Overview
Differentiate bursal, tendon and entheseal pain, recognise sepsis, rupture and inflammatory spondyloarthritis, use imaging or aspiration only for focused questions, and restore tissue capacity through progressive loading with safe selective medicines.
Localise the painful structure before naming it. Ask about change in training, work or footwear; direct pressure, wound or procedure; sudden pop; morning and rest pain; fever; psoriasis, uveitis, bowel inflammation and back pain; diabetes, gout, renal disease and immunosuppression; and fluoroquinolone, steroid or statin exposure. Examine skin and temperature, whether swelling is discrete, passive joint movement, pain with resisted tendon action and passive stretch, insertion tenderness, tendon continuity, gait and the related joint, spine and nerve.
Mechanical tendinopathy is a load-adaptation disorder, not simply ongoing inflammation. Pain during a specific load and the next-day response helps prescribe rehabilitation. Imaging thickening, neovascularity or partial defects can occur in asymptomatic tendons and should not decide activity alone. Brief reduction of provocative load is followed by progressive strengthening and return to energy-storage tasks. Insertional Achilles disease is initially loaded without deep dorsiflexion compression, while mid-portion disease can progress through more range.
Aetiology
Mechanical bursal irritation
Repeated kneeling, leaning on elbows, friction, direct trauma or altered movement irritates superficial or deep bursae; crystal deposition can provoke acute inflammation.
Tendon load mismatch
A sudden increase in running, jumping, gripping or occupational repetition exceeds tendon capacity, especially with age, previous injury, obesity, diabetes or altered biomechanics.
Inflammatory enthesitis
Psoriatic and other spondyloarthritis inflammation targets tendon, ligament and fascial insertions, commonly Achilles, plantar fascia, patellar, pelvic or chest-wall entheses.
Infection and medicine risk
Skin breach can seed olecranon or prepatellar bursae; fluoroquinolones and systemic glucocorticoids raise tendon-injury risk, especially together, with older age or kidney disease.
Pathophysiology
- 1Bursal inflammation
Synovial-lined bursae reduce friction; repetitive compression, crystals or organisms increase fluid and inflammatory cells, producing local fluctuant swelling and painful pressure.
- 2Tendon matrix adaptation
Chronic tendinopathy shows collagen disorganisation, altered tenocytes, neovascularity and failed adaptation rather than simple persistent tendinitis, making progressive load central to recovery.
- 3Enthesis organ inflammation
The insertion, adjacent fibrocartilage, bursa and bone act as a unit; immune inflammation can cause Doppler signal, marrow oedema, erosion and later new bone.
- 4Rupture threshold
Degeneration or medicine-related matrix injury lowers tensile reserve; a sudden force can then produce partial or complete discontinuity with immediate functional loss.
Clinical features and red flags
A discrete fluctuant swelling over olecranon or patella, often more painful with pressure than passive joint movement, identifies the bursal compartment.
Warmth, erythema, tenderness, skin breach, fever or immune risk increases infection probability, although fever may be absent and appearance overlaps gout.
Pain is reproduced by tendon loading and local palpation, with possible morning stiffness or start-up pain that warms during activity then reacts later.
A sudden snap, bruising, palpable gap and immediate loss of the tendon's action distinguishes rupture from gradual load intolerance.
Several spontaneous insertion sites, prolonged morning symptoms and psoriasis, dactylitis, uveitis, IBD or axial pain support a spondyloarthritis phenotype.
Lateral hip pain with side-lying and single-leg load often reflects gluteal tendinopathy within a regional syndrome rather than isolated bursal inflammation.
Investigations
- 01
First-line anatomical examinationFirst stepFirst line - Why
- Distinguish bursa, tendon, enthesis, joint, nerve and bone and identify infection or rupture before rehabilitation.
- Interpretation and limitations
- Local pressure swelling favours bursa, resisted-load pain favours tendon and insertion tenderness suggests enthesis; passive restriction, systemic signs or lost action changes pathway.
- 02
Urgent bursal aspiration - Why
- Confirm or exclude infection and crystal disease in an acutely inflamed superficial bursa when sampling is safe.
- Interpretation and limitations
- Send Gram stain, culture and sensitivities, white-cell count and crystals; no cell threshold perfectly separates sepsis, and crystals can coexist with infection.
- 03
Blood cultures and inflammatory tests - Why
- Assess systemic infection or inflammatory disease when fever, cellulitis, immune risk or multiple entheseal sites are present.
- Interpretation and limitations
- Obtain cultures before antibiotics in systemic illness when feasible, with FBC and CRP; normal markers do not exclude local infection or axial spondyloarthritis.
- 04
Ultrasound for uncertainty or guidance - Why
- Demonstrate bursal fluid, tendon continuity, neovascular change or enthesis abnormality and guide selected aspiration or injection.
