Speaker 1Hey, before we get to the show, I wanted to remind you to check out our Patreon at patreon.com slash curbsiders. If you haven't signed up yet, sign up now to get ad-free episodes, twice-monthly bonus episodes, and a whole bunch of other cool stuff at patreon.com slash curbsiders. Okay, Paul, I'm fairly certain that this pun might have been featured on the show before, but I dare the listeners to figure out which episode it was from. Actually, with AI, it's probably not that hard nowadays.
Speaker 2Dare me to remember it.
Speaker 1I dare you to remember it. Paul, a friend of mine tried to annoy me with bird puns. Oh, no. You know what I realized?
Speaker 2We 100% did this one before, and no, what did you realize? This is killing me.
Speaker 1I realized that Toucan played that game.
Speaker 3Yeah, yeah. The Curbsiders Podcast is for entertainment, education, and entertainment. Information purposes only, and the topics discussed should not be used solely to diagnose, treat, cure, or prevent any diseases or conditions. Furthermore, the views and statements expressed on this podcast are solely those of the host and should not be interpreted to reflect the official policy or position of any entity, aside from, possibly, cash-like moral hospital and affiliate outreach programs. If, indeed, there are any, in fact, there are none, pretty much, we are responsible if you screw up. You should always do your own homework and let us know when we're ready.
Speaker 1Welcome back to the Curbsiders. I'm Dr. Matthew Frank Watto, here with a disappointed Paul Williams that he did not figure out that pun, but he is. He is America's primary care physician, probably the primary care physician.
Speaker 2Hey, Paul. If you'd have given me enough time, I could have done a macaw or something. Like, I feel like I probably could have done a little better than that, but hi, Matt. How are you?
Speaker 1I'm doing well, Paul. Friends of the show, homegrown Dr. Cyrus Askin and a friend of the show, Dr. Nick Mark from the Critical Care Time podcast, are here talking about pulmonary embolism, favorite topic of us and our audience. We've done so many podcasts. We've done so many pulmonary embolism, VTE, DVT episodes, and this is our latest. So, Paul, before we get to introducing our guests, what is it that we do on the Curbsiders?
Speaker 2So, sure, Matt, for our listeners, as a reminder, we are the Internal Medicine Podcast. We use expert interviews to bring you clinical pearls and practice changing knowledge. As you mentioned, Matt, we had a conversation with longtime friends of the show, Dr. Cyrus Askin and Nick Mark. We talked about largely the 2026 updated guidelines on the management of pulmonary embolism. We talked a little bit about pulmonary embolism. We talked a little bit about the new classification system, which is initially bewildering until you look a little bit harder at it, and then it stays bewildering. We talked about who gets what treatment, how to risk stratify patients and decide who gets treated in the hospital, who doesn't get treated at all, who might need a higher level of treatment, like fancy catheter-directed thrombolysis. And we talked about what to do with these patients after they're over that hump and sort of what they should look, how long we should treat in the outpatient setting and with what agents and what doses. So it was a really helpful conversation and a nice update to something that, you know, we obviously encounter a lot in internal medicine.
Speaker 1And I should mention that super producer, Dr. Edison Zhang, put this together. Fantastic job. Things flowed really well. So hope you enjoy this conversation. And a reminder that this and most episodes will be available for CME credit for all health professionals through VCU Health. You can click on the link in the show notes or you can go to patreon.com forward slash curbsiders to sign up for our CME tier to make it really easy to claim CME. Nick. Cyrus, it has been great to have you back on the show, both of you and multiple times for both of you now, I think. And Nick, we'll start with you. What is a hobby or interest that you're currently enjoying outside of medicine?
Speaker 4I am enjoying my periodic rewatch of my favorite TV show. Which is? The Wire, of course. And actually, here's the one quick fun fact I'll give you, which is that I realized that my favorite TV show and my favorite novel are, in fact, telling the same story. That season two of The Wire is The Great Gatsby. And it's just a fantastic adaptation once you realize that. Anyway, to anyone out there who's a fan, I strongly suggest watching season two. It's criminally underrated.
Speaker 1I'm trying to think how the boat cop thing connects with Great Gatsby.
Speaker 4If you want to take a minute, we could do it. I could lay it out for you. So there's the main character. There's the main character, right? Who yearns for this old past, who goes out on the pier, who looks off into the distance, right? At the Francis Scott Key Bridge. In Baltimore or at Daisy's dock in Gatsby, right? He has a helper named Nick, actually, who helps sort of do, you know, do this. He uses bootlegging money or illegal smuggling money, whatever, to try to realize this dream. But ultimately, you can't sail against the current. You can't change the past, right? Gatsby can't win Daisy's love and Sabatka can't bring back the jobs to Baltimore.
Speaker 1Interesting. Paul, are you buying this? I've never seen The Wire. Oh, all right, well, homework assignment. Well, Paul, if you have 60 hours, you can watch all six seasons.
Speaker 2Yeah, I mean, sorry, everyone. Sorry, world. Yeah, see also The Sopranos, see also Mad Men. It just, it gets too daunting. And at this point, I'm like, there's only so much time in my life. So that just will be a masterpiece I might have to forego.
Speaker 1Okay. Cyrus, what are you up to these days?
Speaker 5What's your hobby? I don't know. Nick can probably answer that better than I can. I'm working a lot. That's a big part of life, unfortunately. Sort of exploring and understanding on a daily basis what it means to be a private practice, full-spectrum pulmonary and critical care physician has been certainly a steep learning curve. But it's been fun, and I feel like I'm getting in the hang of it. But I mean, between that, between our own podcast, between other interests adjacent to medicine, and of course, being a husband and a father, it only leaves a little bit of time for me to play video games, which is what I really wish I had more time to do. And hence, it's taken me, like, I don't know, months upon months to make it halfway through Ghost of Yoti. And the list of games that I want to play continues to stack up. Also, Legos. Love Legos. Haven't been able to do as much of that. So I'm trying to right-size my life. That's, I suppose, another hobby of sorts, is trying to figure out where to do what. But yeah, it's good stuff.
Speaker 1It takes some time. The podcast is, like, you know, basically, like, adds another child to the family. So it's a lot to take. It's a lot to take care of.
Speaker 2Yeah. Not to ruin it for you, but the Ghost of Yoti, she just wails on people with a sword a lot. So if that saves you any time.
Speaker 5Yeah, I appreciate that. It's, yeah. I'm kind of committed to finishing it. But then, like, I'd like to revisit, like, the remake of Assassin's Creed Black Flag. I think my son would really enjoy that. But he's still a little young, so I have to figure that out. Anyway, these are not real problems, per se. But yeah, that's me in a nutshell. A lot going on, Cyrus.
Speaker 1But speaking of a lot going on, Paul, let's get to our first case from Cashlack.
Speaker 2Let us discuss Finn. So Finn is a 63-year-old gentleman with a past history noteworthy for type 2 diabetes who's presenting to the ER with dyspnea and pleuritic chest pain. He has recently returned from a long international flight. He is afebrile, has a heart rate of 110, blood pressure of 120 or 75, respiratory rate of 30, that seems high, and an oxygen saturation of 93% on room air. A physical exam is remarkable for right calf swelling and tenderness. So I feel like. So I feel like we're teeing you gentlemen up a little bit, but why don't we start broad and tell us sort of what your diagnostic workup is for a patient for whom you suspect PE, which is, I think, where we're potentially leading with this case.
Speaker 4So, I mean, you know, a lot of what we're going to talk about today is how do you stratify risk in people, right? How do you take somebody and sort of decide what is the most prudent next step? You could either risk stratify once you have a diagnosis of PE to try to figure out what to do, or in this case, we're going to risk stratify what we think the likelihood of PE is. So we can decide what is the most prudent next step. We can decide what tests to do in what order. You know, the rationale for this is that we don't want to just scan everyone who comes into the ED, right? We don't want to expose everybody to the contrast, the radiation, and the cost. So there are many medical decision rules that we can invoke to sort of decide who deserves what testing. In this case, you know, in Finn's case, I should say, we've got a very suggestive story, right? We could talk more about the air travel side, because I love that. But he's. He's got tachycardic, tachypneic, he's got unilateral leg swelling. There isn't really an alternative diagnosis here. So, I mean, we don't even really need a decision rule to know that the likelihood of PE is high. And the way I frame cases like this is like, do you really want to be in front of a jury saying, I didn't think this was a PE, Your Honor? Like, I think we're probably committed to doing some invasive testing here because it's a textbook presentation.
