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Hi everyone, it's Mark.

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We're continuing on with our Mastery Series

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and one of my favorite topics, ground glass.

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We're going to look at the chronic

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ground glass causes, and that one is very

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intimidating, again, to most radiologists.

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Let's see if we can at least

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try and simplify it for you.

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We'll review some of the common differentials

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for these diseases, but a lot of it is

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going to depend on the degree of fibrosis.

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So this session, we're going to talk

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about chronic ground glass, where

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there's not much fibrosis or no

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imaging evidence of fibrosis at all.

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And we'll look at how the distribution

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and just a little bit of clinical

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history can be very useful.

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Okay.

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So this is your differential

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for chronic ground glass.

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It's based on how

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much fibrosis is present.

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So when there's no or minimal

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fibrosis, these are your diseases.

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It looks like a lot, but

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we'll sort through them.

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Don't worry.

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And then we'll talk in the next session

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about when there's a lot of fibrosis.

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Okay, so we'll kind of

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talk about these entities.

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Start off here, gradual decrease in lung

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expansion over one year, progressive dyspnea.

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You can see this patient, remember,

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the degree of inspiration is not based

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on the diaphragm level; it is based on the

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intercostal width. The intercostal width

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is the same; that's the same amount of

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inhalation, but the lungs didn't expand.

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That kind of suggests that this ground glass

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process we're seeing here is, in fact, real.

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And the DLCO was decreased.

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When you look at the CT, there are patchy

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areas of ground glass that are peripheral.

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There is some evidence of emphysema.

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There is no real imaging evidence of fibrosis,

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maybe a little bit, but

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no real imaging evidence of fibrosis.

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And

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you would favor in this

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patient who is a heavy smoker.

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Oh, well, this is going to be

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desquamative interstitial pneumonitis,

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which, when you look at the pathology, is

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actually more of an airspace process.

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That's why I reiterate to you to try to

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avoid using airspace or interstitial.

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Both are almost always present.

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It's kind of an artificial distinction.

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51 years old.

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Again, you see these patchy ground glass.

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You say, "Oh no, I'll give

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this to another radiologist."

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No, you won't.

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You know, just stop for a moment.

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Chronic symptoms over a year.

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Okay.

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Imaging evidence of fibrosis.

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No, I'm not really seeing it.

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Peripheral distribution.

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Hey, you know what?

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You can give a differential,

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maybe three things max.

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It's all you're going to need.

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If the patient's a smoker, and they

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are because there's emphysema, this

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is most characteristic for desquamative

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interstitial pneumonitis, which it was.

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These patients have a different

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appearance to their chronic ground glass.

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These are smudgy.

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Central lobular ground glass

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nodules, and they're very uniform.

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Well, especially this one,

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this one, a little less.

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So they both have a similar

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ground glass smudgy appearance.

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They spare the subpleural.

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There's no imaging evidence of fibrosis.

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When you see central lobular, you're

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thinking, hey, this is a respiratory

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bronchial inhalational problem.

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And you just have to say this.

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If the patient's a nonsmoker, this is most

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consistent with hypersensitivity pneumonitis

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slash extrinsic allergic alveolitis.

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If this patient’s a smoker, and this one

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is, this would be most consistent with

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respiratory bronchiolitis interstitial

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lung disease, or called RBILD.

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So it turns out that smokers don't tend to

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get extrinsic allergic alveolitis, most likely

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because of the immunosuppression that occurs.

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Sometimes they do, but most

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of the time they don't.

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So you have sort of a natural little division

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between two diseases that look very similar.

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Now, the other thing about hypersensitivity

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pneumonitis, and I have to say this

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because I've seen this mixed up a lot.

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It really comes in two major

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forms, two major etiologies.

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There's the extrinsic that is, you breathe

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it in, you breathe that antigen in, and

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then it settles in the respiratory bronchioles

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inducing an inflammatory response, giving

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you those smudgy ground glass nodules.

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It's predominantly seen in

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nonsmokers, as I just said.

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Now the other form of hypersensitivity

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pneumonitis looks different.

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It doesn't settle in the lungs.

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So it's intrinsic things like drug

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toxicity and that manifests as either

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patchy or more of a diffuse ground

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glass process that it's because it's not

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really hitting the respiratory bronchioles.

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So because of that, I separate hypersensitivity

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pneumonitis into an extrinsic etiology that you inhale

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and an intrinsic etiology that's in the blood.

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This patient's got diffuse ground glass.

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Look at the dark bronchus sign.

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No, there's not a lot of

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imaging evidence of fibrosis.

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Would you call this extrinsic allergic alveolitis?

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Not much for smudgy

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nodularity, just a couple of little nodules,

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but it's pretty much a uniform process.

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So this person actually had hypersensitivity

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pneumonitis secondary to her medication.

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It was actually Prozac.

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So there you go.

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Now let's shift gears.

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47 year old with progressive dyspnea, chronic coughs

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who are into the chronic, no evidence really

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here for fibrosis, maybe a little bronchiectasis

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there, but pretty much not much for fibrosis.

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It's a ground glass process

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that's asymmetric and extensive.

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You say, "Gosh, let's give

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this to another radiologist."

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No, you won't.

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Because you're going to look at

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it and say, "Hey, you know what?

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I'm going to look in the areas

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of less involvement here."

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Less involvement.

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What am I seeing?

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Well, when you look in those areas, it's

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more of a ground glass nodule, isn't it?

