AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

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

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

History of the Procedure

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

PTT insufficiency was originally described by Kulowski in a 1936 article.² In 1953, Key intraoperatively identified a PTT rupture that was treated with excision.³ 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.^{4, 5}

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.⁶ The use of a flexor digitorum longus (FDL) transfer was popularized in 1982 by Mann, Specht, and Jahss; however, the original description of using tendon transfer for the treatment of progressive flatfoot deformity is attributed to Goldner in 1974.^{2, 7}

Important clinical signs of PTT dysfunction, the too-many-toes sign and the single-limb, heel-rise test, were discussed by Johnson in 1983.⁸ A widely accepted classification system, proposed by Johnson in 1989 and modified by Myerson in 1997, clarified treatment recommendations based on the severity of the PTT dysfunction and adaptation of the foot to collapse of the medial longitudinal arch.^{9, 10}

Problem

Clinical presentation and progression and severity of AAFD can be extremely variable; a multitude of conservative and surgical options are available for this common clinical entity. A clear understanding of the normal function of the PTT and the static restraints of the medial longitudinal arch is essential to understanding the operative and nonoperative treatment options for AAFD.

Frequency

Although PTT dysfunction is a common clinical entity, a true incidence or frequency is difficult to ascertain secondary to a variety of factors, such as missed diagnoses and coexistent disorders that can make the diagnosis perplexing. However, certain conditions are well known and documented. For example, several authors have noted the incidence of PTT pathology or rupture is higher in middle-aged women who have coexisting obesity.^{8, 11, 12, 13}

Other clinical entities that have been found to contribute to the development of PTT dysfunction include diabetes mellitus, hypertension, steroid exposure, or previous trauma or surgery in the medial foot region. Holmes and Mann studied 67 patients with PTT rupture.¹⁴ The authors noted almost 60% of their patients had a history of at least one of the above-noted conditions.

Etiology

See Pathophysiology.

Pathophysiology

Numerous causes for AAFD have been described; PTT insufficiency is the most common etiology. However, patients must also be evaluated for other possible causes to ensure optimum treatment.

Younger patients who present with rigid flatfoot should be screened for tarsal coalition, congenital vertical talus, or other forms of congenital hindfoot pathology. Patients with asymptomatic flatfeet may eventually progress to symptomatic disease as degenerative processes ensue and turn flexible deformities into rigid ones, although no natural history studies are available to support this often-repeated theory. Biomechanical studies confirm elevated gliding resistance and trauma to the PTT surface in a simulated flatfoot model.¹⁵ These data support the hypothesis that preexisting flatfoot predisposes to AAFD because of chronic mechanical overload.¹⁵

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

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

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

Many vascular and degenerative etiologies have also been proposed to explain PTT failure. Clinical evidence indicates that in the high-stress region where the tendon curves around the medial malleolus, ruptures are common. This region corresponds to a relatively avascular area of the PTT between the navicular bone and the medial malleolus. Nontraumatic tears usually occur in this hypovascular location, suggesting a possible etiology of ischemia and subsequent tendinosis. Histopathologic studies have documented the existence of a fibrocartilaginous zone in this same anatomic location, which not only alters the normal longitudinal collagen arrangement of the tendon, thus compromising the tendon's ability to counteract tensile forces, but also is subject to wear and tear. These changes result in marked disruption of collagen bundle orientation and structure and likely predispose to rupture. Epidemiologic studies have not proven a clear  link  between  a  specific  factor  and  tendon  dysfunction.¹⁶

Clinical

The clinical presentation of AAFD can be extremely variable and directly correlates with the stage of the disease.

RELEVANT ANATOMY

Section 3 of 11  

• Authors and Editors
• Introduction
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

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 lateral longitudinal arch. The medial arch is composed of the calcaneus, talus, cuneiforms, and the first through third metatarsals. The lateral arch consists of the calcaneus, cuboid, and the fourth and fifth metatarsals. The wedge shape of the tarsal bones (wider dorsally, narrower plantarly) provides a stable, keystone arrangement. With weight bearing, tensile forces in the plantar fascia prevent separation of the ends of the medial and lateral arches. Additional arch height is provided by the windlass effect. Dorsiflexion of the toes during the gait cycle results in tightening of the plantar fascia, which ultimately elevates the arch.¹⁷

The spring-ligament complex has received much attention as an important stabilizer of the medial arch.^{1, 18} This calcaneonavicular ligament serves 2 important functions by acting as a support for the head of the talus, thus providing stability to the talonavicular joint, and by maintaining the medial longitudinal arch by acting as a static support.¹⁹ 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.¹

The most frequently affected dynamic stabilizer in AAFD is the PTT, and it is the most powerful invertor of the foot and serves as an important dynamic arch stabilizer.²⁰ The posterior tibial muscle and corresponding tendon are crucial to hindfoot position and foot flexibility during the gait cycle. Originating from the posterior aspect of the tibia, intraosseous membrane, and fibula, the posterior tibial muscle and tendon pass posteromedially behind the medial malleolus and then insert via multiple bands into the navicular, cuneiforms, metatarsal bases (second through fourth), and the sustentaculum tali. Ankle plantarflexion and forefoot adduction-supination with resultant subtalar inversion are key functions of the PTT because of its posteromedial position.

