Section: CME Category: Pathology

Implications of Lymphatic Dysfunction and Failure

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

Heather Hettrick, PT, PhD, CWS, CLT-LANA, CLWT discusses basic principles of lymphatic pathophysiology and it's clinical significance.

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Goals and Objectives
  1. Describe the components of lymphatic pathophysiology
  2. Describe the venous-lymphatic failure process culminating in phlebolymphedema.
  3. Describe why lymphedema results in chronic inflammation.
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  • Lecture Transcript
  • TAPE STARTS – [00:00]


    Hettrick: So we kind of set the stage of its importance, but there are a lot of different implications. So a simple uncomplicated lymphedema results from a mechanical failure of the lymphatic system. So there're two different ways that lymphedema can occur. There's a congenital form, which can be present at birth, or it usually comes on within the first year of life, and that's Milroy syndrome. Also oftentimes you'll see bilateral lower extremity involvement and sometimes an upper extremity involvement with Milroy’s, but you can also have a primary lymphedema, congenital form of lymphedema, that develops during puberty, more common in females, tends to be bilateral lower extremities. And a lot of times these girls will come in, maybe they were doing soccer, maybe it was gymnastics, maybe it was cheerleading, and their legs just start swelling, and it doesn't resolve where they think they sprained their ankle and it's just not resolving.

    And so these are the patients that actually have a primary lymphedema. And we think hormones might be triggering because it does come on right around puberty, and we call this Meige syndrome. It's very, very common, actually. And it's something that's completely manageable if we diagnose it early, and as Pamela was talking about, we tend to miss these things.

    But an interesting thing, just as a caveat is with some of these congenital abnormalities of the lymphatic system, we have to remember the lymphatic system is actually from an embryologic standpoint, it's developed out of our venous system at about three months of gestation. So that's interesting, right? So if our lymphatic system is developing out of our venous system, then how do we separate them from a pathophysiological standpoint? I don't think we can, again.

    But what's interesting, there's also a condition called and I never say this properly, distichiasis. So it's like, you get these accessory eyelashes on the top and the bottom row of the eyelid. And, you know, they're irritating. If you ever had an eyelash in your eye, you know how irritating that is. So a lot of times people will just pluck them out, or they'll go to the eye doctor and they'll remove them, but what they're missing is that this is a symptom of a greater sequela of a complex disease process, which is a primary lymphedema.

    [2:05]

    So if you have somebody that's complaining of weird eyelashes or something along that line, just pay attention to those clues because it's linked to congenital form of lymphedema. So again, what happens when we have an uncomplicated lymphedema, which results from a mechanical failure, what can happen, so we have primary, we have secondary. Secondary is what we probably see more often in clinical practice. These are the patients that might have had breast cancer-related lymphedema. These are patients that might have Kenmall [phonetic] syndrome where they have the fibrosis of the inguinal nodes, or they had prostate cancer; 70% of men treated with prostate cancer and radiation therapy will develop lymphedema of both of the extremities with the genitals and/or the genitals. We can see it for a lot of different reasons. But some trauma, it could be a car accident, it could be multiple surgeries, it can be a lot of different things, radiation therapy, leads to this mechanical failure of the lymphatic system.

    It's just not able to accommodate the load it normally needs to take. So some pathological process has reduced that transport capacity, how much that system is able to transport at any given time, to the point where the system is no longer able to handle that normal lymphatic load. So remember, I said that we have a safety factor. So we have the ability for our system to kick it up a notch when it gets overwhelmed a little bit. But when we have a mechanical failure, this is where we start to develop a true disease of lymphedema.

    And I'd like to talk about it like this. So you know, you might have your pickup truck and you've got a pretty good transport capacity with your pickup truck. But if you get in a car accident and you no longer have your pickup truck, and now you have a smart car, do you have the same amount of transport capacity? No, [laughs] definitely not. Good car, but you're not going to be able to transport the same amount of load at any given time when you've downsized. And this is what's happening when we have trauma to the lymphatic system, whether its primary or secondary. And so what happens when we normally have this clean flowing river, like our lymphatic fluid is moving efficiently, because we have an adequate transport capacity.

