Achilles Tendon Injuries

Achilles tendon pathologies include rupture and tendonitis. Achilles tendon rupture, a complete disruption of the tendon, is observed most commonly in patients aged 30-50 years who have had no previous injury or problem in the affected leg and are typically "weekend warriors" who are active intermittently. (See Etiology and Epidemiology.)

Achilles tendonitis refers to inflammation of the tendon or paratenon, usually resulting from overuse associated with a change in playing surface, footwear, or intensity of an activity. Many experts now believe, however, that tendonitis is a misleading term that should no longer be used, because signs of true inflammation are almost never present on histologic examination. Instead, the following histopathologically determined nomenclature has evolved (See Pathophysiology and Etiology):

• Paratenonitis: Characterized by paratenon inflammation and thickening, as well as fibrin adhesions[1] ; localized thickening of the paratenon, tenderness, crepitus, and pain with active movement also may be present[2]

• Tendinosis: Characterized by intrasubstance disarray and degeneration of the tendon[2, 1, 3]

• Paratenonitis with tendinosis

Patient education

Educating the patient throughout the physical therapy treatment program and at subsequent follow-up visits is very important. Include information on adequate stretching prior to physical activity, as well as on appropriate technique and appropriate and properly fitting footwear. (See Treatment and Medication.)

For patient education information, see Ruptured Tendon and Achilles Tendon Rupture.

The Achilles tendon (tendo calcaneus) is formed from the tendinous contributions of the gastrocnemius and soleus muscles, coalescing approximately 15 cm proximal to its insertion. Along its course in the posterior aspect of the leg, the tendon spirals 30-150° until it inserts into the calcaneal tuberosity.

The spiraling of the tendon as it reaches the calcaneus allows for elongation and elastic recoil within the tendon, facilitating storage and release of energy during locomotion. This phenomenon also allows higher shortening velocities and greater instantaneous muscle power than could be generated by the gastrocsoleus complex alone.

Because actin and myosin are present in tenocytes, tendons have almost ideal mechanical properties for the transmission of force from muscle to bone. Tendons are stiff but resilient, possess a high tensile strength, and have the ability to stretch up to 4% before damage occurs.[10] With stretch greater than 8%, macroscopic rupture occurs.

The tendon's ability to glide is facilitated by the presence of a thin paratenon sheath, which is composed of a visceral layer and a parietal layer, rather than simply a true synovial sheath.

The paratenon can become inflamed and enlarged, this being a form of peritenonitis known specifically as paratenonitis. This condition is often found in runners, with acute crepitus felt over the fusiform swelling (which can originate from the paratenon or from the tendon itself).

Just anterior to the Achilles tendon lies the retrocalcaneal bursa. This can become inflamed, leading to pain anterior to the tendon, especially on dorsiflexion of the foot. It is important to differentiate this type of pain from paratenon inflammation or tendinosis. An enlarged bony prominence at the posterosuperolateral aspect of the calcaneus, called the Haglund process, may be associated with retrocalcaneal bursitis but also with insertional tendonitis as well. This is a reason why plain radiography still has value in diagnosis and management.

On average, Achilles tendons in women have a smaller cross-sectional area than in men. This possibly suggests that less force is generated in a woman’s Achilles tendon, which may account for the lower rate of rupture in women.[11]

Blood supply

The blood supply to the Achilles tendon is derived mainly from vessels traversing the mesotendon. The main blood supply is derived from the vincula, both long and short, via the paratenon and especially from the ventral mesotendon. Small longitudinal supplies from the muscle bellies and the distal insertion are also present. However, blood supply is also derived directly from the muscle bellies themselves and distally from bone where the tendon inserts into the calcaneus.

Microvascular Doppler flow studies have shown that flow is distributed evenly throughout the tendon, but it is less at the insertion.[12] Studies have also demonstrated higher resting blood flow rates in individuals with tendinosis than in healthy control subjects.[13]

Cadaveric studies have shown a relative decrease in the frequency and the total area of vessels in the midportion of the Achilles tendon.[14] Dynamic studies have refuted the once-popular historical theory that the pathology is related mainly to a hypovascular zone at the midtendon. However, the relative lack of blood vessels in the area that usually ruptures has led to the term watershed area, which is still used today. Although the blood supply is a factor in Achilles tendinosis, whether it is causative or reactive is still under debate.

Achilles tendonitis was the term originally used to describe the spectrum of tendon injuries ranging from inflammation to tendon rupture, but it now is seen as more of a garbage term. Current literature has delineated the terminology further to pinpoint the area of injury in hopes of guiding practitioners to more effective treatment of the patient.

Furthermore, through extensive histopathologic study, it has been determined that there is no evidence to support the presence of primary prostaglandin-mediated inflammation in Achilles tendonitis. There are, however, signs of neurogenic inflammation, with neuropeptides such as substance P and calcitonin gene–related peptide present.[15]

Tendon histopathology has been divided into the following 4 categories[16, 17, 18] :

• Cellular activation and increase in cell numbers

• Increase in ground substance

• Collagen disarray

• Neovascularization: However, some more recent studies comparing the degree of neovascularization and the severity of Achilles tendinosis have failed to link a direct relationship[19]

Using this as a guide, a histopathologically determined nomenclature has evolved as follows, to classify Achilles complex pathology:

• Paratenonitis: Characterized by paratenon inflammation and thickening, as well as fibrin adhesions[1] ; localized thickening of the paratenon, tenderness, crepitus, and pain with active movement also may be present[2]

• Tendinosis: Characterized by intrasubstance disarray and degeneration of the tendon[2, 1]

• Paratenonitis with tendinosis

Partial or full tendon ruptures may result from end-stage paratenonitis. Causes of tendon pathologies, including ruptures, are associated with multiple intrinsic and extrinsic factors (see Etiology).[20, 1, 18]

Extracellular and intracellular matrices

Histologic changes in the Achilles tendon include changes to the extracellular and intracellular matrices. These include collagen degeneration, fiber disorientation, and increased mucoid ground substance; however, no increase in inflammatory cells occurs. Focal hypercellularity and vascular proliferation are usually present. The number and morphologic variations of tenocytes increases.[21] Also increased is the number of apoptotic (dead) cells in the degenerate and in the ruptured tendon.[22] The proportion of type III collagen is also increased in the degenerate tendon.