Speaker 1Yeah. And the test that they're putting in the new guidelines, which is part of the impetus to do this episode, they put the WELLS score, the revised Geneva score, or the simplified Geneva score, and now there's this YEARS score as well. So, those are ones that people can look at. And they all ask similar questions and then have a scale to give you the probability. Nick, any comments on those?
Speaker 4I mean, I think, you know, you should use a score that you're familiar with. I think there's WELLS and PERC are pretty well established. Um, they're, uh, the YEARS algorithm is not something that I have used personally, though I think in the ED, it's used a little bit more. You know, I think another thing we should probably talk about is using an age-adjusted D-dimer threshold. So, one of the problems with D-dimer is that it can be a little bit higher in older people. So, normalizing it can avoid some false positives. But I think to sort of step back for a second, the way I think about this is like, if you're low suspicion or very low suspicion, you can use one of these rules to justify the fact that you're why you're not gonna do anything else, or you're just gonna do D-dimer and then you're done. I think for anybody who's low or intermediate risk, you kind of need to start with the years or age-adjusted D-dimer to rule in or rule out. And for somebody who's high risk, you kind of need to just do the test, right? You just go right to the CTPA. I think, you know, you could do other stuff first, but all you're doing is delaying diagnosis in many cases.
Speaker 2Yeah. Can I ask how important is context when using these risk prediction schools? So for instance, you know, being in a primary care office, if I'm working up someone for PE like that, that feels different than someone who arrives in the ER for some, in large part, because some of the tests were not necessarily validated in that particular setting. Like, should I care that much? Is there one that's sort of better for me versus for the ER? How do you think about sort of where the patient's coming from or do you in terms of how you risk stratify
Speaker 4them? I think that's a great point. I mean, context is king, right? So, I mean, two points of context. Most of these tests are developed for the emergency department. So invoking them in a primary care office is a good thing. But I think it's a good thing. I think it's a good thing. I think a care clinic is maybe not right. And, you know, it's hard to know, like, how is the incidence different there? But another point that I would make is that you gave me a detail of this case that makes me very worried, which is you mentioned air travel, right? And we know that air travel is a big risk factor for PE. You said a long flight, which is good because there's no definition of what long is. Different guidelines say different things for long. I think the British Society of Hematology says three hours is long. The American Society of Hematology says four hours is long. The British Thoracic Society says six hours is long. And then in the United States, we say five hours is long. So very confusing, but we'll just say it's long. But the interesting thing about that is that the incidence of VTE after a long flight is quite high. It's something like 0.5 percent. Another way to frame that is that if you are riding on a triple seven, there's a one in three chance somebody else on the plane got a VTE with you, right? So when somebody comes from the airport with unilateral leg swelling, that's a pretty worrisome story. There's kind of a couple other nerdy details that I love because I'm into aerospace medicine, which is that, like, why? Why is air travel so uniquely dangerous? There's a couple theories. One theory is that, like, you get dehydrated with air travel, so your blood is more viscous. But probably the leading theory is that air travel is so uniquely dangerous that the seats are really bad for you. It's got to be the chairs.
Speaker 2It can't be anything else.
Speaker 4They compress the back of your legs. And the supporting evidence for that is that people who are under five foot three or over six foot three have a substantially higher risk of VTE when flying. The other supporting piece of evidence is that people in window seats have something like double the risk of people in aisle seats. And the idea there is you're not getting up. So, you know, if you if you are somebody who is quite tall or quite short, consider consider spending money on that extra leg room, drinking lots of water, but most importantly, get the aisle seat, because that's probably the most proven thing that reduces the risk.
Speaker 1Paul, is it OK to share this with people? Paul's Paul's plane thing is he tries not to go not to use the bathroom at all on a plane. He gets a window seat. I get the aisle seat and I just just pound drinks the whole time. Not alcoholic drinks, just like water. Sure. And that way I could get up and walk anyway, because I just don't want to be like having to. Worry about that. I'm just like aisle seat. I can get to the bathroom when I need it. It's fine. I can drink if I feel like it. So that's my I just I love
Speaker 2the sick thrill of Verschow's triad just threatening me. Well, not that
Speaker 5this is an issue for Paul, but I think in, you know, Nick also failed. Didn't mention this, but but identified this as well. So for your folks, many of whom, let's say, in San Antonio have a BMI of greater than 30. If they're also in a window seat, that's not a twofold risk. But a sixfold risk increase. So pretty germane to many of our patients, I think.
Speaker 1Cyrus, did you have any specific things you wanted to mention about like the any of the scores or anything before we move on to the next part of the case?
Speaker 5Oh, I have a lot to say about the new guidelines in general, the utilization of the tools and the recommendations and how they sort of compare and contrast to the ERS ESC guidelines from a few years ago. I'll sort of pepper that in. Throughout the discussion, I think. Otherwise, this could be a sound like a long winded diatribe. And I want to try to stay away from that. As far as the tools, I think many of the tools that are mentioned are pretty consistently used. They mentioned the Geneva score, which is helpful. I also like the BOVA and the HESTIA criteria. I'll use those for PE. Those can be used to sort of determine also like severity approach to treatment. But sort of on the front end, when you're trying to make your diagnosis, you're going to want to make sure that you're doing it the right way. You're going to want to make sure that you're doing it the right way. So you're going to want to make sure that you're doing it the right way. The years algorithm is sort of in addition to the PERC. So the PERC rule is essentially, does this patient need further testing? Yes or no? It allows you to rule in or rule out with pretty high degree of certainty. I should say it allows you to rule out. Because if you pop positive on any of the elements of the PERC, which include age greater than 50, heart rate greater than 100, oxygen saturation less than 95 on Ramir, you're going to want to make sure that you're doing it like swelling, hemoptysis, recent surgery trauma. So any of those pop positive, you cannot PERC out. And so you have to move on to the next step. Similarly, the years algorithm helps you rule out PE, but it takes into account the increased risk associated with pregnancy. So I do find that to be helpful to some degree, but there also comes a point where you have so many dang tools that it starts to get confusing as to what to use. And this is a recurring theme, I feel like, with the new guidelines is there's so much there, the evidentiary basis is still immature. And it's another situation, and the AHA seems to like to do this, there's another situation where the guideline is sort of outstripping the evidentiary basis. And so, like I said, I'll pause there as far as that goes, because I know we're going to unpack that a bit further. But so the years algorithm that looks at, is the patient pregnant? And so obviously, we're focusing on folks that can get pregnant. And then we're looking for signs of DVT. You're using, you're doing also compression ultrasonography of the symptomatic leg, if they have a symptomatic leg, to sort of evaluate for potential DVT there. You're looking at the D-dimer. So it's, MD-Calc has a great little flow chart, I guess you could say, that you can go through. I'm not sure how much it really adds to the PERC, but I suppose in your pregnant patients, it's a good tool to have. And then you have a lot of other things that you can do. So you're looking at the D-dimer, and you're the Wells criteria as well. That's going to calculate your pretest probability. That looks at several of the same parameters we've discussed. I'm not going to go over all of them. But as you can probably already tell, it can get a little bit confusing as to what to use and when to use it. And so for me, I'm a simple man. I pretty much use the PERC. If they don't PERC out, then I really just try to do the simple calculus of pretest probability. And I have a low threshold to scan most patients if I really think that PE could be on the differential. I approach PE as being, they have PE until ruled out otherwise. And then you can use things also, once you've made the diagnosis, you can look at their PESI or their S-PESI to determine prognosis, so on and so forth. So sorry, I tried to not be long-winded, but there are a lot of tools, and we're trying to sort of figure them all out.
