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Hello and welcome to Noon Conference,

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You can also sign up for a free trial of our premium membership to get access to

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hundreds of case-based micro-learning courses across all key radiology

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subspecialties. Today we are honored to welcome Dr.

0:40

Mark Goslin for a lecture on obstructive pulmonary physiology from the imaging

0:45

perspective, balloons, airway, inflammation, and dynamic collapse.

0:50

Mark Goslin completed his medical school at McGill University Radiology

0:54

residency at the University of Vermont and a cardiopulmonary imaging fellowship

0:58

at Stanford University.

1:00

He spent four years as faculty at University of Utah and 15 years as head of

1:04

Cardiopulmonary Imaging at oh H S U. At the end of the lecture,

1:08

please join Dr.

1:09

Goslin in a q and a session where he will address questions you may have on

1:13

today's topic.

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Please remember to use the q and a feature to submit your questions so we can

1:18

get to as many before our time is up. With that,

1:21

we're ready to begin today's lecture. Dr. Goslin, please take it from here.

1:25

Hello everyone. Nice to be here with you.

1:28

I'm gonna cover a topic here on basically obstructive

1:33

pulmonary physiology. Now,

1:35

I did not use the word C O P D,

1:39

and I do that intentionally, and I'll explain why. So,

1:43

lecture objectives.

1:45

Today I'm gonna introduce the differential of C O

1:49

P D. Now, that term is used a lot. What are the things that actually give it?

1:55

Now I'm gonna look at imaging. I'm gonna look at the pathology literature.

1:59

I'm gonna look at some of the clinical literature,

2:02

and then we're gonna go over some clinical red flags.

2:04

Now the reason I'm doing this is because this is a, it,

2:06

the clinical is gonna be a lot of clinical in this talk,

2:10

and there is gonna be a number of clues that a patient will present with that

2:14

can help us. And as always, um, in my lectures,

2:19

I I believe firmly that we're all think alike. No one thinks very much.

2:23

So there's gonna be some different information here. So let's start off with,

2:29

uh oh, this patient's chest radiograph, hyperinflated, cachexia,

2:35

the clinical information. C O P D,

2:39

what are you gonna say? What's your report impression?

2:45

And I want you to think about that.

2:48

How about this 1 31 year old with dyspnea,

2:52

multiple C O P D admin admissions. These are the,

2:57

these are the cts. What would you say?

3:02

And I can tell you what the report said. And this is a really good radiologist,

3:06

by the way, who read this, uh, findings consistent with C O P D.

3:11

What does that mean? What do you do with that?

3:14

What's gonna happen to this person? Okay,

3:18

I want you to think about that.

3:20

So there's a lot of misconceptions about this, and you know,

3:24

through the years I've heard many different things.

3:27

I've read many different things.

3:29

And it's not that it's completely false,

3:33

but it's not likely true either. Um, you know, pulmonologist,

3:38

hyperinflation alongs with smoking history means emphysema maybe,

3:43

but not necessarily lungs that extend below the 10th rib are hyperinflate and

3:48

represents C O P D. Pulmonologists and radiologists say this, no,

3:52

that's false. That's false. Don't count ribs.

3:56

Emphysema is not diagnosed with imaging. It is a PPF T diagnosis. Wow. Okay.

4:01

That, that's false. That's false.

4:05

So the greatest obstacle discovery is not ignorance people.

4:08

It's this illusion of knowledge.

4:10

We think we know this stuff and then we propagate it on.

4:16

This is the other problem I find, is that when we fo for,

4:21

uh, force this information in,

4:25

then we tend to ignore other problems.

4:27

And we may also be causing problems for the patient by saying some of these

4:32

things. Let me illustrate. So, uh, during round one time,

4:37

patient has emphysema. She was exposed to secondhand smoke.

4:40

That was the response that I got from a pulmonologist. When I said, Hey,

4:44

you know, this person's been admitted multiple times,

4:47

I think they need, they have another diagnosis here.

4:52

And you know, it, it, it was tough to get this information out.

4:57

Uh, this one was interesting. Hyper infl,

5:00

not not uncommon hyperinflated lungs consistent with

5:05

emphysema or C O P D, whatever you wish. You could say, either one,

5:08

that was a radiology report and agreed by the physician.

5:12

What happened to this patient? Well,

5:14

she lost her insurance because she lied about smoking.

5:19

She didn't actually, but she lost her insurance.

5:24

So what we put in a report can have great implications for a

5:29

patient downstream, uh,

5:31

either how they're treated or insurance or you know,

5:34

what goes in their medical record. So we want to be a little careful about that.

5:39

And another quote that I really like,

5:42

we can be absolutely certain only about things we do not understand.

5:46

And that's true. So here we go. This is a patient,

5:50

35 year old non-smoking persistent dyspnea,

5:54

some wheezing two years ago.

5:56

You can see there's a lot of similarity nodules here.

6:00

The diagnosis that she received was poorly responsive asthma.

6:05

And that's okay. I want you to think about that. Poorly responsive asthma. Well,

6:09

I mean that's not asthma, right? Asthma response. So if it doesn't,

6:14

it's gonna be something else. In this case,

6:16

it was sarcoid and sarcoid can present with this wheezing and asthma

6:21

like symptoms, but they don't respond to therapy. Why?

6:24

Because the small granulomas are in the bronchials. They breathe out,

6:29

it traps the air, breathe in, air comes in.

6:34

All right?

6:36

Now what happens when you say C O P D? See, on my reports,

6:41

I never use that word. I never ever use it.

6:45

Because what happens when you say it is that there's this algorithmic thought

6:50

process that goes on. So it's C O P D. Well,

6:53

that leads to the same treatments. It's a reflux, right?

6:57

And the disadvantages is that there are other obstructive pulmonary conditions

7:02

that will be overlooked. All right?

7:05

Those other conditions are different. Physiologically,

7:09

they're different pathologically, they have different treatment options.

7:13

And if the patient doesn't previously have a diagnosis of C O P D,

7:17

they could lose their insurance. So if I could encourage you,

7:22

just try to avoid the term C O P D,

7:27

again, this machine has no brain. Once you say it,

7:32

there's going to be inhalers, steroids, plus or minus antibiotics.

7:37

That's what they'll get. So try not to use it.

7:43

So this is me. This is mine. My call this normal. Um,

7:48

very scientific here, right?

7:50

So this is inspiration and this is expiration.

7:54

What do you see in expiration? Well,

7:57

you see the lungs get more dense as they go back. That's the air coming out.

8:01

There is going to be a higher density dependently.

8:05

The airways are held open by the cartilage so the air can get out.

8:11

All right? And it's a very sort of uniform appearance, not Apache,

8:15

sort of mosaicism. It's very uniform. This is normal.

8:23

Now,

8:24

when you see that a patient has a diagnosis of C O P D from here on in,

8:28

what are you gonna think about? Well, okay, you got emphysema,

8:33

which really represent balloons.

8:35

And I'll explain why you have chronic bronchitis. Hmm?

8:39

You have asthma. That's reversible, right?

8:42

Poorly responsive asthma is not asthma.

8:46

Then you have tricky bronchial lac. That's a dynamic collapse.

8:51

And then you have constricted bronchiolitis. Those are also balloons.

8:56

And then I also throw in bronchiectasis because that gives constricted

9:01

bronchiolitis. Now,

9:02

how many of you have heard these terms constricted bronchitis or trache?

9:06

Bronchia. How common are they?

9:10

They're pretty common. How often are they taught?

9:14

How often have you diagnosed it? All right.

9:20

One of the hallmarks I've learned in medical school was the persistence or

9:23

recurrence of symptoms should alert you to a diagnosis being missed.

9:29

And that's where these two fall in trache, brumation, constricted bronchiolitis,

9:34

they don't respond to the traditional therapy. These people keep coming back.

