Lateral Ankle Instability

Lateral ankle instability is the most common sports injury worldwide, affecting athletes across all sports and age groups. It is chronic mechanical and/or functional instability of the lateral ankle complex after an ankle sprain. This page covers established instability. The acute injury that precedes it - grading, Ottawa rules and functional rehabilitation - is covered in lateral ankle sprains.

How common. There are about 23,000 ankle sprains a day in the United States, 1 per 10,000 person-days in the general population, and they make up up to 30% of all sporting injuries. They are most common in basketball, soccer and volleyball. Incidence peaks at 15-35 years, in the active population; the sex ratio is equal in the general population, with a higher female incidence in specific sports.

How many become unstable. Persistent symptoms and recurrent giving way are common, but reported rates vary widely with the population, the definition used and the length of follow-up. Use validated patient-reported instability measures and functional testing rather than any one population percentage.

Who is at risk.

• Previous ankle sprain, the strongest predictor
• Incomplete or inadequate rehabilitation
• Generalised ligamentous laxity: a Beighton score of 4 or more of 9 is the screening threshold used in the instability literature; the age-adjusted diagnostic cut-off for generalised joint hypermobility is 6/5/4 by age (see generalised ligamentous laxity)
• High-demand sports (basketball, soccer, netball)
• Hindfoot varus malalignment
• Cavovarus foot deformity
• Peroneal weakness or dysfunction

The ligaments. Three ligaments arise from the lateral malleolus and stabilise the ankle against inversion and anterior translation of the talus. They are injured in order of strength, weakest first: ATFL, then CFL, then PTFL, although the sequence is not absolute in every sprain. The PTFL, the strongest, fails only in severe trauma or ankle dislocation.

The ATFL is the one that matters most. It is the weakest of the three, failing at 58-90N, and the most commonly injured. It measures 20-25mm long and 10-12mm wide, has one to three bands (two most commonly), and lies horizontal in plantarflexion, becoming vertical in dorsiflexion.

The CFL is also 20-25mm long and runs 10-45° posterior to the long axis of the fibula, deep to the peroneal tendons. Its unique feature is that it crosses two joints, the ankle and the subtalar joint, so a CFL injury affects subtalar stability as well. That fact returns in concurrent subtalar instability, below.

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Mechanism. The typical injury is inversion in plantarflexion, and combined injuries are common. In plantarflexion the narrower posterior talus sits in the mortise, so there is less bony stability, and the ATFL becomes the primary restraint and the first to fail. With greater force the CFL is injured next, by inversion in dorsiflexion.

Dynamic stabilisers. Peroneus longus and brevis are the primary dynamic stabilisers, with extensor digitorum longus as secondary support. Proprioceptive afferents are critical for neuromuscular control, and peroneal reaction time is delayed in chronic instability.

History. Start with the index injury: its mechanism, and how it was treated and rehabilitated. Then establish the current picture:

• Symptoms: giving-way episodes, pain, swelling
• Functional limitation: sport, uneven ground, stairs
• Prior treatment: duration of physiotherapy, bracing

Red flags. Locking suggests a loose body, medial pain the deltoid, and persistent swelling an osteochondral lesion.

Radiographs. Standard weight-bearing views are the essential first-line imaging:

• Weight-bearing AP: mortise alignment, osteochondral lesion
• Mortise view: lateral clear space
• Lateral: talar dome, anterior impingement

Stress radiographs are for selected cases, when objective documentation will change treatment or clarify the examination. Anterior translation and talar tilt measurements are technique- and position-dependent; side-to-side comparison and image quality matter more than a universal cut-off. Normal stress values do not exclude functional instability.

MRI. Clinical examination remains the primary diagnostic tool, even though MRI has high sensitivity. MRI is indicated for:

• Diagnostic uncertainty
• Suspected osteochondral lesion
• Preoperative planning
• Associated pathology (peroneal, syndesmosis)

The ATFL shows discontinuity, thickening or signal change, and the CFL is often better seen on axial images. MRI also shows talar dome osteochondral lesions, a common association, and peroneal tendon tears or subluxation.

CT and ultrasound are reserved for specific clinical scenarios. CT characterises an osteochondral lesion, assesses bony morphology and plans malalignment correction. Ultrasound is operator dependent but assesses the ligaments and peroneal subluxation dynamically, and is a cost-effective screening test.

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Associated pathology. These are the conditions to exclude:

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The decision runs in four steps:

1. Confirm the phenotype: functional, mechanical or combined, and any associated pathology.
2. Rehabilitate progressively, judging the response by function rather than a fixed number of months.
3. Repair when tissue is repairable; reconstruct when the pattern or the tissue makes repair unreliable.
4. Correct deforming forces and concomitant pathology that would otherwise cause failure.

