Section: CME Category: Vascular

Typical Skin Changes Associated with Various Edemas

Heather Hettrick, PT, PhD, CWS, CLT-LANA, CLWT

Heather Hettrick PT, PhD, CWS, CLT-LANA, CLWT discusses basic principles of various edemas and the different skin changes associated with each pathology.

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Goals and Objectives
  1. Describe the different skin changes related to venous and lymphatic impairments
  2. Describe lipedema and how to differentiate from lymphedema
  3. Describe congestive heart failure classifications and clinical manifestations
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    Heather Hettrick has disclosed that she is a consultant and speaker for 3M and ILWTI.

  • Lecture Transcript
  • TAPE STARTS – [00:00]


    Pamela: Now Dr. Hettrick is going to talk about some of the typical skin changes, and she's already alluded to some of them, but this is a wonderful section. I think you're going to really enjoy this. Thank you for your participation. Yes, ma’am?

    Female Speaker: What are the studies or [Indecipherable] [0:00:16] whenever we try diaphragmatic exercises?

    Pamela: Okay, say the question again.

    Female Speaker: Studies related to the diaphragmatic breathing exercises--

    Pamela: Yes, the question Heather is, are their studies about diaphragmatic breathing?

    Hettrick: There is in the lymphatic literature. And one of the important things with why diaphragmatic breathing is such a simple thing to do, it is not only to stimulates the vena cavas and all of that -- do you remember what structure pierces your diaphragm? Anybody remember? The thoracic duct. Does that ring a bell to anybody? So your thoracic duct is the size if your little finger, it’s your largest lymphatic vessel in the body, it pierces your diaphragm. And the way the lymphatic system works is of with suctioning and siphoning, and this is why diaphragmatic breathing works so well.

    [OFF MIC]

    [Laughs]

    So if you can teach your patients how to diaphragmatic breathe, what they're doing just by the breathing is they're stimulating that thoracic duct, again, the largest lymphatic vessel of the body, which is going to mobilize that lymphedematous fluid from the lower part of the body through the whole body, because of the way it works from suctioning and siphoning. And what you'll start to see even with just basic diaphragmatic breathing is just some patients will start to get a reduction, minimal, but they’ll start to get a reduction in some of that fluid in their lower extremities, and you haven't even touched the patient. And so it's a very effective treatment to do for people. It's also very relaxing. Most people don't breathe properly, most people really don't know how to breathe properly.

    [2:02]

    So teaching them how to do diaphragmatic breathing is one of the simplest, but most effective things you can do to manage or get to start helping manage patients with any form of edema. And I wanted to share what your point was because it's a great comment. And I've heard this before, but it's excellent. It's hard to teach patients sometimes basic things, right? So tell them to smell the rose and blow out the candle. Okay? Smell the rose and blow out the candle, and sometimes that they can put their hands on their abdomen and their chest, the hand on the chest shouldn't move, but the abdominal should move a lot. So they're blowing up that balloon, or whatever works for that patient, to instruct them, but it’s a very effective treatment. Yeah?

    Female speaker: [Indecipherable] [0:02:42] exactly 5 repetitions, like is it numerous times a day.

    Hettrick: You know, the more -- yeah, people always like to give reps, right? Repetition. The more they can do it throughout the day, the better. One of the things I have found though sometimes is patients will concentrate so hard on doing it properly that they kind of can hyperventilate and get dizzy. So you just want to make sure that they just learn how to do it and start to -- when they think about it, just do it. You don't have to stay up to do this five times every 30 seconds, that doesn't work, it has to be meaningful to them, and they have to be able to incorporate it into their life. But if they have little reminders, they can set their phone to remind them maybe once an hour, just to do it for a minute. Or if they're watching television, anytime a commercial comes on, they can do it then. But the more they can do the diaphragmatic breathing, the better. And I'd have to go back and find specifics on those articles, but they do exist. And it's more in the lymphology literature than it is in other places, but it's highly, highly effective. Yes?

    Male Speaker: Can you explain why chest breathing does not accomplish the same thing?

