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Welcome back to Run the List, a medical education podcast in internal medicine. As a quick disclaimer, this podcast is made for educational and informational purposes only and should not be understood as medical advice under any circumstances. Before we get to the show, a quick word on the sponsors for today's episode.
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This episode is brought to you by Open Evidence. Open Evidence is a really incredible resource for people in medicine. It's an AI powered medical information platform that can help you answer clinical questions, provide high quality literature and and so much more. You can ask questions like what are the classic imaging findings for gout? Or Tell me about the landmark trials in lupus nephritis. They recently partnered with the New England Journal of Medicine so they have access to their text, figures and tables within Open Evidence. It's free and unlimited for healthcare professionals, so I highly encourage you to go check it out. Go to openevidence.com to learn more. Today we have with us Dr. Allison Greco. She is an assistant professor at NYU where she's also the Assistant Program Director for the Pulmonary and Critical Care Fellowship Program. And at Bellevue Hospital, she serves as the Director of the Critical Care Consult Service. She's the Director of Quality improvement in the MICU and she's also involved with the PERT team. Dr. Greco, thank you so much for being here with us today.
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Thank you so much for having me.
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Today we'll be talking about pulmonary embolism, a very important topic. Whether you're on the floor, in the icu, in the ed, this is something that's super important to be able to recognize and treat in a timely fashion. So we will dive into our case. We have Mrs. F and she is a 66 year old woman with a history of obesity, hypertension and osteoarthritis of the hip. She had a recent right hip replacement and she's presenting to the emergency room with dyspnea and chest pain. She reports that she has no fever, no cough. This started pretty acutely and she feels like she can't get a deep breath in. She's been home for three days after her surgery and she's been in a good amount of pain, so mostly been laying in bed. Her vitals are notable for a heart rate of 114, a blood pressure of 138 over 80, an oxygen saturation of 93% on room air, and a respiratory rate of 22. So, Dr. Greco, before we actually dive into the details of this case, can you explain what exactly a pulmonary embolism is?
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Sure. This case has me excited. It's an exciting time to talk about pes. There's a lot of research being done, and as you mentioned, it touches all aspects of medicine. There's. There's so much going on right now. So a pulmonary embolism is a blood clot. It conventionally starts in the venous system, so in. In the deep veins of the legs, and blood moving in the venous system returns back to the right side of the heart and then gets pumped to the lungs to be oxygenated. So what happens is a blood clot travels through that circulation from the legs up until the right side of the heart and back into the pulmonary arteries and gets lodged there. I usually explain it to patients. Like, it's like when you put your finger over a garden hose. So there's a blood clot blocking the garden hose. If you've ever done that, the pressure of the water goes up. And so the same thing happens in your pulmonary artery and your heart. It creates high pressure, and that high pressure makes it hard for your heart, specifically the right side of your heart, to pump the blood. What that means, in summary, is that we have a huge spectrum of disease based on where exactly the blood clot is lodged in the pulmonary arterial system, and based on how badly that clot affects the pressure and affects your heart's ability to pump. And so that is why pulmonary embolisms can be so dangerous and life threatening.
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Thinking a little bit more about our patient and her risk factors for PE we know that she had recent surgery, which is definitely a risk factor for forming clots for a number of reasons, both the surgery itself, as well as her reduced mobility after the surgery. What are some of the other risk factors for PE or other important questions to ask her?
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So, yeah, there's a lot of questions we want to ask to figure out. Number one, are we sure this is a blood clot? And two, if it is a blood clot, why does someone have it? And believe it or not, that's the question patients ask me the most, is why do I have this? We can think about it from a pathologic standpoint. We talk about vertis triad, meaning a combination of stasis, hypercoagulability, and endothelial injury. What do I mean by that? Well, when we talk about stasis, we talk about poor venous return, blood pooling, and specifically the deep veins in the legs. So long surgeries, long car rides, long plane rides, immobility from being hospitalized are some examples. When we talk about endothelial injury, it's easiest to think about this like physical trauma to the vessel. But remember, lots of other things can also cause endothelial injury. So infections, infiltration with bacteria, any foreign bodies, implants, medical devices, things like that can cause inflammation and damage to the blood vessels. We talk about hypercoagulability, I think most commonly of true hypercoagulable states, Coagulation factor mutations, protein C, protein S deficiency, nephrotic syndromes, cancer, things like that. But remember, there are other conditions that also cause hypercoagulability. Pregnancy, advancing age, smoking, obesity or other things that we see pretty commonly. And certainly the combination of all of those things together can certainly predispose someone to developing a clot. So our history is going to look at someone's risk for, for all of those things. So I usually ask, does anyone else in your family, has they had blood clots in the past, if a patient has ever been pregnant before, had prior miscarriages, looking at things like APLs, asking about smoking, prior blood clots in the patient themselves, malignancy, any medications? We conventionally think about OCPs and hormone replacement therapy. But remember, folks do use exogenous steroids for weightlifting and things like that. So it's important to ask about. And then recent surgeries, hospitalizations, immobility flights. One thing I actually get a lot of is, is asking folks what they do for work because folks that are at desk based jobs and sitting all day or have more stasis or if folks are drivers, driving Ubers, truck drivers, things like that. So that is another way to think about immobility that folks are probably likely to have more often than taking like transatlantic flights or something like that. So don't forget to ask about those.
