Given the challenges of treating the common condition of adult-acquired flatfoot, this author reviews the literature and shares insights from his clinical experience. He discusses the proper staging of this condition and offers pertinent pearls on the use of conservative therapy.
Aside from calcaneal fractures, adult-acquired flatfoot (AAF) may be the most difficult foot pathology to treat successfully. The complexity surrounding this pathology originates in the continued confusion about etiology, pathology, classification, pathomechanics and surgical and non-surgical treatment.
Accordingly, let us take a closer look at the various classifications of AAF, which has previously been referred to as posterior tibial tendon dysfunction (PTTD), and discuss the pathomechanics, prognosis and treatment options for non-surgical care.
The loss of the active and passive pull of the tibialis posterior tendon is strongly associated with the development of AAF but no one is quite sure of the entire pathomechanics of this clinical disaster.1 Added to the lack of understanding of the etiology is the mystery of why this problem seems to be 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 as an entity in itself?
Although the tibialis posterior must play an important role in the deformity, authors have begun since 1999 to describe this clinical scenario as adult-acquired flatfoot since the dysfunction or non-function of the tendon alone cannot account for the character and severity of the deformity and foot disability.2
In a previous article in Podiatry Today, Douglas Richie, Jr., DPM, postulated that “significant ligamentous rupture occurs” as the flattening of the longitudinal arch and disarticulation of the rearfoot develops along with the attenuation or complete destruction of the spring ligament, superficial deltoid, the plantar fascia and finally the long and short plantar ligaments.2 This may truly be the reason that repair or anastomosis of the tibialis posterior tendon alone is rarely effective in repairing the structural integrity of the foot. Recognizing that a multilevel and interrelated pathology is occurring is essential for the successful treatment of AAF, 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 one would use in the initial stages is not effective. Conversely, treating the early stages with therapies one would employ for the advanced subluxations is probably unpredictable and unsuccessful as well. Which system of classification offers the most appropriate and simplest decision marking opportunities for the clinician?
Although several authors attribute AAF to seropositive or seronegative arthropathies, the overwhelming majority are solely a local lower extremity phenomenon.3,4 Any valid classification should focus on this phenomenon as well as the contributing factors, such as obesity and gender, which seem to determine both the severity and accelerated progression of the deformity.
Clinicians should consider a “pre-stage” to the disease. This may consist of the acute onset of symptoms, characterized by pain, swelling, tendinitis and disability. One must treat these symptoms with immobilization, compression, elevation and ice, or nonsteroidal antiinflammatory medications (NSAIDs). Reducing the initial acute symptoms will allow a more thorough examination. Accordingly, one can determine the extent of the damage and appropriate stage of the disease. Hopefully, this will facilitate a more focused and specific treatment plan.
Proper and effective therapeutic treatment requires periodic assessment and staging of the continuing progression of deformity and pathology. Accurate examination of weightbearing by radiographs, recording accurate rearfoot eversion to the ground and assessing muscle strength and symmetry to the opposite foot are essential. 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.
Observing the change in morphology of the weightbearing foot during a simple heel raise is invaluable as opposed to simply noting a positive or negative response to this test. Most podiatrists realize the significance of performing the first metatarsal rise test, first described by Hintermann, and the supination lag test of Abboud as assessment tools rather than mere diagnostic tests.5,6
The Hubsher maneuver is simply a forced dorsiflexion of the hallux while the patient is bilaterally weightbearing. Plantarflexion of the first ray, supination of the rearfoot and external rotation of the lower leg demonstrates integrity of the rearfoot ligaments. Patients with simple tibialis posterior weakness will have a negative test but patients with disruption of the rearfoot ligaments will have a positive test.
Acknowledging that AAF is not a simple failure of a tendon and recognizing that there are a host of assessment tools, examination tools and criteria to use, we can utilize this information to stage or classify the various forms of the disease before treatment.2,4,7
Stage I AAF. As described by the Richie modification of the Johnson and Strom classification, Stage I demonstrates little or no structural changes weightbearing or non-weightbearing.2,7 The presenting symptom is tendinitis associated with either symmetrical occurring or unilateral flatfoot. Usually, the patient can still raise the heel on the symptomatic side but with more difficulty. Symptoms of Stage I AAF resolve within two weeks with bracing and antiinflammatory therapy, and this response is diagnostic of Stage I. The rearfoot remains flexible and the Hubsher maneuver is negative as are the lag and first metatarsal rise test.
Stage II AAF. This 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 sign of too many toes. 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, creating a positive supination lag test and a positive first metatarsal rise test. The rearfoot remains flexible but the Hubsher maneuver is now positive.
