Board Review Vascular

Compression therapy for non-reconstructible PAD placed in perspective

Paul van Bemmelen, MD, PhD

Paul van Bemmelen, MD, PhD reviews the physiology behind the development of peripheral arterial disease along with the use and benefits of endovascular and bypass approaches. Dr van Bemmelen discusses the role of arterial compression therapy, including how to select the appropriate patient, and provides evidence based studies and case examples in support of this procedure.

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Goals and Objectives
  1. Explain the physiology of peripheral arterial disease (PAD)
  2. Recognize the limitations of endovascular and bypass procedures
  3. Recognize the best patient candidates for compression therapy
  4. Interpret the studies involving compression therapy
  5. Recognize the podiatrist's role in early recognition and treatment of PAD
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  • CPME (Credits: 0.5)

    PRESENT eLearning Systems, LLC is approved by the Council on Podiatric Medical Education as a provider of continuing education in podiatric medicine.

    PRESENT eLearning Systems, LLC has approved this activity for a maximum of 0.5 continuing education contact hours.

    Release Date: 03/16/2018 Expiration Date: 12/31/2018

  • Author
  • Paul van Bemmelen, MD, PhD

    Professor of Surgery at Temple University in Philadelphia, PA.

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    Paul van Bemmelen disclosed that he receives support from ACI Medical, Inc.

  • Lecture Transcript
  • Male Speaker 1: So our next speaker is Paul van Bemmelen. He is a vascular surgeon who received his PhD from the University of Amsterdam, completed his fellowships and open an endovascular surgery at the University of Washington Seattle and at Southern Illinois University. That time, he received a patent for the first arterial assist device after working at the University of New York at Stony Brook and the VA Medical Center. Thank you for your service to veterans. He became a professor at Temple University in Philadelphia. He is going to be speaking to us today on pneumatic compression for non-reconstructible peripheral arterial disease.


    Paul van Bemmelen: Good afternoon. Thank you. I’d like to ask you first with a raise of hands who here has heard me talk before about arterial compression therapy? Okay. Because I’m going to try to put a little new spin on the subject and put it in perspective with the open bypass surgery and endovascular therapy. As a podiatrist, you can control whether referrals go to a vascular surgeon or to interventionalist. You may be currently swept up by the enthusiasm for endovascular gadgets. Or you may be disappointed by the many complications of open bypass surgery. It is hard to keep track of the ever-changing options for each artery. Different gadgets are used for the femoral artery, popliteal artery and tibial vessels. Historically, treatment started off with a balloon. And if that fails, your bail out is a stent. Atherectomy devices and laser are nice to drill through chronic occlusions. Cutting balloons avoid uncontrolled dissections. Super long balloons are nice. And in Europe, drug-coated balloons are available. Whatever is proven not to work today is already history and replaced by something better. It’s just that we don’t have any followup on it yet. Reliable imaging after tibial artery angioplasty is difficult with ultrasound due to acoustic shadowing from calcification. Arteriograms are evasive and rarely repeated unless there’s a problem. Followup with ankle pressures is often unreliable due to incompressible vessels, again due to calcification. Here we see an occluded superficial femoral artery. And if we look carefully here on the close up on the right, you see that the vessel has already been stented before. And here is where the stent ends and another one begins. Another case here on a CAT scan, it looks like a nice stent appear with a Prolim above the stent. But if you look inside the stent on cross-section, this black inside the circle means that it is no contrast and in fact, it’s an occluded stent clot inside. And here is the latest stent technology, the interwoven wire technology. The press release on this was done last month. These patients of ours have already gotten the stent a month before in September. And you can see it is already occluded. The interventionalist can often remain unaware of his own results. Vascular surgeons, on the other hand, are able to reliably study their own vein grafts with ultrasound and they can prove patency rates of around 50% after six or seven years. The problem here is that it started out with 1,032 patients and you can see the little numbers on the bottom. At the end, there are only three patients left at risk. So what happened to the other 1,029? Many of these patients die with their patent bypass, which makes this great result less relevant. You already know that the expected lifespan of patients depends on their initial ABI before intervention. The ABI of about 0.05 is shown here in the middle. And those patients are still 60% alive at five years.


