Stephan Moll, MD, presents the basic concepts of Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE); looking at medical history, diagnostic testing, and treatment options for patients.
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Good morning, everyone. I would like to welcome you to the morning session on benign hematology. I'm Dr Emily Nagler, benign hematologist here at scripts with a specialization in coagulation. It is now my pleasure to introduce Dr Stefan Mole, a professor of medicine in the department of hematology oncology at University of North Carolina School of Medicine who will speak on basic clinical concepts in thrombosis, diagnosis and management refresher and 22 teaching points. Dr. Mullis, a good friend of this conference who has participated in our conference many times and is always very well received. In addition to being a regular speaker, Dr Michael has been a wonderful mentor for faculty here at scripts. Please welcome Dr Stefan Mole. If you have questions you would like to have him address, please use the ask a question chat function to ask your questions during the presentation. Questions will be addressed during the panel session. In the next 30 minutes, I will present some basic clinical concepts about DVT and PE about diagnosis and management. And this is from issues that I see coming up in the thrombosis clinic. The inpatient service, by emails and by phone. I know that a number of these issues that I will mention a basic and self understood for many of you. But I still hope that some of the points that I will raise you will find helpful in your clinical practice. And with that I will make as I go along. 22 teaching points and I will address medical history, diagnostic testing, treatment issues and you will find the 22 teaching points more in detail in your scripts. Conference materials. I have no disclosures. Basics. So this is a real quote. Curbside. Consult to the hematology service. Quick question. How long would you anti choir Great. A 64 year old patient with the basilica vein DVT after, if lobotomy stick See you wonder. Okay, DVT flat bottom e But use struck by the fact basilica vein is not a deep vein. Basilica vein is a superficial vein and what happens not infrequently, is that people confuse the basilica vein the superficial vein with a break in vain Break a vein is the major proximal DVT vein in the arm. So be clear what people are asking about when they ask about advice on antique regulation. The Cilic vein is not a deep vein. This patient has a superficial form of phlebitis. It's associated with a flat bottom. You stick. This patient may not need any anti coagulation, maybe non steroidals. Or if the club is extensive or close to the deep venous system. Maybe a few weeks of anti coagulation, whereas a proximal DVT in the Break Hill, the vein would have to be treated, at least with three months of anti coagulation. And here I've listed the superficial events of the arm and the deep veins by names. So the basilica vein on this side, the break of in on this side. Just be clear about the anatomy. Second type of curbside quick question. And this is a real question again. Superficial clot and the right leg superficial formal vein. Not very symptomatic my plan was to observe, so we step back and think, Okay, superficial femoral vein. Actually, that's the main deep vein in the leg, also called femoral vein. Because superficial is misleading. This is a major proximal DVT that needs to be treated with anti coagulation. This physician thought the superficial femoral vein is a superficial clot, but it's not this patient's proximate activity treat at least with three months of anti coagulation. Here is the leg anatomy. The formal vein right here as a major proximal vein and then in red are the more distal DVT s veins, where DVDs occur. And those are the ones that you may not have to treat with anti coagulation. Unless there's a persistent risk factor such as cancer, persistent immobility or the symptoms are quite pronounced. So the differentiation between proximal vein and distal vein DVT is important. So my teaching point number one, we need to be clear about the arm and leg vein anatomy and what the physician asking us for advice is really asking about some points about imaging studies that we do for DVT pe Doppler ultrasound. There's certain imaging characteristics of a clot that suggests an acute clot and what the Doppler notice on lab cause acute maybe days old, up to three months old, and it takes several weeks for the acute clot to change characteristics to a more chronic clot. The three criteria for an acute clot dilated vein. The cloud appears spongy on compression, and the cloud is hypo eco ick blackish, and when the clot then becomes scar tissue and becomes chronic. The veins scars and gets retracted shrinks. The clot is firm, it's scar tissue, and it's hyper eco ick i e. White. And this can be a clinically helpful distinction between Is this an acute clot, or is it something that pre existed several months ago? And if there is a question, we can pick up the phone and talk to experienced either the apologists and tech or radiologist because not infrequently, the lab report just simply states DVT present. And that does not help because it could be a lot from three or five years ago. That has become scar tissue in a particular challenging situations to diagnose recurrent DVT when a patient with previous DVT now has new legs symptoms swelling pain in the same like whether DVT used to be, we wonder, is a past somatic son norm as the new clot and often the decision, whether we call it a recurrent clot or not, the combination of assessing the clinical symptoms Yes, they're clearly knew. Getting a dime. Er it's positive, suggesting maybe this