Section: New Board Review Category: Wound Care

Clinical Examination and Differential Diagnosis of LE Edema

James McGuire, DPM, PT, LPed

James McGuire, DPM, PT, CPed discusses lower extremity edema, its clinical presentation and etiology. Dr McGuire recommends specific tests and guidelines to recognize and prevent worsening of the condition.

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Goals and Objectives
  1. Identify the clinical signs and symptoms necessary to diagnose phlebolymphedema
  2. Demonstrate an understanding of the differential diagnoses of conditions causing lower extremity edema
  3. Explain the tests necessary to confirm a clinical suspicion of phlebolymphedema as a cause for lower extremity edema
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    Release Date: 03/16/2018 Expiration Date: 12/31/2020

  • Author
  • James McGuire, DPM, PT, LPed

    Leonard Abrams Center for Advanced Wound Healing
    Clinical Professor
    Department of Podiatric Medicine and Orthopedics
    Temple University School of Podiatric Medicine
    Philadelphia, PA

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    James McGuire has disclosed that he is on the Speakers Bureau for Smith & Nephew, BSN Medical, Hollister, Osirus, independant contractor for Medline.

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

    Male Speaker: All right. So we’re going to talk about Clinical Exam and Differential Diagnosis of Edema and I primarily practice in podiatric. Think of it as like doctor’s office but it’s a big one like we see 50,000 patients a year and a lot of them have lower extremity wounds and I’m limited in my – we’re – I was joking a little bit and I’m limited to my treatment to the knees so I will just say I just push all the edema up to the thigh and then send it to somebody in vascular.

    I do get kind of stuck with limitations and then what it points out the importance of having a team to manage this and that you’re not just trying to take care of this in a nice way to place where you’re all alone and you’re dealing with one aspect of it and not really handling at all so that you can take care of these people appropriately. Where is the spot? There we go. So that’s me, some of my interests and other things. I do speak for a number of companies, some of which deal with compression therapies and compression wraps and other things and bone [indecipherable] [0:01:01] I have never gotten any money from, but I do give them advice. Just so you know.

    And learning objectives. I kind of put these together last night so they’re not important. Okay, and these are some of the things that actually Dr. Farrow is here. He’s [indecipherable] [0:01:23] today and he wrote an excellent article on phlebolymphedema. If there was one article that you want, we’ll just grab that one. Common Underdiagnosed and Undertreated Problem in the Wound Care Clinic, Journal with the American College of certification wound – certified wound specialist. Very good little article. My students will all be reading it.

    I’m running out again. Look at this. That goes five ahead. We’ll go back. All right, we really don’t have to do – I think he did a great job in epidemiology and kind of what’s happening out there, how often you see this. Particularly phlebolymphedema, it’s one of those things that – how many people heard the term in their education process, phlebolymphedema? Good. Neither had I.

    Basically, you think venous insufficiency, lymphedema, there’s nothing in between, although, I had always taught that it’s a continuum. It’s a process. When you begin to see fluid moving out of the system into the – into interstitial spaces, it’s got to stress the lymphatic cell. So you begin to see lymphatic changes immediately associated with the fluid overload and if it happens regularly – it’s one thing when you sprain your ankle and you get this massive fluid overload and all the edema goes down. But when – if it happened to you every week you would be getting to see lymphatic changes associated with that constant edema stress to the system and then you would start to see skin changes and all kind of changes in the area where that chronic injury had occurred.

    So you see the same thing with constant edema stress with lower extremity in patients that – and the other thing I was thinking about while we talking is how many of these patients are seen regularly by physicians, therapists, their podiatrist and the symptoms are beginning and nobody does – and I see all these people end stage. They have a wound by the time they come in to the center where I am. They’re already – I laugh at the CEAP classification is this elaborate list of symptoms leading up to the highest classification is CEAP 6 which is ulcer. So the students say, “Well, how do we use this classification system?” I said, “It’s easy. They’re all six.” It doesn’t help with the wounds and the process after the wound had developed.”

    So CEAP is an underutilized evaluation system or classification system because it would lead you to early treatment. I have really bad varicose veins. I inherited them from my mother. They got worse in football because they wrap my right knee every week really tight. So what does that do? It blows out the valves on that vein even when I was 18 years old, I had varicose – superficial varicosities on my right thigh.

