Extremities: Nontrauma

Calcium Hydroxyapatite Deposition Disease

Hydroxyapatite deposition disease is a common entity characterized by pain and periarticular deposition of calcium phosphate crystals. The soft tissues around the shoulder are the most common locations for deposits occurring in tendons, the joint capsule, ligaments, and bursae. Although this disease process has been assigned multiple names, it is mostly known as calcific bursitis/tendinitis. Middle-aged patients are most commonly affected, and the condition is slightly more common in men than in women. More than 30% of persons with calcific deposits in the area of the shoulder are asymptomatic. When the deposits are clinically apparent, patients present with varying degrees of pain and disability, which may last for weeks or months if the condition is untreated. It is important to note that the finding of hydroxyapatite deposits within the rotator cuff tendons (“calcific tendinitis”) has no relationship with the subsequent development of rotator cuff tears.

Calcific deposits are more easily identified and characterized with use of radiographs, computed tomography (CT), and ultrasonography (US) than with magnetic resonance imaging (MRI). On radiographs, most calcific deposits appear as homogeneous and amorphous densities that are ovoid, linear, or triangular in shape, with and without internal trabeculations ( Fig. 5-1, A ). The precise appearance and location varies with the phase of the disease process and specific anatomic structure involved. The supraspinatus is the most frequently affected tendon. US is highly sensitive for detecting even very small calcific deposits and may be used to guide puncture, aspiration, and lavage as therapeutic options. Hyperechoic foci with minimal or no significant posterior shadowing are identified, sometimes as ill-defined and fluffy or as discrete, well-defined calcifications that are linear or rounded ( Fig. 5-1, B ). Calcific deposits may be seen on MRI as nodular foci of low signal intensity in all pulse sequences ( Fig. 5-1, C ) and may be easier to identify on gradient-echo sequences, because they may induce a blooming artifact. Inflammatory changes in surrounding soft tissues may be present and identified as heterogeneous hyperintensity in fluid-sensitive (T2-weighted and short T1 inversion recovery [STIR]) sequences.

Rotator Cuff Abnormalities and Impingement

The concept of extrinsic subacromial impingement was initially described by Neer in 1972 and continues to be a very controversial topic even today. The notion of impingement is based on the anatomic arrangement of the shoulder joint (fixed component) and on the motion of the humeral head relative to the other components of the shoulder joint (dynamic component). In essence, the rotator cuff tendons (primarily the supraspinatus) and muscles, as well as the subacromial-subdeltoid bursa, located between the coracoacromial arch and the humeral head, may be impinged with motion of the arm. It is thought that this repetitive microtrauma from friction will lead to tendon degeneration, bursal inflammation, and, ultimately, a tear of the cuff. The “critical zone” is particularly susceptible to this pathophysiologic process; this critical zone has been described as a hypovascular area located on the anterior aspect of the supraspinatus tendon, approximately 1 cm from its insertion. Other factors described as potential contributors to the impingement process are narrowing of the subacromial space by enthesophytes arising from the undersurface of the acromion, advanced acromioclavicular joint osteoarthritis with hypertrophic changes, a type III acromion (anteriorly hooked), and the presence of an os acromiale (i.e., a secondary ossification center at the tip of the acromion that persists after skeletal maturity as a separate bone). However, impingement can occur without any visible anatomic predisposing factor, and the presence of anatomic variations does not necessarily indicate that impingement is occurring. Thus the diagnosis of shoulder impingement is made mainly on clinical grounds rather than on the basis of radiographs alone. The radiologist should focus on describing, characterizing, and grading rotator cuff disease, as well as on identifying potential contributing sources to the impingement process.

The spectrum of rotator cuff disease includes tendinopathy or tendinosis, partial- and full-thickness tendon tears, and subacromial-subdeltoid bursitis. Most rotator cuff tears are chronic and occur as the result of repetitive microtrauma. Acute rotator cuff tears are rare but do occur, especially in older patients with preexisting chronic impingement and degenerative tendon changes. It is not unusual, however, for patients with acute or chronic rotator cuff tears to seek care at the emergency department on an urgent basis because of severe or acutely worsening shoulder pain.

Radiographs should always be performed initially for evaluation of shoulder pain. However, they often are not contributory to a diagnosis. The presence of gas from the vacuum phenomenon in the glenohumeral joint strongly suggests the absence of a full-thickness rotator cuff tear. The rotator cuff tendons cannot be directly seen on radiographs; rather, a number of radiographic findings serve as indirect evidence of cuff disease and impingement ( Fig. 5-2 ). These findings include superior subluxation of the humerus with a decreased subacromial space (less than 8 mm) and secondary changes in the humeral head, such as sclerosis, flattening, surface irregularity, and cystic changes. Radiographs also may demonstrate potential anatomic causes of impingement ( Fig. 5-3 ).

