Pes Planus (Flatfoot) 

Updated: Jun 18, 2019
Author: Gregory C Berlet, MD, FRCSC, FAOAO; Chief Editor: Vinod K Panchbhavi, MD, FACS 



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 (eg, the too-many-toes sign and the single-limb heel-rise test; see Presentation) 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 (see Treatment).

For information on related topics, see Pes Cavus and Pes Anserine Bursitis.


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.[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] :

  • Acting as a support for the head of the talus, thus providing stability to the talonavicular joint
  • 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.[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:

  • Fracture or dislocation
  • Tendon laceration
  • Tarsal coalition
  • Arthritis
  • Neuroarthropathy
  • Neurologic weakness
  • 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.[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 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.[38]


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 noted that the incidence of PTT pathology or rupture is higher in middle-aged women who have coexisting obesity.[15, 39, 40, 41]

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,[42]  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 in order to gain 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.[43] 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. One study examined 102 stage 2 feet at a mean follow-up of 10 years.[44] These 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.[45]  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 years) who underwent MDCO with FDL transfer and followed them for 2 years.[46] 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.[47]

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.




The clinical presentation of adult-acquired flatfoot deformity (AAFD) can be extremely variable, as can the progression and severity of the condition. Typically, the presentation directly correlates with the stage of the disease (see Staging). Common presenting symptoms include the following:

  • Visible pes planus (flatfoot) deformity (see the image below)
  • Inability or pain upon attempts to perform a single-leg heel rise
  • Pain along the course of the posterior tibial tendon (PTT)
  • Difficulty in walking
Photographs from patient with adult-acquired flatf Photographs from patient with adult-acquired flatfoot deformity (AAFD) show typical features of condition, demonstrated by abducted forefoot and valgus hindfoot.

The usual initial complaint of a patient with PTT dysfunction consists of pain and swelling in the medial ankle and midfoot during weightbearing. Over time, the patient may notice loss of the arch and the tendency to walk on the inner border of the foot. Loss of pushoff strength during gait occurs, and a limp may develop. As the patient's heel displaces into valgus and the forefoot abducts, pressure between the calcaneus and fibula may develop, causing painful impingement between the lateral ankle and calcaneus. Abnormal wear of the medial heel and inner border of footwear may also be noted.

Physical Examination

The patient is first examined while standing so as to facilitate comparison of the symptomatic foot with the asymptomatic foot. The arch heights of the two feet are assessed and compared. In later stages of PTT dysfunction, the arch is lowered and the forefoot abducted. Viewing the patient's foot from behind allows the examiner to evaluate forefoot abduction and heel valgus. The toes visible lateral to the heel are counted. Normally, one or two toes are visible lateral to the heel. In cases of significant forefoot abduction, three or more toes are visible. This "too-many-toes" sign is a test to confirm forefoot abduction (see the image below).

Pes planus (flatfoot). Too-many-toes sign. Three l 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).

The angle that the heel forms with the longitudinal axis of the lower leg (the posterior tibiocalcaneal angle) also should be measured. This angle is increased in cases of significant heel valgus. The patient should then be asked to stand on one foot and rise up on the toes; he or she will usually need to hold on to the examining table or wall for balance during this maneuver. Normally, the heel inverts as the posterior tibial muscle contracts and as the gastrocnemius-soleus complex fires. In cases of PTT dysfunction, the heel does not invert, and the patient finds this single-limb heel-rise maneuver painful, difficult, or impossible (see the image below).

Pes planus (flatfoot). Single-limb heel-rise test. 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.

The patient then is examined seated on the examining table, and the course of the PTT is palpated for tenderness. Swelling along the PTT sheath may be noted, and fluid may be palpated within the sheath. Posterior tibial strength is tested by holding the forefoot in a position of plantarflexion and eversion and asking the patient to invert the foot. During this maneuver, the PTT should be palpated to assess its continuity. The sinus tarsi and distal fibular area also should be palpated for tenderness because in later stages of PTT dysfunction, these areas of impingement may also be painful.

The knee is extended, the foot is held in a subtalar neutral position, and passive ankle dorsiflexion is measured. Usually, 10-20° of dorsiflexion is possible, but in cases of long-standing pes planus, dorsiflexion past neutral is often limited because of the development of a plantarflexion contracture. During the final stages of PTT dysfunction, the subtalar joint may be fixed in eversion, and inversion to neutral may be impossible.

Finally, forefoot flexibility is assessed by pronating and supinating the forefoot while holding the heel in neutral position. Although the subtalar joint may be flexible, the transverse tarsal joint may have become fixed in varus, preventing plantigrade positioning of the forefoot (see the image below). This finding has important implications for surgical treatment.

Pes planus (flatfoot). Fixed forefoot varus is cha Pes planus (flatfoot). Fixed forefoot varus is characterized by elevation of medial side of forefoot, even after heel is placed in neutral position.


Laboratory Studies

Generally, no laboratory studies are warranted for adult-acquired flatfoot deformity (AAFD) unless a systemic metabolic or inflammatory condition is suspected.

A painless, atraumatic flatfoot deformity in an insensate foot is most likely due to neuroarthropathy (Charcot foot). The most common cause of neuroarthropathy in the United States is diabetes. If diabetes mellitus is not already diagnosed, a fasting blood glucose test is indicated.

If the patient has pain in multiple joints, consider a workup for rheumatoid arthritis (RA) or seronegative spondyloarthropathy with rheumatoid factor (RF), erythrocyte sedimentation rate (ESR), and human leukocyte antigen (HLA)-B27.


Plain radiography

As with most foot and ankle deformities, weightbearing radiographs are mandatory in the workup of AAFD.[48]  The authors' protocol includes three weightbearing views for the foot (anteroposterior [AP], oblique, and lateral) and three weightbearing views for the ankle (AP, mortise, and lateral). (See the image below.)

Anteroposterior and lateral radiographs of lower e 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.

Evaluation of longitudinal arch collapse is largely dependent upon weightbearing lateral radiographs. As a flatfoot (pes planus) deformity develops, the arch sags at the naviculocuneiform or talonavicular joint, causing a decrease in calcaneal pitch,[20] a decreased lateral first talometatarsal angle,[49] and depression of medial cuneiform height[50] (see the image below). The forefoot moves laterally into abduction, causing lateral subluxation of the talonavicular joint and an increase in the talonavicular coverage angle.

Pes planus (flatfoot). Standing lateral radiograph 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.

