← The Fellow on Call: The Heme/Onc Podcast
The Fellow on Call: The Heme/Onc Podcast
Episode 131: VTE Series-Approach to workup and initial management
Ronak Mistry, Vivek Patel, Dan Hausrath
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- [00:01]
A
This episode is sponsored by our global research partners. Want to contribute to the advancement of medicine? Make some easy money while sharing your thoughts with market research surveys. Learn more and sign up using the special TFOC link on our website and in the description box below. Hey, friends. This episode of the Fellow on Call is not meant to be used for medical advice and is intended for educational purposes only. Patient information has been modified to ensure privacy. The views expressed in this episode do not necessarily reflect the views of our employers. Enjoy. Welcome to another episode of the Fellow on Call, the Hemong Podcast. We're coming at you from Rouleau University Medical Center. I'm Ronak.
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B
I'm Vivek.
- [00:41]
C
And I'm Dan.
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A
This week we embark on a new journey, starting a new series, a very, very highly anticipated series, one that many of you have been asking about. And this is all about how we approach anticoagulation management after an acute clot. So VT el everyone's favorite hypercoagulable workups.
- [01:00]
B
I'm excited to get into this thrombosis series. It's going to be pretty interesting. We have a lot of good content for everybody, so buckle up. We had a little bit of time off. So excited to get back to it.
- [01:11]
A
So it has been a few weeks at this point since the last time the three of us regrouped to do a recording. What have you guys been up to? What have you been doing with your time? I mean, listeners, I will say before they get started, we acknowledge that it has been a little bit of time. We had just been taking care of ourselves and some things in our personal lives, catching up on work, catching up with family, things that we really need to keep us going. And so hopefully this serves as your reminder that you can't take care of other people if you don't look after yourself. So, Vivek, what have you been up to in the last few weeks?
- [01:42]
B
You know, it's been really good. I've literally done nothing, which is great. I've gone to work, I've come home, not had this extra thing to worry about because we spend so much time making these episodes and we love doing it. It was good to just have that break to just kind of nothing. Went to the gym, you know, watched some good tv, cooked some good food. So it's been a good time. You know, I made some homemade chicken parm from scratch, did a couple of other recipes. So it's been a good time.
- [02:09]
C
Yeah, same here. You know, just visiting some family, doing other things around the house, getting things a Little bit cleaned up, some spring cleaning, all that normal stuff. It's been nice.
- [02:17]
A
I also have been using this time to do things like finally organizing our basement guys. We have finally purchased all of our living room furniture, but it just takes months to get here, so it's not yet it here. We have been catching up on television, which we'll talk about in a future episode, but everything from the White Lotus to Love is Blind. We actually just started Severance. There's a lot of stuff that we have to talk about and debrief because I know that our listeners love listening to our little bits about our favorite TV shows. But it has been good being able to utilize this time to catch up on all of those things has been really, really helpful. But I'm excited to be back. And of course this time we come back with some classical hemes. So I know that our listeners can't see us, but me and Dan grinning from ear to ear. Vivek got a slight smirk on his face. But you know, this is a topic that so many of you have emailed us about, sent us messages on our Instagram and on X and via email asking about guidance about anticoagulation management in the setting of clots and that nebulous hypercoag testing. Who needs it? When do we do it? What are the implications? And so we listen and here we are. We've put together a little series for you all. So Dan, do you want to start us off with a case this time talking about, you know, anticoagulation management after a clot?
- [03:34]
C
I do. I'll start by saying watch Severance immediately. If you haven't done that, you can put this episode on pause. Go watch Severance. Final episode of season two comes out this Friday. Watch Severance. Now that that's out there, we'll start with our case. Yes, we got a 58 year old guy. He's got a history of hypertension, hyperlipidemia, type 2 diabetes and metastatic pancreatic cancer involving his lungs and his liver. He's currently on palliative chemotherapy and he comes in to the emergency room with acute onset shortness of breath and lower extremity swelling. His vital signs on presentation show that he has a normal blood pressure. He's got a heart rate of 110, he's sat in 86% on room air. What kind of things do you find worrisome about this presentation so far? Is there anything you want to do right away? I mean, are we going to be pushing TPA at bedside here or what do you guys want to do?
