e4-10: Flatfoot (Pes Planus)

Flatfoot deformity is common, but most cases are asymptomatic. Flatfoot is also known as adult acquired flatfoot, pes planus, or pes planovalgus. There is a wide range of presenting ages and complaints. Flatfoot is a progressive deformity characterized by the collapse of the medial longitudinal arch with forefoot abduction and hindfoot valgus (Figures E4–6 and E4–7). There are numerous causes of flatfoot including rearfoot equinus, tendon laceration, tarsal coalition, arthritis, neuroarthropathy, muscle imbalances, ligamentous laxity, and neurologic weakness. Most cases of flexible pes planus are associated with generalized ligamentous laxity.

The most common etiology of flatfoot deformity is posterior tibial tendon dysfunction. Even with most causes associated with posterior tibial tendon dysfunction, it is still necessary to evaluate patients for other possible causes to ensure optimal treatment. Patients with congenital ligamentous laxity secondary to Down syndrome, Marfan syndrome, or Ehlers-Danlos syndrome are susceptible to developing flatfoot. Ligamentous laxity seen in pregnancy may also cause flatfoot, but this usually corrects itself soon after delivery. Patients with degenerative or inflammatory arthropathies, rheumatoid arthritis, or seronegative arthropathies are at higher risk for developing flatfoot. A common result in Charcot neuroarthropathy leads to midfoot collapse with a rigid rocker-bottom flatfoot.

Flatfoot is common in the first decade of life, when most infants are born with flatfeet and develop a medial arch during their first decade of life. Children and early adolescents are prone to flatfeet because of ligamentous laxity and lack of neuromuscular control. Most instances of flatfoot in children are flexible, meaning there is an arch present without weight bearing but collapses with weight bearing. Younger patients with rigid flatfoot should be screened for tarsal coalition, congenital vertical talus, accessory navicular, or other hindfoot pathologies. Studies support the theory that asymptomatic flatfoot can progress into symptomatic flatfoot over time as ongoing degenerative processes change flexible deformities into a rigid deformity.

A. Symptoms and Signs

The flatfoot may or may not be symptomatic. Pain coincides variably with the severity or progression of the deformity. Patients may report arch, medial ankle, heel, or pretibial pain. Patients may also report lateral ankle pain due to lateral impingement (sinus tarsi and fibular-calcaneal), which is seen over time as the deformity progresses. When symptoms are present, patients frequently report a dull achy pain at the medial arch or medial ankle. They also may describe a feeling of “muscle weakness” or fatigue with exercises or standing for long periods of time.

The clinical examination should include a generalized overview of the foot type, a gait analysis, and an examination of the foot and ankle in both weight bearing and non–weight-bearing. There is a variable spectrum of presentation from flexible to rigid. Upon inspection, the foot may have an arch while non–weight-bearing but flattens with weight bearing. The arch may reconstitute with toe walking, hallux dorsiflexion at the first MTP joint (activation of the windlass mechanism), or hanging the foot in plantarflexion. Upon weight bearing and gait analysis, there may be collapse of the medial longitudinal arch, the “too many toes” sign, valgus hindfoot deformity, and forefoot abduction. Examination should include an evaluation of the ankle joint and subtalar joint range of motion. In a flexible deformity, the examiner can passively correct the deformity to a plantigrade foot. In a rigid deformity, the examiner cannot correct the deformity. The heel cord can have a contracture (ankle joint equinus) with lateral deviation of the Achilles with weight bearing. Severe Achilles contracture is associated with midfoot breakdown.

If the patient reports pain in the medial ankle or of pain during the examination posterior to the medial malleolus, posterior tibial tendon dysfunction should be strongly suspected. Examination should include a single heel raise, with the heel raising off the ground and inverting (Figure e4–8). If patients are unable to perform the single heel raise or if there is pain with this motion, the posterior tibial tendon is weak and inflamed. The posterior tibial tendon’s strength should be examined by manual muscle testing by positioning the foot in plantarflexion and full inversion. If the patient is unable to maintain this foot position when the examiner applies an eversion force, the posterior tibial tendon is underpowered.

