Tibialis Posterior Tendon Transfer for Foot Drop

Indication. Tibialis posterior tendon transfer is a salvage operation for a permanent foot drop — loss of active dorsiflexion — where the anterior compartment muscles (tibialis anterior, extensor hallucis longus, extensor digitorum longus) are irreversibly paralysed or destroyed but the tibialis posterior remains strong. The classic settings are an established common peroneal (lateral popliteal) nerve palsy with no clinical or electromyographic recovery after at least 12 to 18 months of observation, leprosy (Hansen disease) in which the common peroneal nerve is commonly involved but the tibial nerve (and therefore the TP) is usually spared, and irreversible anterior compartment muscle loss from trauma, compartment syndrome, ischaemia, or a Volkmann-type contracture. Relative indications include post-traumatic deep peroneal nerve injury that has not recovered by 12 months, selected static encephalopathy or cerebral palsy with isolated foot drop, and post-polio residuals with adequate TP power. Prerequisites — confirm every one before listing. The transfer fails if any is missing: - Motor. The TP must be MRC grade 4 or 5, tested by active heel inversion against full resistance with the foot plantigrade; the anterior compartment must be confirmed absent or non-functional (grade 0 to 2). Transferring a grade 3 TP sacrifices the invertor without buying useful dorsiflexion.

• Hindfoot and foot. Plantigrade alignment with a neutral or correctable heel, a mobile subtalar joint (stiffness prevents the TP pull converting from inversion to dorsiflexion), no fixed midfoot collapse, and ankle dorsiflexion to at least neutral. Fixed equinus is corrected (Achilles lengthening or gastrocnemius recession) before or during the transfer.
• Timing. For a nerve palsy, wait at least 12 to 18 months before declaring it irreversible; electromyography showing complete denervation at 12 months, with no clinical recovery, supports the decision. After traumatic muscle destruction the transfer can be considered earlier, once soft tissues have healed. Contraindications. Absolute: TP power less than grade 4, active infection in the leg or foot, and non-reconstructable vascular insufficiency. Relative: any fixed hindfoot deformity (planovalgus or equinus) that must be corrected first, a stiff subtalar joint, severe ankle arthritis, poor compliance or inadequate rehabilitation support, and marked obesity in which the transferred tendon may be overloaded.

Consent specifically for common or deep peroneal nerve injury, anterior tibial vessel injury at the membrane window, failure of the transfer (persistent foot drop), over-correction (calcaneus gait), progression of planovalgus deformity, wound infection, deep vein thrombosis, and the possible need for revision surgery. Setup. Supine with a sandbag under the ipsilateral buttock to internally rotate the leg and bring the medial ankle into view, the foot at the end of the table; thigh tourniquet (250 mmHg for adults); general or spinal anaesthesia (a popliteal block is an acceptable adjunct but not a substitute when a thigh tourniquet is used); cefazolin 2 g intravenous at induction. Prep the whole limb to toes so the medial navicular and the anterolateral leg are both in the field, and mark the navicular tuberosity, the TP course, and both incisions before inflating the tourniquet.

The goal is to harvest the tibialis posterior tendon from the navicular, route it anteriorly — classically through a window in the interosseous membrane — and fix it to the dorsum of the foot (the lateral cuneiform) so that it functions as a dorsiflexor, tensioned with the ankle in neutral. The two incisions and the membrane window, with protection of the anterior tibial neurovascular bundle, are the whole game.

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Rehabilitation | Phase | Timing | Immobilisation | Therapy | |-------|--------|----------------|---------| | 1 | 0–6 weeks | Non-weight-bearing below-knee cast in neutral dorsiflexion (0–5 degrees) | Finger and toe active range of motion only; suture removal at 2 weeks through a cast window; DVT prophylaxis while non-weight-bearing | | 2 | 6–12 weeks | Removable ankle-foot orthosis (AFO) or hinged brace | Progressive weight-bearing from touch-down to full; gentle active dorsiflexion within the AFO; begin training the TP to fire as a dorsiflexor (motor re-learning) | | 3 | 12–24 weeks | Wean from AFO; night/off-load splint for heavy tasks | Progressive resistance dorsiflexion (theraband, weights); gait retraining for normal heel-strike and push-off; stairs, slopes, uneven ground | | 4 | Long-term | AFO for prolonged walking or uneven terrain as needed | Yearly review of hindfoot alignment for planovalgus progression | Most patients regain functional dorsiflexion for everyday walking, with many continuing to use an AFO for prolonged walking or uneven terrain. Long-term AFO use is common and should be discussed in advance. Complications

