Adult acquired flatfoot deformity, primarily posterior tibial tendon dysfunction, in many cases can be successfully managed with conservative treatment modalities including early immobilization, long-term bracing, physical therapy, and anti-inflammatory medications.
By Robert W. Mendicino, DPM, FACFAS, Alan R. Catanzariti, DPM, FACFAS, and Kyle S. Peterson, DPM
Adult acquired flatfoot deformity (AAFD), the painful flatfoot deformity in adults, is a major cause of disability for a patient and can be a challenge for foot and ankle specialists. AAFD is a common condition among patients caused primarily by specific pathology of the posterior tibialis tendon, referred to as posterior tibial tendon dysfunction (PTTD).1,2 PTTD is a progressive musculoskeletal condition that ranges from its simplest form as a localized tenosynovitis to a complex rigid foot and/or ankle deformity. Treatment for PTTD is dependent on the severity of the condition, and clinicians have many conservative and surgical options to choose from.
What is PTTD?
The tibialis posterior muscle is a centralized muscle located in the deep posterior compartment of the leg. The tendon of the tibialis posterior muscle traverses the medial malleolus where it changes direction to insert on the navicular tuberosity, the plantar aspect of all three cuneiforms, the cuboid, and metatarsal bases two through four.3 The tibialis posterior muscle stabilizes the arch of the foot and is also a primary plantar flexor of the ankle and invertor of the subtalar joint.4 Degeneration of the tibialis posterior tendon and associated ligamentous structures can lead to a pathologic flatfoot. As stated previously, PTTD is the most common cause of an adult acquired flatfoot deformity.
Dysfunction of the tibialis posterior tendon occurs from elongation of the tendon as the foot undergoes increased amounts of pronation. This ultimately leads to a functional imbalance of the structural components with an overpowering of the foot’s evertors. As seen on a physical and radiographic exam, the structural components affected by PTTD are: decreased arch height, valgus alignment of the calcaneus, medial subluxation/plantar flexion of the talus, increased forefoot abduction, and equinus contracture (Figures 1 and 2). Early in the condition, a patient may complain of medial foot pain, however, with progression, lateral bony impingement may occur at the subtalar joint and the distal tip of the fibula.5
Johnson and Strom first popularized the most commonly used classification for PTTD, which was subsequently modified by Myerson in 1996.6,7 Stage I patients demonstrate tenosynovitis or tendinosis of the posterior tibial tendon with no structural deformity. Stage II PTTD causes a flatfoot deformity with attenuation or rupture of the posterior tibial tendon. The distinguishing characteristic of Stage II is that the flatfoot deformity still remains flexible and reducible. Early in the course of stage II disease, pain is localized medially along the tendon; later during this stage subfibular impingement and sinus tarsi pain may occur. Stage III PTTD represents a fixed nonreducible deformity with marked calcaneal valgus and midfoot abduction. Stage IV PTTD, as described by Myerson,7 presents as a rigid or flexible flatfoot deformity with associated ankle involvement. Due to deltoid ligament failure, the ankle demonstrates a valgus talar tilt (Figure 3).
Treatment for PTTD
As with other musculoskeletal conditions, many treatment methods are available for PTTD. Numerous studies have assessed operative treatments, including tendon transfer, calcaneal osteotomy, and hindfoot realignment arthrodesis.8-11
Studies of conservative care, however, are much less frequently reported in the medical literature than studies of surgical methods. But, with encouraging results being published,11-18 we feel it is imperative to initiate a solid conservative treatment course initially. Published studies suggest that patient outcomes improve with custom foot orthoses, ankle-foot orthoses (AFOs), physical therapy, stretching and strengthening exercises, and anti-inflammatory medications.
Williams, in 1963, was one of the first to report on a series of 52 patients with a nonspecific tendinitis of the tibialis posterior tendon.19 He utilized many conservative treatment methods, including arch supports, foot baths, plaster of Paris, calipers with T strap, local steroid injections, and activity restriction.
A study in 2008 by Krause et al demonstrated the value of a custom foot orthosis, termed a “shell brace,” for treatment of stage II PTTD. They reported a significant improvement in 83% of patients (15 of 18) within an average of 2.8 weeks once treatment had started with the brace as well as an improvement in mean AOFAS (American Orthopaedic Foot & Ankle Society) ankle-hindfoot score from 55.6 points at baseline to 81.6 after a mean of 61.4 months.
