Fasciae are divided into superficial and deep fasciae. The superficial fascia lies deep to the skin and is composed of fibroareolar tissue. It is of variable thickness and connects the skin to the deep fascia. The superficial fascia may contain superficial muscles or serve as attachment, e.g., platysma myoides. On ultrasound, the appearance of superficial fascia is determined by the content of adipose tissue, hypoechoic, and separated by thin hyperechoic linear bands (Fig. 3.12). MRI demonstrates a low signal intensity band.

The deep fascia is a dense fibrous membrane that invests muscles and deeper structures. It is of variable thickness, becoming thicker on more exposed regions; e.g., it is thicker on the lateral aspect of the leg versus the medial aspect. It forms a sheath for muscles and occasionally as a site of attachment. It gives off the intermuscular septa, which separate various muscles and compartments and attach to the periosteum. In the regions of joints, the deep fascia can become thickened to form the retinacula, as part of fibro-osseous tunnels, maintaining the underlying tendons and nerves in place. On ultrasound, the deep fascia is hyperechoic with an identifiable fibrillar pattern of variable thickness. The hyperechoic intermuscular septa can be seen arising from the fascia. MRI demonstrates the deep fascia as low signal intensity on all imaging sequences. CT can identify fascia, fascial thickening, and perifascial fluid but is less sensitive than MRI; however, CT is excellent at detecting air. NM has no role in imaging fascia.

Plantar fasciitis is a common condition with inflammation of the plantar fascia at its calcaneal origin. It can be diagnosed with ultrasound or MRI (Fig. 3.13). Necrotizing fasciitis is a bacterial infection of the soft tissues that causes rapid tissue necrosis and rapidly spreads via fascial planes. It can be mono- or polymicrobial and may result from minor injuries. If it is clinically diagnosed, surgical debridement should not be delayed. MRI is the gold imaging standard and demonstrates fluid signal intensity along thickened fascial planes with adjacent edema of the musculature. Cellulitis on the other hand demonstrates edema confined to the subcutaneous tissues. CT may demonstrate thickening along fascial planes but is less sensitive than MRI but may demonstrate soft tissue air bubbles, which may not be appreciated on MRI. Radiographs may identify air within the soft tissues. Ultrasound and NM have no primary role in imaging necrotizing fasciitis. Necrotizing fasciitis is reviewed in detail in Chap.​ 13.

Eosinophilic fasciitis, Shulman’s syndrome, is a rare disorder. It is a localized scleroderma-like disease with bilateral peripheral symmetrical skin induration associated with peripheral eosinophilia. MRI is again the gold imaging standard and demonstrates fascial thickening on T1, high SI on T2FS or STIR sequences, and marked enhancement post contrast. MRI findings correlate with disease activity. Ultrasound can be cross-referenced with MRI using bony landmarks and is useful for localizing a biopsy site. Eosinophilic fasciitis is reviewed in detail in Chap.​ 7.

Tendons are composed of tightly packed type I collagen fibers with intervening fibroblasts. Bundles of parallel fibers form primary (subfascicle), secondary (fascicle), and tertiary bundles. They are loosely bound in a loose connective tissue sheath, the endotendineum, and the peritendinal connective tissue. The latter encloses several subfascicles to form a fascicle. The peritendineum also contains the supplying blood vessels and nerves. The epitendineum is a thicker fibroelastic sheath surrounding the whole tendon. At the musculotendinous junction, the sarcolemma intervenes, i.e., there is no direct continuity of muscle and tendon fibers. At the attachment site to bone, the tendon fibers attach to the periosteum, to the fibrocartilage, or directly to the bone. Tendons can also insert onto fascia. Tendons can be round (e.g., biceps), oval (e.g., Achilles), or flattened (e.g., patellar tendon) in cross section. They are surrounded by a synovial sheath in regions that are exposed to friction on motion. The synovial sheath is composed of two layers, one of which is reflected along the surface of the tendon. The sheath contains synovium, which secretes a thick viscid fluid to reduce friction and encourages smooth gliding of the tendon. In areas where a synovial sheath is not required, the tendon is surrounded by the paratenon, a layer of loose connective tissue encasing the epitendineum (e.g., Achilles tendon).

