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Hello and welcome to Lymphedema for the podiatrist. My name is Doctor Wade Farrow and I am the Medical Director for the Texas Wound and Lymphedema Center in Bryan, Texas and I am happy today to come and talk to you about lymphedema. This education module is going to focus on lymphedema for the practicing podiatrist. We are going to cover several areas, anatomy and physiology, clinical practice perils and associated diagnoses. Basically we want to give you familiarity with lymphedema, what is the standard of care to treat it, who has it, who does not, and what should be done about.
Why is lymphedema important? Lymphedema treatment basically, originated in Europe. We are way behind in the United States. Consequently, lymphedema here is widely misunderstood, is misdiagnosed, and is often mistreated. We are basically going to try to cover the basic anatomy, the diagnosis and the treatment options for lymphedema. We will try to cover basic anatomy, diagnosis, and treatment options for lymphedema. Why is there such a problem here in the United States? Basically, there is a lack of education in teaching institutions. If you do not know it, then how can you teach it to your students and the other medical people? Two, there are many myths in the lymphedema such as lymphedema is not something that we can treat. These things are simply not true as we will show in the upcoming lecture.
Why lymphedema? I promise you, you cannot practice podiatry and not encounter patients without lymphedema. Many people think of lymphedema only in terms of arm involvement after breast cancer treatment. Actually, there are many cases of lower extremity lymphedema, and we are seeing more and more of these as the aging population comes and people are living longer with conditions such as chronic venous insufficiency and congestive heart failure. We see lymphedema also after radiation treatment or surgical treatments to the pelvic area. Lymphedema increases the rate of cellulitis. If you have lymphedema, you are at much higher risk of getting an infection, the infection spreads much quicker, and it tends to be much more severe. Also, as you get the infection, this tends to get you more likely to get more infections in the future. The reason is because your lymphatics are already damaged and every infection you get causes more damage to the remaining lymphatics which gives you less, reserves making you more prone to get swelling and more prone to get infections. Untreated, lymphedema tends to worsen and become irreversible, mainly for the reason I just told you about the cellulitis and also because of chronic changes due to the lymphedema fluid which then deposits in the skin and in the subcutaneous tissues. The mainstay of treatment with lymphedema is to reduce the swelling and to prevent the recurrence of swelling. As we will find out, this is not as simple as pitting compression on the leg and we will explain why this treatment does not work.
In order to understand lymphedema, first, you must understand the anatomy and the function of the lymphatic system. If you understand the anatomy, lymphedema then makes sense. The lymphatics largely parallel your venous blood flow system. In the legs, there is a superficial and deep lymphatic system. The superficial system is in the dermal layer of the skin and the deep system contains deep drainage system which drain then back into your deep inguinal lymph nodes. The lymph system basically drains interstitial fluid, filters it through the lymph nodes, and then dumps it back into the venous blood system. There are about 400-700 lymph nodes in the human body. The lymph nodes are concentrated at articulation points such as the groin and the axilla. Also, there are lots of lymphatics in the gastrointestinal tract. So any blockage of the lymphatic system will cause a backup of fluid into the interstitial spaces. If this is severe enough, this leads to the clinical presentation of lymphedema.
The lymphatic system consists of the lymphatic vessels and the lymph organs. The lymphatic vessels drain into the lymph organs which start with the lymph nodes, also include the spleen, the thymus, tonsils, and Peyerâs patches which are located in the gastrointestinal tract. The lymph organs are important immunologically as it help filter the lymphatic fluid and get rid of any bacteria or foreign cells. Where do these bacteria come from? They largely come from breaks in the skin. If bacteria get into your skin, they are going to be floating in the space between the cells to interstitial fluid. This is where the lymphatic fluid is and normally drains into the lymph nodes. This is where your body has hit no points basically to fight infection and to prevent foreign cells such as cancer cells from traveling and moving through the body.
Anatomy of the lymphatic system. The smallest components of the lymphatic system are the lymphatic capillaries. These are leaky, single-cell walls which pick up the interstitial fluid and start to drain it. They drain it to the precollectors and then through the collectors and then they go through the lymph nodes. The lymph nodes filter the lymph fluid and then they also concentrate it. Once they do that, it goes through lymphatic organs and eventually dumps into the cardiovascular system. The lymphatic drainage actually drains quadrants of the bodies. The right arm and right neck drain into the right lymphatic duct, whereas the rest of the body drains into the thoracic duct.
Lower extremity lymphatics. Here you can see a breakdown of the lymphatic watersheds of the lower extremity. There is a medial and a lateral area which drains the thigh and you can also see there is a posterior component which drains the heel and the back of the calf. These watershed areas tend to overlap but they kind of drain generally that portion of the skin. From there, they go into the deep inguinal system and eventually, go through the inguinal lymph nodes and then back into the cardiovascular system.
Here you can see a cross-section of the human skin including the epidermis and the dermis. The lymphatic capillaries are located very superficially in the dermis, just underneath the epidermis as you can see. This is very important as it forms the basis for the Manual Lymphatic Drainage, which is the gold standard of the treatment of lymphedema. You can see the lymphatic precollectors and collectors which are in the deeper dermal regions.
Here, we can see the anatomy of the lymphatic system. We have the arterial on the left and the venial on the right. The blood flows through the arterial and then through the capillary network, and the blood gets picked up back on the venial side. Some of the fluid filters out of the capillaries but then gets reabsorbed. But, no mechanical system is 100% efficient. The human body is not any different. So, some of the fluid which leaks out cannot get back in. This fluid gets picked up by the lymphatic system and that is its job. The lymphatic system basically maintains homeostasis by getting rid of the interstitial fluid which collects.
