Although a variety of surgical treatments are available for adult flatfoot, conservative treatments such as night splints and orthoses can be effective in managing the deformity. These authors provide keys to a thorough clinical exam of these patients, insights on accessing the severity of the flatfoot deformity and a review of conservative treatment options.
The adult flatfoot deformity is a condition that lends itself to many treatment options whether they are conservative or surgical. Formulating a proper treatment must begin with evaluating and categorizing the deformity.
The evaluation of an adult flatfoot requires ascertaining a pertinent patient history that includes the onset of the deformity, the timing of symptoms and the severity of past and current symptoms. One may elicit a family history of flatfoot deformity. Van Boerum and colleagues showed that associated conditions including rheumatoid arthritis, seronegative arthropathies, hypertension or diabetes may be significant in the adult patient with flatfoot.1 Occupation, activity level and obesity are other possible contributory factors. Footwear, the history of trauma and previous treatment are other significant factors. The authors also emphasize a pertinent review of systems.
We can categorize the flatfoot deformity as either a residual flatfoot deformity from a developmental etiology or an acquired deformity. Myerson showed that developmental causes include abnormal joint development, tarsal coalition, a congenital vertical talus, accessory navicular and generalized ligamentous laxity from Marfan’s syndrome or Ehlers-Danlos syndrome.2 As Myerson notes, the acquired flatfoot condition is associated with posterior tibial tendon dysfunction (PTTD), midfoot laxity, subluxation of the talus, traumatic deformities, a ruptured plantar fascia or Charcot foot as well as neuromuscular imbalances from polio, cerebral palsy, closed head injuries or following a cerebrovascular accident.
Importantly, tightness of the triceps surae complex and isolated gastrocnemius tightness have a profound effect on the longitudinal medial arch. Johnson and Christensen performed a three dimensional evaluation of the first ray in cadaver models with variable Achilles tendon tension.3 They found the influence of the peroneus longus on the medial column diminishes with increasing Achilles load. Equinus on an intact longitudinal arch seems to affect the distal components of the medial column, primarily in the frontal plane. Furthermore, the authors say with increased pull on the Achilles, a measurable arch flattening effect occurs with plantarflexion of the talus and navicular, and dorsiflexion of the first metatarsal and cuneiform.
When assessing the extent of flatfoot, clinicians should perform a thorough clinical examination in conjunction with plain film X-rays. With the patient seated in the exam chair, one can focus on the neurological and musculoskeletal portions of the clinical exam. The musculoskeletal examination should account for any gross deformities, symptomatic sites or malalignments. Perform a comprehensive non-weightbearing biomechanical exam including the Silfverskiöld test for equinus, subtalar range of motion and neutral position, forefoot to rearfoot alignment, forefoot hypermobility and first metatarsophalangeal joint range of motion. When it comes to these biomechanical exams, perform these exams with the forefoot both loaded and unloaded.
One must examine the patient while standing and the exam should begin with an evaluation of the legs, ankles and feet. Clinicians should have the patient stand facing directly at them with feet parallel and shoulder width apart. Evaluate the knee and leg for deviation in the frontal and transverse planes, genu varum and hyperextension of the knee. Evaluate the ankle for asymmetrical swelling and proper alignment.
Then evaluate the foot for a pes planus foot type. The hallmark findings of a pes planus foot type are collapse of the longitudinal medial arch, a prominent talar head medially and abduction of the forefoot on the rearfoot. With the patient still facing forward, employ the Hubscher maneuver or toe test of Jack, and the trunk test to evaluate if the deformity is flexible or not.
Observe the patient while walking to look for any gait disturbance, such as an apropulsive gait and an early heel rise. The clinician should then have the patient turn 180 degrees with the feet still parallel and shoulder width apart. Pes planus will present itself once again as a collapsed arch, a prominent talar head medially, a valgus attitude of the rearfoot to the leg and a positive too many toes sign. A double heel rise test in conjunction with a single leg heel rise can help one evaluate the posterior tibialis tendon function and deformity reducibility. Dysfunction of the posterior tibialis tendon will be apparent if there is asymmetrical or incomplete inversion of the hindfoot during this maneuver, and the inability to perform the single leg heel rise.
Lastly, we evaluate the extent of the deformity by using weightbearing plain film X-rays, including lateral, dorsal-plantar, lateral oblique views of the foot and an ankle anterior-posterior view, to evaluate for ankle valgus. Advanced imaging studies, such as computed tomography (CT), ultrasound and magnetic resonance imaging (MRI), are not warranted if one can make the diagnosis clinically and on plain films. Reserve these studies for instances when the diagnosis of posterior tibial tendon dysfunction has come into question or if information from these studies will affect management.
