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Achilles Tendon Ruptures Kenneth J. Hunt, Adam M. Budny and Nicola Maffulli Foot Ankle Spec 2014 7: 199 DOI: 10.1177/1938640014533478 The online version of this article can be found at: http://fas.sagepub.com/content/7/3/199
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〈 Roundtable Discussion 〉 Achilles Tendon Ruptures Acute Ruptures It has been said that an acute rupture of the tendon occurs more commonly in the “weekend” athlete whereby the 40to 50-year-old patient engages in a pick-up basketball game or other endeavor. Yet empirically this does not seem to be the case.
Etiology and Demographics
What is your perception of the demographics in terms of gender, age, and preinjury conditioning level? How do you explain the occurrence of Achilles ruptures in highlevel professional athletes? Budny: Through didactic education and postgraduate training, the “text book” demographics are, as noted, an overweight middle age male “weekend warrior” with an explosive start or stop resulting in an Achilles rupture. I would say that although a substantial number of the patients I have treated for Achilles ruptures fall into this group, a significant minority are not, and I have repaired ruptures in teenagers as well as octogenarians. The “preinjury” conditioning level does not seem to play a significant role in the occurrence of a complete rupture. It has been my experience that a supraphysiologic loading (be it a fall, abrupt start/stop, excessive dorsiflexion, etc) will be the
mechanism leading to the rupture. Athletes are constantly exposed to these loading forces on the tendon, opening the possibility for a traumatic rupture. Given the demands placed on athletes from a physiologic standpoint, their musculoskeletal system, no matter how well trained, will experience loads that ultimately lead to failure. Any avid spectator will be able to recall a catastrophic injury experienced during an event by a star athlete. I find it no surprise that the background incidence of Achilles ruptures is occasionally punctuated by a higher-level athlete incurring this injury.
The Achilles tendon is frequently the subject of the chief complaint when patients present for foot and ankle problems. Problems range from acute ruptures, neglected ruptures, and intratendinous degeneration to insertional calcifications. Yet there is a very wide variety of opinions regarding treatment for all these problems. This symposium will explore some of the controversial and dichotomous philosophies regarding the Achilles tendon.
Hunt: While classic teaching suggests that the most common age group suffering Achilles tendon ruptures is the late 30s to early 50s, I see a number of these injuries occur in running athletes in their 20s and even late teens. The prevalence in contact athletes seems to begin increasing about age 27. This is consistent with publications on NFL injury data and our experience in professional athletes. Achilles ruptures in collegiate football players is very rare, but we see them not uncommonly in gymnasts and jumping athletes. Maffuli: I suspect that this changes from country to country. In the United Kingdom, the most widely practiced sport is soccer, and in physically active individuals, the injury occurs most frequently in soccer players. However, squash and badminton account for a
CONTRIBUTORS Kenneth J. Hunt, MD Department of Orthopaedic Surgery, Stanford University Stanford, CA Adam M. Budny, DPM, FACFAS Blair Orthopedics, 300 Fairway Drive, Altoona, PA 16602 Nicola Maffulli, MD, MS, PhD, FRCP, FRCS(Orth), FFSEM Queen Mary University of London, Centre for Sports and Exercise Medicine, Mile End Hospital, London, UK SECTION EDITOR John M. Schuberth, DPM Chief, Foot and Ankle Surgery, Department of Orthopaedic Surgery, Kaiser Foundation Hospital, San Francisco, CA
DOI: 10.1177/1938640014533478. For reprints and permissions queries, please visit SAGE’s Web site at http://www.sagepub.com/journalsPermissions.nav. Copyright © 2014 The Author(s)
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large number of such patients, probably because some people use them to become fit and do not realize that you have to be fit to play them. Males suffer this injury more often than ladies, but it appears that females are catching up. Schuberth: I have often wondered where this notion of weekend athlete originated insofar that the demographics of patients that have Achilles ruptures are quite diverse. I have seen these injuries from age 16 to 85 with variable degrees of conditioning. Interestingly, an exceedingly low percentage of any of these patients report any prodromal symptoms. We have been taught to caution patients with any Achilles tendonitis about the potential for rupture; yet I cannot recall any patient who presented with a history of preexisting “tendonitis.” Furthermore, none of the patients with nodular enlargement of the tendon have ever progressed to a formal rupture. We really need to differentiate the nature of the intratendinous disease process. In my mind, the inflammatory process generated by overuse and like situations is different from the attritional, degenerative process that is endemic to Achilles tendon rupture.
It is commonly accepted that normal tendons do not rupture. What do you think is the primary intrinsic anatomic “defect” that lends to failure of the Achilles tendon? Budny: In as much as the first scenario questions the “text book” description about patient demographics regarding Achilles ruptures, I do not believe that there is one defect that leads to a failure; but rather, many events must happen in concert. Ground reactive forces, axial load on the tendon from the triceps surae, as well as position of the foot, ankle, and knee all play a part in a rupture. Strain on the tendon during jumping or explosive movements can create several hundreds to thousands of Newtons of force and, when combined with any of the other factors noted, can
lead to a catastrophic failure. Ultimately, I feel that the forces on the tendon combined with a dorsiflexed position of the foot/ankle (and a knee in extension) are likely the most important factors contributing to an Achilles rupture. Collectively, these factors create a “perfect storm,” whereby a tendon that is in a compromised anatomic position is exposed to an extreme force, leading to failure. Anatomically, the Achilles also has an intrinsic rotation created through embryonic development, which may theoretically contribute to increased strain in a supinated position. Hunt: It is probably true that normal tendons do not rupture. However, most patients who suffer ruptures do not have prodromal pain. My teleological assumption is that an injury occurs to the tendon (whether a microtear from a hard fall or hard impact, or from repetitive microtrauma), and repeated use of the tendon weakens this portion of the tendon. This lowers the threshold for failure of the tendon, such that the immense load exerted by the gastrocsoleus, which would ordinarily be accommodated, results in failure of the tissue and rupture of the tendon. Tendon healing simply cannot keep up. This is why ruptures typically occur in the vascular watershed region of the tendon rather than the wellvascularized insertion or musculotendinous junction. Maffuli: Actually, this is only partially true. A histopathologically normal tendon can rupture if the forces exerted on it are high enough. In real life, though, such forces should be so high that they are exceedingly rare. When examining the histopathology and gene expression of these ruptured tendons, we have consistently identified a failed healing response and disordered gene expression of the proteins of the extracellular matrix. The staggering finding is that these changes are not limited to the site of rupture but extend essentially along the whole tendon, even the areas which are macroscopically intact.
Schuberth: I believe it is a combination of an anatomic defect and some sort of occult intratendinous insult, where the limited blood supply (watershed area) is incapable of repair that would otherwise occur. I have always thought that there was a role of the transverse fascial band that courses over the Achilles tendon in the genesis of the so-called watershed area.1 It would seem that this fascial band would compress the tendon and essentially dampen the blood supply. Whether or not this has an intimate role is clinically undetectable in a prospective fashion. Since it has been reported that this band is almost ubiquitous,1 there is probably some genetic contribution as well to the local intratendinous blood supply.
Do you think that there are any preinjury “warning signs” for the patient who sustained an Achilles rupture? If you believe that these warnings exist, what, if anything, do you do to prevent the ultimate rupture? Budny: Unfortunately, most traumatic ruptures are very unexpected, and if there is a prodrome set of symptoms, they are often not reported until after the injury. I do, however, often see patients who have an acute tendonitis or chronic tendinosis as their presenting complaint. The treatment for these of course is very distinct. And as long they are as treated appropriately, the ultimate rupture may be prevented. In an acute scenario, I will restrict the patient from activity and protect the tendon with temporary immobilization with activity modification (rest) and NSAIDs (nonsteroidal anti-inflammatory drugs), either per orum or a topical such as voltaren gel. As the acute inflammatory process resolves, I will begin to resume strengthening but avoid high-impact explosive activities until all symptoms are resolved. In a more chronic scenario of tendinosis, the acute inflammation is resolved (from a physiologic/histologic
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perspective), and the tendon injury has stagnated in the proliferative phase of healing. I will be more aggressive with a home exercise program or formal physical therapy (PT), focusing on eccentric training. This eccentric loading adds strain to the collagen fibrils, which then become aligned with the direction of the long axis of the tendon. By organizing the collagen, a stronger tendon unit is created, which also avoids the significant thickening and disorganized collagen noted histologically with long-term immobilization and scar formation. Although there is conflicting evidence regarding the merits of the eccentric programs, it has worked well in my experience. In certain circumstances, I will perform an autologous platelet injection to stimulate the tendon and create an acute injury to “jump start” the tendon healing process. There is still debate in the literature regarding the use of platelet rich plasma (PRP) for tendon pathology, but I have used it with success as an adjunct therapy. It allows introduction of a supraphysiologic concentration of platelets and, thus, the intrinsic cytokines and growth factors important for healing an injury. When a patient has exhausted all other options and hopes to avoid surgical intervention, I feel it is of benefit to at least have the discussion with a patient about the utility of this technology. Hunt: In my experience, most patients who rupture do not have prodromal symptoms. However, when these warning signs are recognized, I recommend longer periods of stretching and warm-up prior to activities, postexercise stretching, and use of heel lifts, and if the discomfort is severe (or if thickening of the tendon has occurred), consider an MRI to assess for degenerative changes of the tendon substance. Maffuli: Some patients identify a “twinge,” but this is only in retrospect and is not that common, after all. Schuberth: As noted previously, I do not believe that there are prodromal
symptoms. Even if patients did report them, I am not inclined to do anything about them other than have a discussion with the patient. Of course patients want to know what they can do to limit the chance of rupture, and I tell them that I simply do not know. Although it is common practice, I am not convinced that stretching and other preconditioning activities have any effect. On occasion, I have obtained an MRI but have difficulty correlating the level of intratendinous signal change with a cogent recommendation.
