Incidence of LLD

A number of studies have been carried out on the epidemiology of LLD. Most agree that a minor degree of difference in limb length of 1–2 cm is extremely common and occurs in around 90% of the population, and is of little clinical significance (Blustein & D’Amico 1985).

Causes of LLD

Blustein and D’Amico (1985) attributed LLDs to idiopathic unequal development (53%), unilateral coxa vara (3%), pelvic abnormalities (3%), fractures with shortening (11%), fractures with lengthening (7%), postsurgical shortening (3%) and unilateral subtalar joint pronation (1%). The remaining 19% result from a number of diseases and abnormalities, including neurological disorders (e.g. polio, cerebral palsy), rickets, osteomyelitis, slipped capital femoral epiphysis, irradiation-therapy effects and sciatic nerve injury.

Effects of LLD

LLDs are associated with a variety of types of musculoskeletal imbalance, including altered gait patterns, equinus contracture at the ankle and increased energy expenditure in gait (Gurney 2002). However, there is no consistent pattern common to all individuals. LLD alters the magnitude of forces acting through joints and also changes the area of force distribution by altering the area of the joint surface that is subject to load. Runners with LLD tend to present with increased vertebral disc and low-back symptoms, and increased incidence of tibial stress fractures, knee pain, shin splints, painful heel syndrome, symptomatic hallux valgus, and sciatica (Fig. 4.1).

Figure 4.1 Leg-length discrepancy: 3 cm limb-length discrepancy in a 28-year-old man. The patient was unable to give the cause of his limb-length difference, other than he had spent several months in hospital when 12 years old because his ‘left leg was not growing properly’. The patient habitually toe walks on the left foot, and pronates excessively on the right. Examination showed normal sensation and tendon jerks in both legs and no loss of muscle power, although there was a reduction of the muscle bulk on the left side. The forced supination of the left foot is marked by the contraction of the tibialis anterior muscle. He is treated with orthotic therapy to redress the difference in limb length and to control the excessive right foot pronation.

The effects of LLD include:

Symptoms of LLD

Symptoms of LLD include arthritis of the knee, psoasitis, anterior knee pain, shin splints, metatarsalgia, sacroileitis, Achilles tendonitis, quadriceps strain, pes anserinus bursitis, groin (adductor) strain, peroneal tendonitis, neck pain, intermetatarsal neuroma, osteitis pubis, sesamoiditis and sinus tarsi syndrome.

Significance of the degree of LLD

The literature on the degree to which LLD is likely to produce pathological symptoms is contradictory. The view propounded by Subotnick (1981) suggests that the significance of LLD is relative to the patient’s activity levels:

However, even asymptomatic LLD should always be regarded as significant in patients who have lower limb and lower back pathologies.

Assessment and measurement of LLD

There are two presentations of LLD: true LLD and apparent LLD. It is not always straightforward to determine whether the patient has a true or an apparent LLD. True LLD is noted when the patient presents with a difference in the lengths of the tibiae, femurs or both. An apparent LLD will occur when there is pelvic asymmetry, such as a scoliosis and resultant pelvic tilt, or foot asymmetry such as unilateral subtalar joint excessive pronation or supination.

Measurements, made using a standard tape measure with the patient lying supine, include:

The subject can also be assessed in the normal angle and base of gait, and the symmetry of the following may be assessed or measured:

Management of LLD

LLD is managed by applying height correction to the short limb, and the use of orthoses to control problems in the long limb associated with excessive foot pronation.

Coxa valgum, genu vara, tibia vara (bowleg)

Coxa valgum is a frontal plane malalignment of the hip, where the angulation between the femoral neck and the shaft of the femur is greater than 135°. It usually occurs as the outcome of slipped epiphysis of the femoral head. It creates an LLD with relative lengthening of the affected leg. It may induce a limp, together with compensatory pronation within the leg, such as external femoral rotation, internal tibial torsion and pes planus. Cases with coxa valgum usually show genu vara (Hammer 1999).

Genu vara and tibia vara are frontal plane malalignments of the lower limb, which affect foot and limb function in the same way as a rearfoot varus. In genu vara and tibia vara, the anterior aspect of the subject’s thigh will be in a valgus position and the lower leg will be in a varus position when the patient stands in relaxed calcaneal stance. The condition is characterised by ‘bowing’ of the legs and a noticeable gap between the knees when the patient stands erect.

Distal tibia vara is a condition where the lower third of the tibia adopts an inverted (varus) position. When the subject stands erect, the legs will be straight from the hip to the lower third of the tibia, but the lower third of the tibia bows in a varus position. Tibia vara of 5°–10° is normal in the infant and anything up to 5° is probably of little significance in the adult, except perhaps in the overuse situation. Infantile tibia vara usually corrects with maturity. However, not all paediatric or developmental bowlegs will resolve. Pointers for the diagnosis of non-correcting bowlegs are:

Rearfoot varus

Rearfoot varus is defined as a congenital structural abnormality of the rearfoot, where the rearfoot is inverted relative to the weight-bearing surface, when the subtalar joint is in its neutral position and the midtarsal joint is maximally pronated around both axes. A functional rearfoot varus occurs as a result of a varus attitude of the leg (Pickard 1983, Sgarlatto 1971).

Fully compensated rearfoot varus

This condition is characterised by sufficient subtalar joint pronation to allow the plantar aspect of the heel to contact the ground fully, so that ground reaction forces are fairly evenly distributed across the heel and, therefore, the foot.

Signs and symptoms of fully compensated rearfoot varus

These include:

• Significant lowering of medial ‘arch’ height on weight bearing.

• Lateral border lesions are less likely, as this foot is plantigrade. However, there are often signs of excessive lateral shoe wear.

• Varying degrees of Haglund’s deformity (see rearfoot disorders, below) may be present due to irritation of the lateral–posterior–superior border of the calcaneus, lateral to the insertion of the Achilles tendon. The irritation is brought about by rapid and excessive contact-phase pronation. The heel linings of footwear, particularly sports shoes, often wear through at the corresponding point, due to the excessive movement of the foot within the shoe (Fig. 4.2).

• Reduced first MTPJ motion is common, even in the younger subject with no joint pathology (see Stage 1 functional hallux limitus, in the section on hallux limitus/rigidus, below). The excessively pronated foot restricts the ability of the first metatarsal to plantar flex and move backwards to facilitate dorsiflexion of the hallux after heel lift. This causes restriction to passive and/or active dorsiflexion of the MTPJ, and eventually may cause permanent damage to the dorsal surface of the joint, and structural hallux limitus.

