Hi, good evening. My name is Richard Zell. I'm an orthopedic surgeon in Ballier, Maryland, and I'm one of the co-chairs of the LA Health Education Committee. My co-chair is Tracy Herrick from Reno, Nevada. We're very happy to present our third installment of the Putting It Into Practice webinar, and we're going to focus tonight on the complex topic of diabetic management of the foot. We have a great multidisciplinary faculty that will share their insights on Charcot, diabetic wound care, and the musculoskeletal approaches to diabetes. So I'm going to have Tracy introduce our first speaker. Hello, thanks everyone for being here. It is my pleasure to introduce Cheyenne Behar. She's with the Foot and Ankle Service at University of California, Davis School of Medicine in Sacramento, California. She completed a bachelor's degree at UCLA in international development and later her BS and MS in nursing at Salisbury University in Maryland. Her interest in the foot and ankle subspecialty began when she joined the VA San Diego Department of Orthopedic Surgery Podiatric Section in 2009. She then joined UC Davis in 2020. She provides non-operative treatment for a variety of foot and ankle complaints and supports surgeons within her department with the pre-operative and post-operative care. Thanks for that introduction, Tracy. Let me go ahead and share my screen here. Is that working? Yeah, okay. So my name is Cheyenne Behar. I am a nurse practitioner at UC Davis. It's good to be here tonight. Thanks for coming. I'm going to talk about Charcot Foot. And this presentation is intended to be a brief review of Charcot Foot, what it is, how to recognize it and how to treat it non-operatively. I have no disclosures. So first of all, what is Charcot Foot? It is a non-infectious neuroarthropathy which destroys the joints of the foot and ankle in a usually very characteristic way. It has a lot of different names, including Charcot Arthropathy, rocker bottom foot or just simply diabetic foot among others. I've heard patients call it a shark foot as well. The condition is named for Dr. Jean-Martin Charcot who was a neurologist at the Salpetriere Hospital in Paris in the 1860s. And he, when working with patients with tertiary syphilis noted a destructive process in the patient's feet which he determined was related to their neuropathic feet. And he explained this condition with a theory called neurotrophic theory. And what he attributed these changes to was altered bone nutrition caused by peripheral neuropathy. Later on in 1936, Dr. Jordan linked diabetes to peripheral neuropathy and then the rest is pretty much history. So the common thread with patients with Charcot Foot is peripheral neuropathy. In the Western world, in the U.S. diabetes is the most common cause but there are many other causes of peripheral neuropathy. You'll see the same problem with other ideologies of neuropathy. Alcoholics, people with alcohol abuse, RA, Parkinson's and then in certain parts of the developing world where it's endemic, leprosy is still a cause in places like India. And then there's idiopathic peripheral neuropathy which I've seen quite a bit as well. So why does Charcot matter? A large portion of the population is potentially affected. There's 11% of the population in 2019 that had diabetes. More and more people are being diagnosed younger and then the younger you are diagnosed the more potential there is to develop complications down the line, things like Charcot and peripheral neuropathy. It's a really disabling condition. There's difficulty with mobility and function and very low quality of life scores. There've been some studies on that and the quality of life was scored lower than a lot of other chronic illnesses. And then it also matters because with Charcot Foot there's a substantial risk of ulceration. 63% of people with Charcot Foot will develop an ulcer and then a portion of those will go on to develop an infection and be at risk for amputation. So that gets back to the disability. There's also a huge economic cost. Diabetic foot ulcers are a common cause for admission to the hospital for diabetics and that's very costly care. So how will these patients present? Some of the characteristics of the patient is they will all have neuropathy. If diabetic, it usually is a person with longstanding diabetes who will develop this, usually over 10 years. There was one small study that showed that, I have the numbers slightly wrong on the screen, but type one diabetics will develop it. They develop it more frequently, but these patients will show up in their 40s after a mean duration of having diabetes for 24 years, whereas type twos will show up after a mean duration of 13 years in their 50s, not their 60s. And then the hemoglobin A1C does not necessarily need to be sky high in a diabetic. Anything over seven pretty much puts the person at risk in the setting of peripheral neuropathy. They can present with or without pain. When present, there's kind of this paradox. It's an insensate foot, but it's a pain at the same time. So it's often described as a dull aching pain. There may or may not be a history of recent minor trauma or even a big trauma, such as an ankle fracture or an ankle sprain. And then there's also the fact that people are neuropathic and they may not know about a trauma. And then with pure Charcot arthropathy with no complicating factors, there should be no systemic symptoms. That's not to say the diabetes or other conditions wouldn't be causing that. And then men and women are represented equally with this condition. On your physical, the classic presentation is sudden onset unilateral redness, swelling, and warmth of the foot, usually in an obese patient. The patient will fail the monofilament test, meaning one or more of the nine or 10 sites that you test on the foot with a 10 gram monofilament will be insensate and their vital signs should be normal. So there are two main theories of pathogenesis for Charcot foot, neurovascular and neurotraumatic. Neurovascular goes back to Charcot's original theory of neurotrophic theory, the one about altered bone nutrition. This is a modern iteration where autonomic dysfunction, autonomic neuropathy will cause hyperemia, which is an increase in blood flow, which will then result in increased venous pressure, capillary leakage, and then the capillaries leak into the soft tissue, which causes some tissue ischemia. Then that will lead to tendon and ligament compromise, an increased bone resorption, and then ultimately instability and demineralization of the bones. The other main theory is neurotraumatic. This came about around the same time that Charcot was coming up with his theory. This was by his German contemporaries around the same time. They postulated that it was microtrauma caused by altered proprioception, which would start the whole thing in motion. The soft tissues would respond to this trauma with pro-inflammatory cells. Cytokines, which would then set off this cascade reaction, resulting ultimately in osteoplasts being activated. Then the person not being able to feel their foot would keep walking on it and it would keep the cycle going. In reality, it's likely a combination of these things. Most experts now believe it is a combination. There are multiple types of neuropathy at play here. Sensory neuropathy is the loss of predictive sensation we were talking about before. There's motor neuropathy, which results in subtle muscle imbalance and abnormal loading of the foot. That can be a factor as well. Then the autonomic neuropathy, which we already touched on, with altered blood flow and also it can affect skin thickness and integrity, which can also affect the outcome. Ultimately, these processes activate osteoclasts and they start breaking down the bone. Treatment will aim at stopping the inflammation and trauma which would otherwise keep the cycle going. There are several differentials when you see a red, warm, swollen foot. Some of those are listed here. The main ones are infectious, which could be either osteo or aseptic arthritis. If it's in a specific joint or a cellulitis, it could be a crystal disease, which is a variety of inflammatory arthritis or other inflammatory arthritis, something autoimmune, or osteoarthritis, or chronic regional pain syndrome, or even a DVT. Each of these can be differentiated by conducting further testing. In Charcot foot, there are certain characteristics. If you are to measure something like the CRP, ESR, the inflammatory markers, those should be normal unless there's a concurrent infection. The white blood cells can be normal or elevated, but in an acute process, there will be no left shift, whereas with an infection, there could be. Back to the inflammatory markers, those would be more elevated in an inflammatory arthritis, gout, infection, pretty much anything but Charcot. If there's an effusion and it's aspirated in Charcot foot, the fluid will be sterile and not have any crystals present. Another characteristic of Charcot is a temperature difference from the affected foot to the non-affected foot. Usually, it is unilateral. There are many cases when it's also bilateral. I believe it's about 30 percent of the time. But for the sake of this, it's one side to the other is a three to five degree difference. Radiographs, if this has been going on for a while, will show characteristic changes. You'll learn more about that because in the initial phase, you see no changes at all. But if it's been present a couple of months, you'll start to see these changes. Then you can differentiate it from chronic regional pain syndrome because in Charcot foot, there's no significant allodymia, hyperalgesia, vasomotor things going on, no trophic changes, muscular atrophy, nothing like that. The vital signs should be normal. Then if there's a question of a DVT, that can be ruled out, of course, with a duplex, a venous duplex. Imaging. Here are some of the characteristic X-ray changes. You can see after this has been going on outside of the brand new phase. If there's no portal of entry for infection that can be found, this pretty much points to Charcot arthropathy what you see right here. It can be differentiated from osteomyelitis. If it's osteomyelitis, sometimes in a radiograph, it'll be more localized and it'll show a definite erosion, whereas this just starts disintegrating. If there's a question of infection, you can get advanced imaging. An MRI in Charcot will