Interactive Transcript
0:01
All right, it's Mark again, and we're
0:03
going to move on from acute consolidation
0:06
to the chronic consolidated processes.
0:09
Again, consolidation representing
0:11
some clouds in the lung.
0:14
We'll talk about some of the common
0:15
pathologies and etiologies for chronic
0:17
consolidated processes, but overall,
0:20
these are a little less common.
0:22
All right, we're going to understand
0:24
a little bit about the importance of
0:26
when you see traction bronchiectasis
0:28
and irregular visceral pleura
0:30
in a chronic consolidation.
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That's a sign of chronicity.
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And I'm going to give a little bit of a shorter
0:36
differential when you see enlarged lymph nodes.
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So the pertinent findings you want to be
0:42
looking for are traction bronchiectasis, irregular
0:44
visceral pleura, signs of architectural
0:46
distortion, and enlarged lymph nodes.
0:50
So from the concept map in the card,
0:52
we're going to be focusing on this
0:53
area here, chronic consolidation.
0:56
These are going to be your players and start
0:59
you off, and then we'll come back to it later.
1:01
35 years old, chronic cough, no fever.
1:04
These are consolidations, right?
1:06
They're ill-defined.
1:07
There are some air bronchograms.
1:09
They're peripheral, but also notice
1:11
that the mediastinum is convex.
1:13
It's too dense, much more
1:14
dense than the aortic arch.
1:15
The aortic pulmonary recess and
1:17
both hilum are enlarged and dense,
1:19
consistent with enlarged lymph nodes.
1:21
Okay.
1:21
What do you think this is?
1:25
This is going to be one of these.
1:27
These are the more common diseases, and none of
1:30
them are really common, but more common diseases
1:32
that manifest as chronic consolidation.
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Again, you don't have to say airspace or
1:36
interstitial, just, it's consolidated.
1:39
Chronic usually refers to
1:41
greater than maybe two weeks.
1:43
Um, that one to two week period being
1:45
the subacute period where you kind of
1:48
have to think about both acute
1:50
and chronic consolidated opacities.
1:52
Thanks.
1:53
These are your players: the neoplastic
1:55
ones, the granulomatous ones,
1:57
TB, fungal, and alveolar sarcoid.
1:58
Whenever you say TB, you always say fungal
2:01
because they are both granulomatous infections
2:04
and they have a great deal of similarity.
2:07
Imaging-wise.
2:08
Inflammatory causes: COP
2:10
versus eosinophilic pneumonia.
2:11
COP is much more common than
2:13
eosinophilic pneumonia, by the way.
2:14
And, uh, older, I just put older, uh,
2:17
chronic aspiration lipoid pneumonia.
2:19
This will be dependent.
2:21
The big hint: if you have enlarged
2:22
lymph nodes, you think lymphoma
2:24
and the granulomatous diseases.
2:26
So, these patients all have something
2:29
different, uh, oh sorry, all have
2:31
similar consolidation, but they're from
2:34
different causes, different etiologies.
2:36
This patient has consolidation and
2:38
there's traction bronchiectasis.
2:40
And there's a little bit of
2:41
irregularity to the visceral pleura
2:43
and some architectural distortion.
2:45
The same here: a little bit of pulling apart
2:48
of the airways, a little irregular visceral
2:50
pleura here, and some architectural distortion.
2:53
These two are chronic consolidation.
2:56
When you see traction bronchiectasis and scarring,
2:59
that tells us that this most likely is
3:01
something that's more longstanding or chronic.
3:04
And so that's when you would
3:05
start shifting your differential.
3:08
This patient does not have traction
3:10
bronchiectasis, just a lot of consolidation.
3:13
So we would favor, hmm, that might be acute.
3:16
And in fact, that was acute.
3:17
This was a corona, this was COP, and
3:20
this was graft-versus-host disease
3:22
inducing organizing pneumonia.
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So the presence and absence of traction
3:28
bronchiectasis, architectural distortion, irregular
3:30
visceral pleura do support a chronic process.
3:33
Now what is cryptogenic organizing pneumonia?
3:35
That's probably one of the more common
3:36
causes of chronic consolidation.
