Incidence of Recurrent Ankle Instability

Most acute injuries are treated by a rehabilitation program. The remaining 15% to 20% who remain symptomatic may require surgical intervention.¹ In the United Kingdom, 302,000 sprains are treated per year.² Recurrent sprains may result in more lost days of sport than the initial injury.³

Anatomy of the Lateral Collateral Ligaments

The lateral collateral ligaments stabilize the ankle joint to episodes of inversion sprains. The anterior talofibular ligament runs from the anterior aspect of the fibula to the neck of the talus laterally at its junction to the body of the talus.⁴ The calcaneofibular ligament starts just inferior and posterior to the origin of the talofibular ligament, and inserts into the lateral border of the calcaneus running posteriorly.⁵ The talofibular ligament therefore stabilizes the ankle by preventing the talus from subluxing anteriorly in the ankle mortise, whereas the calcaneofibular ligament prevents inversion of both the talus and calcaneus at the ankle joint and subtalar joint, respectively.

Pathoanatomy

Rupture of the lateral ligaments may cause instability in the ankle, in the subtalar joint, or both. During an acute episode of instability, the talus will rotate within the ankle mortise and can subject a shear load onto the cartilage on the dome of the talus. The medial dome may impinge on the medial side of the distal tibia causing a central to posteromedial chondral injury. Alternatively, the lateral dome may impinge on the fibula causing a posterolateral injury. Ongoing instability and the chondral injury can cause further cartilaginous degeneration, allowing the ankle joint to become inflamed with associated synovitis. If long-term instability is persistent, significant ankle degeneration occurs with osteophytes formation, both of which may cause symptomatic impingement. Inversion sprains may also overload the peroneal tendon complex, causing stretching or incompetency of SPR, peroneal subluxation/injury, and synovitis.

The anatomy of the hindfoot has a critical effect on the loading of the lateral ligament complex. A cavus foot position may cause medial displacement of the joint reaction force in the ankle, increasing strain on the lateral collateral ligaments.⁶ Posterior displacement of the tip of the fibula has been hypothesized as being the cause of recurrent instability. These anatomic variations may, however, represent part of a constellation of cavus foot deformity.⁷ Symptomatic chronic instability may be caused by the combination of foot shape and an acute injury. A study of patients with ankle instability awaiting surgery compared with normal control subjects showed that those with instability had a more varus heel.⁶

Limitations of Outcomes Studies

In the Cochrane database review, no evidence was found to support acute lateral ligament reconstruction compared with conservative treatment. However, the studies analyzed were not designed well enough to definitively answer the question.⁹ The obvious limitations of articles on recurrent lateral ankle instability include retrospective design with nonvalidated outcome scores without control groups. Less obvious may be the presence or absence of copathologies with ankle instability. Hintermann and colleagues¹² report on 148 patients with medial or lateral instability. Cartilage injury was found in 66% of patients with lateral instability, and 98% of patients with medial instability. Another study showed a 98% rate of intra-articular pathology is associated with lateral ankle instability. The author notes the most common finding was synovitis with a 25% rate of chondral injuries in the ankle.¹³ Other authors have documented similar findings.^13–15 Injury to the peroneal tendons and tendonitis are associated with recurrent lateral ankle instability^16,17 with 25% of patients having a peroneal tendon injury.

In summary, older studies do not address the copathologies, nor do they discuss or outline their concomitant treatment protocol on finding these associated issues. For this reason alone, the outcomes for ankle ligament stabilization may be improved in recent articles with the advent of routine magnetic resonance imaging (MRI) and ankle arthroscopy, and treatment of osteochondral defects. Based on the Level IV studies, a grade I recommendation exists for the routine use of advanced diagnostic testing, such as MRI. The diagnostic role of routine arthroscopic debridement at the time of lateral ligament reconstruction has not been determined; however, its use is now recommended by some authors^15,18 (grade I). More studies are required in regard to this specific issue.

Nonoperative Treatment of Recurrent Ankle Instability

Nonoperative treatment of recurrent ankle instability may include casting, bracing, anti-inflammatory medication, taping, and physiotherapy. A review of the literature showed a number of studies related physiotherapy, cast, and brace treatment. Most of these modalities are used in combination. Physiotherapy seems to be better studied and the outcomes outlined better than brace treatment.

Surgical Treatment of Recurrent Ankle Instability

After failed nonoperative treatment of ankle instability, patients may opt for surgical stabilization. The ligaments may be repaired or reconstructed. In the Broström repair, the torn ligaments are imbricated and may be augmented by the extensor retinaculum (Gould modification). Karlson modified the Broström technique by recommending repair through drill holes in bone.

Alternatively, the ligaments can be reconstructed. The reconstruction can be either anatomic or nonanatomic. Nonanatomic reconstructions include the Evans procedure (rerouting of the peroneus brevis through the fibula) or the Watson–Jones procedure (peroneal tendon weave). These reconstructions as a result sacrifice the active evertors of the ankle for a static restraint. Because the reconstruction is nonanatomic, joint motion may be restricted, so that the Evans procedure, for example, restricts subtalar joint motion.^37,38 In one retrospective case–control study with long-term follow-up, the rate of arthritis, ongoing instability, and reoperation rate all favored anatomic repair over Evans tenodesis.³⁹ Nine studies recommend against the use of nonanatomic reconstructions.^39–47 Another study showed impaired kinematics after Evans tenodesis and recommended against its use.⁴² In a review of patients undergoing the Broström procedure compared with the Christman–Snook nonanatomic reconstruction, patients with the reconstruction complained of the ankle feeling “too tight.”⁴⁸ Current opinion supports the use of an anatomic reconstruction or repair without sacrifice of the active evertors of the ankle.