show bone marrow edema, which is obviously not specific for Charcot, but is sensitive. Then there are further tests you can do to differentiate the two. Generally, on the MRI, the bone marrow edema will be more diffuse in Charcot neuropathy, the entire midfoot, the entire hindfoot, something like that. Whereas in osteo, it's wherever the portal of entry is, and it starts one bone and keeps going from there. A PET scan can be used when an MRI is contraindicated, and then there's a test which you can use to differentiate between osteo and Charcot if one or both are present, and get a sense for which of those processes going on. It's a tagged white blood cell bone scan, and you essentially remove white blood cells from the patient, tag them with two different tracers, reintroduce them to the body, and then see how each of the tracers uptakes into the bone, and then the results of that would determine what's causing the symptoms. There are various ways of classifying Charcot foot. There are anatomic classifications. Then the modified Brodsky classifications from 1993 are especially useful for determining the order of prevalence that you see these things. Midfoot is very common. It's the most common at 60 percent, followed by hindfoot, ankle, calcaneus, multiple sites, and then the forefoot. It's also worth noting that this is useful in figuring out sometimes when it's more serious, the ankle and the hindfoot tend to lead to more instability. Here are a couple of radiographs we have. On the left, this is an anatomic classification, so you have the midfoot involved here, the hindfoot involved on the right. They're in different stages, but you can see just two of the different regions here. Substantial collapse here of the hindfoot. Then there's also radiographic classification. Then this is something that we, as people who provide non-operative treatment should really pay attention to. The Eichenholz stages, which were modified in 1990, are as follows. There's stage 0. When this shows up out of nowhere, you have a swollen, red, warm foot all of a sudden. There's no radiographic changes. You will see changes on MRI and possibly some stress fracture lines, but no collapse at this point. Stage 1, the bones start to fragment. Things are still red and swollen and warm, and everything just starts falling apart. Stage 2, the redness and swelling starts to go down a little bit. The bones begin to heal. Then stage 3, it gets back to a stable point, and the redness and swelling are gone, and the bone just slowly remodels. At this point, it's considered stable. Here are some examples of some of the stages. Stage 1 shows some fragmentation going on here. Stage 2, it starts to grow back together. Then these are some more stable feet over here. You can tell because it looks like a healed bone, everything is just in the wrong place. Then this is the same patient I saw. He has a little bit of it in the midfoot or the forefoot right here, in the midfoot. It started out stage 0, not showing much, and then he has here some osteopenia and some breakdown of the first TMT. Then obviously, he had other stuff going on as well. The goals of treatment are to make the foot structurally stable so they can get around and be functional, prevent ulceration because we know that that leads down a path we don't want to go down, preserve a plantigrade foot. What that means is that the skin that you're walking on belongs on the bottom of the foot. The mainstay of non-operative treatment, especially in this acute phase, is offloading the Charcot foot. The gold standard is considered to be a total contact cast. It's applied during the acute phase, changed frequently at first to allow for swelling to go down, which it usually does rapidly if it's a good total contact cast and it's being effectively offloaded. That's changed every couple of weeks after the swelling initially goes down. Then you keep doing that pretty much until you reach, I can hold stage 2, and things are looking like it's beginning to heal. While wearing a total contact cast, there are differing opinions on whether the patient should be weight-bearing. I've been told that the gold standard is not to allow weight-bearing, but we know how that goes with certain patients. One advantage of allowing patients to weight-bear is that there's less risk to developing problems with the other side, and it's easier to get compliance. Then of course, non-weight-bearing just allows everything to heal much faster. But personally, I think I would consider weight-bearing over nothing. Then the duration for total contact casting is highly variable, but pretty much you start with 8 to 12 weeks, expecting to cast it for 8 to 12 weeks until the redness, warmth, and swelling go away, and then the radiographic changes kind of halt and start improving. When there's bony consolidation, that's the point at which you would order a custom accommodative insole, which is different from a functional insole. It's custom molded to the patient's foot, shaped exactly like their foot, and often worn in diabetic or extra-depth shoes to just continue offloading that foot once it's stable. If there's ankle involvement, an AFO can be used at this point. So there are some alternatives to a total contact cast for all or part of this treatment. Usually a crow boot, which is, it looks like a big shiny black or white boot with Velcro on it that has two halves. Usually that's used after the immediate acute phase, when the patient's going to be walking around for a few months while everything is solidifying. And that's a custom-made boot that can be ordered through a prosthetist. You wear this after the swelling improves. You can also consider using an Aircast or a pneumatic walker or a CAM boot if a custom boot isn't an option. And then during the initial phase, you can consider making an instant total contact cast, which is basically a CAM boot wrapped in something that's difficult to take off. You can use Coban or fiberglass. So that way you can take it off for visits, but it's easier to get some compliance. And then I put post-op shoe better than nothing, but that's just my opinion. If the patient isn't going to wear anything else, that might just keep it from turning into a convex situation on the bottom of the foot. So medical treatment, let's see. So pretty much the easiest thing to implement here is to check the patient's vitamin D because it's often low in patients with Charcot foot. So check it. If it's low, supplement it. There are other medical options, which are not FDA approved. There's phosphonates, calcitonin. There are some potential severe side effects with the bisphosphonates. Calcitonin has fewer complications. You might have some issues with insurance coverage on these. A bone stimulator. I've also checked a couple of the insurance company guidelines and it's kind of an uphill battle from what I've gathered, but if you can get one, that may be helpful as well. And then most importantly, refer to, to manage the condition causing the neuropathy. So when is it surgical? If there's a non-healing ulcer or a bone spur sticking out, sometimes you can just refer them and the doctor will perform an exostectomy just to cut off the bone spur and kind of take away that pressure point. If there's a non-plantar grade foot where it's kind of turned on its side or things just don't look right in that way, that would be a surgical problem. If the patient's unable to function or ambulate despite the non-operative treatment or for ankles or hind feet, it's worth getting a consultation. And there are surgical options to save Charcot feet and they are worth it for certain patients, but this is, as you'll probably learn in another presentation, it can be kind of a risky endeavor. So that's my introduction to Charcot. These are my references. Thank you, Cheyenne. That was a wonderful overview. Very good. And so I think that we'll move on to Dr. Sinekor. Dr. Sinekor is a professor and director of research in the Department of Physical Therapy at High Point University in North Carolina. His research and clinical practices focuses on musculoskeletal impairments resulting from chronic metabolic diseases such as diabetes. And his clinical practice also specializes in diabetic foot care. His research has been supported by the NIH and he has many awards from the Physical Therapy Association as well as the American Diabetes Association as well as the AOFAS. We're very happy for him to share his thoughts tonight. Dr. Sinekor. Thank you. Can you hear me first? Can everyone hear me? Yes. Okay, great. And can they see the screen? Yes. Oh, major accomplishment. Okay, thank you very much. Well, thank you, Dr. Giselle for that nice introduction and inviting me to talk. I'm gonna kind of do something way out of different than what people are generally hearing, but I'm gonna wanna talk about the skeletal muscle changes that occur in some of the complications with diabetes. And I hope they have implications. I think they have implications for both the assessment of diabetic feet as well as the rehabilitation. And I'll talk a little bit more about that as we go along. So the, let's see, move along. As far as disclosures, I don't have anything, I don't have any financial interest and I received no consultative fees, but I have been blessed and I'll disclose that I've been blessed with a lot of, a number of NIH grant support to study diabetic foot disease. And specifically, I wanna, towards the end of the talk, I wanna talk about an AOFAS, an orthopedic foot and ankle foundation grant that we received back in 2017. And I'll talk about the results of that and the reference for that is in the reference section. So go along. So, yeah, I'm preaching to the choir here, but diabetic neuropathic foot disease in our new millennium, you know, it's all over the place. It's 37.3 million diabetics and increasing daily. So if you do the math and I know you can, it's 74.6 million diabetic feet. And if we get down, drill down, that's 373 million diabetic toes, give or take some that are still, that are all intact. And of course we know that there's a good number of them that may not be intact. So what I wanna talk to you about just quickly is some diabetic complications and there's a variety of them. We all see a variety of these complications that are known to occur in people with diabetes, longstanding chronic diabetes. But specifically, I wanna tell you about peripheral