B (2:42)

A reminder that this and most episodes will be available for CME credit for all health professionals through VCU Health at curbsiders.vcuhealth.org foreign and we are back with the Curbsiders. All right, Jory, this is Lightning Round. We like to do some rapid fire questions to get to know you a little better. So one of the ones we always like to kind of ask is what is one of your like things you like to do that's completely not tied to medicine?

D (3:12)

I am a plant person. I have become very into my house plants and I have accumulated a collection of probably more plants than a person should have in their house. If I'm being honest.

C (3:29)

As there is one behind you, as.

D (3:33)

There is, which it actually has a grow light because it's in an area without a lot of light. But it needed a plant. So I think that's a good testament to my plant problem.

B (3:43)

Do you have like a favorite plant type or plant?

D (3:48)

You know, I like tropicals, so things that you would find in a rainforest. Like I have like a big Monstera which is actually like a variegated version. So the leaves are a little bit green, a little bit white. I have a staghorn fern which like grows almost like antlers. It's a weird, a weird collection I've.

B (4:12)

Accumulated and tropical in Birmingham, Alabama.

D (4:17)

Very valid. I missed them sometimes with a little sprayer. The reason I have started growing more plants is that I moved into a house that actually has a lot of windows so they can get a lot of that hot Alabama sun, which is a positive. So yeah, I don't know. I just started doing it and have been learning about how to care for plants and I find it to be a very calming contrast to medicine because it's like very immediate results. Right? Like you do this and the plant grows or you don't do this and the plant does not grow. And I find it really satisfying in a strange way.

C (4:58)

That is a really good one. I was gifted a plant recently for my birthday and I will have to say it's amazing that it's still alive because I have not cared for it.

D (5:16)

Well, that's the thing. If you get the right and that's the I really like pairing a houseplant with a person. And there are some really good ones that require minimal attention and maybe even thrive a little bit more when you don't pay attention. So it sounds like you and your house plant are really a solid match so far.

C (5:34)

If it needed attention, it would certainly be on the dead or dying spectrum at this point.

D (5:40)

There you go.

C (5:42)

So I guess we'll ask one more maybe let's talk about what is like some meaningful advice or feedback that you've gotten at some point in your career, training, whatever.

D (5:55)

So the thing that always comes to mind for me is from actually my grandfather, he was practicing obgyn for over 40 years. And so it was a really unique experience to go through medical training with him having gone through it in a very different time. And what he always emphasized to me was that it's very easy to get caught up in the path of medicine. Like, we are on this track and we go from step to step. We, you know, we're med school, then we're residency, and then we're fellowship. And he really tried to encourage me to find what I enjoyed at each stage and let that guide my decisions for what I was going to do next, which was a really nice reminder because I. My personality type, I tend to just try to move on to the next thing. And I think in medicine, it was important for me to really figure out what I enjoyed and chase that and has helped me, you know, ultimately find hematology.

C (6:50)

So I think that's a good one. I think it's important to remember that it's really actually a marathon of a career and not the sprint that it often feels like when you're going through training.

D (7:01)

Yeah, totally.

B (7:02)

I think that kind of mindset, though very accidental for me, is probably what landed me on this microphone in this moment. So, yeah, I would agree.

D (7:11)

I love that. Well, and I knew Moni as a trainee, and so it makes perfect sense that she's on a microphone. You're exactly where you should be.

B (7:19)

As are you. We could go a lot of ways, but I think the way we're gonna go is to picks of the week. Meredith, what you got? And I know you're very excited about this.

C (7:28)

I am so trying to really decide where to begin. But we'll start with, as many of you may have heard, the lovely Caroline Coleman's voice on microphone on some of our episodes. Her birthday was this week, and she did the best birthday party, which was a very on theme punk rock birthday party full on with karaoke, of which I did not participate because that's not really my mo. But Moni did because she is always a participator, if that's a word. And do you want to share what you sang?

B (8:02)

Not really.

C (8:04)

At this punk rock themed party, Moni chose Eminem.

D (8:09)

Wow.

C (8:10)

And it brought me so much joy for multiple days, as in still bringing.

B (8:14)

Me joy days later without me. So one of the clownish Eminem tracks. So none of the. I mean, they're all problematic, really, but not one of the truly problematic Eminem songs. Just sort of. At least there's some humor involved.

D (8:27)

That's.

B (8:28)

Yeah, we're not. I can't. I can't excuse that one at all. My pick of the week, really. I might have mentioned this podcast at some point before, but really every, like every two or three episodes is one of my highlights of the week. It's called 60 Songs that Explain the 90s colon the 2000s. Because he did the actually 120 songs for the 90s. And now is streamed into the 2000s. This week's episode was Ms. Jackson by Outkast, which every time I have a patient with a last name Ms. Jackson, that has to come into my head. So that's one and two. It's just. He's a really fun storyteller and just. It's really just one of the highlights of my week. Every time an episode comes out, and especially when it's a song that I know and love, he finds so many weird rabbit holes to go down. And how can you talk about that song for an hour and a half? Well, you don't. He spends about a half hour getting to the actual song he's talking about. So 60 songs that explain the 90s colon, the 2000s, specifically this time, Ms. Jackson by Outkast. All right, Meredith, we have done enough tomfoolery. Please take us to Cash.

C (9:43)

Like I'd love to, Moni. So we'll start here today with Ms. Delvo. She's a 53 year old female with ovarian cancer, currently on chemotherapy. And she has a history of a left sided segmental PE which was diagnosed six months ago. And at that time she was initiated on a Pixaban. She recently traveled with her family to Berlin. So it was a pretty long flight. And with the time changes, she was only like intermittently taking her apixaban. So she thinks that maybe only out of like the seven days she was there. She took like four of the days. And upon return to the States, she started to develop like a three day history of worsening pleuritic. Chest pain and she presents to the ER for further evaluation. Upon arrival, her vitals are noted for tachycardia to 108 and an O2 sat at 91% on room air. She has a CT PE and it shows a left sided segmental PE. Unfortunately, her prior images were done at an outside hospital and cannot be viewed for comparison. So I feel like I see this case or some version of this case on the reg now and just kind of want to maybe start out this conversation with like, are we really talk. Like, how do we define treatment failure and where? What do we do with that?

