Classification

Osteochondritis may be classified in relation to the anatomical location of the enchondral ossification defect (Griffin 1994):

Alternatively, osteochondritis may be classified by the effects brought about by local forces on the area of diseased enchondral bone:

Aetiology

The true aetiology of the various presentations of osteochondritis is unknown, but they have been linked to hereditary factors, local trauma, nutritional factors and local ischaemia within the affected area of bone (Ekman & Carlson 1998, Walsh & Dorgan 1988).

Diagnosis

Plain radiographs are usually used to diagnose osteochondritis, but minor or early-stage lesions may be overlooked as they are difficult to visualise on a plain radiograph. Lesions are identified readily using bone scan, computerised axial tomography scan and magnetic resonance imaging (Bohndorf 1998).

Differential diagnosis

The differential diagnosis for all the osteochondritides can include osteomyelitis, bone tumours and fractures (Caselli et al 1998).

Treatment

The treatment of all presentations of osteochondritis focuses on rest and immobilisation to allow the affected bone to heal with no or only minimal distortion, together with the use of painkillers (such as NSAIDs), as necessary, during the acute or early presentations of the disease.

Rest and immobilisation of the affected bone is essential:

Early initiation of treatment is especially important where the involved osteochondritic bone forms part of a joint, in order to reduce the likelihood of later osteoarthritic changes, pain and dysfunction of the affected joint.

The format, intensity and duration of the regimen of rest is tailored to the presenting problem, and can be achieved by a variety of means, such as rigid splinting, soft splinting and strapping, and other means to reduce weight bearing, and traction and compressive forces on the involved bone.

Pathology

Freiberg’s disease may present uni- or bilaterally, as a focus of ischaemia and bone necrosis within the head of a metatarsal, leading to collapse of both the articular surface and the underlying area of subchrondral bone – the so-called eggshell fracture. The head of the second metatarsal is affected in almost 70% of cases, and the third metatarsal head in almost 30% of cases, but any of the metatarsal heads may be subject to infraction (Griffin 1994). The predominance of osteochondritis affecting the second metatarsal head is thought to be due to the greater length of the second metatarsal in relation to the first and third metatarsals, and its resultant susceptibility to local trauma during the gait cycle, especially at toe-off. It is thought that the blood supply to the epiphyseal plate is interrupted by repeated microtraumata, causing an area of avascular necrosis within the metatarsal head (Manusov et al 1996b).

Clinical picture

The patient presents with increasing pain and associated swelling, and possible bruising on the dorsum of the foot, overlying the affected metatarsal head. Gait is affected and the patient may limp (Caselli et al 1998). The pain worsens on weight bearing and with activity. The range of motion at the affected MTPJ is decreased, particularly when active and/or weight-bearing dorsiflexion of the toes is attempted. Pain and crepitus is likely to be elicited on passive movement of the affected joint.

Diagnosis and differential diagnosis

In the early stages of the disease plain radiographs may show little apparent bone involvement. In the later stages, as healing progresses, new bone growth in the affected area can be seen. The classical radiographic presentation in the adult who has undergone an episode of Freiberg’s infraction as a teenager, or an untreated Freiberg’s disease in a younger person, is of a flattened metatarsal head, with associated signs of osteoarthritic changes, such as bone sclerosis and osteophyte formation, occurring at the metatarsal head (Fig. 4.15). The base of the associated proximal phalanx may also show degenerative changes. The differential diagnoses of an acute presentation in a young person should exclude a march fracture, rheumatoid arthritis, intermetatarsal bursitis and other overuse injuries that may arise in relation to sports or dancing.

Figure 4.15 Freiberg’s disease: radiograph of the foot on initial presentation appears normal.

Treatment

The principal focus of the treatment of Freiberg’s disease is to reduce or eliminate weight-bearing forces to the affected bone area during the 6 weeks of the acute phase of the disease. This is achieved by imposing a regimen of non-weight bearing on the affected foot, with rest and painkillers as necessary. Non-weight bearing during the acute phase of the disease is necessary to ensure that retrograde pressure from the base of the proximal phalanx on the affected metatarsal head at toe-off is minimised, allowing bone healing to proceed without loss of the normal architecture of the affected metatarsal head. Non-weight bearing on the affected foot is achieved by the use of crutches, together with soft splintage of the foot, or rigid splintage of the lower limb and foot.

Freiberg’s disease may cause permanent alteration to or loss of the normal dome shape of the affected metatarsal head, even in cases where the disease has been identified in its early stages. The long-term treatment of these cases includes:

Pathology

It is thought that repetitive minor trauma to the navicular bone causes patchy ossification (Manusov et al 1996b).

Clinical picture

The patient presents with, or the parent notes, pain and possibly swelling in the medial–plantar area of the instep, with focal tenderness in the area of the navicular. Small children may become reluctant to run around or play as normal.

Diagnosis and differential diagnosis

Initially, little shows on radiography, but radiographs from patients who have had Kohler’s disease of the navicular in earlier childhood typically show anteroposterior narrowing (wafering) of the navicular, with increased bone density and loss of normal trabeculation in later life. In this age group, there are few other disease processes that give rise to these presenting features.

Treatment

Some cases of Kohler’s disease are self-resolving. Others require the use of soft splintage, such as semicompressed felt valgus filler pads, or supportive orthoses and appropriate footwear to maintain the architecture of the longitudinal arch of the foot during healing. Paracetamol (e.g. Calpol™) may be used to control pain in young children. Surgery is not usually indicated.

Pathology

The bone lesion is classified in four stages of presentation:

Clinical picture

The patient presents with a painful, swollen ankle. The location of the pain and the swelling can aid the diagnosis of the exact site of the bone lesion. For example, osteochondritis dissicans of the talar head gives rise to focal pain and swelling in the medial area of the midtarsal joint, whereas osteochondritis dissicans of the trochlear surface of the talus will cause pain and swelling that relates to the anterior aspect of the ankle. However, if a loose body has formed within the ankle or talonavicular joints, the site of the pain and swelling is far less constant, and the patient describes episodes of acute focal pain and swelling that change location from day to day as the fragment of bone moves around within the joint cavity. Patients often report that the ankle ‘locks’ or ‘catches’, and that the ankle and subtalar joint area is unstable on weight bearing.

Diagnosis and differential diagnosis

Radiographs may not identify the damaged area, especially in the early stages. Special views may need to be requested to visualise all aspects of the affected bone. Computerised tomography scans and magnetic resonance imaging are much more sensitive than radiography in the early diagnosis of osteochondritis dissicans of the ankle–subtalar–midtarsal joint complex.

Treatment

The treatment of stages I and II includes rest and immobilisation for 6 weeks. This is achieved by the use of a below-knee plaster of Paris cast, an Aircast® boot, or an ankle–foot orthosis, together with the use of crutches to aid in walking. As healing progresses, the use of a firm walking boot, rather than a normal shoe, is of benefit, as it restricts movement of the rearfoot complex, yet allows relatively normal ambulation.

Stages III and IV may require surgical removal of the loose bone fragment, via arthroscopy, or internal fixation to reattach the detached bone fragment.

Pathology

Heel pain in Sever’s disease occurs as the result of an overuse syndrome, and is not a true avascular necrosis. Although it is commonly referred to as an osteochondritis, it is more accurately classified as a traction apophysitis.

The calcaneus has two centres of ossification: the primary centre, which is within the body of the calcaneum; and the secondary centre, which is within the posterior area of the bone. These centres of ossification unite when the bone attains maturity (becomes fully ossified) at about 12 years of age. Traction forces from the Achilles tendon on immature bone can induce epiphyseal distraction, (between the body and the posterior leaflet of the calcaneus) due to its insertion onto the middle third of the posterior surface of the calcaneum. Repetitive contractions of the muscles of the posterior compartment (gastrocnemius and soleus) may also predispose to microfractures at the calcaneal epiphyseal plate. A similar pathology is noted at the insertion of the patellar tendon into the tibial tubercle in Osgood Schlatter’s disease (Madden & Mellion 1996).

Clinical picture

The condition may be unilateral or bilateral. The patient presents with pain and tenderness that localises to the posterior aspect of the calcaneus. Pain is maximal after vigorous or impact exercise, such as running or gymnastics. There may be an associated warmth and oedema at the posterior heel area, and wearing shoes with a close heel counter aggravates symptoms. It affects boys more often than girls, and onset may link with growth spurts, especially in physically active or overweight children (Madden & Mellion 1996). Many patients will also show biomechanical compensation for structural foot anomalies that tend to reduce shock absorption at heel strike and expose the heel to abnormal ground reaction forces (Madden & Mellion 1996).

Diagnosis and differential diagnoses

Diagnosis in the early stages of the disease is based on the history and the presenting symptoms. Diagnostic signs include: increased pain on passive dorsiflexion of the foot at the ankle, and exacerbation of symptoms when standing on tiptoe (a positive Sever’s sign) (Madden & Mellion 1996). Radiographs of the calcaneus appear normal in the early stages of the disease process. As the disorder progresses, the apophyseal area shows sclerosis and fragmentation, although this finding is not necessarily diagnostic as this picture can also been seen in asymptomatic patients (Kaeding & Whitehead 1998).

