Porter & Schon: Baxter's The Foot and Ankle in Sport, 2nd ed.

Section 2 - Sport Syndromes

Chapter 7 - Achilles tendon disorders including tendinosis and tears

Craig I. Title,Lew C. Schon

  

 

Introduction

  

 

Achilles tendinitis

  

 

Treatment of Achilles tendinitis

  

 

Role of ultrasound and shock wave therapy

  

 

Acute Achilles tendon rupture

  

 

Chronic Achilles tendon rupture

  

 

Conclusion

  

 

References

Introduction

The Achilles tendon is formed by a coalescence of fibers from the gastrocnemius and soleus muscles. This complex spans both the knee and ankle joints, making it more susceptible to injury than muscles that span a single joint. The Achilles tendon is notably susceptible to injury with concomitant knee extension and ankle dorsiflexion. The medial and lateral heads of the gastrocnemius originate from the medial and lateral femoral condyles, respectively. The soleus muscle originates from the posterior proximal tibia and fibula. More distally, the medial and lateral gastrocnemius and soleus tendons coalesce to form the triceps surae complex. The Achilles tendon then rotates 90 degrees such that the medial gastrocnemius position is more posterior and superficial. This rotation may result in torque stresses that can increase the risk of tendinitis.[1]After passing distal to the posterior superior calcaneal tuberosity, the Achilles tendon inserts into the posterior and plantar calcaneal tuberosity about halfway between the dorsal and plantar aspects of the calcaneus.

The retrocalcaneal bursa lies between the distal Achilles tendon and the posterior superior calcaneal tuberosity. It is horseshoe shaped and sits around the insertion of the Achilles, which has more fibers centrally and proximally. Anteriorly it is composed of fibrocartilage, whereas posteriorly it blends with the paratenon and commonly connects to the posterior Achilles tendon. The pre-Achilles bursa lies superficial to the Achilles between the Achilles and the skin. These bursae, composed of synovium, provide lubrication to assist with tendon gliding and to minimize tendon irritation. A large, sometimes abnormal prominence of the posterior superior calcaneus, Haglund's deformity,[2] may create repetitive frictional irritation on the Achilles tendon that can lead to tendinitis ( Fig. 7-1, A and B ).

 

 

Figure 7-1  (A) Lateral radiograph of calcaneus demonstrating Haglund's deformity. (B) Sagittal magnetic resonance imaging of the same patient showing changes at Achilles tendon from bony prominence and its effect on Achilles tendon, with thickening and fibrosis as it passes by the bone and more proximally.

 

 

The Achilles tendon is the strongest and longest tendon in the body, measuring approximately 12 to 15cm in length. Although it is the main plantarflexor of the ankle, it also functions to invert the heel during late stance phase and thereby locks the transverse tarsal joint for push-off along with the posterior tibial tendon. It is subject to forces up to 10 times body weight during running, experiencing up to 7000N of force. [0010] [0030] [0040]

The blood supply to the Achilles tendon is segmental and is predominantly derived from anterior branches of the paratenon. Additional sources include intratendinous vessels, the posterior tibial artery, and distal osseous and periosteal branches. A relative zone of hypovascularity exists within 2 to 6cm proximal to the calcaneal insertion, corresponding to the site of most Achilles tendon ruptures and noninsertional tendinitis. [0050] [0060]

Similar to other tendons, the Achilles is composed of predominantly type I collagen. Collagen fibrils are bundled into fascicles, held together by the endotenon, which contain elastin, lymphatics, and neurovascular structures. The epitenon surrounds the group of fascicles, forming the structural unit of the tendon. The paratenon further surrounds the epitenon and consists of an inner parietal layer, lying directly on the epitenon, and an outer, visceral layer. The paratenon, containing a small amount of fluid between its layers, facilitates glide and minimizes posterior adhesion formation.

 

Achilles Tendinitis

Achilles tendinitis is common among athletes, affecting nearly 18% of runners. [0070] [0080] [0090] Repetitive impact-loading activities (overuse) such as jumping are responsible for the majority of cases.[1]Other predisposing factors include poor extremity biomechanics (foot pronation, cavus foot, genu varum), improper training techniques (excessive running, sudden increase in intensity, uphill running), and poor shoewear.[8] Another potential risk factor includes the previous use of fluoroquinolone antibiotics. Athletes commonly affected by tendinitis are involved in running, dancing, tennis, racquetball, basketball, and soccer (unnumbered box 7-1 ).

Achilles tendinitis risk factors

  

   

Repetitive impact-loading activities

  

   

Abnormal lower-extremity biomechanics (foot pronation/supination, stiff joints, genu varum)

  

   

Improper training techniques (intensity, frequency, duration, speed, terrain)

  

   

Poor shoewear selection

  

   

Fluoroquinolone antibiotics

Puddu et al.[10] classified Achilles tendinitis into three categories. Peritendinitis is characterized by inflammation affecting only the paratenon. Peritendinitis with tendinosis refers to inflammation involving both the paratenon and Achilles tendon. Tendinosis reflects isolated Achilles degeneration. Clain and Baxter[1] later created an anatomic classification, separating tendinitis into insertional disorders, affecting the area of the enthesis, and noninsertional disorders, commonly affecting the tendon 2 to 6cm proximal to the calcaneus.

Whereas noninsertional tendinitis occurs more often in younger, more active athletes, insertional Achilles tendinitis develops more often in those athletes who are older, less active, and sometimes overweight. Additionally, the presentation of bilateral insertional tendinitis typically occurs in young athletic men and is commonly associated with inflammatory disorders, including seronegative spondyloarthopathies. [0110] [0120]

Noninsertional tendinitis

Peritendinitis is inflammation affecting only the paratenon. The Achilles tendon itself is uninvolved. In chronic cases, adhesions may form between the paratenon and tendon, leading to more profound pain and tenderness. Pain is noted most often at the initiation of activity (start-up pain) and improves with continued exercise. Acute pain typically resolves with rest. In chronic cases, however, the pain may persist and significantly impair further athletic participation. On examination, a localized, increased diameter that more commonly affects the medial side is appreciated with palpation of the tendon. Tenderness, and at times crepitus, is noted throughout all ankle range of motion ( Fig. 7-2 ). Radiographs generally are unremarkable.

 
 

Figure 7-2  Tenderness with squeezing the Achilles and crepitance with range of motion are hallmarks of peritendinitis. The discomfort related to peritendinitis will be constant in location as the ankle is brought through a range of motion. With Achilles tendinosis the tenderness moves with the thickened tendon during range of motion.

 

 

Peritendinitis with tendinosis represents further inflammation with associated intratendinous degeneration. Pain is more marked and constant. The tendon is thickened and infrequently has palpable intrasubstance calcifications ( Fig. 7-3 ). The painful arc sign may help to distinguish between tenderness associated with peritendinitis and that associated with tendinosis. Tenderness related to peritendinitis will be constant in location as the ankle is brought through a range of motion, whereas tenderness associated with tendinosis will change position with ankle motion.[13]



 

Figure 7-3  (A) Noninsertional Achilles tendinitis with characteristic swelling 2 to 5cm above dorsal aspect of calcaneus. (B) Magnetic resonance imaging shows thickened Achilles tendon. A Haglund's deformity also is noted. (C) Technetium bone scan demonstrating increased uptake in the Achilles tendon; the third phase of the scan, indicative of advanced intrasubstance degeneration.

 

 

Isolated tendinosis, or noninflammatory atrophic degeneration, is associated with normal aging and typically is accelerated by overuse. Most affected are middle-aged, recreational athletes. With repetitive trauma, microtears develop within the tendon, mostly in the hypovascular zone, leading to further fibrosis and degeneration.[14] These athletes complain of weakness in push-off, with pain localized to the area approximately 2 to 5cm proximal to calcaneus. Whereas ankle dorsiflexion commonly is limited, tendon elongation may develop with an associated increase in passive ankle dorsiflexion. Pathologic examination reveals fatty degeneration with disorganized collagen. Calcific deposits may be present (unnumbered box 7-2 ).

Peritendinitis affects the paratenon; the Achilles tendon is not involved:

  

   

Overuse etiology

  

   

Tends to be in younger athletes

  

   

Pain at the initiation of activity (start-up pain)

  

   

Improves with continued exercise

  

   

A localized increased diameter

  

   

Tenderness, and sometimes crepitus, throughout all ankle range of motion

Tendinosis, noninflammatory, atrophic degeneration of the Achilles:

  

   

Associated with normal aging

  

   

Accelerated by overuse

  

   

Pain and weakness in push-off

  

   

Tender thickening 2 to 5cm proximal to calcaneus

  

   

Ankle dorsiflexion commonly is limited

  

   

Less typically, tendon elongation may develop

  

   

Palpation during range of motion reveals tenderness that moves with movement of the tendon

  

   

Calcific deposits may be present

Insertional achilles tendinitis

Insertional tendinitis is an inflammatory reaction within the Achilles tendon affecting the enthesis, or tendon insertion onto the calcaneus. This disorder more commonly affects older, heavier, and less active athletes but can be seen in competitive athletes as well.[12] An abnormally enlarged, bony prominence may aggravate this condition. There is a high association with Haglund's deformity and retrocalcaneal bursitis, but unlike these disorders, insertional tendinitis involves the tendon itself. This most often results from chronic overuse and poor training habits. Improper techniques include inadequate stretching, rapid increase in training, running on harder surfaces, and heel running. Although pain initially follows exercise, particularly uphill running, symptoms may become continuous over time.

