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Speaker: So this is going to be a central concept in Charcot foot. I want to briefly touch because I know you are going to have a separate lecture on differentiating osteomyelitis from Charcot. I think there is even a separate lecture on reconstruction. So I'm just going to try to do my best to highlight the important concepts that we think about. So Charcot foot, we just start off ask ourselves what's in the name and I find this interesting just because initially if you think about different -- you read about this in different papers. Sometimes it's Charcot neuropathic osteoarthropathy, which I think originally was probably the most descriptive because it mentions the neuropathic component and the bone and joint destruction, but I think sort of a better more descriptive, more recent term would be neuropathic inflammatory Charcot osteoarthropathy because it really highlights the inflammatory sort of component of this and we will talk about that or just simply Charcot foot syndrome, which I often discuss with patients. It's an inflammatory syndrome characterized by varying degrees of bone and joint destruction, progressive deformity and that's why we will talk about the importance of early diagnosis and oftentimes results in deformity. Most commonly in the mid foot where we see this classic rocker bottom foot. Why is this important? Well, quality of life is dramatically, negatively affected on these patients and I think not only the patients but also their caregivers. I mean you see these patients either in a wound care center and especially if it's complicated with an ulceration, these patients are coming in every week. Their wife, their husband is bringing them every week and it just has a very negative impact on their lifestyle. Often leads to permanent disability, premature retirement, increased morbidity, mortality and increased amputation rates. Historically, described with complications from syphilis, more recently 1936 it was related to diabetes and now we know really any situation that results in neuropathy is basically a cause for Charcot foot.
So when we think about pathophysiology, traditionally we are always taught the neurovascular and neurotraumatic theories. There is really no single pathway leading to this, it's by combination of the two. If you think just a simple sort of this vicious cycle of uncontrolled inflammation, patients has neuropathy. Maybe there is a traumatic event where it causes a release of pro-inflammatory cytokines and there is up-regulation of that which is going to cause increased osteoclastic activity and then there is down-regulation of the anti-inflammatory cytokines and it results in this mismatch. So diagnostically, unfortunately these are often missed. I mean I am sure you have seen it countless times. Patient goes to the emergency room red hot, swollen foot. Emergency room doc thinks it's cellulitis, gives Keflex, follow up with your primary care doc in a week or so. Patients get the antibiotic, they walk out and they continue to walk on it. There is often a delayed diagnosis that can sometimes reach 29 weeks. They typically present their fourth or sixth decade of life and again it's primarily a clinical diagnosis. We are looking for that red hot, swollen foot. You can use different devices that Dr. Rogers talked about. Last time to assist in diagnosis, I have one of those temp touches in the office and if there is any questions, cellulitis versus Charcot, often times I will take temperature measurements and compare the two.
Just remember classic rocker bottom, hopefully, we are preventing and we don't see this, but think of that as a late deformity. So we want to recognize sort of this Charcot syndrome before the development of the deformities. And then if they do have an open wound, you have to consider concomitant osteomyelitis. And also don't forget trauma. So you get called to the emergency room Lisfranc fracture, ankle fracture in a patent that has neuropathy actually this pretty much as a Charcot foot episode. Whether it requires surgery, so we will get more definitive fusion type procedure. We will do supplemental fixation for ankle fractures. There is going to be a talk on that. There is calcaneal insufficiency fracture. These are very difficult to treat. I used to try to fix them. Now, I just most of the time excise the fragment especially if it doesn't involve the posterior facet and I will just reattach the Achilles. But these patients require close postoperative monitoring usually doubling the patient visits and doubling the time of nonweightbearing. So it's a rapidly progressive condition that results in gross deformity and if left untreated ulceration and then we have risk of infection with amputation. So when we look at -- this was a recent publication by Daniel Gitch [phonetic] -- just looking at -- it highlights the natural progression of Charcot. So he just looked in his practice two groups, patients with Charcot and patients with Charcot-related foot wound. And basically, he found that the presence of Charcot-related foot wound at presentation increased the likelihood of a major lower extremity amputation by factor of 6 and what was interesting is that majority of these feet that presented to his office were already in the Eichenholtz Stage 3.