The differential diagnosis should exclude a duck-bill fracture of the posterior leaflet of the calcaneum, Achilles tendon pathologies and deep retrocalcaneal bursitis.

Treatment

Many authors believe Sever’s disease to be self-limiting, as it tends to resolve spontaneously when calcaneal ossification is completed, usually at about 12 years of age. However, the use of physical therapies such as PRICE (pain control, rest, ice, compression and elevation) is beneficial in the acute phase of the disease. When symptoms are severe, a non-weight-bearing regimen, such as a below-knee cast for 6 weeks, or an Aircast^® boot, and crutches, together with a course of NSAIDs is indicated. When the presenting symptoms are mild, the use of a figure-of-eight bandage to the affected rearfoot with a heel raise in the shoe is useful.

A heel raise should continue to be used after the acute phase has passed, in order to reduce the pull of the Achilles tendon on the posterior surface of the calcaneum. This will also minimise further trauma to the epiphyseal plate during the healing phase. Night splints, such as those used for the treatment of plantar fasciitis (Powell et al 1998) are also of benefit. After healing is complete, a regimen of rehabilitation exercises to stretch the Achilles tendon will be needed to prevent or reduce a tendency to ankle equinus, and a programme of stretching exercises and ice massage should continue to be used after strenuous activity. The patient should undergo a full biomechanical evaluation, and orthoses should be prescribed to correct any noted faults. The routine use of well-fitting trainers with good shock absorption should be recommended.

Pathology

The Achilles tendon inserts into the middle third of the posterior facet of the calcaneus. A bursa readily forms within the soft tissues superficial to the insertion of the Achilles tendon, in response to stress at the central–lateral area of the posterior surface of the heel. This adventitious bursa is known as the superficial retrocalcaneal bursa. Inflammation of the adventitious bursa (superficial retrocalcaneal bursitis) is associated with rearfoot motion in association with compensated rearfoot varus, mobile pes cavus, or in cases where there is an increase in the angle of inclination of the calcaneus. Eversion of the calcaneus (frontal plane motion) occurs during compensation for these pathologies, and the foot rotates about the longitudinal axis of the midtarsal joint. The frontal plane rotation allows the calcaneus to evert, but imposes shear stresses within the soft tissues overlying central–lateral area of the posterior aspect of the heel, as these tissues move relative to the inner surface of the shoe. The continuous compensatory eversion of the heel predisposes to inflammation of the bursa. If the condition is of long standing, there may also be local hypertrophy of the underlying area of the posterior aspect of the calcaneus. The bony prominence thus formed is known as Haglund’s deformity, or a ‘pump bump’. The shear stresses affecting the overlying soft tissues increase in direct proportion to the size of the bony prominence, and the bursitis can become chronic. If the overlying skin is breached, such as in a broken chilblain or a ruptured blister, the bursa may become infected.

Clinical features

The condition usually affects adolescent females, who present with pain in the posterior aspect of the heel, especially when wearing, or having worn a particular pair of shoes, such as high heels or a style with a marked heel counter. The patient may report seasonal fluctuations, as the problem may flare up if there is local perniosis (chilblain) affecting this area of the heel, when it is termed ‘winter heel’. On examination, there will be an inflamed, fluctuant and very tender area at the central–lateral aspect of the posterior surface of the heel, with a palpable hypertrophy of the superficial fascia, and underlying bone in long-standing cases. The patient is often unable to wear a normal shoe, and the pain of the condition causes her to walk with a limp.

Diagnosis and differential diagnosis

The diagnosis is usually made by reference to the presenting signs and symptoms. Oblique-lateral radiographs of the rearfoot will also demonstrate any additional bone formation at the central–lateral heel area. The differential diagnosis should exclude other causes of local soft tissue inflammation, such as chilblain or blisters.

Treatment

Initially, a conservative approach is indicated:

Surgery may be required to reduce the underlying bony prominence. A more laterally placed bony prominence can be reduced, but this becomes more difficult if the area of bone hypertrophy involves the attachment of the Achilles tendon. In those cases, a closing wedge osteotomy may be used to reduce the angle of inclination of the calcaneum.

Pathology

The deep retrocalcaneal bursa is a true anatomical bursa. It is located within the soft tissues at the posterior aspect of the heel, lying between the upper third of the posterior aspect of the calcaneus and the inner aspect of the Achilles tendon, immediately superior to its insertion into the middle third of the posterior aspect of the calcaneus. The bursa is a horseshoe-shaped structure, and in the adult is approximately 2 cm long, 1 cm wide and 0.5 cm deep (Frey et al 1992). Its inferior surface lies on the Achilles fat pad at the posterosuperior aspect of the proximal calcaneus, its anterior surface at the upper third of the posterior surface of the calcaneus, and its posterior surface against the deep aspect of the Achilles tendon.

Pathological changes (deep retrocalcaneal bursitis) can occur in response to local mechanical irritation, such as where the upper edge of a shoe with a marked heel counter traumatises the soft tissues at the superior area of the posterior surface of the heel. The inflamed bursa shows marked thickening and oedema of its walls. The volume of the contained synovial fluid increases, but its viscosity decreases. Deep retrocalcaneal bursitis may also be a feature of inflammatory joint disease, such as rheumatoid disease and seronegative arthropathies. In these cases the area of the calcaneus that receives the insertion of the Achilles tendon may show bone erosions.

Clinical feature

The patient presents with diffuse pain that locates to the posterior aspect of the heel. The pain is exacerbated by active dorsiflexion of the foot, such as when walking upstairs as the inflamed bursa is compressed further, between the overlying Achilles tendon and the underlying calcaneus. The visible signs of inflammation are not obvious, although there may be some local warmth and swelling. The inflamed bursa is usually palpable as a tender, bi-lobed, fluctuant area of soft tissue, to either side of the Achilles tendon at a point just superior to its insertion into the posterior surface of the calcaneus. Palpation of the inflamed tissue may show a fluid ‘thrill’.

Diagnosis and differential diagnoses

The diagnosis is made from the presenting signs and symptoms. The bursa can be identified by bursography (the injection of a radio-opaque dye into the swollen bursa).

The differential diagnosis should exclude:

Treatment

The underlying cause of the bursitis must be established, and in cases where there is evidence of underlying inflammatory joint disease the patient should be referred to a rheumatologist. Conservative therapy focuses on resting the traumatised area. This includes a review of the footwear. The use of a trainer, manufactured with a cut-out at the upper margin of the heel counter is very useful. A simple heel raise, such as a 7 mm semicompressed felt plantar heel pad, placed inside the shoe will prevent or reduce trauma from the upper edge of the heel counter and allow the bursal inflammation to subside. Severe cases may require aspiration of the bursa, and injection of a corticosteroid.

Pathology

Microtears within the distal part of the Achilles tendon (or heel cord) and resultant local inflammation may be precipitated by a sudden increase in activity levels, training on poor surfaces, or using inappropriate footwear. Achilles peritendonitis may be precipitated by a single incident, or can develop gradually as a general overuse phenomenon. It may also affect women who adopt flat-heeled shoes after habitually wearing high heels, and, much more rarely, may present as a later complication of congenital pes valgus. In both these examples, the undue pull on the Achilles tendon causes a reflex spasm of the posterior calf muscles, with increased tension and the development of microtears within the heel cord.

There are three presentations associated with inflammation of the Achilles tendon: peritendonitis (also known as paratendinitis), tendinosis and peritendonitis with tendinosis.

Clinical picture

The patient presents with pain in the distal part of the Achilles tendon that localises to a point approximately 5 cm superior to the point of insertion at the calcaneum. Characteristically the pain develops during strenuous activity and eases with rest. In the later stages of the problem, the pain may be severe and unrelenting even at rest, and prevent normal walking. The soft tissues overlying the affected area may be hot and swollen. If the patient has associated tendinosis, there will be a palpable and tender fusiform thickening along the tendon, or nodule formation at a point approximately 2–5 cm superior to the insertion of the tendon into the calcaneus. Generally the condition has a gradual onset, with mild pain that worsens with continued activity. Patients may also complain of pain on first weight bearing after a period of rest, such as when they first stand up in the morning. Repeated activity in cases of Achilles tendonitis causes an increase in local inflammation and can result in later partial or complete rupture of the tendon. Patients who are prone to this condition often show excessive compensatory pronation, as pronation tends to reduce Achilles tendon traction.

Diagnosis and differential diagnosis

The characteristic pain of Achilles tendonitis can be induced by plantar flexion of the ankle against resistance. This effect occurs as the patient begins to stand up from a sitting position, or by going up on tiptoe. In severe cases the patient will be unable to take the full body weight when asked to stand on the affected leg. These results, together with the presenting symptoms and case history facilitate the diagnosis. Severe cases will show inflammation and even tears with the tendon on magnetic resonance imaging. Radiographs of the tendon (a tenogram) will show local inflammation and deterioration of the tendon quality.

The differential diagnosis should exclude Haglund’s deformity, deep retrocalcaneal bursitis, inflammatory arthritides and partial or total rupture of the Achilles tendon. Patients with marked fatty nodules along the length of the Achilles tendon should undergo blood tests to exclude raised blood cholesterol levels (Citkowitz 2004).