Speaker 1And I can point the audience to, I mean, the guidelines have figure one. It just has a suggested pathway. And as you can see, it's a lot of tools. And I can point the audience to, essentially, like Cyrus said, low probability people, if you do the PERC rule and they can PERC out, then you don't have to do any further testing. But if it's somebody that's like an intermediate risk, you can do the D-dimer, and you could look at like the age-adjusted D-dimer. High probability people were scanning. And then the years criteria, there must be an algorithm, and then there's just like these three criteria. One is clinical signs of DVT. Hemoptysis or PE is the most likely diagnosis. Those are the three criteria. And then they pair that in at least the ones that they're mentioning in the algorithm with like either the D-dimer is less than 1,000 or less than 500, depending on how many years criteria they have. So that one seems like it's a little further down the algorithm. Like the first, you're starting with your like Wells or Geneva to kind of give a sense of like which you go low, intermediate, or high risk. And then you go through the, do you do a D-dimer or do you just go right to testing? But I think what I'm trying to do is, I'm trying to figure out, I think we're all saying kind of the same thing. I thought the aerospace medicine aspect, Nick, that's not something that I've heard of. I haven't heard about that. But I think we've talked about this on our edema episode, Paul, with the Cardi B tweet, right? Where she was all swollen in the legs from the seat kind of cutting off blood flow.
Speaker 2Probably the extrinsic compression. Yeah, exactly right. Still use some presentations to this date.
Speaker 1Okay. So that's where we're at here. So get an aisle seat, make sure you're hydrated on a plane. This episode is brought to you by Figs. Fall is finally here. And if you work in healthcare, you know what that means. It's pumpkin spice everything, baby. Brisk air and of course, busy waiting rooms. It also happens to be the perfect time for a uniform refresh with new styles and colors from Figs. Lightweight, durable, and ridiculously soft, Figs scrubs are hands down what you want to be wearing this fall. I've said this many times. I have five pairs of Figs scrubs when I wear scrubs. I have five pairs of I'm just wearing figs, that's because they're comfortable I like the way they look, and you will too. From underscrubs and scrub wear to outerwear and accessories, you'll be layered up, looking good, and ready to take on anything this season and beyond. Why wear scrubs when you can wear FIGS? If you're in healthcare, we love this time of year for new styles and colors. Get 15% off your first order at wearfigs.com with the code FIGSRX. That's wearfigs.com and use the code FIGSRX. Hey, curbsiders. October is here, which means there are only a few months left to take care of your CME for the year. If you still need credits or have CME funds available that you don't want to leave unused, our friends at Continuing Education Company make it easy to find an option that works for you. You can attend one of their live conferences and combine great education with a great destination. If you need live CME but can't travel, many CEC conferences are also available by live webcast, so you can participate in real time from your home, office, or wherever you choose. And if you need maximum flexibility, CEC offers an extensive library of online CME courses that you can do on your own schedule. CEC also delivers exceptional value for your CME dollars. Attend a live conference and you'll receive a complimentary 15-credit online CME course at no additional cost. But while you're wrapping up this year's CME, it's also a great time to start thinking about 2027. Their 2027 conference schedule is open for registration, and you can reserve your spot now and pay later if you need to wait for your new CME budget. So don't let the end of the year sneak up on you. Take care of CME you need now and start planning where CEC might take you next year. And as a thank you for listening, CEC has a special offer just for curbsiders. Listen up. Use promo code CURB30 for 30% off all online courses and webcasts. That's promo code CURB30 for 30% off all online courses and webcasts. Visit cmemeeting.org forward slash curbsiders to learn more. That's cmemeeting.org forward slash curbsiders to learn more. Continuing Education Company, delivering great education that translates to better care. And now, Paul, let's go to the next part of the case where I think we get back some labs.
Speaker 2Sure. So as a reminder, our gentleman, Finn, after a long flight who has a big hot leg, who's short of breath, who's tachypneic, who actually has a low 2-sat. So it sounds like we're trying to figure out less what the diagnosis is and more how bad things are. So our labs come back, and the troponin is 400. The BNP is 1,200, and there's a lactate of 1.8. We did get the right dose. Right lower extremity ultrasound, which did confirm a DVT, not surprisingly. CT pulmonary angiography shows bilateral, segmental, and subsegmental pulmonary emboli, as well as an RV to LV ratio of 1.3. So a lot of data here. And happily, there's a new classification system, which I think has just a few simple permutations that can help us stratify this patient into one of, I think, two categories. And so I would love to hear a little bit more about how much easier the new system has made things be in terms of how to triage this patient and what to do with them.
Speaker 5But to try to be unbiased here, I think that the AHA-ACC guideline, it's a broad and valuable PE care document in broad strokes. I think that it includes a lot of great elements. I think that the spirit of the stratification that Paul alluded to is great. I actually think of it as sort of a not-ready-for-prime-time version of the SCI classifications, for cardiogenic shock. Unfortunately, they're, like I said, not ready for prime time because of that evidentiary basis kind of lacking. But, you know, I think you could say that the ingredients are familiar, things like clinical risk, RV function, biomarkers, perfusion. But I think the new recipe still needs proof. And that it's really going to change decisions or outcomes, et cetera. That's one way to look at it. Now, to get a bit granular, so the 2011 AHA, AHA guidelines actually had a pretty straightforward breakdown. So you had your low-risk PE patients, your submassive patients. So those were folks with RV dysfunction. Several ways you can sort of make that assertion. And then your massive PE, so your shock, hemodynamic instability. And at that time, that was a time when really these fancy, fairly still unproven catheter-directed therapies were not readily available. And so, you know, really what you're deciding is who gets anticoagulation, a pat on the back and follow-up with their pulmonologist or hematologist. Who comes into the hospital and is on a heparin drip. And who gets TPA in the ER. That's essentially like a lot of what you're trying to decide. In 2019- 2011 was a simpler time. It was a simpler time. 2019 sees the European Society of Cardiology guidelines, which are some of my favorite guidelines ever in all of medicine. But I love PE, so I'm very biased. And that stratifies things into four buckets. So your low-risk, which again, here's your, you know, River-Roxaban or whatever, pat on the back, see you later. And then intermediate-low, intermediate-high, and high-risk. Specifically, your intermediate-high would be presence of an elevated biomarker. So troponin is typically the one that's used. And then evidence of RV dysfunction, which could be based on echocardiography, bedside echocardiography. Could be assumed by, you know, CT scan, whether that's RV to LV ratio distortion, whether that's reflux of contrast back towards the, towards the liver. And so the 2019 guidelines are great because it sort of highlights this weird area where we don't quite know what to do. And it can be very challenging, these intermediate high-risk patients. Not to say that your high-risk patients are a walk in the park, but the treatment algorithm is a little bit more straightforward with those folks. They typically are going to get TPA, maybe something else, but they're going to get thrombolyzed. That brings us to 2026 and the new AHA-ACC guidelines, which was sort of like an attempt to, to, um, up the ante to a degree. Um, and so now we have, we're more granular with five buckets. And like I said, that follows similarly the, the, the sky classifications for cardiogenic shock in that you have A through E. A is sort of your incidentally found PE. B is your symptomatic low severity PE. C is your symptomatic and kind of clinically significant PE with some degree of clinical severity. You could think of that as your intermediate risk. And then we have D and E. D is your sort of incipient cardiopulmonary failure. You could think of that as your quote unquote cryptic shock type patient where they're, they're not quite hypotensive on paper, but there may be trending that way.
Speaker 4Or what used to be called the submassive is kind of what E is. We've kind of reinvented the 2011 guidelines there.
Speaker 5Well, I wouldn't even go so far. I mean, it's, it's like the submassive divided into two category. It's, it's, it's complicated. I don't even really know what to necessarily do with that. Um, and then you have E, which is like this person is, is going down and we need to act quickly. So that's, that's kind of, that's kind of the initial overview of those three guidelines. But then there's more Nick,
Speaker 4right? Yeah. So I think, you know, just stepping back for one quick second, I think the central problem in PE is that it ranges in severity from an incidental, nothing burger you saw on a scan done for something else. Do I even need to treat this to, oh my God, this is the sickest person in the hospital. Call everybody in and that's PE. And so you need a system that will differentiate those, but you need a system that you can actually use. And, and I think to share your criticism, Cyrus, one of my concerns about the system is it is very complicated. So it doesn't just stop at a through E there's, you know, sub segments, uh, so to speak. So there's a one and a two, which correspond to a sub segmental versus segmental incidental asymptomatic PE. There's a similar B one and B two. Then in the C category, uh, we now have C one for a normal RV C two for a normal RV, but with an abnormal biomarker and C three, E which is an abnormal RV function. And then we in D we've subdivided into transient hypotension without organ dysfunction or evidence of organ dysfunction. And then in E they even subdivide this one. So they have refractory. Cardiogenic shock is E one and cardiac arrest is E two. So we, we we've taken it and we've made 11 subgroups and then, yeah. And then to make it even worse, if the person has respiratory distress, we add an R on the end. So you could think about that as now, we have like, you know, C two R might be our classification.
