Achilles Tendon Injuries

Terminology, Pathology, and Etiology

Pathologic changes occur at the insertion of the Achilles tendon onto the calcaneus, the retrocalcaneal bursa, and the midportion of the Achilles. Since the Achilles tendon is a relatively avascular structure, it is relatively resistant to an inflammatory response, making the term Achilles tendinitis generally inappropriate. Besides tendinitis, others terms used include tenosynovitis, tendinosis, paratenonitis, tendinopathy , and peritendinopathy , leaving the reader with significant confusion as to what topic different authors are addressing. In an effort to minimize confusion we prefer to use the term Achilles tendon disorder or dysfunction as described by van Dijk as a global descriptive term. Table 37-1 provides an overview of each Achilles tendon disorder subgroup.

Achilles tendon disorder is often experienced by athletes who participate in impact, running, and jumping sports. Distance runners are particularly at risk. Direct correlation between injuries and the intensity level of a training program has been reported. Clancy concluded that Achilles tendon disorder develops from microtears in the tendon that eventually progress to macroscopic tears without treatment. The incidence of injuries involving the Achilles tendon in athletes varies from 11% to 18%. The common etiologic factor appears to be repetitive impact loading associated with running and jumping. This increased activity can create forces across the Achilles tendon as high as 10 times body weight and vary from 2000 to 7000 N. In athletes, etiology of Achilles tendon dysfunction can be associated with overuse syndromes, postural problems (e.g., pronation, forefoot varus, cavus deformity), surface-related injuries (e.g., training on uneven or excessively hard ground, running on a crowned road bed or slanted surface), training errors (e.g., sudden increase in duration, intensity, or distance), poor footwear (e.g., poor construction, worn-out shoes), or an underlying inflammatory arthropathy. Lagas et al found that in runners, those who had a previous history of Achilles tendon dysfunction and followed a regimented training program were at increased risk of developing an Achilles tendon disorder.

While Achilles tendon disorders are frequently referred to in an athletic patient population, dysfunction and ruptures also occur in sedentary individuals. Holmes and Lin found that obesity, hypertension, and steroid use (including oral contraceptives and hormone replacement therapy) were linked to a higher incidence of Achilles tendon dysfunction. When these risk factors are coupled with the aging process and other extrinsic stresses, degeneration, and possibly rupture, can occur even in a sedentary individual.

An overuse syndrome can develop from accumulated microtrauma with serial impact loading during sports, training, or work. Overuse and/or overload are considered to be the primary etiologic factors in Achilles tendon pathology, but the exact etiology and pathogenesis have never been scientifically proven. At least one study found no correlation between the extent of physical activity and the histopathology, suggesting that activity may be the provocateur of the pain rather than the root cause. Lorimer et al proposed a mechanism of tensile loading, shearing, or hyperthermia ( Fig. 37-1 ). These mechanisms produce an uneven loading distribution that can lead to tissue degeneration. These areas of degeneration can lead to scar formation, which is weaker than the native “normal” tendon. If not given time to heal and remodel, the area of scarring will continue to degenerate, which causes a further mismatch of stress and strain distribution throughout the tendon. This process will cycle and therefore cause increased tendon dysfunction.

An aging tendon associated with poor vascularity is also at risk for degeneration and eventual rupture. However, recent studies have questioned the role of hypovascularity in Achilles tendon dysfunction after observing that neovascularization occurs in chronic Achilles tendinosis, possibly in reaction to degenerative lesions. In response to the anaerobic tissue requirements in the setting of an injured tendon, there is an increase in angiogenic growth factors, which stimulates neovascularization. Injured tendons have increased levels of nitric oxide synthase (NOS) and increased collagen synthesis compared to normal tissue. While the presence of neovascularization and associated neonerves have been proposed as a possible source of pain, their role in Achilles tendon dysfunction are incompletely defined. Clearly, further research is required.

