Posterior tibial tendon dysfunction (PTTD) is the most common cause of adult-ac- Posterior Tibial Tendon quired at foot. (1) Symptoms begin with pain and may progress to degeneration and deformity if left untreated. (1,3) Early recognition and management can lead Dysfunction to signicantly improved outcomes. (1) Evaluation The deep compartment of the leg consists of three muscles: the posterior tibialis (PT), exor digitorum longus (FDL), and exor hallucis longus (FHL). The posterior • Foot & Ankle ROM tibialis is the deepest and largest muscle of the trio – typically comprising almost • Foot Hyperpronation Cluster 60% of the cross sectional area of the entire deep compartment. (4-7) The posteri- • Single Limb Heel Rise or tibialis originates on the interosseous membrane and the posterior surfaces of the tibia and bula. (4) The muscle’s tendon begins several centimeters above the ankle then courses through the deep posterior compartment of the leg behind the Management Soft Tissue medial malleolus before turning toward its main attachment on the navicular • IASTM/ TFM- Posterior Tibialis Tendon tuberosity. (4) Ancillary attachments include the second and third cuneiform, • STM- Posterior Tibialis cuboid, bases of the second, third, & fourth metatarsals, and sustentaculum tali of the calcaneous. (4,8-10) Misc Actions of the posterior tibialis muscle include inversion and plantar exion of the • Arch Support/ Orthotic foot. Because of its size and moment arm, the posterior tibialis is the primary elevator and dynamic stabilizer of the medial longitudinal arch of the foot. Phase I exercises (5,11-15) During the normal gait cycle, the posterior tibialis lifts the medial longitu- dinal arch, thereby interlocking the tarsals (calcaneous, cuboid, talus, and navicu- • Posterior Tibialis Stretch- Standing lar) into a rigid lever for propulsion. (12,17) The role of the posterior tibialis is most • Eccentric Posterior Tibialis signicant during push o. (18,19) • Resisted Posterior Tibialis Strengthening • Single Leg Stance Early literature suggested that up to 50% of PTTD cases arose from trauma. (20,21) More recent literature suggests that the majority of cases begin from repeated micro trauma. (22) Repetitive stressors initiate a cascade of dysfunction that begins Phase II exercises with “normal” inammation but regresses to “failed healing”, brosis, and tendon • Vele's degeneration. Degeneration aects the gliding resistance of the tendon and progressively diminishes the tendon’s ability to support the foot. (22) As the tendon becomes less eective, the longitudinal arch of the foot is allowed to Clinical Pearls collapse; thereby, increasing strain on the posterior tibialis. (22,25,26) The most • Demand on the posterior tibialis is most common site for injury is a zone of relative hypovasulcarity directly posterior to the signicant during push o. medial malleolus. (22,27,28) • The most common site for injury is a zone The continuum of PTTD progresses through the following stages: (29) of relative hypovasulcarity directly posterior I Tenosynovitis without deformity to the medial malleolus. IIA Flat foot deformity • Tenderness and swelling is commonly IIB Flat foot deformity with excessive forefoot abduction located posterior and inferior to the medial III Rigid forefoot abduction and hindfoot valgus IV Deltoid ligament compromise malleolus. • Stage I & II disease are amenable to conser- Like most cumulative trauma disorders, the etiology of posterior tibial tendon vative correction, but once the hindfoot dysfunction is multi factoral. Problems typically arise when repetitive strain deformity has become "rigid" (Stage III) exceeds the tendon’s threshold for injury. Extrinsic factors that contribute to the development of posterior tibial tendinopathy include training errors- particularly management transitions to palliative care. those related to intensity, duration, and/or training on excessively hard surfaces. Stage IV disease may benet from orthope- (30) In addition to the obvious contribution from hyperpronation, other intrinsic dic or podiatric referral. factors that increase the likelihood of developing PTTD include a history of obesity, • Orthotics may help patients in the early diabetes, hypertension, seronegative arthropathy, steroid injection, surgery, or trauma. (1,31-33) A recent prescription of uoroquinolones may increase the risk of stages, but may be less benecial once the tendon rupture. (35) foot has lost stability or has developed a rigid deformity. The stereotypical PTTD patient is an obese, middle-aged female. (1) Some • PTTD patients who do not respond to four researchers estimate that PTTD may be present in up to 10% of this population. (37) PTTD is typically unilateral- bilateral disease is rare. (1) Common