(ii) Flatfoot deformity:an overviewKurt Thomas Haendlmayer

Nick John Harris

symptoms in previously symptom free individuals. A lot has been learned

about flatfoot deformity and a more sensible approach based on symp-

near-

o the

talus. This talo-navicular subluxation is either a contributing

MINI-SYMPOSIUM: FOOT AND ANKLEtoms and expected disability has been adopted.

The adult acquired flatfoot is a complex condition, commonly caused

by posterior tibial tendon deficiency (PTTD). Management of these

patients is based on a thorough assessment of the underlying pathology.

In this article we give an overview of the condition, with emphasis placed

on assessment and management of the more common causes.

Keywords acquired adult flatfoot; flatfoot; paediatric flatfoot; posterior

tibial tendon

Introduction

Flat foot (pes planus) in its various types is a common complaint

in general orthopaedic or more specialised foot and ankle clinics.

A large number of these present in patients without symptoms of

pain or functional deficit. These simply need advice and reas-

surance, especially for the parents of young children under the

age of seven, where flat feet are very common, asymptomatic

and should not cause any concern; they do not need surgical

management, and only very rarely orthotic treatment. Pfeiffer

et al1 found flat feet (valgus 5e20) in 44% of children age 3e6.In the same study group, they found less than 1% pathological

(valgus more than 20) flat feet (7 from 835).1

Kurt Thomas Haendlmayer FRCS (Trauma & Orthopaedics and Sportsmedicine)

Foot & Ankle Fellow Leeds Teaching Hospitals NHS Trust, Leeds General

Infirmary, Great George Street, Leeds, UK.

Nick John Harris FRCS (Trauma & Orthopaedics) Consultant Orthopaedic

Surgeon at the Leeds Teaching Hospitals NHS Trust, Leeds General

Infirmary, Great George Street, Leeds, UK.AbstractFlatfoot deformity is a common complaint with various etiologies. It

causes confusion as to when and how to treat it. Unnecessary treatment

is a problem, especially in asymptomatic flexible paediatric flatfoot. The

human foot is a sophisticated biomechanical structure. Interference

with this complicated system of joints, ligaments, tendons and muscles

has to be based on a sound knowledge of anatomical structures and

their interactions. It is therefore important for every doctor dealing with

this condition to be able to differentiate between cases needing treat-

ment and cases that simply need reassurance. Historically, flatfoot defor-

mities have been over treated with the aim to correct deformity, in the

process not only failing to achieve the desired correction but also creatingORTHOPAEDICS AND TRAUMA 23:6 395factor to pes planus or a biomechanical consequence of existing

flatfoot of other causes. As a consequence of the varying

anatomic conditions, the lateral column of the foot is short in

relation to the medial column.

Recognition of these anatomic factors is especially important

when surgical intervention is indicated.

Paediatric flatfoot

Flexible flatfoot

The physiological flatfoot is usually flexible, and normal arches

can be observed in non-weight-bearing feet and when standing

on tip toes. It is a mostly asymptomatic condition, but mild

symptoms can occur.

Asymptomatic flexible flatfoot: all children are born with flat

feet and it might take until the age of 7e10 before the normal

arch develops fully. The vast majority of these children are

asymptomatic, with no functional deficit. The natural history is

of gradual improvement over time and treatment is not indicated.

Advice to parents is usually sufficient. Even after the age of 10,

a full arch might not develop, accounting for the fact that mostly

asymptomatic flexible flat feet are present in about 20% of the

adult population.2

The management of asymptomatic, non-physiological flat feet

consists of observation initially, to check for progression.might be subluxed in a dorso-lateral direction in relation tcomplete contact with the ground.

Aetiology of flatfoot deformities

Table 1 lists the most common causes of flatfoot deformity in the

adult and paediatric population. By far the most common in both

groups is the physiological or idiopathic flatfoot. The commonest

cause for acquired adult flatfoot is dysfunction of the posterior

tibial tendon.

Anatomical considerations

Flatfoot deformity is always a result of a combination of several

anatomic factors. Hyperpronation and/or increased eversion in

the subtalar joint is often present. The calcaneum in relation to

the talus is in external rotation and valgus. The navicular bonein which the entire sole of the foot comes into complete orTherefore, it is vitally important for the treating orthopaedic

surgeon to be clear about the different types of flatfoot deformity:

congenital or acquired, flexible or rigid, adult or paediatric. It is

also important to understand the biomechanics of the foot and

the relations of forefoot to midfoot to hindfoot in order to identify

and treat the underlying cause correctly.

In this article we give an overview of the current concepts

regarding flatfoot deformity, its diagnosis and management,

bearing in mind that the patients symptoms, disability or

expected disability (if left untreated) are the driving forces to

instigate treatment, not the flatfoot deformity itself, which in the

majority of cases causes no, or minimal, symptoms.

Definition

Flat feet (Figure 1) is a medical condition with varying aetiology, 2009 Elsevier Ltd. All rights reserved.

Patients with a tight Achilles tendon might benefit from

stretching, with the aim of preventing progression. Orthoses are

sometimes helpful.

