs to be biopsied along that

31:30

area of consolidation to get the bug from it.

31:34

Um, so I'll use this example to

31:38

discuss a couple of these signs.

31:39

So, reverse halo is this example where we have

31:43

peripheral consolidation and central ground

31:46

glass or central clearing, or a central lucency.

31:50

Um, when we say a toll sign, it's reverse.

31:54

It's an incomplete reverse halo.

31:56

So, um, an atoll is like a portion of land that

32:01

is partially surrounded by water, um, or partially

32:05

covered by water, just like this example of an atoll.

32:08

Um.

32:10

Or like a sand, sand drift.

32:12

Um, and you can see here that it's an incomplete circle.

32:15

So we use the term reverse halo when it's a complete

32:17

circle, atoll sign when it's an incomplete circle,

32:21

and then a halo sign is when we have consolidation or

32:25

a mass or a nodule with ground glass surrounding it.

32:28

So, um, it, it kind of makes sense if you

32:31

just think about a halo surrounding it.

32:35

Okay, so case 13, we have a

32:38

parts one and two of this case.

32:39

So this is a 36-year-old female

32:41

with shortness of breath.

32:42

We have a chest, a frontal chest radiograph.

32:45

What

32:49

is the imaging finding?

32:52

So is a left lower lobe collapse, right

32:54

upper lobe collapse, right middle lobe

32:56

collapse or right lower lobe collapse.

33:07

Okay, so this can be tricky.

33:11

So this is right lower lobe collapse.

33:14

If we look, I'll go back to this one.

33:16

You can see this opacity here, this kind of a triangular

33:19

shape, and we still have a decent right heart border.

33:23

So the key to right lower lobe collapse is

33:26

finding this or seeing this triangular opacity.

33:29

And it should, the apex of it should

33:31

really point towards the hilum.

33:33

Um, other signs of volume loss could be elevation

33:37

of the hemi diaphragm, crowding of the rib spaces.

33:40

Um, you could, um, have displacement

33:43

of the hilum or the minor fissure.

33:46

Um, and then the right heart border

33:47

should be relatively maintained.

33:49

Um, it can be easy to miss if we only have partial

33:53

or, um, partial collapse or less consolidation,

33:57

or our imaging technique is not perfect.

33:59

Um, obviously a lateral view would

34:02

always be helpful in these scenarios.

34:06

Okay, so same patient.

34:08

We decide to get CT since that was fairly

34:10

abnormal for her to have a lower lobe collapse.

34:14

So this is her CT image.

34:15

We've got coronal on the top, axial on the bottom.

34:19

What is the most likely diagnosis?

34:21

Is it a carcinoid tumor, a hamartoma,

34:25

adenoid cystic carcinoma, or adenocarcinoma?

34:38

Good.

34:38

So the majority of you said carcinoid tumor.

34:41

I were perfect.

34:42

And I think we had a, a chat that I'll just answer

34:44

quickly, um, about which hilum should usually be higher.

34:48

Um, so usually the right hilum is just

34:50

a little bit higher than the left.

34:54

Okay.

34:55

Oops, sorry.

34:57

Okay.

34:57

So this is right lower lobe

34:58

collapse from carcinoid tumor.

35:01

Um, so carcinoid is a low-grade malignant neuroendocrine

35:04

neoplasm, um, that has metastatic potential.

35:08

Typically it's an avidly enhancing central

35:11

nodular, uh, central nodule or mass.

35:15

Um, they can look a little heterogeneous,

35:17

they can have some calcification.

35:18

They can be kind of low-density also.

35:21

Um, but you should think about it when you,

35:23

particularly when you have a younger patient and, um,

35:26

a well-defined central interbronchial, no nodule or a

35:30

well-defined nodule that has an endobronchial component.

35:33

So you see, um, you know, fairly well-circumscribed

35:37

nodule, maybe it's slightly low-density or

35:39

maybe it's well-enhancing, um, and it's along

35:43

a bronchus and maybe has an a, a component that

35:46

looks like it's extending into the, to the airway.

35:50

Um, you can get a dotatate, um, PET scan.

35:53

Um, often we can have false

35:55

negatives on an FDG PET-CT.

35:58

Um, so keep that in mind.

36:01

And then, um, classically you may, you'll hear about,

36:04

um, diffuse idiopathic pulmonary neuroendocrine cell

36:07

hyperplasia or DIPNECH, where you get multiple carcinoid

36:10

tumors or tumorlets when they're really small.

