Could Your Pelvic Pain Be a Vascular Problem? May-Thurner, Nutcracker Syndrome & Pelvic Venous Disorders with Dr. Brooke Spencer

A Pain Source Hiding In Veins

SPEAKER_00
0:00

What if the source of your pain has been hiding in your veins all along? Could Mayturner syndrome, nutcracker syndrome, or pelvic venous insufficiency be behind your nausea, hip pain, back pain, pelvic pain, or even the fatigue no one has been able to explain? And what if you've already had multiple surgeries, multiple diagnoses, and still don't feel better? In this episode of Indobattery, we're joined by the much anticipated Dr. Brooke Spencer to uncover the world of vascular disorders. We talk about diagnosis, stinting, chronic pain, comorbidities, and why recognizing these conditions can be so challenging. Could a vascular disorder be the missing piece you've been searching for? Let's find out. Welcome to Indobattery, where I share my journey with endometriosis and chronic illness while learning and growing along the way. This podcast is not a substitute for medical advice, but a supportive space to provide community and valuable information so you never have to face this journey alone. We embrace a range of perspectives that may not always align with our own, believing that open dialogue helps us grow and gain new tools. Join me as I share stories of strength, resilience, and hope. From personal experiences to expert insights.

Meet Dr. Brooke Spencer

SPEAKER_00
1:26

Welcome back to Indobattery. Grab your cup of coffee or your cup of tea and join me at the table. Today we're diving into a topic that can be incredibly important for people living with chronic pelvic pain, unexplained abdominal or hip pain, leg symptoms, and even years of unanswered questions, vascular compression, and pelvic venous disease. And I am so excited about today's guest, Dr. Brooke Spencer, who is a board-certified interventional radiologist and the medical director and CEO of Minimally Invasive Procedure Specialists, or MIPS, here in Colorado. She has spent more than two decades treating complex venous disease and has performed more than 7,000 venous interventions. But what really caught my attention is her work in pelvic venous disease and chronic pelvic pain, and her commitment to better understand why some patients continue to struggle with symptoms that can be incredibly difficult to explain. Today we're talking about conditions like Maythurner syndrome, nutcracker syndrome, iliac vein compression, pelvic venous disease, and where treatments like stinting fit into that picture. Most importantly, we're going to talk about the questions so many patients are asking. Could a vascular problem be contributing to my pain? Could it explain symptoms that have never had an answer? And how do we know when it's actually time to look beyond the diagnosis we've already been given? Please help me in welcoming Dr. Brooke Spencer to the table. Thank you, Dr. Spencer, for sitting down with me today. It's been a world of busyness and craziness, and we've been working on this for a while. So I know how busy you are, and I just appreciate the fact that you are taking the time to sit down with me.

SPEAKER_01
3:09

Well, thank you. And I'm honored to be here and share uh, you know, important information that we've been learning uh together over time.

SPEAKER_00
3:17

And we're gonna be talking a little about vascular compressions, pelvic venous disease. We're gonna be talking about all of these different things, but this didn't happen overnight for you.

Why Pelvic Veins Are Missed

SPEAKER_00
3:26

What drew you to this field specifically interventional radiology and then also what you're doing now with all of the venous diseases out there?

SPEAKER_01
3:37

Yeah, I think that um, you know, in terms of interventional radiology, I actually went, I decided to be a neurosurgeon when I was eight years old, but I changed my mind when I was 25. And I ended up going into general surgery because I went back and forth between interventional radiology and uh surgery. And then I went to South America and did clef lip and palate surgery for a month with one of the programs called Interplast. And I fell in love and came back and got rid of my radiology applications and went to surgery. Then I did a year of surgery, and then I decided I really wanted to be an interventional radiologist. So it was a little bit of a circuitous route, but I think I ended up where I was supposed to be.

SPEAKER_00
4:13

I would agree with that. I think you ended up exactly where you're supposed to be because all of this information that we are going to talk about today, what is something you hope both providers and patients get out of what we talk about today?

SPEAKER_01
4:26

Well, I think that there is um it's interesting, right? America has a lot of emotion, and America is a bell curve of very conservative and very liberal thinking in all fields and all ways, right? So whenever we're on the forefront of medicine and we're trying to come up with new ideas and new treatments and new therapies, it's inevitable that there will be a lot of people who question the legitimacy of this until there's published data. So, you know, we started recognizing a long time ago, in fact, uh uh when I when a new article came out in 2018 looking at patients that were sent to this group for varicose vein disease in the pelvis or pelvic congestion syndrome, right? They looked at the iliac vein for the first time. And 80% of those patients had more than a 50% compression of their iliac vein or a May Turner lesion. And that was the first time anybody really looked in or published about it uh in patients with pelvic pain. And so the suggestion was wow, well, 80% of the population doesn't have more than a 50% compression of their iliac vein. It's probably 20% or so, and maybe a little more. And uh, and so this must be something. So, in the group of patients within that study where they treated the ovarian vein first or did a coil embolization of the ovary vein, which is the classic gonadal vein embolization or classic pelvic congestion treatment, the average pain scores in that group went from 8.6 to 8. And only 10% of people had any meaningful response at all. And when they went back and stented those patients, their pain scores dropped to 1.3. So this is the first paper that started to raise the question about whether obstructive disease may be more symptomatic or more important than reflux or venous pooling disease, both of which cause elevated venous pressure. So then they flipped the table and they did a study. Now, these are small studies, small numbers of patients. They had 30, I can't remember, six or thirty-eight patients with good data where they stented first, even in the presence of what they called an abnormal pelvic reservoir, beating varicose veins in the pelvis, whether the gnadal vein or whether the pelvic floor. And they saw 76% of patients got complete symptomatic resolution with stenting alone, which was a big flip from 10% of patients responding to varicose vein disease alone to 76% of patients responding to stenting. Now, that's these are retrospective reviews. And, you know, even earlier than uh Dr. Santoshi and Dr. Lockham Paul's papers were published, Dr. Doherty presented 14 patients where they stented the iliac veins, and not only did their leg pain get better, but their pelvic pain got better. So these concepts have been around for a while. I certainly didn't invent them. I'm not the first one to think about this. So I don't want to take credit where credit isn't due. But what has happened is that I have, you know, become a vein expert because over the years I did a lot of work on complex reconstruction of deep vein clots and I really learned how to fix the veins and understand the vein world. And most vascular specialists spent most of their time in training in the arts. So, you know, once I became an expert in that area and became a referral center nationally for that, you know, we started to recognize that clotting people with uh standing people without clots actually had more benefit than just what AI will tell you, which is that Mae Turner causes back pain and leg clots and bad legs.

