• LecturehallMidfoot Ulcers & Charcot Arthropathy treated primarily with Gastroc-soleus Recession (GSR)
  • Lecture Transcript
  • Male Speaker: ____ form these. Have a predilection for developing midfoot ulcerations and many of the treatments that Gary had suggested where also useful in that regard. But I asked Dr. [Monroe] [00:16] aboard to come back and talk to us about his approach to this. Managing midfoot ulcers with the primary gastrocsoleus recession. So let’s ask the expert to give us his insights into this. Thank you.

    Dr. Monroe: Yeah. I’m going to talk to you about something that Dr. Frykberg said generally. Not the usual approach to Charcot arthropathy but I’ve been very happy with it. So I wanted to share it with you. It’s treating both midfoot ulcers and Charcot arthropathy primarily with gastrocsoleus recession. I have no financial relationships to disclose. Basically what I’m going to talk to you about is the evidence that tendon imbalances is the main cause of charcot arthropathy and midfoot ulcers. To describe how midfoot ulcers can be successfully treated with tendon balancing. To also describe preliminary evidence that primary tendon balancing seems to prevent progression of chara. Before I get into that, I wanted to emphasize the fact that this is not something that can be treated by any one specialty or any one person. It requires a team approach. I have fortunately a team of people who can help with the other aspects of the treatment of the diabetic foot. You need medical treatment to manage their medical issues and different surgical specialties for different aspects of the problem and then ancillary treatment. The success rate is much higher together than it is by any one individual. The cascade that I like to use to outline this problem is to think of diabetic foot disease as resulting from the increased glucose which causes a neuropathy. The neuropathy causes the tendon imbalance and the decreased sensation through the neuropathy. Both of these factors increase the stress in the foot. This causes calluses of the skin. It also affects the ligaments and bones and causes deformity. Both of those problems can eventually lead to an ulcer then subsequent infection. Especially if combined with peripheral artery disease, you can get necrosis and end up with an amputation. So different specialties have impact on this cascaded different stages. The medical physicians are the ones that are charged with dealing with the elevated glucose. I think I encourage all my diabetic patients to stretch their calves to try and decrease the development in the high tendons. Use accommodative shoes to decrease the stress in the foot. If they develop progressive callusing and deformity, I will go ahead and do a tendon lengthening on them if they will agree. But by the time they develop ulcers, I think tendon lengthening should be done and combined with wound care. Infection, obviously treated with antibiotics, arterial disease with vascular treatments and then the necrosis would require debridement and wound care. So obviously this is a team approach and not an individual undertaking. I think the success rates that I’ve seen seem to indicate to me that knowing the cause of the problem increases the probability of a successful treatment. That eliminating the cause of the problem is better than only compensating for the result. I think that the results that I’ve seen from using tendon balancing for treatment of diabetic foot problems illustrate this. As I said earlier today, 10 degrees of dorsiflexion is required for normal gait and normal foot pressures. Biomechanically look at the forces in the foot, on the skin, and in the bones. When someone has a tight Achilles, the forces go up dramatically and they are doubled and tripled if not more.


    So these increase forces seem to me to be the primary causes of the foot problems that we see in diabetics. The hallmarks of the tight Achilles tendon that you see on x-ray or illustrated by this x-ray. You’ll see calcifications in the Achilles tendon from the increased stress in the Achilles tendon. You’ll see the spur at the Achilles insertion. You’ll see the spurs that the plantar fascia insertion. Also because of the increase forces in the midfoot, you’ll see arthritic changes in the mid foot and decrease of the arch. Again, if the patients doesn’t have calluses and doesn’t have deformity, I recommend that they do daily eccentric stretching. That’s stretching with the muscle contracted. Seems to be more effective. Again, these are articles which have recommended that diabetics be encouraged to stretch their calves. The classic approach to Charcot arthropathy is offloading and immobilization. The problem with that is that it requires patient compliance. The advantage of tendon balancing is that it doesn’t require patient compliance. So I use both. I use offloading and immobilization and I also use tendon balancing. I think it’s particularly effective in the non-compliant patient. The same cascade occurs in posterior tibial tendon dysfunction. This cascade has been described by the authors listed in this slide. A posterior tibial tendon dysfunction resulting from calf tightness causing subtalar pronation, stretching of the spring ligament and tarsal ligaments, flat foot, plantar fascia sprain. Then you get the posterior tibial tendonitis and tear resulting in the MTP hyperextension hallux valgus and claw toes. This is very similar to the theoretical cause for Charcot arthropathy, also described in by multiple authors listed below where a neuropathy causes calf tightness, decrease sensation. This causes midfoot arthritis or ligament damage which results in arch collapse. Then a midfoot boning prominence. I’m talking about midfoot Charcot. That causes the ulcer under the bony prominence. Again, also listed articles we can hypothesize that equinus is the cause of Charcot arthropathy, and suggesting that Achilles lengthening can be used or should be tried as part of the treatment for Charcot arthropathy. The gastroc recession, many people are afraid to use it because of the potential for weakness. In my hands it’s usually not a problem because these are not athletes. These are usually people who you’re trying to save their foot. But some of the literature on gastroc recession indicates that the strength is basically better than it was before surgery by three months. Then it’s by seven months the strength in the calf is normal. Even in non-diabetic patients I will use this approach to the treatment of foot pain and had not had major problems in weakness in a non-athletic patient. Also, part of the bad reputation of Achilles tendon lengthening comes from the whole procedure, the triple cut procedure where you can get overlengthening. Lengthening the tendon in the Achilles tendon does lengthen and weaken the calf more than gastroc recession and gastrocsoleus recession does. I’m much happier with gastrocsoleus recession than I have been with lengthening the Achilles tendon itself. I have used Charcot, have used gastrocsoleus recession and walking boots successfully for the treatment of Charcot arthropathy and midfoot ulcers. These are some example patients treated with gastrocsoleus recession. They are mobilized in a CAM walker and told not to put weight on their foot but most of them walk on it anyway. Even when they do walk on it, the ulcers usually heal. The same approach can be used in other causes of neuropathy. Not just diabetes but also for example this patient had an ulcer who had Charcot-Marie-Tooth.


