Given the complex pathology associated with adult-acquired flatfoot, this author reviews the pathomechanics of the condition, discusses keys to appropriate staging and offers recommendations for effective, pathology-specific orthotic therapy.
Adult-acquired flatfoot (AAF) may be the most difficult of all foot pathologies to treat successfully with the possible exception of calcaneal fractures. The complexity surrounding this pathology originates in the continued confusion about etiology, classification, pathomechanics and surgical and non-surgical treatment. The loss of the active and passive pull of the tibialis posterior tendon is strongly associated with the development of adult-acquired flatfoot but no one is quite sure of the exact pathomechanics of this clinical disaster.1
Hirano and colleagues performed a cadaveric study to determine whether the abnormal flatfooted position of some individuals increases friction on the tibialis posterior in its sheath, leading to an inflammatory condition that deteriorates or attenuates the tendon.2 Using six lower limbs mounted in a foot simulator and applying axial load to the tendon, they monitored the tendon’s gliding resistance. When they added a functional orthosis to the apparatus, it did not affect this resistance but did somewhat restore the normal anatomic position of the foot. The important aspect of this experiment was the confirmation that the abnormal flatfooted position does create resistance on the tibialis posterior tendon and increases the work of friction. This finding may provide some insight into the etiology of this pathology.
Adding to the lack of understanding of the etiology is the mystery of why this problem seems to have been increasing in prevalence over the last 20 years.2 Is it a result of the increased aging of the susceptible flatfooted population or are we, as clinicians, just starting to recognize the problem more frequently as an entity in itself?
Although the tibialis posterior muscle plays an important role in the deformity, authors since 1999 have begun to describe this clinical scenario as adult-acquired flatfoot, rather than posterior tibial tendon dysfunction, since the dysfunction or non-function of the tendon alone cannot account for the character and severity of the deformity and foot disability.3
In 2004, Richie postulated that “significant ligamentous rupture occurs” as the flattening of the longitudinal arch and disarticulation of the rearfoot develop along with the attenuation or complete destruction of the spring ligament, superficial deltoid, plantar fascia and, finally, the long and short plantar ligaments.3 This may truly be the reason that repair or anastomosis of the tibialis posterior tendon alone is rarely effective in restoring the structural integrity of the foot.3 Recognizing that a multilevel and interrelated pathology is occurring is essential for the successful treatment of adult-acquired flatfoot, whether the treatment is surgical or non-surgical.
The progression from simple weakness of the tibialis posterior through ligamentous disruption and finally rearfoot subluxation creates various stages of pathology that are probably best to approach as individual entities. Treating the more advanced stages with methods used in the initial stages is not effective. As the pathology in adult-acquired flatfoot progresses from moderate to severe, the deformation and dysfunction of the foot pass through several thresholds that conservative and often surgical treatment cannot reverse. It is therefore useful to approach each stage of the deformity as a separate, distinct pathology with the primary objective being to prevent the next more severe stage from occurring.
Conversely, treating the early stages using the therapies for the advanced subluxations is probably unpredictable and unsuccessful as well. Using advanced surgical procedures and highly restrictive orthoses and braces on early stages may well produce the unwanted outcomes of muscle atrophy and additional symptoms. Each stage should have its own treatment protocol that matches the requirements of its specific pathomechanics.
Although several authors attribute adult-acquired flatfoot to seropositive or seronegative arthropathies, in the overwhelming majority of cases, adult-acquired flatfoot is solely a local lower extremity phenomenon.4-6 Any valid classification should focus on this as well as the contributing factors, such as obesity and gender, that seem to determine both severity and accelerated progression of deformity.
Clinicians should consider a “pre-stage” to the disease, consisting of the acute onset of symptoms, characterized by pain, swelling, tendinitis and disability along the course of the tibialis posterior.3 One must treat these symptoms immediately with immobilization, compression, elevation and ice or nonsteroidal anti-inflammatory (NSAID) medications. Reduction of the initial acute symptoms will allow a more thorough examination to help determine the extent of the damage and the appropriate staging of the disease to produce a more focused and specific treatment plan.
