Avascular Necrosis and Total Talus Replacement


Introduction and Etiology

Avascular necrosis (AVN, or osteonecrosis) is death of bone due to lack of blood supply. The talus is at risk for vascular insult due to the nature of its limited and tenuous blood supply.

AVN of the talus is caused by either (1) trauma or (2) nontraumatic causes including hypercortisolism, corticosteroid use, human immunodeficiency virus (HIV), renal transplant, alcoholism or pancreatitis, irradiation, multiple sclerosis, collagen vascular disorders, the technique of subchondroplasty, or idiopathic origin among others. Trauma is the leading cause of talar AVN, accounting for about 75% of all cases. The most common traumatic etiology is talar neck fracture with or without associated peritalar dislocation (see Chapter 46 ). The high association of talar neck fracture and AVN is likely related to the blood supply to the talus that is limited secondary to greater than 60% of the talus being covered by cartilage, and therefore, the majority of vessel entry into the talus is at the talar neck through the tarsal sinus and tarsal canal. The risk of developing AVN is directly related to the severity of the injury, which has been borne out in many studies. The Hawkins classification of talar neck fractures describes the fracture displacement and which joint(s) are dislocated. With increasing Hawkins type, there is increased risk of AVN: Type I, 0% to 13%; Type II, 20% to 50%; Type III, 20% to 100%; Type IV, 70% to 100. The timing of fracture fixation is not related to the risk of developing AVN.

The nontraumatic etiologies of talar AVN are less well understood. Oral corticosteroids are the next most common reason for developing AVN. Dosage and duration of use affect the severity of AVN. The pathophysiology of steroid use causing AVN is unknown but one hypothesis is that steroids increase blood lipid levels leading to occlusion. Other than high lipid levels (fat emboli), sickled red blood cells, hypercoagulable states, and external vessel compression are thought to cause loss of blood supply to the talus. Additional etiologies responsible for loss of blood supply include systemic lupus erythematosus, sickle cell disease, scleroderma, diabetes, multiple sclerosis, protein-S deficiency, and medications.

Imaging and Staging

Imaging is important to understand the extent of AVN within the bone and to determine the sequelae of the disease process such as collapse and surrounding joint arthritis. The main radiographic feature of talus AVN is increased sclerosis. Occasionally, lytic lesions can be seen. However, the presence of a subchondral osteopenic line seen on the anteroposterior (AP) and mortise radiographs of the talus 6 to 12 weeks after talar neck fracture is not AVN. Instead, it represents osteoclast-mediated disuse osteopenia, or the Hawkins sign , suggestive of talus vascularity. Plain radiographs can also demonstrate subchondral collapse, surrounding joint arthritis, and deformity. When AVN is suspected on plain radiographs, further imaging is necessary. Magnetic resonance imaging (MRI) and computed tomography (CT) scans both have utility in supplementing plain radiographs. MRI can better characterize the extent and location of the AVN. In non-talus fracture cases, the MRI can demonstrate AVN in other bones that could be the source of pain and must be considered during treatment. CT can better characterize bony collapse and surrounding joint arthritis.

Treatment of Talar Avascular Necrosis ( )

AVN symptoms do not necessarily correlate with the amount of bony involvement. Some patients may be asymptomatic until sequelae from the AVN process occurs. These sequelae include talar collapse, arthritis of the ankle, subtalar joint, or both, and some may progress to an equinovarus deformity of the foot, whereas other patients may not have any bony collapse or surrounding arthritis but experience pain from the pathology within the bone. Unfortunately, patients with AVN rarely present at early stages of the disease process, but treatment options do exist for these patients.

Treatment considerations for early talar AVN include weight bearing versus non–weight bearing, immobilization versus early range of motion, and conservative versus surgical treatments. Canale and Kelly reported that posttraumatic AVN patients treated with 9 or more months of non–weight bearing fared better than patients treated with a patellar tendon bearing brace or shorter periods of non–weight bearing. Moreover, a recent systematic review reported that prolonged protective weight bearing provided the best outcome in early AVN.

