Lee Rogers, DPM discusses the etiology, epidemiology, pathogenesis, and histopathology of Charcot foot. Dr Rogers also describes technologies available to evaluate patient’s peak plantar pressures as well as reviewing available imaging studies to help diagnose Charcot neuroarthropathy.
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Lee Rogers has disclosed that he is a consultant/speaker for Sanuwave, Kerecis, Advanced Tissue and is and officer/director for RestorixHealth
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Unknown Speaker: Bringing back young Lee Rogers to talk about the most classic diabetic foot deformity. We mentioned earlier today that deformity is part of that very important triad that underlies diabetic foot ulcers. It's also a risk for mortality, as we showed from [Indecipherable] [0:00:21] study in 2010. Today, so I asked Lee to give us a talk on Charcot foot. It's more than just a deformity. Welcome back, Dr. Rogers.
Rogers: Alright. I think that, that many of us get caught up in the thought process around the Charcot foot as being a deformity, because in most cases the Charcot foot is diagnosed at the point of deformity, but in fact, as you'll see, as we go through these slides and I describe the pathophysiology, it's probably more appropriately a disease of inflammation that then later on leads to all the complications that we are familiar with in the Charcot foot, most significantly the deformity and subsequently a high likelihood of amputation.
So, hopefully most of us know that it's an eponym for a disease that was originally described in patients with syphilis that had tabes dorsalis, from Jean-Martin Charcot. And I like to point this out because I just find it interesting, but in his earliest paper, at the very end of his paper, he closed with sera continué, which is French for to be continued. Because he said that there's a lot yet to be discovered about -- he called this diabetic arthropathy, but later was given the eponym named after him, Charcot joint or Charcot foot. But he said there's a lot to be learned about this new condition. And I would argue that you know, some 140 years later, we still have much to be learned about this.
So, a lot of what I'm going to present comes out of the proceeds of the International Task Force, which convened in 2011. Dr. Frykberg and I co-chaired it. It was actually in France at the La Salpêtrière Hospital where Charcot did a lot of his work, not only on diabetic arthropathy, but on a whole host of other conditions. He was a very prominent physician at the time. We actually even had dinner at his house. He didn't attend nor did he cook, but we did have dinner at his house and he was very well paid, I think Bobby, don't you? Because his house, they turned it into a hotel and so his house was kind of a palace.
We got to really get a close look at not only the disease, but also the person who originally had described it and some of his earliest works. This led to the publication from the International Task Force, which broke this into pathophysiology, the definition of Charcot foot, the diagnosis and various treatment options that were available. So here's the La Salpêtrière Hospital, outside the hospital originally, and for about 75 years or so, a big bronze statue of Charcot. The hospital itself is in here, this is the entrance and the gate, but a big bronze statue was there until the Nazis came in and melted it down and used it for something.
And so we met here, a group of about 20 Charcot foot experts. Here's Ed Jude, Andrew Boulton. Bob is over here somewhere, I can't see at this angle, I usually look for his hair. When I see David, I look for no hair and you can tell where David Armstrong is. And so, here's Bob and Dane Wukich who's an orthopedic surgeon from University of Texas. But interestingly enough, going through some of Charcot’s original papers and looking even at some of his original cases that he was treating for these patients. And when you see this, this is an actual note that he wrote from a patient encounter and his notes were pre-printed. So even maybe 15 years ago, if you went to an emergency room in the United States, you'd have a doctor that would use a pre-printed note that fill in the blanks for different things, vitals and whatever. Well, Charcot already was using pre-printed note in the 1860s, and filling in the blanks here off of these presses that he had the notes printed. He would get in big trouble though because you can see the date here 186. And then he forgot the year. At that time, I guess maybe you didn't need a full date and time, you just need to put the year on there, but he would get dinged I think and medical records would send that back to him.
So when we look at where Charcot is today, even though any peripheral neuropathy can lead to Charcot neuroarthropathy, probably the one on the rise is HIV neuropathy and that is not only caused by the infection itself, but also many of the medications that lead to neuropathy, that are treatment for HIV. And we're seeing, interestingly enough, a lot of foot problems in those with HIV that used to be only seen in people with diabetes.