- [04:24]
A
I mean, overall, Dan, this is certainly very worrisome for something like a pulmonary embolism, which if we take a step back for a second, fits into a larger category of venous thromboembolism or VTE. And so VTE as a category, this umbrella term encompasses things like superficial venous thrombosis, deep vein thrombosis, and also pulmonary embolism. But in this case, you know, the patient also has active malignancy and he's presenting with this asymmetric leg swelling as you described, shortness of breath, tachycardia, hypoxemia. And so it's all very, very convincing for a possible VTE diagnosis. That being said, he is normal from what you described, and I didn' a report of chest pain. And so I'm not worried that this patient needs ICU level care. So this is really an important distinction and it demonstrates what we need to do. When we first work up a patient for a pe, we have to categorize the severity of, you know, the burden of disease. And we do this in a few ways. And you'll see terminology used to describe this. So there is massive pe, which means that the clot is large enough that it's causing hemodynamic instability. So remember, the heart is essentially two pumps connected in series. No offense to our cardiology colleagues, but it is in theory that simplistic Two pumps connected in series and the cardiac output of the left ventricle can never exceed the cardiac output of the right ventricle. The right heart is not used to generating high pressures and therefore it can fail if there's a sudden increase in the resistance, causing obstructive shock. So this results in a life threatening situation and requires immediate intervention from cardiac surgery or interventional cardiolog. A submassive PE means that there's evidence of right heart dilation or bowing of the interventricular septum on your echo, or there's biochemical evidence of heart strain like an elevated troponin or an elevated bnp. This may or may not require intervention like a thrombectomy or a catheter directed thrombolysis, and the interventional teams can help make that call. Then there's low risk PEs, which is sort of everything else and by far the largest category of pe. These are patients generally treated with anticoagulation. Many of you probably practice at hospitals that have multidisciplinary teams that are often called PERT teams or PE response teams, which includes a makeup of cardiologists, CT surgeons, interventional radiologists, who can all look at the patient and the imaging data in real time and triage them into one of these categories. So just to highlight there that hematology is usually not involved at this point. So if there is an acute issue, it's important to get these other specialists involved. The other way you've probably seen PE categorized is also by anatomic location. So you may have heard terms like a saddle pe. A saddle PE extends across the bifurcation of the pulmonary artery. In contrast to this, there's also a segmental and a subsegmental pe, and these are more self explanatory that they are involving segmental and subsegmental branches of the pulmonary artery, respectively.
- [07:33]
B
So, getting back to this case, we have a high clinical suspicion for pe. And as you mentioned, the patient's vital signs are a little worrisome, but he's hemodynamically stable. So what are the next steps for workup in this case?
- [07:47]
C
So imaging is of course, very important here, and we can do a bedside echo if we're worried about massive or submassive pe, but if there's less concern for that, you can go straight to CTA of the pulmonary arteries or the sort of CT PE protocol, as it might be called in your system, and this will confirm a diagnosis of penalty. A formal transthoracic cardiogram will also be important during the admission just to assess that right heart function in a more formal way and to get an estimate of what the pressure in the pulmonary vasculature is for patients who are unable to get IV contrast or a CT scan. Of course, we do have the VQ scan, but this is a study with pretty low spatial resolution. And while it can be helpful in the diagnosis of chronic PE, in the acute setting, it'll really only be able to pick out large territory pes much of the time. It's going to come back equivocal for those small and intermediate sized pulmonary emboli. We also want to make sure that we have cbc, CMP and baseline coag labs here. PT and ptt. We want those all documented up front to help inform our anticoagulation plan, especially if there's a possibility that the interventional teams are going to need to do some kind of procedure. We'll often start with a heparin infusion to allow for flexibility around those potential procedures, since we can turn that drip off right away and that heparin metabolizes off relatively quickly. And so, you know, we'll definitely want to have that baseline PTT prior to starting that infusion. But if this case had been different, say, and the patient was instead presenting with evidence of hemodynamic instability, how would that change what we do up front?
