September 2016

Management of athletes with early-stage PTTD

Orthotic-Devices-for-the-Win

By Frank Layman, PT, DPT, EdD, MT; and April Wilson, PTA, BS, CI, CKTP, IASTM

Sponsored by an educational grant from medi USA.

Posterior tibial tendon dysfunction (PTTD), known also as tibialis posterior tendon dysfunction, is one of the leading causes of acquired flatfoot in adults, but the abnormal biomechanics associated with PTTD are often overlooked by clinicians in the condition’s early stages. The post­erior tibial tendon is a major contributor to the structure of the medial longitudinal arch (MLA). The most frequent types of athletes we see with early PTTD are, in order of prevalence, runners, volleyball players, and tennis players. The increasing prevalence of clinic visits for this condition is associated with the continued growing popularity of running and other sports among participants of a range of ages.

PTTD’s precise etiology is not known, but present theories implicate poor vascularization, abnormal foot mechanics (eg, exaggerated antagonist contraction of the peroneus brevis), or bio­mechanical changes.1

Over time, posterior tibial tendinopathies can lead to PTTD, and symptomatic tendon tears are one of the most important causes of pain and joint dysfunction; if the progression is allowed to go uncorrected, vascularization can be negatively affected. Among the intrinsic causes of PTTD, vascularization recently has been recognized as playing a major role.1 In general, tendon blood flow decreases with increasing age and mechanical load. A decrease in vascularization can increase the probability of tissue damage as it decreases tissue flexibility and responsiveness. Another consideration is that the oxygen consumption of ligaments and tendons is 7.5% lower than skeletal muscles, which can contribute to slower healing rates.2,3

Because vascularization and oxygen consumption issues are associated with PTTD, we advocate early intervention in our practice. An evidence-based multimodal approach with an emphasis on good screening and early intervention has enhanced outcomes in our athletes.

9medi-shutterstock_85106908The tibialis posterior muscle, the most deeply seated of the muscles associated with PTTD, originates on the inner posterior borders of the tibia and fibula. The tendon of the tibialis posterior muscle descends posterior to the medial malleolus and terminates by dividing into plantar, main, and recurrent components. The plantar portion inserts into the bases of the second, third, and fourth metatarsals and the first and second cuneiform. The recurrent portion inserts into the sustentaculum tali of the calcaneus. The main portion inserts into the navicular tuberosity. The tibialis posterior also contracts to control inversion and eversion and assist with ankle plantar flexion.

The pain and dysfunction associated with PTTD are related to changes in the biomechanics of the foot and ankle.3,4 The posterior tibial tendon is needed to create biomechanical balance and help sustain a more neutral foot posture. Dysfunction of the tibialis posterior can lead to flat feet and valgus deformity in the rearfoot, associated with unopposed forces.

Early stages of PTTD

The onset of PTTD may be slow and progressive or abrupt. An abrupt onset is typically linked with a trauma, whether it be simple (a misstep) or severe (falling from a substantial height or an automobile accident).5 PTTD is seldom seen in children, and increases in frequency with age.

PTTD is typically described as having four stages. This discussion will focus on the early stages, which progress relatively slowly. In stage I, the tendon is inflamed but intact; no deformity is evident. In stage II, the tendon is dysfunctional, and patients are commonly unable to perform a heel rise; acquired pes planus is evident, but this is passively correctable.

As mentioned, the functions of a healthy posterior tibial tendon are plantar flexion of the ankle, inversion of the foot and elevating the MLA. Elevation of the MLA locks the midtarsal bones, so the midfoot and hindfoot are stiff. All of this allows the gastrocnemius muscle to act more efficiently during gait. When the tendon is not healthy, the surrounding joint capsules and ligaments become weak. There is an eversion of the subtalar joint, abduction of the talo­navicular joint, and valgus of the heel. In addition, the gastrocnemius can’t function properly because of the change in its angle of pull, which affects gait and balance.3,4,6 This can mean the other muscles used in the gait cycle will be overtaxed in patients with PTTD.

Examination

It’s important to examine the whole lower body and not just the foot, as knee valgus can accentuate the appearance of pes planus. The feet themselves should be examined from above, as well as from behind and from the side. A healthy person typically has about 5° of hindfoot valgus; in patients with PTTD, the valgus is increased and the forefoot abduction is also more pronounced.2,5 The post­erior tibial tendon should also be examined from above the medial malleolus to its insertion for pain with palpation and to assess swelling that is common in the first stages of PTTD.7 In later stages the deformity can progress and pes planus may be visible.8

The diagnosis of PPTD can be made clinically based on history and objective testing. Characteristic findings of PTTD include loss of medial arch height, edema of the medial ankle, inability to resist force to abduct the foot, medial ankle pain with weightbearing, inability to rise on the toes without pain, and lateral subtalar joint pain.7,8

Clinical tests that are useful for diagnosis include:

  • The “too many toes” sign (overpronation causes the patient to appear to have extra toes when viewed from behind)8
  • Single- and double-limb heel rise9
  • Plantar flexion and inversion of the foot against resistance9
  • First metatarsal rise sign: Externally rotate the shank of the affected foot while the patient is weightbearing on both feet. The head of the first metatarsal will rise in the presence of PTTD.10

Treatment

Treatment can begin in many cases with nonoperative treatment, which can include orthotic intervention,11-13 immobilization in a short-leg cast or boot, and physical therapy.

