The Achilles tendon complex is composed of contributions from the gastrocnemius, soleus, and plantaris (collectively known as the triceps surae) and inserts directly into the central third of the posterior calcaneal surface. The tendon is round in cross section to a level 4 cm proximal to calcaneus, where it flattens and rotates 90° so that its medial fibers insert posteriorly. This biomechanical “winding” of the fibers increases stored energy for higher shortening velocity and muscle power.1

During dorsiflexion, the tendon articulates with the superior third of the calcaneus. This articulation is cushioned by the retrocalcaneal bursa, which lies between the tendon and the superior third of the calcaneus.

The Achilles tendon does not possess a true synovial sheath. The peritendinous structures of the Achilles are composed of a triple-layered tissue.² The superficial layer of tissue is the most durable and is analogous to the deep fascia. This layer comprises the posterior boundary of the superficial posterior compartment. The middle layer, the mesotendon, provides the major blood supply for the central portion of the Achilles tendon. The deepest layer of tissue is quite delicate and thin; however, it can always be isolated from the most superficial layer of the tendon, the epitenon.

The Achilles tendon is supplied with blood and nutrients by three different sources.² The most abundant supply is at the proximal and distal portions of the tendon, and the poorest is in the central portion of the tendon. As originally demonstrated by Lagerrgren and Lindholm³ and corroborated by others,^4,5 a gradual decrease occurs in the number of blood vessels in the central part of the tendon 2 to 6 cm proximal to the calcaneal insertion (Fig. 31-1).

Nutrient branches emanate directly from the muscle to nourish the distal gastrocnemius aponeurosis and proximal portion of the tendon.⁶ The insertion of the Achilles tendon is supplied by anastomotic branches between the periosteal vessels and the tendon vessels. As already noted, the major blood supply comes from the mesotendon. Vessels enter the tendon itself via a network of fine connections with the deepest peritendinous layer. These vessels come off the deepest layer radially and enter the tendon perpendicular to its long axis. They then course proximally and distally. Because of the external forces that may be encountered by the posterior aspect of the tendon as a result of friction supplied by the skin, most of these fine vessels are found along the anterior aspect of the tendon, where they are afforded more protection (Fig. 31-2).

The theoretic explanation for tendon injuries suggests a continuum of events, including hypovascularity and repetitive microtrauma, that results in localized tendon degeneration and weakness and ultimately rupture with the application of an otherwise normal load that exceeds the tendon’s physiologic capacity. Based on clinical and histologic findings, the traditional description of Achilles tendonitis is not preferred,7 and Achilles tendon pathology is classified into three different categories: (1) paratendinitis, (2) paratendinitis with tendinosis, and (3) pure tendinosis.^8–10

Paratendinitis involves inflammation only in the paratenon, regardless of whether it is lined by synovium. The paratenon thickens, and adhesions may form between the paratenon and the tendon.¹¹ However, patients will rarely have isolated paratendinitis, and some authors believe that this process is the predecessor to tendinosis.⁷

Paratendinitis with tendinosis involves not only inflammation of the paratenon but also a degenerative change within the substance of the tendon. Paddu, Ippolito, and Postacchini¹⁰ and Kvist and Kvist¹¹ have noted thickening, softening, and yellowing of the tendon, as well as cleavage planes and vascular budding during surgery for this condition. As in tendinitis, pain also is commonly noted because of the inflammatory process.

Pure tendinosis often appears as a nodule that is mobile with plantar flexion.⁷ It can present as a chronic nodule in the sedentary middle-aged person or as a contribution to the pathology of rupture in the tendons of persons older than 35 years who have suffered spontaneous rupture.¹² Histopathologic changes such as hypoxic and mucoid degeneration, lipomatous infiltration, and calcifying tendinopathy have been noted at the time of surgical repair of acute ruptures.^10,12