Pain, swelling, and warmth are noted specifically at the tendon-bone junction, the enthesis. In athletes, there often is a localized area of pain with a small spur. Ankle range of motion is painful, with dorsiflexion typically limited because of a tight Achilles tendon. External irritation from a shoe's heel counter plays less of a role in provoking symptoms in athletes with Achilles tendinitis than in retrocalcaneal bursitis and Haglund's deformity. Radiographs generally reveal calcifications or a bony spur at the most distal aspect of the Achilles insertion ( Fig. 7-4, A ). Magnetic resonance imaging (MRI) will show degeneration where the tendon attaches to the calcaneus ( Fig. 7-4, B ).

 

 

Figure 7-4  A lateral x-ray (A) and a series of sagittal magnetic resonance imagings (B, p. 152) of the same patient with insertional degeneration of the Achilles tendon with tendon thickening and fibrosis from about 2cm proximal to its insertion on the calcaneus.

 

 

Haglund's deformity

Haglund is credited with first describing the presence of a prominent posterolateral superior calcaneal tuberosity in 1927.[2] This enlarged superolateral tuberosity predisposes the precalcaneal bursa to be compressed between it and any tightly fitting shoe heel counter, possibly leading to skin irritation and inflammation. Because of the association of shoewear, this disorder also has been referred to as a “pump bump” and “winter heel.” Although there is a frequent association with retrocalcaneal bursitis and insertional Achilles tendinitis, Haglund's deformity generally does not involve the Achilles tendon.

Poorly fitting shoes generally are responsible for the development of symptoms of Haglund's disorder. Other predisposing risk factors include the presence of a cavus foot and hindfoot varus. In rare cases, childhood apophyseal trauma may be a cause. In the nonathletic population, repetitive injury or trauma may result in bone overgrowth. Most affected are young women who wear fashionable high-heeled shoes. In the athletic population, we have observed this condition more commonly in males who participate in running sports. Long-distance runners are susceptible to this condition, as well as to the other Achilles tendon disorders (see Figs. 7-1 and 7-5 [0010] [0050]).

 
 

Figure 7-5  Clinical photograph of Haglund's deformity.

 

 

On examination, the affected heel has a swollen, red, and tender posterior prominence, predominantly on the lateral side of the calcaneus. The Achilles tendon itself is not tender. Numerous radiographic measurements have been used to quantify the size of the posterosuperior prominence. These techniques generally are not used by orthopaedists because they do not always correlate with the clinical findings.

Retrocalcaneal bursitis

Retrocalcaneal bursitis refers to inflammation affecting the bursa immediately anterior to the Achilles tendon. As with Haglund's deformity and Achilles tendinitis, this condition is common in running athletes, including long-distance runners. In the general population, as with insertional tendinitis, those most commonly affected are older, less active recreational athletes. As the disorder becomes chronic, the bursa enlarges and may become adherent to the Achilles tendon. A prominent posterosuperior bony projection may be present.

Athletes typically complain of pain with activities that force the ankle into dorsiflexion, particularly uphill running, and thereby compress the inflamed bursa between the posterosuperior calcaneus and the Achilles tendon. Schepsis et al.[14] described the two-finger squeeze test, in which pain is noted when two fingers compress medially and laterally immediately superior and anterior to Achilles insertion. This area will be warm with a notable soft-tissue bulge. Pain is elicited with passive dorsiflexion. Radiographs often are not useful but may demonstrate loss of the retrocalcaneal soft-tissue shadow, as well as the presence of a posterosuperior bony prominence. MRI demonstrates soft-tissue changes anterior to the Achilles tendon above its insertion in the retrocalcaneal region ( Fig. 7-6 ).

 
 

Figure 7-6  Magnetic resonance imaging demonstrates Haglund's deformity with enlarged posterior superior aspect of the calcaneus.

 

 

 

Treatment of Achilles Tendinitis

Nonsurgical treatment

The initial treatment for Achilles tendinitis is nonoperative. The majority of symptoms respond to rest; activity modification; improved training techniques; stretching; and, at times, shoe modifications and heel lifts. Surgical intervention should be considered only for recalcitrant cases.

Initial treatment should include anti-inflammatory medications and a supervised program of Achilles stretching. At times, a heel lift (one-fourth to three-eighths inch), night splint, or temporary immobilization in slight plantarflexion with a removable walking boot or cast may be required. Relative rest with limitations on intensity, duration, or frequency of training and concomitant institution of nonstressful cross training (exercise bike, pool running, elliptical trainer) also should be helpful. If the athlete has notable foot pronation, a semirigid orthotic may improve overall foot biomechanics by supporting the medial arch. An open-back shoe may benefit those with Haglund's or retrocalcaneal bursitis ( Fig. 7-7 ). Additionally, deepening the heel counter or use of a heel pad or sleeve may be considered.

 
 

Figure 7-7  Shoe alternatives and modifications for patients with Achilles tendinitis. Clockwise from the top left: (A) A higher-heeled, backless shoe, “a mule.” (B) A completely removed heel counter. (C) A partial heel counter cut to relieve external pressure. (D) A backless sneaker.

 

 

Intratendinous corticosteroid injections should be avoided because local use of these injections has been associated with tendon attrition and potential rupture. Although there is no strong evidence of similar deleterious effects after peritendinous corticosteroid injections, there are similar worries with an injection in the bursa. It would be advisable to immobilize the ankle temporarily after a retrocalcaneal injection because the retrocalcaneal bursa has a direct communication to the Achilles and may injure the Achilles tendon. [0120] [0150] [0160] [0170] In general, we advise against corticosteroid injections and use them only in very limited and specific circumstances.

For refractory peritendinitis, we have found that brisement may provide symptomatic relief in a third to half of total cases.[18] Brisement consists of injecting 5 to 10ml of sterile saline or local anesthetic agents into the Achilles tendon sheath; this may forcibly disrupt any adhesions between the paratenon and Achilles tendon. Repeating the injections two to three times over several weeks may be necessary to achieve success. [0140] [0180]

After initial symptoms resolve, it is imperative to correct predisposing factors, including improper technique, excessive training, inappropriate shoewear, and poor flexibility. In addition, it may be critical to temporarily or permanently eliminate provocative, more rigid, and less compliant surfaces and terrain.

Reported results of nonoperative treatment of insertional and noninsertional Achilles tendinitis have been generally successful. Studies have found that 70% to 90% of patients have found symptomatic improvement after corrections in their shoewear, training habits, and mechanics. [0080] [0180] [0190] [0200] [0210] [0220] There are, however, fewer predictable results with nonsurgical management in those with chronic tendinopathy and in the older athlete, as a result of greater degenerative tendon involvement.[21]

In our experience, athletes with isolated Haglund's deformity can be managed with shoewear modification about 50% of the time. We have seen improvement in about 30% of patients with retrocalcaneal bursitis and in about 25% of those with insertional tendinitis. The presence of a prominence does not mandate surgery. One should not perform prophylactic resection because the degenerative process may be improved with mechanical means, rest, and other modalities, as described above.

Surgical treatment

Surgical intervention is considered only after approximately 3 months of good, nonoperative treatment measures. The surgical technique is chosen on the basis of location of pathology. For a symptomatic athlete with a normal tendon, determined by physical examination and possibly by MRI, we generally try to avoid a procedure that may irritate or traumatize the tendon. A medial or lateral approach 5 to 10mm anterior to the Achilles tendon and paralleling its course is best in these cases because it runs through thicker skin with more substantial subcutaneous tissues. If the tendon is involved, an approach directly through the posterior aspect of the tendon is possible. This approach has the additional benefit of obtaining even greater exposure and improved debridement of bone and tendon.

Other issues must be taken into consideration to help guide the surgical approach and choice of technique, such as identifying whether Haglund's deformity, retrocalcaneal bursitis, or insertional tendinitis is involved and determining the extent of tendon involvement (length, width, and depth of pathology). Any prominence of the bone, as well as the location of the prominence relative to the insertion of the tendon (above, at, or below the insertion of the tendon), should be noted, and the surgeon should determine whether the bursa is inflamed and how much additional debridement is necessary. In general, the points of tenderness dictate where the exposure must occur. Thus if there is more medial and central Achilles tendinitis versus lateral, the tendon in the medial and central aspect has to be elevated off the calcaneus, the tendon must be debrided there, and the underlying bone must be resected and recontoured.

