Pulmonary Embolism Diagnosis and Imaging

[Dr. Sabeen Dhand]
How does your practice classify patients with PE?

[Dr. Eric Secemsky]
One thing that we still are getting our heads around is how to classify PE. I think we've kind of got a good criteria in terms of classifying massive, submassive, and non-submassive (some people call it low risk)... But we are trying to understand, particularly within that submassive pulmonary embolism group, what is high risk?

In the AHA criteria right now, it is poorly defined. It says that “submassive” means you have any evidence of RV dysfunction on CT scan or echo, or any signs of RV necrosis with biomarkers of BMP, or cardiac enzyme troponin is elevated.

On the other hand, the European guidelines go a little step further. They first say, “Let's look at your PESI score or your simplified PESI score.” So, let's put your clinical context at the front of that decision. From there, if you have both a high PESI score with RV dysfunction and biomarkers, you fall into the intermediate high risk group. Or, if you have [a high PESI score and] either [RV] dilation or biomarkers that are positive, then you are in the intermediate low risk group.

The PESI score is a little bit more refined in terms of how it classifies these patients. Empirically, when our PE phone calls, we are looking to see if they have any type of vital sign abnormalities. You know, it's a little bit more subjective. We’re asking: What's their heart rate? How much oxygen are they on? Can they complete full sentences? How stable is their blood pressure? Then, we're really looking for evidence of RV dysfunction. If it's overnight, we get a CT scan. If it's daytime, we'll get an echocardiogram. Then, we ask: Are both biomarkers [troponin and BNP] elevated? And we'll get lactate also. We could talk about some refinements, but those are the heart of the patients that we're managing in the hospital.

There's also the massive classification, which is the smaller nugget of the PE patients, but that's where the clinical side is.

[Dr. Sabeen Dhand]
That's good. I'm glad you kind of got into the questions that you ask because there can be a lot of information overload with the European guidelines and the PESI score, and the distinction between intermediate high risk and intermediate low risk. It’s important to look at the real clinical picture. Can the patient finish a sentence? How much are they struggling? That’s a huge source of information. The clinical picture is what really wins in this.

[Dr. Eric Secemsky]
Yeah. The best part of this was, when we first started, we got those PE calls and everything was about how much clot there was. Saddle pulmonary embolism, clot in all the lungs. Then you'd say, "Okay, well how is the patient?" And they're like, "Oh, they're on room air, heart rate is in the 70s, blood pressure's normal." We'd say, “Wow, it's pretty amazing that they're tolerating all this clot burden,” but, on the other hand, it's hard to push yourself to get excited about intervention with some risk, maybe not a ton of risk, but some risk in a patient like that.

Now, our phone calls are really brief about the clot burden, really brief about if it is more about binaries or RV dysfunction or not. Then, it's about the patient interview and how the patient is doing. You know that with a patient who can't finish a sentence or is on a non-rebreather, you're going to have to escalate therapy. On the other hand, there's the stable patient who didn't even know they had a PE, and it is easier to make that decision.

[Dr. Sabeen Dhand]
Clot burden is not the key, but it is all the physiologic effects of what that [clot burden] causes.
The cardiac enzymes used are basically BNP and troponins? Anything else?

[Dr. Eric Secemsky]
The main ones are BNP and troponin. We are starting to get into the weeds of the PERT Consortium Database, looking at how people manage PE across the nation, and it's infrequent that centers order both of those. BNP is a little bit more common than troponin. Troponin often falls a little bit more on the cardiac coronary side, and so it's not always ordered. But we look at both of those.

What I have observed is that when the BNP is elevated but the troponin is not, you have to start thinking more about a subacute PE. Now, again, this is empiric, I don't want anybody to think this is fact. Normally, when I see the troponin elevated, usually it's a more acute PE, a little bit more severe early onset RV dysfunction. When they're both elevated, you know they are a particularly higher risk acute PE patient.

Outside of that, we've been making a push to get lactates as well, and I think that's really helpful to start triaging and risk stratifying the right patient for a more aggressive upfront approach. When the lactate is elevated, we know then any hypoperfusion to these organs is a sign that we might need to really do something to relieve the pressure on the RV. We've been looking to get lactates in addition to the troponin and BNP. Those are the big three. The nice part is that the ER is so used to ordering those.