The Achilles tendon is among the most frequently injured tendons despite it being the strongest and largest tendon in the body. 1 Achilles tendon injuries are common in both athletes and nonathletes, often resulting from predisposing factors such as mechanical injury (repetitive loading), vascular disease, corticosteroids, quinolone antibiotics, inflammatory arthropathies, autoimmune illnesses, hyperpronation, diabetes mellitus, and gout. 2
This article will briefly review the anatomy of the Achilles tendon and discuss the different pathologies and their associated MRI findings.
The Achilles tendon is the strongest tendon in the human body. Its action provides plantar flexion and, to a lesser degree, knee flexion. 1 The Achilles tendon is a common tendon shared by the gastrocnemius and soleus muscles with its distal insertion at the posterosuperior aspect of the calcaneus.
The Achilles tendon is made up of numerous fascicular bundles enclosed almost completely within a paratenon.3,4 The paratenon serves a similar function to synovium, providing nutrition to the tendon. Because the Achilles tendon has a single axis of motion, there is no need for the lubricating function of synovium. 5,6 There is diminished blood supply to the tendon 2 to 6 cm proximal to the calcaneal insertion where the mesotendal vascular anastomosis blood supply is decreased. This portion of the Achilles tendon is called the “critical zone.” This is the most common location for Achilles tendon rupture.7 Distal tears are uncommon because of the blood supplied from the calcaneal insertion periosteal vessels. 5,7 Adjacent structures include the Kager fat pad, which is anterior to the Achilles tendon, and the retrocalcaneal (RC) bursa. The RC bursa is a 1- to 2-cm synovial reflection interposed between the posterior surface of the calcaneus and the Kager’s fat pad anterior surface of the distal Achilles (Figure 1).
The Achilles tendon normally has low-signal intensity on all imaging sequences. On axial images, the anterior margin of the Achilles is concave for most of its course (Figure 2). An exception would be at the soleus insertion where the margin is typically convex and may be focally bulbous.5 The normal fascicular anatomy may be visible as a linear signal on T1-weighted and proton density (PD)-weighted sequences but is not as readily apparent on T2-weighted images (T1WI) (Figure 3). Punctate areas of increased signal can be seen in the distal tendon on axial images representing interfascicular septa containing intratendinous vessels. Also, the anatomic course of the tendon fibers can result in imaging artifact (magic angle effect) on short echo time (TE) sequences. This is generally less well-defined and unlikely to be punctate or linear in morphology.3,6 On sagittal images, the anterior and posterior margins of the Achilles tendon should be parallel below the soleus insertion. On coronal images, the margins of the tendon should be fairly straight with the tendon widening distally.8
Achilles tendinopathy is a broad term describing pathology of the tendon. This can include both tendonitis and tendinosis; however, it is commonly used to describe insertional disease such as insertional tendinopathy. Tendinosis is a more specific term describing noninflammatory degeneration of the tendon, often resulting from repetitive microtrauma, either at the Achilles insertion or midsubstance.6 Tendinosis is the most common abnormality involving the midsubstance of the Achilles tendon and is most often acute in onset and proximal to the RC bursa. This entity usually occurs in older individuals who are less active and overweight.8,9 Conversely, insertional tendinopathy occurs typically in a middle-aged athlete who presents following an increase in training duration, intensity, and frequency with pain in the mid portion of the tendon.10
Histologically, findings of intratendinous mucoid or fatty degeneration are present with a disorganized collagen structure. This tendinous degeneration can progress to stages of microtears, intrasubstance tear, partial tears, and complete tears. 11 Underlying hypoxic degenerative tendinopathy is commonly seen in patients who have acutely ruptured Achilles tendons. These hypoxic changes are likely caused by ischemia due to the relative hypovascularity of the Achilles tendon critical zone with secondary overuse or repetitive microtrauma resulting in a thickened, dysmorphic Achilles tendon 2 to 6 cm proximal to the calcaneal insertion.12,13
MRI will show a thickened tendon > 8 mm in anteroposterior (AP) dimension with an anterior convexity of the tendon contour (Figure 4). 5,8 Intermediate T2-weighted signal secondary to the mucoid deposits or interstitial tearing may be seen. This intermediate signal intensity suggests that a chronic process exists, in contrast to a hyperintense “fluid-like” signal, suggesting an acute component.6
A partial tear of the Achilles is defined as an incomplete disruption of the tendon fibers, often extending to the tendon surface. Partial tears can occur anywhere along the Achilles tendon, but are most common in the critical zone.14 On MRI, partial tears demonstrate alteration in architecture with interruption of tendon fibers. Hyperintense signal on fluid-sensitive sequences and hypointense signal on T1-weighted images (T1WIs) demonstrate the tear (Figure 5). 15,16 Chronic Achilles tendon tears demonstrate intermediate signal intensity on fluid-sensitive sequences with a thickened tendon. The tendon edges will be retracted and there may be ongoing atrophy of the Achilles tendon fibers and muscle. 17
