The inferior tibiofibular joint is the articulation between the fibular notch on the lateral aspect of the tibia and the distal end of the fibula. It is considered to be a syndesmosis because the firm union of the two bones is largely due to the interosseous membrane. Anterior and posterior ligaments reinforce the joint.

The deep part of the posterior ligament is the inferior transverse tibiofibular ligament which passes under the posterior ligament from the tibia into the malleolar fossa of the fibular. It is a thickened band of yellow elastic fibres forming part of the articulating surface of the ankle joint.

The firm union of the inferior tibiofibular joint is a major factor in the inherent stability of the ankle joint mortise. When the ankle joint is in dorsiflexion, the close packed position, the elastic nature of the inferior tibiofibular joint ligament allows the joint to yield and separate, accommodating the wider anterior aspect of the trochlear surface of the talus. In plantarflexion the ligament recoils as the narrower posterior aspect of the talus moves into the mortise, approximating the malleoli to maintain a pinch-like grip on the talus.

Dorsiflexion and plantarflexion of the ankle will induce small accessory movements in the inferior tibiofibular joint which in turn affect the superior tibiofibular joint. Injuries of the syndesmosis usually involve forced dorsiflexion, causing widening or diastasis of the ankle mortise (Edwards & DeLee 1984, Boytim et al 1991, Marder 1994). However, isolated injuries are uncommon and damage usually occurs in association with other major ligamentous disruption and fracture.

The ankle joint (talocrural joint) is a uniaxial, synovial hinge joint between the mortise, formed by the distal ends of the tibia and fibula, including both malleoli, and the dome of the talus. Its function is complex, with the talocrural, subtalar and inferior tibiofibular joints working in concert to allow coordinated movement of the rear foot (Hertel 2002). It bears more weight per unit area than any other joint, and any malalignment or instability may lead to degenerative changes (Sartoris 1994). The joint surfaces are covered with hyaline cartilage and surrounded by a fibrous capsule which attaches to the margins of the articulating surfaces. The capsule is lined with synovium and reinforced by strong collateral ligaments. The congruity of the articular surfaces during loading of the joint, the static ligamentous control and the dynamic control of the musculotendinous units all contribute to the stability of the ankle joint (Hertel 2002).

The collateral ligaments are roughly triangular in their attachments, radiating downwards from the malleoli to a wide base. Each has anterior and posterior components which link with the talus, and a central component that links with the calcaneus.

Movement at the ankle joint occurs about a transverse axis in a sagittal plane and amounts to approximately 20° of dorsiflexion and 35° of plantarflexion, allowing the foot to adjust to the surface on which it is placed. Dorsiflexion achieves the close packed position of the ankle joint and no movement of the talus in the mortise should be possible in this position. In full plantarflexion, the loose packed position, a small amount of side-to-side movement of the talus should be possible.

The medial collateral (deltoid) ligament forms a strong multiligamentous complex spreading out in a fan shape over the medial aspect of the ankle joint. It forms a continuous line of attachment from the navicular in front, along the sustentaculum tali to the talus behind. The origins and insertions of the various parts of the ligament are contiguous and therefore not clearly demarcated, but it is generally accepted to have deep and superficial fibres. The superficial fibres cross the ankle and subtalar joints, while the deep fibres cross the ankle joint (Boss & Hintermann 2002).

As the medial collateral ligament offers such strong support to the medial aspect of the ankle joint, traumatic injuries more commonly cause fracture and disruption of the syndesmosis rather than ligamentous injury. Most strain on the ligament occurs with a dorsiflexion and eversion stress. Biomechanical problems in the foot can, however, lead to a gradual onset overuse lesion of the medial collateral ligament and treatment should be directed to the cause.

The lateral collateral ligament consists of three separate bands which leave the ligament deficient in its support of the lateral aspect of the ankle joint. Consequently forced inversion of the plantarflexed foot commonly affects the lateral collateral ligament (Liu & Jason 1994, Lee & Maleski 2002).

The components of the lateral collateral ligament are as follows (Fig. 12.1):

The contribution of the individual lateral ligaments to ankle joint stability is not constant, but depends on the position of the ankle and foot in space. Ligamentous stabilization is most critical in the unloaded ankle as this is when injury tends to occur as initial contact is made with the ground during the gait cycle. During weight-bearing, stability is maintained by the bony congruency of the mortise. The anterior talofibular ligament has the weakest tensile strength with a load to failure two to three and a half times lower than that for the calcaneofibular ligament which is rarely injured in isolation (Boruta et al 1990, Miller & Bosco 2002).

The tibiofibular syndesmosis is established by the interosseous ligament, the posterior inferior tibiofibular ligament and the anterior inferior tibiofibular ligament, which is the weakest of the three. Post-traumatic antero-lateral laxity following injury to the anterior talofibular ligament may lead to anterior extrusion of the talar dome in dorsiflexion, resulting in impingement of the anterior inferior tibiofibular ligament (Bekerom & Raven 2007).

The foot consists of 26 bones and 57 joints which enable it to act as a rigid structure for weight-bearing, e.g. pointing in ballet, or to be converted into a flexible structure for mobility, e.g. gait activities (Nordin & Frankel 2001). The foot supports body weight and controls posture by maintaining the centre of gravity. It assists propulsion and lift, as well as restraining gait activities and acting as a shock absorber. To provide this variety of functions, arches have developed together with the joints, ligaments and muscles, all contributing to functional activities. The main joints and ligaments of the arches, of clinical concern in orthopaedic medicine, will be described briefly here.

The subtalar (talocalcaneal) joint is a synovial joint between the talus and underlying calcaneus, which works in conjunction with the ankle and mid-tarsal joints to form a functional component. These joints together allow the foot to adapt to the surface of stance and to act as a shock absorber. They allow adjustment of the arches of the foot and, in conjunction with muscle activity, provide spring and propulsion to gait. During walking, the subtalar joint adapts to the side-to-side slope of the ground, accompanied by secondary rotation of the tibia (Evans 1990).

The subtalar joint consists of separate anterior and posterior joint cavities divided by the sinus tarsi (a narrow tunnel running obliquely forwards and laterally between the talus and the calcaneus). Interosseous and cervical ligaments stabilize the subtalar joint and form a barrier between the two joint capsules; they have been described as the ‘cruciate ligaments of the subtalar joint’ (Hertel 2002). This division of the subtalar joint has implications for injection of the joint which will be discussed below.

Movements at the subtalar joint are complex due to the shape of the articulating facets, which allow a degree of play to occur simultaneously in three planes. The calcaneus ‘pitches’, ‘turns’ and ‘rolls’ (Kapandji 1987) under the talus, enabling these accessory movements to contribute to the functional movements of the joint. This results in triplanar motion of the talus around a single oblique axis. The subtalar joint, therefore, is a uniaxial joint with one degree of freedom of movement, supination, which achieves a varus position of the calcaneus, and pronation, which achieves a valgus position of the calcaneus (Levangie & Norkin 2001).

The mid-tarsal (transverse tarsal) joints consist of the calcaneocuboid joint laterally and the talocalcaneo-navicular joint medially. These joints adapt the posture of the foot, keeping the sole of the foot in contact with the ground whatever the slope of the surface or the position of the leg. Together they act as a shock absorber as well as providing elasticity and spring to gait.

