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Home , Achilles tendinitis, Calf (leg)

Disorders of the lower leg 57

CHAPTER CONTENTS Paediatricians’ estimates of the frequency of this diagnosis 1 2 Bone disorders 745 vary from 4% to 20% of all children. During recent decades, several hypotheses have been put forward but none gives a Lesions of the plantiflexors 745 good explanation for the symptoms. As it occurs between the Pain ...... 745 ages of 6 and 12, which is not the period of maximum rate of Weakness ...... 752 growth, ‘growing’ cannot be the real reason for the pain. What- ever the origin of the pain, it disappears spontaneously and Short plantiflexor muscles ...... 753 completely after the age of 12 years.3,4 Lesions of the dorsiflexors 754 Pain ...... 754 Weakness ...... 756 Lesions of the plantiflexors Lesions of the invertors 756 While the patient rises on tiptoe, still the best test of integrity Pain ...... 756 of the plantiflexor mechanism, the examiner notes if there is Weakness ...... 758 any pain or weakness. Lesions of the evertors 758 Pain ...... 758 Pain Weakness ...... 760 Disorders causing neurological weakness of Tennis leg the 760 This is the common term to describe a tear in the triceps. It occurs most often in the medial belly of the , usually some 5 cm above the musculotendinous Bone disorders junction.5 The disorder was first described by Hood in 6 1884. For As this book covers ‘non-osseous’ lesions of the moving parts decades it has been regarded as a ruptured plantaris ,7,8 of the body, little attention will be paid to bone disorders. For but careful clinical examination of patients suffering from this differential diagnostic reasons, however, it is as well to bear in disorder shows this to be false.9 mind that, if the patient complains of continuous localized The history is quite simple. During a vigorous contraction pain, without special clinical findings during functional exami- – for example, when starting to sprint, pushing a car or lifting nation, the possibility of a bone disorder should be considered a heavy weight – the patient experienced sudden severe and a radiograph or a bone scan obtained. Paget’s disease, pain in the calf. From then on, the patient was unable to dors­ metastases, primary bony tumours and osteomyelitis are iflex the foot during walking and needed to tiptoe onthe possibilities. affected side. Children between the ages of 6 and 11 years who complain Examination reveals pain during resisted plantiflexion but of diffuse pain in the legs but have a normal clinical examina- no weakness. In the supine-lying position, dorsiflexion at the tion are very often regarded as suffering from ‘growing pains’. is found to be markedly limited when the is in the

© Copyright 2013 Elsevier, Ltd. All rights reserved. The Lower Leg, Ankle and Foot extended position but becomes normal when the knee is Posterior compartment syndrome flexed. This implicates the gastrocnemius muscle, part of The patient, usually a young man, reports an ache and swelling which is in spasm around the tear. The difference in range in the calf some hours after unaccustomed exercise. Walking between a flexed and an extended knee in a disorder of the is uncomfortable and increases the swelling. Examination gastrocnemius muscle is another example of the constant- shows that rising on tiptoe is not difficult and not really uncom- length phenomenon. of the calf reveals the tender fortable. The calf is diffusely swollen and the skin is red and area in the medial gastrocnemius, with either swelling and warm to the touch. Passive dorsiflexion of the foot is severely haematoma if the lesion is recent, or induration around the limited by loss of elasticity of the calf muscles. Palpation tear if it is old. After a severe rupture, it is possible to palpate reveals uniform tenderness of the whole calf muscle without the gap in the medial gastrocnemius. Ultrasonography is the any localized tender area.20 The symptoms result from muscle imaging technique of choice to demonstrate size and grade of ischaemia, produced by increased tissue fluid pressure in the the lesion.10,11 closed fascial compartment. The difference from tennis leg lies in the discrepancy between marked restriction of passive dor- siflexion and almost painless tiptoe rising. Treatment is surgical Although the diagnosis is obvious, it is as well to bear in mind division of the deep . some other possibilities. Referred pain to the calf High rupture of the This is most frequently the consequence of compression of the Although the similar onset and localization of the pain can S1 nerve root, whether by a primary posterolateral protrusion cause diagnostic confusion, this condition should hardly be of nuclear substance at the fifth lumbar level in a younger a problem if a proper clinical examination is done. Weak patient, or by a compression in a narrowed lateral recess in an resisted plantiflexion and no spasm during passive dorsiflexion older person. When these conditions are suspected, a careful in a ruptured Achilles tendon contrast with the findings in history must be taken and a clinical examination of the lumbar tennis leg.12,13 If there is any doubt, a simple test can be done spine must be performed. Positive findings during lumbar as follows.14 The patient lies prone, the foot hanging over examination, together with painless tiptoe rising, confirms the the edge of the couch. The examiner squeezes the calf diagnosis. muscles. If the Achilles tendon is intact, the foot moves into plantar flexion. When there is total rupture, no movement Treatment results. Different types of treatment have been advocated for tennis Deep venous thrombosis in the calf muscles leg. Most authorities advise partial or total immobilization for Differential diagnosis from this condition is very important. small tears21 and surgical suture for serious ruptures.22,23 Instances have been described of patients with tennis leg In our opinion, surgery for this condition is scarcely ever 15 receiving anticoagulants, which aggravated their condition. necessary and partial or total immobilization by plaster cast or The main historical difference is in the onset. In deep venous strapping is obsolete. When such treatment is instituted, the thrombosis, pain appears after immobilization or after sitting formation of a chronic adherent scar is promoted, which results 16 for a couple of hours, and not during vigorous contraction of in disability lasting several months. The aim of treatment in the calf muscles. Clinical examination does not show limited muscle tears is to allow the torn fibres to heal in such a way passive dorsiflexion, although passive dorsiflexion and resisted that mobile and functional scar tissue is formed. If normal plantiflexion can be painful. The calf muscle and leg are swollen enlargement of the muscle is impaired by adhesions, self- and the foot becomes oedematous because of obstruction to perpetuating inflammation will be the result. Muscle belly venous return. Palpation of the tender spot shows other dif- lesions (tennis leg is an excellent example) therefore need a ferences: in thrombosis the whole calf muscle is painful to the different and more functional approach. The aim must be to touch and sometimes a painful ‘string’ can be palpated deep restore normal movement in the damaged muscle as quickly 17,18 within it. as possible. This can be achieved with combined treatment: Rupture of a Baker’s cyst early compression to decrease the amount of haemorrhage; In long-standing of the knee, chronic aspiration and infiltration with local anaesthetic as soon as the distension with fluid can weaken the posterior ligaments patient is seen; and deep transverse friction and electrically and during exertion these can rupture. Sudden pain in stimulated or active contractions of the muscle during the next the knee, followed by swelling of the leg and oedema few days.24 During the recovery period, the muscle must be of the ankle, strongly suggests venous thrombosis.19 Here, protected by a raised pad, which enables the patient to the long-standing rheumatoid arthritis and the absence of use the unaffected parts of the gastrocnemius without strain injury suggest the diagnosis, which can be confirmed by on the line of healing. arthrography. Technique: infiltration Intermittent claudication As soon as the patient is seen – whether on the day of the The history is characteristic: pain in one calf is brought on by accident or some weeks or months later – local anaesthesia is walking and relieved by rest. Routine clinical examination induced at the site of the partial rupture. The patient lies reveals nothing. Diminished or absent pulsations at the dorsalis prone, the knee slightly bent and the foot plantiflexed, to allow artery of the foot and posterior tibial artery may be found. maximal relaxation of the muscle. The tender spot is located Angiography confirms the diagnosis. and gripped between and index (Fig. 57.1). If

