The answer is D: A synovial fluid analysis
A definitive diagnosis of gout is made by demonstrating negatively birefringent, needle-shaped monosodium urate crystals under a polarizing microscope. Although an elevated serum uric acid concentration is often seen in acute gout, it is neither as sensitive nor as specific a test as the demonstration of uric acid crystals in the synovial fluid under a microscope.
Serum uric acid levels can be normal in patients with acute gouty arthritis. The diagnosis of septic arthritis can be ruled out by appropriate Gram stain and culture of the same specimen of synovial fluid obtained for examination with the polarizing microscope.
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Gout Pearls
Gout involves the accumulation of uric acid in soft tissue of joints and bone
- Attacks are secondary to purine-rich foods (alcohol, liver, oily fish, yeasts) causing rapid changes in uric acid concentration
- Medications: diuretics (thiazides and loop), ACEI, ethambutol, aspirin, ARB’s
- Most common in men 40-60
Clinical manifestations of gout:
- Acute Gouty Arthritis: 80% monoarthropathy with joint erythema, swelling, and stiffness (often extends past the joint). The great toe is often first affected (Podagra).
- Tophi deposition: collection of solid uric acid in soft tissue (helix of ear, eyelids and Achilles tendon)
- Uric acid nephrolithiasis and nephropathy: uric acid stones associated with low urine volume and acidic PH
Diagnosis
Synovial fluid analysis (Gold Standard) demonstrating “needle-shaped” monosodium urate crystals in synovial fluid by polarized light microscopy they have a needle-like morphology and strong negative birefringence.
→ Positive birefringence is pseudogout
Radiographic/ultrasound/CT scan
- Joint destruction, bony erosions (rarely present on the first acute episode)
- Imaging findings become more likely with disease duration
Treatment
Acute management:
- NSAIDs drug of choice – indomethacin, naproxen (NO ASPIRIN = increased serum uric acid)
- Colchicine (inhibits leukocyte migration) is 2nd line treatment, steroids reserved if no response to NSAIDs or colchicine
Chronic management:
- Allopurinol (xanthine oxidase inhibitor): directly inhibits enzyme → urate production, stimulates purine base reutilization → ↓ ↓ ↓ urate concentration
- Uricosuric drugs: probenecid (promotes renal uric acid secretion)
- Uricase medications (rasburicase) mimic enzyme that catalyzes urate conversion → allantoin (more soluble purine degradation product )