Figure 1 Lateral X-ray showing flatfoot with increased talo-metatarsalangle.

MINI-SYMPOSIUM: FOOT AND ANKLESymptomatic flexible flatfoot: symptomatic forms of flexible

flatfoot produce subjective complaints and can have an effect on

function. Patients complain of pain along the medial border of

the foot, in the sinus tarsi, but pain can also be produced in

knees, hips and the lower back. Gait disturbances and reduced

endurance are features. Findings on examination are a prominent

talar head, everted heel and tight Achilles tendon.

Pathological flexible flatfoot is characterised by a more severe

degree of the deformity and progression over time. Other findings

in pathological flat feet can include excessive heel eversion, an

unstable talo-navicular joint, a tight Achilles tendon and on

occasions gait disturbances.

Causes for flatfoot deformity in children and adultsrmalPaediatric flatfoot Adult flatfoot

Physiological Physiological ongoing

from childhood

Inflammatory

- Juvenile rheumatoid arthritis

Inflammatory

- Rheumatoid arthritis

- Seronegative

spondylarthropathies

Connective tissue disorders

- Marfan, Ehlers-Danlos

Posterior tibial tendon

dysfunction

Osteoarthritis

Neurological

Accessory navicular bone

Connective tissue disorders

Post-traumatic

Adult tarsal coalition

Iatrogenic

Neurological disorders

- Cerebral palsy

Tarsal coalition

- Talcalcaneal

- Calcaneonavicular

- Rarer other coalitions

Table 1

ORTHOPAEDICS AND TRAUMA 23:6 396longitudinal arch. Tarsal coalitions are most probably present at

birth but cause symptoms only with increasing maturation of the

skeleton, increasing bodyweight and activity levels. Symptoms

might first present after bouts of vigorous activity. Symptoms in

very young children are rare due to the flexibility of the cartilage

surrounding the primary ossification centres. With progressing

ossification, hindfoot stiffness increases and the ability to with-

stand external stresses decreases, leading to symptoms. Incom-

plete coalitions (fibrous or cartilagenous) often lead to vague,

non-specific foot pain and walking difficulties, especially on

uneven surfaces. Symptoms worsen with increasing age. If

peroneal spasticity due to shortening of the peroneal muscles is

observed, the condition is also called peroneal spastic flatfoot.

Calcaneonavicular coalition e calcaneonavicular coalition

most commonly manifests in children aged 8e12. The coalition

runs from the anterior process of the calcaneus to the lateral and

dorso-lateral extra-articular surface of the navicular bone. It canlittle evidence of pes planus. Most patients, however, have

hindfoot valgus, loss of subtalar motion and loss of the noTreatment consists of activity modification, orthoses and

physiotherapy. In severe cases, non-steroidal anti-inflammatory

medication can be administered. Patients can present with co-

morbidities such as obesity, ligamentous laxity, hypotonia or

proximal limb problems. These need to be identified and

addressed then patients need observation at regular intervals.

If the response to non-operative measures is satisfactory and

the clinical symptoms are resolving, observation and orthoses

might be sufficient. Surgical intervention can be considered if the

clinical response is inadequate.

Surgery can consist of soft tissue procedures, bony procedures

or combinations thereof. Soft tissue procedures alone are rarely

successful in the long term treatment of the flexible flatfoot. Bony

procedures include osteotomies of the forefoot, midfoot and

hindfoot, lateral column lengthening and medial displacement

osteotomy of the calcaneum. These can be combined with

Achilles tendon lengthening and medial plication.

Rigid paediatric flatfoot

Features of rigid flatfoot are a low arch in both weight-bearing

and non-weight-bearing feet, with motion in the midfoot and

hindfoot reduced or absent.

The differential diagnosis includes congenital vertical talus,

tarsal coalition, peroneal spastic flatfoot without coalition,

iatrogenic and post-traumatic flatfoot.

The underlying primary pathology can be diagnosed with

a good history, clinical examination and appropriate imaging.

Tarsal coalition: Tarsal coalition is an abnormal, congenital

union between two or more tarsal bones. It can be osseous

(synostosis), cartilagenous (synchondrosis) or fibrous (syndes-

mosis). The prevalence is 1e2%. Autosomal dominant inheri-

tance with reduced penetrance has been proposed.3,4

Calcaneonavicular and talocalcaneal (middle facet) coalitions are

the most common, accounting for about 90% of tarsal coali-

tions.3 Other rarer coalitions are talonavicular, calcaneocuboid,

naviculocuboid and naviculocuneiform. About 50% of coalitions

are bilateral. The degree of deformity varies, and particularly in

calcaneonavicular coalitions the coalition can be minimal, with

fixed 2009 Elsevier Ltd. All rights reserved.

fibrous or cartilaginous coalitions is, however, recommended by

most authors. As described for calcaneonavicular coalitions, the

presence of arthritic changes makes excision of the coalition

alone less likely to be successful and arthrodesis procedures are

more likely to be required.

The decision making process should be individualised for

each case.