Pathologically, Achilles degeneration has been described as lipoid or mucoid.[23] In mucoid degeneration, the tendon becomes more brown or gray, with mucoid patches and vacuoles. Lipoid degeneration involves increased lipid content in the tendon tissue.[24] Other studies have shown an increase of type I and type III collagen messenger ribonucleic acid (mRNA). Glutamate concentrations also increase in the painful degenerate tendon.[11]

Neovascularization

Neovascularization is often a feature of the degenerate tendon. It is associated with painful tendinosis.[25] Eccentric training leading to good clinical results is associated with a reduction and/or absence of neovascularization, and conversely, poor results are associated with continuing neovascularization.[26, 27] Tendon rupture is almost always the terminal event in the ongoing degenerative process of the tendon, as confirmed in histologic studies of ruptured tendons.[28]

Collagen

Adult tendons are composed of large-diameter type I collagen fibrils. These are 150 nm in diameter, tightly packed with type III collagen, and dispersed in an aqueous gel containing proteoglycan and elastic fibers.[29] The actin and myosin bundles are arranged helically. In healthy tendons, 95% of the collagen is type I.[30] Degenerate tendons have less type I collagen and significantly more type III collagen. The same changes are also seen during the natural aging process, although to a lesser extent. This may be why the tendon is less elastic in older individuals and more prone to rupture.

Type III collagen seems to be the major collagen synthesized in the healing tendon after injury. This observation suggests that the tendon degeneration in tendinosis is an incomplete repair process.

Animal testing has shown that tendons can stretch by 4% of their original length before damage occurs. If they are stretched more than 8%, rupture is likely.[31]

Sport-specific biomechanics

The entire gastrocsoleus musculotendinous unit spans the knee joint, tibiotalar (ankle) joint, and talocalcaneal (subtalar) joint. Contracture of this complex flexes the knee, plantar flexes the ankle, and supinates the subtalar joint. During running, forces equaling 10 times the runner’s body weight have been measured within the tendon.

When there is dysfunction in the gait cycle secondary to Achilles tightness, excessive pronation, or other factors, compensatory posturing up and down the kinetic chain (eg, hip external rotation), functional genu recurvatum, and midtarsal rotation may occur and add not only to Achilles tendinosis but also, in some cases, to a "whipping effect” of the Achilles tendon.[1]

A number of intrinsic and extrinsic factors, including excessive, repetitive strain, appear to be linked to the degeneration and rupture of the Achilles tendon.[32] The exact etiology of such injuries, however, seems to be multifactorial, complicated, and incompletely understood.

Achilles tendinosis is noted more commonly in runners, gymnasts, cyclists, and volleyball players. Hyperpronation may contribute in these cases; moreover, the tendon can be subjected to 8-10 times a person's body weight during strenuous exercise, with Komi having recorded forces of up to 4000 N passing through the Achilles tendon when a person is running on his or her toes.[33, 34]

In cyclists, low saddle height, resulting in extra dorsiflexion of the ankle with pedaling, may be a causative factor in tendinosis.

Intrinsic factors

Systemic diseases that affect the Achilles tendon include the following:

• Chronic renal failure[35, 36]

• Rheumatoid arthritis

• Systemic lupus erythematosus (SLE)

• Gout

• Collagen deficiencies

• Infectious diseases

• Thyroid disorders

• Parathyroid disorders

• Diabetes mellitus

Other intrinsic factors in Achilles tendon injuries include the following[1] :

• Varus alignment with functional hyperpronation

• Cavus foot

• Tibia vara (Blount disease)

• Insufficient gastrocsoleus strength and flexibility

• Limited ankle dorsiflexion

As previously mentioned, age is another factor associated with Achilles tendinosis. Increased incidence of Achilles rupture and Achilles tendinosis has also been associated with having blood group O.[37, 38]

Family history is also a possible risk factor for Achilles tendon disorders. According to a study by Kraemer et al, individuals with a positive family history of Achilles tendinosis have a 5-fold greater risk for such injuries.[39]

Extrinsic factors

Drugs that can play a role in Achilles tendon pathology include the following:

• Steroids: Whether taken systemically or injected around the tendon, steroids appear to increase the rate of acute rupture[40, 41]

• Quinolones: Numerous case reports appear to link the administration of quinolone antibiotics to tendon rupture; these drugs may have a toxic effect on the tenocytes, leading to tendon degeneration[42, 43]

Extrinsic causes of Achilles tendinosis also include the following[2, 1, 44, 16, 45] :

• Overuse

• Activities with jumping and running

• Participation in a new activity

• Increased intensity of activity

• Increased duration of training

• Stairs

• Hill climbing

• Poor conditioning

• Improper shoes

• Improper training surfaces

• Improper stretching exercises

Tendon rupture

Most Achilles tendon tears occur in the left leg in the substance of the tendo-Achilles, approximately 2-6 cm above the calcaneal insertion of the tendon. That the left Achilles tendon is torn more frequently may be related to handedness; right-handed individuals "push off" more frequently with the left foot.

