Disorders of the Ankle and Foot: Posterior

Achilles Tendinopathy

Achilles tendinopathy is one of the most common findings in patients with chronic heel pain. It is a common disorder with an incidence rate of 2.35 per 1000 adult patients in a large Dutch report on GP-registered patients. Most cases are encountered in the middle-aged population (age 41–60 years). It is more a degenerative (tendinosis) than an inflammatory condition, and it is caused by overuse of the tendon fibres, often related to sporting activity, including running. Sport athletes are at high risk but a relationship with sports activity is not always present.

Other factors that can play a role in the pathogenesis of tendinopathy are an imbalance between the gastrocnemius and the soleus individual contributions to the tendon, age, weight, sedentary life, vascularity, associated limb torsion and ankle abnormalities. Symptoms generally develop insidiously. It is difficult to differentiate clinically between tendinopathy and inflammation of the paratenon (para­tenonopathy), all the more since the two conditions can be associated. Patients with tendinopathy present with pain, swelling, morning stiffness and impaired performance in sport activities and with daily living. Ultrasonography has a high-positive predictive value for visualization of tendinopathy, but has a lower sensitivity than MRI for detection of paratenonitis. Ultrasonography shows involvement of the hypovascularized tendon midportion (2–6 cm above the insertion), reflecting the histopathological signs of failed healing response: disruption of collagen fibres, increase in ground substance (proteoglycans), tenocyte proliferation and neovascularization. Bilateral findings are present in more than half the patients,

Most often the degenerative process is diffuse, leading to a painful spindle-shaped hypoechoic enlargement of the Achilles tendon ( Fig. 24.1 ). The fibrillar structure of the tendon is nicely appreciated on longitudinal ultrasound sections, so areas of preserved and thickened fascicles can be seen ( Fig. 24.2A, B ). With progressive involvement, the overall echogenicity of the tendon tends to decrease, as the spacing between fibres tends to increase. It is important to avoid anisotropic artifact during this assessment. This tendon enlargement is quantified by measuring the anteroposterior diameter of the tendon: exceeding 6 mm in tendinopathy. In some patients the tendon enlargement is asymmetrical, often affecting the medial aspect of the tendon more than the lateral ( Fig. 24.3 ). With isolated tendinopathy, there is no discontinuity of the tendon borders. On axial sections ( Fig. 24.2C, D ) the tendon is rounded and hypoechoic, with loss of the normal anterior flat or slightly concave contour. Colour Doppler examination often shows tendinous and/or peritendinous hyperaemia, mostly as small vessels entering the anterior border of the tendon at right angles ( Fig. 24.2 E, F ). This should be performed on a relaxed tendon and without too much transducer compression in order to avoid a false-negative examination due to obliteration of the vessels. Some patients may exhibit focal degenerative abnormalities, involving the anterior or posterior part of the tendon ( Fig. 24.4 ).

When the Achilles tendon is painful at palpation but grossly normal on ultrasound, paratenonopathy should be suspected, and subtle signs of tendinopathy (convexity of the anterior border, slight hypoechogenity or hyperaemia) and/or paratenonopathy (slight thickening of the paratenon, increased echogenicity of the pre-Achilles fat pad) should be carefully sought. Conversely, areas of tendinopathy, with or without increased colour Doppler signal, may be detected in asymptomatic tendons, though there is an increased likelihood that these tendons will eventually become symptomatic. With time, the tendon may become heterogeneous and the hypoechoic areas of degeneration may present very small anechoic, rounded or longitudinally orientated, intratendinous lesions. These are referred to as microtears or delaminations ( Fig. 24.5A, B ). Less commonly, calcifications may be found in the Achilles tendon (calcific tendinopathy, Fig. 24.5C ). Eventually, complete or partial tear of the midportion of the tendon may occur.

Treatment of tendinopathy is essentially conservative with a period of rest, nonsteroidal antiinflammatory medication and heel lift, followed by physiotherapy (eccentric training), and sometimes surgery in resistant situations. Some rare forms of tendinopathy are related to a specific cause and have to be treated accordingly: lipid-storage disorders, rheumatic diseases, treatment by local or systemic steroids, or certain antibiotics.