Stenting Data That Changed Minds

SPEAKER_01
7:54

So after I met Dr. Cutchins, who's a brilliant cardiologist who is at Emory and is now in her own practice in New York City, we started recognizing together, we weren't the first ones again, but that postural orthostatic tachycardia are patients that stand up and feel lightheaded and dizzy and want to pass out, may have a vascular component. So, you know, we started studying that together. And then she was good friends with Dr. Jordan Vaughn, who's like a world expert in long COVID in Alabama, and they were talking, and he's saying, Well, my long COVID patients all of a sudden are getting POTS or orthostatic symptoms, and they have a normal echocardiogram of their heart. They have normal pulmonary function tests, and they can't walk up a flight of stairs. These are normal people. These are these are college athletes, these are moms who are tennis players every day and have to take a two-hour nap after driving their kids to school. These are elderly people, these are Parkinson's patients with severe sleep apnea that developed after getting COVID, that reversed after earlier vein stentic. And so we started to recognize that we think that these uh orthostatic intolerance and difficulty breathing and heart rate issues and adrenal response causing in some people high blood pressure and some people low pressure, causing chest pain, could all be related to decreased venous return to the heart from venous pooling because of compression syndromes like nutcracker that we could talk about later and Mae Thurner and varicose vein disease, pooling in the pelvis, in the uterus and ovaries, or the pelvic floor, or varicose vein disease in the legs that millions of people have. And in fact, in Dr. Kutcheon's registry of patients presenting with POTS, 77% of them had reflux in their legs. And these patients' average ages in their early 30s. They don't show varicose veins. They show a modeling pattern on the legs during showers. They can't take a shower without feeling like passing out. They can't go out into the heat. But they don't show the classic symptoms of varicose vein disease, so nobody looks. But when she looked, 77% of them had reflux in their legs. And then when she started looking, a large percentage of them had iliac vein compression. And so she and I kind of got together, started working. I started treating a lot of her patients. And then after a few years, we've gone back and looked at 275 patients that had the orthostatic hypotension quotient or OHQ questionnaire for orthostasis scores high enough to suggest that they have serious orthostasis. And then we stented these patients and we followed them to see what their quality of life outcomes were, not just for that, but for the International Pelvic Pain Society scores, for the pelvic congestion or PCS score, PUF score, which is the pelvic and pelvic pain and urinary frequency score that looks for, you know, bladder pain syndrome and interstitial cystitis, for the Rome IBS score, which is which is an irritable bowel score, and all of these quality life surveys. So we have a lot of data. And we've now probably treated over 3,000 patients in the last six or seven years and feel like we're learning a lot. We're starting to publish a lot more articles, but I just don't think that people are really comfortable with the concept yet or even aware of what's going on.

SPEAKER_00
10:51

So maybe that's where we start with that, because I think that there's a lot of confusion between all of these venous disorders and compressions and diseases that people are kind of putting in one bubble and under one umbrella.

POTS And Long COVID Connections

SPEAKER_00
11:05

What does go under the pelvic venous disease versus vascular compression syndrome disease umbrellas? So and and what are they? What uh what is Maythurner? What is pelvic congestion? Because I think a lot of people are very confused and think they're interchangeable when they're different in various ways.

