Disorders of the ankle and subtalar joints
The ankle joint
The ankle is a very simple joint, allowing only plantiflexion–dorsiflexion movement. Normally the foot comes into a straight line with the lower leg during plantiflexion and can be moved to less than a right angle during dorsiflexion (Fig. 58.1).
Capsular pattern
The capsular pattern of the ankle joint is slightly more limitation of plantiflexion than of dorsiflexion (Fig. 58.2). In patients with short calf muscles, however, dorsiflexion ceases before the extreme of the possible articular range is reached, which raises the question of whether limitation is capsular or non-capsular. In such a case, a clinical diagnosis of arthritis at the ankle rests entirely on the end-feel. Limitation of plantiflexion with a hard end-feel indicates arthritis. If full dorsiflexion cannot be reached because of short calf muscles, a softer end-feel is detected.
Rheumatoid conditions
Rheumatoid conditions, so often affecting the other tarsal joints, are not found in the ankle joint. If it does become inflamed, this occurs only after a long evolution of rheumatoid disease. Exceptions are psoriatic arthritis and gout, which are not uncommon at this joint. In acute arthritis without an apparent precipitating cause, a gout attack must always be suspected, especially if the patient is a middle-aged man. Gout attacks the ankle joint in almost 50% of all gout patients.1 It responds very well to one or two injections with 20 mg of triamcinolone.
Haemarthrosis
Haemarthrosis of the ankle is not uncommon in ankle sprains. It occurs after direct trauma – for example, in soccer players. A capsular pattern at the ankle joint after an inversion sprain or direct trauma always suggests haemarthrosis. Because blood is a strong irritant to cartilage and provokes early arthrosis, it should be evacuated at once. A radiograph of the talus and/or a magnetic resonance image (MRI) must be taken to exclude osteochondral fracture.2
Avascular necrosis
Avascular necrosis is bone death due to ischaemia. Loss of blood supply to the bone can be caused by an injury (trauma-related avascular necrosis), such as ankle sprain, joint dislocation or fracture of the dome of the talus, or can stem from certain risk factors (non-traumatic avascular necrosis), such as some medications (steroids), blood coagulation disorders or alcohol abuse. The earliest clinical manifestation is the finding of a capsular pattern with a spastic end-feel. MRI is the most sensitive technique for detecting talar avascular necrosis and can be used when the condition is strongly suspected clinically despite normal radiographic findings.3
Osteoarthrosis
Osteoarthrosis is often the result of shearing strains – for instance, after malunion of a tibiofibular fracture. Early arthrosis has also been reported after aseptic necrosis of the talus.4 In sports in which repeated and severe sprains of the ankle occur, such as rugby, American football and judo, osteoarthrosis is common and often occurs early. Clinical examination shows a capsular pattern with a hard end-feel. Radiography may show cartilage loss, a flattened talar dome, subchondral sclerosis, intraosseous cysts and peripheral osteophytes.
The best conservative treatment is to fit the patient’s shoe with a higher heel, which enables walking without much dorsiflexion at the ankle joint. However, conservative treatment of painful osteoarthrosis is seldom satisfactory. Sometimes one or two injections of 20 mg of triamcinolone may help but should not be repeated too often for fear of further destruction of the joint from steroid arthropathy. During the last decade, the use of visco-supplementation (intra-articular injections of high-molecular-weight solutions of hyaluronan to restore the rheologic properties of the synovial fluid) has been shown to be safe and efficacious in the treatment of osteoarthrosis of the ankle.5 If the symptoms warrant and the condition worsens, arthrodesis is the only satisfactory treatment and is usually acceptable, provided the patient is fitted with adequate shoes that permit walking without difficulty.