36:13

Um, and on imaging, we see multiple bilateral lung

36:17

nodules that stay relatively stable over time.

36:20

Um, sometimes one will become a dominant carcinoid

36:23

tumor and will grow and may need treatment.

36:26

Um, but a lot of times they'll kind of

36:28

stay, um, relatively indolent over years.

36:32

Then you'll see a background of mosaic lung attenuation.

36:35

Um, and if we get expiratory images,

36:37

you'll see that that's air trapping.

36:39

Um, so it correlates with constrictive

36:41

bronchiolitis from these, um, carcinoid tumors

36:44

and tumorlets occluding the small bronchi.

36:50

Okay, next case, case 14.

36:52

Um, 46-year-old male with cough and hemoptysis.

36:55

So we've got, um, two mediastinal CT images at the

37:00

level of the trachea and the main bronchi.

37:03

And then, um, axial CT, um, image of

37:07

the right lower lobe on lung windows.

37:14

What is the most likely diagnosis?

37:18

So relapsing polyon, granulomatosis with

37:21

polyangiitis, amyloid, or tracheal bronchial

37:25

pathia, osteochondral plastic, or T-B-E-O-P.

37:40

Okay, good.

37:42

So most people chose granulomatosis

37:44

with polyangiitis or GPA.

37:49

Perfect.

37:50

So this is a necrotizing granulomatous

37:53

vasculitis of the small to medium vessels.

37:56

Um, in the lungs, you can get multifocal

37:59

nodules, masses, consolidations.

38:02

A lot of times they can cavitate, um, they could

38:04

have air-fluid levels from secondary infection.

38:07

Um, sometimes you can get ground

38:09

glass opacity from hemorrhage.

38:12

You can see, like we talked about before,

38:13

sometimes a halo sign, reverse halo sign,

38:16

feeding vessel sign, where you have a, a

38:18

pulmonary artery leading right to the opacity.

38:22

Um, pleural effusions, fibrosis,

38:25

and then airway wall thickening.

38:26

So the key here is seeing that

38:28

this is circumferential thickening.

38:30

We do not have sparing of the posterior membrane.

38:34

Um, so that would, that makes us think less likely.

38:39

Um, relapsing polychondritis, which should only

38:42

be affecting the cartilaginous portions.

38:45

So the key to this is putting together this wall

38:48

thickening, 'cause you know that GPA can affect, um,

38:50

the airway walls and then also the parenchyma down here.

38:57

Okay, 70.

38:58

This is case number 1570,

38:59

6-year-old male with chronic cough.

39:03

So we've got two axial CT images, one on soft

39:06

tissue windows, and then one on lung windows.

39:14

So what is your next best step in management

39:17

for the left lower lobe abnormality?

39:20

Should we do imaging surveillance

39:21

with a non-contrast chest CT?

39:24

Should we biopsy percutaneously, um, EBUS,

39:28

or endobronchial biopsy, or CT chest

39:31

with contrast to further evaluate it?

39:42

Okay, good.

39:43

So we're a little bit split, but most

39:45

of us went with non-contrast chest CT

39:47

surveillance, which is the correct answer here.

39:53

So this is asbestos-related pleural disease

39:57

with round atelectasis in the left lower lobe.

40:00

So the key here is identifying

40:02

these calcified pleural plaques.

40:04

You can see several of them back here and anteriorly.

40:09

Um, so these are virtually pathognomonic

40:12

for asbestos-related pleural disease, which usually

40:15

occurs 20 to 30 years after asbestos exposure.

40:19

Um, and calcifications occur

40:20

in about 15% of these patients.

40:23

The typical locations are posterior lateral chest wall.

40:26

I feel like the dome of the diaphragm is

40:29

one of, um, the best places to see them.

40:31

That's most specific for asbestos, um, along the

40:35

mediastinal pleura. Also, um, when you have other

40:40

things you should think about when you have a

40:42

calcified plaque, particularly when they're layered

40:44

independently, is an emphysema or a previous hemothorax.

40:49

Um, so keep that in mind, particularly

40:52

when it's unilateral or only posteriorly.

40:55

But when we have it bilaterally, you've got anterior

40:58

involvement, involvement of the diaphragms that

41:00

should lead you to asbestos-related pleural disease.

