Heel Bursitis Scans

Tenosynovial Tissue

Fig.4.28 a, b a Transverse scan,dorsum of wrist (compound imaging). Distension with anechoic fluid (*) of the sheath of the 4th extensor's compartment. b MPR reconstruction on a coronal plane. T = extensors ed with fluid the presence of a joint fluid collection must be considered.

In proliferative tenosynovitis hypertrophic proliferation of the synovial tissue is observed, showing various degrees of echogenicity (Fig. 4.29).

Dynamic ultrasound examination and compression of the transducer performed by the operator are helpful to assess the solid nature of the finding. In these cases the power Doppler analysis is very useful to confirm the diagnosis by detecting vascular signals within a thickened tenosynovial sheath (Fig. 4.30). The degree of vascularization is strictly related to the severity of the inflammation and to the "activity" of the synovial proliferation [15,18, 21,36]. These forms of tenosynovitis are often an extra-articular expression of some rheumatic diseases such as rheumatoid arthritis.

Mixed tenosynovitis is the most common form of tenosynovitis. It is characterized by the simultaneous presence of both synovial fluid and pro-liferative thickening of the synovial membrane within the sheath. The US pattern shows several echoic spots of synovial tissue jutting from the sheath expanded by anechoic fluid (Fig. 4.31).

In order to differentiate fluid from the proliferating tissue it is very useful to apply compres

Power Doppler

Transverse scan, finger flexor tendons. Expansion of the tendon sheath with hyperechoic synovial proliferation (*) is shown

Transverse power Doppler scan,finger flexor tendons.Prolifer-ative tenosinovitis with diffuse hypervascularization is shown. S = flexor superficialis tendon; P = flexor profundus tendon

Transverse scan, finger flexor tendons. Expansion of the tendon sheath with hyperechoic synovial proliferation (*) is shown

Transverse power Doppler scan,finger flexor tendons.Prolifer-ative tenosinovitis with diffuse hypervascularization is shown. S = flexor superficialis tendon; P = flexor profundus tendon

Power Doppler Synovitis
Long head of biceps tendon of the shoulder, transverse scan. Fluid expansion (*) of the synovial sheath with synovial proliferation (arrowheads) is shown (mixed tenosynovitis). m = mesoteno-nium; G = intertubercular groove; T=tendon

sion with the transducer. In dubious cases the two components can also be distinguished with power Doppler, because vascular signals exclusively occur within the solid tissue.

In all cases where inflammatory involvement of the tenosynovial sheath is observed, US evaluation of the tendon's morphology and intrinsic structure should be performed. Tendon presenting with an alteration of their echotexture express concomitant pathologic involvement of its parenchyma [15, 44] (Fig. 4.32).

Chronic stenosing tenosynovitis occurs in peculiar anatomical regions, where the tendons run through fibro-osseous canals. The most common US pattern is that of a mixed tenosynovitis, accompanied by thickening of the corresponding retinaculum and consequent stenosis of the canal. From a functional point of view, the dynamic US examination may demonstrate a defective sliding of the tendon within the sheath. Notta-Nela-ton's disease, also known as "trigger finger", and De Quervain's disease are the most common forms of chronic stenosing tenosynovitis [1,45, 46] (Fig. 4.33).

Extensor Pollicis Longus Paratenon
Ankle, longitudinal scan.Tendi-nosis and inflammatory expansion of the sheath.Thickening of fibular tendons and inhomoge-neous echotexture is shown

Chronic stenosing tenosynovitis of 1st compartment of extensors (abductor pollicis longus and extensor pollicis brevis). Enlargement (*) of tenosynovial sheath (20 MHz transducer)

Extensor Pollicis Longus Paratenon

Peritendinitis

The term peritendinitis refers to inflammation of the paratenon of anchor tendons, especially involving the highly vascular loose areolar connective tissue that is found between epitenon and peritenon. In practice, peritendinitis of anchor tendons corresponds to tenosynovitis of sliding tendons, for they both represent a paratenonitis.

Peritendinitis often affects tendons of the lower limbs, particularly the patellar and Achilles tendons. Like tenosynovitis, peritendinitis can be classified as acute, subacute or chronic. The most common cause of peritendinitis is repeated microtrauma [35]. US highlights the inflammatory edema, a hypoechoic thickening of the peritendi-nous wrapping layers (Fig. 4.34) with a hypoechoic ring-like appearance in short axis views. In the classic pattern of peritendinitis, the fibrillar tendon echotexture does not appear altered; it is altered instead in mixed forms where peritendinitis and tendinosis coexist.

