Lower Extremity Arterial Disease (LEAD)

Speaker A: 00:00:10

In this class, we're going to talk about wounds caused by lower extremity arterial disease. We're going to explain the pathology and risk factors for lower extremity arterial disease.

We'll discuss the clinical presentation of arterial insufficiency and ulceration. Well describe guidelines for ABI testing and interpretation.

We'll outline an appropriate management plan for the patient with an arterial ulcer to include indications for hyperbaric oxygen therapy. And we'll explain why debridement of dry, ischemic, uninfected wounds is contraindicated.

Of course, you probably already know that from our previous class where we talked about debridement in general. So you've got the video if you want more in depth content. Chapter 22 is an excellent overview of lower extremity arterial disease and ulceration.

And the learning exercises will be very helpful to you in doing differential assessment of lower extremity wounds. So when you think about the pathology of arterial or ischemic ulcers, it almost always is atherosclerosis.

And you already know a lot about atherosclerosis because it's exactly the same as that involved in coronary artery disease or in cerebrovascular disease.

So you just channel everything you know about coronary artery disease and cerebrovascular disease, apply it to lower extremity arterial disease, and you'll be there. So what is it that causes atherosclerotic heart disease or brain disease or lower extremity ulceration?

It typically starts with high levels of circulating lipids. Now, high levels of circulating lipids damage the blood vessels in two ways.

First of all, they start to accumulate on the inside of the vessel, and they result in plaque formation. And plaque formation, of course, is going to narrow the lumen of the vessel. They also cause endothelial injury.

So let's look at each of those, and then let's look at the end result. So, plaque deposits, as we've already said, narrow the lumen of the vessel.

But the other thing that happens is, over time, those plaque deposits become calcified. So not only is the vessel becoming narrower, but it's also becoming more rigid. Now, let's look at what happens with endothelial injury.

So, high lipid levels damage the lining of the blood vessel. That damage that injury causes release of growth factors and production of collagen.

That, in turn, leads to thickening and hardening of the vessel wall. So you've got two different processes that contribute to narrowing of the vessel and increasing rigidity or fibrosis of the vessel wall.

The third thing that happens is the damaged vessel secretes abnormal levels of vasoconstrictors. The last thing that you need. So what you would need in that situation is vasodilators. But no, you get vasoconstrictors.

Now, a lot of the factors that lead to atherosclerosis also increase blood viscosity and coagulability, so they increase the risk for emboli and thrombi formation. So now you've got narrow vessels that don't dilate well because they're rigid.

You have increased formation of little clots that, as they pass through the narrow vessels, become lodged. And now you can get total occlusion of the damaged vessel.

So the end result, just what we've talked about, a narrow, rigid vessel, you get reduced blood flow at rest. You also tend to get fixed rate blood flow. And we'll talk a little bit more about that.

And also remember, a lot of these patients have increased coagulability, so they're more likely to form clots that get lodged in narrow vessels and totally obstruct the arterial inflow. So reduced blood flow at rest and reduced ability to dilate. So think what that means for the individual.

When you're sitting at rest, the metabolic rate in your tissues and your muscles is pretty low. So the vessels normally constrict partially. You've got kind of maintenance level blood flow until very late in the disease process.

Most of your patients with lower extremity arterial disease will say they're okay as long as they're sitting, and especially if they're sitting with their legs down. But think what happens when you get up and move around.

So let's say you've been sitting at the computer, you've been working on classes or learning exercises or whatever, and then it's like, oh, you know what? I've got to get up. I've got to go to the bathroom. I've got to get something to eat and drink. I've got to answer some messages.

I've got to see what the kids are doing. I guess I better start dinner. So you jump up and you start running around.

Well, now the metabolic demands in your muscles goes way up, and normally that's not no problem, because your vessels are able to dilate and to increase blood flow to meet the increased metabolic demands.

But if you had narrow, rigid vessels that could not dilate when you got up and you started moving around the blood supply, the oxygen delivery would be insufficient to meet the metabolic demands, and you would start to develop cramping pain that would make you stand still or sit down. That's known as intermittent claudication. We'll come back to that. As the narrowing progresses, you can eventually end up with pain, even at rest.

What we see clinically is we see patients coming in, and they either tell us, I don't know. All of a sudden, my toe was looking like this. It was black. Or they'll tell you, I got a little nick on my leg. It was nothing.

I took care of it, I cleaned it up. I put antibody ointment on it, and it just kept getting bigger and bigger. So what do you hear?

You either get spontaneous ulceration and necrosis because of the marked reduction in blood flow and progressive tissue ischemia, or you have a non healing wound because healing requires a lot more blood flow, a lot more oxygen than tissue maintenance. So what are the risk factors for coronary artery disease, cerebrovascular disease, and lower extremity arterial disease? All the same things.

So everything you know about heart disease, transfer it to lower extremity arterial disease is equally relevant. What about smoking? Smoking is a major reversible risk factor. Smoking by itself causes endothelial injury, so it starts that process.

Smoking by itself contributes to lipid accumulation and growth of those plaques that form within the vessel wall. Smoking by itself is a major vasoconstrictor, and smoking by itself causes increased coagulability.

So smoking can cause coronary artery disease, cerebral vascular disease, lower extremity arterial disease.

Even if nothing else is going on, that just underscores the importance of educating our patients, talking to them openly, giving them choices, but seeing if they're ready to attempt smoking cessation and how we can help them. What about diabetes? Diabetes is very much like smoking. It is an independent risk factor for everything.

