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(ii) Flatfoot deformity: an overview
MINI-SYMPOSIUM: FOOT AND ANKLE
(ii) Flatfoot deformity: an overview
Therefore, 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.
Kurt Thomas Haendlmayer Nick John Harris
Abstract Flatfoot 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 treatment and cases that simply need reassurance. Historically, flatfoot deformities have been over treated with the aim to correct deformity, in the process not only failing to achieve the desired correction but also creating symptoms in previously symptom free individuals. A lot has been learned about flatfoot deformity and a more sensible approach based on symptoms 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.
Definition Flat feet (Figure 1) is a medical condition with varying aetiology, in which the entire sole of the foot comes into complete or nearcomplete 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 bone might be subluxed in a dorso-lateral direction in relation to the talus. This talo-navicular subluxation is either a contributing factor 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.
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 reassurance, 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
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.
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.
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Treatment consists of activity modification, orthoses and physiotherapy. In severe cases, non-steroidal anti-inflammatory medication can be administered. Patients can present with comorbidities 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.
Figure 1 Lateral X-ray showing flatfoot with increased talo-metatarsal angle.
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.
Patients with a tight Achilles tendon might benefit from stretching, with the aim of preventing progression. Orthoses are sometimes helpful. Symptomatic 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.
Tarsal coalition: Tarsal coalition is an abnormal, congenital union between two or more tarsal bones. It can be osseous (synostosis), cartilagenous (synchondrosis) or fibrous (syndesmosis). The prevalence is 1e2%. Autosomal dominant inheritance with reduced penetrance has been proposed.3,4 Calcaneonavicular and talocalcaneal (middle facet) coalitions are the most common, accounting for about 90% of tarsal coalitions.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 little evidence of pes planus. Most patients, however, have fixed hindfoot valgus, loss of subtalar motion and loss of the normal longitudinal 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 withstand external stresses decreases, leading to symptoms. Incomplete 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.
Causes for flatfoot deformity in children and adults Paediatric flatfoot
Adult flatfoot
Physiological
Physiological ongoing from childhood Inflammatory - Rheumatoid arthritis - Seronegative spondylarthropathies Posterior tibial tendon dysfunction Osteoarthritis Neurological Accessory navicular bone Connective tissue disorders Post-traumatic Adult tarsal coalition Iatrogenic
Inflammatory - Juvenile rheumatoid arthritis
Connective tissue disorders - Marfan, Ehlers-Danlos Neurological disorders - Cerebral palsy Tarsal coalition - Talcalcaneal - Calcaneonavicular - Rarer other coalitions
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 can
Table 1
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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.
be 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 ‘anteater nose sign’ can be observed on lateral radiographs.5 CT and MRI 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.
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 pointing medially. The calcaneum also takes up an equinus position, causing shortening of the Achilles tendon. The talonavicular 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 manipulations followed by casting. This helps to prevent contractures of the dorsal structures and facilitates surgical correction later. The
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 radiographs unreliable, even when using special angles. Therefore, CT is the gold standard for diagnosis of talocalcaneal coalitions. Treatment consists of activity modification, adjusting footwear or cast immobilisation. Should initial non-operative treatment 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 recommend that only those coalitions involving less than 50% of the talocalcaneal joint should be exicsed.8,9 Excision of early, small
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Figure 2 Clinical photograph showing rocker-bottom deformity in congenital vertical talus.
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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 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 biomechanical 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 deformity, 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.
Figure 3 X-ray showing congenital vertical talus.
talo-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 (3þ years) with severe deformity, excision of the navicular has been described. Children aged 4e8 might need extra-articular subtalar arthrodesis in addition to open reduction and soft tissue releases. Children 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 Flexible adult flatfoot In 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 fixed 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
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Anatomy: the posterior tibial muscle originates from the posterior surface of the interosseous membrane and the adjacent tibia
Figure 4 Intra-operative photograph showing diseased posterior tibial tendon with longitudinal split and synovitis within the opened tendon sheath.
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and 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, especially 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 ligaments 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.
Trauma 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 flatfoot.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 hypovascular 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 mesotenon 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 tendon’s 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
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.
