Retrocalcaneal Bursitis

Retrocalcaneal bursitis is inflammation of the bursa between the Achilles tendon and the posterosuperior calcaneus. It is often associated with Haglund's deformity, a posterosuperior calcaneal prominence, and it has to be told apart from its two neighbours: superficial calcaneal bursitis in the retroachilles bursa between skin and tendon, and insertional Achilles tendinopathy.

The key clinical finding is the two-finger squeeze test. Conservative management (activity modification, NSAIDs, heel lifts) succeeds in 80-90%. The trap is the injection: steroid directly into the bursa risks Achilles rupture. Refractory cases come to bursectomy with or without Haglund resection.

Mechanism. Repetitive compression of the bursa during activity leads to an inflammatory response within the bursal sac.

Haglund's deformity. Named after the Swedish orthopaedic surgeon Patrick Haglund (1928), it is a prominent posterosuperior calcaneal tuberosity, the "pump bump". When it is joined by the other two elements it forms the classic triad of Haglund syndrome:

• Posterosuperior calcaneal prominence
• Retrocalcaneal bursitis
• Insertional Achilles tendinopathy

The geometry of the prominence is quantified on the lateral radiograph, described under Investigations.

The retrocalcaneal bursa. A synovial bursa sitting deep to the Achilles, with the tendon behind it and the posterosuperior calcaneal tuberosity in front, just anterior to the Achilles insertion. Its superior boundary is the substance of the tendon and its inferior boundary the superior aspect of the calcaneal attachment; the insertion itself lies on the posterior calcaneus below the bursa. It does not communicate with the ankle joint. Normally it measures 6mm anteroposterior by 3mm deep and holds less than 1mL of synovial fluid.

What it does. The bursa reduces friction between the Achilles and the calcaneus during ankle dorsiflexion. Compression is greatest at end-range dorsiflexion, and a Haglund prominence on the posterosuperior tuberosity increases the compressive load on it.

The superficial calcaneal bursa. Also called the retroachilles or subcutaneous calcaneal bursa, it lies between the Achilles tendon and the skin, behind the tendon. It develops in response to friction from the shoe counter and produces the pump-bump tenderness of shoe pressure, presents as visible swelling at the back of the heel, and often coexists with retrocalcaneal bursitis.

Vessels and nerves. The bursa is supplied from the adjacent soft tissues. The Achilles tendon has a watershed area 2-6cm proximal to its insertion. The sural nerve is at risk in the surgical approach; its course and how to protect it are set out under Surgical Technique.

There is no validated severity grading system for retrocalcaneal bursitis, and examiners expect you to say so. The condition is classified instead by its cause and by the pathology that comes with it, and it is the presence and extent of associated Achilles and bony disease, not a numeric grade, that drives treatment planning and the choice of surgical approach.

By aetiology. Mechanical, inflammatory or septic.

By associated pathology. This is the axis that guides treatment. Isolated bursitis has the best prognosis and responds better to conservative management than combined pathology.

• Isolated bursitis - bursal inflammation alone, without bony or tendon involvement
• Haglund syndrome - prominence, retrocalcaneal bursitis and insertional Achilles tendinopathy together
• Combined superficial and deep bursitis - both bursal spaces involved

A descriptive gradation follows the same axis: mild is bursal inflammation only with minimal functional limitation, moderate adds a Haglund deformity, and severe is combined pathology with insertional Achilles tendinopathy.

The typical patient. A 40-year-old recreational runner presents with six months of posterior heel pain, worse on running and particularly at push-off, aggravated by rigid-heeled shoes, with a noticeable prominence at the back of the heel.

Why that history fits. Push-off is maximal ankle dorsiflexion under load, which is exactly when the calcaneal tuberosity is driven into the anterior surface of the Achilles and the bursa between them is compressed; pain at push-off rather than at heel strike is the discriminating detail. The rigid heel counter compresses the same area from outside, which is why footwear is both an aggravating factor and the first thing to change. The prominence is the Haglund deformity, a pre-existing bony shape that narrows the space; the running did not create it.