Stage III AAF. The Stage III transition is characterized and easily differentiated from I and II by rigidity of the rearfoot. 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. Of course, the simple heel raise, lag test, first metatarsal rise test and the Hubsher maneuver are all failures.
 Stage IV AAF. This stage is classified as the most dramatic deformity and is resistant to any treatment options other than surgical fusions. The hallmark of this deformity is the 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 lever of the lateral deforming forces.
We know from the literature that AAF is not simply pathology of the tibialis posterior. There are assessment tools one can use to classify this disorder and proper staging of the disorder is necessary to facilitate appropriate therapy.
Goldner suggested tendon repair and Johnson described synovectomies for the early stages of AAF, transfers for the middle stages of AAF and arthrodesis for the later stages.7,8 Few clinicians are satisfied with the surgical approach to this pathology and deformity.
Non-surgical treatments of AAF do not correct the pathology but do seem to slow the progression, reduce symptoms and reverse disability. The course of treatment must, by all accounts, be coordinated with the staging of the deformity. Most authors recommend conservative care for the initial management of symptoms. The Richie update of the Johnson and Strom classification utilizes the appropriate tests and exams to stage the deformity and pathology. This allows practitioners to direct non-surgical care at the specific stage, providing the most effective treatment outcomes.
 The primary pathology in Stage I seems to be, by all accounts, tendinitis of the tibialis posterior tendon and physician should treat this accordingly.1,3,4,7 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 frontal and transverse plane motion only places a greater lever arm of force on this joint and stretches the tendon that 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.
Using a stabilizing functional foot orthosis (FFO) after the reduction of symptoms provides a more stable or rigid “bag of bones,” and provides normal motion with less effort from the tendon. The device should be rigid, deep and should maintain a more normal alignment to the subtalar joint and longitudinal arch while limiting midtarsal joint motion. This reduces the need for the stabilization effort of the tibialis posterior.
In a study of the UCBL type device, made from a neutral negative cast, Imhauser, et. al., demonstrated that the in-shoe device “provided superior restoration of both arch and hindfoot kinematics.”9 The similarly designed Root FFO, with a deep heel cup, top cover and sweet spot for the navicular tuberosity, provides the same support with a much greater acceptance and compliance. The addition of a medial heel skive could only improve such a device by shifting the effective ground reactive force more medially, resisting both eversion of the calcaneus and unlocking the midtarsal joint.10
When it comes to Stage I AAF, the treatment regimen may include:
• antiinflammatory regimen of ice, rest and NSAIDs;
• supportive measures of a rigid walking boot with a high midsole rocker;
• a rigid FFO from a neutral cast with a deep heel cup, 4 to 6 mm medial skive, a stabilizing post, a navicular tuberosity sweet spot and a full length top cover.
The treatment for this more advanced pathology, including the hallmark of tendinosis and the attenuation of the tendon, must be more aggressive than the regimen for Stage I AAF. Physicians must direct treatment to the dysfunction of the rearfoot ligaments as they bear the load of excessive forces and they themselves start to attenuate. However, clinicians can use the continued flexibility of the rearfoot as an advantage in treatment. One should include attempts to maintain this flexibility, especially that of the ankle joint, in the treatment plan if the patient is to maintain function and a relatively normal gait.
 The loss of the subtalar interosseous ligament and the spring ligament make conventional FFO orthoses of little use. Redirecting ground reactive force is ineffective since one cannot transfer this force 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 have the effect of relieving symptoms and preventing or slowing progression of further deformity.
The motivation behind the development of podiatric AFOs was to apply forces below the foot through the foot plate as well as providing uprights attached to the lower leg in order to control the transverse and frontal plane motions above the ankle.
Podiatric AFOs are created from negative casts, which capture the subtalar joint in relative neutral position as well as the orientation of the malleoli. Accordingly, the negative casts capture the position of the ankle joint axis. The neutral cast, similar to the one used for the aforementioned FFO, must reduce the supinatus (false forefoot varus), which almost always occurs as compensation in this pathology.
An orthotic laboratory produces a Root type footplate that has two stirrups with attached leg uprights 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 place an external fixation between the rearfoot and the lower leg in order to compensate for the damaged and attenuated ligaments.
Selecting footwear for the Stage II patient is as important as the brace selection. Rigid athletic shoes with motion control or shoes with stiff shank construction and reinforced heel counters are essential.
