Good evening. Thank you all for joining tonight's webinar. My name is Lori Lazansky. I'm the chairperson for the SVU eLearning Educational Committee. Before we begin, I have a couple of notes from the SVU office to share with you. This webinar will be recorded and available online after tonight for attendees through the SVU website at no charge. Please take a moment to familiarize yourself with the GoToWebinar program. Everyone should see a question section along the side menu on the right side of your screen. It's near the bottom of the column just above chat. So please type in any questions that come to mind during the presentation. And at the end of tonight's talk, we should have some time for discussion. To receive your CMEs from tonight's lecture, you'll need to wait for an email from the SVU office containing an evaluation. You should get that email in about seven days. Once you get the email, complete the evaluation, and your CME certificate will automatically pop up for you on your screen. Tonight, we're privileged to have Dr. Karen Harth joining us for her talk, Venous Thrombosis, Ultrasound, and IVUS Interpretation. Karen Harth is a board-certified vascular surgeon and a registered physician in vascular interpretation. She serves as director of the Center for Comprehensive Venous Care and is the co-medical director of the vascular laboratories at University Hospital's Harrington Heart and Vascular Institute. In addition, she is an assistant professor of surgery at Case Western Reserve University School of Medicine. Dr. Harth earned her medical degree from Stony Brook School of Medicine in New York. She also completed a Master of Health Science at Johns Hopkins Bloomberg School of Public Health and completed a general surgery residency and vascular surgery fellowship at University Hospital's Cleveland Medical Center. Dr. Harth is an active member of multiple national professional organizations, including Society for Vascular Surgery, American Venous Forum, our very own Society for Vascular Ultrasound, American College of Surgeons, and Society for Clinical Vascular Surgery, and she's given multiple lectures at regional, national, and international society meetings. Dr. Harth has been a contributing author on over 100 articles and abstracts in peer-reviewed journals and major societal meetings. She reviews manuscripts for such highly regarded publications as Vascular and Endovascular Surgery, Journal of Vascular Surgery, Journal of Vascular Medicine, and Journal of Vascular Surgery, Venous and Lymphatic Disorders. In her own practice, Dr. Harth treats a wide range of vascular diseases, but is especially interested in the treatment of venous disease. Her research efforts are related to chronic venous thrombosis, ventral hernia repair, and vascular access techniques. She is a recipient of the Faculty Teaching Award from the Division of Vascular Surgery and Endovascular Therapies at UH Cleveland Medical Center, and has been named a top doctor by Cleveland Magazine multiple times. And you can see and hear more from Dr. Harth at SVU's 2022 annual convention. Dr. Harth will be speaking on Thursday afternoon during the conference, during the joint session between SVS and SVU. That session is on the importance of the relationship between the physician and the vascular technologist. Dr. Harth is going to present pelvic venous disorders, how the ultrasound findings help guide the treatment plan during the meeting. So hopefully many of you will get to hear her talk again in a few weeks, this time in person. And now, if you would, please join me in welcoming Dr. Karam Harth. Thanks so much for that very generous introduction. I'm very excited and privileged for this invitation and hope that through this talk I can share some of the sort of pearls of wisdom of how I envision some of the conditions and some of the things that my patients deal with when they have venous thrombosis. And perhaps through a focus on what we know or don't know or hope to know more of in regards to what ultrasound and IVUS shows us, we can bring that knowledge with us as we image patients, as we take care of patients, and kind of help, I think a lot of that helps really guide the therapy choices we make. So with that introduction, a little bit of a prelude, I'll start my talk, which is titled Venous Thrombosis, Ultrasound, and IVUS Interpretation. These are some webinar-related overviews. We'll discuss the venous thrombosis ultrasound criteria and review some cases. These are some disclosures, and my disclosures are noted at the bottom. And if at any point you can't see me or hear me or the slides are not moving or the movies aren't playing, please just let me know. Okay, so just briefly in terms of a talk, I will review the epidemiology of venous thromboembolism, some pathogenesis and phases of thrombosis that I think are important to consider. Sometimes we just have to go back to the basics. I'll introduce this role of aging thrombus, which was actually the initial kind of request in terms of a talk. And so this is, I think we don't really think about it this way very much, but it is, I'll introduce some of the concepts behind it, how to think about it and why it's relevant. I'll review this in light of ultrasound and IVUS imaging. I'll give you some of my perspective on how I do my interpretation, some of the clinical relevance of aging thrombus and why we should think about it that way, and review this in a case-based approach. And then I'm happy to take questions at the end. And so much, again, so much of what I'll try to cover, really we'll just try to touch on some of these things, highlight some of these things, and really just offer some food for thought and use some of these, some of the cases I'll show to kind of highlight these points here on the goals of the talk. So venous thromboembolism, it's not an uncommon problem. It's a significant burden to our society. There's about one to two per 100,000 individuals affected annually, which in the U.S. translates to about 900,000 cases. Over 60 to nearly 100,000 annual deaths from a venous thromboembolic event. And about 25 to 55% of patients will present with a concomitant pulmonary embolism. 20 to 50% will progress to post-thrombotic syndrome, which I'll explain a little more about briefly in the talk. But this is a significant burden and a significant quality of life problem that can be secondary to a lower extremity venous thromboembolic event. It decreases mobility, causes leg swelling, and leads in severe cases to venous ulceration. One-third of patients will have a recurrence of VTE over a 10-year period. Major economic burden with an annualized medical treatment cost of about $25,000 per event. In the bottom right of the screen, you'll see what is considered the Birchhouse Triad, kind of a classic teaching in terms of what predisposes you to a thrombotic event, which includes endothelial injury, hypercoagulability, and abnormal blood flow. So the triad of these factors can lead to a thrombotic event. And some risk factors that are considered to be associated with having an event are listed on the bottom right of the screen. So phases of thrombosis. Again, this is kind of getting back to the basics. So it's really a complex interplay between coagulation, platelets, inflammation, innate immunity, and fibrinolysis. And why this matters is because this is, this really helps us understand how thrombus changes and how we treat it differently secondarily to that and why we, both medically and procedurally, why we treat it differently. And this helps us kind of think about what choices we make. And from a device perspective, and I think from an intervention perspective, this helps me think more about choice of device, which I think is still yet to be teased out because there are so many devices out there. So the process involved, or the phases involved, formation, propagation, and resolution. The formation phase of the triad activates endothelial cells, platelets, neutrophils, and