9:41

So when I look at obstructive pulmonary diseases, I think about, well,

9:46

there's inflammatory conditions. Yep, bronchiectasis, asthma,

9:49

chronic bronchitis. And then there are balloons. Now these are space occupying.

9:54

They're not dynamic, right? They just take up space.

9:57

And that's emphysema and constricted bronchiolitis.

10:01

And then there's the dynamic collapse. That's trache, bronchial lac.

10:06

That's different. Now,

10:08

trache bronchial can be seen in the setting of emphysema and it can be seen in

10:13

the setting without emphysema. It's kind of an independent thing.

10:20

So let's go through this. You're sitting down,

10:23

you're gonna read what are the radiographic? Now cki,

10:27

what are the radiographic signs of hyperinflation? Well,

10:30

I've highlighted the big one. The diaphragm becomes flat.

10:34

That reflects increased trapped residual volume.

10:38

If you were to take the deepest breath,

10:39

you possibly could and take a radiograph. The diaphragm will remain curved.

10:43

When it is flat, that means there's increased trapped residual volume.

10:48

Okay? From whatever cause it just says the lungs are hyperinflated.

10:53

This is obstructive pulmonary physiology.

10:56

Now the sternal diaphragmatic angle is a good way to look at that on the lateral

11:00

projection. Now you can also have increase with the retrosternal space. Sure,

11:05

you can have increased AP diameter, but I don't want you to count ribs.

11:11

Mine go down to T 12. I don't know, what does that tell you?

11:14

It means I have big lungs. Petite people may have smaller lungs,

11:17

but still be hyperinflated.

11:19

You want to be looking at this a little bit more physiologic.

11:23

So this is a normal lung. And you can see in the lateral projection, again,

11:27

the lateral's really helpful here cuz it, it on the a p or pa,

11:31

it takes a bit more hyperinflation to see that flattened appearance.

11:35

So you wanna look at the sternum, diaphragm, sternum and diaphragm.

11:40

It should be, you know, acute angles. As that starts to approach 90 degrees,

11:45

that's an indication that the diaphragm is being compressed down.

11:50

And there should be a nice gentle curve with a deeper posterior salus.

11:56

This is the patient that I showed you before. Now look,

12:00

this is about 90 degrees. The diaphragm is flat. So yes,

12:05

this patient is hyperinflated. They do have obstructive pulmonary physiology.

12:10

What is the cause?

12:13

Find out is there hyperinflation in this patient?

12:16

They go down to the ninth posterior ribs,

12:19

but the sternal diaphragm is about 90 degrees.

12:22

There's a little bit more flattening. So yes,

12:25

this patient does have some element of hyperinflation. All right?

12:29

Even though it doesn't go down to T 10, it doesn't matter.

12:32

People are like snowflakes, right? So don't count ribs.

12:36

Now that flattened diaphragm is an important feature physiologically,

12:40

and I'll get into that later. Now,

12:43

what does it look like on ct? Well or on radiograph? Emphysema,

12:48

it is a vascular attenuation.

12:52

As you destroy or hyperinflate alveoli,

12:56

the vessels also get destroyed. So they tend to get matched.

13:00

You destroy alveolis, you destroy the capillary.

13:03

So you tend to have a VQ match still relative there.

13:07

As you look at it, the vessels usually branch about, you know,

13:11

25, 35 degrees. When you start to lose the vascular bed,

13:16

that branch angle starts to increase, even approaching up to 90 degrees.

13:22

Most of the emphysema tends to be in the upper LOEs, not, uh,

13:25

alpha one antitrypsin and stuff are different.

13:27

But most emphysema in the upper lobes,

13:30

that is a space occupying balloon while will that to the h the hilum get

13:34

depressed and immediately displaced.

13:38

So they're pushed inferiorly immediately.

13:41

And there is a crowding of those vessels in the lower lobes.

13:45

The so-called hyper lucency in the upper lobes really is just the increased

13:49

difference between all of the vascularity going in,

13:52

the lower lobes crowded and the lack of vascularity and increased branch angles.

13:57

You also want to check for pulmonary arteries. Are they getting large?

14:01

Because in the later stages patients develop pulmonary hypertension,

14:05

which is a whole new problem.

14:08

So that's one of the complications to be looking for.

14:10

And cachexia may be present. Why?

14:15

So this would be a person with hyperinflation.

14:19

This is actually emphysema.

14:21

I would actually call this most likely emphysema from the radiograph. Why?

14:26

Well, man, the sternal, uh, diaphragmatic is greater than 90 degrees.

14:30

It's completely flat. Increased AP or, uh, retrosternal space. Okay?

14:34

All of that is hyperinflated. But look at the h,

14:38

this little notch right here from the trunk of interior, the right upper lobe,

14:42

pulmonary artery,

14:44

and the right lower lobe and middle lobe sort of trunk right here.

14:48

There's a little notch that really should be the halfway point as an estimate

14:52

rule of thumb of the right hemithorax. And in this case,

14:57

you can see that it is actually closer to the bottom than it is to the top.

15:01

And you can see the hilum not only are down,

15:04

but they're immediately placed with crowding of the vessels down here.

15:09

This is pretty much going to be, you know,

15:12

hyperinflation statistically most likely emphysema

15:16

on a radiograph. This one's pretty straightforward.

15:19

You can see the large bullet, you can see the hilum pushed down immediately.

15:24

Displaced vascular crowding here in the lower lobes. Um,

15:28

this is a very advanced emphysema. Okay? All right,

15:35

so this patient, what do we think? Two patients, if you look at the notch,

15:39

this one is a little bit pushed down, a little bit of increased vascular,

15:44

uh, branching here. This is emphysema, upper lobes. But this patient,

15:49

you can see it's actually a little bit closer to the upper lobes.

15:54

The hyperinflation, which you can see with the diaphragm here, a bit flat,

15:58

is actually going to be more in the lower lobes.

16:01

Is this emphysema? I wouldn't know that from the radiograph.

16:05

I would just say that there is hyperinflation in both lower lobes.

16:08

I'd actually be thinking this is more likely trache brumation. But, uh,

16:12

the CT showed that there was all emphysema down there and the patient did have

16:16

alpha one 90 tripps in deficiency. But you know,

16:19

there are other causes of emphysema besides that. All right,

16:25

on ct, what you're looking for is essentially the dot,

16:29

a dot or a line cyst doesn't have anything in it.

16:34

And usually you can see a wall,

16:36

but with emphysema there will be some residual interstitial.

16:41

So there will be this hole with either a line or a dot. If you see it,

16:46

just call it emphysema. You don't have to say emphysema is changes, just,

16:49

you know, there's emphysema. And if you want,

16:51

if you wanna get really high tech and go, you know, is it pan lobular bolus,

16:55

central lobular, you don't have to though. Okay, these are cs.

17:01

Okay? You can see the wall. There's nothing in them.

17:04

Emphysema has little lines,

17:07

dots and things in 'em. So that tells you by definition,

17:11

that's not gonna be cyst. And there doesn't tend to be any definable walls.

17:16

Sometimes you may see a vessel around there, it can be confusing,

17:19

but in most cases that this is what emphysema is gonna look like.

17:24

Now, what, why, why does it occur? It is actually,

17:29

the theory is the loss of elastin. Good theory. Um,

17:34

and the bronchi close. The bronchials, sorry, close when they,

17:38

when you breathe out. So what happens is the air tends to get trapped. Well,

17:43

what happens as you accumulate more and more and more air in

17:49

this kind of partially destroyed and um, compromised,

17:54

uh, AVEs, well,

17:56

it tends to come around and it's gonna shut down the bronchial cuz the

18:02

pressure's so high. Okay, now the bronchial shut down,

18:06

take a breath in. Is that gonna open it?

18:08

Is that a higher pressure than the ovulus? No, it's not.

18:13

So it doesn't really have that so-called dynamic,

18:17

what people say,

18:19

it's actually just balloons and it's space occupying,

18:23

which increases the end tial residual void.

