Good evening. Thank you, everyone, for attending tonight's webinar entitled Going for the Juggler. My name is Lori Lozansky. I'm one of the chairpersons for the SUE Learning Educational Committee. It feels like it's been a minute before we – since we've been together, so let me just go over a couple notes from the SUE office about the webinar tonight. It's going to be recorded and available online for attendees through the SUE webinar website at no charge. Please take a moment to familiarize yourself with the GoToWebinar program we're using. Everybody should see a question section along the side menu of your screen. Maybe it's near the bottom of the choices just above chat. Please type in any questions that come to mind during the presentation. And then, at the end of tonight's talk, we should have some time for discussion. Now, in order to receive your CMEs from tonight's lecture – this is important – you need to wait for an email from the SUE office containing an evaluation. And you should get that email in about seven days. When you get it, complete the evaluation, and then your CME certificate will automatically pop up. So that concludes our announcements for tonight. So let's begin. Tonight, we're honored to have Todd Douglas-Hall speaking to us. Todd earned his degree from OIT. He's a registered vascular technologist through ARDMS and a registered phlebology sonographer through CCI. Currently, he is a clinical specialist for MindRay North America. And I just learned he was the first chair for these e-learning sessions. Some of his other previous posts were as technical director for Mercy Vascular Labs in Baltimore, where he maintained a IAC-accredited lab, supervised and managed their hospital vascular lab with multiple satellite locations. Before moving to the East Coast, Todd was located on the West Coast, working out of the Spokane-Washington area as an imaging lab manager and staff technologist. Todd also served the U.S. Marine Corps, working as an Arabic-Farsi linguist and analyst on the Middle East. And besides all of this, Todd has experience in marketing, and he once owned a company that offered automobile surface restoration. Well, let's talk about diversifying. With that, please join me now in welcoming Todd Hall. Lori, thanks so much. I don't know that I'm old enough to have done all that stuff, but if it's on the paper, then I must have done so. Thank you, everyone, for being here this evening. I'd like to once again thank the SVU for continuing to put on this webinar series. A lot of work goes into this and making it all happen, and it's certainly a valuable resource for our membership. So, we appreciate all your effort that goes into doing so. We do have some housekeeping matters to go through. First of all, let's talk a little bit about our discussion this evening. We're going to give an overview of the anatomy and physiology of the jugular venous system, consider the pathology and sonographic presentation of atypical disease states. Upon completion of the course, you should be able to discuss the anatomy of the internal jugular vein and confluencing vessels, explain the overview of atypical disease states that may be encountered during ultrasound, and then describe ultrasound presentation of said disease state. That's kind of the easy part of it. There's going to be a lot more to that, but that's what we have to include for the University of Cincinnati. I have no personal or professional disclosures. I need to do any of the planning committee members, and then we have some additional boilerplate that I'm going to give you about five seconds to read through. And there you're done. So, first of all, for those of you that are looking for introduction to juggling, you're in the wrong webinar. We're going to be talking about the jugular vein. That's this guy right here. And as you look at this graphic, you're going to notice a couple of things. First of all, he is red and carrying oxygen-rich blood. Secondly, that blood is flowing the wrong direction. And I have no idea what he's extravasating down below him, but you should probably get that looked at. So, this graphic really demonstrates the confusion that's often experienced when considering the jugular vein. And it's not just confusion for graphic designers. Physicians can find it very confusing. They're not aware of just how complex the jugular vein can be and how varied the disease states actually are. So, the jugular vein is a little crazy. He's a little kooky. And we're going to spend some time talking about him tonight to see if we can get a little bit better understanding of who he is and what he does. So, again, we're going to talk about the anatomy and physiology of the jugular vein. We're going to step in to do a brief history of deep vein thrombosis in general, mainly because I'm the one who gets to put this together and put in there what I want to. And then we'll talk about some very specific disease states. We'll talk about Lemieux syndrome and ovarian hyperstimulation syndrome, how it plays a role with jugular vein thrombosis. And then we'll look at some other states, jugular vein distension, superior vena cava syndrome, and chronic cerebrospinal venous insufficiency. So, that's what you have