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Operative management options for symptomatic adult aquired flatfoot deformity

H. Zaw, J. Calder
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Pathophysiology

Many factors are associated with the development of adult acquired flatfoot deformity (AAFD) but the most common is posterior tibial tendon dysfunction (PTTD). The tendon is an important dynamic arch stabiliser and a powerful invertor of the foot. It "locks" the talonavicular joint and lengthens the lever arm of the triceps surae, promoting a more efficient toe-off.1 Dysfunction of the tendon results in abnormal loading of the transverse tarsal joints creating excessive biomechanical stresses that lead to midfoot collapse and forefoot abduction with lateral peritalar subluxation of the navicular.2 Loss of the main invertor leaves its antagonist, the peroneus brevis, unopposed to evert the foot. The pull of the Achilles tendon falls lateral to the axis of the subtalar joint creating excessive hindfoot valgus. Progressive tightness of the triceps surae perpetuates the valgus deformity and accentuates the imbalance between the medial and lateral soft tissues. The spring ligament complex is the most frequently torn static stabiliser in AAFD.3 It supports the plantar-medial aspect of the talar head and, along with the plantar fascia and long plantar ligament, helps maintain the congruent bony arches of the foot. The superomedial fibres of the spring ligament are confluent with the anterior portion of the deltoid ligament.3 The deltoid ligament prevents external rotation and abduction of the talus within the ankle mortise.4 It is a static stabiliser of the tibiotalar, subtalar and talonavicular joints, as well as the spring ligament.5 Prolonged hindfoot valgus deformity increases tension on the deltoid ligament and the medial collateral complex, causing lengthening and eventual insufficiency.5,6 Ultimately, these changes lead to degenerative arthrosis of the midfoot and hindfoot.

Presentation

The patient may initially develop medial pain over the posterior tibial tendon or lateral pain from subfibular impingement. Clinical signs of PTTD include hindfoot valgus, arch collapse, forefoot abduction with 'too-many-toes' sign and inability to perform double and single heel-rise tests. Gastrocnemius tightness should be assessed using Silfverskiöld's test.7 The primary clinical determinant dictating surgical management of AAFD is whether the deformity is flexible or fixed. It is then necessary to consider either a joint preservation or joint sacrificing procedure. Factors affecting this decision include patient age, function, underlying pathology, degree of deformity, flexibility, soft tissues status, body mass index and the presence of arthritis.8,9

Classification

Johnson and Strom1 described three stages of PTTD, with a fourth stage subsequently added by Myerson.10 Stage I consists of a painful synovitis but no deformity as the tendon length and function are normal. Stage II describes progressive failure of the tendon with a flexible flatfoot deformity, which is passively correctable. In stage III, the deformity is rigid with degenerative changes in the midfoot and hindfoot. Finally stage IV describes valgus tilting of the talus within the ankle mortise with associated deltoid insufficiency, with or without tibiotalar arthritis. In 2007, Bluman, Title and Myerson11 divided the four main stages into substages with subtle differences in clinical and radiographic findings. More recently, Parsons et al12 subdivided stage II disease with respect to the severity and flexibility of forefoot supination when the hindfoot is brought into neutral position (Table 1).

Non-operative treatment

Approximately 80% of early PTTD (stage I and IIA/B) respond well to non-operative management.13 The biomechanical rationale is to alleviate forces transmitted through the posteromedial hindfoot, thereby preventing medial collapse of the foot and ankle. The patient is encouraged to lose weight, modify loading activities and wear supportive shoes. Footwear modification includes extra-depth shoes, soft leather uppers to accommodate insoles, a high toe box and a cushioned, rocker bottom to reduce ground reaction forces and assist in toe-off.14 A custom-made, semirigid orthosis is useful in stage I or early stage II disease. A more rigid University of California Berkeley Laboratory (UCBL) orthosis is used to hold the subtalar joint in a neutral position and alleviate subfibular impingement pain.14 In stage III disease, when custom-made or UCBL orthoses are no longer capable of stabilising the deformity, an ankle foot orthosis (AFO) can be useful. The AFO stabilises the medial-lateral movement of the ankle by using the leg as an anchor and limits excursion of the PTT by preventing plantarflexion and pronation of the foot.14 Modern, low-profile designs in AFO allow control of the deformity, reduce oedema and protect the soft tissues, whilst increasing long-term compliance.8,14,15 In cases of acute synovitis of the PTT, 6 to 8 weeks immobilisation non-weight-bearing in either a short-leg cast or a fitted removable boot can eliminate symptoms in stage I/II disease by reducing inflammation and oedema. After immobilisation, a custom foot orthosis, UCBL orthosis, or AFO should be applied. Additionally, the patient may be sent for physical therapy for eccentric gastrocsoleus stretching exercises.16,17

