John Schuberth, DPM discusses the myths and realities about healing in the diabetic patient. Dr Shuberth reviews effective management and repair of the ankle fracture, possible complications and ways to avoid these complications.
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John Schuberth, DPM
Chief, Foot and Ankle Surgery
Kaiser Foundation Hospital
San Francisco, CA
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Bob: Our final speaker, I wanted to present you with someone who’s new to Desert Foot. A long time friend of mine, but someone who I consider probably one of podiatry’s best foot and ankle surgeon is as critical as I am I think but probably a little bit more and certainly more cynical than I am. Jack Schuberth is the Chief of Foot and Ankle Surgery at Kaiser Medical Center in San Francisco. He’s got a wealth of experience in very complicated foot and ankle surgical procedures including in diabetes and trauma. He’s a past President of the American College of Foot and Ankle Surgeons and former Editor of the Journal of Foot and Ankle Surgery. I asked Jack to do a podiatric purpurea [Phonetic], if you will, of problems that he’s noted over the years in operating on diabetic patients or specifically neuropathic patients. One of his first topics is going to be the operating patients with the neuropathic ankles and ankle fractures. He’s going to take us through a few assorted topics as well since I’ve asked him to fill in for Guido Laporta who could not come. Believe me, when I say I ask him to fill in Jack and easily, easily do that, he’s going to, as I said, a wealth of experience. I’m really very, very pleased that Jack took time out of his busy schedule to come lecture to us tonight. Let’s finish out the program with a great series of talk with Jack Schuberth.
Jack Schuberth: You have never seen me operate for one but Bob, I do want to thank you. Most of you probably haven’t seen me on a luxury shirt [Phonetic] because I recognize very few people in the room but I’ve been operating on diabetics for 29 years. When I started, I have the fear of God putted in to me about ever touching a diabetic with a 15 blade or a 10 blade and I still have the fear of God. And yet as we evolve and we get better fixatives and better biologics and better knowledge, I think we’re able to take care of a lot more difficult problems. I’ve often told people that I don’t know a damn thing about diabetes and Bob has forgotten more than I’ll ever know. But I know how to fix some of these things and recognizing that my failure rate is probably not any lower than many people that do this. But one thing I’ve learned is to be honest. Be honest with the patients and be honest with your colleagues about the success rate in some of these more complicated problems. I am going to start out with diabetic ankle fractures, I personally have operated over 3,000 fractures as a surgeon of record in 29 years, and whatever the percentage of the population is diabetic pretty much typifies my experience in the diabetic, which one is which here, in the diabetic ankle fracture. We’re going to take an overview. We don’t have enough time to get in all of the nuances of taking care of the diabetic. Well, clearly, it’s a matter of perspective when see these patients with fractures. We have to ask ourselves what makes these patients so different. Should we be afraid and I’ve already answered that question. We should be afraid but we shouldn’t be so afraid that we give them suboptimal care just because they are branded with this diagnosis of diabetes. I think we all come to realize that there is a lot more to it than just fixing the ankle. Many of us know how to put all sorts of stuff on the ankle. In fact, in 3,000 ankle fractures, I’ve yet to use a locking plate and none of them have ever fallen apart. But it’s not to say that we shouldn’t use a locking plate in a diabetic or we shouldn’t do this or that. We have to realize there’s a different dimension of complexity just because the patient is diabetic. And so, we have to of course know how to fix the bone as we mention. We have to modulate the biologic metabolism that is clearly compromised in the diabetic. We have to really worry about end stage renal disease as you all know. This is just a harbinger of disaster. We have to worry about Charcot arthropathy. But to this day I don’t know a single person that can predict if a patient that are going to develop Charcot arthropathy with an ankle fracture other than the fact that they have neuropathy. The other complicating issue is of course soft tissue complications which are pretty much non-existent in the sensate healthy patient in low energy ankle fractures. And so we’ll talk about bone healing and people say all the diabetic doesn’t heal.