    So if your procedure in this case in atherectomy device has less than 50% patency after two years, it’s not long enough for many of our patients. Now some people will say that patency doesn’t matter. It’s only amputation rate that matters. Okay. Well, the tibial angioplasty, there is at least 25% amputation rate after only one year. And this is based on national data from 2011. Another way to look at this is that, the majority of bypass results falls into either a black or white category. So if you have an early bypass occlusion, it usually results in amputation. With endovascular therapy and stents, it’s a little different. Here you see a stent still patent with good flow after two weeks after it’s been put in. And meanwhile, the foot is deteriorated and still had to be amputated. So with stents, there is a lot of gray areas and often a lot of partial results. So another example is here in the tibial. And there’s a lot of tibial disease here. The middle is a very long balloon that is inflated. So you can see the contrast inside the balloon. And then on the right, the balloon has been removed and you see the result. This is a good angiographic result, but I still amputated this leg last week. Even the impact of a good clinical angioplasty result is slow. In fact, it is so slow that it takes 12 months to heal 75% of the foot lesions. The basal trial compared, which strategist should be tried first? And they found endovascular is reasonable but not equal to bypass if the patient is expected to live two years or less. We can’t always see looking at the patient but we start with an eyeball test and then we look if the patient has vein available. And we also have to look at the complexity of the tissue defect. So in this case, a bypass was done. But the bottom line with all our technology is, that we’re doing 300 major amputations above and below the knee a day. So that means about 1,000 leg amputations while you’re having this meeting. Many of these amputations do not come totally as a surprise because patients have had multiple procedures done first. We should try to identify those patients who can benefit from a different approach that increases collateral development. Hereto, we need to be aware of the natural survival of this subgroup. Notice this name on the banner here. It’s also on your program. This retrospective study in diabetics showed patient survival after bypass and angioplasty appear not very different. But in non-reconstructible cases, the survival dropped to 25% alive after two years. And this was regardless of amputation or no amputation. What can be done to stop amputations in this non-reconstructible group? Several arterial pumps are commercially available for home use by the patients. The goal is to treat small lesions before they require major foot surgery. Because real foot surgery requires more blood for healing than the minor debridements. Now it’s not easy to always rule out arterial disease because of the classification, as I mentioned earlier. I like toe pressures but a lot of these patients don’t have toes anymore. Transcutaneous oxygen. Can I ask how many people here are still currently using transcutaneous oxygen in their institution? I see a couple hands but it’s just kind of cumbersome and also not always very consistent. You can get basically a different number every time you put a probe on. So quite often, I have to assume that arteries are at fault if there is a failure to heal. This is to remind you that digital vessels can also get calcified and quite often it’s not recognized. The toe pressure can be falsely elevated because of this.


    So normally, the flow is driven through the capillaries by the difference in arterial pressure and venous pressure. And I’m going to start out with normal numbers that you’re familiar with 120 millimeter mercury for systolic arterial pressure and very minimal venous pressure if you’re looking at a person on an examination table, like a vascular lab. The difference between the two, the driving force, is about 110 millimeter mercury. In endstage arterial disease or critical limb ischemia, the arterial pressure has dropped to about 50 at the ankle, absolute pressure. And therefore the difference between that pressure and the venous pressure is down to about 40 millimeter mercury. Notice that the flow through this connecting tube has slowed down. Now this is going to get a little bit complicated. And I have heard from the audience in the past that they kind of tuned out from this diagram. So, it came up with the milkshake diagram. It’s a little easier. [Laughter] This is a thick milkshake. And I took this picture on a cold day. So if you want to move, the object is to move the milkshakes through the tube, you can either blow or you can suck. Either way, it will move, but I prefer to suck in order to get milkshake. But this is also illustrating that this is a particle suspension. The particles are about the size of the straw. And the same thing is true in human capillaries. We have millions of these tubes in both feet. The red cells barely fit through there. And this point of the circulation is the slowest point in the body. Those much faster flow in the heart, in the aorta, in the femoral artery and even in the veins. But in the capillaries, it moves at 0.7 millimeter per second. And the vessels they can give off their oxygen. They can deliver it really fast, but they have to move along and they’re not moving along. So this is where we have to recognize that we have an issue with the venous pressure. We assume that the venous pressure is minimal in our patients. But our patients are not really walking on a treadmill or uphill. They are not doing a push off. They in fact are either sitting watching TV, sleeping in a recliner. Even if they’re walking, they’re walking with flip-flops. The worst thing you can do, by the way, for a patient is to give them crutches. That will really increase their venous pressure. And so there’s no difference anymore between their arterial and their venous pressure. So does anybody know or realize what the venous pressure is right now and, you, while you’re sitting here, it’s certainly not 10 millimeter mercury. Maybe, when you move your feet, it will come down a little bit but if you’re not really walking, your venous pressure is the height between your heart and the floor. And so, the venous pressure is much higher in real life than it is in a vascular laboratory table situation. About 60 millimeter mercury is the pressure of that column of fluid. Now you also have to add that same number on the arterial side because you have the same height over there. But now we have something we can work one because we can empty this blue cup. Normally, there are two engines going on, there’s the one on the left that’s keeping the red side filled, that is the heart. It keeps the arterial pressure up as long as the heart beats. And on the venous side, as along as our calf muscle contracts and we are weightbearing, it keeps the venous pressure down. It squeezes the blood out of the lake. If you can simulate this or take over with an external machine do it for you, we can resurrect that difference between arterial and venous pressure and create blood flow. And you can demonstrate it instantaneously. This is just to show you the increase again in the difference between arterial and venous pressure. This is a laser Doppler recording which is a minute in a half. The arrow indicates where we turn the machine on. And immediately, after each compression, you see the skin flux increase. It’s nice but you can’t do this 24/7. We can’t do this sort of a life support on a leg just like the patient is on a ventilator machine.


