Shouldering the burden: a case of pain in the middle-aged female athlete
- Correspondence to Dr Bruce B Forster, Department of Radiology, Vancouver General and University of British Columbia Hospitals, Vancouver, British Columbia V6T 1Z3, Canada;
- Accepted 17 March 2013
- Published Online First 19 April 2013
Part 2: Answer
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Shoulder pain is a frequent complaint among patients and diagnosing the cause can be challenging, often requiring imaging studies. As the first-line modality, plain radiography should be ordered for all patients with pain persisting beyond 6 weeks.1 The differential diagnosis for this middle-aged female patient with atraumatic shoulder pain includes arthritis and rotator cuff pathology. However, before considering these more common causes, it is important to exclude infection and malignancy.
Septic arthritis is always a consideration when there is pain at a single joint. Depending on the organism, septic arthritis can either be aggressive causing rapid joint destruction or indolent. The diagnosis is typically made on clinical assessment and laboratory values since radiographs may be normal or demonstrate non-specific findings, especially early in the course.
Musculoskeletal malignancies often present with atraumatic pain. The more common primary bone tumours include multiple myeloma, sarcoma, leukaemia and lymphoma. However, in this age group, metastases are more likely. Radiologically, osseous metastatic lesions can be broadly grouped into osteolytic (eg, renal, lung and thyroid cancer) and osteoblastic (eg, breast and prostate cancer) lesions.
Glenohumeral joint arthritis is classified as degenerative (eg, osteoarthritis) or inflammatory (eg, rheumatoid arthritis) and can generally be diagnosed on a plain film. Radiographic features of osteoarthritis (OA) include focal joint space loss, subchondral cysts, sclerosis and osteophyte formation. Features of inflammatory arthritis include diffuse joint space loss, periarticular osteopenia and erosions.2 OA may be primary, when there is no identifiable cause, or secondary, when there is an initiating factor (eg, trauma, inflammation). (Of note, patients with longstanding inflammatory arthritides are more likely to have radiographic evidence of secondary OA.) Cases of primary OA of the shoulder are rare and may be calcium pyrophosphate deposition disease (CPPD), a metabolic arthropathy in which calcium pyrophosphate is deposited on the articular cartilage and fibrocartilage of joints. In CPPD, radiographs demonstrate features in keeping with OA plus hook-like osteophytes and chondrocalcinosis. CPPD also frequently involves other joints, such as the knee, wrist, pubis symphysis and hip.
Rotator cuff tendon pathology accounts for the majority of shoulder pain in the middle aged and elderly. The glenohumeral joint is stabilised by four rotator cuff tendons (supraspinatus, subscapularis, infraspinatus and teres minor) with the supraspinatus most commonly involved in tendon degeneration. The damage to tendons can range from tendinopathy to partial or full-thickness tears. The exact mechanism by which tendinopathies occur is not well understood but thought to be due to both vascular and cellular mechanisms.3 Tears, which are best appreciated on ultrasound and MRI, result from either a single traumatic event or a repetitive microtrauma.
The rotator cuff may also become painful as a result of calcium deposition within the tendons. In this patient, the imaging is most consistent with hydroxyapatite deposition disease (HADD). HADD is a systemic condition, particularly common in 30-year-old to 50-year-old women, involving the accumulation of hydroxyapatite (HA) crystals, a component of the boney matrix, in the soft tissues around joints.1 ,3 The disease is usually monoarticular and affects large joints, most commonly the shoulder.3 The crystals form a nidus of inflammation in the tendon resulting in tendinopathy or may shed into the subacromial bursa causing bursitis.4
Within the shoulder, 90% of cases of HADD affect the supraspinatus tendon, which originates from the supraspinous fossa of the scapula, passes laterally under the acromion and inserts onto the greater tuberosity of the humerus.1 The site most susceptible to HA deposition lies 1.5–2 cm from the tendon's insertion.5 This ‘critical zone’ is thought to be prone to ischaemia, especially when the rotator cuff muscles contract to hold the shoulder in slight abduction.1 ,5 The mechanism of crystal deposition in this hypovascular area is largely unknown but is suspected to be due to a combination of fibrosis and necrosis leading to degeneration.1 ,5
Plain radiography is often the only imaging test required to diagnose HADD. Typically, amorphous calcific foci are present in the periarticular soft tissues in the expected tendinous regions (figure 1). Up to 50% of patients with plain radiographs demonstrating calcific tendinopathy are symptomatic. On ultrasound, calcifications appear anechoic and display posterior acoustic shadowing (figure 2).1 ,6 Rarely, the posterior shadowing may obscure underling tears. MRI can be used to further assess for associated rotator cuff tears (figure 3), although it is relatively insensitive for demonstrating subtle calcific tendinopathy.1 ,6
The progression of HADD is divided into three stages: (1) precalcific stage in which fibrocartilaginous transformation of the tendon occurs; (2) calcific stage in which there is deposition, extravasation and resorption of HA crystals within the tendon and (3) postcalcific phase in which fibroblasts restore the tendon's collagen pattern.3 Initially, patients with HADD of the shoulder may be asymptomatic with an incidental finding of calcium deposition on imaging studies.1 The disease usually becomes symptomatic at the second stage, likely as a result of repetitive microtrauma with movement and a gradual increase in the size of calcific deposits causing impingement at the acromion.1 ,3 Patients report stiffness, pain and decreased mobility.3 At the time of presentation, clinical assessment is consistent with an inflammatory joint lesion with localised swelling, tenderness, erythema and restricted motion.3 The condition may be self-limiting or chronic.4 Milwaukee shoulder is an uncommon condition in which progressive HADD destroys the joint. Radiographic changes can be dramatic and include intraarticular loose bodies, marked subchondral sclerosis and even fracture.
The goal of HADD treatment is to reduce inflammation caused by extra-articular calcium deposits, either through targeting the local soft tissue reaction or removing the deposit. Non-surgical methods include non-steroidal antiinflammatories, ice, physical therapy and corticosteroid injections.1 The physiotherapy regime consists of rotator cuff strengthening, therapeutic ultrasound and pulsed electromagnetic field therapy.7 The deposit can be removed surgically or by minimally invasive procedures (ie, barbotage).4 ,6 According to some authors, barbotage has been shown to effectively remove calcium deposits in up to 91% of patients4; however, these studies are limited as non-randomised controlled trials have been performed to date. Given the disability caused by HADD and the risks associated with a surgery, this intervention is routinely offered in some institutions to patients failing conservative management.
The patient presented in this case developed shoulder pain secondary to supraspinatus HADD, which was treated successfully with ultrasound-guided barbotage. Shoulder pain is difficult to diagnose by clinical assessment alone because it is a complex joint and pain is often non-specific. Although in this patient, the most likely diagnoses were OA and rotator cuff pathology (eg, age-related tendinopathy, tears, HADD), it is important to rule out the less common aetiologies of infection and malignancy. Conventional imaging plays an integral role in diagnosing these conditions. When plain films clearly demonstrate HADD, it is unnecessary to obtain an ultrasound or MRI. These modalities are typically reserved for the evaluation of complications and prior to therapeutic interventions.
Contributors All authors contributed to the conception, writing, and revising of this article.
Competing interests None.
Provenance and peer review Not commissioned; internally peer reviewed.