D (11:05)

So I get this consult probably as frequently as you see the patients because these are really hard questions to answer. And I think it's very important, right. Defining what we're talking about, which in my mind, anticoagulation failure is definitive evidence of a new thrombus despite adequate anticoagulation. And there's a lot of caveats to that of what is a new thrombus? What is adequate anticoagulation? That ultimately is the most important part on how we approach these cases.

C (11:39)

And so when you are consulted then for anticoagulation failure, what are some of the things you want up front in order to start answering those questions?

D (11:48)

So the way that I approach it is really from a perspective of it's extremely rare for anticoagulation to fail. I think that I have to prove to myself that this is truly adequate anticoagulation and new thrombus. So the first thing is understanding if a patient is adequately anticoagulated. So first of all, are they taking the medication? And oftentimes this is requiring a call to the pharmacy to verify fill history because a patient. I've had examples of patients who think they're taking the medication but actually haven't been putting it in their pillbox. And so even despite our patient's best effort to tell us what they're doing, they may not fully understand. And so really getting a full fill history and understanding if we're filling on time to know if we're taking the anticoagulation appropriately. It's talking about how we're taking anticoagulation. A really common thing is remembering that full dose rivaroxaban really needs to be taken with food to be absorbed adequately. So I want to know when you're taking it and if you're taking apixaban, you're supposed to be taking that twice daily. Are you actually taking that twice daily? I have many patients who've been only taking it once. Daily. So really understanding that are they on the right dose for the indication of anticoagulation. So I find a lot of people who may be on meet criteria for a dose reduction for atrial fibrillation, but their indication for anticoagulation is VTE. So they should be on apixaban 5 milligrams twice daily, and they're on 2.5 milligrams twice daily. So lots of information. There's. So that's kind of the adequate anticoagulation piece, and then the second piece is new thrombus. And really it's trying to understand when and where they had previous thrombosis. It was mentioned in the case that the first thing we often want to know about is if we have old images for comparison, when that's available, it's extremely valuable. Sometimes we think about checking a D dimer. That can be a helpful tool if we're really unsure, is this a new thrombus or not, It's a little harder. It ultimately all depends on the side of the vasculature too. So with ultrasound, we can get some more characteristics about whether a clot is new or old. It's a little bit harder on ct, but those are all the millions of things that are going in my head when I'm first approaching a patient like this.

C (14:02)

And what about for history of hypercoagulable conditions?

D (14:10)

So that is kind of the essential piece of once we've proven to ourselves, is this truly anticoagulation failure? What are the things that can lead to anticoagulation to not work? And I think that's another important thing to recognize is that anticoagulation can only do so much. So what are the things that kind of push anticoagulation beyond its limits? I think about Fearco's triad. We go back to right, hypercoagulability, endovascular injury and stasis. So disruption of flow. What are things that are hypercoagulability states? Things like malignancy, like this patient has antiphospholipid syndrome is always one that comes into play, that comes into our differential in something like this. I think about stasis. So anatomical risk factors. Do they have some sort of anatomical setup that is disrupting flow that's leading to the more likely development of thrombosis? I'm thinking about endothelial injury that can be inflammatory states that cause endothelial injury like antiphospholipid syndrome. Those are the things that I'm thinking about. And so in this patient, malignancy is obviously top of mind. Understanding what type of treatment she's receiving for her malignancy is also important. There are certain chemotherapy agents that do increase thrombotic risk in the ovarian cancer space. Bevacizumab shows up sometimes, which can increase the risk of thrombosis. So all of those things are important to think about and consider in a patient like this.

A (15:36)

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B (18:22)

Yeah, I think that this all makes perfect sense to me. Like I can, can see that wheel turning and try to get it turning when this comes up. But some of the specifics are the part where I get a little, I think a little tied up. So one being like, is there a specific number of doses you have to miss before you are saying that this is just you're not taking it versus treatment failure?

D (18:47)

No. It's so hard. Well, and this is where we're venturing out of, into the data free zone, right? Like there's nothing to tell us. How many doses is a dose? Like how many is too many? The way that I think about it though is kind of based on how we think about holding anticoagulation for procedures. How long does it take for anticoagulation based on the agent to get out of your system? So if we're talking about our oral 10A inhibitors like apixaban and rivaroxaban, we hold one day for a minor procedure, two days for a major procedure. So that's for apixaban. Two missed doses in one day, four missed doses in two days. Rivaroxaban would be two missed doses. Cause that's a daily medication. Dabigatran has some other nuances based on renal failure, but that's kind of how I think about it is, you know, missing one dose once a month probably not gonna make me concerned, right? If I have a patient who missed a solid three days, that to me is kind of more concerning. This patient kind of taking it intermittently in her travels. Hard to know, right? I'm more worried that she has an active malignancy. Is she giving a prothrombotic chemotherapy agent. But there's no. I wish Moni, I could give you an a hundred percent solid rule. But the best thing I can extrapolate from is kind of our data for anticoagulation holds for procedure. And just thinking about, usually you've gotta be off for a day or two for it to really be out of your system.

B (20:13)

Yeah. And I'm gonna kind of reference an episode that came out somewhat recently. I think it was 490. On updates in Antithrombot, they talked a little bit about anti 10A levels potentially being helpful. What are your thoughts on that in particular?

D (20:29)

So it's important to first make sure that your institution has an anti 10A that's calibrated to the direct oral anticoagulants. Right. So a general. At my institution, we don't have access to those assays. We have an anti 10A but it's calibrated to heparin products. And so anti 10A's that are calculated to heparin products cannot give you a quantitative measurement of oral factor XA inhibitor activity. And so it's first really important to understand what assays you have available. Some institutions do have anti 10A assays that are calibrated to assess for oral 10A inhibitor presence or absence. The challenge though is it doesn't tell you what was happening with that patient a week ago. Right. It doesn't tell you what was happening in a couple of days before that. Yes. If you have a patient with a new thrombosis and they come in and they have no detectable anti 10A activity, that definitely makes you feel better. But the challenge is often I find in these patients is that, well, maybe they just weren't taking it consistently a week ago, a month ago. It's a little bit harder. I will say though. So if you are at an institution that has a heparin calibrated anti 10A, I kind of consider it like an on off switch. So if you don't have any detectable anti 10A activity, you can say that your patient does not have a clinically significant amount of an oral 10A inhibitor in their system. It just can't tell you how much it doesn't give you that quantitative piece. So it's kind of like a yes no if they have it in their system or not.

