Stephen Kominsky, DPM reviews the "diabetic foot ulcer". Attention is given to recognition of contributing factors, the importance of thorough documentation and providing appropriate treatment for this common podiatric chief complaint.
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Release Date: 03/16/2018 Expiration Date: 12/31/2018
Stephen Kominsky, DPM
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Male Speaker: I must be old because he keeps telling me that I am. Actually Bob’s [Phonetic] comments are great segue into something that I wanted to share. In 1983, I guess it does make me old, and then again in 1984, I had the opportunity, the privilege and the pleasure to spend a lot of time at the National Hansen’s Disease Center in Carville, Louisiana, which, at that time, was primary Hansen’s Center. But because Hansen’s was on the wane at that point, they really started to focus on neuropathy as it applies to diabetic foot. And I spent quite a bit of time with a gentleman named Dr. Paul Brand, who really was the, if you like a better term, the godfather of diabetic foot. And simply it was really what it can be. There is nothing complex about managing the diabetic foot. All the technologies are fabulous but most of them are unnecessary, quite frankly. If you understand the basic tenets and the principles and the pathomechanics to why a diabetic foot breaks down or why they develop an ulceration, it’s really, really quite simple. I mean I could probably do the whole thing in three slides, but I won’t, because Bob wants a little bit more than that. Let me move on and I’ll kind of highlight what I’m talking about. In this talk, I want to talk a little bit about etiology. I talked about risk factors in my earlier talks so I probably won’t spend much time about that. I will touch on a little bit more detail about neuropathy, very little about angiopathy. Pressure is pretty much everything. I had a slide in a lecture I used to give and the slide said something about “What do you put on the ulcer?” And the following slide was, “It’s not what you put on the ulcer, it’s what you take off of the ulcer,” and that’s pressure. And if you understand that then you go a long way in really healing these patients, but also really preventing breakdown in the first place. Physical exam, we talked a lot this morning about infection versus noninfection and the treatment. This is just a quote from a paper from Andrew Boulton that says, “Every 30 seconds a lower limb is lost somewhere as a consequence of diabetes.” That’s pretty devastating. You all know, of course I’m preaching to the choir here that the role of diabetes and how devastating it is with respect to lower extremity, we know how many billions of dollars a year Medicare alone spends on hospitalizations and rehabilitation and surgical intervention, and shoes, and bracing, and so forth, just for a diabetic patient. So, it’s a big problem. This is a slide I had in my first lecture. Again, one in four people or 25% people with diabetes develop an ulcer. And probably greater than 60% of all nontraumatic amputations in this country are the result of diabetes. That’s a staggering number. I think that if we all just had a better understanding of why these patients get into trouble and hopefully you’ll come away from this talk with that then maybe we can do a little bit to help that. So, we talked about etiology before and, of course, neuropathy, repetitive stress increase pressure. I’ll talk about all those things in more detail in a minute. Again, this is the same slide I showed you earlier about risk factors, which patients in particular are set up for developing an ulceration, whether it’s a digital ulceration or whether it’s a planter ulcer. We talked about that. Again, to quote the old sage from New Jersey, my home state, the ties that bind are neuropathy. Really, I didn’t that Bob. Well. Alright, so neuropathy, there are different presentations for neuropathy. There’s hypoesthesia, there’s hyperesthesia, then of course, there’s motor neuropathy and autonomic neuropathy. We’re going to talk about those and the role that they play in just a second. Sensory neuropathy, for the most part, is the absence of sensation. I like to refer to it as the breakdown or the loss of the protective feedback mechanism. But what does that mean? What that means is that your patient loses the ability to feel pain. I tell my patients when I explain that to them, I said, OK, that sounds like kind of a good thing. If I don’t have pain anymore that’s a good thing. But in reality, it’s a terrible thing because pain is an important response, if you will, to know that there’s a problem. When you have pain, it tells you there’s a problem. If it’s a headache or if it’s a pain on the fifth toe from a corn, you know that there’s something that’s not right. But when you lose that, you loss the ability to protect yourself. There are a lot of studies published over the years about denial, the whole denial concept in diabetes and for neuropathy and the role that it plays in respect to denial. And we find that when you lose the ability to feel a part of your body, your brain in a sense, cuts off that part of your body. It no longer considers that to be attached, if you will. In a sense, your brain amputates that psychologically and so you stop protecting it.
