Clearing Up The Confusion Over Posterior Tibial Tendon Dysfunction

By Douglas H. Richie, Jr., D.P.M.

Addressing etiology myths and raising pertinent questions, the author thoroughly explores the possible causes of this complex condition and offers an array of salient treatment pointers.

Virtually every foot and ankle surgical symposium held in the United States over the past five years has devoted significant sessions to the pathomechanics, surgical and non-surgical treatment of the symptomatic adult flatfoot condition. Unfortunately, the popular name for this condition, posterior tibial tendon dysfunction (PTTD), reinforces a generally accepted notion that a failure of the posterior tibial tendon (PTT) is the primary etiology of the symptomatic adult acquired flatfoot deformity.
       However, there has been recent evidence to the contrary that would, at least, caution us about placing total blame on an attenuated or ruptured posterior tibial tendon as the cause of the painful flatfoot condition. The implications of these recent insights are significant to the degree that we must modify surgical and non-surgical treatment plans accordingly.

According to the author, recent evidence suggests
that DPMS should be wary of assuming that a
ruptured PTT is the primary etiology for adult-acquired
flatfooot (shown above).
Early reports linking a relationship between a ruptured PTT and the developmental flatfoot first appeared in the orthopedic literature during the ‘50s. However, these appeared to be rare, isolated cases.
       Documentation of a developmental flatfoot deformity in an adult patient population (secondary to rupture of the tibialis posterior tendon) appeared several times in the orthopedic literature during 1982 and 1983 (Mann and Specht, Jahss, Johnson). The first report of this condition in the podiatric literature was published by Fredenburg in the Journal of Foot Surgery in 1983. During the next two decades, a virtual epidemic of painful adult flatfeet (secondary to attenuation or rupture of the PTT) was reported in the medical literature. At the same time, numerous theories were proposed regarding the etiology and pathomechanics of this complex condition.
What The Literature Reveals About Causative Factors Of PTTD
Several investigators (Ghormley, Anzel, Kettlekamp, Downey) have linked PTTD to rheumatoid arthritis. Myerson has found a subgroup of patients with seronegative spondyloarthropathy. Other authors have dispelled any link between collagen vascular disease and PTTD.
       An oft-quoted 1992 study from Holmes and Mann found that 52 percent of patients with the adult acquired flatfoot secondary to PTTD had either diabetes mellitus, hypertension or obesity.
       In 1984, Mueller categorized posterior tibial tendon ruptures into three etiologic categories: direct injury, pathologic rupture and idiopathic rupture. Seven years later, Mueller proposed a fourth category, “functional rupture,” which would describe patients who didn’t have complete rupture of the posterior tibial tendon.
       Clearly, during the past two decades, the majority of authors writing about symptomatic adult acquired flatfoot have described an insidious onset of tendinitis symptoms associated with the PTT that progress to attenuation or “dysfunction” of the tendon, and subsequently lead to complete rupture. During this evolution, they noted the affected foot was undergoing a progressive alignment change that lead to significant flatfoot deformity.

Here you can see an example of positive first metarsal
rise. Performing the first metatarsal rise test allows
you to check for ligamentous integrity and movement
transfer mechanisms in the foot of a patient with Stage
II PTTD.
In 1989, Johnson and Strom proposed classifying PTTD into three stages, linking tendon pathology to clinical presentation and radiographic findings. Myerson added a fourth stage later. Currently, this classification system remains the most often quoted system in the literature (see “How To Classify Posterior Tibial Tendon Dysfunction”).

Is The Current Classification Too Broad?
The Johnson and Strom classification attributes the progressive adult acquired flatfoot to gradual attenuation and subsequent rupture of the posterior tibial tendon. However, it ignores other structural changes, specifically ligamentous attenuation, that I will discuss later in this article.
       More often than not, these patients will come into your office, already presenting with Stage II of posterior tibial dysfunction. The Stage II category is too broad in that it encompasses the broad range of a flexible flatfoot, beginning with early attenuation and structural change through progressive ligamentous rupture, rearfoot and midfoot collapse, and finally ending in the rigidity which marks Stage III.
       In my opinion, there should be subcategories of Stage II, based upon levels of ligamentous attenuation and degree of deformity. Clearly, there are non-operative and operative interventions better suited for “early” Stage II than “late” Stage II conditions.