B (21:55)

Okay. Okay. Yeah. No. I would have never thought about calibrate like the calibrations like med specific, but kind of like almost like high sensitivity troponins versus normal troponins to think about it this way.

C (22:07)

Yeah. So Jory, I think the one that this comes up with a lot is apixaban because it's a twice a day medicine. So like, I feel like people will be really good about that morning dose, but then that evening one I'm not so sure.

D (22:18)

About.

C (22:19)

But it sounds like maybe that's not enough if they're missing one or two of those evenings.

D (22:25)

Yeah, I mean, if you're saying maybe one or two evenings a month, but I've had patients like that didn't understand that they were supposed to be taking it twice daily and they were only taking one pill, then to me, you know, the medication is kind of wearing off. So you are inadequately anticoagulated if that's like a consistent pattern. But if I have a patient that's like, you know, once a month, I just forget my nighttime dose. That to me would be less concerning, that that would be a driver of a new thrombotic event.

C (22:53)

Got it. And does that like being anticoagulated to not anticoagulated, does that change their thrombotic risk at all? Like, if there's a lot of, like, that fluctuation going on.

D (23:05)

So kind of to the question, like, is there like a rebound hypercoagulability? You know, I don't think we really know. Again, kind of if we extrapolate from when you stop anticoagulation at the end of, you know, you know, a treatment course for a VTE, you treat for three months, we don't ever taper. We don't really worry about there being any sort of specific rebound. So not. I don't. I don't really consider that in my practice.

C (23:29)

Okay.

B (23:30)

No, I think we kind of covered like, the difference between particular rivaroxaban and apixaban in terms of, like, how you think about their effect in terms of anticoagulation. Are there any other considerations with those two? Like, other than their frequency, Is there any other difference in terms of their anticoagulant effect?

D (23:47)

Yeah, not really. I think it's important to remember we often use the term direct oral anticoagulant. And that includes 2 categories. That includes our oral 10A inhibitors, which is apixaban and rivaroxaban. They have an XA in the name to help you remember that. And then you have your oral direct thrombin inhibitor, which is dabigotran. Edoxaban used to be out there. We don't see much of that anymore, but we often in doac, those are two different mechanisms of action, so I do use them interchangeably. But just important to understand that an anti 10A would not be relevant to a patient on dabigatran. The other thing that's maybe relevant when you're thinking about anticoagulation failure questions is thinking about the sites of absorption of these different medications that are different. And so that's something we haven't really touched on yet. But I think is important to think about when you're talking about anticoagulation failure is considering if your patient has risk factors for that could affect their ability to absorb medications. One thing that's unique about apixaban is that it actually has a significant amount of colonic absorption and so may not be as ideal for a patient who, say, has had a hemicolectomy or has colonic pathology versus rivaroxaban, which does not have colonic absorption. But apixaban is maybe better in someone who's had like a gastric band where rivaroxban is maybe not as good. So there is variation in how the medications are absorbed. That's worth thinking about. And as I did allude to before, that rivaroxaban is dependent on food to be taken with food for absorption, which apixaban is not. So something that you should be thinking about if you do have a patient that you're concerned for. A breakthrough thrombotic event is just understanding do they have altered gastric anatomy for any sort of reason, Any history of bowel surgeries that would be relevant.

C (25:30)

That's really helpful. And I think that's a good segue into kind of the other. The next set of questions I had, which is kind of going back to the underlying conditions that someone may have. And I feel like specifically we can start with some of, like the higher yield ones, but for the doacs, I feel like there's always the question of BMI and if that's a limitation and then what to do with renal failure and where do we kind of draw the line with renal failure?

D (25:56)

Great question. So for bmi, for a long time we were really hesitant to use the direct oral anticoagulants. The International Society of Thrombosis and Hemostasis a few years back came out with kind of a review of the data and expert consensus that it really is probably okay to use these agents in people that are. We're talking more BMIs, 30 plus 40ish. I do still get a little hesitant when we're talking about BMIs of 50 BMIs, 55 BMI 60. We just really don't have any data on that population. So what I sometimes think about, if I do have a patient like that with a new VT el is thinking about, particularly in that early period of time, an alternative anticoagulant, something like warfarin, because if they've had a Big event and I'm just not really sure. And they are at, we're talking a very high bmi. And then long term, we now have some new data from the Renove clinical trial from came out end of last year that basically looked at long term secondary prevention of venous thromboembolism using reduced dose. So rather than a pig span 5mg twice daily, you can use 2.5mg twice daily. Seems to have similar efficacy in thrombosis prevention and a lower bleeding risk that I'm more comfortable kind of long term for secondary prevention. If a patient has a BMI of 5560 that they probably don't need that full dose of apixaban anyway. So I would just keep them on the 5 milligrams twice a day. So it's really kind of what we would consider kind of standard obese patient in that 40 range. We do feel comfortable with the extremes. I do still have a little bit of hesitation. The question about renal function is another great one that comes up all the time. And I think originally, right, we felt like we were going to warfarin for this. And more and more I feel more comfortable using the direct oral anticoagulants. A lot of that comes from data from the atrial fibrillation space of using apixaban in particular because it is less dependent on renal clearance. So I really go to apixaban in patients with renal dysfunction and we've kind of extrapolated that to the VTE space of using apixaban there as well. There's not data to tell us if we need to dose reduce these patients. So I don't tend to dose reduce based on renal function. We don't again have that FDA label guidance that we have for AFIB where we're supposed to dose reduce based on those criteria that do include renal function. But ultimately we know that warfarin's not a good option either. Right. Patients with really severe renal dysfunction don't do well with warfarin either. So in general I am comfortable using a direct oral antiquarian and usually apixaban in patients with renal failure.

