Male Speaker 1: We’ve titled this one problem cases from our high risk clinic. Those of you in the VA all exactly have the same kind of clinics and patients and problems. We’re just going to show you how we manage certain things, certain problems, not that what we do is better than what you do but it’s just how we do it and maybe it’ll provide some insights for you and these are my disclosures, these are our learning objectives. Basically, we know that diabetes has some very important lower extremity complications. I don’t think I’ve had to change this slide in 15 years or so. But ones that give us the most problem obviously are ulceration, infection and peripheral arterial disease, all of which can lead to lower extremity amputation which is what we’re all about preventing even though we all recognize that amputation becomes a very important part of limb salvage when it’s a partial foot amputation so we can save the legs and patients have something to stand on. But most of our infections come about in some way, shape or form through a diabetic foot ulcer which was the pathognomonic lesion going back several hundred years for the diabetic foot. Was it with King Asa in his 29th year of his reign and in chronicles, probably had a diabetic foot ulcer. So foot ulcers, we know this is old statistics, 15% lifetime risk. We know there are multifactorial etiology, of course, and the easiest way to classify them the way that I do in my head is really neuropathic ischemic, or more commonly we’re seeing neuron-ischemic ulcers. Those are the ones that we have most difficulty with. It’s rare that we see a beautiful healthy neuropathic ulcer like we did years ago. I wish we could still find those but they’re very hard because those are the ones we need for all of our research studies. Most importantly from several important studies, we recognize that foot ulcers, DFUs are precursor to amputation in about 85% of cases. In the first paper and I’ve brought this out was Pecoraro’s landmark 1990 paper in May of 1990 in diabetes care where he found that of all those amputations that he studied, there was a foot ulcer that remained unhealed that led to that causal sequence leading to one amputation. I’ve also used this graphic quite a bit over the years and I usually throw it into every one of my presentations to remind us of all the underlying pathophysiologic processes occurring in the diabetic foot. Neuropathy is always the major factor here that leads to amputation, ulceration and infection and of course, Charcot foot. But when you combine the neuropathy with vascular disease, either microvascular disease and/or macrovascular disease and insult or trauma to that, that’s how the pathways start. We have to ultimately be familiar with all these underlying pathophysiologic mechanisms that are interacting in the diabetic foot. Neuropathy is not just sensory neuropathy, it’s also motor and very importantly autonomic neuropathy, and of course the vascular disease is yes, atherosclerotic, major atherosclerosis but also microvascular disease. Microvascular disease is really microvascular disturbances. The neuromicrovascular disturbances that lead to impaired responses to injury so we need to be familiar with all these things because they have a very important role. Unless we understand what’s going on, we’re not going to be effective in treating these problems. This paper came from our Pecoraro lecturer tomorrow was a co-author on this paper that I think was pretty important in diabetes care in 2010 which really they were looking at the acute Charcot foot compared to neuropathic foot ulceration which had been studied in the UK by Moulik in 2003. But here we see if we look at the green bars and we compared the Charcot patients of five-year mortality with the diabetic foot ulcer mortality on the right, we see that they’re about the same. People didn’t really appreciate that years ago. So 41%, five-year mortality for patients with the Charcot foot and DFU, pretty much about the same. We see that these complications in lower extremity from diabetes become very, very important.

[05:05]

