Harold Schoenhaus, DPM discusses tarsal tunnel syndrome in the diabetic patient. Dr Schoenhaus presents the signs and symptoms of the condition, the prevention, treatment and management with surgical and non-surgical techniques, and explains the significant use of amnion nerve wraps.
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Harold Schoenhaus, DPM,
Surgical Editor for PRESENT e-Learning
Penn-Presbyterian Medical Center
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[Dr Frykberg] We asked one of my colleagues and good friends, Harold Schoenhaus, to speak about a interesting application, which Bruce himself had mentioned, and that is on nerve wrapping for tarsal tunnel repairs. So Harold Schoenhaus is the surgical editor for Present E-Learning. He's been a long-time professor at the Temple University School of Podiatric Medicine. He's been around a long time. Gee, I remember when I was a resident, you were speaking too, Harold, so I'm really happy to introduce to you all my friend and colleague Dr Harold Schoenhaus.
[Dr Schoenhaus] I was beginning to wonder whether I'm around longer than that amniotic membrane stuff! Holy Christ!
Certainly thank Dr Frykberg for putting together a program that is spectacular, and to the amount of people that are in this audience, is just representative of how good this program really is and what Present E-Learning does for this profession – second to none in the education of residents and physicians in podiatric medicine and surgery. That being said, I'm going to give a talk dealing with tarsal tunnel syndrome, and some of it's application and how I've approached it over the years. It's certainly a challenging condition, common in diabetics – it's also common in the general population. Interestingly, could not find any true statistics of what the incidence is of tarsal tunnel syndrome truly is.
When we look at etiology of this condition, we realize there are space-occupying lesions that can cause compression within the third canal of laciniate ligaments, through which pass the neurovascular bundle. So we're looking at potential varicosities, ganglia, lipomas, accessory muscles, tenosynovitis of adjacent flexors, bone spiculization, foreign bodies. What results in these type of conditions is nerve entrapment – the nerve is being compressed; scarring; porta pedis compression, which is something that I've looked at very carefully; hyperpronation syndromes; posterior tibial dysfunction; trauma; iatrogenic; and the big one that is left out in there is diabetes – and its influence and effect on nerve tissue.
Nerve is certainly a unique tissue to deal with. When it's traumatized, it does not respond like other tissues within the body that we can predict within a certain amount of time a structure will heal. You break a bone; 8 to 12 weeks it's pretty much healed. You tear a ligament – we know that within a certain amount of weeks it's going to heal a tendon. When it comes to nerve, this is a highly-sensitive tissue that can take months if not a year to demonstrate the final outcome of what is happening to that nerve. And as long as the repetitive trauma, which might be any of these factors continues, the long-term outcome is poor. So early intervention is something that we are beginning to appreciate that much more.
So you can open up the tarsal tunnel and immediately visualize these vascular components that are too large. The vena comitante associated with the posterior tibial artery demonstrating the varicosities that need to be dealt with.
Scarring and adhesions. Unfortunately, I have patients who are referred to me who have had numerous surgical procedures for tarsal tunnel decompression. This is the nightmare. This is the patient you want to send to your best friend – put in parentheses, or enemy, in the community, and say, you handle this! This is a nightmare. The scarring, the adhesions that take place in the canal that typically will not only affect the nerve but now you go in to try and create a lysis of these adhesions and find this little thing called a posterior tibial artery, and the next thing you know you've cut it. So when I do these type of reconstructive procedures, we do it without tourniquet to try to minimize the trauma of adjacent tissues and structures.
The thing that has perplexed me through the years is, after I've done a beautiful resection of scar tissue, what's the body do after I close everything up? Heals with scar tissue. And that will lead us into some of the approaches that I've watched and seen take place. In the diabetic nerve, we realize decreased nerve blood flow caused by increased endoneural pressures changes glucose to sorbitol within the nerve, and you get this increase in endoneural water content. So we're starting to see damage to the nerve because of the diabetes.