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Well defined.

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And that's a pretty good hint.

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If you saw just this on

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a CT, what would you say?

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Oh, I'd say, "Hey, you know, that kind of

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looks like atypical adenomas,

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hyperplasia, well-differentiated adenocarcinoma."

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Oh, that's right, because adenocarcinoma has a

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mucinous form that coalesces and secretes mucin,

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which gives you that ground glass process too.

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And these people often have

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bronchorrhea or coughing up mucus.

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So in this case, I'd come down pretty hard to

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say this is widespread mucinous adenocarcinoma.

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Manifesting as a chronic ground glass

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process, and adenocarcinoma does not induce

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fibrosis, which is why it's not there.

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33-year-old female with widespread ground glass,

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but she has another interesting clue.

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She's got multiple cysts, and these cysts are

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a huge clue to a couple of diseases that, um,

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are present in this case. After treatment, the

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ground glass improved, but the cysts remain.

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And the cysts tend to be permanent.

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This is lymphocytic interstitial

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pneumonitis, commonly seen in the setting of

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autoimmune diseases, especially Sjogren's.

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This patient has ground glass too, very

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subtle, but the dark bronchocyte is present.

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There are

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a lot of perihilar cysts.

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There's also, um, yeah, a lot of

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times these get called emphysema.

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They're not emphysema; they're perihilar cysts.

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And when you have ground glass and cysts,

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it really makes you think of either

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lymphocytic interstitial pneumonitis or DIP.

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This patient was a heavy smoker,

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didn't have an autoimmune disease, so

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it’s DIP, confirmed by biopsy.

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Okay, progressive dyspnea.

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This patient, I think I showed, um, during

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the fibrotic one, has a lot of ground glass.

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There is a little bit of fibrosis here, but

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not a lot of fibrosis in the ground glass.

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So if you don't see a lot of fibrosis

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in the ground glass, that tells you that

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it might be more likely inflammatory.

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This patient did have an open lung biopsy

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and it was diagnosed as cellular NSIP, although

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there are areas of fibrotic NSIP as well.

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That's a spectrum, right?

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The longer the disease is present,

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the more fibrosis there'll be.

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In this patient, it was thought

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to be due to drug toxicity.

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Now, NSIP is a tough one for people to gather.

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It is a spectrum.

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Cellular is more inflammatory.

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Fibrotic has more evidence of fibrosis.

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Please understand, it is not

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a disease or an etiology.

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Just to say they have NSIP as a

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pathology is not a diagnosis.

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You don't stop there.

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You look at the distribution and clues to

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tell you what drove it to the level because

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all of these inflammatory causes, things like

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cryptogenic organized pneumonia, if you don't

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treat it, eventually the scarring gets worse.

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The fibrosis gets worse.

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And then when you do a

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biopsy, you see fibrotic NSIP.

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So remember, it's a pathology, but all

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these different diffuse lung diseases can

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kind of funnel into it if left unchecked.

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Patient, this is the patient who had

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the ground glass, got treated. There's

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the fibrotic stuff that's remaining.

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So again, it's a spectrum,

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but it's mostly cellular.

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How about this patient?

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Avid athlete, worsening dyspnea over one year.

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I'm going to have to confess,

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you're going to see these.

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These are, this is a chronic ground glass

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process, but it doesn't seem to fit any of this.

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There is a little bit of fibrosis,

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but not a lot.

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And it's ground glass, but it doesn't

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seem to have a definite distribution.

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It's not central lobular.

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It's not peripheral.

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It's not bronchovascular.

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I don't see any cysts.

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Um, in this setting, it's progressed.

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You go to an open lung biopsy, open lung biopsy.

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I mean, you just, at some

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points you got to do it.

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And then even then the pathology read was

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unspecified fibrosis, unknown etiology.

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Remember the book about what we don't

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know is bigger than the book we do know.

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You will encounter these occasional cases.

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Even the pathologist may not know.

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Okay.

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Well, that's, that's chronic ground glass.

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This is sort of the more common diseases

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and etiologies that give you ground glass.

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without a lot of fibrosis.

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Clinical history of smoking, autoimmune,

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and medications can be really helpful.

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Remember, hypersensitivity pneumonitis

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comes in two major categories, the type

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you breathe in, extrinsic, and the other

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that's in the blood, the intrinsic.

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And recall that NSIP is not a disease.

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It is a pathology and you don't stop there.

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You look for clues on what could have caused it.

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With that, I will say thank you for

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listening and hope that was helpful.259 00:09:42,280 --> 00:09:43,530 I mean, you just, at some

9:43

points you got to do it.

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And then even then the pathology read was

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unspecified fibrosis, unknown etiology.

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Remember the book about what we don't

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know is bigger than the book we do know.

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You will encounter these occasional cases.

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Even the pathologist may not know.

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Okay.

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Well, that's, that's chronic ground glass.

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This is sort of the more common diseases

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and etiologies that give you ground glass.

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without a lot of fibrosis.

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Clinical history of smoking, autoimmune,

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and medications can be really helpful.

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Remember, hypersensitivity pneumonitis

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comes in two major categories, the type

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you breathe in, extrinsic, and the other

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that's in the blood, the intrinsic.

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And recall that NSIP is not a disease.

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It is a pathology and you don't stop there.

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You look for clues on what could have caused it.

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With that, I will say thank you for

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listening and hope that was helpful.