Proper and effective therapy requires periodic assessment and staging of the continuing progression of deformity and pathology. I believe it is essential to have accurate examination by weightbearing radiograph, recording accurate rearfoot eversion relative to the ground and assessing muscle strength and symmetry relative to the opposite foot. Muscle testing should include weightbearing assessment since the non-weightbearing tibialis anterior’s strength can mislead the examiner into thinking that the tibialis posterior is stronger than it is.
Observation of the change in morphology of the weightbearing foot during a simple heel raise, rather than simply a positive or negative response to this test, is invaluable. Many patients cannot perform the heel raise test but this does not mean they have adult-acquired flatfoot. The total collapse of the arch and dorsiflexion of the forefoot on the rearfoot as the heel lifts on the weightbearing foot are good indications of the progression and worsening of adult-acquired flatfoot.
Most clinicians realize the significance of performing the first metatarsal rise test, which was first described by Hintermann and co-workers, and the supination lag test, discussed by Abboud and colleagues, as assessments rather than mere diagnostic tests.7,8
Hintermann and colleagues observed that radiographs and MRIs were unreliable when it came to diagnosing dysfunction of the tibialis posterior tendon.7 They designed the first metatarsal rise sign to help recognize and treat adult-acquired flatfoot at an early stage when the foot is still supple. Patients perform the test standing with equal weight on both feet. When the leg is passively and externally rotated, the first metatarsal head immediately rises off the ground in a patient with a dysfunctional tibialis tendon while it remains on the ground in a normal patient. Hintermann and co-workers compared the use of this test in 21 patients and found that it was always positive whereas the “too many toes” sign and single heel raise were positive in approximately 80 percent of the patients.
Abboud and colleagues described a test for adult-acquired flatfoot and tibialis posterior function that has a seated patient, with feet dangling above the ground, attempt to touch the plantar surfaces together.8 This attempt at inversion and plantarflexing should happen symmetrically. If one foot lags behind the other, it is a positive sign of tibialis posterior dysfunction.
The Hubscher maneuver is simply a forced dorsiflexion of the hallux while the patient is bilaterally weightbearing.3 Plantarflexion of the first ray, inversion of the rearfoot and external rotation of the lower leg demonstrate integrity of the rearfoot ligaments. Patients with tibialis posterior weakness will have a negative test demonstrated by motion of the rearfoot but patients with disruption of the rearfoot ligaments will have a positive test in which the rearfoot will not move.
By acknowledging that adult-acquired flatfoot is not a simple failure of a tendon and recognizing the host of assessment and examination tools and criteria that one can use, we can utilize this information to stage or classify the various forms of the disease before treatment.3,4,6
Stage I AAF, as described by the Richie modification of the Johnson and Strom classification, demonstrates little or no structural changes, weightbearing or non-weightbearing.3,4 The presenting symptom is tendinitis associated with either symmetrical or unilateral flatfoot. Usually, the patient can still perform a heel raise on the symptomatic side but with greater hesitation and less endurance than an unaffected patient. Symptoms of stage I resolve within two weeks with bracing and anti-inflammatory therapy, and this positive response is diagnostic of this stage. The rearfoot remains flexible and the Hubscher maneuver is negative as are the lag and first metatarsal rise tests.
Stage II AAF is characterized by a change in the weightbearing morphology of the foot, particularly the lowering of the longitudinal arch and abduction of the forefoot distal to the midtarsal joint, producing the signature “too many toes” sign.3 These changes are due to an actual tendinosis, not simply a tendinitis of the tendon. The patient can rarely perform a simple heel raise. These signs are usually a result of the attenuation or rupture of the tibialis posterior tendon, and are associated with a positive supination lag test and a positive first metatarsal rise test. The rearfoot remains flexible but the Hubscher maneuver is now positive.
Stage III AAF is characterized and easily differentiated from stages I and II by the rigidity of the rearfoot.3,4 Forced weightbearing manipulation of the rearfoot into a more neutral position is not possible. Radiographs usually demonstrate moderate to severe arthritic changes at the posterior facet of the subtalar joint and degeneration of subchondral bone at the talonavicular joint. The patient with stage III AAF will fail the heel raise, lag and first metatarsal rise tests as well as the Hubscher maneuver.
