Thanks for having me today; I really appreciate it. Today we’re going to talk about the foot, obviously. It’s an area that gets maybe overlooked or maybe underestimated on its importance on occasion. So, I’ll start off with my first slide. It’s a little graphic for everyone.

I think everyone recognizes the problem, and I thought, since it’s Halloween, a little gore is appropriate. But one of the focuses of today’s lecture, though, is to try to get everyone to recognize things. No one misunderstands this as a problem, but we need to kind of recognize some of the more important things, some of the milder cases, if you will, to get screening. And I think that’s been a nice theme throughout the day today as far as prophylaxis, prevention, and education in the patient population, and for the health providers for that matter, as well, beginning to recognize some of these things before they are a problem.

We’ve got several modalities today that we didn’t have and ways of screening and in improving function of the foot that can improve on function and maintain a patient’s good quality of life and keep all their toes and feet.

The high-risk considerations today that I want to talk about are basically, I’m going to go through three separate areas that I think maybe need attention: diabetic wounds, getting to recognize those appropriately and how to treat those and how to estimate those in the diabetic population; update on peripheral neuropathy, there have been a couple of advances over the last couple of years with regard to treatment with neuropathy that I think deserve some attention; and also Charcot deformity, which is something that we see quite a bit in the office, and we’re very familiar with it, and probably a good deal of you are, too, working with diabetics. But physicians and healthcare providers in general sometimes this is a very overlooked area.

Some diabetic foot statistics. You’ve seen some scary statistics today. The foot’s no different. Approximately 21 million people with diabetes, 189 million people worldwide. And that incidence is growing, like we’ve seen on numerous slides throughout the day today. More than half of all diabetic foot ulcers do become infected, requiring hospitalization. One in five will require an amputation. That’s a pretty scary statistic, considering the number of amputations we see. And one of our goals today is to assess those and reduce that, hopefully.

Sixty or 70 percent of those with diabetes have peripheral neuropathy, which is one of the predetermining factors in development of diabetic foot ulcerations. And 25 percent of those with diabetes will also develop a foot ulceration. After a major amputation, 50 percent of the patients will have their other limb amputated within two years. That’s a very scary statistic to me. Hopefully, it is to you, as well.

Diabetic ulcerations—and these are somewhat dated, as well—numbers, so this may actually be quite a bit higher, approximately $36,000 to heal a foot ulceration in a diabetic patient. That’s not necessarily with a hospital admission. They are 15 times more likely to require amputation. And an average hospitalization for an ulceration or infection is $25,000 to $40,000.

The total cost is more than six billion annually. Foot ulcers are a precursor to 85 percent of amputations. They’re overwhelmingly the largest percentage of amputations. Traumatic amputations are a small minority.

Here’s a similar slide to what was shown earlier today about projected incidence of diabetes and its increasing rates worldwide.

Lower extremity risk, again, this is just to summarize the three things we’re going to be covering: risk factors for diabetic ulcerations, peripheral neuropathy, and sensory impairment, including things like motor neuropathy, which results in foot deformities. Quite frequently, bunions, hammertoes, those types of things are very common in the general population. But with diabetes and the development of neuropathy, it causes an intrinsic muscular wasting. So, the small muscles in the foot lose their input, so they atrophy and die, and it causes them more severe development of foot deformities.

Peripheral vascular disease is an overwhelming cause, and kind of a thorn in our side as far as treating the people with foot ulcerations and gangrene of the foot. But it’s also one of the areas where there are expanding treatment options, too, now. History of ulceration and amputation, over half will require—I guess that’s the same statistic that I had up there earlier. But poor glycemic control is very common in these patients. Development of ulcerations is just kind of a continuation of the diabetes and subsequently the obesity, it’s just a tertiary symptom of the obesity, if you will, and the poor compliance in this patient population.

Here’s the problem. If you put a cigarette in this guy’s hand, you’d be an Indiana native, I think. You lead the nation in those two statistics. But also, I think it puts us in the forefront, since we do have such a bad population, it gives us an opportunity to effect greater change, I think, in the area.

Here’s another slide that I think is pretty interesting. It shows a cross-section of an obese individual and somebody with a more normal BMI. Everyone notices the adipose tissue density, which I think is fascinating. But also notice some of the bone quality in the obese individual. You can see the difference in bone density in the slides and the diameter of those bones, and how that affects more directly what I do.

Here’s a progression of diabetes, which we’ve covered fairly thoroughly today. I’ll skip forward through that.

And again, this is a summary of the overlapping effects of these different metabolic syndromes and how they relate to obesity and diabetes, and subsequently, development of the foot ulcerations and complications.

Assessment of the foot, we’ll go through really quickly. I’ve got several slides with this. But basically, the simple things you can do in your practices.

Just check a pulse in the foot. It’s one of the main, simplest things you can do. When you’re talking to the patient, just lay your hands in the foot. If you’re going to be getting a pulse rate anyway, it’s a simple way to do that. On the dorsalis pedis and the deep posterior tibia behind the ankle joint. Just make sure the pulses are there. If they’re there, that’s one thing that’s a very simple, quick way to assess risk in a patient.

Capillary fill time is another quick thing. Push the tip of the toe and see if it blanches and then it responds very quickly. Ask about symptoms of claudication. Night cramping. If they can only walk a certain distance then they have to sit down and take a break. That’s a good sign of intermittent claudication.

On the venous side, edema and associated chronic skin changes is another more common way people can end up with ulcerations through development of venous stasis ulcerations, which are also very difficult to heal.

Diabetic vascular disease, arterial insufficiency, and it occurs in about 60 percent of diabetics, and is in most cases is present in some level in lower extremity ulcerations. Atherosclerosis, plaque formation within the intima of the wall, is seen in an earlier age in diabetics than it is in the general population. And calcification of the media of the vessel wall, which is hardening of the arteries, doesn’t allow expansion and contraction of the vessel to respond to stresses needed with increased blood-flow requirements of wound healing. Venous insufficiency resulting in edema, caused by CHF and end-stage renal disease, obviously very common in the diabetic patient set. And venous stasis dermatitis and ulcerations associated with that.