neuropathy and some of the changes in skeletal muscles that go on as well as diabetic nephropathy, also known as chronic kidney disease. Those two together, I think really impacted diabetic foot. So I wanted to sort of emphasize both of those changes that occur concurrently in people with diabetes. So I like to think of diabetic foot disease and all of the complications that we see, including amputations, ulcers, fractures, arthropathy, infections that Dr. Behar was talking about really come from three different pathogens, what I call the pathogens, neuropathy, vasculopathy, and the dreaded foot deformity. And the dreaded foot deformity of which Dr. Behar just talked about the worst, guys, is the Charcot foot. But generally what happens in that Charcot foot and in diabetic treatment in general is that the intrinsic and extrinsic muscles and the entire muscles of the lower extremity become very sarcopenic. What does that mean? They waste away, they no longer can produce the power needed for functional activities. So that's kind of what we were gonna sort of talk about a little bit tonight, I thought I'd talk about. Of course, we all know how clinically we can assess peripheral neuropathy and hopefully we're all doing it for every single patient we see because of the prevalence of diabetes. So we can use these SEMS-Weinstein monofilaments. They're very quick, easy, reliable. The way I look at it, if I see one site that a patient can't feel on either foot, I'm gonna call that peripheral neuropathy. Why? Because I know things are gonna potentially progress quickly after that. I know the literature says, no, you have to have three sites or greater. I think I'm really ultra conservative in the sense that only one site will do it for me. The other way we can do it is using this vibration perception threshold. It's a really reliable, quick, easy test. Just put this sort of probe onto the big toe, vibrate it. And if they can't feel 25 volts, then they have peripheral neuropathy. And again, sensory neuropathy, these are really pretty easy tests that we all use. I really wanna quickly review because I know it's not in our nature necessarily, those that deal with the foot, but I wanna review the stages of chronic kidney disease. And we all know, we all learn there's five stages of chronic kidney disease. From stage one, which is essentially no renal dysfunction all the way down to stage five or end stage renal disease. And that's when people require either maintenance hemodialysis or they're requiring a renal transplant in order to continue. But there's a lot in between that happens with the foot. And so we were gonna try to put, I'm gonna try to put the perspective of diabetic foot disease in some of the skeletal muscle complications fitting into this role of not only peripheral neuropathy, which occurs as a complication, but chronic kidney disease as occurs as a complication. All right, so if you go through the bother of looking at people with chronic kidney disease from stage one to stage five, what I'm struck with is that the presence and prevalence of peripheral neuropathy using either of those tests that we do increases dramatically. So about 40% of the people or so in stage one have evidence of peripheral neuropathy, but when they get to stage four and five, just about every one of these people have. So prevalence of peripheral neuropathy increases similarly and directly with the prevalence of chronic kidney disease. And that's sort of a huge take home. Now, the other thing that we have to worry about with these skeletal muscles of the lower extremity in people with diabetes is when their chronic kidney disease becomes so bad that their kidneys are no longer filtering and they become what's called uremic. And uremic can be defined as they have too much nitrogenous waste in their bloodstreams. And you can see that the percentage of uremia in people with diabetic kidney disease really increases dramatically and that defines stage three of chronic kidney disease. So they become uremic in stage three. A portion of them will become uremic in stage two, but far less. Generally normal kidney function in stage one, there's no problem with uremia. By stage four and five, that defines their chronic renal disease. Okay, so keeping those things in mind, what we know then if people are uremic, we wanted to know if they develop muscle function deficits or they become sarcopenic, or in which case they develop a myopathy along with the motor neuropathy that can occur in people with peripheral neuropathy. So we can do tests to find out if the patients are their lower extremity muscles are neuropathic as well as myopathic and due to the uremia. So we can use isokinetic dynamometry like for the knee extensors or the ankle plantar flexors, sort of the important anti-gravity muscles, if you will, and find out if they're not producing enough power in order to perform functional activities. Now, we've gone through the idea using these isokinetic dynamometers for the knee extensors and finding out, is there a value that sort of says, yes, they're uremic and they're weak, or they have power deficits. And yeah, we can come out using knee joint extensors, torque at 60 degrees per second. If they can't produce a force or strength of an 89 foot pounds, they're definitely gonna have this myopathic uremic myopathy. Similarly, with the ankle joint plantar flexors isometric, we can do the same thing. We can get an ROC and we can look at a cutoff value and we can come up with a value. And I've come up and we haven't published this yet, but it's about 46 foot pounds. They can't produce at least 46 foot pounds. They're weak and they're gonna have problems with their function. All right, so that's fun, for people who are interested in research, you got to show some data, but in clinical practice, how do we know that these people have a uremic myopathy as well as a peripheral neuropathy? We perform functional tests of lower extremity. The ones that I like to use are, can they climb stairs and how fast can they climb a flight of stairs? Can they get out of a chair that's 18 inches tall? This is what physical therapists do. And you can see there's weakness if they're delayed or they can't get out of a chair. And we like to use the bilateral or unilateral heel rise test as well. And we'll talk more about those specifically, what they look like in people with peripheral neuropathy as well as with uremic myopathy. So these tests are really simple to do. I mean, all they take is some stairs, a chair kind of thing. We do them in the office all the time. We ask their body weight so we can get a force. We get a vertical distance, how much they increase in terms of vertical distance and time among these things. And we can come out with an estimate of power value based on these very, very simple kind of tests. When we do that in a large number of subjects, this is about 60 or 70 subjects that I'm showing you, in stair power. And I plotted their stair power in watts on the left side of the screen against their stage of chronic kidney disease. And then their chair rise power on the right here in terms of their stage of chronic kidney disease. And you can see there's a rapid drop off in stair power and chair rise power from stage one, no disease to even early stage two. This is in the major muscle groups like the hip extensors and the chair power for the knee extensors kind of thing. But you can see in stage two, there's a drop off rapidly of about 20, 25%, even in stage two. When people get into stage four and five of kidney disease with diabetic peripheral neuropathy as well, now they're almost 45% down compared to stage one in both their powers. So they're losing power in their muscles really, really rapidly. And that's something that we need to concern about. We can come up with values that we did the same thing. For the foot and ankle, the test that we probably all use in our offices is either a bilateral or unilateral heel rise task. And this is a really important one because it tests probably the most important, the ankle plantar flexors as a predominant muscle. And seeing if people can raise up using both legs or even one leg as they do it. And if they don't, what kind of difficulties do they have in doing that? We've looked at this sort of using kinematics as well as clinical tests of heel rise. And you can see on the left, that's kind of what we would expect to see in a normal, healthy individual, young individual, be able to fully sort of heel rise off the ground. This is a person maybe in stage one. You can see that it gets up pretty high and it looks pretty good. By stage three, it looks pretty bad. They can't even get their heel just a little bit off the ground. They can't fully raise up the heel. And in stage four or five, that's downright ugly. And they can't get it. And actually we see a little break between the high foot and the mid foot that we see going on. So that Charcot foot has developed in that particular foot. So knowing the stage, as well as the stage of chronic kidney disease, as well as the evidence of peripheral neuropathy, are really important sort of tasks that we need to assess for. All right, these are just kinematics here. I'm just gonna show you if it'll, hopefully it'll play. And you can see, this is pretty normal foot. You can see the right foot going up a little bit and the heel gets off the ground pretty well. So that's if you were doing some research at it, we can see and mark how high it goes up. Let me just show you what a not so nice and involved one looks like. And you can see it raises up a little bit less. Can you all see that hopefully? And then actually we see that separation between the hind foot and the mid foot in terms of those bones. And that's not a good thing. So those muscles are so weak, the power is really reduced. So that's something we need to sort of address. Oop, let's see if I can stop it. All right, this is a real clinical patient. What you would see, we asked them to do a bilateral heel rise. This is in a 49 year old individual who's got diabetes, peripheral neuropathy. And he is in stage two or early stage three of chronic kidney disease. And you can see, he can barely get his heel off. This is what it looks like from a lateral view looking at that. And yeah, it doesn't look very good. So these are clinical things that we can figure out really pretty rapidly using our simple clinical tests and see how much