Definition
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Excision and replacement of the talus with a patient-specific 3D-printed metallic implant in patients without adjacent joint disease.
Indications
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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).
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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).
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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.
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Malignancy requiring excision of the talus.
Anatomy
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Greater than 60% of the talus is covered with articular cartilage, which limits the surface area for vascular infiltration.
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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.
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The talus has no muscular or tendinous attachments and therefore relies on periarticular ligaments and joint morphology for stability.
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The talar dome is wider anteriorly than posteriorly, and thus mechanically more stable when the foot is dorsiflexed.
Pathogenesis
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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.
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Risk factors for AVN have been identified; however, the precise pathogenesis has yet to be understood.
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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.
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The majority of talar AVN cases occur following neck or body fracture:
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Up to 75% of talar AVN is attributed to trauma.
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The incidence of AVN increases with coexisting adjacent joint dislocation and initial fracture displacement.
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Timing to surgical repair does not appear to influence the risk of AVN.
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The absence of subchondral lucency, referred to as the Hawkins sign, on radiographs 6 to 8 weeks postinjury is concerning for AVN development.
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Multiple atraumatic etiologies exist but are less common for talar AVN. The most common cause of atraumatic AVN is associated with glucocorticoid use.
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An underlying characteristic of AVN is insufficient and/or altered blood supply to the talus, leading to bone cell death.
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Treatment may be more successful in early stages of AVN; however, early-stage AVN is more difficult to diagnose and can be asymptomatic.
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Talar collapse occurs as the avascular process progresses due to the altered structural integrity of the bone.
Patient history and physical exam findings
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History of trauma which required surgical intervention is common.
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Atraumatic history may include prolonged high-dose corticosteroids, alcoholism, prior irradiation treatments, and thrombophilia.
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Initially osteonecrosis is asymptomatic and will typically progress to collapse if untreated.
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Symptoms and presentation vary and may be vague until late-stage AVN, which presents with significant pain, dysfunction, and possibly deformity.
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Patients complain of a deep pain to the talar aspect of the ankle, which is exacerbated with weight bearing and range of motion (ROM).
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Decreased ROM compared to contralateral foot is common if AVN is unilateral.
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Rigid deformity may be present in late-stage talar AVN with collapse ( Fig. 4.4 ).
• Fig. 4.4
Clinical presentation of a patient with advanced talar avascular necrosis, resulting in talar collapse and rigid equinocavovarus deformity.
Imaging and other diagnostic testing
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In the initial stage of AVN, plain radiographs are often unremarkable. If a high index of suspicion exists for talar AVN then it is critical to obtain an MRI, which is the most sensitive and specific test during the early stages ( Fig. 4.5 ).
• Fig. 4.5
Characteristic findings of early-stage talar avascular necrosis on T1- and T2-weighted MRI images in a 51-year-old female with a history of prolonged corticosteroid use.
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In the absence of hardware, MRI can demonstrate the extent of AVN.
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An absence of the Hawkins sign 6 to 8 weeks posttrauma on plain radiographs is concerning for talar AVN.
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As the disease progresses, radiographs may demonstrate talar sclerosis, and in advanced stages may show signs of talar collapse ( Fig. 4.6 ).
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