Posterior Tibial Tendon Dysfunction

Etiology

Historically, Johnson and Strom proposed a 3-stage classification of PTTD based on the condition of the PTT, the position of the hindfoot, and the flexibility of the deformity.[3] Researchers have proposed numerous mechanisms for the degeneration of the PTT, the most common being repetitive loading, which causes microtrauma and progressive failure.

A retromalleolar hypovascular region does exist and may also contribute to the disease. In a study by Manske et al, cadaver specimens showed an area of decreased blood supply from 2.2 cm (SD 0.8 cm) proximal to the medial malleolus to a region 0.6 cm (SD 0.6 cm) proximal to the medial malleolus.[3]

The anatomic course of the PTT likely contributes to the disease, as the tendon makes an acute turn around the medial malleolus. This location puts significant tension on the tendon in the region distal and posterior to the medial malleolus. The adjacent tendons, namely the flexor hallucis longus and the flexor digitorum longus (FDL), do not take this sharp turn.[4]

Metabolic and genetic conditions must also be considered. Diabetes mellitus involves loss of collagen organization, tendon thickening, and calcification, all of which increase the chance of tendon attenuation.[4] Patients with hyperlipidemia have been shown to release proinflammatory cytokines and upregulate matrix-degrading protein, leading to tendon stiffness and decreased healing potential. Moreover, recent studies have demonstrated the influence of genetic inheritance on the predisposition to develop tendinopathy. Genetic predisposition to increased levels of collagen types III and V and matrix metalloproteinases 1, 8, and 13 have been correlated to PTT degeneration.[5] [6]

Although theories of PTT degeneration remain possible causes of PTTD, it is now understood that the deformity can involve a complex combination of midfoot, rearfoot, and ankle deformities not previously described. Furthermore, attenuation or rupture of the plantar fascia, spring ligament, and deltoid ligaments can occur in the absence of PTT rupture, leading to the condition. These factors contributed to the change in nomenclature from PTTD to PCFD.[3]

Isolated spring ligament injury or a combination of spring and deltoid ligament insufficiencies in the absence of PTT degeneration have been shown to cause PCFD.[7] These conditions have been described mainly in small studies, where patients present with normal inversion strength, tenderness anterior to the medial malleolus, and MRI confirmation of spring ligament tear.[8] Other potential culprits include constriction beneath the flexor retinaculum,[5] abnormal anatomy of the talus,[6] degenerative changes associated with osteoarthritis,[7] and preexisting pes planus.[8]

Epidemiology

Although no significant large-scale studies have been performed about the overall incidence of this disease, the prevalence of PCFD is estimated to be between 3.3% and 10%, depending on the sex and age of the patient.[9] A body mass index (BMI) of 25 kg/m² or higher is prevalent in 81.5% of patients and occurs predominantly in females.[9] The classic PCFD patient is a woman with obesity in her sixth decade of life.[9] A case-control study reported a significantly higher prevalence of leg length discrepancy in PCFD patients compared to the control group, suggesting leg length discrepancy as a predisposing factor for PCFD.[10] PCFD is associated with adult-acquired flatfoot deficiency, which can lead to misdiagnosis, potentially resulting in a much higher actual prevalence than reported in the literature. Additionally, underreporting may occur due to the early, asymptomatic stages of PCFD. 

Histopathology

In normal PTT, linear collagen bundles are predominant, accompanied by normal fibroblast cellularity and a low proportion of vascular density. However, in PTTD, the tendon experiences microtrauma, leading to tendinitis characterized by increased mucin content, neovascularization, and fibroblast hypercellularity.[11]

History and Physical

Most patients with PCFD will exhibit medial ankle and foot pain in the early stages of the disease. Later stages may involve lateral pain due to subfibular impingement or peroneal tendon injury.[12]

A comprehensive physical examination is crucial for determining the grading and severity of the disease. The attention should first be turned to grossly inspecting the feet while standing. A weight-bearing examination is essential, as a flexible deformity may normally be present while the patient is non-weight–bearing. The collapse of the medial longitudinal arch leads to pes planus, which is an easily visualized condition. While inspecting the patient, a common observation is the "too many toes" sign; when viewed from behind, more than two toes will flare out laterally due to the valgus alignment of the foot. Equinus contracture is another frequently encountered finding that potentially limits ankle dorsiflexion.