monocytes. It leads to a deposition of fibrin, red blood cells, and immune cells, which ultimately leads to the thrombus. Anticoagulation at this phase really prevents a thrombus propagation. The resolution phase and the recanalization phase, which is much later along the spectrum of the thrombosis phase, we're now involving, or now involved are the inflammatory cells and the fibrinolytic pathways. These things occur simultaneously and over a period of time. It's not seven days, 12 days, 30 days. Sometimes you may read in different papers that describe the chronicity of certain thrombotic events, but really it's over time. We'll talk about that. So fibrinolysis is the most active early in the phase of resolution, and collagen remodeling takes place later in the phase of resolution at its highest level. This really helps restore some of the blood flow to create some channels and really try to recanalize some of the venous portions that are affected by thrombosis. Again, how well the system recanalizes and heals really impacts the development of post-thrombotic syndrome or the long-term significant sequelae that can occur in a certain percentage of patients. So post-thrombotic syndrome, I mentioned that a couple of times already, it's the secondary effects of the inflammatory and healing response to a DVT. We're going to focus on lower extremities, or at least certainly from the IVC down. It has damaging effects to the endothelium and the venous valve that causes venous hypertension below the level of the disease or obstruction level or the area that subsequently has valvular dysfunction, because there's a column of blood and a pooling that occurs, which leads to a venous hypertension, which subsequently impacts the lower extremity and really the endorgan or the skin, and certainly other components such as lymphatics. It's a major source of morbidity after a DVT. One in two to three patients with a prior VTE or throat to suffer from some grade of post-thrombotic syndrome. 10% of these patients will have severe post-thrombotic syndrome. Some of the symptoms of post-thrombotic syndrome include ligatema, ulceration. It can include venous platication, which is a really severe pain and tightening. People describe it as a constricting band, a tightening of their skin, and they have to kind of sit down, take a break, and really elevate the legs. And that rest period takes a long time because it takes so long to drain the legs of the venous blood and all that venous hypertension that's developed from the ambulatory state. There's been studies that are pretty remote, but pretty interesting in terms of looking at how medical management of the different segments of the lower extremity venous system, how they respond to anticoagulation alone. And so when we look at the ILLIAC system, it's thought that only when you have an ILLIAC thrombotic event, only about 20% will achieve full recanalization and long partial recanalization will be at about 20%. The remainder really don't recanalize well. In the femoral segment, about 50% will recanalize with medical treatments and significantly more so in the popliteal and the tibial DVT. And so for me, this has helped me validate how I make choices in terms of who is a good candidate for procedural versus medical and really weigh the risks and benefits, at least to some degree. This isn't the full answer. This is the only answer, but to some degree helped me in my decision-making about who best benefits from a procedure. So aging thrombus, let's first kind of think about, you know, can we age thrombus? And this is a clinical question, an imaging question, a procedural question, as you'll see from some pathology specimens that I'll show. So DVT resolution really resembles the wound healing. And this diagram here is really one for wound healing, but it resembles it in the sense that multiple cellular events, as described earlier, are involved at different to different degrees across time. And it involves profibrotic factors, collagen deposition, MMP expression and activation, and really over a sequence of time. And this time isn't necessarily perfectly defined, and nor is the response to how well someone heals or doesn't heal. So keep that in mind because this really, I think, to me, highlights how each patient really has an individual response, and we should consider that along their care. With regards to aging thrombus, some interesting work here, with regards to aging thrombus, some interesting work here from Nicholas et al. in 2020. At the top of the image, at the top of the screen, shows the three stages. And these are for a mouse model of an IBC occlusive process, looking at recanalization events over time with anticoagulation, and how this may translate and parallel a patient who's had medical management and venous stenting, and they've had venous biopsies, and how their cellular response changes over time after their thrombotic events. And so what we could see is that in the first stage, you see a lot of erythrocytes, the red cell that's in that yellow kind of look and appearance, with significant platelet deposition. And in the mouse model, that's anywhere from two days, and then the human, at least the biopsy timing, is about a week period. This moves on to stage two, which can occur over seven plus weeks, and really here you get fibrin and infiltrating immune cell deposition. And then the last stage, stage three, which in the animal model was around three weeks, but in a human model, or the human biopsy of these patients that underwent therapy, it was about a 54-week time frame, at least when the biopsies were evaluated. And this, as you can see here, the significant collagen deposition and the changes from a histological standpoint, which I think to me is very interesting and certainly something that we're actively discussing with some of the pathologists at my hospital. All right, so how do we optimize ultrasound to help us age thrombus? And can we actually accurately age thrombus using ultrasound? I think hopefully we'll see that the answers are not so obvious and they're not so easy and sometimes a little bit confusing. So let's talk about two common modalities of ultrasound evaluation that certainly most folks on this line will be experienced with or understand or heard of or use in their practice. And this relates to the evaluation of lower extremity thrombotic events. So we'll take a linear transducer and compare that to the standard large catheter intravascular ultrasound catheter that's used for deep venous work, which are much larger vessels in the arterial segments. And so this requires a bigger field of view. So I think it's clear to this group that duplex evaluation for DVT is really the gold standard for diagnosing lower extremity venous DVT. And similarly, amongst common users and expert users and proceduralists of venous thrombotic disease, the IVAS catheter or intravascular ultrasound of the deep venous system is really the gold standard for the guiding therapy and procedural success. Certainly a linear transducer is noninvasive, whereas the IVAS catheter is. It involves cannulating a vein and using a sheath to guide the catheter. The hertz or the strength of the probe usually ranges from 5 to 10 megahertz for the linear transducer, depending on what you have. And in general, the IVAS catheter is about 10 megahertz is common. As you're getting to 20, you're getting to sort of the smaller catheter, smaller vessel type megahertz. So in general, the 035 or 038 catheter for deep venous work is 10 megahertz as well. A linear transducer obviously is mostly for the infrainguinal area. So we're evaluating the stem top and the tibial levels, whereas the IVAS catheter also allows us to evaluate the segments, but then go higher up into the IVC and ILLIAC. And really, we get a look from within and within the channel and really get this very detailed, informative evaluation of the venous system. We have multiple ways of adjusting this and I think this to me is really