Lower Extremity Venous Disease (LEVD): Overview

Speaker A: 00:00:10

In this class, we're going to talk about wounds caused by lower extremity venous disease or lymphedema. In the last class, we talked about arterial wounds. Venous wounds are much more common.

So no matter what your care setting is, you're probably going to care for patients with venous insufficiency and venous ulcers. Our objectives are to explain the pathology, risk factors and clinical presentation of lower extremity venous disease and lymphedema.

To describe the options for management of the patient with a venous ulcer to include the role of compression therapy, elevation medications, surgical intervention and topical therapy, identify contraindications to compression therapy and the implications for pre treatment assessment.

Compare and contrast the various options for compression therapy to include wraps, stockings, and pneumatic devices, describe or demonstrate the correct application of compression wraps and identify indications and options for referral of the patient with lymphedema. So you know the format by now. You're gonna watch the video, you're gonna complete the learning exercises.

And again, there's an excellent chapter in the core curriculum, chapter 21, that goes into a lot of detail about both venous insufficiency and lymphedema. We're going to divide this into two parts because it's a lot of content.

So in part one, we'll cover overview of venous insufficiency and venous leg ulcers. We're going to talk about normal lower extremity venous function and what happens with lower extremity venous disease.

We're going to talk about risk factors for venous disease and the characteristics of both venous insufficiency and venous ulcers.

And we're going to begin our discussion of venous ulcer management with a focus on compression therapy, medications, surgical intervention, but no specific details about compression. We'll get to that in part two. Okay, so when we talk about overview, I just wanted to give you a sense of how common venous leg ulcers are.

Approximately 70% of leg ulcers are thought to be caused by venous insufficiency, which is more common in and of itself than venous ulcers. So there's many, many people walking around with venous insufficiency. You see people with varicose veins, you see people with lower extremity edema.

They might not have ulcers, but they're at risk for ulcers.

So venous insufficiency, very, very common venous ulcer is common and unfortunately, very high rate of recurrence, because even after we get the ulcer healed, they still have the underlying venous insufficiency. So to really understand venous insufficiency, it helps to quickly review normal venous function.

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That's what your veins are doing for you. So let's talk about how they accomplish that, how they push that blood uphill.

So the first thing to remember, you studied this a long time ago, so let's just review it. You have three sets of veins. The deep veins are the femoral, popliteal, and tibial veins. They're thick walled veins.

They're located right against the calf muscle. So if you look at the slide on top, it's the ones in dark blue. And you can see they're immediately adjacent to the calf muscle.

And those veins are characterized by thick walls because they're high pressure veins. So the pressures in the deep veins are high, but they're protected against those high pressures by the thick walls.

Then you have your superficial veins, and those are the ones in light blue on the top slide. Those are your saphenous veins, lesser and greater saphenous veins.

And these veins pick blood up from the tissues, shunt it through the perforator veins to the deep veins. Now, notice that the superficial veins have thin walls and low pressures. They send blood through the perforator.

So look at the slide on bottom, and you see those little connecting channels. Those are the perforator veins. So in the slide on bottom, the dark blue with no valves are your saphenous veins. Those are your superficial veins.

They pick up blood from the tissues. Then they send it through the perforator veins. You have one way valves there, into the deep veins.

And the deep veins propel the blood back to the heart. Now, the perforator veins are the connecting veins between the low pressure superficial system and the high pressure deep system.

They play a very important role. You have a lot of perforator veins, some more than 90 in each leg.

And you need normal function of the perforator veins to maintain a one way path for venous return. So look at how it works. Blood shunts from the perforators, not from the perforators, from the superficial veins into the perforators.

Then the one way valves close to prevent backflow, blood flows into the deep veins. The deep veins contract and push the blood back to the heart. One way valves close.

So those one way valves play a really important role in maintaining that one way path for venous return. So we've already talked about they have to overcome the effects of gravity. That's not very easy.

There are actually three things that help maintain that one way flow. The first is that you do have a lot of smooth muscle in the vein wall.

So that smooth muscle opposes distention of the vein helps maintain tone that promotes venous return.

Secondly, every time you take in a breath, the negative pressure in the thoracic cavity helps pull blood out of the lower extremities and back toward the heart.