to look forward to. Let's get right into it. First of all, let's talk about the anatomy. This is going to be a lot. It's probably more than you'll ever need to know. But I was able to get this video from Dr. Kulkarni, and I always express my appreciation to him for letting me borrow it from him. So, let's talk about the anatomy of the jugular vein. So, the IJV forms intracranially from the sigmoid sinus. It extends, first of all, through the jugular foramen. And then it courses down to terminate at the sternoclavicular joint, where it joins with the subclavian vein to become the brachiocephalic vein. At the origin, there's the first of two dilatations called the superior bulb, which is situated in the jugular fossa of the temporal bone. And then at the other end, there's the inferior bulb, which lies in the lesser supraclavicular fossa. So, let's kind of take a look at some of the adjacent anatomy that we might see. First of all, look superficially. There's the sternocleidomastoid muscle, the posterior belly of the digastric, the superior belly of the oval hyoid, of course, the parotid gland, and there's the styloid process that we might see, and of course, the internal carotid artery. On the posterior aspect, we'll be able to see the transverse process of the atlas, the cervical plexus, the scalenus anterior, and the initial portion of the subclavian artery. Finally, looking medially, we'll have the internal carotid artery again, also the common carotid artery, and the vagal nerve. Now, there's a number of tributaries that we may or may not see confluencing into the internal jugular vein. The inferior petrosal sinus, the common facial vein, the lingual vein, various pharyngeal veins, the superior thyroid vein, and the middle thyroid vein. The only other major thing that we might be interested in, certainly not the thoracic duct, which we probably won't be taking a lot of time to see that, or the right lymphatic duct, but there is a primary communicating vein between the internal and external jugular vein. This is called the oblique jugular vein, and occasionally, especially in pathological states, we might see that come to light. So, that's worth noting. So, what happens when things go bad? Well, whether it's cardiac congestive disease, or any of the processes we're going to discuss today, obviously, we're going to see an increase in venous pressure, which in turn causes distension or diltation of the internal jugular vein. And the speed at which we see the onset of this dilatative process can give us a clue as to the nature of the disease. Obviously, the more rapid the onset of those pressure changes is going to equate to a more acute disease state. Now, there's two things that the animation didn't touch on. One, that there's always a terminal valve. That terminal valve provides the only barrier between the heart and the brain in the jugular venous system. And the other fact is that up to 12% of individuals will have a course that we would classify as hinky. So, it's aberrant. It's atypical. It's not something we're going to normally expect to see. So, that's something we need to keep in mind. So, what does the jugular venous system do? Well, simply put, it empties the head, the face, and the neck directly into the right atrium. Now, because of this direct connection to the right atrium, the jugular vein can give us valuable information as to what might be going on at the level of the heart. For instance, we can determine the central venous pressure. We can observe the venous pulse contour, what we would call the venous waveform morphology. And we can even identify some cardiac pathology. And those are all things we'll discuss throughout the course of the evening. Now, keep in mind that this is initially part of a visual examination. Any attempt to palpate the jugular vein is going to result in a change to that venous pulse rate. So, when we talk about this, we have to look at it in a different way. We're going to look at it in a sonographic way and relate it to our ultrasound. And what we're trying to observe on our ultrasound is what's called an ACXY complex. And obviously that complex consists of four different elements. I know, yikes, right? We always get a little, feel a little dodgy when we see waveforms that we're not familiar with seeing. This represents the jugular venous pressure wave. So, why are we interested in jugular vein pulsatility? Well, simply put, because that pressure wave relates directly to our jugular venous waveform. That wave is what gives us the waveform morphology that we're used to seeing in the jugular vein. So, we need to keep in mind that pulsatility is pressure and pressure impacts flow. So, those cardiac events are reflected within our venous waveform. And there's primarily two events in the cardiac cycle that are going to impact our jugular venous pressure. The first of those is contraction of the heart. And the second of those is filling of those chambers. So, let's talk a little bit about our jugular venous pressure and this pressure wave. So, you'll note there are a wave that represents the beginning of atrial systole. So, that contraction of heart muscle creates a wave of high pressure that increases up to the point where we reach what