Acute gout
A hot, red big toe overnight with previous attacks is gout. Fever or an unusual joint means you must exclude infection first.
A 52-year-old man woke at 4 a.m. with an extremely painful, red, swollen big toe joint. He can't bear the bedsheet touching it. He takes hydrochlorothiazide and low-dose aspirin, and ate a lot of meat and drank sugary drinks at a wedding last night. Temperature 37.6 °C. He had a similar but milder attack last year.
Gout or septic arthritis, what do you give, and when do you start allopurinol?
- Could it be septic?Fever, unwell, prosthetic joint, IV drug use, first attack in a large joint: aspirate.
- Typical goutSudden, very painful, red, swollen joint, often the big toe, reaching its worst within 24 hours.
- Treat earlyNSAID with a PPI, or low-dose colchicine. Prednisolone if both unsuitable.
- Rest, ice, elevateSimple measures help.
- Don't stop allopurinol during an attackIf already taking it, continue.
- After the attackUrate level, kidney function, lifestyle, review drugs, urate-lowering therapy.
- Fever, unwell or possible septic arthritis
- Several joints
- Prosthetic joint
- Kidney failure limiting treatment
- Tophi breaking down or infected
- Septic arthritis (can coexist)
- Pseudogout (older, knee or wrist)
- Cellulitis
- Fracture
- Reactive arthritis
| Naproxen | 500 mg twice daily with a PPI until settled |
| Colchicine | 500 micrograms 2–4 times daily (maximum 6 mg per course, then no more for 3 days) |
| Prednisolone | 30–35 mg daily for 5 days |
| Urate target | Below 0.36 mmol/L (6 mg/dL), below 0.30 mmol/L (5 mg/dL) if tophi or frequent attacks |
| Allopurinol | Start 100 mg daily (50 mg in kidney disease), increase every 2–4 weeks to target |
| Start allopurinol | 2–4 weeks after the attack settles (or sooner with cover), with colchicine cover for 3–6 months |
Check every dose against a current drug reference and your hospital protocol.
On this page
What is gout?
Monosodium urate crystals form in joints when uric acid is high for a long time. A flare is intense inflammation caused by the body reacting to the crystals. The big toe (podagra) is classic, but ankles, knees, wrists and fingers are also affected. Over years, untreated gout causes tophi (chalky deposits), joint damage and kidney stones.
Who gets it?
- Men over 30, post-menopausal women.
- High purine diet (red meat, organ meat, seafood), alcohol (especially beer and spirits), sugary drinks.
- Drugs: thiazide and loop diuretics, low-dose aspirin, ciclosporin.
- Kidney disease, obesity, hypertension, diabetes, metabolic syndrome.
- Triggers for a flare: feasting, alcohol, dehydration, surgery, acute illness, starting or changing urate-lowering drugs.
Gout or septic arthritis?
- Treat as gout
- review in 48 hours
- Aspirate before antibiotics
- Gram stain, culture, crystals
Gout and septic arthritis can coexist. Finding crystals doesn't rule out infection. See septic arthritis.
Differential diagnosis
| Condition | Clues |
|---|---|
| Septic arthritis | Fever, unwell, large joint, risk factors |
| Pseudogout (CPPD) | Older, knee or wrist, positively birefringent rhomboid crystals, chondrocalcinosis on X-ray |
| Cellulitis | Spreading redness beyond the joint, entry wound |
| Reactive arthritis | After diarrhoea or urethritis, several joints, eye symptoms |
| Fracture | Injury |
| Bunion (hallux valgus) | Chronic, deformity |
Investigations
| Test | Why |
|---|---|
| Joint aspiration | Crystals (needle-shaped, negatively birefringent), Gram stain, culture |
| Serum urate | Often normal during a flare; recheck 2–4 weeks after |
| Creatinine | Drug choice and doses |
| CBC, CRP | Inflammation; sepsis if very high |
| Glucose, lipids, BP | Associated conditions |
| X-ray | Chronic gout (punched-out erosions), or other causes |
Treating a flare
- Start earlyThe sooner, the better it works.
- NSAID with a PPINaproxen 500 mg twice daily, if no kidney disease, ulcer or heart failure.
- Or colchicine500 micrograms 2–4 times daily; diarrhoea is the limit.
- Or prednisolone30–35 mg daily for 5 days if NSAID and colchicine unsuitable.
- Rest, ice, elevateContinue allopurinol if already on it.
Long-term: urate-lowering therapy
Offer to anyone with recurrent flares, tophi, joint damage, kidney stones, CKD, or diuretic use that can't stop.
- Allopurinol: start low (100 mg daily, 50 mg in kidney disease), increase every 2–4 weeks until urate is below target.
- Colchicine cover (500 micrograms once or twice daily) for 3–6 months while starting, to prevent flares.
- Febuxostat if allopurinol isn't tolerated (caution in heart disease).
- Review drugs: switch a thiazide to another BP drug (losartan lowers urate a little).
- Lifestyle: less red meat and organ meat, less alcohol and sugary drinks, weight loss, plenty of water.
In people of Han Chinese, Thai or Korean descent, test HLA-B*5801 before allopurinol if available (severe skin reactions). Stop allopurinol at once if a rash appears.
Treatment doses
Common mistakes
- Missing septic arthritis because "it's probably gout".
- Stopping allopurinol during a flare.
- Starting allopurinol at a high dose, or without colchicine cover.
- Using high-dose colchicine regimens (diarrhoea, toxicity).
- Giving colchicine with clarithromycin.
- Never rechecking urate or increasing the allopurinol dose to target.
Frequently asked questions
What is the best treatment for an acute gout attack?
An NSAID (with a PPI) or low-dose colchicine started early. Prednisolone if neither is suitable.
Should allopurinol be started during an attack?
