CME OnDemand - Management of Acute Achilles Ruptures in the Athlete-Foot & Ankle Focus: Management of Acute Achilles Ruptures in the Athlete

Foot & Ankle Focus: Management of Acute Achilles Ruptures in the Athlete

Video Transcription

Good evening. On behalf of AOFAS, I want to welcome you to the fourth webinar of the 2021  Foot and Ankle Focus Series. Tonight's program, Management of Acute Achilles Ruptures in the  Athlete, will be moderated by Dr. Mark C. Dracos. Dr. Dracos will be joined by Dr. Finit Fistiga,  Dr. Martin J. O'Malley, and Johnny Owens, MPT. You can find their full biographies and disclosures  in the program document posted in the chat box and in the PRC. The 2021 webinars are provided  free to AOFAS members and orthopedic residents and fellows with funding from the Orthopedic  Foot and Ankle Foundation, supported in part by a grant from Arthrex, Inc. I'd like to run through  a few housekeeping items before we kick off the presentation. For technical difficulties, we suggest starting with the Help tab to troubleshoot your problem. If you continue  to have issues, try closing all of your browsers and logging back in the same way you did the first  time. Registered physician attendees may earn one hour of AMA, PRA, Category 1 CME credit  by completing an evaluation in CME claim form at the end of the webinar. You can find the link to  Claim CME in the chat tab, and we will also follow up with an email at the conclusion of this broadcast. This webinar is being recorded and will be available for on-demand viewing  on the Physician's Resource Center at www.aofas.org slash PRC in approximately one week. We encourage  you to ask questions during the presentations. To send your questions to the faculty,  click on the Q&A tab on your navigation column. I'll now turn the program over to the moderator, Dr. Mark Dracos, to begin. Thank you.  Okay, thank you, Julie. So it's my privilege to talk about this foot and ankle focus webinar  management of acute Achilles ruptures in the athlete. We have a very distinguished panel,  Valley, Dr. Pinnett Fiscal and Mr. Johnny Owens, who are going to give us each talks about  specifically the treatment of acute Achilles injuries in the athlete. As I was saying before,  these are my disclosures. I have nothing specifically related to the topic of this talk.  So our first speaker is Hollywood Martin O'Malley, who takes care of a bunch of stars. If you are a  NBA player with a foot and ankle injury in the last few years, you most likely had your surgery with Dr. O'Malley. He's an associate attending orthopedic surgeon at HSS, team  orthopedist for the Brooklyn Nets and USA Basketball, foot and ankle consultant to multiple sports teams and leagues. And I'm fortunate enough to call him a colleague and  get to bounce stuff off him all the time. He's going to, he was gracious enough to share his experience with us regarding the treatment of professional athletes. So Marty,  take it away. Thanks, Mark.  Mark asked me to give you the 360 degree overview of the management of Achilles tendon, the things that I've learned over the past 25 years. So I'll try and share that with you over  the next 15 minutes. So can you see my, I have nothing to disclose that relates to this talk.  Achilles tendon ruptures, you know, the instance is increasing. What we can say is we all feel  that recently, certainly the past 10 years increases in our practice of patients rupturing  their Achilles tendons increasing. We don't really know the reason why. Clearly it's the weekend warriors  are the majority of the patients and basketball is clearly the most common sport followed by  racquet sports. It's usually the weekend athlete, this 42 year old radiologist on the left side who  did one Achilles playing basketball. They are so happy to his next Achilles the next year or this banker who was trying to do box jumps off a three foot box and ruptured his. What  gets a lot of press is the Achilles tendons in the professional athletes. We've had a lot of very  notable athletes recently. There's not, there's a lot written about it, but the study in sports  medicine came out in 2013 estimated that 0.78 ruptures per season in the NBA. Well, in 2019,  there were five. I fixed three of them. So the instance is somewhere between 0.78 and five  per season, the NBA, and it's increasing the NFL as well. If you follow the, uh, the league again,  the reasons for this, we can all say maybe they're bigger, they're stronger, they're faster guys are  bigger and more explosive than they were in the past, but we really don't know the reason.  So the diagnosis is pretty straightforward. If someone felt a hurt pop, someone kicked me.  If you have an exam with a palpable gap, increased dorsiflexion and positive Thompson test,  it rarely do you need an ultrasound or MRI. I usually resolve the resort to just for  the questionable exams, a partial rupture with a palpable gap and increased dorsiflexion. A palpable  partial rupture is really not really true. It's really just some fibers are left on some of the  imaging studies. The goal of the treatment, no matter how you treat your Achilles tendon is  restore the muscle tendon integrity and the resting tension. This forced tension relationship  is the crucial thing to a successful treatment of Achilles tendon. You want it to return into  pre-injury level activity and you want to avoid complications. So the Achilles tendon resting  angle relates to tendon length and it really relates to function. So I, I, I have one goniometer  in my office and I'm looking at this all the time, um, and trying to see if that the test,  the resting angle is the same after my treatment for it. And I, and I'm crazy about this because  if they're, if they're not good at three months, they're not, I'll show you later, but that could  be good at a year. So I'm very careful about the resting angle and trying to restore this,  this tension. And I'm, and I'm really a little bit OCD about patients stretching out early on  after an Achilles tendon rupture. So we know that even operative repairs stretch out. If you look at  this study, they did, um, tantalum beads and they split the group into patients who were non-weight  bearing for six weeks in a cast versus early rehab. And they all stretched out and they found  the greatest length in between two and six weeks. So this is really crucial for your patients,  not to get them stretched out between two and six weeks. There's, I don't think I've ever had  a patient who's ever felt from a primary Achilles tendon that they've been too tight. I've had  patients who felt like there's too stretched out. So there's four decisions when you see a patient  with Achilles tendon. The first one is the operator treating the boot, right? When I first started,  we operated, I gave the whole spiel to the patient. We're operating because the re-rupture rate is  lower. That was the reason we operated. And then looking at this, you know, a couple of reviews  came out, well, this complications rate really high from operation. So people started to look  at this non-operative management, revisit it and say, well, maybe non-operative management,  the way we do it is, is the problem. So we know that complete unloaded attendant was detrimental  and this work because it causes decreased healing, increased adhesions. And if you immobilize them  completely, the repair, even for non-operative is not very good. So people started mobilizing them  and they, and the patients did better. Early motion improves the functional outcome. So the landmark trial came out in 2010. They randomized the South Canada, 144 patients,  surgery versus accelerated, accelerated functional rehab. All outcomes including re-rupture rate were  acceptably clinically similar, right? This is a, so this is, this really changed and certainly in  Canada now, it's rare for them to operate on an Achilles tendon rupture. So I consider non-op,  if I get a patient, we can't go through the whole thing, but if they're early, if you're  early presentation within 72 hours from an acute injury, they're compliant, they can access a  functional rehab, any gap size, we don't care about the gap and they're truly acute. They don't have  underlying tendinopathy. And we'll discuss about the weekend athlete versus the elite athlete.  