is a new clot. Negative is an argument against the new clock and getting the Doppler ultrasound and looking at the characteristics that I described C T scans. It's always worthwhile to question the radiology reports with CT scans looking at PES. That could be poor contrast. Filling the timing can be wrong of the contrast that maybe motion artifacts. Um, so if there is a question, it's worth looking at the skin and discussing it with a radiologist. I want to give you an example of a patient we saw a few weeks ago. Real patient, 60 year old smoker came to the E. D was sudden onset of shortness of breath. They thought about P E D. Drama was negative. They did His C T a. P was found did Venus Doppler ultrasound. It was negative for DVT, and they admitted to the patient for treatment of the P E. But the patient also has a history of COPD was wheezing and COPD treatment was initiated and then the patient was sent to the hematologist with a question. How long to anti coagulate? And the thought was well, it's an unprovoked p e. The patient had been ambulatory, so this needs to be long term for years to come into co regulation. But then it was striking that the patient had significant COPD and needed to be treated for the COPD in the hospital. So the hematologist, one of my colleagues, reviewed the C T scan with radiology, radiology and the best chest radiologist. Now she what was called filling defects and you see them listed right here. We really flow artifacts, and the experienced radiologists said this is not a P E. This is a poor contrast study, which you can see it's not well filling. Um, and the patient did not have a P um, and the negative D. Diamond. The negative doctor also argued against a QP, and the patient was treated with COPD and to co regulation one stop. And that's quite a difference. Lifelong long term versus no antique regulation. So questioning the radiology reports, particularly with a sub segmental pes or when the radiologist color report possible PE or low volume PE or cannot rule out PE. In that case, it's always worthwhile to talk to a radiologist so they can have that C t scans. If it does not match the pretest clinical assessment, then the C T A can be wrong in up to 50% of cases, i e. You think it's a PE, but the city is negative. You wonder if the city correct or the symptoms didn't really suggest the P E. But the CT scan is read as positive. The C T scan can be wrong for the reasons that I mentioned earlier and then review with radiologist, particularly if we're dealing with a sub segmental i e. A small PE sometimes radiologist called the pe an acute or chronic p e in a certain criteria that they list that argue. Four cute versus chronic, acute being more central, chronic, more volunteer. And but my experience over the years has been often even the experienced radiologists have different opinions what secured and what's chronic. So take that adjective coming from a radiologist with a grain of salt beacuse skin. So the question is an appropriate test to look for chronic perfusion defects for chronic p e. Um, and the CT scan is not sensitive to pick up old PES and perfusion defects. But the VQ scan is, and this is particularly important when we look for chronic crumble Anabolic pulmonary hypertension III significant perfusion defects from previous either one cloud of multiple clots so the Caravan four VQ scan Cystic Houston's cannot differentiate between acute and chronic PE. All that they can see is perfusion defect that could be old or could be chronic. We need to keep in mind that the Q abnormalities can persist for months after an acute P E. For example, this study showed that two thirds of patients had a VQ abnormality at three months after the P E. So this may not be a new club that we discovered by VQ scan, but an old clot. So the teaching points on the imaging. No, the limitations of Doppler ultrasound and CT A and review imaging with a double a technician or radiologist. If there are any questions, any discrepancies or if this really makes a huge difference for the patient treatment, long term versus short term antique regulation. VT. Treatment So I've shown this before. It's a really good example to highlight that DVD MP a classically multi factorial. So this email from a physician to me reads, Hi, Dr Mall Anita recommendations about a 56 year old man, 2013 right leg DVT and PE had Trezeguet's factor. Five Leiden, long term often and you all know this is really limited information that's being provided. The key determinant. How long to treat with anti coagulation is whether the D. V T o. P was associated with a major transit risk factor and between short term or it was unprovoked and between long term. The fact that the patient is heterocyclic effective have Leiden typically does not change our management. It's a mild from Ophelia. Minimally influences risk of recurrence. And if we talk about long term, often we do need to know. How did the patient total at the antique wagon? Bleeding issues stable in ours because the decision how long to treat is typically conglomerate of VT risk factors and bleeding risk factors. And maybe this is my most important teaching point of my most important slides the multifactorial nature of both these aspects and enlist them as ABC. We want to identify all the contributing risk factors why the patient had a DVT or PE, and this is a recent long distance travel be body mass index of 35 C. Somebody did from affiliate testing heterosexuals, five light and D family history of E. T F. Birth control pill, etcetera, then bleeding risk factors is similarly often multifactorial. A fluctuating iron Osby hemorrhoid C has quite telepathy due to liver disease. D has thrown a subpoena from hyper spline is, um, etcetera. So my teaching point