Acute gout

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Establish onset in hours or days, the first and worst joint, previous self-limited episodes and whether maximum pain occurred within twenty-four hours. Podagra is highly suggestive, as are ankle, midfoot, knee, wrist, finger or olecranon attacks. Ask about fever, rigors, wound, surgery, injection, prosthesis, infection elsewhere, sexual exposure, trauma, anticoagulants, diuretics, kidney disease, transplant medicines, alcohol, dehydration and family history. Review whether urate-lowering therapy was missed or recently changed.

The immediate question is whether aspiration is required. A classic recurrent podagra in a well patient may be diagnosed clinically, but a first atypical attack, deep joint, prosthesis, immunosuppression, systemic illness or meaningful infection probability requires urgent fluid. Aspirate before antibiotics when this is safe and does not delay sepsis care. Divide fluid for Gram stain, culture, white-cell count and polarised microscopy; use blood-culture bottles under local microbiology protocol when appropriate.

Crystal microscopy is the reference confirmation. Monosodium urate crystals are needle-shaped and strongly negatively birefringent under compensated polarised light, appearing yellow when parallel and blue when perpendicular to the compensator axis. Intracellular crystals establish active crystal inflammation, but crystals do not exclude simultaneous bacterial infection. A high synovial white-cell count supports inflammation yet has no threshold that safely separates gout from sepsis.

Treat promptly. NICE does not rank NSAID, colchicine and short oral corticosteroid above one another; choose the safest effective category. Naproxen has a licensed acute-gout regimen of 750 mg once then 250 mg every eight hours until the attack passes, but it is inappropriate with major renal, ulcer, bleeding, cardiovascular or pregnancy risk. Co-prescribe a proton-pump inhibitor when gastrointestinal risk warrants it and avoid concurrent NSAIDs.

The current licensed colchicine regimen is lower than historic repeated dosing: 1 mg then 500 micrograms after one hour, no more for twelve hours, then at most 500 micrograms every eight hours until relief or a total 6 mg course. Do not repeat a course within seventy-two hours. Renal or hepatic impairment and strong CYP3A4 or P-glycoprotein inhibitors can convert a standard dose into marrow, muscle, multiorgan or fatal toxicity.

Do not alter established urate-lowering treatment during the flare. Once pain settles, review the diagnosis, serum urate and why the attack occurred without blaming the patient. NICE recommends discussing long-term urate lowering after any flare and offering it for multiple or troublesome attacks, CKD stages 3–5, diuretic therapy, tophi or chronic gouty arthritis. Provide a written rapid-treatment plan so the next attack is treated early and safely.

Key points

Typical gout is abrupt severe pain, swelling, warmth and erythema reaching maximum intensity within about twenty-four hours, often at the first metatarsophalangeal joint but potentially at any joint or bursa.
Always assess septic arthritis, calcium pyrophosphate disease and inflammatory arthritis; known gout and visible tophi do not remove the possibility of coexisting infection.
Measure serum urate, but a value below 360 micromol/L during a flare does not exclude gout; repeat at least two weeks after the flare resolves when suspicion remains high.
Synovial-fluid identification of needle-shaped, strongly negatively birefringent monosodium urate crystals is the reference confirmation when diagnosis is uncertain; send culture whenever infection remains possible.
NICE offers an NSAID, colchicine or a short oral corticosteroid course as equivalent first-line categories, selected by renal, gastrointestinal, cardiovascular, diabetic, interaction, infection and reproductive safety.
Licensed low-dose colchicine treatment is 1 mg immediately then 500 micrograms one hour later; no further dose for twelve hours, then 500 micrograms up to every eight hours if needed within strict course limits.
Use the lowest effective NSAID dose for the shortest period and add gastroprotection when indicated; avoid NSAIDs in important renal injury, active bleeding and decompensated heart failure.
Aspiration followed by intra-articular corticosteroid is useful for one accessible joint after infection has been reasonably excluded; never inject through cellulitis or into a possibly septic joint.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Sustained hyperuricaemia

When serum urate remains above its saturation threshold, monosodium urate crystals form and persist in cartilage, synovium, tendon, bursa and subcutaneous tissue.