Operative treatment

The treatment of PTTD has been based around the four-stage classification system. In stage I, treatment is typically conservative but may include open or endoscopic tendon debridement,18,19 tenosynovectomy20,21 and possibly calcaneal osteotomy.22 In stage II disease, the aim of treatment is to avoid progression of a flexible flatfoot to a fixed deformity. Increased awareness of PTTD has led to a recent trend in joint preservation techniques for stage II.8,23 Surgical options include reconstruction of the PTT,24 commonly augmented with transfer of the flexor digitorum longus (FDL) tendon25-29 or flexor hallucis longus tendon,30 combined with a calcaneal osteotomy, either a lateral column lengthening (LCL)31-38 or medialising calcaneal osteotomy (MCO).22,26,27 Alternatively, the use of tibialis anterior tendon (Cobb or Young's procedure) to help reconstruct the PTT has also been described.12,39-43 Resulting forefoot supination can be corrected with either a medial cuneiform plantarflexion (Cotton) osteotomy,44,45 or arthrodesis of the first tarsometatarsal (TMT) and/or navicular-cuneiform joints.46,47 The loss of ankle dorsiflexion is addressed with either a tendo-Achilles lengthening (TAL) by open or percutaneous technique, or a gastrocnemius recession.48,49 Additional procedures in stage II disease have been described, such as spring ligament reconstruction with peroneus longus tendon,50 augmentation of the FDL transfer with peroneus brevis tendon,51 and a modified Lapidus fusion of the first TMT joint.46 In stage III disease the hindfoot valgus deformity is fixed, often accompanied by fixed compensatory forefoot supination. The surgical treatment generally consists of a triple arthrodesis52-55 with the fixed deformities in hindfoot and forefoot corrected through the fusion sites. Treatment for stage IV disease is determined by the presence of tibiotalar arthritis and the ability to reduce the deformity. Treatment generally consists of arthrodesis, either tibiotalocalcaneal (TTC) or pantalar,5,56 or realignment procedures of the ankle and hindfoot with deltoid ligament reconstruction.5,57

Summary

The main deforming forces, tendo-Achilles and peroneus brevis, act to promote hindfoot eversion and attenuate structures that stabilise the medial column. More detailed classification systems have been developed in recent years to help clarify treatment recommendations. The commonest surgical management of stage II PTTD is medialising calcaneal osteotomy with FDL tendon transfer. In addition to arthrodesis procedures of the first ray, an opening wedge (Cotton) osteotomy of the medial cuneiform is now a popular alternative and preserves joint motion.

Correcting forefoot abduction deformity has been pivotal to the development of medial and lateral column procedures. When the forefoot is abducted, there is increased uncovering of the talonavicular joint and the lateral column becomes relatively short compared to the medial column. Lengthening of the calcaneocuboid joint with arthrodesis has a higher rate of complication, but lengthening of the anterior calcaneus with an osteotomy proximal to the joint avoids the risk of nonunion inherent in a calcaneocuboid distraction arthrodesis. Furthermore, combination procedures are now more prevalent such as lengthening of the lateral column with simultaneous plantarflexion procedures of the medial column and/or medial soft tissue augmentation. The medial column procedures off-load the lateral column lengthening and prevent symptomatic overload of the lateral column. These combination procedures emphasize the need for careful rebalancing of medial and lateral deforming forces in the surgical correction of a flexible adult acquired flatfoot deformity.

 

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