• Tailor’s bunion deformity due to forefoot hypermobility is common, as a result of the excessive pronation of the subtalar joint, coupled with excessive lateral loading of the foot during the contact period.

• The re-supinator muscles may become fatigued and traumatised as they attempt to supinate the foot rapidly after heel lift. This often presents clinically as anterior or posterior ‘shin splints’.

• Low back pain is also associated with rearfoot varus. The causal mechanism is not well documented but has been hypothesised by Dananberg (1996).

• As in uncompensated rearfoot varus, lateral (inversion) ankle sprains are common, especially in the physically active.

Figure 4.2 Haglund’s deformity. Superficial bursitis and some exostosis formation, particularly on the left heel.

Treatment of rearfoot varus

• Compensated rearfoot varus. In the short term, symptomatic treatment using clinical padding, strapping and physical therapies is appropriate. However, the long-term aim is to negate the need for compensatory pronation of the subtalar joint. This is usually achieved by functional foot orthoses with intrinsic or extrinsic medial posting. In cases where high levels of physical activity compound the symptoms, full-length orthoses may be required (Fig. 4.3).

• Uncompensated rearfoot varus. Feet with uncompensated rearfoot varus lack mobility and thus are less amenable to functional orthoses. Accommodative orthoses, which off-load and protect, with appropriate shoe advice and local treatment strategies are appropriate.

Figure 4.3 Rearfoot varus. (A) uncompensated rearfoot varus; (B) compensated rearfoot varus; (C) pattern of hyperkeratotic lesions in the compensated foot; (D and E) orthotic therapy and shoe modification to control compensation.

Varus rearfoot

Distinction must be drawn between a rearfoot varus (a primary abnormality) and a foot that adopts or functions in a varus position secondary to a malalignment elsewhere in the limb or secondary to another pathology.

The rearfoot may adopt a varus attitude when the subject is standing in a relaxed posture (relaxed calcaneal stance), or the foot may function during gait in a greater degree of varus than is the accepted norm. This may be due to an uncompensated rearfoot varus abnormality, but equally may be due to compensatory movement of the rearfoot as a result of a forefoot valgus or other abnormality that results in compensatory supination of the foot. A varus rearfoot may also be a feature of a neurological pathology.

Forefoot varus

Forefoot varus is a congenital osseous structural deformity in which the plantar plane of the forefoot is inverted relative to the plantar plane of the rearfoot when the subtalar joint is in its neutral position and the midtarsal joint is maximally pronated around both its axes (Bowden 1983, Hlavlac 1971). A true osseous forefoot varus is probably fairly rare, especially in adults, as years of walking in an overpronated manner on a consequently hypermobile foot is likely to result in soft tissue adaptation (Fig. 4.4).

Figure 4.4 Forefoot varus. (A) normal contact in midstance; (B) pronating after midstance; (C) site of hyperkeratotic lesions; (D) (i) adhesive deflective/protective padding on the foot; (D) (ii) the same padding applied in the shoe on an insole; (E) (i) extended heel on sole of shoe (Thomas heel); (E) (ii) medial heel wedging in the shoe and flare (buttress) on the medial side of the heel of the shoe.

Forefoot supinatus

Forefoot supinatus is an acquired soft tissue deformity of the longitudinal axis of the midtarsal joint, where the forefoot is inverted relative to the rearfoot when the subtalar joint is in the neutral position and the midtarsal joint is maximally pronated around both its axes. The condition arises secondary to long-term (>15 years) excessive pronation at the subtalar joint, where eversion of the calcaneum ultimately results in compensatory forced inversion of the forefoot. Initially the foot can recover its normal position when off-loaded, but with time the local soft tissues become stretched and lose their ability to correct the forefoot back to its normal position (Davis’ law), so that the forefoot adopts an abnormal compensatory position (Redmond 2009).

Coxa vara and genu valga/valgum (knock knees)

Coxa vara is a frontal plane malalignment of the hip, where the angulation between the femoral neck and the shaft of the femur is less than 120°. It may occur as the result of trauma or bone disease, or as a congenital abnormality. It causes a limb-length discrepancy, with relative shortening of the affected leg. It usually induces a limp and compensatory supination within the limb, such as internal femoral rotation, external tibial torsion, ankle equinus and pes cavus. Cases with coxa vara usually show genu valgum.

Genu valgum is a frontal plane malalignment of the lower limb, in which the anterior aspect of the subject’s thigh will be in a varus position and the lower leg will be in a valgus position when the patient stands in relaxed calcaneal stance. The condition is characterised by the knees touching or ‘knocking’ on their medial aspects (knock knees) and a noticeable gap between the feet, measured at the medial malleoli, when the patient stands erect. It is a normal developmental feature in many children, showing most commonly from 2–4 years until 6–8 years, and from 11–12 years until 14–15 years. Genu valgum in adults may result in compensatory excessive pronation of the subtalar joint, especially in the overweight or obese patient. During stance and gait, the centre of mass of the body acts medial to the foot, causing the foot to adopt a pronated position.

True rearfoot valgus

A true rearfoot valgus is an exceptionally rare primary congenital osseous abnormality. It is defined as a congenital, structural abnormality of the rearfoot, where the rearfoot is everted relative to the weight-bearing surface, when the subtalar joint is in its neutral position and the midtarsal joint is maximally pronated around both axes. However, it is common for the rearfoot to adopt a valgus attitude in relaxed calcaneal stance, due to a number of conditions that are compensated for by excessive pronation of the subtalar joint.

The valgus rearfoot

A valgus rearfoot, as observed during gait or in relaxed calcaneal stance, is usually a secondary abnormality and appears mostly as a compensation for a primary abnormality elsewhere in the limb or foot, such as forefoot varus, forefoot supinatus, mobile forefoot valgus and genu valgum. A valgus rearfoot can also arise as the result of trauma such as a Pott’s or bi-malleolar fracture, agenesis of the distal aspect of the fibula, congenital absence of a fibula, rupture of tibialis posterior tendon, rheumatoid disease, tarsal coalition, Charcot neuroarthropathy and footballer’s ankle (Zhang et al 2002).

Forefoot valgus

Forefoot valgus is a congenital osseous deformity where the plantar plane of the forefoot is everted relative to the plantar plane of the rearfoot when the subtalar joint is in the neutral position and the midtarsal joint is maximally pronated around both its axes.