The most common mechanisms of injury include sudden, forced plantar flexion of the foot; unexpected dorsiflexion of the foot; and violent dorsiflexion of a plantar-flexed foot. Other mechanisms include direct trauma and, less frequently, attrition of the tendon as a result of longstanding paratenonitis, with or without tendinosis.[6, 20, 16]

Achilles tendon rupture resulting from forced dorsiflexion during active plantar flexion is commonly seen in basketball, diving, tennis, and other sports that require forceful push off from the foot.

Other risk factors for Achilles tendon rupture, aside from those previously noted (ie, age, systemic illnesses, medications, blood type), include the following[46] :

• Poor conditioning

• Fluoroquinolone antibiotic use

• Corticosteroid use

• Overexertion

Although a link between smoking and biceps tendon rupture has been proven, no association between smoking and Achilles tendinosis or rupture is reported in the literature.

Persons who have had an Achilles rupture are more likely than others to have tendinosis and repeat rupture on the contralateral side.[47]

Tendinosis

Traditionally, tendinosis is thought to occur with overuse, causing microtrauma to a degree and at a frequency at which the tendon can no longer heal itself. This situation leads to mechanical breakdown of the tendon.[48]

Several authors have studied factors that may influence the development of tendinosis, such as training mileage, rest periods for military recruits between runs, anatomic alignments of the lower limb, and mechanical factors related to shoes and inserts. As yet, no clear-cut evidence has been found linking these to tendinosis. Further confusion arises because tendinosis also can occur in relatively inactive individuals.[49, 50]

The true incidence of Achilles tendinosis is unknown, although reported incidence rates are 6.5-18% in runners, 9% in dancers, 5% in gymnasts, 2% in tennis players, and less than 1% in American football players. It is estimated that Achilles disorders affect approximately 1 million athletes per year.[1]

Occurrence in the United States

The incidence of Achilles tendinosis is believed to be rising, in terms of tendinosis and acute ruptures. An estimated 10% of Americans are involved in some form of recreational running or in other jumping or pivoting activities, and often for longer periods than in previous generations. No data describe the incidence or prevalence of Achilles tendinosis, but it is known to affect 7-18% of club runners.

International occurrence

The exact frequency of tendon rupture varies, having been reported at 6 cases per 100,000 persons in Scotland and 37 cases per 100,000 persons in Denmark.[51]

Sex- and age-related demographics

Compared with females, Achilles tendon injuries are more prevalent in males by a ratio of 6:1, perhaps due to sports-specific involvement.

These injuries usually are observed in recreational athletes aged 30-50 years. Many persons in this age group are active only intermittently but still challenge their bodies with high-force activities, predisposing them to Achilles tendinosis.

Achilles tendon injury has an excellent prognosis, allowing for some degree of morbidity through reduced range of motion (ROM).

With proper treatment (conservative or surgical) and rehabilitation, most athletes with Achilles tendon rupture are able to return to their previous activity levels. However, individuals who undergo surgical treatment have a rerupture rate of just 0-5%, compared with nearly 40% for patients who opt for conservative treatment.[52]

Surgical repair results following tendon rerupture are poorer than those following the initial operative treatment of an acute tendon rupture. This was borne out by a Swedish study, by Westin et al. Rerupture patients, all of whom underwent surgery and rehabilitation, were followed up at a mean 51 months, with the investigators finding that these individuals had a mean Achilles Tendon Total Rupture score of 78, versus 89.5 for primary rupture patients.[53]

Achilles tendon contracture and/or scarring may result from excessive immobilization. In addition, permanent weakness has been known to occur with as little as 4 weeks of immobilization.

Operative treatments have several potential complications, including wound complications (eg, infection, skin slough, sinus formation), adhesions, and sural nerve injury (especially if surgery is conducted through a lateral longitudinal approach). A retrospective study by Jildeh et al indicated that in patients who undergo surgery for Achilles tendon rupture, longer operative time increases the chance of rerupture, while longer tourniquet time, greater estimated blood loss, and a history of smoking are risk factors for surgical site infection. However, the overall rerupture and infection rates were found to be low (1% and 2.8%, respectively).[54]

Patients with an Achilles tendon rupture frequently present with complaints of a sudden snap in the lower calf associated with acute, severe pain. The patient reports feeling like he or she has been shot, kicked, or cut in the back of the leg, which may result in an inability to ambulate further. In some cases, the patient can ambulate with a limp but is unable to run, climb stairs, or stand on his or her toes. (A very strong athlete usually is able to overcome the gait abnormality of an Achilles tendon rupture by using other plantar flexors to ambulate normally.)

Patient history in Achilles tendon rupture may also include any of the following:

• Chronic, recurrent calf or Achilles tendon ̶ area pain

• Previous rupture of the affected tendon

• Loss of plantar flexion power in the foot

• Swelling of the calf

• Recent increase in physical activity/training volume

• Recent use of fluoroquinolones, corticosteroids, or corticosteroid injections

Family history is a possible risk factor for Achilles tendon disorders. According to a study by Kraemer et al, individuals with a positive family history of Achilles tendinosis have a 5-fold greater risk for such injuries.[39]

Patient history in Achilles tendinosis may also include the following:

• Paratenonitis: Localized/burning pain during or following activity occurs; as the disease progresses, onset of pain may occur earlier during activity, with decreased activity level, or even at rest.

• Tendinosis: Usually, this injury is an asymptomatic, noninflammatory, degenerative disease process (mucoid degeneration); the patient may complain of a sensation of fullness or a nodule in the back of the leg

• Paratenonitis with tendinosis: Activity-related pain and diffuse swelling of the tendon sheath with nodularity is present

With the patient in a prone position and his or her feet off the table, palpate the entire gastrocsoleus complex for tenderness, nodules, swelling, warmth, atrophy, and tendon defects, and note whether ecchymosis is present. Localization of the tenderness should be differentiated between musculotendinous (tennis leg), intrasubstance (Achilles tendon injury), and insertional (eg, Haglund deformity, pump bump).

