The posterior tibial tendon undergoes tearing and degeneration, and as it fails, the foot falls into a planovalgus configuration. Posterior tibial tendon dysfunction (PTTD) is the most common cause of an adult acquired flatfoot deformity.
Most cases occur spontaneously without known antecedent trauma. Women are much more commonly affected than men, with a typical age range older than 50 years.
With time, a rigid deformity develops. The degree and flexibility of the deformity play a key role in determining treatment.
ANATOMY
The posterior tibialis typically degenerates in an area underneath the medial malleolus and distally to its insertion. The process is not inflammatory but is rather characterized by replacement of the normal collagen fibers with amorphous scar and mucinous degeneration.6
As the arch falls, the hindfoot will fall into valgus relative to the leg, whereas the forefoot will abduct through the talonavicular joint. Uncovering of the talar head results as the forefoot pivots laterally.
The sag of the arch and the abduction of the forefoot can be described in terms of the loss of alignment of the first metatarsal and the talus. The long axes of these bones should normally be colinear. A sag of the arch is seen by an angulation in this line on the standing lateral radiograph, whereas abduction of the forefoot is seen by lateral angulation of this line on the anteroposterior (AP) view.
PATHOGENESIS
In most cases, the cause of PTTD is unknown and is not associated with a clear antecedent trauma.
The collapse of the arch is the result of a tendon imbalance. The antagonists to the posterior tibialis are the peroneals and they must be functional for the deformity to develop.
A single study has suggested a correlation of PTTD with the human leukocyte antigen (HLA) B27 genotype, typically associated with seronegative arthropathies.7
Cumulative mechanical factors likely play a role in the development of the disorder; a preexisting planovalgus deformity presumably places extra stress on the tendon and is thought to be a risk factor for degeneration.
The presence of an accessory navicular ossicle within the tendon substance at its insertion into the medial pole of the navicular is also a risk factor for tendon degeneration, likely from local mechanical stress (FIG 1).
NATURAL HISTORY
Dysfunction of the posterior tibialis is thought to be the initiating event in the collapse of the arch.2
Early in the course of the disease, pain along the course of the posterior tibialis or weakness of its function will be present without any arch collapse. This is called stage I disease.
With time, a planovalgus foot deformity develops. Initially, this deformity is flexible and is called stage II disease.
A fixed deformity eventually results; this is called stage III disease. The first component of the deformity to become fixed is usually an elevation of the first ray relative to the fifth ray. This is the result of a compensation of the forefoot for the hindfoot valgus and is called a fixed forefoot varus. Later, the valgus alignment of the calcaneus through the subtalar joint becomes contracted and irreducible.
Rarely, a secondary failure of the deltoid ligament along the medial aspect of the hindfoot develops as the mechanical stresses placed on it by the flattened arch increase. This is called a stage IV deformity.
Achilles tendon contracture is commonly seen in association with PTTD. As the planovalgus deformity develops, the foot collapses through the arch and the Achilles is no longer stretched to its normal length in a standing or walking posture.
Table 1 details the PTTD stages.
PATIENT HISTORY AND PHYSICAL FINDINGS
Most, but not all, patients present with pain along the medial arch.
In some cases, lateral impingement develops as the valgus posture of the hindfoot becomes extreme. The calcaneus impinges against the inferior border of the fibula. This is usually a late finding and is often intractable to conservative management.
The most painful phase of PTTD is usually as the tendon is actively degenerating. Some patients will note a history of intense pain that diminishes once the tendon finally ruptures completely. They may present with deformity or lateral pain as their primary complaint.
Other deformities may coexist, most significantly hallux valgus or midfoot arthritis.
Methods for examining the foot for PTTD include the following:
The single-leg toe rise. The examiner should note the ability to perform the maneuver, the presence of inversion, and the presence or absence of pain. This is a critical and sensitive screening test. Action of the posterior tibialis is required to invert and lock the hindfoot, allowing the foot to act as a rigid lever through which the Achilles powers the ankle into plantarflexion.
The “too many toes” sign. The examiner observes the standing patient from behind. The more abducted forefoot will show more toes visible on the lateral side of the leg. The examiner also notes the presence of forefoot abduction. Abduction of the forefoot occurs as the posterior tibialis fails and must be corrected in treatment.
Power of the posterior tibialis. The examiner isolates the tendon by resisted inversion past the midline with the foot held in plantarflexion. Typical muscle strength grading is used. The result can be normal early in the disease. The patient may attempt to substitute the anterior tibialis; it is also an invertor but will dorsiflex the ankle as well.
Fixed forefoot varus. The examiner holds the calcaneus in a neutral position (out of valgus) and notes any fixed elevation of the first ray relative to the fifth. The severity of deformity is noted in degrees. Fixed forefoot varus must be accounted for in any treatment algorithm and is usually the first component of the deformity to become rigid.
