Progressive Collapsing Foot Deformity

Etiology

Acquired flatfoot was historically attributed to posterior tibial tendon deficiency. However, now the understanding is that the ligamentous structures of the ankle play a role in foot deformity development.[1][7] The dysfunction of the posterior tibial tendon is a multifactorial process. In many patients, preexisting flatfoot is common, and many patients are also obese. Another factor is the relative hypovascularity of the tendon during an abrupt turn posterior to the medial malleolus; this predisposes the tendon to rupture due to insufficient repair.[8] Episodes of previous trauma, corticosteroid injections, arthritis, neuromuscular conditions, and diabetes all predispose to the development of progressive collapsing foot deformity.[9]

Epidemiology

Acquired flatfoot is a common orthopedic condition, although the paucity of literature on the epidemiology regarding progressive collapsing foot deformity is apparent. 5 million people in the United States are affected by the condition. The estimated prevalence in the United Kingdom is over 3% in women over 40.[2][10] Posterior tibial tendon issues are prevalent in older populations, with 10% of patients affected. Ikpeze et al postulated that the geriatric population might be predisposed to more severe progressive collapsing foot deformity due to the degeneration of muscle mass and bone structure.[11] Patients with chronic vascular diseases are at increased risk; this includes patients with diabetes or hypertension.[9]

Pathophysiology

The posterior tibial tendon is critical in maintaining the appropriate gait and function of the foot. Contraction of the tibialis posterior causes the inversion of the foot and locking of the transverse tarsal joints, granting stability for push-off. Deficiency of the posterior tibial tendon leads to an unstable transverse tarsal joint and forefoot abduction, allowing unopposed action of the peroneus brevis. The ensuing abduction of the forefoot and transverse talar joints also displace the force of the calcaneal tendon laterally, accentuating the valgus defect of the foot.[12] The continued strain on the static stabilizing ligaments eventually leads to their attenuation. Most commonly, the spring ligament is affected, and failure leads to medial and plantar subluxation of the talar head relative to the navicular. Failure of the deltoid ligament leads to a valgus position of the talus within the ankle mortise.[1][3][13][9] These events may occur stepwise, corresponding to the Johnson and Strom classification system. However, some patients develop a valgus talar tilt without a fixed flatfoot deformity.[5] In addition, metabolic and genetic conditions can predispose the disorganization of collagen fibers and contribute to polymorphism of collagen types III, V, and matrix metalloproteinases 1, 8, and 13. The pathology contributes to tendon thickening and impaired healing.[14][15]

History and Physical

Evaluating the patient with suspected progressive collapsing foot deformity during weight-bearing is essential. When the patient is standing, excessive forefoot abduction can be noted by the “too many toes” sign. This test is positive if the clinician can see more than the fifth and part of the fourth toe. Inspection and palpation over the posterior tibial tendon at the area of the medial malleolus may demonstrate swelling or pain. Pain may be elicited on the foot's lateral aspect if ligamentous structures are impinged.[16] 

Single and double heel rise tests may be performed to assess the strength of the posterior tibial tendon. Failure to invert the foot on heel rise or perform heel rise indicates posterior tibial tendon dysfunction. Ankle range of motion requires assessment. Efforts should be concerted to correct valgus deformity in a range of motion exercise to evaluate for fixed deformity. A fixed deformity of the subtalar joint or fixed abduction of the forefoot has implications in treatment.[3]

Evaluation

The gold standard for evaluating progressive collapsing foot deformity is weight-bearing radiographs. However, weight-bearing computed tomography is a reliable imaging tool.[17] Radiographs are necessary in the anteroposterior, lateral, and hindfoot views. These views will assess the degree of arch collapse, particularly by measuring the lateral first tarsometatarsal angle and forefoot abduction at the talonavicular joint. Talar head exposure can also be measured in the setting of stage IV disease by the lateral talonavicular angle (see Image. Radiograph of Progressive Collapsing Foot Deformity). Lateral views of the foot can also display naviculocuneiform and first tarsometatarsal collapse. Arthritis should be carefully assessed on all radiographic films as this may have implications for treatment options.[16]

Magnetic resonance imaging (MRI) is typically unnecessary to evaluate progressive collapsing foot deformity; however, imaging may benefit some patients with ligamentous involvement to alter surgical treatment planning. This is particularly relevant for patients with medial peritalar instability, who have improved functional outcomes with deltoid-spring ligament reconstruction.[18] In 2020, MRI was voted for removal in the new classification system.[19] Several studies indicate that ultrasound may be useful in assessing the posterior tibial tendon compared to the more time-consuming and costly MRI. Results from an ultrasonographic evaluation of the posterior tibial tendon were equivalent to MRI in 87% to 94% of patients.[20][21]

