The disorder was first described by Hood in 1884.⁶ For decades it has been regarded as a ruptured plantaris tendon,^7,8 but careful clinical examination of patients suffering from this disorder shows this to be false.⁹

The history is quite simple. During a vigorous contraction – for example, when starting to sprint, pushing a car or lifting a heavy weight – the patient experienced sudden severe pain in the calf. From then on, the patient was unable to dorsiflex the foot during walking and needed to tiptoe on the affected side.

Examination reveals pain during resisted plantiflexion but no weakness. In the supine-lying position, dorsiflexion at the ankle is found to be markedly limited when the knee is in the extended position but becomes normal when the knee is flexed. This implicates the gastrocnemius muscle, part of which is in spasm around the tear. The difference in range between a flexed and an extended knee in a disorder of the gastrocnemius muscle is another example of the constant-length phenomenon. Palpation of the calf reveals the tender area in the medial gastrocnemius, with either swelling and haematoma if the lesion is recent, or induration around the tear if it is old. After a severe rupture, it is possible to palpate the gap in the medial gastrocnemius. Ultrasonography is the imaging technique of choice to demonstrate size and grade of the lesion.10,11

Differential diagnosis

Although the diagnosis is obvious, it is as well to bear in mind some other possibilities.

High rupture of the Achilles tendon

Although the similar onset and localization of the pain can cause diagnostic confusion, this condition should hardly be a problem if a proper clinical examination is done. Weak resisted plantiflexion and no spasm during passive dorsiflexion in a ruptured Achilles tendon contrast with the findings in tennis leg.12,13 If there is any doubt, a simple test can be done as follows.¹⁴ The patient lies prone, the foot hanging over the edge of the couch. The examiner squeezes the calf muscles. If the Achilles tendon is intact, the foot moves into plantar flexion. When there is total rupture, no movement results.

Deep venous thrombosis in the calf muscles

Differential diagnosis from this condition is very important. Instances have been described of patients with tennis leg receiving anticoagulants, which aggravated their condition.¹⁵ The main historical difference is in the onset. In deep venous thrombosis, pain appears after immobilization or after sitting for a couple of hours,¹⁶ and not during vigorous contraction of the calf muscles. Clinical examination does not show limited passive dorsiflexion, although passive dorsiflexion and resisted plantiflexion can be painful. The calf muscle and leg are swollen and the foot becomes oedematous because of obstruction to venous return. Palpation of the tender spot shows other differences: in thrombosis the whole calf muscle is painful to the touch and sometimes a painful ‘string’ can be palpated deep within it.^17,18

Technique: infiltration

As soon as the patient is seen – whether on the day of the accident or some weeks or months later – local anaesthesia is induced at the site of the partial rupture. The patient lies prone, the knee slightly bent and the foot plantiflexed, to allow maximal relaxation of the muscle. The tender spot is located and gripped between thumb and index finger (Fig. 57.1). If there is any fluctuation, an attempt is made to aspirate the haematoma. Once that has been done, 30–50 mL of procaine 0.5% is injected using the usual infiltration techniques. As the spot is never precisely localized (gentle pressure does not reveal tenderness in the deeper part of the muscle, whereas strong pressure is apt to hurt throughout the belly) and the gastrocnemius muscle is a large structure, up to 50 mL of a 0.5% solution may be required.

Fig 57.1 Infiltration with local anaesthesia in tennis leg.

After the injection, pain ceases and a much greater range of passive dorsiflexion at the foot becomes possible within a few minutes. This suggests that the previous limitation was the result of spasm of the muscle. The patient is encouraged to move the foot further up and down while lying on the couch. Never allow the patient to stand up and to put weight on the affected leg after the injection because this might lead to a further tear. A raised heel pad must be given before the patient stands and walks.

Raised heel

While the patient is practising non-weight-bearing movements, a cork pad should be made and fitted into the shoe. By putting the weight on the raised heel, the patient will be able to use the unaffected parts of the temporarily shortened muscle, without straining the healing breach.

For the first few days, a heel pad of 3–4 cm may be needed. Thereafter, as treatment and cure proceed, the height is reduced until the pad becomes unnecessary.

Technique: friction and electrical contractions

The day after the injection, the patient is given the first session of deep friction and electrical stimulation to the muscle.

The patient lies prone with the foot fully plantiflexed. The therapist sits at the level of the patient’s leg. The fingers are placed at one side of the affected area and the thumb is positioned at the opposite side of the leg so as to apply counterpressure. The other hand may reinforce the palpating one (Fig. 57.2). Transverse friction starts deeply. By drawing the fingers upwards over the affected area, the therapist feels the muscle fibres escape from the grip until only skin and subcutaneous tissue remain. In the second stage, the fingers are slightly relaxed and moved backwards into the previous deep position, where the same movement starts again. The procedure is continued for about 15 minutes. During friction, the fingers do not move in relation to the skin – fingers and skin move as a unit over the muscle fibres.

Fig 57.2 Deep friction to the gastrocnemius muscle.

At first, massage is given gently. After 5–10 minutes, friction can be deeper and firmer but must always remain comfortable.

After each session of massage, the muscle is given electrical stimulation and active contractions for about 10 minutes, with the knee flexed and the foot in the plantiflexed position. Deep friction prevents transverse scar tissue formation. Electrically stimulated contractions ensure expansion in the muscle belly without tension on the line of healing.

Massage and electrical stimulation are given daily for the first few days and then three times a week, and for a week after symptoms cease, so as to prevent recurrences.

The diagnosis and treatment of tennis leg is summarized in Box 57.1.

Results

When the patient is seen within the first few days of trauma and this scheme of treatment is followed, one can expect normal sports activities to be resumed after 3 weeks.

A patient who presents with a palpable gap in the muscle belly is sometimes referred for surgery. However, in our opinion, surgery is seldom required when a muscle belly is torn. This contrasts with a tendinous rupture – say, of the Achilles tendon – which often calls for surgical intervention.

