Gout Flare Probability Calculator
Clinical prediction rule for diagnosing acute gout based on clinical features
Clinical Features
Diagnostic Probability
Probability Scale
Gold Standard Diagnosis
Definitive diagnosis requires synovial fluid analysis showing:
- • Needle-shaped, negatively birefringent crystals
- • Monosodium urate (MSU) crystals
- • Examined under polarized light microscopy
Important Notes
- • Normal uric acid doesn't exclude gout
- • Up to 50% of acute flares have normal levels
- • Consider septic arthritis if febrile/ill-appearing
- • Joint aspiration indicated if diagnosis uncertain
💡 Treatment
Acute flare: NSAIDs, colchicine, or corticosteroids. Start urate-lowering therapy (allopurinol, febuxostat) after flare resolves.
Understanding Gout Diagnosis
Gout is the most common inflammatory arthritis, caused by deposition of monosodium urate crystals in joints. While definitive diagnosis requires synovial fluid analysis demonstrating urate crystals, clinical prediction rules can help estimate the probability of gout based on readily available clinical features.
Classic Presentation
- Podagra: Acute monoarthritis of the first metatarsophalangeal (MTP) joint - most classic presentation
- Rapid onset: Symptoms typically develop over 6-12 hours, reaching maximum intensity within 24 hours
- Severe pain: Often described as worst pain ever experienced
- Inflammation: Intense erythema, swelling, warmth, and exquisite tenderness
- Timing: Often begins at night or early morning
Common Sites of Involvement
- First MTP joint (50-70% of first attacks - podagra)
- Midfoot, ankle, or knee
- Wrist, finger, or elbow (less common)
- Polyarticular involvement (more common in chronic/tophaceous gout)
Risk Factors for Gout
- Male gender: Men are affected 3-4 times more often than premenopausal women
- Age: Peak incidence in men 30-50 years, postmenopausal women
- Hyperuricemia: Higher uric acid levels increase risk
- Diet: High purine foods (red meat, seafood), alcohol (especially beer), fructose
- Medications: Diuretics, low-dose aspirin, cyclosporine
- Comorbidities: Hypertension, chronic kidney disease, obesity, diabetes, hyperlipidemia
Diagnostic Approach
The gold standard for gout diagnosis is synovial fluid analysis showing needle-shaped, negatively birefringent monosodium urate crystals under polarized light microscopy. However, joint aspiration is not always feasible or available. Clinical prediction rules can guide empiric treatment decisions.
Important Diagnostic Caveats
- Normal uric acid: 30-50% of patients have normal serum uric acid during acute flare
- Hyperuricemia alone: Not diagnostic - most people with hyperuricemia never develop gout
- Septic arthritis: Must be excluded, especially in ill-appearing patients or those with fever
- Coexistent conditions: Gout and septic arthritis can coexist; gout and CPPD can overlap
Differential Diagnosis of Acute Monoarthritis
| Condition | Key Features | Distinguishing Tests |
|---|---|---|
| Gout | Rapid onset, podagra, male, hyperuricemia | MSU crystals (negative birefringence) |
| Pseudogout (CPPD) | Knee > wrist, elderly, chondrocalcinosis | CPP crystals (positive birefringence) |
| Septic Arthritis | Fever, severe systemic illness, risk factors | SF WBC >50,000, positive culture |
| Reactive Arthritis | Recent infection (GI/GU), younger age | Clinical history, HLA-B27 |
| Trauma/Hemarthrosis | History of injury, bleeding disorder | Bloody synovial fluid |
| Cellulitis | Skin changes, spreading erythema | Clinical diagnosis, imaging if uncertain |
Frequently Asked Questions
Can I have gout with normal uric acid levels?
Yes, absolutely. During an acute gout flare, 30-50% of patients have serum uric acid levels in the normal range. This occurs because the acute inflammatory response can temporarily lower serum uric acid through various mechanisms. Therefore, a normal uric acid level during an acute flare does not rule out gout. Uric acid levels should be rechecked 2-4 weeks after the flare resolves.
Is joint aspiration always necessary to diagnose gout?
While synovial fluid analysis demonstrating urate crystals is the gold standard, it's not always necessary in clinical practice. For a classic presentation (podagra with rapid onset in a patient with risk factors), empiric treatment may be appropriate. However, aspiration should be strongly considered if: (1) diagnosis is uncertain, (2) septic arthritis is a concern, (3) patient is febrile or systemically ill, or (4) this is the first episode without a clear diagnosis.
What is the difference between gout and pseudogout?
Gout is caused by monosodium urate crystals (needle-shaped, negatively birefringent), while pseudogout is caused by calcium pyrophosphate (CPP) crystals (rhomboid-shaped, positively birefringent). Gout typically affects the first MTP joint and has male predominance, while pseudogout more commonly affects the knee and occurs in elderly patients. Both cause acute inflammatory arthritis, but the crystals and demographics differ.
When should I start urate-lowering therapy?
Urate-lowering therapy (allopurinol or febuxostat) should be started after the acute flare has completely resolved, typically 2-4 weeks later. Starting during an acute flare can worsen or prolong the attack. Indications for urate-lowering therapy include: ≥2 flares per year, tophi, chronic kidney disease stage 2 or worse, or urolithiasis. The target serum uric acid is <6 mg/dL, or <5 mg/dL if tophi are present.
What treatments are available for acute gout flares?
Three medication classes are effective for acute gout: (1) NSAIDs (indomethacin, naproxen) - first-line if no contraindications; (2) Colchicine - most effective if started early (<24 hours), use low-dose regimen to minimize GI side effects; (3) Corticosteroids (oral prednisone or intra-articular injection) - excellent option if NSAIDs/colchicine contraindicated. Treatment should be started as soon as possible after symptom onset.
How can I prevent future gout attacks?
Prevention includes both lifestyle modifications and medication: (1) Dietary changes: limit purine-rich foods (red meat, organ meats, shellfish), avoid alcohol (especially beer), limit fructose/sugary drinks, maintain healthy weight; (2) Medications: urate-lowering therapy (allopurinol/febuxostat) to maintain uric acid <6 mg/dL, prophylactic colchicine or NSAIDs during first 3-6 months of urate-lowering therapy; (3) Optimize comorbidities and avoid triggers (dehydration, trauma, rapid weight loss).
Can gout and septic arthritis occur together?
Yes, although uncommon, gout and septic arthritis can coexist in the same joint. This is important because treating gout empirically without aspiration in a patient with septic arthritis can be dangerous. Red flags suggesting possible infection include: fever >100.4°F, systemic illness, immunosuppression, prosthetic joint, recent joint surgery, or injection drug use. When in doubt, aspirate the joint before starting treatment.
What are tophi and when do they develop?
Tophi are deposits of monosodium urate crystals that form solid nodules in soft tissues. They typically develop in patients with chronic, untreated hyperuricemia, usually appearing 10+ years after the first gout attack. Common locations include fingers, toes, elbows, ears, and Achilles tendon. Tophi indicate severe disease burden and are an absolute indication for urate-lowering therapy with a target uric acid <5 mg/dL. With proper treatment, tophi can gradually resolve over months to years.