So if you look at the, the patient reported outcomes after operative versus non-operative  treatment, they're exactly the same. You know, if you look at big studies, patients like the, you know, the operative versus operative, they don't feel like, oh, they, I had an,  I didn't have an operation I didn't do as well. So patient reported outcomes are pretty good  for both treatments. And Wilt's finding again said no difference in re-rupture rate. The only  thing they found was a significant difference in plantar flexion strain at 240 degrees at one in  two years. You know, and how is this really clinically important? We know this weakness in end range plantar flexion after Achilles tendon has been reported for many years.  And if you look at the functional outcomes, they're pretty good for Wilt's study. But if  you look at another perspective study out of Scandinavia, looking at surgical and non-surgical  treatments, they looked at Wilt's study that this Levillade score was the same, but their  isokinetic calf strength was higher through the range of motion in the surgical treated groups.  The peak torque was better at 18 months and the surgical groups had better functional physical  function. So when I look at operative versus non-operative, I compare myself to my son. My son played college soccer and this is him getting a header. If he loses 10 or 18% of his  peak torque, he may not get that ball. This is me doing a layup. I have a 12 inch vertical leap.  If I lose 10 or 18%, I'm still going to get my shot blocked. It's not going to make a difference  for me. So if you have an elite athlete, your hopping, your counter-jump movement, your high  speed plantar flexion torque are all better and your re-rupture rates are lower. So it probably  is worth the slightly increased risk of an operation. The weekend athlete, it's a different  call. It may be, but the soft tissue complication rate may outweigh the small functional gain  achieved at high torque if you do an early weight bearing and rehab program. So that's the first  decision is fix it. So if you decide you're going to treat non-operative, you can go that way. But  if you're going to treat operative, the next step I have to decide do I do mini incision versus do  I make an open incision? So again, our role is to get the appropriate length and tension, but the  least morbidity. So in the best way to take your tension is the opposite side. Now, some people  say, well, I just tighten it up as high as I can and I don't prep out the other way. Bob Anderson  and I have this debate all the time, but I've had patients where I've tightened it up as tight as I  can and I've compared to the opposite side and it's still been too loose. And I've gone back and  redone the whole thing. So I think it probably takes an extra five minutes that it really helps  with comparison. We did a WNBA girl this morning who had really poor plantar flexion, just passive  plantar flexion of her ankle. And if we didn't have the other side to show that it looked good,  we would have been very upset after our repair. We tightened as high as we could. And she only  went down about 20 degrees in full plantar flexion, but her opposite side only went that far  too. So I think it's crucial. If you don't do a lot, just prep out the other side and really set  the tension based on the other side and really look at the first NP joint. Look from the end  of the bed and look at how much inversion you get. You should be slightly inverted. Remember,  they're going to stretch out. Everybody stretches out. Even the patients who were a cast for six  weeks stretched out. So this is a guy of mine who came in and saw me the other day. Three months,  he went through, you know, good non-operative treatment and he's clearly stretched out and they  just moved him a little fast. So he can't do a single heel rise in the right. He's got a lump.  He's got, he's going to need a revision. So surgical treat mini versus open. Mini came out  because of the complications, wound complications of the open incision, but doesn't really have  lower complication rate. This study came out in foot and ankle 2011. That's a retrospective 136 patients. MS had less wound complications and higher patient satisfaction, right?  So Bob Anderson's study, the big study of the PARs versus open, they didn't see a difference  in wounds, dehiscence or seroneuritis, right? No difference in reupturate. So that didn't really  show that the PARs had less complications. They just said it was as the results were as good.  And so if you look at DiGiovanni's study, it's at Harvard, three hospitals, three centers, 215 patients, no difference in complications between MS and open. The only difference was  the trauma surgeon. So the thing you take away from there is don't let your trauma surgeon fix your Achilles tendon. Let your foot and ankle or sports guy fix your Achilles tendon.  So small incisions, patients like it. It's a quicker closure. It feels better, but overall the complication rate is about the same. And what about the strength of the MS  compared to the open? Less locking sutures. Tom Clanton, who's an Arthrex PARs guy, minimally invasive, demonstrates susceptibility to early repair elongation. So if you're doing  this MS technique, then you got to think about the first six weeks. Again, everything stretches out between two and six weeks. So you can probably, with the MS, you probably can't  push them as fast as with an open technique. So my experience, I went MS, they convinced me, Bob Anderson convinced me. I had a friend of mine who had an Achilles and he fell and  re-ruptured and it was a whole disaster. And so I went MS all in. And I had about 30 to 4%  interoperative failure, meaning I didn't like what I got on the MS technique. Maybe it's my  technique, but like one of the sutures would pull out or I didn't feel like I got a good repair.  I always did longitudinal so I can convert it. And so I did this and I did it for 18 months straight.  I thought the results were pretty good, but you get some odd ones. Not all Achilles are the same.  This is a 31 European basketball player. The MRI looked like it was a mid-substance tear.  I'd made a little incision. I'm like looking around, I'm going, oh my God, the guy, I have an MRI. I cannot tell. And I don't know if he did it afterwards because he had some heel  pain before he did it, but he had a sort of mid-substance longitudinal tear and they avulsed it from his Achilles tendon. And I've had this now three times. This is a professional  athlete with an Achilles rupture in this secondary in the middle. And then this is the proximate. So they have been two areas. And so some of these ruptures are not amenable to MIS.  So I think for me in MIS, I think if you get in there and it looks great in two ends, that's  an easy one to do, but you have to be prepared to open it up. So what really changed me was  when I was doing my MIS, I started getting these guys with this discoloration around the wound  site. And I think it's because the locking sutures are on the outside and it's a pretty good suture load right under the skin. And I had a series of three or four guys who had this.  And then I had a 27-year-old dentist who texted me from the ER six months post-op, sorry, who had an open rupture transversely. See all this discoloration? I did straight  parts with fiber wire and he had all this discoloration afterwards and he ruptured transversely through this area. So that sort of put me away from doing the PARs. So I went back  to open and I looked up all this data on suture knots. Every suture has multiple pro-inflammatory  cytokines. So it doesn't really matter what suture it was. Fiber wire has been implicated  in a lot of studies to cause a local tissue wreck, but all of the wires, anything, the magnum wire, the Ticron, the orthocore, they all make a response. And I think it's more of the  location of the sutures versus the actual type of suture. So for my open technique, I stay medial.  My incision is medial the whole time. I do a locked banal. I like it because I think it makes  the Achilles tendon, it makes it narrower. And I think the contour is better. I bury the sutures  inside the knot. So I take this, you don't see any sutures after I'm done. I don't use an Alice.  