Board Review Trauma & Sports Medicine


Ryan Fitzgerald, DPM

Ryan Fitzgerald, DPM gives an in-depth overview of nonunions. Dr Fitzgerald discusses where, why and how nonunions occur and steps to take to avoid them. He also discusses diagnosis as well as medical and surgical treatment options currently available.

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Goals and Objectives
  1. Understand the Etiology of Nonunions
  2. Determine appropriate treatment paradigms to address these challenging patients
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  • Author
  • Ryan Fitzgerald, DPM

    PRESENT RI Associate Editor
    Clinical Assistant Professor of Surgery
    USC GHS Center for Amputation Prevention
    Greenville, SC

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    Ryan Fitzgerald none

  • Lecture Transcript
  • Ryan Fitzgerald: Right. Look to your left and your right, you guys made it. And say all good things come to an end, so we’re going to finish up with nonunions. I’m Dr. Ryan Fitzgerald, I’m at the Center for Amputation Prevention in Greenville, South Carolina. I’m assistant professor of surgery at the University of South Carolina. We did the disclosures thing. And ultimately, with regard to our nonunions, we’re going to talk about the underlying etiology for nonunions and to determine what the appropriate treatment is based on what the etiology. And again, I had the great pleasure of having topics that are not hugely complicated, there’s no math involved. It’s basic principles but it’s helpful sometime for us to revisit these principles and really think about why we’re doing what we’re doing and is what we’re doing supported by the literature. First of all, just some definitions, a delayed union is a fracture that requires more time to heal than as usual. And I think that as usual is an interesting phrase because that’s very subjective, very interesting to think of in that term. And then a nonunion is ultimately a fracture that is not healed and it’s going to heal, not going to heal rather. And really the reality that I think the difference between these two positions is the clinician’s hope. A clinician hopes that delayed union will not be a nonunion. But a nonunion is a delayed union that the clinician has given up hope on, essentially. And there are a variety of factors that can come into play as to when you think one or the other. And one of the take-home points I would argue for this talk would be to consider the progression towards nonunion perhaps sooner than you otherwise might, because there are things you can begin to do to really assess these patients and progress them towards a successful outcome. If you wait until it’s certainly a nonunion, then you’ve lost some ground. Historically, a nonunion has been a fracture that is not healed over a minimum of nine months. And it’s demonstrated in a radiographic progression for more than three months, so that’s a book ending, the reality of that. But again, I would argue that there are nonunions that are going to become nonunions that we should think of sooner rather than the nine-month mark or three months of no radiographic healing. Waiting nine months is inappropriate. And ultimately, this can lead to prolonged morbidity, inability to return to work. And there are some serious financial and psychosocial consequences for this. Often these patients are in pain and so they can progress towards narcotic dependence. And, there’s this emotional impairment and the longer this process is drawn out, the more elaborate this can become. So it’s really important to think in terms of that. And this is interesting, I was sitting and I think it was Dr. Callos [Phonetic] who’s lectured earlier today, and he was talking about some nonunions he had with the tibial rod and that they’re almost exactly like these x-rays. And these are pretty common things to see nonunions in this location. This person comes in, it’s a pretty good chance that they’ve already had some basic workup so you have to think in terms of what are the next step is going to be. You’re not going to just continue on the same path. The best treatment for nonunion is prevention. And so this is important as we’re particularly in the context of the surgeries that we’re doing and the fracture care that we’re providing. It’s really important for us to try to limit the exposure and the risk for patients to progress to nonunion. And there are some factors that can either predispose one towards nonunion or can ultimately try to limit that. And so I would encourage you to, whenever possible, to try to prevent it and think in terms of, “What am I doing today that’s going to try to prevent this complication moving forward?” The designation of delayed union and nonunion is basically surgeon belief and that’s what the American Orthopaedic Surgery Journal said in ‘80 or ‘96 rather. And it’s going to go this concept if the hope. Do you hope it will heal or do you think it’s actually going to heal? There are two important factors to consider when you’re thinking of