41:04

Um, and then keep in mind our terminology here.

41:08

Of asbestos-related pleural disease

41:10

for the calcified pleural plaques.

41:12

And then asbestos is interstitial lung disease related

41:16

to the asbestos fibers, which is usually a UIP pattern.

41:20

Um, but you don't wanna use this term asbestos

41:23

when you're just talking about the pleural disease.

41:26

This is particular to lung fibrosis

41:29

in the setting of asbestos exposure.

41:32

And then round atelectasis, we can

41:33

see this really commonly in patients

41:35

with asbestos-related pleural disease.

41:38

So you, there's several characteristics

41:40

you should meet for round atelectasis.

41:43

Um, you should have an adjacent pleural abnormality.

41:46

You can see a common tail sign where you have

41:49

kinda a curvature of the adjacent bronchovascular

41:52

structures, and there should be some volume loss there.

41:56

Um, the, it's.

41:59

I didn't include in here as an option to

42:01

get a PET because honestly, that would

42:03

be a reasonable, a reasonable thought.

42:06

Um, sometimes on PET, these can have just minimal

42:08

uptake, um, but it shouldn't have a lot of uptake.

42:11

So that could be one of your management options.

42:14

If, if maybe your clinician really needs a, a

42:17

quicker answer and you know you're favoring it

42:19

for round atelectasis, they could get a PET and

42:22

make sure it's not, um, strikingly FDG avid.

42:26

Otherwise, we're just gonna follow

42:27

this on non-contrast imaging.

42:30

There's no use in getting a, a CT

42:32

with contrast or further evaluate it.

42:35

Um, that's not gonna provide

42:37

us any more characterization.

42:39

So, asbestos-related pleural disease with round atelectasis.

42:44

Okay, K 16, 22-year-old female with chest pain.

42:52

So what is the diagnosis?

42:54

You've got a frontal chest radiograph.

42:56

And then, um, an MR Bright

42:59

blood sequence or SSFP sequence.

43:04

So it says, petrology of low transposition of the

43:09

vessels, proximal interruption of the pulmonary

43:12

artery, or congenital absence of the pericardium.

43:22

Okay, good.

43:23

So most of us got this congenital

43:25

absence of the pericardium.

43:29

Good.

43:29

So the key here is identifying this abnormal

43:33

contour on the radiograph, and then on CT and

43:36

MRI, you'll see this levo-position of the heart

43:39

or this, um, turning of the heart to the left.

43:44

So this can be partial or complete

43:47

absence of the pericardium.

43:49

Um, so again, this Levo position, or

43:51

you may hear Snoopy's nose, you can see

43:53

the, my outline of, of the heart here.

43:56

Um, and then another key on CT is

43:59

interposition of the lung between the pulmonic

44:02

trunk and the aorta or the aortic arch.

44:05

Or the ascending aorta?

44:07

Um, so normally your pericardium should be

44:09

extending all the way up here so you wouldn't

44:11

have lung interposed between those two structures.

44:14

Um, MRI can be really useful in, um, trying

44:18

to visualize the pericardium or confirming

44:21

that there's absence of the pericardium.

44:23

Um, so keep that in mind as, um, an option

44:27

if, uh, if they're trying to work this up.

44:31

Okay.

44:31

Case number 17, 24-year-old female with chest pain.

44:44

Okay, so, um, we started with that chest

44:47

radiograph and now you've got, um, mediastinal

44:50

window CT and, um, lung window CT images,

44:55

same answer choices as the previous question.

45:08

Good.

45:09

So most of you got this one also.

45:10

Um, so proximal interruption of the pulmonary artery.

45:13

Perfect.

45:15

So, um, it can, they can fake you out a little

45:19

bit by, you know, you just get this one slice

45:22

of the CT and you don't know, are they just

45:24

not showing me the right pulmonary artery.

45:26

Um, or is this proximal interruption of the PA?

45:30

Um, it is most helpful if they show you an

45:32

additional imaging showing the chronic changes

45:35

that have occurred in the right lung because

45:38

of that absence of the pulmonary artery.

45:40

So you can see even on this radiograph, um, you know,

45:45

if in the correct clinical setting you could suggest

45:47

this diagnosis just on the radiograph because of

45:50

this chronic volume loss in the right lung, you can

45:53

tell that there's some areas of scarring or edema.