Speaker 2C three P O right.
Speaker 1You get a comment from Dr. Paul Williams here, Paul, what are you thinking?
Speaker 2Wow. I, yeah, I think everyone can guess what I'm thinking, but also respiratory distress is defined by what?
Speaker 1I think it's like a respiratory rate above 30.
Speaker 2Would that not qualify as symptomatic or am I just being foolish here?
Speaker 4Yeah. Great, great questions. Yeah. They, they define it based on respiratory rate, but right. There's no acknowledgement of, of like, you know, probably what I think is the single most important criteria, which is, does this person look terrible, right? Like numbers be damned. If this person looks really bad, like I'm gonna treat that very differently. And you know, there's no gestalt anywhere in these guidelines, despite them being incredibly specific. There's no like LLS.
Speaker 5Yeah. Yeah. So, yeah. So if we look at Finn here, he would sort of work out to be a C three R, which I guess means, increased clinical severity, so Category C, with evidence of RV dysfunction, the 3, and he has the respiratory modifier, the C3R. It sounds like a ICD-10 code or something.
Speaker 4Star Wars droid. Yeah, totally. Right.
Speaker 5Yeah. So, or yeah, my C3PO reference. So, yeah, that's kind of what he would work out to be on paper.
Speaker 4And, you know, I think there's a couple of problems here. One is, is this really something that somebody is going to feel comfortable scoring in the middle of the night? I mean, we literally have more categories in this guideline than there are for staging non-small cell lung cancer, which is already kind of complicated, right? So that's a problem. I think another question too is, is it better, right? It's more precise, but is this meaningful? And actually it isn't. So there was a large retrospective data set that they looked at where they compared people in that C category, and they found that C3 actually has lower mortality than C1 or C2. So we have this, but it doesn't predict the thing we care about. So why are we using it? I think it's complicated for the sake of being complicated, not necessarily for prognosticating outcomes or helping us choose what to do.
Speaker 1And in the hospital, I think the patients in the C category, if you're a hospitalist, which a lot of people that listen to this show practice in the hospital, you're getting a lot of those patients. And then you're trying to determine like, is this person in like, I guess, normotensive shock or kind of trending towards shock? And then, and when, when you should do something else or upgrade their level of care. So I think we're going to give you guys a little more information. I know we're going to talk about probably about PERT teams and things like that. Paul, do you want to read the next part of the case here?
Speaker 2Sure. So Finn, our guy Finn, we'll recall, has a PESI score of 113 and falls into category C, as we mentioned. So this is elevated clinical severity score. Also has an elevated RV to LV ratio at 1.3, so greater than one. Elevated biomarkers, which is a little bit more than 1.3, but it's a little bit more than 1.3. So it's a little bit more precisely is category C3, as we alluded to, and the R modifier, as you mentioned it, because of his tachypnea. So what, what, what, what we, we, we touched on this a little bit, but what are we doing here? So does this person need thrombolysis? You know, now that we had the R in the mix, does that change everything? Or we just, are we starting with heparin drip? Like what, how does this change management? I guess is my question. I think you guys touched on this a little bit, but what, who decides where to go from here and sort of what tools can we use to kind of help direct this patient's care from here?
Speaker 5Yeah. So, um, yeah, I don't know, man. I mean, it's, it's like, you have that information.
Speaker 2That's our show, everybody.
Speaker 5Thank you. Yeah. And, uh, and see, um, I will say that the authors, you know, in the, in the context of guidelines, it is, um, acknowledged that there's still a lot of work to be done to answer that very question. You know, we've, we've come up with this very complicated, very granular, um, scoring system. What do you do with the results? There is still a question mark, very, very real question mark. So you're telling me a guy has a PESI, I think you said of one 13. So that would put him as a class five. So that's your very high risk. Um, so someone at the very, in the very high risk category, um, as far as PESI goes, so 30 day mortality is anywhere from 10 to about 25%. Um, so, so those are folks that are, you know, pretty sick, pretty worrisome. That is definitely a patient, that, um, is worthy of a PERT activation. And this is one thing I really like about the guidelines, the new guidelines, um, is the fact that they acknowledge the importance of having a PE response team, um, to help make the decision for a patient like this. What is a PE response team? Um, so that is typically going to be folks of several different disciplines. It's, it's could be, usually there'll be an ICU physician plus, minus a pulmonologist, maybe one in the same. Often there's a cardiologist involved, maybe an interventional cardiologist. Um, there could be a diagnostic radiologist. There could be interventional radiology, vascular surgery, um, potentially even CT surgery, depending on your group, the size of your program and what tools you have in your toolbox. And essentially a well-oiled machine. And I think Nick works in a hospital that has this, a well-oiled machine looks like, um, you know, ED doc triggers the PERT, essentially that gets, uh, called out to all of the constituents. They get on a call, they review the case, they make a collective decision based upon the available data, uh, for that patient and based upon best practices. So my sort of cop-out, but evidence-based answer is, uh, the right thing to do at this point would be to initiate a PERT.
Speaker 1And I just wanted to, to call out here there, figure three in the, in the guidelines, the ACCHA guidelines has the categories across the top and then, down, down the figure, it sort of talks about what you would be doing. So for somebody in the C3 category, and, and you guys tell me if you think this is what we more or less be doing, we've already done a bunch of these things for him, but we would initiate low molecular weight heparin. We've already measured cardiac biomarkers. We'd be measuring lactate. We've already evaluated the RV size and function. And, um, we, we've kind of done a, a risk score. So the PE severity index or the PESI, there's also a simplified, S PESI, uh, Cyrus, we talked about this with Oren Friedman way back in the day, like maybe your first episode you produced or one of the first and, uh, with, with a great guest. And then, uh, we talked about activating the PE response team for most people in this class C category, it would be recommended. So I think the big ticket decision is probably what we're leading to is does this person need thrombolytics or thrombectomy of some sort, but anything you guys disagree with, with just that kind of just general list of things, that, uh, that would be recommended for this category? No, I think that's all right.