Mobile type forefoot valgus

In mobile forefoot valgus heel contact is normal, but the forefoot accepts load under the MTPJs in the order first to fifth (not fifth to first as in the normal foot). The foot is characteristically mobile and distorts under load. The first ray dorsiflexes and the midtarsal joint supinates. There is seldom a need for the subtalar joint to undergo compensatory supination. The net result is forefoot supination, with unlocking of the midtarsal joint and resultant forefoot hypermobility (Fig. 4.5).

Figure 4.5 Pes cavus. (A) forefoot valgus, plantar-flexed first ray; (B) hindfoot varus; (C) (i) and (ii) sites for the hyperkeratotic lesions; (D) (i) and (ii) clinical padding to deflect pressure; (E) (i) and (ii) in-shoe or insole padding; (F) buttressed heel on shoe.

Signs and symptoms of mobile forefoot valgus

The forefoot instability that characterises mobile forefoot valgus (Fig. 4.5A) results in a high incidence of hallux abducto valgus, lesser toe deformities, plantar hyperkeratosis under the central metatarsal heads, fifth toe corns and a tendency to splayed forefoot and tailor’s bunion. Plantar fasciitis, plantar digital neuritis, medial sesamoiditis and first metatarsal–cuneiform joint exostosis may also occur. There is a low incidence of postural lesions as rearfoot function tends to be relatively normal. However, in cases where the calcaneum everts (Fig. 4.5B), postural symptoms may occur, including medial knee pain, shin pain and lower back pain.

Aetiology and presentations of ankle equinus

A range of foot and limb conditions are characterised by ankle equinus. These include:

Compensatory dorsiflexion for ankle equinus takes place at the subtalar joint (Fig. 4.6). As the subtalar joint shows trip-planar motion, compensatory dorsiflexion is accompanied by eversion and abduction of the foot. Thus a foot with insufficient ankle dorsiflexion may compensate for the abnormality by forced and excessive pronation of the subtalar joint. This may be observed during barefoot walking by rapid and increased pronation of the subtalar joint, and a loss of height at the medial longitudinal arch as the support limb passes over the stance foot.

Figure 4.6 Ankle equinus, short or tight Achilles tendon group. (A) Showing relationship between rearfoot and forefoot; (B) the compensation movements that occur; (C) sites for hyperkeratosis; (D) footwear with extra top piece on heel.

Classification of ankle equinus

Ankle equinus, like other functional abnormalities of the foot, is classified by the degree of effective compensation.

Compensation for reduced dorsiflexion at the ankle joint may occur in the lower leg. The subject may show:

Treatment of ankle equinus

The patient must undergo a full biomechanical evaluation to establish the cause of the equinus deformity, in order that the treatment addresses all aspects of the lower limb and foot problem. Therapies include posterior muscle group stretching regimens where soft tissue equinus is diagnosed, orthoses therapy and footwear advice. But care must be taken to ensure that the true ankle equinus is identified and treated, rather than controlling the compensatory pronation at the subtalar and midtarsal joints. The correct diagnosis and treatment of ankle equinus can, however, prevent gross deformity in the longer term.

Aetiology of hallux limitus

Hallux limitus is a chronic degenerative condition that develops over time, in association with a range of intrinsic (within the lower limb and foot) and extrinsic (e.g. systemic disease) factors. The intrinsic and extrinsic factors and variants of normal foot anatomy that predispose to hallux abducto valgus may also predispose to hallux limitus.

Intrinsic factors

• Foot shape: the rectus foot (where the metatarsus adductus angle is <15°) is more prone to develop hallux limitus, whereas the adductus-type foot (characterised by metatarsus primus varus) is more prone to develop hallux abducto valgus (Fig. 4.7).

• Biomechanical factors: these are characterised by excessive pronation at the subtalar or midtarsal joints, where the foot remains in pronation from midstance through to toe-off. The factors include: ankle equinus, flexible or rigid pes plano valgus, rigid or flexible forefoot varus, dorsiflexion of the first ray (metatarsus primus elevatus), an elevated or hypermobile first ray, flexor plate immobility, plantar soft tissue contracture (Durrant and Siepert 1993) and functional hallux limitus (Payne et al 2002).

• Structural anomalies: anomalies within the lower limb that predispose to compensatory excessive foot pronation include external tibial torsion, tibial varum, positional variants of the knee (genu valgum/varum/recurvatum), femoral retroversion, leg-length discrepancy, where the long leg pronates excessively throughout gait, and an abducted angle of gait or wide-based gait.

• Relatively long first toe or long first metatarsal.

• Trauma: such as damage to the articular cartilage at the first MTPJ (e.g. osteochondritis, osteoarthritis), soft tissue tears, and sprains (e.g. ‘turf’ toe) of the soft tissues around the first MTPJ.

Figure 4.7 Foot shape: rectus.

Pathology of hallux limitus

The primary role of the hallux is to dorsiflex on the first metatarsal head during the propulsive phase of gait. It has been calculated that approximately 70° of dorsiflexion is required at the first MTPJ at toe-off during normal bipedal motion, to allow the body’s centre of mass to progress forward with a smooth transfer of weight from the loaded to the opposite foot. The first MTPJ is a major weight-bearing joint, and at toe-off the full forward momentum of the body mass passes through this joint to be dissipated to the supporting surface.

Pathophysiological effects of a reduced range of motion at the first metatarsophalangeal joint

In the normal foot, the hallux remains static when under load (i.e. at toe-off), due to hallux purchase (see above). The articular aspect of the base of the proximal phalanx hallux therefore acts as a dynamic buttress to the forward motion of the body, and in effect functions as a ‘buffer’ to the forward motion of the loaded foot, so that continued onward momentum of the body mass initiates sagittal plane movement at the first MTPJ. There are two components within the sagittal plane movement at the first MTPJ – a hinge movement and a gliding movement – and therefore the first MTPJ is classed as a ginglyomoarthrodial joint (Root et al 1977). The hinge movement occurs as the hallux dorsiflexes at the first MTPJ. The gliding movement (in a plantarwards direction) occurs as the head of the first metatarsal moves down through an arc across the sagittal plane, facilitated by plantar flexion of the first metatarsal at the first metatarsal–medial cuneiform joint. The net result of movement of the first MTPJ is that the first metatarsal moves from a position where is it relatively parallel to the support surface (at midstance), to one where it is almost perpendicular to the supporting surface (at toe-off). As force equals mass/area, the decreased area of foot contact with the support surface at toe-off imposes an increased loading of up to 1.5 times body mass at the first MTPJ. This increased load persists from the latter part of the single support phase of gait until just after the heel strike of the opposite foot, and the weight-bearing limb moves into the swing phase (Dananberg et al 1996).