There we see a graph of capillary filtration and re-absorption. Basically, there are about 16-18 liters of fluid which are filtered out of the capillary and then get reabsorbed everyday which is 90%. This means, that about 3 liters or 10% does not make it back in and has to be picked up by the lymphatic system or you start building up fluid outside the capillary which is in the interstitial space. The main way that the fluid gets driven out is through increased hydrostatic pressure. The main way the fluid gets back into the bloodstream is by increased oncotic pressure which basically oncotic pressure is charges on the proteins which are still inside the capillary. Anything that affects this hemostasis is going to increase the fluids, which gets filtered through the lymphatics, and if the lymphatics are damaged and there is a higher flow and more fluid that has to be reabsorbed, sometimes, they are not going to be able to handle the load. If they cannot handle the load, that is how you develop lymphedema.
Okay, so now we have our fluid building up in the interstitial space as it filters out of the capillary and cannot get back in. This is about 10% of the filtered fluid. And remember, 90% is reabsorbed. The capillaries basically are the smallest unit of the lymphatic system. There are single layer cells which lay down almost kind of like roof shingles with clefts between them. These clefts are actually fairly large and bacteria and even cells can get in them and the anchoring filaments help to hold the shape of these smallest lymphatic system. Remember these anchoring filaments because these are very important to kind of understanding how many lymphatic drainage actually works because it helps to open the space between the clefts and helps push the fluid back into the capillaries and into the lymphatic system. After the fluid gets into the capillary system, it will start flowing down and then eventually will go into the collectors which have little pumps and will pump the fluid and get it back into the bloodstream.
After the fluids goes into the lymphatic capillaries, it goes into the lymphatic collectors. The collectors contain the lymphangion micro pump. This little pump basically has smooth muscle cells on the wall and it constricts almost in the peristaltic motion to help move lymph fluid on through the lymphatic collectors. There is a system one-way valve which helps facilitate this and keeps lymph fluid flow in one way. So what is in the lymph fluid anyway? It actually consists of proteins and some cells and long-chain fatty acids.
Okay, lymphedema can be painful. Remember the lymphangion and the collector, which has smooth muscles. Those smooth muscle cells are innervated by small unmyelinated nerve fibers and while this also can create the peristaltic motion, they also can cause fluid flowing through them to be very painful. Anytime you have lots of edema in which case lymphatic system is handling the load, it still can be painful and especially if you have lymphedema and the system is not working correctly. Also, remember in those smooth muscles; also remember that radiation can cause damage by damaging small nutrient blood vessels and damage to the small nerve fibers which innervate this. If they do not work, then the lymphangions do not work. If they do not work, then you are going to move the lymphedema fluid, so then your fluid which contains proteins, cells and long-chain fatty acids is going to be sitting there and collecting. Now, what happens with that is how you get chronic lymphedema and we will go into that in a minute.
Here we see an example of the lymphatic capillaries and the lymphatic precollector and collector system. On the far left, you see the lymphatic capillaries which have the cleft between the cells. Then you see the lymphangion micro pump which is in the collector system and has a smooth muscle cells on the side and then the one-way valves to help facilitate the flow going through the lymphatic system.
Fluids start coming in to the capillary clefts.
Fluids start going through the one-way valve.
The smooth muscle cells start to contract closing the one-way valve.
The smooth muscle cells contract and forces the fluid out of the lymphangion.
And then the whole process starts again.
Remember that there are several lymphangion; there is one in the middle of the screen and then one on the far right of the screen. Lymphangions work together to help pump the fluid with the peristaltic motion moving it back towards the lymph node and then back into the cardiovascular system.
There are several types of swelling. Basically, there is edema and there is lymphedema. What is the difference? Edema has low protein content. This fluid which is in the interstitium does not have many proteins and is mainly due to capillary hypertension or low oncotic pressure. The fluid there you cannot put compression on and reduce the swelling. Lymphedema on the other hand has high protein content which basically means that it also has its own associated oncotic pressure. So if you try to put compression on the outside and squeeze the fluid to get it to go back into the bloodstream, the proteins are going to hold it and keep it from going back in. Then, that is one of the main reasons why you cannot just use compression on lymphedema and reduce it.
This brings us to the basic definition of lymphedema. Lymphedema is the abnormal accumulation of protein-rich fluid in the interstitium.
This lymphedema fluid contains fat, cells, and protein. There may be bacteria or viruses present. The proteins can consist of cellular residue, matrix metalloproteases or MMPs, cytokines, polysaccharides, glycoproteins, fibronectin, vitronectin, and of course water.
Primary lymphedema. Here is a 15 year old who has early stages of lymphedema. If you look on the picture on the upper left, her left leg is swollen more than the right. Also you will find very small skin papillomas. These are not really visible on the picture but if you run your fingers across the top part of her foot, you will feel them. They are barely visible, but they have little bumps which are hard. These small fibrotic papillomas are basically from the lymphedema fluid. If the lymph fluid cannot drain, these proteins eventually have to deposit somewhere. Inside the dermis, they deposit and form papillomas or little raised fibrotic areas. In the subcutaneous tissue, they deposit as fat. Treatment on this patient is pretty easy because she does not have that much swelling and you cannot do that much with the manual lymphatic drainage to remove the swelling so we focus on education, teaching herself MLD to do it at night to help facilitate the lymphatic fluid that she does have, proper skin care to help prevent infection, and the mainstay is and compliance with compression therapy in order to keep the leg from swelling. We still have the effects of gravity which we have to fight so compression is very important to prevent the lymphedema from recurring.