Not only do you lose the ability to protect it, but in a sense, you stop caring about it. There’ve been a lot of studies that support that so it’s very important that you educate your patients that have peripheral neuropathy and insensitivity about self-examination at home and monitoring and so forth on a daily basis. Autonomic neuropathy, what role does it play? Typically, it involves perspiration and sweat, temperature regulation in the feet. And if that is askew then they stop perspiring, the skin dries out, the skin can crack and fissure, and of course that can be a portal for infection. That’s kind of the role of autonomic neuropathy. In addition to that, I always like to add the whole idea about the GI system though. With autonomic neuropathy, certain antibiotics can be factor with gastroparesis. So you want to make sure that when you have patients that may present with autonomic neuropathy and you’re contemplating either oral, primarily I guess oral antibiotic, you want to make sure that it’s stable for them from a GI perspective. And probably almost as important as sensory neuropathy is motor neuropathy. And the role that motor neuropathy plays is deformity of the foot. You could have atrophy of the intrinsic muscles which can lead to hammertoe deformity of course, claw toe deformity, plantarflexed or displaced metatarsals. Patient can develop bunion deformities, tailor’s bunion deformity, pes cavus, et cetera. Those are all areas for tremendously increased pressure. That opens up a whole discussion, not appropriate for now on the idea of prophylactic surgery in the patient with diabetic neuropathy. I wrote a chapter a number of years ago for a textbook on prophylactic surgery in a diabetic. And as I traveled around the country and I speak, we’re very divided as a profession. Some people really support the notion of prophylactic surgery in a diabetic patient for these reasons and others of us don’t for fear of opening a can of worms when you don’t have to and so forth and so on. So whatever camp you’re in, the bottom line here is the role of motor neuropathy and the appreciation of that in terms of pedal deformity. Angiopathy is pretty straightforward. Clearly, if a patient is dysvascular, they are marginally increased risk for tissue breakdown. Those are patients that either needs to be reconstituted or potentially amputation in the presence of gangrene or liquefaction, necrosis or what have you. But certainly angiopathy does play a role. Pressure, that’s really where I want to spent a few minutes talking about because a minute ago I made the comment about what do you take off of the ulceration. What you take off the ulcer is pressure? What I learned down in Carville from Dr. Brand is the following. That there are basically four ways in which the diabetic foot is destroyed. Number one is direct mechanical disruption of tissue. What does that mean? That means trauma. That means a patient that steps on a thumbtack or a nail or a screw, or they have a golf ball in their shoe, I had a patient that walked around for a whole day with a golf ball in his shoe, or a pill bottle or a twig or a branch. I mean, we’ve all had them. Any kind of foreign body that can penetrate through the bottom of the foot is the first mechanism, if you will, of damage to the diabetic foot. Number two is repetitive stress over a long period of time. What does that mean? That means that the average patient who walks around during the course of the day on a bony prominence. Most of the ulcers that we see are forefoot ulcers and they’re all plantar forefoot ulcers. And probably, with the exception of the mechanical, the direct penetration by virtue of foreign body, they’re all under a bony prominence and most of them are under metatarsal heads and they all start as calluses. I made that comment earlier this morning about having these expensive, sophisticated gait analysis systems which are great for research. But in terms of simple management of the patient, if you just look at the bottom of the foot and look where the callus is, that’s where they’re going to get an ulcer. It ain’t rocket science. That’s why it’s important that these patients come in and have these lesions pared down. That’s why it’s important that they wear accommodative orthotics, not functional orthotics. That’s the role of plastazote, molding and increasing surface area and spreading stress on the bottom of the foot over a greater space. In terms of this point, repetitive stress, so a patient goes out for a walk, they walk on this prominent metatarsal all day long, they develop this callus, the tissue becomes inflamed. That happens to anybody, you don’t have to be diabetic for that. The patient with adequate sensation feels it and it hurts. What do they do about it? They limp, they change their shoe, they wear a pad, they pare down the callus, and the problem goes away. But in the patient population that we’re talking about that has a breakdown in the protective feedback mechanism, that’s neuropathic, they don’t feel it. So, they wear the same shoe. They walk on it all day. It doesn’t hurt. Most likely they don’t check the foot at night. They get up the next day.
