Table of Contents
- 01. Rotator Cuff
- 1. Anatomy and Function
- 2. Pathogenesis
- 3. Terminology
- 4. Natural History
- 5. Ultrasound Technique
- 6. Spectrum of Findings
- 7. Ultrasound Pitfalls
- 8. References
- 02. Postoperative Rotator Cuff
- 03. Long Head of Biceps Brachii Tendon
- 04. Bursae
- 05. Joint Spaces
- 1. Acromioclavicular Joint
- 2. Glenohumeral Joint
- 3. Sternoclavicular Joint
- 4. Scapulothoracic
- 5. References
- 06. Fractures
- 07. Os acromiale
- 08. Adhesive Capsulitis
- 09. Deltoid
- 10. Pectoralis Major
- 11. Web Exclusive: Sternocostal Joints
- 12. Web Exclusive: Musculoskeletal Ultrasound Educational Videos
- a. Best Original Manoeuver
- b. Snapping Film Direction
- c. Actor in a Leading Role
- d. Actress in a Leading Role
- e. Actor in a Supporting Role
- f. Actress in a Supporting Role
- g. Best Correlation Between Clinical and Sonographic Findings
- h. Joint Instability Short Film Documentary
- i. Unedited Film
- j. Real Time Impingement Short Film
- k. Nerve Compression Short Film
- l. Doppler Feature Special Award for Lifetime Achievements
- m. Interventional Feature Special Award for Distinguished Body of Work
- n. Honorary Award
4.1. Subacromial-Subdeltoid Bursa
The subacromial-subdeltoid bursa (SSB) is located deep to the deltoid muscle and the coracoacromial arch and extends laterally beyond the humeral attachment of the rotator cuff, anteriorly to overlie the intertubercular groove, medially to the acromioclavicular joint, and posteriorly over the rotator cuff. The SSB decreases friction and allows free motion of the rotator cuff relative to the coracoacromial arch and the deltoid muscle. The SSB receives nociceptive stimuli and proprioception via the articular branches of the suprascapular nerve posteriorly and the lateral pectoral nerve anteriorly.18,26 Under normal circumstances, it does not communicate with the glenohumeral joint.
4.1.1. Ultrasound Technique
The surface area of the SSB is large and meticulous technique is necessary for full evaluation. US demonstrates the normal SSB as a thin hypoechoic structure surrounded by peribursal echogenic fat. The minimum protocol to evaluate SSB should include (1) long-axis views over the supraspinatus tendon, (2) long-axis views just distal to the supraspinatus tendon, (3) short-axis views over the supraspinatus tendon, and (4) long-axis views over the subscapularis tendon (figure 4-2).
4.1.2. Spectrum of Ultrasound Findings
At US, an abnormal bursa may show (1) fluid distension, (2) synovial proliferation, and/or (3) thickening of the bursal walls. In any case, the magnitude of pathological findings does not correlate with the magnitude of the symptoms.
The diagnosis of subacromial-subdeltoid bursitis based on incompressible hypoechoic thickening of the bursal walls is debated, and there is no consensus agreement on the diagnostic criteria to define pathology.27 In general lines, we consider 2 mm as a reliable cutoff to indicate thickening of the bursal walls. The measurement should not include the peribursal echogenic fat (figure 4-3). Lower thresholds for diagnosis require contralateral asymmetry and correlation with symptoms (figure 4-4). Care must be taken not to confuse the SSB with the deep portion of the normal hypoechoic deltoid muscle surrounded by echogenic fascia (figure 4-5). Also, proximal musculotendinous junction of the supraspinatus may mimic pathological bursa to the inexperienced examiner (figure 4-6). Subacromial-subdeltoid bursitis often coexists with supraspinatus tendinopathy and it may be difficult to sonographically differentiate the hypoechoic bursa from the underlying hypoechoic tendon. Dynamic evaluation during shoulder abduction may help to differentiate between these two structures because it occasionally demonstrates contact between the coracoacromial ligament and the SSB. Nonetheless, as will be discussed later, contact between the coracoacromial ligament and the SSB is not specific to symptoms and can also be found in healthy volunteers.28 Focal or diffuse thickening of the superficial peribursal echogenic fat is occasionally depicted but its clinical relevance is largely unknown (figure 4-7). Theoretically, such areas can result from inflammatory reaction of the fat pad secondary to subacromial impingement. However, controlled studies are needed to correlate this imaging finding with surgical and clinical evaluation. As rotator cuff disease often parallels SSB pathology, asymptomatic bursitis may be as highly prevalent as asymptomatic rotator cuff disorders.