SPEAKER_01
11:23

Yeah, so there's a lot of misinformation out there. So the American Venus Lymphatic Society and some of the venous experts in the world, and I wasn't part of this, uh, and so I try never to take credit where I don't deserve it, right? But I mean, I I was part of the thought process, but I wasn't part of the paper. They went back and did uh SVP classification, which is symptom and like the varicose vein and the pathophysiology. They created a classification so that we could study and look at this. And they are the ones who uh dubbed the name pelvic venous disorders. So it's big P, little E V D. P V D is peripheral vascular disease, which is very confusing because that's an arterial problem, right? So PEVD or pelvic venous disorders, they wanted to take away this concept of pelvic congestion or just pelvic venous insufficiency because it's a nebulous and vague term that doesn't help us study and compare and discuss. So they created a system where they actually look at zone one, two, three, and four. And for me, this is really important. Zone one is the kidney. Are there varicose veins in the kidney? Do we see collateral drainage around a compression of the kidney? Now, what causes a compression of the kidney? Well, in general, everything on the left side of the body, unless you have reverse anatomy, which I've seen. But in most people, everything on the left side of the body has got to cross over to the right side of the body to get to the inferior vena cave and go back to the heart. So the left renal vein has to cross over the aorta and under the superior mesenteric artery. So they call it nutcracker, because in the old days, I don't know if any of you young people know this, but we usually act actually, rather than have the companies crack the nuts for us and put them in a bag, we actually would take rats, crack the shell, and eat them out of there. And I'm a New Englander, so I say it should have been lobster cracker, but it's nutcracker. So um, so yeah, so nutcracker is that compression of the renal vein. So it's a little bit of a tricky concept to understand, but it can cause all sorts of symptoms that we can talk about. But that's the definition is the pinch of the renal vein. Now, classic uh pelvic congestion syndrome was ovarian vein or gonadal vein, because it can happen in men or women, the gonads or the ovaries in women, the testicles in men. So gonadal refers to both. So when the when the gonadal veins, they drain directly on the right side into the inferior vena cava because it's a straight shot back to the heart, but on the left side to the renal vein before it crosses over to get back to the heart. So when we do that, if we have a pinch of the renal vein, we can cause blood to flow backwards into the pelvis down that vein. Blood can go flow backwards down that vein in the absence of compression of the renal vein, and especially in women who've had multiple children. It can happen with one, but it's more common in two, three, or four children to develop reflux in those ovarian veins because we have increased blood flow in the uterus and the pelvis during pregnancy, increased venous pressures, dilate all these veins. And then when the baby's delivered, the pressure's gone, everything flows the wrong way and pulls in the pelvis. So when we look at zone two, we think about compression of the iliac vein. So we have the renal vein going into the inferior vena cava and the mid-abdomen, up under the ribs, about the L2 region, if people know where that is. The bottom of the ribs is T12, and um, and then down closer to L45, which is the lumbar level just above the iliac crests or the bones that are our hips on either side, is where the iliac vein hugs the sacrum, right? Your tush is shaped like this for a reason, right? The sacrum's curved, so it hugs the inside of the sacrum and then comes up across L4 or L5 and kind of gets draped across there. And in some people, the aorta that comes down the left side of the body, where it where the right-sided artery crosses in front of the spine, it it's a it's a high pressure muscular-walled artery against a low pressure wimpy vein against the spine. So you got the artery and the vein and the spine. And the vein doesn't have a chance because especially we think, although this has not been proved yet either, but we think that Ellers Damlow syndrome and other connective tissue disorders experience these problems worse because of potentially because of increased collapsibility of the veins because of the disorganized collagen and vein walls are largely collagen, and because of increased distensibility in response to elevated pressures that may be more than in other patients because of the weakened vein wall. Yes. So this is how we think that the EDS and the hypermobility is related to vascular compression syndromes and venous pooling, and therefore POC.

SPEAKER_00
16:04

Which makes a lot of sense for a lot of us who live with this day in and day out when we're, you know, we hear just that we're bendy and that it doesn't affect, you know, the vascularity of everything, or maybe you have to have the more rare kinds of EDS. And is that in your experience true where it's more the rare kinds of EDS or is it across the board?

SPEAKER_01
16:26

No, it's less the rare kinds of EDS, like vascular. So this is what's confusing for people. So the vascular EDS is a very dangerous type of EDS that can result in rupture of the bowel, rupture of the uterus during pregnancy, massive bleeding problems, arterial aneurysms and dissections and things, right? So that's less than 5% of people with EDS. And that is not who we're talking about, which gets confusing because we're talking about a vascular issue, which is actually just a venous issue that's more common in the hypermobile people or people with collagen disorders. Interesting. So it gets confusing. If they have vascular EDS, it's actually not what we're talking about, yet it's hypermobile EDS that is contributing, we believe, to these vascular compression phenomena. Interesting. Which I think is interesting as well. We have a lot to study here. A lot of this currently is based on theories and you know, helping people. And so that leads to long COVID. So, what does long COVID have to do with anything? Well, um, Dr. Vaughn has been brilliantly studying the blood in people with long COVID and found that many of them have MTHFR, uh, which is a methylated folate problem, and many of them have a plasminogen activator inhibitor deficiency, which say that right. So they call it the Pi 1 gene. And what's happening in COVID is that we're getting micro clots. And so, so the we they they've shown this for sure, that people are getting micro clots or clumping of their blood, and that the shape in COVID clots is actually different than normal and even harder to unclot. So, in the hospitals, when people go in with strokes with COVID, the neuroguys are up in their brain, chasing their tails, trying to dissolve this clot and get this clot out. And it's not the same as someone who just comes in with a regular stroke. Right. And so we've kind of learned more and more over time about these COVID clots. And the problem is that people with these genetic defects cannot unclot their blood. And so we, there is data and literature in the arteries that show that these microclots can clump up the blood supply to the blood vessel wall, if that is not crazy enough in arteries and cause aneurysms and things. So we think that's what's happening with the long COVID is not only is there a spike protein attack on the endothelial lining that we know happens, causing thickening of the veins or malfunction in the vein, but also possibly the blood supply to the vein wall is being compromised and making that these thin walled muscular veins more collapsible and more distensible. So the physiology is the same behind all of this. It's venous pulling, and there was a brilliant article written by the folks at Harvard about another mouthful, something they call hypocapnic cerebral hypoperfusion or hitch. Oh my gosh. Which, yeah, I know. It's on the spectrum with POTS and it's basically dysautonomia without the specific tachycardia criteria for POTS. And they did some tilt table studies where they showed that when the POTS patients and the hitch patients are upright, their carbon dioxide levels drop, right? So we know when we hyperventilate, people pass out, right? So it's hyperventilatory physiology, but all they have to do is stand up to get it. And they actually put ultrasounds on their middle cerebral artery in their brain and showed that there were decreased velocities in the brain when these people sat up. They also looked at some of this population and did some non-invasive testing suggesting that they had an empty right heart. So their conclusion in this paper was that they thought that POTS was was contributed to by venous pooling. Now, in their world, where they, you know, this hadn't yet been studied or wasn't really out there as a concept in that paper, they suggested that the venous pooling was on the basis of small fiber neuropathy, which is another term that enters this field and this world of people, right? But the reality is we frequently see people that have small fiber neuropathy and positive biopsies and things who also have bad iliac vein compression, venous pooling in the legs and the pelvis, nutcracker, and pots. All of it. All of it. All of it. So we've got a very long way to go to really know how all of this is uh interconnected. But at least so far, we have been starting to gather data in patient-reported outcomes and quality of life surveys to see how much people are improving when we stent the iliac vein and return that blood flow to the heart and take that pressure off the pelvis. We saw about 44% of patients no longer met criteria for POTS at all. And about 71% had a statistically significant improvement in their quality of life surveys. And their patient global impression of change as to how their health was was positively affected by the stent at a year in 80% of patients. And when we went back and looked at the people who didn't respond, over half of them have nutcracker. And we didn't specifically look at, well, what percent of them have pelvic venous disease, what percent of them have reflux in their legs. But in general, we're starting to believe collectively, those of us studying this in our prospective areas of COVID and cardiology and neurology. Um, there's a doctor Zach Spiritos in North Carolina who's a neuroGI guy where the gut stuff is definitely connected, who's brilliant about that, who's starting to, you know, I think, uh, believe and consider and send lots of patients for evaluation for this when they're having the gut problems. And we just got an article on 275 patients. That we've written that's not yet published on interstitial

