Arthroscopic Treatment of Osteochondral Lesions of the Talus

Steven M. Raikin, MD

John J. Mangan, MD

Dr. Raikin or an immediate family member has received research or institutional support from Zimmer. Neither Dr. Mangan nor any immediate family member has received anything of value from or has stock or stock options held in a commercial company or institution related directly or indirectly to the subject of this chapter.

This chapter is adapted from Raikin SM, Slenker NR: Arthroscopic Treatment of Osteochondral Lesions of the Talus, in Flatow E, Colvin AC, eds: Atlas of Essential Orthopaedic Procedures. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2013, pp 491-497.

INTRODUCTION

Osteochondral lesions of the talus (OLTs) are a common source of ankle pain and instability. They are defined as a defect in the articular hyaline cartilage, predominantly within the weight-bearing area of the talar dome, and with involvement of the underlying bone. Although trauma is implicated in many cases, it does not account for the etiology of every lesion. The etiology of OLTs has been debated since 1888, when König first described “osteochondritis dissecans” of the knee, which he suggested was the result of spontaneous necrosis.¹ Talar involvement was then described in 1922 by Kappis,² who identified a strong association with prior trauma. The initial classification of talar lesions was described in 1959 by Berndt and Harty,³ who proposed an anatomic rationale for the association of these “transchondral fractures of the talar dome” with intra-articular trauma. In their review that included 582 patients with OLTs, a history of ankle trauma was reported in 76% of patients.³ However, the etiology of OLTs in patients without a history of trauma remains unknown. Repetitive microtrauma, vascular abnormalities resulting in osteonecrosis, and congenital factors have been speculated to play a role.

Historically, most OLTs were described as occurring either posterior-medial or anterior-lateral, and there has been a stronger association between lateral lesions and a history of trauma. More recently, Raikin and Elias et al⁴ developed an anatomic grid that divides the talar dome into nine equal zones. They analyzed MRI examinations of 424 patients with OLTs using this grid and determined that 62% of the lesions were medial and 34% were lateral. More striking was that in the sagittal plane, most of the lesions (80%) were central. They also confirmed an earlier observation that medial lesions were wider and deeper than lateral lesions. This is consistent with the mechanism originally proposed by Berndt and Harty, in which lateral lesions are typically caused by shear between the talus and the fibula that causes shallow, displaced, “wafer-shaped” lesions on the lateral dome of the talus, whereas medial lesions result from torsion and impaction of the tibia on the talus, resulting in deeper, “cup-shaped” lesions.

Symptomatic OLTs typically present with pain, catching, instability, and/or swelling of the ankle. Lesions are commonly seen on radiographic studies but may be incidental findings. Although often nonspecific, a meticulous clinical evaluation is essential to differentiate among the many potential diagnoses, including ligamentous injury, fractures of the fibula, and fractures of the tibial plafond. The index of suspicion should be high in the setting of ankle pain without any recognized trauma or with persistent ankle pain after an acute injury has resolved.

DIAGNOSTIC IMAGING

Diagnostic imaging should begin with AP, lateral, and mortise weight-bearing radiographs of the ankle. However, after an acute injury with a nondisplaced lesion, plain radiographs may be unrevealing. A chronic lesion with displacement, osteonecrosis, or cystic change may be clearly evident on plain radiographs. The limitations of radiographs include a low sensitivity, inability to assess the articular cartilage, and an inability to assess the extent of the lesion. MRI has proven to be very sensitive and specific in the diagnosis of OLTs and allows good visualization of the articular surface.⁵ The benefits of MRI include an accurate assessment of the location and extent of the lesion and the presence of bone marrow edema, which is suggestive of an active lesion, and an evaluation of the vascular status of the fragment. However, excessive edema can sometimes obscure the bony extent of the lesion. Polyaxial CT scanning accurately delineates the bony defect (Figure 1). In clinical practice, MRI is typically obtained before CT to evaluate a patient with unexplained pain because MRI can detect
a variety of pathologic conditions. Frequently, a CT scan is then obtained to characterize bony lesions more fully when the MRI findings are inconclusive.

FIGURE 1 Coronal (A) and sagittal (B) CT scans demonstrate a stage III medial osteochondral lesion of the talus.

CLASSIFICATION

The classification system introduced by Berndt and Harty in 1959 remains the most widely used method of describing an OLT.³ It is based on the appearance of the lesion on plain radiographs and includes four stages. Since its introduction, several authors have revised the original classification to include findings on MRI, CT, and arthroscopy. In particular, a fifth and a sixth stage have been added to describe cystic changes and massive-volume lesions, respectively.⁶^,⁷ The senior author (S.M.R.) has proposed a grading system that is a combination of the various modality-specific systems described previously (Figure 2).