Other observations show that patients rarely sustain bilateral ruptures even at different stages of their lives. How does one explain this phenomenon? Does this conflict with the theory of genetic predisposition? Budny: From an epidemiologic standpoint, this is similar to trying to explain why a patient may only traumatically fracture one ankle in a lifetime. Creating the exact same biomechanical and physiological loads to the contralateral limb to cause such an injury is certainly unusual. There are of course multiple factors that can predispose a patient to bilateral rupture, including but not limited to age, activity level, obesity, other chronic inflammatory diseases, steroid use, exposure to fluoroquinolones, and so on. Hunt: This has been my experience as well. Perhaps it is that activity levels, prehabilitation, and workout routines necessarily change as a result of Achilles rupture and subsequent rehabilitation. Perhaps it is more likely to occur on the dominant leg (ie, more jumping, landing, push-off) than the nondominant leg. Maffuli: Some of us are just predisposed to injuries. We have recently shown that even top athletes have genetic predisposition to developing injuries. It may well be that the rate of developing the failed healing response at the basis of the pathology runs a different course
in the 2 limbs, but eventually it does catch up with you! Schuberth: This is clearly my experience, and in the handful of patients I have treated with bilateral Achilles ruptures, I am unable to detect any reason other than “chance.” One particular patient ruptured both Achilles tendons and both quadriceps tendons, but none of the other 4 had any other history of other ruptures or myofascial disease processes. Certainly, it makes us question the role of a genetic mediated intratendinous defect.
Treatment Philosophy
The treatment of Achilles tendon ruptures is extremely variable, from the fundamental treatment scheme to the ultimate return to activity. In general, in your practice, do you favor operative or nonoperative treatment for the acute rupture? Budny: In general I prefer operative repair for Achilles ruptures. I have developed a consistent surgical approach with good results with minimal surgical time and an aggressive rehab program. My decision making is based on the patient’s preinjury health and fitness levels and what goals they would like to attain postinjury. Hunt: I favor operative treatment for young, active patients who wish to continue participation in athletic activities. For more sedentary individuals, I discuss the risks and benefits of each treatment option and find the best treatment for them. For elderly individuals, I favor conservative treatment. Maffuli: I undertake minimally invasive Achilles tendon repair, using a percutaneous technique that we described more than 10 years ago, under local anesthesia. In general, this is the preferred approach, and most of my patients chose this management option. I am prepared to manage patients
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conservatively, but I have not undertaken an open procedure for an acute rupture for the past 14 years. Schuberth: Over the past 5 years, I have migrated to a nonoperative approach, mostly out of empirical observation that patients seem to do just as well in the long run. Although I do understand the “security” of operative repair, I believe that careful management of the nonoperative rupture is just as effective both in the short and long term. Admittedly, I used to immobilize nonoperative cases longer than operative repairs but now have gained confidence in earlier weight-protected weight bearing.
How would you manage a 23-year-old professional athlete with an acute rupture? How about an obese 48-year-old sedentary factory worker? How about a 74-year-old obese patient with chronic advanced COPD (chronic obstructive pulmonary disease)? Budny: For the first 2 patients in this scenario, I would prefer an open repair. My typical protocol is an open repair approximately 5 to 7 days after the injury (this allows for a Jones wrap and splint application to mitigate any edema). I perform an end-to-end repair, followed by 2 weeks of non–weight bearing in a gravity equinus splint, followed by protected mobilization in a boot, as will be described in further detail later. For both these patients, I think a reasonable goal is resuming their preinjury level of activity without limitation. For the last scenario, I would imagine the long-term goals are much lower and a residual weakness is not going to affect quality of life. In a risk-benefit analysis with the patient, we (the patient and surgeon) would need to decide if an acute repair is indeed going to change, in any significant manner, the way he or she functions from day to day. If there is no improvement to be gained, I would immobilize rather than repair. It is likely
that a person with these preexisting comorbidities would have difficulties even with ADLs (activities of daily living), and the potential risk of DVT (deep vein thrombosis), PE (pulmonary embolism), wound complications, and so on would outweigh any benefit that might be gained.
will significantly increase the risk of infection, wound healing complications, and so on, I will be inclined to treat conservatively. In regard to the follow-up care—I usually increase the frequency of wound check and postoperative appointments for those with increased risk factors.
Hunt: For the 23-year-old professional athlete: open repair; for the factory worker: would discuss risks and benefits of each and leave the option to the patient but would favor open repair; for the 74-year-old patient with COPD: nonoperative.
Hunt: I generally discuss the higher risk of wound complications and delayed healing. I leave the sutures in longer and delay weight bearing in at-risk patients.
Maffuli: For 23- or 48-year-old patients, I undertake minimally invasive Achilles tendon repair, as mentioned above. In 74-year-old patients, movement is even more important. Hence, more of the same. Schuberth: Although I do not take care of any professional athletes, I probably would recommend operative repair in such an instance. This is driven primarily by the expectation of the medical community and most likely the patient. There is a lot of pressure to return these athletes to competition earlier than otherwise and operative repair would probably facilitate that. However, the key distinguishing difference is the capacity to start rehabilitation earlier and load the tendon to the high demands that are usually required to compete. In the other 2 patient scenarios, I would strongly favor nonoperative management.
Do you change your protocol when patients have comorbidities such as diabetes, history of active smoking, or steroid dependence? Budny: I would not say my protocol changes more than my follow-up care and preoperative consult with the patient. Again, I would have a detailed discussion with him or her about the risks/benefits of surgery. If we come to a consensus that the patient does not have that much function to regain postrepair or that his or her particular comorbidity
Maffuli: In these patients, healing is disrupted, and they need even more a method of management that ensures that the tendon stumps are together. We have shown that diabetic patients and older patients can be safely managed by percutaneous techniques, under local anesthesia, with excellent results. Schuberth: I would be even more persistent with nonoperative options as well as slowing the progression to full unprotected weight bearing.
Does your strategy change when the rupture seems to be more proximal than midsubstance? Budny: I do not believe that it changes my surgical approach; however, I will generally be a little more aggressive postoperatively with rehabilitation the more proximal the tendon injury is. The closer to the musculotendinous juncture, the better the vascular supply, and the more confident I am in the potential for healing. If it is a tear near or at the level of the myotendinous aponeurosis, I will likely treat conservatively with a functional rehabilitation program after the acute pain is resolved. Hunt: For MSK junction tears, I am more likely to favor non–up treatment. If it is still within the tendon substance, there is really no change in my approach or repair, just a more proximal incision and extreme caution to identify and protect the sural nerve. Maffuli: If the rupture is more toward the musculotendinous junction, I am
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prepared to manage the patient conservatively. However, there is a recent tendency to operate on elite athletes with this specific location of the tear. In these instances, I use an open approach. Schuberth: In the days when I operated on the overwhelming majority of Achilles ruptures, I was surprised by the high incidence of a more proximal rupture than expected. Perhaps it is not necessarily more proximal, but rather, there is a more distal extension of the soleal muscle fibers, almost to the point of rupture. Nonetheless, this leaves less robust tissue to anchor the sutures proximally. Now, with the availability of high-strength suture materials, the weakest point of repair is the suturetissue interface. The frequency of these so-called proximal ruptures was one of the prompts to gravitate toward nonoperative care.