The calcaneocuboid joint is supported by the dorsal calcaneocuboid ligament, which is a capsular ligament that runs along the dorsolateral aspect of the joint, and the plantar calcaneocuboid (short plantar) and the long plantar ligaments (Levangie & Norkin 2001, Palastanga et al 2006). The dorsal calcaneocuboid ligament is sometimes involved in an inversion sprain of the ankle as it resists inversion and adduction of the mid-tarsal joint.

The talocalcaneonavicular joint is supported by the spring ligament (otherwise known as the plantar calcaneo-navicular ligament) which spans the gap between the sustentaculum tali on the calcaneus and the navicular below the talar head. Consequently, this joint can be visualized as a ball and socket joint with the facet on the head and lower surface of the neck of the talus as the ball. The osseoligamentous socket is formed by the navicular anteriorly, the sustentaculum tali and calcaneus posteriorly and the spring ligament, and supports the head of the talus.

Movements at the mid-tarsal joint (calcaneocuboid and talocalcaneonavicular joint complex) do not occur in isolation (Levangie & Norkin 2001, Palastanga et al 2006). Accessory movements at the mid-tarsal joints consist of dorsiflexion and plantarflexion, abduction and adduction, and inversion and eversion.

A series of arches, ligaments and muscles satisfies the requirements of the foot to be able to provide both strength and mobility.

The arches of the foot depend on ligamentous and muscular support. The important ligaments are the long and short plantar ligaments, plantar aponeurosis and the spring ligament (plantar calcaneonavicular ligament). The intrinsic muscles of the foot maintain the arches, together with some of the long muscles of the leg. Tibialis anterior supports the medial arch, while peroneus longus supports the lateral arch.

The plantar fascia is a strong aponeurosis on the plantar surface of the foot which, together with the mid-tarsal ligaments and intrinsic and extrinsic muscles, withstands loading during weight-bearing. It consists of three variably developed components known as central, medial and lateral cords. The central cord is biomechanically the most important, arising from the medial side of the medial calcaneal tuberosity and consisting of longitudinally arranged fibres of collagen and elastin. The fibres pass distally into the forefoot, widening and thinning before dividing into five distinct bands that extend into the toes (Karr 1994, Yu 2000). At its insertion into the calcaneal tuberosity (the enthesis) it has a thickened ‘cuff’ similar in appearance to the rotator cuff of the shoulder (Yu 2000). This strong connecting cable passing between the pillars of the longitudinal arch has very little ability to lengthen, but under loading gives slightly to act as a shock absorber.

The numerous tendons crossing the ankle joint complex contribute to dynamic stability as well as producing movement of the various joints. The lateral muscles have a role in controlling supination and the anterior muscles probably slow the plantarflexion component of supination, acting to prevent injury to the lateral ligaments (Hertel 2002). As tendons cross the ankle joint, they change their direction from running vertically to horizontally. Several retinacula prevent the tendons from bowstringing under activity, while synovial sheaths protect the tendons as they pass under the retinacula.

The talus provides attachment for ligaments and many tendons pass over it, although it does not itself give insertion to any contractile unit.

All anterior muscles of the lower leg are supplied by the deep peroneal nerve and their principal function is dorsiflexion of the ankle and extension of the toes.

Tibialis anterior (L4–L5) takes origin from the upper two-thirds of the lateral tibial shaft and adjacent interosseous membrane. It becomes tendinous in its lower third, passing across the anteromedial aspect of the ankle joint to insert into the medial aspect of the medial cuneiform and the base of the first metatarsal. Its function is to dorsiflex the ankle during the swing-through phase of gait and to invert the foot. It raises the medial longitudinal arch and works in conjunction with other muscles to counteract gravity and to control foot placement. This tendon runs a relatively straight course and is not a common cause of pain. However, hill running or irritation from tight-fitting boots, for example, may cause lesions of tibialis anterior (Frey & Shereff 1988, Chandnani & Bradley 1994).

Extensor hallucis longus (L5, S1) takes origin from the middle of the anteromedial border of the fibula and passes downwards and medially to a tendon which inserts into the base of the distal phalanx of the hallux. Functionally it dorsiflexes the ankle and extends the hallux to enable the big toe and foot to clear the ground during the swing-through phase.

Extensor digitorum longus (L5, S1) takes origin from the upper two-thirds of the anterior aspect of the fibula and passes downwards under the extensor retinacula, dividing into four tendons which insert into the dorsal digital expansions of the lateral four toes. Functionally, it assists dorsiflexion of the ankle and extends the lateral four toes, to clear the ground during the swing-through phase.

Peroneus tertius (L5, S1), a divorced part of extensor digitorum longus, arises from the lower anterolateral aspect of the fibula and inserts into the base of the fifth metatarsal. It functions as a weak dorsiflexor of the ankle and an evertor of the foot.

The peroneal muscles pass under two rectinacula to reach the lateral side of the foot. The principal function of the lateral muscles is to evert the foot, controlling side-to-side movements in standing and acting as the primary lateral dynamic stabilizers of the ankle (Frey & Shereff 1988). Peroneus longus, together with tibialis anterior, forms a stirrup for the foot, maintaining and supporting the arches. Both peroneus longus and brevis are supplied by the superficial peroneal nerve.

Peroneus longus is the main evertor of the foot and draws the medial side of the foot down, as in plantarflexion and eversion. Peroneus brevis also produces eversion and plantarflexion (Palastanga et al 2006).

Peroneus longus (L5, S1–S2), the more superficial of the two peroneal tendons, arises from the head and upper lateral two-thirds of the fibula. It becomes tendinous just above the ankle and passes behind the lateral malleolus in a sheath common to it and peroneus brevis. Continuing on, it crosses the lateral surface of the calcaneus, passing below the peroneal tubercle, where it leaves peroneus brevis. It occupies a groove on the lateral and plantar surfaces of the cuboid and crosses the sole of the foot obliquely to insert into the lateral side of the base of the first metatarsal and adjacent medial cuneiform.

Peroneus brevis (L5, S1–S2) arises from the lower lateral surface of the fibula. It lies in front of peroneus longus as the tendons pass behind the lateral malleolus in the common sheath. It crosses the calcaneus above the peroneal tubercle to insert into the base of the fifth metatarsal.

Generally, the more superficial posterior muscles are concerned mainly with plantarflexion of the ankle, while the deep muscles flex the toes. Both groups are supplied by the tibial nerve.

Gastrocnemius (S1–S2) is the most superficial of the posterior muscles and gives the calf its characteristic shape. It has two heads of origin from the appropriate posterior femoral condyle. The medial head is larger, extends more distally and is a common site for muscle belly injuries. The two muscle heads come together in a broad tendon which is joined on the anterolateral side by soleus, forming the Achilles tendon. Functionally, gastrocnemius flexes the knee and plantarflexes the ankle.

Soleus (S1–S2) lies deep to gastrocnemius, arising from the upper posterior aspect of the fibula and soleal line of the tibia. The muscle fibres blend into a membranous tendon which lies deep to the gastrocnemius, allowing both muscles to function individually. These tendon fibres then merge with the Achilles tendon.

Plantaris (S1–S2) arises from the posterior aspect of the lateral supracondylar ridge of the femur and descends medially to blend with the Achilles tendon. Its function is to assist gastrocnemius.