Congenital vertical talus: congenital vertical talus (CVT), also

named rocker-bottom flatfoot or congenital rigid flatfoot, can

usually be detected directly after birth (Figures 2 and 3). It can be

isolated or part of a syndromic disorder. It is associated with

arthrogryposis and myelomeningocele.10

The normal longitudinal arch of the foot is reversed to the

extent that the sole of the foot becomes convex. This is caused by

the talus being in abnormal plantar flexion with the talar head

MINI-SYMPOSIUM: FOOT AND ANKLEbe up to 2 cm long and 2 cm wide. Symptoms consist of pain,

often directly over the abnormal coalition, but can be unspecific

and mimic simple sprains. Clinical examination reveals hindfoot

valgus, a reduced longitudinal arch and reduced subtalar

movement, which can be subtle and difficult to determine,

especially in bilateral cases. Some coalitions are asymptomatic

and can present as coincidental findings on radiographs, CT or

MRI scans that have been performed for other indications.

The diagnosis can usually be made with standard radiographs,

including a 45 lateral oblique view. In some cases an anteaternose sign can be observed on lateral radiographs.5 CT andMRI are

also important diagnostic tools. CT is useful for pre-operative

planning. MRI scans show surrounding or intraosseous oedema.

Treatment initially should include activity and footwear

modification or cast immobilisation for 4e6 weeks. If symptoms

are not relieved by these methods, or if they return after initial

success, surgical treatment can be recommended. Early onset of

the symptoms of calcaneonavicular coalitions (below age 10) is

more likely to lead to surgical intervention, as symptoms are

expected to worsen with progressing skeletal maturity.

The chosen surgical procedure depends on the age of the

patient and the presence of secondary degenerative changes in

adjacent joints. Resection of the calcaneonavicular bar, with or

without interposition of fat or muscle tissue, is indicated in

young adolescents after failed conservative treatment and in the

absence of secondary arthritic changes. If beaking of the talar

neck is observed, this indicates early degenerative changes in the

subtalar joint. In these cases simple excision of the bar can still

be attempted but is less likely to lead to a complete eradication of

symptoms. In the presence of advanced arthritic changes in the

subtalar joint, triple arthrodesis is the treatment of choice.

Subtalar coalition e subtalar coalition tends to become

clinically symptomatic in 12e14-year-old children. The most

consistent sign is a reduction or absence of subtalar motion. The

symptoms are similar to calcaneonavicular bars, with pain in the

hindfoot and loss of the longitudinal arch. Peroneal muscle

spasm is more common in talocalcaneal coalition, compared to

calcaneonavicular coalition.

Subtalar coalitions can involve multiple facets but most

consistently affect the middle facet.6 Anterior or posterior facet

coalitions are very rare.

The diagnosis is made on CT scan. Coronal views with the feet

plantarflexed are recommended for best visualisation.7 It is rarely

possible to diagnose subtalar coalitions with X-rays alone. The

great variability in hindfoot anatomy makes standard radio-

graphs unreliable, even when using special angles. Therefore, CT

is the gold standard for diagnosis of talocalcaneal coalitions.

Treatment consists of activity modification, adjusting foot-

wear or cast immobilisation. Should initial non-operative treat-

ment fail, surgery is indicated. Options for the surgical treatment

of subtalar coalition includes excision of the coalition or triple

arthrodesis, with or without calcaneal osteotomy. There is

debate in the literature as to what extent talocalcaneal coalitions

can be successfully excised. Some recommend excision of all

symptomatic coalitions when conservative treatment has failed,

regardless of the extent of the coalition, whereas others recom-

mend that only those coalitions involving less than 50% of the

talocalcaneal joint should be exicsed.8,9 Excision of early, smallORTHOPAEDICS AND TRAUMA 23:6 397pointing medially. The calcaneum also takes up an equinus

position, causing shortening of the Achilles tendon. The talo-

navicular joint is dislocated, with the navicular lying on the

dorsal aspect of the talar head, with resulting dorsiflexion of the

whole forefoot. This causes deep creases on the dorsal and lateral

aspect, in front and inferior to the lateral malleolus. Without

treatment, adaptive changes in bones and soft tissues will occur

and correction of the deformity becomes more and more difficult

with time. Weightbearing leads to callosities underlying the

anterior aspect of the calcaneus and the medial border of the foot

over the talar head. The forefoot becomes severely abducted and

the heel cannot touch the ground. Contractures of soft tissues

occurs. Tendon units will either loose function or adapt to

abnormal function, for example the peroneal tendons come to lie

anterior to the ankle and act as dorsiflexors.

CVT can be diagnosed by clinical examination and adequate

radiographs, which should include anteroposterior views and

plantar flexion lateral stress views. In the normal situation, the

long axis of the first metatarsal passes plantarward to the long

axis of the talus in a lateral plantar flexion stress view, whereas

in CVT the long axis of the first metatarsal runs dorsal to the long

axis of the talus, reversing the normal angle.