Surgical Strategies
Please discuss your surgical treatment plan for a midsubstance tear, including the incisional approach (posterior, medial, minimally invasive), choice, and configuration of suture (Bunnel, Kessler, etc). Budny: My surgical approach is very consistent and reproducible and generally takes under 30 minutes. I perform the procedure under general anesthesia, with a regional popliteal block, in the prone position. My incision is posterior, slightly medial to midline with a midline peritenon incision. I use a #2 fiberwire in a Krakow fashion for end-to-end repair, usually placing the foot in a slight “gravity eqinus” position for the final repair. The regional block helps significantly with postoperative pain and reduces the need for narcotic use. Hunt: I do an open repair through a 4-cm longitudinal incision just medial to midline, centered at the Achilles rupture. The location is confirmed preoperatively
with MSK ultrasound to identify both ends of the rupture. I use a 4 strand modified Krackow technique. Maffuli: I use a percutaneous technique involving a total of 7 stab wounds. We described it in Knee Surg Sports Traumatol Arthrosc, 2008;16:199-203, and reported the biomechanical characteristics of this repair in Knee Surg Sports Traumatol Arthrosc, 2012;20:13921397. Have a look: you will love it! Schuberth: The patient is placed in the prone position under general or spinal anesthesia. Although we place a tourniquet, it is seldom necessary. The incisional approach is just medial to the midline and is linear. I usually wait 7 to 10 days to allow the tissues to settle down as I think that the paratendinous tissues are easier to reflect and preserve for reapproximation. I use a single-strand fiberwire (or equivalent) Kessler technique and try to secure the tendon with an amount of tension such that the position of the foot is equivalent to the uninjured side. I do not drape the other side but memorialize its position in my mind prior to surgery. I am intrigued by these absorbable high-strength sutures because many patients complain about the knot.
Recent meta-analyses have indicated that in the long term, there is little difference between operative and nonoperative treatment. Do you believe that this is true in the short term (first 3 months after injury) versus the long term (6-12 months after injury). What about the rerupture rate and the capacity to mobilize the ankle sooner? Budny: I have read with interest the literature in question. There has been a significant amount of comparison to the treatments in question and a good bit of material is available for review. Most of this evidence shows that the rerupture rates are rather comparable when a functional
rehabilitation program is followed. Of course, complications specifically associated with surgery are present only in the surgical subset of patients, such as wound problems, infections, and so on. Mobilizing a patient quickly when treating nonoperatively is paramount to the improved outcomes noted, and this also requires close monitoring in PT as well as having access to a functional ankle foot orthosis (AFO). In a medicolegal sense, there are some limitations to this geographically; first, the “standard of care” in the area I practice is for operative intervention for acute ruptures in a healthy population. There is a difference in the European literature, where socialized medicine may drive treatment protocols. Second, having near immediate access to a custom-molded AFO to allow protected weightbearing (WB) can also be a challenge for patients with no insurance or specific policy limitations regarding covered durable medical equipment (DME) (from a strictly financial perspective). Finally, beginning a program of functional rehabilitation requires a concerted “team” effort involving the patient, physician, and physical therapist. If the patient is not willing or cannot afford the PT encounters and, thus, does not attend or is not compliant, outcomes will be adversely affected. Often, a patient will have to travel many miles to attend a PT appointment, and not all therapists are equal in their quality or attention to detail. These factors will limit the choice of physical therapists I would refer to, perhaps making the trip to PT impossible or unreasonable for the patient if an acceptable physical therapist is remote from their home or place of employment. Ultimately, in regard to the short-term follow-up, my experience has been that those who are treated operatively have a much more rapid convalescence and their functional outcomes demonstrate better strength and ambulation. I generally mobilize my operatively repaired Achilles within 2 weeks, which helps the patients not only functionally but also from a psychosomatic perspective; they are already making progress, and this helps significantly in their motivation. In the longer term, function is more equal in
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both groups, but the toll on the patient is notable with significant loss of wages (if employed preinjury) or delay in return to sporting activity associated with nonoperative management.
low complication rate and results in a rapid return to activity.
Hunt: In my experience, surgical treatment is functionally superior in the short term and has a much lower rate of rerupture. It is important to recognize that nonoperative treatment still requires treatment (ie, initial immobilization in plantar flexion, functional rehabilitation, etc).
Maffuli: The costs of percutaneous repair are initially higher than the conservative approach, but it should be remembered that conservatively managed patients will need active mobilization under supervision, and by the end of treatment, the costs are comparable. If an open operative approach is pursued, though, there is no doubt that the costs are higher.
Hunt: I do not use these devices. They are associated with a higher complication rate, without evidence of superior outcomes compared to open repair.
Schuberth: I do believe that as more surgeons are pressured to reduce costs, particularly in a closed system, there is a trend. It would be interesting to look at global reimbursement for nonoperative versus operative repairs on a large scale and see if this has any impact on treatment philosophies. No one wants to talk about this, but I believe that in the past, the low complication rate of operative treatment and most likely a higher reimbursement rate fueled the higher incidence of operative care. The European literature favors more functional treatments, and some would argue that it is driven by remuneration. Admittedly, I do worry more about rerupture in the nonoperative patient, but it is fueled by my gradually waning insecurity.
Schuberth: In my mind, they are completely unnecessary and solve a problem that does not exist. I am amazed at the number of these fancy devices now being peddled by industry and the “lecture circuit.”
Maffuli: It should be remembered that a randomized trial is very much an idealized experiment. I am a believer in evidencebased medicine and am ready to change my practice according to the results of well-planned, well-executed, appropriately powered trials that use clinically relevant outcome measures. Real life is different, though. We have shown that although the rate of healing and rerupture is likely comparable between conservative and operative approaches, in reality, patients who were managed conservatively were less likely to return to sport and had less confidence in their limb. I tell the patients what is what, and I leave it to them to decide. The vast majority will choose the percutaneous repair. Schuberth: This is an intriguing subject to say the least. However, as noted previously, I believed that nonoperative ruptures deserved more conservative physiologic progression. Yet with increasing confidence and “pushing” my personal comfort level, I do not believe this to be true after 3 to 4 weeks. If I treat the patient nonoperatively, I immobilize the foot in maximal equinus for 3 weeks and then reexamine the patient. I was surprised by the palpable integrity of the tendon. At this point, I use identical protocols regarding progression to full weight bearing, range of motion, and rehabilitation.
In this era of “cost-containment” have you seen a trend toward more nonoperative approaches? Budny: I have not, and I have found that with sound surgical techniques and brief operating time, the surgery has a
Hunt: I have not yet seen this trend in the western United States.
What do you feel is the place for expensive devices that purportedly make it easier and more reliable to fix the Achilles tendon in a minimally invasive way in the acute injury? Budny: I do not use them nor do I feel they are necessary. Using delicate technique when handling the peritenon and retracting with suture tags limits the soft-tissue injury, and I have not found it necessary to use any auxiliary instrumentation to minimize the incision. Having the tendon exposed also allows complete visualization and primary end-to-end repair. I have also not encountered a reason to dissect the
subcutaneous tissue so far laterally that the sural nerve is at risk. The incision is medial to midline, and little to no soft-tissue dissection is performed outside the peritenon.
Maffuli: There is no evidence that these work or are any better than good old-fashioned surgery in the hands of good surgeons who know their anatomy and their stuff!
Please describe your postoperative (or postinjury if you favor nonoperative care) protocol, including immobilization, time for full weight bearing, and PT specifics. Budny: My postoperative protocol is very basic and is as follows: •• 2 weeks non weight bearing (NWB) in gravity equinus splint to allow swelling to resolve; •• 4 weeks in hinged WB boot with range of motion (ROM) allowing plantarflexion only (no dorsiflexion) and allowing the boot to be removed for PT and eccentric only contracture of the posterior muscle group; •• 4 weeks in a protective brace such as an AchilloTrain; continue PT for strengthening and ROM; no athletic activity, but may begin stationary bike or elliptical machine (no explosive plymetric activity) for cardio; •• begin light jogging and intensify strengthening at 3 months. At any point, I may utilize a graduated compression stocking for management of postoperative edema. This can be
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augmented by the use of cryotherapy (ie, GameReady). Hunt: I immobilize in a splint in resting plantarflexion postoperatively for 2 weeks. I have the patient begin protected weight bearing at 2 weeks in a boot with several heel lifts. I begin limited AAROM at 2 weeks postoperatively (not beyond neutral dorsiflexion with the knee at 90° flexion). Heel lifts get peeled away gradually, and full weight bearing is allowed at 6 weeks. Maffuli: I immobilize the patients with the ankle in full equines in a well-padded below-knee synthetic cast, leaving the metatarsal heads free. I allow them to weight bear on the metatarsal heads as able with crutches from the time they leave my operating theater. I encourage active mobilization of the toes. At 2 weeks, the cast is removed, and a removable boot with 5 wedges is applied. One wedge is removed every other week, and the patients are allowed to weight bear as able, even without crutches. Patients undertake physiotherapy under supervision, avoiding dorsiflexion of the ankle. The boot is removed at 8 weeks from the operation, and the real fun then starts. Schuberth: I always examine the patient with regard to the integrity of the tendon. If I am satisfied with the integrity of the tendon, my protocols are nearly identical. For the nonoperative patient, I immobilize as noted for 3 weeks, followed by serial reduction of equinus in 2 weeks. At 5 weeks postinjury, the patient is usually able to get to neutral dorsiflexion with confidence, and I place them in a weight-bearing cast. At approximately 7 weeks postinjury, I place the patient in a removable boot and start active and passive range of motion. I release the patient to organized PT at approximately 8 weeks, with specific limitations to eccentric load; I direct the physical therapists to “go slow.”
