Adult-Acquired Flatfoot Deformity

Elizabeth A. Cody, MD

Scott J. Ellis, MD

Dr. Cody or an immediate family member serves as a board member, owner, officer, or committee member of the American Orthopaedic Foot and Ankle Society. Dr. Ellis or an immediate family member serves as a paid consultant to or is an employee of Paragon 28 and Wright Medical Technology, Inc. and serves as a board member, owner, officer, or committee member of the American Orthopaedic Foot and Ankle Society.

This chapter is adapted from Ellington JK: Adult-Acquired Flatfoot and Posterior Tibial Tendon Dysfunction in Chou LB, ed: Orthopaedic Knowledge Update: Foot and Ankle 5. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2014, pp 167-179.

ABSTRACT

Adult-acquired flatfoot deformity is a common diagnosis in the fifth and sixth decades of life, arising primarily in individuals with an anatomic predisposition. The deformity involves varying degrees of hindfoot valgus and longitudinal arch collapse, with forefoot abduction and valgus tibiotalar deformity seen in more severe cases. Affected soft-tissue structures can include the posterior tibial tendon, the calcaneonavicular (spring) ligament, and the deltoid ligament of the ankle. Achilles contractures are almost always present. Nonsurgical treatments include a variety of orthotics and braces as well as physical therapy. Surgical treatment is individualized to the deformity and the patient. Typically, joint-sparing procedures (osteotomies and tendon transfers) are performed for flexible deformities without arthritis, whereas hindfoot arthrodesis is performed for rigid deformities and/or arthritis.

Introduction

Adult-acquired flatfoot deformity (AAFD) is a common problem. It commonly leads to progressive posterior tibial tendon dysfunction (PTTD), which usually occurs later in life and mostly in individuals with an anatomic predisposition. Pes planovalgus deformities can also develop in adults following untreated Lisfranc injuries and inflammatory arthropathies, but like congenital pes planovalgus deformities, these are distinct entities apart from AAFD. Symptoms of AAFD usually begin in the fifth and sixth decades of life and treatment is based on the severity of pain and deformity.

Anatomy and Pathophysiology

The posterior tibial tendon (PTT) is the primary dynamic stabilizer of the medial longitudinal arch. The tibialis posterior muscle originates from the posterior tibia and fibula and the interosseous membrane. The PTT courses behind and around the medial malleolus and inserts mainly on the navicular but also has attachments to the cuneiforms and metatarsal bases. The PTT adducts and inverts the foot and plantarflexes the ankle. Adduction of the midfoot provides a rigid lever for progression through the gait cycle during midstance and push-off.

PTTD is caused by an elongated and/or degenerative tendon over the course of its watershed area, which extends from the tip of the medial malleolus to 2 cm distal.¹ Slow degeneration of the tendon decreases its elastic properties and ability to support the foot’s medial column. Inspection of the PTT during surgery usually reveals longitudinal tearing, disorganized collagen, tendinosis, and decreased excursion. Histologically, myxoid and mucinous degeneration is seen.² This degenerative process may be painful, and resection of the diseased tendon is considered a useful adjunct during reconstruction to alleviate pain, although this is controversial.

As the ligaments that support the arch of the foot weaken, the PTT may ultimately lose function leading to plantar flexion of the talus and eversion of the calcaneus. In addition to tendon dysfunction, other plantar structures can attenuate and degenerate as the deformity progresses. The calcaneonavicular (spring) ligament, talonavicular (TN) capsule, and deltoid ligament may all become compromised as the stages of flatfoot progress. The calcaneonavicular ligament has two components, superomedial and inferior, which are collectively referred to as the spring ligament complex. The spring ligament
creates a sling that supports the talar head between the calcaneus and the navicular. In patients with AAFD, the spring ligament is frequently attenuated or fully ruptured.

With attenuation of the PTT and spring ligament, the talus plantarflexes further and the forefoot abducts, resulting in TN uncoverage. In addition, the forefoot supinates to compensate for the valgus hindfoot deformity and maintain a plantigrade foot. The pull of the Achilles tendon on the everted calcaneus works to exacerbate the hindfoot valgus deformity, and a gastroc-soleus contracture typically develops. With advanced disease, flexible deformities can become rigid, limiting treatment options. And finally, with increasing hindfoot valgus, the deltoid ligament can fail, resulting in valgus talar tilt at the ankle.

New research using weight-bearing CT (WBCT) has shown that patients with AAFD may have an anatomic predisposition to developing valgus hindfoot collapse and ligament/tendon failure. A recent study compared patients scheduled for surgical reconstruction of AAFD with control patients and found that the patients with AAFD had significantly more innate talar valgus and more valgus subtalar joint alignment than the control subjects.³ Another study found that patients with peritalar subluxation, as seen in severe AAFD, had greater valgus orientation of the subtalar joint compared with control subjects.⁴ These patients’ tendency toward hindfoot valgus likely puts more stress on the PTT, contributing to development of PTTD. It is possible that in the future, evaluation of bony anatomy will allow surgeons to predict which patients are likely to have progression of deformity and which might benefit from earlier intervention.