Achilles tendinopathy

The terminology used to describe this painful condition of the Achilles tendon is very confusing and terms such as Achilles tendinitis, tendonitis and tendinopathy have been widely used. In this book we use the term tendinopathy as the general clinical label for the combination of tendon pain, swelling and impaired performance. Peritendinitis and tendinosis are the histopathological entities of the disease.²⁵

Achilles tendon problems are very common among athletes as well as the general population.1,2 Tendinitis of the Achilles tendon is chiefly a runner’s problem.²⁶ Non-sporting people can also suffer from this condition and it then starts after unaccustomed exertion or a long walk in inappropriate shoes. Nevertheless, it most often occurs in long-distance runners, and it comes as no surprise that the increase in the number of people running during the past few decades has been paralleled by an increase in the number of cases of inflamed Achilles tendon.^27,28 In a survey of 2002 running injuries seen over a 10-year period at a sports medicine referral clinic, overuse injury to the Achilles tendon was the sixth most common injury.²⁹ The lifetime cumulative incidence of Achilles tendinosis is 5.9% among sedentary people and 50% among elite endurance athletes.³⁰

The site of the lesion lies usually at mid-tendon. Occasionally, the strain occurs level with the upper border of the calcaneus or, very rarely, at the musculotendinous junction. Achilles tendinitis is multifactorial and usually the outcome of a combination of anatomical and biomechanical characteristics, along with poor training technique.³¹ The most important aetiological factors are short triceps (decreased touchdown angle), poor stretching habits and increased plantar flexion peak torque.^32,33 Some authors suggest that there might also be a vascular factor furthering the condition.^34,35 This would explain the usual location of the lesion at mid-tendon, which is the junction of its two vascular systems.^36,37

During the last decade, fluoroquinolone antibiotics have been implicated in the aetiology of Achilles tendinitis and subsequent tendon rupture.38–41

The history in Achilles tendinitis is quite simple.⁴² The patient states that the heel aches during or after walking or running (stage I). Sometimes there is pain at the beginning of exertion, improving after a while and reappearing on fatigue (stage II). Alternatively, there is continuous and worsening pain during exercise (stage III). Sometimes the pain does not cease after exertion but continues at rest (stage IV). As a rule, however, pain eases at rest and increases on running or walking. Nocturnal pain is absent.

Clinical examination shows rising on tiptoe to be painful, although in minor cases pain is only evoked by repetitive tiptoe rising. The rest of the functional examination is completely negative except in lesions at the tenoperiosteal junction, where full plantiflexion hurts slightly as this squeezes the affected part of the tendon between the posterior aspect of the tibia and the upper surface of the calcaneum.

Because we advocate deep transverse friction as the most effective conservative treatment for this disorder and massage only acts where it is applied, the tendon should be palpated very carefully to discover all the tender areas because there may be more than one. The lesion nearly always lies at the inner or outer aspect, or both, of the tendon. Very often, the anterior surface is affected but almost never the posterior.⁴³ Most of the lesions lie 2–6 cm above the tenoperiosteal junction.⁴⁴ The morphological and macroscopic changes in the condition are not always the same. Observations during surgery have led to the description of two separate histopathological types:

• Peritendinitis: the inflammatory changes are confined to the peritenon, which is thickened and shows inflammatory changes, with considerable connective tissue proliferation and adhesions between peritendineum and tendon.45,46

• Tendinosis: this is characterized by inflammatory and degenerative changes in the tendon tissue itself.47,48 Sometimes partial ruptures of deeply situated fibres can be seen, with the superficial parts of the tendon remaining intact. Here there is a visible and palpable enlargement at the tendon from the structural changes of chronic fibrosis.⁴⁹

Imaging methods

Ultrasonography has been used increasingly to examine Achilles tendon injuries. It is a quick, safe and inexpensive method to verify the existence and location of intratendinous lesions but is operator-dependent.50,51 Magnetic resonance imaging (MRI) is useful in visualizing pathological conditions of the tendon but is expensive and time-consuming. It is unwise, however, to rely solely on the results of these imaging techniques. First of all, the normal anatomy of an asymptomatic Achilles tendon may vary, which causes diagnostic misinterpretation.⁵² Secondly, several studies have reported intratendinous changes in up to 34% of cadaver specimens, in ultrasound and MRI images of patients without symptoms.^53–55

Treatment

There are a number of approaches. Initial conservative treatment should be directed towards preventing adhesion formation between tendon and paratenon. Cold packs and stretching comprise most of the treatments proposed in the recent literature and may produce some benefit. Cold therapy is able to control pain and oedema, as well as to reduce regional blood flow and the metabolic demands of the tissue, and thereby helps to prevent further tissue damage at the site of injury. Passive stretching of the Achilles tendon has been advocated as restoring normal ankle joint mobility and decreasing the strain of the Achilles tendon with normal motion.⁵⁶

None of these therapies, however, addresses the problem of breaking the adhesion formation and restoring normal gliding between tendon and paratenon, which is the main reason for the chronic pain.

Steroid injection

The role of corticosteroid injections in the treatment of Achilles tendinopathy is controversial.57–61 Several reports demonstrate disappointing results and injections have also been blamed for causing spontaneous rupture of the Achilles tendon.⁶² However, localized paratendinous infiltrations with small doses of triamcinolone (10–20 mg) still have a place in the treatment of Achilles tendinopathy, provided the correct technique is used. The injection is never made into the body of the tendon but along the surface, between tendon and peritendineum. After the injection, the patient should avoid all exercise during the first 10 days, after which a training programme can gradually be resumed. The injection can be repeated once if there is no cure after 2 weeks. If this procedure is followed and the correct technique is used, as set out below, postinfiltration ruptures are not to be feared.⁶³

Technique: injection

The patient lies prone on the couch. The foot is forced into dorsiflexion over the edge of the couch. This stretches the tendon, which facilitates palpation of the affected area. A 2 mL syringe is filled with 20 mg triamcinolone. A 5 cm needle is fitted and introduced some 3 cm away from the lesion. It is pushed through the skin and moved either upwards or downwards, parallel to the tendon, until the tip reaches the distal edge of the lesion. A small injection is given while the needle is drawn back along the surface of the tendon (Fig. 57.3); the manœuvre is repeated four or five times, each time a little to one side of the previous infiltration line. If the tip of the needle stays superficial to the tendon, no particular resistance to the plunger will be felt during the injection.