Although people don’t die of these problems, their markers are more significant underlying pathophysiology namely cardiac disease associated also with renal disease, et cetera. These are very important problems that we are dealing with and are life changing events for many of our patients even though we might not recognize it and certainly they might not recognize it. This is not even talking about amputation, although many of these patients have amputation makes them with their history. As we’ve said, foot ulcers are major risk factors for subsequent amputations. I always go back to Pecoraro’s 1990 paper so that’s pretty well established. We also know that the risk factors for amputation are fairly much the same as risk factors for ulceration, they’re very closely associated. But if we look specifically for amputation, obviously, neuropathy is always at the top of the list, ischemia, infection, ulceration, gangrene, prior amputation is always a risk factor. Prior amputation is a risk factor not just for further amputation but for ulceration. If it’s a risk factor for ulceration, it’s going to be a risk factor for amputation so we can see how these are so interrelated. We need to know these problems. This is why we pay such an important attention to prevention efforts for our risk-free, high risk individuals because we know they are very much at risk for further problems and we want to try to avoid those. This is published by Lee Rogers, who will also be here at meetings. This is published in a special issue of the Journal of Vascular Surgery in 2010. It’s a diabetic foot issue. It’s just my beloved Led Zeppelin wrote “Stairway to Heaven”, this is stairway to amputation. It’s a simplified way to look at the very difficult problem and I like to keep things simple when we can. At the bottom, we see that neuropathic foot with or without PAD because you don’t need to have PAD, peripheral arterial disease, to go through this whole pathway. We have that high risk foot at the bottom, sustains some type of injury whether it be a callus, thick callus stepping on a nail or a tack that we saw or burns which we see here in Phoenix in the summertime, second and third degree burns from just walking out to the mailbox to pick up the mail on barefoot, we see this all the time. So there is your injury that breaks down the skin envelope, creates a chronic wound. The wound becomes infected when it’s present long enough, develops gangrene. Once we develop gangrene, there’s really no other alternative other than amputation at some level predicated upon the perfusion at that level which is why we have to work so closely with our vascular surgery colleagues and other interventionist and why we need to be so keen on diagnosing underlying PAD when it’s present, even when it’s silent. Most of these patients have silent PAD and very often the presenting sign of PAD is a nonhealing foot ulcer or infection and the PAD had never been recognized before. We see this quite often and it’s very important that we detect this in these patients because it can have major effects on them obviously. But again, we try to make things simplified when we can reduce a complex situation into something simple. We do a systematic approach, at least I do it, it just makes it easier. Etiology, why did that lesion come? Okay, you walk barefoot. Your patients need to be educated. They can’t walk barefoot, especially not in Phoenix, in Florida or in the hot climates. We know they have numerous medical comorbidities that need to be assessed and addressed which is why we always work with our medical team, okay. All of our admissions are co-admitted with a hospitalist team who handle most of the medical issues. We also get nutritional consults on just about every inpatient because these people need nutritional consultations. We know that our patients have neuropathy. It’s almost a given. When a patient walks into you with a hole in their foot or gangrene and they’re not even limping which most of them aren’t, they’ve got neuropathy. You just want to assess to what level do they have autonomic neuropathy, gastroparesis, are there other complications, is it cardiovascular issues as well. Vascular evaluation, we always need to do. We always need to assess for our pulses. We always get our ABIs, at least in our baseline ABIs and you’ll be hearing more about vascular workups and disease later but always look for underlying occult or undocumented ischemic disease, always.

[10:04]

