• LecturehallHeel Pain....When it's not PPF
  • Lecture Transcript
  • Male Speaker: I took over these talks or agreed on. I find this hard to believe that a man of his stature and age would be able to do for these [Laughs]. This is really [Coughs] – it’s a lot. But I enjoy I’m being here with you guys and clearly any opportunity to get out of the frozen state of Alaska which was formerly known as Pennsylvania where I reside is also a benefit. So heel pain when it’s not PPF. Quick talk. And for something I’ve been taking a lot closer look because we all see these heel pain patients we’re all experimenting with. We’ve done everything to the heel. The poor heel has been literally a target of our abuse for over a century. We come in, these patients come in. I mean how I can guarantee if you guys are practicing [Indiscernible] [00:45] are probably one out of every four patients you see is coming in with the complaint of heel pain. When you take a look at it from a historical perspective, we didn’t even know anything was going till this guy happened on the scene. We started shooting x-rays. And then this poor guy who is probably arguably one of the best ball players of the 20th Century, somebody diagnosed him with having a spur, convinced him that it was a good idea to get that thing off, thus ended the career of one of our best, most beloved nationwide baseball players. So we’ve been dealing with this issue for a long period of time. We’ve done everything. We’ve replaced terminology. We’ve had Harvey Lamont say its plantar fasciosis, not fasciitis, because it’s a chronic condition. We’ve changed everything we can think about whether it’s the back or the bottom of the heel where they were doing surgery. We’re not doing surgery. We’ve hit this thing 80 million ways from Sunday. In the end, I don’t know that we know any more about heel pain than we did five years ago. Just probably better ways to treat it sometimes. I know Steve [Bariwel] [01:54]. He was the first guy to introduce the EPF. That was a great answer to a very difficult thing and we all got certified and started doing them and had a bunch of patients end up with calcaneocuboid subluxation syndromes and other things. And Baxter’s nerve entrapments where we whack nerves or we did things and hit things we weren’t supposed to see or do. In the end, a lot of guys that were doing this and it’s inception, me being one of them, doesn’t do it anymore. And it’s not a result of anything that Steve have created because I still think that this test or this surgery is still very viable on a lot of patients. I just don’t do them myself. I refer them to my local podiatrist in my area who do a fantastic job and do them more frequently than I do which is about once every five years. So I would rather have my patients in their hands than in mine with this. So if we take a look at this and we say well, we talked about this and we’ve done the whole toe past thing and jabbing needles in. Now we’re starting to create these grids and we’re talking about amniotic cell derivations, stem cells, what if we put them in there, and we take off the ligament and the plantar fascia and its insertion and irritating and got it to bleed. Now we can throw these other cells in there. That will then take cues from the cells that are existing. I mean geez, we can grow kidneys in dishes at this point as long as we have kidney cells to tell those cells what to become. It’s no different than what we do with bone where we take bone marrow aspirate. These are all hematopoietic cells. We’re basically putting them in an environment and saying hey guys, go to work. This is what you do now. So the same thing is going on here, but does this stuff really identify where heel pain is coming from, and does it really hit everything? Is it a neural origin heel pain? This had been something that I’ve been taking a look at. Clearly things like bone tumors, things like that, they’re pretty straightforward. But take a look at this. Now we’ve all said to our patients, overtime that we know the weight is a big influencer on heel pain. Even you lose five pounds or gain five pounds, we sort of all settle into our weights around the age 30 and 35. When we go over that, we start to feel a lot of things that we wish we didn’t feel or we weren’t feeling previously. In most instances we all know the typical patient population for these and we don’t need to go into that, but the important part is just understanding that when you do put on weight, things are going to start to get stressed and we were sort of built to do another thing. It’s also when we change our lifestyles and become more sedentary and maybe we’re not out walking as many places and certainly not exercising like we did in our 20s or 30s for that matter. We start gravitating more towards the couch or a seat at the office. A Taco Bell for lunch doesn’t seem like such a bad idea anymore. So when these things happen, then we start to get these pains. Stress fracture is clearly so close in terms of a Venn diagram. If you took proximal plantar fasciitis and I say PPF, not just the plantar fasciitis, it’s infecting the right at the origin of that structure. You overlap that with the stress fracture, they really – different, very few ways.