Gastrocnemius, soleus and plantaris form a functional group known as triceps surae; as well as functioning together they also have independent functions. Gastrocnemius works with plantaris to flex the knee and plantarflex the foot, providing propulsion to the push-off phase of gait. Soleus works continuously as a postural muscle through its slow-twitch muscle fibres which maintain the upright posture (McMinn et al 1995). In standing, the ankle is in a loose packed position with the centre of gravity falling anterior to the joint. Soleus counteracts the tendency for body weight to move forwards over the stationary foot (Standring 2009).

The Achilles tendon is a long tendon which receives the fibres of gastrocnemius and soleus. It is about 15 cm long (Standring 2009) and its insertion into the calcaneus is cushioned by two bursae: the retrocalcaneal bursa on its deep surface and the subcutaneous Achilles bursa on its superficial surface (Smart et al 1980). The tendon fibres twist as they pass down to their insertion into the middle of the posterior surface of the calcaneus. This twist in the tendon fibres is understood to be responsible for the tendon’s elastic properties, the stored energy providing propulsion to lift the heel during walking, running and jumping activities (Norris 2004). The tendon has a zone of relatively poor vascularity 2–6 cm above its insertion and is prone to overuse, degeneration and rupture, particularly at this site (Smart et al 1980, Chandnani & Bradley 1994).

Tibialis posterior (L4–L5) arises from the upper postero-lateral surface of the tibia. It passes behind the medial malleolus in its own sheath, crosses the deltoid ligament and inserts into the tuberosity of the navicular. It sends tendinous slips onto every tarsal bone except the talus. Functionally it is the main invertor of the foot, working with tibialis anterior. It gives support to the arches of the foot through its many tendinous insertions. It decelerates subtalar pronation after heel contact (Blake et al 1994). Activities which involve rapid changes in direction (e.g. soccer, tennis, hockey) place increased stress on tibialis posterior and make it vulnerable to injury in these situations (Frey & Shereff 1988).

Flexor digitorum longus (S2–S3) arises from the middle of the posterior surface of the tibia and passes downwards, becoming tendinous above the ankle joint. Behind the medial malleolus it is medial to tibialis posterior and occupies the groove under the sustentaculum tali. Dividing into four tendons, it inserts into the base of the distal phalanx of the lateral four toes. Functionally, flexor digitorum longus works with the lumbricals to keep the pads of the toes in contact with the ground, increasing the weight-bearing surface. It also acts to assist plantarflexion during the toe-off phase of gait, and repeated push-off activity may cause injury to this tendon (Frey & Shereff 1988).

The lumbricals (S2–S3) arise from flexor digitorum longus tendons and insert into the dorsal digital expansions. They flex the metatarsophalangeal joints and extend the interphalangeal joints; this counteracts the clawing tendency of the flexor digitorum longus. Together they maintain the medial arch.

Flexor hallucis longus (S2–S3) arises from the lower posterior surface of the fibula and passes behind the medial malleolus and under the sustentaculum tali to insert into the base of the distal phalanx of the big toe. It functions to provide the final thrust for toe-off and is important in supporting the medial longitudinal arch. Activities which involve repeatedly pushing off from the forefoot (e.g. ballet) may cause lesions in this tendon (Frey & Shereff 1988).

Palpate the short, thick, medial tibial malleolus, appreciating that the apex, anterior and posterior borders are all subcutaneous. Compare this with the longer, slender, lateral fibular malleolus which tends to project further distally and lie slightly more posteriorly.

It is difficult to palpate the tendons lying behind the medial malleolus, but from medial to lateral they are tibialis posterior, flexor digitorum longus and flexor hallucis longus ( Tom, Dick and Harry). You can palpate the posterior tibial pulse by applying light pressure behind the medial malleolus, approximately halfway between it and the Achilles tendon.

Consider the triangular medial (deltoid) collateral ligament which fans down from the medial malleolus to attach by a broad base from the navicular in front, to the talus behind.

Palpate the sustentaculum tali lying approximately one thumb’s width directly below the medial malleolus, where it feels like a horizontal, bony shelf.

Move directly forwards from the sustentaculum tali to the next palpable bony bump, the tuberosity of the navicular. This gives insertion to tibialis posterior and lies at the level of the lip of a slip-on shoe. Move directly forwards from the navicular to palpate the medial cuneiform and the base of the first metatarsal.

Place the ankle joint into plantarflexion and inversion, making the talus both visible and palpable anterior to the lateral malleolus. Palpate along from the anterior aspect of the lateral malleolus and the lower margin of the tibia to the anterior aspect of the medial malleolus to identify the ankle joint line.

Move to the front of the lateral malleolus and feel the depression on the lateral side of the talus; this marks the entrance to the sinus tarsi (the narrow tunnel which runs between the talus and calcaneus in front of the subtalar joint).

Palpate the tibialis anterior, extensor hallucis longus, extensor digitorum longus and peroneus tertius tendons (from medial to lateral) as they cross the ankle joint anteriorly.

Palpate the dorsalis pedis pulse approximately halfway between the malleoli on the dorsum of the foot, just lateral to the tendon of extensor hallucis longus.

Palpate the calcaneus, the largest of the tarsal bones, which forms the bony prominence of the heel.

Palpate the medial tuberosity of the calcaneus, which can be located at the posteromedial edge of the plantar surface of the calcaneus; deep palpation may be necessary. This marks the insertion of the middle cord of the plantar fascia (Fig. 12.5).

Locate the insertion of the Achilles tendon into the middle third of the posterior surface of the calcaneus. Palpate the Achilles tendon, appreciating its thickness, and follow it up to the two fleshy bellies of the gastrocnemius; the medial belly should be felt to extend further distally than the lateral.

Palpate the lateral malleolus. Move approximately one finger’s width below it and slightly anteriorly to locate the peroneal tubercle. This tubercle varies in size and position so may not be obvious. It divides the tendons of peroneus longus and brevis.

Consider the individual components of the lateral collateral ligament which take origin from the lateral malleolus. The anterior talofibular ligament is approximately the width of an index finger and it passes deeply, anteromedially to the talus. Its fibres run roughly parallel to the sole of the foot and it may be palpated in the region of the sinus tarsi. The calcaneofibular ligament passes obliquely downwards and backwards, under the peroneal tendons. The posterior talofibular ligament passes horizontally backwards to attach to the posterior talus; it is difficult to palpate.

Palpate the base of the fifth metatarsal and appreciate its prominent tubercle which gives attachment to peroneus brevis. Placing a thumb vertically behind the base of the fifth metatarsal will indicate the approximate position of the calcaneocuboid joint line. Placing another thumb or finger transversely across the tip of the thumb forms a T and the cross-bar of the T is resting over the dorsal aspect of the joint, indicating the approximate position of the dorsal calcaneocuboid ligament.

Position your hand to resist eversion of the foot, to aid identification of the two lateral tendons, peroneus longus and brevis. Behind the lateral malleolus, peroneus brevis lies in front of longus. They divide at the peroneal tubercle, with brevis running above the tubercle and longus below.

Before proceeding with the history, a general observation of the patient’s face, posture and gait will alert the examiner to abnormalities, particularly of the gait pattern. A limp usually indicates abnormal weight-bearing, but a ‘short leg’ can produce a limp through functional discrepancies of hyperpronation and a flattened medial arch (Kannus 1992).

The age, occupation, sports, hobbies and lifestyle of the patient may give an indication of the cause of the lesion and alert the examiner to possible biomechanical or postural problems.