Considerable controversy exists regarding the timing of the failure of the medial longitudinal arch's static and active supports. Most orthopedic surgeons support the concept that the primary mode of failure is the loss of dynamic arch support, followed by a tension failure of the static restraints. The deformity involves "shortening" of the lateral column, plantar inclination of the talar head, and lateral subluxation of the navicular on the talar head.²¹ Clinically, the arch flattens, the forefoot abducts (ie, too-many-toes sign), and heel valgus occurs. This abnormal foot position has a profound negative impact on the gait cycle.

During the gait cycle, the foot must transition from a flexible construct at heel strike (to accommodate irregular surfaces) to a rigid construct at push-off (to maintain a rigid lever for ambulation).²² At heel rise, PTT initiation of transverse tarsal joint adduction with resultant subtalar inversion causes the talonavicular and calcaneocuboid joint axes to be perpendicular and therefore locked. This process converts the foot into a rigid lever arm against which the powerful gastrocsoleus complex acts to propel the body forward. Patients with AAFD are unable to lock the transverse tarsal joints, thus preventing the formation of a rigid lever arm and transforming the foot into a "bag of bones." Clinical manifestations that ensue include the inability to perform a single-leg heel rise. This inability to invert the heel results in chronic heel valgus and subsequent Achilles contracture. Excessive forefoot abduction further  stresses the static stabilizers of the midfoot. As the static and dynamic stabilizers of the arch are overloaded, the painful clinical spectrum of AAFD develops.²³

CONTRAINDICATIONS

Section 4 of 11  

• Authors and Editors
• Introduction
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

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

An FDL 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.

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Imaging Studies

As with most foot and ankle deformities, weight-bearing radiographs are mandatory. The authors' protocol includes 3 weight-bearing views for the foot (anteroposterior [AP], oblique, and lateral) and 3 weight-bearing views for the ankle (AP, mortise, and lateral).

Evaluation of longitudinal arch collapse is largely dependent upon weight-bearing lateral radiographs. The axis of the talar-first metatarsal angle on the lateral weight-bearing foot radiograph is the most discriminating radiographic parameter in patients with symptomatic flatfoot.²⁴ Alternatively, the distance between the medial cuneiform and the floor is a strong reflection of medial arch collapse and flatfoot.²⁵  Additional features of flatfoot deformity that are noted on the lateral view include talar plantar flexion and decreased calcaneal pitch.¹⁸

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 2 reference lines through the centers of the talar head and navicular bone, respectively—reveals increased angles.

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.{{Ref26} The lateral tibial-calcaneal angle as measured on a standing lateral ankle x-ray identifies patients with Achilles tendon contractures.²⁶

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

Determining the amount of joint degeneration with computed tomography (CT) scanning 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 scans may show 2 frequently occurring extra-articular sources of bone impingement (sinus tarsi and calcaneofibular impingement).²⁷

Staging

The severity of AAFD varies, depending upon 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 3-stage continuum of PTT dysfunction.⁹

• 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.²
• 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 and/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.⁸ 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 gastrocsoleus contracture, hindfoot and midfoot motion testing usually yield normal results.
• 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.^{2, 28}
• In 1997, Myerson added a fourth stage to Johnson and Strom's original description of PTT dysfunction.¹⁰ 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.^{18, 28}

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Medical therapy

Management of the PTT-deficient foot continues to be controversial. Treatment options take many forms, ranging from conservative management with the use of medication and orthotics to various surgical procedures.

Surgical therapy

Operative treatment may involve soft-tissue procedures alone, soft-tissue procedures with the addition of an osteotomy, or arthrodesis. Although the classification discussed above (see Staging) is not foolproof, it can be very useful in the discussion of management of AAFD. Regardless of the stage, operative management should only be considered after conservative management is unsuccessful. The surgical procedure chosen should address all the fixed and dynamic deformities for the individual patient.

Stage 1

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. If the patient is evaluated in an acute state, he or she can be treated with a short-term trial of immobilization. Casting can be supplemented with a trial of nonsteroidal anti-inflammatory drugs (NSAIDs). Often, the casting trial must be for as long as one month before a significant clinical effect is noted. Once the acute symptoms have diminished, the patient can be given a trial of physical therapy, which would consist of stretching and strengthening, and modalities such as iontophoresis. 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, again, is controversial.