Treatments of this are fairly straightforward. Compression through physical therapy, or compression stockings, and diuretics through the primary care doctor. And just compliance education for the patient, getting them to understand how important these things are to address. Typically, these things develop so slowly over time, they tend to just accept it as part of their body, and just go on with it. They don’t recognize the detrimental affects they can have.

Here’s a classic example of chronic venous insufficiency with hemosiderin deposits located on the anterior aspect of the leg there.

Another fairly easy assessment is a neurologic exam with a Semmes-Weinstein. They’re very readily available. It’s a 10-gram monofilament wire you place on several locations throughout the foot. It’s a very quick exam. It takes less than 15 seconds to do, and gives a very easy assessment of neuropathy development in the patient. Oftentimes, the patients are completely surprised when they’re unable to sense that. Vibratory sense is actually the first sense to go, but obviously less important. This is a much more important assessment in determining risk for ulceration in these patient sets.

Proprioception, two-point discrimination, hot cold, deep tendon reflexes. These are all things that become diminished as the disease state progresses in the diabetic.

Sharp-dull, light touch, and eventually, if needed, nerve conductions and EMGs can be obtained in the more recalcitrant neuropathic patient population.

Neuropathy, itself, occurs in about 55 percent of diabetics. That statistic varies a little bit according to the different studies, some as low as 35 and some as high a 75 percent of diabetic populations. But 90 percent of diabetics with an ulceration have an associated neuropathy.

Motor, sensory, and autonomic, these, all three of these factors can be contributing factors that lead to ulceration. As I mentioned earlier, the intrinsic muscular wasting on the motor side, sensory loss of protective threshold, and autonomic decrease in vasomotor tone can either increase or, in most cases, decrease perspiration, resulting in xerotic skin.

This is a great slide. It does a couple of things. This patient actually stepped on this, which they did not feel. It caused quite a bit of pain. But the proprioception is also lost, and so, they didn’t know that they were walking on this until they started walking from carpet to a hard surface and could actually hear that. Proprioception is one of the things that gets avoided and missed quite a bit. So, that’s a nice slide to demonstrate those, I think. I’ll try to keep it to a minimum with those kinds of slides, though.

Diabetic integument. Just do a quick assessment. None of these things take very long. Look at the skin; feel the skin; look for any irregularities, lesions, calluses; and no matter how mild they may be, it’s important to note those and make sure the patient is also aware of those. Look between the toes. Look at the bottom of the foot. Those areas are commonly missed, and you’d think by glancing at the foot, you’d notice something is going on between the toes. Not necessarily the case. Here’s a good example of that.

This is a severe case of tinea pedis. It looks very severe. But in reality, it actually cleans up very nicely with a little bit of light debridement and some topical antifungal cream.

This is a good example of the vascular system, and maybe a little bit out of order. This is someone who had a toenail removed. The person did not bother to check pulses in this patient. This patient had no pulses. And so, you can see that the nonhealing wound there, and she eventually required an amputation, as well.

This is another wound. It looks fairly serious. It’s caused by tinea pedis between the toes again, left untreated, and the callus formation at the bottom of the toe there. It’s a little blurry, but if you can make it out, this is a callus. There’s micromotion that takes place in these calluses. And even though the callus, itself, is fairly mild and not a big deal in some cases—I shouldn’t say it’s not a big deal, but it’s not causing a deep ulceration. It can also cause sheer forces to take place, which causes this large degree of skin slough. And then that can cause subsequent ulceration indirectly that way, as well.

Here’s another very easy thing to miss. A very mild wound. You can easily treat it with conservative care. However, you don’t know it’s there if you don’t look for it. It’s missed. The patient doesn’t look at it. It can lead to bigger, more serious issues.

Musculoskeletal system, hammertoe deformities, things like that are very common in the general population. It can be very detrimental in the diabetic population. Very common areas of pressure, like the area just indicated in the previous slide under the first metatarsal head, the top of the toe where the hammertoe forms, at the PIP joints, and also at the tip of the toe. And you can see, in a case like this, it’s very easy to rub this area on the tip on the top of the shoe, if the patient doesn’t wear a large enough toe box. And also, when they walk, this area of the foot will drive into the ground, causing increased pressure in those areas, as well. Simple things like diabetic shoes are a godsend as far as controlling some of these things in a lot of patients.

Here’s an example of the Charcot deformity and a musculoskeletal deformity. This is a case with some failed internal fixation, and we’ll talk about that a little bit more, later. It’s just one of the severe deformities that takes place in the diabetic patient set.

The University of Texas has a classification system, which is one of the things we use to guide our treatment or actually assign risk to a patient set.

This is another classification system we use quite a bit to differentiate or delineate the different types of surgeries that are available to the diabetic. Classically, people will think, foot surgery in a diabetic is a no-no. Well, in some cases, that’s not the case. In some cases, it’s actually mandatory. The Class I is an elective surgery for something like a bunion or a hammertoe repair to alleviate pain or symptoms, and also improve function of the foot to prevent future ulceration.

Class II is a prophylactic procedure to reduce risk of ulceration or re-ulceration to a patient who has had a previous ulceration. These patients will typically have neuropathy but good blood flow in these two groups, but not always. Curative is a procedure performed to assist in wound healing. That may be a surgical debridement of a skin graft or a reconstructive surgery to reduce plantar pressures, as well, in combination with a skin grafting.

And then Class IV is emergency, which we see more than our fair share of. Once more, the areas we’re trying to work on is eliminating the first slide that you saw, preventing aggressive, large amputations in these patient sets.

The risk categories are broken down by the University of Texas. Classification as a Category 0, which is minimal pathologies present. Patient has a diagnosis of diabetes, sensation is intact, no clinical signs of ischemia, normal noninvasive vascular exams, if those are necessary. Typically, I wouldn’t go to that extent in this patient set, as long as you have palpable pulses. Foot deformity may be present, but it’s typically fairly mild. And no history of ulceration.