Injection or aspiration technique of the ankle joint
This is a simple procedure. The patient lies in the supine position, the knee bent and the foot flat on the couch, which forces the ankle into a degree of plantar flexion. The medial malleolus and the tendon of the tibialis anterior are easily identified. The trochlea tali is found by flexing and extending the talus under the tibia. A 4 cm needle is introduced between the medial malleolus and the tibialis anterior tendon, just under the edge of the tibia (Fig. 58.3). The tip lies intra-articularly when it strikes cartilage.
Non-capsular pattern
Immobilizational stiffness
Limitation of both plantiflexion and dorsiflexion often occurs after long-standing immobilization of the ankle. Only strong and daily mobilization of the joint will afford any benefit. Traction and translation techniques can be of great value in the treatment of this post-immobilization stiffness.6 Some authors report increased motion and pain relief after arthroscopy.7
Loose body in the ankle joint
A loose body with an osseous nucleus is well known as a result of transchondral fracture (osteochondritis dissecans) of the dome of the talus. In most cases, the aetiology is inversion sprain.8,9 The diagnosis is made by radiography or computed tomography (CT), and symptoms may warrant surgery. However, when there is only a loose cartilaginous fragment without an osseous nucleus, radiographs are negative, and the diagnosis must be made almost entirely on the history.
Differential diagnosis
The differential diagnosis is between a loose body in the subtalar joint (p. 1214), distal tibiofibular ligament deficiency (p. 1230), a snapping peroneal tendon (p. 759) or an unstable ankle (p. 1229).
Other lesions with a non-capsular pattern
Sprain of the anterior tibiotalar ligament
In soccer players, new bone may form on the upper surface of the talar neck, as a result of traction at the insertion of the ligament. This has been called ‘soccer ankle’.10 The diagnosis is made from the radiograph. If pain persists, the bone spurs may be removed surgically.
Achilles bursitis
If the bursa, normally found between the Achilles tendon, the upper surface of the calcaneus and the tibia (Fig. 58.5), becomes inflamed, pain will be elicited when it is squeezed between the posterior side of the tibia and the upper surface of the calcaneus at the extreme of passive plantiflexion.11,12 Full plantiflexion evokes pain, this time at the back of the heel. Rising on tiptoe remains negative, thus excluding the Achilles tendon as a cause. Palpation reveals a tender spot anterior to the tendon, close to the superior border of the calcaneus.13
Fig 58.5 The Achilles bursa.
Dancer’s heel (posterior periostitis)
This is a bruising of the periosteum at the back of the lower tibia. The lesion lies at the junction of the cartilage and periosteum, and is caused by pressure from the upper edge of the posterior surface of the talus. It occurs in ballet dancers who, during training, develop a hypermobility in plantiflexion at the ankle joint, usually as a result of pointe work. The repetitive engagement of talus against the posterior tibial edge induces periosteal bruising.14–16 Sometimes the condition results from a single vigorous plantiflexion strain, such as when a soccer player kicks the ball from underneath.
The patient complains of pain at the back of the heel during plantiflexion. Clinical examination reveals an excessive range of movement and pain is reproduced by forced plantiflexion of the ankle. Dancer’s heel must be differentiated from Achilles bursitis.17 In the latter the end-feel is soft, giving the impression of pinching some tissue, whereas in a dancer’s heel the end-feel is normal.
The patient adopts a prone-lying position, the foot over the edge of the couch. The posterior articular margin of the tibia lies approximately 2 cm above the line joining the tips of the malleoli. A 2 mL syringe is filled with a steroid suspension and fitted with a fine needle, 4 cm long. The Achilles tendon is pushed medially (Fig. 58.6). The needle is inserted vertically downwards, lateral to the Achilles tendon, 2 cm above the line connecting the malleoli. The most difficult part of the whole procedure is now to palpate with the tip of the needle and feel for the line at which bone (tibial periosteum) gives way to articular cartilage. The infiltration is now made by placing a line of little droplets all along and just above this cartilaginoperiosteal border.
Fig 58.6 Infiltration of dancer’s heel.