Okay, here is an example of hereditary lymphedema. Here is a mother of age 70 who has had 16 years of leg swelling. Her swelling had never been treated by any other doctor and they did not have any idea what to do. We treated her with manual lymphatic drainage and compression and got the swelling down and then you can see at the bottom picture on the left, her maintenance treatment with custom 30-40 mm compression stocking keep the lymphedema from coming back. Her daughter, who is age 37, you can see on the top right. The daughter actually has had bilateral leg swelling for 17 years. She was actually diagnosed with congestive heart failure which is a misdiagnosis. She actually does not have anything wrong with her heart. They did not know what else would cause such kind of leg swelling. We basically treated her the same way with manual lymphatic drainage and you can see her on the bottom right with compression stockings on and her swelling is well controlled.
Okay, secondary lymphedema. About 2 million people in the United States have secondary lymphedema. This can be caused by surgery such as removal of lymph node and lymph node dissection. This is most commonly seen after breast cancer surgery and seen in the affected arm. It can also be seen in the groin due to lymph node dissection in the groin, radiation for pelvic or prostate cancer. They can be caused by trauma, be caused iatrogenically, or through filiariasis. We no longer see filiariasis in the States but it is seen in third world countries. Radiation is probably one of the most common causes and we are going to see a lot more increased lymphedema due to brachytherapy for prostate, cervical, and rectal cancers, which we are seeing more of now. Cancer tumors which are pressing on and occluding the lymphatics or growing inside the lymph nodes can also cause lymphedema. So it is very important to understand that lymphedema can be the presenting symptom of metastatic cancer. Any of the patients who have swelling like this, need to be worked up and evaluated.
Okay, here is an example of chronic secondary lymphedema. If you look at the far left hand picture, the patientâs left leg is more swollen than the right and they are more affected up in the thigh region. She has a history of hysterectomy for endometrial cancer with post-op radiation for metastasis to her psoas muscle. Her lymphedema has been there for about 8 years and she requires 40-50 mm compression garment to keep it from coming back and she has to use compression at night. So in other words, we are going to see that there are ranges of treatments that people need. Some people can get by with a 30-40 mm compression garment. Some people are going to require a higher compression garment. Some people are going to swell at night and some are not. These patients have to be followed. The mainstay of treatment is going to be to keep the swelling out and to keep her from coming back. Remember, anyone who has swelling, as long as the swelling is there, they are going to get all these proteins and all these long-chain fatty acids are going to deposit on the skin and start leading to irreversible lymphedema. As they go into the dermal layer of the skin, it causes the papilloma which we saw and also, goes into the subcutaneous tissues, and cause increased fatty tissues. As it becomes more and more chronic and irreversible, this also causes further damage to the lymphatics that are remaining and it got harder to get that fluid out and makes it more prone to infection. If you look at the middle picture, there is a JoVi Pak which is a foam garment which has channels to help drain the fluid up. She would put some type of compression on the outer part of this garment in order to keep the swelling. If you look on the far right hand picture, you can see her leg after the treatment for the lymphedema exacerbation and that we got her swelling back down. That is actually her baseline. We cannot get her left leg as small as her right anymore because she has too much irreversible lymphedema.
Okay, so basically, there is a progression of lymphedema. I want you to think about the 15-year-old girl you saw who had the primary lymphedema and how her lymphedema was easily reduced and then her leg was the same size as the unaffected limb. Then the lady we just looked at who had the lymphedema for 8 years due to the surgery and radiation and hers at that point was irreversible and you can never get the limb down to the same size. So there are 4 basic stages of lymphedema and we will go over this. Stage 0 is subclinical. Stage I is reversible. Stage II is spontaneously irreversible lymphedema and Stage III is lymphostatic elephantiasis.
Okay, Stage 0 is the subclinical or latent stage. This can last for years or decades. Good example would be anyone who has had an inguinal lymph node or an axillary lymph node dissection but they do not have any swelling. All these people have decreased ability to drain lymphatic fluid from the leg. They have reduced transport capacity but they do not have any swelling. They do not have any obvious signs of lymphedema and they have a negative Stemmerâs sign which we will go over. They can have subjective complaints which can be fullness or aching in the affected limb and they are all at risk to develop lymphedema. They may or may not develop lymphedema during their lifetime. They do need to be aware that they are at increased risk of getting cellulitis and then developing lymphedema.
Okay, stage I is reversible lymphedema. It has accumulation of protein-rich fluid in the affected limb. This makes a pit. The pitting usually is soft and the tissue is pliable and you do not see any fibrosis there. Also reversible lymphedema typically reduces with elevation. In other words, they can be diurnal or they can vary between the night or the day. When you are lying down flat, it goes down, and during the day, it comes back. This is not always treated. There are some patients whose lymphedema will actually get worse at night, but this is kind of a generalization. As lymphedema becomes more chronic and more severe, you are going to start seeing fibrotic changes and some irreversible swelling. Remember, some of these stages can overlap.
As the lymphedema progresses, it starts to become irreversible. Stage II is the spontaneously irreversible lymphedema which is due to the accumulation of protein-rich fluids. Pitting is becoming progressively more difficult and that is due to the proteins which has higher concentration and are starting to form permanent changes in the dermis and the subcutaneous tissues. We often refer to this as âdoughy pitting.â The Stemmerâs sign is often positive in Stage II and you can reduce the volume of the limb but you have to use proper treatment and you have to reduce the fibrotic tissue which you can do using foam and compression over time. Sometimes, it is not completely reversible. The proliferation of connective tissue is some of the permanent changes that you will see.