Rehabilitation is first-line and remains the foundation for mechanical, functional and combined instability. It is progressive and has five components:

1. Proprioceptive and perturbation training
2. Peroneal and global lower-limb strength
3. Range restoration and calf capacity
4. Bracing or taping for selected activities
5. Running, cutting, landing and sport-specific progression

When has it failed? Duration is response- and goal-dependent, and a calendar alone does not define failure. Document giving-way frequency, patient-reported instability, balance, hop and cutting tasks, strength and confidence. The 3-6 month threshold is pragmatic rather than evidence-defined.

Surgical indications. Consider surgery when:

• Recurrent giving way or instability limits desired function despite a well-delivered rehabilitation programme
• Mechanical laxity or repairable pathology correlates with symptoms
• Alignment and associated osteochondral, peroneal, syndesmotic, impingement or subtalar disease have been assessed
• Patient goals and postoperative rehabilitation capacity support the plan

Athletic level, laxity and patient preference modify treatment but are not stand-alone indications.

Choosing the operation. The options, and when each applies:

• Anatomic repair - direct ATFL ± CFL repair when local tissue quality and excursion permit. Inferior extensor retinaculum augmentation is selective, not mandatory, and open and arthroscopic approaches both have supporting evidence.
• Anatomic reconstruction - consider for poor tissue, failed prior repair, major deformity or laxity, or a multiligament pattern that cannot reliably be repaired. The graft and tunnel strategy should recreate the required ATFL and CFL functions while protecting subtalar motion.
• Alignment and associated pathology - correct clinically important cavovarus or another deforming force when it would overload the repair, and treat osteochondral lesions, impingement, syndesmosis and peroneal pathology in the same plan when indicated.

Historical non-anatomic tenodeses restrict motion and are now salvage rather than routine choices.

Intraoperative. Nerve identification is the key to preventing intraoperative complications; the superficial peroneal nerve is the nerve most commonly injured.

Early (less than 6 weeks). Wound dehiscence occurs in 2-5%, superficial infection in 1-3%, deep infection in less than 1% and haematoma in 1-2%. Careful surgical technique minimises them, and prevention is layered closure, appropriate immobilisation, early mobilisation within the protocol, and DVT prophylaxis. Treat with wound care and antibiotics as needed, and return to theatre for a deep infection.

Late (greater than 6 weeks). Late complications often require revision surgery. Recurrence risk varies with tissue, alignment, laxity, sport and rehabilitation.

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Rehabilitation protocol. Early immobilisation protects the healing repair, and protected mobilisation from two weeks allows healing while preventing stiffness. Proprioceptive training is critical for functional recovery, and a gradual return to sport prevents re-injury.

Return to sport requires:

• Full pain-free range of motion
• Strength equal to the contralateral side
• Completed agility testing
• Sport-specific drills without symptoms

Rehabilitation. Without surgery, 70-80% stabilise. Results are best with supervised physiotherapy; proprioceptive training is key to success and peroneal strengthening essential. Bracing for sport may be permanent.

Repair and reconstruction. The Broström-Gould repair has a lower revision rate than non-anatomic procedures. Anatomic reconstruction has a higher revision rate than a primary Broström and a longer rehabilitation.

Prognostic factors.

Global Epidemiology

• Ankle sprain is among the most common musculoskeletal injuries worldwide; the lateral ankle sprain is the dominant subtype (Doherty meta-analysis of 181 prospective studies).
• Incidence is higher in females than males (13.6 vs 6.94 per 1000 exposures) and in indoor/court sports (basketball, volleyball, netball, handball).
• Approximately 20-40% of acute sprains progress to chronic instability; the Cochrane review cites ~10-20% developing chronic lateral instability.
• A prior sprain remains the single strongest predictor of recurrence regardless of region or healthcare setting.

Side-by-Side Guidelines & Consensus

Registry & Outcome Notes

• Unlike arthroplasty, lateral ankle stabilisation is not tracked in national joint registries (NJR, AOANJRR, SHAR); evidence derives from cohort series, meta-analyses, and consensus statements rather than registry survivorship.
• Reported recurrence after anatomic repair is broadly 5-15%, higher with generalised laxity - the rationale for suture-tape augmentation or reconstruction in selected patients.