C (28:37)

And renal failure being like end stage renal on dialysis or do you stop at a certain point?

D (28:44)

So I do use an end stage renal disease on dialysis. Those are the patients that I'm really looking for an opportunity to reduce their dose. Again, not that I have clear data to do that, but again, pulling from the data that we have now supporting lower doses for secondary prevention, that's the patient that I'm going to dose reduce really quickly in the VT el space just because I worry about bleeding risk.

C (29:06)

And that would be like a standard three months or so.

D (29:11)

Ideal. Yes. Kind of depends on the patient. Right? You know, we do know kind of the standard treatment course for a new VT El is three months. Because we know based on data investigating the natural history of thrombosis, that's how much time it takes for an acute thrombus to heal. That being said, if you kind of think about how we feel about procedures or holding anticoagulation for VTE, sometimes we move it and we're like, well, if they really need a procedure, six weeks is probably okay. So if I have a patient that's really high risk of bleeding, maybe it's six weeks. I might think about it. But I'm in a very data free zone there. And it's really the challenge of hematology is this imperfect balance of bleeding and clotting and how to strike that balance. And I think the reason some people straight don't. I'm not gonna say they don't like it, but hematology makes them nervous. But part of what I love of hematology is there, it is very. There's no right answer. And so it's really having that risk benefit conversation with the patient. It's really understanding your patient's risk factors and just making the best decision that you can with that individual to try and strike that optimal balance.

C (30:13)

Yeah, I think that's helpful. I. Every time I prescribe like a DOAC and they're on dialysis, I feel like I put up a little prayer sign and just hope for the best.

D (30:26)

Well, and I think that's true of all anticoagulation and dialysis patients. Right. Like, we just know that, that dialysis is a huge risk factor for bleeding. So the way that I think about it is I do the exact same thing, but I also review their med list. Like, is there an aspirin that I can get rid of? Like, is there something else that I can do to optimize their bleeding risk and like, do my best to just set this person up for success as much as possible. But I feel you on that.

C (30:52)

Yeah. Okay. And then you kind of alluded to this earlier, but I've had a couple like this recently and I just, I thought they were good reminders for the hospitalist. But the anatomical kind of issues, because in the ones that I've had recently, what I realized was happening is like, those patients were coming in and were just like, Continuously anticoagulating. But like their anatomical feature is really what's kind of driving their acute to really a chronic clot. And one, that was not well explained to the patient. And two, I think it's something that like in hospital medicine, mine were like clot treat, clot treat, but not like, what do you do in this long term situation.

B (31:32)

Yes.

C (31:32)

So I was hoping you could talk a little bit about that.

D (31:35)

Yeah. So those anatomical things I think about, you know, you think about Maith Earner, which is leads to DVT in the left lower extremity due to compression from the overlying artery. We think of thoracic outlet syndrome, where we have compression related to basically all this important stuff that's hanging out in your shoulder. The other thing that I think about and you kind of mentioned is post thrombotic syndrome is so if a patient has had a previous event and they develop scar tissue within the vessel, that disrupts flow as well. And so those are the patients that I kind of come back to. Anticoagulation can only do so much. That's when the stasis piece of your vircos triad just really comes into gear. And I think the challenge in those patients is, I think like you said, we start to just focus on the anticoagulant and we don't think more broadly about if there's anything else that we can optimize. That being said, putting a stents in veins is only something we do if we absolutely have to. Veins do not like to be stented like arteries do. And that is in itself, putting a stent in a vein is an anatomical setup for recurrent thrombosis. So not that we need to be going and doing all sorts of crazy things inside blood vessels, which is usually not a good idea, but I think your point is really important of making sure that we're not just focusing on the anticoagulation not working. Making that kind of bigger question of do we need some broader, you know, it's not just a lower extremity ultrasound that's going to capture May Thurner. We're going to need more proximal imaging of the vasculature in order to see the iliacs. And so someone's got to think about that. Rather than the ultrasound shows another clot and we just prescribe another anticoagulant.

C (33:09)

Yeah, I think that's helpful.

B (33:11)

Yeah. And along the lines of ultrasound, kind of going back to our case a little bit, we don't have a prior imaging, which is incredibly frustrating. And also, like, day one, med school, like, you're taught, right? Like, what's the context? So if you get the read back, like, if you get, like, the little report sheet back and it seems like it's kind of in the same spot, is that sufficient or. Yeah, yeah.

D (33:37)

How do you make that determination of what's new and what's old? It's so true. So the one piece of advice here is to pick up the phone and call your radiologist. And so I really encourage that. I try to do that because oftentimes they have insight that they just can't necessarily put in a report. So there are features of a clot. So if we talk about ultrasound, there are features of a thrombus that make it appear more acute or chronic. So an acute clot tends to be soft. The vein tends to dilate in reaction to that clot, as opposed to a chronic thrombus, which tends to be scarred down. It's kind of scar tissue. It's not clot anymore, and the vein tends to be more contracted. And so a good radiologist can kind of take you through some of that, and you can even just read the report to them and say, hey, there was clot there at this period of time, just, you know, share the information that you have. And they can kind of sometimes glean more out of the images than what the report says. Connecticut has some of that ability as well, maybe not quite as much as ultrasound, because it's not quite as dynamic. But a radiologist who is really knowledgeable is going to be able to give you some clues kind of similarly, in the pulmonary vasculature with a chronic clot, you get some basically, like, changes where it looks more integrated within the vascular wall. At least that's what the radiologists tell me. I'm not a radiologist. But two, they can get some distal changes in the vessel where it kind of scars down that make it look more chron. So don't take the report at face value, I guess, is my advice is so gather whatever information you can, even if it's just a report, and then pick up the phone and talk to the radiologist and say, like, hey, is there anything else you can give me to help determine if this is new or old?

B (35:18)

All right? And say you do have the old imaging and it's bigger, like it's grown. Is that sufficient to say that somebody has had treatment failure?