Fig 57.3 Steroid infiltration parallel to the surface of the tendon in Achilles tendinitis.

Prolotherapy

Recently, promising results have been described in studies of patients with Achilles tendinopathy who were treated with paratendinous injections of a sclerosing agent. On ultrasonography, neovascularization and tendon inhomogeneity decreased significantly as the clinical parameters improved.64–66

Surgery

Operative treatment should only be considered in long-standing cases when rest and conservative treatment (deep transverse friction) have failed. The surgical procedures performed depend entirely on the underlying pathological features.

In simple peritendinitis, the crural fascia and the paratenon are split longitudinally from the musculotendinous junction to the insertion on the calcaneus, and adhesions between the tendon and the sheath are released.⁶⁷

In cases with focal tendinosis and partial rupture of the tendon, the diseased area of the tendon is excised and the tendon repaired by side-to-side suture of the remaining tendinous fibres.⁶⁸ Where excision of the degenerated tissue disrupts the continuity of the tendon, the tendon is reconstructed and reinforced with the fascia of the gastrocnemius.⁶⁹

If there is extensive tendinitis, excessive scar tissue is excised.⁷⁰ Some authors claim better results if carbon fibres are implanted between the tendinous straps.⁷¹

Postoperative care involves between 1 and 4 weeks of non-weight bearing, followed by 1–4 weeks of partial to full weight bearing, depending on the severity of the lesion and the type of surgical intervention.

Results are good to excellent in about 85% of cases.72,73

Deep friction to the Achilles tendon

This was introduced more than 40 years ago by Cyriax ⁷⁴ and is, in our opinion, the best conservative treatment for the condition, provided it is given correctly: (a) at the right point, (b) with a good friction technique, (c) 20 minutes per session and (d) at regular intervals (three times a week). During the period of treatment, the patient must take relative rest.

Technique: friction to the medial and lateral edge of the tendon

The patient lies face downwards on a low couch, with the foot projecting just beyond the edge of the couch. The therapist sits at the foot and pushes the sole into dorsiflexion through a slight pressure of the contralateral knee. At the correct point the tendon is grasped between finger and thumb, or two fingers and thumb, depending on the extent of the lesion (‘a’ in Fig. 57.4). Slight pressure under the tendon is exerted and the hand is drawn upwards until the fingers slip towards the posterior aspect of the tendon (‘b’ in Fig. 57.4). In the final stage of this manœuvre, only skin remains between the two grasping fingers. The pressure is now released slightly and the fingers are pushed downwards until they lie at the starting position (‘a’) and the whole procedure can be repeated. The cycle is repeated for about 15 minutes.

Fig 57.4 Deep friction to the medial and lateral edge of the Achilles tendon.

During friction, fingers and skin are moved as a whole over the tendon. Should there be any movement between the patient’s skin and the therapist’s fingers, the friction will be imparted to the patient’s skin and, if vigorous, will quickly cause a blister.

Friction must be given with sufficient transverse sweep, which means that the amplitude of the to-and-fro movements must be large enough to ensure that the frictional element is paramount. This is the only way to ensure effective separation of each fibre from its neighbour.

Although deep friction to the Achilles tendon is uncomfortable for the patient, especially at first, it should never be intolerably painful. The true art is to give enough friction without too much pressure. The fact that massage is painful is no guarantee that it is correctly given.

Technique: friction to the anterior part of the tendon

This localization should always be sought in addition to other tender spots.

The patient lies face downwards on the couch but further up the couch than in the previous technique, in order to allow the foot to adopt a full plantiflexion position. The relaxed tendon then has good mediolateral mobility. With one thumb at the opposite side, the examiner pushes the tendon over sideways, as far as it will go. The anterior aspect of the opposite side of the tendon can now be reached with the tip of the ring finger of the other hand. The ring finger is reinforced by the long finger, while the little finger is kept out of the way in order not to disturb the pronation–supination movement. This movement is carried out with the elbow flexed and with the finger, hand and forearm in a straight line with the patient’s leg.

Once again, friction is given in two phases. First, the fingertip is placed deeply under the tendon with the forearm in a slightly pronated position (‘a’ in Fig. 57.5). Pressure is exerted in a dorsal and medial direction; meanwhile, the arm moves in full supination, until the lateral fibres escape under the fingertip (‘b’ in Fig. 57.5). Caution is taken not to move the finger on the skin but rather to move the skin and the fingertip as a whole. Now pressure is slightly released and the fingertips replaced in the former position (‘a’), so that the whole procedure can be repeated. The to-and-fro movements are performed for 15 minutes. The fingers must not be allowed to glide on the skin, to avoid the formation of a blister.

Fig 57.5 Deep friction to the anterior aspect of the Achilles tendon.

During the whole procedure, there must be sufficient sweep, which can be achieved by a good pronation–supination movement at the elbow.

Technique: friction to the tenoperiosteal insertion of the tendon

A lesion at the tenoperiosteal insertion lies level with the upper surface of the calcaneus. As in the earlier technique, the tendon must be relaxed; therefore the patient moves upwards on the couch to bring the foot into full plantiflexion.

The tendon is compressed between the therapist’s fingers and the upper surface of the calcaneus. Using both hands, a circle is made round the heel with one index finger, reinforced by the other, at the lesion. Both thumbs cross at the plantar surface. Pressing downwards squeezes the tendon between the fingers and the calcaneus. Deep friction is performed by moving the forearms in opposite directions. The amplitude of the movement must be large enough to reach the whole width of the tendon (Fig. 57.6).