Stage IV AAF is classified as the most dramatic deformity and is resistant to any treatment options other than surgical fusions.4 The hallmarks of stage IV AAF are severe valgus deformity of the talocrural joint, degenerative joint disease of the rearfoot joints and, in dramatic cases, fractures of the fibular malleolus secondary to the huge pathological lever of the lateral deforming forces.
We know from the literature that adult-acquired flatfoot is not a simple pathology of the tibialis posterior muscle or tendon. Staging of the disorder is necessary for proper clinical decision making.
Goldner and co-workers suggested tendon repair and Johnson and colleagues described synovectomies for the early stages, transfers for the middle stages and arthrodesis for the later stages.4,9 However, few clinicians are satisfied with the surgical approach to this pathology and deformity, even in these early stages. Although the appearance of the foot is more normal anatomically, clinical experience has shown that patients are rarely satisfied with functional results. Patient satisfaction with conservative external stabilizers is greater than with surgical intervention.10
Non-surgical treatment of adult-acquired flatfoot using custom foot orthoses does not correct the pathology but does seem to slow the progression to definitely reduce symptoms and limit or reverse disability. One must coordinate the course of treatment with the staging of the deformity. Most authors recommend orthotic therapy for the initial management of symptoms.3,4,6 The proper staging allows physicians to direct non-surgical care at the specific stage, providing the most effective treatment outcomes.
The primary pathology in stage I seems to be, according to most of the related literature, tendinitis of the tibialis posterior tendon and one should treat it accordingly.1,4-6 Immobilization in a rigid walking boot with a high midsole rocker rests the tendon and allows recovery with the least amount of attenuation.
The midtarsal joint, which is stabilized by the tibialis posterior, has significant sagittal plane motion in gait. Using a walking boot that immobilizes the foot in only the frontal and transverse planes places a greater lever arm of force on this joint and stretches the tendon when it really needs to rest. A high midsole rocker on the walking boot allows, during gait, the sagittal plane motion to occur external to the foot, therefore resting the tendon.10
Using a stabilizing custom pathology-specific functional foot orthosis following the reduction of symptoms provides a more stable or rigid “bag of bones,” and restores normal motion with less effort from the tendon. The device should be rigid and deep, and should maintain a more normal alignment of the subtalar joint and longitudinal arch while limiting midtarsal joint motion. This reduces the need for stabilization efforts on the part of the tibialis posterior.
The type of custom device used in one clinical report was the University of California Biomechanics Laboratory (UCBL)-type device, which is made from a neutral negative cast.10 This study demonstrated that the in-shoe device “provided superior restoration of both arch and hindfoot kinematics.” The similarly designed Root custom functional foot orthoses, with a deep heel cup, top cover and sweet spot for the navicular tuberosity, provide the same support with a much greater acceptance and adherence. This is because the Root device fits into most contemporary shoes, which is not the case with the UCBL orthosis. If the patient will not wear the device, then it cannot be effective.
The addition of a medial heel skive would improve such a device by shifting the effective ground reaction force (GRF) more medially, resisting eversion of the calcaneus and unlocking the midtarsal joint.11 Widening the midsection of the orthosis by adding a medial flange expands the surface area of the orthosis and allows better control. The flange also improves orthotic comfort by distributing force over an expanded surface area.
Negative cast: neutral suspension cast
Positive cast correction: perpendicular
Material: rigid polypropylene
Heel cup: deep 18 mm to 22 mm
Width: wide with medial flange
Cast fill: standard
Heel skive: 4 mm to 6 mm medial skive determined by heel eversion
Positive cast modification: no inversion; sweet spot navicular tuberosity
Rearfoot post: flat or 0/0
Top cover: full-length EVA to the toes
Forefoot extensions: none necessary
Treatment for this more advanced pathology, which includes the hallmark of tendinosis and the attenuation of the tendon, must be more aggressive than for stage I. One must direct treatment to the dysfunction of the rearfoot ligaments as they bear the load of excessive forces and start to attenuate. Attempts to maintain this flexibility, especially of the ankle joint, must be included in the treatment plan if the patient is to maintain function and a relatively normal gait.
