Sinus Tarsi Syndrome

Sinus tarsi syndrome is an underdiagnosed cause of chronic lateral ankle pain following inversion injury. O'Connor first described it in 1958 as a clinical entity distinct from lateral ankle ligament injury. It represents chronic inflammation, synovitis and scarring of the soft-tissue contents of the sinus tarsi after they have been disrupted, and because the symptoms are vague and no test is specific, diagnosis is delayed by an average of 6-12 months from injury.

A label, not a lesion. "Sinus tarsi syndrome" is increasingly regarded as a descriptive umbrella term rather than a single discrete pathology (Frey 1999, Willegger 2023).

Who. Typically active adults, with reported series averaging around 30-41 years; the young active patient with an inadequately rehabilitated ankle sprain is the typical case. It is usually unilateral.

The precursor injury. Lateral ankle sprain is the commonest precursor. Ankle sprain incidence in the US general population is approximately 2.15 per 1000 person-years, peaking at 7.2 per 1000 at age 15-19 years, and half of sprains occur during sport, most often basketball, football and soccer (Waterman 2010). In one cohort, 22.5% of patients developed sinus tarsi syndrome after a lateral ankle sprain (Xu 2024).

Aetiology. The conventionally quoted figure is that 70-80% of cases follow an ankle inversion injury. The remaining 20-30% are non-traumatic: pes planus or hindfoot valgus impingement, or inflammatory arthropathy.

Risk factors. The predisposing factors are:

• Previous ankle inversion injury
• Chronic lateral ankle instability
• Repetitive microtrauma (running, jumping)
• Hindfoot valgus alignment
• Generalised ligamentous laxity
• Inflammatory arthropathy (RA, seronegative)

Proper ankle rehabilitation after a sprain, proprioceptive training and ankle bracing during sport are protective.

Sinus Tarsi Anatomy

The space. The sinus tarsi is a cone-shaped tunnel between the talus and calcaneus. Its wide opening faces laterally, anterior and inferior to the lateral malleolus; its narrow apex points medially and becomes the tarsal canal, which contains the posterior tibial neurovascular bundle.

• Superior: neck and body of the talus
• Inferior: superior surface of the calcaneus
• Medial: tarsal canal
• Lateral: opens between the anterior process of the calcaneus and the talar neck

View larger

At the bedside. The sinus tarsi is palpable anterior to the lateral malleolus, approximately 1-2 cm from the skin surface, and its lateral opening is 1-2 cm in diameter. Its rich vascular and nerve supply explains the severity of the pain.

The contents. Two ligaments bridge the space, and they are the structures debridement must preserve. The interosseous talocalcaneal ligament (ITCL) lies medially in the tarsal canal; the cervical ligament lies more laterally. Around them the space is filled with fat, synovium and a dense population of mechanoreceptors, and the inferior extensor retinaculum crosses its lateral opening.

View larger

View larger

Pathophysiology

The acute injury. The inversion injury disrupts the cervical and interosseous ligaments, contuses the fat pad with haemorrhage, inflames the synovial membrane and traumatises the nerve endings. This acute phase lasts 2-6 weeks.

The chronic phase. Chronic inflammation then develops: persistent synovitis, fibrosis and adhesions with scar formation, fat pad degeneration, loss of proprioceptive function and secondary subtalar instability. These changes perpetuate symptoms beyond 3-6 months.

Why it keeps hurting. The proposed mechanisms:

1. Mechanical compression: inversion crushes the lateral sinus tarsi contents between talus and calcaneus
2. Ligamentous disruption: partial tears of the cervical ligament and ITCL lead to microinstability
3. Proprioceptive loss: mechanoreceptor damage causes subjective instability and poor proprioception
4. Inflammatory cascade: chronic synovitis perpetuates pain
5. Scar tissue stenosis: adhesions narrow the sinus tarsi, causing impingement

History. The pain is deep, aching and poorly localised, a vague lateral hindfoot pain anterior to the lateral malleolus. It comes on gradually, weeks to months after an ankle inversion injury, and 70-80% report a sprain 3-12 months before. It is worse on uneven ground, stairs, slopes and lateral movements, with a sensation of instability or giving way.

The triad and its limits. Lateral pain, sinus tarsi tenderness and a sensation of instability make up the classic presentation, but the triad defines a region and a problem, not a specific lesion. Frey's arthroscopic series changed the diagnosis in all 14 feet labelled sinus tarsi syndrome, so treat the triad as the trigger for working out which structure is at fault rather than as the end of the diagnostic process.