The site and spread of pain help to localize the lesion, but, as a peripheral joint, pain is usually well localized. The presence of paraesthesia in the foot or pain in the calf or shin could suggest a more proximal lesion.

The onset of the symptoms may be sudden, due to trauma, or gradual, associated with overuse or arthritis. If the onset is traumatic in nature, the mechanism of injury should be established, particularly to give an indication of the ligaments involved. A ‘snap’ or ‘popping’ sensation at onset may indicate rupture of tendon, ligament or a fracture.

A minor injury is indicated by minimal pain and localized swelling, with the ability to continue weight-bearing activities. More severe injuries will produce diffuse swelling and an inability to weight-bear, suggesting ligamentous rupture or fracture.

The duration of symptoms indicates the stage of the lesion in the inflammatory process. A history of recurrent episodes indicates possible instability, requiring in-depth biomechanical assessment.

The symptoms and behaviour need to be considered. The behaviour of the pain indicates the nature of the lesion: mechanical lesions are eased by rest and aggravated by activity and weight-bearing.

Other symptoms described by the patient could include the ankle giving way; this is a symptom of ligamentous instability or possible loose body in the joint. A clicking or snapping sensation on the lateral aspect of the ankle could be due to disruption of the peroneal retinaculum, allowing subluxation of the tendons.

An indication of past medical history, other joint involvement and medications will aid diagnosis and establish whether contraindications to treatment techniques exist. Rheumatoid arthritis may affect the small joints of the foot. As well as past medical history, establish any ongoing conditions and treatment. Explore other previous or current musculoskeletal problems with previous episodes of the current complaint, any treatment given and the outcome of treatment.

This should be conducted in both weight-bearing and non-weight-bearing postures.

Bony deformity and functional abnormalities, of the medial arch in particular, will usually manifest themselves in the weight-bearing position.

Check the height of the medial and longitudinal arches. Pes planus is a structural flat foot which is visible in both weight-bearing and non-weight-bearing positions, while a functional flat foot is only observed on weight-bearing.

The presence of functional flat foot can be generally estimated by looking for a difference in the height of the medial longitudinal arch in the non-weight-bearing and weight-bearing positions. Estimate the distance between the tuberosity of the navicular and the ground, first in a non-weight-bearing sitting position and secondly in the standing weight-bearing position (Evans 1990).

Observe the position of the Achilles tendon from behind for any deviations in the normal straight alignment, which would indicate postural deformity. Also notice if there is any angulation of the forefoot relative to the hindfoot.

Although it is important to note postural abnormalities of the foot, this should be kept relevant to the patient’s presenting signs and symptoms. A detailed biomechanical assessment is not necessary for uncomplicated lesions, but recurrent symptoms or failure to resolve the patient’s symptoms may require referral to a podiatrist or physio-therapy specialist in lower limb biomechanics.

A bony enlargement of the posterior superior calcaneus may be observed at the back of the heel, known as Haglund’s deformity, which may also be associated with bursitis and soft tissue swellings called ‘pump bumps’ (Stephens 1994) (see page 352).

It is worth inspecting the patient’s shoes for abnormal areas of weight-bearing. This is particularly relevant to athletes and should include their training shoes. In a normal gait pattern, wear is seen on the lateral side of the heel and the medial side of the forefoot (Kannus 1992). Camber running or worn-out or incorrect training shoes can alter angles of contact between the foot and the ground and be an external cause of overuse (Evans 1990). Advice will need to be given regarding the type of shoe best suited to the patient’s activities (Anthony 1987). Abnormal callus formation indicates abnormal weight-bearing.

Colour changes such as cyanosis, erythema or pallor may indicate circulatory involvement and a change in colour in transferring from the weight-bearing to the non-weight-bearing position should be further investigated by palpating for the presence of arterial pulses (Figure 12.7 and Figure 12.8). Bruising is often associated with a recently sprained ankle or gastrocnemius muscle belly lesion and tracks peripherally. A severe sprain of the ankle can cause traction injury of the superficial peroneal nerve and vascular structures. Consideration should be given to these possibilities if changes in skin colour persist (Acus & Flanagan 1991).

Muscle wasting may be seen in the calf or peroneal muscles.

Swelling and any bruising on the lateral aspect of the ankle may be diffuse, indicating a moderate or major ligamentous lesion. Often a rounded mottled egg-shell-like swelling lies in front of the lateral malleolus: this is known as the signe de la coquille d’œuf (Litt 1992).

Minor swelling may be indicated by loss of the hollows behind the malleoli. Local swellings and ganglia should also be noted.

As peripheral joints, the ankle and foot are palpated for signs of activity. The presence of heat is assessed (Fig. 12.9) and synovial thickening is palpated most easily along the anterior joint line (Fig. 12.10). Swelling is usually observed, but it is also possible to palpate for swelling, particularly around the malleoli. If the history indicates major ligament sprain, the malleoli and talus can be palpated for any focal areas of tenderness which may indicate a fracture (Lee & Maleski 2002).

Before any movements are performed, the state at rest is established to provide a baseline for subsequent comparison.

The suggested sequence for the objective examination will now be given, followed by a commentary including the reasoning in performing the movements and the significance of the possible findings. Comparison should always be made with the other side.

The objective examination is carried out in non-weight-bearing with the patient positioned comfortably in supine lying. The joints are examined first, assessing the range of movement, pain and end-feel. Passive dorsiflexion normally has a hard end-feel and to achieve end range it must be performed with the knee in flexion to take the tension off the gastrocnemius muscle complex, which spans both the knee and ankle joints. Passive plantarflexion normally has a firm elastic end-feel due to tension in the tissues on the dorsal aspect of the foot. The presence of the capsular pattern should be noted.

Although individual passive movements can be produced at the ankle joint, it is difficult to produce isolated passive movements at the subtalar and mid-tarsal joints. To assess the small range of movement available at the subtalar joint, grasp the calcaneus with both hands. Flex the knee to allow relaxation of the gastrocnemius complex and push the ankle joint into the close packed position. The varus and valgus stress is then applied to the calcaneus through the heels of both hands, using body weight. The amount of passive movement available at the subtalar joint is limited to a few degrees of supination and pronation and the normal end-feel is hard for both.

To assess movements occurring at the mid-tarsal joints, pull down on the calcaneus to place the ankle joint into dorsiflexion. Place fingers and thumb on either side of the first metatarsal, around the narrow, lateral aspect of the foot, and move the mid-tarsal joint through its range of passive movements, plantarflexion and dorsiflexion, abduction and adduction, inversion and eversion. These movements are minimal, and difficult to produce in isolation.

Assessing passive movements of the toes is not part of the routine ankle examination, but the movements can be applied as necessary to assess for the presence of the capsular pattern.

The most common injury to the ankle involves the lateral ligaments, but other injuries include lesions of the contractile units, subluxation of the peroneal tendons (through partial or complete rupture of the retinaculae), damage to the subtalar and mid-tarsal joints and injury to the various neurovascular structures crossing the region (Marder 1994, Lee & Maleski 2002). Anterolateral impingement is rare, occurring in only 3% of ankle sprains. It can arise from a meniscoid lesion, synovitis or impingement of the distal fascicle of the anterior inferior tibiofibular ligament (Bekerom & Raven 2007). Fractures and dislocations at the ankle are outside the scope of this book.

The main ligaments are tested by two gross composite movements: passive inversion in plantarflexion for the lateral collateral ligament and passive eversion in dorsiflexion for the medial collateral ligament. Should it be necessary, the ligaments can be assessed individually, and accessory tests can be applied for joint instability (see below and p. 334).