Complete restriction of subtalar joint motion places a burden on the ankle joint. The subtalar joint has a small but significant function in the sagittal plane, allowing dorsiflexion of the foot on the leg. If this dorsiflexion is restricted, then ankle dorsiflexion must increase to compensate for it. This extra burden can itself produce deterioration, compensation and deformity, and the device must address this.
The loss of function in the subtalar interosseous ligament and the spring ligament makes conventional functional foot orthoses (FFOs) of little use. Redirecting GRF is ineffective since this force cannot transfer from the calcaneus to any other bone through these ligaments. The unabated internal rotation of the leg requires some sort of mechanical intervention above the ankle to relieve symptoms and to prevent or slow the progression of further deformity.
The motivation behind the development of podiatric ankle-foot orthoses (AFOs) like the Richie Brace was to apply forces both below the foot through the footplate and above the foot through uprights attached to the lower leg in order to control the transverse and frontal plane motions above the ankle.
Richie Brace AFOs are created from negative casts, which capture the subtalar joint in relative neutral position and the orientation of the malleoli (and therefore the position of the ankle joint axis). The neutral cast, similar to the one used for the aforementioned functional foot orthoses, must reduce the supinatus (false forefoot varus) that almost always occurs as compensation in this pathology.
An orthotic laboratory makes a Root-type footplate that has two stirrups with leg uprights attached, producing the lower leg component. The hinges between the stirrups and the uprights allow sagittal plane motion during gait but inhibit frontal and transverse plane motion. The concept is to provide external fixation between the rearfoot and the lower leg to compensate for the damaged and attenuated ligaments.3
Custom-articulated AFOs, in my experience and in a case report, produce greater anatomic alignment than prefabricated or non-articulated AFOs.12 However, it is merely an assumption that anatomic realignment actually delays further deformity or produces any permanent correction. We do know that anatomic realignment, especially of the rearfoot, reduces symptoms.
Selecting footwear for the stage II patient is as important as selecting the brace. Again, in my experience, patient adherence in treatment is primarily a function of orthotic comfort and the ability to wear culturally acceptable footwear. Rigid athletic shoes with motion control or shoes with stiff shank construction and reinforced heel counters are essential. Occasionally, persistent edema in a patient with this pathology will necessitate extra depth shoes.
Negative cast: podiatric AFO fabricated from a neutral cast with the supinatus reduced
Positive cast correction: perpendicular
Material: deep heel cup of 25 to 35 mm
Width: wide with medial flange
Cast fill: standard to maximum dependent on deformity
Heel skive: 6 mm
Hinges: full flexion hinges with bilateral lower leg uprights
Positive cast modification: navicular sweet spot
Rearfoot post: flat or 0/0
Top cover: full-length top cover
The challenges in treating stage III AAF with an orthosis are due to the reality of the foot being deformed and rigid, with seemingly intractable symptoms of pain in the medial arch.3,4 Non-surgical treatment will not reverse or improve the deformity. Treatment goals are limited to reducing symptoms and preventing greater subluxation while attempting to keep the patient ambulatory. These goals also focus primarily on immobilization that allows ambulation.
It is therefore the goal of treatment to restrict motion in all three rearfoot joints while keeping the patient ambulatory. Restricting the subtalar joint while allowing ankle and midtarsal motion does little to relieve symptoms.10 Conversely, clinical experience suggests that controlling sagittal plane motion at the ankle but disregarding midtarsal joint motion only produces greater arthritic degeneration as the midtarsal joint dorsiflexes to compensate for the loss of the ankle sagittal plane motion. This is a plane of motion unsuited for the unstable midtarsal joint.
The gauntlet type of AFO, which combines a custom polypropylene shell interior wrapped in a lace-up leather exterior envelope, allows restriction of motion of all three joints in all three planes without sacrificing the patient’s ability to ambulate and wear reasonable shoes. These braces are individually fabricated on a positive corrected mold of the patient’s foot from a semi-weightbearing cast with the foot at right angles to the leg in the sagittal plane.
