Treatment options for chronic Achilles tendon disorders
Chronic Achilles tendon disorders are a spectrum of disease resulting from a degenerative condition associated with overuse of the Achilles tendon. A Chikate, Yogesh Joshi, Prasad Rao and Asad Syed take a look at some of the options available when treating chronic Achilles tendon disorders
A chronic Achilles tendon disorder is characterised by pain and fusiform swelling along the Achilles tendon within the substance of the tendon or at its insertion. In its severe form it can be incapacitating and sometimes can end an athlete’s career or result in an individual’s loss of independence. Although a common condition, it is a complex and difficult orthopaedic challenge as its pathophysiology is poorly understood. The condition can be either insertional or non-insertional but the microscopic changes essentially are the same. The treatment is largely non-surgical, even though non-surgical management of chronic Achilles tendon disorders has a reported failure rate of 25 per cent. Surgery is reserved for chronic cases not responding to non-operative means. Our understanding of the treatment available keeps evolving and this article serves to highlight some of the treatment options available.
Anatomy
The gastrocnemius and soleus muscle merges to form the Achilles tendon (Figure 1). The Achilles tendon has a round upper part and is relatively flat in its distal 4cm. Fibres of the Achilles tendon spiral 90° as they reach their insertion onto the calcaneus. The Achilles tendon is enveloped by a paratenon, a membrane consisting of a single layer of cells. This anatomic variation contrasts with other tendons that have a synovial sheath. The paratenon originates from the deep fascia of the leg, the fascia cruris, covering the tendon posteriorly. It is highly vascularised and is responsible for blood supply to the tendon. Most of the blood supply is anterior. A microvascular perfusion study in normal Achilles tendons using laser doppler flowmetry has shown that the blood flow is considerably lower – approximately 2–6cm from the calcaneal insertion. In symptomatic Achilles tendon disorder, blood flow is considerably elevated compared with the control tendons [1].
Biomechanics
Tendons are stiff and resilient, with high tensile strength. They can stretch up to 4 per cent before damage. Actin and myosin are present in tenocytes and tendons have almost ideal mechanical properties for the transmission of force from muscle to bone. A tendon loses its wavy configuration when it is stretched more than 2 per cent. As collagen fibres deform, they respond linearly to increasing tendon loads. The normal wavy appearance of the tendon is regained if the strain placed on it remains at less than 4 per cent. At strain levels greater than 8 per cent, macroscopic rupture will occur. The loads imposed on the Achilles tendon can reach up to 9kN during running, corresponding to 12.5 times the body weight, 2.6kN during slow walking, and less than 1kN during cycling.
Pathophysiology
Tendons are subjected to cyclical loads, a major factor in the development of tendon disorders. There is micro-tearing from overuse and proliferation of fibroblasts in response to the tears. The healing response after tendon injury is defined by cell matrix adaptive capability. There are distinct macro-traumatic and micro-traumatic injury patterns and a spectrum of pathologic responses from inflammation to tissue degeneration. Achilles tendon disorders represent a failed healing response. As tendinopathy sets in, there is disruption of collagen fibres and an increase in non-cellular matrix. Macroscopically, the affected portions of the tendon lose their normal glistening white appearance and become grey and amorphous. The thickening that results can be diffuse, fusiform, or nodular.
Risk factors
In athletes, poor technique, sudden increase in exercise or training on hard/ uneven surfaces has been known to increase the risk of developing Achilles tendon disorder