The rest of the history. Onset is gradual, and the pain is worse with activity, running and jumping especially, and with direct pressure on the posterosuperior heel. Morning stiffness that improves with initial activity is part of the picture. Establish the duration, the relationship to activity and sport, the footwear, the treatments already tried, and any systemic symptoms: bilateral disease with morning stiffness suggests an inflammatory cause.

Red flags for another diagnosis. Each of these points somewhere else:

• Acute onset - Achilles rupture
• Night pain - infection or tumour
• Bilateral symmetric involvement - inflammatory arthropathy
• Fever or constitutional symptoms - septic bursitis

Examination

Inspection. Standing, look at hindfoot alignment (varus predisposes to lateral impingement), for a visible posterosuperior prominence, for erythema suggesting superficial bursitis, and for swelling anterior to the Achilles insertion. The two bursae look different from behind: superficial bursitis gives obvious fluctuant swelling superficial to the Achilles, whereas retrocalcaneal bursitis shows only subtle fullness on either side of the tendon.

Gait. Antalgic, with a shortened stance phase and reduced push-off power; the patient may adopt a toe-walking pattern to avoid dorsiflexion. Check for a limb length discrepancy.

Palpation. Work through the posterior heel in order:

1. Achilles tendon substance - nodularity or thickening
2. Achilles insertion on the calcaneus - tenderness here suggests insertional tendinopathy
3. Retrocalcaneal space - anterior to the Achilles on either side
4. Posterosuperior calcaneus - the bony prominence
5. Superficial bursa - between Achilles and skin

Separating bursa from tendon. Palpate with the ankle in slight plantarflexion, which relaxes the Achilles and lets you get in front of it. Tenderness that remains anterior to the slack tendon is bursal; tenderness that moves with the tendon is tendinous. This works because the bursa lies deep (anterior) to the tendon, between it and the calcaneus, so relaxing the tendon uncovers the bursa instead of dragging your finger over it.

The two-finger squeeze test. Compress the area just anterior to the Achilles between thumb and index finger, from medial and lateral; a positive test reproduces the characteristic pain. Its sensitivity is reported as high in clinical teaching, but no validated figure exists. It is more specific than simple palpation of the posterior heel, and done with the ankle plantarflexed it isolates the bursa.

Coexistence. Bursitis and insertional tendinopathy coexist in roughly a third of patients, and the superficial bursa adds a third possible pain generator behind the tendon. Localising the pain decides whether treatment targets the footwear and the superficial bursa, the deep bursa and the bony prominence, or the tendon insertion itself.

Range of motion. Measure dorsiflexion with the knee extended (gastrocnemius tight) and flexed (gastrocnemius relaxed); normal is 15-25° with the knee extended. Ankle equinus, dorsiflexion less than 10°, is present in approximately 60% of patients and contributes to bursal pressure during gait; assessment should include both the gastrocnemius and the soleus contribution. Pain at end-range dorsiflexion suggests bursal compression.

Provocative tests. Four manoeuvres:

• Forced dorsiflexion - passive ankle dorsiflexion compresses the bursa and reproduces posterior heel pain
• Resisted active plantarflexion - may reproduce pain if the Achilles is involved
• Single heel raise - assesses Achilles function and reproduces pain
• Painful arc - pain in a specific arc of ankle motion, typically mid to end-range dorsiflexion, indicating bursal compression during movement; it helps differentiate from Achilles tendinopathy

Excluding the alternatives. Thompson test to rule out Achilles rupture (it should be negative) and Simmonds test for Achilles continuity. Check for sinus tarsi tenderness (lateral hindfoot pathology) and palpate the tarsal tunnel structures (posterior tibial nerve). A complete examination takes in the whole kinetic chain, since hip rotation, knee alignment and foot pronation can all contribute to abnormal heel loading.

Radiographs first. The weight-bearing lateral is the primary study, because it shows the Haglund prominence and the bony anatomy, though it gives no soft tissue detail; weight-bearing is preferred so that the calcaneus sits in its true position. An AP view rules out other hindfoot pathology, and a calcaneal axial view is added if indicated.