When it comes to Stage II AAF, the treatment regimen may include:
• a podiatric AFO fabricated from a neutral cast with the supinatus reduced;
• a deep heel cup of 25 to 35 mm;
• a medial flange foot plate with a 4-mm or greater medial skive;
• full flexion hinges with bilateral lower leg uprights; and
• shoe gear that provides frontal plane rigidity.
The challenge in treating Stage III is the reality that the foot is deformed and rigid. Non-surgical treatment will not reverse or improve this deformity. Treatment goals are limited to reducing symptoms and preventing greater subluxation while attempting to keep the patient ambulatory. Directing treatment at these three goals focuses primarily on immobilization that allows ambulation.
It is therefore the goal of treatment to restrict all three rearfoot joints while keeping the patient ambulatory. Restricting the subtalar but allowing ankle and midtarsal motion does little to relieve symptoms. Conversely, controlling the ankle joint sagittal plane motion but disregarding midtarsal joint motion only produces greater arthritic degeneration by forcing the midtarsal joint to compensate for the ankle’s sagittal plane motion. This is a plane of motion unsuited for the unstable midtarsal.
 The gauntlet type of AFO, which combines a custom polypropylene shell interior with a lace-up leather exterior envelope, allows restriction of motion of all three joints in all three planes without sacrificing the ability of the patient to ambulate and wear reasonable shoes. These braces are individually fabricated on a positive corrected mold of the patient’s foot. The corrected mold comes 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 over a decade, few podiatrists or orthopedic surgeons embraced this therapy until the research of Imhauser demonstrated that the gauntlet, in comparison to other modalities, “completely restored the height of the arch and height of the navicular … .”9 Interestingly, in another study performed in 2003, 95 percent of patients treated nonoperatively for AAF reported a significant reduction in symptoms.11
One must ensure that the gauntlet brace is created 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.
When it comes to Stage III AAF, one should consider the following tips for the treatment regimen.
• The negative cast must be semi-weightbearing 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.
• Select either a solid or cutout heel polypropylene shell. Older patients seem to be more comfortable in the cutout heel design.
• Always select either an 18 cm or 23 cm (from the floor) height of the brace for AAF. A short device only encourages sagittal plane motion of the rearfoot.
• Use a fabrication laboratory that requests the circumference of the patient’s leg, midfoot and malleoli to ensure that a total contact custom device is provided for your patient.
• Request a lace closure with two top straps, either Velcro or D rings. This allows ease of entry and exit of the foot, and contributes significantly to patient acceptance.
The inability of the foot in Stage III to reach 90 degrees with the leg produces a unique challenge. Often, one will note arthritic lipping and ankle joint degeneration affecting the anterior talocrural joint, leading to an osseous equinus. The laboratory must know that the foot does not reach the 90-degree standard and should not accommodate for this in the cast correction.
The resulting gauntlet brace for the equinus patient will be slightly plantarflexed and one must accommodate this deficiency by adding a lift in the shoe or on the sole of the shoe. Failure to observe this deficiency and adjust for it will produce an exceedingly uncomfortable brace or a pending genu recurvatum.
Since the gauntlet type brace immobilizes the ankle, subtalar and midtarsal joints, it prevents motion on the sagittal, frontal and transverse planes. This is all beneficial to reducing symptoms but the patient must find an alternative to sagittal plane motion if he or she is going to ambulate.
 Rather than transfer this sagittal plane motion to the knee, which accepts it poorly, the physician can transfer the sagittal plane motion to the shoe ground interface with the use of a midsole rocker. A pedorthist familiar with rocker placement can easily add a midsole rocker to most shoes. The ideal placement is a 60/40 rocker. Many extra depth shoes are manufactured with this rocker sole.
The non-surgical treatment of AAF 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 and appropriate consideration of all diagnostic tests, observations and examinations. The effective treatment intervention is different for each stage and utilization of the inappropriate treatment for a particular stage is doomed to failure.
The appropriate staging and bracing application for Stage I, II and III AAF can restore mobility, dramatically reduce symptoms and slow progression of a severely disabling disorder.
Dr. Scherer is the Chairman of the Department of Applied Biomechanics at the California School of Podiatric Medicine at Samuel Merritt College. He is also the CEO of ProLab Orthotics in Napa, Calif.