Understand The Nuances Of The Posterior Tibial Tendon And Tibialis Posterior Muscle
Failure of the PTT has been almost universally linked to the progressive symptomatic adult-acquired flatfoot syndrome. However, be aware that knowledge of the true function of the tibialis posterior muscle remains obscure despite considerable research over the past two decades.
       What we do know is that the tibialis posterior muscle and the PTT have the strongest lever-arm for developing supination moment about the subtalar joint axis. The PTT also crosses the oblique midtarsal joint axis, but no one has conducted measurements of moment on this joint.
       The insertion of the PTT on the navicular is intimately involved with the spring ligament complex to prevent plantar-medial migration of the talus head during pronation of the rearfoot complex. Stabilizing the talonavicular portion of the midtarsal joint is probably the most important function of the PTT. Distal insertions of the tibialis posterior tendon into the lesser tarsus and metatarsals provide ligamentous stability to the midfoot and assist with compression and locking of the midtarsal joint.
       In regard to the tibialis posterior muscle, there is a prevalent misconception that this muscle actually supinates the foot during the stance phase of gait. Recent evidence has indicated that the human foot does not actually “supinate” until shortly before heel-rise.
       At this time, the tibialis posterior muscle has already finished providing its most important function: restraining internal rotation of the tibia during the contact phase of gait and stabilizing the midtarsal joint during midstance. This restraint and stabilization occurs through eccentric contractions for which the tibialis posterior muscle is ideally designed.
       Actually, the tibialis posterior muscle has minimal ability to actively shorten, contract and supinate. However, the muscle does resist elongation while contracting eccentrically and provides necessary resistance to considerable internal rotation and pronatory forces imposed on the foot by the tibia.
       There is very little evidence that the PTT has a direct arch supporting function. Conversely, the plantar fascia has a three-fold greater arch-supporting function than the PTT. Therefore, when we see arch collapse in the progressive adult-acquired flatfoot, we must attribute it to the loss of other structures besides the PTT.

Why A PTT Rupture Isn’t The Sole Cause Of Adult Flatfoot
Deland, et. al., evaluated cadaver models that were subjected to axial loads and attempted to reproduce the adult acquired flatfoot by severing the tibialis posterior tendon. When they simply cut the PTT and applied axial load, they saw minimal arch collapse or valgus rotation of the hindfoot. These researchers had to sever the spring ligament complex, plantar aponeurosis, deltoid ligament, talocalcaneal ligament, long and short plantar ligament, and medial calcaneal-cuboid ligament in order to accomplish significant collapse of the hindfoot and midfoot as you would see in Stage II and Stage III PTTD deformities.
       Earlier this year, Chu and Myerson, in their own cadaver studies, also could not create the experimental flatfoot by simply cutting the PTT. They had to sever the spring ligament and plantar fascia in order to re-create the deformity.
The lesson is simple: The adult acquired flatfoot is not caused by a simple rupture of the PTT alone. Numerous significant ligaments must also attenuate and rupture in order for the human foot to assume the alignment you would commonly see in Stage II and Stage III deformities.

Performing A Surgical Transfer Of The PTT: Will The Foot Collapse?
Two surgical studies have been conducted on patients who had a PTT transfer and did not subsequently develop the adult-acquired flatfoot deformity. In a series of 10 patients suffering a traumatic common peroneal nerve palsy, Mizel et. al., followed the patients after they underwent an anterior transfer of the PTT to the midfoot. After a 75-month follow-up, none of the patients exhibited arch contour loss and none of them developed a valgus hindfoot. Mizel concluded that the absence of a functioning peroneus brevis accounted for the failure of these feet to progress to a flatfoot deformity void of a functioning PTT.
       A fascinating counterpoint theory was proposed this year by Yeap et. al.. They followed a group of 17 patients, who had received a PTT transfer to treat a dropfoot condition. These patients had Grade 4-5 eversion strength of the peroneus brevis so you would expect them to progressively develop a flatfoot deformity.
       However, after a five-year follow-up, none of the patients had a clinical flatfoot deformity. Only 6 percent showed any significant forefoot abduction. Eighty-two percent could perform a single heel rise, despite the absence of an intact PTT.
       Yeap et. al., concluded: “The development of a flatfoot in tibialis posterior tendon dysfunction is therefore unlikely to be the result of lack of ‘sling’ support of the medial longitudinal arch from the tibialis posterior tendon only.”
       These investigators suggested that the adult acquired flatfoot is the result of complex biomechanical aberrations in the foot and ankle that ultimately cause overload on the PTT during life. Ideally, we need to correct these poorly understood biomechanical abnormalities before the PTT ruptures.