They put the shoe back on. They walk around and work. I’m in DC, I have a lot of patients that are lobbyist. Those halls in Capitol Hill are miles long. They walk all day long around Capitol Hill. They don’t check their foot. They come back the next day. They do the same thing over and over again. Eventually, via the process called enzymatic necrosis of soft tissue, the tissue under the callus becomes inflamed and starts to liquefy, breaks down and that’s how a plantar ulcer develops. Again, if you understand that and you see that they have callus there and you make the orthotic for them, you accommodate it, you offload it. That’s the term we use today. In the old days, we used to just say relieve pressure, now we offload everything. If you offload that weightbearing area, the problem goes away. You can do it with an orthotic, you can do it with metatarsal osteotomy. That’s the argument for prophylactic surgery. So, repetitive stress over a period of time that leads to ulceration and leads to necrosis, that’s number two for the diabetic foot destruction. Number three, sustained pressure, low pressure over a long period of time leads to tissue ischemia. Now, what does that mean? Basically, what that means is a tight shoe. You have a patient with a bunion. They wear a shoe all day long. They take the shoe off after 10 hours and lo and behold the area over the bunion is inflamed, or there’s a blister, or maybe there’s a beginning of a sinus tract, or worse, even an ulceration. Ulcers over bunions happen for one reason, shoes. Ulcers over tailor’s bunion happen for one reason, shoes. Ulcer on the dorsum of a toe happens for one reason, a shoe. It’s not rocket science. If you understand where these problems arise from, then you as the clinician treating that patient can make the recommendations to reverse or undo whatever that damaging process is. Again, and potentially an argument for prophylactic surgery, straighten the hammertoe, get rid of the bunion, fix the tailor’s bunion, whatever it is. Whether you choose to follow that suit or not, at least address the issue of the shoe. One of the mistakes that we sometimes make and we don’t really have a concept to this is we’ll put a big bandage or a band aid bandage over that ulcer site and put the patient back in their shoe. I’ve seen that over and over again. You take a tight shoe that’s already causing pressure on the bony prominence whether it’s a bunion or a hammertoe, you put a bandage on it which occupies even more space, and then you put them back in the shoe. Does it make a whole lot of sense? Again, be cognizant of sustained pressure over a long period of time leading to tissue ischemia. If you have any of these three mechanisms, direct mechanical disruption of tissue, repetitive stress over a long period of time, which is the plantar ulcer, or sustained pressure over a period of time, which is a tight shoe, you get number four which is tissue breakdown ulceration and potentially a portal for infection. That’s the whole diabetic foot. That’s how it happens. There’s really nothing else. You can move the location around. They can be in the arch under a Charcot foot, it can be under the cuboid, under a Charcot foot, it could be under the heel in equinus or calcaneus gait, whatever it is. But if you have a sense of these basic tenets, then you could treat anything that comes into your office. I teach my residents, there are basically three reasons why an ulcer on the foot doesn’t heal. Number one, there’s an underlying infection that has yet to be identified. Number two, the patient has inadequate circulation. Or number three, we’ve been ineffective in offloading that weightbearing area. That’s pretty much it. I mean, that covers most of them. Obviously there are other co-morbidity issues. There are obviously can be some other extenuating circumstances, serum albumin and nutrition, things like that, but for the most part, that covers the majority of the things that we see in the foot. Having said that, then why do we have all these really, really expensive technologies? And I use them. She mentioned the mesenchymal stem cells. I do a lot with stem cells. I think they’re phenomenal. I think there’s definitely a role for this in these patients. But by far and large, the majority should be able to heal just by simply understanding these basic tenets. I know I’ve jumped way ahead of my slides. But the pathway to ulceration, I talked this morning about neuropathy and that being the tie that binds all these patients together, I truly believe that. Patients that are not neuropathic don’t have these problems generally. Physical exam, I’m not going to bore you with that. Obviously you need to do a vascular exam, a dermatological exam, and of course a neurological exam as well. I think it’s very important in this part of your exam and you should document this because I’ve seen some problems associated with not documenting it. And that’s the shoes. The type of shoe they wear. The stylish shoe they wear. The fit of the shoe, whether it’s a high hill, pointed toe box, rounded toe box. Put you hand inside the shoe, feel whether or not there’s a nail from the sole that has come through, I have found that many times, patient can’t feel if they’re neuropathic, whether there is stitching or lacing in the shoe that may be irritating them.
