Introduction
Pes planus, or flat foot, and its variations are a spectrum of foot and, occasionally, ankle disease. It is one of the core conditions treated by the foot and ankle surgeon. A clear understanding of the true nature of the spectrum of the disease is essential for the successful assessment and treatment of these patients. The adult-acquired flat foot is the commonest pathological cause of flat foot, and is illustrative of the anatomical, pathophysiological, and biomechanical principles of pes planus.
Flat foot is to some extent a maligned term. It has for many years received much attention in musculoskeletal screening, particularly in times of war, where otherwise fit and healthy people are given a “diagnosis” on the basis of having flexible flat feet on the assumption that this will limit their effectiveness. Thankfully, perhaps less so for the reluctant recruit, sense has prevailed with the recognition that the vast majority of flexible planus and planovalgus feet are part of the normal spectrum. In essence, young children are supposed to have flat feet, the bulk of which remain asymptomatic without orthoses or “special shoes.” It is the stiff flat foot or the extreme deformity in the child and the acquired flat foot in the adult that represent true pathology, and it is on the acquired adult flat foot that we shall concentrate our efforts in this chapter.
Definition
Pes planus – flat foot – is a decrease in height of the medial longitudinal arch of the foot. It is often associated with a valgus deformity of the hindfoot – planovalgus.
Pathogenesis/Pathoanatomy
The apex of the medial longitudinal arch of the foot is at the midtarsal joint. The talonavicular joint (TNJ) is most commonly the fulcrum of hindfoot deformity. Classically in the flat foot there is sag at the TNJ with abduction of the forefoot and valgus of the hindfoot, with overall pronation of the foot. Despite this the forefoot is often supinated, to compensate, and produce a plantigrade foot1.
The medial longitudinal arch of the foot has static and dynamic stabilizers.
Static stabilizers of the arch are:
The bony anatomy of the foot, which interlocks to produce a degree of stability. Particular elements include the interlocking “ball and socket” relationship of the TNJ – the “acetabulum pedis” linking the hindfoot to the mid- and forefoot. The sustentaculum tali also supports the bony architecture of the normal arch, as does the “roman arch” arrangement of the tarsometatarsal joints (TMTJs).
Ligamentous structures are also important. The plantar and plantar-medial elements of the talonavicular, naviculocuneiform and TMTJ capsules resist dorsiflexion and abduction of the forefoot on the midfoot. There are two main, named ligaments – the spring and Lisfranc ligaments. The plantar calcaneonavicular ligament (spring ligament) runs between the sustentaculum tali and the plantar surface of the navicular and acts as a check rein to the descent of the medial longitudinal arch in stance. The Lisfranc ligament, running between the base of the second metatarsal and medial cuneiform is also crucial to the maintenance of the tarsometatarsal arch. Failure of these plantar ligamentous and capsular structures leads to the arch sagging, and flattening under load.
Dynamic stabilizers of the arch:
The most important dynamic stabilizer is the tibialis posterior, which arises from the posterior aspect of the proximal third of the tibia, fibula, and the intervening interosseous membrane. Its tendon runs in a groove at the posterior aspect of the distal tibia and angles anteriorly and inferiorly to insert into the tuberosity of the navicular, with slips to the sustentaculum tali, plantar surface of the cuneiforms, cuboid, and the bases of second, third, and fourth metatarsals. The tibialis posterior plantar flexes and inverts the foot, in addition to inverting the subtalar joint and adducting the forefoot2. Importantly for diagnosis, it initiates hindfoot varus on heel rise.