So these are patients that were probably treated somewhere else and they went through the initial stages and we will talk about that classification system. And ultimately, if they were recognized sooner, we could have prevented them from going to that stage 3 with deformity that resulted in the wound. So acute Charcot really think of it as inflammatory syndrome. Red hot swollen foot and sometimes if you see them early enough, radiograph is going to be normal and that's really where MRI comes in. Again not so much just to sort of assist us in the diagnosis. So you cannot rely on MRI for the diagnosis. Diagnosis is clinical. But oftentimes patient comes in red hot swollen foot. It's almost like you have to prove to the patient or the infectious disease doctor or internal medicine that it's actually Charcot and it's not infection. So that's what we do MRI to try to uncover some sort of subtle stress fractures or stress injuries. So early changes usually fractures, subchondral cyst you may get some erosions. This picture here if you look at it quickly. Patient comes in. At first glance, it looks pretty normal. If you look at a little bit closer though, you could see little osteolysis on the dorsal navicula, different scenario. This patient comes in and you could start to see that Lisfranc involvement with that shift at the base of the second metatarsal and I think this is fairly obvious. So typical patterns of involvement, they have been reported and written about with different types of classifications by Dr. Freiburg were basically one, two, three, four and five just based on that anatomic level of involvement with the mid foot tarsometatarsal joint being the most common. So different classification systems that we can use. Eichenholtz is probably the traditional one really based on radiographic changes, stage 1, development stage 2 coalesced, and stage 3 reconstruction where you are getting fusion and ideally without deformity but oftentimes result in deformity.
The problem with this one was that it neglected that initial inflammatory phase where there is no changes on x-ray and therefore it was modified in 1990 with stage 0, red hot swollen foot, no radiographic changes. We actually developed more of a clinical classification system that we would sort of use to help predict amputation, so the more proximal the Charcot if it was in the presence and in combination with the presence of an open wound or osteo, theoretically a greater chance of amputation but this system hasn't been validated. [Indecipherable] [08:52] this is a nice sort of simplified concept of an active versus inactive and this study just looking at MRI, so active and then they sub-categorize it sort of deformity, no deformity, so I tend to think of these as active Charcot versus inactive Charcot and it's good way to sort of determine treatment strategy and we will go over. So clinical suspicion of Charcot red hot swollen foot. You take an x-ray. If there is bony changes, I think you can -- the patient has intact skin, no history of an ulceration, I think you can confidently call it Charcot. What if you do that radiograph and it's normal. Well, then you go on to advance imaging. You could do an MRI or sometimes if there is no open wound, you could just do a simple bone scan and if it lights up, these patients with intact skin have, you can see here, intact skin Charcot. So it becomes difficult and again I know we are going to have a lecture on this, so this is the only slide.
Charcot foot is complicated with osteomyelitis, sometimes that's going to impact treatment obviously, may require more bony resection. So start with radiograph, ask yourself or look if there is an open wound. If there is, then you can consider an MRI, look for those secondary signs, differentiating Charcot versus osteomyelitis. You can do a white blood cell labeled bone scan or you can even do PET scans that are becoming a little bit more popular to help determine if there is underlying osteomyelitis. When we think about treatment, I will try to simplify this with this algorithm here. So we have situation where we have an active Charcot. So it's important to recognize that early inflammatory changes whether you just put your hands on the patient or you have one of those thermometric devices. You have to initiate an offloading plan, gold standard total contact cast but there have been some studies showing effectiveness also of Cam Boot. Oftentimes, I will just make that irremovable instant total contact cast and then I will use thermometry just to sort of monitor the progression. So immobilization is by far the most important. Whether or not patients tolerate wheelchairs, you can consider walkers, roll-about scooters. I still do my best to have these non-weight bear. I mean there have been some studies showing that with a total contact cast, you can have these patients weight bear. Oftentimes it requires frequent cast removal and skin examination. Study published looking at 70 patients treated for Charcot with total contact cast and 30% actually ulcerated. So you just have to be conscious of that.