I use a Xerovicle to pull the ends together. I think an Alice just rips it apart. I prep the  other leg. I set the tension with the Xerovicle and then I kind of maintain it with the open,  with the main repair suture if I have to make it tighter. And then I do, and I'm doing epi,  T-knot stitches, Xerovicle. And my acute wound infection rate in 27 years is one. And I think  it's mostly because I've stayed medial with an open technique. I got one and I got the PARs guy, but I think it's mostly because I keep my incision medial and I bury these sutures.  When I went into practice, all I did was pull at the bottom sutures out of the back of people's  Achilles tendons. They had an incision straight down the back. So right down here and you see  these little sutures sticking through there and I debride them in my office all the time. So  medial incision, here's a guy, he got his Kobe shoes after he got his Achilles fixed. Medial  incision here, you usually don't see it because nice contour. Don't do a lateral incision, that was Kobe's incision. So decision three, the big issue there is post-op management.  How fast do you push them, right? So there's a bunch of studies, development of evidence-based  treatment protocol. They said after the second post-op of the week, controlled ankle mobilization  by free plantar flexion, limited zero dorsiflexion should be applied. I disagree with that. I keep  you quiet before that. And even if you go on the internet, you can find like, this is one guy's,  four guys, and they have six different protocols. And it's probably the same for our office,  right? You can get all these different interventions. But if you look at all these ones, for me, what I do for the first two weeks, you're 30 degrees down and I'm happy. I'll take  you out, if you're a professional athlete, I'll take you out of your split in two days. You'll  start doing plantar flexion exercises with the TheraBands in two days. If your wound looks fine, you can do that. I'll let you at 30 degrees down, put some weight on it. But you go,  you don't go anywhere near past minus 20 of plantar flexion. So you just do that time. I'll  hit their calf. If you have a cold laser on, if you do, but I think the calf muscle needs some  biology to it. So I'll do some, I'll do some laser to the calf muscle. BFR, I won't get into,  we'll talk about later, but we do use that. At phase two to four, hopefully you can recheck in  the office, take the sutures out. We still do touchdown weight bearing, no passive push mass, minus 15 degrees. I am pushing you, working you in plantar flexion the whole time.  When we get to four weeks, you can be with 50% weight bearing, but you can't go minus five weeks.  And I'm really not till eight weeks do I let you go, anyone push you past neutral. If I get to  eight weeks, I know you haven't stretched out and then I'm okay because I can't make it up.  If you've stretched out by eight weeks, then I'm in trouble. So my, my Jomo, they always give me a  lot of grief at the hospital for the journal of Martin O'Malley, which is things that I'm  completely sure of, but have no evidence to back it up. So Achilles stretch out. That's one of my  things. They definitely stretch out. You can work in plantar flexion, but my goal is to get you  neutral by eight weeks. Once you get to 10 weeks, I don't really care. You can do whatever you want,  but by eight weeks, if you're neutral, things are good. The Achilles, and this has been backed up  by some data. If you look at your Achilles tenor rupture score at three months, it'll predict your  ability to return to sport one year. If you have a lousy score at three months, it's not going to  be good at a year. My final thing is, and this is sort of another, this anticoagulation, nothing  versus aspirin versus blood thinners. Instance of DVT and pulmonary embolism after Achilles  rupture. This is a study came out of USC, and they said the overall rate was 0.43 and 0.34 for, for 1,172 patients looking at big HMO in California, right? So they said, you don't  have to anticoagulate. However, this is the study that changed my practice. 2009, there's a study out of Finland. All patients had ultrasound at eight weeks, 95 patients,  32 had a DVT, five proximal, 27 distal, three non-fatal PE. And there's no difference whether  you got operate on or not, or surgery or emergency. And there's lots of these studies out.  So prospective ultrasound data shows operative and non-operative patients have a high rate of DT.  It's unique to Achilles, but it's not surprising if you detach your calf muscle that you'll get  stasis in your calf muscle. I do a pre-op ultrasound for anybody who's had a recent flight, any unusual calf swelling or risk factor. I'll get at least one or two guys a year  who have a pre-op DVT, who have done their Achilles. And I'll still fix it. I'll use a  tourniquet, not an anticoagulant post-op if they need to be fixed. But some of these studies are,  are absolutely scary. And if you look at this out of KSST, they did total DVT instance of  254 patients was 49%. And it didn't matter whether you early immobilized them or didn't  mobilize them. Early mobilization didn't change the rate of DVT. So you just have to assume your  patient's got a DVT to approve it otherwise. So how do they do afterwards? That's the big  question. Do the patients return? Can you return to professional sports? Is it really the worst  injury in sports? I think one of the best studies that I've seen in a while is that one of our  former fellows, Turner Vosser. It's a devastating injury that a lot of patients, a lot of pro  athletes will never recover from, but a lot of pro athletes, this occurs at the end of their  career. A lot of these guys are 34 and 35 years old. They're at the end of their career. Their,  their performance has gone down. They ruptured their Achilles and they just, they just stopped.  They're done. They've had a great career. They're done. If you return, you'll definitely have fewer  games and less performance at one year, but players who do return can perform at a level  at two years. So if you get them to two years, they, they, their stats are pretty much the same.  So the question is how did Kevin Durant beat the worst injury in basketball? So we stayed medial.  We opened it. We fixed him. He was in a splint for probably 48 hours. He started doing BFR.  He started using a cold laser on his calf right away. We're doing all this stuff. We kept his  tension tight the whole time. And then COVID hit. So because COVID hit, he didn't really have to  return at nine months, which is usually the return to play. He didn't return to 16 or 17 months.  So we had a whole nother time for him to recur. So he's doing well because maybe because of the  surgery, I'll take that. But also if you look at these guys who are 16 or 17 months out, they can return fully as long as you take care of them properly at the beginning.  So my, my, my take-home points for you are, if you're going to, if you're going to operate at it,  I don't think it really matters what for me, open or mini incision, whatever you're comfortable with.  Just if you're doing the mini incision, you have to be prepared that there are some Achilles,  not every Achilles tendon is exactly the same and you may have to convert to an open incision.  So for me, a longitudinal incision makes sense for me. Two, I'd like to try and figure out a way  that the suture load is not right under the skin. People have tried to tie it underneath it  from one side to the other. I think that may help, but I think you can get acceptably clinical,  good outcomes with the mini or open Bob Anderson showing good results in his pro-athlete to these  100% PARs, right? I just haven't, didn't have that success. And I'm colored by the four or  five guys who had that discoloration and then the guy who had the further open. And I think the other  thing, you've got to move these guys early, but you, you have to protect them till eight weeks.  You have to think they shouldn't go past neutral till eight weeks, just work them in plantar  flexion. And if you give them to eight weeks, then you don't have to worry about it. And then  the last thing you really have to think about a DVT and these guys, the prospective ultrasound data is really scary.  Thanks, Marty. Next up is Pinnett Fiskel. He is a  He works at Tri-State Specialists. He's a former Clinical Associate Professor of Orthopedic Surgery at the University of Iowa. He is a foot and ankle specialist  with over a hundred peer-reviewed articles. He has extensive experience in high school, collegiate, and professional athletes. He has a passion for minimally invasive approaches  to foot and ankles, so he's going to be the counter argument to Marty's open argument that he just gave.  