- [09:20]
B
So, you know, obviously in that case, the priority, like with any patient being managed for shock, is stabilization and restoring normal perfusion. Since not all patients scream PE when they're being evaluated for shock, bedside echo can be invaluable here to give clues that acute right heart failure from obstructive shock is the driving pathophysiology. So this takes us back to our internal medicine critical care era. We usually would manage this with empiric anticoagulation along with other critical care interventions like pressors, intubation fluids, and even ECMO to try and maintain oxygen delivery to vital organs while a plan is made to intervene on the clot with either thrombectomy or catheter directed thrombolysis. And this idea of catheter directed thrombolytics we'll revisit when we just talk about VTE in general as well. Oftentimes with this severity of illness, it won't be possible to get a CTA of the pulmonary arteries to fully define the clot burden. But if a patient can be stabilized after 15 minutes of resuscitation, they are generally able to have definitive imaging with a CTA after that. So in many cases, if you have a high clinical suspicion, stabilize the patient empirically, anticoagulate them if you have a really high index of suspicion, and then get the scan when they're stabilized. So to continue with this case, the patient's CBC shows the a white count of 13.8, hemoglobin of 12.7, and platelet count of 242. So all relatively unremarkable. Renal function's okay with a GFR of 65 and liver tests are normal. His baseline PTT is normal at 28.4 seconds. He started on a heparin infusion and goes off for imaging, which confirms his diagnosis of pe. And there's no evidence of right heart strain. What about the other component of this patient's presentation, the swollen leg? How do you address this so broadly speaking?
- [11:07]
A
A similar algorithm applies here when you're dealing with what I think you're alluding to is likely going to be a dvt. And it honestly is a very big part of medicine in general. So we need to be very systematic with this. So the first thing is we need to figure out, is there an actual emergency and deal with it if so, and come up with a larger long term plan after that. So what I mean by this is we need to figure out if the DVT is big and bad enough to threaten limb perfusion. Know that a large clot burden may so dramatically impede the blood return from the affected extremity that forward flow is impaired and the limb can actually become ischemic. And this phenomenon is called a phlegmasia presentation. So you may have heard of a diagnosis of phlegmasia coerulea dolens or phlegmasia alba dolans. These are situations where blood flow is being impeded returning to the heart. So really, really severe clot burden. In these cases, you're going to want to talk to your IR or vascular surgery colleagues about undergoing a thrombectomy for your patient to try and improve that blood flow and restore adequate flow to the limb. So once we're sure that we're not in that danger category of limb compromise, we can then get imaging with a Doppler ultrasound to determine the extent and location of the clot. These reports will generally list the veins that are examined and whether or not there are areas that could not be fully compressed. And what that means is that suggests that there's something in the lumen of the vessel. So look out for that. You'll often see in the reporting it'll say compressible, not compressible. That's what they're referring to. So not compressible, as intuitive sense would suggest, means that there's something in the lumen. The Doppler component can also determine if there's absent flow suggestive of a fully occlusive clot. The one thing that ultrasound isn't able to tell us is the age of the clot. So there are features on imaging that can suggest an acute versus a chronic clot. And having comparison imaging is helpful for this, if that's available. But often it'll be difficult to say whether or not a clot is new. So we touched on some of this in our anticoagulation failure episode a while back, and we'll provide a link to that in our show notes, in case you hadn't listened to that before. But it's important to remember that a clot forming inside of a vein is always an abnormal event and often provokes a local and systemic inflammatory response. And so this patient had an elevated white blood cell count, as Vivek had mentioned, which we see often. And many patients will have fevers from their dvts as well, again highlighting the systemic inflammatory response that can happen. The local inflammatory response may manifest as erythema over the area of the clot and so there can be an intense pain that's associated with the DVT as well. If the patient has a non occlusive clot, CNN ultrasound and lacks most or all of these symptoms, I tend to have a hard time believing that the finding represents an acute dvt. But of course there's no real way to prove that.
