Achilles Tendinopathy & Rupture

The Achilles tendon is the largest and strongest tendon in the human body, transmitting the combined force of the gastrocnemius and soleus to the calcaneal tuberosity. Achilles pathology spans a spectrum from tendinopathy (degenerative change without acute rupture) to acute complete rupture. These are among the most common musculoskeletal conditions seen in active adults, and their management — particularly the non-operative vs operative debate for rupture — is one of the most evidence-rich and contested areas in orthopaedic surgery.

• The Achilles tendon has a zone of relative avascularity approximately 2–6 cm proximal to the calcaneal insertion — this is the watershed zone where most tendon ruptures and tendinopathic change occur; blood supply in this zone comes distally from the insertion and proximally from the musculotendinous junction, with a relative paucity in between
• Achilles rupture incidence: approximately 18–40 per 100,000; increasing in recent decades; peak incidence in men aged 30–50 years (recreational "weekend warriors"); male to female ratio approximately 4:1
• Most common mechanism of acute rupture: sudden unexpected dorsiflexion force on a plantarflexed foot (landing from a jump, lunging); eccentric load on a degenerative tendon

Achilles tendinopathy encompasses a spectrum of degenerative change in the tendon (not primarily inflammatory). Two distinct anatomical subtypes have different clinical presentations and management.

• Eccentric heel drop exercise (Alfredson protocol): the gold standard non-operative treatment for non-insertional Achilles tendinopathy — 3 sets of 15 repetitions of eccentric heel drops (standing on the edge of a step, lowering the heel below the step level slowly) twice daily for 12 weeks; evidence of significant pain reduction and functional improvement; mechanism: mechanical loading stimulates tendon remodelling and reduces neovascularisation
• Insertional tendinopathy: eccentric heel drops with the heel below the step are CONTRAINDICATED for insertional type as they increase compression at the insertion — use flat surface eccentric exercises or heavy slow resistance instead

• First-line: load management (activity modification, not rest), eccentric loading programme (Alfredson for non-insertional; heavy slow resistance for insertional), heel lift/raise (reduces tendon load), footwear modification
• Second-line: physiotherapy-directed progressive loading; shockwave therapy (ESWT) — significant evidence for both insertional and non-insertional; GTN patches (glyceryl trinitrate) — some evidence for non-insertional; PRP injection — evidence mixed
• Corticosteroid injection into the Achilles tendon: AVOID — significantly increases risk of tendon rupture; peritendinous injection (into the paratenon) is occasionally used for paratenonitis but intratendinous injection is contraindicated; inform patients clearly
• Duration: minimum 3–6 months of structured non-operative treatment before considering surgery

• Non-insertional surgery: open or minimally invasive tendon debridement (excision of degenerate nodule); longitudinal tenotomies to stimulate healing; paratenon stripping; FHL augmentation if >50% tendon debridement required; good results in approximately 75–85% of patients
• Insertional surgery: posterior heel approach; excision of Haglund`s prominence; retrocalcaneal bursectomy; detachment of the distal Achilles insertion, debridement of calcific enthesophyte, and reattachment using suture anchors; more complex recovery than non-insertional surgery due to tendon detachment
• Haglund deformity: posterior superior calcaneal prominence; compresses the retrocalcaneal bursa; "pump bump" in shoe-wearing patients; excised as part of insertional Achilles surgery; parallel pitch lines on lateral X-ray assess calcaneal shape

• Presentation: sudden "pop" during sporting activity; feels like a kick to the back of the leg; immediate inability to push off; patient often thought they had been kicked
• Thompson (Simmonds) test: patient prone, knee flexed 90°; squeeze the calf; normal = foot plantarflexes (positive test = intact tendon); abnormal = no plantarflexion (negative squeeze test = ruptured Achilles); sensitivity 96%, specificity 93%; most reliable clinical test for Achilles rupture
• Additional tests: palpable gap 2–6 cm above insertion; increased passive dorsiflexion on the affected side (Matles test — knee 90° flexion, affected foot dorsiflexes more than normal side); Copeland sphygmomanometer test (rarely used)
• MRI: confirms rupture, gap length, tendon quality, and degree of retraction — guides choice of repair technique; useful when clinical diagnosis is uncertain or in delayed presentation
• USS: dynamic assessment; confirms gap and tendon ends approximation; useful in acute setting; operator-dependent
• Missed Achilles rupture: occurs in approximately 20–25% of acute ruptures — tendon swelling may obscure the gap; the plantaris tendon can sometimes generate weak plantarflexion, misleading the clinician; Thompson test should be performed in all suspected cases