All right, thanks, Mark, for the nice introduction. And Martin, it's very, very difficult to follow your talk. It's an excellent talk, I learned a lot.  So as you know, I have passion in minimally invasive treatment. Acacia Tendon is one of them, which I actually recommend minimally invasive treatment. I have conflicts of interest,  but nothing pertinent to this talk.  I have personal experience with open surgery, open repair in the past. And I've done, tried to do my best to get the crack cross stitch to get as strong as repair possible.  And I enjoy the skill doing that. But, you know, when something like that happened to me, when a patient of yours that you did yourself,  come back, the tendon poke out from the wound, look at you, the suture everywhere. You start to look at this and you're going to say, damn, I'm not going to do it anymore.  I'm not going to do any more open surgery for Acacia Tendon. That's my last case. So as you know, in the literature, it's up to 34% of wound problems can be ugly,  can be very ugly, can be less ugly. But, you know, almost all of us would have seen at least one or two that you still remember your Acacia Tendon infection.  We talked about this study already, that this is a study that actually sparked my interest in terms of length, tension, balance. So this study as a prospective randomized study  from Finland showing that patient who had surgery did better than conservative treatment with functional rehab. They all have superior peak torque at 18 months.  And we look at this curve again, it's very interesting that when you have a tendon rupture and you did not restore the tension of the Achilles,  the whole thing moved to the left side. The resting length of the muscle unit is shortened. There's no way that kind of calf muscle,  at least Acacia Tendon, can become the same strength. So once you lose the tension, once it heal, it lengthen, it's not going to be the same length.  But if you make it at the perfect tension, that's great. But if you make it too tight, they can still have some passive tension to help with their force.  So Medial Invasive has multiple, it's just a family of multiple things, starting from percutaneous suturing technique, Mount Griffith, MFULI, there's a lot of jigs.  I can show you a few of multiple jigs on the market, endoscopic treatment, which usually I use, and many other new techniques that people describe for MIS.  So MIS is not just a few jigs,  it has the entire philosophy of trying to minimize wound problems. If you look at metamethanolysis in the last 10 years,  series of them have shown that MIS is actually superior to open surgery. This series showed that from six RCTs, 277 repairs, no different in rupture,  adhesion, nerve injury, deep infection, deep end thrombosis, but MIS has decreased superficial wound infection, and then three times greater patient satisfaction.  Another systematic review, this one look at 781 patients. Between open and MIS, they have critical and functional outcome in the comparable zone, but MIS has fewer rupture rate.  This deep and superficial infection are lower, wound disorder are lower, hospitalization time and return to work are shorter. MIS, however, has more neurological complications.  So this is a weakness for MIS. And as Martin pointed out, MIS still not superior to open in terms of the loss of tension in the tendon. This is the latest metamethanolysis  that actually just came out from John Kennedy and his group just a month ago. In summary, they compare surgical treatment versus non-surgical treatment.  Surgery meant significantly favor when we talk about rupture, but non-surgical treatment is actually better when we talking about avoiding complications, especially infections.  When we look at the immediately received surgery versus open repair, they summarize that there was significantly favor on MIS when we consider complications. So my take home is,  can you restore the tension for this athlete?  Can you restore the tension without creating problem with the wound? If you can find those balance and solution, how can you prevent stretching of the tendon?  How can you prevent nerve damage? People who want to do some MIS, but want to do some, you know, one step closer to MIS would be an example like this.  So this surgery converted from a long incision from the posterior aspect to small mini incision to deliver the tendon out and then repair the tendon from the inside.  This series show 24 patients, 87.5% return to activities and no wound complication. This is one step close to the MIS. Many other techniques you can think about.  The echelon is the original jig technique that pass three sutures and then tie them together with six strand construct. Dress strand technique,  design a guide that allow you to palpate on the tip of the instrument so that you can tell where you should pass the suture across the tendon.  You can use ring forceps. It's available everywhere and it's cheap. You can put ring forceps around a tendon, pass sutures to a kid needle and then tie them to small incisions.  You can use commercially available jig, for example, parse on the top left here and you can do transverse incision or long incisions. With the modification of parse technique,  they now added this top fixation using suture anchor.  So without going through the tendon but using suture anchor only.  So those are varieties of MIS technique. Cost is something people need to look at. If you do six strands of ortho cord sutures, you pay 200 bucks.  You start to do jigs, it could be 1,400. Another one would be a thousand. If you add anchors to it, it could be 2,400. So think about cost,  especially if you work in a surgery center. Sural nerve. Sural nerve is the Achilles heel of the MIS Achilles tendon. Sural nerve, can it be avoided? Yes, it can.  But you need to know the technique. The risk of injury is minimized by external rotation of the jig. In the study by I. Bider in FAI,  when they put a jig, this is a echelon jig at neutral, the rate of injury was 15%. When they internal rotate, which is not supposed to be, then the rate would be 25%.  When they external rotate the jig, then the rate was decreased. So you're gonna do jigs, external rotate, rotate it away from the nerves.  When a report from Sue using PARS, they show 0% nerve injury. Again, when you say 0%, it depends on how many cases you do it. You keep doing it more and more in general population.  I think one way or another, people can hit a nerve too. So you need to keep in mind how to prevent nerve injury. Tendon lengthening is a problem. This is a study that in UK,  they show that, look at the curve on the left-hand side. Before the tendon was repaired,  the patient was in dorsiflexion because there's no tension at all. When they repaired completely, their zero has become very tight, five to 10 degrees.  In the next three months, it keeps stretching out, stretching out, and then stabilize a little bit and kind of stretch out a little more or stay about the same until a year.  So that's an issue of stretching. Most of them in the cyclic loading experiment show that the displacement, the stretching of the tendon happened in the first 10 cycles.  So you think about having the patient go and walk one day, first day of walking, it would probably stretch out 80% of the whole stretching already.  So this is something that keep in mind about it, okay? We talk about that a little more. I like to do endoscopic technique, which we do it when it's earlier than two weeks.  We don't want to do it when it's too long. You can see that his tendon has a very well-formed tunnel. It's a fibrous tunnel that we cannot violate it  if we do an open surgery in any way. So kind of want to preserve it, passing suture under direct visualization so that I can just capture the tendon without exposing the,  without opening the tendon sheath. So I can confirm, I can capture the tendon end with the camera. So this is a technique, just use a six-step incisions. Number two, fibro-wide.  I create four-strand repair. I use the arthroscope to help identify the tendon. The problem is that I've seen it a lot of time in the proximal aspect.  