How involved or directive do you get in the PT regimen? Do you have a set protocol? Budny: I have a set protocol that is outlined above.
Hunt: I use a set protocol to direct PT and the home exercise regimen. I generally recommend formal PT to follow, direct, and monitor progression. Maffuli: I do.
Chronic Neglected Ruptures/Reruptures In most cases of a late presentation of an Achilles tendon rupture, the patient did not seek care at the time of the original insult. There is often significant disability and an inability to walk on uneven ground or steps. Most often surgical repair is indicated to restore function.
What is your preferred surgical approach? Please elaborate and include details such as the use of flexor hallucis longus (FHL) transfer, gastrocnemius slide or turndown, end-toend shortening or synthetic/ allograft interposition. Budny: For a neglected rupture, I will consent for many “possible” procedures. I inform the patient and his or her family that this is a salvage-type procedure, through which we are hoping to improve strength and mobility, but it is likely the patient will not return to the prerupture level of strength or activity. I will consent for him or her to have open repair of the Achilles with possible FHL transfer and gastrocnemius recession. I may use a graft or turndown if there is significant loss of length. I will base this decision on preoperative MRI findings as well as intraoperative appearance of the tendon. I use an interference screw technique for the FHL transfer, which I have found provides excellent strength. The FHL transfer with an interference screw has a number of advantages in and of itself. First of all is the ease of access to the musculotendinous unit of the FHL, which is directly anterior to the intermuscular septum after the
Achilles has been dissected free. Again with attention to the details of dissection, the neurovascular bundle can be safely retracted, and there is limited morbidity associated with this procedure. I have also not found it necessary to use a 2-incision approach to the harvesting of the FHL when utilizing the interference screw technique because there is adequate tendon for transfer if the foot and hallux are plantarflexed prior to transection. Postoperatively, there is little to no deficit in the function of the hallux because of redundant intrinsic musculature as well as the flexor digitorum longus through the master knot of Henry. In addition, transferring the FHL with an interference screw allows near anatomic approximation of the insertion of the tendon. I usually attempt to achieve “dead man’s angle” to provide maximal resistance to pull out of the transferred tendon. Close approximation of the FHL muscle belly to the Achilles via this transfer is also important in providing a vascular bed for healing of the repair. Depending on the chronicity of the rupture, the FHL may already be significantly hypertrophied, providing even more strength to the repair. I will usually perform the FHL transfer first to establish a “foundation” for the remainder of the reconstruction, and I will attempt to place the foot in a gravity equinus position equal to the contralateral limb. This will then set the stage, so to speak, for the other procedures. Depending on the residual gap, I will perform a gastrocnemius recession to gain length from the Achilles or perform a turndown at this time to lay over the FHL muscle belly. If the tissue is not adequate at this time, I will use a collagen scaffold or allograft to cover the remaining defect. Hunt: The approach is based on the size of the gap: if 50 years of age. Maffuli: I use minimally invasive techniques, with either a free semitendinosus tendon transfer (Am J Sports Med. 2013;41:1100-1107) or a peroneus brevis transfer (Am J Sports Med. 2010;38:2304-2312). I do not routinely undertake any of the procedures mentioned (FHL transfer, gastrocnemius slide or turndown, end-to-end shortening or synthetic/ allograft interposition), and I believe that the use of synthetic material is to be proscribed. Schuberth: First, I try to determine the size of the deficit. MRI is helpful but not entirely accurate insofar that there is usually some interposed scar tissue. Intraoperatively, I try to be conservative with the degree of debridement of the tendon ends. Once I am satisfied that the tendon ends are “viable,” I determine the method of gap negotiation. In some instances, I am able to do an “end-to-end” repair, using the suture to impart tension to the proximal pole. Sometimes, gradual stretching over a few minutes will give more length. I believe that restoration of the resting length of the muscle fibers is the ultimate key to outcome, and yet we only have empirical observation and experience to guide the tension of the repair. Accordingly, I have tried most of the published turndown techniques in order to reduce the gap when end-to-end approximation is not possible. I do believe that although most of them are suitable to reduce the gap, there is some weakness that otherwise may not be present. However, most recently, I have used an Achilles allograft to fill in the residual gap with satisfactory results. I have never used the FHL transfer, appreciating that this is widely accepted throughout the foot and ankle world with very credible publications regarding the efficacy. A success in my mind is the capacity for the patient to do a single-limb heel rise.
How do you manage the patient with a rerupture after the initial period of immobilization? Is nonoperative care an option? Do you obtain an MRI to help guide treatment or assess the degree of disruption? Budny: Fortunately, acute rerupture is a rarely reported complication in the literature, even more infrequent than rerupture in a delayed setting. This has been reflected in my own experience as well. I will obtain an MRI to evaluate the integrity of the initial repair and to determine if there is possible compromise at a secondary location. Interpretation of this MRI can be difficult due not only to the presence of the most recent tissue trauma but also the surgical trauma and index injury. Hunt: I will get an MRI or ultrasound to assess. If there is no real gap and/or intact fibers, I will treat nonoperatively. If there is a gap (ie, complete disruption), I will revise the repair surgically and immobilize for a longer period of time. Maffuli: I use the same regimen described for acute ruptures.
What is your surgical approach in the patient who sustains a rerupture? Do you feel that some delay is warranted to allow for some healing of the second injury before proceeding with surgery? Budny: I would treat a second injury similar to an initial rupture. I will delay operative intervention for 5 to 7 days, during which time he or she would remain non–weight bearing in a Jones compression wrap and posterior splint to allow edema reduction. To minimize potential further devascularization of the skin, I would use the same incision line. Hunt: I use the same incision, extended slightly. I will use a 4-strand Krackow
repair and a longer period of immobilization and non–weight bearing in these patients to ensure complete healing. Maffuli: I treat them as if they have a chronic tear and use the same minimally invasive techniques with tendon transfer described above. I feel that if the repaired tendon has failed, it needs new biologically sound material to work optimally. A tendon transfer will allow me to do that. Schuberth: I generally like to wait 6 to 8 weeks after the rerupture of the acute rupture. In other words, if the acute rupture occurred in the prior 3 months, I wait because it allows the tissue to reorganize and makes the delayed repair easier. If the patient presents with a neglected rupture (with no prior treatment) older than 3 months, I operate whenever convenient for the patient. Short of a dorsiflexion stop brace, I do not see much of a role for nonoperative treatment in the acute rerupture. A brace does serve some patients well in the chronic neglected rupture, yet there are the expected limitations of function.
Compared to an otherwise uncomplicated course of treatment after an acute rupture, how much additional functional deficit is present after treatment of the rerupture? Budny: Functional deficit after a secondary rupture will usually result in a significant calf atrophy of the leg with a notable weakness. Usual clinical findings are asymmetry in the appearance of the posterior muscle group and significant difficulty when asked to perform a single heel rise. Return to high-level activity or a sport is nearly impossible. There is usually a small amount of soft-tissue “creep” and resultant lengthening of the Achilles even after a primary repair (as noted in previous literature/radiographic studies), which I think contributes significantly to the mechanical weakness of the triceps postinjury. After a secondary injury, this is
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magnified, and it is imperative to maintain physiologic tension on the repair when it is performed. Often, it is also a challenge to manage the inevitable scarring associated with prior intervention, adhesions, and vascular compromise of the surrounding soft-tissue envelope and patient expectations.
same in terms of function in these cases.
Hunt: It takes patients a bit longer to full recovery, but the end result is the
Schuberth: I think that the end point is generally the same but takes longer
Maffuli: I tell my patients that they will have to accept that they will lose some 20% to 30% of the strength of the gastrocsoleus. However, several of them do end up pleasantly surprising me!
to achieve. The calf atrophy seems to be a little worse with nonoperative care.
Reference 1. Saxena A, Bareither D. Magnetic resonance and cadaveric findings of the “watershed band” of the Achilles tendon. J Foot Ankle Surg. 2001;40:132-136.