746 Disorders of the lower leg C H A P T E R 5 7

Fig 57.1 • Infiltration with local anaesthesia in tennis leg. Fig 57.2 • Deep friction to the gastrocnemius muscle. there is any fluctuation, an attempt is made to aspirate the where the same movement starts again. The procedure is con- haematoma. Once that has been done, 30–50 mL of procaine tinued for about 15 minutes. During friction, the do 0.5% is injected using the usual infiltration techniques. As the not move in relation to the skin – fingers and skin move as a spot is never precisely localized (gentle pressure does not unit over the muscle fibres. reveal tenderness in the deeper part of the muscle, whereas At first, massage is given gently. After 5–10 minutes, friction strong pressure is apt to hurt throughout the belly) and the can be deeper and firmer but must always remain gastrocnemius muscle is a large structure, up to 50 mL of a comfortable. 0.5% solution may be required. After each session of massage, the muscle is given electrical After the injection, pain ceases and a much greater range of stimulation and active contractions for about 10 minutes, with passive dorsiflexion at the foot becomes possible within a few the knee flexed and the foot in the plantiflexed position. Deep minutes. This suggests that the previous limitation was the friction prevents transverse scar tissue formation. Electrically result of spasm of the muscle. The patient is encouraged to stimulated contractions ensure expansion in the muscle belly move the foot further up and down while lying on the couch. without tension on the line of healing. Never allow the patient to stand up and to put weight on the Massage and electrical stimulation are given daily for the affected leg after the injection because this might lead to a first few days and then three times a week, and for aweek further tear. A raised heel pad must be given before the patient after symptoms cease, so as to prevent recurrences. stands and walks. The diagnosis and treatment of tennis leg is summarized in Raised heel Box 57.1. While the patient is practising non-weight-bearing movements, Results a cork pad should be made and fitted into the shoe. By putting When the patient is seen within the first few days of trauma the weight on the raised heel, the patient will be able to use and this scheme of treatment is followed, one can expect the unaffected parts of the temporarily shortened muscle, normal sports activities to be resumed after 3 weeks. without straining the healing breach. A patient who presents with a palpable gap in the muscle For the first few days, a heel pad of 3–4 cm may be needed. belly is sometimes referred for surgery. However, in our Thereafter, as treatment and cure proceed, the height is opinion, surgery is seldom required when a muscle belly is torn. reduced until the pad becomes unnecessary. This contrasts with a tendinous rupture – say, of the Achilles Technique: friction and electrical contractions tendon – which often calls for surgical intervention. The day after the injection, the patient is given the first session of deep friction and electrical stimulation to the muscle. Achilles The patient lies prone with the foot fully plantiflexed. The The terminology used to describe this painful condition of the therapist sits at the level of the patient’s leg. The fingers are Achilles tendon is very confusing and terms such as Achilles placed at one side of the affected area and the thumb is posi- tendinitis, tendonitis and tendinopathy have been widely used. tioned at the opposite side of the leg so as to apply counter- In this book we use the term tendinopathy as the general clini- pressure. The other may reinforce the palpating one (Fig. cal label for the combination of tendon pain, swelling and 57.2). Transverse friction starts deeply. By drawing the fingers impaired performance. Peritendinitis and tendinosis are the upwards over the affected area, the therapist feels the muscle histopathological entities of the disease.25 fibres escape from the grip until only skin and subcutaneous Achilles tendon problems are very common among athletes tissue remain. In the second stage, the fingers are slightly as well as the general population.1,2 Tendinitis of the Achilles relaxed and moved backwards into the previous deep position, tendon is chiefly a runner’s problem.26 Non-sporting people

747 The Lower Leg, Ankle and Foot

during exercise (stage III). Sometimes the pain does not cease Box 57.1 after exertion but continues at rest (stage IV). As a rule, however, pain eases at rest and increases on or walking. Summary of tennis leg Nocturnal pain is absent. Diagnosis Clinical examination shows rising on tiptoe to be painful, although in minor cases pain is only evoked by repetitive tiptoe • Acute onset rising. The rest of the functional examination is completely • Limitation of dorsiflexion negative except in lesions at the tenoperiosteal junction, where • Painful tiptoe rising full plantiflexion hurts slightly as this squeezes the affected • Typical localization of pain and tenderness part of the tendon between the posterior aspect of the Differential diagnosis and the upper surface of the calcaneum. Because we advocate deep transverse friction as the most • High rupture of the Achilles tendon effective conservative treatment for this disorder and massage • Deep venous thrombosis only acts where it is applied, the tendon should be palpated • Rupture of Baker’s cyst very carefully to discover all the tender areas because there • Intermittent claudication may be more than one. The lesion nearly always lies at the • Ischaemic inner or outer aspect, or both, of the tendon. Very often, the • Referred pain (S1) anterior surface is affected but almost never the posterior.43 Treatment Most of the lesions lie 2–6 cm above the tenoperiosteal junc- tion.44 The morphological and macroscopic changes in the con- • Infiltration with local anaesthetic dition are not always the same. Observations during surgery + Heel pad have led to the description of two separate histopathological • Deep friction daily during the first week types: + Electrically stimulated and active contractions • : the inflammatory changes are confined to • Deep friction three times a week Peritendinitis the peritenon, which is thickened and shows inflammatory Electrically stimulated and active contractions + changes, with considerable connective tissue proliferation and adhesions between peritendineum and tendon.45,46 • Tendinosis: this is characterized by inflammatory and can also suffer from this condition and it then starts after unac- degenerative changes in the tendon tissue itself.47,48 customed exertion or a long walk in inappropriate shoes. Nev- Sometimes partial ruptures of deeply situated fibres can ertheless, it most often occurs in long-distance runners, and it be seen, with the superficial parts of the tendon remaining comes as no surprise that the increase in the number of people intact. Here there is a visible and palpable enlargement running during the past few decades has been paralleled by an 27,28 at the tendon from the structural changes of chronic increase in the number of cases of inflamed Achilles tendon. fibrosis.49 In a survey of 2002 seen over a 10-year period at a sports medicine referral clinic, overuse injury to the Achil- Imaging methods les tendon was the sixth most common injury.29 The lifetime cumulative incidence of Achilles tendinosis is 5.9% among Ultrasonography has been used increasingly to examine Achil- sedentary people and 50% among elite endurance athletes.30 les tendon injuries. It is a quick, safe and inexpensive method The site of the lesion lies usually at mid-tendon. Occasion- to verify the existence and location of intratendinous lesions 50,51 ally, the strain occurs level with the upper border of the cal- but is operator-dependent. Magnetic resonance imaging caneus or, very rarely, at the musculotendinous junction. (MRI) is useful in visualizing pathological conditions of the Achilles tendinitis is multifactorial and usually the outcome of tendon but is expensive and time-consuming. It is unwise, a combination of anatomical and biomechanical characteristics, however, to rely solely on the results of these imaging tech- along with poor training technique.31 The most important niques. First of all, the normal anatomy of an asymptomatic aetiological factors are short triceps (decreased touchdown Achilles tendon may vary, which causes diagnostic misinterpre- 52 angle), poor habits and increased plantar flexion tation. Secondly, several studies have reported intratendinous peak torque.32,33 Some authors suggest that there might also be changes in up to 34% of cadaver specimens, in ultrasound and 53–55 a vascular factor furthering the condition.34,35 This would MRI images of patients without symptoms. explain the usual location of the lesion at mid-tendon, which is the junction of its two vascular systems.36,37 Treatment During the last decade, fluoroquinolone antibiotics have There are a number of approaches. Initial conservative treat- been implicated in the aetiology of Achilles tendinitis and ment should be directed towards preventing adhesion forma- subsequent tendon rupture.38–41 tion between tendon and paratenon. Cold packs and stretching The history in Achilles tendinitis is quite simple.42 The comprise most of the treatments proposed in the recent litera- patient states that the heel aches during or after walking or ture and may produce some benefit. Cold therapy is able to running (stage I). Sometimes there is pain at the beginning of control pain and oedema, as well as to reduce regional blood exertion, improving after a while and reappearing on fatigue flow and the metabolic demands of the tissue, and thereby (stage II). Alternatively, there is continuous and worsening pain helps to prevent further tissue damage at the site of injury.

748 Disorders of the lower leg C H A P T E R 5 7

Passive stretching of the Achilles tendon has been advocated as restoring normal ankle 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 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 peri- tendineum. After the injection, the patient should avoid all exercise during the first 10 days, after which a training pro- gramme can gradually be resumed. The injection can be repeated once if there is no cure after 2 weeks. If this proce- dure 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 down- wards, 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.

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 ultrasono­ graphy, neovascularization and tendon inhomogeneity decreased significantly as the clinical parameters improved.64–66 Surgery Fig 57.3 • Steroid infiltration parallel to the surface of the tendon in Operative treatment should only be considered in long-standing Achilles tendinitis. cases when rest and conservative treatment (deep transverse friction) have failed. The surgical procedures performed the continuity of the tendon, the tendon is reconstructed and depend entirely on the underlying pathological features. reinforced with the fascia of the gastrocnemius.69 In simple peritendinitis, the crural fascia and the paratenon If there is extensive tendinitis, excessive scar tissue is are split longitudinally from the musculotendinous junction to excised.70 Some authors claim better results if carbon fibres are the insertion on the , and adhesions between the implanted between the tendinous straps.71 tendon and the sheath are released.67 Postoperative care involves between 1 and 4 weeks of non- In cases with focal tendinosis and partial rupture of the weight bearing, followed by 1–4 weeks of partial to full weight tendon, the diseased area of the tendon is excised and the bearing, depending on the severity of the lesion and the type tendon repaired by side-to-side suture of the remaining tendi- of surgical intervention. nous fibres.68 Where excision of the degenerated tissue disrupts Results are good to excellent in about 85% of cases.72,73

749 The Lower Leg, Ankle and Foot

Deep friction to the Achilles tendon This was introduced more than 40 years ago by Cyriax74 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 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 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 pos- (a) (b) terior 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. 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 uncomfort- able 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 Fig 57.4 • Deep friction to the medial and lateral edge of the sideways, as far as it will go. The anterior aspect of the opposite Achilles tendon. side of the tendon can now be reached with the tip of the of the other hand. The ring finger is reinforced by the fingertip (‘b’ in Fig. 57.5). Caution is taken not to move the long finger, while the is kept out of the way in order finger on the skin but rather to move the skin and the fingertip not to disturb the pronation–supination movement. This move- as a whole. Now pressure is slightly released and the fingertips ment is carried out with the flexed and with the finger, replaced in the former position (‘a’), so that the whole proce- hand and in a straight line with the patient’s leg. dure can be repeated. The to-and-fro movements are per- Once again, friction is given in two phases. First, the finger- formed for 15 minutes. The fingers must not be allowed to tip is placed deeply under the tendon with the forearm in a glide on the skin, to avoid the formation of a blister. slightly pronated position (‘a’ in Fig. 57.5). Pressure is exerted During the whole procedure, there must be sufficient in a dorsal and medial direction; meanwhile, the moves sweep, which can be achieved by a good pronation–supination in full supination, until the lateral fibres escape under the movement at the elbow.