When you pass a tendon blindly,  you pass to the tendon, not the, actually you pass to the muscle, not the tendon. When I look at the cross-section of a kid's tendon in the proximal part,  it's actually about 80% muscle, soleus muscle, and about 20% in the back, which is the tendon substance. So you need to make sure you aim for that very well.  So this is a right leg in the back, six incisions, put a camera right there.  So I can see where I'm coming in and out, passing sutures, second one. And then for the distal part is very easily, I just do it percutaneously. Those are the step-by-step,  just left side, put a camera in, debride if I need to, pass sutures, and then tie them, and then at the end on the left side.  What's the key? The most important thing, if people don't listen to me at all, one thing you're gonna take home is that do not forget to do intra-op cyclic loading.  69% to 82% of the gap develop within the first cycles. Why don't we make the first 10 cycles intra-op? So the way I do it, I put one stitch, I do four strands, I put two knots.  So each strand, I tie one knot, and have my assistant hold them tight, and then I do aggressive range of motion of the ankle.  I stretch it out, I make anything that want to cut through, let it cut through, let it reset the tension. And then I reset the suture again with the tension I like to be.  I aim the ankle to be more plantar flexion compared to the other side, about 10 degrees or in that range.  And that's my go-to technique. And I found that if you do cyclic loading initially, let it cut through, and it has less problem cutting through down the road.  I have my series, I report it and publish in arthroscopy. Three years ago, 23 patients, follow-up of 54 months, tourniquet time less than an hour,  patient returned to sport less than six months. We have one superficial infection. There's no sero-nerve damage. And so far I have no sero-nerve damage until nowadays.  But again, I can hit it anytime in the future.  I didn't have DVT in that series, but I have a couple of DVTs in the last couple of years afterwards. So the bottom line, the final take-home,  MIS, if you want to do MIS, it's great. Patients love it. You preserve the biology. You know the functional treatment would let your tendon heal.  It would heal, but MIS create better environment, better mechanics for the tendon with minimized wound complication. Patients love it. They're happy with it.  The cons is that sero-nerve injury. Do it well by rotating your jig. If you use camera like the way I do it, I use camera, use a troll car to go inside the tendon sheath  and actually palpate the nerves. I can tell where the nerve is. So when I make portals, I can avoid the sero-nerve. And then be able to handle tendon lengthening.  Make it lengthen right in your first 10 cycles in the surgery, not to let it happen afterwards. Thank you.  Thanks, Pennant. Really appreciate it. Just a reminder to the group, you can put in your questions after our last speaker. I will throw the questions out to our panel and get them  answered. And finally, we have Mr. Johnny Owens. He's the CEO of Owens Recovery Science. He has  really pioneered this blood flow restriction therapy, which many professional and high-level  athletes have been using to get back into the game faster. He's the former Chief of Human  Performance and Optimization at the Center for the Intrepid. He's done a lot of work with our  veterans dealing with blast injuries. He manages over 40 clinical trials and has extensive publications in both sports and regenerative medicine, and we're really happy to have him.  Thanks, Mark. And thanks, you guys, for having me. It's an honor to be here. So, yeah. So, I'm going to talk about the rehab piece of this and why we think blood flow  restriction really might be kind of perfect for Achilles injuries and Achilles surgery.  Disclosures there. So, here's our rub and rehab. ACSM has a position stand that says, this is what you have to do if you want to increase muscle strength and muscle size.  And it says you have to put load on the muscles. So, 70% of a 1RM done for three to four months is what's necessary. You can look at Dr. O'Malley's like massive weight  set back there. He believes in this guideline, and so he's putting up some weight. And that's  what we're supposed to do if we want to make adaptive changes to muscle. And then rehab,  we kind of fly in the face of this guideline because we can't put load on because of their  injury or surgery. And there's no ACSM strength or hypertrophy guideline that says, if you can't  lift heavy, just lift light, it's going to be okay. So, even if we're allowing our folks to  do some plantar flexion early on post Achilles repair, they're probably not really meeting even  close to the physiological kind of parameters that we need. And I think all of us have seen  most folks, especially these weekend warriors, it just looks like they have a tibia instead of  a gastroc for a muscle after they had an Achilles repair even several years later. So, that's where in the DOD, we really started looking at blood flow restriction primarily for  our combat casualties, our amputees and our limb salvage, because they were very load intolerant.  So, what blood flow restriction is, is it's the application of a tourniquet on the proximal thigh  or the proximal arm. And what we do is we pump these tourniquets up, the systems we use  throughout the pro world, college world, and our trials, they have a built-in Doppler within them.  So, we pump it up to the patient's point where we get 100% of arterial occlusion. And once we  know what that arterial occlusion is, you back it off a little bit to allow a little bit of arterial  blood flow to go in. Right now, there's a lot of research where we're kind of looking at this as  well, like what's the best occlusion pressure that we should shut the artery down. It looks  like the minimum we need in the lower extremities, about 60% of arterial occlusion up to about 80%.  We're also kind of dabbling and looking at using 100% when you can't do really any load at all.  The upper extremity doesn't tolerate that as well. And we've seen strength and hypertrophy changes  happen actually in the upper extremity only at 50%. So, those are kind of the reductions that  we use. Whenever we're closing down the artery that much, we're completely blocking venous return.  And so, it doesn't take much to shut down the veins. And so, you're not really getting blood  flow going back to the heart. It's actually kind of a positive whenever we do that because when we  block the venous return, you limit stroke volume going back to the heart. And the cardiac output  equation is stroke volume times heart rate. If stroke volume goes down, heart rate goes up. So,  even when we got our athletes after Achilles, if they put the tourniquets on and just spin lightly  on a bike or walk on a treadmill, we've seen even in college basketball players and our elite  Air Force pararescuers, we've been able to increase VO2 max just from doing those kind of real basic  aerobic things. What happens whenever we block the blood going into the limb is you can lift at very  light loads. So, BFR is done at either no load, which kind of just slows down atrophy or where  it really kind of shines and starts to put on some strength and some hypertrophy is if you can do it  at a 20% to a 30% of a 1RM. And so, that's really like right in where rehab lives is this no low to  about 30% of a 1RM. And what happens basically is you do this first set. It's a high volume set.  