    And when I went to PT school when I was 21, they told me that those are, you know, like your valves have been destroyed, they’ve been compensated and you need to wear compressor stockings so I started wearing them and I’ve been wearing them since I was – you know, I’m 65 now. I don’t have any hemosiderin, I’ve got other things, but my legs look really pretty good and I look at my patients who are 50 with massive edema wounds and it’s just nobody told them when they were very young to wear something appropriate. So it’s a big problem and look at the number of patients that developed this problem in our society and that are walking around. People that are leading up to some of the things that we’re going to end up having to treat in our wound care centers.


    Diagnosis. Probably the most important is just to sit down and talk to people which we have absolutely no time to do anymore. Anybody would like to say a nasty word about EMRs, just do it now. It’s ruined my life. It’s taken up every second of free time. Yes, sir?

    Male Speaker: [Indecipherable] [0:05:22].

    Male Speaker: Heather and I were talking before and Pamela and we were talking about just what your day like. There’s fun things we would like to do. Wouldn’t you like to do some things to study something? When? You know, I don’t get any – there’s no time left in your day to sit down and ruminate to write, to think, to read even to gather information on a particular patient that you need. We whip to the internet on our phone. We go to the first site. We finally find some piece of information and we try to apply it. If you don’t know something, that’s no way to really self-teach.

    Soft tissue imaging is out there. We’re going to talk about that a little bit. Lymph vessel and lymph node imaging is available if you want to look into this. Conductance, volume measurements which are not really done too much anymore. Genetic testing, which we talked about with children if they have this vascular imaging and then some blood test for other causes mainly to look at some of the inflammatory markers for other conditions that maybe causing lower extremity edema.

    This is a table, causes of lymphedema. It’s by the article that you see down there which you can’t read but that’s even better. Like do you really want to know where I got it? Actually, if you just put in causes of leg ulcers, you will find numerous lists of these things and there is a lot of them and there’s different reasons for edema. We’ve already talked about vascular. There’s neuropathic problems that can lead to the development of an ulcer usually associated with trauma and it’s not just always plantars, sometimes it’s malleolar, sometimes it’s lateral foot, metabolic things, diabetes again, gout, prolidase deficiency, hematological. I have a patient now with thalassemia, a couple with sickle cell, cryoglobulinemia is not seen as often, at least not by me. But these are very difficult ulcers to manage. I keep telling this one – this one woman’s ulcer is horrendous. It’s like her entire leg, its massive white blood cell accumulation, massive inflammation, constant reinfections at the site. And she only has thalassemia trait and her hematologist tells me it can’t possibly be having an effect on this. But there’s no other reason in her. She’s 27 years old with a massive leg ulcer, hemosiderosis and all kinds of problems and it’s a combination of everything that’s going on in her system.

    Trauma, pressure injury, burns, don’t forget that it may – some injury may lead to a blockage of the lymphatics and major outflow for a limb, may scar up, maybe a lot of bleeding into that tissue and afterwards those tissues are significantly compromised.

    Infection. Most of these patients that we see have multiple episodes of cellulitis, which you have to differentiate from vasculitis lots of times because a lot of people get very inflamed. Just associated with all these extra protein in the subcutaneous tissues and the skin gets very red and warm and it’s easily mistaken that – how many patients have you heard they come in and they’ve been on Keflex five times or they’ve been on Cipro four or five times for a cellulitis of their legs. And you ask them, have you ever, ever had fluid coming out of your legs or a wound. And they haven’t had a wound yet. But they’ve had this red, swollen, inflamed legs and to try – and if you white blood cell test them, they don’t have any elevations of white blood cells or sed rate maybe because they have a lot of information. So you have – they present this very confusing picture to you as to how to treat this.

    And some of the antibiotics that we have are actually slightly anti-inflammatory. Keflex is one, which has a little antivasculitic. And doxycycline is another one that’s commonly used in low doses in the lower extremity to help reduce some of the vasculitic inflammation that you see.

