0:02

Hello and welcome to today's Noom conference, hosted

0:04

by modality and provided by the France Foundation.

0:08

Noom Conference connects the global radiology community

0:11

through free live educational webinars that are accessible

0:14

for all and is an opportunity

0:16

to learn alongside top radiologists from around the world.

0:19

Today we're honored to welcome Dr.

0:21

Jonathan Alis for a lecture entitled Mastering HRCT,

0:25

the radiologist Pivotal role in Fibrosing ILD Management.

0:30

Dr. Alis is the director

0:31

of Cardiothoracic Imaging at Jacobi Medical Center in the in

0:34

Bronx, New York, and assistant professor at Albert

0:37

Einstein College of Medicine.

0:39

He's passionate about education, having won teaching awards

0:42

as an attending and during both residency

0:44

and cardiothoracic fellowship at Monte Fiori Medical Center.

0:48

Dr. Alis has research interests in many topics,

0:51

including pulmonary embolism and pulmonary fibrosis.

0:55

At the end of the lecture, please join him in a q

0:57

and a session where he will address questions you may

0:59

have on today's topic.

1:00

Please remember to use that q

1:02

and a feature to submit your questions so we can get to

1:04

as many as we can before our time is up.

1:06

With that, we are ready to begin today's lecture. Dr.

1:09

Alis, please take it from here.

1:12

Good afternoon everybody.

1:13

Very happy to be here today with you.

1:15

We are gonna be discussing CT radiology

1:19

and Fibrosing ILDs.

1:21

Hopefully we'll try to cover a few topics. My name's Dr.

1:25

Alis, Jonathan Alis, I'm a cardiothoracic imager.

1:29

This lecture was prepared with Dr.

1:31

Salvato, the chair of radiology here at Jacobi.

1:33

And um, I hope to spend some nice time today

1:38

with you discussing, you may have seen this just pop up now

1:41

for a few minutes, but we're gonna sort

1:42

of focus essentially on interstitial lung disease.

1:47

Try to sort of differentiate out between

1:48

what the terminologies that clinicians are familiar with

1:52

and guide us a little bit into getting the background,

1:54

background of epidemiology

1:55

and the disease burden so that we understand how we fit in

1:58

as radiologists into the picture.

2:00

We'll move on to discussing the CT findings

2:05

and how we help in ILD management and, and we'll move on.

2:09

We'll basically be pro, you know, the, the crux

2:12

of this will be a few cases that we'll discuss

2:14

and we'll use that as our sort of springboard

2:17

to discuss things

2:18

and hopefully we'll have time

2:19

at the answer to some questions.

2:21

Okay. We're gonna start with a question.

2:24

Um, I think you have a chance to, to do this.

2:27

So how do delays in diagnosis impact the prognosis

2:31

of fibrosing ILD?

2:32

We'll start with an nice easy one. Early diagnosis may lead

2:35

to unnecessary treatments and adverse side effects.

2:38

Delayed diagnosis leads to worse outcomes due

2:41

to continued fibrosis progression

2:43

and delayed diagnosis may result on better symptom

2:45

management due to less aggressive interventions.

2:48

And the prognosis remains stable regardless

2:50

of diagnostic timing

2:51

as currently at the treatment on options are equally

2:54

effective at any stage.

3:01

So interstitial lung disease, somewhat,

3:04

sometimes it can be rather mystical term,

3:07

but it's a broad spectrum.

3:09

It's an umbrella term. It doesn't, there's no specific core,

3:12

there's no specific thing as an interstitial lung disease.

3:14

It's actually en encompasses many,

3:15

many disorders over 200 disorders.

3:17

And the common sort of theme behind it is, is that all these

3:21

diseases that affect the pathological process in the lung

3:25

primarily affect the pulmonary interstitium,

3:27

which is the structural network supporting the alveoli

3:30

capillaries, various degrees

3:33

of inflammation and fibrosis.

3:35

Seems that that's a continuum

3:37

and essentially primarily inviting the interstitial space.

3:41

But also it's even though isn't an interstitial lung

3:44

disease, it doesn't just affect the interstitial lung,

3:46

the interstitial, it affects the entire lung in its own way.

3:50

But their common denominator is it affects the interstitial

3:54

as degrees progresses.

3:55

There's results in essentially as one would expect

3:59

restricted lung function, PU impaired diffusing capacity

4:03

leading towards hypoxemia, progressive DYS dyspnea

4:06

and in many cases unfortunately,

4:08

respiratory failure and death.

4:10

So the sort of big one that we all know about

4:13

or we need to know about or we're aware of, it gets a lot of

4:16

some sort of front and center.

4:17

And it's, so interstitial lung disease is IPF,

4:20

which is idiopathic pulmonary fibrosis.

4:23

I can get a little bit confusing with with radiologically

4:25

because we are gonna be discussing an IPF pattern,

4:29

which is synonymous with a UIP pattern.

4:31

We have to understand though, what IPF is,

4:33

is a disease entity in its own rate.

4:34

It's a chronic progressive fibrosis interstitial pneumonia

4:38

that's idiopathic.

4:39

We don't know currently the unknown, the an unknown cause

4:43

and it is classically associated with it.

4:46

The hallmark radiological

4:47

and histological feature is a UIP pattern, which is one

4:50

of the things that we will sort of make sure

4:53

that we can feel comfortable knowing what is UIP

4:56

and what is not UIP

4:57

and that is gonna lead us to be able to sort of,

5:00

if there is no other cause that would lead them to say that

5:02

that would be idiopathic pulmonary fibrosis.

5:04

What are the, we don't know the cause

5:06

but there we do know that various risk factors,

5:10

it's something that's often seen in older age males

5:14

and those things are helpful because if it's a a, you know,

5:17

a a female younger patient, it, you can take

5:20

that component into your diagnosis thought process.

5:23

But again, obviously not nothing always reads the book.

5:25

But essentially it is an old age male sex.

5:27

There's some genetics involved with the most sort of common

5:31

gen gene associated with be the Muk five B um,

5:36

promoter gene that's commonly in surfactants

5:39

and telomere is more associated

5:40

with short tel is more associated

5:42

with familial interstitial lung disease and IPF.

5:46

And then there are also environmental exposures

5:50

and smoking and also gastroesophageal reflux disease,

5:53

which will also be important for us as radiologists.

5:57

Now that's IPF.

5:58

Now once we put IPF to the side, there's another

6:02

umbrella term as such called progressive pulmonary fibrosis.

6:06

And that's also a, not a distinct disease,

6:08

it's agnostic to the underlying condition.