    [4:08]

    What happens when it's not able to manage the normal load, we get stagnation. And when we have stagnation, it's kind of gross, right. And this is where we end up having a lot of problems, and what we see clinically with these patients is we start to see edema. But over time, when it becomes really chronic, this is where we start to see a lot of those associated skin changes, which we're going to talk about. And it starts to lead to a local area of skin dysfunction or skin failure. And we see this and this is why I believe, and this is my opinion -- but I believe that lymphatic dysfunction is the underlying cause of all forms of wounds. I think there's always going to be a lymphatic failure component when you think about all the different wound pathologies that are out there, when you have disruption to the skin, when you think about where those lymphatic capillaries are, you're disrupting the lymphatic system as well. And it may be overwhelmed temporarily or may become diseased and permanently damaged.

    So this is an interesting slide and I want to share some of the language with you because this is kind of helps to explain why we have so much change to the skin. And so I don't like to read to you, but I'm going to, because I think this is important to convey the importance of why we see these skin changes. So what happens, as we know -- so lymphedema is really a protein-rich edema. That's what separates us from things like an ankle sprain or a congestive heart failure.

    So the complication or the pathophysiology of lymphedema is protein rich, because for whatever reason the system can't pick up those proteins and mobilize them. And what happens when proteins get left behind in the interstitial tissues, they can stay there for a little while. But they can't stay there for very long. And what happens, it's much like if you leave butter out on the kitchen table, it gets rancid, it's going to start to break down. And so what we see is this, we get an inflammatory reaction and it creates a whole host of things to go on. So macrophages start to come in, it leads to excessive collagen deposition.

    [6:03]

    Fibroblasts start to migrate into the connective tissues. They become fibrocytes, creating more collagen tissue and, of course, adipocytes as well, which creates some fatty tissues. So we see all this happening locally where these proteins are being left behind. And this is important because this is what starts that sequelae of leading to these chronic skin conditions. So in addition to the propensity to retain fluid in the tissues, these trapped proteins start to break down, like I just said, like rancid butter. And this leads to a pathohistological state of chronic inflammation. And chronic inflammation is the underlying problem, why we see all these associated skin changes.

    So what happens, these denatured proteins start to oxidize cell membranes, the monocytes become attracted to the area and they change into or differentiate into macrophages. And then these take proteins through pinocytosis, they digest them essentially, which activates macrophages to again release cytokines, especially Interleukin-1, and this in turn activates more fibroblasts. And so again, that cycle of producing more collagen continues to come into play. And so excess collagen formation causes more connective tissue proliferation and fibrosis resulting in that thickened fibrotic skin and that wart-like projection we sometimes see in lymphedema, those papillomatoses.

    So additionally, some fibroblasts might differentiate into adipocytes. This is why sometimes we see some fatty changes associated as well. And this is why in time with this process, and it can take some time, but it becomes chronic, we start to see that hard, fibrotic changes to the skin. It's very similar to lipodermatosclerosis, I think it's a very similar process. And what we're seeing are these significant changes because those proteins aren't getting picked up properly. And that chronic inflammatory state leads to all those associated changes, which is very deleterious to our skin, our skin can't handle that for very long.

    [8:00]

    So what happens is when the lymphatic load is increased, so the demand for fluid mobilization has increased, but our transport capacity is reduced because we now have our smart car instead of our pickup truck. We can start to see very serious swelling. Okay, and what happens you might have somebody with lymphedema, and for whatever reason, but maybe they end up with a cellulitis infection, so we just now induced a whole different exacerbation to that lymphedematous area, and so we put a further demand on their system. And this is why vigilance skincare is so important with these patients, they're very prone to cellulitis and it's the number one reason why they're hospitalized.

    So one of the things we need to be aware of is that because of the immune deficiency due to that fluid stagnation, okay, the lymphedematous regions are very highly prone to infections. And we see this a lot with these patients. So that immune deficiency is caused by a lot of different reasons. The immune cells get congested, the lymph nodes become impaired or diseased, antigen processing is disturbed, the skin can become diseased because those Langerhans cells and those keratinocytes lose their barrier function. And that's critically important as well.

    But one of the things to these areas of congestion, and I'll show you a slide in a little while, become much more prone to malignancies and cancerous changes as well. And so the more infections or immune deficiency our patients with lymphedema experience, the more significant changes in skin morphology we're going to see. And these are the patients that come in with those really hard fibrotic limbs. They just seem to chronically have infections and they're really compromised systemically. But this is so important to think about that link to why the skin can become dysfunctional? Well, it's because the underlying complications associated with the lymphatic system.

    So this is that link. Lymphatic failure produces a region vulnerable to infection, inflammation and carcinogenesis. And this was a great article by Carlson that just came out in 2014.