45:56

Um, even the heart and mediastinum are shifted

45:58

to the right because of that volume loss.

46:02

And then same thing on the CT image, you can see,

46:05

um, how asymmetrically smaller the right lung is

46:08

compared to the left with some areas of scarring.

46:12

Um, so proximal interruption of the pulmonary artery.

46:15

So it's failed development of

46:16

the proximal pulmonary artery.

46:18

It can either be the right or the left.

46:19

Most commonly it's the right, um, on radiograph

46:23

you can see a small ipsilateral lung and hilum.

46:26

And then, um, on CT, the, um, it's interesting

46:32

because the, whichever pulmonary artery is absent,

46:35

um, usually has a contralateral aortic arch.

46:38

So if the right PA is absent, then you

46:41

have a left aortic arch and vice versa.

46:43

Um, in the affected lung, you can have

46:46

bronchiectasis from recurrent infections.

46:48

Um.

46:50

You can get, um, excuse me, mosaic lung attenuation,

46:54

um, parenchymal and subpleural cystic change.

46:57

Um, and then collateral systemic vessels.

47:00

So, um, other differentials to think about, um, when

47:03

you have an asymmetrically smaller lung, um, Swyer,

47:07

James fibrosis, mediastinitis, maybe Scimitar syndrome,

47:11

but those would be the kind of the top things you

47:13

wanna think about with chronic volume loss in one lung.

47:18

Okay.

47:18

Case 18, 23-year-old female

47:21

with enlarging chest wall mass.

47:30

So what is the most likely diagnosis?

47:42

That's, so we're a little bit split,

47:44

um, but chondrosarcoma still won out.

47:49

So yes, this is a classic case of chondrosarcoma

47:52

involving the sternum, um.

47:55

So this is a malignant cartilaginous forming tumor

47:57

and bone, most common primary chest wall malignancy.

48:02

So often you get a fairly well-circumscribed

48:04

anterior chest wall mass, which often involves

48:07

the costal chondral cartilage or the sternum.

48:10

You can get that chondroid calcification with the classic

48:13

rings and arcs and stipple appearance.

48:17

Um, and then often you have the aggressive features too

48:19

with endosteal, endosteal scalloping, cortical destruction, and

48:24

usually there's a soft tissue component with it too.

48:29

Okay, case 19, 28-year-old male with low-grade fever and

48:33

recent travel to Southern California.

48:39

What is the most likely etiology of the finding?

48:51

Good.

48:52

So coccidioidomycosis one.

48:56

So the key to this one is your,

48:58

is your question stem again.

49:00

Um, this, um, hint that he went to Southern California.

49:05

If we saw this imaging finding here in

49:07

the Midwest, um, I live in Kansas City.

49:11

Um, this would most likely be

49:13

histoplasmosis rather than coccidioidomycosis.

49:16

Um, and this map of the US kind of shows

49:20

these areas of endemic fungi really well.

49:22

So down here in the

49:24

The Southwest, you see a lot of coccidioidomycosis.

49:27

In the Midwest, we see mostly histoplasmosis.

49:31

Um, and then these other portions of

49:34

the country, you can see there's kind

49:36

of a mix of coccidioidomycosis and histo down here.

49:39

Um, in Wisconsin you can get blastomycosis, um,

49:42

and histoplasmosis, um, and these other areas, um,

49:45

where you can get blastomycosis more commonly.

49:48

Um, so again, the key to this

49:50

one was that question stem.

49:53

Um, so, um, fungal endemic fungal infection,

49:57

um, in the predominantly in the southwest

50:00

United States, Mexico, South America.

50:02

You get lung nodules and cavitation, um, you

50:06

can get pretty exuberant lymphadenopathy.

50:09

Um, and you can get this classic look of this

50:12

satellite nodularity that extends along the

50:15

bronchovascular structures back to the hilum.

50:17

Um, you can refer to it as ants on a log.

50:20

So just think about like the little ants

50:22

crawling back along the hilum or along the

50:24

bronchovascular structures to the hilum.

50:27

Um, if they did a PET CT, you could get,

50:29

you could see a flip-flop fungus sign.

50:32

Where you're, um, where the hilar lymph nodes or

50:35

mediastinal lymph nodes have greater SUV, um, higher

50:40

SUV levels or greater FDG uptake than the lung

50:44

nodule, um, which is opposite of what you would

50:47

typically see with lung cancer and nodal metastases.