The information obtained with gray-scale US can be usefully integrated with an accurate color and power Doppler analysis that can add further information regarding the presence of peritendi-nous inflammation and hyperemia. It should also be mentioned that in standard conditions the vas-cularization of tendons is very poor with low speed flow, invisible on Doppler analysis. When hyper-emia is detected, a typical hypervascular pattern is observed; this is characterized by several signal spots and typically located in the peritendinous area [47,48] (Fig. 4.35).

Droppler Achilles

Peritendinitis of the Achilles tendon. Longitudinal scan, compound imaging.Thin peritendinous layer of hypoechoic fluid with normal thickness of tendon is shown

Peritendinitis of the Achilles tendon. Longitudinal scan, compound imaging.Thin peritendinous layer of hypoechoic fluid with normal thickness of tendon is shown

Droppler Achilles
Peritendinitis of the Achilles tendon.The power Doppler scan shows some peritendineal vascular signals,expression of hyperemia and inflammation of tendon sheath

Tendinosis

Tendinosis is a degenerative pathology affecting both anchor and sliding tendons, presenting with mild pain or with no symptoms at all. Consequently, US plays a fundamental role in diagnosis, because the patient's history and clinical examination alone cannot accurately implicate the involved tendon. From a histopathologic point of view, fibroblasts are activated with the production of high molecular weight collagen and proteogly cans, causing diffuse edema. Necrosis and fibri-nous exudation occur with a probable consequent fibrocartilaginous metaplasia and calcium deposition. US is able to detect tendon alteration in early phases. The earliest US sign of tendinosis, in long axis views, is disarray of tendon echotexture and its fusiform thickening corresponding, in short axis views, to the rounded appearance with loss of the typical ventral concavity. In early US patterns of tendinosis, fragmentation of the fibrillar echo-texture is observed [49] (Fig. 4.36).

Fragmented Dopler

Low grade tendinosis. The characteristic fragmentation of the fibrillar echotexture is shown

Low grade tendinosis. The characteristic fragmentation of the fibrillar echotexture is shown

In later phases, focal hypoechoic areas, related to mucoid degeneration can be observed (Fig.4.37). Collagen fibers show a lack of organization; several hyperechoic spots can be detected, suggesting the presence of micro and macro-calcification. The largest hyperechoic spots show posterior acoustic shadowing, representing areas of calcific metaplasia within the tendon [50] (Fig. 4.38).

Further assessment of intratendinous hypo-echoic focal areas using color or power Doppler techniques can be useful to detect vascular signals within the degenerative spots, a finding suggestive of the presence of angiogenesis, with a potential consequent substitution of the degenerate area. The absence of vascular signals within the degenerate areas of the tendon suggests necrotic evolution of the degenerative focus. It

Tendonopathy Power Dopper

Tendinosis of Achilles tendon.The tendon is thickened and inhomogeneous with an extensive hypoechoic area (mucoid intratendinous degeneration)

Tendinosis of Achilles tendon.The tendon is thickened and inhomogeneous with an extensive hypoechoic area (mucoid intratendinous degeneration)

Fibrillar Texture Tendons
Transverse scan of Achilles tendi-nosis.The tendon is thickened and inhomogeneous with a small focus of calcification (*)
Calcificaci Tend Aquiles

Fig. 4.39 a-c a Longitudinal scan of Achilles tendinosis.The tendon is thick-ened,inhomogeneous and devoid of its characteristic fibrillar echo-texture. b The power Doppler scan shows some intratendinous vascular signals. c MR scan of the same patient (fat suppression technique). Diffuse hyperintensity of Kager's triangle caused by inflammation of the adipose tissue

Fig. 4.39 a-c a Longitudinal scan of Achilles tendinosis.The tendon is thick-ened,inhomogeneous and devoid of its characteristic fibrillar echo-texture. b The power Doppler scan shows some intratendinous vascular signals. c MR scan of the same patient (fat suppression technique). Diffuse hyperintensity of Kager's triangle caused by inflammation of the adipose tissue should be mentioned that in clinical practice it is common to find cases in which an overlap between degenerative (tendinosis) and inflammatory (paratenonitis) tendon conditions occurs, and in these cases the complex color and power Doppler images can be integrated with gray-scale US to give a more precise assessment [47] (Fig. 4.39 a-c).

It should also be considered that some anatomical regions present peculiar biomechanical characteristics that promote the onset of tendinosis.

For instance, the presence of a prominent postero-superior calcaneal tubercle (Haglund's disease) may cause friction with the pre-insertional portion of the Achilles tendon. In these cases, ultrasound shows the presence of inflammatory and degenerative tendon involvement, especially located at the pre-insertional portion, which appears thickened and inhomogeneous and is often associated with a precalcaneal and retro-calcaneal bursitis [51] (Fig. 4.40 a,b).

