1. INTRODUCTION
The shoulder is one of the most common applications of musculoskeletal US due to the high incidence of rotator cuff disorders related to increasing aging and sporting activities. Many papers dealing with the US scanning technique of the rotator cuff tendons have already been published in the radiological, rheumatologic and orthopaedic literature and US is now widely recognized as an accurate means to evaluate rotator cuff disease (Ptasznik 2001; Bouffard et al. 2000; Brasseur et al. 2000; Thain and Adler 1999; Bretzke et al. 1985; Collins et al. 1987; Crass et al. 1985; Hall 1986; Middleton et al. 1984; Middleton et al. 1986b; Mack et al. 1988a; Middleton 1989; Seibold et al. 1999; Teefey et al. 2000; Naredo et al. 2002). With appropriate equipment and skilled hands, this technique provides assessment of rotator cuff pathology with high sensitivity and specificity in the diagnosis of both partial and full-thickness tears with some specific advantages over MR imaging, such as higher resolution capabilities and the ability to examine tissues in both static and dynamic states and with the patient in different positions.
In addition to the rotator cuff, interest is also growing in the US evaluation of a variety of abnormalities of articular and para-articular structures located in and around the shoulder area (Martinoli et al. 2003). These conditions can mimic rotator cuff tears clinically and most commonly involve the glenohumeral and acromioclavicular joints and the soft-tissue structures around the shoulder, including the joint recesses, the bone and articular cartilage, the subacromial subdeltoid bursa, the labrum, the muscles and the suprascapular and axillary nerves. In these cases, US is able to redirect the diagnosis if a complete examination of the shoulder area is performed instead of a simple rotator cuff assessment. Furthermore, we include in this chapter a specific focus on the US assessment of brachial plexus nerves and the thoracic outlet syndrome as well as the US evaluation of local tumors leading to painful shoulder or snapping scapula syndrome.
As for other sites in the body, a deep knowledge of anatomy, of the proper scanning technique and of the normal imaging findings is essential in order to perform an accurate shoulder examination with US.
2. CLINICAL ANATOMY – OSSEOUS AND ARTICULAR ANATOMY
The shoulder girdle is composed of the scapula, the clavicle and the proximal humerus acting as a single biomechanical unit. Three joints – the glenohumeral, acromioclavicular and sternoclavicular joints – and two gliding planes – the subacromial and the scapulothoracic – allow a greater range of motion in the shoulder than is possible at any other joint in the body, reaching approximately 180° in almost all directions of movement. It is clear that such a wide range of shoulder mobility depends on these joints and gliding planes working together with synchronicity, in order to permit the arm and the hand to be positioned as required in space around the body.
3. GLENOHUMERAL JOINT
The glenohumeral joint is a “ball-and-socket” joint made up of the relatively small and flat glenoid fossa and the large and round articular surface of the humeral head (Fig. 1a,b). Owing to a discrepancy in the size and curvature of the joint surfaces, the glenoid cavity covers only a small portion (about one-fourth) of the humeral head. This incongruity along with the relative laxity of the joint capsule provides wide mobility but makes the joint inherently unstable and, therefore, prone to subluxation and dislocation. The articular surfaces of the humeral head and the glenoid fossa are covered by a layer of hyaline cartilage, which is thicker in its center in the humerus and thinner at its outer edges in the glenoid (Fig. 1b). In the humerus, the articular cartilage reaches the anatomic neck, the site of attachment of the joint capsule. Closely attached at its base to the periphery of the glenoid, a concentric rim of fibrocartilage, the labrum, widens and deepens the shallow concavity of the bony glenoid, providing the joint with inherent stability and restricting anterior and posterior excursions of the humerus. Similar to the meniscus of the knee, the glenoid labrum has a triangular shape and is in direct continuity with the hyaline cartilage of the glenoid cavity (Fig. 1b).
A loose fibrous capsule envelops the joint, extending from the base of the coracoid through the supraglenoid region cranially, onto the anatomic neck of the humerus laterally, and into the labrum posteriorly and inferiorly, whereas its anterior insertion is variable and more complex. Based on its relationship with the glenoid labrum, three types of anterior capsular insertion can be found: type 1, attaching directly on the labrum; type 2, inserting more medially along the scapular neck, but within 1 cm of the labrum; type 3, greater than 1 cm medially from the labrum. With the arm in neutral position, the lower portion of the capsule is lax and redundant, and forms the axillary recess of the joint. The capsule of the glenohumeral joint is invested by the synovial membrane on its deep surface and overlies some intracapsular soft-tissue structures, including the long head of the biceps tendon. Several areas of the capsule are reinforced by ligaments. These are the coracohumeral ligament and the superior, middle and inferior glenohumeral ligaments. The coracohumeral ligament is a strong band of fibrous tissue arising from the coracoid and inserting onto the greater and lesser tuberosities to reinforce the capsule when it passes over the intra-articular portion of the biceps. The glenohumeral ligaments extend from the anterior margin of the glenoid cavity to the lesser tuberosity and act as a check to external rotation and anterior translation of the humeral head. The capsule of the glenohumeral joint has two openings for the passage of the biceps tendon beyond the humeral tuberosities and for communication with the subscapularis recess.
This recess communicates with the joint through an opening in the fibrous capsule located between the superior and middle glenohumeral ligaments (superior subscapularis recess) or between the middle and inferior glenohumeral ligaments (inferior subscapularis recess). This superior subscapularis recess is a small saddle-shaped recess of the glenohumeral joint that overlies the subscapularis tendon. It is located in close relationship with the root of the coracoid and plays a role in protecting the subscapularis tendon during gliding over the scapular neck. The inferior subscapularis recess projects between the middle and inferior glenohumeral ligaments and is located deep to the subscapularis muscle due to its more inferior position (Petersilge et al. 1993). In summary, the anterior glenohumeral joint cavity has three main extensions: the biceps tendon sheath anteriorly, the subscapularis recess medially and the axillary pouch inferiorly (Fig. 2).
4. ACROMIOCLAVICULAR JOINT
The acromioclavicular joint is a small synovial joint located between the medial end of the acromion and the lateral end of the clavicle. It has a limited range of motion, there being approximately 20° between the extremes of shoulder position. The articular surfaces of the acromion and the clavicle are covered with a layer of hyaline cartilage and are separated by a wedge-shaped disk of fibrocartilage which splits the joint cavity either partly or completely. The capsule of the acromioclavicular joint is attached to the articular margins and is reinforced by superior and inferior ligaments. Caudally, it also receives fibers from the coracoacromial ligament, which blends with its undersurface. The acromioclavicular joint is further stabilized against upward dislocation of the clavicle by the coracoclavicular ligament, which joins the coracoid process to the inferior surface of the lateral end of the clavicle. The coracoclavicular ligament consists of two components – the anterolateral trapezoid ligament and the posteromedial conoid ligament – and assumes a fan-shaped appearance with its base located cranially. From the physiologic point of view, the acromioclavicular joint receives cranial-caudal shearing load due to muscle action. Because the articular surfaces of this joint are obliquely oriented, the applied tension leads the clavicle to slide and displace cranially. This tendency is resisted by the coracoclavicular ligaments, damage to which allows the typical superior prominence of the clavicle end.
5. STERNOCLAVICULAR JOINT
The sternoclavicular joint is the only articulation of the shoulder girdle with the thorax. It is a shallow saddle-shaped joint between the manubrium of the sternum and the first rib medially and the medial end of clavicle laterally. The articular surfaces of the manubrium and the clavicle are, at least in part, incongruent, that of the clavicle being wider than that of the manubrium. The sternoclavicular joint houses a fibrocartilaginous disk dividing the joint space into medial and lateral cavities, each of which lined with its own synovial membrane. The costoclavicular and interclavicular ligaments reinforce the joint and oppose to its tendency to anteroposterior instability.
6. SCAPULOTHORACIC PLANE
The scapulothoracic plane separates the body of the scapula and the subscapularis muscle from the thoracic surface, consisting of the superficial aspect of the serratus anterior muscle which overlies the ribs. This gliding plane allows the scapula and the glenoid cavity to tilt anteriorly and posteriorly around the rib cage during shoulder movements. In addition, the scapulothoracic articulation has an important role in shoulder abduction.
7. MUSCLES AND TENDONS
From the anatomic point of view, the muscles of the shoulder may be subdivided into two main groups: intrinsic muscles (subscapularis, supraspinatus, infraspinatus, teres minor, teres major and deltoid), which originate and insert on the skeleton of the upper limb, and extrinsic muscles, which join the upper limb with either the spine (trapezius, latissimus dorsi, levator scapulae and rhomboid) or the thoracic wall (serratus anterior, pectoralis minor and pectoralis major). The clinical relevance is for the most part related to the intrinsic muscles and especially to the rotator cuff muscles and tendons.
8. ROTATOR CUFF
There are four rotator cuff muscles: the subscapularis, which is located on the anterior aspect of the shoulder; the supraspinatus, which lies on its superior aspect; and the infraspinatus and teres minor, which are situated on the posterior shoulder (Fig. 3). They arise from the anterior and posterior aspects of the scapula. The subscapularis muscle takes its origin from the anterior aspect of the body of the scapula. The muscle belly gives rise to a series of two or three intramuscular tendons which direct laterally to join together to form the subscapularis tendon (Fig. 4). This tendon inserts onto the lesser tuberosity in a broad band and acts as an adductor and internal rotator of the arm. Its more cranial fibers are intra-articular in location and some of its superficial fibers overlay the bicipital sulcus and reach the greater tuberosity, merging with the coracohumeral and transverse humeral ligament. The supraspinatus muscle originates from the supraspinous fossa of the scapula and passes underneath the acromion and above the glenohumeral joint before inserting on the upper facet of the greater tuberosity (Fig. 5a). It is separated from the acromion, coracoacromial ligament and deltoid muscle by the subacromial-subdeltoid bursa. Anatomic studies indicate that the supraspinatus consists of two distinct portions: ventral and dorsal (Fig. 5b) (Vahlensieck et al. 1994). The ventral portion takes its origin from the anterior supraspinous fossa and inserts anteriorly onto the greater tuberosity to act as an internal rotator of the arm. This ventral portion may have an accessory site of insertion onto the lesser tuberosity. The dorsal portion of the supraspinatus lies more posteriorly, with muscle fibers arising from the posterior aspect of the supraspinous fossa and spine of the scapula, assuming a strap-like configuration made up of several small tendon slips that coalesce into a broad attachment inserting more posteriorly onto the greater tuberosity. This is the portion that acts primarily as a shoulder abductor. The individual layers of the supraspinatus tendon have different mechanical properties, leading to shearing between them, and can tense and slacken depending on shoulder movements. On the posterior shoulder, the infraspinatus muscle originates from the infraspinatus fossa and gives rise to a wide tendon that extends laterally to insert onto the greater tuberosity, just posterior and inferior to the supraspinatus tendon (Fig. 6). The teres minor muscle, the smallest muscle of the rotator cuff, has a more oblique course than that of the infraspinatus. This latter muscle arises from a narrow strip on the lateral border of the scapula and inserts just posterior and inferior to the infraspinatus into the most caudal segment of the greater tuberosity (Fig. 6). The posterior infraspinatus and teres minor muscles act as external rotators of the arm.
Considered as a whole, the tendons of the rotator cuff muscles are broad and relatively flat, somewhat similar to belts, and converge toward the lesser and greater tuberosity to create a hood – commonly referred to as the “rotator cuff” – that covers the humeral head anteriorly, superiorly and posteriorly (Fig. 7). The subscapularis tendon is separated from the other tendons of the rotator cuff by the ligamentous complex of the rotator interval and the long head of biceps tendon, which is positioned between it and the supraspinatus. The rotator cuff tendons have a constant relationship in the different positions of the humerus and, as a result of their combined activity, play an important role as stabilizers of the humeral head in the glenoid fossa during movements of the arm (for this reason, the rotator cuff tendons have also been referred to as “active ligaments”). The abduction of the arm when the humerus is kept close to the side of the body, for example, is mainly accomplished by contraction of the deltoid muscle, but the force of this muscle is also directed cranially, so that the humeral head would displace upward. The combined action of the supraspinatus, which follows a more horizontal vector force than the deltoid, redirects the humeral head into the glenoid cavity, thus counteracting the tendency to superior translation of the humeral head.
9. BICEPS AND ROTATOR CUFF INTERVAL
The subscapularis and supraspinatus tendons are separated by a free space, which is commonly referred to as the “rotator cuff interval.” This space contains the long head of the biceps tendon, the coracohumeral and the superior glenohumeral ligaments. The long head of the biceps tendon takes its origin at the supraglenoid tubercle with fibers also arising from the superior aspect of the glenoid rim, superior labrum and joint capsule (Fig. 8a,b). The proximal part of this tendon is intra-articular and intrasynovial in location: it has a curvilinear course and reflects over the anterosuperior aspect of the humeral head, between
the margins of the supraspinatus and subscapularis tendons, to descend into the intertubercular groove, also known as the “bicipital groove” or “sulcus”, between the greater and the lesser tuberosity (Cone et al. 1983) (Fig. 8c). Along its course over the humeral head, the biceps tendon has an oval cross-section, whereas it becomes more rounded caudally. In the bicipital groove, the biceps tendon is invested by a synovial sheath as an extension of the synovial lining of the glenohumeral joint which extends down to approximately 3–4 cm beyond the distal end of the intertubercular groove. The biceps tendon sheath communicates with the glenohumeral joint; therefore, fluid distention within it often reflects an underlying joint disease rather than tendon pathology. In the bicipital groove, the biceps tendon is accompanied by the ascending branch of the anterior circumflex artery. Below the bicipital groove, the myotendinous junction of the long head of the biceps is located deep to the flattened tendon of the pectoralis major muscle, which inserts into the lateral lip of the intertubercular groove. The biceps is primarily a powerful supinator and flexor of the elbow, but it also helps to stabilize the glenohumeral joint, as the rotator cuff does, and to flex the shoulder.
Because of its curvilinear course and reflection over the humeral head, the biceps tendon has an intrinsic propensity to displace medially, especially during powerful contraction of the muscle or maximal external rotation. To resist this tendency, the anatomic conformation of the humeral groove and some tendons and ligaments encountered at different levels along its course play a role in retaining it in the proper position. In the rotator cuff interval, a space located between the subscapularis and the supraspinatus tendon – through which arthroscopists enter the glenohumeral joint in order to avoid damaging cuff tendons – the biceps is stabilized by a fibrous plate which courses above it and the joint capsule as a roof. From superficial to deep, this restraining structure consists of the coracohumeral ligament (that extends to the insertions of the subscapularis and the supraspinatus) and some fibers of the supraspinatus and subscapularis (that crisscross the rotator interval to blend into each other and unite with parts of the coracohumeral ligament) (Fig. 9a,b). Strands of loose connective tissue are interspersed with these fibers. At the anterior aspect of the rotator interval, the medial head of the coracohumeral ligament and the superior glenohumeral ligament form an anterior sling around the long head of the biceps tendon which inserts at the lesser tuberosity. This band, which is commonly referred to as the “reflection pulley,” is more flexible than the fibrous plate described above (Weishaupt et al. 1999; Werner et al. 2000; Patton et al. 2001). It assumes a crescentic shape surrounding the anteromedial aspect of the biceps tendon(Fig. 9c). More distally, in the proximal bicipital groove, the biceps tendon lies in close contact with the subscapularis and is stabilized by fibrous bands arising from it. The superficial component of these fibers forms the transverse humeral ligament that, in distal continuity with the coracohumeral ligament, bridges the tuberosities transforming the biceps sulcus into an osteofibrous tunnel. The transverse humeral ligament is thin and weak and its role in stabilizing the biceps just distal to its exit from the rotator interval is not considered important unless the coracohumeral ligament is torn (Patton et al. 2001; Bennett 2001).
The other belly of the biceps, the short head, takes its origin from the tip of the coracoid process of the scapula, in a more medial location than the long head, in close contact with the tendon of the coracobrachialis. The long and short bellies of the biceps continue down in two separate muscle bellies which join together just distal to the middle third of the arm to form a long fusiform muscle. In contrast to the long head of the biceps, the tendon of the short head has a straight course and is not invested by a synovial sheath. In the rare cases when it is involved in shoulder pathology, this is usually injured as a result of trauma (i.e., anteroinferior dislocation of the shoulder) or inflammatory states.
10. DELTOID AND EXTRINSIC MUSCLES OF THE SHOULDER
In addition to the rotator cuff muscles and the biceps, the intrinsic muscles of the shoulder include the teres major and the deltoid. The teres major muscle arises from a raised oval area at the dorsal aspect of the inferior angle and the adjacent lateral border of the scapula and inserts into the medial lip of the intertubercular groove of the humeral shaft. This muscle acts as an adductor and medial rotator of the humerus and plays a role in stabilizing the proximal humerus during abduction. Together with the tendon of latissimus dorsi, the teres major forms part of the posterior wall of the axilla. The deltoid is a thick and powerful muscle supplied by the axillary nerve which forms something of a roof over the rotator cuff tendons and the glenohumeral joint. Its name derives from the fact that its shape is similar to an inverted Greek letter delta (∆). This muscle has a wide origin from the lateral third of the clavicle, the acromion and the spine of the scapula, and inserts on the anterolateral surface of the humerus at the middle third of the arm. The action of the deltoid muscle is multifaceted. In fact, it can be a flexor and medial rotator of the humerus with its anterior fibers (in that assisting the coracobrachialis, the subscapularis and the pectoralis major), an abductor of the humerus with its middle fibers (assisting the supraspinatus) and an extensor and lateral rotator of the humerus with its posterior fibers (assisting the infraspinatus and teres muscles). The primary function of the deltoid muscle, however, is to abduct the humerus. When the supraspinatus is torn, the abduction of the arm becomes the only result of a deltoid contraction, although the upward pull of the deltoid leads to superior subluxation of the humeral head.
The extrinsic shoulder muscles which join the upper limb with the spine are the trapezius, the latissimus dorsi, the levator scapulae and the rhomboids. Among them, the trapezius is the most relevant during examination of the shoulder with US. This muscle is broad, flat and overlies the posterior neck and the superior half of the posterior trunk with a triangular shape (hypotenuse facing the spine). Its name derives from the fact that it becomes a trapezius when the muscles of the two sides are considered as a single muscle. The trapezius has a wide origin from the external occipital protuberance, the ligamentum nuchae and the spinous processes of C7 to T12 vertebrae and attaches to the lateral third of the clavicle, the acromion and the spine of the scapula. The trapezius receives supply from the accessory nerve and some cervical nerves (III–VII), and has its primary function in the elevation and rotation of the scapula. The extrinsic muscles which joint the shoulder with the thoracic wall are the pectoralis major, the pectoralis minor and the serratus anterior. The pectoralis major muscle is a strong fan-shaped muscle covering most of the upper part of the chest wall and forming, with its lateral part, the anterior wall of the axilla. This muscle is separated from the more cranial deltoid by a groove, the deltopectoral triangle, which is traversed by the cephalic vein (Fig. 10a). The pectoralis major has three heads arising respectively from the anterior aspect of the medial half of the clavicle (clavicular head), from the manubrium and body of the sternum and the costal cartilages from II to VI ribs (sternocostal head), and from the aponeurosis of the external oblique muscle (abdominal head). The muscle fibers converge laterally into a broad trilaminar tendon which crosses the myotendinous junction of the long head of the biceps and inserts on the lateral lip of the intertubercular groove of the humerus (Wolfe et al. 1992). The tendon layers fuse and twist 90° just before the tendon insertion at the lateral lip of the bicipital groove, where the posterior lamina inserts cranially and the anterior lamina comprises the most caudal part of the enthesis (Fig. 10a,b). Distal to the humeral tuberosities, the pectoralis tendon participates in retaining the long head of biceps tendon close against the anterior aspect of the humeral shaft. The main action of the pectoralis major is to adduct and internally rotate the humerus. Deep to the pectoralis major, the pectoralis minor is a smaller triangular muscle which takes its origin from the III, IV and V ribs and inserts onto the medial border of the coracoid process. It stabilizes the scapula against the thoracic wall and is a useful landmark for the axillary vessels and nerves as it lies just superficial to them.
Figure 11 illustrates the anatomic relationship among intrinsic and extrinsic muscles of the shoulder and the bones by means of one-to-one correlation between cadaveric specimens and CT images.
11. BURSAE AND GLIDING SPACES
Knowledge of the anatomy of synovial recesses and para-articular bursae is an essential prerequisite to avoid misdiagnoses and pitfalls in the interpretation of pathologic findings. Three main synovial spaces are found around the shoulder area: the glenohumeral joint cavity, the subacromial-subdeltoid bursa and the acromioclavicular cavity. In normal conditions, these spaces are separated from one other because the rotator cuff is interposed between the glenohumeral joint and the subacromial-subdeltoid bursa and the acromioclavicular capsule is found between the acromioclavicular joint and the subacromial-subdeltoid bursa. In some pathologic states, such as a defect in the rotator cuff or in the inferior capsule of the acromioclavicular joint, these spaces can communicate.
The subacromial space, which is located between the coracoacromial arch and the humeral head, contains the rotator cuff tendons, the long head of the biceps tendon, the subacromial-subdeltoid bursa and a variable amount of connective tissue and fat (Fig. 12). The subacromial-subdeltoid bursa is a large synovium-lined structure located inferior to the acromion and the coracoacromial ligament that overlies the superior aspect of the supraspinatus tendon (Fig. 13). It also extends medially to the coracoid (subcoracoid bursa) and anteriorly to cover the bicipital groove, whereas its lateral and posterior boundaries are more variable and reach approximately 3 cm below the greater tuberosity (Bureau et al. 1996). From the functional point-of-view, the main role of the subacromial-subdeltoid bursa is to minimize the attrition of the cuff against the coracoacromial arch and the deltoid during movements of the arm. To facilitate gliding, the bursa is surrounded by a thin cleavage plane of peribursal fat. The subcoracoid bursa may be separated from the subacromial-subdeltoid bursa to form an individual cavity. In these cases, the bursa lies just inferiorly and medially to the coracoid and may simulate a cystic mass when distended by fluid if the examiner is not aware of its existence. In addition, care should be taken not to mistake it for the adjacent subscapularis recess of the glenohumeral joint.
In addition to the subacromial gliding plane, the scapulothoracic plane facilitates movement of the scapula relative to the chest wall and rotation of the scapula during abduction and adduction of the arm.
12. NEUROVASCULAR STRUCTURES
The rotator cuff muscles receive nerve supply from the suprascapular nerve (supraspinatus and infraspinatus), the subscapular nerve (subscapularis) and the axillary nerve (teres minor). The examiner should be aware of the anatomic course of the suprascapular and axillary nerves because these nerves are vulnerable to stretching injuries and trauma and may be involved by extrinsic compression (i.e., paralabral ganglia) leading to well-categorized entrapment syndromes: the suprascapular nerve syndrome and the quadrilateral space syndrome. The musculocutaneous nerve will be described later.
13. SUPRASCAPULAR NERVE
The suprascapular nerve originates from the upper trunk of the brachial plexus (C5–C6 level) and descends through the suprascapular foramen formed by the supraspinous notch of the scapula and the superior transverse scapular ligament to reach the supraspinous fossa (Fig. 14). Then, the nerve continues inferiorly to the supraspinatus muscle passing through the tunnel formed by the inferior transverse scapular ligament and the spinoglenoid notch to distribute in the infraspinous fossa (Fig. 14). In the supraspinous fossa, the suprascapular nerve gives off motor branches to the supraspinatus muscle, whereas the innervation to the infraspinatus muscle is provided by distal branches arising in the infraspinous fossa. Along its entire course, the suprascapular nerve is accompanied by the suprascapular vessels.
14. AXILLARY ARTERY AND NERVE
The axillary artery continues the subclavian artery beyond the outer border of the first rib. It traverses deep to the pectoralis minor muscle and is accompanied by the cords and distal branches of the brachial plexus, and the axillary vein. The axillary artery can be palpable in the inferior part of the axilla, in proximity to the inferior glenohumeral joint capsule. Distal to the lateral border of the pectoralis minor, it sends three branches: subscapular, and anterior and posterior circumflex humeral arteries. The circumflex arteries have a horizontal course and anastomose to form a circle around the anterior and posterior aspect of the surgical neck of the humerus. The anterior circumflex humeral artery is smaller than the posterior and runs deep to the coracobrachialis and the biceps and in front of the surgical neck of humerus. It gives off an ascending branch, the arcuate artery, which accompanies the long head of the biceps tendon in the intertubercular groove. The posterior circumflex humeral artery is larger and crosses the posterior wall of the axilla through the quadrilateral space in association with the axillary nerve. It is a landmark for the US detection of the nerve.
The axillary nerve arises from the posterior cord of the brachial plexus (C5–C6 level) near the coracoid process and proceeds along the inferolateral border of the subscapularis muscle to curve inferior to the glenohumeral joint capsule and pass into the posterior aspect of the arm. The nerve courses in association with the posterior circumflex artery through the quadrilateral space – a squared passageway bounded by the long head of the triceps muscle medially, the surgical neck of the humerus laterally, the teres minor muscle cranially and the teres major muscle caudally (Fig. 15) (Loomer and Graham 1989). It has two terminal branches: anterior and posterior. The anterior branch supplies the anterior deltoid muscle and overlying skin; the posterior branch innervates the teres minor and the posterior deltoid muscle and distributes to the skin overlying the distal deltoid and the proximal triceps muscle.
15. THORACIC OUTLET STRUCTURES
The thoracic outlet region includes the brachial plexus nerves and the subclavian artery and vein. These neurovascular structures traverse restricted spaces in which they can be compressed, the most important of which are the interscalene triangle, the costoclavicular space and the retropectoralis minor space (Fig. 16a) (Demondion et al. 2000). Both subclavian artery and brachial plexus nerves pass through the interscalene triangle, a space bordered by the anterior scalene muscle anteriorly, the middle scalene muscle posteriorly and the first rib inferiorly.