Sometimes you can’t see it so you’ve got to put your hand inside the shoe to feel it. So, evaluating and examining the shoes, I think, is very important and part of the management of these patients. Wound characteristics for documentation purposes, for treatments purposes, it’s critical that you really spend sometime in your charting and really evaluate what you’re looking at. Describe the quality of the tissue. Is it granular? Is it fibrous? Is it red and healthy and beefy? Is it dysvascular? Is it fibrotic? Is there undermining? Is there a sinus tract? Describe the tissues that are visible or that you can see through the wound. Is the plantar fascia exposed? Is there a tendon exposed? Is there a joint capsule exposed? If you put a probe into an ulcer in the forefoot and when you withdraw the probe, if you see it bubbling fluid, that’s typically joint fluid. Joint fluid has hyaluronic acid in it. Hyaluronic acid retards granulation. So, if you’ve got a joint that’s leaking into the soft tissue, you’re probably going to have a very difficult time getting that ulcer to close. You may have to go in and either debride it, open it, incise and drain it, possibly do a mid-head resection in that case. So, understanding the quality of the tissue and what you’re seeing and what you’re evaluating is very important and then documenting it. You’ve got to cover yourself in documentation. This is a huge arena for lawsuits as you know. I mean the whole diabetic foot thing may just blow up if you’re not careful about what you’re putting in the chart. Noninfected versus infected, we’ve had several talks on that already this morning. I’m not going to spend a whole lot of time. I gave you the anecdote this morning about the consult that I was brought in to see, was “an emergency” late at the night, although, I saw it in the morning. It really looked almost just like this. It was just a little bit bigger. There’s no erythema, there’s no cellulitis, it’s very superficial ulceration with a hyperkeratotic rim but basically a viable health, pink margin. No penetration in deeper structures or tissues exposed here, very simple, right under the third metatarsal head. My treatment of choice for an ulcer leg, this would a contact cast. You mentioned contact casting. I am an old fart. They work really well. And that is my gold standard for sure, okay? Same thing for this. Still not infected. Looks a little different. But basically, a clean ulceration versus something that’s starting to look like this where you’ve got cellulitis now dorsally on the toe. Potentially, you’ve got a blow outside proximally, dorsally. There may be some communications along a tendon sheath. I would be very concerned about that patient. That would probably be a patient on the right that I would send for an MRI to see if there’s an abscess dorsally tracking along the extensor tendon there. That would be my concern in that particular case. For something like this which clearly is a surgical scenario, you’ve got to get in there and debride that, open that, unroof that, see what’s exposed, see what you can expose under that, and then make your treatment plan accordingly. I created this very simple algorithm here, we start at the top of the diabetic wound. To the left, it’s infected, to the right, it’s not infected. When it’s not infected, local wound care, debridement, any biologics, if you choose to use them, of course, and then, the key here is offloading. We go to the left side, of course, infection. We have culture, sensitivities, antibiotics, whatever radiographic studies you choose, whether it’s x-rays, MRIs , CT, indium scans, Ceretec scans, whatever you are comfortable doing. But you have to make sure that you evaluate these patients comprehensively more in the infected side of course than the noninfected side, but both are important. Clinical signs of infection, I think, we can skip this. We’ve already kind of talked about this at length this morning. Again, diagnosing infection, very important. On MR, of course, we look for abscess. We look for gas in the soft tissue. Management of infection, I’m not really going to talk about that. We did that earlier. Infected, noninfected chronic wounds, again, for the most part if you understand the mechanics of why this wound has developed in the first place any of the four mechanisms that I highlighted a few minutes ago, then you should be able to implement some treatment plan to reverse that offending issue whether it’s weightbearing stress or a shoe or what have you. Chronic wounds, again, there are hundreds of different ways to treat them with different products. I would absolutely contact cast that foot and that they thing probably close in about three weeks at the most. Debridement of noninfected wounds, of course, there are sharp debridement, enzymatic debridement. I’m a sharp debridement guy for the most part. I like to have the scalpel in my hand. I think I have a lot better control of the wound. I typically debride the wounds. I see the patients generally twice a week. I debride them as necessary of course. But I would say, on average, it’s probably once a week depending on the definite size of the wound of course. Biologic debridement, I don’t have much experience with maggot therapy. I know they use it at Georgetown which is around the corner for me. Dr. Alenger [Phonetic] uses it a lot.