Pinching of the os trigonum
Posterior ankle pain during extreme plantiflexion can also be caused by periostitis of the os trigonum. This accessory bone, located just behind the talus, is found in about 10% of the population.18 Sometimes the ossicle is fused to the talus and is then called Stieda’s process. With extreme plantiflexion, such as in ballet or soccer, the os trigonum may be pinched between talus and tibia and produce periostitis and pain.19 The clinical diagnosis is made when posterior pain during passive plantiflexion is seen in combination with slight limitation of plantiflexion movement and a hard end-feel. Diagnosis can be confirmed by an MRI examination.20 Sometimes a painful outcrop can be palpated in the posterior triangle.21 Martin22 noted not only that this reduced dorsiflexion mobility but that painfully resisted plantiflexion of the big toe was also present. This is caused by fibrosis of the flexor hallucis longus tendon in the fibro-osseous canal behind the talus.
Treatment is infiltration with triamcinolone. If pain persists, surgical removal can be considered.
Anterior periostitis
The converse of a dancer’s heel is periostitis at the anterior margin of the tibia. This is caused by pressure of the anterior lip of the tibia on the talar neck during an extreme dorsiflexion movement at the ankle.23 The typical situation inducing this injury is when a gymnast lands flat on the feet but with the knees bent so that the ankle is forced into extreme dorsiflexion. The result is immediate pain at the front of the ankle. The sharp component of the pain disappears but the lesion does not heal completely, leaving the patient with pain during extreme dorsiflexion movements. In ballet dancers, repeated and extreme dorsiflexion necessitated by the demi-plié position can lead to periostitis of the anterior tibial lip.24,25
Treatment is one infiltration with triamcinolone, along the anterior tibial margin. This is within the reach of a palpating finger and therefore the infiltration is easy to perform. The results are good. In recurrent cases, the patient is referred for arthroscopic removal of the bony impingement.26
Sprain of the posterior talofibular ligament
Sprain of the posterior talofibular ligament (Fig. 58.7) is rare. The diagnosis is difficult to make if the examiner is not aware of the possibility of this lesion being present. The only painful movement during the routine functional examination is passive eversion of the foot during full plantiflexion – a movement performed to test the anterior fasciculus of the deltoid ligament. If the pain is posterolateral instead of anteromedial, it is obvious that a tissue is being pinched rather than stretched and the condition can be considered.
Fig 58.7 The posterior talofibular ligament.
Jumper’s sprain (lateral periostitis)
This is one of the classic lesions sustained by high jumpers. Before the athlete takes off to jump, the foot is forcefully twisted in valgus and dorsiflexion. Apart from lesions at the inner side of the ankle (strain of the deltoid ligament and elongation of the tibialis posterior tendon), compression at the outer side can result. During this extreme movement, the superolateral aspect of the anterior margin of the calcaneus can impinge against the inferior and anterior edge of the fibula and produce bruising, which results in traumatic periostitis.27 Sometimes the impingement leads to chronic inflammation of the talofibular ligament, resulting in hypertrophic scar tissue.28
Examination reveals nothing if only the standard functional tests are performed. When the possibility of this lesion is suspected, combined dorsiflexion–valgus movement is performed to reproduce the pain (Fig. 58.8). If this manual stress is not sufficient to elicit the usual pain, the patient is asked to stand, squat with the foot flat on the ground and twist the heel into valgus. Palpation reveals localized tenderness at the anterioinferior surface of the fibula.
Fig 58.8 Accessory test in jumper’s sprain.
One or two injections of triamcinolone bring total relief, provided the athlete avoids sustaining the same trauma. Normally, a slight inner wedge (0.5 cm) within the shoe is needed, which prevents further bruising of the fibula during ‘take-off’. Those patients refractory to conservative treatment require arthroscopic debridement.29,30
Disorders of the ankle joint are summarized in Table 58.1.
Table 58.1
The subtalar (talocalcaneal) joint
The subtalar joint allows movement in two directions only: varus and valgus. Motion takes place around an axis through the talus (Fig. 58.9), the axis being at a 15° medial angle to a line drawn through the calcaneus and the second metatarsal.