Reduced renal urate excretion

Chronic kidney disease, dehydration, diuretics, ciclosporin, tacrolimus and genetic transporter variation commonly reduce renal clearance and raise the body urate pool.

Increased urate production

High cell turnover, myeloproliferative disease, chemotherapy, psoriasis and uncommon enzyme disorders increase purine breakdown; alcohol can alter production and excretion.

Flare-provoking crystal disturbance

Rapid urate change, intercurrent illness, surgery, trauma, fasting, dehydration or starting urate-lowering therapy can expose or shed crystals and activate an acute attack.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Crystal nucleation
Persistent supersaturation permits needle-shaped monosodium urate crystals to form preferentially in cooler peripheral tissues, explaining first-metatarsophalangeal and distal-joint susceptibility.
2
Inflammasome activation
Phagocytosed crystals activate the NLRP3 inflammasome and interleukin-1 signalling, rapidly recruiting neutrophils and generating extreme pain, warmth, swelling and erythema.
3
Self-limited resolution
Neutrophil apoptosis, crystal coating and anti-inflammatory mediators eventually damp the flare even when crystals remain, so symptom resolution is not crystal clearance.
4
Tophus development
Continued deposition creates organised crystal masses with chronic macrophage and giant-cell inflammation, eroding bone, distorting joints and compressing nearby tissue.
5
Urate fluctuation paradox
Both rising and falling extracellular urate can destabilise deposits, which explains early flares after effective urate-lowering treatment and the need for prophylaxis.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Podagra

Explosive nocturnal pain, erythema and exquisite tenderness at the first metatarsophalangeal joint is the most recognisable acute gout presentation.

Other crystal sites

Ankle, midfoot, knee, wrist, fingers, olecranon bursa and periarticular tissue can flare, and longstanding disease may become oligoarticular or polyarticular.

Septic overlapRed flag

Fever, prosthesis, recent joint procedure, skin breach, immunosuppression or bacteraemia increases infection risk, but sepsis can occur without any of these.

Tophaceous burden

Firm chalky nodules at ears, fingers, toes, elbows or tendons indicate prolonged urate deposition and strengthen the need for long-term crystal dissolution.

Atypical deep-joint attackRed flag

Hip, shoulder, sternoclavicular or spinal symptoms require imaging and guided sampling because examination and superficial aspiration cannot secure the diagnosis.

Red flags requiring action

Fever, rigors, hypotension, delirium, rapidly spreading erythema or systemic toxicity requires immediate septic-arthritis and sepsis assessment.
A prosthetic joint, recent operation or injection, penetrating wound, bacteraemia, immunosuppression or intravenous drug use materially increases infection probability.
Inability to bear weight with a large hip, shoulder or deep-joint effusion requires urgent imaging-guided aspiration and orthopaedic involvement.
Severe pain after trauma, anticoagulation, sickle disease or vascular compromise widens the emergency differential to fracture, haemarthrosis, osteonecrosis or ischaemia.
Acute kidney injury, dehydration, gastrointestinal bleeding, decompensated heart failure or pregnancy changes the safety of NSAID and colchicine treatment.
New gout during chemotherapy or profound systemic illness can accompany tumour lysis and requires metabolic emergency assessment rather than routine flare care.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Reference synovial-fluid microscopyFirst step
Why
Confirm monosodium urate crystals when the diagnosis is uncertain.
Interpretation and limitations
Needle-shaped strongly negatively birefringent crystals support gout; observer skill and prompt analysis matter, and absence in one sample does not absolutely exclude disease.
02
Synovial Gram stain and culture
Why
Exclude septic arthritis in any aspirated joint where infection remains plausible.
Interpretation and limitations
Send culture even when crystals are present; Gram stain has limited sensitivity and antibiotics before sampling can reduce culture yield.
03
First-line serum urateFirst line
Why
Support diagnosis and establish a future treatment baseline.
Interpretation and limitations
A level of 360 micromol/L or higher supports gout; if lower during an attack, repeat at least 2 weeks after resolution because acute inflammation can lower it.
04
FBC, CRP, renal profile and glucose
Why
Assess infection probability, systemic inflammation and treatment safety.
Interpretation and limitations
No inflammatory-marker value separates gout from sepsis; eGFR, potassium, glucose and blood count constrain NSAID, colchicine and steroid choice.
05
Plain radiography
Why
Identify trauma, late gout damage and another structural diagnosis.
Interpretation and limitations
Early gout films may be normal; established disease can show preserved joint space until late, punched-out erosions with overhanging margins and soft-tissue tophi.
06
Ultrasound or dual-energy CT
Why
Demonstrate urate deposition when aspiration is not feasible or remains non-diagnostic.
Interpretation and limitations
Double-contour or tophus on ultrasound and colour-coded urate on DECT support deposition, but artifacts and asymptomatic deposits require clinical context.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Septic arthritis