Our multimodal treatment approach includes manual therapy, modalities focused on improving vascularization, therapeutic exercise (with an emphasis on eccentric contractions4,12,13), flexibility (stretching), and foot orthoses. We based this approach on the aforementioned evidence related to the mechanisms underlying PTTD and the effectiveness we have seen in clinical practice.

The most prolonged benefits of our approach have been changes in the biomechanics of the foot and ankle with the use of orthoses, which is consistent with the literature.12,13 We have found success in the clinic with machine-grade orthotic devices that are comfortable, supportive, and can be posted to improve lower extremity biomechanics. Changing the biomechanics of the foot and ankle can improve efficiency and decrease trauma of tissue, particularly in patients with PTTD.6,14

Alvarez et al12 and Kulig et al13 suggested many patients with early PTTD can be effectively treated nonoperatively with orthotic management combined with exercise.

Alvarez et al demonstrated that patients with stage I and stage II PTTD had successful outcomes—including significant improvement in strength, biomechanics, and function at four months12—after completing this multimodal rehabilitation protocol:

  • Wearing a short articulated ankle foot orthosis or foot orthosis
  • Supervised high-repetition exercises, including plantar flexion exercises
  • An aggressive high-repetition home exercise program that included gastroc-soleus tendon stretching

Success was defined as a strength deficit of no more than 10%, the ability to do 50 single-leg heel raises with minimal or no pain, the ability to walk 100 feet on the toes with minimal or no pain, and the ability to do 200 repetitions of the home exercises for each muscle group. After a mean of 10 visits over a median period of four months, 83% of patients had successful outcomes.12

Kulig et al also found that, while the use of foot orthoses and stretching was associated with significant improvement in pain and disability in patients with early PTTD, combining custom foot orthoses with eccentric and concentric progressive and resistive exercises accentuated those improvements.13 The combination of interventions appears to be important for targeting the tibialis posterior muscle: In a previous study of patients with pes planus, the same group found the most effective and selective activation of the tibialis posterior during a closed-chain resisted foot adduction exercise occurred when the study participants wore arch-supporting orthoses.15

Clinical bottom line

PTTD is one of the most common problems of the foot and ankle in our patients who are runners and other athletes.6 The tendon provides stability for the medial longitudinal arch of the foot. Depending on the patient’s disease stage, PTTD can result in a flat foot (stage II, III, and IV) caused by inflammation or strain of the posterior tibial tendon. Early detection and intervention is key to mitigating progression. Early stage PTTD responds to a well-rounded treatment approach that includes orthotic management.

Frank Layman, PT, DPT, EdD, MTC, is an administrator and clinician at Randolph Specialty Group in Asheboro, NC, an adjunct faculty member of the Department of Physical Therapy at High Point University in North Carolina, and a vice president of business development for Tapout Fitness in Raleigh, NC. April Wilson, PTA, BS, CI, CKTP, IASTM, is a physical therapy assistant at Randolph Specialty Group and the owner of Footwise, a company that offers individualized foot fittings for athletes, also in Asheboro, NC.

REFERENCES
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  2. Patla CE, Abbott JH. Tibialis posterior myofascial tightness as a source of heel pain: diagnosis and treatment. J Orthop Sports Phys Ther 2000;30(10):624‐
  3. Vailas AC, Tipton CM, Laughlin HL, et al. Physical activity and hypophysectomy on the aerobic capacity of ligaments and tendons. J Appl Physiol 1978;44(4):542-546.
  4. Ringleb SI, Kavros SJ, Kotajarvi BR, et al. Changes in gait associated with acute stage II posterior tibial tendon dysfunction. Gait Posture 2007;25(4):555-564.
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  8. Johnson KA, Strom DE. Tibialis posterior tendon dysfunction. Clin Orthop Rel Res 1989;(239):196-206.
  9. Papalia R, Moro L, Franceschi F, et al. Endothelial dysfunction and tendinopathy: how far have we come? Musculoskelet Surg 2013;97(3):199-209.
  10. Hintermann B, Gächter A. The first metatarsal rise sign: a simple, sensitive sign of tibialis posterior tendon dysfunction. Foot Ankle Int 1996;17(4):236-241.
  11. Neville C, Flemister AS, Houck JR. Effects of the AirLift PTTD brace on foot kinematics in subjects with stage II posterior tibial tendon dysfunction. J Orthop Sports Phys Ther 2009;39(3):201-209.
  12. Alvarez RG, Marini A, Schmitt C, Saltzman CL. Stage I and II posterior tibial tendon dysfunction treated by a structured nonoperative management protocol: an orthosis and exercise program. Foot Ankle Int 2006;27(1):2-8.
  13. Kulig K, Reischl SF, Pomrantz AB, et al. Nonsurgical management of posterior tibial tendon dysfunction with orthoses and resistive exercise: a randomized controlled trial. Phys Ther 2009;89(1):26-37.
  14. Basmajian JV, Stecko G. The role of muscles in arch support of the foot. J Bone Joint Surg Am 1963;45:1184-1190.
  15. Kulig K, Burnfield JM, Reischl S, et al. Effect of foot orthoses on tibialis posterior activation in persons with pes planus. Med Sci Sports Exerc 2005;37(1):24-29.
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