750 Disorders of the lower leg C H A P T E R 5 7

(a)

(b)

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

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, Fig 57.5 • Deep friction to the anterior aspect of the Achilles whereas superficial lesions without palpable changes respond tendon. quite well to friction. Recently, there has been increasing interest in the use of eccen- tric 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 Technique: friction to the tenoperiosteal insertion once-daily, 6-week eccentric loading programme led to com- of the tendon plete relief of pain in 44% and a marked improvement in A lesion at the tenoperiosteal insertion lies level with the upper symptoms in a further 43% of patients. More recently, others surface of the calcaneus. As in the earlier technique, the tendon have confirmed the efficacy of eccentric loading for mid- must be relaxed; therefore the patient moves upwards on the substance lesions of the Achilles tendon,76,77 and high success couch to bring the foot into full plantiflexion. rates (at least 60% either good or excellent) have also been The tendon is compressed between the therapist’s fingers reported in prospective randomized trials.78–80 However, the and the upper surface of the calcaneus. Using both , a mechanism for the efficacy of eccentric loading remains circle is made round the heel with one , reinforced unknown.81 by the other, at the lesion. Both cross at the plantar surface. Pressing downwards squeezes the tendon between the Prevention fingers and the calcaneus. Deep friction is performed by moving Raised , shock-absorbing heels and correction of a valgus the in opposite directions. The amplitude of the deformity are usually prescribed.82 As the triceps is also a movement must be large enough to reach the whole width of slight invertor, a valgus deformity must always be corrected to the tendon (Fig. 57.6). relieve excessive strain on the tendon.83 Although these meas- Results of deep friction. Provided massage is given at the ures are certainly beneficial, it is important to remember that right point and the technique is adequate, the results of deep they are prescribed for prevention only because they do not transverse friction are good. Usually, a schedule of 15 minutes, lead to substantial and histological changes at the site of three times a week over 2–4 weeks, is required. In the adhesions.

751 The Lower Leg, Ankle and Foot

Many authors pay a great deal of attention to the preventive Weakness value of stretching exercises before running.84,85 Although they may have such value, the worth of stretching techniques alone Weakness of the plantiflexor mechanism is detected by an should not be overestimated when they are used as therapy in inability to rise on tiptoe. actual lesions. Stretching is a good method of prevention but, Apart from neurological lesions, which are discussed at the in our experience, has no therapeutic value. end of this chapter, the commonest cause of weakness is a rupture of the Achilles tendon, most frequent in athletes 90 Achilles tenovaginitis over 30 years of age. The tear lies in the ‘critical zone of poor vascularization’, which is 2–6 cm above the calcaneal Although the Achilles tendon does not have a sheath, inflam- insertion.91 mation can sometimes occur between the tendon and It is surprising that this simple and easy-to-detect condition the peritenon and create a so-called tenovaginitis of the very often remains undiagnosed for a time. Between 30 and Achilles tendon. This can take two forms: rheumatoid and 41% of Achilles tendon ruptures remain undiagnosed for more xanthomatous. than 2 weeks.35,92,93 The history is typical. During a sudden contraction – for Rheumatoid arthritis and example, at the start of or during a sprint, lifting a heavy object In these conditions, the contrast between the mild symptoms or pushing a car – the patient hurts the heel. There is a snap, and the marked signs is striking. It is also important to remem- followed by a dull pain in the heel. This eases fairly quickly ber that gout can sometimes affect the Achilles tendon. The but, from then on, the patient finds that only hobbling on main complaint is not, as in tendinitis, pain during contraction a flat surface is possible. Alternatively, there may not have of the triceps but pain during local pressure, e.g. catching the been a sudden contraction of the triceps but rather a severe heel against the edge of the shoe. Examination shows that elongation caused by excessive and sudden dorsiflexion at rising on tiptoe is indeed just uncomfortable rather than painful the ankle. but the tendon is warm, swollen and very tender to the When the patient lies on the couch, the clinical examination 86,87 touch. Local treatment consists of infiltration with 20 mg reveals little. There is usually no haematoma or visible thicken- of triamcinolone between the sheath and the tendon. The ing. Passive movements are painless. An alert examiner will technique is the same as described for Achilles tendinitis. probably detect an excessive range of dorsiflexion. In the Xanthomatous tenovaginitis supine, non-weight-bearing position, resisted plantiflexion remains possible because the plantaris, flexor hallucis longus The Achilles tendon is a common site of xanthomatous lesions. and flexor digitorum muscles still contract. Rising on tiptoe, Similar swellings can be seen and palpated at the extensor however, immediately reveals the diagnosis. The squeeze test on the dorsum of both hands or occasionally on the is also positive: the patient lies prone, with both feet suspended tendons crossing the dorsum of the foot and on a line at the over the edge of the couch; compressing the triceps surae upper part of the ulna and tibia. Small nodules can also be seen causes plantiflexion of the foot when the tendon is intact but in the upper . There is only slight discomfort during not when it is ruptured.14 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. Differential diagnosis Treatment consists of restoring normal lipid metabolism The differential diagnosis from tennis leg is quite simple. In a with clofibrate 1.5 g daily, or fenofibrate 300 mg daily. patient with a minor tear in the medial gastrocnemius muscle, there is pain in the calf and the foot is fixed in plantiflexion. Calcaneus apophysitis This contrasts very strongly with the absence of pain, the inability to plantiflex against resistance and the excessive dor- Apophysitis of the calcaneus (Sever’s disease, Osgood’s disease) siflexion range at the ankle that are characteristic of a rupture occurs in boys between 6 and 12 years of age and is often of the Achilles tendon. bilateral. The disorder has been classified among the general Although the history of sudden pain and disability may osteochondrosis syndromes, such as Legg–Calvé–Perthes suggest a sprained ankle, a rupture of the Achilles tendon disease at the or Osgood–Schlatter disease at the tibial will not be missed if the clinical examination is executed tuberosity. The child complains of sharp pain in the heel, properly. 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 Treatment usually tender to the touch. The radiological appearances are There is still controversy concerning the best treatment for characteristic – ‘slight fragmentation of the apophysis’ – and Achilles tendon ruptures. It appears that a satisfactory outcome confirm the diagnosis. Spontaneous recovery occurs in a year may be achieved with either non-operative or operative or two, often with the development of a slight permanent treatment but surgical repair appears to provide better func- prominence on the posterior aspect of the calcaneus.88 tional capacity94 with better scores of strength, power and There is no treatment except relative rest, slightly raising endurance95–97 and lower re-rupture rates. The advantages of the heel and inserting shock-absorbing heel pads in the shoe.89 the conservative approach are that there are no risks of

752 Disorders of the lower leg C H A P T E R 5 7 anaesthesia, infection, skin adhesions and sural nerve injury.98,99 Reports in the literature indicate that in active, young, very Box 57.2 demanding individuals, surgical repair should be considered, with non-surgical treatment reserved for elderly or sedentary Short calf muscles 100–102 However, conservative treatment can also be patients. Symptoms considered in athletically active patients, as treatment should always be individualized to the concerns and health of the • Pain on standing/muscular fatigue patient.103,104 • Outward position of the feet There is no single, uniformly accepted surgical technique Complications for Achilles tendon repair. Most acute ruptures have been treated successfully with excision of the devitalized tendon • Achilles tendinopathy tissue and simple end-to-end suture. However, various aug- • mentation procedures, such as reinforcement of the suture • Plantar with a triceps surae tendon tip-over graft, have been combined • Mid-tarsal strain and arthrosis 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 Clinical examination reported to be promising, although not without failures and 108,109 This shows the dorsiflexion range at the ankle joint to be pain- complications. lessly limited. A gastrocnemius equinus is typically character- Several recent studies have reported functional benefits of ized by less than 10° of ankle dorsiflexion with the knee early postoperative tendon mobilization in well-motivated extended.117 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 Complications Conservative treatment consists of 8 weeks in a plaster Because the patient cannot bear weight adequately on the cast with the foot in equinus position, followed by the use heels, mid-tarsal and later painful strain will of a 2.5 cm heel for an additional 1 or 2 months.112,113 The result. Limited dorsiflexion at the ankle can also lead to various thickened and enlarged scar tissue resulting from conservative compensations in the lower extremity that ostensibly cause treatment can be massaged twice a week for 2–3 months. secondary problems, including Achilles tendinopathy,118 The fibrous swelling at the point of the rupture never seems flat foot, chronic metatarsalgia119 and strain of the plantar to disappear, however, and some residual disability can be fascia.120 permanent. Symptoms and complications associated with short planti- It can be concluded that the treatment of choice in the flexor muscles are summarized in Box 57.2. athletically active patient is primary surgical repair.114 Con- servative treatment is chosen in middle-aged or less active Treatment patients.115 Younger patients The mid-tarsal must be protected, together with the Short plantiflexor muscles and the forefoot. Therefore the heel must be raised temporarily by a horizontal surface. The child is taught Short calf muscles, resulting in equinus deformity, are among to do stretching exercises for soleus and the gastrocnemii, the most common complications in children with cerebral several times a day, for 2–6 months. These lengthen the calf palsy.116 Sometimes, shortening of calf muscles is an isolated muscles so that the raised heel on the shoe can be discarded. finding and may easily be overlooked. The 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, History the patient is encouraged to lean further and further forwards Usually, the parents bring the child’s gait to attention. They so as to stretch the soleus more. notice that the youngster turns the feet outwards during To stretch the gastrocnemii muscles, the child stands in walking or running, adopting a ‘Chaplin’ style of moving. front of a wall, with feet fully dorsiflexed and extended, Because the child cannot dorsiflex the ankle joint during the heels remaining on the ground. The patient then leans walking, the feet must be turned outwards to take off. As this forwards, keeping the knees firmly in full extension (Fig. is not the best technique for running, the child will run con- 57.7b). spicuously more slowly than healthy peers. Sometimes the parents also notice that the child tends to Adults tilt backwards on standing. The poise around the centre of The same treatment can be tried but the process of stretching gravity is incorrect, which leads to muscular fatigue. Therefore the calf muscles is tedious and tends to fail. Here, the shorten- the child will complain that prolonged standing is tiring. ing can only be compensated by raising the heel of the shoe.