Noninsertional tendinitis

For noninsertional tendinitis, the choice of procedure is based on whether the disease involves the paratenon, tendon, or both. In peritendinitis, all adhesions are excised, and the surgeon also performs a limited resection of any thickened paratenon. The extremity is immobilized for 3 to 5 days, followed by a range of motion program to limit the recurrence of scar formation ( Fig. 7-8 ).

 
 

Figure 7-8  Release of the paratenon. Note that the incision is made 1cm anterior to the margin of the Achilles tendon. The incision can be made much smaller than shown in this case.

 

 

When there is tendinitis and peritendinitis, elliptical excision of the tendon and longitudinal paratenon release is performed. Maffulli et al.[23] have reported a success rate of approximately 70% after percutaneous longitudinal tenotomy of the middle third of the Achilles tendon. In this technique a no. 11 or no. 15 blade is introduced posteriorly through the skin and tendon. With the blade held stationary, the ankle is dorsiflexed and the tendon is cut longitudinally. Next the blade direction is reversed 180 degrees and the ankle is plantarflexed. The process is repeated through four additional incisions in the zone of the degenerative tendon ( Fig. 7-9 ).

 
 

Figure 7-9  The Maffulli technique: an incision is made with a no. 11 or no. 15 blade. The blade is held stationary and the ankle is dorsiflexed creating a longitudinal cut in the tendon. The blade then is turned 180 degrees, and the ankle is plantarflexed. The process is repeated until there are five longitudinal cuts.

 

 

Tendinosis

The type of procedure chosen for treatment of tendinosis depends on many factors, the largest, in our experience, being the extent of tendon involvement, determined by clinical findings, ultrasound, or MRI. When less than 50% of the tendon is involved, we longitudinally ellipse the diseased tendon; and when more than 80% of the tendon is involved, a debridement and tendon augmentation (e.g., turndown) or transfer is recommended ( Fig. 7-10 ). When there is between 50% and 80% involvement, the decision is determined by the patient, the sport, and the surgeon's preference.

 
 

Figure 7-10  Magnetic resonance imaging cross section of the Achilles tendon demonstrating more than 80% tendon involvement. This would indicate the need for tendon augmentation or transfer following debridement.

 

 

Debridement of tendon. For tendinosis, typically the degenerative portion of the Achilles tendon is debrided and the paratenon is released. If less than 50% of the tendon width is debrided, then the remaining section of intact longitudinal tendon should be strong enough to withstand stresses.

Typically a medial incision is made just anterior and parallel to the border of the tendon that is thickened, and the paratenon is entered. On the basis of maximal tenderness, MRI, or ultrasound localization of the degenerative zone of the tendon, an elliptical longitudinal excision of the diseased tendon is performed, leaving intact the anterior and posterior surfaces of the tendon. Essentially the zone of ellipsed tissue should include the degenerative fibers and the thickened tendon ( Fig. 7-11 ). The tendon then is repaired with internally placed, nonabsorbable sutures with buried knots. The subcutaneous tissues are apposed, followed by closure of the skin. The leg is immobilized for 3 to 5 days in a splint, followed by range of motion exercise, strengthening, and nonimpact activities. A boot brace is worn for 6 to 12 weeks during ambulation to unload the healing tendon. Jogging and running may be introduced at 3 months, depending on the extent of involvement and the nature of the patient's athletics.

 
 

Figure 7-11  Intraoperative photo of debridement of the Achilles tendon. Once the degenerative tissue is ellipsed from within the substance of the tendon, buried sutures are used to close the defect.

 

 

Tendon transfer. If more than 50% of the tendon width is involved, then one must consider the risks and benefits of either longitudinal tenotomy, debridement, or tendon transfer. The decision to consider tendon transfer is determined by the structural weakening of the tendon that may result from a large debridement.

Because most athletes use all their tendons for ultimate, lower-extremity performance, it is difficult to justify harvesting a working structure to improve the function of the Achilles. Thus depending on the demands of the athlete and nature of his or her skills, we have to balance the pros and cons of using the tendon transfer. If 50% to 80% of the width of the tendon is resected, we consider these factors. However, if 80% or more of the tendon is involved, our experience has been that the transfer becomes more critical to restore function. Alternative procedures in this latter scenario include a turndown procedure, tendon allograft, and V-Y advancement.

The flexor hallucis longus (FHL), flexor digitorum longus (FDL), or, less commonly, the peroneal tendons can be transferred. We prefer to use the FHL tendon in a nonsprinting athlete, nondancer, or rock climber. Transferring the FHL or any other tendon in a sprinting athlete or ballet dancer could lead to loss of agility, power, or balance. In these athletes, it is better to consider performing a turndown procedure, a V-Y advancement, or an allograft if a wide area of tendon is involved.

The patient is positioned prone and both legs are prepped for any tendon transfer, turndown procedure, or V-Y advancement because it usually is necessary to compare resting tensions with those of the contralateral side. In a tendon transfer, our preferred technique is to use a medial approach to the Achilles tendon, typically staying 1cm anterior to the medial edge of the tendon. The incision is extended more inferiorly. The paratenon is opened, the degenerative tendon is excised, and the deep fascia between the superficial and deep compartment is released. It is felt that, by opening the fascia and exposing the deeper FHL muscle belly, there is an improved vascular bed for the Achilles. Ranging the big toe should facilitate identification of the moving FHL muscle belly and tendon. The FHL tendon may have a more distal origin and may not be viewed readily in the wound. Care should be taken while dissecting along the course of the muscle because the tibial nerve runs immediately medial to the tendon ( Fig. 7-12, A through E ).





 

Figure 7-12  (A) A medial approach 1cm anterior to themedial edge of the Achilles tendon. (B) The deep fascia between the superficial and deep compartment is released. Ranging the big toe should allow palpation and identification of the moving flexor hallucis longus (FHL) (marked with two arrows). The tibial nerve runs immediately medial to the tendon, therefore dissection of the tendon must be carefully performed. (C) The tendon is released distally and secured with a whipstitch. The degenerative Achilles tendon is excised. (D) 4-0 or 2-0, nonabsorbable suture is buried within the tendon. (E) The defect is closed and the FHL tendon is sewn to an anchor into the calcaneus. This area of the calcaneus is prepared by locally elevating the periosteum. In this case the Achilles tendon length was normal, so the FHL was tensioned to permit full dorsiflexion.

 

 

Follow and release the FHL tendon from the sheath (fibroosseous tunnel) as it travels between the medial and lateral tubercles of the posterior talus. Continue to release the tendon for as much length as possible from the posterior approach, dissecting toward the underside of the sustentaculum tali. Cut the tendon as distally as possible, again avoiding the tibial nerve. The FHL tendon then is either sewn to the Achilles repair or inserted into the calcaneus or its periosteum, depending on tendon length. A useful technique involves drilling a hole the width of the tendon (typically 5mm) through the calcaneus from dorsal to plantar ( Fig. 7-13 ). A small incision made over a K-wire passed through this tunnel can facilitate placement of a small-bore suction tip over the wire from plantar to dorsal and out the planned entry point for the tendon. The whip suture in the FHL tendon then can be passed through the suction tip and pulled plantarly to permit tensioning. An interference screw can be inserted through the tunnel. Alternatively, an anchor can be placed obliquely in the tunnel wall just distal to the opening but not obscuring the passageway. After the proper tension has been determined, the tendon is secured. Occasionally there is a need to resect the posterior superior calcaneus; this procedure is determined by the presence of Haglund's deformity and bursitis. We do not close the deep fascia between the compartments because the FHL muscle belly may provide for improved healing following the Achilles repair.







 

Figure 7-13  (A) Following debridement of the Achilles and harvest of the flexor hallucis longus (FHL),the thickness of the FHL is determined to properly select the drill size. (B) A guidewire is passed through the calcaneus and then is advanced to pierce the plantar soft tissues. The exit point plantarly is just anterior to the fat pad of the heel. (C) A drill matching the width of the FHL is used to create a channel in the calcaneus but should not penetrate the soft tissues. (D) A small incision is made and a small-bore suction tip is placed over the wire from plantar to dorsal and out the planned entry point for the tendon. (E) The whip suture in the FHL tendon then can be passed through the suction tip and pulled plantarly to permit tensioning. (F) An interference screw is inserted through the tunnel. As an alternative, an anchor can be placed obliquely in the tunnel wall just distal to the opening but not obscuring the passageway. (G) A corkscrew anchor is inserted to repair the Achilles tendon onto bone.