18:27

So people breathe up here, right?

18:31

Sometimes they use their shoulders. Oh, that just reflects,

18:34

the lungs are markedly hyperinflated. The diaphragm is flat.

18:38

So there's very little diaphragmatic excursion.

18:41

That's a space occupying process. When you look at pathology, look,

18:46

go to an autopsy and a patient with an emphysematous lung.

18:50

When they take the lungs out of the body and put it on the table,

18:53

the lung collapses, but not the emphysema. See,

18:57

they still remain hyperinflated, they're locked. Nothing gets in,

19:01

nothing gets out. When you see patients like this,

19:06

oh, there's emphysema, there's your dots. And this is a ground-glass process.

19:10

Cellular N S I P. That's okay. Nothing gets in. It's, it's avoiding it,

19:15

it's going around it. This is a consolidated pneumonia. Is this cavitation?

19:20

No, these are areas of emphysema. The consolidation goes around it.

19:24

Nothing gets in. Nothing gets out.

19:28

So another patient with a consolidated pneumonia,

19:30

that's why you got that sort of Swiss cheese appearance.

19:34

It just doesn't tend to get in. So once it locks,

19:38

it locks. What is the surgery for?

19:43

Advanced emphysema? What's it called? Right?

19:48

Lung reduction surgery. See, it's in the name,

19:52

it's in the name.

19:53

You're removing this portion of all this emphysematous lung.

19:59

Now the diaphragm starts to come up,

20:02

the space occupying balloons are less.

20:05

And the patient goes from here

20:09

to a more normal breathing pattern because the end title residual volume has

20:14

been improved. So remember the surgical therapy, it's in the name.

20:20

Now why the cachexia with severely hyperinflated lungs?

20:23

This patient is cachectic. You can see there's hyperinflation.

20:26

Is this emphysema? You look here. Well, that looks about halfway. I don't know,

20:31

may I guess it could be. But this isn't clearly emphysema.

20:35

So you wanna be careful about that.

20:36

And you also wanna be careful about calling it C O P D. Could be something else,

20:40

right? Could be traum milia, which is a form of it,

20:44

but it's something else. Now, why do they get cachectic?

20:48

I want you to look at this diaphragm again. When we breathe,

20:52

the diaphragm goes down.

20:53

There's a huge amount of negative pressure in the intrathoracic cavity.

20:57

This accentuates the inflow from the superior venava and inferior venava.

21:01

And when the diaphragm is down like this, there's no diaphragm excursion.

21:05

The pressures are high within the lungs, okay?

21:10

They're high. Now remember, the venous inflow is a low,

21:15

low pressure state. It relies on the increase in negative,

21:19

negative intrathoracic pressures to sort of basically suck it right on into the

21:23

right atrium and then move it through. But in these patients,

21:30

yeah, venous return might be compromised. Hey, now of course,

21:34

one of the theories that was given, and it's not given as a theory,

21:37

it's told to you that it's known, is that, oh, they can't eat enough.

21:42

Okay? That's made up. That's made up stuff.

21:45

Let's go back to basic science.

21:47

Let's try to figure this out physiologically.

21:52

When you take a breath in, this is my liver, by the way. Um,

21:56

this is the inferior cava expiration. When you take a breath in,

22:00

that's what it does. And it does. So suddenly don't believe me.

22:04

Put an ultrasound on your liver, take a breath out and hold it.

22:08

Look at the I B C. Now take a breath in, watch what happens. Closes,

22:14

suck the, uh, venous flow right into the right atrium. Okay?

22:20

These patients have,

22:21

with their high intrathoracic pressures and high right atrial filling pressures.

22:26

Well, this isn't gonna happen very well. So the venous blood flow is reduced.

22:31

I mean, you can see some patients here, the cachectic patient, um,

22:35

the kidneys are enhancing, still a little bit arterial,

22:37

but they do have the venous in flow. The spleen is pacified,

22:41

but the superior cava still hasn't really opacified yet. Now,

22:46

CT is just an indirect way, but if and when I was a, uh, resident,

22:51

way back when we used to do mesenteric angiograms, the conventional,

22:56

and when they would inject these patients, you would see this, uh,

23:00

superior mesenteric flow moving like this. Very slow,

23:06

very slow

23:08

because it can't get in the intrathoracic cavity.

23:12

So a more likely explanation here for why patients with severely hyperinflated

23:16

lungs for whatever reason,

23:18

is that they get this chronic venous ischemia, mesenteric ischemia,

23:23

you can't eat very much because then you get pain. That's more likely, I think,

23:28

as a hypothesis for why patients get cachectic.

23:33

In hyperinflated states, this patient is cachectic,

23:36

lost 30 pounds over four days, diagnosed with C O P D. Um,

23:41

they put in, uh, a feeding tube,

23:44

fed her aggressively because she's malnourished. What happened? Well,

23:49

pneumatosis, small bowel infarct.

23:54

Why venous ischemia? Most likely they did do a vascular,

23:59

um, ultrasound. The arteries were normal, but they didn't look at the veins.

24:05

Okay, severe tricuspid regurgitation. Why is this patient cachectic? Again,

24:10

there are other reasons that can block and limit the filling of the right

24:15

atrium. So it's a hypothesis,

24:18

but it seems to make a lot more physiologic sense. Uh,

24:23

I quote this truth passes through three stages. People, first it is ridiculed.

24:27

Second, it is violently imposed. Third,

24:30

it is eventually accepted as being self-evident. All right,

24:35

let's move on. Arthritis, severe arthritis, rheumatoid arthritis.

24:40

The patient has had three C O P D admissions. Okay, what's, what's the key here?

24:45

The, when you were sitting down and reading these things, what did you notice?

24:49

Immediately, let, let me take you back.

24:52

The persistence or recurrence of symptoms often indicates that a diagnosis

24:57

is being missed. The key here is three C O P D admissions.

25:03

That kind of is a red flag that says, you know,

25:07

I think this patient has something else.

25:10

You can see the severe erosions of rheumatoid arthritis. Well,

25:13

what are chronic rheumatoid arthritis treated with often? Well,

25:17

she was treated with steroids for a l um, a long time.

25:21

What does steroids do? Well, you know, they do a lot of harm in many ways.

25:25

They can also be helpful, but they also, uh, have their, have their problems.

25:30

So she's got these areas of ground, glasss, nodularity,

25:34

little cysts. And I would've said, okay, that's probably follicular bronchitis.

25:38

I won't get into what, what that is, but it is associated rheumatoid arthritis.

25:43

The other thing that came up is that she breathes through per slips.

25:48

Now what does that mean when you hear someone breathe through per slips,

25:52

they're auto peeping. They're auto peeping.

25:57

That is classically associated with emphysema.

26:00

But we've just noted that emphysema is not a dynamic process.

26:04

It is just a space occupying.

26:07

So if they're breathing through per lips, what does that probably tell you?

26:12

You're gonna find on ct? Well,

26:15

you're gonna find trachea, bronchia,

26:19

and this is her in expiration. This is the tr the bronch eye,

26:23

and there is the bronch eye when she takes breath out. Notice as you go back,

26:28

it doesn't get more dense. It is global air trapping.

26:32

And when you have global air trapping, the obstruction is more central.

26:36

So you look very carefully at the airways,

26:41

okay? Mm-hmm. This is a so-called frown sign. I don't,

26:45

I don't use those signs. Um, I just look and I see, okay, that is trachea,

26:50

bronchia, moia, it's severe. There is global air trapping.

26:54

Now that latter part is important.

26:56

There are some people who have collapsible airways, trachea bronchi,

27:00

but they don't have any air trapping.

27:02

They don't have chronic alesis and they don't really have symptoms.

27:06

So you really wanna be looking closely when you see trache,

27:10

bronchia are there,

27:12

is there evidence of global air trapping and or chronic

27:17

asis? Because that's what you would expect when the airway collapses.

27:21

Now how well will the standard C O P D therapy work for this patient?