Hippocrates was the first to record an injury to the Achilles tendon, while Ambrose Pare was the first to describe Achilles tendon ruptures in 1575, and Gustave Paoaillon was the first to report operative repair of the tendon.^1,2,13 Theories implicating the degenerative changes that take place in the Achilles tendon with the increased mechanical loads associated with various activities are the most common explanations of the pathogenesis of these ruptures.^13,14 A combination of hypovascularity and repetitive microtrauma results in degenerative changes and inflammation, putting the tendon at risk for rupture. Healing and regeneration are hindered or halted because of poor blood supply to the tendon and recurrent microtrauma. Alfredson, Thorsen, and Lorentzon¹⁵ have shown that microtears in the tendon lead to areas of chronic damage that lack normal levels of prostaglandin E2, which are needed for healing. The combination of these factors may account for the fact that most ruptures occur 2 to 6 cm proximal to the tendon’s insertion into the calcaneus. Associated intrinsic factors include age (which leads to decreased vascularity and decreased deoxyribonucleic acid [DNA] synthesis),^16–18 endocrine function, and nutrition.¹⁹ Extrinsic factors of compression and friction on the posterior aspect of the tendon (from the skin and inappropriately compressive footwear) further hinder vascularity, healing, and regeneration. Fluoroquinolone antibiotics are also associated with Achilles tendon rupture. Their use inhibits transcription of decorin, a protein important in collagen architecture, and the odds ratio for tendon rupture in patients taking the medication is 4.2.²⁰ Acute Achilles ruptures are also often the result of corticosteroid injection for chronic inflammation of the tendon.⁷

Normally, tendons are able to tolerate high forces associated with daily activities and athletics. However, if degenerative changes take place, then the mechanical load usually tolerated may exceed the tendon’s physiologic capacity. Mechanically, a tendon may be damaged or ruptured by a sudden application of force. This often involves a forceful lengthening or eccentric muscle contraction. Sudden maximal muscle activation results in a larger than normal force that is applied rapidly to the tendon, causing the rupture. The high load forces that cause such rupture are usually associated with vigorous activities such as sports. The forces to which the Achilles tendon is exposed during activities such as running and jumping have been calculated to be between 4000 and 5500 N^21–23; they are summarized in Fig. 31-3.¹⁹ Arner and Lindholm²⁴ describe three activities that can rupture a tendon:

Curwin¹⁹ best summarized the possible progression of tendon injury (Fig. 31-4).

Although spontaneous tendon ruptures are rare, the Achilles tendon appears to be the one that is most frequently ruptured. Kannus and Jozsa12 report that 44.6% (397 out of 891) of tendon ruptures treated surgically between 1968 and 1989 involved the Achilles tendon, whereas the biceps brachii accounted for 33.9%. Achilles tendon ruptures are usually traumatic and occur between the ages of 30 and 40 years,^25–27 which is younger than for other tendon ruptures (Fig. 31-5).

Most ruptures are suffered by recreational athletes rather than highly competitive, very active athletes. Of the 105 patients with Achilles ruptures described by Nistor,²⁸ only 9 participated in competitive sports. Of the remaining patients, 35 exercised twice a week, 41 once a week, 20 took walks and occasionally exercised, and two were physically inactive. Of the 111 patients who ruptured their Achilles tendon while participating in a sports activity in Cetti and colleagues’ report,²⁶ 92 (83%) averaged only 3.6 hours of athletic activity per week. Of the 292 Achilles tendon ruptures documented by Jozsa and associates,²⁷ 59% occurred during recreational athletic activity—141 of these (83.2%) in men and 29 (16.8%) in women. No patients in this study by Jozsa and colleagues participated in competitive athletics. In their study, more than 625 of the Achilles tendon ruptures occurred in professional or white collar workers who tended to have generally sedentary lifestyles except when involved in sports. A review of numerous studies demonstrates that athletic activities that require sudden acceleration or deceleration are most likely to cause a rupture (Table 31-1). Ruptures not attributed to athletic activity are usually caused by falls or stumbles that also produce sudden acceleration and deceleration movements. Overall, Achilles tendon ruptures have been demonstrated to be more common in men than in women. Ratios of 2 : 1,²⁹ 4 : 1,³⁰ 1.6 : 1,³¹ 8.7 : 1,²⁸ 10 : 1,²⁵ and 12 : 1¹⁰ have been reported.