Treatment

People, especially those in middle age, who intend to embark on a jogging or running programme should be reviewed for appropriate orthotic therapy, and undergo a programme of stretching exercises before carrying out sporting activity in order to reduce the likelihood of developing Achilles tendonitis. In the earliest stages of presentation, a simple heel raise to minimise the pull on the Achilles tendon, together with advice on training and prestretching may be sufficient to resolve an incipient Achilles tendonitis. Of course, it will be necessary to rest from strenuous sports activity until all symptoms have cleared, and to undergo a programme of gradual rehabilitation when sports are resumed. Attention should be paid to the footwear, in particular the shape of the heel counter, to reduce the likelihood of further trauma. More advanced cases, where there is a degree of tendon degeneration, require more active intervention. Steroid injections are contraindicated because of the danger of causing further tendon deterioration, and subsequent rupture. Physical therapies such as the use of pain control, rest, ice and strapping (PRICE) in the acute stages, and a course of twice-weekly ultrasound and contrast footbaths to reduce inflammation are beneficial. Heavy-load, eccentric calf muscle training is very effective (Alfredson et al 1998), but immobilisation in a below-knee cast or Aircast® may be necessary to allow tendon healing, followed by a rehabilitation programme of intensive stretching and exercises, as an essential adjunct to treatment to allow the patient to get back to full weight bearing. After the acute injury has resolved the patient should undergo biomechanical evaluation and any identified faults should be corrected by the prescription of functional orthoses.

Pathology

The Achilles tendon may rupture as the result of an isolated severe traumatic event, or as the culmination of repeated episodes of peritendonitis. The tendon rupture in either case may be partial or total.

Clinical picture

Patients with either acute or chronic Achilles tendon rupture present ultimately with a similar set of clinical signs. These include a palpable painful swelling overlying and surrounding the distal part of the tendon, a discontinuity along the length of the tendon just superior to its insertion (Fig. 4.16), and inability to stand on tiptoe or plantar flex the foot against resistance, or bear weight normally on the affected foot. In an acute presentation of Achilles tendon rupture, the patient gives a characteristic history of a severe pain and a sudden sensation of something ‘snapping’ at the back of the heel, usually occurring during an episode of strenuous or sports activity. They experience severe localised pain, usually fall over, and are unable to use that foot to walk normally, as they will have lost the ability to plantar flex the foot against ground resistance. Sometimes they think that someone must have kicked them in the back of their heel. In a chronic presentation, the onset of symptoms is more gradual, as an increasingly severe Achilles tendonitis, leading to eventual partial or total rupture.

Figure 4.16 Achilles tendon rupture. This male patient, aged 74 years, developed a rupture of the Achilles tendon several months after experiencing pain at the posterior area of his right heel/lower leg. He was diagnosed as having type 2 diabetes mellitus at age 68 years, with associated chronic hypertension, hypercholesterolaemia, peripheral sensory neuropathy, chronic venous insufficiency and mild obesity. In view of his overall medical condition, the vascular status of the lower limb, and the chronicity of the Achilles tendon injury, the orthopaedic surgeon recommended that surgical repair of the tendon was not in the patient’s best interest. The case was managed initially by the use of an Aircast™ walking boot for 6 weeks, followed by prescription orthoses worn in walking boots.

Treatment

In cases of partial Achilles tendon rupture the affected limb must be immobilised in a below-knee cast or Aircast® boot for several weeks to allow the tendon to heal. The patient will need to follow a programme of rehabilitation once the cast is removed and tendon repair is complete in order to regain full strength in the posterior calf muscles, reduce the chance of re-rupture, and prevent the development of ankle equinus due to any contraction of the posterior soft tissue structures that may have occurred during the healing period. More severe cases of partial rupture are corrected surgically.

Cases of full rupture of the Achilles tendon may be corrected surgically. The tendon ends are resutured together, sometimes including the additional use of donor tendon, such as a plantaris tendon graft. The foot is immobilised in a cast for 6–8 weeks, in a plantar-flexed position, and the patient not allowed to weight bear until tendon healing is complete. Wound healing in Achilles tendon repairs can be prolonged. In cases of total Achilles tendon rupture, immobilisation without surgery, even for several months, is not usually successful, and the risk of re-rupture is high in those few cases that do achieve a degree of repair solely by immobilisation.

Pathology

Prolonged and continuing traction on the plantar fascia results in inflammation, swelling and pain, especially at its origin at the medial calcaneal tuberosity.

It is thought that the repetitive excessive tensile forces created by walking or standing cause microtears in the fascia, leading to acute and eventual chronic inflammation. If the inflammation affects the entire plantar fascia, it is referred to as a plantar fasciitis; however, if it is isolated to the heel alone, it is called heel pain. Involved tissues undergo changes that typify chronic inflammation. These include collagen necrosis, angiofibroblastic hyperplasia (i.e. overgrowth of local fibrous tissue and blood vessels), chondroid metaplasia (i.e. their transformation into a cartilage-like tissue) and eventual calcification, especially at the origin. In some cases, the first branch of the lateral plantar nerve, known as Baxter’s nerve, may become entrapped within the fibrous tissue, causing symptoms of distal sensory neuropathy.

Where the inflammation also affects the periosteum of the medial plantar calcaneal tubercle, an enthesopathy occurs (the insertion of ligamentous or fascial tissues into a bone surface is termed an ‘enthesis’). The pull of both the origin of the flexor digitorum brevis muscle and the proximal part of the plantar aponeurosis on the periosteum of the calcaneus acts as a stimulus to new bone formation at their points of insertion, resulting in the formation of a plantar calcaneal or heel spur. A heel spur is usually very painful during its formation, but later may become asymptomatic, as once formed it effectively reduces the tractional forces applied to the medial calcaneal tubercle by the plantar aponeurosis. The presence or absence of a heel spur is not diagnostic of heel pain, as 16% of people with heel spurs do not have heel pain, and 50% of people with heel pain do not have a heel spur (Crawford & Snaith 1996).

Clinical picture

The patient reports a gradual and increasing pain at the medial–central heel area, which often radiates into the medial longitudinal arch. There is not usually a history of local trauma. The pain, which is usually described as sharp or severe, is worse on weight bearing, especially on first standing in the morning. Typically, the pain subsides gradually after the patient has walked about for a while, but tends to re-establish towards the end of the working day, and recur during the day after periods of rest or non-weight bearing. It is thought that the paradox of pain apparently increased by rest is due to the combined effects of accumulated inflammatory oedema and the sudden traction applied to the inflamed plantar tissues by weight bearing (Wapner & Sharkey 1991). The gradual reduction in the initial pain after walking about is thought to relate to the dispersion of the oedema by the ‘massage’ effect of walking.

On physical examination, the patient often has tightness of the Achilles tendon, due to the close anatomical relationship of the heel cord with the plantar fascia. Pain is elicited by the examiner applying traction to the plantar fascia by passively extending or dorsiflexing the toes at the MTPJ with one hand whilst palpating along the length of the now tightened medial band of the plantar fascia with the thumb of the other hand from distal to proximal. The examiner’s thumb comes to directly palpate the origin of the plantar aponeurosis at the medial plantar calcaneal tubercle (Fig. 4.19). Characteristically, the patient will grimace or verbally indicate pain as the thumb pressure is applied to the point of insertion of the plantar fascia at the medial–plantar heel area, and will also usually describe a sensation of pain as the thumb is moved down the taut plantar fascia.

Figure 4.19 To test the exact site of tenderness of plantar heel pain, dorsiflex the great toe, run a thumb from distal to proximal along the plantar fascia until it meets the calcaneum, and apply firm pressure.

Diagnosis and differential diagnosis

The characteristic pattern of pain, tenderness in the medial longitudinal arch and the response to direct compression of the tissues at the origin of the plantar aponeurosis in a sedentary, overweight patient is largely diagnostic. The diagnosis can be confirmed by using ultrasonography and radioisotope bone scans to demonstrate inflammation and early new bone formation at the medial calcaneal tubercle. The presence of a heel spur on plain lateral radiographs is not necessarily diagnostic, as asymptomatic heel spur is noted in 10% of people aged over 50 years (Banadda et al 1992) and can be considered as a normal variant when the spur is small and well defined. Large, ill-defined or fluffy heel spurs are seen in conjunction with plantar enthesopathy, especially in cases with seronegative rheumatoid disease (Fig. 4.20).

Figure 4.20 Lateral radiograph of a large, irregular and painful plantar heel spur in a patient with psoriatic arthropathy.

The differential diagnoses should consider:

Other causes of plantar heel pain

Treatment of plantar heel pain

The treatment of plantar heel pain involves isolating the cause of the problem, measures to reduce the painful symptoms, and actions to resolve, where possible, the underlying mechanical or other pathologies. A variety of conservative measures will allow four out of five cases to make a full recovery within 6–9 months of onset of the symptoms, with the podiatric intervention providing palliative care to reduce mechanical stresses on the heel during the painful period. However, the recalcitrant one-fifth of plantar heel pain cases presents a considerable challenge to successfully treatment (Wolgin et al 1994).

Podiatric palliation includes the provision of:

Figure 4.21 Cobra pad.