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Yeah, that's really interesting. I know we think about, you know, the classic board question will be about a 12 hour flight. But sadly in this current day and age we have a lot of immobility just in our day to day. So getting a thorough history is really, really important. And this also plays into, I know later the duration of anticoagulation. It will depend very much on whether we deem this PE to be provoked or unprovoked. So, so back to our patient, what are we looking for? I know I mentioned that she's dyspneic and tachycardic. What other things are we kind of looking for on exam?
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I think in the initial phases you're still sort of risk stratifying and I think one important thing is to look for could this be something else? Right. If the patient, if you're examining the patient and they have like slam dunk pneumonia. I'm going to be less worried about pe. I will say most commonly the thing I see is a completely normal physical examination. The other things commonly that they're going to have is they're going to be very tachypneic, they're going to be tachycardic. Folks that have classic DVT symptoms, you know, may have unilateral lower extremity swelling and skin changes depending on how occlusive a DVT might be. But for the most part, that's really it. Most folks have a very bland or even a normal exam that makes sense.
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So we have a good idea of what might be going on with her, but we're not a thousand percent sure and we don't want to expose her to unnecessary testing and radiation. Are there any risk scores that we can kind of use to help risk stratify for her?
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Yes, there's two big things that we talk about. So we talk about a Wells score and we talk about a D dimer test. I think there's often a lot of confusion about, like, how we use both of those things together. Do we use them together? And so essentially you use the Wells score, which is a constellation of clinical findings that help us risk stratify the patient's likelihood of having a pulmonary embolism. This is where, like, making sure there's not an alternate diagnosis. Have they had a prior clot before? And there's lots of clinical calculators you can use. You can look these up and essentially based on that pretest probability, you decide whether or not one of several things. If your pretest probability based on your well score is high enough, actually the guidelines and a lot of folks would recommend actually initiating treatment while you pursue additional diagnostic testing. If your well score is intermediate, you might hold off on that initial treatment and then pursue additional diagnostic testing. But if your well score is low risk, a score of 0 or a lower score, you would then use your D dimer. So it is in those patients that are low risk, obtain a D dimer level. If the D dimer level is low, you've essentially ruled out vte. But if your D dimer is elevated, then you would also want to pursue diagnostic testing. So you can see that the discriminatory decisions are really only made in those, like, low risk populations. When you think something else might be going on, if you're really not sure, but in those higher risk patients, patients who you really clinically suspect a pe, you should probably just go ahead and initiate treatment. While you pursue additional diagnostic testing.
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And speaking of, let's get into some of the labs and imaging and EKG findings that we might see in a patient who are working up for pe. What kinds of labs do you look for?