The axis of the talar–first metatarsal angle on the lateral weightbearing foot radiograph is the most discriminating radiographic parameter in patients with symptomatic flatfoot.[49]  Alternatively, the distance between the medial cuneiform and the floor is a strong reflection of medial arch collapse and flatfoot.[50]

An AP standing foot projection is primarily used for evaluating talar head uncoverage secondary to lateral deviation of the navicular. As peritalar lateral subluxation increases, the talonavicular coverage angle—created by two reference lines through the centers of the talar head and navicular bone, respectively—reveals increased angles (see the image below). Alternatively, using the talonavicular incongruency angle to measure forefoot abduction results in improved interrater reliability.[51]

Pes planus (flatfoot). Standing anteroposterior ra 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.

Standing AP radiographs of the ankle are evaluated for evidence of valgus talar tilt with resultant subluxation, arthrosis, or both. The ankle view is particularly important in patients who have fixed hindfoot valgus. Hindfoot alignment can be further evaluated in the axial plane with the so-called Buck view, as described in a 1995 study by Saltzman and el-Khoury.[26]  The lateral tibial-calcaneal angle as measured on a standing lateral ankle x-ray identifies patients with Achilles tendon contractures.[52, 53]

A study by Dyal et al compared weightbearing radiographs of symptomatic feet with posterior tibial tendon (PTT) dysfunction with those of the contralateral asymptomatic feet.[31]  The measurements of the two feet were strongly correlated, leading the authors to suggest that a predisposing constitutional flatfoot may be an etiologic factor in the development of dysfunction. The authors cautioned against using radiographic measurements alone for diagnosis.

Ellis et al concluded that weightbearing multiplanar imaging also provides a reliable means of assessing lateral pain in patients with flexible flatfoot deformity.[54]


Tenography has been used to diagnose PTT rupture, with limited success. For this test, 5 mL of radiopaque dye is injected into the sheath between the medial malleolus and navicular tuberosity. In later stages of dysfunction, the tendon and sheath become adherent, and injection of dye becomes impossible. After tendon rupture, the sheath often is not palpable, and injection is very difficult.

Magnetic Resonance Imaging

Although highly dependent on technique and the experience of the interpreter, magnetic resonance imaging (MRI) can be extremely sensitive and specific in the evaluation of AAFD, providing highly detailed evaluations of both bony and soft-tissue anatomy. (See the image below.) In most instances, however, PTT dysfunction can be adequately diagnosed with a thorough physical and radiographic examination. Because of the expense of MRI, the cost-to-benefit ratio must be considered; most MRI examinations should be reserved for patients who have a confusing clinical picture.

Pes planus (flatfoot). Axial magnetic resonance im Pes planus (flatfoot). Axial magnetic resonance image demonstrating medial calcaneal shift.

Conti et al used MRI to describe three types of PTT degeneration, as follows[55] :

  • Type I - A partially torn tendon with tendon enlargement and vertical splits
  • Type II - A partially torn attenuated tendon
  • Type III - A complete rupture with a tendon gap

Although it is sensitive, MRI can cause overestimation of the degree of tendon degeneration as compared with surgical assessment, with a mere 40% correlation between MRI findings and surgical findings. This MRI classification is useful in predicting the outcome of tendon transfer, with higher grades of tendon degeneration faring worse than mild grades.

Computed Tomography

Determining the amount of joint degeneration with computed tomography (CT) in patients who have chronic disease may be beneficial; however, this modality does not provide comprehensive information on tendon pathology. In patients with late-stage AAFD and lateral hindfoot pain, CT may show two frequently occurring extra-articular sources of bone impingement (sinus tarsi and calcaneofibular impingement).[56] Weightbearing CT scans allow the surgeon to view multiplanar images in a weightbearing mode with less radiation and shorter image acquisition times.[57]

Several studies have demonstrated that weightbearing CT allows improved prediction of AAFD through analysis of angles presenting hindfoot valgus, along with improved deformity appreciation in those with a definitive diagnosis.[58, 59]


The severity of AAFD varies, depending on the degree of pathologic anatomy and the resultant changes in biomechanics. Therefore, staging the spectrum of dysfunction can be extremely helpful in guiding treatment protocols. In their 1989 report, Johnson and Strom described an initial three-stage continuum of PTT dysfunction.[16] In 1997, Myerson added a fourth stage to Johnson and Strom's original description.[17]

Stage 1 dysfunction

Initial stage 1 findings include mild tenderness along the inframalleolar course of the PTT, with minimal (if any) loss in tendon strength as assessed by the single-limb heel-rise test. When the patient bears weight only on the involved extremity, performing the heel-rise test demonstrates not only adequate strength but also initiation of heel inversion, which signals an intact tendon. The foot and ankle typically demonstrate normal alignment without fixed deformity.[7]

Stage 2 dysfunction

The key to diagnosis of stage 2 disease is a dynamic deformity, typically hindfoot valgus with forefoot abduction.

Palpation along the course of the PTT demonstrates pain and possibly hypertrophy or defects. Observing the patient's stance from behind reveals increased visualization of the lateral toes (too-many-toes sign) on the affected extremity secondary to weakness.[15] Single-limb heel rise may not be possible due to weakness, and if performed, corrective heel inversion is generally absent. With the exception of possible gastrocnemius-soleus contracture, hindfoot and midfoot motion testing usually yield normal results.

Stage 2 disease has been further subclassified according to the degree of talonavicular coverage, as originally proposed by Vora.[60] Radiographic measurements quantify talar head uncovering as either mild deformity with less than 30% uncovering (2A) or more severe deformities with greater than 30% uncovering (2B).[4]

Stage 3 dysfunction

As the continuum of disease progresses to stage 3, chronic dysfunction and lengthening of the PTT lead to fixed hindfoot deformity. In order to achieve a plantigrade foot in the setting of a fixed hindfoot valgus, the forefoot typically compensates into a fixed supination position. With stage 3 disease, patients often present with lateral pain secondary to subfibular impingement as the calcaneus subluxes and the flatfoot deformity progresses.[7, 61]

Stage 4 dysfunction

In stage 4, as described by Myerson, long-standing hindfoot valgus places increasing stress on the deltoid complex, with eventual loss of competence. The resultant valgus tilt of the talus leads to eccentric loading of the ankle with subsequent tibiotalar arthrosis.[20, 61]



Approach Considerations

Posterior tibial tendon (PTT) insufficiency with different degrees of deformity at different joints in the foot is a challenge to manage. Indications for treatment of PTT dysfunction include the following:

  • Disabling pain
  • Deformity
  • Footwear problems
  • Difficulty with ambulation

A painless deformity that can be accommodated by normal footwear and allows for normal gait does not require treatment.

