Progressive Arch Collapse
Painful Progressive Arch Collapse
This month we focus on the posterior tibialis tendon that, when healthy, serves as the key support for the foot, but when dysfunctional, it may lead to a plethora of problems related to the progressive arch collapse. Posterior tibial tendon dysfunction (PTTD) is the most common cause of adult-acquired flat foot. 1 Symptoms begin with pain and may progress to degeneration and deformity if left untreated. 1,3 Early recognition and management can lead to significantly improved outcomes. 1
Anatomy
The deep compartment of the leg consists of three muscles: the posterior tibialis (PT), flexor digitorium longus (FDL), and flexor hallucis longus (FHL). The posterior tibialis is the deepest and largest muscle of the trio, typically comprising almost 60% of the cross-sectional area of the entire deep compartment. 4-7 The posterior tibialis originates on the interosseous membrane and the posterior surfaces of the tibia and fibula. 4 The muscle’s tendon begins several centimeters above the ankle then courses through the deep posterior compartment of the leg behind the medial malleolus, before turning toward its main attachment on the navicular tuberosity. 4 Ancillary attachments include the second and third cuneiform, cuboid, bases of the second, third, & fourth metatarsals, and sustentaculum tali of the calcaneous. 4,8-10
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Actions of the posterior tibialis muscle include inversion and plantar flexion of the 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. 5,11-15 During the normal gait cycle, the posterior tibialis lifts the medial longitudinal arch, thereby interlocking the tarsals (calcaneous, cuboid, talus, and navicular) into a rigid lever for propulsion. 12,17 The role of the posterior tibialis is most significant during push off. 18,19
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 microtrauma. 22 Repetitive stressors initiate a cascade of dysfunction that begins with “normal” inflammation but regresses to “failed healing,” fibrosis, and tendon degeneration. Degeneration affects the gliding resistance of the tendon and progressively diminishes the tendon’s ability to support the foot. 22 As the tendon becomes less effective, the longitudinal arch of the foot is allowed to collapse; thereby, increasing strain on the posterior tibialis. 22,25,26 The most common site for injury is a zone of relative hypovasulcarity directly posterior to the medial malleolus. 22,27,28
Stages
The continuum of PTTD progresses through the following stages: 29
I Tenosynovitis without deformity
IIA Flat foot deformity
IIB Flat foot deformity with excessive forefoot abduction
III Rigid forefoot abduction and hindfoot valgus
IV Deltoid ligament compromise
Like most cumulative trauma disorders, the etiology of posterior tibial tendon dysfunction is multi-factorial. Problems typically arise when repetitive strain exceeds the tendon’s threshold for injury. Extrinsic factors that contribute to the development of posterior tibial tendinopathy include training errors, particularly those related to intensity, duration, and/or training on excessively hard surfaces. 30 In addition to the obvious contribution from hyperpronation, other intrinsic factors that increase the likelihood of developing PTTD include a history of obesity, diabetes, hypertension, seronegative arthropathy, steroid injection, surgery, or trauma. 1,31-33 A recent prescription of fluoroquinolones may increase the risk of tendon rupture. 35
Typical Patient
The stereotypical PTTD patient is an obese, middle-aged female. 1 Some researchers estimate that PTTD may be present in up to 10% of this population. 37 PTTD is typically unilateral; the bilateral disease is rare. 1 Common presenting complaints of an irritated (but intact) posterior tibial tendon include insidious onset unilateral pain and swelling along the course of the tendon, most notably behind the medial malleolus. 38-41Symptoms 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 biomechanical 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 an incursion of the distal fibula and calcaneous. 46
Evaluation
Clinical evaluation will typically demonstrate tenderness and swelling posterior and inferior to the medial malleolus. 38,43,47-49 A significantly fallen arch with minimal pain and swelling over the posterior tibial tendon could indicate a rupture. 50 Patients with PTTD demonstrate hindfoot 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 flexion. 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 flexion to help differentiate tendinopathies involving the adjacent flexor digitorum longus and flexor hallucis longus.
Clinical evaluation should seek to classify the stage of the disease. The collapse of the medial longitudinal arch corresponds to Stage IIA, while excessive forefoot abduction (“too many toes” sign) signifies progression to Stage IIB. Hindfoot valgus that has progressed from flexible to rigid signifies 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 affected foot for 8-10 repetitions. The inability to complete this test correlates to the degree of PTTD. 1,47
Diagnosis
PTTD is primarily a clinical diagnosis. 53 In general, plain films have little diagnostic value for soft tissue lesions. 53 Nonetheless, radiographs may be needed to exclude other possibilities from the differential diagnosis. Plain films would include weight bearing, AP and lateral views of the foot and ankle. 55 The collapse of the medial longitudinal arch is a classic radiographic finding associated with PTTD. As the disease progresses, films may demonstrate the valgus misalignment of the talus and subtalar 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 Diagnostic 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 defining PTTD. 59
The differential diagnosis for PTTD includes flexor hallucis longus or flexor digitorum longus tendinopathy, posterior impingement, stress fracture, deltoid ligament injury, osteoarthritis, Lisfranc injury, and tarsal tunnel syndrome. 60,61
Early identification of PTTD is essential to limit the 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 benefit from anti-inflammatory modalities and NSAIDs. 62-65 NSAIDs may not be a good choice for more chronic “tendinopathies.” 66
Treatment
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 “flexible” deformities, i.e. maintain the medial arch and correct hindfoot 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 alignment or gliding resistance of the posterior tibialis. 69,73
Active rehab should be directed at strengthening the posterior tibialis tendon as well as the peroneals, anterior tibialis, and gastroc/soleus. 84Specific exercises would include resisted plantar flexion, heel rises, toe walking, inversion, and adduction. 84 Strengthening the posterior tibialis via eccentric exercise leads to more rapid improvements in symptoms and function. 80 Stretching of the gastroc/ soleus is appropriate. 84Exercises should be performed while wearing shoes and arch supports or orthotics. 62,74,75 Soft tissue manipulation and myofascial release should address the posterior tibialis and associated musculature. IASTM may be appropriate to stimulate the healing of degenerated tendons.
Conclusion
Conservative care (including stretching, strengthening, modalities, NSAIDS, and support ranging from orthotics to a rigid boot) has shown success rates ranging from 67-90%. 81-84 PTTD patients who do not respond to four weeks of conservative care may benefit from a walking cast or cam boot to immobilize the foot. 62,76 Those who have failed four months of conservative care and those with advanced disease (i.e. beyond Stage II, with non-correctable deformity and joint degeneration) may benefit from orthopedic or podiatric referral. 62,77,78
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