Achilles-tendon rupture and tendinopathy

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

Separate an acute event from chronic load pain immediately. Rupture follows a jump, sprint start, sudden change of direction or unexpected dorsiflexion and may be described as a kick from behind. Ask about the exact time, ability to continue, previous Achilles symptoms, fluoroquinolone or steroid exposure, diabetes, inflammatory disease, smoking, renal disease and baseline sport or work. Chronic tendinopathy causes morning stiffness and load-related pain either two to six centimetres above the insertion or directly at the calcaneus.

Inspect both legs from behind for swelling, bruising, tendon contour and resting ankle angle. With the patient prone and knees flexed, compare spontaneous plantar flexion, then squeeze each calf and observe ankle movement. Palpate the entire tendon for a gap, recognising that swelling can fill it. Test a single-leg heel rise only when rupture is not strongly suspected; do not repeatedly stretch a likely fresh rupture. Examine the calcaneus, calf, sural sensation, pulses and skin.

A typical rupture is diagnosed clinically. Ultrasound can confirm discontinuity, dynamic approximation and an alternative lesion when examination is obscured or equivocal. Its reported gap depends on ankle position, so the scan must state position and answer a management question. MRI is reserved for unusual chronic rupture, complex insertional disease or operative planning. Plain radiographs are for suspected avulsion fracture, bony insertional disease or another traumatic diagnosis, not routine tendon confirmation.

Protect length from the first encounter. Immobilise in plantar flexion using the local acute rupture boot or backslab protocol, ensure the heel wedges or splint position are correct, and avoid an unsupported neutral ankle. Local services differ on immediate weight-bearing, but modern functional pathways commonly permit protected weight-bearing in a boot when the specialist protocol specifies it. Arrange urgent review rather than a routine physiotherapy referral and assess VTE risk under NICE guidance for lower-limb immobilisation.

Shared treatment choice should not be reduced to young equals surgery. Functional non-operative treatment with early protected loading has narrowed rerupture differences when adherence is good and avoids wound and nerve risk. Surgery may be favoured for selected athletes, delayed or gapped ruptures, rerupture, open injury or where the specialist judges functional demand and anatomy justify it. Explain infection, wound breakdown, sural injury, rerupture and persistent weakness for both routes. Rehabilitation quality strongly influences outcome.

Rehabilitation follows biological protection: plantar-flexed immobilisation, staged wedge removal, controlled ankle range, progressive weight-bearing, then calf strength, balance, running and sport-specific power. Never accelerate dorsiflexion or abandon the boot because pain has eased. Measure calf circumference, ankle range, bilateral heel-rise height and endurance. Return to running or jumping requires strength and reactive capacity rather than a date alone; recovery commonly extends across many months.

For tendinopathy, explain that load is treatment as well as trigger. Reduce provoking volume temporarily, correct abrupt training changes and begin isometric or slow calf raises, progressing from bilateral to unilateral and from level ground to greater range for midportion disease. Insertional symptoms often tolerate a heel lift and calf raises from the floor better than heel drops over a step. Footwear modification and addressing proximal strength, sleep, weight and metabolic health support loading but do not replace it.

Short topical or oral analgesia may enable exercise, but long NSAID courses do not remodel tendon. Extracorporeal shockwave therapy may be considered for persistent appropriately diagnosed disease within a specialist pathway. Surgery for debridement, insertional bone work or reconstruction is uncommon and follows prolonged failed rehabilitation. Older age, pregnancy and anticoagulation change thrombosis, analgesic and operative planning; they do not make acute rupture safe to stretch or delay.

Key points

Acute rupture typically feels like being kicked in the heel, with a pop, weak push-off and inability to perform a normal single-leg heel rise; pain may settle quickly and should not reassure.
The high-yield bedside tests are a reduced resting plantar-flexion angle and absent or markedly reduced plantar flexion when the calf is squeezed with the patient prone and knees flexed.
Residual active plantar flexion does not exclude rupture because tibialis posterior, toe flexors and peroneal muscles can still point the foot.
First-line investigation is a confident clinical examination; ultrasound is used when findings are equivocal or gap and anatomy affect the plan, while routine MRI usually adds delay without changing acute care.
First-line emergency management is immediate immobilisation in plantar flexion, avoidance of repeated dorsiflexion, urgent specialist pathway referral and documented VTE-risk assessment.
Both functional non-operative bracing and operative repair can produce good outcomes; select treatment through shared decision using age-independent activity goals, gap, presentation delay, skin, comorbidity and rerupture versus wound risk.
Achilles tendinopathy is treated first with education, temporary load adjustment and progressive calf loading for at least twelve weeks; insertional disease begins on level ground without forced heel-drop dorsiflexion.
Do not inject corticosteroid into or around the Achilles tendon routinely because tendon weakening and rupture can outweigh temporary symptom relief.