6:09

There's gonna be many underly underlying conditions

6:11

of progressive pulmonary fibrosis,

6:13

but essentially it's defined as non I-P-F-I-L-D-I-L-D

6:17

with signs of pulmonary progression, pulmonary pro fibrosis,

6:21

that with evidence of progression

6:23

and the criteria that we use within one year.

6:25

So there's gonna be, there's a,

6:26

there's a clinical criteria worsening respiratory symptoms,

6:29

there's physiological progression.

6:31

So that's more what they pulmonologists gonna be seeing at

6:34

in when they do pulmonary function tests.

6:36

And from what we see is radiological progression.

6:38

So that's gonna be something we want to touch on is

6:39

how do we define progression in pulmonary fibrosis.

6:45

Some suggest using a, you know,

6:47

a more nuanced PPF despite management as such,

6:49

meaning is it progressing even

6:50

though the patient, so management.

6:51

But that's just as a side to get an idea.

6:54

We're talking about close to a third of the patients with

6:58

non I-P-F-I-L-D.

6:59

They're going to progress

7:01

and that will be something that we expect over time

7:03

as we're following these patients.

7:05

Now this slide here

7:09

shows you the causes of this is, this is ILD other than IPF

7:13

'cause we're looking at progressive pulmonary fibrosis.

7:15

So IPF apathic pulmonary fibrosis is not within this slide,

7:18

but the other entities that do cause it.

7:20

So you can see here there's a lot of different diseases

7:24

and what's in blue is the sort of prevalence of how many

7:28

of these disease entities are likely to lead

7:31

to progressive fibro pulmonary fibrosis.

7:33

It's just worth sort of taking a quick look to see.

7:35

Let's, if we just focus on, so

7:37

to the left we have the idiopathic ones.

7:39

There's a lot of idiopathic causes again,

7:40

but once we do know causes, so the most common causes,

7:43

what we're gonna see, a lot of the ILDs are gonna be caused

7:45

by autoimmune diseases, rheumatoid arthritis

7:47

and systemic sclerosis up there at the top,

7:49

mixed connecting, dis mixed, mixed connect

7:52

to connective tissue disease, excuse me,

7:54

and various autoimmune IDs.

7:56

And then there's gonna be exposure related

7:58

with hyper pneumonitis being a very common one,

8:01

occupational exposures.

8:03

And then you can move over.

8:05

There are some cysts or airspaces a definition,

8:07

but then sarcoidosis.

8:08

So really as if we, if we sort of have in our, in our sort

8:11

of mindset that we, we have an IPF

8:13

and then outside IPF within PPF, the sort of things

8:16

that we are thinking, you're going to always sort

8:18

of lead down to the processes, you know,

8:21

always generally gonna speak

8:22

to lead down a autoimmune workup, seeing a rheumatologist

8:26

or, or coming the other way if they know the patient has an

8:29

autoimmune disease, we're likely going to see the, i,

8:32

you know, the CT chest from these patients

8:35

with rheumatoid arthritis systemic sclerosis as a way

8:38

to determine did they get

8:39

or are they expressing inte interstitial lung disease from

8:42

their incidents

8:45

and prevalence to get an idea.

8:48

Really just to see how IPF tends

8:52

to be a little bit more in North America, Europe, Europe

8:55

as opposed to the South America Asia.

8:59

And we can see the prevalence is about, sorry,

9:02

the incidence is about between three

9:04

and 900,000 patients per year.

9:10

So delayed diagnosis, you'll hear this a few times from me,

9:14

the, and we'll see a few slides on this,

9:16

but really the, one of the key points

9:18

to take away at currently the management

9:20

that we have does not reverse interstitial lung disease.

9:23

It's an irreversible lung lung disease

9:26

with irreversible lung damage.

9:28

And therefore the earlier we pick it up,

9:30

the more likely we are to help the patient

9:33

as they can start antifibrotics.

9:35

The treatments that we have available to us generally

9:39

slow the decline of respiratory function,

9:42

but they can't reverse it.

9:44

So earlier the better.

9:46

And then obviously downstream there later on there are

9:48

significant risks of complications such

9:50

as pulmonary hypertension

9:51

and that's also gonna be things that we're gonna be looking

9:53

out for radiologically as well.

9:56

As you can imagine, those PE patients

9:58

with PPF progressive primary fibrosis as opposed

10:01

to non-progressive primary fibrosis are more likely to have

10:04

associated much higher ILDs and

10:08

therefore we are, um, are going to be able to

10:13

see though there'll be serial PTs

10:15

and high um, res resolution cts.

10:17

There'll be an antifibrotics oxygen therapy

10:22

and eventually lung transplant is going to be the causes

10:24

of these, um, these healthcare resource utilizations.

10:27

Okay. Generally speaking,

10:29

the disease burden is gonna be similar for IPF

10:31

and PPF with expect with the symptoms of shortness of breath

10:34

and dry cough being something similar by all of them and,

10:36

and a result of their negative impact on their quality

10:39

of life and these things that we don't necessarily

10:40

may not think about at radiological.

10:41

But it's important to realize that these things

10:44

lead downstream to eventually affecting these people in a

10:47

very lot, in a very significant way across their, their life

10:50

of there is a lot of, um, transplantation

10:56

constraints towards the end

10:57

and we really try to get a catch it before that

11:00

and we try to collect the, the, you know, sort out the,

11:04

the essentially the comorbidity management early on as well.

11:07

So pulmonary hypertension we mentioned good, those type

11:09

of things we're trying to think about and we try

11:11

to pick up at the fact that these patients are going

11:13

to have acute exasperations

11:15

and that's gonna throw, you know,

11:17

throw up in our imaging interpretation as well.

11:20

So it is really the backdrop of how all

11:22

of this management is taking place.

11:24

And so now we're going to um, have a look at the,

11:27

look at the sort of role of ct.

11:29

So we have a question, which

11:32

of the following hhl t's finding is most characteristics

11:35

of UIP, the hallmark of IPF?

11:39

Is it upper low predominant fibrosis

11:40

with grand gloss opacities?

11:43

Is it peripheral basal predominant

11:44

fibrosis with honeycombing?

11:46

Is it diffuse consolidation throughout both lungs

11:50

or is it central lung fibrosis sparing the periphery?

12:00

Okay, great. As we've mentioned, early detection

12:03

and inter intervention can improve patient outcomes

12:05

and we're pivotal with making those,

12:07

identifying those characteristics also important to sort

12:11

of help diagnosis

12:12

and move them into an ILD specialistic specialist center if

12:14

you, if they're not being imaged in one

12:16

or to have multidisciplinary team teams in that, in that way

12:19

to timely initiate fibrotic.

12:21

So how do we image patients the most?

12:25

Essentially what, you know, HR ct,

12:27

high resolution CT and ct.

