Bursitis, enthesitis and tendinopathy

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

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.

Enthesitis needs systemic context. A single lateral elbow or Achilles insertion after a clear load change is usually mechanical. Several sites, spontaneous onset, prolonged morning stiffness or associated psoriasis, dactylitis, uveitis, IBD and inflammatory back pain raise spondyloarthritis. Ultrasound Doppler or MRI can support inflammation but mechanical load also changes the enthesis, so imaging never replaces phenotype. Treat confirmed systemic disease through rheumatology while restoring local capacity.

Key points

Bursitis produces local swelling and pressure tenderness over a bursa; tendinopathy produces load-related tendon pain; enthesitis localises at an insertion and may be mechanical or inflammatory.
A hot olecranon or prepatellar bursa with skin breach, fever or immune risk needs aspiration for Gram stain, culture, cell count and crystals when safe, plus prompt anti-staphylococcal treatment.
Do not aspirate or inject an uncomplicated mechanical bursa routinely; repeated needle entry can introduce infection and fluid reaccumulates unless pressure or loading changes.
Diagnose most tendinopathy clinically from location and reproducible load pain; ultrasound or MRI is useful for uncertainty, suspected tear or procedural planning, not routine severity scoring.
Initial tendon care uses relative load modification followed by progressive isometric and isotonic, heavy-slow or eccentric loading appropriate to the tendon; complete rest delays recovery.
Avoid intratendinous corticosteroid and do not inject around Achilles or patellar tendon routinely because relief may be brief and rupture risk is concerning.
Persistent enthesitis at multiple sites or with psoriasis, uveitis, bowel disease, dactylitis or inflammatory back pain requires rheumatology referral and systemic assessment.
A pop with immediate weakness, palpable gap, absent heel rise or abnormal Simmonds-Thompson test indicates rupture until excluded; protect and refer urgently.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

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.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Bursal inflammation
Synovial-lined bursae reduce friction; repetitive compression, crystals or organisms increase fluid and inflammatory cells, producing local fluctuant swelling and painful pressure.
2
Tendon matrix adaptation
Chronic tendinopathy shows collagen disorganisation, altered tenocytes, neovascularity and failed adaptation rather than simple persistent tendinitis, making progressive load central to recovery.
3
Enthesis 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.
4
Rupture threshold
Degeneration or medicine-related matrix injury lowers tensile reserve; a sudden force can then produce partial or complete discontinuity with immediate functional loss.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Superficial bursitis

A discrete fluctuant swelling over olecranon or patella, often more painful with pressure than passive joint movement, identifies the bursal compartment.

Septic bursal pattern

Warmth, erythema, tenderness, skin breach, fever or immune risk increases infection probability, although fever may be absent and appearance overlaps gout.

Tendinopathy pattern

Pain is reproduced by tendon loading and local palpation, with possible morning stiffness or start-up pain that warms during activity then reacts later.

Complete rupture pattern

A sudden snap, bruising, palpable gap and immediate loss of the tendon's action distinguishes rupture from gradual load intolerance.

Inflammatory enthesitis

Several spontaneous insertion sites, prolonged morning symptoms and psoriasis, dactylitis, uveitis, IBD or axial pain support a spondyloarthritis phenotype.

Greater-trochanteric pattern

Lateral hip pain with side-lying and single-leg load often reflects gluteal tendinopathy within a regional syndrome rather than isolated bursal inflammation.

Red flags requiring action

Spreading erythema, fever, rigors, immunosuppression, a skin wound or systemic instability with superficial bursal swelling requires urgent septic-bursitis or sepsis management.
A sudden snap, immediate weakness, palpable tendon gap, inability to perform a straight-leg raise or abnormal calf-squeeze test suggests complete rupture and needs urgent protection and referral.
Disproportionate night pain, a mass, weight loss or persistent focal bone tenderness requires imaging for malignancy, fracture or infection rather than repeated soft-tissue treatment.
Multiple entheses, inflammatory back pain, psoriasis, dactylitis, uveitis or inflammatory bowel disease warrants timely spondyloarthritis assessment instead of serial local injections.
Calf swelling with breathlessness, chest pain or thrombotic risk may be venous thromboembolism rather than Achilles or calf tendinopathy and requires acute care.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

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.
Interpretation and limitations
Thickening and Doppler signal are nonspecific and occur with mechanical adaptation; dynamic continuity and the clinical question matter more than an isolated report.
05
MRI for deep or surgical questions
Why
Define a major partial tear, occult rupture, bone stress, deep infection, mass or refractory condition being considered for surgery.
Interpretation and limitations
MRI gives anatomical extent but can overdiagnose degeneration; protect a clinically suspected major rupture while awaiting imaging.
06
Targeted SpA assessment
Why
Identify systemic inflammation when enthesitis is persistent, multifocal or accompanied by psoriasis, axial or extra-articular features.
Interpretation and limitations
Use CRP or ESR and HLA-B27 selectively, then rheumatology-directed imaging; negative biomarkers do not exclude a convincing phenotype.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

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.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

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.