Prolonged non–weight bearing is not practical in today’s society. The majority of other nonsurgical treatment methods have been studied in femoral head AVN and not necessarily in talar AVN. Alendronate, calcium, vitamin D, and pulsed electromagnetic field therapy have demonstrated promise in early AVN of the femoral head. Extracorporeal shockwave therapy and injection of concentrated iliac crest bone marrow aspirate have demonstrated efficacy in talar AVN ( Video 24-1).

When the talar AVN is severe and talar collapse with associated adjacent joint arthritis has ensued, management is less controversial. Severe AVN leads to structural changes in the architecture of the talus as well as compromise of hindfoot alignment. In addition to the subtalar joint, these deformities often spread to the tibiotalar joint. Many techniques have been described to manage these issues, including gradual correction with external fixators, osteotomies, and allograft bone blocks shaped to correct the deformity.

Preoperative Evaluation

Operative treatment options are dependent on the extent of the disease within the talus, cortical deformation, whether the adjacent joints are involved, and the condition of the patient. Advanced or severe AVN of the talus indicates significant bone loss or collapse of large portions of the talus. This can result in structural collapse of the hindfoot, poor function, and pain.

The preoperative evaluation includes a comprehensive patient medical history, relevant nutrition and metabolic laboratory values, physical examination and assessment of hindfoot alignment, standard radiographs, and obtaining advanced imaging. Pertinent laboratory studies might include vitamin D, calcium, albumin, and pre-albumin, and complete metabolic panel can offer insight into whether a patient is even a candidate for surgery and if they have the healing potential as a host to undergo these complicated procedures. A detailed physical exam including neurovascular status, muscle strength, physical deformities, and prior incisions must be performed. Skin contractures as well as scars from previous injuries or surgeries must be considered when determining the most appropriate approach.

Standard radiographic imaging should include weight-bearing AP, lateral, and oblique views of the foot and ankle. These images help to identify bony collapse, deformity, and arthritis of the surrounding joints. A hindfoot alignment view is also important, especially in cases of AVN from a talus neck fracture (varus malalignment). Identifying preoperative malalignment is necessary to achieve optimum surgical outcome for either motion sparing of fusion techniques outlined below.

MRI demonstrates the extent of necrosis and can elucidate the areas of bony edema. Low signal intensity of T1-weighted images occurs secondary to adipocyte death while high or mixed signal intensity on T2-weighted images occur due to increased bony edema. Often the patient presents with an MRI ordered by another provider. If the MRI is more than 6 months old, then a new MRI should be obtained to determine if the AVN has progressed. The surrounding bones must also be assessed for AVN. In nontraumatic cases of AVN, the tibia is often involved as well. MRI combined with CT scan provide two complementary components to evaluate bony necrosis. Moreover, CT imaging can provide a better three-dimensional (3D) understanding of collapse and bone loss as well as complement standard radiographs in identifying deformity and adjacent joint arthritis. If consideration is given to a 3D printed implant (discussed below), a CT of the contralateral limb (assuming pathology is not bilateral) provides the 3D printing company a template for baseline dimensions and height restoration. The contralateral CT data will be “mirror imaged” to provide a baseline template for the 3D printed implant.

Finally, an assessment of the patient’s goals for surgery and realistic outcomes must be set. Operative treatment can be classified into two main categories: (1) arthrodesis and (2) motion sparing procedures. Arthrodesis can consist of isolated tibiotalar or subtalar joint(s) based on the location of talar collapse, deformity, arthritis progression, and source of pain. However, the majority of the time both the tibiotalar and subtalar joints require arthrodesis (tibiotalocalcaneal arthrodesis, TTC). The choice of treatment is dependent on the overall condition of the patient, the condition of the hindfoot, extent of AVN, patient’s wishes, treating surgeon’s comfort level with the desired treatment, and the available technology. Both arthrodesis and motion sparing options have recently benefited from the introduction of 3D printing to orthopaedic surgery. See Chapters 22 and 25 for further discussion of arthrodesis techniques.

Motion sparing, through the use of a total talus replacement (TTR), will be a focus of the remainder of this chapter. The following sections will outline 3D printing technology, the available evidence behind the use of TTR, and techniques of designing and performing a TTR.