This patient will typically be seen once or twice a year. Once to three times a year depending on the risk and how compliant the patient is with their overall medical care. Possible shoe accommodations or orthotics, as well. And again, we spend quite a bit of time on patient education with these people.

Category 1 is essentially the same as category zero, except now the patient has developed neuropathy, in which case, it puts them at a slightly higher risk for development of calluses and ulcerations, because of the development of the neuropathy.

Treatment guidelines are the same as the previous category, except possibly, more aggressive shoe accommodations and monitoring of the temperature changes in the foot over time. And also, you may want to step up the timing of the visits throughout the year.

Insensate foot with deformity. Again, increasing risk. A patient has diabetes, the same developments as the previous one, but they have more deformity present, but no history of plantar foot ulceration and no history of Charcot’s arthropathy at this point.

Treatment guidelines, consultation for possible custom-molded diabetic shoes at this point. This patient set typically is not acceptable to have over-the-counter orthotics or custom over-the-counter orthotics. They should actually move on to a custom-molded diabetic shoe at this point. And possible prophylactic surgery pending circulatory status to alleviate any severe deformities.

Summary, the Category 3 would demonstrate a pathology. This is the patient that has history of deformity or history of ulceration or a possible structural deformity, which is in a stable state.

Treatment guidelines for this would be more aggressive shoe combinations and possibly some AFL bracing. Anything to keep the foot planting grade and reduce plantar weight bearing pressures. Also, again, more increased visits, as well.

Here’s the Pecoraro and Reiber study, which is fairly famous as far as assessing this triad of the things necessary to cause an ulceration in a diabetic set, be it ischemia or neuropathy; you need a trauma, either acute or repetitive trauma. And probably in most cases of most ulcerations, it’s repetitive trauma. There’s repetitive wear and tear on the callus area or pressure points.

The classification system we use once someone has developed an ulcer, because it’s also very simple, there are multiple classification systems out there, but we really like this, because it’s very easy to use once an ulcer develops.

Grade 0 is also basically a callus. It’s a thickened area of skin, which may or may not have some pinpoint dermal bleeding within the tissue itself.  A Grade 1 is a superficial ulceration without involving the deeper tissues, tendon, bone, that sort of thing.  It typically will have, once the callus is debrided, will have more of a beefy-red appearance to it. Grade 2 does involve tendon or bone, extending into the deeper tissues or possibly joint capsule. And then Grade 3 is a deeper ulceration with abscess and/or possible osteomyelitis. Grade 4 is gangrene of the toes or forefoot, which will require aggressive amputation. And then Grade 5 is a sufficient gangrene to cause loss of the distal lower extremity.

Here’s a good example of a Grade 0. Typically, the treatment for this would just be to involve debridement, to ensure whatever is causing all the callus to develop can be reduced as much as possible.

Grade 1 ulcerations are typically treated with debridement, assuming the patient has intact sensation. Converting the chronic to an acute wound is critical to getting these wounds to heal. Wounds, ulcerations, which many of you probably know, in a diabetic patient set, they’re lacking certain growth factors, and they become more of a chronic state. And so, they need to be converted back to an acute wound in order to facilitate healing.

 

Here’s a good example of a Grade 1 ulceration. You can see the beefy-red central aspect. And that’s a very healthy tissue in there. It doesn’t probe the bone and there’s not probing to deep tissue. This is a mild amount of hyperkeratosis around that area. And so, typical treatment for a wound like this would be to offload it. Surgical shoes with the combinations and cut-outs. And once the ulceration heals, prevent future ulcerations, and typically we use like a surgical shoe or an orthotic in some patients, as well.

Here’s that same wound healed once the offloading has taken place, or nearly healed, I should say. You can see how much reduced it is in size.

Grade 2 is the same, but prevention of infection becomes more of a priority at this stage. It may also require more aggressive amputation. And in some cases, depending on the presence of osteomyelitis or suspected osteomyelitis in these patients, preventive surgeries, like bunions and hammertoe corrections and other reconstructions may be necessary at that point.

Here’s an example of a Grade 2. It’s not a true Grade 2, because this is an ischemic foot. The ulceration has developed because of ischemia. But you can see the tendon present within the wound. This would require vascular intervention of some type to restore circulation prior to any kind of debridement or curative efforts.

Grade 3, typically that’s kind of like the first slide we saw. It’s an aggressive forefoot gangrene. But that generally always requires amputation, which may or may not be present with osteomyelitis. Gangrene typically is, people a lot of times will assume it’s always osteomyelitis. But it’s not always the case. Sometimes there’s just tissue loss. And the tissue loss is sufficient, which will also require amputation. In the case of infection present, an extended course of antibiotics may be needed. Convention states six weeks. There’s actually been no studies done to assess the efficacy of the six-week treatment. It’s just the rote, over time it’s been accepted. Not many people are willing to volunteer for that study.

Here’s a good example. This is the fifth metatarsal right here in this area exposed. This will require an aggressive resection of the metatarsal bone back to healthy, bleeding margin. And typically, when we do something like that, we’ll also obtain a culture at the site to determine the pathogen from the deep tissue. Then also once we resect back in this margin here, typically to a healthy bleeding margin, following copious irrigation in the interop, we’ll also obtain interop cultures at that time to, hopefully, assess that the bacteria is clear. And then that also might reduce the length of the antibiotic needed, as well.

In Grade 4, basically to keep the dry gangrene from becoming wet gangrene until an adequate amputation can be performed.

Grade 5 involving the rear foot usually requires a below-knee amputation, as well. And then here’s the same patient I showed you a little earlier, just a little different angle. That’s a classic Grade 4.

Factors affecting healing. I think we’ve discussed those quite a bit today, or at least touched on them at some point. Adequate peripheral perfusion is key for a lot of these. Control of infection. And offloading of pressure sensitive areas. And then overall controls of systemic disease, including the diabetes.