Symptoms Beyond Pelvic Pain

SPEAKER_01
22:03

cystitis. So we took that PUF score and people with a score of 13 or higher, which would suggest they have a more than 90% chance of having interstitial cystitis. Um, and we pulled those people out and looked at them. And again, we're seeing about a 75% improvement or resolution or statistically significant improvement in patients who are stented with IC, and about 80% saying that their patient's global impression of change at a year was significantly improved. And these are diseases that don't have great treatment options. Now, there are multifactorial causes that lead to all this. I'm not saying it's a vascular problem in 100% of patients for all of this, but I'm saying in a large number of these people, we really believe there's a vascular contribution to symptoms. So I'll be presenting that data at the AUGS meeting, an American Urogynecological Society meeting in October in Denver.

SPEAKER_00
22:52

What are, I mean, we're talking a little bit about these symptoms, and you've and you've mentioned bladder and bowel and IC and all these other things. What are some of these symptoms that you see on repeat for these patients that they can say, ah, maybe this is not one area, maybe it's something like a venous disease, or what are the most common symptoms that people should be paying attention to across the board?

SPEAKER_01
23:16

Yeah, and I think what's really tricky about this, right? Before I go through that, I'll tell you. There's also intracranial compression symptoms. So people are having transverse sinus stenosis in their brain, and Dr. Fargen and Dr. Hepworth and Dr. Huey are doing a beautiful judge of studying that. Dr. Bolognese's group in New York, there aren't as many people, but there are other people starting to get on board with this. And I just went to the Society of Neurointerventional Surgery so I could learn more about the CSF leaks that are associated with these connective tissue people and CSF venous fistulas. And people are starting to think that for the intracranial stuff, it's not always high pressure or low pressure. Sometimes it's this waxing and waning high pressure, low pressure, which can be super confusing for those symptoms. So those patients, and even some patients without intracranial compression, where we think it's coming from the compressions below, they get symptoms of, you know, chronic daily headaches, frequent migraines, sometimes pulsatile tinnitus or ringing in the ear, sometimes just ringing in the ears. They get visual disturbance, they get blurry vision, they get difficulty focusing their eyes, they get brain fog and fatigue. They're sleeping for a very long time. And at different periods of time, they have a very difficult time thinking, forming sentences, thinking of words, and thinking the way they used to. So we're this is happening to long COVID patients from children to adults as well, right? So is this a direct neurologic effect or is it a vascular effect where we're getting elevated venous pressures in the brain, or we're not getting blood return to the heart? So we're not perfusing the brain as well. Right. Uh, which is also something we're seeing. So in our patients that we're stenting for orthostatic problems or back pain and pelvic pain that we can talk more about in a second, you know, we're seeing that people's brain fog and fatigue improves. And so, you know, we're starting to study, you know, is it just that we're pulling deoxygenated blood with all this evil stuff in it that's, you know, people are keeping this in their system and it's causing immune triggers and those immune triggers and those mast cell activation and all this autoimmune stuff is lingering. And when we clear that at Spezzer, is it that we're improving blood flow to the brain, to the arms, to the gut, right? To all of the organs. And so, like I've now seen over the last two months, people that come in with freezing cold hands and a diagnosis of Reno, freezing cold feet, and their loved one is holding their hand, saying, This is how they always feel. Then I've had three patients that I've stented and they come out and their hands are like sweating. They're hot. I think it's a reactive phenomenon. Um, some of it may be anesthesia and drugs we give them and things like that, but they do report later that that was sustained, that their Raynaus and their freezing whole cold hand and feet thing is better now. So I I mean, I all think that when we think about all these symptoms and we think about how they may be caused by these vascular compression syndromes, it all comes back to decreased blood return to the heart, decreased perfusion to all the organs in the brain. And it's fairly simple and we can simplify it