Speaker 4I think there's a couple other things that when I'm sort of leading the, the, um, PERT we're going to look at. So we're going to look at the imaging and we're going to look for some signs that aren't necessarily captured in these other scores. So one thing that I always look for is the size of the RV. I also look at the size of the PA, if that's big, that tells you something about the pressure there. Um, and then I also like to look for contrast in the IVC. So remember that contrast is usually injected in the arm, and it should go into the RV, and then it should go out into the pulmonary vasculature. If instead you see contrast squirted back out into the IVC, it tells you that the RV is experiencing pressure volume overload. So even before you've gotten an echo, you've got a functional analysis of how the RV is doing on the CT scan. The other thing that I'm going to look at, we're going to pull up and look at together is, um, where are these clots, right? If these are a lot of little clots that are all in the periphery, those that, that there's fewer options for those, right? You can't go in with a catheter and suck those out. In contrast, if it's a big central clot, that may be more amenable to some of these other catheter directed interventions. So that's another thing. And then finally, another thing that we're really going to be talking about is like, uh, is this person a good candidate for, for anticoagulation? And so, you know, things like, oh, they had a, you know, big subdural yesterday. Uh, that's an important factor. So it's not just would they benefit from this intervention? It's like, what, what is the likelihood that they would be harmed by this intervention? And so you sort of have to weigh both sides. Um, at my institution, we do, we do per as sort of a tiered response. So we have like a consult versus an activation, a consult, meaning the ED physician or hospitalist or whoever calls the C this cardiac ICU intensivist and runs through the case. If we score the case together, and if we meet our activation criteria, the things we've talked about, then I'll bring together the whole group. We'll look at the whole case together, and then we'll come back with recommendations to your point, Matt, those recommendations are almost always gonna be low molecular weight Heparin. Um, in 2026, that's, that's almost always the right answer over unfractionated Heparin. Um, and then, you know, the options might vary from admit them, we'll monitor, uh, bring them in, uh, admit them and we will plan to go to the cath lab or give thrombolytics or, uh, or sometimes, you know, we'll say, okay, you know, we're gonna, we're gonna monitor now and plan to go in the morning. But if things change, maybe we'll speed that up. So it's sort of like a range of options. Uh, to Cyrus's point, you know, there are a few cases where you may think, you know, is this a surgical case or would this person need advanced therapies like ECMO, which is why we, we often will involve a cardiothoracic surgeon. If that's potentially in the cards, not, not so much in this case,
Speaker 1this one is for the practice owners out there. If you own a practice, you've probably been through practice. financing before, and you may have learned what bad banking looks like a lender that treats your practice. Like any other small business runs it through a standard model and hands you an answer. Most of us did not go through medical school to learn how to run a business. So it's hard to know what to ask what's negotiable and whether the deal you're getting is actually a good one. That's why if I was opening a new practice, I wanna work with a bank that knows what it's like to build a practice. They have experience. They have a dedicated person that's gonna help me. And then they have credibility because they've already worked with lots of other doctors. And that's why Panacea approaches practice financing differently. Panacea was built for doctors by doctors. Instead of fitting you into a standard lending model, they start by understanding your practice and what you're trying to do, whether that's expanding, buying or building your space, acquiring another practice, bringing in a partner or refinancing. Then they work out the right way to finance it. So you get a dedicated, experienced banker backed by a healthcare specialized team who gets to know your practice, advocates for you inside the bank and with you as your practice grows. Panacea is trusted already, like I said, by more than 7,000 doctors and is funded over a billion dollars in doctor loans. And as an AMA preferred provider, AMA members get quarter point interest rate discount and no origination fees on practice loans. Visit panaceafinancial.com forward slash curbsiders to talk with a practice finance specialist about what you're planning next. Terms and conditions apply for new customers subject to credit approval and AMA membership verification. Panacea Financial is a division of premise member FDIC. Paul, let's go to the next part of the case. And I know we're going to be talking about, I do want to swing back and talk a little bit more about the thrombolytics and thrombectomy, but Paul, let's go to the next part.
Speaker 2All right. I'm going to trigger Nick and say the PERT team has been The PERT team, the PE
Speaker 1response team team has been
Speaker 2Sure. Exactly. As I go to my ATM machine and enter my PIN number.
Speaker 4Exactly. This is a faux pas that will, you know, like, you know, get me on my soapbox, like saying PJP pneumonia. Just, you know, it's
Speaker 5For Matt and I, the trigger, the trigger would be the CAC card.
Speaker 2Yeah, right. All right. Well, now that I've done that, the PE response team is activated. The decision to start low molecular weight heparin on the medical floor is made. Finn feels objectively better and is no longer ticked Nick. Overnight, however, he is noted to have a decrease in urine output and morning lab show creatinine bump from 1.0 to 1.6. Probably not the contrast. A repeat lactate is ordered by the night team comes back at 2.1. His vitals, however, remain relatively stable with a heart rate of 100 and a blood pressure of 101 over 55. So kind of a reassuring looking blood pressure in isolation. But I guess in sort of the larger context, what, how should we think about this and how concerned should we be about this patient?
Speaker 5Yeah, so I think this is always, um, this is a, this is great, right? So the first thing you need to do is determine, um, whether the change that you're seeing is most likely related to the PE or, or something else. For example, you know, if, if this patient had underlying coronary artery disease, and this was just enough to tip them over into having a coronary event, on top of their PE, that could manifest like this. If this person also, um, for example, maybe wasn't on a plane, but is sort of chronically sick, maybe has sick contacts, and they might have PE in the context of their evolving septic shock. Um, I just think it's important to realize that none of these pathologies exist in a vacuum. And so you, you always have to, I think, take a step back and try to look at the whole picture before you assume that the progression is related to the pathology. And so I think it's important to realize that none of these pathologies are related to the, um, the admitting diagnosis.
Speaker 4You can have fleas and lice, as they say.
Speaker 5Right. Exactly. Yeah. Fleas and lice. Exactly. Um, so we can sort of assume for the purposes of our discussion here that this is evolution of PE. Although I would say most of the time, the vast majority of the time, if you identify the patient using the tools we've discussed, and you start them on anticoagulation, they follow a pretty predictable course, of getting better. So, so this is a bit odd to me, but fine. Um, now we talk about this concept a lot in our podcast. You know, we spend a lot of time talking about shock, but not surprisingly. And so it's important to know that hypotension and shock are not synonymous. And this gets to the idea of sort of cryptic shock. Remember, shock is defined as a state of inadequate oxygen delivery to meet the needs of the body at a given time, whereas hypotension is a blood pressure. It's an arbitrary number. We'll say systolic blood pressure less than 90, MAP less than 65 or 60, depending on which church you, uh, attend. Um, and, and so, um, the point being is that shock is a situation where you're not perfusing and that results eventually in inordinate dysfunction. And in fact, we make the diagnosis by assessing end organs and determining if there's evidence of dysfunction. Hypotension is a number. And furthermore, context is king, as Nick said earlier, a patient with a blood pressure of 110 over 70, who typically takes five blood pressure medications, you know, that's, that's very worrisome. Right. Um, and so I think you need to take all of that into account. Um, in a patient like this, I would be looking at things like urine output. I would look at their lactate, um, which, you know, we did get a repeat lactate. It wasn't terribly helpful in this case. I don't, it was rising though. It was rising. I think that's actually quite, quite helpful. It's, um, the two. Yeah. I mean, the 2.1 in and of itself is not terribly helpful, but like everything in critical care medicine, we trend it. Right. And so you're seeing it increase. That's worrisome. All else being equal. I don't worship at the altar of lactate, but I think it's important to know, um, a lot of religious metaphors. I'm sorry. Um, I think it's, I think it's important to know when it's useful. And in this case, I think it is useful. Other thing, if, if this patient happens to be in the IV, uh, in the ICU and you have like a CBP monitor and you see their CBP is rising all of a sudden that could indicate progressive right heart failure. So all of those are tools you can use. The other thing that anyone can use to help you sort of suss this out on the ward or what have you, is the shock index. And really that's just looking at their heart rate over their systolic blood pressure. And so anywhere 0.5 to 0.7, we think of as normal greater than 0.7, um, can be worrisome. We think of 0.8, 0.9 as being early decompensation and greater than one would be suggestive of shock. And so all of that is to say, so, so
Speaker 4we look, so we look at this guy, by the way, right? His heart rate was a hundred and his SVP is one Oh one. So that's a shock index of like 0.99 repeated. So that's pretty worrisome, right? If you think about yourself at let's say your heart rate is 60 and your systolic blood pressure is one 20, you know, you're 0.5, that's normal. So this guy is very abnormal compared to you. And so, you know, I think that that is a strong clue that even though neither of those vital sign numbers are red in the computer, um, the, the ratio of them is worrisome and more so just the trajectory of this patient is worrisome. You know, it's the middle of the night, this person's sleeping in a hospital bed and their vitals look worse. Their lactate looks worse. You know, everything is moving in the wrong direction, the right direction. So that, that should be getting you nervous.
Speaker 1Yeah. And you also mentioned before, just like the eyeball test, like, does the person look sick? You know, that's, that's a very important thing as well to, to take into account. So I just wanted to highlight that when I'm, when
Speaker 4I'm, when I'm in the ICU and I'm hearing about these patients, even when these patients don't come to the ICU, I like to go eyeball them, you know, introduce myself, say, Hey, you know, here's what we're thinking. We'll talk to you more about this, you know, in the morning we'll see, you know, and, and potential we, you know, we'll talk to you about doing a procedure. Um, because then when, when I get called by the hospitalist, you know, at 2 AM and they're, they're nervous, I have a reference point like, Oh yeah, this person looks great when I talked to them four hours ago and now they don't.
