Key clinical clues
- A monoarthritis of the knee at four in the morning, after two past attacks in the big toe
- Thiazide started four months ago, heavy beer intake, and stage 3 kidney disease
- Fever and a CRP of 148 with 42 000 synovial white cells, but a sterile stain and culture
- A firm painless nodule in the rim of the ear
- Needle crystals inside neutrophils, yellow along the compensator axis and blue across it
First-line treatment
Colchicine or an NSAID
A hot swollen knee with a temperature of 38.1, a CRP of 148 and 42 000 white cells per microlitre of joint fluid is septic arthritis until the aspirate says otherwise, which is why the joint is tapped before the first antibiotic dose: a dose given first can sterilise the culture and leave the question open. The crystals answer it. Needles that turn yellow along the compensator axis and blue across it are negatively birefringent: monosodium urate. Calcium pyrophosphate, the other crystal that inflames a knee at this age, is the mirror image, rhomboid and positive where this is needle-shaped and negative, so one field separates gout from pseudogout. Crystals inside neutrophils rather than merely beside them is what makes them the cause rather than an old deposit. Two findings mislead at face value. The fever and neutrophilia belong to the attack: crystal-driven inflammation is a real innate immune response and runs systemic, so neither argues for infection, and the negative Gram stain with sterile fluid and blood closes that door. The urate of 0.38 is the more dangerous trap, because it is squarely normal, and urate commonly drops into the normal range during an acute attack; a normal level excludes nothing, and the value worth acting on is measured weeks later. The rest of the history explains why the disease arrived: a thiazide started four months ago cuts urate excretion, beer supplies purine and ethanol together, 12 kg adds insulin resistance, and stage 3 kidney disease removes the main route of clearance. The ear nodule is a tophus, which dates the problem well before tonight. For the attack, colchicine or an NSAID, and here colchicine, because an eGFR of 48 makes an NSAID a poor bargain; colchicine itself needs a reduced dose in renal impairment. An intra-articular or oral corticosteroid is the answer when neither drug is safe. Allopurinol is the definitive treatment and the wrong drug tonight: urate-lowering starts once the joint is quiet, introduced slowly under colchicine cover, because dropping urate abruptly sets off fresh attacks. The thiazide should be exchanged for something else.