Okay, I have been talking about the Stemmerâs sign but what is it? Actually, the Stemmerâs sign is very important for the diagnosis of lymphedema. Lymphedema is mainly a diagnosis of history and physical exam and the Stemmerâs sign is a very important component. Basically, the Stemmerâs sign is when you have difficulty pinching or lifting the skin between your thumb and your index finger. You typically do it over the bony prominence such as the base of the second toe. If you can pinch the fluid together, then that means that there is not that much protein in the fluid and therefore, the Stemmerâs is negative which means that you may or may not have lymphedema but if it is positive, and when you pinch the tissue, you cannot pinch together, and you cannot lift it up, it does not tent in other words, then that is always diagnostic of lymphedema and the reason for this is basically that the protein content does not allow the fluid to redistribute quickly between the cells and the interstitial space so when you pinch together, therefore you cannot and you cannot redistribute the pressure quick enough and that is why you pick up a larger area of tissues. In other words, the tents and the Stemmerâs sign is negative if you have trouble picking it up because there is too much tissue in between your fingers, then that means the Stemmerâs sign is positive.
Okay, to go over this one more time, we got about 16-18 liters of interstitial fluids that are produced every day. Of this, about 80-90% of the fluid which filters out of the capillaries is reabsorbed which means we got about 3 liters per day of interstitial fluid that has to filter, and the hydrostatic pressure is what drives it out of the precapillaries on the arterial side, and the oncotic pressure of the protein charges is what drives it back in and goes back into the capillary vein. So the rate of the flow into the lymphatic system is mainly determined by the interstitial pressure which is outside of the capillary area and the degree of activation of the lymphatic pumps into the lymphangion.
Okay, stage III is lymphostatic elephantiasis. This basically means that the limb volume is increased and you get more progression of the tissue changes. You get fibrosis which is becoming increasingly more firm and you get other skin changes, papillomas, cysts, hyperkeratosis, you can get mycotic infections, and you can get ulcerations. You may or may not get pitting and the skin folds also deepen as you can see here in this patient, the crease between the anterior ankle site which is very deep, and this area becomes moist, wet, macerated, tends to get fungal infections, and obviously, this person is going to have a positive Stemmerâs sign. You are never going to be able to pick up the tissue and have it tent in between your fingers. There is little to no pitting, extensive sclerosis or fibrotics in the skin and loss of skin changes.
Okay, so factors affecting lymphatic filtration. Anything that increases the lymphatic filtration, or the fluid, going into the lymph system basically. This can be due to cardiovascular exercise, you get more blood flow to the capillaries, therefore you can filter more fluid out; increased venous pressure which means you have more difficulty reabsorbing the fluid; passive range of motion or hyperemia, both of these can lead to increased blood flow through the capillaries so therefore, you get more fluid go into the lymphatic system; infection; or even decreased cabin pressure. Decreased cabin pressure is kind of interesting because basically you get decreased pressure on the interstitial fluid and so there is less pressure in the interstitial fluid and there is less drive to drive that fluid back into the lymphatic capillaries which we saw in the picture. Therefore, the fluids start to collect and you get lymphedema. This is how people who have lymphedema or who are at the subclinical stage who will sometimes manifest themselves after plane flights pretty classic and that is due to the increased cabin pressure that we talked about. Any low pressure activity could cause these symptoms.
Okay, so how do we diagnose lymphedema? We do this by taking a good history, the physical exam including the Stemmerâs sign we saw and the lymphoscintigraphy.
Okay, first looking at the history. Lymphedema can be symmetrical or asymmetrical. There are lots of symmetrical causes of swelling though and these can be due to cardiac problems, renal problems, liver problems, due to pulmonary problems. What is the nature of the history of swelling? What is the duration of it? Has it been a week, a month, a year? Is it diurnal? Does it vary at night. Do they have any family history of lymphedema? Do they have any history of cancer? Anytime they get rapid onset of swelling, then you get a little bit more worried about malignancy being possible. Also you want to look at coexisting health problems. Do they have thyroid disease, any kidney dysfunction, heart disease, pregnancy, and things like that.
Okay, physical examination. The distal extremity is usually involved in the lymphedema, in other words, the foot and the toes are usually involved in the lower extremities, whereas in the venous insufficiency, it is much less likely to be involved. Classically, you are going to get the little toes squared or swollen sausage-shaped toes. You can also get color changes where the skin can be reddish or brown. This is called lymphedema nigra and this is more common with people who have fibrotic changes or lipodermatosclerotic changes. Lipodermatosclerotic changes are basically where you get the hardening or kind of woody change to the skin but you do not necessarily have any papilloma that is kind of a different thing that you can see. So this is obviously the sign that someone has the lymphedema.
Okay, testing. This is something that I do not do very often. Maybe if you get a case and you cannot quite figure out or you are not sure. With the lymphoscintigraphy, this is basically we get radioactive tracer. You inject it intradermally to the skin, and you will look at the rate of movement and basically if you lymphedema, then you are not going to move the radioactive tracer very quickly because you have a damaged transport and if itâs normal, then you are going to move the radioactive tracer out quicker and is to be taken up to the lymph nodes. So basically, we look at the speed which is measured, itâs kind of a neat way, and you can diagnose lymphedema that way if you are not sure or if your insurance company is giving you a hard time.