753 The Lower Leg, Ankle and Foot

Lesions of the dorsiflexors

Pain

If resisted dorsiflexion of the foot elicits pain, a resisted move- ment of the hallux, and then of the , identifies the offend- ing 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.

(a) 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 , 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 rheu- matoid condition. Apart from pain, a localized swelling can be seen and occasionally crepitus can be felt. In traumatic teno- , 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 (b) The only parallel condition in the body is myosynovitis of the bellies of the abductor pollicis longus and the extensor pollicis Fig 57.7 • Stretching of the left soleus (a) and left gastrocnemii (b). 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, Alternatively, surgery can be advised. Recently, good who are unaccustomed to wearing heavy boots.123 Resisted results have been reported with endoscopic release of the dorsiflexion hurts above the front of the ankle. Painless resisted gastrocnemii.121,122 dorsiflexion of the big toe and outer toes points to the tibialis

754 Disorders of the lower leg C H A P T E R 5 7

Box 57.3

Summary of treatment of lesions of the dorsiflexors Muscle • Either 10–30 mL procaine 0.5% • Or deep friction 3 times a week, 10 sessions Tendon • Deep friction 3 times a week, 10 sessions Tenoperiosteal junction • Either 1 mL triamcinolone (10 mg/mL) • Or deep friction 3 times a week, 10 sessions

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 Fig 57.8 • Deep 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 con- ducted by an adduction movement of the . 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 – vol- untary 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 Fig 57.9 • The anterior compartment (colour indicates the fascia). in the closed fascial compartment which is formed by the tibia, the fibula, the interosseous membrane and the anterior produces relative muscle ischaemia and therefore temporary fascia (Fig. 57.9). During exercise, muscle volume may expand paralysis and pain. The swelling may also trap the superficial by 20%, from both increased blood flow and capillary peroneal nerve at its exit through the fascial foramen at mid-leg filtration.126,127 If the superficial fascia is not lax enough to and cause paraesthesia in the outer foot. accommodate the greater volume, the intramuscular pressure After some minutes’ rest, blood flow recovers and symp- rises to levels that compress the anterior tibial artery. This toms resolve. Because the patient is asymptomatic between

755 The Lower Leg, Ankle and Foot occurrences and not chronically disabled, some authors prefer the suffix ‘recurrent’ rather than ‘chronic’ to identify anterior 1 2 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 plan- tiflexion 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 entrap- ment syndromes and claudication.131 The gold standard of diagnosing anterior compartment syndrome is the measure- Fig 57.10 • Tendons and insertions of the main invertor muscles: ment of intracompartmental pressures before and after 1, tibialis anterior; 2, tibialis posterior. exertion.132,133 A resting pressure > 15 mm Hg, and 5 minutes post-exercise pressures > 20 mm Hg are diagnostic of compart- ment syndrome.134–136 Posterior tibial tendinitis is usually caused by overuse, which Acute and severe anterior compartment syndromes may occurs frequently in a valgus deformity at the .145 develop after a tibial fracture137 or a direct blow.138 Within a Resisted inversion of the foot hurts and dorsiflexion does not. few hours, pain at the mid-leg becomes intense and is not Because the tibialis posterior has an additional function in relieved by immobilization. The overlying skin sometimes stabilizing the hindfoot during rising on tiptoe, this test may becomes shiny and warm. Together with the palpable tender- also be painful. Palpation then discloses whether the lesion lies ness, this may give the false impression of cellulitis. Making at the insertion on the navicular bone, at the tendon (distal or this error is a disaster because, if the diagnosis is not made at proximal to or under the medial malleolus), at the muscle belly once and the fascia divided immediately, ischaemic necrosis or at the proximal musculotendinous junction. will ensue. Complete paralysis with a permanent drop foot will Sometimes the tendon sheath rather than the tendon is then result. There are also documented cases of bilateral com- inflamed, causing . This occasionally occurs in partment syndrome with permanent drop foot complicating rheumatoid arthritis. surgery of long duration in the lithotomy position.139 Tendinitis usually recovers with a few sessions of massage Treatment but the valgus deformity at the heel must be corrected in order Apart from altering the patient’s activities or training pro- to prevent recurrences. Pain resulting from overuse secondary grammes, surgery seems to be the only effective treatment for to a valgus deformity will never be relieved unless a combined recurrent compartmental syndromes. The surgical procedure approach is used consisting of deep friction and correction of consists of a subcutaneous fasciotomy.140–142 the valgus deformity with a support at the heel. In acute cases, surgical decompression must be performed In rheumatoid tenosynovitis, 10 mg of triamcinolone is as soon as possible. As in a strangulated inguinal hernia, the injected between the tendon and its sheath. motto is: ‘operate before sunset or sunrise’.143 Sheridan and Matsen144 found that fasciotomy performed within 12 hours Deep friction techniques of onset of a compartment syndrome resulted in normal func- The technique differs according to the site of the lesion: above tion in 68% of cases. However, in those decompressed after or below the medial malleolus. In both instances, the patient 12 hours, only 8% recovered normal function. lies on the couch with the hip in external rotation so that the inner surface upwards. Weakness Technique: friction to the upper part of tibialis posterior Painless weakness of dorsiflexion results from neurological The therapist sits lateral to the patient’s foot. With the con- lesions that are discussed at the end of this chapter. tralateral 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 Lesions of the invertors only be reached if the pronation–supination technique is used. The of the ipsilateral hand, reinforced by the index finger, is thus laid flat on the affected part ofthe Pain tendon, just behind the edge of the tibia (Fig. 57.11). The ring and little fingers are kept extended. The fingers, the and The main invertor muscles are the anterior and posterior tibia- the forearm are brought into line with the tibia. Friction is lis muscles (Fig. 57.10). The flexor hallucis longus and the imparted with a supination movement, which is continued triceps are weak invertors as well. until the tendon escapes from the finger. Pressure is then

756 Disorders of the lower leg C H A P T E R 5 7

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

(a) (b)

released a little and the finger returned to the original position stress syndrome’. Few conditions have caused as much contro- by pronation. versy. The term has been used to cover a variety of conditions, This alternating pronation–supination movement is contin- such as stress fractures,146–148 periostitis and inflam- ued for about 20 minutes. Usually 10 sessions, three times a mation.149 The American Medical Association subcommittee week, suffice to resolve the condition. for classification of sports injuries restricts the name shin Technique: friction to the lower part of splints to musculotendinous lesions of the tibialis posterior 150 tibialis posterior muscle. The patient’s foot is dorsiflexed and the therapist sits level The disorder appears as an overuse phenomenon in runners with the affected foot. The thumb of the contralateral hand is and is one of the most common causes of exertional leg pain, 151 placed at the lateral side of the foot. The tips of one or two accounting for 6–16% of all running injuries. fingers are placed on the affected length of the tendon, just The most common complaint is diffuse pain of the lower beyond it. Friction is now given with an extension movement extremity, along the middle-distal tibia, associated with exer- at the wrist (Fig. 57.12), using the thumb as a fulcrum. The tion. In the early course, pain is worse at the beginning of fingers ride over the whole width of the tendon until the latter exercise but gradually subsides during training and within escapes from the pressure. Using flexion of the wrist, without minutes of cessation of exercise. As the injury progresses, losing contact with the skin, the fingers are then moved to the however, pain presents with less activity and may occur at 152 original position behind the tendon, and the whole procedure rest. is repeated. Clinical examination shows little pain during resisted inver- Friction is continued for 20 minutes, twice a week, for 1 or sion of the foot. Palpation reveals tenderness and sometimes 2 weeks. 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 Pain at the posterior medial edge of the tibia in athletes and striking the heel or tapping the anterior tibia, or the bone is long-distance runners is called ‘shin splints’ or ‘medial tibial tender to direct pressure. During the initial weeks, a stress

