Primary total ankle total talus replacement

Surgical treatment of end-stage ankle arthritis with concomitant avascular necrosis (AVN) of the talus utilizing a combination of patient-specific 3D-printed and off-the-shelf (OTS) components for joint preservation and restoration of function.

3D printing has evolved and now allows surgeons to partner with technology that facilitates a continuity of care to maintain ankle joint range of motion (ROM) and avoid the need for tibiotalar calcaneal joint arthrodesis.

This chapter focuses on the niche situations that involve significant talar body loss from AVN or posttraumatic changes where plafond and arthritic changes are evident.

The talus is a uniquely shaped bone that articulates with the tibial plafond, fibular malleolus, calcaneus and navicular bones.

The talus is without tendon attachments therefore stability is provided by its articulations and ligament attachments.

Sixty percent of the talar surface is covered by cartilage, thus minimizing available area for vascular perforators.

The primary source of vascular influx is provided by the posterior tibial artery via perforators within the deltoid ligament and to the tarsal canal. The dorsal neck and sinus tarsi rely on vascular supply from the dorsalis pedis artery while the perforating peroneal artery serves the posterior body.

AVN results from a temporary or permanent loss of vascular supply to a bone. Interruption in any part of the vascular supply (arteries, capillaries, sinusoids, or veins) can lead to AVN. Bones with a single terminal vascular source are known to be at higher risk for AVN.

Within 3 hours of vascular impairment, anoxia causes osteocyte necrosis. Over time the resultant osteonecrosis can progress to subchondral fracture, loss of normal bony architecture, and collapse, leading to cartilage destruction and arthritis.

Much of the pathogenesis is not fully understood, although trauma, drug-induced, and idiopathic causes can result in vascular impairment. Trauma remains the most common cause of talar AVN. The more severe talar trauma, the more likely AVN will develop.

The physiologic response to AVN is to resorb necrotic bone by revascularization and reossification, which can be observed radiographically.