Fig 57.6 Deep friction to the insertion of the Achilles tendon.

Results of deep friction.

Provided massage is given at the right point and the technique is adequate, the results of deep transverse friction are good. Usually, a schedule of 15 minutes, three times a week over 2–4 weeks, is required. In the meantime, the patient should not run or walk any further than necessary. The only failures are in nodular scarring around an old partial rupture. Our experience is that Achilles tendinitis with macroscopic fibrous changes in the deep layers of the tendon often remains refractory to conservative treatment, whereas superficial lesions without palpable changes respond quite well to friction.

Eccentric training

Recently, there has been increasing interest in the use of eccentric loading in treatment of chronic Achilles tendinopathy. (In an eccentric contraction, the muscle–tendon unit lengthens as a load is applied to it.) In 1986 Stanish et al⁷⁵ reported that a once-daily, 6-week eccentric loading programme led to complete relief of pain in 44% and a marked improvement in symptoms in a further 43% of patients. More recently, others have confirmed the efficacy of eccentric loading for mid-substance lesions of the Achilles tendon,^76,77 and high success rates (at least 60% either good or excellent) have also been reported in prospective randomized trials.^78–80 However, the mechanism for the efficacy of eccentric loading remains unknown.⁸¹

Prevention

Raised heels, shock-absorbing heels and correction of a valgus deformity are usually prescribed.⁸² As the triceps is also a slight invertor, a valgus deformity must always be corrected to relieve excessive strain on the tendon.⁸³ Although these measures are certainly beneficial, it is important to remember that they are prescribed for prevention only because they do not lead to substantial and histological changes at the site of adhesions.

Many authors pay a great deal of attention to the preventive value of stretching exercises before running.84,85 Although they may have such value, the worth of stretching techniques alone should not be overestimated when they are used as therapy in actual lesions. Stretching is a good method of prevention but, in our experience, has no therapeutic value.

Achilles tenovaginitis

Although the Achilles tendon does not have a sheath, inflammation can sometimes occur between the tendon and the peritenon and create a so-called tenovaginitis of the Achilles tendon. This can take two forms: rheumatoid and xanthomatous.

Rheumatoid arthritis and ankylosing spondylitis

In these conditions, the contrast between the mild symptoms and the marked signs is striking. It is also important to remember that gout can sometimes affect the Achilles tendon. The main complaint is not, as in tendinitis, pain during contraction of the triceps but pain during local pressure, e.g. catching the heel against the edge of the shoe. Examination shows that rising on tiptoe is indeed just uncomfortable rather than painful but the tendon is warm, swollen and very tender to the touch.86,87 Local treatment consists of infiltration with 20 mg of triamcinolone between the sheath and the tendon. The technique is the same as described for Achilles tendinitis.

Xanthomatous tenovaginitis

The Achilles tendon is a common site of xanthomatous lesions. Similar swellings can be seen and palpated at the extensor tendons on the dorsum of both hands or occasionally on the tendons crossing the dorsum of the foot and on a line at the upper part of the ulna and tibia. Small nodules can also be seen in the upper eyelids. There is only slight discomfort during walking and tiptoe rising is painless. Both tendons can be seen to be thickened, and palpation reveals enlargement and diffuse nodularity. The nodules are painless to the touch.

Treatment consists of restoring normal lipid metabolism with clofibrate 1.5 g daily, or fenofibrate 300 mg daily.

Calcaneus apophysitis

Apophysitis of the calcaneus (Sever’s disease, Osgood’s disease) occurs in boys between 6 and 12 years of age and is often bilateral. The disorder has been classified among the general osteochondrosis syndromes, such as Legg–Calvé–Perthes disease at the hip or Osgood–Schlatter disease at the tibial tuberosity. The child complains of sharp pain in the heel, occurring during contraction of the triceps. The pain starts suddenly, can last a couple of hours or days, and may disappear and reappear. Rising on tiptoe can be negative but the bone is usually tender to the touch. The radiological appearances are characteristic – ‘slight fragmentation of the apophysis’ – and confirm the diagnosis. Spontaneous recovery occurs in a year or two, often with the development of a slight permanent prominence on the posterior aspect of the calcaneus.⁸⁸

There is no treatment except relative rest, slightly raising the heel and inserting shock-absorbing heel pads in the shoe.⁸⁹

Weakness

Weakness of the plantiflexor mechanism is detected by an inability to rise on tiptoe.

Apart from neurological lesions, which are discussed at the end of this chapter, the commonest cause of weakness is a rupture of the Achilles tendon, most frequent in athletes over 30 years of age.⁹⁰ The tear lies in the ‘critical zone of poor vascularization’, which is 2–6 cm above the calcaneal insertion.⁹¹

It is surprising that this simple and easy-to-detect condition very often remains undiagnosed for a time. Between 30 and 41% of Achilles tendon ruptures remain undiagnosed for more than 2 weeks.35,92,93

The history is typical. During a sudden contraction – for example, at the start of or during a sprint, lifting a heavy object or pushing a car – the patient hurts the heel. There is a snap, followed by a dull pain in the heel. This eases fairly quickly but, from then on, the patient finds that only hobbling on a flat surface is possible. Alternatively, there may not have been a sudden contraction of the triceps but rather a severe elongation caused by excessive and sudden dorsiflexion at the ankle.