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Achilles Tendon Ruptures Kenneth J. Hunt, Adam M. Budny and Nicola Maffulli Foot Ankle Spec 2014 7: 199 DOI: 10.1177/1938640014533478 The online version of this article can be found at: http://fas.sagepub.com/content/7/3/199
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〈 Roundtable Discussion 〉 Achilles Tendon Ruptures Acute Ruptures It has been said that an acute rupture of the tendon occurs more commonly in the “weekend” athlete whereby the 40to 50-year-old patient engages in a pick-up basketball game or other endeavor. Yet empirically this does not seem to be the case.
Etiology and Demographics
What is your perception of the demographics in terms of gender, age, and preinjury conditioning level? How do you explain the occurrence of Achilles ruptures in highlevel professional athletes? Budny: Through didactic education and postgraduate training, the “text book” demographics are, as noted, an overweight middle age male “weekend warrior” with an explosive start or stop resulting in an Achilles rupture. I would say that although a substantial number of the patients I have treated for Achilles ruptures fall into this group, a significant minority are not, and I have repaired ruptures in teenagers as well as octogenarians. The “preinjury” conditioning level does not seem to play a significant role in the occurrence of a complete rupture. It has been my experience that a supraphysiologic loading (be it a fall, abrupt start/stop, excessive dorsiflexion, etc) will be the
mechanism leading to the rupture. Athletes are constantly exposed to these loading forces on the tendon, opening the possibility for a traumatic rupture. Given the demands placed on athletes from a physiologic standpoint, their musculoskeletal system, no matter how well trained, will experience loads that ultimately lead to failure. Any avid spectator will be able to recall a catastrophic injury experienced during an event by a star athlete. I find it no surprise that the background incidence of Achilles ruptures is occasionally punctuated by a higher-level athlete incurring this injury.
The Achilles tendon is frequently the subject of the chief complaint when patients present for foot and ankle problems. Problems range from acute ruptures, neglected ruptures, and intratendinous degeneration to insertional calcifications. Yet there is a very wide variety of opinions regarding treatment for all these problems. This symposium will explore some of the controversial and dichotomous philosophies regarding the Achilles tendon.
Hunt: While classic teaching suggests that the most common age group suffering Achilles tendon ruptures is the late 30s to early 50s, I see a number of these injuries occur in running athletes in their 20s and even late teens. The prevalence in contact athletes seems to begin increasing about age 27. This is consistent with publications on NFL injury data and our experience in professional athletes. Achilles ruptures in collegiate football players is very rare, but we see them not uncommonly in gymnasts and jumping athletes. Maffuli: I suspect that this changes from country to country. In the United Kingdom, the most widely practiced sport is soccer, and in physically active individuals, the injury occurs most frequently in soccer players. However, squash and badminton account for a
CONTRIBUTORS Kenneth J. Hunt, MD Department of Orthopaedic Surgery, Stanford University Stanford, CA Adam M. Budny, DPM, FACFAS Blair Orthopedics, 300 Fairway Drive, Altoona, PA 16602 Nicola Maffulli, MD, MS, PhD, FRCP, FRCS(Orth), FFSEM Queen Mary University of London, Centre for Sports and Exercise Medicine, Mile End Hospital, London, UK SECTION EDITOR John M. Schuberth, DPM Chief, Foot and Ankle Surgery, Department of Orthopaedic Surgery, Kaiser Foundation Hospital, San Francisco, CA
DOI: 10.1177/1938640014533478. For reprints and permissions queries, please visit SAGE’s Web site at http://www.sagepub.com/journalsPermissions.nav. Copyright © 2014 The Author(s)
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large number of such patients, probably because some people use them to become fit and do not realize that you have to be fit to play them. Males suffer this injury more often than ladies, but it appears that females are catching up. Schuberth: I have often wondered where this notion of weekend athlete originated insofar that the demographics of patients that have Achilles ruptures are quite diverse. I have seen these injuries from age 16 to 85 with variable degrees of conditioning. Interestingly, an exceedingly low percentage of any of these patients report any prodromal symptoms. We have been taught to caution patients with any Achilles tendonitis about the potential for rupture; yet I cannot recall any patient who presented with a history of preexisting “tendonitis.” Furthermore, none of the patients with nodular enlargement of the tendon have ever progressed to a formal rupture. We really need to differentiate the nature of the intratendinous disease process. In my mind, the inflammatory process generated by overuse and like situations is different from the attritional, degenerative process that is endemic to Achilles tendon rupture.
It is commonly accepted that normal tendons do not rupture. What do you think is the primary intrinsic anatomic “defect” that lends to failure of the Achilles tendon? Budny: In as much as the first scenario questions the “text book” description about patient demographics regarding Achilles ruptures, I do not believe that there is one defect that leads to a failure; but rather, many events must happen in concert. Ground reactive forces, axial load on the tendon from the triceps surae, as well as position of the foot, ankle, and knee all play a part in a rupture. Strain on the tendon during jumping or explosive movements can create several hundreds to thousands of Newtons of force and, when combined with any of the other factors noted, can
lead to a catastrophic failure. Ultimately, I feel that the forces on the tendon combined with a dorsiflexed position of the foot/ankle (and a knee in extension) are likely the most important factors contributing to an Achilles rupture. Collectively, these factors create a “perfect storm,” whereby a tendon that is in a compromised anatomic position is exposed to an extreme force, leading to failure. Anatomically, the Achilles also has an intrinsic rotation created through embryonic development, which may theoretically contribute to increased strain in a supinated position. Hunt: It is probably true that normal tendons do not rupture. However, most patients who suffer ruptures do not have prodromal pain. My teleological assumption is that an injury occurs to the tendon (whether a microtear from a hard fall or hard impact, or from repetitive microtrauma), and repeated use of the tendon weakens this portion of the tendon. This lowers the threshold for failure of the tendon, such that the immense load exerted by the gastrocsoleus, which would ordinarily be accommodated, results in failure of the tissue and rupture of the tendon. Tendon healing simply cannot keep up. This is why ruptures typically occur in the vascular watershed region of the tendon rather than the wellvascularized insertion or musculotendinous junction. Maffuli: Actually, this is only partially true. A histopathologically normal tendon can rupture if the forces exerted on it are high enough. In real life, though, such forces should be so high that they are exceedingly rare. When examining the histopathology and gene expression of these ruptured tendons, we have consistently identified a failed healing response and disordered gene expression of the proteins of the extracellular matrix. The staggering finding is that these changes are not limited to the site of rupture but extend essentially along the whole tendon, even the areas which are macroscopically intact.
Schuberth: I believe it is a combination of an anatomic defect and some sort of occult intratendinous insult, where the limited blood supply (watershed area) is incapable of repair that would otherwise occur. I have always thought that there was a role of the transverse fascial band that courses over the Achilles tendon in the genesis of the so-called watershed area.1 It would seem that this fascial band would compress the tendon and essentially dampen the blood supply. Whether or not this has an intimate role is clinically undetectable in a prospective fashion. Since it has been reported that this band is almost ubiquitous,1 there is probably some genetic contribution as well to the local intratendinous blood supply.
Do you think that there are any preinjury “warning signs” for the patient who sustained an Achilles rupture? If you believe that these warnings exist, what, if anything, do you do to prevent the ultimate rupture? Budny: Unfortunately, most traumatic ruptures are very unexpected, and if there is a prodrome set of symptoms, they are often not reported until after the injury. I do, however, often see patients who have an acute tendonitis or chronic tendinosis as their presenting complaint. The treatment for these of course is very distinct. And as long they are as treated appropriately, the ultimate rupture may be prevented. In an acute scenario, I will restrict the patient from activity and protect the tendon with temporary immobilization with activity modification (rest) and NSAIDs (nonsteroidal anti-inflammatory drugs), either per orum or a topical such as voltaren gel. As the acute inflammatory process resolves, I will begin to resume strengthening but avoid high-impact explosive activities until all symptoms are resolved. In a more chronic scenario of tendinosis, the acute inflammation is resolved (from a physiologic/histologic
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perspective), and the tendon injury has stagnated in the proliferative phase of healing. I will be more aggressive with a home exercise program or formal physical therapy (PT), focusing on eccentric training. This eccentric loading adds strain to the collagen fibrils, which then become aligned with the direction of the long axis of the tendon. By organizing the collagen, a stronger tendon unit is created, which also avoids the significant thickening and disorganized collagen noted histologically with long-term immobilization and scar formation. Although there is conflicting evidence regarding the merits of the eccentric programs, it has worked well in my experience. In certain circumstances, I will perform an autologous platelet injection to stimulate the tendon and create an acute injury to “jump start” the tendon healing process. There is still debate in the literature regarding the use of platelet rich plasma (PRP) for tendon pathology, but I have used it with success as an adjunct therapy. It allows introduction of a supraphysiologic concentration of platelets and, thus, the intrinsic cytokines and growth factors important for healing an injury. When a patient has exhausted all other options and hopes to avoid surgical intervention, I feel it is of benefit to at least have the discussion with a patient about the utility of this technology. Hunt: In my experience, most patients who rupture do not have prodromal symptoms. However, when these warning signs are recognized, I recommend longer periods of stretching and warm-up prior to activities, postexercise stretching, and use of heel lifts, and if the discomfort is severe (or if thickening of the tendon has occurred), consider an MRI to assess for degenerative changes of the tendon substance. Maffuli: Some patients identify a “twinge,” but this is only in retrospect and is not that common, after all. Schuberth: As noted previously, I do not believe that there are prodromal
symptoms. Even if patients did report them, I am not inclined to do anything about them other than have a discussion with the patient. Of course patients want to know what they can do to limit the chance of rupture, and I tell them that I simply do not know. Although it is common practice, I am not convinced that stretching and other preconditioning activities have any effect. On occasion, I have obtained an MRI but have difficulty correlating the level of intratendinous signal change with a cogent recommendation.