we call peak systole. That's something we're all familiar of seeing in our arterial waveform morphology. There's a downslope then of that wave as we go into diastole, which would be atrial filling. And then we arrive at our C wave, which is ventricular systole. This causes the tricuspid valve to inflect towards the right atrium, creating a second, although smaller, reduced pressure increase that's reflected in the waveform. After that, we have that deep trough, that X wave that follows that. This is where the tricuspid valve closes, the atrium relaxes, and ventricular systole occurs. And from that point, pressure then begins to build once again in the atrium until reaching peak pressure just before the tricuspid valve opens. That's called the V complex, but we don't typically consider that as part of our wave. Finally, there's the Y wave. This is where the tricuspid valve opens, the right atrium empties into the right ventricle, what we call ventricular diastole. So did you get all that? That's a lot. And we're not used to typically talking about that venous waveform in relation to our waveform morphology in our venous system. So that's the complex, mind-bending, mind-breaking version. Let's see if we can relate it to something that we're a little more familiar with, perhaps an ECG tracing, which might give us some greater clarity. Okay, so here is what we recognize as a normal ECG tracing. And superimposed below that is the normal jugular vein pressure tracing. And so we can see how each of those aspects relates to that cardiac cycle. So we're used to looking at the cardiac cycle to give us an idea of cardiac morphology, or pathology rather. But at the same time, those same changes are reflected in our venous waveform. And that is also used to give us an idea of what pathology might be occurring within our heart. Okay, so let's relate this then to our jugular vein waveform morphology. And to really understand this, I know we're used to looking at the actual color. But in this case, I want you to look at the negative. I want you to look at the black portion of the waveform so we can better understand that pressure wave. Because remember, peak pressure means lower flow. So we can see as that pressure increases in the A wave, we are getting that reduction of flow. And we can follow that all the way up to the ACX5 complex. So as we said, since they're connected, we can also see heart issues within our jugular waveform. Now, I know that might be as clear as mud. It takes some time to digest that and really understand it. And there's lots of different opportunities on the internet to look up other explanations that go into more detail on that. But here's an example of the types of things we can see in that jugular waveform. Given whatever might be reflected in that morphology, we can see if it's a valve issue, we can see if it's some type of dissociative issue, we can identify atrial flutter, we can see tamponade, all manner of things that we can tend to see within the cardiac waveform we can see also in that unit's waveform. All right. So I'm sure you're all either understand what we're talking about or you're completely flubbexed. But we're going to move on. We're not going to spend a lot of time on that. It's just to help us understand what goes into creating that waveform a little bit. Let's talk pathology now. And I added this in here just because I haven't attended a talk on DVT in some time where there was actually historical consideration of that. So I thought I'd throw some of the basic history of DVT and its treatment in here as well. So let's talk about that just for a little bit here. So for those of you who work with varicose veins. Both art and literature from ancient history depict that aspect of venous disease pretty prolifically. That makes sense to us. Varicose veins are outwardly visible. For medical personnel and artists and writers at the time, it was very easy for them to see what they were, that they were veins that for some reason had gone bad. They may not have understood the process that was causing it, but they thought to include it within their writing and their artwork. Physicians also took the time to understand what was going on and to deal with it. Thrombosis is a little bit different prospect historically. It's an internal process. And the only way we know something is going on is by the symptoms that it presents. As such, deep vein thrombosis remained mostly hidden through ancient history. That changed, however, in the Middle Ages. In 1271, a young Norman cobbler was experiencing pain and swelling in his right calf. Now, if you know anything about cobbling, making shoes means you sit all day long at a little table and repair or make shoes. Now, just as an aside to that, if you want a really excellent read, there is a keynote address for SVS back from many years ago entitled, The Chair and the Venous Thrombus. Look it up online. It's an excellent consideration coinciding the rise of thrombosis with the use of the chair. Makes an excellent read, and I certainly encourage you to look that up. Anyway, this 20-year-old Norman cobbler went to see his doctor, and his surgeon adopted a wait-and-see attitude, probably since there wasn't a vascular lab