Osteochondral Lesion of the Talus

An osteochondral lesion of the talus is a focal injury to the articular cartilage and underlying subchondral bone of the talar dome. It follows ankle sprains and fractures (up to 50% show a lesion on arthroscopy after severe sprain) and is also caused by repetitive microtrauma, ischemia and, rarely, genetic factors. Peak age is 15 to 35 years.

Two typical sites:

• Medial (posteromedial) lesions: deep, cup shaped, often atraumatic, and more common (about 60%)
• Lateral (anterolateral) lesions: shallow, wafer shaped and nearly always traumatic

Staging by MRI: 1. Bone marrow edema and an intact cartilage surface 2. Partial cartilage tear with a subchondral cyst or an attached fragment 3. Detached but undisplaced fragment, with fluid around it 4. Displaced fragment 5. Subchondral cyst

Lesions over 100 mm2 in area, over 10 mm in diameter, or over 5 mm in depth, and uncontained shoulder lesions, have worse outcomes. Cartilage cannot heal, and untreated lesions can progress to ankle osteoarthritis.

• Deep ankle pain with weight bearing and activity, persistent beyond 6 weeks after a sprain
• Intermittent swelling, stiffness, catching, locking and giving way
• Tenderness at the anterolateral talar dome with the ankle plantarflexed, or posteromedial with the ankle dorsiflexed
• Effusion and reduced range of motion
• Red flags: a locked ankle (loose body), recurrent effusion, a persistent sprain beyond 6 weeks, and bilateral lesions

• Weight bearing radiographs (anteroposterior, mortise, lateral and plantarflexed views). They may be normal early.
• MRI is first line: marrow edema, fragment size and stability (a high signal line under the fragment suggests instability), cysts and associated ligament injury.
• CT for bone detail, loose bodies and quantifying lesion size and depth.
• SPECT-CT for activity in equivocal cases.
• Arthroscopy as both diagnostic and therapeutic step.

Differentials: chronic lateral ligament instability, anterolateral impingement, peroneal tendon pathology, talar or tibial stress fracture, ankle osteoarthritis, osteonecrosis, os trigonum syndrome.

Stage 1 and 2, stable, undisplaced lesions:

• Cast or boot, non-weight-bearing for 4 to 6 weeks, then progressive weight bearing with physiotherapy. About half of patients respond.
• Ibuprofen 400 mg orally every 8 hours with food for up to 7 days, and paracetamol 1 g every 6 hours.

Surgery after 3 to 6 months of failed conservative care, or for unstable or displaced fragments:

• Lesion under 100 mm2 (about 1 cm2) with no large cyst: arthroscopic debridement with bone marrow stimulation by microfracture (awls 1 to 2 mm, 3 to 4 mm apart, 3 to 4 mm deep) or drilling. Success about 80 to 85%.
• Large lesions (over 100 mm2), failed marrow stimulation or cystic lesions: osteochondral autograft transfer (often from the knee), osteochondral allograft, matrix induced autologous chondrocyte implantation or particulated juvenile cartilage.
• Unstable large fragment with viable bone: fixation with bioabsorbable pins or screws.
• Posteromedial lesions may need a medial malleolar osteotomy for access, fixed with two 3.5 or 4.0 mm screws.
• Cefazolin 2 g IV before incision. Enoxaparin 40 mg SC daily while non-weight-bearing.

Postoperative: non-weight-bearing for 2 to 6 weeks (6 weeks after osteotomy or graft), with early motion, then progressive weight bearing. Return to sport at 4 to 6 months after marrow stimulation and 6 to 12 months after grafting.

Complications: persistent pain, fibrocartilage of lower quality, donor site pain, nonunion of the osteotomy, infection and arthritis.

Follow up at 2 weeks, 6 weeks, 3 months and 6 months, with MRI at 12 months in selected cases. Counsel on activity modification.