757 The Lower Leg, Ankle and Foot

Box 57.4

Leg pain: differential diagnosis Posterior leg pain Anterior leg pain • Tennis leg • Myosynovitis of the tibialis • Achilles tendinitis at the anterior musculotendinous junction • Shin splints • Deep venous thrombosis • Stress fracture • Rupture of Baker’s cyst • Tight fascial compartment • Intermittent claudication • Lesion of a dorsiflexor • Ischaemic contracture of muscle belly the calf muscles • L3, L4 referred pain • L5–S2 referred pain

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 progres- sive, unilateral, acquired flat foot, with increasing valgus of the heel, plantar flexion of the talus and subluxation of the talona- vicular 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 Fig 57.12 • Deep friction to the lower part of the tibialis posterior. typical sequence. First the TPT is activated, which inverts the foot and locks the heel and the mid-tarsal joints. Then the fracture is not visible on a plain radiograph153 but can be triceps muscle pulls on the now-rigid calcaneus, the heel rises detected with ultrasound.154 In case of doubt, a bone scinti- and the body weight is imparted to the ball of the foot. With gram can be obtained that easily distinguishes an inflammatory a rupture of the TPT, however, the initial varus movement at 155,156 the heel is impossible and the patient rises up with the heel in shin splint from a stress fracture. 161,162 The condition responds effectively to a series of sessions of valgus or does not get up on to the ball of the foot at all. Conservative treatment includes a medial heel wedge and a deep transverse friction. Good results have also been obtained 163 with weekly infiltrations of procaine (10–20 mL) over 3 con- longitudinal arch support. secutive weeks. Surgical treatment must be considered when the patient is For a stress fracture, only rest is effective. A 6- to 8-week young and active. A plantaris or extensor tendon graft may be pause in training is usually necessary. used to bridge the defect. Recently, the transfer of the flexor digitorum longus tendon into the sheath of the tibialis posterior Differential diagnosis between posterior and anterior leg 164,165 pain is summarized in Box 57.4. has been used for larger defects.

Weakness Lesions of the evertors

Neurological lesions are discussed at the end of this chapter. Pain 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 Tendinopathy critical zone with a low degree of vascularity, posterior to the If there is pain on resisted eversion of the foot, the peroneal medial malleolus.158 muscles are at fault. Peroneal tendinosis is usually a simple

758 Disorders of the lower leg C H A P T E R 5 7

Fig 57.13 • Deep friction to the peroneal tendons under the Fig 57.14 • Deep friction to the peroneal tendons level with the malleolus. malleolus. overuse phenomenon in runners and skaters,166,167 although the peroneus tendon (Fig. 57.14). Friction is started with the it may also appear as a complication of ankle sprain (see finger behind the tendon. Pressure is exerted and, with a supi- p. 774).168,169 nation movement of the forearm, the tendon is pressed ante- As tendinosis occurs anywhere, from the lower fibula to the riorly until it escapes from the finger and slips backwards. The cuboid and the fifth metatarsal base, the exact position of the now-supinated hand is manœuvred back to the pronated posi- lesion can only be disclosed by palpation for tenderness along tion behind the tendon, where the movement restarts. the whole tendon. Friction is imparted by rotating the forearm in full supina- tion and full pronation for about 15 minutes. Three sessions a Treatment week over 3–4 weeks are usually sufficient to cure the lesion. Peroneal tendinosis is seldom sufficiently localized to be treated by steroid injection. However, it responds very well to deep transverse massage. Other conditions Technique: deep friction above and below ‘Snapping ankle’ 170 the malleolus Sometimes patients complain of a slight pain, together with a The patient lies supine, with the leg medially rotated. The snapping feeling at the outer side of the ankle, during certain therapist sits at the opposite side. The foot is brought into movements. The reason is a loosening of the peroneal tendons inversion; this stretches the tendon. Two or three fingertips of in the groove of the posterior surface of the fibula. They slip the therapist’s ipsilateral hand are now placed on the tendon. forwards over the malleolus when the ankle is dorsiflexed and The fingers are slightly flexed, thereby pressing the tendon ‘jump back’ during plantiflexion.171 This ‘snapping ankle’ is against the fibular shaft. The thumb is placed at the medial usually not painful, just uncomfortable. Sometimes, however, side of the lower leg or ankle to provide counterpressure it is the origin of a superimposed tendinitis. Non-surgical treat- (Fig. 57.13). Friction is given with a to-and-fro movement of ment should always be instituted first and consists of holding the forearm, during which the fingers ride over the tendon. the tendons reduced in their anatomical positions while the The friction is in two phases: an active phase, during which the superior peroneal retinaculum heals by scarring.172 If consider- tendon is pressed and pulled, and a relaxed phase, during able discomfort remains, surgery can be advised. Different which the fingers are placed in the previous position to restart methods of repair have been described.173,174 Usually, a new the movement. retinaculum is constructed behind the lateral malleolus or the Three sessions a week over 2–4 weeks may be required. calcaneofibular ligament is transposed to the lateral side of the During the course of treatment, the patient should avoid exer- peroneal tendons.175 cise but complete rest is not required. The results are uniformly good. Mucocele Technique: deep friction level with the malleolus A mucocele can form in the sheath of the tendon. It results in The therapist sits by the patient’s foot, facing it. The foot is localized swelling and can be associated with a considerable held in inversion and plantar flexion is produced by slight pres- ache. The diagnosis is obvious because the swelling is located sure of the ipsilateral hand. The therapist holds the contralat- in the sheath and can be made to fluctuate upwards and down- eral hand and forearm in line with the leg. The middle finger, wards along the malleolus by digital pressure. Treatment is reinforced by the index finger, is placed in the sulcus, behind aspiration. Because the viscous fluid has a high density, the

759 The Lower Leg, Ankle and Foot aspiration is difficult to perform unless a wide-bore needle and Table 57.1 Innervation of neurological weakness of the foot 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 Muscle Segmental Peripheral are injected into the now-empty synovial space. Sometimes innervation nerve this procedure has to be repeated after a year or so. Tibialis anterior L4 (L5) Deep peroneal Peroneal spasm Extensor digitorum longus L4, L5 Deep peroneal This is not an intrinsic disorder of the peroneal muscles but results from arthritis of the talocalcaneal and mid-tarsal joints. Extensor hallucis longus L4, L5 Deep peroneal If the arthritis is cured, the spasm disappears immediately. Peronei L5, S1 Superficial peroneal Tibialis posterior L4, L5 Tibial Weakness Flexor digitorum longus L5–S1 Tibial Weakness of the peronei usually results from neurological Flexor hallucis longus L5–S1 Tibial lesions. Triceps surae S1, S2 Tibial

Disorders causing neurological In lesions of the nerve root (sciatica caused by disc protru- sion), the distribution is segmental. There is or there has been weakness of the foot considerable pain in the respective dermatomes before the appearance of the weakness. Although weakness can be signifi- Weakness of the calf muscles is best detected by asking the cant, especially if two consecutive nerve roots are involved, it patient to stand on one foot and to rise on tiptoe. Slight weak- is almost never complete. ness can only be identified by repetitive rising on tiptoe, com- In lesions of a peripheral nerve, weakness follows the normal paring one leg with the other. afferent distribution of the nerve. Very often, the pain appears Dorsiflexion, eversion and inversion are tested in the supine- silently, without previous pain in the innervated area. As the lying position. As described in Chapter 55, it is very important peripheral nerves in the lower behave in the same way as to give strong counterpressure, with the leg in a neutral posi- a nerve trunk, paraesthesia will only appear when pressure on tion. Normally, the extrinsic muscles of the foot are very strong the nerve is released and not during the actual period of com- and their pull cannot be overcome by the examiner’s force. pression (see release phenomenon in Ch. 2).176,177 Both sides should be compared. In central or upper motor neurone lesions, the weakness is gross and distributed over different muscles and muscle groups Access the complete reference list online at (Table 57.1). www.orthopaedicmedicineonline.com