Measuring the prominence. Several measurements quantify the posterosuperior calcaneus on the lateral view:

• Parallel pitch lines - a first line along the plantar aspect of the calcaneus, a second from the posterior plantar calcaneus to the posterosuperior corner, and a third from the posterior plantar calcaneus to the medial tubercle; Haglund deformity is present if the posterosuperior corner lies above the second line
• Fowler-Philip angle - the intersection of a line parallel to the calcaneal undersurface and a line from the posterosuperior corner to the medial tubercle. Normal is 44-69°. More than 75° indicates a prominent posterosuperior tuberosity, and angles less than 44° are associated with increased retrocalcaneal pressure and an increased risk of retrocalcaneal bursitis
• Posterior calcaneal angle (Chauveaux-Liet angle), increased in Haglund deformity
• Calcaneal inclination (pitch) angle

How far to trust them. Treat these thresholds with caution. In Tang's series of operated Haglund deformities (see Evidence Base), the Fowler-Philip angle and parallel pitch lines did not separate patients from asymptomatic controls, whereas bump height and the bump-calcaneus ratio did.

View larger

Ultrasound, MRI and CT. MRI is for diagnostic uncertainty or surgical planning; ultrasound assesses the bursa and guides injection.

Reading the MRI. A standard ankle protocol with sagittal, axial and coronal sequences; T2-weighted and STIR images best show bursal fluid. The finding is a triangular area of high signal between the Achilles and the calcaneus on the sagittal images, the bursa taking the shape of the space it occupies.

Two cautions. A small amount of fluid in this bursa is normal, and asymptomatic bursal fluid is present in 20% of normal subjects on MRI, so the diagnosis rests on distension plus surrounding inflammatory change and always on correlation with the clinical findings. And the scan should answer a specific question: is the Achilles insertion itself diseased, is there intratendinous change or a partial tear, and is the posterosuperior prominence the driver? Those answers decide whether treatment is bursa-directed or must address tendon and bone, and they are the reason to image a diagnosis that is otherwise clinical.

Blood tests. Order them for bilateral involvement, recurrent or refractory disease, constitutional symptoms, features of inflammatory arthropathy, or a young patient with no clear mechanical cause:

• ESR and CRP - elevated in inflammatory arthropathy
• Rheumatoid factor and anti-CCP antibodies
• HLA-B27 for seronegative spondyloarthropathy
• Uric acid if gout is suspected
• Full blood count if infection is a concern

Aspiration. Rarely indicated; consider it if septic bursitis is suspected. Send the fluid for cell count, Gram stain, culture and crystal analysis. Cloudy fluid with an elevated white cell count suggests infection, and crystals may indicate gout or pseudogout.

The sequence. Structured conservative care comes first and fixes most patients. The programme is staged, with a minimum trial of 12 weeks and reassessment at 3-6 months, and surgery is considered only after at least 6 months of failed treatment.

Activity. Reduce or stop the aggravating activities, avoiding hill running and excessive dorsiflexion, and cross-train with low-impact exercise such as cycling or swimming. Return to sport follows a gradual protocol once symptoms resolve.

Footwear. A soft heel counter, or none at all, and a wider heel box to reduce compression. Heel lifts of 6-12mm reduce dorsiflexion stress. New or poorly fitted shoes are avoided.

Physiotherapy. Eccentric Achilles strengthening, gastrocnemius and soleus stretching, manual therapy for soft tissue mobilisation, and ultrasound therapy for its anti-inflammatory effect. Biomechanical factors such as equinus and a varus hindfoot are addressed.

Medication. NSAIDs for 2-4 weeks if there is no contraindication, with topical NSAIDs as an alternative, and simple analgesics for pain. Oral corticosteroids are avoided (limited evidence).

Injection. The Achilles lies immediately adjacent to the bursa and corticosteroid weakens tendon structure. High-quality evidence for steroid injection is limited, and the rupture risk outweighs the potential benefit in most cases. Evidence for PRP or autologous blood injection is insufficient.