The scalene muscles are respiratory muscles and act by raising the first rib and bending and rotating the neck. The anterior scalene takes its origin from the anterior tubercles of the transverse processes of C3 to C6 and inserts into the scalene tubercle of the first rib; the middle scalene, the longest and the largest of the scalene muscles, originates from the posterior tubercles of the transverse processes of C2 to C7 and has a broad insertion onto the first rib, between the groove for the subclavian artery and the scalene tubercle; the posterior scalene, which is not responsible for upper extremity neurovascular compression syndromes, is deeper in location, arising from the posterior tubercles of C5 and C6 (possibly C7) and attaching onto the second and third ribs. Within the interscalene triangle, the brachial plexus nerves lie posterior, lateral and superior to the artery. The lower roots (C8 and T1) have the closest relationship with the artery. They lie behind it. In contrast to the artery, the subclavian vein courses in front of the anterior scalene muscle, just inferior and lateral to the costoclavicular ligament and over the first rib. Several anatomic variants in the scalene region, including accessory muscles, abnormal origin or insertion of the anterior and middle scalene muscles, intermingled muscles and a variety of fibrous bands, can cause narrowing of this space and subsequent entrapment of the neurovascular bundle. After traversing the scalene triangle, the neurovascular structures pass across another restricted space, the costoclavicular space, between the clavicle and the first rib. In this space, the nerve cords maintain a constant relationship with the axillary vessels. Then, nerves enter the retropectoralis minor space, which is a passage delimited by the anterior pectoralis minor muscle and the posterior subscapularis muscle, near the coracoid. In this tunnel, the nerve cords course just above and posterior to the axillary artery (Demondion et al. 2000).
16. BRACHIAL PLEXUS NERVES AND VERTEBRAL ANATOMY
The anatomy of the brachial plexus is complex, with many nerves interconnecting involved. Because the plexus nerves exit the spinal canal through the neural foramina, a preliminary description of the transverse processes of the cervical vertebrae is essential for a better understanding of the US scanning technique required (Martinoli et al. 2002).
The transverse processes of the cervical vertebrae project from the junctions of the pedicles and laminae and act primarily as attachments for muscles, such as the scalene muscles. Each process has a “U” shape formed by two prominent bony tubercles, anterior and posterior, which form its walls, and a thin lamina, which forms its floor (Guha et al. 1996). This lamina is pierced by the vertebral artery, which ascends through the foramina transversaria of C6 to C3. This configuration is repeated uniformly from C2 down to C6, whereas C7 appears different. As the C7 vertebra represents a transition between cervical and thoracic configuration, it has a larger transverse process in which the posterior tubercle is larger and more prominent and the anterior tubercle is absent or rudimentary (Fig. 17). More caudally, the T1 vertebra differs from the cervical ones since its transverse processes are directed more posteriorly to articulate with the head of the first rib. The rib overlaps the vertebra immediately inferior to the foramen, thus giving a flat and smooth appearance to its lateral aspect. As the nerve roots leave the spine, they cross the groove between the tubercles. One has to consider that each root leaves the intervertebral foramen sliding on the transverse process of its corresponding vertebral level (Guha et al. 1996). Then, because there are eight cervical nerves and only seven cervical vertebrae, the C8 root lies at the level of the T1 vertebra, and so forth.
Brachial plexus nerves include several components, including roots, trunks, divisions, cords and finally peripheral nerves of the upper limb which derive from the union of the ventral roots from C5 down to T1. In the paravertebral area, each root has an individual (monofascicular) structure.
Proceeding toward the interscalene area, the roots of C5 and C6 join together to form the upper trunk, the root of C7 emerges by itself as the intermediate trunk and, in the lower neck, the roots of C8 and T1 form the lower trunk of the plexus. More distally, in the supraclavicular region, each trunk gives off two divisional branches, named the anterior and posterior divisions, which innervate the flexor and extensor muscles of the upper extremity respectively. In the axilla, these divisions join in various combinations to form the cords of the brachial plexus. The relationship of the cords with the axillary artery determines their names: the lateral, medial and posterior cords. The axillary and radial nerves originate from the posterior cord, the musculocutaneous and part of the median nerve arise from the lateral cord, whereas the other contribution of fibers to the median nerve and the ulnar nerve originate from the medial cord.
17. ESSENTIALS OF CLINICAL HISTORY AND PHYSICAL EXAMINATION
Initially, the examiner should perform a brief clinical assessment based on the patient’s history, a short physical examination and a review of previous imaging studies.
18. ROTATOR CUFF PATHOLOGY
First, the examiner should check whether previous shoulder accidents, including acute trauma, chronic microtrauma, sport-related injuries and episodes of shoulder instability, have occurred. Special attention should be given to the location, type, severity and circumstances of the referred pain. Patients with rotator cuff pathology typically complain of night pain and inability to sleep on the affected side. Generally speaking, the location and irradiation of shoulder pain is not related to involvement of a specific tendon. Most patients are fairly accurate in localizing pain. Often, patients with supraspinatus tendon tear complain of pain irradiated along the lateral aspect of the upper and middle third of the arm, in proximity to the insertion of the deltoid muscle. Pain distal to the elbow level in association with paresthesias is usually related to cervical or brachial plexus disorders rather than an isolated rotator cuff pathology. Next, the patient should be asked what kind of movement produces discomfort, or the examiner should attempt to produce pain with different maneuvers. In anterosuperior impingement syndrome, pain is reported during activities or maneuvers that require active abduction and forward elevation of the arm. Exacerbation of pain can also be noted during maximal elevation of the arm and internal rotation in posterosuperior impingement and during maximal internal rotation and adduction of the arm in anteromedial impingement.
A basic physical examination of the affected shoulder for rotator cuff assessment is part of the routine US study (Moosikasuwan et al. 2005). The examination begins with observation on how the patient is undressing, because the act of slipping the shirt off is an indicator of the full range of movements that the patient is able to perform and is typically limited in rotator cuff disease. Then, the overall range of shoulder motion can be assessed by asking the patient to place the dorsal aspect of the hand behind the back as cranially as possible, between the scapulae (internal rotation and extension), and behind the neck (external rotation and abduction). With the patient seated, the affected shoulder is inspected and simultaneously palpated by the examiner. Swelling and tenderness around the shoulder, especially when located over the anterior aspect of the joint, more likely reflects an effusion in the subacromial subdeltoid bursa rather than an intra-articular effusion. In chronic cuff tears, palpable crepitus over the cranial aspect of the shoulder can be produced by rotation of the shoulder with the arm in 90° of elevation. A localized soft-tissue lump over the cranial aspect of the acromioclavicular joint is often related to a cyst arising from the acromioclavicular joint which develops following massive rotator cuff tear (Geyser Sign). Care should be taken to correlate it with the tear because patients usually take medical advice for the lump and not for the underlying disorder (Fig. 18a). Ecchymosis over the anterior aspect of the shoulder and arm is typically correlated with an acute tear of the long head of biceps tendon but it may also be appreciated in cases of traumatic enlargement of a previous tear of the supraspinatus or subscapularis tendons. Except for the subscapularis, atrophy of rotator cuff muscles can be appreciated by inspection and palpation. Although the occurrence of a bilateral cuff rupture should be always kept in mind, comparative examination of the two shoulders for asymmetry may help the examiner to evaluate muscle atrophy. On the lateral shoulder, deltoid atrophy may reveal wasting from axillary neuropathy or from previous surgery with deltoid detachment for rotator cuff repair. On the posterior shoulder, wasting of the infraspinatus and teres minor muscles may derive from chronic rotator cuff tears, disuse, glenohumeral arthritis and suprascapular nerve palsy (Fig. 18b). In patients with biceps tendon tear, the retracted muscle can be palpated as a soft-tissue lump over the anterior aspect of the middle third of the arm, possibly mimicking a hypertrophied muscle, the so-called Popeye sign (Fig. 18c). Detection of the retracted biceps can be difficult in obese patients. Rotator cuff tendons may be palpated systematically for focal tenderness starting anteriorly with the subscapularis and the biceps and then moving posteriorly to evaluate the insertions of the supraspinatus and infraspinatus into the superior and posterior facets of the greater tuberosity. Finally, the acromioclavicular joint is assessed by applying a firm pressure over it with the thumb. If this pressure generates pain, the ache should be compared with that recalled by the patient to ensure matching of symptoms. A painful acromioclavicular joint may indicate an arthritic or traumatized joint. Acromioclavicular joint separation is noted by the painful prominence of the distal end of the clavicle associated with excessive mobility of the joint.
The overall range of shoulder motion is frequently affected in patients with rotator cuff disorders. In these cases, examination of passive motion may be helpful to differentiate a real impingement syndrome with rotator cuff pathology from adhesive capsulitis (frozen shoulder). Whereas in rotator cuff disease without secondary adhesive capsulitis the range of motion is restricted during active but not passive motion, shoulder motion in adhesive capsulitis is always lost. In this disorder, the motion is for the most part restricted in external rotation tested in both 0° and 90° of abduction, although all directions are usually involved to some extent. Specific clinical tests to evaluate the strength of individual rotator cuff tendons have been described in the orthopaedic literature (Hawkins and Hobeika 1983). Supraspinatus function can be evaluated by testing the patient’s ability to resist a downward force applied to the humerus with the elbow extended and the arm in a position of internal rotation and 45° of forward flexion (Fig. 19a). If positive, the test generates pain, weakness or both symptoms. Then, two impingement maneuvers, which may be performed with the patient standing or supine, may help the examiner to assess shoulder pain related to rotator cuff disease or biceps tendinitis. The first, which is referred to as Neer’s test, is obtained with maximal passive glenohumeral forward flexion with the shoulder in neutral rotation to obtain impingement of the supraspinatus and the biceps against the anterolateral margin of the acromion (Neer 1983). The second, Hawkins’ test, is performed with 90° forward flexion, slight horizontal adduction and internal rotation to compress the insertion of the supraspinatus and the subacromial bursa under the coracoacromial ligament (Hawkins and Hobeika 1983). The internal rotation of the shoulder reflects the action of the subscapularis tendon and can be assessed by means of the “lift-off test” (Gerber and Krushell 1991). To avoid the contribution of other muscles (i.e., pectoralis major, teres major) to internal rotation, this test measures the strength of the subscapularis in isolation by positioning the forearm behind the patient’s back. The patient is then asked to lift her or his hand off of the lumbar region, an action that requires the active contraction of the subscapularis (Fig. 19b). Inability to perform this maneuver indicates subscapularis tear. The combined action of the infraspinatus and teres minor cannot be differentiated during external shoulder rotation. The ability of these muscles considered as a whole can be estimated using the “horn-blower sign,” in which the patient’s arm is passively brought into 90° of abduction and full external rotation. The examiner holds the elbow while the patient is asked to maintain maximal external rotation. Any loss of active external rotation represents weakness of the posterior rotator cuff, whereas failure to maintain full external rotation of the abducted arm suggests a large posterior rotator cuff defect. Posterior deltoid contraction could give a false negative Hornblower‘s sign. Performing the test bilaterally is useful to avoid this potential pitfall (Hawkins and Hobeika 1983). Although strength tests are useful to support the clinical suspicion of rotator cuff disease, they have been found to have varying sensitivity and specificity in the diagnosis. Sonologists must at least be familiar with them because the orthopaedist can cite these maneuvers in the request for a US examination. In patients who have undergone previous surgery for rotator cuff tears, the examiner should spend some additional time reviewing the surgical report before starting the US examination, because surgical procedures can alter the local anatomy. One should also keep in mind that the surgical intervention may have consisted of acromioplasty and bursectomy without any suture of the torn tendons. In these cases, discontinuity of the rotator cuff must not be misinterpreted as a retear.
Although conventional radiography is somewhat limited in evaluation of the rotator cuff and its findings become pathognomonic only in patients with chronic tear, previous imaging studies should be reviewed before starting the US examination. Advising the patient or the referring physician the day before the examination will usually ensure these studies available. Standard radiographs are the most common imaging studies performed before US examination. Pathologic changes associated with rotator cuff disorders include intratendinous or bursal calcifications, acromial spurs, erosions and sclerosis of the tuberosities, a reduced subacromial space with superior subluxation of the humeral head and a lateral downsloping or low-flying acromion. Inferior humeral osteophytes, osteoarthritic changes and undersurface osteophytes of the acromioclavicular joint, and bony changes related to previous surgical procedures can be appreciated as well. In anterior shoulder dislocation, a compression fracture on the posterolateral aspect of the humeral head – commonly referred to as the Hill-Sachs fracture – is seen as the result of impaction of the displaced humeral head against the anterior aspect of the glenoid rim. Similarly, in the setting of posterior shoulder dislocation, a compression fracture on the anteromedial aspect of the humeral head, the so-called reversed Hill-Sachs or McLaughlin lesion, can be encountered due to the impaction of the humerus against the posterior glenoid rim. Both abnormalities can be detected on plain films and should redirect the US examination toward an instability problem. The examiner should be aware that the availability of standard radiographs is time-saving and essential for the adequate interpretation of troublesome US images related to disorders that can be more obvious on plain films.
19. THORACIC OUTLET AND BRACHIAL PLEXUS PATHOLOGY
Thoracic outlet pathology is conventionally divided into two main types – vascular and neurogenic – although vascular and nervous entrapment signs and symptoms, such as pain, numbness, tingling, weakness and other disturbances in the upper limb, often coexist as a single clinical picture. In general, brachial plexus nerves are more often involved than subclavian vessels. Brachial plexus syndromes often resemble more distal entrapment neuropathies and are often mistaken for a lower level (i.e., carpal tunnel, cubital tunnel) compression. To distinguish them from distal entrapment of individual nerves, one should consider that sensory and motor system abnormalities encountered in brachial plexus pathology are, in general, not clearly attributable to a single nerve. Patients with upper plexus involvement (C5–C7 level) complain of pain in the region of the trapezius and shoulder, with symptoms radiating along the lateral aspect of the extremity down to the territory of innervation of the median nerve. Motor symptoms include weakness of shoulder abduction (involvement of the deltoid and supraspinatus) and external rotation (involvement of the infraspinatus and teres minor). In overt cases, patients exhibit an extended and internally rotated arm, a pronated forearm and a flexed wrist. On the other hand, patients with lower plexus involvement (C8–T1 level) feel pain in the supraclavicular region, in the back of the neck and in the axilla down to the area of the hand innervated by the ulnar nerve, with sensory disturbances in the fourth and fifth fingers. In longstanding disease, muscle weakness may involve the ulnar-innervated muscles of the hand and forearm (flexor carpi ulnaris) resulting in a claw-hand deformity. Trauma to the neck, shoulder girdle and even the upper limb is often associated with the onset of a thoracic outlet syndrome related to brachial plexus involvement. Brachial neuritis (Parsonage Turner syndrome) may also be suspected when the onset of shoulder pain and disability follows a viral illness or unrelated previous surgical procedure. Apart from nerves, if the subclavian vein is selectively compressed, symptoms are mostly related to increased venous pressure in the upper extremity. Entrapment of the subclavian artery is rare and usually presents with arterial insufficiency and a cold extremity.
When examining a patient with suspected thoracic outlet syndrome, objective findings are, in many cases, few. The physical examination should include general evaluation of the musculoskeletal and vascular systems of the upper extremity looking for temperature changes and areas of muscle atrophy. The supraclavicular and infraclavicular area should be palpated for tenderness and a radiating Tinel sign. Several provocative tests may be performed both before and during the US examination, including the Adson maneuver (Adson and Coffey 1927), the hyperabduction test or Wright maneuver (Wright 1945), the Eden maneuver, or military position (Eden 1939), and the Roos maneuver (Roos 1976). In particular, the Adson maneuver is performed by holding the patient’s arm down and checking the radial pulse while the patient inspires deeply and keeps the head extended and turned toward the involved extremity. The Wright maneuver is obtained with the patient seated or standing and the shoulder hyperabducted and rotated externally. If the test is positive, the patient complains of paresthesias in the extremity and any change in arterial pulse. The Roos test is performed by means of a 3-minute abduction with exercise (clenching fists). While performing these tests, the examiner must be aware that positive findings may also occur in normal subjects.
20. NORMAL ULTRASOUND FINDINGS AND SCANNING TECHNIQUE
When examining the shoulder with US, appropriate positioning of the patient is essential to allow the examiner access to the patient’s shoulder and the US keyboard simultaneously. Positioning should be comfortable for the patient and the examiner, and allow examination of the shoulder in as short a time as possible. Different patient positions have been reported for the US examination of the shoulder, likely reflecting the preference and habit of the examiner. Many sonologists examine the shoulder using an anterior approach, standing in front of the patient while he or she is seated on the examination bed. Generally speaking, the anterior approach is easier to learn for the beginner and offers greater opportunity to correlate US images with probe positioning based on skin landmarks. At least in our opinion, this is particularly true while evaluating anterior structures, such as the biceps tendon and the rotator interval. Other sonologists prefer to perform the examination by a dorsal approach with the patient seated on the bed or on a revolving stool. This approach allows the examiner to perform a brief physical examination and prevents excessive backward curvature of the spine, thus improving the US assessment of the supraspinatus (Lyons and Tomlinson 1992). In addition, the dorsal approach makes guiding the patient to assume different arm positioning easier and increases stability during scanning (Allen and Wilson 2001). Depending on the examiner’s and patient’s height, an appropriate adjustment of the bed level allows a more comfortable examination, while a revolving stool makes the approach to the different aspects of the joint easier. An additional technique in which the patient is examined supine with the arm hanging down the side of the bed has been described for a better evaluation of the internal structure of the supraspinatus (Turrin et al. 1997; Turrin and Capello 1997). The US examination is well tolerated by patients and even preferred to MR imaging (Middleton et al. 2004A). The main reasons for this preference probably include a shorter examination time, the lack of discomfort related to positioning within the magnet, and a free environment with contact with the medical personnel and absence of the sense of isolation and anxiety which is typically produced during MR imaging examinations (Middleton et al. 2004a).
Because most indications for shoulder US are concerned with the rotator cuff, most of this section will focus on the examination of these tendons. Before discussing the normal US anatomy and examination technique of the cuff, some important points should be taken into account:
- Rotator cuff US needs a rigorous standardized technique to obtain systematic and comprehensive assessment of the individual tendons within a short examination time.
- While examining the rotator cuff with US, it is essential to perform the assessment of each of the four tendon–muscle units and the biceps tendon by means of scanning planes oriented according to their long-axis and short-axis. Although this approach might seem boring and time-consuming, it is the only way that ensures subtle pathologic findings are not missed. This is true even for skilled examiners.
- Each tendon should be evaluated systematically from its myotendinous junction to the bony insertion and in the proper position during maximal tendon stretch so that the bony structures that limit US access, such as the acromion and the coracoid process, are moved away from it.
21. BICEPS TENDON AND ROTATOR CUFF
Apart from the type of approach used, we perform a standard US examination of rotator cuff tendons starting with the long head of the biceps tendon as the initial key reference. The examination of the biceps is then followed by scanning the anterior (subscapularis), superior (supraspinatus) and posterior (infraspinatus and teres minor) aspects of the rotator cuff. To avoid confusion with the spatial planes of the body, we prefer to use the terms “long-axis” and “short- axis” rather than “longitudinal” and “transverse” to indicate the orientation of the scanning plane according to the axis of the examined structure.
22. LONG HEAD OF THE BICEPS TENDON
In most patients, the biceps tendon is assessed with the arm in neutral position. In most instances, a slight internal rotation of the arm can be helpful for a more accurate assessment. The first landmark to identify is osseous: the intertubercular sulcus, which is also referred to as the “bicipital groove.” It lies between the lesser and the greater tuberosities and has a well-defined concave appearance (Fig. 20a,b). Once the groove is found, one should check its appearance, looking at its depth and presence of focal cortical erosions (Fig. 20c–e). The two tuberosities do not have the same appearance, the lesser having a more pointed and the greater a more rounded look. Care should be taken to examine the content of the bicipital groove. This cavity holds the long head of the biceps tendon invested by its proper synovial sheath, along with the ascending branch of the anterior circumflex artery, located on the lateral side of the tendon, and fatty tissue (Fig. 21). Visualization of the arcuate artery depends on its size and flow volume. In younger patients, it is almost invariably found. Awareness of its presence can avoid misdiagnosis of tendon sheath hyperemia. The transverse humeral ligament appears as a very thin hyperechoic band overlying the sulcus (Fig. 20b).
Short-axis scans are the most useful planes for evaluating the biceps tendon. Because this tendon courses from cranial to caudal and from superficial to deep, a careful scanning technique is needed to distinguish it from both the adjacent fat (which is not affected by anisotropy and always appears hyperechoic) and the sheath fluid (Middleton et al. 1985). In fact, if the transducer is not maintained parallel to the tendon, this may appear artifactually hypoechoic mimicking fluid (Fig. 22a–c). Often, the transducer must be rocked slightly to ensure the best visualization of the fibrillar echotexture. In particular, a slight tilting of the probe (short-axis scans) or a slight pressure exerted with its caudal end on the skin (long-axis scans) may be helpful for this purpose (Fig. 22c,d,f). Once the tendon has reached maximum reflectivity, the orientation of the transducer should maintained constant while shifting the probe up and down. Cranially, at the intra-articular level, the biceps tendon assumes a more oval or crescent shape while reflecting over the humeral head and overlies the anechoic hyaline cartilage. Because the biceps is intrinsically much more reflective and anisotropic than the adjacent supraspinatus and subscapularis, slight continuous changes in transducer orientation may be useful to recognize the tendon in its intra-articular portion on short-axis scans. The origin of the biceps tendon is not visible due to problems of access. Therefore, the anatomic variants of the biceps tendon origin cannot be detected with US. Positioning the patient in posterior flexion may, however, be helpful to visualize part of its most proximal portion emerging from underneath the cover of the acromion. Distal to the humeral tuberosities, the long head of the biceps tendon lies in front of the proximal humeral metaphysis. It is important to examine this level because even small effusions tend to fill the most dependent portion of the tendon sheath (Fig. 23).
In this area, a small amount of intrasheath fluid, not sufficient to encircle the tendon, is a normal finding and should not to be indicated in the report. More caudally, the myotendinous junction of the biceps tendon can be appreciated as a gradual decrease in the size of the tendon and a parallel increase in the size of the muscle. It lies deep to the tendon of the pectoralis major and lateral to the short head of the biceps muscle (Fig. 24a). The distal portion of the biceps should be always evaluated because a tear or calcification may occur at this level. In the evaluation of the long head of the biceps tendon, the importance of long-axis scans is limited to confirm the tendon integrity in doubtful cases based on visualization of its fibrillar echotexture. The pectoralis tendon is a broad flattened tendon which crosses anterior to the biceps to insert into the lateral lip of the intertubercular groove, receiving contributions from the three heads of the muscle: clavicular (superficial layer), sternal (intermediate layer) and abdominal (deep layer). When the arm is internally rotated, this tendon assumes an arcuate course over the biceps, whereas it becomes straight in external rotation (Fig. 24b,c). It is best evaluated with the arm abducted and externally rotated to stress the myotendinous region (Rehman and Robinson 2005). US is able to distinguish the three heads of the pectoralis major muscle but not the individual components of the tendon because the three tendon layers blend with no significant intervening connective tissue (Rehman and Robinson 2005).
23. SUBSCAPULARIS TENDON
After the biceps has been examined, the patient is asked to rotate the arm externally in order to evaluate the subscapularis tendon on the anterior aspect of the shoulder. This maneuver stretches the subscapularis and helps to move its tendon from underneath the coracoid process into a more superficial position for an adequate examination (Fig. 25). Dynamic scanning during passive internal and external rotation with the arm adducted may also be helpful to assess the integrity of the subscapularis. While the arm is in external rotation, the examiner must remember to neutralize the tendency for the patient to lift and abduct the elbow from the lateral chest wall. This can be easily avoided by keeping the hand in supination while rotating the arm externally. Conditions limiting external rotation, such as shoulder casting, may lead to a poor delineation of the anterior structures. Any of these constraints should be indicated in the report.
When examined on its short axis, the multipennate structure of the normal subscapularis tendon creates a series of hypoechoic clefts among the fascicles that should not be confused with tendon tears (Fig. 26). In fact, these cleft are related to muscle fibers interposed with tendon fascicles. On short-axis scans, the lesser tuberosity has a flat appearance ending in a smooth downsloping contour located just caudal to the tendon insertion (Fig. 26). Such a bony landmark would be helpful when assessing partial tears of the subscapularis because it indicates the caudal limit of the tendon insertion. Because partial tears often involve the cranial portion of the tendon and preserve its caudal portion, checking the shape of the lesser tuberosity would increase the confidence in excluding a complete tear. On its long axis, the subscapularis tendon has a convex shape over the curvilinear profile of the humeral head and is outlined by an echogenic layer representing subdeltoid fat (Fig. 27). In the most medial scans, the humeral head appears covered with a layer of articular cartilage. When examining the subscapularis tendon on long-axis planes, one must be aware that this tendon is broad and, therefore, requires the transducer to be swept up and down until its full width is demonstrated (Fig. 27b). In addition, it must be known that the actual insertion of the subscapularis tendon involves a limited portion of the lesser tuberosity which is placed laterally, in proximity to the bicipital groove (Fig. 27a). Moving the probe medially on transverse planes, the coracoid process appears as a rounded hyperechoic structure. With internal rotation of the arm, the subscapularis tendon can be seen disappearing beneath the acoustic shadowing of the coracoid (Fig. 25a–c). The insertions of the short head of the biceps (lateral), the coracobrachialis and the pectoralis minor (medial) onto the coracoid process can be appreciated by shifting the probe caudally to the bone: the tendon of the short head of the biceps is longer than that of the coracobrachialis muscle (Fig. 28). Deep to these extrinsic structures, the muscle belly of the subscapularis, the anterior surface of the glenoid and the anterior labrum can be demonstrated in slender subjects. When short-axis planes are obtained, care should be taken not to confuse the belly of the subscapularis muscle for a hypoechoic effusion in the dependent anterior portion of the subacromial subdeltoid bursa or the anterior joint recess. Especially in obese patients, the US assessment of these latter structures may be problematic and requires low-frequency probes (7.5–5 MHz).
