• LecturehallEquinus Doesn't Exist
  • Lecture Transcript
  • TAPE STARTS – [00:00]

    Speaker: Okay, so this is really changing gears and we are going to move kind of into the speculative realm. I will ask you to try to keep your minds open. If you have happen to have been reading podiatry today or podiatry management, you would see some discussion between different folks about equinus being the root of all evil versus equinus not being such a big deal. I think it's still a big deal but -- thank you so much -- much better -- I don't think equinus really doesn't exit. That's just a provocative title, so I don't have any disclosures and we are going to talk about this. So here is the hypothesis I am going to give you today. So I am going to tell you that gastrocnemius equinus is normal. It's a normal physiological part of the body. It's not a pathological contracture of either the Achilles or the calf muscle complex. When you measure this with the Silfverskiold test, you are measuring something called passive insufficiency, which is something that exists on all of us in various parts of our body. What is really happening is that we have a normal triceps complex that's acting on an abnormal foot. So we are going to talk about how that's going to create pathology. So this was Nils Silfverskiold. You guys have all heard of the name, I am sure. He is a handsome guy. He is an orthopedic surgeon who happened to be pretty good athlete. He won a gold medal in the Olympics. I thought gymnastics is currently a women's sport but maybe it was a men's back then, I am not sure. He happened to work under Patrick Schanz. If you know the Schanz pin, then Dr. Schanz and he also worked under Dr. Haglund, Haglund's disease.


    He was married four times, which might make him an actor in our society. Interestingly, he was an anti-Nazi advocate, which in where he lived in Stockholm it took some pretty cojones to stand up to folks like Nazis and he actually did and he helped Jewish refugees get out of camps. That's a pretty special guy. So I think he is pretty cool. So if you look back to his paper, in which he discussed the test that now has his name. This is kind of you know sort of a quote from his paper and what he was really looking at were kids with spastic equinus that neurological causes of equinus. So he described that the test that was passive and active dorsiflexion of the foot with a knee bent and knee stretched. It's very similar to what we talked about today. So the problem is that we have misinterpreted the use of his test. So in the research there is a lot of variability with how equinus is defined whether it's five degrees, zero degrees, 10 degrees or something else. How it's measured is really variable and in fact it's really difficult to measure. You know dorsiflexion of foot in the office is really easy but from a research standpoint, trying to do that and get really reproducible result is not the easiest thing to do from a research standpoint. So for those who do research, I applaud them on this. This is not an easy thing to do. Overall, our evidence will be considered relatively weak. So where does it come from, where do we as podiatrist learned about this? So this is Root's books, the two of them. And in his book, he describes how to do the test or what is necessary for this test and you will note that he relates to a citation number 33.


    If you look in his book, citation 33 refers to his biomechanical examination book and down there is where he says it. So there is no actual research citation or evidence about the test itself. And there is no real research or evidence that shows that 10 degrees is really normal. So we haven't really answered this question yet. So that's an issue. How about looking at sort of how this thing is tested. So the inter-assessor reliability of this you know different people assessing the gastroc Silfverskiold test is actually considered pretty low. So between examiners, we have poor reliability. So if I measure it, I might get one thing. If you measure it, you are going to get something different. Well, that's hard to really do in a research study where you are going to show this. So that's really not reliable. So this literature review looked at various things and they looked at bunch of studies and don't read the whole slide because your eyes are going to burn out of your head if you do. But really, these two tables are [indecipherable] [00:05:17] reliability. So from all the studies that we have we know that there is some pretty good reliability for the same examiner. So the more you do it, the better you get and the more reliable your own examination gets. But there is really weak reliability between examiners. So for the rest of this, I am going to define the sort of the way Root and folks did. So less than 10 degrees of passive ankle joint dorsiflexion with the knee extended, that improves to at least 10 degrees with the knee flexed. You can kind of see this picture that's exactly what I am doing here. I tend to slightly invert the foot as I am doing this to kind of lock the subtalar and mid tarsal joint.


