Hi, everyone. We'll go ahead and get started. Thanks for coming to the last grand rounds of the 2019 calendar year. We'll close out this year with a great presentation from Dr. Ziv Haskell. Dr. Haskell is a professor of radiology. He's the Fellowship Director for Interventional Radiology and Vice Chair for faculty development here at the medical school. 

Got his MD from Boston University, and completed his residency and fellowship at University of California San Francisco, and has had quite their career since then. Has had over 500 invited presentations worldwide, has designed and participated in more than 40 research trials, and has greater than 400 scientific manuscripts, chapters, review articles, and editorials. He also co-founded the world's largest scientific Congress on embolization and is the Editor In Chief of the two journals that you see listed below. So please join me in welcoming Dr. Haskell. 

[APPLAUSE] 

So we think a lot about veins, finally, as interventional radiologists, from deep vein thrombosis to other types of interventions. And kind of a way to think about things in medicine are things we do well but not enough, things we can do well but we should stop doing because there's evidence or science that does otherwise, things that we could do. 

You think about TIPS, which has been a larger part of my career for the last 20 something years. I've treated upwards of 1,000 patients. The idea occurred to somebody in 1969 as a Eureka moment doing an experiment in dogs trying to make maps of the bile ducts, and the light bulb went off and said, this could actually be a percutaneous portosystemic shunt. It took 20 years until it happened because there weren't metal stents. So a lot of things are echoes again and again, roads not taken, perhaps. But the one I'm going to touch on today is things we do badly or could do better, but perhaps we're less aware than we might be. 

So what is it? The crippling and mundane toll of venous obstruction that we cause by the lines. It's not the exciting gee whiz or something else, but it is actually. And as an interventional eventual radiologist, I spend a lot of my time doing dramatic procedures to restore veins for these patients who have obstructions. And they're exciting and they look great, and you make them feel better. And my phone is full of before and after pictures of patients over the years, but really, we wanted to kind of take it back earlier to see what the problem is. So iatrogenic venous obstruction are what I'm calling the deforestation of our patients' veins. 

So if you take care of patients with end-stage renal disease, then this is a daily part of business. Every access in removed is a transaction that has a cost in terms of venous narrowing or thrombosis. And a walk through any dialysis outpatient dialysis center is going to show you patients who have under-recognized superior vena cava syndrome, who are just passed off as this is how you are when, in fact, they're living with venous hypertension because of central vein obstructions and a hypertensive arm because there's a fistula, there's an AV shunt for dialysis. 

So the drama is more exciting to talk about, and here's sort of an example. This is a woman with an incredibly swollen arm. The arm is essentially non-functional. About seven years before I met her, before I came here, somebody had tried to open this central vein obstruction. 

Wow, that's quite a pointer. OK, that pointer did not-- there we go. Let me try that again. 

So where the arrow is, so this is the axillary vein. There should be a vein that goes from here down to here, and that's missing. She has a fistula in that arm. The arm has been passed off as lymphedema. Somebody tried to cross that seven years ago. They weren't able to, and she has basically-- it's a dysfunctional arm. Can't type, can't use a phone, can't hold a steering wheel, and just the chronic pain. 

And I somehow met her and said, you know, there's some different techniques. There's something else that I can do, some new equipment, actually, a wire that becomes red hot at the end that you can burrow through things a little bit, good things and bad things. You can see that I fuse a picture of her aorta together with where we were so that we might try to avoid big blood vessels and go through small ones, and put a stent at the very end, which is that sleeve that you can see is over there. 

And that is extravascular. It's just gone through tissue. There is no vein in between. And gradually, her arm becomes better. It took a couple of months, but it it's a new arm, so great, exciting. 

The problem is that we're now dealing with the secondary interventions of the stent. Or it turns out that she has an unrecognized thoracic outlet syndrome that you wouldn't know is compressing it because it's been blocked for so long, and it's been called lymphedema. So only by opening it and seeing the effect on the stent, which is fracturing, do we realize that there's been compression. There wasn't another way to think about it. You wouldn't operate just because. 

She's since had the surgery. But she still has chronic pain and now some neuropathy. In other words, we haven't really solved this by doing this great intervention. And I've told her that I'm going to be dealing with this with you lifelong, in some way. 

And then there's this kind of drama in which there's a central venous obstruction. And the black arrow is the superior vena cava, and you can see the veins coming down from the chest, massively swollen head. And somebody actually took an aortic endograft, which is what you put into the aorta for an aneurysm. And put it in upside down into the veins. 

That's a $20,000, seven-hour procedure, which is a little bit more like Willem Dafoe in the Platoon thing, which is a bit closer to futility. If that's where we're going, to think that this is a durable intervention for somebody other than publishing it and probably never do it again, we should be backing it up to earlier. 