 

 

V-Y advancement. A V-Y advancement may be required if more than 80% of the tendon width and 2 to 3cm in length is involved. With this large amount of tendon involvement, the remaining normal tendon may not be thick or wide enough to safely flap. The V-Y advancement is accomplished by extending the initial posterior incision more proximally toward the musculotendinous junction ( Fig. 7-14,A through C ). A V-shaped fascial incision is made with the apex proximal. With traction on the tendon distally, an advancement of 2 to 3cm then can be achieved; this should close the distal gap sufficiently. The distal repair can be performed with a modified Krackow or whipstitch, and then balancing of the tendon tension is performed by checking for the resting posture of the foot and testing the “springiness” of the foot as it sits in the normal, slightly plantarflexed position.



 

Figure 7-14  The V-Y advancement. (A) The section of the diseased Achilles is debrided, and the new edges are sutured with a whipstitch for anastomosis. (B) A V-shaped fascial incision is made with the apex proximal. With traction on the tendon distally, an advancement of 2 to 3cm can then be achieved. (C) The final tendon tensioning is performed by checking the resting posture of the ankle and testing the “springiness” of the foot as it sits in the normal slightly plantarflexed position. A comparison with the other side is helpful. The V-Y is then sutured. If it appears that there is too large a gap to close, a turndown or a tendon transfer may span the defect.

 

 

The V-Y advancement is performed with the patient prone. Because it usually is necessary to compare resting tensions with those of the contralateral side, both legs are prepped as for any tendon transfer or turndown procedure. However, the tendon may begin to tear and pull off the muscle base beyond an advancement of 3 to 5cm. If it appears that there is not enough fascia/tendon substrate or if too large a defect exists for advancement, then a turndown or an allograft tendon transfer such as with a semitendinosus tendon may be used as a connecting bridge.

Turndown procedure. A turndown procedure provides substrate for healing and may limit the possibility of rerupture when there is between 50% and 80% of tendon width involvement. The patient is positioned prone with both legs prepped to compare the two and re-create normal resting tension. A medial incision is used, with care taken on deeper exposure to avoid branches of the sural nerve. After the rupture or degeneration site is exposed, the end of the proximal tendon is mobilized, then grasped with Alice clamps and gently distracted by pulling distally on the Alice clamps for 5 to 10 minutes (Fig. 7-15, A ).







 

Figure 7-15  The turndown procedure. (A) After the rupture or degeneration site is exposed, the end of the proximal tendon is mobilized and then grasped with Alice clamps, and tension is pulled. (B) The size of the gap is measured while the foot is maintained in a neutral position. (C) An additional 4cm then are added to the tendon defect (a 2-cm distal hinge that is overlapped by the turned-down flap, or 2cm plus 2cm). Another 1cm is added to account for the intended 1-cm overlap of the tendon ends distally. Thus the flap begins proximally at a point 5cm more than the size of the gap. (D) A strip of tendon 1cm wide is harvested centrally. (E and F) The tendon graft now can be turned distally to span the void. (G) Two no. 1 Ethibond sutures are used to anchor the corner of the turned-down graft (arrows) reinforcing the high stress junction. The central slip typically is passed anteriorly deep to the tendon to decrease the bulk. The distal tendon end then is secured to the remaining viable Achilles or to the bone. Comparison with the nonoperative side facilitates tensioning of the graft.

 

 

The size of the gap is measured while the foot is maintained in a neutral position ( Fig. 7-15, B ). An additional 4cm then is added to the tendon defect (a 2-cm distal hinge that is overlapped by the turned-down flap, or 2cm plus 2cm). Another 1cm is added to account for the intended 1-cm overlap of the tendon ends distally ( Fig. 7-15, C ). Thus the flap begins proximally at a point 5cm more than the size of the gap. For example, if the gap is 6cm, then a flap is initiated 11cm proximal to the gap ( Fig. 7-15, D ). A strip of tendon approximately 1cm wide and 1cm thick is harvested centrally. The tendon graft now can be turned distally to span the void ( Fig. 7-15, E and F ). At approximately 2cm proximal to the defect, two no. 1 Ethibond sutures are used to anchor the corner of the turned-down graft, reinforcing the high stress junction so there is no propagation of the split between the strip and the main body of the tendon ( Fig. 7-15, G ). To decrease the bulk created by this method, the tendon then is passed anteriorly deep to the tendon instead of posteriorly.

The distal tendon end then is secured to the remaining viable Achilles or to the bone. Tensioning of the graft requires checking the range of motion and the springiness of the operative side versus the normal side. Usually, the foot should have a resting position of 15 degrees of plantarflexion. The graft and the turned-down flap are held in place by hand or by suture. Once the appropriate tension and position are established, whipstitches are used for final anastomosis. The resting tension and springiness are checked once again at the end of the procedure (unnumbered box 7-3 ).

Noninsertional tendinitis surgical alternatives

  

   

Paratendinitis: release paratenon

  

   

Tendinosis: degree of width involved

  

   

<50% ellipse and repair

  

   

>80% ellipse and augment

  

   

Tendinosis: degree of length involved

  

   

1-3cm V-Y

  

   

3-5cm turndown

  

   

>5cm turndown with consideration for FHL or FDL tendon transfer

Insertional tendinitis

Insertional tendinitis is surgically treated by excising the retrocalcaneal bursa and any prominent posterosuperior bone. Additionally, the Achilles tendon is debrided of any intratendinous calcifications and degenerated tissue, including detachment of part of the tendon's insertion. Achilles tendon reattachment through calcaneal bone tunnels or with suture anchor is advised. A central splitting or paralateral Achilles approach both have been advocated.[12] Our preference is a central approach for optimal visualization ( Fig. 7-16, A through H ). The direct posterior central approach for the distal Achilles tendonopathies requires an incision through thick, well-vascularized skin. This is distinct from the thinner skin found proximal to the calcaneus that is potentially more problematic with delayed healing of a wound.








 

Figure 7-16  Insertional Achilles tendinitis. (A) Sagittal magnetic resonance imaging of a patient with insertional Achilles tendinitis and retrocalcaneal bursitis. Note the bony prominence, the fluid in the bursa anterior to the tendon, and the abnormal signal at the insertion consistent with degeneration at the interface. (B) A central incision is made through the site of maximal tenderness through the tendon down to the bone. (C) The tendon is released from its insertion posteriorly and the posterior superior calcaneus is exposed. (D) Two human retractors are placed, and the chisel is used to resect the insertion site and the posterior superior bony prominence. (E) A side view of the chisel angle to resect the bony prominence. Care is taken not to inadvertently penetrate too anteriorly and end up in the subtalar joint. The medial lateral and dorsal edges are checked for remaining bone. (F) The bone has been resected and the suture anchor is placed centrally into the calcaneus about 5 to 8mm proximal to the previous insertion site. (G) An intraoperative image demonstrating the anchor placement. (H) The sutures are placed close to the midline, penetrating the tendon directly over the anchor with very minimal divergence to maximize tendon apposition to the bone. The knots should be buried so that postoperative irritation is avoided.

 

 

Through the central incision, we debride both the bone and the tendon at the junction and resect the posterior superior process. Tendon augmentation may be required, depending on the extent of debridement. When more than 80% of the tendon is involved or when the Achilles is degenerative at the insertion and proximally, an FHL graft should be considered ( Fig. 7-17, A through C ). The FHL can be harvested in the arch of the foot or, as we prefer, behind the ankle. After the FHL is attached to the bone through a tunnel or into a trough, the Achilles tendon is reattached with one or two suture anchors.



 

Figure 7-17  When the Achilles is degenerative at the insertion and proximally or when more than 80% of the tendon is involved a flexor hallucis longus (FHL) graft should be considered. (A) The central approach is used to detach the Achilles posteriorly, and the prominent bone is resected. (B) The degenerative tendon is debrided. (C) The FHL tendon is harvested from behind the ankle and will be reattached through a tunnel or into a trough before repairing the Achilles tendon.

 

 

A biomechanical study by Kolodziej et al.[24] demonstrated that as much as 50% of the Achilles tendon may be safely resected through this approach. Despite this study, we still recommend placing suture anchors to optimize tendon bone contact and healing. When reattaching the tendon, it is important to restore normal resting tension, using the remaining intact portions of medial and lateral slips of tendon as a guide. Inadvertent overtensioning of the repair when using anchors could cause an equinus contracture or difficulty squatting or lunging.

Haglund's deformity

Surgical treatment for Haglund's deformity and retrocalcaneal bursitis focuses on resecting the enlarged posterior bony prominence, including the attached precalcaneal bursal projection. Any inflamed retrocalcaneal bursa also is excised. Because the lateral side is more commonly affected, it is easier to approach through a lateral incision ( Fig. 7-18, A ). A medial approach is warranted when the bony prominence is found medially ( Fig. 7-18, B ). When the tendon is not involved, the insertion can be avoided through the lateral or medial approaches. Either way, it is critical to resect a sufficient amount of bone to prevent impingement on the tendon and avoid creating a sharp edge after resection that may irritate the tendon ( Fig. 7-18, C and D ). Too much resection can weaken the tendon insertion, and the subtalar joint may be penetrated if the surgeon is not careful. Jones and James[25] advocated a combined medial and lateral approach to ensure a thorough bony resection ( Fig. 7-18, E ). This exposure helps to avoid inadvertent creation of a sharp, bony edge.