Factors affecting wound healing. This gets complicated in the diabetic patients who may have rheumatoid arthritis, who may be on steroid medications, betadine, Dakin’s solution; these are all older medications that were used, but are typically updated now. We have more updated treatment options for these people.

Inadequate use of offloading, which we see quite a bit. People just simply don’t get the pressure off their foot. There are a couple of studies that looked at offloading devices, such as a surgical boot or shoe versus the ulceration. And most patients felt a greater anxiety or stress level from wearing the boot than from actually having the wound. Which kind of stems back to their underlying disease state.

Smoking, caffeine, stress, anxiety. All these things affect wound healing. I really stress to the diabetic patient, which I do to a lot of patients, is, in general, smoking and diabetes is a terrible combination, and it severely affects the perfusion of the lower extremity.

Extrinsic offloading is accomplished by removable walking casts, half shoes. Total contact casting is the gold standard. Patient compliance and risk of complications are increased with a total contact cast, as well. And then intrinsic debridement, which is debridement of the keratotic tissue.

Here’s an ulceration or preulcerative area. You can see the pinpoint hemorrhages in the center.

Then here it is postdebridement. That type of debridement actually reduces the pressure under the area, and it reduces the skin breakdown.

Offloading can be accomplished, as I mentioned before, through bunion correction, hammertoe, metatarsal head resection, and Charcot reconstruction. Anything to make the foot plantar graded and reduce plantar pressures is one of the mainstays of treating these patients in a lot of the cases.

I’ll skip through the debridement.

There are different types of debridement.

There’s surgical and sharp debridement. There’re also other types of debridement, as well. And there’re a couple of slides here which kind of summarize those different debridement modalities.

You can use things like papain-urea ointments, which are appropriate for patients who can’t undergo surgical debridement because of inadequate perfusion or who can’t tolerate the pain of those debridements. Biosurgical, which is also maggot therapy, and you may or may not have heard of that. Typically, people make a face when they hear about that, but it actually works amazingly well.

We haven’t classically used it here. But the people I’ve talked to who do use it, they have good results with it. And typically, it’s not the patient that’s resistant to it, it’s the healthcare providers that send them.

Physical therapy is another modality that can be used. They can use whirlpool treatments and things for painful wounds. That’s another effective means of debridement.

Here’s an example of surgical debridement of a wound. You can see a large degree of hyperkeratotic tissue surrounding that. Then debrided back to a healthy margin. It stimulates bleeding and brings back growth factors, agents necessary to heal the wound.

Enzymatic debridement, as I mentioned. Papain-urea products work very well for those patients who can tolerate that.

Planning wound treatment, you need to consider the anatomic site, amount of exudate, dead space, surrounding skin, the person’s ability to care for the wound themselves is also a huge factor in this. If they can’t do that, they need to get some kind of assistance or maybe come in more frequently for visits. I don’t know how many of you feel comfortable doing these kinds of treatments in your office, or you can send them over to see us. We’re happy to help. Cost is also an issue in that—I guess I should mention that, too—in a lot of these. There are a lot of wound modalities that help patients heal, but they’re also very expensive. And traditionally, insurance companies are very resistant to paying for a lot of these modalities, as well. It does limit our ability to treat in some cases.

Now, infection, the sequelae, the untreated or improperly treated ulceration contamination, possible cellulites and abscess, and osteomyelitis, in some cases, necrotizing fasciitis.

Here’s a list of the common pathogens associated with the development of the ulcerations. And it kind of helps give you a guideline to begin imperative treatment with IV antibiotics if it’s a hospital admission, or antibiotic oral agents depending on the level of cellulites. I’ll show you a couple of examples in just a second of different levels of cellulitis and assessment of how the wound can be treated or how you know if you need to admit the patient to the hospital.

Non–limb-threatening infections. Typically, it’s a wound site that has less than two centimeters of cellulitis surrounding it. It’s a superficial ulceration, maybe like the grade 1 I showed you earlier, but with the addition of some cellulitis surrounding the area. It does not probe to bone; no bone or joint involvement, and no systemic toxicity and no significant ischemias present.

A limb-threatening infection is greater than two centimeters of cellulite with or without lymphangitis. Edema, a person may have systemic infections, a fever, odor from the wound, or a deeper wound which probes to bone or tendon or deeper tissues, and also purulent drainage at the site. These were classic examples of reasons for hospital admission to treat this.

Here is a good example of that. This is a deep wound. Actually, it probes deep into the heel. And you can see the surrounding cellulitis around the wound. That’s definitely a reason for admission. That’s a very limb-threatening infection, especially in the position it is on the foot. Obviously, that area of the foot does not lend well to a more distal amputation.

Diagnostic evaluation of diabetic foot infections. When you’re in the presence of an infection, you should always get deep cultures from the base of the wound or ulcers, as much as you can. Diagnostic imaging may be helpful. X-ray, looking for cortical destruction of bone, or an MRI for bone marrow edema, and also more sensitive for cortical destruction, as well. Bone scans and other arteriography, serologic exams, CBCs, sed rate. All those types of testing sometimes are misleading; in the diabetic patient population with their compromised immune system, they won’t always have markers on the serologic exam. Blood cultures if the patient exhibits systemic symptoms. And sed rate and CRP.

And also, it’s always a multispecialty approach. We typically work very closely with infectious disease and vascular in assessing these patients, it gets the patient assessed in a timely fashion, and it also helps prevent a larger degree of tissue loss.

Again, this summarizes our plan of treatment. Hospital admission, which usually in most cases will require some kind of surgical debridement and possibly an amputation once it reaches this stage. Exploration of the site, and then whatever modalities are necessary to help heal the wound.

I guess, one of the things I should mention, too, that I see quite a bit, is when you’re suspicious of—I think you need to use good clinical judgment if you’re worried about infection in an ulceration. Typically, if a wound is simply not an infected wound, it looks like that Grade 1 I showed you earlier, which is a fairly healthy-looking wound. You probably shouldn’t culture those, because they’re always going to grow something, and then you’re obligated to treat those.