Okay, here is the clinical pearl and that is the distal foot is usually involved in lymphedema. We kind of went over that. The toes would be sausage-shaped although a bit swollen and you get a good example. The picture on the left-hand side has tons of papillomas. You also see a little fat sausage toes. This is from very severe chronic lymphedema. The patient on the right-hand side is more of a secondary lymphedema. In other words, this person actually has chronic venous insufficiency as her main problem, but they are likely to have been so swollen for so long that the swelling started blocking out the lymphatic, it could not drain, and they develop secondary lymphedema, then you can see how they have swelling over the dorsum of the distal part of the foot and they also have some swelling of the toes.
Okay, here is a good example of lymphedema versus chronic venous insufficiency. As we say, the lymphedema typically has the feet and the toes involved. You have skin changes, if you can look on this patient, you saw the foot and the closer picture on the last slide and now you can see the skin changes on the leg which is red. There also has some ulceration and diurnal variation that is changing at night and the proximal is also involved. In other words, the swelling just is not distally, it is also more proximally up to thigh as well. However, in chronic venous insufficiency, sometimes you see the champagne bottle leg which is where the calf is swollen but the you can add to the little bit skinny ankle, they usually have hemosiderin deposit in the leg and have all those skin changes.
Okay, lipedema. Lipedema is kind of interesting. It was first described around 1940 and it is basically people who have a proliferation of adipose tissue. It is symmetrical. It is almost always in the lower extremities and is seen with basically flaps of tissues that typically overhang the ankles and the knees. It is almost exclusively seen in women. It is almost exclusively in the lower extremities. Feet usually are uninvolved which is very important to differentiate it from lymphedema and typically, onset is in puberty. These people are hypersensitive to touch and have pain and they also get very easy bruising. It is caused by proliferation of the adipose tissue in the limb and basically, these people are at higher incidence to develop lymphedema which they actually call lipolymphedema, and usually takes about 17 years of lipedema and in a way it gets very severe. The lipedema is often mistaken for lymphedema and get people come into my clinic. Sometimes, they have lipedema and no lymphedema and these are people who basically have normal lymphangiogram to accept it or kind of have a corkscrew shaped collectors rather than straight one because they have to get around all the fat cells.
Here is an example of patient who is 62 years old who has early lipedema and note that she has skin folds which is just above the ankles and that is classic to get those area above the knees. And despite the fact that their ankles look swollen, there is no dimpling and you cannot get any pitting. And the Stemmerâs sign is negative. And the patient shows little or no improvement with compression therapy. That is a classic lipedema patient.
Okay here you get a really severe case of Lipolymphedema. You can see in the upper parts of the thighs that you can almost see a total fat nodule and in the lower part of the leg, you can see what is thicker, you get the fibrotic changes, you already got the liposclerotic changes with the skin that is red and this person obviously has developed lymphedema. So this is called lipolymphedema. This person obviously needs to be treated for lymphedema with a manual lymphatic drainage and they also would need bandaging and then they will need some type of compression garment to keep it from coming back. And this is kind of the result of not getting treatment.
Okay, before we go on, the lymphedema as we talked about before is something that you cannot treat, it does not really respond to compression although that can decrease the chance of developing the lipolymphedema. I just want to make sure we got that point across that the lymphedema is not something that you treat with just manual lymphatic drainage and that is why we want to make a distinction about it. Okay, things that exacerbate lymphedema basically are bacteremia, the plane flights with a negative pressure that we talked about which decreases the flow into the lymphatic system, anything that increases the capillary permeability and gets more flow, any kind of venous blockage because that is going to make more fluid stay out in the interstitial space, and anything the increases the arterial blood flow.
Okay this is another Clinical Pearl in anyone with lymphedema. Good skin care is essential. You can look at the patient on the left-hand side. They have lots of cracks in their skin, then they are developing some lymphorrhea or weeping skin. They are getting mycotic infections which are highly prone to inside the skin folds and so doing good skin care and keeping the skin moist and preventing cracks in the skin goes a long way to its preventing infections and keeping the lymphedema under control
Okay, so what is the morbidity of having lymphedema? Basically, you have a swollen limb. This can decrease your range of motion; can get constant medical care due to swelling and due to infections. You get increased expenses to treat it. The longer it goes, the more it becomes irreversible, the longer hospital course, longer treatment course. Cosmetic problems because you have clothes that do not fit. Also, it takes a lot of psychic issues with people not feeling like they can get along as well doing their activities of daily living or not feeling normal or feeling weird because their limb is not in the normal shape. Also, increased weakness due to heavy limb and problems moving around, which leads to decreased mobility.
Okay, so the chronic lymphedema morbidity is caused by fibroblast proliferation which increases the collagen, causes the fibrotic changes, and this increases the subcutaneous fatty tissue.
Factors that contribute to making the lymphedema worse are developing infection, surgery, any kind of post-op infection, radiation therapy, obesity, infections such as insect bites, athleteâs foot, sedentary life style, tight clothing, trauma.
Controlling lymphedema, you want to avoid hot temperatures which will increase the blood flow and could lead to more swelling, anything that disrupts the skin integrity, trauma, you want to keep a good nutrition, exercise, good hygiene with a good skin care that we talked about and then elevation of the limbs or even wrapping the limbs at night and of course, you will need daytime compression.