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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
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, fullness 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 symmetrically 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
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 paragraph is simply a guideline. In our unit we follow the look, feel, move principle with inspection first, then palpation and finally examination of movement followed by specific tests. As with all foot and ankle problems, the patient’s shoes should be inspected for abnormal wear patterns.
Figure 5 Examination of hindfoot movement. Note shift from valgus to varus when tiptoeing. (Reproduced with kind permission of Cambridge University Press from ‘‘Advanced Examination Technique in Orthopaedics’’).
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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 patient’s 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 body’s 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 examiner’s 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.
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 talocalcaneal angle (normal ¼ 25e30 ), the talo-metatarsal angle (normal ¼ 4 to þ4 ) 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.
Classification: The system used the most in PTTD is the classification system proposed by Johnson and Strom, which originally included stages 1, 2 and 3.31 More recently, stage 2 was subclassified into stages 2A and 2B and then in 1996 Myerson added a stage 4.32 The staging includes clinical presentation, disorder and radiographic findings (Table 2).
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 oedema. 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 scanning. 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
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 clinical, pathological and radiological features Stage
Clinical findings
Pathology
Imaging
I
Medial pain and swelling Single-limb heel rise þ
Normal tendon length Tenosynovitis
X-ray: normal MRI/USS: tenosynovitis
IIA
Obvious but flexible deformity Medial pain and swelling Single-limb heel rise þ Too many toes sign þ
Tendon elongation Tenosynovitis Flatfoot deformity
X-ray: lateral increased talo-metatarsal angle AP: uncovering of talar head MRI: tenosynovitis, splits USS: tenosynovitis, splits
IIB
Obvious deformity Medial and lateral pain Single-limb heel rise ve Too many toes sign þ
Tendon elongation Degenerative changes Lateral impingement
X-ray: arthritic changes MRI: soft tissue changes
III
Rigid valgus deformity forefoot varus >15 Tight tendo Achilles Lateral pain Pain at rest
Subtalar osteoarthritis Lateral impingement
X-ray: arthritic changes CT: pre-operative planning of fusion procedures MRI: soft tissue changes
IV
Lateral ankle pain Rigid deformity
Advanced osteoarthritis Now also in ankle joint
X-Ray: ankle OA with ankle tilt CT/MRI: pre-operative planning
Table 2
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MRI 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 costeffective tool for diagnosing PTT pathology. It has the advantage of allowing dynamic examination. It is, however, very dependant on the radiologist’s 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.
Figure 6 Intra-operative photograph showing FDL transfer with fixation of the FDL in a drill hole through the navicular bone with biotenodesis screw.
Treatment e Operative: surgical treatment is dependant on the stages of the disease. There are different principles and procedures for each stage. This article cannot go into great detail about individual 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 procedures. 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 forefoot 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.
Imaging e Computed Tomography: CT has largely been replaced by MRI and is now mainly used if MRI is contraindicated. It shows anatomy well but has limitations in distinguishing 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 immobilisation 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 activation 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 management 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.22
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Other causes for acquired adult flatfoot Other causes for acquired adult flatfoot include post-traumatic flatfoot, osteoarthritis and Charcot arthropathy. In all of these 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 physiological 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
