DISORDERS OF THE POSTERIOR TIBIAL TENDON

Posterior tibial tendon dysfunction (PTTD), increasingly referred to in contemporary literature as Progressive Collapsing Foot Deformity (PCFD) or Adult-Acquired Flatfoot Deformity (AAFD), represents a spectrum of pathology ranging from acute tenosynovitis to rigid, arthritic hindfoot collapse. The posterior tibial tendon (PTT) is the primary dynamic stabilizer of the medial longitudinal arch. Loss of its continuity or function—whether through chronic degeneration, inflammatory arthropathy, trauma, or anatomical variants such as an accessory navicular—renders the tendon insufficient to perform its critical tasks of plantar flexion, hindfoot inversion, and arch stabilization.

Other than the Achilles tendon, the loss of no single muscle-tendon unit distal to the knee produces as profound a functional deficit and symptomatic burden as the loss of the posterior tibial tendon.

Anatomy and Biomechanics

To comprehend the pathophysiology of PTT insufficiency, the orthopaedic surgeon must first master the intricate biomechanics of the normal foot and ankle.

The tibialis posterior muscle originates from the posterior surfaces of the tibia, fibula, and interosseous membrane. Its tendon courses posterior to the medial malleolus within a fibro-osseous groove, constrained by the flexor retinaculum. It has a broad, complex insertion, primarily attaching to the navicular tuberosity and the plantar surface of the medial cuneiform, with secondary slips to the bases of the second, third, and fourth metatarsals, the cuboid, and the sustentaculum tali.

Clinical Pearl: The PTT possesses a critical "watershed" zone of hypovascularity located approximately 1 to 1.5 cm distal to the medial malleolus. This region is the most frequent site of degenerative tearing and spontaneous rupture.

During the normal gait cycle, the PTT fires during the stance phase. Its contraction inverts the subtalar joint, which subsequently locks the transverse tarsal joint (Chopart's joint). This locking mechanism transforms the midfoot into a rigid lever arm, allowing the gastrocnemius-soleus complex to generate effective forward propulsion during heel-off. When the PTT is insufficient, the transverse tarsal joint remains unlocked, leading to a profound loss of push-off power and the progressive collapse of the medial longitudinal arch.

Pathomechanics of the Deformity

Any pathological condition that reduces the effective excursion of the PTT can produce the typical asymmetrical flatfoot deformity. The classic triad of this deformity includes:
1. Hindfoot Valgus: Driven by the unopposed pull of the peroneus brevis.
2. Midfoot Abduction: Occurring primarily at the talonavicular joint as the talar head plantarflexes and medially rotates.
3. Forefoot Pronation/Supination Paradox: A complex rotational deformity that requires careful clinical assessment.

The Forefoot Supination Paradox

The nomenclature describing the components of PTTD deformity is notoriously confusing. In a weight-bearing posture, the heel is in valgus, the midfoot is abducted, and the forefoot appears pronated relative to the floor. However, this is an illusion of weight-bearing compensation.

In reality, if the examiner anatomically reduces the subtalar and midtarsal joints to a neutral position (provided the deformity is supple), the forefoot is revealed to be not pronated, but supinated. In severe, long-standing deformities, this fixed supination (also termed forefoot varus) may measure 60 to 70 degrees in the non-weight-bearing position. Restated, when examining the foot end-on with the hindfoot held in neutral, there is a relative elevation of the first ray out of the neutral plane. Failure to recognize and surgically correct this fixed forefoot supination during hindfoot reconstruction will result in lateral column overload and surgical failure.

Secondary Ligamentous Attenuation

Recognition of secondary changes in the hindfoot and forefoot is paramount. As the hindfoot drifts into valgus and the midfoot abducts, immense stress is transferred to the static ligamentous restraints of the medial arch. The superomedial calcaneonavicular (spring) ligament undergoes significant stretching and elongation, gradually losing its ability to support the talar head. Concurrently, the plantar fascia, the long and short plantar ligaments, and eventually the deltoid ligament may attenuate, leading to progressive, multi-planar collapse.

CLINICAL EVALUATION

A meticulous history and physical examination are the cornerstones of diagnosing PTT insufficiency. Patients typically present with medial ankle pain, swelling along the course of the tendon, and a progressive loss of the arch. In later stages, patients may report lateral hindfoot pain due to subfibular impingement (the calcaneus abutting the lateral malleolus).