50:50

Um, so some classic imaging findings

50:53

of endemic fungal infection.

50:54

Like I said, usually when I see this, it's histo.

50:57

Um, but depending on where in the country you're,

51:01

you're living or where your patient has traveled,

51:03

um, you need to think about these other endemic

51:05

fungi and also consider this when a patient's being

51:08

treated for community acquired pneumonia and they're

51:10

not responsive to the typical antibiotic treatment.

51:14

Okay.

51:15

Case 20, 30, 4-year-old female with arthritis,

51:22

what is the best initial treatment?

51:35

Perfect.

51:35

So most of you said corticosteroids.

51:37

So another great example of AOL signs or reverse halos.

51:42

I'd call this an atoll.

51:43

Maybe these two could be reverse halos.

51:47

Um, but, um, it's one of the, um, CT

51:50

imaging appearances of organizing pneumonia.

51:53

So I'll, I'll show on a different slide for organizing

51:57

pneumonia, there can be many different CT patterns, but

52:00

this is one of our classic patterns, um, associations.

52:04

Most commonly when we see organizing pneumonia,

52:07

it's from an underlying autoimmune disorder, or it

52:10

could be from drug reactions such as immunotherapy

52:13

that the patient's on, um, occasionally infection.

52:17

COVID-19 presented a lot of times

52:19

with an organizing pneumonia pattern.

52:21

Um, and then radiation, um, radiation, lung injury

52:24

can have an organizing pneumonia appearance.

52:28

Um, so this slide shows a few different examples of

52:31

those examples of what we mean by organizing

52:33

pneumonia and how different it can look.

52:35

So you can see in COVID-19, um, it was really a lot

52:38

of just perioral and peripheral ground glass here.

52:42

This was a drug-induced, um, OP from, um,

52:46

an immunotherapy and really pretty AOL sign.

52:51

Um, this was OP associated with ulcerative

52:53

colitis, and you can see it's really just

52:55

kind of these smudgy nodules here and there.

52:58

And then radiation, um, you can see this nice

53:02

like perlobular thickening, so consolidation

53:05

that kind of surrounds the secondary pulmonary

53:07

lobe and, um, kind of has this arcadian appearance.

53:12

So varying appearances of organizing pneumonia,

53:15

but can really help limit your differential

53:17

if you can recognize these patterns.

53:20

Okay, case 21, 42-year-old female with a dry cough.

53:30

What is the distribution of micronodularity?

53:36

Is it central lobular, perilymphatic, random, or miliary?

53:50

Good.

53:50

So a few of us said central lobular, but the majority

53:53

of us said perilymphatic, which is the correct answer.

54:00

Perfect.

54:00

So this is a case of sarcoidosis with

54:03

classic perilymphatic micro nodularity.

54:05

And I didn't show you this image with

54:08

the first one, um, but you can see

54:10

they've got mediastinal lymphadenopathy.

54:13

Um.

54:14

So sarcoid is a systemic granulomas

54:18

disease characterized by non-KC granulomas,

54:21

usually involving multiple organs.

54:23

Um, the lung and the mediastinum

54:24

are most commonly involved.

54:26

You can have, um, the, you can have lung

54:29

involvement with or without lymphadenopathy

54:32

or lymphadenopathy without lung involvement.

54:35

So you don't have to have both for it to be sarcoidosis.

54:37

You could have one or the other.

54:39

Um, but it's an immune-mediated disease that's

54:42

triggered by some environmental antigen that's

54:44

usually unknown in a genetically susceptible host.

54:47

Usually, these are younger patients,

54:50

higher prevalence in African-Americans.

54:53

Um, so other things you would want to think about are

54:56

other ulous infections like we just talked about with

54:59

COI and histo because we've got kind of that similar

55:02

appearance of that satellite nodularity that ants on a

55:06

log along the, um, str the bronchovascular structures.

55:10

Silica can look identical, and you would

55:12

need, um, pathology to identify the, um,

55:17

the silica nodules in the specimen.

55:20

Borreliosis can also look similar and

55:22

there's a blood test that you can do.

55:24

Um, and then lymphangitis carcinomatosis

55:27

should always be considered when we've got,

55:28

um, kind of septal thickening fis nodularity.

55:33

So sarcoid, you usually get the symmetric

55:35

hilar mediastinal lymphadenopathy.