So it's associated with increased plaque formation.

It's associated with increased blood viscosity, hypercoagulability, increased risk of clot formation, hyperinsulinism, which we see in patients with type two diabetes, where you have constantly high circulating insulin levels.

Insulin acts like a growth factor, so it causes hypertrophy of the smooth muscle in the vessel wall, thickens the vessel wall, narrows, the vessel lumen. So what if you have a patient who's a poorly controlled diabetic and a smoker?

Then they're almost doomed unless we start to get diabetes under control and work on smoking cessation. Hyperlipidemia.

We've already talked about how high levels of circulating lipids cause endothelial damage and begin the whole process of plaque formation. What about hypertension? That's the fourth reversible or controllable risk factor. But with hypertension, the mechanism of injury is unclear.

It's not clear whether hypertension increases the risk of lower extremity arterial disease and coronary artery disease, or if hypertension and arterial disease are caused by the same underlying etiologic factors. For example, maybe increased production of vascular smooth muscle contribute both to hypertension and to arterial disease.

Maybe activation of the renin angiotensin aldosterone system contribute to both, maybe vasoconstriction. We definitely know it contributes to hypertension. We know it contributes to coronary artery disease. Lower extremity arterial disease.

So are they both a result of the same pathologic pathway, or is hypertension an independent contributing factor? Not sure. We just know that what we need to do is work with the patient on smoking cessation.

If they have any interest at all, work with the patient on tight glycemic control, get the patient on medications to reduce levels of circulating lipids and manage blood pressure. Now, there are other risk factors. Some of these are controllable, most of them are not. Age is not a controllable risk factor.

But we do know that there's a definite correlation between age and lower extremity arterial disease. If you're over 66, there's a much greater incidence, like increase, more than 30% prevalence in the older population as a whole.

So if you're working in an outpatient wound center, you are going to see a lot of patients with lower extremity arterial disease. Obesity is a risk factor for lower extremity or arterial disease, and we know that obesity is epidemic in our country.

Family history not modifiable, but a major predictor of what's going to happen. So if you have a family history of lower extremity arterial disease, coronary artery disease, critical for you to avoid smoking or stop smoking.

Control glucose levels, manage your hypertension, manage your lipid levels.

Now, an interesting area of research is the link between autoimmune and inflammatory states that have found consistently increased incidence of lower extremity arterial disease and coronary artery disease among patients with inflammatory or infectious states, like chlamydia and pneumonia. But we don't know precisely what the link is.

We just know inflammatory states do need to be controlled and maybe in part to protect the heart and the arterial system. Elevated homocysteine levels are another risk factor that tends to be population specific.

So some individuals and some groups of individuals are high risk for elevated homocysteine levels, which track to increased incidence of coronary artery disease and lower extremity arterial disease. The good thing about elevated homocysteine levels is that they can be easily treated with vitamins b twelve, b six, and folic acid.

So reversible risk factors, major reversible risk factors. Smoking, hyperglycemia associated with diabetes, hyperlipidemia, and hypertension. Age, not controllable. Obesity can be modified.

Family history, not controllable. Autoimmune and inflammatory states can be diagnosed, managed, and hopefully rendered reversible.

And elevated homocysteine levels, definitely reversible.

Now, when most of us think about coronary artery disease or lower extremity arterial disease, we link it in our heads to diabetes, and that's very accurate because diabetes is such a major risk factor. We know that this also occurs in non diabetics.

But there are big differences when you look at arterial disease in the diabetic, arterial disease in the non diabetic. So we know lower extremity arterial disease has earlier onset in the diabetic population.

If you're seeing a patient with an arterial ulcer in the outpatient clinic and they're non diabetic, they're likely to be in their sixties, seventies, eighties. But if you're seeing someone who is diabetic, they might be in their thirties, forties, fifties. Male to female ratio is essentially the same.

But diabetics are much more likely to have bilateral and multisegmental disease. So they're likely to come in, both legs are bothering them.

When you do vascular workup, you find that there's multiple vessels and multiple segments of an artery that are involved, which means it's more difficult to treat, more difficult to bypass, because there's multiple areas of involvement.

Diabetics are more likely to have disease that involves the mid sized vessels of the lower leg, whereas the non diabetic is more likely to have disease involving the larger vessels. So you think how many patients come in every day in hospitals across this country for femoral popliteal bypass grafts?

Okay, well, that involves larger vessels, typically with one area of involvement. But diabetics know it's likely to be mid sized vessels, multiple areas of involvement, much more difficult to bypass.

Probably the most important things are the last two bullet points.

Lower extremity arterial disease in the diabetic is much more likely to progress to limb loss, and the diabetic population is also at risk for small vessel disease.

So you can have a diabetic patient, they come in, they have necrotic areas on their toes, but when you assess their foot, their foot feels pretty warm. They've got palpable dorsalis pediatric pulses. Well, how could you have a palpable DP and necrotic toes?

Because that dorsalis pedis vessel then feeds into smaller and smaller and smaller vessels. So if you have small vessel disease, you can get necrotic areas on the toes, even though the larger vessels are patent.

So specifically the mid sized vessels you can see here, that is the tibial vessels that are likely to be involved in lower extremity arterial disease in the diabetic, as opposed to femoral and popliteal.

And also, I put that bottom slide in, so you can just see that it can also be the very small arterioles that feed into the capillary bed, and those cannot be bypassed.

