Practice Essentials
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, Specht, and Jahss [12] ; however, the original description of using tendon transfer for the treatment of progressive flatfoot deformity is attributed to Goldner in 1974. [7, 13]
Important clinical signs of PTT dysfunction (eg, the too-many-toes sign and the single-limb heel-rise test; see Presentation) were discussed by Johnson in 1983. [14] 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. [15, 16] Most treatment strategies continue to focus on the PTT as the weak link in AAFD (see Treatment).
The overall medical condition of the patient, the patient's expectations, and the stage of the disease determine the recommended treatment. For example, if the patient has low physical demands or has serious underlying medical problems, he or she should be treated nonoperatively. Operative management should be considered only after conservative management (see Nonoperative Therapy) has proved unsuccessful. The surgical procedure chosen should address all the fixed and dynamic deformities for each patient. Comparative outcome trials are needed to provide better data for evaluation of the various therapeutic options.
For information on related topics, see Pes Cavus and Pes Anserine Bursitis.
Anatomy
The 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, the 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. [17] Dorsiflexion of the toes during the gait cycle results in tightening of the plantar fascia, which ultimately elevates the arch. [18]
The spring-ligament complex has received much attention as an important stabilizer of the medial arch. [4, 19] This calcaneonavicular ligament serves the following two important functions [20] :
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Acting as a support for the head of the talus, thus providing stability to the talonavicular joint
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Maintaining the medial longitudinal arch by acting as a static support
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. [21, 22] 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.
Pathophysiology
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). [23] 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. [24]
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. [25] 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. [26, 27]
Etiology
There are numerous causes of AAFD, including the following:
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Fracture or dislocation
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Spring ligament tear
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Tendon laceration
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Tarsal coalition
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Arthritis
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Neuroarthropathy
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Neurologic weakness
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Iatrogenic causes
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. [28]
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 this often-repeated theory has not been confirmed by natural history studies. [29, 30] Biomechanical studies confirm elevated gliding resistance and trauma to the PTT surface in a simulated flatfoot model. [31] These data support the hypothesis that preexisting flatfoot predisposes to AAFD because of chronic mechanical overload. [31, 32]
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. [33] (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. [34]
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. [35]
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. [36] One patient group was younger and had associated enthesopathies at multiple sites, a higher incidence of human leukocyte antigen (HLA)-B27 positivity, and a significant family history for inflammatory disease and psoriasis; these factors suggested a seronegative spondyloarthropathy. The other group was older and had isolated dysfunction; these factors suggested a purely mechanical degenerative cause.
It was previously postulated that AAFD could be iatrogenically introduced via a PTT transfer utilized for correction of foot drop or cavovarus foot reconstruction. Pecheva et al studied 10 patients who underwent a PTT transfer for either foot drop or cavovarus reconstruction; at 45 months' follow-up, none of the patients had developed AAFD radiographically, and only one had findings consistent with spring-ligament strain on physical examination. [37]
Epidemiology
Although PTT dysfunction is a common clinical entity, its true incidence or frequency is difficult to ascertain for a number of reasons, including missed diagnoses and coexisting disorders that can make the diagnosis perplexing. However, certain conditions are well known and documented. For example, several authors noted that the incidence of PTT pathology or rupture is higher in middle-aged women who have coexisting obesity. [14, 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 et al, 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.
Prognosis
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 in order to obtain the best functional outcome for the individual patient.
Prospective data on the outcome of surgical intervention for stage 2 AAFD (see 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.
There is a paucity of literature regarding the long-term follow-up of patients who undergo reconstruction for AAFD. In a study that examined 102 stage 2 feet at a mean follow-up of 10 years, [43] patients were treated with several combinations of techniques, including FDL transfer, direct repair, medial displacement calcaneal osteotomy (MDCO), and/or lateral-column lengthening (LCL). (See Surgical Therapy for Stage 2 AAFD.) The authors reported a mean American Orthopaedic Foot and Ankle Society (AOFAS) hindfoot score of 89 ± 10 and noted that 86% of patients were satisfied with their foot.
Patients older than 65 years, previously considered only for arthrodesis (see Surgical Therapy for Stage 3 AAFD), have been shown to do well with stage 2 joint-sparing reconstruction. With a minimum follow-up of 2 years, Conti et al demonstrated that older patients showed similar improvements in Foot and Ankle Outcome Score subscales to those seen in young and middle-aged patients. [44] Although they were shown to need additional corrective procedures at the time of initial operation, they were not at significantly increased risk for revision surgery.
Return to the prior athletic level after stage 2 joint-sparing reconstruction has also been demonstrated. Usuelli et al studied 42 patients (mean age, 41 y) who underwent MDCO with FDL transfer and followed them for 2 years. [45] As a whole, these patients were able to engage in their sporting activities for longer periods than they could before surgery, with the significant majority reporting good pain and symptoms scores during performance. However, this ability may be limited to recreational activities; one study of military patients reported that only 4% returned to the prior level of function before deformity onset, and 40% required medical discharge from the military. [46]
Patient Education
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 6-12 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.
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Photographs from patient with adult-acquired flatfoot deformity (AAFD) show typical features of condition, demonstrated by abducted forefoot and valgus hindfoot.
