Lindsay Wagahoff, MA | Aug 19, 2020 | 0
Achilles Injuries and Tendinopathy
Introduction & Etiology
The Achilles tendon is the largest and strongest tendon in the human body but is simultaneously a vulnerable link in the locomotion chain. (1) The tendons’ structural prowess is relentlessly confronted by functional demands that can be up to 12 ½ times body weight while running. (2)
The Achilles tendon may be acutely strained or ruptured as the result of an excessive stretch or eccentric force. Consistent with other types of acute strains, Achilles tendon injuries may occur when the musculotendinous unit transitions from eccentric deceleration to concentric propulsion. This happens during the “mid-stance” phase of gait. (3) Strains occur when collagen fibers are stretched by more than 4%. Ruptures occur when stretch exceeds 8%. (4,5)
Unlike acute injuries that cause inflammation, tendinopathy is characterized by repeated overloading, micro-tearing, failed healing, and subsequent tendon degeneration. (3,4,6,7) The process begins with collagen fiber disruption and ends in a disorganized healing process that fails to regenerate a “normal” tendon. Failed healing is blamed on a hyperplastic, but ineffective, microvascular system. (8,9)
An appreciation of gait mechanics is germane to understanding Achilles tendon injuries. During normal gait, the foot approaches the ground with 3-4 degrees of supination, allowing ground contact to occur on the lateral portion of the calcaneus. As a shock-absorbing mechanism, the foot initially relaxes into subtalar pronation. At mid-stance, the foot converts into a rigid lever and begins to supinate in anticipation of propulsion. Tibial external rotation accompanies ankle supination. Inefficient conversion from shock absorber to rigid lever results in hyper pronation, which stresses the medial calcaneotendinous attachment of the Achilles tendon. (10)
Classifications of Injuries
Injuries to the Achilles tendon may be classified as “insertional” or “non-insertional.” Insertional tendinopathy, as its name implies, describes damage to tendon fibers at their insertion on the posterior calcaneus. This process may result in calcification and bony exostosis, producing a prominent enlargement of the posterior calcaneus, also called a “Haglund deformity” or “pump bump.” Non-insertional Achilles tendinitis most commonly involves the vulnerable “watershed area,” 2-6 cm proximal to the calcaneal insertion. (11) This region of the tendon has a smaller cross-sectional area, is relatively hypovascular, and is subject to a repetitive “wringing” motion during supination/ pronation. This susceptible mid-section is the most common site for degeneration and rupture. (12,13)
Achilles tendon injuries affect between 250,000 and 1 million people per year in the United States. (14,15) Most are middle-aged males in their third or fourth decade of life. (14,16) Interestingly, Achilles tendon injuries occur more frequently on the left side. (16) Injury rates are highest in the spring months and lowest in the fall. (93) Patients who have suffered prior Achilles tendon rupture are at significantly higher risk for contralateral tendon rupture. (17)
Two-thirds of all Achilles tendon injuries involve athletes. (18) Runners are up to 10 times more likely to suffer Achilles tendon injuries, compared to age-matched controls. (18) The Achilles is the most common site of tendinopathy in runners. (77) Athletes are at greater risk during speed training or sprinting. (19) Runners who assume a midfoot or forefoot strike pattern may be at even greater risk of injury. (20) Not surprisingly, a higher risk has been identified in other sports that involve running or jumping. The estimated incidence of Achilles tendinopathy is: running sports, 53%; soccer, 11%; dance, 9%; gymnastics, 5%; racquet sports, 2%; football, 1%. (14,21)
Extrinsic risk factors for Achilles injury include improper warm-up, overtraining, cold-weather training, running on hard surfaces, excessive stair or hill climbing, improper arch support/ footwear, poor conditioning and abruptly returning to activity after a period of inactivity. (19,22-26,94) Wearing high-heeled shoes may lead to shortening of the gastrocnemius/soleus, predisposing women to Achilles tendinopathy. (27) Intrinsic factors include, prior lower limb fracture, hyper pronation, pes planus, cavus foot, gastrocnemius/soleus inflexibility or weakness, limited ankle dorsiflexion, and limited subtalar motion. (14,22-26,94,96) Systemic risk factors include diabetes, hypertension, inflammatory arthropathy, gout, obesity, and the use of corticosteroids or quinolones (broad-spectrum antibiotics). (28,81,84,94)
Patients may present with symptoms from an acute strain or a more gradual onset of repetitive irritation. Complaints include pain or tenderness in the tendon or heel that intensifies with activity, especially walking or running. Patients may report difficulty when attempting to stand on their toes or walking steps, particularly down stairs. Morning pain and stiffness are common. Patients may report warmth and swelling that increases throughout the day, related to activity. Symptoms may be tracked using the VISA-A questionnaire. (29)
Palpating the point of maximum tenderness can help localize the site of injury to either the “watershed area,” or the calcaneal insertion. Mid tendon pain suggests non-insertional tendinitis, whereas posterior calcaneal pain suggests insertional tendinitis. Fusiform swelling and tendinous or bony enlargement are common in cases of chronic tendinopathy. Those with insertional tendinopathy may demonstrate evidence of bony enlargement or spurring on the posterior calcaneus.