the classifications of nonunions and ultimately these are the presence or absence of infection because that’s obviously going to be something that’s going to impact your bone’s ability to heal. But also, is there vascularity. If there’s no circulation, then it doesn’t matter how strong the construct or how well oppose the bones may be. No vascularity is no vascularity. Both of these can influence the bone’s healing and it’s important to consider both options. In terms of classification, the Weber classification system breaks it down into three different types of nonunions, a hypertrophic and oligotrophic and avascular. And these have different clinical presentations that you can see radiographically. And so, we won’t go through all the details because I know everybody is ready to move on. But, you can see essentially in the pictures, the A, B and C, the different types of nonunion. A Weber hypertrophic nonunion is one that is pretty vascularized and often it can create a fairly significant amount of callus formation but it’s just not healing. You get that elephant foot callus that an abundant callus or a horse foot callus which is abundant callus but not as abundant as elephant foot. And suggest that you have adequate biological response, but the mechanical environment is not such that the bone can heal. The bones have the capacity to heal, but for whatever reason, there’s increased motion at the site. And there’s a mechanical reason that you’re progressing to nonunion.


    On an oligotrophic, actually there’s no real callus that shows up on the x-ray and there’s vascularity to the bone but there’s not enough biological response. And this is one that becomes more of a biochemical problem. This, you can have a stable construct but if you’re progressing in the absence of the biological component, then the bone is not likely to heal. And in the avascular is obviously avascular and atrophic and those will certainly not heal, because it’s ischemic. This is just a progression, you can see the horse foot or elephant foot progression here, this hypertrophic bone. Then, less so but still hypertrophic here and then this oligotrophic, atrophic sort of an absence of activity. In terms of avascular necrosis and atrophic necrosis, there’s essentially three or four kinds depending on which version of the literature you read, but essentially there are going to be wedges and torsion wedges that can occur. It’s more a function of the defect in the bone. There’s an avascular component because there has been significant bone fragmentation of the fracture pattern and such, that the individual pieces of bone become devascularized. Even if you put them all back together again, this is particularly of consequence in a pilon fractures and things like that, where you have a high impact, small fragments. Even if you get them loosely reapproximated anatomically, there’s a strong likelihood that those individual pieces may progress to nonunion because they’re simply not vascularized. Also in the context of periosteal stripping if you have aggressive, either traumatic injury or in a surgical correction. In terms of the incidence of nonunions, you can get a sense here of which bones are progressing towards nonunion. Many of the studies have been done in long bones and you can get a sense that depending on which version anywhere from 30 to 60% of tibial fractures progress to nonunion. And there's a variety of reasons for that and if you look at the actual studies, the data is all over the map, really. But, just to get a sense that there is some incidents that some bones progress to nonunion more than others. And so that’s important as you were managing whether or not these fractures are one that are likely to progress to nonunion or not. And that’s part of step one in preventing the problem is recognizing that you have a situation that could be a problem. In terms of pathophysiological risk factors, the systemic status of the patient, so what the patient brings to the table is always going to be a challenge in the management of these patients, particularly important to know the local limb status before the injury. In the context of trauma as opposed to surgical nonunions, it’s important to know what was going on with them the minute before they had the injury. Because if they had very poor circulation to start with, and then they had a big traumatic injury, that’s going to play a factor more so than many of the others. And you have to get a sense of what their local post response is going to be. What is their capacity to heal? Much likely, wound healing, there are biological markers for whether or not a wound will heal. Do they have the appropriate protein, the albumin levels, the circulatory levels? Similarly, bones heal in very similar way so they need to have the appropriate biochemical capacity to be able to do this. And then depending on the orthopedic fracture care, how are these fractures being managed. Are they stable? Is the fixation adequate? Things like that. And then some pharmacological variables. Are they