We tend, even on patients with pulses that I can feel because I don’t trust residents or students when they said it’s one plus. They're usually feeling their own pulse so I like to make sure it’s documented, that I carry a Doppler. My research coordinator, Jim Nelly [Phonetic] always has my gel ready for me. Right, Jim? I find that extremely useful, and I encourage you. I don’t understand why everybody doesn’t carry a Doppler quite frankly because we are listening not just to see if there’s a signal but what’s the quality of the signal. Is the signal absent in the dorsopedal or the deep plantar arteries? What’s the quality? Is it monophasic, is it stenotic, is it a weak signal or is it a strong signal? And then, of course, we order our ABIs including our PVR waveforms. We always look for infection. We always probe looking for penetration of bone or tracking of wounds because you’ll track all and you need to know where you’re going. We always get our x-rays. We’re very keen on getting PET scans now because PET is easier for us to get than an MRI by far. We’re quite comfortable with using PET to make our diagnosis of osteomyelitis especially when Charcot is not present. When Charcot is present concurrent with an ulcer as we’ll see, that’s a little bit more difficult obviously. Of course, you are looking for deformities. Because deformities lead to high pressure point. We know that these deformities are going to need to be corrected at some point. Then, when we do our assessment then we have our classification. You can use any classification you want. The University of Texas, I tend to Wagner because it’s easier for me. Or you can just go, is this neuropathic, is it ischemic, or is it neuroischemic? If it’s neuroischemic, you have to get a vascular consultation. If it’s ischemic, you better get a vascular consultation. Then, it facilitates your treatment. By a thorough systematic approach and assessment, you address each one of these points. You take care of them if there is a problem. I don’t view this as being terribly difficult. You just have to be thorough in your approach and look for these underlying problems. Whoop, what did I do here? Here we go. Alright, so this is an algorithm that I put together. Just for a simplified algorithm for infection which is our main focus this morning. A diabetic foot infection, as you can see, we’re probing the wound. You can see you got some soft tissue necrosis on that picture. We do the clinical exam, look, feel and listen. We look for cellulitis, we look for bullae. We look for necrosis, look for cellulitis, feel it, is there any crepitus. Can we hear crepitus? Is there fluctuance when we feel it? So look, listen and feel. Cellulitis, lymphangitis, bullae, et cetera, probe to bone pulses. This is just basic. This is done within the first couple of seconds that we’re evaluating a patient. We get our imaging of both soft tissue and bone. Always get your x-rays. Believe it or not, they’re not always done. Always get your x-rays and then additional scans as necessary to supplement your evaluation. This also includes your angiography in ischemic patients. We got our routine lab studies, of course, always looking at creatinine, always looking at the glucose and, of course your white count. The problem with the white count is that in the diabetic patient, it’s often suppressed. It’s not always a good indicator of severe infections. This has been shown by several studies, even by Magnus Eneroth back in I think 1997, 50% of his severely infected patients had a normal white count. You can’t rely on the white count nor a fever. But when they are present, I think they’re very important signs. Okay, so the absence of leukocytosis is not something that you can rely on in all cases. But when you do have leukocytosis, when you do have fever, you need to really pay attention to it. And then, based on that evaluation then we’ll classify and treat accordingly, so I don’t view this as anything that’s very, very difficult. We tried to simplify things as best as we can. With that brief introduction to our approach, we’ll just go some cases over. Most of us are podiatrists and we all grew up on just looking at the pictures so we want to do that. My residents will recognize these patients. This man is still under our care and that he came in, in the summer with acute necrotizing soft tissue infection. Javier Aragón Sánchez has done some nice papers. He comes from the Canary Islands in Spain. He is a general surgeon who focuses on diabetic foot infections. He’s done some great papers on infection and soft tissue infections and management in osteomyelitis and so I like to use his terminology, necrotizing soft tissue infections. You can see the amount of necrosis on the lateral side, dorsal and plantar side.

[15:03]