24. SUPRASPINATUS TENDON
Because of its peculiar position between the acromioclavicular arch and the humeral head, only the distal part of the supraspinatus tendon can be examined while keeping the patient’s arm in neutral position (Fig. 29a). To obtain a more complete visualization of this tendon, the patient is asked to extend the arm posteriorly, placing the palmar side of the hand on the superior aspect of the iliac wing with the elbow flexed, directed posteriorly and toward the midline, so that the acromion is moved away from it (Fig. 29b). With this maneuver (commonly known as the modified Crass or Middleton position), the tendon is depicted in its full extent, even including visualization of its myotendinous junction (Crass et al. 1988b; Middleton et al. 1992). When the patient assumes this position, the supraspinatus rotates and becomes a more anterior structure (Fig. 29b). Some authors have also suggested forced internal rotation for imaging the supraspinatus tendon under stress. This position, which is referred to as the stress maneuver or the Crass position, is obtained by keeping the shoulder extended, adducted and internally rotated with the elbow flexed, the palm facing out, and the fingers pointing toward the contralateral scapula (Crass et al. 1987). There should not be any space between the elbow and the lateral chest wall. We believe this latter position has a role in increasing diagnostic confidence in the interpretation of subtle pathologic findings (i.e., partial-thickness tear) by applying more tension on the intact tendon fibers or shifting the bursal fluid away from a tear to better delineate its width. However, examining the supraspinatus under stress has some drawbacks: this position is often not well tolerated by the patient and, in many cases, does not allow a proper and complete visualization of the entire width of the supraspinatus because the excessive internal rotation leads to a more difficult assessment of its anterior third and the structures of the rotator cuff interval, which are displaced too medially. In addition to static scanning, dynamic assessment of subacromial impingement can be attempted by placing the probe in the coronal plane with its medial margin at the lateral margin of the acromion. The patient is asked to abduct his or her arm while it is in internal rotation. With this maneuver, the supraspinatus and the bursa can be seen passing deep to the coracoacromial arch. In degenerative conditions, this maneuver helps appreciation of the difficult gliding of the thickened tendon and subacromial bursa under the acromion (Fig. 30).
On long-axis scans, the supraspinatus tendon appears as a convex beak-shaped structure extending deep to the subdeltoid fat and the subacromial subdeltoid bursa and superficial to the articular cartilage, which appears as a smooth hypoechoic band ending at the edge of the convexity of the humeral head, the humeral neck, where the greater tuberosity begins (Fig. 31a). The shape of the humeral head is an essential landmark when examining the supraspinatus tendon and its insertion onto the cranial aspect of the greater tuberosity (Fig. 32). Similar to other cuff tendons, the supraspinatus lies between two cavities: the glenohumeral joint, which extends between it and the cartilage up to the humeral neck, and the subacromial subdeltoid bursa that lies just over the tendon and is usually separated from it by a thin hyperechoic layer of peribursal fat (Fig. 32). In normal states, these cavities are collapsed and, therefore, not visible. Often, the bursa cannot be separated from the tendon and may occasionally be seen bulging beyond the lateral edge of the tuberosity (Fig. 31a). In such cases, it cannot be confused with superficial tendon fibers. Then, one should not mistake the hypoechoic muscle fibers in the area of the myotendinous junction for a proximal tear. The deltoid overlies the bursa and is seen inserting in the lateral border of the acromion through a very short tendon (Fig. 29a,b). The normal supraspinatus tendon is approximately 6 mm thick. Larger tendons may occasionally be seen in athletes, whereas the rotator cuff thickness in women and old patients tends to be less than that of younger active men (Crass et al. 1988).
When the shoulder is examined in posterior flexion, doubts may arise, especially in beginners, as to whether the probe is correctly oriented along the real long-axis of the tendon. To solve this problem, a trick of the trade is to refer to the intra-articular portion of the biceps as a landmark to obtain proper transducer positioning for imaging the supraspinatus (Fig. 6.33). In fact, the two tendons run parallel to one another and the intra-articular biceps is easily recognized due to its more clearly defined fibrillar pattern. The examiner should first rotate the transducer until the biceps is as elongated as possible in the US image (approximately 45% between the coronal and sagittal planes) (Fig. 33a,b). Then, the probe is moved posteriorly over the supraspinatus without changing its orientation (Fig. 33c,d). The resulting image will be along the axis of the supraspinatus. On long-axis scans, a typical site where anisotropy may create pitfalls is the tendon area overlying the anatomic neck of the humerus. In this area, anisotropy is produced by a curved diverging course of the articular fibers of the tendon as they approach the insertion and should not be confused with a partial tear of the rotator cuff (Fig. 34). It is important to rock the transducer gently to visualize this portion of the tendon correctly, in a plane perpendicular to the US beam. In fact, partial-thickness tears commonly occur at this site and have a similar appearance. In contrast to the subscapularis, the normal supraspinatus tendon is composed of a homogeneous matrix of medium-level echoes, an appearance somewhat different from other tendons in the body, which have a well-defined fibrillar structure (Fig. 31a). This pattern seems to be the result of varied orientation of the fibers because the supraspinatus and the infraspinatus splay out and interdigitate (Fig. 35).
In other words, when scanning is obtained along the tendon axis, the plane may not be in the real axis of the tendon fibers to produce intense specular echoes. Nevertheless, there is a tendon portion more fibrillar in echotexture and anisotropic in the supraspinatus: it is located anteriorly and seems to be related to a cylindrical bundle of fibers with a straight course arising from the anterior part of the muscle belly. This tendon portion can mimic a biceps tendon due to its strong anisotropy (Fig. 35b,d). The other flat portion of the tendon tapers posteriorly and infiltrates the undersurface of the cylindrical tendon. A hypoechoic band may sometimes be seen separating the flat and cylindrical parts of the tendon: it should not be mistaken for a rotator cuff tear.
In its short axis, the supraspinatus exhibits a convex shape and is composed of a homogeneous texture of medium-level echoes (Fig. 31b). Like the rest of the cuff, the supraspinatus generally appears more echogenic in comparison with the overlying deltoid muscle. The different portions of the tendon (anterior and posterior) should be examined separately to avoid problems related to anisotropy. While the anterior edge of the supraspinatus is clearly appreciated, there is no clear interface between the supraspinatus and the infraspinatus due to the interwoven structure of these tendons. In fact, the supraspinatus and infraspinatus form a continuum and cannot be clearly distinguished at either US imaging or arthroscopy. If the probe is shifted too posteriorly on short-axis planes, a multilayered disposition of tendon fibers can occasionally be appreciated with a different orientation relative to the supraspinatus (Fig. 36). These fibers belong to the infraspinatus and are, therefore, imaged out-of-plane. One should not confuse them with the most posterior part of the supraspinatus. To separate the contribution of the two tendons, some authors have suggested that the supraspinatus is approximately 1.5 cm in width; therefore, on short-axis planes the first 1.5 cm of the rotator cuff located just posterolateral to the biceps tendon is believed to represent the supraspinatus tendon and the next posterior cuff portion the infraspinatus (Fig. 37a,b) (Teefey et al. 1999, 2000a). We believe that this method has limitations related to the different body mass of subjects and the complex structure of these tendons. As an alternative, one could attempt to obtain US images more proximally, over the myotendinous junctions of these tendons: a plane of separation between them may occasionally be observed (Fig. 37c,d).
Shifting the transducer on a more proximal level, the coracoacromial ligament can be seen as a fibrillar band joining the acromion with the coracoid. This ligament is normally straight or slightly convex and can be seen overlying the myotendinous junction of the supraspinatus and the biceps (Fig. 38). On its short axis, the coracoacromial ligament is more difficult to be appreciated due to a similar echogenicity with the surrounding fat and can be demonstrated only in cases of bursal distension related to impingement and septic bursitis as a notch sign on the bursal wall. Medial to the coracoacromial arch, the supraspinatus muscle can be seen as a trapezoid hypoechoic structure that lies beneath the flat trapezius. In continuity with the cylindrical tendon, the intramuscular tendon can be demonstrated as a hyperechoic structure located in the anterior portion of the supraspinatus muscle. The overall volume of the muscle and its echogenicity can be evaluated with US to assess atrophy and fat infiltration. In a quantitative study of healthy subjects, the cross-sectional area of the supraspinatus muscle was found to be larger on the dominant side and progressively decreased with aging (Katayose and Magee, 2001).
25. INFRASPINATUS AND TERES MINOR TENDONS
The examination of the infraspinatus and teres minor tendons requires transducer positioning on the posterior glenohumeral joint either with the forearm in a supination on the ipsilateral thigh or with the patient’s hand on the opposite shoulder. We believe the first approach works better as it avoids repositioning of the tendon too anteriorly, which may make it difficult to separate its fibers from the supraspinatus. Using such a posterior approach, the spine of the scapula may be a useful landmark to distinguish these tendons (Fig. 39). First, one should palpate the scapular spine and place the transducer over it, in a more medial position relative to the greater tuberosity (Fig. 39a): shifting the transducer up on the sagittal plane, the supraspinous fossa and the supraspinatus muscle can be found deep to the trapezius muscle (Fig. 39b). After that, the infraspinatus and teres minor muscle can be depicted as individual structures deep to the deltoid muscle by shifting the transducer down to the scapular spine (Fig. 39c).
Each of these muscles is characterized by a central aponeurosis and should be evaluated and compared for size and echogenicity (Fig. 40a). The teres minor muscle is smaller than the infraspinatus and has a rounded cross-section while the infraspinatus is more oval in appearance. In some cases, these muscles are fused together and exhibit a common elongated central aponeurosis (Fig. 40b). Systematic scanning over these muscles may help to rule out echotextural changes related to tendon tears and nerve pathology. In fact, certain shoulder diseases, such as suprascapular neuropathy, can be recognized on the basis of muscle atrophy detected in these scans. After scanning the muscles, the transducer is swept toward the greater tuberosity on sagittal planes and the two tendons can be appreciated as individual hyperechoic structures arising from the respective muscles, the larger and more cranial being the infraspinatus, and the smaller and caudal, the teres minor (Fig. 41). Often, the profile of the posterior aspect of the greater tuberosity can demonstrate two separated facets at the insertion of these tendons (Fig. 41).
On long-axis scans, the infraspinatus tendon appears as a thick beak-shaped structure coursing deep to the deltoid and superficial to the posterior aspect of the humeral head, the posterior labrum and the bony glenoid (Fig. 42a). The teres minor tendon, the smallest tendon of the cuff, has a more oblique course than that of the infraspinatus and arises eccentrically with respect to the muscle (Fig. 42b). Therefore, the probe should be oriented obliquely to image it in its long axis. Each tendon must be examined separately. Care should be taken to evaluate the infraspinatus tendon up to its insertion. In fact, at least when the arm is kept in internal rotation, the tendon may project over the lateral rather than the posterior aspect of the shoulder. Dynamic scanning during passive internal and external rotation with the arm adducted may help the examiner to assess the insertion level and the integrity of both tendons.
26. ROTATOR CUFF INTERVAL
Before entering the bicipital groove, the biceps tendon passes across the “rotator cuff interval”, a free space delimited by the subscapularis and supraspinatus tendons. In this space, the biceps tendon is retained in its proper location by the coracohumeral ligament, which courses above it as a roof, and by the superior glenohumeral ligament (Fig. 43a, 44a). At US, the coracohumeral ligament can be appreciated as a thick homogeneous echogenic band of tissue, tightened between the subscapularis and the supraspinatus and located just over the biceps (Fig. 43b). Often, a thin hypoechoic layer is seen arising from the deep edge of the supraspinatus tendon and intervening between the ligament and the biceps tendon, a finding that may represent the joint capsule (Fig. 43b). The coracohumeral ligament is best depicted on short-axis scans while the arm is kept in posterior flexion, because this position causes maximal opening of the rotator cuff interval, stretches the biceps against the humeral cartilage and tightens the ligament. Careful scanning technique is needed to adjust the orientation of the transducer to avoid anisotropy: typically, the biceps is much more anisotropic than the coraco- humeral ligament.
Occasionally, the interval structures may form a large gap on either side of the biceps which should not be misinterpreted as a tear. Less than 1 cm distally, the anterior (medial) part of the coracohumeral ligament joins the superior glenohumeral ligament to form the “reflection pulley,” which inserts into the lesser tuberosity (Fig. 44a,b). At this level, the biceps is elevated relative to the bone and assumes an oblique orientation due to the pulley which surrounds it with a curvilinear shape. It is conceivable that the deep medial fibers of the pulley that infiltrate the undersurface of the biceps on this plane may reflect contributions from the superior glenohumeral ligament. Because the process of subluxation of the tendon tends to initiate at this location, the relationships among the biceps, the cranial segment of the groove and the superior portion of the subscapularis tendon must be carefully evaluated. Care should be taken not to confuse the double image produced by the pulley structures for a longitudinal split of the biceps. More distally, in the proximal bicipital groove, the biceps lies in close contact with the subscapularis and is here stabilized by fibrous bands arising from it (Fig. 44c,d). These fibers form the transverse humeral ligament, which can be depicted as a thin echogenic layer overlying the sulcus.
27. SHOULDER BEYOND THE CUFF
Once the systematic evaluation of rotator cuff tendons is completed, the US examination should be focused to assess other structures around the shoulder joint, including the glenohumeral joint space, the subacromial subdeltoid bursa and the acromioclavicular joint. In selected cases, additional scans can be obtained to image the fibrocartilaginous labrum (to rule out paralabral pathology), the morphology of the acromion (to exclude an os acromialis) and the axilla (for assessment of joint effusions and disorders in the axilla, including intra-articular loose bodies).
28. GLENOHUMERAL SYNOVIAL SPACE
As stated before, the glenohumeral joint capsule extends from the margins of the labrum and glenoid rim to the anatomic neck of the humerus. The capsule is lax and redundant to allow a wide range of movement of the arm. The large axillary recess arises, for instance, from a deep folding of the capsule that permits a complete elevation of the arm without stretching the inferior capsule. The same is true for the anterior and posterior recesses, which allow maximal external and internal rotation of the arm. In normal states, the small amount of synovial fluid contained in the joint space cannot be recognized with US. On the other hand, US has high sensitivity for appreciating even a minimal amount of pathologic fluid inside the main synovial recesses (i.e., the dependent axillary pouch, the posterior and anterior recesses and the sheath of the long head of the biceps tendon).
Although a caudal approach through the axilla has been described to evaluate the axillary pouch, posterior transverse scans are usually preferred for better accessibility. Once the teres minor tendon is localized, the transducer is shifted more caudally to investigate the space intervening between the humeral metaphysis and the inferior neck of the scapula, where the axillary pouch lies. If distended by considerable effusion, this pouch is visible as a fluid-filled area.
The posterior recess is best examined on transverse scans by placing the transducer over the infraspinatus tendon (Fig. 45). An effusion filling the posterior recess appears as a hypoanechoic crescent surrounding the tip of the posterior labrum. In larger effusions, the infraspinatus tendon can be seen displaced posteriorly by the fluid contained in the recess. In doubtful cases, the examiner can induce changes in the shape of the recess by passively moving the patient’s arm externally and internally, which results in reduced/increased tension of the posterior capsule and the overlying infraspinatus. Due to the lack of intervening vessels and easy accessibility, procedures of needle aspiration or injection in the posterior recess can be safely performed under US guidance while the patient is seated or prone (Fessell et al. 2000; Zwar et al. 2004). This recess can be selected for a safe US-guided needle placement for shoulder arthrography (Cicak et al. 1992; Valls and Melloni 1997).
US evaluation of the anterior recess is more complex due to its deep location, and often requires a small curved-array transducer, lower frequencies and a careful scanning technique. When fluid is present in the anterior recess, it can be appreciated on transverse scans as a hypoechoic halo surrounding the anterior labrum. Similarly, the subscapularis recess (also known as the subscapularis bursa) is difficult to evaluate reliably with US because of its small size and problems of access related to its location deep to the coracoid tip. This is a small saddle-bag-shaped recess located between the anterior neck of the scapula and the subscapularis tendon which may extend above the tendon to overlie its anterior aspect. Using transverse or sagittal scans, the main landmark to find is the coracoid: an effusion in the subscapularis recess can be demonstrated as a small hypoanechoic area located just caudally and posteriorly to the bone and adherent to the subscapularis tendon (Fig. 46). The subscapularis recess should not be confused with the larger subcoracoid bursa that extends more caudally and does not communicate with the glenohumeral joint as it is an extension of the subacromial subdeltoid bursa (Figs. 46b, 47) (Grainger et al. 2000). The subcoracoid bursa lies deep to the conjoined tendon of the short head of the biceps and the coracobrachialis, in a more medial location relative to the subscapularis tendon and the coracoid, and may contain abundant effusion in cases of anterior rotator cuff tears (Fig. 47c). It is best examined while keeping the patient’s arm adducted by scanning just inferiorly and medially to the coracoid. The distinction between the subscapularis recess and the subcoracoid bursa is relevant because the causes of a subscapularis recess effusion may be different from the causes of a subcoracoid bursa effusion (which is most often associated with rotator cuff tears, including tears of the rotator cuff interval) (Grainger et al. 2000).
Finally, the synovial sheath of the long head of the biceps tendon is formed by an extrusion of the articular synovial membrane. As the sheath is merely an extension of the joint cavity, intra-articular effusion can lead to fluid in the sheath. Fluid secondary to an isolated biceps tendinitis is rare.
29. SUBACROMIAL SUBDELTOID BURSA
The subacromial subdeltoid bursa appears as a 2 mm thick complex comprised of an inner layer of hypoechoic fluid between two layers of hyperechoic peribursal fat (van Holsbeeck and Strouse 1993). In normal states, the synovial membrane of the bursa cannot be depicted with US. Hypoechoic thickening of the bursal walls can be observed in a variety of shoulder disorders, among which anterosuperior impingement is the most important (Fig. 48a). In these instances, the bursa assumes a pseudosolid appearance and may be difficult to delineate from the underlying supraspinatus tendon, somewhat mimicking a degenerative tendinopathy. A notch sign in the upper profile of the bursa at the point where it passes deep to the coracoacromial ligament may help this differentiation (Fig. 48b,c). Because intrabursal fluid can migrate depending on gravity and arm positioning, the various bursal portions should be systematically assessed. Care should also be taken not to apply excessive pressure with the probe over the bursa, so as not to overlook small effusions.
When the patient is standing or seated, fluid tends to accumulate in the most dependent portions of the bursa and, more commonly, along the lateral edge of the greater tuberosity, producing a typical “teardrop” sign (Fig. 49a) (van Holsbeeck and Strouse 1993). When effusion is contemporarily present in the glenohumeral joint and the bursa, anterior transverse planes are the best suited to demonstrate fluid in both cavities. Using these planes, the intra-articular fluid can be appreciated as a hypoechoic halo surrounding the long head of the biceps tendon, while the bursal fluid appears as a crescent-shaped collection located just deep to the anterior deltoid muscle (Fig. 49b). The two effusions are separated by a thin hyperechoic structure which represents the bordering walls of the biceps tendon sheath and the bursa. More abundant collections tend to fill the bursal portion located posterior to the infraspinatus tendon. In these cases, detection of the infraspinatus may help to distinguish superficial bursal effusions from deep joint effusions (Fig. 49c). Demonstration of an effusion in both synovial spaces is, for the most, an indicator of full-thickness tear of the rotator cuff. Dynamic scanning performed with the probe placed over one cavity – either the bursa or a joint recess – while compressing the other with the hand can reveal communication between the two compartments as a result of rotator cuff tear.
30. ACROMIOCLAVICULAR JOINT AND OS ACROMIALE
To examine the acromioclavicular joint, the transducer is placed over the top of the shoulder in a coronal plane. The width of the joint is measured and compared with that of the contralateral side. The evaluation of the acromioclavicular joint has to be included as part of the routine study of the shoulder, because its lesions can mimic rotator cuff disease. In fact, this joint is intimately related to the supraspinatus tendon, which runs directly underneath the joint. In spite of a similar echogenicity, the superior acromioclavicular ligament can be distinguished from the underlying joint cavity using high-frequency probes and dynamic scanning (Fig. 50a,b). This ligament forms an external inextensible band joining the mobile ends of the clavicle and the acromion, an appearance quite different from the content of the acromioclavicular joint which is limp and can change shape and width with shoulder movements. In young healthy subjects, the internal fibrocartilaginous disk can seldom be appreciated as a slightly hyperechoic structure, an appearance somewhat similar to the knee menisci or the glenoid labrum (Fig. 50c,d). The coracoclavicular ligaments are difficult to be detected with US due to the acoustic shadowing of the overlying clavicle.
An os acromiale can occasionally be recognized as an incidental finding while scanning the acromioclavicular joint with US (Fig. 51). This accessory bone derives from the nonfused epiphysis of the anterior part of the acromion, has an overall frequency of approximately 8% of general population and is bilateral in one third of cases (Sammarco 2000). The os acromiale is triangular in shape and has a variable size (mean 22 mm). It can articulate with the acromion and the clavicle with a distinct articulation, a fibrocartilaginous union or a nearly complete union (Sammarco 2000). The deltoid muscle inserts on its anterolateral edge. The os acromiale is a potential source of anterosuperior impingement, either as a fragment mobilized by deltoid pulls or from osteophyte lipping. US is a sensitive means to identify or confirm this anomalous bone (Boehmet al. 2003). The diagnosis is based on detection of a well-defined cortical discontinuity on the superior aspect of the acromion, often mimicking a double acromioclavicular joint (Figs. 51, 52). At US, an os acromiale may exhibit flat bony margins (type I), marginal osteophytes (type II) or inverted bony margins (type III) (Boehm et al. 2003). A confident identification of the os acrominale from the adjacent acromioclavicular joint can easily be accomplished by shifting and rotating the probe over the acromion in order to identify two articulations instead of one. In case of an associated rotator cuff tear, the treatment is varied. In patients with impingement symptoms, a small mobile os acromiale can be resected, a large stable os acromiale treated by acromioplasty and a large unstable os acromiale by fusion to the acromion. The postoperative outcome is good.
31. GLENOID LABRUM
The fibrocartilaginous labrum can be demonstrated at US as a triangular homogeneously hyperechoic structure capping the bony rim of the glenoid (Schydlowsky et al. 1998a). The different portions of the labrum lie at various depths, the inferior being the most superficial and the anterior the deepest. Consequently, an adequate US scanning technique should first include a dynamic adjustment of the focal zone, based on the characteristics of each individual quadrant to be examined. The anterior labrum is best scanned with curved-array transducers and low frequencies (down to 5 MHz) using an anterior transverse approach (Fig. 53a). The patient’s arm is maintained adducted or abducted at 90° with the elbow flexed or with an axillary transverse approach placing the arm in the same position as before (Hammar et al. 2001). While evaluating the anteroinferior quadrant of the glenoid, difficulties may arise in patients who are obese or unable to put their arm in the proper position because of pain or apprehension. Contrary to the anterior labrum, the posterior labrum is more superficial in position and can be easily imaged at US using transverse planes while placing the patient‘s hand on the opposite shoulder (Fig. 53b). It appears as a triangular structure with the base directed medially and the apex pointing laterally. Changes in the shape of the labrum can be observed in different rotations of the arm. A more pointed appearance is noted when traction is applied on it by the capsule (during internal rotation for the posterior labrum). The superior labrum is very difficult to visualize due to problems of access related to the acoustic shadowing of the acromion. A tentative approach can be made in slender subjects by placing the probe just behind the head of the clavicle while abducting the arm to better differentiate the static glenoid from the moving humeral head (Fig. 53c). Even with appropriate technique, high-end equipment and skilled hands, US is unable to demonstrate superior labrum abnormalities, such as anterior to posterior (SLAP) lesions. MR or CT arthrography are the techniques of choice to depict this condition. Wherever its location, the labrum is demonstrated more easily when surrounded by joint effusion. A thin (<2 mm) hypoechoic zone at the base of the labrum – an image somewhat equivalent to the sublabral transitional band of intermediate signal intensity visible at MR imaging (Loredo et al. 1995) – is a normal finding related to a band of cartilage and should not be confused with a tear.
32. NERVES AROUND THE SHOULDER
Using high-resolution transducers, the suprascapular nerve may occasionally be visualized with US in slender young subjects. Short-axis planes are the most useful to reveal it. In the supraspinous fossa, the nerve can be visualized as a small rounded hypoechoic structure lying between the scapla and the supraspinatus muscle (Fig. 54a). In the spinoglenoid fossa, the nerve is identified in a shallow depression of the scapula, the splinoglenoid notch, filled with hyperechoic fat (Fig. 54b). At both sites, the suprascapular nerve appears as a thin hypoechoic structure lying over the bony floor (Bouffard et al. 2000; Martinoli et al. 2003; Martinoli et al. 2004). Doppler imaging may help to identify the nerve by showing color flow signals from the adjacent suprascapular artery (Fig. 54c) (Bouffard et al. 2000).
US detection of the axillary nerve is a challenging task due to its small size and deep course. Doppler imaging is an essential step in the examination as it aids the identification of the nerve position by demonstrating flow signals from the adjacent posterior circumflex artery (Martinoli et al. 2004). With the arm elevated, the axillary neurovascular bundle is first imaged in the posterior axillary fold as it passes between the teres major and the triceps muscle (Fig. 55a,b). Then, both artery and nerve can be followed across the posterior shoulder with the patient seated and keeping the arm in neutral position (Fig. 55c,d). In certain instances, some orthopaedic surgeons may ask the examiner to mark the lateral skin at the level of the axillary nerve to avoid inadvertent nerve lesion during skin incision for repair of rotator cuff tears. If the nerve is not clearly detectable, the skin can be marked at the level of the circumflex artery.
33. BRACHIAL PLEXUS AND OTHER NERVES OF THE NECK
US has recently proved to be an effective means to depict normal brachial plexus anatomy at several levels, including the paravertebral, interscalenic, supraclavicular, infraclavicular and axillary regions (Yang et al. 1998; Sheppard et al. 1998; Apan et al. 2001; Retzl et al. 2001; Martinoli et al. 2002; Demondion et al. 2003). The US examination of brachial plexus nerves is based on detection of some anatomic landmarks in the neck, including bones (roots), muscles (trunks) and vessels (divisions and cords). After exiting the neural foramina, the roots pass between two prominent apophyses of the transverse processes of the cervical vertebrae – the anterior and posterior tubercles – in close relationship with the vertebral artery and vein (Fig. 56). Each root emerges as an individual (monofascicular) hypoechoic structure, an appearance quite different from that of nerves in the extremities, which are composed of clusters of hypoechoic fascicles. Coronal planes are able to depict the nerve roots in the paravertebral area using the same longitudinal scan for the study of the vertebral artery and vein as a landmark (Fig. 57a,b). In these planes, the picture of the vertebral vessels is obscured at regular intervals by the acoustic shadowing from the anterior tubercles of the transverse processes. Moving the transducer slightly posteriorly, the vessels disappear and the roots appear as elongated hypoechoic images exiting the neural foramina, each of which is located over the costotransverse bar of the vertebra (Fig. 57c,d). Nevertheless, transverse planes are ideal to depict the relationship of the roots with the transverse processes at any given level. Based on the peculiar appearance of the transverse process of C7, in which the posterior tubercle is absent, US is able to assess the level of the nerve roots (Martinoli et al. 2002).