Understanding the function of tibialis posterior is key to understanding the adult-acquired flat foot deformity. The line of pull of the posterior tibial tendon (PTT) is medial to the axis of the sagittal plane of rotation of the subtalar joint, giving it a mechanical advantage in inverting the heel. The line of the tendo Achillis (TA) pull is just lateral to the axis2–3. Should the tibialis posterior muscle or its tendon become abnormally lengthened this mechanical advantage may be lost. In addition, the excursion distance of the PTT is short and lengthening of 1 cm, or more, causes dysfunction. Defective PTT function results in its antagonist, the peroneus brevis, which everts the foot, becoming dominant and abducting the forefoot with resultant gradual attenuation of the TNJ capsule and the spring ligament, leading to a plantar flexion of the talus with a loss of arch height. Associated with this is the development of heel valgus, which lateralizes the insertion of the TA, which in turn worsens the heel valgus. The hindfoot valgus also leads to the development of gastrocnemius–soleus tightness and contracture4.
Etiology
Pes planus has many causes (Table 10.1). The flexible flat foot is a normal variant and rarely, in itself, causes serious symptoms or disability. The infant is born with a flat foot, and the arch develops in the first decade, therefore flat foot is commoner in childhood and often resolves spontaneously. Nevertheless, the adult-acquired flat foot, which is usually caused by PTT dysfunction, is a cause of pain and disability. Planovalgus foot deformity in the adult may be caused by failure of any of the structures named above, but these are far less common than PTT dysfunction.
Table 10.1 The causes of flat foot. This is not an exhaustive list
Physiological, flexible flat foot
Pathological
Tibialis posterior tendon insufficiency
Degenerative and inflammatory arthritis: TMTJ, subtalar
Tarsal coalition and congenital vertical talus
Trauma: Lisfranc injury, spring ligament injury, plantar fascia
Charcot neuroarthropathy
Neuromuscular: cerebral palsy, polio
Ligamentous laxity: Marfan, Ehler–Danlos
In normal gait the foot is supple at heel strike, as the subtalar joint is everted and the tibia is relatively internally rotated, “unlocking” the transverse tarsal joint. Conversely, during toe-off the tibia is externally rotated and under the influence of the tibialis posterior the subtalar joint inverts locking the midtarsal joint, causing the foot to become more rigid. Thus the normal foot is “flatter” at heel strike, when it is positioned for shock absorption, whereas at toe-off it is stiffer with a varus heel and a locked midtarsal joint. The stiffer foot is more efficient for the transfer of muscle forces to the ground, which is better for an effective push-off; the supple foot is better for the shock absorption of heel strike. Thus the flat foot is ineffective for the transference of force in late stance phase, which leads to a feeling of weakness and fatigue in the foot.
Epidemiology
There is considerable disparity across the scientific literature as to the incidence and prevalence of pes planus. A population study of 75 000 people in the United States identified that adult pes planus was associated with being male, a military veteran, African American, having a high body mass index, and other foot abnormalities, such as bunions and hammer toes. Pes planus is associated with poverty, although this is thought to be through the association of poverty with ill health, with “ill health” having a strong association with pes planus5–6. There is also, rather surprisingly, an association between pes planus and white-collar work; this conflicts with the other socioeconomic findings.
Posterior tibial tendon dysfunction occurs almost exclusively in feet that have an underlying planus morphology. There is a bimodal peak of occurrence of PTT dysfunction with age, with a subgroup of traumatic PTT dysfunction in the young and a second larger peak of degenerative PTT dysfunction in the older patient. The cause is thought to be hypovascularity of the tendon in the vascular watershed zone posterior and distal to the medial malleolus7. It is interesting to note that PTT dysfunction is associated with hypertension, obesity, diabetes, steroid exposure, and trauma or surgery to the medial side of the foot and ankle, with 60% of patients having one or more of these conditions8. Hypertension, obesity, diabetes, and steroids are all associated with an acceleration of the micro- and macrovascular degeneration seen with aging. The effect of local trauma or surgery to this area is probably also likely to be as a result of its effect on the vascularity of this critical tendon zone.
Classification
For a classification system to be accepted in clinical practice, it must reflect the natural history of the disease, identify specific clinical stages, and guide treatment. In general terms, pes planus can be thought of as being: congenital or acquired; symptomatic or asymptomatic; pediatric or adult; traumatic or atraumatic; and fixed or flexible.
