Achilles tendinitis is the symptomatic inflammatory and degenerative disorder of the Achilles tendon — the thick fibrous cord linking the calf muscles to the heel and the largest tendon in the human body. Modern terminology favors Achilles tendinopathy because chronic histology shows degeneration rather than classical inflammation.
Achilles tendinitis (ICD-10: M76.6) — more accurately Achilles tendinopathy — is a clinical syndrome of pain, swelling, and impaired function of the Achilles tendon. Histopathologically, the chronic tendon shows degenerative changes (collagen disorganization, increased ground substance, neovascularization) rather than classical inflammatory cells, hence the modern preference for 'tendinopathy.' Two anatomical patterns are recognized: mid-portion (non-insertional) tendinopathy involves the watershed area 2-6 cm proximal to the calcaneal insertion where the tendon has poorest blood supply; insertional tendinopathy involves the tendon attachment to the calcaneus and often coexists with Haglund's deformity (posterior superior calcaneal prominence) and retrocalcaneal bursitis. Paratenonitis describes inflammation of the paratenon surrounding the tendon, sometimes coexisting with tendinosis. The pathogenesis is mechanical overload exceeding the tendon's ability to remodel, with secondary changes in cellularity, matrix composition, and tendon vascularity.
The key symptoms of Achilles Tendinitis are: Localized pain along the Achilles tendon, most pronounced 2-6 cm above the heel (mid-portion) or directly at the heel attachment (insertional)., Morning stiffness and pain on the first few steps after rising, gradually easing as the tendon warms up., Pain at the start of exercise that initially improves with warm-up, then returns with prolonged activity or after cool-down., Palpable thickening, tenderness, and sometimes a fusiform swelling of the tendon — visible nodule in long-standing cases., Crepitus or a grating sensation along the tendon during ankle movement in paratenonitis., Reduced push-off power during walking, running, jumping, or climbing stairs., Worsening pain during hill running, sprinting, or jumping activities; relative comfort during low-impact activity such as swimming or cycling..
Diagnosis is primarily clinical. The patient describes typical pain pattern — morning stiffness, exercise-related pain, often a recent training change or systemic risk factor. Examination shows localized tenderness, palpable thickening, and pain with the Royal London Hospital test (pain on tendon palpation with foot dorsiflexed, no pain with foot plantarflexed) or with the squeeze test. The painful arc test distinguishes mid-portion from insertional disease — pain moves with the ankle in tendinopathy but stays fixed in paratenonitis. The Victorian Institute of Sport Assessment-Achilles (VISA-A) questionnaire (0-100 scale) quantifies symptom severity and tracks response. Imaging supports the clinical diagnosis when symptoms are atypical, severe, or refractory: musculoskeletal ultrasound shows tendon thickening (mid-portion diameter above 6-7 mm), hypoechoic areas, neovascularization on Doppler, and intratendinous calcifications in insertional disease; MRI quantifies degenerative changes and excludes partial tear. Plain radiographs detect Haglund's deformity, calcaneal spurs, and calcifications in insertional disease. The differential diagnosis includes posterior ankle impingement, partial or complete Achilles rupture, retrocalcaneal bursitis, plantaris tendon disorders, peroneal tendon injury, calcaneal stress fracture, and systemic conditions (spondyloarthropathy with enthesitis, gout). HbA1c, lipid profile, uric acid, and inflammatory markers screen for systemic contributors when symptoms are bilateral, insidious in a non-athlete, or atypical. The Thompson calf-squeeze test rules out complete tendon rupture — failure of plantarflexion when the calf is squeezed indicates rupture and warrants urgent referral.
Most patients with Achilles tendinopathy respond to non-operative care. Approximately 60-90% of mid-portion tendinopathy patients achieve substantial improvement with 12 weeks of structured eccentric loading; 40-60% of insertional tendinopathy patients respond to modified loading and heel lifts. Shock wave therapy adds 60-80% response in refractory cases. Surgical outcomes for the 5-10% who require operation are good: 75-90% return to previous activity level in mid-portion disease and 65-85% in insertional disease. Recurrence is common, particularly with rapid return to running or untreated systemic risk factors. Untreated chronic tendinopathy increases the risk of Achilles tendon rupture (lifetime risk 5-15% in chronic tendinopathy versus 0.1% in healthy tendons). Predictors of better outcome include shorter symptom duration, mid-portion location, athletic patient with good adherence to rehabilitation, and adequate management of systemic risk factors.
See a sports medicine physician, podiatrist, or physical therapist if pain persists more than 6 weeks despite rest, if symptoms are bilateral or systemic, or if you cannot perform single-leg heel raises. Refer to an orthopedic surgeon when 6-12 months of structured rehabilitation, shock wave, or injection therapy have failed, when a partial tear of more than 50% is suspected, or when full rupture is documented.
Find specialists →Pain typically reduces by 30-50% within 6-8 weeks of consistent eccentric loading. Functional recovery (single-leg heel raises, return to walking and gentle running) at 12-16 weeks. Return to previous athletic activity at 4-6 months. Post-surgical recovery: 4-6 months for tendon debridement, 6-12 months for tendon transfer. Tendon thickness on ultrasound takes 12-24 months to remodel.
Maintain cardiovascular fitness with low-impact activities (cycling, swimming, elliptical, deep-water running) during active rehabilitation. Eccentric and heavy slow resistance exercises form the core rehabilitation program. Return to running follows a graduated walk-run program once single-leg heel raises are pain-free; start with 1-2 minute run intervals progressing weekly. Avoid hill repeats, sprinting, and plyometric work until VISA-A score exceeds 80 and pain provocation tests are negative. Strength training of the entire lower limb and hip musculature reduces re-injury risk.
Choose a sports medicine physician, podiatrist, or orthopedic surgeon with experience in tendon disorders and access to musculoskeletal ultrasound. A physical therapist trained in progressive eccentric loading and heavy slow resistance is essential for the rehabilitation phase. Ask about VISA-A score tracking, return-to-sport criteria, and surgical experience for refractory cases.
Medically reviewed by AIHealz Medical Editorial Board · May 13, 2026
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