    Hettrick: You're not getting the same amount of intrathoracic pressure. It's not stimulating the diaphragm in a way that's conducive to support venous return or also lymphatic return. It's still important. I mean, a lot of people are chest breathers, but we want to teach them how to be diaphragmatic breathers, because it's not the same amount of changes in the intrathoracic pressure to get the benefit to mobilize the fluids as much.

    [4:03]

    That’s a basic response, but that's the gist of it, essentially. And there's somebody else had a question.

    Female Speaker: [Indecipherable] [0:04:09]

    Hettrick: You know, it's interesting too, because there's a lot of patients, some of our morbidly obese patients have a lot of compression on the vena cava. And what do we see with that? Edema, right, and so that's why it's another incentive to help get them in behavior modification or lifestyle modifications. See if they can lose some of the weight to take the pressure off the vena cava. But the same idea we see a lot of edema for different reasons. But they can even benefit significantly by teaching them how to do diaphragmatic breathing, because it can help mobilize some of that fluid and get that out of there a little bit more efficiently. Okay. Is there another question? Yeah. Okay. Okay, great.

    Okay, so skin changes. We've all seen this. But one of the basic things is to always do your edema assessment, right, just part of comprehensive skin assessment. And we want to look for pitting and rebound. And we basically graded according to the depth and to the time it takes to rebound. And this is a really classic example. So here's a lymphedematous limb with a lot of those fibrotic changes we talked about. And you can see with this finger, she's trying to pit that tissue, it's not going anywhere. It's kind of like pushing on a candle or pushing on tree bark, it's just not going to go anywhere. But up here, it's still kind of soft and pitting, and so the fibrotic changes haven’t occurred up here as well.

    So we want to really know, like, how much pitting did we note? Now, you're not going to sit there and measure this, right? It’s clinical judgment. But we can use pitting scales, because it's always good to try to quantify our information when we're doing our tests and measures. But the other thing that's important to note is if we are pitting that tissue and pushing it in and leaving an indentation, how long does it take to rebound and come back to normal?

    [6:00]

    That's important because really anything over, I believe, it's 20 seconds or 30 seconds is indicative of a lymphedema. Okay, so similar to like -- you can use that diagnostically just like a Stemmer sign. But it's really important to consider that non-pitting edema. Now remember early on, this is chronic. This has been around a long time, and this is why we see those fibrotic changes, but early on you might still get a pitting response and you still might get a negative Stemmer sign, but it doesn't exclude the diagnosis of lymphedema. We just need to monitor them and think about -- okay, if they don't respond the way they should to conventional therapies, we need to start thinking about it being a lymphedema component.

    So tissue texture helps a lot with differential diagnosis. So normal tissue should feel elastic, supple, pliable, maybe a little bit different in patients over the age of 65 because the gerontodermatological skin changes, but we can also find watery edema, and these are really palpable pockets of fluid. This is typical of what we find with congestive heart failure and that is really mobile fluid. You can just push that all over the place. The skin can sometimes be translucent, you can even manually displace it, move it around, sometimes even see blisters. We can have a softly pitting edema, it feels like dough. We can have brawny fibrotic tissue, which is starting to become difficult to pit, it's very thick skin. So again less fibrotic, it's going to feel a little bit like toothpaste, okay. Or more fibrotic, it's going to feel firm and leathery. And then you can have all the way to that hard non-compressible, that's the advanced lymphedema that we see here, the lipodermatosclerosis.

    So I do a tissue texture lab with my students and they hate me because I put everything related to food. So I ruin a lot of the food that they like, so bear with me. So when we talk about this, sometimes what I like people to appreciate, especially if they've never worked with patients like this, is if you have an unripe avocado that's very analogous. That texture and the hardness and a lumpy-bumpy texture to it is very much like chronic lymphedema with fibrotic changes.

    [8:01]

    When we start doing manual lymph drainage and complete decongestive therapy, and we start to break down that fibrosis, it starts to feel like a ripe avocado because now it's soft. We still have that lumpy bumpy tissue a little bit but it's softer and it's more pliable. Another thing that I have them do is have them palpate a cantaloupe, because the cantaloupe has a very similar texture to some of these fibrotic changes, particularly lipodermatosclerosis. And other things like play doh or bread dough or pizza dough is very analogous to that softly pitting fluid. Then there's a lot of times we’ll feel that with like congestive heart failure and things like that.

