ACHILLES TENDINOPATHY

have been implicated. Free radical damage occurring on reperfu- sion after ischaemia, hypoxia, hyperthermia, impaired tenocyte apoptosis, cytokines, prostaglandins and fluoroquinolones have all been linked with tendinopathy (10). Pain is the main symptom of Achilles tendinopathy, but the underlying mechanism causing pain is not fully understood. Traditionally, pain has been thought to arise through inflammation, or via collagen fibre separation or degeneration (11). However, chronically painful Achilles tendons have no evidence of inflammation, and many tendons with intra- tendinous pathology detected on MRI or ultrasound, are not painful (11). As tendinopathies are the result of a failed healing response, and are not inflammatory conditions, pain may originate from a combination of mechanical and biochemical causes (12).

HISTOPATHOLOGY Tendinopathy is characterised by a disorganised impaired healing response and inflammation is not a typical feature. As a result we advocate the use of the term tendinopathy as a generic descriptor of the clinical conditions in and around tendons arising from overuse, and suggest that the terms tendinosis, tendonitis and tendinitis be used only after histopathological examination. Histologically, tendinopathy is characterised by an absence of inflammatory cells and a poor healing response, with non-inflam- matory intratendinous collagen degeneration, fibre disorientation and thinning, hypercellularity, scattered vascular ingrowth, and increased interfibrillar glycosaminoglycans (9).

CLINICAL PRESENTATION Pain is the cardinal symptom of Achilles tendinopathy. Generally, pain occurs at the beginning and end of a training session, with a period of diminished discomfort in between. As the pathological process progresses, pain may occur during exercise, and, in severe cases, it may interfere with activities of daily living. In the acute phase, the tendon is diffusely swollen and oedematous, and on pal- pation tenderness is usually greatest 2 to 6 cm proximal to the ten- don insertion. Sometimes, fibrin precipitated from the fibrinogen- rich fluid around the tendon can cause palpable crepitation. In chronic cases, crepitation and effusion diminish, and a tender, nodular swelling is present at the site of the failed healing response lesion. The diagnosis of the Achilles tendinopathy is mainly based on a careful history and detailed clinical examination. However, diagnostic imaging may be required to verify a clinical suspicion or, occasionally, to exclude other musculoskeletal disorders.

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IMAGING Ultrasonography is commonly employed to examine tendon disor- ders. It is readily-available, quick, safe, and inexpensive. However, ultrasound is operator-dependent, has somewhat limited soft tis- sue contrast, and is not as sensitive as MRI. In acute para- tendinopathy, ultrasound reveals fluid accumulation around the tendon. MRI provides extensive information on the internal mor- phology of the tendon and the surrounding structures, and is use- ful to evaluate various stages of chronic degeneration. Excellent correlation between MRI and pathological findings at surgery has been reported (13). A recent longitudinal ultrasound study showed that mild-to-moderate changes were observed frequently in both the involved and uninvolved Achilles tendons, but the occurrence of these changes was not clearly related to the patients' symptoms (14). Given the high sensitivity of these imaging modalities, an abnormality should be interpreted with caution and correlated to the patient’s symptoms before making any management recom- mendations.

MANAGEMENT In the early phase of Achilles tendinopathy, various forms of con- servative management are used. Seeking medical attention at an early stage may improve outcome, as treatment becomes less pre- dictable when the condition becomes chronic. Surgical manage- ment is recommended for patients who do not adequately respond to a conservative treatment programme over a period of 3 to 6 months. The initial conservative programme is directed towards presumed aetiological factors or towards relieving symptoms. Most commonly, it consists of a combination of strategies, including abstention from the activities that caused the symptoms, and cor- rection of training errors, foot malalignments, decreased flexibili- ty, and muscle weakness (15).

Decreasing the intensity, frequency and duration of the activity that caused the injury, or modification of that activity, may be the only necessary action to control symptoms in the acute phase. Collagen repair and remodelling is stimulated by tendon loading, and complete rest of an injured tendon can be detrimental. Modified rest, which allows activity in the uninjured body parts and reduces activity in the injured site has been recommended (15). Cryotherapy has been regarded as the single most useful intervention in the acute phase of Achilles tendinopathy. Cryotherapy is used for its analgesic effect, to reduce the metabolic rate of the tendon, and to decrease the extravasation of blood and protein from new capillaries found in tendon injuries (16).

Therapeutic ultrasound may also reduce swelling in the acute inflammatory phase and improve tendon healing. Deep friction massage has been advocated for tendinopathy and paratendinopa- thy. In chronic cases, this should be accompanied by stretching to restore tissue elasticity and reduce the strain in the muscle-tendon unit with joint motion. Augmented soft tissue mobilisation (ASTM) is a non-invasive soft tissue mobilisation technique which has been successfully used in chronic tendinopathy patients, probably through controlled application of microtrauma which would increase fibroblast proliferation (17).

Stretching and strengthening of the triceps surae muscle and Achilles tendon are important to preserve function of the triceps surae musculotendinous unit by restoring normal ankle joint

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