Enthesopathy Calcaneal Tuberosity Thickening The Achilles Tendon

Haglund disease.a Longitudinal scan.The pre-insertional segment of Achilles tendon appears inhomogeneous and thickened, with inflammation of the retro-calcaneal bursa (B). b MR scan of the same patient (gradient echo (GE) T2W sequence).The US diagnosis is confirmed by the presence of a prominent postero-superior calcaneal tubercle. T=tubercle

Enthesopathy

Enthesopathy, also known as insertional tendinopa-thy, is an inflammatory-degenerative pathology involving the osteo-tendinous junction, usually caused by functional overload. It typically affects anchor tendons submitted to continual and intense mechanical stress. The affected anatomical region, therefore, varies according to the athletic task, resulting in the onset of typical pathologies associated with specific sports, such as tennis elbow and jumper's knee.

In standard conditions the enthesis consists of intertwined tendon fibers and fibrocartilage, with slow flowing vessels that cannot be visualized on Doppler analysis. In enthesopathies, the earliest pathologic finding is local hyperemia and angio-genesis; with Doppler techniques the increase of vascular signals can be identified early, when the matrix of tendons is not yet altered. US is a highly sensitive technique for identifying and quantifying the tendon insertional thickening, the hypoe-choic pattern and the inhomogeneous echotex-ture. Insertional calcification and hypoechoic focal areas, corresponding to myxoid degeneration within the tendon, may be observed [52] (Fig. 4.41).

An inflammatory reaction of the adjacent serous bursa and the presence of erosions and of an irregular cortical bone outline at the insertion are often associated. On US, erosions appear as interruptions of the hyperechoic cortical bone outline. In advanced cases, an MR examination should be per-

Verdikking Achillespees
Longitudinal scan of Achilles tendon (T) enthesopathy.Diffuse disarray of the fibrillar echotexture, calcifications (arrowheads) and thickening of peri-calcaneal soft tissues (*)
Achille Peri

MR of the ankle,sagittal scan (fat suppression technique).Reac-tive hyperemia of calcaneus at the Achilles tendon insertion

MR of the ankle,sagittal scan (fat suppression technique).Reac-tive hyperemia of calcaneus at the Achilles tendon insertion formed, because it represents the only technique capable of determining the insertional bone involvement appearing as medullary edema within the bone in high contrast sequences (Fig. 4.42).

A peculiar form of enthesopathy is that affecting patients in adolescence. During growth, the tendon insertion does not occur on the bone, but on the growth plate cartilage, that represents a weaker structure of the enthesis compared to bone and tendon, and is less resistant to mechanical stress. Impact is therefore mostly absorbed by the growth plate cartilage, and the corresponding bone and tendon are relatively spared. Typical clinical conditions that follow this situation are some juvenile osteochondroses, such as Osgood-Schlatter's disease (affecting the patellar tendon at its distal insertion), Sinding-Larsen-Johansson's disease (affecting the patellar tendon at its proximal insertion) and Haglund-Sever's disease (affecting the Achilles). All these patients present with pain at the enthesis level and functional loss. The typical US pattern shows thickened growth plate cartilage and fragmented nucleus of ossification, suggestive of irregular enchondral ossification [53, 54] (Fig. 4.43 a,b).

Fragmented Dopler

Sinding-Larsen-Johansson syndrome in a young patient. a The plain film shows fragmented appearance of the ossification centre of the lower patellar pole. b The US scan shows an irregular bone outline and swelling at the patellar tendon insertion

Sinding-Larsen-Johansson syndrome in a young patient. a The plain film shows fragmented appearance of the ossification centre of the lower patellar pole. b The US scan shows an irregular bone outline and swelling at the patellar tendon insertion

Tendon tears

A tendon tear may be observed after an acute injury or as a poor outcome of tendinosis, with a spontaneous rupture. Mechanical overload, especially when excessive and repetitive, may eventually cause partial or total tears within a degenerative tendon structure. Such tears are often incomplete, but they still alter the tendon continuity and, consequently, its integrity. Histological samples show degenerative involution of the collagen fibers, with necrotic foci. On US scans, a tear appears as a hypo to anechoic spot that interrupts the fibrillar structure of the tendon (Fig. 4.44 a,b). In complete tears, US allows the discontinuity of the fibers, the two tendon stumps and the hemorragic collection within the retraction gap to be visualized [14-16, 55]. In these cases it is important to perform a dynamic US examination for a more accurate evaluation of the tear location.

In some regions, the US signs of tendon tears can be very complicated. A clear example is represented

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