55:37

It can calcify, usually upper low

55:40

predominant perilymphatic nodularity,

55:43

sometimes these form conglomerate masses.

55:46

And the key is identifying the

55:48

surrounding satellite nodularity.

55:51

And then this is just a, a quick depiction,

55:53

um, from radiology assistant to show you

55:55

guys to remind you of those different, um.

56:00

Um, patterns of micro nodularity.

56:02

I found that the best way to kind of narrow this

56:05

down when you're going through is to look along

56:07

the fissures, look along the subpleural lung.

56:10

If you have, if you have nodules there,

56:12

then you can take out central lobular.

56:14

And then you just have to decide

56:15

Is it para, lymphatic or random?

56:17

And then look along the bronchovascular structures.

56:20

Are the nodules clustered along the bronchovascular

56:22

structures, or is there no clustered areas?

56:26

Is it all just pretty diffuse and random?

56:29

And hopefully, that can help you narrow down, um,

56:31

which pattern of micro nodularity you're looking at.

56:35

Okay, case number 22, 40 8-year-old

56:38

male with dry cough and low-grade fever,

56:51

So, most likely diagnosis.

56:54

You've got an axial CT image and then a MIP

56:58

maximum intensity projection image next to it.

57:06

Okay, great.

57:07

You guys, nearly the majority definitely got this one.

57:12

So this is non-fibrotic hypersensitivity pneumonitis.

57:16

So, um, antifibrotic HP, it's an allergic inflammatory

57:20

response to the lung to an inhaled antigen.

57:23

Um, we used to classify it as, um, acute and chronic.

57:27

We no longer do that anymore.

57:28

It's either fibrotic or non-fibrotic.

57:31

Um, so the non-fibrotic form most commonly presents

57:34

with the diffuse central lobular nodularity, which can

57:38

be pretty faint, but, um, your MIPs often kind of bring

57:41

it out a little bit better, so use those to help you.

57:44

Um, and then fibrotic HP, I've got an

57:47

example down here of, um, a fibrotic HP case.

57:51

Um.

57:53

And, um, the three densities, this sign

57:56

replaced the previous head cheese sign,

57:59

um, if some of you had heard of that.

58:01

And it just refers to areas of lucent

58:03

lung, relatively normal lung, and then

58:06

lung with more ground-glass attenuation.

58:08

So, three different densities all within,

58:10

um, like one lobe or one slice of a CT.

58:15

Okay, we got, just have a couple more to get through.

58:18

Um, so this is a 28-year-old female

58:20

with post-stem cell transplant.

58:24

What is the diagnosis?

58:35

Okay, good.

58:36

So the key to this one is recognizing

58:38

what images you're looking at.

58:40

So on the top here, we have an inspiratory CT.

58:44

On the bottom, we have expiratory.

58:45

You can see that the posterior membrane

58:47

of the trachea is bowed inward.

58:49

Um, which tells us an ex, it's

58:51

an expiratory phase imaging.

58:53

So on the inspiratory view, you can see that there's

58:56

subtle mosaic attenuation, like this area looks a

58:58

little more ground-glassy than the adjacent lung.

59:01

And then all those areas become more, um, more obvious

59:05

or more contrasted on the expiratory phases, telling us

59:10

that this is air trapping, um, causing this abnormality.

59:16

So bronchiolitis obliterans

59:17

or constricted bronchiolitis.

59:19

Um, and it's obstructive lung disease of the small

59:22

airways often seen in, um, post-lung transplant

59:26

or, um, stem cell transplant patients as a, um,

59:29

as a manifestation of graft-versus-host disease.

59:33

Um.

59:34

Other things that can cause it, um, are

59:37

infection, like Swyer-James syndrome,

59:39

some medications, some autoimmune disorders,

59:41

particularly, uh, rheumatoid arthritis.

59:44

Um, so the key here, keep in mind that when we say

59:47

mosaic attenuation, that's our, um, inspiratory CT term.

59:52

And then we need the expiratory images

59:54

to confirm that it's air trapping.

59:55

So expiratory air trapping, mosaic attenuation is your expiratory term.

60:03

Okay?

60:03

58-year-old male with chronic cough and hemoptysis.

60:10

What, um, malignant transformation can occur most

60:13

commonly to what cell type in this underlying diagnosis?

60:27

Good.

