He has a 20 year history of rheumatoid arthritis, which was managed initially with gold injections and subsequently methotrexate, despite which he accumulated typical small joint deformities. In the past two years with the addition of etanercept his disease has been very well controlled and he enjoys an active and independent retirement. His only other background medical history is of hypertension, for which he takes bendroflumethiazide. He is an ex-smoker.
He now presents with a one week history of mildly productive cough as well as an acute and polyarticular flare of arthritis.
He is fully responsive but noted to be pale and in pain. His temperature is 37.8˚C, blood pressure 100/50, pulse 90, respiratory rate 16. Mucous membranes are dry. Right basal crackles are heard, though his CXR is clear. Both knees are noted to be swollen, red and tender.
- What are the key investigations to be sent and following these what treatment is indicated?
Many thanks to Dr Philip Riches for this case, and for taking part in the discussion. If you want to find out what happened in this case, click below.
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Here is a summary of Dr Riches’ thoughts on this case.
My initial question was “What are the key investigations?” The answer is synovial fluid analysis. You cannot assume it is his rheumatoid until you have worked very hard to exclude other possibilities. This patient is immunosuppressed and there needs to be a high index of suspicion of infection as well as a recognition that this is not a typical presentation for a rheumatoid flare. Specifically many of the signs of sepsis may be masked by disease modifying therapy. TB is important to consider since reactivation is well recognised with anti TNF therapies.
On review this patient had raised his temperature to 38.5 C and lowered his blood pressure to 90/50 despite being given IV fluids.
His initial blood results were Urea 14.8, creatinine 140, eGFR44
Hamoglobin 112, WBC 18.2, platelets 238
CRP 165, ESR 32
Urate 0.34 mmol/l.
A joint aspirate was performed and obtained 2ml of blood stained fluid which was been sent for culture (no organisms or crystals seen).
His methotrexate and etanercept were stopped appropriately and he was commenced on IV Tazocin and fluids. He developed multiple new, very painful and very swollen red joints.
He was reviewed the next day by rheumatology and had aspirates of both knees and wrists performed. In total over 100ml of highly turbid synovial fluid was obtained and sent for culture and crystal examination.
The aspirates revealed … polyarticular gout. Urate crystals were seen in all aspirates and culture of these was negative. To muddy the water a little the initial (and almost certainly traumatic/inadequate) aspirate that was performed came back on day 3 of culture with 3cfu of staph aureus and we were obliged to treat him as septic arthritis with 2 weeks of IV flucloxacillin and a subsequent 4 weeks of oral therapy. We could not rely on the subsequent negative aspirates since he was already on antibiotics by the time they were performed. He was also commenced on colchicine and although it took the best part of 2 weeks his joints did finally settle down. His renal function returned to normal. His CRP peaked at 233. His respiratory symptoms also settled with antibiotics, and the crackles heard on auscultation on admission seemed to be a red herring.
The case was an unusual one – you will not often see coexisting gout and rheumatoid arthritis. I hope it illustrates a couple of important lessons. Firstly, a red hot joint should be considered septic until proven otherwise. Remember that patients with pre-existing joint damage and immunosuppressants are at increased risk, and this describes a large number of RA patients. Also, please make every effort to get adequate cultures before antibiotics are started as it is very hard to establish the diagnosis after antibiotics. But septic arthritis is potentially fatal, and if there is genuinely no-one around who can aspirate the joint then all you can do is take blood cultures and get on and give antibiotics.
The main differential is crystal arthritis. Up to 50% of patients with acute gout have normal levels of serum urate so this is a poor diagnostic test for gout. Joint aspirate is the gold standard but if this is blood stained, and the microbiology technician is not looking specifically these are often missed.
Gout is on the increase – we are all living longer, fatter and getting more drugs than is good for us. Polyarticular gout occurs in 10% of cases in the young and is more prevalent still in the elderly in whom it may present in less typical ways. (NB Septic arthitis will present often enough as polyarticular disease so do not rely on this to exclude it).
The patient was discharged and started on allopurinol with colchicine cover. His methotrexate and Etanercept were stopped on admission and this will be reviewed in clinic.