27:28

It won't. Okay.

27:32

Patients often state that too. Steroids don't seem to help at all.

27:36

I've had a number of patients who have gone to meet after seeing their scans and

27:40

they say the same thing.

27:41

There's this little FEV one portable device that blow into and

27:46

they use it like 30 to 50 times a day. Well, that's a form of auto peep,

27:51

right? That's a form of peep. Much like burst lip breathing,

27:56

right? So what is trache bronchia? Well,

27:59

the official DEF definition greater than 70% narrowing of the trachea and or

28:03

bronchi.

28:04

But the key here with global air trapping or chronic appearing aex,

28:10

this often can, can be from cartilage weakness.

28:13

You can have the so-called excessive dynamic trachea posterior wall collapse,

28:18

uh, two hallmarks clinically per lip breathing and vocal cord dysfunction.

28:24

So if you see C O P D and then over here you see vocal cord dysfunction, you go,

28:29

Hmm, because they use their vocal cords to auto peep.

28:33

Classically, they have a chronic cough. They'll even say this,

28:37

they have difficulty clearing secretions. Why?

28:40

Every time they cough the airway collapses.

28:44

Can't get the secretions out. They get exercise intolerance.

28:47

They may have some wheezing. Uh, dyspnea though is the big one.

28:51

And chronic cough. Patient has a diagnosis of C O P D 30 pack,

28:56

year of smoking, yes. Yep. Emphysema. And there's your, uh, resolving pneumonia.

29:01

Again, not getting in the emphysema. Nothing gets in, nothing gets out.

29:06

But look what happens here. The trachea and the,

29:09

or the bronchi collapse and there's global air trapping.

29:14

She has developed trachea bronchia in addition.

29:19

So you can have trache bronchia without emphysema or with em. It,

29:23

it's its own entity.

29:27

So some of the call marks,

29:28

poorly responsive asthma or recurrent C U P D exacerbations.

29:32

These are your clues, right? Those are your red flags associations. Oh,

29:37

look at, there it is. Chronic steroids. That's it. Chronic steroids.

29:42

So that's why these patients with autoimmune diseases, if you look carefully,

29:46

you'll probably see this. Now of course to diagnose trium, malacia and ct,

29:51

you really have to have some expiratory scans.

29:54

You won't see it on the inspiratory, you see it on the expiratory.

29:58

If the patients are breathing, then you'll see it. If they're not,

30:02

then you really won't be able to make that diagnosis unless you get expiration

30:07

scans. The other causes, uh, patients have constricted bronchiolitis.

30:13

Okay? Get chronic steroids. They develop trache, brumation next. All right?

30:18

And then the third one, sleep apnea. Now sleep apnea is tracheal lac,

30:23

but it's more in the hypopharynx, right? But when you get into the chest,

30:28

it goes the opposite. So it's actually those two are related.

30:31

So sleep apnea patients also tend to have trache, bronchial ceia.

30:36

Now what about steroids?

30:37

Now this was a study and it's done just with inhaled steroids.

30:40

But the same thing can be seen with the systemic steroids.

30:44

The steroids wreck the cartilage. They inhibit chondrocyte formations.

30:48

So formation of more,

30:50

they cause vascular congestion and then they cause the smooth muscle atrophy

30:55

and thinning of the bronch eye. What happens next? Oh boy. Yeah.

31:00

Trache, bronchia. So a lot of these patients with C O P D, oh,

31:05

they're not responding. What do we do? Well, let's give more steroids. Time out,

31:10

time out, slow down. Um,

31:12

because you actually end up making it worse.

31:17

And that's kind of what tends to happen. Now this is a patient,

31:21

and I'm gonna bring this to the real life. Now,

31:23

how many CTAs do you read for pulmonary embolus? Hmm. Way too many probably.

31:28

So when you have a patient with a CTA for pulmonary embolus because

31:34

of C O P D, shortness of breath dyspnea,

31:39

you know, um, this sort of thing,

31:42

you have to look at the trachea and the bronchi. I look there first.

31:47

I hardly, I look at the pulmonaries last, uh,

31:49

because this is oftentimes where you'll see it.

31:54

They may not be able to hold their breath.

31:56

So this patient had per lip breathing rule out pulmonary embolus. Well,

32:01

the trachea is completely collapsed and on the expiration,

32:05

you see there's no increasing area of density that it's all globally air

32:09

trapped. Couple of areas here, got some air out, this is their problem.

32:15

What would you recommend to this person? A trial, A BiPAP, right?

32:19

What's BiPAP? Right?

32:22

It's another way to auto or a way to peep and it holds the airway open longer

32:27

so that they can get some more air out. Maybe secretions, BiPAP.

32:32

And one of the hallmarks is, is that when you see people like that and you know,

32:36

I call the ER and tell 'em this is what the God give a trial,

32:38

a BiPAP within about 15 minutes,

32:41

the patients often are like feeling much better. That's a pretty good sign.

32:46

You have a dynamic collapse. What is the incidence? Well,

32:51

of all CTAs, this is from uh, 2003. So, uh,

32:56

one out of 10 had trache bronchia, all pulmonary CTAs, one outta 10.

33:02

I actually think it's a little higher,

33:03

but maybe that's just the patient population. I'm reading red flags,

33:07

shortness of breath. C T A for shortness of breath.

33:10

Gotta look at the trac in the bronch eye chest pain.

33:14

And you gotta look at the heart pericardium aorta. Yes,

33:18

but with shortness of breath you have to look at the trachea.

33:23

Okay? Or when they have C O P D as listed,

33:27

you gotta have expiration.

33:29

When they have a C O P D diagnosis for their ct pulmonary angio two outta 10 had

33:34

tracheal bone lac. When they had severe asthma,

33:37

seven out of 10 had trache brumation the cause.

33:42

So is this common? Yes it is.

33:46

It will not take you long till you see this. I'm,

33:51

I promise you. Okay,

33:54

so this patient shortness of breath rule pe known pe,

33:58

severe trachea lac, global air trapping, uh,

34:02

the patient and I called the ER and told him and I go, yeah,

34:06

that person probably can't cough up their secretions, right?

34:08

Cuz they have these secretions here. And he goes, yeah, yeah,

34:11

that patient said that. Yeah. Yep. Um,

34:15

did improve quickly on BiPAP. Actually the,

34:19

this patient particularly was discharged. He was about to get admitted.

34:24

All right, this patient who severe tracheal lac,

34:29

they are intubated, they are unable to extubate. There is global air trapping.

34:34

Why can't they extubate at this point? Well,

34:37

it's because they need that peep to hold their airways open.

34:42

This was, you know, interesting too because in in rounds it was, you know,

34:46

this patient had been in chronic steroids for C O P D.

34:50

This probably made the trachea bronchial malacia much worse at this

34:55

point, they cannot extubate. Now what will happen?

35:00

Chronic steroids, they're chronically ext, uh, they,

35:03

they're intubated for multiple days. Yeah, they develop a,

35:07

a pneumonia, well we gotta get them off the steroids.

35:11

So you start to taper the steroids,

35:13

but the adrenals don't work and they're in crisis because of the pneumonia.

35:16

What happens? Well, their blood pressure drops,

35:18

they become unstable and then you put 'em back in the steroids and things

35:21

stabilize. The conclusion was, oh,

35:25

well that's why steroids are good for C O P D. Right? Circular reasoning.

35:29

Gotta be careful about this, right? So the more you start to understand,

35:34

the more you say, you know, this stuff is hard, it is confusing.

35:39

It's not that simple. Uh oh,

35:42

mark Twain education is a progression from a cocky ignorance to a miserable

35:46

uncertainty. Yeah. Amen. All right,

35:51

well let's shift gears. 58 year old LDS woman. Uh, and you,

35:55

I would, I worked at the University of Utah, so I saw a lot of L d s patients.

36:00

Uh, persistent dyspnea started eight years ago. All right, stop.