    But I think it's important for people to have that context of what this feels like, so that when they encounter it in clinical practice, they can remember sort of what it's like. And most of us have experience with food, so we can relate to that a little bit better. But there's a whole spectrum basically of how tissue texture can help us with differential diagnosis. And so with skin changes, the more common forms of edema we see in clinical practice are venous insufficiency, lipedema, which we'll talk about in congestive heart failure.

    And so it's very important that -- we often look obviously at our patients and visually assess them, but we have to use all of our senses. We really have to feel and palpate those tissues to pick up those subtle changes. Whether it's tissue consistency or texture, we have to really look. We have to talk and ask questions, get a good history. One of the side effects of doing wound care, of course, we have to smell. And we really need to actively listen. Because if we really listen to our patients, they will tell us what's wrong. They may not have the medical terms to tell us, but they always know what's wrong with them, so we need to really listen to be able to glean some of those clues.

    [APPLAUSE]

    Okay. CVI pathophysiology, so this is again just to review insufficiency of the venous system, usually due to failure of the deep veins, the perforating veins, or superficial failure.

    [10:04]

    And it results in that regurgitation of the blood. The valves aren’t working properly, the blood leaches out of the vessels into the skin, the hemoglobin breaks down, releasing the iron, and we end up with that biological tattoo or the hemosiderin deposits that are classic telltale sign of venous insufficiency. But what happens we get this dermal backflow, but not just a venous congestion or blood, but we get a dermal backflow of lymphatic congestion as well. And this is why we start to see the edema. And this impairs the capillary function due to increased pressure.

    So again, it's that arterial venous lymphatic relationship. So when there's impairment in one system, we're going to see impairment in the other, and the trick comes in, whoever asked that question about, I think it was you, with compression, is most of our patients don't just have one comorbidity. Did anybody have a patient who has like one thing wrong with them? Just remarkable, right? It doesn't happen, and Dr. Keystep [phonetic] in Canada did a study with his lymphedema patients and this was over 200 or 400 patients. On average, they had seven co-morbidities. Seven and they're all contributing. So how do you know when to compress? Because you have to figure out what's the most involved system to know how to adequately compress because some compression is better than no compression. But it's got to be done safely, and we'll talk about that.

    So we can have superficial vein failure. Again, this is just meant for your review. But it can lead to the pathophysiology of venous disease. This is more common and it tends to be bilateral. But we can also have deep vein failure, and this can oftentimes lead to blow out syndrome, and this can be much more fast acting and come on much more quickly, that we can see with patients as well and you can end up with perforator failure. So you end up then also involving the system ultimately as well. But whether you're dealing with a superficial venous dysfunction or a deep venous dysfunction, there's going to be an associated lymphatic dysfunction.

    [OFF MIC]

    [12:02]

    Okay, so with the CVI, we know typically with traditional venous insufficiency that early on with venous hypertension, it leads to that low-protein, watery edema, and tell us dysfunction of the lymphatic system. That's when it converts to high-protein edema, and a true lymphedema. With classic venous insufficiency, you might not have a Stemmer sign, it might be negative initially until there's more fibrotic changes that persist. Typically, with CVI, it's going to be symmetrical, but patients with lymphedema, this is one of the telltale signs that it's lymphedema. If it's bilateral, it's always asymmetrical. And this is a differential diagnosis between lymphedema and lipedema. So if it's bilateral lower extremity lymphedema, it will be asymmetrical.