nearby. However, Raoul's symptoms worsened to the point of, first of all, ulceration, and then ulceration with exposed bone. He was getting worse rather than better. He saw a bunch of different people. There were a number of failed, unspecified treatments. We don't know what they were. But eventually, someone suggested that he visit the tomb of King St. Louis. So he did, and he did so praying for several days. At the end of that week of prayer, he gathered up dust from around the altar, and he spread it into that open ulceration. Now, the account reports that he was miraculously healed, and he was still alive 11 years later. So that's the first known historical account of the presence of deep vein thrombosis. It's interesting that revered physicians from Greece and Rome made absolutely no mention of it. It showed up nowhere in the art or writing of Egypt or Persia or Babylon. And yet, we have to assume, knowing what we know about the disease, that history was replete with those who suffered from the disease. So following this initial description back in 1271, the medical community started to make notes and began to look for this process that was causing these difficulties. At one time, it was attributed to evil humors and bloodletting was used to treat it. In postpartum women, it was blamed on milk length, which is a buildup of excess breast milk in the legs. And the treatment for that was increased breastfeeding. That was supposed to fix those symptoms. It wasn't, however, until 1676 that progress began to be made. Dr. Wiseman was the first to postulate that thrombosis was due to an alteration in the blood's chemical makeup. So he was the first one to really start us off on the right path of identifying DBT and figure out how it might be treated. In 1793, Dr. Hunter identified clot causing venous occlusion. And he actually began performing ligations to stop the progression of the thrombotic disease. In 1856, a guy we know really well, Dr. Versho, described the relationship between DBT and PE. There was a detailed description of jugular deflating thrombosis, specifically in 1912, which was likely a case of Lamiere's disease, which we will discuss a little bit further in our talk tonight. Although the understanding of the disease was progressing, its treatment was stalled. It wasn't progressing along with the understanding of what was going on. In addition to bloodletting, they would cup their patients. They would purge their patients. They would apply ice and give ice baths. They would apply blisters to them in the hopes of rectifying them. They were on the right path. They would do tight wraps around the affected limb, hoping to stop that spread. But they would also immobilize them completely, so they weren't able to move until the disease passed. They would also suspend them, either upside down or right side up, thinking that that might make a difference. They used zinc chloride, they used quinine, they used mercury, they used autumn crocus, all in an attempt to treat these symptoms of what they considered to be a blood clot, all with very minimal effect. However, jump forward to 1933, crystallized heparin was finally created. And that was the first major step into actually being able to treat deep vein thrombosis. Subsequently, in 1941, vitamin K antagonists were introduced, specifically dicoumarol. And then in 1948, warfarin was initially introduced as a rat poison. Because of the properties of that, we know we all have patients that say, I don't want to be put on a rat poison. But it was those initial observations that led physicians to realize that it might be beneficial as a therapeutic agent. And finally, in 1954, it was released as such, particularly to combat deep vein thrombosis. Finally, in 1996, the first research on the safety of low molecular weight heparin began to demonstrate efficacy and show that it was safe for patients to be treated at home, not have to have hospital stays. And that kind of brings us up to where we are today. So that's just a brief history. Obviously, there's a lot more to go on there. But that kind of gives us a framework by which we're going to consider specifically our jugular vein thrombosis. So let's go ahead and move on to that. As we said, it was first described in the jugular vein in 1912 in conjunction with a paratonsillar abscess. And while it makes up a small portion of overall DVT exams, it has a relatively high morbidity rate. 13, 31, and 40% at 1, 3, and 12 months. Of those that die from the disease, 25% of them experience sudden death. 