So, you do 30 reps with the tourniquet on reducing the arterial blood flow. And that's a really easy  set because you still have oxygen all perfused within the muscle. And so, it feels like a light  load. But what that does is that really taps out the Krebs cycle and taps out the slow twitch  fibers. So, you get rid of slow twitch right off the bat. From a muscle physiology standpoint,  your body hates to use the fast twitch fibers because fast twitch fibers are reserved for really doing big mean things. Cavemen didn't lift weights for fun. And we're still in a  hunter-gatherer kind of evolution. And so, the more muscle you put on, the more that muscle  drives metabolism and forces you to use energy and have to search for more food. So, your body  really wants to make you earn it to put on the muscle. So, we force the slow twitch fibers,  which your body wants to use for that light load, to be done after that first set of 30. Then you  take a 30-second rest. We keep the tourniquets on so you don't reperfuse. And then the kind of magic  happens in these last three sets. So, we do three sets of 15. At this point, there's not enough  oxygen on board for the Krebs cycle to work. Your body has to switch over to using an anaerobic  pathway, which is your fast twitch fibers. And you start to force our patients to recruit fast  twitch fibers, which is beautiful because most of our patients in rehab never see their fast  twitch fibers even being touched, especially these first two to three months post-surgery,  post-Achilles repair. So, you do that. You get done with that final set of 15. You hope the muscle's  fatigued or gone to failure. If you take a muscle to failure, you kind of hit the anaerobic jackpot.  And that's where we see all the benefits from this. That whole 30, 15, 15, 15 with 30-second  rest with the tourniquet on is about a six-minute bout of ischemia with the exercise. And not only  can this be done, as I mentioned, with resistance exercise aerobically has really, it looks like a  lot of good potential. And I'm going to talk about maybe what's really good for the Achilles repairs  is this passive application where you're doing it on another part of the body, but it's helping  with the area that's immobilized to maybe slow down atrophy could be very powerful for this.  There's a lot of papers out there, surprisingly, that have looked at using blood flow restriction.  This is my bib list. I've got almost 1,700 papers that are specifically looked at using blood flow  restriction or some sort of hypoxia on a limb for muscle changes. In the DoD, when we were first  looking at this, we found a paper in 1937 in JAMA that had actually used this kind of technique with  peripheral arterial disease patients. There's been a lot of systematic reviews and meta-analysis  done, fortunately, so we don't have to go through all those papers. If I just put that into my  search list on my bib, there's been 32 systematic reviews and multiple meta-analyses as well.  The majority of systematic reviews on meta-analysis have been compared low-load to low-load with the  tourniquet on. And hands down, it's not even really debatable anymore. If you do low-load  with a tourniquet, it's going to beat low-load. This paper just came out on the end of last year,  though, which was really kind of interesting. And this is from Denmark, Per Argaard, who's kind of one of the leaders in just muscle physiology. They looked at comparing BFR to the  trials that compared it to lifting heavy. And whenever they ran the stats and looked at them,  there was no difference in strength gains between lifting heavy and doing low-load BFR when they  took all the good studies that had kind of done it in a well-done fashion. So their conclusion on  the basis of this meta-analysis, low-load BFR training and high-load strength training appear  equally effective in producing gains in maximum muscle strength in healthy adults, which is huge if we're talking about these people who cannot really load after an Achilles repair,  that they can maybe apply this and get similar benefits as lifting heavy. Also, the clinical  patients really shine. So this is a systematic review on meta-analysis that was in BMJ that  looked at all the BFR studies that compared doing it with a tourniquet on it, low-load versus  low-load for the clinical trials. So the ACL trials, NEOA, idiopathic myositis, etc. And every  study trended over to the BFR side. And so basically, if you look at those trials and you did the same exercises and just threw a tourniquet on the patients, they had about a 70%  better chance of getting stronger just by having that tourniquet applied. One of the main things  that we looked at in the DOD, and this is what's huge, I think, for Achilles repairs as well, is this thing called anabolic resistance. And basically, that is just what happens to  muscle whenever you go into disuse. So this is atrophy. And this is from some of the leaders  in the physiological space who have done these anabolic resistance trials. And basically, what  they've done is they've taken healthy individuals and they put them in a cast for two weeks with  their knee flexed, where they can't walk on their limb or use their limb for a two-week period to  see what happens to the muscle. Muscle either does protein synthesis, where it's synthesizing  protein to either rebuild or try and put muscle on, or it's going through muscle breakdown  throughout the day. And that kind of goes through this sinusoidal wave for a few hours throughout  the daily cycle. Whenever they looked at these individuals' limbs, the limb that was immobilized  during two weeks of disuse, the muscle protein synthesis on the limb not being used dropped about  30%. What that teased out to is when they looked at primarily, they were looking at the thighs in  this, but it was also the thigh and the gastroc. They lost about 350 grams of muscle tissue just  from being in that disuse from that muscle protein synthesis drop. I hate the metric system. I have  no idea what 350 grams is. So I looked up a surrogate. The human heart weighs about 300 grams.  So you can tell your patients just after they have the surgery and they're going to be in a  cam boot and then this period of disuse in two weeks, they're going to lose more than the size  of their heart and muscle in that limb. They also, when they looked at just quad strength in these  studies, you'd lose about 30% of your quad stream just from that, that drop in muscle mass and  muscle protein synthesis. So what we were looking for in the DOD, because our people were all in  this anabolic resistant state with some sort of way to get a muscle protein synthetic response  from exercise. There's no muscle protein synthesis pill. If you lift heavy, it does drive muscle  protein synthesis, but BFR consistently in studies that have looked at it, it looks like  it also drives muscle protein synthesis. So this is an older study in journal of applied physiology  done at UTMB Galveston that did leg extensions at 20% of a one rep max in individuals without a tourniquet. And it did not increase muscle protein synthesis at all. So if your  people come in and they do 30% or 20% of a one rep max, just exercises, mad exercises,  band exercises, you're not doing a thing to slow down the anabolic resistance or the atrophy that  they're seeing their Achilles. If they brought those people back and they did the same exercise  and they put the, put BFR on them, it drove muscle protein synthesis up by 46%. So again,  if these people are losing it by about 30%, just putting the tourniquet on in this low level  exercise, you've put them into a net positive. And it's not just for young, healthy individuals  at the same lab at UTMB. Chris Fry looked at this in older folks. And so 70 year old individuals,  they did the same study. And what they found is at that three hour time point that their muscle  protein synthesis in that limb was up 51%. That's huge for rehab. That's a big anabolic drive that  can help fight atrophy. That's with exercise. BFR with exercise is a no brainer. If you can get that  load, the 20 to 30%, you're going to be low load exercise. The problem that you guys have in the  foot and ankle world, and we have in rehab in this foot and ankle injuries is a lot of times  they're in a mobilization and in disuse. I agree with Dr. O'Malley. I never want to stretch out  one of these Achilles. I'm perfectly happy leaving the cam boot on and doing minimal things in the  lower leg. But is there a way that we can do thigh exercises and keep the thigh strength and size,  but also maybe spare the loss of muscle? And there's some studies that have looked at this and is really kind of fascinating. So this is what we call passive BFR. And so this is,  if you have people go into a disuse state and you put the tourniquets on and you don't do exercise  at all, is there a way that that could spare muscle and strength? And most of these have  been done in healthy models, but this one, they put people in a cast for two weeks. One group,  they just had the tourniquets inflated and deflated for five rounds. They didn't do any  exercise at all. The other group did nothing. And after two weeks, they reassessed their strength.  