60:27

So we are a little bit split, but most of us still said

60:29

squamous cell carcinoma, which is the correct answer.

60:33

So I, I could have made this obvious

60:35

to you guys and given you an image of

60:37

the trachea with some papillomas in it.

60:39

Um, but I wanted you to just see the long

60:41

findings, um, of disseminated papillomatosis.

60:45

Um, so this is tracheobronchial papillomatosis

60:47

due to HPV (human papillomavirus).

60:52

Um, and these, these patients have multifocal

60:57

cavitary nodules in the lungs.

60:59

Um, they can grow really large and get

61:02

really, um, have big areas of nodularity and

61:06

mass-like thickening and wall thickening.

61:08

Um, and we continue to watch 'em because of the trans,

61:12

the risk of transformation to squamous cell carcinoma.

61:15

Um, so often one of these will become

61:18

a dominant, um, nodule or mass and will

61:21

need to be biopsied or evaluated by PET.

61:25

Um, so the key is just knowing the

61:28

risk of squamous cell transformation.

61:33

Okay, in our last case, case 25, so this

61:37

is just a normal lateral chest radiograph.

61:40

So what normal structure is the arrow pointing to?

61:52

Okay, great.

61:54

Um, so we had some people saying bronchus intermedius,

61:56

but most of us saying left upper lobe bronchus and

61:59

left upper lobe bronchus is the correct answer.

62:04

So, um, I tried to label some of these for you.

62:07

Um, so your most superior rounded lucency is

62:11

gonna be your right upper lobe, uh, bronchus.

62:14

And then below that will be

62:15

the left upper lobe bronchus.

62:16

Your bronchus intermedius.

62:18

This I, I'll be honest, is not the best example of

62:20

bronchus intermedius, um, but it would be right here.

62:24

The posterior wall of the bronchus

62:25

intermedius is your intermediate stem line.

62:28

You'll see it referred to that, um, or it could be asked

62:31

a question on an exam, um, about what that is.

62:35

And that's a posterior wall of the bronchus intermedius.

62:38

And then remember your right pulmonary artery

62:40

sits um, anteriorly there, and your left

62:43

pulmonary artery will drape posteriorly back here.

62:47

So nice review of your lateral chest radiograph anatomy.

62:52

And that's it.

62:52

We got through all 25 cases.

62:54

Thank you guys for joining us.

62:56

You guys all did really great.

62:57

I wish you all the best with your core exam.

63:00

Um, and if we have any questions, I think I, I answered

63:05

one earlier, but if we have any other in the chat, um,

63:09

I can, I have a few minutes to answer some questions.

63:14

Thank you so much for that case review.

63:15

Yeah.

63:16

We'll wait a minute or two to

63:17

see if any questions come in.

63:19

Sometimes it takes a second, uh, that to come in.

63:25

Got a lot of thank yous.

63:28

Thank you guys for being here.

63:34

Okay.

63:34

You got a question in the Q and A box there for you?

63:40

Okay.

63:41

Is NSIP and OP similar in pathology or

63:44

is, or OP is NSIP differential diagnosis?

63:49

So a lot of times there can be overlap.

63:51

Um, a lot of our inflammatory myopathies present with

63:55

an NSIP OP overlap on CT and even on pathology.

64:00

Um, when you're taking cases and when you're,

64:04

um, reading studies, most of the time, if it's

64:07

a purely basal predominant peronial, central

64:11

ground glass with traction bronchiectasis,

64:13

you're probably gonna just call it NSIP.

64:16

Um, I tend if there's, if there's more upper lobe

64:18

involvement with, with ground glass opacities that

64:22

look more classic for OP, but still has the basal

64:26

disease, um, then I may suggest that an NSIP OP overlap.

64:31

Um, but they're really different

64:33

things on, on pathology.

64:37

Hopefully that answered your question.

64:40

I think you got it all.

64:41

Dr. Caroll, thank you so much you guys.

64:44

Thank you for being here.

64:45

Yeah, thank you for, for this case review

64:47

and for everyone else for participating.

64:48

And be sure to join us on Wednesday, April 24th.

64:52

We are having Dr. Mohammed Umar, who will lead

64:55

us in a rapid review of cardiac imaging cases.

64:58

You can register for that at

64:59

the link provided in the chat.

65:00

Follow us on social media for future case reviews.

65:03

Thanks again for learning with

65:04

us and we will see you soon.