So when you think arterial disease, you think ischemic ulcers, you think primarily atherosclerotic heart disease, same process as coronary artery disease, cerebrovascular disease. But we want to remember that there are less common causes of ischemic ulcers, and they're listed here.

A lot of you will have patients with sickle cell disease, and you know that they have abnormally shaped red blood cells. You know that those abnormally shaped red blood cells are likely to sickle and to obstruct blood vessels, especially in any kind of crisis.

So they get sick with anything, they have any kind of febrile illness, and it frequently pushes them into crisis. Sickling and vessel obstruction with resultant ischemic ulcers.

Your septic patients, how many of you have had critically ill patients who were septic, and then they had necrotic toes, or they had necrotic areas on their toes and maybe on their fingers and maybe other areas of the body. It's because they can shower microenvoli, and those microenvoli keep moving until they get to a vessel too small for them to pass through.

So that's why we typically see evidence of microemboli showers on the digits. When they get to very small vessels. You can have patients with vasculitis and vasculopathy.

We're going to talk about that more in a later class, where there's direct damage and inflammation of the vessel wall.

That can definitely cause ischemic ulcers, because what happens, either they obstruct the vessel and get an acute ischemic area, or the vessel wall perforates and you get an acute area of ischemia.

So vasculitis definitely causes wounds that have an arterial component that's not the only thing going on with them, but there is an arterial component. And finally, and those of you who are working inpatient are seeing this a lot.

Now, we have so many patients who are hemodynamically unstable and who require vasopressor therapy. And we know that use of vasopressors causes shunting of blood away from smaller vessels and away from the cutaneous circulation. We very commonly see.

I know you see this, too, where we're fighting to keep a patient alive. We've got them on multiple vasopressors, and we're starting to see ischemia of the digits, of the toes, of the fingers.

And sometimes they lose those digits. Sometimes we can salvage them by using topical nitroglycerin. Sometimes we can't.

Okay, so we've talked about causative factors for lower extremity arterial disease.

Now let's talk about clinical presentation, because when a patient comes in with a lower extremity wound, you're going to do the history, you're going to do the assessment, you're going to put all of your clues together to determine what caused this wound. Was it lower extremity arterial disease? Was it venous disease? Was it neuropathic disease or something else?

So, first of all, ask them about their pain. Remember that intermittent claudication is pain with activity that is typically relieved by ten minutes of rest.

So you can ask the patient, you know, are you able to walk distances without pain? Can you walk the same distances today without pain that you could one year, two years, three years ago? So I recently had a patient on the chart.

His diagnosis was venous disease. When I walked in, he had his legs down. I could see that he had dependent ruber, which we'll get to in a minute.

So I asked him, how do your legs feel best? Are you sitting in the chair with your legs down? Because that's how they feel best? Yes. What happens when you get up and walk?

Well, I can't walk as far as I used to. I can't walk to the mailbox anymore. I have to stop several times on the way to the mailbox because my legs are so heavy. Heavy and kind of crampy.

I can stand there for a few minutes and it'll get better, and then I can walk a little further than I have to stand and wait again. That's classic intermittent claudication. Patients may report pain, they may report cramping.

They may tell you that their legs are heavy and it's hard for them to walk. Progressive disease results in progressive pain. So how much reduction in blood flow do they have? You start out with intermittent claudication.

You're fine at rest. Pain occurs with activity. Then you get to nocturnal pain. You go to bed now, you put your legs horizontal.

Now you don't have that gravity assist to the arterial circulation. The tissues become ischemic. You start to develop pain. You sit up on the side of the bed.

A lot of you, if you ask your patients, they will tell you they sleep in recliners because then they can sleep with their legs down. I once had a patient and I asked him, I was asking about his pain.

I asked him what made it better and what made it worse, and he's like, well, you won't believe me. I don't even want to tell you. And I'm like, I'm really listening. I'm really going to try to believe what makes it better. What makes it worse?

Well, what made it worse was going to bed and putting his legs up. What made it better, he said, was cigarettes. Lucky strikes. And I'm thinking to myself, I don't believe that.

And he's like, see, I can see it on your face. You don't believe me. But let me tell you, here's what happens. I go to bed, I wake up, my legs are killing me.

Sit up on the side of the bed, grab my cigarettes, light it up. By the time I'm on my third drag, my pain's better. Well, why was his pain better? Because now he has gravity assist.

You think I ever convinced him of that fact? No. Lucky strike's got all the credit for that. So you start out with pain, with activity. Then you progress to nocturnal pain and eventually rest pain.

So rest pain means I'm just sitting here with my legs down, but I'm delivering such low volumes of blood and oxygen to my tissues that they're chronically ischemic. And they hurt. I have pain even at rest. Typically, when you get to rest pain, you've got 90% vessel occlusion. So it's very advanced.

We've already talked about. They might tell you that their legs hurt. They might tell you that they have muscle cramping. They might just say that their legs are heavy.

They can't walk very far.

Now, one thing to think about is that the very same patients who are highest risk for lower extremity or arterial disease also have diabetes and are at risk for neuropathic pain. So how do you sort out, is the pain they're having caused by ischemia, by the arterial disease?

Or is it caused by neuropathy, you go back to what makes it better? What makes it worse. Neuropathic pain is frequently worse at night. Arterial pain is frequently worse at night.

But what makes neuropathic pain better is I get up and I walk, because when I walk now, I'm bombarding the nerve pathways with different signals, and that drowns out the pain signals. But if I'm dealing with arterial disease, what makes it better is to sit with my legs down. So if walking makes it better, it is not ischemic pain.