If an injection is given at all, it is under imaging guidance and the patient is counselled about the rupture risk.

Shockwave therapy. Low to moderate energy ESWT, typically 3-5 sessions over 6-12 weeks, may stimulate healing and reduce inflammation. The evidence for it in retrocalcaneal bursitis specifically is limited; there is more for insertional Achilles tendinopathy, and there the highest-level trial (Mansur, in the Evidence Base) found that adding shockwave to eccentric loading did not improve the outcome at 24 weeks.

Surgery

Indications. Surgery is considered for:

• Failure of conservative treatment for a minimum of 6 months
• Significant functional impairment affecting daily activities or sport
• MRI-confirmed retrocalcaneal bursitis, with or without a Haglund deformity
• Patient understanding of the post-operative rehabilitation requirements
• Optimisation of comorbidities - smoking cessation and diabetes control

Matching the operation to the pathology. Three patterns, three operations:

• Isolated bursitis - bursectomy alone may suffice
• With Haglund deformity - bursectomy plus calcaneal ostectomy
• With insertional tendinopathy - may require Achilles detachment and reattachment

FHL transfer to augment the insertion

When. Augment when more than 50% of the Achilles insertion has to be detached or debrided. The transfer adds strength and brings blood supply, and it guards against post-debridement rupture.

Why the FHL. It is the strongest expendable posterior-compartment tendon. Its muscle belly is low-lying and vascularised, bringing blood supply to a poorly vascular insertional zone; it is in phase with the gastrocnemius-soleus (both plantarflex); and it lies immediately deep to the Achilles, so it is harvested through the same wound.

Harvest. The FHL is found deep to the Achilles through the posteromedial part of the exposure. A single-incision harvest divides it as far distally as can be reached behind the ankle; a two-incision technique adds a medial midfoot incision for extra length, and then the medial and lateral plantar nerves must be protected at the master knot of Henry, where the FHL crosses the FDL.

Fixation. After the bursectomy, Haglund resection and tendon debridement, the FHL goes into a calcaneal bone tunnel or is fixed with an interference screw or anchor just anterior to the debrided Achilles footprint, tensioned with the ankle in slight plantarflexion. The residual Achilles insertion is then reattached over it with suture anchors.

The cost. Loss of independent hallux interphalangeal flexion, which is well tolerated because the FDL and the intrinsics compensate. The FHL transfer for chronic Achilles rupture is developed in the Achilles-rupture topic.

Protecting the sural nerve

Course. The sural nerve is the structure most at risk in posterolateral hindfoot surgery, with an injury rate of about 3%. It forms in the calf from the medial sural cutaneous nerve (from the tibial nerve, between the two heads of gastrocnemius), usually joined by a peroneal communicating branch. It pierces the deep fascia in the mid-calf, runs alongside the small saphenous vein, and passes about 1-1.5cm posterior (and slightly inferior) to the lateral malleolus. It then curves forward below the malleolar tip toward the base of the fifth metatarsal, supplying sensation to the posterolateral leg, lateral heel and lateral border of the foot.

Why it is at risk. In a posterolateral approach to the retrocalcaneal space the nerve lies just anterolateral to the Achilles at the operative level. A too-lateral incision, retractor pressure or a distal-lateral endoscopic portal can catch it, producing lateral heel and foot numbness or a painful neuroma.

Staying safe. Keep the incision just lateral to the Achilles midline but posterior to the nerve's course, and dissect bluntly straight down to bone. For endoscopic calcaneoplasty, place the lateral portal at the superior calcaneal level with care, respecting the small saphenous vein: it is the surface marker, because the nerve runs with it.

Open or endoscopic

Reading the two studies together. The pooled review below reports markedly fewer complications and failures endoscopically, while a single-unit cohort comparing both techniques found no difference in any score. Pooled series compare surgeons who chose the technique they favour, so the honest position is that endoscopy is at least equivalent and probably lower-morbidity; the choice rests on the extent of Achilles involvement and on the surgeon's expertise.