Other observations show that patients rarely sustain bilateral ruptures even at different stages of their lives. How does one explain this phenomenon? Does this conflict with the theory of genetic predisposition? Budny: From an epidemiologic standpoint, this is similar to trying to explain why a patient may only traumatically fracture one ankle in a lifetime. Creating the exact same biomechanical and physiological loads to the contralateral limb to cause such an injury is certainly unusual. There are of course multiple factors that can predispose a patient to bilateral rupture, including but not limited to age, activity level, obesity, other chronic inflammatory diseases, steroid use, exposure to fluoroquinolones, and so on. Hunt: This has been my experience as well. Perhaps it is that activity levels, prehabilitation, and workout routines necessarily change as a result of Achilles rupture and subsequent rehabilitation. Perhaps it is more likely to occur on the dominant leg (ie, more jumping, landing, push-off) than the nondominant leg. Maffuli: Some of us are just predisposed to injuries. We have recently shown that even top athletes have genetic predisposition to developing injuries. It may well be that the rate of developing the failed healing response at the basis of the pathology runs a different course
in the 2 limbs, but eventually it does catch up with you! Schuberth: This is clearly my experience, and in the handful of patients I have treated with bilateral Achilles ruptures, I am unable to detect any reason other than “chance.” One particular patient ruptured both Achilles tendons and both quadriceps tendons, but none of the other 4 had any other history of other ruptures or myofascial disease processes. Certainly, it makes us question the role of a genetic mediated intratendinous defect.
Treatment Philosophy
The treatment of Achilles tendon ruptures is extremely variable, from the fundamental treatment scheme to the ultimate return to activity. In general, in your practice, do you favor operative or nonoperative treatment for the acute rupture? Budny: In general I prefer operative repair for Achilles ruptures. I have developed a consistent surgical approach with good results with minimal surgical time and an aggressive rehab program. My decision making is based on the patient’s preinjury health and fitness levels and what goals they would like to attain postinjury. Hunt: I favor operative treatment for young, active patients who wish to continue participation in athletic activities. For more sedentary individuals, I discuss the risks and benefits of each treatment option and find the best treatment for them. For elderly individuals, I favor conservative treatment. Maffuli: I undertake minimally invasive Achilles tendon repair, using a percutaneous technique that we described more than 10 years ago, under local anesthesia. In general, this is the preferred approach, and most of my patients chose this management option. I am prepared to manage patients
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conservatively, but I have not undertaken an open procedure for an acute rupture for the past 14 years. Schuberth: Over the past 5 years, I have migrated to a nonoperative approach, mostly out of empirical observation that patients seem to do just as well in the long run. Although I do understand the “security” of operative repair, I believe that careful management of the nonoperative rupture is just as effective both in the short and long term. Admittedly, I used to immobilize nonoperative cases longer than operative repairs but now have gained confidence in earlier weight-protected weight bearing.
How would you manage a 23-year-old professional athlete with an acute rupture? How about an obese 48-year-old sedentary factory worker? How about a 74-year-old obese patient with chronic advanced COPD (chronic obstructive pulmonary disease)? Budny: For the first 2 patients in this scenario, I would prefer an open repair. My typical protocol is an open repair approximately 5 to 7 days after the injury (this allows for a Jones wrap and splint application to mitigate any edema). I perform an end-to-end repair, followed by 2 weeks of non–weight bearing in a gravity equinus splint, followed by protected mobilization in a boot, as will be described in further detail later. For both these patients, I think a reasonable goal is resuming their preinjury level of activity without limitation. For the last scenario, I would imagine the long-term goals are much lower and a residual weakness is not going to affect quality of life. In a risk-benefit analysis with the patient, we (the patient and surgeon) would need to decide if an acute repair is indeed going to change, in any significant manner, the way he or she functions from day to day. If there is no improvement to be gained, I would immobilize rather than repair. It is likely
that a person with these preexisting comorbidities would have difficulties even with ADLs (activities of daily living), and the potential risk of DVT (deep vein thrombosis), PE (pulmonary embolism), wound complications, and so on would outweigh any benefit that might be gained.
will significantly increase the risk of infection, wound healing complications, and so on, I will be inclined to treat conservatively. In regard to the follow-up care—I usually increase the frequency of wound check and postoperative appointments for those with increased risk factors.
Hunt: For the 23-year-old professional athlete: open repair; for the factory worker: would discuss risks and benefits of each and leave the option to the patient but would favor open repair; for the 74-year-old patient with COPD: nonoperative.
Hunt: I generally discuss the higher risk of wound complications and delayed healing. I leave the sutures in longer and delay weight bearing in at-risk patients.
Maffuli: For 23- or 48-year-old patients, I undertake minimally invasive Achilles tendon repair, as mentioned above. In 74-year-old patients, movement is even more important. Hence, more of the same. Schuberth: Although I do not take care of any professional athletes, I probably would recommend operative repair in such an instance. This is driven primarily by the expectation of the medical community and most likely the patient. There is a lot of pressure to return these athletes to competition earlier than otherwise and operative repair would probably facilitate that. However, the key distinguishing difference is the capacity to start rehabilitation earlier and load the tendon to the high demands that are usually required to compete. In the other 2 patient scenarios, I would strongly favor nonoperative management.
Do you change your protocol when patients have comorbidities such as diabetes, history of active smoking, or steroid dependence? Budny: I would not say my protocol changes more than my follow-up care and preoperative consult with the patient. Again, I would have a detailed discussion with him or her about the risks/benefits of surgery. If we come to a consensus that the patient does not have that much function to regain postrepair or that his or her particular comorbidity
Maffuli: In these patients, healing is disrupted, and they need even more a method of management that ensures that the tendon stumps are together. We have shown that diabetic patients and older patients can be safely managed by percutaneous techniques, under local anesthesia, with excellent results. Schuberth: I would be even more persistent with nonoperative options as well as slowing the progression to full unprotected weight bearing.
Does your strategy change when the rupture seems to be more proximal than midsubstance? Budny: I do not believe that it changes my surgical approach; however, I will generally be a little more aggressive postoperatively with rehabilitation the more proximal the tendon injury is. The closer to the musculotendinous juncture, the better the vascular supply, and the more confident I am in the potential for healing. If it is a tear near or at the level of the myotendinous aponeurosis, I will likely treat conservatively with a functional rehabilitation program after the acute pain is resolved. Hunt: For MSK junction tears, I am more likely to favor non–up treatment. If it is still within the tendon substance, there is really no change in my approach or repair, just a more proximal incision and extreme caution to identify and protect the sural nerve. Maffuli: If the rupture is more toward the musculotendinous junction, I am
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prepared to manage the patient conservatively. However, there is a recent tendency to operate on elite athletes with this specific location of the tear. In these instances, I use an open approach. Schuberth: In the days when I operated on the overwhelming majority of Achilles ruptures, I was surprised by the high incidence of a more proximal rupture than expected. Perhaps it is not necessarily more proximal, but rather, there is a more distal extension of the soleal muscle fibers, almost to the point of rupture. Nonetheless, this leaves less robust tissue to anchor the sutures proximally. Now, with the availability of high-strength suture materials, the weakest point of repair is the suturetissue interface. The frequency of these so-called proximal ruptures was one of the prompts to gravitate toward nonoperative care.