    [10:00]

    And he calls this the Locus Minoris Resistentiae, the path of least resistance. I think it's kind of interesting. And he states that lymphedema is not only a site of chronic inflammation, it's also a region of immune deficiency. That's important. Lymphostasis leads to persistence and accumulation of antigens, foreign material and immune complexes in those interstitial spaces. Because again, remember, it's not picking it up the way it's supposed to. So it's getting left behind, we have that stagnant river now. And this can ultimately cause chronic localized inflammation. We see this, those red limbs with our patients, that chronic inflammatory state.

    So lymphatic failure causes disruption of adaptive immunity by decreasing or obstructing all that on immune trafficking; all those structures that we need them to normally do, they're kind of on hold and they're not working the way they need to. And what this does is it causes a cutaneous region of immunosuppression.

    So think about your patients with different types of wounds and what that tissue looks like. We see this immunosuppression. But what this is, all these abnormalities lead to a condition called lymphostatic dermopathy, which is actually failure of the skin as an immune organ. So this is skin failure, but presented in a different way. It's because of the lymphatic component. And so this is why I think that a lot of wounds that we're seeing, regardless of the etiology, have an underlying lymphatic component associated with them, because of this link. So it's kind of an interesting thing. So that integration or understanding the important connection between the lymphatic system and the integumentary system is critically important too. If you do not have a healthy lymphatic system, you may not have a healthy integumentary system in that regional area. So again, this could be a contributing factor to all wounds and skin dysfunction.

    So the lymphatic system is organized into a one-way drainage system, as we talked about, to allow recirculation of tissue fluid, macromolecules and all those other things back into the vascular system. It's the only way that fluid gets backed in and dumps it back in, about 4 Liters a day, like I said, into the venous angle. And if there's actually excessive demand on the lymphatics or congenital or acquired anomaly, there's lots of tissue fluid homeostasis, and this is where we clinically start to see edema.

    [12:10]

    And this can be recognized clinically and it's actually a feature of severe chronic venous insufficiency, and this is why there's a movement out there to call all CVI, especially when there's an edematous component, phlebolymphedema, because of that interconnection. We'll talk about this, the CEAP classification soon, but anything CEAP-3 or higher on the CEAP classification is considered a phlebolymphedema.

    So the excessive demand can also be fatigue from obesity and fat disorders. And I'll talk about that later. But we start to see with obesity and things like lipedema and Dercum's disease and some of the other fat disorders out there is that the stretch on those lymphatic capillaries due to the adiposity actually leads to fatigue of the lymphatic system and ultimately down the road is secondary lymphedema. So they're not always just “obese,” they actually have clinical complications not only associated with their obesity or their lipedema, but also secondary lymphedema.

    So this is a slide just to help you appreciate why there's that link again between lymphatic dysfunction and venous dysfunction. So if we start with our diagnosis of chronic venous insufficiency, and I believe it’s the Framingham Study that came out and said almost 20% of Americans actually have some form of CVI or chronic venous insufficiency, particularly varicose veins. So what happens is with chronic venous insufficiency, we get a high filtration pressure increased. What we have is a venous hypertension.

    And so we're getting increased pressures and hemodynamic changes in the lower extremities, which is causing fluid to actually leak out. And similar with some of the blood too because we get that backflow that congestion. And so the fluid is getting pushed out of the venous system at a more rapid rate and we start to see the edema, and that water load now is going to exceed the normal lymphatic transport capacity.

    [14:07]

    Now our lymphatic system is still intact, it's still functional, but it's overwhelmed. So we start to see the edema that we have commonly associate with chronic venous insufficiency. So what this does is we start to develop a low-protein edema. So it's kind of stagnant, it's hanging out there. The lymphatic system is trying to work as hard as they can, but it can't always keep up, and in time, especially if we're not addressing the chronic venous insufficiency component with adequate compression, we start to see a lymphatic hypertension develop.

    So now the lymphatic system isn't working properly. It ends up leading to those fibrotic changes we talked about, which we kind of now call lipodermatosclerosis or we see those venous skin changes, which is actually due to lymphatic hypertension. And what we start to see now is a lymphatic damage. And that lymphatic damage now is going to lead to a high-protein edema. So we're starting to get those skin changes too with that non-pitting response. And what it does is, it basically tells us that lymphedema now, because of the system, this process, is the underlying pathology contributing to the formation of venous ulcers. Because remember those slides, a couple of slides ago, it talks about -- it creates that local area of skin barrier failure. And so I think that's the connection that when we have venous hypertension, it ultimately leads to lymphatic hypertension, which can ultimately lead to skin barrier failure, and we end up getting these venous insufficiency ulcers.