here is and this is, as I said, probably the most important one, because it's a concept that helps not just with D v t of the lake and pe the common VTs, but also with the unusual clothes, the portal vein thrombosis, Sinus vein thrombosis. Define the clock first and then list all the thrombosis risk factors and the way that looks in my clinic note is as follows. The Venus from embolism. I define it right leg proximal DVT, proximal versus distal matters regarding risk of recurrence in 3 2020 video risk factors and then my ABC. So another point that comes up on the in patient service, for example, and we get the consultations submitted for GI bleed on warfarin and the consultation hematology is when to restart anti coagulation. But certainly Lee, there are a number of factors that determine when to restart. What was the iron out when the patient was admitted? The other risk factors for bleeding aspirin, et cetera. But the first question, really is that we should ask. Well, does this patient really still need to be on long term anti coagulation? What was the indication for the warfarin and revisit what led to the initiation of anti coagulation? So my teaching point there is question and revisit the indication with a detailed history of each clot in the past. It's not that revealing to just say, Oh, the patient had recurrent DVT. All those could have been a distal DVT with a hip replacement and another distal with a knee replacement surgery. That patient does not need long term antique regulation. You may need to get objective records of the double largest sounds and then always questioned the diagnosis of protein. C. Protein is an anti thrombin deficiency and anti fossil lipid syndrome because, as I will show a little bit on many factors, acute Claude being on an antique wagon, influence the levels of these tests. Family history. So in our history, taking residents may come back from the patient's room of fellows and say, there's no family history of bleeding or clotting. When nobody in the family had a clot, what I really want to know is, is the family history. Is it a small tree, or is it a huge tree here? The red is the program, the patient with a V T if he or she only has two parents but no uncles, aunts, no siblings. That's a small family history tree and a negative family. History is not very meaningful, whereas if it's a huge family tree, a negative family history of no bleeding, no clotting is meaningful to rule out or to make it quite unlikely that there's an inherited familiar from Ophelia or, in the case of bleeding, inherited familial bleeding disorder. So the teaching point is to obtain a detailed family history and not just asking the patients to anybody in your family who has a history of blood clothes, social history. That's important to me, not only because that's how how I remember patients and engage with them and see that they're not just patients but have some real life behind the medical issues, but also because it gives me a chance to talk about anti coagulation management at times of their professional activity or their hobbies that they love to do, like contact sports or situations that lead to a high risk for bleeding. And we can discuss temporary interruption of anti coagulation for two or three days while they go skiing or skipping the morning and the evening. Those prior to going mountain biking or bungee jumping, etcetera, physical examination place not that future role in thrombosis care. And that's why I'm doing this virtual visit time that we've experienced in the last year. Many of the thrombosis patients can be seen as an outpatient, particularly the question. Should I be a long term anti coagulation or not? But what is important to me is typically measuring the calf circumference, and I go to the superior board of the patella. Easy to feel to the mid calf wherever the camp is the biggest and measure the circumference. Now compare left to right side. And that's how I documented in my chart, right more than left by two centimeters. It allows me in the future in a year when they come back and they say I have more swelling to objectify that, or if they come back with a suspicion new symptoms. Could this be a new clot? I can compare it to the baseline what they had when I saw them in clinic and then the other part of the examination. Self understood, but, um, sometimes not appropriately done. Yes, Linford and apathy to look for malignancy and abdominal exam That's often done, but breast exam may not be routinely done artistically. Examined the young person. But we need to think about those malignancies in patients with new D. V, T O. P. And then the patient may have problematic sunrun swelling, pain, etcetera. And what can we offer? The patient compression stockings? And they do not prevent the past symbiotic Sonam. But they can be beneficial treating the past symbiotic Sonam leading to symptom relief. And while we used too often say and I did that to recommend the tight ones 30 to 40 millimeters of mercury well, patients can also try the 20 to 31st. They are not quite as tight. There may be more comfortable because these may be too tight to be comfortable, but it's really up to the patient to wear whatever they feel comfortable and give some symptom relief. And if neither one of them does, they do not have to wear them. And if the swelling is below the knee. I recommend or suggest that bologna stocking. The swelling also involves the thigh I would suggest and above thigh stocking and see how they tolerate it. The other thing that we can do is we think about pelvic vein narrowing from the thrombosis or, on the left side, the main furnace syndrome. So to all the CCTV anagram or MRV anagram, whichever your institution does better and more reliably is appropriate