Jack was a 69-year-old Irishman. He had red cheeks, which I first imagined were from working outside as a bricklayer and from consuming frequent draughts of bitter.
He showed me a bursa of the elbow about the size of a goose egg. It had appeared recently without any history of trauma. On examination it was quite tense and caused discomfort when palpated. There was, however, no erythema and the overlying skin looked normal.
I asked Jack if he was still laying bricks. He laughed and said: ‘I’m 69, doctor. The heaviest thing I lift now is a paintbrush. I’ve taken up painting watercolours. I hardly think that’s going to cause this.’
I decided not to push my luck and talk about student’s elbow, a condition caused by persistent rubbing of the joint on a table.
There were no cuts or bruises near the bursa to suggest an entry for infection. The movement of the joint was relatively pain-free, except at the extreme of flexion, making a fracture unlikely.
I asked Jack about his alcohol intake. He looked affronted: ‘I’m teetotal. Apart from the odd drink at Christmas, I have been all my life.’
Another stereotype bit the dust. I looked at my teetotal, ex-bricklaying watercolourist with renewed puzzlement. He had no fever or systemic symptoms or signs, and all the other joints were normal.
I felt I could not risk sending Jack away without aspirating the joint to exclude infection. I explained what I was going to do and plunged an 18-gauge needle into the bursa, using a zigzag approach to avoid fistula formation.
The fluid that filled the syringe was clear. I had most likely excluded infection and haemarthrosis.
I sent the fluid off for culture, sensitivity and microscopy just in case, and sent the patient for an FBC, uric acid and rheumatoid factor.
The aspirate results confirmed that culture and sensitivity were normal but microscopy showed gout crystals. The diagnosis was confirmed by a uric acid result of 470mmol/l.
Gout can be caused by myeloproliferative and lymphoproliferative disorders, thyroid disease, psoriasis, chemotherapy, haemolytic anaemias, dehydration, excessive exercise and obesity.
Jack was thin, was not the world’s most active man and hadn’t had any chemotherapy. His normal FBC made proliferative disorders unlikely.
When I asked him about alcohol, Jack’s reaction had seemed genuine. He seemed to have a healthy diet and I was aware that apart from alcohol, the evidence for the role of diet in the aetiology of gout was somewhat minimal.
When I next saw Jack I remembered that I had diagnosed him with hypertension a few months ago and had put him on bendroflumethiazide. I stopped this immediately and put him on an ACE inhibitor.
The bursa had come back so I aspirated it again and this time instilled some corticosteroid.
I asked Jack to have another uric acid test done a month later. I added U&Es to the list to make sure his renal function could cope with an ACE inhibitor and that his gout was not secondary to kidney disease.
I reviewed him a week later with the results. Both his serum urea level and his bursa had gone down. His U&Es had been normal.
Jack has not developed another bursa and his uric acid levels have remained normal. Now we have stopped the bendroflumethiazide.
I do not think we need bother with prophylactic allopurinol again.
However, I will keep the situation under review. This case taught me a lot, but mainly never to jump to conclusions about a patient’s lifestyle from their appearance.
Dr Knott is a GP in Enfield