Traditionally, stage 1 disease has been addressed with debridement and tenosynovectomy of the diseased PTT. 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."²⁹ Debridement should be reserved for patients who show no clinical deformity or weakness.

Stage 2

Many patients with stage I and II AAFD can be effectively treated nonoperatively with orthoses (either a short, articulated ankle-foot orthosis [AFO] or foot orthosis) and structured exercises.³⁰ Alvarez et al studied patients with stage 1 and 2 AAFD (without complete tendon rupture). 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]."

Surgical management of stage II disease typically involves both a soft-tissue (FDL transfer) and a bony (medializing calcaneal osteotomy) reconstruction (see Image 2). This procedure has yielded excellent results with minimal complications and a high satisfaction rate.³¹ The osteotomy (and subsequent medial shift) of the calcaneal tuberosity shifts the moment arm of the gastrocsoleus complex medial to the subtalar axis. (See Image 3  for an axial MRI that demonstrates a calcaneal shift.) This then generates an inversion force that protects the medial soft-tissue reconstruction. The transferred FDL muscle hypertrophies  significantly as it compensates for the diseased PTT.³²
 
More advanced stage II 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 lateral column lengthening (LCL) through the anterior process of the calcaneus (joint sparing) and calcaneocuboid distraction arthrodesis (non–joint sparing). Lengthening of the lateral column through the anterior process of the calcaneus can be successfully performed with either autografts or allografts.³³ Both 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.³⁴
 
Medial column bony procedures are indicated when residual forefoot varus exists after lengthening of a lateral column. 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.^{35, 36} 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.³⁷
 
An additional procedure that is designed to correct the pes planovalgus deformity is subtalar arthroereisis. This procedure involves the placement of a plug or screw-type implant in an effort to correct the rotational malalignment of the subtalar joint. The long-term outcome of subtalar arthroereisis has been questioned; a significant number of patients develop persistent sinus tarsi pain that requires implant removal.³⁸ The limited research on this procedure in adult patients means that there is insufficient evidence to make a recommendation for or against this procedure.²³

Stage 3

In stage 3 disease, conservative management is limited to NSAID treatment and orthotic management with an Arizona Brace (Arizona AFO, Inc, Mesa, Ariz) (see Image 4). These orthotics must be accommodative rather than corrective because of the fixed deformity. Shoe modifications (larger size, rocker sole) are often required. The chances of success in relieving pain despite these measures are relatively low.

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. 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.²² 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. Long-term follow-up studies have shown that triple arthrodesis is associated with increased wear in the ankle joint andahigher rate of  degenerative ankle arthrosis.³⁹

To the authors' knowledge, no comparative studies to date have demonstrated a lower rate of adjacent joint arthrosis with the above limited fusions relative to triple arthrodesis. For this reason, triple arthrodesis continues to be the criterion standard for treatment of stage 3 AFDD.⁴⁰ (See Image 5, which consists of a preoperative radiograph of a stage 3 AFDD and another radiograph 3 months after triple arthrodesis with bony union.)

Stage 4

Stage 4 disease is rare and often requires a pantalar arthrodesis or tibiotalocalcaneal arthrodesis. Conservative management is similar to that for stage 3 disease and often utilizes accommodative braces that immobilize the ankle as well as the foot. Tibiotalocalcaneal arthrodesis involves fusion of the ankle joint and the subtalar joint. Pantalar arthrodesis involves fusion of the ankle and the subtalar, talonavicular, calcaneocuboid, and tibiotalar joints. These surgeries are technically demanding in nature and are considered salvage procedures. (See Image 6 for AP and lateral radiographs of a stage 4 PTT dysfunction with valgus tilt at the ankle.)

COMPLICATIONS

Section 7 of 11  

• Authors and Editors
• Introduction
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Although some complications that are associated with AFDD 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.⁴¹ Similar long-term failure rates were noted for FDL transfers to the navicular that were performed for stage 2 PTT dysfunctions.⁴²

Bony procedures such as a calcaneal osteotomy and various arthrodeses can also be associated with significant complications. Although nonunion of the calcaneal osteotomy is exceedingly rare, placement of the transosteotomy screw 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 nonunion—in some cases in excess of 20%—and also malposition, both in hindfoot alignment and in forefoot rotation.⁴² Longer-term complications involve arthrosis of adjacent joints.

OUTCOME AND PROGNOSIS

Section 8 of 11  

• Authors and Editors
• Introduction
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Proper treatment of adult-acquired flatfoot deformity requires a comprehensive knowledge of foot biomechanics and astute clinical judgment. No single solution is appropriate for all patients and all degrees of dysfunction; rather, a continuum of treatment options must be considered to gain the best functional outcome for the individual patient.

