Tendinopathy General Principles

Universal clinical features (across all tendinopathy sites):

History:

• •Localised tendon pain with loading - the cardinal feature, provoked by activities that load the affected tendon (especially energy-storage activities such as running, jumping for lower limb; gripping, lifting for upper limb).
• •Load-dependent pain pattern: worse at the start of activity ('warm-up' pain that may initially improve), returns after activity or the following morning; progresses to pain earlier in activity and eventually at rest.
• •Morning stiffness - the first few steps or movements are stiff and typically improve within minutes (fluid redistribution after sleep).
• •Pain at a specific anatomical site - the patient can usually point precisely to the location.
• •Insidious onset over days to weeks during increased loading; a precipitating training error is often identifiable.
• •Ask about training history (load changes - the most important), occupation, sport, previous tendinopathy, diabetes, fluoroquinolones, and corticosteroids.

Examination:

• •Localised tenderness at the tendon, maximum at the site of pathology.
• •Tendon thickening or nodularity - compare contralaterally.
• •Pain with loaded testing - isometric holds against resistance are a useful initial provocation; eccentric testing is also provocative.
• •Reduced capacity (strength, endurance, power) compared with the contralateral side.
• •ROM is usually preserved (unlike arthritis).
• •Assess the kinetic chain (proximal and distal biomechanical contributors).

Common tendinopathies - site-specific highlights:

• •Achilles mid-portion: pain 2-6 cm above the calcaneal insertion; thickened tender tendon; worse with running and stairs.
• •Achilles insertional: pain at the calcaneal insertion; associated with Haglund's deformity; compressive loading (dorsiflexion) worsens it.
• •Patellar ('jumper's knee'): pain at the inferior pole of the patella; common in jumping sports.
• •Lateral elbow ('tennis elbow'): pain at the lateral epicondyle, worse with gripping and lifting - the most common upper limb tendinopathy.
• •Rotator cuff (supraspinatus): shoulder pain with overhead activity; painful arc.
• •Greater trochanteric pain syndrome (GTPS): lateral hip pain; GTPS is a regional pain syndrome - gluteal tendinopathy is often a component but GTPS is broader. More common in women, particularly post-menopausal.
• •Proximal hamstring: deep buttock or ischial tuberosity pain; worse with sitting, running, lunging.
• •Tibialis posterior: medial ankle or arch pain; progressive flatfoot in advanced cases (posterior tibial tendon dysfunction).

Related but distinct: De Quervain's is a stenosing TENOSYNOVITIS of the 1st extensor compartment (a tendon-sheath disorder, positive Finkelstein's test), not a simple tendinopathy.

Tendinopathy is predominantly a clinical diagnosis. Imaging supports the diagnosis, assesses structural change, and excludes alternative pathology - but imaging abnormalities are common in asymptomatic tendons and must be interpreted alongside the clinical picture.

• •Clinical diagnosis is primary: localised tendon pain provoked by loading, localised tenderness, and a typical load-related history are usually sufficient. Imaging is not mandatory for every presentation.
• •Ultrasound (the most commonly used modality in UK MSK practice): accessible, dynamic, relatively inexpensive, and clinic-based. Demonstrates tendon thickening, hypoechoic areas, neovascularisation on Doppler, calcification, tears, and peritendinous fluid. Dynamic assessment is a major advantage. Operator-dependent. Critical caveat: ultrasound abnormalities are common in asymptomatic tendons.
• •MRI: more useful for deep tendons (proximal hamstring, deep gluteal), assessing partial tear extent, pre-surgical planning, and excluding intra-articular pathology. Same caveat about asymptomatic abnormalities.
• •Plain radiographs: do not image the tendon directly. Useful for enthesophytes, calcification (calcific tendinopathy, particularly supraspinatus), and excluding bony pathology.
• •Bloods: not routine. Consider ESR and CRP if inflammatory enthesopathy is suspected; HbA1c if diabetes is suspected; lipid profile if hypercholesterolaemia. Persistent or multi-site enthesitis with back pain, uveitis, psoriasis, IBD, or family history - refer per NICE NG65 for spondyloarthritis assessment.

Progressive loading rehabilitation is the cornerstone of tendinopathy management. The evidence consistently shows that tendons need to be LOADED, not rested, to recover. Site-specific UK guidance differs for some tendinopathies - management is not identical for every tendon. There is no single overarching NICE guideline.

Core principles:

• •Load management (the most important principle): identify and modify the provocative load. Complete rest leads to deconditioning and is counterproductive. RELATIVE rest reduces the provocative load to a manageable level while maintaining other activities.
• •Pragmatic pain monitoring: pain during loaded exercise is acceptable if it remains manageable (typically 5/10 or less), does not progressively worsen during the session, and settles within 24 hours. If morning-after pain is worse than baseline, the previous day''s load was too much.
• •Progressive loading rehabilitation is THE treatment: the single most effective intervention. Loading is progressed through isometric, isotonic (heavy slow resistance or eccentric), energy-storage (plyometric), then sport-specific phases. Takes months, not weeks - 3 to 6 months for significant improvement. Setting realistic expectations prevents dropout.
• •Education and self-management: explain that tendinopathy is not a simple inflammation, that the tendon is not 'damaged beyond repair', and that loading is therapeutic. Address fear-avoidance and catastrophising.