Heterozygous familial hypercholesterolemia is an autosomal dominant disease, characterized by elevated low-density lipoprotein cholesterol plasma levels, premature coronary artery disease and cholesterol deposits in extensor tendons (xanthomas) with the Achilles tendon as the most frequently affected tendon ( Fig. 24.6 ). The presence of Achilles tendon xanthomas is pathognomonic of the disease but 25% of patients present with a normal tendon at palpation. Ultrasonography may demonstrate focal anechoic areas, confluent hypoechoic areas or an enlarged heterogeneous tendon. Ultrasonography has thus been advocated as a screening tool in clinically silent tendons in patients with hyper­lipidaemia or with a family history of occurence. Achilles tendinopathy, paratenonopathy, enthesitis, retrocalcaneal bursitis and/or joint synovitis are frequent findings in rheumatic disorders such as rheumatoid arthritis, gout or spondylarthritis. Ultrasonography can also show subcutaneous rheumatoid nodules (well-circumscribed focal hypoechoic area) in rheumatoid arthritis and intratendinous tophi in gout (heterogeneous hyperechoic areas with shadowing). Achilles tendon tears have been reported as a complication of local or systemic steroids. Severe tendinopathy can also occur as a complication of the administration of fluoro­quinolone antibiotics, with a higher risk in patients with renal dysfunction. It is most frequently seen at the Achilles tendon, often bilateral and leading to tendon tear in nearly half the cases.

Achilles Paratenonopathy

Paratenonitis means inflammation of the paratenon. The most common cause is mechanical and secondary to an overuse injury, either isolated (initial stage) or associated to tendinopathy (late stage). Paratenonosis fibrous adhesions can develop in chronic situations (paratendinosis), limiting tendon movement. Other causes of paratenonitis are rheumatic diseases and especially spondylarthropathies.

Palpation is painful and thickening of the Achilles tendon is often suspected clinically. Ultrasonography may show an echo-poor thickening of the paratenon, best seen on axial scans ( Fig. 24.7 ). The paratenon surrounds the Achilles on three sides: posterior, medial and lateral. This explains the shape of paratenonopathy: U-shaped with no enlargement anteriorly. This thickening of the paratenon is often subtle. In rare acute cases, a small amount of fluid in the paratenon can be identified. Some patients with inflammatory joint diseases exhibit a marked enlargement, often with associated tendinopathy. MRI is also sensitive for the diagnosis of paratenonitis, as diffuse soft tissue oedema around the tendon is easy to detect. In some cases, ultrasonography may show soft tissue oedema in the pre-Achilles fat pad (diffuse hyperechogenicity and heterogeneity) or the subcutaneous tissue, with careful comparison to the contralateral side. Peritendinous hyperaemia demonstrated with colour Doppler examination is also helpful for the diagnosis.

Achilles Enthesopathy

Achilles enthesopathy is caused by inflammation at the site of insertion of the tendon on the inferior part of the posterior aspect of the calcaneus. This area comprises the most distal part of the tendon, the enthesis fibrocartilage, as described by Benjamin and McGonagle, and the adjacent bone. The causes of Achilles enthesopathy are most often mechanical and related to age, overweight, sport activity, compression by hard footwear, or a short Achilles tendon, but can also be inflammatory. Inflammatory enthesitis is seen in seronegative spondylarthropathies, such as ankylosing spondylarthritis and psoriasis. Regardless of the cause, chronic enthesopathy changes can be subtle and asymptomatic.

Key Point

The typical ultrasound findings of enthesopathy are enlargement of the tendon insertion, which becomes hypoechoic, sometimes with calcifications or spur, and often hypervascularized on colour Doppler examination ( Fig. 24.8 ).

Disturbances of the interface between the tendon and the posteroinferior aspect of the calcaneus are well demonstrated on ultrasonography, sometimes better than with plain radiography or MRI. Ultrasound shows irregularity of the enthesis fibrocartilage and the underlying bone surface and posterior bone spur. On the other hand, MRI can demonstrate a focal area of bone oedema in the posteroinferior calcaneus, close to the enthesis and/or in the bone spur. Bone spur is a common asymptomatic finding.

In addition, ultrasonography enables precise placement of the tip of the needle for local steroid injection, which can be very helpful as the subcutaneous soft tissues often are adherent to the enthesis.

In spondylarthropathies, enthesitis is predominantly encountered in the lower limbs, and especially at the Achilles tendon insertion. Achilles enthesopathy is often underestimated clinically.

Ultrasonography is especially useful to demonstrate erosions of the posterior calcaneus, but cannot visualize associated bone oedema. Local soft-tissue hyperaemia on colour Doppler may also be found and is an important feature for treatment monitoring. Adjacent bursitis, bilateral involvement and joint involvement with synovitis also occur.

The main differential diagnoses are Haglund's disease, calcaneal stress fracture, heel pad syndrome, and plantar fasciitis. Calcaneal tumours are rare but calcaneal stress fracture is not and may be seen in runners. Plain radiography is normal with stress fractures, and the diagnosis is usually made using MRI, which shows focal bone oedema around a fracture line. Ultrasound is positive only if the cortex is involved. Isotope bone-scan has been advocated but carries a high radiation dose. CT is used to assess healing.