    Panniculitis or that, you know, like a necrobiosis lipoidica, fat necrosis, breakdown of the fat tissues, pyoderma and we see pyodermic gangrenosum in our clinic a little more because we have a trial going on right now. We’re beginning to attract these patients into the clinic, but I find that again, to be a very difficult wound to manage because there’s massive inflammation, massive autoimmune reaction happening at the site, and a triggered massive edema which ends up with a lymphedema, phlebo–lymphedema associated with the – all the trauma and inflammation that goes with the pain and inflammation with the skin disorder that’s occurring.


    And then special cases such as a hypertensive ulcer.

    Venous insufficiency, the most common cause of these ulcers, accounts about 80% of the cases that we see. So your mind goes there immediately but you don’t always know. What’s not on there are any of the metastatic things, the squamous cell carcinoma, basal cell carcinoma, some of the other skin carcinoma that might be producing a wound on the lower extremity. And you can never be sure that you’re not dealing with something cancerous, so biopsies are always indicated. If you don’t know, just take some biopsies.

    I mean I usually discouraged by biopsies because I’m sure something bad’s going on. Couldn’t be my treatment and then it’s – all you get is what? Inflammatory cells consistent with venous and venous ulcers or venous insufficiency. Very uncommital. Most VLUs are completely healed at six months. I wish. But 50 to 65 are, but the recurrence rate is very, very high so many of them are reulcerated within the year or within the next six months afterwards for one reason or another.

    And I was – you were – I was laughing about what you’re saying like, you know, doing a trampoline. Well, most of my patients would break a trampoline. They could never – they couldn’t do it alone. They’d have to have somebody with them because their balance is horrible. They can’t even reach their toes. They can’t see their toes to determine whether they’re sausage or not. And they’re not the patients that are going to easily be coaxed into a rehab program. They give up. They just – I can’t do that, I can’t do that. I can’t get stockings on. I can’t wear a – I can’t wear shoes anymore. I can’t get my feet up. I can’t, I just can’t do it. And you spend most of the time coaching and coaching takes time and we don’t have any time. You’re coaching like this – you should try that.


    That would be really good for you. You’re on diuretic? Which one are you taking? No, isn’t it life? It’s where we are. It’s – this is medicine today. When I retire, I’m going to get on my computer and I’m just going to go on, “Hi, this is Dr. [McGuire] [0:12:17], I’ll answer any question you have about medicine. Then I’ll try to help you take care of yourself with an aloe plant. What are we talking about? You need an aloe plant, electrical stem and other thing and you could take care of yourself forever.

    Well, what, vitamin C – silver – yeah, you’ll turn gray. This is – there’s a little list over here which is very, very hard for anybody to read but it’s small because it’s a big one which is differential diagnosis of edema of the lower extremity. Like, if you see swelling, what can it be? And it’s everything, it’s malabsorption of protein, it’s obstructive disease. Obstructive sleep apnea can result in lower extremity edema. Renal disease, localized – like cellulitis, chronic venous insufficiency, compartment syndromes, which you may see from an injury. Complex regional pain syndrome, which can result in swelling or response to this chronic kinds of pain. DVT, iliac vein obstruction or May-Thurner Syndrome, which was – I find it more often than not. And it’s so easily fixed, they just stent the vein. So that it can’t be collapsed and it seems to do great.

    Lymphedema and then again, May-Thurner. This is lymphedema, again, fairly classic picture. Nice normal feet, big fat legs. Big heavy, heavy legs and the feet look – they’re fitted in to their regular footgear. It’s a dead giveaway for lymphedema.

    But you’re right, in the sense that it never stands alone. Like that much like adipose accumulation in the lower extremity begins to affect your lymphatic outflow, begins just like both – affect both arterial inflow, venous outflow which – and then you have the fluid buildup, you get protein extravasation into the spaces. You get all the triggering that occurs and they begin to see many of the skin changes associated like lipodermatosclerosis and other skin changes associated with lymphedema. May-Thurner is unilateral and it’s – all you have to do is like check out the system and see if it’s being included.

    Okay. Is it sudden? Is it delayed? Or is it intermittent? Intermittent would be venous insufficiency or some condition that’s producing a momentary blockage which then release itself. Is it up and down during the day? Does it go away at night? Does it stay there at night? Is it improved in the morning or is there a component of it that’s not improved? Where is it locating? We already talked about that.

