Chronic Achilles Reconstruction with FHL Transfer

Indication. Reconstruction with a flexor hallucis longus (FHL) transfer is offered for a chronic, neglected or re-ruptured Achilles tendon in which primary end-to-end repair is impossible — classically a gap greater than 3 cm after debridement, with retracted, degenerate tendon ends — and for large insertional defects left after Haglund resection or debridement of calcific tendinopathy. The common endpoint is persistent weakness and a positive functional deficit (a palpable gap, a positive Matles test, inability to perform a single-leg heel rise) after a neglected rupture that has failed conservative care. Absolute indications.

• Chronic rupture with a gap greater than 3 cm after debridement where primary end-to-end repair is impossible.
• Re-rupture after previous repair with retracted, degenerate tendon ends.
• Large insertional Achilles defect after debridement of calcific tendinopathy or Haglund resection.
• Failed conservative management of a neglected rupture with persistent weakness and functional deficit. Relative indications.
• A high-function patient (sports, manual work) with a 2-3 cm gap and poor tendon quality.
• A diabetic or vasculopathic patient in whom bringing vascularised tissue into the repair zone improves healing.
• Revision reconstruction after a failed primary repair or augmentation. Contraindications. Absolute: active infection at the surgical site; severe peripheral vascular disease with a non-palpable posterior tibial pulse; a non-ambulatory patient or one unable to comply with protected weight-bearing. Relative: isolated great-toe pathology (hallux rigidus, prior FHL tenodesis) where donor morbidity would be unacceptable; severe osteoporosis compromising calcaneal tunnel fixation; a heavy smoker unwilling to cease smoking perioperatively. The one decision that matters. Having debrided the rupture to healthy tendon and measured the gap, the reconstruction is chosen by the size of the defect and the quality of the tendon:

Consent specifically for sural nerve injury (up to 15 percent), wound breakdown (5-15 percent), great-toe weakness (20-30 percent strength loss, rarely symptomatic), under- or over-tensioning, re-rupture (5-10 percent), and the need for protected weight-bearing for 8-12 weeks. Setup. Prone with the ankles at the end of the table and a small bump under the ipsilateral hip if internal rotation is needed; a thigh tourniquet inflated to 300 mmHg after exsanguination; bilateral leg preparation so the resting tension can be compared with the contralateral side. Anaesthesia is general or spinal; a popliteal or ankle block may be added for analgesia, but avoid a complete motor block if intraoperative tension testing is planned. Equipment: a standard foot-and-ankle tray, 7.0 and 8.0 mm cannulated reamers, 7-8 mm interference screws (PEEK or bioabsorbable), fluoroscopy, and a headlamp or loupes.

The goal is to bring a vascularised, in-phase motor unit into an avascular chronic-rupture bed and to fix it strongly enough to allow early protected weight-bearing. The exposure is posteromedial: it is laid out in full below (and in depth on the Achilles tendon approaches page), and the structures at risk are identified at the step where each is encountered.

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Rehabilitation | Phase | Timing | Immobilisation | Activity | |-------|--------|----------------|----------| | 1 | 0-2 weeks | Below-knee cast or boot, ankle in 10-15 degrees of plantarflexion; non-weight-bearing for the first 2 weeks | Wound review at 10-14 days; gentle active plantar- and dorsiflexion within the boot (0-20 degrees plantarflexion); no active great-toe flexion against resistance | | 2 | 2-6 weeks | Removable boot; touch weight-bearing progressing to 50 percent, then full weight-bearing by week 6-8 | Gentle dorsiflexion stretching to neutral from week 4-6 once the wound is healed; active plantarflexion strengthening with a theraband (low resistance); great-toe active flexion to maintain FDL function | | 3 | 6-12 weeks | Wean from the boot to a supportive shoe with a 1-2 cm heel lift at week 8-10 | Progressive plantarflexion resistance; single-leg heel raises begin at week 10-12 when pain-free; gait retraining (push-off and eccentric control); proprioception and balance | | 4 | 12-24 weeks | Full weight-bearing without support by week 12; a permanent 0.5-1 cm heel lift for high-impact activity | Sport-specific training at week 16-20 when heel-rise strength reaches 80 percent of the contralateral side; return to running at week 20-24; full sport at 6-9 months | Long-term. A permanent heel lift (0.5-1 cm) for high-impact activity; a maintenance plantarflexion strengthening programme; monitoring for contralateral Achilles tendinopathy (increased risk after a unilateral rupture); and education on activity modification and a gradual return to sport. Expected outcome. Most patients reach full weight-bearing without support by week 12, return to running at 5-6 months and to full sport at 6-9 months. Published series report greater than 80 percent patient satisfaction, a typical AOFAS improvement of 30-40 points, and a re-rupture rate of 5-10 percent. Single-leg heel-rise strength is usually 60-80 percent of the contralateral side and great-toe push-off is reduced by 20-30 percent, but donor morbidity is tolerated in greater than 90 percent. Complications

Why chronic ruptures are hard. A neglected Achilles rupture retracts: the tendon ends fibrose, become degenerate and avascular, and a direct repair under tension will stretch out and fail. The mid-portion of the tendon is a relatively avascular watershed zone, and the paratenon — normally a loose gliding layer — is scarred and adherent. The surgical problem is therefore to bring healthy, vascularised tissue into a poor-quality bed and to restore a plantarflexion motor unit. Why FHL is the transfer of choice. The flexor hallucis longus is preferred over FDL or peroneus brevis because it is in-phase with the Achilles (both plantarflex the ankle), its independent vascularised muscle belly extends distally to the ankle joint and so brings a blood supply into the repair zone, it lies immediately adjacent to the Achilles (minimal dissection for harvest), and its donor morbidity is low — great-toe push-off strength falls by 20-30 percent but is rarely symptomatic provided the FDL is intact and the transfer is tensioned correctly. Reference anatomy. The Achilles is the largest tendon in the body, formed by the confluence of gastrocnemius and soleus, inserting on the posterior calcaneal tuberosity about 2 cm distal to the superior calcaneal margin; its blood supply comes proximally from the musculotendinous junction and distally from the calcaneal insertion, leaving the mid-portion relatively avascular. The FHL arises from the posterior fibula and interosseous membrane, its muscle belly extends to the ankle joint, its tendon passes behind the medial malleolus in its own fibro-osseous tunnel and crosses the FDL at the knot of Henry (2-3 cm distal to the navicular), and it inserts at the base of the distal phalanx of the hallux. At the ankle the posterior tibial neurovascular bundle lies between FHL and FDL (medial to FHL); at the knot of Henry the medial and lateral plantar nerves lie on the plantar surface of the FHL; the sural nerve runs subcutaneously along the lateral Achilles border; and the medial calcaneal nerve branches from the tibial nerve and is at risk in medial dissection.

Key evidence. Multiple Level III-IV series of FHL transfer for chronic Achilles defects report greater than 80 percent patient satisfaction, AOFAS improvement of 30-40 points and re-rupture rates of 5-10 percent, with donor morbidity tolerated in greater than 90 percent. The single-incision technique gives reliable pain relief for chronic tendinopathy, while the modified two-incision transfer addresses large-gap ruptures. The consistent message — a vascularised, in-phase transfer reliably restores function where primary repair is impossible — is why FHL is the transfer of choice and a perennial viva favourite.