- [14:10]
C
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- [14:23]
B
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- [14:42]
A
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- [14:50]
B
Yeah, and that's really, really important that distinguishing acute from chronic clot you can't just do easily on an imaging test. I mean, we always want the radiologist to tell us, oh yeah, this one's chronic. Oh, this one's acute. It's way harder to do that. Clinical judgment plays an important role here, and reviewing prior imaging also plays an important role. And it's really important to note this. In an acute event, often you have this inflammatory response. And that's why even when you start a patient on anticoagulation, they may still be having symptoms a couple days later. It takes some time for inflammatory response to die down. So in this case, our patient's leg is indeed tender and very obviously swollen, although there's no dusky color to the foot or other findings to suggest compromised blood flow, the primary team calls you and asks whether to call IR for placement of an IVC filter. After the ultrasound shows extensive thrombosis throughout the deep veins of their right leg and the common femoral down to the calf veins. So, Dan, what do you think about IVC filters?
- [15:50]
C
Yeah, it's going to be a hard pass for me. IVC filters can be a great tool, but like any other tool, they need to only be used in the specific situations which they're helpful. First off, the name IVC filter is kind of a misnomer. They probably can stop really large clots from causing a massive pee. If you've ever seen these things, they look kind of like an umbrella without any of the meshing over it. We'll have a picture of one in our show notes. But what they actually do most of the time is serve to break up these very large clots into smaller pieces that that wouldn't represent a risk for hemodynamic compromise. So in that way you're converting what might have been a massive pulmonary embolus into a bunch of smaller, low risk PEs. The second thing is you gotta remember that these devices are a foreign material in the lumen of the vein and therefore they themselves represent a potential nidus for thrombus formation. I usually only reach for a filter if a patient has an absolute contraindication to anticoagulation and has a large lower extremity clot. That represents a high risk for causing a bad peak. I've had patients develop, for example, large DVTs right after having a brain tumor resected. And yes, those folks need a filter until we can safely anticoagulate them. The other important thing about filters is that they should be removed when they're no longer needed. Our IR doctors here at Rouleau University are really good about following up their patients with IVC filters. But I always strongly recommend that any hematologist who is recommending filter be placed closely follow those patients to make sure that a plan gets put in place to have that filter taken out. If a filter has been in place for too long, it'll kind of get fixed and scarred into the vessel wall and then it can't be safely removed. So it's important to get them out while you can after a patient is able to be started on a blood thinner.
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B
And one other thing I want to point out is that the question always comes up for catheter directed thrombolytics. And earlier we brought up the idea that if you have limb ischemia, you're going to be reaching for that tool because you really need to reperfus that organ. Well, another thing that's really important in VT's is that there's something called post thrombotic syndrome where patients, after they get a DVT in a proximal leg vein, like a femoral vein or something proximal, that they can have chronic swelling, chronic edema, potentially leg ulcers, and that can be debilitating. This is an uncommon event, but it happens. So there was a thought that what if for the patients who have these femoral vein dvts, these proximal lower extremity dvts, that we gave them catheter directed thrombolytics, we improved their outcomes. So there's a randomized clinical trial that was published in New England Journal of medicine in 2017 that took patients and they randomized them to anticoagulation alone or anticoagulation with catheter directed thrombolytic therapy for those who had a proximal vein DVT with the primary endpoint of reducing post thrombotic syndrome. They ultimately randomized 692 patients and found that there was no difference in outcomes for post thrombotic syndrome between 6 and 24 months of follow up. And there was an an increased risk of bleeding within 10 days of the incident event, which makes sense because you're doing this procedure. So ultimately, we found that the use of catheter directed thrombolytics does not need to be done for any proximal DVT in the femoral vein unless you have limb compromise.
- [19:09]
C
Really, really important distinction to make. I'm so glad you brought that up. And so now that we're kind of beyond this acute phase of management for the patient, what kind of questions are important to ask to try and help us figure out how to manage a patient with VTE beyond this initial presentation, what kind of stuff are you gonna wanna get on history? Or when you interview the patient, what kind of questions are you asking?