3:38
It's a little confusing.
3:40
The body is reacting as if a pulmonary infection
3:42
is present, although there are different
3:44
etiologies, and you never know, there might
3:47
be an infection there, we just didn't find it.
3:51
It's reacting, and it's usually going to be
3:55
subacute to chronic, and there'll be some
3:57
evidence of traction bronchiectasis or scarring.
4:01
Now this, uh, organized pneumonia response,
4:05
even when the etiology is removed, is still
4:07
occurring, so it's kind of like a computer
4:11
that's just kind of flipping through
4:13
and not stopping, and now this is coming.
4:15
How do we stop this?
4:17
I don't know.
4:17
Let's reboot the dang thing, right?
4:19
And so that's kind of what corticosteroids
4:21
are doing: it's kind of shutting down
4:24
that immune reaction, and then it resets.
4:28
Now, if it comes back, you know, the so-called
4:31
resistant cryptogenic organizing pneumonia,
4:33
that probably tells us that whatever the
4:35
etiology is that's causing it is still present.
4:40
So, BMT patient, there are some areas of
4:42
consolidation, maybe a little traction
4:45
bronchiectasis, but there's definitely some
4:47
irregularity here and architectural distortion.
4:50
So this is a patient who's got
4:52
some chronic consolidation.
4:54
Uh, I would say, yeah, this is
4:56
an organizing pneumonia reaction.
4:58
Maybe there's an infection there,
5:00
but you'd start thinking graft
5:01
versus host or some other etiology.
5:05
This is a patient with alveolar proteinosis.
5:07
Now, this is different.
5:09
Alveolar proteinosis gives a
5:11
consolidation and ground-glass
5:13
process, the so-called crazy paving.
5:16
Crazy paving just means that there
5:17
are lines here and surrounding
5:20
ground-glass and consolidation.
5:22
Okay.
5:23
Now this usually, or we feel, is related
5:27
to poor alveolar macrophage clearing
5:29
(macrophages), pulmonary macrophages
5:31
clear the surfactant and debris.
5:33
And in these patients, the pulmonary alveolar
5:36
macrophages are, uh, they're on strike, right?
5:38
So this stuff kind of
5:40
slowly accumulates in the lung.
5:42
One of the hallmarks
5:43
though, is that this has no
5:46
imaging evidence for scarring,
5:48
no traction bronchiectasis.
5:51
The others that do this would be things like
5:53
lipoid pneumonia or mucinous adenocarcinoma.
5:56
These are forms of chronic
5:57
consolidation that do not give fibrosis.
6:01
16-year-old with Rett syndrome
6:04
aspirates, has a consolidation in the
6:08
right middle lobe and left lower lobe.
6:11
And it's unchanged from two years ago.
6:14
And when you look at the CT, you'll
6:16
see, yeah, that's consolidated,
6:18
but it's really low density.
6:19
It's actually close to the subcutaneous fat.
6:22
This is lipoid pneumonia.
6:24
The patient was given mineral oil and she
6:27
aspirated it two years ago, and it's just kind
6:29
of hanging in there, not a lot of fibrosis here.
6:34
Another patient, more of a ground
6:35
glass to consolidative appearance.
6:38
There is no real evidence, maybe a
6:40
little bit there, but no evidence
6:41
for real traction bronchiectasis.
6:44
Um, you know, what do you think?
6:45
Well, when you see such widespread
6:48
disease like this, it's usually best to
6:51
look in the areas of less involvement.
6:54
And you'll see that the underlying process
6:56
here is one of ground-glass nodules that are
7:00
sharply defined that then probably coalesced.
7:05
In this patient, no fibrosis.
7:09
Panic progressive kind of consolidation,
7:11
some ground-glass, um, ground-glass
7:14
nodules that are well defined.
7:16
Well, yeah, this turned out to be mucinous
7:19
secreting adenocarcinoma, and the adenocarcinoma
7:22
is growing, secretes the mucus, which then
7:24
accumulates in the, uh, lung parenchyma, giving
7:27
you that kind of ground-glass consolidated
7:29
process without imaging evidence of fibrosis.