36:06

What's the thing here that says, whoa, okay, that was helpful.

36:11

There's a huge clinical clue here. In fact,

36:14

I don't even need really to image this patient.

36:16

You already sort of know what the diagnosis is. It started eight years ago.

36:22

She has hyperinflated lungs. You can see that sternal diaphragms 90 degrees,

36:26

not much here, uh, for curvature.

36:29

But I don't see that sort of emphysema kind of look the vessel attenuation that

36:34

these are branching.

36:35

Normally she has something else that's causing this obstructive pulmonary

36:39

physiology. What had happened now with this patient too,

36:44

is that she lost her health insurance for lying about smoking.

36:48

Now at the University of Utah,

36:49

there was a clinic every Thursday afternoon run by the pulmonary department that

36:54

took in patients who had lost their insurance to uh,

36:58

something pulmonary based and the vast majority of them.

37:02

And it was like a six week waiting list. That, that,

37:05

so it's common because we would say as radiologists all findings consistently

37:09

with C O P D and

37:14

no insurance. So they come to the University of Utah,

37:17

we image 'em and then you see this is the patient. Is this emphysema? No,

37:21

this is mosaic. This is a mosaic lung attenuation.

37:24

The vessels are really shrunk here. There is actually going to be air trapping.

37:29

And this is the inspiration and expiration. It's not trachea.

37:33

Bronchial moia in this one. And remember trache,

37:36

bronchial moia tends to cause global air trapping cause the obstruction is

37:39

central. This is more peripheral.

37:42

And so you get these areas of mosaicism and that's the air trapping

37:46

scene.

37:47

Cons consistently with constricted bronchiolitis used to be called

37:52

bronchiolitis o litter,

37:54

but it got changed to constricted bronchiolitis because there was some confusion

37:58

between bronchitis o litter and bronchitis O litter with organizing pneumonia

38:02

now called cop. Okay?

38:05

So the key here was she knew when this started.

38:11

If you ask a patient with emphysema, when did your breathing problem start?

38:14

I go, I dunno, trigger bronch. Maybe, uh, you know,

38:19

a few months ago with constricted bronchiolitis,

38:22

there is an insult to the airways and it's usually a specific event.

38:27

Oftentimes it's a respiratory viral infection like influenza or mycoplasma or

38:32

something. And it causes the bronch osa to uccr and then heal with a scar.

38:38

And then the hyperinflation distally occurs through the collateral aird drift of

38:43

the pores of con and canals of lamber until it gets so hyperinflated.

38:48

It also manifests as balloons or space occupying. It's not dynamic,

38:53

it's not gonna be like the purse lip breathing thing.

38:56

She did regain her insurance by the way.

39:00

Now bo I just do this cuz it's funny. Um,

39:04

it's common but it's not commonly diagnosed. And this one's more subtle,

39:08

especially on inspiration.

39:10

So the pathology is the permanent scar and that's the key.

39:14

The terminal bronchials, whenever there's an injury, wound necrosis,

39:17

this can occur. The most common is airway infections,

39:21

but smoke or chemical inhalation to autoimmune diseases,

39:25

drug toxicity and a big one is bronchiectasis cuz bronchiectasis destroys

39:30

the bigger airways. But this inflammatory process is,

39:34

is hitting the small airways too.

39:37

And this is a nice sort of sequence of what happens. This is normal.

39:42

You can see the lv i, it gets markedly inflamed. Let's just say it's influenza.

39:48

And then what happens is it tends then to Neros

39:54

scar starts to form. Whoops,

39:56

scar starts to form and then it plugs up and that's it.

40:01

It's done.

40:01

Now notice the alveoli here compared to here they are hyperinflated.

40:07

This is permanent, okay? It's done. You,

40:11

it's done.

40:14

So usually what they'll be diagnosed with is poorly responsive asthma or

40:19

non episodic asthma. Uh, recurrent C O P D.

40:24

They have a persistent dyspnea. It doesn't respond to steroids.

40:27

Usually there may be a transient response, but it'll be back.

40:31

The major clue is the patient can usually tell you when the difficulty began.

40:35

That's the clay. Now look at the infections.

40:38

R S V infections in pediatric patients, right? Less than two really severe.

40:43

They get the hyperinflation, they get the inflammation,

40:45

they go into their tents. Um,

40:47

and then what does the physician say appropriately? Hey,

40:50

there's gonna be some asthma risk of increased risk of asthma.

40:54

Well the increased risk of asthma really is only about six weeks.

40:59

But the persistence tells us that it's constricted bronchiolitis.

41:03

But they also say that they tend to outgrow it.

41:06

That is true because in these younger kids, two-year-olds,

41:10

these areas of constricted bronchiolitis, they don't grow.

41:14

So the rest of the lung grows and then compensates for it.

41:18

Now what if this was an older person, say a 15 year old?

41:22

Well now they can't outgrow it, right?

41:24

They are stuck with this constricted bronchiolitis.

41:29

This patient nine 2017. Okay?

41:33

She's now comes in here from 2019, she's had weight loss,

41:37

difficulty exercising. Okay? She was caught in a house fire.

41:43

What happened? Look at, look at the difference.

41:47

Why is she becoming cachectic? Well we talked about that

41:52

she was caught in an house. Fire.

41:53

Fire and the smoke is had high heat caused

41:58

this generalized broncho mucosa necrosis.

42:01

And then over the ensuing six weeks,

42:04

this plug all these plugs form and now she's hyperinflated.

42:07

So she's C O P D, uh,

42:10

because she's got a 14 pack year of smoking history. No,

42:13

she knows it started at the time of this house fire.

42:18

Now the imaging is patchy areas of air trapping. Now that's the key.

42:21

The mosaicism, it tends to be patchy tra your bronchial milias more global.

42:26

Now here's the confounding variable. You might see both there.

42:30

You might see some bronco malacia in the smaller airways,

42:34

but you'll see areas of, um, air trapping, um,

42:38

that's more patchy.

42:40

So constricted bronchiolitis and broncho lac, especially the bronchials.

42:44

Smaller segmental bronchials can coexist,

42:48

especially if they've been on more of chronic steroids.

42:52

All right, this is what it looks like.

42:54

Now it's tough on inspiration but the vessels tend to be larger in the

42:59

areas of the parent ground glass.

43:02

And they are vaso constricted in the areas of constricted bronchiolitis.

43:09

And these are balloons, okay? These are balloons.

43:13

They also tend to have a little less hypoxia in the emphysema. But that's,

43:17

there's a lot of overlap there. Now this person's a little different.

43:21

This person's had a cough and dyspnea for five weeks and you see all these

43:25

terminal bronchial nodules, terminal bronchial nodules.

43:29

This is the active form of bronchiolitis obliterating.

43:34

So remember that sequence of histology I showed you,

43:37

they're sort of still in the middle there and you are starting to see some

43:42

areas of air trapping or mosaicism that's beginning to form.

43:47

Now this person,

43:49

if you hit them hard with steroids for about a week to two weeks, okay?

43:54

Not, not not chronic, just hit it hard.

43:57

You can actually stop that sequence

44:02

in most cases and they won't be left with that debilitating sort of constricted

44:07

bronchiolitis. Cuz once you see that mosaicism, it's,

44:11

it's permanent, okay? In fact,

44:16

what's the most common um,

44:18

way to D treat severe tra constricted bronchiolitis while you give 'em a lung

44:22

transplant. What's the most common chronic complication of lung transplant?

44:27

Constricted bronchiolitis, right?

44:30

So this is a patient with asthma cuz this, there's a lot of misinformation here.

44:35

So in asthma they can get the hyperinflation. This patient had it,

44:39

it's got a little bit of airway thickening.

44:41

They got the treatments that felt better within a couple hours,

44:45

but they still did a C T A. And even though it's like, look,

44:49

the diaphragm is back now you see it's a transient, it's reversible.