There was an interesting case. The first case of vancomycin-resistant staph aureus was in a case in Michigan, and that was from a noninfected wound. So, they were obligated to treat this. It caused quite a bit of uproar and things. But it was actually not an infected wound. It was just a contaminant at the wound site. So, it kind of underscores the need to have a good clinical judgment before you actually culture.

On to diabetic neuropathy. Diabetic polyneuropathy affects greater than 50 percent of diabetics with diabetes. Fifteen to 50 percent of these suffer from painful neuropathy. No available cure is available for diabetic neuropathy, as no one completely understands the underlying ideology of the disease process. We know that tight glycemic control is important, but it’s not gong to completely prevent, in most cases, people from progressing with their neuropathy.

The three most common areas of distal symmetric polyneuropathy are: areas of entrapment—excuse me, three nerve components: the small and large fibers, fiber loss; small results in pain or loss of pain and temperature, and difficulty to—this is a test—it’s difficult to assess with an EMG or a nerve-conduction study. Large fibers control proprioception and vibratory gait, which results in sensory ataxia and is also usually affected first. One of the things people don’t often ask about in the diabetic patient set is, how often do you fall? And when we’re actually asking these patients, it actually is recorded a fairly high incidence rate.

The sensory presentation with the development of neuropathy, patients will often come in at first, they won’t complain a lot of pain, they’ll usually mention that they feel like they’re walking—their sock is rolled up under the ball of their foot or they’re walking on a stone. Or they may or may not have some cramping in the feet. A lot of times, too, they’ll also complain about a mild tingling in the toes. And in some cases, that’s the way we diagnose diabetes. They come in and we start to do a little more thorough history on these patients, and turns out, they actually have diabetes.

Occasionally, they’ll describe increased pain with non-noxious stimuli, like they’ll feel they can’t stand to have the bed covers touch their feet because it’s too painful. Or they can’t find a pair of shoes that feels comfortable. These kinds of signs should be tipping you off that the patient may have neuropathy.

And the motor presentation: the patient may have drop foot, weakness, and an inability to balance. The deformities become more severe with development of the intrinsic muscular wasting.

The autonomic presentation is also important. Altered sweat gland function, hyperhydrosis or hypohydrosis, where the impaired vasomotor tone affects the vascular system to the point where the sweat glands don’t work appropriately. And impaired vasomotor tone and hypervascularity is one of the possible ways that Charcot deformity develops in the diabetic patient set, as well.

Risk factor reduction for the patients is, in general, some of the things we’ve already covered today. It’s regular visits, compliance, education. Can’t stress these things to people enough. It’s a lot of material for them to remember, too, which I think is part of the problem. You’re inundating them with information all the time  about these things they should and shouldn’t do. And I think it needs to be kind of handed out in small doses. And that’s what I try to do in the office, take a proactive approach, which it sounds like a lot of you are doing, as well, and just get the job done that way.

The proposed etiology for development of neuropathy is not fully understood. There’s a metabolic pathway where glucose breakdown products accumulate in the axon and cause damage. And it causes water to follow the breakdown products, and it causes swelling in the nerves, and it may cause what resembles a carpal tunnel-type syndrome in the small fibers and in the large fiber nerves.

Vascular, the ischemic-hypoxic theory, which may or may not be an autoimmune response to the build-up of the breakdown products in the nerve.

The double crush theory relates back to that inositol flow into the nerve that causes an altered osmotic gradient, which results in endoneurial edema in areas of anatomic narrowing. The tarsal tunnel, the fibular neck, and the dorsal midfoot are three common areas; very similar presentation to a carpal tunnel-type situation. Results in what’s called a double crush phenomenon, which as it goes on can result in ischemic changes and impaired nerve repair, and then axonal damage.

Treatment, tight glycemic control may slow the progression of the disease, but it, unfortunately in most cases, doesn’t typically eliminate it. Oral medications, which I’ll go through a little bit. Peripheral nerve decompression, which is somewhat of a controversial area, has received a lot of debate in the literature lately; and we’ll talk about that a little bit, as well.

Tricyclic antidepressants are one of the methods typically used. It used to be, I guess, amitriptyline was one of the few options that we had. It was off-label use; it wasn’t FDA approved, but it seemed to improve patients’ neuropathy. It has some side effects of hypertension, sedation, and seizures, and weight gain, as well. Nortriptyline, it’s included in the list, but I have not actually typically used that.

Prozac and the SSRIs are also sometimes used in patients with this, and also somewhat effective, because typically, a lot of the diabetics will also be depressed, as well.

Tegretol, Dilantin, these are medications that are anticonvulsants that have been used and documented in the literature. I have not used those personally. One of the large ones I’m sure all of you are familiar with is Neurontin (gabapentin). Efficacy with this medication, however, decreases with dosing, and it also—lost my train of thought—but it should be considered as a first line of therapy because it’s been very well documented. It’s not FDA approved for treatment of diabetic neuropathy, but typically, it should be one of your first considerations, also, because of cost.

Anti-arrythmics, topical lidocaine transdermal patches, also known as Lidoderm. They may be effective, and there’s relatively little risk with these in the patient set. You can apply up to three patches per day at 12-hour intervals. And that’s be on for 12 hours, and off for 12 hours. Local reaction is possible. Anaphylaxis is fairly rare. It has been documented, local erythema and skin rash is the main side effect with using a topical medication like this.

Non-narcotic analgesics, tramadol, also can be considered a first-line therapy with relatively mild neuropathy. One study showed us significant improvement after six weeks of use. Side effects, again, they are similar to other NSAIDs with possible seizures, anaphylaxis, angioedema, and respiratory depression.

Nonsteroidal antiinflammatories also can be considered. I typically don’t start with these, and it’s not something I usually use in practice, because in most cases, the patient has already tried these under most situations. And kidney function is also important, as well, with these patients; that you need to watch with these kind of medications in your renal-compromised patients.

