Achilles Tendinopathy and Rupture

• Tendinopathy is an overuse degeneration presenting with posterior heel pain and morning stiffness, tenderness and often fusiform thickening in the mid-portion. Insertional disease at the calcaneus behaves differently and responds less well to the same measures.
• Rupture typically occurs in a middle-aged intermittent athlete during sudden push-off. The history is characteristic: a sudden "pop" with the sensation of being struck or kicked in the back of the ankle, followed by difficulty walking and pushing off.
• Examination of a rupture: a palpable gap, weakness of plantarflexion, and a positive Thompson (Simmonds) test — squeezing the calf with the patient prone fails to produce plantarflexion. Note that a patient with a complete rupture can often still plantarflex weakly using the other flexors, so the ability to move the foot does not exclude it.
• Risk factors worth naming: fluoroquinolone antibiotics and corticosteroids (systemic or injected), which is why steroid injection directly into the Achilles is avoided; also gout, hyperlipidaemia and chronic kidney disease.
• Imaging: ultrasound or MRI where the diagnosis is uncertain; the diagnosis of rupture is primarily clinical.
• Management: tendinopathy is treated with eccentric loading exercises, load management and footwear modification. Rupture may be managed operatively or non-operatively in a functional rehabilitation protocol; surgery lowers re-rupture rates at the cost of wound and infection risk.

Mechanical/overuse mechanisms (tendinopathy)

• Training error: abrupt increases in mileage, hill or interval work, and hard or uneven surfaces load the mid-substance faster than the tenocytes can remodel it.
• Biomechanical factors: gastrocnemius–soleus tightness with limited ankle dorsiflexion, hindfoot malalignment, and worn or minimally cushioned footwear concentrate strain on the watershed zone.
• Insertional disease: often accompanies a Haglund deformity (prominent posterosuperior calcaneus) with retrocalcaneal bursitis, or enthesitis in seronegative spondyloarthritis.

Sudden-load mechanism (rupture)

• Eccentric overload: forced dorsiflexion of a plantarflexed foot or explosive push-off, classically in the middle-aged "weekend warrior" returning to court or racquet sports.

Modifiable risk factors — the ones examiners plant

• Fluoroquinolones: ciprofloxacin and levofloxacin carry an FDA boxed warning for tendinitis and tendon rupture; risk is greatest in patients over 60, transplant recipients, those with renal impairment, and those on concurrent steroids. Rupture may occur within days of starting and sometimes after the course ends.
• Corticosteroids: systemic therapy or peritendinous injection impairs collagen synthesis and provides analgesia that permits continued loading — this is why intratendinous Achilles injection is avoided.
• Obesity, diabetes, hyperlipidaemia, and smoking: all impair tendon microvascular supply and matrix quality.
• Anabolic steroid use and deconditioning with sporadic intense activity.

Non-modifiable / disease-associated

• Age 30–50 for rupture (older cohorts for tendinopathy), male sex, and prior tendinopathy or contralateral rupture.
• Chronic kidney disease and dialysis, secondary hyperparathyroidism, and solid-organ transplantation.
• Gout (tophaceous deposition) and familial hypercholesterolaemia, where bilateral Achilles xanthomas produce nodular thickening — a classic stem clue pointing to an LDL-receptor defect.
• Inflammatory arthritides, including rheumatoid arthritis and spondyloarthritis with enthesitis.

The vascular substrate

• The tendon receives blood proximally from muscular branches, distally from calcaneal periosteal vessels, and along its length from the paratenon. The region 2–6 cm above the insertion sits between these supplies — a watershed zone with the lowest capillary density, so repetitive microtrauma outpaces repair precisely where rupture occurs.

Tendinopathy is degeneration, not inflammation

• Repetitive tensile load induces tenocyte apoptosis and a failed healing response: disorganised collagen with a shift from type I to weaker type III, mucoid ground-substance accumulation, and neovascularisation with accompanying sensory nerve ingrowth. Histology shows few or no inflammatory cells — hence tendinosis is the more accurate term, and why NSAIDs modify symptoms but not the disease.
• The ingrowing nerves and neuropeptides explain load-related pain; the disordered matrix explains the fusiform mid-portion thickening and the morning stiffness that eases as the viscoelastic tendon warms up.

How drugs weaken the tendon

• Fluoroquinolones chelate magnesium and disrupt integrin-mediated tenocyte–matrix signalling, upregulate matrix metalloproteinases, and generate oxidative stress — accelerating collagen degradation, so rupture can occur at submaximal load.
• Corticosteroids suppress fibroblast collagen synthesis and proteoglycan production; injected intratendinously they create a focal weak zone.

