Acute Monoarticular Ankle Arthritis: Most Likely Gout
This presentation is most consistent with acute gouty arthritis (gout flare), and you should initiate anti-inflammatory treatment immediately while arranging joint aspiration to confirm the diagnosis and exclude septic arthritis.
Clinical Reasoning
The rapid onset of ankle swelling, redness, and pain reaching maximum intensity within hours to a day is highly characteristic of crystal-induced inflammation, particularly gout. 1, 2 The EULAR guidelines emphasize that rapid development of severe pain, swelling, and tenderness reaching maximum within 6-12 hours, especially with overlying erythema, is highly suggestive of crystal inflammation. 1
Why Gout Is Most Likely
Occupational risk factor: Standing 12 hours daily on concrete creates significant lower extremity venous stasis and repetitive microtrauma, which can precipitate crystal deposition and acute gout flares in susceptible individuals. 3, 4
Classic presentation: The ankle is a common site for gout flares (second only to the first MTP joint), and the rapid onset with marked erythema strongly favors gout over other causes. 2, 3, 5
Demographic likelihood: If this patient is male and middle-aged, gout becomes even more probable given the 7% prevalence in men over 65. 3
Why Shrimp Is a Red Herring (Not Allergic Reaction)
Timing mismatch: True IgE-mediated shellfish allergy manifests within minutes to 2 hours of ingestion with urticaria, angioedema, and potentially systemic symptoms—not isolated joint swelling 12+ hours later. 2
Localization: Allergic reactions cause diffuse swelling, not monoarticular inflammation confined to one ankle joint. 2
However, shrimp IS relevant: Shellfish are purine-rich foods that can trigger gout flares by raising serum uric acid levels, making this dietary history supportive of gout rather than allergy. 6, 4
Why Not Trauma-Related
The patient explicitly denies injury or trauma, and the rapid inflammatory presentation with erythema is inconsistent with simple overuse edema from prolonged standing. 1
Immediate Diagnostic Approach
Joint aspiration with synovial fluid analysis is mandatory to confirm gout and exclude septic arthritis, which can present identically. 2, 7
When Aspiration Is Required
Septic arthritis cannot be excluded clinically—gout and infection can coexist, and missing septic arthritis carries substantial morbidity and mortality risk. 1, 2, 7
First suspected gout attack in this patient requires definitive crystal confirmation. 2, 7
Send fluid for:
If Aspiration Cannot Be Performed
Ultrasound is the first-line imaging modality, looking for the "double contour sign" (74% sensitivity, 88% specificity for MSU crystal deposition). 2, 7
Clinical diagnosis can be made with >80% accuracy using validated criteria when aspiration is not feasible: rapid onset (<24 hours to maximum pain), joint erythema, male gender, and cardiovascular comorbidities. 2, 7
Laboratory Tests to Order
Serum uric acid: Essential for long-term management but cannot confirm or exclude acute gout—10% of patients with acute gout have normal levels during the attack. 1, 7, 8
CBC, ESR, CRP: Assess inflammation severity and help differentiate from infection. 8
Renal function (creatinine, eGFR): Guides medication selection and identifies chronic kidney disease as a gout risk factor (RR 4.95). 7, 8
Immediate Treatment
Initiate anti-inflammatory therapy within 12 hours of symptom onset for maximum effectiveness. 2
First-Line Options (Choose Based on Comorbidities)
NSAIDs at full anti-inflammatory doses (e.g., indomethacin 50 mg TID or naproxen 500 mg BID) with PPI if GI risk factors present. 2, 3, 6
Colchicine: Loading dose 1.2 mg, then 0.6 mg one hour later (low-dose regimen equally effective with fewer adverse effects than high-dose). 2, 6
- Contraindicated in severe renal impairment and with strong P-glycoprotein/CYP3A4 inhibitors (risk of fatal toxicity). 2
Corticosteroids: Oral prednisone 30-35 mg daily for 3-5 days, OR intra-articular injection after aspiration. 2, 3
- Preferred in patients with heart failure where NSAIDs are contraindicated. 3
Risk Factor Assessment and Long-Term Planning
Evaluate for Gout Risk Factors
Medications: Thiazide/loop diuretics (RR 1.72), low-dose aspirin, cyclosporine, tacrolimus. 7, 3, 6
Comorbidities: Obesity (RR 3.81), hypertension (RR 3.93), chronic kidney disease (RR 4.95), metabolic syndrome. 7, 3, 4
Dietary factors: Alcohol (especially beer), purine-rich foods (red meat, shellfish), high-fructose corn syrup beverages. 6, 4
When to Start Urate-Lowering Therapy
Initiate ULT if the patient has: 2, 7, 4
- ≥2 gout flares per year
- Tophi on examination or imaging
- Chronic kidney disease stage 2 or higher
- Radiographic evidence of gouty arthropathy
Target serum uric acid <6 mg/dL (or <5 mg/dL if tophi present), starting allopurinol 100 mg daily and titrating by 100 mg every 2-4 weeks. 2, 7, 4
Provide flare prophylaxis with low-dose colchicine 0.6 mg daily or NSAID for at least 6 months after starting ULT. 2, 7
Critical Pitfalls to Avoid
Do not delay treatment waiting for laboratory or imaging confirmation—clinical diagnosis is sufficient to initiate therapy in typical presentations. 2
Do not assume infection is excluded based on clinical appearance alone—joint aspiration with culture is mandatory if septic arthritis cannot be ruled out. 2, 7
Do not rely on serum uric acid alone for diagnosis—normal levels during acute attack do not exclude gout. 1, 7, 8
Do not attribute symptoms to shellfish allergy without appropriate allergic features (urticaria, angioedema, systemic symptoms within 2 hours). 2