And finally, and critically important, every time that you dorsiflex, whether you're standing in place and doing calf muscle exercises or you're walking with that heel toe configuration, every time your calf muscle contracts. And when your calf muscle contracts, it melts the deep veins and rapidly propels blood back to the heart.

And then those valves close so you do not get backflow. So the valves maintain the integrity of each compartment, the deep veins, the perforator veins.

Now, when the venous system is working correctly, if you're walking, you're constantly milking the deep veins and you're propelling blood back to the heart. It keeps venous pressures very low. So you have low walking pressures because you're constantly emptying the venous system.

But if I just stand here and my calf muscle relaxes, then I don't have nearly the same push to propel blood back to the heart, and the pressure starts to build up within the venous system.

So sometimes you'll see the venous system characterized high standing pressures because the veins are full, low walking pressures because you're constantly emptying the veins. So walking is a really great thing when it comes to venous function.

So go back to the fact that we said normally, the superficial system is a low pressure system shunts blood through the perforators to the deep veins. Those are high pressure vessels, but they're protected by thick walls.

Now, those perforators and those valves play a really important role because they keep the superficial system and the deep system separated, that's normal function.

But if you develop valvular incompetence, either because you get direct damage to the valves or because you spend so much time just standing that those veins dilate and pull the valves apart, either way, once the valves fail, you start getting backflow of blood from the deep systems to the superficial system. Now, the superficial system dilates. You start to get all kinds of changes in the superficial veins. That's known as venous insufficiency.

At the same time, the high pressures in the deep system start to be transmitted to the superficial veins, which are then walled, remember? And that's called ambulatory venous hypertension.

So, basically, you get reflux of blood into the superficial, into the superficial system, and you get back pressure into the superficial system.

So venous hypertension and venous insufficiency, once the valves fail, once blood starts to move out of the deep system, back into the superficial system, you get back pressure on the capillary beds.

Because, remember, the capillary beds, if you look at this slide, blood flows in from the arterial system into the capillary bed, out of the capillary bed, and back into the venous system. But if the venous system is congested, then there's back pressure on the capillary bed.

Once the capillary bed distends, stretches the walls, the walls become much more permeable. Now, fluid leaks out of the capillary bed into the tissues. White blood cells leak out into the tissues. Red blood cells leak out into the tissues.

Tissues, and plasma proteins leak out into the tissues. And this is how the whole cycle of tissue damage begins. So when fluid leaks out of the capillary bed into the tissues, you get edema.

That's a very visible indicator of venous insufficiency. When red blood cells leak out of the capillary bed into the tissues, they break down, they release hemoglobin, hemosiderin.

So you get that brown, gray, black staining of the tissues that's known as hemosiderosis. Patients frequently ask, will that go away? And because that actually involves deeper tissues, it involves the subcut tissue.

Most of the time, that staining does not go away.

When you get capillary, I mean, when you get plasma proteins and white blood cells migrating out of the capillary bede into the surrounding tissues, now you get an inflammatory response. When you get an inflammatory response, you get increased collagen deposits. And now you end up with a lot of chronic changes in the tissue.

You get fibrosis of the tissue, and you get chronic inflammation that may be manifest as a dermatitis. So you don't want that. So let's look at who's at risk for venous disease and what can be done about those risk factors.

So there are some conditions that cause chronic resistance to venous return.

Obesity is one especially truncal obesity because it puts so much pressure on the large veins that it interferes with venous return from the lower extremities to the heart.

So if we could help a patient with venous insufficiency and venous ulcerations to lose weight, that would be very beneficial to them for many reasons.

If you have a patient who has had multiple or very closely spaced pregnancies, again, look at third trimester, look at the interference to Venus return. Look how common it is for pregnant women to complain of swelling. And a lot of them develop varicosities. You impair venous return.

The veins dilate, you pull the valves apart. The valves become incompetent.

You get reflux of blood back into the superficial system, you get varicosities, you get back pressure on the capillary system, you get edema formation, anything that damages the valves. The valves are critical to that one way flow pattern.

So if you have a deep vein thrombosis that is almost always going to damage the valve, it's going to cause major obstruction to venous return that's going to pull the valves apart. What if you have thrombophlebitis, inflammation that can damage the valves?