Speaker 1Paul Williams, you want to go to the next part of the case? Maybe we'll, we'll make a fin a bit
Speaker 2sicker. I mean, as is the curbsiders way. Yeah. Over, over the morning, Finn becomes progressively hypotensive requiring small fluid boluses. I don't mission patient work and also begins requiring two liters of oxygen via nasal cannula for mild hypoxia. The PE response team team reconvenes and decides on catheter directed thrombolysis for this category D two patient approaching category E, which as a reminder is cardiopulmonary failure. Finn does well after the procedure and starts asking about discharge planning, especially with anticoagulation. So he's ready to go out the door. Now we did so well. So talk to us about what his care trajectory looks like moving from here.
Speaker 4Okay. So first of all, arguably, maybe we should have, shouldn't have waited until morning, you know, that that's the whole reason why we have a, uh, uh, perch team, team, team, team, um, so that we can do this expeditiously. Um, but that said, glad he did well. Um, you know, so I, you know, I think, I think this is a question that often comes up, which is like, okay, now what we fix the problem. How long do I have to stay on these, these pills for, I will say, you know, it's 2026. So do acts are, you know, are, are pretty established. That's pretty much the way to go here. Um, in the guidelines, it is a class one recommendation, but there are situations where, um, vitamin K antagonists are still used. Maybe Cyrus, do you want to talk about those a bit?
Speaker 5Yeah. So assuming you're not going to send your patient home with low molecular weight, heparin injections, then you're pretty much left with your vitamin K antagonists. So, um, you know, warfarin, Coumadin, the, the times when we might use those could be severe renal or hepatic dysfunction. Um, you know, a patient that already has, uh, a valve replacement is probably, it might already be on one of those agents, uh, as, as they're, uh, also patients that have certain pathologies like, you know, antiphospholipid, uh, antibody syndrome, they, they would already be on it. So that's generally a case. And, uh, yeah. So in, in most patients, I think of severe renal and hepatic dysfunction, um, maybe if they have issues with absorption, you know, the nice thing about, the nice thing about your vitamin K antagonist is that you can, uh, test the INR and then adjust as, uh, as indicated, whereas that gets a little dicier. Like you can try to look at 10 A levels and you can sort of like, but, but we still, we don't really have an FDA approved alternate dosing strategy for your medications like Rivaroxaban and Apixaban. The, I mentioned low molecular weight heparin, um, also in, in pregnancy, that would be sort of the move there. Um, so yeah, those are, those are the agents we use. Uh, one other quick thing, just to get back to the decision making, the whole, like, don't get me wrong. I love toys just as much as everybody else. And I think that there is a place for catheter-directed interventions. I just have yet to figure out what that place is. And so, you know, I think it's important to know this patient, you could certainly make an argument to give them a dose attenuated, maybe like a quote-unquote half-dose systemic thrombolysis, assuming they don't have a, you know, strong contraindication to that, although dying is a pretty compelling motivator to do things, even if there might be a relative contraindication. I think, at least in my experience and from my understanding of the literature, when you do intervene in a patient like this, what you certainly do is you improve their RV to LV ratio faster, you improve their hemodynamics faster. The long-term benefits are very sus, as the kids say. It's unclear as to whether that's really anything that you're gleaning. But really, in patients who maybe have a more worrisome story as it relates to systemic thrombolysis, in theory at least, especially with devices like some of the suction catheters that don't use any sort of thrombolytic, there's a device out there that does that, that might be a compelling indication to move in that direction. So that's all right. That's a soapbox I just had to climb on for a little while.
Speaker 1What Cyrus is getting into here, so basically, the standard of care has been systemic thrombolysis, where you just give it, you know, you give a thrombolytic through a vein and it goes through the whole body. Then we thought, well, maybe catheter-directed lysis is safer because you can give smaller doses. You can direct the catheter where the clot is. And then the competing therapy with that that's also an intervention is mechanical thrombectomy, where you're sucking the clot out or, I don't know, like drilling through the clot, whatever, to reopen the area. Yeah, rotor-rooter. So, but when you actually look at the evidence, even of the systemic thrombolysis and these other ones, like, none of these have been, like, really effective. I mean, I don't know if it's really established with what we would now say is, like, really high quality evidence, but there's a lot of, like, case series, uncontrolled studies, registries, and things like that. So, Nick, what do you make out of this whole world?
Speaker 4Yeah. So, I think it's a challenging thing to study because there's going to be crossover in these studies. So, the sickest patients in the control group get the intervention. So, and in many of these studies, like, 30% or more will cross over. So, it's basically impossible to do a good study. So, it's not that nobody's tried. It's just that, you know, it's really hard to show that doing an intervention is better than doing an intervention a little bit later, which is what often happens. My institution, we do tend to use a lot more catheter-directed thrombolysis these days. You know, I think systemic lysis is a great option, though, and we probably need to be using that more. It can be done quickly. It can be done far away. It can be done before transporting somebody. So, I think we probably ought to do more of it. There's also one more intervention on the list, which is surgical embolectomy. Which we don't do that often, but occasionally there's indications for it. I say all this just because it's good to be at a center that has expertise in all of these things. And often what we do is we sort of use a hub-and-spoke model where sick patients diagnosed with PE at, like, an outlying ED get transferred in so that they have all these options available. I think that's kind of, that's kind of the takeaway. Like, if you are, if you are somebody in the ED or in the hospital diagnosing PE, it's not your job to decide exactly what the treatment is. It's your job to get the patient where they can get the, whatever treatment they end up needing.
Speaker 1Yeah. And Cyrus kind of hinted at this. Like, I think that whatever trial, I can't remember the name of it right now, that, that was looking at this, that actually had, like, a proper randomized trial. They, they really, I think it was with catheter-directed lysis. They looked at RV to LV diameter. They didn't look at, like, mortality or quality of life.
Speaker 5Yeah. There's, like, Seattle 2 and Optalyse are some of the big studies that were done with that. So, if I can take a quick moment to just talk about the data briefly, you know, the world of PE management from an interventional standpoint has grown a lot in the last few years, from 2023 to 2026. The big studies have been, you know, Flame in 23, Peerless in 25, Storm PE in 26, Hypitho in 26, many of which, if not all of which, were industry-sponsored studies looking at the benefits or potential benefits of devices, either head-to-head or, versus anticoagulation. And
Speaker 4by the way, listeners, if you're wondering if it is a industry-sponsored trial, if it has an awesome name like Flame, Flame Peerless, it's probably industry-funded. If it has a lame name, it's probably a bunch of academics who did the study. Right.
Speaker 5Yeah. So, definitely industry-funded. Storm PE was most assuredly industry-sponsored. And so, the long story short here, and you guys can definitely, I think the show notes, we're is that, yes, there's a signal for benefit, but the signals always seem to be short-term wins. So, like, you know, reversal of RV to LV strain ratio, improvement in hemodynamics, which may or may not have occurred with anticoagulation or thrombolysis via, you know, intravenous administration. We just don't have that data. You know, Flame in particular, I would say, it's an encouraging signal in a study. Treatment was not randomized. The comparison arm had far more advanced shock. Statistical adjustment can help to sort of address this, but it can't erase the selection bias or the unmeasured differences. And so, these studies are challenging to interpret as much as maybe the device companies want us to really buy into it. Briefly, I'll say, on the horizon, there are some very exciting studies. So, Persevere and Torpedo NL, both with badass names too, are looking at some more, I think, clinically relevant or maybe patient-centered data, looking at, you know, initiation of ECMO, major, like, death and sort of bad outcome stroke, things like that. So, look for those studies in the coming years. That's Persevere and Torpedo NL.
Speaker 1Nick, any comments on those before we move on?
Speaker 4Yeah, I think just to reiterate the point that it's actually pretty hard to study this because these are often patients that have to be in enrolled emergently. It's not ideal for study recruitment. There's a lot of crossover. There's potential, you know, bias of patient selection. So, you know, just because there isn't amazing evidence doesn't mean these aren't amazing therapies if it's done in the right way for the right patient. I am a believer in many of these. We do a lot of these at my institution. The challenge is who gets what when, and that's where PERT is really important.
Speaker 1Paul, what do you want to get to next? I know there's a couple different things we can ask about
Speaker 2here. Yeah, let's talk about duration of therapy once we actually have someone done sort of out of the acute phase because I feel like those recommendations, I don't know if they changed or not or not, but just in terms of who gets anticoagulated for how long, and I was reading about some rules of extending coagulation and reduced doses and kind of who gets that. So, you just sort of talk us through our menu of options and what's appropriate for whom according to the newer guidelines.