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

Sudden eccentric overload

Rupture commonly occurs during acceleration, jumping or an unexpected forced dorsiflexion when gastrocnemius-soleus force exceeds the tendon's remaining tensile capacity.

Degenerative tendon susceptibility

Age-related matrix disorganisation, obesity, diabetes, inflammatory disease and previous symptoms may weaken tendon, although many ruptures occur without warning pain.

Medicine-related risk

Systemic glucocorticoids and fluoroquinolone exposure increase tendon injury risk, especially together and in older age, renal impairment or transplant recipients.

Repetitive load mismatch

Tendinopathy follows a mismatch between running, jumping or occupational demand and recovery capacity, modified by calf weakness, training error and metabolic health.

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

1
Acute fibre discontinuity
Rupture interrupts force transfer from gastrocnemius and soleus to calcaneus, reducing plantar-flexion power and the ability to push off or rise on one heel.
2
Gap and lengthening risk
Unprotected dorsiflexion separates tendon ends; healing in an elongated position leaves persistent calf weakness even when continuity later returns.
3
Tendinopathic matrix remodelling
Collagen disarray, increased proteoglycan and altered tenocyte signalling thicken the tendon and create load-related pain without a purely inflammatory mechanism.
4
Insertional compression
At the calcaneal insertion, tensile load combines with compression against the posterosuperior calcaneus, so rehabilitation may initially need to avoid deep dorsiflexion below floor level.

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

Kick and pop history

Sudden posterior-ankle impact sensation during push-off followed by weak gait is a classic rupture history even when pain decreases before review.

Positive calf-squeeze test

Squeezing the relaxed calf fails to produce the normal brisk plantar flexion when Achilles continuity is lost.

Altered resting angle

With knees flexed prone, the injured foot hangs less plantar-flexed than the opposite side, indicating loss of tendon tension.

Midportion tendinopathy

Load pain and morning stiffness with focal thickening several centimetres proximal to the insertion identifies the common midportion pattern.

Insertional tendinopathy

Pain and tenderness directly at the calcaneal insertion, aggravated by shoe pressure or deep dorsiflexion, requires a compression-sensitive loading plan.

Thrombosis warning

New diffuse calf swelling, disproportionate pain, breathlessness or pleuritic symptoms during immobilisation requires urgent venous-thromboembolism assessment.

Red flags requiring action

A sudden acceleration, jump or push-off followed by a pop, weak gait and positive calf-squeeze test is an acute rupture until proved otherwise, even if the patient can still point the foot.
An open posterior-ankle wound over a suspected rupture requires immediate antibiotics, tetanus assessment and orthopaedic washout and repair planning.
Pale or cool foot, altered sensation, severe escalating pain, tense swelling or passive-stretch pain requires emergency neurovascular and compartment assessment.
Calf swelling, pleuritic pain, breathlessness, haemoptysis or unexplained tachycardia during immobilisation requires urgent venous-thromboembolism assessment.
Insertional pain with fever, skin breach, rapidly spreading erythema or systemic illness suggests infection rather than uncomplicated tendinopathy.