Nodules should be palpated for tenderness, boundaries, mobility, and size. Calf atrophy, determined by comparison of calf circumference on the affected side with that on the contralateral side, may provide information as to the chronicity of the disease process (acute vs chronic). Gaps, or areas of tendon discontinuity, are often signs of partial or complete tendon rupture.

A patient with Achilles tendon rupture will be unable to stand on his or her toes on the affected side. Upon presentation, however, the individual may be able to weakly plantar flex his or her ankle due to the intact peroneal muscles, posterior tibialis tendon, or flexor hallucis tendons; therefore, misdiagnosis or delay in treatment may occur because the condition is believed to be just a strain.

Ascertain active and passive ROM and strength of the knee, ankle, and subtalar joints. Patients with overuse Achilles tendon injuries typically have decreased motion and strength in the ankle and/or subtalar joints.

Note the resting alignment and motion of the forefoot and ankle. Forefoot and heel varus, pronated feet, cavus feet, and tibia vara are known predisposing risk factors for Achilles tendinosis.

Clinical tests for Achilles tendon rupture

These include the following:

• Hyperdorsiflexion sign: With the patient prone and knees flexed to 90°, maximal passive dorsiflexion of both feet may reveal excessive dorsiflexion of the affected leg

• Thompson test: With the patient prone, squeezing the calf of the extended leg may demonstrate no passive plantar flexion of the foot if its Achilles tendon is ruptured

• O’Brien needle test: Insert a needle 10 cm proximal to the calcaneal insertion of the Achilles tendon; with passive dorsiflexion of the foot, the hub of the needle will tilt rostrally when the Achilles tendon is intact.

Tendinosis

Tendinosis is often pain free. Typically, the only sign of the condition may be a palpable intratendinous nodule that accompanies the tendon as the ankle is placed through its range of motion (ROM). Occasionally, a thickening along the entire tendon may develop in chronic conditions.

Paratenonitis

Patients with paratenonitis typically present with warmth, swelling, and diffuse tenderness localized 2-6 cm proximal to the tendon's insertion. Crepitation may also be felt if paratenonitis presents acutely. As the condition becomes more chronic, symptoms may be provoked by decreased amounts of physical activity.

Paratenonitis with tendinosis

Paratenonitis with tendinosis is diagnosed in patients with activity-related pain, as well as swelling of the tendon sheath and tendon nodularity.

Laboratory studies usually are not necessary in evaluating and diagnosing an Achilles tendon rupture or injury, although evaluation may help to rule out some of the other possibilities in the differential diagnosis. These laboratory tests, all of which are normal in Achilles tendinosis, include the following:

• Complete blood count (CBC) with differential

• Coagulopathy panel

• Erythrocyte sedimentation rate

• Arthritis panel

Imaging studies can aid in the diagnosis and evaluation of Achilles tendon pathology, but typically they are not needed. Like laboratory studies, however, they can be helpful in evaluating possibilities in the differential diagnosis and should be ordered as clinically indicated.

Plain radiography

Radiography may reveal tendon calcifications in tendinosis or spurs at the calcaneal insertion site, but neither is diagnostic for Achilles tendinosis.

Radiographs are more useful for ruling out other injuries than for ruling in Achilles tendon ruptures. The bones appear normal in patients with a ruptured Achilles tendon, although soft tissue swelling may be evident.[55]

Radiographs of the tibia and fibula often are indicated when the patient’s history shows trauma that may have resulted in fracture of these long bones. Radiographs of the knee and ankle may help to discover findings of degenerative or inflammatory arthropathies.

Ultrasonography

Ultrasonography of the leg and thigh can help to evaluate the possibility of deep venous thrombosis and also can be used to rule out a Baker cyst. Moreover, in experienced hands, ultrasonography can identify a ruptured Achilles tendon or the signs of tendinosis.

Unlike magnetic resonance imaging (MRI), ultrasonography cannot distinguish a partial tear from tendinosis.

In a small study, De Zordo et al concluded that, in terms of revealing the characteristics of Achilles tendinosis, the ultrasonographic technique known as sonoelastography was comparable to clinical examination and ultrasonography only in the identification of distinct softening of the Achilles tendon. However, very early changes in tissue elasticity in Achilles tendinosis may cause mild softening, which should be assessed in follow-up studies.[56]

MRI

MRI can facilitate definitive diagnosis of a disrupted tendon. This is especially useful when considering the possibility of partial disruption of the Achilles tendon. Partial disruption often is undetectable clinically and may be misdiagnosed as simple Achilles tendinosis; however, partial Achilles disruption often responds to surgical intervention. Imaging the knee can confirm a Baker cyst, as well as the probable underlying pathology causing the Baker cyst.[57]

MRI can also distinguish between paratenonitis, tendinosis, and bursitis.[55] In paratenonitis, MRI can reveal fluid in and around the tendon, while in chronic paratenonitis, the paratenon may be seen as thickened and fibrotic.

In tendinosis, increased MRI signal is evident in the tendon and degenerative changes, and partial tears may occasionally be seen. Keep in mind that these MRI findings may also be present in asymptomatic individuals.

Medical therapy for a patient with an Achilles tendon rupture consists of rest, pain control, serial casting, and rehabilitation to maximize function.[58] Ongoing debate surrounds the issue of whether medical or surgical therapy is more appropriate for this injury.[4, 5]

Surgical techniques for rupture repair are varied but usually involve reapproximation of the torn ends of the Achilles tendon, sometimes reinforced by the gastrocsoleus aponeurosis or plantaris tendon.