The other topicals that are readily available that I also will typically add before I start the patient on a long-term medication: capsaicin, which is derived from pepper plants, and it depletes substance P. It’s also marketed in the pharmacy. It’s an over-the-counter medication marketed for arthritis control. But it’s also fairly effective in controlling neuropathy in some patients. One double-blind study noted significant improvement in a fairly large patient population. It’s also relatively inexpensive, and the side effects are minimal. The main thing to caution your patients with this medication, not to rub your eyes after you apply it.

B12 deficiencies. Diabetics have gastroparesis, altered absorption. And B12 and B6 levels tend to be low in these patients. A relatively new medication, Metanx, which is kind of a later-on cousin of Foltx, many of you may be familiar with. I’ve actually started using this quite a bit and have very good results with patients in various state of medication. There are very little side effects with it, and it is very well tolerated. The main detractor with this is cost. A lot of insurance companies won’t pay for it, and it’s a relatively expensive medication. But I’ve had several patients who have been through the whole gamut of treatment options for their diabetic neuropathy, and then they come in to see us, and we try them on Metanx, and they have fairly good results. They’ve got some studies to back that up.

Also, with the folic acid, you can use it to improve perfusion of the lower extremity, and also it’s been shown and been demonstrated to reduce ulcer healing times, as well.

Of the two medications that I use primarily now, I really like pregablin. It’s an alpha2 channel ligand. It’s a very safe medication. It’s sort of a cousin of neurontin, if you will. It’s very effective. I have very good results with this. I typically will start patients off on a fairly low dose, maybe 50 milligrams b.i.d., and then titrate them up a little bit at a time as they can tolerate the side effects. Primarily, the main side effects are drowsiness or altered mental status, to a certain extent. Also, lower extremity edema is one of the possible side effects, which is fairly important to watch because a lot of these patients have a fair amount of edema to begin with. So, you don’t want to enhance that effect.

But it’s also a fairly safe medication. Renal impairment, you can use it in a renal patient, but it’s not excreted from the body as readily as it is in someone who has functioning kidneys. And so, you have to start them off on a smaller dose, because the medicine tends to hang around in the system a little longer.

Cymbalta (fluoxetine) that’s a dual serotonin/norepinephrine reuptake inhibitor. I also use this a fair amount. And I guess I would say I probably use the pregablin a little bit more consistently, just because the side-effect profile is a little bit safer, I suppose, and also—but it depends on the patient population. I screen the patients a little bit, and ask about their mood history and things like that, too, because it’s also an antidepressant medication, obviously. And so, I do use this a fair amount, as well.

Surgical decompression is one of the hot topics right now. Dellon in Baltimore came out with a large paper several years ago, proposing that these nerves should be decompressed in the diabetic patient population. He had a decent-sized patient population. I don’t remember the exact number of patients in the study. But he actually had very good results, and he would decompress the nerves in the common areas of entrapment, which I mentioned earlier, at the tarsal tunnel, the fibular head near the knee, and also at the dorsal aspect of the foot.

In one of the groups, I want to say there were 200 patients in the set, he had approximately 80 percent reduction in pain. Not everybody received a complete reduction in pain, but an 80 percent improvement, or 80 percent of the population received an improvement in pain; as well as 60 percent of the population actually experienced some improvement in sensation. Which was pretty amazing and people got pretty excited about that study.

More recently, though, some of the contraindications of the procedure have come out, and a lot of people say that this is not appropriate use of surgical technique in a diabetic patient population. And so, it’s become kind of a shouting match between two sets of groups in the neurology community.

We do use it in our group, actually. And I have a small patient set I’m actually putting together, and basically, in order to meet the criteria for it, you basically have to have failed every other option. And your options are either this or long-term narcotic use, which I feel like, in my opinion, is sort of a failure. If I have to keep these people on long-term narcotic use, I feel like I’ve failed them in some ways. And they also have to be relatively low risk. It’s a relatively low-risk surgery, but I also want to make sure the patient understands that they may not be improved. And so, we go through a fairly thorough screening process before we enroll the patients in the study.

Typically, we’ll get an EMG or nerve conduction study to try to eliminate any of the other possible etiologies of the neuropathy prior to the surgical decompression, as well. If they have any other spine-related issues, radiculopathies, sciatica, then we’ll also have those worked up and eliminated first.

The common areas of nerve entrapment, common peroneal, as it courses around the distal fibular or proximal fibular head. The deep peroneal, as it dives between the first and second metatarsal heads. And then the tarsal canal along the medial aspect of the foot.

In the group that I have currently put together, I have 11 patients that I have performed this on; it was 17 legs. VAS, every single patient was 10 out of 10, and the VAS post-op in four of the patients was actually zero out of 10. Two to four of the patients—excuse me, two to four out of 10 VAS, and six of the patients. And I did have one complication. I had one of the tarsal tunnel incisions dehisce a little bit with resultant scar tissue formation. And she developed some recurrent pain at the site, which was fairly severe. And so, we actually went back in and excised the scar tissue and found in that procedure, her pain actually dropped. Her pain is higher than the rest of the group, but she’s actually still pleased at the procedure, that she feels like she can bear this level of pain, even though it is fairly severe.

One of the most interesting things, which either undermines Dellon’s original etiologies on this, is I get quite a few referrals from pain centers. And so, when these people have chronic pain and no underlying foot or musculoskeletal etiology to account for this, I’ve actually done this procedure on four nondiabetic patients with chronic pain in the lower extremity. And those patients actually had the greatest results. Sort of interesting. I don’t know that it suggests an etiology, necessarily, but it’s somewhat interesting.

Ancillary treatments to control the neuropathy, tight glycemic control, pressure reduction, and diabetic shoes. Sometimes sclerosing agents will help, injections around the nerve sites, vitamin B12, nutrition. And there are other treatment modalities, near-infrared photo waves and then TENS-like units. One common one is called the Rebuilder, which some people experience good success with.