So here's the example of what I mean. This is a 26-year-old woman in Baltimore, actually, that I met with this swollen arm for yet another balloon angioplasty of something. This is how she looks. And she has been stretched five times by good people, taken care of by smart nephrologists in the same dialysis center. 

40%-- that's four out of 10 patients-- will have some central vein obstruction because of repeated access. That's almost 150,000 US patients a year, pretty big number. That's three times as many patients that have colon cancer metastatic to the liver in the US. 

That's the same person. She hasn't looked like this for four years. The only difference was that the interventions that we'd been doing, which were stretching it, were completely non durable. She never-- in other words, the vein just recoiled. It never really had improvement of any sense. And then she just lives as you're an obese African-American woman in dialysis when, in fact, it's all superior vena cave syndrome. Same patient. Two years it stays the same. That's what I mean by under-recognizing it or walking through a dialysis center. 

So things we can do well, but less of, or at least think about more. Well, we spend almost half a billion dollars on central venous access. The number is actually higher than this. And some years ago in 2006, the Fistula First Movement, our initiative in the US said the US needs to create native AV fistulae instead of placing dialysis prosthetic AV access grafts like the rest of the planet already did, second world countries and first world, well ahead of the US, because of a four to five times less infection rate from not having the prosthetic, and if you have a mature fistula, a dramatically longer patency, far better, things that can function for years. 

So surgeons were basically said, if you don't make your quota, we have the ability to reduce your reimbursement because they're all Medicare patients. And remarkably, it actually worked. 

The downside of being pushed is that fistulas are created and still are in patients in whom they won't mature because I've gotta get a fistula in because that's what I measured by. So Fistula First has actually resulted, as we've known now for years, as Catheter First. A lot of people are carrying dialysis catheters for a longer time in hopes that this fistula will become usable, will mature, will turn into something, or eventually abandon and a second one made. So we have people with catheters for longer than we did. 

And we're starting to learn that there are subgroups of people who shouldn't have fistulae, that should have grafts. Older patients, diabetic patients, ones that don't mature do not work as well. So it's swinging back slowly as large-scale studies are occurring. But the end result is that we still have and continue to have a lot of patients with prolonged catheter use. 

But this isn't really a problem of dialysis only. And I've just given you a short list of examples because all of you are going to see patients in here that resonate with you from cystic fibrosis, heart failure, congenital heart disease, transplant patients, any chronically ill patient with either some gut or other disorder who's going to have chronic infusions, pulmonary hypertension patients, pacemaker patients with wires. 

So much of our daily business at UVA is making pictures of venograms of patients with pacers who need upgrades of wires because there are stenoses or occlusions, and we're going to have to do something so that something new can be pushed through. It's not a durable solution, but it's basically just find a way to upgrade it, and a lot other examples as well. 

Everything has a consequence. Every catheter causes an injury by contact. That contact leads to thrombosis, intimal injury, and the resulting fibrotic reaction, that fibrin sheath that you may have heard about, or if you've taken out a line and you see a little bit of glistening tissue. Sometimes it can even return out like a sock around the catheter, or when the catheter that you're pulling out a PICC line or others, it is hard to pull out, and you feel, oh my goodness, it's going to tear. It's bound in a fibrin sheath. This will happen within days. 

The picture-- and this is the sleeve around the catheter over here in white. And this entire thing, which looks like a scabbard, is actually a sleeve of tissue that is formed around the catheter that has been withdrawn to that vertical thing. So that is iodine liquid constrained within a fibrin sleeve that has developed around it like a sock around the foot, has encased it. 

And these things don't really go away. We do fancy things like stretch them, but they kind of come back like those plastic curtains that you walk through that insulate the front of a restaurant with those sleeves. So we really can't cut them free. 

So just another example on the young end of the spectrum, 7-year-old with two prior PICCs. You see the axillary vein, and at the asterisk, that's an occluded vein. That PICC, at 7, has occluded that vein. 

The picture on the other side over there, further over, that's an eight-year-old with one prior PICC, and we're now completely occluded from the subclavian vein, through the innominate, to the top of the IVC. That's one PICC in a kid. 

So part of the problem with thinking about it is that you need a language. A common language lets things get studied and talked about and data get pooled. And as the plumbers who work with these things, we haven't really had a consistent language. People have talked about central veins as including all the way from here to the center, and these are completely and utterly different pathologies and causes of things. The superior vena cava is not a vein that might be compressed with motion or have anything to do with the arm. 

So after some years, we have what's called a reporting standard and a categorization, which means now future papers can be pushed into using categories. And we can actually define therapies or severities of things by a standard nomenclature. Completely absent because we haven't thought about this methodically. 