Patients who have thrombophilic conditions, they're very high risk for clot formation, for dvt formation, that again obstructs venous return, pulls the valves apart. So patients with protein s are protein c deficiency, patients with factor five leiden mutation, they're very high risk.

Finally, inflammatory autoimmune conditions like lupus, that can affect vessels, that can cause, end up resulting in venous insufficiency, prolonged standing, sedentary lifestyle.

So if you've ever had a job where you're just on your feet, but you weren't walking, as nurses, we're protected because, yes, we're on our feet, but we're walking all day. So we're constantly engaging our calf muscle pump, propelling blood back to the heart.

A lot of us also wear support stockings, so that helps protect us. But what if you were a cashier and you were just standing there all day and nobody had taught you the importance of doing calf muscle pumps?

Then you'd just be standing there. The veins would dilate because you're not propelling blood back to the heart.

Veins would dilate, valves would be pulled apart, you get venous insufficiency, backflow of blood, venous hypertension, and the whole process of vein damage and tissue damage would begin.

So prolonged standing, sedentary lifestyle, a lot of you in home health probably go in to see patients who are going to do compression wraps or whatever. And where are they? They're in their recliners. And where do they spend the day? In their recliners.

And if they're also morbidly obese, it's very, very difficult for them to get up and move around.

But you can see what an uphill battle you have trying to get those wounds to heal because it's so difficult to correct the underlying pathology, anything that adversely affects calf muscle function. So what if I sustain spinal cord injury and I have lower extremity paralysis, then my calf muscle never works.

You can teach me to literally dorsiflex to improve venous return, but that might be really hard for me to do. Depending on the level of my injury, you might put me in compression stockings to try to limit the venous reflux and hypertension.

But the bottom line is I'm going to have some degree of venous insufficiency because I've lost the calf muscle pump.

Even if I'm not paralyzed, if I'm much older and I have gait changes and I'm no longer doing heel strike toe off when I walk, if I'm just kind of shuffling along, I'm at risk for venous hypertension, venous reflux, because I'm not really engaging the calf muscle pump, I'm not propelling blood back to the heart. Okay, so we've talked about what causes venous insufficiency.

Anything that interferes with bowel function is what it comes down to, whether it's a sedentary lifestyle, whether it's morbid obesity, whether it's hypercoagulability with DVT formation, whether it's paralysis. The bottom line is I'm not getting blood back to the heart. My calf muscle pump is compromised or my valves are compromised. So I start to get reflux.

Now I get venous insufficiency, so my veins are dilated. I might have varicosities, I might not, but my veins aren't working normally.

We know a lot about what causes venous insufficiency, but why is it that some people develop ulcers and others don't? And we don't totally understand that.

The current thinking is that venous ulceration is probably caused by a combination of venous hypertension, so abnormal pressures in the superficial veins that cause the varicosities and everything, plus the impact of extravasated molecules.

So remember we said if the veins are not emptying effectively, if you have venous insufficiency, backflow of blood into the superficial system, distention of the superficial system, back pressure on the capillaries. Now you leak fluid, plasma proteins, red blood cells, white blood cells out into the tissue. Okay?

Once you start breaking those cells down, breaking down the protein molecules, then you are starting to attract multiple white blood cells to the area, because the breakdown products are chemo attractants for the white blood cells. Once you have activated white blood cells in the area, remember, white blood cells are troublemakers. They love fights.

They're looking for a fight all the time. They want somebody to kill, like bacteria, but anything will do. So you start attracting these activated white blood cells.

Now, they produce inflammatory molecules like mmps, and they produce growth factors, because in their mind, there's tissue injury, and we've got to start the repair process.

And the end result is chronic tissue inflammation and fibrotic changes, because those plasma proteins and the resulting inflammatory response cause collagen production. So you've got chronically inflamed tissues that are also somewhat fibrotic. They're not nearly as supple as they used to be, and they're edematous.

So very minor trauma can result in ulceration that is very hard to heal. So you'll hear patients say, I don't really know what happened. I think maybe I bumped it or, you know, I think this started when I scratched.