Usually start 2–4 weeks after the attack settles, with colchicine cover. If already taking allopurinol, continue it during an attack.
What is the target uric acid level?
Below 0.36 mmol/L (6 mg/dL), or below 0.30 mmol/L (5 mg/dL) with tophi or frequent attacks.
Can uric acid be normal during a gout attack?
Yes. It often falls during a flare, so check it again 2–4 weeks later.
Test yourself
Exam-style questions on this guide, from our two question banks. Choose an answer to see why each option is right or wrong.
1. A man has a hot, swollen big toe joint after a wedding feast. He takes a thiazide. Which crystals are expected on aspiration?
Answer: Negatively birefringent needle-shaped crystals. Monosodium urate crystals are needle-shaped and negatively birefringent.
- Positively birefringent rhomboid crystals: Pseudogout.
- No crystals: Gout shows urate crystals.
- Cholesterol crystals: No.
- Calcium oxalate: No.
2. A patient on allopurinol for a year has an acute gout attack. What should be done with the allopurinol?
Answer: Continue it. Continue urate-lowering therapy during attacks and treat the attack separately.
- Stop it permanently: No.
- Stop it until the attack settles: Stopping causes urate swings.
- Double the dose immediately: Can prolong the attack.
- Switch to febuxostat: Not needed.
3. Which is a suitable first-line treatment for an acute gout attack in a patient with normal kidneys?
Answer: Naproxen with a PPI. An NSAID with a PPI, or colchicine, started early.
- Aspirin: Raises urate.
- Furosemide: Raises urate.
- Antibiotics: Not infected.
- Allopurinol 300 mg now: Not for the acute attack.
4. A 60-year-old with CKD stage 3 has an acutely red, hot, swollen first MTP joint; joint aspirate shows negatively birefringent needle-shaped crystals. He is not on urate-lowering therapy. Which is the best acute treatment?
Answer: Low-dose colchicine or short oral steroid. Acute gout: monosodium urate crystals (negatively birefringent needles). Treatment within 24 h: NSAIDs (avoid in CKD, heart failure, peptic ulcer), low-dose colchicine (500 µg two–three times daily; reduce in CKD; diarrhoea), or corticosteroids (oral prednisolone, intra-articular). Rest, ice. Urate-lowering therapy (allopurinol, febuxostat) for recurrent attacks, tophi, CKD, stones — start low, titrate to urate < 360 µmol/L (< 300 with tophi), with flare prophylaxis; can be started during/after flare, don’t stop if already taking.
- Start allopurinol 300 mg immediately alone: Allopurinol does not treat a flare.
- High-dose NSAID for 2 weeks: High-dose NSAIDs carry renal risk.
- IV antibiotics: This is not septic arthritis.
5. How does colchicine work in acute gout?
Answer: Blocks neutrophil microtubules. Colchicine binds tubulin → inhibits microtubule polymerisation → reduced neutrophil migration, degranulation and NLRP3 inflammasome activation. Uses: acute gout (low dose — 1 mg then 0.5 mg after 1 h), gout flare prophylaxis when starting urate-lowering therapy, familial Mediterranean fever, pericarditis (reduces recurrence), Behçet. Adverse: diarrhoea, vomiting; toxicity — multi-organ failure, myopathy, marrow suppression; reduce dose in renal impairment; interactions with CYP3A4/P-gp inhibitors (clarithromycin, ciclosporin).
- Inhibits xanthine oxidase: Xanthine oxidase inhibition is allopurinol’s action.
- Increases renal urate excretion: Increasing urate excretion is probenecid’s action.
- Converts urate to allantoin: Converting urate to allantoin is rasburicase’s action.
6. How does paclitaxel kill cancer cells?
Answer: Stabilises microtubules. Taxanes (paclitaxel, docetaxel) bind microtubules and stop them depolymerising, freezing cells in M phase. Vinca alkaloids (vincristine, vinblastine) do the opposite: they block microtubule assembly. Both cause peripheral neuropathy; vincristine is especially neurotoxic.
- Prevents microtubule assembly: Vinca alkaloids.
- Inhibits dihydrofolate reductase: Methotrexate.
- Alkylates DNA: Cyclophosphamide, cisplatin (cross-linking).
- Inhibits topoisomerase II: Etoposide, doxorubicin.
7. Molybdenum is a cofactor for which enzyme involved in purine breakdown?
Answer: Xanthine oxidase. Molybdenum is part of the molybdenum cofactor (molybdopterin) for xanthine oxidase (hypoxanthine → xanthine → uric acid), sulfite oxidase and aldehyde oxidase. Allopurinol and febuxostat inhibit xanthine oxidase (gout prophylaxis; azathioprine and 6-mercaptopurine doses must be reduced with allopurinol). Molybdenum cofactor deficiency causes seizures and sulfite toxicity in infants. Adenosine deaminase deficiency causes SCID; HGPRT deficiency causes Lesch-Nyhan syndrome.
- Adenosine deaminase: Deficiency causes SCID.
- HGPRT: Salvage enzyme; Lesch-Nyhan.
- Ribonucleotide reductase: Makes deoxyribonucleotides; hydroxyurea target.
- PRPP synthetase: Purine synthesis.
References and dose sources
- NICE NG219 — Gout: diagnosis and management
- Naproxen dosing: Drugs.com: Naproxen dosage (see also our naproxen dose page)
- Colchicine dosing: Drugs.com: Colchicine dosage (see also our colchicine dose page)
- Prednisolone dosing: Drugs.com: Prednisolone dosage (see also our prednisolone dose page)
- Omeprazole dosing: Drugs.com: Omeprazole dosage (see also our omeprazole dose page)
International guidance is linked where it reflects good practice. Where your hospital’s protocol differs, follow your hospital.