Over a million PICCs a year in the US. That's a lot of PICCs. And there are giant businesses that have been created to provide picks on an outpatient basis, patients you'll never see from nurse- or technologist-driven businesses that will basically go to long care facilities or otherwise with a EKG or other types of systems that allow you to tell how far the PICC has gone in, which means you'll never see them placed. They just kind of occur. It's a big, profitable business. 

And I can show you pages and pages of literature that will show you that stenoses in large trials are essentially inevitable. Now, the fact that the patient is asymptomatic is not really a comfort because they're future access, and it doesn't take much to tip them over if they're stenotic to occlusion. And then they become symptomatic, and then we ramp up and say, my goodness, it's occluded. Do we now need to anticoagulate? What's the PE rate from a little bit of clot on top of a [INAUDIBLE], all those things that kind of get us excited. 

And here's just another measure of how far this has gone beyond the point of being able to think about it. This is a paper that was published my journal out of University of Toronto at the Children's Center, in which they performed venography, contrast injections on 100 children who've had PICCs, during the PICC, so an opportunity to basically make maps as part of a study, and then driven by history, prior numbers of PICCs, histories of PICCs, sizes of PICCs as well, materials, how many had different positioning or malpositionings as well. The point of all this is they've created an algorithm to figure out how to manage the inevitable abnormalities that are going to be found in children because they may have add 1 or 1.3 prior PICCs and how to categorize them for more complex interventions to put more accesses into them. 

So this whole superstructure and this interesting analysis is built on the problem that we've created on the other side. So part of this is to really to be aware. And then this sentence which is kind of blithely written in the discussion, counseling regarding the risk of future venous compromise should be considered for the parents. I don't know what you exactly say. 

So here's a patient from here. It's a 14-year-old girl with cystic fibrosis. That means long term accesses of all types. At 14, all her right-sided veins are gone, from here to the jugular, subclavian, innominate vein are chronically out. There is nothing to reconstruct. 

The left side, you can see, that's the axilla with that valve there. Let's see if I can get the pointer to-- this is what we call in radiology a low resolution pointer, that big a circle. 

So here's a catheter running through it. But you can see that from the clavicle centrally, it's completely occluded. So she needs and access. And the only other thing is we're going to put a leg catheter in an otherwise functioning kid who's living a daily life and going to school? Not an option. But this one remaining vein in her is completely occluded, all the way to the superior vena cava. There's nothing there. 

And she's got a swollen head, which has been under-recognized. I came across her incidentally. She's got a red eye, she's got a swollen head, she's got some tinnitus because blood flows toward that side across the veins in her head. Higher flow on the open side from the other side will cause tinnitus. Ask your patients. You'll find this finding, and it's exciting when you can make that better. Imagine what that would do. 

So in this case, trying not to place stents and things like that. We've stretched it, dilated. Each one of these procedures in her is general anesthesia. 

So three weeks afterwards. And a whole lot of drama of pushing the port out of the way-- it's a port, so it's not something easy to take out. Pushing it out of the way, stretching, pulling it back down, we get something that starts to look a little bit better. And her face has gone down and she feels better, and there we go. That's exciting. 

The problem is that I have since repeated these interventions five times on her, and ultimately had to place a stent, which means talking about whether this will or won't have an impact for a hopeful eventual lung transplant or otherwise. So at 14, she's already got end-stage access. We've got stents in place, and we're re-intervening again. 

There is no clean solution. There's no reason to think that a drug-coated balloon, regardless of the controversy, would make a difference. This is just the problem, so it is a thing. 

And in fact, in cystic fibrosis-- and I've made this in a small font not because I expect you to read the references, but to impress upon you that I could run the list of these papers below double the length of the slide below on papers talking about the complexities of central vein stenosis and occlusion in cystic fibrosis patients, particularly as to what surgical requirements there are. 

Imagine that you're going to operate to replace a lung on somebody with a central vein occlusion, which not only, how do you manage access afterwards, but everything are collaterals throughout the chest. So there are surgical risks. There are conversations about reconstructions of the superior vena cava in the setting of large hemorrhage. These are all things that we're making as a secondary cost of having to have access in patients. 

So intentional blindness. So when you find a paper that says, what's the rate of injury from a catheter or the thrombosis rate? It's anywhere from 1% to 70%. How do you get a number like that? You write the paper saying, this is what I saw in my last 10 patients because you found something dramatic, so that paper gets written. 

But actual incidence is something else. This is what retrospective reporting is. It's a non-methodical means of-- I remember when I was in med school, when we were learning epidemiology in Boston, that someone was describing in The Boston Globe a cancer, a pediatric cancer cluster of tumors. And we analyzed it as a case study. 

