Achilles Tendon Rupture

Carrie A. Jaworski, MD, FAAFP, FACSM

Melissa Faubert, DO

BASICS

Achilles tendon ruptures are caused by laceration or by indirect forces applied to the tendon.
Three types of indirect forces have been described:
- Pushing off with the weight-bearing forefoot while extending the knee, such as with sprint starts and the push off in basketball
- Sudden, unexpected dorsiflexion of the ankle, as when the foot slips in a hole
- Violent dorsiflexion of a plantarflexed foot, as with a fall from a height

DESCRIPTION

Achilles tendon rupture is a complete disruption of the Achilles tendon, usually occurring 2 to 6 cm proximal to its calcaneal insertion, where blood supply is the poorest.
It can be associated with preexisting tendon degeneration and microtrauma.
It most commonly occurs in 30- to 40-yr-old men.
Synonym(s): heel-cord rupture; Achilles tear

EPIDEMIOLOGY

>75% of Achilles tendon ruptures occur in patients 30 to 40 yr old while they partake in sports activities.
Males > females: Ratio ranges from 1.7:1 to 19:1.
Left Achilles > right Achilles: thought to be due to higher prevalence of right-side dominant individuals using left lower limb to push off during activity
Yearly incidence is around 2 in 10,000.

ETIOLOGY AND PATHOPHYSIOLOGY

Is the largest tendon in the human body and is designed to endure stresses up to 10 times the body’s weight
Is formed by the confluence of the tendons of the gastrocnemius and soleus muscles. The gastrocnemius medial and lateral heads originate from the medial and lateral femoral condyles, respectively. The soleus originates from a large attachment on the posterior tibia and fibula. Together, these tendons insert onto the calcaneus and form the Achilles tendon.
Receives its blood supply intrinsically from both the musculotendinous junction and the osteotendinous insertion site
Additional vascular supply comes from an external source known as the paratenon. The paratenon is a thin layer of areolar tissue that encases the Achilles tendon. The further the tendon is from its musculotendinous origin and calcaneal insertion, the more it relies on the paratenon for vascular support.
The area with the poorest vascular supply is ˜ 2 to 6 cm proximal to the calcaneal insertion site.
Prior to inserting into the calcaneus, the Achilles tendon internally rotates, which imparts a structural torque stress in the tendon. This is thought to contribute to decreased vascularity in the tendon and ensuing tendon failure.

RISK FACTORS

Disease processes: connective tissue disorders, seronegative spondylopathies, rheumatoid arthritis, collagen vascular disease, diabetes mellitus, gout, hyperparathyroidism, renal insufficiency, hypothyroidism

Disuse atrophy and sedentary lifestyle
Prolonged immobilization
Advanced age
History of Achilles tendonitis/tendinosis, regardless of history of injection therapy
Mechanical imbalances (i.e., decreased flexibility of gastrocnemius-soleus complex)
Body weight/obesity
Possibility of genetic predisposition (possibility of association with human leukocyte antigen [HLA]-B27, blood group 0)

DIAGNOSIS

HISTORY

Patients commonly report feeling as if they have been kicked or struck in the back of the heel, only to find no one is nearby.
May feel or hear a “pop” or snap
Pain with weight-bearing
Weakness or stiffness of posterior ankle
May give history of chronic Achilles tendinitis with or without history of injection therapy

PHYSICAL EXAM

Acute complete rupture of the Achilles tendon involves a sudden, sharp pain behind the ankle, usually associated with a painful, palpable defect in the tendon.
Swelling and/or ecchymosis
“Hatchet strike” defect: palpable, tender defect, usually 2 to 6 cm from the tendon insertion site
Positive Thompson test is diagnostic. Have patient lie prone or kneel with ankles clear of the table. Perform on uninvolved side first for comparison. Squeeze bulk of calf muscle and observe for plantar flexion. Absence of plantar flexion is consistent with complete tendon rupture (sensitivity 0.96, specificity 0.93) (1).

Plantar flexion strength and ability to toe rise may be decreased compared to unaffected side.
Passive dorsiflexion may be increased compared to unaffected side.
These signs may be absent because of recruitment of other intact muscles, such as tibialis posterior, plantaris, peroneus longus and brevis, and flexor digitorum and hallucis longus.

DIAGNOSTIC TESTS & INTERPRETATION