taking medications as a consequence of systemic disease that may progress them towards nonunion as well. Generally speaking, nonunions are more common in men than in women, more so in obese patients and postmenopausal patients. And that makes sense if you consider that because there are some hormonal factors in play. Age plays a role. Young periosteum is much more healthy than old periosteum. And so if you think about the fractures that you’ve managed and particularly the nonunions that you’ve managed, young healthy people rarely go to nonunion if the fracture is adequately addressed and there’s appropriate vasculature. Older patients, patients with diabetes, patients that are taking the systemic steroids, these are the ones that have a tendency to have problems. There’s certainly a genetic component and that comes to play. I don’t know why that’s yellow, I apologize. The systemic status of the patient is important, and it’s important to get a sense overall of where they are from a nutritional standpoint. Do they have the capacity to heal tissue? Is there vitamin D level as such that they can heal bone? There’s a significant incidents of vitamin D deficiency in the patient populations these days. Any fractures that I’m managing, I get a vitamin D level on anybody that I’m going to do any osteotomy on, I get a vitamin D level. And you’d be surprised how many patients will come back low. Prior to doing that, we would do a triple or something and it would just in that delayed union where you’re still hoping it’s going to come through. One of the workups I would do is I would order a vitamin D level and they would often be low. You get them on the supplemental therapy and they start doing much, much better. You really have to consider the patient as a whole. And recognize that the literature suggests that many of these patients are going to be malnourished even if they don’t seem to be, up to 50% of patients in urban areas who sustain [indecipherable] [10:06] fractures are.


    That’s a reality. Protein deficiencies as well, either external or internal, if they have some storage deficiencies, that can be a problem as well. In terms of malnutrition, you want to have the protein because you need it. Your body is trying to build the bone. You have to lay down your bone and your body has to have the inner view to do that. And so, there are screening tests, checking the serum albumin, the total lymphocyte count is important. And albumin less than 35 and a lymphocyte less than 1500 cells is a significant reality. And that’s going to likely progress somebody on to progression towards nonunion. If you have patients with significant traumatic injuries that you’re assessing, it’s important to assess these values because supplemental therapy may be adequate to stave off these more significant complications. Anemia can be significant for this patient in the same context that your vascular supply is a supply and demand issue. Patients can be adequately and functionally vascularized right up into the level of their incident. And then once they’ve had a traumatic injury, the demand for new oxygenation as a consequence of the injury may be more than they can supply. They get a functional ischemia even on a cellular level. And this can create a low oxygen tension environment. And that is very poor environment to promote healing. A high-oxygen tension is far more necessary for faster healing and the literature supports this again and again. It’s not just, is there blood getting there in a macrovascular sense but on the tissue level is the oxygen tension in that location adequate to provide healing. Patients with diabetes are a tremendous example. We all know patients with diabetes have a tendency for delayed healing and slow healing in nonunions. And part of this is why, because they had this macrovascular disease in the context of overall metabolic syndrome. It’s important to consider these patients similarly to the hormone deficiencies, postmenopausal patients, these systemic issues that can be a factor. Patients with diabetes have these neuropathic fractures. We talked briefly about Charcot this morning. And, this neuroarthropathy is not entirely result of unpredicted weightbearing. There’s certainly factors that are coming into play either whether you ascribed to the vascular theory or the traumatic theory. The reality becomes there’s a dysregulation in the formation of bone and this inability to control that response creates a situation where your body can’t lay down new bone or can’t lay it in an organized fashion to get a good rebuilt of any fracture tissue. And that’s essentially where you get this disconnect between the osteoclastic activity and osteoblastic activity. And that’s more common to patients with neuropathy than not. Smoking is obviously one and we all know this and the literature supports it again and again. But the reality is that smoking decreases your peripheral oxygen retention. Again, you need to have that appropriate oxygen tension for your body to be able to do the things that it needs