33% of them will have a recurrent episode within 10 years. And 5% to 8% of them will have thrombophilia for the remainder of their life. So these are important exams. But why is it at the lower end of deep vein thrombosis? Why are we seeing so few of those? Well, it's primarily because unless we have actually stuck something into the jugular vein, it's less likely to thrombose. One, it's less susceptible. It experiences gravity. There's that pressure wave that we just discussed. It has a relatively short course. All of those work together to mean that there's a lower risk of developing thrombus without other corroborating pathology. These next two really kind of go together. It can be somewhat elusive to detect clinically. The symptoms can sometimes be very quiet. And it can be a result of numerous disease states. So we can see how physicians can have a difficult time diagnosing what's going on with issues in the jugular vein. So we can make the assumption then that it's likely substantially underdiagnosed. So when we complain about getting those very odd referrals for jugular vein DVT, we should have some understanding for the physician and what they're trying to deal with. So what is the etiology of jugular vein thrombosis? This is certainly not a complete list, but you can see the wide range of processes that can contribute to thrombosis. First of all, whiplash and seatbelt injury are perhaps the most common causes of traumatic injury. So when we're doing these post-motor vehicle accident carotids, we should always take time to make sure we take a quick peek at the jugular vein and make sure there's not something going on there. Of course, the number one cause at 60% is placement of central venous catheters. That's something we see on a routine basis. And that's what most of our referrals are going to be for. Two decades ago, there was only 5% to 8% of all IV drug use associated with vessels in the neck. And depending on the study that you read, that number has now reached up to 35% in the past decade. And that's a disturbing trend. And it's a concern in the healthcare community due to the broad range of sequelae that resolve from that. So in addition to deep vein thrombosis and deep neck abscess that we might typically see in those patients, IV drug use causes a wide range of other complications. There are reported cases of airway obstruction, vocal cord paralysis, pneumothorax, mycotic subclavian aneurysm, even paraplegia. So although it may have once been uncommon to see these patients for upper extremity DVT exams, we can sadly expect an increasing number if this trend continues. Add to that any neck procedure as an inherent risk of thrombus. So anytime they're in the neck, around the mouth, anything like that, we can expect that there's a degree of improved chance that they will develop DVT. Next is our second most common cause, cancer of the head and neck, resulting primarily from radiotherapy. That accounts for 37% of all jugular vein deep vein thrombosis. Obviously, clotting disorders, hemophilia, von Willebrand disease, inherited clotting disorders, all create a risk of thrombosis. And the list continues up to the point where sometimes we just don't know what happened. Idiopathic deep vein thrombosis in the jugular vein, I think that probably accounts for a lot more than we expect. We just don't know why that happened. So since we don't have sufficient time to consider all of these, we're going to focus in on just two of them. Now, first of all, we referred to it earlier, Lemire's disease. So let's talk about that. So in the mid-30s, Dr. Lemire, who was a French bacteriologist, published a study involving 20 patients who all shared three primary characteristics of their clinical history. One, they each had a form of oropharyngeal infection, tonsillitis, or infectious abscess due to dental work. All of them had thrombus within the internal jugular vein, which was confirmed either clinically or radiologically. And each patient had septicemia caused by a very specific bacterium, Fusobacterium necrophorum. And I know that sounds kind of like a great name for a gut, doesn't it? So it wasn't until my big hair era, the 80s, that the disease state became associated with his name. And why was that so? Why did it take so long to get his name attached? Well, it's probably due to the fact that there was a significant decline in the syndrome in the 40s. And I hear you all asking why. Well, I'll tell you. We're going to briefly digress again, going into an interesting chapter in bacteriology. So penicillin was being researched in 1909 and 1910 by a team at St. Mary's Hospital in London. But it wasn't until 1929 that one of the members of that team, a Dr. Fleming, published his findings, first calling this effective antibiotic penicillin. Yet, as is the case within the fickle world of clinical research, no one really paid much attention to what was going on. That is until World War II had engulfed the planet. In 1940, Drs. Florey and Chain demonstrated that penicillin could be used to treat a broad spectrum of bacterial diseases. As such, it went into large-scale production in both the UK and the US. And by the time D-Day was launched in 1944, every medical unit was adequately equipped to deal with all manner of battlefield infections. So this resulted in a substantial decline in the incidence of various bacterial infections, including septic thrombophobitis. So much so that many researchers began referring to it as a forgotten disease. And it was in that setting that they finally gave Dr. Lemieux credit for its description. So then, why are we even talking about it, you ask, if it's forgotten? Well, simply because it is inexplicably been on the rise since the 1990s. So back to our story. What does Lemieux's disease look like? Well, you note that it is typically a younger patient population than what we would normally expect with typical jugular vein thrombosis. It really