Well, who says they don’t heal? What’s the difference between diabetic bone and your bone? Well, no one really knows the metabolism per se. We appreciate that it’s probably a little bit more brittle, particularly in the diaphysial areas. But whether it’s more brittle in the metaphyseal areas which is really the business end of the tibia and fibula with respect to ankle fractures, I’m not so sure about that. Remember that these patients have more body mass and so the same maneuvers or shifts in body weight in the diabetic patient versus the average patient made of in part more force to the diabetic bone and yet we extrapolate that and say, well, the bone is weaker. I’m not so sure about that. Certainly, the healing rate is going to be compromised if you have nutritional deficits or glucose metabolism deficits as you’re all well aware of here. But we have yet to define a concrete difference in the way diabetic bone heals or breaks compared to the normal population recognizing that just because you’re diabetic doesn’t mean your blood sugar is in the 400s and your hemoglobin A1c is over 6. And so, we have to sort these things out and recognize that they are not necessarily universally applied to the entire diabetic population. Yet, we appreciate that the local biology does change. Although we can’t necessarily define it, we have to take it into consideration when we apply our fixatives. Now, I’m going to talk a little bit about Charcot after this talk here. Nothing makes my blood pressure go up more than somebody who comes up and gets on the lecture and says, “If you operate on a diabetic foot, you’re going to cause Charcot arthropathy.” That’s just simple fiction. It can but it can also be just a straightforward ankle fracture culminate in the disastrous complication without anybody ever laying a knife on it. And so, I’m always wary of Charcot arthropathy. I like to watch for it but until someone can come up concretely with predictors that are going to make a difference in taking care of the diabetic population, I’m not going to change the way I’m doing things realizing that I probably among the far left end of taking care of these patients which for reasons which should become clear in a second. We do appreciate as Dr. Navone [Phonetic] has just pointed out, there is a higher incidence of infection. Bob Fieberg’s [Phonetic] paper pointed this all very nicely. We’ve known this empirically. Bob’s proved it and there is not a damn thing we can do that about that other than practice good surgical technique here. What are these myths? Well, the bone is soft. Well, we don’t know that. We don’t know that the bone is soft at the distal metaphysis. It won’t heal. Many of these diabetics have excellent circulation. If they don’t have good circulation, we’re not going to operate on them. It’s that simple in my mind. The circulation is poor. Well, they do. Some of these patients do have poor circulation and they just don’t heal any operation that we provide for them. And anesthesia says no. This is the one that just kills me. Any numbskull can put a patient to sleep if they’re healthy. But we need an anesthesiologist to put people that aren’t so healthy to sleep. I trained in Seattle as some of you know. And in the days where the trauma world was evolving, and Ted Hansen [Phonetic] used to say this patient is too sick not to operate on it. And I think that that’s very, very true in the diabetic patient when you get these 300 plus patients which primary their fractures that are just incapable of being non-weightbearing, they’re confined to bed. There is tremendous physiologic cause and cardiopulmonary cause to someone that’s bedridden. We try to mobilize these patients whether or not we let them walk on this with personal preference. But we need to get them functional instead of just plopped them in the bed and say, “Hey lady, we’ll get you up when your fracture heals.” That may be six or eight weeks for now and they may not survive it. And so, we also have been told, well, she can’t be non-weightbearing. Well, can’t and won’t are two completely different verbs. People can be non-weightbearing if they break both tibias, they will be non-weightbearing. And so we have to get pass all of these stuff that’s kind of been propagated is the can and won’t, and should and wouldn’t. Because it does come into play when we take care of the diabetic patient and I already talk about that. So what’s the real deal here? The basic difference is the complications are more common, we all know that. No one is going to dispute that. The dilemma is how to stratify the risk over the long-term. What I mean by the long-term is from the time the patient breaks their ankle until the time they assume their pre-injury functional levels.