Single-limb heel raise is an important clinical test that can differentiate stage I disease from stage II and beyond. A patient with stage I disease should be able to perform this test without pain. In stage II disease, patients may be able to perform the test but will likely have pain. In advanced stages, rigid deformities may prevent the patient from completing the test. Additionally, foot flexibility warrants examination during evaluation.[12]

Evaluation

Imaging is critical in determining the severity of PCFD and subsequent treatment. Anteroposterior (AP) and lateral radiographs of the foot are necessary. Increased talonavicular uncoverage and increased talo-first metatarsal angle (or Simmons angle) will be evident on the AP radiograph. The normal talo-first metatarsal angle is around 7 degrees, and angles over 16 degrees indicate flatfoot deformity.[11] Talonavicular coverage is expressed as the proportion of the talus not in contact with the navicular medially, with values surpassing 30% to 40% typically suggestive of forefoot abduction, characteristic of stages II to IV PCFD.[9] A cutoff value of 25.4 degrees of talonavicular coverage serves as a discriminator between patients with or without sinus tarsi impingement.[13] On the weight-bearing lateral radiograph, assessment should include the evaluation of an increased talo-first metatarsal angle (or Meary angle), which typically measures 0±4 degrees but exceeds 20 degrees in cases of flatfoot deformity.[10]

When considering advanced imaging, options such as weight-bearing computed tomography (WBCT) and magnetic resonance imaging (MRI) are available. WBCT has demonstrated an enhanced ability to recognize deformities, accompanied by excellent inter-rater reliability.[14] Although the orthopedic consensus group opted against incorporating MRI into a classification system,[3] it remains a valuable tool for assessing the condition of affected soft tissue (see Image. MRI of Posterior Tibial Tendon Dysfunction).

Treatment / Management

The treatment approach outlined for PTTD stages is historically suitable for the new PCFD nomenclature.

• All stages (initially):
  • Conservative management with nonsteroidal anti-inflammatory drugs (NSAIDs) and activity modification. This is also indicated for nonsurgical candidates or low-demand, older patients.[15]
(B2)

• Stage I:
  • Conservative management through immobilization in a walking boot or cast for up to 3 to 4 weeks may be warranted to allow for healing of the PTT, followed by eccentric strengthening with physical therapy.[1]
  • If immobilization and physical therapy are successful, transitioning to custom-molded orthotics or ankle-foot orthosis (AFO) is appropriate to maintain relief, with a crucial emphasis on medial forefoot posting. University of California Biomechanics Laboratory (UCBL) orthoses, featuring a custom insert with a lace-up component, can help maintain midfoot height.[16]
  • Conservative therapy is recommended for 3 to 4 months overall, with surgical intervention being considered if conservative measures fail. A tenosynovectomy, coupled with tubularization, may be indicated in such cases.
(A1)

• Stage IIA:
  • Conservative management includes immobilization and physical therapy, following the recommendations for stage I, along with the use of orthotics or AFO.
  • Surgical treatment involves medial calcaneal osteotomy with posterior tendon debridement and repair. Ancillary procedures may include any or all of the following: FDL transfer, spring ligament reconstruction, or Achilles tendon lengthening.[17]
(B2)

• Stage IIB:
  • All previously listed procedures in stage IIA are considered +/- lateral column lengthening or isolated subtalar joint arthrodesis.

• Stage III:
  • Conservative therapies, as mentioned above, are typically used.
  • Surgical treatment is often warranted due to rearfoot arthritic changes. Common procedures include medial double arthrodesis or triple arthrodesis (subtalar, calcaneocuboid, and talonavicular arthrodesis), with or without deltoid ligament repair.[18]

• Stage IV:
  • Conservative therapies, as mentioned above, are typically used.
  • Surgical treatment is often necessary due to arthritic changes in the ankle and rearfoot. Surgical options may encompass a variety of procedures, including triple arthrodesis with Achilles tendon lengthening, deltoid ligament reconstruction, and total ankle arthroplasty with replacement.[18] Alternatively, medial double arthrodesis, deltoid ligament reconstruction, and total ankle arthroplasty with replacement can be considered if ankle deformity is reducible. A staged approach is recommended for patients deemed suitable candidates for total ankle arthroplasty. This involves performing rearfoot arthrodesis and soft tissue balancing initially, followed by a second stage for total ankle arthroplasty 4 to 8 weeks later.
  • Tibiotalocalcaneal arthrodesis is indicated for a rigid hindfoot with a significant valgus alignment of the talus within the ankle mortise.[19][20] Pantalar Pantalar arthrodesis, which involves triple arthrodesis with the addition of ankle arthrodesis, is also considered in such cases.