I was itching and I scratched, and I think that's what started it. I'm not sure what you will hear patients say who have had a recurrence is I was doing really well.

We got that first wound healed up, but then I quit wearing my stockings on a routine basis, I guess, and the swelling came back. And it wasn't too long after the swelling came back that I got the sore again. So, definitely associated with edema.

Okay, now what are you going to see when the patient comes to you? You're looking for characteristics of venous insufficiency and characteristics of venous ulcers.

So the number one characteristic of venous insufficiency, of course, is going to be edema, because fluid is leaking out of the capillary bed into the tissues. So typically you have pitting edema, primarily from the ankle to the knee, because that's where the failure typically occurs in the venous return.

So you have a major perforator right at the ankle. That perforator is frequently involved. It frequently becomes dysfunctional. And so your primary swelling is from the ankle to the knee.

You're going to see evidence of that. Ambulatory venous hypertension. You're going to see telangiectasias, which are those little spider veins.

You're going to see reticular veins, which are slightly larger than the spider veins. You might see varicosities. So you all know what varicosities look like. You probably all know what spider veins look like.

So any evidence that there's back pressure on the superficial veins, you're going to see those little tiny telangiectasia spider veins, but then you might see a little bit larger ones. And then finally those big gnarly varicosities.

Hemocityrosis, like you see on the top slide, very, very common, because, remember, red blood cells leak out, they break down, they release hemoglobin. It breaks down to cause that tissue staining. Aching pain relieved by elevation, very different from the pain of arterial insufficiency.

So with, for patients with arterial insufficiency, pain is worsened by activity and relieved by rest and dependency.

But if you have venous insufficiency, elevation makes the pain better, because with elevation, you start to drain fluid out of the tissues back into the bloodstream. You eliminate a lot of that congestion that contributes to the aching pain. So aching pain relieved by elevation.

People will frequently tell you, I feel good in the morning because I sleep with my legs up, and in the morning my legs are the smallest, they are all day, and I feel good.

But by the end of the day, my legs are swollen and I have all this aching pain, and I can't wait to get home and get in my recliner and put my legs up. Venous dermatitis is very common.

So look at the middle slide and you see that you've got all of this erythema and kind of scalene pruritic rash in what they call the gator area, which is the sock area. So that's venous dermatitis.

It's due to the inflammatory response, but it can cause intense itching and it certainly leaves the tissues very vulnerable to minor trauma. You might see ankle flare. Ankle flare is a group of abnormally prominent blood vessels right around the ankle.

Remember, that's where a major perforator is. So if that perforator fails, very common. To see ankle flare, you might see atrophy.

Blanche, that's where you have this ivory white scar tissue from previously healed ulcers. And you might have little pinpoint areas where you see evidence of capillaries.

So it might be ivory white with little red spots throughout, and then with long standing venous disease, you can get fibrotic changes in the skin and soft tissues, and that's called lipodermatosclerosis. So break it down. Lipo is fat. Dermato is skin. Sclerosis is hardening. So hardening of the fat in the skin so the tissues become, yes, very rigid.

So they lose their softness, they lose their suppleness, and it feels like you're just touching a concrete wall when you touch the skin, when you have lipodermatosclerosis.

We'll talk later about the fact that chronic venous insufficiency causes a secondary lymphedema, and lymphedema contributes to fibrosis of the tissue as well. So how do you know you have venous insufficiency?

You've got edema, you might have hemocytosis, you might have spider veins, reticular veins, varicosities.

You probably have aching pain that's worse toward the end of the day, worse when the edema is bad, much better early in the day when the edema is minimal, typically relieved by leg elevation. You might see dermatitis from the ankle to mid calf. What about a venous ulcer?

How would you know that an ulcer was caused by venous disease and not by arterial disease? Remember we said location is really important?

So with arterial wounds, they're going to be located either distally, the point farthest from the heart, like toes or distal foot, or in areas of trauma that lack enough blood flow and oxygen heal. Venous ulcers are very different.

Venous ulcers are located between the ankle and the knee, most commonly around the ankles and especially around the medial malleolus, the inner ankle bone. That's the most common sight. You do not typically have venous ulcers on the foot. You definitely don't have them on the toes.