Wound healing. Delayed healing follows from the tenuous soft tissue coverage of the posterior heel. Most infections are superficial wound infections; deep infection is rare but serious.

Sural nerve injury. Numbness over the lateral heel and foot, and painful neuroma formation. Management is stepped: observation and desensitisation first, neuropathic medication such as gabapentin for persistent pain, and surgical excision of a symptomatic neuroma with burial of the nerve.

Achilles rupture. The key modifiable risk factor is the extent of debridement: the risk rises with aggressive debridement and is higher when more than 50% of the insertion is debrided. Limit debridement of the insertion to less than 50%, and protect weight-bearing after surgery.

Recurrence. Inadequate Haglund resection is the most common cause; failure to address the biomechanical factors is another. Revision means reassessing the adequacy of the first resection, performing an adequate calcaneal ostectomy, and dealing with any contributing factor left untreated. The resection should be adequate but not excessive.

Milestones. Wound healed and sutures out at 2 weeks, full passive range at 6 weeks, a pain-free single heel raise at 12 weeks, and return to running and sport at 4-6 months.

If the Achilles was detached. Everything slows down: plantarflexion positioning is extended to 4 weeks, active range of motion is delayed to 4-6 weeks, strengthening progresses more gradually, and return to sport is typically 6-9 months rather than 4-6. Where more than 50% of the insertion was detached or debrided and FHL augmentation used, weight-bearing is protected for 6 weeks, and early aggressive rehabilitation risks Achilles rupture.

Conservative treatment. Resolution takes on average 3-6 months, and 10-15% recur on returning to previous activity levels. Early intervention, good compliance and modification of the risk factors predict success. Complications of conservative care are minimal, and return to sport after it is variable.

Surgery. Good to excellent results in around 85% at 3-5 year follow-up (approximate, from pooled surgical series), with 90% achieving significant pain improvement and satisfaction of 88-91%. AOFAS hindfoot scores improve from 52 to 88. Return to the previous activity level is 75-80%, and the overall complication rate is 11%.

What predicts the result. Outcomes are better with isolated retrocalcaneal bursitis without Achilles pathology, a mechanical rather than inflammatory cause, an adequate non-operative trial before surgery, good surgical technique with complete resection, excellent rehabilitation compliance, and not smoking. They are worse with inflammatory arthropathy as the underlying cause, extensive Achilles pathology requiring detachment, a workers' compensation claim or litigation, smoking or uncontrolled diabetes, and previous failed surgery. Workers' compensation claims and smoking are independent predictors of a poor outcome. Address the modifiable factors before operating.

Recurrence risk factors. Recurrence is more likely with:

• Inadequate Haglund resection
• Persistent equinus contracture
• Returning to high-impact activities too quickly
• Failure to modify footwear
• An underlying systemic inflammatory condition

In the long term. Most patients keep a good result if they continue their activity modifications, and a small percentage develop insertional Achilles tendinopathy later. Ongoing Achilles flexibility and strength work matters, with reassessment if symptoms recur.

Related pages: Haglund Syndrome is the same clinical territory approached from the bone rather than the bursa, and the two pages should be read together - Haglund's is the posterosuperior prominence, retrocalcaneal bursitis is the inflamed bursa it impinges, and most operated patients have both; Achilles Tendinopathy for the insertional disease that completes the triad and that most of the evidence carded here actually studied, since the trials enrol "insertional Achilles tendinopathy" rather than bursitis alone; Achilles Tendon Rupture for the complication that limits how much insertion can safely be debrided and the reason FHL transfer exists; Calcaneal Fractures and Calcaneal Tuberosity Fractures for the traumatic causes of posterior heel pain that must be excluded on the lateral radiograph; Septic Bursitis for the infected bursa, which is a different and urgent problem; and Seronegative Spondyloarthropathy for the inflammatory enthesitis that presents bilaterally in a young patient and is the reason bilateral disease prompts blood tests rather than an operation.