High- vs Limited-Resource Practice Variation

• High-resource settings: Ready access to MRI, stress imaging, arthroscopy, and suture-tape/InternalBrace augmentation; arthroscopic Broström increasingly favoured for lower wound morbidity.
• Limited-resource settings: Diagnosis is largely clinical (Ottawa rules, stress testing); supervised neuromuscular rehabilitation and bracing carry the management burden, with open anatomic repair the mainstay where surgery is indicated.
• The conservative-first, rehabilitation-led pathway is universal and equally valid across all settings - the major global driver of good outcomes.

The biomechanical problem. In a varus or cavovarus hindfoot the ground-reaction force passes medial to the subtalar joint axis, generating a constant inversion (supination) moment across the ankle and hindfoot. The lateral ligaments are chronically loaded, which predisposes to the original recurrent sprains.

Why the repair fails. After surgery the same moment places a persistent stretching force on a Broström-Gould repair, so an isolated soft-tissue repair on an uncorrected varus hindfoot is prone to gradual stretch-out and recurrent instability. Failing to recognise and correct hindfoot varus is one of the leading causes of an otherwise technically sound repair failing.

Sorting out the deformity. The assessment itself belongs to the cavovarus foot work-up: standing hindfoot alignment, a standing hindfoot-alignment (long-axial) radiograph, and the Coleman block test. The block decides whether the varus is forefoot-driven, a plantarflexed first ray that corrects on the block and is flexible, or a fixed hindfoot varus that does not correct. This topic's job is deciding which bony procedure, if any, must accompany the ligament surgery.

The surgical corollary. The ligament repair or reconstruction is done on a balanced, plantigrade foot:

• Fixed hindfoot varus - add a lateralising, valgus-producing calcaneal osteotomy (Dwyer lateral closing-wedge, or a lateral-translation/Z-type osteotomy) to move the weight-bearing axis lateral to the subtalar joint and unload the lateral repair
• Forefoot-driven varus (Coleman block positive, correcting on the block) - a dorsiflexion (dorsal closing-wedge) osteotomy of the first metatarsal addresses the plantarflexed first ray
• Peroneal balance - consider a peroneus longus-to-brevis transfer, strengthening eversion, where longus overdrive plantarflexing the first ray is driving the varus

Symptoms. The patient describes the hindfoot "rolling" or giving way on uneven ground, sometimes with a medial-hindfoot ache, persisting despite an apparently competent ATFL. The instability may feel deeper or more posterior than a pure ankle giving-way.

Examination is difficult because ankle and subtalar motion couple. Look for a medial subtalar glide or tilt and reproduction of the "rolling" sensation; CFL insufficiency (a positive talar tilt) should raise suspicion.

Imaging. Broden views and subtalar stress radiographs are described to demonstrate talocalcaneal tilt, but normative values are poorly standardised and the tilt is difficult to separate from ankle (talar) tilt, so the diagnosis remains substantially clinical. CT and MRI mainly exclude other hindfoot pathology and coalition.

Treatment. Rehabilitation comes first, exactly as for the lateral ankle, with proprioceptive and peroneal work. At surgery, because the CFL is the shared restraint, an isolated ATFL-only Broström is inadequate: the reconstruction must extend distally to the calcaneus and recreate the CFL, and an anatomic reconstruction reproducing both the ATFL and CFL footprints is preferred.

Why not a tenodesis. The older non-anatomic tenodeses (Chrisman-Snook, Evans) did restrain subtalar motion, but at the cost of subtalar stiffness and later arthritis, a key reason anatomic techniques that preserve subtalar motion are now favoured.

Open versus arthroscopic repair. Meta-analyses show comparable stability with lower wound morbidity arthroscopically. Longer-term durability and learning-curve data are still maturing, and no high-level RCT establishes clear superiority of either approach.

Suture-tape (InternalBrace) augmentation. It is biomechanically stronger and allows earlier loading, but its clinical benefit over standard repair is small and short-term. Concern about over-constraint and cost-effectiveness remains unresolved.

Repair versus reconstruction in laxity. Direct repair has a higher failure rate in generalised laxity (Beighton ≥4), but the optimal threshold for choosing graft reconstruction is not standardised. Augmented repair may bridge the gap but lacks long-term comparative data.

Early surgery in elite athletes. Whether acute repair of complete grade III ruptures in high-level athletes shortens return to sport compared with functional treatment remains debated; most evidence still favours rehabilitation first.

Rehabilitation dose. The ideal duration, supervision intensity and balance or neuromuscular protocol are not standardised across guidelines.

Imaging. The role of weight-bearing CT and dynamic imaging in routine assessment is evolving and not yet consensus practice.