When you perform the Hubscher maneuver,
be aware that effective ligamentous integrity
and movement transfer will cause a one-to-one
external rotation of the tibia as you passively
dorsiflex the hallux.
Raising Questions About A Pre-Existing Flatfoot Deformity
Many authorities have linked the presence of a pre-existing flatfoot in patients developing PTTD. In his 1991 series, Jahss found a pre-existing flatfoot in 100 percent of patients with PTTD.
       It is commonly reported in the literature that most patients with various stages of PTTD have an asymptomatic flatfoot on the contralateral side. This makes side-to-side radiographic interpretation difficult as both feet will appear abnormal in terms of radiographic alignment of the rearfoot. What has not been answered by any investigator, thus far, is why only one foot breaks down and begins following the progressive cascade of events leading to the symptomatic adult-acquired flatfoot.
       These insights into the etiology of the adult acquired flatfoot should change our approach in selecting non-operative and operative interventions.
About 10 years ago, performing a direct transfer of the flexor digitorum longus tendon to the navicular was a popular surgical procedure for correcting painful adult flatfoot (secondary to PTTD). While initial reports by Johnson and Mann on this procedure were quite promising, a follow-up survey of patients (published by Sobel in 1993) showed a 50 percent failure rate of the flexor digitorum longus transfer to the navicular among patients with Stage II PTTD.
Clearly, the evidence in subsequent years has validated the fact that, unless you address the underlying biomechanical abnormality, surgically replacing the damaged PTT is doomed to failure.
       Correcting the pre-existing flatfoot deformity appears to be the most reasonable surgical approach to providing long-term favorable outcomes. However, as I’ve discussed, there is no consensus on the primary biomechanical deformity or force that causes the cascade of events leading to collapse of the foot. Is the primary deformity in the transverse plane? Should we correct the calcaneus through frontal plane and transverse plane repositioning (i.e., medial displacement calcaneal osteotomy)? Or should we aim the surgical approach at the midtarsal joint with a calcaneal lengthening procedure (i.e., Evans osteotomy)? These questions continue to be debated in the literature and at surgical symposia throughout the country.

How Do Researchers Feel About Using Conservative Measures?
Non-operative interventions give us the greatest opportunity for applying new insights into the pathomechanics of the adult-acquired flatfoot. In 1985, Mann and Thompson advocated repairing or reconstructing the damaged PTT since conservative interventions were largely disappointing.
       However, in 1996, Chao et. al., published the results of a prospective study that evaluated 49 patients with Stage II and Stage III PTTD. With a mean follow-up of 20 months, researchers found that out of 40 patients using an ankle foot orthosis (AFO), 67 percent had good to excellent results. Thirty-three percent had stopped using the AFO and had remained asymptomatic for over six months. Indeed, an AFO appeared to offer a much greater opportunity for successful treatment than traditional foot orthoses that had been used in the past.
       Keep in mind that functional foot orthotics rely on ligamentous integrity between the bones of the feet to direct ground reaction forces and initiate movement transfer between the major pedal joints. In treating PTTD, DPMs commonly modify the heel cup of the orthotic to direct ground reaction forces medial to the axis of the subtalar joint. This notion is based upon the fact that the subtalar joint will have a profound influence on the remainder of the rearfoot and forefoot in terms of providing stability. More importantly, it is based upon the fact that the calcaneus is directly coupled to the rearfoot complex, which includes the midtarsal, subtalar and ankle joints.
       In a 1995 study, Hintermann, Sommer and Nigg demonstrated in a cadaver study that the foot becomes mechanically disconnected from the tibia after you transect the deltoid ligament. They found that it becomes even further disconnected after you transect the interosseous talocalcaneal ligament. Both of these ligaments are attenuated or ruptured by end-stage II PTTD. Therefore, you lose movement transfer between the calcaneus and the leg after such ligamentous attenuation.

It would appear reasonable to assume that the only chance of assuring coupling between the tibia and the rearfoot complex is by using an AFO that applies forces both above and below the essential joints of the rearfoot complex itself.