1. Beals TC, Manoli I. An unusual cause of posterior tibial tendon degeneration. Foot and Ankle International, 19(3):177,1998
2. Richie DH. A new approach to adult-acquired flatfoot. Podiatry Today 17(5):32-46,2004.
3. Kettlecamp DB. Spontaneous rupture of the posterior tibial tendon. Journal Bone Joint Surgery, 51A(4):759,1969
4. Myerson MS. Adult acquired flatfoot deformity. Journal Bone Joint Surgery, 78A:780,1996
5. Hintermann B, Gachter A. The first metatarsal rise sign: A simple sensitive sign of tibialis posterior tendon dysfunction. Foot and Ankle 17:237,1966
6. Abboud J, Kapcha P. Supination lag as an indication of posterior tibial tendon dysfunction. Foot and Ankle 19:570,1998
7. Johnson KA, Strom DE. Tibialis posterior dysfunction. Clinical Orthopedics and Related Research 239:196,1989
8. Goldner JL, Keats PK, Bassett FH, Clippinger FW. Progressive talipes equino valgus due to trauma or degeneration of the posterior tibial tendon and medial plantar ligaments. Orthopedic Clinics North America 5:39,1974
9. Imhauser CW, Abidi NA, et. al. Biomechanical evaluation of the efficacy of external stabilizers in conservative treatment of acquired flatfoot deformity. Foot and Ankle International 23(8):727-37, 2002
10. Kirby KA. The medial heel skive technique: Improving pronation control in foot orthoses. JAPMA 82:177,1992
11. Augustin A, et. al. Non operative treatment of adult acquired flatfoot with the Arizona brace. Foot and Ankle Clinics North America 8:491,2003.
For related articles, see “A New Approach To Adult Acquired Flatfoot” in the May 2004 issue of Podiatry Today, “Clearing Up The Confusion Over Posterior Tibial Tendon Dysfunction” in the December 2001 issue, or “Key Insights On Surgical Correction Of Pediatric And Adult Flatfoot” in the January 2007 issue.
Also check out the archives at www.podiatrytoday.com .
CE Exam #153
Choose the single best answer to the following questions.
1. When one performs the Hubsher maneuver, plantarflexion of the first ray, supination of the rearfoot and external rotation of the lower leg demonstrates …
a) disruption of the rearfoot ligaments
b) integrity of the rearfoot ligaments
c) severe tibialis posterior weakness
d) none of the above
2. In regard to Stage I adult-acquired flatfoot (AAF) …
a) there are little or no structural changes weightbearing or non-weightbearing
b) the presenting symptom is tendonitis associated with either symmetrical or unilateral flatfoot
c) symptoms resolve within two weeks with bracing and antinflammatory therapy
d) all of the above
3. In regard to the presentation of Stage II AAF …
a) radiographs usually reveal degeneration of subchondral bone at the talonavicular joint
b) the patient can usually perform a simple heel raise
c) the rearfoot remains flexible but the Hubsher maneuver is now positive
d) all of the above
4. In regard to the presentation of Stage III AAF …
a) the simple heel raise and lag test are positive but the Hubsher maneuver is negative
b) forced weightbearing manipulation of the rearfoot into a more neutral position is not possible
c) radiographs usually reveal mild arthritic changes at the posterior facet of the subtalar joint
d) all of the above
5. In regard to Stage IV AAF …
a) physicians should still try conservative modalities prior to surgical fusions
b) one will see severe valgus deformity of the talocrural joint
c) physicians will see degenerative joint disease of the rearfoot joints in rare cases
d) none of the above
6. When it comes to treating Stage I AAF …
a) one should incorporate a walking boot that immobilizes the frontal and transverse plane motion but not the sagittal as this facilitates rest of the tibialis posterior tendon
b) in a study of the UCBL type device, Imhauser, et. al., found that the in-shoe device was markedly deficient in restoring hindfoot kinematics.
c) a stabilizing functional foot orthosis should maintain a more normal alignment to the subtalar joint and longitudinal arch while limiting midtarsal joint motion
d) all of the above
7. In regard to treating Stage II AAF, the author recommends modalities including …
a) a podiatric AFO fabricated from a neutral cast with the supinatus reduced
b) fusion of the talonavicular
c) a heel cup of 10 to 20 mm
d) all of the above
8. In regard to treating Stage III AAF, treatment goals are limited to …
a) reducing symptoms and facilitating greater subluxation while attempting to keep the patient ambulatory
b) limited weightbearing and shoe gear that prevents frontal plane rigidity
c) reducing symptoms and preventing greater subluxation while attempting to keep the patient ambulatory
d) none of the above
9. When it comes to treating Stage III AAF …
a) short braces are encouraged as they reduce sagittal plane motion of the rearfoot
b) older patients seem to be more comfortable with a solid heel polypropylene shell.
c) a negative cast must be semi-weightbearing on foam with the foot at 90 degrees to the leg or fully dorsiflexed at the ankle
d) all of the above
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