7:33
Well, let's compare it to this person.
7:36
She has chronic productive cough.
7:38
She has consolidation and clearly
7:40
has some traction bronchiectasis.
7:43
And you'll notice the
7:44
distribution is bronchovascular.
7:47
Well, geez, to me, this is, uh,
7:49
organized pneumonia, COP, organized
7:51
pneumonia, COP, organized pneumonia, COP.
7:53
I mean, that's what it is.
7:56
It progressed.
7:57
It's progressed quite a bit, in fact.
7:59
And in bronchoscopy, they
8:01
got a lot of lymphocytes.
8:03
So, it turns out that this is actually
8:05
a form of primary pulmonary lymphoma.
8:08
This is very uncommon.
8:11
You might see it sometime in your career.
8:14
The clues here were that it's bronchovascular,
8:16
it's consolidated, and it turns out lymphoma is
8:21
a, gives a form of sort of scarring as opposed
8:25
to the mucinous secreting adenocarcinoma.
8:28
So, unlike the other tumors.
8:30
This one does induce evidence of scarring.
8:33
The other thing that's notable about
8:35
primary pulmonary lymphoma is only about
8:36
half of them have enlarged lymph nodes.
8:41
So, let's go back to this person.
8:43
Consolidation enlarged lymph nodes,
8:46
chronic, no fever, this, and you
8:50
can see the air bronchograms.
8:51
This is an example of, um, alveolar sarcoid.
8:56
Do you want to call this airspace?
8:57
No.
8:58
Do you want to call it interstitial?
8:59
No, don't bother.
9:00
It's, it's chronic consolidation in
9:02
the setting of enlarged lymph nodes.
9:04
I would think about histoplasmosis
9:07
or some fungal infections.
9:09
I would consider things like,
9:10
um, non-Hodgkin's lymphoma.
9:12
Not the primary pulmonary,
9:13
but more of the systemic.
9:15
But in this case, this was, this is pretty
9:18
characteristic for alveolar sarcoid,
9:20
especially in the setting of no fevers.
9:24
This patient has enlarged lymph
9:26
nodes and a chronic consolidation.
9:29
They're from Vietnam.
9:30
And this turned out to be primary tuberculosis.
9:35
Primary tuberculosis gives you
9:36
that chronic consolidation with
9:38
associated enlarged lymph nodes on CT.
9:41
The clue about this, that it's not sarcoid, is
9:44
that those lymph nodes will be necrotic, right?
9:49
Sarcoid lymph nodes are not necrotic.
9:53
And then we'll finish with this
9:55
one, uh, multifocal areas of
9:57
consolidation, kind of unusual.
9:59
This is sort of the reverse
10:00
halo sign or the atoll sign.
10:03
Um, I don't use signs like that very much.
10:05
I just say, hey, that's consolidated.
10:07
I know that they have two months of dyspnea.
10:09
This is a chronic process.
10:11
There were no enlarged lymph nodes.
10:13
I really don't see too much
10:14
here to suggest scarring.
10:16
Um, you know, an infection-induced
10:19
organizing pneumonia and indolent infection.
10:23
Maybe, uh, you know, in the end,
10:27
um, you know, drug toxicity?
10:29
No, not really.
10:30
In the end, what do you do?
10:31
Well, you go to biopsy, and when they
10:34
removed it, they found cryptogenic
10:36
organized pneumonia and cellular SIP.
10:38
Um, these are unusual diseases, but they do
10:42
tend to manifest with that consolidated process.
10:45
Um, and that's what it is.
10:46
Sometimes, though, you have to go to biopsy.
10:49
So, chronic consolidations
10:52
are not common, but when they are,
10:54
they have a few common pathologies.
10:57
Cryptogenic organized pneumonia,
10:58
perhaps being the most common.
11:00
Look for evidence of tracheobronchial
11:02
cysts or scarring, uh, that is associated
11:05
with chronic inflammation, the presence
11:07
of pathologically enlarged lymph nodes,
11:09
a very useful clue for lymphoma, not the
11:12
primary, but the lymphoma and granulomatous.
11:16
And with that, I thank you very much.
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