    Now sometimes, it's really hard to tell looking at your patients that it's asymmetrical. But if you take your circumstantial girth measurements, one limb will always be more involved than the other. Lipedema, which we'll talk about later, is symmetrical. And it's an abnormality of adipose tissue, which we'll talk about, but if you're trying to decide, “Well, what's going on with this patient?” look for symmetry

    Another one we’ll start to see with classic CVI, a lot of the changes in the skin typically start to occur around that ankle or gaiter area. The texture of the tissue can be brawny, again that cantaloupe [laughs]. It progresses, typically, distal below the knee, and responds to elevation. The edema does reduce with elevation or overnight when sleeping, and so this is why early on this might be like a stage 1 lymphedema. It can be spontaneously reversible lymphedema. But we start to see this classic presentation at some of these skin changes. And when you're at this point, there is lymphatic dysfunction. And you can see the various studies in this patient as well and the hemosiderin staining.

    [OFF MIC]

    [14:06]

    Okay, so I think we've all seen this, and I think it's just an important reminder to note. One of the things we’ll start to see with CVI too is that contracting down by the ankle. And if you do any range of motion assessments on your patient, you'll find that they actually often have limited ankle range of motion, due to the bounding down at the tissue.

    [OFF MIC]

    Also what we start to see is typically with pure CVI, the onset is going to be fairly slow with superficial involvement but more rapid with the deep involvement. Pain, it's uncomfortable, right? They get that distention type achiness, it's uncomfortable, it gets worse as the day progresses, especially if they do prolonged standing or sitting. And this is why it's important for people to vary up their activity. If they're sitting, get up and walk around. If they're standing, they should be doing ankle pumps and doing heel raises. Those types of things, taking breaks. And what we’ll start to see too is that even without an obvious wound, sometimes that fluid will just weep right out and/or it can lead to a venous ulcer. So it’s a classic hemosiderin-staining, atrophie blanche lipodermatosclerosis; all of these things that we see all the time.

    Now with pure CVI and that's debatable if it's really a pure CVI anymore, cellulitis is uncommon but dermatitis is very common. Now with lymphedema, cellulitis is very common. But either way these patients are prone to infection because of the skin barrier dysfunction that they’re now experiencing. So with venous skin changes, we see a lot of telangiectasias, we’ll see that medial ankle flare, we might see a lot of these tortuous, superficial veins. But these patients even though they don't look like it, they need compression. We need to support that hemodynamic system because there's dysfunction in that venous system, and in time, they're going to develop edema. Because in time, they're going to develop a secondary lymphedema, because of the fatigue and the breakdown because of that association.

    [16:01]

    But these patients really, really should benefit from some type of compression as well. And the trick with that is, it's going to be compression for life. I mean, that's the trick, and it's really behavior modification and explaining to them why it's so important that they comply. When it gets to this point, these are not reversible. Hemosiderin staining is irreversible. The champagne bottle or the inverted bowling pin lipodermatosclerosis is not modifiable. We can work on modifying some of the fibrotic changes. We can soften those over time with some very specific manual techniques and using different types of foam under compression. But the staining of the tissues is not something we can change nor is the atrophie blanche that we can see in some of these patients as well, the classic telltale signs. The other thing too that we’ll see and I listed some of these before. One of them is this venous eczema that's common. They get very sensitive to products, just because of the skin barrier dysfunction. So we want to make sure that we're using things that doesn't have a lot of alcohol or perfumes or other sensitization additives like lanolin or benzocaine or neomycin, because they do become very sensitive.

    Now patients with this crusty skin, there's some newer products out on the market now that are monofilament debridement pads. If you've ever seen those, they work extremely well to remove all of that tissue. What's nice about it is, it's a form of debridement but it's painless, essentially. And you could remove a tremendous amount of these crusty things that you often see with these patients. So these monofilament debridement pads that are available now are very, very effective in managing skin like this, okay. But the skin does need to be protected and we need to manage it and care for it before we put it under compression. It's not saying you hold off on compression, but you treat the skin, you treat the wound, then you put them in the compression. And with lymphedema, we see this too. Now these all also have a venous component but we see this hyperkeratosis that over-proliferation, and you see a lot of this crusting; it’s that lymphorrhea that weeping, that just comes out and builds up a hyperkeratinization on that tissue.

