VTE Unplugged Episode 3: Enhancing Anticoagulation Approaches — Factors to Consider in Patients with Altered Parameters
I'm going to put in a little bit of a spot now. So my question will be, does one shoe size fit all? So if you've got a patient with a deranged parameters in the liver or kidney or platelets, how do you go about choosing the drug? Let's talk our profile access first. How will you choose which drug you're going to use? Because we've got quite a few drugs available to us either in the treatment arena or profile access. Yeah, so I think DOACs are coming on board for profile access. I'm still not comfortable, especially in patients with deranged parameters. I think that there are reasonable treatments in patients who otherwise would be outside of the hospital, but maybe are undergoing some sort of treatment in the hospital for various reasons. So no one with deranged parameters will get a DOAC from me. Also no one with a high risk of decompensation in the near future. So I'm giving a therapy that I know will cause renal failure in this patient. I would not be giving a DOAC in them. So I almost need a reason to give a DOAC rather than to not give a DOAC in these patients. The then treatment options are the Heparin-based therapies. So I love low-menolicular weight Heparin for a lot of reasons, but because it's lost frequently dose and because it has a lower incidence of hit than regular Heparin, I think it is a, and it has a slightly higher efficacy because probably because of the pharmacology. So I want to give low-molecular weight Heparin in most of my patients. If I am really worried about bleeding, the half-life makes me a little hesitant about the low-molecular weight Heparin. I will switch over to unfractionated Heparin. That's beautiful. Thank you so much. I'm also a huge proponent for the use of low-molecular weight Heparin, especially in hospitalized patients, for the same reasons that you mentioned. And I find a lot of comfort in the fact that it's drug interactions at least. And I've used it in patients with GI bleeding where anticoagulation was used in very high-risk and that's why I found it's beneficial for me. So thank you very much for those thoughts. We'll come to chronic kidney disease. What are the provoking risk factors that are commonly present in patients with moderate to severe CKD that contribute to a higher risk of VTE? And we have all physicians and intensivists have appeared that they might be a higher risk of bleeding because of latent dysfunction. So what is the provoking risk factor? And how do I take care of this situation to anti-coding the patient? Yeah, so I think, you know, we often will think about patients who have renal failure as maybe having a bleeding risk. We don't think there's true bleeding risk unless there's actual ureaemia in these patients, which can cause platelet dysfunction. So an ureaemia is usually a reason to dialyse someone. And so it is also a transient risk factor, I would say. And I think that ureaemia, in general, I would say over 100 is where I start to get really worried about. And that's a ballpark, you know, 80s could maybe be true, but it is a profound ureaemia. It's not just a small elevation of the BUN. So that is something that I think about, but not necessarily something that makes me not anti-cragulated patient. Because CKD and you kind of were talking about this, CKD is very, is a chronic inflammatory condition and inflammation is actually what causes thrombosis in a lot of cases. And it's actually the buildup of urea in the blood and the urea solutes themselves, which can kind of cause this cardiovascular toxicity and cause prothrombosis in these patients. So as a whole, the risk for thrombosis is much higher than the risk of bleeding. There is one caveat of patient that I get concerned about with ureaemia and that is pericarditis or urinic pericarditis in these patients. Those, if I hear a rub or if I'm worried and I have my ultrasound, I find a patient with a high BUN and a large pericardiofusion or a moderate pericardiofusion. Those will be patients that I really want to get dialized, make sure that I have kind of decreased the inflammatory condition in the heart, around the heart, so that I don't transform that to a hemorrhagic pericardiofixture. And that is the one time that I do get concerned. Right. Like I think you've kind of answered a couple more questions that I had on chronic kidney disease. So I'm going to quickly shift on to another situation of deranged parameters and that's the liver. So so far, the listeners have heard you speak about thrombocytopenia and your cut-offs and about the beautiful explanation of CKD and how to manage. Let's come to liver. In liver, especially in a serotic liver, there is a re-balanced hemostasis. The pro-quagulants and the anticoagulants, which is balanced out each other. And therefore, it's a little bit difficult, especially for me to find out what is the real risk of bleeding or clotting in these patients. And sometimes the tests that we do don't give us good quantification parameters to understand the pathophysiology better. So in patients who got serosis of liver, how do you thromboprophilize them? And is there any such marker that predicts that this serotic is a higher tendency to clot rather than beat, so be more aggressive in anticoagulant? Yeah, this is a great question and something we struggle with a lot. And I think that there is a false sense of security. So in an INR therapy, in an INR level. So we were just saying, you know, when a patient comes in with liver failure, I look at a couple of things to figure out whether I think that the elevation in the INR, the PT is related to liver dysfunction or something else because if I don't have any other clues, this could be the biggest help. So I asked the patient if they're eating okay. So that would be a nutritional component where the patient might be vitamin K deficient from that, from lack of food. And I see if the patient has been on warfarin in the past or are supposed to be taking that for a reason. If that's the case, if they have not eaten in the week and they have warfarin on board, I tend to believe the INR a little bit more. But if they have just liver failure, or I'm not sure, I believe the INR, I then look for if the patient's actively bleeding. So the patient came in with