That’s how morbidity is measured in hip fractures, tibia fractures, and every other orthopedic injury in the world and that’s how we need to do this. Pre-injury function, post-injury function, that’s the long-term. It may not be years, it may be a matter of weeks or months, but we have to appreciate that the mortality of these patients is clearly not zero just like it isn’t zero in a total hip. When my residents come up here and I’ve heard some of these fiction, I said, “You should ask if patient how fast and or how soon and how do you want to die? Do you want to die laying in bed or do you want to die from an anesthetic complication?” I’ll take the anesthetic complication any day because I know that that’s very, very uncommon. That people aren’t going to get off the table. So what are we trying to do? Well, we are trying to preserve life. You may say that sensationalistic but I’ve had a number of patients die. In fact, in 2012, I’ve had three people die on my service after taking care of fractures. It’s not much fun, believe me, to go tell the family that auntie, Auntie Lee [Phonetic] is no longer with us. So we are in a sense trying to preserve life. We’re trying to preserve the limb. The next slide is behind it. We’re trying to restore to stable plantigrade platform. It can be an insensate plantigrade platform but it has to be stable and it has to be plantigrade as you all well know. It may be up the expense of anatomic reduction. So if a patient is insensate, all I want is the foot under the leg. I don’t care if the ankle has arthritis or not. If it moves a little bit, great but that’s a good result in many of these patients because they still have their leg and they still can assume their pre-injury levels. So someone ask, “Well why even operate on this patient that they’re diabetic? What’s wrong with non-operative care?” Well, not a lot is wrong with it except if you’re 300 pounds, got cardiopulmonary compromised and there is no way that you can transfer from bed to wheelchair without walking on that ankle. So closed reduction cast in a hotel stay used to be modus operandi. When I was a resident here, we just put these patients in a cast, put them in bed for six weeks. And we recognize there was a fair amount of morbidity. And so the problem in my mind is weightbearing. If we can get that patient to bear some sort of weight after we treat their ankle fracture, whether it’s operative or not, then we have basically circumvented some of the cardiopulmonary compromise that’s inevitable in these patients. And we all understand that weightbearing in a diabetic patient is difficult. And we can argue for hours whether it’s because their brain isn’t working or whatever, but I don’t think it’s that. I think it’s because they’re just physically incapable of being non-weightbearing and so I don’t fight it. I just assume that I’m going to fix this fracture so that you can get out of bed and put some weight on it immediately after the injury. We all know that even though they may last or, you know, while they’re in the hospital or not and weight bearing, when they get home, they’re going to pounce on it. What are the mechanical issues? Well, the bigger they come, the harder they fall, as you know. And it not only affects the severity of the fracture but the postoperative management. Obviously, energy in equals energy out. We have to deal without that. We can’t control but we can control the postoperative management. And so, is there a correlation of diabetes in the ability to be non-weightbearing. I don’t think so. I think there’s clearly a relationship with body habitus and overall health which we appreciate is different. But certainly, we have to understand that weightbearing doesn’t potentiate Charcot. We’ve seen Charcot in non-operative and operative. If we do get Charcot and we recognize it and it doesn’t go on to collapse, we can take care of it. I personally believe the answer to this question is yes. I do believe that these patients will decompensate over the six to eight week period. And in my mind, that’s the real issue. Can we prevent that decompensation that we see in the elderly sick patient after trauma? As I mentioned, the model in the orthopedic world is hip fractures and yet we have to study this in more detail. Let’s look at some of the things here. Upper arms strength, as we talk about cardiopulmonary restraints, immediate weight bearing. And I’ve been told that I’ve committed malpractice. Well, I probably committed it 3,000 times because out of the 3,000 fractures I’ve done, I’ve operated well over 2900 of them within two weeks of surgery. I’m not including Pilon fractures. And knock on wood, haven’t been accused of malpractices yet.
So we look at how the ankle breaks and we have to realize it taluses the weapon of insult. This is what causes the fracture of the malleoli because of the morbid motion within the mortis. We appreciate that it’s a rotational sequence, alright? The PABs and [indecipherable] [15:21] SADs are extremely uncommon. These are rotational injuries and we have to keep that in mind. And so when the foot rotates on the leg or the leg rotates on the foot, we’re going to cleave off the malleoli in a fairly recognized pattern and we need to put it back together. Of course, we all like to put in screws and plates and all sorts of paraphernalia here. It’s a lot of fun to do this. My point is it doesn’t matter what you do, you have to make a stable construct. You can use screws and plates. You can use locking plates and waste our money but the point is you need to get the forces of the foot up through the tibia and have it absorbed by the long axis of the tibia. And there’s lot of fixation alternatives as I mentioned here. I’ve been told that you can never put tension bands in oblique fractures. I’ve been doing that for years and this lady got three of them or two of them, and a plate, and this is a very, very stable construct. It’s called miss-a-nail technique where you bolster the screws on either side. And this woman was diabetic. We got her out of bed the next day when she did remarkably well. I saw her 20 years later, she was senile as I am. After fixing her ankle fracture, she broke the other side but she never had a single problem with this and there it is on the side there. And so, we have to modify our technique sometimes. We can’t just look in the book and say, well, that needs a semi-tubular plate and the interfrag