From degeneration to rupture

• A degenerated tendon fails under an eccentric spike in load. Discontinuity produces the palpable gap, and the audible pop reflects sudden release of stored elastic energy.
• The Thompson (Simmonds) test works because squeezing the calf deforms the gastrocnemius–soleus mass and tugs the tendon; with continuity lost, that force is no longer transmitted and the foot stays still.
• Plantarflexion is not abolished, because tibialis posterior, the peroneals, FHL and FDL still act across the ankle — the patient can plantarflex weakly against gravity but cannot perform a single-leg heel raise.

Tendinopathy — the insidious presentation

• Posterior heel/calf pain and morning stiffness: worst with the first steps out of bed and after periods of inactivity, easing with warm-up then returning after prolonged activity — the signature of a degenerative, load-responsive tendon rather than an inflammatory one.
• Fusiform mid-portion thickening and focal tenderness 2–6 cm above the calcaneus, corresponding to the watershed zone.
• Arc sign / painful arc: the tender swelling moves with ankle dorsiflexion–plantarflexion in intratendinous disease but stays fixed in paratendinitis.
• Insertional disease: tenderness at the calcaneal attachment, often with a bony Haglund prominence, retrocalcaneal bursal swelling and pain aggravated by rigid heel counters. It is more common in older, less athletic and inflammatory-arthritis patients.
• Bilateral nodular thickening in a young patient with tendon xanthomas should prompt a lipid panel.

Rupture — the acute presentation

• Stem demographic: a man in his 30s–50s, sedentary during the week, playing basketball, tennis or squash; or an older patient recently started on a fluoroquinolone or taking systemic corticosteroids.
• Sudden pain with the sensation of being kicked or shot in the back of the ankle, sometimes with an audible pop; patients often turn around expecting to find someone behind them.
• Inability to push off, run or climb stairs; an antalgic, flat-footed gait.
• Palpable gap 2–6 cm above the insertion, sometimes obscured within hours by haematoma and swelling; ecchymosis tracks distally.
• Positive Thompson (Simmonds) test with the patient prone and feet over the table edge — calf squeeze produces no plantarflexion.
• Matles test: with knees flexed to 90° prone, the affected foot rests in neutral or dorsiflexion instead of the normal resting plantarflexion, because tendon resting tone is lost.
• Inability to perform a single-leg heel raise — a more reliable functional sign than simple plantarflexion, which is preserved by the deep flexors and peroneals.

Step 1 — the diagnosis is clinical

• Acute rupture is diagnosed at the bedside. The AAOS clinical practice guideline supports diagnosis using two or more of: positive Thompson (Simmonds) test, decreased resting ankle plantarflexion (Matles test), palpable gap, and decreased plantarflexion strength. The Thompson test is highly sensitive; imaging is not required when the examination is unambiguous.
• Always test the contralateral side for comparison, and document sural nerve sensation before any intervention.

Step 2 — plain radiographs, selectively

• Lateral ankle films do not show the tendon but exclude a calcaneal avulsion fracture (important in diabetics and the elderly, and it changes management to fixation), demonstrate a Haglund deformity or insertional enthesophytes, and may show loss of the normal Kager fat pad triangle.

Step 3 — ultrasound as first-line imaging when the picture is unclear

• Operator-dependent but cheap and dynamic: it shows fibre discontinuity, the gap and whether the ends appose with plantarflexion — the finding that informs non-operative treatment. In tendinopathy it shows hypoechoic fusiform thickening with neovascularity on power Doppler, correlating with pain.

Step 4 — MRI as the confirmatory/gold-standard study

• Reserved for equivocal examinations, suspected partial tears, chronic or neglected ruptures, and preoperative planning. It defines tendon gap length, degree of retraction, and muscle atrophy or fatty change.

Severity and outcome scoring

• The VISA-A (Victorian Institute of Sport Assessment – Achilles) questionnaire is the named instrument for grading tendinopathy severity and tracking rehabilitation response.

Targeted labs when the stem hints at it

• Fasting lipid panel for bilateral nodular tendons (familial hypercholesterolaemia), serum urate for tophaceous disease, and inflammatory markers plus HLA-B27 considerations for young patients with bilateral insertional enthesitis.

Immediate management of suspected acute rupture

• Immobilise in equinus (plantarflexion) in a posterior splint or a boot with heel wedges, keep the patient non-weight-bearing or protected-weight-bearing, and refer urgently to orthopaedics. Plantarflexion apposes the torn ends; splinting in dorsiflexion is a management error.
• Stop the offending drug: discontinue the fluoroquinolone and avoid further corticosteroid exposure. Assess VTE risk, since immobilisation of a lower limb is itself a thrombotic risk factor.

