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Isolated total talus replacement


Definition

  • Excision and replacement of the talus with a patient-specific 3D-printed metallic implant in patients without adjacent joint disease.

Indications

  • Avascular necrosis (AVN) of the talus without significant arthritic changes ( Fig. 4.1 ).

    • Fig. 4.1, Preoperative radiographs (A) and CT images (B) of talar avascular necrosis with early collapse in a 53-year-old female with history of long-term corticosteroid use for lupus. The patient failed to respond to nonoperative treatment for nearly 2 years and then underwent total talus replacement. At 1-year postoperative follow-up the patient demonstrated a significant improved in pain and function (C).

  • Complex talus trauma ( Fig. 4.2 ).

    • Fig. 4.2, Initial radiographs and CT scan of a 69-year-old male after a 10-foot fall from a ladder resulting in a comminuted talar body fracture (A). Due to the high rate of avascular necrosis and longer recovery associated with open reduction with internal fixation (ORIF) surgery, the patient decided to undergo total talus replacement (TTR). The injury was reduced and placed into a spanning external fixator (B). While the soft tissues recovered, a patient-specific 3D-printed total talus implant was designed and manufactured. Roughly 2 weeks after the injury, the patient underwent TTR. Functionally the patient remains at a preinjury activity level without a brace or assistive device at 2-year follow-up (C).

  • Large osteochondral lesions with cystic formation which have failed traditional surgical procedures ( Fig. 4.3 ).

    • Fig. 4.3, Radiograph and CT scan of a 24-year-old male who failed to improve following multiple procedures for a large osteochondral defect of the medial talus (A). Due to worsening pain and function preventing the patient’s ability to work, the patient elected to undergo total talus replacement (TTR). At 2 years follow-up, the patient has shown significant improvement compared to preoperative pain and function scores (B). He returned to work 4 months following TTR and remained very satisfied with his outcome.

  • Malignancy requiring excision of the talus.

Anatomy

  • Greater than 60% of the talus is covered with articular cartilage, which limits the surface area for vascular infiltration.

  • Extraosseous circulation loops all arise from branches of the posterior tibial, anterior tibial, and peroneal arteries. Vasculature within the sinus tarsi and tarsal canal in addition to deltoid branches all play vital roles for talar blood supply.

  • The talus has no muscular or tendinous attachments and therefore relies on periarticular ligaments and joint morphology for stability.

  • The talar dome is wider anteriorly than posteriorly, and thus mechanically more stable when the foot is dorsiflexed.

Pathogenesis

  • Shah et al. classified AVN etiology into six categories ( Table 4.1 ).

    TABLE 4.1
    Avascular Necrosis Etiologies as Categorized
    Category Etiology
    Direct cellular toxicity

    • Chemotherapy

    • Radiotherapy

    • Thermal injury

    • Smoking

    Extraosseous arterial

    • Fracture

    • Dislocation

    • Iatrogenic/postsurgical

    • Congenital arterial abnormalities

    Extraosseous venous

    • Venous abnormalities

    • Venous stasis

    Intraosseous extravascular compression

    • Hemorrhage

    • Elevated bone marrow pressure

    • Fatty infiltration of bone marrow (prolonged high-dose corticosteroid use)

    • Cellular hypertrophy and marrow infiltration (Gaucher’s disease)

    • Bone marrow edema

    • Displaced fractures

    Intraosseous intravascular occlusion

    • Coagulation disorders (i.e., thrombophilia, hypofibrinolysis)

    • Sickle cell crises

    Multifactorial A combination of two or more etiologies
    Shah KN, Racine J, Jones LC, Aaron RK. Pathophysiology and risk factors for osteonecrosis. Curr Rev Musculoskelet Med. 2015;8(3):201-209.

  • Risk factors for AVN have been identified; however, the precise pathogenesis has yet to be understood.

  • It is probable that AVN occurs due to a combination of risk factors and conditions. Modifiable risk factors include excessive alcohol consumption, nicotine use, poor diet, and obesity.

  • The majority of talar AVN cases occur following neck or body fracture:

    • Up to 75% of talar AVN is attributed to trauma.

    • The incidence of AVN increases with coexisting adjacent joint dislocation and initial fracture displacement.

    • Timing to surgical repair does not appear to influence the risk of AVN.

    • The absence of subchondral lucency, referred to as the Hawkins sign, on radiographs 6 to 8 weeks postinjury is concerning for AVN development.

  • Multiple atraumatic etiologies exist but are less common for talar AVN. The most common cause of atraumatic AVN is associated with glucocorticoid use.

  • An underlying characteristic of AVN is insufficient and/or altered blood supply to the talus, leading to bone cell death.

  • Treatment may be more successful in early stages of AVN; however, early-stage AVN is more difficult to diagnose and can be asymptomatic.

  • Talar collapse occurs as the avascular process progresses due to the altered structural integrity of the bone.

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