Correction of CVT is difficult and can rarely be achieved

without surgery. Non-surgical methods involve gentle manipu-

lations followed by casting. This helps to prevent contractures of

the dorsal structures and facilitates surgical correction later. The

Figure 2 Clinical photograph showing rocker-bottom deformity in

congenital vertical talus. 2009 Elsevier Ltd. All rights reserved.

military recruits did not find significant differences in injury rates

for different arch heights.13 Jones et al concluded after an

extensive search of the literature, that arch height is likely to be

a risk factor for metatarsal fatigue fractures.14

Posterior tibial tendon dysfunction (PTTD)

PTTD (Figure 4) is the most common cause of adult acquired

flatfoot. It has been suggested that PTTD is not solely responsible

for causing acquired adult flatfoot, and that other structures are

also failing in the development of acquired flatfoot. Deland et al15

examined cadaver models after severing the PTT. They then

subjected the foot to axial loads in an attempt to reproduce the

adult acquired flatfoot. Cutting the PTT alone produced minimal

arch collapse or valgus rotation of the hindfoot. To achieve

significant collapse of the hindfoot and midfoot (as seen in Stage

II and Stage III PTTD), the spring ligament complex, plantar

aponeurosis, deltoid ligament, talocalcaneal ligament, long and

MINI-SYMPOSIUM: FOOT AND ANKLEIn the adult population, flexible flatfoot deformity is common,

and in most cases it is asymptomatic. It usually represents

a progression from paediatric flatfoot.

The most common cause of acquired adult flatfoot is

dysfunction of the posterior tibial tendon, which is typically

unilateral and progresses from flexible to rigid adult flatfoot.

Other causes are trauma, types of arthritis, prolonged or

unusual stresses to the foot, defective biomechanics or it can

simply develop as part of the normal ageing process. Most

commonly, it is a combination of several of these factors. Flat

feet can also develop during pregnancy, due to increased

elasticity combined with increased strain due to increased

weight. Flat feet acquired as an adult will usually remain flat as

normal arches can only develop in the growing skeleton. The

adult flexible flatfoot can develop into a rigid flatfoot, where the

soft tissue structures are stretched out and as a result in the end

stage, the bony skeleton develops arthritic changes, with fixedFlexible adult flatfoottalo-navicular joint cannot usually be reduced by manipulation

alone and needs open reduction in almost all cases.

Surgery depends on the age of the child and the severity of the

deformity. Children from 1 to 4 years old are treated with open

reduction of the talo-navicular and subtalar joints, which

involves extensive dorsal soft tissue releases, posterior capsular

releases of the ankle and subtalar joint and lengthening of the

Achilles tendon with a Z-plasty. In older children (3 years) withsevere deformity, excision of the navicular has been described.

Children aged 4e8 might need extra-articular subtalar arthrod-

esis in addition to open reduction and soft tissue releases. Chil-

dren older than 12 years need triple arthrodesis for deformity

correction.

Procedures are often performed in several stages in order to

allow the soft tissues to adapt to the new position.

Adult flatfoot

Figure 3 X-ray showing congenital vertical talus.positions.

Treatment of adult flexible flatfoot should be reserved for

symptomatic cases, as it will not make any difference to

asymptomatic patients. It will not create a lasting arch and

overenthusiastic treatment can even be the cause of symptoms.

No amount of exercise, however useful it might be overall for the

individual, can change the appearance of a flatfoot. Studies

comparing two groups of individuals with high arches and low

arches found a tendency to a lower injury rate in individuals with

low arches.11 A study of Israeli soldiers found an almost four

times higher incidence of stress fractures in those with high

arches compared to those with low arches.12 Other studies of

ORTHOPAEDICS AND TRAUMA 23:6 398Figure 4 Intra-operative photograph showing diseased posterior tibial

tendon with longitudinal split and synovitis within the opened tendon

sheath.short plantar ligament, and medial calcaneal-cuboid ligament

had to be cut as well.

This supports the theory that the adult acquired flatfoot is not

caused by rupture of the PTT alone. Other ligaments must also

fail to produce deformities and the clinical pictures seen in Stage

II and Stage III deformities.

Similar conclusions have been drawn from examinations of

feet after PTT transfer that did not develop a flatfoot deformity

after 6 years of follow-up.16

The development of a flatfoot in tibialis posterior tendon

dysfunction is unlikely to be the result of PTTD alone. The adult

acquired flatfoot is more likely the result of complex biome-

chanical failures in the foot and ankle that ultimately cause

overload of the PTT during life.

The underlying pathology is within the posterior tibial tendon

itself, which is usually unilateral. Typically, it affects women aged

45e65years. The history often reveals pre-existing flatfoot defor-

mity, positive family history for flatfoot, or minor trauma. Patients

often report overuse activity before the onset of initial symptoms.

Symptoms may present at any stage of this condition, but are

often not immediately recognised as relating to PTTD, which can

lead to delayed diagnosis.

Anatomy: the posterior tibial muscle originates from the poste-

rior surface of the interosseous membrane and the adjacent tibia 2009 Elsevier Ltd. All rights reserved.