TABLE 1 Clinical Staging of Posterior Tibial Tendon Dysfunction

Stage I	Pain over the posterior tibialis with no deformity
Stage II	Deformity is flexible 1. Medial pain only 2. Lateral pain
Stage III	Deformity is not flexible
Stage IV	Deformity is not flexible and changes at the ankle
Reproduced from Alvarez RG, Price J, Marini A, Turner NS, Kitaoka HB: Adult acquired flatfoot deformity and posterior tibial tendon dysfunction, in Pinzur MS, ed: Orthopaedic Knowledge Update Foot and Ankle, ed 4. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2008, pp 215-229.

Classification

PTTD staging was first described in 1989,⁵ was later modified in 1996, and refined in 2007⁶^,⁷ (Tables 1 and 2). Other classification systems have been described.⁸^,⁹ It is important to note that the classification system was created to describe the pathology of the PTT but is commonly used to describe progression of AAFD. The flatfoot deformity itself, as noted earlier, occurs with certain anatomic predispositions as well as ligament failure, involving far more than just the PTT.

Stage 1 PTTD is defined as tenosynovitis with retained strength (eg, the patient can still perform a single-limb heel rise). No alteration of foot alignment is noted clinically or radiographically. Stage II PTTD is characterized by progressive pes planovalgus deformity, which remains flexible, and decreased strength, demonstrated by the inability to perform a single-limb heel rise. Stage III PTTD is defined by a rigid planovalgus deformity, and stage IV involves changes to the ankle joint with deltoid laxity, resulting in ankle valgus deformity.

Patients presenting with stage I PTTD usually report medial ankle and hindfoot pain. Their foot remains flexible and they are able to perform a single-heel rise; however, a patient may have pain with repetitive rising. The tendon has normal function and length. Stage I PTTD is relatively rarely seen in clinical setting.

Most patients with AAFD who seek evaluation have stage II PTTD. Patients report progressive pain and deformity in most cases, and they are unable to perform a single-limb heel rise on the affected extremity. However, the deformity remains flexible and they usually can perform a double-limb heel rise. The hindfoot typically does not invert during heel rise in cases of PTT dysfunction. Patients may also report lateral hindfoot pain, which is usually attributable to development of subtalar arthritis and/or calcaneofibular (subfibular) impingement.¹⁰ Fibular stress fractures also can occur with severe deformity because of calcaneofibular abutment.

Stage III PPTD is characterized by a rigid deformity. The hindfoot is fixed in valgus and patients cannot perform a single-heel rise. Often, the subtalar joint is arthritic. Varying degrees of TN and calcaneocuboid arthrosis and deformity may also be present. With advanced disease, deformity may develop further down the medial column, extending to the naviculocuneiform (NC) joints and the first tarsometatarsal (TMT) joint. This can be observed on a lateral radiograph or WBCT with collapse at the NC joint and plantar gapping at the first TMT joint (Figure 1).

Stage IV PTTD is defined by involvement of the deltoid ligament (Figure 2). With prolonged AAFD, the deltoid becomes attenuated and valgus talar tilt

develops. The foot deformity may be flexible or rigid. Once AAFD has progressed to this stage, treatment becomes much more difficult. For this reason, weight-bearing anterior-posterior (AP) ankle radiographs should always be obtained in patients with AAFD to ensure ankle congruity and to assess for arthritis. Patients with ankle involvement may present with either isolated deltoid stretching or tearing, or frank arthritis in the ankle joint itself with lateral cartilage loss contributing to valgus talar tilt. The distinction between these two scenarios has important implications for surgical management.