If rest and dependency make it better, that is ischemic pain. So first of all, pay attention to pain. That's a huge indicator in terms of what's going on. Then look at the skin and the tissues. Skin, hair, nails.

That will tell you a lot about adequacy of blood flow, because when you think about it, it takes blood flow to replace hair, to grow hair, it takes blood flow to replace skin cells. It takes blood flow to grow a normal nail. So if you have chronic tissue ischemia, you're going to have diminished hair growth.

Now, this is a valid finding, but it's nonspecific because a lot of people have diminished hair growth just with age, and that's due in part to hormonal changes. So very significant if they have had major reduction in hair growth over the past few months or years. But again, you don't hang your hat on that.

You just note that as a finding. What about nails? If you have chronic ischemia, most of the time the nails will be very thin and you'll see ridges in the nails.

Again, sometimes this assessment finding is obscured because many of our patients have fungal infections involving the nails. Fungal infections cause thickening and discoloration of the nails.

If they have a fungal infection, then you cannot use nail assessment as a contributing factor. You won't know if there's underlying thinning of the nails, but you will see thin, shiny skin.

You've all seen this thin, shiny skin, minimal or no hair. You'll also see color changes. So if you put the leg up, keep it up until blood drains out, then you're going to see elevational pallor or cyanosis.

You'll see a definite change in color compared to other areas of the body. And then when you put the leg down, you'll see that dependent ruber. So you see that in the slides on top.

What causes dependent ruber that dark kind of blue red color to the tissues? It's because the chronic ischemia causes all the vessels to stay dilated. Trying to increase oxygen flow to the tissues.

So when you place the legs in a dependent position, those dilated vessels result in dependent. Ruber tissues are never getting their oxygen needs really met. So the vessels stay dilated, and that's what you see.

There's something else you can check on. You can check on venous filling time. That's what you see at the bottom. So venous filling time.

What you do is you raise the leg, pretend this is my leg. I'm raising the leg till my veins collapse. So now my veins are collapsed.

Once my veins are collapsed, I lower the leg and I count the number of seconds for the veins to refill, because, of course, where's the blood coming from to refill the veins from the arterial circulation. If it takes more than 20 seconds to refill the veins, that is independently indicative of lower extremity arterial disease. What about pulses?

Pulse is a very objective finding, something we always include in our vascular assessment. So we should be checking both the dorsalis pedis and the posterior tibialis.

If you have significant impairment of both the dorsalis pedis and the posterior tibialis, that's independently predictive of lower extremity arterial disease.

In contrast, if I have a very weak dorsalis pedis, or maybe I cannot even palpate it and I can barely hear it on Doppler, but my posterior tibialis is normal, that tells you that the DP artery just runs deeper to the soft tissues and can't be palpated or auscultated. But as long as your pt is normal, then that tells you you have adequate perfusion to the lower extremity.

Probably the most definitive screening test for lower extremity arterial disease is the ankle brachial index. You'll have a lot of questions on this in clinical practice. You'll have questions on this, on our exams and on the certification examined.

So you want to be really clear about what ankle brachial index tells you, how to perform it, how to interpret the results.

So, essentially, what you're doing, you're comparing the blood pressure in the arms, which is almost always normal, to the blood pressure in the lower extremities. Normally, blood pressure in the arms and the lower extremities should be essentially the same or very close to the same number.

But with advancing lower extremity arterial disease, you get deviation from that normal 1.00.

So as the ABI drops away from 1.00 or rises above 1.00, then the farther from 1.00 your ABI is, the more likely it is that you have significant faster disease. So let's talk about how you get the number and then we'll talk about how you interpret it.

So you want your patient to rest supine for ten minutes so that everything has a chance to normalize. Then you're going to get your systolic brachial in both the right and the left arms using a Doppler stethoscope.

So you apply the cuff, find the pulse, apply the gel again, find the pulse with the Doppler, inflate the cuff till you obliterate the signal. Gradually deflate until the systolic signal recurs, and that's your systolic. And that's the only one you'll get, is the systolic.

So you write down right systolic is this, left systolic is this. Let's say that when you did my brachial pressures, you got 120 in the right and 140 in the left.

You're going to use 140 as the comparator for both right and left lower extremity findings. So you'll always use the highest of the two brachial pressures for all your calculations.

I think I got this slide out of order, so let me just finish telling you how you would do your abi.

So then after you've gotten your brachial pressures, then you're going to put the cuff around each lower extremity and you're going to get systolic pressure over the DP, systolic pressure over the PT. Then you're going to take the highest pedal pressure on the right and you're going to divide it by the highest of the two brachial pressures.

You're going to take the highest pedal pressure on the left and divide it by the highest of the two brachial pressures. We're going to actually do this when you come on site for bridge week.

So let's say I already said that the highest systolic pressure in the brachial arteries was 140. So let's say that the highest pedal pressure on the right was 140. Okay, great. 140 over 141.00. That's as good as it gets, right?

But what if the pedal pressure was 0.170? Okay, well, that's not so good, right? 70 over 140 is 0.5. That can't be good. That's only 50% of what it should be.

So basically, you're taking the highest pedal pressure in that lower extremity, dividing it by the highest brachial pressure. Now, here's your interpretation. Anything between 0.9 and 1.3 is considered to be normal.

Anything less than 0.9 is considered to be some degree of lower extremity arterial. Lower extremity arterial disease. So 0.8 to 0.9 would be very mild. Blood flow would definitely be enough for healing and for standard compression.