They're almost always between the ankle and the knees. What does the ulcer bed look like? Well, remember, it's the very opposite of arterial wounds. With arterial wounds, there's not enough blood flow.

With venous wounds, there's a lot of venous congestion. And so the wound bed typically looks dark red, kind of a ruddy appearance.

Sometimes you have this recurrent layer of yellow film from high levels of bacteria and bacterial activity. Ulcer edges are usually irregular. The wound is usually shallow, superficial, just like you see here. They are wet.

So arterial ulcers tend to be dry because there's no blood flow. Venous ulcers tend to be very wet because there's so much congestion.

So keeping up with exudate is a major challenge in managing a venous, and most of the time your feet are going to be warm with palpable pulses, unless there's some coexisting arterial disease. So with arterial disease, what do you see? You see distal location or areas of trauma.

You see thin skin, no hair, dry wound bed, pale wound bede venous. You see a shallow wound, you see a very wet wound bed. You see a dark red wound base.

You typically have warm feet, good pulses, very, very different presentation. Now, can you have mixed disease?

Yes, and we'll talk in a later class about, in that situation, how you determine which is the primary cause and which is contributing. Now, there's something called the CEAP classification system.

Now, we're not going to test you on this in any kind of detail, but we just want you to be aware of it, because if you're reading any kind of chapter or article about venous insufficiency, you're probably going to see CEAP mentioned. On my last certification examined, they asked me something about CEAP classification.

So it's a classification that takes in all the elements of venous disease. C is the component of the CEAP classification system that's most relevant to us because it addresses clinical manifestations.

So c one, you see, you've got evidence of venous hypertension and reflux, you've got telangiectasias, reticular veins, ankle flare. C two, now you have the large veins involved, varicosities.

C three, now you've got evidence of back pressure on the capillary bed and you've got edema, but no significant skin changes.

C four, now, you do have skin changes that tell you that cells are migrating out into the tissues, triggering inflammatory responses, triggering previous wounds that have healed. So this is where you see hemocityrosis, you see atrophy. Blanche, you see dermatitis. C five, you have a healed ulcer and c six is an open ulcer.

Now, of course, most of the time we're dealing with patients with c six disease, but sometimes we're dealing with patients who might have anywhere from c three to c five. Now, e addresses etiologic factors. So what caused this? Was it caused by morbid obesity? Was it caused by a sedentary lifestyle?

Was it caused by deep a thrombosis? What was it? We don't focus on that as much a is anatomic factors that simply, which system is involved?

Does it involve the deep system, perforator system or superfluous system? And pathologic factors get into. Okay, exactly what's going on at the level of the vein. Do you have valve failure or do you have dilatation?

What's going on? I'm going to go back to that for just a minute. So when you look at the ceap system, I don't want you to focus on anything except c.

It's the clinical manifestations that are most relevant to us. I just wanted you to know about that classification system. Now, what about diagnostic studies for the patient with lower extremity venous disease?

These are not always done, but if you're doing an in depth workup, any surgeon who might be contemplating endovascular procedures will do a venous duplex ultrasound.

And what this will do is it will identify the presence of venous reflux out of the deep system, through the perforator vein, back to the superficial system, and the site of any obstruction to venous returns.

So once you have a venous duplex ultrasound, you know which perforator veins are nonfunctional, you know what the issue is, and it allows you to go in and to intervene with an endovascular procedure. The other diagnostic study, and we talked about this when we talked about arterial disease, you need an ABI.

Now you're probably thinking, well, why do you need an ABI for venous disease? I understand why you need it for arterial disease. Cause it tells you how severe it is.

It's a screening test for the severity, helps you differentiate people who need an urgent vascular consultant and people who have mild to moderate, and they can be worked up in the next few weeks or months. But remember that the primary management for the patient with venous disease is compression therapy.

And before you initiate compression therapy, you need to assure that there's no significant arterial disease. You need to be sure that compression therapy is safe.

So, yes, we routinely do Abi as part of the workup for a patient with venous disease to determine their eligibility for compression therapy and whether they can tolerate standard compression or whether we should modify the level of compression. Okay? So now let's move on to management.