Considerable controversy remains about the appropriate treatment of all stages of PTT dysfunction. Therapeutic options take many forms, ranging from conservative management with the use of medication and orthotics to various surgical procedures.[62, 63, 64]  Comparative outcome trials are needed to provide better data for evaluation of the various options. To the authors' knowledge, such trials have not yet been completed.

Operative treatment may involve the following:

  • Soft-tissue procedures alone
  • Soft-tissue procedures with the addition of an osteotomy
  • Arthrodesis

Contraindications for surgical intervention in adult-acquired flatfoot deformity (AAFD) are similar to those for any other foot or ankle surgery and include the following:

  • Active or chronic infection
  • Open ulceration
  • Inadequately perfused foot
  • Insensate foot
  • 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.

A flexor digitorum longus (FDL) 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.

Nonoperative Therapy

Medical or nonoperative therapy for PTT dysfunction involves the following[65, 66] :

  • Rest
  • Immobilization
  • Nonsteroidal anti-inflammatory drugs (NSAIDs)
  • Physical therapy
  • Orthotics
  • Bracing

Such therapy is especially attractive for patients who are elderly, who place low demands on the tendon, and who may have underlying medical problems that preclude operative intervention.

During stage 1 PTT dysfunction, the predominant manifestation is pain, rather than deformity. Cast immobilization (with NSAIDs if warranted) is indicated for patients with acute tenosynovitis of the PTT or for those whose main presenting feature is chronic pain along the tendon sheath. A well-molded short leg walking cast or removable cast boot should be used for 6-8 weeks. Despite the need for prolonged below-knee immobilization, chemoprophylaxis for venous thromboembolism (VTE) typically is not necessary unless three or more VTE risk factors are present.[67]

With three-dimensional (3D) gait analysis, electrical stimulation has also been shown to demonstrate improved arch height along with increased tibial external rotation with forefoot inversion in patients with pes planus (flatfoot).[68]

Weightbearing is permitted if the patient is able to ambulate without pain. If improvement is noted, the patient may be placed in custom full-length semirigid orthotics. He or she may then be referred to physical therapy for stretching of the Achilles tendon and strengthening of the PTT. Steroid injection into the PTT sheath is not recommended, because of the possibility of causing a tendon rupture.

Gait analysis also supports improved foot kinematics with the use of orthoses.[69]  However, the literature remains unclear as to whether a custom-molded orthosis or a conventional off-the-shelf orthosis provides a better outcome; a randomized controlled trial comparing the two demonstrated similar pain and functional scores.[70]

In stage 2 dysfunction, a painful flexible deformity develops, and more control of hindfoot motion is required. In these cases, a rigid University of California at Berkeley (UCBL) orthosis or a short articulated ankle-foot orthosis (AFO) is indicated.

Once a rigid flatfoot deformity develops, as in stage 3 or 4 dysfunction,[71] bracing is extended above the ankle with a molded AFO, a double upright brace, or a patellar tendon–bearing brace. (See the image below.) The goals of this treatment are as follows:

  • To accommodate the deformity
  • To prevent or slow further collapse
  • To improve walking ability by transferring load to the proximal leg away from the collapsed medial midfoot and heel
Arizona Brace. Image courtesy of Don Pierson, CO o Arizona Brace. Image courtesy of Don Pierson, CO of Arizona AFO, Inc.

Because of the fixed deformity, these orthotics must be accommodative rather than corrective. Shoe modifications (eg, larger size or rocker sole) are often required. The chances of success in relieving pain despite these measures are relatively low.

In a study of nonoperative therapy for stage 2 and 3 PTT dysfunction, Chao et al used a rigid UCBL orthosis with a medial forefoot post in nonobese patients with flexible heel deformity correctible to neutral and less than 10° of forefoot varus and used a molded ankle foot orthosis in obese patients with fixed deformity and forefoot varus greater than 10°.[72] Average length of orthotic use was 15 months.

In this study, nonoperative therapy yielded good-to-excellent results in 67% of patients.[72] Four patients ultimately elected to have surgery. The authors concluded that orthotic management is successful in older low-demand patients and that surgical treatment can be reserved for those patients who fail nonoperative treatment.

Conservative treatments for AAFD may be summarized as follows:

  • Stage 1 - NSAIDs and short-leg walking cast or walker boot for 6-8 weeks; full-length semirigid custom molded orthosis, physical therapy
  • Stage 2 - UCBL orthosis or short articulated ankle orthosis
  • Stage 3 - Molded AFO, double-upright brace, or patellar tendon–bearing brace
  • Stage 4 - Molded AFO, double-upright brace, or patellar tendon–bearing brace

Surgical Options

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.

Although the four-stage classification cited earlier (see Staging) is not foolproof, it can be very useful in the discussion of management of AAFD. Regardless of the stage, however, operative management should only be considered after conservative management (see Nonoperative Therapy) has proved unsuccessful. The surgical procedure chosen should address all the fixed and dynamic deformities for each patient.[73, 74]

Treatment of stage 1 PTT dysfunction is straightforward. The goal is to halt the progression of tenosynovitis through conservative or operative methods in order to prevent tendon rupture. The rigid deformities of stages 3 and 4 necessitate operative correction and fusion of the involved joints in order to produce a plantigrade balanced foot. The principle of fusing the fewest number of joints possible should be followed.

Surgical treatment of stage 2 PTT dysfunction generates the most controversy among foot and ankle surgeons. Many different surgical procedures have demonstrated good short-term relief of pain and improved function but have shown only limited ability to correct the deformity.

For example, a tendon transfer using FDL or flexor hallucis longus (FHL) tendon yields satisfactory short-term pain relief, but it does not achieve arch correction. The addition of a medial displacement calcaneal osteotomy (MDCO) improves heel valgus position, but it may not produce complete correction of the medial longitudinal arch. Lateral-column lengthening (LCL) through the anterior calcaneus or through the calcaneocuboid joint achieves arch correction, but it requires an iliac crest tricortical graft and risks nonunion or overcorrection.

In large or obese patients, subtalar or talonavicular fusion may be needed to achieve long-term correction, though these procedures limit hindfoot motion significantly. The most biomechanically sound surgical treatments may be those that use tendon transfer to substitute for the deficient PTT, with LCL to restore alignment of the subtalar and talonavicular joints and medial fusion of the sagging naviculocuneiform joint or first metatarsocuneiform joint. These procedures require multiple steps, multiple incisions, and prolonged recovery time. Perhaps the most important unanswered question is whether arch correction is required to achieve a long-term satisfactory outcome.