D (35:29)

So, yeah, these are so important. And so the. The important thing to remember is there. There was actually a really nice publication by Sven Olson, who is at Oregon. This was a couple years back in research and practice in thrombosis and hemostasis. That basically looked back at studies in VTE and basically showed it's not uncommon to have asymptomatic propagation within the first month of starting anticoagulation for VTE when we're looking by ultrasound. So the important thing is sometimes I get consults of, you know, the patient was still having some symptoms, but not necessarily any worse. They're just still in the recovery phase from an acute dvt. Somebody gets another ultrasound to see what the clot is doing, and it looks like it's bigger. That, to me, is not that the anticoagulation is not doing its job. That publication kind of says, keep doing what you're doing. Like, that's just kind of clot evolution. If you're a couple years down the line and the patient has new symptoms associated with it and you have a D dimer elevation, let's say that's more helpful. The important thing to remember, though, is that patients do. Many patients do have post thrombotic syndrome. Right. They have symptoms related to scar tissue within their blood vessel. And so it is helpful to have a really detailed conversation with them to understand, do you have chronic swelling? Like, is this day maybe still on the spectrum of, you know, are your symptoms you're having consistent with what you've been having for the past two years? Or is this like, no, I haven't had any previous swelling. Now my leg is huge. It's red. This is all brand new. Those are two very different conversations. Because the most common thing that I see is those patients. And you, you know, once you take the time to talk to them, you say, yeah, I actually swell a lot of times today it just, like, felt a little bit more different. And like, maybe the clot on the ultrasound doesn't look that much different than it did before. So it's all about getting that, like, full picture, I think.

C (37:16)

Yeah.

B (37:16)

And along those lines, the example you kind of used was about a month. And I think one of the things that we read in preparation started around three months before you really start thinking that this. That treatment failure or recurrence was kind of. Is that roughly around the timeline you start thinking about recurrence and. Or like.

D (37:38)

Yeah, I mean, you know, it's like I said, there's remodeling that happens. So it's like, by imaging, it's really hard to know. So your. Your symptoms are. Are so important in that. In that piece. And I do find Again, I, I don't necessarily have any. This is maybe my practice. No data to tell me that this is a helpful tool. But a D dimer is kind of helpful, right? If you have like a stone cold normal D dimer and you feel like the symptoms are that different and you're just like the ultrasound looks a little bit different. Like I'm not too worried about that. And again, coming from the space that I said in the beginning, anticoagulation works the majority of the time. Like you really have to convince me that it's not working. And so before making a change. Because what I see a lot of times is it's a very quick switch to say, well, new clot on apixaban, I've got to put this patient on warfarin. And committing a patient to warfarin, which is an agent that we know comes with more risk, leads to a lot more difficulty for a patient. There's a really high bar I have to meet before I'm thinking about that for a patient. So I think like coming to these clinical encounters with it in mind that anticoagulation works the majority of the time. Should frame how you're viewing all that information, if that makes sense.

B (38:52)

Yeah, it does. And I'm going to avoid the get off my lawn about how kids don't know about warfarin anymore to ask a question along the lines for doacs, which is when warfarin we know if someone's taking it and that kind of thing. But with doacs, do we have something similar to kind of help us with that?

D (39:09)

Yeah. So I mean we have, like we mentioned, we have the anti 10A and like I said, know what you have available. But if you only have a heparin anti 10A, if they have detectable drug, that means they have taken some of it somewhat recently. But I think it's important, I think for particularly when the DOACS first came out, there was this thought that like if we're not sure if a patient takes is taking their medication, that we need to put them on warfarin. And I think that pendulum has really swung because we're just not setting people up for success because taking warfarin is really hard. And so knowing that a patient is taking your medication, to me I depend on fill history like that's the most reliable way for me. And I validate that myself. I pick up the phone and call. And so for me a question of if concern about being able to comply with medication is not a reason to put on warfarin and it's a reason to put on a once a day oral medication that requires no monitoring.

A (40:06)

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C (41:55)

So Jory, you've mentioned several times now using dimers and my hospitalist brain is like why would I get another dimer? I already know they have a clot. So can you be specific as to like when it's valuable to you? Cause I think I have a feeling you're using it much more than we are.

D (42:15)

Well, and opening the dime or can of worms is always a scary one. But the time that I'm using it is if I have a patient and I'm unsure if this is a new thrombus or not. And it's really to kind of reassure me if I am looking at the imaging, it doesn't look that different to me. And their D dimer is stone cold normal. Like I'm less concerned that this is a new rip roaring thrombus. That means I need to change. Their anticoagulant versus imaging is maybe a little bit different. Their D dimer is quite high. They're really having symptoms. That to me is more of a concern that I need to make a change.

C (42:56)

And you would only be checking that after that like three month time frame?

D (43:03)

Yes, well, and yes, like theoretically though, like, I guess it's kind of tricky, but I would really be using it only in those questions where I'm concerned that we're talking about like a new recurrence. Like kind of if we're still on the tail that I think this is like the existing clot. You're right. In that first three months, like hard to know, but three months out, like your D dimer probably should be normal at that point. But it's not the only. The important thing is that's not the solo decision maker. Right. This is a piece of the puzzle. Because I think where we get into trouble is when D dimer as this like crystal ball to tell us what's happening with a thrombus. And it's not that for all the things that you know even better than me, um, but it's a tool in my toolbox. When I just really don't think that this is a new thrombus. If I have a normal D dimer, it just makes me a little more reassured that I'm on the right track.

C (43:55)

So hypothetically, you're gonna really make me.

D (43:59)

Put my finger down, which I respect.

C (44:00)

Um, well, it's not that I think the one that one of the ones that I get called a lot and I'm wondering if the dimer would be helpful. Patient got new diagnosis of dbt, got put on a Pixaban, comes back somewhere in that four to eight weeks later time frame saying symptoms are worse. And so then they get readmitted. And like while I'm trying to figure out, you know, because inevitably they've mostly been taking the Apixaban, but you know, they're. And so you're trying to like rationalize, is that enough to have caused something worse? So in those, like in that timeframe, would that dimer be helpful or that's still too early?