They have great success with it. It’s just not something that I have much experience with. Offloading, we could talk about this for hours. Contact cast, there’ve been lots and lots of papers published over the years as the gold standard for offloading for the ulceration. I have seen many times, affectionately, in my lectures over the years, any idiot can get the ulcer to close. It’s really the smart person that keeps it close. We get it closed, but then you have to figure out what to do to keep it closed. And that’s where the role of shoes and orthotics comes in. It’s very important to understand the different materials that are available. Unfortunately, I see patients come in a lot of times, or sometimes I should say with functional orthotics, a hard rigid graphite orthotic that’s been made for them either by another podiatrist, hopefully not, or a physical therapist or some other physician in order to either heal or control or prevent from recurring a previous ulceration. And that isn’t going to do it. There’s a whole talk about why offloading works. Offloading works because you’re spreading weightbearing stress over a greater area. The example that I like to use is take the average 150-pound person, okay, and have them stand on a 1-inch square block of wood. That’s 150 pounds per square. It’s a pressure for the skin that’s in contact with that block of wood. Now, make that block of wood 5 inches. You’ve reduced the weightbearing by factor five so now it’s down to 30 pounds per square inch. You spread the surface area over a much greater area. That’s how the contact cast works and that’s how a plastazote molded, accommodative orthotic works. It spreads the weightbearing stress over a much greater surface area thereby reducing the pounds per square inch. That’s it in a nutshell. Any bony prominence can be accommodated by doing that. There’s really not much of a place for a rigid orthotic when you’re managing this patient population. I’m not talking about the patient that happens to have diabetes that has plantar fasciitis or something like that. I’m talking about the high risk neuropathic patient should be in tri-density or four-layer density, plastazote, pili, corex, whatever materials you’re comfortable working with but a molded and molded is the key accommodative orthotic. Total contact casting, we could talk about that for days. There’ve been chapters written on this topic. I think, again, the key to understanding it is increasing the surface area on the bottom of the foot, spreading stress. And the other thing that it does is it eliminates the vertical forces of gait by locking the ankle, so there’s no push off, so there’s no forefoot pressure for this patient. They have to ambulate with a flat bottom, flat foot so that you’ve eliminated all the vertical stress going through the metatarsals through the forefoot which is a great step forward, no pun intended, in terms of taking pressure off of the ulcer, “offloading” it, and allowing this to go on the heel. Again, there’s all kinds of devices. You’ve got the darker shoes, the CROW walker, extra-depth shoes. There’s a place for all of these things in your practice and for this patient population. I’m not going to talk about surgery. We’ve talked about that already. In my conclusion, I think you just have to make sure you understand that the role of neuropathy and the breakdown of the protective feedback mechanism, understand about weightbearing stress, repetitive stress over a period time leads to tissue inflammation under a bony prominence where the callus is on the bottom of the foot, about the role of constant low-grade pressure over a bony prominence like a bunion or a tailor’s bunion or a toe that leads to localized tissue ischemia and that comes from the shoe, so you want to reverse that process, and then, prevention. And that’s pretty much it. It’s that simple. Thank you.