to do if you’re a smoker. Or if you’re treating a smoker, then that person just does not have the capacity. And it is very well understood. I tell my patients that are smokers particularly preoperatively that 100% of smokers have some complication. It’s just a matter of what, whether it would be bone healing issues or wound healing issues. And unfortunately, it’s not necessarily a reason not to do it, sometimes you don’t have a choice. But, it’s something that they need to understand going into it that smoking is a significant risk factor across all areas. There have been no specific randomized studies with regard to smoking because the reality is that it would be very difficult to ethically do so. But retrospective studies have shown significant delays in union radiographically and clinically in patients who are smoking. So if you ever have somebody who wants to argue the point, they say, “My grandmother smoked for 70 years and she broke her hip and she did just fine.” She’s the outlier, she’s not the common. There’s certainly literature to support it. We’ve talked about neuropathic fractures a little bit and we’ll glaze over this. There’s no great accepted algorithm in terms of how do you manage it. There are some medications that have been extrapolated like the bisphosphonates. And these can be utilized to improve bone healing by decreasing the osteoclastic response. There’s a lot of opportunity for research here and I don’t know that I would go prescribing bisphosphonates on everybody. But, recognize that this is something that’s coming down the pipe. There are some fairly significant consequences that can come from these medications. I would judiciously do that. In fact, I would encourage you to work with a primary care physician or whoever’s managing them globally with regard to this. I don’t know that you want to be the ones on the hook for writing for bisphosphonates, but there’s a lot of opportunity there. In terms of the type of injury, there are some injuries that are more prone to nonunion than others. Among them, we talked about pilon fractures, high impact injuries, lot of fragmentation, particularly if there’s a lot of periosteal stripping that can compromise the vasculature for the bones.


    And so, it’s important to consider your basic bone anatomy when you’re thinking about the types of fracture that you’re seeing. Remember where the blood supplies come. The metatarsal blood supplies have a very unusual vascularization among other things. It’s important to think in terms of that as you’re thinking about how you’re going to correct them surgically and how you’re going to make your incisions if you’re doing elective surgery, things like that. The nature of the injury is something that can predispose it. High trauma injury or high impact injuries are far more likely to progress towards nonunions, likely a consequence of the soft tissue envelope injury as compared to lower impact injuries. Ones that have an infectious component, they’re far more likely to progress towards nonunion as well. And the presence of infection can increase the soft tissue damage. It’s a one-two punch. High impact injuries with the damage tissue envelope, can then get infected which further damages the soft tissue envelope. And both can alter the chemical properties of the macro and microenvironment in a way that can progress you towards nonunion. There are nerve disruptions and it has been shown that in animal models, when you disrupt a nerve, that can slow bone healing down. So when you think about that and extrapolate back towards that neuropathic wounds, that makes more sense to the context of the global metabolic syndrome associated with patients with metabolic diseases that have a tendency to progress towards nonunion as well. The immunocompromising these patients even with a nerve damage has been correlated with this delay in healing. Patients that have a back fracture and they have neuropathy, again, a one-two punch in terms of their capacity to heal these wounds. The local postinjury response is important because there are what should happen when you have an injury and then there’s what actually happens. When you have a local injury, there’s an immediate inflammatory response that progresses to a less acute inflammatory response over the course of tissue remodeling and then ultimately progression towards bone healing. Each steps in this process require a fairly significant and complicated interplay of cytokines and growth factors. And if there’s a dysregulation or some other malpositioning of these types of signal markers, then you can progress towards a chemical nonunion which can disrupt the mineralization. That’s important. Again, consider when you’re thinking about these patients in global setting. Orthopedic fracture care, one of the biggest reasons that people get nonunions apart from just the metabolic issues and patient care issues is poor fracture care. If you don’t put the fracture back together well, if there’s too large gap between fracture fragments then it’s not likely to