Pes Planus 

Progressive pes planus, or flatfoot, deformity in adults is a common entity that is encountered by orthopedic surgeons. Despite the significant incidence of this condition, the pathophysiology is still debated. The failure of one anatomic entity alone is unlikely to explain the clinical presentation of adult-acquired flatfoot deformity (AAFD). Instead, a mismatch between active and passive arch stabilizers is a more likely scenario (see Pathophysiology). See the images below.

The term "acquired" implies that some physiologic or structural change causes deformity in a foot that was structurally normal at one point. Insufficiency or dysfunction of the posterior tibial tendon (PTT) has historically been thought to be the most common cause of AAFD.^[1] Later research has focused more on the static restraints of the medial longitudinal arch. Patients with PTT insufficiency demonstrate extensive ligament involvement, particularly the spring-ligament complex and the talocalcaneal interosseous ligament.^[2] Because ligament pathology is nearly as common as PTT pathology, the authors favor the use of AAFD to accurately describe this condition.

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Adult-acquired flatfoot deformity (AAFD) has received increased attention in the medical literature. In the past 2 to 3 decades, interest in the biomechanics and anatomic contributions to this deformity has led to greater insight into its etiology. Most treatment strategies continue to focus on the posterior tibial tendon (PTT) as the weak link in AAFD.

PTT insufficiency was originally described by Kulowski in a 1936 article.^[3] In 1953, Key intraoperatively identified a PTT rupture that was treated with excision.^[4] This was followed by articles by Fowler and Williams, who each presented posterior tibial tendinitis as a syndrome, with the suggestion that surgical intervention may play a role in the treatment of this condition.^{[5, 6]}

Results from a 1969 study by Kettelkamp and Alexander revealed that when patients demonstrated tendon rupture and surgical correction was delayed, a poor outcome with surgical exploration resulted.^[7] The use of a flexor digitorum longus (FDL) transfer was popularized in 1982 by Mann, Specht, and Jahss; however, the original description of using tendon transfer for the treatment of progressive flatfoot deformity is attributed to Goldner in 1974.^{[3, 8]}

Important clinical signs of PTT dysfunction, the too-many-toes sign and the single-limb, heel-rise test, were discussed by Johnson in 1983.^[9] A widely accepted classification system, proposed by Johnson in 1989 and modified by Myerson in 1997, clarified treatment recommendations based on the severity of the PTT dysfunction and adaptation of the foot to collapse of the medial longitudinal arch.^{[10, 11]}

Clinical presentation and progression and severity of adult-acquired flatfoot deformity (AAFD) can be extremely variable; a multitude of conservative and surgical options are available for this common clinical entity. A clear understanding of the normal function of the posterior tibial tendon (PTT) and the static restraints of the medial longitudinal arch is essential to understanding the operative and nonoperative treatment options for AAFD.^[12]

Frequency

Although posterior tibial tendon (PTT) dysfunction is a common clinical entity, a true incidence or frequency is difficult to ascertain secondary to a variety of factors, such as missed diagnoses and coexistent disorders that can make the diagnosis perplexing. However, certain conditions are well known and documented. For example, several authors have noted the incidence of PTT pathology or rupture is higher in middle-aged women who have coexisting obesity.^{[9, 13, 14, 15]}

Other clinical entities that have been found to contribute to the development of PTT dysfunction include diabetes mellitus, hypertension, steroid exposure, or previous trauma or surgery in the medial foot region. Holmes and Mann studied 67 patients with PTT rupture.^[16] The authors noted almost 60% of their patients had a history of at least one of the above-noted conditions.

See Pathophysiology.

Numerous causes for adult-acquired flatfoot deformity (AAFD) have been described; posterior tibial tendon (PTT) insufficiency is the most common etiology. However, patients must also be evaluated for other possible causes to ensure optimum treatment.^[17]

Younger patients who present with rigid flatfoot should be screened for tarsal coalition, congenital vertical talus, or other forms of congenital hindfoot pathology. Patients with asymptomatic flatfeet may eventually progress to symptomatic disease as degenerative processes ensue and turn flexible deformities into rigid ones, although no natural history studies are available to support this often-repeated theory.^[18] Biomechanical studies confirm elevated gliding resistance and trauma to the PTT surface in a simulated flatfoot model.^[19] These data support the hypothesis that preexisting flatfoot predisposes to AAFD because of chronic mechanical overload.^{[19, 20]}

Arthritides, both inflammatory and degenerative, must also be examined as a possible underlying etiology of AAFD. Degenerative arthritides typically have signs and symptoms in and around the midfoot region with accompanying pain and exostosis. Rheumatoid and other inflammatory arthritides (eg, seronegative spondyloarthropathies, gout) have deformity progression that is primarily dependent upon disease control.

Trauma, both bony and soft tissue, can lead to the development of AAFD. Fracture-dislocation that involves the medial column (navicular and first metatarsal), Lisfranc joints, and calcaneal fractures have been noted to cause AAFD, usually because of malunion or chronic joint subluxation. There has also been increasing interest in soft-tissue injury as a cause of flatfoot deformity. Ruptures of either the spring ligament or the plantar fascia (traumatic and iatrogenic) have been reported to lead to progressive collapse of the medial longitudinal arch.^[21]

Neuropathic-induced pes planus is perhaps the most concerning etiology of this condition, ranging from diabetes mellitus–induced Charcot arthropathy to spinal cord injuries. Midfoot collapse secondary to Charcot neuroarthropathy with a resultant rockerbottom foot may require a completely different route of intervention and treatment from those that are used for patients with PTT-insufficiency disease. The discussion of this complex topic, however, is beyond the scope of this article. [For more information, see the eMedicine articles Charcot Arthropathy and Neuropathic Arthropathy (Charcot Joint).]

