Achilles tendinitis exists along the spectrum of peritendinitis to tendinosis or tendinopathy. This is a painful, swollen, and tender area of the Achilles tendon and peritenon usually secondary to repetitive activity or overuse.
Athletes with particularly tight heel cords are predisposed to injury. This condition commonly affects middle-aged men who play tennis, basketball, or other quick start-and-stop sports. Collagen vascular disease and diabetes may also be risk factors.
The two main categories of Achilles tendon disorder are broadly classified by anatomical location to include non-insertional and insertional conditions.
Achilles tendinopathy is a soft tissue disorder causing pain, stiffness, and swelling of the Achilles tendon. It is more common in people who participate in recreational or competitive sports, but can also affect less active individuals. Repetitive strain and microtrauma to the Achilles tendon during activities such as running and jumping make it susceptible to injury and degeneration. Most patients can be managed with conservative treatments but in some cases injection treatments may be considered. Corticosteroid injections are generally not recommend due to risk of tendon rupture, where as high volume saline injections and platelet rich plasma therapy are being increasing used now a days.
This condition may affect 9% of recreational runners and causes up to 5% of professional athletes to end their careers. The underlying cause is multifactorial.
The dogma has been that the relative avascularity of the region 5 to 7 cm proximal to the calcaneus insertion is the primary predisposing risk factor; however, there is some question as to the role of thinning and twisting of the tendon at this midsection and whether vascularity is the primary factor.
In the acute phase there may be an inflammatory cellular reaction in the peritenon, with circulatory impairment and oedema. The peritenon may become filled with fibrinous exudate, perceived as crepitus, and may form adhesions, causing the more chronic condition of paratendinopathy. Injury within the tendon itself will also lead to an initial inflammatory response but an imbalance between matrix degeneration and synthesis may lead to tendinopathic changes.
Disorders of the Achilles insertion account for around 20% to 25% of tendo Achilles disorders. Predisposing factors are increasing age, inflammatory arthropathies, corticosteroid use, diabetes, hypertension, obesity, gout, hyperostotic conditions, lipidaemias and quinolone antibiotics. Other factors include genetic susceptibility and extrinsic factors such as increased repetitive loading or inadequate footwear can contribute, with uneven wear causing excessive subtalar joint movement or poor shock absorption; uneven or sloping surfaces also play a role. Intrinsic hindfoot and lower limb malalignment and altered biomechanics of the subtalar joint in particular can result in micro-tears and tendinopathic changes.
A posterosuperior calcaneal prominence, originally described by Haglund, has been associated with tendon attrition, pain and swelling. However, insertional spurs are probably an adaptive process of formation rather than being due to tendon micro-tears or inflammatory changes.
The anterior aspect of the insertion is commonly affected more than the posterior aspect in tendinopathy. As the posterior aspect undergoes a higher strain on dorsiflexion, it has been thought that stress shielding and potential under-use phenomenon have a role to play in the aetiology of insertional tendinopathy. However, the fact that fibrocartilaginous endochondral ossification of the insertion is more likely to occur on the anterior stress-shielded side means that the precise role of loading is complex.
The retrocalcaneal bursa is lined with sesamoid and periosteal fibrocartilage. During dorsiflexion of the ankle these layers are apposed and the tendon is compressed against the calcaneal prominence. Changes such as
synovial fold hypertrophy, calcification of the sesamoid fibrocartilage and cellular degeneration with bursal debris have been demonstrated.
The essential element in the physical examination is the localization of swelling and tenderness in the Achilles tendon in the critical zone or at the insertion. Exquisite tenderness to palpation is a classic examination finding. Palpable heat is usually not evident unless peritendinitis is a major component. The Achilles is usually tight, with ankle dorsiflexion rarely extending beyond 90 degrees. Associated findings may include abnormal foot posture (pes planus or cavus), tight hamstrings, and muscle weakness of the entire hip and leg. Heels may not move into a normal varus position when standing on toes. Neurologic evaluation, including strength, sensation, and deep tendon reflexes, is normal.
The examination should also include observation for a palpable defect and the Thompson test (squeezing the calf, which should result in plantar flexion in an attached tendon) to rule out rupture of the Achilles tendon.