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19 De Zwart DF, Davidson JS. Rupture of the posterior tibial tendon associated with fractures of the ankle. A report of two cases. J Bone Joint Surg Am 1983; 65: 260e2. 20 Myerson M, Solomon G, Shereff M. Posterior tibial tendon dysfunction: its association with seronegative inflammatory disease. Foot Ankle 1989; 9: 219e25. 21 Kirkham BW, Gibson T. Comment on the article by Downey et al. Arthritis Rheum 1989; 32: 359. 22 Jahss MH. Spontaneous rupture of the tibialis posterior tendon: clinical findings, tenographic studies, and a new technique of repair. Foot Ankle 1982; 3: 158e66. 23 Keenan MA, Peabody TD, Gronley JK, Perry J. Valgus deformities of the feet and characteristics of gait in patients who have rheumatoid arthritis. J Bone Joint Surg Am 1991; 73: 237e47. 24 Holmes GB, Mann RA. Possible epidemiological factors associated with rupture of the posterior tibial tendon. Foot Ankle 1992; 13: 70e9. 25 Frey C, Shereff M, Greenidge N. Vascularity of the posterior tibial tendon. J Bone Joint Surg Am 1990; 72: 884e8. 26 Petersen W, Hohmann G, Stein V, Tillmann B. The blood supply of the posterior tibial tendon. J Bone Joint Surg Br 2002; 84(1): 141e4. 27 Supple KM, Hanft JR, Murphy BJ, Janecki CJ, Kogler GF. Posterior tibial tendon dysfunction. Semin Arthritis Rheum 1992; 22(2): 106e13. 28 Delmi M, Kurt AM, Meyer JM, Hoffmeyer P. Calcification of the posterior tibialis tendon: a case report and literature review. Foot Ankle Int 1995; 16: 792e5. 29 Mueller TJ. Acquired flatfoot secondary to tibialis posterior dysfunction: biomechanical aspects. J Foot Surg 1991; 30: 2e11. 30 Trevino S, Gould N, Korson R. Surgical treatment of stenosing tenosynovitis at the ankle. Foot Ankle 1981; 2: 37e45. 31 Johnson KA, Strom DE. Tibialis posterior dysfunction. Clin Orthop Relat Res 1989; 239: 196e206. 32 Myerson MS. Adult acquired flatfoot deformity: treatment of dysfunction of the posterior tibial tendon. J Bone Joint Surg Am 1996; 78: 780e92. 33 Rosenberg ZS, Jahss MH, Noto AM, Norman A, Leeds NE. Rupture of the posterior tibial tendon: CT and surgical findings. Radiology 1988; 167(2): 489e93. 34 Wacker JT, Calder JD, Engstrom CM, Saxby TS. MR morphometry of posterior tibialis muscle in adult acquired flat foot. Foot Ankle Int 2003; 24: 354e7. 35 Gerling MC, Pfirrmann CW, Farocki S, et al. Posterior tibial tendon tears: comparison of the diagnostic efficacy of magnetic resonance imaging and ultrasonography for the detection of surgically created longitudinal tears in cadavers. Invest Radiol 2003; 38(1): 51e6. 36 Kulig SA, Burnfield JM, Requejo SM, Sperry M, Terk M. Selective activation of tibialis posterior. Evaluation by magnetic resonance imaging. Med Sci Sports Exerc 2004; 36(5): 862e7. 37 Wacker JT, Hennessey MS, Saxby TS. Calcaneal osteotomy and transfer of the flexor digitorum longus for stage-II dysfunction of tibialis posterior. Three- to five-year results. J Bone Joint Surg Br 2002; 84-B: 54e8.
acquired flatfoot deformity is only the endstage of a complicated sequence of biomechanical failures in the architecture of the normal foot and ankle. A
REFERENCES 1 Pfeiffer M, Kotz R, Ledl T, Hauser G, Sluga M. Prevalence of flat foot in preschool-aged-children. Pediatrics 2006; 118: 634e9. 2 Staheli LT, Chew DE, Corbett M. The longitudinal arch. A survey of 882 feet in normal children and adults. J Bone Joint Surg Am 1987; 69: 426e8. 3 Newman JS, Newberg AH. Congenital tarsal coalition: multimodality evaluation with emphasis on CT and MR imaging. RadioGraphics 2000; 20: 321e32. 4 Leonard MA. The inheritance of tarsal coalition and its relationship to spastic flat foot. J Bone Joint Surg Br 1974; 56B: 520e6. 5 Chapman VM. The anteater nose sign. Radiology 2007; 245: 604e5. 6 Sartoris DJ, Resnick DL. Tarsal coalition. Arthritis Rheum 1985; 28: 331e8. 7 Herzenberg JE, Goldner JI, Martinez S, Silverman PM. Computerized tomography of talocalcaneal tarsal coalition: a clinical and anatomic study. J Foot Ankle 1986; 6: 273e88. 8 Kumar SJ, Guille JT, Lee MS, Couto JC. Osseous and non-osseous coalition of the middle facet of the talocalcaneal joint. J Bone Joint Surg Am 1992; 74: 530e5. 9 Scranton Jr PE. Treatment of symptomatic talocalcaneal coalition. J Bone Joint Surg Am 1987; 69: 539e53. 10 Lloyd-Roberts GC, Spence AJ. Congenital vertical talus. J Bone Joint Surg Br 1958; 40B: 33e41. 11 Esterman A, Pilotto L. Foot shape and its effect on functioning in Royal Australian Air Force recruits. Part 1: Prospective cohort study. Mil Med 2005; 170: 623e8. 12 Giladi M, Milgrom C, Stein M, et al. The low arch, a protective factor in stress fractures: a prospective study of 295 military recruits. Orthop Ref 1985; 14: 709e12. 