Several classification schemes have been proposed for Achilles tendon pathology. One is based on the duration of symptoms: acute with symptoms less than 2 weeks, subacute with symptoms for 3 to 6 weeks, and chronic with symptoms longer than 6 weeks. Another more comprehensive classification scheme for Achilles tendinopathy that is helpful not only in defining the problem but also in determining a rational method of treatment is that of Clain and Baxter, who separated Achilles tendon dysfunction into insertional and noninsertional tendinosis. Noninsertional tendinosis occurs proximal to the tendon insertion within or on the periphery of the tendon. Insertional tendinosis occurs within or around the tendon at its calcaneal insertion. It may be associated with a bony prominence on the superior aspect of the calcaneus (Haglund deformity) or with the development of a calcaneal spur within or along the periphery of the Achilles insertion. Puddu et al proposed three stages of paratenon inflammation: stage 1 is paratenonitis, stage 2 is paratenonitis with tendinosis, and stage 3 is tendinosis ( Table 37-2 ).

Paratenonitis (stage 1) occurs with pathologic inflammatory changes localized to the paratenon. Although the tendon is typically normal in appearance, the paratenon may be thickened, fluid can accumulate adjacent to the tendon, and adhesions can develop.

Paratenonitis with tendinosis (stage 2) is characterized by macroscopic tendon thickening, nodularity, softening, yellowing of the tendon, decreased luster, and fibrillation. Microscopically, there is inflammation in the paratenon but also focal degeneration within the tendon itself. The earliest changes appear to be fragmentation of collagen fibers within the substance of the tendon. At surgery there are regions of macroscopic tendon thickening. It has been hypothesized that these are areas of focal degeneration or of partial tendon rupture and that these patients are at risk for complete tendon rupture. These areas are associated with poor vascularity, mucoid degeneration, and are absent of any reparative process.

Achilles tendinosis (stage 3) is characterized by degenerative lesions of the tendon without evidence of paratenonitis. Microscopically, with tendinosis, there is an altered tendon structure with decreased luster, yellowish discoloration, and softening of the tendon. As described above, Puddu observed that a rupture of the Achilles tendon was often associated with intermittent symptomatic paratenonitis with tendinosis. Without a prodromal period, less paratenon inflammation appears to occur, and histologic changes demonstrate areas of mucoid degeneration within the tendon. Decreased cellularity and fibrillation of collagen fibers are often observed. They also found that even the tendon distant from the site of an Achilles tendon rupture was abnormal.

History and Physical Examination

With Achilles tendinosis, patients typically complain of pain in the area of the distal Achilles tendon, 2 to 6 cm proximal to the Achilles tendon insertion. Pain is often experienced with initial morning activity and increases with exercise. With increased tendon involvement, pain becomes associated with both walking and running. Early symptoms are generally characterized by sharp transient pain or recurrent episodes of sharp pain with running. Over time, less activity incites symptoms. Some patients eventually develop pain even at rest.

Clain and Baxter stated that insertional Achilles tendinitis is an entirely separate entity that overlaps with the condition known as a Haglund deformity or “pump bump.” Van Dijk et al later coined the term superficial calcaneal bursitis. With this condition, discomfort is mainly noted over the posterolateral prominence of the calcaneus and is often associated with tight constricting footwear or shoes with a closely contoured heel counter. Noninsertional Achilles tendinosis is infrequently associated with a pump bump.

On physical examination it is important to determine the precise area of tendon pain. The location and magnitude of soft tissue swelling should be noted. The patient should be asked to do a single-limb heel-rise test. Many patients demonstrate a loss of at least 5 degrees of dorsiflexion compared with the contralateral side. The calf should be examined for atrophy and a Thompson test performed to demonstrate that the Achilles tendon is intact. The tendon should be palpated for any area of defect or nodularity. In cases of paratenonitis, the area of nodularity does not move, while in cases of tendinosis, the nodularity will move with ankle plantarflexion and dorsiflexion. To determine gastrocnemius contracture involvement, the SilfverskiÖld test should be performed by comparing ankle dorsiflexion when the knee is flexed versus fully extended. Kvist noted that pain was localized to the lower part of the tendon in 24% of patients, the middle region in 51%, and the upper region in 10% ( Fig. 37-2, A–C ). Diffuse tendon involvement was noted in 15% of cases and nodularity in 40%. Localized tenderness to palpation, swelling, decreased range of motion, tendon thickening, increased temperature, edema, and erythema all may be noted on physical examination.

