Rheumatology Unit, Royal Cornwall Hospital, Truro, UK
Correspondence to: R. Mascarenhas, Rheumatology Unit, Royal Cornwall Hospital, Truro, Cornwall, R1 3LJ, UK. E-mail: ravik25{at}hotmail.com
SIR, A 41-yr-old Caucasian man was referred with a 4-yr history of bilateral groin pain. This had increased in severity in the preceding year, more so on the right, resulting in him having to give up his job as a labourer. On X-ray in 2002 there was patchy sclerosis, osteolysis and collapse of the right femoral head. There was relative preservation of the joint space. The left femoral head showed patchy sclerosis with a subcortical crescentic lucency and a break in the cortex (Fig. 1). The findings were consistent with bilateral avascular necrosis (AVN).
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Avascular necrosis is the term given to death of bone resulting in the collapse of the architectural bony structure, leading to joint pain, bone destruction and loss of function. It is most commonly associated with trauma. Non-traumatic associations include prolonged corticosteroid use, alcoholism, infections, hyperbaric events, storage disorders, marrow infiltrating diseases, coagulation defects and some autoimmune diseases [1]. In this man's initial history there was little to suggest any recognized cause for his bilateral AVN. There was no history of alcohol abuse, major trauma to the hips, connective tissue disease or chronic oral corticosteroid use. His corticosteroid use has been limited to a single 1-week course of oral prednisolone (30 mg daily) 16 yr previously and regular use of a Becotide inhaler (500 µg twice daily) for his mild asthma.
Further investigations included a normal full blood count and autoimmune profile, normal levels of anticardiolipin antibodies and a negative test for lupus anticoagulant. There seemed to be no obvious explanation for the bilateral hip AVN described here.
However, a more detailed occupational history resulted in a possible explanation for his presentation. He had previously worked at the Falmouth shipyard for a period of 3 yr, ending 2 yr prior to his being seen in the rheumatology clinic. His job consisted of stripping paint from ships using an ultra-high-pressure water-blaster. He used this device by resting one end in either groin while directing the other end into the air so that the paint was blasted away. The device vibrated and caused mild discomfort in both groins during its use. This work was undertaken for 5 h per day for 3 yr. His persistent groin pains began 1 yr into the use of the water-blaster.
There are scanty reports of AVN occurring in the bones of workers handling vibrating machinery. This has occurred principally in the lunate and capitate [2, 3]. In these cases, delayed onset of symptoms was noted after the patient began to use the vibrating machinery, as was the case here.
The most well-known complication of handling vibrating machinery is the development of vibration white finger [2]. This is thought to occur principally due to vibration-induced vasospasm. The accepted final common pathway for avascular necrosis of bone is compromise of the blood supply to that bone [1]. Kakosy's review article [2] suggests that vibrating machinery may induce a similar process, with the circulatory disturbance resulting in interruption of the bone vasculature. In this case we propose that the hips were involved because of the particular method of use of the vibrating machinery. It is our suggestion that this man's AVN is a result of vibration-induced injury.
This case illustrates the necessity of taking a thorough current and past occupational history. We therefore suggest that a thorough current and past occupational history is taken for all patients presenting with AVN.
We, the authors, declare that there are no conflicts of interest and that we have contributed equally to the planning and writing of the report. Both of us have seen and approved the final version.
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References