Skip to content

BASICS

Description

  • Acute inflammatory arthritis with red, hot, swollen joints.
  • Caused by deposition of monosodium urate (MSU) crystals.
  • Commonly affects first metatarsophalangeal joint (podagra), foot, ankle, knee.
  • Chronic disease can cause tophi, joint destruction, urate nephropathy, nephrolithiasis.
  • Flares usually monoarticular; polyarticular flares can have systemic symptoms.

Epidemiology

  • Prevalence 0.68% to 3.9% in adults.
  • More common in males.

Etiology and Pathophysiology

  • Four stages:
  • Hyperuricemia (overproduction or decreased excretion).
  • MSU crystal deposition triggered by local factors (cold, trauma, acidosis).
  • Acute inflammatory response causing gout flare.
  • Chronic gout with tophi and joint damage.
  • Genetic association: HLA-B*5801 allele (esp. in Asians).

Risk Factors

  • Age >40 years.
  • High purine diet: alcohol (beer), red meat, seafood, sugary beverages.
  • Metabolic syndrome, diabetes, obesity, hypertension.
  • Medications: thiazide diuretics, loop diuretics, niacin, aspirin.
  • Transplant recipients on calcineurin inhibitors.
  • Tumor lysis syndrome.

Prevention

  • Diet modification: avoid purine-rich foods and alcohol.
  • Maintain hydration.

DIAGNOSIS

History

  • Rapid onset severe joint pain, swelling, erythema.
  • Joint intolerance to touch, often waking patients at night.
  • Precipitating factors: infection, injury, dehydration, alcohol/purine intake.
  • Chronic gout: tophi at joints, ears, olecranon, tendon.

Physical Exam

  • Tender, swollen, warm joint(s).
  • Tophi: firm nodules on joints, ears, olecranon, Achilles tendon.

Differential Diagnosis

  • Septic arthritis
  • Pseudogout (calcium pyrophosphate deposition disease)
  • Cellulitis
  • Osteoarthritis
  • Rheumatoid arthritis
  • Traumatic arthritis
  • Hemarthrosis

Diagnostic Tests

  • Synovial fluid analysis: negatively birefringent needle-shaped MSU crystals (pathognomonic).
  • Uric acid levels (may be normal during attacks).
  • Serum inflammatory markers (WBC, ESR, CRP) may be elevated.
  • 24-hour urine uric acid in early onset or history of stones.
  • Imaging:
  • X-rays: periarticular erosions in chronic disease.
  • Ultrasound: double contour sign, tophi.
  • DECT: urate deposits.

TREATMENT

General Measures

  • Supportive care: rest, ice, hydration.

Acute Attack

  • Initiate treatment within 12-24 hours, continue 1-2 days after symptom resolution.
  • NSAIDs: naproxen 500 mg BID, meloxicam 7.5-15 mg daily, indomethacin, diclofenac, ibuprofen.
  • Corticosteroids: oral (15-35 mg prednisone daily for 5 days) or intra-articular.
  • Colchicine: loading dose 1-1.2 mg, then 0.5-0.6 mg 1 hr later, then 0.5-0.6 mg q8h; max 6 mg/course.
  • Combination therapy for severe attacks.

Chronic Management

  • Urate-lowering therapy targeting serum uric acid <6 mg/dL.
  • First line: allopurinol (start low, titrate up), febuxostat.
  • Uricosurics: probenecid (avoid if CrCl <50 or history of stones).
  • IL-1 inhibitors (anakinra, canakinumab) if contraindications/intolerance.
  • Continue anti-inflammatory prophylaxis during initiation (low-dose colchicine or NSAIDs).

Additional Therapies

  • Losartan and fenofibrate for uricosuric effects in hypertension or lipid disorders.
  • Surgery for large tophi causing functional impairment or infection.

Complementary Medicine

  • Vitamin C (>500 mg daily) may reduce serum uric acid.

ONGOING CARE

Follow-Up

  • Monitor serum uric acid q2-5 weeks during titration.
  • Periodic renal, liver, CBC tests.
  • Reinforce lifestyle and dietary advice.

Diet

  • Avoid organ meats, high fructose corn syrup, excessive alcohol.
  • Limit red meat, shellfish, sweetened beverages.
  • Encourage coffee, high-fiber foods, dairy, cherries.
  • Weight loss in overweight patients.

Patient Education

  • Flare-ups may increase during urate-lowering therapy initiation.
  • Early treatment of acute flares improves outcomes.
  • Adherence to lifestyle modifications is essential.

Prognosis

  • Generally well-managed with appropriate treatment.
  • Chronic gout can cause joint damage and nephropathy if untreated.

Complications

  • Chronic arthritis and joint destruction.
  • Uric acid nephropathy, kidney stones.

Clinical Pearls

  • Podagra is the classic first presentation.
  • MSU crystals on synovial fluid are diagnostic.
  • Treat acute flares within 24 hours.
  • Asymptomatic hyperuricemia does not require treatment.

References

  1. Abhishek A, Roddy E, Doherty M. Gout—a guide for the general and acute physicians. Clin Med (Lond). 2017;17(1):54-59.
  2. Rogenmoser S, Arnold MH. Chronic gout: Barriers to effective management. Aust J Gen Pract. 2018;47(6):351-356.
  3. Neogi T, Jansen TLTA, Dalbeth N, et al. 2015 Gout classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Arthritis Rheumatol. 2015;67(10):2557-2568.
  4. daSilva MT, de Fátima Haueisen Sander Diniz M, Coelho CG, et al. Intake of selected foods and beverages and serum uric acid levels in adults: ELSA-Brasil (2008-2010). Public Health Nutr. 2020;23(3):506-514.
  5. Lamb KL, Lynn A, Russell J, et al. Effect of tart cherry juice on risk of gout attacks: protocol for a randomised controlled trial. BMJ Open. 2020;10(3):e035108.
  6. Choi HK, Atkinson K, Karlson EW, et al. Obesity, weight change, hypertension, diuretic use, and risk of gout in men: the health professionals follow-up study. Arch Intern Med. 2005;165(7):742-748.