    Sooner or later, we’ll have to be turned off. So, it would be kind of useless unless we have a long-term effect. And the long-term effect is similar as the fact of training which is collateral formation. Blood vessels develop, they increase in size. And this can be proven with angiograms and with the PVR, the pulse volume recording amplitude. I’ll skip the PVR because less and less people are using it. This is the same patient before and after where you see the same collaterals but they are reduced here, the sizes increase and this is not just a matter of giving more contrast. Here’s another patient before and after. This patient had multiple bypass as you can see from staples in the corner over here. So how do you select somebody for an arterial pump? I put “old” in quotation marks because we see patients that are 40 years old and they are biologically 80 years old. Obviously, it’s bad genes and it’s a bad lifestyle. But if the patient is biologically old and maybe not a good candidate for surgery anymore, you should keep this in mind. It’s not intended for acute onset ischemic legs. It’s for slow onset chronic problem. People that already have an amputation on one side and, therefore, are not very ambulatory anymore, are good candidates for this. You want to start out with a limited tissue loss and I’ll illustrate that. I’ll show you some feet. I’m sure you’re looking forward to seeing some feet now. But the therapy takes a couple of months to really work. So if you were starting out with a complex tissue infection that involves a tendon, muscle and bone, then you’re a little bit behind the eight ball. Patients that have had multiple very extensive procedures like heart transplants, the renal failure and so on, they may be candidates. Typically, the patients that I worked on already have had multiple bypasses and they don’t have any veins left. So, this is an example of a heel ischemic lesion. This is not a decubitus. This is not on the posterior part of the heel. This patient was not in bed. This just develops on that watershed area right on the edge of the heel, where the vessels come from both sides. And then that’s after treatment. This is a patient with diabetes and dialysis where I had personally done the amputation on the other side and it was getting very pessimistic. This looked horrible for months and then we started the treatment, worked well. Here’s a patient where we exhausted the bypasses. He had no more veins left. Hopefully, you notice that the little toe is missing, the fifth toe is missing. That was the indication for one of the previous bypasses. And then we couldn’t do another one, so we gave him a pump. And basically it works on every side of the foot. So, whether it’s on the medial or the lateral side, it’s basically all pretty much the same thing but it has to be somewhat limited, ideally. The evidence and hopefully, I’ll say it right, because the people from Mayo are here, one of the studies looked at 48 patients and compared 24 controlled patients with the same topical to 24 patients that had compression. And they had criteria to exclude mixed ulcers and stuck to the ischemic patients. Their compression was six hours a day and it was supervised, so that’s important to recognize. They had three times as many people heal their toe amputations with compression as without it. And conversely, they had twice as many below knee amputations in the controlled group so that looked pretty convincing.


    I’ll skip couple of studies and go to last year when the city from Ireland was published on paper. They had a five-year followup because they started on 2004. Three of the 170 legs and looked at the cost savings that are possible and it’s about $32,000 per patient. And obviously, the quality of life was much better if you were able to have no pain and your leg at the same time. So to start summarizing, both the open bypasses and the endovascular approach have limited ability to stop all amputations. They’re still doing 300 amputations a day. And you have to remind yourself after every product that you’re going to hear about, every antibiotic, every biological dressing, there’s still 300 amputations a day. The non-reconstructible patients have a very limited lifespan. Twenty five percent are going to be alive after two years. If you can give them something to get through those two years, usually you don’t have to worry about the leg anymore. Limb salvage has been demonstrated in studies and resting, I realize sometimes you have to rest a foot when you do reconstructive surgery on the bones. But resting will decrease your arterial flow because it’s going to increase your venous pressure. Last slide, the podiatry can start the treatment early because they recognize the early stages of ischemia. They can avoid immobilization. They can refer patients to either a center where both therapies are available open and endovascular hybrid and you can also suggest compression yourself if you have a patient that runs into a problem. Thank you very much.