How often do we see patients that are what we consider pre-diabetic who are complaining of tarsal tunnel syndrome or symptoms associated with it, that may be the harbinger or the indicator that diabetes is right in the threshold of what is causing these problems. So we see decreased axoplasmic flow and cannot transport rebuilding proteins. We get advanced glycosylation of the end product, with age, with build-up. And you get stiffness and decrease in elasticity, increased tension and decreased blood flow – all through the nerve. We think of a nerve as that little piece of spaghetti that you see in the wound – not identifying the fact that you have these little blood vessels that are almost like hairs that are supplying the nerve, the vasa nervorum, and often we just ignore the fact that there may be a blood supply. It's a living tissue – it has to be nourished. So the diabetic susceptibility comes from a lot of work from a guy by the name of Dylan. Years ago at Hershey seminars in Pennsylvania, Dylan started to talking to podiatry as a profession, recognizing that we see tons of neuropathy associated with diabetes. And he published numerous articles comparing diabetics versus non-diabetics, and what happens over time with certain types of trauma, conduction velocities, with the change in the diabetic nerve versus the normal nerve. And he did numerous studies to indicate what would happen with compression, inducement of diabetes and compare it to the normal, and these were done usually in rats.
All right? And here's a good example of two groups of diabetic rats versus control, with tarsal and plantar tunnel release versus no surgery, and evaluated walking patterns in one year identifying a major difference. And we saw the decompression, no neuropathic walking pattern, similar to control, no decompression and you've got this walking pattern abnormality. So compression and what is happening in the canal must be recognized early and addressed early. And I've yet to see a technique other than
surgical decompression that is going to allow for this reduction of pressure against the nerve.
So in diabetic decompression the goals are prevention of ulcer and limb loss. Why? Because of the effect of that nerve which is supplying sensorium to the plantar aspect of the foot as well as the motor components to all your intrinsics planarly. So we see marked changes in digits, digital contractures, increased areas of pressure, reduction of sensation. These are conditions that probably are preventable. That may be the day that we're going to be injecting the material that Bruce just talked about, this amniotic fluid, into the canal to prevent the need for surgical decompression. Obviously we want to diminish pain, treatment and restoration of sensory and motor function. Early intervention in my opinion is incredibly important. So the prophylaxis of what we're doing is to prevent the neuropathy, which is a continuous process accelerated by the fact that you have compression and abnormality of the nerve. And you can look at numerous articles that Dylan has put out since 1992 and earlier, with long-term follow-up of decompression of nerves in various aspects of the body. When I first heard Dylan talk, he was talking about decompression of three primary nerves in diabetics, which he felt were mandatory. Common peroneal, by the head of the fibula. Posterior tibial nerve, and the deep peroneal nerve. Identifying major nerve function that influences lower extremity capacity to deal with stress and reactivity. So ultimately obviously, you want to try and improve and decrease these side-effects. And you can read that as well as I can.
All right? So we can go through literature and identify very clearly the association with healthy nerve function. And you can see it by numerous articles, numerous authors have identified the importance of decompression of the tarsal tunnel canal.
Interestingly, we do these diagnostic test things – Semel-Weinstein, the monofilament, can determine if in fact this is really going to be indicative of something going on. And he found that in diabetics these were not the most diagnostic when one's looking for these compressive type of neuropathies.
Patient presenting with tarsal tunnel syndrome, diagnostic testing is helpful. And these are the typical tests that I will get – an MRI, provocative nerve conduction velocity, EMGs, specially of the abductor digiti quinti in the interossei; CT scans, ultrasound. It's interesting, nerve conduction velocities are not always totally reliable. You can have a good number of false negatives. I am more concerned about a Tinel sign over the tarsal tunnel, and Dylan points this out as well. And if you percuss the tarsal tunnel and elicit a radiating pain, you know you've got a problem related to that nerve, because it's not been picked up on NCV does not mean it doesn't exist.
A provocative NCV is the test that I asked for, in that the patient walks, creates the symptoms, and then do the NCV test – not the patient sitting in a chair waiting for the
technician to come in, and a half hour later they do the test and it comes out negative. So patients with provocative testing demonstrate a different effect.
EMG with diabetics, useful in determining presence, exact site of neuropathy. And to detect left to right differences, differentiate between myopathy and neuropathy. Interesting, in peripheral diabetic neuropathy, EMG usually shows bilateral reduced nerve action potential and conduction velocities. The patient has an occupying lesion on one side – obviously he's not going to demonstrate bilateral abnormality.
Interestingly, with nerve compression syndromes, the value of EMG is doubtful. And false negative results, 50% of the cases. That's pretty significant.
Wyman pointed out decompression surgery in peripheral diabetic neuropathy is essential, but he showed no electrophysiologic improvement. Two point discrimination and subjective functioning did improve. I think this clearly demonstrates early intervention.