Nutcracker Vs MALS Confusion

SPEAKER_01
26:16

that way. So then we go down to nutcracker and we say, well, what symptoms does that cause? Well, the classic nutcracker symptoms are flank pain and blood in the urine. We're also told this is rare. It's exceedingly common and grossly underdiagnosed. But if the patient reroutes their blood flow really well in the veins around the spine and throughout the spinal cord, we're finding they can get all sorts of other symptoms that mimic other illnesses. For example, when someone comes in with this, they are have this differential diagnosis of median arcuate ligament syndrome, superior mesenteric artery syndrome, and nutcracker. So mediate arcament ligament syndrome is where the cruise of the diaphragm or the median arcuate ligament of the diaphragm, the inside part of the diaphragm, inserts pretty low on top of the celiac artery on the aorta. And when you breathe in and out, in theory, that gets worse and compresses those nerves or more, which is why they sometimes feel differences with inspiration and expiration. But we think that people with hypermobile EDS might have more hypermobile diaphragms, and that may be related to that as well. We know that their rips, ribs slip in and out, and they have rib slipping problems, right? But the classic teaching for mouths is that we do these inspiratory expiratory ultrasounds, and we have to see elevated velocities or blood flow rapidity, like how fast is the flow going through the celiac artery that we actually have to see a kinked celiac artery for someone to have mouths. And there is a new thinking that mouths is a neurogenic problem, and it's the nerves surrounding celiac artery being pinched by the diaphragm with inspiration and expiration. And that makes more sense than the idea that it's a blood flow problem. Because we know in elderly people that get what's called intestinal ischemia or mesenteric ischemia. So, you know, a heart attack is an aching heart on the basis of not enough blood flow to the heart. Well, abdominal angina or intestinal ischemia is the same thing. It's an aching gut every time you eat when there's an increased need for blood flow and you don't get that blood flow, it causes pain. So that happens in elderly patients, but in order for that to happen, they have to have a complete blockage of two of the three main arteries in the abdomen. And they often have narrowing of the third from atherosclerosis, right? So it doesn't make sense that it's a vascular supply problem. There is interconnectivity between all these arteries in the abdomen. They can easily reroute blood flow. And, you know, usually this resolves with breathing in or breathing out, right? Um, so it doesn't make sense to me that it's a vascular phenomenon. I'm on board with the people who think this is a neurologic phenomenon, and it's causing mid-epigastric pain. So right under your ribs in the front, in the middle, it causes very intense pain that is usually constant, although it can be intermittent, and usually made worse with eating and food. So what happens is these patients go in and they say I have severe abdominal pain and I and I'm I'm starving to death. They're some of them are very thin. Some of them even require feeding tubes to feed them. And it can be associated with gastroparesis. And and the sad teaching to me about Nutcracker and Mae Thurner is that by gaining weight, they can just make this go away or feel better. As as if increased fat, which is a very soft, squishy thing. We all know that. We all know that.

SPEAKER_00
29:55

A little too well for some. We all know about that, right?

SPEAKER_01
29:59

Yeah. Um, rock hard abs don't come from fat. Right. Um, that that would actually splay the arteries apart and give us some improved blood flow. And I'm just not a believer that that's really a thing. There may be some people that put some weight on and get a little bit of improvement in that nutcracker syndrome, but it's not common. And telling a person who's starving to death because they have severe abdominal pain and food fear that they need to eat more and put on weight or they're not going to feel better is pretty brutal. It's cruel. It's pretty brutal. So there's something that's called a celiac plexus block. So Dr. Shu in Connecticut, and I hope he's not mad for me saying this because I think this is what I interpreted correctly, but you can ask him yourself, has done, you know, close to a thousand median arcuate ligament surgeries to release the median arcuate ligament. And, you know, I asked him to help me be better at identifying these patients on imaging, because I am a radiologist. So he helped me see this bulky diaphragmatic cruise that can be sitting on top of the celiac artery that doesn't have to show a kink in the artery, that that could be clinically significant. Interesting. So when we see that and we match that with the symptoms, then we get patients to get a celiac plexus block, which is a CAT scan guided needle procedure that goes next to the celiac artery, usually from the back, it can be done from the front. They inject a little X-ray dye and make sure it's right around the base of the celiac artery where the nerves are, and they inject long-acting numbing medicine. Now, patients are mildly sedated for this procedure. It's a small procedure. And when they wake up, if they can go out and eat a cheeseburger for three days or two days or one day, and they have no abdominal pain, they probably have mouse. If it doesn't improve their symptoms at all, it's unlikely their symptoms are gonna be from males. So there's a simple test we can do to check the pretest probability that fixing mouse is gonna fix our symptoms. So why would someone have all those symptoms and not have mouse? Well, what we're learning is that if the nutcracker or the compression of the kidney vein is very severe, which is up at the same level as the stomach, if you reroute blood flow in and around the spine and through the spinal canal, around the spinal cord, and all of the nerve roots in that mid-thoracic spine, which is the same place that the innervation from the stomach comes from. We sometimes are seeing people with referred pain that sounds like mouths, that's coming from nutcracker. So, how can you tell? You can do a renal hilar block, which is a CAT scan guided procedure where you put a needle next to the nerves that are that are innervating the kidney and you can try to block that. Now, is that going to be 100% accurate? Maybe not, because the symptoms may actually be coming from the dilated veins pushing on the spinal cord of the nerve root away from that. So we're not really sure. Not everybody believes in renal hyalur blocks for nutcracker, but if they're positive, they can be very helpful. When they're negative, it can be a little bit more confusing. The other study that some urologists or transplant docs do is called a markane study, where they go into the bladder, they do a cystoscope, put a catheter in the kidney, the ureter to the kidney, and they blow up a little balloon and they infuse markane, a long-acting numbing medicine, for 10 or 15 minutes throughout the whole ureter and kidney and numb that whole system from the inside. Same thing. Do they get better or not? Now, if it's flank pain and hemateria, that's a great test for nutcracker. When the symptoms are more vague or they involve back pain and they involve upper abdominal pain and food fear and nausea, that has really not been worked out. It hasn't really even been published yet, although the people in the nutcracker world frequently talk about this as the same way Mae Turner was always thought to be just left leg pellet swelling and pain in varicose veins. They're now talking about the fact that maybe this is actually contributing to neurologic symptoms in the brain. Maybe this is contributing to orthostatic symptoms in the chest with heart racing and brain fog and all of this. And, you know, maybe it's also contributing to, you know, uh nutcrackers contributing to upper abdominal pain, food fear, nausea, and other symptoms, not just flank pain and blood in the urine. But like I said, we got a lot of studying to do.

Imaging Limits And Gold Standard Tests

SPEAKER_00
34:14

I feel like I just got a like a brief synopsis of like you're better than Chat GPT right now because you're giving the brief synopsis of all of this. But one of the things that I think people are confused about is how do we tell if someone has, for instance, Maythurner? How do what is the imaging look like? How do we tell, you know, if someone has that as opposed to something else going on? And specifically, we see this a lot within the endometriosis community, is like, is it mathurner or is it endometriosis causing some of these pains? Because a lot of the symptoms can be very similar, if I'm not mistaken, correct?