comes down to anyone that has a bacterial infection of the neck and is not taking antibiotics is at a risk for developing Lemieux's disease. So what is the progression of the disease? Well, that infection, regardless of the cause, initially affects the deep tissue of the neck. And then it progresses to infect the tissue of the internal jugular, resulting in thrombophobitis. And if it is undetected or untreated, it can go on to cause septicemia throughout various organs, typically causing abscess. And if it reaches the point of this systemic infection, it can also result in septic shock. In later stages, patients may exhibit respiratory distress, whether they have PE or not, and they can also develop osteomyelitis or meningitis. So treatment obviously involves anticoagulation for the thrombus, requires antibiotics for the infection. And when abscess is present, it needs to be drained. That affected region needs to be drained of that abscess. Now, the rate of mortality in these patients, depending on the source, ranges from 5 to 18 percent. So obviously, as sonographers, our primary concern is identification of the thrombus so that that first treatment strategy can begin. However, knowing indicators in the patient history that may tip our suspicions to the presence of a disease is always a benefit for us. So we need to make sure we're taking good patients. The next one we're going to talk about is ovarian hyperstimulation syndrome. For the past 20 years, in vitro fertilization has demonstrated a steady and significant increase. By the end of last year, it was a $25 billion industry, and it's projected to reach 43 billion in just the next 10 years. And this is significant for us since one of the complications of this treatment is deep vein thrombosis. Well, why is that? Well, there are a number of drugs that work either on their own or in conjunction with one another to ensure that the maximum number of viable eggs are available for in vitro fertilization. What is of interest to us are the gonadotropins since they are hormones and we know the effect that hormones can have on coagulability. Most significantly are human chorionic gonadotropin, HCG. So HCG is really designed to increase systemic blood viscosity. And as a result, it also increases the concentration of coagulation factors. And it's a very complicated process. Basically, capillary walls become more permeable, which is a good thing since we are trying to achieve increased fertility, in this case, egg production, which depends upon adequate blood flow. In addition, there's various kinds and means and factors that contribute to angiogenesis at the capillary level. Now, when this process results in overstimulation, there is a compensation that takes place. There's a transfer of fluid into the extravascular compartment resulting in hypovolemia, which means we have both low blood volume and as a result, a hypercoagulable state. So we have to just check two out of three boxes on virtual trials. So just how present is DVT within virtual fertilization? Well, in the study we're talking about, 80% of those presenting with internal jugular vein thrombosis had a confirmed diagnosis of ovarian hyperstimulation syndrome. So it's worth taking note of, again, in our patient history. So that's a brief overview of two atypical disease processes that can contribute to internal jugular vein thrombosis. Now, regardless of the cause, what do we look for as a presentation of thrombosis? Well, all of these are possible. Generalized neck swelling, neck pain. They're going to be swelling along the course of the jugular. They can complain of headaches or visual disturbances. Or as we often see, they can have no complaints at all. We're used to that sometimes. We've all asked that question, well, why are we seeing you today? Only to have the patient tell us, well, they feel fine, but their doctor wanted us to look at their jugular vein. So it can be easy for us to be frustrated with these referrals. But if we stay focused on how many disease states can contribute to jugular vein thrombosis and how elusive their symptomology might be, we might then have a greater appreciation for what their physicians are up against when trying to make a diagnosis. So let's look at some examples. How do you feel when you plop the probe down and see this? That acute looking luminal gook that is poorly adhered to the vein wall. Does that give you the heebie-jeebies a little bit maybe? How about this one? Does that set your heart aflutter just a bit here? Let's let's make it an action adventure movie. Yeah, so that's our typical run-of-the-mill jugular vein deep vein thrombosis. And if you've been doing this long enough, you've seen that classic floating tail thrombus. Catch your breath a little bit and finish up your exam, toddle off to make the call to the physician, letting them know that it's a positive examination. How about this one? This is an interesting case. This is a 28-year-old female who had been in two months previously for an upper extremity DVT exam due to left arm swelling. Looking back at that exam, images of the contralateral right internal jugular were completely normal. However, two weeks ago, she had her wisdom teeth removed, which resulted in