Surgical treatments for AAFD may be summarized as follows:

  • Stage 1 - Tenosynovectomy, tendon debridement, and tendon repair of partial tears
  • Stage 2 (add Achilles tendon lengthening or gastrocnemius recession in cases of equinus contracture) - PTT repair; FDL or FHL transfer alone; FDL or FHL transfer and calcaneal osteotomy; FDL transfer and LCL; FDL transfer, LCL, and medial-column fusion; FDL transfer, LCL, and calcaneal osteotomy; subtalar fusion; talonavicular fusion; medial cuneiform opening wedge plantar flexion osteotomy (Cotton)
  • Stage 3 - Subtalar fusion; triple arthrodesis; double arthrodesis of talonavicular and subtalar but sparing the calcaneocuboid joint 
  • Stage 4 - Tibiotalocalcaneal fusion; pantalar fusion

Surgical Therapy for Stage 1 AAFD

By definition, patients with stage 1 pes planus do not demonstrate clinical deformity and are the group with the highest likelihood of responding to conservative management (see Nonoperative Therapy). If the patient's condition does not improve with conservative management or if the patient's symptoms are sufficiently chronic in nature, then consideration can be given to surgical intervention. The exact nature of this intervention has been debated.

Traditionally, operative treatment of stage 1 disease has involved release of the PTT sheath, tenosynovectomy, debridement of the PTT with excision of flap tears, and repair of longitudinal tears. A short-leg walking cast is worn for 3 weeks postoperatively. Teasdall and Johnson reported complete relief of pain in 74% of 14 patients undergoing this treatment regimen for stage 1 disease.[75] A retrospective review of young athletes with stage 1 disease who were treated with surgical debridement revealed an "excellent likelihood to return to the previous level of athletic activity."[76]

Debridement should be reserved for patients who show no clinical deformity or weakness. It has been suggested that surgical debridement of tenosynovitis in early stages may prevent progression of disease to later stages of dysfunction.

Surgical Therapy for Stage 2 AAFD

Treatment of the flexible deformity of stage 2 PTT dysfunction is controversial. Many patients with stage 2 AAFD, like those with stage 1, can be effectively treated nonoperatively with orthoses (either a short articulated AFO or a foot orthosis) and structured exercises (see Nonoperative Therapy). Alvarez et al studied nonoperative management of patients with stage 1 and 2 AAFD (without complete tendon rupture).[77] At the conclusion of the treatment protocol, most patients had "minimal or no pain, could walk on tiptoes, were not limited by walking distance, and could perform a painless SSHR [single-sided heel rise]."

If appropriate conservative treatment fails for patients with stage 2 disease, surgical management may be considered. The exact surgical procedure chosen for stage 2 varies widely, and numerous bone and soft-tissue reconstructive surgeries have been described to treat the various presentations of stage 2 pathology. The multitude of surgical procedures proposed for stage 2 dysfunction is evidence of the difficulty of obtaining an excellent surgical result in this setting. Procedures that have been reported to yield satisfactory outcomes include the following:

  • Direct repair of the torn tendon
  • Tendon transfer or tenodesis using the FDL or the FHL
  • Spring-ligament repair,
  • MDCO
  • LCL
  • Medial cuneiform opening wedge plantar flexion osteotomy (Cotton osteotomy)
  • Limited arthrodeses of the hindfoot or midfoot

Achilles tendon lengthening is recommended if ankle dorsiflexion is limited to 10° or less. 

Typically, surgical management of stage 2 disease involves both a soft-tissue reconstruction (FDL transfer; see the image below) and a bony reconstruction (medializing calcaneal osteotomy) reconstruction.[78, 60] This procedure has yielded excellent results with minimal complications and a high satisfaction rate.[79] Additionally, it yields significant and lasting improvement in radiographic parameters, including the lateral talometatarsal angle and the tibiocalcaneal angle.[80]

Intraoperative images from patient with pes planus Intraoperative images from patient with pes planus (flatfoot). (A) Flexor digitorum longus (FDL) transfer to navicular bone. (B) Torn spring ligament.

The osteotomy (and subsequent medial shift) of the calcaneal tuberosity shifts the moment arm of the gastrocnemius-soleus complex medial to the subtalar axis. This then generates an inversion force that protects the medial soft-tissue reconstruction and corrects the hindfoot alignment.[81] The transferred FDL muscle hypertrophies significantly as it compensates for the diseased PTT.[82]

Stage 2 surgical intervention also typically involves a lengthening of the gastrocnemius-soleus complex. This can be achieved by means of either a percutaneous Achilles lengthening or a gastrocnemius recession. Prospective data reviewing the gastrocnemius recession have demonstrated no loss of plantarflexion strength at 1 year and, in fact, improved strength in comparison with the preoperative strength of the ipsilateral extremity.[43]

More advanced stage 2 disease may be associated with medial-column instability, severe forefoot abduction, or severe forefoot varus. In this clinical scenario, additional reconstructive techniques include both lateral- and medial-column bony procedures. The lateral-column bony procedures include LCL through the anterior process of the calcaneus (joint-sparing) and calcaneocuboid distraction arthrodesis (non–joint-sparing).

LCL through the anterior process of the calcaneus can be successfully performed with autografts, allografts, or metallic implants.[83] These techniques provide powerful corrective forces through medial and plantar translation of the navicular on the talar head, effectively restoring the longitudinal arch and correcting the forefoot abduction.[84, 85]  Moore et al followed 34 feet for a mean of 16.1 months that underwent LCL for AAFD. A porous titanium wedge was utilized in all to lengthen the lateral column, resulting in significant radiographic correction in all parameters without any cases of nonunion, removal of hardware, or wedge migration.[86] The authors reported a 14.7% rate of calcaneocuboid joint pain.

Medial-column bony procedures are indicated when residual forefoot varus exists after lengthening of a lateral column. In particular, the Cotton osteotomy has been demonstrated to have no effect on hindfoot alignment when performed but to be a valuable tool for bringing the first ray plantigrade.[87, 88] Residual forefoot varus prevents the creation of a plantigrade foot and results in symptomatic lateral-column overload. To reduce this overload, which is associated with LCL, clinical and biomechanical research has supported the use of medial procedures to redistribute load to the medial column.[89, 90]  

Such medial-column bony procedures include plantarflexion opening wedge medial cuneiform osteotomies (joint-sparing) and plantarflexion arthrodesis of the first tarsometatarsal articulation (non–joint-sparing). Alternatively, medial soft-tissue reconstructive techniques have also proven useful for correcting associated forefoot supination deformities. The Cobb procedure involves use of a partial anterior tibial tendon graft that is rerouted through the first cuneiform to the proximal stump of the PTT.[91]

An additional procedure that is designed to correct the pes planovalgus deformity is subtalar arthroereisis,[92, 93, 94] which involves placement of a plug or screw-type implant in an effort to correct the rotational malalignment of the subtalar joint.[95] The long-term outcome of this procedure has been questioned; a significant number of patients develop persistent sinus tarsi pain that necessitates implant removal.[96] The limited data on this procedure in adult patients are insufficient to permit a recommendation for or against this procedure.[27]

Various procedures performed to treat stage 2 dysfunction are described in more detail below.