Dynamic therapies include:

Pathology

Synovitis of the tibialis posterior tendon, often in association with underlying rheumatoid disease, causes a local chronic inflammation and swelling of the synovial sheath of the tendon as it passes beneath the sustentaculum tali. The resultant local fibrosis causes the tibial nerve to become tethered within the fibro-osseous tunnel formed by the flexor retinaculum of the ankle and the medial malleolus (Cimino 1990). Either direct pressure on the nerve from the fibrous swelling and/or the indirect pressure of rearfoot pronation causes a relative local neuroischaemia, and resultant neural dysfunction, such as sensory neuropathy. The affected area of nerve shows fibrous thickening (Hadjari Hollis et al 2008).

Clinical features

The patient experiences a burning pain and paraesthesia in the sole of the foot and toes in the distribution of the distal part of the tibial nerve. The patient often reports paraesthesia affecting the whole of the plantar surface, with maximal symptoms at the medial longitudinal arch and the metatarsal heads area. Alternatively, the patient may describe paraesthesia, including tingling, pins and needles, and cramp-like feelings in the medial longitudinal arch area. Symptoms are exacerbated by weight bearing, and are often worse at night. Percussion over the inferior–medial aspect of the heel at the site of the entrapment, or sustained direct digital pressure to the nerve in the area of the medial malleolus will reproduce the symptoms (a positive Tinel’s sign). Long-standing cases may also show frank plantar and digital sensory neuropathy with weakness of intrinsic muscles subserved by the affected nerve.

Treatment

Treatment of tarsal tunnel syndrome focuses on therapies that reduce the unpleasant and painful symptoms. Clinical padding, such as valgus filler pads or medial heel wedges either affixed to the foot or an insole, helps reduce nerve compression or stretching. Excess rearfoot pronation should be controlled as far as possible by the use of moulded cushioned orthoses, housed within appropriate bespoke shoes, to minimise local pressure at the medial aspect of the heel. The inflammation occurring as the result of the rheumatoid process should be controlled by the relevant drug therapies, including NSAIDs together with disease-modifying antirheumatic drugs (DMARDs) as prescribed by the general practitioner or rheumatologist, but many patients with rheumatoid or other inflammatory arthropathies who develop tarsal tunnel syndrome are already on high doses of NSAIDs, to control other aspects of their disease. Surgical treatment including the decompression of the nerve by freeing it from the surrounding fibrotic tissues, with excision of local fibrous tissue, is indicated in cases that do not respond to conservative measures (Takakura et al 1991).

Aetiology

The cause of tibialis posterior dysfunction is unclear, but a number of factors are associated with the development of the condition. These include:

Pathology

The presentation of tibialis posterior dysfunction may be classified into four stages:

Alternatively, the pathology of tibialis posterior dysfunction may be classified by the duration and severity of the presenting signs and symptoms:

Clinical picture

Approximately 50% of cases present with a history of local trauma, such as a forced eversion of the rearfoot. The typical sufferer of tibialis posterior dysfunction is a female aged over 40 years, although the condition may also affect younger athletes.

Diagnosis and differential diagnosis

The integrity of the tibialis posterior tendon can be assessed by palpating the tendon whilst the patient actively plantar flexes and adducts the foot and the examiner applies an abductory force to the forefoot. It is important to determine the exact site of the injury within the tendon, and it is important to compare the problematic foot to the asymptomatic foot. Direct pressure along the course of the tendon will elicit pain, and active inversion of the foot against resistance will show reduced tibialis posterior muscle power. If a partial tendon rupture has occurred, a distinct defect along the integrity of the tendon can be palpated. If the tendon has fully ruptured, the tendon cannot be palpated along its normal course, and the patient is unable to invert the foot against resistance. A partial or complete rupture of the tendon, secondary to trauma, is accompanied by distinct pain at the navicular tuberosity. Overuse injuries and tendon degeneration present with pain just distal to the medial malleolus.

Magnetic resonance imaging is the most useful method of imaging tendons around the ankle, and it is highly sensitive and specific for the detection of a tendon rupture. Other diagnostic tests include bone scans and injection of radio-opaque material into the tendon/tendon sheath. The early diagnosis is not enhanced by a plain radiograph, although views of the foot will show the extent of structural changes in Stage 3 presentations. A standard weight-bearing anterior–posterior view shows an increase in the angle between the longitudinal axis of the talus and the longitudinal axis of the calcaneus, with an anterior break in the cyma line, abduction of the forefoot and displacement of the second metatarsal. The long axis of the forefoot no longer bisects the rearfoot angle. The normal linear relationship of the talus, navicular, medial cuneiform and the first metatarsal is seen to be lost when the foot is viewed on a lateral radiograph. As the condition progresses, osteoarthritic changes may become evident at the first MTPJ, secondary to the development of hallux limitus.

The differential diagnoses should exclude bone anomalies such as os naviculare (os tibiale externum) syndrome, os trigonum syndrome, navicular avulsion, stress fracture of the navicular; osteochondritis or avascular necrosis of the head of the talus or the navicular, fracture of the medial malleolus, subtalar tarsal coalition and medial sinus tarsitis. Soft tissue anomalies such as strain of the deltoid ligament, medial ankle capsulitis and synovitis, tarsal tunnel syndrome, strain of the flexor hallucis longus or flexor digitorum longus, and retrocalcaneal bursitis should be excluded. Other causes of unilateral flat foot, such as true or apparent leg-length inequality and tarsal coalition, should also be considered in the differential diagnosis.

Treatment

The most appropriate treatment for tibialis posterior dysfunction is dependent on the stage or phase of the pathology, the presenting symptoms and the severity of the pain reported by the patient. Treatment should always be implemented rapidly and aggressively to prevent further deterioration of the tendon. If the patient is seen in the early stages, conservative methods that focus on reduction of inflammation, joint stabilisation and pain control are indicated for up to 8 weeks. In advanced cases or recalcitrant mild cases, surgical repair of the tendon together with joint fixation may be the options of choice.

Pathology

The most common presentations of tarsal coalitions include fusion of the calcaneus with another rearfoot or midfoot bone. These include coalition of the calcaneus and the talus (talocalcaneal coalition), the cuboid (calcaneocuboid coalition) or the navicular (calcaneonavicular coalition) (Fig. 4.22). The condition is normally asymptomatic in early childhood. It becomes symptomatic later in childhood or during adolescence, when the cartilaginous anlage undergoes ossification, and the flexibility between the conjoined bones is lost. Presentations of tarsal coalition in adulthood have been reported.

Figure 4.22 Oblique radiograph of a calcaneonavicular coalition.

The normal motion of the subtalar joint during weight bearing involves both rotation and gliding. During the stance phase of gait, the axis of the subtalar joint rotates from a position of 4° external valgus to 6° internal varus to compensate for the internal rotation of the tibia. The loss of or reduction in internal rotation at the subtalar joint causes loss of the height of the medial longitudinal arch, flattening of the foot and fixed calcaneal eversion (a valgus heel). The plantar aspects of the midtarsal joints widen, and their dorsal aspects narrow. The navicular tends to override the head of the talus when the foot is in a position of maximum dorsiflexion, causing traction and elongation of both the deep midtarsal and spring ligaments and the talonavicular joint capsule. The overall flattening of the longitudinal profile of the foot leads to adaptive shortening of the peroneal tendons, with reactive spasm of the peroneal muscles – the so-called ‘peroneal spastic flatfoot’. Prolonged subtalar joint restriction of motion may lead to long-term degeneration of the posterior facet or arthrosis of the subtalar joint.

Clinical presentation

The patient with a tarsal coalition presents with a flat foot and marked restriction of available hind- and midfoot eversion. There is associated pain in the foot and lateral compartment of the leg that is usually relieved by rest and aggravated by activity. The patient may also complain of recurrent eversion ankle sprains.

The varying forms of tarsal coalitions ossify at different ages, and thus the age of onset of symptoms is an indicator of the site of the coalition. For example: talonavicular coalitions begin to ossify, and thus become symptomatic, in children aged 3–5 years; calcaneonavicular coalitions begin to ossify in children aged 8–12 years; and talocalcaneal unions become symptomatic during adolescence, most commonly between the ages of 12 and 16 years. The loss of subtalar joint motion and the increasing valgus position of the hindfoot become more apparent as ossification progresses, leading to the development of pes planus. Coalitions involving the middle facet of the subtalar joint are associated with the greatest loss of midtarsal joint motion and are the most likely to cause marked valgus deformity of the foot.

Diagnosis and differential diagnoses

Tarsal coalitions are most readily identified by computerised axial tomography or magnetic resonance imaging scans. Plain radiographs require special views to visualise tarsal coalitions. Calcaneonavicular coalition is suggested by the presence of an elongated anterior calcaneal process, and a talocalcaneal coalition is best visualised on a Harris–Beath (also known as an axial or ‘ski-jump’) view of the hindfoot.

The examiner can evaluate a loss of subtalar joint movement: In the normal weight-bearing foot the tibia and patella externally rotate and the foot supinates when the medial border is raised, the lateral border maintained in contact with the floor, and the heel maintained in the neutral position. When this examination technique is carried out on patients with limited or decreased subtalar joint motion, the amount of available external rotation of the tibia is decreased and the patella does not rotate externally. A loss of subtalar joint motion can also be demonstrated by the absence of or reduction in normal hindfoot inversion and a lack of increase in the height of the medial longitudinal arch when the patient attempts to stand on tiptoe on the affected foot.