There is an overwhelming amount of literature stating that PTTD is the most common cause of an adult-acquired flatfoot. It is a good practice to classify your flatfoot patients.
We use the Johnson and Strom staging system in our clinic.4 Sizensky and coworkers noted that Johnson and Strom’s 1989 staging system for PTTD is based on the clinical presentation and severity of deformity as the disease progresses along a continuum.5
Stage I is characterized by tenosynovitis of the posterior tibial tendon without tendon elongation or clinical deformity.4 A patient in this stage is able to perform a single-limb and double-limb heel rise. Stage II is marked by tendon elongation, incompetence and degeneration as well as a flexible pes planovalgus deformity. Stage II patients frequently are not strong enough to perform a single-limb heel rise although these patients typically demonstrate heel inversion on double-limb heel rise, which indicates a supple deformity. Patients with stage III have a fixed, irreducible flatfoot deformity and cannot perform a single-limb or double-limb heel rise.
Myerson modified this classification and proposed a stage IV, a progression of stage III disease characterized by deltoid insufficiency and valgus ankle instability.6 Researchers have proposed a stage IIb to describe a stage II deformity with residual forefoot supination (varus) of more than 10 degrees when the hindfoot has been reduced to a neutral position.7
Coupling the patient’s history of present illness with the results of the clinical exam, the clinician should be able to formulate a proper treatment plan. It is paramount that the initial treatment plan seeks to relieve the patient’s pain and discomfort. We treat stage 1 and stage 2 posterior tibialis tendon dysfunction with night splints, low Dye strappings, Medrol Dosepaks and RICE (rest, ice, compression, elevation) therapy at initial contact.
Night splints may be effective initial treatments as many clinicians’ treatment plans seem to under-address equinus. Van Boerum and colleagues showed that biomechanically, the deforming force of a tight triceps surae acts on the midfoot instead of the metatarsal heads during the propulsive phase of the gait cycle, which collapses the arch.1 With a collapsed arch, the authors note the foot rolls forward like a rocker bottom and loses the force that is necessary for efficient gait. This puts chronic stress on the posterior tibial tendon and puts the foot at risk for a pes planus foot type, which physicians must address.
We instruct the patient to use the splints one or two hours a night for two to three months with augmentation one day a week for long-term care. The arch has the external support of low Dye strapping and usually stays in place for four to five days. We also prescribe a Medrol Dosepak and provide written instructions for RICE therapy. If the patient is unable to tolerate oral prednisone, we use Duexis (Horizon Pharma) or Mobic (Boehringer Ingelheim). The patient then presents to the office in one week for further evaluation.
The majority of the patients do well with this initial treatment plan. Getting the patient’s initial symptomology under control allows the clinician not only to formulate a proper treatment plan but allows one to access the apex of the deformity and address the root cause of the pain.
However, if the flatfoot deformity is severe, we may see at the next office visit that the initial treatment plan has been nullified. In these cases, we opt to place the patient in a controlled ankle motion (CAM) walker or a below-the-knee hard cast for four to six weeks or until symptoms subside. In our clinic, immobilization in a walking boot in conjunction with low Dye taping for two to four weeks has been effective in reducing many of our patients’ painful conditions and gets us to square one to move forward with long-term treatment. We do not use steroid injections into the tendon although some clinicians utilize this treatment modality.
Once the initial symptomology is under control, we then employ external supportive devices to control the excessive pronation the patient is experiencing. Our first line of therapy is a custom orthotic that has a deep heel cup, an extra 1/8th inch of ethylene vinyl acetate (EVA) forefoot padding, and a perforated EVA top cover with a non-slip rubber bottom. This is a semi-rigid device.
A foam box helps to obtain the impressions. We invert the rearfoot as we drive the foot into the foam. Once the heel is all the way down, we then plantarflex the first metatarsal as the forefoot drives into the foam as well. This essentially builds correction into the cast and in theory recreates the patient’s arch to allow the device to combat the strong plantarflexory force of the triceps surae complex at the naviculocuneiform joint complex.
If we feel the patient will pronate over the top of this device, we utilize a Blake inverted orthotic. The Blake inversion refers to balancing the positive cast more than 10 degrees inverted. This device has a high medial flange. A high medial flange is an increase in the height of the medial side of the device starting just distal to the heel and extending to the distal edge with the apex near the navicular.8 This modification also makes the orthosis slightly wider at the area of the medial arch. We also add a deep heel cup to the device to try to control eversion of the rearfoot. The Blake orthotic can correct a significant amount of deformity. This device is less cumbersome than conventional bracing and lends itself quite well to fitting into a tennis shoe or extra-depth shoe.