12:29

Nowadays all cts are essentially high resolution,

12:31

so it's a little bit misleading,

12:33

but essentially we're going to be getting three thin

12:35

sections of one to two millimeters

12:37

and we are going

12:39

to be imaging these patients in end inspiration

12:42

without contrast.

12:45

The reason why without contrast helps is often when you give

12:47

a patient contrast, they can have a, uh, tachycardia

12:49

or they become tnic when they contrast goes in.

12:52

And that obviously we would like them to hold their breath

12:55

standard cts that performed in supine.

12:57

And a lot of interstitial lung disease centers will also do

13:01

expiratory imaging and prone imaging

13:04

and we can discuss that a little bit,

13:05

but as a general that may be an additional.

13:09

So just to point out this role of our HRCT

13:12

and diagnosis here, you can see here our patients suspected

13:14

of having IIPF generally speaking

13:19

HRCT pattern, what if you can see a UIP pattern

13:23

or an I, um, essentially that's gonna lead us down

13:26

of the MDD of the multidisciplinary team into IPF

13:30

and be able to, if we can definitively say the patient has

13:33

U-P-U-I-P, they can, it can

13:35

result in them not requiring a biopsy.

13:40

Uh, this slide's a little busy, I'm just,

13:42

bear with me one second.

13:43

So this slide is essentially the guidelines

13:45

and if you mind 20, we're not gonna go through the details

13:47

of all of this, but what I,

13:48

because we will in as as the base of the cases,

13:51

but what I really wanna bring out is how

13:53

the guidelines basically form towards can you determine if

13:58

there's a UIP pattern or not?

13:59

So is on one extreme is a definite UIP pattern. There it is.

14:02

And on the other side, is it an alternative diagnosis?

14:04

And that really is what I wanna give over in this lecture.

14:06

Can we comfortably say what UIP is?

14:08

And then if we don't think it's UIP,

14:10

what do we think it could be?

14:11

And that's going to be our sort of main job

14:14

of really saying, is it UIP

14:16

or if it's not UIP, can we sort of

14:20

know the common patterns that are significant

14:23

of a suggestive alternative diagnosis in between UIP

14:27

and an alternative diagnosis, you can have probable UIP,

14:30

which could someone may suggest that

14:31

that could just be early UIP and that will transition over

14:34

and that will be fall into our discussion of

14:35

how do we see the progression

14:37

and then in determine is where we're not so sure.

14:40

As we mentioned before, when we're looking

14:42

for progressive pulmonary fibrosis,

14:44

the radiological evidence of pro,

14:46

pro progressive fibrosis is going

14:48

to be really looking at do we, we see the, the sort

14:52

of hallmarks of interstitial lung disease

14:53

and do we see progression of them?

14:54

So do we see traction bronchiectasis and bronchiectasis?

14:58

Do we see progression of that?

14:59

Do we see progression of reticulations?

15:01

Do we see increased honeycombing or increased volume loss?

15:04

All of these things that we should be thinking about

15:05

as we're looking at it and we'll look

15:06

at these images very soon.

15:08

Okay, so let's do some questions.

15:12

So a 60-year-old, 61-year-old man with worsening dyspnea,

15:17

what is your diagnosis?

15:20

Is it NSIP? Is it UIP?

15:23

Is it PPFE or is it organizing pneumonia?

15:34

Okay, next.

15:39

Okay, so this is a 40-year-old female.

15:43

Let's have a look at the images first with a chronic cough

15:46

presents to the emergency DIS department

15:48

with dyspnea, 40-year-old female.

15:51

What is your diagnosis? Is it N-S-I-P-U-I-P

15:54

HP or organizing pneumonia?

16:03

Okay. All right.

16:11

Mixed. Okay, you have two, we have two images for this.

16:14

So just one, we'll just look at these first.

16:15

So this says 63-year-old female with shortness of breath.

16:18

So they have an axial slice and a sagittal slice.

16:21

This was in 2016.

16:24

Okay, so the patient then returned in 2021.

16:28

Yes, five years later. What is your diagnosis?

16:31

Is this N-S-I-P-U-I-P HP

16:35

or organizing pneumonia?

16:38

Just have a look at that poll

16:39

for a little bit when that comes up.

16:42

Let's get a quick look at

16:50

okay rate.

16:55

Okay, 60-year-old female with shortness of breath,

17:01

a 60-year-old female with shortness of breath.

17:03

You can look at the two axial slices here.

17:05

The one on over here is at the base of the lungs.

17:07

This is higher up at the lungs

17:09

and as you come this is gonna be the corona images.

17:12

What is your diagnosis? Is this U-U-I-P-I-P-F?

17:15

Is this CT DUIP or is this type sensitive pneumonitis?

17:19

Is this cystic lung disease?

17:30

Okay, so let's get, let's get to the meat

17:31

of things now, UIP.

17:33

So UIP, we've touched base,

17:35

we've discussed the key findings.

17:36

We're looking for when we're seeing any

17:37

interstitial lung disease.

17:38

Do we see reticular? Opacities?

17:39

Is this a sort of, so one way I would look at this a

17:42

thing, is this a diffuse disease?

17:43

Do I see bilateral? Is it we're not looking

17:44

for something focal that's around an osteophyte

17:47

or something that could be scarring.

17:48

So so is it a diffuse, is it a bilateral disease?

17:52

And then we're gonna try to determine where is it?

17:55

CRAN cranial cord cran, quarterly

17:58

and centrally and peripherally.

18:00

So if we were gonna focus on a UIP pattern,

18:03

very straightforward subpleural bas lip predominant.

18:06

So we're gonna look at the basis

18:07

and we're gonna look at the peripheral.

18:10

I either looking at the sagittal

18:12

or the axles, depending what you're more comfortable with.

18:13

The coronals look for a distribution.

18:15

Ideally what we're looking for is aran cord A

18:18

where be more bas on and nothing always, it doesn't have

18:20

to just be, but if you have basal sparing then we're not

18:23

gonna be going with UIP.

18:24

You will likely see other areas as well.

18:26

But does it involve the air, the basal liver is

18:29

and is it subfloor that we're looking

18:30

for reticular opacities.

18:31

And to make the the UIP definite pattern,

18:34

we're looking at honeycombing

18:36

and we'll discuss that momentarily

18:38

and absence of features to suggest alternative diagnosis.

18:41

So that's really gonna define our UIP.

18:43

What about pro honeycombing? So let's discuss honeycombing.

18:46

So as you can see here, honeycombing essentially is a lot of

18:50

stacked cysts and you can imagine it like a brick wall,

18:52

the way you make a brick wall.