MINI-SYMPOSIUM: FOOT AND ANKLEand fibula. The tendon curves at an acute angle around the

posterior medial malleolus in a shallow groove. The groove is

covered by the flexor retinaculum, which ties the tendon firmly

down. It passes underneath the calcaneonavicular ligament and

inserts into the navicular tuberosity, but it is unique in that it also

has insertions into the sustentaculum tali, all the cuneiforms, the

cuboid and into the bases of metatarsals two, three and four. It

passes posterior to the axis of the ankle joint and medial to the

subtalar axis, therefore acting as plantar flexor and inverter of the

hindfoot. Through its many insertions into the midfoot, it acts as

a forefoot supinator and adductor. The posterior tibial tendon

runs in a synovial sheath, which extends from approximately

4e5 cm proximal to 3 cm distal to the tip of the medial malleolus.

Its sheath is unique as it does not contain a complete mesotenon,

and the tendon therefore relies on its blood supply via other

routes.

Apart from inversion, plantar flexion, supination and forefoot

adduction, the posterior tibial tendon also acts as a hindfoot

stabiliser against valgus forces. It is active in the stance phase of

the gait cycle, from heel strike to toe lift-off, decelerating the

pronation forces to the subtalar joint after heel contact, and then

it stabilises and locks the transverse tarsal joint at midstance.

This maximises the effects of the soleusegastrocnemius complex

during plantar flexion. By adducting and supinating the forefoot,

the PTT also allows the soleusegastrocnemius complex to

become the primary invertor of the subtalar joint. This optimises

the leverage so that forces can be transferred efficiently, espe-

cially in the propulsive phase of the gait cycle. The peroneus

brevis muscle is the primary antagonist, abducting the midfoot

and everting the hindfoot.

Stabilisation of the longitudinal arch is provided by static and

dynamic forces. There is still debate whether the static forces act

as a truss or a beam. A truss has two struts meeting at an apex,

represented in the foot by the arch.17 These struts are connected

at their base by a tie, the plantar aponeurosis, and as long as the

tie remains intact the arch cannot collapse. This is closely

represented by a windlass mechanism. A beam is a less rigid

structure. In the foot the beam is curved, which on loading

creates compression at the convex side and tension on the

concave side. Tension therefore directly affects the plantar liga-

ments stabilising the arch, namely the long and short plantar

ligament, the spring ligament (calcaneonavicular) and the

bifurcate ligament. All of these ligaments are insertion sites for

the posterior tibial tendon.18

The posterior tibial tendon and the intrinsic muscles of the

foot act as dynamic arch supports.

Aetiology: the cause of posterior tibial tendon dysfunction is

subject to much debate. It is most likely multifactorial. Although

many underlying causes have been identified, a clear uniform

opinion does not exist. Possibilities are spontaneous rupture,

progression from congenital flexible flatfoot, trauma, repetitive

microtrauma, inflammatory causes, collagen disorders, vascular

causes or the presence of an accessory navicular bone.

Spontaneous rupture of an intact tibialis posterior tendon is

unlikely, and what might appear to be a spontaneous rupture is

likely to be the endstage of a degenerative process within the

tendon that might not have caused noticeable symptoms until

rupture occurs.ORTHOPAEDICS AND TRAUMA 23:6 399Trauma is rare as a cause for PTT rupture but cases have been

reported, especially with medial malleolar fractures.19 Reports of

an initiating traumatic event leading to rupture range from 14%

in elderly patients20 to 50% in a younger patient group.21 Again,

trauma leading to rupture of the PTT is more likely on the basis

of an already diseased tendon, even in the absence of pre-existing

symptoms.

Repetitive microtrauma to the tendon can lead to tendon

disruption through an inflammatory response. Microtears can be

caused by overloading and if these are repetitive, the damage

cannot be repaired and chronic inflammation can result.

Inflammation as a primary cause for PTT dysfunction and

rupture is also debated. In rheumatoid arthritis it is difficult to

ascertain which pathological process is responsible for PTT

failure. It is most likely a combination of effects specific to

rheumatoid arthritis. Rheumatoid disease can lead to flatfoot via

several pathways, e.g. joint destruction with resulting hindfoot

valgus and destruction of the ligament complexes of the subtalar

and talo-navicular joints. The resulting valgus deformity puts

enormous stresses on the PTT to counteract the deformity. Several

studies suggest that rheumatoid arthritis might not be linked

directly to destruction of the PTT. Kirkham and Gibson found no

PTTD in 50 patients with rheumatoid arthritis, collapsing

arches and hindfoot valgus.21 Similarly, Jahss found a normal

PTT in patients undergoing arthrodesis for symptomatic flat-

foot.22 There is evidence that the PTT is actually working harder

to counteract the valgus forces caused by rheumatoid arthritis, as

shown in an electromyographic study by Keenan et al.23

An epidemiological study by Holmes and Mann found

a correlation between PTTD and obesity, hypertension, diabetes

and steroid use.24 All of these conditions can compromise the

blood supply to the posterior tibial tendon directly or indirectly.