- [19:30]
A
So this is often the conversation that, you know, a lot of our listeners that don't take care of patients in the office may actually not be having all the time because they may make the initial diagnosis and then they are told to go see their friendly neighborhood hematologist for further discussion. And so, as the friendly neighborhood hematologist, these are sorts of the things that are being discussed in our clinic room. So first off, we need to get some basic history from the patient on their VTE symptoms, as well as information about the medical history in general. Really the things that we are trying to understand from this is things like how high of a risk is this patient for having bleeding complications if they are put on anticoagulation, how long does this person need to be on anticoagulation? And if anticoagulation is indicated, what is the best option for the patient? So things that we want to know include things like when did the leg swelling start, Was there any shortness of breath that happened in association with leg swelling either before or after. Was the shortness of breath onset insidious or was it sudden? So then we want to know about whether or not there's any provoking risk factors for VT and more to come on that in just a second. We want to know, did the patient ever have a VT eliagnosis before? And we also want to know, has the patient had any serious bleeding concerns like a GI bleed or a brain bleed in the past? Has the patient had any operations on their intestines or any diagnoses of GI disorders that may impair the ability to absorb certain medications in different parts of the gut or the stomach? And has there been anybody else in the family with a VT, eliagnosis or history of other blood disorders? So, again, really, really important questions to sort of just internalize and make sure that you sort of rattle these off when you see your patients. Because. Because ultimately, the question that doctors are trying to ask their hematologists to help them answer is trying to understand the pros and cons of anticoagulation for that particular patient. And so, yes, blood thinners will help with the blood clot, but blood thinners also mean an increased risk of bleeding.
- [21:31]
B
So the most important thing that you mentioned there, I think, are the provoking risk factors. And everybody knows this, who's gone through any training in internal medicine, what's provoked and what's unprovoked, and that's in the eye of the beholder. So in this case, I would say his metastatic cancer and active chemotherapy represent major provoking risk factors. But what other risk factors are there? Are we asking about long car trips and flights to Australia? What really is a major provoking risk factor? What's a minor provoking transient risk factor? What does all this stuff mean? And this gets really, really confusing, even if you're a hematologist. So, Dan, can you walk us through some of that that?
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C
Sure, yeah. We do tend to break down these provoking risk factors into a couple of large bins. There's the major provoking risk factors and minor provoking risk factors. And then we also think about, is that a risk factor, a transient risk factor, something that's only there for a limited period of time? Or is this a permanent thing for the patient? Is this risk factor going to be there for the duration? And so for major risk factors, the main things we're thinking about here are major surgeries, pregnancy or recent delivery, and so delivery within six weeks, exposure to exogenous estrogens, including hormone replacement therapy, the estrogen containing Birth control, or even selective estrogen receptor modifiers like tamoxifen. Traumatic orthopedic injuries. So traumatic injuries that involve bone fractures, metastatic cancer diagnosis, chemotherapy, treatment, severe obesity, paraplegia, nephrotic syndrome. Remember that you lose those anticoagulant proteins preferentially, they're smaller than the procoagulant ones. So nephrotic syndrome is a high risk for VTE, inflammatory bowel disease, other severe autoimmunity, and extended hospitalization. So hospital stays of three or more days. And although we hear about long flights and drives, that's like the thing in med school that triggers you to think about pulmonary embolism and dvt. Those are actually considered minor risk factors. And some other minor risk factors are things like minor surgery, traumatic injuries that don't involve bone fractures, hospital stay of less than three days, fewer than three days, or being sick at home and immobile for five days or more, those are considered minor risk factors. And this determination of whether a clot is provoked or unprovoked is so important for figuring out how long a patient should be treated for their VTE. If a patient has a major transient provoking risk factor and it's their first VT el, I'm usually going to recommend they have a limited duration of anticoagulation. Almost all of these patients will really only need three months of therapeutic anticoagulation to keep them protected and safe. By contrast, patients with an unprovoked VTE or a VTE in the setting of a permanent major risk factor, I almost always recommend that they remain on therapeutic anticoagulation indefinitely. The risk of recurrence is just so high in those cases that it's hard to justify telling them that they only need it for a limited period of time. Time. For patients with recurrent provoked VT EL or with VT EL provoked by minor risk factors, the decision is a little bit less clear cut. It really is an individualized discussion at that point on a patient's risk tolerance, what the risk of bleeding is and how well they're tolerating any coagulation so far to figure out what the best duration to recommend is. And this is also sort of a tedious linguistic distinction that I make, but I generally always talk about indefinite anticoagulation and not lifelong. People's lives change, right? Like decisions about anticoagulation are always about balancing the risk of bleeding against the benefits of preventing recurrent VTE. And as that balance changes throughout the course of someone's life, they may need to come off anticoagulation Even if there's a fairly high risk of recurrence for vte, you gotta keep the conversation going with your patients as you follow them in clinic over the long term, so you have a full and current understanding of what that balance of risk and benefit is. So let's say we talk with our patient and he can't identify any additional provoking risk factors for thrombosis besides his active cancer and chemo. He's never had any major bleeding in the past and has never had a VT eliagnosis before this. No one in his family has had a VTE to his knowledge. He does mention that his father died of a stroke at age 74, but he's not sure that counts. And as you talk with him about blood thinners, he asks, you know, is this heparin that he's on actively, quite, quote, busting up the clot in his leg or in his lungs? How do you talk to him about what the blood thinner is actually doing and why we think it's important?