Muscle atrophy can be a manifestation of a chronic tendon tear, with irreversible atrophy presenting as a fatty infiltrated or “marbled” muscle.5,16 Atrophy occurs first in the soleus because of the predominance of slow-twitch fibers. Because the soleus muscle is part of the Achilles tendon unit, soleus atrophy can be thought of as a predictor of a dysfunctional myotendinous unit. Therefore, when imaging the Achilles tendon, sagittal images should include at least 3 cm of the distal soleus muscle belly to assess for fatty infiltration of the muscle. Gastrocnemius atrophy can be seen but is rare.5,16
Treatment typically consists of initial nonsurgical management such as casting, nonweightbearing, and functional bracing. Platelet-rich plasma injections have been proposed for refractory cases of tendinopathy, with evidence supporting efficacy of these Achilles injections.17 If conservative management fails, an open or percutaneous surgery may be performed.18,19
Achilles ruptures, or a full-thickness tear involving the entire width of the tendon, are defined as a complete discontinuity of the tendon. Complete tears occur in a bimodal distribution in individuals aged 25 to 40 years and those older than 60. 6 The mechanism leading to rupture is not fully understood; however, some pathological factors are known such as activities that require a dorsiflexed position while running or jumping, degenerative changes, recurrent microtrauma, corticosteroids, fluoroquinolone use, chronic renal failure, rheumatoid arthritis, and systemic lupus erythematosus.2
Complete tears will demonstrate a T2-weighted hyperintense signal defect of the tendon with fluid-signal or a heterogeneous signal hematoma filling the tendon gap. The torn tendon fibers are commonly distracted or overlapping (Figure 6). 14 T1WI will demonstrate a hypointense stump just above the fluid-filled gap and is also useful to visualize potential avulsed osseous fragments (Figure 7). These avulsion fractures are best seen on x-ray, highlighting one of the many important reasons MRI interpretation should be done with an available x-ray correlation. Of note, the size of the tendon gap, quality of the torn tendon, estimation of cross-sectional involvement, and presence of atrophy of the soleus and gastrocnemius muscles are useful descriptors for the surgeon and should be recorded in the radiology report.16
Treatment remains controversial. In general, operative treatment allows improved functional outcome with greater likelihood of returning to the same performance level and decreased repeat rupture rate in athletes.6 The possibility of surgical complications and the greater cost are the obvious disadvantages. Nonoperative management has a greater likelihood of patient dissatisfaction and outcomes are heavily dependent on patient compliance to the rehabilitation protocol.2
Peritendinitis, also referred to as “paratenonitis,” is defined as an inflammatory condition of the paratenon surrounding the tendon and is most commonly seen in active athletes due to repetitive overuse injuries. It can also arise from disorders such as seronegative arthritis and infection.20 On MRI this presents with hyperintense T2-weighted and short-TI inversion recovery (STIR) signal surrounding the Achilles tendon (Figure 8). Additionally, in the acute phase, fluid-signal may be seen between the tendon and the paratenon, and inflammatory changes commonly extend into the subcutaneous fat and Kager fat pad.8
Tendinitis is most commonly located at the distal tendon calcaneal insertion and frequently coexists with adjacent soft-tissue and osseous pathology. It is common in runners and frequently leads to the development of a calcaneal enthesophyte. 21
MRI demonstrates thickening of the distal tendon with vague, ill-defined longitudinal T1-weighted postcontrast, T2-weighted, and STIR hyperintense signal (Figure 9). This signal may be intense and can mimic a partial tear, albeit fairly distally. Edema within enthesophytes correlates with more acute symptoms. 21 RC bursitis is a frequent accompanying finding.
Tendinitis and peritendinitis usually respond to nonsurgical measures including rest, ice, compression, training modifications, NSAIDs, heel lifts, orthotics, and night splints.2 Local injections of pharmacologic agents have not proven efficacious. In recalcitrant cases of peritendinitis, brisement (injection of fluid between the tendon and the paratenon) has been advocated.6
Haglund deformity is a somewhat common cause of heel pain that predominantly affects middle-aged women and is often bilateral. It was first documented in 1927 by Swedish orthopedist Patrick Haglund. While it is largely considered idiopathic, there are several known contributing factors.22 For instance, the Haglund deformity is also known as the “pump bump.” The “pump” refers to the low-back, high-heeled shoes commonly associated, and the “bump” refers to the prominent calcaneal projection that results.14 Other common causes include repetitive use or chronic stress such as excessive running, poor biomechanics due to cavovarus deformities, or a stiff heel-counter of footwear (eg, dress shoe) that can compress the bursa against the calcaneus.23
The posterior calcaneal tuberosity serves as a partial site of attachment for the Achilles tendon as it extends down the posterior calcaneus. The RC bursa cushions the tendon from the tuberosity. When exposed to chronic stress over time, the posterosuperior aspect of the tuberosity hypertrophies resulting in a Haglund deformity.14 Eventually this results in a cycle of painful inflammation of the RC bursa and Achilles tendon known as Haglund syndrome.24
In general, lateral radiographs will show a bony projection along the posterosuperior aspect of the calcaneal tuberosity. MRI will show excess fluid in the RC and retro-Achilles bursae on STIR and T2WI as well as bone marrow edema in the hypertrophied calcaneal tuberosity.14 (Figures 10 and 11).