With paratenonitis (stage 1) the patient has notable tenderness and thickness that remains fixed with active range of motion. With a lesion of the tendon itself (tendinosis stage 3), the movement of the ankle and foot into dorsiflexion and plantar flexion is characterized by the area of tenderness moving along with the tendon (painful arc sign) ( Fig. 37-2D and E).

The tendon should be examined with the ankle joint both plantar flexed and dorsiflexed. With pain localized to the insertion of the Achilles tendon, there is often increased pain with plantar flexion. Grasping the heel and dorsiflexing the foot can compress the Achilles bursa and incite pain.

With insertional tendinosis, pain and tenderness are present at the Achilles tendon insertion and usually worsens with provocative exercise. With chronic irritation, the tendon insertion can become thickened ( Fig. 37-3 ).

In patients suspected of having retrocalcaneal bursitis, pain may be elicited just anterior to the Achilles tendon. A two-finger squeeze test elicits pain by squeezing in a medial to lateral direction just superior and anterior to the Achilles tendon insertion. Pain is localized at the bone tendon interface and may be increased with eversion and dorsiflexion ( Table 37-3 ).

Radiographic Examination

In the evaluation of Achilles tendon disorders, routine radiographs should be obtained. Radiographs can demonstrate cortical erosion associated with inflammatory arthropathy, calcification within the tendon, or at the Achilles tendon insertion. On a lateral radiograph, a Haglund deformity, which has been associated with retrocalcaneal bursitis, may be present ( Fig. 37-4 ). Pavlov described a method of measuring the magnitude of a prominent posterosuperior calcaneal tuberosity by using parallel pitch lines ( Fig. 37-5 ). With a Haglund deformity, the superior surface of the calcaneus projects beyond the superior calcaneal line.

Ultrasound or MRI can demonstrate a partial Achilles tendon tear, paratenon thickening, tendinosis, nodularity, cystic change, or calcification ( Figs. 37-6 and 37-7 ). While these diagnostic tools are extremely useful for determining the location and extent of the disorder in preoperative surgical planning, they lack the ability to guide clinical decision making. More recently, the advent of ultrasound sonoelastography (SES) has been described, which allows the clinician to measure tendon stiffness of the tendon both with shear wave and strain wave. The stiffness of the tendon has been shown to closely correlate to patient symptoms. SES has also been shown to correlate to response to treatment, thereby potentially providing a tool for the clinician to follow treatment response. Further studies are required to fully evaluate the full application of this technology.

Nonoperative Treatment

Most cases of noninsertional Achilles tendinopathy are successfully managed nonsurgically. To the contrary, nonoperative treatment of insertional Achilles tendinopathy can be time consuming and often unsatisfactory, with only about half of the patients satisfied with their outcome. One of the most significant factors influencing prognosis and recovery with nonoperative treatment is duration of symptoms. If tendinosis has been present for 6 months or more, the condition is more difficult to treat nonsurgically. Kvist and Kvist observed that failed treatment often results from adhesions in the paratenon. They noted that chronic paratenonitis was much more difficult to treat successfully when it had been present 8 to 12 weeks. Nicholson et al, looked at 157 patients with insertional disease. Of those patients, 53% of patients responded to nonoperative treatment. Those who failed nonoperative treatment were more likely to have insertional Achilles tendon pain without signs of inflammation. The authors concluded that earlier identification of these patients may help identify earlier those who would benefit from surgical treatment.