For this purpose, scanning first reveals the C7 level and then moves either up or down on axial planes. The C7 root is detected in the same plane as the C7 vertebra is bordered by the posterior tubercle only (Fig. 58a–d). Shifting the transducer upward, the C6 vertebra is recognized due to the presence of prominent anterior and posterior tubercles: the C6 root appears as a hypoechoic structure held in between them (Fig. 58e–h). The transverse processes of C5 have basically the same shape as those of C6 and can be identified as successive steps cranial to the C6 level by taking into account the number of transverse processes encountered while sweeping the transducer cranially from C7. From the anatomic point of view, the higher the level, the smaller the space between the tubercles. Then, moving the transducer downward from C7, the lateral aspect of the T1 vertebra is flat without any tubercle; at this level, the C8 root can be appreciated near the foraminal outlet. More caudally, identification of the T1 root is not always feasible due to problems of access related to the too deep location of the intervertebral foramen between the T1 and T2 vertebrae. The T1 root shows a curving course below the first rib, and can be examined by using an axial oblique plane of approximately 45°. In addition to determining whether a lesion is preganglionic rather than postganglionic, or infraclavicular rather than supraclavicular, attributing a given level of nerve involvement is an important component of the imaging report since the list of possible clinical syndromes in a patient with brachial plexopathy is different according to the pattern of the injured roots and trunks (e.g., upper partial: C5, C6 [C7]; lower partial: C8, T1; complete: C5–T1) (Narakas 1993). Sweeping the transducer down to the interscalene region on short-axis planes, the nerve trunks are visualized as they pass in between the scalenus anterior and scalenus medius muscles (Yang et al. 1998).
Visualization of the trunks in the interscalene space depends on the amount of fat between these muscles, and a careful scanning technique is needed because nerve fascicles can easily be confused with muscle fascicles. The upper and middle trunks are more readily identified with US (Fig. 59). They are arranged in series from superficial to deep and receive contributions from the C5 and C6 levels (upper trunk) and C7 level (middle trunk). One has to consider that the progression of the roots is anatomically constant down to the interscalene region, where they unite to form the three trunks: upper (C5 and C6), middle (C7) and lower (C8 and T1). Therefore, the ability of US to recognize the root levels in the paravertebral area also reflects on a confident identification of the trunks by simply following the nerves from where these latter arise. In the supraclavicular region, the nerves are visualized as a cluster of hypoechoic rounded images that represent the divisions (Yang et al. 1998). The divisions follow, for the most part, the posterior aspect of the subclavian artery, just over the straight hyperechoic appearance of the first rib and apical pleura (Fig. 60) (Sheppard et al. 1998; Yang et al. 1998).
Crossing down the clavicle, in the infraclavicular area, the nerve cords continue their course along the axillary artery and behind the pectoralis minor muscle (Fig. 61). An individual identification of divisions and cords of the brachial plexus distal to the interscalene region is less feasible on US because these branches anastomose with each other in various combinations. Overall, we believe that the main advantage of US in brachial plexus imaging is its ability to follow up continuously each individual component of the plexus through the lateral neck by shifting the probe back and forth in short-axis plane. Similar to other sites in the body, anatomic variants of brachial plexus nerves and surrounding tissues possibly predisposing to compressive neuropathy can be demonstrated with US, including cervical rib, hypertrophied transverse process of C7 and variations in the scalene muscles (Fig. 62). Detection of a discrete arterial branch arising from the subclavian artery and encroaching on the brachial plexus nerves in the supraclavicular region is a normal finding. This blood vessel is the dorsal scapular artery (Fig. 63).
In addition to brachial plexus nerves, US is also able to image other nerves running in the lateral cervical region, including the vagus nerve (Giovagnorio and Martinoli 2001), the recurrent laryngeal nerve (Solbiati et al. 1985) and the spinal accessory nerve (Bodner et al. 2002). The vagus nerve (CN X), the main parasympathetic nerve to the organs of the body, leaves the skull through the jugular foramen and passes inferiorly in the posterior part of the carotid sheath, in the angle between and posterior to the internal jugular vein and the carotid artery (Fig. 64a). In this location, it can be appreciated with US as a thin (<2 mm in cross-sectional diameter) vertically oriented cord-like structure containing three or four very small fascicles (Fig. 64b) (Giovagnorio et al. 2001). Its secondary branch, the recurrent laryngeal nerve, reaches the posteromedial aspect of the lower pole of the thyroid after looping the subclavian artery (on the right) and the aortic arch (on the left). Then, it proceeds cranially in the tracheoesophageal groove to supply the intrinsic muscle of the larynx (Fig. 64a). Using a high-resolution transducers, small segments of this nerve may be recognized in a few patients with lean necks, deep to the thyroid (Fig. 64c) (Solbiati et al. 1985). The spinal accessory nerve (CN XI) is a motor nerve consisting of spinal and cranial roots which leaves the skull base through the jugular foramen and traverses the lateral cervical triangle, a space bordered by the sternocleidomastoideus muscle anteriorly, the trapezius posteriorly and the clavicle inferiorly, to supply the trapezius muscle. Its palsy causes limited shoulder elevation and retraction, the so-called drooping shoulder. The spinal accessory nerve passes underneath the sternocleidomastoideus muscle and, in the lateral cervical triangle, it becomes superficial, coursing immediately deep to the fascia and adjacent to superficial lymph nodes. At this site, it may be injured during lymph node biopsy or procedures of carotid surgery. US is able to depict the normal nerve as a small (1 mm in size) linear structure traversing the lateral cervical triangle and can reveal its traumatic damage in the appropriate clinical setting (Bodner et al. 2002).
34. SHOULDER PATHOLOGY
Knowledge of the complex pathophysiology and biomechanics underlying rotator cuff impingement and shoulder instability is an essential prerequisite for a correctly executed US examination and interpretation of the imaging findings.
35. PATHOPHYSIOLOGIC OVERVIEW – IMPINGEMENT AND ROTATOR CUFF DISEASE
Rotator cuff disease is the commonest cause of shoulder pain and dysfunction in adults. It derives from a wide range of pathologic conditions, including acute and chronic trauma, arthritis and shoulder instability (Laredo and Bard 1996). Most tears, however, occur in patients who lack a definite clinical history of trauma or systemic disease. In these cases, rotator cuff disease is believed to be secondary to local causes. From the pathophysiologic point of view, tendon ischemia was the first factor hypothesized to play a causative role in the pathogenesis of rotator cuff disease (Codman, 1934). This theory was supported by the histologic evidence of a relatively hypovascular area in the supraspinatus tendon, the so-called “critical zone”, which is located approximately 1 cm medial to the tendon attachment on the greater tuberosity (Fig. 65a). Microangiographic studies demonstrated that this zone is located at the limit between the tendon vasculature deriving from the myotendinous junction and that arising from the teno-osseous junction of the supraspinatus (Chansky and Iannotti 1991). The critical zone is, therefore, prone to ischemia and more susceptible to develop degenerative changes. More recently, tendon damage secondary to chronic contact of the supraspinatus tendon with the undersurface of the coracoacromial arch, the so-called “impingement syndrome”, was proposed as the main causative factor leading to rotator cuff tears (Neer, 1972). The clinical success of combined procedures of rotator cuff repair and anterior acromioplasty led to the widespread acceptance of this hypothesis. A consensus is now emerging that the causes of rotator cuff disease are manifold, including various combinations of extrinsic factors, such as morphology of the coracoacromial arch, tensile overload, repetitive overuse and kinematic abnormalities, and intrinsic factors, such as altered tendon vascular supply (Soslowsky et al. 1997).
The degenerative process in the tendon substance may progress toward partial and complete tendon tears. As demonstrated on autopsy studies, rotator cuff pathology becomes more prevalent with increasing age. A disease prevalence of approximately 10% at 30 years, 50% at 60–70 years and 80% at 80 years has been reported and it is well known that asymptomatic rotator cuff lesions are not so uncommon, particularly in elderly subjects who do not realize the shoulder failure given their reduced demands (Leach and Schepsis 1983; Yamaguchi et al. 2001). Depending on the location of the contact, three main types of shoulder impingement have been described: anterosuperior (the most common), anteromedial and posterosuperior. As described above, the supraspinatus tendon lies in the subacromial space between the humeral head and the cover of the coracoacromial arch, which is formed (from posterior to anterior) by the anterior portion of the acromion and the acromioclavicular joint, the coracoacromial ligament and tip of the coracoid. In normal states, the tendon glides smoothly in the subacromial space during abduction and anterior elevation of the arm. The subacromial subdeltoid bursa, which is interposed between it and the structures of the coracoacromial arch, reduces the local attrition during shoulder movements. In anterosuperior impingement, the conflict between the bursal side of the tendon and the undersurface of the arch occurs during shoulder abduction and elevation of the arm (Fig. 65b).
From the pathophysiologic point of view, the anterosuperior impingement syndrome may be secondary to several anatomic and dynamic factors. Anatomic factors mainly refer to the incongruence between the size and shape of the subacromial space and the structures contained within it. Any lesion leading to a decrease in the cross-sectional area of the subacromial space or an increase in the volume of the structures housed within it makes tendon impingement more likely. Congenital variants in the acromial slope and shape or occurrence of an os acromiale can be predisposing factors for the onset of an anterosuperior impingement syndrome (Mudge et al. 1984; Bigliani et al. 1991). According to the classification system of Bigliani and coworkers (Bigliani et al. 1986), the shape of the acromion can be classified into three main types as it appears based on “outlet view” radiographs: the type I acromion (18.6%) has a flat undersurface (Fig. 66a,d); the type II (42%) has a curved under-surface that parallels the convexity of the humeral head (Fig. 66b,e); and the type III (38.6%) has an anteriorly projecting hook, resulting from either a spur at the site of attachment of the coracoacromial ligament or a congenital abnormal configuration (Fig. 66c,f).
Although some interobserver variability in such assessment has been described, both plain films (Lamy’s view, outlet view) and MR imaging (sagittal oblique planes) are able to assess the acromial type (Mayerhoefer et al. 2005). The type III acromion causes narrowing of the subacromial space and seems to be related to a higher frequency of tendon impingement (Bigliani et al. 1986). A fourth type of acromion shape (type IV) with a convex inferior surface has also been described (Vanarthos and Monu 1995). The importance of the slope of the acromion in the pathogenesis of shoulder impingement syndrome has been reported (Edelson and Taitz, 1992). In particular, it is believed that lateral or anterior downsloping of the acromion relative to the clavicle may contribute to narrowing of the supraspinatus outlet. The os acromiale derives from a failed fusion of the anterior ossification center of the acromion with the acromial body. In most cases, a strong fibrous bridge firmly joins the ossicle to the acromion preventing its movement. In some cases, however, the tip of the os acromiale may be pulled inferiorly during contraction of the deltoid, which attaches over it, causing impingement on the underlying supraspinatus tendon (Mudge et al. 1984). In addition to congenital causes, a variety of acquired disorders may result in a restricted subacromial space. Among them, osteoarthritis of the acromioclavicular joint with osteophytes extending inferiorly can cause scraping and damage of the bursal side of the supraspinatus tendon. These osteophytes are found in approximately half of patients with supraspinatus tendon tears compared with 14% of patients with no tear (Peterson and Genz 1983).
Spurs on the acromial attachment of the coracoacromial ligament are also considered signs of shoulder impingement. A poorly consolidated fracture of the greater tuberosity can lead to an abnormal upward displacement of the bony fragment and subsequent narrowing of the subacromial space. Anterosuperior impingement may occur in the absence of any evidence of anatomic abnormalities that may explain it. Unlike impingement syndrome related to alterations in the coracoacromial arch, these cases occur in athletes involved in sporting activities which require overhead motion of the arm (e.g., volleyball, throwing) and are somewhat related to glenohumeral joint instability (Jobe et al. 1989). During anterior instability, repetitive overload leads to some degree of anterior and superior translation of the humeral head with secondary restriction of the subacromial space and local attrition of the supraspinatus tendon against the anterior acromion and the coracoacromial ligament when the arm is abducted and externally rotated. In general, these patients have less advanced rotator cuff disease (i.e., tendinosis, partial-thickness tears) and benefit from therapy directed to the underlying instability, including strengthening of the rotator cuff. The same often occurs in slender young females who have weak scapular rotators. Once the impingement syndrome is established, chronic mechanical microtrauma induce progressive tendon degeneration and tearing as well as changes in the subacromial subdeltoid bursa. In the anterior impingement syndrome, three stages of increasing tendon damage have been described (Neer, 1972). Stage I is mainly appreciated in young adults in whom impingement leads to subacromial bursitis and absent or minimal tendon changes: this stage is usually reversible. Stage II is characterized by progressive thickening and an irregular appearance of the supraspinatus tendon and the subacromial subdeltoid bursa as a result of the degenerative process: surgery is usually considered (i.e., removal of the thickened bursa and release of the coracoacromial ligament) if conservative management fails. Stage III indicates progression of tendon damage to partial- and full-thickness tears: acromioplasty and cuff repair are often required.
Far less common than anterosuperior impingement, anteromedial impingement (subcoracoid impingement) derives from encroachment of the superior portion of the subscapularis tendon and the long head of the biceps tendon against the tip of the coracoid during maximal internal rotation and forward flexion of the arm (Gerber et al. 1985). Laxity of the anterior capsule and ligaments and congenital anomalies of the coracoid process and the lesser tuberosity seem to be implicated as predisposing factors. Finally, a third type of shoulder impingement, the posterosuperior impingement (posterosubglenoid impingement) occurs as a result of pinching of the rotator cuff at the junction of the supraspinatus and infraspinatus tendons, between the greater tuberosity and the posterosuperior aspect of the glenoid rim, during maximal abduction and external rotation of the arm (Walch et al. 1991). This kind of impingement causes degenerative changes and partial tears of the posterior supraspinatus tendon, typically involving its undersurface.
36. INSTABILITY
Due to its peculiar anatomy, the shoulder joint is inherently unstable. Several shoulder structures may be involved in the pathogenesis of instability, including bony surfaces, joint capsule, ligaments and the fibrocartilaginous labrum (static restraints) and the rotator cuff tendons (dynamic constraints). In addition to anatomic factors, a combination of other predisposing factors related to both developmental and acquired diseases, often combined with one another, can be responsible for glenohumeral joint instability. The degree of glenohumeral joint instability ranges from subluxation to dislocation and indicates that the humeral head slips out of its socket during movements. In this setting, the clinician must realize whether a subluxation or dislocation has occurred and has to assess the state of the anatomic structures responsible for joint stability to establish a proper treatment. Based on its direction, shoulder instability can be defined as anterior, posterior or inferior to the glenoid, or multidirectional (Zarins and Rowe, 1984). Anterior instability accounts for approximately 96–98% of all shoulder dislocations. Although often encountered in subjects with a loose anterior capsule and ligaments, anterior instability usually follows an acute injury that weakens the para-articular structures responsible for joint stability. The mechanism associated with anterior instability is abduction, extension and external rotation. Recurrent subluxations or dislocations may occur even after trivial trauma. The diagnosis of anterior instability is based on physical examination and plain films (Fig. 67).
In most cases, anteroposterior views are sufficient to detect the anterior dislocation of the humeral head and no additional projections are needed. Unlike dislocation, a subluxation of the humeral head may be a subtle transient event that may be difficult to recognize. Posterior instability may be secondary to shoulder trauma and, when bilateral, is frequently observed in seizures as a result of the stronger convulsive contraction of the posterior muscles (infraspinatus and teres minor) relative to that of the subscapularis. The diagnosis is often missed because this condition is uncommon (4% of all shoulder dislocations) and may present with subtle clinical and radiographic findings. Standard radiographs, including anteroposterior and lateral views, may often be inadequate for detection of posterior dislocation and additional projections, such as the axillary view, may be required for this purpose. However, these projections are not easily obtained in the acutely injured patient. Approximately 50% of posterior shoulder dislocations go unrecognized and some authors have reported an average interval from the injury to the diagnosis of 1 year, particlarly in the case of a “locked” posterior dislocation which occurs when the posterior glenoid causes an impaction fracture on the humeral head preventing its repositioning (Hawkins et al. 1987). If not recognized early, posterior dislocation can lead to chronic joint stiffness, pain and reduced range of motion. Chronic longstanding dislocations are most often found in the elderly. In these cases, the prognosis is not good and the decision may often be to leave the shoulder dislocated and attempt to regain as much motion as possible with physical therapy or the insertion of a shoulder prosthesis.
37. ROTATOR CUFF PATHOLOGY
Initially and for many years, investigators reported contradictory results, either enthusiastic or poor, in the ability of US to diagnose rotator cuff pathology (Mayer 1985; Mack et al. 1985; Middleton et al. 1985, 1986b; Hodler et al. 1988, 1991; Burk et al. 1989; Brandt et al. 1989; Soble et al. 1989; Hall 1989; Ahovuo et al. 1989a,b; Miller et al. 1989; Drakeford et al. 1990; Vick and Bell 1990; Misamore and Woodward, 1991; Nelson et al. 1991; Wulker et al. 1991; Wiener and Seitz, 1993; Guckel and Nidecker 1997). In many cases, the first studies made use of US criteria that nowadays have either been refined or are no longer accepted, examinations were performed with a scanning technique that has since been modified to improve visualization of the cuff, and old low-resolution equipments were employed. In the context of technological improvements, higher resolution capabilities and new criteria to diagnose rotator cuff tears, the current US technology is now increasingly able to reliably provide good accuracy in the assessment of rotator cuff tears (Teefey et al. 1999, 2004; Bouffard et al. 2000; Leotta et al. 2000; Roberts et al. 2001; Moosikasuwan et al. 2005). In addition, this technique allows the assessment of most of the stages of rotator cuff disease and the classification of rotator cuff tears based on the extent of tendon involvement, size and location of the tear. As already described, the supraspinatus is the rotator cuff tendon most commonly involved by either partial- or full-thickness tears as a result of subacromial impingement. In a large series of surgically proven rotator cuff ruptures, isolated tears of the supraspinatus tendon were found in 62% of cases, accounting for 18% of partial-thickness and 44% of full-thickness tears (Walch et al. 1999). Early degenerative changes and tears of the supraspinatus are typically observed in the anterior half of the tendon, just behind the long head of the biceps tendon (Fig. 68a). The smallest forms of rotator cuff tears are partial-thickness tears, which can in turn be located at either the articular (12%) or the bursal (5%) surface of the involved tendon. Intrasubstance tears occur more rarely (1%). If untreated, partial-thickness tears can enlarge to become full-thickness tears (Fig. 68b). Overall, one should consider that partial-thickness tears are more common than full-thickness tears and those involving the articular side of the rotator cuff are slightly more common than those of the bursal side. Beginning in the anterior third of the supraspinatus, most tears then propagate in a posterior direction to involve the middle and posterior tendon, eventually in some cases causing complete supraspinatus rupture (Fig. 68c). In more advanced disease, other rotator cuff tendons may additionally rupture as a result of excessive tensile forces due to the altered shoulder biomechanics related to the supraspinatus tear (Fig. 68d). The involvement of other tendons together with the supraspinatus has been reported in an additional 30% of patients (Walch et al. 1999). In these combined tears, the posterior extension of a supraspinatus tear to the infraspinatus occurs in approximately 20% of cases, whereas the anterior involvement of the subscapularis from a supraspinatus tendon tear is less common and accounts for approximately 10% of cases (Walch et al. 1999). As the lesion expands anteriorly into the subscapularis, disruption of the stabilizers of the biceps tendon (i.e., rotator cuff interval structures) occurs. Isolated rupture of the subscapularis tendon occurs in another 8% of cases: such ruptures are more common in sport traumas due to forceful stretching on an abducted and externally rotated arm. On the other hand, isolated rupture of the infraspinatus is rare and occurs in the spectrum of posterior posterosuperior subglenoid impingement.
The classification of rotator cuff tears is somewhat confusing because different terms have been inappropriately used with the same meaning. In an effort to better understand the type of tendon tear and to standardize the observations of various examiners, the rotator cuff should be thought of in a three-dimensional view. A tear must be considered incomplete when it involves only a part of the tendon width on short-axis planes (Fig. 68a,b). Incomplete tears may be in turn subdivided into partial-thickness (Fig. 68a) or full-thickness (Fig. 68b) types depending on whether they result in an abnormal communication of the glenohumeral joint and the subacromial subdeltoid bursa. According to their depth, partial-thickness tears may involve the bursal side, the articular side or the midsubstance (intrasubstance) of the tendon (Ellman 1990). When a full-thickness tear involves the full width of a tendon, it becomes a complete tear (Fig. 68c). Then, it can become a massive tear as it spreads to involve more than one tendon with a total width of the affected cuff more than 3 cm (Fig. 68d).
38. CUFF TENDINOPATHY
Rotator cuff tendinopathy is thought to be an early result of anterosuperior impingement (Neer stage II) and, at first, affects the supraspinatus tendon along with the subacromial bursa. The US appearance of tendinopathy includes swelling of the affected tendon and abnormal tendon echotexture with a heterogeneous hypoechoic appearance (Fig. 69).
Tendon swelling can be appreciated with US as either a focal or – most often – a diffuse increase in tendon thickness (Farin et al. 1990). Because long- axis planes give a panoramic depiction of the tendon as a whole, they are the most adequate to recognize its thickening. Bilateral examination may occasionally be used to improve diagnostic confidence when only small changes in the tendon size occur. In these cases, care should be taken to evaluate the same level on both sides because the supraspinatus tapers toward the greater tuberosity and from anterior to posterior. Dynamic scanning obtained by placing the probe in the coronal plane over the lateral margin of the acromion while the patient abducts their arm in internal rotation may demonstrate difficult gliding of the thickened tendon and subacromial bursa underneath the acromion (Read and Perko 1998). Some thresholds in tendon size between the unaffected side and the affected supraspinatus (thickness difference ranging from 1.5 to 2.5 mm) or a tendon thickness greater than 8 mm have been proposed as indicators of tendinopathy (Crass et al. 1988a). Similar to other applications of musculoskeletal imaging, we believe US findings in rotator cuff pathology should be interpreted in the light of clinical data rather than on the basis of differences in measurements. In fact, measurements are not so reliable and their value is poor in the absence of clinical correlation. In addition, supraspinatus tendinopathy is often associated with diffuse wall thickening of the subacromial subdeltoid bursa and a small reactive bursal effusion. In many instances, a cleavage plane is lacking between these two structures and, therefore, it may be difficult to exclude the contribution of the bursa when measuring the tendon thickness. As regards the abnormal echotexture in tendinopathy, US findings seem to be related to subtle fibrillar tears and areas of mucoid degeneration intermixed with the reparative process occurring in the tendon substance. Nevertheless, a definite pathologic correlation of these abnormalities is lacking in the imaging literature because these patients are treated conservatively. Mild cortical changes in the greater tuberosity can also be observed.
39. PARTIAL-THICKNESS TEARS
Partial-thickness tears account for approximately 13–18% of all rotator cuff tears and occur in a younger age group compared with full-thickness tears (Walch et al. 1999). US detection of these tears and their differentiation from focal tendinopathy is often challenging because the appearance of the two conditions may be similar. It must be noted, however, that the therapeutic approach is conservative for both, so their differentiation is clinically worthless. On the basis of the US findings, we believe that an accurate diagnosis of a partial-thickness tear should be made when a true defect or cleft within the tendon substance is clearly delineated on both long- and short-axis planes. As previously stated, partial tears most frequently affect the anterior third of the supraspinatus tendon. The main US finding is a localized hypoechoic area affecting only part of the tendon thickness. Because the echogenicity of the different tendon portions can vary depending on the incidence of the US beam, a reliable diagnosis of partial-thickness tears should be made only when the area does not change its hypoechoic appearance on short- and long-axis scans and while tilting the transducer over the tendon (van Holsbeeck et al. 1995). The size of the tear must be measured on long and short-axis planes and should be indicated in the report as a measurement (in mm) or a percentage of the tendon diameter (thirds of tendon thickness). In our opinion, the second option is more practical because it gives an estimate of the lesion with respect to the tendon size. With reference to partial-thickness tears may have either a bursal or articular or intratendinous extension. Bursal surface tears are better visible on US and typically appear as hypoechoic concave defects located at the bursal surface of the supraspinatus, in most cases close to the greater tuberosity (Figs. 70, 71). Focal herniation of hypoechoic bursal fluid or hyperechoic peribursal fat within the defect is often seen and represents a useful sign for detecting such tears (Fig. 72).
Bursal effusion is usually moderate and needs accurate scanning technique for its detection: graded pressure with the probe can make fluid herniation into the tear more evident. In bursal tears, visualization of the integrity of the deep articular fibers is always required so as not to confuse these tears with full-thickness tears. Articular surface tears are more common than bursal ones, but are also more difficult to detect with US. They appear as a discontinuity of the articular line of the tendon filled with joint effusion and are associated with a normal insertion of the superficial bursal fibers (Fig. 73). Often, they appear as a deep mixed hyperechoic and hypoechoic focus at the humeral neck, due to the separation of the retracted distal segment of the tendon from the surrounding intact tissue, resulting in a new acoustic interface within the tendon substance (Fig. 74) (van Holsbeeck et al. 1995; Teefey et al. 1999; Bouffard et al. 2000; Yao et al. 2004). Articular side tears are often accompanied by bone irregularities in the greater tuberosity. Intrasubstance tears may be appreciated as subtle intratendinous longitudinal splits oriented from the bony insertion proximally without exiting onto either the bursal or the articular side of the tendon. They appear as thin fluid-filled intratendinous lines and must be assessed in their long and short axis to avoid pitfalls related to anisotropy and confusion with focal tendinopathy (Fig. 75). In other cases, these tears may be characterized by a linear high-level echo surrounded by a hypoechoic halo of fluid or edematous tendon, the so-called “rim rent” tears (Fig. 76) (Bouffard et al. 2000).
In a series of 52 shoulders with arthroscopic correlation, US had 93% sensitivity, 94% specificity, 82% positive predictive value and 98% negative predictive value for detecting partial-thickness tears of the rotator cuff (van Holsbeeck et al. 1995). Another more recent study, performed with high-end equipment in which the US findings were controlled with arthroscopic findings, reported 67% sensitivity, 85% specificity, 77% positive predictive value, 77% negative predictive value and 77% accuracy in the diagnosis considering partial-thickness tears as true-positives and no tears as true-negatives (Teefey et al. 2000a). Compared with US, MR arthrography has a higher sensitivity for depicting small partial-thickness tears, particularly those occurring on the articular side of the cuff (Ferrari et al. 2002).
