Nicholas J Bevilacqua, DPM discusses the common finding for Charcot foot as well as discusses why there is often a delay in diagnosis. Dr Bevilacqua also reviews the treatment options for both active and inactive Charcot foot.
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Male Speaker: So next topic is Charcot foot. And I think the biggest challenge with this talk was, you know, figuring out what to include in 20 minutes, but I'll do my best to focus more on the diagnosis and the treatment options and I'll try to make it sort of as clinical as possible. Learning objectives basically understand the pathogenesis because again, by understanding the causes, we can sort of help direct the treatment, identify the diagnostic sort of clinical signs and symptoms that we'll look for and goals of treatment, whether it's surgical or nonsurgical. So we hear this term differently, Charcot neuropathic osteoarthropathy. Its, you know, a traditional name. It encompasses the neuropathic component and the bone component. William Jeffcoate [phonetic] recently suggested maybe we call it neuropathic inflammatory Charcot osteoarthropathy incorporating inflammation because you'll see that this is sort of an uncontrolled inflammatory state and the Charcot being the soft tissue. But I think, you know, that's a mouthful, so most people call it Charcot foot syndrome. So really, it's categorized by varying degrees of bone and joint destruction. We think about the classic rocker bottom foot, but just understand that that's kind of late. That's sort of a misdiagnosis, that's a late deformity. Ideally, we catch these patients before they get this significant boney breakdown. Historically, named after the French neurologist, Dr. Jean-Martin Charcot, originally described encephalus 1868 in larger joints. It wasn't until 1883 where he first described it in the foot. It was linked to diabetes in 1936. And today, we know, obviously, diabetes is the most common cause because it's the most common cause of neuropathy, but really, anything that causes neuropathy, potentially you can have a patient develop a Charcot foot and we've seen it with alcohol induced neuropathy. We even described a case in a patient with HIV positive that developed Charcot foot. So there's no singular cause. I'm not going to get into too much of the details here because I think a lot is still unknown in terms of the causes of this. But you know, really it's an uncontrolled inflammatory states. So we have these patients that have neuropathy. You know, there's some sort of a trauma. Again, it could be, you know, an ankle sprain. It could be surgery. It could be gout. It could be, you know, just from walking where they get the, you know, inflammation at least of proinflammatory cytokines and then they continue to walk on it because of the neuropathies, so it becomes this sort of vicious cycle. And the inflammation releases these proinflammatory cytokines. And you know, there's different pathways that have been looked at because they're sort of involved with the osteoclastic activity. One of them is the RANKL/OPG pathway. So you get this inflammation. You get the release of these cytokines and it up-regulates or it messes with the regulation system between the two. So you get sort of unregulated RANKL, which causes the maturation of the premature osteoclast to the matured osteoclast which are responsible for, you know, boney resorption and bone breakdown. You know, there are other pathways that are being sort of looked at as potential causes of this. Clinically, you know, at times, it could be a challenge. And you know, hopefully, not for us. But you know, oftentimes, these patients present to their primary care doctor or the emergency room. And I'm sure you've seen this many of times especially, you know, when you're a resident in the hospital. They come in red hot swollen foot, ER doc, primary care doc think it's cellulitis, gives him a prescription for an antibiotic. So oftentimes it's misdiagnosed cellulitis, DVT or gout. You know, they'll treat those. You know, they'll work them up but the patients are continuing to walk. They're not thinking about Charcot. And oftentimes, there's a delay in diagnosis and it's been shown that an average is almost 30 weeks. And the longer the delay, the worse the outcome is. So whenever you see a red hot swollen foot, you know, in my opinion, it's always Charcot foot until proven otherwise. And sometimes, it's, you know, a challenge talking to the internist. You know, they're insisting that it's cellulitis, and fine. You know, we can treat the cellulitis but let's offload these patients at the same time. Let's not burn any bridges. You know, patient with diabetes and neuropathy, you know, trauma can cause Charcot. I'll treat these patients the same. If there's displacement, you know, I'll do an open reduction internal fixation and it's just closer follow-up, longer follow-up. These calcaneal insufficiency fractures, I think, in this population are really tough. I've been burned many times. You know, oftentimes if it's a smaller fracture, it doesn't involved a posterior facet of the subtalar joint. I'll just excise it and reattach Achilles. If it is larger, I'll try more of like a percutaneous approach. So again, some of the diagnosis, you know, classic rocker bottom recognize it's kind of a late deformity. We'll talk about sort of an active and inactive and we always have to think about underlying osteomyelitis. Different classification schemes, traditionally Eichenholtz. I think traditionally, it's more of a radiographic sort of progression of the deformity.