The non-operative vs operative debate for acute Achilles rupture is one of the most rigorously studied questions in orthopaedic surgery. Current evidence supports functional non-operative management as the first-line approach in most patients when early functional rehabilitation is initiated.

• UKSTAR trial (2020): major UK RCT of non-operative vs operative management of acute Achilles rupture; no significant difference in Achilles Tendon Rupture Score (ATRS) at 9 months; non-operative with functional rehabilitation equivalent to surgical repair; surgical group had higher complication rate; conclusion: functional non-operative management is first-line for most patients
• Percutaneous repair: small stab incisions reduce wound complication vs open; Ma-Griffith technique; risk of sural nerve entrapment; suitable for patients where surgery preferred but open complications to be minimised
• Delayed presentation (>4 weeks): significant tendon retraction; operative repair with augmentation (FHL tendon transfer, V-Y gastrocnemius advancement, peroneus brevis transfer) may be required

• Fluoroquinolone-associated tendinopathy and rupture: ciprofloxacin and other fluoroquinolone antibiotics increase risk of Achilles tendinopathy and rupture up to 3–4× — mechanism involves inhibition of tenocyte metabolism and matrix metalloproteinase (MMP) activity leading to tendon degeneration; risk highest in elderly patients and those on concurrent corticosteroids; warn patients prescribed fluoroquinolones; avoid strenuous activity and consider stopping if tendon pain develops
• FHL (flexor hallucis longus) transfer for chronic Achilles rupture and massive tendon defects: FHL is the preferred augmentation tendon — strong, adjacent, expendable (minimal functional deficit); harvested from its tunnel behind the medial malleolus or from the midfoot; transferred to calcaneal insertion; provides a functional motor replacement; used for gaps >3 cm after debridement of degenerate tendon
• Sural nerve anatomy in Achilles surgery: the sural nerve runs approximately 1 cm lateral to the Achilles tendon at the level of the musculotendinous junction and closer to the tendon distally; percutaneous repair is the most common procedure to inadvertently capture the sural nerve; always confirm nerve is free before percutaneous suture passage
• Tendon lengthening after conservative management: non-operative treatment carries risk of healing in a lengthened position if boot is not maintained at adequate equinus; lengthened tendon = reduced plantarflexion strength = worse functional outcome; the boot must be maintained at 20° equinus initially and the protocol followed precisely to prevent this

• Watershed zone: 2–6 cm proximal to insertion — most common site of rupture and tendinopathy; relative avascularity
• Thompson (Simmonds) test: squeeze calf → no plantarflexion = positive rupture; sensitivity 96%, specificity 93%
• UKSTAR trial: functional non-operative management equivalent to surgical repair for most patients; lower complication rate non-operatively; surgical preferred in elite athletes, large gap, delayed presentation
• Non-insertional tendinopathy: Alfredson eccentric heel drop protocol (3 × 15 twice daily × 12 weeks); gold standard non-operative treatment
• Insertional tendinopathy: do NOT use eccentric drops below step level — increases insertion compression; use flat surface or heavy slow resistance instead
• Corticosteroid injection INTO Achilles tendon: contraindicated — significantly increases rupture risk; peritendinous injection only if used at all
• Haglund deformity: posterior superior calcaneal prominence; retrocalcaneal bursitis; insertional Achilles disease; excised at surgery
• Fluoroquinolones: 3–4× increased rupture risk; inhibit tenocyte metabolism; warn patients; especially elderly + steroids
• FHL transfer: preferred augmentation for chronic rupture or large gap (>3 cm); strong, adjacent, minimal donor deficit
• Missed rupture: 20–25% of acute ruptures missed clinically; plantaris can simulate weak plantarflexion; always perform Thompson test