weakness the individuals might have. All right, let's stop this. All right, so when we look at how many people have dynopenia or power deficits across the stages of diabetes, you can see that nearly 50% by stage three are gonna have some power deficits in heel rise or in using dynamometry. Also in stage two, more than a third of those individuals are gonna be rather weak and they're not gonna be able to do a bilateral and certainly a unilateral heel rise because of the power deficits that we see in the lower extremity. All right, I'm just gonna sort of switch gears a little bit now and maybe come up with a reason why does this happen? Well, we, a graduate student and I took some muscle biopsies of a quadriceps femoris in people with chronic, with diabetes, peripheral neuropathy and different stages of chronic kidney disease. So we took out there a little piece of their quadriceps muscle, we isolated the stem cells which are satellite cells in muscles and then we cultured those satellite cells in really good medium so that the muscles would grow. In stage one on the far left, these are muscles from stage one, the blue dots that you're looking at, those are nuclei. Those are those satellite cells and nuclei that will form new muscle cells. And in the red bands here, those are new myotubes that are forming and you can see it's a robust formation from the satellite cells and form new myotubes within three to four days, very, very quickly. In stage three individuals, we still see some myotube formation, but it's mostly impaired. And so they do form myotubes, it takes a little longer, five to six days to get this kind of development, but you can see that those satellite cells do work and be able to form new muscle cells. By the time stage five comes along and a person's in stage five, those satellite cells, those muscle stem cells, they don't work nearly as well in culture. When you try to culture them, they form really thin myotubes, they're not as contractile, they're not producing as much power in those individuals. So this is a problem due to the chronic kidney disease. So we've kind of sort of said the satellite cells are the problem with this in regenerating new muscle. Now, to get to the AOFAS grant that we received, we wanted to look at some of the changes in the skeletal muscles that occur in people who were metabolically normal. In other words, didn't have diabetes, didn't have peripheral neuropathy. And these are muscles that we sampled from surgery, people who are having either, in this case, the MNC person, he was having, or I think it was he, had a traumatic trans-tibial amputation. Whereas in the DPN, the diabetic peripheral neuropathy group, moderate and severe, these are people who had a trans-tibial amputation. And we sampled a piece of the muscle from the medial gastrocnemius in the abductor hallucis muscle. We took right during surgery, during the amputations, we were able to harvest some of these muscles. So what you're looking at here is on the left side, you're looking at the medial gastrocnemius and the abductor hallucis in the metabolically normal or unimpaired individual. And it all looks really good. The muscles all look about the same size. There's a good amount of type one and type two muscle fibers, the fast powerful, as well as the slow twitch. But in the moderate DPN, even up into the calf muscles, the medial gastrocnemius, the muscles are smaller. There's a lot more type two fast twitch muscle fibers that are going on. In the abductor hallucis, the intrinsic muscles, they're totally looking really impaired. We don't see good muscle fibers at all inside them. In fact, when we do see them, and even in the severe diabetic peripheral neuropathy and the abductor hallucis, we start to seeing muscles that regenerate very embryonically, very rudimentary in terms of forming their myosin heavy chain components, which allow for power to be executed. In the next slide, you can see the same kind of idea that I showed you in the previous one for the quadriceps. These are the metabolically normal ones. This time, the myotubes are in green. The satellite cells and the nuclei are in blue here. You can see in the normal individuals, they form robust myotubes, but in the diabetic peripheral neuropathy group, even in the media of gastrocnemius, it's starting to look like there's a little bit more impaired trying to grow these muscles. Certainly in the intrinsic muscles where the neuropathy takes the most effect, it's starting to be well impaired. And in severe diabetic peripheral neuropathy, again, these satellite cells do not make and regenerate new muscle. So we're having a problem, not only with the CKD or the chronic kidney disease and the aremic myopathy, but we're coming in now on top of it with a diabetic peripheral neuropathy. And this creates for a real difficult problem for patients and their feet. All right, I'm telling you a lot of bad news, but what can we do about good news? Well, the good news is, I think is, we might be able to intervene early in people, let's say stage two and stage three, and salvage these muscles. The way we can do it, probably from a rehabilitative point of view, is getting these people identified and putting them on some resistance training. High intensity resistance training, doesn't have to be done daily, but at least once, twice per week is potentially gonna save those muscles. And it might even improve their kidney function and might salvage them. So the idea, we need to start developing people early on in their disease and trying to catch them. So I'm gonna stop here and sort of say, I think we should, from a clinical point of view, we should continue to assess and document the presence of peripheral myopathy in our patients, but also their stage of CKD. We need to pay more attention to their chronic kidney disease and diabetic neuropathy. We can use dynamometry tests or clinical tests to characterize. We continue to use the bilateral and unilateral heel rise and see what kind of power deficits the extrinsics have in terms of being able to provide some heavy resistance training kind of thing. But we really need to start early in the disease. We need to start people in their stage two and early stage three to make any difference to prevent some of those bad deformities and maintain function of the foot. Okay, I'm gonna stop here and thank you for listening. Thank you, Dr. Zinogre, that was excellent. So I think we'll get going right into Lynn. I'll let you go. All right, so next up is Lynn Johnson. She has been a nurse since 1996 and is certified in wound ostomy incontinence. As a nurse practitioner, she helped develop a multidisciplinary limb preservation service and has managed diabetic foot patients, both in and outpatient. Thank you, Lynn, for being here. Hi, well, I gotta get my notes up. Got my tech support here. As Tracey said, I'm a nurse practitioner specializing in wound care. I've been in wound care now for the past 19 years, seeing tons of changes in the modalities in that time. Currently, I'm working at a hospital-based outpatient wound clinic in Reno, Nevada. In 2014, I helped to establish our limb preservation service, which over the years has grown and has become an integral part of our wound care program. I have no disclosures of the challenge. As all of you know, these ulcers can be extremely challenging. Typically, they present on the plantar aspect of the foot. These patients don't have all the sensations, so they don't have any problem walking on these ulcers all day long. As alluded to in the previous two presentations, these patients are prone to deformities such as hammer toes, prominent metatarsal heads, and charcoal deformities. They get these weird prominences. They get calluses, which develop into ulcers, and these horrible wounds. These wounds seem to be heavily draining, which causes a lot of maceration. They also are prone to infections. To top it all off, a lot of these patients have very poor lower extremity perfusion and therefore very poor healing potential. As with everything in health care, start with the history. After you get a good history, then hone in on the history of the ulcer itself. How long has the ulcer been present? How did it start? Has a patient had previous ulcers or amputations? If so, they're much more prone to have more. Are they offloading the foot? Can they offload the foot? What kind of work do they do? Do they have to wear certain types of footwear for their jobs? Do they have to stand a lot or walk a lot? What can really be eye-opening is to ask the patient what they've been doing to treat the wound. A lot of these patients are doing exactly what they shouldn't be doing, such as pouring hydrogen peroxide or alcohol on the wound on a daily basis, or soaking their feet in epsom salts, which believe it or not, still a lot of doctors are telling them to do. Assessing the foot, start off by assessing for those structural changes. Do a sensation test with a monofilament. Feel the foot. Look for those hot spots or those cold spots. Assess the color. Pulses. Palpation is great, but it's very subjective. If you have a doppler available, you should always assess the pulses with that. Look for skin changes that can give you some clues as to whether or not the patient has arterial insufficiency and or venous insufficiency. Edema is a big problem with most of these patients, and they often have gait abnormalities. Diagnostics, arterial studies, the ABIs and TBIs, PPGs and TCPO2s can be helpful. Imaging. I always like to start with a three-view x-ray of the foot and hopefully with a weight-bearing view if possible. MRIs and CTs can also be helpful. If you're worried about infection, grab a culture. Always do it after you debride the wound and clean the wound. If you keep getting infections that just don't respond to antibiotics, send a piece of tissue off for culture. Inflammatory labs, CRPs, ESRs are helpful. Albumins, most dieticians don't put much stock in those these days. Referrals. Based on your assessment findings, make appropriate referrals. Send in a vascular if they require improvement in their blood flow. Orthopedics for debridement of bone, correction of some of those structural abnormalities or amputations. Infectious diseases, if IV antibiotics are indicated. Plastics for soft tissue coverage, once you get to that part of the healing where that is appropriate. If your patients are... Diabetes is really out