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 bilateral Simmonds-Thompson examinationFirst stepFirst line
Why
Confirm functional tendon discontinuity and avoid false reassurance from residual active plantar flexion.
Interpretation and limitations
Reduced calf-squeeze movement plus altered resting angle strongly supports rupture and should trigger protection before imaging.
02
Diagnostic ultrasound when clinical findings are uncertain
Why
Assess continuity, location, dynamic end approximation and competing calf or tendon lesions.
Interpretation and limitations
Document ankle position because apparent gap changes with plantar flexion; scanning must not delay protective immobilisation.
03
Plain ankle and calcaneal radiographs
Why
Investigate avulsion, fracture, insertional calcification or bony prominence when history and tenderness suggest them.
Interpretation and limitations
Normal radiographs neither exclude rupture nor establish uncomplicated tendinopathy, which remain predominantly clinical diagnoses.
04
MRI for complex chronic disease
Why
Map chronic rupture, extensive insertional degeneration, tumour or anatomy required for reconstructive planning.
Interpretation and limitations
MRI is not a routine first-line acute rupture test and should not postpone referral or plantar-flexed protection.
05
VTE and pre-treatment assessment
Why
Identify thrombosis risk, bleeding risk, renal function and contraindications to prophylaxis during immobilisation.
Interpretation and limitations
Follow the current local tool and NICE NG89; prescribe prophylaxis only when individual VTE risk outweighs bleeding risk.

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

Calf muscle tear

Medial gastrocnemius injury produces proximal calf tenderness and pain but retains a normal tendon contour, resting angle and calf-squeeze response.

Deep-vein thrombosis

Diffuse swelling, venous risk and tenderness without an acute mechanical event requires thromboembolic assessment; rupture and immobilisation can also precipitate thrombosis.

Posterior ankle impingement

Pain during forced plantar flexion, often in dancers or kicking athletes, localises deeper at the posterior joint rather than within a thickened tendon.

Calcaneal stress or avulsion fracture

Bony squeeze pain, trauma, inability to bear weight or focal calcaneal tenderness warrants radiographs and sometimes advanced fracture imaging.

Inflammatory enthesitis

Bilateral insertional pain, prolonged morning stiffness, psoriasis, uveitis, bowel disease or several entheses suggests spondyloarthritis rather than isolated mechanical overload.

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

01ImmediateProtect a suspected ruptureFirst stepAn acute event produces weak push-off, abnormal resting angle, palpable gap or positive calf-squeeze test.

1Stop further dorsiflexion testing, document skin and neurovascular status and place the ankle in the approved plantar-flexed boot or backslab.
2Give mobility and weight-bearing instructions that match the local acute rupture protocol and check the device before discharge.
3Assess VTE and bleeding risk, provide thrombosis and pressure-area safety-netting and arrange urgent specialist review.
4Use ultrasound only when examination is equivocal or the specialist pathway needs gap information; do not wait for MRI routinely.

02Shared treatmentChoose functional bracing or repairThe diagnosis is confirmed and acute protection has been established.

1Discuss functional non-operative care and surgery using activity goals, timing, tendon apposition, skin, comorbidity and adherence rather than age alone.
2Explain rerupture, wound, infection, nerve injury, elongation and residual weakness in absolute and personally relevant terms.
3Continue plantar-flexed protection until the chosen protocol begins, avoiding unplanned neutral casting or stretching.
4Record the rehabilitation schedule, wedge removal and contact route so transitions do not create an unprotected gap.

03RehabilitationRestore length, strength and powerHealing has entered a functional brace or postoperative programme.

1Progress protected weight-bearing and wedge removal exactly to protocol while maintaining hip, knee and foot conditioning.
2Introduce ankle range without exceeding the permitted dorsiflexion, then build seated and standing calf strength progressively.
3Measure bilateral heel-rise height, repetitions, gait and balance before adding running, hopping and change of direction.
4Delay sport return until strength and reactive tasks are adequate and the specialist team agrees, not simply until pain is absent.

04TendinopathyRebuild tendon load capacityGradual load-related pain occurs without rupture findings, infection or fracture concern.

1Classify midportion versus insertional disease and modify the specific provoking load while retaining tolerable activity.
2Start progressive calf loading, avoiding below-floor heel drops initially for insertional compression and using a temporary heel lift when helpful.
3Review adherence, exercise dose, training error, footwear, systemic disease and medicine exposure over at least twelve weeks.
4Refer persistent major disability for diagnostic review and selected shockwave or surgical discussion rather than serial injections.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Provides early analgesia without affecting platelet function while the tendon is protected and the definitive plan is arranged.

Paracetamol for acute rupture pain

Take 500–1000 mg orally when needed, separated by at least 4 hours and limited to 4 g in 24 hours; use a lower maximum with body weight below 50 kg, frailty, malnutrition or liver risk.