- [25:54]
B
Yeah. So I try to make a distinction between the clot buster drugs, quote unquote, like TPA and anticoagulants. And remember that the goal of anticoagulation is twofold. Prevent extension and embolization of the acute clot and to prevent additional thrombosis from developing elsewhere in the body. As we mentioned before, the formation of a blood clot in the lumen of a blood vessel is an abnormal event. Under normal circumstances, the body's clotting system functions as a self sustaining chain reaction to allow a clot to expand to cover a defect in the vessel wall. When a clot forms inside an intact blood vessel, those activated clotting factors are thrown into circulation throughout the body. As a result, the presence of an acute VTE makes it much more likely for other venous clots to form. So this makes a lot of sense about why we need the anticoagulation to help mitigate that risk. So what I tell patients is that the body's own fibrinolytic system will work to digest away enough clot to restore blood flow, but that the restoration of blood flow is really the only thing the body cares about. If there's sufficient collateral flow or the body can increase the blood flow through other collateral vessels. Some residual clot may end up being there permanently and is slowly transitioned to kind of scar tissue over time. So it's important for people to know that your body's own janitor crew is doing its best. We have bypass hot that are Going to bypass this. We might leave a little bit of a scar left behind, and that's okay. And that's what you might pick up on these ultrasounds. When we had talked about earlier for that chronic clot where the patient, you know, we just did these dopplers and it's like, okay, well is that a real clot? Is that not. That could be a scar from a prior event. Which is why a thorough history reviewing prior images are really, really important for these patients. So getting back to this case, our patient's doing well on his heparin infusion over the first couple days of his admission. And with his oxygen saturation normalizing, decision is made that he will not need any kind of thrombectomy or catheter directed thrombolysis in terms of his pe. And remember from the ATTRAK trial, it does not improve post thrombotic syndrome and proximal leg dvts. The patient is switched over to therapeutic enoxaparin. The primary team tells you that the patient's aunt works at a warfarin clinic and wants to know if he can go home with warfarin instead of staying on the shots. So what do you guys think about this?
- [28:14]
A
Whenever the conversation of warfarin comes up, patients always go one of two ways. Most of them though are like, ugh. And what I tell patients is that warfarin's a great drug. And the reason we still use warfarin today, even though it's been around forever, is because, honestly, it works. And it really is the comparator that we compare most of our other drugs to. So I do use it a fair amount in my clinic for a variety of reasons. But in this case, I think we should avoid it. And to do this, I think we should look back at the data showing that warfarin was actually inferior to enoxaparin in patients with active malignancy to say that we probably should avoid warfarin if possible in this setting for this particular patient. Fortunately, DOACs appear to be non inferior to enoxaparin in patients with cancer. So we can offer this to patients as something that's not a shot and even easier to take than warfarin. And in fact, DOAC medications are a good choice for the majority of patients with a new vt, else they're convenient compared to twice daily injections. They don't have many interactions with dietary things like dietary vitamin K and don't really require any special monitoring. In most cases. The lack of requirement for monitoring is sort of a double Edged sword, however, because we also can't monitor these drugs. While many labs can report a DOAC level, the medications aren't studied in that way as to give us a well established therapeutic range for those drugs. And so there's really no protocol for titrating a patient's dose to achieve a target level. As a side, you know, this question does come up often of whether or not we should be checking DOAC levels really from experience. The only time that that level lab is really helpful is in situations where you're trying to for instance, take somebody off of anticoagulation for a procedure or they had, you know, a life threatening bleed and you just sort of want to know whether or not there's any effects of drug in their system. So instead of using that test as more of a yes, this person's therapeutic, it's almost more of a binary test like yes, it's either in the system or it's not just some side words of wisdom. But back to our case, you know, as a result, it's really, really important to make sure that there's nothing that could impair medication absorption. And so you'll remember that one of the questions that I had said to ask your patients is whether they've had any prior bowel surgeries, right? Or any for instance, gastric surgeries like gastric slee gastrectomies, because any of these situations may impair the absorption of the DOACs, which would essentially make them less effective.