of control, call in your endocrinologist, your diabetes education, and your dieticians. By all means, if you have a wound clinic available, refer to them. Assessing the wound. In order to track the progress of a wound, of course, we have to be able to keep track of assessment. A wound assessment includes, of course, the location of the wound, dimensions, type, and amount of drainage presence or absence of odor. You need to describe the types of tissue at the base of a wound. Obviously, if you see bone, you want to be suspicious for osteomyelitis. The peri-wound of the wound will tell you an awful lot about the condition of the wound. Is it macerated? That means there's too much moisture. Callus means there's too much pressure to that part of the foot. Is there erythema? An induration indicates there's probable infection. There we go. It's going crazy. Where were we? Photos and measurements should be done pre and post debridement. Thankfully, with digital photography, this has gotten much easier. We want to document at least weekly so that we can track our progress. Treatment of the diabetic foot. Start off with debridement. Select appropriate topical therapy or dressings. Control infection always. Consider using some adjunctive therapies. We'll talk about those later. Biologics are coming on strong these days, are being used much, much more. Offloading is always a key element to treating a diabetic foot. Debridement. Debridement is an essential component of wound care, of course. Necrotic tissue increases the risk for infection. It also inhibits proliferation of new tissue. We've got to get that tissue, that necrotic tissue, out of the wound before we can expect any healing. Typically, we think of surgical or excisional debridement when we think of debridement, but there are many other types that are widely used. Enzymatic debridement with collagenase being the primary enzymatic debrider. It's a prescriptive product. It's been around forever. It works by degrading excess collagen in the wound. Medical-grade honey dressings can be considered enzymatic. This is manuka honey, not just regular table honey, but it also works by degrading necrotic tissue. Autolytic debridement is the most conservative and probably the least painful of all types of debridement. It utilizes the body's own phagocytic cells and proteolytic enzymes to break down necrotic tissue. Dressings that promote autolytic debridement include hydrocolloids, caudexamer iodine, and again, medical-grade honey dressings. Sorry, chemical debridement. I know Daikin's has gotten a bad rap over the past few years, but I still like Daikin's for those really smelly, contaminated wounds. Never stronger than quarter strength and only used for five to seven days, sometimes 10 at a stretch. It's just dilute bleach, but it does work very well. Acetic acid or vinegar is useful for treating pseudomonas topically, usually diluted to 50-50 strength. Mechanical debridement, wet-to-dries, really not best practice, but still widely used. I don't know if we'll ever see it go away completely, but it's here. Other mechanical debridement methods are pulsal botch and ultrasonic mist. Not seeing those used quite as much these days. The patient shows up with a red-hot swollen foot with advancing cellulitis, purulent drainage, odor. You need to get them into the OR ASAP for surgical IAD and IV antibiotics. A lot of surgeons choose to do a staged approach with serial debridements. They will also often use adjunctive therapies such as the wound vac or some of the newer skin substitute products, which they will use often in conjunction with the vac or so into the wound itself. Excisional debridement at the bedside is what we do mostly in the clinic. It's not only important to remove all the non-viable tissue you can from the wound bed, but to pay attention to the peri-wound as well. You need to read that callus down to skin level, and you need to open up those rolled wound edges. Don't be afraid to make them bleed. Bleeding starts that inflammatory process and can often stimulate a wound out of a senescent phase into inflammatory and proliferative phases. Probably one of the biggest mistakes newer clinicians make is they don't debride aggressively enough. Probably because they're worried about the bleeding. As my mentor once told me, he says all bleeding eventually comes to an end, and he is right. Debridement should be done at least weekly until the wound bed is clean and the wound is progressing steadily. Even though a lot of these patients don't have much sensation, we always use topical lidocaine prior to debridement. We do 2% lidocaine, leave it on for 5 to 10 minutes before we start debriding. If that's not sufficient to manage their pain, we'll sometimes use subcutaneous lidocaine, 2% with or without epinephrine. The patient presents with dry, stable eschar, meaning there is no drainage, there's no fluctuance, there's no bogginess, no radiating erythema. Leave it alone. Typically, this is due to arterial insufficiency, and the blood flow issue needs to be addressed first. Once that is addressed, then you can start debriding or just let the wound go on to progress on its own, which it will. Now we need to select our dressings. For some reason, this is very intimidating to people. We have known since the 60s that wounds need to be moist in order for optimal wound healing to occur. Not only does it need to be moist, but it needs to be normal body temperature and protected from trauma and infection. Advanced wound care dressings are designed to do just that. They decrease healing times and reduce costs. To figure out what kind of dressing you need, you just need to know these three things. If the wound is wet or highly exudative, select dressings that absorb. If the wound is dry, which is not very common in diabetic foot ulcers, but it happens, you want to select dressings that hydrate the wound bed. If it's just right, keep doing what you're doing. Dressings that absorb for highly exudating wounds include alginates, which are made from sea weeds, hydrofibers, which are synthetic absorptive dressings, foams. Some of the newer foam dressings absorb incredible amounts of drainage. Gauze can be considered as absorptive, but not your best choice. All of these dressings come in antimicrobial forms as well, such as silvers, medical honey, and codexamariodines. For wounds without so much drainage, you want to choose dressings that hydrate the wound bed. Hydrogels, honey dressings, again manuka honey, hydrocolloids for shallow wounds, or wet to dries. Again, not my favorite, but it's still out there. These are also available in antimicrobial forms. All of these products you want to be able to leave in place for three to seven days. We have found that changing a dressing daily or twice a day is actually detrimental to wound healing. I should have added on here collagen, which is really helpful for increasing granulation in wounds that are clean. So that's one of the dressings you might add once the wound has progressed to a certain point. Advanced products. These are just flooding the market right now. Skin substitutes. The AHRQ just recently published some data identifying 76 commercially available skin substitutes for the treatment of chronic wounds. Some of these have been around for a long time, such as the animal tissue products made from porcine bladder or intestines. Donated human dermis. These are products such as apograph or dermagraph. They've been around for at least 20 years. Coming on strong these days are the amniotic products made from human placental membrane. Not only the membrane, but the cord. Seeing tons of products come out and they are very effective. All of these products are intended to stimulate the host to regenerate lost tissue and replace the wound with functional tissue or functional skin. Not just skin or not just scar formation as you see with regular healing. Most insurance companies will require that you try traditional wound care for at least 30 days before they'll authorize payment for these. Adjunctive wound therapies such as negative pressure wound therapy or the VAC and hyperbaric oxygen therapy are quite common in treatment of the diabetic foot. Negative pressure wound therapy has been around a long time now and has become a staple in wound care. It is indicated for treatment of diabetic foot ulcers and tons of other wounds as well. It has been shown to accelerate wound closure by up to 40 to 50 percent. It's often used to prepare a wound bed for primary closure. We're using it now quite a bit over split thickness skin grafts to increase take of the graft. And we're seeing it used a lot over skin substitutes these days. Hyperbaric oxygen therapy is the deliverance of high 100 percent oxygen in a pressurized chamber. This serves to increase partial pressure of oxygen into all tissues of the body. It's thought to restore fibroblast growth and collagen production, decrease swelling, and improve circulation. The evidence for how effective this is in treating the diabetic foot is pretty mixed. Several of our clinics in Reno have hyperbaric chambers. We don't at this time. Offloading is critical. You cannot heal a wound when a patient is walking on it constantly. The gold standard of course is total contact casting or TCC. This works by immobilizing the foot and redistributing the forces and weight to other parts of the leg. It can increase healing tremendously with healing rates as high as almost 90 percent. A lot of, most of clinics are going to these roll-on type casts. They tend to be lighter because of the honeycomb design. They're easy to apply. There's an outer boot that you can apply to this so that the patient can walk on it. Getting patients to buy into this is the hard part because if it's on their right foot and they want to drive, they won't go for this. So your second best option is to go for a removable boot such as a Bledsoe, a Kamwalker, or a Crow boot. These, I'm sure you guys are all familiar with these. They're ski boot looking things. They do work well. If a patient wears them like they're supposed to, they work just as well as the TCC. Unfortunately, they don't always do that. The only reason they don't work as well as the total contact cast is that patients can remove them and just take a few steps, which we know turns into a lot of steps. Other offloading options include a knee scooter, which can be rented or purchased. This can be a