The PCFD classification does not outline a treatment algorithm similar to the former PTTD, but the orthopedic consensus agreed on the following statements:[21](B3)

• Preservation of range of motion and mobility should be a primary goal.

• Talonavicular (TN) joint fusion should be considered in cases of arthritis, joint stiffness, significant sagittal plane deformities, severe deformities, and inadequate correction of TN abduction with other procedures.

• Patients with a BMI exceeding 30 experience poorer outcomes with reconstructive surgery compared to hindfoot fusions.

• Joint preservation procedures should be attempted for young patients.

Differential Diagnosis

Although PCFD is the most prevalent cause of adult-acquired flatfoot deformity, numerous related conditions exist. The following diagnoses can manifest with striking similarity to PCFD and thus warrant consideration during evaluation:[22]

• Tarsal coalition
• Inflammatory arthritis
• Charcot arthropathy
• Neuromuscular disease
• Traumatic disruption of midfoot ligaments

Staging

The Johnson and Strom classification for PTTD insufficiency, modified by Myerson and described below, defines radiographic findings, physical examination findings, and associated deformities. This classification has been widely accepted for many years.

Stage I: Normal radiographs, able to perform single-heel raise, and mild tenosynovitis.

Stage IIA: Arch collapse on a radiograph, unable to perform single-heel raise, and a flexible flatfoot deformity.

Stage IIB: Arch collapse and talonavicular uncoverage (over 40%) on a radiograph, unable to perform single-heel raise, flexible flatfoot deformity, and characteristic forefoot abduction or "too many toes" sign.[23]

Stage III: Subtalar arthritis on a radiograph, unable to perform single-heel raise, flatfoot deformity with rigid forefoot abduction, and hindfoot valgus

Stage IV: Valgus deformity of the talus in the ankle mortise, visualized on an AP radiograph of the ankle with talar tilt due to deltoid ligament compromise; subtalar arthritis on radiographs; unable to perform a single-heel raise; flatfoot deformity with rigid forefoot abduction; and hindfoot valgus.[23]

In 2020, Myerson et al, together with the consensus group, proposed the newest accepted classification with the nomenclature change to PCFD:

• Stage I is flexible
• Stage II is rigid

Both stages I and II can be subdivided into classes A through E.

Class A: Hindfoot valgus deformity

• Hindfoot valgus alignment
• Increased hindfoot moment arm, hindfoot alignment angle, foot and ankle offset

Class B: Midfoot/forefoot abduction deformity

• Decreased talar head coverage
• Increased talonavicular coverage angle
• Presence of sinus tarsi impingement

Class C: Forefoot varus deformity/medial column instability

• Increased talus-first metatarsal angle
• Plantar gapping first tarsometatarsal (TMT)/naviculocuneiform (NC) joints
• Clinical forefoot varus

Class D: Peritalar subluxation/dislocation

• Significant subtalar joint subluxation/subfibular impingement

Class E: Ankle instability

• Valgus tilting of the ankle joint

Prognosis

PCFD is a progressive disorder that worsens without intervention. Early detection and intervention are crucial for slowing its progression. Patients who receive custom orthotics and undergo rehabilitation typically experience significant improvement. In a recent study conducted by Alvarez et al, approximately 89% of patients with stages I and II PCFD responded positively to orthotics and physical therapy, with nearly all regaining full strength within 4 months.[20] 

Orthotic management has also shown promising outcomes for injuries to the spring ligament.[7] However, analyses of surgical outcomes reveal less predictable results, with no assurance of returning to the pre-disease state. Patients may experience residual effects even after reconstructive surgeries.[24]

Complications

General complications of surgical reconstruction include thromboembolic events, infection, wound dehiscence, neurologic injury, and painful hardware, either individually or in combination. Reports indicate that up to one-third of patients undergoing flatfoot reconstruction experience wound-healing complications, underscoring the paramount importance of diligent wound care.[25]