The contractile structures are assessed by resisted tests for pain and power. The joints are placed in the mid-position and maximum resistance applied. Resisted dorsiflexion tests mainly tibialis anterior and resisted plantarflexion tests gastrocnemius and the Achilles tendon. Testing the gastrocnemius group in lying may not produce symptoms and the test may need to be repeated in standing against the resistance of body weight. Resisted inversion tests mainly tibialis posterior and resisted eversion tests the peroneal muscles.

Accessory ligament and instability tests are applied if appropriate. The gross ligament test of passive inversion mainly tests the anterior talofibular ligament which crosses the ankle joint and is taut in plantarflexion. It is the most common ligamentous injury found at the ankle. It is further assessed by the drawer test which assesses its integrity (Marder 1994). Flex the leg to allow the foot to rest on the couch. Position yourself to view movement of the fibula on the lateral side of the ankle. Place one hand over the talus to fix it and the other just above the ankle joint. Apply pressure backwards against the fibula and tibia, comparing the degree of posterior movement of the fibula with the other side. Increased posterior movement of the fibula is a positive sign and indicates laxity or rupture of the anterior talofibular ligament. There is no standardized score for assessing abnormal displacement on the anterior drawer test, with some texts suggesting a grading system of 1–3 in excessive movement relative to the contralateral ankle. A ‘suction sign’ or dimple may be observed on the lateral aspect of the ankle if the anterior talofibular ligament is ruptured (Lee & Maleski 2002, Hattam & Smeatham 2010).

In a cadaver study, Beumer et al (2003) were unable to demonstrate significant displacement during various clinical tests, including the anterior drawer test, suggesting that syndesmotic injury is unlikely to be detected by such tests. However, the mean age of the 17 cadaver specimens was 78.4 years which may have had a bearing on ankle mobility and this was not addressed in the study. They conclude that pain rather than increased displacement should be considered as the outcome measure of these tests, but admit that how increased displacement relates to pain has not been demonstrated. Fujii et al (2000) similarly used elderly cadavers to assess the accuracy of the anterior drawer and talar tilt tests and, although both tests demonstrated reasonable displacement of the hindfoot, neither was sufficient accurately to diagnose specific ligament involvement. It was concluded that these conventional stress tests are not sensitive due to a substantial amount of difference between movement of the cadaver specimens, examiner agreement and positions of the ankle for the tests. To our knowledge, these ligament tests have not been evaluated in vivo.

The calcaneofibular ligament crosses both the ankle joint and the subtalar joint. Injury to this ligament does not often occur in isolation, but is usually in conjunction with the anterior talofibular ligament. The calcaneofibular ligament resists varus stresses to the calcaneus in dorsiflexion. Combined rupture of these ligaments results in an increased talar tilt (Boruta et al 1990, Wilkerson 1992, Marder 1994). With the knee straight, passively dorsiflex the ankle (this allows it to fall just short of the close packed position) and apply a strong varus stress to the calcaneus; compare the range of movement with the other side. This test may also be graded 1–3 relative to the contralateral ankle and again dimpling may be observed (Lee & Maleski 2002).

Disruption of the inferior tibiofibular joint may be due to a forced dorsiflexion injury which can cause widening (diastasis) of the ankle mortise (Marder 1994). In clinical practice, such an injury would usually only occur in conjunction with other major ligamentous damage and possible fracture, but the talar tilt test can also be applied to test the integrity of the mortise. Apply the talar tilt test as above (it can only be applied accurately if the lateral collateral ligaments are intact). If there is any widening of the mortise, pain and excessive movement will be appreciated. A ‘click’ may be felt as the talus tilts excessively in the enlarged mortise (Cyriax & Cyriax 1993, Hattam & Smeatham 2010).

The dorsal calcaneocuboid ligament crosses the calcaneocuboid joint, part of the mid-tarsal complex, and may be involved in a lateral collateral ligament sprain or injured in isolation. To assess its involvement, apply passive adduction and inversion of the mid-tarsal joints looking for increased pain.

Sprain of the lateral collateral ligament is the most common ankle injury, accounting for approximately 85–90% of ankle sprains (Stanley 1991, Liu & Jason 1994). The anterior talofibular ligament is the weakest of the ligaments in the lateral ligament complex and is involved in nearly all lateral ligaments sprains. The calcaneofibular ligament is involved in 50–75% of all lateral ligament injuries and the posterior talofibular ligament in less than 10% (Ferran Maffulli 2006).

The basic mechanism for lateral ligament sprain is a forced inversion injury (Sartoris 1994, Kerkhoffs et al 2002). Injury occurs commonly in sport, when a player may land on another player’s foot, stumble on uneven ground; or, apart from sport, the patient may simply have tripped or slipped. The most common predisposition factor to suffering a lateral ligament injury is a history of at least one previous strain and an estimated 55% of patients do not seek treatment for a sprained ankle (Hertel 2002).

Diagnosis of sprain can be made on clinical grounds and X-ray investigation is only necessary if there is clear clinical evidence of fracture, e.g. marked bony tenderness to palpation (Auletta et al 1991, Litt 1992). The so-called ‘Ottawa ankle rules’ have also been developed as a guideline to help to decide whether an X-ray is necessary and are based on the identification of bone tenderness in specific areas (Patel & Subramanian 2007). The fibular end of the ligament is more likely to be involved in avulsion fractures than the talar end, which is protected by greater bone density (Kumai et al 2002). Forced inversion may cause avulsion of lateral structures or undisplaced fracture of the lateral malleolus, while impactive forces may stress medial structures (Sartoris 1994).

Lateral collateral ligament sprains most commonly involve the anterior talofibular ligament, with more severe injuries also involving other ligaments and structures on the lateral side of the ankle (Litt 1992, Liu & Jason 1994, Hertel 2002). Lateral collateral ligament sprains are graded according to the severity of the signs and symptoms (Boruta et al 1990, Stanley 1991, Litt 1992, Wilkerson 1992, Liu & Jason 1994, Kerkhoffs et al 2002).

Eversion sprains of the ankle represent 5–15% of all ankle injuries and are not common, as the medial collateral ligaments are 20–50% stronger than the lateral ligaments. The mechanism of injury involved is eversion with possible damage to the syndesmosis, or fracture of the malleoli, as well as injury to the medial ligament (Roberts et al 1995, Lee & Maleski 2002).

The treatment principles are applied as for the acute and chronic stages of the lateral collateral ligament if the injury is traumatic. The various directions of the ligament fibres need to be borne in mind, to be able to apply the frictions transversely. A Grade C manipulation is not applied in the chronic stage, due to the multidirectional nature of the fibres.

A secondary medial ligament sprain may develop through postural overuse. This is especially evident with flattening of the medial arch in the elderly. A biomechanical assessment of the foot may be indicated, together with orthotic correction to address the cause.

The retrocalcaneal bursa is described as saddle-shaped, horseshoe-shaped or shaped like an inverted boomerang. It lies between the distal end of the Achilles tendon, near its insertion, and the superoposterior surface of the calcaneus (Stephens 1994, Bottger et al 1998). It rests against the Achilles fat pad superiorly and blends with the Achilles tendon posteriorly (Frey et al 1992).