And in fact, what was happening, because childhood cancers are so rare that you get to report them all together in some papers because it's so rare to have the single one again and again to make numbers, that it was kind of like the president's Sharpie including Pensacola. Every time there's a new cancer, you just enlarge the circle and then include another one and include another one. And there's one in Fall River. We include that, and suddenly we have a cluster, a cancer epidemic. That's a bias as to reporting. That's not actually an incidence. 

So when we actually look at it methodically, then the numbers are really different. And here's a paper that I accepted to be published for reasons that were very different than what the authors thought they were doing. They did the standard sort of thing. You have a company that'll pay you to do an industry-sponsored trial, which means you get paid to enroll every patient. 

What was the study? We're going to try one PICC line that has a little bit of a hub over here versus another one that has a different type of hub. Really? You really want to enroll patients and try to identify a difference because of the external hub, and that that's a good project for an assistant professor to spend a year and a half on, enrolling? I guess it pays for the research coordinator. It's silly. 

But the difference in this is that they built in asymptomatic ultrasound of each of these patients' arms. We're just going to do an ultrasound of the arm in the patient that has a PICC, in everybody. So suddenly, there's a methodical, prospective look at what's happening in the vein. 

So what did they find? Of course, no functional difference between either of these two PICCs. They're hoses of the same size. The hub makes no difference at all. 

What's fascinating is that it's a 70% demonstration of peri-PICC thrombus or occlusions developing in these veins, three out of four occlusion in the vein. So when you see the RM DVT called around the PICC, that's the routine. This occurs reliably, and it's a lot more than 1%. 

So people have done large-scale studies, tens of thousands of patients and some analysis as well trying to say, what are the things that guide it, so every single risk factor that you can imagine. Every paper has a home somewhere, it's going to get published somewhere. There's always room for one more. 

And every single factor that you can imagine, here are just some of them in patients in studies up to 5,000. Is that the basilic vein? Is it the cephalic vein? Are they trauma patients? Are they special, somebody who's had radiation? If they're really sick, does that make a difference? 

What about being in a certain ICU? What about a certain medication? Why should that make a difference? It's delivered downstream. Well, who knows? Maybe there's something systemic. 

What about the number of lumina? What about the size? Everything has been looked at and some themes. There is no safe dwell time. In other words, in for shorter does not guarantee safety. That was the point of showing you those examples in children as well. 

What we do know is that larger number of lumina and larger PICCs are more likely to be related to catheter thrombosis, and also PICC size to cross-sectional lumen. If that's the PICC, and that's the cross-sectional lumen in my hand, that's a lot different than if it's something like that. There's flow around it. That is less likely. 

So smaller patients, bigger PICCs, small veins-- . Older patients often have smaller veins. Older women have smaller veins. Repeated accesses are going to have smaller veins. You want one lumen or do you want two? 

Well, of course we want two. Why wouldn't we get two? It costs the same amount. Let's get double, super size it. That's not a good thing. Higher infection rates with more lumina, and also potentially a larger catheter. These are decisions that we can actually make. 

So then there are stories that say that middle lines are safer. What's a midline? It's a PICC, essentially, that goes about this far. And this is somehow supposed to be safer for patients for infusion of things. And these are stories that go around. 

And if you kind of look at the literature to find out, there is this echoing thing where somebody will write this somewhere, and then it gets cited again and cited again and cited again. And if you trace back to find out where these things to get cited, you can often find that the very first report of it was simply somebody's opinion in an editorial, and then it just gets repeated and echoed again. It becomes a given fact. What's myth and what's fiction in medicine. It's kind of interesting to look at citations. 

So recall that the silent DVT rate for [INAUDIBLE] picks is 27.2%. In contrast, midlines, it's less than 2%, and all these citations in this publications. So then I go and I look at these citations because multiple papers have quoted this one back originally. So two of them are conference posters that never got published. One of them in the Journal of Vascular Access, which may or may not ever get an impact factor. But it is, I can tell you, a retrospective poorly conducted study. In other words, the quality of the literature does not allow you to make these conclusions. 

But if you look at other larger papers that have actually made these comparisons methodically, and there are ones that have actually compared them, then the outcomes are very different, and there is no clear safety with the midline. It's not a safer thing. You get the same thing, plus you have the potential exposure of the downstream vein to whatever hypertonic or irritating solution that you're infusing. So it's a sort of a devil's bargain as to which one. 

So there are things that we can control that are worth remembering, and subclavian vein catheters and left-sided catheters are evil when it comes to venous thrombosis. The single vein that has a better outcome is the right internal jugular vein. It is a straight line. It may have as much as an order of magnitude lower thrombosis rate, and it's simply contact. 