And again, because diabetes used to be a disease in which it was a death sentence when you were diagnosed with diabetes, but after the advent of insulin, now we have people living even -- the longest living person with Type I Diabetes, lived over 85 years with Type I Diabetes. So now we're developing complications of a disease process that last decades. And the same thing now we're seeing with HIV where these complications that didn't exist before because people had just died, we're now seeing these complications. But still, in the Western world, diabetes is still the major cause of peripheral neuropathy that leads to Charcot foot. The prevalence is very difficult to pin down because there are studies, none of which very large, but there are studies where the prevalence varies from 0.15% of those with diabetes or 1 in 680 to one study that showed over 20% of those with diabetes when x-rays were taken in looking for evidence of some type of joint activity in the feet, there is definitely increase in morbidity.
Dr. Frykberg did mention the [Indecipherable] [0:07:27] study where there was an increase in mortality. But there's also been another study that showed there was no increase in mortality. Increase in the amputation rate, 40,000 new cases estimated yearly in the United States estimated by the ADA, and there may be as many as 250,000 undiagnosed cases. So we know that those with Charcot has 36 times increased risk of a foot ulcer. There is a 30% incidence of bilateral Charcot foot, and this is not because the Charcot process starts of both feet at the same time. Almost always one foot becomes inflamed, has some type of trauma, and while that foot is being treated or favored by the patient, then all the factors that led to the occurrence of Charcot on one side are present in the contralateral side, and usually the other side starts then within a year or two.
So, we know that the quality of life is dramatically affected in those with Charcot deformity, and it commonly leads to permanent disability and premature retirement.
So, when we think about the pathogenesis, the two theories that were at one point conflicting with one another; the French theory, which was described by Charcot himself is one, that is a neurovascular theory that the innervation to the blood vessels has been impaired because of neuropathy. It leads to an increase in the blood flow because the sphincter muscles are not being innervated. So it leads to an increase in blood flow, which washes out the minerals in the bones because of that bones become soft and then the foot can dislocate. That's the French theory. Even back then they were in disagreements with the Germans.
So the Germans, this was Virchow, he said, “No, it's neurotraumatic because there's neuropathy present, patients are getting trauma and walking on it. And this continued walking is causing all of these problems.” But really what we believe is that it's more of a unified theory that there are parts of both of these that are true, and that's the modern day theory of the pathogenesis of Charcot foot, and it becomes a vicious cycle where we have diabetic neuropathy, which results in hyperemia. There's an exaggeration of blood flow.
There can be in many cases, just a minor trauma. Many patients will recall some type of trauma, nothing very severe, but they may recall just twisting their ankle or slipping in the shower, catching their foot on a stair. And then that is enough to cause inflammation. There could be also a foot ulcer or some other type of surgical insult to revascularization. There's also case reports of patients who have an increased risk of Charcot foot after pancreas and/or kidney transplants, which I'm not sure I understand the pathway there. But those reports are out there as well. There, then, are fracture dislocation of the joints, continued insult because of neuropathy and continued ambulation. And this vicious cycle just continues and leads to this worsening deformity, which then can cause ulceration and amputation.
We look at the histopathology, and we have great bone for histopathology because during Charcot foot reconstruction, there's usually a lot of bone that's being removed, a lot of diseased bone. And so we can look both of the joints and at the bone itself. And we can see here this is an example of a bony trabecula that was taken from a Charcot foot patient that we operated on. And this whole thing is trabecula here, but we take this little peninsula and we blow it up, you can see that these large multinucleated cells are the osteoclasts and they're eating away the bone, and so this should be nice smooth edges, and instead the bone is being eaten by the osteoclasts. And there's an imbalance in the osteoclasts to the osteoblasts, which are building the bone. That's probably due to a molecule that we know about, that it governs bone reabsorption and regeneration, called RANKL and OPG.
We also have noticed that the Haversian canals in many cases are widened, and you can tell that this is actually good bone. The edges of this trabecula are nice and smooth. There osteocytes have nuclei in them, in the bone itself. And the matrix surrounds this here but the Haversian systems in early Charcot are widened because there's more blood flow getting through the bone.