In addition, Augustin and colleagues presented the effectiveness of an AFO for use in 21 patients with PTTD stages I through III. At an average follow up of 12 months, 90% of patients had a statistically significant improvement in symptoms and quality of life.13 Mean AOFAS hindfoot scores increased from 37.7 before the use of the brace to 76 after brace use. Foot Function Index scores (FFI) and Short Form Health Survey (SF-36) scores also improved significantly with the AFO.
In 2008 Lin and colleagues published their long-term results of a study in which participants with stage II PTTD used a double upright AFO after six weeks in a walking cast.14 Investigators defined patients with successful outcomes as those who were brace-free and avoided surgery; at 8.6 years of follow up 70% of the cohort met this definition.
In 2009 Kulig et al examined the effectiveness of orthoses and resistance exercises in the early treatment of stage I or II PTTD.15 They demonstrated the greatest improvement in patients’ pain and activity limitation with the combined treatment of orthotics, stretching of the gastrocnemius and soleus muscle complex, and performing an eccentric exercise regimen focused on the tibialis posterior tendon.
Similarly, Alvarez et al studied the effectiveness of a structured rehabilitation protocol in 47 patients with stage I or II PTTD for a median treatment period of four months.16 Their program included the use of a short articulated AFO or foot orthosis and strengthening exercises for the posterior tibial, peroneal, anterior tibial, and gastroc-soleus muscles. The program also included isokinetic exercises, exercise bands, heel rises, and toe walking. After an average of 10 physical therapy sessions, 83% (39 of 47) patients had successful subjective and functional outcomes, and 89% (42 of 47) were satisfied with their treatment.
Lastly, Chao et al found that 67% of 49 patients with stage II or III PTTD had an improvement in pain, function, ambulation distance, and satisfaction with a molded AFO or University of California Biomechanics Laboratory (UCBL) shoe insert after an average of 15 months of use.17
Our hospital’s approach
In order to better understand patient satisfaction with conservative care for PTTD and to evaluate our treatment methods, we undertook a retrospective chart review that was recently published in The Journal of Foot and Ankle Surgery.20 We reviewed 64 consecutive patients with stage I through II PTTD seen from 2007 through 2009. The goals of our research were to support the previous studies and to demonstrate that, if treated early in the course of PTTD, conservative care improves patients’ symptoms. We made treatment decisions based on individual patients’ chief complaint and their relative severity of pain and potential contraindications to oral medications. We also tailored treatment course based on each patient’s previous care.
Our overall success rate with nonsurgical treatment was 87.5% (56 out of 64 patients). Twenty eight patients (47.46%) were immobilized with a cast-boot (CAM walker) for a median of two weeks, and 50 (78.12%) were braced (low articulated AFO) for a mean of 3.51 months. Forty-four (74.58%) underwent physical therapy, and 27 (46.55%) were prescribed foot orthoses. Twenty (31.25%) received nonsteroidal anti-inflammatory drugs (NSAIDs), six (9.38%) received oral corticosteroids, and 38 (59.38%) received both. Eleven patients (18.97%) also received corticosteroid injections into their sinus tarsi region for secondary complaints.
Further investigation revealed the use of any form of immobilizing brace (cam walker or LAFO) was significantly (p=.003) associated with successful nonsurgical treatment in 83.93% of cases. We feel that bracing—in particular the LAFO for longer use—is a crucial addition for nonoperative treatment because it combines a foot orthosis with extra support around the ankle.
Of all the fabricated and off-the-shelf devices utilized, we found our patients most often prefer the LAFO device. Patients’ reported reasons for this preference were the ability to wear LAFOs with their own shoe gear and the brace’s allowance for ankle joint range of motion (Figure 4). We work closely with a pedorthist to ensure proper fabrication and fitting.
Interestingly, we found that in 27 patients (46.55%) who underwent magnetic resonance imaging (MRI) for their PTTD, the presence of a split-tear of the tibialis posterior tendon (13 of 27 patients, 48.15%) was significantly associated with failed nonsurgical treatment (odds ratio, 0.016). This finding is not surprising, however; when a torn tendon is present, conservative treatment will likely fail, and the patient may require surgical repair. Although we are not quick to order advanced imaging, such as an MRI, we do so in approximately 50% of our patients with PTTD, as demonstrated in our study. Most MRI evaluation is performed on patients who are not responding to the initial conservative care modalities.