If you think about the course of the catheter coming across, every place that it makes contact as it makes that turn is an intimal injury that I showed you on the histology slides. From the left side, you get a point of contact here, across the innominate vein. And then the worst is where it turns into the superior vena cava so you get a narrowing that actually inflicts pain on the right side as well because the two then come together. 

So if I'm placing a large caliber catheter, or even a small one that's tunneled, I'm going to use that right every single time. And even if it's partly thrombosed and I can see it, I'm still going to try to reopen that right-sided catheter. So the cost of removing a catheter and then placing it back for a magic day of holiday is that it may have thrombosed in the interim, and we may not have that. Simple location choice. 

In a potential dialysis patient, future dialysis patient, a subclavian catheter is a deadly thing because we're going to develop a narrowing in that vein, and that's the outflow to the arm. And those are the patients that I showed you at the beginning. We should never see subclavian dialysis catheters. Translumbar sooner than anything else. 

This has been a project here, actually. You can make teams who think about this and get better. So here's some data from UVA for the team that has been thinking about it, multidisciplinary group that has started to look at education and intervention-- and that's just one graph of the efforts-- has reduced lumina use in PICC lines, which generally means smaller catheter and lower infection rates. That's a good thing. We can actually effect change. See how the lines are going? This is here. 

The other place that is an opportunity to think about is this endless cycle of taking catheters out, having this sort of holiday, and then putting them back in. And most often they go in and another site, which means you burn one site, and then you go to another one that's less ideal as well. And you get the kind of hardship that I showed you in some of the earlier case examples as well. 

We have national guidelines from dialysis access guidelines, the KDOQI guidelines that will have another revision coming out soon, Infectious Disease Society guidelines that say that in the absence of a tunnel infection or frank cellulitis, mild you can try to treat through, that you can give the patient antibiotics and changed the catheter in situ. 

That's not treat in place. Treat in place has a very poor success. But exchange over a guide wire after defervescing after antibiotics can be, depending on what series you look at, 80 plus percent success rates for gram-negative, gram-positive in the absence of a tunnel infection. So the automatic thing of it must come out and then we're placing another catheter in a high-risk patient for access, like the patients I've shown you, from all those different conditions, is not the way to go. We should be doing line exchanges and try to preserve access because of the costs of these. 

And we know this type of thing in the corner over here. You're supposed to cure the infection, not become it, which means you have a patient who has a bacteremia or an osteomyelitis. You put the PICC in so they can get their four weeks, and then they spike another fever and you say, the PICC line must be infected. The PICC line is the tool to treat it. It didn't suddenly become the nidus of infection. 

And yet, we know that we create these cycles. So then the thing comes out, and then we burn another vein as well. So just understanding the arc of it more than just the immediate can reduce these types of things as well. We have greater opportunities to improve our hard accesses, preserve accesses in patients here as well, particularly, and not just the ones who are basically down to one femoral vein, and that's their only access. 

And we talk about doing sort of tough cases of trying to exchange it and see if we can get away with antibiotics. We should be thinking about that more broadly for these types of patients where we can, not the septic patient by true criteria of sepsis, but the ones that defervesce with a dose and can be changed in situ with a high expectation of success. 

So removing a catheter from the right side [AUDIO OUT] side, if at all possible, even if it's blocked, if we have to give it up. Here's someone in which the right side has become blocked down to the superior vena cava. He's had a left-sided catheter. He gets a stent because of a swollen face. 

And you can see that the right side is jailed. It doesn't drain into the stent. It's still occluded. This stent has done something for the left side, but done nothing for the right. And his superior vena cava syndrome doesn't improve. 

You could look at that man and say, that's just how you look. And the answer is no, that's half-treated superior vena cave syndrome, which means some fancy intervention to put this into that. And that's still a work in progress because he's going to have repeated interventions. Those are those contact points that I showed you that you get from the left-sided catheters. 

Fibrous encapsulation-- that's that fibrin sheath has been reported since at least '66 with pacer leads. Happens in almost everybody, that a pacer lead is going to cause this problem. Be great pace or leads could come in on the right side and come down the jugular, and we could change that approach. And we'd have less of that. 

But this is how it's practiced, so out of my business at UVA is dealing with the narrowings and reopening these things or helping the interventional cardiologist get across it so they can put a new lead. It's not a durable solution. It's just get the new lead in, and don't ask about the arm. So this is a real thing. 

So I said I'd show you sort of dramatic things. Here is a man with an incredibly swollen arm and an occlusion that extends all the way from here all the way up to there. That's about 20 centimeters. So this is all blocked vein. This is actually after an angioplasty. There's nothing there. 

So this is a stent graft. This is a whole series of basically Teflon, PTFE, Gore-Tex, the other company that makes it, and sleeves all the way there. And you can see that his arm is now better. This is nine-month follow-up. But I'm still doing periodic little interventions at the edges. This isn't the solution. 