Differential diagnosis
Septic or crystal arthritis
A hot joint has deep pain and restricted passive movement rather than clearly extra-articular swelling; joint aspiration is urgent and crystals do not exclude infection.
Cellulitis and abscess
Diffuse skin inflammation or focal collection can mimic superficial bursitis; ultrasound and aspiration route are selected to avoid traversing infected skin.
Tendon tear or fracture
Acute loss of force, a gap, bruising or focal bony tenderness after trauma suggests structural discontinuity rather than uncomplicated chronic tendinopathy.
Neurological or referred pain
Radiculopathy, peripheral nerve entrapment and referred joint pain may produce regional tenderness but add sensory, reflex or movement findings beyond one tendon.
Inflammatory arthritis
Persistent multiple entheses, synovitis, psoriasis, inflammatory back pain or extra-articular disease supports spondyloarthritis; rheumatoid disease can cause tenosynovitis and rupture.
Management
01First-line localisationName structure and mechanismFirst stepFirst lineA focal periarticular pain syndrome presents without systemic instability or obvious complete rupture.+
- 1Map bursa, tendon course and insertion, test passive joint movement and resisted action, and examine skin, neurology and adjacent bone.
- 2Establish whether onset follows pressure or load, is infectious or crystal-like, or clusters with systemic inflammatory features.
- 3Use no imaging for a clear uncomplicated mechanical pattern; request ultrasound, radiography or MRI only for uncertainty, trauma, mass, failed care or procedure.
- 4Give safety-netting for fever, spreading redness, sudden power loss, calf swelling or mass and set a functional review.
02Preferred tendon rehabilitationReload rather than rest indefinitelyPreferredClinical tendinopathy is present without complete rupture, infection or bone stress injury needing protection.
Complications
Bacteraemia and deep spread
Untreated septic bursitis can extend to cellulitis, joint, bone or bloodstream, particularly with diabetes, immunosuppression or delayed presentation.
Tendon rupture
Progressive matrix failure, premature high load or corticosteroid exposure can culminate in partial or complete rupture with prolonged functional loss.
Persistent load intolerance
Rest without graded reloading reduces muscle and tendon capacity, making return to work or sport repeatedly provoke symptoms and reinforce avoidance.
Unrecognised systemic inflammation
Treating each enthesis locally can delay diagnosis of axial or psoriatic disease, allowing pain, damage, uveitis and functional restriction to progress.
Monitoring and follow-up
- For tendon rehabilitation, record a reproducible task, load and next-day response, then progress resistance or energy-storage demand only when recovery is acceptable.
- Review suspected septic bursitis within 24 to 48 hours for fever, erythema spread, reaccumulation, culture and antibiotic tolerance; escalate non-response.
- After injection, give infection advice and reassess whether relief enabled activity; do not repeat after no meaningful functional gain.
- Track tendon power and continuity after acute injury; increasing bruising, a gap or lost function requires imaging or surgical reassessment.
- In enthesitis, monitor number of sites, morning stiffness, spinal symptoms, skin, nails, eyes and bowel disease so systemic phenotype is recognised.
- Review fluoroquinolone or steroid exposure and avoid unnecessary repeat courses while never stopping essential glucocorticoids abruptly.
Special situations
Tendinopathy is not tendinitis
Chronic tendon pain reflects failed load adaptation and matrix change more than persistent neutrophilic inflammation, explaining why strengthening outperforms rest.
Greater trochanter is regional
Lateral hip pain labelled bursitis often centres on gluteal tendon compression and weakness, so progressive abductor loading is important.
Crystals do not exclude sepsis
Gout or calcium-pyrophosphate crystals may be found in an infected bursa or joint; culture and severity still determine antimicrobial care.
Insertional loading differs
Deep dorsiflexion compresses the Achilles insertion against calcaneus, so early exercises may use a flat surface rather than heel drops below a step.
Enthesitis can be systemic
One loaded insertion is usually mechanical; multiple spontaneous sites plus psoriasis, uveitis, IBD or axial symptoms changes the diagnostic frame.
Common pitfalls
- 01
Do not inject or repeatedly aspirate a hot bursa before infection assessment; corticosteroid worsens sepsis and needle entry can introduce organisms.
- 02
Do not prescribe complete prolonged rest for tendinopathy; load reduction without rebuilding produces a weaker tendon that relapses.
- 03
Do not inject corticosteroid into tendon substance or routinely around Achilles or patellar tendon.
- 04
Do not treat an ultrasound abnormality rather than the patient; asymptomatic thickening, neovascularity and partial defects are common.
- 05
Do not call multifocal enthesitis repetitive strain without asking about psoriasis, inflammatory back pain, uveitis, bowel disease and dactylitis.
- 06
Do not begin strengthening a suspected complete rupture; protect the limb, confirm continuity and obtain urgent guidance.