18:53

So this is the most periphery,

18:55

you lay the bricks on top of each other.

18:57

So too the cysts start the most periphery

18:59

and they go sort of centrally.

19:01

So you are gonna see more stacked cysts.

19:04

Yes, it can become confusing when you are looking at

19:07

traction bronchiectasis and the periphery.

19:09

But I often find sometimes helping using a mini ip,

19:12

which is a minimum intensive protection projection,

19:15

you can sometimes see that if the,

19:17

what looks like holes are actually a dilated bronchial.

19:21

And if we're looking for stax cysts along the periphery, um,

19:25

we will invoke, um, honeycombing.

19:29

Now if it's less than two

19:30

or you have evidence of paraseptal emphysema, that's

19:33

where there's a sort of thing but a sort

19:35

of question backwards and forward.

19:37

But generally emphysema paraseptal should not have the Stax

19:41

cyst appearance and therefore this would lead

19:43

you to think of honeycomb.

19:45

Probable U IP is essentially the same

19:47

as U IP other than you don't have honeycomb.

19:49

So you have the same subpleural basal predominant fibrosis,

19:52

you see the reticulations

19:53

and again, the absence of features

19:55

to suggest alternative diagnosis.

19:56

So you'll see traction bronchiectasis as you can see out

19:59

to the periphery here.

20:00

And generally that means that you'll see

20:02

as you go out towards the end, you don't expect to see the,

20:05

the bronchial tree AOR rises and becomes more

20:08

and more peripheral, more becomes more and more smaller.

20:10

So if you start to see a beating

20:11

or you see the bronchial, the bronchial is right out

20:13

of the periphery, you can and associated, um,

20:17

parenchymal de um, abnormality, you could suggest that

20:20

that is tran traction bronchiectasis.

20:23

What are features that are considered to be alternative

20:26

to UIP?

20:27

So this is mnemonic from Dr. Salvador. Cannot be UIP.

20:31

So if you like mnemonics, then use mnemonic.

20:33

If you don't just, we'll go through them briefly anyway just

20:35

to sort of cover the, the areas.

20:37

Generally speaking, consolidate consolidations says

20:40

something superimposed on A UIP,

20:42

but as as it being part of the ILD process,

20:44

you don't expect to see that.

20:46

You don't expect to see air trapping, you don't expect

20:49

to see knowledge nodules, nonsolid nodules or nodules.

20:53

You don't exist here as represented by an O cysts.

20:57

We're thinking of something of a

20:58

cystic lung disease instead.

21:00

And top meaning the, if the, if the cranial cord focal,

21:04

you know, the distribution is more

21:06

of a an upper low predominance, we're not gonna be thinking

21:08

of UIP, we're gonna be thinking more

21:10

for an upper low predominance

21:11

of two ones that have in your back pocket.

21:13

If you see an upper load that would be sarcoid

21:15

and hyperemia pneumonitis and we'll discuss them

21:17

and they're a little bit better essentially just now just

21:19

to habit it, there would be the way I would differentiate

21:20

those two I, again, these all just not always like this,

21:24

but an upper lobe

21:25

and with, you know, with a lot of lymphadenopathy,

21:27

you could think of sarcoid or an upper lobe with a lot

21:29

of air trapping, you could think of hyper pneumonitis

21:32

otherwise in terms

21:33

of not just the cranial cord distribution,

21:35

you'd have the central distribution.

21:36

So while UIP is a peripheral,

21:38

once we're looking at the peripheral, something

21:40

that's more central, or we could call it bronchovascular

21:43

or airway centered, we're gonna be thinking

21:45

of other institutional lung disease.

21:47

Similarly, for example,

21:48

sarcoid would be more bronchovascular or a hyper sensor.

21:51

Mitis would be more airway centered.

21:56

This is really just to demonstrate to you how

21:59

the reticular opacities often can appear ground glass

22:03

and UIP having an extensive amount

22:06

of grand classes is not something that you would expect

22:08

to see with UIP and that would point

22:09

to towards an alternative diagnosis.

22:12

But reticulations themselves often can appear obviously

22:15

whiter than the normal lung.

22:18

I'm gonna slip the sky for now.

22:22

We mentioned this before and I'm trying to just reiterate,

22:27

one of our jobs is not just necessary.

22:30

So ideally picking up interstitial lung disease early

22:33

as we've mentioned and then being able to characterize it

22:35

and then also be able to determine if there's progression.

22:39

So we are going to look for early fibrosis,

22:41

which we'll see here as traction bronchiectasis.

22:44

You can see these periphery here.

22:46

You would expect these little, so you see sort of lucencies

22:49

that you would expect by this point the bronchial tree

22:51

would've ized and would be much smaller

22:53

and you will not tend to see normal bronchi.

22:55

Now for it to be called traction bronchi is when you invoke

22:58

the word traction bronchi is what you're saying,

23:00

or traction bronchial exis, which is really differentiating

23:02

where the bronchial or the bronchial, what you are really

23:06

trying to invoke.

23:08

That should be a terminology that you are going

23:10

to be using only in an interstitial lung

23:11

disease or a fibrosis.

23:13

Because the, the concept behind this is, is

23:15

that the bronchiectasis

23:17

or bronchiectasis is being caused by traction.

23:19

Meaning the primary issue is the lung parenchyma around it,

23:24

it's pulling on the bronchi.

23:26

But if you, you can have bronchiectasis that are, you know,

23:29

where that's being the, the centered focus of it.

23:32

Ground gloss opacities again can appear not often with UIP,

23:37

but you can see as often be it gets hard sometimes

23:39

to differentiate from fine reticulation.

23:41

And as it progresses you will expect

23:44

to see the bronchiectasis is transitioning

23:46

into honeycombing.

23:49

And this one, I, I threw it in here

23:52

because it was part of the questions as well.

23:54

It is a nuance thing, but it's something worth no noting.

23:57

So we mentioned that

24:00

and we will discuss this as we go forward.

24:02

UIP is a pattern, excuse me, is a pattern that the lung,

24:07

uh, pathology in the lung.

24:08

Now UIP doesn't necessarily mean the patient has IPF,

24:12

it's just a pattern that it can be associated with IPF.

24:15

So once you invoke a UIP pattern,

24:17

if the patient has no known cause

24:19

for this UIP, then it's feasible.

24:21

Then this patient has IPF, that would be our process.

24:24

But if you do invoke a UIP pattern

24:27

or any lung disease, there will be a workup.

24:29

And if the patient has a, a specific type of appearance

24:32

of A UIP like this, this is often helpful.

24:34

And as I find this pretty useful,

24:37

tell you which one I find the most that if you see this type

24:40

of pattern, you can invoke UIP

24:43

in a connected tissue disease.