Seventy-eight percent of our patients studied were classified as obese (BMI ≥ 30). Five of eight (62.5%) of patients who failed nonoperative therapy were obese, although this finding was not statistically significant. In general, we find that educating patients about weight loss can be a helpful adjunct to a treatment regimen.
Lastly, it is important to have a good working relationship with a physical therapist to discuss proper stretching and strengthening exercises for PTTD. We ensure instructions are given to physical therapists because we have found that, in certain situations, physical therapy can aggravate the symptomatic tendon and impede successful treatment. These instructions include the recommendation that stretching of the posterior muscle group be done with the LAFO in place, so as not to put excessive strain on the posterior tibial tendon. Also, strengthening of the posterior tibial tendon must be performed from a neutral rather than an everted position, as an everted position can put undo strain on the tendon.
We found our nonoperative modalities of initial immobilization, anti-inflammatory medications, physical therapy, and longer duration bracing to be useful in the early management of PTTD. We rely on a thorough history and physical to accurately diagnose PTTD and classify it according to Johnson and Strom.6 We believe the degree of flexibility or rigidity of a flatfoot deformity dictates the choice of conservative versus surgical treatment. Essentially, if the flatfoot is in an early flexible stage, patients respond better to conservative treatment, whereas rigid later stages more often require surgery.
When conservative care fails, surgical treatment should be employed. The literature describes a wide variety of surgical procedures that are currently used for treatment of adult acquired flatfoot and PTTD.8-11
Stage I and II PTTD may present with collapse of the medial longitudinal arch of the foot and/or significant tendinopathy or a tear of the posterior tibial tendon. If conservative treatment is unsuccessful popular treatment for stage I and early stage II includes tenosynovectomy, direct posterior tibial tendon repair, flexor digitorum longus (FDL) tendon transfer, and gastrocnemius muscle recession.5 We frequently utilize the FDL tendon transfer with or without direct repair of the posterior tibial tendon when treating early stage II PTTD.21,22
Late stage II PTTD demonstrates varying degrees of medial arch collapse, forefoot abduction, and hindfoot valgus (Figure 2). When presented with a flexible deformity and a compromised posterior tibial tendon, the majority of the indicated procedures focus on single or double calcaneal osteotomies with the use of a FDL tendon transfer.21-25 We have previously shown that a double calcaneal osteotomy can re-establish proper alignment in a stage II flexible flatfoot (Figure 5).26 In a patient with significant medial column instability, a naviculocuneiform arthrodesis may also be performed as an isolated procedure or combined with a calcaneal osteotomy (Figure 6).27-28
Stage III PTTD is a rigid flatfoot condition. Arthrodesis of the hindfoot is required to realign the joints and stabilize the foot. Most often, fusion of all three hindfoot joints is performed; however, isolated fusions are indicated when isolated degenerative joint disease is present without marked structural deformity.29-31 Our preferred method of treatment for end-stage flatfoot deformity is a triple arthrodesis (Figure 7).
Few reports have been published on the treatment of stage IV PTTD, and no specific standard has been set for comparisons. Surgical treatment has included pantalar arthrodesis, ankle fusion, total ankle replacement with a triple arthrodesis, and deltoid ligament reconstruction.32 Given the complexity of the deformity of the foot and ankle, stage IV PTTD is challenging to treat and generally has less than desirable outcomes.
PTTD is a common condition treated by foot and ankle specialists. Although there is a role for surgical treatment of PTTD, conservative care often can prevent or delay surgical intervention. Decreasing inflammation and stabilizing the affected joints associated with the posterior tibial tendon can decrease pain and increase functional levels. With many different modalities available, aggressive nonoperative methods should be considered in the treatment of PTTD, including early immobilization, the use of long-term bracing, physical therapy, and anti-inflammatory medications. If these methods fail, proper evaluation and work-up for surgical intervention should be employed .
Robert W. Mendicino, DPM, FACFAS, is chair, Alan R. Catanzariti, DPM, FACFAS, is director of residency training, and Kyle S. Peterson, DPM, is a second-year resident in the Division of Foot and Ankle Surgery at The Western Pennsylvania Hospital in Pittsburgh, PA.
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