Addressing The Biomechanics Of Stage II Adult-Acquired Flatfoot

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Understanding The Progression Of The Adult-Acquired Flatfoot Deformity

1. Preexisting flatfoot deformity
2. Pronated position of the subtalar joint creates increased friction and gliding resistance of the posterior tibial tendon
3. Posterior tibial tendon gradually attenuates and ruptures
4. Pronated subtalar joint creates increased mobility of the forefoot on the rearfoot, increasing strain on the supportive ligaments
5. Sequential ligament rupture occurs beginning with the spring ligament and followed by the long and short plantar ligaments as well as the superficial and deep deltoid ligaments
6. Progressive flatfoot deformity occurs and is characterized by hindfoot valgus, lowering of the medial longitudinal arch and forefoot abduction

Douglas Richie, Jr., DPM, FACFAS, FAAPSM

Given the common presentation of adult-acquired flatfoot in podiatric practice, this author discusses the pathomechanics of the condition, offers diagnostic insights on the spring ligament and the heel raise test, and shares perspectives from the literature on the efficacy of treatment interventions.

Adult-acquired flatfoot represents one of the most challenging clinical conditions facing the podiatric physician. With insights gained from recent biomechanical studies, clinicians can more accurately design and target treatment strategies for a more positive patient outcome.

   The adult-acquired flatfoot is a symptomatic, progressive deformity, which is the result of loss of integrity and function of the posterior tibial tendon as well as key supportive ligaments of the ankle and hindfoot.1 While this condition was previously known as posterior tibial tendon dysfunction (PTTD), we now know that simply attributing this deformity to a single anatomic structure is shortsighted and will overlook the more important role of ligamentous disruption, which leads to the true disability of this disorder.

   Adult-acquired flatfoot appears to be a common, if not epidemic, condition presenting to podiatric practice. However, few studies have been conducted to verify the true incidence in the general population. In a survey of 1,000 women over the age of 40 in the United Kingdom, 3.3 percent had symptoms and other clinical evidence of adult-acquired flatfoot.2 Many studies have verified that women over the age of 50 are most at risk for developing adult-acquired flatfoot. Other contributing factors include diabetes, hypertension and obesity.3

   Staging of the adult-acquired flatfoot deformity has traditionally followed the classification proposed by Johnson and Strom.4 Stage I adult-acquired flatfoot is characterized by symptoms of pain and swelling along the posterior tibial tendon without visible changes of foot alignment. Stage II deformity shows asymmetry of alignment with hindfoot valgus and forefoot abduction exaggerated on the symptomatic foot. Patients with stage II adult-acquired flatfoot have weakness with inversion and difficulty performing a single foot heel raise, indicating attenuation or rupture of the posterior tibial tendon. Stage III adult-acquired flatfoot represents a progression of all the clinical signs of stage II but the deformity has now become rigid. Myerson proposed Stage IV to include a valgus deformity within the ankle joint itself.5

   According to Tome and coworkers, patients in stage II AAF will demonstrate the following clinical findings:
• palpable tenderness of the posterior tibial tendon;
• swelling along the distal sheath of the posterior tibial tendon;
• pain or inability to perform the single limb heel rise;
• flexible valgus deformity of the hindfoot in static stance; and
• increased abduction of the forefoot during gait.6

Can Orthotic Interventions And Modifications Help Address The Pathomechanics Of Adult-Acquired Flatfoot?

A sequence of events in the development and evolution of adult-acquired flatfoot is presented in the table “Understanding The Progression Of The Adult-Acquired Flatfoot Deformity” at right.

   As we evaluate each of the steps in this pathomechanics scheme, I will discuss the biomechanics and treatment interventions along with supportive references from the medical literature.

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