 

Figure 7-18  The incisions for treatment of the Haglund's deformity. (A) A lateral incision is more common because the prominence is usually more pronounced on this side (B) A medial approach is warranted for a medial bony prominence. (C and D) Radiographs preoperatively and postoperatively show sufficient bone resection without impingement at the tendon insertion. (E) A combined medial and lateral approach ensures a thorough bony resection and edge contouring.

 

 

We recommend a lateral approach or the combined medial and lateral exposure. The central posterior approach for Haglund's deformity should not be used because it is better to avoid disrupting the insertion of the tendon unless there is a clinically relevant component of insertional tendinitis ( Fig. 7-19, A through D ). Bone resection should be performed just proximal to the insertion of the tendon (Fig. 7-19, E ). A power reciprocating rasp should be used to help contour the cut edges by the tendon ( Fig. 7-19, F ). A mini-C arm should be used to help identify any remaining prominences ( Fig. 7-19, G).







 

Figure 7-19  (A) through (C) This athlete's x-rays and sagittal magnetic resonance imagings demonstrate a Haglund's deformity, retrocalcaneal bursitis, posterior calcaneal bony edema, and some insertional Achilles tendon changes. (D and E) Because all the tenderness and prominence were lateral and there was no tenderness as the Achilles insertion, a lateral approach was chosen, with the intraoperative option of an additional medial incision to contour the sides. (F) Bone resection should be performed just proximal to the insertion of the tendon. A power reciprocating rasp should be used to help contour all edges by the tendon. (G) A mini-C arm should be used to help identify any remaining prominences.

 

 

Endoscopic Haglund's resection as presented by Niek van Dijk (see Chapter 16 ) recently has gained popularity. In this technique, the patient is placed in a prone position, and a lateral incision is made just dorsal to the calcaneus and anterior to the tendon ( Fig. 7-20 ). A 4.5-mm, 30-degree arthroscope is introduced. A spinal needle then is introduced medially just dorsal to the calcaneus, and the 5.0-mm full-radius resector is inserted. With the shaver on the superior surface of the bone, the periosteum is removed. In plantarflexion the Haglund's prominence can be resected with the shaver. A burr may be needed to remove bone at and near the insertion point of the tendon. The site of the burr placement should be confirmed with fluoroscopy. Adequate decompression is achieved at the posterior medial and lateral edges by alternating portals. The portals are sutured after the bursa and Haglund's prominence have been removed with fluoroscopic assistance. This technique avoids the creation of tender scars in this region, has low morbidity, and may shorten recovery relative to the open procedures.



 

Figure 7-20  Endoscopic portal landmarks. With the patient in a prone position, the lateral incision is made just dorsal to the calcaneus and anterior to the tendon. (A) The posterior view demonstrating the lateral portal (black arrow) and the medial portal (white arrow). The area of pain is marked on the patient's skin. A dotted line is marked at the superior site of the Achilles insertion below the area of pain. (B) The lateral perspective of the portal site. (C) The medial perspective of the portal. A 4.5-mm, 30-degree arthroscope is introduced laterally. A spinal needle is introduced medially just dorsal to the calcaneus. The 5.0-mm. full-radius resector then is inserted.

 

 

Alternatively, some authors have advocated a dorsal closing wedge osteotomy of the posterior tuberosity of the calcaneus. It is rarely used in athletes because of inherent complications with this procedure, including nonunion or malunion, potentially longer recovery times, difficult fixation, painful prominent hardware, broken hardware, and altered mechanics. This procedure may have a role if an athlete has a noticeably deformed posterior and superior calcaneal prominence, which we call the “pregnant heel” ( Fig. 7-21 ). It should be reserved for atypical cases (unnumbered box 7-4 ).

 
 

Figure 7-21  Top left corner shows the preoperative appearance of this large posterior prominence. It is uncharacteristically inferior, although the patient did not have insertional tendinitis. Title calls this the “pregnant heel.” This is a rare exception to consider, a dorsal closing wedge osteotomy of the posterior tuberosity of the calcaneus. Top left shows the lateral approach anterior to the Achilles tendon. Bottom left shows the preoperative radiograph. The bottom right demonstrates the calcaneus following the resection of the dorsally based closing wedge and fixation with a screw. The technique is used rarely because of inherent complications with this procedure, including nonunion or malunion, potentially longer recovery times, difficult fixation, painful prominent hardware, broken hardware, and altered mechanics.

 

 

Symptoms and surgery

Haglund's/retrocalcaneal bursitis

  

   

Tender over posterior superior bony prominence and/or anteromedial and anterolateral Achilles

  

   

Surgery: resect bone through medial and/or lateral incision over prominence

Insertional Achilles tendinitis

  

   

Tender at the insertion of the Achilles halfway between the dorsal and plantar aspect of the calcaneus

  

   

Surgery: central posterior Achilles splitting incision, debride tendon and bone

Postoperative management

Our postoperative management for the athlete is determined on the basis of the extent of tendon involvement. If there is no tendon repair or reconstruction, a nonweight-bearing posterior and U-splint is applied in mild plantarflexion for the first 10 days. The sutures then are removed, and progressive, full weight bearing is permitted with a boot brace in neutral position. Between 6 and 12 weeks, the athlete is weaned out of the boot as tolerated. Early range of motion and strengthening exercises are encouraged. Impact activities are avoided for about 8 to 12 weeks. Swimming and exercise bicycling are encouraged by 3 weeks, followed by the elliptical trainer by 4 weeks. Beyond 12 weeks, the athlete may progress to sports-specific activities. Our average time for athletes to return to sports has been 3 to 6 months.

If the tendon was repaired or reconstructed or if a tendon was transferred, a postoperative splint is applied in a relaxed resting position (25 to 45 degrees of equinus). At 10 days, the sutures are removed, and a boot brace is applied in 20 degrees of plantarflexion. We permit active dorsiflexion progressively up toward the neutral point but recommend reaching the neutral point at 6 weeks. Exercises are encouraged with the knee flexed to eliminate extra pulling of the gastrocnemius muscle during dorsiflexion. Ankle inversion and eversion strengthening may be performed. Flexing the toes against resistance is avoided if a tendon transfer was performed but encouraged if no transfer was done.

Partial weight bearing in a boot is allowed while maintaining the “triple flex walk” ( Fig. 7-22 ) (flexion of hip, knee, ankle). With the ankle in plantarflexion and the ipsilateral leg remaining anterior to the body at all times, the patient leads with that leg in gait and keeps the sole of the foot in contact with the ground by flexing the knee and hip, similar to a fencer's advance. Although the appearance is awkward, this method permits ambulation without crutches.

 

 

Figure 7-22  Partial weight bearing in a boot in plantarflexion is allowed while maintaining the “triple flex walk” (flexion of hip, knee, ankle). (A) With the ankle and the ipsilateral leg remaining anterior to the body at all times, the patient leads with that leg in gait and keeps the sole of the foot in contact with the ground by flexing the knee and hip, similar to a fencer's advance. (B) The back leg is now brought forward but does not advance beyond the front healing leg so that the Achilles can be kept unloaded. Next the braced leg is advanced again as in A. This method permits ambulation without crutches.

 

 

Ankle neutral position is achieved by 6 weeks, permitting full weight bearing with the boot adjusted at a right angle to the leg. Then progressive dorsiflexion exercises beyond neutral are performed, with caution not to overstretch. Dorsiflexion is progressed slowly, depending on the integrity of the repair. Swimming, bicycling, and other nonimpact activities are commenced at 6 weeks. At 12 weeks, the boot is discontinued, and lower-impact activities such as the elliptical trainer are instituted and increased. The patient then is progressed to jogging and then running. It may take 4 to 6 months to return to play, or perhaps more than 9 months, depending on the extent of the tendon disease and the integrity of the repair.