Physical Examination

• Inspection: Observe the patient standing. The "too-many-toes" sign is pathognomonic for midfoot abduction; when viewed from directly behind, more toes are visible on the lateral side of the affected foot compared to the normal side.
• Single-Limb Heel Rise Test: Ask the patient to stand on the affected leg and elevate the heel. A normal PTT will invert the calcaneus. In PTTD, the patient will either be unable to perform the maneuver or the heel will remain in valgus during elevation.
• Hubscher Maneuver (Jack's Test): Passive dorsiflexion of the hallux should recreate the medial longitudinal arch via the windlass mechanism. Failure to do so indicates a rigid deformity or severe ligamentous incompetence.
• Silfverskiöld Test: Essential to evaluate for concomitant gastrocnemius equinus, which is present in a vast majority of PTTD patients and acts as a deforming force.

IMAGING AND DIAGNOSTICS

Radiographic Evaluation

Weight-bearing radiographs of the foot and ankle are mandatory.
* Anteroposterior (AP) View: Assess the talonavicular coverage angle. Uncovering of the talar head indicates midfoot abduction. Evaluate the AP talocalcaneal (Kite's) angle.
* Lateral View: Assess Meary's angle (the intersection of the longitudinal axis of the talus and the first metatarsal). A normal angle is 0 degrees; in PTTD, the angle is directed apex-plantar. Evaluate calcaneal pitch and the distance from the medial cuneiform to the floor.
* Hindfoot Alignment View: Quantifies the degree of calcaneal valgus.

Surgical Warning: The weight-bearing lateral radiograph may occasionally show no collapse and appear identical to the asymptomatic foot, despite obvious clinical evidence of an asymmetrical pes planus. Treat the patient, not just the radiograph.

Advanced Imaging

• Magnetic Resonance Imaging (MRI): Highly sensitive for evaluating PTT tendinosis, partial tears, and complete ruptures. MRI is also invaluable for assessing the integrity of the spring ligament complex and the deltoid ligament.
• Ultrasound: A dynamic, cost-effective modality for assessing tendon excursion, tenosynovitis, and peritendinous fluid, though highly operator-dependent.

CLASSIFICATION OF PTT DYSFUNCTION

The Johnson and Strom classification, modified by Myerson, remains the standard framework for guiding treatment:

• Stage I: Tenosynovitis without deformity. The tendon is intact, and the patient can perform a single-heel rise.
• Stage II: Tendon elongation or rupture with a flexible flatfoot deformity. The patient cannot perform a single-heel rise.
  • Stage IIa: Hindfoot valgus with minimal midfoot abduction.
  • Stage IIb: Hindfoot valgus with significant midfoot abduction (>30% talonavicular uncoverage).
• Stage III: Rigid flatfoot deformity. The hindfoot is fixed in valgus, and the subtalar joint cannot be passively reduced.
• Stage IV: Flatfoot deformity with ankle joint involvement. Attenuation of the deltoid ligament leads to valgus tilt of the talus within the ankle mortise.

SURGICAL MANAGEMENT

Surgical intervention is indicated when conservative measures (custom orthotics, Arizona braces, physical therapy) fail to halt progression or alleviate symptoms. The surgical strategy is dictated strictly by the stage of the disease and the flexibility of the deformity.

Stage I: Joint-Sparing Soft Tissue Procedures

For patients with recalcitrant tenosynovitis without deformity, a tenosynovectomy is indicated.
* Technique: A medial incision is made over the PTT. The flexor retinaculum is incised, and inflamed synovium is aggressively debrided. If a longitudinal split tear is identified, it is excised, and the tendon is tubularized using a running non-absorbable suture.

Stage II: Joint-Sparing Reconstruction

Stage II represents a flexible deformity and is treated with a combination of soft tissue reconstruction and bony osteotomies to correct the biomechanical axes. The "workhorse" reconstruction typically involves a Flexor Digitorum Longus (FDL) transfer combined with a Medial Displacement Calcaneal Osteotomy (MDCO).

1. Flexor Digitorum Longus (FDL) Transfer

The FDL is the ideal transfer candidate as it is phase-matched to the PTT, lies in close anatomical proximity, and its harvest results in minimal donor-site morbidity.
* Harvest: The FDL is identified posterior to the PTT and traced distally to the Master Knot of Henry. It is transected as distally as possible.
* Transfer: A drill hole is created dorsal-to-plantar through the navicular. The FDL tendon is passed through the tunnel from plantar to dorsal.
* Tensioning: The foot is held in maximal plantar flexion and inversion. The tendon is secured using a bio-tenodesis screw or sutured back onto itself.