little bit dangerous for some of our older patients or some of our less coordinated patients. A wheelchair. It'll work, but it can be pretty much, it can be a hassle for a lot of patients, but I do have patients that are willing to do it. But I do have patients that are willing to do it. Hang on. Didn't mean to do that. Technical difficulties. Anyway, if you're not seeing healing in the wound within four to six weeks, can you go back? I just want to finish up my last thought on this. Am I still on? I'll go backwards. I don't know why my thing is doing that. Okay. If a wound is not healing within four to six weeks, it's considered refractory. Ideally, you want to see 50% reduction in the size of the ulcer within four weeks. If not, you need to review the plan, regroup, refigure. In our clinic, we do limb preservation service rounds every other week where we take some of these patients that are not progressing. We bring in an orthopedic foot and ankle surgeon, orthotist, a limb preservation service nurse practitioner, a wound RN, and hopefully soon again, we will have an infectious diseases nurse practitioner. We all gather, we meet with a patient, we collaborate, we come up with a new plan, and hopefully come up with something to help the patient heal faster. No, it's not going. It truly is a team effort. As everybody knows, it is multidisciplinary. With that, I end. Thank you. Thank you, Lynn. That was really a wonderful talk and solved some of the mysteries of wound care for me. I still use wet to dry, but I'm not going to do that anymore. Thank you. Our next speaker is Dr. Joseph O'Neill. He's a proud graduate of Notre Dame. Then he went to Thomas Jefferson and Rotman in Philadelphia. After some time in Baltimore with Dr. Schoen and Dr. Guyton, he came back to Philadelphia. He's going to share his thoughts on surgical management of the diabetic Charcot ankle and foot. Dr. O'Neill, I think you're still under mute. Sorry about that. Got the video, but not the mic. But I just wanted to say thank you to everyone for joining us tonight. Hopefully, you find this helpful and valuable to your practices. As Dr. Zell mentioned, I'm an orthopedic surgeon, did my fellowship in foot and ankle surgery, and I'm now in the Philadelphia area. We'll finish this multidisciplinary panel by talking about surgical management of Charcot. Honestly, this is a topic we could spend days talking about, so we're just going to scratch the surface, just a basic introduction and hopefully leave time for questions at the end here. I don't have any conflicts of interest to disclose. I do want to send a special shout out to Dr. Lu Shon, who, as Dr. Zell mentioned, I did fellowship under, who provided some of the images that you're going to see here. As was mentioned in Cheyenne's talk at the beginning, there's two main classification systems we use when we're talking about patients with Charcot. I want to do briefly go through them again, just because I will reference them in the talk in terms of the decision-making process for how to go about treating these patients. I think anytime you have a talk about surgical management of a problem, you also need to talk about non-surgical management and also preoperative optimization. We'll briefly touch on that, although it has been briefly touched upon already. Just like Cheyenne mentioned, again, trying to be brief here, the Brodsky classification is exclusively an anatomic system. We know from that, that type 1 or involvement of the midfoot is most common, less common to have involvement of your ankle and your hind foot. You can have a combination, but that's pretty rare. It's also possible to have involvement of the forefoot, but again, pretty rare. Then we have the Eichenholz classification, which is more referring to the natural history of the disease. Stage 0, you have some joint edema, you have swelling, but generally normal radiographs. I will tell you as an orthopedic surgeon, I very rarely see patients at this point. Most of the patients are referred to me from outside institutions, and so I very rarely see patients at this stage. Honestly, I'll tell you, probably not many patients actually even present at this stage. Advanced imaging may or may not be positive, but you typically have normal radiographs. More commonly, when you're going to be seeing these patients show up in your office, is at stage 1, in the fragmentation stage. They have joint edema, but significant soft tissue swelling, oftentimes a red swollen foot can easily be mistaken for infection. And certainly there can be concurrent infection, so you do need to be aware of that possibility. And oftentimes you see destructive process on their radiographs. And then they progress to stage 2, so they start to coalesce, you have decreased swelling at this point, and you start to see some resorption of some of the smaller fragments and some coalescence of the destruction. And then finally you get stage 3, which is the consolidation phase. And by this point, most of their swelling has resolved, and you start to get some consolidation and remodeling of the destructed bone. So in terms of our goals here, no matter whether it's surgical or non-surgical, we are trying to achieve a stable foot or ankle. We are trying to avoid bony prominences, and by avoiding that, we ultimately can allow for healing of ulcers and any other associated wounds. And so just as Lynn touched on, we try to do everything we can with these patients to treat them non-surgically, because obviously surgery is a big undertaking. And so if they do have soft tissue wounds, total contact casting is generally the way I approach these patients, if at all possible, to try and get their soft tissue wounds to heal. And if we can do that, and they have a stable foot and or ankle, and we don't have any significant bony prominences, well then the goal is to get them into a customized brace with an additional customized orthotic. Now, most commonly in my practice, the brace that I typically would most commonly use is a double upright brace. And especially if there's involvement in the midfoot, as part of that brace is a steel shank that is inserted into their, that is built into their shoe, and then in combination with a customized plastazote lined orthotic insert. We obviously will also try to modify their shoes, particularly when we talk about diabetics, extra depth shoe wear is kind of the buzzword. And so if we can accomplish our goals with that treatment regimen, then that's a win. But obviously there are patients where we cannot accomplish our goals with that regimen. And so therefore surgery becomes the next step. I will tell you, it's incredibly important to have these patients prior to undertaking surgery, particularly if you're undergoing reconstructive surgery, they need to be medically optimized. Now, there are certainly gonna be cases where that's not possible. They have an acute infection and you need to get them to the operating room on a more urgent basis. But in the absence of infection, it's very important to get them medically optimized, not just their diabetic control, but as Dr. Senecor had mentioned, they oftentimes have a lot of other comorbidities at play and making sure that those are all being well-managed and as optimized as possible will only benefit the patient in the long run. And as has been mentioned in multiple talks so far in this panel, these patients oftentimes do have vascular compromise. It sometimes can be difficult to assess their vascularity in the office because they can be quite swollen. I have a very low threshold to obtaining vascular studies, usually starting with ABIs and PBRs with toe pressures, and they can be falsely elevated in diabetics. So you do need to be mindful of that. So it's very important that, again, I think you should have a low threshold to involve your vascular surgery colleagues and do everything you can to optimize their vascularity because ultimately, if they don't have good blood flow to the foot, you can perform the world's greatest surgery ever, but it will fail if they don't have good blood flow to the foot. And that's not just from a soft tissue healing perspective, but also from a bone healing standpoint. So when we talk about surgery, indications are a foot that's just not amenable to bracing. It was mentioned earlier by Cheyenne, particularly when we have Charcot in the hind foot and the ankle, it is much more common to have significant instability there that's just not going to be successfully braced. Obviously, these patients can have pain, even though a lot of them are insensate, they can still have pain, and that is a relative indication for surgery, again, if they failed appropriate non-surgical management. Timing of surgery is important. I will tell you, it's not clearly defined, although most surgeons, if you ask them, ideally would like to wait until stage three, that consolidation phase. This is primarily based on retrospective studies that have been done in the past, as well as expert opinion. There are some cases where you do have to act sooner, but if you can get a patient to stage three, I think ultimately you'll have a better outcome. Once again, we want to optimize their vascularity too, so that's got to be part of their workup. And when we talk about surgical management, I kind of break it up into three main categories. Exostectomy, or simply going in and removing bony prominences. Arthrodesis, where we're completely reconstructing the foot and performing extensive fusions. And then ultimately, amputation has to be part of the surgical discussion with these patients. So when we talk about exostectomy, what I'm referring to is basically, these patients have bony prominences that is leading to either pain and or soft tissue wounds. And so we're talking about just removing the bony prominence. These are patients that typically have a stable deformity. They obviously would have failed bracing and or orthotics. They can have open wounds at the time that you see them. And so you can consider a concurrent, obviously excision of the ulcer. And that would be done in situations where you think you have adequate soft tissue to close. Following the excision, you can also place a vac after excising the ulcer versus simply debriding the ulcer and potentially placing a wound back over that. And then performing your exostectomy through a separate incision. And the theory there would be if you're getting rid of the