Surgical results typically correspond to the athlete's age, with patients younger than 50 years generally having less tendon involvement, more rapid return to work and sports, and fewer postoperative problems. Patients older than 50 years typically have more tendon involvement, require greater debridement, and have longer postoperative recovery. [0180] [0210]

Expected success rates and return to sport

Success rates have ranged from 50% to 90%, depending on the extent and location of tendon involvement. Surgical debridement for Haglund's syndrome and chronic tendinosis generally has less favorable results. [0260] [0270] Watson et al.[28] reported that those with insertional tendinosis are older athletes, have greater tendon involvement, take a longer time to recover, and often do not achieve results as satisfying as those with isolated retrocalcaneal bursitis. Leach et al.[29] reported in a small series of athletes that the long-term success rate was 85% following surgical treatment. However, the authors noted that symptoms recurred in two patients and required reoperation. A study by Schepsis et al.[26] also demonstrated initially high satisfactory results, mostly in athletes with paratendinitis, although long-term results deteriorated with time. In a recent study by Saxena,[30] return to activity was fastest in elite athletes requiring only soft tissue procedures, particularly peritenolysis. Return to competition was approximately 6 months. Although many studies in the literature have quoted high success rates, this optimism for surgical treatment must be tempered by the fact that these were retrospective analyses that often did not differentiate among the various Achilles tendon disorders. [0140] [0180] [0210] [0250] [0260] [0270] [0290] [0310] [0320]

 

Role of Ultrasound and Shock Wave Therapy

The use of extracorporeal shock wave therapy (ESWT) for the treatment of Achilles tendinitis has not been widely studied. Most information on shock wave therapy comes from research on kidney stone lithotripsy, upper extremity tendinitis, and plantar fasciitis. Shock wave therapy works by creating a pressure change that propagates rapidly through a medium. When transmitted through a water medium, it can either directly create high tension at a given structure or indirectly create microcavitations. Theories behind its analgesic effect in orthopedic applications include an alteration of the permeability of neuron cell membranes and induction of an inflammatory-mediated healing response by increasing local blood flow.[33] Studies on ESWT on Achilles tendinitis have shown a success rate of approximately 30% to 40%. [0340] [0350] In our experience, we have found a similar success rate of approximately 30% in athletes, although more severe cases are indicated for surgery. Even with this lower success rate, we try ESWT for 3 months on all patients before surgery because this treatment has minimal side effects. Depending on the immediate results, we may allow sports play with only 1 or 2 weeks off. If the athlete is in midseason, then this modality is his or her best chance to resume play. If the athlete is at the end of the season, then we may try shock wave therapy and a boot brace for 2 to 6 weeks and then allow the athlete to resume impact activities. After the season, when there is more time for recovery, decisions regarding further treatment can be made. Contraindications to ESWT quoted in the literature include pregnancy, coagulopathies, bone tumors, bone infection, and skeletal immaturity.[33]

Saggini et al.[36] noted successful outcomes after two treatments with no complications using shock wave therapy on Achilles tendinitis. Several later studies reported promising results after ESWT with those affected with chronic Achilles tendinitis. [0370] [0380] [0390] The cost of shock wave treatment can be an important consideration because the therapy may not be covered by insurance. With lower-energy shock wave machines, three treatments are used, at a cost of $500 to $800 each. One treatment (at a cost of about $1500) is the norm for the higher-energy machines. The temporary pain with this procedure is considerable and requires an ankle block or general anesthesia, which increases both the risk and the cost.

 

Acute Achilles Tendon Rupture

Although the incidence of Achilles tendon ruptures has increased over the past few decades, many still are missed on initial presentation. Achilles tendon ruptures typically occur in men in their 30s and 40s, with more than 75% of these injuries occurring during athletic participation. Most of these patients are recreational athletes. Those engaged in abrupt repetitive jumping or sprinting sports, such as basketball, football, and soccer, are particularly at risk.[40]

Sports-related injuries are most often the result of a rapid eccentric load that is applied to a tensioned tendon with ankle dorsiflexion and simultaneous knee extension. This occurs during the loading phase of a rapid push-off or sudden jump. Most ruptures occur in an area of relative hypovascularity of the Achilles tendon, 2 to 4cm proximal to the superior aspect of the calcaneus.[41] Additional risk factors include intratendinous degeneration, vascular impairment, corticosteroid or fluoroquinolone use, mechanical malalignment, and systemic disorders such as gout, hyperthyroidism, and renal insufficiency.[0400] [0410]

An athlete typically reports an audible snap and a sensation of being struck or shot from behind following a misstep or sudden jump. The player will note significant loss of push-off strength and normally will be unable to continue sports participation. Diffuse swelling, ecchymosis, and residual strength from remaining ankle plantarflexors can make diagnosing an initial injury difficult. However, findings consistent with an acute Achilles tendon rupture include a palpable tendon gap ( Fig. 7-23 ), positive Thompson test (absence of passive ankle plantarflexion with calf squeeze in prone position; Fig. 7-24 ), loss of the normal plantarflexion resting tone while prone in comparison with the unaffected side, inability to perform a single toe heel rise, and weak active plantarflexion. Although imaging generally is unnecessary in acute cases, lateral radiographs may show an avulsion fracture ( Fig. 7-25 ). MRI and ultrasound are useful in equivocal or late cases ( Fig. 7-26 ).

 

 

Figure 7-23  (A) The side with the Achilles rupture has a visible indentation (white arrow)(B) The normal side. (C) The ruptured side has a palpable defect.

 

 

 
 

Figure 7-24  A positive Thompson test in the near leg with the Achilles tendon rupture. The calf muscles are squeezed and there is an absence of passive ankle plantarflexion in the prone position.

 

 

 
 

Figure 7-25  A lateral radiograph shows an avulsion fracture in a patient with a history of retrocalcaneal bursitis. There was no history of steroid injection.

 

 

 
 

Figure 7-26  The sagittal magnetic resonance imaging shows a long, complex Achilles tear (white arrows).

 

 

Nonsurgical treatment

Although the treatment of choice for most athletes with an acute Achilles tendon rupture is surgical repair followed by early, protected range of motion and weight bearing, nonoperative treatment of Achilles ruptures using cast immobilization has some advocates. The ill effects of “cast disease” [0420] [0430] include calf atrophy and resultant muscle weakness, as well as the consequences of immobilizing joints, ligaments, and uninvolved muscles and tendons. Furthermore, nonoperative management of an Achilles tendon rupture typically does not restore the normal functional length of the tendon, and the athlete will note significant muscle weakness. Although operative management is associated with inherently potential surgical risks, including poor wound healing, infection, and nerve injury, the risks are balanced by a lower incidence of tendon rerupture rates, less than 2%, compared with 13% to 35% after nonoperative care.[42] Further, studies have demonstrated improved strength and ankle motion with a greater potential of sports resumption following surgical repair. [0420] [0440]

Nonoperative management generally is better than operative management in those with systemic disorders, such as diabetes, peripheral vascular disease, lower-extremity edema, or overlying skin conditions. However, these comorbidities are not often found in the athletic population. Following nonoperative management, a short-leg, nonweight-bearing cast in slight equinus is used for 6 weeks. This is followed by a weight-bearing cast or walking boot with progressively increased dorsiflexion.

Results similar to those of operative management have been reported for nonoperative treatment with a functional boot brace guided by ultrasound.[45] Ultrasound is used to ensure that the ends of the torn tendon remain apposed as the ankle is progressively dorsiflexed during the first 6 weeks. Additionally a successful nonoperative protocol has been reported using a functional brace to minimize the ill effects of immobilization and to shorten the time needed for rehabilitation and return to activities.[46] A more recent study found similar success with operative and nonoperative treatment in the athlete.[47]

More recent postoperative trends have focused on a functional rehabilitation program with early controlled range of motion and strengthening exercises. [0480] [0490] [0500] Early mobilization limits the dystrophic effects of prolonged cast use and has been shown to reduce tendon adhesion, improve healing, and maximize tendon strength without increasing the risk of rerupture or infection. We favor operative repair unless contraindicated.

Surgical treatment

Athletes with well-controlled systemic disorders, such as diabetes, should be considered for operative treatment. This higher-risk situation requires close attention to wound closure and postoperative management, including meticulous and frequent follow-up.

Standard technique

Acute Achilles tendon ruptures in an athlete should be treated operatively with the goal of recreating normal tendon length and tension. After positioning the patient prone, the contralateral leg is additionally prepped to help match resting ankle tension. A medial approach 1cm anterior to the Achilles tendon border avoids injury to the sural nerve and is located in relatively thick tissues, which are biomechanically better suited to provide a healthy closure farther away from the tendon ( Fig. 7-27 ). Care is taken to minimize soft-tissue handling. A Krackow-type stitch technique with nonabsorbable, no. 2 sutures is used to reapproximate the “mop end” rupture ( Fig. 7-28 ). Whenever possible, the paratenon is reapproximated to minimize scar formation and improve tendon glide. Additionally, reapproximation of the fat pad anterior to the tendon can be performed. Initially, we immobilize the leg for 10 days until the wounds have healed. The same postoperative protocol described above for tendon reconstructions is used. Return to sport for the athlete after repair is 4 to 6 months.





 

Figure 7-27  (A) An acute Achilles tendon rupture repair is performed with the patient in a prone position, (B) A medial approach made 1cm anterior to the Achilles tendon avoids injury to the sural nerve. (C) The approach is with the scalpel, avoiding blunt dissection. (D)The exposure is through relatively thick tissues, which are biomechanically better suited to provide a closure that provides a barrier to the tendon, which is 1 to 1.5cm away from the incision. (E) The exposed mop ends of the tendon.