24:44

So then I would invoke suggest, you know,

24:47

rheumatological workup

24:48

and that would be a UIP pattern

24:49

that has what's called exuberant honeycombing.

24:52

So it often looks like cysts.

24:53

It's an extensive amount of honeycombing that you don't tend

24:56

to see with IPF.

24:57

And more importantly, what I find is what I find

24:59

to be quite helpful is the anterior upper lobe sign.

25:03

So you'll have the basis, you'll have your IP sort

25:06

of UIP pattern, but you're gonna have a lot more anterior

25:08

upper lobe honeycombing and disease.

25:11

And that I often see with patients with u

25:13

with connected tissue disease.

25:14

The other signs here is just

25:15

to point out you have straight edge signs.

25:17

So if you look at the coronals, it's such a differentiation

25:19

between the, the, the, the AP code, um, the,

25:22

the CRAN cord gradient.

25:24

But this is a UIP patent,

25:26

but not a UIP patent that you would expect

25:28

to see in I pf this is a UIP associated

25:29

with connected tissue disease.

25:32

So we've mentioned this and we're just gonna review just

25:34

to sort of, you know, come from a different angle.

25:40

This is a pattern of lung disease that UIP.

25:43

So you see a lot of the extracellular matrix build up here

25:47

and it is a, it's a disease that is a per,

25:49

so if we're looking at the lung, parenchyma will be

25:50

a peripheral disease.

25:52

It's a peripheral disease. The airways is the

25:53

bronchovascular bundles, you see peripheral involvement and

25:58

therefore you'd expect it to be subpleural on a, on a ct.

26:01

That's A-U-I-P-N-S-I-P patent.

26:03

So an NSIP patent is a much more hetero, sorry,

26:07

homogeneous as opposed to a heterogeneous appearance

26:10

that you would, you would see in UIP.

26:13

It's gonna diffusely involve the alveoli spaces

26:16

and you'll often see a lot of ground gloss opacity

26:19

as you do here and it's more homogeneous.

26:21

So a homogeneous pattern, as you can see is involving not,

26:24

it's not just focused to the peripheral,

26:25

but it's homogeneously involved.

26:26

That would be thinking something of NSIP.

26:28

Now the third pattern that I really want to talk about

26:31

and we, we will mention is hyper pneumonitis.

26:34

And hyper pneumonitis is what we can, so what in terms

26:39

of a a, a fibrotic pattern,

26:42

we have UIP which was peripheral, we had a homogeneous NSIP

26:46

and hyper hyper percentage pneumonitis is gonna be more

26:48

of an airway centered for fibrosis.

26:51

So we tend to see it around the airways.

26:54

And this would often be either, you know,

26:55

call it peri bronchial or per

26:56

bronchovascular or airway centered.

26:58

We tend to use the terminology airway centered

27:00

and it again, you can see very clearly the

27:03

periphery of the lung is spared here.

27:04

So this was the way we would see an image like this

27:06

and you say, well look, this is very central.

27:08

I don't see it on the periphery.

27:10

So I'm leaning more towards a hyper pneumonitis

27:12

where the hyper pneumonitis you're gonna be looking.

27:15

Therefore, since it is a broncho process,

27:17

it's an airway centered, you will often see air trapping

27:21

and that's gonna help you because that's gonna be from the

27:24

differences in the different airways being affected.

27:28

Now the hyper humanis would be one of the images

27:31

that you would consider doing expiratory images imaging that

27:34

that would bring that out even more

27:37

and you would be able to see the air trapping the mosaic

27:39

attenuation and prove that is really from the airway.

27:42

So I, that is a helpful thing to use.

27:44

Um, which would be exploratory imaging when you're concerned

27:46

about air, air trapping

27:48

and in a situation of airway center fibrosis.

27:52

So they're the main sort of key findings

27:55

and sort of, um, patterns I want to talk about.

27:58

And I wanna just touch base the things that,

28:00

the other things that are just gonna help us.

28:02

Hiatal hernias. I tend

28:03

to see hiatal hernias in everybody maybe,

28:05

but generally speaking and these patients having reflux is,

28:10

can the acid reflux not is it associated with IPF,

28:12

but it can significantly worsen the disease.

28:15

So making somebody aware of that, making, you know,

28:18

making sure that that's just clear if the patient has,

28:22

uh, evidence of reflux.

28:23

That's an important thing to point out.

28:24

Lymphadenopathy, it's a tough one, meaning IPF patients

28:29

and we always have to just remember this, anybody

28:30

with any chronic inflammatory

28:32

or fibrotic lung disease is gonna have a higher

28:34

chance of malignancy.

28:36

So therefore we're always gonna be keeping an extra, um,

28:39

eye out for malignancy in these patients.

28:42

But also lymphadenopathy seems to be a run of the process.

28:46

So you will tend to see, we see a lot

28:47

of lymphadenopathy just in a patient with IPF alone.

28:50

And obviously if they have a systemic disease

28:52

that's causing their interstitial lung disease like

28:54

rheumatoid arthritis or systemic sclerosis,

28:56

you're gonna see a lot of lymph nodes, you know as well.

28:59

Often you'll see auxiliary lymph nodes

29:00

with those type of patients as well.

29:02

Pulmonary hypo artery hypertension,

29:04

you can see here in the top image this patient has extensive

29:06

pulmonary hypertension with

29:07

calcifications in the pulmonary tree.

29:09

Important because this is a downstream effect

29:11

and causes a lot of comorbidities.

29:14

Pulmonary hypertension for me, I, you know,

29:15

I use the main pulmonary artery,

29:17

I use 32 millimeters looking at the main pulmonary artery

29:20

literature, something up to, you know, from 29 up.

29:22

But essentially pay attention

29:24

for your looking at pulmonary

29:26

evidence of pulmonary hypertension.

29:27

And then you could, as we mentioned,

29:29

there are other things you could think about mosaic

29:31

attenuation if you are looking for air trapping to try

29:33

to determine do I think this is a, a hyper mitis?

29:36

And then you can think of other things like cirrhosis.

29:38

If you see cirrhosis with an I

29:39

with this sort of IPF picture.

29:40

Could you think, could you think

29:41

of something like short tel bear syndromes?

29:43

Is this, does this patient have a familial issue

29:46

or is there other causes

29:49

from looking at the attenuation of the liver?

29:51

Could speak from a drug induced interstitial lung disease,

29:56

quantifying fibrosis.

29:58

We'll discuss this briefly, it's important as, as right now.

30:02

And I think things will change as, as the,

30:05

as AI becomes more and more useful in these matters.

30:09

Right now we don't really have a very good way

30:12

of quantifying it clinically.