important because most of us are experienced or know that we can adjust things with a linear transducer when we use the ultrasound but there's not a lot of discussion at least that I hear and certainly there's not a lot of experience unless someone physically takes you through it in adjusting and optimizing an image when you use an IVIS catheter but they both have the opportunity to adjust the gain. You can adjust the field of view or the depth of view and in the case of a linear transducer. Both allow for B-mode evaluation and change of gain. So I think gain as we all know is very to the beholder of the eye it's very important in optimizing the image and so that's I think to me critical because how we interpret the echoes that we're receiving on ultrasound really may change how you interpret the ages from it. So both have the gain opportunity to adapt. Color flow is an option for linear transducer it is not a current modality available for IVIS catheter at least not for the large catheter the large diameter catheter. With linear transducer you can certainly evaluate directionality with spectral Doppler with an IVIS catheter. There is no you know spectral Doppler so directionality is not really an option as it is with a linear transducer. Both have different dynamic things you could do. I think some of the things that we do for venous insufficiency studies certainly we're not doing and are not part of protocol and we're standard for a DVT scan but you know in terms of positioning a linear transducer and someone who's having a DVT scan is supine. You can do dynamic you can do color evaluation again see if there is any flow partial partial compression with partial flow through a channel or completely occlusive you can change the color the chroma and things to help you visualize things better. With an IVIS catheter you really rely on the physician so patients either usually supine or prone and that really to me is a big predictor or at least influences how you look at certain parts along the venous system because you can't have changes such as that are induced from external compression. Respiration can affect how pliable or non-pliable because they're full of thrombus how the vessels are so respirations really affect what we see and if we when we evaluate specifically for compression issues we can get a sense of volume. It's very affected by volumes and some are very volume depleted you may have more than normal collapsed vein and that can alter how you make a decision at the time of the procedure so that has to be considered the volume status. You can certainly augment the leg you know calf level if you're working from below to see if there's any kind of movement of blood and again this is just B-mode you can kind of sometimes see a little bit of rule changes if you have a stagnant column. And a lot of this what we see on IVUS is based on access sites so where you access the vessel dictates how much you can or can't see so if you're going from the jugular approach or if you're going from a femoral or popliteal approach you're limited because if your catheter really just goes up in one direction away from your access site so that limits what you could see and obviously we want to see the most we can so sometimes the choice is to pick the site furthest from where you're going to intervene. Procedure wise you know linear transducer again diagnostic with an IVUS catheter can be used pre and post intervention so it can also just be used from a diagnostic standpoint. So most folks likely know some of this but I always like to kind of think about you know why do I see what I see when I use ultrasound so I like to go back to the basics with this as well so we know that our ultrasound machines are calibrated to the velocity of sound which is about 15-40 millimeters per second and B-mode provides a view of all of the reflected echoes we receive when we evaluate a structure so ultrasound blood and acute thrombus appear anechoic because versus aging thrombus where they'll be more hyper echoic. Acute thrombus has a high red blood cell composition and the earlier it is in its formation certainly they'll be more anechoic and over time these red blood cells decrease the content of fibrin and eventually collagen increase and that will give you more reflective echoes giving you more hyper echoic changes. This just compares some of these things like echogenicity across an acute DVT or chronic DVT which we'll talk about some of that terminology when you have a linear transducer or a lower extremity ultrasound evaluation and IVAS both in general have this hypoechoic look when it's an acute thrombotic event and more hyper echoic or changing in progressive echogenicity as you get to the more chronic phase. In acute DVT you'll have a larger more extended lumen both on ultrasound. IVAS you obviously don't compress but you will see a distended fixed immobile vessel from within that's not respondent to maneuvers like valsalva or holding breath. In a chronic state in ultrasound you'll have a small irregular lumen and the variability of that depends on whether the vessel was able to recantalize from the DVT or a contracted and fixed vessel as well on a IVAS evaluation. You know and so generally this is the two extremes right and I think those sometimes seem obvious so I think we're much better at the acute thrombotic events evaluation but the middle is a very broad base and it's a long period and I think this is really where the art of interpretation affects you know we all have our own different experiences that we bring to the table. I think this has a little bit more art to this and certainly some subjectivity to this part. Ultrasound imaging for lower extremity is really the gold standard for evaluating lower extremity DVT as mentioned with good sensitivity. As we get to the calf veins the sensitivity decreases and I think with this aging thrombus or an attempt to age the thrombus it's estimated that about 30% of DVT may be wrongly staged using you know common modalities and criteria again because perhaps we're not these subtle findings are not being aged or accurately evaluated. So I think I just this brings something of importance to me which certainly I talk about with my colleagues and in our group in our vascular lab which is this sort of interpretation of chronic DVT which I think can certainly confuse the the more sort of common provider or the referring provider who orders an ultrasound from your vascular lab but I think it can cause an overtreatment because if they see chronic DVT they may forget the chronic part or not understand that it's the post thrombotic change and then the patient may remain on anticoagulation for you know because of the usage of this language. So this is a really interesting and good paper which I encourage you folks to read which really based on an expert panel and a large group of expert physicians and thrombotic imaging they recommend using the term chronic post thrombotic change and I think that's something important to consider and something certainly that we consider for our lab. So then the next few questions is does age of thrombus matter clinically? Does knowing the age of thrombus help guide interventions? And I think that there is a role to that. So why is it of interest? Well there are different clinical therapies that work best under different circumstances. The venous field is rapidly growing and there are many many devices in the pipeline, many new devices that have just come out in you know in the last decade and these are going to continue to grow. How thrombus appears may predict and I think can help now that we have so many different options may help us decide well which device should we use or which therapy should we try first and this is not just an imaging to treatment kind of translation obviously primarily we have to think about the patient's symptoms. Do they even would they benefit from any therapy? So that's probably the largest group of patients but I'm kind of focusing on