Typical history of fever, chills, malaise, important signs, I call that diabetic foot flu when they have that malaise. They are not complaining of pain in the foot. They just don’t feel right. We see gangrene, cellulitis and sepsis. We always get our blood cultures, of course. Of course, this is no surprise. This is a surgical problem far above antimicrobial therapy, although we do everything altogether. I think this was after his first initial debridement where you’re just trying to control infection. Recognize we’re not always going to get all the necrotic infected tissue out at one time. This is after the first debridement, then we took him back a second time and, of course, he had to have his lateral ray amputated. Because I mean, we can see a little bit more than healthy wound bed here. Again, we can look at the image in the center to the bottom so the second debridement were improving. We always expect multiple debridements on these patients. Always expect that. I tell patients, “We’re going to have to do this several times. If you want to save a leg, it’s much harder to save it than it is to cut it off.” We focus on multiple debridements as appropriate, as necessary. But the main job, control that infection. Once you’ve got the infection controlled, then you have time to settle back and do your other investigations. But I like to know am I dealing with an ischemic infection or not, first of all. To me, the vascular assessment concurrently is important. But job one is to control the infection. There's not going to be any revascularization while there’s acute raging infection so you must control that in the presence of ischemia or not. You have to control the infection and that requires several debridements, of course. Then we see further improvement. Once we get rid of much of the necrosis and the drainage, that we start putting these patients on negative pressure. I’m a big fan of negative pressure for many years. We are now using the installation negative pressure devices because they will help clean these infections out as well, also to give us time to see how they will respond. Then we recognize we need to go back and debride further. We’d narrow our broad spectrum antibiotic coverage. Remember, you are covering gram positive, gram negatives, as well as anaerobes but the main goal is to adequately treat those gram positive. The gram positive ones are the organisms that drive the whole system. MRSA is a problem but not as much of a problem as beta hemolytic strep or alpha streptococci. Those are the so-called flesh-eating bacteria so I actually pay more attention to those than MRSA, although we routinely cover for MRSA initially. On this case, once he was appropriate, once we have no necrosis, even though we have underlying exposed deep structures, we tend to use this bi-layer matrix tissue, Integra. I’m trying not to use a lot of brand names but Integra is very popular overseas for this application as well as here. We use an Integra and I use it under negative pressure. Now, it looks soupy here but that’s because you’re looking at the silicone top layer under negative pressure. Always get soupy and it always lifts up from the wound bed. But what we’re trying to do is provide coverage for that wound bed obviously. Here is immediately, you have to remove that silicone layer. Now, look at the difference, we see we have a nice granular wound bed. And we’ll just continue using further negative pressure. We could see negative pressures continue until we get a nice, healthy wound bed ready for split thickness skin graft. Over a skin graft, we use a negative pressure therapy. I usually use it for about five days. This guy had a pretty good take. Not 100%, we’re still working on some areas down on his fifth ray area which was so problematic. But we can see where we’ve gone from a horribly necrotic foot, we’ve got him down to one small ulcer in pretty healthy coverage. He had about 95% coverage of his wound area. This is in a neuropathic individual who did have good perfusion luckily. That’s why there was no vascular intervention here. Once in a while, we do get a nice, healthy infection. He has done fairly well and we’ll do well but these take months. You have to be prepared and the patient has to be prepared to work months on these things. But these patients are outpatients. Makes a big, big, big difference. One further amputation, one further hospitalization might cost $25,000, $30,000 just for that one episode. So even though we’re going a long time and a lot of visits and using some advanced products, we’re actually saving money in the long run by avoiding further amputations, especially major amputation.

[19:59]