B. Imaging

Plain radiographs are used to determine the severity of a flatfoot deformity or to rule out other mimicking conditions. Weight-bearing anteroposterior, oblique, and lateral radiographs of the foot are the most useful images (Figure e4–9). On weight-bearing anteroposterior view of the foot, the following will be evaluated: talar head coverage, increased talocalcaneal angle, cuboid-abduction angle, and talar-first metatarsal axis. The oblique view is to help rule out a tarsal coalition. Another view called the Harris-Beath view can help rule out a tarsal coalition. A weight-bearing lateral radiograph of the foot can evaluate for decrease in calcaneal inclination angle, increased talar declination angle, increased first metatarsal declination angle, anterior break in the Cyma line, and the Meary angle.

MRI in later stages of this deformity may show a varying amount of posterior tibial tendon degeneration and arthritic changes in the talonavicular, subtalar, and tibiotalar joints.

Since the severity of the deformity varies depending on the pathological anatomy and changes in biomechanics, staging can be helpful in guiding treatment protocols. Johnson and Strom (later modified by Myerson) is a widely used classification system, which also gives recommendations on possible procedures to be performed according to the stage of the deformity. Johnson and Strom published their three stages in 1989, and Myerson added the fourth stage in 1996. It is very common to perform a combination of procedures because this is a complicated deformity with multiple planes of motion affected. The classification system focuses on deformity, flexibility or rigidity, and muscle strength and degeneration.

Stage I

Stage I includes tenosynovitis with mild tendon degeneration. Findings might include tenderness along the course of the posterior tibial tendon. The tendon strength may have a mild weakness, if any, assessed by the single heel raise. The foot usually demonstrates normal alignment with a flexible hindfoot. With gait analysis, there will be an absence of the “too many toes” sign.

Stage II

Stage II includes elongation of the posterior tibial tendon with tendon degeneration. The hindfoot deformity remains flexible. There is marked weakness and pain of the posterior tibial tendon with the single heel raise. There may be pain with palpation along the course of the posterior tibial tendon. In this stage, the disease is a dynamic deformity with hindfoot valgus and forefoot abduction. With gate analysis, a positive “too many toes” sign will be present (visualization of the lateral toes with gate analysis of the patient from behind).

Stage III

Stage III includes chronic dysfunction with elongated and possible rupture of the posterior tibial tendon. The lengthening of the posterior tibial tendon leads to a rigid hindfoot valgus deformity. Because of this rigid hindfoot valgus deformity, the forefoot usually compensates with a supination. There is marked weakness and pain with single heel raise test or inability to perform the test. Also, the “too many toes” sign is seen with gait analysis. There can be lateral ankle pain due to lateral impingement (sinus tarsi and fibular-calcaneal impingement).

Stage IV

Stage IV includes the same findings of stage III but with ankle joint valgus. Longstanding hindfoot valgus places increasing stress on the deltoid complex with eventual failure, which results in a valgus tilt of the talus. This change in the biomechanical forces of the ankle joint results in arthrosis of the joint.

A. Conservative

Conservative care entails patient education of the natural history of the deformity and biomechanical support, which is appropriate for some flexible and asymptomatic patients. Also, conservative treatment is indicated for patients who are not candidates for or not amenable to surgical intervention. Stretching, muscle strengthening, shoe gear modifications, and orthotics are all types of conservative treatments. For shoe gear, a supportive “motion control” type of shoe is recommended. Functional orthotics includes custom or prefabricated orthotic device, which can aid in providing arch support, changing the heel strike position, and heel support during the gait cycle. Orthotics may help the patient’s discomfort but will not change the natural progression of the deformity or reverse the flatfoot deformity. Anti-inflammatory medications, such as nonsteroidal anti-inflammatory drugs, may provide symptomatic relief.

B. Surgical

Pain, discomfort, and rigid deformity are the major considerations for surgical correction. Many different surgical treatments have been described in the literature to correct flatfoot deformities, and because this deformity affects multiple joint and planes of motion, a combination of procedures are typically performed together. Because it is a disorder with a spectrum of deformity, there is controversy over surgical options throughout the stages of the deformity. Surgical options may include procedures of tendon debridement, tendon balancing (including lengthening or transfer), osteotomy, or arthrodesis.

• If the patient has not responded to conservative treatment.

• There is severe deformity or fixed deformity.

• There is severe pain or posterior tibial tendon weakness.

• There is difficulty with ambulation or footwear problems.