When the patient lies on the couch, the clinical examination reveals little. There is usually no haematoma or visible thickening. Passive movements are painless. An alert examiner will probably detect an excessive range of dorsiflexion. In the supine, non-weight-bearing position, resisted plantiflexion remains possible because the plantaris, flexor hallucis longus and flexor digitorum muscles still contract. Rising on tiptoe, however, immediately reveals the diagnosis. The squeeze test is also positive: the patient lies prone, with both feet suspended over the edge of the couch; compressing the triceps surae causes plantiflexion of the foot when the tendon is intact but not when it is ruptured.¹⁴

Differential diagnosis

The differential diagnosis from tennis leg is quite simple. In a patient with a minor tear in the medial gastrocnemius muscle, there is pain in the calf and the foot is fixed in plantiflexion. This contrasts very strongly with the absence of pain, the inability to plantiflex against resistance and the excessive dorsiflexion range at the ankle that are characteristic of a rupture of the Achilles tendon.

Although the history of sudden pain and disability may suggest a sprained ankle, a rupture of the Achilles tendon will not be missed if the clinical examination is executed properly.

Treatment

There is still controversy concerning the best treatment for Achilles tendon ruptures. It appears that a satisfactory outcome may be achieved with either non-operative or operative treatment but surgical repair appears to provide better functional capacity ⁹⁴ with better scores of strength, power and endurance^95–97 and lower re-rupture rates. The advantages of the conservative approach are that there are no risks of anaesthesia, infection, skin adhesions and sural nerve injury.^98,99 Reports in the literature indicate that in active, young, very demanding individuals, surgical repair should be considered, with non-surgical treatment reserved for elderly or sedentary patients.^100–102 However, conservative treatment can also be considered in athletically active patients, as treatment should always be individualized to the concerns and health of the patient.^103,104

There is no single, uniformly accepted surgical technique for Achilles tendon repair. Most acute ruptures have been treated successfully with excision of the devitalized tendon tissue and simple end-to-end suture. However, various augmentation procedures, such as reinforcement of the suture with a triceps surae tendon tip-over graft, have been combined with simple suture and have had satisfactory outcomes.105–107 To minimize the complications typically associated with open surgery, percutaneous techniques to repair the ruptured Achilles tendon have been advocated, and the results are reported to be promising, although not without failures and complications.^108,109

Several recent studies have reported functional benefits of early postoperative tendon mobilization in well-motivated patients, as treatment results are determined not only by the method of repair but also, and perhaps more importantly, by the early postoperative functional rehabilitation.110,111

Conservative treatment consists of 8 weeks in a plaster cast with the foot in equinus position, followed by the use of a 2.5 cm heel for an additional 1 or 2 months.112,113 The thickened and enlarged scar tissue resulting from conservative treatment can be massaged twice a week for 2–3 months. The fibrous swelling at the point of the rupture never seems to disappear, however, and some residual disability can be permanent.

It can be concluded that the treatment of choice in the athletically active patient is primary surgical repair.¹¹⁴ Conservative treatment is chosen in middle-aged or less active patients.¹¹⁵

Short plantiflexor muscles

Short calf muscles, resulting in equinus deformity, are among the most common complications in children with cerebral palsy.¹¹⁶ Sometimes, shortening of calf muscles is an isolated finding and may easily be overlooked.

History

Usually, the parents bring the child’s gait to attention. They notice that the youngster turns the feet outwards during walking or running, adopting a ‘Chaplin’ style of moving. Because the child cannot dorsiflex the ankle joint during walking, the feet must be turned outwards to take off. As this is not the best technique for running, the child will run conspicuously more slowly than healthy peers.

Sometimes the parents also notice that the child tends to tilt backwards on standing. The poise around the centre of gravity is incorrect, which leads to muscular fatigue. Therefore the child will complain that prolonged standing is tiring.

Clinical examination

This shows the dorsiflexion range at the ankle joint to be painlessly limited. A gastrocnemius equinus is typically characterized by less than 10° of ankle dorsiflexion with the knee extended.¹¹⁷

Complications

Because the patient cannot bear weight adequately on the heels, mid-tarsal hypermobility and later painful strain will result. Limited dorsiflexion at the ankle can also lead to various compensations in the lower extremity that ostensibly cause secondary problems, including Achilles tendinopathy,¹¹⁸ flat foot, chronic metatarsalgia¹¹⁹ and strain of the plantar fascia.¹²⁰

Symptoms and complications associated with short plantiflexor muscles are summarized in Box 57.2.

Treatment

Younger patients

The mid-tarsal joints must be protected, together with the plantar fascia and the forefoot. Therefore the heel must be raised temporarily by a horizontal surface. The child is taught to do stretching exercises for soleus and the gastrocnemii, several times a day, for 2–6 months. These lengthen the calf muscles so that the raised heel on the shoe can be discarded.

The soleus muscle is stretched in the following way. The child performs knee flexion exercises and tries to keep the heels on the ground (Fig. 57.7a). Once this can be done easily, the patient is encouraged to lean further and further forwards so as to stretch the soleus more.

Fig 57.7 Stretching of the left soleus (a) and left gastrocnemii (b).

To stretch the gastrocnemii muscles, the child stands in front of a wall, with feet fully dorsiflexed and knees extended, the heels remaining on the ground. The patient then leans forwards, keeping the knees firmly in full extension (Fig. 57.7b).

Adults

The same treatment can be tried but the process of stretching the calf muscles is tedious and tends to fail. Here, the shortening can only be compensated by raising the heel of the shoe.

Alternatively, surgery can be advised. Recently, good results have been reported with endoscopic release of the gastrocnemii.121,122

Lesions of the dorsiflexors

Pain

If resisted dorsiflexion of the foot elicits pain, a resisted movement of the hallux, and then of the toes, identifies the offending muscle: tibialis anterior, extensor hallucis longus or extensor digitorum longus. Further palpation then discloses the precise localization, which can be at the muscle, the tendon or the tenoperiosteal insertion.

Lesions of the muscle bellies respond equally well to local anaesthesia and deep friction (Box 57.3). Three injections, each of 10–30 mL of procaine 0.5%, at weekly intervals usually give good results. Friction is given according to the general principles that it should be deep and transverse, with sufficient sweep on a relaxed muscle, three times a week for 6–10 sessions.