• When normal first MTPJ motion is reduced, as in hallux limitus, the amount of active dorsiflexion of the hallux at the first MTPJ (the hinge movement) is decreased and its gliding component forms the majority of available first MTPJ motion. The smooth transfer of body weight from the loaded to the opposite foot is compromised. Newton’s second law of motion (i.e.: force = mass × acceleration) dictates that, as the patient’s body mass remains constant, the force passing through the first MTPJ must increase when the acceleration of the hallux over the head of the first metatarsal is reduced, and forces of forward motion at the head of the first metatarsal and base of the proximal phalanx reciprocally increase.

• In cases where there is reduced movement at the first metatarsal–medial cuneiform joint (e.g. where there is a degree of arthritis at that joint) the plantarwards glide of the first metatarsal head across the sagittal plane is reduced, so that only the dorsiflexion component of the first MTPJ movement is available to facilitate forward momentum of the body from midstance through toe-off (Dananberg et al 1996), with a net restriction of the normal amount of dorsiflexion at the first MTPJ.

• In a normal joint, a feedback mechanism operates to prevent extremes of movement. At the limit of the normal range of movement, nerve endings within the joint secrete substance P and other inflammatory mediators, to initiate the feedback mechanism that prevents the joint moving beyond its normal range. Where the first MTPJ habitually is forced to work at the limits of its (pathologically decreased) range of movement (as outlined above), levels of substance P rise within the joint, triggering a neurogenic inflammation, with pain, swelling, heat, redness and loss of joint function (Light 1996). Thus the feedback mechanism creates and perpetuates the joint pathology, so that inflammation within the first MTPJ leads to even further limitation of joint movement, chronic inflammation, an increasing joint pathology, degenerative changes, the gradual reduction or loss of joint space, osteoarthritis and osteophyte formation, especially at the dorsal aspect of the joint (itself further compromising normal first MTPJ movement) (Fig. 4.8).

Figure 4.8 Pathophysiology of hallux limitus. Impingement of the base of the proximal phalanx during gait in a foot with metatarsus primus elevatus and the genesis of hallux limitus.

Classification of hallux limitus

The clinical presentation of hallux limitus varies with the stage of the pathology, and thus the progress of the condition can be classified according to the range of the presenting signs and symptoms (Table 4.1).

Table 4.1 The Classification of hallux limitus/rigidus (after Camasta 1996)

MTPJ, metatarsophalangeal joint.

Clinical picture of hallux limitus

The typical patient presenting with hallux limitus is 30–50 years old (Coughlin & Shurnas 2003), with increasing great toe pain and stiffness, especially after walking or exercise involving dorsiflexion at the first MTPJ. There may or may not be a history of minor injury. The first MTPJ area is swollen, tender to touch and painful on passive movement. There may be joint crepitus on movement. The hallux is usually hyperextended (dorsiflexed) at its interphalangeal joint, but in cases where dorsiflexion at the first MTPJ is especially tender and restricted by pain and joint immobility the hallux may be held in slight flexion at the first MTPJ. Gait is modified to accommodate the first MTPJ dysfunction and weight is shifted laterally to the outer border of the foot (Fig. 4.9A and B).

Figure 4.9 A typical presentation of Stage 3 (moderate) structural hallux limitus. (A) Radiograph showing a reduction of the first MTPJ space and bone sclerosis, degenerative changes of the subchondral bone, hypertrophy of the sesamoids and marginal osteophytosis. (B) Photograph showing the typical clinical presentation of late-stage structural hallux limitus, with hyperextension of the hallux at the interphalangeal joint, elevation of the first metatarsal (metatarsus primus elevatus), the dorsal ‘bunion’ and an increase in the depth of the foot at the first MTP joint area (reflecting the underlying dorsal osteophytosis).

The early clinical signs of functional hallux limitus (Stage 1) are subtle and may go unnoticed: the patient is likely to be free of foot pain, but may show a mildly apropulsive gait and an abductory forefoot twist at toe-off. Patients with Stage 2 mild structural hallux limitus show reduced dorsiflexion at the first MTPJ and reduced heel lift. They tend to compensate for the lack of efficient toe-off by excessively pronating the foot. In Stage 3, severe structural hallux limitus or early hallux rigidus, dorsiflexion at the first MTPJ is much reduced. In Stage 4 the first MTPJ becomes virtually or actually fused/ankylosed. To walk, the patient must pronate, abducting and everting the foot throughout gait, walking in a ‘duck-footed’ manner. Alternatively, where the ankylosed first MTPJ effectively extends the length of the medial column, it increases the angulation of the line of axis of the MTPJs in relation to the frontal plane, and allows the foot to supinate about the interphalangeal joint of the hallux late into toe-off.

Gait and posture effects of structural hallux limitus

As walking is modelled as an inverted pendulum system, in which the centre of mass ‘vaults’ over the rigid stance limb (Lee & Farley 1998), a full range of dorsiflexion at the first MTPJ is an essential component of the normal walking mechanism. During stance, dorsiflexion at the first MTPJ allows the joint to form the pivot to the ‘lever arm’ of the leg, allowing the transfer of body mass from the loaded to the opposite foot, whilst maintaining a smooth forward momentum. The loss of normal first MTPJ dorsiflexion in hallux limitus causes marked changes to gait and body posture. The normal response of the first MTPJ is to dorsiflex in direct response to the leverage imposed by heel lift. Where heel lift is reduced secondary to decreased available dorsiflexion at the first MTPJ, the foot is obliged to pronate about the oblique axis of the midtarsal joint, and the patient has to make an abductory twist to assist toe-off. The patient adopts an abnormally abducted angle of gait. Excess pronation imposes changes on limb and skeletal relationships, which include internal tibial torsion, internal rotation and transverse plane motion at the knee, internal rotation at the hips, a forward pelvic tilt (pelvic nutation) due to an increased lumbar lordosis, a thoracic kyphosis and a forward tilt of the cervical spine. Thus the patient with structural hallux limitus or hallux rigidus adopts a short stride length and early knee flexion, shows decreased thigh extension, a hunched back (‘bad’ posture or thoracic kyphosis), a diminished arm swing (to match the shortened stride length) and tends to either hyperflex the upper cervical spine, in order to face forward, or looks down to the ground whilst walking (Dananberg et al 1996).

