Treating Posterior Tibial Tendon Dysfunction
April 2007 Issue
Although there are many lower-extremity diagnoses presented to O&P for consideration and treatment, few are as common as posterior tibial tendon dysfunction (PTTD). This condition is more prevalent than ever, due to factors such as an increasingly overweight population along with an aging population. If left unchecked, PTTD can be a seriously disabling condition; however, proper and early use of orthotics and AFOs along with the correct shoes can halt and even reverse its effects.
The posterior tibial (PT) muscle originates from the deep posterior compartment of the leg. The PT tendon passes posterior to the medial malleolus, slightly posterior to the ankle joint axis. It then passes medially and plantar to the subtalar joint (STJ) axis. Just posterior to the navicular, the tendon divides into three branches: anterior, middle, and posterior. Collectively, these insert deep onto the plantar arch of the foot including the navicular, all three cuneiforms, the cuboid, and the metatarsals. Due to its location, multiple insertions, and influence over several axes of the foot, the PT muscle plays a critical function in weight-bearing activity.
Four Stages of PTTD
Stage I: In the mildest cases, you may or may not see structural changes in the foot. There will be a flatfoot condition, but if the deformity has not progressed too far, the patient may still be able to complete the heel rise test. The primary symptom is tenosynovitis of the PT tendon.
Treatment Options: Initial treatment will include short-term immobilization with a rigid walking boot and subsequent use of a foot orthotic.
Stage II: Visible changes will occur in the foot structure due to the PT tendon attenuation and the loss of function of one or more of the critical ligaments in the hindfoot. The patient will have difficulty or be unable to perform the single heel rise. Inversion strength of the hindfoot is compromised.
Treatment Options: Foot orthotics may help, but with the loss of hindfoot ligament integrity, it may be necessary to consider some type of AFO that provides control above and below the ankle joint. Physical therapy can also help to improve strength and restore some loss of range of motion.
Stage III: The deformity becomes rigid, and the patient cannot perform the single heel rise test. Radiographs will reveal arthritic changes are starting to occur.
Treatment Options: Ankle and rearfoot motion needs to be severely restricted; gauntlet type braces may be necessary. Surgical options such as an osteotomy, a fusion, or arthrodesis need to be considered.
Stage IV: Complete tear or rupture; end-stage deformity.
Treatment Options: Surgery, if feasible, and/or conservative bracing are necessary.
All treatment options need to be considered across each stage. Factors to consider include the patient's weight, activity level, general health, and commitment to rehabilitation. A Stage III or IV patient with a low activity level may respond surprisingly well to conservative measures, whereas bracing may not be successful for a highly active Stage II.
The PT tendon plays a major role in the gait cycle and, among other things, is responsible for decelerating the internal rotation of the tibia, thus limiting pronation of the foot following heel strike. The PT muscle is considered to be a plantarflexor as well as an inverter of the hindfoot. Loss of function of the PT tendon results in a foot that is unable to stabilize the midtarsal joint, has a reduced supination moment across the STJ axis, can no longer adequately support body weight, and demonstrates increased STJ pronation.
Patients with PTTD may present symptoms of a partial tear, complete tear, or a restriction of the gliding motion of the tendon along the medial ankle. There are several etiologies for PTTD:
- Traumatic, or direct injury.
- Pathologic rupture, due to degenerative conditions such as rheumatoid arthritis.
- Functional rupture, where the tendon remains intact but is not functioning correctly.
More recent literature indicates that for older adults, PTTD may be considered part of a greater progressive flatfoot condition called adult acquired flatfoot (AAF), which can ultimately result in multiple ligamentous ruptures. Contributing factors include obesity, diabetes, and age. It also tends to be more common in women. Often these patients are poor surgical candidates, so any and all conservative measures should be fully explored.
PTTD more often occurs unilaterally, and clinical diagnosis usually reveals an obvious asymmetry between the feet, with noticeable edema and a medial bulge of the talonavicular joint on the affected side. There will also be an observable internally rotated position of the malleoli and a significant heel valgus. The patient will be unable to perform the single heel rise test, and palpation will reveal tenderness along the course of the tendon. Radiographic examination will support the findings and help to determine the stage of the deformity and also to see if there are any degenerative changes to the foot structures.
There is strong evidence to suggest that equinus plays a significant role in the progression of AAF. Equinus contracture breaks down the midtarsal joint and the medial longitudinal arch, reducing the effectiveness of the PT tendon. Physical therapy can be very helpful to both stretch the gastrocsoleal complex and strengthen the PT muscle. Surgical options may include some posterior muscle group and tendon lengthening, which will establish proper correction and alignment of the hindfoot.
At the outset, patients will usually have pain, tenderness, and swelling along the PT tendon. Ice therapy done for 20 minutes, three times a day should help to reduce some of the inflammation. Doctors may also prescribe non-steroidal anti-inflammatory drugs (NSAIDs).
In the mildest cases, custom foot orthotics should be considered. I prefer to use orthotics with a high medial flange to support the entire midfoot. The orthotics can be made from thermoplastics such as subortholen or polypropylene although not all patients will be able to tolerate the rigid control. More accommodative orthotics can also be made from Thermocork or Ethylene Vinyl Acetate (EVA), again incorporating a high medial flange to prevent midfoot collapse. Furthermore, these orthotics can be posted extrinsically to provide more medial varus support. Some practitioners will favor a UCBL-type device to get maximum control. Incorporating a slight heel raise will help decrease any tension in the Achilles tendon if equinus is present.
Proper Shoes Required
As was learned at Pisa, a weak foundation will not support a sturdy building. Foot orthotics are only as useful as the shoes in which they are placed. The midfoot collapse associated with AAF and subsequent medial deviation of the STJ axis requires that the patient wear the proper shoes with firm shanks and stiff medial counters. Hiking boots are ideal for this patient. The strong counters, an upper that extends above the malleoli, lace closures, and firm soles provide better control for the entire foot. A foot orthotic exerts control below the STJ axis, while a hiking boot works above the STJ axis. In addition, depth boots will allow patients to comfortably substitute their custom foot orthotics in place of the removable inlays. There are other shoe modifications that may help stabilize the foot such as a Thomas Heel (an extension of the medial heel), a medial flare, or an external medial buttress.
More advanced cases need more rigid control. Traditional AFOs, unlike foot orthotics, will control the foot throughout the entire gait cycle, both in the stance and swing phases. They also exert control above and below the ankle and can control in all three planes of motion. Once again, it is essential that AFOs are worn with proper and well-fitting shoe gear.
In summary, the literature indicates that PTTD can be managed quite successfully non-operatively using combinations of the techniques discussed above, including foot orthotics, proper footwear, AFOs, and physical therapy. Depending on the severity of the case, results may be seen in as little as six weeks, or they may take up to a year. Surgical treatment can be reserved for those patients who fail an adequate trial of conservative measures.