Surgical Strategies
Please discuss your surgical treatment plan for a midsubstance tear, including the incisional approach (posterior, medial, minimally invasive), choice, and configuration of suture (Bunnel, Kessler, etc). Budny: My surgical approach is very consistent and reproducible and generally takes under 30 minutes. I perform the procedure under general anesthesia, with a regional popliteal block, in the prone position. My incision is posterior, slightly medial to midline with a midline peritenon incision. I use a #2 fiberwire in a Krakow fashion for end-to-end repair, usually placing the foot in a slight “gravity eqinus” position for the final repair. The regional block helps significantly with postoperative pain and reduces the need for narcotic use. Hunt: I do an open repair through a 4-cm longitudinal incision just medial to midline, centered at the Achilles rupture. The location is confirmed preoperatively
with MSK ultrasound to identify both ends of the rupture. I use a 4 strand modified Krackow technique. Maffuli: I use a percutaneous technique involving a total of 7 stab wounds. We described it in Knee Surg Sports Traumatol Arthrosc, 2008;16:199-203, and reported the biomechanical characteristics of this repair in Knee Surg Sports Traumatol Arthrosc, 2012;20:13921397. Have a look: you will love it! Schuberth: The patient is placed in the prone position under general or spinal anesthesia. Although we place a tourniquet, it is seldom necessary. The incisional approach is just medial to the midline and is linear. I usually wait 7 to 10 days to allow the tissues to settle down as I think that the paratendinous tissues are easier to reflect and preserve for reapproximation. I use a single-strand fiberwire (or equivalent) Kessler technique and try to secure the tendon with an amount of tension such that the position of the foot is equivalent to the uninjured side. I do not drape the other side but memorialize its position in my mind prior to surgery. I am intrigued by these absorbable high-strength sutures because many patients complain about the knot.
Recent meta-analyses have indicated that in the long term, there is little difference between operative and nonoperative treatment. Do you believe that this is true in the short term (first 3 months after injury) versus the long term (6-12 months after injury). What about the rerupture rate and the capacity to mobilize the ankle sooner? Budny: I have read with interest the literature in question. There has been a significant amount of comparison to the treatments in question and a good bit of material is available for review. Most of this evidence shows that the rerupture rates are rather comparable when a functional
rehabilitation program is followed. Of course, complications specifically associated with surgery are present only in the surgical subset of patients, such as wound problems, infections, and so on. Mobilizing a patient quickly when treating nonoperatively is paramount to the improved outcomes noted, and this also requires close monitoring in PT as well as having access to a functional ankle foot orthosis (AFO). In a medicolegal sense, there are some limitations to this geographically; first, the “standard of care” in the area I practice is for operative intervention for acute ruptures in a healthy population. There is a difference in the European literature, where socialized medicine may drive treatment protocols. Second, having near immediate access to a custom-molded AFO to allow protected weightbearing (WB) can also be a challenge for patients with no insurance or specific policy limitations regarding covered durable medical equipment (DME) (from a strictly financial perspective). Finally, beginning a program of functional rehabilitation requires a concerted “team” effort involving the patient, physician, and physical therapist. If the patient is not willing or cannot afford the PT encounters and, thus, does not attend or is not compliant, outcomes will be adversely affected. Often, a patient will have to travel many miles to attend a PT appointment, and not all therapists are equal in their quality or attention to detail. These factors will limit the choice of physical therapists I would refer to, perhaps making the trip to PT impossible or unreasonable for the patient if an acceptable physical therapist is remote from their home or place of employment. Ultimately, in regard to the short-term follow-up, my experience has been that those who are treated operatively have a much more rapid convalescence and their functional outcomes demonstrate better strength and ambulation. I generally mobilize my operatively repaired Achilles within 2 weeks, which helps the patients not only functionally but also from a psychosomatic perspective; they are already making progress, and this helps significantly in their motivation. In the longer term, function is more equal in
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both groups, but the toll on the patient is notable with significant loss of wages (if employed preinjury) or delay in return to sporting activity associated with nonoperative management.
low complication rate and results in a rapid return to activity.
Hunt: In my experience, surgical treatment is functionally superior in the short term and has a much lower rate of rerupture. It is important to recognize that nonoperative treatment still requires treatment (ie, initial immobilization in plantar flexion, functional rehabilitation, etc).
Maffuli: The costs of percutaneous repair are initially higher than the conservative approach, but it should be remembered that conservatively managed patients will need active mobilization under supervision, and by the end of treatment, the costs are comparable. If an open operative approach is pursued, though, there is no doubt that the costs are higher.
Hunt: I do not use these devices. They are associated with a higher complication rate, without evidence of superior outcomes compared to open repair.
Schuberth: I do believe that as more surgeons are pressured to reduce costs, particularly in a closed system, there is a trend. It would be interesting to look at global reimbursement for nonoperative versus operative repairs on a large scale and see if this has any impact on treatment philosophies. No one wants to talk about this, but I believe that in the past, the low complication rate of operative treatment and most likely a higher reimbursement rate fueled the higher incidence of operative care. The European literature favors more functional treatments, and some would argue that it is driven by remuneration. Admittedly, I do worry more about rerupture in the nonoperative patient, but it is fueled by my gradually waning insecurity.
Schuberth: In my mind, they are completely unnecessary and solve a problem that does not exist. I am amazed at the number of these fancy devices now being peddled by industry and the “lecture circuit.”
Maffuli: It should be remembered that a randomized trial is very much an idealized experiment. I am a believer in evidencebased medicine and am ready to change my practice according to the results of well-planned, well-executed, appropriately powered trials that use clinically relevant outcome measures. Real life is different, though. We have shown that although the rate of healing and rerupture is likely comparable between conservative and operative approaches, in reality, patients who were managed conservatively were less likely to return to sport and had less confidence in their limb. I tell the patients what is what, and I leave it to them to decide. The vast majority will choose the percutaneous repair. Schuberth: This is an intriguing subject to say the least. However, as noted previously, I believed that nonoperative ruptures deserved more conservative physiologic progression. Yet with increasing confidence and “pushing” my personal comfort level, I do not believe this to be true after 3 to 4 weeks. If I treat the patient nonoperatively, I immobilize the foot in maximal equinus for 3 weeks and then reexamine the patient. I was surprised by the palpable integrity of the tendon. At this point, I use identical protocols regarding progression to full weight bearing, range of motion, and rehabilitation.
In this era of “cost-containment” have you seen a trend toward more nonoperative approaches? Budny: I have not, and I have found that with sound surgical techniques and brief operating time, the surgery has a
Hunt: I have not yet seen this trend in the western United States.
What do you feel is the place for expensive devices that purportedly make it easier and more reliable to fix the Achilles tendon in a minimally invasive way in the acute injury? Budny: I do not use them nor do I feel they are necessary. Using delicate technique when handling the peritenon and retracting with suture tags limits the soft-tissue injury, and I have not found it necessary to use any auxiliary instrumentation to minimize the incision. Having the tendon exposed also allows complete visualization and primary end-to-end repair. I have also not encountered a reason to dissect the
subcutaneous tissue so far laterally that the sural nerve is at risk. The incision is medial to midline, and little to no soft-tissue dissection is performed outside the peritenon.
Maffuli: There is no evidence that these work or are any better than good old-fashioned surgery in the hands of good surgeons who know their anatomy and their stuff!
Please describe your postoperative (or postinjury if you favor nonoperative care) protocol, including immobilization, time for full weight bearing, and PT specifics. Budny: My postoperative protocol is very basic and is as follows: •• 2 weeks non weight bearing (NWB) in gravity equinus splint to allow swelling to resolve; •• 4 weeks in hinged WB boot with range of motion (ROM) allowing plantarflexion only (no dorsiflexion) and allowing the boot to be removed for PT and eccentric only contracture of the posterior muscle group; •• 4 weeks in a protective brace such as an AchilloTrain; continue PT for strengthening and ROM; no athletic activity, but may begin stationary bike or elliptical machine (no explosive plymetric activity) for cardio; •• begin light jogging and intensify strengthening at 3 months. At any point, I may utilize a graduated compression stocking for management of postoperative edema. This can be
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augmented by the use of cryotherapy (ie, GameReady). Hunt: I immobilize in a splint in resting plantarflexion postoperatively for 2 weeks. I have the patient begin protected weight bearing at 2 weeks in a boot with several heel lifts. I begin limited AAROM at 2 weeks postoperatively (not beyond neutral dorsiflexion with the knee at 90° flexion). Heel lifts get peeled away gradually, and full weight bearing is allowed at 6 weeks. Maffuli: I immobilize the patients with the ankle in full equines in a well-padded below-knee synthetic cast, leaving the metatarsal heads free. I allow them to weight bear on the metatarsal heads as able with crutches from the time they leave my operating theater. I encourage active mobilization of the toes. At 2 weeks, the cast is removed, and a removable boot with 5 wedges is applied. One wedge is removed every other week, and the patients are allowed to weight bear as able, even without crutches. Patients undertake physiotherapy under supervision, avoiding dorsiflexion of the ankle. The boot is removed at 8 weeks from the operation, and the real fun then starts. Schuberth: I always examine the patient with regard to the integrity of the tendon. If I am satisfied with the integrity of the tendon, my protocols are nearly identical. For the nonoperative patient, I immobilize as noted for 3 weeks, followed by serial reduction of equinus in 2 weeks. At 5 weeks postinjury, the patient is usually able to get to neutral dorsiflexion with confidence, and I place them in a weight-bearing cast. At approximately 7 weeks postinjury, I place the patient in a removable boot and start active and passive range of motion. I release the patient to organized PT at approximately 8 weeks, with specific limitations to eccentric load; I direct the physical therapists to “go slow.”