13 Kaufman KR, Brodine SK, Shaffer RA, Johnson CW, Cullison TR. The effect of foot structure and range of motion on musculoskeletal overuse injuries. Am J Sports Med 1999; 27(5): 585e93. 14 Jones BH, Thacker SB, Gilchrist J, Kimsey CD, Sosin DM. Prevention of lower extremity stress fractures in athletes and soldiers: a systematic review. Epidemiol Rev 2002; 24: 228e47. 15 Deland JT, Arnoczky SP, Thompson FM. Adult acquired flatfoot deformity at the talonavicular joint: reconstruction of the Spring ligament in an in vitro model. Foot Ankle 1992; 13: 327e32. 16 Mizel MS, Temple HT, Scranton Jr PE, et al. Role of the peroneal tendons in the production of the deformed foot with posterior tibial tendon dysfunction. Foot Ankle Int 1999; 20(5): 285e9. 17 Lapidus PW. Kinesiology and mechanical anatomy of the tarsal joints. Clin Orthop Relat Res 1963; 30: 30e6. 18 Saraffian SK. Anatomy of the foot and ankle. Philadelphia: JB Lippincott, 1983. pp. 43e61; 216e19; 375e425.
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(ii) Flatfoot deformity: an overview
Therefore, 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.
Kurt Thomas Haendlmayer Nick John Harris
Abstract Flatfoot 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 treatment and cases that simply need reassurance. Historically, flatfoot deformities have been over treated with the aim to correct deformity, in the process not only failing to achieve the desired correction but also creating symptoms in previously symptom free individuals. A lot has been learned about flatfoot deformity and a more sensible approach based on symptoms 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.
Definition Flat feet (Figure 1) is a medical condition with varying aetiology, in which the entire sole of the foot comes into complete or nearcomplete 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 bone might be subluxed in a dorso-lateral direction in relation to the talus. This talo-navicular subluxation is either a contributing factor 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.
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 reassurance, 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
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.
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.
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Treatment consists of activity modification, orthoses and physiotherapy. In severe cases, non-steroidal anti-inflammatory medication can be administered. Patients can present with comorbidities 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.
Figure 1 Lateral X-ray showing flatfoot with increased talo-metatarsal angle.
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.
Patients with a tight Achilles tendon might benefit from stretching, with the aim of preventing progression. Orthoses are sometimes helpful. Symptomatic 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.
Tarsal coalition: Tarsal coalition is an abnormal, congenital union between two or more tarsal bones. It can be osseous (synostosis), cartilagenous (synchondrosis) or fibrous (syndesmosis). The prevalence is 1e2%. Autosomal dominant inheritance with reduced penetrance has been proposed.3,4 Calcaneonavicular and talocalcaneal (middle facet) coalitions are the most common, accounting for about 90% of tarsal coalitions.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 little evidence of pes planus. Most patients, however, have fixed hindfoot valgus, loss of subtalar motion and loss of the normal longitudinal 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 withstand external stresses decreases, leading to symptoms. Incomplete 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.
Causes for flatfoot deformity in children and adults Paediatric flatfoot
Adult flatfoot
Physiological
Physiological ongoing from childhood Inflammatory - Rheumatoid arthritis - Seronegative spondylarthropathies Posterior tibial tendon dysfunction Osteoarthritis Neurological Accessory navicular bone Connective tissue disorders Post-traumatic Adult tarsal coalition Iatrogenic
Inflammatory - Juvenile rheumatoid arthritis
Connective tissue disorders - Marfan, Ehlers-Danlos Neurological disorders - Cerebral palsy Tarsal coalition - Talcalcaneal - Calcaneonavicular - Rarer other coalitions
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 can
Table 1
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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.
be 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 ‘anteater nose sign’ can be observed on lateral radiographs.5 CT and MRI 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.