Capsular pattern
The capsular pattern (Fig. 58.10) is progressive limitation of varus with, eventually, fixation in valgus. The valgus position is maintained by spasm of the peronei muscles.
Rheumatoid disorders
In addition to the limitation of movement towards varus by muscle spasm, local heat is present and synovial thickening can be palpated. Very often, the midtarsal joint is affected as well. In rheumatoid arthritis, the arthritis is often accompanied by characteristic changes in other joints. The possibility of early ankylosing spondylitis should be kept in mind when a young patient presents with arthritis of the subtalar joint. An early manifestation of arthritis in the subtalar and midtarsal joints is also a common finding in juvenile idiopathic arthritis.31,32 In the case of an acute joint inflammation, gout should not be forgotten.
Treatment
A 2 mL syringe is filled with steroid suspension and fitted with a thin 2 cm needle. As there may be muscle spasm, the joint is fixed in valgus to create room to insert the needle from the medial side, which must be done just above the sustentaculum tali and parallel to the joint surface. The index finger of the palpating hand is placed at the lateral end of the sinus tarsi (Fig. 58.11). The needle is moved in the direction of and slightly anterior to the palpating finger. Usually it meets bone after 1 cm. The needle must then be manœuvred until it is felt to slip in further without resistance. The tip then lies within the anterior chamber of the joint, and 1 mL of the suspension is injected. The needle is then partly withdrawn and reinserted in a 45° posterior direction, where it enters the posterior chamber, and the remaining 1 mL is injected.
Non-capsular pattern
Immobilizational stiffness
The patient lies face upwards on the couch. The therapist stands at the patient’s foot. The fingers are clasped behind the heel and the calcaneus is grasped as strongly as possible between the palms of the hands. The elbows are brought forwards in order to dorsiflex the foot. This position (Fig. 58.12) immobilizes the talus in the mortice. Mobilization is performed by swinging the body from one side to the other. This forcing must be repeated for 10–20 minutes at each session, with the greatest possible vigour.
Loose body
The patient lies prone, pulling himself or herself upwards at the upper edge of the couch until the dorsum of the foot engages the lower edge. This forces the foot into slight plantiflexion. The manipulator stands behind the patient and locks both hands around the heel, so that the crossed fingers are placed between the dorsum of the foot and the edge of the couch. The fingers are protected by a thick layer of foam. The thumbs are crossed at the dorsum of the calcaneus. In order to exert the utmost possible traction, the feet are placed against the legs of the couch and the body leans backwards. The elbows stay in line with the calcaneus, the abdomen close to the patient’s foot (Fig. 58.13). The traction produced by the body weight is reinforced by a pronation movement of both forearms. Varus–valgus movements are forced at the joint by repeatedly swinging the shoulders from one side to the other. During the whole procedure, the patient is told to maintain the pulling position and not to allow any downward movement of the body.
Disorders of the subtalar joint are summarized in Table 58.2.
Table 58.2
Painful conditions at the heel
Plantar fasciitis
Plantar fasciitis is most commonly a disorder of middle age, and men and women are affected equally. Risk factors include obesity and spending prolonged periods standing or walking, particularly on hard floors.33 It is also more common among middle-aged athletes, in whom it accounts for about 10% of running injuries.34 The lesion is usually an overuse phenomenon, occurring in the presence of predisposing anatomical, biomechanical or environmental factors that put too much strain on the plantar fascia.35,36 The condition seems to be more common in people with a valgus deformity, because this flattens the foot and puts more strain on the fascia.37 Short calf muscles can also be the cause of an overstrained fascia. In this condition, the Achilles tendon tends to pull the heel upwards during standing, which stresses the longitudinal arch and the fascia.38
Functional examination of the foot and the ankle is negative. The only positive sign is the detection of a point of deep tenderness, usually situated at the anteromedial portion of the calcaneus – the origin of the plantar fascia. Exceptionally, the tenderness is not at the tenoperiosteal junction but in the body of the fascia, between its origin on the calcaneus and the forefoot. Ultrasound examination can objectively confirm the clinical diagnosis39–41 but is usually not needed.
