Progressive pes planus (flatfoot) deformity in adults is a common entity that is encountered by orthopedic surgeons. A deformity that develops after skeletal maturity is reached is commonly referred to as adult-acquired flatfoot deformity (AAFD). AAFD should be differentiated from constitutional flatfoot, which is a common congenital nonpathologic foot morphology.[1, 2] The use of the term acquired implies that some physiologic or structural change causes deformity in a foot that previously was structurally normal.
Over the past few decades, interest in the biomechanics and anatomic contributions to this deformity has led to greater insight into its etiology. Despite the significant incidence of this condition, there is still some debate regarding its pathophysiology. The failure of one anatomic entity alone is unlikely to explain the clinical presentation of AAFD. Instead, a mismatch between active and passive arch stabilizers is a more likely scenario (see Pathophysiology and Etiology).
Insufficiency or dysfunction of the posterior tibial tendon (PTT) has historically been thought to be the most common cause of AAFD.[3] Later research has focused more on the static restraints of the medial longitudinal arch. Patients with PTT insufficiency demonstrate extensive involvement of ligaments, particularly the spring-ligament complex, the talocalcaneal interosseous ligament, and the deltoid ligament.[4, 5] Because ligament pathology is nearly as common as PTT pathology, the authors favor AAFD as the term that most accurately describes this condition.
PTT insufficiency was originally described by Kulowski in 1936.[6, 7] In 1953, Key intraoperatively identified a PTT rupture that was treated with excision.[8] 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.[9, 10]
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.[11] The use of a flexor digitorum longus (FDL) transfer was popularized in 1982 by Mann,[12] Specht, and Jahss[13] ; however, the original description of using tendon transfer for the treatment of progressive flatfoot deformity is attributed to Goldner in 1974.[7, 14]
Important clinical signs of PTT dysfunction, the too-many-toes sign and the single-limb, heel-rise test, were discussed by Johnson in 1983.[15] A widely accepted classification system, proposed by Johnson in 1989 and modified by Myerson in 1997, clarified treatment recommendations on the basis of the severity of the PTT dysfunction and the adaptation of the foot to collapse of the medial longitudinal arch.[16, 17] Most treatment strategies continue to focus on the PTT as the weak link in AAFD.
For information on related topics, see Pes Cavus and Pes Anserine Bursitis.
NextThe function and structure of the medial longitudinal arch are affected by numerous anatomic structures, all offering potential contributions to the pathophysiology of 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 a lateral longitudinal arch. The medial arch is composed of the calcaneus, the talus, the 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 weightbearing, 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.[18] Dorsiflexion of the toes during the gait cycle results in tightening of the plantar fascia, which ultimately elevates the arch.[19]
The spring-ligament complex has received much attention as an important stabilizer of the medial arch.[4, 20] This calcaneonavicular ligament serves the following two important functions[21] :
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.[4]
The most frequently affected dynamic stabilizer in AAFD is the PTT. This structure is the most powerful invertor of the foot and serves as an important dynamic arch stabilizer.[22, 23] The posterior tibial muscle and the 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 the PTT pass posteromedially behind the medial malleolus and then insert via multiple bands into the navicular, the cuneiforms, the second through fourth metatarsal bases, 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.
Contraction of the PTT causes inversion of the midfoot and elevation of the medial longitudinal arch. The PTT also indirectly affects hindfoot inversion by virtue of its course running behind the medial malleolus and its close association with the deep deltoid and spring ligaments.
During the gait cycle, the foot must transition from a flexible construct at heel strike (to accommodate irregular surfaces) to a rigid construct at pushoff (to maintain a rigid lever for ambulation).[24] At heel rise, PTT initiation of transverse tarsal joint adduction with resultant subtalar inversion causes the talonavicular and calcaneocuboid joint axes to diverge and the transverse tarsal joint (Chopart joint) to become locked. This process converts the foot into a rigid lever arm against which the powerful gastrocnemius-soleus complex acts to propel the body forward.[25]
Loss of posterior tibial function due to stretching or rupture of the PTT removes the primary inverter of the foot and leaves the primary and secondary everters of the foot, the peroneus brevis and the peroneus longus, relatively unopposed. Thus, posterior tibial dysfunction leads to flattening of the medial longitudinal arch, forefoot abduction, and hindfoot valgus.
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.[26] Three-dimensional computed tomography (CT) of patients with AAFD has documented subluxation of the subtalar joint with less contact between all three facets of the calcaneus and talus as compared with control subjects.