Pain associated with hallux limitus and hallux rigidus

The presenting symptoms of hallux limitus and hallux rigidus vary depending on the stage of the pathology:

Shoe-wear marks

The foot with hallux limitus and hallux rigidus causes characteristic wear marks on the upper and the sole of the shoe. These are more readily visualised in a lace-up shoe, with a leather upper and sole:

Diagnosis and differential diagnoses

The diagnosis of hallux limitus and hallux rigidus is made from the clinical signs and the patient’s symptoms, and confirmed by radiography.

Radiographs (anteroposterior, oblique and lateral views) of a foot with structural hallux limitus show narrowing of the first MTPJ space, with bone sclerosis and formation of dorsal osteophytes (dorsal spur formation). In moderate structural hallux limitus there is progressive enlargement of the sesamoids, increasing osteophytosis and metatarsus primus elevatus. In hallux rigidus, the first MTPJ shows ankylosis and loss of differentiation of the sesamoids, marked metatarsus primus elevatus, decreased inclination of the calcaneum and loss of the cyma line.

The differential diagnoses should rule out inflammatory joint diseases such as rheumatoid arthritis, gout and psoriatic arthropathy, as well as osteochondritis dissicans (in adolescents) and flexor hallucis longus tenosynovitis.

Treatment of hallux limitus and hallux rigidus

Hallux limitus and hallux rigidus can be treated conservatively, or by surgery, after taking the history and making a full examination and biomechanical evaluation of the patient to determine the extent of the pathomechanical processes associated with the condition. In the past, immobilisation of the first MTPJ was advocated as the principal treatment for hallux limitus and hallux rigidus, in order to unload the joint, promote rest and preserve the remaining joint function (Laing 1995). But Dananberg et al (1996) advocate that the conservative therapy should include manipulative therapy to enhance first MTPJ movement, reduce pain and improve and maintain overall joint function, in order to avoid later gait and postural disturbances.

Pathology of hallux flexus

The typical acute hallux flexus patient is a young person who presents with a recent history of trauma to the foot, usually as the result of an accident such as stubbing the toe against a kerb or tripping over a heavy or immovable object. The sudden deceleration of the body mass due to the impact imposes an excessively high load at the articular surfaces of the first MTPJ, resulting in an acute inflammatory response in and around the joint. It is a very painful condition, in which the flexor hallucis brevis muscle goes into spasm as a protective mechanism, creating a metatarsus primus elevatus and excess pain on attempted movement of the first MTPJ. The hallux is held in plantar flexion until the pain, inflammation and muscle spasm subside. Repeated episodes of hallux flexus can predispose to developing structural hallux limitus in later life.

Diagnosis of hallux flexus

The diagnosis is made from the clinical signs together with the patient history. Radiography will exclude any concomitant fractures caused at the time of the original trauma to the foot.

Treatment of hallux flexus

Treatment involves pain control, rest, ice, compression and elevation (PRICE):

Classification of pes planus

Pes planus may be classified according to its aetiology; that is, whether it is of functional, congenital, acquired or neurological origin:

Consequences of pes planus

Flexible flat foot causes, or is associated with, many foot and lower limb pathologies, including:

Treatment of pes planus

Flexible flat foot is often amenable to treatment, provided the underlying cause has been diagnosed and is addressed by the management strategy. However, some cases of very severe flat feet, particularly those involving late-stage tibialis posterior dysfunction (see plantar heel pain), especially in the elderly, and flat foot of congenital or traumatic origin, are less amenable to conservative treatments. These cases should be referred for an orthopaedic or podiatric surgery opinion. The reader is referred to the wide range of texts (and the considerable debate) available in the literature on surgery for the flat foot.

The rigid flat foot causes a range of symptoms, which will be related in general to the underlying pathology and consequent gait difficulties. Treatment is mostly palliative, but can maximise the function that is available. Referral for surgery may be the option of choice.

Aetiology of pes cavus

Pes cavus is often related to neuromuscular dysfunction, congenital abnormality or familial predisposition. For example:

However, in a significant number of cases no clear aetiology can be identified, and these cases are classed as being of idiopathic cause. Idiopathic presentations of highly arched feet that do not arise in association with neuromuscular dysfunction, congenital abnormality or familial predisposition are often associated with functional abnormalities and malalignments, which include:

Mobile pes cavus is a term used to describe a foot in which, in the non-weight-bearing state, the medial arch appears excessively high but flattens to a more normal profile when the patient stands. This type of pes cavus is mostly associated with a mobile forefoot valgus foot type. The constant adaptive changes in the foot shape between weight-bearing (stance) and non-weight-bearing (swing) result in excessive movements occurring in the foot joints proximal to the first metatarsal. Over time, and as the patient ages, the tarsal joints undergo degeneration, leading to reduced tarsal joint mobility, loss of the weight-bearing adaptation and increased weight-bearing arch height (see tarsal arthritis).

Treatment of pes cavus

The treatment of pes-cavus-type feet will depend on the presenting symptoms, the resultant gait dysfunction, and the degree of foot-joint mobility. The rigid-type pes cavus foot requires orthoses that cushion and increase shock absorption. The mobile-type pes cavus foot requires dynamic orthoses that maximise foot function and minimise joint deformity. The increase in height of the midfoot means that it can be difficult to obtain footwear that is a good fit and does not traumatise the foot. There are a number of surgical procedures that are indicated to reduce some of the deformity of rigid pes cavus, or to correct the secondary pathologies that characterise mobile pes cavus. The reader is referred to the abundance of literature on this topic.

Normal anatomy of the first ray

The first ray is formed by the medial column of the mid- and forefoot; that is, by the medial cuneiform, the first metatarsal, and the proximal and distal phalanges of the hallux, and their interposed joints i.e. the first metatarsal–cuneiform joint, the first MTPJ and the interphalangeal joint of the hallux.

The first metatarsal–cuneiform joint is a synovial joint that forms the articulation between the base of the first metatarsal and the medial cuneiform bone. The axis of the first metatarsal–cuneiform joint is oriented from proximal–medial–plantar to distal–lateral–dorsal.

The first MTPJ is a synovial joint that forms the articulation between the head of the first metatarsal and the base of the proximal phalanx of the hallux, and of the plantar aspect of the head of the first metatarsal and the sesamoid bones that are embedded within the tendon of the flexor hallucis brevis muscle.