The differential diagnoses should exclude bone tumours, rheumatological disease and fractures about the subtalar joint. Tarsal coalitions have been shown to be a feature of other foot deformities, such as talipes equinovarus, and are associated with fibular hemimelia (a congenital abnormality characterised by total or partial absence of the distal half of the limb), Nievergelt–Pearlman syndrome (a rare, autosomal-dominant, inherited bone disease that affects males more than females, characterised by upper limb and hand deformities, symmetric dysplasia of the lower limbs, with genu valgum, clubfoot and deformed great toes, and crura rhomboidei) and Apert’s syndrome (acrocephalosyndactylia – a rare developmental condition with characteristic craniofacial and limb anomalies including craniosynostosis (premature fusion of the skull bones), midface underdevelopment, and gross syndacylisation of the fingers and toes).

Treatment

The early treatment of a non-ossified tarsal coalition includes immobilisation of the foot in rearfoot neutral by the use of an ankle–foot orthosis or ankle callipers to restrict movement of the affected joints and minimise pain. Surgery is indicated after full ossification of the coalition is complete. The procedure of choice is determined by the degree and location of the coalition, and includes resection of the bone bar, or fixation and arthrodesis of the affected degenerate and painful joints.

Pathology

The true pathology of plantar fibromatosis is unclear. Adherent fibrous nodules or fibromae develop, usually within the superficial parts of the plantar fascia, and the associated fascial tissues undergo a degree of contraction. The condition follows a similar pathology to Dupuytren’s contracture of the palmar aspect of the hand. Plantar fibromatosis is less common, and generally less disabling than Dupuytren’s contracture, as weight-bearing forces prevent the plantar tissues from undergoing the same degree of contraction as the palmar tissues.

Clinical features

Patients present with single or multiple, painful or asymptomatic nodules, or discrete firm, fluctuant swellings within the soft tissues overlying the plantar aspect of one or both feet.

Diagnosis and differential diagnosis

The diagnosis is made from the clinical signs and symptoms. Patients presenting with plantar fibromatosis may also have a history of Dupuytren’s contracture affecting the hands, and there is a weak association with alcohol abuse.

Treatment

Asymptomatic cases do not require treatment. Painful presentations may be treated with accommodative orthoses to reduce pressure over the tender nodules. More problematic cases can be treated by an injection of hydrocortisone into the nodule. Surgery may be indicated to excise multiple painful or large nodules, but fibromata tend to recur.

Pathology

Degenerative changes occur at the first metatarsal–medial cuneiform and the cuneionavicular joints in feet with pes cavus and pes valgus:

Clinical picture

The patient presents with a pain in the dorsal midfoot area that radiates to the plantar aspect of the medial longitudinal arch. There is a palpable thickening of the bony architecture of the first metatarsal–medial cuneiform joint and the cuneionavicular joint, with the development of exostoses at the joint margins (Fig. 4.23). There is a loss of or reduction in the normal gliding movement within the joint, and possible crepitus. The overlying dorsal tissues may become inflamed, and a dorsal adventitious bursa may develop over these joints due to shoe pressure. In extreme cases, the bursa may even perforate through the overlying dorsal skin. In cases of pes valgus or mobile pes cavus the area of plantar skin overlying the exostoses may develop hyperkeratosis, or even ulcerate, especially in patients with sensory neuropathy or those on parenteral steroid therapy.

Figure 4.23 Osteoarthritic changes at the first metatarsal–medial cuneiform joint.

Diagnosis and differential diagnoses

The condition can be confirmed, and the extent of the exostoses and joint degeneration visualised, by plain lateral radiographs of the foot.

The differential diagnosis should exclude midtarsal Charcot arthropathy, such as the neuroarthropathy that arises with diabetes mellitus, other causes of distal sensory neuropathy and midfoot fractures.

Treatment

Clinical pads may be used to reduce pressure on painful areas. These include cavitied or holed semicompressed felt ovals applied to the dorsal or plantar areas of the midfoot, and fleece ovals, which are used to reduce sheer stress to a dorsal bursa. Shoe-style advice is essential, as the patient should obtain a style that will both accommodate the altered foot shape and reduce trauma to the painful area. Temporary or permanent orthoses can be made to control or reduce the effects of the underlying biomechanical anomaly. The exostoses can be excised surgically, with or without fixation of the affected arthritic joint.

Pathology

The pathology of plantar fasciitis resembles that of heel-pain syndrome. Biomechanical anomalies that predispose to excess tension along the medial column of the foot, together with obesity and prolonged standing predispose to chronic inflammation within the medial band of the plantar fascia.

Clinical picture

The patient presents with a history of a gradual increase in discomfort or pain radiating along the medial band of the plantar fascia. The pain is worse on first weight bearing in the morning, or after periods of prolonged sitting or rest, and may radiate proximally to the central area of the heel, or distally to the MTPJs. The pain may become intractable and constant, especially by the end of the day. Pain can be induced by asking the patient to stand on tiptoe, or by the examiner palpating the medial band of the plantar fascia with the thumb whilst dorsiflexing the hallux at the first MTPJs. The medial band of the plantar fascia can be easily palpated as a tight, tender cord. Inflammation is not usually obvious. One or both feet may be affected, and sufferers may become quite debilitated, depressed and disabled by the chronic and intractable nature of their foot pain.

Diagnosis and differential diagnosis

The diagnosis is made on the basis of the presenting signs and symptoms.

The differential diagnosis should exclude heel-pain syndrome, plantar fibromatosis, march fracture and tibialis posterior dysfunction.

Treatment

Treatment of chronic foot strain is not straightforward, as the patient may have had the condition for several months before seeking treatment. The patient should be advised that they have a chronic soft tissue injury that has probably been present for some considerable time, and is caused by the movements and tensions that occur within the foot during standing and walking. Absolute rest of the foot is impossible to achieve in an ambulant patient, and thus there is no one ‘quick fix’ treatment for their problem. The recovery period may be protracted, and may not necessarily follow a smooth path to resolution. Thus the patient is likely to have ‘good’ and ‘bad’ days. The practitioner is advised to encourage the patient to use combinations of the therapeutic measures listed below, rather than to rely on one type of therapy alone, and to keep on with the treatment for as long as it takes to resolve the symptoms. Empirically, it appears that most cases will respond to a multitherapy approach and the condition will become tolerable within 1–2 months and fully resolve in 6–9 months.

• A daily regimen of ‘triple therapy’ is an effective form of home physical therapy, especially when used in conjunction with antipronatory insoles. The ‘triple therapy’ is used at least once a day and consists of:

The use of contrast foot baths (i.e. alternating immersion in warm water at 45°C for 5 minutes, and very cold water at 5°C for 1 minute) for a total of 30 minutes.

This is followed by a 5-minute period of toe ‘scrunching’ exercises, where the patient attempts to gather a tea towel under the foot using only the toes. The towel is laid out on the floor and the toes repeatedly plantar flexed at the MTPJs so that the towel is gradually drawn under the plantar surface of the foot.

Finally, the patient rolls the medial longitudinal arch area back and forth for 5 minutes across a cold cylinder (e.g. a bottle of water or a can of cola that has been kept cool in the refrigerator).

Classification of metatarsalgia

‘Greater metatarsalgia’ is a term that may be used to describe pain that relates to first-ray pathology, and ‘lesser metatarsalgia’ for pain relating to pathology in the area of the second to fifth rays. Alternatively, metatarsalgia may be classified as functional or non-functional.

Pathology

Persistent intermittent abnormal compression of the plantar tissues results in contusion and inflammation of soft tissues, and predisposes to the formation of focal, nucleated plantar keratoses. Abnormal compression forces at the plantar fibrofatty pad of the forefoot are associated with:

Clinical presentation

Persistent abnormal shear stress predisposes to the development of plaques of diffuse plantar hyperkeratosis of skin overlying the MTPJs, and formation of adventitious bursae especially beneath the -first MTPJ. Abnormal shear stress primarily arises as the result of hypermobility. The hypermobility may affect the whole foot, such as is seen in generalised whole-body hypermobility. But it is also associated with biomechanical anomalies such as mobile pes cavus and fully compensated rearfoot varus. Associated excessive compensatory pronation at the subtalar and midtarsal joints causes a reduction in the height of the medial longitudinal arch, with a resultant relative lengthening of the foot on weight bearing and abnormal shear stress of plantar soft tissues. The forefoot is stabilised, in part, by the transverse metatarsal ligament and the tone of the transverse head of the adductor hallucis muscle, which together control the transverse spread of the metatarsal heads when under load. The first and fifth metatarsals are unable to resist metatarsal splaying in the hypermobile foot, with the development of metatarsus primus varus and metatarsus qinque valgus, a resultant increase in the width of the forefoot and associated hallux abducto valgus and digitus quintus varus deformities. In these cases the medial aspect of the first MTPJ and the lateral aspect of the fifth MTPJ are subjected to shoe-related shear stress, with resultant bursa formation at these sites. Over-large or slip-on shoes also predispose to shear stresses at the skin surface, with resultant development of painful diffuse plantar keratoses at the forefoot.