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Oftentimes, what happens when it comes to diagnostic testing? Folks are being seen in the emergency department or in the office. So a lot of the diagnostic testing is happening at the same time. So while from an academic standpoint, we talk about the Wells score and determining our pre test probability, a lot of the diagnostic testing we should acknowledge is, you know, pragmatically going on at the same time. So with that said, tests that often get ordered in these patients, CBC I think is very helpful. It will allow us to look at the patient's hemoglobin, their, their platelets and think about their bleed risk. While we're talking about anticoagulation. A CMP is helpful. What's their creatinine doing? What's the best imaging test we can order based on their creatinine? And we'll talk about that in a second. As an ICU doctor, I am essentially, primarily, always taking care of the sickest of these patients with right heart failure. So they may have end organ dysfunction as evidenced by elevated LFTs or elevated creatinine and lactate. I mentioned the lactate. It has been shown to correspond to mortality risk in these folks. So I do think that also has some value. As we talk about risk, stratification and evidence of right heart failure. We think about troponin as evidence of RV ischemia. We talk about BNP as evidence of RV strain and dysfunction. Most oftentimes, these folks are also going to have a D dimer ordered at the same time as the rest of their labs. Like I said, for just pragmatic reasons, I want to specifically talk about risk stratification. Part of the job of the multidisciplinary team in evaluating these patients is quantifying the degree, if any, of RV dysfunction and if, if it's present, what to do about it. And so the only way to tell if there's RV dysfunction. I mentioned checking things like a troponin and a bnp. We can look at the EKG to see if there's right heart strain. Most commonly, you're going to see sinus tachycardia. You may see S1, Q3, T3. It's great. When we find it, we all ooh and ah over it. But the majority of cases, you're not going to see it. Folks can have T wave changes. They might have right axis deviation and a right bundle branch block. A CTPE is the diagnostic test of choice in these cases. I specifically say ctpe. It's important to know that contrast has to be timed to opacify the pulmonary arterial system. It's confusing. Not all CTs with contrast are able to effectively evaluate the pulmonary arterial circulation. So CTPE will diagnose whether or not there's a clot present. But in the initial studies, the Seattle 2 trial, looking for markers of RV strain, they actually looked at the RV to LV ratio on the ctpe. So the CT itself can also diagnose right heart strain. Finally, I would order TTE if there's any concern for right heart strain based on elevated troponin BNP on the ctpe. The definitive test to look at the RV itself and see how the heart is functioning is an echo. And then you can talk about the utility of lower extremity dopplers. On one hand, if you have a very low risk PE and someone who you're really thinking is appropriate for outpatient treatment. I don't know that diagnosing like a very distal DVT is going to change anything. However, I do use it to make clinical decisions when I have folks with intermediate or high risk pe. Because if someone's pulmonary embolism has caused right heart strain and their heart is already struggling a little bit, if they have a risk for additional embolic phenomena, meaning a DVT in their lower extremity breaks off and forms a new pe, that makes me more worried than someone who doesn't have it. So I think lower extremity dopplers are useful for thinking about treatment decisions in sick patients, but it does not formally risk stratify in terms of looking for RV strain or something like that.
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All right, so in our patient, we send her to radiology and we get a call back that they see an acute saddle PE with evidence of right heart strain. So, moving now into treatment, I know that there is really a whole spectrum of treatment here as well. How do you kind of think about what the priorities are in treating this patient?
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The mainstay of treatment for all comers, Anyone with a pulmonary embolism is going to be anticoagulation. The question is, how fast do we need to remove the clot? And this is where risk stratifying the patient comes in. Folks that are low risk, essentially, you can just start a doac. The evidence behind that is that patients get therapeutic relatively quickly. They stay in therapeutic range quickly. We don't need to monitor levels. So for low risk PEs, that's the way to go. On the opposite end of the spectrum, if someone has a large pulmonary embolism and they have evidence of hypotension, meaning systolic blood pressure less than 90 or drop in 40 from baseline, or they've had a cardiac arrest, things like that, we're going to talk about thrombolysis. This means this person's right heart has failed, their cardiac output has dropped and we need to relieve obstruction quickly. So all of the guidelines are going to recommend systemic thrombolysis for these patients in patients that can tolerate it. Right. And we know, especially in this patient who just had a recent surgery, if this patient developed hypotension, that is a conversation I would be having with her surgeons. Is it safe to give this person systemic thrombolysis or not? So I think those two ends of the spectrum are fairly straightforward. Low risk, get anticoagulation, DOAC's preferable. High risk patients are going to get systemic thrombolysis if it is safe. That leaves us with this middle group of patients, the intermediate risk group, depending on the guidelines that you're looking at. The European Society of Cardiology, HURT Consortium, Pulmonary Embolism Response Team, American College of Chest Physicians Chest, American Heart association, we have the hematology guidelines. Depending on the, on the group you're looking at, they recommend further risk stratifying that intermediate risk group of patients. Some groups use the PESI score. There's another calculator you can look up, you can use at the bedside. It takes into account things like history of malignancy, age. You can also look at hemodynamic data. This is my personal preference. In those cases you look at the echo and do they have both an elevated troponin and BNP or just one? And you can further risk stratify the intermediate risk group into intermediate high risk and intermediate low risk. And so in that group, based on multidisciplinary discussions, other things like I mentioned, is their lactate elevated? Do they have a big