And this is a recent case of somebody who had a fistula created. Left arm is swollen. Five weeks later, it's still swollen. Why is that? 

Because downstream of this left arm fistula, he has a chronic central vein occlusion from prior catheters that wasn't recognized. So of course, the arm blows up because we're now pouring high flow arterialized blood into the vein. The arm swells. For five weeks, he's basically had a swollen arm, saying, walk it off. 

And he's got a superior vena cava occlusion, which now has a stent. And the fish flow has not matured which means he still has a catheter on the right side, which I had to put back through the stent. So we've got a stent, a non-matured fistula, and still a catheter abusing that same thing going through it. 

Be nice if it were simpler and we hadn't gotten him this occlusion to begin with, and planned his fistula much earlier at imminent dialysis. And that's really how we reduce our continued catheter use in dialysis patients, which is early referral for official a creation before they actually have a full requirement of hemodialysis. When we see the inevitability, they should have a fistula created so there's time to mature, which may be 30 to 120 days, depending on the patient. So it's seeing ahead of it. 

And another sort of example of drama. That's full-fledged SVC syndrome. You can also see how the collateral's extremely swollen. That's without the swelling, and kind of reconstruction of everything being blocked from nothing moving centrally to all of these things. Looks exciting, lot of stents in there, a lot of metal. 

But in fact, if you look down the barrel of them, they're not perfectly good circles. They're actually ovals because they're squeezed against each other, which means this is not a long-term solution as well. It's great, but it's not-- it's operatic in the thing, but the tenor is going to miss the high note sooner or later. 

So we're missing the-- new devices are not going to solve this. Is it going to be new hoop strength, flexibility, precision? We have stents that are stronger now, so now there's a lot of excitement to sell people like me and vascular surgeons the new veins stents. But in actual fact, there's no difference in their patency, their outcomes. They're simply better able to press against occlusions. There's more radial force. 

So we can do this kind of extraordinary stuff, and this is the first reported case of a percutaneous creation of a vena cava. This is a woman who was born without a vena cava from below the liver to her heart. So her entire liver drains by that horizontal vein downwards. You put contrast into her inferior vena cava, and it goes reverse because blood is coming out of her liver and going retrograde because there is no up vein. So she actually has portal hypertension, Budd-Chiari syndrome, because she has outflow obstruction, hepatic vein outflow block, essentially. 

So she's got ascites, young woman, massive collaterals, swollen legs since childhood. I met her because she thrombosed everything. We cleaned it out and figured out her anatomy, and then essentially created her vena cava that carried through. Let me see if I can show you that picture. 

There is the missing piece. This is the hepatic vein going down the vena cava. That's the superior vena cava above the diaphragm, and this is some sort of plumbing procedure somewhere through her diaphragm and something else in her retroperitoneum. 

Scared the heck out of me to do. Took me about two months to get the courage to do this. I called the cardiothoracic surgeon, I said, she would do it in the operating room? He said, don't bother because if she bleeds out, she'll be dead by the time I make an incision. So do it where you want. I said, that's very comforting. OK, thank you. 

So that was 2013. So I can say that now because that's when I published the case. So that seems great. I have done six or seven re-interventions on her since that time for other aspects of her thrombophilia, as well as working with this. And every year at a conference, I update this just to remind people that you can do cool stuff, but. 

And here's another example because I was feeling good. So this is somebody who has-- all of those white things are stents, and there's a vena cava filter that is in a densely occluded vena cava. So it's deep in clot. Her legs are very swollen. Somebody put all these stents in that are a complete mess. 

And I said, I can probably get through this without all these tools. Two sessions of 6 and 1/2 hours, and I basically construct her a vena cava, dig out the filter from within the occlusion with those bronchial forceps. That's what that big jaws of life thing was at the top. Placed all these stents, make her a new vena cava, and the thing promptly thrombosis. 

Throw every med at it. One week later, it's gone. A lot of money, a lot of time, no solution. Not worth a thing. 

So we can make these beautiful sort of castles in the sky, and they're exciting. We show them [INAUDIBLE] in conference. But really, the point of this is it's prevention, it's recognizing thrombophilia, it's recognizing that these low-flow states, that cross-sectional error, the number of lumina, and the prevention. Thinking about the cost of each one of these upfront is the reason. 

Here's a company that was sold for, I think, estimated $60 million, will come to the US market. We were in a trial. This is a fancy device in which we bring something up from the groin. Put a washer on the skin at the neck, and then fire a needle that comes out through the skin, through the neck, looks like Sigourney Weaver an alien when the alien comes out of the belly. 