Objectively it is difficult to diagnose a retrocalcaneal bursitis differentially from an Achilles tendinopathy, with which it may coexist. It presents with posterior heel pain and a muddle of signs which may include pain on passive dorsiflexion which squeezes the inflamed bursa under the stretched Achilles tendon and/or passive plantarflexion which may squeeze the bursa between the Achilles tendon and the calcaneus. Swelling and tenderness to palpation may be present, just anterior to the insertion of the Achilles tendon. Retrocalcaneal bursitis may be a manifestation of rheumatoid arthritis or one of the spondyloarthropathies such as Reiter’s disease (Hutson 1990, Frey et al 1992, Baxter 1994).

Frey et al (1992) demonstrated the existence of the retro-calcaneal bursa on X-ray using an injection of contrast medium. The normal bursa contains approximately 1 mL of fluid. Patients suffering from retrocalcaneal bursitis accepted less of the contrast medium than normal subjects, leading the authors to propose that this was due to inflammatory fluid, thickened oedematous bursal walls, hypertrophic synovial infoldings and pain. Bottger et al (1998) demonstrated the normal retrocalcaneal bursa to be 1 mm in an anterior–posterior dimension, 6 mm in the transverse dimension and 3 mm in the craniocaudal dimension; bursal dimensions greater than these were seen in symptomatic subjects.

Treatment consists of a local corticosteroid injection.

Position the patient in the prone position with the foot in a degree of plantarflexion. Palpate for the tender area anterior to the distal end of the Achilles tendon and insert the needle from either the medial or lateral aspect, running parallel to the anterior aspect of the Achilles tendon (Figure 12.47 and Figure 12.48). Give the injection as a bolus if possible, or pepper it if you feel the resistance of the synovial folds. The patient is advised to maintain a period of relative rest for approximately 2 weeks following injection.

The subcutaneous Achilles bursa lies between the skin and insertion of the Achilles tendon. It may be an adventitious bursa developing as a result of external friction (Gibbon & Cassar-Pullicino 1994). Inflammation of this bursa presents with subcutaneous swelling and tenderness over the heel and may be due to abnormal pressure from heel counters. Treatment consists of relative rest and advising the patient about footwear, with particular regard to the height and rigidity of the heel counter (Stephens 1994).

Plantar fasciitis produces a typical history of a gradual onset of pain felt over the medial plantar aspect of the heel at the enthesis of the central cord into the calcaneal tuberosity (Yu 2000). Its particular characteristic is pain under the heel when the foot is first put to the floor in the morning, easing after a few steps have been taken (Kibler et al 1991, Karr 1994). It is worse after prolonged periods of standing and on initial exercise, easing as the foot warms up.

Plantar fasciitis usually occurs in middle age, with obesity as a predisposing factor (Gibbon & Cassar-Pullicino 1994). It may be precipitated by an alteration in footwear, e.g. wearing flip-flops or other similar unsupporting shoes, or seen as a relatively common injury in the running athlete, where it constitutes approximately 10% of running injuries seen (Kibler et al 1991).

Postural foot deformity such as pes planus and overpronation lowers the medial longitudinal arch and may overstretch the plantar fascia. Tightness of the Achilles tendon limits dorsiflexion and may contribute to the overpronation (Evans 1990, Karr 1994). Due to the constant-length phenomenon, extension of the toes increases the height of the longitudinal arch – the ‘windlass’ effect of the plantar fascia (Canoso 1981, Sellman 1994) – so that activities involving long-term tip-toe standing, e.g. high heels, may excessively stress the plantar fascia. It may also be associated with rheumatoid arthritis or the spondyloarthropathies.

Diagnosis is made on the typical history and the absence of other findings on examination of the foot and ankle. Passive extension of the toes, with the foot in dorsiflexion, may reproduce the pain by its ‘windlass’ effect on the plantar fascia and tenderness to palpation is usually found over the medial calcaneal tuberosity.

The mechanism of the lesion is thought to be repetitive microtrauma through overloading of the longitudinal arch, which produces focal tears and fascial and perifascial inflammation at the insertion of the plantar fascia at the bone–fascia interface (the enthesis) (Kibler et al 1991, Gibbon & Cassar-Pullicino 1994, Karr 1994). It may be a traction injury occurring through repeated intrinsic muscle contraction against a stretched plantar fascia during the push-off phase of gait, the plantar fascia acting as an aponeurotic attachment for the first layer of the plantar muscles. Both mechanisms could possibly lead to the development of calcaneal spurs (Gibbon & Cassar-Pullicino 1994). Cole et al (2005) note that calcaneal spurs are present in 50% of patients with plantar fasciitis and in up to 19% of patients without, suggesting that the presence or absence of heel spurs is not helpful in diagnosis.

Differential diagnosis should exclude fat pad syndrome which tends to occur acutely following a fall onto the heel or chronically through poor heel cushioning (Brukner & Khan 2007). The patient will experience pain on palpation of the heel and treatment is aimed at addressing the cause, advice on footwear and activity modification.

Plantar fasciitis usually responds to conservative management and Thomas et al (2001) state that 90–95% of cases get better in under 1 year without surgery. However, if symptoms do persist, surgery may be an option, with careful consideration paid to maintaining the load-bearing capacity of the longitudinal arch (Kulthanan 1992, Kim & Voloshin 1995). Tissue examined at the time of surgery has shown a hypercellular inflammatory response, reactive fibrosis and degenerative areas (Kibler et al 1991).

The chronic nature of the condition produces changes in the strength of the plantarflexors with loss of range of dorsiflexion and there may be alterations in the length of the stride (Kibler et al 1991, Chandler & Kibler 1993). All components of dysfunction should be considered when planning a rehabilitation programme.

Treatment of plantar fasciitis is local corticosteroid injection or transverse frictions. Either treatment is combined with rest from overuse activities and a full rehabilitation programme which may include intrinsic muscle exercises and correction of foot posture, if appropriate. DiGiovanni et al (2006) advocate specific stretches to the plantar fascia combining dorsiflexion of the metatarsophalangeal and ankle joints. They conclude that stretches applied in this way are more effective than Achilles tendon stretches in the management of chronic plantar fasciitis.

Although unusual, cases of spontaneous rupture of the plantar fascia have been reported, particularly among athletes. It usually occurs during rapid acceleration as the foot forcibly pushes against the ground, or may occur over time in association with sustained activity such as walking. The patient may report specific injury and a snapping sensation together with the appearance of a painful lump. The plantar fascia may be tender to palpation and bruising may be evident. Occasionally infection may occur, but this is usually associated with systemic disease such as diabetes mellitus with heel ulcerations, or extension from a surrounding soft tissue infection or through penetration by a foreign object. The calcaneus is the most commonly infected tarsal bone (Yu 2000).

An ultrasound scan is sometimes performed prior to injection to assess the degenerative state of the fascia prior to injection, as a safeguard against possible rupture. More research is needed to assess whether this should be performed more routinely.

Position the patient in prone lying with the knee flexed and the lower leg resting on a pillow. Hold the foot in dorsiflexion to apply some tension to the plantar fascia. Insert the needle at the medial border of the heel, anterior to the point of tenderness, and angled posteriorly towards the site of tenderness (Figure 12.49 and Figure 12.50). Deliver the injection to the origin of the plantar fascia by a peppering technique, with the needle point in contact with bone at the anterior edge of the medial tubercle. The patient is advised to maintain a period of relative rest for approximately 2 weeks following injection.

