Gout
An inflammatory arthritis caused by monosodium urate crystals; treat the flare promptly, exclude septic arthritis when the diagnosis is uncertain, and prevent recurrence with treat-to-target urate-lowering therapy.
Definition
Gout is an inflammatory arthritis caused by deposition of monosodium urate crystals in and around joints, driven by sustained hyperuricaemia.
Epidemiology
Gout becomes more common with age and is associated with renal impairment, obesity, alcohol excess, diuretic therapy and cardiometabolic disease. The first metatarsophalangeal joint is a classic site, but other peripheral joints can be involved.
Pathophysiology
Sustained hyperuricaemia allows monosodium urate crystals to deposit in and around joints. When crystals trigger innate inflammation, a neutrophil-rich acute flare develops; persistent deposits can form tophi and damage joints. Lowering serum urate below target gradually reduces the crystal burden.
First principles
Hyperuricaemia permits monosodium urate deposition
Gout is caused by deposition of monosodium urate crystals in and around joints after sustained hyperuricaemia. The usual problem is reduced renal urate excretion, with renal impairment, diuretics, alcohol, obesity and dietary factors contributing in some people. Crystal deposition can persist between attacks, so controlling the flare does not remove the need to consider long-term urate lowering.1,2
A typical flare is rapid, severe and often peripheral
Gout commonly presents as a rapidly developing red, hot, swollen and exquisitely tender first metatarsophalangeal joint, although other joints can be affected. The pattern supports the diagnosis but is not sufficiently specific to replace assessment for infection or calcium pyrophosphate crystal arthritis.1,2
Crystals trigger intense innate inflammation
Monosodium urate crystals activate innate inflammatory pathways and recruit neutrophils, producing the abrupt pain, warmth and swelling of a flare. Anti-inflammatory treatment suppresses this response but does not remove the underlying urate burden; long-term urate lowering is the separate strategy that gradually reduces crystal deposition.1,2
The immediate safety question is septic arthritis
A crystal flare and septic arthritis can look alike, and infection can coexist with crystals. If the diagnosis is uncertain, aspiration for microscopy and culture is central; if septic arthritis is suspected, follow the local emergency pathway immediately rather than reassuring yourself with a history of gout.1,3
Long-term treatment is treat-to-target
When urate-lowering therapy is indicated, use a low starting dose, increase it according to monthly serum urate results until target is reached, and provide flare prophylaxis. The usual target is below 360 micromol/L; a lower target below 300 micromol/L can be considered for tophi, chronic gouty arthritis or ongoing frequent flares despite a level below 360.1,4,5
Presentation
Acute onset of a red, hot, swollen and severely painful joint, classically the first metatarsophalangeal joint, with the diagnosis supported by the clinical pattern and serum urate but confirmed by aspiration when uncertainty or infection is a concern.1,2,3
Cardinal features
- Rapid-onset severe monoarthritis, often reaching peak severity within 24 hours
- First metatarsophalangeal joint involvement (podagra), although any peripheral joint may be affected
- Marked erythema, warmth, swelling and tenderness
- Previous self-limiting attacks or a history of raised serum urate
- Tophi, chronic gouty arthritis or urate stones in established disease
Red flags
- Fever, systemic upset or an acutely ill patient: assess urgently for septic arthritis
- Prosthetic joint, immunosuppression, recent joint procedure or bacteraemia risk
- Diagnostic uncertainty or failure to respond as expected
- Polyarticular or rapidly destructive disease
- Chronic kidney disease, cardiovascular disease, anticoagulation or other comorbidity affecting anti-inflammatory choices
Investigations
Serum urate
Use serum urate to support the diagnosis and to monitor urate-lowering therapy. A level below 360 micromol/L during a flare does not exclude gout; repeat it at least 2 weeks after the flare has settled when clinical suspicion remains high.
Expected finding: A level of 360 micromol/L or more supports a clinical diagnosis; the result may be lower during an acute flare.
1Synovial-fluid aspiration, microscopy and culture
Offer aspiration when the diagnosis is uncertain. Send fluid for crystal analysis and microbiology, because identifying crystals does not by itself exclude coexisting infection.
Expected finding: Needle-shaped, negatively birefringent monosodium urate crystals support gout; Gram stain and culture are used to assess septic arthritis.
1,3Ultrasound or dual-energy CT when aspiration is not possible or remains uncertain
If aspiration cannot be performed or the result does not settle the diagnosis, consider imaging to look for urate deposition. Use local expertise and interpret imaging alongside the clinical picture.
Expected finding: Imaging may show urate deposition, but a positive finding does not remove the need to consider infection in a hot acutely inflamed joint.
1Renal function and treatment-safety blood tests
Assess renal function and relevant comorbidity before selecting and dosing anti-inflammatory or urate-lowering treatment. Review current medicines, particularly diuretics, anticoagulants and drugs that may interact with colchicine or allopurinol.
Expected finding: Chronic kidney disease or cardiovascular disease may narrow acute treatment choices and influence the urate-lowering plan; medicine-specific checks are required.