The control group and their quad lost almost 27%. The group that just put the tourniquets on only  lost 10%. The hamstrings three and a half percent in the BFR group versus 19% in the control group.  And if you look at this, this is probably the most fascinating one for our talk tonight. The  calf lost really nothing whenever they applied this to it. So it spared the loss of calf strength.  There's also been studies that have shown that they've spared the loss of calf size, not even  from doing the exercise. They were just immobilized and it was these repeated bouts  of the tourniquets on and off that seemed to have this protective effect. It's also been looked at  in an ACL model. So this one, after they got done with their ACL exercises from day three to two  weeks out, the one group just put the tourniquet on and inflated it for five minutes on and five  minutes off, no exercise, just put them in that hypoxic state. The other group didn't do that.  And whenever they looked at MRM gene on the thigh muscle, the group that put them in the  hypoxic state lost only about 9.4% of their quad size compared to about 20.7% in the control group.  And the overall loss of thigh size was only about 6% in the group that put the tourniquet on  versus about 14.5% in the control group. So that got a lot of people interested in what's the  mechanism. Is that hypoxic state driving muscle protein synthesis like we see in the other BFR  trials? And a study out of Denmark from Van Loon's lab showed that, no, when you do this passive BFR,  that muscle protein synthesis didn't go up. And then the end of last year, this study came out  that might've explored this and given us a little bit of a mechanism. So they put two groups into  cast immobilization for two weeks. They were non-weight bearing on crutches. The control group did nothing. The BFR group put the tourniquets on and just inflated and deflated.  It was a good study because they were able to get some biopsies, which were able to give us  some gene expression, as well as MRI. The group that was immobilized, that put the tourniquets  on and inflated them, spared the hamstring significantly. They didn't reach significance  on the quad, but it definitely trended that way. But the biopsy is what you really look at. And  if you look at just the sparing of the loss of fiber size in the quad, just by getting those tourniquets on those first two weeks of immobilization, it's pretty striking. So they  only lost about 6% of overall muscle fiber size if they were able to just put the BFR on,  versus almost loss of about 13% of fiber size. So this is this huge muscle dump. You see this  first two weeks when your patients come back versus this potential sparing of muscle. And simply all you had to do was get the tourniquet on them. They didn't have to add exercise.  From the gene expression standpoint, we were able to see that it's not muscle protein synthesis  that might be sparing the calf muscle for your Achilles patients. If you can get it on early,  it's the blocking of the catabolic pathways. And the one that was significant was this one  muscle ring finger one. So if you don't know what MRF1 is, as soon as you go into immobilization,  MRF1 is a catabolic gene and it tells your body to start dumping the muscle. It peaks at about  seven to 10 days. And it says, if we're not using this, get rid of it. So MRF1 is the thing that  starts telling muscle protein synthesis, stop happening, get rid of this muscle. For some  reason, we're not using it. We don't need it. If you put that tourniquet on, you got them in  hypoxia, the BFR significantly blunted that MRF1 catabolic protein almost down to baseline level.  So that might be this protective effect that we're seeing. Just kind of want to also throw out,  we're looking at a lot of other things from gene expression and there's an interesting paper that  just came out of maybe why we're seeing some responders versus non-responders and the capillary beds play a role in this. So this was Chris Fry again. And what they did is they took  elderly people and have them do 12 weeks of heavy exercises. And when they went back and looked at  it, basically the group that had more capillary beds within their limb made changes in muscle.  The group that had low capillary beds within their limb made no changes in muscle at all. And so basically what they said is we need to look at, you need a baseline capillarization,  especially if you're older, also with these injured people. If you rupture your Achilles,  you go into disuse, you go into atrophy, you lose this capillarization within the limb and that we  need to do something to get this capillarization up to give our people a fighting chance, even if  they lift heavy. You see these people like, I'm trying, I'm trying, I've been trying to lift  weights. My calf isn't getting stronger. It's not getting bigger. It might be they just don't have  the capillarization there to even make these adaptive changes. And so standing on the shoulders  of giants here in 2019, the Nobel prize in physiology was given to these three gentlemen  who showed that with hypoxia around cells, you can really make adaptive changes in gene expression.  And one of the main things that they really showed was this thing called HIF1A. So if you  take a limb from a normal oxygen state down to a low oxygen state, hypoxia inducible factor 1A  comes out of the bone and it does a million like amazing things. But one of the things it really  does is it drives what's called VEGF, vascular endothelial growth factor. And if VEGF goes up,  you build up angiogenesis and you build capillary beds. And over and over in BFR studies, when you  look at VEGF, if you do it, it goes up. And so if you can get our, your people on BFR, you might,  in this first few two to four weeks, get their capillarization up, get that baseline ability  for them to put some muscle on. And just a study that looked at this, this is just four weeks of  doing calf presses with or without tourniquets on in elderly folks. The strength was significantly  better in the elderly folks, as long as they use the tourniquet for their low load calf presses,  but also when they looked at capillarization after just a month of it, they significantly  improved capillarization only in the BFR group. So in summary, what we think right now is if you  can get BFR on early, even while they're immobilized, they can be doing BFR exercises on their thigh. That passive hypoxic event will be benefiting the calf muscle and hopefully  slowing down that catabolic pathway. Then when they're able to actually put on some low loads,  that's whenever you start to really see this increase in strength and hypertrophy that we, we hope can start to restore them back to baseline. And this hypoxia might also even  promote some gene expression, such as angiogenesis. We're also looking at things like  improving muscle stem cell, the satellite cells, as well as slowing down some things like myostatin  that block the body from putting muscle on. Just to kind of put the landscape out here,  we're trying to put our money where our mouth is. These are just some of the clinical BFR trials  that we're involved with or tracking. ACL is really the big one. We have more ACL trials  than we can shake a stick at right now, but we have a lot of DOD funding. And I'll just kind of  throw a plug out. Dr. Dracos has the Achilles repair trial going on. We're seeing this done  a ton in the pros colleges in the clinical setting. And we really think that this is something that  could use maybe even a multi-center. So I would love to look at DOD funding next year and going  after this in a bigger way. Thanks. Oh, thanks, Johnny. That was outstanding. And certainly,  you've made a believer out of me, and we continue to appreciate the work that you've done. And  other studies coming out to show the best way to use this in our post-operative patients.  We're getting a little short on time. Some of the questions were answered in the Q&A box.  If you have any questions, go to the panel. You can send them to me. My email is dracosm at hss.edu. Again, that's D-R-A-K-O-S-M at hss.edu. And some of the other questions,  we'll answer in the Q&A box. But I just want to thank everybody here for participating.  And everybody, have a nice night. Thanks. Thank you.