• The sesamoids are two small bones that reinforce the tendon of the flexor hallucis brevis muscle at the point where it crosses the plantar aspect of the first MTPJ. The deep aspects of the sesamoids articulate with the grooves at the plantar aspect of the head of the first metatarsal. The sesamoids have a number of ligamentous attachments to adjacent structures:

the medial (tibial) sesamoid ligament inserts into the medial collateral ligament of the first MTPJ and the lateral (fibular) sesamoid ligament inserts into the lateral collateral ligament of the first MTPJ (Fig. 4.10C);

the sesamoids have strong fibrous attachments with the deep transverse ligament (Fig. 4.10D);

the sesamoids have a number of functions that are essential to normal walking and weight bearing. They increase the strength and prevent wear and tear of the flexor hallucis brevis tendon, provide a groove through which the flexor hallucis longus tendon passes as it crosses the plantar aspect of the first MTPJ, increase the functional depth of the head of the first metatarsal, increase the relative length of the lever arm of the foot and lower limb and, most importantly, provide an articular surface against which the head of the first metatarsal can plantar flex at toe-off. When the sesamoids are compressed into the grooves of the plantar aspect of the first metatarsal head, the first MTPJ is stabilised and abduction of the hallux at the first MTPJ is restricted (Phillips 1994).

Figure 4.10 The first metatarsal head: functional anatomy. (A) Sagittal plane motion of the hallux (dorsiflexion/plantar flexion) occurs about the transverse axis of the first MTRJ. Transverse plane motion of the hallux (abduction/adduction) occurs about the vertical axis of the first MTPJ. (B) The articular cartilage at the head of the first metatarsal covers the dorsal, medial/lateral and plantar elements. (C) The joint capsule is thickened at the medial and lateral aspects to form the medial and lateral collateral ligaments of the first MTPJ. (D) The sesamoid bones that lie within the paired tendons of the flexor hallucis brevis have ligamentous attachments to the medial and lateral collateral ligaments of the first MTPJ and the base of the proximal phalanx.

The sesamoid complex helps maintain the integrity of the first MTPJ and its associated soft tissue structures:

Figure 4.11 Proximal phalanx of the hallux.

Tendons crossing the first MTPJ insert into the proximal phalanx and the sesamoids complex:

Figure 4.12 Fibrous attachments of the sesamoid complex and the proximal phalanx (ligamentous structures around the first MTPJ).

Planar movements at the normal first metatarsophalangeal joint

Active weight-bearing movement at the normal first MTPJ includes:

Incidence of hallux abducto valgus

Hallux abducto valgus affects approximately 1% of all adults. It occurs more often in females, with a male/female ratio of incidence of 1 to 4 (Ferrari et al 2004). There is an age-related increase in incidence, such that 16% (approximately 1 in 6) of people aged over 60 years have a degree of hallux abducto valgus (Gould 1988). There appears to be a genetic predisposition to the development of hallux abducto valgus, although congenital hallux abducto valgus (i.e. hallux abducto valgus noted at birth) is rare.

Aetiology of hallux abducto valgus

There is no one single cause of hallux abducto valgus, rather the condition develops over time, in association with a range of intrinsic (within the lower limb and foot) and extrinsic (e.g. systemic disease) factors. Variants of normal foot anatomy can also predispose to the development of hallux abducto valgus (Ferrari & Malone-Lee 2002). Contrary to popular lay opinion, shoes, such as high-heeled shoes with a small toe box, or tight-fitting shoes, do not cause hallux abducto valgus. However, high-heeled and tight, narrow shoes exacerbate the signs and symptoms of an existing hallux abducto valgus and its associated soft tissue pathologies, and facilitate intrinsic features within normal foot anatomy and function that predispose to the development of hallux abducto valgus.

Factors that predispose to the development of hallux abducto valgus

Factors that predispose to the development of hallux abducto valgus include intrinsic features of the lower limb and foot, extrinsic features related to systemic pathology, and certain variants of normal foot anatomy.

Pathology of hallux abducto valgus

There are a number of pathomechanical factors that contribute to the pathology of hallux abducto valgus. These include:

The influence of the position of the sesamoid complex (Fig 4.13)

Sesamoid function is severely compromised by the deformities and foot dysfunction that characterise hallux abducto valgus, and sesamoid dysfunction exacerbates hallux abducto valgus. When the relationship of the sesamoids within the first MTPJ complex is altered, as in hallux abducto valgus, joint stability is decreased and the ability of the hallux and first ray to further resist deforming forces is greatly reduced.

• A tendency to first metatarsal eversion at toe-off, as in metatarsus primus varus, imposes an unequal loading on the sesamoid complex at the plantar aspect of the first MTPJ, so that the medial (tibial) sesamoid receives a greater proportion of ground reaction forces than the lateral sesamoid.

• In an adductus foot, the distal (head) end of the first metatarsal moves medially at toe-off. Tension is created within the plantar joint capsule, generating pressure between the lateral (fibular) side of the medial sesamoid and the medial aspect of crista (the ridge of bone that separates the medial and lateral sesamoid grooves on the plantar aspect of the metatarsal head). The crista tends to undergo resorption, allowing the sesamoids to maintain their normal orientation within the flexor hallucis brevis tendon but becoming disarticulated from their normal position on the plantar aspect of the head of the first metatarsal. There is an apparent lateral drift of the sesamoids.

• The location of the medial sesamoid into the lateral sesamoid groove and the lateral sesamoid to the space between the first and second metatarsals effectively decreases the dorsiplantar dimension of the medial part of the head of the first metatarsal, so that an even greater degree of foot pronation will occur at toe-off.

• The lateral deviation of the hallux on the head of the first metatarsal is characterised by disuse atrophy of the articular cartilage, erosion of the subchondral bone, medial bone proliferation at the head of the first metatarsal, and thus increasing compromise of joint function.

• Adduction of the head of the first metatarsal, as in metatarsus primus varus, causes tension in the medial part of the capsule of the first MTPJ, in the medial collateral ligament and in the medial sesamoid ligament. The structures within the medial capsule stretch and allow the head end of the first metatarsal to adduct further.

• Under the principles of Davis’ law, soft tissue structures at the lateral side of the first MTPJ contract and shrink, and thus maintain the abducted position of the hallux.