Haglund's Disease

Haglund's disease is a mechanical disorder causing heel pain, first described in 1928, and classically based on the Haglund's triad: hypertrophy of the posterosuperior portion of the calcaneal tuberosity (Haglund's deformity), retrocalcaneal bursitis and focal changes in the anterior distal Achilles tendon. These pathological findings are located in the proximal, preinsertional part of the enthesis, and not at the level of the tendon insertion. On clinical examination, pain and swelling are found in the angle between the calcaneal tuberosity and the Achilles tendon. It is believed to be related to impingement of the tendon on the hypertrophied tuberosity during dorsal flexion of the ankle, often related to sport activity in young subjects (running, soccer, racket sports and gymnastics). The use of rigid shoes has also been incriminated in the pathogenesis.

On ultrasonography the diagnosis is based on the soft tissue changes ( Fig. 24.9A, B ): retrocalcaneal bursitis and a focal hypoechoic area in the anterior part of the distal Achilles tendon, corresponding to the sesamoid fibrocartilage described by Benjamin and McGonagle. Bone irregularities can be detected on the surface of the calcaneal tuberosity (corresponding to the periosteal fibrocartilage), but plain radiography is needed to demonstrate the hypertrophy of the tuberosity. Different radiological measurement techniques have been developed to quantify this hypertrophy. MRI has the ability to show all the elements of the diagnostic triad, but also areas of focal oedema in the posterosuperior calcaneus and/or the pre-Achilles fat pad ( Fig. 24.9C ).

Haglund's disease often leads to partial tearing of the anterior part of the distal Achilles tendon and rarely to complete tearing. It can also be associated with signs of Achilles tendinopathy or signs of enthesopathy. In some patients, the calcaneal tuberosity is either not or minimally hypertrophied, and impingement can be suspected on the presence of bone oedema at the tuberosity or an abnormal calcaneus tilting. Retrocalcaneal bursitis is not always obvious on ultrasound in chronic situations and the diagnosis can be based on the other signs of Haglund's disease or bursal calcifications.

If conservative treatment (rest, nonsteroidal antiinflammatory medication, change of shoe and heel lift) is not effective, surgical treatment with calcaneal osteotomy can be considered.

Achilles Tendon Tear

Tears of the Achilles tendon are most often complete/full thickness. Partial thickness tears are uncommon and an initial impression of a partial tear is often upgraded to full thickness on dynamic assessment. Tears most commonly occur secondary to a preexisting tendon abnormality, which explains the different locations and types of tears and their frequencies. Tears can thus be located at three different levels: the midportion, the musculotendinous junction, and the distal part of the tendon.

Tears of the midportion occur in the third to fifth decade, often related to sport activity (especially racket sports), more commonly in males, and with a second peak in the eighth decade. The onset is often acute, with a sharp sensation and sometimes a snap in the hind-foot as if the patient has just been kicked (or struck by an arrow fired by Paris and guided by Apollo). The patient cannot stand on his toes on the affected side. After a short period a characteristic haematoma develops, tracking inferiorly on either side of the tendon. The patient may consult de novo with tendon rupture or will often present with a preexisting history of Achilles tendon pain. A complete Achilles tendon tear is often suspected on clinical examination: spontaneous slight dorsal flexion of the ankle at inspection, tendon defect at palpation, and positive Thompson's test (no plantar flexion of the ankle during compression of the calf). However, it is not infrequent that Achilles tendon tears are overlooked at the initial clinical examination (20–25%). Thompson's test is negative in partial tears and can be false-negative if the presence of a plantaris tendon produces a plantar flexion during the test, as there may be infiltration by haematoma and inflammation in chronic cases.

Ultrasonographic diagnosis is based on the detection of a complete or partial interruption of the tendon fibres with loss of tendon volume and alteration of its borders. Signs of underlying chronic Achilles tendinopathy are common. With complete tears retraction occurs and the gap is filled with anechoic blood and heterogeneous haemorrhage or other debris.

In partial tendon tears, a substantial portion of the Achilles tendon is disrupted, with focal loss of function. Dynamic ultrasonography can reliably detect these partial Achilles tendon tears and distinguish them from Achilles tendinopathy or from the rare tears of the midportion of the plantaris tendon. Very small anechoic areas in the Achilles tendon, without impact on tendon contours and without loss of function (microtears), should not be referred to as partial tears, but are changes associated with the underlying tendinopathy. The accumulation of these microtears at one site may be expected to weaken the tendon and eventually lead to partial or full-thickness tear.

Overlooked tendon tears are not infrequent and can lead, like insufficiently treated tears, to chronic complications, such as a focal area with reduced solidity, lengthening of the tendon, pain, or muscle atrophy with fat degeneration (echo-rich muscle tissue seen mainly in the soleus muscle). Interposition of the plantaris tendon and/or anterior fat pad into the tendon gap occurs and needs to be reported as it may prevent spontaneous healing. Healing with in situ plantaris interposition has been described.