a select patient population that we may potentially consider therapies for and who are these right correct patients and I think there's a lot of really great research trying to answer that question because certainly a therapy is only as good as the benefit it offers the patient so we don't want to have a patient undergo unnecessary procedures. So in a very rough and very you know crude if you would overview we can say that we treat DVT in the infertile region with anticoagulation and ileofemoral disease with anticoagulation and you know selectively procedurally as again indicated based on the clinical picture as long as we feel that there are some benefits to preventing post thrombotic syndrome which is what we generally want to prevent in the acute phase. In a chronic phase we would say that a good indication is someone with a venous ulcer or healed venous ulcer. I think there's a lot of pretty good data for that. In my practice certainly I pick a therapy and or device that will help me clear the most thrombus based on timeline of patient symptoms based on the imaging how the patient feels is there a clear indication am I going to offer a benefit as I want the best long-term result for any stenting that I may perform at the time of my procedure. Certainly I think with such an enthusiasm and devices and therapy development choice of device can be confusing so I think it's important to be very thoughtful about that. And so when we actually age thrombus at various stages of a patient's evaluation you know we do it clinically we do it based on imaging with ultrasound and the latest iteration of devices. We also do it with the specimens that are extracted with some of these new devices. Yet with all of these three scenarios you likely have a different definition in your mind about what's acute what's the subacute or chronic and what's post thrombotic if that's the language you're using. So I just I kind of put this here as a way of showing that there's a range of time frames and not everyone is speaking the same language when they see acute subacute or chronic and so just consider that and take that into account when you're considering discussions about DVT. In the lower half these are just some specimens and now you know we're talking about aging specimens and I it's interesting at the American Venus Forum recently there was some discussion about this which I found interesting and made me think about well I say this looks chronic and truthfully ever since then I kind of stopped thinking that middle part looks chronic. So what is chronic? You know again thinking about this in the phase of thrombosis but certainly we know the acute DVT is really red cell rich and so that's on the far extreme of the bottom of the screen left and on the far bottom right. These are these really chronic post thrombotic changes that we see that are the end result that can be the end result in some patients where the the vein is significantly impacted by their thrombotic event. All right so with that information and with those thoughts we just move on to some cases. So I'll start off with some just quick look at infertile DVT using a linear transducer. So here we have a femoral vein that is not compressible so the vein can be either non compressible or partially compressible. When you have an acute DVT the thrombus appears soft or deformable with the probe. The surface is smooth. There could be some edema outside or the wall that's affected. The vein can be dilated more than larger than normal size and sometimes you can see some free-floating edge of the end of the thrombus. On the bottom right of the screen you see here there's no detectable color flow in this case. Here we have a Sine where we have a partially compressible acute DVT of the palpateal vein. There's not much echogenicity here. Overall I think the gain is pretty good and I mean it's almost non-compressible in this image here on the screen right of the slow shot. So similar to those characteristics we just described. Here we're looking at a case of partially occlusive DVT. When we look up higher at the mid femoral vein we see nice compression. No evidence of thrombosis at this level and as we move down to the palpateal level we have a partially compressible vein with some echogenicity but overall not hyper echoic. With some partial compression here we see some what I would describe as a continuous flow with a response to augments distally and this was a sort of a bit of a loose extension of the thrombus noted on long view here at the palpateal vein. So as we progress through the phases of thrombosis and as the thrombus ages you can see here that we have some more echogenicity changes occurring. This is a palpateal, we'll call it subacute DVT. Here it's non-compressible. There's intraluminary material. It gets more rigid, more echogenic, somewhat deformable depending on the extent of involvement. The surface is fairly irregular with a variable thickness. More chronic disease and really not in this phase but likely a later stage you may see some calcification changes from the prior DVT as evidence of DVT. And some of these really appear like those thin webs or thick bands which are called senechiae which I showed in that earlier pathologic image I showed earlier on the last slide. I thought this was an interesting image. We have a patient who had an acute DVT here on screen left, an image where you have a fairly anechoic, hypoechoic thrombotic finding which then was re-evaluated about five weeks later and here you start to see some of that recanalization or changes and collagen deposition, fibrin deposition making this look more echogenic with some channel, open channel here occurring and more of this laminated, layered, thicker look to what's occurring in the inside which is essentially a scar. This is a case of images showing an acute DVT which then about a year later with some edema was noted to just have mostly post-thrombotic changes. Likely has, you know, we would suspect that if you looked at this you certainly may see some deep venous reflux and this patient went on to subsequently have a recurrent DVT and so now you have some anechoic segments, some dilation of the vein with then some layering of the chronic prior events in that same segment and I think certainly we're not going to talk much about recurring disease and interpretation there but that, you know, certainly can add another layer of complexity and challenge when we evaluate these scans. Here we have a patient, same patient, to the right leg, left leg. Time frame is about a year to from DVT and you can see how nice and normal the screen left is which is the right leg and it's normal. The femoral vein, mid and distal segments are easily compressible. Walls are soft or supple. You get a full nice wink when you compress and on the contralateral side is an affected, the affected same segment of the other leg where you have a partially compressible segment and along different parts of the femoral vein with an irregular thickness along the views. So that's just some kind of basics. I think probably most folks in this line are very good at looking at those cases and now I just like to show you some of iliofemoral DVT cases where they either underwent procedure or not and how we look at that both from with ultrasound, how IVAS helped me confirm what what I suspected, how it helps me guide the therapy, how it's so important to looking from within to understand the anatomy and culprit lesions and what may have predisposed somebody to have a extensive DVT and how these things can change over time and how I use some of these things to help me decide how to approach some of these cases. So here we have a 67 year old female with a one-day history of sudden left leg pain, which was severe and actually caused some numbness or paresthesias, and this is a condition called phlegmasia. She actually woke up with a symptom, and preceding this she actually had about a three-week period of significant weight loss, which was