Pharmacological management (adjunctive - symptom relief, not disease-modifying):

• •Topical NSAIDs may provide short-term relief for superficial tendons.
• •Oral NSAIDs may facilitate engagement with rehabilitation - short courses; do not address the underlying pathology.
• •GTN patches: limited and mixed evidence; not routine UK first-line.

Injection therapy - a nuanced area with site-specific guidance:

• •Corticosteroid injection is NOT a routine first-line treatment for most tendinopathies. Provides short-term pain relief but does NOT improve long-term outcomes and may worsen them. Inhibits collagen synthesis and may weaken the tendon; repeated injections increase rupture risk.

- NICE CKS advises against corticosteroid injection for lateral elbow tendinopathy due to worse medium-term outcomes. - For rotator cuff disorders, NICE CKS states that subacromial corticosteroid injection may be considered in selected cases. - AVOID corticosteroid injection around the Achilles tendon (rupture risk - widely accepted consensus). Patellar tendon injection is also generally avoided. - Injection without rehabilitation is poor practice.

• •PRP (platelet-rich plasma) and autologous blood injection: evidence is mixed and inconsistent; not routinely available on the NHS; should not be presented as standard first-line.
• •Shockwave therapy (ESWT): may be considered in selected chronic tendon-related conditions - evidence is most established for calcific supraspinatus tendinopathy (NICE IPG742) and refractory Achilles tendinopathy (NICE IPG311). Not a universal treatment for all tendinopathies.
• •High-volume image-guided injection (HVIGI) is specialist-level care, not standard first-line.

Surgery is reserved for tendinopathies refractory to at least 6 months (some guidelines 12 months) of structured loading rehabilitation. Options vary by site - debridement, stripping of neovessels/paratenon, tendon repair, tendon transfer, decompression. Post-operative rehabilitation still requires progressive loading.

SEM relevance: training load monitoring, periodisation, biomechanical assessment, and return-to-sport criteria based on FUNCTION (capacity testing, symptom response to loading) rather than imaging appearance.

Progressive loading rehabilitation IS the treatment for tendinopathy. Everything else is adjunctive. The programme is individualised, progressive, and sustained over months.

The four-stage loading progression:

Stage 1 - Isometric loading (load introduction and pain modulation): sustained isometric holds (typically 45 seconds, 4-5 reps, 2-3 times daily). A safe, low-risk starting point that allows tendon loading without high demand. Useful for pain relief in the reactive stage. Examples: wall sit (patellar), heel raise hold (Achilles), isometric wrist extension (lateral elbow), isometric shoulder external rotation (rotator cuff). Progress when isometric loading is comfortable and pain is manageable.

Stage 2 - Isotonic loading (heavy slow resistance, HSR, or eccentric-focused): slow controlled concentric and eccentric movements with progressively increasing resistance to stimulate tendon remodelling and strengthen the muscle-tendon unit. Heavy load, slow tempo (3 seconds concentric, 3 seconds eccentric), moderate repetitions progressing to heavier load and lower reps. Both HSR and eccentric-focused protocols are acceptable - the evidence does not clearly favour one universally, and adherence matters most. Typically 8-12 weeks before advancing.

Stage 3 - Energy-storage loading (plyometrics and elastic recoil): prepare the tendon for elastic, energy-storage demands of sport. Progressive plyometric loading - low to high amplitude. Examples: double-leg hops to single-leg hops to multidirectional hops (lower limb); progressive throwing (upper limb). Only begin when HSR is comfortable and the muscle-tendon unit has adequate strength.

Stage 4 - Sport-specific and return to full activity: progressive return to sport-specific training; volume before intensity. Ongoing tendon loading as maintenance. Return-to-sport guided by symptom response, restoration of tendon capacity, functional testing, sport demands, and psychological readiness - NOT by imaging appearance.

Key rehabilitation principles: load management not rest; pragmatic pain monitoring (manageable during, settles within 24 hours); progressive overload as the therapeutic mechanism; recovery takes 3-6 months minimum; address the kinetic chain (proximal weakness, biomechanical factors, training errors). Compressive loading caution for INSERTIONAL tendinopathies (insertional Achilles, proximal hamstring) - avoid end-range positions that compress the insertion early in rehabilitation.

• •Cook and Purdam tendinopathy continuum (2009) - the widely used clinical framework for staging tendinopathy and guiding rehabilitation (reactive then dysrepair then degenerative).
• •NICE CKS topic pages for site-specific tendinopathies (tennis elbow, shoulder pain, GTPS) - the UK primary-care reference; corticosteroid injection guidance is site-specific.
• •NICE IPG742 - shockwave therapy for calcific supraspinatus tendinopathy.
• •NICE IPG311 - shockwave therapy for refractory Achilles tendinopathy.
• •MHRA fluoroquinolone safety guidance - stop immediately if tendon symptoms develop; restrict prescribing when alternatives exist; Yellow Card reporting.

• •Tendinopathy = failed healing, NOT simple tendinitis; Cook-Purdam continuum is reactive then dysrepair then degenerative.
• •Progressive LOADING (isometric, isotonic/HSR or eccentric, energy-storage, sport-specific) is the treatment - not rest.
• •Both HSR and eccentric-focused protocols are acceptable; adherence matters most.
• •Fluoroquinolones risk tendinopathy and rupture - stop immediately if tendon pain develops (MHRA).
• •Corticosteroid injection is NOT routine first-line; avoid around the Achilles and patellar tendons.
• •Imaging abnormalities are common in asymptomatic tendons - treat the patient, not the image.