Attention should be drawn to any focal thinning of the tendon, with loss of volume and concavity of the contours. Complete tears are prone to retraction, leading to better visualization of tendon ends by their edge artifacts (posterior shadowing associated with refraction of the ultrasound waves). Visualization of the two tendon ends is important to measure the length of the defect and the degree of proximal tendon retraction ( Fig. 24.10A, B ) as, in many centres, this impacts on surgical decision making. Small gaps, less than 5 mm, may be treated by conservative measures, whereas larger gaps are often managed surgically, either by open or percutaneous methods. If surgery is likely, the location of the tendon ends can be marked on the patient's skin. As contact gel can make this difficult, an initial impression can be made using an unfolded paperclip moved under the probe until its shadow lies at the tendon end, then pressed into the skin to make an indentation ( Fig. 24.11 ). Once the two ends are marked, the skin is dried and the indentations can be augmented with a skin-marking pen. An alternative method is to mark the centre of the tendon gap. Colour Doppler examination does generally not add much to the diagnosis.

In complete tears a longitudinal fibrillar structure can often be seen in the medial part of the defect. This represents an intact plantaris tendon ( Fig. 24.10C, D ) and should not be mistaken for residual Achilles tendon fibres and a partial tear misdiagnosed. In axial sections of the tendon gap, the heterogeneous haematoma is often still contained by the intact paratenon, with a small echo-rich rounded plantaris tendon in the medial part of the gap. Because of the proximity of the sural nerve, just lateral to the Achilles tendon, injury to this nerve may accompany Achilles tendon tears.

The second most frequent type of Achilles tear is an epimyseal tear of the musculotendinous junction of the medial gastrocnemius muscle, often seen in young athletes. This lesion has been called ‘tennis leg’ and occurs typically after a forced push-off with concomitant rotation of the leg.

In the acute phase, an anechoic fluid collection is seen between the medial gastrocnemius and the soleus muscles, with slight retraction of the distal part of the medial gastrocnemius muscle. The tear is often small and difficult to visualize as an irregularity of the deep aponeurosis of the distal gastrocnemius muscle. Treatment is conservative, and can include ultrasound-guided fluid aspiration followed by compression. Less frequently the musculotendinous lesion is located at the distal aponeurosis of the soleus muscle. Ultrasonography shows changes at the level of the distal soleus muscle with a complete tear of both the gastrocnemius and the soleus aponeurosis (including a defect in the soleus muscle). Differential diagnoses of all these Achilles musculotendinous lesions are deep venous thrombosis, ruptured Baker's cyst and musculotendinous tears of the plantaris tendon. Patients with tennis leg may develop chronic pain, if the injury is overlooked. On ultrasound a hard, heterogeneous, hypoechoic layer of scarred tissue is found between the medial gastrocnemius and the soleus muscles.

The third and least common type of tear is situated in the distal part of the Achilles tendon, and is most often a partial tear of the anterior distal tendon in patients with Haglund's disease. A bone avulsion of the insertion of the Achilles tendon is rare. It is generally related to an abnormality of the os calcis. Predisposing factors include steroid therapy, diabetes, rheumatoid arthritis, metabolic bone disease and renal failure. The diagnosis is made on ultrasonography and standard radiography.

The Postoperative Achilles Tendon

In postoperative patients, ultrasonographic follow-up shows a markedly enlarged, hypoechoic and heterogeneous, sometimes with small residual cystic areas or calcifications. Sutures can be visualized as thin intratendinous double lines, with or without acoustic shadowing. Intratendinous colour Doppler signal is often visualized and difficult to interpret. With time the tendon becomes less hypoechoic and tendon hypervascularization should vanish, but this can take many months. Ultrasonography can be performed for postoperative tendon complications (pain and limping) or for tendinopathy in a previously uninvolved contralateral Achilles tendon.

Ultrasonography is performed for detection of tear recurrence or necrosis, signs of infection, residual tendon lengthening, or lesion of the sural nerve.

Local infection is a more severe complication. Ultrasonography may show subcutaneous oedema and fluid collections in or around the tendon. The most important role for ultrasonography is, however, to perform an ultrasound-guided diagnostic aspiration of such collections. The sural nerve is a sensory nerve crossing the upper part of the Achilles tendon to become lateral to it. Because of this anatomical proximity, injury to this nerve may occur as a complication of tendon suturing, particularly under minimally invasive surgery.

After calcaneal osteotomy in patients with Haglund's disease, a focal bone defect is seen on the calcaneal tuberosity. With time, pain can recur due to fibrotic tissue between the calcaneus and the Achilles tendon (hypoechoic mass). When symptomatic this tissue is painful at palpation and can be hypervascularized on colour Doppler examination. Hyperaemia can also be found in the focal hypoechoic area of the anterior part of the distal Achilles tendon, and this area should be carefully explored for possible tendon tear.