Figure 4.13 The position of the medial sesamoid in relation to the midline (crista) on the plantar aspect of the head of the first metatarsal (Palladino 1991). Positions 1–3 allow the medial sesamoid to articulate with the medial plantar groove on the plantar aspect of the head of the first metatarsal and maintain the stability of the first MTPJ. A medial sesamoid in position 4–7 cannot locate to the medial groove. The crista becomes eroded and the medial sesamoid ‘drifts’ laterally. The stability of the first MTPJ is lost and, together with the ‘bow string’ effect of contraction of the extensor hallucis longus and flexor hallucis longus muscles, there is little to oppose further abduction of the hallux.

Clinical picture in hallux abducto valgus

The patient presents with pain in and around the first MTPJ area. Pain is exacerbated by activity, aggravated by tight or high-heeled shoes, and relieved to some extent by rest or a change of shoe style. The patient is usually concerned about the unsightly appearance of the medial ‘bunion’, the lesser toe deformities and associated nail pathologies characteristic of the foot with hallux abducto valgus, and the difficulty of obtaining shoes to accommodate the increased width of the forefoot. In addition to the symptoms that the patient reports, the clinician notes: metatarsus primus varus and hallux abducto valgus; a medial eminence at the head of the first metatarsal, which is often overlain with a large bursa; a reduced range of dorsiflexion at the first MTPJ, with pain and/or crepitus on passive movement of the hallux; palpable marginal osteophytes at the first MTPJ; second-toe hammer deformity with associated subluxation of the second toe at the second MTPJ; clawing and/or varus rotation (supination) of the third/fourth/fifth toes; rearfoot and/or forefoot varus; a range of nail pathologies; and hyperkeratotic lesions on the toes and plantar forefoot (Fig. 4.14).

Figure 4.14 The typical pattern of deformity and forefoot lesions with hallux abducto valgus.

Clinical examination in hallux adducto valgus

The underlying, principal cause of the hallux abducto valgus deformity must be determined. This is achieved from the patient history, from a physical examination of the foot and limb (both weight bearing and non-weight bearing) and a biomechanical evaluation of lower limb and foot function.

In the relatively healthy patient, the development of hallux abducto valgus is usually associated with biomechanical and intrinsic factors. Extrinsic factors associated with hallux abducto valgus will either predispose the patient to develop the condition as a direct result of the systemic disease process, or exacerbate any natural tendency to hallux abducto valgus due to inherent intrinsic factors. For example, patients with rheumatoid disease tend to develop marked eversion of the rearfoot, due to the effects of inflammatory arthritis within the subtalar joint. The resultant excessive whole-foot pronation, together with the generalised connective tissue inflammation that characterises the disease (e.g. vasculitis, synovitis, capsulitis, tendonitis, bursitis), predisposes to instability at all forefoot joints, with severe hallux abducto valgus and marked lesser toe deformities.

The biomechanical evaluation should include examination of the lower limb and foot to note:

Non-weight-bearing examination

With the patient in a non-weight-bearing position, the following should be assessed:

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• The position of the hallux on the horizontal plane, in relation to the second toe.

Lateral deviation of the hallux may result from subluxation of the hallux at the first MTPJ, or relate to structural changes within the hallux, such as hallux interphalangeus valgus.

The hallux may override, underride, abut, or not contact the second toe.

Where the extensor hallucis longus has a greater pull than the flexor hallucis longus, the hallux tends to hyperextend and rotate in relation to the frontal plane, so that the medial (tibial) nail wall becomes weight bearing, and the plantar aspect of the pulp of the hallux tends to override the dorsum of the second toe, causing the second toe to adopt a hammer position.

Where the flexor hallucis longus has a greater pull than the extensor hallucis longus, the hallux tends to underride the second toe, and the second toe tends to dislocate at the second MTPJ.

• The medial eminence: this is formed by the hypertrophy of the medial and dorsomedial aspects of the head of the first metatarsal. Its junction with the dorsomedial aspect of the head of the first metatarsal is marked by a ‘sagittal groove’.

The medial eminence is usually associated with the formation of an adventitious bursa within the overlying soft tissues.

The bursa may become very large and fluctuant and be subject to inflammation (bursitis), chilling, tissue breakdown and infection. It is often termed a ‘bunion’.

• The available range of motion at the first MTPJ: the first MTPJ complex should be taken through its full range of movement (dorsiflexion and plantar flexion, adduction and abduction, inversion and eversion, clockwise and anti-clockwise circumduction) to identify pain, crepitus, restriction or excess movement.

The normal non-weight-bearing range of motion at the first MTPJ is 65–70° of dorsiflexion and 15–20° of plantar flexion. The range of dorsiflexion is usually decreased in hallux abducto valgus.

The quality of the motion at the first MTPJ should be noted, especially the presence of pain and/or crepitus, which indicates damage to the intra-articular cartilage. Pain on movement without crepitus is indicative of synovitis at the first MTPJ.

The degree of abduction of the hallux at the first MTPJ is examined to determine whether the abduction deformity can be corrected passively. An abducted hallux that cannot be passively placed into a corrected (rectus) position indicates contracture and shrinkage of soft tissues at the lateral aspect of the first MTPJ.

• The range of motion at the first ray: the normal range of motion of the first ray at the level of the first MTPJ is 5 mm dorsiflexion and 5 mm plantar flexion (10 mm overall). The resting position of the first ray with the foot in subtalar joint neutral should be assessed by comparison to the position of the second ray, and both should lie in the same plane, and parallel to the ground surface.

With hallux abducto valgus, the first ray may be plantar or dorsiflexed relative to the second ray.

Transverse motion at the first metatarsal–cuneiform joint and the first MTPJ should be assessed: in a normal foot there is little to no transverse motion available in the medial column, but transverse plane motion is usually noted with hallux abducto valgus.

• The prominence of extensor hallucis longus tendon, and the path taken by the tendon should be noted.

The path of the extensor hallucis longus tendon on the dorsum of the first MTPJ reflects the path of the flexor hallucis longus tendon at the plantar aspect of the joint, and thus shows the degree of ‘bow-stringing’ of the extrinsic muscle tendons occurring in association with hallux abducto valgus.

A prominent extensor hallucis longus tendon indicates soft tissue contracture, hyperextension of the hallux at the first MTPJ, and/or hyperextension of the hallucal interphalangeal joint. It characterises a long-standing hallux abducto valgus deformity.

• The presence of plantar keratoses.

Hyperkeratosis in the plantar first MTPJ area indicates excessive plantar pressure at that site secondary to ankle equinus, rigid forefoot valgus, non-mobile pes cavus, a non-reducible plantar-flexed first metatarsal, prominent sesamoids, and/or atrophy of the plantar fat pad below the first MTPJ.