SPEAKER_01
34:52

Yeah. So, you know, we talked about the neck cracker and and the mouths, but Maythurner, from what we're understanding from these studies that we're publishing in the patients we've treated, is causing pretty severe back pain in young patients. And it can also cause the bladder of the bowel, like we talked about, groin pain, pelvic floor, vaginal pain, pain with intercourse, and all of these things. And endo can cause a lot of these things, but I think correct me if I'm wrong because I may be and I may be speaking out of turn, but I don't think classically endo causes neuropathic pain in the legs. Unless it's within the SI area area in the presacral venous plexus, not as commonly, right? And that's very rare. Yeah. So Dr. Petra Klinga at Brown is one of the world experts on occult tethered cord or just tethered cord. Now we're calling it occult because most of these people's MRIs are red as normal, right? But she can look at the MRI and she can see the thickened phylum, the low-lying cord, and I'm not sure why that hasn't reached the whole radiologic community, but it's not dissimilar to iliac vein compression and renal vein compression. So we order MRIs, and this is very controversial still, but I'm hoping we'll prove that this is important. When we went back and looked at Dr. Cutcheon's patients in the registry who had uh were thought to have pelvic venous disorder, 89 of them went on to venogram and intravascular ultrasound, which is considered the gold standard for diagnosing iliac vein compression. Okay. We went back and looked at those patients, ultrasounds, CAT scans, and MRIs to see what percent of the time these lesions were missed on these screening tools. Right. On CAT scan, it was missed 50% of the time. And this is with the intention for the CAT scan to be looked at by an interventional radiologist to say whether this patient has iliac vein compression. Ultrasound missed it 50, 46% of the time, and MRI missed it 17% of the time. So the MRIs were a lot more accurate in general compared to ultrasound and CT. Now, when I've made this claim before, people get very angry at me because ultrasound is less expensive and it can these things can be diagnosed on ultrasound, and that's absolutely true. If you have an advanced vascular lab, these things can be diagnosed on ultrasound. But it's very, they have to do multiple ultrasounds to look at the renal vein, the gnadal vein, the iliac vein, the pelvic floor, they take hours of time and they take a skilled sonographer. And that's just not as widely available as MRI is, to be honest. And I will tell you that if you're trying to make a decision about what someone has endo, has varicose vein disease, has compressive disease, or has tethered cord, you need more information than just a pelvic ultrasound saying whether or not they're dilated veins around the ovaries. Even then, most pelvic ultrasounds are not performed with valva or specifically with spectral traces put on the dilated veins around the uterus and the ovaries. So they just look at the anatomy and frequently ignore that. So part of the problem is that the concept of these things being diagnosable and treatable needs to be accepted, which requires better data than we've had and then we have. And then that has to translate into actually relearning how to read these exams and identify these problems. Because even with people who are starting to buy into this concept, that we should be looking for this. And it's not a small