- [30:51]
B
And Roanoke, that's super, super important that we're talking about. The patient who you might prefer warfarin in is that patient who we worry about absorption issues. And you know, in a future episode in the series we'll talk about reversal of anticoagulation in general and we can talk about the nuances for the DoACs versus warfarin versus even how do you reverse heparin, for example, when somebody's on enoxaparin at. And so we'll get into that in a future episode. So this patient is switched to apixaban at discharge. 10mg PO bid for 7 days as a loading followed by 5mg PO bid indefinitely. He sees you in clinic for follow up and has a few additional questions for you. He really wants to know if he needs a hypercoagulable workup and somebody mentioned to him about this Factor 5 Leiden and he's interested to know if this should be tested.
- [31:39]
C
I, I think we should probably leave that discussion for another day. Ultimately, it's a pretty Complex question. There are still roles for hypercoagulable testing, certainly, but it's something that has really fallen out of fashion in hematology. It's one of these things that it's a question that really makes a lot of hematologists skin crawl when you're faced with the question of whether or not we should be doing testing for these prothrombotic states. And so I think maybe we can follow up that discussion in another episode. Is there anything else you want to know?
- [32:10]
B
The last thing I want to know. Dan, as we wrap up this episode, what dietary things do we need to consider at all when somebody is taking a doac? And what about lab monitoring for these patients?
- [32:20]
C
Okay, that we can talk about. I'd say we do still need to do some degree of lab monitoring. For folks who are on a doac. They need at least yearly measurement of their liver and kidney function to make sure it's still safe to give them these meds. Generally speaking, a pixaban we can use kind of regardless of kidney function. And as long as their liver is okay, a lot of it's hepatically metabolized. So we can use apixaban for those folks. For people with good kidneys but impaired liver function, dabigatran is kind of where I go for that. It is mostly renally cleared. And there are no dietary restrictions for apixaban. And unlike rivaroxaban, which requires a sort of fatty meal for optimal absorption, there's no requirement that apixaban be taken with food either. So it's kind of one of the easier ones, although it is twice a day. In fact, even for patients who are on warfarin, I generally don't tell them that they need to completely avoid vitamin K containing foods. Instead, it's just important that they try and maintain this stable amount of vitamin K in their diet. Consume the same amount of vitamin K containing foods week to week. That's what'll help avoid those really labile INRs. You know, if they eat a lot of vitamin K, if they have a diet that's rich in vitamin K, as long as it's stable, we can always give them just a higher dose of warfarin. We're not running out of the stuff anytime soon. So that's something we can work around. But no dietary restrictions, certainly for our apixaban patients.
- [33:41]
B
All right, that's great. So I think we covered a lot of ground today. In this episode, we introduced VT's, we talked about provoking risk factors and the nuances behind that. And a long car ride is not necessarily a provoked clot at all. And there's a lot of controversy on how you deal with these patients who got a clot on a long flight. Should you anticoagulate them forever or should it be fixed duration? You ask 10 hematologists, you'll get probably 50% of them will say one thing, 50% of them might say another thing. And so it's really nuanced and difficult. Listen to this episode, check out our show notes and really we'll lay it out for everybody. So we had a fantastic discussion today. Let's wrap it up for today and we'll see everybody next week.
- [34:20]
C
And remember that a long flight or car ride may only be a minor risk factor for VT el, but it's a major opportunity to listen to your favorite hematology and oncology podcast. So remember to download those episodes before you hop on the plane.
- [34:33]
A
All right, guys, until next time. We'll see you all later.
- [34:35]
B
See you later.
- [34:36]
C
Peace.