Overall healing rates with serial casting are similar to those of surgical reanastomosis, yet the return-to-activity benefits of surgery are debated.

Medical therapy for Achilles tendinosis and paratenonitis includes activity modification, orthotic therapy, physical therapy, and analgesic anti-inflammatory medication.[59, 60, 61, 3]

As with gastrocsoleus muscle strains, prevention of Achilles tendon injuries involves adequate stretching and conditioning prior to physical activity, especially for new activities or ones at higher levels of intensity.[62]

Nonoperative treatment for Achilles tendon rupture is usually indicated for patients who are elderly and/or inactive, as well as for those with systemic illnesses or poor skin integrity. Patients with diabetes, wound healing problems, vascular disease, neuropathies, or serious systemic comorbidities are encouraged to opt for nonoperative treatment because of the significant risks of operative treatment (eg, infection, wound breakdown, repair dehiscence, neurovascular injury, perioperative complications).

Activity modification for a ruptured Achilles tendon requires crutch ambulation without weight bearing. Once initiated, serial casting dictates the activity level.

Overall healing rates with casting are similar to those associated with surgical reanastomosis, yet the return-to-activity benefits of surgery are debated. Nonetheless, this is viable therapy, especially for more sedentary patients and older persons. The initial cast applied is a long-leg cast with some knee flexion and ankle plantar flexion to allow free edges of the Achilles to approximate. The cast is changed in series, decreasing the plantar flexion and eventually moving toward short-leg casts in a neutral ankle position. This treatment lasts 6-12 weeks.

Serial casting usually results in some Achilles contracture, and heel lifts are used afterwards. Depending on the degree of shortening and rate and aggressiveness of physical therapy, initiate use of 1- to 2-inch heel lifts with gradual weekly or biweekly adjustment directed toward weaning the patient off of them.

Advantages of nonoperative treatment include no wound complications, decreased hospital costs and physician fees, lower morbidity, and no exposure to anesthesia.

Disadvantages of nonoperative treatment include a higher incidence of rerupture (up to 40%) and more difficult surgical repair following rerupture. In addition, the tendon edges may heal in an elongated position because of a gap in the unapposed tendon ends, resulting in decreased plantar flexion power and endurance.

In a randomized, controlled trial by Maempel et al, patient-reported outcomes at mean 15.7-year follow-up indicated that nonoperative therapy for acute Achilles tendon rupture is just as effective as surgical treatment. For example, between the operative (33 patients) and nonoperative (31 patients) groups, the investigators found no statistically significant difference in scores for the Short Musculoskeletal Function Assessment (SMFA) Dysfunction Index, the SMFA Bother Index, the Achilles Tendon Total Rupture Score (ATRS), and the five-level EuroQol five-dimension (EQ-5D-5L) instrument. Moreover, in contrast to the statement in the previous paragraph, rerupture rates did not demonstrably differ between the two groups.[63]

Similar to the Maempel trial, a study by Ecker et al found good functional outcome and patient satisfaction following nonoperative treatment for acute Achilles tendon rupture. The study, in which 114 patients were followed up for at least 12 months, reported a mean Thermann score of 82 in these individuals, with 90% of patients rating their subjective satisfaction with the treatment results as “good” or “very good.” The therapy combined the use of an equinus cast and a rehabilitation boot, allowing patients to immediately bear full weight, as well as undergo early functional rehabilitation. The study found tendon length and muscle strength to be inversely proportional but stated that the equinus cast and boot can discourage excessive lengthening of the healing tendon.[64]

Paratenonitis

Relative rest from activities that involve forceful and repetitive ankle plantarflexion are recommended. In athletes wishing to maintain conditioning while waiting for the injury to heal, cross training with activities that do not involve forceful plantarflexion can be employed. Examples of these exercises are swimming, biking (with the pedal on the heel), and aqua jogging. In mild cases, runners may continue to run and still allow their injury to heal by simply reducing their mileage and eliminating hills for a while. In severe cases, complete rest with crutches or a walking cast or boot may be needed for a short time.

Initially for acute Achilles paratenonitis, icing and nonsteroidal anti-inflammatory drugs (NSAIDs) to reduce inflammation and pain are often helpful.[7]

Heel lifts of 10-15 mm for short-term use my reduce symptoms by reducing the stress and excursion of the tendon.

Fluoroquinolones should be avoided, as these agents have been associated with Achilles tendinosis and rupture.

Tendinosis

The initial treatment for tendinosis is similar to paratenonitis (above), although tendinosis tends to be less responsive to NSAIDs and ice, unless there is concomitant paratenonitis. Treatment has shifted away from traditional treatments and focuses more on intense eccentric strengthening exercises.[7]

Some clinicians feel that patients with Achilles tendinosis are predisposed to rupture and should be protected, but this is controversial.

Physical therapy

Physical therapy for patients with Achilles tendinosis consists of the following stages:

• In the first and part of the second phase of physical therapy, pain is used to guide the intensity of exercise; active ankle dorsiflexion with gentle calf stretching is performed

• In the intermediate phase, strengthening replaces active ROM, and neuromuscular control programs are initiated

• In the third phase of rehabilitation, progressive stress is applied under good control to allow the collagen to form appropriately; as pain resolves, aggressive stretching and active resisted motion are performed

Achilles tendinosis is best prevented and treated by preserving good ROM in the heel cord complex. Such motion can be gained with the use of an incline board, wall leans, or "foot-on-chair" stretching exercises. Application of moist heat or compresses before workouts and at night is beneficial. Cold modalities should be used following strenuous activities to provide pain relief and anti-inflammatory effects.