presenting weeks of conservative care may benet complaints of an irritated (but intact) posterior tibial tendon include insidious from a walking cast or cam boot to immobi- onset unilateral pain and swelling along the course of the tendon – most notably lize the foot. behind the medial malleolus. (38-41) Symptoms often begin following an increase in training intensity or duration. (42) Symptoms may be exacerbated by weight bearing activity, particularly, standing tiptoe and walking stairs or on uneven surfaces. (39,43) Loss of arch height and other associated biomechani- cal deformities may become evident as the condition progresses however, tendon degeneration begins long before physical deformity. (44) Patients who have altered gait may demonstrate abnormal shoe wear. (39) As the condition nears end-stage, patients may describe the feeling that they are walking on the inside of their ankle, and pain may transfer to the lateral ankle due to incursion of the distal bula and calcaneous. (46) Clinical evaluation will typically demonstrate tenderness and swelling posterior and inferior to the medial malleolus. (38,43,47-49) A signi- cantly fallen arch with minimal pain and swelling over the posterior tibial tendon could indicate rupture. (50) Patients with PTTD demon- strate hind foot eversion proportionate to the degree of posterior tibialis weakness (48) Isometric strength testing may reproduce pain or weakness during resisted inversion (supination), and/or plantar exion (43,49,50) Motion assessment may demonstrate a rigid hindfoot valgus deformity in later stages. (47) Clinicians should assess for pain and/or weakness of toe exion to help dierentiate tendinopathies involving the adjacent exor digitorum longus and exor hallucis longus. Clinical evaluation should seek to classify the stage of the disease – collapse of the medial longitudinal arch corresponds to Stage IIA, while excessive forefoot abduction, (“too many toes” sign) signies progres- sion to Stage IIB. Hindfoot valgus that has progressed from exible to rigid signies Stage III. Tenderness below the lateral malleolus from bony incursion is a sign of Stage IV disease. The single limb heel rise is a sensitive test to detect PTTD. (47,48) The test is performed by allowing the single leg standing patient to balance with one hand on the wall while attempting to rise on the toes of the aected foot for 8-10 repetitions. The inability to complete this test correlates to the degree of PTTD. (1,47) PTTD is primarily a clinical diagnosis. (53) In general, plain lms have little diagnostic value for soft tissue lesions. (53) Nonetheless, radio- graphs may be needed to exclude other possibilities from the dierential diagnosis. Plain lms would include weight bearing, AP and lateral views of the foot and ankle. (55) Collapse of the medial longitudinal arch is a classic radiographic nding associated with PTTD. As the disease progresses, lms may demonstrate valgus mal-alignment of the talus and sub talar degeneration. (55-57) MRI may better demonstrate soft tissue lesions as well as the sub-tendinous bone marrow edema that often accompanies the condition. (55,57) Diagnos- tic ultrasound is a useful, low cost alternative for the diagnosis of PTTD. (55,58) Studies have shown that diagnostic ultrasound is only slightly less sensitive than MRI for dening PTTD. (59) The dierential diagnosis for PTTD includes exor hallucis longus or exor digitorum longus tendinopathy, posterior impingement, stress fracture, deltoid ligament injury, osteoarthritis, Lisfranc injury, and tarsal tunnel syndrome. (60,61) Early identication of PTTD is essential to limit progression of the disease. (1) Conditions that advance may ultimately require surgery for the resultant instability, impingement, degeneration, and deformity. (1,3,79) Optimal management is partially dependent upon the stage of the disease. (1) Patients with acute tendon irritation (Stage I) may benet from anti-inamatory modalities and NSAIDs. (62-65) NSAIDS may not be a good choice for more chronic “tendinopathies” (66) Arch supports and orthotics are mainstays of management, but have shown varying degrees of success. (67,68) The intended purpose of orthotics is to correct “exible” deformities, i.e. maintain the medial arch and correct hind foot position, thus decreasing stress on the posterior tibial tendon. (69,70) Orthotics may help patients in the early stages of PTTD, but may be less beneficial once the foot has lost stability or has developed a rigid deformity. (69) Studies have shown that for unstable feet, orthotics do not consistently improve align- ment or gliding resistance of the posterior tibialis. (69,73) Active rehab should be directed at strengthening the posterior tibialis tendon. Specic exercises would include