Infection remains the critical alternative in every acutely hot swollen joint; systemic signs, risk factors and purulent fluid increase probability, but their absence cannot exclude it.

Calcium pyrophosphate arthritis

Acute CPP crystal disease often affects knee or wrist in an older adult and shows weakly positively birefringent rhomboid crystals rather than urate needles.

Trauma and haemarthrosis

Injury, fracture, anticoagulation or a bleeding disorder can produce rapid pain and effusion; fluid may be bloody and imaging addresses structural damage.

Cellulitis or bursitis

Skin infection and inflamed prepatellar or olecranon bursa can resemble joint inflammation; careful passive movement and aspiration of the correct compartment distinguish them.

Inflammatory arthritis flare

Rheumatoid, psoriatic or reactive arthritis can begin asymmetrically, especially when several joints or entheses and extra-articular features are involved.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First diagnostic priorityExclude joint infectionFirst stepA hot, swollen, very painful joint presents acutely.

1Check observations, sepsis, prosthesis, skin breach, recent procedure, immunosuppression, bacteraemia and joint depth before assuming a crystal flare.
2Refer immediately and aspirate for culture and crystals when infection is plausible, drawing blood cultures and starting antibiotics according to sepsis timing.
3Use imaging-guided aspiration for a deep joint and arrange drainage with orthopaedics when septic arthritis is suspected or confirmed.

02NICE first-line treatmentChoose one safe anti-inflammatoryFirst lineGout is secure or likely and septic arthritis has been reasonably excluded.

1Select colchicine, an NSAID or a short oral corticosteroid course from renal, gastrointestinal, cardiac, diabetic, interaction, infection and patient factors.
2Start promptly, add protected ice, rest and elevation and add a proton-pump inhibitor when an NSAID recipient has gastrointestinal risk.
3Review response within several days and re-aspirate or revisit infection and CPPD if pain, fever or swelling fails to improve as expected.

03Local-joint optionAspirate then injectOne accessible large joint remains very inflamed and systemic treatment is unsuitable or inadequate.

1Aspirate completely where possible and send microscopy and culture when diagnosis or infection remains a concern.
2After septic arthritis and overlying infection are reasonably excluded, inject an appropriate intra-articular corticosteroid using strict asepsis.
3Give post-injection infection warnings and avoid fixed repeat scheduling; recurrence should trigger diagnosis and prevention review.

04Post-flare preventionUse the attack as a review pointAcute inflammation is resolving and the patient can engage with long-term decisions.

1Repeat serum urate at least two weeks after resolution, assess CKD and cardiovascular risk and reconcile diuretics and adherence.
2Discuss treat-to-target urate lowering and offer it for troublesome recurrence, CKD stages 3–5, diuretic use, tophi or chronic gouty arthritis.
3Provide a patient-held early-flare treatment plan and arrange prophylaxis when urate-lowering therapy will be started or titrated.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

One of three NICE first-line anti-inflammatory categories for a gout flare and often useful when an NSAID is unsafe.

Colchicine 500 microgram tablets

Take 1 mg orally at flare onset, then 500 micrograms 1 hour later. Take no more for 12 hours; if needed after that, take 500 micrograms no more often than every 8 hours until relief or a total course dose of 6 mg.

Do not repeat a course within 72 hours and stop immediately for diarrhoea or vomiting. Reduce or avoid with renal or hepatic impairment and never combine in high-risk impairment with strong CYP3A4 or P-glycoprotein inhibitors; macrolides, azoles, ciclosporin and statins raise fatal marrow and neuromuscular toxicity risk.