in patients with significant part symbolic syndrome. Because if you find narrowing, you may send the patient to the interventional lists for angioplasty and possible standing, which in some patients helps. We can offer home compression, pump the lymphedema pumps to be worn in the evening for half an hour, an hour pain clinic appointment to manage chronic pain and disability assistance. And if a patient had a significant P E or at three months or six months still has significant respiratory symptoms. Chest pain, shortness of breath, fatigue just can do what they used to do when we start to think about some chronic damage to the lung, which in the most severe cases a chronic from anabolic pulmonary hypertension. But if it's not for my attention. It can be the chronic from metabolic discipline. So I take a good history. I walk or run with the patient three flights of stairs with the pulse oximeter and see how they do. Compared to me, I do a cardiac echo not very sensitive, but it may pick up a right heart strain, and the VQ scan is the gold standard of perfusion defects. And if these are not normal and there's suspicion that there may be some chronic damage and I send the patients with pulmonary hypertension clinic, they do a formal six minute walk test, and they may do a right heart cat for pulmonary pressure measurements. An angiogram to see whether Parmley and direct me might be appropriate. So teaching points here, plus somebody soon on treatment, offers stocking. We don't make patients wear them, but we offer them and suggest them and then consider venogram and possible stenting and then recognize the post pe syndrome in a patient with P E, either as chronic from anabolic pulmonary, a display here without significant hypertension or the chronic from anabolic pulmonary hypertension that requires or should be evaluated for pulmonary endarterectomy and how long to treat with anti coagulation. Many of you have seen me present this recurrence triangle, and I continue to use it and find it very helpful. I modified as new data come up, but there's nothing new, really. In the last year. This really reflects if a patient has been treated with anti coagulation for three or six months and then stops and the risk of recurrence is low that patients in the Green Zone tip of the triangle low risk for recurrence three months short term of anti equalization is appropriate. That would be a DVT LP due to a major transit risk factor. Hip replacement hysterectomy, etcetera. Down in the broad red zone of the triangle, high risk for recurrence is a man with an unprovoked DVT, or pe high risk for returns. Long term entry correlation. A woman with unprovoked VT. Has a somewhat lower risk than in men, but still high enough that it's in the red zone. Still, long term enter co regulation if they tolerate the blood thinner well, and then we have some patients here in the intermediate zone not low enough to stop, not high enough to feel comfortable continuing for years to come. What do we do? Women with VT. On hormones, birth control pill, non major transit risk factors, some outpatient, arthroscopic knee surgery or a clock maybe four weeks after long distance travel? Not really close to it. Well, I draw the patient that I see in clinic into the triangle, wherever by history and by the multiple risk factors the patient fits and where I think the patient fits in recurrence rate, and then we can use the deed. I'm, er, these intermediate zone patients. The negative diamond pushes the patient to a lower risk for recurrence. Positive diamond pushes patient down in the triangle here, up here, we can stop in the red zone. You continue, and this is a diorama on anti coagulation. If it's negative, we stop anti coagulation. Repeat the dilemma four weeks later, and if it's still negative, the patient is in the Green Zone. We continue without anticoagulants, but if the patient was positive or turns positive, highest risk for recurrence. Continue anti coagulation or restart. Also, it's this patient population where think about it from a failure. Work up. I'm looking for a strong from Ophelia protein C protein s anti thrombin deficiency. Hamas, I guess. Five laden doubleheaders, I guess. State or strong or anti fossil lipid syndrome? Not the simple heterosexuals factor. Five Leiden or simple heterosexuals. Pastrami Mutation. The Strong from Assyria pushes the patient down in the triangle as one of the reasons to consider long term mental co regulation only finding heterosexual factor. Five. Leiden barely changes. The patient's position pushes the patient down a little bit, typically not enough for decision makings and a strong predictor of recurrences. Anti foster lipid antibodies, particularly the triple positive patients and below that, the positive Lupus center requirements. But we also need to look at the degree of positivity of the anti foster lipid antibodies and certainly the repetitive testing. It's a teaching point on this topic. Try the Recurrence triangle and see how that works for you and then getting back to the decision. How long to treat We've talked about these two aspects. The third one is the patient preference, and many of you know that I used the war from hate factor. Ask the patient on the scale from 0 to 10. How much do you have to be on warfarin? Zero means it's just a pill. I don't mind it. 10. I hated incredibly, and ask them to take together the need for monitoring the dietary interactions, the risk for bleeding, the cost. And then they give you a number, and then the typically spill out why they either don't mind being on it or why they hated so much. Now do the same with the individual direct oil anticoagulant there on What's your arcade factor? And then I make sure that they address what the copay