a down trending hemoglobin. The patient said that they have gingival bleeding or the patient's telling you somehow, I cut myself and I'm just bleeding a ton. Those are great hints to know if the patient has a bleeding risk related to the INR. Otherwise, I in general don't believe the INR in a patient with liver failure. And I actually will run a thromboelastogram or a tag scan, which is actually an ex vivo actual process of whether the thrombosis, how a thrombosis is formed. And so there is basically a thing that's inserted to a blood sample, a metal rod, and it sees kind of how the blood clots and breaks, ultimately breaks down the clot. And based on that, I can determine whether the blood has been linked to a clot or tendency not to clot or to what we would say to bleed. And if the patient's tag is totally normal or even hypercrogulable with an elevated INR, I will give that patient thromboprophylaxis. Right. Thank you. I mean, there was talk of doing a thrombin generation test to see whether there is a potential for thrombosis higher than that of bleeding, I for one don't have the facility in the institution where I work. Have you all looked at that maybe from a research angle whether serotics should have a thrombotic potential general assessed prior to deciding therapy? I have not personally looked at that. I will say that is not something standard in practice within our hospital setting. But I do think that it comes to the question and the exact point you are making is that the classic laboratory parameters that we have for serotics are not adequate at predicting either they are bleeding or they are clotting. Another question which our physicians asked, I think you are very hands on. So I am asking this question because if the INR is prolonged, most of the physicians would want to correct the INR mainly through fresh frozen plasma. Is this something we should be doing or we should be telling them this is an inappropriate way of looking at things? Yeah, there is no reason to correct an INR in a patient that is not bleeding if the INR is under five definitely. When we get closer to ten or then perhaps it might be prudent. If you have evidence of the patients at increased bleeding risk, there is no need to correct the number. I will let patients have an INR of five if they are not bleeding and I am not worried about bleeding. I will then assess whether they are even likely to bleed using other parameters. So it is clear that we should not transfuse a fresh frozen plasma just for an INR number. It may be detrimental to the patient's health. Of course that can definitely increase thermobotecris. The one thing that I will say is if you think that the INR is real and it is nutritional, then a little bit of PO vitamin K is possible. It is a lot less thrombogenic while FFP is very thrombogenic. That is excellent. Thank you. I am going to give you this situation now where you have a patient who has got a pancreatic mass detected on a CT scan. It is found to be malignant. The patient has a cancer-associated thrombosis. That is partially occlusive thrombosis in the left femoral vein. And now you want to initiate anticoagulation. So how do you approach a patient with CAT, cancer-associated thrombosis? How do you go about deciding which drug and because we have to remember this patient is going to get chemotherapy. There is going to be upper GI complaints. There might be nausea, vomiting, diarrhea, a little bit of mucocytus. So how should we grow about approaching a therapeutic anticoagulation in this CAT patient? Yeah, no, I think this is a great question. So the first thing I think of is if any of my drugs will interact with the chemotherapy. And if there is any thought that the chemotherapy will cause thrombocytopenia or anything like that, those will be things that I kind of work with my heme-onc colleagues to discuss and to figure out and to plan. If there is no contraindication and the patient is not at high risk for bleeding, you can use any of the therapies dosing. Remember, because this patient has a thrombosis, so all of them are possibilities. There are pluses and minuses to each one that we are going to have to talk about and individualize to the patient. But they can be given. And if there is a large GI gastric mass that was super friable and doss can be diagnosed, that might not be a patient that I go with a doak on. But otherwise, I think in the setting of a lung-relignancy, no hematocyst, something like that, liver-malignancy, those are patients that we can consider doing doax and if it makes the most sense for the patient and for the medications being used. Right, thanks. So despite our best effort, we used either the low-malignancy or the doak. Despite that, if there is an extension of thrombosis or there is a recurrence of thrombosis, then if the patient was on the doak or low-malignancy or the doak, then how do you go about then creating this extension or repair? Yeah, so I think you kind of brought this up a little bit earlier with the doak. So I think the question is, is this doak failure or was the patient not getting the right amount of drugs? So maybe the patient had horrible mucositis, maybe the patient was vomiting, maybe it's not true doak failure in this patient, maybe it's that the patient actually cannot tolerate the drug. Additionally, if the patient was having any kind of, if the patient is an extreme of weight to very obese or has very poor perfusion to their skin or soft tissue, low-malignal weight heparin might not be the treatment of choice. Definitely not once a day dosing that could, dividing that up into twice a day dosing for treatment is always what I do, but definitely in a patient with deranged parameters. So those are kind of the options. The one thing that I will say is a patient with heparin, you are 100% sure how anticoagulated they are because you can check the levels and you can be sure and you can bolus. When a patient has a large amount of clots, they actually can inactivate heparins and those patients can be somewhat heparin resistant. So those patients sometimes need to be bolus multiple times to get, to get adequately anticoagulated. In those cases, those cases with large thrombose or those cases that are very likely to bleed, those will be patients that I have moved directly to heparins in. Thank you very much for that.