not clear as to why. She also had significant GI symptoms, diarrhea, and so she was in a fairly weak and dehydrated state. Prior to this, notably, she had or she denied any leg symptoms, any unilateral edema, or otherwise. She was also in the midst of working up a breast lump. So we, you know, she was, she presented to the emergency room. She had a DBT scan of the left leg, which was the first thing they wanted to rule out, and you can see here as high up as the left iliac vein, there's a non-compressible, fairly anechoic segment of the external iliac vein. As we move down to the common femoral vein, you see that it involves not just the common femoral vein, which is pretty dilated and distended, but you also have GSV thrombus occurring at that same level near the sapheno-femoral junction. As far down as the popliteal vein, she actually had some partial compression, and so she, you know, her thrombus really was of a proximal type, multi-segments, mostly ileo-femoral. So, you know, to me this needs to be addressed urgently because she's having sensory deficit. Again, this is a phlegmasia case. So we expedited her. First things first, you know, she got anti-coagulation, hydration and anti-coagulation. I proceeded to take her to the operating room. We accessed her popliteal vein, going from a prone approach, and confirmed some interesting things, which I show here on my venogram. Let me kind of show it from this segment here. So, you know, as we talked about in this series of images here, the similar image that was obtained for the common femoral vein was actually obtained for the mid-femoral vein, but my venogram looked significantly different. And so this highlights a point here. If you look at the screen left here, the third series of ultrasound images, the femoral vein didn't have any of this slight echogenicity within the lumen, but it was deemed non-compressible. And so this was read out as an acute thrombus. On venogram, the lumen felt completely fine. There's a very distended and dilated valve just before the profunda vein, which is seen here right at the level of the lesser trochanter joint, the femoral vein, just behind the common femoral vein. Actually, this segment was actually free of thrombus. And this is a classic, not common, but I do see it on occasion, where the severe venous hypertension that can occur from extensive proximal BVT can actually impair the ability to compress the vessel. And so that's one component that affects it. Certainly, as you get towards the adductor hiatus, it's harder to compress that segment. So there's also patient-related issues, there's pain-related issues, edema. But this is not, you know, just think about that as you're trying to evaluate different segments. Sometimes you may not be able to compress it because of this severe venous hypertension from a very large proximal acute BVT. And when you compare the ultrasound images with the IVUS images, really they kind of look somewhat similar, where you have lack of exogenicity on the IVUS catheter. So here, for those that don't understand, have not personally done IVUS imaging, you have a wire that goes up the vein, and once you get your wire up, then the catheter follows. And the catheter, which is a little tiny probe that sits right at the segment you're evaluating that you can match with a fluoro image or an x-ray, you are physically looking within. So here's the IVUS catheter, here is the edge of the wall, and whatever's in the middle between the catheter and the wall is either an open vessel or thrombus or whatever it is that you're looking at from within. So here, we're at the common iliac vein level. It's not very echogenic. As we move down, sorry, that was common iliac vein. Common femoral vein here by the femoral head, also not very echogenic. A little bit of an enhancement of the wall of the common femoral vein, significant for inflammation, inconsistent with the findings on duplex. As we move down, we can see that perfunda comes off of you here at the nine o'clock position. And I want to show this sort of interesting cine here of what things look like here at the valve. So hopefully this image is playing. You can actually see the little red cells moving. This is what I call, what's called Rouleau flow. And actually when I give a calf squeeze, you can actually see the little valves opening and closing. So here we go again, there's that Rouleau flow. And you'll see there's the valve opening with augments at the calf. This may be a little bit of thrombus maybe behind that valve leaflet. But here as we pull down towards the femoral vein, that echogenicity gets less and less. And that's actually where the vein will open. As I mentioned, gain can be something that can be adjusted. And here we could see that by changing the gain on either from 41 to 50 using the same diameter. Things look very different here. You really make things look quite bright on the screen, right? And you could perhaps overestimate how, you know, what age the thrombus is. But this is just an example of how gain affects how you view things. You know, it's very subjective. But you try your best to try to balance out the gray, the black, the white, and the gray echoes. In this case, this patient's under one thrombectomy. We're pulling back the catheter. We're coming from the IDC on the screen left. And as we pull back, there's this compression point. You lose the lumen. It kind of winks at you like if you're compressing on the leg. I'll go over this a little bit slower. But as we're pulling back, we've achieved a nice clearance of the vein. This now, we're at the common femoral vein. Again, this is a prone case. And I'll share what that means there. But when we look at this case after sensing, we treated that compression point, which is called the Maeferner compression. That may be something you've heard about. We then place the sense to maintain the lumen and keep an open channel and a good outflow for that leg. And interestingly, I'll play this again. But here's that common femoral compression, which when you actually elevate the patient on prone, who's prone off of there, rested. Usually, we put them on these gel rolls or bumps, which tend to go end at the groin. And when we lift them up, lo and behold, that compression point goes away, which I think is a really important maneuver, certainly something I use every time I have a patient prone because I don't want to over-stent and necessarily stent segments that are not true compressions. The ones to stent and the ones to treat are really the fixed lesions. And so this is from external compression. You can see here how everything just kind of opens up. And that's when I lifted the patient off the bed. And so again, I'm getting this nice look from within when I'm doing my ivis catheter to really give me all the detail possible. Here's the same thing looking at it, same position. Catheter is in that position, not moving. And all I did was lift the patient off the bed. That's another nice maneuver to use when using ivis catheter is to evaluate any lesion or something that's concerned is just keep your catheter right in that spot and decide for yourself based on different maneuvers, whether it's moving the patient, hydrating the patient, which takes some time, so that's not really a good use of time, but giving a nice sal-salvo or an augment or a leg squeeze and seeing what happens to that lesion to determine if it's a fixed lesion. There's certainly other maneuvers, but that's one nice one. And so this patient, you know, after looking at the ultrasound, after the ivis and doing a thrombectomy, we could see that actually in this case it was failure acute DVT. This is some of the specimen that we retrieved from this case. You can see it's mostly red cell filled rich thrombus. And at two months, she's doing excellent on anticoagulation with no leg edema. She's been worked up for any concern for hypercoagulable disease and or cancer, and none of which have been positive, and so she'll remain on