    Pain and discomfort. Now that’s one that I find very confusing because they tell you venous-like ulcers generally are not painful and arterial are.


    And I’ve seen some horrendously painful inflammatory venous ulcers. Just, you know, maybe ideal with a group of people with a very low tolerance and high vitamin P need, which is Philadelphia in general has a real high Percocet intake. So people know, they come in in agony and sort of roll around and cry. And then they tend – and they’re already on, but the status do – we have a nice program now where we’re really monitoring morphine, Percocet, you know, all the opioids have to be – they’re in a registry now. So I just go in and I look up the patient, I see, “Oh, you’ve gotten seven prescriptions on the last six, you know. You’re going to be getting this from your primary only now.” Not me. For pain. And then the primary can send them to the pain center, so we’re getting out of it a little bit but that doesn’t excuse the fact that these – many of these ulcers are extremely uncomfortable where they’re very – they’re not non- painful so then we have to get into the how are we going to manage this pain and is it appropriate to use opioids for a short period of time in a very, very painful wound, pyodermas, other things that are just incredibly painful.

    When somebody tells you that they’re willing – a younger person tells you they’re willing to go and have their limb amputated, then you know they’re in agony and you need to do something about this.

    Certain medications across swelling, we have a list of them in a minute. The course of the disease process which I think Heather has laid out very, very succinctly is that it starts one way but it progresses and it’s a slow progressive development of edema and skin changes and limb changes. That can easily be headed off at certain points, but when you get to that brawny edema, that mitosis of the skin, that bar flake changes in the skin, you have a tremendous amount of protein in the subcutaneous spaces and in the limb that is inducing a massive inflammatory response, it’s not easily managed at that point. You have to go backwards. And you got there in little steps, you have to go backwards in little steps and the discussion with the patient is just take a simple step.

    Well, I learned something today. I didn’t know diaphragmatic breathing would help people. You know, when they said would you like to talk, I said sure, I’ll come and listen and I learn something from everybody I’m talking with. Fact is associating with this, with swelling, you know, cancer. Don’t rule out that there are some other cancerous problems causing – I’m a prostate cancer survivor and after hearing all this and seeing one of those pictures up there, I’m extremely happy that my results are as they are.


    Very happy. Okay. Histories in infections, CHF. My students always ask me, the patient has a history of congestive heart failure, how can you use compression on them? And I said take your finger and push on the limb and it’s completely brawny with very little like pitting component at this point in the secondary. So you can easily compress them because they’re not – they’re very, very, very slowly going to leech that fluid out of that limb. They’re never going to overwhelm the cardiovascular system with the amount of fluid that we’re going to remove. And you can – and I said, can you titrate your compression? You have to do exactly what it says on the box, you know, full compression, you know, wrap it on tight. You can wrap it on lighter. So you get just a small fluid movement and then gradually bring – you can do one limb today and one limb next, few days later you can go back and forth. So you don’t overwhelm the system but you can still get the edema out of the limb.

    Kidney disease, liver, malnutrition and hypoalbuminemia all produce problems. Thrombogenic events, presence of malignancy again, insect bites. Well, in Philadelphia, we do have a problem with either ticks or flees producing constant biting of the extremity, which produces a lymphangitis and it’s not exactly elephantiasis but it does end up with a lymphatic problem of the lower extremity because they’ve had multiple like lymphatic-related infections associated with insect bites. Not a lot of mosquitoes flying around but there are a lot of fleas.

    Medications that can cause edema. Well, we all know like if you take a lot of NSAIDs, your ankles are going to swell. But they don’t use to use any opioid related pain medicines, so now we just tend to like shoot a little bit toward NSAIDs to reduce inflammation in the tissues and recue discomfort.


    Then you say, “No, you can’t use.” So we use Tylenol but that’s going to overwhelm the liver, so you have hepatic dysfunction. So we really are like saying just suffer and we’ll try to get your legs down. And there’s very little… you know, I do find I’m throwing these terms around and we’re kind of laughing about it a little bit, but it’s a frustration I have almost every day, is do I make the jump over to an opoid a little bit for a short period of time.