If the patient needed compression, you would probably send that patient for vascular workup because they are beginning to develop arterial disease, but it would not be urgent. What if they're somewhere between 0.5 and 0.8? This is moderately severe disease, also considered to be borderline perfusion.

Most of these patients would retain the ability to heal a wound if managed correctly. You could use low level compression, modified compression if needed, for edema control, but definitely they should get a vascular consult.

As you drop below 0.5, the level of ischemia becomes progressively more severe, and the urgency of the vascular consult follows right along. So if I did an ABI and you had an ABI of 0.4, I would be setting you up a vascular consult immediately.

Because you fall into the range of critical ischemia less than 0.4, you're high risk for limb loss. And then as it rises above 1.3, you have a different process going on.

Now you have calcification of the vessels, making it very difficult to compress the vessel wall. That's particularly common in the diabetic population. So I want you to think about what's happening here.

So let's take the patient who has a very low abI. So maybe their ABI is 0.5 or less. What they have are very fragile vessels that are very easily compressed.

There's minimal blood flow to keep the vessel open. That patient would be very high risk for tissue damage if you wrap them up in a compression wrap. Now, let's take the patient whose ABI is 1.41.5.

They have vascular disease, but it's another type. Their vessels are calcified, they're rigid, they're very difficult to collapse. I don't know how much blood flow they're getting.

I'm going to have to send them to the vascular lab to find out.

But if someone did compress them, probably nothing would happen because they have rigid vessels, so low Abi, very fragile, easily compressed vessels, elevated ABi, rigid, hard to compress vessels. Both result in diminished blood flow to the tissues, diminished oxygenation, increased risk of ulceration and potential failure to heal.

Notice that if you cannot obliterate the signal at 250 mercury, your vessels are considered to be non compressible and you can't get an ABI. So any patient who has an abnormal ABI goes for a vascular consult. Anybody who has an ABI of less than 0.5 to 0.6.

If the goal is healing patients with an ABI greater than 1.3, any patient who has significant indicators of ischemia. So even if their ABI didn't look so bad, let's say their ABI is 0.7. But they're telling me they can just walk very short distances.

They can't sleep in bed at night. They have to sleep in their recliner. They have a non healing wound, they have dependent rubr. They're diabetic.

I'm going to recognize that their ABI is probably not an accurate reflection of tissue perfusion because of the level of calcification. I'm going to send them to the vascular lab. I'm going to get an urgent vascular consult.

So vascular consult anytime your ABI is abnormal, anytime you have significant clinical indicators of ischemia. Okay, so let's say that the patient came in, I did my initial workup, I did pulses, I checked skin, hair, nails, I did venous refill.

I have all of these indications of vascular disease, of arterial disease. Then I do the Abi, but my Abi is elevated. It's like 1.5. So it doesn't really tell me anything.

It just tells me my vessels are calcified and not very compressible. But I still don't know really anything about how much blood flow is getting through how well my tissues are oxygenated.

So what could I use to assess oxygenation perfusion in the patient with calcified vessels and elevated Abi? When we send them to the vascular lab, they're likely to do a toe brachial index.

So in doing a toe brachial index, you literally put a little tiny cuff around the great toe, and you compare toe pressures to brachial pressures. Now, they've tried doing these at the bedside. They're not accurate at the bedside. They need to be done in the vascular lab.

Why do toe pressures give you more accurate readings than pedal pressures? And the answer is that the toe vessels are much less likely to be calcified. So you get a much more accurate measure if you use toe pressures.

And if the toe pressures are less than 30, they're indicative of lower extremity or children's disease. Another great test to do is transcutaneous oxygen measurements so that you actually measure how much oxygen is getting out to the tissues.

One thing that makes TCPO two so beneficial is that it will tell you if there's a problem either with large vessels, mid sized vessels, or small vessels, because it tells you what happens at the end of the delivery. Okay, what happens out at the tissues. That's what we really want to know about.

And delivery of oxygen to the tissues requires patent large vessels, mid vessels, and small vessels. So a very helpful test to do if you have access. Now, this is usually done in the vascular lab.

Normal levels are considered to be higher than 40 mercury. And we have good data that says as long as the tissue oxygen levels are higher than 40, you've got enough oxygenation for wound healing.

If you have tissue oxygen levels between 30 and 40, that's considered to be an indeterminate zone. Some patients will heal, some won't.

If your tissue oxygen levels are less than 20, pretty much you're not going to heal unless we can improve perfusion through revascularization, medications, whatever. So ABI is where we start.

You do a TBI if you have an elevated ABI, if you want really accurate information that reflects both small vessel patency as well as mid vessel patency, and you have access, get a TCPO two cap refill time. Yes, we know that normally if you press the nail bed or the toe pad, that you should get refill of the vessels within 3 seconds.

And if it's delayed, we know that's indicative of lower extremity arterial disease. It's not considered to be as helpful as venous filling time, but it does give you a little bit of information.

If you have the ability, you can literally take a stethoscope and auscultate over larger arteries, listening for bruise, which tells you you've got vessel damage, and sensory assessment. So you're probably thinking sensory assessment, what does that have to do with arterial function?

Well, if your tissues are chronically ischemic, it's going to negatively impact on sensory function. So a lot of centers are incorporating monofilament testing, sensory testing into their arterial workup.

And we'll talk more about sensory testing, monofilament testing in a later class. Now, there is a particularly severe form of lower extremity arterial disease known as critical limb ischemia, and this is advanced disease.