issues. I asked them, What is your copay? And that's often the reason why people mind the docks. But it gives me the chance to talk to them about the patient support programs that all the door companies have. Where people with insurance can often get the drug for $10 a month, at least for the first month. Um, for the first year, sometimes for 2nd and 3rd year, it's a teaching point Here. Try the often hate factor and the do arcade factor and see how it works for you at the patient and with the dark. In fact, to make sure you ask What is your copay? How much do you pay at the pharmacy and then from affiliate testing. What are the key points there? We have told you in whom I consider from affiliate testing. Those are the people in the intermediate range in the Recurrence triangle. I want to find a strong from affiliate, but I have four general rules who and when not to test and number one do not test during an acute from Batic episode because the acute thrombosis changes many other functional coagulation tests, particularly protein C s anti thrombin, a Lupus and requirement. So you get falsely low values and falsely positive tests. Similarly, don't test the hospitalized patient because the activity is sick and therefore the sickness, whatever it is infection the acute illness, it gives you false abnormal tests and tippy finding. Economically, it does not change the acute management. The patient with an acute TV t p needs antica regulation. Yes, As a hematologist, we see the occasional patient with catastrophic anti fossil lipid syndrome. The patient we consider P N. H. Or a mile of proof of neo plasm. But a general rule applies not to test acute traumatic episode in hospitalized patients and then similarly, the don't test the patient is on an anti CO. Ireland because anticoagulants influence many of the clotting tests. And if you don't know how to interpret the test or what to do with the results, don't test. And that's really referring. Mostly, if I may say that to our surgical and E D colleagues, So I've put together a table. Here are the from a phileas here, the acute thrombosis unfriend champion therapy lawmaker, heparin, warfarin therapy, the dogs and how these situations influence the test results. And you see the number of them that are listed as unreliable elevated may be low, and it reflects that we have to interpret labs with caution in these situations. And I want to particular highlight the Lupus anticoagulant as a hematologist. I think while it's good to look at the lab result and see okay, fast, Philip, it dependent inhibitor demonstrated. So there is a Lupus anticoagulant. I think it's good for the hematologist to be able to tell what was actually done in. How positive is this Lupus anticoagulant? It can be quite confusing with all the numbers and abbreviations list that. But if I just take this patient right here, a real patient who had a key values. Are these two right here? The DVD ratio was 1.27 In our patient, normal is up to 1.26 So this is a barely pause of Lupus anticoagulant. The SCT ratio is 1.2 and that's where the normal. So this patient has a minimally pause of Lupus anticoagulant, very unimpressive, possibly probably the false positive at the time of an acute clot or while being on an anti choir land. And if the anti capitalist and anti beta twos are negative. I'm extremely unimpressed by that, However, if this test was strongly positive, but both tests plus, maybe there's an anti Catholic and anti better to I'm much more impressed that this may be true anti fossil lipid syndrome and that I have to be more cognizant about risk for recurrence, retesting, maybe using Worf in instead of a direct anticoagulant for the acute D. V. T. R. P. So teaching point here. Be clear whom to test and went to test. I've presented you my four rules. Be aware of the influence of anticoagulants and from affiliate tests and with Antifa selected tests, understand what exactly the lab did. And then finally, whenever we stop anti coagulation after 36 months or whenever the treatment ends, it's been recommended appropriately to get a baseline. Follow up the plotter son of the legs to have a baseline study in case trouble comes up in the future. In a year, there's new leg swelling. They scan, they find a clot so that, you know, is that a new cloth since antiquity was stopped, or is it the old scar tissue? While the Doppler lab and publications often talk about residual clot, I don't like that term, and patients don't like it. Often they think clot can still break off, but this is really scar tissue after a few weeks or months, so I like to call the residual cloud. Rather, yes, you have some scar tissue left, but there's no risk for breaking off. And then people ask, and typically, healthcare professions. What does a long term into coagulation really mean what it means extended? It means kind of lifelong, long term, but a re evaluation every so often, maybe once per year. What are the new data? The new studies, the new drugs? What is the new risk benefit. What events have happened regarding bleeding, etcetera? What hobbies of profession Influence the anti organization management. What does Doc Full dose versus lower dose have been studied and FDA approved. So with that, the main points of my talk have been I've summarized in the 22 teaching points that are in your conference materials. You can read up on them but if you really ask me what are the three key points? And they're very self understood and nut high powered as a Terek, but really clinically, I noticed they do help people think about dvt pe define the DVT PE first list the risk practices ABC Try the recurrence triangle and use the warfarin or the dark hate factor with the patient that I thank you very much for your attention.