    And has anybody ever ordered like Percocet or Percodan Demi? Have you ever written a script for the half dose instead of 5… 3 to 25 year old for 2.5? You can’t get it. So how can you titrate anybody up or down or just sort of use a small amount of medication to maybe help them if you can’t even get the medication, it’s not available.

    Calcium channel blockers can lead to edema, corticosteroids, Pioglitazone and Rosiglitazone. Pramipexole, this is one that we use a lot, Gabapentin, Pregabalin, Lyrica and Neurontin. It has a tendency to produce edema of lower extremities. And if you’re getting that, you may have to back them off of that medicine, [indecipherable] [0:21:12], various chemotherapies also will result in increased edema. So go through their medication list, pull the meds up, and at least that’s one good thing we can do in the MRs. I can always pull the meds up and look at the things that are associated with those medications.

    As a podiatrist, there are always like mystical medications that I’ve never heard of before, so I have to do… I have to look them up. And if you’re a person that does prescribe medicines very consistently, you need to look them up.

    Yes, ma’am?

    Personally, I… well, okay. Everybody that has obstructive apnea that I’ve seen is very overweight or associated with a great ill. So we already heard that increased adipose tissue in the abdomen interferes with that nice flow of the lymph up out of the system. Apnea is, again, you know, breathing. You’re obviously probably not taking a nice deep belly breath while you’re sleeping, you’re breathing very high and then you stop for a while. So just a lack of diaphragmatic movement would result in a decrease in lymphatic flow, but it’s also going to… just that amount of adipose in the legs, in the abdomen, especially when you’re lying down, it’s going to compress the abdomen, it’s going to decrease flow. So I would suspect that’s the main reason why this is occurring.

    Anything to add? All right.

    Yes, go ahead.

    Yes. I would say, go to your primary. Remember, I’m a podiatrist. So I say, go to your primary and get evaluated for sleep apnea, get sleep apnea treated. We run into a lot with when we take patients in for surgery and they have a problem with apnea and they have to be… they have to get general there, and there’s a significant risk during the case for some of the anesthesia patients, so a lot of patients that have inventory diff for anything. They have apnea, they have never been… they have never admitted it and or talk to it with their physicians. So you can ask them. I have said a patient, yes, they asked their wife or their partner, sometimes there’s a better person to talk to. Like do you think this… like somebody asked me one time, “Do you think you have sleep apnea?” I said, “No, I don’t think so.” My wife goes, “You might.” She says, “I thought you died a few times at me.” She goes like, “Are you awake?” But I just stopped breathing for a couple of seconds. But I think it’s just frustration with life.

    Symptoms, ask [indecipherable] [0:24:07], what I think about the election. I think it would be better for you to just stop breathing. I had to get one political remark. If you know me, it’s hard for me not to.

    All right. Leg fatigue, burning, swelling, throbbing, cramping, aching, heavy and restless legs, they all fall into that component. Although every time I see restless legs, I spend a little time talking to patient about spinal problems, if they have numbness, tingling, shooting pains, because I see that kind of night jumpy legs and restless legs very much associated with spinal stenosis, so it’s often a trigger for that for me, but it can be for this too.

    I mean that leg has got to hurt. It’s got to be uncomfortable. It has to be uncomfortable to try to live with that. Clinical science starts with varicosities.


    You might see some hyperpigmentation from, you know, repeated small inflammations, edema or swelling, venous dermatitis or chronic dermal disruption, ulceration, much of those little tiny itty-bitty ulcerations on the skin where it just kind of breaks open in a lot of places and it kind of weeps that fluid through the skin. Lipodermatosclerosis, ankle flare or starts with small varicosities in the ankle and then proceeds to deeper and up to superficial system into the larger vessels.

    Once the deep system changes, that’s when you really, really see some changes in the limb. I think it’s very rapid after the deep system becomes compromised. And then the characteristics of the ulcer and location of the dorsal skin. I mean we have a patient with a venous leg ulcer on the dorsum or the foot right now, it extends down the inner spaces because it involved one of the inner spaces and they get interdigital inflammation and infection that kind lives in that tight space between sausage toes which infects their wound all the time. They’re constantly getting pseudomonas is a real big one, it just keeps growing on these wounds that they’re black or green. They have a terrible look to them. We’re always fighting an infection to try and stay ahead.