40. FULL-THICKNESS TEARS
Full-thickness tears extend from the bursal to the articular surface of the tendon. As previously stated, the term “full-thickness” may refer to either a complete (full-width) or an incomplete (partial-width) tendon rupture (i.e., a tear located in the anterior third of the supraspinatus which allows communication between the glenohumeral joint space and the bursa is a full-thickness tear but not a complete tear because the middle and posterior third of the tendon is unaffected). In general, full-thickness tears have a greater extension than partial tears and are, therefore, easier to be detected with US. A classification of full-thickness tears has been proposed in both the radiographic and clinical literature (Lyons and Tomlinson 1992). In small (<5 mm wide) full-thickness tears of the supraspinatus tendon, a thin hypoechoic cleft can be seen connecting the joint cavity and the bursa (Fig. 77). The identification of these tears may not be easy because of the lack of tendon retraction (the supraspinatus is maintained in the correct position by its intact portions) and the absence of changes in the inferior boundaries of the deltoid and subdeltoid fat. A focal bursal thickening or a small amount of fluid collected just over the lesion can increase the examiner’s confidence that a lesion is present. In this regard, some authors have even proposed performing the US examination after arthrography to obtain a better assessment of rotator cuff tears as a result of the induced bursal-joint distension (Fermand et al. 2000; Lee et al. 2002). Otherwise, small tears should always be confirmed on both long- and short-axis planes to avoid any confusion with the distal prolongation of supraspinatus muscle tissue. In some cases, a differential diagnosis between a partial-thickness tear and small full-thickness tear cannot be achieved even with high-resolution transducers. Larger full-thickness tears usually affect the anterior portion of the supraspinatus tendon at the level of the critical area (Fig. 78). When the tear is localized in this area, the posterior supraspinatus can appear completely normal. In these cases, US proved to be accurate for predicting the size of the tear. Long- axis scans may be used to measure the amount of retraction of the torn tendon end from the greater tuberosity, whereas an estimate of the tear width can be obtained on short-axis scans from the distance between the torn tendon ends (Fig. 79) (Farin et al. 1996b). The accuracy of these measurements is worse in large-sized tears (Teefey et al. 2005), and may be somewhat related to shoulder positioning (Ferri et al. 2005). When scans using the Crass and Middleton positions were compared with the operative findings, the former appeared to reflect more accurately the true size of full-thickness tears in the long-axis plane, whereas both were equally accurate in evaluating the tear size in the short-axis plane (Ferri et al. 2005). Conversely, the Middleton position tended to overestimate, at any extent, the size of the tear. It is conceivable that the two positions can create a different tension across a cuff tear, thus affecting its measured size. In particular, the component of internal rotation in the Middleton position could contribute to increased tension along the tendon length and the subsequent overestimation of tear size (Ferri et al. 2005).
The US appearance of full-thickness tears depends on the amount of joint effusion. When a large effusion is present, the tear appears as a focal hypoechoic area due to the fluid that fills in the tendon discontinuity (Figs. 80, 81). In these cases, graded pressure with the probe may be helpful to distinguish the hypoechoic fluid from the tendon. When the effusion is small, it tends to collect in the most dependent portions of the bursa and the joint cavity, thus not filling the tear. In these cases, the diagnosis is based on focal non-visualization of tendon fibers. In the absence of effusion or tendon retraction, tilting the probe and pressing it over the tendon can demonstrate the detachment of the fibers from their humeral insertion. Full-thickness tear lead to a naked appearance of the greater tuberosity as the bone is no longer covered by the retracted tendon (Fig. 80). In these patients, care must be taken not to mistake the deltoid muscle for the supraspinatus. Among the indirect signs of supraspinatus tendon tears, the most important include focal herniation of the deltoid muscle and peribursal fat into the space created by the tear (Fig. 82a,b). This sign is more pronounced in full-thickness than in partial-thickness tears and can be appreciated even better when pressure is applied with the probe. In addition, there may be prominent reflection of the US beam at the interface of fluid and the articular cartilage, a sign which is commonly referred to as the “uncovered cartilage sign” or the “cartilage interface sign” (Fig. 82c,d). Although this latter sign can be seen in large partial tears affecting the articular surface of the supraspinatus, it is most frequently encountered in full-thickness tears when there is anechoic fluid overlying the articular cartilage. One should be aware, however, that this latter sign is subjective and can also be appreciated in normal states (Jacobson et al. 2004). The occurrence of bone irregularities in the profile of the greater tuberosity is an important finding to be routinely sought because it is not simply related to aging but also significantly associated with rotator cuff tears, particularly with full-thickness supraspinatus tendon tears (Wohlwend et al. 1998; Huang et al. 1999; Jiang et al. 2002; Jacobson et al. 2004). This sign has been found to be very important, as it has the highest sensitivity and negative predictive value in the diagnosis of supraspinatus tendon tear (Jacobson et al. 2004). On the other hand, contradictory results are reported in literature as to whether the US finding of bursal fluid combined with a joint effusion may be considered a specific predictive sign for a rotator cuff tear (Hollister et al. 1995; Arslan et al. 1999). This could be explained by the fact that bursal or joint fluid is common in patients with shoulder impingement even in the absence of a rotator cuff tear (Jacobson et al. 2004).
Considering full-thickness tears as true-positives and no tears as true-negatives, a recent study performed with high-end equipment in which the US findings were controlled with arthroscopic findings has reported 100% sensitivity, 85% specificity, 96% positive predictive value, 100% negative predictive value and 96% accuracy in the diagnosis (Teefey et al. 2000a). In terms of study reproducibility, a low level of interobserver variability was demonstrated in the US detection, characterization and localization of rotator cuff tears by comparing the results of two expert blinded observers in a group of 61 patients (Middleton et al. 2004). In the few discrepant cases, the disagreement concerned whether there was a full-thickness or a partial-thickness tear or whether a tear involved both the supraspinatus and infraspinatus tendons or one or the other of these tendons (Middleton et al. 2004b). Other diagnostic errors also occur in distinguishing tendinopathy from partial-thickness tears (Teefey et al. 2005). These data seem particularly important given that US is generally regarded as one of the more operator-dependent imaging techniques. On the other hand, poor agreement is expected when there is marked disparity between the operators’ experience levels (O’Connor et al. 2005).
Compared with MR imaging, US has been demonstrated to have a comparable accuracy for identifying and measuring the size of full-thickness and partial-thickness rotator cuff tears if performed by an experienced examiner using high-end equipment (Jacobson 1999; Martin-Hervas et al. 2001; Teefey et al. 2004). When the examiner has comparable experience with both imaging tests, the decision regarding which test to perform for rotator cuff assessment does not need to be based on concerns about accuracy (Chang et al. 2002; Teefey et al.2004). Instead, it can be based on other factors, such as the importance of ancillary clinical information (regarding lesions of the glenoid labrum, joint capsule, or surrounding muscle or bone), the presence of an implanted device, patient tolerance and cost (Teefey et al. 2004).
41. COMPLETE AND MASSIVE TEARS
When a full-thickness tear spreads to involve the full width of the supraspinatus, the tendon retracts medially. The amount of tendon retraction depends mainly on the age of the tear. In acute lesions, the tendon is less retracted and its tip can still be detected with US (Fig. 83a–c). In the more common chronic ruptures, the tendon end disappears beneath the coracoacromial arch as a result of involutional processes in the tendon substance and upward displacement of the humeral head (Fig. 83d,e). This condition can be promptly recognized with US. The main US findings include nonvisualization of the tendon and herniation of the deltoid, which shows a rectilinear or convex inferior margin facing the humeral convexity. A broad area of the upper convexity of the humeral head appears uncovered by the supraspinatus, the so-called “naked head” sign. Joint and bursal fluid is often absent (Teefey et al. 2000b). Especially in cases of mild retraction of the torn tendon end, short-axis planes are essential to distinguish complete (full-thickness, full-width) from incomplete (full-thickness, partial-width) tears of the supraspinatus tendon (Fig. 84). A number of possible pitfalls may mask or simulate a complete tear of the supraspinatus tendon. Although most of these pitfalls are easy to recognize and, therefore, unlikely to present a diagnostic problem, others are potentially confusing. Among them, the continuous layer of hypoechoic humeral cartilage resting on a naked humeral head may create confusion with an intact tendon (Fig. 85a). Similarly, massive calcific deposits in the supraspinatus tendon related to calcifying tendinitis should not be mistaken for a naked humeral head (Fig. 85b) (Middleton et al. 1986a). Familiarity with these imaging findings, coupled with the knowledge of the normal US anatomy of the rotator cuff, can facilitate recognition of true disease and help avoid misdiagnosis.
After assessing a complete rupture of the supraspinatus tendon, attention should always be directed to the infraspinatus and subscapularis tendons to detect any possible posterior or anterior extension of the lesion leading to a massive tear of the rotator cuff. Not uncommonly, a complete tear of the supraspinatus can be seen expanding in the posterior direction to involve the infraspinatus tendon. US findings of infraspinatus full-thickness tears are often similar to those already described for the supraspinatus (Fig. 86). Dynamic scanning during internal and external rotation of the arm can be helpful to demonstrate the torn infraspinatus tendon detached from its insertion on the humeral head. In these cases, atrophic changes in the infraspinatus muscle and a slight hypertrophy of the teres minor muscle can be appreciated on posterior sagittal scans (Fig. 87). The examiner should be aware, however, that infraspinatus muscle atrophy may also occur with either an intact tendon as a result of disuse in patients with full-thickness anterior cuff tendon tears or suprascapular neuropathy (Yao and Mehta 2002). Therefore, this finding does not imply that the infraspinatus tendon is ruptured.
Due to the intrinsic interwoven structure of the supraspinatus and infraspinatus tendons, some full-thickness tears of the supraspinatus may progress at the posterior margin of the defect along a horizontal cleavage plane causing a complex pattern of delamination (Fig. 88a). These horizontal tears are probably related to shearing stress forces generated by the defect in the supraspinatus tendon. They consist of a fissuration parallel to the plane of the articular side of the tendon and appear as linear hypoechoic defects in the middle thickness of the tendon. Detection of horizontal tears has clinical relevance because it changes the surgical approach. Unlike arthro-CT or arthro-MRI, US does not easily reveal these tears. Changes are usually subtle and experience is needed to correctly recognize this entity. When visible, horizontal tears appear as focal linear hypoechoic defects in the middle of the tendon (Fig. 89). In rare cases, insinuation of fluid into the tear can generate intramuscular cysts which appear as well-defined hypoanechoic masses inside the belly of the supraspinatus or infraspinatus muscle (Fig. 88b). Tears of the teres minor tendon are extremely rare and usually result from acute shoulder trauma rather than caudal progression of a tear from the infraspinatus.
While tears of the infraspinatus tendon are almost invariably associated with rupture of the supraspinatus, subscapularis ruptures can also be encountered as an isolated problem. Subscapularis tendon tears are mainly related to acute traumatic lesions produced with the arm abducted and in external rotation. Similar to other rotator cuff tendons, complete tears of the subscapularis are revealed by the absence of tendon fibers and the concavity of the deltoid over the naked anterior surface of the humeral head. Incomplete tears of the subscapularis tendon often involve the cranial and preserve the caudal portion of the tendon (Fig. 90). This pattern should not be mistaken for complete tears. For this purpose, the morphology of the lesser tuberosity as seen on sagittal planes may help to establish the caudal limit of the tendon and avoid any confusion between incomplete and complete tendon ruptures (Fig. 91). In addition, because of the peculiar insertion of the subscapularis on the lesser tuberosity and relationships of this tendon with the long head of the biceps tendon, subscapularis tears usuallycause secondary instability of the biceps tendon. A more detailed explanation of the mechanism of involvement of the biceps tendon will be given later.
Once a complete evaluation of rotator cuff tendons has been performed, the size and location of the tear has been determined and the degree of retraction of the torn tendon has been assessed, the status of the rotator cuff muscles should also be evaluated to rule out possible hypotrophy and fat degeneration (Sofka et al. 2004a). In fact, the orthopaedic literature has confirmed that recognition of muscle atrophy may contribute to a more precise choice of either surgical or conservative treatment for patients with rotator cuff tears, and may be useful for proving that a post-traumatic lesion is not true but related to a pre-existing degenerative state. Furthermore, presence of muscle atrophy following surgical repair of a torn cuff may indicate that lack of functional recovery is due to the state of the muscles and is not related to unsuccessful surgery.
42. CUFF TEAR ARTHROPATHY
In massive rotator cuff tears, the medial retraction of the torn thinned tendons and the contraction of the deltoid muscle cause upward displacement of the humeral head resulting in an increased conflict between the superior facet of the greater tuberosity and the inferior aspect of the acromion (Fig. 93a). Chronic local trauma leads to degenerative bony changes such as sclerosis, subchondral cysts, spurring and thinning of the acromion and cortical irregularities. In longstanding disease, subacromial changes are followed by a direct involvement of the glenohumeral space related to the incongruity between the articular surfaces. The resulting condition is referred to as eccentric (because of the upward displacement of the humeral head) osteoarthritis or “cuff tear arthropathy” (Neer et al. 1983b). This state can be considered an end-stage irreversible destructive arthropathy consisting of a reduced or absent subacromial space, thinning and loss of the articular cartilage at the lower third of the humeral head and the superior aspect of the glenoid cavity, inferior osteophytes of the humeral head, a rounded and irregular greater tuberosity due to abrasion during abduction of the arm with flattening of the bicipital sulcus and a reduced thickness of the acromion. In chronic longstanding disease, the occurrence of a stress fracture of the acromion can occur as a result of local trauma induced by the humeral head (Hall and Calvert 1995). It has been suggested that rotator cuff arthropathy may derive from both mechanical factors and reduced cartilage nutrition due to the increased volume of the articular cavity and subsequent decrease in intra-articular pressure (Neer et al. 1983b).
The diagnosis of rotator cuff arthropathy basically relies on its radiographic appearance. We believe standard radiographs are mandatory before a US study because examining a patient with rotator cuff arthropathy with US as a first examination may be a challenge, especially for the beginners. The main US findings include a massive tear of two or more rotator cuff tendons associated with a markedly reduced or absent subacromial space, loss of the articular cartilage, a rounded and irregular greater tuberosity due to abrasion during abduction of the arm with flattening of the bicipital sulcus, a reduced thickness of the acromion and marginal osteophytes on the inferior humeral head (Figs. 93, 94). Joint and bursal effusions may contain echogenic debris. The close contact of the humeral head with the undersurface of the acromion may make differentiation between these structures less immediate with US. The best way to separate these structures is by dynamic scanning on coronal planes (somewhat oriented along the long axis of the supraspinatus) over the tip of the acromion while abducting the patient’s arm in internal rotation. This maneuver may help to distinguish the moving humeral head from the stationary acromion and to appreciate the reduced distance between them. An additional problem may be related to the localization of the bicipital sulcus which is, at least in part, effaced by the abrasions in the greater tuberosity. This can lead to some technical problems even for the experienced examiner because the sulcus is a main landmark for rotator cuff evaluation. In the case of an intact subscapularis tendon, its identification may be helpful to localize the position of the flattened sulcus. A reduced thickness of the acromion may also be observed. These patients have a proximal migration of the humeral head such that it contacts the undersurface of the acromion. This contact point functions as a fulcrum, allowing for near-normal elevation of the shoulder with deltoid contraction, despite the absence of the rotator cuff.
43. ACROMIOCLAVICULAR CYSTS
Acromioclavicular cysts appear as well-demarcated painless masses overlying the acromioclavicular joint (Cvitanic et al. 1999). Physical examination typically reveals a painless elastic slightly tender mass. Acromioclavicular cysts can be found in association with several arthropathies affecting the acromioclavicular joint (Cooper et al. 1993; De Sanctis et al. 2001; O’Connor et al. 2003) or, more commonly, may develop in patients presenting with longstanding massive rotator cuff tears (Cvitanic et al. 1999; Mellado et al. 2002; Steiner et al. 1996). The pathogenesis of acromioclavicular cysts is still debated. Chronic friction of the humeral head against the undersurface of the acromioclavicular joint due to a full-thickness tear of the supraspinatus tendon has been suggested as the cause of progressive damage to the inferior capsule and communication between the glenohumeral and degenerated acromioclavicular joint (Craig 1986). Then, the cyst in the soft tissues at the superior aspect of the shoulder develops from progressive passage of glenohumeral joint fluid through the acromioclavicular joint (Fig. 95).
This mechanical theory does not, however, explain some pathologic findings that are often associated with these cysts, such as their mucoid content and fibrous wall. In addition, similar to ganglia, the intramuscular extension of these cysts inside the trapezius has also been reported (Montet et al. 2004). Based on these findings, chronic instability of the acromioclavicular joint could also be hypothesized to play a causative role in the development of the cyst. This observation is supported by the fact that patients with massive rotator cuff tears often exhibit widening of the acromioclavicular joint space at arthrography and dynamic US during arm movements. Although we can only speculate on this subject, massive rotator cuff tears could generate acromioclavicular cysts through the following sequence of events: upward displacement of the humeral head, tearing of the inferior capsule of the acromioclavicular joint due to chronic microtrauma against the greater tuberosity, acromioclavicular instability, tearing of the articular disk or of the superior capsule related to chronic compressive and pulling forces exerted on the articular structures and, finally, formation of the cyst (Montet et al. 2004). According to this theory, acromioclavicular cysts would be somewhat similar to meniscal cysts. At US, acromioclavicular cysts may exhibit thickened walls and internal septa that can partially fill in the lesion. In some cases, acromioclavicular cysts are associated with calcium pyrophosphate dehydrate deposition disease or synovial hypertrophy leading to a echogenic appearance of the mass (Tshering Vogel et al. 2005). These findings may evoke a solid tumor rather than a cystic lesion and care should be taken not to propose a biopsy for such a benign lesion (Fig. 96).
In rare instances US can demonstrate communication of the acromioclavicular joint space with the cyst and, on exerting pressure with the probe on the cyst, debris may be seen moving to and fro across the acromioclavicular joint (Craig 1984), the so-called “Geyser sign”. Treatment of acromioclavicular cysts depends on the patient’s age and functional requirement. In the elderly or when disability is negligible, conservative treatment is the most appropriate. Surgical treatment can be proposed in younger active patients and must also be directed toward the underlying disorder. Combined excision of the cyst and rotator cuff repair is the treatment of choice for patients with functional impairment because simple aspiration or resection of the cyst is almost invariably followed by recurrence if the rotator cuff itself is not addressed (Groh et al. 1993). In cases complicated by degenerative osteoarthritis of the glenohumeral joint, shoulder arthroplasty can prevent recurrence (Groh et al. 1993).
44. POSTOPERATIVE CUFF
In the early stages, the impingement syndrome is treated conservatively with restriction of activities, physical therapy, anti-inflammatory drugs and, possibly, steroid injections in the subacromial subdeltoid bursa (Bokor et al. 1993). When conservative treatment fails, surgery is indicated. A basic knowledge of the type of surgical intervention performed and its extent is critical for the examiner to reach a correct interpretation of the US images. Before the examination, details of the surgical intervention should always be collected from the surgical reports or the patient’s records. Generally speaking, the main surgical techniques for impingement syndrome and rotator cuff disease involve subacromial decompression and rotator cuff repair or debridement. In patients with subacromial impingement but without rotator cuff tears, subacromial decompression may be performed with either an open procedure through an anterolateral deltoid splitting incision or arthroscopy (Fig. 97a,b). The open approach consists of excision of the anteroinferior aspect of the acromion, including the distal end of the clavicle, and resection or debridement of part of the coracoacromial ligament (Fig. 97c,d).
If prominent osteophytes are present, the acromioclavicular joint and the distal 2.5 cm of the clavicle may be removed. On the other hand, arthroscopic subacromial decompression is carried out by resecting the anterior edge and inferior surface of the acromion along with the subacromial subdeltoid bursa and the subdeltoid fat. The coracoacromial ligament is released and the distal clavicle is resected as well. Combined open and arthroscopic approaches may be used in the event of large full-thickness tears of the rotator cuff. Although arthroscopy does not require deltoid incision (leading to secondary weakness of the muscle), this technique is more often associated with persistence or recurrence of pain (procedure failure reported in up to 3–11% of cases), as a result of insufficient excision of the acromion. Other complications include progression of rotator cuff tendinosis, residual or recurrent rotator cuff tears and postoperative adhesions. In patients with rotator cuff tear, the type of intervention mainly depends on the location, thickness and severity of the tear. In small partial-thickness tears, treatment ranges from debridement of frayed tendon tissue to a combined excision of the defect and repair of the adjacent healthy margins of the cuff. In full-thickness tears, repair may be performed with either a side-to-side suture (small tears) or tendon-to-bone reattachment (large tears), both associated with acromioplasty. Usually, these procedures are carried out arthroscopically using three bursal portals (anterior, lateral and posterior) or with a mini open repair (least possible split in the deltoid, preserving the acromial origin of the muscle). In large full-thickness tears, a tendon-to-bone repair is usually performed, reattaching the tendon at a more proximal site (humeral neck) relative to the greater (supraspinatus) or the lesser (subscapularis) tuberosity (Figs. 98, 99). Nonabsorbable sutures or metallic anchors (arthroscopic repairs) are used for this procedure. Massive tears are, for the most part, treated with debridement alone.
The diagnostic role of MR imaging of a shoulder that has undergone surgical treatment is controversial due to sutures, suture anchors and osseous changes that may alter signal intensities within the acromion, humeral head and rotator cuff tissue (Magee et al. 1997). US has the advantage that it is unaffected by the presence of intraosseous hardware. Nevertheless, postoperative shoulder US may be a challenge, especially if the operative details are not available. At US examination, a repaired supraspinatus usually appears much more heterogeneous than normal. The superficial tendon boundaries may assume a slightly concave profile when the supraspinatus is scarred and reduced in volume. In addition, the bursal surface of the tendon is often undefined as a result of bursal removal. Intratendinous nonabsorbable suture material and suture anchors may be seen as bright linear echoes with faint reverberation artifact (Figs. 98c, 100a). The examiner should be conscious that the retracted torn tendon is often implanted in the humeral neck rather than in the greater tuberosity. As a result, some bare bone in the region of the greater tuberosity should not necessarily be regarded as a recurrent tear. The most reliable US signs of a re-torn supraspinatus are: nonvisualization of the cuff because of complete tendon avulsion and retraction under the acromion, presence of a focal defect in the rotator cuff, a variable degree of tendon retraction from the surgical trough and detection of sutures floating freely in the fluid (Fig.100b) (Crass et al. 1986; Hall 1986; Mack et al. 1988b; Prickett et al. 2003). In difficult cases, dynamic scanning may be helpful to distinguish the impairment related to a recurrent tear from adhesive capsulitis as well as to assess the functional result of acromioplasty. Overall, the diagnostic accuracy of US for detection of postoperative rotator cuff tears is similar to that for imaging of shoulders that have not been operated on (Mack et al. 1988; Furtschegger and Resch, 1988; Prickett et al. 2003). The most recent series based on newer equipment, current US criteria for tears and complete surgical validation of the results reported 91% sensitivity, 86% specificity and 89% accuracy for US identification of rotator cuff integrity postoperatively (Prickett et al. 2003).
45. CALCIFYING TENDINITIS
Rotator cuff calcifications are a common finding (occurring in as many as 3% of adults with a prevalence in females in their fourth to sixth decades of life) when examining the shoulder with US. Generally speaking, calcifying tendinitis refers to deposition of calcium, predominantly hydroxyapatite, in the rotator cuff tendons: the most commonly affected tendon is the supraspinatus (80%), followed by the infraspinatus (15%) and the subscapularis (5%). However, deposits can also be found in unexpected locations around the shoulder, such as the teres minor, the pectoralis major and the myotendinous junction of the long head of the biceps tendon (Goldman, 1989; Cahir and Saiffuddin, 2005). In the cuff, the lower third of the infraspinatus tendon, the critical zone of the supraspinatus and the preinsertional fibers of the subscapularis are the most commonly involved sites. Although the pathogenesis of calcifying tendinitis is not completely understood, this condition seems to be related to hypoxic areas or metabolic factors in tendons and is typically associated with an intact rotator cuff. Local hypoxia is believed to lead to fibrocartilaginous metaplasia that is turn produces the calcifications (Flemming et al. 2003). Four stages of the disease can be recognized: precalcific, calcific, resorptive and postcalcific (Uhthoff and Sarkar 1989). In the resorption phase, the tendon develops increased vasculature and the calcium deposits are removed by phagocytes. There is significant correlation between acute pain attacks and histologic evidence of calcium resorption. At the time of diagnosis, patients may be asymptomatic or may present with either acute or chronic pain. Typical symptoms include either subacute low-grade shoulder pain increasing at night (formative phase) or a sharp acute pain limiting shoulder movements and seldom accompanied by fever due to rupture of the calcification in the adjacent structures (resorptive phase). The diagnosis of calcifying tendinitis is based on plain films (anteroposterior views in internal, neutral and external rotation, outlet view) which can accurately assess the size and location of the calcifications. Radiographs can also detect calcific deposits inside the bursa and the occurrence of focal erosions on the humeral head. Asymptomatic rotator cuff calcifications do not require treatment. In symptomatic cases, calcifying tendinitis can be managed conservatively with physical therapy and a short course of nonsteroidal anti-inflammatory drugs. Complications are best treated with more aggressive therapy including systemic steroids.
At US, rotator cuff calcifications appear as intratendinous hyperechoic foci. Three main types of calcium deposits can be identified with US depending on the amount of calcium contained in the deposit. Type I calcifications appear as hyperechoic foci with well-defined acoustic shadowing, similar to gallstones (Fig. 101a). These calcifications correspond to the formative phase of calcium deposition and account for approximately 80% of cases. Type II and type III calcifications (“slurry” calcifications) look like hyperechoic foci with a faint (type II) or absent (type III) shadow and can be referred to the resorptive phase, in which the deposits are nearly liquid and can be successfully aspirated (Fig. 101b,c). In symptomatic patients, these deposits are more often associated with local hyperemia at color Doppler imaging (Chiou et al. 2002). Often, semiliquid deposits are difficult to diagnose because they appear nearly isoechoic with the tendon (Fig. 101d). An oval area of fibrillar loss and small hyperechoic dots within the affected tendon is the main criterion for detecting them. The shape of the calcification is quite variable, ranging from well-defined chunks of calcium to thin hyperechoic strands in the cuff (Fig. 102).