These are patients who have chronic breast pain. They have non healing ulcers. They might have gangrenous changes in the tissues.

Their ankle pressures are very low, their ABI is less than 0.4, their TBI is low, and their TCPO two is under 30 and usually under 20. So that tells you very minimal perfusion to the lower extremity. And here's the implications? Look at the one year mortality rate.

So a lot of these patients actually die once they get to this level of lower extremity arterial disease. 20% one year mortality rate, 50% are going to require some kind of revascularization procedure, 40% are going to require amputation.

Bottom line, if you have any of the signs of critical limb ischemia, they have chronic breast pain, they have non healing wounds. There's any degree of gangrenous changes, they have low abi, they have low tbI, they have low tcpO, two, they have to see vascular.

They have to see vascular now. Okay, so we've talked a lot about the pathology of lower extremity aorterial disease.

We've talked about the presentation of lower extremity arterial disease. We've talked about diagnostic studies. Now let's talk about the characteristics of arterial ulcers and management of arterial ulcers.

So when it comes to lower extremity wounds, location is very instructive. If it is an arterial ulcer, the wound is going to be located either over the distal toes or foot or in an area of trauma.

And let's talk about why that is. So you think, okay, blood originates from the heart. The toes are the farthest point from the heart.

So if there's compromise in blood flow, if the delivery system is impaired, who's going to get in trouble first? Well, who's at the end of the line? The toes are at the end of the line, the distal foot's at the end of the line.

So with advancing ischemic disease, you can get spontaneous necrosis, spontaneous ulceration of the distal foot and the toes. And that's the patient that's going to say, I don't know, I don't think I did anything, but all of a sudden this is what happened.

More commonly a patient will say, well, I bumped into something when I was working in my basement, or I bumped into the coffee table when I was vacuuming, and it started out as a little bitty thing and just kept getting bigger. That makes sense, right?

Because if you get a traumatic injury, you're not going to have enough blood flow, you're not going to have enough oxygen to heal the wound, and it's going to get progressive, larger. Now, what if I have a patient with known lower extremity arterial disease? They've got all the clinical indicators.

They've got maybe dependent rubr, minimally palpable pulses, delayed capillary refill, delayed venous filling time, low abi, all of those things, and then they develop a heal ulcer, but all the surrounding tissue is viable. It's just the heel. And their history includes that they've been bed bound and they weren't keeping their heel off the bed.

Is that due to lower extremity arterial disease or is that a pressure injury? And the answer, of course, is it's a pressure injury. Yes.

The lower extremity arterial disease made them higher risk because their tissue was somewhat ischemic at baseline. But notice that the area of necrosis, the area of tissue loss, is concentrated over the bony prominence where the tissues were compressed.

So I've seen people try to classify heel pressure injuries as arterial wounds. But if the surrounding tissue is intact and the area of injury is over the bone in a bed bound patient, that's a heel pressure injury.

Okay, back to characteristics of arterial ulcers. What's the wound bed going to look like? We'll go back to the fact very inadequate levels of blood flow. So are you going to have a pink red wound bed?

No, it's going to be pale, it might be necrotic. The wound edges typically look punched out.

There's usually minimal etudate because etudate arises from the bloodstream and infection is very, very common.

But these signs of infection are very muted because all of those classic signs of infection, erythema and duration heat, those are, that's all part of a vascular response to inflammation. They're not going to get much of a vascular response. So they're going to have a faint halo of erythema. They're going to have slight induration.

So that tells you you have to maintain a pretty high index of suspicion for infection with arterial wounds. So these are all arterial wounds. So you can see on the top left you've got spontaneous necrosis of the second toe.

So they actually called me from a facility where I was doing consults, and they're the, they didn't tell me the toe was black. They told me the toe was shrinking.

And then when I got there, I'm like, oh, not only is it shrinking, it was shrinking because, of course, it was dead and atrophic. It was also completely dry and black. So you cannot salvage that toe. That toe is gone. That toe is dead.

Then you look at the one on the top, the mid slide on the top, and here you have a wound that's covered with Eschar, but you clearly see that erythema. That halo of erythema is faint, but it's definitely there. Same thing, top right, that halo of erythema. I just want you to see how muted it is.

And then the slides on the bottom, same foot. So the patient came in, had what looked like a relatively small wound.

But you can see that when they used the cotton tipped applicator to explore, the applicator went way in. So then they did a CT of the foot, and they debrided based on CT findings, and look how extensive that wound was. So arterial wounds can be very bad.

They can result in major tissue loss. They can deteriorate very quickly. Okay, so the last thing we want to talk about is management.

And you think, well, the causative factor is inadequate perfusion. So I've got to focus on improving perfusion.

If you can do something surgically to improve perfusion, that might be the key to getting that wound to heal and to preserving that limb.

Our goal is a vascular consult, because we're not taking the patient to surgery, but we want to make sure that patient gets a prompt workup by someone who can determine, is this patient a candidate? Can they be bypassed? Are there distal vessels that are patent? Can they do angioplasty?

So is there a compressible plaque that they could literally open up the vessel and maybe they could put a stent in? We can't make those decisions, but we can make sure that we get the patient to the group who can make those decisions.

So you just think, okay, priority number one, vascular consult for the vascular team. Their primary priority is going to be to determine, what can we do? Can we bypass? Can we do angioplasty? Can we get a stent in place?

Now, bypass always sounds like the perfect way to go. Just go around the blockage. Take a patent vessel, either a native vein or a synthetic vessel.