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 pointing medially. The calcaneum also takes up an equinus position, causing shortening of the Achilles tendon. The talonavicular 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 manipulations followed by casting. This helps to prevent contractures of the dorsal structures and facilitates surgical correction later. The
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 radiographs unreliable, even when using special angles. Therefore, CT is the gold standard for diagnosis of talocalcaneal coalitions. Treatment consists of activity modification, adjusting footwear or cast immobilisation. Should initial non-operative treatment 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 recommend that only those coalitions involving less than 50% of the talocalcaneal joint should be exicsed.8,9 Excision of early, small
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Figure 2 Clinical photograph showing rocker-bottom deformity in congenital vertical talus.
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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 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 biomechanical 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 deformity, 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.
Figure 3 X-ray showing congenital vertical talus.
talo-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 (3þ years) with severe deformity, excision of the navicular has been described. Children aged 4e8 might need extra-articular subtalar arthrodesis in addition to open reduction and soft tissue releases. Children 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 Flexible adult flatfoot In 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 fixed 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
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Anatomy: the posterior tibial muscle originates from the posterior surface of the interosseous membrane and the adjacent tibia
Figure 4 Intra-operative photograph showing diseased posterior tibial tendon with longitudinal split and synovitis within the opened tendon sheath.
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and 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, especially 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 ligaments 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.
Trauma 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 flatfoot.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 hypovascular 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 mesotenon 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 tendon’s 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
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.
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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
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, fullness 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 symmetrically 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
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 paragraph is simply a guideline. In our unit we follow the look, feel, move principle with inspection first, then palpation and finally examination of movement followed by specific tests. As with all foot and ankle problems, the patient’s shoes should be inspected for abnormal wear patterns.
Figure 5 Examination of hindfoot movement. Note shift from valgus to varus when tiptoeing. (Reproduced with kind permission of Cambridge University Press from ‘‘Advanced Examination Technique in Orthopaedics’’).
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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 patient’s 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 body’s 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 examiner’s 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.
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 talocalcaneal angle (normal ¼ 25e30 ), the talo-metatarsal angle (normal ¼ 4 to þ4 ) 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.
Classification: The system used the most in PTTD is the classification system proposed by Johnson and Strom, which originally included stages 1, 2 and 3.31 More recently, stage 2 was subclassified into stages 2A and 2B and then in 1996 Myerson added a stage 4.32 The staging includes clinical presentation, disorder and radiographic findings (Table 2).
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 oedema. 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 scanning. 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
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 clinical, pathological and radiological features Stage
Clinical findings
Pathology
Imaging
I
Medial pain and swelling Single-limb heel rise þ
Normal tendon length Tenosynovitis
X-ray: normal MRI/USS: tenosynovitis
IIA
Obvious but flexible deformity Medial pain and swelling Single-limb heel rise þ Too many toes sign þ
Tendon elongation Tenosynovitis Flatfoot deformity
X-ray: lateral increased talo-metatarsal angle AP: uncovering of talar head MRI: tenosynovitis, splits USS: tenosynovitis, splits
IIB
Obvious deformity Medial and lateral pain Single-limb heel rise ve Too many toes sign þ
Tendon elongation Degenerative changes Lateral impingement
X-ray: arthritic changes MRI: soft tissue changes
III
Rigid valgus deformity forefoot varus >15 Tight tendo Achilles Lateral pain Pain at rest
Subtalar osteoarthritis Lateral impingement
X-ray: arthritic changes CT: pre-operative planning of fusion procedures MRI: soft tissue changes
IV
Lateral ankle pain Rigid deformity
Advanced osteoarthritis Now also in ankle joint
X-Ray: ankle OA with ankle tilt CT/MRI: pre-operative planning
Table 2
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MRI 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 costeffective tool for diagnosing PTT pathology. It has the advantage of allowing dynamic examination. It is, however, very dependant on the radiologist’s 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.
Figure 6 Intra-operative photograph showing FDL transfer with fixation of the FDL in a drill hole through the navicular bone with biotenodesis screw.