30:13

There are some, the stocks use this in terms

30:16

of a grading fibrosis for a research basis

30:18

for the idea really is just to demonstrate the point being

30:21

that the higher the fibrosis it correlates likely

30:24

with the patient having a increased, um,

30:27

a decreased diffusing lung coefficient.

30:29

And so essentially worsening lung functions.

30:31

So we need to be able to come up with a way

30:34

to dis demonstrate when we're,

30:36

when we're demonstrating progression,

30:38

which right now is a little hard,

30:39

but right now, we'll you know,

30:41

generally either looking at progression of do we see

30:44

more extensive lung disease

30:46

and do we see progression from not just the extent

30:48

but like we spoke about before that the bronchiectasis

30:51

or bronchiectasis is now transition into honeycombing.

30:54

So we can see here this is an example

30:57

of a progressive fibrosis.

30:59

So you can see how this was the original image

31:01

and later on is you can see clearly that there's now more,

31:04

there's increased honeycombing

31:05

and you can see how the fibrosis is while once was more

31:09

peripheral and less honeycombing.

31:11

Now the honeycombing is,

31:12

so this obviously would lead under progressive fibrosis

31:16

similarly, often it doesn't necessarily appear that the more

31:20

of the lung is involved now the same area

31:22

amount of the lung is involved.

31:24

However, it's transitioned more from a,

31:26

a bronchiectasis appearance now to now you can see here, so

31:29

how you can see these bronchials periphery

31:31

or this would be a bronchiectasis here

31:33

and now you can start to see these more stacked cysts.

31:36

Appearance of honeycomb said again this would be progression

31:39

even though the actual extent of the lung hasn't progressed.

31:43

This is an example of progressive hyper pneumonitis.

31:47

You could see very clearly here so very clearly,

31:49

but you do see mosaic attenuation in air trapping.

31:52

But what you do note is that the bulk of the process

31:55

as you can appreciate is not a peripheral

31:58

process, it's a central process.

31:59

It's around the airways, it's

32:00

around the broncho para bronchovascular bundles.

32:03

You can see how you have sparing of the load.

32:04

So here happens to be an upper lobe, a central,

32:07

and you can see progression of what once was just mosaic

32:11

and ground gloss.

32:12

And now you can appreciate

32:14

how there's traction bronchiectasis

32:16

and traction bronchiectasis.

32:17

So there's progressive fibrosis.

32:23

NSIP often NSIP can transition from

32:28

being, so we mentioned NSIP is more of a diffuse homogeneous

32:32

pattern and you see ground gloss, which is one of the things

32:35

that would, yeah, an extensive amount

32:37

of ground gloss would be something would take you away from

32:38

thinking of a UIP pattern.

32:40

So often that concept of having a homogeneous appearance

32:44

with a lot of ground graft would be a cellular pattern,

32:46

however often they appear together and makes,

32:49

but as you move away from a cellular pattern

32:51

or move away from ground graft and you see more

32:52

and more traction bronchiectasis,

32:54

you're gonna be thinking more of a fibrotic pattern.

32:55

So you can see progressive NSIP can transition from a

32:59

cellular to a more fibrotic pattern

33:02

and often you can have a fibrotic pattern

33:04

and then you can get a flare up

33:05

where you can have a mixed cellular and

33:06

that affects their treatment courses.

33:09

Okay, do a question.

33:16

What is considered the gold standard ILD diagnosis

33:18

and management and the HRCT

33:21

and content notes, HLCT and lung biopsy.

33:24

Is it HLCT and serological testing

33:27

or is it multidisciplinary discussion?

33:34

Okay, great.

33:40

The radius radiologist role in multidisciplinary care.

33:43

So we saw this before, but essentially just to bring out

33:48

how we sort of from a different component,

33:50

but the guidelines emphasize multidisciplinary approach

33:53

for diagnosis and management

33:55

and multidisciplinary discussion.

33:56

Multidisciplinary teams is recognized as the gold standard

33:59

for IILD diagnosis and management.

34:02

We are part of that discussion

34:03

and the reason why it's so important is

34:05

because there are so many components.

34:06

Now we've discussed the main factors of appearances here,

34:09

but often there will be requirements to make a,

34:14

as we've mentioned, for example,

34:15

A UIP pattern doesn't necessarily mean IPF and

34:18

therefore we need to ensure the patient's had a good

34:20

rheumatological workup.

34:21

Often we don't know the findings or the findings are mixed

34:25

and will lead to biopsies.

34:26

Hopefully we, you know, as we progress

34:28

with our diagnostic skills, we the less requirement

34:32

of biopsies, but the core team

34:34

really has the patient in mind.

34:35

It takes the pulmonologist, the pathologist, the radiologist

34:38

and rheumatologist and that really leads to the management.

34:40

Strong collaboration is crucial

34:43

and often, um, you know, HLCT features

34:48

of UIP can be found, um,

34:50

with often there's histological diagnosis of UIP

34:53

that we won't necessarily see.

34:54

So depending on the, obviously the circumstances

34:57

and the requirement to make that diagnosis early, um,

35:01

involving pathology

35:03

and necessary the necessary, the necessary requirements

35:07

of having biopsy is important.

35:11

Benefits of a, of, of collaboration has shown

35:14

to demonstrate improved diagnostic accuracy and confidence.

35:18

Guideline concordance optimize management,

35:21

tailoring the treatment plan specifically to when

35:24

to consider antifibrotics, when

35:25

to consider immunosuppression.

35:26

These are discussions that we have quite regularly in the,

35:28

in the, in our teams of and and at what point do you start?

35:32

What point do you, you sort of watch

35:34

and then enhance patient care as they,

35:36

as we've discussed at the beginning,

35:37

they often will need a long, a long-term follow up.

35:41

Okay, so what have you learned?

35:45

Go through this slowly now

35:47

and this will be part of our review.

35:50

So 61-year-old man

35:54

with worsening dyspnea.

35:56

What is your diagnosis?

35:58

N-S-I-P-U-I-P-P-P-F fee or organizing pneumonia.

36:11

Okay, great. So we'll we'll go with the 85%.

36:14

We're doing great. So what do we have here?

36:17

We have a peripheral disease.

36:22

It is affecting the, the base.

36:24

We can see how there's some stacked areas

36:26

here, cystic spaces.

36:27

So we see honeycombing

36:28

and the peripheral and the basal area.

36:30

So this would point towards attraction bronchiectasis,

36:34

a peripheral basal and honeycombing.

36:38

This would be very good for a UIP pattern.

36:41

Why would we go away from NSIP would like NSIP

36:43

because this is not so homogeneous

36:45

and we don't like to see more of a ground glass appearance

36:49

and more of a homogeneous appearance

36:50

as opposed as heterogeneous.

