Acute Gout Flare in the Left Ankle: Diagnosis and Management
Diagnosis
Joint aspiration with synovial fluid analysis demonstrating needle-shaped, negatively birefringent monosodium urate (MSU) crystals under polarized light microscopy is the gold standard for diagnosing gout and should be performed when clinical judgment indicates diagnostic testing is necessary. 1
When Joint Aspiration is Mandatory
- Perform arthrocentesis immediately if septic arthritis cannot be clinically excluded, as gout and bacterial infection can coexist—even when MSU crystals are identified, Gram stain and culture must still be performed. 2
- Aspiration is also required when this is the patient's first suspected gout attack or when the clinical presentation is atypical. 2
Clinical Diagnosis When Aspiration is Not Feasible
If joint aspiration cannot be performed (common in primary care settings), clinical algorithms incorporating the following features achieve >80% sensitivity and specificity for diagnosing gout: 1, 2
- Maximum inflammation developing within 1 day (pain reaching peak intensity within 6-24 hours) 2
- Redness (erythema) observed over the affected joint 1, 2
- More than one previous attack of acute arthritis 1
- Male sex 2
- Presence of cardiovascular comorbidities (hypertension, cardiovascular disease) 2
- Hyperuricemia (serum uric acid >5.88 mg/dL)—though approximately 10% of patients with acute gout have normal uric acid levels during an attack 2
Imaging When Diagnosis Remains Uncertain
- Ultrasound is the first-line imaging modality, with the "double contour sign" demonstrating 74% sensitivity and 88% specificity for detecting MSU crystal deposition; always scan the first metatarsophalangeal joint bilaterally even if asymptomatic. 2
- Dual-Energy CT (DECT) should be considered as second-line imaging when ultrasound is negative but clinical suspicion remains high, particularly in patients with disease duration >2 years, with sensitivity of 85-100% and specificity of 83-92%. 1, 2
Essential Laboratory Tests
- Obtain serum uric acid, complete blood count, inflammatory markers (ESR, CRP), renal function (creatinine, eGFR), and liver function tests. 3
- Remember that hyperuricemia alone cannot diagnose gout, and normal serum uric acid does not exclude it during an acute flare. 2, 3
Acute Management
Initiate anti-inflammatory therapy immediately with colchicine, NSAIDs, or corticosteroids—the choice should be guided by the patient's comorbidities and contraindications. 2, 4
First-Line Treatment Options
Colchicine (preferred for most patients):
- Loading dose of 1.2 mg (two tablets) at the first sign of flare, followed by 0.6 mg (one tablet) one hour later—maximum 1.8 mg over one hour. 5
- Low-dose colchicine (1.8 mg total) is equally effective as higher doses with significantly fewer adverse effects. 2, 5
- Do not repeat treatment course more frequently than every 3 days. 5
NSAIDs (alternative first-line):
- Use full anti-inflammatory doses immediately upon symptom onset. 6, 4
- Avoid in patients with significant renal impairment, cardiovascular disease, or gastrointestinal risk factors. 2
Corticosteroids (when NSAIDs/colchicine contraindicated):
- Oral prednisone 30-35 mg daily for 3-5 days, OR 2
- Intra-articular injection after joint aspiration (particularly useful for monoarticular involvement). 2
Dose Adjustments for Renal Impairment
- Mild to moderate renal impairment (CrCl 30-80 mL/min): No dose adjustment required for acute treatment, but monitor closely for adverse effects. 5
- Severe renal impairment (CrCl <30 mL/min): Treatment course should be repeated no more than once every two weeks. 5
- Dialysis patients: Reduce total dose to single 0.6 mg dose; do not repeat more than once every two weeks. 5
Long-Term Management
Indications for Urate-Lowering Therapy (ULT)
Initiate ULT in patients with: 2, 4
- Two or more gout flares per year
- Presence of tophi (visible or on imaging)
- Radiographic evidence of gouty arthropathy
- Chronic kidney disease
- History of urolithiasis
ULT Initiation Strategy
- Start allopurinol at 100 mg daily and titrate upward by 100 mg every 2-4 weeks until serum uric acid is <6 mg/dL (or <5 mg/dL for severe disease with tophi). 2
- Do not start ULT during an acute flare—wait until the acute attack resolves, typically 2-4 weeks. 2
- If patient is already on ULT when flare occurs, continue the medication; do not stop during acute attack. 2
Flare Prophylaxis During ULT Initiation
- Provide prophylaxis with low-dose colchicine 0.6 mg daily or low-dose NSAID for at least 3-6 months after initiating ULT and continuing until serum uric acid reaches target. 2, 5
- This prevents acute flares triggered by mobilization of urate from tissue deposits. 5
Risk Factor Modification
Address modifiable risk factors systematically: 2, 6
- Dietary modifications: Limit purine-rich foods (organ meats, shellfish), avoid alcohol (especially beer), eliminate beverages with high-fructose corn syrup, encourage low-fat dairy products and vegetables. 6
- Medication review: Consider alternatives to thiazide and loop diuretics (relative risk 1.72 for gout); losartan may have uricosuric properties. 2, 6
- Weight management: Obesity carries a relative risk of 3.81 for gout. 2
- Comorbidity screening: Assess for hypertension (RR 3.93), chronic kidney disease (RR 4.95), cardiovascular disease, diabetes, and dyslipidemia. 2
Common Pitfalls to Avoid
- Do not diagnose gout based on hyperuricemia alone—up to 80% of patients with hyperuricemia never develop gout, and 10% of acute gout patients have normal uric acid during attacks. 2
- Do not assume fever is merely a gout manifestation—septic arthritis and gout can coexist; always perform joint aspiration with Gram stain and culture when infection cannot be excluded. 2
- Do not stop febuxostat or allopurinol during an acute flare—this can prolong the attack and delay urate lowering. 2
- Do not rely on plain radiographs for acute diagnosis—they are useful only for assessing chronic structural damage or excluding alternative diagnoses. 2