Diuretics for lymphedema. The National Cancer Institute 1998. âDiuretics encourage vascular fluid depletion, but do nothing for excess protein deposits and could hasten connective tissue fibrosis. Therefore, diuretics should be used with caution and only for treatment of excess vascular fluid due to other causesâ. Basically, the National Cancer Institute is saying do not give diuretics for someone who has pure lymphedema. If you take the interstitial fluid which already has too many proteins in it and then you give them the diuretics, then you are going to have less fluid but the same amount of proteins so you are going to have a higher protein concentration which is going to tend to pull more fluid out of the capillaries to compensate for it. It is also going to increase the risk of infection because you are going to have more proteins there for bacteria to feed on and if they do break the skin, and since you have a higher protein content, it is going to be more likely to form fibrotic tissue. This is a mistake I see time and time again and unfortunately we do not have a good education system about lymphedema so this mistake keeps happening so I really would like you to take this Pearls home and help stop this from happening.
Okay, surgical treatments for lymphedema. There are some people out there who advocate in this and historically, these things have been failure. This is a patient who had a something called a Littâs procedure where they strip the lymphatics on the left leg and you can see the other limb look smaller than the right. They actually have had a severe fibrotic reaction on the toes and severe papillomatosis, so generally, there are lots of other surgical treatments, but generally, we do not recommend these and they do not work.
Okay, here is a patient who has been treated for lymphedema and you can see the lymphedema rubra on the picture on the left-hand side with the redness that is not due to infection, that is actually due to lymphedema itself and this is resolving after treatment and after compression therapy, they will require a lifelong compression and we get about 50% reduction on average with the lymphedema treatment.
Treatment for lymphedema consists of combined decongestive therapy. This has two phases. One is a manual lymphatic drainage which would go for the subtle technique where we basically open those clefts in the lymphatic capillaries and moves the fluid in and helps stimulates the lymphangions to move the fluid and we do that in conjunction with the bandaging which consists of special bandages called short-stretch bandages along with foam. And then thereâs phase II which is after we do the treatment and get the limb back down kind of as small as we can get it, and then we go to the maintenance phase. In the maintenance, this is where you are going to need a long-term compression daily and then bandaging as needed. As I said before, some people will swell and some will not where you may get an exacerbation during plane flight and sometimes they use bandaging intermittently. People with severe lymphedema will actually have the bandages in their limbs every single evening.
The Combined Decongestive Therapy is basically done 3â5 times a week, each treatment takes about 60 minutes to 2 hours to do, they go over skin care. We do the manual lymphatic drainage, we put on the compression bandage, we do education with the patient, and whenever the patient is ready, we put him in a compression garment. Basically we want someone who has been trained especially with manual lymphatic drainage and who has gone on to specialized training course and ideally, you want like a month long course but people who had at least 2 weeks with a specialized course, otherwise they do not know how to do the bandaging part correctly and also their technique is not really that accurate in many cases with the manual lymphatic drainage.
Okay, hereâs another Clinical Pearl. All that swells is not lymphedema. This is 52 y/o female who has 4 years after having stroke, and she developed a left-sided hemiparesis and you can see the picture on the left-hand side, her left leg is more swollen than the right and she was having a significant pain in the left leg maybe due to the stroke that she has what we call hyperesthesia or increased sensitivity to touch and basically the one key here is that she was having a prolonged leg elevation, reducing the swelling and was relieving the pain. We actually reduce her swelling with compression wraps and put her in a compression stocking and she had significant improvement in the pain.
And here is an example of a patient who develops severe cellulitis which required hospitalization and got 1 week of IV antibiotics. She had basically secondary of lymphedema from chronic venous insufficiency and basically she would probably benefit from prophylactic treatment in order to prevent the recurrence so she did not have to go back in the hospital.
Okay, so protein fluid is the perfect culture medium. These people who get bad infections like this will go to the hospitals. We recommend them going on prophylactic antibiotics typically if you have more than 2 episodes of cellulitis per year and this goes for anyone whose primary diagnosis is chronic venous insufficiency or maybe they have heart failure and leg swelling. These people probably have some secondary lymphedema and if they have more than 2 episodes of cellulitis per year, then we recommend them going on penicillin and you can give them penicillin V, you can give a low dose at 250 mg and you can do this once a day or twice a day. This actually comes from the guidelines that were developed in England by some famous lymphologist there.
Okay, here is an unusual case of postop lymphedema. This is a 72-year-old patient who underwent bunionectomy and arthroplasty of the first metatarsal. She also has neuropathy and starting about one year post-op, she started developing multiple episodes of cellulitis and developed an ulceration on the bottom of the left toe and she basically was recommended to get an amputation and she presented to me for a second opinion. She has chronic regional lymphangitis basically which is postop lymphedema isolated to the big toe. You can see the severe papillomatosis on the toe and you can also see the redness which is the chronic skin color changes that we see with the lymphedema. I offloaded her with a DH walking boot, debrided some of the dead skin with the papillomatosis to reduce it, and I did wound care with the antimicrobial dressings, and some white Molelast gauze for compression, and she healed up completely. We kept her on prophylactic penicillin. She never had any further episode and you can see at the bottom right-hand corner where the papillomatosis is fully resolved and there is no sign of infection. The ulcer is healed. So were able to prevent amputation on this patient
Here is an example of a 58-year-old paraplegic female. She basically developed it from a car accident and developed progressive leg swelling. She has the edema due to chronic venous insufficiency and neurogenic edema. And then secondarily, she has developed lymphedema as you can see with the dorsal foot swelling she has also a positive Stemmerâs sign, she has small ulcer there and again the swelling under control is very important to decrease the drainage or the lymphorrhea in the ulcer and get it to heal.