1,6,4,5Assessment for tophi, chronic gout and comorbidity
Examine joints and skin for tophi, assess functional impact, and review cardiovascular, renal and metabolic comorbidity. These findings influence the indication for long-term urate lowering and the target selected.
Expected finding: Tophi, chronic gouty arthritis, frequent troublesome flares, chronic kidney disease or diuretic therapy support offering urate-lowering therapy.
1,2Management
| Step | Detail | Source |
|---|---|---|
| Exclude septic arthritis when the presentation is not clearly typical | Assess the whole patient and examine the joint. If septic arthritis is suspected, use the local emergency pathway; if the diagnosis is uncertain, aspirate for microscopy and culture. Do not allow a previous history of gout to close the differential.1,3 | NICE NG219; Oxford University Hospitals joint aspirates |
| Treat the flare promptly with one first-line anti-inflammatory option | Offer an NSAID, colchicine or a short course of an oral corticosteroid, selected using comorbidities, co-prescriptions and patient preference. If using an NSAID, consider gastroprotection and check the BNF for contraindications, interactions and renal dosing.1,6,7 | NICE NG219; BNF colchicine and naproxen |
| Use specialist or local alternatives for an unsuitable first-line option | If an NSAID, colchicine and corticosteroid are contraindicated, not tolerated or ineffective, consider intra-articular or intramuscular corticosteroid where appropriate. Interleukin-1 inhibitors are specialist options only after other treatments have been considered.1 | NICE NG219 |
| Review after the flare and discuss prevention | After the flare, review serum urate, renal and cardiovascular risk, comorbidities, current medicines, lifestyle factors and whether urate-lowering therapy is appropriate. Explain that treatment is usually long term and that the aim is to prevent further flares and dissolve deposits.1,2 | NICE NG219; NHS gout |
| Offer urate-lowering therapy when the risk-benefit is clear | Offer urate-lowering therapy to people with multiple or troublesome flares, tophi, chronic gouty arthritis, chronic kidney disease stage 3 to 5 or diuretic therapy. Discuss it after a first or subsequent flare even when these features are absent, using shared decision-making.1 | NICE NG219 |
| Start and titrate urate-lowering therapy to a serum-urate target | Usually start at least 2 to 4 weeks after a flare has settled; if flares are frequent, it can be started during a flare. Start low and increase the dose using monthly serum urate measurements until below 360 micromol/L. Consider below 300 micromol/L for tophi, chronic gouty arthritis or ongoing frequent flares despite a level below 360.1,4,5 | NICE NG219; BNF allopurinol and febuxostat |
| Choose the urate-lowering drug and prevent treatment-related flares | Offer allopurinol or febuxostat as first-line options, choosing allopurinol first when there is major cardiovascular disease. Give flare prophylaxis with colchicine unless contraindicated; consider a low-dose NSAID with gastroprotection or low-dose oral corticosteroid when colchicine is unsuitable. Check BNF cautions, renal function and interactions.1,6,4,5 | NICE NG219; BNF colchicine, allopurinol and febuxostat |
| Support adherence and address modifiable contributors | Explain that urate-lowering therapy is usually lifelong and should not be stopped without advice. Encourage a balanced diet, weight management where appropriate and avoidance of excessive alcohol; NICE does not recommend a specific diet as proven to prevent flares or lower serum urate. Review medicines that may contribute, while balancing their other clinical indications.1,2 | NICE NG219; NHS gout |
| Monitor the target and refer when specialist input is needed | Continue monthly serum urate checks while titrating, then consider annual monitoring once target is stable. Seek rheumatology advice when the diagnosis remains uncertain, standard treatment is contraindicated, not tolerated or ineffective, or there is chronic kidney disease stage 3b to 5 or a renal transplant.1 | NICE NG219 |
Illustrations
Differentials
Septic arthritis
A hot swollen joint with fever, systemic upset or risk factors for infection; aspirate for culture when suspected or uncertain, and remember that infection can coexist with crystals.
Acute CPP crystal arthritis
Often affects a knee or wrist in an older person; calcium pyrophosphate crystals are rhomboid and weakly positively birefringent.
Cellulitis
Superficial erythema and warmth without a true intra-articular effusion, although the two can coexist.
Reactive or psoriatic arthritis
A different joint pattern, preceding infection or psoriasis, and no urate crystals on aspiration.
Complications
- Recurrent disabling flares
- Chronic tophaceous gout and joint damage
- Urate nephrolithiasis
- Treatment toxicity or interactions
- Missed or coexisting septic arthritis
Prognosis
Gout is controllable with sustained urate-lowering therapy titrated to a serum-urate target. Without prevention, recurrent flares can progress to tophi and chronic joint damage. Renal, cardiovascular and metabolic comorbidity should be addressed in parallel.
Guidelines
- Gout: diagnosis and management (NG219) (NICE, 2022)
References
Evidence checked: 2026-08-03
This page is exam revision material, not medical advice, and must not be used for patient care. Always check drug doses against the BNF and current guidance. Full disclaimer.