bony prominence, in theory, you should be able to heal the ulcer once the insult from below has been removed. Obviously, you wanna have a low threshold to perform a biopsy or culture of the bone, particularly if there is an open wound and you have concern for infection. You do need to be careful here that you don't destabilize the foot. So you wanna be aggressive, but not overly aggressive. You wanna remove enough bone that you have allowed for the overlying soft tissues to be decompressed, but not that you destabilize the foot. And you also have to be very mindful of your major ligamentous and tendinous attachments and avoiding removal of those. These patients can have variable postoperative regimens. It's all dependent on where your incisions are, where the wounds are, and whether they have wounds. But this can be a much easier recovery for a patient than a complex reconstruction. Typically, we try to err or try to make our incisions either medial or laterally, try to avoid a plantar incision when possible, but we do try to skirt the plantar aspect of the foot to get to the exostosis and then remove that prominent bone with or without. And sometimes this can be done in combination with a fusion procedure, but can also be done in isolation if the deformity is stable. So then we can move forward with talking about arthrodesis or fusion. Indications for this would be a persistent or recurrent ulceration in association with deformity in a patient who has failed an appropriate course of nonoperative management. Once again, our goals are to realign and stabilize, produce a plantigrade foot, and relieve pressure on the surrounding soft tissues. Once again, we could do a concurrent ulcer excision versus debridement in combination with this. And there are multiple ways in which we can accomplish our fusion. We can use exclusively internal fixation, exclusively external fixation, or a hybrid in which we utilize a combination of internal and external fixation. The overall goal here is to provide as rigid a construct as possible. We wanna make sure that we correct deformity here. What you're seeing here in this patient, this was a patient who had midfoot involvement who had an AD duction deformity combined with a rocker-bottom deformity through their midfoot. It's very common for these midfoot patients to have rocker-bottom deformities. And so you want to be, again, aggressive, but not overly aggressive in terms of your deformity correction. If you're doing a fusion in situ, you're really not helping that patient. So this is an example. Oftentimes your corrective osteotomies are biplanar in nature. And in this patient, they underwent a combined lateral and plantar closing wedge osteotomy. It's my opinion, and I think it's shared by the majority of individuals that a closing wedge osteotomy where you've removed bone is much more ideal than any sort of opening wedge osteotomy in these patients. And then obviously proceeding with your fusion once you've been able to correct your deformity. And so, you know, internal fixation is optimal if you can perform exclusively internal fixation. Obviously you want to, you know, the ideal patient would be someone who doesn't have any overlying soft tissue wounds and certainly no active infection. Construct options are highly variable. You can utilize constructs that are exclusively comprised of all screws. You can augment with plates. And there are intramedullary devices, whether you use rods or nails. And there are also beams and bolts, particularly for midfoot involvement. So these are two cases here depicting all screw involvement. Particularly this patient on the left is the proverbial heel with steel example where we are trying to provide as rigid and as stable of a contract as possible. The depiction on the right is someone who had more hindfoot involvement, Charcot. Obviously not as impressive of an X-ray, but certainly trying to provide maximum stability for these patients. And you can see that, especially in this patient on the right, if you can see, it's kind of the middle X-ray, so to speak. We have traversed the navicular cuneiform articulation, but not necessarily involved it in our fusion. That joint has not been prepared, so to speak. So sometimes you do need to traverse joints that you haven't necessarily prepared in order to try to get good bone stock and ultimate stability of your fusion construct. I mentioned that we can augment with plates. These are some examples of that. I think it's ideal, particularly we use plates most commonly in the midfoot. I don't typically use plates when we're dealing with Charcot in the ankle or hindfoot, but in the midfoot, it can be an option. But, and ideally a plantar based plate can be used. The reason for that is a lot of these patients have a rocker bottom deformity. And if you've done an adequate deformity correction, you've done a plantar closing wedge osteotomy. And so the plantar side is essentially what we call your tension side of the deformity. And so putting a plate on the tension side can increase the stability of your construct. So it can be a little bit footsie to do, but if you can perform it, it can be beneficial. And in addition, there's a lot, oftentimes the soft tissue coverage on the plantar side is much more adequate than dorsally or medially. And so that is another benefit of doing a more plantarly based plate construct. Oftentimes this will be augmented with three standing screws, as you can see in all of these radiographs. The radiograph on the right side depicts a medial column plate. And in certain situations that can be done, but I will say you need to be careful with using a construct like this because oftentimes the soft tissue envelope on the medial side is not as robust. And so putting a, and these plates typically, because we're trying to provide maximum stability, these plates are not necessarily what we would call low profile. And so that can add a lot of bulk to the soft tissues on the medial side of the foot and can increase your risk of wound complications and issues there. So you use them judiciously, but in certain circumstances they can be, they are called for. And then we can talk about intramedullary fixation. This is a patient who came to me from elsewhere who had had midfoot charcot that was previously attempted to be managed with the dorsal plates that ultimately failed. I revised her to essentially bolts that are inserted through the metatarsal heads. These are incredibly strong and provide excellent stability. You can see on her AP and her oblique radiograph. So she didn't completely heal her first TMT or her medial NC joint. But the nice thing with a lot of these patients and with these constructs is they don't oftentimes have a whole lot of pain, even though they may not have fused all of their joints. The most important thing for these patients is you provided them with stability and a plantigrade foot that even if maybe they didn't heal all their joints, they may not be painful. If they are painful, you've at least given them a braceable foot and the brace can oftentimes alleviate whatever discomfort they're having. And then this is a patient with more hind foot and then specifically in this case, ankle involvement, where she was managed with an intramedullary nail in combination with fusing her tail and avicular joint. And so you can see there's a variety of constructs when we talk about internal fixation. But obviously no talk about surgical management of Charcot would be complete without talking about the role of external fixation. Obviously any presence of open wound, it should be seriously considered because of the fact that any internal hardware in the setting of an open wound or in the setting of active infection is a very high risk factor for persistent infection and loss of limb. And so the external fixation devices allow us to provide stability to the foot and the ankle while minimizing the risk of hardware associated infection. External fixation can and should always be considered as an augment to internal fixation, particularly in patients with very poor bone quality, particularly your Charcot patients who have end stage renal disease. As one of my surgeons that I learned from once said that it is also veterinary medicine and that can seem a little bit crass and crude, but at the end of the day, as Lynn mentioned, unfortunately these patients aren't always compliant with what you tell them. And I try to be very frank with them in the office about their risk of loss of limb. And in a way, almost try to read them the riot act and scare them into obedience, but it doesn't always work. And so putting an external fixator on their leg, and I'll show you some pictures of what this would look like. You can see it, it is oftentimes a detractor to walking because it is very difficult to get around with an external fixation device. These can be static or dynamic. Oftentimes these are multi-planar and circular frames that are comprised of thin fine wires drilled through the foot along with half pins in the tibia, but you do need to warn patients. It is very common that these injure their other leg because they routinely bang them into their other leg. These definitely take a mental health toll on patients. These in my world, typically I leave on for a minimum of three months, but sometimes longer. And patients by the end of that time are absolutely miserable. So you do need to warn them about that. And there is a high risk of complications. So if I can get away without using it, I will, but sometimes your hands are tied. These are a couple examples of these devices. So you can see they are bulky. They look like medieval torture devices. They are not fun for the patients. They're not fun to look at and they're not fun to manage. And they're certainly not fun for a patient to have to deal with, but sometimes they're a necessary evil. But as I said, they look like a torture device. It's almost like a human hell razor around their foot. So lastly, again, amputation should always be part of the surgical discussion, particularly in patients who have significant deformity, especially in the setting of either active infection or a concurrent ulceration that did not respond to non-surgical management. This is typically reserved for patients where reconstruction is just not an option, recalcitrant infection, wounds, especially someone who has vascular compromise that is not amenable to revascularization