Alright, let’s do another case. When you’re presented with a leg like this, we don’t even know what’s underneath that wrap yet but this is extensive cellulitis, extensive lymphedema, an obese types 2 diabetic, neuropathic man. Progressive swelling, erythema on his left leg, chronic lymphedema, he has pumps at home but not really using the pumps. Regularly use the pumps but he again complained of malaise, hyperglycemia. He did have leukocytosis but denied fevers, okay. We didn’t find any fever. Negative sign for a fever is not always reliable as we said. His Doppler waveforms did not indicate ischemia and waveforms, to me, sometimes just means PVR and listening to the Doppler signals. Of course, his venous ultrasound was negative for a DVT. We get a lot of ultrasound scans for DVT. We take off the dressing and we see a nice, again, soft tissue necrotizing infection on the plantar lateral foot. This was more towards the summer so we tend to see a lot of these infections festering in this area. Obviously, this is a surgical problem far, above and beyond that of any antimicrobial therapy. Of course, he's going to require operative debridement and culture-directed antimicrobial therapy. This is nothing new, but it’s the process of getting this done as quickly as you can and that’s almost an oxymoron when we talk in the VA system which is marked by horrible inefficiencies but we try to move these as long as fast as possible. Antibiotics are easy to start but getting them in the operating room sometimes takes a longer time, which is why many times, we’ll do operative debridement, surgical debridement right at bedside because these people are neuropathic. As long as you’re draining that pus and controlling that infection, you’re doing the patient some good until you can get them into the operating room for formal debridement. Here he is, after initial debridement, not very healthy. He had a lot of bleeding. He was well perfusing so you have big clot on the bottom of his foot there but at least we’ve gotten rid of a lot of the soft tissue necrosis. Here is another view but a very deep wound, obviously still swelling going down, cellulitis improving with these debridements. But once again, we expect multiple debridements, not necessarily everyday but multiple debridement, maybe once or twice every week until we control this problem. Once we get rid of the necrosis, there is no more purulent drainage. We all tend to use negative pressure as I said. This one is an installation negative pressure device because the installation can really help expedite the clearance of the infection. To a point, I mean, sometimes, I don’t use the installation completely through the whole course of negative pressure. But I use it initially to clean up the infection. Once we have a fairly healthy wound be, I’ll stop the installation and just continue on with the negative pressure therapy, traditional negative therapy. Now we’re seeing a little bit better wound bed here. What we’re trying to do is prepare the wound bed for soft tissue coverage. Now, those of you looking at this, that’s not ready for any skin graft and it’s not because we’ve got either exposed bone or tendon or fascia here and you can’t throw a skin graft on there. We rely on many of our soft tissue substitutes. Here was a bovine neonatal dermis that we use on a debrided wound bed, covered over with negative pressure therapy, okay, and several weeks of negative pressure therapy because we are trying to develop granulation tissue above that. That bovine collagen or you can use human collagen here or human dermis will become incorporated into the wound. I’m looking for some soft tissue coverage, some bulk there. As you can see over the course of weeks of negative pressure, we develop a nice, healthy granular wound bed. Then we move the patient to the outpatient setting and I like to use mechanical negative pressure therapy when possible, when it’s appropriate as an outpatient because it’s just a little bit easier. Here, we have a much healthier bed compared to what we had had before. This is right after removing the negative pressure device. Then we continue. He’s at home, we’ve continued it until we get a nice, healthy, superficial wound bed. Then we’re ready for skin grafting. I failed years ago because we didn’t move quickly to skin graft. Now, our premise is let’s get skin graft on as soon as it’s appropriate because the longer these wounds are open, the more susceptible they are to infection so I like to move them through to a nice, healthy bed like this.

[25:09]

Remember, you had a nice necrotic deep wound before but now we have a nice granular superficial wound by using these multiple modalities to get to this point. Then we applied a split thickness skin graft. I usually use sutures, absorbable sutures. A lot have gone more to stapling lately. But almost invariably, we’ll use negative pressure therapy on our skin graft for a take, usually for five days or so. If they’re inpatient, it’s not a problem or I’ll send them home with this and then they’ll come back and then we’ll just take it off and then you’re done with negative pressure. This is a perfect application for some of these disposable negative pressure devices that are good for seven days. There’s a couple of companies probably here who have them. I think it’s a perfect application for those kinds of negative pressure devices because you’re going to use it once for five days or so and then it’s done. Here, we can see we had a full take of his skin graft starting from where we did to now and his edema has come down, he’s starting to use his pumps. This is the way that we would normally progress through managing these very severe limb and life threatening infections. I’m sorry, I didn’t go back and tell you what the organisms were. But once again, I worry more about beta hemolytic streptococcal infections than I do MRSA. I just think that you have much more soft tissue necrosis, not that you can deny the importance of MRSA but for soft tissue necrosis, I think streptococcal infections are very, very significant and severe and we pay particular attention to those. Luckily, they are very easily treated with the first generation cephalosporins or penicillins, if you like so, they’re very easy. But you need to treat them properly. Okay. Here is case 3, how will would we manage this? Fifty-seven-year-old non-diabetic man with a history of ETOH abuse and clinically fairly profound neuropathy which we see, not diabetes, ETOH abuses are the most common reason for a neuropathy. Mild PAD but no revascularization was gained necessary by our vascular surgery team. He had chronic forefoot ulcers, chronic recurrent forefoot ulcers despite previous attempted operative intervention, bone resection, debridement, et cetera. He had recalcitrant recurrent osteomyelitis. He had almost predictable complications, if you think about it, they’re almost predictable as we’ll see here. Okay. Here we go. Here is our start. First metatarsal ulceration and he’s treated appropriately with appropriate offloading and local care, negative pressure wound therapy as we can see here. A subsequent required sesamoidectomy because he developed osteomyelitis, his wound just would not heal with good proper care, maybe he was not good with his offloading at this point. He subsequently learned but it was not good, so we did a sesamoidectomy which I don’t often do it but it’s well-illustrated in the literature. The sesamoidectomy is a fairly reasonable approach to a localized ulceration. I’m not that big on sesamoidectomies myself anymore but it’s certainly something that’s worth trying in appropriate circumstances. Well, he failed. He failed and got acutely infected then we had to proceed with a first ray amputation because he developed osteomyelitis of the metatarsal head and the joint. You see a funny shape to that flap because I had to go around the ulceration to do it. Designing flaps for your amputation is an art in and of itself but you’re doing the flap that seems to work best to get that wound closed. I don’t like doing open amputations unless it’s for a drainage. I want to do a definitive procedure, I want it closed so we did this and we had a nice result. And he initially healed. This is back in February of this year. But then he had started to develop persistent swelling. This was in April. Completely healed, yes, you’re worried about deep infection, but there’s really not a lot of erythema there. But let’s see, first ray amputation, you lose the first ray, biomechanical instability. Then we have to start thinking about other problems that have been illustrated in the medical literature and then what do we have here? We’re looking for that minor slip, that minor dislocation, the second metatarsal, the keystone joint there. The second metatarsal with the second middle cuneiform, so this is the onset of an acute Charcot foot.