    This is the CEAP classification. This is the C part or the clinical part. C0 is no visible or palpable signs. C1 or little telangiectases of those reticular veins. And what you’re really looking at is a progression of venous disease. C2 is varicosities. C3 is edema. When edema begins to show up, you see pigmentation and eczema of the skin. Then you see lipodermatosclerosis or atrophie blanche. Atrophie blanche is sort of healed skin where they’ve had inflammation and a healing process that goes on, a fibrotic process that goes on that leaves you with sort of a non-pigmented area of skin, which is actually scar tissue. Healed venous ulcer, active venous ulcer.

    So by the time they get here, they walk in your clinic, they’re here. They’re already six. And then they have S is symptoms, and we’ve already talked about those. A is – if you get further into this, it gets very deep, if you look at CEAP. I didn’t put it all up here. I just put a couple of things. There are numeral classifications for which veins, the anatomical location, whether it’s telangiectases, greater saphenous, greater saphenous below, lesser saphenous, non-saphenous veins, they each get a number. Whether they’re in the perforate and then this is the deep veins, which one is involved and where it is, it gets a number. Also, it becomes a little complicated to administer the classification, so really we just look at – we’re just looking at the C part and using that fairly regularly.

    Differential diagnosis of a venous leg ulcer. Think basal cell carcinoma if it’s been around a very long time and it’s not responding. Think that you may get a conversion of the lesion over to a cancerous condition and go ahead and do biopsies. And when you do biopsy, you don’t biopsy in one place. You probably should biopsy in quadrants for around the wound at least three or four of them out of wound to make sure that you’re catching any of the tissues that might be involved.

    Cellulitis is not always, you know, due to venous insufficiency. You can have a cellulitis which is [indiscernible] [0:28:26], which is from a puncture of the skin inflammation that then results in an inflammation up into the subcutaneous spaces. But with that you’ll see a massive amount of fluid move in, erythema, redness, it’s going to – it’s painful. But I want to show you a picture in a minute which is not cellulitis, you know, but just like it.

    Dermatologic manifestation. Cardiac again. Renal, generalized essential telangiectases are not venous leg ulcers, but they are a condition which mimics that. [Indiscernible] [0:29:00] now or webber, squamous cell, stasis dermatitis and from just constant, you know, fluid accumulation in legs.

    And then you could also say on there that you might contact dermatitis which is – and that’s up there, allergic. And the most common contact dermatitis that we see are patients putting Neosporin, Bacitracin on some little wounds that become very, very inflamed because they become sensitive to Neosporin. They don’t know it and they just keep putting this, quote, “antibiotic” on because it looks worse. I looks I guess more and more infected, so they use more and more of it and it gets worse and worse.

    Pitting edema, again, we’ve kind of gone through this. Just another list, more of the same. We already talked about all of them. So duplex ultrasound, study choice for evaluation of venous system and DVTs. Real-time B-mode or two dimensional sonographic image. Consider the new gold standard to diagnose clinically significant DVT.


    This is the test we usually order to rule out when they have leg pain or discomfort in the legs, sort of recent onset of swelling. I can’t tell you how many times people say, you know, my legs hurt, the [indecipherable] [0:30:15] tabs and tests, it’s uncomfortable. I’ll probably go five over. But I will go 500 on the next one, so you’ll be lucky. And just send them and get the test. It doesn’t hurt anything to order this. And you’ll be able to rule out the possibility of a DVTs, the source of their discomfort.

    But a lot of legs, when you compress them and, you know, you do the dorsiflexion test and you do the cap compression, if they have lymphangitis or lymphatic pain or just pain from edema, they’re going to have a lot of discomfort so it will throw you off.

    Magnetic resonance stenography is available. It’s a sensitive test and it’s very specific to test the deep and superficial venous disease of the lower extremity. It gives you a very nice picture of the venous system and the arterial system depending on how it’s read. Direct contrast stenography is available where you inject a dye and watch the proximal flow. I think the newer one which is available which is cyanic dye, we’ll get to that. cyanine die, whatever. It’s, yeah, the green thing.