    [18:08]

    We see this papillomatosis, this lumpy bumpy skin that we can see, or these wart-like projections on the skin, which tend to be benign. And we start to see that thickened fibrotic skin that resembles alligator skin or like a tree bark, which is interesting. So I mentioned I'm doing a study with sea turtles. You’re probably like, “what does that have to do with anything?” Well, we see this papillomatosis, right, in our patients with lymphedema that lumpy bumpy skin, which is really indicative of a longstanding lymphedema. We know it's because of a lymphatic dysfunction. Well in sea turtles, particularly green sea turtles, they have a condition called fibropapillomatosis, looks identical to papillomatosis we see in humans, but the prevailing theory in marine biology, it's due to herpes. I’m like, I think the herpes is opportunistic. I think what's happening is the turtles have a lymphatic dysfunction because of contamination to their food and water supply. And they're developing lymphatic dysfunction manifesting as this fibropapillomatosis and then the herpes is saying, “Hey, look what we can enjoy.” And so we're kind of doing a study, a comparative pathology study, right now to see if there is actually lymphatic pathology with the sea turtles, but the problem is nobody knows anything about sea turtle lymphatics. So we have to start by imaging that first. And one of the prevailing theories is that because they are subject to hydrostatic pressures, being in the water all the time, they have an underdeveloped system, which makes sense, because the hydrostatic pressures of the water can promote fluid flow. Whereas on land, we've developed a pretty robust lymphatic system to promote fluid flow. And then what we're finding in space, with our astronauts that are in space for over three months at a time, they're coming back with a condition called puffy-head bird-leg syndrome. And what's happening is like a toothpaste tube, all their lymphatics are getting squeezed up into their head, because they don't have the effects of gravity to countereffect to work on the lymphatic system.

    [20:00]

    So they're coming back with visual disturbances, plaques on the brain and a whole bunch of other complications, because their lymphatic system isn't working properly, because there's no gravity. So interestingly, there is some connection between sea turtles, the lymphatic system on land, and space. And we're just trying to figure out what that is, because it's kind of interesting. I like pattern recognition, but that's even pushing it a little bit. So lymphatic skin changes, we see this -- you know, typically patients with lymphedema, it's not painful. It's very uncomfortable. It's heavy. I mean, imagine carrying around 40 or 100 pounds in your limb, it's heavy, it's uncomfortable. If they're complaining of pain, work them up either for an orthopedic condition or potentially metastasis. Something like a tumor could be encroaching on vascular structures, nerve structures or something of the like. But typically, it's uncomfortable, it's not painful.

    Now wounds again, they can have wounds of different etiologies, but the lymphorrhea, the leaching of the skin where it's just weeping out can cause like a chemical burn. We often will get infections, fungal infections and cellulitis infections are very common. We’ll see that progressive fibrosis, lichenification.

    And typically with lymphedema, the progression is distal to proximal, okay, so distal to proximal. And it's important, because differentially, if somebody is presenting with a proximal to distal, that's usually a sign of a malignant lymphedema that usually there's a tumor encroaching on the structures, usually in the groin, sometimes in the arm. But if it's a proximal to distal progression, it's usually pretty quick, and it is painful, you want to work them up for a malignant lymphedema. And response to elevation -- you know, early on in stage 1 lymphedema, it tends to go away overnight, but it's progressive. And so for not managing it properly, will go on to -- so it doesn't resolve overnight. But typically, the onset is pretty slow unless it's a malignant form of lymphedema, so it's a progressive condition.

    This is just a slide and we, as Pamela has said, can email this presentation to you but some of the different skin changes that are common that we see with our patients with lymphedema.

    [22:05]

    And another thing I just want to touch on is the lipedema. Are you familiar just with a show of hands what lipedema is?

    Some people -- very few, okay good. Good, learning opportunity.

    Okay, so this is a pathological deposition of fatty tissue. And what's interesting with this, it's from the waist to the ankles, the feet are spared. Unfortunately, it's more common in the female population. So at least progressive enlargement, almost exclusively in women. We believe there's a genetic component, it's frequently misdiagnosed as lymphedema or obesity. So it's not always called lipedema. And it's a true disease in and of itself. And we make this diagnosis clinically. And you really have to know what to look for. But when you do, you’ll see this, and you will actually see this in a lot of places, and interesting that here -- where am I? I was in New Mexico last weekend. In Arizona. At the University of Arizona in Tucson, Dr. Karen Herbst is one of the leading researchers in the world dealing with lipedema, right here. So those of you that live in this area, you have tremendous access to a wonderful, wonderful woman and researcher.