Nonoperative treatment includes NSAIDs, rest, immobilization, decreased activity, ice, contrast baths, stretching, backless shoes, and heel lifts ( Fig. 37-8 ). A medial arch support or other orthotic devices may be used to decrease overpronation. Night splints to keep the ankle dorsiflexed during sleep are another option that can encourage healing and mitigate the painful morning symptoms. However, one study reported no benefit to their use in a randomized controlled trial (RCT). We have used topical applications such as ketoprofen and diclofenac gel and patches, nitroglycerine patches, and lidocaine patches with mixed results. Topical glyceryl trinitrate has been effective in Achilles tendinopathy in a double-blind and placebo-controlled RCT. An intratendinous injection of corticosteroid is discouraged because of the increased risk of tendon rupture.

A paratenon injection of local anesthetic (lidocaine or bupivacaine) and/or normal saline can be attempted in cases of paratenonitis. This technique, called brisement , involves injecting 5 to 10 mL into the pseudosheath to break the adhesions between the mesotendon and the tendon itself. A series of two or three injections can decrease the symptoms in paratenonitis about 50% of the time. Platelet-rich plasma (PRP) can also be used instead of normal saline. Results of this treatment within the literature are sparse. Alternatively, a high-volume injection (HVI) treatment with normal saline, local anesthetic, and steroid has also been described. The solution is placed into the peritendinous area between the Achilles tendon and Kaeger’s fat pad. The treatment is thought to have a mechanical effect on neurvascular ingrowth as well as breaking up adhesions between the tendon and the paratenon. Either PRP or HVI, when combined with eccentric exercise,s have been found to be more effective than exercises alone.

Activity modifications are a time-honored nonoperative treatment that will almost always reduce symptoms. This can be done with or without reduced weight bearing and with or without a walking boot or cast immobilization. The latter simply reinforces the rest principle in those patients who are tempted to not adhere to the treatment regimen.

Our preferred method of nonoperative treatment is a walking boot either with a slight heel lift or in neutral position. The boot is worn for 2 to 3 months for resolution of symptoms. A general rule is to use the boot until there are no symptoms for 2 weeks or until the improvement has plateaued for 2 weeks. Then the boot should be gradually discontinued, with more time spent out of the brace for progressively longer and more frequent intervals throughout the day. Patients remove the boot several times a day for gentle range-of-motion exercise. We also use eccentric exercise and stretching programs since they have been shown to be effective in the treatment of chronic Achilles tendinopathy in several RCTs. It has been reported that the high-frequency oscillations in the tendon with eccentric exercises are the basis for the therapeutic benefit seen with this type of rehabilitation. One study reported on 190 athletes with Achilles tendinosis. They were put through a 6-week eccentric stretching program resulting in a high degree of patient satisfaction, reduced pain levels, and a successful return to premorbid activity levels. Other studies have shown similar results in the nonathletic population. It has even been shown that patients can continue exercise involving running and jumping while monitoring pain and still see significant improvements with an eccentric training program. This eccentric training program can reduce tendon thickness and restore the tendon appearance to one that is more normal both by ultrasonography and MRI.

Extracorporeal shock wave therapy (ESWT) for the treatment of Achilles tendinosis is now being widely studied. Most information on ESWT comes from research on kidney stone lithotripsy, upper extremity tendinitis, and plantar fasciitis. ESWT 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. ESWT has also shown to decrease expression of several matrix metalloproteinases (MMPs) and cytokines (e.g., IL6) that have been found in human tendinopathy-affected tenocytes. More studies have come to a common conclusion that use of ESWT as an adjunct to conservative treatment of Achilles tendinopathy is effective when typical nonoperative treatment fails. In an RCT comparing eccentric therapy to ESWT, Rompe et al found that eccentric loading showed inferior results to low-energy shock wave therapy with chronic recalcitrant insertional tendinopathy at 4 months of follow-up. In another RCT, ESWT in conjunction with eccentric loading therapy was found superior to eccentric loading alone. In the short term, low-energy ESWT is thought to produce an analgesic effect by changing the permeability of neuron cell membranes and in the long term to cause increased blood flow in the chronic tendinopathy, thereby improving symptoms. Contraindications to ESWT include pregnancy, coagulopathies, bone tumors, bone infection, and skeletal immaturity. Previous literature reviews, including a Cochrane review, have shown an overall benefit in utilization of ESWT for Achilles treatment. More research must be conducted to determine the most effective type of ESWT, low or high energy. Furthermore, indications and contraindications have to be defined to select the most appropriate patients for this treatment.