Definitive management of rupture

• The AAOS guideline supports either operative repair or non-operative treatment within an early functional rehabilitation protocol (progressive weight-bearing and controlled range of motion in a boot with graduated heel-wedge removal), and recommends shared decision-making. With modern functional rehab the re-rupture difference narrows considerably.
• Operative repair (open or percutaneous end-to-end) is favoured for young, high-demand athletes, delayed presentation, large gaps that do not appose on dynamic ultrasound, and re-rupture. It reduces re-rupture but adds wound infection, dehiscence and sural nerve injury risk.
• Non-operative care is favoured in older, sedentary, diabetic, vasculopathic or smoking patients in whom wound healing is the greater threat.
• Chronic/neglected ruptures require reconstruction — V-Y lengthening, turndown flap, or flexor hallucis longus tendon transfer.

Tendinopathy

• First line — mechanotherapy: a supervised eccentric heel-drop programme (Alfredson protocol) over roughly 12 weeks, with relative rest, load modification, heel lifts and calf stretching. This is the intervention with the best evidence.
• Adjuncts: short-course NSAIDs (for example naproxen) for analgesia only; extracorporeal shockwave therapy for recalcitrant cases; nitroglycerin patches and platelet-rich plasma have inconsistent evidence.
• Surgery (debridement, Haglund resection, gastrocnemius recession, FHL transfer) after failure of a genuine six-month rehabilitation trial.

Contraindicated

• Intratendinous corticosteroid injection — precipitates rupture.
• Continuing a fluoroquinolone in a patient with tendon pain, and immobilising a rupture in dorsiflexion.

Of the disease and of non-operative care

• Re-rupture: highest risk in the first months as the healing tendon remodels and after return to sport; higher with non-operative treatment, particularly if functional rehabilitation is not used. Signalled by a repeat pop, a new gap and a again-positive Thompson test.
• Tendon elongation (healing in a lengthened position): the ends heal apposed but stretched, producing permanent loss of push-off power, inability to single-leg heel raise, and calf atrophy — the main functional penalty of casting in insufficient equinus.
• Missed or neglected rupture: up to a quarter of acute ruptures are missed initially because the patient can still weakly plantarflex. Retraction and scar interposition then require reconstructive tendon transfer rather than simple repair.
• Chronic tendinopathy with insertional calcification, retrocalcaneal bursitis and adhesions between tendon and paratenon.
• Venous thromboembolism — immobilisation plus lower-limb injury is a recognised risk; new calf swelling out of proportion, or pleuritic chest pain and dyspnoea, is an emergency requiring evaluation for DVT/PE.

Of surgery

• Wound dehiscence and infection: the posterior heel has thin, poorly vascularised subcutaneous cover; risk is amplified by diabetes, smoking and steroid use. Deep infection involving the repair can require debridement and is limb-threatening — treat as urgent.
• Sural nerve injury: the nerve crosses lateral to the tendon and is at particular risk with percutaneous techniques; presents as numbness or dysaesthesia over the lateral foot and fifth toe.
• Adhesions and scar sensitivity limiting footwear tolerance; complex regional pain syndrome rarely.
• Anaesthetic and positioning complications from prone surgery.

• The watershed zone is the answer to "why here?": 2–6 cm above the calcaneal insertion, between the proximal muscular and distal calcaneal blood supplies. Both tendinopathy and rupture cluster there.
• Preserved plantarflexion does not exclude rupture — the classic distractor. Tibialis posterior, the peroneals and the long toe flexors still plantarflex the ankle. Ask instead for a single-leg heel raise, which the patient cannot do.
• Positive Thompson (Simmonds) test — prone calf squeeze producing no plantarflexion — is the single most tested physical sign. The Matles test (foot resting in neutral/dorsiflexion with knee flexed 90° prone) is its companion.
• Single best next step for a convincing history and positive Thompson test: splint in equinus (plantarflexion), non-weight-bearing, urgent orthopaedic referral — not MRI. Imaging is for equivocal cases, partial tears, or chronic ruptures.
• The drug association examiners love: fluoroquinolones (FDA boxed warning), amplified by concurrent corticosteroids, age over 60, renal impairment and transplantation. A stem describing heel pain days after starting levofloxacin wants "stop the antibiotic."
• Never inject corticosteroid into the Achilles tendon — it suppresses collagen synthesis and precipitates rupture.
• Bilateral nodular Achilles thickening in a young patient = tendon xanthomas of familial hypercholesterolaemia; order a lipid panel and think LDL-receptor defect.
• Tendinopathy is degenerative, not inflammatory (tendinosis: collagen disarray, type III collagen, neovascularisation, no inflammatory infiltrate). This is why eccentric loading, not NSAIDs, is first-line therapy.
• Post-repair numbness of the lateral foot and fifth toe = sural nerve injury, especially after percutaneous repair.
• Get a lateral radiograph in an elderly or diabetic patient to exclude a calcaneal avulsion fracture, which is fixed rather than rehabilitated.