These stripe-like deposits are typically located at the preinsertional level (calcific enthesopathy) and should not be confused for intratendinous partial-thickness tears, such as rim rent tears. Although standard radiographs can establish the tendon in which the calcific deposit is located, US examination is valuable to determine which portion of the tendon is affected, the distance of the calcification from an arthroscopic landmark such as the biceps tendon (particularly useful when the deposit does not bulge over the tendon surface) and, most importantly, whether the calcification cause impingement (Figs. 102a,d, 103). Dynamic examination can reveal the impingement of the calcification against the acromion while abducting the arm in internal rotation. In the case of semiliquid deposits, local compression and tilting the probe over the calcific focus can induce movements of the fluid calcium.
Types II and III calcifications may appear at one site initially and migrate to another location subsequently. In such cases, US can identify the sub-bursal and intrabursal extrusion of the calcification, when the deposit exits the tendon and slides between it and the bursa or enters the subacromial subdeltoid bursa itself causing an acute microcrystalline bursitis. These painful conditions can be reliably diagnosed with US. In sub-bursal migration, the calcific deposit relocates between the subacromial subdeltoid bursa and the tendon from which it derives. These deposits are usually isoechoic or slightly echogenic relative to the tendon, displace a collapsed bursa and are associated with edematous changes in the surrounding fatty spaces (Fig. 104). In cases of intrabursal penetration of the calcification, the subacromial subdeltoid bursa shows thickened walls and appears completely filled with hyperechoic fluid containing calcium and debris. In some cases, a fluid-calcium level in the dependent pouch of the bursa can be observed: the hypoechoic upper layer of the level relates to the reactive synovial fluid while the lower level is due to sedimentation of calcium material (Fig. 105a–c). Although subtle, these findings may explain the severe exacerbation of pain that usually accompanies the extrusion of calcium. Bursal-side partial-thickness tendon tear has been reported after extrusion of calcium in the subacromial bursa (Fig. 105d) (Gotoh et al. 2003).
The intraosseous loculation of the calcification may occur in the tuberosities as a result of migration of the intratendinous deposit into the bone (Chan et al. 2004). The pathomechanism is not completely understood: it seems to be somewhat mediated by acute inflammation and local vasculature at the tendon insertion or by mechanical effects of muscle traction causing bone destruction (Durr et al. 1997). Fever, raised white cell counts and local tenderness are often associated. US diagnosis of intraosseous loculation of calcifying tendinitis is difficult. A focal bone erosion in continuity with a tendon calcification and partially filled by hyperechoic dots should make the lesion suspected if the patient complains of intense pain without a specific injury (Fig. 106). This finding requires confirmation with other imaging modalities, including radiography, scintigraphy, CT or MR imaging: detection of an intraosseous lytic area with a focus or faint calcification, ill-defined calcification in the overlying tendon and periosteal reaction is diagnostic (Figs. 106, 107).
There is a general consensus that CT is the optimum imaging modality to depict the continuity of the tendinous, cortical and medullary processes (MR imaging is superior in evaluating marrow involvement but intratendinous calcification may not be appreciated) (Flemming et al. 2003). Among uncommon complications of calcifying tendinitis, inferior glenohumeral joint subluxation (drooping shoulder) has been described as a result of a large-sized calcific deposit within the supraspinatus tendon (Prato et al. 2003). In the reported case, the deposit pushed inferiorly against the humeral head, overcoming the resistance of the muscles and the capsuloligamentous structures given the rigid roof formed above by the coracoacromial arch. Direct removal of part of the calcification by needle aspiration, together with the passage of the residual portion into the subacromial subdeltoid bursa, decreased the compression on the humeral head, allowing its relocation with respect to the glenoid fossa (Prato et al. 2003).
46. BICEPS TENDON PATHOLOGY – BICEPS TENDINOPATHY
Tendinopathy of the long head of the biceps tendon, including tenosynovitis and tendinosis, derives from two main mechanisms: impingement and attrition. In the first, the intracapsular portion of the biceps is pinched between the humeral head and the coracoacromial arch during abduction and rotation of the arm. The mechanism is similar to that leading to supraspinatus impingement. In addition, if the supraspinatus is torn, the humeral head is displaced upward by the action of the deltoid so that the biceps tendon is pulled by the humeral head and becomes its main depressing structure (Fig. 108a). Chronic tension related to this overload may be contributory to tendon degeneration (Wallny et al. 1999). The second mechanism derives from chronic conflict between the intertubercular portion of the biceps and a narrowed bicipital groove caused by local periostitis, osteophytes and bony irregularities in the lesser tuberosity (Pfahler et al. 1999).
The main signs of tendinopathy are biceps tendon hypertrophy related to edema and heterogeneous echotexture with fissurations (Fig. 108b,c). These abnormalities are maximal at the level of tendon reflection over the humeral head and at the proximal portion of the bicipital sulcus. Color flow signals may be recognized around the swollen tendon as well. In some cases, the extra-articular portion of the biceps may appear normal and this finding may be misleading if scanning does not systematically include its intra-articular portion. In biceps tendinopathy, effusion in the tendon sheath is an ancillary finding. Care should be taken not to diagnose biceps tendinopathy when a sheath effusion surrounds an otherwise normal tendon, because the fluid merely reflects an intra-articular effusion which may extend into the tendon sheath. When the fluid in the tendon sheath is out of proportion to that visible in the posterior joint recess, it can be regarded as an expression of biceps tendinopathy. In attrition tendinosis, the biceps tendon may appear thinned and frayed across the intertubercular sulcus. Due to repeated friction against the irregular bone, biceps tendinosis may eventually progress to longitudinal spits. These may either create a central cavity within the tendon substance or may divide the biceps into two cords, giving the appearance of two tendons lying adjacent to each other over a variable length (Fig. 109a–f). In this latter instance, one must be sure the second tendon is actually an elongated structure because synovial folds and loose bodies in the sheath might mimic the appearance of two tendons in cross-section. Care should be taken not to mistake a partial longitudinal tear of the biceps for a bifid tendon, which represents an anatomic variant. Distinction of a tear from such a variant can be potentially difficult because US is unable to follow the tendon up to its attachment into the supraglenoid tubercle. In the case of sheath effusion, detection of two individual mesotendons in the bicipital groove can be regarded as an indicator of a bifid tendon (Fig. 109g–i). Evaluation of the labral attachment should also be important to differentiate an isolated longitudinal biceps tendon tear from a biceps tear associated with a SLAP lesion. In this respect, MR imaging is superior to US in making a correct diagnosis.
47. BICEPS TENDON RUPTURE
The rupture of the long head of the biceps tendon is not a difficult clinical diagnosis. It typically generates a soft-tissue lump in the anterior aspect of the middle arm, the so-called “Popeye’ sign”, accompanied by decreased strength during flexion and supination of the forearm (Fig. 110a). Often, the shoulder pain ceases as the tendon tears and the patient is amazed to see such a hypertrophied muscle in the arm which paradoxically leads to a diminished strength. Diagnostic difficulties can be encountered in a few cases, especially in obese patients with thick arms. US can identify the disruption of the tendon, which usually happens at the intra-articular level and retracts distally leaving an empty groove (Fig. 110b–e). On short-axis scans obtained at the intra-articular level, the coracohumeral ligament may assume a concave profile over the humeral head due to the absence of the underlying biceps (Fig. 111).
In acute ruptures, the tendon stump is retracted down into the arm and appears surrounded by fluid (Middleton et al. 1985; Ahovuo et al. 1986). At the site of rupture, the sheath of the biceps tendon may fill in with debris, making it difficult to distinguish a torn from an irregular but intact tendon. In such circumstances, we believe there is no real need to explore the biceps sulcus to make a correct diagnosis. Instead, the examiner should consider the level of insertion of the pectoralis major tendon relative to the myotendinous junction of the biceps. In fact, when the biceps tears, its myotendinous junction falls down in a more distal location than the level of the pectoralis (Fig. 112). In an acute setting, the retracted muscle is usually surrounded by fluid and retains its normal echotexture. Cranial to it, a hyperechoic image surrounded by a hypoechoic halo corresponds to the retracted tendon encircled by an effusion. In chronic ruptures, the muscle belly shows a decreased volume and becomes hyperechoic compared with the adjacent short belly as a consequence of atrophic changes.
The difference between the two biceps heads may be so striking that a “black and white” appearance is often noted on transverse scans (Fig. 113). Occasionally, there may be self-attachment of the ruptured tendon stump into the groove without retraction and care should be taken not to mistake it for a normal tendon. In these cases, the reattachment of the torn tendon in a more distal location may prevent muscle degeneration. The muscle may exhibit a globular appearance as a result of retraction but usually retains a normal internal echotexture (Fig. 114a,b). Finally, in rare instances biceps tendon tears may occur at the myotendinous junction with a normal-appearing tendon inside the groove (Fig. 114c–e). If the biceps tendon is examined without evaluating the muscle, such tears can be missed completely. Although the US findings of biceps tendon tears are multifaceted, the essential point is to establish whether the tendon is intact or torn: further information on position and echo-texture of the tendon ends and the muscle does not affect the therapeutic decision (surgical vs. conservative), which is essentially based on clinical findings such as the patient’s age and activity. In general, biceps tendon ruptures are significantly associated with supraspinatus (96.2% of cases) or subscapularis (47.1% of cases) tendon tears as a result of the same impingement forces and tensile injuries (Beall et al. 2003).
48. BICEPS TENDON INSTABILITY
Due to its curvilinear course and reflection over the humeral head, the biceps is intrinsically predisposed to instability. As a rule, the biceps does not undergo medial subluxation or dislocation out of the bicipital groove when the coracohumeral ligament is intact. If the coracohumeral ligament is torn, as may occur in association with anterior supraspinatus tears, the biceps may dislocate over the intact subscapularis. In such cases, the ruptured lateral part of the coracohumeral ligament can be seen (Fig. 115a,b). Dynamic examination during rotational movements of the shoulder can reveal abnormally increased motion of the intra-articular portion of the biceps tendon, which is no longer stabilized by the pulley formed by the coracohumeral and superior glenohumeral ligaments. In these cases, abnormal stress forces can produce early local degeneration with biceps tendon thickening and fissurations. More caudally, the biceps may appear perched over the lesser tuberosity (Fig. 115c). Careful scanning technique is needed to image the subluxed long head of the biceps tendon because instability occurs at first cranially, at the intra-articular level.
In addition, the slight medial positioning that the tendon normally assumes as it enters the bicipital sulcus should not be mistaken for a pathologic finding. We believe that a proper diagnosis of biceps tendon subluxation can be made with US only when the tendon is seen overlying the lesser tuberosity on transverse scans in which the bicipital sulcus is clearly depicted. When the sulcus is not clearly seen, the apparent subluxation of the biceps tendon can be the result of either an incorrect scanning technique or anatomic variations. In the rare cases of intermittent instability, “to-and-fro” displacement of the tendon out of the groove can be seen. Dynamic scanning with the shoulder in maximal external and internal rotation may help the diagnosis (Farin et al. 1995). In these patients the biceps groove should be accurately imaged on transverse planes to assess its shape (Farin and Jaroma 1996). A congenital shallow intertubercular groove (<3 mm deep) with a flat medial wall predisposes the long head of the biceps tendon to instability (Levinshon and Santelli 1991). In rare instances, dislocation of the biceps tendon can be secondary to a combined tear of the lateral portion of the reflection pulley and the transverse ligament even if the subscapularis is normal. In these patients, the biceps can dislocate superficial to the subscapularis (Fig. 116) (Patton et al. 2001; Bennett 2001). When the biceps is subluxed, spurring in the lesser tuberosity may contribute to worsening the tendinopathy as a result of attrition. In these cases, the biceps may be markedly swollen and predisposed to longitudinal splits, as already described. The pathogenetic mechanism of this abnormality is similar to that occurring in the peroneus brevis at the ankle as a result of intermittent anterior subluxation over the lateral malleolus.
Disruption of the cranial third of the subscapularis tendon, either in isolation or associated with supraspinatus tendon tear, is often associated with biceps instability (Bennett 2001). When the cranial third of the subscapularis is torn, the biceps tendon tends to sublux superficial to it on cranial transverse scans and to rest in a normal position on caudal transverse scans (Fig. 117). When the subscapularis tear becomes complete, the biceps slips medially within the glenohumeral joint (Ptasznik and Hennesy 1995; Farin et al. 1995; Farin 1996; Prato et al. 1996). The US diagnosis of biceps tendon dislocation relies on demonstration of an empty groove and a medially displaced tendon. In many cases, US is able to identify the biceps tendon on the outside slope of the bicipital groove (Fig. 118).
However, the displacement of this tendon may be so medial and deep as to make its demonstration difficult due to the acoustic shadowing of the coracoid. In these cases, a careful scanning technique may be necessary to recognize the dislocated tendon in proximity to the anterior glenoid labrum to avoid a false diagnosis of tendon rupture. In doubtful cases, tilting the probe up and down may help to detect the dislocated biceps on the basis of anisotropy. A trick of the trade is to refer to the pectoralis major tendon as a landmark to identify the myotendinous junction of the biceps. Unlike biceps tendon tears, the dislocation of this tendon does not cause changes in position of the myotendinous junction. The probe should be swept from caudal to cranial following the tendon course: if the biceps is seen deflecting from its normal route, tendon dislocation must be considered. On short-axis images, a dislocated biceps tendon typically appears as a hyperechoic rounded image surrounded by a hypoechoic rim due to peritendinous effusion. Also, care must be taken not to mistake the displaced long head of the biceps tendon for the short head: they can be differentiated by sweeping the probe upward to reach the insertion of the short head into the coracoid. Finally, one should not confuse the echogenic debris and fibrous scarring that are often found in the empty groove for a normally positioned tendon (pseudobiceps tendon) (Farin 1996). In these cases, diagnostic confidence may be enhanced by the lack of fibrillar echoes detectable on longitudinal scans over the bicipital groove (Teefey et al. 1999). Overall, distinguishing between biceps tendon tear and instability is clinically relevant because a tear is usually treated by conservative measures, whereas biceps dislocation is frequently associated with a tear of the subscapularis, a condition that requires surgical treatment: debridement in the case of incomplete tears of the subscapularis, repair of complete tears and tenodesis of the biceps tendon to the intertubercular groove (Fig. 119).
49. SHOULDER PATHOLOGY BEYOND THE ROTATOR CUF
Although most examinations of the shoulder are performed to evaluate the rotator cuff, US can evaluate other structures around the shoulder girdle (Peetrons et al. 2001; Martinoli et al. 2003). In general, people are poorly informed about the contributions of US in shoulder instabilities, joint disorders and nerve entrapment syndromes, and US probably remains underutilized in this area. As regards intra-articular diseases, there is no doubt that they are better diagnosed by MR imaging and CT and MR arthrography, because of better assessment of anatomic structures such as the capsule, the ligaments, the glenoid labrum and the bone. However, US is quick to perform and has specific advantages over MR imaging that warrant its wider use, including its higher resolution and ability to examine different structures in both static and dynamic states and in different patient positions.
50. PECTORALIS AND DELTOID LESIONS
Complete traumatic rupture of the pectoralis major is a very uncommon sport injury which mainly occurs in young male athletes. Typically, the injury occurs while performing bench presses with the arm in forced external rotation, extension and abduction of the humerus. Because the lowest fibers of the muscle insert at the highest point on the humerus, this mechanism causes an eccentric stretching and lengthening of the inferior (abdominal) part of the muscle, predisposing it to rupture (Wolfe et al. 1992). Forced external rotation and abduction (ABER position) applied across the contracted muscle of an outstretched arm while breaking a fall, or accidents in wrestling, rugby and waterskiing, have also been reported as possible mechanisms of injury (Äärimaa et al. 2004). Patients report sudden pain in the arm and shoulder with or without a “pop” sensation. The classification of tears depends on the degree (complete vs. partial) and location (tendon-bone junction, myotendinous junction, intramuscular) of injury. In the acute phase, distinguishing among these types of tears is important because partial injuries are treated conservatively whereas complete tears require surgical repair to restore strength and have a better patient outcome. This differentiation, however, is often difficult to do without imaging studies, because of local edema and soft-tissue swelling and tenderness. In chronic phases, loss of the anterior axillary fold can be found with asymmetry of the muscle in comparison with the uninjured side (Fig. 120a). US has proved able to diagnose traumatic injuries to the pectoralis major muscle, as well as to obtain an accurate grading of the tear (Rehman and Robinson, 2005). If the tendon is avulsed from the humeral bone, the most common occurrence (Connell et al. 1999), US findings include either a wavy appearance or nonvisualization of the tendon (Martinoli et al. 2003; Rehman and Robinson, 2005). Hypoechoic fluid adjacent to the humeral cortex and along the tendinous bed related to the hematoma can help the diagnosis (Fig. 120b,c). The long head of the biceps tendon and its myotendinous junction are surrounded by fluid. As the tendon of the pectoralis major is a stabilizer of the long head of the biceps tendon distal to the humeral tuberosities, its rupture leads to elevation of the biceps from the humerus (Fig. 120d) (Martinoli et al. 2003). If the lesion occurs at the distal myotendinous junction, US demonstrates a normal tendon insertion on the humerus and swelling and a heterogeneous echotexture at the tendon-muscle junction related to disrupted muscle fibers and intervening hypoechoic hematoma, just deep to the deltoid muscle. In complete ruptures, the muscle belly is retracted medially and may exhibit atrophic changes. With time, adhesions may form a pseudotendon between the retracted muscle and actual tendon stump (Rehman and Robinson, 2005). When differentiation between partial and complete tears is doubtful with US, MR imaging is an accurate means to confirm the diagnosis (Connell et al. 1999; Lee et al. 2000; Carrino et al. 2000).
Apart from traumatic injuries, the pectoralis major and minor muscles are the most common congenitally absent muscles (Fig. 121). Patients typically have a flattened chest wall with hypoplastic ribs and an elevated nipple. Agenesis of these muscles is often partial and may be part of a syndrome associated with other anomalies: the Poland syndrome (Demos et al. 1985). This syndrome is an autosomal recessive condition with an incidence of 1:30,000 live births, in which the absence of the pectoralis is unilateral and associated with syndactyly and hypoplasia of the ipsilateral upper extremity. US diagnosis of pectoralis agenesis is mainly based on the absence of a muscle belly and tendon. Transverse planes over the anterior chest wall and the myotendinous junction of the biceps are obtained on both sides for comparison. In pectoralis agenesis, a fibrous remnant of the tendon and muscle may occasionally be observed; this finding should not be mislead the examiner into thinking that a congenital absence of the muscle does not exist.
There are few reports in literature dealing with spontaneous rupture of the deltoid muscle. In the reported cases, the injury occurred in patients with chronic, massive rotator cuff tears and was in some instances responsible for an acute onset of shoulder weakness. One of the possible causative factors claimed to explain rupture or detachment of the deltoid muscle is a history of repeated steroid injections for frozen shoulder and longstanding rotator cuff tears (Allen and Drakos 2002). Because, in patients with deltoid rupture and massive rotator cuff tear, contraction of the intact deltoid can lead the humeral head to protrude through the defect (a type of boutonnière) – most commonly in the anterior or middle third – humeral impingement on the undersurface of the deltoid could be regarded as another possible causative factor (Blazar et al. 1998; Bianchi et al. 2006). Upward displacement of the humeral head may lead to it causing attrition at different sites. If impingement acts on the anteromedial part of the acromioclavicular arch, it more likely generates acromioclavicular cysts (Tshering Vogel et al. 2005); if it affects the posterior part of the acromioclavicular arch, it may lead to stress fractures of the acromion (Dennis et al. 1986). It is conceivable that a more lateral location of impingement forces (possibly secondary to a small acromion size or to a large humeral head) may cause weakening and even tears of the deltoid attachment (Figs. 122, 123) (Bianchi et al. 2006). Detachment of the deltoid insertion from the anterolateral acromion is a frequent surgical practice that improves exposure during acromioplasty. Postoperative detachment of the deltoid is a potential complication after this procedure. US can identify this condition, which can be repaired surgically if recognized early.
Intramuscular injection through the deltoid muscle is common practice to treat shoulder pain and infection. Repeated injection of drugs, however, can lead to fibrosis of the injection site, even evolving into contracture status of muscles (injection myopathy). Deltoid muscle contraction is an uncommon, often unrecognized, clinical entity which usually involves the intermediate portion of the muscle, this being the preferred site for intramuscular injection (Chen et al. 1998). Clinical findings include a palpable fibrous cord within the deltoid muscle, skin dimpling overlying the cord, wingling of the scapula and a restricted range of shoulder motion, in particular limited adduction of the glenohumeral joint. US is able to reveal multiple hypoechoic small-caliber fibrotic cords (diameter <1 cm) oriented along the long-axis of the muscle (pattern I), reflecting the initial stage of small focal fibrotic foci (Fig. 124) (Huang et al. 2005). As the injections continue or the abnormality evolves over time, the small-caliber cords may coalesce into larger hypoechoic areas (pattern II) or even develop into calcified masses (pattern III) (Huang et al. 2005). In advanced disease, treatment is based on distal release of the deltoid fibrous cords.
51. ADHESIVE CAPSULITIS (FROZEN SHOULDER)
Adhesive capsulitis, also referred to as “frozen shoulder,” refers to an insidious syndrome of shoulder pain and restricted movement in the absence of shoulder impingement and rotator cuff injury. The patient generally complains of loss of the normal shoulder range of motion, particularly arm elevation and external rotation. This condition tends to occur in perimenopausal women and is associated with diabetes mellitus, some drug treatments (i.e., isoniazide and barbiturates), trauma and prolonged immobilization after reduction for shoulder dislocation. Although the pathophysiology of adhesive capsulitis is unknown, hypervascular synovial proliferation followed by deposition of collagen and formation of capsular adhesions is typically found in these patients, leading to a reduced articular volume and, as a consequence, to pain and severely restricted joint motion. Treatment includes physiotherapy, steroid injections and closed manipulation in the operating room. In refractory cases, hydrodilatation and anterior capsulotomy is indicated (Gam et al. 1998).
The clinical diagnosis is not easy in the early phases. It rests on physical findings and demonstration of reduced joint capacity at arthrography (glenohumeral articular capacity <7 ml). In the early stages, however, this condition may be difficult to diagnose as it mimics rotator cuff pathology and impingement syndrome. Although US is not able to depict adhesions or measure the degree of restriction of the joint cavity, frozen shoulder must be considered in the differential diagnoses when limitation of sliding movements of the supraspinatus tendon underneath the acromion during arm abduction or its persistent visualization during lateral elevation of the arm is observed (Ryu et al. 1993). In fact, during arm abduction these patients tend to elevate the shoulder as rotation of the humerus is hindered by capsular adhesions (Fig. 125). Other findings include thickening of the soft-tissue structures in the rotator cuff interval and increased vasculature depicted at color Doppler imaging around the intra-articular portion of the biceps tendon and the coracohumeral ligament (Fig. 126) (Lee et al. 2005). Mild fluid distension of the biceps tendon sheath and the subscapular recess are also seen. Nevertheless, these signs are operator- and equipment-dependent and, for the most part, difficult to quantify. In doubtful cases, MR imaging and MR arthrography are valuable to diagnose this condition (Mengiardi et al. 2004).
52. GLENOHUMERAL JOINT INSTABILITY
Although the value of US in assessing glenohumeral joint instability is poor, this technique can incidentally detect a variety of instability injuries affecting the glenoid labrum and the bone (Rasmussen 2004). In anterior shoulder instability, the main criteria for anterior labral tear are an enlarged (>2 mm) hypoechoic zone at the base of the labrum, a hypoechoic cleft within an otherwise homogeneous labrum, a truncated, eroded, frayed, irregular shape or absence of the labrum and an abnormal motility of the labrum when dynamic scanning is performed; altered labral echogenicity seems to be an inaccurate finding (Fig. 127) (Loredo et al. 1995; Hammar et al. 2001; Schydlowsky et al. 1998b; Rasmussen 2004). On the other hand, a small altered labrum seems to indicate degenerative changes (Schydlowsky et al. 1998c; Hammar et al. 2001; Taljanovic et al. 2000). In patients with acute traumatic or recurrent anterior shoulder dislocations, US has a reported 88–95% sensitivity and 67–70% specificity for the diagnosis of labral tears (Schydlowsky et al. 1998b; Hammar et al. 2001; Rasmussen 2004). Nevertheless, even using high-end transducers, the anterior capsular complex (capsule and inferior glenohumeral ligament) cannot be distinguished clearly from the anterior labrum. Although some attempts have been made to assess the capsular tightness during dynamic scanning, US seems unable to reliably identify the discontinuity of the anterior capsuloligamentous complex in cases of traumatic avulsion of the capsule from its glenoid insertion, so-called capsular stripping or shearing. In contrast, fragmentation of the anteroinferior rim of the glenoid, representing a Bankart lesion, may occasionally be identified with US as a V-shaped bony defect over the anterior aspect of the glenoid (Hammar et al. 2001). Overall, we believe that US has a intrinsic limitations in the evaluation of the fibrocartilaginous glenoid labrum. It may exclude labral tears when the labrum appears normal. In suspected abnormalities, MR and CT arthrography are the most reliable and specific technique to confirm a labrum tear by depicting contrast material extending into the labral defect.
A scanning technique for documenting the presence, direction and extent of glenohumeral translation has been described in patients with voluntary posterior shoulder subluxation or dislocation (Bianchi et al. 1994). Although rare, this condition is often unrecognized clinically and may be misdiagnosed as a frozen shoulder. In this technique, the examiner stands behind the patient and acquires transverse images over the posterior glenohumeral joint. The distance between the dorsal bony glenoid and the tip of the humeral head is measured at rest and during subluxation. The patient is examined in different positions (neutral, 90° flexion, abduction and external rotation), including the one in which he/she perceives the shoulder has become subluxed. The measured distances are compared between the affected shoulder and the healthy one: distances between 12 and 18 mm are indicative of subluxation (Fig. 128). It is important, however, to point out that assessment of associated intra-articular lesions essentially depends on the use of contrast-based imaging modalities (CT arthrography and MR arthrography). In posterior shoulder dislocation, the relationship of the coracoid (anterior approach) or the posterior glenoid surface (posterior approach) with the dislocated humeral head can be assessed and the distances between these structures are measured without the need of painful rotation or abduction of the arm using both anterior and posterior approaches (Fig. 129) (Hunter et al. 1998; Bize et al. 2003).