You know, they added stage zero which incorporates that red hot swollen foot, but it's kind of, you know, the early sort of bony resorption and the fragmentation and the coalescence. Dr. Freiberg and Sanders, they talked about an anatomic classification, which I think is helpful. Just recognizing which joints are involved and the percentages of the involvement. And I think recently, you know, people have questioned, you know, Eichenholtz, do we really need that. You know, how about just inactive versus active. So active being that red hot swollen foot, because you may see these patients at different points and you know, what may be acute might not be acute for them. So I always just think is it an active sort of syndrome that's happening or is it inactive. And we'll talk about some of the treatment for both scenarios. So you know, the workup for these patients, sometimes it's simple, sometimes it's not. Well, I think the diagnosis of Charcot is simple, but differentiating it, maybe they have sort of superimposed osteomyelitis, it's tough. Patient red hot swollen foot, let's say you do an x-ray. You know, if you look closely, you know, we can see little boney changes at the navicular, but let's just say that this x-ray was completely normal. You know, oftentimes, I'll consider either a bone scan or most often now, we just do an MRI because you know, it's good to reveal some of these "hidden injuries." So this patient has no boney destruction. So we consider advanced imaging and you could see that navicular lights up. And this really to me shows the patient, look, there's this underlying sort of process happening. We need to get you off the foot because oftentimes, they don't feel pain. So it's hard to convince them that, you know, something bad potentially is happening. So there is changes on MRI. Is there an open wound, no. So that's clearly Charcot foot. So we offload these patients. You know, this again is very obvious, midfoot breakdown, but you'll be surprised. You know, sometimes the radiologist will read this and cannot rule out osteomyelitis. And once they say that osteomyelitis term [phonetic], we almost have to prove to them and to the internist that there is no bone infection because infectious disease, you're going to want to put this patient on long-term antibiotics. So we'll think about, you know, there are radiographic changes. There's no wound, any sort. You know, Dr. Freiberg quote Dr. Lavery's [phonetic] study. Ninety-nine percent of these infections are going to come from an underlying ulcer. So if this patient never had an open wound and the boney destruction is in that midfoot there. You're pretty confident saying it's Charcot. But how do we determine if there is overlying osteomyelitis. Well, sometimes we combine modalities. So that patient clearly has Charcot. If you look, there is boney destruction. He does have an open wound. So again, we can consider an MRI, which isn't sort of diagnostic for infection. It's more to determine extended [phonetic] infection. You can look at some secondary signs. You combine it. You could do a tech-99 bone scan, which is very sensitive, not specific. Maybe you white blood cell labeled scan and use the two to see if, you know, there is increase. In this case, it was, which clearly does tell us that there is underlying osteomyelitis. So this is going to play a role in treatment because you're going to potentially stage the treatment. You want to, you know, aggressively remove that infected bone, maybe a packet with some antibiotic beads and you take them back at a second date, confirm the infection is gone and maybe reconstruct it at that point. So just, you know, differentiating factors between osteomyelitis and Charcot foot. I think the most common is presence of an ulcer. Obviously, very common in osteo, not common initially in Charcot. Unfortunately, when you have a deformity and there's an open wound. That's when it becomes tough. PET scan as Dr. Freiberg said, I think, you know, most hospitals, hopefully you have access to this. I think that's kind of where their future is, is heading for, you know, especially diagnosis of osteomyelitis, especially in the foot and the bones just to help differentiate treatment. So we'll just kind of use this algorithm and talk about treatment. So nonsurgical treatment options in the active Charcot foot. By far, the most important is immobilization. So we're going to use either a total contact cast or an instant total contact cast. Ideally, you get these people. I try to get them off their foot. So you know, some people put them in a total contact cast and let them walk. I mean, I just, you know, do everything I can to try to get them off, whether it's a wheelchair. Again, I know it's not practical to put these patients on crutches, but you know, the scooters. Whatever you can do just to limit the pressures on the foot. And there have been studies looking at duration. I mean, there's a study out in the U.K. which you know, was greater than six months of immobilization. But you know, Armstrong, their study showed about four months. So I tell patients to expect anywhere from four to six months to be either in this boot or cast. And really, you're just looking for resolution of those clinical signs of the active Charcot, resolution of the warmth, the swelling. You know, you can use the dermal thermometer. It's described once it's within two degrees Celsius, which is, you know, four degrees Fahrenheit, maybe a little less three-and-a-half degrees Fahrenheit. When you get them, you know, within that range to the contralateral limb, then you're confident that you can start to wean them out.