Abnormal tensile stresses occur as the result of chronic strain on fascial tissues. Examples of metatarsalgia associated with abnormal tensile foot stresses include chronic foot strain, and strain on the transverse intermetatarsal ligaments with associated fatigue of intrinsic musculature due to splaying of the metatarsals, such as is seen in pes cavus and hallux abducto valgus.

Management

The successful management of functional metatarsalgia depends on the identification and elimination, or mitigation, of the underlying pathomechanical cause of pain. In cases where metatarsalgia is symptomatic of a forefoot (rather than hindfoot) malfunction, the management focuses on the promotion of maximum function of the lesser toes and their MTPJs, by the use of clinical padding, the use of correctly fitting shoes, the use of functional orthoses and surgery.

Categorisation of non-functional metatarsalgia

Metatarsalgia can be considered within three broad causative categories:

Focal hyperkeratoses

Ganglia/ganglionic cysts

Weakness in the wall of a synovial tendon sheath or a joint capsule predisposes to the formation of a local fluctuant swelling, often at the dorsum of the foot, especially at the point where the tendon sheath emerges from the overlying retinaculae.

Capsulitis

Capsulitis is the term used to describe inflammation of a joint capsule. Capsulitis frequently arises secondary to osteoarthritis and rheumatoid arthritis, or as the result of ongoing, low-grade joint trauma.

Gouty tophus

Gout is a crystal deposition disease that predisposes to arthropathy in susceptible subjects.

Problematic bursae

Adventitious bursae form over bony prominences in relation to local shear stresses. In the long term they may become fibrous, distended, inflamed, infected or even calcified. The skin overlying the bursa may be prone to chilling. Patients with forefoot deformities, such as hallux abducto valgus, are prone to develop adventitious bursae over the medial exostosis at the first metatarsal head, and patients with rheumatoid arthritis tend to develop very large and distended bursae over the bunion joint and the plantar aspects of the MTPJs (see below).

Rheumatoid nodules and rheumatoid bursae

Patients with rheumatoid arthritis are prone to develop large adventitious bursae within the plantar tissues overlying the MTPJs, and fibrinoid nodules over bony prominences (see Ch. 8).

Plantar plate rupture

The plantar plate is a tough, rectangular, fibrocartilaginous structure that overlies the plantar aspects of the MTPJs. It is formed from the distal part of the plantar aponeurosis and the plantar aspects of the capsules of the MTPJs. It has a weak origin at the plantar aspects of the necks of the metatarsals and a strong insertion into the plantar aspect of the base of the proximal phalanges. Its function is to reduce load at the plantar aspects of the metatarsal heads, stabilise the digit in association with the collateral ligaments and the intrinsic and extrinsic muscles, and guide the line of pull of the tendons that insert into the digits, such as the tendons of the lumbrical and flexor digitorum longus muscles. The plantar plate acts as an attachment for the distal part of the plantar fascia and has a role in the windlass mechanism (Hicks 1954), resisting hyperextension of the MTPJ. The loss of the integrity of the plantar plate is implicated in the genesis of hammer toe. When rupture of the plantar plate occurs at the first MTPJ the condition is termed ‘turf toe’, and commonly affects young men who engage in vigorous sports (see Ch. 13).

Diagnosis and differential diagnoses

The clinical diagnosis is made from the history and presenting symptoms. A positive vertical stress test allows the affected toe to be elevated in a dorsal direction at the MTPJ, when the associated metatarsal is stabilised. Translocation of the digit by more than 2 mm in relation to the associated metatarsal head is indicative of rupture of the plantar plate. The tear within the plantar plate and the resultant leak of synovial fluid out of the joint space can be visualised on a radiograph when a radio-opaque dye is injected into the affected joint space (arthrography). The lesion shows on a magnetic resonance imaging scan as an increase in signal intensity in and around the plantar plate (Fig. 4.25), with discontinuity of the integrity of the plate, synovitis of the MTPJ and flexor tendon sheath, and persistent hyperextension of the proximal phalanx.

Figure 4.25 Magnetic resonance image of the second MTPJ, showing loss of integrity of the plantar plate.

The differential diagnosis should exclude synovitis in association with rheumatological disease, traumatic subluxation of the toe, osteochondritis of the metatarsal head (Freiberg’s disease), stress fracture and plantar digital neuroma.

Sensory problems, paraesthesia and painful neuropathy

Patients with painful neuropathy or hyperalgesia experience radiating burning, sharp or shooting pains in the distribution of the affected nerve. Their symptoms are usually exacerbated by movement. Tinel’s sign (i.e. distal tingling and paraesthesia) or Valleix’ sign (i.e. proximal tingling and paraesthesia) may be noted when the affected nerve trunk is percussed or palpated. Patients with abnormal sensory function will have altered nerve conduction rates on testing. Painful neuropathy or hyperaesthesia may be a feature of diabetic sensory neuropathy, and often precedes severe loss of peripheral sensation.

Nerve entrapment/Morton’s neuroma

Morton’s neuroma, also known as plantar digital neuroma, causes spasmodic neurological pain in the forefoot. It is a common condition, often affecting middle-aged women. Durlacher first described the painful syndrome in 1845, although it is named after TG Morton who wrote on the condition in 1876. In 1883, Hoadley was the first person to identify a nerve lesion at a symptomatic area. Many clinicians have theorised on the true nature and cause of the pain of plantar digital neuroma: some theories are feasible, but others are anatomically incorrect. Plantar digital neuroma affects women more often than men, and the most likely age band of onset is 40–60 years. Sufferers show a tendency to the upper limit of the normal body mass index (BMI). The BMI is calculated as the body weight in kilograms divided by the square of the height in meters. The normal BMI range is 20–25. Patients with plantar digital neuroma tend to the upper levels of the normal BMI (i.e. a BMI of 25 or greater). Neuroma can affect either foot, but bilateral presentation is less common, as is the occurrence of more than one lesion in the same foot. The neuroma lies approximately 5–10 mm deep to the plantar skin, just proximal to the point of division forming the plantar digital nerves proper. Plantar digital neuroma arises as an entrapment pathology affecting an intermetatarsal nerve, causing focal thickening of the nerve at the point where it divides to form the plantar digital nerves. Approximately 90% of cases affect either the second–third or third–fourth web spaces, and only 10% affect the first–second or fourth–fifth interspaces.

Pathology

Branches of the tibial nerve give rise to the lateral and medial plantar nerves, which subdivide to form paired plantar digital nerves proper. The lateral plantar nerve gives off digital branches that supply both sides of the fifth toe and the lateral side of the fourth toe. The medial plantar nerve gives off digital branches that supply both sides of the first, second and third toes, and the medial side of the fourth toe. There is often a communicating branch of the lateral plantar nerve that anastomoses with the medial plantar nerve, and also supplies the third web space. Other communicating branches anastomose with nerves deeper within the foot, and thereby tether the nerve in the third–fourth web space (Fig. 4.26). The metatarsal heads are separated by bursae, which lie superior (dorsal) to the transverse plantar ligament. The neurovascular bundles and lumbrical muscles lie within the intermetatarsal spaces, deep (plantar) to the transverse metatarsal ligament (Fig. 4.27).

Figure 4.26 Plantar digital neuritis: the plantar nerves.

Figure 4.27 Illustration of a cross-section through the level of the metatarsal necks 2–5.

Factors that predispose to the development of plantar digital neuroma include nerve compression and tension, especially in the third–fourth interspace, the distal extension of the intermetatarsal bursa at toe-off, transient nerve ischaemia and biomechanical factors.

Compression and tension of the plantar digital nerves

There are a number of factors that predispose to compression and tension of the plantar digital nerves. These include:

• Nerve thickness: the third common digital nerve is thicker than other common digital nerves, as it is formed of branches from both the medial and lateral plantar nerves.

• Movement between the medial and lateral columns of the foot: the third metatarsal is relatively immobile in comparison to the range of sagittal plane movement available to the fourth metatarsal. Thus, the third common digital nerve is tensioned by sagittal plane movement of the fourth metatarsal relative to the more static third metatarsal.

• Hyperextension of the toes at the MTPJs: for example, shoes with high heels pitch the centre of gravity of the body forward towards the forefoot, and decrease the area of foot–ground contact. They impose hyperextension of the MTPJs, so that the digital nerve is forced upwards against the inflexible transverse intermetatarsal ligament.

Distal extension of the intermetatarsal bursa

The intermetatarsal bursae lie between adjacent metatarsal heads (Fig. 4.27). The distal margins of the intermetatarsal bursae project just distally to the associated MTPJ and the distal limit of the transverse intermetatarsal ligament, to lie between the bases of the proximal phalanges. At toe-off the bursal fluid tends to move into the more distal parts of the bursae. This effect is implicated in the pathogenesis of plantar digital neuroma:

• hypermobility of the forefoot, associated with abnormal subtalar joint pronation and compounded by lateral compression from constricting footwear, creates shear and friction on the intermetatarsal bursa, inducing inflammation and an increased volume of fluid within the bursa

• the rise in fluid pressure within the bursa causes it to extrude distally and impinge against the neurovascular bundle, leading to an entrapment neuropathy, compression of the local artery and resultant ischaemic pain

• the resultant chronic inflammation leads to perineural fibrosis, where fibrous tissue develops around and compresses the nerve.