760 Disorders of the lower leg C H A P T E R 5 7

References

1. Naish JM, Appley J. ‘Growing pains’. A 22. Franke K. Traumatologie des Sports. 41. Casparian JM, Luchi M, Moffat RE, clinical study of nonarthritic limb pain Stuttgart: Thieme; 1980. Hinthorn D. Quinolones and tendon in children. Arch Dis Child 1951;26: 23. Dürig M, Schuppiser JP, Gauer EF, ruptures. South Med J 2000;93(5): 134–40. Muller W. Spontaneous rupture of the 488–91. 2. Oster J, Nielsen A. Growing pains – gastrocnemius muscle. Injury 1977;9: 42. Schepsis AA, Jones H, Haas AL. Achilles a clinical investigation of a school 143–5. tendon disorders in athletes. Am J Sports population. Acta Paediatr Scand 1972;61: 24. Kwak HS, Lee KB, Han YM. Ruptures Med 2002;30:287–305. 134–40. of the medial head of the gastrocnemius 43. Ohberg L, Lorentzon R, Alfredson H. 3. Baxter MP, Dulberg C. ‘Growing pains’ (’tennis leg’): clinical outcome and Neovascularisation in Achilles tendons in childhood. A proposal for treatment. compression effect. Clin Imaging with painful tendinosis but not in normal J Pediatr Orthop 1988;8:402–6. 2006;30(1):48–53. tendons: an ultrasonographic investigation. 4. Harel L. Growing pains: myth or reality. 25. Khan KM, Cook JL, Kannus P, et al. Knee Surg Sports Traumatol Arthrosc Pediatr Endocrinol Rev 2010;8(2): Time to abandon the ‘tendinitis’ myth 2001;9:233–8. 76–8. [editorial]. BMJ 2002;324:626–7. 44. Paavola M, Kannus P, Järvinen T, et al. 5. Miller A. Rupture of the 26. Biedert R. Beschwerden im Current concepts review: Achilles musculotendinous juncture of the medial Achillessehnenbereich. Ätiologien und tendinopathy. J Bone Jt Surg 2002;84A: head of the gastrocnemius. Am J Sports therapeutische Äberlegungen. Unfall 2062–76. Med 1977;5:191–3. Chirurg 1991;94(10):531–7. 45. Kvist MH, Lehto MU, Jozsa L, et al. 6. Hood WP. On lawn-tennis leg. Lancet 27. Devereaux MD, Lachmann SM. Athletes Chronic Achilles paratenonitis: an 1884;i:728–9. attending a sports injury clinic – a review. immunohistologic study of fibronectin and 7. Gilcreest EL. Ruptures and tears of Br J Sports Med 1983;17:137–42. fibrinogen. Am J Sports Med 1988;16: muscles and tendons of the lower 28. Kvist DR, Järvinen M. Zur Epidemiologie 616–23. extremity. JAMA 1993;100:153–60. von Sportverletzungen und 46. Järvinen M, Jóa L, Kannus P, et al. 8. Cornwell HE, Allredge RH. Ruptures and Fehlbelastungsformen. Patienten-analyse Histopathological findings in chronic tears of tendons and muscles. Am J Surg einer Sportmedizinischer Poliklinik. Med tendon disorders. Scand J Med Sci Sports 1937;35:22–33. Sport 1980;20:375–8. 1997;7:86–95. 9. Golding D. Tennis leg. BMJ 1969;4: 29. Taunton JE, Ryan M, Clement DB, et al. 47. Clement DB, Taunton JE, Smart GW. 243. A retrospective case-control analysis of Achilles tendinitis and peritendinitis. 10. Gaulrapp H. ‘Tennis leg’: ultrasound 2002 running injuries. Br J Sport Med Etiology and treatment. Am J Sports Med differential diagnosis and follow-up. 2002;36:95–101. 1984;12:179–84. Sportverletz Sportschaden 1999;13(2): 30. Kujala UM, Sama S, Kaprio J. Cumulative 48. Åström M, Rausing A. Chronic Achilles 53–8. incidence of and tendinopathy. A survey of surgical and 11. Bianchi S, Martinoli C, Abdelwahab IF, tendinopathy in male former elite athletes. histopathologic findings. Clin Orthop et al. Sonographic evaluation of tears of Clin J Sport Med 2005;15:133–5. 1995;316:151–64. the gastrocnemius medial head (’tennis 31. McCrory JL, Martin DF, Lowery RB, et al. 49. Auquier L, Siaud JR. Tendinites nodulaires leg’). J Ultrasound Med 1998;17(3): Etiologic factors associated with Achilles du tendon d’Achille. Rev Rhum 1971;38: 157–62. tendinitis in runners. Med Sci Sports Exerc 373–81. 12. Werken van der C, Marti RK. Rupturen 1999;31(10):1374–81. 50. Schie HT, de Vos RJ, de Jonge S, et al. van de Achillespees. Ned Tijdschr 32. Scioli MW. Achilles tendinitis. Orthop Ultrasonographic tissue characterisation Geneeskd 1980;124:1321–2. Clin North Am 1994;25(1):177–82. of human Achilles tendons: quantification 13. Visser JD. Achillespeesruptuur. Ned 33. Reinschmidt C, Nigg BM. Influence of tendon structure through a novel Tijdschr Geneeskd 1980;124:1340–2. of heel height on ankle joint moments non-invasive approach. Br J Sports Med 2010;44:1153–9. 14. Thompson TL, Doherty JH. Spontaneous in running. Med Sci Sports Exerc rupture of tendon of Achilles, a new 1995;27(3):410–6. 51. Paavola M, Paakkala T, Kannus P, diagnostic clinical test. J Trauma 1962;2: 34. Lemaire M, Miremad C, Combelles F. Järvinen M. Ultrasonography in the 126–9. Tendinite du tendon d’Achille du sportif. differential diagnosis of Achilles tendon injuries and related disorders. A 15. Gauer EF, Düring M, Müller W. Die Méd Sport 1981;55:6. comparison between preoperative proximate Ruptur im Triceps surae, eine 35. Zuinen C. Ruptures du tendon d’Achille. ultrasonography and surgical findings. typische, aber oft verkannte Verletzung. Méd Sport 1980;54:6. Acta Radiol 1998;39:612–9. Chirurgie 1976;47(4):236–40. 36. Logengren C, Lindholm A. Vascular 52. Soila K, Karjalainen PT, Aronen HJ, et al. 16. Scurr JH, Coleridge-Smith PD, Hasby JH. distribution in the Achilles tendon. Acta High resolution MR imaging of the Deep venous thrombosis: a continuing Chir Scand 1958;116:491–5. asymptomatic Achilles tendon: new problem. BMJ 1988;297:28. 37. Schmidt-Rohlfing B, Graf J, Schneider U, observations. AJR Am J Roentgenol 17. Lambie JM, Mahaffy RG, Barber DC, Niethard FU. The blood supply of the 1999;173:323–8. et al. Diagnostic accuracy in venous Achilles tendon. Int Orthop 1992;16(1): 53. Haims AH, Schweitzer ME, Patel RS, thrombosis. BMJ 1970;ii:142–3. 29–31. et al. MR imaging of the Achilles tendon: 18. Kakkar W, Howe CT, Flance C, Clarke 38. McGarvey WC, Singh D, Trevino SG. overlap of findings in symptomatic and MB. Natural history of postoperative Partial Achilles tendon ruptures associated asymptomatic individuals. Skeletal Radiol . Lancet 1969;ii:230– with fluoroquinolone antibiotics: a case 2000;29:640–5. 2. report and literature review. Foot Ankle Int 54. Khan KM, Forster BB, Robinson J, et al. 1996;17(8):496–8. 19. Baker WM. Chronic synovial cysts 1887; Are ultrasound and magnetic resonance Report. St Bartholomew’s Hospital, 39. van der Linden PD, van de Lei J, Nab imaging of value in assessment of Achilles London. HW, et al. Achilles tendinitis associated tendon disorders? A two year prospective 20. Cyriax JH. Textbook of Orthopaedic with fluoroquinolones. Br J Clin study. Br J Sports Med 2003;37: Medicine, vol. 1. 8th ed. London: Baillière Pharmacol 1999;48(3):433–7. 149–53. Tindall; 1982. 40. Lewis JR, Gums JG, Dickensheets DL. 55. Emerson C, Morrissey D, Perry M, Jalan 21. Colson JHC, Armour WJ. Sport Injuries Levofloxacin-induced bilateral Achilles R. Ultrasonographically detected changes and their Treatment. London: Stanley Paul; tendonitis. Ann Pharmacother 1999;33 in Achilles tendons and self reported 1975. (7–8):792–5. symptoms in elite gymnasts compared