Although this brace has been available for more than a decade, few podiatrists or orthopedic surgeons embraced this therapy until the research of Imhauser and colleagues in 2002 demonstrated that, in comparison to other modalities, the gauntlet “completely restored the height of the arch and height of the navicular.”12
They compared the efficacy of insole orthoses and gauntlet ankle braces by evaluating their stabilizing effect on the motion of the medial longitudinal arch and calcaneal position of six cadaveric subjects.12 Researchers simulated a flatfoot condition by sectioning the structures of the medial arch. They tested each specimen with six different devices: UCBL foot orthoses, a molded polypropylene AFO, an Arizona-type gauntlet and three prefabricated stirrup-type braces. The UCBL in-shoe orthoses provided superior restoration of both arch and hindfoot kinematics. The molded polypropylene AFO performed poorly. The Arizona-type gauntlet restored the height of the midfoot but had little effect on the orientation of the calcaneus. The prefabricated stirrup-type braces were basically ineffective in stabilizing the hindfoot and arch.
Interestingly, in another study performed in 2003, 95 percent of patients treated conservatively with restrictive devices for adult-acquired flatfoot reported a significant reduction in symptoms.13
The gauntlet brace that is recommended for stage III adult-acquired flatfoot must be made to specific parameters in order to have a positive clinical outcome. Accurate casting is absolutely essential if the brace is to be comfortable and produce good patient acceptance and tolerance.
The inability of the foot in stage III to reach 90 degrees with the leg poses, in most patients, a unique challenge. Often, arthritic lipping and ankle joint degeneration affecting the anterior talocrural joint produce an osseous equinus. The laboratory fabricating the brace must know that the foot does not reach the 90 degrees standard and should accommodate for this in the cast correction.
The resulting gauntlet brace for this equinus patient with adult-acquired flatfoot will be slightly plantarflexed and one must accommodate this deficiency by adding a lift in the shoe or tilt on the sole of the shoe. Allowing the patient with an equinus deformity to remain plantarflexed without raising the heel with extra material to support the heel will cause the anterior aspect of the leg to experience great pressure against the front of the brace at midstance as the tibia attempts to pass over the foot. Making the brace more rigid and confining to relieve this pressure redirects the sagittal plane motion requirement proximally and may produce a genu recurvatum.
Since the gauntlet-type brace immobilizes the ankle, subtalar and midtarsal joint, it prevents motion in the sagittal, frontal and transverse planes. This is all beneficial for reducing symptoms but the patient must find an alternative to sagittal plane motion in order to ambulate.
Rather than transfer this sagittal plane motion to the knee, which accepts it poorly, one can transfer motion to the shoe-ground interface with the use of a midsole rocker. A pedorthist who is familiar with rocker placement can easily add this rocker to most shoes. The ideal placement is a 60/40 rocker. Many extra-depth shoes are manufactured with this rocker sole.
• Semi-weightbearing negative cast on foam with the foot at 90 degrees to the leg or fully dorsiflexed at the ankle. The deep foam board compresses the plaster or STS sock into the arch and snugly around the heel, producing a more accurate and comfortable brace.
• A heel cutout in the polypropylene shell produces a more comfortable design, especially for older patients.
• The brace height should be at least 18 cm from the floor for a 150 cm tall patient and 23 cm for a 180 cm tall patient. One would measure this from the floor to the collar of the brace.
• A fabrication laboratory that requests the circumference of the patient’s leg, midfoot and malleoli to ensure a total contact custom device is provided for your patient.
• A lace closure with two top Velcro straps. This allows ease of entry and exit of the foot, and contributes significantly to patient acceptance.
The non-surgical treatment of adult-acquired flatfoot requires a firm understanding of the pathomechanics of this disorder. It is not simply a function of tibialis posterior dysfunction. Successful treatment is dependent on accurate staging of the disorder, utilizing all tests, observations and examinations. The effective treatment intervention is different for each stage and utilization of inappropriate treatment for a particular stage is doomed to failure.
The appropriate staging and bracing application for stages I, II and III of adult-acquired flatfoot can restore mobility, dramatically reduce symptoms and slow the progression of a severely disabling disorder.
Dr. Scherer is a Clinical Professor within the College of Podiatric Medicine at the Western University of Health Sciences in Pomona, Calif. He is also the CEO of ProLab Orthotics/USA. Dr. Scherer is the author of the book “Recent Advances In Orthotic Therapy.”
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Editor’s note: This article is adapted with permission from the book “Recent Advances in Orthotic Therapy” by Dr. Scherer and published by Lower Extremity Review.