    So what this is feeling of heaviness in the legs and aching dysesthesia, easy bruising. They tend to bruise very easily with minor, minor trauma, minor contact, very sensitive to touch. So this has been referred to in the literatures as painful fat syndrome. And they'll get orthostatic edema. So over periods of, you know, sitting during the day or standing during the day, they'll get an associated edema. And they’ll start to have these oatmeal changes to the skin. Now usually it comes on around puberty, we do believe it's a hormonal component, but it can come on before or during pregnancy or during menopause. And we do find that there is a hereditary component. So it's really better to ask questions more about who has large legs in your family versus who's fat, because that's just not a nice question to ask.

    [24:01]

    But who has big legs in your family, because there is a familial predilection. What's interesting is there's a disconnect between the upper body and the lower body in these patients. Now you can have somebody with lipedema that also has obesity, but I'll show you some pictures where you can see that disconnection. So clinically, they end up too with a hypermobility, particularly of the knee joints. Their knee joints are hyper-mobile, part of the disease process. The fat pads above, inside, and below the knees, and the outer region of the upper thighs become very enlarged. And it can put a lot of stress on the joints.

    And 30% to 90%, also have an associated component with the upper extremity and you can see it here, in here, in here. But most of it is really confined to the lower extremity from the hips, the iliac crest down to the ankle bones, but not the feet. The feet are spared all the time. So if you see swelling or edema in a patient with lipedema, they likely have a lymphedema as well, secondary lymphedema, so that would be like lipo-lymphedema. So 50% are overweight or obese, but may have a normal appearance, appear at the waist. So the upper and lower bodies do not match. And that's what I mean, okay. And so weight loss may decrease the upper body but the size of the legs does not decrease.

    And what's frustrating with this condition is it's a diet and exercise resistant condition. Diet doesn't work, exercise doesn't work. Because it's an abnormal fatty deposition. There's newer wet tumescent liposuction technique, specifically for this. It not cosmetic liposuction, cosmetic liposuction sucks out your lymphatic capillaries. But these newer techniques are aimed at really reducing the lipedematous fat and are having some good outcomes with that. So it's bilateral and symmetrical, and you see how the feet are spared. And you can see these oatmeal changes in the skin. And you can see the over-proliferation of some of these fatty lobules.

    [26:00]

    So the skin is soft and pliable, but it will bruise easily because there's capillary fragility, they get a malleolar fat pad sign. So instead of that sulcus, it bulges out, but the feet are spared. And that's one of the telltale signs here. Okay. And this is kind of what it looks like too. Early on, the only sign is the disappearance of the concave spaces on the sides of the Achilles tendon. So they call it the fat pad sign or the filling of the retromalleolar sulcus. And you can see that there. So it is staged and you'll see variations in the literature and resources about how lipedema is staged. I did give you some resources on this one sheet, we're going to do later today, fat disorders.org. The disease they call fat, there's some really excellent resources online that you can learn more about not only how to assess and diagnose, but how to treat. Yeah?

    [OFF MIC]

    Hettrick: Well, what's interesting -- if it's purely lipedema, it really doesn't pit because it's not a fluid problem, it's an adipose problem. But if you're seeing pitting or you're seeing edema, you want to start thinking there's probably a lymphatic component. And it makes sense when you think about the stretch that it's causing on those lymphatic capillaries and that increase diffusion distance that blood has to travel to provide the oxygen and the nutrients to support adequate perfusion and other things. A lot of times they will develop a secondary lymphedema. So if you're feeling that there's fluid present, it's likely a lipo-lymphedema, so they do have a secondary lymphedema thing.

    [OFF MIC]

    Hettrick: It depends on the patient. But basically, they do respond to complete decongestive therapy, which is the standard of care for managing patients with lymphedema. So even if it's just pure lipedema, they do respond to complete decongestive therapy. But the caveat with that is to make sure that you reduce the amount of compression because it's uncomfortable for them because of how sensitive their skin is.