heal. If there’s too much motion, it’s not likely to heal, things like that. It’s your basic AO techniques that we all were taught about. You want to make sure that you limit your gap to be no more than about two millimeters and here’s an akin that clearly is larger than that. And to no one’s great surprise, it progress to nonunion. You have to think about, don’t set yourself up for failure. If they had had more appropriate bony apposition in this patient, then it’s very likely that this would not have failed. Motion at the fracture site can also be an issue. You want it to be, the bone is well approximated together. And you want them not to be moving around. Every time your body tries to build new bone tissue, if it moves and it breaks off, you’re never going to get any bone that forms in that spot. You’ll remember from your physiology that there is two ways the bones are healing, both primary and secondary bone healing and both are important to the context of bone healing overall. Dysregulation in either situation can progress you to nonunion. Controlled weightbearing can ultimately make you heal faster because it does stimulate the bones and that’s the concept of dynamization on a rod. But, you have to have some motion but not too much. And so you have to dial it in the way you need it to be. For the local factors, we talked about infection, the energy, the mechanism of injury, the anatomic location, some bones are more likely to go to nonunion just as a function of their vasculature. Wolff’s law, that’s the law that says that the bones need to be stressed a little bit to stimulate them to heal. Lack of physiologic stress, if you just put somebody completely immobile and don’t stress them at all, their bones can also progress to nonunion. Of the things that can cause a nonunion and be a prognostic indicator overall bad outcome, infection is usually the worst. And that was what Nicole [Phonetic] and Cannibery [Phonetic] said in the ‘70s. And that still holds true today. In terms of the bad things that can happen to somebody who has a nonunion, an infected nonunion is significantly worst. Mechanism of injury, we talked about fracture pattern. This is reiterating. And I bring it about only to remind you as you’re thinking of these things as you’re getting calls from your residence and getting calls from the ER and places.


    Think in terms of what fracture patterns are more likely to progress you towards nonunion and what are the things that can ring that bell for you. You started thinking in terms of how you’re going to prevent it. Delayed union and nonunions are more likely in tibial fractures with moderate to severe displacement, that makes sense. The more displaced fracture is more likely there is a vascular injury. And the greater risk of vascular injury, the greater the risk for nonunion. It does fit together. Fracture patterns, certainly a more fragment of fracture pattern can predispose you to nonunion also because there’s a higher degree of segmental tissue loss and bone ischemia. Gustilo-Anderson talked about this and we’re not going to go in, and you’ve had a day of Gustilo-Anderson conversations. But, essentially as you progress to Gustilo-Anderson, there is more soft tissue injury and there is worst fracture. And so those higher level of Gustilo-Anderson fractures are far more likely to progress towards nonunion. And so that’s important. There’s a soft tissue classification as well called the Tscherne classification. And this suggests that not all high energy fractures necessarily progress to nonunion but rather it’s the soft tissue injury that the component is going to progress. It’s not the soft tissue injury to the bone per se, rather the fracture injury, the bone that progresses you to nonunion but the concomitant soft tissue injury. And they talked about the degrees of these. And you can see this pretty well, but a grade zero through three and increasing amounts of soft tissue injury over the bone to progress towards nonunion. You can see this here in the Word version. But the grade 3 injuries are with extensive soft tissue loss. And these are very, very likely to lead towards nonunions. Mechanical factors, through successive motion of the site, we’ve talked about that and that’s, again, is really important. You got to be able to put it all back together again in a way that’s not excessive motion but does allow for some physiologic splinting. It’s your basic AO techniques. Some areas of the skeleton are more likely and more easy to do this than others. Some are not. And some are more anatomically designed as a function of the blood supply to be weak spots. The fifth met base is always a common joint fracture, it’s a very poor healing as a consequence of that. Femoral neck as well is another location that’s very poor healing. In terms of the diagnosis of nonunion, the history is important so you got to get a good history in physical. I was like this a couple of years ago. I had a patient who related that rap music made his condition worse. I encouraged him to stay away from