Testing For Ligamentous Integrity
A traditional functional foot orthosis relies on the direction or re-direction of ground reaction forces through the plantar surface of the foot, and then relies on ligamentous integrity to affect transfer of moment or movement within the pedal joints. In the Stage II adult-acquired flatfoot, you’ll often find ligamentous attenuation. Therefore, you need to determine which patients in Stage II PTTD are candidates for traditional functional foot orthosis therapy and which patients are better off with AFO therapy.
       In order to determine ligamentous integrity and the presence of movement transfer mechanisms within the foot of a patient diagnosed with Stage II PTTD, there are two reliable tests you can use. The first test, the “first metatarsal rise,” was described and published by Hintermann in 1996. With this test, you have patients sit on the edge of the examination table with their feet partially weightbearing on the floor and knees flexed to 90º. Then you externally rotate the leg or invert the heel of the affected foot.
       When the first metatarsal rises off the supportive surface, your patient has TPPD and a loss of ligamentous integrity. When the ligaments are intact, this same maneuver will simply raise the arch of the foot while supinating the subtalar joint, and the first metatarsal will remain on the supportive surface through tensioning of the long and short plantar ligaments.
       The second test is the familiar Hubscher maneuver. As your weightbearing patient is in a relaxed stance, passively dorsiflex the hallux to end range of motion. This activates the windlass mechanism and, through movement transfer, plantarflexes the first ray, and supinates both the subtalar joint and the midtarsal joint. Effective ligamentous integrity and movement transfer will cause a one to one external rotation of the tibia as you passively dorsiflex the hallux.
       On the other hand, if you passively dorsiflex the hallux and you see no effective external rotation of the tibia or raising of the medial arch, you can presume there is a significant loss of ligamentous integrity in the rearfoot and midfoot. Be aware that, in this situation, a traditional functional foot orthosis will fail to control pronation moments applied to the rearfoot complex.

Key Orthotic Pointers For Treating PTTD
If your patient has had ligamentous disruption and loss of movement transfer through the midfoot and rearfoot, you should emphasize an AFO to treat the symptoms and prevent progression of the deformity. There are several ways that AFOs differ from traditional foot orthoses in terms of their ability to control lower extremity forces and movements (see the table on page 44).
       In Stage II and Stage III PTTD, the tibia becomes a dominant lever, conveying the massive body weight through a long lever into the shorter lever, known as the foot. By controlling sagittal plane and transverse plane rotation of the tibia, the powerful force can be applied above the axis of both the subtalar and midtarsal joints while still combining the benefits of a traditional functional foot orthosis below these axes.
       In addition, AFOs enable you to control the foot through the swing phase of gait. With an unopposed peroneus brevis muscle, the dysfunctional PTT foot will function in a markedly everted position during the swing phase of gait and will be placed in an abnormal severely everted position at the moment of foot strike. At this point, no traditional functional foot orthosis can redirect forces adequately to the joints of the rearfoot complex.
       When patients have early Stage II PTTD, using traditional foot orthoses is clearly indicated as they can help you decrease pain, improve mobility and prevent further deformity. When you institute functional foot orthotic therapy or AFO therapy in managing any stage of PTTD, the role of adequate foot wear cannot be over-emphasized. Your patient must be willing to make a lifetime commitment to using lace-up, Oxford-style shoes with deep, stable heel counters, slight heel elevation and a stable shank through the midfoot. Many “motion-control” running shoes will meet these criteria.
       You can also use functional foot orthoses on the contra-lateral, asymptomatic foot, which is at risk for developing PTTD. Although there are no published studies to validate the preventive benefits of orthoses and shoes for the development of PTTD, there appears to be a common sense notion that you proceed with this intervention for patients at risk.
       When you’re using AFO therapy to treat patients with late Stage II and Stage III PTTD, it’s important to remind patients that using an AFO may not be a lifetime commitment. In my experience and the aforementioned Chao study, one-third of patients receiving an AFO for Stage II PTTD will be able to discontinue using their brace after one year of treatment.
       These patients can progress to a traditional functional foot orthotic coupled with appropriate footwear and remain asymptomatic for several years, if not a lifetime. This may be due to the fact that foot and ankle ligamentous structures will heal when you’ve properly braced the affected joints. You’ll see that this lesson is reinforced when you’re treating patients who suffer lateral collateral ankle ligamentous injuries.
       However, in the case of PTTD, you must address the biomechanical forces and the acquired flatfoot deformity with aggressive functional orthotic therapy and appropriate footwear if there is any hope of keeping the condition in an asymptomatic, non-progressive state.

Final Notes
Clearly, the adult-acquired flatfoot, secondary to PTTD, has an etiology far more complex than a simple tendon rupture. Poorly understood biomechanical abnormalities cause extensive overload of the posterior tendon and the supportive ligaments of the rearfoot complex during the first six decades of life, ultimately leading to structural failure and progressive disability.
       Questions still remain. Specifically, if nearly all patients developing a debilitating adult-acquired flatfoot deformity had a pre-existing flatfoot all of their life, could early surgical or non-surgical intervention prevent such a catastrophic event later in the patient’s life? Hopefully, further research will give us better insights into this question so preventive interventions for the asymptomatic, juvenile flatfoot will become a more acceptable clinical practice.

       Dr. Richie is a Director of the American Academy of Podiatric Sports Medicine.

REPRINTED WITH PERMISSION FROM Podiatry Today.