So, as I said, it doesn't start with a deformity and in fact, once the deformity occurs, the diagnosis had been missed in some times months, but it always starts with inflammation though, and that inflammation usually manifests as a hot, red and swollen foot. Not only a physical deformity, but also muscle tendon imbalance from equinus is a contributing factor in the dislocation and subluxation of the mid foot and also in ulceration. But the Achilles tendon has been studied in those with Charcot, and the Charcot patients versus diabetic controls found that the tensile strength and elasticity are significantly altered in those with Charcot. And when we look at electron microscopy of the Achilles tendon, it's morphologically different from those that are non-diabetic controls.
Actually, this is a schematic that came out of one of David Armstrong's articles. And this was a photo of an x-ray from one of my patients during residency, but that matched almost exactly this schematic here.
So you have the Achilles tendon pulling on the calcaneus, which is causing an increase in pressure underneath the forefoot, but dislocation and subluxation forces that are occurring across the mid foot. And again, this is why the Achilles tendon is part of the treatment plan in many patients with Charcot foot deformity during undergoing surgery.
So when we look at it in the laboratory, this is another patient that we studied in the laboratory, and you could see in this case where the heel is not even touching the ground, the Achilles pull. We have the tail of first metatarsal angle and the calcaneal inclination angle. In this case, might even call it a calcaneal declination angle, because it's negative. But you can put these people in devices to measure the peak plantar pressures, and just to look at the dynamic pressures on the plantar surface of the foot. You can see the heel barely touches the ground here, big spike of pressure at the mid foot, and still some increased pressure actually off the forefoot during gait.
So, this inflammation and this increase in blood flow results in a reduction in the bone mineral density. But these bone mineral density changes are local and they're not systemic. Because when we compare those with diabetes and neuropathy to those with diabetes and Charcot foot, we see that in the vertebra versus the calcaneus. In the vertebra, their reduction in their T-scores is relatively the same. There's no statistical significance in the difference here. But when we look at their calcaneus, those Charcot foot have a T-score of -3.0 compared to those with diabetes and neuropathy of around even.
So that this change in bone mineral density may, in fact, drive the pathway of whether a patient develops a fracture pattern or dislocation pattern of their Charcot foot. So the DEXA scans of 50 some patients with Charcot foot were evaluated. And what was found is that the odds ratio for developing Charcot with a fracture pattern was 10 times greater in those who had evidence of peripheral osteopenia on a DEXA scan. So when we look at this dislocation pattern, fracture pattern, and then those patients that had both fractures and dislocations, and you compare that to the T-score, you can see those that had neutral T-scores really just dislocated, but those that had negative T-scores all the way down -1.5 almost, they had a higher incidence of fracture, which makes sense. But you will miss this if you're doing a bone mineral density scan and they're scanning the wrist or the femur or the vertebra, you're not going to see a difference. But it requires actually looking at the calcaneus.
So when we're looking at the diagnosis of Charcot foot, and I'd argue that in many cases, the diagnosis can be made clinically with no added imaging aside from x-rays, but in some cases, some imaging is required. And so when you think about which tests to run to look for Charcot foot, the question is really what kind of Charcot are you looking at, and are you looking at an acutely formed Charcot, something that just recently happened, that's a hot red swollen foot?
Are you looking at one that has obvious fracture subluxation/dislocation, or you're looking at a foot that has an open wound with exposed bone, and this is where I would argue that your decision making, as far as the test goes, is going to be different, because in those patients that come in with no deformity but hot red swollen foot, many times just radiographs, thermography, sometimes you do conventional bone scans, sometimes we do MRI, although not always needed, even in this case. And this is not really, I don't think, standard in the United States. There're some places in Europe where this is really being talked about a lot more doing bone densitometry early on.
And then if you have a patient that has an open wound with exposed bone where you're really trying to differentiate Charcot foot from osteomyelitis or possibly at Charcot foot with osteomyelitis, there's the need for possible bone scan combinations, MRI and now possibly even a PET scan where we've seen that there's a difference in the uptake based on the activity in the foot and those that have Charcot foot have actually a higher metabolic need in the bone than those that have osteomyelitis and maybe because of bone necrosis. And then those that are kind of in the middle here, you might need a test somewhere in this range if it's just a fracture dislocation, but no open wound.