Go from here above the blockage here below the blockage, and everything's good. But notice the last bullet point. The problem is that a lot of those grafts become occluded within a matter of months to years.

That's particularly common with your synthetic grafts.

So when you think about our patients who come back with coronary artery bypass grafts, and they have suture lines up and down the legs, that's because they were harvesting veins to use for the bypass to minimize the risk of graft occlusion. Okay, so priority one fastener consult. What can be done there?

And the vascular team is going to look to see, can we do anything with an open procedure? Can we do anything with endovascular approaches? What can we do with medications?

So these are the primary medications used for patients with arterial disease and arterial ulcers solastazole platol is probably the most commonly used. We have great data for this drug. We know that it reduces pain, reduces that intermittent claudication, improves walking tolerance.

That tells you in and of itself that you've got better perfusion, but unfortunately, is contraindicated for a lot of patients with heart failure. And a lot of patients with lower extremity or arterial disease also have coronary artery disease and heart failure.

All of these patients should be on statinse to get their circulating lipid levels back into normal range. So we know that statins improve ABI findings. They improve walking tolerance, they reduce the incidence of cardiovascular events like MI.

You can use aspirin also to reduce the risk of disabling or fatal stroke, and it can help reduce the risk of cardiovascular events as well.

So aspirin's primary effect is in reducing the incidence of cardiovascular and cerebrovascular events, not so much the impact on lower extremity arterial disease or lower extremity wounds. What about. I can never say this, clopidogrel. It's an antiplatelet drug. Well, you can see how an antiplatelet would be very helpful.

So you prevent aggregation of the platelets, you reduce the risk of emboli thrombus formation, you keep vessels patent. So again, just like aspirin, clopidogrel is associated with reduced risk of cardiovascular and cerebrovascular events.

Unfortunately, it can be given in combination with aspirin so that you get enhanced effects.

So when you see patients on aspirin, when you see patients on clopidogrel, what's the intent to protect that patient against cardiovascular and cerebrovascular events? Statins are used to reduce circulating lipid levels, improve ABI, improve walking tolerance, and reduce cardiovascular events.

Solosazole, specific to lower extremity arterial disease, but unfortunately, contraindicated with heart failure. What else can we do?

So vascular is going to be in charge of determining whether or not any kind of surgical procedure can be done and for determining which combination of medications would be most effective. There's also behavioral therapy that can be very beneficial, and there's actually behavioral measures that can improve perfusion.

And the most effective is a progressive walking program. So patients think, what you want me to walk? That's what causes pain.

But what we've learned is that with progressive walking, you reduce pain, you improve walking tolerance and walking distance. Just like if you've taken on any kind of physical fitness program the first time, how much could you do?

But over time, you build tolerance so what we know is that with a progressive walking program, you improve collateral circulation, so you develop collateral vessels. You also improve the muscles ability to utilize oxygen very effectively.

So we typically delay this progressive walking program until after any open wounds have healed, because as long as you've got an open wound, we want all the oxygen going to the wound bed, not so much to the muscles.

But once the wounds have healed, we want to put them on a supervised walking program where they walk on a treadmill, okay, about three times a week for about 30 to 60 minutes, they should walk to the point of discomfort, then rest, then walk to discomfort, then rest, then walk to discomfort, then rest. And what are they doing? They are building collaterals. They're building tolerance.

Now, interestingly, studies have shown that if patients are in a supervised program, it's more effective than if they just do it themselves.

So, in other words, if they come to a center and there's a lead instructor or physical therapist or whatever, they're much more likely to get good results than if they say, I'll just walk at home on my treadmill. Why do you think that is? It's because it builds in and promotes compliance.

If I go to the center, it's very obvious whether I went or not and whether I participated or not. But if it's my treadmill at home, I've got all kinds of reasons why I'm waiting till tomorrow, right?

So if at all possible, get them into a supervised progressive walking program and help them understand how beneficial it is. The other critical thing we keep coming back to this is tobacco cessation, smoking cessation. So I know patients get so tired of hearing this.

I've had patients say, don't even start on me again. So what should our message to them be? I don't want to harass you. This is your decision. This is your life.

I just want to make sure you understand the relationship between tobacco use and what's going on with your legs. I want to find out what your goals are in relation to these wounds and see if we can help you meet your goals.

Well, I want them to heal, but I don't want to quit smoking. If you had to pick one, if you knew that you could not get those wounds to heal and continue to smoke, which one would you pick?

Would you pick save your leg or keep smoking? And I've had patients who said I would pick keep smoking. Okay, then that's their decision, as long as it's made based on correct information.

So you want to talk to them?

You want to leave them in the decision making seat, find out what their priorities are, see if they're interested in smoking cessation, and if so, do absolutely everything you can to help nicotine replacement.

So work with prescribing provider to make sure they've got adequate nicotine replacement therapy, that they've got appropriate medications, that they're enrolled in a support group, all of those things. What else can we do to improve perfusion hydration? So make sure that people are drinking enough.

Interestingly, a lot of adults, and especially older adults, don't drink enough, so they've got increased blood viscosity. That is not helpful for somebody with arterial disease. So simply increasing fluid intake, tight glucose control, low cholesterol diet.

Some studies suggest that supplemental niacin can be beneficial because it's a vasodilator. That's not typically a first step or a primary recommendation. Okay, so goal number one, do everything we can to optimize perfume perfusion.

Second priority, prevent further injury. Their legs are going to be high risk, probably for the rest of their lives unless we can make major changes in perfusion.