anticoagulation. Here, moving along the spectrum, we have a patient with subacute DVT. She's 26 years old and an extensive iliofemoral left leg DVT during pregnancy just two weeks prior. She was full term. She was at that time managed medically. She did not have phlegmasia. She had significant swelling and impairment of the mobility in addition to her gravid state. She ultimately underwent a filter, got anticoagulated, and underwent an elective C-section. Unfortunately, after her delivery and despite anticoagulation and compression, she continued to have severe pain and so we offered her a single session therapy with some obvious risk discussion given that she was two weeks post C-section. And here we see a static picture of her left common femoral vein, which shows a very dilated common femoral vein that still remained with some echogenic changes. She was brought in for a venogram and intervention. On the screen left, you could see how she had a significant thrombus filled common femoral just around the level of the profunda all the way to the iliac vein. And here you could see where this osteochondroma is. It's right where the lesser trochanter is, which is around the level of the profunda. Actually, if you look back at the last image, it was a little bit difficult to evaluate down by the femoral vein segment, mostly because of this osteochondroma. So we started off with an intravascular ultrasound. And so here we have a very collapsed IVC, but this is the IVC segment. This patient is prone. What we all see here coming on screen right from 12, which will probably go down towards the six o'clock position, is the common iliac artery. So here's IVC. Common iliac artery over the catheter and over the vein with, again, no lumen, no visible lumen. A lot of echogenic tissue changes outside of that catheter and outside of that compressed vein, which was her culprit lesion. She had a mason or lesion on the outflow side. And as we pull back our ivis catheter, you'll see it now, a dilation or return of what looks like a channel with a lot of echogenic changes. You know, I would even say that today looking back, I might change the gain here a little bit. Maybe it's a little too bright, but definitely a variability in the echogenicity that we could see in her iliac segment. And this was due to the fact that, you know, this started now about a month ago because she had these symptoms about two weeks pre-delivery state. Let's see, I can just move this along here a little bit. As we head down, here we have the common femoral vein and the profunda is about to come off center screen here on the 11 o'clock position. And below that, it gets much brighter and echogenic. And actually if you put the catheter here and do a calf squeeze, you'd see that there's actually real low flow. And this is that segment that was actually not involved with DDT, but just had stagnant column of blood with venous hypertension. So she underwent single stage thrombolytic therapy and angiothermectomy, which was again, a different approach than the first case. You can still see that there's a venogram, there's some residual thrombus. This is just a reconstruction of how things look after some stenting. Again, her osteochondroma was right around the profunda and so I was a little hesitant to extend any stenting down to that area. And she had nice emptying and brisk emptying. So I thought it was reasonable to stent the outflow and treat the rest medically. On the screen right, we see here the IVF catheter in the vein, the outer edge was the stent. So I'll go back to that real quick here. So let's start with the IVC. You see here the stent just going into the IVC a little bit with the contralateral iliac vein coming off view here at the eight o'clock position. That common iliac artery on the top here goes over the stent and no compression seen because of stenting. As we move down, you'll see that there's nice open channel, no echogenicity within the stent, suggestive of no thrombus, indicative of no thrombus with good emptying consistent with what we see on venogram. This stent ended at the external iliac vein and we could see that a little bit of that layering thrombus that's residual here, variable echogenicity, certainly not acute DVT because acute DVT responds very well to lytics and this part just did not. And so I think for me, this really highlights how the therapies have changed over time and how, you know, things were able to clear things, I think better with the therapies we have today. Just for the interest of time, I'm going to move on to this next case. But before I go to the next one, here's just her segments and her evaluation that, you know, she's about two and a half years out, three years out. And if you look on screen, right, this is that left leg. Her stent remains open. Her leg looks great. Her osteochondroma remains fairly stable with no issues. Let's see here. And if it would play. Well, all right, I can't show you, but I mean, it's like that she has had a complete remodeling of her common femoral vein with no residual to nickeate or thrombosis or chronic changes that are seen. And so, you know, I think that's a really nice result. And so that lower segment was treated medically with treatment of the stent of the outflow segment. Um, let me, uh, I know we're kind of running out of time a little bit, but what I want to show is one other case, like a chronic case. And if we have another few minutes, I can show, um, one of the, one more case. But here, if we go to the other extreme, you know, I think this to me highlights the role of ultrasound and a really good detailed image. And when we collaborate with our sonographers, at least from my perspective as a surgeon, when I collaborate with my sonographers, I mean, it's a win-win. So we get beautiful images. There's a lot of education to be done. There's a lot of information you can gather, which really allows you to see what maybe you didn't see before. If a patient is a candidate, one minute, they were not a candidate for endovenous reconstruction or open surgical reconstruction. And when you get a good look and a good image, and you do it together, you can really, uh, uh, you know, go, I would say, go as far as really get good detailed information that you could come up with a solution for a patient that is otherwise struggling to find an answer or a home for a therapy. So here we have a patient who's got a very, very extensive, uh, severe occlusive, multi-level occlusive disease, consistent with, uh, his prior history of, um, trauma that led to an IBC filter that never got removed. He has a greenfield filter for like probably 30 years. He's occluded all the way from his cava down to his popliteal veins, essentially. And I took him for a venogram because he suffers from post-thrombotic syndrome, venous claudication, recurrent ulceration. And I was trying to find a solution. And so I thought, let me just do a venogram and an IVA. And this is, um, the patient is, um, supine for this. Uh, if you look at, um, I'll do this top screen since it's playing. Uh, I have my catheters down. Um, I couldn't get very far up into the groin because he's occluded at the mid-thrombal vein segment. But you could see here that, uh, actually he's prone. So I'm going from the popliteal. On the right side, so, um, uh, in a prone case, the right side is here. Um, you know, I could see that the common femoral vein looks diseased. Um, he has massive collaterals. These are all abdominal collaterals. There is no cava flow. And you can see a little bit of a wisp of an iliac vein here that's residual, which is nice, uh, hopeful view there for me. But on the left side, you know, I could not really, uh, make heads or tails about what this patient had in terms of, is there even a profunda? Uh, is there something for me to land a stent in? Can I do an endovinectomy? Should I consider that on one side and, um, endovenous reconstruction on the right? Um, and I just, I couldn't, uh, feel confident even with this image and