I know that MRI is probably the most frequently ordered test outside of an x-ray, as far as imaging goes, for Charcot foot, but I will caution you about using an MRI to try to differentiate Charcot foot from osteomyelitis because many of the changes on the MRI are similar. And if the radiologist doesn't have the entire clinical picture, they may not even be able to distinguish the two but the good news is that there are secondary signs of osteomyelitis that can really help you to make this determination whether or not osteomyelitis is present instead of Charcot foot.
So the first thing to know is just that over 90% of cases of osteomyelitis have a contiguous spread evident on MRI. That means that they're going to have a sinus tract that you can see on the MRI that goes all the way to bone, and 90% of cases you'll be able to see that if there's osteomyelitis. Then we look for secondary signs of osteomyelitis and we know that osteomyelitis primarily only affects one bone. If you see multiple bones involved on an MRI, it's more likely to be Charcot. Deformity is common with Charcot, but it's very rare with osteomyelitis. If you see some type of mid foot deformity, it's unlikely to be osteomyelitis by itself. And then Charcot foot is more common in the mid foot and I would argue probably the ankle. And osteomyelitis more common in the toes and the forefoot because the soft tissue thickness is smaller, so the distance after you have an ulcer to get from the skin to the bone, it doesn't take as long and the bacteria travels that a lot easier. So osteomyelitis more common in the toes and the forefoot, Charcot foot more common in the mid foot. So you look for the secondary signs to help make your diagnosis.
I'd argue that thermometry is probably one of the best techniques and tools you can use to not only make the diagnosis of Charcot foot but also track your therapy, to determine whether or not this patient is going into remission, or they're going from an active state to an inactive state. And in thermometry, the older thermometers like these -- there is only for one patient, not single use, but just for one patient to use because they contacted the skin.
And these goose neck thermometers would contact the skin, beep, give you a number. You would go to the exact same point on the contralateral extremity, do the same thing, compare the temperatures. What we're looking for is a difference of roughly 4 degrees Fahrenheit or around 2.5 degrees Celsius. That difference is significant for inflammation. If it's not, doesn't mean that there's Charcot foot, because it could also be gout or infection or some other type of trauma. So it's significant for inflammation is what it is. It's diagnostic for inflammation. A Charcot foot is one of those conditions that causes a lot of inflammation, so you'd be looking for that in the diabetic foot.
Many cases the temperature difference is about 10 degrees and that's noticeable by palpation. The reason why we use thermometry is based on another study that was done, where they took water bottles and heated them up to different temperatures, and they had doctors test the temperatures of the water bottles with their hands to see if they could tell which one was warmer. And they found that it wasn’t until about 8 degrees or 10 degrees before you could actually tell the temperature difference with your hands. And so it's important to use a more objective measure in this case.
We can advance now another few years or so from there, and now we have thermal imaging. This is even an older thermal imager. I think I have a picture of a newer one on here as well, but this is an older thermal imager. When we got this one, it was $15,000. Now you get one for $250 that fits on your iPhone or your Android, and just as good. And these were originally developed and commercialized publicly for mechanics to look at auto parts and things like that, to see if they were too hot to touch. Or inspectors doing a home inspection could see behind walls and see if there's a leaky pipe, that type of thing. The military used to use them to find AL Qaeda in caves or the police can see people behind walls. It's useful if you're running a clinic, because you can find where your nurses are. You just like go around the clinic like this, you see where everybody is.
I remember when I first got this. I always try out everything on my family first, any new tests that I have, and so I took this thing home, in the basement shut all lights off. And your phone imager will do the same thing, this is even more advanced than this now, because you swipe your finger across it and it'll go infrared, visual spectrum, infrared, visual spectrum; just back and forth, and you could stop halfway in between, really see what point you're looking at that's elevated. And you can touch your finger on a point and it'll tell you what the temperature is of that point. But in this case, we're just looking at the visual spectrum image in the basement with the lights shut off. And the hottest thing in the room is 95.5 degrees, it’s marked right there. And then when you look at the infrared spectrum, it's the eyeball of my cat. So it's that specific. And these things are cool, because you see, when the cat gets pretty bored pretty quickly and sneaks away, but he leaves footprints behind him, that you can see in the heat signature on the carpet.
