Soft tissue mass around the shoulder

Gratuitous

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  1. H S Reid,
  2. Due east McNally,
  3. A Carr
  1. Nuffield Orthopaedic Centre NHS Trust, Oxford
  1. Dr H S Reid, Nuffield Orthopaedic Centre NHS Trust, Windmill Route, Headington, Oxford OX4 4LD.

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  • shoulder
  • diagnostic imaging
  • soft tissue

Clinical history

A previously fit 47 year old female person school instructor presented with a half-dozen month history of a painful swelling over her correct shoulder. There was rapid evolution of the swelling initially, which so stabilised. On test she was apyrexial with a large, firm, not-tender mass around the right shoulder, which clinically had some cystic features. There was no significant limitation of movement. Other findings on clinical examination included some small-scale soft tissue capsular swelling of the second and third metacarpophalangeal joints of the right hand. Otherwise the remainder of the locomotor system was normal.

Her erythrocyte sedimentation rate was increased at 51 mm 1st h, only C reactive protein remained normal at <0.vi. Full blood count was normal with a haemoglobin of xiii.4 g/dl, white blood jail cell count 7.5 × 10nine /l, platelet count 424 ×109/l. The rheumatoid cistron, nonetheless, was positive with a titre of ane:1280.

Imaging

QUESTIONS

(ane) What does the plain film (fig 1) evidence? Suggest a list of diagnoses that would fit this clinical context.

(ii) Which of your diagnoses does ultrasound (fig 2) support?

(3) Describe the magnetic resonance imaging findings (figs3-5).

(4) Using all the evidence what are the nearly probable diagnoses?

Plain picture show

There is a large, homogeneous soft tissue mass superolateral to the right shoulder articulation, in the region of the subdeltoid bursa. There is no calcification or ossification within the mass. Irregularity of the inferior surface of the acromion and the greater tuberosity suggests some caste of impingement syndrome otherwise there is no bony or joint aberration.

The diagnostic possibilities in this case tin can exist divided into those conditions arising from the synovium of the joint or subacromial bursa and those arising from muscle or related tissues. Synovial based lesions such equally pigmented villonodular synovitis (PVNS) can present as a soft tissue mass, as tin can synovial osteochondromatosis or soft tissue chondromas. Synovial sarcomas are rare malignant tumours but characteristically arise next to joints and grow slowly. With the exception of PVNS, all these conditions typically show some degree of calcification on evidently film.one Most cases of synovial osteochondromatosis show a blueprint of fibroid calcification and 1 third of cases of synovial sarcomas show spotty calcification.1 Cystic lesions such as a ganglion or synovial cyst tin occasionally reach this size.

A lipoma would fit the clinical context just fat is of lower density on plain film than muscle and consequently would announced blacker on apparently film. Other benign neoplasms such equally a haemangioma or an angiolipoma could give this appearance and sarcoma has to be considered.

Ultrasound

The ultrasound examination shows that the soft tissue mass is located inferior to the acromium and deltoid, and superior to the greater tuberosity and supraspinatus tendon. This is the region of the subdeltoid bursa. It contains multiple heterogeneous echoes, indicating that information technology is either a solid mass or a circuitous cyst. Ultrasound has the advantage of being a dynamic test and differentiation between a solid or complex cystic lesion can sometimes be made by watching the effect of force per unit area on its components. In this case, every bit indeed was suggested clinically, the lesion was idea to be a complex cyst, thus favouring the diagnosis of synovial osteochondromatosis or PVNS. Nonetheless, the ultrasound does not definitely exclude a synovial sarcoma or a liposarcoma (that is, an extra-bursal lesion).

Fat is characteristically reflective which reinforces the determination reached on the plain film that this is non a simple lipoma.

Magnetic resonance imaging (MRI)

Effigy 3, a coronal T1 weighted paradigm, shows gross enlargement of the subacromial subdeltoid bursa. The lumen is filled with intermediate signal intensity material, which on the T2 weighted axial images (fig4) is seen more conspicuously to represent multiple filling defects outlined by the high signal of fluid within the bursa. The filling defects themselves are intermediate bespeak on T2 weighting. After gadolinium injection (fig v) the synovial lining of the bursa enhances but no change occurs in the advent of the filling defects.