Many vascular and degenerative etiologies have also been proposed to explain PTT failure. Clinical evidence indicates that in the high-stress region where the tendon curves around the medial malleolus, ruptures are common. This region corresponds to a relatively avascular area of the PTT between the navicular bone and the medial malleolus. Nontraumatic tears usually occur in this hypovascular location, suggesting a possible etiology of ischemia and subsequent tendinosis.

Histopathologic studies have documented the existence of a fibrocartilaginous zone in this same anatomic location, which not only alters the normal longitudinal collagen arrangement of the tendon, thus compromising the tendon's ability to counteract tensile forces, but also is subject to wear and tear. These changes result in marked disruption of collagen bundle orientation and structure and likely predispose to rupture. Epidemiologic studies have not proven a clear link between a specific factor and tendon dysfunction.^[22]

The clinical presentation of adult-acquired flatfoot deformity can be extremely variable and directly correlates with the stage of the disease.

The function and structure of the medial longitudinal arch are affected by numerous anatomic structures, all offering potential contributions to the pathophysiology of adult-acquired flatfoot deformity (AAFD).

The structural arrangement of the foot starts with 26 individual bones, each with a specific shape and function. The foot has both a medial and lateral longitudinal arch. The medial arch is composed of the calcaneus, talus, cuneiforms, and the first through third metatarsals. The lateral arch consists of the calcaneus, cuboid, and the fourth and fifth metatarsals. The wedge shape of the tarsal bones (wider dorsally, narrower plantarly) provides a stable, keystone arrangement. With weight bearing, tensile forces in the plantar fascia prevent separation of the ends of the medial and lateral arches. Additional arch height is provided by the windlass effect. Dorsiflexion of the toes during the gait cycle results in tightening of the plantar fascia, which ultimately elevates the arch.^[23]

The spring-ligament complex has received much attention as an important stabilizer of the medial arch.^{[2, 24]} This calcaneonavicular ligament serves 2 important functions by acting as a support for the head of the talus, thus providing stability to the talonavicular joint, and by maintaining the medial longitudinal arch by acting as a static support.^[25] The complex ligamentous support and congruent bony anatomy that surrounds the talonaviculocalcaneal joint have created comparisons to the ball-and-socket of the femoral head and acetabular articulation. This "acetabulum pedis" maintains the medial longitudinal arch and acts as an important static stabilizer. The spring-ligament complex is the most frequently affected static stabilizer in symptomatic AAFD.^[2]

The most frequently affected dynamic stabilizer in AAFD is the posterior tibial tendon (PTT), and it is the most powerful invertor of the foot and serves as an important dynamic arch stabilizer.^[26] The posterior tibial muscle and corresponding tendon are crucial to hindfoot position and foot flexibility during the gait cycle. Originating from the posterior aspect of the tibia, intraosseous membrane, and fibula, the posterior tibial muscle and tendon pass posteromedially behind the medial malleolus and then insert via multiple bands into the navicular, cuneiforms, metatarsal bases (second through fourth), and the sustentaculum tali. Ankle plantarflexion and forefoot adduction-supination with resultant subtalar inversion are key functions of the PTT because of its posteromedial position.

Considerable controversy exists regarding the timing of the failure of the medial longitudinal arch's static and active supports. Most orthopedic surgeons support the concept that the primary mode of failure is the loss of dynamic arch support, followed by a tension failure of the static restraints. The deformity involves "shortening" of the lateral column, plantar inclination of the talar head, and lateral subluxation of the navicular on the talar head.^[27] Clinically, the arch flattens, the forefoot abducts (ie, too-many-toes sign), and heel valgus occurs. This abnormal foot position has a profound negative impact on the gait cycle.

During the gait cycle, the foot must transition from a flexible construct at heel strike (to accommodate irregular surfaces) to a rigid construct at push-off (to maintain a rigid lever for ambulation).^[28] At heel rise, PTT initiation of transverse tarsal joint adduction with resultant subtalar inversion causes the talonavicular and calcaneocuboid joint axes to be perpendicular and therefore locked. This process converts the foot into a rigid lever arm against which the powerful gastrocsoleus complex acts to propel the body forward.^[29]

Patients with AAFD are unable to lock the transverse tarsal joints, thus preventing the formation of a rigid lever arm and transforming the foot into a "bag of bones." Clinical manifestations that ensue include the inability to perform a single-leg heel rise. This inability to invert the heel results in chronic heel valgus and subsequent Achilles contracture. Excessive forefoot abduction further stresses the static stabilizers of the midfoot (see image below). As the static and dynamic stabilizers of the arch are overloaded, the painful clinical spectrum of AAFD develops.^{[30, 31]}

Contraindications to surgical intervention in adult-acquired flatfoot deformity (AAFD) are similar to those for any other foot surgery. Absolute contraindications include an inadequately perfused foot, an insensate foot, or a nonambulatory patient. Otherwise, specific contraindications depend on the stage of the disease and an appropriate preoperative diagnosis. For example, performing a stage 1 procedure (ie, synovectomy) on a patient with stage 2 disease would most likely result in long-term postoperative failure. The same holds true for the other stages.

An FDL (flexor digitorum longus) transfer and calcaneal osteotomy would be contraindicated in a patient with fixed deformities or severe arthrosis of the hindfoot. A triple arthrodesis (fusion of the subtalar, talonavicular, and calcaneocuboid joints) alone or any lesser procedure would also be contraindicated in a patient with stage 4 disease. Proper diagnosis of the etiology and staging of disease are critical in the prevention of postoperative failure.