Examination. Inspection is usually normal, perhaps with mild lateral swelling. Exquisite point tenderness over the sinus tarsi is the most reliable sign, though it localises the lesion rather than naming it. Subtalar motion is painful at the extremes of inversion and eversion, and the anterior drawer is usually negative unless there is a coexisting ATFL injury.

Differential diagnosis. Exclude these before settling on sinus tarsi syndrome:

• Lateral ankle instability: positive anterior drawer and talar tilt. It may coexist, is found in 30-40%, and should be addressed surgically if present
• Subtalar arthritis: older age, crepitus, reduced subtalar motion; radiographs show joint space narrowing
• Peroneal tendinopathy: tenderness posterior to the lateral malleolus, pain with resisted eversion
• Extensor tendinitis (EDB)
• Stress fracture of the calcaneus or talus: keep a high index of suspicion in athletes; MRI shows bone marrow oedema
• Tarsal coalition: congenital, rigid flat foot, usually a younger patient; CT is diagnostic
• Inflammatory arthropathy: rheumatoid, seronegative
• L5-S1 radiculopathy: back pain, dermatomal sensory loss, weakness
• Bone tumour: red flags of night pain and systemic symptoms

View larger

Clinical first. The diagnosis is primarily clinical, made on post-inversion lateral hindfoot pain and sinus tarsi point tenderness. With a typical presentation and a good response to initial conservative treatment, no investigation is required.

Radiographs. Weight-bearing AP, lateral and mortise ankle views are normal in isolated sinus tarsi syndrome, though they may show signs of chronic lateral instability. Their purpose is to:

• Exclude fractures, arthritis and tarsal coalition
• Assess hindfoot alignment (valgus, varus)
• Check for talar tilt (lateral instability)

View larger

MRI. MRI is the gold standard for diagnosis, with a sensitivity of 80-90% for sinus tarsi pathology, and it is how subtalar arthritis is excluded. The normal high T1 fat signal of the sinus tarsi is lost, replaced by low T1, high T2 inflammatory fluid and fibrotic tissue. On T2-weighted sequences look for:

• High signal intensity in the sinus tarsi (oedema, inflammation) and fat pad signal change
• Disruption or thickening of the cervical ligament
• ITCL signal abnormality
• Synovitis, synovial thickening and fluid in the subtalar joint

Read the report alongside the clinical picture. In Lektrakul's series MR over-called ligament tears against cadaveric specimens, and it confirmed the diagnosis in only 18 of 37 patients who carried it clinically.

View larger

Ultrasound. A dynamic, real-time and cost-effective assessment, though operator-dependent. It evaluates the sinus tarsi soft tissues, assesses the integrity of the cervical ligament, identifies fluid collections and guides injection.

View larger

View larger

Diagnostic injection. Under ultrasound or fluoroscopic guidance, 2 mL of 1% lidocaine is injected into the sinus tarsi. Immediate pain relief confirms the sinus tarsi as the pain source, with a specificity over 90%, and corticosteroid can be added for a therapeutic effect.

The pathway. Red flags and alternative diagnoses (fracture, infection, tumour, inflammatory arthropathy, peroneal pathology, subtalar arthritis) are investigated or referred first. Almost everyone is then treated non-operatively. If pain persists past 3 months, weight-bearing radiographs and an MRI confirm sinus tarsi inflammation and rule out subtalar arthritis, and a targeted local anaesthetic and corticosteroid injection is then both diagnostic and therapeutic. Only a minority, with six months of failed conservative care, an injection response that fades, MRI-confirmed pathology and activity-limiting pain, proceed to arthroscopic debridement.

Algorithm

View larger

How well it works. With activity modification, anti-inflammatory measures, physiotherapy and orthotics, 50-60% improve within 3 months. The 70-80% response rate refers to the full conservative package of physiotherapy, injections and proprioceptive training. Durability is the weak point: in the one cohort with 12-month follow-up, corticosteroid injection gave good relief at 1-3 months but around 65% of symptoms had recurred by a year (AOFAS falling 88.7 to 79.1). Physiotherapy with proprioceptive training is the part that lasts, so read the injection primarily as a diagnostic test that also buys time, and judge the response at 12 months, not 3.