In most situations the history is diagnostic. Patients describe hearing a pop as though someone had shot them in the back of the ankle. Prodromal symptoms of Achilles aching have been reported in 5% to 30% of cases.12,32 The rupture commonly occurs in the “watershed area,” between 2 and 6 cm proximal to the calcaneus.³ Avulsion fractures of the calcaneus are relatively uncommon.⁴ A careful history and physical examination are important because it has been shown that 22% of primary care physicians miss the diagnosis of acute Achilles rupture.²⁶ The physical examination is characterized by palpation of the defect and documentation by Thompson test,³³ which indicates discontinuity and loss of plantar flexion when the calf is squeezed. The Thompson test is performed by asking the patient to kneel on a chair with the feet hanging over the edge and the calf muscles relaxed. In this prone position, the examiner can usually denote a difference in resting angle from the contralateral side. Radiographic evaluation rules out the presence of a bony injury. Magnetic resonance imaging (MRI) can be helpful in demonstrating the presence, location, and severity of tears of the Achilles tendon. MRI also is helpful in assessing the status of an Achilles tendon repair.³⁴ Ultrasonography has been used to define Achilles tendon discontinuity³⁵ in countries where MRI is not routinely used. No one clinical test has been shown to be superior; however, a combination of a complete history and physical examination along with radiographic studies (if necessary) will lead to an accurate diagnosis.³⁶

After an accurate diagnosis is made, a definitive physical therapy and rehabilitation program can be implemented by establishing the objectives for management. If any questions remain regarding the diagnosis or severity of the tear, then MRI and ultrasonography can be used to enhance diagnostic accuracy. The physical therapist (PT) should define the patient’s functional and athletic goals, personal needs, and temporal priorities before making therapeutic judgments.

Treatment for Achilles tendon ruptures was nonoperative until the twentieth century. It included immobilization with strapping, wrapping, and braces for varying periods of time.37 In 1929 Quenu and Stoianovitch³⁸ stated that a rupture of the Achilles tendon should be operated on without delay. Christensen³⁰ (1953) and Arner, Lindholm, and Orell⁴ (1958) compared patients treated surgically and those managed nonoperatively; the surgical group had better results. As the field of sports medicine progressed with new surgical techniques, including rigid internal fixation combined with rehabilitation, the optimal treatment for Achilles tendon rupture became controversial. Some studies supported nonoperative management of Achilles ruptures,^28,39 as shown in the following editorial statement made in 1973: “In view of the excellent results obtainable by conservative treatment, it is doubtful whether surgical repair in closed rupture of the Achilles tendon can be justified.⁴⁰” In an updated meta-analysis of reports on Achilles tendon injury, Khan and associates⁴¹ found that open operative treatment of acute Achilles tendon ruptures significantly reduces the risk of rerupture compared with nonoperative treatment, but it produces a significantly higher risk of other complications, including wound infection. Significance varied among studies included. In total, reruptures in the operative groups were 3.5% vsersus 12.5% in the nonoperative groups. Rates for other complications (infection, adhesions, disruptions in sensation) in the operative groups were 34% versus 2.7% in the nonoperative groups.

In 2003, Weber and colleagues⁴² compared the results of acute ruptures in 23 patients treated nonoperatively to 24 patients treated operatively. Patients in the nonoperative group were allowed full weight bearing in 20° patellofemoral casts for 6 weeks and were verified with weekly ultrasonography and cast changes. Patients in the operative group were placed in casts and were non–weight bearing for 6 weeks with variable rehabilitation protocols. The results showed a decreased return to work and crutch time for nonoperative cases, with 4 of 23 reruptures at 7 to 12 weeks. Patients in the operative group had only 1 of 24 reruptures at 3 years. This study demonstrates that nonoperative treatment may be acceptable for some patient populations, but that operative treatment, even with traditional postoperative immobilization, yields a lower rerupture rate. The surgeon must explore the goals and expectations of the patient and decide which treatment is most appropriate. Indications for nonoperative treatment include concomitant illness in the patient, a sedentary lifestyle, or lower functional and athletic goals.

Early nonoperative options were well accepted and tolerated. But in the past 20 years, patient expectations and functional goals have increased so that surgical options have gained acceptance and preference.

Less invasive surgical procedures were first noted in the literature by Ma and Griffith.⁴³ A lower overall rate of complications (particularly infection) in the percutaneously treated group has been noted.^41,44,45 Studies comparing open versus percutaneous techniques have a relatively small number of subjects, limiting their reliability.

The patient selected for operative repair should be an individual who is extremely interested in optimal functional restoration.

In 2010 the American Academy of Orthopaedic Surgeons published guidelines on the treatment of acute Achilles tendon ruptures. A meta-analysis of all existing literature showed similar outcomes in operative and nonoperative treatment. The study demonstrated two moderate-strength recommendations that included suggestions for early postoperative protective weight bearing and for the use of protective devices that allow for postoperative mobilization in those patients who have surgical treatment.³⁶

Functional postoperative treatment programs, regardless of surgical technique, avoid cast immobilization and are well tolerated, safe, and effective with well-motivated athletes and patients who especially desire the highest functional outcome.^13,46–50

In the last century, the literature has proposed numerous approaches to the management of acute Achilles tendon ruptures. The most important design principles of the option selected should include the following:

The categorical options for the surgical treatment of acute Achilles tendon rupture include repair, repair with augmentation, and reconstruction.

