Hot Swollen Knee: Gout Versus Septic Arthritis
A 62-year-old man with a history of two gout attacks and stage 3 chronic kidney disease (eGFR 44 mL/min/1.73 m²) presents with 3 days of worsening right knee pain, swelling, and inability to bear weight. He takes hydrochlorothiazide 25 mg daily and allopurinol 300 mg daily; he has not had an injection or recent antibiotic. Temperature is 38.3°C, blood pressure 142/86 mmHg, and heart rate 96 beats/min. The knee is warm, tense, and exquisitely tender with a large effusion and markedly limited range of motion. White blood cell count is 13,800/µL, C-reactive protein 128 mg/L, and serum uric acid 8.9 mg/dL. Arthrocentesis yields turbid fluid with 45,000 white blood cells/µL, 88% neutrophils; Gram stain shows no organisms and the first wet mount shows no crystals. The clinician must decide whether this is gout or infection and act while cultures are pending.
1. How do you interpret the synovial fluid, and what is your immediate management?
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The synovial fluid cannot be dismissed as gout. A white cell count of 45,000/µL with 88% neutrophils is in the septic range; gout can produce 2,000–50,000/µL, so the count overlaps and does not discriminate. The absence of crystals on one wet mount does not exclude gout-crystals can be missed, especially by an inexperienced examiner-and it certainly does not exclude infection. Gram stain is negative in a substantial fraction of septic arthritis. A normal or elevated serum uric acid also cannot separate the two; his uric acid is 8.9 mg/dL, but gout flares can occur with normal levels and infection can occur in a patient with gout.
Treat as septic arthritis until proven otherwise. Admit, obtain blood cultures, send synovial fluid for culture, cell count, and crystal analysis, and involve orthopedics for aspiration or lavage. Start empiric IV antibiotics covering staphylococci and streptococci-vancomycin (renally dosed, preferably by AUC) plus ceftriaxone 1 g daily, or cefazolin if MRSA risk is low; adjust for gram-negative risk. Do not inject intra-articular steroids. Repeated aspiration helps decompress the joint.
2. What would you do with his allopurinol and hydrochlorothiazide, and how would you confirm the diagnosis over the next 48–72 hours?
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Stop hydrochlorothiazide: thiazides raise uric acid and are a plausible trigger. Switch to an alternative such as losartan, which is uricosuric, or amlodipine; do this after the acute admission when blood pressure is stable. Continue allopurinol-stopping it during a flare can cause urate shifts, and it should not be restarted later without prophylaxis. However, 300 mg is probably too high for an eGFR of 44 mL/min/1.73 m²; a renally adjusted dose around 150–200 mg daily is more appropriate, with titration to a serum urate below 6 mg/dL. Do not start a new urate-lowering drug during an acute flare unless it is covered by anti-inflammatory prophylaxis.
Over 48–72 hours, follow the clinical course, CRP, and white count, and review the synovial culture. If cultures are negative, the patient is afebrile and improving, and repeat polarized microscopy shows negatively birefringent needle-shaped crystals, gout becomes the working diagnosis. If cultures are positive, infection is confirmed and he needs a full antibiotic course even if crystals are also present. Both can coexist.
3. At 72 hours, blood and synovial cultures are negative, he is afebrile and improving, and repeat polarized microscopy shows negatively birefringent needle-shaped crystals. What now?
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At 72 hours with negative cultures, clinical improvement, and confirmed negatively birefringent needle-shaped crystals, stop the antibiotics and treat the gout flare. Negative cultures are less reassuring if antibiotics were given before the cultures were obtained, so the decision should be made jointly with orthopedics and infectious diseases; but improvement off antibiotics plus crystals supports gout. Use a short course of oral glucocorticoids (for example, prednisone 30–40 mg daily for 5 days) or intra-articular glucocorticoid after infection has been excluded; avoid NSAIDs because of CKD. If colchicine is used, reduce the dose for renal impairment.
Continue allopurinol with a renally appropriate dose and titrate to urate <6 mg/dL; add colchicine or low-dose steroid prophylaxis for 3–6 months after any urate-lowering change. Remove triggers: replace thiazide, counsel on alcohol and dehydration, and review other medications. Arrange follow-up for urate monitoring and recurrent-flare prevention, and document that septic arthritis and gout can mimic each other and coexist.