Direct visualization of the rotator cuff tendons is achieved with MRI or US. One of these two methods is usually required to accurately diagnose and characterize rotator cuff tears. Selection of the modality depends on availability, individual expertise, and preference of the interpreting radiologist. Both offer relative advantages and disadvantages, which determine preference, and practice trends vary among different world countries. For example, in the United States, MRI is used more commonly than US, perhaps because of its faster learning curve and because the method is easily reproducible and less operator dependent than US. On the other hand, US is a great cost-effective alternative in experienced hands and is the first alternative in many institutions throughout the world.

Rotator cuff tendinopathy (tendon degeneration) is characterized on MRI by increased signal within the tendon on low echo time (TE) sequences (T1 and proton density). The tendon may demonstrate associated focal or diffuse thickening, but this finding is not consistent ( Fig. 5-4, A ). Abnormal signal within the rotator cuff tendons in low TE sequences may be seen in a variety of normal situations, and thus the need exists for close clinical correlation—most commonly, magic angle artifact as an area of increased signal at 55 degrees from the main magnetic field, which, on oblique coronal planes, coincides with the supraspinatus “critical zone.” Cuff tendon tears present as disruption (interruption) of fibers and may be either partial thickness or full thickness in the craniocaudal plane. High signal fluid is seen separating the disrupted fibers. This fluid may extend from the articular (inferior) surface superiorly in varying degrees to the bursal (superior) surface ( Fig. 5-4, B ). Partial-thickness tears affecting the articular surface are more common than isolated bursal surface tears. In full-thickness tears, fluid invariably extends across the tendon ( Fig. 5-4, C ) into the subacromial-subdeltoid bursa. Subacromial-subdeltoid bursitis may occur in isolation or in conjunction with rotator cuff tears.

Figure 5-5, A, shows an intact supraspinatus and its relation to the humeral head and deltoid muscle. The primary or direct signs of a full-thickness supraspinatus tear in US include nonvisualization of the tendon and a hypoechoic or anechoic full-thickness defect filling the gap of the torn tendon ( Fig. 5-5, B ). Secondary or indirect signs that are helpful to correlate with the primary signs include sagging of the peribursal fat, cortical irregularity at the greater tuberosity, fluid in the subacromial-subdeltoid bursa, and muscle atrophy. Partial-thickness tears manifest sonographically as focal areas of hypoechoic or anechoic tendon defects involving the bursal or articular surface ( Fig. 5-5, C ). An adequate examination requires evaluation of the extension of the defect on two orthogonal planes to confirm the findings. Tendon degeneration is demonstrated as internal heterogeneous echogenicity.

Acromioclavicular Joint Disease (Osteolysis and Osteoarthritis)

The incidence of acromioclavicular joint disease as a cause of shoulder pain is higher than generally realized. The acromioclavicular joint is often ignored, to the point that it has been termed the “forgotten” or “overlooked” joint. Osteolysis and osteoarthritis are two of the most common causes of shoulder pain arising from the acromioclavicular joint.

Osteolysis

Destruction of bone (osteolysis) may be seen as the result of multiple localized or generalized conditions. Destruction of the distal end of the clavicle is not uncommon and may be idiopathic, posttraumatic, or caused by rheumatoid arthritis, hyperparathyroidism, metastatic disease, multiple myeloma, primary osteolysis syndromes, and infection.

Posttraumatic osteolysis deserves special attention because of its relative frequency as a cause of debilitating pain and painful shoulder motion and because very often it is unrecognized. This entity can occur after a single or multiple episodes of minimal or major injury to this region. Most important is the recognition that posttraumatic osteolysis can occur without an obvious acute or known traumatic episode, and in those situations it is thought to be due to repetitive stress, as seen in weightlifters, judo practitioners, and pneumatic tool workers. The pathogenesis is poorly understood, and several theories have been formulated, including a neurologic and/or vascular mechanism, hyperemia, and autonomic phenomenon. More recently it has been proposed that osteolysis may be the result of a reactive process originating in the synovium or a subchondral fracture.

When it is advanced, resorption of the distal clavicle may be easily recognized radiographically ( Fig. 5-6 ), with loss of up to 3 cm of bone and widening of the acromioclavicular joint. However, the radiologist should focus on identifying early signs, because immobilization seems to diminish the amount of bone loss and shorten the natural course of the lytic phase. Early radiographic signs include soft tissue swelling, demineralization, and loss of the subarticular sclerotic cortex at the distal end of the clavicle. MRI findings usually precede radiographic findings. Initially periarticular soft tissue swelling/edema is present, and a bone marrow edema pattern may be evident. The marrow signal abnormality can be limited to the distal end of the clavicle or involve the acromion as well, albeit to a lesser degree. An associated joint effusion may be present, although this finding is variable. The disease process then progresses to bone erosion and frank destruction. Other MRI findings include cortical irregularity, subchondral erosion or cystic changes, and a subchondral line suggestive of a subchondral fracture.