36:51

PPFE is gonna be more of a apical involvement

36:54

and organ organ organizing pneumonia just often would

36:57

necessarily not have these areas

36:59

of high uh, fibrosis or honeycomb.

37:01

We, but more sort of per focal consolidations.

37:10

Okay now a 40-year-old female

37:15

with chronic cough presents

37:17

to the emergency department with dyspnea.

37:20

So here we have this homogeneous appearance,

37:22

ground glass opacities throughout the lung.

37:26

So extensive homogeneous ground glasss opacities.

37:35

Is it NSIP? Is it UIP HP or organizing pneumonia?

37:42

Excellent. Okay. 80% 0.4, close to 80%.

37:46

So again we we're gonna the homogeneous

37:49

ground gloss appearance.

37:51

So also it is a lower low performance.

37:53

Now just to point this out, it's not really part

37:55

of the thing, but you see how there's one cystic space here.

37:58

Generally speaking, there's another point I wanna point

38:00

out that's relevant on this thing.

38:01

So first of all, the patient's female, it's helpful

38:04

and then you can see also this, you can see

38:06

how the patient has a dilated esophagus.

38:08

So dilated esophagus, this patient has scleroderma.

38:11

So in a dilated esophagus scleroderma picture

38:13

with NSIP pattern, I pointed out that cyst.

38:16

'cause often you can see LIP um,

38:18

and I don't really wouldn't call that

38:20

unless I saw maybe three cysts or so.

38:22

I don't know if that's a, uh, an academic finding,

38:24

but I try not to, if there's one cyst I would not invoke it.

38:27

But if the, once I start to see three I question is there,

38:29

uh, 'cause you can often see LIP

38:32

and an SIP together, especially in someone

38:33

with an autoimmune disease.

38:37

Okay, this is a two, two slide question.

38:42

Started off in 2016.

38:44

Patient has a lot of air trapping, a lot

38:46

of mosaic attenuation you can see is central

38:48

and you can see around this area.

38:50

So a lot of air trapping

38:51

and as it progressed five years later

38:54

we can see there's a very lot of, there's a lot of

38:58

per bronchial fibrosis, airway centered.

39:03

What is your diagnosis?

39:05

Is this NSIP, this is UYP is

39:08

or is this a hyper pneumonitis or an airway centered

39:10

or is this organizing pneumonia?

39:22

Okay, excellent.

39:24

Okay, so this is hyper pneumonitis

39:26

and again, the, the reason why we were focused on this now

39:29

for organizing pneumonia, they have it in a certain area.

39:31

Maybe this slide made you feel like it's more

39:33

of a focal consolidation,

39:34

but it really well was just for the demonstration

39:36

of the progression of fibrosis, which is more

39:38

of an airway center focus.

39:39

You see the air trapping,

39:40

I think based on the original image that you saw,

39:44

the mosaic attenuation, the air trapping

39:46

and it progressed to be a more of a airway center as opposed

39:50

to a peripheral fibrosis be.

39:51

And an upper lobe would be very helpful

39:54

and very good diagnosis for I sense United is this

39:57

68-year-old female, if I recall had a parrot

40:00

that she did not want to say goodbye to.

40:02

So often if I have a rule, if anybody has a parent,

40:06

it's hyper humanoid, it's irrelevant of the imaging.

40:09

But that's a side. Okay, this one tends

40:14

to throw people but hopefully we'll go over it again.

40:16

So we have a lot of what seems to be extensive.

40:20

Honeycombing could be full, but cysts,

40:23

but you also see anterior upper lobe involvement.

40:26

And if you look on the coronal you can see a

40:29

very clear straight edge.

40:31

So is this A-U-I-P-I-P-F pattern and a 60-year-old female?

40:34

Is this A-C-T-D-A connective tissue disease UIP pattern?

40:38

Or is this a hypersensitive pneumonitis

40:40

or cystic lung disease?

40:43

Serant honeycombing anterior upper lobe

40:46

involvement, straight edge side.

40:54

Okay, good. 51% went for, well it is a tough question.

40:58

It says cystic lung disease, it is not cystic lung disease.

41:00

However, I understand why

41:02

and that's the reason why it's there.

41:03

But the reason why this is based this is would be the A

41:08

UIP pattern that is more classically seen

41:11

with a connected tissue disease.

41:13

And again, the, the, the sort of tip offs I like

41:16

to see is have a look at the anterior upper lobe.

41:19

Often you can see, so the exuberant honeycomb, you'd expect

41:21

that very later on.

41:22

Often you can see that someone like a rheumatoid arthritis

41:25

ILD, um,

41:26

but if you see the anterior upper lobe, you can often see

41:28

that earlier and you can, you can suggest at least

41:31

that should be in your differential.

41:33

So the key takeaways I hope we have taken away is

41:37

that it's pivotal for early diagnosis

41:39

and for the ongoing monitoring of fibrosis, including IPF

41:42

and progressive pulmonary fibrosis, early detection

41:45

and intervention can improve outcomes.

41:47

Accurate identification of CT patterns like UIP is crucial

41:50

and can obviate the need for biopsy.

41:51

So the guidelines are gonna often say is it a UIP pattern

41:54

because it's gonna be a UIP slash ipf,

41:57

but remembering UIP can show up in other, in other forms

42:01

and other causes of UIP.

42:04

And then when on the other extreme, is it not UIP.

42:07

So do we think of something like NSIP is this,

42:09

is this hypersensitive pneumonitis

42:13

and how our key role in the multidisciplinary management

42:17

of these patients and of ILD.

42:19

So I think that we're just gonna do a knowledge

42:20

check of the last few questions.

42:22

I maybe and I, I believe they come along now.

42:25

So first one,

42:27

how does the delay in diagnosis impact the prognosis

42:29

of fibrosing ILD?

42:30

Early diagnosis may lead

42:31

to unnecessary treatments and adverse side effects.

42:34

Delayed diagnosis leads to worse outcomes due

42:37

to continued fibrosis progression.

42:39

Oh, excuse me,

42:44

delayed diagnosis may.

42:45

Okay, you're good? I think we're good.

42:46

Everyone's in Very good. Okay. Excellent. Next question.

42:54

Next question. Which

42:56

of the following findings is most characters of UIP?

42:59

Is it upper or predominant peripheral per

43:02

fibrosis with ground glass?

43:03

Is it peripheral basal predominant fibrosis

43:05

with honeycombing or is it diffuse consolidation throughout

43:07

the lungs or central fibrosis sparing the periphery?

43:10

What is, what is UIP? The whole market of ip.