The blood supply to the PTT arises mainly from the posterior

tibial artery, with the most distal portion of the tendon receiving

a supply from the dorsalis pedis artery. Several authors have

examined the blood supply to the PTT. Frey et al found a hypo-

vascular zone of approximately 14 mm length at a distance of 40

mm from insertion.25 This corresponds roughly with the tip of

the medial malleolus. In this zone the authors found no meso-

tenon and also a hypovascular synovial sheath. This theory is

supported by the fact that the common location for tendon

rupture falls within this zone. Peterson et al found this zone to be

avascular using a different method.26 The avascular area is

exactly where the PTT is in direct contact to the bone at the level

of the medial malleolus. Further anatomical factors restricting

the tendons blood supply have been suggested. Jahss states that

the overlying flexor retinaculum can cause compression and

constriction through synovial swelling and as a consequence

causes degeneration of the tendon.22 Other authors state that

excessive friction at the sharp turn around the medial malleolus

can contribute to an inflammatory process.27

Another contributing factor to PTTD is thought to be changes

in the collagen content, type and orientation of the fibres. Given

the fact that in a normal tendon the collagen works perfectly, any

changes in the collagen content or type or orientation may reduce

the elastic qualities. Ageing changes the collagen structure.

Myxoid degeneration with increased mucin content, alters the

normal linear orientation of the collagen bundles of the tendon,

leading to a haphazard configuration of the collagen, which leads 2009 Elsevier Ltd. All rights reserved.

to decreased tensile strength with the potential endpoint of

spontaneous rupture. Several authors found a wavy and irregular

configuration of the collagen in histopathological examinations

of diseased posterior tibial tendons.28e30

Another detiological factor is congenital pes planus. The

abnormal position of the hindfoot and forefoot places greater

stresses on the posterior tibial tendon, which in line with the

theory of repetitive microtrauma, can ultimately lead to PTTD.

The presence of an accessory navicular bone is also associated

with development of PTTD.

Posterior tibial tendon dysfunction is also correlated with

seronegative spondyloarthropathies. Especially in younger

patient groups with PTTD, Myerson found HLA markers in the

majority of patients, whereas in the older age group HLA markers

are rarely found. Seronegative inflammatory disease affects

tissues outside the synovium, and involves multiple attachment

sites of tendons, ligaments and capsules to bone (enthesopathy).

The younger patient group is mostly female, and in this group

a disproportionately high number of concurrent connective

tissue disorders such as inflammatory bowel disease, psoriasis,

urethritis, uveitis, conjunctivitis and oral ulcers are found.20

Physical examination and findings: the physical examination of

the foot and ankle should follow a systematic approach in order

to get a complete picture without missing physical signs. Every

surgeon can create their own system, and the following para-

graph is simply a guideline. In our unit we follow the look, feel,

The patient is first inspected standing with the lower

extremities exposed to above the knee from the front, the sides

and from behind. The gait is observed from front, back and sides.

With the patient sitting on the examination couch, the sole of the

foot can be inspected. Features of PTTD on inspection are flatfoot

deformity (unilateral or bilateral), swelling along the PTT, full-

ness around the medial aspect of the ankle, lateral skin wrinkling

(lateral impingement), too-many-toes sign when inspected from

posterior, and hindfoot valgus. All these should be observed with

the patient standing. With the patient seated the sole can be

inspected for callosities, which in PTTD are typically plantar to

the talar head.

Palpation must again follow a systematic approach, with

special attention paid to the course of the posterior tibial tendon

around the medial malleolus to its insertion into the midfoot. In

stages of active inflammation, palpation along the course of the

PTT can be extremely painful but in later stages it might be

painfree. Palpation is performed along all the hindfoot and

midfoot joints to detect potential signs of arthritis. The examiner

should also look for warmth and increased fluid within the

tendon sheath.

The range of movement is examined for ankle, subtalar and

midfoot joints bilaterally.

Specific tests concerning the function of the tibialis posterior

tendon are the heel rise test and direct strength testing. The heel

rise test is first performed bilaterally with the examiner

observing from posterior. The hindfeet should inverse symmet-

s w

MINI-SYMPOSIUM: FOOT AND ANKLEmove principle with inspection first, then palpation and finally

examination of movement followed by specific tests. As with all

foot and ankle problems, the patients shoes should be inspected

for abnormal wear patterns.

Figure 5 Examination of hindfoot movement. Note shift from valgus to varu

Press from Advanced Examination Technique in Orthopaedics).ORTHOPAEDICS AND TRAUMA 23:6 400rically from a valgus position going into slight varus (Figure 5).

Asymmetry indicates an insufficient PTT unable to invert the

subtalar joint, lock the transverse tarsal joint and thereby allow

the soleusegastrocnemius complex to lift the heel off the

hen tiptoeing. (Reproduced with kind permission of Cambridge University 2009 Elsevier Ltd. All rights reserved.

ground. The examiner must exclude primary pathology in the

subtalar or talo-navicular joints, which can give similar results

on testing. Confirmation is obtained by asking the patient to

perform a single-limb heel rise. For single-limb heel rise the

patient is allowed to rest some fingers against a wall or table for

balance, but the examiner must be aware of the patients overall

position, which must be upright without leaning forward or

bending the knee. The PTT is mainly used to initiate heel rise,

which is then maintained by the soleusegastrocnemius complex.