Speaker 4Yeah, so I think this has evolved a bit with the use of DOACs more. It used to be that, you know, the risk of bleeding was considered significant enough with Warfarin that, you know, we were like, how long do we have to continue this for? And I think that's changing a bit with DOACs. The way I approach it is if there's no apparent risk factors, if this is a truly unprovoked PE, extended anticoagulation is reasonable. And the idea here is there's nothing that we can point to and we can be like, okay, don't do this. Don't sit in this window seat again and you'll be fine. If there's nothing that we can point to, we can't modulate that risk. We want to prevent it. If there is a persistent risk factor, a known persistent risk factor, somebody has cancer, autoimmune disease, IBD, chronic immobility, then that's also an indication for extended anticoagulation, right? The idea here is, well, we can't fix this risk factor. The place where it gets a little trickier is if somebody has a reversible risk factor. So like, for example, somebody had surgery, somebody had a C-section, somebody had a limb fracture and they were in a cast. This is a situation where you could potentially say a three to six month course of treatment might be appropriate. And then it gets even trickier because there are also minor reversible risk factors where we could say, oh, well, it's not as obvious that that was the thing. You had a vaginal delivery and then you had a clot. That's not as high risk as C-section. We just don't know. And this is an indication for shared decision-making, which honestly is kind of how we should approach all of these. It's just, we have less good data to guide us in that shared decision-making.
Speaker 1If you're watching, you'll notice that Nick is gone for a moment, but he will magically reappear in just a few minutes due to parenting duties. But Cyrus, I wanted to ask about reduced dose because I know, okay, so we just talked about how long to treat someone for, but is there a time after that initial three to six month initial treatment period where you would do a reduced dose of a DOAC? Yes, it's a great question.
Speaker 5And this is something that I think the, um, ACC AHA multi-society guideline actually does a great job of. So I don't want to totally poo-poo the guideline because I actually think they do a good job here. So they've made the extended phase strategies substantially clearer. Uh, if you're continuing anticoagulation beyond the initial three to six months, um, so usually we usually use six months, I think in practice, half dose apixaban or rivaroxaban is now a class one level A recommendation to reduce bleeding. Um, and so I will often use that dosing strategy at the six month, maybe, you know, sometimes it becomes 12 months just because you don't see that patient until, you know, whenever you see them, but I'm a big fan of doing that. um whichever agent they're on sort of going to a half dose um the the guidelines also say as far as who should enter that extended phase so your first pe with no major reversible provoking factor it's a class 1a indication to continue if there's a persistent risk factor it's a class one indication it's like a class 1c indication if they have a major reversible provoking factor then you are generally going to stop after the initial three to six month treatment period and if it's a minor reversible provoking factor that's when it gets into what nick was saying you use those those shared decision uh making skills that we we all have or should all be fostering um to help make the determination so long story short yes big fan of dose reduction i think the data is pretty supportive of that paul
Speaker 1do you want to read the next part of the case and let's let's see what's happening to
Speaker 2finn sure so finn is eventually discharged from the pixaban he sees you in clinic one week post hospitalization he is doing well overall though he still has some mild shortness of breath that has not gone away you counsel and continue the pixaban to treat his pulmonary embolism and reiterate the risk of bleeding you make a three month follow-up he is a good patient and comes back well we should not be voting value judgment finn comes back to see us in three months he
Speaker 1is a good boy and you pat him on the head
Speaker 2he listens to his doctor so we like him because that's how medicine should work
Speaker 5paternalistic medicine for the week it's perfect yeah
Speaker 2just cancel me now um at three months finn notes he still gets short of breath when taking the stairs so all this is to say cyrus so this this patient's now three months out from treatment of his acute pe he is still actually having symptoms so what point should we be concerned about something like chronic thromboembolic pulmonary disease and does this patient need a repeat ct pulmonary angiogram just to just to make sure we really treated him appropriately or not so what what do we do with this this the symptomatic patient who's still symptomatic status post treatment i
Speaker 5think really we should be getting q i'm just kind of track track the clot as it's dissolving every step of the way for all patients um okay so um that's a joke by the way for our audience so all kidding aside um this is a really great question this is something we encounter not infrequently in the world of pe i think the important time point is around three months after acute pe it is very common for patients to still have some dyspnea or exercise intolerance after pe most of those patients don't have ctef but if you're you know three months after acute pe you're still going to have some dyspnea or exercise intolerance after pe so if you're three or more months down the road and the symptoms are persistent or they're kind of maybe uh evolving or they're clearly out of proportion to their baseline that's when we need to consider some sort of chronic thromboembolic disease um not just like say they're deconditioned because that's a very easy thing to do and like i said at the very beginning of this i um you know nick is essentially an octensivist he does a lot of he basically does all critical care and some pulmonary consults i find myself doing it all so like i see these patients in the icu i see them in clinics so this is a very common very real scenario for me and so if i see this person in my clinic really my first step is to do an echocardiogram uh in my current clinic i don't have the bedside uh ultrasound uh readily available but um you know in other places you might have one and you can throw a probe on their chest take a look see what you see use your skills if you have them um but then ultimately those patients should get a a you know a full checkup and they should be able to get a full checkup and they should be able to get a full study uh done by an echoconographer um and so you'll you'll get that done and really what you're looking for is evidence of pulmonary hypertension evidence of right ventricular dysfunction uh god forbid evidence of right heart failure and you're also going to want to at that same time consider other causes for their dyspnea things like heart failure um lung disease that was hitherto undiagnosed is that patient anemic and and yes deconditioning is a thing right i mean a lot of these folks don't do a lot of exercise uh during the first few months of their months after a pe diagnosis now if the question is specifically could this patient have chronic thromboembolic pulmonary disease um or pulmonary hypertension so that's your c ted versus your c tef then the screening imaging that you're going to want to obtain is a vq scan not simply another ct pulmonary angiogram because the vq or the ventilation perfusion scan is really going to identify whether there are regions of lungs where there is a mismatch in terms of ventilation and as good as they are in 2026 isn't really going to get far enough out there to give you that answer and remember that your ct pulmonary angiography is dependent on timing as well um so i think the vq scan is really the test of choice here
Speaker 1paul this just it just wowed to me that the vq scan just shines so much in this situation because if you ever look at them they just look like you're like oh yeah it's a little more gray there
Speaker 2i yeah i remember you know back in the day when we had to get them because someone was thought to not be appropriate for ib contrast like oh we'll get a vq scan i'll come back and determine it then we won't know what to do so it's interesting that this as this has developed our knowledge has broadened we actually have found real utility in these things i'm going to ask a half joke question cyrus i heard you say c ted so but there's a p in there so just when i'm talking to my pulmonology colleagues i just want to make sure i sound smart is it are we going c ted not c pita oh gosh yeah
Speaker 5okay so um you don't
Speaker 2actually have to respond
Speaker 5i'll respond to it in the context of the the rest of the answer which is really i think my practical takeaway for for this particular question is is basically if you have persistent unexplained dyspnea for three months or more after pe you should think about some sort of um long-term sequelae from your pe that could be something like like um as quote-unquote simple or not simple as deconditioning or it could be true chronic thromboembolic pulmonary hypertension or um or pulmonary disease and so we use that echo we talk about pulmonary perfusion we use the vq scan and really what you're looking for on the vq is persistent mismatch defects which if you have that plus an abnormal echo then you're thinking more along the lines of that group for pulmonary hypertension i.e your c tef whereas if you have um let's say an abnormal echo or some other abnormal signal without pulmonary hypertension then you're leaning more towards c ted and uh potentially like some some places can do pulmonary angiography to identify some subtle changes to the pulmonary vasculature and also to the lung parenchyma which might be more in the c ted category but that's kind of coloring outside the lines a little bit but yeah really the the key difference is does that person have pulmonary hypertension or not and the gold standard is going to be your right heart cath so if you if you're really concerned you're going to progress in that manner if they have it you can treat it we have medications like rea saguat which you can use for um chronic thromboembolic pulmonary hypertension they don't have that you're not going to reach for rea saguat but instead you're going to be able to use it for things like um trying to you're really trying to optimize whatever else you can optimize in that patient from a whole holistic standpoint pulmonary rehabilitation is a good option in those folks um those sorts of things