D (44:44)

Probably not. I mean, cause at that point, like we talked about, like imaging is still remodeling, Lots of things are still changing. So that's still in that period of time where I would not consider calling it a failure. What I do sometimes in these patients is, and we haven't talked about like agent switching yet. And I'm sure that's where we're going at some point. Point is if I do have a patient and they feel like their symptoms are getting worse and I'm not really sure what to do, sometimes I think about putting them on something like a parenteral agent like Enoxaparin for a period of time. Not saying that they can't, not saying they have failed apixaban and they can never be on a Pixaban ever again, but saying, well, let's get something that we know can be consistently administered. I can know if the patient is receiving it. I can see if that can help in the short period of time, help relieve some of their symptoms. And then once we're out of that three month window, then I switch them back to apixaban. And so I do think from a hospitalist perspective, what from a hematologist, the thing that I ideally don't want to happen is for this person to be put on a heparin drip, which is what I see sometimes. Right. Heparin drips, which is a whole nother soapbox I could get on. Right. Are not a. They're no more powerful than anything else and they have very variable pharmacokinetics. And you often end up in times when people are either over anticoagulated or under anticoagulated. And if you're at an institution that uses ptts to monitor your heparin, it becomes, even if you're using anti 10A's, it's really inaccurate. But your PTT can sometimes be affected by direct oral anticoagulants. So for all of those reasons, heparin is not your friend. And so that to me is the potential for a miss. I think in that situation, what I would talk about with the patient is if they are amenable, if they're concerned that the apixaban is leading to changes that we would consider a period of time on Enoxaparin and that ultimately long term, once their symptoms stabilize, once their clot has stabilized, that we would ultimately switch them back to an oral agent.

C (46:44)

Okay, I can get on board with this.

D (46:46)

Okay.

C (46:52)

All right. Do you have anything else from.

B (46:55)

No, I think the, the monkey. The elephant in the room. Not the monkey and the elephant. The elephant in the room is what you're about to ask.

C (47:01)

Yeah.

D (47:01)

Is agent change?

C (47:03)

Yep. Yeah, let's just go there.

D (47:05)

Yeah, let's do it. No, and we've already, I think, started touching on some different things. I think it's worth Mentioning that, you know, there are some conditions that we want to make sure that a patient doesn't have where we worry about certain anticoagulants not working. And the one that I think most people are familiar with and comes to mind is antiphospholipid syndrome. We do have data that compares warfarin to both apixaban and rivaroxaban, and we see an increased risk of arterial thrombosis in those patients. That being said, there is a lot of debate in the hematology community. I think there the pendulum has kind of swung and we're now saying every patient with antiphospholipid syndrome needs to be on warfarin. I think there's hopefully still some nuance to that, that there will be ideally some patients that we can identify that can be on direct oral anticoagulants. There's patients out there with antiphospholipid syndrome that have been on it and haven't had problems. But in general, that is something that I'm thinking about. In a patient with a recurrent thrombus, the important thing to remember and to familiarize yourself with is the diagnostic criteria for antiphospholipid syndrome. There was new diagnostic criteria published by ACR in Eular. It's E U L A R, which I should remember what rheumatologic professional society that is. But I'm a hematologist and I forgot was published in 2023 and basically updates. It's really research criteria. But many people are extrapolating to the clinical space but gives more nuance to what we call antiphospholipid syndrome. Because the other thing that I see happening, unfortunately, is a patient has a mildly elevated anticardiolipin, IgM, doesn't meet diagnostic criteria, and that patient is then committed to lifelong warfarin. And that's what we don't want either. So that is something to think about when we're talking about picking agents. But ultimately, if I have a patient and let's say we've jumped through all these hoops and we really think that they were, let's say, on one of our oral 10A inhibitors, and they have a new thrombus, what do you do? There's no data to tell us what to do here. We have no data to tell us that one agent is better than another. Do you switch from apixaban to rivaroxban? Do you switch to a different mechanism? So do you switch from apixaban to dabigatran? We don't know do you have to switch to something like warfarin? Oftentimes, kind of alluding to what we just talked about. I try to think about putting them on enoxaparin for a period of time as I start to figure out what other things could be causing them to have a breakthrough thrombus. Right when we're looking for those anatomical causes, when we're looking for hypercoagulable conditions, like, that's something. Rather than getting, like, rushing them to warfarin, which is a big life transition and requires a lot of resources, an ox parent, I can kind of control and manage as long as my patient is comfortable with injections, which is important to, of course, make sure if ultimately I have a patient that I really don't have another explanation. It's a conversation with them. Do they think warfarin is feasible for them? As Moni mentioned, warfarin is a great anticoagulant. Many people are afraid of it, but it's been around for a long time and works really well for a lot of people. I have plenty of patients that are on chronic warfarin, and they do fantastic, but it has to be the right patient. And so I think it's ultimately a conversation with them. Sometimes it does make me feel a little bit better if I'm switching from a 10A to a direct thrombin inhibitor. Maybe it's a different mechanism of action. If I have a patient who really can't be on warfarin for whatever barrier they might have. But it's a evidence no man's land, there's no right answer. So it's really talking to your patient and figuring out what they think is going to be most feasible for them.

C (50:48)

Do you ever switch apixaban to rivaroxaban or vice versa?

D (50:54)

I guess, yeah, probably not. I mean, I think unless there's kind of something that, you know, really the only time that I'm switching is like, a patient, like, can't take a medicine twice a day, so once a day works better. You know, there's. There's really. I don't think we have any data to say that one is gonna work any better than the other. So again, it's just asking those questions as, like, what's the driver? What's the problem here? But in my mind, like, I'm not sure that that's any better. And what I see sometimes is, like, again, the focus on just, like, switching to another medication and not, like, doing the broader question of, like, why, like, what was the original, you know, what's the source of the problem. Do they have a myeloproliferative disorder? Do they have pnh? Like, do they have something else that's going on that needs something more than anticoagulation? So it's not a switch that I usually make unless it's just easier for a patient to take a different medication.

C (51:46)

And when would you favor, like, I feel like I never see dabigatran. I know we, like, talk about it, like, but to me, it really feels like it's in an esoteric state space.