So when you when you use this in the clinic, you can see that here's the visual spectrum image and I made a box where the infrared image is. Here's a big difference. This is a 10-degree difference between extremities and, again, it's not the actual temperature of the skin. Because skin temperatures can be a lot lower than body temperature, and especially extremity skin temperature, but it's the difference between the same point on the other side that is important. And so we see a 10-degree difference here, 89 to 79 degrees. And then looking at a period of time with treatment of total contact cast. In this case, I think it was somewhere around 20 weeks.
I'll caution you when you're talking to patients about the length of time that they need for total contact cast. We think about Charcot foot and deformities, and we kind of relate this to fracture healing. And patient will ask, “How long do I have to be in this cast?” And you say, “Oh, six to eight weeks” and I see that commonly written in notes that I'm reviewing. And when you look at the literature, the literature shows that on average, patients require 18 weeks plus or minus 10 weeks of total contact casting before they have normalization of skin temperatures in their foot. And that's important because you need to set reasonable expectations upfront with your patients, so that they don't get disappointed and you're trying to compromise with them later on. And so it needs to be explained to them that this is a very serious condition that commonly leads to amputation, you're going to work together, but they have to understand that this is a long-term process and it's going to require commitment for them for that long period of time.
So we've even looked at some things written more recently at cryotherapy. Like using Cryo/Cuff, for example. Orthopedic surgeons use it all the time after hip and knee replacements to cool the area after surgery. They have an ankle version of the cuff and you can fill up a cooler full of ice water or whatever else you might want to put in that cooler, as long as there's ice in it as well, that's what you're going for, some type of liquid and ice. You can put that liquid into this bladder that goes around the extremity. The foot doesn’t get wet. So even if there's an ulcer, it's okay, that's not getting wet.
And the question that we have really is how long and how many times a day? We don't know the answer to this yet, but this we started with 30 minutes, three times a day. And you can see this is just immediately after 30 minutes, already the same temperature even at the hottest point on that foot. It's already the same temperature as it is on the contralateral extremity. But is this going to make a big difference in cooling the foot down and arresting the process early? We don't know yet. But I think this is very interesting and probably one of the cheapest things that we could do for those with Charcot foot.
Our statement from the Joint Task Force on how to diagnose Charcot foot, and I think this is important because we need to reiterate that this is primarily a clinical diagnosis. You have to have a very high index of suspicion for this. It's going to be a red, hot, swollen foot in the presence of neuropathy. In any case, that's going to be considered Charcot until proven otherwise. Inflammation is the earliest finding. When you find a patient with rocker bottom deformity, that's a late finding, somebody missed that diagnosis or the patient didn't come in early enough. Acute fractures and dislocations in those with diabetes and neuropathy is actually Charcot foot. And that's because it's the fractures and the trauma that led to the inflammation. And inflammation is occurring in this case, and it's the inflammation that’s starting the Charcot process and that's why we consider that to be Charcot foot.
There are lots of classifications out there. A lot of these classifications are either pathology based or radiographic based, or Bob and Lee Sanders have a classification that's anatomically based. Our recommendation is really the one that make probably makes the biggest difference in the treatment plan is whether or not this Charcot foot is active or inactive. If it's active, it's actively inflamed. If it's inactive, the temperature difference is less than 4 degrees Fahrenheit.
And that's a better descriptor than acute and chronic. You hear people talk sometimes about acute Charcot foot or chronic Charcot foot. Acute and chronic are medical terms that relate to time. If it’s acute, it recently happened. If it's chronic, it’s been going on for a long time. There's no differentiation point that's been really described in the literature that makes any sense about when somebody has acute Charcot, when they have chronic Charcot. And then they can have chronic Charcot and get another injury. And then have acute-on-chronic Charcot, and that makes things confusing. So our recommendation is really looking, just going and referring to this as active or inactive as defined by inflammation. So, thank you very much.
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