Lesions of the tendons respond to deep friction, on a stretched tendon, three sessions a week, for 6–10 sessions.

Lesions at the tenoperiosteal junction respond to deep transverse friction and to infiltration with 10 mg of triamcinolone.

Special conditions

Ischaemic contracture or adherence of the extensor hallucis longus

The muscle may develop ischaemic contracture or become adherent after a fracture at mid-tibia. This results in a constant-length phenomenon. Each time the foot is plantiflexed, the shortened extensor hallucis muscle extends the big toe, which is forced against the tip of the shoe. This may result in extreme soreness of the big toe. The treatment is tenotomy level with the first metatarsophalangeal joint.

Tenosynovitis of the extensor digitorum longus or the extensor hallucis longus

This rare condition occurs level with the ankle and is usually a sequel of a sprained ankle. Sometimes it is seen as a rheumatoid condition. Apart from pain, a localized swelling can be seen and occasionally crepitus can be felt. In traumatic tenosynovitis, infiltration with 1 mL of triamcinolone between the tendon and sheath and deep friction have equally good results. In rheumatic conditions, infiltration is the only method of symptom relief.

Myosynovitis of the tibialis anterior muscle

The only parallel condition in the body is myosynovitis of the bellies of the abductor pollicis longus and the extensor pollicis muscles in the forearm. The lesion occurs as an overuse phenomenon in skaters, skiers and long-distance runners. It has also been described in army recruits after a long march, who are unaccustomed to wearing heavy boots.¹²³ Resisted dorsiflexion hurts above the front of the ankle. Painless resisted dorsiflexion of the big toe and outer toes points to the tibialis anterior muscle but palpation fails to reveal any tenderness in the anterior tibial tendon itself. If the palpating finger moves upwards to the musculotendinous junction, a painful area is detected close to the bone. If the foot is moved gently up and down, crepitus may be felt.

Treatment consists of deep transverse friction, which solves this problem very quickly: 2–4 sessions at intervals of 2 days usually give lasting relief.

Technique: deep transverse friction to the tibialis anterior muscle

The therapist sits opposite the patient. With one hand, the foot is brought into full plantiflexion and eversion in order to stretch the muscle. The thumb of the other hand is placed at the medial aspect of the leg and the fingers on the lesion (Fig. 57.8). The thumb is used as a fixed point and the fingers move in a transverse direction over the anterior aspect of the anterior tibial muscle. To allow sufficient sweep, the movement is conducted by an adduction movement of the shoulder.

Fig 57.8 Deep friction to the tibialis anterior muscle.

Tight fascia syndrome of the anterior compartment

This disorder may resemble intermittent claudication but the patient is much younger and physically active. After exertion – for example, kicking a football for about 10 minutes – voluntary dorsiflexion becomes impossible and what seems like a drop foot develops. This is accompanied by vague pain at the front of the leg and sometimes by pins and needles over the dorsum of the foot and the inner four toes. After a short rest, the muscle recovers and pain and weakness disappear.¹²⁴ When the patient is examined at rest, nothing special is revealed: dorsiflexion is strong and painless, and the arterial pulsations are normal. In long-standing cases, it is sometimes possible to palpate fascial hernias over the front of the leg.¹²⁵

The symptoms result from increased tissue fluid pressure in the closed fascial compartment which is formed by the tibia, the fibula, the interosseous membrane and the anterior fascia (Fig. 57.9). During exercise, muscle volume may expand by 20%, from both increased blood flow and capillary filtration.^126,127 If the superficial fascia is not lax enough to accommodate the greater volume, the intramuscular pressure rises to levels that compress the anterior tibial artery. This produces relative muscle ischaemia and therefore temporary paralysis and pain. The swelling may also trap the superficial peroneal nerve at its exit through the fascial foramen at mid-leg and cause paraesthesia in the outer foot.

Fig 57.9 The anterior compartment (colour indicates the fascia).

After some minutes’ rest, blood flow recovers and symptoms resolve. Because the patient is asymptomatic between occurrences and not chronically disabled, some authors prefer the suffix ‘recurrent’ rather than ‘chronic’ to identify anterior compartment syndromes.¹²⁸ However, if the minute vessels in the belly of the muscle themselves gradually become silted up with cells, the disorder may become irreversible.¹²⁹

The diagnosis is made on the typical history in combination with a negative clinical examination. However, if the athlete is examined after completing the exercise that reproduces the symptoms, clinical examination will show pain on passive plantiflexion and weak dorsiflexion. The anterior compartment is also tender on palpation.¹³⁰

The differential diagnoses of an anterior compartment syndrome include shin splint, stress fracture, nerve entrapment syndromes and claudication.¹³¹ The gold standard of diagnosing anterior compartment syndrome is the measurement of intracompartmental pressures before and after exertion.^132,133 A resting pressure > 15 mm Hg, and 5 minutes post-exercise pressures > 20 mm Hg are diagnostic of compartment syndrome.^134–136

Acute and severe anterior compartment syndromes may develop after a tibial fracture ¹³⁷ or a direct blow.¹³⁸ Within a few hours, pain at the mid-leg becomes intense and is not relieved by immobilization. The overlying skin sometimes becomes shiny and warm. Together with the palpable tenderness, this may give the false impression of cellulitis. Making this error is a disaster because, if the diagnosis is not made at once and the fascia divided immediately, ischaemic necrosis will ensue. Complete paralysis with a permanent drop foot will then result. There are also documented cases of bilateral compartment syndrome with permanent drop foot complicating surgery of long duration in the lithotomy position.¹³⁹

Treatment

Apart from altering the patient’s activities or training programmes, surgery seems to be the only effective treatment for recurrent compartmental syndromes. The surgical procedure consists of a subcutaneous fasciotomy.140–142

In acute cases, surgical decompression must be performed as soon as possible. As in a strangulated inguinal hernia, the motto is: ‘operate before sunset or sunrise’.¹⁴³ Sheridan and Matsen¹⁴⁴ found that fasciotomy performed within 12 hours of onset of a compartment syndrome resulted in normal function in 68% of cases. However, in those decompressed after 12 hours, only 8% recovered normal function.