Despite this the adult-acquired flat foot is most commonly caused by PTT dysfunction. It was initially described in 1969 by Kettelkamp et al.1 and classified by Johnson and Strom (1989)9. The classification was modified by Myerson (1997), who added stage IV disease10. This classification is the most widely accepted and used, relating specifically to acquired PTT dysfunction.
Stage I: Inflammation and dysfunction of the intact PTT – minimal deformity with symmetrical heel shape – single heel rise is possible.
Stage II: Elongation or rupture of the tendon leading to established, but flexible or correctable, planus/planovalgus deformity – a single heel rise is usually possible, but is painful and the patient fatigues in comparison to the other side.
This is a large group with significant variation in severity, which Myerson’s group11 has further subdivided into subgroups:
Stage IIA-1: Upon correction of the hindfoot valgus, the remaining forefoot supination is either corrected completely or is minimal.
Stage IIA-2: Upon correction of the hindfoot valgus, the forefoot supination does not correct.
Stage IIB: There is abduction of the forefoot, either at the TNJ or TMTJ.
Stage IIC: The medial rays is unstable. This instability may occur at the TNJ, naviculocuneiform joint, or the TMTJ.
Stage III: Deformity that is usually more severe but, importantly, is fixed and the hindfoot valgus is no longer passively correctable.
Stage IV: In stage IV disease the ankle tilts into valgus as a result of the chronic planovalgus deformity of the foot. The ankle joint develops valgus degenerative change.
This group is further subdivided into (a) and (b), based on the correctability of the tibiotalar joint deformity and the presence or otherwise of ankle joint arthrosis:
Stage IVa: Correctable valgus tilt within the tibiotalar mortise without major degenerative changes.
Stage IVb: The more advanced stage with fixed deformity and established tibiotalar arthrosis.
Presentation
The history is usually of a gradual, or insidious, onset of pain and swelling on the medial side of the midfoot or ankle, below and behind the medial malleolus. There is often no specific traumatic incident and although some patients may recall an injury, only a small number of these represent a true, acute tendon injury. Many patients are overweight, older, and have a background of asymptomatic flat feet; many also have other medical conditions including diabetes mellitus and hypertension, as well as other foot conditions such as hallux valgus. Patients also often describe a vague “soreness” and “weakness” in the foot, which is increased by activity and limits their ability to exercise. As the condition progresses the patient may notice their foot “changing shape” with a progressive loss of the medial longitudinal arch.
Examination should commence as the patient walks into the office, assessing age, height, weight, and general health. This is followed by a more specific examination of the gait.
Patients should be inspected standing, with their lower limbs exposed above the knee. The shoe-wear pattern and any orthoses should be noted. Look for overall lower limb alignment and rotation, particularly knee valgus and lower limb internal rotation, both of which can be associated with the planovalgus foot. Observe the calves from behind for muscle bulk and symmetry. Swelling, scars, the quality of the skin, and a general impression of vascular status should be noted.
Observing from behind, the heel alignment is noted. Hindfoot valgus of 5 to 7° is normal. On a heel rise the heel moves to neutral or a few degrees of varus. The “too many toes sign” is observed from behind. This is a record of the number of lesser toes that are not obscured by the hindfoot and can be seen from behind – one and a half toes are considered normal. In reality the “too many toes sign” is of limited use as it is dependent upon the position of the examiner’s head and the rotation of the patient’s leg. After inspection ask the patient to walk toward a wall in the office and look for dynamic increases in deformity during gait.