I couldn't get my catheter any higher up for diagnostic studies, uh, because it was occluded. So we took this patient back to the lab and we got some really amazing images with one of our excellent sonographers and really did a focus evaluation right from the external iliac to that, into the profunda, to the bifurcation of the profunda and into the proximal femoral vein. And we could see here on the right side, which we felt was pretty good, here's some nice findings of what looks like that chronic post-thrombotic change. You have a common femoral vein with some webbing. When you look at it on the longitudinal view, you can see this very hyper-echoic band right smack in the middle of the common femoral vein, which is important for me to know because it's, depending on how my wire goes in, if I push that valve or that funiculae over to the profunda, it could act like an occlusive valve. So we get this great information about, that could help maybe directionality of how I proceed with my intervention. We got a really great look at the profunda. We could see that in the right side, you know, there was a nice profunda where I could plant my stent anere that will feed the stent and keep that stent open. And then we got some nice measurements here, some long views with that web or that nice chronic, well it's not nice, but there's chronic funiculae change from the chronic changes from extensive DVT. The profunda on the right side was fairly good and there's continuous monophasic flow. The left, unlike the right, very diseased, but there is hope. More post-thrombotic, smaller caliber, profunda caliber is pretty good. And actually, you know, his profunda had quite a bit of funiculae, so this will change how I approach things. Perhaps I need to do prolonged balloon angioplasty or extend my stent into the profunda, but I felt confident that there was a profunda that was patent despite my inability to tell that with all the collaterals on his venogram, so this to me is a win-win kind of collaboration with my sonographers. And with that, I'll just end, because I think I've run out of time, and I'll just share that, you know, clinical presentation matters. You have to consider the prior history and imaging of the patient. We're better at aging and interpreting acute thrombosis, but I think aging thrombus is relevant and implications in the choice of the therapy, choice of device, the timing of device, or even avoiding use of certain devices. Maybe we pick better devices based on how we age thrombus. And I think there's certainly room for lots of evaluation, and with that, I'll be happy to take questions. Thank you. Thank you. Dr. Hart, that was so interesting, very informative, and one of my committee members, Melinda, she said the very same thing I was thinking. She's like, oh, would you be interested in giving another webinar with maybe some more question-and-answer time? Missy, will you let me? Yeah, no, absolutely. I'm sorry. I kind of maybe took a little, I definitely took a little more than I wanted, so there's a lot to share. It was riveting. Missy, can we take some questions? Can we go over a few minutes? I'm going to take your silence as a yes, Missy. So I'm going to ask a couple questions here quickly. How long after the initial ultrasound, which is positive for DVT, would you be able to use IVUS? Sorry, so how long after? Yeah, like... Ultrasound? Yeah, so if we do an ultrasound and we say it's an acute DVT, like, do you, how long would you have to wait to go in with IVUS, or do you, you just do one or the other? Yeah, so IVUS is not, so they're not dependent on each other, if you would. You know, DVT scans, the ultrasound is diagnostic as part of the workup of the patient. And then the IVUS part is, again, for deep venous work, a mandatory component of how I treat patients. So how I like to get a look, get a baseline look, so once I get my wire up, I get my IVUS catheter and I look at everything, see if I can tell why there was this event, see if I can anticipate what I need to clear, how extensive of these thrombus, and then I try to clear the thrombus with a device of choice, and then I proceed with another look, because it's very good compared to the enogram at residual thrombus, and identifying compressive lesions or chronic changes, which you can't get with a 2D planar venography, it's just misleading. And you can size the veins, size the stents, and choose a device and choose a stent. So to me, it's, you know, they each have a separate role, and there's no timing restrictions, if you would, from one based on the other. I mean, I could, you know, do a DVT scan, do my procedure IVUS, and I don't do it now, but you know, you could check a DVT scan the next day to see how things look, if you're curious to get that directionality information that you don't get with IVUS, but just to get like a baseline look, I think, you know, again, you could do that as early as post-op. Okay. How do you avoid procedural embolization during IVUS? So there's not a lot of, there's not significant risk or much that I'm aware of with, certainly With any wire manipulation or catheter manipulation, there is a risk, but when we do these procedures, the patients are heavily anticoagulated, and I think the risk is fairly small. I never stop anticoagulation, I never reverse anticoagulation. And so, you know, if there was, let's say, a small embolic event, that's usually not clinically symptomatic, but I don't use filters, and I've not seen significant issues with IVUS catheter or procedural devices in the legs in the way I, in that scenario. What are the key things you look for on post-venous stent duplex? So I look for phasic flow, so most of the time, so I'll tell you what I do, so I get a duplex of the stent at one month, and I want to see a nice restrophasic flow, particularly, sometimes you don't see that within the stent because it's rigid, so you lose that phasicity, but I want to see restrophasic flow changes with augments on the inflow, particularly on the inflow side, and you want to look up above the stent and the IVC or wherever you land the stent above it. You also, I think, to me, which is certainly an area I think that we could look a little more at is how does that profunda flow look, because the profunda is more critical than the femoral vein in terms of feeding flow through the stent, which is really what keeps things open, you don't want any stagnant areas feeding the stent or else your stent clogs up, so I want to look at the profunda flow and if the femoral vein is open, certainly that. Most of the stents are landed in the iliac segment, sometimes they go down into the common femoral vein, but you just want to consider that flow, and certainly you want the vein right behind the stent or on the inflow side of the stent to be nice and compressible in addition to the collar flow and spectral Doppler analysis. Okay, the next question is how often does echogenic material respond to lysis? Does this mean it's subacute, do you think? Yeah, so lysis, you know, certainly I think, so if I look at my practice, I've gone from being pretty much a lysis only provider, if you would, in terms of procedures to no longer, really in very selective cases, use lytics. I think lysis does well for acute DVTs and you really get the best results if you capture them within the first week, and then beyond that you may leave some of that thrombus, sort of the evolving thrombus behind, which is what I showed in the second case that you can't clear with lytics alone or certain mechanical thrombectomy devices. And so for me, some of the newer devices offer the ability to, in single-stage fashion, clear more of that evolving thrombus, subacute, more rubbery, collagen-filled, fibrin-filled thrombus, which in addition to removing the acute stuff, I think is significantly, in my mind, is going to improve the patency and the durability of whatever stent and therapy I offer that patient. Okay, do you think IVUS can cause valve damage? The audience