rap music and he got better. But, a good history is important in terms of what they’ve had and particularly their medical history in terms of any potential sources that can be an issue for metabolic syndromes that could predispose these patients to nonunion. Have they had any history or symptoms of infection, any other things that would be risk factors in that context. And then the examination, if there’s gross deformity, is the soft tissue intact, the basic stuff with particular concern paid towards, is there vascularity. And if there’s adequate vascularity to manage these wounds appropriately, and then if there’s stability at the fracture site. The diagnosis is almost always a clinical diagnosis that is confirmed with our various imaging studies either plain x-rays, CT, MRI, bone scan. Bone scan is useful if you’re trying to determine if patient has avascular necrosis versus atrophic nonunion versus a hypertrophic nonunion to see if the bone ends with that. If you have AVN on the talus and a talar fracture, you get that dead center talus and you know it’s not going to heal no matter what you do, unless you do something fairly dramatic. It’s important to think in terms of what options do you have available to use. Basic radiographs, we don’t have to go in the details and all this, but essentially just take them, use them. CT, very few people do linear tomograms anymore, it’s all computerized with CT and that’s good and it’s much easier for us. They’re replacing that and MRI is becoming increasingly good for this as well. Biopsy is an interesting concept. It’s important to patients particularly if they come to you with biopsy. Because remember that the potential for infected nonunion is a fairly higher prognostic indicator for bad, bad outcome or a role. In patients who have a nonunion, particularly nonunions who had a history of a soft tissue injury, it should be on the table to consider the possibility that they have a very low virulent osteo that’s down in that site and infected nonunion. And it’s worth doing a biopsy to just rule it out because if you have an infected nonunion, you don’t notice it. Nothing else you’re going to do is going to make it any better until you address them. So you want to always consider the possibility for infection. Bone scans, again, we talked about mostly in the context of determining if they have appropriate vascularity at the site themselves. And you can do tech 99 scans, gallium and there’s a variety of options and each hospital has a different protocol.


    It’s more just knowing what you have available at your facility. But it’s not going to be as useful necessarily in terms of, is it infected or not more just as a vascular or not. You can use the indium-labeled scan to some degree for infection. But again, the gold standard for that is going to be biopsy. And, MRI is an option as well. This can help sometimes depending on how good your radiologist is and how good the MRI machine you have is. But, it is sensitive but not specific so there’s going to be a lot of things that you can see in there and you can get a sense of what’s going on. But it’s not going to tell you definitely if it’s infectious or not. I would say, I would lean on biopsy is the key. If you’re not doing a lot of biopsies, you’re not doing enough biopsies ultimately is the reality on this. In terms of the treatment for nonunions, and I know we’re running over a little bit so we’re going to breeze through this. But essentially, there’s nonoperative care and the reality is, by the time somebody has come to you, they’ve probably already progressed through that. Nonoperative care is essentially going to be things like continuing to immobilize them or perhaps may be starting to progress them into a little bit of dynamization depending on the nature of their injury. There are things like nonoperative bone stimulators, either ultrasound, electronic stimulator, bioactive adjuvant therapies, things like that. And there’s a lot of research to describe it, we’re taking another day to discuss. But, ultrasound is shown to be fairly effective in some fractures and can shorten the time for healing. This is an EXOGEN bone stimulator on a fifth metatarsal fracture. There are some studies that can do this and I won’t read it to you, but there are some studies that support the use of ultrasound for fractures. And they’ve had some good success. Electronic stimulation uses it, it’s the same idea as Coke versus Pepsi to a degree. It’s still electronic stimulation. But, what it does is it uses the electrical properties of the bone to create a magnet and de-stress the bones with a magnetic field. And this electromagnetic field ultimately can stimulate the osteoblasts to become more active and to do what they need to do for proliferation and matrix formation for bone healing. And there’s, again, a variety of versions of this, there’s direct occurrence and then also capacitated coupling which is a variation on a theme. But the basic principle is that you’re using electricity, creating electromagnet to stimulate