The two heads of gastrocnemius (medial and lateral) arise from the condyles of the femur, the fleshy part of the muscle extending to about the midcalf. As the muscle fibers descend, they insert into a broad aponeurosis that contracts and receives the tendon of the soleus on its deep surface to form the Achilles tendon.³

The Achilles tendon is the thickest and strongest tendon in the body. About 15 cm long, it originates in the midcalf and extends distally to insert into the posterior surface of the calcaneum. Throughout its length, it receives muscle fibers from the soleus on its anterior surface.⁴

To date, the etiopathogenesis of Achilles tendinopathy remains unclear.

Tendinopathy has been attributed to a variety of intrinsic and extrinsic factors.⁶

It has been linked to overuse vascularity, dysfunction of the gastrocnemius-soleus, age, gender, body weight and height, endocrine or metabolic factors, deformity of the pes cavus, lateral instability of the ankle, the use of quinolone antibiotics, excessive movement of the hindfoot in the frontal plane, marked forefoot varus, changes in training pattern, poor technique, previous injuries, footwear, and environmental factors such as training on hard, slippery, or slanting surfaces.¹,²,³,⁴,⁵,⁶

Most of the previously mentioned factors should be considered associative, not causative, evidence, and their role in the cause of the condition is therefore still debatable.⁸

Although Achilles tendinopathy has been extensively studied, there is a clear lack of properly conducted scientific research to clarify its cause, pathology, natural history, and optimal management.⁹

The management of Achilles tendinopathy lacks evidence-based support, and tendinopathy sufferers are at risk of long-term morbidity with unpredictable clinical outcome.¹⁰

Most patients respond to conservative measures, and the symptoms can be controlled, especially if the patients accept that a decreased level of activities may be necessary.¹⁰

In 24% to 45.5% of patients with Achilles tendinopathy, conservative management is unsuccessful and surgery is recommended after exhausting conservative methods of management, often tried for 3 to 6 months. However, longstanding Achilles tendinopathy is associated with poor postoperative results, with a greater rate of reoperation before reaching an acceptable outcome.⁷,¹¹

As the biology of tendinopathy is being clarified, more effective management regimens may come to light, improving the success rate of both conservative and operative management.¹²

Patients typically present with pain located 2 to 6 cm proximal to the insertion of the tendon and felt after exercise.

As the pathologic process progresses, pain may occur during exercise and, when severe, may interfere with activities of daily living.

Runners experience pain at the beginning and at the end of a training session, with a period of diminished discomfort in between.

The foot and the heel should be inspected for malalignment, deformity, obvious asymmetry in the size of the tendon, localized thickening, a Haglund heel, and any previous scars.¹¹,¹²,¹³

The tendon should be palpated to detect tenderness, heat, thickening, nodularity, and crepitation.

The “painful arc” sign helps to distinguish between lesions of the tendon and paratenon. In paratendinopathy, the area of maximum thickening and tenderness remains fixed in relation to the malleoli from full dorsiflexion to plantarflexion, whereas lesions within the tendon move with movement of the ankle.¹⁴

Plain soft tissue radiography is useful in diagnosing associated or incidental bony abnormalities.¹⁰

Ultrasound is the primary imaging method because it correlates well with the histopathologic findings despite being operator-dependent.¹²

Ultrasound promptly identifies hypoechoic areas, which have been shown at surgery to consist of degenerated tissue, and increased thickness of the tendon.

Magnetic resonance imaging (MRI) studies should be performed only if the ultrasound scan remains unclear.

MRI provides extensive information on the internal morphology of the tendon and the surrounding structures and is useful
in evaluating the various stages of chronic degeneration and in differentiating between peritendinitis and tendinosis. Areas of mucoid degeneration are shown on MRI as a zone of high signal intensity on T1- and T2-weighted images.¹³

Paratendinopathy of the Achilles tendon

Acute or chronic rupture of the Achilles tendon

Rerupture of the Achilles tendon

Tear of the musculotendinous junction of the gastrocnemiussoleus and the Achilles tendon¹²

There is weak evidence of a modest benefit of nonsteroidal anti-inflammatory drugs (NSAIDs) for the alleviation of acute symptoms.⁵

Low-dose heparin, heel pads, topical laser therapy, and peritendinous steroid injection produced no difference in outcome when compared with no treatment.⁹

Medications shown to be effective in randomized controlled trials include peritendinous injection of aprotinin, topical application of glyceryl trinitrate, and the use of ultrasoundguided sclerosing injections in the area of neovascularization.¹⁰

Painful eccentric calf muscle training can be an effective treatment for noninsertional Achilles tendinopathy.¹³

Eccentric loading and low-energy shockwave therapy show comparable results.¹⁴

Conservative management is unsuccessful in 24% to 45.5% of patients with tendinopathy of tendo Achilles.¹⁴

Surgery is recommended after at least 6 months of conservative management.¹¹

The objective is to excise fibrotic adhesions, remove degenerated nodules, and make multiple longitudinal incisions in the tendon to detect intratendinous lesions and to restore vascularity, possibly stimulating the remaining viable cells to initiate a response in the cell matrix and healing.¹⁴