The rationale for any repair method is to restore continuity of the ruptured tendon end, facilitate healing, and restore muscle function. The technical difficulty is taking relative “mop ends” and opposing them in a stable fashion. Bunnell51 and Kessler⁵² were the first to popularize the end-to-end suture technique for ruptured tendons. Ma and Griffith⁴³ described a percutaneous repair in 1977; however, a higher rerupture rate also occurred in their series. Beskin²⁵ introduced the three-bundle suture, and Cetti⁴⁶ demonstrated the suture weave in 1988, which was further modified by Mortensen and Saether⁵³ in 1991 as a six-strand suture technique. Nada⁵⁴ described the use of external fixation for Achilles tendon ruptures in 1985. Richardson, Reitman, and Wilson⁵⁵ described good results using a pull-out wire, which has the advantage of minimal suture reaction but requires a second procedure for suture removal. More recently, a commercial device has become available that allows for the percutaneous passing of a suture to repair a rupture through a minimally invasive incision. Jung and colleagues evaluated 30 patients with limited open repair for Achilles tendon rupture using a commercial device with an average 18 months follow-up and found that 16 patients were very satisfied, 11 were satisfied, and 3 were dissatisfied.⁵⁶

Each of these techniques has advantages and disadvantages, hence the wide spectrum of options. The surgeon’s selection of a method should be based on technical training, an accurate pathoanatomic diagnosis, and the patient’s goals and desires.

Historically, augmentation procedures evolved to supplement the repair construct of mop ends plus suture. Most augmentation procedures involved the local use of gastrocnemius fascia flaps or the plantaris tendon if available. Christensen30 described the use of the gastrocnemius aponeurosis flap to augment Achilles tendon repair in 1981. Silfverskiold⁵⁷ described a central rotation gastrocnemius flap, and Lindholm⁵⁸ devised a method of two turndown flaps. Lynn⁵⁹ used the plantaris tendon, fanning it out to use the membrane to reinforce the repair. Kirschembaum and Kellman⁶⁰ modified the technique in 1980 by placing the fascial flaps centrally rather than separating them. Chen and Wertheimer⁶¹ demonstrated the use of suture anchors distally at the calcaneus to repair the gastrocnemius turndown flap with semirigid fixation. Overall, these methods can facilitate the continuity and strength of the repair construct when doubt persists concerning the repair’s integrity. In practice these techniques are applied only in limited situations, but they should still be in the surgeon’s armamentarium.

Acute ruptures are usually managed with the repair techniques already described with or without augmentation. Usually these are appropriate to promote continuity and healing of acute ruptures. Neglected, chronic ruptures, however, require reconstruction with endogenous or exogenous materials. Endogenous materials include fascia lata,62 peroneus brevis transfer,⁶³ flexor digitorum longus,⁶⁴ and flexor hallucis longus.⁶⁵ Exogenous materials include carbon fiber,⁶⁶ Marlex mesh,⁶⁷ Dacron vascular grafts,⁴⁹ polylactic acid implant, and a polypropylene braid.⁶⁸ Once again, the surgeon must be familiar with these procedures and understand their advantages and disadvantages before applying them in appropriate scenarios.

Prolonged cast immobilization has been used with both operative and nonoperative treatment of Achilles tendon ruptures. Although cast immobilization may promote healing, it also promotes one or more of the following manifestations of “cast disease69,70”:

Immobilization after tendon surgery was considered the single factor most responsible for postsurgical complications as long ago as 1954.^24,30,43 Various clinical studies in the literature document residual isokinetic strength deficits between 10% and 16% after cast immobilization of Achilles tendon injuries, regardless of whether they were managed operatively or nonoperatively.^9,28,71–73

The AO Group of Switzerland found that stable and rigid internal fixation of bone fractures allows early range of motion (ROM) and maximal rehabilitation, thus minimizing atrophy and the manifestations of cast disease. This principle indicates that early mobilization of tendon ruptures should be promoted as long as stable fixation is ensured. In support of this concept, it has been demonstrated that early motion limits atrophy,⁷⁴ promotes fiber polymerization to collagen,⁷⁵ and increases the organization of collagen at the repair site, leading to increased strength.^76–79 Krackow, Thomas, and Jones⁸⁰ initially described a suture technique that allows “rigid” internal fixation without tendon necrosis. This technique, coupled with complete repair of the peritenon, should result in progressive and successful healing of the Achilles tendon rupture without postoperative cast immobilization.