A rapid NSAID option within NICE first-line treatment when renal, gastrointestinal, cardiovascular, bleeding and reproductive risks are acceptable.

Naproxen

For the licensed acute-gout regimen, take 750 mg orally once, then 250 mg every 8 hours until the attack has passed; use for the shortest necessary period and review if ongoing treatment is needed.

Avoid active ulcer or bleeding, severe renal, hepatic or heart failure, NSAID hypersensitivity and concurrent NSAIDs; review anticoagulants, antiplatelets, ACE inhibitors and diuretics. Add gastroprotection when indicated. Avoid from 20 weeks of pregnancy unless essential and use is contraindicated in the final trimester under product advice.

NICE first-line category when NSAID or colchicine is unsuitable, especially for several joints, after septic arthritis and other infection are assessed.

Prednisolone

A common evidence-supported off-label flare regimen is 30 to 35 mg orally once daily with food for 5 days; a short course of this duration does not usually require tapering.

May mask or worsen infection and raise glucose, blood pressure, mood and fluid retention. Review diabetes, psychosis, ulcer and heart-failure risk. Prednisolone may be used in pregnancy when needed after individual review; repeated courses require cumulative bone and adrenal assessment.

A local option for acute monoarticular inflammation when oral medicines are contraindicated, poorly tolerated or ineffective.

Intra-articular triamcinolone acetonide

After aspiration and infection exclusion, inject 5 to 10 mg into a small joint or up to 40 mg into a large joint using strict asepsis; the exact volume depends on the 40 mg/mL product and joint size.

Never inject a septic joint, through infected skin, into an unstable joint or into the Achilles tendon. Warn about post-injection flare and infection; account for systemic glucose and steroid effects and do not repeat at fixed intervals. Pregnancy requires an individual benefit-risk review.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Recurrent disabling flares

Untreated crystal burden produces increasingly frequent, prolonged and polyarticular attacks that disrupt sleep, mobility, work and adherence.

Tophaceous joint damage

Chronic deposits erode bone, restrict movement, deform digits, ulcerate through skin and damage tendon or nerve.

Renal and cardiovascular association

Gout commonly coexists with CKD, hypertension, obesity, diabetes and cardiovascular disease, which influence treatment safety and overall long-term risk.

Treatment toxicity

NSAIDs can cause bleeding, renal failure and fluid retention; colchicine can cause fatal interaction toxicity; systemic steroid can worsen infection, glucose and pressure.

Missed septic arthritis

Attributing infection to known gout can lead to bacteraemia, rapid cartilage loss, osteomyelitis, surgery, permanent disability and death.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Review pain, swelling, temperature, function and systemic features within several days; failure to improve requires reconsideration of sepsis, CPPD, fracture and adherence.
Repeat serum urate at least two weeks after a low acute value and use the settled baseline for long-term prevention decisions.
Check renal function after NSAID exposure in CKD, dehydration, older age or renin-angiotensin and diuretic combinations and ask about bleeding or fluid retention.
After colchicine ask specifically about diarrhoea, vomiting, weakness and interacting antibiotics and review renal and hepatic function before another course.
After steroid treatment monitor glucose when diabetes or hyperglycaemia risk is meaningful and investigate new fever rather than assuming an inflammatory rebound.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Normal urate can coexist

Serum urate may fall during acute inflammation, so a low result at peak pain requires a settled repeat rather than diagnostic rejection.

Crystals do not sterilise fluid

Bacteria and urate can coexist in the same joint; microbiological culture remains necessary whenever infection is plausible.

Redness can cross the joint

Gout erythema may resemble cellulitis and extend beyond the capsule, so passive movement, ultrasound and aspiration answer localisation better than colour.

Keep established ULT going

Stopping allopurinol or febuxostat creates another urate shift and offers no immediate anti-inflammatory benefit.

11Common pitfallsFrequent interpretation and management errors.

01
Assuming a known history of gout excludes septic arthritis in a new hot joint.
02
Using a normal serum urate during the flare to rule out crystal disease.
03
Sending synovial fluid only for crystals and omitting Gram stain and culture when infection remains possible.
04
Prescribing colchicine without checking renal function and newly prescribed macrolide, azole, ciclosporin or statin interactions.