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Intraoperative images from patient with pes planus (flatfoot). (A) Flexor digitorum longus (FDL) transfer to navicular bone. (B) Torn spring ligament.
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Pes planus (flatfoot). Axial magnetic resonance image demonstrating medial calcaneal shift.
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Arizona Brace. Image courtesy of Don Pierson, CO of Arizona AFO, Inc.
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Radiographs of foot in patient with pes planus (flatfoot). (A) Preoperative radiograph of stage 3 posterior tibial tendon (PTT) dysfunction. (B) Radiograph obtained 3 months after triple arthrodesis with bony union.
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Anteroposterior and lateral radiographs of lower extremity in patient with pes planus (flatfoot). Images demonstrate stage 4 posterior tibial tendon (PTT) dysfunction with valgus tilt at ankle.
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Pes planus (flatfoot). Too-many-toes sign. Three lateral toes are visible on symptomatic left foot, compared with only two toes on right foot (black arrow). Medial midfoot is prominent and swollen (yellow arrow).
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Pes planus (flatfoot). Single-limb heel-rise test. Patient with posterior tibial tendon (PTT) dysfunction is unable to rise up on toes because of inability to invert hindfoot.
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Pes planus (flatfoot). Fixed forefoot varus is characterized by elevation of medial side of forefoot, even after heel is placed in neutral position.
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Pes planus (flatfoot). Standing lateral radiograph of foot of patient with posterior tibial tendon (PTT) dysfunction. A = lateral first talometatarsal angle (normal value, 0°). B = calcaneal pitch (normal value, 20-25°). C = Distance from medial cuneiform to floor (normal value varies with foot size). As deformity increases secondary to PTT dysfunction, talus plantarflexes and medial border of foot is lowered. Therefore, lateral first talometatarsal angle decreases, calcaneal pitch decreases, and medial cuneiform is depressed closer to floor.
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Pes planus (flatfoot). Standing anteroposterior radiograph of patient with posterior tibial tendon dysfunction shows talonavicular coverage angle; navicular axis is formed by perpendicular line connecting medial and lateral aspects of navicular proximal articular surface. Talonavicular coverage angle is formed by talar and navicular axes. As forefoot abduction increases, talonavicular coverage angle increases.
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Pes planus (flatfoot). Flexor hallucis longus (FHL) tendon is identified under sustentaculum tali and is pulled proximally. FHL and flexor digitorum longus (FDL) tendons then are sutured to each other with 2-0 nonabsorbable suture prior to division of FHL tendon.
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Pes planus (flatfoot). Flexor hallucis longus (FHL) tendon is rerouted anterior to posterior tibial tendon (PTT) and sutured to navicular tuberosity with suture anchor. Multiple No. 2 nonabsorbable sutures also are used to suture FHL tendon to PTT stump and navicular tuberosity periosteum.
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Pes planus (flatfoot). Incision for calcaneal osteotomy is made posterior to peroneal tendon sheath and sural nerve. Incision is made at 45° angle to plantar aspect of foot.
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Pes planus (flatfoot). Calcaneal osteotomy is distracted with laminar spreader to spread medial soft tissues. This permits easy medial displacement of calcaneal tuberosity.
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Pes planus (flatfoot). Lateral radiograph of fixated calcaneal osteotomy. After tuberosity is displaced medially 1 cm, two screws are inserted perpendicular to osteotomy site under fluoroscopic control.
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Pes planus (flatfoot). Intraoperative axial view of fixated calcaneus documents satisfactory medial translation of tuberosity and satisfactory screw position.
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Pes planus (flatfoot). Preoperative anteroposterior view of foot prior to lateral-column lengthening (LCL). Note forefoot abduction and increased talonavicular coverage angle.
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Pes planus (flatfoot). Distraction arthrodesis of calcaneocuboid joint with tricortical iliac crest graft results in lengthening of lateral column. Osteotomy is fixated with laterally placed cervical plate. Note correction of forefoot abduction and correction of talonavicular coverage angle.
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Pes planus (flatfoot). Outline of extended Z-cut osteotomy.
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Pes planus (flatfoot). Axial model of extended Z-cut osteotomy demonstrating medialization of calcaneal tuberosity and lengthening of lateral column simultaneously through rotation of horizontal osteotomy arm.
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Pes planus (flatfoot). Preoperative lateral radiograph of stage 2B adult-acquired flatfoot deformity (AAFD) prior to reconstruction with extended Z-cut osteotomy.
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Pes planus (flatfoot). Preoperative anteroposterior radiograph of stage 2B adult-acquired flatfoot deformity (AAFD) prior to reconstruction with extended Z-cut osteotomy.
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Pes planus (flatfoot). Postoperative lateral radiograph of stage 2B adult-acquired flatfoot deformity (AAFD) after reconstruction with extended Z-cut osteotomy displaying restored radiographic parameters and osteotomy union.
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Pes planus (flatfoot). Postoperative anteroposterior radiograph of stage 2B adult-acquired flatfoot deformity (AAFD) after reconstruction with extended Z-cut osteotomy displaying restored radiographic parameters.