Range of motion testing will likely reveal deficits in passive dorsiflexion, with pain on resisted plantar flexion. In some patients, single-leg heel raises will elicit pain, while in others, repetitive hopping may be needed to elicit complaints. The Silfverskiold test can help differentiate Achilles vs. gastrocnemius tightness in patients with limited dorsiflexion. Clinicians may perform the “calf squeeze test” (Thompson test) to exclude tendon rupture in those who have difficulty ambulating. The test has excellent validity and is performed by squeezing the calf of a prone patient and observing for passive plantar flexion of the foot. (30) Clinicians should perform motion palpation of the subtalar joint to assess mobility and identify restrictions.
Plantaris tendon pathology is associated with chronic mid-portion Achilles tendinopathy. (87-89) The plantaris tendon typically resides deep and adjacent to the Achilles medial border. Repetitive irritation of either tendon may lead to inflammation, scar tissue formation, and adhesion. This restricts gliding and leads to painful tethering when load is applied. (90) In some cases, the plantaris tendon has been known to thicken or even invaginate into the Achilles tendon, thereby thwarting traditional conservative management of Achilles tendinopathy. Tenderness on the medial mid-tendon is suggestive of plantaris involvement, while ultrasound or MRI may be necessary for a definitive diagnosis.
Assessing for Deficits
Clinicians must assess for contributory functional deficits throughout the kinetic chain. Runners with non-insertional tendinopathy demonstrate an increased incidence of foot hyperpronation (subtalar eversion). (76) Foot hyperpronation manifests as loss of the medial longitudinal arch, forefoot abduction (i.e. “too many toes sign”), calcaneal eversion, and navicular drop. Assess for weakness in the posterior tibialis by observing for calcaneal eversion during heel raises. Gastrocnemius/soleus flexibility may be assessed by measuring and comparing passive ankle dorsiflexion. Clinicians should assess knee flexor/hamstring strength, as weakness in this muscle is a known risk factor for Achilles tendon pain. (31) Weakness or delayed activation of the hip abductors (gluteus medius) should be identified and corrected. Functional orthopedic testing for hip abductor weakness would include the Trendelenberg sign, overhead squat test, and single-leg squat test. Weakness or delayed activation of the gluteus medius is associated with ankle dysfunction. (32)
Hallux limitus (limitation in passive dorsiflexion of the first metatarsophalangeal joint) disrupts normal foot functional stability and has been associated with Achilles tendon pain. (33) Functional hallux limitus assessment is performed on a long-sitting patient. The clinician places a thumb under the patient’s first metatarsal head and forces the patient’s foot into maximum dorsiflexion and pronation to simulate a ground reaction force. The clinician then pinches the patient’s great toe with their opposite hand and passively moves the toe into dorsiflexion. Dorsiflexion of the great toe should be fluid and produce concurrent plantar flexion of the patient’s metatarsal head into the clinician’s thumb. A sense of “jamming” or “locking” upon dorsiflexion or a lack of concurrent first metatarsal plantarflexion suggests hallux limitis. Assessment of the patient’s shoe insole may help to identify hallux limitus by revealing a lack of wear under the first metatarsal head with disproportionate wear under the second through fifth metatarsal heads and pad of the great toe. (34)
Diagnostics & Differential
Radiographs are often unnecessary for the diagnosis of Achilles tendinopathy. (35) The Ottowa Ankle Rules define the appropriateness for imaging patients with ankle or midfoot pain, following trauma. (36-38,74,75) No clearly defined rules exist for imaging non-traumatic heel pain. Clinicians may consider radiographs in cases of significant trauma with altered gait or when necessary to rule out other pathology, including calcaneal epiphysitis/avulsion. Radiographs of Achilles tendinopathy may demonstrate tendon calcifications and spurs/ enthesophytes on the posterior calcaneus. Ultrasound may be an efficient cost-effective means of evaluating the Achilles tendon. (39) Ultrasound or MRI may help identify and define tendon pathology.
The differential diagnosis for Achilles tendinopathy includes fracture, avulsion, neoplasm, infection, ankle sprain, retrocalcaneal bursitis, posterior ankle impingement, Os-trigonum syndrome, tenosynovitis, tendon dislocation, gastrocnemius musculotendinous strain (tennis leg), sural neuroma, systemic inflammatory disease, and calcaneal apophysitis (Sever’s disease). In children and adolescents, the epiphyseal growth plate is 2 to 5 times weaker than in adults. This group is more likely to suffer epiphyseal injuries in the form of calcaneal apophysitis (Sever’s disease) from stressors that would likely cause Achilles tendinopathy in adults. (40)
Nonoperative treatment is the mainstay for Achilles tendinopathy. (81) “Traditional” treatment plans based solely on rest, therapy modalities, orthotics, and NSAIDs have failed to demonstrate benefit for Achilles tendinopathy patients. (41) Passive modalities including ice, ultrasound, electrical stimulation, and low-level laser also lack support. (42) The current standard of care for Achilles tendinopathy includes a combination of rest, eccentric rehabilitation, and correction of mechanical faults. Studies have demonstrated excellent results in up to 85% of patients undergoing appropriate conservative care. (43) Initially, patients may need to limit or stop activities that cause pain. Significant strains may require the use of crutches or a boot. Runners may need to switch to swimming, cycling, or other activities that limit stress to the Achilles tendon. Less stiff shoe soles will help to dissipate force and decrease Achilles strain when landing. (97) Patients should avoid shoes with an excessively rigid heel tab to reduce irritation.