Transient ischaemia

The vasa nervosum (the artery serving the affected nerve) and the digital artery (which lies within the same neurovascular bundle as the affected nerve) are subject to intermittent compression during gait, by the distal distension of the intermetatarsal bursa, causing a local transient ischaemia, and acute ischaemic pain.

Biomechanical influences

Empirical observation indicates that a majority of cases with plantar digital neuroma present with inversion of the forefoot when the foot is non-weight bearing. This is compensated at toe-off by sagittal plane movement between the second–third or third–fourth metatarsals. That is, the lateral column of the foot moves dorsally, and the medial column moves relatively in a plantar direction when the forefoot comes under load, leading to stretching of the intermetatarsal tissues, chronic inflammation and the development of local fibrosis around the plantar nerve at the point where it divides to form the plantar digital nerves. The fibrous tissue ensheaths the nerve, exacerbating the condition.

The affected plantar digital nerve shows a fusiform thickening of the perineural tissues, and hypertrophy of the plantar digital nerves – a neuroma. The neuroma is white to yellow in colour, and shiny. Microscopically, there is juxtaneural fibrosis of the nerve that is continuous with the intermetatarsal bursa, intraneural fibrosis and collagen deposition, subperineural hyalinised nodules (Renault’s bodies), fibrosis of endoneural blood vessels (endarteritis), demyelination of the involved nerve fibres and axonal loss. These pathological changes to the plantar digital nerve confirm the diagnosis of Morton’s neuroma, and indicate that the lesion forms as the result of degenerative processes, consistent with an entrapment neuropathy.

Clinical picture

The patient typically reports a sudden, sharp, shock-like, burning, paroxysmal, spasmodic debilitating pain at the plantar aspect of the second–third or third–fourth intermetatarsal webbing area. The pain is often triggered by prolonged standing, walking or running, and may also occur during rest. The pain may be acute and disabling. Patients often report urgent need to remove the shoe and massage the foot to try to reduce the pain. Pain can be induced or aggravated by wearing tight or narrow shoes, thin-soled shoes or high-heeled shoes. Pain can also occur spontaneously and during the night. The pain often radiates into the toes that lie to either side of the affected web space, to the dorsum of foot and/or into the lower part of the back of the leg. The patient often describes a sensation of walking on a ‘lump’ or ‘pebble’ in the vicinity of the focal point of the pain at the plantar webbing, and has disturbed sensation, such as paraesthesia, tingling and numbness in the toes to either side of the affected web space. Sometimes the pain of plantar digital neuroma may present as an isolated apical pain. There may be a palpable thickening and oedema of the affected webbing area, which can be detected by palpating the dorsal–plantar dimension of the webbing tissues and comparing this with the same site on the other foot or the adjacent web space. Local oedema may cause the toes at the affected web space to diverge slightly, especially on weight bearing (the sunray sign).

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CASE STUDY 4.8 MORTON’S NEUROMA

The patient was a 47-year-old woman, who was in good general health and worked as a home help. She presented with acute pain at the tip of the left fourth toe. The pain had been present for approximately 6 months, beginning gradually, but recently increasing to almost intolerable levels. She was otherwise in good health, although inclined to asthma and eczema.

On examination, the left fourth and fifth toes were in a marked varus position, with a large Durlacher’s corn deep in the lateral sulcus of the left fourth toe. Enucleation of the lesion gave almost instantaneous relief. However, as the pain re-established within 2 months, the outer segment of the left fourth nail was later excised under local anaesthetic, and the exposed pocket of matrix phenolised to prevent nail regrowth. Healing was uneventful, and the left fourth toe was pain free.

However, 1 year later, the patient returned, complaining of exactly the same apical pain in the left fourth toe. The pain was worse when wearing court shoes, and was described as like ‘toothache’ in its sudden and unpredictable onset. There was no sign of nail regrowth, or hyperkeratotic lesion. However, thumb pressure to the left thirrd/fourth plantar webbing whilst simultaneously applying lateral compression across the forefoot (Mulder’s test, Fig. 4.28) triggered the pain spasm. She was diagnosed with plantar digital (Morton’s) neuroma.

Figure 4.28 Mulder’s test: Apply pressure to the third and fourth web spaces, using the thumb, to elicit pain. The forefoot should simultaneously be compressed laterally to test for a palpable, painful ‘Mulder’s’ click.

A temporary insole with a medial heel/instep/forefoot (cobra) pad was made, and this gave some considerable, but short-lived, relief of the symptoms. Finally, the patient underwent day-case surgery, and a large neuroma was excised from the left third/fourth interspace via a web splitting incision. The area healed well, and the patient has been symptom-free in the 10 years since.

This was an unusual presentation of Morton’s neuroma, as the typical signs and symptoms were not obvious, and the treatments of the primary lesions gave good, but only temporary, relief. As the pain of the diagnosed neuroma was no different to that of either the Durlacher’s corn and nail trauma, it was assumed that the neuroma was the underlying cause of the forefoot pathology.

Diagnosis and differential diagnosis

The diagnosis of plantar digital neuroma is generally made on the basis of the highly characteristic presenting symptoms, together with elicitation of the pain by lateral compression of the metatarsal heads whilst simultaneously applying direct pressure in a dorsal–proximal direction with the thumb at the affected web space (Mulder’s test) (Fig. 4.28). The patient will also characteristically show a degree of paraesthesia or hypoaesthesia in the associated interdigital cleft, in comparison to the unaffected interdigital areas (Fig. 4.29). Unambiguous loss of sensation at the affected interdigital space and adjacent toes can be taken as strong supportive evidence of a positive diagnosis of plantar digital neuroma. The patient with plantar digital neuroma or neuritis will experience a full reduction of pain, even when the action that normally triggers the pain is undertaken, by the injection of local anaesthetic, such as 2 ml of 1% lignocaine plain solution, into the area of the neuroma via the interdigital space. The nerve lesion is not visible on radiography, unless it is very large, when the adjacent metatarsal heads may show divergence. The lesion can be well visualised on magnetic resonance imaging, and high-resolution ultrasound imaging is a very useful indicator of the presence of plantar digital neuroma, showing the lesion as a hypoechoic mass, varying in density from the surrounding tissue and oriented parallel to the long axis of the metatarsals (Fig. 4.30A and B). Nerve conduction tests are not always conclusive in the diagnosis of Morton’s neuroma.

Figure 4.29 The affected interdigital space should be tested for loss of sensation using a sharp instrument e.g. a neurotip.

Figure 4.30 (A) Ultrasound scan of the third–fourth intermetatarsal space revealing a large neuroma. (B) An MRI scan of the same site, however, failed to identify the neuroma.

(Photographs printed with kind permission of Miss A. Wilson, The London Foot Hospital.)

The differential diagnosis of Morton’s neuroma or plantar digital neuritis should exclude forefoot pain arising as the result of: lumbar radiculopathy, tarsal tunnel syndrome, metatarsal or stress fracture, Freiberg’s infraction, peripheral neuritis or neuropathy, intermetatarsal bursitis, arthritides, metatarsal and soft tissue tumours, rupture of the plantar plate and MTPJ capsulitis.

Stress fracture

Stress fractures are hairline cracks that develop in bone as the result of the repeated application of low-level forces – such as the forces arising during prolonged exercise, or unaccustomed activity. Stress fracture of a metatarsal is given as an example of this process, and the principles of the recognition and treatment of stress fractures elsewhere in the foot are discussed.

Diagnosis

The diagnosis of a stress fracture is made from the history and the presenting signs and symptoms. These include an insidious onset of pain or aching that is increased by activity, together with local swelling with or without bruising. The patient may limp. There may be generalised foot or local oedema. The clinician will be able to palpate an isolated, excessively tender point in relation to the underlying bone. In cases of metatarsal fracture, pressure applied under the forefoot induces pain, as will the use of ultrasound over the fracture site, or attempting to move the opposing sides of the fracture in relation to one another.

Early-stage stress fractures do not usually show on plain radiographs, although a technetium-90 radioisotope bone scan will show an area of increased uptake of contrast medium, or ‘hot spot’, at the fracture site, early in the case. From weeks 3–4 onwards the fracture shows as a dark line surrounded by an area of diffuse bone callus on plain radiograph (Fig. 4.31). The fracture line may follow an oblique, transverse, longitudinal or spiral course through the bone tissue. Once healing is complete, the bone callus resorbs, but the cortical bone may remain permanently thickened around the site of the earlier fracture.

Figure 4.31 Osteopenia of the lateral sesamoid and avascular necrosis.

March fracture

The typical stress fracture in the foot affects the second, third or fourth metatarsal shaft, and is termed a ‘march’ fracture. The fault develops within the shaft of the metatarsal, at the point one-third from the head and two-thirds from the base, but stress fractures of the first and fifth metatarsals tend to affect the more proximal part of the bone shaft. Classically, the lesion develops at the medial aspect of the affected metatarsal. Usually only one metatarsal per foot is affected at any one time. The patient rarely gives a history of an exciting incident or trauma, although he or she may have undergone a period of extra exercise or standing, or have experienced weight gain in the weeks prior to the problem developing.

Principles of recognition and treatment of stress fractures elsewhere in the foot

Other bones in the foot may be prone to develop stress fracture.