Focal plantar hyperkeratosis at the second metatarsal head can indicate a short first metatarsal (bradymetatarsal), a relatively long second metatarsal, a dorsiflexed first metatarsal (metatarsus primus elevatus), hypermobility of the first metatarsal and first ray, and retrograde pressure at the second metatarsal head secondary to deformity of the second toe (a hammered, clawed or retracted second toe).

Plantar hyperkeratosis in the second, third, fourth and fifth MTPJs area is associated with lesser toe deformities, where imbalance between the pull exerted by the extensor digitorum longus and the flexor digitorum longus muscles allows the toes to retract, claw or hammer, with resultant dorsiflexion of the proximal phalanges at the MTPJ. The base of the proximal phalanx exerts a plantarwards piston-like action at the dorsal aspect of the head of the metatarsal, and the metatarsal is forced into plantar flexion at toe-off, causing an increase in ground reaction forces at the overlying plantar skin and distal drift of the plantar fibrofatty padding.

Diffuse plantar hyperkeratosis in the second/third/fourth MTPJs area is associated with hypermobility of the foot, where the foot fails to supinate fully at toe-off. The height of the medial longitudinal arch is decreased in a pronated foot, and there is a relative lengthening of the foot at midstance that persists into toe-off. Shear forces at the plantar skin overlying the second/third/fourth MTPJs promote the formation of diffuse callosity.

• The presence of digital keratoses.

Hyperkeratosis at the medial–plantar aspect of the interphalangeal joint of the hallux indicates excessive foot pronation at toe-off.

Hyperkeratosis at the lateral (fibular) aspect of the hallux interphalangeal joint/medial (tibial) aspect of the proximal interphalangeal joint of the second toe indicates abduction of the hallux at toe-off.

The lesser toe deformities that characterise a foot with hallux abducto valgus predispose to apical, dorsal and interdigital callosity and corn formation. A deep helloma molle may form at the depth of the fourth/fifth interdigital sulcus, especially in association with sagittal hypermobility of the fifth ray.

• The presence of paraesthesia or reduced sensation at the medial and dorsomedial quadrant of the hallux.

Some patients note paraesthesia, pain or reduced sensation in the distribution of the cutaneous nerve, which serves the dorsomedial quadrant of the hallux. The nerve can be chronically irritated by exostoses at the medial/dorsal area of the first MTPJ (Camasta 1996).

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• The presence of pain and/or onychophosis and/or onychocryptosis at the hallux nail.

Pain in the medial or lateral nail sulcus arises in conjunction with axial rotation of the hallux, where the medial sulcus becomes weight bearing and/or the lateral sulcus is compressed against the medioplantar aspect of the second toe.

Subungual pain or a subungual corn indicates that the hallux is in a hyperextended position at toe-off.

• The presence of other forefoot deformities that form the classic clinical presentation of hallux abducto valgus include:

lesser toe deformities, such as hammered second and third toes; clawing of the third, fourth and fifth toes; axial rotation or supination of the third, fourth and fifth toes; and associated dorsal, interdigital and apical hyperkeratoses

tailor’s bunion formation, a similar but more minor deformity than hallux abducto valgus, affecting the fifth ray at the fifth MTPJ

a ‘diamond’-shaped forefoot due to first ray (metatarsus primus varus and hallux valgus) and fifth ray (metatarsus quinque valgus and digiti minimi varus) deformities, and flat foot (Fig. 4.14).

Diagnosis of hallux abducto valgus

The diagnosis of hallux abducto valgus is based on the clinical observation of the typical forefoot deformities, and associated hyperkeratotic skin lesions, together with reported pain in and around the first MTPJ, metatarsalgia and the presence of characteristic lesser toe deformities. The differential diagnoses should exclude inflammatory joint disease and other extrinsic factors that predispose to hallux abducto valgus.

Weight-bearing plain radiographs are taken to determine the extent of joint pathology and forefoot deformity prior to carrying out corrective surgery. Views include anteroposterior, lateral oblique, lateral and axial projections.

Table 4.2 First ray relationships (from an anteroposterior view radiograph)

Treatment of hallux abducto valgus

Treatment of hallux abducto valgus includes the conservative and symptomatic management of the soft tissue and nail pathologies that are associated with the forefoot deformities, orthotic therapy to address the biomechanical dysfunction that predisposes to the development of the condition, and surgical correction of the deformity.

Conservative and symptomatic management of nail and soft tissue pathologies

• Reduction of onychauxic nails and sharp debridement of onychophosis that forms in relation to the chronic trauma due to digital deformity.

• Regular sharp debridement of the areas of corn and hyperkeratosis that develop in relation to forefoot deformity, in association with the use of deflective and cushioning digital padding:

helloma molle at the interdigital aspects of the proximal and distal interphalangeal joints of adjacent toes and in the depth of the interdigital web spaces

digital helloma durum at the dorsum of the proximal interphalangeal joint in a hammer toe, the dorsum of the distal interphalangeal joint in mallet toe, or the apex in clawed toe

Durlacher corn at the lateral nail sulcus area in varus toe

plantar helloma durum at the MTPJ area of a toe with an associated fixed hammer deformity

diffuse plantar callosity at the lesser MTPJ areas.

• Anti-shear measures to reduce trauma to bony prominences:

clinical padding/strapping to reduce shear stress to the bursa at the medial aspect of the first MTPJ (see Ch. 16)

the use of an appropriate shoe style, such as flat shoes with a wide, deep toe box and positive fixing (laces) to accommodate the breadth of the forefoot, any clinical padding and in-shoe orthoses.

• The provision of bespoke or semi-bespoke shoes that will accommodate both the deformity and an orthotic, and/or shoe adaptations to the first MTPJ area:

stretch of the shoe upper to accommodate the medial eminence and lesser toe deformities

provision of a false bursa or balloon patch to accommodate the medial eminence and lesser toe deformities.

Orthotic therapy

• Palliative devices to correct non-fixed digital deformity, and to cushion and deflect plantar pressure, such as:

silicone orthodigita

moulded cushioned insoles to compensate for loss of the plantar forefoot fibrofatty pad

deflective plantar pads to support the medial longitudinal arch and reduce pressure on isolated plantar lesions.

• Dynamic orthoses to stabilise the rearfoot and midfoot and reduce excessive foot pronation. These are not indicated for patients with fixed rearfoot deformity or inflammatory arthritis.