[30:00]

Predictable, predictable, although not always occurring but we’ve seen this commonly and it is in the literature. Here we are, so we instituted offloading whether it be seriously an initial cast nonweightbearing or a CAM boot. Both are acceptable based on the literature, evidence in the literature. Here’s a Charcot foot, it was properly diagnosed early on so offloading with a CAM boot and a TCC. Fairly good structure it means. Now, the patient remains off the foot, just keep him immobilized, he should be okay. However, progressive changes, remember these are neuropathic patients. Even though he had been immobilized the whole time, which is why I like casting and nonweightbearing although some people will weightbear people. I like to keep them off because I see this time and time again despite diagnosis, despite proper early therapy, they progress, he progressed. . Remember he wasn’t diabetic but he had alcoholic neuropathy. Alright, we have a picture of a CT scan on the bottom left there which shows the disorganization at the midtarsal area, so a complete dislocation there. Then he developed ulceration with his rocker bottom foot. This was predictable, acute infection, you can see that middle picture. He’s got an infection abscess up around the lateral side of his foot requiring drainage, debridement, et cetera. Negative pressure therapy after. We’re talking a year or so into treating this man or two years. We had done our proper antibiotic therapy, our antibiotics, operative debridement, bone cultures, et cetera and you could see the negative pressure therapy on him. Here we are, here we are, an infected Charcot foot. There’s a PET scan that you can see in the middle showing his entire midfoot lighting up and he’s got abscess there. He’s got osteomyelitis. You can see the progressive changes on that x-ray on the left. He’s got his Charcot foot easily visible there, so what would you do in this case? Anybody want to shout out what would you do in this case. Pardon?

Male Speaker 2: BK.

Male Speaker 1: Okay, we had BK, very viable, very viable option. [Indecipherable] [32:19], would you do a BK? Anybody else? That whole midfoot now is infected. Any other alternatives? Yes.

Male Speaker 3: [Indecipherable] [32:34]?