Eccentric exercise programs are effective in treating Achilles tendinopathy. (41,44-54) Eccentric training is more effective than concentric training for reducing pain and improving function. (52,55) In fact, research suggests that eccentric strength training programs are more than twice as effective as concentric programs for the treatment of Achilles tendinopathy. (52) A proven program by Alfredson (45) incorporates single leg eccentric heel drops off the edge of a step. Heel drops should be performed with the knee both straight and bent, three sets of 15 repetitions, twice per day for 12 weeks. One study suggested that deficits are more prevalent in the soleus as compared to the gastric so rehab must include bent-knee exercises that target this muscle. (96) Heel drops should occur slowly on a 4-10 second count. (56) The patient should use the non-injured leg to return to the “heel up” start position, thereby avoiding concentric contractions. Moderate pain during this exercise is acceptable but if the pain is excessive, the patient should assist downward motion with the non-injured leg.
The goal of tendinopathy rehab is to carefully balance stimulating a controlled musculotendinous inflammatory response without causing greater injury or exacerbating symptoms. Rehab should begin with moderate effort and low repetitions. Response to tensile loading may be assessed by the patient’s change in night pain. Increases in night pain indicate the current rehab load is excessive. Progression advances when the patient tolerates a given level of tensile load. (92)
Soft tissue manipulation, stretching, and myofascial release techniques are necessary to promote flexibility of the calf muscles. Stretching of the calf muscles should be performed with the knee straight to address the gastrocnemius and with the knee bent to lengthen the soleus. Clinicians should consider the use of IASTM to release adhesions within the Achilles tendon. As an additional benefit, IASTM may accelerate healing, possibly via controlled microtrauma. (57,78-80) Manipulation may be necessary to eliminate restrictions in the kinetic chain, particularly within the ankle. (58) Clinicians may consider the use of a 7-15 mm heel lift (bilaterally) to minimize dorsiflexion stress. Arch supports or orthotics may be necessary to correct hyperpronation. (76) Patients with hallux limitus may benefit from wearing shoe inserts with a “cut out” beneath the first metatarsal head. (59)
The treatments described thus far are directed at a “contractile dysfunction” model. If the patient’s complaints are not resolving as intended, it is important to consider the Mechanical Diagnosis Therapy (MDT) concept of “derangement”. Many cases of “derangement” tendinopathy have responded to end-range plantar flexion, although a recent review of the literature provides no clinical trials of this concept. End range plantar flexion is performed on a regular basis, 10 repetitions every 2-3 hours. A clinical indicator that the patient may respond well to repetitive end-range movements is worsening of symptoms after dorsiflexion exercises.
Athletes should introduce new activities slowly and avoid increasing activity, particularly running, by more than 10% per week. Runners should begin on smooth, shock-absorbent surfaces and start out at a lower intensity and distance, first increasing distance, then pace. Athletes should avoid training on hard or unlevel surfaces, including hills.
Return-to-play criteria for Achilles tendon strains or ruptures include the “Triple 5”:
1. Ankle dorsiflexion is within 5 degrees of the uninjured side,
2. Calf circumference (measured 10 cm distal to the tibial tuberosity) is within 5 mm of the uninjured side, and
3. The patient is able to perform 5 sets of 25 single leg heel raises. (60)
Patients who fail a trial of conservative care should be referred, but proven alternatives are scarce. Medical co-management is of limited benefit. NSAIDs may relieve symptoms but have little long-term effect on outcome. (61,62) Cortisone injections are unproven for the treatment of Achilles tendinopathy and carry a possible increased risk of tendon rupture. (63,64) Extracorporeal shock-wave therapy (ESWT) or platelet-rich plasma (PRP) injections are controversial alternatives. (65-68) ESWT (originally developed as lithotripsy) is thought to break up calcific deposits and stimulate fibroblast activity to encourage healing and may be appropriate for Achilles tendinopathy. (81,82,91). PRP treatments consist of injecting platelet-rich plasma into a tendon to create a concentrated trigger of growth factors and chemoattractants for macrophages and fibroblasts, which gradually repair the damaged collagen. (69) Some clinicians suggest benefit from PRP injections, but others refute its usefulness for Achilles tendinopathy, (81,83) including at least one randomized clinical trial. (70)
Conservative care has shown to be as effective as surgery for long-term pain relief, ROM, function, tendon force, and quality of life in cases of chronic tendinopathy. (98) In the event of Achilles tendon rupture, several studies report at least equivalent results between surgical and conservative management. (59,71,72,85)
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