Video Summary

The video is a recording of a webinar titled "Management of Acute Achilles Ruptures in the Athlete." The webinar is part of the 2021 Foot and Ankle Focus Series hosted by AOFAS (American Orthopedic Foot and Ankle Society). The moderator is Dr. Mark C. Dracos, and the panel includes Dr. Finit Fistiga, Dr. Martin J. O'Malley, and Johnny Owens, MPT. The panel discusses various aspects of managing acute Achilles ruptures in athletes, including surgical techniques, rehabilitation strategies, and the use of blood flow restriction therapy. They also address common challenges, such as preventing stretching of the tendon and minimizing complications like wound infections. The panelists draw on their own experiences and research findings to provide insights and recommendations for treating acute Achilles ruptures in athletes. The webinar is supported by funding from the Orthopedic Foot and Ankle Foundation, with a grant from Arthrex, Inc. The webinar is recorded and will be available for on-demand viewing on the Physician's Resource Center website of AOFAS.

Asset Subtitle

Moderator: Mark C. Drakos, MD
Faculty: Phinit Phisitkul, MD; Martin J. O'Malley, MD; Johnny Owens, MPT

Description
This interactive discussion takes a close look at the treatment and rehabilitation of acute Achilles ruptures in athletes. Our expert faculty will examine minimally invasive management of acute Achilles tears, management of acute Achilles tears in the elite athlete, and rehabilitation of Achilles injuries using blood flow resistance training.

Course Objectives
At the conclusion of this webinar, you will be able to:

Understand state-of-the-art practices when treating high-demand athletes with acute Achilles ruptures
Investigate more minimally invasive approaches to Achilles injuries and how this may expedite recovery
Recognize the potential advantages of early physical therapy and advanced rehabilitation to reduce atrophy with respect to Achilles injuries

Keywords

Acute Achilles Ruptures

Athlete

Webinar

Surgical techniques

Rehabilitation strategies

Blood flow restriction therapy

Preventing stretching

Wound infections

Insights

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