Who Should Get Stented And Why

SPEAKER_01
38:19

number of people. I will tell you that in the recommendations, so the American Venus Lymphatic Society again, the American Venus Forum and the Veins Meeting in Vegas, the docs all got together, reviewed all the data and literature, and put out a position paper in 2025 on what we should be doing for non-thrombotic iliac vein lesions based on all the data that's been published and the experts on that panel. And in that is the first time that there is a recommendation to consider iliac vein stending for people with chronic pelvic pain. But then they said also with parametrial varices, which was confusing to me. Because when we see an iliac vein compression, we see rerouting through the presacral venous plexus, through the epidural venous plexus, and through the ascending lumbar vein. When we see varicose vein disease, we see dilated veins around the uterus and ovaries in the pelvic floor. And I I sometimes see iliac vein compression cause dilated veins in the pelvic floor or contribute to it in young patients. So I have seen that, but it's rare and it's not what I'm seeing routinely and grossly and regularly. So the bottom line is I think we still have a long way to go to figure all this out. But the key is if I could teach Dr. Cutchins, who's brilliant, so it's not that hard to teach her anything, and Dr. Vaughn, who's an internist, how to look at MRIs and see whether someone has nutcracker or iliac vein compression, and they can routinely do it. Anyone can routinely do it. But right now is what's in question is that, you know, I'm very used to having having now correlated thousands of MRIs with venography and intravascular ultrasound. I'm very comfortable looking at MRI and saying, I think this is clinically significant. We need to do the definitive diagnosis of venography and intravascular ultrasound. There are a lot of other specialists that aren't comfortable with this concept yet, and I understand that's why we stopped doing everything else and started just doing this. So I'm grateful for you saying that I'm the best. There are lots of good doctors in the country that can do this and know how to do this. Many of them aren't comfortable stenting the younger patients yet, understandably. There are unfortunately some doctors who aren't very adept at sizing and placing stents and following like the Venus rules. And there's no way to know. It's very hard for patients to know who knows how to do this technically correctly and who doesn't. Right. And there's only one of you to teach everyone. Well, so I mean, I now have Dr. McDermott who's just as good as I am. She's been with me for a couple of years, and Dr. Bailey is joining us. She's the former uh president of the Canadian IR Society with 20 years of experience. She's been down here over the years learning complex venous reconstruction work that she's been doing up there for me. She's been putting in stunts in patients, and she's amazing. So she's joining us. And, you know, we're gonna try to move into a big building, expand here, hire more docs, and I'm you know, looking to help with that. But there are very competent and capable doctors out there. The problem is we've got to do a better job of standardizing the approaches to this and standardizing the way that we that we measure veins. And and even I just presented uh data at the Society of Interventional Radiology, which I'm pretty sure is fairly controversial in April. But there's one study called the video trial, which was a multi-center trial of interventional radiologists, vascular surgeons, and cardiologists. And the goal was to get data on 100 patients using venography and intravascular ultrasound. So this was back when we weren't using IVIS very much. And they were looking at, you know, symptoms, but those symptoms were all leg swelling, pain, seep classification symptoms in the legs. Right. Right. They weren't looking at pelvic pain or any of the other symptoms. But in that study, they had complete data on 68 patients, or 64 or 68, and 48 of them were treated for non-thrombotic, non-clot-related iliac vein stenting. And what they saw was that a 61% diameter compression by diameter, not cross-sectional area, in this study, correlated mostly with symptom improvement in that population. The problem with that study is that despite the fact that we were doing intravascular ultrasound, the reference vessel that the percent stenosis was being calculated on was made up in the literature and not actually measured in the patient in 29% of the patients. So the gold standard for deciding what the cutoffs should be for stenting people is based on a study with 48 patients with non-thrombotic disease, at least 19 of whom had made-up data. So that's pretty bad. Right. And then when you look at the paper that Santoshi published where they stented patients, that was a 50% cross-sectional area reduction that they used as their cutoff to stent people in that retrospective review we talked about, where there was ovarian vein problems, varicose vein problems, and iliac vein compression. So those that's the data we have. I mean, it's pretty limited. So I just presented data on 875 patients. 500 of them had extensive collaterals on their venogram. 375% did not. They had a compressed or funnel-shaped vein where the artery was causing the compression, but on a on a supine, meaning flat venogram on a sedated patient, we did not see, we saw maybe flash filling into a vein or no filling at all of collateral veins. And when we compared the quality of life surveys in the group with extensive collaterals and the group with no collaterals, there was zero difference. Interesting. The quality of life survey lines were statistically significant in both groups at three months that lasted to a year. And they overlapped each other pretty much imperceptibly. There wasn't even a trend of difference. So there are a lot of doctors out there that have made up their own criteria for whether someone should get stented or not. And they say if they don't see extensive collaterals, it's not clinically significant. But that's not what the data that is there would suggest. Right. So, you know, I know that I'm heavily criticized for being aggressive. And where this came from is that since we had no clear data, in patients who were truly severely debilitated, they'd had multiple endosurgeries, they'd seen 20 doctors, they were in severe pain every day, they had horrible orthostatic symptoms, some of them in a wheelchair, and their life was ruined. We took them and said, if you're equivocal in that 50 to 60% range by cross-sectional area, do you want to be stented or not? Because you don't let the patient decide in general, but we didn't have any data. So in some of those patients, they said, I want you to stent me. I understand you don't know if this is going to work. And I started keeping track of those patients. And out of the first 38 patients that I did like that, 95% of them had a positive response in some way, and over 80% of them were a statistically significant improvement, which is what we're seeing in all the other patients, right? So I became more comfortable stenting people with a lesser degree of stenosis who had the classic symptoms who had been worked out and had other diagnoses expected. Okay, so people can say that's crazy, but that's where that came from. And so we put all 875 of those patients back together because there was no difference. And we looked at what happens to the people's quality of life surveys if they had a 50 to 60 percent narrowing, 60 to 70, 70 to 80, 80 to 90, or 90 to 100. Is there a range in here where we should be considering a cutoff? And I don't know the answer to this information before we look at the data to help guide us as to who we should be stenting and who we shouldn't be stenting. And guess what? There was a statistically significant improvement in all of these ranges at three months that lasted to a year. But as one might be able to guess, the quality of life scores, a high score is bad, a low score is good. The quality of life scores were higher in the people with a 70 to 80, 80 to 90, and 90 to 100% compression than it was in the people with 50 to 60 or 60 to 70. But the amount of drop in the scores and the continued improvement over time was the same in all the groups.

SPEAKER_00
46:34

Interesting.

SPEAKER_01
46:35

So we're trying, we're we're in the process of I had to scramble to get that data together in time for the meeting. And so we have over a thousand patients that we have this data on. And we would like to continue, we're continuing to collect the data on the other 250 patients till we get to over a thousand, and then we're gonna publish this, hopefully, in a peer-reviewed journal, and it will be the largest number of patients that have been published for non-thrombotic iliac vein stenning. In fact, in 2015, there was a meta-analysis done of all the published data, and there were 1,200 patients with non-thrombotic iliac vein stenning in all of the literature published in all of the articles ever written at that point. In comparison, not enough. It's not enough. None of it's enough. But I still think that trying to base what we're doing off of patient-reported outcomes and over a thousand patients makes more sense than each individual practitioner making up what their criteria are for stenting. So when patients come to me and they say, well, why would this doctor say I don't have a significant compression? And, you know, I mean, I have a friend who's a very good doctor who cares very much about patients, but says, I won't stent any of these patients unless they have a 75% compression. And so that's his criteria. So if you go to that doctor and you don't have more than a 75% compression, you're not going to get stented. Interesting. But if you come to me and you have the classic symptoms and you've been worked up appropriately, you will get stented. And the question is, is he right or am I right? And the answer is the reason I'm trying to study this and publish this data is that it doesn't matter who's right, it matters what's right. Right. Data and scientific publications help us understand what's true and what's accurate. So there is a lot of emotion in this space. Yes. And like we talked about, you know, Americans live on a bell curve of, you know, risk adverse to ri worry about everything, from conservative in general to the way they live their lives to very aggressive or, you know, uh, or very liberal in the way they live their lives. We're not talking about politics here. We're talking about the way people are. And so people in a are gonna react and respond to what's happening through their own lens.

unknown
48:44

Right.