Manual Lymphatic Drainage. This is the specific manual movement that we use along lymphatic pathways and our goal is to empty and decompress the obstructed lymph vessels. We want to use the subcutaneous lymph vessels which will just go to the superficial dermal part and use the existing anastomoses and basically get those anastomoses to widen over time, and then drain from the areas that are included. So in other words, you take areas that are already draining and you kind of do the treatment and you can actually get these little anastomotic regions to dilate, and the analogy that I use is kind of like lifting weights, you know if you lift weights, your muscle are going to get bigger. If you do the manual lymphatic drainage and try to get the small anastomotic vessel to drain more lymph fluid, your body will react in those areas to dilate, and you will feel they generally drain more fluid to this areas
Benefits of Decreasing Edema. Basically, if you decrease edema, you will increase the PO2 or the oxygen delivery to the wound. This increases a collagen cross-linking, increases angiogenesis, increasing epithelialization, improves neutrophil function. Remember that the super oxide dismutase requires oxygen in order to function. So, neutrophils can ingest bacteria, but if you do not have the oxidated burst, then you cannot kill the bacteria so you got to have oxygen to do it, and having the increased oxygen therefore improves resistance to infection. So we are now going to start over compression things and I really think that this is very important because I want to make sure we emphasize importance of what we call short-stretch compression, and why it is very important for many types of the swelling and it is the safer and smarter type of compression.
The Laplace mathematical formula basically defines the relationship between pressure, the number of layers of your bandage, the tension applied, and the radius of the limb. And basically what it tell us is that the smaller the limb is, the more pressure that you are going to have. So if you take a bandage and put it on a limb that has normal geometry, since the ankles are smallest, you are going to have higher pressure there automatically. So you are kind of already achieving gradient compression by a putting the bandage on. Also, if you increase the number of layers, then obviously you are going to increase the compression in that area. And then of course the tension in which you apply the bandage is also important
Classic contraindication for compression are arterial disease with an ABI below 0.8, cardiac edema or edema due to congestive heart failure, anyone who has an active infections or people with a malignant lymphedema. What you will find is that using the short-stretch bandages however, in some cases and under close supervision, and with highly trained therapist that you can use these bandages somewhat with arterial disease, somewhat with cardiac edema, and somewhat with infections in order to help the patients heal quicker. This is something that is not widely accepted. It is controversial but there are a lot of very smart doctors out there who are doing this and we found in our clinic that in some cases, this can be done safely and improve the patient outcomes
Compression Safety Guidelines. If the patients are developing pain in the leg, if they have paresthesias, which comes from the lack of neurotransmitter flow to the neurons due to compression, decrease capillary return, visible skin trauma or you know the one turning dark, then you definitely need to remove the compression. It all comes down to reassessment and using lots of padding allowing you to use compression safely. If you cannot do that, then you should not be putting compression on the patient.
There are lots of benefits of compression. You can increase the cardiac preload and by increasing the pressure going into the heart, it can increase the cardiac output by about 5%. Also, it is important to remember that laying down, levels compression of only about 10 mm are needed to reduce swelling and basically if you go above 30 mm, it is really not helping any additionally you do not always need a super high level of compression to be effective which is important. In the upright position, however, due to gravity, you have leg pressures which will fluctuate from 20â100 mm due to the calf muscles contracting, gravity and the effects of the bandage.
Compression bandaging types. Short-stretch bandages such as Comprilan or LowPress have less than 70% extension. Medium stretch such as Coban wraps have 70-140% extension and then the long-stretch such as Ace wraps have greater than 140% extension, and we really want to kind of focus on teaching you about some of these different types and why they are important.
Multilayer compression wraps basically consist of four layers of weak elastic bandages. The second layer is kind of a short-stretch and does not stretch very much and the third layer is a medium-stretch which has a little bit more of active compression and basically together, this is to give some padding and to provide a certain level of compression around 30-40 mm while the patient is resting and also to have some inelasticity such that when the patientâs legs try to expand and the compression goes up. These all required trained technicians to put them on. They are very useful in the clinic and they are very useful to use over wounds that are draining and over dressings.
Bandages such as short-stretch require specific training and you can use up to 6 to 8 of these for lymphedema. Also you can use foam to break up fibrotic areas and usually use cotton batting underneath the short-stretch to put them on. This bandage stretch around 30%.
The reason the short-stretch bandages are so important is because you can really think of them as a flexible Unna boot with a low grade compression built-in. When you apply them, since they only stretch 30%, you can stretch them as much as it will stretch when you wrap them around the leg. So, once they are on, they are providing basically a low amount of resting compression on the leg. But importantly, they cannot stretch anymore, so if the patient tries to stand and the calf muscle contracts and expands against the bandage, the compression level goes up, so what you get is a bandage which has a lower level of resting compression but a higher level of working compression when the patient needs it. This is a very important concept and this is what we call smarter and safer compression. There are much different ways to overlap and basically if you overlap the bands 33%, then you get basically 2 layers of the short-stretch. And if you overlap it 50%, you get 3 layers. Most of these bandages provide slightly less active compression in a four-layer system. I kind of think of the short-stretch you can put on in a 20-30, it is almost impossible to get higher than that with 2 layers and the multilayer however, you can get usually up to 40 mm if you put it on tight. Then I see about short-stretch too is that you can put it on even more easily. So if you wanted to put it on a bandage that was 8-15 mm compression bandage for instance, you can actually do it if you are trained and you know what you are doing and how do you experience.