Review of Traditional and 3D Printed Arthrodesis for AVN of the Talus

Before discussing TTR, it is important to present the evidence behind arthrodesis procedures for talus AVN. The techniques of hindfoot arthrodesis procedures are described in Chapters 22 and 25 . He we will specifically discuss hindfoot arthrodesis options related to AVN of the talus. The majority of literature regarding the treatment of this pathology focuses on tibiotalar, tibiotalocalcaneal (TTC), or tibiocalcaneal arthrodeses with minimal reports on isolated subtalar arthrodesis (discussed later). Although the pathologic talus does not provide healthy bone, successful fusions have been achieved with the avascular talus, complete talectomy, cadaver bone, and even non-3D metal implants borrowed from other areas of orthopaedic surgery. To make interpretation of the literature more complicated, hardware constructs have consisted of external fixators, internal plate and screw fixation, and intramedullary nail fixation.

The avascular talus may aid in maintaining hindfoot height during fusion, and, with supplementation, its retention leads to high fusion rates. DeVries et al reported on 14 patients who underwent retrograde intramedullary nail arthrodesis for talus AVN. Most of the tali were left in place with variable treatment techniques regarding biologic augmentation. Thirteen patients went on to union and the remaining patient had a braceable pseudoarthrosis. Another study reported on 14 TTC arthrodeses in which 10 of them used the avascular talus. All cases used some type of biologic supplementation, including autograft (majority). Arthrodesis was achieved in all cases. These studies support the use of the avascular talus. If the avascular talus is used, the author suggests some type of biological supplementation when using the avascular talus. Moreover, the avascular talus should only be used if it is not collapsed. There are other options to restore hindfoot length.

One option to restore length, when the avascular talus is not used for the arthrodesis procedures, is to use bulk autograft. In a series of talus AVN after fracture, Abd-Ella et al reported successful treatment with bulk autograft from the iliac crest and intramedullary nail arthrodesis in 12 patients. At a mean of 23 months, solid osseous fusion was achieved in only 8 (67%) of the patients. Autograft was chosen over allograft because of biological superiority. While autograft could have biological superiority, it lacks in volume, shape, and structural integrity when compared to other options and is not the author’s preferred treatment.

The prevailing method to replace the avascular talus is the use of bulk allograft, typically a femoral head. Jeng et al reported on the results of 32 patients who underwent TTC arthrodesis using bulk femoral head allograft to fill large bony voids. The defects were the result of talar AVN, failed total ankle replacement, trauma, osteomyelitis, Charcot, or failed reconstructive surgery. Sixteen patients healed their fusion for an overall success rate of 50%. Diabetes mellitus was a predictive factor for failure. All nine patients with diabetes developed a nonunion. Structural bone graft requires healing through the interfaces between the graft and the native bone and risks future collapse if this incorporation is not successful. Over time, even with successful fusion, some collapse is common.

As previously mentioned, the avascular talus can be completely excised and not replaced with any graft. Dennison et al reported on six cases of talar AVN treated with complete talectomy and shortening using Ilizarov ringed-external fixator arthrodesis. Five of six patients reported good results and all six patients went on to union. However, the long-term results of shortening are not known but will likely result in gait abnormalities.

A subset of patients with talus AVN develops isolated or primarily symptomatic subtalar arthritis and may benefit from isolated subtalar arthrodesis instead of ankle or TTC arthrodesis. In a series of 148 isolated subtalar arthrodeses for various pathologies, Easley et al reported that all nonunions developed in patients who were found to have 2 mm of avascular subchondral bone at the time of surgery (although the preoperative diagnosis of AVN was not specified). On the contrary, Devalia et al reported on isolated subtalar arthrodesis in the setting of talar AVN as an intermediate step to total ankle arthroplasty to prevent talar subsidence. They demonstrated a 100% fusion rate in seven patients with improvement in pain and decreased talar component subsidence.

With the advent of 3D printing technology, the opportunity to design custom implants has provided another option to manage the treatment of symptomatic talus AVN.

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