Figure 4-4. Subacromial-subdeltoid bursitis.
Figure 4-7. Diffuse thickening of the peribursal fat.
The diagnosis of subacromial-subdeltoid bursitis based on fluid distension of the bursal cavity is more intuitive since sonographic detection of any amount of compressive fluid is considered abnormal (video 4-1). When the patient is standing or in sitting position, fluid tends to accumulate distally in the most dependent anterolateral aspect of the bursa (figure 4-8). Another dependent area is located anteriorly over the intertubercular groove, often included in the field of view when evaluating the long head of biceps brachii tendon for disease. Care should be taken not to apply excessive pressure with the probe because bursal fluid may become undetectable if displaced (figure 4-9). In long-standing cases, the bursa may develop loculi (figure 4-10; video 4-2) and septations (figure 4-11). Fluid distension of the SSB may also result from its communication with the glenohumeral joint via a full-thickness tear of rotator cuff tendons. In such cases, graded compression with the free hand of the examiner can reveal fluid passing from the SSB to the glenohumeral joint and vice versa during real time evaluation. Communication with the glenohumeral joint allows the SSB to serve as a reservoir for loose bodies (figure 4-12; video 4-3).
Figure 4-9. Subacromial-subdeltoid bursitis.
Figure 4-10. Subacromial-subdeltoid bursitis.
Figure 4-11. Subacromial-subdeltoid bursitis.
Figure 4-12. Loose body.
Complex hypo- or hyperechoic fluid may also be detected, but these characteristics do not accurately predict inflammatory, hemorrhagic or infectious process (figure 4-13). Synovial proliferation must always be included in the differential diagnosis of complex fluid, though both conditions can usually be confidentially differentiated at US because the former shows poor compressibility, lack of internal movements during graded compression, and occasional internal vascularization on Doppler interrogation. Synovial proliferation is especially common and can be massive in patients with systemic inflammatory arthropathies, mimicking an intrabursal mass (figure 4-14). Synovial chondromatosis should be considered in the differential diagnosis of intrabursal masses as it courses with a variable degree of synovial proliferation or hyperplasia. First described by Leannac in 1813,29 synovial chondromatosis can be differentiated into a primary and secondary form. The primary form represents an idiopathic benign neoplastic process affecting subintimal cartilage of a joint, tendon sheath, or bursa.30 In contrast, secondary chondromatosis does not show the cytogenetic aberrations observed in the primary form, probably represent metaplasia of synovial tissue into cartilaginous tissue, and occurs in association with preexisting traumatic, inflammatory, and degenerative conditions. In some cases, it may be difficult to differentiate primary from secondary synovial chondromatosis because long-standing primary synovial chondromatosis also predisposes to degenerative changes. Primary synovial chondromatosis is relatively rare and invariably presents as a monoarticular disease. Polyarticular involvement suggests the more common secondary form. Knees are the most commonly affected joints, possibly because of their abundance of synovial tissue. The extra-articular form is particularly rare and is frequently referred to as tenosynovial or bursal chondromatosis. Regardless of location and etiology, the resultant subintimal nodule of hyaline cartilage may detach from the synovium and produce chondral loose bodies within the joint, bursa, or tendon sheath. In primary synovial chondromatosis, the numerous chondral bodies are usually similar in size, which suggests a similar time frame origin. Conversely, chondral fragments generated by secondary synovial chondromatosis are fewer in number and more variable in size when compared with the fragments observed in primary disease. Because cartilage is nourished by absorption of nutrients and oxygen from the synovial fluid, detached chondral bodies may gradually increase in size. Fusion or coalescence of multiple chondral bodies may also occur, creating a soft tissue mass appearance.31 Most chondral bodies calcify over time, and a small proportion progress further and undergo ossification.32 Malignant transformation of primary synovial chondromatosis to chondrosarcoma occurs in 5% of cases and is suggested by multiple recurrences and marrow invasion depicted on MRI. In fact, the pathological appearance of primary synovial chondromatosis may simulate chondrosarcoma because of significant histologic atypia, and imaging correlation to localize the process as synovially based is vital for correct diagnosis.30 At US, synovial chondromatosis may present as a calcified heterogeneous avascular mass with variable shadowing (figures 4-15 and 4-16). Extrinsic erosion of bone may also be present. Extensive shadowing from calcified or ossified lesions may obscure the soft tissue mass and the multiplicity of the loose bodies. Dynamic evaluation is helpful to document change in position of unstable loose bodies. Treatment of primary disease is surgical synovectomy with removal of loose bodies. Recurrence rates are estimated between 3% and 23%33-35 and usually secondary to incomplete resection. The differential diagnosis of synovial chondromatosis includes pigmented villonodular synovitis, which represents an uncommon benign neoplastic process that affects the synovium. The extra-articular form of pigmented villonodular synovitis is even rarer and can involve tendon sheaths (pigmented vilonodular tenosynovitis) and bursae (pigmented villonodular bursitis).36,37 Histologically, the hypertrophic synovium is villous, nodular, or villonodular and contains variable amounts of hemosiderin.38 At US, pigmented villonodular bursitis usually appears as a fixed mural nodule (figure 4-17).39 MRI is helpful to diagnosis because it typically shows low signal foci on T2-weighted images and susceptibility artifact on gradient echo sequences due to the paramagnetic effect of hemosiderin-laden synovial tissue, which is usually very prominent in pigmented vilonodular bursitis.32
Figure 4-13. Subacromial-subdeltoid bursitis.