760.e1 The Lower Leg, Ankle and Foot

with controls – an observational study. 74. Cyriax JH. Textbook of Orthopaedic 90. Jozsa L. The role of recreational sport Man Ther 2010;15:37–42. Medicine, vol. II. Treatment by activity in Achilles tendon rupture. Am J 56. Sandmeier R, Renström PA. Diagnosis and Manipulation, Massage and Injection. Sports Med 1989;3:338–43. treatment of chronic tendon disorders in London: Baillière Tindall; 1986. 91. Shields CL, Kerlan RK, Jobe FW, et al. sports. Scand J Med Sci Sports 1997;7: 75. Stanish WD, Rubinovich RM, Curwin S. The Cybex II evaluation of surgically 96–106. Eccentric exercise in chronic tendinitis. repaired Achilles tendon rupture. Am J 57. Daniel U, Skeoch MD. Spontaneous Clin Orthop Relat Res 1986;208:65–8. Sports Med 1978;6(6):369–72. partial subcutaneous ruptures of the tendo 76. Alfredson H, Pietilä T, Jonsson P, 92. Kennedy R, Inglis J, Malcolm L. Late Achilles. Am J Sports Med 1981;9(1): Lorentzon R. Heavy-load eccentric calf reconstruction of the Achilles tendon. 135–7. muscle training for the treatment of J Bone Joint Surg 1979;61A(6):653–8. 58. Bedi S, Ellis W. Achilles tendon ruptures. chronic Achilles tendinosis. Am J Sports 93. Rodineau J. La Rupture du tendon Ann Rheum Dis 1970;29:494. Med 1998;26:360–6. d’Achille. Pratique Médicale 1982. 59. Visser JD. Achillespeesruptuur. Ned 77. Mafi N, Lorentzon R, Alfredson H. 94. Majewski M, Rickert M, Steinbruck K. Tijdschr Geneeskd 1980;124(32):1344–7. Superior short-term results with eccentric Achilles tendon rupture. A prospective 60. Krahl H, Plaue R. Sehnenrupturen nach calf muscle training compared to study assessing various treatment Cortisoninjektionen. Med Sport 1971;11: concentric training in a randomized possibilities. Orthopade 2000;29(7): 264. prospective multicenter study on patients 670–6. with chronic Achilles tendinosis. Knee 61. Mahler F, Fritschy D. Partial and complete 95. Inglis AE, Scott WN, Sculco TP, Patterson Surg Sports Traumatol Arthrosc 2001;9: ruptures of the Achilles tendon and local AH. Ruptures of the tendo Achillis: an 42–7. corticosteroid injections. Br J Sports Med objective assessment of surgical and 1992;26(1):7–14. 78. Silbernagel KG, Thomeé R, Thomeé P, non-surgical treatment. J Bone Joint Surg Karlsson J. Eccentric overload training for 62. Shrier I, Matheson GO, Kohl HW. 1976;58A:990. patients with chronic Achilles tendon pain Achilles tendonitis: are corticosteroid 96. Jacobs D, Martens M, Van Audekercke R. – a randomised controlled study with injections useful or harmful? Clin J Sport Comparison of conservative and operative reliability testing of the evaluation Med 1996;6(4):245–50. treatment of Achilles tendon rupture. methods. Scand J Med Sci Sports 2001;11: Am J Sports Med 1978;6:107. 63. Read MT, Motto SG. Tendo Achillis pain: 197–206. steroids and outcome. Br J Sports Med 97. Percy EC, Connochie LB. The surgical 79. Sayana MK, Maffulli N. Eccentric calf 1992;26(1):15–21. treatment of ruptured Achilles tendon. muscle training in non-athletic patients Am J Sports Med 1978;6:132. 64. Maxwell NJ, Ryan MB, Taunton JE, et al. with Achilles tendinopathy. J Sci Med 98. Stein SR, Leukens CA. Closed treatment Sonographically guided intratendinous Sport 2007;10:52–8. injection of hyperosmolar dextrose to treat of Achilles tendon ruptures. Orthop Clin 80. Rompe JD, Nate B, Fuira JP, Maffulli N. chronic tendinosis of the Achilles tendon: North Am 1976;7:241. Eccentric loading, shock-wave treatment, a pilot study. AJR 2007;189:947. 99. Fruensgaard S, Helmig P, Riis J, Stovring or a wait-and-see policy for tendinopathy JO. Conservative treatment for acute 65. Alfredson H, Öhberg L. Sclerosing of the main body of the tendo Achilles: a rupture of the Achilles tendon. Int Orthop injections to areas of neo-vascularisation randomized control trial. Am J Sports Med 1992;16(1):29–31. reduce pain in chronic Achilles 2007;35:374–83. tendinopathy: a double-blind randomised 100. Nistor L. Surgical and non-surgical 81. Rees JD, Lichtwark GA, Wolman RL, controlled trial. Knee Surg Sports treatment of Achilles tendon rupture. Wilson AM. The mechanism for efficacy Traumatol Arthrosc 2005;13:338–44. J Bone Joint Surg 1981;63A:394. of eccentric loading in Achilles tendon 66. Ryan M, Wong A, Taunton J. Favorable injury; an in vivo study in humans. 101. Carden DJ. Rupture of the calcaneal outcomes after sonographically guided (Oxford) 2008;47(10): tendon: the early and the late intratendinous injection of hyperosmolar 1493–7. management. J Bone Joint Surg 1987;69B: dextrose for chronic insertional and 416–20. 82. Subotnick SI. Orthotic foot control midportion achilles tendinosis. AJR Am J and the overuse syndrome. Physician 102. Popovic N, Lemaire R. Diagnosis and Roentgenol 2010;194(4):1047–53. Sportsmed 1975;3(1):75–9. treatment of acute ruptures of the 67. Schepsis AA, Leach RE. Surgical Achilles tendon. Current concepts 83. James SL, Bates BT, Ostering LR. Injuries management of Achilles tendinitis. Am J review. Acta Orthop Belg 1999;65(4):458– to runners. Am J Sports Med 1978;6(2): Sports Med 1987;15(4):308–15. 71. 40–50. 68. Saxena A. Surgery for chronic Achilles 103. Lo IK, Kirkley A, Nonweiler B, Kumbhare 84. Möller MHC, Ekstrand J, Oeberg BE, tendon problems. J Foot Ankle Surg DA. Operative versus nonoperative Gillquist J. Duration of stretching effect 1995;34(3):294–300. treatment of acute Achilles tendon on range of motion in lower extremities. ruptures: a quantitative review. Clin J 69. Schepsis AA, Wagner C, Leach R. Surgical Arch Phys Med Rehabil 1985;65: Sport Med 1997;7(3):207–11. management of Achilles tendon overuse 171–3. injuries. Am J Sports Med 1994;5: 104. Gorschewsky O, Vogel U, Schweizer A, 85. Wiktorsson-Möller M, Oeberg B, Ekstrand 611–9. van Laar B. Percutaneous tenodesis of the J, Gillquist J. Effects of warming up, Achilles tendon. A new surgical method 70. Nelen G, Martens M, Burssens A. Surgical massage and stretching on range of motion for the treatment of acute Achilles tendon treatment of chronic Achilles tendinitis. and muscle strength in the lower rupture through percutaneous tenodesis. Am J Sports Med 1989;17:754–9. extremity. Am J Sports Med 1983;11: Injury 1999;30(5):315–21. 71. Jenkins DHR, Forster IW, McKibbin B, 249–52. 105. Ralston EL, Schmidt ER. Repair of the Ralis ZA. Induction of tendon and 86. Gerster JC, Vischer TL, Bennanin A, ruptured Achilles tendon. J Trauma ligament formation by carbon Fallet GH. The painful heel. Ann Rheum 1971;11(1):15–21. implantation. J Bone Joint Surg 1977;59B: Dis 1977;36:343–9. 53–7. 106. Winter E, Weise K, Weller S, Ambacher T. 87. Rask MR. Achilles tendon disease owing Surgical repair of Achilles tendon rupture. 72. Leach RE, Schepsis AA, Takai H. to rheumatoid disease. JAMA 1978;239 Comparison of surgical with conservative Long-term results of surgical management (5):435–6. of Achilles tendinitis in runners. Clin treatment. Arch Orthop Trauma Surg 88. Rodman GP, McEwen C, Wallace SL. Orthop 1992;282:208–12. 1998;117(6–7):364–74. Primer on rheumatic diseases. JAMA 107. Zell RA, Santoro VM. Augmented repair 73. Maffulli N, Testa V, Capasso G, et al. 1976;224(suppl5):67–8, 116–7. Results of percutaneous longitudinal of acute Achilles tendon ruptures. Foot 89. Taunton J, McKenzie D, Clement D. The tenotomy for Achilles tendinopathy in Ankle Int 2000;21(6):469–74. role of biomechanics in the epidemiology middle- and long-distance runners. Am J 108. Cretnik A, Kosanovic M, Smrkolj V. of injuries. Sports Med 1988;6:107–20. Sports Med 1997;25(6):835–40. Percutaneous suturing of the ruptured