First-line treatment of symptoms associated with Haglund’s syndrome is typically nonsurgical, such as wearing appropriate footwear and orthotics, reducing activity, stretching the gastrocnemius and soleus, and taking NSAIDs. If nonsurgical treatment fails, the recommended procedures include surgical osteotomy with removal of the superolateral deformity and calcaneal step with decompression of the RC bursa. 24
The RC bursa is a saddle-shaped structure that is deep to the Achilles tendon and its paratenon and is posterosuperior to the posterior calcaneal tubercle and Kager’s fat pad. RC bursitis is most commonly due to repetitive trauma and is frequently found in runners. Other causes include rheumatoid arthritis and seronegative spondyloarthropathies.14 Normal-sized RC bursa on asymptomatic patients measures approximately 1 mm (AP) x 6 mm (transverse) x 3 mm (craniocaudal).24 There is measurable T2-weighted and STIR hyperintense fluid signal on MRI. In symptomatic patients, the RC bursae will typically measure > 1 mm AP x 11 mm transverse x 7 mm craniocaudal.25
When the bursa is enlarged with fluid it will obscure the RC fat.26 Therefore, the presence of the RC recess on lateral plantar flexion radiographs essentially excludes the possibility of RC bursitis. On plain film, RC bursitis can be diagnosed by a normal Achilles tendon, normal superficial soft tissues, and normal calcaneal cortex in the setting of an obliterated RC recess.27
An enlarged bursa with hypointense T1-weighted and hyperintense fluid-sensitive signal is a key finding on MRI (Figure 12).14 Some studies suggest that an AP measurement > 2 mm seen on MRI may be considered diagnostic for RC bursitis. However, in some chronic cases, fibrosis and scarring may eventually shrink the inflamed bursa, making the dimensions inconsistent with the diagnosis.25
Resection of the posterosuperior aspect of the calcaneus has been shown to be up to 92% effective in treating RC bursitis if performed within 1 year of symptom onset, but the most common treatment is corticosteroid injections.28
The retro-Achilles bursa is located between the Achilles tendon and the skin. Inflammation usually is caused by repetitive trauma/irritation from the posterior heel counter of a shoe. MR imaging demonstrates hyperintense signal posterior to the Achilles tendon on a fluid-sensitive sequence (Figure 13).29 As with RC bursitis, treatment is typically nonsurgical with progression to corticosteroid injections if necessary.
Achilles xanthoma is a reactive lesion due to hyperlipoproteinemia most commonly found in the Achilles tendon. It is often painless and slow growing and will cause diffuse tendon enlargement over time. MRI demonstrates intermediate T1-weighted, STIR, and T2-weighted signal between low-signal tendon bundles. There may be a speckled appearance on axial images (Figure 14).30
On a macroscopic level in the Achilles, tendon ossification occurs more frequently than tendon calcification and is relatively more common in the Achilles than in other tendons in the body. Nevertheless, it is a rare condition that is usually associated with prior surgery or history of repetitive running-related tendonitis. Tendon ossification predominates distally in the tendon, appearing as focal fatty marrow. It will demonstrate the same signal as bone on MRI and may have an appearance of a fractured enthesophyte (Figure 15).31
Infection of the Achilles tendon occurs most often in people with diabetes and vasculopathy from postsurgical complications and more commonly direct extension of calcaneal osteomyelitis from heel ulcers.32 In the setting of osteomyelitis, the distal aspect of the tendon is most commonly involved due to proximity with the overlying soft-tissue infection (Figure 16). Contrast enhancement of the Achilles tendon and the presence of peritendinous fluid-signal on T2WI are not specific for the presence of a tendon infection; these findings can also be seen in patients with inflammatory conditions, degenerative disorders of the tendons, and in patients who have sustained trauma. However, circular enhancement of a tendon passing through an area of cellulitis from an infected pedal ulcer may be a specific sign of infection.33,34
Achilles tendon injuries are common and increasing in frequency due to their association with an aging and active population. Having a firm understanding of the normal anatomy and pathology of the Achilles tendon with the associated MRI findings is paramount in helping guide the clinician to a more accurate diagnosis and earlier treatment for patients.
Young D, DeGiacomo C, Fisher S, von Borstel D. Overcoming Your Achilles Heel: A Review of Achilles Tendon Anatomy, Pathology and Associated MRI Findings. J Am Osteopath Coll Radiol. 2020;9(3):5-13.