So now if we get the patient through that active phase, the temperatures are now normalizing, signs of inflammation are subsiding, then you have to sort of look what you are left with and you ask yourself if there is a deformity, can it be accommodated? If it can be, then obviously we are going to do a nonsurgical approach. We are going to accommodate them either in extra-depth orthopedic shoe with a custom insert, a custom shoe, a CROW device, anything to just keep these patients from ulcerating and really if it's braceable, there is really no indication for surgery at this point. The problem is if it's a non-braceable and you are unable to accommodate it or if they have this chronic non-healing wound because we know a total contact cast would adequately offload it and most likely get the wound to heal but once they are out of the cast back into any sort of shoe or boot, the risk of reulceration is very high. And this is when we consider surgical intervention and options; tendon-Achilles lengthening, exostectomy, fusions or amputations. So Lee spoke about tendo-Achilles lengthening for Charcot foot, so I can skip this. This is just radiographs showing and I will often use that in combination with an exostectomy. So they are useful when you have these patients that are in stage 3 of the Eichenholtz classification. So they are fused and they have a rigid deformity, but they have that rocker bottom with bony prominence. So you do tendo-Achilles lengthening to help weaken the posterior muscle group to lessen up plantar forces and combine that with exostectomy of that bony prominence and Cantaserini [phonetic] and his group in West Penn showed that it's very successful for those medial wounds or medial prominences, less successful for laterally.
Because the theory is that you resect and you have to cautious that you don't resect too much bone because you can destabilize it. So they are destabilizing a lateral column and patients wouldn't do well. But if you have a patient like this, it's a rigid deformity, they'll do great with just a simple exostectomy. Reconstruction indications and deformed unstable foot and ankle for skin breakdown. So these patients are severely unstable with pending skin breakdown or they have an open wound or history of an open wound. And the goal is to obtain a stable plantar great foot. We are not going for the sexiest postoperative x-ray. I just want it to be plantigrade. We want to, as Dr. Rogers mentioned, try to restore Meary's angle, try to restore that calcaneal inclination angle. We are going for osseous fusion, although it has been shown that a pseudo fusion is sometimes just as effective. So Lee talked about this comparing with total contact cast. He showed a study combining with tendo-Achilles lengthening. This is one comparing fusion with total contact casting for mid foot ulcerations. And really the key is that last point on the bottom also recurrence. Zero in the fusion group, 33% the total contact cast because not only we're initially offloading these patients but we're addressing the underlying deformity, so we are reducing the risk of reulceration. So for mid foot deformities, which is the most common, we want to identify the apex of deformity and correct malalignment.
Oftentimes, I will do a biplanar wedge and with this biplanar wedge, you can actually get triplanar correction. So these are initially started with sagittal saw and then oftentimes completed with an osteotome and mallet. I will totally sort of separate that forefoot segment to the hind foot and this allows me now to correct in the transverse plane, in the sagittal plane and even dial in frontal plane correction as well. So we are just looking pre and post correcting Meary's angle in terms of fixation, internal, external or combination of both. Lee mentioned that there is sort of some people it's like religion where they will sort of standby their technique but I think it's just beneficial to be proficient in both options because oftentimes my indications for external fixation, patients with an open wound, history of an open wound, osteomyelitis. If they have intact skin, never ulcerated, I am happy doing internal fixation. So Marco talked about some super constructs. So it gets away from the traditional sort of AO technique and some of the surgical principles that were taught. Now, we are doing extended fusions, we're bridging sort of beyond the area of involvement with thinking about plantar plates and also beaming techniques. There are some companies that have these pre-contoured plates but I think it's important just to span the fusion at least a joint proximal and distal and any joint you are crossing with fixation, you have to fuse because otherwise it's just a non-union and you can use these bolt screws. And you can even use combinations of -- so the bolt screws, just the medial bolt screw not as effective, so you have to use two or more.