D (51:56)

Yeah, it's so funny. And the one place that's really interesting in the dabigatran column is it seems to be based on the limited data that we have best for menstrual bleeding. So in people who menstruate, it seems that dabigatran actually has the best profile for not, you know, worsening menstrual bleeding. Apixaban is second in that. Rivaroxan is third. So. So that's one place where I will think about Dabigatran is if I have a patient who menstruates and struggles with heavy menstrual bleeding on anticoagulation. But other than that, you're right. We don't necessarily go to it. You have to think about renal function is another thing. It's just that you have to pay attention to. And so many of our patients are complex. But in a young menstruating patient, it is a good option.

C (52:44)

I don't have a lot of those, so that might be.

D (52:46)

Why don't you. I think that's why it doesn't come up very much. But yes, in your practice inpatient medicine, you probably wouldn't see a lot of that.

B (52:58)

Specifically at the va. Yeah.

D (53:01)

Oh, gosh, yes, There you go. But for those in other spaces, it is an option. And again, it is a different mechanism of action. Do I know that that mechanism of action is any better than inhibiting? Inhibiting 10A. I do not.

C (53:17)

So, okay, so then I think you kind of were alluding to this. But just for like, the one other conversation I get into, which is specifically into the risk benefit of it is like, if I have someone who already has adherence at shoes, like, something is hard, whether it is a pixaban or rivaroxaban, I personally don't see how warfarin is going to be better because I don't see how the adherence plus clinic physics are going to be better. And so sometimes I wonder if, you know, just then making sure they are on rivaroxaban to Be, this is a once daily. You don't have to do clinic visits. And if this still doesn't work, I have no ideas left. But I just like, how do you really weigh that risk and benefit? Or is that just kind of the best options that we got right now?

D (54:08)

Yeah, no, I think, I think you really nailed it. I do think that that was kind of the older approach, but I'm with you. I mean, I don't think I could take warfarin consistently. Like, it's really difficult and it's a huge ask for patients. And so I really think it's really describing to them what warfarin is and what warfarin means. And some people are really motivated. Thrombosis can be really scary. And so I have a lot of patients who are really, if they have any concern for recurrence, they want to know that it's not going to happen again. And so for that person, sometimes warfarin is the right answer because it's something they can measure. It's something where they do have more feeling of control and agency. And it is a really different change. And I feel comfortable saying that, you know, this is probably, if we do have a true failure, this is probably what most people would recommend doing. But I think you're exactly right. If I have a patient, I have any concern that they're not gonna be able to stick with what warfarin requires or even you put a patient on warfarin and then some people are just really hard to control. And like for a patient who's had breakthrough thrombosis, like, that's not ideal. When I know I can have a patient taking a medication once a day and that's better. I do have some colleagues who sometimes, you know, if we have these really severe patients with thrombosis that venture very far out of the evidence zone and we're talking about things like adding aspirin to a direct oral anticoagulant or using a higher dose of a direct oral anticoagulant. But that's something that I would say, like working closely with a hematologist just because they're going to have some more experience doing that. Makes sense. Because I don't think warfarin is the holy grail of anticoagulation failure because it is in itself, as you mentioned, is just a setup for a lot of barriers to adequate anticoagulation.

C (55:54)

Yeah.

B (55:55)

All right, I'll take us to our second case. Mr. Hitz is a 65 year old man with a history of diabetes, hypertension who comes in with a one week history of intermittent palpitations associated with dizziness and generalized fatigue. Upon arrival at the ed, he is found to be tachycardic and he's an AFIB and basically everything else checks out. He's stable, his labs are unrevealing, he's admitted to medicine and cardiology, remained recommends a cardioversion because he's been having symptoms for a week. They do a TEE and they find an LV thrombus, which is always fun. And he started on a heparin drip. Jory's favorite.

D (56:32)

You know, I feel okay about starting.

B (56:35)

DOACs and patients with DVTS and PEs and AFib and stroke prevention, but basically any other indication and I turn off my brain and call you. So can you help me navigate this situation? Because I really just never know what to do here.

D (56:53)

Yeah, no, it's tough because the conversation continues to evolve and change. And so we can talk specifically about LV thrombus. There was a lot of concern based on some initial, really retrospective observational data. And the cardiologists always have fancy names for their trials. There was the Red Velvet trial that looked. I know, right. Good name. But that suggested or raised concern that direct oral anticoagulants were not effective as warfarin. That literature has really shifted and there was actually, I think it was like a scientific statement from AHA a couple of years ago that came out and said that direct oral anticoagulants are an acceptable alternative to warfarin. And so it does suggest that the data supports that it is safe to use the direct oral anticoagulants for LV thrombus. And pretty consistently the data has supported that. The other thing that sometimes comes up that I get questions about is, you know, thrombus in abnormal locations. So cerebral venous sinus thrombosis or splanchnic thrombosis. And at this point I feel comfortable based on observational data that it's okay to use the direct oral anticoagulants. What I'll often do is if I have any concerns is it is a kind of a quick literature search of direct oral anticoagulants in this area of the vasculature, like just as a double check. But there's nothing that really comes comes to mind for me, like anatomically as a specific area, aside from. Right. We're talking mechanical valves, things that we know we have to use the warfarin over the direct oral anticoagulants. But aside from that, from like an anatomical consideration, there's nothing that really stands out to me that I say I can't use a direct oral anticoagulant in this patient.

C (58:32)

And so really then based on our last case, antiphospholipid syndrome and mechanical valves and like, anatomical things are kind of our two most obvious contraindications.

D (58:46)

Yeah, those are kind of the two big ones. And then we alluded to this earlier, but the like, really extreme obesity, I'm talking BMIs 55, 60, gives me pause. No data there, but that's another population that I sometimes think about. But aside from that, I think fortunately we have enough data at this point to support use in the majority of indications.

C (59:11)

And for those that like, you're referring to, where you're like maybe new hepatic vein thrombus or something like that, like, that's not the most commonplace or LV thrombus or whatever, do you still have a conversation of risk benefit with the patient and still talk about warfarin or are you still like, I feel good about the doacs and I am still going to favor the doacs over warfarin?