Figure 4-14. Subacromial-subdeltoid bursitis.
Figure 4-15. Synovial osteochondromatosis.
Apart from thickening of the bursal walls, synovial proliferation, and fluid distension of the bursa, rice bodies may also be detected. Rice bodies consist of concentrically laminated masses of fibrin and represent an end product of synovial proliferation, inflammation or degeneration40 There are many different theories about their pathogenesis, including bleeding within the bursa and fibrinous degeneration of the infarcted synovial tissue. Rice bodies are not exclusively found in chronic disorders and can occur early or late in the course of disease.41 They are usually present in large numbers, resemble rice grains (hence the name) and are depicted as isoechoic to hyperechoic nodules that may mimic complex fluid containing blood or debris (figure 4-18). Rice bodies can induce symptoms from chronic irritation that subside after effective removal by aspiration, lavage, or instillation of fibrinolytic agents.
Figure 4-18. Rice bodies.
The Role of Doppler
Doppler evaluation may be useful to investigate SSB disorders because blood flow rates in normal bursae are relatively low and neovascularization suggests an active process that can correlate with symptoms.42 Adequate settings are essential to maximize low flow detection, and the color box must be sized to the area of interest to reduce background noise and optimize system resources (figure 4-19). Subacromial-subdeltoid bursitis may develop neovascularization via numerous mechanisms, including high concentrations of vascular endothelial growth factor and the combination of substance P and interleukin-1 (video 4-4).43
The Role of Dynamic Evaluation
The role of dynamic sonographic evaluation to detect subacromial impingement is not free of controversy. Although earlier studies have demonstrated bursal thickening following shoulder abduction in symptomatic shoulders,44-47 a more recent investigation found no significant difference in the degree of gathering of the SSB in impingement patients compared with healthy volunteers (figure 4-20).28 Anecdotal experience also suggests that slight contact between the coracoacromial arch and the SSB can occur in healthy individuals (video 4-5). However, significant contact (figure 4-21; video 4-6) or snapping (video 4-7) between these two structures are not common in the absence of symptoms and suggest clinically relevant subacromial impingement.
4.1.3. Grading of Subacromial-Subdeltoid Bursitis
We generally do not report measurements of the bursal thickness because it has no proven influence on prognosis and may not correlate with the magnitude of bursal distension (figure 4-22). We also do not subjectively grade subacromial-subdeltoid bursitis, except for the very mild (e.g.: asymmetric incompressible hypoechoic thickening of the bursal walls < 2mm) or very severe cases (e.g.: fluid distension > 10mm in thickness). Although the amount of fluid does not correlate with symptoms, patients with more severe fluid distension typically show more advanced rotator cuff pathologies as an associated finding (figure 4-23).
Figure 4-23. Severe subacromial-subdeltoid bursitis.
4.1.4. Follow-up of Subacromial-Subdeltoid Bursitis
From the several presentations of subacromial-subdeltoid bursitis, only fluid distension, synovial proliferation, and neovascularization can completely disappear on follow-up. Conversely, hypoechoic thickening of the bursal wall likely represents an irreversible finding. Small submillimetric variations in bursal wall thickness on follow-up mostly correspond to interpersonal or intrapersonal variations and are probably best considered of no clinical significance. The efficacy of treatment should be assessed on clinical grounds and not based on the magnitude of imaging findings.