So, just like with arterial ulcers, the number one goal was to improve tissue perfusion, improve the patient's ability to get oxygenated, oxygenated blood out to the tissues. With venous ulcers, our number one priority is to get venous blood back to the heart. How are we going to do that?

So, big picture, leg elevation and compression therapy. And you look at the little asterisk, it tells you compression and elevation remain the cornerstones of effective venous ulcer. Management.

Is there anything we can do with medications? Well, pentoxify is used in selected cases, typically refractory venous disease. So we'll come back to that.

What about surgical measures to reduce venous hypertension? Could we obliterate the damaged perforator, for example? Yes. So there's a procedure called Seps subfascial endoscopic perforator surgery.

That means you identify the perforator vein that is nonfunctional, that is permitting reflux, and typically, you do ablation of that perforator. Just shut it down. All of the other perforators will pick up for that one nonfunctional perforator. Or sometimes they'll do endovenous laser ablation.

So they'll find, okay, here's the vein is this superficial saphenous vein. We're going to do ablation for that vein and just shut it down.

So there's enough redundancy in the venous system that if there's a section not working, you can literally destroy that section, and the rest of the system will take over and fill in the gap. So we said compression therapy is the cornerstone of effective venous ulcer management.

So let's talk a little bit more about what compression therapy does. Now, we're talking about stockings. We're talking about wraps. Sometimes we're talking about orthotics. So let's.

As a nurse, you have probably worn support stockings. So what happens when you put on a support stocking? What happens when we wrap that patient's leg?

Well, as soon as I wrap the leg or put them in a support stocking, I partially collapse the distended vein. And when I partially collapse the distended veins, I improve valve function because, remember, they've been pulled apart.

Now I partially collapse the vein, and now I improve valve function, so it helps to reverse that pathology. Also, it supports the calf muscle pump, which improves venous return to the heart.

And by increasing interstitial pressure, I push fluid out of the tissues, back into the capillary bed, back into the venous system, so I help to reduce and reverse edema.

Now, there's also some very interesting research that says it's possible that compression therapy actually reduces pro inflammatory enzymes out in the tissues and might help to reverse those inflammatory changes that eventually result in tissue fibrosis. Bottom line, it pretty much does what you need done.

Collapses the distended veins, improves valve function, that improves venous return, supports the calf muscle pump, improves venous return, drives fluid out of the tissues back into the bloodstream. So it eliminates edema and may also have an anti inflammatory effect on the tissues.

When I put a patient in compression therapy, what am I trying to do? Number one, I want to get their ulcer to heal. Number two, I want to control symptomatology.

I can control venous insufficiency and venous hypertension. With compression therapy, I won't eliminate the underlying pathology. I'll just be compensating. And, you know, all the options. So I could do wraps.

You've all seen wraps. Most of you have probably done wraps or bandages. There are garments like stockings and there are devices like orthotics.

And we're going to talk about those in more detail in part two of this class. Okay, so if I'm going to use compression therapy, what differentiates between therapeutic level support stockings and something like TEDs?

Given the information we have at this point in time, the therapeutic level of compression is thought to be 30 to 40 mercury at the ankle. And that's appropriate for a patient who has no coexisting arterial disease.

If you do have a patient who has primary venous insufficiency but mild to moderate lower extremity arterial disease, if their ABI falls between 0.5 and 0.8, you should use reduced level compression, specifically, 23 to 30 mercury at the ankle. So think why? So if I have an ABI between 0.5 and 0.8, it tells me that those vessels are more easily compressed.

I do not want to cause arterial compression and tissue ischemia, so I have to downgrade the level of compression to keep those vessels open.

Now, there are a number of studies that have been done looking at compression therapy, and in a recent Cochrane review, they summarized the findings of all of these studies. So here are the general principles that should be guiding your practice.

First of all, across the board, multi layer systems have been shown to be more effective than single layer systems. So anytime you're doing a wrap, it's better if you have two layer, three layer, four layer than just a single layer. Also, some.

Also, systems that have elastic components are generally more effective than those with inelastic only. So you think about Oona's boot. So Oona's boot is that paste bandage. We'll talk more about it in the next section of this program.

But it's an inelastic base bandage. That's a band folded, wrapped around the leg to form a conformable boot. No active compression, no elasticity.