Traction spurs, projecting forwards at the anterior border of the calcaneus, are commonly seen on radiographs and traditionally have been implicated as the cause of the painful heel.42 However, there is no relation between the spur and pain. The cause of the pain is the plantar fascial tendinitis resulting from excessive tension. The presence of a spur does not determine whether or not the patient has symptoms because a spur is very often not found in patients with obvious signs and symptoms of plantar fasciitis. Therefore a radiograph is of no particular assistance in the diagnosis of plantar fasciitis.
Treatment
The classic conservative treatment methods range from application of a heel cup, heel cushion, night splints, walking cast and steroid injection to rest, ice and anti-inflammatory drugs.43–45 Recently, extracorporeal shock wave therapy (ESWT) has been advocated for treatment of this condition. While the first placebo-controlled trials of ESWT in chronic plantar fasciitis reported benefit of variable magnitude,46,47 later studies concluded that shock-wave treatment was no more effective than conventional physiotherapy when evaluated 3 months after the end of treatment.48,49 Another study showed that treatment with corticosteroid injections was more efficacious and several times more cost-effective than ESWT in the treatment of plantar fasciitis.50
We have found the combination of alleviating the strain on the plantar fascia and one or two localized infiltrations with triamcinolone to be effective in almost every case of plantar fasciitis. The most important measure to alleviate tension on the plantar fascia is to raise the heel horizontally by 5–10 mm, which will drop the forefoot during weight bearing. This has a double effect: first, it shortens the distance between metatarsus and calcaneus and therefore directly relieves the fascia of strain; second, it removes the tension on the Achilles tendon and therefore indirectly relaxes the tension on the fascia. A high heel can afford immediate relief, provided the upper surface is horizontal and not wedge-shaped, as is the case in women’s shoes (Fig. 58.14); in the latter, a wedge that is thicker anteriorly is placed in the shoe to render the upper surface of the heel horizontal.
Results of the infiltration depend entirely on its accuracy. It is extremely important to localize exactly the site and the extent of the lesion before the needle is introduced. Palpation and infiltration should therefore be done with great care. Some authors even suggest placing the needle under ultrasound guidance,51,52 although this is seldom really necessary.
In the exceptional case when conservative treatment fails, the patient is sent for operative plantar fascia release. The results in terms of symptomatic relief are generally good.53
If an abnormal valgus position of the heel is present, a small inner wedge should be built in as well.54,55
The patient’s foot is held in dorsiflexion, either with the dorsum of the injecting hand or by an assistant. This position renders the plantar fascia taut and creates more room for the needle, which aims towards the palpating thumb on the tender spot. After traversing the resistant fascia, it touches bone (Fig. 58.15). The affected area at the tenoperiosteal border is now infiltrated.
Fig 58.15 Injection in plantar fasciitis.
Alternatively, tenotomy of the fascial origin at the heel under local anaesthesia may be required.56 This minor operation is followed by a couple of days’ bed rest and exercises for the short plantiflexor muscles of the foot.
Plantar fascial tear
Like a ruptured Achilles tendon, a plantar fascial tear occurs mostly in middle-aged athletes.57 The presentation is sudden pain in the midfoot during a sprint or a jump. There is an area of ecchymosis on the sole.58 Palpation reveals a tender and swollen area at the medial plantar aspect of the foot.59
Heel pad syndrome
Inflammation of the heel pad between the calcaneus and the skin of the heel is also called superficial plantar fasciitis.60 The heel pad (Fig. 58.16) consists of fatty tissue and elastic fibrous tissue, enclosed within compartments formed by fibrous septa; these connect the skin of the heel with the calcaneal periosteum. The fat pad acts as a shock absorber.61 It can become inflamed after a direct blow or repeated minor injuries.62 The pain is felt all over the posterior part of the sole, especially during weight bearing.