 

 



 

Figure 7-28  (A) Another acute Achilles repair with exposure of the frayed tendon ends. (B) Care is taken to minimize soft-tissue handling. A Krackow-type stitch technique with nonabsorable, no. 2 sutures is used to reapproximate the “mop end” rupture. (C) The edges of the anastomosis should be made neat with a 2-0 or 4-0, absorbable suture. The resting tension should be restored.

 

 

Mini-open technique

To minimize the possibility of injury to the sural nerve inherent in a purely percutaneous suture technique, a mini-open approach can be used. A small stab incision is made, and then the subcutaneous soft tissue is spread bluntly before passing the suture/wire. A mini-open technique using a new instrument, the Achillon (Newdeal SA, Vienne, France), or Giannini's device (Citieffe, Calderara di Reno, Bologna, Italy), combines the advantage of direct visual repair with minimizing potential complications of wound and nerve problems. A small skin incision is made, and the Achillon or Giannini's device is introduced under the paratenon. A needle with suture is passed from the external guide through the skin into the tendon and out the opposite side. Three sutures are passed through the proximal tendon end, and three are used in the distal tendon end. The device and the suture ends are pulled out from under the paratenon and incision such that the ends of the sutures grasping the tendon now rest entirely within the paratenon. The tendon ends are reapproximated, and the sutures are tied. Assal et al.[51] reported their experience using the Achillon device in 82 patients, noting that all patients who were elite athletes were able to return to their same level of competition.

Expected results of acute surgical repair

One may expect return to sports generally at 4 to 6 months after acute repair and a program of early protected weight bearing. [0140] [0440] [0520] [0530] Cetti et al.[42] previously showed less calf atrophy and improved ability to resume preinjury level of athletic play after surgical repair as compared with nonoperative treatment. [0420] [0440] [0480] [0490] [0500] [0520] In a meta-analysis of acute Achilles tendon treatment, Bhandari et al.[54] confirmed a statistically significant reduction in rerupture rates after surgical repair (3.1%) as compared with nonoperative treatment (13%). However, infections occurred only in the surgically treated group (infection rates ranging from 4% to 20%). The proportion of patients who regained normal function was similar in the operative and nonoperative treatment groups.

In another meta-analysis, Kahn et al.[55] identified 12 suitable papers for inclusion. They found that the relative risk of rerupture was 0.27 with operative versus nonoperative treatment. Complications including infection, adhesions, and altered skin sensitivity had a relative risk of 10.6 (operative vs. nonoperative). Functional bracing postoperatively had lower complications than casting postoperatively (relative risk 1.88). They concluded that operative treatment significantly reduced the risk of rerupture but significantly increased the risk of complications.

 

Chronic Achilles Tendon Rupture

More than 20% of patients with an Achilles tendon rupture are missed on initial examination,[14] and it therefore is not uncommon to diagnose a late injury. Chronic Achilles tendon ruptures generally present for delayed diagnosis or after a failed acute repair. Chronic ruptures typically are defined as those diagnosed more than 4 to 6 weeks after initial injury.[53] After this period, the gap between the separated tendon ends fills with fibrinous material. This scar tissue contains disorganized fibroblasts and does not possess the same biomechanical strength as normal tendon. Over time, the tissue will elongate and lead to further functional weakness.[14]

Typically, a patient will complain of loss in push-off strength and be unable to perform toe walking and repetitive heel rise. When the patient lies prone, the injured extremity will demonstrate less resting plantarflexion tone as compared with the contralateral ankle. The involved ankle will display a relative increase in passive dorsiflexion and significantly less plantarflexion with calf squeeze. A palpable tendon gap is not typically evident, but the contour of the tissues will be altered, with thickening and loss of defined margins. The appearance of the affected calf muscle can be different from the contralateral side. Often the muscle belly is more proximally situated (“balled up”) as a result of its detachment distally. MRI and possibly ultrasound evaluation are useful in evaluating the size of the tendon gap and assist in surgical planning.

Nonsurgical treatment

Nonoperative management may be considered in those without functional deficits or potentially high-risk patients, but surgical management is the treatment of choice for the athlete.

Surgical treatment

Operative reconstruction generally will restore optimal musculotendinous length and improve strength and endurance. Direct repair often is not possible because of the relative immobility of the separated tendon ends with associated muscular retraction and atrophy. The size of the gap after debridement of interposed scar tissue determines whether a repair or reconstruction should be done and also determines which type of reconstruction should be done.

If the delayed diagnosis is made within 4 to 6 weeks of injury, we perform tendon end debridement. We then mobilize the tendon by applying tension, holding the tendon in a stretched position for 10 minutes, and attempt a direct repair. After the tendon apposition, if it appears that the repair is too tight, we do a V-Y lengthening proximally to adjust the tension.

After 6 to 12 weeks postinjury, it is not likely that the tendon ends can be mobilized sufficiently for direct repair with proper tension. If the gap is between 1 and 3cm after debridement and mobilization, a V-Y procedure can be performed (see Fig. 7-14 ). To perform the V-Y advancement, a direct reapproximation is performed using a no. 2, nonabsorbable suture in a Krackow or whipstitch. This allows further ability to stretch out the tendon. If reapproximating the tendon ends results in too much tension, we then proceed with the V-Y advancement. We allow the V-Y gap distance to reduce the contraction and restore proper tension as compared with the contralateral side.

For more chronic cases seen more than 12 weeks after a missed rupture or after a previous completely failed repair, a V-Y advancement or turndown likely will be required, depending on the size of the defect after repair. For defects between 2 and 3cm, a V-Y advancement is possible, as mentioned previously. For defects longer than 3 to 5cm, a turndown procedure with possible tendon augmentation is required, as discussed earlier (see Fig. 7-15 ).

For those cases with preoperative atrophy of the gastrocnemius/soleus muscle, an FHL tendon transfer may be considered (see Figs. 7-12 and 7-13 [0120] [0130]). The FHL can be harvested from the posterior ankle in the depths of the posterior approach ( Fig. 7-29, A ) to the Achilles, or, if a longer graft is felt to be advantageous, from the arch of the foot. The graft harvest can be performed through a medial approach just plantar to the posterior tibial tendon and the talonavicular joint ( Fig. 7-29, B ) or through the plantar aspect through the plantar fascia ( Fig. 7-29, C ). For the latter approach, once the incision is made through the plantar fascia, care is taken to avoid the medial plantar nerve. The FHL and FDL tendons can be found in the depth of the wound next to the first metatarsal and medial cuneiform. Once the tendons have been identified, the FHL is sutured to the FDL distal to the point at which the tendon will be transected (at or near the knot of Henry). A suture placed in the FHL proximal to the transection is helpful in case the tendon does not pull through into the proximal wound.

 

 

Figure 7-29  (A) The flexor hallucis longus (FHL) can be harvested from the posterior ankle in the depths of the posterior approach to the Achilles. (B) The graft harvest through a medial approach just plantar to the posterior tibial tendon and the talonavicular joint. (C) The graft harvest through the plantar aspect of the foot. After incising the plantar fascia and reflecting the medial plantar nerve, the FHL and flexor digitorum longus (FDL) tendons can be found next to the bones. The FHL is sutured to the FDL distal to where the tendon will be transected. Next, the FHL is cut proximal to the tenodesis and withdrawn out the proximal ankle incision.

 

 

Den Hartog[56] described a technique of harvesting the FHL tendon near the tip of the medial malleolus for chronic Achilles tendinosis. Good to excellent results were reported in 23 of 26 treated patients without any deficit to first-toe function. A recent biomechanical study showed little pressure change under the first or second metatarsophalangeal (MTP) joint and no clinical functional deficit after FHL harvesting.[57] Prior studies also showed promising clinical results. [0580] [0590]

 

Conclusion

Achilles tendon disorders are common in the athlete. If diagnosed early, the process usually is a tendinitis and is amenable to nonoperative treatment such as intermittent immobilization, stretching, modalities such as ultrasound and iontophoresis, and use of anti-inflammatoriy medication. More chronic cases take longer to treat and have a higher risk of requiring operative intervention. Operative treatment typically is 70% to 90% successful but requires 3 to 6 months for return to athletic participation. Achilles rupture typically will require operative treatment in the athlete, and 6 to 9 months can be a typical recovery period.