The patient is instructed to face the wall and place the hands flat against it at approximately shoulder height. She is then asked to perform a double heel rise. Observe for restoration of medial longitudinal arch height and movement of the heel into varus. Restoration of the arch is a variation of Jack’s test – the plantar fascia comes under tension with MTPJ extension, drawing the anterior and posterior extremes of the arch closer together with a resultant ascent of the apex of the arch. The patient is then asked to perform repeated single heel rises on both sides, in turn. If she gets pain, ask “is that the pain you get?” Patients may also complain of pain on the medial side of the ankle. In the presence of significant PTT dysfunction the patient is unable to repeatedly perform a single heel rise, as the tibialis posterior is the “initiator” of heel rise.
We prefer to complete the examination with the patient sitting on the edge of the examination couch with the legs hanging over the side and the examiner seated. Palpate over the course of the PTT with particular emphasis on the portion distal to the medial malleolus: there may be tenderness, thickening, or fullness. Palpate for tenderness in the other key structures of the ankle, hindfoot, and midfoot. Active and passive range of motion should be assessed in the ankle, subtalar, and midtarsal joints. Noting whether the deformity is fully correctable, or not, is important, as this has a bearing on treatment. Long-standing and severe deformities will tend to be uncorrectable, or “fixed.”
The strength of the tibialis posterior muscle is best established with the patient sitting. Active inversion or resistance to passive eversion is tested in plantar flexion. Plantar flexion defunctions the tibialis anterior muscle, which can function as an inverter if the ankle is dorsiflexed, masking tibialis posterior weakness. Placing a thumb firmly over the tibialis anterior tendon can diminish its action and one can also feel it working. In terms of quantifying weakness, a useful rule of thumb is simply that a lower limb muscle should be stronger than one in the forearm, and therefore the examiner should not be able to overpower the normal tibialis posterior.
Establishing the relationship between the forefoot and the hindfoot is important. If the subtalar joint position is corrected, and moved from valgus to neutral, the forefoot position should be noted. In some cases the forefoot supination does not correct; in these cases surgery to correct the subtalar joint may well be inadequate, and further surgery to correct the forefoot supination may be required.
In summary, the patient can be seen to progress through the stages outlined in Johnson and Strom’s classification.
Stage I: Patients present with medial pain and swelling around the medial ankle along the distal course of the PTT. With the patient standing “square” they have no deformity and symmetrical hindfeet.
Stage II: As the tendon elongates hindfoot valgus develops and the medial arch descends. This is flexible and can be passively corrected by the examiner. In the later stages, abduction occurs through the midfoot with a progressive uncovering of the talar head. There may be medial midfoot callosities where patients have walked on the uncovered, flexed talar head. The forefoot also abducts with callosities under the medial border of the first ray.
Stage III: The deformity becomes more pronounced and with time there is joint degeneration, especially of the subtalar and TNJ, leading to the deformity becoming fixed.
Stage IV: Finally, with longstanding abnormal loading of the medial ankle joint, the medial soft tissue stabilizers of the ankle gradually fail, and valgus ankle arthrosis develops.
Finally, assessment of the patient’s lower limb neurological and vascular function should be performed, particularly if surgery is being considered.
Investigation
The first-line investigation of the acquired flat foot is good quality plain radiographs. Weightbearing views of the ankle mortise, and AP, lateral, and oblique views of the foot are obtained.
The AP weightbearing radiographs of the foot should be assessed for talonavicular coverage, talar–first metatarsal angle, talocalcaneal angle, degree of forefoot abduction, and joint degeneration.
Talonavicular coverage angle: the edges of the articular surface of the talar head are marked, and the two points joined by a line (Figure 10.1). A similar process is undertaken for the navicular. The angle between these two lines indicates the degree of talonavicular lateral subluxation. The coverage angle is normally less than 7°.
Figure 10.1 The talonavicular coverage angle. This is normally <7°.
The AP talar–first metatarsal angle is a measure of forefoot alignment, by comparing the relative relationship of the long axes of the talus and the first metatarsal (Figure 10.2). The long axis of the talus should be almost parallel to that of the first metatarsal. If the talar axis passes medial to the first metatarsal axis the forefoot is abducted. Forefoot abduction is usually caused by pes planus.