The distances measured in the affected shoulder are compared with those in the contralateral shoulder (care should be taken not to misdiagnose a bilateral dislocation) and a difference greater than 20 mm indicates dislocation (Bianchi et al. 1994). Quantitative measurements performed during dynamic US scanning have also been suggested for measuring increased laxity in patients with anterior and multidirectional shoulder instability (Jerosch et al. 1989; Krarup et al. 1999) as well as for assessing anterior and posterior glenohumeral translation in a selected series of swimmers (Borsa et al. 2005b) and professional baseball pitchers (Borsa et al. 2005c). Based on these studies, dynamic US seems to be a promising means for measuring glenohumeral joint laxity, replacing stress radiography for this purpose (Borsa et al. 2005a).
A variety of surgical procedures, both open and arthroscopic, can be used to repair the capsulolabral complex and to thicken and tighten the glenohumeral ligaments in patients with post-traumatic glenohumeral join instability (Mohana-Borges et al. 2004). Detailed description of these procedures is beyond the scope of this chapter. In the postoperative setting for glenohumeral instability, however, suture materials and anchors used for fixation along the capsuloligamentous complex can be visualized with US (Fig. 130).
53. HUMERAL HEAD FRACTURES
Despite its limitations in assessing bones, US can accurately detect the humeral head injuries which accompany glenohumeral joint instability, including the Hill-Sachs and McLaughlin fractures and avulsions of the tuberosities. The Hill-Sachs lesion is a depressed intra-articular compression fracture located on the posterolateral aspect of the humeral head typically observed after episodes of anterior glenohumeral dislocations. It can be regarded as a hallmark of anterior glenohumeral joint dislocation because it occurs in up to 47% of patients after the first episode of dislocation and up to 100% in patients with recurrent disease (Resnick et al. 1997). The pathomechanism of Hill-Sachs fracture consists of a powerful contraction of the para-articular muscles that pull the humeral head against the anteroinferior glenoid rim (Calandra et al. 1989; Resnick et al. 1997). The size and location of the fracture must be evaluated because a large defect can facilitate new episodes of dislocation. US has a reported sensitivity of 91–100%, specificity of 89–100% and overall accuracy of 84–94% in detecting this lesion (Farin et al. 1996a; Pancione et al. 1997; Cicak et al. 1998). For this purpose, the posterolateral aspect of the shoulder is examined with the transducer in transverse planes. Deep to the infraspinatus tendon, the humeral head at this level should have a smooth, curvilinear surface. The Hill-Sachs lesion typically appears as a wedge-shaped shallow defect of the hyperechoic bony contour of the humeral head at the point where the anterior portion of the infraspinatus inserts into the greater tuberosity (Jerosch et al. 1990) (Fig. 131).
Its size and shape can be accurately assessed with US. Dynamic examination with back and forth rotation makes it possible to judge whether the lesion reaches the glenoid cavity during movement and the extent to which the motion of the limb is hindered. It is important to avoid confusion between the smaller and superficial erosions that occur commonly in rotator cuff tendinopathy and a true Hill-Sachs lesion. Usually, the latter makes contact with the dorsal glenoid rim at 10–20° of external rotation. Also, care should be taken, at least by the beginner, not to misinterpret the normal depression of the humeral neck (bare area) located on a more caudal plane for a Hill-Sachs fracture (Bouffard et al. 2000). Similarly, in the setting of posterior shoulder dislocation, a fracture of the anterior portion of the humeral head may occur as a result of its impaction against the posterior aspect of the glenoid rim. This lesion is commonly referred to as “reversed Hill-Sachs lesion” or McLaughlin fracture. In these patients, anteroposterior standard radiographs reveal two parallel lines of cortical bone the medial aspect of the humeral head, the lateral one corresponding to the margin of the anterior impaction fracture. This line, which is known as the “trough line,” is created when the anterior aspect of the humeral head strikes the posterior glenoid rim during the dislocation. The diagnosis of posterior glenohumeral joint dislocation is often delayed and this fracture may be radiographically unsuspected unless additional projections (i.e., axillary view) are performed. US can demonstrate the reversed Hill-Sachs lesion as a bone defect on the anterior aspect of the humeral head located medial to the lesser tuberosity and deep to the subscapularis tendon (Fig. 132). This lesion should be searched with the patient’s arm in external rotation because in neutral position the fracture can be masked by the coracoid.
Avulsion lesions of the tuberosities can also be encountered in shoulder instability. Greater tuberosity fractures are the commonest and derive from an excessive pulling force exerted by the supraspinatus on its bony insertion. The examiner must be aware that these fractures can also be secondary to a direct blow on the shoulder and that they are often missed on standard radiographs. Therefore, in a post-traumatic setting, US examination of the shoulder must include a careful search of bone irregularities in the greater tuberosity, even in the presence of previous normal radiographs. When undisplaced, these fractures appear as a double discontinuity of the cortical bone located at the notch between the humeral head and the greater tuberosity (humeral neck) and over the external slope of the greater tuberosity, often at the junction of the humeral shaft and the anatomic neck of the humerus, suggesting an elevated fragment (Fig. 133) (Patten 1992). In displaced fractures, the uplifted fragment may be angled or overlapping, and the supraspinatus tendon in continuity with it appears abnormally thickened and heterogeneous due to edema and contusion (Fig. 134). In these cases, visualization of a well-demarcated defect on the surface of the greater tuberosity can avoid misdiagnoses with calcifying tendinitis. Avulsion fractures of the lesser tuberosity can also be found in posterior shoulder dislocations as a result of subscapularis traction (Fig. 135) (Ross et al. 1989; Martinoli et al. 2003). Once a possible fracture of the tuberosities is found, additional radiographic views, particularly under fluoroscopic control, must be obtained to confirm the US findings.
54. DEGENERATIVE ARTHROPATHIES AND LOOSE BODIES
Degenerative osteoarthritis of the glenohumeral joint may be idiopathic or secondary to a longstanding massive tear of the rotator cuff. Although plain films are the mainstay for the diagnosis, the examiner should become familiar with the US appearance of shoulder osteoarthritis in order to recognize this condition even in absence of a previous radiographic study. Main US findings include narrowing of the joint space, osteophytes and intra-articular loose bodies. Humeral osteophytes are more prominent form a sort of “crown” around the cartilage-bone junction (humeral neck), whereas glenoid osteophytes are less conspicuous and more difficult to be identified. At US, they appear as hyperechoic bony spurs arising from the joint surface which are typically covered by a thin hypoechoic rim of cartilage (Fig. 136). Intra-articular effusion and, in more severe cases, reactive synovial hypertrophy can be detected.
Intra-articular loose bodies are the end result of progressive disintegration of the articular cartilage and subchondral bone which leads to release of fragments within the joint cavity. While bony fragments are avascular and undergo necrosis, cartilaginous fragments can increase in size because they are nourished by synovial fluid. Loose bodies usually remain entrapped in the most dependent portions of the glenohumeral joint, including the axillary pouch, the biceps tendon sheath, the posterior glenohumeral recess and some bursal recesses (i.e., lateral, subcoracoid bursa) which communicate with the joint cavity as a result of a rotator cuff tear (Fig. 137). Most intra-articular loose bodies appear as hyperechoic images with posterior acoustic shadowing (Fig. 138).
In some cases, however, a layer of hypoechoic cartilage may be identified over the echogenic interface corresponding to the subchondral bone (Bianchi and Martinoli 1999). The size and position of the fragments can be reliably determined with US. Their exact number, in contrast, cannot be established with certainty. Estimating the size of loose bodies is important before planning arthroscopic surgery because fragments that are too large cannot be removed arthroscopically and may make the procedure difficult and time-consuming. However, such an assessment may also be problematic using standard radiographs, because the unossified portion of the fragment leads to an underestimation of its actual size. Differentiation between loose bodies secondary to osteoarthritis, trauma and osteochondromatosis is mainly based on clinical and radiographic findings. In general, US detection of innumerable loose bodies of nearly equal size without joint space narrowing more likely reflects osteochondromatosis, whereas identification of a single fragment or a few fragments of different size and appearance is more likely associated with an osteoarthritis-related process or a posttraumatic nature (Campeau and Lewis 1998). In idiopathic synovial osteochondromatosis, the age range of the affected patients is wide but, in most cases, disease onset occurs in the fourth or fifth decades. Men are affected more frequently than women. At US, different patterns may be noted depending on whether the loose bodies contain cartilage alone, cartilage and bone or mature bone (Fig. 139a,b). When entirely cartilaginous (synovial chondromatosis), the intra-articular nodules are hypoanechoic and difficult to distinguish from surrounding effusion. Furthermore, cartilage-containing masses of synovial chondromatosis may be difficult to differentiate from “rice bodies,” which are seen in patients with chronic rheumatoid arthritis or tuberculosis (Mutlu et al. 2004). At US, rice bodies may appear as hypoanechoic spherules a few millimeters in size (Fig. 139c,d).
They may fill the subdeltoid bursa and, in most cases, are distinguished with difficulty from the adjacent hypoechoic synovial pannus due to similar echogenicity. The pathogenesis of rice bodies is different from that of loose bodies. In the late stages of rheumatoid arthritis, rice bodies seem to derive from chronic articular inflammation leading to formation of elongated synovial villi which then become covered by fibrin and may snap off, producing fibrin grains similar to polished rice (Law et al. 1998; Reid et al. 1998). With increasing age, rice bodies undergo a degree of organization and may contain a core of mature collagen. Identification of rice bodies is clinically relevant as they are a persistent reason for continuing synovial inflammation. Their removal is usually associated with clinical improvement (Propert et al. 1982).
Among the degenerative arthropathies that typically involve the shoulder, there are a variety of conditions related to crystal deposition diseases, including renal osteodystrophy, milk-alkali syndrome, hypervitaminosis D and the so-called “Milwaukee shoulder syndrome”. This last condition, which is also known as apatite-associated destructive arthritis, hemorrhagic shoulder or rapid destructive arthritis of the shoulder, consists of massive rotator cuff tear, osteoarthritic changes, blood-stained noninflammatory joint effusion containing calcium hydroxyapatite and calcium pyrophosphate dihydrate crystals, synovial hyperplasia and extensive destruction of cartilage and subchondral bone (Llauger et al. 2000). Osteophytes are not characteristic of Milwaukee syndrome. This destructive arthropathy most commonly affects elderly patients, predominantly women, and manifests clinically as a rapid progressive and destructive arthritis of the shoulder with localized pain, swelling, variable limitation of joint motion and joint instability. Occasionally, there is rupture of the shoulder capsule with drainage of blood-stained fluid into the para-articular soft tissues lasting for weeks or months (Fig. 140).
Radiographically, this condition resembles a neuropathy-like arthropathy with high-riding humeral head. Pseudoarthrosis between the humeral head, the coracoid and the acromion is commonly seen (Nguyen 1996). Although US is able to demonstrate a marked distension of the joint space by effusion and echogenic debris reflecting synovial proliferation and blood clots, calcified deposits, destruction of the cartilage and osteolysis of the subchondral bone, it is not reliable for differentiating this disorder from the more common osteoarthritis related to rotator cuff disease. Therapy includes analgesic drugs and repeated arthrocentesis followed by intra-articular steroid administration. In advanced disease, shoulder arthroplasty may be considered. In patients with chondrocalcinosis, US can depict deposition of pyrophosphate crystals in the cartilage of the humeral head (Peetrons et al. 2001). These deposits appear as a blurry hyperechoic line on the outer margin of the cartilage surface (Fig. 141).
Grossly echogenic thickening of the synovium, especially prominent in the subacromial subdeltoid bursa, para-articular nodules within the soft tissues surrounding the cuff and deep bony erosions may be observed in dialysis-related shoulder arthropathy reflecting amyloid deposition of ß2-microglobulin, which is an amyloid protein that is not filtered by standard dialysis membranes (Kay et al. 1992; Sommer et al. 2002; Cardinal et al. 1996; Llauger et al. 2000; Slavotinek et al. 2000). US features of shoulder amyloidosis are varied and may include a heterogeneous and thickened rotator cuff, especially involving the supraspinatus and the subscapularis tendons (McMahon et al. 1991; Malghem et al. 1996). Based on these findings, US offers an early diagnosis and should be a useful tool to follow up the disease. In these patients, para-articular calcifications are often observed as a result of calciumphosphorus imbalance.
55. INFLAMMATORY ARTHROPATHIES
As a result of a widespread involvement of synovial tissues, rheumatoid arthritis usually affects the glenohumeral joint in association with the acromioclavicular joint and the synovial bursae around the shoulder. Radiographically, rheumatoid arthritis may cause uniform narrowing of the joint space, marginal erosions, erosions of the greater tuberosity, osteophytes, flattening of the glenoid cavity and sclerosis of apposing surfaces of the glenoid and humerus and pseudowidening of the acromioclavicular joint related to reabsorption of the distal end of the clavicle (Fig. 142a). US has proved able to reveal synovitis both at the early stages of disease, when no radiographic changes are yet evident (Alasaarela and Alasaarela 1994; Chhem 1994; Alasaarela et al. 1997; Gibbon and Wakefield 1999), and in an asymptomatic population with arthritic shoulder (Naranjo et al. 2002). This technique is used for the evaluation of shoulder girdle arthritis in an attempt to assess which synovial cavity is involved by the inflammatory process, to differentiate between effusion and synovial pannus and evaluate the extent of such involvement, as well as to detect subtle bone erosions that cannot be imaged on standard radiographs (Fig. 142b) (Speed and Hazleman 1999). In a selected group of patients with symptomatic disease, US assessment of synovitis has demonstrated subacromial subdeltoid bursitis as the most common finding, occurring in up to 69% of cases, followed by glenohumeral joint involvement in 58% and biceps tendinitis in 57% (Alasaarela et al. 1998a).
Overall, no correlation exists between these findings and either the duration or stage of disease. A quantitative assessment of synovitis may be attempted by measuring the widest distance between the humeral head and the joint capsule in the axillary pouch and posterior recesses (Alasaarela and Alasaarela 1994; Alasaarela et al. 1998a; Koski 1989, 1991). Difficulties may arise with US when trying to distinguish effusion from the pannus in the posterior recess, because graded compression with the probe is not always able to squeeze the fluid away from this site. In addition, when pressure is applied over the pannus, this can be mobilized similarly to joint fluid. Doppler systems may be helpful to assess the activity of the inflammatory process by showing hyperemic blood flow within the synovial tissue (Alasaarela and Alasaarela 1994). In the biceps tendon sheath, hyperemic flow is detected to a greater extent in rheumatoid arthritis rather than in patients with degenerative disease (Strunk et al. 2003). The reliability of these findings seems, however, too limited for an objective assessment, particularly when Doppler imaging is used as an indicator of the response to therapy. It is possible that US contrast agent will have a role in this field (Wamser et al. 2003). Loss of definition and thinning of the articular cartilage can be demonstrated in advanced disease as well. As regards the bony surfaces, US is able to reveal erosions as well-defined cortical defects filled by hypoechoic pannus: they may be isolated, confluent or generalized (Fig. 142c,d) (Alasaarela et al. 1998b; Gibbon and Wakefield 1999; Hermann et al. 2003). As mentioned earlier, US is useful when obtaining a sample of fluid or synovium because it can identify the ideal puncture site (where the fluid accumulates more or the pannus is thicker) and can provide easy guidance for directing the needle. The intra-articular injection of corticosteroids or the lidocaine test can be performed under US guidance, thereby avoiding the risks of inadvertent intratendinous steroid injection or para-articular injections of anesthetic. In these circumstances, the procedure of needle placement is more accurate and less painful under US guidance than when performed blindly. The structures involved by the inflammatory process in polymyalgia rheumatica have also been investigated using US (Lange et al. 1998; Koski 1992; Cantini et al. 2001). Most studies report a frequency of bursitis (14–16%) lower than that of glenohumeral joint synovitis (57–66%) in this disease (Lange et al. 1998; Koski 1992).
56. SHOULDER ARTHROPLASTY
Glenohumeral joint arthroplasty has become the procedure of choice to treat patients with pain and articular damage who do not respond to conservative therapy. Regardless of the underlying disease (e.g., osteoarthritis, rheumatoid arthritis, rotator cuff arthropathy, avascular necrosis, proximal humeral fractures), the procedure is performed to relieve pain and improve the range of shoulder motion. The prosthesis is composed of a metallic stem with a modular humeral head that articulates either with the native glenoid (shoulder hemiarthroplasty) or with a poly-ethylene or metal glenoid component (total shoulder arthroplasty) (Taljanovic et al. 2003). Reverse shoulder prostheses are also obtained by reversing the position of the ball (implanted on the glenoid) and the socket (implanted on the humeral head). Many types of devices are available. Criteria for selection of a given type depend on the patient’s condition, the surgeon’s preference and the surgeon’s experience, and are beyond the scope of this chapter. The main complications with shoulder arthroplasty are loosening, superior migration, subluxation or dislocation of the humeral head and postoperative rotator cuff tear. After shoulder arthroplasty, MR imaging is of limited value owing to the artifact created by the metallic implant. US has proved able to provide information about the para-articular soft tissues and the rotator cuff after shoulder arthroplasty, especially in cases of poor postoperative outcome and absence of radiographic signs of loosening and migration (Westhoff et al. 2002; Sofka and Adler 2003). In this setting, the metallic hardware of the humeral component of the prosthesis is readily demonstrated, enabling one to recognize the following landmarks arranged in series: acromion, humeral component, greater tuberosity (Sofka and Adler 2003). The prosthesis itself does not hinder examination of the rotator cuff. Its metallic component appears as a linear echogenic interface with moderate posterior reverberation artifact. The examiner should remember that moderate to severe regional muscle atrophy – often involving the deltoid and the teres minor – is frequently encountered in patients who have undergone shoulder replacement and that the subscapularis tendon (but not the supraspinatus) has often been taken off the lesser tuberosity to allow surgical access (deltopectoral approach). After placement of the prosthesis, the subscapularis tendon is usually reinserted more medially, at the site of humeral head resection rather than at the anatomic insertion site: however, this tendon may retear leading to an anteriorly unstable shoulder. In general, preservation of the rotator cuff tendons in these patients correlates with a good clinical outcome. In patients with loosening of the cup, dynamic examination can depict some degree of instability of the metallic hardware relative to the bony humerus (Fig. 143).
57. SEPTIC ARTHRITIS AND BURSITIS
Septic arthritis of the glenohumeral joint has predilection for very young infants or elderly patients with chronic debilitating disorders, such as diabetes, cirrhosis and alcoholism. The intra-articular injection of corticosteroids greatly increases the likelihood of infectious disease because of steroid-induced reduction in the host defences. In addition, septic arthritis may derive from accidental introduction of bacteria during nonsterile arthrocentesis procedures. Although US is a sensitive means for detection of even small glenohumeral joint effusions, US imaging findings usually do not allow the conclusive differentiation of a noninfected joint effusion from septic arthritis (Cardinal et al. 2001). Definitive diagnosis requires analysis of the fluid, possibly aspirated under US guidance, and must be performed in every patient in whom the likelihood of infection is present. As described in Chapter 18, large-bore (16–18 gauge) needles are ideal for this purpose, because purulent material can be too thick and viscous to be aspirated with a small needle. Although the most adequate puncture site may vary among patients, the posterior approach is usually preferred. Using this access, the needle should be inserted at mid-glenohumeral level and directed into the posterior recess through the infraspinatus. Septic arthritis is usually not associated with bursal infection unless a full-thickness tear of the rotator cuff is present and allows free communication between these two spaces. Nevertheless, the two entities may overlap and clinical differentiation may be difficult. At US examination, an infected subacromial subdeltoid bursa may appear distended by a complex effusion containing debris and septations (Fig. 144a) (Cardinal et al. 2001; Lombardi et al. 1992; Rutten et al. 1998). The bursal walls may be thickened and peribursal hypoechoic strands reflecting edema in the surrounding soft tissues may be associated findings (Fig. 144b).
Although color and power Doppler imaging may show hyperemic flow in the synovial walls and around the bursa, this is not regarded as a specific sign of infectious disease. When the joint recesses are free of fluid, US is a reliable means to obtain a correct diagnosis of isolated bursal involvement, thus avoiding arthrocentesis procedures with their potential complications (Lombardi et al. 1992). During aspiration of the infected bursa, US guidance may avoid inadvertent contamination of the underlying sterile joint by traversing the infected bursa with the needle. In sepsis of the acromioclavicular joint (Blankstein et al. 1985), US is a useful modality to exclude the involvement of the adjacent subacromial subdeltoid bursa and glenohumeral joint. Main US findings include superior bulging of the joint capsule, widening of the joint space with erosions of the bony edges and debris moving freely within the joint space (Widman et al. 2001). Although aspiration of the infected joint can be performed blindly, US allows this procedure to be carried out more confidently.
58. ACROMIOCLAVICULAR JOINT TRAUMA AND INSTABILITY
Subluxation or dislocation of the acromioclavicular joint may be a source of shoulder pain which is often mistaken for a post-traumatic rotator cuff lesion because of the close proximity of this joint with the rotator cuff tendons. US is more sensitive than standard radiographs in detecting low-grade sprains of the acromioclavicular joint. These lesions appear as widening of the joint cavity, distended by hematoma or effusion, and bulging of the superior capsule and ligament (Fig. 145). When the acromioclavicular joint is more severely injured with rupture of the coracoclavicular ligaments, an upward displacement of the distal end of the clavicle can be appreciated (Fig. 146). Although direct imaging of the coracoclavicular ligaments is not feasible with US because of the overlying clavicle, a hematoma in the soft tissues between the clavicle and the coracoid may be regarded as an indirect sign of injured ligaments.
In addition, measurement of the coracoclavicular distance using anterior sagittal scans may increase confidence in the diagnosis (Sluming, 1995). In severe dislocations with gross displacement of the clavicle, disruption of the muscular insertion of the deltoid and/or the trapezius with a hematoma developing anteriorly (deltoid lesion) or posteriorly (trapezius lesion) to the cranial edge of the clavicle can also be demonstrated (Heers and Hedtmann 2005). Short-axis planes over the distal clavicle are useful to evaluate the common fascia of both muscles in order to avoid injuries being missed (Heers and Hedtmann 2005). These structures are important stabilizers of the acromioclavicular joint. Although US is not routinely used as the screening modality for acromioclavicular joint separation, some attempts have been made to correlate US findings in acute and chronic unstable acromioclavicular joints of varying severity with the radiographic scale described by Tossy (Tossy et al. 1963) and the Rockwood (Rockwood 1984) classification. At US, the width of the joint is measured using a coronal approach and compared with the contralateral side. Theoretically, measurements are best obtained with the patient’s arms hanging down and holding a 10 kg weight in each hand to increase stress on the capsuloligamentous structures and allow identification of subtle changes. Since variants can exist in the joint width among normal subjects, the measure must be related to the normal uninjured side. An index is then calculated by dividing the acromioclavicular joint width on the affected side by that on the normal side. In normal subjects, the acromioclavicular joint width should be no wider than 6 mm and the acromioclavicular index 1.0; patients with Tossy II instability have a mean acromioclavicular joint width of 10.2 mm on the injured side and an acromioclavicular index of 0.5; patients with Tossy III instability and indication for surgery have a mean acromioclavicular joint width of 22.3 mm on the injured side and an acromioclavicular index of less than 0.25 (Kock et al. 1996). As defined by Rockwood (Rockwood 1984), Tossy III type injury can be further subdivided depending on posterior displacement of the clavicle (type IV), marked increase in the coracoclavicular distance by 2 or 3 times and the scapula displaced inferiorly (type V) and dislocation of the clavicle inferior to the acromion or the coracoid (type VI). Although coracoid process fractures may be secondary to anterior shoulder dislocation, they most frequently occur in association with type III acromioclavicular joint dislocations (Ogawa et al. 1997). The mechanism of these rare fractures seems related to the occurrence of direct trauma to the shoulder girdle and sudden strong pull of the short head of the biceps and the coracobrachialis inserting at the coracoid process, leading to an avulsion (Fig. 147). In most cases, conservative treatment is appropriate. In the case of large avulsed fragments or persistent pain, open reduction is advised with coracoid screw and acromioclavicular fixation.
Post-traumatic osteolysis of the clavicle is a self-limiting disorder with gradual reparative changes over a period of 4–6 months that may occur several weeks up to several years after acromioclavicular trauma (Dardani et al. 2000). The key to diagnosis is the fact that changes occur only at the clavicular end while the acromion remains normal. Although the diagnosis is usually based on the patient’s history and radiographic findings, US is able to detect the same abnormalities seen on plain films. At US, the clavicular tip exhibits irregular cortical erosions associated with joint space widening, joint effusion and soft-tissue swelling, whereas the acromion remains intact (Fig. 148). Post-traumatic osteolysis of the clavicle should be considered in the differential diagnosis when a patient experiences chronic pain or soft-tissue swelling beyond the acute phase of the injury. Care must be taken not to confuse this condition with shortening of the clavicle secondary to resection of the distal end of clavicle, which can be performed to treat acromioclavicular osteoarthritis with secondary impingement, rheumatoid arthritis, ankylosing spondylitis and infection. Both the patient’s history and local inspection allow a reliable differentiation between these conditions.
59. STERNOCLAVICULAR AND COSTOSTERNAL JOINT PATHOLOGY
Injuries to the sternoclavicular joint are uncommon given the strong ligamentous support of this joint. Traumatic sternoclavicular instability, including subluxation and dislocation, is always secondary to a well-defined traumatic event. In these patients, disability has a longer duration in cases of posterior dislocation than anterior dislocation, presumably because of coexistent injury to the mediastinal soft tissues posterior to the sternum. US has proved able to identify posterior sternoclavicular dislocation as well as to evaluate its reduction in the operating room (Benson et al. 1991; Pollock et al. 1996). In addition to traumatic injuries, other atraumatic conditions affecting the sternoclavicular joint are amenable to US examination, including degenerative osteoarthritis (Hiramuro-Shoji et al. 2003). Similar to that observed in the acromioclavicular joint, degenerative osteoarthritis of the sternoclavicular joint is characterized by narrowing of the joint space, osteophytes and para-articular cysts (Fig. 149a,b). This condition usually affects the dominant arm of women between the ages of 40 and 60 years. Previous neck surgery with spinal accessory nerve lesion is also claimed as a predisposing factor, as it causes downward and forward drop of the shoulder leading to additional stress on the sternoclavicular joint (Hiramuro-Shoji et al. 2003). In rheumatoid arthritis, sternoclavicular joint involvement shows irregularities of the osseous surfaces with osteolysis of the medial end of the clavicle and synovial inflammation (Fig. 149c,d). Tietze’s syndrome, which is also referred to as costosternal syndrome or anterior chest wall syndrome, is a benign, self-limiting condition characterized by swelling of the costal cartilages and gradual onset of pain in the anterior chest wall exacerbated by coughing and sneezing. US is able to reveal an increased volume of the costal cartilages with irregular calcifications and perichondral soft-tissue swelling in clinically and radiographically apparently normal costochondral joints of patients with anterior chest pain (Choi et al. 1995; Kamel and Kotob 1997). In these patients, US has been proposed as a means to guide local steroid injection for treatment (Kamel and Kotob 1997).