Posterior tibial tendinitis is usually caused by overuse, which occurs frequently in a valgus deformity at the subtalar joint.¹⁴⁵ Resisted inversion of the foot hurts and dorsiflexion does not. Because the tibialis posterior has an additional function in stabilizing the hindfoot during rising on tiptoe, this test may also be painful. Palpation then discloses whether the lesion lies at the insertion on the navicular bone, at the tendon (distal or proximal to or under the medial malleolus), at the muscle belly or at the proximal musculotendinous junction.

Sometimes the tendon sheath rather than the tendon is inflamed, causing tenosynovitis. This occasionally occurs in rheumatoid arthritis.

Tendinitis usually recovers with a few sessions of massage but the valgus deformity at the heel must be corrected in order to prevent recurrences. Pain resulting from overuse secondary to a valgus deformity will never be relieved unless a combined approach is used consisting of deep friction and correction of the valgus deformity with a support at the heel.

In rheumatoid tenosynovitis, 10 mg of triamcinolone is injected between the tendon and its sheath.

Deep friction techniques

The technique differs according to the site of the lesion: above or below the medial malleolus. In both instances, the patient lies on the couch with the hip in external rotation so that the inner surface faces upwards.

Technique: friction to the upper part of tibialis posterior

The therapist sits lateral to the patient’s foot. With the contralateral hand, the foot is fixed in dorsiflexion. As the tendon lies deeply between the posterior aspect of the tibia and the tendon of the flexor digitorum longus, the proper spot can only be reached if the pronation–supination technique is used. The middle finger of the ipsilateral hand, reinforced by the index finger, is thus laid flat on the affected part of the tendon, just behind the edge of the tibia (Fig. 57.11). The ring and little fingers are kept extended. The fingers, the wrist and the forearm are brought into line with the tibia. Friction is imparted with a supination movement, which is continued until the tendon escapes from the finger. Pressure is then released a little and the finger returned to the original position by pronation.

Fig 57.11 Deep friction to the upper part of the tibialis muscle: (a) starting position; (b) end of the movement.

This alternating pronation–supination movement is continued for about 20 minutes. Usually 10 sessions, three times a week, suffice to resolve the condition.

Technique: friction to the lower part of tibialis posterior

The patient’s foot is dorsiflexed and the therapist sits level with the affected foot. The thumb of the contralateral hand is placed at the lateral side of the foot. The tips of one or two fingers are placed on the affected length of the tendon, just beyond it. Friction is now given with an extension movement at the wrist (Fig. 57.12), using the thumb as a fulcrum. The fingers ride over the whole width of the tendon until the latter escapes from the pressure. Using flexion of the wrist, without losing contact with the skin, the fingers are then moved to the original position behind the tendon, and the whole procedure is repeated.

Fig 57.12 Deep friction to the lower part of the tibialis posterior.

Friction is continued for 20 minutes, twice a week, for 1 or 2 weeks.

Shin splints

Pain at the posterior medial edge of the tibia in athletes and long-distance runners is called ‘shin splints’ or ‘medial tibial stress syndrome’. Few conditions have caused as much controversy. The term has been used to cover a variety of conditions, such as stress fractures,146–148 periostitis and soft tissue inflammation.¹⁴⁹ The American Medical Association subcommittee for classification of sports injuries restricts the name shin splints to musculotendinous lesions of the tibialis posterior muscle.¹⁵⁰

The disorder appears as an overuse phenomenon in runners and is one of the most common causes of exertional leg pain, accounting for 6–16% of all running injuries.¹⁵¹

The most common complaint is diffuse pain of the lower extremity, along the middle-distal tibia, associated with exertion. In the early course, pain is worse at the beginning of exercise but gradually subsides during training and within minutes of cessation of exercise. As the injury progresses, however, pain presents with less activity and may occur at rest.¹⁵²

Clinical examination shows little pain during resisted inversion of the foot. Palpation reveals tenderness and sometimes induration at the musculotendinous junction of the tibialis posterior muscle, usually between its upper and medial thirds.

Differential diagnosis must include exertional compartment syndrome and stress fracture. Here, pain is elicited by sharply striking the heel or tapping the anterior tibia, or the bone is tender to direct pressure. During the initial weeks, a stress fracture is not visible on a plain radiograph ¹⁵³ but can be detected with ultrasound.¹⁵⁴ In case of doubt, a bone scintigram can be obtained that easily distinguishes an inflammatory shin splint from a stress fracture.^155,156

The condition responds effectively to a series of sessions of deep transverse friction. Good results have also been obtained with weekly infiltrations of procaine (10–20 mL) over 3 consecutive weeks.

For a stress fracture, only rest is effective. A 6- to 8-week pause in training is usually necessary.

Differential diagnosis between posterior and anterior leg pain is summarized in Box 57.4.

Box 57.4 Leg pain

Differential diagnosis

Weakness

Neurological lesions are discussed at the end of this chapter.

Weak resisted inversion is often caused by a rupture of the tibialis posterior tendon (TPT), secondary to a combination of degenerative changes and trauma.¹⁵⁷ It is usually located in a critical zone with a low degree of vascularity, posterior to the medial malleolus.¹⁵⁸

Rupture of the TPT does not initially cause pain and usually the patient cannot recall an acute trauma. The main symptom that draws attention to the possibility is a gradual deformity of the foot. The triad of deformity appearing during weight bearing is:

• Valgus deformity of the heel

• Loss in height of the medial longitudinal arch

• Abduction of the forefoot, which is detected by the ‘too many toes sign’¹⁵⁹: more of the lateral toes are seen on the affected side when the patient is inspected from behind.