Figure 10.2 The AP talar–first metatarsal angle. (a) Normal; (b) abnormal.
The AP talocalcaneal or “Kite’s” angle is a measure of hindfoot valgus and is an angle formed by the intersection of the long axis of the talus and the lateral border of the calcaneus (Figure 10.3). It can be difficult to measure, as under- or overexposure may obscure the calcaneal outline.
Figure 10.3 The AP talocalcaneal, or Kite’s, angle. Normal 15 to 30°.
The AP cyma line (Figure 10.4) is a sigmoid line drawn through the midtarsal joint and should be smooth or unbroken. A broken line, or line with a step, suggests “shortening” of the lateral column or adduction or flexion of the talus. The term “cyma” is borrowed from the world of architecture where it refers to the junction of two differing curves as seen in the architrave of classical architecture.
Figure 10.4 The cyma line, the broken line shown in (b) is abnormal.
Lateral weightbearing radiographs of the foot should be assessed for calcaneal pitch, Meary’s angle, talocalcaneal angle, midtarsal, naviculo-cuneiform or tarsometatarsal joint “sag” or break, height of medial cuneiform from the ground, degree of talar flexion, and joint degeneration.
The calcaneal pitch is the angle between the undersurface of the calcaneus and the floor (Figure 10.5), in essence it is the angle of the “posterior portion” of the arch. Put simply, the flatter the angle or pitch, the flatter the foot.
Figure 10.5 The calcaneal pitch angle. Normal 10 to 20°.
Meary’s angle (Figure 10.6) is the angle between the long axis of the talus and the first metatarsal, which should be linear. A “break” in the foot between the talus and the metatarsal is abnormal. An increase in Meary’s angle may be caused by sagging of the midfoot joints with gapping on the plantar surface. On the lateral weightbearing view it is also possible to appreciate “descent” of the cuboid toward the floor when there is significant loss of arch height.
Figure 10.6 The lateral talo–first metatarsal angle. Normal 0 +/– 4°.
The lateral talocalcaneal angle is measured between the central axis of the talus and the undersurface of the calcaneus. An increase in the angle greater than 45° suggests hindfoot valgus (Figure 10.7).
Figure 10.7 Lateral talocalcaneal angle. Normal 25 to 45°.
The lateral cyma line (Figure 10.8) should be continuous, as on the AP radiograph.
Figure 10.8 The lateral cyma line.
When assessing the plain radiographs of the patient with adult-acquired flat foot, the presence or absence of degenerative change must be noted. This is for two reasons. Firstly, the flatness of the foot may be resultant on arthritis, in particular of the midtarsal joint, naviculocuneiform, or tarsometatarsal joints and, secondly, as the presence of degeneration, even if the primary diagnosis is PTT dysfunction, will alter management, with fusion surgery being favored.
A standing mortise view of the ankle should also be obtained. Valgus ankle tilt is seen in stage IV PTT dysfunction.
Ultrasound and MRI
MRI has a sensitivity of 95%, a specificity of 100%, and an accuracy of 96% in the diagnosis of disorders of the PTT12. The MRI findings have been classified by Conti et al.13. Ultrasound is cheaper and more widely available but is more operator dependent, albeit with sensitivity and specificity approaching that of MRI14 in the best hands. Ultimately the diagnosis is very much clinical in nature with tests having a confirmatory role, also aiding in the quantification of structural damage, such as degenerative change.
Treatment
In most cases the treatment of PTT dysfunction is initially non-operative. If surgical treatment is required, the nature of the surgery depends on many factors. These include the patient’s level of pain, physiological age, medical comorbidities, and their expectations and activity levels. The soft tissue, vascular, and neurological integrity of the foot and ankle are also important, as are the degree of deformity, its correctability, and which joints are involved. Degenerative joints are more likely to be fused. On balance treatment is principally dictated by the stage of disease.
Stage I: Tendinosis of PTT but no deformity.