    [28:06]

    So usually you're going to use less compression initially with them and build up their tolerance a little bit. Now they're not going to have drastic changes in size, like our lymphedema patients are when we start doing complete decongestive therapy, but it is going to help manage the condition, make it a little bit more comfortable. And if they do have a lymphatic component, it will help manage that piece completely. But these patients -- I don't want to say as bad as we are, but as difficult as it is to diagnose patients properly with lymphedema, it's these patients are missed all the time, absolutely all the time.

    But we see patients like this all the time, and people just assume it's obesity, it's not. This is a separate entity in and of itself. Now they can also have obesity, but both are disease processes. Obesity is a disease much like lipedema is a disease. And these are some of the different distribution patterns that it can present with. So you can have just the upper thighs, you can have thighs and a little bit of the calves. You can have full leg or you can have just the lower leg for lipedema, but the most common is usually full leg presentation. So they can develop that secondary lymphedema, as I talked about, and usually it's due to that microangiopathy because that adipose tissue leads to increased capillary permeability, leads to proteins and capillary fragility and because of that relationship of the AVL systems, then the lymphatic system becomes fatigued, they can break down. And once the transport capacity is then mechanically disrupted, you now have a lymphedema.

    So again, one of the prevailing mechanisms they believe here is that mechanical pressure from fat and capillary leakage affect the operation of the lymphatics, and that's how ultimately leads to what we call a lipo-lymphedema, much like we talked about phlebolymphedema. This is the combination of lipedema and lymphedema, but you can also have obesity and lymphedema, and that would be considered a lipo-lymphedema as well. Yes.

    [30:00]

    Male Speaker: Can you talk about what decongestive therapy is?

    Hettrick: I will. Yes, I will. Good question. So, will I talk about complete decongestive therapy? Absolutely yes, fair question.

    So, again, what's important to remember -- adipose tissue is an endocrine organ, right, and adipokines actually impact the lymphatics. So too many can cause lymphatic leakage, and decreased contractility of the vessels. And we need that contractility to mobilize lymphatic fluid. So patients with obesity and lipedema are at risk for developing a secondary lymphedema. And I'll tell you a lot of my patients, when I was in clinical practice, have phlebo-lipo-lymphedema. They have chronic venous insufficiency, lipedema or obesity, and lymphedema, but you can treat it and it's manageable. Okay. There's no cure for any of these conditions but it is manageable and it is treatable with the complete decongestive therapy, which I will talk about.

    So again, this is a classic presentation of phlebolymphedema. And again, a lot of times people will say this is venous insufficiency ulceration. It's actually just the fluid leaking out and leading to skin barrier dysfunction, it's that lymphorrhea.

    This is lipo-lymphedema. And again, you can still kind of see that demarcation of where the feet are spared, but look at the knees and how those fat lobules are presenting. It's not quite symmetrical. So that's indicative of whether something else other than lipedema going on here, and note there's involvement of the feet. So now we have a lipo-lymphedema. And these are what most of my patients look like, it’s the phlebo-lipo-lymphedema. There's a CVI component, you can see the venous changes, you can see the hemosiderin staining, you can see the feet are fairly spared, you can see the lipedema changes here and the asymmetry, which is indicative more of the lymphedema. And if you did a Stemmer sign, this patient had a positive Stemmer sign. So a whole combination of things.

    But what's interesting, regardless of how they're presenting, it's manageable. And that's the good news, because so many of these patients are told, you're just going to have to live with it, there's nothing that can be done. And that's not the case. That's not the case.

    [32:05]

    [OFF MIC]

    Hettrick: Can you guys hang in with me for a few more minutes. Yes?

    Male Speaker: [Indecipherable] [0:32:12] lymphedema patients to plastic surgeons?

    Hettrick: Yeah, okay. That's a fair question. It requires special training to be able to treat patients with lipedema. It's not your typical plastic surgery procedure. Same with some of the microvascular techniques that they're doing now for managing lymphedema. So there's some newer anastomosis procedures, there's lymph node transfers, there's a whole bunch of newer techniques coming out. But it's a very specialized training, because we're talking about micro, microvascular surgery. And for these patients with the lipedema, for the practitioners that are trained in how to treat them, it's highly effective, but it's really not for just a general plastic surgeon to do. Does that make sense?