Dasgupta & Bowles (1995) conducted bone scans on 15 patients with a diagnosis of plantar fasciitis, to localize the inflammatory focus. In 80% of patients, an area was localized to the medial aspect of the plantar surface of the calcaneus. An accurately placed injection into this area abolished the pain and tenderness. An accurate injection technique is important to prevent the need for repeated injection, as cases of plantar fascia rupture associated with corticosteroid injection have been reported (Sellman 1994).

Although relatively rare, loose bodies can occur in the ankle or subtalar joints. They may be due to degenerative changes in the joint or be associated with fragmented spurs on the tibial or talar side, or by avulsion from the dome of the talus or either malleolus (Scranton et al 2000). The patient presents with a history of twinging pain with giving way or a momentary inability to weight-bear; this symptom may also be indicative of mechanical ankle instability due to ligamentous laxity. On examination, a non-capsular pattern may be present. The principle of treatment for a loose body is applied – strong traction and Grade A mobilization. The direction selected for the mobilization is not important.

Peroneal tendinopathy may be a chronic overuse injury, e.g. walking or training on unaccustomed surfaces, predisposed by altered foot biomechanics, or have an acute onset as tenosynovitis if the tendons are involved in an inversion sprain of the ankle. A few cases of rupture of the peroneus longus tendon secondary to repetitive inversion injury or forced eversion injury against resistance have been reported, presenting as chronic lateral ankle instability (Patterson & Cox 1999).

On examination pain is felt on the lateral side of the ankle on resisted eversion of the foot. Acute tenosynovitis may also produce pain on passive inversion. The exact site of the lesion is determined by palpation and may be at the musculotendinous junction, the tendons above, behind or below the malleolus, or at the insertion of peroneus brevis into the base of the fifth metatarsal. Disruption of the retinacula may cause snapping of the peroneal tendons due to subluxation or dislocation which may be obvious. However, to confirm this the ankle should be actively dorsiflexed and everted against resistance, which dynamically recreates the subluxation or dislocation of the tendons (Lee & Maleski 2002).

Transverse frictions are applied with the tendons on the stretch if the lesion involves the tendons in their common sheath behind or below the malleolus. If the lesion lies in the common sheath below the malleolus, corticosteroid injection can be applied as an alternative treatment modality.

The Achilles tendon is the longest tendon in the body; it is up to 1.5 cm wide and less than 1 cm in anteroposterior thickness (Chandnani & Bradley 1994). It has the capacity to withstand high tensional forces with forces of 12.5 times body weight recorded (Alfredson & Lorentzon 2000). It consists of approximately 95% type I collagen fibres and elastin embedded in a matrix of proteoglycans and water. These fibres adopt a wavy ‘crimp’ configuration at rest and the primary response to tendon and fibre elongation is straightening out of the collagen fibre crimp. It is not surrounded by a true synovial sheath, but by a paratenon, a thin gliding membrane, which permits free movement of the tendon within the surrounding tissues. The blood supply is from the musculotendinous junction, the teno-osseous junction and the surrounding paratenon (Paavola et al 2002).

The Achilles tendon is a common site for injury and rupture. Symptoms include posterior heel pain with stiffness before, during and after exercise. The tendon is usually sore and thickened, impairing gait (Alfredson et al 2002, Koenig et al 2004). Chronic symptoms are usually of gradual onset (Ohberg & Alfredson 2004).

Achilles tendinopathy can involve a range of lesions at different sites in the tendon. Lesions of the Achilles tendon usually occur about 2–6 cm proximal to its insertion, which is the zone considered to be of relatively poor vascularity (Lagergren & Lindholm 1958, Smart et al 1980, Chandnani & Bradley 1994). Lesions can also exist at the musculotendinous and teno-osseous junctions and the peritenon itself can be involved.

Differential diagnosis should include retrocalcaneal or superficial bursitis, impingement between the posterior part of the calcaneus and the Achilles tendon (Haglund’s deformity), calcification or avulsion fracture, or occasionally mixed pathology (Alfredson & Lorentzon 2000). Ohberg & Alfredson (2003) used ultrasound and colour Doppler to scan patients with chronic heel pain and identified thickened retrocalcaneal bursae, calcifications, bone spurs and loose fragments in the adjacent tissues.

An abnormally large bony bump (exostosis), known as Haglund’s deformity, may be present on the supero-posterior surface of the calcaneus. Soft tissue swellings are often associated with Haglund’s deformity and are known as ‘pump bumps’ (Stephens 1994). The deformity itself may be asymptomatic but the prominence predisposes to mechanical irritation of the retrocalcaneal bursa and strain on the Achilles tendon insertion. Treatment can include NSAIDs, heel raise or change of footwear to avoid friction, intrabursal corticosteroid injection or surgery for resistant cases.

A combination of pain in the Achilles tendon, swelling and impaired performance, together with pain on resisted plantarflexion, provides a clinical diagnosis of Achilles tendinopathy (Paavola et al 2002). Lesions of the Achilles tendon can be a tendonitis, an early acute condition which may be reversible, responding to conservative treatment, or a tendinosis, i.e. focal degenerative lesions within the tendon itself which may be irreversible (Williams 1986, Mahler & Fritschy 1992, Paavola et al 2002). Partial or complete rupture may also exist. The condition has been considered to be a continuum of a degenerative process which may eventually progress to total rupture (Fox et al 1975, Read & Motto 1992).

Overuse has been suggested as a cause of Achilles tendinopathy, especially amongst athletes, although not just in the more elite group. Symptoms are common in recreational athletes within the 35–50 age group, particularly in those who participate in middle- or long-distance running, but they can be caused by less strenuous activities or may even develop without an obvious cause (Alfredson et al 2002, Ohberg Alfredson 2004). There is a higher incidence in older postmenopausal women (J. L. Cook, conference lecture 2008). The condition also occurs in the general population, often in those with a sedentary lifestyle (Alfredson & Lorentzon 2000, Paavola et al 2002). Koenig et al (2004) note that malalignment of the rear foot leading to functional overpronation has been proposed as a cause of Achilles tendinopathy, which supports the value of assessing the biomechanics of the lower limb as part of the objective examination of the ankle and foot. Achilles pain or spontaneous rupture can be associated with spondyloarthropathies (Jebaraj & Rao 2006), a further consideration in causative factors.

Several other aetiological mechanisms are suggested in the various texts for Achilles tendinopathy: incorrect or worn-out footwear, pressure from heel counters, one-off incidents of direct trauma, inappropriate or changes in training surfaces, excessive training, training errors or indirect trauma, muscle weakness and/or imbalance, reduced flexibility, joint stiffness, male gender, obesity or leg length discrepancy.

Frey & Shereff (1988) suggest that since the fibres of gastrocnemius and soleus do not insert into the Achilles tendon in a parallel direction, abnormal shear stresses may be set up, creating an area of weakness and making it susceptible to injury. September et al (2007) have examined the genetic component in tendon and ligament injuries and blood group O or the A/O ratio appears to be associated with Achilles peritendinitis and tendon rupture in some studies. Variation in genes that encode structural proteins including various types of collagen, proteoglycans and glycoproteins may also be involved in Achilles tendon injuries. These findings are interesting but are probably not as relevant as the causative factors that can be identified and addressed as part of rehabilitation.