is wondering what some complications of post-IVUS scan might be. So I don't think there's much risk with IVUS. That doesn't significantly cause damage. I think there's discussions about whether some thrombectomy devices can cause valvular damage when you're doing the thrombectomy itself. I have not been impressed with the deep venous reflux changes anecdotally, subjectively, not in a studied fashion amongst the patients I've treated with mechanical thrombectomy devices that I use. So I don't think there's a lot of great data saying that that actually occurs, but certainly probably room for evaluation. Do you think transducer compression might transform thrombus ecogenicity from fresh to sort of an older thrombus? It shouldn't. So I think if you have the right 90-degree angle for B-mode evaluation for your tissue plane, I think sometimes in the legs it gets a little hard, so you got to always consider that. That gives us the best B-mode image. I think the compression shouldn't change acute to subacute or more age, but it may change, you know, the angle may change how you view the thickness of the wall or any chronic changes. So I think just considering that angle when you're doing your compressions are important. So you don't want to come in at an angle because that'll change, you know, that may not be optimal for getting a good B-mode picture. What's the most common IBIS approach? I think most commonly I would say is the popliteal approach. So I think a prone popliteal access approach is likely the most common, but there are a multitude of access points. And number one is what are you trying to clear? You need room to work. That should drive, you know, what your access point is and then ease of access. So I tend to now do kind of mid to mid femoral vein if I can get a good window between my superficial femoral artery and femoral vein that I can cannulate it from a supine anterior approach. But I would probably say prone and the popliteal is likely the most common. Okay. You can always flip the patient too. Right. Can you tell us a little bit can we use shear wave elastography to age thrombus, do you think? So that's a very interesting question. You know, I did have that as a part of a talk I gave with a similar theme. And elastography, there is definitely research in this arena for aging thrombus because it uses stress and strain physics to try to age the tissue or define the tissue better. But I think there's certainly a lot more work that needs to be done before that could be translated into practice. But it's a very interesting topic. Yeah. Do you think thrombus is different in your experience when it develops like post saphenous ablation or, you know, some other intervention methods? And does it look different? Right. No, but I also don't look very much at my post ablation superficial veins. But I tell you what does look different. I think, you know, there's a lot of different ablation therapy, there's laser ablation, thermal ablation, bone sclerotherapy, there's cyanacrylate or blue ablation. And certainly, when you look at cyanacrylate versus like thermal ablations, it's very different, right? So one, it's just thermal damage to the endothelium causing a thrombosis. And cyanacrylate or venaseal, that's a foreign body, it's an implant. You get a very different look. And you get a very echogenic change. And you actually see it right away shortly after the ablation on the table before completing your procedure. And so that changes echogenicity. If you use any of the other modalities, I mean, once the vein thrombosis is off, I don't think there's, you know, my impression is that they wouldn't really look any different. And eventually, the goal being eventually to occlude it and involute and become the tritic. Can you elaborate a little bit more? You were talking about lifting the patient off the bed during IBIS. What's that all about? Yeah. So it's, I mean, I like, literally move their head off anything that I think may be externally compressing them. So we have these, you know, fake gel rolls that we use along the chest line, just lateral to the nipple line. And it, you know, protects the shoulders, the collarbone, and it goes right down to the inguinal crease. It's just to say that perfect length, but it's rigid. It's the ones we have in the operating room table for like padding for sacral pressure prevention and heel prevention. So I have now, I don't use those anymore. I use pillows and other padding. But I just lift the hip off the bed with my catheter in the position of interest. So if I'm curious as to is there an external source to this finding, I leave my catheter there and I'll just lift that body part off the bed. So we kind of angle it off and then just see what happens to the vein. Does it open? Is it a fixed lesion or is it opening and, you know, responding to removing that pressure? If it's fixed, it's fixed. If the vein becomes normal like it did in that image, when I move that external pressure from the patient, then it's not a sensible lesion. It should not be sensitive. It's not a fixed lesion. Okay. How about when you're reading an ultrasound study, what makes you call it acute on top of chronic DVT? So there's that art of interpretation. I mean, I think I use my best judgment of the image and the best images I get. And if it's, I do, I like looking. So compared to prior, I think it's very important. You look at prior images. I tend to look at the history a little bit. So I think that's where it's really important to include some of that history in your report. You know, I have access to the medical records. So I use that as well. Have they had prior DVTs? That's that compared to prior importance and relevance. And really just try my best to look at that echogenicity, the compression, and how I put that information together as best as I can using that. Again, it's a little bit of an art, but I think if you optimize the gain, if you optimize the angles and how you're doing the compression, I think that helps significantly. Okay. Let's take one more question here. Early in the talk, you mentioned immune cells. And the audience member said they recently found out discoid lupus causes plaque buildup in the arteries. Do you feel patients afflicted with this pathology would also have increased incidence of thrombus in their vein? Lupus patients, repeat that part again. That patients with discoid lupus seem to have plaque buildup in their arteries. Do you think they also might have an increased risk of thrombus in the vein? Oh, I don't. So not in my understanding, but I'm not a vascular medicine specialist, so I don't want to mislead. But it's not like a particularly higher risk population for me in treating venous thrombosis. Okay. Okay. They have lupus patients that, you know, just in general, higher risk profile with regards to that. All right. I think if you want to close your screens off, Dr. Harth, I have a couple of announcements. Before we sign off, I want to remind everyone that this webinar was recorded and it will be available online through the SVU website at no charge for attendees. Watch your inbox for that email from SVU to get your CME certificate. And then we hope to see you all at the 45th annual conference being held August 3rd to the 6th at Disney's Coronado Springs Resort in Orlando, Florida. The conference will feature didactic lectures, live scanning, super panel discussions designed to provide interaction with attendees. And remember, early registration closes June 27th, so sign up soon to get that discounted conference rate and take advantage of the opportunity to hear great talks like this one and earn up to 18 CME. You can visit the SVU website for more information. And until then, take care, stay well, and we'll see you next time. Thank you again, Dr. Harth. That was great. Thank you. Have a great night.

venous thrombosis

ultrasound

IVUS interpretation

webinar

Lori Lazansky

Dr. Karen Harth

vascular surgeon

pelvic venous disorders

DVT

imaging

thrombus