the bones to function. And there are a variety of times how long it takes to do this and a variety of different studies, and there are studies that support this as well. I would encourage you, if you’re interested in looking to read the studies and decide what seems to work for you when you have availability. In terms of contraindications, they’re relatively few. The only thing that’s not really going to work for this nonoperative care is if you have a patient who does not have the physiologic capability to heal a wound or a fracture. They’re not going to heal it no matter how you stimulate it because you haven’t addressed the underlying biochemical property. That’s again as you’re thinking about your patients with nonunion, you have to really consider the patient as a whole. Surgical treatment, essentially going to be trying to remove the nonunion and stabilize the fracture. You can see this is a pretty wicked distal tibial fracture and nonunion. And depending on where it is in the body, whether you try to fix the fracture, whether you try to progress it to a fusion, whether you do an amputation, there are some arguments for that as well. It depends on what your training is and what you need to do for each specific encounter. Bone grafting is important. Obviously, if you’re going to resect out an area of nonunion, you got to put something in that hole. Better to put in something that’s going to be both osteoconductive and inductive so it’s going to stimulate bone healing while also providing scaffolds so that’s important as well. We’ve talked about this and it’s a pretty basic concept. But, the idea is that if you’re taking something out, you need to put something good back and not necessarily from the patient. If patient’s got very poor systemic responses to fracture healing, you don’t necessarily want to take their bad bone and stick it back in there, or maybe get argument for taking some allograft or something like that. In occasions, again, patients that have these fractures that have progressed to nonunion, you do need to have vascularity. An atrophic nonunion is not necessarily likely to work. And if you have a fairly significant segmental defect more than about 6 centimeters, it’s not likely to work. But, up to about 6 centimeters, you can do a segmental defect as well. And you have to create a stable environment which is usually at this point, a combination of both internal and external fixation. There are a variety of techniques for stabilization and that, again, surgeon’s choice. Whatever you can do to get the job done is what I would encourage you to do. Plate osteosynthesis, this is, again, the AO technique. You want to stabilize the fracture and put all the pieces back together. Intramedullary fixation, this is just a guy who had a bad fracture, he had arthritis, we just brought him in and he’s better. The nonunion was distal tibia and we just went ahead and progress him towards a TTC fusion because he had subtalar joint arthritis as well.


    Again, here’s more proximal intramedullary nailing where the tibial plafond was intact. The fracture was higher up. A rod that was higher in the leg, keeping the ankle joint intact. External fixation, Dr. Caleb gave a good talk about that, particularly the parallels of external fixation. And I would say, it’s like waltzing with the grizzly bear or something. It can be interesting and it can be useful. But it can also get you in a lot of trouble. You definitely want to be judicious in the use of external fixation. And be very ready to treat any complications as soon as they occur. Fibular osteotomy, I don’t think this is much but it’s something that you can do, particularly for tibial nonunions because the idea is that it awful as the tibia. I have other ways that I deal with this but I put in there because it’s something that you might read in the literature. And then ultimately in summary, the reality becomes you have to get the good diagnosis and you have to figure out why these things are not healing. And it’s usually going to be one of a couple of things. Either there’s too much motion at the site, they don’t have adequate circulation or they don’t have the metabolic opportunity to heal these things. And, if you address one of those but not the other or two, but not all three, the reality is you’re very likely to progress towards nonunion. It’s really important for you to consider the patient as a whole and figure out what individually is going on in that location. Early intervention is key, particularly in high risk groups, patients with diabetes, patients that are taking steroids for rheumatological issues, psoriasis, RA, things like that. And so it’s important to really to get on them quickly. In the context that we started with the surgeon’s hope that something will heal, I would say, start your clinical experience by having relatively little hope. Expect that it would go to nonunion, start working it up like it is even before it’s become one and that’ll save you a lot of trouble in the long run. Are there any questions? Okay.