Traditionally, tenoscopy has been an option for surgical intervention in stage 1 AAFD. Bernasconi et al described tenoscopy for 16 stage 2 AAFD patients who were followed for 25 months.[97] Eighty percent of these patients did not require further surgery, demonstrating significant improvement in the visual analogue scale (VAS) for pain and in both the physical and the mental components of the Short Form (SF)-36 survey. The authors' experience was positive, and their recommendation in this instance was to attempt tenoscopy during this stage if the tendon is intact and there is no aberrant navicular pathology.

Direct repair

The torn tendon may be directly repaired by suturing the ends of an acute rupture. If the tendon is avulsed distally, it can be repaired to the navicular, or the portion of the tendon that is attenuated can be excised and the proximal and distal tendon stumps repaired end to end. Proximal Z-lengthening of the PTT may be needed to achieve direct repair. The distal half of the anterior tibial tendon can be detached proximally and left attached to its insertion into the base of the first metatarsal and used to reinforce the directly repaired tendon.

Tendon transfer

The PTT often has an irreparable gap or is attenuated and scarred to the tendon sheath. The posterior tibial muscle may function poorly, even if the tendon can be directly repaired. This has led several authors to recommend tendon transfer to substitute for the dysfunctional or irreparable PTT.

Jahss described side-to-side tenodesis of the proximal and distal stumps of the PTT to the intact FDL tendon in five patients, reporting short-term satisfactory results, though all patients had residual heel valgus.[13] Transfer of the FDL tendon to the distal stump of the PTT or directly into the navicular tuberosity through a vertically oriented tunnel has been advocated by several authors ,with good short-term subjective results. The procedure uniformly failed to correct the flatfoot deformity but functioned well in relieving pain and improving inversion strength.

Some authors have emphasized the importance of spring-ligament (calcaneonavicular-ligament) repair or reconstruction in conjunction with FDL transfer. A retrospective study of spring-ligament repair/reconstruction and FDL transfer demonstrated excellent functional results in 14 of 18 patients, though arch correction on radiographs was inconsistent.

Goldner et al reported using the FHL for transfer into the distal stump of the PTT in two patients, of whom one had a previous laceration of the tendon and the other a chronic tear.[14] The younger patient had a full and complete recovery, and the outcome in the other patient was not reported.

Procedural details: FHL tendon transfer

An 8-cm incision is made along the course of the PTT from a point just proximal and posterior to the medial malleolus to the navicular tuberosity. The PTT sheath is opened, and a tenosynovectomy is performed. Partial tears of the PTT are repaired with 2-0 nonabsorbable Dacron sutures. If the PTT is attenuated and irreparable, it is excised, leaving a 1-cm stump attached to the navicular tuberosity. If the spring ligament is torn or attenuated, it is repaired and imbricated with 2-0 nonabsorbable sutures.

The FDL tendon is identified in its sheath just deep to the PTT sheath. The FHL tendon is identified deep to the sustentaculum tali. The FHL tendon is sutured to the FDL tendon distally with 2-0 nonabsorbable sutures and then divided proximal to the anastomosis (see the image below).

Pes planus (flatfoot). Flexor hallucis longus (FHL 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.

A suture anchor is placed in the navicular tuberosity, and the transferred FHL tendon is sutured to the navicular and to the distal stump of the posterior tibial tendon with No. 2 nonabsorbable sutures (see the image below). Tension on the FHL tendon is adjusted with the foot in inversion and plantarflexion. The tendon sheath, subcutaneous tissue, and skin are closed in layers. Percutaneous triple-cut Achilles tendon lengthening or gastrocnemius recession is performed if the foot cannot be easily dorsiflexed past neutral.

Pes planus (flatfoot). Flexor hallucis longus (FHL 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.

After surgery, the foot is placed in a posterior splint in a position of equinus and inversion. A short leg nonweightbearing cast is applied 3 days after surgery to maintain the position of equinus and inversion and is worn for 4 weeks. The foot then is placed in a short leg walking cast in a neutral position, which is worn for an additional 2 weeks. A Cam walker boot is worn beginning 6 weeks postoperatively and is removed for range of motion (ROM) and strengthening exercise. Immobilization is discontinued 10 weeks postoperatively.

Procedural details: FDL tendon transfer

A similar approach is used for the FDL tendon transfer. In this case, the distal FDL is sutured into the FHL, and the FDL is released just proximal to the suture to give adequate length to the tendon. A vertical hole then is drilled into the navicular bone. The surgeon should be careful to leave an adequate bridge of bone in place medially. The plantar hole is rounded smooth proximally to take any sharp edge away that may damage the tendon.

With the aid of a suture passer, the FDL tendon is routed from plantar to dorsal and sutured to itself (if enough tendon length is available) and to the surrounding tissue. The foot is held in an inverted position during this maneuver to place appropriate tension on the FDL tendon. Closure and postoperative care are similar to those for FHL transfer.

Calcaneal osteotomy

Follow-up examination of patients who have undergone FDL tenodesis or transfer alone has not shown consistent correction of deformity.[98] Because of a concern of deteriorating clinical results over time with soft-tissue procedures alone, some surgeons added bony procedures to the soft-tissue reconstruction, theorizing that the restoration of arch height and heel position might produce more durable and improved clinical results. The ideal bony procedure to treat acquired pes planovalgus corrects the foot deformity, decreases strain on the spring and deltoid ligaments, and protects the soft-tissue reconstruction.

Gleich first described a medial and inferior displacement osteotomy of the posterior third of the calcaneus in 1893.[99] Koutsogiannis first described the medial displacement calcaneal osteotomy as a treatment of valgus hindfoot deformity.[100]

The addition of a medial displacement osteotomy through the posterior portion of the calcaneus moves the valgus heel under the weightbearing axis of the leg. The osteotomy also decreases the heel valgus–producing deforming force of the Achilles tendon by shifting the Achilles insertion medially. In-vitro studies showed that a 1-cm medializing osteotomy of the calcaneal tuberosity decreases strain on the spring ligament and deltoid ligament. A 1-cm translational calcaneal osteotomy actually moves the center of pressure in the ankle joint 1.58 mm medially.