Rupture of the tibialis posterior tendon thus leads to a progressive, unilateral, acquired flat foot, with increasing valgus of the heel, plantar flexion of the talus and subluxation of the talonavicular joint.157,160

It is difficult to detect weakness of the tibialis posterior during manual testing because the synergistic action of the other invertors of the foot substitutes for the power of the ruptured muscle. Weakness of the tendon is best detected during rising on tiptoe. In a normal foot, this test shows a typical sequence. First the TPT is activated, which inverts the foot and locks the heel and the mid-tarsal joints. Then the triceps muscle pulls on the now-rigid calcaneus, the heel rises and the body weight is imparted to the ball of the foot. With a rupture of the TPT, however, the initial varus movement at the heel is impossible and the patient rises up with the heel in valgus or does not get up on to the ball of the foot at all.161,162

Conservative treatment includes a medial heel wedge and a longitudinal arch support.¹⁶³

Surgical treatment must be considered when the patient is young and active. A plantaris or extensor tendon graft may be used to bridge the defect. Recently, the transfer of the flexor digitorum longus tendon into the sheath of the tibialis posterior has been used for larger defects.164,165

If there is pain on resisted eversion of the foot, the peroneal muscles are at fault. Peroneal tendinosis is usually a simple overuse phenomenon in runners and skaters,166,167 although it may also appear as a complication of ankle sprain (see p. 774).^168,169

As tendinosis occurs anywhere, from the lower fibula to the cuboid and the fifth metatarsal base, the exact position of the lesion can only be disclosed by palpation for tenderness along the whole tendon.

Treatment

Peroneal tendinosis is seldom sufficiently localized to be treated by steroid injection. However, it responds very well to deep transverse massage.

Technique: deep friction above and below the malleolus ¹⁷⁰

The patient lies supine, with the leg medially rotated. The therapist sits at the opposite side. The foot is brought into inversion; this stretches the tendon. Two or three fingertips of the therapist’s ipsilateral hand are now placed on the tendon. The fingers are slightly flexed, thereby pressing the tendon against the fibular shaft. The thumb is placed at the medial side of the lower leg or ankle to provide counterpressure (Fig. 57.13). Friction is given with a to-and-fro movement of the forearm, during which the fingers ride over the tendon. The friction is in two phases: an active phase, during which the tendon is pressed and pulled, and a relaxed phase, during which the fingers are placed in the previous position to restart the movement.

Fig 57.13 Deep friction to the peroneal tendons under the malleolus.

Three sessions a week over 2–4 weeks may be required. During the course of treatment, the patient should avoid exercise but complete rest is not required. The results are uniformly good.

Technique: deep friction level with the malleolus

The therapist sits by the patient’s foot, facing it. The foot is held in inversion and plantar flexion is produced by slight pressure of the ipsilateral hand. The therapist holds the contralateral hand and forearm in line with the leg. The middle finger, reinforced by the index finger, is placed in the sulcus, behind the peroneus tendon (Fig. 57.14). Friction is started with the finger behind the tendon. Pressure is exerted and, with a supination movement of the forearm, the tendon is pressed anteriorly until it escapes from the finger and slips backwards. The now-supinated hand is manœuvred back to the pronated position behind the tendon, where the movement restarts.

Fig 57.14 Deep friction to the peroneal tendons level with the malleolus.

Friction is imparted by rotating the forearm in full supination and full pronation for about 15 minutes. Three sessions a week over 3–4 weeks are usually sufficient to cure the lesion.

Other conditions

‘Snapping ankle’

Sometimes patients complain of a slight pain, together with a snapping feeling at the outer side of the ankle, during certain movements. The reason is a loosening of the peroneal tendons in the groove of the posterior surface of the fibula. They slip forwards over the malleolus when the ankle is dorsiflexed and ‘jump back’ during plantiflexion.¹⁷¹ This ‘snapping ankle’ is usually not painful, just uncomfortable. Sometimes, however, it is the origin of a superimposed tendinitis. Non-surgical treatment should always be instituted first and consists of holding the tendons reduced in their anatomical positions while the superior peroneal retinaculum heals by scarring.¹⁷² If considerable discomfort remains, surgery can be advised. Different methods of repair have been described.^173,174 Usually, a new retinaculum is constructed behind the lateral malleolus or the calcaneofibular ligament is transposed to the lateral side of the peroneal tendons.¹⁷⁵

Mucocele

A mucocele can form in the sheath of the tendon. It results in localized swelling and can be associated with a considerable ache. The diagnosis is obvious because the swelling is located in the sheath and can be made to fluctuate upwards and downwards along the malleolus by digital pressure. Treatment is aspiration. Because the viscous fluid has a high density, the aspiration is difficult to perform unless a wide-bore needle and a large syringe are used. Sometimes up to 50 mL of fluid can be removed. If there is any pain, 1 or 2 mL of triamcinolone are injected into the now-empty synovial space. Sometimes this procedure has to be repeated after a year or so.

Dorsiflexion, eversion and inversion are tested in the supine-lying position. As described in Chapter 55, it is very important to give strong counterpressure, with the leg in a neutral position. Normally, the extrinsic muscles of the foot are very strong and their pull cannot be overcome by the examiner’s force. Both sides should be compared.

In central or upper motor neurone lesions, the weakness is gross and distributed over different muscles and muscle groups (Table 57.1).

Table 57.1

Innervation of neurological weakness of the foot

Muscle	Segmental innervation	Peripheral nerve
Tibialis anterior	L4 (L5)	Deep peroneal
Extensor digitorum longus	L4, L5	Deep peroneal
Extensor hallucis longus	L4, L5	Deep peroneal
Peronei	L5, S1	Superficial peroneal
Tibialis posterior	L4, L5	Tibial
Flexor digitorum longus	L5–S1	Tibial
Flexor hallucis longus	L5–S1	Tibial
Triceps surae	S1, S2	Tibial