    Also use it in rheumatoid arthritis and spinal patients who have nerve damage from a spinal surgery, stroke, cerebral palsy, various causes of neuropathy. Basically the same approach can be used. I published an article in Foot and Ankle International on the use of gastrocsoleus recession for midfoot ulcers. It’s also published in Podiatry Today in addition. Let me go back. Basically just using primary gastrocsoleus recession, 90% of the midfoot ulcer is healed. One of the ten recurred. When you compared this to using bony procedures, exostectomy, the healing rate for gastrocsoleus recession was higher and the complication rates were lower comparing it both to exostectomy and to fusion. Also the even more aggressive surgical procedures, the osteotomy infusion, these procedures are very technically demanding. You can imagine the complication rate of the gastrocsoleus recession compared to some of these more extensive procedures would be very different, especially in these high risk patients who are smokers, who have ulcers, peripheral artery disease. I would much rather initially treat them of the gastrocsoleus recession than I would with one of these very large bony procedures. I think there’s much less chance of amputation in those patients. So basically tendon surgery in the calf, even in someone who has gangrene of the foot and no pulses is relatively safe certainly compared to bony procedures in the foot. So I prefer to do the tendon procedures first especially in patients with no pulses, foot ulcers, infection, necrosis, smokers, elderly patients and diabetics which is almost all of the patients that I treat. My standard approach is to do the tendon procedure first. Then when that fails, then I consider bony procedures. It only fails in about 10% or less of the patients. The conclusion of the article that I published in Foot and Ankle International is that gastrocsoleus recession is a primary treatment for diabetic midfoot ulcers as a low risk method for promoting ulcer resolution and decreasing recurrence. Gastroc recession may stop progression of Charcot arthropathy because in the patients that I treated with Charcot, I noticed that the ones that had gastrocsoleus recession, their deformity stopped progressing. They didn’t go usually on to ulcer and amputation. My midfoot ulcer treatment basically is to first try and heal the ulcer with the soft tissue procedure, gastrocsoleus recession. Sometimes I’ll add posterior tibial lengthening if the ulcer is lateral. Sometimes if they have good circulation, I may transfer flexor digitorum longus to posterior tib is the ulcer is medial. But I’ll only do that if they have good circulation, they don’t have infection, and they don’t have an ulcer, or they don’t have an infected ulcer. I think gastrocsoleus recession is safe, even in patients who have ulcers infection and Baxter disease. If the ulcer doesn’t heal or recur, that’s when I go to bony procedures, usually mainly exostectomy and sometimes fusion if they’re unstable. The patients who don’t have ulcers sometimes progress like this with a red swollen foot and some pain. Even though they don’t have a wound, they’re frequently diagnosed with cellulitis and admitted and put on antibiotics. This is an example patient that I saw in the hospital who was admitted because he had so much foot pain that he was – and he had pain and swelling in both feet and he was totally unable to walk. So he was put in the hospital and put on IV antibiotics. His x-ray that you see there was read by the radiologist as being normal. Although I do think that maybe some increase space between some of the tarsal bones. So what I did with him was I put him on the schedule the following day for a bilateral gastrocsoleus recession and gave him, immobilized him in CAM boots. I gave him a wheelchair and told him not to walk on his feet.