    So what are we not talking about when we talk about equinus and the case of the rest of this lecture, we are not talking about bony equinus, pseudo equinus, anything traumatically induced and anything neurological. So the rest of that's not the stuff that we are going to talk about. Those are the real equinus that actually exist and are pathological. So the important thing is to consider what many-joint muscle is. And the gastroc is a many-joint muscle. So this is defined as a muscle intending complex that passes across two or more joints and that's a many-joint muscle. So these are all many-joint muscles. Rectus femoris, the hamstring, there is lots of them and we have a ton of them in the foot and ankle and the gastroc is one of those as well. So what Silfverskiold was originally talking about was he was measuring something called muscular insufficiency. So there is two kinds. There is active and passive. With active insufficiency, the muscle itself is just not able to shorten enough to provide a full range of motion. With passive insufficiency, it's that the antagonist muscle is working and it can't allow the muscle to allow that full range of motion. And I am going to show you that this happens all over the place. So let's look at rectus femoris. So this is one. I am not going to have you do this and I am not going to do it either if you lay down and you flex your hip and you try to dorsiflex your foot, you try to extend the knee, you are going to have a really hard time doing it. So if you flex the hip, you are going to have a hard time raising your knee.


    You feel the kind of tension. You can get to it but you have to really fight it to do it. This one you can do sitting there if you want. So these are your finger extensors. So if you put your hand like so and then you try to elevate your fingers, you can do that really easy. That's very easy to do. Put your hand back and then try to extend your fingers, it's really hard to do. So that is passive muscular insufficiency. And that's exactly the same thing that's happening in the gastroc when you try to dorsiflex a foot with a knee extended. So at the gastroc, if you extend the knee, you are using up some of the available movement of the gastroc muscle belly and then when you try to dorsiflex the ankle, it doesn't do it as well. If you bend the knee, you will just relax the gastroc and then you can dorsiflex the foot and it becomes easier. So you are having a many-joint muscle where the amount of movement has been used up by the knee joint and then you can't move the ankle. So here is an example, same thing. This is a perfectly normal student of mine at the school. He has no pathological problems. He has no complaints. We extended his knee. You can see he has got, I don't know, maybe -5 degrees or so looking at that and then we dorsiflex then, he gets up to about 90 degrees. So most of us would say he has got gastroc soleus equinus. But really, we are just giving him more range of motion because we are just loosening the gastroc. That's all normal. Do I have any evidence for this other than this is what happens? Well, I am going to show you some of it. So if you have this normal gastroc insufficiency on a normal foot, the foot is what I would consider stable or preloaded.


    You know I just think of subtalar joint is supinated, the mid tarsal joint is maximally pronated, the foot is locked and when the gastroc fires, the Achilles pulls the foot up and it causes plantar flexion. The foot moves as a unit. It's exactly what we want to see, that's normal. We even see that if you look at EMG studies, you will see that the tibialis posterior is firing little bit before and almost about at the same time as gastroc. So for patients with flatfoot condition, their tibialis posterior is firing, it's supinating the foot, it's creating a stable foot and then the gastroc is firing on that stable foot and everything works well and the patient doesn't come in to your office. What about abnormal feet? So here is one. So if the subtalar joint axis off, you have an unstable mid tarsal joint. The muscles that normally support the foot are not working well and then when you fire the gastroc on this unloaded foot, you are going to get dorsiflexion at the foot. That's pretty common. We see this lots of times, right? This happens to be the foot of a ballad dancer who stretches all the time and you think that person would have really good gastroc motion, yet they still have a flatfoot and that's the problem. So Kevin Kirby has done a lots of work about subtalar joint axis and you can even see that in the case here if you look at these sort of two on your right images, the triceps surae is on the medial side in the normal foot. So when it fires, it's going to supinate. That's nice and normal. And if the subtalar joint axis is medially deviated, then everything is lateral to it. So the foot is a malfunctioning foot on a normal gastroc complex.


    So here you have same power, so the gastroc doesn't change its power. It's just doing its thing but you have a different lever arm that's occurring and because of that lever arm being shorter on the dysfunctional foot, it's going to cause the foot to break in the middle. The foot is not able to handle it. So there is another model for this. These are hammertoe and we all love treating hammertoes. So how many people say that the long extensor tendon became somehow pathologically contracted like in the normal person's foot. Really, most of these are like flatfoot conditions and it's the intrinsic muscles that cause problems. You get overloading with a normal extensor tendon until you get the contracture and then maybe over time, the extensor tendon starts to shorten [00:12:59] [indecipherable] So that's a current model. That's a normal EHL or EDL tendon. That's working on the toe that doesn't have appropriate support. Maybe the plantar plate went and that cause some problem. No one is saying that the EHL or EDL is dysfunctional. So there is some evidence to this if you kind of think through. So this is a cadaver study that was done and they looked at different surgical procedures what they do to the foot. So in this particular study, they found that the patients with PTD and a foot that had a PTD sort of created, the forced exerted by the Achilles tendon was increased. So the amount of force that it pulled with was increased when the foot was dysfunctional. And then when they did a medial displacement calcaneal osteotomy and normalized the foot, they found that that decreased the force that the Achilles tendon was pulling on the foot.