X-rays are usually normal. Diagnostic ultrasonography or magnetic resonance imaging is capable of defining the extent of both tendinosis and peritendinitis.
The mainstay of treatment for non-insertional Achilles tendinopathy is conservative, with initial rest, modification of training regimes, specific exercises and correction of underlying lower limb malalignment with orthoses. Most patients will be able to return to previous activities.
Immobilisation is frequently used in the acute setting in insertional Achilles tendinopathy to control exacerbating factors, but prolonged immobilisation should be avoided. A rational treatment plan following any immobilization should involve a gradual integration of reduced load-bearing activities and a monitored physical therapy or stretching regime.
Patients who suffer from insertional disorders often have heel pain on loading. This can be due to ankle dorsiflexion causing retrocalcaneal bursa compression and impingement of the anterior fibres of the tendon. A graduated shoe raise or heel lift can alleviate pressure on the insertion by plantarflexing the heel. This may potentially accelerate healing of a degenerate tendon insertion. Hindfoot malalignment associated with insertional disorders can be corrected by insoles. if thought to be a provocative factor. Correction of eversion and pronation can improve symptoms.
Non steroidal anti-inflammatory drugs (NSAIDs) have been shown to have a modest effect on symptoms, but this was not supported in a randomised study including a placebo arm. The scientific basis of NSAIDs use in chronic tendinopathy is questionable in the histological absence of inflammatory cells in the tendinopathic tissue. Any short-term benefit is likely to be due to their analgesic effect. Some studies have highlighted the possible detrimental effects of NSAIDs: celecoxib inhibits tendon cell migration and proliferation, and NSAIDs increase leukotriene B, which may contribute to the development of Achilles tendinopathy.
Conflicting results have been reported for extracorporeal shockwave therapy (ESWT), usually of low energy, but a recent randomised controlled trial (RCT) demonstrated significant improvement when this was combined with eccentric exercises compared with eccentric exercises alone, and a further RCT reported improved scores after ESWT, particularly in women.
The increasing evidence in support of ESWT for the treatment of insertional tendinopathy, and the development of smaller, cheaper machines, is leading to an increased use of this method. ESWT can stimulate a tissue response at variable depths under the targeting device. Many applications for the treatment of tendo Achillis disorders use a low-energy therapy (< 0.2 mJ/mm2) over multiple sessions. Another important parameter is the number of impulses emitted per treatment: often up to 2000 impulses in low-energy treatment and 3000 to 4000 in high-energy treatments.
How ESWT works is a matter for speculation, but it is known to cause selective dysfunction of sensory unmyelinated nerve fibres, and changes in the dorsal root ganglia have also been reported. Cavitation may also play a role in interstitial and extracellular disruption leading to a healing response.
Corticosteroid injections are reported to reduce pain and swelling and improve the ultrasound appearance of the tendon but their vasoconstrictive action via prostacyclin, adrenoceptors and inhibition of nitric oxide synthase might be responsible.
Corticosteroid injections may have some early benefit but adverse effects were reported in up to 82% of corticosteroid trials; these include tendon rupture and decreased tendon strength is reported in animal studies. Any possible benefit of corticosteroid injection appears to be outweighed by potential risks.
Platelet-rich plasma (PRP) has become widely used in various areas of orthopaedics, with some studies demonstrating improved tendon healing using PRP compared with controls but significant improvement in symptoms has not been found when using PRP to treat Achilles tendinopathy. A randomised double-blind placebo-controlled study evaluating eccentric exercises and PRP or saline injection showed no difference in improvement in pain and activity at six months, and a recent meta-analysis concluded that although there may be benefit in using PRP to increase the healing strength in tendo Achilles repair following acute rupture, there was no evidence of any benefit in using PRP in the treatment of Achilles tendinopathy.
Small studies with limited follow-up have demonstrated reduced pain and improved function following high-volume injections of 10 ml 0.5% bupivacaine and 40 ml normal saline into the paratenon.
Intratendinous hyperosmolar dextrose (prolotherapy) is thought to produce a local inflammatory response and increase in tendon strength, but evidence to support its use is lacking.
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