    A few weeks later, he walked back into my office without his boots and no longer had any foot pain. Two and a half months later, he came back. I did x-rays on his feet and he had spontaneously fused his tarsal metatarsal joints. So I think he was in acute onset Charcot that was treated acutely with gastrocsoleus recession successfully and he has had no recurrences and no additional problems with his feet in the last three years. Other patients with gastrocsoleus recession who have abnormal x-rays. I have noticed that the gastrocsoleus recession decreases their pain and swelling. Usually they will go on to spontaneous fusion without additional development of deformity. I did review some of my midfoot Charcot arthropathy patients, as many as I can find. There were 28 feet. 11 of the patients had ulcers. Some were lost to follow up that left 25 feet and 21 patients. Average follow up was 37 months. The post op x-ray showed no progression of deformity and further arch collapse. There was one patient whose ulcer did not heal because he had severe disease when I first saw him. One patient had an amputation for another problem. In the remaining patients, basically there were no other patients who had deformity progression, arch collapse. No patients developed new ulcers and no patients other than the ones that are described above had amputation. If you compare these results to this article by [Fabern] [17:04] in diabetes care, treatment of Charcot arthropathy with crutches and therapeutic shoes, 36% progression, 37% ulceration at 48 months. When they added gastrocsoleus recession to that, they noticed that the ulceration and progression rates decreased to 4% which is basically the same results that I had. So I think that the two articles are in agreement. There was another article published in General Bone and Joint Surgery. 15 patients had progression of deformity on x-ray at one year despite total contact casting and boots. Fractures develop in four of 15 patients in two years. The recommendation of this author was that this supports surgery to progressive deformity ulceration and amputation. So if you compare the results that I had using gastrocsoleus recession, the new ulcer rate was 5% compared to 40% in one article, 37% in another. Then another article, also using gastrocsoleus recession, had 4% new ulcers. Progression of the deformity. In one article 36%. Another one 100%. Again with gastrocsoleus recession 4%. Very similar to the 5% that I found with using gastrocsoleus recession. Basically I had no new fractures in this small study that I did compared to 27% new fractures in another article. Another article recently published in Foot and Ankle International described that Charcot arthropathy treated with total contact cast in which the arch collapsed, patient sustained a calcaneus fracture. So they treated the patient with Achilles lengthening and the alignment improved, the fracture healed. They noticed that the deformity decreased. So they felt like Achilles lengthening decreases deformity and ulceration in the presence of Charcot arthropathy. Also I think this is consistent with the Medicare data, showing major amputation decreasing 47% between 2000 and 2010. The number of gastroc recessions increasing during the same time, 575%. This author felt there was a connection between those two numbers although that is somewhat controversial. Basically in conclusion, the approach of using tendon balancing for Charcot arthropathy, the results are preliminary.


    It’s been noted that most patients who have gastroc recession did not progress deformity or developed additional arch collapse and new ulcers. I suggest that gastrocsoleus recession heals ulcers and may stop progression of a Charcot arthropathy. May prevent further arch collapse, midfoot ulceration and amputation. Tight Achilles and decreased sensation may be the main causes of Charcot foot disease. Also I use gastrocsoleus recession combined with decreased weight bearing as my initial offloading treatment as soon as Charcot arthropathy is recognized. As I said, gastrocsoleus recession has the advantage over a decreased weight bearing and non-operative offloading techniques, and that it doesn’t require patient compliance. Whereas all of the non-operative approaches do require patient compliance. This is a list of articles describing of the opinion, mostly undocumented, that equinus is the cause of Charcot arthropathy, and that recommending Achilles lengthening as at least part of the treatment for that problem. Just a review of the approach to Charcot arthropathy, basically if the patient has infection, they need debridement. If they have an ulcer, subluxation or arthritis, I believe, and the tendon lengthening. If they have a bony prominence, it’s definitely combined. If there were current ulcer, then ostectomy is good for patients with bony prominences where patients with deformity and instability sometimes need osteotomy infusion. Amputation is for failure of these treatments but the gratifying part of tendon lengthening is that only a small percentage of patients will need bony procedures. Earlier today I talked about using tendon lengthening and tendon balancing for forefoot ulcers, metatarsal and toe ulcers, and the level one evidenced from metatarsal ulcers. Also using it for ulceration of transmetatarsal amputation. Using it for foot and ankle pain, Achilles tendonitis, plantar fasciitis, metatarsalgia, posterior tibial tendonitis, arterial forefoot wounds, calluses and corns. I also like to add midfoot ulcers and Charcot arthropathy. So basically there’s very little about the diabetic foot that can benefit from tendon lengthening and tendon balancing. My general approach to patients with foot problems in non-athletes, not just diabetics, is to check to see if the patient has some dorsiflexion of their ankle within the extended. If they don’t, I recommend if they stretch their calf. If that doesn’t work, then I will usually proceed to gastrocsoleus recession either alone or in combination with another procedure. I think there’s level one evidence for this approach in forefoot ulcers. Level four evidenced for Achilles tendonitis, plantar fasciitis, metatarsalgia, midfoot ulcers and Charcot arthropathy. Only level five evidence in posterior tibial tendonitis, midfoot arthritis, and stretch fractures. These are articles which describe and support this information. Thank you.