TABLE 2 Clinical Classification System for Posterior Tibial Tendon

Stage	Substage	Characteristic Clinical Findings	Radiographic Findings	Treatment
I	A: Inflammatory disease	Normal anatomy, tender PTT	Normal	NSAIDs, immobilization, ice, orthoses, tenosynovectomy, treat specific systemic disease
	B: Partial tear	Normal anatomy, tender PTT	Normal	Same as for substage A
	C: Partial tear with mild HF valgus	Slight HF valgus, tender PTT	Slight HF valgus	Same as for substage A
II	A1: HF valgus with flexible FF varus	Flexible HF valgus, flexible FF varus ± tender PTT	HF valgus, Meary angle disrupted, calcaneal pitch lost	Orthoses, medial slide calcaneal osteotomy, Strayer or Achilles tendon lengthening, FDL transfer (if deformity corrects only with ankle PF)
	A2: HF valgus with rigid FF varus	Flexible HF valgus, rigid FF varus ± tender PTT	Same as A1	Same as for substage A1, Cotton osteotomy
	B: FF abduction	Same as for substages A1 and A2 with FF abduction	HF valgus, talonavicular uncovering, FF abduction	Medial slide calcaneal osteotomy, lateral column lengthening, Strayer or Achilles tendon lengthening, FDL transfer
	C: Medial ray instability	Flexible HF valgus, fixed FF varus, medial column instability, first ray dorsiflexion with HF correction, sinus tarsi pain	HF valgus, first TMT joint plantar gaping	Medial slide calcaneal osteotomy, FDL transfer, Cotton osteotomy, or first TMT joint fusion
III	A: Rigid HF valgus	Rigid HF valgus, sinus tarsi pain	Decreased subtalar joint space, angle of Gissane sclerosis	Triple arthrodesis, custom AFO if not a surgical candidate
III	B: FF abduction	Same as for substage IIIA, FF abduction	Same as for substage IIIA, FF abduction	Triple arthrodesis with lateral column lengthening, custom AFO if not a surgical candidate
IV	A: Rigid HF valgus, flexible ankle valgus, deltoid ligament insufficiency, minimal ankle arthritis	Flexible tibiotalar valgus	Tibiotalar valgus, HF valgus	Correct HF valgus, reconstruct deltoid ligament
IV	B: Significant ankle arthritis, with or without rigid ankle valgus	Rigid tibiotalar valgus	Tibiotalar valgus, HF valgus	Pantalar fusion, TTC fusion, or triple arthrodesis and TAR
Adapted from Bluman EM, Title CI, Myerson MS: Posterior tibial tendon rupture: A refined classification system. Foot Ankle Clin 2007;12:233-249. Copyright 2007, with permission from Elsevier. AFO = ankle-foot orthosis, FDL = flexor digitorum longus, FF = forefoot, HF = hindfoot, NSAIDs = nonsteroidal anti-inflammatory drugs, PF = plantar flexion, PTT = posterior tibial tendon, TAR = total ankle replacement, TMT = tarsometatarsal, TTC = tibiotalocalcaneal

FIGURE 1 Weight-bearing CT sagittal image demonstrating first tarsometatarsal plantar gapping (arrow), representing instability, as well as degenerative arthritis.

FIGURE 2 Stress radiograph demonstrating significant deltoid laxity. (Reproduced with permission from Ellington JK, Myerson MS: The use of arthrodesis to correct rigid flatfoot deformity. Instr Course Lect 2011;60:311-320.)

Clinical Presentation

Patients with AAFD typically present with medial hindfoot pain. However, in some patients, lateral foot pain predominates, and more rarely, patients will present with only ankle pain. Typically, prolonged ambulation and uneven terrain aggravate symptoms. Patients may report uneven shoe wear, with the medial aspect of the heel wearing out faster, or difficulty finding shoes that fit. Some patients report a prior injury, sometimes having heard or felt a “pop,” and many have been treated by their primary physicians for an “ankle sprain.” Some patients state that they have had a flatfoot their entire life, which has worsened. Comorbidities, particularly inflammatory conditions and diabetes mellitus, should be documented.

Physical Examination

Patients should be evaluated in both the standing and seated positions. In the standing position, a patient with AAFD will have a decreased arch, increased hindfoot valgus (Figure 3), and the “too many toes sign” (attributable to forefoot abduction) when viewed from behind. In the seated position, the flexibility of the hindfoot and that of the gastrocnemius-soleus complex are assessed. Findings should be compared with those of the opposite foot/ankle. A flexible deformity allows for osteotomies and tendon transfers, whereas rigid deformities require arthrodesis procedures.

The Silfverskiold test is performed to distinguish between contracture of the Achilles tendon and isolated gastrocnemius contracture. It is important to assess ankle dorsiflexion with the hindfoot held reduced in a neutral position; if this is not done, dorsiflexion will be overestimated. The test is performed by first assessing ankle dorsiflexion with the knee in full extension. The knee is then flexed. If ankle dorsiflexion increases when the knee is flexed, this indicates an isolated gastrocnemius contracture (because of the gastrocnemius origin being above the knee joint). If ankle dorsiflexion does not increase with knee flexion, then the entire gastrocnemius-soleus complex/Achilles tendon is contracted. This detail is important for surgical planning. If the gastrocnemius is contracted, then it is lengthened as part of the surgical procedure. Several gastrocnemius fascia lengthening procedures have been described, including the Strayer¹¹ recession. If the entire complex is contracted, then Achilles tendon lengthening is performed. This procedure often involves a percutaneous triple-cut hemisection of the Achilles tendon.¹²

Swelling and pain with palpation over the course of the PTT and its insertion on the navicular are also documented. An accessory navicular may become obvious when a painful prominence is present at the PTT insertion. Localized edema over the PTT is common in AAFD and has been
shown to be an excellent predictor of PTTD confirmed with MRI. In a study of 49 patients, pitting edema in the distal PTT area had a sensitivity of 86% and specificity of 100% for PTT degeneration.¹³ Additional examination findings associated with AAFD include a callus that may develop under the medial column and a medial rocker-bottom deformity. Tenderness may be noted in the sinus tarsi, in the subfibular area, and over the peroneal tendons.

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