60. QUADRILATERAL SPACE SYNDROME
In neuropathies around the shoulder, the small size of nerves, the complex regional anatomy and problems of access due to the acoustic shadowing from superficial bone structures, makes direct evaluation of nerves difficult with US. Axillary neuropathy may be caused by stretching injuries (anterior dislocation) or extrinsic compression in the quadrilateral space caused by fractures of the upper humerus, improper use of crutches, casts, fibrous bands and inferior (from the 9 to 7o’clock positions) paraglenoid cysts (Linker et al. 1993; Chautems et al. 2000; Tung et al. 2000). Static (fibrous bands, occlusion of the posterior circumflex artery, muscle hypertrophy) and dynamic (nerve stretching in some arm positions, such as occur in throwing athletes at the extremes of joint motion) traction and compression on the axillary nerve seem play a role in this syndrome (Perlmutter 1999). Iatrogenic damage during arthroscopic procedures around the coracoid or by posterior surgical arthroscopic portals has also been reported outside the quadrilateral space (Lo et al. 2004). When the entrapment of the axillary nerve occurs in the quadrilateral space, there is selective denervation of the teres minor muscle because the anterior branch of the nerve (supplying the deltoid) is spared. Clinically, axillary neuropathy is often found as an occasional finding during an examination of the shoulder for other symptomatic abnormalities. This would suggest that the disease may exist in an asymptomatic or sub-clinical entity (Sofka et al. 2004b; Cothran and Helms 2005). When symptomatic, it is associated with vague, often nonspecific, posterior shoulder pain, paresthesias over the external aspect of the shoulder and weakness exacerbated by abduction and external rotation of the arm. Because the teres minor is the only muscle involved, this condition can be difficult to recognize on the basis of clinical grounds alone, because the action of the teres minor cannot be clearly separated from the contribute of the infraspinatus. Even without any detectable soft-tissue abnormality along the course of the nerve, the diagnosis of axillary neuropathy is based on the evidence of volume loss and hyperechoic changes of the involved muscles in the absence of a tendon tear (Martinoli et al. 2003). These signs are particularly suggestive given that teres minor tendon disruptions are extremely rare, even in cases with massive rotator cuff tears. At US, the atrophy of the teres minor is best assessed by comparing the appearance of this muscle with that of the adjacent infraspinatus on sagittal scans (Fig. 150). On the other hand, atrophy of the deltoid can be revealed by a reduced thickness of this muscle relative to the contralateral one on coronal scans (Fig. 151). In addition, US is able to demonstrate any possible space-occupying lesion in the quadrilateral space, such as paralabral cysts extending off the inferior aspect of the glenoid in association with a tear of the inferior labrum (Sanders and Tirman 1999; Robinson et al. 2000). The main differential diagnosis of quadrilateral space syndrome is the Parsonage-Turner syndrome, in which the involvement of muscles usually relates to more than one nerve distribution.
61. SUPRASCAPULAR NERVE SYNDROME
Suprascapular neuropathy is an unusual syndrome leading to chronic shoulder pain and weakness (Fehrman et al. 1995). This condition may be secondary to a constriction of the suprascapular nerve at the suprascapular notch or at the spinoglenoid notch as a result of a variety of condition, including stretching injuries, ligament abnormalities, overuse or space-occupying lesions. From the pathophysiologic point of view, if the suprascapular nerve is entrapped at the supraspinous notch, both supraspinatus and infraspinatus muscles undergo denervation changes; if it is compressed at the spinoglenoid notch, denervation is limited to the infraspinatus muscle whereas the supraspinatus is spared. Because the suprascapular nerve is a purely motor nerve, there is no sensory loss. Paralabral cysts are the leading cause of suprascapular neuropathy (Takagishi et al. 1991; Bousquet et al. 1996; Bredella et al. 1999; Tung et al. 2000; Weiss and Imhoff 2000; Ludig et al. 2001; O’Connor et al. 2003). Two possible theories have been hypothesized to explain the origin of these cysts. The first assumes that they are secondary to tears of the glenoid labrum allow- ing the joint fluid to extrude into the periarticular tissues; the second suggests that they would arise from areas of myxoid degeneration of para-articular structures following labral tears, a pathogenesis somewhat similar to that of other ganglion cysts. In the shoulder, paralabral cysts are usually associated with tears of the superior and posterior glenoid labrum (from the 8 to 11 o’clock positions), as a result of a SLAP lesion or posterior instability, respectively. Only rarely they extend off the anterior and inferior aspect of the glenoid. Once developed, paralabral cysts can show a progressive enlargement due to a one-way valve mechanism leading to the passage of the joint fluid into the cyst through a thin pedicle (Fig. 152a,b). During their expansion, they spread into the spinoglenoid notch, the suprascapular notch, or both notches of the scapula lying deep to the myotendinous junction of either the supraspinatus or the infraspinatus, and may or may not cause nerve entrapment and muscle denervation (Fig. 152c) (Tung et al. 2000). US can easily recognize secondary changes of nerve damage, including loss in bulk and increased reflectivity of the innervated muscles due to edema and fatty replacement (Figs. 153, 154).
A correlation was found between the size of paralabral cysts and the onset of denervation symptoms, significantly more muscle denervation occurring with larger cysts (volume 6.0 cm3; diameter 3.1 cm) compared with all other paralabral cysts (volume 2.2 cm3) (Tung et al. 2000). A careful scanning technique is recommended for imaging the posterior shoulder, starting with near-field settings to examine the rotator cuff tendons and then adjusting both the focal zone and image magnification to the far-field in order to explore the scapular notches (Martinoli et al. 2003). In fact, even large cysts could be easily missed while performing a standard US examination of the shoulder due to their deep location, far from the rotator cuff tendons. In many cases, spinoglenoid cysts develop in the most cranial portion of the notch, in close proximity to the scapular spine. Placing the hand on the opposite shoulder during scanning may be helpful to decrease the depth of the posterior fossa and to make this area more readily examined with US. US demonstrates paralabral cysts as rounded or oval hypoechoic lesions with well-defined margins, relatively fixed in location and shape during active and passive shoulder movements (Hashimoto et al. 1994; Bouffard et al. 2000; Martinoli et al. 2003). The continuity of the cyst with a defect in the posterior labrum can be revealed with US. A mass effect on the adjacent tendon and muscle is often demonstrated as well. Then, a careful evaluation of rotator cuff tendons should be carried out to exclude a possible tendon rupture as the cause of the muscle atrophy. The main differential diagnosis of paralabral cysts includes varicosities in the spinoglenoid notch (Carroll et al. 2003). Although enlarged spinoglenoid notch veins appear as hypoechoic round or oval images mimicking a cyst, they are not stationary and change shape and size during shoulder movements (an increased venous size is typically appreciated while the arm is in external rotation, whereas these vessels tend to collapse in internal rotation) (Fig. 155).
On the other hand, Doppler imaging does not demonstrate flow signals within these veins because the flow velocities are too low. In recent papers, the association of vascular abnormalities in the spinoglenoid notch area with suprascapular neuropathy has been described (Bredella et al. 1999; Ludig et al. 2001; Carroll et al. 2003). In these cases, it is not still clear whether the dilated venous plexus and the compressed nerve are a separate expression of a narrow suprascapular tunnel or whether the varicosities themselves may lead to nerve impingement. In cases of suprascapular neuropathy caused by paralabral cysts, percutaneous needle aspiration of the cyst can be attempted under US guidance (Hashimoto et al. 1994; Chiou et al. 1999). The procedure has three main goals: to confirm the diagnosis by showing a viscous mucoid content; to drain the fluid as much as possible to reduce the internal pressure of the cyst; and to disrupt the cystic wall with repeated to-and-fro movements of the needle tip to avoid recurrence. Although this procedure is not definitive, marked improvement or relief of patients’ symptoms has been reported in up to 86% of cases (Chiou et al. 1999). The real efficacy of an addition of steroids within the cyst after aspiration is unknown and can increase the risk of local infection.
62. THORACIC OUTLET AND BRACHIAL PLEXUS PATHOLOGY
Generally speaking, the clinically relevant structures of the thoracic outlet region are the brachial plexus nerves, the subclavian artery and the subclavian vein. The causes of brachial plexopathy include trauma, intrinsic and extrinsic tumors, radiation plexopathy and Parsonage-Turner syndrome. The neurovascular structures of the thoracic outlet can also be involved by compressive lesions due to congenital or acquired changes in the surrounding fibro-osseous and fibromuscular structures, leading to the thoracic outlet compression syndrome.
63. BRACHIAL PLEXUS TRAUMA
Brachial plexus traumas account for more than half the cases of brachial plexopathies. The nerve damage is usually caused by trauma mechanisms that cause simultaneous traction of the arm and throwing of the head to the opposite shoulder, as most often occurs in the adult population during a motorcycle accident. Different types of histopathologic lesions may occur depending on where the stretching injury takes place. Preganglionic injuries derive from avulsion of the nerve rootlets from the spinal cord or from nerve root avulsion at the level of neural foramina (Fig. 156a,b). In the case of nerve root avulsions, pseudomeningoceles may occur as a result of breakage of the dura and arachnoid membranes and extravasation of cerebrospinal fluid outside the neural foramen (Fig. 156b). These lesions are characterized by the worst prognosis because surgical reconnection of the nerve rootlets with the spinal cord is not feasible. Since preganglionic injuries are located inside the spinal canal, they are not visible with US and require MR imaging for their depiction. On the other hand, postganglionic injuries are almost invariably associated with disrupted nerves and traumatic neuromas in the interscalene triangle or in the area between the interscalene triangle and the costoclavicular space (Fig. 156c). Neuromas may derive from either injury of a trunk, the upper one (C5–C6 level) being most commonly affected, or avulsion and retraction of nerve roots outside the spine (Fig. 156d). In both cases, the location of neuromas is almost invariably at the level of the scalene muscles.
In preganglionic injuries, pseudomeningoceles can be appreciated as hypoanechoic collections located in proximity to the intervertebral foramina instead of the nerve roots. In our experience, however, US seems less sensitive than MR imaging for detecting them. At least in part, this could be explained by the fact that these collections are not extruded so far outside the neural foramina. In addition, avulsed frayed roots without pseudomeningoceles can have a very similar US appearance. The examiner must also be aware that nerve root avulsions can occur without traumatic pseudomeningoceles and that traumatic pseudomeningoceles can exist in the absence of nerve root avulsions (Ochi et al. 1994). In postganglionic injuries, three main types of US findings can be detected: disruption of nerve continuity of one or more roots and trunks, possibly associated with swelling of the proximal and distal stumps and a “wavy” course of the retracted distal segment; irregular scar tissue encasing one or more nerves; segmental fusiform thickening of the roots and trunks of the plexus representing traumatic neuromas (Fig. 157) (Shafighi et al. 2003; Graif et al. 2004). These latter lesions consist of a mass of scar tissue and retracted nervous tissue in continuity with the nerves and can be regarded as a real marker of disease. They may derive from a partial or complete injury of a root or a trunk outside the spine and typically occur in relation to the inter- scalene triangle. Often, they bulge over the lateral margins of the scalene muscles. As regards the best scanning technique to image them, long-axis planes over the affected nerves are not so easy to perform due to the oblique course of the nerves. We therefore recommend the use of short-axis planes (Fig. 158). On these planes, US demonstrates neuromas as hypoechoic masses filling the fat plane between the scalene muscles. They appear isoechoic or slightly hyperechoic compared with the adjacent muscles depending on their different content of fibrous tissue. Remember that difficulties may arise when examining the brachial plexus in the acute setting due to the possible occurrence of diffuse subcutaneous emphysema related to thoracic trauma.
Overall, we believe US is more accurate than MR imaging for establishing the level of involvement, namely whether the upper or the lower plexus are injured, in patients with postganglionic injuries. On the other hand, MR imaging is more sensitive for detecting pseudomeningoceles and lesions occur- ring in the inner spine. In clinical practice, we suggest a combined approach with MR imaging and US to evaluate the traumatized patient, the first technique to evaluate the spine and the foramina, the second to assess the nerves outside the spine. Detection of nerve abnormalities with US may have clinical implications. It may provide an early assessment of the status of the plexus in the immediate phases after the trauma, when clinical findings are not yet conclusive as to whether or not brachial plexus damage requires intervention. In general, patients with total plexopathy have the largest neuromas, as these probably reflect the sum of more than one lesion. On the other hand, patients with small neuromas are usually managed conservatively and show the best functional recovery without surgery.
64. NEOPLASTIC INVOLVEMENT OF THE BRACHIAL PLEXUS
Imaging of brachial plexus tumors should consider two main classes of disorder: metastatic disease and radiation plexopathy, and neurogenic primary tumors. Although many histotypes have been reported to metastasize to the brachial plexus, including breast cancer, bronchogenic carcinoma, lymphoma and squamous cell carcinoma of the head and neck, the nerve involvement in patients with breast cancer is far more common – accounting for approximately 24% of all nontraumatic brachial plexopathies – because one of the major lymphatic drainage routes of the breast is through the apex of the axilla (Wittenberg and Adkins 2000). In some patients, the metastatic tumor appears as a well-defined solid mass usually located in the soft tissues of either the suprascapular or the infraclavicular area (pattern I). It may exhibit irregular margins and a hypoechoic echotexture and can be seen encasing the nerves with an abrupt nerve-to-tumor interface (Fig. 6.159a,b) (Graif et al. 2004). Most often, the neoplasm invades the brachial plexus leading to a segmental thickening and hypoechoic appearance of the involved nerves without causing a clear mass effect (pattern II). The infiltrative spreading of the tumor causes an abnormal fusiform thickening of the nerve (Fig. 159c–e).
Satellite lymph nodes are often associated. Color Doppler imaging can depict intratumoral vessels and may help in depicting displacement and infiltration of the subclavian vessels and distinguishing the infiltrated cords from the adjacent blood vessels. Compared with MR imaging, US seems better able to delineate the tumor tissue and the nerve involvement in the interscalenic and supraclavicular area owing to its higher spatial resolution capabilities. On the other hand, MR imaging has the advantage of a panoramic view with the possibility of delineating both vertebral and pleural involvement. In patients who have received radiation therapy to the axillary region, radiation-induced damage to the brachial plexus nerves is a common cause of brachial plexopathy, accounting for approximately 30% of the cases of nontraumatic plexopathies (Wittenberg and Adkins 2000). The distinction between recurrent or residual disease and radiation-induced neuropathy can be difficult both clinically and on imaging studies. Neurologic damage after radiation therapy may be observed several months to years after treatment. Common symptoms of radiation neuropathy include upper brachial plexus involvement, doses in excess of 60 Gy, a latency period of less than 1 year (peak at 10–20 months), absent pain and lymphedema in the upper limb. On the other hand, neoplastic plexopathy seems more typically associated with symptoms related to the lower plexus nerves, early and severe pain, hand weakness, a dose of less than 60 Gy and a period of latency after completion of radiation therapy of more than 1 year (Wittenberg and Adkins 2000). In radiation fibrosis, US demonstrates diffuse thickening of the nerve fascicles in the absence of a focal mass. Unlike tumor infiltration (see for comparison Fig. 159c,d), the nerve thickening is more uniform and some faint fascicular pattern is preserved (Fig. 160). However, this finding is far from being specific to radiation fibrosis and the differentiation between radiation damage and residual tumor or recurrence can be problematic as the two conditions may coexist (Graif et al. 2004). Postirradiation plexus lesions should be operated on as early as possible to stabilize the clinical course (as soon as paresthesias appear and before the onset of pain). US can provide a useful means to monitor changes in the cross-sectional volume of the affected nerve fascicles over time.
Neurogenic primary tumors of the brachial plexus, including for the most neurofibromas and schwannomas, are far less common than metastatic disorders (Graif et al. 2004). The US characteristics of these tumors are the same as those already described in other locations of the body. The feature of value in distinguishing them from other soft-tissue masses – and especially from enlarged supraclavicular lymph nodes – is demonstration of the continuity between the tumor and the nerve of origin (Fig. 161) (Shafighi et al. 2003).
65. PARSONAGE-TURNER SYNDROME
Parsonage-Turner Syndrome, which is also known as “acute brachial plexus neuritis,” is a rare clinical entity of unknown cause consisting of sudden severe shoulder pain followed by the onset of profound muscle weakness and flaccid paralysis of the shoulder girdle and upper arm. This disorder has a peak rate of incidence between the third and fifth decades and a slight male predominance. Although different factors, including viral infection, trauma, surgery and autoimmunity have been suspected to play a causative role, the etiology of the disease remains unknown. There is usually no loss of
sensation associated with the weakness. Several patterns of weakness are reported, the involvement of the suprascapular nerve being the most common. The most frequent pattern relates to the multiple involvement of the axillary (deltoid and teres minor), suprascapular (supraspinatus and infraspinatus), long thoracic (serratus anterior) and musculocutaneous (coracobrachialis, biceps brachii, brachialis) nerves. Regarding the nerve root involvement pattern, C5 and C6 are the most commonly affected. The prognosis is generally benign, with approximately 75% recovery within 2 years, and treatment is symptomatic (analgesic drug and physical therapy). Electrodiagnostic studies may indicate the complex pattern of muscle involvement. Imaging studies may be helpful to rule out any other local abnormalities, such as rotator cuff tears, shoulder impingement syndrome and calcific tendinitis, thus preventing unnecessary surgery in some patients owing to diagnosis failure (Helms et al. 1998; Helms 2002). At US examination, the affected muscles appear smaller in volume as a result of atrophy and diffusely hyperechoic in relation to denervation edema and fatty infiltration (Fig. 162). Although US is able to confirm the clinical diagnosis, MR imaging seems more reliable for depicting the overall extent of muscle atrophy around the shoulder (Bredella et al. 1999; Helms, 2002).
66. THORACIC OUTLET SYNDROME
Thoracic outlet syndrome is a range of disorders arising from the passage of the subclavian artery and vein and brachial plexus nerves through the three anatomic spaces of the thoracic outlet – the interscalene triangle, the costoclavicular space and the retropectoralis minor space (subcoracoid tunnel) – the narrowing of which can lead to arterial, venous or nervous compression (Demondion et al. 2000). Compression of these neurovascular structures with related onset of symptoms may occur at rest or during dynamic maneuvers, such as during holding the arm overhead and backward (hyperabduction). Typical symptoms include upper limb ischemia, pallor, coolness, fatigability, pain, muscle cramp and pulselessness. In the arterial thoracic outlet syndrome, color Doppler imaging and waveform analysis must be obtained from both subclavian and axillary arteries. These techniques can demonstrate high peak systolic velocities in the subclavian artery at the compression site and diminished or absent blood flow in the axillary artery (or the distal arteries of the arm) with hyperabduction maneuvers (Fig. 163) (Longley et al. 1992). This latter sign actually seems to be more reliable because the vessel stenosis most often occurs at the level of the costoclavicular space as a result of fibro-osseous or fibromuscular abnormalities and, therefore, cannot be directly depicted with US due to problems of access. A rebound increase in velocities on release of abduction can also be noted (Wadhwani et al. 2001). On the other hand, in the venous thoracic outlet syndrome, the patient complains of edema, cyanosis, fatigability and heaviness. In these cases, long-axis planes over the axillary vein can reveal gradual tapering of the vessel lumen in proximity to the clavicle and distal venous dilation (Fig. 164).
This sign can be observed either at rest and with a hyperabduction maneuver or during hyperabduction only. When compression occurs during provocative tests, the lumen becomes more echogenic as a result of blood flow stasis. For the most part, the causes of venous compression are related to fibrous bands or anomalies around the costoclavicular space and, therefore, cannot be delineated with US (Longley et al. 1992). Venous compression, however, must be interpreted very carefully because it is often observed in the asymptomatic population (Demondion et al. 2003a). In addition, care should be taken to exclude a cervical rib or an elongated transverse process of the C7 vertebra, both of which are often associated with fibrous bands. In these patients, tight contact and impingement of the subclavian artery against the tip of the cervical rib can be revealed while performing the postural maneuver. Compression of neural structures with paresthesia, numbness, tingling, progressive weakness and pain can be associated findings (mixed neuroarterial syndrome). However, detection of dynamic nerve compression in this area is difficult with US, either in its isolated form or associated with vascular disease. Overall, we believe that MR imaging has important advantages over US for clearly depicting the different compartments of the thoracic outlet by directly measuring the size of the interscalene triangle, the costoclavicular space and the pectoralis minor space with the arm alongside the body or after a postural maneuver, as well as for demonstrating the location and cause of compression (Demondion et al. 2000, 2003).
67. SHOULDER MASSES
Depending on the age of presentation, up to 60% of benign soft-tissue tumors arising around the shoulder are lipomas (Kransdorf 1995). US detection of superficial lipomas arising in the subcutaneous tissue (Fig. 165a,b), within the fat planes of the axilla or deep in the anterior deltoid muscle (Fig. 165c,d) is generally not a diagnostic problem. In contrast, deep-seated lesions within or among shoulder muscles may be difficult to recognize with US (Fig. 165e-g). In these cases, contact of the mass with the surrounding anatomic structures during certain movements of the arm may lead to symptoms that can mimic a true impingement syndrome. If arising in the region of the neurovascular bundles, lipomas may also cause nerve entrapment, resulting in weakness, pain and numbness. Apart from lipomas, the other soft-tissue tumors arise around the shoulder with a similar incidence as elsewhere in the body. A peculiar tumor-like condition which has a predilection for the shoulder area is elastofibroma dorsi, which is almost invariably located in the inferior part of the thoracoscapular space elevating the inferior angle of the scapula. It merits a separate discussion.
68. ELASTOFIBROMA DORSI
Elastofibroma dorsi is a slow-growing reactive pseudotumor composed of a mixture of fibroelastic tissue and fat which usually arises on the back, deep in relation to the rhomboid major, serratus anterior and latissimus dorsi muscles and adjacent to the inferior angle of the scapula. The disorder has a predominance in women, is often associated with hard manual labor and more commonly occur in the elderly (Kransdorf et al. 1992). Based on histopathologic data, elastofibroma dorsi is composed of several alternating fatty and fibrous tissue planes containing thick elastic fibers, which result in the typical striated appearance of the mass. It has been speculated that elastofibroma dorsi results from periosteal fibroblasts with deranged elastogenesis, but it is not known whether this change is primary or results from repeated mechanical friction between the tip of the scapula and the chest wall (Kransdorf et al. 1992). In more than half the cases, elastofibroma dorsi is bilateral and asymptomatic, suggesting that many elastofibromas are clinically occult. In fact, when the arm is in the neutral position, the scapula may overlie the tumor and completely mask it (Fig. 166a,b) (Kransdorf et al. 1992): at least in part, this may explain the discrepancy between the relatively rare incidence of these masses found clinically and the higher prevalence reported in large autopsy series (Jarvi and Lansimies 1975). At US examination, elastofibroma dorsi should be examined while keeping the arms adducted and internally rotated, to reposition it from underneath the scapula for an adequate examination (Bianchi et al. 1997; Dalal et al. 2002). The lesions appear as ill-defined crescent-shaped masses growing in the fat plane interposed between the extrinsic back muscles and the costal plane (Fig. 166c,d).
Their boundaries are not clearly separated from those of the superficial muscles, since the tumor echotexture blends with that of skeletal muscle. Elastofibromas have a peculiar texture composed of an inhomogeneous echogenic background with interspersed linear or curvilinear hypoechoic strands, reflecting the histology of the tumor: these strands are typically arrayed in series with oblique orientation throughout the mass. One-to-one comparison with the CT, MR imaging and gross pathology findings revealed that the hypoechoic strands are compatible with areas of fat, whereas the echogenic background reflected the predominantly fibroelastic bulk of the mass (Fig. 167) (Bianchi et al. 1997). It is known that fat can assume a variable echogenicity at US, including an anechoic appearance (pure fat) or a hyperechoic appearance (fat interspersed with other tissues). It has been clearly shown that pure fat is anechoic, whereas fat interspersed with other tissues tends to become hyperechoic (Fornage et al. 1991). The fat within the stripes is relatively homogeneous. Therefore we can expect it can be hypoechoic. In contrast, the higher echogenicity of the fibroelastic background of the mass could result primarily from the amount of acoustic interfaces caused by fibrous tissue against interspersed fat or by intrinsic heterogeneity of the fibrous tissue itself, reflecting varying proportions and distribution of degenerated elastic fibers and collagen. Although elastofibromas have been shown to have increased fluorodeoxyglucose (FDG) metabolism at positron emission tomography (PET) and PET-CT (Pierce and Henderson 2004), color Doppler imaging does not usually detect blood flow signals within them (Bianchi et al. 1997). The main differential diagnoses for parascapular masses are lipomas and metastases (Fig. 168a–c).
However, elastofibroma has a typical US appearance which should allow it to be distinguished from these lesions on the basis of a well-defined multilayered pattern. Diagnostic pitfalls might be encountered with US in cases of parascapular hemangiomas. In fact, hemangiomas may exhibit a complex ill-defined appearance with prominent hyperechoic components reflecting fat and prominent hypoechoic vascular channels (Fig. 168d,e). The hypervascular appearance of these masses at color Doppler imaging and the detection of phleboliths (which occur in approximately 50% of cases) should help the differential diagnosis. The distinction between elastofibromas and extra-abdominal desmoids, which contain variable amounts of collagen and may also be found around the shoulder, is essentially based on the absence of well-defined striations at US. Overall, we believe that, in the appropriate clinical setting, the US-based diagnosis of elastofibroma can obviate unnecessary patient anxiety and the need of further imaging and unnecessary surgical procedure or biopsy.