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KembaraXtra-Medicine: Achilles Tendon Rupture
Achilles tendon rupture is a disruption of the continuity of the Achilles tendon, most commonly occurring after an eccentric loading event when the ankle is plantarflexed or when plantarflexion is forced against resistance. It is often an acute sports-related injury and can be missed initially, sometimes being mistaken for an ankle sprain. Relevant ICD-10-CM codes include S86.011 (right), S86.012 (left), M66.871 (nontraumatic right), M66.872 (nontraumatic left), and S86.0 (unspecified injury of Achilles tendon).
In the general population, Achilles tendon ruptures occur at an estimated rate of 18 per 100,000 people per year and are the most common large tendon rupture, accounting for approximately 20% to 35% of major tendon injuries. They most often occur in adults aged 30 to 55 years, with peak incidence in males aged 30 to 40 years, particularly those who participate in recreational athletics.
Risk is highest in people involved in “stop-and-go” sports such as basketball, tennis, and soccer, especially when there is a sudden increase in training intensity or duration. Additional risk factors include preexisting Achilles tendinopathy, advancing age, male sex, poor running mechanics, and a sedentary baseline followed by abrupt strenuous activity. Certain medications and substances are also associated with rupture risk, most notably fluoroquinolone antibiotics, where rupture tends to occur within the first 90 days, and steroid exposure, including prescribed corticosteroids and illicit anabolic steroid use.
The classic presentation is a middle-aged recreational athlete who feels a sudden “pop” in the posterior ankle or calf during pivoting, sprinting, jumping, or rapid deceleration, followed by acute pain and difficulty continuing activity. Pain may be severe, but some patients present primarily with weakness rather than pain and may still be able to walk. On examination, there may be swelling, bruising, and tenderness, and a palpable gap is often appreciated in the distal third of the tendon, typically 2 to 6 cm proximal to the calcaneal insertion. Patients may have an antalgic gait and are often unable to perform a single-leg heel raise due to loss of plantarflexion strength. When the patient lies prone with the feet hanging off the table, the injured side may rest in a more dorsiflexed position than the uninjured side. The Thompson test (calf squeeze test) is highly useful: squeezing the calf fails to produce normal plantarflexion when the tendon is ruptured. The Matles test (knee flexion test) provides additional support, with the injured foot falling into a more dorsiflexed or neutral position when the knees are flexed to 90 degrees.
Mechanistically, rupture is usually due to indirect trauma and reflects a combination of mechanical overload, relative hypovascularity in the classic “watershed zone” 2–6 cm above the insertion, and poor tendon tissue quality. Chronic tendinosis (degenerative change from repetitive microtears) and tendinitis can weaken the tendon, making it more susceptible to rupture during abrupt loading.
The differential diagnosis includes Achilles tendinopathy, retrocalcaneal bursitis, ankle sprain, calcaneal avulsion fracture, partial gastrocnemius tear, plantaris rupture, os trigonum syndrome, and calcaneal apophysitis. Diagnosis is largely clinical when history and exam findings are classic, but imaging can help in unclear cases or when partial tears are suspected.
Ultrasound is often used at the bedside and can identify tendon discontinuity, tendinopathy, and hematoma, making it a practical first-line study in many settings. MRI provides the greatest anatomic detail and is particularly helpful for confirming partial tears, defining the extent of injury, and assessing associated tendinopathy; a complete rupture typically shows fiber discontinuity and fluid signal at the tear site.
Initial management includes RICE (rest, ice, compression, elevation), along with analgesia such as acetaminophen or NSAIDs as appropriate. The ankle should be immobilized in a posterior slab splint with the foot in resting equinus (plantarflexion) to reduce tension on the tendon. Definitive treatment may be nonoperative or operative, and modern care increasingly uses accelerated functional rehabilitation protocols rather than prolonged casting alone.
Nonoperative treatment traditionally involved immobilization for 8 to 12 weeks, but newer accelerated protocols typically begin with about 2 weeks of immobilization, followed by progressive weight bearing in a walking boot with heel wedges to limit dorsiflexion, plus early supervised physical therapy emphasizing gradual range of motion and strengthening. These protocols have improved outcomes compared with older prolonged immobilization approaches.
Surgical repair is considered especially for acute complete ruptures, often aiming for repair within 4 weeks, and ideally within 7 to 14 days, to optimize healing and tendon length restoration. Techniques include open repair and percutaneous or minimally invasive approaches. Percutaneous repair may reduce operative time and deep infection risk but carries a higher risk of sural nerve injury. Postoperative care similarly relies on structured rehabilitation with early controlled motion and progressive strengthening.
Orthopedic referral is recommended for suspected acute or complete ruptures, as early evaluation helps guide operative versus nonoperative management and facilitates timely rehabilitation planning. Clinically important pearls include remembering that some patients may have minimal pain and may still walk, so careful palpation for a defect and performance of the Thompson test are crucial. Although surgery can reduce rerupture rates, it has higher complication risks, and randomized trials show that with modern functional rehabilitation, nonoperative treatment can achieve outcomes comparable to surgery at 12 months. Platelet-rich plasma (PRP), despite common use, has not shown benefit over placebo in several studies for acute rupture.
Prevention focuses on addressing modifiable risk factors, including maintaining conditioning, using proper training progression, continuing eccentric and concentric calf strengthening (especially after prior tendinopathy or rupture), and reducing training intensity during fluoroquinolone or anabolic steroid exposure.
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