44:54

The diaphragm's back, it's normal, but they still did the C T A.

44:59

Where's the mosaicism? Here? This is at, this is the, this patient.

45:05

Well there isn't any a little bit of con ground glass consolidated,

45:08

but there's no mosaicism.

45:10

This is constricted bronchiolitis in a patient who's diagnosed with poorly

45:14

responsive asthma,

45:18

you don't see this mosaicism or this vascular attenuation in

45:23

the acute setting. So you really don't see it with asthma.

45:28

When you see mosaic lung attenuation,

45:30

that indicates a chronic airway obstruction. If it's patchy,

45:35

it's probably constricted bronchiolitis.

45:37

Does the patient know when their breathing problems start? Yeah,

45:40

I was burning leaves outside and then got sick and didn't feel well and I've

45:45

been having trouble breathing since that's constricted.

45:48

Bronchiolitis asthma does not give you

45:52

mosaic lung attenuation. We'll finish with bronchiectasis. Uh,

45:57

very severe uh, cystic fibrosis here. Airway destruction.

46:01

But what are you also noticing? Look at the lungs. Look at the diaphragm.

46:06

Right? Severely hyperinflated. Why

46:11

bronchiectasis induces hyperinflation through constricted bronchiolitis.

46:17

You can see the mosaicism here, the vascular attenuation.

46:22

This area is a little bit better little ground glass,

46:25

but this is all constricted bronchiolitis at this point and

46:30

this when a bronchiectasis gets real severe,

46:33

it can actually collapse eventually another patient with cystic

46:38

fibrosis hyperinflated lungs. Why constricted bronchiolitis.

46:42

What's your differential? Constricted bronchitis.

46:46

It is because that the airway infection is recurrent and it

46:51

keeps hammering the smaller bronch osa eventually inducing the necrosis,

46:56

the scar and the hyperinflation which becomes permanent.

47:01

So cystic fibrosis or patients with bronchiectasis, I don't know,

47:06

put it on your macro or something. Uh, look for constricted bronchiolitis,

47:11

it's going to be there.

47:12

In fact it's evolving as a more common cause of morbidity and mortality for

47:16

these patients cuz they're living longer.

47:19

You always try to mention the degree and extent of constricted bronchiolitis

47:24

in any patient with bronchiectasis, but especially cystic fibrosis.

47:28

These three patients with cystic fibrosis, why do you see the mosaicism?

47:33

What does that tell you? This one's a bit more mild.

47:36

This one's a bit more moderate to severe. This is quite severe,

47:41

okay? These are common.

47:44

They're just not commonly diagnosed and constricted. Bronchiolitis.

47:47

You really would like to have expiration scans again, but you know we do.

47:52

You do what you can. So now let's go back to that first one.

47:57

After this,

47:59

what are you gonna say on your report of this patient?

48:05

Okay, well I'm looking here at the notch. Looks about halfway.

48:10

I don't see any deviation. There's definitely hyperinflation.

48:14

This patient has obstructive pulmonary physiology.

48:17

What if you say this patient has C O P D? What are you telling people?

48:21

What if you say, you know, this patient has emphysema?

48:23

What are you telling people? Why is this patient cachectic?

48:29

See, this patient has obstructive pulmonary physiology. Uh,

48:34

it is not clearly emphysema consideration for trick your bronchia or constricted

48:38

bronchiolitis CT scan with expiration may be helpful.

48:43

Okay, what about this patient? 31 year old dyspnea.

48:50

What are you gonna say?

48:53

A report findings consistent with C O P D. No, don't,

48:57

don't say C O P D. This is a mosaicism.

49:01

It's mosaic vascular attenuation. You get,

49:04

there's even a little bit of bronchiectasis here. You get expiration.

49:08

It's all air trapping.

49:09

This is constricted bronchiolitis differential constricted bronchiolitis.

49:13

This patient was also in a house fire.

49:20

How about this one? My DI patient got diagnosed with um,

49:25

C O P D.

49:26

She developed her breathing problems after she was cleaning her bathroom with a

49:29

heavy chemical solvent. Got sick then got a bit more disnic. What is that?

49:34

I don't even need to look. That's constricted Bronchiolitis.

49:38

Then the pulmonologist put her on steroids, wasn't responding,

49:43

kept the steroids going.

49:45

After a few years she noticed that her dyspnea was getting worse and that she

49:50

could no longer walk two miles.

49:51

She could only walk a mile and she was starting to breathe through her slips.

49:55

Why? What does she have? Well,

49:59

she's got the patchy areas of constricted bronchiolitis and she's now also

50:03

developed trache bronchia most likely because of the steroids.

50:09

Every one of these, the shoes image multiple times three pulmonologists,

50:13

like five radiologists. Everyone missed it.

50:18

This is something you can have an impact from your first day of working.

50:25

Watch out for these red flags.

50:28

Recurrence of symptoms or persistent multiple C O P D exacerbations.

50:34

The patient can identify the time period when breathing uhs constricted

50:37

bronchitis.

50:39

Breathing through purse lips or vocal cord dysfunction indicates a dynamic

50:43

collapse in auto peeping. That's bronchial lac.

50:48

They may have emphysema, they may not, but that's a separate thing.

50:52

Suggest a trial, a BiPAP.

50:55

I also have to suggest in my reports and to thing that trache bronchial

51:00

LAC is most likely the etiology pulmonary consultation

51:05

for workup of trachea bronchia is recommended.

51:09

Pulmonary consultation for workup of constricted bronchiolitis is recommended.

51:14

I specifically say this because in the clinical realm

51:18

that these diagnosis of trache bronchia constricted bronchiolitis are also not

51:23

considered by many pulmonologists.

51:26

The pediatric pulmonologists are much more aware of this,

51:29

but not as much in the adult. It just didn't make its way into the curriculum.

51:35

So, you know, we diagnose what we know. Take home points,

51:40

they're common. You will see this and you can have an impact.

51:45

All right, try to avoid the term C O P D.

51:48

It can lead to inappropriate therapy and if the patient doesn't

51:53

previously have that diagnosis, they can lose their insurance.

51:57

Consider something like there's obstructive pulmonary physiology. You know,

52:00

I don't, not sure the underlying etiology considered Turkey bronchia or,

52:04

you know, something pulmonary consultation for further workup of this. Okay,

52:10

with that, this is, uh, my dog Willow,

52:12

who I don't know if you heard barking or trying to get in here. Um,

52:17

and I will stop at that point when radiologist take ACI selfie.

52:22

Now, these are my email.

52:24

Please feel free to email me if you have any questions or something comes up

52:28

later. Um,

52:31

I can take a look at some of these questions and see if I can help you out here.

52:36

Um, when did the surgery for advanced emphysema become an option for treatment

52:40

patients? Oh, that's been a while actually. Um, geez,

52:45

I remember that back when I was a resident and that was,

52:49

that was the early nineties that they started to do that.

52:53

And we would do cts looking at the degree of emphysema.

52:57

Is it uniform then? They didn't do the surgery,

53:01

but if a lot of it was upper lobe,

53:03

then they would resect the upper lobe and then you would see the diver come back

53:07

and the patients felt so much better. Okay,

53:12

when do you consider expiration? I love expiration scans. I mean,

53:16

I love them, I just do 'em. And,

53:20

but when you really want to do it is this recurrence of C O P

53:25

D admissions per, you know, poorly responsive asthma or asthma,

53:30

C O P D, um, persistent shortness of breath, chronic cough,

53:35

um, and you should also be doing it for the ILDs. Okay.

53:40

All right. Do we have expirations? No. See do we,

53:45

do we have to take expiration scans and all pa Well,

53:51

yeah, do it. Do it. Just do it. Um,

53:56

but I will tell you in real life,

53:58

in real life at night when I'm reading most of those CT pulmonary

54:03

angiograms, these patients are breathing. Um, so I see it,

54:08

but yes, I be,

54:11

be liberal with getting expiration scans on anyone with

54:15

persistent pulmonary problems. Um,

54:19

is there a rule about vascular size that they are small? Hmm,

54:24

they will be smaller than the bronchi for sure.