    So in this, the Achilles was never touched. The gastroc wasn't touched. All they did was you know sort of created a flatfoot and then they did a medial displacement calc osteotomy and they found that because it re-established the foot, there was more function associated with it. So normal Achilles tendon. Here is one that's similar. Same kind of thing, they did in Evans on a cadaver flatfoot model. And in the normal foot, the Achilles force was 240 N. In the created flatfoot, they found that the Achilles had 259 N and after they did the Evans, it went back to basically normal. So again nothing was done with the Achilles or gastroc, it's function changed based on the poorly functioning foot. Here is another one, same thing, they had a cadaver, they created a flatfoot model by suctioning the ligament, they cyclically loaded it and then they did medial displacement osteotomy, same thing, normal Achilles, abnormal foot. When they changed it back to "normal foot", you had better function. So that's some surgical evidence that shows maybe it doesn't matter about the gastroc. Maybe that's kind of a normal action. So what about prevalence? So these are three studies that found the prevalence of gastroc equinus is in the very high ranges; 96% in one, 100% in one, 87% in one. These are pretty high prevalence. Now, in all of these studies, the researchers suggested that this was pathological. A 100% of pathological adolescent patients. So how many pathological patients do you see?


    How many of them are adolescents? How many of them have really tight Achilles tendon? In Dr. Saxena's study, 100% of them did. And he mentioned that this might be somehow beneficial to them as an athlete. Maybe give them stronger push. So that's an awfully high prevalence of something that we are calling a pathological problem. If we had 100% of, I don't know, say cancer, everybody in this room is going to die from cancer. Well, that's silly, right? That's not going to happen and it seems kind of odd to call something that has 100% prevalence pathological. There is some counter arguments that you can look at from the literature and kind of the most significant one is Digiovanni's article where what they did was they were looking for gastroc equinus in patients who had forefoot problems. So they had 68 patients. They created a device called an equinometer, which is basically just a goniometer that is attached to a computer that tells them how much force they are dorsiflexing the foot with so that there could be consistent every time they dorsiflexed it. So it's just a sort of flat plate on the bottom of the foot and then a plate on the side and then that's attached to the computer. They had two groups. They had 34 patients with forefoot and mid foot problems. These varied with things like Lisfranc issues, first ray problem. Most of them were first ray issues. And then they had 34 controls, which were mostly their spouses, which I find kind of funny because I have done stuff to my spouse to test stuff that I learned while I was in school on her and she to this day will not let me lift it down. So I think it's kind of interesting that they used their spouses in these things. Apparently, the spouses don't have any foot problems.


    So what they found was a prevalence of equinus in 88% in the patients who had the patient group, the ones with the problems and 44% of the patient who had "normal feet". Now, one of the problems is that on their physical exam, they talked about a "normal foot" or a structurally sound foot, which I think was what how they said it. But they never said what that means. They never did any measurements to show what a structurally sound foot would look like. So that's an issue. This is really too small to read but basically one of the issues that they had is that they mix their groups and a bunch of the patients in the normal group had ligamentous laxity, so about five of these patients. Now remember there is only 34 patients in each group. So five of the patients in the normal group had diagnosis of ligamentous laxity. Now, that would mean if they have ligamentous laxity that they are not going to have equinus no matter what, right? You are going to push and they are going to dorsiflex great. So that's going to completely change the numbers that they are reporting. So this study had lots of confounders and that makes this a really difficult study to use to say that gastroc equinus is both normal and prevalent, which is exactly how this has been used over the years. Now just to sort of finish this up here. These are their kind of results and in the patient group you can see this knee in 0 degrees of flexion. It's just a fully extended knee. Those patients had 4.5 degrees of ankle dorsiflexion and it went up to 17 degrees when they flexed the knee to 90. So that's equinus according to what we have been taught. And their control group had 13, so they had better range of motion but they also increased their ankle range of motion when they had the knee flexed.