Conservative Management (First-Line)

Indications for Surgery

Arthroscopic TechniqueOpen DebridementSubtalar Arthrodesis

Arthroscopic debridement. Compared with open surgery it offers smaller incisions, less soft-tissue disruption, faster recovery, better visualisation and a lower complication rate. The aim is to debride pathological tissue while preserving ligamentous stability.

Surgical Steps

SetupPositioning

• Lateral decubitus, affected side up
• Beanbag or lateral positioning device
• Thigh tourniquet
• Ankle and foot prepped free
• C-arm available for portal placement

Step 1Portal Placement

• Anterolateral portal (visualisation): just anterior to the tip of the lateral malleolus, at the level of the ankle joint
• Sinus tarsi portal (instrumentation): 1-2 cm anterior and inferior to the lateral malleolus, directly into the sinus tarsi opening

Mark portals before inflation to identify landmarks.

Step 2Arthroscopic Debridement

• Insert a 2.7 mm 30-degree arthroscope via the anterolateral portal and navigate to the sinus tarsi
• Inspect the contents: synovitis, adhesions, scar tissue
• Switch to the sinus tarsi portal for direct access
• Debride inflamed synovium with a shaver, thoroughly and gently to avoid iatrogenic damage
• Remove scar tissue and adhesions
• Preserve the cervical ligament and ITCL (do not excise)
• Irrigate thoroughly

Step 3Assess Subtalar Joint

• View the subtalar joint through the sinus tarsi and assess the articular cartilage
• If there is significant arthritis, reconsider the surgical plan; arthrodesis may be required instead

Step 4Closure

• Irrigate portals
• Close skin only, with nylon suture
• Soft compressive dressing
• Non-weight bearing for the first week in a boot

View larger

When to open. Failed arthroscopic debridement, the need for extensive debridement, surgeon preference or lack of arthroscopy equipment, and concurrent lateral ligament reconstruction. Recovery is slower than after arthroscopy, and immobilisation longer, but it allows lateral ligament reconstruction at the same sitting.

Open Technique

Step 1Incision

• Oblique incision over the sinus tarsi, 3-4 cm long
• Anterior and inferior to the lateral malleolus, parallel to the peroneal tendons

Step 2Exposure

• Dissect through subcutaneous tissue
• Identify and protect superficial peroneal nerve branches
• Retract extensor digitorum brevis
• Identify the sinus tarsi opening

Step 3Debridement

• Explore the sinus tarsi contents
• Excise the inflamed fat pad
• Debride synovium and scar tissue
• Preserve the cervical ligament and ITCL
• Curette any bony spurs

Step 4Concurrent Procedures

If lateral ankle instability is present:

• Brostrom repair of ATFL and CFL
• Tighten lateral structures
• Augment with suture tape if needed

Step 5Closure

• Irrigate wound
• Absorbable subcutaneous sutures, nylon to skin
• Below-knee cast or boot, non-weight bearing

When arthritis coexists. Subtalar arthrodesis is the definitive treatment for sinus tarsi syndrome with concomitant subtalar arthritis. Debridement alone has a 40-60% failure rate when arthritis is present; fusion addresses both pain sources and gives higher patient satisfaction than debridement in arthritis.

Technique. A lateral approach to the subtalar joint, debridement of the articular cartilage to subchondral bone, and two 7.0 mm cannulated screws, with bone graft if there is bone loss.

Return to activity. After arthroscopic debridement, walking returns at 6-8 weeks, running at 3-4 months and full sport at 4-6 months, with proprioceptive retraining critical to preventing recurrence. Open debridement is slower because of the soft-tissue disruption, typically adding 4-6 weeks, with full return at 5-6 months.

Red flags after surgery. Early identification prevents complications. The patient should contact the surgeon with:

• Increasing pain after initial improvement
• Signs of infection (fever, drainage, erythema)
• No improvement by 3 months
• New instability or giving way
• Numbness or tingling (nerve injury)
• Inability to bear weight by 6 weeks

Results. Arthroscopic debridement gives 70-80% good to excellent results and open debridement 65-75%. The best outcomes are in post-traumatic sinus tarsi syndrome without arthritis, treated early, in a patient who complies with proprioceptive training and responded to the diagnostic injection. Failed multiple injection attempts, like subtalar arthritis and inflammatory arthropathy, mark the patients who do worst.

Global Epidemiology

Guidance & Evidence Synthesis Across Bodies

Practice Variation

Differential Diagnosis