    Stress fractures actually will not get better after being up on the first 20 or 30 minutes, like post-static dyskinesia. They will get worse or that pain gets worse as the day goes on monotonically increasing over the weeks. Usually it will not be in the patient that you would suspect who would have a plantar fasciitis. It’s going to be your lighter patient. Maybe it’s even a female athlete and you have to have concerns of dysmenorrhea and all these other different types of syndromes associated with that. Is she really eating enough? What’s her bone quality and strength, etcetera, period. So what is the causal influence in this? I remember I was speaking at ACFAS a couple of years ago. I think we’re back, I think we’re down to Florida and I was on the heel pain track with Sam Mendicino. He basically looked at a hundred patients from his own clinic and he basically went through everything and we’ll get to what he found at the end. But it was a pretty amazing stuff to present. When we take a look at the things that can be going on in that Venn diagram that I talked about earlier, really the only thing that separates it is when these things hurt. Typically we’ve got different individuals here but both of them could be having heel pain. Clearly the ones more obvious and the one you would all pick is the obvious one but in addition that other patient can do too. So I just got a squeeze test. Clearly this is one of the tests you should be performing. If you’re not, you want to make sure that when you’re squeezing now on the other side, you want to make sure that you’re not grabbing that tarsal tunnel and pressing down there. Because if they do have a tarsal tunnel-type pain or some sort of impingement in that region you may actually be causing the pain with your fingers that you’re not looking at. You should be pressing there. I’m squeezing on the side of the heel but look where my fingers are up, coming around the other side. I can’t see them and neither can you. So you got to make sure that in these instances you’re almost taking your thumb and just pressing right on that lateral wall and that usually gives you your information. So there’s a typical spot where we’re going to feel for heel pain which is going to be plantar medially and at that tubercle. That should give us our answer and PPF certainly can be there. You still can feel a stress fracture there but mostly likely you’re looking at proximal plantar fasciitis. So now we’re moving in to another area. So now we moved over. We’ve done our direct central and we’ve done our plantar medial and we’ve done our lateral wall, but we still can’t reproduce this pain that this patient is complaining about. So what we’re going to do is move almost a fingerbreadth laterally and then press in that region. What are we looking for there? Now we’re looking for entrapment of Baxter’s nerve. Baxter’s nerve entrapment, especially in a thin athletic individual, is very, very common. It’s often times a misread or misdiagnosed as PPF and we continue to treat these patients with orthosis and every imaginable thing, injection, splints, whatever. We know it’s not a stress fracture. We’re pretty fairly sure it’s PPF but they’re just not getting better. This is probably why they’re not getting better because that nerve branch is going to fire off laterally right there. That’s the ADQM nerve branch. That’s where you’re going to get your greatest pain and sensitivity is in that region. Now we move up to the tarsal tunnel. We press there and simultaneously you can also press down on the bottom and see if you’re actually reproducing both at the same time. Sometimes they actually will come in concert with each other. I’m not a big proponent of that whole diagnosis of tarsal tunnel syndrome and we’ll go over that in a second why. But from my perspective, there’s a very few people that have isolated tarsal tunnel syndrome. It’s usually related to something if they do have it in fact. What are the clinical findings that we see? Well, it’s really tough. Unlike proximal plantar fasciitis and even for stress fracture, in most cases you can pick out a pinpoint area where they’re having an exorbitant amount of pain. The neural pain is very different. It’s sort of all over the place. It’s more like globally located than direct pinpoint pain. So if you have a patient that you see and you’re pressing on his areas and you’re not getting a real response in one particular area where you’re pushing but sort of fanning out from that spot, the first thing I would look at, are you looking at a nerve pain issue? The other thing is hyperhidrosis. The Tinel’s sign is always very subjective thing whether you see or whether they feel it. But one of the things that I look for is do they have varicosities? I’m not talking about big, ropey, thick varicose veins. In most of these instances they’re just spider veins, just telangiectasia. But what we find is when we do finally go in and if we do a tarsal tunnel release on these patients as we see these rosary bead varicosities, and we’ll see that in the upcoming slides, but these are anatomic considerations.