Mandelbaum, Myerson, and Forster¹³ reported on the successful use of the Krackow modified suture technique in a series of 29 athletes with acute Achilles tendon rupture. Postoperatively the patients were not rigidly immobilized and were started on early ROM and conditioning programs. No patients in this series experienced rerupture, persistent pain, frank infection, or skin necrosis as a complication. By 6 weeks after surgery, 90% of patients had full ROM. By 6 months, 92% had returned to sports participation; strength deficits were less than 3% on isokinetic testing. Rigid internal fixation of Achilles tendon tears allowed a more functional rehabilitation process in this series, including early motion and weight bearing. Maffulli and colleagues,³² who reported on the operative results of 42 patients who were randomized to a traditional protocol of postoperative immobilization or a full weight bearing protocol, strengthened these results. In the full weight-bearing group, patients were placed in a full weight-bearing cast for 2 weeks, then a full weight-bearing dorsiflexion splint for 4 weeks. In the traditional protocol, the patients were immobilized in a cast for 4 weeks, then a full weight bearing cast for 2 more weeks. They found that the full weight-bearing group had no crutch use at 1.5 weeks, a quicker return to work, less calf atrophy, greater patient satisfaction, less patient visits, and isometric strength equal to the traditional group.³² This method of accelerated but controlled postoperative management has proven to be safe and highly effective at returning the athlete and patient to activities of daily living (ADLs) and sports with the highest level of function.^13,14,81

Surgery is performed with the patient in the prone position under general, regional, or local anesthesia. Care should be taken to note the resting tension of the opposite foot. To be most accurate, both feet can be prepped to allow accurate side-to-side comparison of tendon length. Either a straight midline or an anteromedial incision is made just medial to the gastrocnemius. A direct incision is made through the peritenon, which is split and tagged. Before repair of the tendon, any adhesions between the anterior surface of the muscle and tendon unit and the paratenon are removed. A relaxing incision in the anterior surface of the paratenon is made down to the muscle of the flexor hallucis longus, which will facilitate closure of the paratenon. Each end of the tear is sewn with a No. 2 nonabsorbable suture using the Krackow suture technique (Fig. 31-6). The recently introduced synthetic, polyethylene sutures such as Fiberwire^* or Orthocord^† are now commonly used for the repair and have been shown to have superior strength to traditional braided sutures.⁸² The sutures are tensioned appropriately to achieve the same resting angle as the contralateral extremity. If any doubt exists regarding the amount of tension, then the contralateral side may be used for comparison. The suture knots are passed to the anterior aspect of the tendon and secured. The peritenon is then closed anatomically with 4-0 absorbable suture. The ankle is taken through a ROM to evaluate the stability of the repair construct. The wound is closed with dermal mattress sutures, with the knots based on the medial side to protect the tendon; a posterior splint is applied. On the second day after surgery, the splint is removed and the ankle is taken gently through active range of motion (AROM). Gentle ROM exercises are begun. The sutures are removed by about day 14, and a progressive weight-bearing program is initiated using a walker boot.

The major complication with nonoperative treatment is a higher rerupture rate and an incomplete return of function and performance. Complications associated with the surgical technique include infection, anesthetic problems, rerupture, deep vein thrombosis, and an incomplete return of function. Infection can be a disastrous complication because soft tissue coverage is a major problem and can only be resolved with vascularized flaps and a reconstructive tendon procedure.88

The use of early motion during postoperative rehabilitation requires the PT to have a working knowledge of the process of tissue healing. With this knowledge, the therapist can apply appropriate amounts of stress at the correct times, progressing the rehabilitation program at an optimal pace and ensuring a good clinical outcome. Extensive summaries by Leadbetter,89 Curwin,¹⁹ and Curwin and Stanish²² fully describe tendon physiology and healing.

Fig. 31-7 summarizes the stages of the healing process and the implications they have for traditional postoperative management of Achilles tendon repairs and motion in the early postoperative period. Tendon healing occurs in four consecutive, related phases, with somewhat overlapping time frames.