Check combination products and alcohol or liver history; adequate analgesia must not encourage removal of the boot or premature dorsiflexion.

May reduce pain enough to begin graded calf loading, while exercise remains the disease-focused treatment.

Topical diclofenac for tendinopathy pain

For a short trial, place 2–4 g of diclofenac 1.16% gel on intact painful skin at each dose; remain within the product limit of three or four daily applications.

Avoid damaged skin and NSAID hypersensitivity, consider other NSAID exposure and pregnancy, and do not use symptom relief to accelerate tendon load abruptly.

Reduces immobilisation-associated venous thrombosis when VTE risk is judged to outweigh bleeding risk under NICE NG89.

Pharmacological VTE prophylaxis when risk assessment supports it

Use the locally approved prophylactic low-molecular-weight heparin or fondaparinux regimen for lower-limb immobilisation only after weight, renal function, pregnancy and bleeding assessment, continuing for the locally specified period and considering stopping if immobilisation exceeds 42 days.

Confirm renal dosing, body weight, platelet history, active bleeding, interacting antithrombotics and neuraxial plans; provide injection training and urgent advice for bleeding or thromboembolic symptoms.

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

Tendon elongation and weakness

Healing with excessive length reduces plantar-flexion torque, heel-rise height, running efficiency and eventual return-to-sport capacity markedly.

Rerupture

Premature dorsiflexion, unprotected loading, poor adherence or another injury can disrupt healing, particularly during the vulnerable transition out of the boot.

Venous thromboembolism

Lower-limb injury, reduced mobility and immobilisation increase deep-vein thrombosis and pulmonary embolism risk, requiring individual prophylaxis assessment and safety-netting.

Wound and nerve problems

Operative repair can cause wound breakdown, infection, adhesions and sural-nerve injury, risks amplified by smoking, diabetes and compromised posterior skin.

Persistent tendinopathy

Continuing load mismatch, fear, calf weakness or missed inflammatory disease can produce prolonged symptoms and deconditioning despite structural continuity.

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

At every early rupture review, check boot position, heel wedges, skin pressure, swelling, neurovascular status and adherence to loading instructions.
Screen for new calf swelling, pleuritic pain or breathlessness and reassess VTE and bleeding risk when mobility, surgery or medicines change.
Follow resting angle, tendon continuity, calf circumference and ankle range without forcing dorsiflexion during vulnerable healing.
Use heel-rise height, endurance, gait, balance and later hopping or sport tasks to progress rehabilitation objectively.
For tendinopathy, record morning stiffness, load tolerance, exercise dose and next-day response rather than imaging thickness alone.
Review smoking, diabetes, kidney disease, steroid or fluoroquinolone exposure and analgesic harm when recovery is slower than expected.

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

Plantar flexion can survive rupture

Several deep and lateral muscles still point the foot, so voluntary movement must never replace calf-squeeze and resting-angle assessment.

Pain can fade while the gap remains

Acute pain often settles before assessment; function, contour and tendon-tension tests determine urgency rather than current pain intensity.

Length matters as much as continuity

A healed but elongated Achilles transfers force poorly, which is why early plantar-flexed positioning and protocol-controlled dorsiflexion are essential.

Insertion changes the exercise range

Floor-level calf raises reduce compression at the calcaneus, whereas step drops may aggravate insertional disease despite helping selected midportion loading.

Boots create systemic risk

Pressure injury, falls and venous thrombosis must be considered alongside tendon healing whenever mobility is reduced.

Fluoroquinolone risk can persist

Tendon symptoms can occur during or after exposure; stop the medicine and seek prescriber review promptly when suspected, especially with systemic steroids.

11Common pitfallsFrequent interpretation and management errors.

01
Excluding rupture because the patient can plantar-flex or walk with a limp.
02
Stretching a fresh rupture to demonstrate range or placing it unsupported in neutral before the pathway begins.
03
Waiting for MRI when bedside findings already justify urgent protection and referral.
04
Choosing surgery or non-operative treatment solely from chronological age without discussing goals, gap, skin and adherence.
05
Progressing rehabilitation by time and pain alone without heel-rise strength, gait and power criteria.
06
Injecting corticosteroid around a painful Achilles tendon or prescribing fluoroquinolone without acting on new tendon symptoms.