an infection in one of the sites. In fact, she had a prescription for antibiotics in her hot little hand since she saw her physician's assistant that morning, that's who ordered this examination. Now, because this is obviously acute DVT, and you can see how wonky that presentation is for acute DVT, it looks kind of atypical. I chatted with our chief of surgery, and I made my case for Lamiere's disease. He was willing to call the results of the physician directly and asked if he could look for our Gocfan, that fusobacterium nucleatum, in her bloodwork. When that bloodwork came in, the diagnosis was confirmed as Lamiere's disease the next day. All right, let's look at one more. This one's another freaky one. This is a 24-year-old female who was in the initial stages of in vitro fertilization and was on human chorionic gonadotropin. Don't ask me why this looks so inky, I couldn't tell you, but you can tell for an acute thrombus, it looks atypical. It's not what we would normally expect. So, that brings our consideration of jugular vein thrombosis to a close. What else is there? Well, how many of us have seen a patient that presents like this, a big, chonky vein, and I challenge you to use that descriptor in your next report. So, it's a big, chonky vein, but when you palpate it, it's soft and yielding. This is a classic presentation of jugular vein distention due to the increased central venous pressure. And there's many things that can contribute to this pressure increase. Many, if not most of them are related to the heart. What we are going to be most interested in is a potential superior vena cava obstruction. What else do we look for? Well, there's any number of additional symptoms that may be present, and you will again notice that most of them are, again, typically cardiac in nature. So, this stresses, again, the importance of a complete patient history so that we are aware of any comorbidities. Diagnosis is usually by determining the jugular venous pressure. ECG can also help to determine pathological states that may contribute to increased central venous pressure, and it can help us to rule out other cardiac issues that might present the same symptoms. Remember that venous pressure wave is connected. So, how about ultrasound? Well, we might not know DVT to be unlikely based on the clinical exam. We have to rule out proximal obstruction, though, to complete the diagnostic picture. Now, just as an aside, pressure measurement, as we mentioned, is the gold standard for diagnosis. Unfortunately, the trend is for pressure estimation rather than direct measurement. It's never a good thing to stick a needle into something unless we can avoid doing so. I'm not going to go into great detail on the methods other than to say that both of them are increasingly using ultrasound, especially if it has onboard ECG capabilities to synchronize the measurements with the cardiac cycle. Now, while there are challenges in performing the exam since probe pressure will have an effect on the results, it has been proven to be more accurate than observation alone. So, another opportunity, ultrasound for the win. Now, how about this guy? Same presentation as the previous patient, chunky complaint veins, but these are in a different location. Now, this is classic presentation for superior vena cava syndrome. That's a syndrome that's due to reduced inflow of blood through the SBC. And as you look for these symptoms, again, four out of five are respiratory in nature. So, you can see why a referring physician might be concerned for pulmonary embolism. And there's an interesting history for SBCS. Remember Dr. Hunter? Well, he first published a description of SBCS in 1757 in connection with a patient with syphilitic aneurysm. This and primarily tuberculosis were the primary causes from that point forward up until the 1900s when our old buddy penicillin once again reduced infectious etiologies for the disease. From that point forward, then malignancy was the primary cause. So, what happens in those patients that we're likely to see? Well, in large tumors, whether it's from the lung, from the chest wall, from the lymphatic system, from the breast, these tumors encroach upon the SBC causing restriction of blood flow and a subsequent backup of pressure. But we're going for the jugular, right? Well, let's think back to our jugular venous pressure. Remember that since the SVC empties directly into the right atrium, it carries that pressure wave up into the jugular vein. This is why the jugular venous pressure is observed primarily in the right jugular vein. It has that straight shot up from the SVC, not having to go through the anomina vein. Now, imagine if there is compressive obstruction of our SVC. How is that JVP and therefore our venous waveform affected? It's going to be flattened, right? Or at least it's going to be extremely attenuated. When that happens, that flow has to find another way to get to the heart. And there's really only two pathways to do so. It's either through the SVC or through the inferior vena cave. And look at all these collateral pathways that can go into the unaffected segment of the SVC if possible, or by finding a pathway to the IVC. That is why we look for that presentation, either