Treatment / Management

Treating progressive collapsing foot deformity is complex. Multiple treatment options are available, and the treatment of foot deformity has been the focus of most recent research. However, first-line therapy for the condition remains non-invasive. Treatment with orthotic devices, such as low-articulating ankle-foot orthosis, cast-boot walkers, and other ankle-foot orthoses, in conjunction with nonsteroidal anti-inflammatory drugs (NSAIDs) and physical therapy, have a resolution of symptoms in 87% of patients, according to one study. Other studies have demonstrated results with success rates of 67% to 90% using conservative measures.[16]

Surgical treatment is indicated in patients who have attempted conservative therapy and are not satisfied with their results. Surgical treatment depends on the stage of the disease, as well as other factors, including medical comorbidities, functional status, and use of tobacco. Surgical management of stage I disease is uncommon, but if required, patients should undergo posterior tibial tendon tenosynovectomy, debridement, or flexor digitorum longus tendon autograft. Repair of the posterior tibial tendon may cause complications with long-term failure; therefore, surgical treatment should be carefully considered before any intervention.[13] 

Stage II disease treatment has succeeded by medializing calcaneal osteotomy and a flexor digitorum longus transfer. Results from one study showed 87% patient satisfaction with this treatment after a mean follow-up of 15 years.[22] Stage III disease is more challenging to treat due to the fixed nature of the defect. Arthrodesis is the standard of care, with common double and triple arthrodesis. Double arthrodesis entails a fusion of the subtalar and talonavicular joints. Triple arthrodesis involves the calcaneocuboid joint and the 2 joints mentioned above. Double arthrodesis has the advantage of reduced arthritic complications and reduced joint stiffness associated with calcaneocuboid fusion. Unfortunately, joint fusion has an inherent loss of mobility, and patients may struggle on uneven ground. Risk of nonunion, deltoid insufficiency, and ankle valgus is also present.

Stage IV disease management depends on whether rigid flatfoot has developed. Some patients progress to stage IV disease without rigid disease due to the failure of the deltoid ligament. In this setting, patients may have treatment with a deltoid ligament repair. Patients with rigid stage IV disease will require an ankle fusion, which is associated with significant morbidity. Ankle replacement is an alternative to arthrodesis.[3][23](B2)

A recent meta-analysis of surgical treatments for progressive collapsing foot deformity was conducted to study therapy efficacy further. This study analyzed different radiographic angles to measure the effectiveness of each procedure, including medial calcaneal osteotomies, lateral column lengthening, and double and triple arthrodesis. The results suggested that all treatment types result in significant improvements for the patient.[24](A1)

The orthopedic consensus agreed on 3 statements concerning the operative treatment of progressive collapsing foot deformity: mobility and range of motion should always be prioritized, especially in younger patients. Talonavicular joint fusion should be considered only in arthritic joints, important sagittal plane sagging, severe deformity, inadequate correction of talonavicular abduction, and patients with higher body mass index will generally do worse with reconstructive osteotomies when compared to arthrodesis.[25](B3)

Differential Diagnosis

While the diagnosis of progressive collapsing foot deformity is relatively straightforward, the treating clinician needs to rule out several diagnoses when acquired flatfoot is suspected. These include adult flexible flatfoot, tarsal coalition, Charcot foot, neuromuscular flatfoot, and arthritic, post-traumatic, and iatrogenic deformity. A careful history and physical can rule out most of these etiologies.[26]

Staging

Johnson and Strom Classification (1989) Modified by Myerson (1997):

Stage 1: Normal radiographs, able to perform single-heel raise and mild tenosynovitis

Stage 2A: Arch collapse on a radiograph, unable to perform single-heel raise, and a flexible flatfoot deformity

Stage 2B: Arch collapse and talonavicular exposure (over 40%) on a radiograph, unable to perform single heel raise, flexible flatfoot deformity, and characteristic forefoot abduction or “too many toes” sign

Stage 3: Subtalar arthritis on a radiograph, unable to perform single heel raise, flatfoot deformity with rigid forefoot abduction, and hindfoot valgus

Stage 4: Valgus deformity of talus in the ankle mortise visualized on an anterior-posterior radiograph of the ankle-talar tilt due to deltoid ligament compromise, subtalar arthritis on radiographs, unable to perform single heel raise, flatfoot deformity with rigid forefoot abduction, and hindfoot valgus [19]

Orthopedic Consensus Group (2020 Classifications)

Stage 1 is flexible, and stage 2 is rigid. Both stages 1 and 2 can be subdivided into classes A to E listed below:

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 joint or naviculocuneiform 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

The prognosis for most patients with progressive collapsing foot deformity is positive. Most patients do not require surgery. Approximately 10% of patients who require surgery can expect favorable outcomes.[16] The higher-grade diseases require more extensive surgery, with stage IV progressive collapsing foot deformity requiring ankle fusion or total ankle arthroplasty.[3]

Complications

If left untreated, progressive collapsing foot deformity can progress to more severe stages that require more invasive treatments. Early diagnosis is critical and can even help avoid surgery in some patients. As the disease progresses into the late stages, the need for the patient to get an ankle fusion increases. With an ankle fusion, the patient essentially has an immobile ankle joint, and many recreational activities are affected.