2. Medial Displacement Calcaneal Osteotomy (MDCO)

The MDCO corrects hindfoot valgus by shifting the mechanical axis of the Achilles tendon medially, converting it from an evertor to an invertor of the heel.
* Approach: An oblique lateral incision is made posterior to the sural nerve and peroneal tendons.
* Osteotomy: An oscillating saw is used to create an osteotomy in line with the incision, perpendicular to the lateral wall of the calcaneus.
* Displacement: The posterior tuberosity is translated medially by 10 to 15 mm.
* Fixation: The osteotomy is secured with one or two large-fragment (6.5 mm or 7.3 mm) cannulated headless compression screws directed from the posterior heel into the anterior calcaneus.

Pitfall: Failure to protect the neurovascular bundle on the medial side during the calcaneal osteotomy can result in catastrophic injury to the tibial nerve or posterior tibial artery. Always use a blunt retractor medially to protect these structures.

3. Addressing Midfoot Abduction (Lateral Column Lengthening)

If severe midfoot abduction is present (Stage IIb), an Evans calcaneal osteotomy is indicated.
* An osteotomy is performed 1.5 cm proximal to the calcaneocuboid joint.
* A trapezoidal tricortical bone graft (autograft or allograft) is impacted into the osteotomy site, lengthening the lateral column and swinging the midfoot out of abduction.

4. Addressing Forefoot Supination (Cotton Osteotomy)

As previously discussed, correcting the hindfoot may unmask a fixed forefoot supination. If the first ray is elevated after hindfoot correction, a medial cuneiform opening wedge osteotomy (Cotton osteotomy) is required.
* A dorsal opening wedge osteotomy is made in the medial cuneiform.
* A structural bone wedge is inserted to plantarflex the first ray, restoring the tripod mechanics of the foot.

Stage III: Hindfoot Arthrodesis

When the deformity becomes rigid, joint-sparing osteotomies are contraindicated. The goal shifts to achieving a plantigrade, painless foot through arthrodesis.
* Triple Arthrodesis: Historically the gold standard, involving fusion of the subtalar, talonavicular, and calcaneocuboid joints.
* Isolated Subtalar or Double Arthrodesis: Modern trends favor sparing the calcaneocuboid joint if it is not arthritic, focusing on fusing the subtalar and talonavicular joints to correct the deformity and relieve pain.

Stage IV: Complex Ankle and Hindfoot Reconstruction

Stage IV disease involves failure of the deltoid ligament and valgus tilt of the ankle.
* Flexible Ankle: Deltoid ligament reconstruction combined with a Stage III hindfoot arthrodesis.
* Rigid/Arthritic Ankle: Tibiotalocalcaneal (TTC) arthrodesis using a retrograde intramedullary nail, or a pantalar arthrodesis in severe cases.

POSTOPERATIVE PROTOCOL

Successful outcomes in PTTD surgery rely heavily on strict adherence to postoperative rehabilitation protocols.
* Weeks 0-2: The patient is placed in a well-padded short leg splint, strictly non-weight-bearing (NWB). Elevation is critical to manage edema.
* Weeks 2-6: Sutures are removed. The patient is transitioned to a short leg cast or a rigid CAM boot, remaining strictly NWB.
* Weeks 6-10: Radiographs are obtained to confirm osteotomy/fusion healing. The patient begins progressive weight-bearing in a CAM boot. Active and active-assisted range of motion exercises for the ankle and toes are initiated.
* Weeks 10-12: Transition to regular footwear with a custom medial arch support or UCBL orthosis. Formal physical therapy focuses on strengthening the FDL transfer, peroneal stretching, and proprioceptive training.
* Return to Activity: Maximum medical improvement and return to high-impact activities may take 9 to 12 months.

By meticulously evaluating the components of the deformity and applying a staged, biomechanically sound surgical approach, the orthopaedic surgeon can effectively restore function and alleviate pain in patients suffering from posterior tibial tendon dysfunction.

📚 Medical References

• posterior tibial tendon dysfunction: a preliminary report, Foot Ankle Int 24:600, 2003.
• Vogler H: Subtalar joint blocking operations in pronation syndromes. In McGalmery ED, ed: Textbook of foot surgery, Baltimore, 1987, Williams & Wilkins. Zaret DI, Myerson MS: Arthroerisis of the subtalar joint, Foot Ankle Clin 8:605, 2003.