Clinically, the arch flattens, the forefoot abducts, and heel valgus occurs. (See Presentation.) This abnormal foot position has a profound negative impact on the gait cycle. The inability of patients with AAFD to lock the transverse tarsal joints prevents the formation of a rigid lever arm and transforms the foot into a "bag of bones." Patients will be unable 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. As the static and dynamic stabilizers of the arch are overloaded, the painful clinical spectrum of AAFD develops.[27, 28]
There are numerous causes of AAFD, including the following:
The most common cause of AAFD is PTT dysfunction. The etiology of PTT dysfunction is varied; it is attributed to degenerative, inflammatory, and traumatic causes.
Although most cases of AAFD are attributable to PTT insufficiency, it is still necessary to evaluate patients for other possible causes so as to ensure optimal treatment.[29]
Younger patients who present with rigid flatfoot should be screened for tarsal coalition, congenital vertical talus, or other forms of congenital hindfoot pathology. It is theorized that patients with asymptomatic flatfeet may eventually progress to symptomatic disease as ongoing degenerative processes turn flexible deformities into rigid ones, though no natural history studies are available to support this often-repeated theory.[30, 31] Biomechanical studies confirm elevated gliding resistance and trauma to the PTT surface in a simulated flatfoot model.[32] These data support the hypothesis that preexisting flatfoot predisposes to AAFD because of chronic mechanical overload.[32, 33]
Trauma to bone, soft tissue, or both 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.[34] (See Plantar Heel Pain and Plantar Fasciitis.)
Arthritides, both inflammatory and degenerative, must also be examined as a possible underlying cause of AAFD. Degenerative arthritides typically give rise to signs and symptoms in and around the midfoot region with accompanying pain and exostosis. Rheumatoid arthritis (RA) and other inflammatory arthritides (eg, seronegative spondyloarthropathies and gout) have a deformity progression that is primarily dependent upon disease control. In one study, 11% of 99 RA patients were found to have PTT pathology.[35]
Neuropathy-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 necessitate 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 Charcot Arthropathy and Imaging in 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. A zone of tendon hypovascularity exists 1-1.5 cm distal to the medial malleolus, continuing 14 mm distally. Poor blood supply in this area of the tendon, where it takes a sharply curving course around the medial malleolus, could result in tendon degeneration and may explain a mechanical cause for tendon rupture. 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 established a clear link between a specific factor and tendon dysfunction.[36]
In one study, 60% of patients were obese or had diabetes mellitus, hypertension, previous surgery or trauma to the medial foot, or treatment with steroids. Myerson described two subsets of patients with PTT dysfunction.[37] One patient group was younger and had associated enthesopathies at multiple sites, a higher incidence of HLA-B27 positivity, and a significant family history for inflammatory disease and psoriasis; these factors suggested a seronegative spondyloarthropathy. The other patient group was older and had isolated dysfunction; these factors suggested a purely mechanical degenerative cause.
Although PTT dysfunction is a common clinical entity, its true incidence or frequency is difficult to ascertain secondary to a variety of factors, such as missed diagnoses and coexisting disorders that can make the diagnosis perplexing. However, certain conditions are well known and documented. For example, several authors have noted that the incidence of PTT pathology or rupture is higher in middle-aged women who have coexisting obesity.[15, 38, 39, 40]
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, in a study involving 67 patients with PTT rupture,[41] noted that almost 60% of their patients had a history of at least one of the above-noted conditions.
Proper treatment of AAFD requires a comprehensive knowledge of foot biomechanics and astute clinical judgment. No single solution is appropriate for all patients and all degrees of dysfunction; rather, a continuum of treatment options must be considered to gain the best functional outcome for the individual patient.
Prospective data on the outcome of surgical intervention for stage 2 AAFD (see Workup, Staging) demonstrated significant improvement of all outcome measures utilized including high patient satisfaction.[42] The authors noted that patients should be aware that maximal improvement takes at least 1 year.
The patients who are best suited for an optimal return to full function have mild changes of the dynamic structures but maintenance of the static restraints of the hindfoot. These patients are most tolerant of nonoperative treatment modalities and, if surgery is necessary, can reasonably expect a return to near-normal function if joint-sparing options are utilized.
Patients should be advised about the prolonged length of recovery following surgical reconstruction of the foot. Generally, 6 weeks of no weightbearing is required for soft-tissue procedures and osteotomies, and up to 3 months of no weightbearing is required for fusions. Swelling of the foot should be expected for 4-10 months after surgery. Finally, although high rates of good-to-excellent results are reported for most surgical procedures, there is often some foot discomfort with prolonged standing or walking after surgery, and patients should be advised of this possibility.
Clinical Presentation
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