A retrospective study of 32 patients undergoing FDL transfer and calcaneal osteotomy with an average of 20 months follow-up showed 94% pain relief, improved function, and significant improvement in radiographic arch measurements. Sammarco and Hockenbury reported satisfactory results in 19 patients undergoing FHL transfer and MDCO.[101] Although the FHL is stronger than the FDL, postoperative radiographs did not show significant arch correction, indicating that a medial soft-tissue procedure in conjunction with calcaneal osteotomy may not result in arch correction.

Procedural details 

Calcaneal osteotomy is employed in conjunction with FDL or FHL transfer and is performed before the tendon transfer. A 5-cm oblique incision is made along the lateral heel from posterosuperior to anteroinferior, running posterior to the peroneal tendon sheath and sural nerve (see the image below). Sharp dissection is used to proceed directly down to bone. Skin flaps are kept thick. The lateral wall of the calcaneus is exposed subperiosteally with a Key elevator. Small Hohmann retractors are placed over the superior aspect of the calcaneus anterior to the Achilles tendon and at the plantar aspect of the calcaneus anterior to the plantar fascial attachment.

Pes planus (flatfoot). Incision for calcaneal oste 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.

A straight, wide power osteotome (eg, Micro-Aire, Inc) or sagittal saw is used to make a cut across the calcaneus in line with the incision at a 45° angle to the plantar surface of the foot and perpendicular to the surface of the calcaneus. C-arm fluoroscopy is used to document proper osteotomy position before the bone cut is made. The medial aspect of the heel is palpated to gauge the depth of the osteotomy and to avoid overpenetration of the osteotome, which could cause injury to the tibial nerve and vessels. The depth of the osteotome cut also can be judged with a Freer elevator during completion of the cut.

After completion of the osteotomy, the medial soft tissues are spread by inserting a large Key elevator into the osteotomy site and levering the calcaneal tuberosity downward. A laminar spreader also can be placed into the osteotomy site and used to spread the medial soft tissues (see the image below).

Pes planus (flatfoot). Calcaneal osteotomy is dist Pes planus (flatfoot). Calcaneal osteotomy is distracted with laminar spreader to spread medial soft tissues. This permits easy medial displacement of calcaneal tuberosity.

If the medial soft tissues are adequately mobilized, the tuberosity should be easily translated medially 1 cm. It is important to ensure that the plantar surface of the osteotomy has been adequately mobilized. Otherwise, the posterior calcaneal fragment rotates internally rather than slides medially. The calcaneal tuberosity then is translated 1 cm medially, with care taken to avoid superior translation of the fragment. A surgical assistant then holds the osteotomy in a corrected position while it is fixated with two 4.0-mm diameter partially threaded cancellous screws placed perpendicular to the osteotomy cut (see the image below). Typically, no washers are used.

Pes planus (flatfoot). Lateral radiograph of fixat 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.

Placement of the screws into the subtalar joint should be avoided, and the screw heads should be kept off the weightbearing surface of the heel. Screws are placed in a parallel fashion. Because the tuberosity has been shifted medially, the screws should be aimed slightly laterally in order to hit the main calcaneal body; if this is not done, the screw(s) may miss the anterior calcaneus. Screw position is documented by means of intraoperative fluoroscopy (see the image below).

Pes planus (flatfoot). Intraoperative axial view o Pes planus (flatfoot). Intraoperative axial view of fixated calcaneus documents satisfactory medial translation of tuberosity and satisfactory screw position.

The wound is closed in layers. Postoperative care is the same as for FDL transfer, except that weightbearing is not allowed until radiographs indicate that the osteotomy has healed (usually 6-8 weeks postoperatively).

Lateral-column lengthening

The Evans anterior calcaneal lengthening osteotomy lengthens the lateral column of the foot by inserting a 10- to 15-mm bone graft 10-15 mm proximal to the calcaneocuboid joint. This lateral column-lengthening procedure radiographically improves forefoot abduction and hindfoot valgus and restores the medial longitudinal arch.

Cadaveric studies show that LCL protects the calcaneonavicular (spring) ligament form overload during weight bearing. A retrospective study of 19 patients undergoing Evans calcaneal osteotomy in conjunction with posterior tibial tendon repair or shortening and deltoid ligament repair or reconstruction reported six excellent, 11 good, and two fair results. Significant radiographic arch correction was noted at 23-month follow-up.[102]

The calcaneocuboid was shown to have remodeled in a series of 21 consecutive AAFD patients. The resulting deformity was a short, laterally/dorsally facing calcaneal side of the joint. In this instance, the senior author recommends LCL to not only restore length to the column but to redirect the calcaneal portion of the joint medially and plantar.[103]  

Variations on traditional Evans osteotomy

Several variations on the traditional Evans procedure have been developed, including the following.

StepCut lengthening calcaneal osteotomy

Saunders et al presented a comparative case-control series of Evans osteotomy vs StepCut lengthening osteotomy (SCLO) for stage 2B AAFD.[104] Functional outcomes and correction ability were the same for the two osteotomies; however, SCLO demonstrated faster time to union, lower nonunion rates, smaller graft size needed, and less removal of hardware. SLCO incorporates a horizontal arm to create a "Z" type osteotomy that theoretically provides improved stability and union ability.[105]

Hintermann calcaneal lengthening osteotomy 

A Hintermann calcaneal lengthening osteotomy is similar to an Evans osteotomy, except that the cut is directed more posteriorly/proximally than a traditional Evans cut,  starting just anterior to the posterior facet of the calcaneus and angling posteriorly. In a comparative case series comparing the two osteotomies with short-term follow-up, radiographic correction and clinical scoring were similar between the two procedures.[106] The Hintermann group displayed less radiographic calcaneocuboid joint arthritic change, but this finding was not clinically relevant.

Calcaneocuboid joint distraction arthrodesis

A cadaver study of Evans calcaneal LCL in normal feet showed elevated calcaneocuboid joint pressures postoperatively, raising questions about potential long-term degenerative arthritis of the calcaneocuboid joint after the procedure. This concern led to the recommendation of lengthening the lateral column through distraction arthrodesis of the calcaneocuboid joint. However, results of another cadaver study failed to confirm elevation of calcaneocuboid joint pressure after Evans calcaneal LCL in preexisting flatfeet and, in some cases, actually showed lowering of calcaneocuboid pressure after LCL. 

A retrospective study of 41 feet undergoing LCL through distraction arthrodesis of the calcaneocuboid joint in conjunction with FDL transfer and selective medial midfoot arthrodesis found satisfactory outcomes in 85% of cases and a uniform radiographic correction of flatfoot, butit also documented a calcaneocuboid nonunion rate of 20%.[107] It should be noted that this series included several patients who also had fusions of the naviculocuneiform or first metatarsocuneiform joints and that distraction arthrodesis of the calcaneocuboid joint was not the only bony procedure performed.