SPEAKER_00
48:45

And it and it goes back to the risk versus benefit when it comes to the patients,

What Iliac Vein Stenting Looks Like

SPEAKER_00
48:50

right? And so when we're talking stinting, I think maybe one of the things that we can do is clarify what is stinting, first of all, because I think for those people that are just hearing about this for the first time, they're that could seem a little scary when approached with that. What is stinting and what are the risks versus benefits that you see in your practice and what you are doing? Because you are going to be more aggressive in helping these patients who are like, I'm at my wit's end with what I'm dealing with. I need help. Can you please help me? And you're like, of course I will, because I'm amazing like that. I mean, you're very sweet like that, but I said that for you.

SPEAKER_01
49:26

So well, I appreciate that. And, you know, I I think so. What iliac vein stenting is is for me, so everybody does things a little differently, right? But I use the saphenus vein for access in most patients. So, what is the saphenus vein? It's a superficial vein in the thigh, it's outside the muscular compartment. It's easy to put compression to control any bleeding issues and access site complications are very rare. Some people use the femoral vein and they go in deeper, but I've found that people recover more quickly, get up, and have less discomfort if we use the saphenus vein. So, on average, we use a saphenous vein. Now, people who've had their saphenous vein ablated or closed because they have reflux or blood flowing the wrong way in their legs, we can still use it. There's usually a stump that people leave behind. So, if not, we go in the femoral vein. Okay. And then what I do, and this is very important, like, you know, I know this isn't a super technical field, but you asked me. So I'm going to tell you. So I put a micropuncture catheter in, and I immediately do a venogram because the veins are very sensitive to spasm. And you touch them, they can spasm, and I immediately get to see on a venogram what size the vessel is and what it looks like. Then I put the intravascular ultrasound catheter into the inferior vena cava over a wire that slides up there usually, even when there's a compression, there's not usually a circumferential fixed lesion. So the wire usually goes up fairly easily. And then we put the intravascular ultrasound catheter up and pull it down from the heart all the way through the inferior vena cava and through the iliac venous system. And then, you know, we measure that. We measure the size of the inferior vena cava, we measure the compression, we measure the normal size of the common iliac vein. Sometimes there's a prestenotic dilation or a poof in response to the pressure. And we measure the external iliac vein. So while all that's being measured, what I do is take a catheter and go into the renal vein. Most of these patients have both compressions. They can both contribute to some of the symptoms that are seen in these people. So I had one patient say to me, This doctor said you did a drive-by renal venogram. And I said, Okay, so that concept comes from the fact that years ago, when patients had high blood pressure, we knew that narrowing of the kidney arteries could cause that. And so every time cardiologists were doing a heart catheterization, some of them were also looking at the renal arteries. And it got dubbed this term a drive-by. Okay, so for this, I think those people maybe don't understand that most people with an iliac vein compression have some degree of renal vein compression. And the the definitive way to evaluate this is with venography, pressure measurements, and intravascular ultrasound. Now, why pressures in the kidney and not in the iliac region? Because I don't do pressures in the iliac region. My answer is the iliac region has innumerable collaterals all over the place that we can see that can decompress the iliac vein. The kidney is an end organ. Right. Right. And it drains through one vein on average. So I think, personally, that the pressure measurements may be more helpful in the kidney than they are in the iliac vein. That being said, some of the very worst nutcrackers I've ever seen that have collaterals everywhere where there's no flow going out the kidney vein itself actually don't have very elevated pressures in the kidney vein because the body's rerouted it. But the symptoms are on the basis of a location of those collaterals. Now, a lot of docs in interventional radiology are taught that nutcrackers associated with blood flowing the wrong way down the ovary vein or pelvic congestion syndrome. But they're not taught that it's actually more common, in my experience, from doing venograms on all these patients, to see rerouted blood flow along the ascending lumbar vein and the epidural venous plexus through the spinal canal up into the chest, which can contribute to chest pain and postural orthostatic tachycardia and upper abdominal pain and mid-epigastric pain. So all these things are interconnected. And I think all the docs out there that are seeing patients are well-meaning. I think the docs that tell young patients you absolutely should not have a stent put in are well-meaning. I think they really believe this because the reality is we've been putting in stents since 1998 in the venous system. Charlie Semba and Mike Dake, brilliant interventional radiologists at Stanford, were the first to publish stenting the iliac vein after blood clot removal on the left side. And that was in the 90s. So we haven't been doing it for 50, 60, or 70 years. So we don't have data on what happens to these stents in 50, 60 to 70 years. But a stent is like you can look it up online, right? There are lots of different set. Look up Venus stent. So a stent is almost like an open chicken wire design, right? So it's metal with holes in it, like a crocheted shirt. It's not a solid tube. Okay. It's flexible, it bends, it can twist a little bit, and it even elongate and foreshorten a little bit. So the new FDA approved venous stents, and there's several of them on the market, were designed to specifically help resist the compression and to be more flexible and to be the right size for the iliac veins, which are twice as big as arteries, by the way. I have lots of people come to me and say, I thought the stent was going to be this big, and they see that it's this big and they're like, oh my gosh, that's huge. And they are. The average size of a stent in a woman is probably 14 millimeters or 1.4 centimeters, and in a man is probably about 16. But stents have been placed anywhere from 10 to 20 millimeters in the iliac vein.

SPEAKER_00
54:35

Interesting. Because I think that's one of the things that people are concerned about is the longevity of it. But then also for those who maybe have had a stent placed before and maybe it wasn't done correctly, or maybe it was the wrong stint. Who knows what the case is for those people? But I think there's a lot of concern with putting other stents in to someone without knowing what the long-term outcome is going to be.

SPEAKER_01
54:57

Well, then I think we have to decide what's a legitimate concern, what are the concerns, and let's identify them.

Part One Wrap And Part Two Tease

SPEAKER_00
55:02

And that brings us to the end of part one. But we're not done yet. In part two, we're getting into the risks of stinting, other pain generators, and of course, the question I know you've all been waiting for. What role does endometriosis play in all of this? So come back for part two. You won't want to miss it.