1Temporarily reduce provoking work, running, jumping or gripping while maintaining tolerable movement and addressing footwear, technique and recovery.
2Begin isometric or low-load isotonic exercise when irritability is high, then progress slow resistance and finally tendon-specific speed and return-to-task loads.
3EscalationUse pain during and the following day to adjust dose rather than insisting on zero pain or exercising through escalation.
4Refer to physiotherapy or specialist care when diagnosis, progression, partial tear, occupational demand or six-to-twelve-week response remains uncertain.

03Infection pathwaySample and treat a septic bursaA superficial bursa is hot, erythematous and tender with a wound, fever, immune risk or no mechanical explanation.

1Assess sepsis severity and adjacent joint, obtain bursal fluid and blood cultures when safe, mark erythema and check FBC, CRP, glucose and renal function.
2Start anti-staphylococcal antibiotics promptly after samples in a stable patient and immediately if unwell, using intravenous treatment and admission for severe disease.
3Review culture and response within 24 to 48 hours, repeat drainage or seek orthopaedics for loculation, failure, joint involvement or osteomyelitis.
4Never inject corticosteroid into an infected or incompletely assessed bursa and protect any wound while reducing recurrent pressure.

04Inflammatory escalationMove from local lesion to systemic phenotypeEscalationEnthesitis is persistent at several sites, has no mechanical explanation or accompanies psoriasis, uveitis, IBD, dactylitis or inflammatory back pain.

1Document the full spondyloarthritis phenotype, family history, skin and nails, joints, spine and extra-articular organs rather than treating each insertion separately.
2Refer to rheumatology under NICE criteria; use a short NSAID trial when safe without allowing normal CRP or negative HLA-B27 to block referral.
3Continue local load management while rheumatology treats active systemic disease with conventional or biologic therapy according to axial or peripheral involvement.
4Avoid repeated local steroid around weight-bearing tendons, particularly Achilles or patellar sites, when systemic treatment is needed.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

Provides short-term local analgesia so load can be modified and rehabilitation started.

Topical diclofenac gel

Apply the product-directed amount over focal pain, commonly 2–4 g of 1.16% gel three or four times daily for one to two weeks initially, without exceeding the product maximum.

Avoid broken or infected skin, NSAID allergy and excess combined NSAIDs; systemic harms remain possible. In pregnancy use only when clearly necessary and avoid during the third trimester.

Controls short-term regional pain or inflammatory enthesitis when topical treatment is unsuitable; it does not rebuild tendon capacity.

Naproxen with gastroprotection

Use 250–500 mg orally twice daily with food for the shortest course; add omeprazole 20 mg orally once daily when gastrointestinal risk indicates protection.

Assess ulcer, bleeding, anticoagulants, eGFR, hypertension, heart failure and cardiovascular disease; avoid severe renal impairment and apply pregnancy restrictions from 20 weeks.

Provides empirical anti-staphylococcal treatment after aspiration when local resistance and allergy history support it.

Flucloxacillin for uncomplicated septic bursitis

For a clinically stable adult managed orally under the local infection pathway, use flucloxacillin 500 mg orally four times daily for 14 days, adjusting by severity, culture response and microbiology advice.

Admit for intravenous therapy if septic, rapidly spreading, immunocompromised or unable to absorb; avoid immediate penicillin hypersensitivity and check liver history, renal dosing and cultures.

A selective short-term option for persistent non-infectious bursal pain obstructing rehabilitation after pressure and load factors are addressed.

Bursal triamcinolone acetonide

After infection exclusion, trained clinicians may inject 10–20 mg into a selected small bursa and up to 40 mg into a larger deep bursa under local protocol; never inject tendon substance.

Do not inject through cellulitis, into infected bursa, Achilles or patellar tendon; discuss skin atrophy, depigmentation, transient hyperglycaemia, flare, tendon injury and rare infection.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

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.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

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.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

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.

11Common pitfallsFrequent interpretation and management errors.

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.