Correction of strength and flexibility deficits of the muscle-tendon unit in Achilles tendinosis, along with ultrasonography, phonophoresis, and other modalities, can be used.[7, 65] This can be done under the supervision of a physical therapist or from instructions or handouts from the physician. Calf stretches should be done with the knee in both extension (to stretch the gastrocnemius muscle) and flexion (to stretch the soleus muscle).

The cornerstone of strengthening is now the use of eccentric exercises, with most patients achieving 60-90% pain relief.[7, 8, 9] As with stretching, strengthening should be done with the knee in extension and flexion. A heavy-load, eccentric, calf-strengthening program has been shown to be highly beneficial for treating resistant tendinosis in runners and for getting them back to full activity.[66, 67] Investigators have evaluated the close correlation between good clinical results with eccentric training and a marked reduction in neovascularization of the tendon.[26]

Cross training with low-impact exercises can begin during this phase. If pain develops, the athlete should decrease the amount of activity 1 level to alleviate the pain.

If the individual is pain free with low-impact activity, the athlete can begin sport-specific training. If pain develops as activity is escalated, the patient should decrease the level of activity to one that does not cause pain.

Care must be taken to not commit another training error if that is what initially caused the tendinosis. The patient should warm up the muscle-tendon unit well before engaging in vigorous activity, such as sprinting and jumping.

In chronic, refractory cases of paratenonitis and tendinosis with a tight heel cord despite stretching, a “night splint” can be used.[68] This orthosis is similar to an orthopedic boot and is worn at night, keeping the ankle at 5° dorsiflexion.

In refractory cases with hyperpronation, a custom orthotic with a medial heel posting may be tried.

Orthotics

Orthotic therapy in Achilles tendinosis consists of the use of heel lifts; however, lifts usually are not used to the extent they are after serial casting for rupture. The goal is for the patient eventually to use conventional shoes.

Orthotic devices most often are used bilaterally to prevent a gait imbalance. Since overpronation and cavus foot deformities can cause tendinosis, custom orthotics to correct overpronation or shock-absorbing shoes for cavus deformities can alleviate pain as well.

NSAID therapy

Paratenonitis

Initially for acute Achilles paratenonitis, icing and nonsteroidal anti-inflammatory drugs (NSAIDs) to reduce inflammation and pain are often helpful.[7]

Tendinosis

Logic dictates that anti-inflammatories should not help in tendinosis because this is not an inflammatory condition. Indeed, studies have shown no clinical benefit from NSAIDs. However, they do appear to have some effect, and most physicians use NSAIDs in nonoperative treatment regimens. This practice persists because NSAIDs enable the patient to ignore mild symptoms.

Results of laboratory studies have suggested alternate roles for the NSAID effect, wherein tendon healing is improved. Findings from other studies have suggested that a reduction in the neutrophil and macrophage count occurs within the tendon; however, these counts are known to be limited in true tendinosis anyway.[69]

Steroid injections

Steroid injections are still controversial. They can certainly provide short-term relief of painful symptoms; however, whether steroids can aid healing and should still be used as part of the tendinosis treatment regimen is open to debate.[40]

Moreover, steroid injections, especially multiple injections, may weaken the tendon, leading to tendon rupture. Indeed, Astrom found that corticosteroid injection was the only predictor of partial tendon tears in a large series of chronic Achilles tendinoses that eventually required surgery.[49]

Sclerosis of vessels

A small study has shown improvement in symptoms after the injection of a sclerosing agent (polidocanol) in painful Achilles tendinosis. The assumption is that the sclerosant reduces neovascularization and, therefore, pain. In this trial, 10 patients were monitored for 6 months, with 8 having a reduction of symptoms.[70] In a similar study of 25 patients (26 tendons) injected with polidocanol for Achilles tendinosis, 19 patients (20 tendons) reported good-to-excellent results at 6-12 months’ follow-up.[71]

Platelet injections

Platelet-rich plasma (PRP) injections have become popular for refractory tendinosis, particularly chronic lateral epicondylitis. Results of studies on the effectiveness of PRP injections have been mixed. With regard to Achilles tendinosis, some study results have indicated no difference in outcome between intratendinous PRP injections and saline injections at 1 year, whereas other studies have shown moderate (>50%) improvement of symptoms.[72, 73, 74]

Nitric oxide

Nitric oxide has been shown to “stimulate collagen synthesis in fibroblasts”—the major cell population found in healing tendon tissue—and “promote tendon remodeling.”[75, 76] Many studies have shown that increasing nitric oxide in the area of injury “improved tendon healing through collagen reorganization and tissue mass loss.”[75, 76]

Nitric oxide is used most frequently in the form of a nitroglycerin transdermal patch. One quarter of a 5-mg patch used daily for 12-24 weeks has been suggested. However, it should not be used in combination with drugs used to treat erectile dysfunction or pulmonary hypertension (eg, sildenafil, tadalafil). In addition, precaution should be observed with coadministration of rosiglitazone, certain drugs used to treat migraine headaches (ergot alkaloids such as ergotamine), and drugs that lower blood pressure (including alpha blockers such as tamsulosin).

Shock-wave therapy

Extracorporeal shock-wave therapy (ESWT) has been a source of interest for treating chronic insertional and noninsertional Achilles tendinosis. Evolving data have been extremely positive, indicating that low-energy ESWT can improve pain and function by increasing blood flow to the chronic tendinosis.[77]

High-energy ESWT has also shown promise as a treatment for insertional Achilles tendinosis. One study demonstrated that a single treatment was more effective than traditional conservative treatment in improving pain and enabling patients to return to their activities.