Male Speaker 1: Syme amputation, very good. That’s obviously something. We’ve done that. To address your concerns, his flap would be perfect. There’s no wound on that heel. These are the things we have to think about. Because we’re not going to putz around with further debridement and antibiotic therapy where you’ve been that route. So we did a Chopart amputation because we had reasonable flaps because I think his amputation site or his infection was distal to the midtarsal joint. Here we can see the postoperative film. Because we had that plantar ulcer, it’s always a challenge to try to get that close. When you design your flap, you’re trying to close the plantar ulcers so they’re really hybrid amputations. We took these pictures just yesterday and he happened to come in the clinic so the bottom two pictures we can see, he’s completely healed now and this has been several months since his amputation, completely healed. Now he’s getting ready for his Chopart prosthesis. The other alternative for me would have been a Syme amputation. Yes. Okay, because I think you can save it. This poor man, many, many problems but we’ve saved his leg. I think we did everything appropriately. He just developed one complication after another including Charcot foot then the infected Charcot foot and so Chopart amputation. Now he is healed. Hopefully with this prosthesis, he’ll get on and move on, no further problems. This is my final case, I didn’t know if I’d have time for this or not but we do. Let’s go over this last case here, another Charcot foot. Not that we see Charcot feet everyday but we all see Charcot feet that come in, sometimes acute, sometimes chronic. This patient had previously been treated for an ulceration that is infected first MTP joint on other foot and then a year later, he comes back in with an acute Charcot foot, with this nice nasty ulcer that probes right to bone. He’s a type 2, 59-year-old, neuropathic man. Again, I’m not presenting any patients with significant ischemia here. Okay, these just happen to be neuropathic patients or neuroischemic patients. Nice nasty large ulceration that probes from the bottom ulcer that looks fairly good all the way to the lateral side as you can see in that top right picture, a little bit of soft tissue necrosis, but there’s a fluctuant abscess.

[35:08]

When you feel a fluctuant abscess, you know you have to drain that right away even if it was right at bedside. There, we can see the probe directly through. The first job is obviously control infection, debride it, let the pus out, clean it out first. Again, this man had an acute Charcot foot, fairly acute and then he developed this ulcer consequently but he had palpable pedal pulses with good waveforms. We did get our ABIs as we always will do. I call this a subacute chronic unstable Charcot foot. He was unstable at the midfoot and offloading had not been successful and so he just developed progressive changes and got the infection. Here we are after one or two bone debridements and you can see the large ulcer still remaining on the bottom of the foot. His infection though had been controlled with the debridement. I think we did use the installation negative pressure and also systemic culture-directed antibiotic therapy. Here we are at this point. Now what do we do? We see, we got the foot, the wound is probed right to bone. These are two images of PET scans showing probable osteomyelitis in the midfoot. Okay, this is two separate images on the bottom left and right. I presume it was infected we had an acute soft tissue infection and we’re probing right into the joint, right into the midfoot joints which were unstable. What are our options now? Just shout out what you think we might need to do. Nobody has any ideas? He’s in your clinic, he’s your patient. Chopart is one. Yeah, yeah, we might thought about that. Hyperbaric and antibiotic, probably that might be used, I don’t think that hyperbaric and antibiotic. We don’t have hyperbarics first of all. Antibiotic therapy, he had had. He’s well perfused. Now he wasn’t ischemic or neuroischemic so I don’t know. Although one of the indications for hyperbaric is chronic osteomyelitis, chronic recalcitrant osteomyelitis. Possibly yeah, I wouldn’t say no but possibly. Anybody else?

Female Speaker: [Indecipherable] [37:39]?

Male Speaker 1: Alright, a fusion. Anybody want to go for a fusion here?

Female Speaker: Not really.