Platelet rich plasma (PRP) has also been studied for its effectiveness in treating chronic tendinopathy. PRP is platelet-rich blood that is derived from whole blood through centrifugation. The highly concentrated platelets release several growth factors, including transforming growth factor beta 1 (TGF- β1) and insulin-like growth factor (IGF), which promote a healing response at wound sites. PRP has become a promising treatment option for a variety of reasons, including its convenient extraction and excellent safety profile. While PRP has several attractive qualities, the evidence of its efficacy has been mixed and is highly dependent on composition and preparation. Many studies have found that PRP injections do not result in clinical improvement in chronic midportion Achilles’ tendinopathy, compared with a placebo. However, due to the heterogeneity of preparations along with variations in treatment protocol and administration, it is difficult to interpret existing literature and make definite conclusions on the efficacy of PRP.

In general, with all forms of nonoperative therapy, patients with severe tendinosis should be treated until symptoms subside and rehabilitation can be initiated. A patient with only paratenonitis is at low risk for rupture. With increasing tendinosis, the risk of rupture increases. A physician should have a frank discussion with an athlete regarding any predisposing factors that may have led to acute paratenonitis, including training techniques and footwear. The amount of time to recovery is variable, but subacute tendinopathy (3–6 weeks in duration) can take a similar amount of time (3–6 weeks) to resolve with a conservative program. Chronic tendinopathy can take much longer to resolve. Clancy recommends at least 3 to 6 months of conservative treatment before surgical intervention ( Table 37-4 ).

Surgical Treatment of Paratenonitis ( Videos 37-1 and 37-2 )

We differentiate between paratenonitis and tendinosis because of the prognosis. Patients with paratenonitis respond more quickly than those who have paratenonitis with associated tendinosis. Paratenonitis with additional tendinosis requires not only resection of the paratenon but also debridement of the tendon and possibly augmentation with either a turn-down flap or FHL tendon graft.

Some surgeons advocate for paratenon resection and debridement. Nodules on the paratenon that are removed are thought to have formed secondary to a previous partial tear along the Achilles tendon. Resection and debridement have been shown to alleviate pain. Other surgeons feel that this method of removal and debridement of the paratenon devascularizes the area and makes the Achilles tendon even more susceptible to failure. Their treatment method includes longitudinal incisions along the paratenon, which stimulates healing and vascular ingrowth. Additional techniques to supplement the defective tissue involve tendon transfers that augment the native tissue and potentially bring a new vascular network to the area to aid in the healing process.

Surgical Treatment of Insertional Achilles Tendon Dysfunction

The determination of whether surgery is indicated depends on the duration and level of patient discomfort. We consider surgical intervention in the athlete with symptoms of insertional Achilles tendinosis who have not responded to an adequate conservative treatment program of 4 months’ duration, including a period of relative immobilization. Angerman and Hovgaard recommended surgical treatment if the athlete has been treated conservatively for 3 to 6 months without progress. A walking boot is used for immobilization to allow continued use of physical therapy modalities and gentle stretching exercises. When the patient remains significantly disabled regarding previous lifestyle, surgery is offered as an alternative ( Fig. 37-11 ).

There have been many methods and surgical approaches described for surgical treatment, but the principles remain consistent. Excision of the retrocalcaneal bursa, excision of the prominent tuberosity, debridement of the degenerative tissues, and repair of the tendon if necessary are advocated.