54:27

What you'll also see is not just the size,

54:31

but you'll look out in the parenchyma and you won't see those little branching

54:36

vessels. So when you look in the area of the apparent ground glass,

54:39

the vessel size is bigger.

54:41

It'll probably be the same size or bigger than the bronchus,

54:44

but you will see lots of little dots and branching structures of the small

54:48

vessels in the areas of hypo, of,

54:52

of hypo attenuation. The vessels, you'll see almost none,

54:58

none of those small vessels that tells you they're all just sort of vaso

55:02

constricted and out. Okay?

55:05

Her lip breathing is primarily an inspiration ex, uh,

55:08

her lip breathing is expiration. It's all expiration

55:13

and you can feel it if you do it yourself.

55:16

You can feel how it keeps the tries to keep the airway open.

55:21

All right. Uh, dynamic airway collapse. Uh,

55:26

people like to separate them. I don't, but strictly speaking,

55:31

the cartilage is destroyed. The whole trachea bronchi go.

55:36

But in dynamic, excessive dynamic collapse, it's the posterior wall.

55:41

Remember the trachea, the cartilage is a horseshoe,

55:44

but the posterior wall has no cartilage. So when they breathe out,

55:49

it just kind of occludes that lumen. I think they're both kind of the same.

55:54

So I don't split,

55:56

but some the purest like to separate those two out.

56:00

Okay? Um,

56:03

you can differentiate constricted bronchitis from inflammatory bronchiolitis.

56:07

They really are interchangeable in, well, no, they're not inflammatory.

56:12

Bronchitis is more the active phase. So it was that one I showed you with.

56:17

You can see the little terminal bronchial nodularity and branching in a patient

56:22

with six weeks of symptoms. That's an active inflammatory bronchitis.

56:28

If it persists,

56:29

that inflammatory bronchitis will eventually become constricted.

56:34

Bronchiolitis constricted bronchitis is permanent.

56:38

It does not reverse. It does not respond to steroids.

56:42

Does not respond to antibiotics, right?

56:46

And a lot of these people will be mislabeled because again,

56:50

I'm not blaming anyone.

56:52

We just don't teach this in the curriculum and we diagnose what we know.

56:57

And especially with C O P D people just, you know, oh,

57:02

it's another C O P D and just give them this rather than just, okay,

57:06

wait a minute, time out. This patient's come in multiple times for this.

57:10

We should probably slow down. Um,

57:15

peep, peep pressures, uh, vocal cord.

57:17

You can constrict your vocal cords when you breathe out,

57:20

and that's how come you get vocal cord dysfunction with some of these patients

57:24

per lip breathing.

57:27

If you have these patients blow up balloons, you know, that can help.

57:31

They did a study in Australia if you're interested, uh,

57:33

where they had patients play the doddery tube, remember that tube?

57:38

And they played it for about, I think it was like, you know, uh, a couple hours,

57:43

three or four times a week.

57:45

And what they found at the end of six weeks is these patients with the sleep

57:49

apnea, trache, bronchial LAC kind of combo,

57:51

they actually did better than the patients who didn't

57:56

do that. So all of this peeping is what's needed.

58:01

And that tells you there's a dynamic collapse. It does not reflect emphysema.

58:07

It does not reflect emphysema. It reflects trache bronchia.

58:12

Um, can excessive airway be limited to central bronchi with air trapping,

58:17

but the trachea is relatively unaffected or normal? Yes.

58:22

Yes, it can. Yeah. Usually it'll be the whole thing, but the,

58:26

it can just be the bronch eye. It could be the segmental bronch eye,

58:30

and that's when it gets really tough. Like, Hmm, is this constricted bronchitis?

58:35

Or, you know, segmental broncho lac, I don't know. Same Both.

58:41

Same both pulmonary consultation for workup of constricted bronchitis and

58:45

broncho LAC trial of BiPAP. All right.

58:50

What is your opinion on using the parenchymal analysis software

58:55

available workstations? Uh, I'm an old fart, so,

59:00

um, go for it. Um, if you think it helps,

59:05

uh, I tend to see it and I don't know,

59:10

I think it's just because I looked at so many, I just, it just pops out to me.

59:14

But I understand it's hard. Uh, give it a try.

59:17

If you think the software can identify the mosaicism in the parenchyma,

59:22

then it's useful. But after

59:27

I just looked at so many that y you know, when I, the exam pops up, it just,

59:33

I just see it. Okay, but expiration,

59:37

just get expiration when you're not sure. Uh,

59:40

is imaging in the prone position useful? I'm not a big prone position fan. Um,

59:48

you can do it.

59:49

I would just rather have supine inspiration expiration and I think you can

59:54

diagnose most things.

59:56

I think you can tell the difference between alesis and fibrosis personally. Um,

60:00

irregular visceral pleura is not ASISs that's gonna be myelofibrosis.

60:04

If the asis looks like it's going up laterally, that's not ays. But you know,

60:09

either way in bronchitis is steroid used at some point

60:15

as it is a cause of factor. Yes,

60:17

steroids in the short term can be helpful,

60:22

but it's when you start, cuz the body heals, right? We insult the body,

60:27

but if you give it a chance, it'll heal.

60:30

When you keep that insult in injury going, that's when you run into problems.

60:35

If you were to drink a lot of alcohol tonight, have fun,

60:39

your liver's gonna take a hit, but it's gonna recover.

60:43

But you drink a lot of alcohol every single day,

60:45

your liver can't repair and then things start to spiral out.

60:51

Okay, so steroids short term. Yeah, go for it.

60:56

Just don't keep in mind. All right.

61:01

What is the treatment, uh, for tracheal,

61:04

bronchial lac constricted bronchitis? Not much.

61:10

Um, if it's very severe for constricted bronchitis, you get a lung transplant,

61:16

uh, tracheal, bronchial malacia, you could try some different airway, uh,

61:20

peeping, uh, processes,

61:22

like what I just said with the f even one or ballooning balloons or trumpet,

61:26

you can try that C P A P, um, you can try that.

61:30

The key here is you don't want them going on chronic steroids,

61:34

which often happens. That's the key. The other thing is,

61:38

there are some places that if it's excessive airway collapse,

61:42

you can do a Cy Lastin, uh,

61:45

implant as an outpatient and you're fine.

61:50

Some people have tried stents that could work.

61:53

But if the broncho LAC gets out too far,

61:56

then the stents won't work because you're still collapsing out here.

61:59

Still air trapping, even though centrally it's open. Um, uh,

62:04

you know,

62:04

there are some institutions that are recognizing this more and thoracic surgeons

62:09

are starting a tracheal,

62:10

bronchial malacia clinic where they do all this workup and then treatment

62:13

options. Um, if you don't have that at your own institution, you know,

62:17

you can always look at it, look at starting it on its own. Okay.

62:23

Um, is there a way to differentiate infectious bronchitis from inflammatory

62:27

radiologically as the former is treated with antibiotics later are treated with

62:31

steroids? No, uh, not usually,

62:33

but the time will tell in infection usually will run its course

62:38

within usually a week to two, um, antibiotics,

62:43

you know, a week to two usually is it, if it's still there.

62:48

Okay, the, the infection's gone. That's,

62:51

that's an inflammatory bronchiolitis and that needs to get hit with steroids.

62:56

So the time will tell, believe me,

63:00

most of the of those terminal bronchial things that you saw, that'll be gone,

63:05

that'll be gone in a, you know, after antibiotics.

63:09

It's those that are persistent. That's when you go, okay, stop the antibiotics.

63:13

This is a steroid hit. Let's see. About preventing a future complication,

63:18

which is much worse of constricted bronchiolitis. Okay.

63:22

And then hopefully that answered the question. Uh,

63:26

treatment of constricted bronchitis.