So I never do anything cold turkey. Everything is slow progression. You wean them out of the boot. You put them in good therapeutic shoes, sometimes a custom brace and I have them start walking on it. So the nonsurgical methods. We talked about offloading bisphosphonates. You know, when I was a resident, that was all the rage and you know, we would infuse these patients. You know, I had promising results, but unfortunately, it's been shown to possibly prolong the Charcot sort of process or episode. So there's really no evidence to have these patients be treated with bisphosphonates. Intranasal calcitonin work directly on that RANKL/OPG pathway, but it's off the market now. You know, there was a link to malignancy for that, so it's hard. You know, you can't get that. I think future agents are going to be more directed towards kind of those specific pathways. But really, the nonsurgical most important is immobilization and offloading. So when they have inactive, that's kind of when I take a step back and I think, alright, it's inactive, we can get them out. You know, whether you've seen the patient at this point or whether they have progressed at this point during your treatment, you ask yourself, can the deformity be accommodated. Is it stable, is it a relatively plantigrade foot. If it is, great. We put them in accommodated footwork close follow-up. If it cannot be accommodated whether there is just a boney prominence or getting impending skin breakdown or they do get skin breakdown or it's just completely unstable and we can't successfully manage these patients for the brace. You know, that's when we consider surgery. Surgery, you know, goes sort of on the simple to the complex. Oftentimes, you know, I talk about an equinus component. You know, most of these patients have equinus deformity that we're going to address. We can combine that with an exostectomy, which you know, potentially could be very useful "simple procedure." I mean, there's no such thing as a simple procedure, but at least you're not, you know, doing the big reconstruction. This is a great example, patients coalesce. It's a rigid deformity and you can see that big boney prominence medially and also plantarly. And [indecipherable] [00:12:18] show that doing exostectomies for those medial wounds do well. We have to be careful. You don't want to reset too much bone because you don't want to destabilize it. None is successful when it's under the lateral part of the foot. So I have a patient like this where the ulcer or the wound is medial. I'll sort of plane it. I'll do an exostectomy and I'll combine it with a tendo Achilles lengthening and these patients, they do well. So reconstruction, the goals are stable plantigrade foot. Again, we're not recreating the errors. They're not going to have a perfect asymmetrical foot to the opposite side. Really, the goals are prevent ulcer or augment healing and prevent ulcer recurrence. We want to try to get these patients in a off-the-shelf shoe. So when we think about reconstruction, really what we're doing is looking at the apex of deformity. We want to correct the malalignment. So that's kind of where this biplanar wedge comes in. Oftentimes, you know, this is an example of the midfoot. So you're going to take a wedge out, looking at the sagittal or that lateral x-ray, wider on the plantar aspect so we can sort of dorsiflex. You know, if they have that rocker bottom, we want to plantar flex the forefoot and they're often abducted. So we want to adduct the foot and then we take off more bone medially. And by doing this through and through, this all started with, you know, power instrumentation. I'll usually finish it with an osteotome and mallet. But by completing that through and through, we can sort of dial down the deformity. So I think of a biplanar wedge with triplanar correction. So we can address the sagittal deformity, the transverse abduction deformity and also, we can rotate it to correct that frontal plane deformity. So you want to reduce the medial column. You want to basically realign Meary's angle. That's been shown to be sort of the most important predicator of ulceration, provisionally fixated with [indecipherable] [00:14:14] guide wires, where I'm getting the x-ray in there and I'm looking at, you know, all my views to make sure I have a plantigrade foot and I've corrected Meary's angle. And then you want to think about definitive fixation. We can do this either internal or external or both. If there is an open wound, I tend to do external. If there's intact skin, I'll consider internal fixation. Traditionally, have been fraught with complications, but I think with newer devices and some changes in our thought process, you know, Sammarco [phonetic] describes it is super construct. So we sort of, you know, extend the working area of the plate. We go beyond that sort of boney, sort of dissolution and we sort of fuse joints proximal and distal to it. You can think about plantar plating and even beaming. So you know, I use these big strong heavy-duty locking plates.
I'll do an extended needle column fusion. You want to lay it before your look and you're going to lock proximal and distal to it. And you can combine that with different techniques. You can do plantar plating and medial plating. You can do beaming screws and a locking plate. You know, you really just want this super construct because oftentimes, it's a race, you know, between fixation failure and boney fusion. So external fixation, I'll just end it with this. A logical choice for Charcot, you know, in my hands, it's with an open wound. Maybe, you know, osteomyelitis that we stage the procedure, because it does allow direct access to the wound. Whether you do sort of a simple plastic surgery procedure to get immediate closure or you're going to put a wound vac on and later skin graft. You can do this all while you're sort of stabilizing the skeletal structures osseous structures. We obtain compression with a [indecipherable] [00:16:01] technique. So we just put that fine wire distal to the fusion, walk it back and turn it. You can see that video on the right here. You can see the nice wrinkles on the skin when we get compression here. And then my son -- you could prebuild these constructs -- he always checks to make sure that I followed sort of proper Ilizarov technique. So I'll just finish with a case, 43-year-old male, Charcot with result in rocker bottom foot. He's got longstanding diabetes, unstable midfoot with a history of an ulceration. And the ulceration recurred despite, you know, good accommodated footwear. So you can see that abduction deformity. Also, that sagittal plane deformity with the rocker bottom. You look at his pressure analysis there. You see that spike beneath the cuboid bone. You know, our goal is to offload the midfoot there. So we do this biplanar wedge. Again, triplanar correction fixated. In this case, open wound. So I did do external fixator. But you can see kind of before and after restoration of Meary's angle. Here, he is six months, you know, intact skin. And then when we compare before and after reconstruction, you can see right now the spike on the left and we offloaded that on the right side. So the spike was basically heel contact and tall. So we took the pressure, you know, beneath the cuboid. So take-home points, basically, Charcot foot. Sorry if I went through it pretty fast, but early diagnosis is by far the most important. Red hot swollen foot Charcot until proven otherwise. Conservative management, really focuses on offloading and immobilization and surgery for deformed foot, you know, especially for ankle. We didn't discuss ankle as much, but those are very unstable, often requiring surgery. For either impending skin breakdown of those wounds that are reluctant to heal. Thanks.