Other important points are that the glenohumeral and acromioclavicular joint, seen in the coronal plane in figure 3, announced uninvolved and the rotator cuff intact.

Differential diagnoses

SYNOVIAL STEOCHONDROMATOSIS

This is most commonly a monoarticular process, which presents in the tertiary to fifth decade with a 2:ane male preponderance. The condition is thought to be acquired by a disorder of the metaplasia of the synovial membrane.1 Radiologically almost cases exhibit calcification on the plainly film and therefore this example would be atypical.

PIGMENTED VILLONODULAR SYNOVITIS

This is an unusual proliferative disorder of synovium, which typically presents equally a non-painful soft tissue mass arising in the synovial lining of joints, tendon sheaths, fascial planes or ligaments. Calcification is not a characteristic and the ultrasound appearances would be similar to figure 2. MRI, withal, characteristically shows areas of very low betoken on T2 weighted images, which correspond haemosiderin deposition.2

Operative findings

The subacromial bursa was lined by proliferative synovium and filled with numerous loose bodies (fig vi).

Histological examination showed thickening of the synovial membrane with intimal hyperplasia and a heavy subintimal infiltrate of numerous lymphocytes and plasma cells. Giant cells and lymphoid aggregates were also axiomatic in the deeper subintima.

The loose bodies were composed near entirely of fibrin with surrounding organising cellular fibrous tissue.

Concluding diagnosis

Multiple rice bodies (fibrin bodies) in the subacromial bursa caused by rheumatoid disease.

Clinical issue

The patient fabricated a adept recovery afterward the synovectomy and has had no recurrence of her symptoms. She has not required any further treatment.

Discussion

Rice bodies were originally described past Reise in 18953 in association with tuberculous arthritis. They were chosen rice bodies because of their macroscopic similarity to grains of polished white rice. In 1993 Stein et al 4reported a case that first described the MRI appearances of subacromial bursitis with massive rice body formation.

In 1982, Popert et al 5 studied the frequency of rice bodies occurring in seropositive and seronegative rheumatoid arthritis. In the seropositive group, 72% of 50 joints aspirated using a large diameter needle, contained rice bodies. None were seen in the 31 joints of the seronegative group. There are just case reports elsewhere in the literature of rice bodies occurring in seronegative arthritis6 and also in hypogammaglobulinaemic arthritis.7

Rice bodies vary in size from 2–7 mm (55%) to greater than vii mm (10%).5 In 1977, Berg et al 8divided rice bodies into two types. Both type 1 and blazon ii consist of amorphous or coarsely reticular and condensed fibrin merely type 2 also contain a core of mature collagen. It has been suggested that with increasing age, rice bodies undergo a degree of organisation and begin to resemble mature connective tissue.v

The precise aetiology of rice bodies remains controversial. In the afterwards stages of rheumatoid arthritis, the full synovial surface expanse is vastly increased past proliferation and hypertrophy of synovial villi. Fassbender et al 9 suggest that fibrin accumulates in these villous structures, which then go elongated and snap off.

Popert et al 5 argue that information technology is the precipitation of fibronectin and fibrin, stimulated by the glycosaminoglycans released from eroded cartilage, which is responsible for rice body formation. This theory seems less probable in our instance, where the glenohumeral articulation was normal both on imaging and at surgery.

A further theory, put forward past McCarty and Cheung, suggests that microcirculatory deficiencies within the synovium and consequent hypoxia, result in synovial microinfarcts.10 The infarcted fragments then drop off into the articulation crenel and their surface becomes covered by fibrin layers.

The final and perhaps most important question is what is the clinical relevance of rice bodies? It is known that fibrin itself is irritant. Therefore rice bodies themselves have been implicated as one of the stimuli for continuing synovial inflammation.11 It is certainly truthful that their constructive removal tin can produce clinical improvement.5 Glynn has gone a step further to suggest that persistent fibrin deposits may provide a continuous stimulus to antibody germination to other inverse body constituents.12

Conclusion

The imaging characteristics of a huge collection of rice bodies on plain moving picture, ultrasonography, and MRI have been demonstrated. Although uncommon, we propose that this diagnosis should exist borne in listen equally a differential of atypical synovial ostechondromatosis.

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