chest wall or abdominal wall, those distended veins. It helps us to identify the location and the extent of obstruction. Now, note the location of the zygus vein, which carries deoxygenated blood from the abdomen and chest wall. It's located on the right side of the midspine and is part of the greater zygus venous system, which includes the intercostal venous. And that's really what's used to determine classification. It's either going to be suprazygous or prezygous or infrazygous, post-zygous. McIntyre and Sykes came up with another classification in 1949, but we don't really have to spend any time taking a look at that. There's also two different methods of classification. One is based on the anatomical location and the degree, in the case of Doty and Stanford, or based on the physiologic impact, in this case, of you. And it's not really necessary to commit these to memory unless your intent is to become a subject matter expert on SVCS. You would certainly wow the reading physician, though, if they read a suspected type 3 SVC obstruction. So that might be worth taking some time to understand. And there's one other classification that's an operative classification that the physician might use as part of this workup. Other than collaterals, what are we looking for? Well, go with your high percentage. We're looking for facial puffiness. We're looking for dyspnea. We're looking for dilatation in the neck and the chest. Here's a great example of the facial puffiness. And you'll note that this is the same day series. The first picture was taken at 7 a.m. So remember, the gravity has an effect on the venous system. So as the patient gets up and begins to move around, collateral pathways work more effectively and they alleviate that puffiness. What are we looking for sonographically? Well, unless you have a good cardiac probe, something with a small footprint and a smaller aperture, it might prove to be difficult to visualize the SVC directly, especially given the difficulties we have with patient body evidence. It's really going to be indirect waveform morphology that's going to give us our first clues as to its presence. So here's a case, a 63-year-old female referred for new onset facial and right arm swelling. She has a history of breast cancer. Clinical examination reveals prominent veins to the chest right there to the left. We can see that the right IJV is absolutely absent of color flow. It's Doppler silent, although you can pick out just a little bit of wall plump. You have low amplitude near continuous flow in the right subclavian vein. Again, the left IJV is low amplitude with accentuated cardiac morphology. And the left subclavian vein proximally is Doppler silent again. So this is reported as bilateral brachycephalic occlusion with less likely involvement to the proximal SVC. The patient went on to have a CT and our diagnosis was confirmed. So ultrasound, once again, successfully identified the clinical issue. One of the things we're going to talk about quickly, specifically chronic cerebrospinal venous insufficiency. Back in 2009, Dr. Zamboni in Italy published some initial research linking CCSVI with multiple sclerosis. We all know that multiple sclerosis is an insidious disease that has yet to find a cure. So anytime they think they found a potential treatment for the disease, it sets the worldwide community on fire with excitement and anticipation. And with Zamboni's research, they finally thought they had a smoking gun. The treatment was venoplasty, specifically valvuloplasty in a procedure they call liberation therapy. Wasn't just hearing that name of the procedure give you a little bit of hope? And it was a thing for a while. They would go in and they would scan those areas of narrowing and then hold their breath to see what happened. So what were the results? Well, multiple sclerosis societies sponsored numerous studies and every single one of them found the exact same thing to be true. My favorite is this last one, November, 2017, venous PTA has proven to be a safe but largely ineffective technique. This was by Dr. Paolo Zamboni. So that brings us to one of my favorite quotes, do not be afraid to be a failure like Christopher Columbus. What is the takeaway? Well, we never know where research might lead us. We never know how our knowledge of an atypical disease process might direct our patient to better care. Whether we've been in the field, whether we're new or whether we've been in the field far too long, be curious, never stop having a passion for vascular disease and a role in its detection. A good friend of mine, Dale Aspen, always said the three most important things we do is number one, answer the clinical question. Number two is answer the clinical question. And number three, answer the clinical question. So be that healthcare professional that makes a difference in your patient's paradigm of care. And the next time you're on someone's neck, don't be afraid to go for the judgement. That's all I have. Any questions? Yeah. Thank you, Todd, the presentation. We have a couple of questions. We have a few minutes left.

webinar

Lori Lozansky

Todd Douglas-Hall

jugular vein anatomy

Lemierre's disease

ultrasound images

vascular health

diagnosis

treatment