Treatment: orthoses/physiotherapy/temporary immobilization/surgical debridement.
Stage II: Tendon rupture or functional failure leading to varying degrees of passively correctable pes planus.
Treatment: Corrective orthoses/physiotherapy/surgical procedures to correct the deformity, but maintain joint motion. The commonest procedure is a flexor digitorum longus (FDL) tendon transfer to the navicular combined with a medial-displacement calcaneal osteotomy. Alternative and supplementary procedures include lateral column lengthening procedures, Cobb procedure, Cotton procedure, extended medial column fusion, and spring ligament repair.
Stage III: The planovalgus deformity becomes fixed as a result of a combination of joint degeneration with soft tissue contracture.
Treatment: Soft accommodative orthoses/surgical treatment with realigning arthrodesis procedures – classically a triple arthrodesis is used, although increasingly more selective fusion is being used15–17.
Stage IV: In this stage there is failure of the medial ankle stabilizers leading to valgus arthrosis of the ankle joint proper.
Treatment: Surgical treatment at this stage may be ankle arthrodesis, which may form part of a pantalar arthrodesis; however, there are also procedures to reconstruct the deltoid ligament with tendon graft.
Non-Operative Treatment
Non-operative treatment is the first line of treatment for most with acquired pes planus. The degree of deformity and the flexibility of the foot are key factors. In Stage I patients with PTT pain, but symmetrical heel alignment, immobilization for six weeks, oral anti-inflammatory medication, followed by the use of an AFO is tried. Surgical debridement, open or tendonoscopic, is reserved for those patients who fail non-operative treatment.
In the patient with a flexible, stage II, deformity non-operative treatment is initially with corrective orthoses. The key elements of the deformity requiring correction are hindfoot valgus, forefoot abduction, and supination with first-ray dorsiflexion and loss of the medial longitudinal arch. The corrective orthosis is generally a shoe insert or insole. There should be a medial heel wedge to correct the subtalar joint valgus and a lateral forefoot post to correct the forefoot abduction. Incorporation of a medial-arch support can be useful, but care must be taken with the selection of the material used – in severe deformity there may be a sag at the talonavicular, naviculocuneiform, or tarsometatarsal joint, leading to a bony prominence in the medial-plantar foot, under which a callosity may form. In particular, a TNJ break, with uncovering of the head of the talus as a result of forefoot abduction, can lead to patients walking on the talar head. These patients need a cushioned, non-corrective insole. Trying to drive the medial arch back up with a rigid, corrective insole leads to pain under the prominence, making the orthosis unwearable. In summary, an uncorrectable deformity requires treatment with a soft, accommodative orthosis, with the harder, corrective orthoses being reserved for patients with correctable deformities.
More severe hindfoot and forefoot deformity may be addressed with the University of California Biomechanics Laboratory (UCBL) orthosis. This has a deep heel cup, which grips the posterior calcaneus, controlling the heel valgus and arch height. It can also be molded about the lateral forefoot, reducing the forefoot abduction and controlling the first metatarsal.
Ultimately the severity of the deformity may outstrip the ability of in-shoe orthoses to control the foot and it is necessary to employ an AFO, which is more rigid and extends more proximally across the ankle, providing a more efficient and powerful lever to hold the hindfoot. Good results have been shown in the medium term for resolution of symptoms with the use of a low-articulating AFO. It has been shown that stage I and II PTT dysfunction, without tendon rupture, can be effectively treated non-operatively with an orthosis and a structured exercise program in over 80% of cases18. Nevertheless in younger patients and individuals with severe symptoms, refractory to non-operative treatment, surgery may be the only option19.
Although some clinicians offer steroid and local anesthetic injection into the PTT sheath for symptomatic relief, most avoid injection as PTT dysfunction is a degenerative, not an inflammatory, condition. Furthermore steroid injections are associated with tendon rupture and therefore most feel that injection should be avoided.
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