    Soft tissue imaging, you can use an MRI, CT or ultrasound. You can’t tell edema from these tests, like what’s causing it. Just that’s it’s there. But you can pick up tumors and other things, injury to vessels and that kind of thing.

    Lymphoscintigraphy where you’re able – this is where you inject it into the limb. It’s a radial pink dye, it goes up through the lymphatic system. And if you’re looking for places where pools, dermal pooling as it flows to the limb, it helps you identify, you know, certain nodes that may be a significant problem if there’s any – if there’s nodal cancer for some reason from a proximal spread of the cancer cells if you had a squamous on the foot, it may be up in the node. You can diagnose that with this test.

    Indocyanine green, ICG, we’ll give you that really pretty picture of flow through the limb and it’s real-time, inject it, you watch it on the screen and you actually see it flow through the limb and you’re seeing the flow, you’re seeing where it is, it’s very helpful in determining therapies. Like where the – where you see your lymph edema therapies is going to – how they’re going to perform MLD, where they’re going to do it, where they’re going to focus, it can be based easily on the flow that you see on one of these tests. They’re not as common. The device is not as common yet. But I’d like to see it used a lot more. It’s very helpful in mapping arterial changes in the lower extremities as well.

    Bio measure is not done too much. It used to be the gold standard a long time ago where they put you in a pool and measure how much water you displace, but that takes a big pool, takes a lot of time and it really is not – it’s very – it’s actually quite accurate in looking at limb volume.

    [Parametry] [0:33:07] is infrared optical scanner. It sort scans a limb and does you a volume. And then the regular old tape measures are there for you too. Which you should be doing on a regular basis to see how patients are, if they’re getting bigger every week, do they go up and down? Are they changing? What’s happening?

    Electrical conductants is available. They do a biopedance spectroscopy which looks at sort of how does the electricity flow through the limb and you can extrapolate water volume from that. I’ve never seen that test done. I know it’s available. But nobody does it at Temple. It changes the biomechanical properties of the tissues.

    Physical exam, we’ve already talked about the induration and the Stemmer’s sign that you do. Tonometry is actually a measurement of the force required to dent the skin. So you have a tonometric measurement that takes a pressure indentation of the skin and looks at how much pressure does it take to indent the skin a certain amount. The dielectric constant you can measure.

    And again, these are primarily research tools and they’re hard to do a consistent test on people because they got to be same position, same amount of force, you use same temperature, all the kind of thing.

    Genetic test, we already talked about. And traditional vascular assessment, which is – this is a classic, you know, ABI PVR test where you’re looking for any kind of blockage in the system. It’s not particularly helpful sometimes with diabetics who have calcification of the arteries, so you have to look for toe pressures or TBIs which are a little more accurate because the toe arteries don’t calcify as quickly or as easily.

    The SensiLase skin perfusion pressure is a fairly accurate test. We’re looking at microflow, ultrasound, the PVR testings and then transkinase activity takes a little longer.


    It’s just a longer test to do. We actually don’t have that. This is just kind of what your typical read would look like with a test. And often, there’s no TBIs because they either couldn’t get a reading and couldn’t get it appropriate was either too fat or too swollen and it just wouldn’t read.

    These are the readings for ABI. That’s that, the header are the same ones, which if is it’s over 1.4 Sometimes you see 1.2, 1.4 is vastly eliminated. Think calcification of the internal wall. Normal 1.4, 0.9 in there is borderline PAD. 0.8 to 0.9 is mild PAD. But this is already a cut point for –or at least where – they’re used to be called a cutoff point.

    I would say it’s at least where you start thinking about how much pressure you’re going to apply. If you’re getting readings below 0.8, you have to really think about when I apply pressure, am I going to reverse the flow near the ulceration or I put so much pressure on the outside of the wound that the perfusion of the periwound and, you know, in wound care, the wound heals from the edges in and the bottom up. So if you occlude the area around the wound so that it’s easier for the capillary flow and lymphatic flow to move away from the wound, the wound will stagnate, it goes completely deoxygenated and the tissue breakdown more and you’re actually making the wound worse.

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