proximal DVT that's at risk for further embolization? You can make decisions about should this patient be treated with systemic anticoagulation alone or should we think about some of our catheter based options? I describe them to patients. As I say we're going to go in and roto rooter and we're going to remove a clot. So that would be a mechanical thrombectomy versus catheter based thrombolysis where we go in with catheters and drip tiny little amounts of localized TPA to treat the clots. And there's lots of studies looking at which of these catheter basis approaches is better. That's like a whole podcast in and of itself. But what the data does show is that in this intermediate group, thrombolysis is not the answer. So systemic thrombolysis, meaning tpa, that is not the answer. It just essentially comes with a higher bleed risk than clinical benefit. So these decisions, I think are best made as part of a multidisciplinary team looking at a constellation of clinical variables is, I guess, the short answer. If someone cannot be anticoagulated and they have a dvt, all the guidelines recommend an IVC filter. There's no evidence to support the use of IVC filter in folks that can otherwise tolerate anticoagulation. I often get asked, well, which agent should I start? In these intermediate and high risk folks, folks, and in these patients, some of the guidelines, there's some dissent. Heparin is probably the most commonly recommended. I will say there are some caveats. You have to actually get a patient therapeutic quickly. So without use of a bolus, it's going to take you a long time to get into the therapeutic window. Studies have shown that folks have a lot of time outside the therapeutic window with peaks and troughs. Because of this, some of the organizations chest, et cetera, recommend using low molecular weight heparin or Lovenox as the initial therapeutic dosing. However, not all interventionalists are comfortable doing procedures on that. So if the patient is a candidate for some sort of procedure, whether it be a thrombectomy, or whether they need additional hemodynamic support, like mechanical circulatory support, that might not be the best option. And then it's obviously has renal clearance issues. So in folks that are really sick and having AKI and the like, it's probably not the best choice. So those are the conversations that we also have as a multidisciplinary PERT team.
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Mrs. F is ultimately started on Lovenox. She's feeling much, much better than when she first came in. Now you start to talk to her about discharge planning. So what are we telling her about the medications that she'll need to be on when she goes home and her outpatient follow up and how long she's gonna have to stay on anticoagulation?
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Good question. So I actually have a little spiel I go over with folks when we're at this point, point the good news for our patient is she's not going to need to self inject or give herself low molecular weight heparin at home. I think this is an appropriate point to transition her to a doac. I usually counsel them on risk of bleeding with their blood thinners. Fortunately, the doacs don't have as many side effects as warfarin. But. But I do go through that with everyone. And then most folks, the next natural question is how long do I need to be on this medication? And this gets back to thinking about provoked versus unprovoked. So it used to be that provoked clots, folks that had true transient identified risk factor, they had a hip fracture in surgery a long flight. Folks with provoked clots would historically get at least three months of anticoagulation and then folks that had no identified risk factor would get lifelong anticoagulation because we didn't really know why they had the clot. I will say we're starting to move away from that in thinking about transient risk factors versus unmodifiable risk factors. Folks that have large hemodynamically significant clots probably do benefit from longer term anticoagulation. There's actually a number of different scoring systems you can do to determine whether people need longer term anticoagulation. So I usually say at least three months of anticoagulation, if not more depending on how you do. All patients with intermediate and high risk PEs also additionally need a follow up echo at about three months as well to make sure that that RV dysfunction has normalized. It can take some time to get back to normal. And in folks who don't get back to normal or have ongoing pulmonary hypertension would need to see specialists for longer term follow up.
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Awesome. She's very grateful for the thorough explanation and your wonderful care in the hospital. So Dr. Greco, this has been a phenomenal episode. We've all learned a ton about caring for patients with peace. Do you have any final pearls that you want to share with our audience?
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Sure. This has been fun. Thank you again for having me. One of the things that kind of like a must read is a paper. It's. It is now an old paper. It's called the golden hour. The terminology used in the risk stratification of pulmonary embolisms that is this massive submassive that we have moved away from. So some of the nomenclature is outdated. However, it goes through the hemodynamic effects of PES in such great detail. It's such a wonderful pathophysiologic read. So I do recommend it for focus on pathophys, less on nomenclature. And the other pearl, when we talk about specifically the intermediate risk group, I do want to point out that their highest risk for decompensation in the first 12 to 24 hours. If you think about how anticoagulation works, whether it's heparin, aluminolicular, what happener, doac doesn't matter. It works by first stabilizing the clot and then your body's natural thrombolytic mechanisms are what's going to actually break it down. So in the first 12 to 24 hours, while you're becoming therapeutic on those agents, patients are highest risk for clot propagation or further embolization of the clot. These are the patients you want to have on the bare minimum telemetry in our institution. We bring them to the ICU. Know that once you've gotten through that first 12 to 24 hours, if the patient's symptomatically improved, that's when we can start having those discharge conversations.
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That's very, very helpful. Thank you again for all of your expertise. We hope to have you back again soon on Run the List.
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Thanks so much. Some content from this episode was generated with the assistance of artificial intelligence.