On ultrasound, the tendon is composed of dense linear hyperechoic bands forming a fibrillar pattern, when evaluated in the tendon’s longitudinal axis (Fig. 3.14). On transverse images, the tendon is hyperechoic with multiple hyperechoic foci or dots. The hyperechoic appearance is due to the specular reflections at the interface between the fascicles and the peritendineum. Normal tendons are not compressible. The paratenon is identified as a thin hyperechoic line surrounding the tendon (Fig. 3.14b). The synovial sheath is best visualized when fluid is present between its layers (Fig. 3.15). A small amount of fluid may normally be present. In some tendons, the fibers have to change course slightly prior and at insertion and often appear hypoechoic due to anisotropy. Realigning the transducer so it is perpendicular to the change in orientation will resolve most of the hypoechoic appearance in normal tendons; the remaining hypoechoic appearance is related to the interdigitating fibrocartilage.

On MRI, tendons are of low SI on all imaging sequences (Fig. 3.16). Magic angle is a common MRI imaging artifact and occurs when a structure, commonly tendons and ligaments, lies at 55° to the main magnetic field. This creates apparent increased SI within the tissue, simulating pathology. Common sites are the critical zone of the supraspinatus tendon proximal to its insertion onto the greater tuberosity, the proximal patellar tendon, and the peroneal tendons as they course under the lateral malleolus (Fig. 3.17). Magic angle is present only on sequences with a short TE such as T1, PD, and GE. Magic angle is not evident on long TE sequences such as T2 and STIR, and this allows differentiation from true pathology.

Tendinopathy or tendinosis refers to tendon degeneration and is usually hypoxic or myxoid in origin. The term tendinitis is usually avoided, as there is usually no acute inflammatory component. On ultrasound, the tendon may be enlarged, be attenuated, or be of normal caliber. The normal fibrillar pattern is usually lost and is replaced by hypoechogenicity (Fig. 3.18). The tendon may demonstrate increased internal flow on Doppler interrogation. Comparison with the contralateral tendon can be helpful to identify subtle findings. On MRI, the tendon may be enlarged, be attenuated, or be of normal caliber. Increased internal signal intensity on T2-weighted sequences is in keeping with increased water content (Fig. 3.19). Post-gadolinium imaging demonstrates abnormal enhancement within the tendon and may also demonstrate enhancement of the tendon sheath or paratenon. Note that enhanced studies are not required for the diagnosis of tendinopathy. CT is not as sensitive or specific as ultrasound or MRI in assessing morphological change. It may demonstrate tendon enlargement, attenuation, split tendons, or complete tears. Current imaging description will therefore concentrate on ultrasound and MRI imaging appearances of tendon pathology.

Tendon tears may be partial, full thickness, or complete (Fig. 3.20). Partial tears may be contained within the tendon, interstitial tears. Interstitial tears on ultrasound are identified as a hypoechoic or anechoic cleft within the tendon. On MRI, linear internal clefts of fluid signal intensity are identified (Fig. 3.21). Tears may progress and develop a longitudinal split of the tendon. Ultrasound and MRI will then demonstrate more than one tendon bundle. The number of tendon bundles, percentage of involved tendinous fibers, and positional relationship to the parent tendon should be noted. Be aware of accessory muscles and tendons which can simulate a split tear, e.g., peroneus quadratus is an accessory tendon adjacent to the peroneus longus and brevis at the level of the lateral malleolus and usually inserts upon the calcaneus and has its own muscle belly. It may simulate a tear of the peroneus brevis or longus tendons to the unwary.

Alternatively the tear may extend and involve the superficial fibers, a surfacing partial tear. Ultrasound and MRI both demonstrate fiber discontinuity. The defect may be occupied by granulation tissue or fluid. The defect appears hypoechoic/anechoic on ultrasound and demonstrates a fluid signal intensity defect on MRI. A full thickness tear requires extension to the opposite tendon surfaces, e.g., superficial to deep surface. It implies however that some tendinous fibers remain intact. Tendon tear area should be measured in orthogonal planes and include the percentage of fibers involved. When all fibers are disrupted, it is termed a complete tear. Measurement retraction between the tendon ends, residual distal tendon fibers remaining attached to bone, and bony avulsions should be assessed.

Tenosynovitis is active distension of the tendon sheath with fluid or synovium. Fluid may normally be present in tendon sheaths but is usually minimal. Some tendon sheaths communicate with joints and may have significant fluid within, e.g., flexor hallucis longus communicates with the ankle joint. The tendon sheath in these cases is not thickened and there is no synovial thickening. OMERACT has developed definitions for tenosynovitis on ultrasound and MRI based on literature reviews, expert reviews, and consensus (Table 3.3).