D (59:38)

Yeah, you know, I, I typically am just going to the, the oral 10A inhibitors. You know, I think, because when we have, you know, again, we're extrapolating from the VT space, but warfarin is associated with a higher bleeding risk. The literature consistently shows that. And so, so I, I do feel comfortable that the data supports that generally it is a safer and more effective option. You know, the other thing that we didn't talk about is consideration of bleeding and how to make that, like, transition. Like, when do you feel comfortable? Maybe that's another situation where, like, I want a parenteral agent like enoxaparin as opposed to a direct oral anticoagulant that, you know. You know, you mentioned, like hepatic artery when we're thinking of like, you know, massive portal vein thrombus and you're worried about big varices and bleeding, like, that's maybe something else where you might be thinking about another agent and enoxaparin might come to mind. I didn't mention pregnancy and breastfeeding, which I should mention as well, is just to remember that our direct oral anticoagulants should not be used during pregnancy or during breastfeeding, that enoxaparin is really our best option in pregnancy. During breastfeeding, enoxaparin or warfarin can be used. So in people who are breastfeeding, warfarin is an option. So that's Another population to think about. But overall, I do still go to the doacs first. And I don't necessarily introduce warfarin into the conversation unless I feel like there's a specific situation that warrants it.

C (61:11)

I'm gonna ask one other like, rogue question. What about so, and this has never really come up for me, but I just remember like, because I was definitely in training when DOACs were coming out and like warfarin coming into favor or not Warfarin coming into favor, warfarin falling out of favor, and I'm in. But one of the things we would talk about with patients is like reversibility and the ability to just have that reversible agent available. And I know, like, there's some, I don't know, questions around, like all the stuff right now. And so I'm just curious if that like it comes into this conversation at all, like with the rest of the benefit.

D (61:59)

Great thing to think about. And that's actually what I get. A lot of people who've been on warfarin for a long period of time are hesitant to think about direct oriented coagulants because they like that idea of having a reversal agent. I think that was the initial concern. I think more and more what we understand is that particularly if we're dealing with like really severe catastrophic bleeding events, things like intracranial hemorrhage, we're not really sure that reversibility makes a significant difference in clinical outcomes. It's once you have the bleed, it's the bleed itself that leads to the significant morbidity and mortality. And we know that warfarin is associated with a higher bleeding risk than the direct oral anticoagulants. But that being said, so what does it mean to how do we reverse the direct oral anticoagulant? So remember that our oral 10A inhibitors, apixaban and rivaroxaban do have a currently FDA approved agent for the reversal index in an alpha that has come under a lot of scrutiny based on recent trial results from Annexa I due to particularly concern for thrombotic risk associated with that agent and that it's only really available at large centers. And so kind of a small community place is not going to have access to that. So what is reversal for a placement? It doesn't have that. Usually it is a four factor PCC and four factor pcc. There's kind of different dosing and strategies for that. But I would consider that kind of the standard reversal for the oral 10A inhibitors. Remember that dabigatran is a different mechanism of action. It has a medication called iterucizumab that is approved for reversal. It too may only be available in specialized centers. But again, that to me, and when I have a conversation with patients, to me it's all about the concern is the initial is the bleed itself and trying to prevent the bleed itself. Because I do think once the bleed happens, oftentimes whether or not we can, you know, reverse that in a certain way is often not the biggest driver of morbidity and mortality.

C (64:01)

I think that was great. Do you have any take home points for the listeners?

D (64:07)

Well, I think that it's just acknowledging that these cases are really tough. So I think you guys highlighted some really important questions that we get, is that, you know, what is anticoagulation failure? I think to come into that encounter saying that anticoagulation really doesn't fail. So, like, what are the things that you really have to do to prove to yourself that this, that you really need to change agents for this patient? Like, is this new? Can I talk to a radiologist? What other information do I need to get? Do I need to call the pharmacy and make sure that this patient was taking it as they should? Because making that change is a really big deal and not something that should be done unless we're really confident that the patient can't be on an agent that is proven to be effective and safe. But if that's the case, you venture into a data free zone. So think about involving a friendly hematologist if you have that option, but thinking about switching to a different mechanism of action, but really understanding your patient's ability to take these different agents and what that means for them and thinking about what other things other than the anticoagulation are at play. Do they have a hypercoagulable condition? Is there an anatomical issue? Do you need to send more testing to consider other etiologies? Because oftentimes when anticoagulation fails, it's because there's something else that's going on. So I think those are my take home points. And hopefully folks listening feel a little bit more equipped to encounter these really challenging cases. But hopefully just a therapy session to say it's hard and we all feel.

C (65:43)

You, that's what we're here for, the therapy.

D (65:46)

There we go. Thanks, doctor.

C (65:53)

So this has been another episode of the Curbsiders, bringing you a little knowledge food for your brain hole.

B (65:58)

Yummy.

C (65:59)

Still hungry for more?

D (66:00)

Yep.

C (66:01)

Join our Patreon and get all episodes ad free, plus twice monthly bonus episodes at patreon.com curbsiders you can find show notes@the curbsiders.com and sign up for our mailing list to get our weekly show notes in your inbox, including our Curbsiders Digest, recapping the latest practice, changing our Articles, guidelines and News, and internal medicine.

B (66:19)

Here at the Curbsiders we're committed to high value practice changing knowledge and to do that we need your feedback so please email us@askcurbsidersmail.com it also helps a ton when you subscribe, rate and review the show on YouTube, Spotify or Apple Podcasts. A reminder that this and most episodes are available for CME credit for all healthcare professionals through VCU health@curbsiders.vcuhealth.org A special thanks to our whole Curbsiders team. Our technical production is done by the team at Podpaste. Elizabeth Croto runs our social media, Jen Watto runs our Patreon, Chris the Chew Man Chew moderates our Discord, and Stuart Brigham composed the theme music. And with all of that, until next time, I've been Moni Amin and I'm.

C (66:57)

Still Dr. Meredith Trubitt. Thank you and good.

D (67:08)

Sa.