So I'm going to just keep going into some more specifics of the clinical component. Symptoms – tingling, burning, paresthesia, intrinsic atrophy, clawing of digits, numbness, heel pain, bulging in the retinaculum.
The anatomic considerations as the posterior tibial nerve enters the canal and divides or bifurcates into the medial lateral plantar nerve, medial calcaneal branch also comes off of that nerve, either above the canal, in it or below.
Your dissection into the tarsal tunnel should be proximal and distal to expose the entire canal where the nerve enters the canal itself as well as where it enters into the foot. I think the tendency is to be too timid in our dissection. And part of that is by the abductor hallucis. The porta pedis is a canal. It's a ring through which the neurovascular structures pass into the arch. They kind of protect the area. But if I have a diabetic with a collapsed arch and a flat foot and you're getting compression of the abductor against the calcaneus, that canal becomes a compressive environment.
So we need to identify the canal and actually opening it up. Non-operative approaches I think are rarely of significant benefit – certainly the NSAIDs, unless there's an acute trauma that you bump the area and you're calming it down. Lyrica – I've used an extensive amount of Lyrica, and I would say that in my tarsal tunnel patients it's helped minimally. I do use it post-operatively, by the way. Steroid local injections, orthotics, I think are minimal benefit. But if you're going to go conservative you could certainly approach it. Treatment surgical has released the canal. Release the abductor, so your dissection is rather extensive. Identify the branches of the nerve, recognizing there are two canals, and the nerve may go through one canal, and the other branch going
through the other, and there's a septum in between. So your dissection has to be rather extensive, bold but careful.
And here we are, just identifying the structures, looking at how the nerve appears – the color of the nerve, the presentation, the thickening of the epineurium. Does that nerve show flattening? The changes that one would see with disease. So the treatment surgically has released the ligament, the abductor, into muscular septum. If there's other associated abnormality, deal with it. Now the problem comes in as to what do you do if you've done this extensive dissection. Are you careful to cut through the sineate ligament and then attempt to sew it back together? I've never felt comfortable in doing that. If you leave it exposed you're going to get scarring in the area, which definitely is going to influence the nerve and possibly the blood vessels. So I've always looked into what material, what can I do to protect the nerve to prevent additional scarring?
And there's a couple of materials that I've used over the years. One's collagen. There's a number of companies that do have it. You simply wrap the nerve – it looks like a little cocoon round which you will protect the nerve. All right? Now I've used that very effectively, but then when I was introduced to amniotic membrane, and I've heard Bruce talk about his success with amnion, I decided that it might be a better approach. And here I am just using amniotic membrane to wrap the nerve. And there's a number of companies who have amnion, and that's going to be the decision you make as to who you utilize, what their method of presentation is, how they prepare it, how viable is it and how easy is it to use? And cost is always a factor in today's world, 'cause the hospital is going to immediately say, what did you use before and how does it compare in price? Not so much thinking in terms of what the long-term benefit is, with the use of these type of products. There's a thicker version of the membrane, and then there's a thin version, and it's almost like cellophane, that you can wrap around peripheral nerves. I've used it effectively, not only in the tarsal tunnel, but also in the area of the dorsum of the foot or anywhere that I have provided a surgical approach to a patient and ended up with an entrapped nerve. 'Cause the only alternative's, once you've performed a neurolysis, is to either resect the nerve or protect the nerve. And here's where the amnion has worked beautifully to protect the nerve.
That's what it looks like. It's a little bulky. The thinner membrane makes it a little thinner, but I need enough material to protect that nerve and let the environment quiet down.
So my experience with amniotic membrane in tarsal tunnel is about two years now. I have used it primarily on my re-dos, and I've now switched my thinking completely to every tarsal tunnel decompression I perform. The nerve is wrapped with amnion, and that can extend proximally and down into the canal. And actually two days ago, before I left, a good friend of mine, a judge, called me. He's had decompression at least two to three times for tarsal tunnel, and he said, “I cannot believe how good my foot feels, without the feeling of something tight and binding down in that canal,” he said. “I don't
know what you did there, but this is far different than anything I've ever experienced.” And this is what I am seeing: reduction of pain, restoration of sensation, and a happier patient.
So references are available – tarsal tunnel syndrome is something one should consider every diabetic has the potential of presenting with. And certainly, thank you for your time and enjoy the rest of this seminar.