Diabetic neuroarthropy, classically known as the Charcot foot. It originally was described in leprosy, but the overwhelming majority worldwide now, it may still be leprosy, but it probably won’t be long before it’s diabetes as the underlying cause for this condition, as well. I guess I put that in the slide, too, that most likely it will be the worldwide cause by 2025.

The osteoarthropathy of Charcot foot has an incidence ranging from .16 percent to 13 percent in all the patients with diabetes. It leads to increased risk of ambulation especially if it’s not addressed appropriately or early on in its disease process.

The etiology is not well understood, actually, and the one consistency within it is, there needs to be lack of protective sensation. There’re two theories: the neurotraumatic, which is either an acute or a repetitive trauma to the foot, which causes a small breakdown in the osteoplastic/osteoblastic activity of the normal balance in bone metabolism between those bones. Then the neurovascular theory the cause is a state of hyperemia, which causes a vasomotor autonomic neuropathy, which affects bone metabolism. Most people agree at this point that probably it’s a combination of these two factors which cause the development of this.

One theory that’s recently proposed in the actual literature just a month or so ago, was cytokine-mediated response or a proinflammatory response that takes place at these areas prior to the development of the actual clinical findings, which suggests that it may be a type of autoimmune factor related.

The classification by Eichholtz is a stage I. This is the classic stage, and this is actually the most important stage, or later on the stage 0, which has been added more recently. It’s the red, hot, swollen foot. If someone presents to your office, and quite frequently we see this in the ER. Someone will go to the ER with a red, hot, swollen foot. There may or may not be pain. Classically, it’s described as no pain. But in a lot of cases, people will describe pain, and especially in neuropathic patients, that should be kind of a trigger for you to think about Charcot.

When the patient presents to the ER, they’ll automatically assume that it’s cellulitis or an infection. However, the patient has no source of infection. There won’t be any wounds on the foot or any other assumption. So, they’re typically admitted to the hospital, but they’re allowed to continue to bear weight on the foot. And that’s the key difference there. If someone suspects Charcot in a foot, the most important thing you can do is get the patient off the foot immediately. Once its bony breakdown process takes place, the bone becomes like putty, and they can actually walk right through their foot. And I’ll show you a couple of slides in a minute. And it results in huge degrees of deformity. And then you’re also covered, because if it turns out to be a cellulitis, and you made the patient un-weight bearing, then you haven’t actually hurt yourself at all.

Stage II is referred to as the coalescent phase. This is where the bony fragmentation has taken place in the soft tissue. It begins to resorb and reattach to the bone, and the sclerosis of the bone ends and coalescence of the fragments in the soft tissue.

Stage III can go on for months to years following the acute phase, which is called the remodeling phase. And there’s a marked decrease in the symptoms and clinical findings. You’ll notice radiographic findings decrease, and the foot basically becomes more of a solid bony block at this point.

Stage 0 is added more recently in the Eichholtz Classification. And this has also been done to help people assess this, or to more readily recognize the symptoms of Charcot deformity, in which the foot is described as a clinically warm and edematous and most likely painful. And you may or may not notice fractures on radiograph. In the earliest stage, which is also the stage which is most preventable, you won’t see a lot of radiographic changes. The bone isn’t always destroyed. Sometimes there’s just simple ligament disruption, in which a bone may become dislocated through part of the foot. But prior to this is when it’s important to assess this. And you need to know you need to get this patient off of this foot.

As I mentioned before stage 0 and stage I are often mistaken for cellulitis and possible osteomyelitis. So, if you get an x-ray of this red, hot, swollen foot, and you see these bony changes taking place, most people will think that it’s an osteomyelitis or an infectious process taking place. However, this patient will not have an open sore source or a wound. While it’s possible to cause a cellulitis or infection in the lower extremity without a wound source, you’ll see in hematology, those events are fairly rare. And so, in most cases, it’s going to be a Charcot.

Imaging may also not be of very much help at this stage, because MRI and bone scans also look very similar between osteomyelitis and Charcot. White blood cell–labeled scans may be the most beneficial. And there’s some debate about this as well between white blood cell–labeled scans and MRI. One of the things we do typically, especially in the presence where we think someone has Charcot, but also has an ulceration, which is not infected, you can get a contrast printed, indium Tech 99 scan and a white blood cell–labeled scan and then compare the difference in uptake on those two tests. It may help you to differentiate infection versus a Charcot attack.

Basically, just use good clinical judgment.

Here’s a good, classic example of a couple of Charcot feet. You can see on the top, the collapse, and this is a real, classic area where it takes place. The bones simply become soft and it dislocates, as well. And the midfoot just collapses. This results in a large prominence in the bottom of the foot, which then, down the road, will also cause ulceration. If the patients are allowed to be non–weight-bearing prior to the development of this or even after development of this, it really limits the severity while all of this takes place.

The drawback for the patient is that this may go on. A Charcot attack may last from a week to a year. And so, that may mean immobilization for up to a year in some cases, which is a very hard thing for patients to be compliant with, especially in the obese patient population.

Here’s another severe example of a Charcot deformity, which you can just see that the leg bone has actually, because the bone is so soft, it’s crushed right through the talus. This bone here should be here, and it’s completely destroyed because of the Charcot process.

Treatment, the primary goal of treatment is early recognition. It’s essential for use in the complications down the road from this. Recognize the appearance of cellulitis without a wound, unilateral edematous, erythematous foot with calor, with or without pain, and no source of infection. You should always think Charcot.

Recognition is important because this is a prolonged healing time with these in most cases. It requires a prolonged period of immobilization. If you wait, if it takes you a couple of weeks to see the radiographic changes taking place, it’s usually too late. Secondary deformities that develop, we had shown you earlier. And gait disturbances, altered weight-bearing pressures, and increased potential for amputation. That previous slide, this foot actually is at a high risk even though there is no infection present there. That’s actually a high risk for limb amputation because what happens is, this will a lot of times not be a braceable foot or will be a reconstructable foot. And that patient is just at high risk for amputation and limb loss as is someone who has an infection. That’s what makes this such a severe, serious condition, and why an early recognition is very important.