And sometimes if you are just using a medial bolt screw, you could supplement that either with a plate or an external fixation whichever you are more confident with. This was the patient where basically it was a failed locking plate and I took them back to the medial bolt. This is just an intraoperative fluoroscopy, so I did add a second bolt there. So what about external fixation? Obviously, it's a logical choice. It gives us access to soft tissue. If they have a wound that needs debridement, if there is osteomyelitis with any defect that were -- and typically these are pre-built frames, two tibial rings with a foot plate. Oftentimes, I will bring the frame home, have my kids give me the okay. Dad, it looks good. So typically if it's a mid foot Charcot, temporarily fixated with Steinmann pins and then I will just use the Russian technique or the walk-back technique just to get uniform compression at the fusion site where we place a skinny wire distal to the fusion and one proximal and then when we attach it to the foot plate, we sort of walk it down, tension it and by tensioning it, it brings that forefoot segment down. You could see in this video here. So the wire is already placed distal to the osteotomy. We brought it back about two or three holes on the foot plate and then we are going to tension it and you can actually see sort of like wrinkling of the skin where we are getting good compression. So these devices typically stay on for about three months or so. Just to finish it up with case study, we have a 43-year-old male, Charcot with resultant rocker bottom foot. So you ask yourself, is it braceable, if it's non-braceable, if he has history of recurrent ulcerations? These patients are going to go on to reconstruction. So again goals of treatment, decreased pressure. We are treating the underlying deformity, so ideally we want to --if there is a wound, we want to augment wound healing.
But ultimately lessen the risk of reulceration, increase function. Obviously, we want these patients to walking ideally in a non-customized shoe and allow for -- So I think Lee showed yesterday using the dynamic pressure analysis. So when are in fellowship, we had access to all this fancy technology. I think it's great obviously for presentation but I don't have this in my office now. I don't think it's necessary but it really just highlights the benefit of really what we are trying to accomplish here. So this is kind of a pre-op analysis. So patient hits that pressure mat and you could see that spike in pressure right beneath the cuboid and that's either where he ulcerated or have the history of the ulcer. So by plantar wedge just like we talked about and you can see here pre on the left, post on the right and then if we compare now pre-reconstruction versus post-reconstruction, you can see that spike underneath the cuboid has been completely eliminated post-reconstruction. So on the six-month post-reconstruction, we get the spike heel and toe off where we would expect it. So hopefully, we put this patient in the best position to function well and lessen the chance of reulceration. So more rear foot and hind foot, again same principles. If they are braceable, they are usually in a CROW device but unfortunately, they are oftentimes unstable and unbraceable and that's where we will consider surgical reconstruction. In this situation, it's usually going to be fusion. So if it's hind foot, we are thinking triple arthrodesis or some people even coin the term like pan pedal fusion where pretty fusing all the joints in the foot. If it's subtalar joint, you do a subtalar fusion.
If it's an ankle, you are going to do an ankle fusion and oftentimes TTC fusion as well. So you know incision placement based on sort of presentation, this patient had varus deformity in the ankle, ulceration on distal fibula. So TTC fusion worked out well because we were able to just excise that distal fibula, correct the deformity using IM nail. You can use plates, you can Ex-Fix. I don't think fixation is as important of just correcting the deformity. So some take-home points; first and foremost to clinical diagnosis, early diagnosis is paramount. Red hot swollen foot in a patient with neuropathy is Charcot foot until proven otherwise. Consider advanced modalities to identify hidden or stress injuries, conservative management or I should say it shouldn't be conservative, it's just nonsurgical management, focuses on offloading and immobilization, frequent followups, checking temperature differentials, surgical management, identify apex of deformity whether it's mid foot, hind foot, ankle and ultimately, correct the underlying deformity so we can limit -- I just added this in sort of last minute so this was just a current concept, foot and ankle international with Mickey Penzer [phonetic]. And just looking at the evidence, so I know Dr. Rogers talked about sort of lack of evidence, especially when it comes to Charcot foot reconstruction and he is just sort of looking at diagnostic images and grade 1, meaning insufficient evidence using a PET scan just because the studies -- the trials haven't been performed yet. And then when we go down looking at the operative management, they are all grade B and grade C. So they are all level 4, level 5 studies. So I just sort of emphasized with Dr. Rogers talking about last talk. Alright. Thanks for your patience and bearing with me for the hour.
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