    All the different nerve branches that are coming in and off and around that area. There’s a lot of them. There’s a lot of different variations. But that Baxter’s nerve is the one that’s going to be right there, right at that origin, and it’s going to – basically it’s the proximal originating fascia of the quadratus plantae that is actually incarcerating that nerve in that area. This is again that mechanical neuritis. You cannot put your finger on what is going on until you actually go in there one time and see it for yourself. You see how the nerve which should be this nice little thin strand. It’s very difficult to even isolate in a non-pathologic state. When it’s in a pathologic state, you’re talking about the difference between a piece of angel hair pasta and a piece of linguini. That’s how much the size increase and the caliber of the nerve changes. So here’s all the different variations and patterns and we don’t need to get too crazy about that. You can see they’re all in the very low, they’re all less than 5%. But you can see there’s all different types of branches coming off here, coming off there. Some are splits. Some are divergent. Again, there’s just so many different cross sectional changes that occur in that region, the tarsal tunnel and the nerves. So is x-ray really going to help us in this instance? It’s probably not. MRI, if we got a stress fracture, most definitely. Baxter’s nerve, I’m sure you’ve all gotten reports that say fat pad atrophy or ADQM atrophy maybe consistent with Baxter’s neuropathy. This could be painless or it could be painful. But I have a nice slice of an MRI that’ll show you what a normal MRI should look like and what the abnormal ones do. Clearly in cases if it’s a diabetic or a neuropathic patient you’re going to see sleeves of fat throughout all that plantar musculature. But this is for the patient that’s not a diabetic and you’re just picking up that isolated area where it just looks different, and we’ll get to that. Sometimes you can have a fractured – intensified on the plantar aspect. They’ve got a spur that sometimes cracks. This is really thinner, older patients, especially older women that don’t have a lot of fat pad to begin with. Hit something the wrong way and they’ll get a little crack there. Again, these things can linger around for a long period of time. Does EMG and NCV really help us with anything other than just putting our patients through torture? I think it does if we’re looking for drop foot or we’re looking for some crazy – or if we’re looking radicular pain or some plexopathy or some mononeuritis multiplex or something like that. But really isolating whether Baxter’s over a tibial nerve issue, is going to be picked up on EMG and NCV is probably pretty limited. So you see, that’s a normal MRI slice. You see that ADQM. Now you see it on the abnormal version. You see how it looks, like the surrounding fat. In fact you don’t even pick up the muscle belly. That is very indicative of or should be indicative to you that what you’re looking at is a Baxter’s neuritis or Baxter’s neuropathy for that matter. Other things you can find in that area, accessory muscles, clearly. You can have accessory flexor tendons. We always have no problems believing that we can have extra muscles and tendons on the lateral side of the ankle, like a [cortius] [13:13], etcetera. But on the medial side we really don’t think too much about it but clearly they can be there and they can insert right under the heel bone where they could be the thing that’s occupying the tarsal tunnel itself. You’ve got this extra muscle that should not be there. So here’s your non-surgical treatments for these conditions. I have never found any one of these to work consistently for everybody. So it’s basically a process of elimination like most of the things we do, where you see if it will work. If it works, great. If it doesn’t, you move on to the next thing. Sometimes it’s a combination of things as long as they don’t interact or counter-manage each other, I think you’re in pretty good shape. So you can do an immediate decompression. You can see that’s the neural triangle that we always refer to. That tarsal tunnel pretty much bisects. It goes right through the middle of that. You can follow that incisional plain. I’ve heard everything from go to the medial, always one fingerbreadth back. That seems to be pretty accurate. Once you’re in there, isolating all these different structures and making sure that you’re getting everything released is imperative. But also understanding that that lateral plantar nerve is going to come off before you get down to that abductor halluces. When that does occur and you’ve not released that fascia for the abductor halluces, you’re basically doing the proximal part of the release but you’re doing nothing distally as the nerve is plunging into the foot. So oftentimes they will still remain with “tarsal tunnel pain.” That flexor retinaculum must be cut. Once it’s cut, you could be very, very gingerly getting underneath there. A nice way to do that is basically just come up there with a blunt instrument that you can see as getting right underneath it and then just cut down on the metal. Don’t cut straight down. There are those rosary bead or thickened vena comitans that we see with patients with varicosities.