Treatment, the classic treatment for this is the non–weight-bearing total contact cast is the gold standard. It varies a little bit from the standard cast in that there’s very little padding, and it’s a total contact to the plantar weight-bearing surface of the foot, designed to reduce the pressure and also maintain the position of the foot. This is typically done in the stage I and stage 0s. Surgical intervention could be entertained at this point prior to the deformities to help stabilize the foot with external fixation devices. And that’s somewhat of a hot issue right now, too, and there’s a lot of debates surrounding that. Classically, people say you should not do that. But there are a couple of researchers out there now who are proponents of that and have been doing it with reasonably good success.

Bisphosphonate therapy is also somewhat on the forefront. Pamidronate used to treat bone cancer. This is also shown to be of some benefit in treating Charcot patients with this, as well. Bone stimulators, there’s a small amount of research out there available to show that use of bone stimulator will help the bone coalesce in these early stages sooner and prevent further deformity or long-term active stage.

Here’s a couple of examples of total contact casts. This is a very good example of a total contact cast right here. This also happens to have a foot wedge or a foot plate in the bottom of it to help the patient weight bear, because the patient is unable to be totally non–weight bearing. I picked this up from a family practice journal, actually. This was marketed as a total contact cast. It’s actually not a total contact cast. This is a standard cast, and you can kind of see the differences, where there’s a larger degree of padding surrounding the foot. And also, the toes are open, so it doesn’t actually affect a great reduction in plantar weight-bearing pressures.

For long-term use, this is what’s actually called a crow walker. This is essentially a total contact cast the patient is able to weight bear in once they enter the coalesce stage and the remodeling stage, where it helps to maintain the foot position long term. Typically, these will be worn for a long period of time following coalescence or decrease in the active phase. And they may wear these actually up to 18 months in some cases. So, you can see why compliance is an issue with this. It’s a very debilitating problem.

Bone stimulates. Again, I mentioned there’re limited controlled studies on these but promising early results. PEMF technology and continuous magnetic field technology are the most well studied. And again there, they have fairly small patient populations. The upside of this is, there are few contraindications for this. There are very little side effects from using bone stimulator. It won’t hurt the patient. In some cases, when I can’t get the patient to stabilize, I have them use a bone stimulator, especially in a patient who can’t be non-weight bearing, we’ll put them in a crow walker boot and you have them use the bone stimulator and try to get the foot stabilized that way.

Bisphosphonates, pamidronate, administered in 30-milligram infusion over four hours for three consecutive days. You need to monitor renal function. This is excreted through the kidneys. Also, prior to use of this medication, you need to have any dental work completed before, because there have been several cases of osteonecrosis of the jaw reported with the use of this medication.

The goals of Charcot reconstruction which would be to repair a nonbraceable foot. This is only to be undertaken under extreme situations where the foot has not maintained a good position, is not braceable, the patient is not ambulatory. Very complicated surgery, and even with the surgery, the patient is still at high risk for limb loss. Wang identified three main goals: to correct the ankle equines that takes place, restore the calcaneal inclination angle, and maintain the rear foot to leg relationship. Basically, keep the foot under the leg and keep it flat on the ground. That will help reduce any risk of future ulcerations.

Progression of management, produce a plantigrade braceable foot. Nonoperative prolonged immobilization is, again, the mainstay. And in those cases where it failed, there’re a variety of surgical procedures you can perform. Something simple as a bumpectomy, basically, where you remove the plantar prominence for an effective flat surface for the foot to walk on, to a more aggressive reconstructions and surgical interventions where the foot is fused in a more plantigrade position. More and more these days, people are going toward, in the literature, toward use of external fixation and with or without internal fixation and stabilize this. This has the added advantage that external fixation, that the patient is actually able to bear some weight on this when they can’t be compliant with non-weight bearing.

Here’s an example of an external fixator frame in a post-Charcot reconstruction. You can see how the foot is relatively plantar grade. It’s not a pretty foot, and no one is attempting to make it a pretty foot. It’s basically just trying to get this foot flat on the ground and reduce any plantar pressure across the area. The patient will typically wear these for up to three months, as well, and so compliance and pin site infection is one of the drawbacks to using a device like this. The patient needs to be educated in how to control the pin sites and how to clean the pin sites to keep those clean to prevent any sort of infection.

Here’s a preoperative view of this patient’s foot with a Charcot. This would be very similar to that x-ray I showed you earlier where this midfoot collapse takes place and it results in this plantar prominence along the aspect of the foot. Here he is post-Charcot reconstruction with a frame that’s been applied. We’ve actually made some osteotomy or cuts in the bone here to reduce the plantar prominence here and increase this angle and this angle of the foot, so the foot approximates more of a normal architecture.

Here’s the closing thought. I came across this thought, and it came out a few months ago, I actually noticed this. We always hear these scary statistics about diabetes and things. And I thought this was actually a fairly interesting. The five-year mortality after a limb amputation is 50 percent, which actually would compare to cancer, is the second-highest rate of mortality of all the cancers except for lung cancer. Which is a pretty scary statistic. And I think—I’ve heard the statistics, and I know what the mortality rates are. But when you look at it in those terms, it actually makes it seem more scary or more impressive. And I think that maybe sometimes, especially in the general media, these things get precedence over diabetes in general. Which is probably trending in the other direction, of course, but I still think that we need to do more to get the education out there to help these people prevent some of these changes.

We would like to see these patients not at this stage, in some of these nasty slides I showed you today, but we would like to see them before they actually have problems so we can prevent that, and keep them active, keep them healthy. And I know a lot of people probably, especially with a lot of exercise, they mention things like, they can’t exercise because their feet hurt. Well, get them in at that point before they have a problem. Don’t wait until they have a dead toe or an ulcer before you send them over to see us. It’s one of the ways we can help cut down. We’d much rather have those patients instead of having to perform so many amputations and things.

Thank you.

 

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