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Avascular necrosis of bone can be almost silent until it comes under unusual strain. We report a case in point and lessons learned.
A woman aged 25 reported left hip pain for the past two weeks with diminishing ability to bear weight through the left leg. On enquiry she disclosed that for the past year she had been amenorrhoeic and had noted proximal muscle weakness in all her limbs. Her facies was cushingoid, there was widespread bruising and she was hypertensive. Radiographs revealed not only a basicervical fracture of the left femur but also generalized osteopenia. The fracture was treated with dynamic hip screw and plate fixation; a bone biopsy specimen taken at operation showed unusually thin trabeculae suggestive of osteoporosis.
On subsequent biochemical testing serum cortisol was 1081 nmol/L (normal 218-867) and urinary free cortisol was 311 nmol/24h (28-124). A 48-hour low-dose dexamethasone test gave a normal result but a 48-hour high-dose test showed suppression of corticotropin (ACTH) secretion. The suspected pituitary adenoma was confirmed by magnetic resonance imaging and was resected trans-sphenoidally.
Six months later, on review in the orthopaedic clinic, she complained of pain in her right shoulder. The pain had been present at the time of the hip fracture but she had not mentioned it. The pain had become worse when she used crutches after internal fixation of the hip fracture and was exacerbated by tasks above shoulder height. On examination there was minimal restriction in all arcs of shoulder motion, with abduction most obviously diminished. Anteroposterior radiographs in two planes of humeral rotation showed probable avascular necrosis (AVN) of the head of the humerus (Figure 1). Magnetic resonance imaging, including short tau inversion recovery sequences, revealed irregularity of the articular surface of the humeral head and subchondral oedema consistent with AVN. With physiotherapy and restriction of overhead activity the symptoms resolved and 6 months later there is no evidence of radiographic progression.
In populations without endemic sickle cell disease, AVN of bone is most often due to exogenous steroid therapy. High levels of corticosteroids from tumours seldom cause AVN. In the small number of cases associated with either tumours or steroid therapy, the main site was the femoral head1,2,3,4. There are two reported cases of AVN of the humeral head secondary to tumours: in one the tumour was an adrenal adenoma5, in the other a pancreatic tumour secreting ACTH6. In a series of four patients with AVN secondary to Cushing's disease, Phillips et al. described two patients with AVN involving the humeral head, one of whom also had AVN of the femoral head1.
Our patient was already experiencing symptoms from her shoulder at the time of her hip fracture. Seemingly, the use of crutches worsened these symptoms. A similar observation has been made in patients with steroid-therapy-associated AVN involving both humeral and femoral heads. From our experience in this case we suggest that, in a patient with Cushing's disease or AVN at other sites, shoulder symptoms should be enquired about and investigated radiographically. This is particularly important if the shoulder is to come under the weightbearing strain of crutches.