    So if they really know, if they’ve had advanced training on how to manage or treat or do this tumescent liposuction, then yes. So it's just finding who in the area might be beneficial. And Dr. Karen Herbst, down at the University of Arizona, has a lot of resources on her website for places to do that. But not everybody's going to be a candidate, but definitely there's hope for these patients. And one of the best things that's come out of this movement is there's a lot of new support groups called the Lipo Ladies. And so there's wonderful support groups, for these women to get together and share their stories and share successes and what works, what doesn't work, and at least to know that they're not alone in this process.

    I'm not going to spend a lot of time on CHF, but this is another one of the common things that we see with edema. And one of the best ways that we manage this right is with diuretics. Well, it's great at mobilizing the fluid, but if you also have a lymphedema component, it's not going to mobilize those proteins. Okay. And so this is the problem that happens what Pamela related to is if somebody is coming in with true lymphedema and the practitioner doesn’t really know what to do, but sees the edema and says, “We’ll just give you a diuretic to get rid of that fluid,” it’s going to mobilize the fluid, but it's not going to do anything with the proteins.

    [34:09]

    So those proteins are going to get left behind and they “love” water, they’re hydrophobic, so they're going to attract more water to the area and they're going to over-proliferate, you're going to lead to actually more fibrotic changes over time. So it's really important that if somebody needs to be on a diuretic that they're on the diuretic for a medical condition that warrants being on a diuretic, but if it's just to manage the lymphedema, that's not recommended, because that will make lymphedema worse.

    With congestive heart failure, lot of different reasons why there's congestive heart failure, a lot of different medical conditions that can lead to congestive heart failure. We see this a lot. A lot of patients with lymphedema have congestive heart failure. And the trick with that is like, well, what's safe to do with these patients? Because they need compression, but how much compression is safe? Can we do manual lymph drainage? We don't want to overload the heart. And the short answer is yes, we can treat these people but we have to do it conservatively, and we have to do it in a team approach with the cardiologist.

    So again, just for your review, there's left-sided heart failure. Right-sided heart failure is the one we typically see with the peripheral edema, okay, that watery form of edema. And it can be complicated sometimes to discern, you know, clinically what type of edema we're dealing with. But that's why your histories are just so important to take with these patients. So, the left-sided heart failure is the patients that often have the dyspnea, the restlessness, the confusion, whereas the right-sided heart failure is whoever we're going to see more of the ascites, the dependent edema, and this is where sometimes it gets confused to be a lymphedema. Doesn't mean they don't have a lymphedema, but sometimes it's just CHF and should be managed according for CHF. But a lot of these patients will also present with a concomitant lymphedema.

    So there's systolic heart failure. There is diastolic heart failure. Again, this is just meant to be kind of a review, but it's important to bring it up because so many patients do have congestive heart failure, and we see this a lot, and the tricky part is being safe with your compression with these patients.

    [36:09]

    But can you compress them? Yes, but we have to do it carefully. Again, some compression is better than no compression, we have to be able to justify why we're doing the compression. They do respond to complete decongestive therapy, manual lymph drainage, but what we’ll tend to do especially if it's a bilateral presentation, is just focus on the more involved extremity first, monitor cardiac output, make sure medications may need to be adjusted, work with the cardiologist to say, “Hey, we're going to be mobilizing a lot of fluid. We don't want to overwhelm the heart.” And we need to look for some of the signs too to see if we're potentially overwhelming the heart with our interventions.

    And again, so the different clinical manifestations -- that could go here. So just some of the symptoms and signs, so again the swelling is usually one of the first things that people report. There's an ad out now recently too where you see a woman getting out of bed and she's trying to put on her shoe, and she's just like, do we have to do this today? It's so sad because there's so many things that we can do to help with these patients, but the edema component can be pretty debilitating for some of these patients.


    TAPE ENDS [0:37:16]