    Now what happens is it’s sort of like a fat guy like two fat guys in an elevator with a skinny guy. It’s a close environment. The skinny guy can’t go anywhere. As these veins expand, they also put pressure on the arteries which then read that pressure, counter expanding, and the expansion keeps going until the nerve is the poor little guy in the corner getting squeezed into the corner. That’s what takes place in these areas. It’s usually related to the veins. Patients with chronic stasis are definitely patients you want to look at as if their heel pain has a neural origin or a concept of that. These are patients that you’re probably going to see this type of phenomenon where they’ve got this very thickened valvular disrupted veins that are really swollen and they’re basically draped all over the place and hanging all over the nerve pressing it. Remember that nerve can’t get out of there. In these instances it almost does you better just to remove the vein in that area and get rid of it. You can see there there’s a nice carotid vein. And isolating these things with vassal lubes is important so you can trace out the branches. And believe me. A lot of times there are things that look just like everything else. You have to be very, very meticulous in your dissection. Clearly the veins will be always a little bit darker, more purple. But what if you have a neuroma-in-continuity? So basically this is a long neuroma of the tibial nerve. No different than a Morton’s neuroma in the forefoot. Only it happens to be back around the ankle. This sucker goes all the way down in the abductor hallucis fascial shoot right there, right down in the plantar aspect of the foot. So what do we do? In those instances with the neuroma, you definitely don’t want to be cutting that neuroma out as we do in the forefoot. That’s not going to work ever well for your patient. They’re going to lose sensation on the bottom of their foot. So you have to do other procedures like epineurolysis and other things to try to shrink down that area. Also removing possibly some of the epineurolysis in the medial plantar nerve there, lateral plantar nerve there, and the calcaneal branch, all stemming off before we’ve even – you see that Dr. House his muscle belly in the picture in the button next to the adjacent to bottom loop. You see all this stuff could take in place before it’s even made its way into the foot. Gary Jolly was a big proponent of doing this procedure with this incision. He always felt it healed better and that it really led him to sort of map out that calcaneal branch. There is definitely some viability to doing your incisions this way. There’s certainly nothing wrong with doing your incisions this way and it does heal nicer because you’re sort of going with the skin tension lines instead of across them. These can heal very poorly or just they take a while to get together. This is where you can see, you can see space occupying lesions such as this that are in that tarsal canal. They are also the primary forces behind your tarsal tunnel or your neurotic heel pain. So when we have feel of our tarsal tunnel issues, the things that we always look at or to feel a tarsal tunnel surgery, what do we get? What do we achieve? Did we get things to scar down? Did we close that retinaculum back over top of it again? Resealing it in that vault where it could still be impinged upon. So we don’t want to repair that. We want to just close subcu and close the skin and that’s it, and leave that area open, things like double crush syndrome. All these things can place with tibial nerve decompression. That’s why I’m not a big believer in isolated tarsal tunnel syndrome. There’s always something behind it if you are truly getting those symptomatology or you’re getting that symptomatology. Again, when we look at the majority of these things, they all fall under that algorithmic incorrect diagnosis. So did we get it right the first time? A lot of these instances we didn’t. Getting to the end of this, this was the Sam Mendicino talk or comment that I was referring to earlier. So these are patients that he took a look at. You can see, almost complete resolution of almost a hundred patients with no injections, minimal conservative measures. Just basically dietary were his recommendations. Want to see if the patients can get rid of it on their own. So 92 of the hundred got better without us doing anything. You can see with the eight remaining, they had other issues as well that could not be resolved conservatively. I think understanding the origin of all these things is tantamount to your success. Again, stressing the point that there’s no one treatment for anybody. Nobody fix into perfectly one column and you say, “Well, they’ve got that, that’s going to work.” Clearly everybody’s different and they’re going to respond to different things. But understanding that there’s sometimes more going on and plantar fascia is important especially if they’re accounting for probably one out of four, one out of five patients that we see in our office every day. Okay. Thank you.