Acute and Chronic Gout

Related Subjects: |Rheumatoid arthritis |Systemic Sclerosis (Scleroderma) |RA vs OA |Acute and Chronic Gout |Calcium Pyrophosphate Deposition (Pseudogout) |Hyperuricaemia |Allopurinol |Rasburicase |Lesch-Nyhan syndrome

⚠️ It is very rare for acute gout to occur in a rheumatoid joint. 👉 Continue treatment until 1–2 days after the attack has resolved and ensure follow-up. 🚑 Admit if septic arthritis is suspected (always exclude this). 📌 Remember: serum urate may be normal during an acute attack, so repeat later.

🔎 About

• 💎 Gout is due to deposition of monosodium urate monohydrate crystals in joints and tissues.
• ⏳ Chronic hyperuricaemia may cause renal failure, nephrolithiasis, and tophi.
• 💊 Drugs in the elderly (thiazides, low-dose aspirin, ciclosporin) are common contributors.

🧬 Aetiology

• ⬆️ Overproduction of uric acid (purine metabolism disorders, haematological malignancy).
• ⬇️ Impaired excretion of urate (genetic predisposition in >90%).
• 💡 Crystals are needle-shaped, negatively birefringent under polarised light.
• 👣 Classically affects 1st MTP joint → Podagra.
• 💊 Precipitating drugs: thiazides, ciclosporin, aspirin.

⚡ Effects of Hyperuricaemia

• Often asymptomatic
• Acute gouty arthritis
• Chronic interval gout → repeated flares on background inflammation
• Polyarticular tophaceous gout → pain, deformity, joint damage
• Renal urate stone formation and chronic kidney disease

📊 Epidemiology

• Male predominance (M:F ≈ 10:1)
• Prevalence: ~1–2% of UK population, especially older men & postmenopausal women
• Attacks often linked to lifestyle factors (alcohol, obesity, diet rich in purines)

🦶 Podagra – 1st MTP joint (classic site)

• 👨 Male sex (risk ×5–10 compared to women)
• Age <30 → suspect enzyme defects or renal disease
• Obesity, alcohol, hypertension, hyperparathyroidism
• 💉 Post-chemotherapy tumour lysis & tissue breakdown
• Pb poisoning (saturnine gout)
• Haematological malignancy, haemolysis, extreme exercise
• Lesch–Nyhan syndrome (HGPRT deficiency)

🔺 Causes of Excess Urate

• Reduced excretion: CKD, thiazides, aspirin, hypertension, lactic acidosis (alcohol, starvation), glycogen storage disease, lead toxicity, hypothyroidism
• Overproduction: HGPRT deficiency, PRPP overactivity, myeloproliferative or lymphoproliferative disorders, psoriasis

🩺 Clinical Presentation

• Sudden onset (often nocturnal/early morning)
• Severe localised pain, swelling, erythema – maximal in 6–12 hours
• Extreme tenderness, sometimes mimicking cellulitis
• Attack lasts 5–14 days if untreated
• Systemic features: fever, malaise, raised CRP

🚨 Complications

• Chronic tophi → visible lumps, joint deformity, disability
• Renal stones in ~20% of patients
• Chronic urate nephropathy → CKD

🧪 Investigations

• Bloods: FBC, U&E, CRP, ESR (raised in acute flares)
• Serum urate: may be normal during flare; repeat later
• Joint aspiration: strongly negative birefringent, needle-shaped crystals
• Radiology: punched-out erosions, soft tissue tophi, osteoporosis

💊 Management

• Acute Attack:
  • Rest, elevate, ice, avoid trauma
  • Exclude septic arthritis (may need aspiration)
  • NSAIDs (e.g. indomethacin, diclofenac) + PPI if tolerated
  • Colchicine (1mg stat, then 0.5mg BD/TDS) – caution diarrhoea
  • Oral steroids (prednisolone 10–15mg for 5–7 days) if NSAIDs/colchicine unsuitable
  • ⚠️ Do not stop allopurinol/febuxostat during an acute attack
• Prevention:
  • Lifestyle: weight loss, reduced alcohol, avoid dehydration
  • Stop thiazides/aspirin if possible
  • Urate-lowering therapy if recurrent attacks, tophi, renal impairment, or nephrolithiasis
• Drugs:
  • Allopurinol (start 50–100mg, titrate to 300mg+; dose adjust in CKD)
  • Febuxostat (80–120mg OD if allopurinol fails/intolerant)
  • Pegloticase (IV uricase) for severe refractory gout
  • Cover initiation with colchicine or NSAID for 3–6 months (prevents flares)

📚 References

• British Society for Rheumatology Gout Guidelines (2017)
• NICE CKS – Gout (2018)