The outer layer is coban and it's stretched, but once it's locked down, it doesn't tighten up.

So that's not going to be as effective as a layer system that maintains stretch and the capacity to at least partially adjust to changes in calf muscle circumference. We have two layer systems, three layer systems and four layer systems. Are four layer better than three layer? Is three layer better than two layer?

Because two layer and four layer are the most commonly used. Those are the ones that have been compared, and current data suggests that two layer is just as effective as four layer.

Out of the data we have so far, healing has been found to generally be faster with a four layer than with short stretch. So four layer retains elastic components that can compensate for changes in calf muscle circumference. Short stretch are addressing that.

You stretch them to provide the right amount of compression and then wrap them, but you pretty much use up all the stretch and they don't really adapt. So layered compression better than one layer component or systems with elasticity? Better than systems with minimal or no elasticity.

Let's talk about static compression versus dynamic compression. So static compression is usually first line therapy. Static compression is stockings. It's wraps, it's garments. So you wrap it. There it is. That's it.

There's no pump involved. There are contraindications to static compression.

First of all, what if you have a patient who's in heart failure, they're symptomatic at baseline, so maybe they come into clinic and they're dysne, they're short of breath, they're wheezing.

You're not going to put that patient in static compression because you would be pushing fluid out of the legs, back into the heart, onto the right side of the heart, which communicates with the lungs. We do not want to take fluid out of the legs and put it in the lungs when the patient's already struggling.

So symptomatic heart failure is a contraindication to stay. Static compression associated lower extremity arterial disease with an ABI less than 0.5.

If the ABI is less than 0.5, you have minimal arterial inflow and you should not be using compression at all. Not static compression, because static compression, you put it on, it squeezes, it's squeezing the arteries as well as the veins.

What if you have a patient with coexisting lower extremity arterial disease and their ABI is between 0.5 and 0.8? You can use compression, but you have to be cautious and you have to reduce the level of compression.

So instead of providing compression between 30 and 40 mercury at the ankle, you're looking to provide compression. Compression that provides 23 to 30 mercury at the ankle.

In other words, yes, you want to support venous return, but you want to avoid arterial collapse. Arterial compression.

You would monitor the patient for tolerance, so you would tell the patient, okay, we're going to try to use low level compression to manage the swelling. Swelling to help get the blood back to the heart. We want to make absolutely sure we're not interfering with your circulation.

So if you start having pain in your toes, if your toes start turning blue or purple, first of all, I want you to sit down or lie down with your legs elevated, because most often that happens with swelling. If elevation for 30 minutes doesn't reverse the symptoms, I want you to either take off the wrap or call me now.

I want you to notice that low ABi is not a contraindication to dynamic compression. So right now we're talking static compression. Stockings. Wraps. Garments. So what are the contraindications to static compression?

Symptomatic heart failure. Low ABI. ABI between 0.5 and 0.8. You used a modified compression wrap. AbI, less than 0.5, no compression.

What about contraindications to dynamic compression? Those are your pumps. So those are very much like the sed devices we use in the hospital for DVT prevention.

Would you want to use that pump for a patient with symptomatic heart failure? Do you want to actively move fluid out of the legs, back into the heart? No.

So uncompensated heart failure is a contraindication for both static and dynamic. You do not want to use dynamic compression therapy for the patient with an active DVT because you don't want to risk embolus formation.

And if you're doing compressed, relax, compress, relax, compressed, relax, you run the risk that you'll knock an embolus loose from that thrombus, and then it will cause a pulmonary embolism or something else terrible. So you do not use dynamic compression if the patient has symptomatic heart failure.

You do not use dynamic compression if the patient has an active DVT and we don't use active compression with acute cellulitis. So you want to be very clear about your contraindications for static compression. Let's go back.

What are the contraindications with static compression? Symptomatic heart failure, lower extremity arterial disease. ABI less than 0.5. Total contraindication. ABI 0.5 to 0.8. Dial it down.

Modified compression, dynamic compression. Your pump therapy, three contraindications. Symptomatic heart failure, active DVT due to the risk of embolus formation and acute cellulitis.

We're going to stop there, and in a few minutes, we'll go back and start again, and we'll do part two.