Achilles contracture. The examiner holds the calcaneus in a neutral position and notes dorsiflexion of the ankle, with the knee both flexed and extended (the Silfverskiöld test). The result is measured in degrees of ankle dorsiflexion. A significant Achilles contracture limits the degree of correction possible with bracing and may require surgical correction.
IMAGING AND OTHER DIAGNOSTIC STUDIES
Plain radiographs should be obtained with weight bearing to adequately describe the alignment of the foot. The talo–first metatarsal angle describes the sag of the arch when drawn on the lateral view and the abduction of the forefoot when drawn on the AP view.
Plain foot radiographs should also be examined for the presence of hindfoot arthritis, midfoot arthritis or instability, and an accessory navicular.
A standing ankle mortise view should be obtained to rule out deltoid laxity (stage IV disease).
Magnetic resonance imaging (MRI) is not routinely necessary and may underestimate the severity of disease, but it may be useful in ruling out other pathologies. Findings of PTTD typically include fluid in the sheath, dramatic thickening of the tendon, and a heterogeneous signal within the tendon substance indicating the presence of interstitial tears (FIG 2).
DIFFERENTIAL DIAGNOSIS
Midfoot arthritis resulting in pes planus through tarsometatarsal joint collapse
Medial ankle arthritis
Medial osteochondral lesion of the talus
Neurogenic failure of the posterior tibialis through spinal or central pathology
NONOPERATIVE MANAGEMENT
The flatfoot that results from posterior tibial tendon failure is irreversible, but symptoms may be controllable in many patients by nonoperative means.
A simple in-shoe semirigid or rigid foot orthotic may provide sufficient arch support to reduce symptoms in some patients.
The gold standard for nonoperative management is the use of a cross ankle brace. This allows direct control of the tendency of the calcaneus to fall into valgus. The most commonly used and best tolerated is a leather ankle lacer with an incorporated custom-molded plastic stirrup, often referred to as an Arizona brace after a common brand name.1
Other options that may be suitable for higher demand situations or patients with edema control problems include a hinged molded ankle–foot orthosis or a conventional double metal upright ankle–foot orthosis with a leg strap.
Steroid injections into the posterior tibial tendon sheath are contraindicated, as they may directly or indirectly precipitate frank rupture and further collapse.
No brace, physical therapy regimen, or medication has been shown to modify the course of the disease or the ultimate outcome for the tendon. These are all best thought of as modalities to control the symptoms.
SURGICAL MANAGEMENT
Surgery is indicated when the symptoms cannot be controlled by a nonoperative means acceptable to the patient. An active patient in his or her 50s, for instance, may find the use of an Arizona brace for the remainder of his or her life to be intolerable and may choose to pursue a surgical remedy.
Preoperative Planning
The patient’s size must be considered before any motion-sparing tendon reconstruction in the hindfoot is considered. Although not rigorously proven in the literature, the morbidly obese patient with an acquired pes planus deformity is at greater risk to break down the repair and may be better served by a triple arthrodesis.
The presence of hindfoot arthritis similarly requires a fusion rather than an osteotomy and tendon reconstruction.
A fixed forefoot varus should be addressed, either as part of the procedure through a medial column osteotomy or by a triple arthrodesis if severe.
Tightness of the gastrocnemius should also be assessed to determine if a fractional lengthening of the gastrocnemius (Strayer procedure) will be required.
Positioning
The patient is positioned supine with a bolster under the ipsilateral hip. This internally rotates the leg to allow access to the lateral aspect of the calcaneus, which is addressed first. The bolster may then be removed to allow the leg to externally rotate and allow access to the medial aspect of the foot.
A tourniquet is applied to the thigh.
Approach
The posterior tibial tendon is débrided directly and augmented or replaced by transferring the flexor digitorum longus (FDL) to the navicular. This procedure alone was first described in the 1980s and proved quite effective at pain control in most cases, although static correction of the arch was minimal.2,5
A medial displacement calcaneal osteotomy is then used to provide a measure of arch correction, directly addressing the hindfoot valgus. Indirectly, this raises the sag along the medial column of the foot as well and helps correct the talo–first metatarsal angle. Correcting the mechanics of the arch is thought to confer an element of protection to the FDL transfer.3,8,9,11
If necessary, up to about 20 degrees of forefoot varus may be corrected by a plantarflexion osteotomy of the medial column through the medial cuneiform (the Cotton procedure). This allows the indications for a motion-sparing procedure to be expanded to a wider patient population, and the need for this step is assessed after the other components of the correction are complete.4
Once the arch is corrected, a final check of the tightness of the gastrocsoleus complex is made to ensure that a lengthening is not required.
TECHNIQUES
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