procedures. And obviously it's a consideration for those who have failed prior arthrodesis attempts and are not good candidates for attempts at a revision or salvage arthrodesis procedure. Certainly you do not forget about the Achilles tendon in these patients. Almost all of them will need some either release or lengthening of the Achilles tendon because the vast majority of them have a contracted Achilles tendon. This will help to offload the forefoot and the forefoot and improve outcomes. And just be very mindful, these patients have as prolonged of a postoperative course as any patient that will walk into at least my clinic. I typically keep them off of foot for at least 10 to 12 weeks. And then that is followed up by progressive weight bearing in either a boot or a walking cast. So it's a very long and drawn out process, but if it means that we salvage the limb, then a lot of patients will get on board with that. But you do have to warn them, this is a very long and drawn out process and they will at times regret their decision, but ultimately our goal is to allow them to salvage their limb, give them at the very least a braceable foot and allow them to be as active as hopefully they can be. So just to rehash, your principles are first and foremost, you got to optimize these patients preoperatively for a number of reasons. Timing of surgery, if you're going to move forward in that fashion is important. Be very meticulous with your handling of the soft tissues. You want to make sure you are adequately correcting deformity. Consider the use of auto versus allograft to help fill any bone voids that may or may not result from your correction. You want rigid fixation. Do not forget about the Achilles tendon. It should be dealt with in pretty much every case you do for these patients with Charcot and very prolonged demobilization and weight bearing restrictions. So thank you for your attention. Sorry for going a little bit over. Hopefully didn't lose too many of you here. And hopefully we have time for some questions here if anyone does have any. Thanks, Dr. O'Neill. That was really a great talk. And I liked all the Hellraiser pictures too. Those were cool. I want to thank all the speakers. They were really wonderful talks and from many different perspectives. I'm not sure if we have time for questions. We're a little over, but if we can take some if we have a couple of minutes. Looks like there's one in the chat. I don't know if you guys can see that. Yep. Looks like I can handle the first two. Well, so yes, I definitely will accept a fibrous union and oftentimes you do get that. And so I met, that's what I mentioned that one who I showed who had the midfoot bolts in place. And I do try to prep the joints, but if they don't heal with a bony union, I'm not necessarily upset about it. The big goal for me is getting them a plantigrade foot that is braceable. And so they may not have pain with a fibrous union, but if they do, if you've done a good adequate deformity correction, at the very least, you can get them into a brace and or orthotic. And hopefully that will help with any residual pain that they have. And then for the second question, certainly, I am not in these patients a big fan of lengthening. I tell them specifically for the foot. I mean, you saw that one midfoot case with that biplanar osteotomy, they end up with a different, their foot is, their shoe size is gonna be different potentially. I would much rather treat that with a customized shoe lift or if they need some sort of filler in their shoe to deal with a discrepancy in their shoe size. I just think their healing rates are better with shortening than trying to do some sort of lengthening procedure. But I'm sure there's individuals out there who have a different opinion. That's just my opinion with dealing with these patients. And I do warn them, particularly if I think I do have to do a pretty significant deformity correction that they may end up with a shorter limb or a foot size discrepancy. Lynn, I don't know if you can help answer the other question about the active ulcer, but are there any options besides total contact casting? I think you're muted. I'm not very technical. TCC is the best, but if that's not an option, the boot is your next best option, but you really need to stress with that patient that they need to wear it constantly. If your foot's hitting the floor, that boot had better be under it. If that's not an option, if you have a patient that's relatively coordinated and motivated, the knee walkers work great. There is a pogo stick type thing I've seen that patients will use, but you have to be pretty coordinated to do that. I just ran over, I'm still in the office. And have you guys ever used this? My past tech just ordered this for us. It's this like offloading insole that the post-op shoe people make. They're like $20. And they have these little honeycomb things that you pick out to like offload the ulcer. And then you stick it in the, whether it's post-op shoe or boots. We have a hard time getting diabetic boots in the office. I think it's more insurance than anything, but these have been kind of a godsend lately for us. And they're fairly inexpensive and the cast techs can do it. They don't last very long. I mean, they're, you know, it's foam. So it breaks down pretty quickly, but they can, you know, kind of get gross. And while they're going through the wound changes, this works pretty well as that intermediary before they get their sort of permanent insert. I don't know if you guys ever used this in clinic, but this is sort of new to us and I like it. Any thoughts on crow boots? My orthotist always wants me to order that and the patients don't seem to tolerate them all that well. And so I often order them, but any success with them in the past? Is that towards me? Any of the panel? I don't do a whole lot of it. I typically will transit, just have them, if they need to be in a boot, just using a regular boot. I've had a couple of patients where I've done a crow just for various compliance and deformity reasons, but I don't honestly do a whole lot of it. For me, the crow boot is in place of surgery. So to me, mostly like my ankle charcoals are unstable and I'm having the discussion. So the people that I have that are in chronic crow boots are ones that are terrified of surgery and they'll do anything to avoid the risk of amputation. So they do it because the alternative is a surgery that they really want to avoid. So I don't have a lot, but again, I'm not using a crow for like a hind foot. Usually I'm usually using it for an ankle that, you know, I offer them surgery and they don't want it. Sure. Yeah, I would agree with that. All right, Dr. Sinecourt, your talk was very interesting. I was, should we be sending a lot of our diabetic patients or to a physical therapy and will most therapists want to see those patients or will insurance cover it? Yeah, I would think certainly there is. I mean, I just looked at the numbers, you know, just in passing kind of thing. And I looked at, you know, Dr. O'Neill and you are really unusual. I mean, it looks like there's only about 1,100 foot and ankle, you know, specialists, orthopedic surgeons in the nation kind of thing, you know, where there's, and again, not surgical cases, but early on kind of thing. And there's only about 18,000 podiatrists in the nation. And there's 578,000 physical therapists in the nation. So, I mean, I would think that, you know, physical therapy could be utilized in certain cases, you know, in terms of prepping for surgeries or just sort of doing things, getting people early to do some exercises and to not just stuff them into shoes, you know, but actually start using these muscles instead of just wearing these muscles, they got to start using these muscles a little bit more. So, yeah, I think, I think physical therapists should be more educated on the foot and some of the complications that we see, we can maybe have an earlier role in helping avoid these complications that we all see. Do you ever have problems getting approved by insurance just because it's not, because you're not going to see measurable improvement. And I find that in patients at this point where you're not seeing progress, right? Cause they never, it's more preventative. Do you see that or is insurance covering it? Yeah, no, insurance is a problem. I think, you know, the way that often people are going towards is let's get them early on, let's set them up and let's just see them sort of infrequently, just like somebody else with would be a regular checkup kind of thing. So in those cases, again, once they get to stage four and stage five and they've had peripheral neuropathy, these are the kinds of things that I think Dr. O'Neill and everybody's seeing in the clinics, you know? So we got to see them early on in order to have any kind of impact. Thank you. Johnny, you mentioned that you checked the temperature of the skin. Does that, do you follow the patients, you know, in your visits and take a temperature? And does that help you at all to decide when patients can get on a total contact cast or when they can, you know, progress to braces or, you know, orthotics? That's more theoretical for me because I rarely see them in stage zero. Usually it's something later on, but we do have the tool available and in addition to radiographs, that would be something that could be utilized. Usually I just kind of, you know, use my hands to see if they feel about equal. And I usually decide when patients have had enough in a total contact cast. Is there anything specific you look for on x-rays or is it just really the whole clinical picture? Coalescence or later. Take it out of the total contact cast and into an accommodative orthotic. Sure. So I just got a message from Julie, it says, we need to wrap up due to CMA criteria. So, and I guess we were more than 15 minutes over. So Tracy and I wanted to thank all the speakers. They're really wonderful talks and I learned a lot this evening and hope everybody else did and hope everybody has a nice holiday season. Thank you. Thank you. Thanks everyone. Good night.

diabetic foot ulcers

Charcot foot

management

recognizing Charcot foot

treating Charcot foot

muscle changes

complications

peripheral neuropathy

chronic kidney disease

comprehensive assessment

multidisciplinary approach

early recognition

non-operative treatment

chronic metabolic diseases