    And there were so many times I got referrals in New York for venous insufficiency. But it was really -- yeah, it was venous insufficiency and the presence of lymphedema, and it really doesn't matter what comes first. It's just a combination of complication, right. The phlebolymphedema.

    And the hard part is that even today you have a lot of lymphedema therapists, you know what to do to manage the lymphedema, but don't know what to do about the wound care. And then you have wound specialist who know what to do about the wounds, but don't know what to do about the lymphedema. And we need to bring those two specialties together so that we can treat these patients holistically back to your point, because there's no reason we should separate them out.

    [16:09]

    So it's kind of an interesting pathophysiology relationship there. And so we see this. And one thing I want to say, sometimes we wait till we see patients starting with the mild edema here or more severe and definitely more severe. But even here, what we need to be doing, you don't have to wait until you see edema to start using compression. Sometimes it's too late by that time, you’re still beneficial, but we want to catch them much more early to support the hemodynamics. So when I talk about the hemodynamics, not just the venous system, but also the lymphatic systems. Because think about your lymphatic system having a hemodynamic component, even though it's not blood based, it's lymphatic based, but it's still a hemodynamic component.

    So again, you see patients like this all the time, right? It’s a typical patient, and these are the patients that come referred to you for venous insufficiency, right?. And yeah, there's definitely a venous component here. But these all are phlebolymphedema patients, and one of the ways you can tell is you can see the toes here. This is not what I -- I didn't name this, but these are called sausage toes, okay. And the reason being that if you try to tent the skin on the toe -- tent that tissue, you're not going to be able to pick up that tissue. It's hard and fibrotic, that's the Stemmer sign, okay.

    And when you have a positive Stemmer sign, it's a positive valid tool to diagnose the presence of lymphedema. But by that time, the changes have been going on for so long, it's very chronic, so you get those fibrotic changes. Sometimes you can do a Stemmer sign early on in a patient and you might still be able to tent that skin. But that doesn't exclude the diagnosis of lymphedema. It just means that maybe the lymphedema hasn't been around long enough to lead to those fibrotic changes. But if you know with these patients, they're not responding to traditional like compression, elevation, rest, ice, all those things; if the edema is persisting, start thinking it's likely a lymphedema.

    [18:06]

    Because regular swelling will respond to basic interventions, because there's not a lymphatic pathology. It's overwhelmed, but it can manage. Once the system has impairment, whether it's congenital or secondary impairment, then we start to see this. And this is where we'll start to see those really complicated patients. This is where that skin barrier failure starts coming in to play. A lot of these patients -- this patient does -- this was the patient I had in New York and this was not my patient, but you can see the skin here. These really aren't actually wounds per se, there's just such a fluid burden, the lymphorrhea is weeping out. It's just leaching right through the tissues. And because lymphorrhea is so caustic, think about the metabolic products that are in it, all those cellular components, and it's very caustic material, it breaks down the skin.

    It leads to this crusting, particularly this yellow crusting, and you can also see that reddened response and that’s the chronic inflammation we see with these patients. So again, there's that link between the venous and the lymphatic systems. So this was just interesting. Sklesi [phonetic] looked at an art, it's a while ago, 1994. But he went back way back in the days and even showed long time ago that relationship, because he looked at chronic venous insufficiency in particular that what we used to call stasis dermatitis. And he found what happens at that point is that the lymphatic capillary lumen collapses and we have a derangement of these anchoring filaments.

    So looking at the lymphatics here, so here's our artery or arteriole and our veins, and here's our lymphatic capillary. And these are all cut in half, so you're looking inside of them. But the lymphatic capillary itself is a one-cell layer. They're very, very fragile. And this is why they don't do well with regular massage. And we don't call manual lymph drainage as massage, it's a manual technique, because it's a totally different approach. But what happens is these cells then are attached by these anchoring filaments, you can see these black little like finger, hand like projections that attach the lymphatic capillary cell walls to interstitial tissues.

    [20:14]

    And with exercise, with breathing, with muscle contraction, these anchoring filaments get pulled. And what it does is, it opens up those lymphatic capillaries and it allows that fluid then to come into the lymphatic capillary and get picked up. And when that vessel fills up, it then closes. But when you end up getting CVI and all those associated skin changes, you start to get collapse of that capillary lumen and derangement of the filaments. So now you have lymphatic dysfunction on top of this venous dysfunction. So again, there's that interrelationship of what's going on there.