Treatment e Operative: surgical treatment is dependant on the stages of the disease. There are different principles and procedures for each stage. This article cannot go into great detail about individual 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 procedures. 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 forefoot 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.
Imaging e Computed Tomography: CT has largely been replaced by MRI and is now mainly used if MRI is contraindicated. It shows anatomy well but has limitations in distinguishing 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 immobilisation 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 activation 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 management 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.22
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Other causes for acquired adult flatfoot Other causes for acquired adult flatfoot include post-traumatic flatfoot, osteoarthritis and Charcot arthropathy. In all of these 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 physiological 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
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19 De Zwart DF, Davidson JS. Rupture of the posterior tibial tendon associated with fractures of the ankle. A report of two cases. J Bone Joint Surg Am 1983; 65: 260e2. 20 Myerson M, Solomon G, Shereff M. Posterior tibial tendon dysfunction: its association with seronegative inflammatory disease. Foot Ankle 1989; 9: 219e25. 21 Kirkham BW, Gibson T. Comment on the article by Downey et al. Arthritis Rheum 1989; 32: 359. 22 Jahss MH. Spontaneous rupture of the tibialis posterior tendon: clinical findings, tenographic studies, and a new technique of repair. Foot Ankle 1982; 3: 158e66. 23 Keenan MA, Peabody TD, Gronley JK, Perry J. Valgus deformities of the feet and characteristics of gait in patients who have rheumatoid arthritis. J Bone Joint Surg Am 1991; 73: 237e47. 24 Holmes GB, Mann RA. Possible epidemiological factors associated with rupture of the posterior tibial tendon. Foot Ankle 1992; 13: 70e9. 25 Frey C, Shereff M, Greenidge N. Vascularity of the posterior tibial tendon. J Bone Joint Surg Am 1990; 72: 884e8. 26 Petersen W, Hohmann G, Stein V, Tillmann B. The blood supply of the posterior tibial tendon. J Bone Joint Surg Br 2002; 84(1): 141e4. 27 Supple KM, Hanft JR, Murphy BJ, Janecki CJ, Kogler GF. Posterior tibial tendon dysfunction. Semin Arthritis Rheum 1992; 22(2): 106e13. 28 Delmi M, Kurt AM, Meyer JM, Hoffmeyer P. Calcification of the posterior tibialis tendon: a case report and literature review. Foot Ankle Int 1995; 16: 792e5. 29 Mueller TJ. Acquired flatfoot secondary to tibialis posterior dysfunction: biomechanical aspects. J Foot Surg 1991; 30: 2e11. 30 Trevino S, Gould N, Korson R. Surgical treatment of stenosing tenosynovitis at the ankle. Foot Ankle 1981; 2: 37e45. 31 Johnson KA, Strom DE. Tibialis posterior dysfunction. Clin Orthop Relat Res 1989; 239: 196e206. 32 Myerson MS. Adult acquired flatfoot deformity: treatment of dysfunction of the posterior tibial tendon. J Bone Joint Surg Am 1996; 78: 780e92. 33 Rosenberg ZS, Jahss MH, Noto AM, Norman A, Leeds NE. Rupture of the posterior tibial tendon: CT and surgical findings. Radiology 1988; 167(2): 489e93. 34 Wacker JT, Calder JD, Engstrom CM, Saxby TS. MR morphometry of posterior tibialis muscle in adult acquired flat foot. Foot Ankle Int 2003; 24: 354e7. 35 Gerling MC, Pfirrmann CW, Farocki S, et al. Posterior tibial tendon tears: comparison of the diagnostic efficacy of magnetic resonance imaging and ultrasonography for the detection of surgically created longitudinal tears in cadavers. Invest Radiol 2003; 38(1): 51e6. 36 Kulig SA, Burnfield JM, Requejo SM, Sperry M, Terk M. Selective activation of tibialis posterior. Evaluation by magnetic resonance imaging. Med Sci Sports Exerc 2004; 36(5): 862e7. 37 Wacker JT, Hennessey MS, Saxby TS. Calcaneal osteotomy and transfer of the flexor digitorum longus for stage-II dysfunction of tibialis posterior. Three- to five-year results. J Bone Joint Surg Br 2002; 84-B: 54e8.
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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