Examination shows nothing in particular except uniform tenderness over the whole inferior surface of the heel. It was recently demonstrated that the affected heel pad in plantar heel pain syndrome was stiffer under light pressure than the heel pad on the painless side, and it was hypothesized that this was caused by the changed nature of chambered adipose tissue.63
Treatment
The patient lies prone, with the knee flexed at a right angle. The physician stands at the foot and encircles the heel with one hand. A 10 mL syringe is filled with procaine 0.5% and fitted to a needle 5 cm long. The needle is thrust in horizontally between calcaneus and skin (Fig. 58.17). The tip of the needle is then pushed in for some centimetres until it lies at the centre of the heel. The solution is injected there and diffuses over the whole area, forming a large, tense swelling. Significant pressure is needed to force in the last millilitre.
Fig 58.17 Injection in heel pad syndrome.
Subcutaneous bursitis
There is no anatomical bursa between the posterior aspect of the calcaneus and the skin, but in some circumstances a bursa may form, particularly when narrow and ill-fitting shoes are worn, and especially if they are curved in at the upper posterior edge.64 Friction of the hard border against the calcaneus results in an adventitious bursa. Chronic irritation will thicken the walls of the bursa and also the overlying skin. Palpation reveals a very tender spot at the posterior and upper surface of the calcaneus or at the lower extent of the Achilles tendon. The bursa is usually visibly inflamed and may contain some fluid. An excessive prominence of the bursal projection on the posterosuperior aspect of the calcaneus, in combination with a swollen and painful bursa, is called Haglund’s disease.65
The initial treatment is to alter the back of the shoe and introduce a rubber pad at the lower half of the back of the calcaneus, which keeps the upper half away from the pressing edge. If this does not succeed, the bursa can be drained by aspiration, followed by infiltration of 10 mg of triamcinolone. If such conservative treatment does not succeed, excision may be advised. The results of surgery are satisfactory, provided adequate bone has been resected.66,67
Ligamentous disorders – ankle sprains
‘Sprained ankle’ is the general name for a variety of traumatic lesions to the posterior segment of the foot. It is a very common sports injury. Several conditions are so described, varying from a simple strain of the ligaments to avulsion fractures and fracture–dislocations. Sometimes only one structure is injured, and sometimes several.68
Sprained ankles have been classified according to the causative stress (varus–valgus), the tissue damaged (ligament, tendon or bone) or the degree of damage (grade I, II or III) and the time elapsed since the causative accident (acute, subacute or chronic) (Box 58.1 and Tables 58.3 and 58.4).
Table 58.3
Classification of ankle sprain according to time since accident
Stage | Time |
I Traumatic inflammation | 24–48 hours |
II Repair period | 48 hours to 6 weeks |
III Adherent scar tissue | > 6 weeks |
Table 58.4
Classification of ankle sprain by severity of lesion
Grade71 | Lesion |
I | Elongation of ligaments without macroscopic rupture |
II | Partial and macroscopic ligamentous rupture |
III | Complete ligamentous rupture |
Inversion sprain
Lateral ankle sprain injury is the most common acute sport trauma, and accounts for about 14% of all sport-related injuries.72 It is also reported to be the most common injury in college athletics in the United States.73 Athletes involved in soccer, basketball, volleyball and long-distance running are especially plagued by these injuries.74–76
Mechanism
The origin of an inversion sprain is usually an indirect force produced against an inverted and plantiflexed foot, when the weight of the body forces the talus to rotate77 and twists the forefoot into supination and adduction. Hirsch and Lewis78 demonstrated that a rotational force of only 5–8 kg can produce a rupture of the anterior talofibular ligament.
The site of the lesion will depend largely on the degree of plantiflexion during inversion79