Male Speaker 1: Not really? Okay. Here’s what we did. A fusion, I should say, we’re attempting a fusion. We did a full frame. I don’t know, it’s a lot of hardware there. Remember, he’s no longer acutely infected. We had managed that infection. If you look at Nikki Kinzer’s [Phonetic] work, we did like a midfoot tarsectomy as she calls it, a wedge resection and then try to push it altogether with a frame. We did some axial wires there to maintain position. I think we also did a TAL. I do TALs, not the gastrocsoleus resection which everybody loves to do, I just go TAL. Okay, so we did a TAL so we can move the talus up. Here we are not perfect, they’re never perfect in my mind. You can see his plantar ulceration which we treated concurrently with negative pressure wound therapy. He’s still on antibiotics because he’s still infected so we have him treating for osteomyelitis for six week, concurrent antibiotic therapy. You can see this, he was in our CLC, our skilled nursing facility. We’re treating him with negative pressure therapy. That plantar wound progressively improved. He left, went home. We still use negative pressure therapy. The picture on the lowest one on the bottom center there was yesterday. He just happened to come in yesterday so I threw this in. His plantar ulcer is essentially completely healed. What are we? I think we’re 10 weeks post fusion now and I plan to keep him in the frame for about 14 to 16 weeks. But he’s also on a bone stimulator because this guy is notorious. They’re going to slow to fuse. I’m not quick to remove the frame because I don’t want it to fall apart. While he’s at home, but we’ll probably plan on removing this frame next month. Okay, so this is where we are. Nothing is perfect. This is the way that we heal it. Yes, a Chopart amputation I could have done very easily on this patient too but I felt we had a chance with this.

[40:02]

He had gone through a year or so of failed treatments. That comes to play as well. Somebody who’s gone through repeated operations over and over and over again with failure, I tend to be more with let’s get it done. But this man, this is the first episode with the infection here so we’re going to give this a good shot. He’s got a plantigrade foot. It’s not fused yet, but it’s plantigrade, a little shorter but I think he’s going to do okay. The basic tenets of limb salvage 2015 are the same as they were in 2010, 2000 and 1995. Medical management, stabilization, diabetes control, treat infection early and aggressively with operative incision and drainage, debridement, antibiotics, et cetera. Look for osteomyelitis and treat it. Treat ischemia when present, do your good clinical assessment, always get your ABIs. Go back to the 2003 ADA consensus panel on PAD with our recommending any diabetic patient older 50 should have an ABI baseline just so you have something to compare it to. We tend to get them on baseline just so I can compare it for future events. We practice foot-sparing surgery, partial foot amputations when indicated, certainly better than major amputation because people will live longer generally. We’ll do reconstructive procedures, ablative procedures, amputations, et cetera, whatever really we feel the patient needs and depending on the soft tissue coverage and the perfusion. Wound care always, debridement always, offloading. Offloading is where we all fall short. Look at Stephanie Wu’s paper, about 2% of the people practice with TCCs, 2% of the entire wound care population practitioners treat with TCCs. We’re more aggressive with TCCs. I think we could be even a little bit more aggressive so we tend to use a lot of CAM boots. But for those of you who are CAM boot fans, the literature shows exactly the same effect so there’s no problem there. But sometimes, you have more control with the TCC. Of course, prevention, once you heal these people, they must get into your prevention program. That’s also where we fall short. We’re always writing patients with prior ulcers, amputations, Charcot but we haven’t seen for three years. We should be seeing them every three months. You want to make sure your prevention program is up to speed as well. I use this for many, many years in the VA system, we use our system, podiatry is the gatekeeper. Anything in the lower extremity, we tend to get. Anything below the knee, we get. We manage all the diabetic foot infection. We manage all the prevention, et cetera. When we have a problem, we work very closely with our vascular surgeons, our internists, hospitalists and all the other services functioning to save that limb, get these people healed and keep them healed. Simpler than what it sounds as we all know but anyway, some kind of a model is necessary depending on where you practice. In summary, diabetic foot complications are leading causes for diabetes-related hospitalizations as we know. Neuropathy, PAD, ulceration and infection, major risk factors for amputation, they’re all related. Proper assessment, we’ll facilitate proper management because if you find a problem, you need to address the problem. Limb salvage requires patients and persistence as you’ve seen. Multiple operative debridements are often necessarily as we’ve seen. You can’t do it at one time. Always follow the basic tenets of wound care. Treat ischemia. Do your adequate debridement. Treat your infection. Treat your underlying medical comorbidities. This is not rocket science really, you just have to be persistent and do what is necessary. Of course, multidisciplinary management is always essential. Here’s our classic diabetic VA patient. With that, I want to thank you.