I had a medical student up there. The needle came out of the neck, and he jumped back and screamed at the time. It was very exciting. I wish I had it on tape. 

And then we can follow that back and basically place a catheter through the skin, through the subcutaneous tissue, into the vena cava. This whole thing has been designed because we have 150,000 patients with central vein occlusions, so we've built this new procedure and device that's going to be sold all over the planet because we're creating these occlusion. That doesn't really seem right. 

So as I'm sort of wrapping up, I'll show you a couple more examples, and then try to pull it all together. This is a patient from here, a 36-year-old woman with a heart transplant, which means lots of biopsies, lots of catheters, pacers, pulmonary hypertension. You know she's had catheters. 

I meet her incidentally. I don't know what the luck was, but she's in the emergency room repeatedly for crippling migraines, hospital admissions for opiates because of this. Severe tinnitus, gets worse when she picks up her right arm. Her tinnitus gets worse. Something changes in the vein that changes flow that magnifies her tinnitus. To me, it's kind of a provocative question to ask. 

And her head is foggy. She's got slightly swollen face, but she feels stupid. That's what she describes herself. Dropped out of school, has a low-end job. Everything is occluded. Everything is occluded centrally, from her head down. That's a collateral. 

So I basically reconstructed the single central vein out of her head, which is the right internal jugular vein. That's what that is over there. You can see it's narrow at the bottom. This is after a bunch of work on it over here. That's after reopening it. 

And she becomes smart. That's what she says. She goes back to school. Everything lifts. She starts driving a car. This brain fog is a manifestation of chronic venous outflow obstruction. 

They're not nuts. This is real. Unless we ask and recognize these questions, we're not going to elicit the opportunity. So all these symptoms disappear, and that's exciting. And now it's been two years of repeated interventions, sometime urgently, and now stance that I've desperately had to place inside to keep this thing open. And we're now having kind of end-stage conversations because at some point, I'm not going to be able to keep this thing open. 

Now there's a stent graft. Now they're narrowing that are happening above. And now the last thing is that the vein that is the inflow has diffusely narrowed over time, which it wasn't before. There's some other pathology, and I can't stent up to her top of her ear. So when this goes and she feels like-- what's that book, Flowers For Algernon, like she has gone back to that in the beginning, then she becomes suicidal, and there's our end-of-life conversations. She wants to go off for immunosuppressions, and that's it. 

This is all iatrogenic venous obstruction. That's what that is. We get stenosis at the edges of things. We don't have devices that manage it. We have catheters, we have stents that keep things open beautifully. But at the edge, we create some sort of change in the elastic modulus of behavior with shear stresses, and veins narrow there. And then you can imagine this bionic arm of stents extending out is not a solution because we really don't have devices or ways to even think about that. We just have a new stent that is bigger and stronger, and this must be the venous stent. So that's what the market's going to do. 

So in closing, I'll show you maybe a surprising and hopeful picture and wrap up over here, which was a patient that I took care of quite some time ago and just came back to me by email, of all things. So I share this with us an update from just two or three weeks ago. 

So seven-month-old with life-threatening SVC syndrome. Intubated because of difficulty ventilating, short gut syndrome, a left subclavian catheter-- I'm sorry, protein losing enteropathy within one month of birth. You can see the catheter coming up in the tip of it, right over there at the tip of the arrow. 

So it's short. It's hitting the vein like here, it's going to create some sort of narrowing, and we're putting non-isotonic fluids right at that point of contact as well. So everything becomes occluded, no results. She's in hospital. She can't be anticoagulated, and she can't be lysed because of bloody bowel movements as well. So this is kind of a life-threatening situation. There's no book for what you do and these kinds of things. 

So I clean her out over a series of days, trying to get away without placing stents. I finally place one that you see, that ends in that jugular vein. That's the white arrow going down to the black. And that wasn't enough. Her swelling didn't get better because that little point in between simply didn't work, so I places then into her jugular vein. So this kid basically has one vein coming out of her head. And it has a stent from the jugular vein going into her atrium at this age, and that's it. 

Nine days later, her SVC syndrome is better. And her dad, who's an orthopedic surgeon in New Jersey, sent me this pictures. And I asked him, and he said that I could use them. 1.5 months. 

As she's growing, she's got 95% head circumference on the chart, big head, some chronic venous hypertension. Did one intervention on her at the stent, and I get these pictures now. 

So here she is at 6, and this is the coolest part. 13, this is the one that came by. No visible issues. 

And she happened to get a chest X-ray at some point. You can see all those stents, and you can see the gaps. She has essentially grown the stents apart. There is no way that those stents are open. It's not possible. So sometimes we get lucky. Kids are different. 