Speaker 1yeah i'm glad you said that drug name and we didn't have to prompt you uh prompt you for it uh okay so the so basically as a primary care if we're seeing these people number one we want to see people a week after they leave the hospital make sure they're doing okay they're taking the anticoagulate uh anticoagulation okay and then within three months we want to check in with them see if they're still having symptoms if they are still having symptoms then at that visit we might order an echocardiogram looking for pulmonary hypertension but if that comes back abnormal or if our risk our suspicion is really high we might be sending them to someone like yourself and getting a vq scan to see if how high our suspicion is for um chronic thromboembolic pulmonary disease or pulmonary hypertension and i think that's i think that's most of what we had to ask about here the the follow-up with pe is and and getting the anticoagulation you mentioned like sometimes you would reduce the dose at the 12 months but the the primary care doctor i think should feel empowered either to reach out to you or to reduce the dose if they see them you know if it's been after six months and there's no reason for them to be on that high dose anymore we can we can potentially
Speaker 5lower it i agree i think we have enough data to support that so i think that's a good point to support that position
Speaker 1paul any other questions you wanted to ask before we get to our take-home
Speaker 2points yeah while we're in ctef land or or cted or whatever we're calling it cyrus i did want to ask i i think i heard years ago sort of the the excitement around potentially doing catheter directed thrombolysis might be to reduce ctef as a sequelae of of having a pe and i i don't know where the data are with that if they support that or not because i i it sounds like the outcomes are fairly challenging to sort of study with these kind of trials but is there any data to suggest that sort of earlier intervention with these sort of more fancy pants therapies might actually reduce the outcome of ctef or cted
Speaker 5yeah so so that's a that's a great question and um of course we would love to see um that signal unfortunately it doesn't exist as far as i'm aware and so you know we we just we don't have that convincing evidence that there's a reduction in the rates of cted or um or a ctef uh as compared with anticoagulation alone there's of course this strong mechanistic argument that's made cdt or thrombectomy is going to rapidly lower your thrombus burden your pa pressure your rb strain so i think it's very tempting to sort of make that leap and say okay well if you fix things earlier they're going to do better um you're going to improve things and they're going to do great and they're going to run marathons and so on and so forth um just we have yet to see that in any randomized long-term outcome data that i'm that
Speaker 1i'm aware of so nick i don't know if you have any with paul was asking about the the catheter directed lysis the mechanical thrombectomy does it reduce the incidence of ctef it looked like you were nodding along there have you yeah aware of any evidence suggesting that it doesn't
Speaker 4work? As far as I'm aware, there's no great randomized trial showing that it is. There are a couple, you know, case series showing good outcomes, but those are heavily biased by selection. So I think, you know, it's going to be a hard thing to ever prove just because, you know, getting people to enroll in this study, following them for the long term, getting a device company to pay for a study like this, it's a big lift. You know, I do agree with the point that Cyrus made that, you know, mechanistically, it's really hard to get CTF if you sucked out all the clot. So I think, you know, that is a compelling argument. But one unfortunate thing that we've learned in medicine is that things that seem obviously true sometimes aren't. And, you know, just because that sounds really compelling, you know, it's not. It's not a substitute for actual clinical trial data. So I do think it's reasonable to offer in many patients who qualify for it, but there's no proof that it's going to be better in the long
Speaker 1term. Yeah. Like we just learned that from lowering LP little a, which we know we can lower it, but it did not reduce cardiovascular events. So you got to, you got to study these things. Well, guys, this has been fantastic. We covered so much ground. I was, I didn't think we were going to be able to do it in the time allotted, but we did. So, Nick, we'll start with you. Favorite take home points, maybe one or two that you wanted to leave the audience with, and then we'll go to Cyrus for his.
Speaker 4I guess I'll just make one point about the duration of anticoagulation, you know, which is just to say that I think that as the therapies have gotten better, the risks of lifelong anticoagulation have gotten a lot smaller, but the benefits remain. You know, somebody who has had a PE once is at significant risk for it happening again. And so I think there's a really compelling argument that lifetime, actually, I hate the term lifetime anticoagulation. That would be another point. That, that long-term anticoagulation is beneficial. You know, obviously you have to customize this to your patient. You know, if they are like an MMA fighter or sword swallower, or they sleep on a bed of nails, the risks are higher. But if, you know, they are like a long haul truck driver, or they had an uncle who died mysteriously. You know, that kind of pushes me towards, you know, maybe you should be on this. And the reason why I don't like lifelong is because we should be evaluating these things consistently and continuously. Right. And so like, if something changes, if they have a big GI bleed, maybe, maybe the risk benefit changes. But, you know, I think in 2026, it's not that many patients where I think stopping at three months is the right move.
Speaker 1Cyrus, what are your take-home points?
Speaker 5Yeah. So I think as far as the guideline goes, I think a big part of this podcast was talking about the new guideline. It's pretty, pretty topical, right? I think there's a, there's obviously I have, I have a number of critiques that I shared. I think some of the really important things to know, they're actually positive. So even though there's a lot of discussion of catheter-directed interventions, it does reserve reperfusion for those with clear clinical failure, especially in those categories D and E. And, and so there is sort of a conservative slant there that I think is, is a push for early follow-up for long-term surveillance, which is refreshing. This discussion of CTEF, discussion of bleeding risk. I think that's really big. It legitimizes the, the PERT in a very meaningful way. And like I said before, I think the framework is, I guess, conceptually strong, but it's complex and it hasn't really been prospectively validated. So as far as my sort of, sort of take-home regarding the guideline, I think that's, sort of my, my feeling on it as, as far as PE and the, the disease itself. I mean, I could talk about this for days. I won't bore the audience, but I'll just say- But where could they hear you talk about it, Cyrus? You guys have any, I was trying to look
Speaker 1for a PE episode. I didn't see any, but they, where can they hear you guys talk about all sorts of fun critical care topics?
Speaker 5Yes. Well, I'll say briefly, I think respect the PE, think about it in your patients and whether you use these guidelines or the old guidelines, I think as long as you approach the patient with sort of open eyes and you focus on what they're telling you, I don't think you're going to be led astray. Now, to get to your other leading question. You know, Nick and I, when we're not here, there, and everywhere else, we're working on our own podcast, which is Critical Care Time. And hopefully we'll be able to maybe cross post this or something over on our channel there and try to get it out to some of the folks that listen to us. But, but yeah, we have several PE episodes that we've talked about that we've done. I think, I think maybe in season three, three episodes. Yeah. Two. Yeah. Certainly in one. And then I imagine as we start to do some more ECMO episodes and some other content, PE will continue to come up over and over again.
Speaker 1All right. So check them out at Critical Care Time. And thanks so much to both you guys for, for giving us your time.
Speaker 5Thanks for having us. Had a great time, Matt. Thank you. And thank you, Paul.
Speaker 2That has been another episode of The Curbsiders, bringing you a little knowledge food for your brain. Oh, yummy. I feel like you've given up the whole holes thing. I'm not mad about it, but I'm just, I'm a little bit surprised. The whole holes thing, Paul. That's something you just said. Not proud of that sentence. The internet is forever. Are you still hungry for more? Join our Patreon to get all of our episodes ad-free plus twice monthly bonus episodes at patreon.com/curbsiders. You can find our show notes at thecurbsiders.com and sign up for our mailing list to get our weekly show notes in your inbox. This includes our Curbsiders Digest, which recaps the latest practitioner articles, guidelines, and news in internal medicine.
Speaker 1And you can send us your feedback at [email protected]. You can click on the link in the show notes, or you can go to patreon.com/curbsiders, where you can sign up for our CME tier, where you can get quarterly CME bundles. It's a really easy way to claim your CME credit. A special thanks to our writer and producer for this episode, Dr. Edison Jang. And to our whole Curbsiders team, our technical production is done by the team at Podpaste, Elizabeth Proto does our social media, Jen Watto runs our Patreon, Krista Chumanchu moderates our Discord, Stuart Brigham composed our theme music, and with all that, until next time, I've been Dr. Matthew Frank Watto. Speaker 2And as always, our main Dr. Paul Nelson-Williams, thank you and goodbye. Dr. Paul Nelson- And as always, our main Dr. Until now, the data your AI depends on has been trapped
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