    So this is really just showing the same kind of thing. It's just a passive ankle dorsiflexion except in those other patients, they had dysfunctional feet to begin with. They were there for problems, so they had feel that didn't work and that was really the problem. So there are couple of other interesting studies. So Dr. Frykberg did one and Dr. Lavery and these were on diabetic patients. And they found a prevalence of 24.5% in Dr. Frykberg group and in Dr. Lavery's group, these diabetics had a prevalence of 10%. On both studies, they said these are pretty high prevalence rate, which I guess I am going to agree with except they are not 95 like I was saying before. The problem is that in both of these studies they defined equinus as 0 degree of ankle dorsiflexion. They don't say whether it was the knee extended or flexed. So if they had to find equinus as 10 degrees, then there would have been more patients who they would have diagnosed with equinus and this is more about a definition of equinus and you know if you have very sort of low kind of threshold or high threshold for diagnosing this, then you are going to get a low prevalence. Now, I wonder with your numbers if they had actually changes that, then there would be -- they probably would have seen a much higher prevalence rate if they had said 10 degrees of dorsiflexion. So my question to you is, are noses pathological? Everyone body has one. Thank god, mine isn't really that big. Everybody has one. If there is 100% prevalence of noses in human population, then we don't call that pathological, we call those noses. So that's an interesting thing. So there may be some use to this and maybe this is just a little silly little thought process kind of thing but there potentially is an issue with this. So this is a study that looked at the medial calcaneal displacement osteotomy.


    What they did -- this is a cadaver study and they did two versions of a medial displacement osteotomy. One was just a kind of classic one, cut the calc, move it over medially. In the other one, they cut the calc and they put a graft in after they moved it over medially. So they change in the lever arm of how this works. Now, in both cases, they decreased the force of the PT tendon that was needed to create a heel rise. So they also found that the Achilles tendon force that was needed to raise the heel was lower. So what they did was they created a normal foot from their flatfoot model and the gastroc was never touched. The Achilles was never touched. So the same thing that we are saying is pathological if you fix the foot, it becomes non-pathological all of a sudden. That seems kind of suspicious. So I am going to finish this up with a patient of mine. So this is a patient who on the right anatomical left side. She has PTD. You can see that she is kind of pronated. You see the talar head. You can see that she is everted and kind of how prominent she is medially. She is really flexible, so when she rotates and you can really put her back into a neutral calcaneal stance position pretty easily and she is kind of big lady. She weighs quite a bit. So we fixed her. This is from pre-op. You could see her talar head uncovering, her increased calcaneal abduction, you know her calcaneal inclination angle maybe is like low normal to normal and she has kind of NC bridge. So here is her post-op. So if you look at her TN covering, that's almost 100%. So what we did with this patient was a double calcaneal osteotomy and we did a spring ligament reconstruction. So we used a cadaver graft and some anchors to recreate her spring ligament complex and the double calc osteotomy and I didn't do a gastroc recession.


    I used to do gastroc recessions for every flatfoot reconstruction I did, all of them. But I did nothing with them in this particular patient. Here is again her pre-op and her post-op, just pretty rectus. There she is from the back. It's just in case you don't believe me. So whether you are a double calc person or Kidner person or whatever you are, it doesn't matter. What matters in this particular patient is that we didn’t do a gastroc recession. What we did was we re-lateralized the subtalar joint axis and we turned the gastroc into an inverter instead of the evertor that it was before. So if I had weakened it, it would have done maybe less of a good job as an inverter. So by leaving it strong, she now has a rectus foot. So to finish this up, what does this mean for us? Well, it may or may not change any of your treatment methods. You may decide there is a just a bunch of bunk and you are going to keep doing your gastroc. I still do gastroc on diabetic patients, I do TALs for TMAs. I do all those things. I do gastroc for patients who have retrocalcaneal problems. All of those things that hasn't changed. There is a lot of researches that still needs to be done to confirm the truth of this. We really need to do an actual study that looks just at the prevalence of what we think is equinus in the normal population. Everything that's in here is just on pathological patients. Should we stop the Silfverskiold? I don't do it because every patient seems to have it. I have access to a bunch of young healthy students and all of them have it. So I don't know what that means for the reality of this but should you stop the Silfverskiold? I used it to really test the sort of severity of contracture. And that might help me to learn a little bit more about the patient. So there is a lot more to come on this. I think we will see a bit more in the future. Thank you very much for your attention. Alright. I think we are -- thank you. I think we are done for the evening.

    TAPE ENDS - [26:22]