How involved or directive do you get in the PT regimen? Do you have a set protocol? Budny: I have a set protocol that is outlined above.
Hunt: I use a set protocol to direct PT and the home exercise regimen. I generally recommend formal PT to follow, direct, and monitor progression. Maffuli: I do.
Chronic Neglected Ruptures/Reruptures In most cases of a late presentation of an Achilles tendon rupture, the patient did not seek care at the time of the original insult. There is often significant disability and an inability to walk on uneven ground or steps. Most often surgical repair is indicated to restore function.
What is your preferred surgical approach? Please elaborate and include details such as the use of flexor hallucis longus (FHL) transfer, gastrocnemius slide or turndown, end-toend shortening or synthetic/ allograft interposition. Budny: For a neglected rupture, I will consent for many “possible” procedures. I inform the patient and his or her family that this is a salvage-type procedure, through which we are hoping to improve strength and mobility, but it is likely the patient will not return to the prerupture level of strength or activity. I will consent for him or her to have open repair of the Achilles with possible FHL transfer and gastrocnemius recession. I may use a graft or turndown if there is significant loss of length. I will base this decision on preoperative MRI findings as well as intraoperative appearance of the tendon. I use an interference screw technique for the FHL transfer, which I have found provides excellent strength. The FHL transfer with an interference screw has a number of advantages in and of itself. First of all is the ease of access to the musculotendinous unit of the FHL, which is directly anterior to the intermuscular septum after the
Achilles has been dissected free. Again with attention to the details of dissection, the neurovascular bundle can be safely retracted, and there is limited morbidity associated with this procedure. I have also not found it necessary to use a 2-incision approach to the harvesting of the FHL when utilizing the interference screw technique because there is adequate tendon for transfer if the foot and hallux are plantarflexed prior to transection. Postoperatively, there is little to no deficit in the function of the hallux because of redundant intrinsic musculature as well as the flexor digitorum longus through the master knot of Henry. In addition, transferring the FHL with an interference screw allows near anatomic approximation of the insertion of the tendon. I usually attempt to achieve “dead man’s angle” to provide maximal resistance to pull out of the transferred tendon. Close approximation of the FHL muscle belly to the Achilles via this transfer is also important in providing a vascular bed for healing of the repair. Depending on the chronicity of the rupture, the FHL may already be significantly hypertrophied, providing even more strength to the repair. I will usually perform the FHL transfer first to establish a “foundation” for the remainder of the reconstruction, and I will attempt to place the foot in a gravity equinus position equal to the contralateral limb. This will then set the stage, so to speak, for the other procedures. Depending on the residual gap, I will perform a gastrocnemius recession to gain length from the Achilles or perform a turndown at this time to lay over the FHL muscle belly. If the tissue is not adequate at this time, I will use a collagen scaffold or allograft to cover the remaining defect. Hunt: The approach is based on the size of the gap: if 50 years of age. Maffuli: I use minimally invasive techniques, with either a free semitendinosus tendon transfer (Am J Sports Med. 2013;41:1100-1107) or a peroneus brevis transfer (Am J Sports Med. 2010;38:2304-2312). I do not routinely undertake any of the procedures mentioned (FHL transfer, gastrocnemius slide or turndown, end-to-end shortening or synthetic/ allograft interposition), and I believe that the use of synthetic material is to be proscribed. Schuberth: First, I try to determine the size of the deficit. MRI is helpful but not entirely accurate insofar that there is usually some interposed scar tissue. Intraoperatively, I try to be conservative with the degree of debridement of the tendon ends. Once I am satisfied that the tendon ends are “viable,” I determine the method of gap negotiation. In some instances, I am able to do an “end-to-end” repair, using the suture to impart tension to the proximal pole. Sometimes, gradual stretching over a few minutes will give more length. I believe that restoration of the resting length of the muscle fibers is the ultimate key to outcome, and yet we only have empirical observation and experience to guide the tension of the repair. Accordingly, I have tried most of the published turndown techniques in order to reduce the gap when end-to-end approximation is not possible. I do believe that although most of them are suitable to reduce the gap, there is some weakness that otherwise may not be present. However, most recently, I have used an Achilles allograft to fill in the residual gap with satisfactory results. I have never used the FHL transfer, appreciating that this is widely accepted throughout the foot and ankle world with very credible publications regarding the efficacy. A success in my mind is the capacity for the patient to do a single-limb heel rise.
How do you manage the patient with a rerupture after the initial period of immobilization? Is nonoperative care an option? Do you obtain an MRI to help guide treatment or assess the degree of disruption? Budny: Fortunately, acute rerupture is a rarely reported complication in the literature, even more infrequent than rerupture in a delayed setting. This has been reflected in my own experience as well. I will obtain an MRI to evaluate the integrity of the initial repair and to determine if there is possible compromise at a secondary location. Interpretation of this MRI can be difficult due not only to the presence of the most recent tissue trauma but also the surgical trauma and index injury. Hunt: I will get an MRI or ultrasound to assess. If there is no real gap and/or intact fibers, I will treat nonoperatively. If there is a gap (ie, complete disruption), I will revise the repair surgically and immobilize for a longer period of time. Maffuli: I use the same regimen described for acute ruptures.
What is your surgical approach in the patient who sustains a rerupture? Do you feel that some delay is warranted to allow for some healing of the second injury before proceeding with surgery? Budny: I would treat a second injury similar to an initial rupture. I will delay operative intervention for 5 to 7 days, during which time he or she would remain non–weight bearing in a Jones compression wrap and posterior splint to allow edema reduction. To minimize potential further devascularization of the skin, I would use the same incision line. Hunt: I use the same incision, extended slightly. I will use a 4-strand Krackow
repair and a longer period of immobilization and non–weight bearing in these patients to ensure complete healing. Maffuli: I treat them as if they have a chronic tear and use the same minimally invasive techniques with tendon transfer described above. I feel that if the repaired tendon has failed, it needs new biologically sound material to work optimally. A tendon transfer will allow me to do that. Schuberth: I generally like to wait 6 to 8 weeks after the rerupture of the acute rupture. In other words, if the acute rupture occurred in the prior 3 months, I wait because it allows the tissue to reorganize and makes the delayed repair easier. If the patient presents with a neglected rupture (with no prior treatment) older than 3 months, I operate whenever convenient for the patient. Short of a dorsiflexion stop brace, I do not see much of a role for nonoperative treatment in the acute rerupture. A brace does serve some patients well in the chronic neglected rupture, yet there are the expected limitations of function.
Compared to an otherwise uncomplicated course of treatment after an acute rupture, how much additional functional deficit is present after treatment of the rerupture? Budny: Functional deficit after a secondary rupture will usually result in a significant calf atrophy of the leg with a notable weakness. Usual clinical findings are asymmetry in the appearance of the posterior muscle group and significant difficulty when asked to perform a single heel rise. Return to high-level activity or a sport is nearly impossible. There is usually a small amount of soft-tissue “creep” and resultant lengthening of the Achilles even after a primary repair (as noted in previous literature/radiographic studies), which I think contributes significantly to the mechanical weakness of the triceps postinjury. After a secondary injury, this is
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magnified, and it is imperative to maintain physiologic tension on the repair when it is performed. Often, it is also a challenge to manage the inevitable scarring associated with prior intervention, adhesions, and vascular compromise of the surrounding soft-tissue envelope and patient expectations.
same in terms of function in these cases.
Hunt: It takes patients a bit longer to full recovery, but the end result is the
Schuberth: I think that the end point is generally the same but takes longer
Maffuli: I tell my patients that they will have to accept that they will lose some 20% to 30% of the strength of the gastrocsoleus. However, several of them do end up pleasantly surprising me!
to achieve. The calf atrophy seems to be a little worse with nonoperative care.
Reference 1. Saxena A, Bareither D. Magnetic resonance and cadaveric findings of the “watershed band” of the Achilles tendon. J Foot Ankle Surg. 2001;40:132-136.
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