63:28

Don't give them on chronic steroids if it gets severe enough. Lung transplant,

63:32

that's pretty much what we got. Try to prevent it from happening.

63:38

Uh, should we give constricted bronchiolitis differential of all cases with yes,

63:42

shortness of breath, mosaic lung attenuation,

63:44

constricted bronchitis needs to be there might be pulmonary hypertension,

63:48

but it'll probably be constricted bronchiolitis. Absolutely. Absolutely.

63:55

Um, please elaborate on Hyler position and x-ray with emphysema.

63:59

Yeah, remember that little line I drew?

64:03

Remember that line I drew with a pulmonary artery up?

64:05

Pulmonary artery down right side, that's should be normal.

64:11

Patients who have conventional emphysema most in the upper lobe,

64:15

those are balloons in space occupying the hilum will go down.

64:20

Okay? You'll have increased distance to the apex. Decrease to the diaphragm,

64:25

all right?

64:26

Then it will go medial and you will see the,

64:31

the vessels that look like this, they will be like this and curved.

64:38

Okay? So they go down, they go medial

64:43

vascularture gets crowded together and curved.

64:48

If you don't see that, it still could be emphysema,

64:51

but you don't want to say that.

64:53

You just say it's obstructive pulmonary physiology or something of that sort.

64:59

And you know, further workup for this if, if you think it's worthwhile,

65:03

especially if you see that they keep coming back,

65:05

then absolutely further workup. Okay.

65:08

Differential for patchy mosaic. Um, mosaic attenuation,

65:13

small airway trapping, pulmonary hypertension, that's your two.

65:19

Okay. Pulmonary hypertension be from chronic thromboembolic disease,

65:23

primary pulmonary hypertension. Um,

65:25

there will be no air trapping seen with the pulmonary hypertension.

65:28

Both will increase in density with air trapping. When you do expiration,

65:33

the wider areas will get wider. The dark areas stay the same.

65:37

The accentuates the difference. Okay.

65:40

Small airways disease is bronchiolitis, constricted bronchiolitis,

65:45

asthma, sometimes, you know, these are what we term small airways disease.

65:51

Um,

65:51

and how do you differentiate pulmonary hypertension in a scenario of emphysema

65:55

and vessel size? Um hmm. Pulmonary hypertension,

65:59

emphysema often coexist,

66:01

especially with advanced emphysema because of the loss of vascular bed,

66:05

usually maybe some chronic hypoxia. Um, differentiating it well,

66:10

uh, what you're gonna do is measure the main pulmonary artery.

66:13

Look at the ASIN aorta, look at the main pulmonary artery.

66:16

Is the main pulmonary artery much bigger? If it's much bigger,

66:19

there's pulmonary hypertension. Okay, you can say three centimeters,

66:24

but I've seen a lot of people with three centimeters and it's normal cuz the

66:27

aorta is three centimeters, they've just got bigger vessels.

66:30

People are like snowflakes. So I usually go that route. Look centrally.

66:35

Is the pulmonary artery much bigger than the aorta at the same level? Yeah,

66:40

probably pulmonary hypertension in the setting of emphysema. Okay.

66:45

Is chronic bronchitis or radiologic? Not really. It,

66:48

it can be if you see a lot of airway thickening in mucus plugging,

66:52

that one to me is a bit more clinical and it's probably not as common as what we

66:56

suggest, but, uh,

66:59

all you'll really see is a lot of airway thickening and maybe some mucus

67:02

plugging. Um, that's pretty much it. And look for pulmonary hypertension,

67:07

for sure.

67:08

In chronic bronchitis that tends to develop earlier than emphysema because these

67:12

patients tend to be chronically hypoxic because of the VQ mismatch.

67:19

Um, asthma, small airway or large airway disease? Both.

67:22

I actually consider it more both, but it's more of a small airway.

67:25

It gives the main problems, but those receptors are, you know,

67:30

they're, they're seen throughout the trachea, brum, mucosa,

67:34

but the real problems clinically, it's from the small airways.

67:39

Okay. Uh, when do you ask for a cta, a mosaic lung attenuation?

67:44

Oh, um hmm. I don't usually ask for CTAs. Uh,

67:49

I guess the only time I would is if you think there's pulmonary hypertension,

67:52

which again, you can see on a, on a, on a CT scan without contrast. You know,

67:57

there's your aorta, there's your pulmonary artery. Same size. Yeah.

68:00

Don't go to a c t a get an expiration scan. Um,

68:05

if you see there's no air trapping, you can go to it,

68:07

but there'll be our trapping.

68:09

If that pulmonary artery is much bigger in diameter,

68:12

then you're in the pulmonary hypertension.

68:16

Now you order the c T A for workup of pulmonary hypertension,

68:20

which it is a pretty good mo uh, test for that.

68:23

So you've now shifted because you've seen something that requires a separate

68:29

evaluation. All right.

68:32

Most of the AE patients ae, Hmm.

68:36

What's ae, I dunno, with the request for C T A,

68:40

have breathing difficulties and lungs invariably show abnormal density.

68:43

Do you suggest additional lung specific high re No, no. Don't do high res, uh,

68:48

CTAs for pulmonary embolus or what have you. Um,

68:53

the sections are thin enough, you'll be able to see something. Um,

68:57

most of the time the, it's an acute problem.

69:00

It's when you start to notice that they like God,

69:04

this is their third CT pulmonary angiogram in, in one year.

69:08

That's when you want to say, Hmm,

69:10

I wonder if they should probably get a separate workup from a pulmonologist or

69:14

something. A lot along those lines. And that also says,

69:18

look very carefully at the trachea.

69:19

And the bronchi look very carefully for mosaic lung attenuation.

69:23

Even if it's just inspiration,

69:25

you can suggest an expiration scan and stuff like that.

69:28

If you see the pulmonary arteries big, then work up a pulmonary hypertension,

69:33

which you're already doing a really good test for. All right.

69:37

How do you differentiate artifact from pathology? Ground glass. Oh,

69:41

that's a good one.

69:42

That gets hard when the patient is halfway breathing out.

69:47

Now, if they're half expiration, you're gonna see a higher density,

69:52

slightly higher density. Okay. Now when you breathe out,

69:57

it should get more dense as you go posterior. Remember that picture of my ct,

70:02

it, the, that ground glass or higher density,

70:05

not as high anteriorly as you went back,

70:07

it got progressively and uniformly more dense.

70:11

If you have a partial expiration ct,

70:14

which is pretty common and you notice that it's subtly ground glass,

70:18

but it's got that increasing density,

70:21

that is overwhelmingly likely going to be normal.

70:25

But if you see a subtle ground glass and you don't see that

70:29

increasing density,

70:32

but it looks like it's either patchy or more uniform,

70:37

you wanna suggest a diffuse lung disease.

70:41

Or if it's patchy, a small airways disease like constricted bronchiolitis,

70:46

you can suggest A D L C O,

70:48

which is really helpful because if it's normal, blow it off.

70:54

If it's abnormal, you made a great catch of a diffuse lung disease.

70:59

So it has everything to do with seeing that normal increasing density.

71:05

Okay. It's tough by the way. Sometimes you just can't tell,

71:09

and that's okay. Sometimes I can't tell either. Okay.

71:15

Um, okay. I guess that's it for the questions. Uh, geez,

71:20

I hope you enjoyed it. Please feel free to email me if you have any questions.

71:26

Um, it, you know, um, I'll do the best I can to answer it. Okay.

71:31

Thank you Dr.

71:32

Dr. Goslin.

71:33

Thank you so much for that amazing lecture and answering all those questions.

71:37

Thank you to everybody for all those really fantastic questions.

71:41

Really appreciate you being here.

71:43

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71:46

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71:49

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71:54

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71:55

Deborah Baumgarten for a lecture on urothelial cancer and beyond CT urography

72:00

interpretation, including pitfalls.

72:02

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72:09

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