Thomas et al reported on 25 patients who underwent FDL transfer to the navicular and lateral column lengthening with two different methods.[108] Postoperative American Orthopedic Foot and Ankle Society (AOFAS) scores were 87.9 for the osteotomy group and 80.9 for the calcaneocuboid distraction arthrodesis group, but the difference was not statistically significant. Significant improvement in radiographic parameters was seen in both groups. Complication rates were high in both groups, with an especially high rate of nonunion and delayed union in the calcaneocuboid distraction group.

A combination of FDL transfer to medial cuneiform, MDCO, and Evans LCL produced good short-term results in a retrospective study of 17 patients with stage 2 PTT dysfunction. Significant improvement in the AOFAS hindfoot score was seen, and radiographs showed significant improvement in arch measurements at 17.5-month follow-up.

LCL by distraction arthrodesis of the calcaneocuboid joint is illustrated in the images below.

Pes planus (flatfoot). Preoperative anteroposterio Pes planus (flatfoot). Preoperative anteroposterior view of foot prior to lateral-column lengthening (LCL). Note forefoot abduction and increased talonavicular coverage angle.
Pes planus (flatfoot). Distraction arthrodesis of 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.

The postoperative course is the same as for the calcaneal osteotomy, except that weightbearing is delayed until fusion is confirmed radiographically.

Combination calcaneal osteotomy

A subsequent development is the extended Z-cut osteotomy, described in detail by Ebaugh et al.[109] This osteotomy combines MDCO and traditional Evans osteotomy into a three-plane Z-cut osteotomy with an elongated horizontal limb. It uses a single incision and maintains a long horizontal arm, allowing for deformity correction through rotation and providing a large surface area of bony apposition for union. In a retrospective case series of 16 patients, the extended Z-cut osteotomy yielded significant improvement in both radiographic correction and clinical outcomes while achieving a union rate of 100% with acceptably low complications.[109]

The extended Z-cut osteotomy is illustrated in the images below.

Pes planus (flatfoot). Outline of extended Z-cut o Pes planus (flatfoot). Outline of extended Z-cut osteotomy.
Pes planus (flatfoot). Axial model of extended Z-c 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.
Pes planus (flatfoot). Preoperative lateral radiog Pes planus (flatfoot). Preoperative lateral radiograph of stage 2B adult-acquired flatfoot deformity (AAFD) prior to reconstruction with extended Z-cut osteotomy.
Pes planus (flatfoot). Preoperative anteroposterio Pes planus (flatfoot). Preoperative anteroposterior radiograph of stage 2B adult-acquired flatfoot deformity (AAFD) prior to reconstruction with extended Z-cut osteotomy.
Pes planus (flatfoot). Postoperative lateral radio 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.
Pes planus (flatfoot). Postoperative anteroposteri 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.

Medial-column procedures

When residual forefoot varus persists after addressing the valgus hindfoot and forefoot abduction, medial-column procedures, in the form of Cotton osteotomy of the medial cuneiform or midfoot arthrodesis,[87]  may be performed. The use of these procedures is often left to the individual surgeon's preference; however, in many instances, the Cotton osteotomy is favored by virtue of its joint-sparing nature and ease of performance. In addition, Wang et al, in a case-control series that followed 40 feet for 12 months, demonstrated that fixation is not required to achieve a satisfactory outcome with the Cotton procedure, reporting no difference in radiographic correction, union, or functional outcome.[110]  

The literature has also given surgeons a means of linearly dialing in correction of residual forefoot varus. One group showed that a preoperatively measured cuneiform articular angle can be used to choose the appropriate graft size for restoring the radiographic parameter.[111]  In a subsequent study of 61 feet, they further defined the importance of appropriate correction, noting that those who underwent mild correction achieved greater improvement in Foot and Ankle Outcome symptoms and daily and sport activities scores.[112]  If medial-column instability is seen through the first tarsometatarsal (TMT) joint in conjunction with AAFD, a first-TMT arthrodesis is often used to correct forefoot varus.[113]


The difficulty of achieving consistent and lasting correction of the flatfoot deformity with soft-tissue procedures, whether alone or in conjunction with osteotomies, has led some surgeons to recommend fusion as a treatment of stage 2 deformity.[114] Some surgeons feel that soft-tissue procedures are less successful in patients who are obese and that obesity is an indication for joint fusion.

Kitaoka et al compared subtalar arthrodesis with FDL transfer in vitro and found a more consistent correction of deformity after subtalar arthrodesis.[115] A retrospective study of 21 feet treated with subtalar arthrodesis for PTT dysfunction yielded good-to-excellent results in 16 of 21 feet and significant correction of flatfoot deformity according to radiographic measurements. Stephens et al emphasized the need for reducing the subtalar joint prior to fusion and for differentiating a subtalar repositional arthrodesis from a subtalar fusion in situ.[116]

Another in-vitro study compared subtalar fusion alone, calcaneocuboid fusion alone, talonavicular fusion alone, double (talonavicular and calcaneocuboid) arthrodesis, and triple arthrodesis with respect to their abilities to correct an experimentally corrected flatfoot deformity. Talonavicular or double arthrodesis resulted in better correction of flatfoot deformity than did subtalar fusion alone. A retrospective study of 29 patients with PTT dysfunction treated with isolated talonavicular fusion found good-to-excellent results in 86% of patients at an average follow-up of 26 months.

Combination treatments

Johnson et al used subtalar fusion, FDL transfer, and spring-ligament repair in 17 feet with stage 2 dysfunction.[117] At an average follow-up of 27 months, they reported excellent radiographic correction of pes planus deformity and improvement in AOFAS hindfoot scores.

Chi et al reported on 65 feet that underwent FDL transfer with LCL and/or medial-column fusion.[118] Lateral-column fusion was performed for calcaneovalgus deformity with a flat calcaneal pitch angle. Naviculocuneiform or first metatarsocuneiform joints that showed sag on lateral radiographs were also fused. At 1- to 4-year follow-up, 88% of the feet that had LCL, 80% of those that had medial-column stabilization, and 88% of those that had medial and lateral procedures were less painful or pain-free. Significant radiographic correction of the deformity was seen in all groups. The authors concluded that fusion of these unessential joints effectively corrected deformity and relieved pain.

Surgical Therapy for Stage 3 AAFD

Because fixed deformity is often associated with symptomatic arthrosis, an arthrodesis is often required for proper correction of stage 3 disease. The goals of surgery are to relieve pain and to restore proper alignment of the foot. The principle of fusing the smallest number of joints possible should be followed.