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.

FUTURE AND CONTROVERSIES

Section 9 of 11  

• Authors and Editors
• Introduction
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

PTT insufficiency with different degrees of deformity at different joints in the foot is a challenge to manage. Considerable controversy remains about the appropriate treatment of all stages of PTT dysfunction. Comparison-outcome trials are needed to provide better data to evaluate the treatment options. To the authors' knowledge, to date, these trials have not been completed.

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Media file 1:  Photographs from a patient with adult-acquired flatfoot deformity. These images show the typical features of the condition, which are demonstrated by an abducted forefoot and valgus hindfoot.
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Media type:  Photo

Media file 2:  Intraoperative images in a patient with pes planus. (A) Flexor digitorum longus transfer to the navicular bone. (B) Torn spring ligament.
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Media type:  Photo

Media file 3:  Axial magnetic resonance image that demonstrates a medial calcaneal shift.
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Media type:  MRI

Media file 4:  The Arizona Brace. Image courtesy of Don Pierson, CO of Arizona AFO, Inc.
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Media type:  Image

Media file 5:  Radiographs of the foot in a patient with pes planus. (A) Preoperative radiograph of a grade 3 posterior tibial tendon dysfunction. (B) Three months after triple arthrodesis with bony union.
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Media type:  X-RAY

Media file 6:  Anteroposterior and lateral radiographs of the lower extremity in a patient with pes planus. These images demonstrate grade 4 posterior tibial tendon dysfunction with valgus tilt at the ankle.
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Media type:  X-RAY

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

1. Deland JT, de Asla RJ, Sung IH, Ernberg LA, Potter HG. Posterior tibial tendon insufficiency: which ligaments are involved?. Foot Ankle Int. Jun 2005;26(6):427-35. [Medline].
2. Pomeroy GC, Pike RH, Beals TC, Manoli A 2nd. Acquired flatfoot in adults due to dysfunction of the posterior tibial tendon. J Bone Joint Surg Am. Aug 1999;81(8):1173-82. [Medline]. [Full Text].
3. Key JA. Partial rupture of the tendon of the posterior tibial muscle. J Bone Joint Surg Am. Oct 1953;35-A(4):1006-8. [Medline]. [Full Text].
4. Fowler AW. Tibialis posterior syndrome. J Bone Joint Surg Br. 1955;37:520-6.
5. Williams R. Chronic non-specific tendovaginitis of tibialis posterior. J Bone Joint Surg Br. Aug 1963;45:542-5. [Medline]. [Full Text].
6. Kettelkamp DB, Alexander HH. Spontaneous rupture of the posterior tibial tendon. J Bone Joint Surg Am. Jun 1969;51(4):759-64. [Medline]. [Full Text].
7. Goldner JL, Keats PK, Bassett FH 3rd, Clippinger FW. Progressive talipes equinovalgus due to trauma or degeneration of the posterior tibial tendon and medial plantar ligaments. Orthop Clin North Am. Jan 1974;5(1):39-51. [Medline].
8. Johnson KA. Tibialis posterior tendon rupture. Clin Orthop Relat Res. Jul-Aug 1983;177:140-7. [Medline].
9. Johnson KA, Strom DE. Tibialis posterior tendon dysfunction. Clin Orthop Relat Res. Feb 1989;239:196-206. [Medline].
10. Myerson MS. Adult acquired flatfoot deformity: treatment of dysfunction of the posterior tibial tendon. Instr Course Lect. 1997;46:393-405. [Medline].
11. Mann RA, Thompson FM. Rupture of the posterior tibial tendon causing flat foot. Surgical treatment. J Bone Joint Surg Am. Apr 1985;67(4):556-61. [Medline]. [Full Text].
12. Funk DA, Cass JR, Johnson KA. Acquired adult flat foot secondary to posterior tibial-tendon pathology. J Bone Joint Surg Am. Jan 1986;68(1):95-102. [Medline]. [Full Text].
13. Myerson M, ed. Posterior tibial tendon insufficiency. Current Therapy in Foot and Ankle Surgery. St Louis, Mo: Mosby-Year Book; 1993:123-35.
14. Holmes GB Jr, Mann RA. Possible epidemiological factors associated with rupture of the posterior tibial tendon. Foot Ankle. Feb 1992;13(2):70-9. [Medline].
15. Uchiyama E, Kitaoka HB, Fujii T, et al. Gliding resistance of the posterior tibial tendon. Foot Ankle Int. Sep 2006;27(9):723-7. [Medline].
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Article Last Updated: Sep 27, 2007