This means the patient with a PTTD can appear to have PTT

function by altering the bodys centre of gravity and recruiting

adjacent muscles to get the heel to rise and then maintaining the

position.

The power of the PTM is assessed in the seated patient. To

isolate the PTT the ankle is placed in a plantarflexed position and

the foot everted. This eliminates the effect of the anterior tibial

tendon. The examiners hand is placed against the medial aspect

over the first metatarsal and the patient is asked to invert the foot

against the examiners resistance. The strength is noted and

compared against the contralateral side. Pain when performing

the test is also noted.

Classification: The system used the most in PTTD is the classi-

fication system proposed by Johnson and Strom, which originally

included stages 1, 2 and 3.31 More recently, stage 2 was sub-

classified into stages 2A and 2B and then in 1996 Myerson added32

In patients with congenital flatfoot, X-rays of the contralateral

foot are recommended for comparison. Radiographs are usually

normal in stage I disease, but are useful as a screening tool to

look for other pathology contributing to the patients symptoms

like arthritic changes, tarsal coalition, an accessory navicular

bone or Lisfranc injury. Characteristic changes are seen with

progressing disorder. The talo-navicular joint will show lateral

subluxation on an AP view and sag on lateral views. The first

tarso-metatarsal joint is viewed in the lateral view, as it can

contribute to the flatfoot deformity through subluxation and

arthritis. Subluxation of the subtalar joint is difficult to detect on

a lateral view, as it only shows as an indistinct joint surface.

Radiography is also used to quantify deformity by measuring

angles, which can then be used for monitoring progression of

disease and for pre-operative planning.

The angles measured on lateral radiographs are the talo-

calcaneal angle (normal 25e30), the talo-metatarsal angle(normal 4 to 4) and the cuneiform height.

On AP radiographs the relevant angles are the talocalcaneal

angle, the talo-metatarsal angle and the articular congruity angle

for the talo-navicular joint.

Imaging e Magnetic Resonance Imaging: MRI scanning is

excellent in detecting detailed changes in the PTT. It is superior

to computed tomography for showing tissue degeneration,

tendon definition, highlighting synovial fluid and soft tissue

clin

logy

l te

yno

n e

yno

ot d

n e

era

l im

lar o

l im

ced

lso

MINI-SYMPOSIUM: FOOT AND ANKLEa stage 4. The staging includes clinical presentation, disorder

and radiographic findings (Table 2).

Imaging e Radiography: radiographs are the first line of

investigation in suspected PTTD. Weight-bearing films should be

obtained of the foot in three planes and the ankle in two planes.

Johnson and Strom classification of PTTD with associated

Stage Clinical findings Patho

I Medial pain and swelling

Single-limb heel rise Norma

Tenos

IIA Obvious but flexible deformity

Medial pain and swelling

Single-limb heel rise Too many toes sign

Tendo

Tenos

Flatfo

IIB Obvious deformity

Medial and lateral pain

Single-limb heel rise veToo many toes sign

Tendo

Degen

Latera

III Rigid valgus deformity forefoot varus >15

Tight tendo Achilles

Lateral pain

Pain at rest

Subta

Latera

IV Lateral ankle pain

Rigid deformity

Advan

Now a

Table 2ORTHOPAEDICS AND TRAUMA 23:6 401oedema. The sensitivity of MRI is 95%, compared to 90% for CT.

The specificity is 100% for both MRI and CT.33 MRI detects

longitudinal splits easily, which often do not show on CT scan-

ning. Rosenberg et al also found the percentage of tears correctly

diagnosed and classified with MRI to be 73%, with CT as low as

59%.33

ical, pathological and radiological features

Imaging

ndon length

vitis

X-ray: normal

MRI/USS: tenosynovitis

longation

vitis

eformity

X-ray: lateral increased talo-metatarsal angle

AP: uncovering of talar head

MRI: tenosynovitis, splits

USS: tenosynovitis, splits

longation

tive changes

pingement

X-ray: arthritic changes

MRI: soft tissue changes

steoarthritis

pingement

X-ray: arthritic changes

CT: pre-operative planning of fusion procedures

MRI: soft tissue changes

osteoarthritis

in ankle joint

X-Ray: ankle OA with ankle tilt

CT/MRI: pre-operative planning 2009 Elsevier Ltd. All rights reserved.

bout

diagnoses, the aim is to provide the patient with a functional,

stable, plantigrade foot with operative or non-operative methods

as appropriate.

Conclusion

From reviewing the literature, it is clear that a great deal of

progress has been made in the diagnosis and treatment of flatfoot

deformity. There is now a consensus about flexible or physio-

logical paediatric flatfoot that treatment is not necessary in the

vast majority of cases and simple observation and advice to

parents and their children is sufficient.