Ok, to explain this a little bit better, we will take a picture on the left-hand side. At rest, you have the muscle, then the lymphatics and the skin and then you have the compression. Now what happens when the calf muscle contracts, in the middle, we have the elastic bandage. When the calf muscle contracts, it expands. The lymphatics are then squeezed underneath the skin by the elastic bandage. But the elastic bandage if you can remember can stretch many times its length, so it still has the ability to stretch more. So when the calf muscle contracts, it is going to continue stretching because it has more stretch left in it. This is going to result in a lower working pressure than you would get with an inelastic bandage which you can see on the right-hand side. This bandage has already been stretched as much as it will stretch when you put it on. So, when the calf muscle contracts, it basically becomes like an Unna boot and the compression level goes way up. And this is why I love the short-stretch bandages so much because they are flexible, like to go on the limb, but at the same time they can provide much higher working pressures with someone who has an active calf muscle pump.
So edema will improve the tissue gas exchange, increasing the oxygen delivery to the tissues, improves your acid-base balance, and it will improve the bacterial dynamics and the ability to kill bacteria because you have more oxygen which as you know, oxygen is required for the neutrophils to kill the bacteria, and it will also improve the cellular transport.
I want you to avoid the compression myths. The first is that you cannot put a compression on a patient with cellulitis. There are some practitioners who think that this is the case, and yet, when you think about it, the bacteria replicate and they propagate through the interstitial fluid, which is like a culture medium. Also, there are there fewer white blood cells in the interstitium and there is less PO2 delivery to fight the infection if you have edematous leg. So if you have the patient who is already on antibiotics, and therefore, when you squeeze them, you are not going to be pushing any bacteria into the blood stream, then use of monitored compression can reduce the treatment times and reduce the severity of the patients with cellulitis. I have seen many patients kept in the hospital for even 9 days because of simple cellulitis and yet they did nothing to put compression on the limb. I really believe that if the patient has been kept on antibiotics for 24 hours and then use some supervised compression using short-stretch bandages, then they might have gotten the patient out of the hospital much quicker.
The next thing is congestive heart failure. In someone who has heart failure, we have to avoid fluid shifts, in other words, avoid moving large amounts of fluid back into the blood stream. It is true that the legs are in some ways are reservoir for the fluid in which case, though we do not want the legs to get so swollen that they would rupture and open up in the wounds. So using a short-stretch type of compression on a patient with congestive heart failure and monitoring the patient closely for signs of breathing problems, and using a trained therapist, you can actually slowly reduce the swelling in the legs, get the swelling under control, and as we discussed, you can increase the cardiac output.
The next is peripheral vascular disease. Yes it is true that someone who has ABI of less than 0.8, you do not want to be putting 40 or 50 mm compression. But what about 8-15 mm? What about 15-20? There actually is probably a range here that is safe to use. If you have a patient who has mild or moderate peripheral arterial disease, I think you probably can use a short-stretch bandage with a trained therapist and safely reduce the swelling in the patient. A perfect example would be taking a patient who is diabetic and has some swelling and putting a Jobst stocking on them. The stockings have 8-15 mm of compression. They are not going to hurt the patient and yet reducing the swelling can prevent them from getting wounds and as we discussed before with this cellulitic, it can help prevent infections. That also goes for diabetes, we just covered this.
Okay so I want you to use smart compression. Use short-stretch bandages and avoid long-stretch bandages. Ace bandages have no place in compression therapy. Let me repeat this, Ace bandages have no place in compression therapy. They stretch 3x their length. They have a horrible spring constant. Basically, you put them on the leg, you can put them on too tight, and then within 6 hours, the bandage has fallen off, and they basically are worthless. I also want you to remember pad - pad â pad!! Padding is very important in order to prevent pressure wounds over places like the malleoli and other pressure points. And I want you to avoid the compression myths. I want you to start thinking about short-stretch and thinking about using compressions safely.
Maintenance compression. Compression stockings such as from Juzo, Jobst, Sigvarus, and Medi-Van can be used. Also, I want you to remember the short-stretch bandages by Jobst, and I also want you to remember inelastic bandage such as by Circaid, also short-stretch basic compression garments such as Farrow Wrap which I invented. My company Farrow Medical Innovations distributes this and this basically is a garment that is worn on the limb and is based upon the similar amount of compression that is two-layers of short-stretch. Nighttime garments for lymphedema. I only recommend this if the limb is swollen at night. If your limb is not swollen at night, then you do not need to wear a nighttime garment. Also, intermittent pneumatic compression. Intermittent pneumatic compression pumps for lymphedema are usually only if the patientâs lymphedema is not controlled using the manual lymphatic drainage and then the short-stretch wraps to get it down. If after that period, the patient goes into compression stocking and the limbs start re-swelling, then you can consider intermittent pneumatic compression. If you do get a pump for your patient and recommend it, do not get a pump for a lymphedema patient unless it has at least 3 chambers. Preferably 8 chambers if you are using it for lymphedema in the lower extremity. If you want to use portable intermittent pneumatic compression pump for someone with venous stasis as her primary diagnosis who has some secondary lymphedema, then I can fully support this. There are a number of portable intermittent pneumatic compression devices which are coming on the market and they are very exciting. They have a very good option for people with chronic venous ulcerations of greater than 6 months duration. One type of product is made by DVT Care which is based in Michigan and weighs less than 2 pounds, and the battery would last over 10 hours on the patient. So there are lots of new and exciting things going on there.
Okay, that concludes our presentation. If you have any questions, please feel free to contact me at email@example.com and I will do the best I can to answer them. Thank you very much.
|Goals and Objectives|
After participating in this activity, the viewer should be better able to:
1. Understand the anatomy and pathophysiology of the lymphatic system
2. Recognize primary
Estimated time to complete this activity is 65 minutes.
Physicians, diabetes educators, and other health care professionals who treat patients with diabetes.
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