Isolated arthrodesis of the subtalar joint is indicated in patients with subtalar arthrosis or fixed hindfoot alignment with flexible forefoot deformity. Isolated talonavicular arthrodesis is indicated for management of an unstable talonavicular joint in the presence of a flexible subtalar joint in patients older than 50 years.[24]

On the other hand, a double arthrodesis (fusion of the calcaneocuboid joint and the talonavicular joint without addressing the subtalar joint) is indicated in younger patients. A triple arthrodesis is indicated for cases of a rigid subtalar joint and fixed forefoot varus deformity.[119] Long-term follow-up studies showed that triple arthrodesis is associated with increased wear in the ankle joint and a higher rate of degenerative ankle arthrosis (ie, disease or degeneration of an adjacent joint or segment, as the forces normally seen in the fused joints or segments are transferred to the next adjacent joint or segment).[120, 121]  Often, the resulting deformity created by these forces is a valgus ankle joint.

Miniaci-Coxgead et al analyzed 187 patients who underwent hindfoot arthrodesis, the majority of which were triple arthrodeses for AAFD.[122] They found that an increased preoperative Meary angle or a Meary angle that was left undercorrected postoperatively predicted the likelihood for creating a valgus tibiotalar joint, which was displayed in 27% of patients at a mean of only 3.6 months after the operation. The authors recommended counseling those at risk and careful correction of hindfoot and forefoot alignment.

To the authors' knowledge, no comparative studies to date have demonstrated a lower rate of adjacent joint arthrosis with the aforementioned limited fusions in comparison with triple arthrodesis. For this reason, triple arthrodesis continues to be the criterion standard for treatment of stage 3 AAFD (see the image below).[123]

Radiographs of foot in patient with pes planus (fl 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.

Complex rigid deformity

In some patients, the apex of their AAFD is through the naviculocuneiform joint. This presents a surgical dilemma, in that extension of a triple arthrodesis to include the naviculocuneiform joint creates a very stiff medial column, making accommodation to ambulation on uneven ground increasingly difficult. Steiner et al described an approach combining subtalar and naviculocuneiform joint fusion with or without an MDCO, which showed promising results.[124] In their study of 34 feet followed for 2 years, 80% of radiographic parameters showed significant improvement, and 94% of patients achieved fusion. 

Surgical Therapy for Stage 4 AAFD

Stage 4 AAFD is rare. The valgus ankle in stage 4 dysfunction develops because of deltoid ligament instability. The deltoid ligament is difficult to reconstruct with a tendon transfer. Arthritic valgus ankle deformities secondary to deltoid ligament insufficiency have not been treated successfully with a total ankle arthroplasty, because of the inability to achieve ligamentous balance.

Treatment of a fixed subtalar deformity and degenerative ankle valgus requires tibiotalocalcaneal arthrodesis, which involves fusion of the ankle joint and the subtalar joint.[125] If fixed forefoot varus is also present, pantalar arthrodesis may be necessary to realign the foot adequately; this procedure involves fusion of the ankle and the subtalar, talonavicular, calcaneocuboid, and tibiotalar joints.[125]

Either tibiotalocalcaneal arthrodesis or pantalar arthrodesis results in a stiff foot, which results in an altered gait. Shoe modifications and bracing are often required after surgery. These operations are technically demanding and are considered salvage procedures.[126, 127]


Although some of the complications associated with AAFD treatment may be related to poor surgical planning and improper choice of procedure, others may be inherently related to the procedure itself. For example, a flatfoot deformity that is secondary to an arthritic Lisfranc joint may be wrongly diagnosed as a PTT-deficient foot and therefore be treated as such.

Other complications may be related to inadequate surgical intervention. For example, in a study by Michelson et al, tenodesis of the FDL to the diseased PTT proved to have a 50% failure rate after 2 years.[128] Similar long-term failure rates were noted for FDL transfers to the navicular that were performed for stage 2 PTT dysfunctions.[129]

Bony procedures such as a calcaneal osteotomy and various arthrodeses can also be associated with significant complications.[130] Although nonunion of the calcaneal osteotomy is exceedingly rare, placement of hardware to stabilize these osteotomies can be associated with postoperative morbidity. Penetration of the subtalar joint or a prominent screw head may cause postoperative symptoms. Risks associated with a triple arthrodesis include higher rates of nonunion—in some cases exceeding 20%—and also malposition, both in hindfoot alignment and in forefoot rotation.[129] Longer-term complications involve arthrosis of adjacent joints.

The major concern with any reconstructive procedure on the foot is to achieve a painless plantigrade foot that fits into a shoe. Undercorrection or overcorrection of a deformity can easily occur. Soft-tissue procedures alone do not correct the pes planus deformity of PTT insufficiency. Caution must be exercised intraoperatively to ensure that the heel is in slight valgus and that the forefoot is plantigrade and not left in varus. An ankle equinus contracture should not be left untreated.[131]

As with any medial midfoot procedure, care must be taken to avoid neurovascular injury during PTT debridement or FDL or FHL tendon transfer. Many surgical techniques involve suturing the distal stump of the transferred FDL tendon to the adjacent FHL tendon at the knot of Henry. The neurovascular bundle is at significant risk during this anastomosis because of its close proximity. Medial skin flaps should be kept thick to minimize the risk of wound dehiscence.

During MDCO, the sural nerve is at risk if the lateral incision is made too far anteriorly. The calcaneal osteotomy is made at a 45° angle to the long axis of the calcaneus through the calcaneal tuberosity. If the osteotomy is made too far anteriorly, the posterior facet of the subtalar joint could be damaged. If the osteotomy is made too far posteriorly, the Achilles insertion could be disrupted. If the osteotome overpenetrates the medial calcaneal wall, the neurovascular bundle could be damaged.

Superior translation of the tuberosity during medial translation of the posterior calcaneal tuberosity must be avoided; if it occurs, the calcaneal pitch could be decreased and the arch flattened further. Two screws are recommended for fixation of the calcaneal osteotomy to prevent rotation of the calcaneal fragment and to enhance fixation, though single large cancellous screws have been used successfully. The screws should be inserted perpendicular to the osteotomy plane, and the subtalar joint should not be penetrated.

LCL achieves arch correction both clinically and radiographically. However, overlengthening of the lateral column is possible, with creation of painful lateral forefoot overload. The Evans calcaneal osteotomy places the sural nerve, peroneal tendons, and anterior and middle subtalar facets at risk. Ideally, the calcaneal osteotomy should be made 10 mm proximal to the calcaneocuboid joint so as to avoid damage to the anterior and middle facets. The high rate of calcaneocuboid joint nonunion during calcaneocuboid distraction arthrodesis also is a concern.