Special situations. In leprosy, the TP is usually spared because the tibial nerve is less commonly affected than the common peroneal nerve, which is why TP transfer is the gold standard for leprosy foot drop — but screen for concurrent tibial nerve involvement (a weak TP will fail), complete or advance multidrug therapy before elective surgery, and assess protective sensation because insensate feet need modified wound care and footwear. With a concurrent fixed hindfoot deformity, never transfer the TP in isolation (removing it accelerates the collapse); correct the hindfoot first with a Dwyer or medialising calcaneal osteotomy or a triple arthrodesis, then transfer the TP — or do both at one sitting in carefully selected cases. For a failed transfer, distinguish the mechanisms: an under-powered or under-tensioned transfer (persistent drop), an over-tensioned transfer (calcaneus gait), adhesion at the window, fixation pull-out, or progression of the underlying disease — each points to a different revision strategy, and a marginally grade 4 TP may benefit from a supplementary Bridle procedure or an AFO rather than a simple re-do.

Surgical anatomy. The tibialis posterior muscle arises from the posterior tibia, fibula, and interosseous membrane in the proximal third of the leg. Its tendon passes behind the medial malleolus in the tarsal tunnel (in a groove covered by the flexor retinaculum), turns anteriorly, and inserts chiefly on the navicular tuberosity with slips to the sustentaculum tali, all three cuneiforms, the cuboid, and the bases of the second to fourth metatarsals. It is the dominant invertor and the primary dynamic support of the medial longitudinal arch. Its total length from musculotendinous junction to navicular is about 14 to 18 cm — enough to reach the dorsum when harvested as proximally as possible. Motor supply is the tibial nerve (L4, L5, S1); the posterior tibial artery gives segmental branches to the sheath, with a vascularised zone at the insertion and a hypovascular zone about 1 to 2 cm proximal to it. The interosseous membrane and what lies on it. The membrane spans the tibia and fibula in the middle and proximal thirds, with fibres running obliquely from proximal-medial (tibia) to distal-lateral (fibula). On its anterior surface run the anterior tibial artery and the deep peroneal nerve, immediately deep to EHL and tibialis anterior — the very structures paralysed in the indication for this procedure, and the structures at risk when the window is cut. The safest zone for the window is the proximal third, about 4 to 6 cm distal to the fibular head, where the bundle is more mobile and retractable; the window must stay proximal to the distal tibiofibular syndesmosis to avoid destabilising the ankle mortise. Fixation sites on the dorsum. The lateral cuneiform is the usual target — strong cancellous bone accessible through a dorsal incision, giving a good line of pull for dorsiflexion and taking an interference screw or anchor well. The third metatarsal base is an alternative if the lateral cuneiform bone stock is poor or a more lateral attachment is wanted. On the dorsum the deep peroneal nerve and dorsalis pedis artery run between EHL and EDL and must be identified and protected at the fixation site; the transferred tendon is brought to the site subcutaneously or beneath the superior extensor retinaculum.

Why leprosy is the classic indication. In leprosy the common peroneal nerve is commonly thickened and infiltrated by Mycobacterium leprae, producing foot drop from anterior compartment paralysis, while the tibial nerve — and so the TP — is much less often affected. That anatomical selectivity leaves a strong, functioning donor tendon available to replace the paralysed dorsiflexors, which is why TP transfer is the gold standard reconstruction for leprosy foot drop; large worldwide series (Carayon and successors) report good functional outcomes in the majority of well-selected patients. Key evidence. Watkins and colleagues (1954) described the original transfer through the interosseous membrane and established the unchanged principles — TP harvest from the navicular, a membrane window, and dorsal fixation. Carayon and colleagues (1972) established the procedure as the standard for leprosy foot drop. Yeap, Birch and Singh (2001) reported long-term results across aetiologies, stressing that outcome hinges on patient selection — adequate TP power and a supple hindfoot. Vigasio and colleagues (2008) refined the routing and identified long-term planovalgus progression as a concern. Johnson and colleagues (2015) evaluated the Bridle procedure (combined TP, FDL and peroneus longus), showing stronger dorsiflexion force than isolated TP transfer at the cost of sacrificing extra tendons — useful when TP power is borderline.