    This is interesting too. Now there's a huge new area coming into play using indocyanine green and near-infrared fluoroscopy in the world of lymphedema. And this was work done by Rasmussen and Eva Sevick as well out of Houston. And here's a classic patient with chronic venous insufficiency, not a wound right now. And this is just a marker, this is not a wound, and they injected her with indocyanine green and look at the stagnation.

    Okay, so normal lymphatic should be moving up towards regional nodes. But look at the stagnation that's happening around the areas. it's hard to tell because of the darker complexion, but around areas of hemosiderin staining and just that lymphatic congestion. So again, this is showing you that relationship with venous impairment, how there's a lymphatic impairment because you should see nice linear lines of the lymphatic vessels going up to the popliteal node and then ultimately up into the inguinal nodes.

    This is a different patient with actual venous ulcer. And if you look at them under the ICG near-infrared fluoroscopy, you can see there are actually no functional lymphatics now, because ICGs picked up it's lymphatic load, no functional lymphatics at that wound base, but look at the stagnation around that wound.

    [22:02]

    So again, it's showing you that appreciation of that when you have a wound or venous congestion, you also have lymphatic congestion.

    What's interesting with this new technique is, as lymphedema therapists, what we can do is, we can go in and we can manually mobilize the fluid and see if we're taking it to regional places, functional places that's working. It's actually changing the way we're treating patients now, because we're finding unique ways to manage patients on an individual basis based off of their own anatomy and physiology with our lymphatic system. And the ICG has a very low toxicity. I mean they use it on infants. I'm actually doing a study with sea turtles right now, you're looking at ICG in sea turtles. So it's kind of an interesting process. And I think it's going to be a game changer for manual lymph drainage and for therapists training with the edema out there.

    So again, this is that slide I alluded to that all in edema, including chronic venous insufficiency, is actually a secondary lymphedema. Because it's an impairment to the system, we have the venous hypertension, which leads to the lymphatic hypertension. So what a lot of the researchers starting to say now is that anytime you have see CEAP-3 or higher, it's actually a secondary lymphedema, we should be calling it a phlebolymphedema.

    And with that, it goes back to 1991 and even ’98 where they were starting to show that connection with CVI and lymphatics. And this was backed using lymphoscintigrams, we don't use them as much anymore. But even back in that time, they were starting to show that there were abnormalities in the lymphatic system, even though their focus was on the venous system.

    Here we go, I don't know if this is going to work, but this is something you can look up as well. And this is from Ava Sevick’s work.

    So what it shows you is healthy system at the elbow in an unhealthy system.

    [OFF MIC]

    What it shows you and its time lapses sped up a little bit, but you can see the flow going up towards the axillary lymph nodes, and that's what we want it to do.

    [24:08]

    What you see in the one with the damaged system is you get this backflow and you get the regurgitation. Much like we see when we talk about venous congestion and venous hypertension, you get that backflow, and so you can see just how damaged that system is.

    Now this slide just again talks about lymphedema results in the presence of a chronic wound. You get that chronic inflammation and stagnant wound milieu because, again, the lymphatic system is not picking up those substances and normally does. So think about all the crud that's in a wound, right. The MMPs, the biofilms, all these other types of things. So that stagnating high-protein edema develops this pathohistological state. Again that chronic inflammation just like those pictures we saw those legs with infiltration of the tissue by mononuclear cells, angiogenesis, proliferation of connective tissue, fibrosis, and fibrosclerosis, all those fibrotic changes we see.

    And what's happening again, is that what I just read to you a little bit while ago, is that leads to that collagen tissue proliferation and also triggers those adipocytes leading to fatty tissue proliferation.

    And so this is a very interesting process that happens due to breakdown from the lymphatic system, but how it directly impacts the integumentary system. So I think it's an important consideration. So interesting thinking points and I think these are kind of those paradigm shifts we talked about.

    Mortimer recently came out and said that all edema indicates an inadequacy, or failure of lymphatic drainage. And if you think about that, it actually kind of makes sense because that's telling us when we have any type of edema, our system is overwhelmed. Now, it could be that it's just temporarily fatigued or it's overwhelmed, or it could mean that it's actually diseased or impaired. And when it does become diseased or impaired, this is when we actually have a lymphedema. This is when we have a disease, without a cure, but something that's manageable.

    [26:03]

    They further go on in the International Union of Phlebology, and their consensus statement talks about lymphatic failure, and it can be regional, is responsible for all forms of peripheral edema. Not all swelling is equal and so we have to consider how involved or how damaged is that system? Is it just temporarily overwhelmed where it can accommodate and go on after some time and appropriate care to manage itself? Or is it truly impaired, and now it's going to be a lifelong problem for that individual?

