Gout Diagnosis
Gold Standard Diagnostic Approach
The definitive diagnosis of gout requires identification of monosodium urate (MSU) crystals in synovial fluid aspirated from the affected joint or from tophi, visualized under polarizing microscopy as needle-shaped crystals with negative birefringence. 1, 2, 3
When to Perform Synovial Fluid Analysis
- Perform arthrocentesis in any patient with undiagnosed inflammatory arthritis, particularly when septic arthritis cannot be excluded clinically, as gout and septic arthritis may coexist 2
- The procedure requires a polarizing microscope and a trained operator to properly identify MSU crystals 3
- Sensitivity and specificity of MSU crystal identification are 85-100% and 83-92%, respectively 3
- Always perform Gram stain and culture even when MSU crystals are identified, as infection and gout can occur simultaneously 2
Important Caveat About Serum Uric Acid
- Serum uric acid alone is insufficient for diagnosis because many patients with hyperuricemia never develop gout, and up to 30-40% of patients with acute gout have normal serum uric acid levels during an attack 2, 4
- Serum uric acid is essential for ongoing management and monitoring treatment efficacy, but not for initial diagnosis 2
Clinical Diagnosis When Crystal Analysis Is Not Possible
When synovial fluid analysis cannot be performed, use validated clinical prediction algorithms that demonstrate sensitivities of 84-99% and specificities of 66-96%, depending on disease duration. 5
2015 ACR/EULAR Classification Criteria (Most Current)
This is the most validated and comprehensive clinical algorithm available. 5
- Entry criterion: At least one episode of swelling, pain, or tenderness in a peripheral joint 5
- If MSU crystals cannot be identified, apply a hierarchical scoring system across clinical, laboratory, and imaging domains 5
- Score ≥8 points is diagnostic for gout (sensitivity 92%, specificity 89% with imaging; 85% sensitivity, 78% specificity without imaging) 5
Key high-value clinical features (weighted by predictive value):
- Presence of tophi (odds ratio 7.29) 5
- Resolution of pain within 2 weeks (odds ratio 3.58) 5
- Involvement of first metatarsophalangeal joint (podagra) 1
- Maximal joint inflammation within 24 hours 1
- Erythema over the affected joint 1
- Male sex 1
- Cardiovascular disease comorbidities 1
- Hyperuricemia 1
Clinical Gout Diagnosis (CGD) Algorithm
- Using ≥4 of 8 clinical criteria has 97% sensitivity and 96% specificity in established disease (>2 years duration) 5
- In early disease (<2 years), sensitivity drops to 87-89% with specificity of 66-82% 5
- This algorithm performs better in later-stage disease and should be interpreted cautiously in recent-onset symptoms 5
Janssens Diagnostic Rule
- Demonstrates 88% sensitivity in early disease (<2 years), making it the best-performing clinical algorithm for recent-onset gout 5
- Specificity ranges from 66-88% depending on disease duration 5
Imaging Studies for Diagnosis
Dual-Energy Computed Tomography (DECT)
DECT is the most accurate imaging modality for non-invasive detection of MSU crystal deposits, with sensitivity of 85-100% and specificity of 83-92%. 5, 1, 3
- Allows visualization of urate deposits in joints and soft tissues 1
- Major limitation is accessibility and cost 5
- Most useful when clinical diagnosis is uncertain and synovial fluid analysis cannot be performed 5
Ultrasonography
Ultrasonography has high specificity for urate deposits and can detect subclinical disease. 1, 3
- The "double contour" sign on cartilaginous surfaces is the most specific finding (pooled sensitivity 74%, specificity 88%) 5, 1
- Overall sensitivity ranges from 37-100% and specificity from 68-97%, depending on which ultrasound signs are assessed 5, 1, 3
- Can identify non-clinically evident tophi 1
- More accessible and less expensive than DECT 5
- Requires trained operator for accurate interpretation 1
Plain Radiography
- Often normal in early-stage gout 5
- May show characteristic punched-out erosions with overhanging edges in chronic disease 5
- Not recommended as a primary diagnostic tool 5
Diagnostic Algorithm for Clinical Practice
Step 1: Attempt Synovial Fluid Aspiration
- This is the reference standard and should be attempted whenever feasible, especially if septic arthritis is in the differential 2, 3
- Send for MSU crystal analysis, Gram stain, and culture 2
Step 2: If Aspiration Not Possible or Negative
- Apply 2015 ACR/EULAR classification criteria (score ≥8 diagnostic) 5
- In early disease (<2 years), consider Janssens diagnostic rule for higher sensitivity 5
Step 3: Consider Advanced Imaging
- Order DECT if available and diagnosis remains uncertain (highest accuracy) 1, 3
- Use ultrasonography if DECT unavailable (look for double contour sign) 1, 3
Step 4: Obtain Supporting Laboratory Tests
- Serum uric acid (for management, not diagnosis) 2
- Renal function tests (creatinine, BUN) 2
- Consider 24-hour urine uric acid in patients with early-onset gout (<25 years), family history of young-onset gout, or history of renal stones 2
Common Diagnostic Pitfalls to Avoid
- Never rely solely on serum uric acid for diagnosis—it may be normal during acute attacks 2, 4
- Do not assume monoarthritis of the first MTP joint is always gout—this presentation has only 8% specificity (though 99% sensitivity) 5
- Failing to perform synovial fluid analysis in atypical presentations leads to misdiagnosis 2
- Remember that gout and septic arthritis can coexist—always culture synovial fluid even when MSU crystals are present 2
- Clinical algorithms perform poorly in early disease (<2 years)—specificity drops significantly, increasing false-positive diagnoses 5
- Consider medication effects on uric acid levels (thiazides, loop diuretics, low-dose aspirin, niacin can elevate levels) 2
Risk Factors and Comorbidity Assessment
Evaluate the following risk factors in all patients with suspected gout: 1, 4
- Chronic kidney disease 1, 4
- Obesity 1, 4
- Hypertension 4
- Cardiovascular disease 1
- Medications: diuretics, low-dose aspirin, cyclosporine, tacrolimus 1
- Excessive alcohol consumption (especially beer) 1, 4
- Diet high in purine-rich foods (organ meats, shellfish) 1, 4
- Consumption of fructose-rich beverages 1, 4
- Ethnicity (higher risk in Taiwanese, Pacific Islander, New Zealand Maori populations) 4