So what's the point? The point is summarized in slide over that picture in the corner. It really is our job. So we have to be thinking about these patients in terms of the points that I've kind of tried to share with you, which is, what's the actual access need? How long is it necessary? 

If it's longer than anything at all, should we be tunneling in the right jugular? Should we be rigid about not pulling it out when we don't have to, and trying to treat in situ if it's possible, reducing lumina, staying out of subclavian veins, specifying sites, determining is a PICC absolutely necessary? How many lumina can we get by? What veins are most suitable? 

All these kinds of things can actually be used to reduce, and they have been in hospitals as well. So the opportunity is there for us to think about this, and not to think that the PICC is the throwaway. If anything, PICC are evil. And yet, it's so important for patients. 

And lastly, if you'll allow me the editorial to realize that source control is an incredibly important thing. But once we say that, sometimes the blinders can come on so that source control, at the cost of everything. And in certain patients, that's a desperate cost as well. 

So ask us what you need. Tell us what you need. Engage in the conversation, and that's our upside opportunity. Thanks very much for having me. 

[APPLAUSE] 

We have time for a couple questions, if anybody has any. 

Thanks. Great talk. You mentioned pacer wires being an issue, and you kind of gave alternatives for PICCs and things like that. Are there things that should be thought about when we're talking about pacemakers? 

No. Pacer leads have in some cases gotten thicker, as well as they have multifunction or multiple leads as well. So we have that issue that doesn't seem to be a solution. I can't say that I know what the innovations are in pacers, or whether they could be moved to a different vein. We've changed to a jugular approach. 

I don't know why they couldn't because all the things that we place go into the jugular. But on some level, that would actually be a good. And who wants to start that and drive that? That's an opportunity. 

Infectious disease guidelines would say if you had Staph aureus growing out of the central line, all the central line, Pseudomonas [INAUDIBLE]. Are you suggesting that maybe we should try to treat through that, guidelines are only guidelines, and see if you can clear it? 

So there are papers that show almost every bacteria-- not spirochetes, not yeast, not patients who are hypertensive but stable, including Staph. Treating in situ doesn't necessarily move that glycocalyx that hides the bugs around the catheter, but exchange seems to disrupt it as well. So absolutely, Staph species, gram-negatives as well. 

Gerry Beathard, who's an interventional nephrologist, wrote one of the earliest papers looking-- and I grant you that the quality of these papers is not necessarily the ones that we need, ideally. But there are going to be circumstances and we just have to make these kinds of decisions. And for dialysis patients, it's much easier to make these routinely exchanging in situ, which we still underutilize. But in other hard-to-treat ones and stable ones, particularly if they defervesce, that's in guidelines, including Staph. 

[INAUDIBLE]. 

So depending on how you want to view it, it's treat if they defervesce, then change over a wire, exactly. So you can take that as early signal. And the cost is essentially a day and a half or so, or two days. So if there's a time in the setting of a hospitalization, then that's an acceptable shot to take if you're thinking long view. 

If you think about from the dialysis side and the cost of an intervention, even a venipuncture causes a narrowing, and that may impair a radiocephalic fistula. So if any of us are going to be plagued by elevated renal function and worry that that's in our future somewhere, and we see a creatinine rising, which means thinking about our patients, we shouldn't even have any acute blood draws. Forget IVs. Everything should be from down here. 

And there are hospitals who make this routine, that blood draws should simply be from the hand and anyone with a rising creatinine or high risk because even the blood draw's a problem. It's down to that level. 

Thank you. Excellent talk. Thank you for sharing our data on the [INAUDIBLE] reduction project. One of the things we've learned qualitative interviews with some of the people [INAUDIBLE] was that no one cared about making the decision personal. A lot of the reasons I think the project was so successful is most physicians are willing to defer decisions about vascular access to an expert [INAUDIBLE]. That's usually not the case when you try to change practice. 

So I came to the conclusion that what we really want is a consult. And I know that Jenny, Caleb, and [INAUDIBLE] all feel the same way. So I think however we can figure out a way to make this a true team sport here and a consult, where we tell you what our patient's situation is, and you strongly advise but not tell us what's the safest, best way to do get vascular access. 

I think we can get there. I think the speed bumps that we can both simply acknowledge so we can move through them is that there are going to be variations on the IR side as well, in terms of the engagement. Not everybody cares the same way about every single thing. But we can groove people toward-- we all grooved into time out after years of resisting it. These are public goods. 

And so the other arm of that consult are going to be the infectious disease folks who are going to say, yes, we understand that, and we'll support these kinds of things. And then it may be a bicameral one, or it may narrow down to us knowing that everybody has each other's backs. I think I'd be proud to be seeing that happen. 

Great. Thank you, everybody. Happy holidays. Thanks for coming out. 

[APPLAUSE]