Leadbetter (cited in Paavola et al 2002) suggests a mechanical theory for tendon degeneration, called the ‘tendinosis cycle’, as the tendon continues to fail to adapt to excessive changes in load either during a single incident or over a prolonged period of time. The vascularization of tendons is relatively sparse compared to muscles and there are relatively few cells available for oxidative metabolism, resulting in a low circulatory and metabolic response to loading (Alfredson et al 2002).

When the tendon is subjected to 4–8% repeated strain (or possibly to 12% (Wang et al 2006)), it is unable to bear further tension. Injury occurs as the tendon tissue becomes fatigued and it is overwhelmed by repetitive microtrauma and thus unable to repair the fibre damage. The structure of the tendon is therefore disrupted and collagen fibres begin to slide past one another, weakening and breaking the collagen cross-links. Alfredson & Lorentzon (2000) emphasize that no inflammatory cells are seen histologically in tendinosis, but increased amounts of interfibrillar gel and glycosaminoglycans with changes in the collagen fibre structure. However, inflammation may affect the paratendinous structures leading to scar tissue development and this will need to be addressed during the treatment programme (Brukner & Khan 2007).

Rees et al (2006) put forward mechanical, vascular and neural theories to explain the aetiology of tendinopathy suggesting that pain may arise from a combination of factors rather than from one alone. They propose that underuse rather than overuse can be responsible and that tendinopathy is a failure of healing with the damaged tendon being subject to fibroplasias resulting in scar tissue formation and a weakened tendon. Both chronic pain and rupture occur most frequently 3 cm above the calcaneal insertion, an area that has been shown to be hypovascular in normal tendons (Pufe et al 2001, Alfredson et al 2002).

Pufe et al (2001) have hypothesized that the lack of vascularity compromises the nutrition required by tendon cells, making it more difficult for the cells to synthesize the extracellular matrix required for repair and remodelling of the fatigue damaged tendon (Tasto et al 2003). Alfredson et al (2002) have a different view, however, and note that blood flow is evenly distributed in the normal Achilles tendon under resting conditions and that the flow is unaltered by age and exercise. If that is so, factors other than peritendinous flow will need to be investigated to account for the increased incidence of lesions of the mid-portion of the Achilles tendon in middle-aged individuals.

Patients present with a history of a gradual onset of pain felt locally at the back of the heel. They may or may not recall the causative factors. In the early phase of the condition pain usually follows strenuous activity, whereas in the more chronic condition pain occurs during all activities and can be present at rest (Paavola et al 2002). The pain is worse when the foot is first put to the floor in the morning, easing after several steps (the different location of the pain distinguishes it from plantar fasciitis). Pain is increased by activity and the tendon itself may show some thickening. It is tender to palpation. Crepitus may be present, due to movement of the tendon within the paratenon which may be filled with fibrin exudate (Paavola et al 2002).

Khan & Cook (2000) initiated the debate of ‘Where does the pain comes from’ in overuse tendon injuries. The traditional inflammatory cause of pain was challenged and the ‘myth’ of tendonitis was dispelled for ‘not withstanding scrutiny’ (Khan et al 2002). Collagen fibre injury was cited as an obvious component and the biochemical irritant model of pain was put forward. Neovascularization and growth of new nerve fibres were later proposed as the cause of the pain.

This has been supported by the pain relief achieved by sclerosant injections that appear to destroy new capillary and nerve growth (Ohberg & Alfredson 2003) and eccentric exercises have also been shown to abolish neovascularization with an accompanying decrease in pain (Ohberg & Alfredson 2004). This does lead to a tension in the aims of treatment techniques however, since Tasto et al (2003) suggest that any treatment modality that stimulates local blood supply and addresses the deficit of angiogenesis may be beneficial in the treatment of tendinosis. More work needs to be done to resolve this apparent conundrum.

On examination, pain is felt on resisted plantarflexion, which should be performed against gravity with body-weight resistance to reproduce the symptoms in minor or chronic lesions. If the history indicates Achilles tendinopathy, but pain cannot be reproduced on examination, the patient may have to perform some sort of provocative exercise to produce symptoms before assessment to allow accurate diagnosis.

Rupture of the Achilles tendon rarely occurs if the tendon is healthy, but may occur if there is existing tendinosis with fibrous degeneration (Smart et al 1980). Rupture, whether partial or complete, may occur through indirect violent trauma, e.g. push-off with knee extension during weight-bearing as in sprinting, unexpected forced dorsiflexion, e.g. missing a step or stumbling, or forced dorsiflexion of the plantarflexed foot, as in falling from a height. It is accompanied by a sudden onset of pain (Smart et al 1980, Mahler & Fritschy 1992). Partial rupture and tendinosis may coexist, however, or possibly be regarded as the same condition (Alfredson & Lorentzon 2000).

Total rupture presents with a history of intense pain at the time of injury, as if being kicked or shot in the tendon, but little pain following injury. Function is disrupted and the patient is unable to tip-toe stand. A gap may be palpable immediately after injury, and the Thompson’s test (also known as Simmond’s test) may be positive. Position the patient in prone lying with the foot hanging off the couch and squeeze the bulk of the calf muscle. If intact, the Achilles tendon plantarflexes the foot (Hattam & Smeatham 2010). Matles test is a further aid to diagnosis of rupture, particularly if chronic. The patient is placed in prone lying and requested to flex the knee to 90°. Normally the foot should be slightly plantarflexed in this position and the test is positive if the foot falls into a neutral or a dorsiflexed position (Frey & Shereff 1988, Lee & Maleski 2002).

X-ray can be used to confirm complete rupture of the Achilles tendon. Kager’s triangle is a triangular space filled with fatty tissue bordered posteriorly by the inner contour of the Achilles tendon, anteriorly by the deep flexor tendons and inferiorly by the upper border of the calcaneus (Grisogono 1989, Cetti & Andersen 1993). In total rupture, Kager’s triangle loses its normal contours on the X-ray picture (Smart et al 1980). Ultrasound and magnetic resonance imaging have since become much more commonly used to confirm diagnosis.

The condition is treated by immobilization in plaster, usually after surgical repair, followed by early mobilization to achieve rapid recovery and to return to normal strength (Saw et al 1993).

Apply the principles of treatment for acute lesions, with protection, rest, ice, compression and elevation (PRICE) being applied as soon as possible after the onset and for 2–3 days after injury. Gentle transverse frictions are given to the full extent of the lesion, at a depth judged to be appropriate for the irritability present, with the muscle belly in a relaxed position (Fig. 12.69). This imitates the normal function of the muscle belly fibres, which is to broaden as the muscle contracts. Transverse frictions are followed immediately by Grade A mobilizations. The patient is taught to maintain a normal heel–toe gait, with the aid of crutches if necessary. A heel-raise takes the pressure off the muscle belly and can be gradually reduced as movement is regained.

The patient is seen ideally on a daily basis. An increasing depth of transverse frictions and greater range of Grade A mobilization is applied until full painless function is restored.

Deep transverse frictions are applied with the muscle belly in a relaxed position (Fig. 12.69), to facilitate the broadening of the fibres, having first gained analgesia with a more gently graded technique. Vigorous Grade A exercises are performed. The patient is treated until normal painless function is restored. Should the muscle need to be stretched, it is applied once the muscle is pain-free on resisted testing.

If the lesion is in the musculotendinous junction it may be treated with transverse frictions. Locate the tender site and apply the principles with regard to depth, sweep and extent of the lesion and with consideration for the irritability of the lesion (Fig. 12.70).