Gout is an acute-onset, crystal-induced arthritis that is characterised by intense joint pain and swelling – typically in the first metatarsal-phalangeal joint – when monosodium urate crystals are deposited.
Definition of terms
| Term | Definition |
|---|---|
| Asymptomatic hyperuricaemia | Elevated serum urate level without signs and symptoms. It can progress to gout if it is not treated. |
| Acute polyarticular gout | Interstitial nephritis and chronic kidney disease are caused by the deposition of urate crystals in the renal tubules. |
| Tophaceous gout | Chronic gout is characterised by deposition of monosodium urate crystals in soft tissue, e.g., the pinna. Tophi cause deformity and disability if they are located near joints. They can also ulcerate. |
| Gouty nephropathy | Interstitial nephritis and chronic kidney disease are caused by the deposition of urate crystals in the renal tubules. |
Crystals in gout vs pseudogout
| Gout | Pseudogout | |
|---|---|---|
| Crystal type | Monosodium urate | Calcium pyrophosphate |
| Shape | Needle shaped | Rhomboidal |
| Birefringence | Negatively birefringent | Positively birefringent |
- Risk factors
- Reduced urate excretion
- Advanced age
- Male sex
- Post-menopausal
- Renal impairment
- Hypertension
- metabolic syndrome
- Diuretics
- Antihypertensives
- Aspirin
- Excess urate production
- Alcohol
- Red meet
- Sea food
- Sweetners
- Genetic disorders
- Myeloproliferative disorders and lymphoproliferative disorders
- Psoriasis
- Tumor-lysis syndrome
- Drugs, e.g., warfarin and cytotoxics
- Reduced urate excretion
- Precipitating factors
- Trauma
- Surgery
- Starvation
- Infection
- Diuretics
- Associated conditions
- Cardiovascular disease
- Hypertension
- Diabetes mellitus
- Chronic renal failure
- Pathophysiology
- Reduced excretion or increased production of urate → monosodium urate crystal formation → deposition of crystals in joints → acute inflammatory response
- Chronic inflammation → tophi, joint damage, and chronic pain
- Signs and symptoms
- Acute monoarthritis
- Acute onset
- Severe pain, redness, swelling, and tenderness
- May be polyarticular
- Podagra commonly affects the first metatarsophalangeal joint
- Other joints include the ankle, foot, small joints of the hand, wrist, elbow, and knee
- Acute monoarthritis
- Differentials
- Septic arthritis
- Reactive arthritis
- Haemarthrosis
- Calcium pyrophosphate deposition (CPPD)
- Investigation
- Synovial fluid analysis
- Monosodium urate crystals
- WBCs > 2000/uL
- Serum urate: measured 4 – 6 weeks after an acute gout attack.
- Elevated
- It may be normal during an acute attack since crystals have been deposited in the joint(s)
- Plain radiograph
- Soft-tissue swelling in the early stages
- ‘Punched-out’ erosions in juxta-articular bone
- Joint spaces are preserved in the early stages
- Ultrasound to visualize tophi
- Hyperechoic structures
- Urea, electrolytes, and creatinine to properly dose allopurinol
- Complete blood count
- WBC count may be raised
- Fasting glucose and lipid profile, since gout is associated with metabolic syndrome
- Synovial fluid analysis
- Treatment
- Rest and elevate the joint
- Ice packs
- High-dose NSAIDS +/- PPI or colchicine (first-line)
- Colchicine is slower to work
- Oral or intramuscular steroids if NSAIDs and colchicine are contraindicated
- Continue allopurinol during the acute attack if already established
- Prevention
- Weight loss and exercise
- Avoid prolonged fasting
- Reduce alcohol intake
- Reduce consumption of purine-rich meats
- Low-dose aspirin
- Urate-lowering therapy
- Allopurinol (first-line) – prescribed 3 weeks after an acute episode since it may trigger an attack.
- Febuxostat (second-line)
- Rasburicase in refractory cases
- Indications for urate-lowering therapy
- 1 attack in 12 months
- Tophi
- Renal disease
- Uric acid nephrolithiasis
- As prophylaxis, if the patient is receiving cytotoxics or diuretics
- Complications
- Tophi
- Degenerative arthritis
- Osteoporosis
- Nephrolithiasis
- Chronic pain and incapacitation