43:16

Excellent. Very good. Okay.

43:18

And I believe what is considered the gold standard ILD

43:23

diagnosis, is it HLC imaging with consult notes,

43:26

with lung biopsy with s

43:27

or is it multidisciplinary discussion?

43:39

Okay, excellent.

43:42

I believe thank you so much for spending time with me.

43:46

I hope we, um, reviewed some things that were helpful

43:50

and um, if anybody would like to reach out to me,

43:52

always welcome to get my email either through modality

43:55

or France Foundation and I can answer questions that way.

43:58

Thank you so much for your lecture Dr.

44:00

Alis, that was wonderful. We have a couple extra minutes if

44:04

you're okay to answer some questions that have come in.

44:07

Okay. Let's see if I can go through these questions. Okay.

44:12

PPF does not include any IPF in decision logical

44:15

progression when occurs to the IPFA?

44:16

It's a great question. I think I would

44:17

just the same technology.

44:19

I think it's a semantics thing,

44:20

but in terms of progression, I think I would

44:21

utilize the same concept.

44:23

So really we're, we're focusing on, um, um,

44:29

the looking at the, so really the, the,

44:31

the main factors are just sort of recap that briefly.

44:35

We're looking for reticular opacities, we're looking

44:36

for early on we're gonna see traction bronchiectasis.

44:39

So that's really what I look at very early on.

44:42

So the combination of reticular opacities

44:43

and traction bronchiectasis and then moving

44:47

and then moving forward you can see, um,

44:51

traction bronchitis turn into honeycombing or get worse

44:54

or volume loss, those type of things

44:56

that would use use as progression.

44:59

Um, do you have lung pain transplant at your institution

45:01

as part of your practice lung transplant?

45:03

For our institution we refer out to in to, um, part of the,

45:07

the health network if, if needed.

45:09

But it is often on, you know, for people especially,

45:12

you know, further down the line who are not

45:15

either get picked up very early when we pick them up

45:18

before treatment or so they have extensively

45:22

or especially young patients, that would be the ones

45:23

that we, we refer out to.

45:26

Can a lymph node in scleroderma rated

45:28

NSIP increase uptake in PET scan?

45:30

It's a good question. I don't wanna say yes

45:32

or I would assume yes,

45:33

but I don't know definitively what the research is.

45:35

I'm happy to look into that. It's an interesting question,

45:36

but I would assume that, um, it has to be taken into mind,

45:41

but I believe that all

45:42

of these inflammatory things could

45:43

necessarily, um, increase uptake.

45:45

But I, that's a good question

45:46

and I, I would like to look into that question as well.

45:49

What the exact, if there's a way to differentiate

45:51

between PET avidity in a lymph node that would be concerned

45:55

to be more of something suspicious as opposed to a backdrop

45:58

of having an inflammatory disease.

46:03

Okay. Yes, great question.

46:07

Commenting on I-L-I-L-A spec specifically

46:09

how you calculate 5% involvement,

46:11

which is the requisites of diagnosis.

46:12

So we actually just had a

46:14

very interesting discussion about this.

46:15

I would prefer if there's a way to get to, to touch base

46:18

with you about in how ILA is a, is a, is a subject

46:21

that I would need more of a discussion on

46:24

and that's something that I'm happy to discuss

46:25

and you know, I can email you with you how we do that.

46:27

But again, I, I do feel that, um, that way forward is going

46:32

to be with, um, it's gonna help with a lot

46:35

of AI is gonna help us, you know,

46:36

trying to make these involvements.

46:39

Thank you for the presentation. If I mention in the last

46:41

case of CCRD,

46:42

why is it honeycombing in the anterior pillows and not cyst?

46:46

I believe it's a progression if it's, I think it's,

46:48

it is honeycombing it, you know,

46:50

and I think that that probably leads to the same questions

46:52

of why people will go for cystic lung disease.

46:54

Um, and I think the progression is often what

46:56

what we see is it starts with,

46:58

if you see the progression over time, I often see

47:01

what starts, what looks like reticulars in the anterior

47:03

upper lobe and then moves on

47:05

to traction bronchiolitis and then generates.

47:08

So they have to end up having this exuberant honeycombing,

47:10

but I think it's more on their

47:11

progression as opposed to a one-off.

47:13

The, the questions were not meant to sort

47:16

of, they may not be great.

47:17

Um, they were more just to bring out that point.

47:20

But I agree with you on a one-off you could invoke cysts,

47:22

but I think putting it all together and the, the extent

47:24

of the exuberant honey, the lows I would go with.

47:30

I'm gonna jump through some of these questions

47:31

because I think I, I sort of adjust some of that.

47:34

Um, generally speaking, cystic lung disease, you, you,

47:38

again, I would put it into perspective,

47:39

but if you have a transition of things

47:41

and you can see volume loss

47:42

or you do see um, various other factors of towards ILD,

47:47

I would, I would, you know, I would in, I would consider,

47:49

uh, you, uh, a ct DILD in this case

47:52

following after starting.

47:55

I think that is also dependent on our

47:56

multidisciplinary discussion.

47:57

Depending on how the patient's

47:58

resolving, we're generally seeking.

47:59

We do follow up in a few months

48:00

and then, you know, we act, we extend that,

48:02

but generally speaking, at least, at least six months or so.

48:04

But I think that is every institution differently

48:06

and how that patient's revolving organizing pneumonia.

48:09

What we did look for did not touch upon it as much.

48:11

You're correct. Wasn't the main I,

48:13

but essentially for organizing pneumonia,

48:15

I generally would think of, you know, the way I was sort

48:18

of in, in a backdrop look of thinking about consolidations.

48:21

Often it could be per bronchial consolidations with, uh,

48:24

broncho grams, but there would be more consolidative

48:26

opacities as opposed to, um, an ILD picture.

48:30

The, the sort of honeycombing, the traction bronchiectasis

48:33

that we've been discussing today.

48:36

Okay. Hopefully that's answered some of those questions.

48:38

I think you got 'em all. Thank you so much Dr.

48:40

Hali, world record.

48:42

Alright. I try to do my best.

48:43

Thank you so much for everybody. Um,

48:45

please reach out if you want to.

48:47

Awesome. Thank you so much to Dr.

48:48

Aless and specifically the France Foundation

48:51

for providing this new conference.

48:53

Be sure to join us next week, Thursday,

48:55

September 25th at 11:00 AM Eastern, where Dr.

48:58

Ssh McCury will deliver a lecture entitled Anatomy

49:01

and Pathology of the Central Skull Base.

49:03

You can register for that@modality.com

49:06

and follow us on social media

49:07

for updates on future noon conferences.

49:09

Thanks again for learning with us and have a great day.