So you've got to treat them like a diabetic. You've got to tell them and teach them.

Any traumatic injury is going to be very difficult to heal and could potentially, potentially result in limb loss. So we've got to do everything possible to protect your legs and your feet. What does that mean?

It means you're never out of bed without protective footwear. You don't want to stub your toe. You don't want to step on something. You don't want to cut your foot.

It means if you're a cleaning house, working in your basement, maybe you should wear shin guards like people wear when they're playing soccer. It means you should have professional nail care. You're going to have to break up with your girl at the mall. It's too risky.

You've got to inspect your feet and legs daily, and you've got to promptly intervene for any minor injury. So you get a little cut, clean it well, put a topical antibiotic, watch it. If it starts to deteriorate at all, you've got to get in to be seen.

What about hyperbaric oxygen therapy?

So we mentioned this in a previous class on refractory wounds, and we said, yes, if you have a patient who has arterial disease, they have a wound that is viable but non healing. They should be evaluated for potential benefits from hyperbaric oxygen therapy. So they should check, they should see what kind of response they get.

Comparing tissue oxygen levels on room air, tissue oxygen levels on 100% oxygen, possibly tissue oxygen levels on hyperbaric.

Many vascular surgeons are starting to look at a one two approach, where they first do whatever can be done with an open or an endovascular procedure to improve perfusion.

So, first of all, let me see how much blood I can get going to the area, and then I'm going to send you for hyperbaric oxygen so that every bit of plasma that gets through is hyperoxygenated. Dynamic compression therapy can be helpful.

So this is essentially a variation of the sequential compression device, things that we use in the hospital all the time to prevent dvts. This is called art assist, and it works because when it cycles on, you can see you wrap it around the lower legs.

When it cycles on, it compresses the veins and it drives blood out of the veins back to the heart. So now the vascular bed is open, which enhances arterial inflow. Then you pump the venous blood out and bite the arterial blood in.

So we don't have a lot of data, but the data that we do have suggests that, yes, this can be beneficial in promoting healing.

And then the last set of decisions we have to make relate to topical therapy, because whenever you go see a patient with a wound, the staff is going to want to know, what do I do? What do I put on it? So let's say that you have a wound that is covered with dry aspirin and there are no signs of infection. Okay.

At this point in time, when we know the wound is ischemic, it has not yet been revascularized. So it's ischemic, it's closed and protected. It's not infected. So you go back to your decision making pathway about necrosis and when to debris.

If your goal is maintenance or comfort and the wound is dry and sealed and there is no evidence of infection, you leave it alone. Debridement would be contraindicated because it would turn a closed wound into an open wound, and that wound would be very high risk for infection.

So these are wounds that we paint with betadine. We either wrap them with dry gauze, or we leave them open to the air and we monitor.

But what if I have a necrotic wound that's infected or a necrotic wound that is no longer sealed? It's now draining. Then you have to debris to control the infection to minimize the risk of limb loss.

Of course, you would also place the patient on systemic antibodies, antibiotics. Would I debride this wound using instrumental debridement? No, that would be crazy and very high risk.

So I'd be sure the patient was on antibiotics, and then I would initiate debridement, probably with a chemical agent, because I'm trying to kill bacteria. I need an agent that works independently of blood flow or white blood cell function.

If the wound is open or if the wound has been revascularized, then I should move ahead. I should follow all of my principles of moist wound healing. So I should eliminate necrotic tissue.

I should implement measures to control bacterial loads. I should absorb any excess exudate while keeping the wound surface itself moist and monitor the wound. Followed along one thing I wanted to emphasize.

When it comes to arterial wounds, prompt elimination of necrotic tissue and effective management of bacterial loads is absolutely essential to promotion of healing and prevention of any deterioration in wound status.

So that's one of the things that they've found over and over with diabetic wounds and ischemic wounds, is there's that correlation between necrotic tissue and infection and limb loss. So necrotic tissue supports bacterial growth, then you can get overwhelming infection.

Overwhelming infection frequently tips the balance and you end up with amputation.

So if you have an open wound, or if you have any arterial wound, really whether it's open or not, you have to be very careful in terms of managing necrotic tissue. Preventing infection, managing infection the only time it's appropriate to just leave eschar in place is when your goal is maintenance or comfort.

The wound is completely sealed and dry. There's no drainage, and there are no signs of infection. That's the only time you leave necrotic tissue alone.

When we're dealing with arterial wounds, we're always very aware that these wounds are very, very high risk for infection. So if we are dealing with an open wound, we're likely to use antimicrobial dressings, and we will use occlusive dressings with tremendous caution.

So, to summarize what's going on with arterial ulcers, basically you have diminished blood flow to the tissues.

Diminished oxygenation of the tissues renders those tissues very vulnerable to spontaneous ulceration or necrosis, or to failed healing of traumatic wounds. Always.

Our goal is to improve perfusion, either through vascular interventions, bypass or angioplasty, to flatten plaque through use of medications, through use of smoking cessation, through use of progressive walking programs. Topical therapy comes down to the adequacy of perfusion and the status of the wound.

If you have poor perfusion, you have a closed, dry wound and no infection. Keep it there. Maintain the status quo.

If you have poor perfusion but an open or infected wound, you have to move ahead with eliminating necrotic tissue, managing bacterial loads. Once you have adequate perfusion, you manage with moistwinthialing. Okay, so that's it for arterial.

And in the next class, we'll flip and we'll talk about venous ulcers and lymphedema.