screw here. This bone may or may not be any good. And there is no law that says we can’t just fire Steinmann Pins in there or whatever it takes. There’s just a couple of other options here. Two K-wires that are buried under the skin or poke into the skin or two transsyndesmotic screws. And this is the technique that I favor the most which is called the fibula pro-tibial technique where a simple little rotational fracture that I deem unstable. I’m just going to fire several transsyndesmotic screws through the plate, tighten them down and get the patient up. There’s no place for that bone to go. The fibula cannot escape because it’s incarcerated by the fibula. And so regardless of how we fix it, if we can dampen the rotational forces, then we can allow the patient to put some weight up through the tibia. In rare instances, I will supplement my construct with an external fixer if a patient is polytraumatized, I’ll usually put a fixator on it so we can get them out of bed and get their lungs functioning better and everything else functioning better. But it is probably even five times in 29 years where I put a fixator on a diabetic fracture just to allow them to walk. We try to minimize the exposure if we can because we don’t necessarily need anatomic reduction. We can capitalize on the neuropathy and modulate the biology if it all possible. So you say, well, big deal, rotational fractures, any sort of fixation, we’ll take care of it if we can dampen the rotatory torque. How do we do that? Well, we can neutralize the disruption by simply transferring the weight up the tibia, one of the simple, short leg cast. There is no way that that foot can rotate and put pressure on the fibula or the medial malleolus when it’s incarcerated in the cast, it’s impossible. If you hold the ankle still, the fibula will absorb very, very little if any load with full weight bearing up the tibia. And that’s pretty been the premise of my thought process for many, many years. Transfer the weight up the fibula. This is the only one that I’ve ever had fall apart in 29 years I’ve operated on these patients. And it fell apart in a manner that I still defies me to this day, whether I missed the interfrag or whatever or she had distal lateral osteonecrosis of the distal tibia, I don’t know but this is the only one that fell apart. Here is just a couple of other techniques here. This guy was numb as a brick and I didn’t even open the fracture. I just put this plate on through a percutaneous corridor and fired three transsyndesmotic screws, put him in a cast. And it’s not perfect but he loves it. He has absolutely no pain and he was non-weightbearing. Exactly, that hour it took me to put the hard wiring [Phonetic]. So does this always work? Well, of course not. We always have complications. And when these complications occur, they’re often catastrophic.
And as I mentioned, I had three deaths on my own service this year. And I lost a lot of sleep over this and still just dizzy by this whole thing here. And many of these patients end up with amputation but not as many as you think whether sound and judicious approach to these ankle fractures. We’ve talked about soft tissue complications, you all know how to take care of this far better than I do. I don’t know very much about wound care. My residents take care of it all and they don’t even bother. They ask me anymore because I don’t know. They just do what they do and most of these things heal. This is another woman that got out of bed before we even got the cast on him and busted this one apart, but that one I don’t count. And she ended up in another emergency room. And I could have strangled the surgeon that did this putting these two Steinmann Pins up right through the heel. This is his way of fixing it. Obviously, this lady is going nowhere with those two pins that were protruding through the plantar aspect of the heels. So I finally wrestled her back into my clinic and put a fixator on her, centralized the tibia, excuse me, the talus and let her walk. This guy, he was a model. He built airplanes and you can see that he probably wasn’t very good at it, diabetic, bilateral Pilon fractures from a plane crash that he built. This is from Southern California and this was just a mess. And we ended up doing a fusion on him. This is probably about 15 years ago. And so we can’t saw all with these patients if they have good blood flow. Is it pretty? No, it’s ugly. But the point is these patients still have their limb and they can get back into their pre-injury levels. I’m not sure what that one is there for. Anyway, remember the foot of stone [Phonetic], that’s our goal in the diabetic fracture. The last case I’m going to show you was catastrophic. This is another woman that did not make it out of the hospital. Simple little rotational fractures, end stage renal disease, closed reduction once, closed reduction twice. Finally, I gave up and I stuck a pin right through the heel just to hold it there. She’s about 120 pounds, soak and wet, 40 years old, with a creatinine in double digits. And this is her first post-op visit and that’s what her leg look like and she went under a DIC and died within about three days of this ankle fracture. It was just a tragic situation. So these are difficult patients as you all know and you all have your horror stories on how this happened. And so in my mind, the ideal practice protocol is the chief stable fixation, immediate short leg walking cast with careful surveillance for any migration of the hardware. And whether or not you let him bear a full weight or partial weight, it’s up to you. But get them out of bed and get them moving so that they don’t decompensate and improve or graduate their physiologic stress whether it’s weightbearing or cardiopulmonary, and decide what the patient needs for the best functional outcome. Don’t be pigeonholed into taking care of this by the book. You can’t deal corrupt the physiology, it’s what it is. But if you’re uncomfortable of having a non-weightbearing, at least mobilize him. So again, you take care of their entire patient rather than just the fracture. What have we resolved? We resolved that the diabetic will break their ankle and there is clearly no cookbook approach. We have to discard many of the traditional mentalities and I don’t want to get diabetes and I certainly don’t want to get an ankle fracture because of the morbidity. So we’ll stop there with this and then go on.