Sesamoid pathologies

Sesamoids are small bones that occur within tendons, especially at points where the tendon crosses a joint. The sesamoid reinforces the tendon, and facilitates its movement across the joint as the deep aspect of the sesamoid is covered with cartilage and articulates with the other bones of the joint complex. Sesamoid bones are classified as constant or variant. Constant sesamoids are found in almost all humans. Examples of constant sesamoids include the patella that forms part of the knee joint complex, and the paired sesamoids that form part of the first MTPJ complex. Variant sesamoids, and bi- or tripartite sesamoids within the foot occur far less often, and their incidence and presentation varies from person to person.

All sesamoids are subject to all bone pathologies. These include subluxation, dislocation, fractures of all types, osteochondritis, chondromalacia, osteoarthritis and osteoarthrosis, osteomyelitis, bone tumour and associated bursitis.

There are paired, constant sesamoids that form part of the first MTPJ. These are each approximately the size of a grapefruit pip and lie within the tendon of the flexor hallucis brevis muscle to articulate at their deep aspects with the medial (tibial) and lateral (fibular) grooves on the plantar aspect of the first metatarsal head. Their function is to form part of the first MTPJ and contribute a channel on the plantar aspect of the first MTPJ through which the tendon of the flexor hallucis longus muscle courses as it passes to its insertion at the plantar aspect of the distal phalanx of the great toe. The sesamoids reinforce the flexor hallucis brevis tendon, increase the relative depth of the first metatarsal head so that tension within the flexor hallucis longus tendon is maintained, even at toe-off, and increase the functional length of the lever arm of the lower limb at the first MTPJ. Thus the paired sesamoids of the first MTPJ stabilise the joint and increase foot function during gait. The medial sesamoid tends to be larger than the lateral one, but either may present in a mono- or multi- (bi-, tri-, or quadri-) partite form. Bipartite sesamoids are encountered twice as often as multipartite sesamoids, and whilst up to one-third of medial sesamoids are noted as bipartite, only 2% of lateral sesamoids show bipartitism.

Metatarsalgia in the area of the plantar aspect of the first MTPJ may relate to sesamoid pathology.

CASE STUDY 4.9 SESAMOID PATHOLOGY DUE TO OSTEOCHONDRITIS OF THE LATERAL SESAMOID

A 31-year-old woman presented with pain in the first metatarsophalangeal joint of the right foot. The area had been symptomatic for just over 1 year and the pain was becoming progressively worse. The patient was otherwise in good health, and normally a very active individual. She used to play netball for an amateur league team but since the onset of the right forefoot problem had had to give up sport altogether.

The patient presented with fixed pes cavus, with rearfoot inversion and a plantar-flexed first ray. Movement and direct palpation at the right first metatarsophalangeal joint (MTPJ) area was warm, puffy and very painful, with an exquisitely tender point at the lateral plantar aspect of the first MTPJ. A dorsiplantar weight-bearing radiograph showed osteopenia of the lateral sesamoid and a healing stress fracture of the fourth metatarsal.

Osteopenia of the lateral sesamoid and avascular necrosis.

A diagnosis of avascular necrosis of the lateral sesamoid was made. It was presumed that the metatarsal fracture had developed as stress fracture due to lateral forefoot overload and the patient’s inability to load the medial area of the right forefoot, secondary to the sesamoid problem.

The patient presented with fixed pes cavus, with rearfoot inversion and a plantarflexed first ray (partial forefoot valgus). Movement and direct palpation at the first metatarsophalangeal joint (MTPJ) area was warm, puffy and very painful, with an exquisitely tender point at the lateral plantar aspect of the first MPTJ. A dorsiplantar weight-bearing radiograph showed osteopenia of the lateral sesamoid shown in figure, indicating a continuing pathology. As her pain was so debilitating and unrelenting she was referred to a podiatric surgeon, who excised the lateral sesamoid, to good outcome.

Sesamoid osteochondritis

See the section earlier in this chapter on osteochondritides (Fig. 4.32).

Figure 4.32 (A) Lateral radiograph of plantar and posterior heel spurs. This patient was later diagnosed as having ankylosing spondylitis. (B) subsequent radiograph taken during disease remission shows remodelling of the calcaneum and reduction of the spurs.

Freiberg’s infraction

Freiberg’s infraction, or osteochondritis of the metatarsal head, causes metatarsalgia most commonly in the area of the second MTPJ area. It may present as a primary problem in teenagers, or as a secondary degenerative arthrosis in later life. See the section earlier in this chapter on Freiberg’s disease.

Complications following metatarsal surgery

Metatarsalgia may develop as the result of forefoot or metatarsal surgery. Complications arising after metatarsal surgery can include delayed union, malunion, non-union and the development of a pseudoarthrosis, recurrence of the original metatarsal problem, or the development of plantar hyperkeratotic ‘transfer’ lesions over adjacent MTPJs. Where the integrity of the MTPJ is lost as the result of surgery, such as a Keller’s arthroplasty, used to correct hallux abducto valgus, the patient may develop a ‘floating’ digit. Other postsurgical complications can include the overexuberant formation of bone callus, with loss of the normal bone architecture; displacement of the metatarsal head and loss of MTPJ integrity; aseptic necrosis of the capital fragment of the metatarsal following osteotomy; and osteomyelitis (bone infection).

Rheumatological diseases

Any generalised pathology that affects the locomotor system is likely to give rise to pain in the foot, and thus can be a cause of metatarsalgia. Diseases of the locomotor system fall into two broad categories:

The text in the following section gives only a summary of the main features of these diseases. For greater detail the reader is advised to consult a textbook on general medicine.

Arthropathies

Plantar fibromatosis

The development of fibrous nodules on the plantar fascial structures is reviewed in the section on plantar fibromatosis (see earlier in this chapter).

Altered tissue perfusion and reduced vascular drainage

This can cause forefoot and generalised foot pain.

Generalised muscular pathology

Myalgia or muscle pain of a muscle unit or group is characterised by muscular stiffness and pain on movement. Myalgia may occur as a feature of repetitive movements, intermuscular sensory neuritis (also known as fibrositis, fibromyositis and myositis) tendonitis, muscle strains, traumatic injury and contusions. Symptoms vary from a transient stiffness, to agonising pain, and can be set off by pressure at trigger points within the affected muscle. Acupuncture of the trigger and more proximal pressure points, or trigger point massage, is a useful therapy to reduce the pain of myalgia (Sandberg et al 2004).

Neoplastic disease

Neoplasm is rare in the foot, accounting for less than 0.05% of foot lesions. There are a number of relatively benign neoplasms that affect the foot and may possibly cause metatarsalgia. These include squamous-cell papilloma, dermatofibroma, naevi, eccrine poroma, angiokeratoma, giant-cell tumour of tendon sheaths, lipoma, benign fibrous histiocytoma, chondroma, leiomyoma, myxoma and lipoblastoma. Primary malignancies within the foot and lower limb are rare. Those that do arise may provoke metatarsalgia, and include synovial sarcoma, melanoma, verrucous carcinoma, squamous-cell carcinoma, basal-cell carcinoma, fibrosarcoma, malignant fibrous histiocytoma, leiomyosarcoma, chondrosarcoma, myosarcoma, lymphangiosarcoma and malignant neurofibroma. Those malignant neoplastic tumours that affect the bones of the foot tend to occur as a secondary tumour to a primary tumour of lung, breast or kidney. However, the possibility of bone tumours in the foot cannot be ignored, as, although bone tumours below the knee are very rare, 25% of those malignancies that do arise in the lower leg affect the bones of the foot.

Back pain

Lumbar pain can cause pain in the legs and feet, referred within the distribution of the sciatic nerve. Classically, heel pain can be a feature of spinal nerve compression at the S1 level.

Soft tissue effects of rheumatic disease

Large plantar bursae are a feature of rheumatoid arthritis. Tenosynovitis and plantar enthesiopathies characterise rheumatoid diseases and Reiter’s syndrome. Nerve-compression syndromes, such as tarsal tunnel syndrome, can arise as the result of local autoimmune-mediated inflammation and vasculitis of the vasa nervosum.

Miscellaneous systemic causes of metatarsalgia

Paget’s disease, which is characterised by bone pain, enlargement of the medullary cavity and thinning of the cortex of long bones, can predispose to stress fractures. Bone infections, such as osteomyelitis and tuberculosis, are very painful, even in cases with sensory neuropathy, and are difficult to treat, requiring surgery and prolonged courses of antibiotics. Neoplastic disease, muccopolysaccharide disorders, skeletal dysplasia (e.g. achondroplasia, osteomalacia), and hereditary diseases such as osteogenesis imperfecta and osteopetrosis all predispose the patient to fractures that are as likely to affect the bones of the foot as elsewhere in the skeleton.

Obese patients with a BMI of over 30, and/or a waist measurement of more than 1 m may experience foot pain due to chronic tension on the plantar fascia. Foot pain can be a feature of the later stages of pregnancy. Any biomechanical anomalies are exaggerated by the increase in body weight, the change in the centre of gravity of the body due to the gravid uterus, and the generalised ligamentous laxity that characterises late pregnancy. Patients who suffer from alcoholism often develop painful neuropathies that affect the feet and legs.