760.e2 Disorders of the lower leg C H A P T E R 5 7

Achilles tendon under local anesthesia. J 126. Arai M, Endoh H. Blood flow through 143. Swierstra JCC, Klasen HJ. Het tibialis Foot Ankle Surg 2004;43(2):72–81. human skeletal muscle, during and after anteriorsyndroom. Geneeskd Sport 109. Mertl P, Jarde O, Van FT, et al. contraction. Tohoku J Exp Med 1970;2(3):45–6. Percutaneous tenorrhaphy for Achilles 1974;114:379–84. 144. Sheridan GW, Matsen FA. Fasciotomy in tendon rupture. Study of 29 cases. Rev 127. Schissel DJ, Godwin J. Effort-related the treatment of the acute compartmental Chir Orthop Reparatrice Appar Mot chronic compartment syndrome of the syndrome. J Bone Joint Surg 1976;58A: 1999;85(3):277–85. lower extremity. Mil Med 1999;164(11): 112–5. 110. Buchgraber A, Passler HH. Percutaneous 830–2. 145. Conti SF. Posterior tibial tendon problems repair of Achilles tendon rupture. 128. Reneman RS. The Anterior and Lateral in athletes. Orthop Clin North Am Immobilization versus functional Compartment Syndrome of the Leg. 1994;25(1):109–21. postoperative treatment. Clin Orthop Mouton: The Hague; 1968. p. 176. 146. Devereaux MD, Parr GR, Lachman SM, 1997;341:113–22. 129. Harman W. Significance of local vascular et al. The diagnosis of stress fractures 111. Bring DK, Kreicbergs A, Renstrom PA, phenomena in ischaemic necrosis in in athletes. JAMA 1984;252:531–3. Ackermann PW. Physical activity skeletal muscle. Am J Path 1948;24: 147. Batt ME, Ugalde V, Anderson MW, modulates nerve plasticity and stimulates 625. Shelton DK. A prospective controlled repair after Achilles tendon rupture. 130. Humphries D. Exertional compartment study of diagnostic imaging for acute J Orthop Res 2007;25(2):164–72. syndromes. Medscape Gen Med 1999;3: shin splints. Med Sci Sports Exerc 112. Lea RB, Smith L. Non-surgical treatment 1–7. 1998;30(11):1564–71. of tendo Achilles rupture. J Bone Joint 131. Bong M, Polatsch D, Jazrawi L, et al. 148. Anderson MW, Ugalde V, Batt M, Surg 1972;54A:1394. Chronic exertional compartment Gacayan J. Shin splints: MR appearance 113. Angermann P, Hovgaard D. Chronic syndrome: diagnosis and management. in a preliminary study. Radiology Achilles tendinopathy in athletic Hosp Joint Dis 2005;62:77–84. 1997;204(1):177–80. individuals: results of nonsurgical 132. Mubarak SJ, Hargens AR, Owen CA, 149. Jackson D. Shinsplints: an update. Phys treatment. Foot Ankle Int 1999;20(5): et al. The wick catheter technique Sports Med 1978;6:51–61. 304–6. for measurement of intra-muscular 150. American Medical Association. Standard 114. Singer K, Jones D. Soft tissue conditions pressure. A new research and clinical Nomenclature of Athletic Injuries. Chicago: of the ankle and foot. In: Nicholas J, tool. J Bone Joint Surg 1976;58A: American Medical Association; 1976. Hershman E, editors. 1016–20. The Lower Extremity 151. Bronfort G, Haas M, Evans R, et al. . St Louis: and Spine in Sports Medicine 133. Pedowitz RA, Hargens AR, Mubarak SJ, Effectiveness of manual therapies: the Mosby; 1986. p. 418–25. Hershuni DH. Modified criteria for UK evidence report. Chiropr Osteopat 115. Fruensgaard S, Helmig P, Riis J, Stovring the objective diagnosis of chronic 2010;18:3. JO. Conservative treatment for acute compartment syndromes of the leg. Am J 152. Kortebein P, Kaufman K, Basford J, Stuart rupture of the Achilles tendon. Int Orthop Sports Med 1990;18:35–40. M. Medial tibial stress syndrome. Med Sci 1992;16(11):33–5. 134. McQueen M. Acute compartment Sports Exerc 2000;32(3 suppl):S27–33. 116. Fontenrose A, Miller J, Hallum A. syndrome. Acta Chir Belg 1998;98(4): Physicians’ and physical therapists’ 166–70. 153. Prather JC, Nuzynowitzi ML, Snody AJ, et al. Scintigraphic findings in stress evaluation of cerebral-palsied children for 135. Verleisdonk EJ, van den Helder CJ, fractures. J Bone Joint Surg 1977;59A:896. Achilles tendon lengthening. Dev Child Hoogendoorn HA, van der Werken C. Neurol 1984;26:208–14. Good results of fasciotomy in chronic 154. Gilaldi M. Comparison between 117. McGlamry ED, Banks AS. McGlamry’s compartment syndrome of the lower leg. radiography, bone scan and ultrasound in Comprehensive Textbook of Foot and Ankle Ned Tijdschr Geneeskd 1996;140(50): the diagnosis of stress fractures. Milit Med Surgery, 3. Philadelphia: Lippincott 2513–7. 1984;149:459–61. Williams & Wilkins; 2001. p. 722. 136. Simon R, Sherman S, Koenigsknecht S. 155. Holder LE. Radionuclide bone-imaging in 118. Lamm BM, Paley D, Herzenberg JE. Compartment syndrome. Emergency the evaluation of bone pain. J Bone Joint Gastrocnemius soleus recession: a simpler, orthopedics: the extremities. New York: Surg 1982;64A:1391–6. more limited approach. J Am Podiatr Med McGraw Hill; 2007. p. 76–8, 441–3. 156. Young A, McAllister D. Evaluation and Assoc 2005;95:18–25. 137. Wiggins H. The anterior tibial treatment of tibial stress fractures. Clin 119. Hill R. Ankle equinus: prevalence compartment syndrome. A complication Sports Med 2006;25(1):117–28. and linkage to common foot pathology. of the Hauser procedure. Clin Orthop 157. Mann RA, Thompson F. Rupture of the J Am Podiatr Med Assoc 1995;85:295– 1975;113:90–4. posterior tibial tendon, causing flat foot. 300. 138. Leach RE, Corbett M. Anterior tibial J Bone Joint Surg 1985;67A:556–61. 120. Heim M, Blankstein A. Congenital short compartment syndrome in soccer players. 158. Frey CC, Shereff MJ. Tendon injuries Achilles tendon. Orthop Rev 1992;21(1): Am J Sports Med 1979;7(4). about the ankle in athletes. Clin Sports 105–7. 139. Duflo F, Allaouchiche B, Mathon L, Med 1988;7:103–18. 121. Trevino S, Gibbs M, Panchbhavi V. Chassard D. Bilateral anterior tibial 159. Johnson KA. Tibialis posterior tendon Evaluation of results of endoscopic compartment syndrome from prolonged rupture. Clin Orthop Rel Res 1983;117: gastrocnemius recession. Foot Ankle Int surgery in the lithotomy position. Ann Fr 140–7. 2005;26:359–64. Anesth Reanim 1999;18(7):779–82. 160. Funk DA, Cass JR, Johnson KA. Acquired 122. Saxena A, Widtfeldt A. Endoscopic 140. Blackman PG. A review of chronic adult flat foot secondary to posterior tibial gastrocnemius recession: preliminary exertional compartment syndrome in the tendon pathology. J Bone Joint Surg report on 18 cases. J Foot Ankle Surg lower leg. Med Sci Sports Exerc 2000;32 1986;68A:95–102. 2004;43:302–6. (3 suppl):S4–S10. 161. Ness ME, Long J, Marks R, Harris G. 123. O’Donoghue DH. Treatment of Injuries to 141. Schepsis AA, Gill SS, Foster TA. Foot and ankle kinematics in patients with Athletes. 3rd ed. Philadelphia: Saunders; Fasciotomy for exertional anterior posterior tibial tendon dysfunction. Gait 1976. compartment syndrome: is lateral Posture 2008;27(2):331–9. Epub 2007 Jun 124. Shah S, Miller B, Kuhn J. Chronic compartment release necessary? Am J 20. Sports Med 1999;27(4):430–5. exertional compartment syndrome. Am J 162. Tome J, Nawoczenski DA, Flemister A, Orthop 2004;33(7):335–41. 142. Kitajima I, Tachibana S, Hirota Y, et al. Houck J. Comparison of foot kinematics 125. Veith RG, Matsen FA, Newell SG. One-portal technique of endoscopic between subjects with posterior tibialis Recurrent anterior compartmental fasciotomy: chronic compartment tendon dysfunction and healthy controls. syndromes. Physician Sportsmed syndrome of the lower leg. Arthroscopy J Orthop Sports Phys Ther 2006;36(9): 1980;8(11). 2001;17(8):1. 635–44.

760.e3 The Lower Leg, Ankle and Foot

163. Kulig K, Reischl SF, Pomrantz AB, et al. 168. Anderson E. Stenosing peroneal tendons. Results of rerouting the tendons Nonsurgical management of posterior tenosynovitis symptomatically simulating under the calcaneofibular ligament. Am J tibial tendon dysfunction with orthoses ankle instability. Am J Sports Med Sports Med 1986;14(2):148–50. and resistive exercise: a randomized 1987;157:258–60. 174. Das De S, Balasubramaniam P. A repair controlled trial. Phys Ther 2009;89(1): 169. Sammarco GJ, DiRaimondo CV. Chronic operation for recurrent dislocation of 26–37. Epub 2008 Nov 20. peroneus brevis tendon lesions. Foot Ankle peroneal tendons. J Bone Joint Surg 164. Hansen ST, Clark W. Tendon transfer to 1989;9(4):163–70. 1985;67B(4):585–7. augment the weakened tibialis posterior 170. Bisschop P, Deconinck R, Ombregt L, 175. Ferran NA, Maffulli N, Oliva F. mechanism. JAMA 1988;78:309–402. Van de Velde T. Workbook for the Cyriax Management of recurrent subluxation of 165. Mendicino SS, Quinn M. Tibialis posterior Course in Orthopaedic Medicine. the peroneal tendons. Foot Ankle Clin dysfunction: an overview with a surgical De Haan: Belgian Scientific Society of 2006;11(3):465–74. case report using a flexor tendon transfer. Orthopaedic Medicine; 1986. 176. Guarantors of Brain. Aids to the J Foot Surg 1989;28:154–7. 171. McLennon JG. Treatment of acute and Examination of the Peripheral Nervous 166. Sammarco GJ. Peroneal tendon injuries. chronic luxations of the peroneal tendons. System. London: Baillière Tindall; 1986. Orthop Clin North Am 1994;25(1): Am J Sports Med 1980;8:422–36. 177. Brügger A. Die Erkrankungen des 135–45. 172. Stover CN, Bryan DR. Traumatic Bewegungsapparates und seines 167. Jackson MA, Gudas CJ. Peroneus longus dislocation of the peroneal tendons. Am J Nervensystems. Stuttgart: Gustav Fisher; tendinitis: a possible biomechanical Surg 1962;103:180–6. 1980. etiology. J Foot Surg 1982;21(4):344–8. 173. Martens MA, Noyez JF, Mulier JC. Recurrent dislocation of the peroneal

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