Controversy still exists about the aetiology of acquired adult

flatfoot, especially concerning the events leading up to posterior

tibial tendon dysfunction or rupture. The large number of

potential contributory causes for posterior tibial dysfunction

makes it clear that the cause is most probably multifactorial. The

MINI-SYMPOSIUM: FOOT AND ANKLEMRI is also used to assess the muscle belly of the posterior

tibial muscle, which helps with pre-operative planning. In

a physiological study by Wacker et al, the muscle underwent

significant fatty degeneration only 10 months after complete PTT

rupture, and atrophy in incomplete tears.34 At the same time the

muscle belly of the flexor digitorum longus hypertrophied as

a compensatory mechanism. This is especially important since

the FDL is used in reconstructive procedures for PTTD.

Imaging e Ultrasound: ultrasound is a very accurate and cost-

effective tool for diagnosing PTT pathology. It has the advantage

of allowing dynamic examination. It is, however, very dependant

on the radiologists skill and experience, which might be the

reason why the interobserver reliability was found to be poor

with USS (0.37) and excellent with MRI (0.86).35 In some units

ultrasonography is used as the primary diagnostic tool for

detection of PTTD.

Imaging e Computed Tomography: CT has largely been

replaced by MRI and is now mainly used if MRI is contra-

indicated. It shows anatomy well but has limitations in dis-

tinguishing tenosynovitis from tendon rupture. Longitudinal

tears, in particular, are frequently missed.33

Treatment e Non-operative: a multidisciplinary approach is

useful, including services from physiotherapy, podiatry, and the

orthotic department. The non-operative options should be

exhausted before surgical reconstruction is planned. These

include rest, anti-inflammatory medication, physiotherapy and

orthotics. Rest should include unloading of inversion excursion,

which can be achieved in ankle crossing braces or walker boots,

although this is only successful in mild cases. If more immobi-

lisation is required for pain relief, a period in a below knee cast

provides best rest for the PTT. Weightbearing can be allowed

according to pain tolerance. Cast immobilisation can be

combined with anti-inflammatory medication.

Physical therapy can also reduce inflammation. Iontophoresis

with dexamethasone, cryotherapy or pulsed ultrasound can be

used. Strengthening exercises aimed at the PTT are limited by

pain and can only be started once other methods have greatly

reduced or eliminated the pain. According to Kulig et al, resisted

adduction with elastic bands had the greatest effects on activa-

tion of the posterior tibial muscle.36

Orthotics and braces aim to reduce stresses and strain on the

PTT by elevating the arch and reducing PTT excursion. The type

of orthosis used depends on the stage of disease and whether the

deformity is flexible or fixed. With flexible deformities (stages 1

and 2A), the orthotics are corrective tools, whereas fixed

deformities require accommodating rather than correcting

devices. Examples of devices used are the UCBL (University of

California Biomechanics Laboratory) for flexible deformities, and

the moulded ankleefoot-orthosis (AFO) for rigid deformities.

These are only a few examples out of a wide variety of orthotic

tools available. Each surgeon treating patients with PTTD should

be familiar with the type of devices available in their unit.

There is debate whether prolonged non-operative manage-

ment allows the condition to worsen, but most authors agree that

a 3e6-month trial of non-operative treatment is indicated unless

there is significant structural deformity present.22ORTHOPAEDICS AND TRAUMA 23:6 402individual surgical procedures but instead focuses more on the

principles and aims.

Although stage 1 should be reserved for conservative

management, tenosynovectomy can be indicated.

Stage 2 dysfunction usually requires a combination of proce-

dures. Meticulous pre-operative assessment is mandatory for

surgical planning and choice of procedures. Flexor digitorum

longus tendon transfer (Figure 6) is often combined with medial

displacement calcaneal osteotomy.37 These can be combined

with spring ligament repair or reconstruction and gastrocnemius

slide. A plantar flexion opening wedge osteotomy of the medial

cuneiform is added if, after correction of the hindfoot, the fore-

foot remains in a supinated position with the first ray not

touching the ground. In more advanced stages (2B), a lateral

column lengthening procedure might be indicated. Subtalar

arthrodesis is performed if inversion is restricted but a stable

correctable transverse tarsal joint is present. If the transverse

tarsal joint is in fixed abduction, or if there is fixed forefoot

varus, then triple arthrodesis is indicated.

Other causes for acquired adult flatfoot

Other causes for acquired adult flatfoot include post-traumatic

flatfoot, osteoarthritis and Charcot arthropathy. In all of thesestages of the disease. There are different principles and p

dures for each stage. This article cannot go into great detail aTreatment e Operative: surgical treatment is dependant on the

roce-

Figure 6 Intra-operative photograph showing FDL transfer with fixation ofthe FDL in a drill hole through the navicular bone with biotenodesis screw. 2009 Elsevier Ltd. All rights reserved.

acquired flatfoot deformity is only the endstage of a complicated

sequence of biomechanical failures in the architecture of the

normal foot and ankle. A

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(ii) Flatfoot deformity: an overviewIntroductionDefinitionAetiology of flatfoot deformitiesAnatomical considerations

Paediatric flatfootFlexible flatfootRigid paediatric flatfoot

Adult flatfootFlexible adult flatfootPosterior tibial tendon dysfunction (PTTD)Other causes for acquired adult flatfoot

ConclusionReferences