In a randomized, controlled study of the use of eccentric loading versus the use of eccentric loading plus shock-wave treatment for chronic midportion Achilles tendinosis, at 4-month follow-up, eccentric loading alone was less effective than the combination therapy (56% vs 82% completely recovered or much improved on the Likert scale). At 1-year follow-up, however, the difference had greatly diminished.[78]

Actovegin therapy

Pforringer compared subcutaneous injections of Actovegin (a deproteinized calf-blood extract) with subcutaneous injections of placebo. The Actovegin treatment significantly reduced pain, but the patients were monitored for only 3 weeks.[79]

Friction massage

Sparse clinical evidence supports the use of deep friction massage. A Cochrane review in 2002 showed no obvious benefit, although the reviewers were not evaluating Achilles tendons in particular.[80]

Acupuncture

For patients who want to also use complementary and alternative medicine modalities, studies have shown that acupuncture improves pain and function compared with eccentric exercises alone.[81] This can be a beneficial adjunct to offer patients.

Conservative versus surgical treatment

Surgical techniques are varied and usually involve reapproximation of the torn ends of the Achilles tendon, sometimes reinforced by the gastrocsoleus aponeurosis or plantaris tendon. Controversy exists regarding whether to conservatively manage a first-time Achilles tendon rupture or to surgically reconstruct the ruptured tendon. There are distinct benefits and risks associated with each approach.[4, 5, 82, 6, 83, 84, 85]

Advocates of conservative treatment cite the similar results between conservative and surgical treatment when looking at ROM, strength, power, and functional levels as a reason for avoiding surgery. Surgical advocates argue that full function is achieved more quickly with surgical therapy than with conservative therapy, especially for athletic individuals. The surgical approach is supported by a lower rate of rerupture, greater postoperative power, and low infection rate.[86]

A systematic review by Erickson et al of Achilles tendon rupture meta-analyses indicated that surgical treatment is associated with fewer reruptures and, possibly, an earlier return to work than conservative therapy, while nonoperative treatment reduces the risk of minor complications.[87]

A meta-analysis by Amendola of randomized, controlled trials found a rerupture rate of 8.8% in nonoperative Achilles tendon rupture repair, compared with 3.6% in patients treated operatively, over a 10- to 36-month follow-up period. However, the nonrupture complication rates, as follow, tended to be higher in surgical repair than in nonoperative treatment[88] :

• Deep infection: 2.36% (surgical); 0% (nonsurgical)

• Noncosmetic scar complaints (pooled rate): 13.1% (surgical); 0.62% (nonsurgical)

• Sural nerve sensory disturbances (pooled rate): 8.76% (surgical); 0.78% (nonsurgical)

• Deep venous thrombosis (pooled rate): No significant difference

Conservative clinicians state that, with early application and prolonged duration of casting, the rerupture rate is decreased significantly in nonsurgical repair. A study by Twaddle and Poon indicated that the use of controlled, early motion in the rehabilitation of patients receiving either surgical or conservative treatment results in comparable functional outcomes and low rerupture rates.

Open surgical repair

Open reconstruction is undertaken using a medial longitudinal approach. Medial incisions have the advantage of better visualization of the plantaris tendon, as well as avoidance of injury to the sural nerve. Midline incisions are rarely used because of higher rates of wound complications and adhesions.[89]

After application of the tourniquet and palpation of the rupture gap, the incision is made through the skin and subcutaneous fat to the paratenon. The paratenon is then divided longitudinally to expose the ruptured ends, which are irrigated and debrided. The ends are then reapproximated and sutured with a heavy, nonabsorbable suture using a modified Kessler, Krackow, or Bunnell technique, with the surgeon being careful not to overtighten.

If the repair is insecure and reinforcement is required, a pull-out wire or multiple interrupted sutures may be used. These may be augmented with a turn-down fascial graft or a woven tendon graft; however, a study by Pajala et al found no advantage for augmented techniques in the surgical repair of fresh complete Achilles tendon rupture.[90]

A study by Park et al suggested that absorbable sutures may be just as effective as non-absorbable ones when repairing acute Achilles tendon ruptures. Thirty-seven patients were treated via the Krackow technique, using either braided absorbable polyglactin sutures or braided nonabsorbable polyethylene terephthalate sutures. The investigators found that at 12-month follow-up, both groups demonstrated comparable results with regard to isokinetic plantar flexion strength, the Achilles tendon Total Rupture Score (ATRS), the visual analogue scale (VAS) score for pain, and the EuroQoL five-dimension health questionnaire (EQ-5D). Re-rupture was found in neither group.[91]

Augmented repair

Although use of a down-turned gastrocnemius fascia flap (augmented repair) offers the theoretical advantage of stronger pullout strength, Pajala et al's randomized trial in 60 patients who underwent the Krackow locking loop technique showed that mean operative time was 25 minutes longer and the incision was 7 cm longer with augmented versus nonaugmented repair.

Moreover, no significant difference in outcome between the augmented and nonaugmented repair groups was evident at 3- and 12-month checkups with regard to pain, stiffness, subjective calf muscle weakness, footwear restrictions, range of ankle motion, overall outcome, isokinetic calf muscle strength, mean peak work-displacement relationships, or tendon elongation.[90]

Postsurgical care

Following surgery, the ankle is maintained in flexion as a cast or rigid orthosis is applied. After a period of immobilization, the foot is brought into neutral or slight plantar flexion in a rigid orthosis, and the patient is allowed partial weight bearing. Immobilization is typically discontinued 4-6 weeks after repair. At that point, active and active-assisted range of motion (ROM) exercises (20 min twice daily), swimming, stationary cycling, and walking in a shoe fitted with a heel lift can be initiated. In most cases, patients can progress to full activity within 4 months of surgery.[89]

Percutaneous surgery

Studies indicate that patients who undergo percutaneous, rather than an open, Achilles tendon rupture repair have a minimal rate of infection but a high rate of sural nerve entrapment (16.7% of treated cases).[6]

In paratenonitis, fibrotic adhesions and nodules are excised, freeing up the tendon. Longitudinal tenotomies may be performed to decompress the tendon. Satisfactory results have been obtained in 75-100% of cases.

