Early Detection Strategies for Interstitial Lung Disease in Rheumatology: Janet Pope, MD, MPH

Janet Pope, MD, MPH, FRCPC, professor of medicine in the division of rheumatology at the University of Western Ontario and division head of rheumatology at St. Joseph's Health Centre in London, Ontario, shares how she approaches early detection of interstitial lung disease (ILD) in rheumatology practice. She explains tailored screening strategies for conditions such as systemic sclerosis, lupus, and rheumatoid arthritis, emphasizing the role of patient history, physical examination, pulmonary function testing, and collaboration with pulmonologists to guide timely intervention.

This transcript has been lightly edited; captions were auto-generated.

Transcript

What are the most effective strategies for early ILD detection in patients with connective tissue diseases like systemic sclerosis or rheumatoid arthritis?

When we're looking at strategies of early detection for patients that I would see—so as a rheumatologist—we're really thinking about systemic sclerosis, rheumatoid arthritis, and some of the other connective tissue diseases.

If we're thinking about interstitial lung disease, there's kind of 2 approaches. One is in systemic sclerosis, which we call scleroderma. We will screen these patients. We're screening them for interstitial lung disease to detect early; we're screening them as well for pulmonary arterial hypertension. We're usually doing an echocardiogram, which won't be helpful for interstitial lung disease, looking for their pulmonary pressure, but we're looking at the full PFTs [pulmonary function tests], the flows and volumes, and the diffusing capacity gas exchange—because as the DLCO or the diffusing capacity gas exchange goes down, they're more apt to have early interstitial lung disease, pulmonary arterial hypertension, or many other things such as having a recent cold or something, a URI [upper respiratory infection].

That's a strategy of screening with tests as well as doing a history and a physical. Early on in disease, asking if someone is short of breath, the question that they'll answer is, "Thinking right here today now while I'm sitting here?" And they'll go, "No." You really have to say, "Compared to a year ago or compared to last visit, when you're carrying in your groceries and unloading them, or when you're walking with your friend, is it different than it used to be? Have people commented that you're short of breath? Do you have a cough?" Things like that.

When we're looking at other diseases—lupus, rheumatoid arthritis, Sjogren's, etc.—we're really trying to detect early disease by not just screening regularly but instead history and physical and then test where appropriate. Again, listening to the bases of everyone's lungs who has rheumatoid arthritis, if you hear crackles, you should start investigating even when there's no dyspnea so that we can determine what's the cause of this. Is it heart failure? Is it early interstitial lung disease? Is it scarring from an old pneumonia, etc.?

I think we have 2 kinds of approaches, and the whole idea is we want to treat where appropriate, so we want to detect, make the proper diagnosis—usually with the help of the pulmonologist—and then where appropriate, I will determine [if] I think I can improve symptoms, level them, or slow worsening.

When someone doesn't have progressive pulmonary fibrosis but has interstitial lung disease that we feel is clinically relevant—they're dyspneic or they have a moderate restrictive pattern, even if it's an NSIP pattern, so no scarring or honeycombing, but inflammation, a nonspecific interstitial pneumonia pattern—we will get on with treatment, and our outcomes and goals will be dependent on what we think we can achieve.