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Failed arthroplasty of the ankle due to
Primary loosening of component
Late loosening of component
Progressive nonmanageable malalignment
Nonmanageable instability
Avascular necrosis of underlying bone
Deep infection
Periprosthetic fracture
Breakdown of soft tissues
Chronic pain syndrome
Others (e.g., metal allergy or intolerance, dysfunction)
Active infection
Neuroarthropathy (Charcot arthropathy)
Controversy about appropriate salvage procedure
Revision arthroplasty
Tibiotalar arthrodesis
Tibiocalcaneal arthrodesis
Revision arthroplasty
Tibiotalar arthrodesis
Tibiocalcaneal arthrodesis
While the patient is standing, perform a thorough clinical investigation of both lower extremities to assess
Alignment
Deformities
Foot position
Muscular atrophy
Soft tissue condition (e.g., existing scars)
While the patient is sitting with free-hanging feet, perform an assessment of
Extent to which a present deformity is correctable
Preserved joint motion of the ankle and subtalar joints
Ligament stability of the ankle and subtalar joints with anterior drawer and tilt tests
Supination and eversion power (e.g., function of posterior tibial and peroneus brevis muscles)
Plain weight-bearing radiographs, including anteroposterior (AP) views of foot and ankle and lateral view of the foot, to determine/rule out
Component position
Lucency zone beneath component
Extent of destruction of underlying bone stock (e.g., tibia, talus, fibula)
Status of neighboring joints (e.g., associated degenerative disease)
Deformities of the foot and ankle complex (e.g., heel alignment, foot arch, talonavicular alignment)
Bony condition (e.g., avascular necrosis, bony defects, osteoporosis)
Fig. 59.1 shows a 67-year-old male patient, 5.8 years after primary arthroplasty, evidencing cyst formation on AP ( Fig. 59.1A ) and lateral ( Fig. 59.1B ) plain radiographs.
Computed tomography scan may be obtained for assessment of
Bone-implant interface
Bony defects
Cyst formation
Avascular necrosis
Fig. 59.2 shows coronal ( Fig. 59.2A ) and sagittal ( Fig. 59.2B ) views of the same patient as in Fig. 59.1 .
Single-photon emission computed tomography with superimposed bone scan may be used to visualize
Bone-implant interface
Stress reaction (e.g., medial malleolus, fibula)
Bony impingement
Morphologic pathologies and associated activity process
The superior extensor retinaculum is a thickening of the deep fascia above the ankle, running from the tibia to the fibula ( Fig. 59.3 ). It includes, from medially to laterally, the tendons of the tibialis anterior, extensor hallucis longus, and extensor digitorum longus.
The anterior neurovascular bundle lies roughly halfway between the malleoli ( Fig. 59.4A ); it can be found consistently between the extensor hallucis longus and extensor digitorum longus tendons.
The neurovascular bundle contains the tibialis anterior and the deep peroneal nerve. The nerve supplies the extensor digitorum brevis and extensor hallucis brevis and a sensory space (interdigital I–II).
On the height of the talonavicular joint, the medial branches of the superficial peroneal nerve cross from lateral to medial ( Fig. 59.4B ). This nerve supplies the skin of the dorsum of the foot.
On the posterior aspect of the ankle, the medial neurovascular bundle is located behind its posteromedial corner, and the flexor hallucis longus tendon on its posterior aspect ( Fig. 59.4C ).
A self-retaining distractor may be helpful; care must be taken, however, that no tension is applied to the skin.
The patient is positioned with the feet on the edge of the table.
The ipsilateral back is lifted until a strictly upward position of the foot is obtained.
The tourniquet is mounted at the ipsilateral thigh.
The affected foot is underlet with a block to facilitate fluoroscopy during surgery.
Usually, the scar from the previous incision is used.
The scarred extensor retinaculum is exposed through a 10–12-cm incision.
The retinaculum is dissected along the lateral border of the anterior tibial tendon, and the anterior aspect of the distal tibia is exposed.
While the soft tissue mantle is dissected with the periosteum from the bone, attention is paid to the neurovascular bundle that lies behind the long extensor hallucis tendon.
A capsulotomy and capsulectomy are made, and a self-retaining retractor is inserted to carefully keep the soft tissue mantle away.
The prosthesis is exposed and explored with regard to instability, dysfunction, loosening, bony impingement, and wear. The components are then removed.
In most instances, the polyethylene insert is removed first.
The tibial component is removed next, taking care not to damage the bone stock ( Fig. 59.5A ).
The talar component is then removed, again taking care not to damage the bone stock ( Fig. 59.5B ).
The remaining bone surfaces are carefully débrided from any soft tissue formation and avascular bone. Fig. 59.5C shows the talar surface after débridement, and Fig. 59.5D shows excised cyst material from the same patient as in Fig. 59.1 .
The medial and lateral compartments are also débrided.
While the foot is held in a neutral position, the overall defect is measured.
To remove a tibial component with stem fixation, a window at the anterior tibial cortex may be created.
To remove a talar component, a small impactor may be inserted percutaneously from the lateral foot sole to gain access to the anterolateral corner of the implant ( Fig. 59.6 ).
If old scars from previous surgeries or injuries are not respected, breakdown of critical areas may occur.
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