We have the patient utilize a break-in period for all of our custom orthoses. Patients get instructions to wear the devices for 30 minutes to an hour at the time of dispensing and after a seven- to 10-day period, they should have them in their shoes for the entire day. We have them follow up in one month for an orthotic check and instruct them to call the office if they notice any redness, irritation, blistering or an increase in pain.
An ankle-foot orthosis such as an Arizona AFO (Arizona AFO) may be necessary for severe flatfoot cases. The brace extends proximally to the midshaft of the tibia and distally to the metatarsal heads. One can fabricate the leather upper using a standard Velcro closure, lace-up design or a combination of the two. Once one has ensured proper fitting of the Arizona AFO, he or she can insert the Arizona AFO inside the patient’s shoe for daily wear in keeping with its low-profile appearance.
As Augustin and Sheldon note, the Arizona AFO functions by decreasing hindfoot valgus alignment, lateral calcaneal displacement and medial ankle collapse.9 During casting of the mold for the brace, the calcaneus reduces to its proper anatomic alignment underneath the tibia and talus. The authors note the brace maintains this relationship via three-point fixation, which is similar in a well-molded cast.
Some patients may tolerate an articulated ankle-foot orthosis such as a Richie Brace. This brace is effective at controlling foot drop and valgus rotation at the ankle although some patients do not tolerate the brace well. The patient must have complete information about the brace before prescription. It is imperative that the patient is aware that it may not fit well in existing shoe gear. One should only use this type of orthosis to correct the flexible aspect of the deformity. In our experience, a brace cannot correct the rigid components of adult flatfoot. Pain and problems with the skin may increase if the brace provides too much correction in a patient with a rigid deformity.10
Formulating a proper non-surgical treatment plan for an adult flatfoot can be challenging although many patients with an adult flatfoot in association with PTTD can have effective treatment with conservative management protocols as we have described above. At first patient contact, the clinician’s goal should be to alleviate or significantly decrease the patient’s pain and discomfort. When this happens, the clinician should institute long-term treatment options to decrease the progression of the deformity and limit future discomfort.
Dr. DeHeer is a Fellow of the American College of Foot and Ankle Surgeons, a Fellow and member of the Board of Directors of the American Society of Podiatric Surgeons, and a Diplomate of the American Board of Podiatric Surgery. He is also a team podiatrist for the Indiana Pacers and the Indiana Fever. Dr. DeHeer is in private practice with various offices in Indianapolis.
Dr. Warnock graduated in 2013 from the Kent State University College of Podiatric Medicine and is completing a preceptorship with Dr. DeHeer.
1. Van Boerum D, Sangeorzan B. Biomechanics and pathophysiology of flat foot. Foot Ankle Clin. 2003; 8(3):419-430.
2. Myerson MS. Adult acquired flat foot deformity. J Bone Joint Surg Am. 1996; 78(5):780–92.
3. Johnson C, Christensen J. Biomechanics of the first ray part V: the effect of equinus deformity a 3-dimensional kinematic study on a cadaver model. J Foot Ankle Surg. 2005; 44(1):114-120.
4. Johnson KA, Strom DE. Tibialis posterior tendon dysfunction. Clin Orthop Rel Res. 1989; 239:196-206.
5. Sizensky J, Marks R. Medial-sided bony procedures: why, what and how? Foot Ankle Clin. 2003; 8(3):539-562.
6. Myerson MS. Adult-acquired flatfoot deformity: treatment of dysfunction of the posterior tibial tendon. Instr Course Lect. 1997; 46:393–405.
7. Lee MS, Vanore JV, Thomas JL, et al. Diagnosis and treatment of adult acquired flatfoot. J Foot Ankle Surg. 2005; 44(2):78–113.
8. Blake R, Ferguson H. Foot orthoses for severe flatfoot in sports. J Am Pod Med Assoc. 1991; 81(10):549-55.
9. Augustin JF, Sheldon SL, Berberian WS, Johnson JE. Nonoperative treatment of adult acquired flat foot with the Arizona Brace. Foot Ankle Clin. 2003; 8(3):491-502.
10. Noll K. The use of orthotic devices in adult acquired flatfoot deformity. Foot Ankle Clin. 2001; 6(1):25-36.
11. Meehan RE, Brage M. Adult acquired flat foot deformity: clinical and radiographic examination. Foot Ankle Clin. 2003; 8(3):431-452.
For further reading, see “A Guide To Conservative Care For Adult Flatfoot” in the January 2011 issue of Podiatry Today or the DPM Blog “Why Conservative Treatment Is The Standard Of Care For Adult-Acquired Flatfoot” at http://tinyurl.com/43fsr3u  . For an enhanced online experience, check out Podiatry Today on your iPad or Android tablet.