    So just some good thinking points, but what I really want to convey is how important it is to consider the lymphatic system when we're dealing with patients with edema, any form of edema, and how it'll change our plans of care. Okay, so we're going to transition now back to Pamela.

    [OFF MIC]

    Pamela: You have an exercise sheet. Now, we as in all of us, when we do these exercises, you have the choice of doing them sitting down or standing up. And the reason for this is, you're going to have patients who say “I can't walk, I can't do that, my legs too heavy, I'm too weak.” They can do this, but in different postures where you take gravity out of the component. So it is important that you as healthcare providers teach your patients.

    [28:00]
    Everyone in this room needs -- unless you're sending them to physical therapy, you need to teach your patients basic exercises that are going to help with the venous return back to the central system. And it's important that they do this while they're wearing their compression garments. So when you teach them this, and I've given you a very good sheet, a basic sheet, that you can literally copy and give to your patients if you would like to. And so we're going to do all of this together in just a moment. You're going to have on your patients a short stretch or an elastic material, because that's going to give the best return of fluids back to the central system. And again these movements, most of the movements can be done lying down, supine, sitting, or standing. And we're going to start with the diaphragmatic breathing.

    Steve, are you back there?

    Steve, would you put this video on please for 3 minutes and 25 seconds.

    [OFF MIC]

    Pamela: Yes, sir. And when you do your breathing, you teach your patients how to breathe, they're breathing through the nose, inhale through the nose, exhale through the mouth. And this wonderful physician I’ve just have fallen in love with this physician from England for several different reasons. And he's going to teach us diaphragmatic breathing.

    [VIDEO STARTS 0:29:25]

    Male Speaker in Video: So, in the previous clip, we considered the components of venous return, contributing to venous return, which are contraction of skeletal muscles, movement of blood from the superficial to the deep venous systems and the pulsatization of the adjacent arteries. But how else does blood get back from the periphery back to the center of the body? Well, another mechanism is the respiratory pump.

    Pamela: So it's the respiratory pump.

    Male Speaker in Video: So when you breathe in, if you put your hands like that, that's your diaphragm, isn't it?

    [30:03]

    And so when you breathe in, your diaphragm is going to flatten. When you breathe out, it's going to go up. Breath in, diaphragm flattens. Breathe out, diaphragm goes up. So when you breath in, the diaphragm flattens, that's going to increase the pressure in the abdominal cavity. And of course on the right side, running up the abdominal cavity you have the inferior vena cava. So as you breathe in, the diaphragm goes down, compresses the abdominal contents that's going to press on the inferior vena cava. And the valves, because of the increased pressure in the inferior vena cava, mean the blood will go from the abdominal through to the thoracic cavity.

    And at the same time, as I breathe in the diaphragm is going to go down that's going to reduce the intrathoracic pressure. It's going to reduce the pressure in the thorax and that's going to help to suck the blood from the abdominal vena cava through to the thoracic vena cava. So the increased pressure in the abdomen is pushing, the reduced pressure in the thorax is sucking. So increased pressure in the abdomen is pushing, reduced pressure in the thorax sucking. That's going to increase venous return.

    Pamela: I'm sorry, I didn't get to see this gentleman doing it. He's just a wonderful educator. So this is diaphragm breathing, which is one of the very basic fundamental things that you want to teach your patients with venous insufficiency, lymphedema, and phlebolymphedema; one of the first things that you're going to teach them.

    And we're going to save this, actually Heather is going to lead you in some exercises to teach you some basic clearing exercises for some of the different regions where we have a lot of lymph nodes, and she's going to help you with this in a little while. So here's your diaphragmatic breathing; the exercise as you inhale through your nose, you breathe in, the stomach pushes out. The person can do it sitting, they can do it standing, they can do it lying down.

    You can do diaphragmatic breathing and I do diaphragmatic breathing all day, whether I'm standing, sitting, whether I’m on an airplane. How many of you fly a lot? If you're on an airplane, you want to sit there and do some diaphragmatic breathing because your feet are going to swell when you fly. There's no way around unless you wear compression. The upper chest needs to stay mostly still. So when you do your diaphragmatic breathing, you're not breathing up here. It’s when you want your -- tell me to [indecipherable] [0:32:46] actually, so then you're going to let your air out and your stomach's going to sink back. And this particular instructor and I've not seen this before, but it seemed reasonable to me, as you bending forward when you're sitting to help exhale more of the air.


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