 

References

  1. Clain MR, Baxter DE: Achilles tendinitis.  Foot Ankle Int1992; 13:482.
  2. Haglund P: Beitrag zur Klinik der Achillessehne.  Z Orthop Chir1997; 49:49.
  3. Burdett RG: Forces predicted at the ankle during running.  Med Sci Sports Exerc1982; 14:308.
  4. Scott SH, Winter DA: Internal forces of chronic running injury sites.  Med Sci Sports Exerc1990; 22:357.
  5. Carr AJ, Norris SH: The blood supply of the calcaneal tendon.  J Bone Joint Surg1989; 71B:100.
  6. Langergren C, Lindholm A: Vascular distribution in the Achilles tendon: an angiographic and microangiographic study.  Acta Chir Scand1959; 116:491.
  7. Clancy WG, Neidhart D, Brand RL: Achilles tendonitis in runners: a report of five cases.  Am J Sports Med1976; 4:46.
  8. Clement DB, Taunton JE, Smart GW: Achilles tendonitis and peritendinitis: etiology and treatment.  Am J Sports Med1984; 12:179.
  9. Krissoff WB, Ferris WD: Runner's injuries.  Physician Sportsmed1979; 7(12):54.
  10. Puddu G, Ippolito E, Postacchini F: A classification of Achilles tendon disease.  Am J Sports Med1976; 4:145.
  11. McGonagle D, et al: Enthesitis in spondyloarthropathy.  Curr Opin Rheumatol1999; 11:244.
  12. Myerson MS, McGarvey W: Disorders of the Achilles tendon insertion and Achilles tendonitis.  Instructional Course Lectures1999; 48:211.
  13. Marks RM: Achilles' tendinopathy.  Foot Ankle Clin1999; 4:789.
  14. Schepsis AA, Jones H, Haas AL: Achilles tendon disorders in athletes.  Am J Sports Med2002; 30:287.
  15. Fredberg U: Local corticosteroid injection in sport: review of literature and guidelines for treatment.  Scand J Med Sci Sports1997; 7:131.
  16. Paavola M, et al: Treatment of tendon disorders. Is there a role for corticosteroid injection?.  Foot Ankle Clin2002; 7:501.
  17. Shrier I, Matheson GO, Kohl 3rd HW: Achilles tendonitis: are corticosteroid injections useful or harmful?.  Clin J Sport Med1996; 6:245.
  18. Johnston E, Scranton Jr P, Pfeffer GB: Chronic disorders of the Achilles tendon: results of conservative and surgical treatments.  Foot Ankle Int1997; 18:570.
  19. Angermann P, Hovgaard D: Chronic Achilles tendinopathy in athletic individuals: results of nonsurgical treatment.  Foot Ankle Int1999; 20:304.
  20. Gerken AP, McGarvey WC, Baxter DE: Insertional Achilles tendonitis.  Foot Ankle Clin North Am1996; 1(112):237.
  21. McGarvey WC, et al: Insertional Achilles tendinosis: surgical treatment through a central tendon splitting approach.  Foot Ankle Int2002; 23:19.
  22. Paavola M, et al: Long-term prognosis of patients with Achilles tendinopathy. An observational 8-year follow-up study.  Am J Sports Med2000; 28:634.
  23. Maffulli N, et al: Results of percutaneous longitudinal tenotomy for Achilles tendinopathy in middle- and long-distance runners.  Am J Sports Med1997; 25:835.
  24. Kolodziej P, Glisson RR, Nunley JA: Risk of avulsion of the Achilles tendon after partial excision for treatment of insertional tendonitis and Haglund's deformity: a biomechanical study.  Foot Ankle Int1999; 20:433.
  25. Jones DC, James SL: Partial calcaneal ostectomy for retrocalcaneal bursitis.  Am J Sports Med1984; 12:72.
  26. Schepsis AA, Wagner C, Leach RE: Surgical management of Achilles tendon overuse injuries. A long-term follow-up study.  Am J Sports Med1994; 22:611.
  27. Schneider W, Niehus W, Knahr K: Haglund's syndrome: disappointing results following surgery—a clinical and radiographic analysis.  Foot Ankle Int2000; 21:26.
  28. Watson AD, Anderson RB, Davis H: Comparison of results of retrocalcaneal decompression for retrocalcaneal bursitis and insertional Achilles tendinosis with calcific spur.  Foot Ankle Int2000; 21:638.
  29. Leach RE, Schepsis AA, Takai H: Long-term results of surgical management of Achilles tendonitis in runners.  Clin Orthop Relat Res1992; 282:208.
  30. Saxena A: Results of chronic Achilles tendinopathy surgery on elite and nonelite track athletes.  Foot Ankle Int2003; 24:712.
  31. Schepsis AA, Leach RE: Surgical management of Achilles tendinitis.  Am J Sports Med1987; 15:308.
  32. Tallon C, et al: Outcome of surgery for chronic Achilles tendinopathy. A critical review.  Am J Sports Med2001; 29:315.
  33. Chung B, Wiley JP: Extracorporeal shockwave therapy: a review.  Sports Med2002; 32:851.
  34. Heller KD, Niethard FU: [Using extracorporeal shockwave therapy in orthopedics—a meta-analysis].  Z Orthop Ihre Grenzgeb1998; 136:390.
  35. Kvist M, et al: Chronic Achilles paratenonitis in athletes: a histological and histochemical study.  Pathology1987; 19(1):1.
  36. Saggini R, et al: Experimental study of shock wave therapy on Achilles tendonitis to investigate treatment parameters,  2000.
  37. De Pretto M, et al: A retrospective multi-centre experience report of shock wave therapy on Achilles tendonitis,  2000.
  38. Galasso O, et al: Chronic achillodynia,  2000.
  39. Ogden JA, Cross GL: Application of electrohydraulic orthotripsy for chronic Achilles tendinopathy,  2003.
  40. Title CI, Katchis SD: Traumatic foot and ankle injuries in the athlete.  Orthop Clin North Am2002; 33:587.
  41. Thermann H: Treatment of Achilles' tendon ruptures.  Foot Ankle Clin1999; 4:773.
  42. Cetti R, et al: Operative versus nonoperative treatment of Achilles tendon rupture. A prospective randomized study and review of the literature.  Am J Sports Med1993; 21:791.
  43. Soma CA, Mandelbaum BR: Achilles tendon disorders.  Clin Sports Med1994; 13:811.
  44. Mandelbaum BR, Myerson MS, Forster R: Achilles tendon ruptures. A new method of repair, early range of motion, and functional rehabilitation.  Am J Sports Med1995; 23:392.
  45. Thermann H, Zwipp H, Tscherne H: [Functional treatment concept of acute rupture of the Achilles tendon. 2 years results of a prospective randomized study].  Unfallchirurg1995; 98(1):21.
  46. McComis GP, Nawoczenski DA, DeHaven KE: Functional bracing for rupture of the Achilles tendon. Clinical results and analysis of ground-reaction forces and temporal data.  J Bone Joint Surg1997; 79-A:1799.
  47. Weber M, et al: Nonoperative treatment of acute rupture of the Achilles tendon: results of a new protocol and comparison with operative treatment.  Am J Sports Med2003; 31:685.
  48. Mortensen HM, Skov O, Jensen PE: Early motion of the ankle after operative treatment of a rupture of the Achilles tendon. A prospective, randomized clinical and radiographic study.  J Bone Joint Surg Am1999; 81:983.
  49. Solveborn SA, Moberg A: Immediate free ankle motion after surgical repair of acute Achilles tendon ruptures.  Am J Sports Med1994; 22:607.
  50. Speck M, Klaue K: Early full weightbearing and functional treatment after surgical repair of acute Achilles tendon rupture.  Am J Sports Med1998; 26:789.
  51. Assal M, et al: Limited open repair of Achilles tendon ruptures: a technique with a new instrument and findings of a prospective multicenter study.  J Bone Joint Surg Am2002; 84-A:161.
  52. Maffulli N: Rupture of the Achilles tendon. Current concepts review.  J Bone Joint Surg1999; 81A:1019.
  53. Myerson MS: Achilles tendon ruptures.  Instructional Course Lectures1999; 48:219.
  54. Bhandari M, et al: Treatment of acute Achilles tendon ruptures: a systematic overview and metaanalysis.  Clin Orthop2002; 400:190.Jul
  55. Kahn RJ, et al: Treatment of acute Achilles tendon ruptures: a meta-analysis of randomized, controlled trials.  J Bone Joint Surg Am2005; 87-A:2202.
  56. Den Hartog BD: Flexor hallucis longus transfer for chronic Achilles tendinosis.  Foot Ankle Int2003; 24:233.
  57. Coull R, Flavin R, Stephens MM: Flexor hallucis longus tendon transfer: evaluation of postoperative morbidity.  Foot Ankle Int2003; 24:931.
  58. Wapner KL, et al: Repair of chronic Achilles tendon rupture with flexor hallucis longus tendon transfer.  Foot Ankle1993; 14:443.
  59. Wilcox DK, Bohay DR, Anderson JG: Treatment of chronic Achilles tendon disorders with flexor hallucis longus tendon transfer/augmentation.  Foot Ankle Int2000; 21:1004.