Achilles Tendon Rupture

The Achilles tendon is the largest and strongest tendon in the body. It is formed by the confluence of the gastrocnemius and soleus tendons and inserts on the posterior calcaneus.

Rupture is the commonest tendon rupture of the lower limb, with an incidence of about 11 to 37 per 100,000 per year. It peaks in men aged 30 to 50 who take part in intermittent sport (football, basketball, racquet sports). The male to female ratio is about 5 to 10:1.

Most ruptures occur 2 to 6 cm proximal to the calcaneal insertion, in the relatively avascular "watershed" zone. The mechanism is sudden forceful plantarflexion (push off or sprint), unexpected dorsiflexion (misstep into a hole), or violent dorsiflexion of a plantarflexed foot. Rupture typically occurs in a tendon with pre-existing degenerative changes (tendinosis), although the patient often has no prior symptoms.

Risk factors:

• Fluoroquinolone antibiotics (ciprofloxacin, levofloxacin), especially in those aged over 60 and those who take corticosteroids; the effect may occur within days or up to months after treatment
• Local or systemic corticosteroids (injection into or near the tendon, oral steroids)
• Age, male sex, obesity, diabetes, gout, rheumatoid arthritis, renal disease, hyperparathyroidism, and statins in some data
• Prior tendinopathy, leg length discrepancy, poor flexibility, and intermittent high intensity loading
• Anabolic steroid use, and familial predisposition (blood group O in some series)

Patients describe a sudden "pop" or sensation of being kicked or struck in the back of the calf, followed by pain, swelling and weakness in plantarflexion. They may be able to walk with a limp, and may still plantarflex weakly using toe flexors and tibialis posterior, so the diagnosis is missed in up to 20 to 25% at first presentation.

Examination findings:

• Palpable gap in the tendon 2 to 6 cm above the heel, best felt in the first hours before swelling and haematoma obscure it
• Weak plantarflexion and inability to perform a single leg heel raise
• Thompson (Simmonds) test: with the patient prone and knees flexed or the legs hanging off the couch, squeezing the calf fails to produce plantarflexion; a positive test has a sensitivity of over 95%
• Matles test: with the patient prone and knee flexed to 90 degrees, the injured foot falls into neutral or dorsiflexion rather than remaining in slight plantarflexion
• Copeland sphygmomanometer test: cuff inflated to 100 mmHg around the calf, passive dorsiflexion produces less pressure rise on the injured side
• Increased passive ankle dorsiflexion compared with the other side
• Ecchymosis later at the heel and ankle

Differential diagnosis: partial tear, gastrocnemius tear (tennis leg), plantaris rupture, deep vein thrombosis, ankle sprain, Achilles tendinopathy, posterior ankle impingement, and Baker cyst rupture. Calf swelling and tenderness after a pop sensation should prompt consideration of DVT as a secondary complication.

The diagnosis is clinical. Imaging is used when the diagnosis is uncertain, in partial tears, chronic injuries, or when planning surgery.

• Ultrasound: dynamic assessment of the tendon gap and the tendon ends in dorsiflexion and plantarflexion; sensitivity above 90%
• MRI: confirms complete and partial tears, shows tendon quality, and detects associated pathology; useful for chronic ruptures
• Radiographs are not required routinely but exclude calcaneal avulsion fracture (a "fleck sign" or Kager fat pad changes)

Consider diabetes screening (HbA1c), review of drug history (fluoroquinolones, steroids), and thromboprophylaxis assessment.

Both operative and non-operative treatment are acceptable. Modern evidence shows that, with early functional rehabilitation, non-operative management gives similar functional outcomes to surgery with a lower complication rate. Rerupture rates have historically been higher with non-operative cast immobilisation (about 10 to 13% versus 2 to 5% with surgery in older studies). With accelerated functional protocols the difference narrows to about 1 to 3%.

Immediate care. Apply a posterior splint or boot in about 20 to 30 degrees of plantarflexion (equinus). Give rest, ice and elevation. Prescribe analgesia: paracetamol 1 g four times daily, with a short NSAID course if there is no contraindication. Some data suggest NSAIDs could affect tendon healing, so many advise limiting use.

Refer to orthopaedics within 24 to 72 hours. Consider thromboprophylaxis with low-molecular-weight heparin (enoxaparin 40 mg daily) during immobilisation in those with risk factors, or for the whole non-weight-bearing duration. Stop fluoroquinolones.

Non-operative functional rehabilitation protocol.

• Weeks 0 to 2: boot with heel wedges (about 3 to 4 cm raising the heel), protected weight bearing as tolerated with crutches
• Weeks 2 to 4: weight bearing as tolerated in the boot, remove one wedge layer every 2 weeks
• Weeks 4 to 6: reduce wedges progressively towards neutral
• Weeks 6 to 8: boot to neutral, begin gentle range of motion exercises and then physiotherapy
• Weeks 8 to 12: wean from the boot into shoes with a heel raise, strengthening, proprioception
• Months 3 to 6: progressive strengthening, running at about 4 to 6 months, return to sport at about 6 to 9 months, with the full strength recovery taking up to 12 months

Surgical repair. Indicated for:

• Younger and athletic patients who wish to minimise rerupture risk
• Delayed presentation (over 4 weeks)
• A retracted or irreducible gap in plantarflexion on ultrasound
• Rerupture
• Insertional or proximal avulsions

Techniques:

• Open repair with Krackow, Bunnell or Kessler type core sutures (number 2 non-absorbable braided or absorbable suture) with a running epitenon stitch
• Mini open or percutaneous repair (Ma and Griffith), with a lower wound complication rate but a higher sural nerve injury risk

Chronic ruptures or defects over 2 to 3 cm need augmentation: flexor hallucis longus transfer, V-Y advancement (Abraham and Pankovich), peroneus brevis transfer, or allograft. The postoperative protocol is similar to the non-operative functional rehabilitation protocol, starting weight bearing in a boot at 2 weeks.

Complications.

• Rerupture (about 2 to 5% operative, 3 to 12% non-operative, depending on protocol)
• Wound infection or necrosis (up to 5 to 10% with open repair)
• Deep vein thrombosis (up to 5 to 10% without prophylaxis)
• Tendon elongation with persistent weakness (push off strength about 80 to 90% of normal)
• Sural nerve injury, adhesions, calf muscle atrophy, and chronic pain

Patients should be counselled that complete recovery of strength may not occur.

Prevention. Avoid fluoroquinolones in patients at risk, avoid local steroid injection near the Achilles, warm up and use eccentric calf strengthening for tendinopathy.