Stage I lesions involve an isolated cartilaginous flap, without subchondral bony compromise. Radiographs and CT scans are usually negative. MRI demonstrates edema in the underlying bone without evidence of fracture. Symptoms are commonly mechanical and include painful catching and giving way of the ankle.

Stage II lesions involve an incomplete or completely nondisplaced fracture of the underlying bone (Berndt and Harty stage I and II). This is often not visible on plain radiographs, but it is clearly discernible on MRI or CT scans. These lesions are stable and unlikely to displace, and they may respond best to nonsurgical treatment.

Stage III lesions are unstable and displaced. The fragment usually remains in its bed or crater, covered by dysmorphic cartilage, and can be balloted arthroscopically. These lesions are clearly visible on plain radiographs, MRI, or CT. Large acute fragments may maintain their vascularity and can potentially be reduced and fixed with a bioabsorbable pin, particularly in the acute traumatic setting. If the fragment is avascular, treatment is by arthroscopic resection, débridement, and microfracture of the lesion base.

Stage IV lesions involve a defect devoid of any remaining bony fragments. The fragments may be free floating within the joint as loose bodies or crushed and no longer present. The lesion base may still be covered by damaged cartilage or unstable fibrocartilage that, in symptomatic cases, should be arthroscopically débrided and the base microfractured.

Stage V lesions are subchondral cysts, often with an intact cartilaginous cap. These have been shown to do poorly with arthroscopic débridement and microfracture.⁷ Treatment options include retrograde drilling and bone grafting of the lesion (arthroscopic confirmation of an intact and healthy cartilage cap is an essential part of the procedure) or osteochondral autologous transfer.

Stage VI lesions are very large and include either a large surface area of chondral damage and/or a large subchondral cyst communicating with the joint (ie, osteochondral cyst). These lesions are too large to treat arthroscopically or with an osteochondral autologous transfer procedure and require fresh osteochondral allograft transplantation.⁸^,⁹^,¹⁰

TREATMENT OPTIONS/INDICATIONS

A trial of nonsurgical management is advocated for all nondisplaced OLTs.¹¹ The main contraindication to nonsurgical management is acute injuries with displaced osteochondral fragments. In these cases, immediate surgical management is warranted to either resect or reduce and internally fixate the fragment. Generally, nonsurgical treatment involves an initial period of non-weight bearing with cast immobilization, followed by progressive weight bearing and mobilization to full ambulation by 12 to 16 weeks. Studies by Shearer et al¹² and Elias et al⁵ demonstrated 54% and 45% success rates, respectively, for nonsurgical treatment of OLTs. Although good results may be obtained without surgery, some lesions remain symptomatic after a course of nonsurgical management. The indications for surgical intervention include symptomatic
lesions refractory to nonsurgical care regardless of the stage. The presence of advanced grade III or IV lesions often necessitates surgical intervention as well.¹³^,¹⁴ A meta-analysis conducted by Tol et al¹¹ in 2000 showed only a 45% success rate in nonsurgical treatment of grade I, grade II, and medial grade III osteochondral defects of the talus. Furthermore, the results of excision and drilling were encouraging compared with nonsurgical treatment. They found excision, curettage, and drilling to have had good to excellent results in 88% of patients with grade III and higher lesions (16 studies, 165 patients). However, simple excision and curettage without drilling (9 studies, 111 patients) had a success rate of 78%, and excision alone (5 studies, 63 patients) had a success rate of 38%.

FIGURE 2 Illustrations show the senior author’s (S.M.R.’s) grading system for osteochondral lesions of the talus (shown as medial lesions). See text for descriptions.

Multiple surgical treatment options exist, including débridement with or without bone marrow stimulation, autologous chondrocyte implantation, allograft transplantation, and osteochondral autograft transplantation or mosaicplasty. Despite advancements in some of these options, arthroscopic débridement combined with bone marrow stimulation remains one of the most effective treatments.¹³^,¹⁴ It is considered the treatment of choice for primary lesions not exceeding 15 mm in diameter.¹¹ Van Bergen et al presented the longest term follow-up study of patients 8 to 20 years after undergoing bone marrow stimulation. They demonstrated that 78% had excellent to good functional outcome scores at long-term follow-up.¹⁵ The International Consensus Group on Cartilage Repair of the Ankle 2018 statement on OLTs reported a consensus statement that repeat bone marrow stimulation can be considered for when there is concern about the efficacy of the débridement and stimulation, or the patient is unwilling to undergo more extensive procedures.¹⁶

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