In tendinosis, in addition to the above procedures, the degenerated portions of the tendon and any osteophytes are excised. Haglund’s deformity, if present, is removed. If the remaining tendon is too thin and weak, the plantaris or flexor hallucis longus tendon can be weaved through the Achilles tendon to provide more strength. The outcome is generally less favorable than it is in paratenonitis surgery.

Operative brisement (ie, injection of dilute anesthetic into the paratenon sheath under ultrasonographic guidance to break up adhesions) may be useful in patients with paratenonitis or tendinosis with paratenonitis.

More complex surgical problems, such as concurrent partial rupture of the tendon, may require the use of synthetic allografts or autografts from the flexor hallucis longus, semitendinosus, or gracilis muscle.[92]

While the reasons are not precisely known, surgery tends not to be as successful in nonathletic individuals with chronic Achilles tendinosis. Nonathletic patients tend to have a more prolonged recovery and a greater risk of complications, and they are more likely to need further surgery.

In a study of 78 patients with ruptured Achilles tendon, Silbernagel et al concluded that in evaluating the efficacy of treatment for tendon rupture, measuring both the number of heel-rise repetitions that patients could perform and the height of each heel rise was a better means of determining differences between injured and uninjured legs than was measurement of heel-rise repetitions alone.[93]

Employing a limb symmetry index (LSI) to determine differences in calf muscle strength between the patients' injured and uninjured legs, the authors found that 6 months after tendon rupture, the patients' mean LSI for the number of repetitions was 84%, but the mean LSI for the height/repetition combination was only 61%. At 1-year follow-up, the mean heel-rise repetition LSI was 95%, but the height/repetition LSI was only 76%.

Two major categories of drugs used in Achilles tendon rupture and Achilles tendinosis are analgesics (opioid and nonopioid) and nonsteroidal anti-inflammatory agents (NSAIDs). Consider side effects and patient profiles when choosing medications. Acetaminophen can result in liver damage. Opioids can result in gastrointestinal (GI) distress, constipation, and sedation and have addictive potential. NSAIDs can result in GI upset and bleeding, as well as renal damage and impaired coagulation. A new generation of cyclo-oxygenase 2 (COX-2) ̶ inhibiting NSAIDs may have fewer side effects. Currently, the only available COX-2 inhibitor is celecoxib.

In chronic cases of paratenonitis, some authors have advocated bupivacaine injection into the sheath to disrupt adhesions. Others have suggested that 2 mL of saline injection into the sheath may lift the paratenon off the tendon and lead to improvement; this is possibly more effective when performed with ultrasonographic guidance.

Class Summary

Pain control is essential to quality patient care. It ensures patient comfort, promotes pulmonary toilet, and aids physical therapy regimens. Many analgesics have sedating properties that benefit patients who have sustained trauma.

Acetaminophen (Tylenol, Feverall, Aspirin Free Anacin)

Acetaminophen is the drug of choice (DOC) for pain in patients with documented hypersensitivity to aspirin or NSAIDs, who have upper GI disease, or who are taking oral anticoagulants.

Hydrocodone and acetaminophen (Vicodin, Lorcet, Lortab, Norco)

This drug combination indicated for moderate to severe pain.

Acetaminophen and codeine (Tylenol #2, Tylenol #3, Tylenol #4)

This combination is indicated for the treatment of mild to moderate pain. The available dosage strengths are as follows:

• Tylenol #2: 300 mg Tylenol/15 mg codeine

• Tylenol #3: 300 mg Tylenol/30 mg codeine

• Tylenol #4: 300 mg Tylenol/60 mg codeine

Class Summary

NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclo-oxygenase (COX) activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.[94]

Naproxen (Naprosyn, Aleve, Naprelan, Anaprox)

Naproxen is used for the relief of mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing COX activity, which results in decreased prostaglandin synthesis.

Ibuprofen (Motrin, Advil)

Ibuprofen is the DOC for patients with mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Indomethacin (Indocin)

Indomethacin is used for relief of mild to moderate pain; it inhibits inflammatory reactions and pain by decreasing the activity of COX, which results in a decrease of prostaglandin synthesis.

Diclofenac (Voltaren, Cataflam XR, Zipsor, Cambia)

Diclofenac inhibits prostaglandin synthesis by decreasing COX activity, which, in turn, decreases formation of prostaglandin precursors.

Ketoprofen

Ketoprofen is used for relief of mild to moderate pain and inflammation. Small dosages are indicated initially in small patients, elderly patients, and patients with renal or liver disease. Doses higher than 75 mg do not increase the therapeutic effects. Administer high doses with caution, and closely observe the patient's response.

Class Summary

COX-2 inhibitors are used to control pain and inflammation, especially in cases of contraindication to conventional anti-inflammatories. Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeds is clearly less with COX-2 inhibitors than with traditional NSAIDs. Ongoing analysis of cost avoidance of GI bleeds will further define the populations that will find COX-2 inhibitors the most beneficial.

Celecoxib (Celebrex)

Celecoxib inhibits primarily COX-2, an isoenzyme that is induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity, but at therapeutic concentrations, COX-1 isoenzyme is not inhibited and thus, GI toxicity may be decreased. Seek the lowest dose of celecoxib for each patient.